Motion-Secondary: ROBERT ROSS et al VS. C.C. MOORE & CO. ENGINEERS

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                                Hake Law
‘A PROPESSIONAL CORPORATION

ELECTRONICALLY
wiliam M, Hake, Esq. (State Bar No. 110956) F I E D
Melissa. Ippolito, Esq. (State. Bar No. 239811} . a
Kathryn L. Hoff, Esq, (State Bar No. 260420) Se ean cable
HAKE LAW, .A PROFESSIONAL CORPORATION
655 Montgomery Street, Suite 1000 FEB 22 2013
San Francisco, CA 9411} Clerk.of tHe Court
Tek: 415-926-5800 BY: WESLEY 3. RAMIREZ
Fax: 415-926-5801 } Deputy Clerk

bili@hakelaw.com
melissa@hakelaw.com.
lucy@hakelaw.com

Attorneys for Defendants

COLLINS ELECTRICAL COMPANY, INC; EMIL J. WEBER ELECTRIC CO,;

BELL PRODUCTS, INC; ADVANCE MECHANICAL CONTRACTORS;

BRAGG INVESTMENT COMPANY, INC; ANDERSON, ROWE, BUCKLEY, INC.
IN THE SUPERIOR COURT OF THE STATE OF CALIFORNIA

COUNTY. OF SAN FRANCISCO.

ROBERT ROSS. AND JEAN ROSS, 1. Case No" CGC-10-275731

Plaintiffs, DECLARATION OF ROBERT W. =
MORGAN, M.D-IN SUPPORT OF
WS. : MOTION FOR SUMMARY JUDGMENT

CC, MOORE. & CO.; ENGINEERS, et-al:; Complaint: December 17, 2010
‘Trial Date: June:10, 2013
Defendants:

I, Robert W. Morgan, M.D., declare as follows:

1. Lhave personal knowledge of each fact set forth in this Declaration and, if called upon. to
testify, could and. would competently testify thereto.

2. Lat a physician, board certified in. Occupational and Environmental Medicine anda
Fellow of the American College of Epidemielogy. | am thus qualified in both
occupational medicine and epidemiology. Attached as Exhibit A is a teue and correct
copy of my Curriculum. Vitae,

3. To study risk of disease from a potential hazard, epidemiologists use two major types of
scientific study: the cohort and the case-control, In a cohort study, we follow over years
a group of people with a common exposure (e.g., asbestds), ascertain their causes of

death, and compare the death rates in the exposed group to another (presumably

alyHake LAW

A PROBESSIONAL CORPORATION

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unexposed) group. The group of exposed persons is called the cohort. A case-control
study works backward in time by first identifying persons with the disease of interest
(e.g. bowel cancer) and ascertaining thei previous exposures, Another group of people
(conirols).without the disease is selected and goes through the same ascertainment
process, usually by questionnaires. Both types of study are useful. However, in studying
diseases for potential association with asbestos, the cohort study is much stronger
because exposure ascertainment is more certain since if begins with identifying exposed
individuals (typically from’a trade or job) and then following to ascertain all causes of
death. "The case-control study however relies on. patients or next-of-kin to identify the
exposures of several decades earlier. Studies have shown that many people cannot
correctly identify their asbestos exposure-(or non-exposure) more than twenty years
earlier. As in many areas of. aoience, there is conflicting evidence. For this reason,
scientists and government agencies urn io metd-atatysis, which is amethod of
combining ail available studies into a single estimate of risk. Meta-analysis is widely

accepted and-used.as the basis for evidence-based medicine.

.: Lhave reviewed the voluminous medical records and ‘expert roports of Mr. Ross,

inchiding records from Carondelet St. Joseph's Hospital: Tucson Surgery Center;
Gastroenterology Associates, PC. Amold Hollander, M.D. PC; Wilmot Center for
Diagnostic Imaging and Treatment, Tucson, Arizona; and R.M. Luros, M.D, M.P:HL;
dealing with bis chest conditions and his colorectal cancer. [ will not opine on his chest

conditions. -T am not disputing his diagnosis of adenocarcinoma of the colon:

. Most epidemiologic evidence (especially meta-analyses of dozens of cohort studies)

indicates no relationship of calon carcinoma to asbestos. (Morgan & Foliart!, Goodman
& Morgan’, [OM 20067.) To examine the risk of bowel cancer after asbestos exposure, 1

have relied on three meta-analyses of the issue. | published the first meta-analysis of

+ Morgan, RW, et al; Asbestos and Gastrointestinal Cancer ~ A Review of the Literature. West. Med 1985 July:
143:60-65.

* Goodman, M, ef ali Cancer in Asbestos-Exposed Occupational. Cohorts: A Meta-Analysis. Cancer Causes.and
Conirol 10:453-465, 1999.

