[Senate Hearing 110-1096]
[From the U.S. Government Publishing Office]
S. Hrg. 110-1096
EXAMINING THE HUMAN HEALTH EFFECTS OF ASBESTOS AND THE METHODS OF
MITIGATING SUCH IMPACTS
=======================================================================
HEARING
before the
COMMITTEE ON ENVIRONMENT AND PUBLIC WORKS
UNITED STATES SENATE
ONE HUNDRED TENTH CONGRESS
FIRST SESSION
__________
JUNE 12, 2007
__________
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COMMITTEE ON ENVIRONMENT AND PUBLIC WORKS
ONE HUNDRED TENTH CONGRESS
FIRST SESSION
BARBARA BOXER, California, Chairman
MAX BAUCUS, Montana JAMES M. INHOFE, Oklahoma
JOSEPH I. LIEBERMAN, Connecticut JOHN W. WARNER, Virginia
THOMAS R. CARPER, Delaware GEORGE V. VOINOVICH, Ohio
HILLARY RODHAM CLINTON, New York JOHNNY ISAKSON, Georgia
FRANK R. LAUTENBERG, New Jersey DAVID VITTER, Louisiana
BENJAMIN L. CARDIN, Maryland LARRY E. CRAIG, Idaho
BERNARD SANDERS, Vermont LAMAR ALEXANDER, Tennessee
AMY KLOBUCHAR, Minnesota CHRISTOPHER S. BOND, Missouri
SHELDON WHITEHOUSE, Rhode Island
Bettina Poirier, Majority Staff Director and Chief Counsel
Andrew Wheeler, Minority Staff Director
C O N T E N T S
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Page
JUNE 12, 2007
OPENING STATEMENTS
Boxer, Hon. Barbara, U.S. Senator from the State of California... 1
Inhofe, Hon. James M., U.S. Senator from the State of Oklahoma... 3
Lautenberg, Hon. Frank R., U.S. Senator from the State of New
Jersey......................................................... 5
Isakson, Hon. Johnny, U.S. Senator from the State of Georgia..... 6
Vitter, Hon. David, U.S. Senator from the State of Louisiana..... 8
Baucus, Hon. Max, U.S. Senator from the State of Montana......... 213
WITNESSES
Murray, Hon. Patty, U.S. Senator from the State of Washington.... 9
Prepared statement........................................... 12
Weissman, David N., M.D., Director, Division of Respiratory
Disease Studies, National Institute for Occupational Safety and
Health, Centers for Disease Control and Prevention, U.S.
Department of Health and Human Services........................ 23
Prepared statement........................................... 25
Responses to additional questions from Senator Boxer......... 30
Miller, Captain Aubrey, M.D., M.P.H., U.S. Public Health Service,
Region 8, U.S. Environmental Protection Agency................. 31
Prepared statement........................................... 33
Marty, Melanie, Ph.D., chief, Air Toxicology and Epidemiology
Branch, California Environmental Protection Agency, Office of
Environmental Health Hazard Assessment......................... 37
Prepared statement........................................... 39
Castleman, Barry, Sc.D., Environmental Consultant................ 65
Prepared statement........................................... 66
Responses to additional questions from:
Senator Boxer............................................ 71
Senator Inhofe........................................... 74
Wylie, Ann G., Ph.D., Professor of Geology, University of
Maryland....................................................... 84
Prepared statement........................................... 84
Response to an additional question from Senator Inhofe....... 90
Weill, David, M.D., Associate Professor, Division of Pulmonary
and Critical Care Medicine, Stanford University Medical Center,
Stanford, CA................................................... 91
Prepared statement........................................... 93
Responses to additional questions from Senator Inhofe........ 96
Lemen, Richard A., Ph.D., M.S.P.H., former director, Division of
Standards Development and Technology Transfer, Assistant
Surgeon General, U.S. Public Health Service (Retired), Rear
Admiral, U.S. Public Health Service (Retired).................. 96
Prepared statement........................................... 98
Reinstein, Linda, executive director and co-founder, Asbestos
Disease Awareness Organization................................. 169
Prepared statement........................................... 170
Response to an additional question from Senator Boxer........ 190
ADDITIONAL MATERIAL
Article, Responding to a Harsh Business Environment: A New
Diaphragm for the Chlor-Alkali Industry........................ 16
Survey, 2005 Minerals Yearbook, Asbestos, U.S. Geological Survey. 44
Letters:
El Dorado County Office of Education, Vicki L. Barber.,
Ed.D., Superintendent...................................... 58-64
Signatory Groups in the United States.......................176-189
Other Groups................................................190-204
EXAMINING THE HUMAN HEALTH EFFECTS OF ASBESTOS AND THE METHODS OF
MITIGATING SUCH IMPACTS
----------
TUESDAY, JUNE 12, 2007
U.S. Senate,
Committee on Environment and Public Works,
Washington, DC.
The committee met, pursuant to notice, at 10 a.m. in room
406, Dirksen Senate Office Building, the Hon. Barbara Boxer
(chairman of the committee) presiding.
Present: Senators Boxer, Inhofe, Carper, Lautenberg,
Isakson, Vitter, and Klobuchar.
Also present, Senator Murray.
STATEMENT OF HON. BARBARA BOXER, U.S. SENATOR FROM THE STATE OF
CALIFORNIA
Senator Boxer. The committee will come to order. We welcome
Senator Patty Murray.
Senator Murray, I want to congratulate you on your
leadership on this issue. I also want to say, I know Senator
Isakson has been working closely with you and I want to thank
him for trying to reach some agreement on your bill. This is an
important hearing for millions of Americans who have been
exposed to asbestos, for their families and especially for the
thousands of American families who have lost family members to
asbestos-related lung disease and cancer.
Millions of Americans are still being exposed to asbestos
today. If we don't act, countless more people will get sick and
die in the future.
Your legislation, Senator, the Ban Asbestos in America Act
of 2007, would place the United States clearly on the side of
protecting the health of the public from this dangerous
substance. It would ban nearly all uses of asbestos in
products. I am proud to be an original co-sponsor of this bill,
as is Senator Baucus, who you know has had so many issues with
asbestos in the town of Libby, MT.
We must take every reasonable step we can to end exposure
to asbestos, when we see our fathers, mothers, sisters and
brothers dying from asbestos. There is no justification for
allowing the number of dead to continue to mount. Just this
past year, we lost a Congressman, we lost Eli Segal, who was
exposed at a very young age to asbestos. This is a deadly
situation.
Asbestos fibers can be 1,200 times smaller than a human
hair. These microscopic fibers can stay invisible and suspended
in the air for days. People, including children, can breathe
these fibers deep into their lungs, where they cause their
damage. We see the results of this in communities across our
country.
This nationwide, actually worldwide tragedy, has hit my
State of California especially hard. According to the National
Institute of Occupational Safety and Health, or NIOSH, between
1993 and 2002, more than 1,000 people died from asbestosis
caused by exposures at their work. From 1999 to 2002, NIOSH
reports 1,001 people died from mesothelioma, a rare cancer and
deadly cancer generally caused by asbestos. These figures do
not include the deaths from lung cancer and other diseases that
asbestos can cause, or the deaths that the Government tracking
system may have missed.
The deaths of hard-working people exposed to asbestos at
their work only tell part of the story. Workers can take
asbestos into their homes on their clothes. After a hard day at
work, they go home and hug their children or sit with their
families at the dinner table. Their spouses may handle their
asbestos-laden clothes. Nobody can see the fibers, but they can
still kill.
We have a picture here of Rebecca Martinez. She lived in
Baldwin Park, CA. This is a picture of Rebecca Martinez.
Margarito Martinez lived in Baldwin Park, CA with his wife of
39 years, Rebecca, pictured here on the right. Margarito worked
as a plasterer, and Rebecca would clean his asbestos-covered
clothes when he came home, breathing in the dust as she shook
them out and did the laundry. They say they were never warned
about the dangers of asbestos.
Rebecca was diagnosed with the deadly cancer mesothelioma
in 2002. She died 4 months later.
Now we have a picture of Georgina Bryson. She lived in
Riverside, CA when she died of mesothelioma. From 1962 until
1980, Georgina lived downwind from two cement companies that
used asbestos to manufacture their products. She was also
exposed to asbestos when she lived with her dad, who worked
with gaskets that contained asbestos. She was only 40 years old
when she died from mesothelioma.
I have a picture of a lung damaged by mesothelioma, just
one of a number of devastating diseases caused by asbestos.
Despite all of this death, we continue to allow the
importation and use of asbestos and products that contain
asbestos. What is interesting about it, Senator Murray, you
know this as well as I, people think we have already banned
asbestos. But we continue importing it.
World production of asbestos actually increased in 2005,
from 2.36 million metric tons in 2004, to 2.40 million metric
tons in 2005. In the United States, we imported 2,530 metric
tons of asbestos, and we imported more than 90,000 metric tons
of products that may contain asbestos, products like cement and
gaskets, as well as brakes and clutch parts for autos. Even the
Environmental Protection Agency acknowledges that people who
work on cars should be careful because of the danger of
breathing in asbestos.
The good news is that there are safer alternatives to
asbestos that are available today. Because of this and the
continuing risks to people's health, many nations have adopted
bans on asbestos. Countries that have banned or phased out
asbestos, we have a chart, I won't read it, but it is available
for everyone to see, how many countries have banned asbestos.
Due to the on-going dangers of using asbestos, the WHO reports
that more than 40 countries have banned or are phasing out the
use of asbestos. I believe the United States should squarely
address the problem. That is why, again, I am so proud to be a
sponsor of Senator Murray's bill, S. 742.
In scores of nations, products that used to be made with
asbestos now are being made without it. I have great faith in
American ingenuity, and I strongly believe that these products
can be made here from safer materials as well. This hearing's
focus is clear. It is on people, and the terrible price they
continue to pay because asbestos is being used, despite the
availability of safer alternatives.
Senator Inhofe.
STATEMENT OF HON. JAMES M. INHOFE, U.S. SENATOR FROM THE STATE
OF OKLAHOMA
Senator Inhofe. Thank you, Madam Chairman.
The health effects of exposure to certain kinds of asbestos
are well-known and tragic. As you pointed out, I don't know
that there is any debate there, in fact, there is no doubt.
This is why the United States has essentially eliminated the
use of most dangerous forms of asbestos, and our use of other
forms is severely limited to those critical areas for which
there is no readily available substitute. It is also why
bipartisan language to ban asbestos has been included in the
bills in the last two Congresses.
It may sound simplistic, but the debate is not over true
asbestos minerals and their health effects. That has been
extensively studied and we now have an entire legal liability
system built around it. But rather, any debate here, if there
is one, has to do with the potential effects of other types of
minerals. These non-asbestiform minerals have the same chemical
makeup as asbestos but have entirely different physical
structures, similar to coal and diamonds or water and ice.
However, our primitive analytical techniques used for
indoor remediation of commercially produced asbestos falsely
identifies these rocks as asbestos. In fact, the U.S.
Geological Survey said that, ``The counting criteria developed
for analysis of asbestos in the workplace or in commercial
products may not be appropriate for direct application to what
is currently referred to as naturally occurring asbestos.'' Let
me show you what I mean. Put that chart up that has the rocks.
As you can plainly see, dangerous asbestos minerals consist
of fibers that are long, skinny, very flexible. That would be
columns 1 and columns 3. Research has shown that these fibers
are hard for the human lung to eliminate. They essentially get
trapped in the lung, sometimes causing disease decades after
the initial exposure.
Non-asbestiform minerals, these rocks here, that is columns
2 and 4, break up into particles called cleavage fragments,
which are short, fat and bulky. Studies have shown that these
cleavage fragments do not pose the same health risks as the
fibrous asbestos counterparts.
We do not know if these non-asbestiform minerals have
specific health risks, but yet they are regulated currently as
airborne particle by the U.S. EPA, OSHA and the Mineral Safety
and Health Administration, thereby protecting against
occupational exposure. But what we do know is that these
cleavage fragments do not cause the same diseases as asbestos.
Therefore, they must be treated differently. It should be noted
that the National Institute of Occupational Safety and Health
has recently begun an effort to collect and analyze available
data on asbestos and other materials. Other agencies are
working on this, too, including the EPA, OSHA, Mining Safety
and Health Administration, Agency for Toxic Substance and
Disease Registry, and the U.S. Geological Survey.
The previous bipartisan language to ban asbestos recognizes
these fundamental mineralogical and medical differences, and
banned the true culprit. Despite the fact that this language
was not debated here in the Environment and Public Works
Committee, as it should have been, I have never stood in the
way of the substance of that language as it represented a
carefully constructed agreement providing a process for
critical use exemptions and was scientifically sound with
respect to the mineralogy of asbestos.
The ban language was supported by the affected industries
and negotiated with Senator Murray and her staff and has held
intact through two Congresses. Any legislation that comes
through this committee in this Congress should do the same
thing.
So I guess what we really need to do is recognize that this
is a different form and treat it differently, if our
investigation warrants it. Thank you, Madam Chairman.
[The prepared statement of Senator Inhofe follows:]
Statement of Hon. James M. Inhofe, U.S. Senator from the
State of Oklahoma
Thank you Madame Chair for holding this hearing today.
The health effects of exposure to certain kinds of asbestos are
well known and tragic. Chest, lung and gastrointestinal cancers are
horrible diseases. On that, there is very little debate. This is why
the United States has essentially eliminated the use of the most
dangerous forms of asbestos and our use of the other forms is severely
limited to those critical uses for which there is no readily available
substitute. That is also why bipartisan language to ban asbestos has
been included in the bills addressing the asbestos liability situation
in the last two Congresses.
It may sound simplistic but the debate is not over true asbestos
minerals and their health effects. That has been extensively studied
and we have an entire legal liability system built around it. But
rather, any debate here, if there is one, has to do with the potential
health effects of other types of minerals. These non-asbestiform
minerals have the same chemical makeup as asbestos but have entirely
different physical structures. Similar to coal and diamonds or water
and ice.
However, our primitive, analytical techniques used for indoor
remediation of commercially produced asbestos falsely identify these
rocks as asbestos. In fact, the U.S. Geological Survey said that ``. .
.the counting criteria developed for analysis of asbestos in the
workplace or in commercial products may not be appropriate for direct
application to what is currently referred to as naturally occurring
asbestos.''
Let me show you what I mean. (SEE EXHIBIT). As you can plainly see,
dangerous asbestos minerals consist of fibers that are long, skinny,
and very flexible. Research has shown these fibers are hard for the
human lung to eliminate. They essentially get trapped in the lungs,
sometimes causing diseases decades after the initial exposure. Non-
asbestiform minerals, these rocks here, break up into particles called
cleavage fragments, which are short, fat and bulky. Studies have shown
that these cleavage fragments do not pose the same health risk as their
fibrous asbestos counterparts.
We do not know if these non-asbestiform minerals have specific
health risks but yet they are regulated currently as airborne particles
by the U.S. EPA, OSHA and the Mining Safety and Health Administration,
thereby protecting against occupational exposure. But what we do know
is that these cleavage fragments do not cause the same diseases as
asbestos and therefore, they must be treated differently. It should be
noted that the National Institutes of Occupational Safety and Health
has recently begun an effort to collect and analyze available data on
asbestos and other minerals. Other agencies are working on this too,
including EPA, OSHA, Mining Safety and Health Administration, the
Agency for Toxic Substances and Disease Registry, and the U.S.
Geological Survey.
The previous bipartisan language to ban asbestos recognized these
fundamental mineralogical and medical differences and banned the true
culprit. Despite the fact that this language was not debated here in
the Environment and Public Works Committee, as it should have been, I
have never stood in the way of the substance of that language as it
represented a carefully constructed agreement, provided a process for
critical use exemptions, and was scientifically sound with respect to
the mineralogy of asbestos. The ban language was supported by the
affected industries and negotiated with Senator Murray and her staff
and has held intact through two Congresses. Any legislation that comes
through this committee in this Congress should do the same. I believe
there is real potential here for bipartisan compromise if we don't go
beyond what the science shows to be true.
I look forward to hearing from the witnesses today and to further
understanding the various minerals and the differences in their health
effects.
Senator Boxer. Thank you so much.
Senator Lautenberg, you have 5 minutes.
STATEMENT OF HON. FRANK R. LAUTENBERG, U.S. SENATOR FROM THE
STATE OF NEW JERSEY
Senator Lautenberg. Thank you very much, Madam Chairman.
I commend you for holding this hearing and Senator Murray
in particular for her aggressive action to try to get rid of
this threat in our State and our communities.
I have some degree of familiarity with problems with
asbestos. When I went to high school in Patterson, New Jersey,
a lot of the kids who I went to high school with worked in the
asbestos factory, it was call Raybestos Manhattan. A friend
mine, who spent 20 years practicing law after having been in
high school, was called by a member of a union and asked if he
had any x-rays of his chest in recent years. He said no, he
hadn't. The fellow from the union suggested that he does that
promptly because there have been signs of illness from people
in that class group.
Well, the story had a terrible ending, because my friend
the lawyer was dead in a year from mesothelioma. When they took
an x-ray, they found out that the asbestos had started the
process of spoiling his health. The Chairman, Senator Boxer,
talked about, showed pictures of a family that got sick from
asbestos brought home in clothing. I met a family where the
father worked for Johns Manville down in central New Jersey and
would bring home his clothes for laundry. He came in with his
son, who is about 30 years old, and the man's wife, and all
three of them had asbestosis as a result of just cleaning his
clothing.
So we know the terrible toll that asbestos takes. With more
than 2,000 Americans dying premature and painful deaths from
exposure to asbestos. Needless to say, the consequence of this
to these families is terrible, terrible, and to the people who
were exposed. We have had enormous reluctance by the industry,
any of the companies that we have had contact with, have fought
fiercely to reduce any legislation that would impact the
ability of those who work there to collect damages who worked
in the asbestos factories and would do little if they weren't
pushed to deal with the problem forthrightly.
We went through a series here a few years ago where ads
were run in the papers, Roll Call and the Washington papers,
about stopping any legislation that would enable those who were
rendered ill from having compensation. I picked up a piece of
material that shows an exchange of letters in 1935, 1935,
between Raybestos Manhattan and Johns Manville, alerting the
companies, from a lawyer working for Johns Manville, to the
concern about asbestos. In 1935, one letter says, ``After
discussing the hazards of asbestos, as I see it personally, we
would be just as well off to say nothing about it. I think the
less said about asbestos, the better we are.'' Once again,
October 1, 1935. That is a letter from one president, from the
president of Raybestos Manhattan, to a Manville attorney.
So we could continue with the exchange, but all of them
suggest that they were fully aware of how dangerous asbestos
was, and chose, like the tobacco companies with cigarettes way
back in the 1930's, to ignore it and hope that the problem
would go away.
So thank you again, Senator Boxer, and you, Senator Murray,
for your persistence here. I am glad to be a co-sponsor of your
legislation. I hope we can get it through.
[The prepared statement of Senator Lautenberg follows:]
Statement of Hon. Frank R. Lautenberg, U.S. Senator from the
State of New Jersey
Madam Chairman, thank you for holding today's hearing on the health
effects of asbestos. Let me welcome Senator Murray to the committee and
thank her for working to keep Americans safe from asbestos.
Every year, more than two-thousand Americans die premature and
painful deaths from exposure to asbestos. Their deaths leave children
without parents, and families struggling to make ends meet.
New Jersey has America's sixth-highest number of deaths from
asbestos. From asbestos used in ship insulation at shipyards to
asbestos used to insulate pipes at refineries and factories, at least
two-thousand seven-hundred and seventy-five New Jerseyans died because
of asbestos exposure from 1979 to 2001. Just last week, a school in
Asbury Park was closed because part of the ceiling fell and asbestos
was found. This toxin's presence in offices, schools and homes could
pose health risks for years to come--ranging from breathing problems to
lung damage and cancer.
One of the leading researchers on the link between asbestos and
lung disease was Dr. Irving Selikoff, who lived in New Jersey. Dr.
Selikoff did his research on workers across my state, including those
in my home town of Paterson. In 1979, Dr. Selikoff showed that one in
five asbestos workers developed a fatal lung disease. Senator Murray's
bill is a strategy for real action to reduce asbestos in the places we
live and work.
The bill will ban the use of asbestos to the maximum extent
possible and benefit companies who are producing safer alternatives. It
also calls for more research on the health affects of asbestos, as well
as the best treatment options for asbestos-related illnesses and better
coordination among federal agencies. Congress owes our children and
grandchildren action now to protect them from asbestos in the future.
I look forward to hearing the testimony of today's witnesses.
Thank you Madam Chairman.
Senator Boxer. Thank you, Senator.
Senator Isakson.
STATEMENT OF HON. JOHNNY ISAKSON, U.S. SENATOR FROM THE STATE
OF GEORGIA
Senator Isakson. Thank you, Madam Chairman. It is my
privilege to serve as Ranking Member on the Occupational Safety
Subcommittee of the Health Committee, which is chaired by
Senator Murray.
Over the course of, in particular the last 6 or 8 months,
but over a number of years on Senator Murray's instigation,
this issue has been brought forward. I want to commend her for
both the intensity of her effort as well as her willingness and
the willingness of her staff to work together to find common
ground, which I think in large measure is about to take place.
There have been a couple of issues in terms of the natural
occurrence of asbestos and in terms of a reasonable transition
out of asbestos and in terms of the couple of remaining uses
that it has in the United States. Our staffs have talked and I
have talked and have the greatest of respect for Senator
Murray.
So it is my belief that it is very important that this
hearing take place today as sort of the foundation, hopefully,
for a common sense agreement that reflects the majority of the
Congress and the majority of American people and the majority
of all those, the absolute majority of all those in health
care.
So I just want to commend Senator Murray, thank her for her
willingness to work together. I look forward in the next few
days ahead to trying to complete those negotiations to have a
significant bill for this Senate to deal with very quickly.
[The prepared statement of Senator Isakson follows:]
Statement of Hon. Johnny Isakson, U.S. Senator from the State of
Georgia
Thank you Madam Chairman. I welcome Sen. Murray before the
committee. I am pleased to work with her as her Ranking Member on the
Subcommittee on Employment and Workplace Safety which she chairs in the
HELP Committee. On March 1 of this year, we held a hearing on just this
topic in the subcommittee, and I am pleased to be able to participate
again in a hearing on this issue.
Of course, there is no debate that certain forms of asbestos are
toxic and deadly.
Over the past 30 years, we have learned the sad truth that exposure
to some airborne asbestos fibers pose potentially serious health risks.
Continued exposure to airborne asbestos can increase the amount of
fibers that remain in the lung. Once embedded in lung tissue, these
fibers over time may cause serious lung diseases including asbestosis,
lung cancer, or mesothelioma.
As we will hear today, there are several kinds of asbestos.
Different forms of asbestos pose different health risks. Any ban passed
by Congress must recognize these differences.
The EPA initially proposed a ban of most asbestos-containing
products in the late 1970s. At the time, the U.S. consumed over 500,000
tons of asbestos, about 7 percent of which was the very toxic amphibole
asbestos.
The rule was then struck down the 5th Circuit, because EPA had
``failed to muster substantial evidence'' in support of the ban. The
Court of Appeals remanded the matter back to EPA, demanding the Agency
demonstrate that all asbestos poses an ``unreasonable risk'' to
Americans.
During the 1990s, the worldwide trade of the most hazardous form of
asbestos, amphibole asbestos, ceased. Thus, this very toxic form of
asbestos is no longer available to the United States. Essentially,
there is a de facto ban on amphibole asbestos already in place.
Today, asbestos is still used in the United States, albeit very
sparingly. According to the U.S. Geological Survey, the U.S. consumes
about 2,000 tons of chrysotile asbestos yearly, down from almost
800,000 tons consumed in mid-1970s. Take note: consumption of asbestos
decreased 99.75 percent without government fiat. Amphibole asbestos,
the most dangerous kind, is not used. Chrysotile asbestos is used for
three purposes only: roof coatings, NASA shuttle motor parts and
specialized filters used in the manufacture of chlorine.
Last Congress, I was happy to support Senator Specter and Leahy's
``FAIR Act.'' As part of that important legislation, Senators Specter
and Leahy included a workable, reasonable asbestos ban that recognized
the important distinctions between various kinds of asbestos.
In closing, there are many different kinds of asbestos. It comes in
many different forms. There is room for bipartisan compromise on this
issue, as Senators Specter and Leahy have demonstrated. I hope to work
with all sides to resolve this issue.
I yield my time.
Senator Boxer. Senator, I just want to thank you so much
for your positive attitude, and Senator Murray, too. Sometimes
an author of the bill will just say, I have done all I can, I
don't want to discuss it further. But Senator Murray was very
open to your common-sense thoughts on this and I am very
hopeful that we will have this agreement, we can have, I am
just suggesting my dream ticket, of a Murray-Isakson bill. It
would really be wonderful for this committee to take up such a
bill.
Senator Vitter.
STATEMENT OF HON. DAVID VITTER, U.S. SENATOR FROM THE STATE OF
LOUISIANA
Senator Vitter. Thank you, Madam Chair. Thanks for this
hearing and thanks also to Senator Murray for her leadership.
I want to echo what so many folks have said. There is
absolute consensus and unanimity about the deadly nature of
asbestos. Certainly in most industrial uses in the past, the
obvious example of these uses where you had airborne asbestos,
which has killed thousands upon thousands of people. I look
forward to legislation that builds on that clear consensus.
I hope we focus in large part in this hearing on the more
difficult issues, issues like brought up by Senator Inhofe in
terms of different types of material, non-asbestos material on
which there are different interpretations and rulings, even
among Federal agencies.
Second I want to bring up that I hope we can focus on and
come to a good resolution on, based on sound science, and that
is the use of asbestos in chlor-alkali production. I am very
concerned that we might ban this completely, when the science
does not justify it, because the chlor-alkali industry relies
on technology that safely uses asbestos diaphragms. That is
really for two reasons. One is the use of asbestos there is
confined in asbestos diaphragms and produced in a continuous
wet environment that remains in a closed process, so there is
minimal to no release of asbestos and absolutely no worker
exposure. So I think again, two things are significant: wet
environment and completely closed process.
Again, it is significant that this use in this production
is also in accord with OSHA and EPA standards. This was
specifically allowed in the final rules on this issue on
asbestos from EPA in 1989.
It is important to get this right and base whatever we do
on sound science, because of the significant uses of this in
this country. There are 16 chlor-alkali plants operating in 9
States that rely on this technology, that is Louisiana,
Alabama, Indiana, Kansas, Nevada, New York, Texas, West
Virginia and Wisconsin. But it really goes well beyond that in
terms of impact, because this provides critical benefits to
society and the economy. Today, over 60 percent of U.S.
chlorine production uses this technology. About 93 percent of
pharmaceuticals sold in the United States rely on chlorine
chemistry. So this has a major, major impact on society and the
economy.
Now, if this were harming people or potentially killing
people, that would be the end of the argument, we should outlaw
it. But there is no known case of asbestos-related disease from
the chlor-alkali industry using this technology. So I hope in
part our discussion can focus on that, so we delve into those
details as we finalize a consensus on the issue.
Thank you again, Madam Chair, for the hearing.
Senator Boxer. Thank you.
Senator Murray, we would love to hear from you for 10
minutes.
STATEMENT OF HON. PATTY MURRAY, U.S. SENATOR FROM THE STATE OF
WASHINGTON
Senator Murray. Thank you so much, Chairman Boxer, for
holding this hearing and for your longstanding support of my
efforts to ban asbestos in the United States. I want to thank
all of our committee members who are co-sponsors, potential co-
sponsors. I especially want to recognize Senator Isakson and
his staff, who have worked very long and hard with us to reach
a consensus, which I hope we can do fairly quickly.
I am very pleased as well to be here this morning with the
distinguished group of witnesses that you have assembled for
this hearing. I especially want to acknowledge the efforts of
three of your witnesses: Dr. Barry Castleman, Dr. Dick Lemen
and Linda Reinstein. Without their tireless work, we would not
be where we are today, on the verge of finally protecting
Americans from deadly asbestos.
You have called this hearing to examine the health effects
of asbestos and ways to minimize its harm. I have worked now on
this issue for 6 years, and I can tell you, asbestos is deadly.
It is devastating to families and communities. Every day that
we wait to ban it we are sentencing more Americans to an early
and avoidable death. Asbestos exposure, as studies show, kills
up to 10,000 Americans each year. I want to take a minute to
introduce you to two of them.
This is Fred, his real name is George, but Fred Biekkola.
He is from Michigan. Fred served in World War II, and for
almost 30 years, he worked for a mining company in Michigan,
where he was exposed to asbestos. Fred testified at my very
first hearing on asbestos 6 years ago. I will never forget what
he told us.
He said, ``Senators, please make sure what happened to me
won't happen to anyone else. Workers like me are counting on
you to protect us. Please don't let us down.''
Well, I am said to say that we have let Fred down. We
didn't ban asbestos. We didn't warn the public. We didn't
invest in research and treatment. Fred died of asbestos and
mesothelioma on April 7, 2004.
Sadly, Fred is not the only friend and advocate that I have
now lost over the years because Congress has failed to act.
This is Brian Harvey. He is a teacher from Marysville, WA.
Brian stood by my side when I introduced my very first bill to
ban asbestos back in July 2002. Now, most asbestos victims die
within a year of being diagnosed.
But amazingly, Brian stood with me and lived for 6 years.
He knew he was living on borrowed time. So he told me he was
using his time to help fight for others. He stood by my side
again in 2004 at a press conference we held here to try and ban
asbestos. Sadly, I lost Brian to this fight as well in July
2005.
Well, Fred and Brian aren't with us any more. But their
words and their spirit hang over this hearing. As I said, it is
estimated that up to 10,000 Americans die every year from
asbestos-related causes. Now, I have been at this for 6 years.
This is my third bill, and I know we can't wait another year to
fix this problem, because the stakes are just too high. To
anyone who says, we don't need this bill, I would pose one
question: how many more Americans like Fred, like Brian, like
the pictures you showed, Madam Chairwoman, how many more have
to die before our Government finally does the right thing and
bans asbestos? We have to do the right thing and we need to do
it now.
Now, as I look at this issue, four problems stand out.
First, asbestos is deadly. It is so deadly that there is no
known safe level of exposure. It only takes a tiny bit of fiber
to cause disease.
Second, asbestos is everywhere. It is put into consumer and
industrial products on purpose every day.
Now, my staff bought these brake pads in an automotive
repair shop in my home State of Washington. They contain
asbestos. They bought these off the shelf. It says on the sign,
warning, contains asbestos. Brake pads like these are in tens
of thousands of cars in this country today. Any time one of the
cars with brake pads like this goes in for maintenance, a
mechanic could unknowingly be exposed to deadly asbestos.
Now, Madam Chairwoman, there are alternatives. These brake
pads, which we also bought here, don't contain asbestos, and
they work just as good as the ones that do. We should not keep
selling asbestos products and putting workers and countless
consumers at risk. Madam Chairwoman, there are thousands of
other products that contain asbestos today in this country,
floor tiles, roofing material, cement pipes and even hair
dryers.
Deadly asbestos is still putting construction and
maintenance workers at risk. Today in this hearing room we have
some of the workers who work in the tunnel of the Capitol
Building, right below this room. They know asbestos exists,
they have been exposed to it, and that is wrong. For them alone
we should be doing a lot more. But the very least we can do is
to ban asbestos so other workers are not put at risk as well.
Third, we know asbestos is still legal. Now, many
Americans, as you alluded to, assume as I did that asbestos has
already been banned in this country. But it is not. In 1989,
the EPA did try to ban asbestos. But most of those regulations
were overturned by a court in 1991. As a result, while new
applications for asbestos were banned, asbestos is still being
imported and used in consumer and industrial products that are
on our shelves today.
Fourth, research and treatment for asbestos diseases is not
very far along. Doctors have been hampered by a lack of funding
for research on how asbestos fibers actually cause disease and
what treatment strategies work best. Industrial hygienists have
been hampered by lack of research on how to best measure
asbestos fibers in the air.
I know that the Mesothelioma Applied Research Foundation
has privately awarded over $4 million in grants and their
investment in research is helping to motivate brilliant
investigators to study mesothelioma. But the foundation seed
money is not enough. Federal funding is critical to the
research effort if we truly are going to help people. That is
why my bill requires collaboration among the 10 research and
treatment centers established under the bill, along with the
National Cancer Institute, the Department of Veterans Affairs
and the National Institute for Occupational Safety and Health.
Because nearly one-third of mesothelioma victims were
exposed to asbestos while serving in the U.S. Navy, my bill
directs the Pentagon to conduct additional research on asbestos
disease, early detection and treatment as well. I am also very
encouraged that NIOSH has embarked on an ambitious research
road map to better answer current scientific questions about
appropriate occupational levels of exposure.
To address the national scourge of asbestos, I have again
this year introduced the Ban Asbestos in America Act of 2007,
S. 742. My bill basically does three things. First of all, it
bans asbestos. It prohibits the importation, manufacture,
processing and distribution of products containing asbestos.
Unfortunately, some 2,500 metric tons of asbestos was used in
the United States in 2005, and imports of products containing
asbestos in cement pipe, tiles, brake gaskets and linings
continue unabated today.
Second, my bill dramatically expands research and treatment
and creates a $50 million, 10-center Asbestos-Related Disease
Research and Treatment Network. It creates a new National
Asbestos-Related Disease Registry. And it supports research at
the Department of Defense and launches a study to determine the
most promising areas for new research.
Third, my bill launches a very important public education
campaign to better inform all Americans of the dangers of
exposures to asbestos in the workplace and in the environment
while also providing helpful steps so all of us can better
protect our families.
I know we can and we should be making progress in banning
asbestos. As you stated, Madam Chairwoman, more than 40 other
industrialized countries have already banned asbestos. Around
the world, chlorine producers are phasing out dangerous and
inefficient methods in favor of safer and more environmentally
responsible technology. We need to help our U.S. companies
embrace those new greener approaches today.
I am also very grateful that industry leaders have stepped
up to the plate to work with me in achieving a goal that
everyone supports: a ban on the production and importation of
asbestos in the United States. These corporate leaders also
strongly support the need to better educate the public and to
provide more for research and treatment dollars to better
mitigate the effects of asbestos on workers and their families.
I look forward to working with all of the members of this
committee to achieve a bipartisan consensus on banning asbestos
in the United States in this Congress. Chairwoman Boxer, I know
this hearing will help us go a long way in achieving that goal,
and I really want to thank you. We have lost enough people,
Fred, Brian and others, and we have a responsibility to protect
tens of thousands of people just like them. So thank you very
much for this opportunity to testify and for your hearing on
this important legislation. Thank you.
[The prepared statement of Senator Murray follows:]
Statement of Hon. Patty Murray, U.S. Senator from the
State of Washington
Thank you, Chairwoman Boxer, for convening this hearing and for
your long-standing support of my efforts to ban asbestos in the United
States.
I'm so pleased to be here this morning with the distinguished group
of witnesses you have assembled for this hearing.
I especially want to acknowledge the efforts of three of your
witnesses, Dr. Barry Castleman, Dr. Dick Lemen and Linda Reinstein.
Without their tireless work, we would not be where we are today--on the
verge of finally protecting Americans from deadly asbestos.
You've called this hearing to examine the health effects of
asbestos and ways to minimize its harm. I've worked on this issue for 6
years, and I can tell you that
asbestos is deadly,
it's devastating families and communities,
and every day that we wait to ban it, we're sentencing
more Americans to an early and avoidable death.
Studies show that asbestos exposure kills up to 10,000 Americans
each year. I want to introduce you to two of them.
This is George ``Fred'' Biekkola from Michigan. Fred served in
World War II.
For almost 30 years, he worked for a mining company in Michigan,
where he was exposed to asbestos. Fred testified at my first hearing on
asbestos 6 years ago. I'll never forget what he told us. He said:
``Senators, please make sure that what happened to me won't happen
to anyone else. . . . Workers like me are counting on you to protect
us. Please don't let us down.''
I'm sad to say that we let Fred down. We didn't ban asbestos. We
didn't warn the public. And we didn't invest in research and treatment.
Fred died of asbestosis and mesothelioma on April 7, 2004.
Sadly, Fred is not the only advocate we've lost over the years
because Congress has failed to act.
This is Brian Harvey, a teacher from Marysville, Washington. Brian
stood by my side as I introduced my first bill to ban asbestos in July
2002.
Most asbestos victims die within a year of being diagnosed.
Amazingly, Brian lived for 6 years. He knew he was living on borrowed
time, so he used his time to fight for others. He stood by my side
again in 2004 at another press conference, but sadly Brian died in July
of 2005.
Fred and Brian are not with us, but their words hang over this
hearing.
As I mentioned, it's estimated that each year, up to 10,000
Americans die every year from asbestos-related causes. I've been at
this for 6 years, this is my third bill, and I know we cannot wait
another year to fix this problem. The stakes are just too high.
To anyone who says, ``We don't need this bill,'' I would just pose
one question:
``How many more Americans have to die before our
government finally does the right thing and bans asbestos?''
We have to do the right thing, and we have to do it now. As I look
at this issue, four problems stand out.
1. Asbestos is Deadly
First, asbestos is deadly. It's so deadly that there is no known
safe level of exposure. It only takes a tiny bit of fiber to cause
disease.
2. Asbestos is Widespread
Second, asbestos is everywhere. It's put into consumer and
industrial products on purpose every day.
My staff bought these brake pads in an automotive repair store in
my home state. They contain asbestos. Brake pads like these are on tens
of thousands of cars. Anytime one of those cars goes in for
maintenance, a mechanic could be unknowingly exposed to deadly
asbestos. Fortunately, there are alternatives.
These brake pads are made without asbestos, and they work just as
well. We shouldn't keep selling asbestos products and putting workers
and countless consumers at risk. There are thousands of other products
that contain asbestos including floor tiles, roofing material, cement
pipes, and even hair dryers. And deadly asbestos is still putting
construction and maintenance workers at risk. Below this hearing room
and under the Capitol there are tunnels where we know asbestos exists
and workers have been exposed.
3. Asbestos is Still Legal
Third, asbestos is still legal. Many Americans assume--as I did--
that asbestos is already banned, but it's not. In 1989, the EPA tried
to ban asbestos, but most of those regulations were overturned in court
in 1991. As a result, while new applications for asbestos were banned,
asbestos is still being imported and used in consumer and industrial
products.
4. Strong Need for Research and Treatment
Fourth, research and treatment for asbestos diseases are not very
far along. Doctors have been hampered by a lack of funding for research
on how asbestos fibers actually cause disease and what treatment
strategies work best. Industrial hygienists have been hampered by the
lack of research on how to best measure asbestos fibers in the air.
