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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 

Printed for the use of the Committee on Environment and Public Works 

( 

Available via the World Wide Web: http://www.gpo.gov/fdsys/browse/ 

committee.action?chamber=senate&committee=environment 
(II) 

COMMITTEE ON ENVIRONMENT AND PUBLIC WORKS 

ONE HUNDRED TENTH CONGRESS 

FIRST SESSION 

BARBARA BOXER, California, Chairman 

MAX BAUCUS, Montana 

JOSEPH I. LIEBERMAN, Connecticut 

THOMAS R. CARPER, Delaware 

HILLARY RODHAM CLINTON, New York 

FRANK R. LAUTENBERG, New Jersey 

BENJAMIN L. CARDIN, Maryland 

BERNARD SANDERS, Vermont 

AMY KLOBUCHAR, Minnesota 

SHELDON WHITEHOUSE, Rhode Island 

JAMES M. INHOFE, Oklahoma 

JOHN W. WARNER, Virginia 

GEORGE V. VOINOVICH, Ohio 

JOHNNY ISAKSON, Georgia 

DAVID VITTER, Louisiana 

LARRY E. CRAIG, Idaho 

LAMAR ALEXANDER, Tennessee 

CHRISTOPHER S. BOND, Missouri 

BETTINA POIRIER, Majority Staff Director and Chief Counsel 

ANDREW WHEELER, Minority Staff Director 
(III) 

C O N T E N T S 

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 
Page

IV 

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 
(1) 

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. 
2 

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 
3 

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. 
4 

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 nonasbestiform 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 
5 

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 xray, 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 
6 

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 asbestosrelated 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 Sub-
7 

committee 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. 
8 

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. 
9 

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 chloralkali 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 
10 

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. 
11 

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 
12 

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 longstanding 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 includ-
13 

ing 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 pri- vately 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. 
14 

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. 
15 

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:] 
16 
17 
18 
19 
20 
21 
22 
23 

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 stu-
24 

dent 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 nonasbestiform 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 microscopi-
25 

cally 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: 
26 

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 
27 

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 
28 

Table 1—Number of mesothelioma deaths, U.S. residents age 15 and over, 1999–2004— 

Continued 

Year Deaths 

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 fibercontaminated 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 reanalyzed 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 
29 

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 manmade 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 
30 

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 asbestosrelated 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.’’ 
31 

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 asbestoscontaining 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. 
32 

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 indistinguish-
33 

able from typical asbestos fibers, can be generated from these nonfibrous 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). 
34 

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 solidsolution 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 in-
35 

clude the conditions of interstitial pulmonary fibrosis (asbestosis), benign asbestosrelated 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 μm are more likely to cause injury than fibers with lengths 

less than 2.5μm. (1 μm 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 μm 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 re-
36 

search plan for these projects was initiated from the recommendations of a multiagency 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. 
37 

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 expo-
38 

sure 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 
39 

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 ENVIRON- MENTAL 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 subse-
40 

quent 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 amphibolecontaining 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. 
41 

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:‘ 
42 

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—Guid- ance 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 lin-
43 

ings for tractors. I am going to put this into the record without objection. 

[The referenced material follows:] 
44 
45 
46 
47 
48 
49 
50 
51 

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. 
52 

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 
53 

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 
54 

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. 
55 

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, rocklike 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. 
56 

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. 
57 

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:] 
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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, nongovernmental 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 hydroblasting for removal and replacement of the asbestos is another 

possible source of area contamination and drying and airborne ex-
66 

posure. 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 
67 

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 asbestoscontaining 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 
68 

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 nonasbestos 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 Min-
69 

ing 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 
70 

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 
71 

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.] 
72 
73 
74 

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 populationat-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 
75 

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 
76 

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 
77 

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 
78 

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 
79 

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 
80 

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 
81 

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 
82 

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 
83 

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. 
84 

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 asbes-
85 

1OSHA’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) 2Leidel et al., 1979 

3 Addingley, C.F., 1966; Lynch et al., 1970 4OSHA, 1992 

5 NIOSH, 2007 

6 NIOSH, 2007 

tos 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

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 method2, 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. 

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. 

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 disease5. 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. 

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. 

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. 
86 

7Wylie, 1979, 1993, 1988; Verkouteren and Wylie, 2002 

8Wylie et al.,1993 

9See Zoltai, 1981, for an excellent discussion. 

10Polygonal serpentine fibers may have diameters up to 10,000A. Baronnet and Devouard, 

2005. 11Wylie et al., 1993 12Warnock, 1989 13Siegrist and Wylie, 1980 14 1995 

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’’. 

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 cummingtonitegrunerite 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

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

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

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. 