* Institute of Medicine of the National Academies. Asbestos ~ Selected Cancers.: National Academy of Selences,
2006;Hake LAW
A PROFESSIONAL CORPORATION

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ashestos and gastrointestinal cancer in 1983. Asbestos and Gastrointestinal Cancer — A
Review of the Literature reviewed 45 published studies on mortality data of asbestos-
exposed workers, concluding as to. colorectal cancer, there is no discernible relationship
to asbestos exposure. In 1999, Dr. Goodman and 1 published a much larger meta-
analysis. Cancer in Asbestos-Exposed Occupation Cohorts; A Meta-Analysis reviewed .
data trom 69 asbestos-exposed occupational cohorts reporting om cancer morbidity and
mortality, concluding as to gastrointestinal cancers (including eolon.cancer); there is no
evidence of a significant association to asbestos. and no dose-response effect. I 2006,
the. Institute of Medicine of the National Academies.was charged with conducting a
comprehensive study of the then existing medical studies regarding asbestos exposure as
a possible cause of various eanicers including colon cancer. In evaluating whether or
not there is a causal link between asbestos-exposure and colon cancer, the Institute:
reviewed 32 cohort studies, 11 case-control studies.and 11 animal studies, As part of this
comprehensive ‘analysis, the Institute considéred all availablé evidence.. The Institute
concluded that the scientific evidence is suggestive but not sufficient to infer a causal
relationship between asbestos exposure and colon cancer, The category of “suggestive
but not sufficient” is defined by. the Institute as one that potentially comprises a range of |
evidence and uncertainty that does not rise to the level of certainty needed for the
designation of causality. From the three studies referenced above, and.a reading of most
of the dozens of published papers on the topic, Lagree with the Institute of Medicine that
there has been established no causal telationship between asbestos and colorectal cancer.
Attached as Exhibits B-D, respectively, are true and correet-¢opies of Morgan & Foliart,
Goodman & Morgan, and 1OM 2006.

DECLARATION OF ROBERTHake Law
A PROFESSIONAL CORPORATION

SO wD WOR Rw

6, Toa reasonable degree of medical and scientific certainty, the evidence does not support
arelationship or causal connection between asbestos exposure and colon cancer, °
therefore asbestos exposure neither caused nor contributed to. Mr. Ross’s
adenocarcinoma.

I declare under penalty of perjury under the laws of the State.of California that the

foregoing is true and-cortect:’ Executéd on February ™ 2013 at Aiken, South Carolina,

Robert W. Morgan, oe =

SUPPORT OF MOTION FOR

“BECLARATION OF ROBERT W. MORGAN, MD.Exhibit A
to the Declaration of
Robert W. Morgan, M.D.Robert W. Morgan, M.D., S.M. HYG, FACPM, FACE
CURRICULUM VITAE

Current Address: EPIDOC, LLC
241 Magnolia Lake Rd
Aiken, SC 29803
(803) 643-3938 (ph)
(803) 643-2721 (fax)
bobepidec@amail.com

Professional Profile

Robert W. Morgan, MD is a Fellow of the American College of Epidemiology and board-certified in
occupational and environmental health. He holds a medical degree from University of British
Columbia and a master of science in epidemiology from Harvard School of Public Health. His
professional career has included research on the health effects from non-ionizing radiation, paint
and solvents, and asbestos. He has also studied cancer and reproductive outcomes in both
communities and worker populations in the petroleum, chemical, paint, fibrous glass, and electronic
industries, with over seventy peer-reviewed publications. He has served as a consultant to city,
provincial, state, and national governments, trade unions, and most Fortune 100 companies and
has testified as an expert in several jurisdictions for both plaintiffs and defendants.

Or. Morgan has been a principal in two previous scientific consulting firms. He was founder and
President of Environmental Health Strategies. Earlier, he was President and CEO of
Environmental Health Associates. He also served as Director of the Center for Community Health
Studies at SRI (formerly Stanford Research Institute). During his academic career, Dr. Morgan
taught epidemiology and preventive medicine at the University of Toronto, where he was Professor
and Chairman of the Department of Preventive Medicine.

Current Position
At Epidoc LLC, Dr. Morgan is currently an independent consultant in both Occupational and

Environmental Health and Epidemiology, specializing in litigation support and expert witness
testimony.