I know that the Mesothelioma Applied Research Foundation (MARF) has
privately awarded over $4 million in grants.
The Foundation's investment in research is helping motivate
brilliant investigators to study mesothelioma. But the Foundation's
seed money is not enough. Federal funding is critical to the research
effort if we are truly going to help people.
My bill also requires collaboration among the 10 research and
treatment centers established under the bill along with the National
Cancer Institute, the Department of Veterans Affairs and the National
Institute for Occupational Safety and Health (NIOSH).
Because nearly one-third of mesothelioma victims were exposed to
asbestos while serving in the U.S. Navy, my bill directs the Pentagon
to conduct additional research on asbestos disease, early detection and
treatment as well.
I am very encouraged that the NIOSH has embarked on an ambitious
research roadmap to better answer current scientific questions about
appropriate occupational levels of exposure.
the ban asbestos in america act of 2007
To address the national scourge of asbestos, I've again introduced
the Ban Asbestos in America Act of 2007 (S. 742).
My bill does three things:
First, my bill bans asbestos. It prohibits the importation,
manufacture, processing and distribution of products containing
asbestos. Unfortunately some 2,500 metric tons of asbestos was used in
the U.S. in 2005 and imports of products containing asbestos in cement
pipe, tiles, brake gaskets and linings continue unabated today.
Second, my bill dramatically expands research and treatment. It
creates a $50 million, 10-center ``Asbestos-Related Disease Research
and Treatment Network.'' It creates a new National Asbestos-Related
Disease Registry. It supports research at the Department of Defense and
launches a study to determine the most promising areas for new
research.
Finally, my bill launches a public education campaign to better
inform Americans of the dangers of exposures to asbestos in the
workplace and in the environment, while also providing helpful steps
all of us can take to better protect our families.
other countries are protecting their citizens
I know we can and should make progress in banning asbestos. More
than 40 other industrialized countries have already banned asbestos.
Around the world, chlorine producers are phasing out dangerous and
inefficient methods in favor of safer and more environmentally
responsible technology. We need to help U.S. companies embrace new,
greener approaches today.
I am very grateful that industry leaders have stepped up to the
plate to work with me in achieving a goal everyone supports--a ban on
the production and importation of asbestos in the U.S.
These corporate leaders also strongly support the need to better
educate the public and to provide for more research and treatment
dollars to better mitigate the effects of asbestos on workers and their
families.
I look forward to working with all of the Members of the
Environment and Public Works Committee to achieve a bipartisan
consensus on banning asbestos in the U.S. in this Congress. Chairwoman
Boxer, I know this hearing will go a long way in helping us achieve
that goal.
We've lost enough people like Brian and Fred, and we have a
responsibility to protect tens of thousands of people just like them.
Thank you again for the opportunity to testify.
Senator Boxer. Senator Murray, thank you once again for
your testimony.
I don't have any questions for you, I just want to tell you
my intent as Chair, and I think Senator Inhofe knows this, is
to really move this bill as quickly as I can, with the great
hope that you and Senator Isakson can reach an accord. I think
it would be a proud day for this committee, and I think it
would be a proud day for the Senate if we finally did something
that frankly most Americans think we have already done in the
past, and do it in a wise way and make a statement to all those
people out there who have lost loved ones and those who fear
for the future that we are relevant to their lives. And we are
going to do this.
So I don't have any questions. I guess I have one. Are you
ready to work with us to get this bill to the floor, for as
long as it takes?
Senator Murray. I am ready to go. I again want to thank
Senator Isakson and his committee staff for working with us on
this.
Senator Boxer. Very good.
Senator Isakson, do you have any questions for Senator
Murray?
Senator Isakson. Just to thank her for her diligence and
hard work and courtesy to me and my staff. I think we can put
this together quite quickly.
Senator Boxer. Senator Lautenberg, any questions?
Senator Lautenberg. Just to commend Senator Murray for, as
I said before, her persistence in doing this, and alerting the
country to the danger of this product, and to take it away as
quickly as we can, so that people aren't exposed to it. My
congratulations.
Senator Boxer. Senator Vitter.
Senator Vitter. I would just ask Senator Murray her
thoughts on the chlor-alkali issue in particular and where you
are perhaps with Johnny and others on discussion of that aspect
of the bill.
Senator Murray. Senator Vitter, as you know, a number of
the chlorine producers are coming up with alternative methods.
Part of our bill hopes to help provide support for them to do
that.
But I think the important thing in our bill that will help
everyone is that not enough research has been done. Senator
Inhofe mentioned a number of different fibers that people don't
know enough about. We want to make sure that we do the right
thing. That is why the research that is part of this bill is
absolutely critical.
You mentioned a number of times that it is important to be
science-based. If you don't have the science, it is very
difficult to make a decision. Meanwhile, people are dying
because we are not doing the right thing. So I think that you
will be satisfied that Senator Isakson has addressed a number
of those issues that you raise concerns about.
Senator Vitter. As that science is being done or whatever
you are describing, would use of asbestos in chlor-alkali
production under the parameters I was describing, with the
process fully enclosed, no humans in contact, would that be
allowed or not?
Senator Murray. Let me refer to my staff on the latest
reiteration of the language that we have been working with.
Perhaps we can have my staff work with yours as we are working
through the committee process and get you an answer so we are
all accurate.
Senator Vitter. OK.
Senator Boxer. Let me say, Senator Vitter, if I might have
your attention for a second, Senator Murray, I know Senator
Murray's staff has been meeting with Dow and others to see if
there is a way to do this right. I wanted to place into the
record, without objection, an article, Responding to A Harsh
Business Environment: a New Diaphragm for the Chlor-alkali
Industry. It talks about a new industry, PPG Industries has
responded by developing a new separator for its diaphragm cells
operating at its plants at Natrium, West Virginia and Lake
Charles, LA. The new separator is asbestos-free, energy
efficient and durable. The new separator is named Tephram.
In any case, I am going to put this into the record for you
to read.
[The referenced material follows:]
Senator Boxer. As usual, the entrepreneurship spirit has
kicked in here, and there are alternatives coming. So I would
love to share this with you.
Senator Vitter. I have looked at many things like that and
I would love to read that. I guess the question in my mind is
not, is there an alternative. The first question is, is there a
safety issue and if there is, we need to do something about it.
But if there is not, then we need to think.
Senator Boxer. A safety issue with the alternative?
Senator Vitter. No, with the use of asbestos in chlor-
alkali production under an enclosed, wet process.
Senator Murray. I believe you have a number of witnesses
who will be able to help you answer that question.
Senator Vitter. OK. Because I am not aware of any known
cases of asbestos-related disease from that. If there is a
safety issue, great.
Then the second question is, certainly there are
alternatives. At what cost?
Senator Boxer. Senator Vitter, I think we will explore this
in the next panels. My understanding is that there is a danger
if bags rip and you have to clean up the asbestos, so it is not
as clean as one would think. Certainly this is something that
Senator Murray is trying to work on. If we can find
alternatives, we ought to encourage alternatives. That is for
sure.
OK, why don't we call up our next panel. Senator Murray, we
thank you very much. We will let you know how the rest of the
hearing went.
David Weissman, M.D., Director, Division of Respiratory
Diseases at National Institute for Occupational Safety and
Health; Captain Aubrey Keith Miller, M.D., Senior Medical
Officer, Toxicologist, U.S. Public Health Service and
Environmental Protection Agency; Melanie Marty, Ph.D., Chief
Air Toxicology and Epidemiology Branch, California EPA, Office
of Environmental Health Hazard Assessment.
So we welcome you to panel one. Your titles are very
impressive and we welcome you here. Dr. Weissman, from NIOSH,
why don't you begin? We will give you 5 minutes.
STATEMENT OF DAVID N. WEISSMAN, M.D., DIRECTOR, DIVISION OF
RESPIRATORY DISEASE STUDIES, NATIONAL INSTITUTE FOR
OCCUPATIONAL SAFETY AND HEALTH, CENTERS FOR DISEASE CONTROL AND
PREVENTION, U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Dr. Weissman. Thank you. Madam Chair, members of the
committee, thank you for giving me the opportunity to testify
today. My name is David Weissman, and I direct the Division of
Respiratory Disease Studies in the National Institute for
Occupational Safety and Health, NIOSH.
For the last 21 years, I have been a pulmonary disease
physician, serving in both academic medical centers and in
Government. When asked to testify, I couldn't help but think of
a colleague who recently died of mesothelioma. He was a very
distinguished physician whose only known exposure to asbestos
was as a college student during a summer job. Forty years
later, he developed mesothelioma and died at the age of 62.
In my oral comments today, I will focus on three of the
issues addressed in the written testimony. First, I will
describe the continued burden of asbestos-related diseases in
the United States. Second, I will mention several issues
relevant to prevention efforts in the occupational setting.
Finally, I will address NIOSH's efforts to identify key
research needs and strategies to address them as described in
the draft NIOSH Road Map document.
A substantial number of people still die from asbestos-
related disease in our country. Asbestosis deaths increased
almost 20-fold from the late 1960s to the late 1990s and have
plateaued since the year 2000 at about 1,500 per year. By
contrast, mesothelioma deaths since 1999 have increased each
year, up to 2,657 deaths in 2004, the most recent year for
which we have data.
It should be noted that because the latency between
exposure and disease onset is so long, current disease, to a
large degree, reflects past exposures. Asbestos usage, as we
have heard, hasn't been completely eliminated. Although
domestic production of asbestos has ceased and importation of
raw asbestos fibers has markedly declined, finished asbestos-
containing products continue to be imported into the United
States.
Asbestos-related diseases can be prevented by eliminating
or limiting exposures to asbestos. The OSHA Permissible
Exposure Limit, or PEL, for asbestos is 0.1 fibers per cubic
centimeter of air. This limit was set in part based on the
limit of detection of the exposure assessment method, a light
microscopic method called phase contract microscopy, or PCM.
Exposure limits are usually set to reduce risk associated with
exposures to a level at or below 1 per 1,000 working lifetimes
with exposure every day over the working lifetime. Over such a
working lifetime, exposure at the asbestos PEL is estimated to
be associated with excess risk of cancer of 3.4 per 1,000, an
excess risk of asbestosis of 2.5 per 1,000.
A major recent NIOSH effort has been the development of a
draft road map document that details key scientific issues in
asbestos and identifies research directions. One key question
is which minerals should be treated as asbestos. Most
regulatory definitions of asbestos do not explicitly include
fibers of minerals such as winchite, richterite and erionite,
despite their known similar health effects to asbestos.
In addition, significant controversy exists regarding other
types of mineral particles that have the dimensions of fibers.
For example, El Dorado, CA, is a site with natural mineral
deposits that have been disturbed by construction and crushing
of rock. Analyses of air and rock samples have identified
structures called acicular actinolite. These particles have a
different crystalline structure from that of fibrous actinolite
asbestos. Research is needed to be better characterize their
toxic potential.
Asbestos minerals have analogs that are crystallized in
non-asbestiform or massive forms. A controversial type of
mineral particle that we have heard about is the cleavage
fragment, which can be generated from massive forms during
their handling, crushing or processing, as occurs in mining and
construction. Using current analytical methods, these cleavage
fragments are often microscopically indistinguishable from
asbestos fibers of asbestos mineral counterparts.
Another key question is whether the specified dimensions of
asbestos fibers are appropriate. Currently, a mineral particle
is detected by PCM and counted as a fiber if it has a length to
width or aspect ratio of 3:1 and a length of at least microns.
These counting rules include particles with diameters greater
than 3 microns, which are unlikely to reach the airways or gas-
exchange regions of the lung.
Also, PCM can't detect particles with diameters less than
.25 microns, which although not visible by PCM are capable of
causing harm. Finally, although longer fibers have been
associated with greater potential for carcinogenicity, studies
of fibers deposited in human tissues suggest that fibers less
than 5 microns in length may also contribute to human disease,
including cancer.
In order to address these questions, NIOSH has put forth a
draft document called the Roadmap. It is developing a range of
partnerships to address the goals in the Roadmap, including
with other Federal agencies, labor, industry, academia and
interested parties.
To summarize, asbestos-related diseases continue to be an
important problem. Fortunately, much progress has been made.
However, there is room to do better and several key issues
remain to be fully addressed.
Thank you for the opportunity to testify today. I would be
happy to answer any questions.
[The prepared statement of Dr. Weissman follows:]
Statement of David N. Weissman, M.D., Director, Division of Respiratory
Disease Studies, National Institute for Occupational Safety and Health,
Centers for Disease Control and Prevention, U.S. Department of Health
and Human Services
Madam Chair and members of the committee, I am Dr. David Weissman,
and I direct the Division of Respiratory Disease Studies in the
National Institute for Occupational Safety and Health (NIOSH), a part
of the Centers for Disease Control and Prevention (CDC) within the
Department of Health and Human Services (HHS). NIOSH is the federal
agency responsible for conducting research and making recommendations
to identify and prevent work-related illness and injury. I am also a
pulmonary diseases physician, and over the last 20 years have seen
firsthand the human suffering caused by asbestos. Thank you for the
opportunity to provide testimony on the health effects of asbestos and
efforts by NIOSH to address this important problem.
My testimony today will address current scientific knowledge about
the health risks posed by exposure of workers to airborne asbestos. I
will also provide an update on NIOSH's recent activities in this area,
including NIOSH efforts to define key areas for research as described
in the draft NIOSH document released in February for public comment,
Asbestos and Other Mineral Fibers: A Roadmap for Scientific Research.
background
Asbestos is a term that is generally used to refer to a group of
fibrous silicate minerals with exceptional resistance to degradation by
heat, acids, bases, or solvents. The minerals are not combustible and
have a high melting point and low thermal and electrical conductivity.
Their fibers can be woven or incorporated into other materials. These
and other useful properties resulted in their widespread commercial
application during much of the 20th century. Unfortunately, widespread
use of asbestos was followed by a marked increase in asbestos-related
disease.
The definition of asbestos in many Federal regulations is limited
to the fibrous forms of six specific commercial types of asbestiform
minerals. One is from a class of minerals called serpentines, which
have curved fibers: chrysotile. The other five are members of a class
of minerals called amphiboles, which have straight fibers: crocidolite,
amosite, tremolite asbestos, actinolite asbestos, and anthophyllite
asbestos. The elemental composition of the six asbestos minerals can
vary slightly, even within a single fiber, as a result of geological
conditions such as pressure, temperature, or proximity of other
minerals. Recognizing these variations in elemental composition, the
six asbestos minerals can be defined by their ``solid-solution''
mineral series. For example, the mineral series tremolite-
ferroactinolite contains the asbestos mineral actinolite. These mineral
series are considered solid-solutions in which cations (i.e., sodium,
calcium, magnesium, iron, etc.) are replaced by other cations which can
affect the elemental composition of the mineral without significantly
altering the structure. As another example, the Libby, Montana
vermiculite ore body contains amphibole asbestos fibers of the
tremolite-actinolite-richterite-winchite solid solution series. The
minerals in the solution series have only minor differences in chemical
content and have similar, if not identical, health effects. A third
example of a mineral that produces similar diseases as asbestos is
erionite, a fibrous mineral that is neither a serpentine nor an
amphibole. It belongs to an entirely different class of minerals called
zeolites.
asbestos-related diseases
Exposure to asbestos significantly increases the risk of developing
several types of cancer and non-cancerous diseases. Most asbestos-
related diseases, particularly the cancers, have long latency periods
often extending 10-40 years from initial exposure to onset of illness.
These include:
(1) Asbestosis--a non-cancerous disease characterized by scarring
of the air-exchange regions of the lungs. Progressive lung damage can
cause progressive shortness of breath and inability to engage in
physical activity, as well as other symptoms such as coughing and chest
pain;
(2) Lung cancer--for which asbestos is one of the leading causes
among non-smokers, and which occurs at dramatically high rates among
asbestos-exposed smokers;
(3) Malignant mesothelioma--an almost invariably fatal cancer of
the tissue covering the lungs and chest wall (called the pleura) or
abdomen (called the peritoneum) for which asbestos and similar fibers
are the only known cause; and
(4) Non-malignant pleural disease--asbestos exposure can affect the
pleura in several ways. It can cause a painful accumulation of bloody
fluid surrounding the lungs. It can cause a circumscribed thickening,
fibrosis, and sometimes calcification of pleural tissue--a condition
called pleural plaques. Finally, it can cause a more severe condition
with more extensive and sometimes constricting scarring of the tissue
surrounding the lungs called diffuse pleural thickening.
In addition, asbestos exposure is associated with excess mortality
due to cancer of the larynx and cancer of the gastrointestinal tract.
The various types of cancers caused by asbestos are often fatal within
a few years after initial diagnosis. In contrast, asbestosis deaths
typically occur only after many years of suffering from impaired
breathing.
The risk of developing adverse health effects from asbestos is
related to the amount and duration of exposure to airborne asbestos
fibers. Exposure occurs in the occupational setting when microscopic
asbestos fibers become airborne during various industrial processes or
from handling of asbestos-containing materials. The fibers can then be
inhaled and/or swallowed. In the lungs, asbestos fibers can interact
with cellular targets such as alveolar macrophages and alveolar
epithelial cells, inducing a chain of events leading to scarring and/or
cancer in the lungs. Fibers can also translocate through the lungs to
the pleura, where they can cause malignant mesothelioma and
nonmalignant pleural disease. Key factors associated with the
carcinogenic potential of asbestos fibers include: particle length
(longer fibers are more toxic than shorter fibers); diameter (fibers 3
micrometers in diameter are more likely than thicker fibers to be
inhaled into the lungs, and fibers <0.5 micrometers in diameter are
more likely to migrate through lung tissue to the pleura); and
biopersistence (fibers able to persist in the lung and not be cleared
from the lung by physiological lung defense mechanisms are more likely
to cause adverse health effects).
Asbestos-related diseases can be prevented by eliminating or
limiting exposures to asbestos. The Occupational Safety and Health
Administration (OSHA), the Mine Safety and Health Administration
(MSHA), and the Environmental Protection Agency (EPA) regulate the six
asbestos minerals. The OSHA permissible exposure limit (PEL) for
asbestos is 0.1 fibers per cubic centimeter (cc) of air. This limit was
set in part based on the limit of detection of the exposure assessment
method specified in the standard (phase contrast microscopy (PCM)) and
is not completely protective against asbestos-induced disease.
Occupational exposure limits are generally set to reduce risk
associated with exposures to a level at or below 1 per 1,000 working
lifetimes.
The risk analyses upon which the OSHA PEL and MSHA's proposal to
revise its PEL are based were recently detailed by MSHA in its proposed
rule. It should be noted that these risk analyses make the maximally
protective assumption that exposure would be at the PEL every work day
over an entire 45-year working lifetime. Over such a working lifetime,
exposure at the OSHA asbestos PEL is estimated to be associated with an
excess risk of cancer (lung, mesothelioma, and gastrointestinal) of 3.4
cases per 1,000 exposed individuals and an excess risk of asbestosis of
2.5 cases per 1,000 exposed individuals. In mining, the current MSHA
PEL for asbestos is 20-fold higher at two fibers per cc air. Were
exposure to the current MSHA PEL to occur every day over a 45-year
working lifetime, it would be associated with an excess risk of cancer
of 64.1 cases per 1,000 exposed individuals and an excess risk of
asbestosis of 49.7 cases per 1,000 exposed individuals. Fortunately,
the U.S. mining industry does not currently mine or produce asbestos
and asbestos sampling data presented in MSHA's proposed rule showed low
exposures for the mining population. MSHA has proposed to reduce its
PEL to make it consistent with the OSHA PEL, and NIOSH has provided
public comments in support of this proposed rule.
burden of asbestos-related diseases
NIOSH has tracked annual U.S. asbestosis deaths since 1968 and
malignant mesothelioma deaths since 1999 using death certificate data
in the National Occupational Respiratory Mortality System (NORMS). Data
from NORMS show that asbestosis deaths increased almost 20-fold from
the late 1960s to the late 1990s and have apparently plateaued only
since 2000 at approximately 1,500 per year (Figure 1). By contrast,
mesothelioma deaths continue to rise (Table 1). Current asbestos and
mesothelioma mortality reflect past exposures because the latency
between exposure and disease onset is long, particularly for
mesothelioma, and asbestosis is a chronic disease, with affected
individuals typically living for many years with the disease before
succumbing.
Figure 1. Number of asbestosis deaths, U.S. residents age 15 and
over, 1968-2004. Source: National Occupational Respiratory Mortality
System (NORMS), found at: http://webappa.cdc.gov/ords/norms.html.
Table 1--Number of mesothelioma deaths, U.S. residents age 15 and over,
1999-2004
------------------------------------------------------------------------
Year Deaths
------------------------------------------------------------------------
1999....................................................... 2,484
2000....................................................... 2,531
2001....................................................... 2,509
2002....................................................... 112,573
2003....................................................... 112,625
2004....................................................... 112,657
1999-2004 (total).......................................... I15,379
------------------------------------------------------------------------
Source: NORMS (http://webappa.cdc.gov/ords/norms.html)
Over time, the annual number of deaths should decrease
substantially as a result of reductions in exposures. However, asbestos
usage has not been completely eliminated. Although domestic production
of asbestos has ceased and importation of raw asbestos fibers has
markedly declined, many finished asbestos-containing products continue
to be imported into the United States. These include asbestos-cement
sheets, panels, and tiles; corrugated sheets; and automotive friction
products. In addition, a reservoir of asbestos-containing materials
remains in place in older buildings and machinery. Thus, even with
limitations or exclusions from new use, occupational exposures to
asbestos will continue, albeit at a far lower level than in the past.
update on niosh activities related to asbestos
NIOSH continues to work actively to address issues related to
asbestos-induced lung disease. We are continuing to track asbestosis
deaths, mesothelioma deaths, and occupational exposures to asbestos and
have plans to include updated findings in an upcoming new edition of
the recurring NIOSH document, the ``Work-Related Lung Disease
Surveillance Report.'' Updates are also available on the NIOSH Web
site.
NIOSH recently reported updated information on the occupational
respiratory disease mortality among workers who mined, milled, and
processed vermiculite contaminated with asbestiform fibers, including
winchite, richterite, and tremolite from the mine near Libby, Montana.
These workers had significantly increased rates of death from cancer,
including lung cancer and malignant mesothelioma. They also had
significantly increased rates of death from nonmalignant respiratory
disease, including asbestosis and chronic obstructive pulmonary
disease. Exposure-response relationships were demonstrated, with
increasing fiber exposure associated with increasing mortality from
lung cancer, asbestosis, and noncancerous chronic respiratory disease.
This report adds to the growing body of literature documenting the
adverse effects of exposure to Libby amphibole fibers.
With regard to Libby, the activities of the Agency for Toxic
Substances and Disease Registry (ATSDR), an important partner of NIOSH,
should be noted. A medical screening program conducted by ATSDR in
Libby revealed an unusually high rate of asbestos-related disease among
participants. Although many of these participants were former mine
workers, others were their household contacts or community members with
possible environmental exposures. Based on these findings, ATSDR
established a Tremolite Asbestos Registry, which will complement
NIOSH's work by tracking the health outcomes of exposed individuals
over time. To date, ATSDR has enrolled more than 4,000 individuals--
comprising 83 percent of former Libby mine workers, their household
contacts and a defined set of other local residents--and will
administer follow-up interviews and medical screenings on a regular
basis. ``Take-home'' exposures--involving family members of workers who
bring asbestos home on their hair, clothing, or shoes--is a well-
recognized hazard addressed by NIOSH in a 1995 report to Congress
(http://www.cdc.gov/niosh/contamin.html), so ATSDR's inclusion of
household contacts in the registry will contribute important
information to the body of research. In addition to research, ATSDR
will use the registry to provide participants with information about
new therapies that may become available in the future. ATSDR is also
studying exposures to asbestiform fiber-contaminated vermiculite ore
from Libby that was processed at sites in California, Ohio, Minnesota,
New Jersey, New York and Wisconsin. ATSDR plans to use the findings of
the registry and studies conducted at processing sites to develop a
research agenda for Libby amphibole-related research.
NIOSH is doing research to clarify the relationships between fiber
dimensions (length and diameter) and the risk for developing lung
cancer or asbestosis through follow-up studies of a cohort of
chrysotile-exposed South Carolina textile workers. NIOSH originally
reported on this cohort in the 1980s. Exposures were originally
evaluated by PCM. Since then, archived samples collected by NIOSH have
been re-analyzed by transmission electron microscopy (TEM) to better
evaluate fiber dimensions, including fibers too small to be seen by
PCM. Also, mortality information about the cohort has been updated.
Based on these data, fiber size-specific exposure estimates have been
developed for the cohort. Analyses are underway to determine the
influence of fiber length and width on lung disease risk. These
findings will help to inform approaches to quantitative risk
assessment, particularly the potential utility of risk assessment based
on fiber size.
NIOSH is also doing research in the area of exposure assessment. A
recently published American Society for Testing and Materials (ASTM)
International Standard--``Method for Sampling and Counting Airborne
Fibers, Including Asbestos Fibers, In Mines and Quarries, by Phase
Contrast Microscopy'' (D7200-06)--contains a proposed methodology for
separating fiber-like particles other than asbestos from probable
asbestos fibers. The new ASTM procedure has not yet been validated to
confirm that it produces accurate, reproducible results. A current
NIOSH study will address this issue by documenting the performance of
the ASTM procedure. Another important issue in asbestos exposure
assessment is sampling in dusty environments, such as mines.
Traditional filter samplers quickly become overloaded with dust,
limiting the ability to detect asbestos fibers. One approach to
reducing this problem is to use a sampler that only collects particles
small enough to reach the airways of the lung when inhaled, and not
larger particles that mostly deposit in the mouth, nose, and throat.
NIOSH is currently evaluating two such ``thoracic'' particulate
samplers in comparison to the traditional filter sampler in two
different mining environments.
NIOSH is pursuing research relevant to the detection of asbestos-
related respiratory diseases. Traditionally, film-based chest
radiographs have been used in epidemiological studies evaluating
workers for pulmonary and pleural disease associated with asbestos
exposure. This is because only film-based chest radiographs may be
systematically classified for changes of dust-induced lung disease
(pneumoconiosis) using the widely accepted International Labour
Organization (ILO) classification system. However, in the United
States, digital chest radiography has largely replaced film-based
radiography. NIOSH has funded research to evaluate the impact of
classifying digital, instead of film-based, chest x-rays on the
detection and classification of pulmonary and pleural disease. Initial
results suggest that the two methods do not differ significantly in
detection of interstitial (lung tissue) processes, but do differ in
detection of pleural processes, with fewer pleural changes detected in
those undergoing digital chest radiography. In follow up to this
finding, NIOSH is assisting ATSDR in performing a study to compare
detection of pleural changes in those exposed to Libby amphibole by
film-based and digital radiography, with findings of computed
tomography scans of the chest serving as a ``gold standard.''
In 2006, NIOSH published a Recommended Exposure Limit (REL) for
another type of inorganic fiber, refractory ceramic fibers (RCF).
Although RCF are man-made fibers which differ from asbestos in
toxicity, many of the same issues relevant to asbestos such as fiber
length, diameter, and biopersistence were considered in developing the
NIOSH REL of 0.5 fibers per cc.
asbestos and other mineral fibers: a roadmap for scientific research
A major recent NIOSH effort has been the development of a draft
``Roadmap'' document that details key scientific issues in asbestos and
identifies research directions to address these issues. Key issues
include the following:
Which minerals should be treated as asbestos?
As already described, most regulatory definitions of asbestos do
not explicitly include minerals such as winchite, richterite, and
erionite, despite the known similar health effects of their fibers to
those of the explicitly listed asbestos minerals. In addition,
significant controversy exists regarding other types of mineral
particles that have the dimensions of fibers. For example, El Dorado,
California, is a site with natural deposits of amphibole that have been
disturbed by construction and crushing of rock. Analyses of air and
rock samples have identified the presence of actinolite in the form of
needle-like crystalline structures called ``acicular/prismatic
actinolite.'' Although many of these amphibole particles meet the
dimensional criteria of asbestos fibers, they have a different
crystalline structure from fibrous actinolite asbestos. A recent report
by investigators from the University of California found that
residential proximity to deposits of ``naturally occurring asbestos''
such as those in the vicinity of El Dorado was associated with
increased risk for mesothelioma, implicating these minerals as a
possible health hazard. It should be noted that this report did not
include actual measurement of fiber exposures associated with residence
in these areas.
Asbestos minerals have analogs that are crystallized in non-
asbestiform (massive) structures. A controversial type of mineral
particle is the ``cleavage fragment,'' which can be generated from
massive forms of these analog minerals during their handling, crushing,
or processing, as occurs in mining and construction. Using current
analytical methods based on light microscopy, these ``cleavage
fragments'' are often microscopically indistinguishable from
asbestiform fibers of their asbestos mineral counterparts. The toxic
potential of these mineral particles, in particular their
carcinogenicity, has been an area of great controversy.
Are the specified dimensions of asbestos fibers appropriate?
Currently, a mineral particle is detected by PCM and counted as a
fiber if it has a length to width (``aspect'') ratio of 3:1 and length
of at least 5 micrometers. These counting rules include particles with
diameters greater than 3 microns, which are unlikely to reach the
airways or the gas-exchange regions of the lungs when inhaled. Also,
PCM cannot detect particles with diameters less than about 0.25
micrometers, which, although not visible by PCM, are capable of causing
harm. Finally, although longer fibers have been associated with greater
potential for carcinogenicity, studies of fibers deposited in human
tissues suggest that fibers less than 5 micrometers in length may also
contribute to human disease, including cancer.
The broad goals of the research outlined in the Roadmap are to: (1)
provide a scientific framework for evidence-based worker protection
recommendations; (2) address the broad range of mineral fibers to which
workers are exposed; and (3) refine our understanding of fiber
characteristics associated with toxicity. Strategic goals identified by
the Roadmap are to: (1) develop improved sampling and analytical
methods for mineral fibers; (2) develop information and knowledge on
occupational exposures to the range of mineral fiber types and their
health outcomes; and (3) develop a broader understanding of the
important determinants of fiber toxicity. In particular, it would be
useful to develop approaches that would make it possible to predict the
ability of various mineral fiber types to cause human disease and apply
this information for risk management.
NIOSH has solicited public comment on the draft Roadmap document
via docket submissions and a public meeting. The draft document was
first made available to the public on February 28, 2007, and public
comments were accepted into the docket from the time of posting until
May 31, 2007. The public meeting was held on May 4, 2007. Peer
reviewers have been selected and are being provided with a copy of the
public comments as well as the draft Roadmap document. Revision of the
document will take into account both public and peer review comments.
The goals expressed in the Roadmap are ambitious. NIOSH plans to
develop a range of partnerships to address these goals, including with
other Federal agencies, labor, industry, academia, and other interested
parties. Although NIOSH will focus on occupational safety and health,
we will pursue opportunities to ensure that the results of research
arising from the Roadmap can be extended outside of the occupational
setting.
conclusion
Despite the ability to prevent asbestos-related diseases by
preventing exposure, they continue to be an important problem in the
United States. At least in part because of the long lag in time between
exposure and mortality, deaths from asbestos-related diseases such as
asbestosis and mesothelioma have not yet declined. Furthermore,
asbestos exposure continues to occur due to the presence of asbestos in
older buildings and continued importation of asbestos-containing
products from other parts of the world. Asbestiform erionite, a non-
serpentine, non-amphibole mineral fiber that is well-established as
having toxicity similar to asbestos, is not included within regulatory
definitions that are limited to the six commercial types of asbestos.
Controversy surrounds the toxic potential of several other mineral
fiber types, in particular acicular/prismatic actinolite identified in
El Dorado, California; and ``cleavage fragments'' of non-asbestiform
amphibole minerals encountered especially in mining and construction.
NIOSH continues to work actively in this area and has developed a draft
Roadmap describing current issues and research strategies to address
these issues. Working with a range of partners, our ultimate goal is to
develop, disseminate, and facilitate the adoption of evidence-based
recommendations to better protect workers from diseases caused by
asbestos and other mineral fibers.
Thank you again for the opportunity to testify before you today. I
would be happy to answer any questions you may have.
______
Responses by David N. Weissman, M.D., to additional questions
from Senator Boxer
Question 1. Your testimony states, ``using current analytical
methods . . . cleavage fragments are often microscopically
indistinguishable from . . . fibers of their asbestos mineral
counterparts.''
Please describe what that tells us about most federal definitions
of asbestos, particularly given the need to protect public health from
diseases associated with asbestos.
Response. Phase contrast microscopy (PCM) is a light microscopy-
based method that is specified by OSHA and MSHA for use in determining
the level of exposure to asbestos fibers. There is insufficient data to
suggest that this method can accurately or reproducibly distinguish
between asbestiform fibers of the six asbestos minerals on one hand;
and ``cleavage fragments'' formed by handling, crushing, or processing
of amphibole minerals crystallized in a massive habit on the other
hand. Thus, no current practical definition of asbestos could
distinguish between asbestiform fibers and cleavage fragments unless it
specified the use of other analytical methods, such as electron
microscopy, and provided guidance on how the analytical method would be
performed and when it would be used.
The public health impact of PCM's inability to distinguish between
asbestiform fibers and cleavage fragments is not entirely clear, given
the uncertainties about the toxicity of cleavage fragments. Those who
believe that cleavage fragments are likely to have similar toxicity as
asbestiform fibers would view the inability of PCM to distinguish
between them as unimportant. Those who believe that cleavage fragments
have less toxicity than asbestiform fibers would take the opposite
view. Specifically, they would feel that undercounting of asbestiform
fibers in mixed dust would result in underestimation of risk; and over-
counting of asbestiform fibers would result in over-estimation of risk.
Definitive resolution of these differing viewpoints will require
research to better document the ability of cleavage fragments to cause
toxicity. In response to this need, CDC has nominated dusts containing
a variety of mineral fibers for laboratory toxicology studies by the
National Toxicology Program (NTP).
Question 2. U.S. Geological Survey data indicates this country
still imports more than 2,500 metric tons of asbestos a year as well as
products that contain asbestos.
Can you describe the types of diseases that may be associated with
the use of these materials, and whether these diseases may be a concern
for people who use these products in or around their homes?
Response. Many finished asbestos-containing products continue to be
imported into the U.S. These include products such as: asbestos-cement
sheets, panels, and tiles; corrugated sheets; and automotive friction
products. Asbestos exposure associated with these products could
potentially occur in either work or home settings. Regardless of
country of origin, sufficient exposure to asbestos in either setting
would be associated with the potential to develop any of the diseases
caused by asbestos. A special concern for exposure in the home setting
is that children can inhale asbestos, which could potentially remain
within their lungs for a lifetime. Another special concern for
exposures in the home is that exposures can potentially occur at any
time and are not limited to a 40-hour work week. Since asbestos is a
carcinogen, even low exposures are of concern for their potential to
cause malignancies. An important consideration in older homes is past
installation of asbestos-containing products, such as tiles, shingles,
or insulation. Libby vermiculite was widely used as loose attic
insulation. Installation of newer asbestos-containing materials would
also be a concern.
When asbestos-containing products are identified in the home
setting, steps must be taken to prevent exposure. The materials can
either be removed or ``managed in place.'' Management in place involves
prevention of exposure by encapsulation of asbestos-containing
materials so they cannot break down and become aerosolized, resulting
in exposure of home occupants.
Senator Boxer. Thank you, sir.
Captain Miller, U.S. Public Health Service and EPA.
STATEMENT OF CAPTAIN AUBREY MILLER, M.D., M.P.H., U.S. PUBLIC
HEALTH SERVICE, REGION 8, U.S. ENVIRONMENTAL PROTECTION AGENCY
Dr. Miller. Good morning, Madam Chairman and members of the
committee. I am Captain Aubrey Miller, a physician in the U.S.
Public Health Service and currently a senior medical officer
and toxicologist with the U.S. EPA in Denver. I am board
certified in occupational medicine and have cared for patients
with asbestos-related disease prior to beginning my Federal
career.
Over the last 8 years I have worked for both the Department
of Health and Human Services and for EPA in their Denver
offices, where my efforts have been largely focused on
improving our understanding of the health effects associated
with asbestos exposure in Libby, MT. During this time, I have
also worked toward strengthening the health care infrastructure
of the Libby community and helped to establish a new community
health center to provide primary care for those in need.
I have personally come to know the pain, suffering and
courage of the good folks in Libby, like Les Skramsted and Mick
Mills, who finally succumbed to this terrible disease. Our work
is about these individuals and the countless others across
America with ongoing exposures or illnesses from asbestos.
Thank you for the opportunity to discuss EPA's perspective and
progress in understanding the human health effects associated
with exposures to asbestos.
Asbestos is a general term for fibrous silicate minerals in
the serpentine and amphibole classes, and include chrysotile,
amphiboles, amosite, crocidolite, antophylite, tremolite and
actinolite. Asbestos has been classified as a human carcinogen
by the EPA and the World Health Organization. Mesothelioma and
lung cancers are the malignancies most consistently and
strongly associated with such exposures.
The non-cancerous conditions related to asbestos exposure
may be more prevalent than cancer and just as debilitating and
lethal. The American Thoracic Society defines non-malignant
asbestos-related disease to include conditions of interstitial
pulmonary fibrosis, or asbestosis, benign pleural effusions,
pleural fibrosis, both circumscribed and diffuse, and
obstruction of pulmonary airflow.
Asbestos diseases have a latency period ranging from 1 year
to several decades, depending upon the health endpoints of
concern. Once established, asbestos-related fibrosis can remain
static or progress in severity in the absence of continued
exposure. But they rarely regress.
As a natural mineral, serpentine and amphibole deposits may
be present as natural outcroppings and can be found in native
soils in a number of communities in the United States and
abroad. As a result, community members can be exposed to
asbestos during various activities outdoors or in their homes.
Studies of communities with such environmental exposures have
found health effects similar to those observed in asbestos-
exposed workers. EPA is currently evaluating several sites
impacted by such natural outcroppings.
There is a scientific debate concerning the differences in
the extent of disease caused by different fiber types and
sizes. Some of these differences may be due to the physical and
chemical properties of the different fiber types. For example,
several studies suggest that amphibole asbestos types may be
more harmful than chrysotile, particularly for mesothelioma.
Studies also indicate that fiber size dimensions, the length
and diameter, are important determinants in the risk for
disease.
Asbestos minerals can also occur in a non-fibrous or so-
called massive form that can be found geologically in some ore
deposits in which fibrous asbestos minerals also occur.