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 
87 

15Siegrist and Wylie, 1980 16Stanton et al., 1981 17 Bertrand, and Pezerat, 1980, Davis et al., 1991, Smith et al., 1979, Pott et al., 1974. 18 Baris, 1987, Wagner et al., 1985 19 Amandus et al., 1987; Sullivan, 2007. 20 IARC, in press; Honda et al., 2002; Gamble, 1993; Stille and Tabershaw, 1982 21For 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. 22Leake et al., 1997, 2004 23McDonald 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 

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. 

Cleavage fragments are different. Cleavage fragments, formed by crushing rock, 

get wider as they get longer and width is therefore dependent on length15. 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. 

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 results17. 

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 exposed19. 

However, we also know from the experience of miners exposed to other durable 

long, thin fibers such as fibrous talc20 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. 

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 composition22, 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

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 
88 

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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90 

1There are other recognized methods of identification, but x-ray d most reliable and its results 

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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 flax2 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. 

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: 
91 

(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 legisla-
92 

tion 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 opin-
93 

ion, 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 xrays 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 
94 

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 
95 

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 ‘‘nonasbestiform’’ 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 impor-
96 

tant 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 nonoccupational 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 asbestosrelated 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 asbestosrelated 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 asbestosrelated diseases is beginning to slow down. However, this is not 
97 

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. 
98 

1Lemen, 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. 2Lemen, 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. 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. 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). 

[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

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

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

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

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 
99 

5OSHA, 1986. OSHA, 1986. Final Rule: Asbestos. 51 FR 22612. U.S. Department of Labor. 

Occupational Safety and Health Administration, Washington, D.C., June 20. 6Glustavsson P, Nyberg F, Pershagen G, Sche ́ele 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. 7 IPCS, 1998. Environmental Health Criteria 203: Chrysotile Asbestos, International Program 

on Chemical Safety, World Health Organization. 8WHO, 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. 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 fiContinued 

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. 

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! 

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
100 

bers are about 0.2μm in diameter while the finest asbestos fibers may be as small as 0.2μm 

in diameter. For some exposures, substantially more fibers may be present than are actually 

counted.’’ 11Dement 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. 12See Appendix 1—Short Fibers, Richard A. Lemen, Ph.D. 13 See Appendix 2—Mesothelioma Surveillance, Richard A. Lemen, Ph.D. 14 Bellman B, Muhle H, Pott F, Konig H, Kloppeel H, Spurny K, 1987. Persistence of manmade fibers (MMF) and asbestos in rat lungs. Annals of Occup Hyg, 31: 693–709. 15Suzuki, 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. SepOct;29(5):415–33. 

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

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. 

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 pleura15. 

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 con-
101 

16Malomi, 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. 17Levresse, 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. 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. 19McDonald 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. 21Kamp DW, Weitzman SA, 1999. The molecular basis of asbestos induced lung injury. Thorax.54:638–652 22 Hull MJ, Abraham JL, Case BW, 2002. Mesothelioma among workers in asbestiform fiberbearing 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. 

tributes 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

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 doseresponse 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 asbestosinduced disease. Therefore, future research should continue to look at all asbestosinduced diseases when determining recommended regulatory actions for the prevention of asbestos-related diseases. 

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

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 pa-
102 

24Fitzgerald 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. 25Dement 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. 

renchymal fibrosis and pleural changes. The data also suggest that individuals in 

the paper industry and construction trades may be at risk.’’24

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 5μm 

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

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. 
103 

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. 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. 31Stanton, M.F., and Wrench, C., 1972. Mechanisms of mesothelioma induction with asbestos 

and fibrous glass. J. Natl. Cancer Inst., Vol. 48, p. 797. 32Stanton, 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. 

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 length27

and thus are less harmful.28

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 5μm 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 [<0.2μm 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. 

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 
104 

33Greenberg, M, 1984. S Fibers. Am J Indust Med, Vol. 5, p. 421–422 & Personal correspondence from Dr. Morris Greenberg, 23 May 2003. 34Suzuki, 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. 35Dement, 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. 36Oberdorster, 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. 37Dement, 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. 38Davis 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. 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. 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 

probability, might be more hazardous than fewer long fibers, individually of high 

probability.33

Studies have also found that the majority of asbestos fibers in lung and 

mesothelial tissues were shorter than 5μm 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 5μm in length outnumber the longer fibers by a 

factor of 10 or more.35

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

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 μm in length 

as ‘‘Structures <5 μm 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. 

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. 

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 
105 

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. 41Price 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 & 42Pinheiro 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. 43World Health Organization, 1992. ICD–10 International Statistical Classification of Diseases and Related Health Problems Tenth Revision: 1; 201. 44Pinheiro 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. 45Steenland 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. 46Magnani 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. 

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. 

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

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. 

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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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 asbes-
170 

tosis 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-yearold 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) 
171 

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 asbestoscaused 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. 
172 

• 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. 
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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:] 
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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 dif-
206 

ferent 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 cleavagetype 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 
207 

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. 
208 

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. 
209 

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 
210 

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 
211 

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—— 
212 

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? 
213 

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 
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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. 

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