Citizenship: CanadianRobert W. Morgan, M.D., S.M. HYG, FACPM, FACE

Curriculum Vitae (continued)

Page 2 of 10

Professional Background

1999 - Present Independent Consultant, occupational and environmental health

1989 - 1999 Founder and President
Environmental Health Strategies, inc., San Mateo, CA (sold to
Exponent Corporation)

1988 - 1989 President

Senior Physician Epidemiologist, ENSR Health Sciences

1985 - 1988 Chairman & CEO
Environmental Health Associates, Inc. (sold to ENSR Corporation)

1980 - 1985 Principal and Senior Physician Epidemiologist
Environmental Health Associates, inc., Oakland CA

1979 - 1980 Director
Center for Community Health Studies
SRI (formerly Stanford Research institute)
Pato Alto, California

1971 - 1980 Professor
Department of Preventive Medicine and Biostatistics
University of Toronto

1972 - 1980 Professor

Department of Medicine, University of Toronto

4972 - 1975 Professor
Department of Epidemiology, University of Toronto

1971 - 1980 Staff Physician
Department of Medicine, Toronto General Hospital

1971 - 1975 Professor and Chairman
Department of Preventive Medicine, University of Toronto.

1970 - 1971 Assistant Professor and Director
Division of Epidemiology and Biometry
Department of Health Care and Epidemiology
University of British Columbia

1969 - 1970 Research Associate, Department of Health Care and Epidemiology
University of British ColumbiaRobert W, Morgan, M.D., S.M. HYG, FACPM, FACE.

Curriculum Vitae (continued)

Page 3 of 10

1968 - 1869

1967 - 1968

1962 - 1967
Board Certification
1983

1984

Medical Licensure
Education

1961

1962

1970

1985 ~ 1989

Awards and Honors

Instructor
Department of Health Care and Epidemiology
University of British Columbia

Research Fellow

Department of Health Care and Epidemiology
University of British Columbia

Vancouver, British Columbia

General Practice
Victoria, British Columbia

Fellow, American College of Epidemiology
Certified (FACPM) in Occupational and Environmental
Medicine by the American Board of Preventive Medicine

California (retired)

M.D.
University of British Columbia

Internship
St. Joseph's Hospital

S.M. Hyg. (Epidemiology)
School of Public Health
Harvard University

Courses in Business Administration at Stanford
University and University of California, Los Angeles

Doctor Lavell H. Leeson Memorial Scholarship
Hamish Heney Mcintosh Memorial Prize

MRC of Canada Fellowship (for study at Harvard)
Samuel McLaughlin Foundation Fellowship

Eli Lilly International FellowshipRobert W. Morgan, M.D., S.M. HYG, FACPM, FACE
Curriculum Vitae (continued)
Page 4 of 10

Other Professional Activities

Reviewer, numerous scientific journals

Former Member, Epidemiology Study Section, NIH

Grant reviewer, numerous agencies

Consultant to various governments, trade associations, corporations, and unions
Member, Board of Directors - York/Toronto Lung Association (1975-1978)
Member, Board of Directors - Metropolitan Toronto Zoo (1977-1979)

Member, Board of Directors - Paperback Software intemational (1989-1991)
Former Member, Environmental Health Council, Harvard School of Public Health
Former Member, Editorial Advisory Board ~ Medical Epidemiology Newsletter
Former Member, Scientific Committee on Epidemiology, International Commission on
Occupational Health

PUBLICATIONS

Books and Chapters

1.

Morgan RW. Medical Records in Community Health Centers, The Community Health Center in
Canada, Vol. 1 July 1972, Community Health Center Project, Department of Health and
Welfare, Information Canada, Ottawa, 1972.

Morgan RW. Medical Education in British Columbia, Working Paper 38, National Security for
British Columbians. Report to Minister of Health, Province of British Columbia, December
1973.

Morgan RW. Biochemical Changes in Carcinoma, Chapter in the Biochemistry of Women, by
Dr. Alan Curry. CRC press, Cleveland Ohio, 1974.

Morgan RW. Prevention in Clinical Practice, Editor and Chapter: Epidemiology, Department of
Preventive Medicine, Toronto, 1974.

Morgan RW and Vakil DV. Opportunities for Prevention, in Risk Factors in Breast Cancer, Vol.
ll, Patients at Risk (Basil A. Stoll, Ed.) Heinemann Medical, London, U.K.,1976; 226-238

Morgan RW. Prospects for Preventive Medicine. A Catalogue. Ontario Economic Council,
1977.

Morgan RW, Choi BCK, and Corey PN. Mutagens, Carcinogens and Probability, InVitro
Toxicity Testing of Environmental Agents. Proceedings: NATO Advanced Research Institute,
Plenum Press, 1983, Part B: 319-327.

Morgan RW and Larson SR. Newer Occupational Lung Carcinogens, Chapter in Occupational
Lung Disease, (JBL Gee et al, eds.}, Raven Press, New York, 1984.Robert W. Morgan, M.D.. S.M. HYG, FACPM, FACE
Curriculum Vitae (continued)
Page § of 10

Journal Articles

1.