Cleavage fragments, small mineral shards that are often
microscopically indistinguishable from typical asbestos fibers,
can be generated from these non-fibrous forms of asbestos
minerals during crushing or processing.
Based upon scientific evidence from studies suggesting that
the dimension, specifically length and diameter, as well as
durability, may be more critical factors in causing disease
than chemical or elemental composition, NIOSH and the Centers
for Disease Control have recommended that the definition of
asbestos encompass cleavage fragments from the non-fibrous
forms of these minerals. EPA recognizes there is considerable
controversy regarding the toxicity of fiber-like cleavage
fragments. Because of this uncertainty, more work needs to be
done to understand which of the many forms of asbestos or
asbestos-like fibers are associated with adverse health
effects. To this end, EPA is engaged in a number of activities
to update and improve our understanding of the human health
effects associated with asbestos exposure.
EPA is currently developing a set of toxicological and
epidemiological research projects to address data gaps and
scientific uncertainty regarding the health effects from
exposure to the Libby amphibole and other asbestiform fibers. A
more detailed description of the Agency's efforts has been
included in my written testimony.
In conclusion, EPA will continue its efforts to increase
our understanding on the health effects from asbestos and
mineral fiber exposure. These efforts by EPA and its partners
will provided needed health effects data and help inform
Federal, State and local decisionmaking on how best to reduce
and mitigate potential exposures.
I will be pleased to answer any questions that the
committee may have on these issues. Thank you.
[The prepared statement of Dr. Miller follows:]
Statement of Captain Aubrey Miller, M.D., MPH, U.S. Public Health
Service, U.S. Environmental Protection Agency
Good morning Madame Chairman and members of the committee. I am
Captain Aubrey K. Miller, MD., MPH, a physician in the U.S. Public
Health Service and a Senior Medical Officer and Toxicologist for the
U.S. Environmental Protection Agency (EPA), Region 8 Office. In
addition to my experiences prior to working for the federal government
caring for patients suffering from asbestos-related disease as a Board
Certified occupational physician, over the last eight years my work has
been directly focused on improving our understanding of the health
effects associated with asbestos exposure in Libby, Montana. Further,
the early activities of my involvement, while employed in the
Department of Health and Human Services (DHHS) Region 8 Office, were
focused on strengthening the health care infrastructure of the Libby
community to better care for those affected by this terrible tragedy.
Thank you for the opportunity to discuss EPA's perspective and progress
in understanding the current state of the science concerning the human
health effects associated with exposure to asbestos.
definitions of asbestos
Asbestos is a general term for fibrous silicate minerals, including
minerals in the amphibole and serpentine classes. A 1971 National
Academy of Sciences (NAS) report distinguished the general term
``asbestos'' and commercial varieties as follows:
``Asbestos'' is a generic term for a number of hydrated
silicates that, when crushed or processed, separate into
flexible fibers made up of fibrils. [footnote omitted].
Although there are many asbestos minerals, only six are of
commercial importance: Chrysotile, a tubular serpentine
mineral, accounts for 95 percent of the world's production; the
others, all amphiboles, are amosite, crocidolite,
anthophyllite, tremolite, and actinolite. (NAS 1971).
With respect to a definition of asbestos which is most relevant to
our current understanding of health effects, the Centers for Disease
Control, National Institute for Occupational Safety and Health (NIOSH),
in 1990 testimony before the Occupational Safety and Health
Administration (OSHA), and reiterated again in 2001, broadened its
science-based definition of ``asbestos'' as a result of concerns about
the microscopic identification of the six commercial forms of asbestos
minerals. The six minerals can also occur in a non-fibrous (so-called
``massive'') form. The non-fibrous mineral forms of the six asbestos
minerals can be found geologically in the same ore deposits in which
the fibrous asbestos minerals occur or in deposits where other
commercially exploited minerals are mined (e.g., industrial grade
talc). ``Cleavage fragments,'' small mineral shards that are often
microscopically indistinguishable from typical asbestos fibers, can be
generated from the non-fibrous forms of the asbestos minerals during
their handling, crushing, or processing, and these ``cleavage
fragments'' are often microscopically indistinguishable from typical
asbestos fibers of the (fibrous) minerals.
The elemental composition of the six asbestos minerals can vary
slightly as a result of geological conditions such as pressure,
temperature, or proximity of other minerals. Recognizing these
variations in elemental composition, NIOSH stated that the six asbestos
minerals can be defined by their ``solid-solution'' mineral series. For
example, the mineral series tremolite-ferroactinolite contains the
asbestos mineral actinolite. These mineral series are considered solid-
solutions in which cations (i.e., sodium, calcium, magnesium, iron,
etc.) are replaced by other cations which can affect the elemental
composition of the mineral without significantly altering the
structure.
NIOSH bases this expanded ``asbestos'' definition--encompassing the
entire solid-solution mineral series for each of the six currently
regulated asbestos minerals and including cleavage fragments from the
non-fibrous forms of these minerals--on scientific evidence from
cellular and animal studies suggesting that dimension, specifically
length and diameter, as well as durability, may be more critical
factors in causing disease than chemical or elemental composition [CDC
2001]. EPA recognizes that there is considerable controversy regarding
the toxicity of fiber-like cleavage fragments, and additional research
will help to improve understanding of important health determinants.
where asbestos occurs naturally
As a natural mineral, serpentine and amphibole deposits may be
present as natural outcroppings. The fibers present may exhibit a range
of mineral forms and morphologies. There are many communities where
these minerals are present in native soils. Community members have been
exposed to elevated ambient levels of these materials in outdoor air,
to materials brought into the home (e.g., fibrous clays used for
interior wall coverings), and during outside activities like farming.
Residents in communities exhibit health effects similar to those noted
in the occupation cohorts including pleural fibrosis, asbestosis, lung
cancer, and mesothelioma. These deposits in some cases include minerals
which were commercially mined and milled (chrysotile and crocidolite).
In addition, health effects have also been seen in communities that are
exposed environmentally to actinolite, tremolite, and erionite.
Erionite, which is not asbestos, represents a third class of silicate
minerals, zeolites or framework silicates. EPA is currently evaluating
sites impacted by natural outcroppings of silicate minerals including
actinolite-tremolite, anthopholyte, chrysotile, anthopholyte and
erionite.
health effects
Asbestos has been classified as ``carcinogenic to humans'' by EPA
(1986) and as a ``Class A'' carcinogen by the World Health
Organization. Although mesothelioma and lung cancer are the
malignancies most consistently and strongly associated with such fiber
exposures, cancers of the gastrointestinal tract (Jarvholm et al. 1984;
Kolonel et al. 1985; Sanden, Naslund, & Jarvholm 1985), larynx (Blot et
al. 1980; Burch et al. 1981; von Bittersohl 1977; Rubino et al. 1979),
pancreas, (Selikoff and Seidman 1981), and ovary (Acheson et al. 1982;
Wignall and Fos 1982) have also been identified. A recent review by the
National Academy of Sciences Institute of Medicine concluded there was
sufficient evidence to infer a causal association for laryngeal cancer;
but, the evidence for pharyngeal, stomach and colorectal cancers is
only suggestive, not sufficient (NAS 2006).
The noncancerous conditions related to asbestos exposure may be
more prevalent than cancer and just as debilitating and lethal.
Exposure to asbestos fibers via inhalation is associated with noncancer
diseases to the pleura and lungs. The American Thoracic Society (ATS)
recently defined nonmalignant asbestos-related disease to include the
conditions of interstitial pulmonary fibrosis (asbestosis), benign
asbestos-related pleural effusions, pleural fibrosis (both
circumscribed fibrosis, or plaques, and diffuse fibrosis), and
obstruction of pulmonary airflow (ATS Documents 2004). Rounded
atelectasis, a benign form of subpleural lung collapse, has also been
associated with asbestos exposure (Terra-Filho et al. 2003). Asbestos
diseases have latency periods ranging from a year to several decades,
depending on the health endpoint of concern. The latency varies for
nonmalignant effects, from approximately a year for pleural effusion to
several years for asbestosis (Cugell and Kamp 2004). Once established,
asbestos-related nonmalignant interstitial and pleural disorders may
remain static or progress in severity in the absence of continued
exposure, but they rarely regress (Becklake 1994). Asbestos-related
pleural effects are often found in individuals without occupational
exposures and even asbestosis has been noted in some communities where
materials may have been brought into homes (Luce et al. 2000; Luce et
al., 2004; Bernardini et al. 2003; Luo et al. 2003; Baumann et al.
2007; Metintas et al. 2003).
There is a scientific debate concerning the differences in the
extent of disease caused by different fiber types and sizes. Some of
these differences may be due to the physical and chemical properties of
the different fiber types. For example, several studies suggest that
amphibole asbestos types (tremolite, amosite, and especially
crocidolite) may be more harmful than chrysotile, particularly for
mesothelioma. Other data indicate that fiber size dimensions (length
and diameter) are important factors for cancer-causing potential. Some
data indicate that fibers with lengths greater than 5.0 mm are more
likely to cause injury than fibers with lengths less than 2.5mm. (1 mm
is about 1/25,000 of an inch). Additional data indicate that short
fibers can contribute to injury. This appears to be true for
mesothelioma, lung cancer, and asbestosis. However, fibers thicker than
3.0 mm are of lesser concern, because they appear to have less of a
chance for penetrating to the lower regions of the lung. (ATSDR Tox
Profile for Asbestos (2001), p. 6.)
Because of this uncertainty, more work needs to be done to
understand which of the many forms of asbestos or asbestos-like fibers
associated with adverse health effects require additional study. To
this end, EPA in engaged in an asbestos toxicology research program.
epa's health assessment activities for asbestos and silicate mineral
fibers
EPA's Integrated Risk Information System (IRIS) database provides
health assessments and tools for quantitative risk characterization
which represent a consensus agency position. The current asbestos
assessment was posted on IRIS in 1988 and provides cancer risk
estimates based on a meta-analysis of 14 studies of workers exposed to
commercial asbestos (primarily chrysotile, amosite, and crocidolite).
The risk estimate represents both lung cancer and mesothelioma risk. At
that time, EPA discussed many of the complexities regarding the health
effects of asbestos, including: mineral form, fiber dimension, and
fiber morphology. However, the exposure data available in the
epidemiologic literature did not allow for refinement of the cancer
risk estimate based on these factors (EPA 1986).
In 1991, the EPA published a Health Assessment on vermiculite,
reviewing the studies available at that time on workers exposed to
amphibole asbestos-contaminated vermiculite (Libby, MT and the Enoree
region of South Carolina). The document concluded that weight of
evidence for asbestos-contaminated vermiculite is sufficient to show a
causal relationship for increased lung cancer in miners and millers
(EPA 1991).
In preparation to update the asbestos health assessment, EPA held
several conferences regarding asbestos toxicity, convening national
experts on the mechanisms of fiber toxicity: ``Asbestos Health Effects
Conference'' in 2001 and ``Mechanisms of Toxicity Workshop'' in 2003.
In 2004 EPA initiated a health assessment focused on the noncancer
effects of asbestos. In February 2006, EPA announced that it would
begin a cancer health assessment for asbestos as well. In expectation
of updating the cancer assessment, EPA has coordinated with NIOSH to
reanalyze historical worker cohorts with state of the art exposure
measurements for a key chrysotile study (Dement et al. 1994). EPA is
continuing this collaboration and is working with nationally recognized
experts from academia to conduct similar reanalysis, using state-of-
the-art exposure measurements for key studies of workers exposed to
amosite (Levin et al. 1998; Seidman et al. 1986).
As part of its ongoing activities, EPA is developing a set of
research projects to assess the dosimetric and toxicologic effects of
amphibole fiber-containing vermiculite ore from Libby, Montana. The
objective of these projects is to address data gaps and scientific
uncertainty for the quantitative characterization of health risks from
exposure to the Libby amphibole and other asbestos-form fibers. The
research plan for these projects was initiated from the recommendations
of a multi-agency meeting in January 2007 and is now being revised in
response to external peer review. Funding has been approved and
research is anticipated to commence by July 2007. The research involves
the following assessment studies:
Libby Amphibole RfC Development;
Libby Amphibole Cancer Assessment;
Fiber Size Distribution in Libby Vermiculite;
Dosimetry Model Development and Simulation Studies;
In Vitro Dissolution Assays;
In Vitro Toxicity Endpoints;
Comparative Toxicology In Mice and Rats;
Inhalation Toxicology In Rats;
New Epidemiologic Information From Libby, Montana and
other cohorts; and
Interim Risk Methodology For Quantification Of Cancer Risk
From Inhalation Exposure to Asbestos.
exposure and exposure mitigation
Over the past several years, EPA conducted research designed to
reduce uncertainties in asbestos exposure scenarios. This work was a
collaboration among ORD's National Exposure Research Laboratory,
National Risk Management Research Laboratory, and National Health and
Environmental Effects Research Laboratory. A report addressing the
state-of-the-science for various exposure scenarios was completed in
2006. Additionally, a database of exposures, doses, and physical-
chemical properties has been developed for more than 40 asbestos
fibers. An air sampling study was also completed, as was an analysis of
the Comprehensive Soil Method.
Workplace exposure mitigation practices have been in place for
decades. To minimize exposure from building demolition, EPA has been
working on an alternative to the National Emissions Standards for
Hazardous Air Pollutants (NESHAP) method for demolition of buildings
containing asbestos. Also, the California Air Resources Board and the
Agency for Toxic Substances and Disease Registry (ATSDR) provide advice
for limiting exposure to naturally occurring asbestos.
closing
EPA will continue its efforts to increase our understanding on the
health effects from asbestos and mineral fiber exposure. These efforts
by EPA and those of its Federal, state, and local partners will provide
needed health effects data and help inform Federal, state, and local
decision making on how best to reduce and mitigate potential exposure.
I will be pleased to answer any questions that the committee may have
on these issues.
references:
Acheson, E.D., Gardner, M.J., Pippard, E.C. & Grime, L.P. (1982).
Mortality of two groups of women who manufactured gas masks from
chrysotile and crocidolite asbestos: a 40-year follow-up. Br. J. ind.
Med., 39, 344-348.
Baumann F, Rougier Y, Ambrosi JP, & Robineau BP (2007). Pleural
mesothelioma in New Caledonia: an acute environmental concern. Cancer
Detect Prev. 2007;31(1):70-6.
Becklake, M. R. (1994). ``Symptoms and pulmonary functions as
measures of morbidity'', Ann.Occup.Hyg., vol. 38, no. 4, pp. 569-80,
418.
Bernardini P, Schettino B, Sperduto B, Giannandrea F, Burragato F,
& Castellino N. (2003). [Three cases of pleural mesothelioma and
environmental pollution with tremolite outcrops in Lucania] G Ital Med
Lav Ergon. 2003 Jul-Sep; 25(3):408-11. Italian.
Blot, W.J., Morris, L.E., Stroube, R., Tagnon, I. & Fraumeni, J.F.,
Jr (1980). Lung and laryngeal cancers in relation to shipyard
employment in coastal Virginia. J. Natl Cancer Inst., 65, 571-575.
Burch, J.D., Howe, G.R., Miller, A.B. & Semenciw, R. (1981).
Tobacco, alcohol, asbestos, and nickel in the etiology of cancer of the
larynx: a case-control study. J. Natl Cancer Inst., 67, 1219-1224.
CDC 2001 Testimony of Kathleen M. Rest, Ph.D., M.P.A.
Acting Director, CDC's National Institute for Occupational Safety
and Health Before the committee on Health, Education, Labor and
Pensions, U.S. Senate July 31, 2001; http://www.cdc.gov/washington/
testimony/ws073101.htm]
Cugell, D.W. & Kamp, D.W. (2004). ``Asbestos and the pleura: a
review'', Chest, vol. 125, no. 3, pp. 1103-1117.
Dement, J. M. & Brown, D. P. (1994). ``Lung cancer mortality among
asbestos textile workers: a review and update''. Ann.Occup.Hyg., vol.
38, no. 4, pp. 525-32, 412.
Jarvholm, B., Holmberg, E., Naslund, P. E., Sanden, A., &
Zettergren, L. (1984). ``[Mesothelioma of the peritoneum--a neglected
diagnosis?]''. Lakartidningen, vol. 81, no. 8, pp. 644-645.
Kolonel, L. N., Yoshizawa, C. N., Hirohata, T., & Myers, B. C.
(1985). ``Cancer occurrence in shipyard workers exposed to asbestos in
Hawaii''. Cancer Res., vol. 45, no. 8, pp. 3924-3928.
Levin, J, McLarty, J., Hurst, G., Smith, A., & Frank, A. (1998).
Tyler asbestos workers: mortality experience in a cohort exposed to
amosite. Occupational and Environmental Medicine, 55:155-160.
Luce D, Billon-Galland MA, Bugel I, Goldberg P, Salomon C, Fevotte
J, Goldberg M. (2004). Assessment of environmental and domestic
exposure to tremolite in New Caledonia. Arch Environ Health.;59(2):91-
100.
Luce D, Bugel I, Goldberg P, Goldberg M, Salomon C, Billon-Galland
MA, Nicolau J, Quenel P, Fevotte J, & Brochard P. (2000). Environmental
exposure to tremolite and respiratory cancer in New Caledonia: a case-
control study. Am J Epidemiol.;151(3):259-65.
Luo, S., Liu, X., Mu, S., Tsai, S. P., & Wen, C. P. (2003).
``Asbestos related diseases from environmental exposure to crocidolite
in Da-yao, China. I. Review of exposure and epidemiological data''.
Occup Environ Med, vol. 60, no. 1, pp. 35-41.
Metintas, M., Metintas, S., Hillerdal, G., Ucgun, I., Erginel, S.,
Alatas, F., & Yildirim, H. (2005). ``Nonmalignant pleural lesions due
to environmental exposure to asbestos: a field-based, cross-sectional
study''. Eur.Respir.J., vol. 26, no. 5, pp. 875-880.
National Academy of Sciences (1971). Asbestos - The Need for and
Feasibility of Air Pollution Controls. NAS Press, Washington, DC.
National Academy of Sciences (2006). Asbestos: Selected Cancers.
NAS Press, Washington, DC.
Rubino, G.F., G. Piolatto, M.L. Newhouse, G. Scansetti, G.A.
Aresini and R. Murrary (1979). Mortality of chrysotile asbestos workers
at the Balangero mine, Northern Italy. Br. J. Ind. Med. 36: 187-194.
Sanden, A., Naslund, P.E., & Jarvholm, B. (1985). ``Mortality in
lung and gastrointestinal cancer among shipyard workers''.
Int.Arch.Occup.Environ.Health, vol. 55, no. 4, pp. 277-283.
Seidman, H., Selikoff, I.J., & Gelb, S.K. (1986). ``Mortality
experience of amosite asbestos factory workers: dose-response
relationships 5 to 40 years after onset of short-term work exposure''.
Am.J.Ind.Med., vol. 10, no. 5-6, pp. 479-514.
Selikoff, I.J. & Seidman, H. (1981). Cancer of the pancreas among
asbestos insulation workers. Cancer, 47 (Suppl.), 1469-1473.
Terra-Filho, M., Kavakama, J., Bagatin, E., Capelozzi, V. L., Nery,
L. E., & Tavares, R. (2003). ``Identification of rounded atelectasis in
workers exposed to asbestos by contrast helical computed tomography''.
Braz. J. Med. Biol.Res., vol. 36, no. 10, pp. 1341-1347.
U.S. EPA. (1986). Airborne Asbestos Health Assessment Update.
Prepared by the Environmental Criteria and Assessment Office, Research
Triangle Park, NC. EPA 600/8-84/003F.
U.S. EPA. (1991). Health Assessment Document for Vermiculite.
Office of Health and Assessment, Washington, DC. EPA/600/8-91/037.
von Bittersohl, G. (1977). On the problem of asbestos-induced
carcinoma of the larynx (Ger.). Z. ges. Hyg., 23, 27-30.
Wignall, B.K. & Fos, A.J. (1982). Mortality of female gas mask
assemblers. Br. J. Ind. Med., 39, 34-38).
Senator Boxer. Thank you very much.
Our next and last panelist is Dr. Melanie Marty, chief, Air
Toxicology and Epidemiology Branch from the California EPA. We
welcome you.
STATEMENT OF MELANIE MARTY, Ph.D., CHIEF, AIR TOXICOLOGY AND
EPIDEMIOLOGY BRANCH, CALIFORNIA ENVIRONMENTAL PROTECTION
AGENCY, OFFICE OF ENVIRONMENTAL HEALTH HAZARD ASSESSMENT
Ms. Marty. Good morning, Madam Chair and members of the
committee. I am a toxicologist with Cal/EPA.
My testimony today focuses on naturally occurring asbestos
in California, the assessment of potential health impacts from
exposure and ways California is addressing exposure to
naturally occurring asbestos.
Asbestos was identified as a toxic air contaminant in 1986
in California, based on the evidence that you just heard,
asbestosis, lung cancer and mesothelioma in workers, and on the
ubiquitous presence of asbestos in urban air due to its
widespread use.
The health effects assessment conducted for the
identification of asbestos as a toxic air contaminant was based
on studies of workers exposed to asbestos in a number of
industrial settings. We evaluated the relationship between the
extent of exposure to asbestos and the subsequent development
of asbestos-related disease in the workers with a focus on the
cancers caused by asbestos in order to assess cancer risk from
exposure to asbestos of the general population in urban air.
The workers in the occupational studies we used in our risk
assessments were exposed to mixed forms of asbestos from
relatively pure chrysotile to predominantly amphibole. Both
types of asbestos are found naturally in the Sierra foothills
and elsewhere in California and frequently together.
When asbestos fibers become airborne, they can be inhaled
deep into the lung. Some are cleared by normal physiological
processes, but many fibers remain in the lung tissue
essentially forever. Inhaled asbestos fibers can migrate to the
lining of the chest wall, the pleura, and also be transported
to other organs. There is no question that asbestos is a human
carcinogen. You have heard my colleagues mention that as well.
It is regulated as such in the United States by OSHA, in
California and other countries.
While many researchers consider the amphiboles to be
substantially more potent than chrysotile in causing
mesothelioma, toxicology studies in animals and human studies
show that all forms of asbestos can cause mesothelioma,
including chrysotile, and that further, are more or less
equally potent in producing lung cancer, which accounts for the
majority of the asbestos-induced cancers.
The disease that has been most well investigated in
relation to exposures to naturally occurring asbestos is
mesothelioma, in part because it is a rare cancer and it is
strongly associated with asbestos exposure. There are many
studies that describe mesothelioma in people exposed as a
result of the presence of asbestos in the soil in their
communities in Greece, Turkey, New Caledonia, China and
elsewhere. Many but not all of the mesotheliomas in these
populations were related to use of the amphibole-containing
soils in the community in various ways.
Further, some studies have shown elevated mesothelioma and
lung cancers in populations in close proximity to mines or
asbestos factories where predominantly chrysotile asbestos-
containing products were made. It is difficult to use these
studies to develop quantitative estimates of risk that
Californians may face from naturally occurring asbestos, but
these studies heighten concern about environmental exposure.
The typical approach for assessing risk from environmental
exposure is to use a long-term average concentration of the
carcinogen in air. That gets difficult in the case in El Dorado
County, where you have asbestos in the soil, because the
exposures of concern are primarily episodic, short-term
exposures to relatively high levels of asbestos occurring from
activities that release soil-borne fibers into the air, for
example, driving down a dirt road or playing baseball in
asbestos-contaminated soil, making it difficult to actually
quantitatively assess risk. However, episodic exposures are
important in view of the long time asbestos fibers can remain
in the body and the cumulative nature of the injury and risk.
Also, there is general concern about exposing children to
any carcinogen. Children breathe more on a body-weight basis
than adults, thus experiencing higher exposures in the same
setting. Cancer has a long latency between exposure and
manifestation of the disease. So when exposure occurs during
childhood, the risk from carcinogens, including asbestos, is
higher, because there is more time to develop the disease.
Cal/EPA estimated risks from episodic exposures related to
serpentine rock used for surfacing unpaved roads. The agency
conducted a number of studies, measuring fibers that became
airborne after vehicles drove down such roads. Furthermore, EPA
Region 9 conducted activity-based sampling and showed elevated
levels of airborne fibers released by soil-disturbing
activities, including sports and mountain biking, running and
so forth.
As a result of such investigations, the California Air
Resources Board promulgated two airborne control measures
designed to reduce the allowable level of asbestos in aggregate
use for surfacing and to reduce dust generation during
construction and grading activities. Cal/EPA also has mandates
to ensure school sites are free of asbestos. Furthermore, we
worked with local air districts and EPA Region 9 to educate
citizens on the presence and dangers of asbestos in the soil
and how they can reduce their exposures.
In closing, many studies have found mesothelioma, lung
cancer and pleural abnormalities in populations exposed to
naturally occurring asbestos. The presence of asbestos fibers
in soil can pose elevated risks of cancer when the fibers are
released into the air from activities that disturb the soil,
such as construction activities, driving on unpaved roads and
sports. These episodic exposures are important and mitigation
measures are necessary to reduce exposure to naturally
occurring asbestos.
Thank you.
[The prepared statement of Dr. Marty follows:]
Statement of Melanie Marty, Ph.D., Chief, Air Toxicology and
Epidemiology Branch, California Environmental Protection Agency, Office
of Environmental Health Hazard Assessment
Good morning Senator Boxer and Members of the committee. My name is
Melanie Marty. I am a toxicologist in the California Environmental
Protection Agency and I direct the Air Toxicology and Epidemiology
Branch in the Office of Environmental Health Hazard Assessment, or
OEHHA. We are the Cal/EPA department mandated to assess the health
risks of exposure to chemicals in our environment. My testimony today
focuses on naturally occurring asbestos, or NOA, in California, the
assessment of potential health impacts from exposure, and ways
California is addressing exposure to NOA.
Asbestos was identified as a Toxic Air Contaminant in 1986 in
California, based on the evidence that asbestos causes asbestosis, lung
cancer and mesothelioma in workers, and the ubiquitous presence of
asbestos in urban air due to its widespread use in brake lining,
building materials and so forth.
The health effects assessment conducted for the identification of
asbestos as a Toxic Air Contaminant was based on studies of workers
exposed to asbestos in a number of industrial settings (such as textile
and other products manufacturing). We evaluated the relationship
between extent of exposure to asbestos and subsequent development of
asbestos-related disease in the workers, with a focus on the cancers
caused by asbestos, in order to assess cancer risk from exposure to
asbestos in ambient air.
The workers in the occupational studies we used in our risk
assessments were exposed to mixed forms of asbestos ranging from
relatively pure chrysotile to predominantly amphibole. Both types of
asbestos are found naturally in the Sierra foothills, frequently
together.
When asbestos fibers become airborne, they can be inhaled deep into
the lung. While some are cleared by normal physiological processes,
many fibers remain in the lung tissue forever. Inhaled asbestos fibers
can migrate from the lung to the pleura (the lining of the chest wall),
and can be transported to other organs as well.
There is no question that asbestos is a human carcinogen, and it is
classified as such by the International Agency for Research on Cancer,
and the U.S. EPA. Asbestos is regulated as a human carcinogen by OSHA,
as well as by many countries around the globe.
As you have heard from other witnesses, in occupational settings,
chrysotile and amphibole asbestos exposure causes lung cancer and
mesothelioma, a rare and fatal cancer of the lining of the chest wall
and abdomen, and nonmalignant respiratory disease such as asbestosis.
While many researchers consider the amphiboles to be substantially more
potent than chrysotile in causing mesothelioma, all forms of asbestos
can cause mesothelioma and are more or less equipotent in producing
lung cancer, which accounts for a majority of asbestos-induced cancers.
The disease that has been most well investigated in relation to
exposures to naturally occurring asbestos is mesothelioma, in part
because it is a rare cancer and strongly associated with asbestos
exposure.
Although initial studies focused on workers, there are many studies
that describe mesothelioma in people exposed as a result of the
presence of asbestos in the soil in their communities in Greece,
Turkey, New Caledonia, and China. Many but not all of the mesotheliomas
in these populations were related to use of the amphibole-containing
soils in the community in various ways. Further, some studies have
shown elevated mesothelioma and lung cancers in populations in close
proximity to mines or asbestos factories where predominantly chrysotile
asbestos-containing products were made. I submitted a short
bibliography of key papers (there are many more studies) regarding
environmental exposures to asbestos and cancer as well as a copy of
some of these papers for your information. While it is difficult to use
these studies to develop quantitative estimates of risks that
Californians may face from naturally occurring asbestos, these studies
heighten concerns about environmental exposures to asbestos.
I'd like to make a few comments on the difficulties of assessing
risk from exposure to naturally-occurring asbestos present in the soil.
The typical approach for assessing risk from environmental exposure to
airborne carcinogens is to use long-term average concentrations of the
carcinogen in the air in the calculation.
But in the case of naturally-occurring asbestos in the soil, the
exposures of concern are primarily episodic short-term exposures to
relatively high levels of asbestos occurring from activities that
release soil-borne fibers into the air, for example, while driving down
a dirt road, or playing in asbestos-contaminated soil. It is difficult
to determine an average air concentration to use in the typical cancer
risk assessment calculation. However, episodic exposures to asbestos
are important, in view of the long time asbestos fibers can remain in
the body and the cumulative nature of the injury and risk.
There is general concern among scientists about exposing children
to any carcinogen. Children breathe more on a body weight basis and
thus experience higher doses than an adult in the same setting. Cancer
has a long latency between exposure and manifestation of the disease;
this is particularly true with asbestos-induced mesothelioma where
there appears to be a long average latency, on the order of 30 to 40
years in most cases. When exposure occurs during childhood, as opposed
to adulthood, the risk from carcinogens including asbestos is higher
because there is more time to develop the disease.
Cal/EPA has tried to estimate risk from episodic exposures related
to serpentine rock used for surfacing unpaved roads. The Agency
conducted studies which measured asbestos fibers in the air after
vehicles have driven down such roads. Any way one cuts the data, it is
clear that asbestos fiber exposures are elevated, particularly very
close to these roads, and the cancer risk is elevated as well. Further,
USEPA Region 9 conducted activity-based sampling, measuring the
airborne fibers released by soil-disturbing activities including
playing baseball, riding a mountain bike or running along an unpaved
trail. These measurements clearly indicate that activities that disturb
the soil result in locally elevated asbestos fiber concentrations.
I would like to touch briefly on some of the mitigation measures
that have been put in place in California. The California ARB
promulgated an airborne toxic control measure designed to reduce the
allowable level of asbestos in aggregate and other materials used for
surfacing unpaved roads. The local Air Pollution Control Districts in
areas with asbestos in the soil have adopted measures to reduce dust
generation during construction and grading activities. The Dept of
Toxic Substances Control as part of its mandate to ensure that school
sites are safe to build on, evaluates sites for the presence of
asbestos in the soil, and requires mitigation and maintenance of such
sites to reduce as much as is practicable the exposure of children
attending these schools. In addition, there has been an effort by ARB
and the local air districts to educate citizens on the presence of and
dangers of asbestos in the soil, and on ways they can reduce their
exposures. Information including fact sheets on these activities have
been submitted for your review. And finally, we have been actively
working with USEPA Region 9 to evaluate exposures and risk and provide
information to the public in El Dorado County about asbestos in their
soil.
In closing, many studies have found mesothelioma, lung cancer, and
pleural abnormalities in populations exposed to naturally occurring
asbestos. The presence of asbestos fibers in soil can pose elevated
risks of cancer (above background asbestos risks) when the fibers are
released into the air from activities that disturb the soils.
Construction activities, driving on unpaved roads surfaced with
asbestos-containing rock, and other activities that people do
(including sports) can elevate the concentration of airborne fibers in
the immediate vicinity and expose individuals engaged in those
activities to elevated fiber levels. These episodic exposures are
important and increase the risk of asbestos-induced cancers to a level
that is of regulatory concern. Finally, mitigation measures are
necessary to reduce exposures to NOA.
Thank you for the opportunity to testify.
______
Some Key References for Cancer from Environmental
Exposures to Asbestos
Berry M. (1997) Mesothelioma incidence and community asbestos
exposure. Environ Res 75:34-40.
Horton K et al. (2006) A review of the Federal Governmen's Health
Activities in Response to Asbestos-Contaminated ore found in Libby,
Montana. Inhalation Toxicol 18: 925-40.
Luce D et al. (2000) Environmental exposure to tremolite and
respiratory cancer in New Caledonia: A case-control study. Am J
Epidem151:259-65.
Luo S, et al. (2003) Asbestos related diseases from environmental
exposure to crocidolite in Da-yao, China. I. Review of exposure and
epidemiological data. Occup Environ Med 60:35-42.
Magnani C et al. (1995) Pleural malignant mesothelioma and non-
occupational exposure to asbestos in Casale Monferrato, Italy. Occup
Environ Med 52:362-7.
Maule MM, et al. (2007) Modeling mesothelioma risk associated with
asbestos exposure. Environ Health Perspect. Doi:10.1289/ehp.9900
(available at http://dx.doi.org/) online March 22, 2007.
Metintas S, et al. (2002) Malignant mesothelioma due to
environmental exposure to asbestos:Folow-up of a Turkish cohort living
in a rural area. Chest 122:2224-9.
Paoletti L et al. (2000) Unusually high incidence of malignant
pleural mesothelioma in a town of Eastern Sicily: An epidemiological
and environmental study. 55:392-8.
Sakellariou K et al. (1996) Malignant pleural mesothelioma from
nonoccupational asbestos exposure in Metsovo (north-west Greece): slow
end of an epidemic? Eur Respir L 9:1206-10.
Smith A and Wright C. (1996) Chrysotile asbestos is the main cause
of pleural mesothelioma. Am J Ind Med 30:252-66.
california government web sites related to naturally occurring asbestos
1. The California EPA, Air Resources Board has a number of fact
sheets and posted documents related to the identification of asbestos
as a Toxic Air Contaminant and the presence of asbestos in California
soils:
http://www.arb.ca.gov/toxics/asbestos/asblinks.htm
http://www.arb.ca.gov/toxics/asbestos/asbestos.htm
The following provides a link to the 1986 health effects assessment
for asbestos as a Toxic Air Contaminant:
http://www.arb.ca.gov/toxics/id/summary/summary.htm
2. The California EPA, Office of Environmental Health Hazard
Assessment has a fact sheet on asbestos health hazards:`
http://www.consrv.ca.gov/cgs/minerals/hazardous--minerals/asbestos/
index.htm
3. The California EPA, Department of Toxic Substances control
school site assessment program evaluates school sites for presence of
naturally occurring asbestos as part of their program to ensure
adequate protection of public health at schools. They have several
documents regarding activities to reduce exposure located at the
following link:
http://www.dtsc.ca.gov/Schools/index.cfm#Environmental--
Advisories--and--Guidance
4. The California Geological Survey web site contains numerous
publications regarding the presence of asbestos in California soils
including maps of various areas with known asbestos in the soil.:
http://www.consrv.ca.gov/cgs/minerals/hazardous--minerals/asbestos/
index.htm
__________
Senator Boxer. Thank you very much.
I want to thank the panel. Let me try to cut to the chase
here. I have a few questions for Dr. Weissman.
Dr. Weissman, this country still imports more than 2,500
metric tons of asbestos a year, as well as products that
contain asbestos. Can you describe the types of diseases
associated with the use of these materials and whether these
disease may be a concern for people who use these products in
or around their homes?
Dr. Weissman. As we have heard, the types of diseases that
are caused by asbestos exposure break into cancerous conditions
and non-cancerous conditions. Among the non-cancerous
conditions are asbestosis, which is a fibrosing lung disease
that causes shortness of breath and impaired respiratory
function. Also, asbestos can damage the pleura, which is the
tissue lining the surfaces of the lung and chest wall,
resulting in fibrosis. It can either by plaques or more
extensive fibrosis that can constrict the lungs.
From the side of carcinogenic effects, lung cancer,
mesothelioma, there are also associations with cancer of the
larynx and cancers of the gastrointestinal tract.
With regard to the impact of continued exposure to
asbestos, in protecting workers, there is something called the
industrial hygiene hierarchy of controls, which is the approach
to reducing exposure to reduce disease. Really the No. 1 best
way to reduce disease caused by a hazardous exposure is to
eliminate the exposure. The No. 2 thing that we think about is
whenever possible substituting for other products that are less
hazardous. Then we get into other kinds of controls, like
engineering controls and respirators.
Senator Boxer. So limiting exposure would certainly be
achieved if we were to, I am not asking your opinion on this,
stop the importation so the products wouldn't have it, that
would limit the exposure, obviously, to the products that were
still on the market. So I ask you specifically if it would
impact people around the home, who might be exposed. I am
assuming you would say yes. You are not making a distinction
between workers and people in their homes. You are saying if
you are exposed to it, it could be a problem, is that correct?
Dr. Weissman. That is correct.
Senator Boxer. OK. I just wanted to note, I am taking this
from the USGS Minerals Yearbook, the importations include
corrugated cement sheet, flat cement panel sheet, cement pipe,
tube and pipe fittings, other cement products, yarn and thread,
cord and string, woven or knitted fabric, articles for us in
civil aircraft gaskets, other building materials, brake lining
and pads, mounted brake linings for tractors. I am going to put
this into the record without objection.
[The referenced material follows:]
Senator Boxer. I guess as I listen to you, and I so
appreciate the panel, we had some questions from Senator Vitter
and raised by my Ranking Member on a certain type of product
that perhaps that is a safe form. I wanted to ask you about
chrysotile. What I want to know is whether exposure to this
type of asbestos has adverse health impacts.
Dr. Weissman. Yes.
Senator Boxer. What would they be?
Dr. Weissman. Yes, chrysotile asbestos is hazardous and has
the same health impacts as other types of asbestos. There is a
debate in the literature over the potency, over whether you
need the same dose of chrysotile to cause one of the health
effects, which is mesothelioma. But it certainly causes all of
the same health effects.
Senator Boxer. So you would agree with Dr. Marty, who made
that point. And I see that Dr. Miller is shaking his head.
OK. I guess my last question is this. In a lot of these
issues, the more vulnerable populations are more at risk. Have
you found that in this whole thing of asbestosis? For example,
if a worker comes home and hugs a child, and he had asbestos
fibers on him, have you had any studies that indicate that the
more vulnerable populations would be more apt to get sicker
earlier, or have there been no studies of that?
Dr. Weissman. We don't have any information from NIOSH
about take-home exposures of families. I would defer to Dr.
Miller on that.
Senator Boxer. Dr. Miller or Dr. Marty, either.
Dr. Miller. With respect to that, our concern is certainly
that children, being exposed at an earlier age, at a minimum
would have a longer period of life to express disease. Those
fibers get into their lungs, they are durable, they are going
to stay in their lungs and they will have that.
