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IN THE SUPREME COURT OF OHIO
MARK SCHWARTZ, et al.,
Appellees,
v.
HONEYWELL INTERNATIONAL, INC.,
Appellant.
:
:
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:
:
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Supreme Court Case No. 2016-1372
On Appeal from the Cuyahoga County
Court of Appeals, Eighth Appellate District
Court of Appeals Case No. CA-15-103377
BRIEF OF 51 CONCERNED PHYSICIANS, SCIENTISTS, AND SCHOLARS
REGARDING CAUSATION OF ASBESTOS-RELATED DISEASE,
AS AMICI CURIAE IN SUPPORT OF APPELLEES
Joshua P. Grunda (0084266)
*Counsel of Record
Thomas W. Bevan (0054063)
Patrick M. Walsh (0075966)
BEVAN & ASSOCIATES LPA, INC.
6555 Dean Memorial Parkway
Boston Heights, Ohio 44236
Phone: (330) 650-0088
Fax: (330) 467-4493
Counsel for Amicus Curiae
51 Concerned Physicians, Scientists,
and Scholars Regarding Causation of
Asbestos-Related Disease
James L. Ferraro (0076089)
John Martin Murphy (0066221)
Anthony Gallucci (0066665)
Shawn M. Acton (0072675)
KELLEY & FERRARO LLP
Ernst & Young Tower
950 Main Avenue, Suite 1300
Cleveland, OH 44113
Phone: (216) 202-3450
Fax: (216) 575-0799
Counsel for Appellee, Mark
Schwartz, et al.
Steven G. Blackmer (0072235)
Melanie M. Irwin (0086098)
WILLMAN & SILVAGGIO LLP
One Corporate Center
5500 Corporate Drive, Suite 150
Pittsburgh, PA 15237
Phone: (412) 366-3333
Fax: (412) 366-3462
Michael W. Weaver (PHV 2612)
MCDERMOTT WILL & EMERY
227 West Monroe Street
Chicago, IL 60606
Email: [email protected]
Counsel for Appellant, Honeywell
International Inc.
Supreme Court of Ohio Clerk of Court - Filed July 17, 2017 - Case No. 2016-1372
ii
Douglas R. Simek (0075988)
SUTTER O’CONNELL CO.
1301 East 9th Street
3600 Erieview Tower
Cleveland, OH 44114
(216) 928-4519 phone
(216) 928-4400 facsimile
James N. Kline (0007577)
ULMER & BERNE LLP
1660 West 2nd Street
Cleveland, OH 44114-1406
(216) 583-7000 phone
(216) 583-7161 facsimile
Counsel for Amicus Curiae
Ohio Association of Civil Trial Attorneys
Victor E. Schwartz (0009240)
SHOOK, HARDY & BACON L.L.P.
1155 F Street, NW, Suite 200
Washington, DC 20004
Tel: (202) 783-8400
Fax: (202)783-1211
William L. Anderson (PHV 18357)
CROWELL & MORING LLC
1001 Pennsylvania Avenue, NW
Washington, DC 20004
Tel: (202) 624-2942
Fax: (202)628-5116
Counsel for Amicus Curiae
Coalition for Litigation Justice, Inc.
Richard D. Schuster (0022813)
Daniel E. Shuey (0085398)
Damien C. Kitte (0084057)
VORYS, SATER, SEYMOUR AND PEASE
LLP
52 East Gay Street, P. O. Box 1008
Columbus, Ohio 43216-1008
Telephone: (614) 464-5475
Facsimile: (614) 464-6350
Counsel for Amici Curiae Ohio
Manufacturers’ Association;
Ohio Council of Retail Merchants; Ohio Tire
& Automotive Association; Ohio Alliance for
Civil Justice; and the Honorable William
Seitz
iii
TABLE OF CONTENTS
Page
TABLE OF AUTHORITIES ........................................................................................................ iv
STATEMENT OF THE FACTS ....................................................................................................1
STATEMENT OF AMICI’S INTEREST ......................................................................................1
SUMMARY OF THE ARGUMENT .............................................................................................2
ARGUMENT IN OPPOSITION OF PROPOSITION OF LAW NO. 1 .........................................3
Proposition of Law No. 1: A theory of causation based only upon cumulative
exposure to various asbestos-containing products is insufficient to demonstrate
that a particular defendant’s product was a “substantial factor” under R.C.
2307.96................................................................................................................................ 3
I. ALL EXPOSURES TO ASBESTOS CONTRIBUTE TO A PERSON’S
CUMULATIVE LIFETIME DOSE .......................................................................3
II. CUMULATIVE LIFETIME EXPOSURE TO ASBESTOS,
INCLUDING SECONDARY HOUSEHOLD EXPOSURES,
CAUSES MESOTHELIOMA ................................................................................5
III. ASBESTOS RESEARCHERS EMPLOY A MULTI-FACETED
APPROACH TO ASSIGN CAUSATION OF ASBESTOS-RELATED
DISEASE, BUT NEVER REQUIRE A PRECISE QUANTIFICATION
OF A PERSON’S EXPOSURE LEVEL ..............................................................15
A. SIGNIFICANT EXPOSURE HISTORY .................................................15
B. INDIVIDUAL SUSCEPTIBILITY ..........................................................19
C. BIOLOGICAL PLAUSIBILITY ..............................................................20
D. CASE REPORTS AND SENTINEL EVENTS/SIGNATURE
DISEASES ................................................................................................22
E. EPIDEMIOLOGICAL STUDIES ............................................................24
CONCLUSION .............................................................................................................................29
PROOF OF SERVICE ..................................................................................................................31
iv
TABLE OF AUTHORITIES
Page(s)
AUTHORITY
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551 (2008) ...............................................................................................................................21
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(1974) ................................................................................................................................11, 15
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Hillerdal, Mesothelioma: Cases Associated with Non-Occupational and Low Dose
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565 (2000) ...............................................................................................................................15
vii
Huncharek, M., et al., Pleural Mesothelioma in a Brake Mechanic, 46 Brit. J. Ind.
Med. 69 (1989) ........................................................................................................................27
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Asbestos from the Joint Policy Committee of the Societies of Epidemiology
(JPC-SE) (2012) ......................................................................................................................24
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Epidemiol. 695 (2011) ............................................................................................................24
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Asbestos Exposure. Am. J. Respir. Crit. Care Med. Vol 178 .................................................13
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Perspectives 118:897-901 (2010) ...........................................................................................28
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Ind. Med. 229 (2004) ....................................................................................................4, 27, 28
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(2015) ........................................................................................................................................7
viii
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Canada, 26(4) Cancer 914 (1970) ..........................................................................................27
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1
STATEMENT OF THE FACTS
Because this brief is intended to present an objective discussion of the relevant generally
accepted, reliable science, the particular facts of this case do not affect our analysis.
STATEMENT OF AMICI’S INTEREST
The undersigned Amici collectively possess hundreds of years of experience
researching, diagnosing, and treating asbestos-related diseases in workers and their families. We
have published extensively in this field for more than forty years and have conducted dozens of
epidemiological and other studies concerning asbestos and disease or are well aware of the
issues. Many of us have testified before legislative and regulatory bodies, in the United States
and abroad, regarding asbestos and disease, as well as in court proceedings. We have reviewed
and been given an opportunity to comment upon this brief and have asked to be listed as
signatories because we agree with its contents.1 We have not received any compensation for our
participation in this scientific endeavor.
We understand that causation is a key contested issue in lawsuits involving people who
are suffering or have died from asbestos-related diseases. As this Court addresses the legal
issues before it, our goal is to educate the Court about how scientists, researchers, and physicians
like us attribute causation of asbestos-related diseases in our day-to-day work. We discuss the
practical realities of causal attribution — including the impossibility of precisely quantifying an
individual’s asbestos exposure in the vast majority of situations — and strive to eliminate any
confusion sometimes found in court decisions discussing the subject. In the end, we know this
Court must apply Ohio law to reach a decision. We seek only to ensure the Court does so with
the benefit of an accurate view of the relevant science.
1 A list of the Amici and their titles and affiliations is attached hereto as Exhibit A. The titles
and affiliations listed with names of the Amici are provided for identification purposes only.
2
SUMMARY OF THE ARGUMENT
We discuss the science with respect to three discrete, relevant areas. First, we explain the
undeniable scientific fact that all exposures to asbestos contribute to a person’s cumulative total
dose of a known carcinogen. Numerous studies have shown that cumulative dose drives both the
risk and causation of asbestos-related diseases. We distinguish that from the narrative advanced
by the asbestos industry, which is that an expert who embraces this unremarkable proposition is,
in reality, stating that “each and every exposure,” no matter how de minimis (or even a single
fiber of asbestos) is enough to cause mesothelioma. Second, we discuss the medical and
scientific consensus that so-called low-level cumulative exposures to asbestos, as qualitatively
estimated by both intensity and duration, are capable of causing mesothelioma. As
acknowledged by numerous agencies, including but not limited to, the National Institute for
Occupational Safety and Health (“NIOSH”), the United States Environmental Protection Agency
(“EPA”), and the United States Occupational Safety and Health Administration (“OSHA”), even
exposures well below federal regulatory exposure limits have been shown to be sufficient to
cause mesothelioma. This principle has also been acknowledged by purely scientific groups like
the Collegium Ramazzini2 and the National Institutes of Health
3. Third, scientists and physicians
employ a multi-faceted methodology when assigning causation of asbestos-related disease. In
general, reliable exposure histories provide the most practical and useful qualitative measure of
2 Collegium Ramazzini, Asbestos Is Still with Us: Repeat Call for a Universal Ban (2010).
http://www.collegiumramazzini.org/download/15_FifteenthCRStatement(2010).pdf (Accessed
June 5, 2017).
3 National Institutes of Health, et al., Asbestos: Worker and Employer Guide to Hazards and
Recommended Controls.
https://portal.hud.gov/hudportal/documents/huddoc?id=IEPWG_asbestos_worker.pdf (Accessed
June 5, 2017).