10.

11.

12.

13.

14.

15.

Morgan RW. Thanatology - Meaning? Archives of the Foundation of Thanatology 1968;
20.

Morgan RW and Mansfield PJ. Geographic Distribution and Availability of Physicians in
Vancouver, Cam Fam Physician 1989; 123-127.

MacMahon B, Cole P, Brown JB, Aoki K, Lin TM, Morgan RW, Woo NC. Estrogen Profiles
of Asian and North American Women. Lancet 1971; Vol fl, No.7730:900-902.

Morgan RW. Open Angle Glaucoma: An Epidemiologist's View. Can J Ophthalmol1972;
7(1): 75-79.

Morgan RW. Prevention, Anyone? (Editorial) Can J Public Health 1972; 62(5): 361- 363.

Drance SM, Morgan RW, and Sweeny VP. Shock Induced Optic Neuropathy: A Cause of
Non-Progressive Glaucoma. New Engl J Med 1973; 288:392-395.

Morgan RW and Munro M. Refractive Problems in Northern Natives. Can J Ophthalmol
1973; 8:226-228.

Vakil DV and Morgan RW. Etiology of Breast Cancer, |. Genetic Aspects. Can Med Assoc
J 1973; 109:29-32.

. Vakil DV and Morgan RW. Etiology of Breast Cancer, |!. Epidemiologic Aspects. Can Med

Assoc J 1973; 109:201-206.

Drance SM, Sweeney VP, Morgan RW, and Feldman F. Studies of Factors involved in the
Production of Low Tension Glaucoma. Am Arch Ophthalmol 1973, 89:457-465.

Morgan RW and Vakil DV. Endocrine Profiles and Breast Cancer (Letter). Lancet 1973;
1:546,

Rock WJ, Drance SM and Morgan RW. Visual Field Screening in Glaucoma. Arch
Ophthalmol 1973; 89.

Drance SM, Morgan RW, Bryett S, and Fairclough M. Anterior Chamber Depth and
Gonioscopic Findings Among Eskimos and Indians in the Canadian Arctic, Can J
Ophthalmol 1973;8(2): 255-259,

Morgan RW, Vakil DV, and Chipman ML. Breast Feeding, Family History and Breast
Disease, Am J Epidemiol 1974:99(2):117-122.

Morgan RW and Jain MM. Bladder Cancer: Smoking, Beverages and Artificial Sweeteners.
Can Med Assoc J 1974; 111:1067-1070.Robert W. Morgan, M.D., S.M. HYG, FACPM, FACE.
Curriculum Vitae (continued)
Page 6 of 10

16. Morgan RW and Vakil DV. Etiology of Breast Cancer, Ill. Opportunities for Prevention. Can
Med Assoc J 1974; 114:1105-1107,

17. MacMahon B, Cole P, Brown JB, Aoki K, Lin TM, Morgan RW, and Woo NC. Urine
Estrogen Profiles of Asian and Northern American Women. Int J Cancer 1974; 14:161-167.

18. Morgan RW and Drance SM. Chronic Open-Angle Glaucoma and Ocular Hypertension: An
Epidemiologic Study. Br J Ophthalmol 1975; 59(4): 211-215.

19. Shettigara PT and Morgan RW. Asbestos, Smoking and Laryngeal Carcinoma. Arch
Environ Health 1975; 30:517-519.

20. Morgan RW, Speakman J, and Grimshaw S. Inuit Myopia. An Environmentally induced
Epidemic? Can Med Assoc J 1975; 112:575-577.

21. Morgan RW and Shettigara PT. Occupational Asbestos Exposure, Smoking and Laryngeal
Carcinoma. Ann NY Acad Sci 1976; 271:308-319.

22. Coronary Artery Surgery, (Task Force, Federal-Provincial). Can Med Assoc J 1977;
417:451-459.

23. Jain M, Morgan RW, and Elinson L. Hair Dyes and Bladder Cancer, (Letter). Can Med
Assoc J. 1977; 117:1131-1133.

24. Morgan RW, Grimshaw-Levesque S, Elinson L, Vakii DV, and Brown JB. Estrogen
Fractions and Breast Cancer Risk in Canadian Inuit and Whites. Clin Invest Med 1978;
4(4): 33-35.

25. Morgan RW, Vakil DV, Brown JB, and Elinson L. Estrogen Profiles in Young Women:
Effect of Maternal History of Breast Cancer. J Nat! Cancer Inst 1978; 60(5): 965-967.