Another part of that concern is, are children just more
susceptible, at the developmental time of their life.
Senator Boxer. That is why I asked the question. I wrote a
bill called The Children's Environmental Health Protection Act.
It makes the point that when we set standards for anything,
when we do laws about anything, we have to focus on the
children, because they are developing and it may be more
dangerous.
Dr. Marty, do you have any comment on that, exposure to
most vulnerable, like our children?
Ms. Marty. Yes. I think for children, we also have to
recognize that they probably have higher exposures in the same
setting as an adult, simply because they breathe more on a body
weight basis and particle deposition appears to be higher. This
would probably be the same for fiber in a child's lung than in
an adult's lung.
Senator Boxer. So it is more a proportion of their body,
because of their size. I think the point that Dr. Miller makes
is important as well, that because they would be exposed at
this early age, the disease would take shape at a younger age
than an adult.
Ms. Marty. Yes.
Senator Boxer. So if an adult is exposed at age 30, it may
take how many years on average to get mesothelioma?
Ms. Marty. Thirty, approximately.
Senator Boxer. But if it is a child, they could die at 36
or 40.
Ms. Marty. And there are definitely case reports in the
literature of children being exposed from take-home exposure or
from environmental exposure and having mesothelioma at a
relatively young age.
Senator Boxer. I think, colleagues, this is a really
important point, that when we ban asbestos and we ban materials
like asbestos, we are really protecting the children, in
addition to everybody else.
Senator Vitter.
Senator Vitter. I just wanted to ask all the panelists
their impression or summary of the science on specifically
chlor-alkali production.
Dr. Weissman. I don't have any comments on that. I come at
it purely from my expertise as a physician. And as a physician,
any potential exposure creates the potential for disease. But
as to the criticality of use of asbestos in the process and the
viability of alternatives, it is outside of my expertise.
Dr. Miller. I don't have specific knowledge of that
production. But concerns would be the production, processing,
transportation of these materials and the disposal of it. While
it may be controlled in the work environment, and that can be
done with a lot of toxic substances we deal with, our concerns
with this situation, as with other asbestos products in
commerce would be the concerns of how it is handled, what is
done with it and who may be exposed outside of those controlled
conditions.
Ms. Marty. In other words, someone mined it, someone milled
it, someone packed it in bags before it ever got into the
diaphragm.
Senator Boxer. Senator, do you have any further questions?
Senator Vitter. No, I am fine.
Senator Boxer. OK, thank you.
Senator Lautenberg.
Senator Lautenberg. Thank you, Madam Chairman.
I may have defined the disease incorrectly in my earlier
statement. I used the term asbestosis. I kind of thought that
was a coverall for all forms of the illness derived from
exposure. But the people who came to see me, the family I
described, who, three of them were terminally ill, it was
mesothelioma. And a very close personal friend of mine was a
physician named Dr. Irving Selikoff. He had a practice in
Patterson, NJ, where I earlier described the fact that high
school mates of mine worked in an asbestos factory and suffered
some terrible results as a consequence of that very short
exposure. As I hear you talk, the latency period suggests that
there is a time bomb in the body of these folks who have been
exposed. And when it is going to go off, we are not sure. But
we are sure of one thing, that it is going to explode.
I would ask you this, Dr. Miller. Prevention is the ideal
program to avoid this. Is treatment available for mesothelioma
or related lung disease?
Dr. Miller. Just going back to the first element of your
question, we certainly see asbestos exposures, low exposures,
resulting in disease of great concern. As a matter of fact, we
have been working closely with Dr. Selikoff at Mount Sinai on
research on this. They had actually done work at Patterson and
looked at the households, the home contacts of these workers,
and even people that worked there for just a short time and
looked at the household contacts of those workers. They found
that there was very high elevation of disease in these folks in
their homes, just as a result of the workers' contamination,
and bringing it home.
They even looked at some folks that were either born in the
house or came into the house subsequent to the workers'
stopping, with just that residual contamination. It would
suggest that residual contamination of asbestos in their home
is producing this, not even having an active worker coming in
and out and shaking off their clothes and washing them. So that
is of great concern.
Certainly the efforts are to prevent this, to prevent these
diseases from occurring. I am not familiar with the current
treatments of mesothelioma, and I wouldn't be the best to try
and comment on that. I am not sure if my colleagues here could
do that.
Senator Lautenberg. Do either one of our friends at the
table have any comments on treatment possibilities?
Dr. Weissman. The bottom line is that the pulmonary
fibrosis caused by asbestos exposure, asbestosis, the treatment
is only symptomatic. There is no treatment for the underlying
process. That is also the case for diffuse pleural thickening,
the pleural fibrosis that constricts the lungs, and of the
treatment results for the cancers that are caused by asbestos
are dismal.
Senator Lautenberg. It is essentially a death sentence if
exposed.
Dr. Miller, based on your work at EPA, is there any safe
level of exposure to asbestos that would not cause disease to
follow?
Dr. Miller. Thank you for the question, Senator. Asbestos
is one of the first diseases I studied on entering occupational
health and it is one that I thought we had resolved. A
situation like Libby, MT came up and caused me to go back in
and try to reevaluate this and look at the evidence that is
available. Asbestos was first described to cause disease back
in 50 A.D., by Pliny the Elder. So the fact is, we have been
struggling with this for a long, long time.
The issue of what is safe, to our understanding there is no
safe level that has been identified. The more you are exposed
to asbestos, the more it increases your risk for disease. The
fact is, we have seen disease, while fairly rare, resulting
from people that had relatively inconsequential exposures, very
short exposures, children of a parent that worked in an
asbestos factory for a short time.
So at this point in time, we do not know of a safe level
with respect to asbestos.
Senator Lautenberg. Madam Chairman, may I take 1 more
minute?
Senator Boxer. Yes.
Senator Lautenberg. I would ask this, also. Dr. Miller,
last week a New Jersey school was forced to close its doors
because asbestos was found in one of the classrooms. Are there
Federal resources available to assist State and local school
districts in helping to prevent exposure as a result of that
condition?
Dr. Miller. I can't comment entirely. I know that EPA has
been involved in a number of situations in providing technical
assistance and certainly I personally provide technical
assistance to schools, as you have mentioned, with respect to
trying to do appropriate testing and evaluation and assisting
with discussions about appropriate remediation.
So as far as active programs from the Federal side, I think
it mostly resides in the domain of technical assistance in
trying to help folks evaluate these situations and provide
technical assistance in that respect.
Senator Lautenberg. Thank you. Thank you, Madam Chairman.
Senator Boxer. Thank you. Senator Carper.
Senator Carper. Thank you. My thanks to our witnesses for
coming this morning.
I missed your testimony. I am going to ask you a question,
I will ask you all the same question. I apologize for missing
your testimony. But I just want you to take maybe a minute
apiece and give me what you think should be our takeaway from
your testimony. If we remember nothing else of what you said,
what might that be?
I understand, while they are thinking about that, I
understand, Madam Chair, that Senator Murray is moving forward
with the legislation. I think that is good. I understand that
they are making at least one modification with respect to
production of chlorine and trying to model it after what they
are doing in the European Union. I think that makes sense. I
understand that there is some issue maybe involving last year's
definition involving common rocks to try to make an
accommodation there. Going back to last year's definition, I
think if those two changes are made, I think we have a bill
that is going to roll right out of here and get to the Senate
floor and through the Congress.
With that having been said, let me ask of our panelists,
any takeaway you would like to share with me? Let's start with
Dr. Marty, if we could.
Ms. Marty. I think the upshot is that all forms of asbestos
cause asbestos-related disease, chrysotile, amphiboles, and
even things that aren't quite called asbestos, at least yet.
Environmental exposures are a concern. We have studies across
the world showing an epidemiological way that mesothelioma
incidence is elevated in populations that have naturally
occurring asbestos in their soil and we must reduce exposures
as much as is practicable.
Senator Carper. All right, thank you.
Captain? I used to be a captain in the Navy.
Dr. Miller. I think it is important with respect to this
issue, a lot of what we have been focusing on has kind of been
defined by mineralogists and by techniques that have been
available, older techniques that were available at the time we
started into this. And what we really want to focus on is
capturing those fibers which are causing illness and not being
limited by either antiquated methods or older understandings of
disease and exposure.
So with that, I really want, I guess, to further the
understanding of what are the fibers, what are the minerals
that are causing this problem. There are things about the
fibers we measure, that we measure a certain sector. As Dr.
Weissman mentioned, these phase contrast optical microscopy
fibers. But we know that there are fibers outside of that phase
contrast optical microscope, looking at things under a
microscope versus a big microscope, a TEM microscope, which we
use and have been using in our environmental situation in Libby
and across the country.
So to use this, we see a lot more. Our understanding is
there are a lot of these fibers that have toxic effects. As a
matter of fact, the shapes and what the fibers look like, I
believe Senator Inhofe provided a diagram of pictures of rocks
and fibers. Rocks and fibers, it is not one or the other. They
run across a gamut. They have different sizes and shapes, from
one extreme of being a willowy looking fiber to another extreme
of being kind of a short, stubby, rock-like material.
Senator Carper. Captain, I asked for a 1-minute takeaway. I
want to make sure Dr. Weissman gets to speak. So finish up.
Dr. Miller. So in between, these fibers all have health
effects that we need to be concerned about and captured in
whatever efforts we make to control and ban asbestos.
Senator Carper. Thank you.
Dr. Weissman?
Dr. Weissman. Senator, I have three big points. First,
there are still a lot of people getting disease because of past
exposures. We need to think about them.
Second, even at our permissible exposure limit for
asbestos, there is still an appreciable, detectable risk of
developing diseases, including lung cancer. It is a very
hazardous thing to be exposed to.
Third, and finally, we need research. We need better
exposure assessment methods that include all of the hazards,
that count all of the hazardous fibers to which people are
exposed, not just those that we can see under a light
microscope. And we need to understand the toxicities of all the
different fiber types and drive our public policy based on
that. So there is still room to do better.
Senator Carper. Good. Thank you very much for that
response. My thanks to all of you and thank you, Madam Chair.
Senator Boxer. Let me thank the panel. For my takeaway,
Senator Carper, I took away that there is no safe level of
exposure and the kids are the most vulnerable.
In terms of people still getting sick, I thank you, Dr.
Weissman, because Patty Murray's bill does get help to those
people. I think that is a very important point.
We thank this panel. You have been just terrific, thank you
very much.
We invite our last panel--oh, I forgot that we have been
joined by the wonderful Senator Klobuchar, who I missed, even
though I shook her hand on the way in. I am sorry. Senator, you
are welcome to sit over here. The floor is yours, you can use
it either for questions or an opening statement. You have 5
minutes.
Senator Klobuchar. I just have a few quick questions. That
is of you, Dr. Weissman, first, and about your work with NIOSH.
You talked about the need for research. So I was wondering what
type of monitoring and tracking system NIOSH has in place now
for asbestos-related diseases?
Dr. Weissman. It is not a perfect system by any means. The
primary stream of data that we rely upon for surveillance is
mortality data, which is based on death certificates. Death
certificates are well known to incompletely capture all of the
cases of disease. In addition, since 1999, the electronic data
bases that are abstracted from death records don't include
information about usual occupation and usual illness.
So we can track things that are tightly related to asbestos
exposure, like asbestosis and mesothelioma. But things like
lung cancer that have a background in the population can be
caused by other things than asbestosis. We have some trouble
tracking that. But death data is really the main thing that we
have to work with.
Senator Klobuchar. So do you think there is potential for
under-reporting of asbestos-related illnesses, then?
Dr. Weissman. That is right, because we depend upon the way
that people fill out death certificates. It is well known that
death certificates under-report.
Senator Klobuchar. And you were talking about how there are
more cases being diagnosed from the past, people have gotten
this from the past. Is there a large amount of asbestos-related
product still in existence in the United States?
Dr. Weissman. Yes. There are reservoirs of asbestos in
older buildings where the asbestos is being managed in place
but can still be encountered when buildings are demolished or
renovated. Then there is still important of asbestos-containing
products.
Senator Klobuchar. What kinds of products are those?
Dr. Weissman. Things like automotive friction products,
cement products that contain asbestos.
Senator Klobuchar. Does better equipment, I guess I would
ask all of you this, like ventilators or some kind of personal
dust respirators, does that result in lower illness? Have any
of you looked into this?
Dr. Weissman. Respirators are considered in one of the, in
what we call the industrial hygiene hierarchy. They are the
least preferred method of control, because even if someone
wears them, they might not work. Then also, people have to wear
them whenever they are exposed, and they might not always know
when they are exposed.
So respirators are the least preferred method to protect
people.
Senator Klobuchar. Do you want to add anything to that?
Dr. Miller. I think with respect to protection, NIOSH-
approved personal protection equipment and controls are the
most appropriate.
Senator Klobuchar. I have heard, I think one of the other
witnesses who is going to testify talked about the need to
better coordinate with States to improve the surveillance of
fiber-related illnesses. In fact, I guess I would ask you as
well, Dr. Weissman, about how NIOSH, OSHA, both of them are
currently coordinating with State governments to address
asbestos-related diseases?
Dr. Weissman. NIOSH has an activity with the States to do
State-based surveillance for occupational diseases. So we have
a granting program. Not every State has a grant under that
program. But it supports State-based surveillance for diseases.
Different States have somewhat different portfolios of what
they monitor for. But that is the main NIOSH interaction with
States in terms of surveillance.
In terms of OSHA, our interaction is largely from hazard
surveillance. OSHA, under an agreement with NIOSH, provides us
with their compliance data and allows us to track levels of
exposure, which appears in our surveillance report that we put
out at intervals.
Senator Klobuchar. Thank you very much.
Senator Boxer. Senator Inhofe said he had no questions for
this panel. So we are going to thank you again, and I am sorry,
Senator Klobuchar. I am so pleased that you are here and to
have you on this committee is just so fortunate for America.
Senator Klobuchar. Thank you very much. I am glad you are
here, too.
[Laughter.]
Senator Boxer. Now we will call up our third panel, or our
second panel but third group of witnesses. Barry Castleman,
Sc.D., Environmental Consultant; Ann Wylie, Ph.D., University
of Maryland, Department of Geology; David Weill, M.D.,
director, Lung and Heart-Lung Transplant Program, Stanford
School of Medicine; Richard Lemen, Ph.D., M.S.P.H., former
director of Division of Standards Development and Technology
Transfer at NIOSH, Assistant Surgeon General, U.S. Public
Health Service, retired; and Linda Reinstein, executive
director and co-founder, of the Asbestos Disease Awareness
Organization.
We will start with Dr. Castleman, an environmental
consultant. We will ask each of you to speak for 5 minutes. We
will put your full statement into the record and then we will
start with questions.
Senator Inhofe. Madam Chairman?
Senator Boxer. Yes.
Senator Inhofe. Let me do a U.C., here, first if I could.
Senator Boxer. Of course.
Senator Inhofe. We received just yesterday a letter from
the El Dorado County Office of Education regarding this hearing
and their experience with non-asbestiform rock that has been
mistaken as dangerous asbestiform. I would like to include this
in the record.
Senator Boxer. Of course, without objection, it will be
done.
[The referenced material follows:]
Senator Boxer. Dr. Castleman, we welcome you. Please
proceed.
STATEMENT OF BARRY CASTLEMAN, Sc.D., ENVIRONMENTAL CONSULTANT
Mr. Castleman. Thank you, Senator Boxer.
I have worked for 35 years with U.S. Government agencies,
non-governmental organizations, international agencies on
asbestos issues. I also testify as an expert witness about the
public health history of asbestos, the subject of my doctoral
thesis.
I work with other public health workers all over the world
on asbestos, and we all hope to see the United States join
about 40 other countries that have banned asbestos.
The World Trade Organization has concluded that controlled
use of asbestos products is unrealistic, supporting national
asbestos bans. Here, as we have noted, the EPA tried to ban
asbestos, but the rules were overturned in a court challenge.
There is broad support for banning asbestos in the United
States today. A statement in support of the Ban Asbestos in
America Act has been endorsed by 18 groups, including leading
American unions, environmental groups and asbestos victims
groups, groups including the AFL-CIO, the Service Employees
International Union, the Natural Resources Defense Council, the
White Lung Association, Asbestos Diseases Awareness
Association. There are also a number of groups from around the
world that have also joined in this, showing the tremendous
impact on the rest of the world of the United States having not
up until now banned asbestos. So I offer this for the record,
the statement and the groups that have endorsed it.
U.S. consumption of asbestos annually is now what it used
to be in a single day in 1973. It is about one 400th of what it
was at its peak. There is practically nothing left of the
asbestos industry here. The main use appears to be in roofing
products and one process for making chlorine. The European ban
on asbestos has no exemption for roofing products and they
don't seem to have any problem with that. Here too we have
plenty of alternative materials.
As for chlorine, it is made by two processes, two old ones
and one modern one. One of the old processes is the diaphragm-
cell process, in which an asbestos diaphragm has been used. The
newer membrane-cell process is the only type used in new plant
construction since 1987 around the world, because it is much
more energy efficient and it doesn't use mercury or asbestos.
There were questions raised about the exposures that you
can get in this industry, Senator. Asbestos exposures arise
from transport and storage of sacks of asbestos involving tears
in the sacks that must be identified and sealed and the
spillage cleaned with special vacuum cleaners; cutting open and
emptying sacks of asbestos; transferring sacks into slurry
mixing tanks can cause additional exposures; if there is any
spillage of the slurry, that has to be cleaned up very
carefully or you have the drying of the material and the
creation of an airborne asbestos hazard.
Then the diaphragm has to be properly handled and stored
again, providing for the possibility of exposure. Then the
hydro-blasting for removal and replacement of the asbestos is
another possible source of area contamination and drying and
airborne exposure. Then you have the waste asbestos from all of
this that has to be dealt with as well as the personal
protective clothing that workers may wear, throw away garments
that then are hazardous waste themselves. I have comments on
this in my prepared statement, Senator.
The diaphragm-cell chlorine plants can also be operated
with non-asbestos diaphragms, as Senator Boxer pointed out
there, available from companies including PPG in the United
States, which has used it in their own plants. So they can
replace the asbestos diaphragms with non-asbestos, or they can
convert to the membrane process. In Japan, the chlorine
industry is solely membrane cell. In Europe, I think there are
only three plants left using asbestos diaphragms.
I would say that there shouldn't be a statutory exemption
for the chlorine industry. They should have to justify that
based on current technology to the EPA along with any other
party that wants to have an exemption to the ban that Senator
Murray has put into her bill.
The main problem, as pointed out, is the import of asbestos
products. I simply would point out that these products compete
against safer products made in the United States. There is just
no reason why they should be allowed to be continuing to be
imported.
As for contaminant asbestos, there are problems with talc.
Four months ago I sent a letter with several other scientists
to the Consumer Product Safety Commission. There is a notorious
talc in upstate New York that is contaminated with asbestos.
People have died with asbestosis, lung cancer and mesothelioma
from mining the stuff. Yet the company that makes it persists
in selling the stuff as if it doesn't have asbestos, and making
mineralogical arguments to that effect. Meanwhile, this product
is being used in consumer products used all over the United
States.
Senator Boxer. Can you wrap up, Doctor?
Mr. Castleman. Sure. So I think that it is very important
for the Government to deal with the issue of contaminant
asbestos and talc, vermiculite and construction stone. We can
definitely deal with a ban on commercial forms of asbestos very
quickly and I hope you will proceed to do that.
[The prepared statement of Mr. Castleman follows:]
Statement of Barry Castleman, Sc.D., Environmental Consultant
Members of the committee, thank you for inviting me to testify
about public health issues related to asbestos exposure in America
today. I have worked on public health issues surrounding asbestos for
35 years, including product bans at the Consumer Product Safety
Commission and regulations at EPA, OSHA, and FDA. My bachelor's degree
is in chemical engineering, my masters is in environmental engineering,
and my doctorate is in public health policy from the Johns Hopkins
School of Hygiene and Public Health. I will discuss public health
issues related to present asbestos hazards and banning asbestos in the
U.S.
background
The public health and corporate history of asbestos were the
subject of my doctoral thesis and a 900-page book (asbestos: Medical
and Legal Aspects). The book is in its 5th edition and has been cited
in judicial opinions up to the Supreme Court. I have testified about
this history as an expert witness in courts across this country since
1979.
It is tragic that so much of the public health catastrophe we are
seeing now was not only foreseeable but foreseen long ago. The cancer
hazard of breathing asbestos dust was noted in The New York Times,
Business Week, Scientific American, and Newsweek all before this time
in the year 1950. But it would not be until after social developments
led Congress to establish the EPA, OSHA, and NIOSH in 1970 that workers
and the public were first protected from or even warned about the
dangers of most asbestos products. So it was not until 1973 that our
use of asbestos peaked, at around 800,000 metric tons. U.S. consumption
of asbestos for the year 2006 was down to around 2000 metric tons,
approximately the amount we used each day in 1973.
Americans are now dying from asbestos cancers and asbestosis at the
rate of 10,000 per year, as a result of past asbestos use. That is more
than one death per hour. The medical literature is replete with tragic
cases of mesothelioma in people with minimal occupational and
environmental exposures to asbestos. The World Trade Organization has
rejected the idea that there is really such a thing as ``controlled
use'' of asbestos, citing do-it-yourself home repair as a prominent
example of something no government can make safe through regulations.
Starting in the early 1980s, Sweden and other countries pressed
manufacturers to substitute asbestos in vehicle brakes so they could
impose national asbestos bans.
The U.S. EPA tried to phase out the major uses of asbestos in
regulations published in 1989, but the rules were overturned in a court
challenge. EPA was unable to persuade the Department of Justice to
appeal the court's 1991 decision, leaving the matter to Congress to
resolve.
u.s. asbestos use today
The main problem now is imported asbestos products, commercial
asbestos product manufacture is almost extinct in the U.S. Because
there is practically no restriction on what can be sold with asbestos
in the U.S., we continue importing asbestos-containing brake linings,
asbestos gaskets, asbestos yarn and thread, etc., despite the fact that
these products are no longer made in the U.S. Given the abject lack of
OSHA enforcement of asbestos product labeling requirements, there is a
real concern that some imported asbestos products are not even labeled
with the required health warnings.
The last U.S. asbestos mine closed in 2002. U.S. consumption of
commercial asbestos in domestic manufacturing seems to be limited now
to roofing felts and related products, and chlorine manufacturing (see
below). No asbestos roofing products are needed or allowed in the many
countries of Europe where asbestos has been banned for over 10 years
(e.g., Sweden, Germany, Italy, France, Denmark, Holland), and
alternative non-asbestos roofing products are widely available here.
U.S. brake manufacturers no longer use asbestos, and the auto industry
has already stopped using asbestos brakes in new vehicles and
replacement parts throughout Europe and elsewhere.
asbestos exposure in chlorine manufacturing
Asbestos has long been used in the diaphragm-cell process for
making chlorine. This process and the old mercury-cell process are
still operated, although a newer and more environmentally and
technically superior membrane-cell process has been the only type built
anywhere in the world for the past 20 years. Some diaphragm and mercury
cell plants have been converted to membrane cells. Power requirements
are substantial for chlorine manufacture, and the membrane cell process
requires 15-20 percent less energy than diaphragm cells.
Asbestos exposures in the chlorine industry arise from transport
and storage of sacks of asbestos, typically involving tears in the
sacks that must be identified and sealed, with spillage cleaned with
high-efficiency vacuum filters. Cutting open and emptying sacks of
asbestos and transferring asbestos into slurry mixing tanks can cause
additional exposures. The empty sacks are an additional exposure
source, they must be carefully gathered up, placed in sealed
containers, and landfilled at approved sites. Storage and handling of
partially used sacks are also sources of exposure. If the slurry is
spilled, this has to be meticulously cleaned up right away, because
once it dries it becomes a source of airborne asbestos exposure.
Handling and storage of prepared or purchased pre-deposited asbestos
diaphragms can cause additional exposures. Hydro-blasting for removal/
replacement of asbestos diaphragms is another possible source of area
contamination, drying, and airborne exposure. The water used for hydro-
blasting has to be contained and the asbestos filtered from it. The
waste asbestos from this water and the spent diaphragms have to go to a
landfill that accepts asbestos.
To some degree, workers can be protected against these asbestos
exposures if they wear respirators that will remove some of the
asbestos from the air they breathe, and if they wear personal
protective clothing such as disposable coveralls. But these safeguards
are partial. The respirators must be fit-tested and properly
maintained; and even the protective clothing is a hazardous waste that
requires special precautions for disposal. Chlorine Institute pamphlet
137, Guidelines: Asbestos Handling for the Chlor-Alkali Industry,
recommends personal protective clothing and respirators only for
workers exposed in excess of the permitted limits in the OSHA standard,
which is all that is legally required. But OSHA has admitted that
compliance with its limits will not fully prevent deaths from asbestos.
Dr. Richard Lemen and NIOSH epidemiologists estimate that exposure at
OSHA's permissible exposure limit for asbestos will still cause 5
deaths from lung cancer and 2 deaths from asbestosis in every 1000
workers exposed for a working lifetime. (L. Stayner et al., Exposure-
Response Analysis of Risk of Respiratory Disease Associated with
Occupational Exposure to Chrysotile Asbestos. Occ. Env. Med. 54: 646-
652, 1997).
While company manuals may state that the workers are supposed to
observe various precautions to minimize asbestos exposure, there is
virtually no OSHA inspection of these workplaces, and the usual
combination of production demands, Gulf coast heat and humidity, and
carelessness will assure that things are not always done ``by the
book'' to minimize workers' asbestos exposure.
In the past 15-20 years, non-asbestos diaphragms have become
available for relatively simple replacement in asbestos diaphragm cell
plants. These are sold by Eltech/DeNora and PPG Industries in the U.S.
The non-asbestos diaphragms cost more and last longer than asbestos.
Although two-thirds of the chlorine made in the U.S. in 2006 was from
diaphragm cells, I don't know how many of these used non-asbestos
diaphragms. The technology continues to advance, however, and has had
wide acceptance in Europe, where the European Union's temporary
exemption allowing asbestos use in chlorine manufacturing comes up for
reconsideration next year. I understand that there are only 3 chlorine
plants in Europe still using asbestos diaphragms.
PPG Industries has been a leader in the development of non-asbestos
``Tephram'' diaphragms, and PPG is also a major producer of chlorine in
the U.S. I understand that PPG routinely replaces non-asbestos Tephram
diaphragms in its asbestos diaphragm-cell units when they are taken
down for periodic maintenance. I do not know of any technical reasons
why other diaphragm-cell chlorine manufacturers could not do the same
thing.
Therefore, if chlorine manufacturers want extra time to convert to
non-asbestos technology, perhaps that could be allowed but with the
requirement that when the equipment is shut down for maintenance
overhauls, the new diaphragms used be non-asbestos. A similar several-
year time frame might be allowed for diaphragm-cell units that
manufacturers want to convert to membrane cells.
contaminant-asbestos in talc, vermiculite, stone, and other minerals
1. Talc
Aside from commercial asbestos minerals that have been used for the
past century in various products, asbestos also occurs as a contaminant
in other minerals. This has been long recognized, and at times the
occurrence of asbestos fibers in these products has even been noted in
advertisements for them. For example, it was repeated that
``asbestiform varieties are common'' in a 1966 brochure describing
NYTAL, the trade name for a talc mined in New York by R. T. Vanderbilt
Company.
Health officials had long ago noted that New York talc miners were
dying from lung scarring, including asbestos bodies in the scarred lung
tissues and pathology ``similar to [findings] reported in asbestosis.''
(FW Porro et al., Pneumoconiosis in the Talc Industry. Am. J. Roent.
Radium Therapy 47: 507-524, 1942. Quote from FW Porro et al., Pathology
of Talc Pneumoconiosis with Report of an Autopsy. North. N. Y. Med. J.
3: 23-25, 1946). New York state labor protection officials noted that
other writers had attributed talc lung scarring to the fibrous
varieties of talc, and observed that, for New York talc miners, ``In
general, the clinical, [chest X-ray], and pathological findings were
similar to those observed in asbestosis.'' (M Kleinfeld et al., Talc
Pneumoconiosis. Arch. Ind. Health 12: 66-72, 1955; M Kleinfeld et al.,
Talc Pneumoconiosis/A Report of Six Patients with Postmortem Findings.
Arch. Env. Health 7: 101-115, 1963) So it should have come as no
surprise that these talc miners also had an excessive death rate from
cancers of the lung and pleura (M Kleinfeld et al, Mortality among Talc
Miners and Millers in New York State. Indust. Hyg. Review 9: 3-12,
1967).
Starting in 2002, there have been published reports of cases of
mesothelioma, considered a signal tumor for asbestos exposure, among
New York talc miners. An epidemiology report sponsored by R. T.
Vanderbilt Company found 2 cases among the 782 white men who had been
employed for at least one day at the New York talc mines between 1948-
1989 (Y Honda et al., Mortality among Workers at a Talc Mining and
Milling Facility. Ann. Occup. Hyg. 46: 575-585, 2002) R. T. Vanderbilt
Company has stipulated that, subsequent to the period covered in this
study, at least 5 more cases of mesothelioma have occurred among its
employees (Hirsch vs. RT Vanderbilt Co. Middlesex Co. NJ Superior
Court, Nov. 2, 2006). It appears that some of these cases were the
subject of workers' compensation claims.
Meanwhile, independent pathologists reported finding at least 8
confirmed cases of mesothelioma among New York state talc miners and
millers as of 1986, and added 5 new cases (MJ Hull et al., Mesothelioma
among Workers in Asbestiform Fiber-bearing Talc Mines in New York
State. Ibid. Suppl. 1, 132-136, 2002) Commercial amphibole asbestos
fibers were virtually absent in the lung tissues of all 10 cases
subjected to pathological examination, indicating that other
occupational asbestos exposures (e.g., in construction) were not
responsible for these mesotheliomas of these workers.
R. T. Vanderbilt denies that there is asbestos in its talc and that
its talc causes asbestos diseases. It is interesting to read internal
memoranda of the Johns-Manville Corporation, the country's largest
asbestos company, shortly after J-M bought a talc mine in the early
1970s. J-M's talc had asbestos in it, and J-M labeled it accordingly,
pursuant to the 1972 OSHA asbestos regulations. This upset executives
at Vanderbilt, who claimed that J-M placing asbestos warnings on
containers of talc was causing a ``big stink'' and ``irreparable
damage'' to Vanderbilt in 1974. J-M laboratories proceeded to examine
the Vanderbilt talc product grades microscopically. Their comments on
what they found were expressed in internal memos that only came to
light in recent years, after the consummation of the J-M bankruptcy
plan in 1988.
The J-M people found plenty of asbestos in the New York talc and
used very strong language about Vanderbilt's insistence that there was
no asbestos in its talc:
It is apparent that the R. T. Vanderbilt presentations to OSHA,
NIOSH, FDA, MESA, etc. are based on something less than the truth. I
feel it difficult to believe that they could be so grossly misinformed
as to what their materials really are.
(RS Lamar, J-M Internal Correspondence, Oct. 11, 1974)
The R. T. Vanderbilt position with respect to labeling must be
deliberately perfidious; they cannot be this misinformed. Slim
Thompson, their technical director, has a Ph.D. in mineralogy. At the
moment, Vanderbilt is misleading their customers and confusing ours
with the decision not to label. Ultimately, the truth will out, and
they will be forced to label.
(RS Lamar, ``An Assessment of the J-M Position with Talc,'' J-M
Internal Correspondence, Mar. 20, 1975)
The truth still hasn't won out, I am sorry to say. Fully 32 years
after this was written by a morally offended official at the largest
asbestos corporation in America, R. T. Vanderbilt still sells talc that
they say has no asbestos hazards.
As a result, this talc is used commercially in an unknown number of
industrial processes and consumer products, endangering thousands,
perhaps millions, of unwitting workers, consumers, and children. Along
with two other scientists, I filed a complaint with the Consumer
Product Safety Commission about Durham's Water Putty, a product sold
across the country in Ace Hardware stores, because it exposes users to
airborne asbestos arising from the product's ingredient of Vanderbilt
talc (Jan. 29, 2007). The Center for Environmental Health, in Oakland,
filed a complaint last month with the California Attorney General's
Office, asserting that Durham's product has violated state law because
it has been sold without cancer warning labeling. The Connecticut
Department of Public Health filed another complaint with CPSC about
asbestos hazards to school children from Vanderbilt talc in art clay
products (Feb. 6, 2007). In 2006, a jury awarded $3.3 million to the
estate of a New Jersey potter, finding that Vanderbilt's talc was a
substantial cause of his death. Only Vanderbilt knows what other
commercial uses and products expose the American people to this talc.
The people in this country urgently require the government's
protection against the sale of such products by manufacturers who
prefer to play semantic games over what mineralogists and government
regulations call ``asbestos'', while people continue to be unknowingly
exposed to mortal peril. The grossly excessive number of mesotheliomas
among the New York talc mine and mill workers is very powerful evidence
that this material is lethal and should be regulated as asbestos and
banned when asbestos is banned.
2. vermiculite
We have seen this suppression of contaminant-asbestos health
warnings in other cases. WR Grace sold vermiculite insulation that was
contaminated with asbestos until 1990, ultimately placing it in
millions of homes in the U.S. and Canada. The company had been called
the Vermiculite and Asbestos Corporation when it opened in 1919, and
Montana State Board of Health reports on the high asbestos exposures of
the workers were sent to the company in the 1950s and 1960s. WR Grace
sold this material without applying OSHA asbestos warning labels first
required in 1972. By 1985, a ``Personal and Confidential'' memo
reviewed the serious business problems from Grace continuing to sell
vermiculite products that contained asbestos (RC Walsh, Feb. 2, 1985).
Noting the difficulty of continuing to obtain insurance, one of the
parties to this exchange commented that this ``increases attractiveness
of setting business up as a subsidiary or some other legal form to
distance it from Grace assets.'' Criminal proceedings are currently
pending against Grace executives for selling this product as they did,
but it was a public health failure that the government had not taken
earlier action to prevent the widespread sale and exposure of millions
of people to this deadly product. (A. Schneider, Big Asbestos
Prosecution in Jeopardy, U.S. Argues. Seattle Post-Intelligencer, June
5, 2007) http://seattlepi.nwsource.com:80/local/318479--
grace05.html?source=rss
Vermiculite is still mined in the U.S. by Virginia Vermiculite.
Mine Safety and Health Administration (MSHA) officials have raised
concern about asbestos exposure of workers at this site and at plants
receiving and processing this material. Vermiculite has been widely
used in such products as potting soil, insulation, and cat litter.
(A. Schneider, Virginia Miners at Risk from Asbestos. Seattle Post-
Intelligencer, Oct. 4, 2000) http://seattlepi.nwsource.com/
uncivilaction/asb04.shtml
3. stone
Asbestos can also be present in basic stone used in construction.
In 2005, research was published linking residence in areas of
California with naturally-occurring asbestos outcrops and increased
risk of mesothelioma (Pan et al., Am. J. Resp. Crit. Care Med. Oct.
2005). Dr. Marc Schenker, one author of this study, expressed concern
about the health hazard faced by people with environmental exposure in
areas where land development was proceeding in El Dorado County,
California, and other areas where asbestos minerals are known to be
present in the soil in significant amounts. http://
www.medicalnewstoday.com/medicalnews.php?newsid=32149
iron ore
There has been controversy for at least 35 years over asbestos-like
material in the host rock of ore mined in the Iron Range of Minnesota.
By March 2006, State officials identified 35 deaths from mesothelioma
among the miners, in addition to 17 fatal cases previously known to
have occurred between 1988-1996. http://www.startribune.com:80/462/
story/1250516.html
What is needed is a process whereby the EPA does surveillance of
possible sources of contaminant-asbestos around the country, starting
with Vanderbilt talc and Virginia Vermiculite, using USGS mineral
survey maps to help identify hot spots. Then, as operations of concern
are discovered, there needs to be a process of investigation, first for
the government to realistically sample the products of these operations
and do bulk sample analysis. Then, if there is any concern over public
and worker exposure, the company should have to disclose its commercial
customer list to EPA. EPA could then contact the customers to see how
the material is handled, ask what products it is used to make, and
assess what asbestos exposures result for workers, consumers, and
people living where the stuff is shipped, processed, and put to end
use. In annual reports, EPA should disclose what operations it has
under investigation, and summarize the state of these investigations,
describing the commercial uses of the suspect materials. And of course,
the EPA needs the authority to close operations and stop the sale of
products that are deemed a threat to public health.
broad support for banning asbestos in the u.s. and international
implications
A statement in support of the Ban Asbestos in America Act of 2007
has been endorsed by groups that have been active on asbestos issues
for many years in the U.S. and around the world. These include trade
unions, leading environmental groups, asbestos victims' groups, and
medical and public health groups. I ask that this statement and list of
supporters be made a part of the record of this hearing.
You can see that there are many groups from other countries that
signed the statement in support of banning asbestos in the U.S.,
countries where asbestos is still used and is the subject of public
health struggles. I work with people all over the world on asbestos,
and everywhere the local asbestos industry points to the U.S. and says,
``But asbestos is not banned in the United States.'' It would be great
value to public health workers the world over if the U.S. finally
banned asbestos. It would significantly assist efforts in Brazil,
India, South Africa, Thailand, and many other countries. So, on behalf
of the rest of the world and the people in our country, I urge you to
ban asbestos in the U.S. now. It is long past time for the U.S. to take
a 21st century position on this issue and catch up to Croatia by
banning asbestos.
I have not been paid by anyone for my preparation and testimony
here today. Nor do I represent anyone but myself, a public health
worker. Thank you for inviting me to speak.
______
Responses by Barry Castleman to Additional Questions from Senator Boxer
Question 1. What benefits do businesses get when developing or
using alternatives to asbestos?
Response. Businesses benefit by developing safer alternatives to
asbestos products in a number of ways. They have improved labor and
community relations, compared to firms persisting in asbestos use. They
avoid damaging publicity that often comes with resistance of employees,
consumers, and plant neighbors to asbestos use. They don't have to
spend money complying with EPA and OSHA asbestos standards (e.g.,
industrial ventilation system fixed and operating costs, periodic
employee medical exams and air sampling, 30-year retention of medical
records, cancer warning product label requirements, hazardous waste
disposal requirements, etc.). They save money on group life, group
health, workers' compensation, and product liability insurance. They
will be around a lot longer than companies still using asbestos,
because asbestos is hazardous, discredited technology losing markets
worldwide.