3
asbestos exposure and causality as it is virtually impossible to obtain an accurate numerical
quantification of the asbestos fibers inhaled.
ARGUMENT IN OPPOSITION OF PROPOSITION OF LAW NO. 1
Proposition of Law No. 1: A theory of causation based only upon cumulative exposure to
various asbestos-containing products is insufficient to demonstrate that a particular
defendant’s product was a “substantial factor” under R.C. 2307.96
I. ALL EXPOSURES TO ASBESTOS CONTRIBUTE TO A PERSON’S
LIFETIME CUMULATIVE DOSE
There is a generally accepted scientific consensus that in an individual diagnosed with
mesothelioma, and with a history of exposure to asbestos, the cause of that disease is the
person’s lifetime cumulative exposure to asbestos. Scientists also agree that every exposure to
asbestos (including so-called “low dose” exposures) contributes to the cumulative dose. But that
is not to suggest that every exposure to asbestos, no matter how small, must be considered a legal
cause of mesothelioma. Said differently, there is a clear difference between the irrefutable fact
that all exposures contribute to the total dose and the unverifiable conclusion that “one fiber” or
some infinitesimally small exposure to asbestos has made a significant or appreciable
contribution to causing a given case of mesothelioma.
While the “one fiber” or “one hit” scientific concept may indeed be true on some
theoretical plane,4 the theory has no practical application in the real world of asbestos exposures;
public health experts agree that both direct occupational exposures to asbestos and second-hand,
4 The “one hit” hypothesis for cancer genesis is that each molecule of a cancer-causing
substance has a very tiny but not zero chance of inducing via mutation one fully cancerous cell
that leads to a cancerous tumor. It is one possible explanation on how cancers might form and
would provide some additional biological explanation for how the low dose cancers caused by
radiation or asbestos occur. It may or may not ultimately be proven to be true, but it is a separate
issue from determining what constitutes a significant exposure for the purpose of attributing
causation. Goldstein, Bernard D. & Henifin, Mary Sue, Reference Guide on Toxicology, in
Reference Manual on Scientific Evidence, 642 (Federal Judicial Center, 3rd
ed. 2011).
4
bystander asbestos exposures in the household, may be intensive enough to cause mesothelioma.
These types of exposures involve the inhalation of many millions of asbestos fibers, a portion of
which will be retained in the patient’s body; a single gram of pure asbestos contains as much as
one trillion asbestos fibers.5 To suggest a qualified expert’s opinion that these types of real
world significant exposures is unreliable by falsely claiming that the expert’s opinion is based
on the theory that any exposure/single fiber is a substantial contributing factor is, at best, a clear
misstatement of the actual testimony. At worst, it is intellectual dishonesty and an attempt to
deceive the Court. The consensus that lifetime cumulative exposure to asbestos is the cause of
mesothelioma is a corner-stone of medicine and science; what makes for a significant or
“substantial” exposure under the law is a different topic altogether. This is no different than the
dose response concept that applies to human disease for most exogenous sources.
It is our understanding that the legal test employed in Ohio and some other states already
requires that a plaintiff present evidence of the manner, proximity, and frequency of exposure to
the defendant’s products. Given this requirement, and given the reality that direct and bystander
exposures to asbestos (including those secondary household exposures experienced by family
members) typically involve billions or trillions of asbestos fibers,6 the suggestion that an expert
5 Abraham, J, Letter to the Editor, re: When Science Crosses Politics: The Case of Naturally
Occurring Asbestos, J. Environ. Health 67:3 40-41 (2004) (“[a] simple calculation based on the
size and mass of an average asbestos fiber will tell you that in a single gram of pure (100%)
asbestos, there will be on the order of one trillion fibers (1,000,000,000,000 fibers/gram in pure
asbestos)”).
6 Lemen, Richard A., Asbestos in Brakes: Exposure and Risk of Disease, 45 Am. J. Ind. Med.
229 (2004) (“Studies conducted by General Motors’ researchers of brake wear debris
demonstrated that 90,000 asbestos fibers per ng remain in that dust [citation omitted]. Fibers less
than 5 µm in length out number fibers greater than 5 µm by a ratio of 300:1. This translates to
approximately 300 billion asbestos fibers greater than 5 µm per g of wear debris and 90 trillion
asbestos fibers less than 5 µm.”); (“Even the so called ‘controlled’ use of asbestos containing
brakes poses a health risk to workers, users, and their families.”).
5
who testifies that regular and proximate exposure to an asbestos product is a substantial
contributing factor is relying on the “any exposure/single fiber” theory, is without basis in fact or
logic. Thus, the Court should scrutinize carefully lawyers’ attempts to portray an expert’s
opinion in those terms.
II. CUMULATIVE LIFETIME EXPOSURE TO ASBESTOS, INCLUDING
SECONDARY HOUSEHOLD EXPOSURES, CAUSES MESOTHELIOMA
To date, scientists have not been able to identify a level of exposure to asbestos that does
not carry with it a risk of mesothelioma. Rather, over the past several decades, as the amount of
data available for analysis has increased, peer-reviewed published epidemiological studies have
demonstrated a substantial, statistically significant, increased risk of mesothelioma even at low
cumulative levels — that is, levels that can be reached in short periods of time or in
environments containing relatively low amounts of asbestos.
Government regulators, relying on the best available scientific data, have always
recognized that there is no “safe” level of exposure at which mesothelioma will not occur. For
example, NIOSH declared the following almost four decades ago: “Excessive cancer risks have
been demonstrated at all fiber concentrations studied to date. Evaluation of all available human
data provides no evidence for a ‘safe’ level of exposure to asbestos.”7 Currently, OSHA states as
follows on its website:
There is no “safe” level of asbestos exposure for any type of
asbestos fiber. Asbestos exposures as short in duration as a few
days have caused mesothelioma in humans. Every occupational
7 National Institute for Occupational Safety and Health, Workplace Exposure to Asbestos:
Review and Recommendations: NIOSH-OSHA Asbestos Work Group Recommendations.
Department of Health and Human Services, 1980:81-103. https://www.cdc.gov/niosh/docs/81-
103/pdfs/81-103.pdf (accessed May 10, 2017). Just recently, NIOSH once again recognized
“that there is no safe level of exposure to a carcinogen.” Department of Health and Human
Services, Centers for Disease Control and Prevention, Current Intelligence Bulletin 68: NIOSH
Chemical Carcinogen Policy DHHS (NIOSH) Publication No. 2017–100 (2016).
6
exposure to asbestos can cause injury of [sic] disease; every
occupational exposure to asbestos contributes to the risk of getting
an asbestos related disease.8,9
This maxim was reiterated in Volume II (Neoplastic Lung Disease) of Dail and Hammar’s
Pulmonary Pathology, a well-regarded textbook:
No lower (minimum) threshold of exposure to asbestos has been
delineated below which there is no increase in the risk of MM
[malignant mesothelioma] and most authorities approach causation
of mesothelioma by asbestos from the perspective of a no threshold
model.
***
One factor that emerges from the Peto model and its modifications
is that when there are multiple asbestos exposures, each
contributes to cumulative exposure and hence to the risk and
causation of MM, within an appropriate latency interval of 15
years10
As discussed below, the constantly growing body of high quality scientific data only reinforces
these observations.
8 U.S. Dept. of Labor, Occupational Safety & Health Administration, Safety and Health Topics –
Asbestos, https://www.osha.gov/SLTC/asbestos/ (accessed May 10, 2017) (citations omitted).
9 The World Health Organization stated the following:
No threshold has been identified for the carcinogenic risk of
chrysotile [citation omitted].
***
Bearing in mind that there is no evidence for threshold for the
carcinogenic effect of asbestos and that increased cancer risks have
been observed in populations exposed to very low levels [citations
omitted], the most efficient way to eliminate asbestos-related
diseases is to stop using all types of asbestos.
World Health Organization, Elimination of Asbestos-Related Diseases (2006)
http://www.who.int/occupational_health/publications/asbestosrelateddiseases.pdf (Accessed June
5, 2017). 10
Hammar, Samuel P., et al., Neoplasms of the Pleura, in 2 Dail and Hammar’s Pulmonary
Pathology Volume II: Neoplastic Lung Disease (Joseph F. Tomashefski, Jr., et al., eds., 3rd
ed.
2008) at p. 587 (emphasis added).
7
Substantial, reliable evidence supports the conclusion that there is excess risk of
mesothelioma at low cumulative exposure levels. Dr. Yasunosuki Suzuki, a pathologist and
asbestos researcher from Mount Sinai School of Medicine in New York City stated:
It is well accepted that asbestos fibers are the cause of virtually all
cases of malignant mesothelioma. It is also known that all asbestos
types, including chrysotile and amphiboles, have been shown in
epidemiological and toxicological studies to be fully capable of
inducing the tumor. In addition to heavy (occupational exposure),
milder asbestos exposure (bystanders and family contact) can also
induce the tumor. Presently, no data are available to support a
threshold limit for asbestos exposure below which there is no risk
of malignant mesothelioma [citations omitted].11
In a 2015 peer reviewed article, Dr. Steven Markowitz concluded that “[t]he risk of
malignant mesothelioma due to asbestos is dose dependent,” but that “no ‘safe’ threshold risk of
cancer has been demonstrated.”12
Dr. Markowitz discussed the findings of several large case-
control studies that evaluated the risk of mesothelioma based on estimated occupational asbestos
exposure and showed a sharp rise in risk with increasing asbestos exposure.13
This pattern
illustrates the dose-response relationship between increasing cumulative asbestos exposure and
an increased incidence of disease in a population of workers. Three of the studies reviewed by
Markowitz concluded as follows:
11
Suzuki, Yasunosuke, et al. Asbestos Fibers Contributing to the Induction of Human
Malignant Mesothelioma, Ann. N.Y. Acad. of Sci. 982:160-176 (2002).
12 Markowitz, Steven, Asbestos-Related Lung Cancer and Malignant Mesothelioma of the
Pleura: Selected Current Issues, Semin. Respir. Care Med. 36:334-346 (2015).