26. Morgan RW, et al. A Comparison of Dietary Methods in Studies. Am J Epidemiol 1978;
107:488-498,

27. Choi NW, Howe GR, Miller AB, Matthews V, Morgan RW, Munan L, Burch 0, Feather J,
Jain M and Kelly A. An Epidemiologic Study of Breast Cancer. Am J Epidemiol 1978;
407(6): 510-521.

28. Miller AB, Kelly A, Choi NW, Matthew V, Morgan RW, Munan L, Burch JD, Feather J,
Howe GR, and Jain M. A Study of Diet and Breast Cancer. Am J Epidemiol 1978; 107(6):
499-509.Robert W. Morgan, M.D., 5.M. HYG, FACPM, FACE
Curriculum Vitae (continued)
Page 7 of 10

29. Vakil DV and Morgan RW. Pre-and Postmenopausal Breast Cancer: Differences in Risk
Factors, Proceedings of the Third International Symposium cn Detection and Prevention of
Cancer, Vol. ll, Prevention and Detection of Cancer (H.E.Nieburgs, ed.). Marcel Decker,
inc., New York 1978; 839-1550.

30. Reid EL and Morgan RW. Exercise Prescription: A Clinical Trial. Am J Public Health 1979;
8016); 691-595.

31, Morgan RW. Skin Cancer after PUVA Treatment for Psoriasis (Letter). New Eng J Med
1979; 301(10): 564.

32. Schottenfeld D, Morgan RW, and Zauber AG. Questions raised by a Study on Cancer
Mortality in Oil Refinery Workers (Letter). J Occup Med 1980; 22(2): 89-70.

33. Vakil DV, Morgan RW, Elinson L, and Cory PN, Pre-menopausal and Post-menopausal
Breast Cancer: Epidemiologic Similarities. Clin Invest Med 1980; 2(4): 161-164.

34. Morgan RW, Kaplan SD, and Bratsberg J. Mortality Study of Fibrous Glass Production
Workers. Arch Environ Health 1981; 36(4): 179-183.

35. Morgan RW, Kaplan SD, and Gaffey WR. A General Mortality Study of Production Workers
in the Paint and Costings Manufacturing Industry. J Occup Med1981; 23(1) 13-21.

36. Morgan RW, Claxton KW, Divine BJ, Kaplan SD, and Harris VB. Mortality Among Ethylene
Oxide Workers. J Occup Med 1981; 23(11): 767-770.

37. Vakit OV, Morgan RW, and Elinson L. Benign Breast Disease: Estriol Proportions and
Family History of Breast Cancer. Cancer Detection and Prevention 1981; 4:517-523.

38. Vakil DV, Elinson L, and Morgan RW. Cystic Disease, Family History of Breast Cancer,
and Use of Oral Contraceptives. Cancer Detection and Prevention 1981; 4:511-515,

39. Kaplan S and Morgan RW. Airborne Carcinogens and Human Cancer. Rev Environ Health
(tsrael) 1981; 3(4): 329-368.

40. Clarke EA, Morgan RW, and Newman AM. Smoking as a Risk Factor in Cancer of Cervix:
Additional Evidence From a Case-Control Study. Am J Epidemiol 1982; 115(1}: 59-66.

41, MacMahon B, Trichopolous D, Brown J, Andersen AP, Aoki K, Cole P, deWaard F,
Kauraniemi T, Morgan RW, Purde M, Ravinhar B, Stormby N, Westlund K and Woo NC.
Age at Menarche, Probability of Ovulation and Breast Cancer Risk. Int J Cancer 1982;
29:13-16.Robert W. Morgan, M.D., S.M. HYG, FACPM, FACE
Curriculurn Vitae (continued)
Page 8 of 10

42. Morgan RW, Kaplan SD, and Bratsberg JA. Mortality Among Fibrous Glass Production
Workers, in: Biological Effects of Man-Made Mineral Fibres. Report of The WHO/IARC
Meeting, Copenhagen, Denmark, 1982.

43. Morgan RW. Artificial Sweeteners and Bladder Cancer, in European Toxicology Forum,
transcript of the Third European Toxicology Forum, Geneva, Switzerland, 1983.

44. Vakil DV, Morgan RW, and Halliday M. Exogenous Estrogens and Development of Breast
and Endometrial Cancer. Cancer Detect Prev 1983; 6(4-5) 15-424.

45. Morgan RW and Wong O. Evaluating Diagnostic Devices: An Epidemiologic Perspective.
Medical Device & Diagnostic Industry, April 1983; 28-31.

46. Morgan RW, Kheifets L, Obrinsky DL, Whorton MD, and Foliart DE, Fetal Loss and Work
in a Waste Water Treatment Plant. Am J Public Health 1984; 74(5): 499-501.