Question 2. Your testimony contained disturbing references to
individuals in business that potentially hid information on health
threats related to their products that may contain asbestos. In your
experience, have other businesses potentially tried to hid information
that their products may contain material that cold cause diseases
associated with asbestos?
Response. There are widespread examples of businesses that hid
information that the use of their products could cause asbestos
diseases. Many examples are given in my book, Asbestos: Medical and
Legal Aspects (5th Ed., 2005). Despite published reports between 1932-
1964 from around the world that commercial asbestos products were
causing death and disease, and despite workers' compensation claims
around the country by workers harmed by asbestos products in
construction in the 1940s and 1950s, no asbestos products appear to
have borne even mild health warning labels before 1964. No manufacturer
placed health warnings on brake linings, drywall patching compounds,
and many other asbestos products until after they were required to by
OSHA in 1972, sometimes many years after (e.g., Ford, Chrysler). OSHA
has failed for 35 years to monitor the marketplace to assure that
required labels were placed on asbestos products, so that products we
import today may well contain asbestos that is not disclosed by foreign
manufacturers and distributors. This problem is mainly confined to
imports, as there are practically no commercial asbestos products made
in the U.S. anymore.
Other businesses selling products with contaminant-asbestos have
withheld information from consumers to this day, and the scale of this
menace is unknown. I gave examples in my statement of asbestos-
contaminated talc from R. T. Vanderbilt and vermiculite from Virginia
Vermiculite. These companies deny that there is asbestos in their
products, which are sold to commercial customers. At the customers'
plants, workers are consequently unaware of the danger they face in
handling these materials. The products go out to the public with no
labeling warning of the cancer danger that the dust can pose. Workers
are also endangered by disturbing, extraction, and construction
involving iron ore in Minnesota, where there have been a large number
of mesotheliomas among the workers, and extracting stone in El Dorado
County, California.
One product containing Vanderbilt talc is Durham's Water Putty,
which has been analyzed and shown to contain asbestos; airborne
asbestos is released in alarming concentrations when the product is
used. With two other scientists, I urged the Consumer Product Safety
Commission to get this product off the market on January 29, 2007; we
also urged CPSC to investigate all other commercial applications of
Vanderbilt talc. No reply has yet come from CPSC, and this appears to
be a matter of considerable public health importance.
Question 3. Please submit a copy of the statement of support for
Senator Murray's bill that you discussed a the hearing.
Response. [The ``Statement in Support of the Ban Asbestos in
America Act of 2007'' follows.]
Response by Barry Castleman to an Additional Question from
Senator Inhofe
Question. Please describe, to the best of your knowledge, every
instance in which you testified or were deposed as an expert witness
for any party in asbestos litigation or were officially retained to
provide expert advice to any party involved in asbestos litigation. For
each instance provide the following:
(a) The name of the case, (b) Court (and whether State or Federal);
(c) The name of the party that retained you or for whom you provided a
deposition or testimony; (c) The dates on which you were deposed or
testified or were otherwise retained; (d) What service you provided
(testimony, deposition, etc.); (e) An explanation of the nature of your
testimony or deposition; (f) Who paid you, and please provide the
invoice (if you have the records).
Response. My records of my work as an expert witness in asbestos
litigation are limited, and I am providing what I can. I have kept a
running listing of trial and deposition testimony since starting this
work in 1979. There is a one-line entry for each testimony, listing the
name of plaintiff, whether trial or deposition, location of State or
Federal court where the case was filed, and date. (Attachments:
``Castleman Testimony 1979-1993''; and for 1993 to date, ``trials'')
In all cases but one in which I have testified, I was retained by
plaintiffs. In that one, I was a witness for the United States of
America in the U.S. Court of Claims. There, Johns-Manville Corporation
was suing the government for partial reimbursement for damages paid by
J-M to workers with asbestos diseases, arising from J-M's sale of
asbestos products (without health warning labels) for shipbuilding
during World War II. This was in 1987.
Two of the cases I have testified in were property damage cases,
the rest were personal injury cases brought by workers, their family
members and survivors. The property damage claims were brought by the
State of Maryland and by Chase Manhattan Bank. The State of Maryland
and Chase were suing asbestos product sellers for the costs of
carefully removing and replacing asbestos products in their buildings.
My testimony in asbestos litigation is referred to as ``State-of-
the-art'' testimony. It is about the public health and corporate
history of asbestos, the subject of my doctoral thesis at Johns
Hopkins. I trace the history of knowledge about the dangers of
asbestos, describing the earliest and most significant reports of
asbestosis, then various forms of cancer, tracking the development of
knowledge as the population-at-risk was gradually recognized to be
increasing with the addition of different populations of workers and
other individuals over time. I describe what individual corporations
and industries did as the problem of asbestos disease arose in
different ways for them, based on a historic record replete with
documents from institutional, governmental, and corporate archives.
The knowledge available in medical writings, safety publications,
government publications, laws, industry trade magazines, major
newspapers, encyclopedias, etc. is, on the whole, the standard against
which the defendants' conduct is judged. In these cases, the
manufacturers are held to the knowledge of experts about the hazards of
the products they are selling to the public, and the product seller has
the duty to warn about lethal, non-obvious hazards. Similarly, premises
owners, such as oil and chemical companies, that bring in contract
workers, have a duty to warn and protect these workers against hazards
that the premises owners know or should know are there.
Payment for my services in litigation has been by the law firms
that have hired my services, the U. S. Treasury, Chase Manhattan Bank,
and the State of Maryland. I do not retain invoices after receiving
payment of my bills, I am just a single person working as an
independent consultant in occupational and environmental health. I try
to minimize paperwork burdens for myself, as I have not employed any
full-time employees since starting as a consultant in 1975.
______
Trials
Asner, trial, Baltimore s.c., Nov. 17
Asbestos Cases III, deposition, Charleston WV s.c., Dec. 8
1994
Dikun, trial, Ft. Lauderdale s.c., Jan. 24
Adams, trial, Baltimore s.c., Feb. 23, 24, 28
Gordon, deposition, Austin s.c., Feb. 25
Chavers, deposition, Mobile s.c., Mar. 24
Rones, deposition, Washington DC s.c., Apr. 21
Hannon, trial, Baltimore s.c., Apr. 27
Purcell, trial, Portland s.c., May 3-4
Monahan, trial, L.A. s.c., June 16, 17, 20,21
Norris, trial, Wilmington s.c., June 30
One Wilshire, deposition, L.A. s.c., Sept. 13
Chase Manhattan, deposition, New York f.c., Nov. 1; and Feb. 22,
Oct. 9, 1995
Olson, trial, Sydney Australia Dust Diseases Tribunal, Dec. 10-11
1995
Adams, deposition, Baltimore s.c., Jan . 5, 12
Wiggins, trial, San Francisco s.c., Jan. 10-11
One Wilshire, trial, Los Angeles s.c., Mar. 20, 22
White, trial, Austin s.c., April 13
In Re Asbestos, deposition, Travis Co. TX, May 12
Bowser, trial, San Francisco s.c., May 26-27
Adams, trial, Baltimore s.c., June 6-7
Richmond, trial, San Francisco s.c., June 14
Boyd, videotaped evidence deposition, Spokane s.c., June 29
Automobile worker asbestos cases, deposition, Birmingham MI s.c.,
Sept. 7
Hicks, deposition, Bloomington IL s.c., Oct. 12
Zumas, trial, Baltimore s.c., Oct. 25, 30, Nov. 6
Heisler, deposition, Cincinnati s.c., Oct. 26
Dye, trial, San Francisco s.c., Oct. 31-Nov. 1
White, trial, Austin s.c., Nov. 2
Hicks, trial, Bloomongton IL s.c., Nov. 7-8
Sirbaugh, trial, Martinsburg WV s.c., Nov. 15
Drake, trial, San Antonio s.c., Dec. 5
1996
Crabtree, trial, Bloomington IL s.c., Jan. 17
Sloan, deposition, San Francisco s.c., Feb. 13
Butler, deposition, San Francisco s.c., Feb. 14
Lee, trial, Brunswick GA s.c., Mar. 14
Chaney, deposition, San Antonio s.c., Mar. 14
Greive, deposition, Baltimore s.c., April 2
Sherer, trial, Bloomington s.c., May 20
Pusey, trial, Wilmington s.c., May 23
Anderson, deposition, Little Rock, June 6
Danilowicz, trial, San Francisco s.c., June 13-14
Williams, deposition, San Francisco, June 13
Williams, trial, San Francisco s.c., June 14
Roa, trial, Portland OR f.c., July 19
Perepechko, deposition, Chicago s.c., Sept. 4
White, deposition, El Paso, Sept. 5
Biebel, trial, Baltimore, Oct. 7-9
Buyard, trial, Los Angeles, Oct. 31
Overly, deposition, San Francisco, Nov. 4
Adams, videotaped deposition, Houston s.c., Nov. 6
Overly, trial, San Francisco, Nov. 12-13
Childress, deposition, San Francisco, Nov. 13
Becknell, trial, Bloomington, Nov. 15, 18
Childress, trial, San Francisco, Nov. 21, 22, 25
Ronzini, trial, New York s.c., Dec. 9-10
Scanlon, deposition, Chicago s.c., Dec. 20
1997
Arthur, trial, Wilmington s.c., Feb. 21, 24
Ehret, deposition, L.A. s.c., May 9
Crowe, trial, Cleveland s.c., May 21
Ehret, trial, Los Angeles, May 28
Driver, trial, Dallas s.c., June 25
Derr, deposition, Wilmington, July 8
Sanchez, trial, SF s.c., July 30-31
Abshire, deposition, Charleston WV, Sept. 22
Britton, French, depositions, Bloomington s.c., Oct. 13
DeBolt, trial, Bloomington s.c., Nov. 13
Pruitt, trial, San Francisco s.c., Nov. 19
Varga, trial, Fairfield CA s.c., Nov. 20
Trujillo, deposition, Albuquerque s.c., Dec. 5
Harpham, deposition, L.A. s.c., Dec. 6
MONMASS, deposition, Morgantown WV, Dec. 29
1998
Armstrong, deposition, San Francisco s.c., Jan. 2
Group 119, deposition, San Francisco s.c., Jan. 2
Valadez, deposition, San Francisco s.c., Jan. 2,5
Armstrong, trial, San Francisco s.c., Jan. 6
Group 119, trial, San Francisco s.c., Jan. 7-8
Burgess, trial, Bloomington, Jan. 26
Schedel, trial, Bismarck ND, Jan. 28
Valadez, trial, San Francisco, Feb. 4-5
Burks, trial, San Francisco, Feb. 5-6
Lowery, trial, Baltimore, Feb. 10
Ball, trial, Cleveland s.c., Feb. 25
Group 129, trial, San Francisco s.c., Mar. 9-11
Group 131, deposition, San Francisco, Mar. 12
Silveira, trial, San Francisco, Apr. 23
Woods, deposition, Chatanooga s.c., Apr. 27
Cosey, trial, Fayette MS s.c., May 21
Brady, deposition, Buffalo NY s.c., June 4
Gramley, trial, Cleveland, July 10
Frost, deposition, Bloomington IL, July 28
Cavitt, deposition, Cameron TX, July 30
Padron, evidence deposition, Cameron TX, Aug. 3
Charley, deposition, Cedar Rapids Iowa, Nov. 2
Henderson, deposition, Charlotte NC, Nov. 9
Corbal, deposition, L.A., Dec. 8
Briggs, evidence deposition, Beaumont TX, Dec. 10
1999
Missik, deposition, Cleveland s.c., Jan. 15
Lilienthal, deposition, San Francisco s.c., Jan. 16-17, Feb. 15
Salke, deposition, Bridgeport CT s.c., Feb. 11
Luevano, deposition, Oakland CA s.c., Feb. 19
Lilienthal, trial, S.F. s.c., Feb. 22
Raper, deposition, Dallas s.c., Mar. 11-12
Brittin, trial, Bloomington s.c., Mar. 15-16
Sanford, deposition, S.F. s.c., Apr. 2
Harris, deposition, Waycross GA s.c., Apr. 14
Zeleny, deposition, Chicago s.c., Apr. 15
Epperson, trial, Dallas s.c., May 28
Taylor, deposition, San Francisco s.c., June 1, 1999
Malang, deposition, San Francisco s.c., June 2
Townes, trial, Augusta GA s.c., June 16
Shank, trial, Cleveland s.c., June 28-29
Sanchez, trial, El Paso s.c., July 29
Rasmussen, deposition, San Francisco s.c., Aug. 9, 15
Powell, deposition, San Francisco s.c., Aug. 24
Miller, deposition, Bloomington s.c., Aug. 30
Thompson, deposition, Seattle s.c., Aug. 31
Widing, deposition, San Francisco s.c., Sept. 10
Ball, trial, Cleveland s.c., Sept. 23
Albright, deposition, Salisbury NC s.c., Oct. 3
Thompson, trial, Everett WA s.c., Oct. 12
Jones, deposition, Cleveland s.c., Oct. 22
Hoppmann, deposition, San Francisco s.c., Oct. 22
Chiasson, deposition, Los Angeles s.c., Nov. 2
Castillo, trial, El Paso s.c., Nov. 4
Raigoza, deposition, S.F. s.c., Nov. 11
Haig, deposition, S.F. s.c., Nov. 15
Hart, trial, Canton NY, Nov. 16
Hedrick, deposition, Fayette MS, Nov. 22
Grizzle and McElheney, depositions, S.F. s.c., Nov. 23
Gotter, deposition, Bloomington, Dec. 17
2000
Cicchillo, trial, Cleveland s.c., Jan. 27
Hollis, trial, Wilmington s.c., Feb. 1
Chavers, deposition, S.F. s.c., Feb. 2-3
Chavers, trial, S.F. s.c., Feb. 3
Peralta, deposition, El Paso s.c., Mar. 27
McLeod, deposition, Buffalo NY s.c., Apr. 3
Hines, deposition, SF s.c., May 1
Burnside, deposition, WV s.c., May 12
Ockerman, deposition, Oakland CA s.c., May 21
Ockerman, trial, Oakland s.c., May 22
Thornton, deposition, San Francisco s.c., June 9
Kasun, trial, Milwaukee s.c., June 16 and 19
Pavolini, deposition, San Francisco s.c., June 21
Pavolini, trial, San Francisco, June 25-26
Davis, deposition, San Francisco s.c., June 26
Perez, trial, San Francisco s.c., July 10-12
Tolbertson, trial, San Francisco s.c., July 20
Chiasson, trial, Los Angeles s.c., Aug 1-2
Chiasson, deposition, L.A. s.c., Aug. 1
Davis, trial, San Francisco s.c., Aug. 21-22
Pickle, deposition, San Francisco s.c., Aug. 25
Atchison, deposition, Oakland CA s.c., Aug. 28
Kinsman, deposition, San Francisco s.c., Sept. 7
Bouldin, deposition, Houston s.c., Sept. 8
Lyons, deposition, Washington D.C., Sept. 11
Emrick, trial, Portland OR s.c., Oct. 9-11
Moro, deposition, San Francisco s.c., Nov. 7
Moore, deposition, Daingerfield TX s.c., Dec. 29
2001
Gault, deposition, San Francisco s.c., Jan. 3
Overly, trial, San Francisco s.c., Jan. 5
Vasen, deposition, SF s.c., Jan. 8
Jestes, deposition, SF s.c., Jan. 12
Hoskins, deposition, Kansas City MO s.c., Jan. 22
Jacobs, deposition, Dallas s.c., Jan. 25
Lambertson, deposition, SF s.c., Feb. 13
Hoskins, trial, Kansas City MO s.c., Mar. 1
Jones, trial, New York NY s.c., Mar. 2
Dunn, trial, Oakland CA s.c., Mar. 5
Lee, trial, SF s.c., Mar. 6
Edwards, deposition, SF s.c., Mar. 8 and 12
Watkins, deposition, SF s.c., Mar. 9
Highsmith, deposition, Brunswick GA s.c., Mar. 21
Branscum, deposition, SF s.c., Mar. 27
Padalecki, deposition, Houston s.c, Apr. 9
Kingsland, trial, New York s.c., May 21
Peterman, trial, Portland OR s.c., May 24-25
Alexander, deposition, SF s.c., May 29
Chandler, deposition, SF s.c., June 11
Calhoun, deposition, Bloomington s.c., June25
Smith, trial, SF s.c., June 27
Stanfill, deposition, SF s.c., July 2
Wass, deposition, Seattle s.c., July 13
Rasmussen, deposition, SF s.c., July 16
Thompson, deposition, El Paso s.c., July 20
Moore, trial, Daingerfield TX s.c., July 23
Shingle, deposition, SF s.c., July 24
Miller, deposition, Salisbury NC s.c., July 27
Carter, deposition, SF s.c., Aug. 3
Shingle, trial, SF s.c., Aug. 14
Novo, deposition, Baltimore s.c., Aug. 17
Hunt, deposition, Bloomington IL s.c., Aug. 21
Petruzzelli, deposition, New Haven CT s.c., Aug. 24
Steenberger, deposition, Marshall TX s.c., Aug. 24
Alber, deposition, Boulder CO s.c., Aug. 27
Amos, deposition, Charleston WV s.c., Aug. 28
Book, deposition, S.F. s.c., Sept. 6
Skinner, deposition, Austin s.c., Sept. 7
Peterson, deposition, SF s.c., Sept. 14
Kiber, trial, Bloomington IL s.c., Sept. 25
Kinsman, deposition, Seattle s.c., Sept. 28
Turley, deposition, S.F. s.c., Sept. 28
Henderson, trial, Greenville SC s.c., Oct. 10
Dressler, deposition, SF s.c., Oct. 12
Jernigan, trial, Wilmington s.c., Oct. 16
Wilson, trial, Baltimore s.c., Oct. 18
Gerke, deposition, Oakland s.c., Oct. 19, 24
Stringfellow, trial, Little Rock s.c., Oct. 23
Colwell, deposition, Oakland CA s.c., Oct. 23
Guerra, deposition, Oakland CA s.c., Oct. 26
Cargile, deposition, Baltimore s.c., Oct. 30
Kiber, trial, Bloomington s.c., Nov5
Elliott, deposition, S.F. s.c., Nov. 6
Henderson, deposition, Oakland CA s.c., Nov. 6
Weiner, trial, Bethlehem PA s.c., Nov. 28
Jordan, deposition, San Francisco s.c., Dec. 11
Wells, deposition, SF s.c., Dec. 13
Brown, deposition, SF s.c., Dec. 14
2002
Jacques, deposition, Chicago f.c., Jan. 3
Campbell, deposition, SF s.c., Jan. 15
Franklin, deposition, SF s.c., Jan. 15
Burns, trial, SF s.c., Jan. 22
Todak, deposition, SF s.c., Feb. 14
Jones, trial, Atlanta s.c., Feb. 20
Tolbertson, deposition, SF s.c., Mar. 1
Meiers, deposition, Cleveland s.c., Mar. 4
Meiers, trial, Cleveland s.c., Mar. 7
Todak, trial, SF s.c., Mar. 12-13
Totman, deposition, Providence s.c., Mar. 21
Cave, deposition, SF s.c., Mar. 22
Peterson, deposition, Oakland s.c., Mar. 29
Matteson, deposition, New York s.c., Apr. 22
Matteson, trial, New York s.c., Apr. 24
Brown, deposition, Oakland CA s.c., Apr. 25
Anderson, deposition, Port Gibson MS s.c., Apr. 26
Flores, deposition, Corpus Christi TX s.c., May 1
Farrell, deposition, SF s.c., May 3
Peterson, trial, Oakland s.c., May 6
Anderson, deposition, Port Gibson MS s.c., May 10
Kuhn, deposition, SF s.c., May 17
Robinson, deposition, SF s.c., May 20
Trinchese, deposition, SF s.c., June 3, 17
Rivenbark, trial, Galveston s.c., June 4-5
Highsmith, trial, Atlanta s.c., June 6
Bennett, deposition, SF s.c., June 7
Caruso, trial, Springfield IL s.c., June 11-12
McCarthy, deposition, Los Angeles s.c., June 19
Trinchese, trial, SF s.c., June 28
Roca, deposition, Wilmington DE s.c., July 1-2
McCarthy, trial, Los Angeles s.c., July 11
Sledz, deposition, Baltimore s.c., July 29
Schmidt, deposition, Cleveland s.c., Aug. 5
Probst, deposition, Cleveland s.c., Aug. 9
Jensen, deposition, SF s.c., Aug. 16
Otten, deposition, SF s.c., Aug. 19
Nelson, deposition, SF s.c., Aug. 21
Barry, deposition, Galveston TX s.c., Aug. 29
Hansen, deposition, SF s.c., Aug. 30
Anderson, trial, Port Gibson MS s.c., Sept. 5
Frederick, deposition, SF s.c., Sept. 16
Kuhl, deposition, SF s.c., Sept. 17 and July 25, 2003
Langford, deposition, Center, TX s.c., Sept. 26
Graham, deposition, S.F. s.c., Oct. 2
Lansford, trial, Center TX s.c., Oct. 9
Gunderson, deposition, SF s.c., Oct. 11
Shauan, deposition, Providence RI s.c., Oct. 14
Campbell, trial, Seattle s.c., Oct. 17
Vincent, deposition, Wilmington s.c., Oct. 21
Flood, deposition, Chicago s.c., Nov. 7
Bottner, deposition, S.F. s.c., Nov. 8
Couch, deposition, S.F. s.c., Nov. 8
Consolini, deposition, Providence RI s.c., Nov. 18
Gunderson, trial, S.F. s.c., Nov. 19
Scott, deposition, S.F. s.c., Nov. 19
Wallstrom, deposition, S.F. s.c., Nov. 20
Wirt, deposition, Dallas s.c., Nov. 25
Yoakum, deposition, Cameron TX s.c., Nov. 26
Rhynes, deposition, S.F. s.c., Nov. 27
Skelton, deposition, S.F. s.c., Dec. 2
Miller, trial, Austin s.c., Dec. 3-4
Cash, trial, Wilmington s.c., Dec. 10
Kruchuk, deposition, SF s.c., Dec. 27
2003
Kubik, deposition, Warren OH s.c., Jan. 3
Clark, deposition, S.F. s.c., Jan. 13
Hofstetter, deposition, Alton IL s.c., Jan. 16
Sargent, deposition, Amarillo s.c., Jan. 17
Roseman, trial, Indianapolis s.c., Jan. 21-22
Falcone, trial, New Haven CT s.c., Jan. 30
Wells, deposition, S.F. s.c., Jan. 31
Kavanaugh, deposition, West Palm Beach s.c., Feb. 1
Kubik, trial, Warren OH s.c., Feb. 4
Davis, trial, Cleveland s.c., Feb. 5
Richardson, deposition, SF s.c., Feb. 6
Lundsford, trial, SF s.c., Feb. 14
Kavanaugh, trial, Palm Beach FL, Feb. 18
Lee, deposition, SF s.c., Feb. 21
Niemeier, deposition, SF s.c., March 3
Mintz, deposition, SF s.c., March 7
Dexter, deposition, NYC s.c., March 17
Sparks, trial, Beaumont TX s.c., March 26-27
Lilly, deposition, Charleston WV s.c., Apr. 4
Griffith, deposition, SF s.c., Apr. 30
Curtright, deposition, SF s.c., May 1
Wajer, deposition, Baltimore s.c., May 9
Kelley, deposition, SF s.c., May 12
Green, deposition, SF s.c., May 19
Marr, deposition, Dallas, May 23
Brackett, deposition, Orange TX, May 27, 2003
Lukac, trial, Warren OH, May 28
Pernowsky, deposition, Cleveland s.c., May 29
Toma, deposition, SF s.c., June 2
Gomez, trial, NY s.c., June 3, 9
Gartner, trial, Minneapolis s.c., June 19-20
Miller, deposition, Bloomington IL s.c., June 24
Andrade, deposition, SF s.c., June 24
Connor, deposition, SF s.c., June 24
Prasel, deposition, Cameron TX s.c., July 1-2, 21-22
Marshell, trial, Alameda CA s.c., July 9
Bangs, deposition, SF s.c., July 14
Tripp, deposition, SF s.c., July 25
Robinson, trial, Marietta GA, Aug. 12
Nolan, deposition, Chicago s.c., Aug. 15
Keyser, deposition, SF s.c., Aug. 22
Waishes, deposition, Wilmington s.c., Sept. 8
Wirts, trial, Baltimore s.c., Sept. 15
Bertucci, deposition, New Orleans, Oct. 3
Huck, deposition, Oakland s.c., Oct. 6
Weller, deposition, Cleveland s.c., Oct. 20
Robinson, deposition, Wilmington s.c., Oct. 21
Martin, deposition, Houston s.c., Oct. 24
Davis, deposition, Houston s.c., Oct. 31
Polito, trial, Rochester NY s.c, Nov. 21
Anzulis, deposition, Baltimore s.c., Nov. 24
Mikolich, deposition, SF s.c., Dec. 1
Chauvin, deposition, New Orleans s.c., Dec. 15
Lombardo, deposition, San Francisco s.c., Dec. 16
Baker, deposition, San Francisco s.c., Dec. 16
Ward, deposition, Belton TX s.c., Dec. 19
2004
Jameson, deposition, Seattle, Jan. 6
Harris, deposition, SF s.c., Jan. 12
Ross, deposition, SF s.c., Jan. 16
Smith, deposition, SF s.c., Jan. 16
Williamson, deposition, Jacksonville s.c., Jan. 19
Douglas, deposition, Orange TX s.c., Jan. 20
Jones, deposition, New Orleans s.c., Jan. 26
Ford, deposition, Wilmington s.c., Jan. 30
Korenek, deposition, Cameron TX s.c., Feb. 9
Amento, trial, Philadelphia s.c., Feb. 10
Munro, deposition, Indianapolis s.c., Feb. 23
Mason, deposition, Beaumont s.c., Feb. 24
Logston, deposition, Louisville s.c., Mar. 1
Stephens, trial, Angleton TX, Mar. 2
Prather, trial, Dallas, Mar. 3
Dori, deposition, Sweetwater TX s.c., Mar. 5
Kubic, deposition, Warren OH s.c., Mar. 8
Wise, trial, SF s.c., March 11
Dori, trial, Sweetwater TX s.c., Mar. 19
Braden, deposition, SF s.c., Mar. 22
Stover, deposition, SF s.c., Mar. 22
Donahue, deposition, SF s.c., Mar. 28
Roberts, deposition, Houston s.c., Apr. 2
Rhines, deposition, Covington Co. MS, Apr. 12
Burdo, deposition, Cleveland s.c., May 7
Whitney, trial, Los Angeles s.c., May 19
Mills, deposition, Corpus Christi, June 1
Kolson, trial, Ebensburg PA, June 9
Compton, deposition, Bloomington, June 10
Garzee, trial, Peoria, June 11
Wilson, deposition, SF s.c., June 14
Coleman, deposition, Cleveland s.c., June 25
Carter, deposition, Oakland s.c., July 2
Kell, deposition, SF s.c., July 13
Odum, deposition, Copiah Co. MS, July 16
Carter, trial, Oakland s.c., July 20
Wilson, deposition, SF s.c., July 27
Hinchman, deposition, Houston s.c., July 28
Kruger, deposition, SF s.c., Aug. 3
Pisani, deposition, SF s.c., Aug. 9
Pretko, deposition, Dallas s.c., Aug. 20
Kennedy, deposition, Portsmouth OH, Aug. 26
Ocegueda, deposition, SF s.c., Sept. 7
Lorenzino, deposition, Oakland s.c., Sept. 24
Barone, deposition, Warren OH s.c., Sept. 27
Cameron, deposition, Bloomington IL s.c., Sept. 30
Tracy, deposition, Oakland s.c., Oct. 1
Anthony, trial, NY s.c., Oct. 6
Gadeleta, trial, NY s.c., Oct. 8
Bearer, deposition, SF s.c., Oct. 11
Giesick, deposition, SF s.c., Oct. 11
Bishop, deposition, New Orleans s.c., Oct. 18
Marco, deposition, St. Louis s.c., Oct. 19
Cullison, deposition, Austin s.c., Oct. 22
Gendreau, deposition, SF s.c., Nov. 4
Coen, deposition, Milwaukee s.c., Dec. 20
Brown, deposition, SF s.c., Dec. 21
McWard, deposition, Peoria s.c., Dec. 23
2005
Bruner, deposition, SF s.c., Jan. 10
Hamilton, trial, Cleveland s.c., Jan. 13
Zavacky, deposition, Cleveland s.c., Jan. 14
Walsh, deposition, S.F. s.c., Jan. 14
Walraven, deposition, Boston s.c., Jan. 17
Hargrave, deposition, Edwardsville IL, Jan. 31, Feb. 28
Aukland, deposition, Cleveland s.c., Feb.4
Poore, deposition, Houston s.c., Feb. 7
Plathe, trial, St. Paul s.c., Feb. 16
Bruner, trial, SF s.c., Feb. 23
Miller, deposition, SF s.c., Mar. 14, 30
Flax, deposition, Baltimore s.c., Mar. 21
Hoover, deposition, SF s.c., Apr. 5
Konecny, deposition, SF s.c., Apr. 8
Coffey, trial, Buffalo s.c., April 13
Bouhanna, deposition, Boston s.c., Apr. 15
Clark, deposition, SF s.c., May 19
Pendergast, deposition, NY s.c., May 20
Rizzi, trial, NY s.c., May 26-27, 31
Goodman, deposition, Tacoma s.c., June 10
Nisselius, deposition, SF s.c., July 7
O'Halloran, deposition, SF s.c., July 8
Hartford, deposition, SF s.c., July 11
Lightsee, deposition, Brunswick GA s.c., July 15
Ammons, deposition, Brunswick s.c., July 15
Dawson, trial, Wilmington s.c., July 14 and 18
Cotton, deposition, Beaumont s.c., Aug. 5
Grisez, deposition, SF s.c., Aug. 10
Lantz, trial, SF s.c., Aug. 12
Ballenger, deposition, SF s.c., Aug. 15
Dukes, deposition, Bloomington s.c., Aug. 17
Schadt, deposition, Edwardsville IL s.c., Sept. 1
Coca, deposition, SF s.c., Sept. 2
Orlando, trial, NY s.c., Sept. 8
Kleineke, deposition, Cleveland s.c., Sept. 9
Dukes, trial, Bloomington IL s.c., Sept. 26
Lightsee, trial, Atlanta f.c., Sept. 27
Barnhill, deposition, SF s.c., Sept. 29
Hicks, deposition, Newport News s.c., Sept.30
Dodson, deposition, Kansas City MO s.c., Oct. 4
Fletchner, deposition, NY s.c., Oct. 14
Richardson, deposition, Baltimore s.c., Oct. 28
Jellum, trial, St. Paul s.c., Nov. 8
White, trial, Bloomington IL s.c., Nov. 15-16
Franklin, deposition, Louisville s.c., Nov. 18
Riggle, deposition, Dallas s.c., Nov. 21
Adamson, deposition, Atlanta s.c., Nov. 22
Demster, deposition, SF s.c., Dec. 5
Cerny, deposition, Cleveland s.c., Dec. 6
Parsons, deposition, Ft. Lauderdale s.c., Dec. 9
Saenz, deposition, Cameron TX s.c., Dec. 19
Jacobelly, deposition, SF s.c., Dec. 22
Thalman, deposition, Galveston s.c., Dec. 27
2006
Whiting, deposition Cleveland s.c., Jan. 4
Pisani, deposition, SF s.c., Jan. 5
Konecny, deposition, SF s.c., Jan. 9
Potts, deposition, Cleveland s.c., Jan. 13
Horr, trial, Oakland s.c., Jan. 18
Robinson, deposition, Angleton TX, Jan. 30
Thalman, trial, Galveston s.c., Feb. 1
Betti, deposition, SF s.c., Feb. 13
Smyth, trial, NY s.c., Feb. 16
Stroker, deposition, Oakland s.c., Feb. 21
Ryan, trial, Edwardsville IL s.c., Feb. 23-24
Woolston, deposition, Wilmington s.c., Feb. 27
Garrison, trial, Cleveland s.c., Mar. 1
Wallace, trial, Austin s.c., Mar. 2
Kovacevich, deposition, Houston s.c., Mar. 3
Troncali, deposition, Galveston s.c., Mar. 10
Jagid, deposition, New Brunswick NJ s.c., Mar. 13
Hellen, trial, Angleton TX s.c., Mar. 16
Brent, deposition, Edwardsville IL s.c., Mar. 22
Gortney, deposition, Beaumont TX s.c., Mar. 23
Slanina, deposition, Houston s.c., Mar. 24
Gregory, deposition, Kansas City MO s.c., Apr. 3
Miller, deposition, SF s.c., Apr. 6
Stone, deposition, Great Falls MT s.c., Apr. 10
Terrance, deposition, Baton Rouge s.c., Apr. 11
Burgeson, deposition, SF s.c., Apr. 12
Halsema, deposition, Oakland s.c, Apr. 13
Campbell, deposition, SF s.c., Apr. 13, 18
Miller, deposition, SF s.c., Apr. 17
Spurgeon, deposition, Edwardsville s.c., May 1
Sells, deposition, Cleveland s.c., May 3
Faulkoner, deposition, Wagoner OK s.c., May 8
Robinson, trial, Houston s.c., May 10
Flexner, trial, NY s.c., May 12
Fulton, deposition, SF s.c., May 15
Finnefrock, deposition, Cleveland s.c., May 18
King, deposition, Angleton TX s.c., May 19
Dancho, deposition, Chicago s.c., May 22
Haanstra, deposition, SF s.c., May 26
Bolen, trial, Garden City NY s.c., May 30
Giero, deposition, Los Angeles s.c., June 1
Jones, deposition, SF s.c., June 5
Gibson, deposition, Beaumont s.c., June 19
Loboda, deposition, NY s.c., June 26
Pitts, deposition, Fredericksburg VA s.c., June 28
Price, deposition, Oakland s.c., July 10, Aug. 12
Jones, trial, Newport News VA s.c., July 12
Jones, trial, SF s.c., July 31
Poindexter, deposition, Angleton TX s.c., Aug. 3
Christian, deposition, SF s.c., Aug. 10
Sutterfield, deposition, Houston s.c., Aug. 11
Hoser, deposition, New Brunswick NJ s.c., Aug. 14
Hegele. deposition, SF s.c., Aug. 17
Reese, trial, Bloomington IL s.c., Aug. 28
Siegwald, deposition, Dallas s.c., Aug. 29
Ferrera, deposition, Dallas s.c., Aug. 29
Bergin, deposition, SF s.c., Sept. 7
Adair, deposition, Orange TX, Sept. 8
Copenhaver, deposition, Dallas s.c., Sept. 8
Ard, deposition, Beaumont s.c., Sept. 8
Price, trial, Oakland s.c., Sept. 11
Pounds, deposition, SF s.c., Sept. 11
Homewood, deposition, Houston s.c., Sept. 18
Voight, deposition, Houston s.c., Sept. 18
Lindquist, deposition, Providence RI s.c., Sept. 22
Anderson, deposition, Denver s.c., Sept. 25
Rodriguez Negron, deposition, L.A. s.c., Sept. 28
Sheffield, deposition, Oakland s.c., Oct. 2
Shreiner, trial, Wilmington s.c., Oct. 3-4
Colella, trial, New York s.c., Oct. 10, 12, 17
Luckey, deposition, Houston s.c., Oct. 13
Hewitt, deposition, SF s.c., Oct. 16
Whitlock, deposition, SF s.c., Oct. 16
Boyer, trial, Boston s.c., Oct. 20
Johnson, deposition, Memphis s.c., Oct. 23
Cable, deposition, Bridgeport CT, Oct. 24
Hogan, deposition, Oakland s.c., Nov. 6
Stewart, trial, Wilmington s.c., Nov. 9
Oney, deposition, Houston s.c., Nov. 13
Blessing, trial, Bloomington s.c., Nov. 16
Young, deposition, Seattle s.c., Nov. 20
Whitlock, trial, SF s.c., Nov. 21
Duncan, deposition, Dallas s.c., Dec. 12
Morell, deposition, Edinburg TX s.c., Dec. 19
2007
Anzulis, deposition, Baltimore s.c., Jan. 5
Dodd, deposition, Edwardsville IL s.c., Jan. 8
Duncan, deposition, Edwardsville IL s.c., January 16
Boyle, deposition, SF s.c., Jan. 18
Link, deposition, Cleveland s.c., Jan 19
Knight, deposition, Houston s.c., Jan. 22
Gomez Gonzales, trial, NY s.c., Jan. 24
Foster, deposition, Angleton TX s.c., Jan. 26
Malcolm, deposition, Bloomington IL, Jan. 29
Lathrop, deposition, SF s.c., Feb. 2
Drinkwater, deposition, SF s.c., Feb. 2
Jones, deposition, Boston s.c., Feb. 5
Pollard, trial, Galveston s.c., Feb. 7
Metzger, deposition, Wilmington s.c, Feb. 12
Irvin, trial, Edmonton KY s.c., Feb. 15
Lee, deposition, Salisbury NC, Feb. 20
Pinedo, deposition, SF s.c., Feb. 26
Melon, deposition, Dallas s.c., Mar. 2
Murray, trial, Oakland s.c., Mar. 5
Farmer, deposition, SF s.c., Mar. 9
Rincon, trial, SF s.c., Mar. 16,19
Ridgley, deposition, Baltimore s.c., Mar. 22
Graves, deposition, Edwardsville IL, Mar. 23
Monroe, trial, Edwardsville IL, Mar. 27
Beckler, deposition, Dallas s.c, Mar. 30
Bock, deposition, Richmond s.c., Apr. 2
Melon, trial El Paso s.c., Apr. 5
Justice, deposition, Wilmington s.c., Apr. 9
Martin, trial, NY s.c., Apr. 25-26
Cox, trial, Cleveland s.c., May 4
Rodamer, deposition, SF s.c., May 7
Felker, trial, SF s.c., May 8
Passig, deposition, SF s.c., May 10
Asworth, deposition, Orange TX s.c., May 14
Heppe, trial, Bloomington s.c., May 15
Gilson, deposition, Atlanta s.c., May 18
Lucadamo, deposition, Providence s.c., May 25
Stirm, deposition, SF s.c., June 4
Ormonde, deposition, SF s.c., June 6
Dachauer, deposition, SF s.c.,June 11
Matel, deposition, SF s.c., June 21
Cook, deposition, Baltimore s.c., June 22
Buttitta, deposition, Hackensack NJ, July 2
Dachauer, trial, SF s.c., July 9-10
Scott, deposition, SF s.c., July 13
Gardner, deposition, Houston s.c., July 16
Eubanks, deposition, SF s.c., July 17, 25
Venturini, trial, Bloomington s.c., July 18-19
Lagrone, deposition, Wilmington s.c., July 23
Lagrone, trial, Wilmington s.c., July 24
Senator Boxer. Thank you, sir. Thank you very much.