13 Three of the studies discussed in depth by Markowitz are: Lacourt, A., et al., Occupational
and Non-Occupational Attributable Risk of Asbestos Exposure for Malignant Pleural
Mesothelioma, Thorax 1 (2014); Rödelsperger, Klaus, et al., Asbestos and Man-Made Vitreous
Fibers as Risk Factors for Diffuse Malignant Mesothelioma: Results from a German Hospital-
Based Case-Control Study, 39 Am. J. Ind. Med. 262 (2001); and Iwatsubo, Y., et al., Pleural
Mesothelioma: Dose-Response Relation at Low Levels of Asbestos Exposure in a French
Population-based Case-Control Study, 148(2) Am. J. Epidemiol. 133 (1998).
8
Lacourt, et al.: “A clear dose-response relationship was observed between
occupational asbestos exposure and pleural mesothelioma…for men exposed at
less than 0.1 f/ml-year.” (Odds Ratio (“OR”) of 4.0 for those exposed to ˃0 - 0.1
f/ml-year).
Rödelsperger, et al.: “[O]ur results confirm the previously reported observation of
a distinct dose-response relationship even at levels of cumulative exposure below
1 fiber year.” (OR of 7.9 for those exposed to ˃0 - 0.15 f/ml-year).
Iwatsubo, et al.: “We found a clear dose-response relationship between
cumulative asbestos exposure and pleural mesothelioma in a population-based
case-control study with retrospective assessment of exposure. A significant
excess of mesothelioma was observed for levels of cumulative exposure that were
probably far below the limits adopted in most industrial countries during the
1980s.” (OR of 4.2 for those exposed to 0.5 - 0.99 f/ml-year).
Because the dose-response relationship shows increased risk at low levels of cumulative
exposure, the data demonstrates that all significant exposures to asbestos increase the likelihood
of developing malignant mesothelioma.
Additionally, two other epidemiological studies, Offermans, et al. (2014)14
and Ferrante,
et al. (2007),15
also found substantially increased risk of mesothelioma at very low cumulative
levels of asbestos exposure. Offermans, et al. (2014), found excess risk as follows: ≤ 0.2
f/cc/years, Hazard Ratio (HR) 2.69 (95% CI 1.60 - 4.53). Ferrante, et al. (2015), a population-
based case-control study on pleural mesothelioma in the Casale Monferrato area of Italy,
reported an increased incidence of pleural mesothelioma at all levels of exposure studied: <1
fiber/cc/years, Odds Ratio (“OR”) 4.4 (95% CI 1.7 – 11.3). It should be pointed out that as
exposure, and therefore risk, decreases, the size of the population being studied has to increase in
order to have adequate statistical power to detect an increase in risk. At very low levels, the size
14
Offermans, N.S., et al. Occupational asbestos exposure and risk of pleural mesothelioma,
lung cancer, and laryngeal cancer in the prospective Netherlands cohort study, J. Occup.
Environ. Med. 56(1):6–19 (2014).
15 Ferrante, et al., Cancer Mortality and Incidence of Mesothelioma in a Cohort of Wives of
Asbestos Workers in Casale Monferrato, Italy, Environ. Health Perspectives 115:10; 1401-1405
(2007).
9
of the cohort necessary to detect an increased risk in a rare disease like mesothelioma would be
enormous, and for all practical purposes, render the use of epidemiology impossible.
To give some context to the exposure numbers discussed above, OSHA regulations
currently set a “Permissible Exposure Limit” or PEL of 0.1 fiber per cubic centimeter (0.1
f/cc)16
of air as an eight-hour time-weighted average. While OSHA’s PEL is intended to
mitigate risks of asbestos exposure, the agency recognizes that significant risk remains at the
PEL of 100,000 fibers/cubic meter.17
Thus, the epidemiological studies discussed above confirm
OSHA’s assessment that there remains substantial excess risk of mesothelioma, even at very low
levels. In fact, OSHA requires that mandatory work practices be followed when performing
brake work even when the PEL is being met, in order to reduce the risk of cancer as much as
humanly possible under the circumstances. Scientific organizations’ and OSHA’s long standing
position that there is no safe level of cumulative asbestos exposure directly refutes the asbestos
industry’s suggestion that OSHA’s PEL is a mere overly precautionary measure.
The excess risk of mesothelioma posed by low-level exposure to asbestos is not confined
to persons who worked directly with asbestos. Reliable studies dating back more than fifty years
have found a substantially increased risk of mesothelioma in persons who suffered non-
occupational exposures such as living with someone who worked with asbestos and brought the
16
Many of the studies discussed in this brief measured exposure in terms of fibers per milliliter.
A milliliter and a cubic centimeter are equivalent measures of volume.
17 U.S. Dept. of Labor, Occupational Safety and Health Administration, Letter of Interpretation
https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=INTERPRETATIONS&p
_id=22884 (Accessed June 5, 2017) (“The statement from the interpretation letter mentioned
above is imprecise. It definitely does not accurately capture OSHAs position on those
permissible exposure limits which have been established for most carcinogens, including the
PEL for asbestos. With these substances, a significant risk of harm frequently persists at even
very low levels of exposure.”).
10
substance home on their clothing or person. 18, 19
In the first large case series discussing
mesothelioma and asbestos, Wagner, et al. (1960)20
reported one case of mesothelioma in a
patient whose environmental exposure to asbestos was from secondary household contamination
and living in the mining area. Indeed, of the thirty-three individual cases of mesothelioma
discussed by Wagner, almost half involved persons with no first-hand exposure to asbestos.
Newhouse, et al. (1965), reported mesothelioma from household and environmental exposures to
asbestos, in addition to occupational exposures.21
Anderson, et al. (1979), and Anderson (1983)
reported on familial exposure to asbestos and disease, showing both non-malignant and
malignant disease occurring in family members not otherwise exposed to asbestos.22
One early
epidemiological study documented a substantially elevated (10-fold) incidence of mesothelioma
in family members of asbestos workers, including a woman whose husband worked as a brake
18
Wagner, J.C., C.A. Sleggs and P. Marchand, Diffuse Pleural Mesothelioma and Asbestos
Exposure in North Western Cape Province. Br. J. Ind. Med. 17 (4):260- 271 (1960) (reporting
on cases of mesothelioma due to occupational, household and environmental exposures to
asbestos).
19 See also Hamilton, Alice. The Fight Against Industrial Diseases – The Opportunities and
Duties of the Industrial Physician. Pa. Med. J. Vol. XXI, No. 6, 378–381 (1918). It was
recognized very early that companies should provide adequate medical facilities at work, that
changes of work clothing should be furnished by the employer, that showers should be provided
to reduce exposures, and that ventilation to remove hazardous dusts is recommended. The need
to keep clean work areas, to use wet methods, to use ventilation, to avoid dry sweeping during
cleanup, and to provide respirators was well known where toxic dusts were present.
20 Wagner, J.C., supra note 18.
21 Newhouse, et al., Mesothelioma of Pleura and Peritoneum Following Exposure to Asbestos in
the London Area, Br. J. Ind. Med. 22 (4):261-269 (1965).
22 Anderson, Henry A., R. Lilis, et al., Household Exposure to Asbestos and Risk of Subsequent
Disease. Dusts & Disease. 145-146 (R.A. Lemen and J.M. Dement eds., 1979); Anderson, Henry
A., R. Lilis, et al., Asbestosis Among Household Contacts of Asbestos Factory Workers. Ann.
N.Y. Acad. Sci. 330:387-399 (1979); Anderson, Henry A., Family Contact Exposure.
Proceedings of the World Symposium on Asbestos 349-362 (Canadian Asbestos Information
Center) (1983).
11
lining worker.23
Bourdes, et al. (2000) found a relative risk of pleural mesothelioma for
household exposures ranged between 4.0 and 23.7, and the summary risk estimate was 8.1.24
Magnani (2000) found domestic exposure was associated with an increased risk (Odds Ratio of
4.81 with a 95% CI of 1.8 to 13.1).25
Many other publications recognize the real and deadly risk
posed by domestic second-hand exposure to asbestos.26
In light of all these studies, it is no surprise that NIOSH27
reported to Congress that
“families of asbestos-exposed workers have been at increased risk of pleural, pericardial, or
peritoneal mesothelioma…and non-malignant pleural and parenchymal abnormalities as well as
23
Vianna, Nicholas J. and Adele K. Polan, Non-Occupational Exposure to Asbestos and
Malignant Mesothelioma in Women. Lancet. 311 (8073):1061-1063 (1978).
24 Bourdes, V., P. Bofetta, P. Pisani, Environmental Exposure to Asbestos and Risk of Pleural
Mesothelioma: Review and Meta-Analysis, European J. of Epi., 16:411-417 (2000).
25 Magnani, et al., Multicentric study on malignant pleural mesothelioma and non-occupational
exposure to asbestos, Br. J. Cancer 83(1), 104-111 (2000).
26 See, e.g., Champion, P., Two Cases of Malignant Mesothelioma after Exposure to Asbestos,
Am. Rev. Res. Dis. 103(6):821-826 (1971); Lillington, Conjugal Malignant Mesothelioma
[letter], New Engl. J. Med., 291(11):581-585 (1974); Greenberg & Davis, Mesothelioma
Register 1967-1968, Brit. J. Med. 31:91-104 (1974); Li, Familial Mesothelioma After Intense
Asbestos Exposure at Home, JAMA 240(5):467 (1978); Epler, Asbestos-Related Disease from
Household Exposure, Respiration, 39:229-240 (1980); Tagnon, Mesothelioma Associated with
the Shipbuilding Industry in Coastal Virginia, Cancer Research, 40:3875-3879 (1980); Hammar,
Familial Mesothelioma: A Report of Two Families, Human Pathology, 20:1-7-112 (1989);
Schneider, Pleural Malignant Mesothelioma and Household Exposure, Review Environ. Health,
11:65-70 (1996); Dodson, et al., Quantitative Analysis of Asbestos Burden in Women with
Mesothelioma, Am. J. Ind. Med. 43:188-195 (2003); Rake, Occupational, Domestic and
Environmental Mesothelioma Risks in the British Population: A Case-Control Study, Brit. J.