47. Morgan RW and Larson SR. Potential Effects on Humans of Long-Term Exposure:
Possibie Reproductive and Carcinogenic Effects. AAMI Technology Assessment Report
No. 8-84:31-34

48. Wong 0, Morgan RW, and Whorton MD. An Epidemiologic Surveillance Program for
Evaluating Occupational Reproductive Hazards. Am d Ind Med 1985; 7:295-306.

49. Morgan RW, Claxton KW, Kaplan SD, Parsons JM, and Wong 0. Mortality of Paint and
Coatings Industry Workers: A Follow-up Study. J Occup Med 1985; 27(5): 377-378.

50. Wong O, Morgan RW, Kheifets L, and Larson SR. Comparison of SMR, PMR and PCMR
in a Cohort of Union Members Potentially Exposed to Diesel Exhaust Emissions. Br J ind
Med 1985; 42(7): 449-460.

51. Wong O, Morgan RW, Kheifets L, Larson SR, and Whorton MD. Mortality Among Members
of a Heavy Construction Equipment Operators Union with Potential Exposure to Diesel
Exhaust Emissions. Br J Ind Med 1985; 42(7): 435-448.

52. Cranmer JM, Morgan RW, et al. International Workshop on Neurobehavioral Effects of
Solvents: Consensus Workshop Summary. "Neurotoxicology" 1985; 6(4): 101-102.

53. Morgan RW, Foliart DR, and Wong O. Asbestos and Gastrointestinal Cancer; a Review of
the Literature. West J Med 1985; 143:60-65.

54. Morgan RW and Wong O. A Review of Epidemioiogical Studies on Artificial Sweeteners
and Bladder Cancer. Food and Chemical Toxicology 1985; 23(4/5); 529-533.

55. Wong O, Morgan RW, Bailey W, Swencicki RE, Claxton K and Kheifets L. An
Epidemiologic Study of Petroleum Refinery Employees. Br J ind Med 1986; 43:6-17.Robert W. Morgan, M.D., S.M. HYG, FACPM, FACE
Curricutum Vitae (continued)
Page 9 of 10

56. Whorton MD, Larson SR, Gordon NJ and Morgan RW. Investigation and Work-Up of Tight
Building Syndrome. J Occup Med 1987; 29(2): 142-147.

57. Whorton MD, Morgan RW, Wong ©, Larson SR, and Gordon NJ. Problems Associated
with Collecting Drinking Water Quality Data for Community Studies: A Case Example,
Fresno County, California. Am J Public Health 1988; 78(1): 47-51.Fresno County,
California. Am J Public Health 1988; 78(1): 47-51.

§8. Wong O, Whorton MD, Gordon NU, and Morgan RW. An Epidemiologic investigation of the
Relationship between DBCP Contamination in Drinking Water and Birth Rates in Fresno
County, California. Am J Public Health 1988; 78(1): 43-46,

59. Whorton MD, Wong 0, Morgan RW, Gordon NJ. An Epidemiologic Investigation of Birth
Outcomes in Relation to Dibromochioropropane Contaminations in Drinking Water in
Fresno County, California. Int Arch Occup Environ Health 1989; 61,403-407.

60. Wong 0, Morgan RW, Whorton MD, Gordon N, Kheifets L. Ecological Analysis and Case-
Control Studies of Gastric Cancer and Leukemia in Relation to DBCP in Drinking Water in
Fresno County, California. BR J Ind Med 1989; 46(8): 521-528.

61. Morgan RW. Meta-Analysis of Asbestos and Gastrointestinal Cancer (Letter). Am J ind
Med 1991; 19:407-408.

62. Morgan RW. Whodunit? Liability For Mesothelioma Cases, J Occup Med 1991; 3(9). 956-
957.

63. Morgan RW. Dioxin and Mortality from Cancer (Letter). New Engl J Med 1991; 324:1809-
4810.

64. Morgan RW. Attitudes about Asbestos and Lung Cancer (Commentary).Am J Ind Med
1992; 22:437-441.

65. Morgan RW, Elcock M. Update on Artificial Sweeteners and Bladder Cancer. Regul Toxicol
Pharmacol 1993; 17:35-43.

66. Morgan RW. Tracking and Surveillance of Patients with Medical Devices and Implants.
Med Device Tech 1993; 4:38-43.

67. Morgan RW. Medical Device Trials of the Future. Applied Clin Trials 1994; 3(7):3741.

68. Morgan RW and Zhao K. Study of Occupational Lung Cancer in Asbestos Factories in
China (Letier}. Occup Environ Med 1994; 51:719-720.