Now, Dr. Ann Wylie, University of Maryland Department of
Geology.
STATEMENT OF ANN G. WYLIE, Ph.D., PROFESSOR OF GEOLOGY,
UNIVERSITY OF MARYLAND
Ms. Wylie. Thank you, Madam Chairman and members of the
committee.
I am pleased to be here today to speak to you about
definitions, in particular, the definition of asbestos and the
definition of asbestos fiber. I have been a professor for 35
years, and I have developed over this time expertise on the
properties of minerals that produce human disease when inhaled.
I provided a written text from which the following short
summary is taken.
The Federal definitions of fiber and asbestos both date
back to the early 1970s. Let me first address the definition of
fiber.
As defined, a fiber is any particle that fits into a
particular size and shape category. The category is large, and
it includes a wide range of particle sizes and shapes. Included
in this range are rock fragments as well as asbestos fibers.
The size and shape category is not specific for asbestos.
These non-asbestos particle that fit this category are very
common. They may be found in bedrock in large portions of the
United States. Epidemiological studies of miners exposed to
these particles have found no excess of asbestos-related
diseases.
The first pictures that I have shown over here are
particles in both of these that fit the definition of fiber.
The one on the left is asbestos; the one on the right is rock
fragments. Rock fragments meeting the fiber definition from
South Dakota are shown in this photograph. This is the site at
Leeds, SD of one of the negative studies for asbestos-related
diseases among the miners.
Asbestos is well-studied and well-characterized. A better
dimension definition of asbestos fiber would be relatively
simple to construct.
I also mention the definition of asbestos. The Federal
description of asbestos, in my view, needs to be amended. It
needs to explicitly include these asbestos fibers from Libby,
MT. These are the mineral winchite, and it is not listed in the
Federal regulatory definition of the minerals that make up
asbestos. As you can see from this photomicrograph, this is
actually an electron micrograph, these are clearly asbestos.
A more comprehensive description of asbestos and an
accurate, scientific definition of asbestos fiber will exclude
non-asbestos particles. They can be incorporated into
regulatory policy without compromising protection against
asbestos-related diseases. I would be happy to answer
questions.
[The prepared statement of Dr. Wylie follows:]
Statement of Ann G. Wylie, Ph.D., Professor of Geology at the
University of Maryland
My name is Ann G. Wylie. I hold a baccalaureate degree from
Wellesley College and a Ph.D., from Columbia University. I am Professor
of Geology at the University of Maryland. I have spent more than 30
years studying asbestos and the minerals that compose it.
I am here today to discuss the both the scientific and the federal
regulatory definition of asbestos.
regulatory history
In the early 1970s the United States lagged behind the rest of the
world in the strict regulation of occupational exposure to airborne
asbestos. Regulation of asbestos was one, if not the first, major
initiative of both EPA and OSHA when they were formed at this time.
Needless to say, these two agencies were in a hurry.
OSHA wrote a definition of asbestos and specified a method for its
measurement; both were incorporated into law. Together these comprise
the federal regulatory definition of asbestos.
The federal regulatory definition was written without any
consultation with the mineral experts at the United States Geological
Survey or the U.S. Bureau of Mines, and, consequently, it was not
mineralogically correct.\1\
---------------------------------------------------------------------------
\1\ OSHA's list of asbestos is also incomplete. One very public
effect of the latter mistake is that most of the asbestos occurring at
Libby Montana is not technically covered by asbestos regulations.
(Verkouteren and Wylie, 2000)
---------------------------------------------------------------------------
OSHA's regulatory definition identified mineral names without
specifying the asbestiform character. This is the same as saying that
hail and snow are the same thing. Both are ice, but everyone knows that
they are not the same and that have different potentials for harm.
The measurement method, called the membrane filter method\2\,
compounded the definitional problem. The foundation for the membrane
filter method was developed in the 1960s in British factories that
utilized asbestos. The particles included in exposure estimates were
specified by both a minimum length and a minimum length to width ratio.
A length of >5 micrometers was chosen to reflect an acceptable level of
reproducibility among analysts.\3\ A length to width ratio of 3:1 was
also specified, but its choice was not explained. Whatever the reason,
3:1 was arbitrary. It is not a scientific definition of a fiber, it
does not reflect the length to width ratio of asbestos fibers, and it
was not chosen because of any studies linking it to health effects.
---------------------------------------------------------------------------
\2\ Leidel et al., 1979
\3\ Addingley, C.F., 1966; Lynch et al., 1970
---------------------------------------------------------------------------
Because of the membrane filter method, particles longer than 5
micrometers with a length to width ratio of 3:1 or higher meet what has
become known as the Regulatory Fiber Definition (RFD). They are also
referred to as ``federal fibers.''
The effect of these two specifications, a mineralogically incorrect
definition of asbestos and the development of an arbitrary Regulatory
Fiber Definition (RFD), is that sometime during the 1970s, rock
fragments, sometimes called cleavage fragments, became fibers and
fragments of six minerals became de facto asbestos.
In 1992, OSHA examined this issue in detail. They concluded that
there was no scientific evidence that cleavage fragments have the same
health potential as asbestos. OSHA removed them from the asbestos
standard.\4\ I am not aware of any epidemiological, animal or cellular
studies that have been done since the OSHA decision that would change
this conclusion.
---------------------------------------------------------------------------
\4\ OSHA, 1992
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NIOSH disagreed with OSHA, and up to this time, it has been the
practice of NIOSH to assume that the RFD describes the size and shape
of fibers that correlate with their potential to cause human
disease\5\. The RFD was also recently applied by EPA in the El Dorado
Hills, CA, study. It is clear that there is disagreement within the
regulatory community of the appropriateness of the RFD in the
protection of health.
---------------------------------------------------------------------------
\5\ NIOSH, 2007
---------------------------------------------------------------------------
NIOSH has just opened this question for study.\6\ This year, NIOSH
issued a White Paper outlining in detail a research agenda to examine
this question and held public hearings on it last month. The adverse
health effects of asbestos are widely known and, with the exception of
the differences between chrysotile-asbestos and amphibole-asbestos, are
not in dispute. What the NIOSH White Paper addresses is the need to
examine the health effects of nonasbestos particles that meet the RFD.
---------------------------------------------------------------------------
\6\ NIOSH, 2007
---------------------------------------------------------------------------
While the NIOSH White Paper does not provide evidence that
challenges OSHA's 1992 decision, it calls for study of the issue,
including, animal inhalation studies, epidemiological studies of
miners, and cell culture studies. These are necessary before the health
effects of nonasbestos particles that meet the RFD can be understood
fully.
Why is this issue still in debate after the 1992 OSHA decision?
Partly, I believe, that it comes from (1) lack of knowledge about the
nature of asbestos, (2) acceptance of the hypothesis that only the
size, shape, and durability of mineral particles affect their
carcinogenic potential, and (3) a reluctance to change.
the nature of asbestos
Asbestos is unusual.\7\ It is a mineral habit, like snow and hail
are habits of ice. Habit is a form of ``growth''.
---------------------------------------------------------------------------
\7\ Wylie, 1979, 1993, 1988; Verkouteren and Wylie, 2002
---------------------------------------------------------------------------
Asbestos grows as bundles of single fibers, (referred to as
fibrils), that are easily separated from each other by hand pressure.
The geologic environment that enables asbestos to form is limited and
involves the presence of warm, water-rich conditions and open
underground spaces.
Fibrils have narrow widths and extraordinary tensile strength
imparted to them by their strong outer layers. They are difficult to
break and their strength makes them flexible and almost impossible to
grind. They are able to enter the body because of their narrow widths
and they are retained because their lengths (as much as several hundred
micrometers) thwart the body's mechanisms to remove them.
Asbestos can form from a number of different minerals. A mineral
name implies only a particular atomic arrangement of a fixed set of
elements in particular proportions. Mineral names are not synonyms for
asbestos, just like ice is not a synonym for snow although snow is made
of ice. To specify asbestos, the mineral name is followed by the term
asbestos, e.g., tremolite-asbestos. Two forms of asbestos have a
specific name, e.g., crocidolite is riebeckite-asbestos, and amosite is
cummingtonite-grunerite asbestos.
The dimensions of asbestos fibrils found in occupational air and in
the lung of asbestos workers are published in the literature, providing
the basis for a dimensional definition of asbestos fibers. Although
accurate dimensional definitions of asbestos may have been unnecessary
in monitoring asbestos factories, mills and mines where what was in the
air was only asbestos, they are essential in a mixed dust environment,
essential when dealing with environmental exposures, and essential if
asbestos were to be banned in the United States
Published data on the width of asbestos fibers found in bulk
samples, on air monitoring filters, and in lung tissue show that
asbestos is composed of mineral fibrils that are less than 1 micrometer
in width.\8\ Fibrils wider than 1 micrometer are brittle (lack tensile
strength) and cannot be used as asbestos.\9\ The widths vary somewhat
within and among asbestos deposits, but the range is narrow. The
dimensions of the most abundant forms of asbestos are similar:
crocidolite fibrils are about 500 to 2000 A in width, amosite and
anthophyllite-asbestos are about 2000 to 10,000 A in width, and
chrysotile-asbestos is about 200-650 A.\10\
---------------------------------------------------------------------------
\8\ Wylie et al.,1993
\9\ See Zoltai, 1981, for an excellent discussion.
\10\ Polygonal serpentine fibers may have diameters up to 10,000A.
Baronnet and Devouard, 2005.
---------------------------------------------------------------------------
Other types of asbestos have equally narrow widths. Actinolite-
asbestos has fibril widths of 600-2000 A and tremolite-asbestos fibrils
range from about 2000 to 6000 A. At Libby Montana, mean widths are
about 5000A and the range is 2000 to about 10,000A.\11\
---------------------------------------------------------------------------
\11\ Wylie et al., 1993
---------------------------------------------------------------------------
Studies of the lung burden of asbestos workers also report very
narrow fibers. Martha Warnock measured 3723 fibers from lung tissue
from 27 mesothelioma cases and identified them as crocidolite,
tremolite-asbestos, anthophyllite-asbestos, actinoliteasbestos,
chrysotile-asbestos, amosite, or other by TEM. More than 60 percent of
the fibers are either amosite or chrysotile-asbestos. The mean width of
the entire population was 2600 A; for amosite it was 2300 A and for
chrysotile-asbestos, 600 A. Similar dimensions were observed by Warnock
in asbestosis and lung cancer cases.\12\
---------------------------------------------------------------------------
\12\ Warnock, 1989
---------------------------------------------------------------------------
The width of asbestos fibers is independent of length.\13\ Width is
the same no matter how long the fibers because width is an independent
characteristic imparted during the ``growth'' of the fibers.
---------------------------------------------------------------------------
\13\ Siegrist and Wylie, 1980
---------------------------------------------------------------------------
Berman et al.\14\ extensive and careful evaluation of the 13
different rat experiments conclude that the fibers that contribute to
tumor risk are <4000A in width or they are bundles and aggregates of
such fibers. Stanton and others also find that fibers less than 5000 or
less in width are most likely to be carcinogenic. The NIOSH White Paper
states: ``Fibers and particles with diameters less than 0.5um (5000 A)
are more likely to cross membranes and translocate to pleural and
peritoneal spaces and are more likely to enter the lymphatic and
circulatory systems.'' Thus, not only is the width of asbestos a
defining characteristic, it is key to its carcinogenicity.
---------------------------------------------------------------------------
\14\ 1995
---------------------------------------------------------------------------
Cleavage fragments are different. Cleavage fragments, formed by
crushing rock, get wider as they get longer and width is therefore
dependent on length\15\. They do not possess the asbestos
characteristic of high tensile strength and their surfaces are
different in fundamental ways. While a 40 micrometer asbestos fiber
could easily have a width of 0.2 micrometers, such dimensions could
never be formed by breakage and no cleavage fragments have such
dimensions.
---------------------------------------------------------------------------
\15\ Siegrist and Wylie, 1980
---------------------------------------------------------------------------
size and shape hypothesis
The hypothesis that only dimensions and durability (biopersistence)
determine a mineral particles potential to cause mesothelioma, lung
cancer, laryngeal cancer, and asbestosis is known as the Stanton
Hypothesis. It was based on a large number of experiments in which
Stanton and coworkers at the NCI implanted a number of different
fibrous materials in rats.\16\ They found that the number of long thin
fibers highly correlated with the sarcomas that developed after
implantation. Other researchers have found similar results\17\.
---------------------------------------------------------------------------
\16\ Stanton et al., 1981
\17\ Bertrand, and Pezerat, 1980, Davis et al., 1991, Smith et al.,
1979, Pott et al., 1974.
---------------------------------------------------------------------------
If the Stanton Hypothesis is correct, then any biopersistent
particle that has the dimensions of real asbestos should have the same
carcinogenic potential as asbestos. In fact, we know that this is often
the case for asbestiform fibers. Long thin fibers of erionite, a
mineral not regulated as asbestos, are thought to be responsible for a
high incidence of mesothelioma among several small villages in
Turkey.\18\ Furthermore, the long, thin fiber (not specifically
regulated as asbestos by the federal government) from Libby ,Montana,
has been identified as the agent in a number of mesothelioma cases
among those occupationally exposed\19\.
---------------------------------------------------------------------------
\18\ Baris, 1987, Wagner et al., 1985
\19\ Amandus et al., 1987; Sullivan, 2007.
---------------------------------------------------------------------------
However, we also know from the experience of miners exposed to
other durable long, thin fibers such as fibrous talc\20\ that all
durable long, thin fibers are not the same. Many studies have shown the
importance of the surface in the biological activity of mineral
fibers.\21\ Understanding the basis of the carcinogenicity of mineral
fibers requires further study.
---------------------------------------------------------------------------
\20\ IARC, in press; Honda et al., 2002; Gamble, 1993; Stille and
Tabershaw, 1982
\21\ For example: Chamberlain and Brown, 1978; Feuerbacher et al.,
1980; Flowers, 1980; Marchisio and Pernis, 1963; Schlipkoter et al.,
1963; Brown et al., 1990; Weitzman and Graceffa, 1984; Weitzman and
Weitberg, 1985; Hochella (1993) provides an excellent discussion of the
variability of surface chemistry, structure and reactivity of mineral
surfaces that may affect biological activity.
---------------------------------------------------------------------------
Can the Stanton Hypothesis be used to justify concern for
nonasbestos, durable, RFD particles? If the RFD corresponds to a high
carcinogenic potential, then many mineral particles would be potential
carcinogens. Many common durable minerals break into elongated
particles that conform to the RFD even though they are not asbestiform
and do not have the dimensions of asbestos fibers. These include
pyroxenes, feldspars, zeolites, some sheet silicates, and many other
mineral groups. In fact, the Appalachian and Rocky Mountain Chains
contain abundant minerals that would form particles meeting the RFD
when crushed.
What does the epidemiology tell us? The studies that have examined
the epidemiology of workers exposed to dusts that contain nonasbestos
amphibole particles that meet the RFD have found no asbestos-related
diseases. Amphiboles make up 5 percent of the Earth's crust and,
although a large group of minerals of variable chemical
composition\22\, most amphibole fragments exceed 3:1 in length to width
ratio if they are longer than 5 micrometers. These studies include
miners and millers from a talc mine in New York, gold miners from Lead,
South Dakota; vermiculite workers at Enoree, South Carolina; and iron
miners from the Minnesota taconite iron district.\23\
---------------------------------------------------------------------------
\22\ Leake et al., 1997, 2004
\23\ McDonald et al., 1988, McDonald et al., 1978, Brown et al.,
1986, Higgins et al., 1983, Cooper et al., 1992, Honda et al., 2002,
Gamble, 1993, Steeland and Brown, 1995, Stille and Tabershaw, 1982
---------------------------------------------------------------------------
Asbestos fibers do meet the RFD. They exceed the 3:1 length to
width ratio. But because of their narrow widths, they also exceed a 5:1
and a 10:1 and most exceed a 20:1 ratio. Therein lays the problem.
While asbestos fibers conform to the RFD, they are not DEFINED by it,
and they cannot be separated from other mineral particles by it. While
we know that it is very likely that among amphiboles it is the size and
shape that affects their carcinogenicity, the question is ``What size
and what shape?''
reluctance to change the regulatory fiber definition
Neither OSHA nor MSHA consider cleavage fragments to be asbestos.
NIOSH has put the issue up for discussion. It is time for this issue to
be resolved.
conclusions
I conclude by asking you to support the work that NIOSH has
proposed to address unanswered questions about the carcinogenicity of
nonasbestos mineral particles. I also ask that the National Institute
of Standards and Technology (NIST) be funded to develop new analytical
methods for identifying and monitoring asbestos, and that NIEHS fund a
comprehensive risk assessment. At the present time, these issues are
being decided in the courts, not the appropriate venue for scientific
discourse.
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Health of vermiculate miners exposed to trace amounts of fibrous
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February 2007 draft, presented at Public Meeting, Washington , D.C, May
4, 2007, 47 pages.
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Siegrist, H.G. and Wylie, A.G., 1980, Characterizing and
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Stanton, M., Layard, M., Tegeris, A., Miller, E., May, M., and
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______
Response by Ann G. Wylie to an Additional Question from Senator Inhofe
Question. Are there universally accepted methods by which minerals
with asbestiform morphology can be distinguished via testing from
chemically similar cleavage fragments?
Response. Asbestos is a commercial term describing a group of
highly fibrous silicate minerals composed of very narrow fibrils that
easily separate by hand pressures yet possess tensile strength that is
higher than the same minerals in a different form. These physical
properties are universally understood as the characteristics necessary
for the term asbestos to apply. It has been in use for at least 130
years. E. S. Dana, then curator of the Mineral Museum at Yale, and J.D.
Dana, Professor of Physics, also at Yale, published a Textbook of
Mineralogy in 1877 in which they gave the following definition of
asbestos:
``Trernolite, actinolite, and other varieties of amphibole,
excepting those containing much alumina, pass into fibrous varieties,
the fibres of which are sometimes very long, thin, flexible and easily
separable by the fingers and look like flax. These kinds are called
asbestos.''
Since this definition was written, it is known that the form of
serpentine known as chrysolite can also be asbestos. The properties the
Danas describe are the same for both chrysotile-asbestos and amphibole-
asbestos and are distinctly different from chemically similar materials
that fragment by cleavage.
The identification of a mineral as amphibole or serpentine is
readily accomplished by a chemical analysis and an x-ray diffraction
pattern, the universally recognized basis for mineral
identification.\1\ In hand specimens of known amphibole or serpentine,
where long thin fibers that look like flax\2\ are visible and hand
pressure can be applied to determine if the fibers are flexible and
easily separable, the Dana definition of asbestos is universally
accepted.
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\1\ There are other recognized methods of identification, but x-ray
d most reliable and its results are unequivocal.
\2\See photographs attached.
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Another definition has been developed over the past 20 years for
identification of asbestos in material taken from bulk samples and
examined under the optical microscope. To apply this definition, the
identification of the mineral as serpentine or amphibole must be known.
It has never to my knowledge been criticized and it is widely used;
applying the term ``universal'' however, suggests that it would be
accepted by mineralogists worldwide and I cannot say that it has been
so widely discussed. It would probably surprise mineralogists not from
the United States that a definition is needed at this level since the
Danes' definition is so clear and has served so well for so long. This
definition of asbestos at the microscope level for ao rp--ption of
asbestos fibers is as follows:
The following characteristics of a population of asbestos fibers
can be observed by light microscopy and enable it to be distinguished
from a chemically similar population of cleavage fragments:
(1) Aspect ratios of 20: I and greater for particles longer than 5
micrometers are common.
(2) Fibers are composed of very thin fibrils, often less than 0.5
micrometers, which occur in bundles.
(3) Fibers wider than 0.5 micrometers display splayed ends,
demonstrating their fibrillar structure.
(4) Matted masses of individual fibers may be found in some samples
(5) Long fibers frequently display curvature, a sip of flexibility.
There is no accepted method by which asbestos can be distinguished
from cleavage fragments on a particle by particle basis on air
monitoring or water filtration filters. The NIOSH fiber definition is
not specific for asbestos. However, I believe, and I so testified, that
it is possible to develop a method that will enable a sufficiently
accurate distinction between asbestos fibers and cleavage fragments
found on air and water monitoring filters such that reliable exposure
estimates/concentrations of each can be made. The method would be based
on the unusual and distinctive dimensional characteristics of asbestos
that are already well known and well described in the published
literature. The National Institute of Standards and Technology has the
experience and knowledge to develop such a method.
Senator Boxer. Thank you very much.
Dr. Weill.
STATEMENT OF DAVID WEILL, M.D., ASSOCIATE PROFESSOR, DIVISION
OF PULMONARY AND CRITICAL CARE MEDICINE, STANFORD UNIVERSITY
MEDICAL CENTER, STANFORD, CA
Dr. Weill. Good morning, Senator Boxer and members of the
committee. Thank you for the opportunity to testify.
I will comment today specifically on the differences in
toxicity associated with a variety of inhaled fibrous and non-
fibrous minerals. These minerals are often grouped under the
broad category of asbestos, but there are fundamental
differences among these minerals in terms of their potential to
cause human disease.
My testimony is from a clinician's point of view, using
appropriate support from the scientific background. As was
mentioned, I hold several positions at the Stanford University
Medical Center, including Director of the Lung and Heart-Lung
Transplant Program. I am also a ``B Reader,'' certified by
NIOSH as competent to classify chest x-rays for lung conditions
such as those caused by exposure to asbestos dust.
I have also had the opportunity to testify before the U.S.
Senate Judiciary Committee when it was considering the FAIR Act
legislation in 2005 as well as the Texas State legislature when
it was considering legislation addressing the handling of
asbestos and silica claims. It is of course a privilege to
testify before you here today.
Asbestos exposure, as you have heard today, can lead to
both non-malignant and malignant diseases, such as lung cancer
and mesothelioma. The asbestos-related diseases, and for that
matter, all pneumoconiosis, are dose-dependent, meaning that
increased level and total amount of exposure results in
increased risk and/or severity of the disease. Conversely, as
workplace exposures have been substantially reduced in the last
several decades, asbestos-related health effects have also
become less prevalent.
While our focus here today is to discuss the differences
between asbestiform and non-asbestiform substances, it is
important to note that there are important differences, even
among various asbestos fiber types, and considerable evidence
that different types of asbestos have different potentials to
cause disease. While many epidemiologic studies have
demonstrated an association between asbestos exposure and
mesothelioma, the asbestos-mesothelioma association is
particularly strong in occupations that involve heavy amphibole
exposure, such as shipyard workers and insulators.
The message of these studies is simple: different asbestos
fiber types have different potential to cause disease.
Now, examining the health effects of amphibole minerals
more closely. There has been a considerable body of literature
about the health effects of cleavage fragments derived from
non-fibrous amphibole minerals, specifically whether or not
they can cause human disease.
Although I am by no means a mineralogist, I have some
understanding about the physical properties of these fibers and
cleavage fragments. Most amphibole minerals are non-
asbestiform, designated as such because they have different
characteristics that make them behave differently. Cleavage
fragments result from a physical manipulation of these non-
asbestiform particles.
They are sometimes difficult to distinguish from amphibole
asbestos fibers using standard counting procedures. Based on
the scientific literature in my experience as a clinician, I
have three general opinions regarding the health effects of
cleavage fragments. No. 1, the different properties of
asbestiform amphibole fibers and non-asbestiform cleavage
fragments impact human health differently and should not be
considered as the same. No. 2, animal data reveal lack of
pathogenicity; and No. 3, human epidemiologic studies have
established no association between cleavage fragments and human
disease.
Others testifying here today will describe in detail the
differences in physical properties of asbestos fibers and
cleavage fragments. In the interest of time, I will skip any
discussion of these physical properties, except to say that the
fundamental physical difference between amphibole asbestos
fibers and cleavage fragments results in each having very
different health effects. That is my first opinion that I want
to express.
Now my second opinion, specifically that there are animal
studies involving exposure to cleavage fragments, not finding
any adverse health effects from these exposures, I have also
outlined in my written testimony. I wanted to be able to skip
to my third opinion, looking at human epidemiologic studies
involving exposure to cleavage fragments, specifically that
they have not found any adverse health effects. The
occupational settings for these studies include gold, nickel
and taconite mines, as well as talc and pottery workers and
tunnel diggers. In each of these cohorts, no excess
mesothelioma, lung cancer of pneumoconiosis risk could be shown
from exposure to cleavage fragments.
Fortunately, with the institution of policies which limit
occupational exposure to asbestos, the incidence of asbestos-
related lung conditions is decreasing. Further, it is my
opinion that not all types of asbestos have the same potential
to cause human disease. Even further, cleavage fragments are
naturally occurring and rarely meet the regulatory definition
of asbestos fiber.
Currently, there is no existing evidence that cleavage
fragments are pathogenic for the reasons that I reviewed. The
impetus to perform----
Senator Boxer. Doctor, could you just wrap up?
Dr. Weill. Sure.
Senator Boxer. Thank you.
Dr. Weill. The impetus to perform epidemiologic studies on
substances that may have a human health risk evolve from
hypothesis-generating information that suggest there might be a
risk. I do not believe such data exists with regard to cleavage
fragments.
I feel my opinions today are based on the scientific
evidence already available. Thank you for the opportunity to
testify, and I hope my perspective is helpful.
[The prepared statement of Dr. Weill follows:]
Statement of David Weill, M.D., Associate Professor, Division of
Pulmonary and Critical Care Medicine, Stanford University Medical
Center, Stanford, CA
Senator Boxer, Senator Inhofe, and Members of the committee: Thank
you for the opportunity to testify before you about the health effects
of asbestos. I will comment today specifically on the differences in
toxicity associated with a variety of inhaled fibrous and non-fibrous
minerals. These minerals are often grouped under the broad category of
``asbestos,'' but there are fundamental differences among these
minerals in terms of their potential of each mineral to cause human
disease. My testimony is from a clinician's point of view, using
appropriate support from the scientific literature.
I'll begin by telling you a bit about my background. I am board
certified in Pulmonary and Critical Care Medicine. Currently, I hold
several positions at the Stanford University Medical Center, including
Associate Professor of Medicine in the Division of Pulmonary and
Critical Care Medicine, and I am the Director of the Lung and Heart--
Lung Transplant Program.
I am also a ``B Reader,'' which means I have been certified by the
National Institute of Occupational Safety and Health (``NIOSH'') as
competent to classify chest x-rays for lung conditions such as those
caused by exposure to asbestos dust. At Stanford, we are referred and
treat patients with both common and rare respiratory conditions. Such
referrals include patients with both occupational and non-occupational
diseases.
I have also had the opportunity to testify before the United States
Senate Judiciary Committee when it was considering the FAIR Act in 2005
and the Texas State Legislature regarding legislation addressing the
handling of asbestos and silica claims. It is of course a privilege to
testify before you here today.
heath effects of asbestos
Asbestos exposure can lead to nonmalignant conditions such as
asbestosis (a parenchymal fibrotic lung disease) and pleural changes
(pleural effusion, pleural thickening, pleural plaques, and rounded
atelectasis), as well as malignant conditions such as lung cancer and
mesothelioma. The asbestos-related diseases and, for that matter, all
pneumoconiosis, are dose-dependent, meaning that increased level and
total amount of exposure results in increased risk and/or severity of
the diseases. Conversely, as workplace exposures have been
substantially reduced in the last several decades, asbestos-related
health effects have become less prevalent.
health effects of different asbestos fibers
Asbestos is the commercial designation for 6 fibrous minerals of
two broad types: serpentine and amphibole. Chrysotile is the only type
of serpentine asbestos, while there are five different amphibole
asbestos fibers: crocidolite, amosite, tremolite, actinolite, and
anthophyllite. While our focus here today is to discuss the differences
between asbestiform and non-asbestiform substances, it is important to
note that there are important differences even among various asbestos
fiber types and considerable evidence that different types of asbestos
have different potentials to cause disease. While many epidemiologic
studies have demonstrated an association between asbestos exposure and
mesothelioma, the asbestos-mesothelioma association is particularly
strong in occupations that involved heavy amphibole asbestos exposure,
such as shipyard workers and insulators.
The message of these studies is simple: different asbestos fiber
types have different potential to cause disease.
health effects of cleavage fragments
Now, let's examine the health effects of amphibole minerals more
closely. There has been a considerable body of literature about the
health effects of cleavage fragments derived from non-fibrous amphibole
minerals, specifically whether they can cause human disease. Although I
am by no means a mineralogist, I have some understanding about the
physical and chemical properties of asbestos fibers and cleavage
fragments, particularly as they are important to the development of
human lung disease.
Most amphibole minerals are ``non-asbestiform'', designated as such
because they have different characteristics that make them behave
differently. Cleavage fragments result through the physical
manipulation of these non-asbestiform particles and are sometimes
difficult to distinguish from amphibole asbestos fibers using standard
counting procedures.
Based on the scientific literature and my experience is a
clinician, I have three general opinions regarding the health effects
of cleavage fragments:
(1) The different properties of asbestiform amphibole fibers and
non-asbestiform cleavage fragments impact human health differently and
should not be considered as the same;
(2) Animal data reveal a lack of pathogenicity;
(3) Human epidemiological studies have established no association
between cleavage fragments and human disease
physical properties of amphibole asbestos fibers and cleavage fragments
First, a bit about the different properties of asbestos fibers and
cleavage fragments. Although the non-asbestiform and asbestos
amphiboles are chemically similar, they differ with regards to
morphology. Asbestiform amphiboles are made up of fiber bundles that
run parallel to each other, which when they split, form single fibrils.
Each individual fibril is long, thin, and very flexible. Non-
asbestiform amphiboles are not unidirectional fibers but run in two or
more different planes, forming a prism. These non-asbestiform
structures do not break down into fibers or fibrils but instead into
cleavage fragments that are thick and short and therefore not likely to
be inhaled into the more distant (or deep) parts of the lung.
If one then compares more closely asbestiform and non-asbestiform
amphiboles, they differ with respect to three important
characteristics: surface properties, tensile strength, and dissolution.
1. Surface properties. The outside surface of amphibole asbestiform
fibers is smooth, free of defects, and very strong, largely because
there are no crevices or cracks in the fiber surface that can be
subject to degradation strategies present after inhalation into the
lung. This is not the case in non-asbestiform structures that have
mechanical planes that can be exploited and lead to degradation.
2. Tensile strength. Amphibole asbestos fibers have inherent
flexibility, giving them great tensile strength. Cleavage fragments,
however, are inflexible and brittle, making them vulnerable to physical
stress.
3. Dissolution properties. The human body's natural defenses,
particularly macrophages, generate an acidic environment to break down
inhaled particles in the lungs. Amphibole asbestos fibers are resistant
to acidic dissolution and are said to be biopersistent, meaning they
remain in the lungs indefinitely. Cleavage fragments have surface
defects or cracks that make these fragments amenable to acidic
dissolution, which enables the body's natural defenses to expel them.
These fundamental physical differences between amphibole asbestos
fibers and cleavage fragments result in each category of minerals
having different health effects. Cleavage fragments are generally too
wide to penetrate into the deep parts of the lung, particularly when
longer than 5 microns. If shorter than 5 microns, as is commonly the
case, there is a body of literature that suggests that, even if they
shared the same properties as those of asbestos fibers, that these
smaller particles have no pathologic effect, either in terms of
fibrosis or mesothelioma development. In fact, the epidemiology and
basic science literature (beginning in 1968) demonstrates that fiber
length correlates strongly with development of asbestos-related
diseases. This proposition is described as the Stanton hypothesis and
assumes that fibers greater than about 8 microns in length and less
than a quarter of a micron in diameter are the most potent in producing
mesothelioma.
Highlighting this point, the EPA in 2003 reviewed the available
literature to devise a protocol to assess asbestos-related risk. The
expert panel agreed with the development of a protocol that considered,
for purposes of evaluating asbestos-related risk, that fibers less than
0.5 microns in diameter and greater than 5 microns in length were more
important in disease development. Fibers with greater diameters were
believed to be unlikely to be inhaled to the more distal parts of the
lung.
animal studies involving exposure to cleavage fragments
Let's move on to my second opinion, specifically that animals
studies involving exposure to cleavage fragments have not found any
adverse health effects from such exposures. It should be noted that
there are limitations of the findings of any animal studies of this
nature. First, animal studies generally use direct intrapleural or
intraperitoneal injection of the substance being studied, bypassing the
lung's natural defense mechanisms. And secondly, the amount of a
substance administered to the animals (i.e. the dose) is usually
massive and well beyond what could be observed in any occupational
setting. However, notwithstanding these limitations, there are several
animals studies that have been conducted that show no carcinogenic
potential for cleavage fragments. This is very different from similarly
conducted studies when true amphibole asbestos fibers were instead
injected.
human studies involving exposure to cleavage fragments
Finally, my third opinion is that the body of human epidemiological
studies involving exposure to cleavage fragments has not found adverse
health effects from exposure to cleavage fragments. The occupational
settings for these epidemiological studies included gold, nickel, and
taconite miners, as well as talc and pottery workers and tunnel
diggers. In each of these cohorts, no excess mesothelioma, lung cancer,
or pneumoconiosis risk could be shown from exposure to cleavage
fragments.
The largest study of workers exposed to cleavage fragments has been
the Homestake gold mining cohort. In this study, there was no excess
lung cancer risk identified. In fact, as exposure levels increased, the
lung cancer risk tended to decrease, indicating no association of
exposure with lung cancer development. Importantly, there were no
mesothelioma deaths in this group. A study was also conducted of the
Minnesota taconite miners who were exposed to grunerite cleavage
fragments and this cohort showed no evidence of an excess of asbestos-
attributable diseases. Other studies of cohorts exposed to cleavage
fragments have reached similar conclusions. Therefore, the health risks
demonstrated to be associated with amphibole asbestos exposure should
not be assumed to apply to cleavage fragments.
Fortunately, with the institution of policies which limit
occupational exposure to asbestos, the incidence of asbestos related
lung conditions is decreasing. Further, it is my opinion that not all
types of asbestos have the same potential to cause human disease. Even
further, cleavage fragments are naturally occurring and rarely meet the
regulatory definition of an asbestos fiber. Therefore they are
designated as ``non-asbestiform'' and have fundamentally different
properties than amphibole asbestos. Currently, there is no existing
evidence that cleavage fragments of nonasbestiform fibers are
pathogenic for the reasons that I reviewed in my testimony, and there
is no animal or human data that implicates these fragments as a cause
of disease.
The impetus to perform epidemiologic studies on substances that may
have a human health risk generally results from hypothesis-generating
information to suggest that there might be a health risk. I do not
believe such data exists. Further, with the asbestos exposure levels so
low currently and the inability to study in isolation the health
effects of cleavage fragments, I do not feel that human studies could
be conducted which would result in meaningful conclusions. The medical
literature is already informative on non-asbestiform fragments, and
while it is always important to gain new scientific knowledge, I feel
my opinions expressed today are based on the sound scientific evidence
already available.
I hope that my perspective is helpful to the committee's efforts.
Thank you.
______
Responses from David Weill, M.D., to Additional Questions from
Senator Inhofe
Question 1. Can you please clarify your response during the hearing
regarding questions posed to you associated with scientific methodology
and acceptable risk?
Response. Science, through epidemiologic study, provides society
with risk assessments of various elements of our society. These
elements are broad and include non-occupational activities, such as
driving a car, drinking the water, and flying in an airplane, just to
name a few. Epidemiology has also given us information about the risks
present in a variety of occupational settings and informs employers,
employees, and society in general about the risks that might be present
in a particular work environment. Science can quantitative these
occupational and non-occupational risks, but it cannot determine what
is an acceptable risk. Instead, the determination of acceptable risk is
a societal function.
Question 2. Do you believe it is the proper role for scientists and
data analysts to make policy, regulatory, and legislative decisions
regarding health protections or is it the role of these technical
professionals to fairly and without bias evaluate scientific data to
inform the public policy debate?
Response. I clearly think it is our job as scientists to provide
the scientific data and analysis to policy makers, who then have the
responsibility to set policy that reflects societal values and
concerns. I do not think it is my place as a physician to make
determinations about what risks are acceptable in non-occupational or
occupational settings. This should be a function of our policy makers.
Senator Boxer. Thank you, Doctor.
Dr. Lemen.
STATEMENT OF RICHARD A. LEMEN, Ph.D., M.S.P.H., FORMER
DIRECTOR, DIVISION OF STANDARDS DEVELOPMENT AND TECHNOLOGY
TRANSFER, ASSISTANT SURGEON GENERAL, U.S. PUBLIC HEALTH SERVICE
(RETIRED), REAR ADMIRAL, U.S. PUBLIC HEALTH SERVICE (RETIRED)
Mr. Lemen. I would like to thank you, Chairman Boxer,
Ranking Member Inhofe and Senator Lautenberg and the rest of
the committee for inviting me here today. My name is Dr.
Richard Lemen. I am a former Assistant Surgeon General of the
United States, and was former Acting and Deputy Director of the
National Institute for Occupational Safety and Health.
As we address asbestos during this hearing over the next 2
to 3 hours, approximately three to four people will die of an
asbestos-related death. These diseases could have been
prevented. Unfortunately, these diseases represent an under-
estimate because there are no nationwide surveillance systems
that capture adequately the true nature of asbestos-related
diseases.
For example, one of our premier surveillance systems, the
Surveillance Epidemiology and End Results data base of the
National Cancer Institute has been found to under-report
mesothelioma in some areas of the United States by as much as
80 percent. We need to fix this and perfect better systems to
capture all asbestos-related diseases, if we are ever to have
data to measure the true impact of asbestos and to determine if
our public health efforts to prevent asbestos-related diseases
are effective.
As we will see in countries that have banned or placed
strict regulations on the import and use of asbestos, the trend
of asbestos-related diseases is beginning to slow down.
However, this is not true in the United States, according to
the National Institute for Occupational Safety and Health,
where asbestosis is the only one of the induced lung diseases
that continues to increase. This is also true for mesothelioma.
While this country is still experiencing asbestos-induced
and disease epidemic that continues to get worse and shifting
from occupational to non-occupational victims, proponents of
asbestos usage are trying to influence the regulatory agencies
with efforts to exclude some forms of asbestos, as well as
rewrite the definition of asbestos to exclude exposures to non-
asbestos materials that are contaminated with fibrous asbestos.
These issues include the relaxation of regulatory standards for
the main commercial asbestos fiber type chrysotile.