Cancer, 1-9 (2009); Gao, et al., Asbestos Textime Production Linked to Malignant Periotoneal
and Plueral Mesothelioma in Women: Analysis of 28 Cases in Southeast China, Am. J. Industr.
Med. 58:1040-1049 (2015) (Hospital-based study showing an overrepresentation of peritoneal
mesothelioma in women exposed to chrysotile asbestos at home and work).
27 NIOSH is primarily viewed as a scientific advisory body for OSHA with very little regulatory
authority of its own. NIOSH’s mission is: “[t]o develop new knowledge in the field of
occupational safety and health and to transfer that knowledge into practice.”
https://www.cdc.gov/niosh/about/ (Accessed June 5, 2017).
12
asbestosis.”28
In that report, which reviewed the available literature at the time, including twelve
epidemiological studies and multiple case reports, NIOSH further concluded that mesothelioma
has occurred following short term asbestos exposures of only a few weeks (including household
exposures), and can result from very low cumulative levels of exposure.29
In part because of
these low dose issues, over fifty nations have banned asbestos since 1983.30
Second-hand household asbestos exposures are not necessarily low-level exposures.
Rather, as Hillerdal (1999) explained in a review of the literature concerning low-level exposure:
“fibre concentrations in domestic exposure might in fact be as high as in occupational exposure”
and “[b]rushing clothes might give peaks of ≥ 100 fibres/ml.”31
Hammar, et al., in a well-
regarded pulmonary pathology textbook, advised that “lung tissue asbestos body and fiber
concentrations as a consequence of domestic exposure approached those found in some patterns
of occupational exposure.”32
The effect of domestic exposures is magnified by the fact that
fibers persist in contaminated homes and rooms, which can result in repeated or even constant
exposure of those who live there:
Ordinary vacuum cleaning is not effective in removing asbestos
fibres, which can remain for years in the house and be airborne
again whenever disturbed. Thus, domestic exposure is not low
exposure.33, 34
28
National Institute for Occupational Safety and Health, Report to Congress on Workers’ Home
Contamination Study Conducted Under the Workers’ Family Protection Act (29 U.S.C. 671a)
(Sept. 1995).
29 See NIOSH, supra note 7.
30 Collegium Ramazzini. The Global Health Dimensions of Asbestos and Asbestos-Related
Diseases. 2015.
31 Hillerdal, Mesothelioma: Cases Associated with Non-Occupational and Low Dose Exposures,
Occup. Environ. Med., 56:505-513 (1999).
32 Hammar, supra note 10 at p. 566.
33 Hillerdal, supra note 31.
13
The work of Selikoff has documented that even persons moving into a household after a
worker has stopped bringing in asbestos leaves enough residue that some individuals develop
asbestosis. This shows that even residual dust from years before can significantly contaminate
living spaces.35
Ampleford, et al. (2007) recognized a five-fold increased risk of mesothelioma
in people exposed to asbestos in the household as compared to “non-exposed” controls and stated
the following:
Bystander exposure can occur through contact with asbestos
contaminated occupationally exposed individuals (or their
belongings), through contact either with fibers resulting from…
exposure to products made with asbestos such as…brake pads,
clutch pads,…
***
Bystander exposure is often sustained by women and children who
may be at increased risk for mesothelioma compared with men.36
Environmental exposures, such as living near an asbestos mine or a factory using
asbestos, have further demonstrated that direct occupational exposure is not required for excess
mesothelioma risk. Studies of numerous environments including California,37
Japan,38
34
D’Agostin et al., Pleural Mesothelioma in Household Members of Asbestos Exposed Workers
in Friuli Nenezia Guilia, Italy, Inter’l. J. Occ. Med. And Environ. Health 30:426 (2017)
(Moreover, while fiber dose may be lower in non-occupational settings, the duration of
exposure may be much longer in the non-occupational settings as compared with
occupational setting because the asbestos fibers permeate the environment. Therefore,
cumulative exposure may be comparable between occupational and non-occupational
cases.”) (emphasis added)
35 Anderson H.A., Lilis R., Daum S.M., Selikoff I.J. Asbestosis among Household Contacts of
Asbestos Factory Workers. Annals New York Academy of Sciences. 387-399 (1979).
36 Ampleford, et al., Mesothelioma: You Do Not Have to Work for it, Diagnostic Cytopathology
35:774-777 (2007).
37 Pan et al., Residential Proximity to Naturally Occurring Asbestos and Mesothelioma Risk in
California, Am. J. Respir. Crit. Care Med. 172 1010-25 (2005).
38 Kurumatani et al., Mapping the Risk of Mesothelioma Due to Neighborhood Asbestos
Exposure. Am. J. Respir. Crit. Care Med. Vol 178 (2008).
14
Italy,39
England,40
and elsewhere,41
have provided strong evidence that asbestos pollution from
remote sites such as factories can and does cause mesothelioma. One early investigation in the
United States, Lieben and Pistawka (1967), reported several cases from both neighborhood and
household asbestos exposures that resulted in mesothelioma.42
Just two years ago, Stayner
explained the significance of a previous study by Ferrante, et al. (2015), summarizing it as
follows:
An approximately twofold increase in risk was observed for having
lived with a family member who worked in the Eternit asbestos
cement plant (OR=2.4, 95% CI1.3 to 4.4), or having been exposed
from domestic or environmental sources (OR=2.0, 95% CI 1.2 to
3.2).
***
What is new is that this study considers the exposure-response
relationship between pleural mesothelioma and cumulative
exposure to asbestos from domestic, environmental and
occupational. Not surprisingly, the study found strong evidence of
an exposure-response relationship between higher cumulative
exposure to asbestos from all sources and increased risk of pleural
mesothelioma. Of particular concern is their finding of an
approximately fourfold (OR=4.4, 95% CI 1.7 to 11.3) increased
risk of pleural mesothelioma at relatively low levels of asbestos.43
39
Barbieri et al., Asbestos Fibre Burden in the Lungs of Patients with Mesothelioma Who Lived
Near Asbestos-Cement Factories, Ann. Occup. Hyg. 56(6) 660 – 670 (2012).
40 Newhouse, supra note 21. That study showed, among other things, that a number of
individuals developed mesothelioma simply from living near an asbestos-utilizing facility in
London.
41 Camus et al., Nonoccupational Exposure to Chrysotile Asbestos and the Risk of Lung Cancer,
New England Journal of Medicine 338:1586 (1998) (mortality study finding “significant
elevations” in mesothelioma cases with residence in chrysotile mining areas).
42 Lieben, J. and H. Pistawka. Mesothelioma and Asbestos Exposure. Arch. Environ. Health.
Apr. 14 (4):559, 559-563 (1967).
43 Stayner L.T., Para-Occupational Exposures to Asbestos: Lessons Learned From Casale
Monferrato, Italy. Occup Environ. Med. 73(3), 145-146 (2016).
15
In sum, the concept of low-level environmental and domestic exposure to asbestos causing
mesothelioma is neither novel nor controversial in the scientific community.
Regulatory bodies, including OSHA, after conducting comprehensive reviews of the
medical and scientific literature, have cited case reports showing very short exposures as capable
of causing mesothelioma: “Asbestos exposures as short in duration as a few days have caused
mesothelioma in humans.” (Emphasis added.)44
III. ASBESTOS RESEARCHERS EMPLOY A MULTI-FACETED APPROACH
TO ASSIGN CAUSATION OF ASBESTOS-RELATED DISEASE, BUT
NEVER REQUIRE A PRECISE QUANTIFICATION OF A PERSON’S
EXPOSURE LEVEL
As the Court evaluates the opinions rendered by the causation experts in this case and
attempts to determine whether they create a fact issue on causation under Ohio law, we discuss
below the generally accepted standard practices employed by scientists and physicians
investigating the causal relationship between asbestos exposure and mesothelioma. Although the
specifics may vary from case to case, experts employ a multi-faceted methodology that includes
studying the subject’s exposure history and accounting for individual susceptibility.
A. Significant Exposure History
Using exposure histories to identify significantly harmful exposures is at least as ancient
as the field of occupational medicine itself, as evidenced by this advice from the father of
occupational medicine, Bernardino Ramazzini, in 1713:
44
U.S. Dept. of Labor, Occupational Safety & Health Administration, Safety and Health Topics,
Asbestos, https://www.osha.gov/SLTC/asbestos/ (Accessed June 5, 2017), citing: E. Skammeritz,
et al., Asbestos Exposure and Survival in Malignant Mesothelioma: A Description of 122
Consecutive Cases at an Occupational Clinic, 2(4) Int. J. Occup. Environ. Med. 224 (2011).;
Morris Greenberg & T.A. Lloyd Davies, Mesothelioma Register 1967-68, 31 Brit. J. Ind. Med.
91 (1974).; World Health Organization, International Agency for Research on Cancer (IARC),
IARC Monographs on the Evaluation of the Carcinogenic Risks to Humans, Overall Evaluations
of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, Supplement 7 106-116
(1987); and Hodgson, John T. & Darnton, Andrew, The Quantitative Risks of Mesothelioma and
Lung Cancer in Relation to Asbestos Exposure, 44(8) Ann. Occup. Hyg. 565 (2000).