69. Morgan RW and Eicock M. Artificial Implants and Soft Tissue Sarcomas. J Clin Epidemiol
1995; 48(4): 545-549.Robert W. Morgan, M.D. S.M. HYG, FACPM, FACE
Curriculum Vitae (continued)
Page 10 of 10

70. Rothman KJ, Chou CK, Morgan RW, Balzano Q, Guy AW, Funch DP, Preston-Martin S,
Mandel J, Steffens R, Carlo G. Assessment of Cellular Telephone and Other Radio
Frequency Exposure for Epidemiologic Research. Epidemiology 1996; 7:291-298.

71. Morgan, RW. Risk of Endometrial Cancer After Tamoxifen Treatment. Oncology 1997; 11
{2, supp.1): 25-33.

72. Morgan RW, Keish MA, Zhao K, Heringer S. Mortality of Aerospace Workers Exposed to
Trichloroethylene. Epidemiology, July 1998; 9:424-431.

73. Morgan, RW, Goodman, M. Re: Nonoccupational Exposure to Chrysotile Asbestos and
the Risk of Lung Cancer, (letter) NEJM, Oct. 1998, 339:14, p.1001.

74. Goodman M, Morgan RW, Ray R, Malloy CD, Zhao K. Cancer in Asbestos-Exposed
Occupational Cohorts: A Meta-Analysis. Cancer Causes and Control; 1999 10: 453-465.

75. Morgan RW, Kelsh MA, Zhao K, Exuzides A, Heriner S, Negrete W. Radiofrequency
Exposure and Mortality from Cancer of the Brain and Lymphatic/Hematopoietic Systems.
Epidemiology March 2000, Vol. 11: No. 2.Exhibit B
to the Declaration of
Robert W. Morgan, M.D.The Western
Journal of Medi

Clinical Medicine
errr cence ener eneemnaemenenietnepereneeNETEREREERSNESLe RONEEORERINNEEDANEE

Asbestos and Gastrointestinal Cancer

A Review of the Literature

ROBERT W. MORGAN, MO, SMHyg; DONNA E. FOLIART, MD, MPH, and
OTTO WONG, ScD, Oakland, California

Exposure to asbestos is among several factors cited as possible causes of esophageal, gastric and
colorectal cancer. More than 45 published studies have presented mortality data on asbestos-ex-
posed workers. For each cohort, we listed the observed and expected rates of deaths from types of
gastrointestinal cancer based on the latest published follow-up. Summary standardized mortality
ratios (SMRs) were then derived. Finally, we calculated summary SMRs for total gastrointestinal
tract cancer for three occupational groups: asbestos factory workers, insulators/shipyard workers
and asbestos miners.

Statistically significant elevations in summary SMRs were found for esophageal, stomach and
total gastrointestinal tract cancer in ail asbestos-exposed workers. Esophageal cancer summary
SMR remained significantly elevated when data were reanalyzed to include only those cohorts with
death certificate diagnoses for cause of observed deaths. However, summary SMRs were not
Statistically significant for stomach and total gastrointestinal tract cancer after reanalysis. Summary
SMRs by occupational group showed a significant elevation for total gastrointestinal cancer in
insulators/shipyard workers. The elevation was not significant after reanalysis,

Based on the results after reanalysis, the elevations in summary SMRs for stomach and total
gastrointestinal tract cancer are of a magnitude that could result from diagnostic and investigator
error. We conclude that more studies are required before stomach and colorectal cancers are
documented as asbestos-related diseases.

(Morgan RW, Foliart DE, Wong O: Asbestos and gastrointestinal cancer—-A review of the litera-
ture. West J Med 1985 Jul; 143:60-65)

TSS Snails NGaSssniis

Ww causes gastrointestinal cancer is far from clear
Cited as possible causes are factors as diverse as diet.
race, blood group, alcohol intake and exposure to asbestos
This review will examine the relationship of occupational
asbestos exposure to the risk of developing carcinoma of that
portion of the gastrointestinal tract including the esophagus.
stomach and colon-rectum. The association of asbestos and
peritoneal mesothelioma is well documented, does not involve
the gastrointestinal tract and will not be reviewed here.

Esophageal cancer is a relatively uncommon cancer for
which death rates have remained stable over time: 4.17
160,000 in 1955 and 4.3/ 100,000 in 1975, for US white men.
Higher death rates have been reported in areas of Africa anc.
Eastem Europe. In the United States, esophageal cancer is
found predominantly in men and is associated with cigarette
smoking and alcoho! intake.