In doing this, two issues will be accomplished. First, the
ability to continue to use chrysotile asbestos in this country
and to promote new markets in developing countries not having
regulations or adequate knowledge of the hazards of this form
of asbestos.
Second, by redefining asbestos and eliminating types of
fibrous particles such as cleavage fragments that are
contaminants of talc mines and other types of mines such as
vermiculite mines, allow these operations to continue exposing
their workers and spreading their contamination and deadly
products to unsuspecting consumers. Such shenannery must be
exposed.
Chrysotile asbestos is dangerous and no exposure threshold
has ever been established for its safe use. It causes all
asbestiform-related diseases. Regulation of asbestos has been
historically dependent upon the definition of asbestos, and as
you heard from NIOSH, even at the current standard of .1 fiber
per cc, 3.4 per 1,000 workers will die over a working lifetime.
I would like to provide some data which may shed some light
on the arguments for a better fiber definition which comes to
materials contaminated to fibrous asbestos. For many years,
NIOSH has been looking at this issue. NIOSH's Dement and co-
workers found from one mine and mill reported by a company to
be producing non-asbestiform talc air samples of 5 fibers per
cc as time-weighted averages in 6 job categories containing 48
percent mineral talc, tremolite and phosolyte, serpentine,
lizardite, antigorite. Thus, the TWA for asbestos was exceeded
by both the OSHA and the Federal Mine Safety and Health
Administration.
I would like to end this testimony by saying that in some
of the testimony that has come before, we have heard that the
mines that have some of these fibers, such as the gold mine,
have not had related diseases. I would like to correct that,
because there is a threefold excess in the study that I was
conducting with my NIOSH colleagues in 1976 for respiratory
cancer, and a twofold excess for respiratory disease.
In the study that was done by Dr. McDonald, when you look
at the----
Senator Boxer. We need you to wrap up now.
Mr. Lemen. When you look at the latency period, which is an
important, critical factor, and those highest latency periods
disease did occur.
Thank you, and I will have the rest of my comments
submitted to the committee.
[The prepared statement of Dr. Lemen follows:]
Statement of Richard A. Lemen, Ph.D., M.S.P.H., Former Director,
Division of Standards Development and Technology Transfer, Assistant
Surgeon General, U.S. Public Health Service (Retired), Rear Admiral,
U.S. Public Health Service (Retired)
I would like to thank Chairman Boxer, Ranking Member Inhofe and the
entire EPW Committee for the honor and opportunity to testify today.
My name is Dr. Richard A. Lemen. I am retired from the United
States Public Health Service where I was an Assistant Surgeon General
of the United States. At the time of my retirement I was also Deputy
Director and had been Acting Director of the National Institute for
Occupational Safety and Health (NIOSH). I have spent my entire career,
since 1970, studying the epidemiology of asbestos-related diseases and
have conducted numerous epidemiology studies, written many scientific
papers, advised the World Health Organization, various other National
governments, and have testified before the United States Congress on
several occasions concerning the health risks from exposure to
asbestos. I am an adjunct professor of environmental and occupational
medicine at Emory University and a consultant in occupational health
and epidemiology. I also testify in asbestos-related litigation on
behalf of plaintiffs. My CV, which I have supplied the committee, will
give you further information concerning my studies on asbestos.
Often asbestos is referred to as the ``magic Mineral'' having at
least 3000 or more uses, such as being woven into cloth, with vegetable
fibers; for wrapping the corpuses, referred to by Pliny as the funeral
dress of kings prior to cremation in order to help collect the ashes;
in making clay pots some 4000 years ago; and was even mentioned by
Marco Polo, during his travels to the far east, where he found it
called ``salamander'' skin which was mined from the mountains,
extracted then crushed, by subjects of the Great Khan, into a fibrous
like wool that was then spun and made into cloth of which some were
used for table cloths, that when soiled, were thrown into the fire and
came out ``white as snow'' for use again; one was sent to the Pope, in
Rome, ``in which cloth he keeps the Sudarium of our Lord.'' Benjamin
Franklin even bought a purse from the ``northern part of America'' made
from woven asbestos.\1\
---------------------------------------------------------------------------
\1\ Lemen, RA, 2005. Epidemiology of Asbestos-Related Diseases and
the Knowledge that Led to What is Known Today. In: ASBESTOS Risk
Assessment, Epidemiology, and Health Effects, Eds. RF Dodson, SP
Hammar. CRC Taylor & Francis, 201-308.
---------------------------------------------------------------------------
Our modern knowledge of asbestos usage and asbestos-related disease
began in the early 1900s, with reports of lung diseases among asbestos
workers in the United Kingdom as well as the United States. By 1930,
the disease asbestosis was well established as a lung disease
contracted from exposures to asbestos. Unfortunately, by the mid-1930s
it was suspected that, in addition to asbestosis, cancer may also
result from exposure to asbestos. Today we know that various cancers,
including lung cancer, gastrointestinal cancers, and mesothelioma are
all causally associated from exposure to asbestos. We know that all
forms of commercially used asbestos, including chrysotile, as well as
the amphiboles cause all of the asbestos-related diseases including
asbestosis, lung cancer, mesothelioma and gastrointestinal cancers.\2\
---------------------------------------------------------------------------
\2\ Lemen, RA, 2005. Epidemiology of Asbestos-Related Diseases and
the Knowledge that Led to What is Known Today. In: ASBESTOS Risk
Assessment, Epidemiology, and Health Effects, Eds. RF Dodson, SP
Hammar. CRC Taylor & Francis, 201-308.
---------------------------------------------------------------------------
Asbestosis is a progressive disease which can eventually result in
death after much disability and suffering, even after occupational
exposures have ceased. Asbestosis does not respond to medical
treatment, only palliative care can be given.\3\
---------------------------------------------------------------------------
\3\ ATSDR, 2001. Agency for Toxic Substances and Disease Registry
Questions and Answers Exposure to Asbestos. Department of Health and
Human Services, Atlanta, GA, July 26.
---------------------------------------------------------------------------
Asbestos-induced cancers are not confined to just the workers
exposed at work, but asbestos exposures can be brought home to family
members, as a result of contamination of their work clothes, prompting
asbestos-induced disease in them as well. Asbestos-related diseases can
also occur to residents living near asbestos sources.\4\
---------------------------------------------------------------------------
\4\ NIOSH, 1995. Report to Congress on Workers' Home Contamination
Study Conducted Under The Workers' Family Protection Act (29 U.S.C.
671a). U.S. Department of Health and Human Services, Public Health
Service, Centers For Disease Control And Prevention, National Institute
for Occupational Safety and Health (NIOSH), Cincinnati, OH 45226,
September. See sections on Asbestos p. 6-11; 45-46; 55; 62-63; 86-87;
tables 2-6 (pp. 145-159).
---------------------------------------------------------------------------
In the United States it is estimated that between 189,000 and
231,000 deaths have occurred since 1980 due to workplace exposure to
asbestos. Another 270,000 to 330,000 deaths are expected to occur over
the next 30 years and for those workers exposed, over a working
lifetime, to the current Occupational Safety and Health administration
(OSHA) standard of 0.1 fibers/cc--3.4/1000 workers are estimated to die
as a result of asbestos-related diseases.\5\ A more recent study
suggested the use of linear extrapolation, as used by OSHA, from high
exposure levels may underestimate the risks at low doses (Gustavsson et
al., 2002).\6\ Unless asbestos use in the United States is not banned
there is no end of its ability to exposure workers and consumers to its
dangers.
---------------------------------------------------------------------------
\5\ OSHA, 1986. OSHA, 1986. Final Rule: Asbestos. 51 FR 22612. U.S.
Department of Labor. Occupational Safety and Health Administration,
Washington, D.C., June 20.
\6\ Glustavsson P, Nyberg F, Pershagen G, Scheele P, Jakobsson R,
Plato N, 2002. Low-dose exposure to asbestos and lung cancer: Dose-
response relations and interaction with smoking in a population-based
case-referent study in Stockholm, Sweden. Am J Epi, Vol. 156 (11);
1016.
---------------------------------------------------------------------------
Products containing asbestos can still be found in things found in
the home such as lamp sockets, floor tiles, cat box fill, braking
mechanism in washing machines and cars, furnaces, and other products.
Because these products are not only manufactured by workers, but are
also used, maintained, and repaired by workers--they (workers) suffer
additional exposure from consumer products as do the consumers using
these products.
The most recent Criteria Document from the World Health
Organization's (WHO) International Programme for Chemical Safety (IPCS)
states in 1998 that no threshold has been identified for carcinogenic
risks to chrysotile asbestos.\7\ Chrysotile is the main commercially
used asbestos in the World. This 1998 WHO statement is consistent with
the WHO's earlier conclusion in 1989 ``[T]he human evidence has not
demonstrated that there is a threshold exposure level for lung cancer
or mesothelioma, below which exposure to asbestos dust would not be
free of hazard to health''.\8\ The WHO recognizes what NIOSH concluded
31 years ago, in 1976, that ``. . . (only a ban can assure protection
against carcinogenic effects of asbestos)''.\9\ I cannot tell any of
you, on this committee, why some will develop asbestosis or other
asbestos-related cancers and why others won't. But what I can tell you
is that asbestos-induced diseases are preventable. Each and every one!
---------------------------------------------------------------------------
\7\ IPCS, 1998. Environmental Health Criteria 203: Chrysotile
Asbestos, International Program on Chemical Safety, World Health
Organization.
\8\ WHO, 1989. Occupational Exposure Limit for Asbestos. WHO/OCH/
89.1, Office of Occupational Health, World Health Organization, Geneva.
\9\ NIOSH, 1976. Revised Recommended Asbestos Standard. DHEW
(NIOSH) Publication No. 77-169. U.S. Department of Health, Education,
and Welfare. Public Health Service. Centers for Disease Control.
National Institute for Occupational Safety and Health. December.
---------------------------------------------------------------------------
The first criteria document from the newly formed NIOSH of 1970,
was on asbestos, after NIOSHs first Director Dr. Marcus Key had sent a
letter to OSHA stating the inadequacy of OSHAs new start-up standard
for asbestos, based on the then ACGIH TLV. NIOSH was the first federal
agency to call for a ban on asbestos in its 1976 Revised Criteria
Document. NIOSH has maintained this position to the present, while
suggesting in the interim that the only reliable and practical
analytical method, in 1976, was 0.1 fiber/cc using the NIOSH Phase
Contrast Method (PCM) 7400 asbestos analytical method. Unfortunately
chrysotile cannot be seen in the light microscope when it occurs in the
fibril form and thus most chrysotile is not counted in an air sample
using a NIOSH 7400 count scheme-diameter resolution of approximately
0.25 microns where as most individual fibers of crocidolite and
chrysotile are 0.02-0.05 microns in diameter. OSHA describes the
advantages and disadvantages of the Phase Contrast Microscope (PCM) as
can be seen in the footnote.\10\
---------------------------------------------------------------------------
\10\ Rules and regulations--Dept Labor--OSHA 29 CFR Parts 1910,
1915, 1926-Occupational Exposure to Asbestos--Final rule--Aug. 10, 1994
59FR4096
``1.3 Advantages and Disadvantages
There are four main advantages of PCM over other methods:
(1) The technique is specific for fibers. Phase contrast is a fiber
counting technique which excludes non-fibrous particles from the
analysis.
(2) The technique is inexpensive and does not require specialized
knowledge to carry out the analysis for total fiber counts.
(3) The analysis is quick and can be performed on-site for rapid
determination of air concentrations of asbestos fibers.
(4) The technique has continuity with historical epidemiological
studies so that estimates of expected disease can be inferred from
long-term determination of asbestos exposures.
41066 The main disadvantage of PCM is that it does not positively
identify asbestos fibers. Other fibers which are not asbestos may be
included in the count unless differential counting is preformed. This
requires a great deal of experience to adequately differentiate
asbestos from non-asbestos fibers. Positive identification of asbestos
must be performed by polarized light or electron microscopy techniques.
A further disadvantage of PCM is that the smallest visible fibers are
about 0.2mm in diameter while the finest asbestos fibers may be as
small as 0.2mm in diameter. For some exposures, substantially more
fibers may be present than are actually counted.''
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Any definition of asbestos should include all respirable
asbestiform fibrous minerals, including fibrous cleavage fragments
which are respirable.\11\ This should only be changed if there exist
irrefutable data, both human and animal, showing the safety of any such
fibrous mineral being excluded. Valid methodologies now exist to sample
for all size fibers, including those less than 5 um in length, not
currently addressed in regulatory standards. These smaller fibers
should be included in any asbestos definition. Both animal and human
data support such an inclusion as can be seen by the attached Appendix
1.\12\
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\11\ Dement J M, Zumwalde RD, Gambel JF, Fellner W, DeMeo MJ, Brown
DP, Wagoner JK, 1980. Occupational exposure to talc containing
asbestos-Morbidity, Mortality, and environmental studies of miners and
millers. NIOSH Technical Report-DHEW (NIOSH) Publication No. 80-115,
Feb.
\12\ See Appendix 1--Short Fibers, Richard A. Lemen, Ph.D.
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Federal and State governments should work together to address,
refine, and/or develop surveillance of fiber-related diseases,
including those from asbestos. For example it is well known that the
National Cancer Institutes Surveillance Epidemiology and End Results
(SEER) data base underreports mesothelioma.\13\ NIOSH should be funded
to continue its Respiratory Disease Surveillance System and should
assure that other NIOSH surveillance systems become more comprehensive
and inclusive. None of the systems should rely solely on Proportionate
Mortality/Morbidity Analysis for determining mortality or morbidity
data, as this type analysis underreports low incidence diseases, albeit
important diseases i.e. mesothelioma.
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\13\ See Appendix 2--Mesothelioma Surveillance, Richard A. Lemen,
Ph.D.
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Research should determine how much of background mesothelioma and
other asbestos-related diseases are related to the increased
consumption of asbestos in any reference populations used for
comparison and thus adjust expected rates accordingly in order to
determine the true risk of asbestos-related diseases.
Epidemiology literature on all fibrous materials, not just those
related to the currently regulated asbestiform fiber types should be
reviewed and new research conducted when necessary. Such research
should address all respirable fiber types and all size parameters of a
respirable nature, including short respirable fibers less than 5
microns in length.
Since biopersistence has been used as a surrogate for exposure and
fiber type of exposure through identifying their persistence in the
lung as a critical factor in causation, toxicological studies should
evaluate whether the external airborne concentrations of fibers are
actually representative of the fiber concentrations and morphologies
once the fibers have been inhaled into the lung. Data suggest that the
correlation of breathing zone samples of chrysotile may not represent
the actual fiber concentration of chrysotile fibers once in the lung as
they break apart from fiber bundles and multiply within the lung, while
the amphiboles do not.\14\ This is important not only as it means a
higher dose of chrysotile within the lung but a higher number of fibers
that can translocate from the lung to other parts of the body, such as
the pleura. Because dose plays a significant role in the toxicity of
chrysotile as compared to amphiboles such findings would be important
in determining the actual role of chrysotile in asbestos-related
diseases such as mesothelioma. Translocation of chrysotile asbestos
from the lung indicates a specific role for chrysotile in the etiology
of mesothelioma since the chrysotile fibers reach the areas where the
tumor develops. Mesotheliomas develop in the pleura, peritoneum and
other serosal surfaces of the body. It is universally accepted that
chrysotile is a cause of cancer in the lung and migrates to and is
concentrated in the pleura\15\. Since chrysotile is carcinogenic and is
present in high concentrations in the pleura where the mesothelioma is
induced, it is biologically plausible that it causes or contributes to
the cause of mesothelioma. This is also shown by many mechanistic and
molecular studies that indicate how chrysotile may cause mesothelioma.
Fiber penetration can rearrange the cytoskeletal apparatus of the cell
and this could indicate an interaction between the chrysotile fibers
and the normal mitotic process, since giant multinucleated cells are
formed. These studies indicate that chrysotile penetrates the cell,
enters the nucleus and induces abnormal chromosome formations in
dividing cells.\16\ Some of these abnormalities include the deletion of
the P53 gene that controls cell growth.\17\
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\14\ Bellman B, Muhle H, Pott F, Konig H, Kloppeel H, Spurny K,
1987. Persistence of man-made fibers (MMF) and asbestos in rat lungs.
Annals of Occup Hyg, 31: 693-709.
\15\ Suzuki, Y. & Kohyama, N., 1991. Translocation of Inhaled
Asbestos Fibers from the Lung to Other Tissues. Am J Ind Med, Vol. 19,
p. 701-704; Kohyama, N. & Suzuki, Y., 1991. Analysis of asbestos fibers
in lung parenchyma, pleural plaques, and mesothelioma tissues of North
American insulation workers. Ann N Y Acad Sci, Vol. 643, p. 27-52;
Suzuki, Y., Yuen, S., Ashley, R. & Calderaro, A., 1998. Asbestos fibers
and human malignant mesothelioma. Advances in the Prevention of
Occupational Respiratory Diseases, Eds. Chiyotani, K., Hosoda, Y., &
Aizawa, Y., Elsevier Science B.V., p.709 and Sebastien, P., Janson, X.,
Gaudichet, A., Hirsch, A. & Bignon, J., 1980. Asbestos retention in
human respiratory tissues: comparative meas urements in lung parenchyma
and in parietal pleura. IARC Sci Pub, Vol. 30, p. 237-246; Dodson RF,
Graef R, Shepherd S, O'Sullivan M, Levin J, 2005. Asbestos burden in
cases of mesothelioma from individuals from various regions of the
United States. Ultrastruct Pathol. Sep-Oct;29(5):415-33.
\16\ Malomi, W., Loai, F., Falchi, M., and Donnelli, G., 1990. On
the mechanism of cell internalization of chrysotile fibers: An
immunocytochemical and ultrastructural study. Environmental Research,
Vol. 52, No. 2, pages 164-177.
\17\ Levresse, Renier, Fleury-Feith, Levy, Moritz, Vivo, Pilatte,
Jaurand, 1997. Analysis of Cell Cycle Disruptions in Cultures of Rat
Pleural Mesothelial Cells Exposed to Asbestos Fibers. Am J Respir Cell
Mol Biol, 17: 660-671.
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Additional research should include evaluation of the synergistic
effects between amphibole and serpentine fiber exposures, since it is
highly unlikely that uncontaminated serpentine exposures exist in
occupational and environmental settings. To date such findings have
suggested such a synergistic action between the mixed fiber types.\18\
It has been suggested by some that the fibrous tremolite contamination
of chrysotile, usually less than 1 percent, is the cause of
mesothelioma among predominately chrysotile exposed persons.\19\ New
evaluation of the South Charleston chrysotile exposed population of
textile workers has confirmed a dose-response relationship between
asbestosis and lung cancer.\20\ This is important as entities
suggesting that chrysotile is the ``safe asbestos'' are basing their
conclusions on only one outcome, that being mesothelioma. While it is
generally recognized that chrysotile on a dose-by-dose basis is less
potent than the amphiboles in producing mesothelioma; this does not
appear the case in its ability for causing other asbestos-induced
disease. Therefore, future research should continue to look at all
asbestos-induced diseases when determining recommended regulatory
actions for the prevention of asbestos-related diseases.
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\18\ Nicholson WJ, Landrigan PJ, 1994. The carcinogenicity of
chrysotile asbestos, In : The Identification and Control of
Environmental and Occupational Diseases : Asbestos and Cancer. Eds. M
Mehlman, A Upton: Princeton Scientific Publishing Co., Inc. Vol XXII;
Acheson ED, Gardner MJ, 1979. Mesothelioma and exposure to mixtures of
chrysotile and amphibole asbestos.
\19\ McDonald J.C., McDonald AD, Chrysotile, Tremolite and
Mesothelioma. Letter published in Science, 10 Feb 1995, Vol. 267:775
\20\ Hein MJ, Stayner L, Lehman E, Dement JM, 2007. Follow-up study
of chrysotile textile workers : cohort mortality and exposure-response.
Occup Environ Med (published online 20 Apr. 2007), 031005.
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The current OSHA regulations govern exposure to minerals defined in
the regulations as asbestos; however, formations that contain tremolite
asbestos also have tremolite cleavage fragments. Thus, just because the
cleavage fragments are not covered under the current OSHA regulations,
as regulated fibers, does not mean that they are biologically inactive.
The emphasis of the fiber pathogenicity being related to the fact that
any asbestos structure is a fiber is only one explanation of how it
causes disease. The fact is that the non-asbestiform cleavage fragment
is an analog of the fibrous asbestos structure and is chemically made
of the same composition. The complexity of asbestos induced lung
disease/injury includes a wide array of issues other than just physical
features (Kamp and Wiseman, 1999).\21\
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\21\ Kamp DW, Weitzman SA, 1999. The molecular basis of asbestos
induced lung injury. Thorax.54:638-652
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Next I will provide some data which may shed more light on the
arguments for including a broader fiber definition when it comes to
materials contaminated with asbestos. As former Deputy and Acting
Director of NIOSH I know the agency has been dealing with the issue of
talc contaminated with fibrous asbestos for many years. Researchers
found among miners and millers from two counties in Northern New York
eight talc miners identified as having mesothelioma and now Hull,
Abraham and Case (2002) have added five new cases.\22\ Rohl and Langer
(1974) have stated ``Talc because of its composition, conditions of
formation and geological occurrence, is frequently contaminated with
asbestos fibers.''\23\ ``The data, however, support earlier studies
that indicate that talc miners and millers experience excess
parenchymal fibrosis and pleural changes. The data also suggest that
individuals in the paper industry and construction trades may be at
risk.''\24\
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\22\ Hull MJ, Abraham JL, Case BW, 2002. Mesothelioma among workers
in asbestiform fiber-bearing talc mines in New York State Ann Occ Hyg,
46, (Supplement 1):132-135
\23\ Rohl AN, Langer AM, 1974. Identification and quantitation of
asbestos in talc. Env Health Perspectives, Dec., 9; 95-109.
\24\ Fitzgerald EF, Stark AD, Vianna N, Hwang S-A, 1991. Exposure
to asbestiform minerals and radiographic chest abnormalities in a talc
mining region of upstate New York. Archives of Environmental Health.
May/Jun, 46 (3); 151-154.
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Dement et al., in 1980 found from one mine and mill, reported by
the company to be producing non-asbestiform talc, air samples of 5
fibers/cc as time weighted averages (TWA) in six job categories
containing 48 percent mineral talc, 37-59 percent tremolite, 4.5-15
percent anthophyllite, and 10-15 percent serpentine, lizardite,
antigorite. Thus the TWA exposures to asbestiform amphiboles
(anthophyllite and tremolite) were found to be in excess of the present
U.S. Occupational Safety and Health (OSHA) and Mine Safety and Health
Administration (MSHA) occupational exposure standards. They also found
that in many mine and mill operations more than 90 percent of the total
airborne fibers were less than 5mm in length. They found asbestiform
tremolite, anthophyllite and in a couple of samples chrysotile and
found they were fibers when using Analytical Transmission Electronic
Microscope (ATEM) as well as PCM and not cleavage fragments.\25\
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\25\ Dement J M, Zumwalde RD, Gambel JF, Fellner W, DeMeo MJ, Brown
DP, Wagoner JK, 1980. Occupational exposure to talc containing
asbestos-Morbidity, Mortality, and environmental studies of miners and
millers. NIOSH Technical Report-DHEW (NIOSH) Publication No. 80-115,
Feb.
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I recommend that that all fibrous asbestiform minerals and that all
other minerals or materials contaminated with fibrous asbestos be
treated as hazardous and regulated as asbestos.
Finally when new epidemiology studies are conducted strict criteria
must be followed to assure the best quality studies possible. These
criteria should include, but not limited to areas such as:
(1) Determine actual exposure to the fibrous material and not allow
dilution of any effect finding by including hose in the cohort not
exposed to the fibrous material;
(2) Allow sufficient size of the study population to assure
sufficient power to detect adverse effects if they exist;
(3) Conduct sufficient follow-up to assure that at least 95 percent
of the cohort is traced and vital status known and evaluated;
(4) Allow sufficient latency to determine if adverse effects do
develop, this is important since known traditional latency periods may
be extended due to lower level cumulative exposures experienced today;
(5) Identify and account for any possible confounders that may
affect the outcome of the study;
(6) If case-control analyses are conducted make sure that all
matched controls are selected so that confounding factors will not skew
the outcome, including adequate occupational histories to rule out
other causative agents or past occupational exposures; and
(7) Dose-reconstruction should not be allowed unless adequate data
points exist, from actual exposure samples taken at multiple points
during the entire exposure period, as extrapolation from more recent
exposures will often reflect control technologies not in place earlier
in the persons exposure history, thus resulting in an under estimate of
the individuals true exposure. Dose-reconstruction should never be
applied from one work situation to another without adequate working
conditions being explained and/or described by the affected worker or
from actual witnesses to the workers exposure conditions, including an
explanation of both environmental or personal control-technologies
applied in the specific workplace(s).
I would hope all who have testified here today have disclosed their
own affiliations and potential conflicts of interest. Since my
retirement I have testified numerous times for plaintiff's attorneys in
asbestos litigation, I am also Co-Science Director to the Asbestos
Disease Awareness Organization (ADAO) which has covered some of my
expenses to attend this hearing today, and no expenses for my testimony
or preparation for it have been covered by plaintiff attorneys or any
other entity other than myself.
Last, I would encourage members of this committee to support the
Ban Asbestos Act introduced by Sen. Murray to include a ban on all
commercial uses and importation of asbestos to or within the United
States. I look forward to be of assistance should further questions
arise.
______
Appendix 1
Short Asbestos Fibers, Richard A. Lemen, Ph.D.
EPA reported that millions of asbestos fibers can be released
during brake and clutch servicing and that such asbestos can linger
around the garage long after brake jobs are done and can be breathed in
by everyone inside the garage which can present a hazard for months or
years. Grinding of used brake block linings has been shown to release
up to 7 million fibers per cubic meter and beveling new linings up to
72 million fibers and even light grinding of the new linings up to 4.8
fibers.\26\ It has also been reported that during this decomposition
process the majority of fibers that remain are of small diameter as
well as below 5 micron in length\27\ and thus are less harmful.\28\
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\26\ USEPA, 1986. Guidance for Preventing Asbestos Disease Among
Auto Mechanics. United States Environmental Protection Agency. EPA-560-
OPTS-86-002, June.
\27\ Rohl, AN, Langer, AM, Wolff, MS & Weisman, I, 1976. Asbestos
exposure during brake lining maintenance and repair. Environ Research,
Vol. 12, p. 110; Sheehy, J. W., Cooper, T. C., O'Brien, D. M.,
McGlothlin, J. D., & Froehlich, P. A., 1989. Control of Asbestos
Exposure During Brake Drum Service. National Institute for Occupational
Safety and Health, Public Health Service, Centers for Disease Control,
U. S. Department of Health and Human Services, August; & Yeung, P,
Patience, K, Apthorpe, L, & Willcocks, D, 1999. An Australian study to
evaluate worker exposure to chrysotile in the automotice service
industry. Appl Occup Environ Hyg, Vol. 14, No. 7, July, p. 448.
\28\ Hatch, D, 1970. Possible alternatives to asbestos as a
friction material. Ann Occup Hyg, vol. 13, p. 25.
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Any assumption that short fibers, less than 5 micron in length, are
not hazardous cannot be justified based on the available science.
Because the analytical method of choice, for regulatory purposes, has
been the phase contrast method [PCM] which counts only fibers greater
than 5 um in length, epidemiology studies therefore have been forced to
compare doses of exposure within their cohorts only to fibers greater
than 5mm in length. It must be noted that the PCM analytical method was
chosen based on its ability to count fibers only and not on a health
effect basis.\29\ While PCM has been the international method for
analysis, it should also be noted that it is not able to detect thin
diameter fibers [<0.2mm in diameter]. The evidence suggests that PCM
may underestimate exposures and the health risks as found in the
analysis of brake residue,\30\ or other such exposures where short
fibers may be found and because of this, it has been suggested that
transmission electron microscopy [TEM] should be an adjunct to PCM.
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\29\ ``The first decision made concerned that part of the dust
spectrum which should be counted and it was agreed that only fibers or
fiber bundles having a minimum length of 5 microns and a maximum of 100
microns should be counted, the definition of a fiber being arbitrarily
taken as a particle whose length was at least three times it diameter.
This decision was taken in the light of evidence to the effect that the
particle size distribution or spectrum of an asbestos dust cloud was
reasonably constant over a wide range of textile processes, although
later work has suggested that this might not be strictly true.'' This
decision represent the conclusions made for use of the Thermal
Precipitator Method in collecting asbestos-containing dust and when the
Membrane Filter Technique came into use, the basis for the method
referred to as the PCM method, it was determined that the 5 micron in
length would remain the standard as ``The filter on the other hand,
having a pore size in the region of 0.45 micron, would appear to be
quite adequate for trapping fibers in the length range 5-100 microns.''
While it was thought the Membrane Filter Technique would be more
representative in assessing the ``true health hazard to which an
operative is subjected'' it did not rely upon knowledge that fibers
less than 5 micron in length had been shown harmless. Holmes S, 1965.
Developments in dust sampling and counting techniques in the asbestos
industry. Ann NYA Sciences: 132(1); 288-297.
\30\ Yeung, P, patience, K, Apthorpe, L, & Willcocks, D, 1999. An
Australian study to evaluate worker exposure to chrysotile in the
automotice service industry. Appl Occup Environ Hyg, Vol. 14, No. 7,
July, p. 448.
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Stanton and Wrench (1972)\31\ and Stanton et al. (1981)\32\ found
that the longer, thinner fibers were more carcinogenic, but they could
not identify a precise fiber length that did not demonstrate biological
activity. It must be kept in mind that Dr. Stanton has never said long
fibers are bad and short fibers are good. In fact, he appreciated that
a large number of short fibers, individually of low tumorogenic
probability, might be more hazardous than fewer long fibers,
individually of high probability.\33\
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\31\ Stanton, M.F., and Wrench, C., 1972. Mechanisms of
mesothelioma induction with asbestos and fibrous glass. J. Natl. Cancer
Inst., Vol. 48, p. 797.
\32\ Stanton, M.F., Laynard, M, Tegeris, A, et al. 1981. Relation
of particle dimension to carcinogenicity in amphibole asbestoses and
other fibrous minerals. JNCI, Vol. 67, No. 5, November, p. 965.
\33\ Greenberg, M, 1984. S Fibers. Am J Indust Med, Vol. 5, p. 421-
422 & Personal correspondence from Dr. Morris Greenberg, 23 May 2003.
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Studies have also found that the majority of asbestos fibers in
lung and mesothelial tissues were shorter than 5mm in length, thus
indicating the ability of the shorter fibers to reach the tumor site,
remain there, and therefore their role in the etiology of disease is
implicated.\34\ Research has found in typical occupational environments
fibers shorter than 5mm in length outnumber the longer fibers by a
factor of 10 or more.\35\
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\34\ Suzuki, Y. & Yuen, SR., 2002. Asbestos fibers contributing to
the induction of human malignant mesothelioma. Ann NY Acad Sci, Vol.
982. pp. 160-176 & Dodson, RF, O'Sullivan, MF, Brooks, DR & Bruce, JR,
2001. Asbestos content of omentum and mesentery in nonoccupationally
exposed individuals. Tox Indust Health, Vol. 17, p. 138.
\35\ Dement, JM & Wallingford, KM, 1990. Comparison of phase
contrast and electron microscopic methods for evaluation of
occupational asbestos exposures. Applied Occ Env Hyg, Vol. 5, p. 242.
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Shorter fibers must be studied in more depth and they should not be
disregarded especially when clearance is retarded.\36\ That chrysotile
fibers tend to spit longitudinally as well as partially dissolve,
resulting in shorter fibers within the lung, was reported in a review
of several articles.\37\
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\36\ Oberdorster, G, 2001. Fiber characteristics, environmental and
host factors as determinants of asbestos toxicity. 2001 Asbestos Health
Effects Conference, May 24-25, Oakland, CA, U. S. Environmental
Protection Agency.
\37\ Dement, JM & Brown, DP, 1993. Cohort mortality and case-
control studies of white male chrysotile asbestos textile workers. J
Occup Med Toxic, Vol. 2, No. 4, p. 355.
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Davis et al., 1986, 1988 and the Berman et al., 1995 reanalysis of
the Davis data and the McDonald et al., 1989 papers examine both the
toxicity or lack thereof for short fibers.\38\ The Davis papers show
that: (1) long fibers produced 6 times more fibrosis and 3 times more
tumors than the short fiber preparations after inhalation; (2)
injection studies, at the highest dose levels 25 mg, found little
difference in the numbers of tumors produced by both long and short-
fibre chrysotile, while at lower levels there was a significant
difference between the long and short-fibre preparations with the
longer fibers being more carcinogenic; (3) the mean tumor induction
period was longer for the short-fibre preparation in producing
mesotheliomas at both the 25mg and 2.5mg dose level and the authors
conclude ``. . .would probably have been seen with the 0.25mg dose if
the short-fibre chrysotile had produced any mesotheliomas at this
level.''; and (4) the authors state that the alteration of the short-
fibre chrysotile produced by ball-milling is subject to a level of
crystal damage which is sufficient to make results difficult to
interpret in relation to hazards resulting from short fibres produced
during the manufacture of asbestos products or during the subsequent
usage of these materials. Berman et al., 1995, using a risk analysis
model of their choice choose to eliminate all fibres less than 5 mm in
length as ``Structures <5 mm in length do not appear to make any
contribution to lung tumor risk.'' Such an assumption is unwarranted
given the conclusions of the Davis et al. papers along with the other
data, discussed in this affidavit, showing toxicity for the short
asbestos-fibers.
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\38\ Davis JM, Addison J, Bolton RE, et al. 1986. The pathogenicity
of long versus short fibre samples of amosite asbestos administered to
rats by inhalation and intraperitoneal injection. Br J Exp Pathol 67:
415-430; Davis JM, Jones AD. 1988. Comparisons of the pathogenicity of
long and short fibres of chrysotile asbestos in rats. Br J Exp Pathol
69: 717-737; Berman DW, Crump KS, Chatfield EJ et al. 1986. The sizes,
shapes, and mineralogy of asbestos structures that induce lung tumors
or mesothelioma in AF/HAN rats following inhalation. Risk Analysis 15:
181-195; & McDonald JC, Armstrong B, Case B et al. 1989. Mesothelioma
and asbestos fiber type: Evidence from lung tissue analyses. Cancer 63:
1544-1547.
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McDonald et al., 1989 examined 78 cases of mesothelioma from
autopsy between 1980 through 1984 with matched referents to evaluate
the lung burden of long vs. short fibers, concluded that the role of
short-fibers was nil. Looking only at lung burden analysis for
chrysotile short-fibers is not the only way nor is it the most
appropriate analysis to determine the role of either chrysotile or
short-fibers, as they are cleared from the lung rapidly compared to
longer non-chrysotile fibers. This same criticism is applicable to the
Butnor et al.,\39\ analysis of 10 cases of mesothelioma among brake
exposed workers where analysis was only made of lung tissue.
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\39\ Butnor KJ, Sporn TA, Roggli VL. 2003. Exposure to brake dust
and malignant mesothelioma: A study of 10 cases with mineral fiber
analyses. Ann Occup Hyg 47: 325-330.
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Butnor et al. also dismiss the `hit-and-run' hypothesis for
chrysotile as `flimsy' and having no solid scientific support and cite
Hesterberg et al., 1994, 1995, 1996 studies,\40\ of man-made vitreous
fibers, as their proof for this contention. While there is clear proof
of the biopersistence for amphibole asbestos, the lack of such
biopersistence of other fibers, as shown in the Hesterberg et al
papers, provide support to the contrary, and are an indication that
pathogenicity of a fiber is dependent upon more than simply the dose,
dimension, and the durability of the fibers found with in the lung. It
is also important to note that chrysotile asbestos produced fibrosis,
lung tumors and mesothelioma in rats after inhalation studies as shown
in the Research and Consulting Company (RCC) studies cited in the
Hesterberg et al., 1995 paper.
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\40\ Hesterberg TW, Miiller WC, Mast R, McConnell EE, Bernstein DM
& Anderson R. 1994. Relationship between lung biopersistence and
biological effects of man-made vitreous fibers after chronic inhalation
in rats. Env Health Perspect 102(S); 133-137; Hesterberg TW, Miiller
WC, Thevenaaz P, & Anderson R. 1995. Chronci inhalation studies of man-
made vitreous fibres: Characterization of fibres in the exposure
aerosol and lungs. Ann Occup Hyg 39 (5): 637-653 percentHesterberg TW,
Miiller WC, Musselman RP, Kamstrup RD, Hamilton RD & Thevenaz P. 1996.
Biopersistence of man-made vitreous fibers and crocidolite asbestos in
the rat lung following inhalation. Fund Appl Toxico 29: 267-279.
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______
Appendix 2
Mesothelioma Surveillance, Richard A. Lemen, Ph.D.
Two recent papers have concluded the beginning of a decrease in
mesothelioma rates in the United States.\41\ Their data analyses bring
to the fore additional questions about the reliability of surveillance
data for mesothelioma based solely on death certificate analysis or
mortality data without pathological confirmation of mesothelioma. SEER
data, for example, prior to the implementation of the new ICD 10 codes,
are inaccurate and underestimate the true incidence of mesothelioma in
the U.S.\42\
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\41\ Price B & Ware A, 2004. Mesothelioma trends in the United
States: An update based on surveillance, epidemiology, and end results
program data for 1973 through 2003 &
\42\ Pinheiro GA, Antao VCS, Bang KM & Attfield MD, 2004. Malignant
mesothelioma surveillance: A comparison of ICD 10 mortalaity data with
SEER incidence data in nine areas of the United States. Int J Occup
Environ Health: 10; 251-255.
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The new ICD-10 codes for mesothelioma are C45.0 for pleural and
C45.1 for peritoneal.\43\ Before the new ICD-10 codes went into effect
in 1999 the reporting based on incidence data was likely underreported
and thus analysis using such data is likely to have underreported the
incidence of mesothelioma. In some cases, SEER data reported only 12
percent of the mesothelioma cases were accurately reported and even
with the new ICD 10 codes it is estimated that only about 80 percent
will be detected through SEER data, indicating that mesothelioma
reporting will still be problematic but much less so than in the
past.\44\ The new ICD 10 codes have only been in existence for the past
8 years and any trends based on this data are unwarranted at this time
and it will be many years until a more accurate picture can be seen as
to mesothelioma trends within the U.S. It is important that NIOSH
address this underreporting gap.