16
When a doctor arrives to attend some patient of the working
class...let him condescend to sit down...if not on a gilded chair...on
a three-legged stool... He should question the patient carefully...So
says Hippocrates in his work ‘Affections.’ I may venture to add
one more question: What occupation does he follow?45
Qualitative history of exposure has also been the driving force behind the discovery and
development of knowledge regarding the dangers of asbestos. The seminal 1960 Wagner study
is a good case in point.46
The study identified thirty-three individual cases of mesothelioma in a
South African asbestos mining town, thirty-two of whom had a known qualitative history of
exposure to asbestos. There were no exposure measurements, nor epidemiological/statistical
analyses. Despite limitations that many industry advocates would now proclaim fatal to
ascribing causation, many scientists believe the Wagner study established that asbestos causes
the very rare disease mesothelioma, and that environmental or household exposures alone were
adequate — all based on after-the-fact, qualitative exposure histories alone.47
Indeed, in the
seminal 1965 paper on causation, The Environment and Disease: Association or Causation?, Sir
Austin Bradford Hill emphasized the importance of exposure history used in conjunction with
existing literature to establish a causal link.48
45
Ramazzini, Bernardino, De Morbis Artificum Diatriba (1713), Trans. by W.C. Wright in A.L.
Birmingham, Classics of Medicine Library (1983), in Medicine in Quotations: Views of Health
and Disease through the Ages, 276 (Edward J. Huth & T.J. Murray, eds., 2nd
ed. 2006).
46 Wagner, supra note 18.
47 The first cohort study on mesothelioma was published in 1963. This landmark study provided
to epidemiologists and other public health professionals proof of a statistical association.
Mancuso, Thomas F., et al., Methodology in Industrial Health Studies: The Cohort Approach,
with Special Reference to an Asbestos Company, 6 Arch. Env. Health 210 (1963).
48 Hill, Sir Austin Bradford, The Environment and Disease: Association or Causation?
Proceedings of the Royal Society of Medicine 295 (1965).
17
A group of internationally respected asbestos disease specialists reached a scientific and
medical consensus, originally in 199749
and reaffirmed in 2014,50
on the requirements for experts
to attribute a given mesothelioma to asbestos exposure. The original 1997 committee consisted
of nineteen participants of various disciplines from eight countries, with more than 1,000 articles
published between them. The resulting “Helsinki Consensus” agreed with the traditional,
generally accepted conclusion in occupational medicine that “a history of significant
occupational, domestic or environmental exposure will suffice for attribution.” The Helsinki
Consensus also stated that the following points need to be considered in determining attribution
of a given mesothelioma to asbestos exposures:
“The great majority of mesotheliomas are due to asbestos
exposure.”
“Mesotheliomas can occur in cases with low asbestos
exposure. However, very low background environmental
exposures carry only an extremely low risk.”
“About 80% of mesothelioma patients have had some
occupational exposure to asbestos, and therefore a careful
occupational and environmental history should be taken.”
“An occupational history of brief or low-level exposure should
be considered sufficient for mesothelioma to be designated as
occupationally related.”
“A minimum of 10 years from the first exposure is required to
attribute the mesothelioma to asbestos exposure, though in
most cases the latency interval is longer (e.g., in the order of
30-40 years).”
These generally accepted principles serve as the basic framework for occupational medicine and
public health professionals when they are making determinations of both whether the total
49
Tossavainen, A., et al., Consensus Report: Asbestos, Asbestosis, and Cancer: The Helsinki
Criteria for Diagnosis and Attribution, 23(4) Scand. J. Work Environ. Health 311 (1997).
50 Wolff, Henrik, et al., Consensus Report: Asbestos, Asbestosis, and cancer, the Helsinki
Criteria for Diagnosis and Attribution 2014: Recommendations, 41(1) Scand. J. Work Environ.
Health 5 (2015).
18
cumulative exposure was capable of causing mesothelioma and whether some subset of the total
exposure was a significant or appreciable exposure.
It is important to note that experts in our fields routinely attribute causation without the
benefit of a numerical quantification of an individual’s asbestos exposure. That is because it is
usually impossible to have reasonably precise quantification of the amount of asbestos actually
inhaled by any given person. Indeed, the only way to measure a person’s actual inhaled dose is
to have contemporaneously measured the asbestos in his or her breathing zone every time the
asbestos exposure occurred – i.e., if the exposed person wore a personal asbestos monitoring
device throughout the duration of his or her exposures. This detailed quantitative information is
almost never available and is not needed for a sound attribution of causation to asbestos. “The
best indicator of past asbestos exposure (the gold standard) remains the detailed past work
history.”51
In any event, from the medical and scientific perspectives, no bright-line quantitative
tests can ever be applied in such causation evaluations. To require quantification where it is
almost always impossible and unnecessary to do so would be a public health travesty. Not only
would it be contrary to scientifically reliable and generally accepted scientific practice, but it also
would create an impossible burden of proof, and no valid claim would be able to meet this
impossible standard. As Goldstein and Henifin explained in an effort to assist judges and
lawyers in understanding scientific evidence:
[O]nly rarely are humans exposed to environmental chemicals in a
manner that permits a quantitative determination of adverse
outcomes…Human exposure occurs most frequently in
occupational settings where workers are exposed to industrial
51
Bégin, R., & Christman, J. W. (2001). Detailed Occupational History. Am J Respir Crit Care
Med, 163(3), 598-599. doi:10.1164/ajrccm.163.3.ed09-01b
19
chemicals such as lead or asbestos; however, even under these
circumstances, it is usually difficult, if not impossible, to quantify
the amount of exposure.”52
Perfect and complete exposure data is virtually never available. But, using professional
judgment based on the available evidence — including a qualitative asbestos exposure
assessment — is the generally accepted standard practice in the medical and scientific
community.
B. Individual Susceptibility
Another important factor to consider in what constitutes a significant exposure is the
concept of individual susceptibility. The great weight of evidence suggests that there are widely
varying levels of susceptibility to asbestos, much as there is with tobacco and lung cancer. For
example, even with very high exposures such as those experienced by insulation workers, less
than 10% of the insulators developed mesothelioma.53
Dodson, et al. (2008) pointed out that:
All asbestos-related diseases are dose-response related, which
means that increased exposure to asbestos increases the risk of
developing an asbestos-related disease. However, even in
individuals who are exposed to high concentrations of asbestos
(e.g., heat and frost insulators), only about 10% develop
mesothelioma. There is no factual information on how much
asbestos it takes to cause an asbestos-related disease such as
mesothelioma in any given individual. One could argue that
individual susceptibility (genetic susceptibility) is as important as
asbestos concentration in determining who develops an asbestos-
induced disease.54
52
Goldstein, Bernard D., & Henifin, Mary Sue, Reference Guide on Toxicology, in Reference
Manual on Scientific Evidence, 639-640 (Federal Judicial Center, 3rd
ed. 2011).
53 Ribak, J., et al., Malignant Mesothelioma in a Cohort of Asbestos Insulation Workers:
Clinical Presentation, Diagnosis, and Causes of Death, 45 Brit. J. Ind. Med. 182 (1988).
54 Dodson, et al., A Technical Comparison of Evaluating Asbestos Concentration by Phase
Contrast Microscopy (PCM), Scanning Electron Microscopy (SEM), and Analytical
Transmission Electron Microscopy (ATEM) as Illustrated From Data Generated from a Case
Report, Inhalation Toxicology 20:723-732 (2008).
20
Low level exposure to chrysotile asbestos via home contamination, without any direct
occupational exposure, has been shown to induce high incidences of mesotheliomas in family
groups that also have a germ-line BAP1 genetic mutation.55
Additionally, a diagnosis of
mesothelioma combined with a Helsinki Consensus sufficient exposure history is certainly proof
of the body’s defenses being overwhelmed and defeated. The capacity of the body’s defense is
certainly influenced heavily, if not defined by, individual susceptibility. This is true for most
human diseases.
C. Biological Plausibility
The concept of biological plausibility examines whether scientists understand the
mechanisms by which a disease develops and whether a theory of causation is consistent with
existing knowledge. The emerging consensus among physicians and scientists is that most forms
of cancer develop in a multistage process. This process typically involves a number of mutations
and these mutations must follow in some particular sequence for the cell(s) in question to
become a fully cancerous cell, which over time develops into a tumor:
It is now recognized that asbestos fibers themselves are
carcinogenic, mainly by indirect mechanisms, and that malignant
transformation is a multi-stage process…Direct effects are related
to the physical interaction of fibers with target cells or by the
generation of free radicals and reactive oxygen species (ROS) at
the surface of fibers. Indirect effects are related to an
inflammatory response to fibers, including the generation of
factors, such as ROS and cytokines as a consequence of attempted
but incomplete phagocytosis of fibers by macrophages (“frustrated
phagocytosis”). There is now substantial scientific evidence for the
indirect model, as discussed in several reviews.56
55
Testa, Joseph R., et al., Germline BAP1 Mutations Predispose to Malignant Mesothelioma,
43(10) Nature Genetics (2011). This does not mean the BAP1 mutation causes mesothelioma;
rather people with this mutation may be more susceptible to the carcinogenic effects of asbestos.
56 Hammar, supra note 10 at pp. 587-588 specifically, and 589-599 generally.
21
Although, as in most areas of medicine, there is much to be learned, scientists have
identified “established mechanistic events” in the development of asbestos-induced
mesothelioma. These include: “impaired fiber clearance leading to macrophage activation,
inflammation, generation of reactive oxygen and nitrogen species, tissue injury, genotoxicity,
aneuploidy and polyploidy, epigenetic alteration, activation of signaling pathways, [and]
resistance to apoptosis.”57
Cumulative exposure — the idea that all exposures contribute to a person’s cumulative
dose thereby increasing the risk of disease — is merely an extension of the ancient concept of
dose-response. As Goldstein wrote, “‘the dose makes the poison’ is the oldest maxim in the
field.”58
However, the existence of a dose-response relationship does not mean that there is
necessarily a “threshold level” below which a substance cannot cause harm, as Professor
Goldstein explained:
Toxicologists generally posit two main dose-response curves:
those that have a “threshold” and those that do not…The second
general type of a dose-response curve is one that is considered to
have no threshold. The most important example for toxic torts is
that of cancer. The underlying cause of many cancers is a
persistent genetic mutation allowing the unbridled growth of a cell
which then results in a clone of cancer cells.59
57
World Health Organization, International Agency for Research on Cancer (IARC), Special
Report: Policy: A review of human carcinogens - Part C: metals, arsenic, dusts, and fibres, 10
The Lancet, 453 (2009).