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\43\ World Health Organization, 1992. ICD-10 International
Statistical Classification of Diseases and Related Health Problems
Tenth Revision: 1; 201.
\44\ Pinheiro GA, Antao VCS, Bang KM & Attfield MD, 2004. Malignant
mesothelioma surveillance: A comparison of ICD 10 mortalaity data with
SEER incidence data in nine areas of the United States. Int J Occup
Environ Health: 10; 251-255.
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Since it has been generally reported that the incidence of
mesothelioma in women is much less associated with asbestos exposure,
Steenland et al.\45\ suggest that if take-home asbestos exposure were
considered the attributable risks may rise to around 90 percent. Price
and Ware (2004) unjustly suggest that because the female lifetime
mesothelioma risk across birth cohorts has remained constant this
supports a threshold exposure for mesothelioma, which is yet to be
shown and no epidemiological study to date has been able to demonstrate
such a threshold. Trends in mesothelioma are on the rise in many
countries and a large multicentric study on malignant pleural
mesothelioma and non-occupational exposures to asbestos projects that
low-doses from the home and general environment may carry a measurable
risk of mesothelioma over the next few decades.\46\ The findings of
this multicentric study have direct implications to the risk of
mesothelioma from exposures to asbestos among end-product user of
asbestos-containing products, e.g. brake mechanics, as their exposures
have generally been of a lower magnitude that those encountered by the
various highly exposed and predominately studied trades including
insulators, construction workers, shipyard workers, pipefitters to name
a few.
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\45\ Steenland K, Burnett C, Lalich N, Ward E & Hurrell J, 2003.
Dying for work: The magnitude of U.S. mortality from selected causes of
death associated with occupation. 43; 461-482.
\46\ Magnani C, Agudo A, Gonzalez CA et al., 2000. Multicentric
study on malignant pleural mesothelioma and non-occupational exposure
to asbestos. Br J Cancer: 83(1); 104-111.
Senator Boxer. Thank you, and we will have some questions.
Ms. Linda Reinstein. We welcome you and we are so sorry for
your loss.
STATEMENT OF LINDA REINSTEIN, EXECUTIVE DIRECTOR AND CO-
FOUNDER, ASBESTOS DISEASE AWARENESS ORGANIZATION
Ms. Reinstein. Thank you, Madam Chairman Boxer and Ranking
Member Inhofe and the entire EPW Committee for the honor and
opportunity to testify today.
My name is Linda Reinstein. I am the executive director of
the Asbestos Disease Awareness Organization, ADAO, and now a
mesothelioma widow. My husband, Alan Reinstein, lost his 3-year
battle with mesothelioma, a deadly asbestos cancer, in May
2006. I am neither a lobbyist nor an attorney, just a
volunteer.
Today, I somberly represent the victims and their families
who have suffered the traumatic effects of asbestos diseases.
For many of us, this is an especially difficult week, as
Fathers Day is on Sunday.
Hundreds of thousands of asbestos victims around the world
pay the ultimate price for asbestos exposure: their lives.
These diseases are all preventable. Before I share the faces,
it is important to understand the facts. We cannot alter
history or bring back the dead, but we can learn from the past
to save lives and money.
Most Americans trust that their air, soil and water are
safe from toxic contaminants. But as victims, we know the
truth. For a century, asbestos exposure has been linked to
incurable diseases. Yet we continue to face an enormous man-
made public health crisis. Just walk the streets of Libby or
New York City, or talk to the U.S. Capitol tunnel workers, here
today. They all know too well about the irreversible effects of
asbestos poisoning.
The stress and trauma is life-altering for those Americans
with known exposure, waiting for time to reveal their medical
fate. The IARC declared asbestos as a human carcinogen nearly
30 years ago. The EPA, WHO, IRO agree. There is no safe level
of asbestos exposure. The simple truth: asbestos kills.
The penny slide on the easel compares the nearly invisible
deadly fibers just under President Lincoln's nose to grains of
rice and human hair. These virtually indestructible fibers are
700 times smaller than human hair and can remain suspended in
the air from seconds to days. Asbestos is an equal opportunity
killer. Its dust doesn't discriminate. Inhaling or swallowing
the fiber can cause malignant or non-malignant diseases.
Asbestos diseases are difficult to diagnose and treat. The
evolution from exposure to death can take 10 to 50 years.
Children are even more susceptible to carcinogens. It is
important to focus on all asbestos-caused diseases, not just
mesothelioma. The Samia 7-year study on the board shows 65
percent of the victims suffered from asbestos-caused cancers
and the remaining 35 percent from asbestosis. Lung cancer and
mesothelioma accounted for 25 and 11 percent, respectively, of
all asbestos diseases.
Although asbestos safety measures have been in place since
the 1970s, exposure continues. The CDC reports an increase in
asbestosis deaths from 1968 to 2000. These and other related
diseases are not going away, only the victims who die.
Victims suffering from pulmonary diseases and cancer feel
like they are breathing through a pinched straw every breath,
every minute, every day. When victims' oxygen levels become
critically low, they are tethered to supplemental oxygen to
prolong life, like my husband. Lack of oxygen can cause death
by respiratory failure or cardiac arrest.
To prolong a victim's life, many cancer patients opt for
radical treatments, such as having their entire diseased lung
and diaphragm surgically removed. We call this death by a
thousand cuts. Victims living with these painful, aggressive
and hopelessly incurable diseases sometimes commit suicide or
ask their spouses to commit mercy killings.
Mesothelioma patients' medical expenses can exceed a
million dollars before death. The physical and financial
devastation is immeasurable to victims and their families. Each
time a patient dies, a shattered family is left behind. The new
patient profile is now a 51-year-old woman. Younger victims are
dying. There is a 16-year-old girl newly diagnosed in New York.
Federal surveillance in the United States under-report.
So what is a human life worth? Certainly banning asbestos
and investing in safe alternatives. Without an asbestos ban,
death and litigation will continue. To profit over people is
unconscionable. It is time to eliminate asbestos exposure and
invest in research to improve treatment.
We applaud Senator Patty Murray for the Ban Asbestos Act.
An immediate worldwide ban on the production and use of
asbestos is long overdue, fully justified and absolutely
necessary.
Support for my testimony comes from some of the most well-
respected members of the science community and an outpouring
from victims around the world. I have included a list of these
endorsements in my written testimony. Thank you.
[The prepared statement of Ms. Reinstein follows:]
Statement of Linda Reinstein, Executive Director, Co-founder and
Mesothelioma Widow
I would like to thank Chairman Boxer, Ranking Member Inhofe and the
entire EPW Committee for the honor and opportunity to testify today.
My name is Linda Reinstein, Executive Director of the Asbestos
Disease Awareness Organization (ADAO) and now a mesothelioma widow. My
husband, Alan Reinstein, lost his three year battle with mesothelioma,
a deadly asbestos cancer, on May 2006. I am neither a lobbyist nor an
attorney, only a volunteer.
Today I somberly represent the victims and their families who have
suffered the traumatic effects of asbestos diseases. Hundreds of
thousands of asbestos victims around the world paid the ultimate price
for asbestos exposure: their lives. These diseases were preventable.
Before I share the faces, it is important to understand the facts.
We can not alter history or bring back the dead, but we can learn from
the past to save lives and money.
Most Americans trust that their air, soil and water are safe from
toxic contaminants--but as victims, we know the truth. For a century,
asbestos exposure had been linked to incurable diseases, yet we
continue to face an enormous man-made public health crisis. Just walk
the streets of Libby or New York City or talk to the U.S. Capitol
Tunnel Workers--they also know all too well about the irreversible
effects of asbestos poisoning. The stress and trauma is life altering
for those Americans with known asbestos exposure waiting for time to
reveal their medical fate. The International Agency for Research on
Cancer (IARC) declared asbestos as a human carcinogen thirty years ago.
The Environmental Protection Agency, (EPA) World Health Organization
(WHO) and the International Labor Organization (ILO) agree--there is no
safe level of asbestos exposure. The simple truth is--asbestos kills.
The Penny slide compares the nearly invisible deadly fibers just
under President Lincoln's nose to grains of rice and human hair. Once
known as the ``The Magic Mineral'', these virtually indestructible
asbestos fibers can be 700 times smaller than human hair and remain
suspended in air from seconds to days.
Although asbestos safety measures have been in place since the
1970s, The Center for Disease Control (CDC) reported that deaths from
asbestosis, a debilitating lung disease, increased from 77 deaths in
1968 to 1,493 deaths in 2000. These and other asbestos-related diseases
are not going away, only the victims who die.
The World Health Organization estimates 125 million workers are
exposed to asbestos and 90,000 workers die annually. There is no global
data estimating deaths from non-occupational or environmental exposure.
Asbestos is an equal opportunity killer and the dust does not
discriminate. Inhaling or swallowing asbestos fibers can cause
malignant and nonmalignant diseases.
Asbestos diseases are difficult to diagnose and treat. Evolution of
disease, from exposure, screening, surveillance, detection, treatment
and death can take 10-50 years. Children are even more susceptible to
carcinogens and have a shorter latency period.
It is important to focus on all asbestos-caused diseases, not just
mesothelioma. The Sarnia seven year study sited: 65 percent of the
victims suffered from asbestos-caused cancers and the remaining 35
percent suffered from asbestosis. Lung cancer and mesothelioma
accounted for 25 percent and 11 percent respectively of asbestos
diseases.
Asbestosis is the scarring of lung tissue resulting only from the
inhalation of asbestos fibers which reduces oxygen transfer to the
blood as well as the removal of carbon dioxide. Asbestosis is a
painful, progressive and incurable lung disease with no effective
treatment.
Victims suffering from pulmonary diseases and cancer feel like they
are breathing through a pinched straw, for every breath, every minute,
every day. When the victims' oxygen levels become critically low, they
are tethered to supplemental oxygen to prolong life. Lack of oxygen
causes death by respiratory failure and/or cardiac arrest.
To prolong a victim's life, many cancer patients opt for radical
treatments such as having their entire diseased lung and diaphragm
surgically removed. We call this, death by 1,000 cuts. Victims living
with these painful, aggressive and hopelessly incurable diseases
sometimes commit suicide or ask spouses to commit mercy killings.
Mesothelioma patients' medical expenses can exceed $1 million--
until death.
medical expenses include:
Tri-modal Cancer Treatment, Surgery, Radiation
Chemotherapy
Medication & Oxygen
Home Health/Hospice
Psychiatry
Interstate Travel to Medical Surgery Centers
The physical, financial and physiological devastation are
immeasurable to the victims and their families. After the patient dies,
financial and psychological problems continue to plague the family. For
each life lost, a shattered family is left behind.
Psychological issues are tormenting--as victims hold hands with
death.
Constantly facing death is debilitating for both the
patient and family.
Constantly facing death is debilitating for both the
patient and family.
Caregivers face both mental and physical
exhaustion--Alan needed 24-hour care for 12 months.
Depression is a common factor.
Physical pain and treatments are brutal; the prognosis is grim
Screening, surveillance, and detection are
exhausting and remain a constant reminder of exposure and
possible terminal diseases.
Late stage diagnosis is common, as many victims are
asymptomatic.
Victim has baffling and radical treatment options to
navigate.
Dangerous surgeries and toxic medicine--if the
diseases don't end your life, the treatments may.
Financial issues devour assets and threaten financial stability
Expensive medical treatments. One month of Alan's
prescriptions, oxygen and chemotherapy averaged $104,000.
Lost jobs or reduced income results when victims are
too ill to work.
Health benefits are also terminated as a result of
losing a job.
Constant fear and extreme isolation magnifies these three factors.
In 1990, the average patient was a male, age 70. Our data shows the
new patient profile to be a 51 year old woman. Younger victims are
dying from diseases. Recently, a 16 year-old girl was diagnosed with
mesothelioma. Patients diagnosed with asbestos-caused diseases are
completely innocent. They are firefighters and veterans, construction
workers and engineers. They are the women who became exposed washing
their husbands' work clothes. They are children whose loving hug turned
deadly.
Surveillance in the U.S. continues to under report asbestos-related
disease. Without disease registries, effective outreach and well
implemented surveillance programs; we can not accurately forecast the
magnitude of disease.
deadly contamination continues today
Asbestos was widely used in the construction and attic insulation
in millions of homes in the U.S. and Canada built before 1975. More
than 30 million homes, schools and office building are still
contaminated with deadly asbestos.
In 2002, the collapse of the World Trade Center towers led to the
release of hundreds of tons of asbestos from the towers. An estimated
20,000 responders, workers, volunteers and residents suffer from
respiratory diseases. The annual direct treatment costs are $140
million dollars. We can only extrapolate the cost of human tragedy and
treatment expenses from the Hurricane Katrina disaster one of whose
consequences is poorly controlled asbestos exposure in the buildings
being repaired and demolished. The World Health Organization has
started an asbestos action program to help countries all over the world
develop national plans, based on the conclusion that ``the most
efficient way to eliminate asbestos-related diseases is to stop using
all types of asbestos.''
Asbestos continues to be mined and exported from Canada. The United
States and Canada remain the only two industrialized nations that have
not yet banned the use of asbestos in common products while more than
40 countries have banned asbestos. Consumers are at risk with imported
products contaminated with asbestos such as brakes and asbestos-cement
building panels. The asbestos ban will only be as effective as the laws
that are enforced. Presently, minimal fines and lack of enforcement
make our existing laws weak and deadly asbestos exposure continues.
What is a human life worth? Certainly banning asbestos and
investing in safe alternatives. Without an asbestos ban, deaths and
litigation will continue. To profit over people is unconscionable. It
is time to eliminate asbestos exposure, while simultaneously investing
in research for a cure and improved treatments. An immediate worldwide
ban on the production and use of asbestos is long overdue, fully
justified and absolutely necessary. We applaud Senator Patty Murray for
the Ban Asbestos in America Act, and hope that this is only the start
of a ban across the globe.
Support for this critical issue comes from some of the most well
respected members of the scientific and medical community from around
the world. I have included a list of these endorsers in my written
testimony.
Thank you.
Response from Linda Reinstein to an additional question
from Senator Boxer
Question. You have a number of health professional and other people
who have signed on in support of your statement. Can you please
describe how widespread this support is?
Response. [The names in support of the statement follow:]
Senator Boxer. Thank you for your powerful testimony.
Senator Inhofe has asked to be recognized first, since he
needs to go to a very important meeting. So Senator, the floor
is yours.
Senator Inhofe. I appreciate it, Senator Boxer. I will just
take a couple of minutes, I won't take the whole time.
I have a few problems with this. It is always difficult
when you have a panel of scientists and you are expected to
make determinations by listening to two opposing views. One
thing that I noticed, Dr. Lemen, in your written testimony, you
talk about, you do testify occasionally in asbestos-related
litigation on behalf of the plaintiffs.
One of the problems I have is that when you get into
something like this, like we have gone through with asbestos,
there are big winners, and the big winners are the trial
lawyers. In asbestos claims, so far it has now exceeded $70
billion claims, and there is a remaining liability of somewhere
between $145 billion and $200 billion. More than 70
bankruptcies have taken place, and most of the current
defenders are users and not manufacturers of asbestos. That was
a Rand report.
So 60 cents out of every dollar goes to the lawyers. This
bothers me.
Second, and let me start with you, Dr. Wylie, if we were to
count these non-asbestiform minerals as asbestos in the
regulatory definition, change your definition, include them
all, what would that mean in terms of the land area of the
world? Put up that one chart that shows the United States. This
would be, as I understand it, just the United States part, but
go ahead. Do you have a percentage that you could use?
Ms. Wylie. What is shown there in green roughly outlines
the areas in the United States where amphiboles are naturally
occurring. And amphiboles make up about 5 percent of the
earth's crust overall. So these are extraordinarily common
rock-forming minerals. These minerals, when crushed, do form
elongated particles.
Senator Inhofe. I see. In his testimony, Dr. Lemen stated,
I am going to read this and then I am going to ask both of you
to respond to it, ``Any definition of asbestos should include
all respiratory asbestiform fibrous materials, including
fibrous cleavage fragments that are respirable.'' Now, I will
start with you, Dr. Wylie, to respond to that just real
briefly. Because I want to get it in the record in terms of his
exact quote.
Ms. Wylie. I believe that that quote suggests that cleavage
fragments are asbestiform fibers, that that is not true.
Senator Inhofe. OK. Dr. Weill, would you respond to the
same quote there?
Dr. Weill. Yes, I also agree that cleavage fragments have
not been shown to be pathogenic to humans.
Senator Inhofe. As the only practicing lung physician here
today, could you briefly discuss the differences in how
asbestiform minerals and non-asbestiform minerals and cleavage
fragments affect the human body?
Dr. Weill. Yes, I think the large majority of cleavage
fragments aren't even respirable, because of their width. They
are not able to make it into the distant parts of the lung,
where they do most of their damage. The physical properties of
these fragments are different from asbestos fibers. There have
been animal studies that have shown that they are not
pathogenic whereas asbestos fibers clearly are in animal
studies.
Also, there have been several studies, human epidemiologic
studies, of thousands of workers exposed to these fragments
demonstrating no disease.
Senator Inhofe. I think that is extremely significant. What
I would like to ask you to do for the record is to elaborate on
that, showing the studies by name, where they were conducted,
who was involved, so that we will have that in the record, not
today but for the written record, if you would be good enough
to do that.
Dr. Wylie, you made a statement concerning the mining, that
it has not been such a case found after a period of time, those
who work in the minds. I think that was refuted by Dr. Lemen.
Would you like to have a chance to refute the refute?
Ms. Wylie. I am not a medical scientist. But as I read the
studies, I find no excess of asbestos-related diseases. There
are in some of these studies some excesses in lung cancer. But
there are other compounding variables, such as the smoking
history of the workers, radon daughters that can reasonably
account for these excesses in lung cancer.
I know of no cases of mesothelioma associated with exposure
to cleavage fragments.
Senator Inhofe. Thank you very much. Thank you, Madam
Chairman.
Senator Boxer. Yes, Senator, thank you very much.
I am going to ask Dr. Lemen and any others, Dr. Castleman,
to respond to this. I just want to say for the record that
Senator Isakson and Senator Murray are working on some of these
definitions, too. But if you would like to respond, Dr. Lemen,
to the other two who challenged your point.
Mr. Lemen. I agree with Dr. Weill, yes, with Dr. Weill,
that some of the cleavage fragments will not get into the lung.
It is not those that we are concerned about. What we are
concerned about are the respirable ones.
Senator Boxer. Right.
Mr. Lemen. And the respirable ones can get into the lung.
They do have the same mineralogical characteristics as
asbestos. We are concerned about what gets into the lung that
can cause disease.
As far as the gold mine that was talked about, as I said in
my brief comments, when you look at the latency, you do find,
in two different studies, both the study that NIOSH conducted
and the study that the McDonalds conducted, that after a long
latency in the higher exposed groups, you do see an excess of
respiratory cancer as well as respiratory disease.
So finally, the animal studies that have been conducted are
basically negative. However, there are some cellular studies
that have shown cellular reaction with these types of small,
short cleavage-type fibers.
Senator Boxer. You are saying that if those fibers get
loose, that is a problem?
Mr. Lemen. That is right.
Senator Boxer. So I don't know that there is any
disagreement whatsoever here. I think that is a phony kind of
distinction without a difference. If they break off, and they
are inhalable, I am sure both Dr. Weill and Dr. Wylie would
agree, if they are inhaled, they are a danger, is that correct?
Dr. Weill. Inhaled and reach the distant parts of the lung?
Senator Boxer. Yes.
Dr. Weill. No, they are----
Senator Boxer. They are not a danger?
Dr. Weill. No, the chemical properties may be similar
between asbestos fibers and cleavage fragments. But their
physical morphology is different and the body can handle them
differently----
Senator Boxer. This is important, because NIOSH disagrees
with you, sir.
Dr. Weill. I understand that.
Senator Boxer. NIOSH believes that durable inhalable fibers
with characteristics similar to asbestos should be considered
potentially harmful. Exposure to these fibers should be avoided
if possible or otherwise minimized through standard industrial
hygiene practices.
I am going to move on. I wanted to ask the Capitol workers
here, who we know are exposed to asbestos, if they would stand
up, just to be recognized by the audience, if they would stand
up. The reason I want to ask you to stand is because I want you
to know that all of us are very determined to make sure that
your problem, (a) has been stopped, in other words, there is no
more exposure; and (b) if there was exposure, which you I think
were informed there was, we are going to stand with you on
this. I just want to thank you very much for coming.
I want to get to a couple of other things, and you can
start my clock now at 5 minutes and I will just come back to
it.
Dr. Weill, describe the health effects of asbestos. Have
you ever treated or personally evaluated a patient who had
asbestos-related disease?
Dr. Weill. Yes. The health effects of asbestos, as I
mentioned in my testimony, can include both malignant and non-
malignant diseases. I have----
Senator Boxer. How many patients have you personally
evaluated and treated?
Dr. Weill. Somewhere in the neighborhood of 50 to 100, I
would say, with true asbestos-related disease.
Senator Boxer. OK. Did you co-author a commentary on the
American Thoracic Society's statement on the diagnosis and
initial management of non-malignant disease related to
asbestos?
Dr. Weill. Yes, I did.
Senator Boxer. Did the Society point out that your
commentary cited a 1993 study by William Weiss to make a point
which the study specifically stated is not the question
considered in this review?
Dr. Weill. I am not certain I understand your question.
Senator Boxer. OK, well, this is--are you aware that the
Society pointed out in response to your story that your
commentary cited in a 1993 study by William Weiss, which the
study specifically stated is not the question considered in
this review, did you hear from the Society on this point?
Dr. Weill. Yes, I did.
Senator Boxer. Thank you.
Have you worked for businesses that make money selling
products that may have caused lung disease?
Dr. Weill. I have been retained by lawyers who represent
these companies.
Senator Boxer. Well, thank you for your honesty in
answering this question, because I believe it is important that
this information be so stated in the record.
Now, Dr. Wylie, are you a doctor, are you a geologist or do
you treat patients?
Ms. Wylie. I am a geologist.
Senator Boxer. OK. Then do you agree with the statement by
the U.S. Geological Survey, ``It is absolutely not the role of
the analytical or mineralogical communities to make health-
based decisions or to make independent analytical assessments
that directly or indirectly influence health-based outcomes''?
Do you agree with that statement?
Ms. Wylie. I am not sure that I do. I think that is the
role of mineralogists to make clear the nature of the materials
to which pele are exposed. And in that regard, it is an
independent analytical assessment that might indirectly
influence the outcomes of some studies. But it is only our job
to tell about the materials, what they are like----
Senator Boxer. Well, that is not what you did. I find
aspects of your testimony troubling, including your statement,
not only is the width of asbestos a defining characteristic, it
is the key to its carcinogenicity. That you are stepping into
another field that your own profession says you should avoid.
So I am rather shocked by your statement. I have another
question. Have you worked for business that makes money selling
products that may have caused disease associated with asbestos?
Ms. Wylie. No.
Senator Boxer. Well, I have a number of receipts that show
you have worked as a paid defense witness for business in
asbestos litigation. I ask unanimous consent that these
documents be placed into the record.
[The referenced documents are retained in the committee's
file.]
Senator Boxer. Why didn't you answer my question honestly?
Ms. Wylie. I did. I have never worked for an asbestos
manufacturer.
Senator Boxer. I didn't say that.
Ms. Wylie. Or an asbestos fabricator.
Senator Boxer. I didn't ask you that. I said, have you
worked as a paid defense witness for a business in asbestos
litigation?
Ms. Wylie. I have testified on about three occasions for,
on the nature of materials involved----
Senator Boxer. Who paid you?
Ms. Wylie. R.T. Vanderbilt, three times or thereabouts.
Senator Boxer. So your original answer was incorrect?
Ms. Wylie. I misunderstood----
Senator Boxer. Well, let me be clear. I think it is very
important that we be totally honest before this committee.
Ms. Wylie. I agree.
Senator Boxer. Senator Lautenberg.
Senator Lautenberg. I am a little bit astonished to say the
least at what we hear from two of our witnesses, Dr. Weill and
Dr. Wylie, in terms of the contradictory nature of your views
and those for instance, Dr. Lemen's presentation. The 1998 WHO
statement, consistent with their early conclusions, 1989, human
evidence has not demonstrated there is any threshold exposure
level for lung cancer or mesothelioma below which exposure to
asbestos dust would not be free of hazard to health. Do you
disagree with that conclusion, Dr. Weill?
Dr. Weill. I think I would just state it differently. I
think it is very difficult scientifically to render something
``safe.'' I think all we can do is estimate the risk as best we
can and try to determine, and this is more of a public policy
question, how much risk is tolerable. I think it is very
difficult to say something is safe, whether it be air travel,
water, asbestos fibers----
Senator Lautenberg. Those comparisons are not valid, air
travel, that--you are not risking exposure when you get in an
airplane that is commonly thought to be a dangerous exercise.
Dr. Weill. No, but I think my point really was, and maybe
it wasn't a perfect analogy, was that all science can do really
is estimate risk. It can't render something safe or unsafe.
Because the circumstances that somebody is exposed to something
differs, what they are exposed to differs. I think that is why
we have to really rely on the scientific evidence to assign
risk to these different exposures.
Senator Lautenberg. Is mesothelioma directly connected with
asbestos exposure or are there other exposures?
Dr. Weill. There are other causes of mesothelioma that are
very uncommon.
Senator Lautenberg. Dr. Lemen, is mesothelioma typically a
result of exposure to asbestos, the larger share, let's say, of
cases that we see?
Mr. Lemen. Yes. And there are some other causes, they are
very small, related to asbestos. But in man, about 80 percent
of the mesotheliomas have been related to exposure to asbestos.
That is somewhat less in women, because we just don't have good
surveillance data on women. But when I was at NIOSH, we put out
a paper and we titled mesothelioma as a signal tumor. That is,
once you see the disease, look closely to see if there is any
asbestos exposure. Because in almost all cases, there is some
exposure to asbestos.
Senator Lautenberg. So Dr. Weill, I get the suggestion from
you that we are just alarmists with our concerns about this,
and that it is not, the threats are not really what we think we
are talking about here?
Dr. Weill. No, Senator, I am sorry if I left that
impression. I don't think you are alarmist at all. I think,
though, what is important, particularly as it relates to
asbestos, given the long history of looking at this disease,
both scientifically and in the public policy arena, is that we
rely on the science. We keep coming back to risk assessment and
not just tend to lump everything together without regard to the
scientific evidence that is available.
Senator Lautenberg. I ask each of you again, Dr. Wylie and
Dr. Weill, and the Chairwoman asked you about whether or not
you have testified on behalf of companies, helping to protect
companies that are facing lawsuits. You both agreed that you
have testified in those cases.
Now, who brings these suits? Are these people who are sick,
people who are at risk from exposure to asbestos?
Dr. Weill. As you can imagine, in litigation, some are sick
and some are not.
Senator Lautenberg. But have you, are you familiar with the
condition of your physician and the condition of the people who
are bringing this suit who were trying to prove that they were
sick? Were you invited to examine these people?
Dr. Weill. In some instances?
Senator Lautenberg. And you found that, you testified that
they weren't really sick?
Dr. Weill. Sometimes yes, sometimes no.
Senator Lautenberg. Even though other physicians said they
were sick?
Dr. Weill. There has been disagreement.
Senator Lautenberg. Dr. Lemen, where do we get differences
like this? How is that possible? Are you so blindsided that you
think these things really relate to exposure to asbestos
cleavage in particular, et cetera?
Mr. Lemen. I believe, and I have been in this field for a
long time, that when you have a respirable fiber, and if you
look at the issues about fiber size, length and diameter, we
see that these types of fibers get into the lung, are capable
of causing damage. So I pointed out a particular facility, R.T.
Vanderbilt facility, where our agency went into in the 1970s,
where the company claimed that they were having a non-
asbestiform talc. But when we went in, we actually found two
types of asbestos fibers in that talc, and they were above the
OSHA and MSHA risk.
So it lies a lot in the definition. As I say in my extended
testimony, a lot of this depends upon getting a good
definition. I would agree with all the panelists here that we
need to get a good definition and come to some conclusion
amongst ourselves of what that definition is. But as a health
scientist, I am concerned when fibers get into the lung and
stay in the lung and have the characteristics of asbestos
fibers that they can cause damage. And that is where I am
coming from and have been from that point of view for the whole
time that I was with the Federal Government, 26 years. I still
believe that.
I would like to say one thing about the lawsuit. I think
that there is a lot of concern about frivolous lawsuits. But
there are a lot of real lawsuits. It was the real lawsuits that
brought the attention of the asbestos issue, your friend, Dr.
Selikoff, that I had the privilege of working with for many
years, brought this to the attention when the Occupational
Safety and Health Act passed in 1970, and asbestos was a major
issue because the companies were not doing their part to
prevent these diseases. I would end with that.
Senator Lautenberg. I thank you very much, Madam Chairman,
for having this hearing. I would ask that the record be kept
open so that we have a chance to review in a little more detail
the differences that we see, the testimony differences. I am of
the view that with the exposure from my high school days and
friends that I know and people who worked in New Jersey had a
lot of work on Johns Manville in the Raybestos Manhattan, the
shipyards and the whole thing.
So thank you to all of the witnesses. Madam Chairman, that
concludes my questions. Thank you for permitting me the extra
time.
Senator Boxer. Always happy to. And I think that gets
really back to the heart of the matter I was trying to get at.
I have a couple more points.
I think the point that Senator Inhofe, whom I have great
respect for, my Ranking Member, and my good friend, when he
says that this is all about the trial lawyers, I don't know
what he is thinking. We want to ban asbestos. That would put
the trial lawyers out of business at the end of the day. So
let's get it straight. We are going to ban it, at least in this
committee, and we are going to get the ball rolling. That is
going to put the trial lawyers out of business eventually. So
that is point No. 1.
Dr. Weill, you said it is an issue of how much risk is
tolerable, which is something I hear a lot from people who
always defend the folks who are pushing poison on the public,
if you will. So how much risk is tolerable to you? Are you
married with a family?
Dr. Weill. Yes.
Senator Boxer. Is it tolerable for your child to get
mesothelioma? Would that be tolerable for you, sir?
Dr. Weill. Of course not. And----
Senator Boxer. Would it be tolerable if you knew the
company knew they could use an alternative but yet you came
home and you had asbestos on your clothes, like one of these
guys might have done, and your child got close to you and
breathed it in, is that tolerable? Would that be tolerable to
you, sir?
Dr. Weill. I don't understand the specific----
Senator Boxer. Would it be tolerable to you if you worked
in a place where you were exposed to asbestos, the kind you
admit is dangerous, and your child breathed it in, and pretty
soon she or he had some kind of asbestos-related disease and
could die from it, would that be tolerable to you?
Dr. Weill. No. If there is amphibole asbestos in a dose
that is important, that would not be tolerable.
Senator Boxer. So you would support banning this product, I
assume?
Dr. Weill. By banning it, we would have to define what we
are talking about in terms of the----
Senator Boxer. Banning a product that was dangerous, you
wouldn't have objection to that?
Dr. Weill. Products that are dangerous shouldn't----
Senator Boxer. You would support that?
Dr. Weill. Absolutely.
Senator Boxer. Because I don't know what--that sort of
contradicts what you said before, how much risk is tolerable,
which indicates to me that some of the risk is tolerable. So I
am trying to ask you, how many people a year could die from
mesothelioma, and it would be tolerable to you, sir?
Dr. Weill. I answered the question, though, to look at a
certain type of asbestos in a certain dose. That is----
Senator Boxer. Well, I am asking you a different question.
I am asking you, how many people dead every year from
mesothelioma would you consider tolerable?
Dr. Weill. I would hope that none would die from
mesothelioma. It is a personal tragedy for the families----
Senator Boxer. So no deaths are tolerable?
Dr. Weill. That is right.
Senator Boxer. So that contradicts what you said, how much
risk is tolerable.
Dr. Weill. No, we are not saying that deaths are tolerable.
We are saying that risk assessments are a sign in the
scientific literature for a variety of things.
Senator Boxer. Sir, what if the risk is 1 per 300, 1 per
1,000, 1 per 500,000? What is tolerable? You started this. You
said before it is a question of how much risk is tolerable.
Dr. Weill. And I----
Senator Boxer. You know what risk benefit means. Some
people die. What is tolerable?
Dr. Weill. I think that is a public policy question, not a
question----
Senator Boxer. Oh, OK, so you are ducking it. So you don't
sit here and tell me, it is a question of how much risk is
tolerable and then refuse to answer it, because that is wrong.
That is just saying, I can testify in front of any court and
then I can say, well, my Senator, Barbara Boxer, I am your
Senator, oh, God, I think I lost a vote here----
[Laughter.]
Dr. Weill. I have a very open mind about that, Senator.
Senator Boxer. About voting for me?
Dr. Weill. Sure.
Senator Boxer. OK. It seems to me, if you are going to say,
it is a question of how much risk is tolerable, you have to
then be prepared to answer the question. Because let me tell
you what is intolerable, I agree with what you said, any death,
whether it is your kid, my kid or any kid or any worker or
anybody. And here we have Linda Reinstein sitting here, having
lived through this experience with her husband. And here we
have, you know, deaths going down? Doesn't look that way, sir.
But you can take a look at it. It looks like we have lost
10,000, and this is under-reported, from NIOSH, they admit it
is under-reported, 10,000 since 1999, 10,000 dead. Close your
eyes and think about 10,000 families.
In my case, I raised my kids in Marin County. And a lot of
those towns just had 11,000 people. So just think about what
that means.
So I agree with what you said, it is intolerable to lose
anyone. I don't agree with saying, well, it's a public policy
decision as to how much risk. I think everyone is responsible,
if you are in this game and you are in the game, you have money
in the game, you have to be prepared to tell me how much risk
is tolerable.
Was it worth Ms. Reinstein losing her husband? And maybe
she will want to talk about--do you have a daughter? Do you
want to talk about what it is like, to tell people who go and
testify on behalf of the industry, please tell us what it is
like.
Ms. Reinstein. Are you asking me to tell you?
Senator Boxer. Yes, I am asking you to please tell us what
it was like for your child.
Ms. Reinstein. I think it is really important for the
record and I thank you for asking. Because there are hundreds
of thousands of women just like myself, we go from wife to
widow. Our children are raised by single parents. Emily walked
Alan's oxygen around the house. He struggled for a year with
chemotherapy. I stayed home lovingly to walk my husband to the
bathroom, he was too weak. He was a brilliant businessman, a
mountain climber and a marathoner who died a shell of a man who
weighed 135 pounds. Emily stood there over her father's body as
he gasped for his last breath. He got to her bat mitzvah, he
died 5 months later.
None of these deaths are tolerable. And the victims and the
families want a ban and education. It is heartbreaking, Senator
Boxer. It really is painful.
Senator Boxer. Let me just thank you very much for that.
I know I sounded harsh. And I feel concerned that people
have talked themselves into a position where they are part of
the problem and don't see it. It is not right. I don't think
geologists should talk about what causes cancer. I don't think
the USGS said they should and I don't think they should appear
before here and do it and I don't think they should deny they
got paid until they are reminded. Call me old-fashioned, I
don't think it is ethical. I don't.
I will just say this. The facts are in. We are going to
have a bill. It is going to ban asbestos. We are going to do
that. We are not going to allow this moment, this opportunity,
to pass us by. Because if we do, we are part of the problem,
Senator Lautenberg and I. We don't want to be part of the
problem. I can't speak for other Senators, except I know
Senator Isakson wants to be part of the solution.
So let me just say to all the panelists, whatever side you
are on, that I appreciate the fact that you came here. I know
it isn't easy. There are some withering questions sometimes. I
know it is emotional. I saw people in the audience with tears,
and I know that Linda is fighting them back at the moment.
But just think about what it will mean, the memory of your
husband, when we get this signed, thanks to Patty Murray's
bill, thanks to Senator Isakson for working with her. And
thanks to the happenstance that I am holding the gavel. This is
good. These are good things. And we can spare other people what
you went through. And I will give it all I have.
So I want to thank everybody on all the panels. Again, the
Capitol workers who are here as a reminder that this is hitting
right close to our home right here, to our family right here at
the Capitol.
We stand adjourned, and hopefully we will be marking this
bill, Senator Lautenberg, in the near future. We stand
adjourned.
[Whereupon, at 12:18 p.m., the committee was adjourned.]
[Additional statement submitted for the record follows.]
Statement of Hon. Max Baucus, U.S. Senator from the State of Montana
After the field hearing this committee held in Libby, Montana, this
last April, an outraged constituent approached me to talk about
asbestos. He didn't want to talk about WR Grace's disgraceful history
of poisoning the town of Libby. Nor did he want to discuss the ongoing
EPA cleanup in Libby. What outraged him, and rightly so, was that given
all the dangers of asbestos, the heartache it has causes thousands of
families throughout the country, and the over 200 confirmed asbestos
disease related deaths in Libby alone, the United States continues to
use over 2000 metric tons of asbestos every year. We here on the
committee ought to share that constituent's outrage.
Madame Chairman, I want to thank you for calling this hearing. It
is beyond comprehension that after years of studies and thousands of
deaths we are still fighting to ban this deadly substance. It is an
affront to all those who have suffered throughout the country to not
learn the lessons from places like Libby.
Libby epitomizes what happens to a town devastated by the health
effects of asbestos. As I mentioned previously, there have been over
200 confirmed deaths due to asbestos exposure in Libby. And it is not
only the former employees of WR Grace that have been victims. For years
miners came home with their clothes covered in the deadly fibers. The
WR Grace mill spewed 5,000 pounds of asbestos into the air every day.
The entire community was exposed. This resulted in ``take home'' and
environmental exposure on a frightening scale. According to an Agency
for Toxic Substances and Disease Registry, asbestosis mortality in
Libby is 60 times higher than in the rest of the U.S.
We must learn from this tragedy and prevent asbestos exposure. We
must prevent more asbestos exposure. We must do two things. First, we
need to continue to fund research on asbestos and non-asbestiform
structures as well as minerals such as erionite, richterite, and
winchite. With a better understanding of the toxicity of these
materials, we will be better able to protect public health.
Secondly, we must pass Senator Murray's ``Ban Asbestos in America
Act.'' This bill would put an end to this dangerous product that has
been used for far too long. Senator Murray has been a champion of this
issue, and I'm proud to have joined her as an original cosponsor of the
``Ban Asbestos in America Act.'' This is an important piece of
legislation, and I look forward to working with her to bring an end to
asbestos use in America.
We must learn from history. In Libby and across the country too
many lives have been devastated by asbestos related diseases to
continue asbestos use in this country. It is an outrage, an affront to
the victims of asbestos related disease, and we ought to put an end to
it.