58 Goldstein, Bernard D., Toxic Torts: The Devil is in the Dose, 16(2) J.L. & Pol’y. 551 (2008).
Bernard D. Goldstein is Professor of Environmental and Occupational Health and former Dean
of the University of Pittsburg Graduate School of Public Health.
59 Id. at 554-555.
22
In other words, when considering the carcinogenic effect of asbestos, which exerts its toxicity by
causing mutations, there is no “threshold” below which there is no observable effect.60
Research to date confirms the findings of case reports and epidemiological studies: total
body burden (i.e., cumulative exposure) has a significant effect on the carcinogenic process and
all forms of commercial asbestos are genotoxic and mutagenic (i.e., a dose-response curve
without a threshold).
D. Case Reports and Sentinel Events/Signature Diseases
Case reports can be a powerful form of evidence that researchers consider when
evaluating causation, along with cell and animal studies, autopsy studies, and epidemiology
studies. They are particularly useful when studying rare diseases that are considered sentinel
events/signature diseases for a given exposure.61
Decades of case reports and case series also
support the attribution position taken in the Helsinki Consensus.
Mesothelioma is a signature malignancy for asbestos exposure,62
sometimes called a
signal or sentinel cancer. This has been generally accepted in the scientific community based on
studies conducted decades ago.63,64,65,66
In fact, more than thirty years ago, mesothelioma was
60
See also Goldstein, Bernard D., & Henifin, Mary Sue, Reference Guide on Toxicology, in
Reference Manual on Scientific Evidence, 669-670 (Federal Judicial Center, 3rd
ed. 2011) (“For
agents that produce effects other than through mutations, it is assumed that there is some level
that is incapable of causing harm… If the level of exposure was below this no observable effect,
or threshold, level, a relationship between the exposure and disease cannot be established… This
analysis, however, is not applied to substances that exert toxicity by causing mutations leading
to cancer.”) (Emphasis added).
61 Checkoway, Harvey, Pearce, Neil & Crawford-Brown, Douglas J., Research Methods in
Occupational Epidemiology, at p. 60 (London: Oxford Univ. Press 2d ed. 2004).
62 Id. at p. 248. (“Certain conditions, known as ‘sentinel’ health events, are so closely associated
with the occupational exposures that the occurrence of any cases serves as an indication of an
occupational hazard [citation omitted]. Malignant mesothelioma (which is nearly always
attributable to asbestos exposure), silicosis, and adult lead poisoning, fit this description.”).
63 Wagner, supra note 16.
23
listed as a sentinel health event of occupational origin in the United States.67
There is no other
proven major cause of malignant mesothelioma for persons living in the United States.
Phillip Enterline, M.D., in a report funded by and generated for the industry group,
Asbestos Information Association, observed as follows regarding the usefulness of case reports
in studying asbestos-related cancer:
Among the things I gained from this research was a deep respect
for the clinicians and pathologists who contributed to the early
literature…I became far less sure that the sharp distinction made
by many writers between epidemiological as contrasted with
clinical-pathological observations served a useful purpose. Even
a single case report is a kind of epidemiological observation, since
the basis of such reports is usually a feeling, unexpressed, that the
case is somehow aberrant for a human population.68
Indeed, case reports have played an important role historically in the study of asbestos-
related disease. Wagner’s seminal 1960 paper discussed above — which many scientists in our
field credit with establishing that asbestos causes mesothelioma, and that environmental and
household exposures alone are sufficient to cause the disease — was based on thirty-three case
reports from a South African mining town.
64
Selikoff, Irving J., Opening Remarks, 132 Ann. N.Y. Acad. Sci. 7 (1965).
65 Becklake, Margaret R., Asbestos-Related Diseases of the Lung and Other Organs: Their
Epidemiology and Implications for Clinical Practice, 114 Am. Rev. Resp. Disease 187 (1976).
66 World Health Organization, International Agency for Research on Cancer (IARC), IARC
Monographs on the Evaluation of the Carcinogenic Risks for Humans, Chemical and Industrial
Processes Associated with Cancer in Humans: IARC Monographs, Volumes 1 to 20, Supp. 1
(1979); World Health Organization, International Agency for Research on Cancer, IARC
Monographs on the Evaluation of Carcinogenic Risks to Humans, A Review of Human
Carcinogens, Part C: Arsenic, Metals, Fibres, and Dusts 1-40, 219-309 (2012).
67 Rutstein, David D., et al., Sentinel Health Events (Occupational): A Basis for Physician
Recognition and Public Health Surveillance, 73(9) Am. J. Public Health 1054 (1983).
68 Enterline, Philip E., Asbestos and Cancer: The First Thirty Years (1978).
24
E. Epidemiological Studies
Asbestos industry advocates often state that epidemiological studies are the “gold
standard” for evaluating causation. We agree that epidemiology is an important component in
the multi-faceted methodology that scientists in our field employ to determine causation,
although we caution against focusing on epidemiology to the exclusion of the other factors
discussed above. In any event, there is overwhelming consensus in the medical and scientific
communities that exposure to all forms of commercial asbestos can induce mesotheliomas based
on peer-reviewed, published epidemiological studies.69
For example, Kanarek (2011), reviewed
studies and cases from all over the world in which chrysotile asbestos was the only or
overwhelming asbestos exposure.70
Based upon his comprehensive review, Kanarek (2011)
concluded that:
By 2011, there are numerous occupational epidemiology and
registry case studies clearly linking all types of asbestos, including
chrysotile, to pleural and peritoneal mesothelioma.
***
The authors of multiple studies have shown that all levels of
exposure can increase the risk of mesothelioma. Because there is
no known threshold, then current regulatory levels for asbestos
may be capable of mesothelioma carcinogenicity. Brief or low
exposures to asbestos are capable of mesothelioma
carcinogenicity.71
69
IARC 2009, supra note 57; IARC 2012, supra note 66; Joint Policy Committee of the
Societies of Epidemiology, Position Statement on Asbestos from the Joint Policy Committee of
the Societies of Epidemiology (JPC-SE) (2012) (“…[t]here have been examples of relatively
“pure” exposures, and again, such epidemiological data are consistent with the proposition that
all forms of asbestos can cause mesothelioma.”).
70 Kanarek, M., Mesothelioma from Chrysotile Asbestos: Update, 21 Ann. Epidemiol. 695
(2011).
71 Id.
25
Mesothelioma is caused by the inhalation of respirable asbestos fibers, not by the exposed
person performing a particular task or being exposed to a specific product type. Just as there is
no scientific “rule” that occupational or secondhand household exposures be quantified in order
for attribution, there is no “rule” that a product-specific or task-specific positive epidemiology
study be available for attribution.
As discussed above, nearly all adequately powered human asbestos epidemiology that has
looked at the question has determined that asbestos-induced mesothelioma follows a dose-
response pattern, generally with the greater the total cumulative dose, the greater the risk of
mesothelioma.72
Researchers have found some additional factors important in analyzing the
asbestos mesothelioma dose-response curve, such as time since first exposure, but total
cumulative dose consistently is the best indicator of risk.73
Studies have shown that working on brakes can release significant levels of airborne
asbestos fibers. A table published by Dr. David Egilman in the International Journal of
Occupational and Environmental Health illustrates this point:
TABLE 2 Studies Showing High Asbestos Exposures During Brake Work
Author Year Exposure Type Exposures Reported
Lee[citation omitted] 1970 Blow out 3-5 f/cc
Boillat & Lob[citation
omitted]
1973 Brake work undefined 0.3-29.2 f/cc
72
Hammar, supra note 10 at p. 587 (“…when there are multiple asbestos exposures, each
contributed to cumulative exposure and hence to the risk and causation of MM [malignant
mesothelioma], within an appropriate latency interval…”).
73 Bignon, Jean, et al., History and Experience of Mesothelioma in Europe, in Mesothelioma 29-
53 (Bruce W.S. Robinson & A. Philippe Chahinan, eds., 2002) (“In this study…the dose-
response seemed to be described best by Cumulative Exposure Index.”).
26
Castleman & Ziem[citation
omitted]
1985 Damp rag
Squirt bottle
Stoddard Solvent
Dry rag
Brake washer
High: 2.6 f/cc; TWA: 0.28 f/cc
High: 0.54 f/cc; TWA: 0.21 f/cc
High: 0.68 f/cc; TWA: <0.1 f/cc
High: 0.81 f/cc; TWA: 0.2 f/cc
High: 1.1 f/cc
Hatch[citation omitted] 1970 Compressed Air Fibers >5 um: 2.1-8.2; 10
minute avg: 0.8
Rodelsperger[citation
omitted]
1986 Passenger car (various
operations)
Truck (various
operations)
Mean: 3.8-4.7 f/cc
Mean: 4.4-9.9 f/cc
Kauppien &
Korhonen[citation omitted]
1987 Truck (various
operations)
Grinding
<0.1-125 f/cc; TWA: 0.1-0.2
f/cc
7 f/cc
Hickish[citation omitted] 1968 Auto blow out Peak exposure: 7.09 f/cc
Hickish [citation omitted] 1968 Auto brake work,
various
TWA: 1.57-2.55 f/cc
Clark[citation omitted] 1976 Auto disc brake
change
0.2-1.9 f/cc
Hatfield & Longo[citation
omitted]
1998 Bendix Chrysler
(filling and cleaning)
8.53-14.57 f/cc
Hatfield & Longo[citation
omitted]
n.d. Bendix Ford (filling
and cleaning)
5.47-12.67 f/cc
Hatfield & Longo[citation
omitted]
2000 Sweeping and
cleaning brake shop
Personal Samples: 7.5-8.8 f/cc
Area Samples: 2.0-2.4 f/cc
Hatfield, Longo &
Newton[citation omitted]
2000 Grinding 4.83-12.51 f/cc
Hatfield, Longo &
Newton[citation omitted]
2000 Hand grinding 12.57-21.43 f/cc
Hatfield, Newton &
Longo[citation omitted]
2001 Hand sanding 0.5-0.96 f/cc
Rohl et al.[citation
omitted]
1977 Blowing dust
Beveling
6.6-29.4 f/cc
23.7-72.0 f/cc
Osborn[citation omitted] 1934 Grinding 17 mppcf
Roberts &
Zumwalde[citation
omitted]
1982 Compressed air 0.14-15.0 f/cc
Lloyd[citation omitted] 1975 Servicing brakes 3.75-37.3 f/cc
Longo, Mount &
Hatfield[citation omitted]
2004 Hand sanding and
grinding and other
operations
19.7-35.7 f/cc 74
74
Egilman, David, Fiber Types, Asbestos Potency, and Environmental Causation, A Peer
Review of Published Work and Legal and Regulatory Scientific Testimony, IJOEH 15:202-28
(Table 2) (2009).
27
The U.S. EPA determined that merely hitting a brake drum with a hammer or wiping a brake
drum with a dry rag or brush can release millions of asbestos fibers.75
Moreover, human evidence, including positive epidemiological studies and numerous
case reports, provides additional support for a weight-of-the-evidence conclusion that asbestos
from brakes can and does cause mesothelioma.76
These and other asbestos exposure and disease
studies in brake workers were reviewed by Dr. Richard Lemen, Assistant Surgeon General of the
United States (Ret.) in 2004, who wrote:
Fiber release studies of actual brake repair and replacement and the
laboratory simulation studies both demonstrate the ability of
encapsulated asbestos containing brake products, to release
respirable asbestos fibers at concentrations capable of causing
asbestos related disease.
***
A review of the published peer reviewed literature reveals at least
165 cases of mesothelioma in end-product users of friction
products. Additional government studies have reported other
cases. These numbers cannot be attributed ambient air exposure or
to chance alone [citations omitted].77
Dr. Lemen concluded that “[e]ven the so called ‘controlled’ use of asbestos-containing brakes
poses a health risk to workers, users, and their families.” (Emphasis added.)78
Likewise, the
National Cancer Institute—which is part of the National Institutes of Health (NIH), and is the
75
U.S. Environmental Protection Agency, Guidance for Preventing Asbestos Disease Among
Auto Mechanics, EPA-560-OPTS-86-002 (June 1986).
76 See, e.g., McDonald, D., et al., Epidemiology of Primary Malignant Mesothelial Tumors in
Canada, 26(4) Cancer 914 (1970); Anderson, A.E., et al., Asbestos Emissions from Brake
Dynamometer Tests, SAE Technical Paper 730549 (1973); Rödelsperger, Klaus, et al., Asbestos
Dust Exposure During Brake Repair, 10 Am. J. Ind. Med. 63 (1986); Huncharek, M., et al.,
Pleural Mesothelioma in a Brake Mechanic, 46 Brit. J. Ind. Med. 69 (1989); Iwatsubo, supra
note 13; Teschke, Kay, et al., Mesothelioma Surveillance to Locate Sources of Exposure to
Asbestos, 88(3) Canadian J. Pub. Health 163 (1997).
77 Lemen, supra note 6.
78 Id.
28
United States government’s principal agency for cancer research and training—has concluded:
“Studies evaluating the cancer risk experienced by automobile mechanics exposed to asbestos
through brake repair are limited, but the overall evidence suggests there is no safe level of
asbestos exposure.”79
Finally, when analyzing epidemiological studies, it is important that those studies be
properly designed to examine the relevant relationship. For example, brake manufacturers and
their consultants frequently cite a collection of purportedly “negative” brake studies and
industry-financed meta-analyses to support their claim that asbestos in brakes does not cause
mesothelioma. In order for a study or studies to be truly “negative” in the sense suggested by the
brake industry and its advocates, the study must (i) be large enough to have sufficient “power” to
detect an increase in risk, (ii) include sufficiently reliable exposure histories to establish exposure
or lack thereof, and (iii) be followed for a sufficiently long time to account for mesothelioma’s
long latency period.80
It is also highly preferable that the study be specifically designed to detect
an increase in risk for the disease in question. The studies relied upon by the brake industry and
its advocates fail on all of the above counts.81
79
National Cancer Institute, Asbestos Exposure and Cancer Risk (2009) (citations omitted)
https://www.cancer.gov/about-cancer/causes-prevention/risk/substances/asbestos/asbestos-fact-
sheet (Accessed June 5, 2017).
80 Median latency since first exposure for mesothelioma is 38.4 years. See Reid, A., et al.,
Mesothelioma Risk after 40 Years since First Exposure to Asbestos: A Pooled Analysis, Thorax 1
(2014).
81 A comprehensive survey of the brake literature is not the intent of this brief. For a thorough
criticism of the articles relied upon by the brake industry, Amici refer the Court to the following:
Lemen, Asbestos in Brakes, supra note 6; Egilman, David S., & Billings, Marion A., Abuse of
Epidemiology: Automobile Manufacturers Manufacture a Defense to Asbestos Liability, 11 Int. J.
Occup. Environ. Health 360 (2005); LaDou, et al. “The Case for a Global Ban on Asbestos,
Environ. Health Perspectives 118:897-901 (2010); and Welch, Laura S., Asbestos Exposure
Causes Mesothelioma, But Not This Asbestos Exposure: An Amicus Brief to the Michigan
Supreme Court, 13 Int. J. Occup. Environ. Health 318 (2007).
29
A recent editorial by the editor of Annals of Occupational Hygiene, asked the proper
rhetorical question in the context of an asbestos-industry expert study of the risks of cancer from
asbestos in brakes:
So when are risk analyses on job titles informative? Analyses on job titles can be
informative in the situation where job titles entail unknown carcinogens or a mix
of known and unknown carcinogens. In these situations, job-title-based analyses
can provide information on the role of new or suspected occupational
carcinogens. However, as exposures vary considerably within job titles depending
on their job activities, they can at best be regarded as crude measures of exposure.
As such, positive results may provide new information; however, null results
cannot be used to exclude that there is no effect of a known carcinogen within that
occupation.82
Vermeulen explained the correct approach to causality when it comes to asbestos exposure:
So how should we view these analyses on job titles with known carcinogenic
exposures? Clearly, such analyses cannot be used to inform on the carcinogenicity
of known carcinogenic exposures. In other words, we would not, based on the
absence of an association between working as a motor vehicle mechanic and
mesothelioma, conclude that there is no association between chrysotile exposure
and mesothelioma.83
Thus, a person exposed to a known carcinogen, such as chrysotile asbestos used in brakes, is at
increased risk of mesothelioma, just as is the insulator or pipe fitter exposed to chrysotile
asbestos from products used in their trades. Ultimately, it is the exposure, not the job title or
trade, that causes mesothelioma.
CONCLUSION
In evaluating the legal issues presented in this case, the Amici urge the Court to bear in
mind the following principles, which we have gleaned from our decades of experience
researching, diagnosing, treating, and writing about asbestos and asbestos-related diseases. The
82
Vermeulen, R, When are Risk Analyses on Job Titles Informative?, Ann. Occup. Hyg., Vol. 60,
No. 8, 913–915 (2016) (emphasis added).
83 Id.
30
idea that a person’s lifetime cumulative exposure to asbestos causes mesothelioma is an
irrefutable scientific fact, and an expert’s agreement with that principle should not adversely
affect a court’s view of his or her causation opinion. Science has been unable to identify a “safe”
level of asbestos exposure below which mesothelioma will not occur and, in fact, very low-level
exposures have been shown to cause mesothelioma. Finally, the generally accepted practice
employed by experts in our field to attribute causation is a multi-faceted approach that centers on
a person’s qualitative exposure history and how that exposure compares with the published
scientific and medical literature in this area. The actual number of asbestos fibers that someone
has inhaled is essentially never available, and is not required from a medical and scientific
perspective to attribute causation.
By: /s/ Joshua P. Grunda
Thomas W. Bevan (0054063)
Patrick M. Walsh (0075966)
Joshua P. Grunda (0084266)
BEVAN & ASSOCIATES LPA, INC.
6555 Dean Memorial Parkway
Boston Heights, Ohio 44236
Phone: (330) 650-0088
Fax: (330) 467-4493
Counsel for Amicus Curiae
51 Concerned Physicians, Scientists,
and Scholars Regarding Causation of
Asbestos-Related Disease
31
PROOF OF SERVICE
I HEREBY CERTIFY that a true and correct copy of the foregoing was served on this
17th
day of July, 2017 on all counsel of record at the addresses listed below:
James L. Ferraro (0076089)
John Martin Murphy (0066221)
Anthony Gallucci (0066665)
Shawn M. Acton (0072675)
KELLEY & FERRARO LLP
Ernst & Young Tower
950 Main Avenue, Suite 1300
Cleveland, OH 44113
Phone: (216) 202-3450
Fax: (216) 575-0799
Counsel for Appellee, Mark
Schwartz, et al.
Douglas R. Simek (0075988)
SUTTER O’CONNELL CO.
1301 East 9th Street
3600 Erieview Tower
Cleveland, OH 44114
(216) 928-4519 phone
(216) 928-4400 facsimile
James N. Kline (0007577)
ULMER & BERNE LLP
1660 West 2nd Street
Cleveland, OH 44114-1406
(216) 583-7000 phone
(216) 583-7161 facsimile
Counsel for Amicus Curiae
Ohio Association of Civil Trial Attorneys
Victor E. Schwartz (0009240)
SHOOK, HARDY & BACON L.L.P.
1155 F Street, NW, Suite 200
Washington, DC 20004
Steven G. Blackmer (0072235)
Melanie M. Irwin (0086098)
WILLMAN & SILVAGGIO LLP
One Corporate Center
5500 Corporate Drive, Suite 150
Pittsburgh, PA 15237
Phone: (412) 366-3333
Fax: (412) 366-3462
Michael W. Weaver (PHV 2612)
MCDERMOTT WILL & EMERY
227 West Monroe Street
Chicago, IL 60606
Email: [email protected]
Counsel for Appellant, Honeywell
International Inc.
Richard D. Schuster (0022813)
Daniel E. Shuey (0085398)
Damien C. Kitte (0084057)
VORYS, SATER, SEYMOUR AND PEASE
LLP
52 East Gay Street, P. O. Box 1008
Columbus, Ohio 43216-1008
Telephone: (614) 464-5475
Facsimile: (614) 464-6350
Counsel for Amici Curiae Ohio
Manufacturers’ Association;
Ohio Council of Retail Merchants; Ohio Tire
& Automotive Association; Ohio Alliance for
Civil Justice; and the Honorable William
Seitz
32
Tel: (202) 783-8400
Fax: (202)783-1211
William L. Anderson (PHV 18357)
CROWELL & MORING LLC
1001 Pennsylvania Avenue, NW
Washington, DC 20004
Tel: (202) 624-2942
Fax: (202)628-5116
Counsel for Amicus Curiae
Coalition for Litigation Justice, Inc.
/s/ Joshua P. Grunda
Joshua P. Grunda (0084266)
Counsel for Amicus Curiae
51 Concerned Physicians, Scientists,
and Scholars Regarding Causation of
Asbestos-Related Disease
1
EXHIBIT A
Eula Bingham, M.S., Ph.D.
Professor Emerita College of Medicine
Adjunct Professor Department of Biology
University of Cincinnati
College of Arts and Sciences
Assistant Secretary of Labor, 1977-1981
Cincinnati, Ohio, USA
Francesco Barone-Adesi
Associate Professor of Public Health
Department of Pharmaceutical Sciences
University of Eastern Piedmont
Largo Donegani n. 2, 28100 Novara, Italy
Telephone: +39 032166068
Prof. Dr. Med. Xaver Baur, MD
University of Hamburg, School of Medicine, former Chair of Occupational Medicine
President of European Society for Environmental and Occupational Medicine (EOM Society)
Hamburg, Germany
Dr. Nachman Brautbar
Emeritus Clinical Professor of Medicine, University of Southern California
Los Angles, California
Massimiliano Bugiani
Consultant of prosecutor's office in Turin, Professional tumor section
Section of Judicial Police Professional Cancers of the Prosecution of the Republic of Turin
Republic of Turin, Italy
Roberto Calisti
Occupational Physician
Local Unit for Occupational Safety and Health
Occupational Epidemiology
ASUR MARCHE - area vasta 3 (Regional Health Service)
Civitanova Marche (Italy)
Barry Castleman
Environmental Consultant
Garrett Park, MD
2
Dr. Dario Consonni, MD, PhD
Epidemiology Unit, Fondazione IRCCS Ca'
Granda Ospedale Maggiore Policlinico
Milan, Italy
Carl Cranor
Distinguished Professor of Philosophy
Faculty Member Environmental Toxicology Graduate Program
Department of Philosophy
University of California
Riverside, CA 92521
Naransukh Damiran, PhD, MSPH
Chair at Department of Environmental Health, School of Public Health, Mongolian National
University of Medical Sciences,
Fellow of Collegium Ramazzini
Mongolia
John Dement, Ph.D., CIH
Professor
Duke University Medical School
Division of Occupational & Environmental Medicine
Department of Community & Family Medicine
Durham, North Carolina, USA
Anders Englund, MD
Former Director of Medical and Social Department of the Swedish Work Environment Agency
Stockholm, Sweden
Arthur L. Frank MD, PhD
Professor
Drexel University School of Public Health
Philadelphia, Pennsylvania, USA
Professor Bìce Fubini
President of the "G.Scansetti" Center for the Study of Asbestos and Other Toxic Particulates,
University of Torino, Italy
Thomas H. Gassert, MD, MSc
Assistant Professor of Medicine, University of Massachusetts Medical SchoolVisiting Scientist,
Occupational & Environmental Medicine, Harvard School of Public Health Massachusetts, USA
Fernanda Giannasi
Civil, Safety, Health and Environmental Engineer.
Labour Inspector (retired), CR Fellow
São Paulo, Brazil
3
David F. Goldsmith, PhD
Georgetown and George Washington Universities
Washington DC 20057
Morris Greenberg, Extramural
London, United Kingdom
Birger G.J. Heinzow
Head of the Department of Environmental Health at the State Agency for Social Services of
Schleswig-Holstein(LAsD)
Kiel, Germany
John Heinzow
Reg.-Med.-Dir. aD
State Agency for social Services Sleswig-Holstein
D 24105 KIEL
Germany
James Huff, Ph.D.
National Institute of Environmental Health Sciences
Research Triangle Park, North Carolina, USA 27709
Peter F. Infante, Dr.P.H., F.A.C.E.
Peter F. Infante Consulting, LLC
200 S. Oak Street
Falls Church, VA 22046
Formerly, 1978-2002, Director, Office of Standards Review,
Occupational Safety and Health Administration,
Washington, District of Columbia, USA
Tushar Joshi
Director, OEM Programme
Centre for Occupational and Environmental Health, New Delhi
Fellow, Collegium Ramazzini, Italy
Karl T. Kelsey, MD, MOH
Professor of Epidemiology and Pathology and Laboratory Medicine
Director of the Center for Environmental Health and Technology
Brown University
Providence, Rhode Island, USA
Richard Kradin, MD
Department of Pathology and Pulmonary Medicine
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts, USA
4
Philip J. Landrigan, MD, MSc, FAAP
Dean for Global Health
Professor of Environmental Medicine, Public Health and Pediatrics
Arnhold Institute for Global Health
Icahn School of Medicine at Mount Sinai
New York, New York, USA
Bruce Lanphear, MD,. MPH
Professor, Simon Fraser University
Vancouver, British Columbia, Canada
Richard A. Lemen, Ph.D., M.S.P.H.
Assistant Surgeon General, United States Public Health Service (Ret.)
Eugene J. Mark, MD,
Professor of Pathology, Harvard Medical School, Boston, MA
Pathologist, Massachusetts General Hospital, Boston, MA
James Melius MD, DrPH
NYS Laborers Health and Safety Fund
Albany, New York, USA
Atul C. Mehta, M.D., F.A.C.P., F.C.C.P.
Professor of Medicine, Lerner College of Medicine
Buoncore Family Endowed Chair in Lung Transplantation
Staff, Department of Pulmonary Medicine, Respiratory Institute
Senior Editor, Journal of Bronchology and Interventional Pulmonology
Cleveland Clinic, Cleveland, Ohio, 44195, USA
Sigurd Mikkelsen, DrMedSci
Senior consultant, emeritus
Specialist in Occupational and Environmental Medicine
Onsgårdsvej 19
DK-2900 Hellerup
Denmark
Dario Mirabelli, MD
Cancer Epidemiology
Città della Salute e della Scienza Hospital, Turin (Italy)
Celeste Monforton, DrPH, MPH
Professorial Lecturer
Milken Institute School of Public Health
George Washington University
5
Annie Thebaud Mony
Emerite director of research, National Institute for Health and Medical Research (INSERM)
Interdisciplinary Research Group on Occupational Cancer (GISCOP 93)
Paris-13 University
Bobigny (France)
David Ozonoff, MD, MPH
Professor of Environmental Health
Boston University School of Public Health
Boston, MA, USA
Dr. Smita Pakhalé, MD, FRCPC, MSc (Epi & Biostat)
Associate Scientist - Ottawa Hospital Research Institute
Assistant Professor - University of Ottawa
Staff Respirologist - Division of Respiratory Medicine
The Ottawa Hospital
Ottawa, ON, Canada
Rolf Petersen
Chief Physician, PhD
Department of Occupational Medicine
Slagelse Hospital
Slgelse, Denmark
Laxminarayana C. Rao, M.D., F.C.C.P, F.A.C.P
Pulmonologist and NIOSH Certified B-Reader
Hinckley, Ohio, USA
Kenneth Rosenman MD, FACE, FACOEM, FACPM
Professor of Medicine, Chief, Division of Occupational and Environmental Medicine
Michigan State University
East Lansing, MI, USA
Kathleen Ruff
Honorary Fellow, Collegium Ramazzini
Smithers, BC, Canada
Sheldon W. Samuels
Director Emeritus, Industrial Unions, AFL-CIO
Alvin J. Schonfeld, D.O., F.A.C.O.I., F.C.C.P.
Board Certified- American Board of Internal Medicine
Board Certified- American Board of Internal Medicine- Pulmonary Medicine
Fellow- American College of Osteopathic Internists
Fellow- American College of Chest Physicians
6
NIOSH Certified B-Reader
Chicago, Illinois, USA
Michael Silverstein, MD MPH
Clinical Professor, University of Washington
Department of Environmental and Occupational Health Sciences
Seattle, Washington, USA
Craig Slatin, Sc.D., MPH
Professor Emeritus, University of Massachusetts Lowell, Department of Public Health
Lowell, MA, USA
Colin L. Soskolne, PhD (Epidemiology)
Professor emeritus, University of Alberta, Edmonton, Canada; Adjunct Professor, Health
Research Institute, University of Canberra, Australia
Daniel Thau Teitelbaum, MD
Adjunct Professor,
Occupational and Environmental Health.
Colorado School of Public Health
Aurora, Colorado, USA
Benedetto Terracini
Former Processor of Biostatistics
University of Torini, Italy (Currently retired)
Yv Bonnier Viger
Médecin spécialiste en santé publique et médecine préventive,
Directeur régional de santé publique de la Gaspésie et des Îles
Professeur, Département de médecine sociale et préventive
Faculté de médecine, Université Laval
Quebec, QC, Canada
Professor Andrew Watterson PhD CFIOSH
Head of the Occupational and Environmental Health Research Group
Centre for Public Health and Population Health Research
Faculty of Health Sciences and Sport
Pathfoot Building R E010
University of Stirling
Stirling, Scotland FK9 4LA
Laura Welch, MD
Adjunct Professor of Environmental and Occupational Health
George Washington University School of Public Health and Health Services
Washington, DC, USA