Gastric cancer is a slightly more common disease of con-
siderable geographic variation, with some countries, notably
Japan, having rates significantly higher than those of the
United States, Dietary factors have been implicated in the
pathogenesis of the disease. In the United States both mor-
tality and incidence of stomach cancer in white men have
fallen consistently and dramatically over a 20-year period.
For example, the mortality rate dropped from 17.2/100,000
in 1955, 10 8.2/100,000in 1975,

Colorectal cancer presents an etiologic puzzle distin-
guished more by the number of hypotheses than by discovery
of causative agents. In addition to asbestos, associations are
postulated for intake of fiber, fat and specific foodstuffs. For
US white men, death rates for colorectal cancer were 23.4/
100,000 in 1955 and 24.4/100,000 in 1975,

Attempts to study the relationship of asbestos to gastroin-

From the Environmental Hewith Associates, Ine, Oakland, California.
Submitted, revised. December 17. 1984.
Reprint requests to Robert W. Morgan. MD, Environmental Health Associates,

60

Ine. $20 Third Street, Suite 208, Oakland. CA 94607,

THE WESTERN JOURNAL OF MEDICINE

Reprinted from the Western Journal of Medicine, © 1985ASBESTOS AND GASTROINTESTINAL CANCER

ABBREVIATIONS USED IN TEXT

AR attributable risk
SMR standardized monality ratio

testinal cancer are frustrated by a number of factors. First, for
any specific site (for example, stomach), the disease is suffi
ciently uncommon that few work forces can be expected to
account for enough cases from which to draw conclusions.
Perhaps more important, there is considerable opportunity for
misdiagnosis or inaccurate certification of death, in that some
gastroimestinal tract cancers will be certified as mesothe-
lioma, and vice versa. This question has been addressed by
both Newhouse ' and Selikoff * in their examinations of death
certificate accuracy in asbestos workers’ deaths. In the New-
house series, half of the deaths certified as gastrointestinal
cancer were actually due to mesotheliomas. In Selikoff’s se-
ries, only 24 deaths were originally certified as peritoneal
mesotheliomas; after examining further clinical and patho-
logic evidence from other deaths in the cohort, investigators
classified 112 deaths as due to that cause, with a pronounced
reduction in number of deaths due to “al other cancer” and
“all other catises.””

Although diagnostic inaccuracy is troubling, it is not
easily remedied. Selikoff has used “best evidence”’ from nu-
merous sources, rather than the certified cause of death, to
calculate standardized mortality ratios (SMRs). However,
“best evidence’ data cannot properly be compared with na-
tional mortality statistics, which are derived solely from death
certificates. Unless one can also correct the statistics from the
US reference population, comparisons are invalid because of
the underlying principle that both study and reference popula-
tions should have similar ascertainment and classification of
death. Another statistically questionable practice is attrib-
uting to cancer those deaths previously certified as due to a
cause other than cancer, but where cancer was present (Seli-
koff communication quoted by Miller’). Again, without a
similar mechanism for including cancer as a contributing
cause of death in the national mortality statistics, such com-
parisons will either create an apparent excess of cancer in the
study population or will exaggerate any excess already there.

Most of the evidence concerning asbestos and disease
comes from the retrospective cohort mortality studies of as-
bestos-exposed workers, In all of these studies, a cohort ex-
posed to asbestos has been identified from employment, union
or other existing records and then followed prospectively over
time to compare their rate and pattern of mortality with a
reference population with presumably no exposure or less
exposure, The reference population is frequently that of
county, state or country. In general, national statistics are
used because of availability and the stability imparted by large
numbers. Smaller jurisdictions tend to produce statistics that
can be heavily influenced by relatively few deaths, including
those occurring in the work force under study.

Methods

‘To determine the role of occupational asbestos exposure in
the risk of gastrointestinal cancer, we attempted to identify all
relevant publications from the indexed literature. From each
report, we extracted the details concerning cohort definition,
exposure of concern and gastrointestinal cancer deaths (both

JULY 1985 + 143 6 1

observed and. expected). We did not include any judgment
concerning scientific merit in selecting papers to be included,

A summary of published studies of asbestos-exposed
workers is presented in Table 1, Some 45 publications have
described about 22 different cohorts, although within them
there is some overlap. Deciphering the Interwoven cohorts is
complicated because in many cases a single data set has been
repeatedly published, sometimes for an alternative analysis.
In other cases, there appears to be no clear reason for the
republication. Further confusion is introduced when papers
do not specify that the data, or portions thereof, were previ-
ously reported. Some of the cohort studies reported do not
mention gastrointestinal cancer, let alone specific sites, so
contribute little to a quantitative analysis.

‘Table 2 summarizes the results of those studies which are
informative as to the possible relationship of asbestos to gas-
trointestinal cancer. Studies were included in Table 2 when
the number of gastrointestinal tract cancer deaths was avail-
able and the cohort discrete. Because of the problem of data
overlap, we have used the latest published follow-up of each
cohort rather than numbers from earlier papers. When avail-
able, observed deaths based on death certificates, rather than
“best evidence," are presented in Table 2. Several of the
studies****** in Table 2 grouped deaths from peritoneal meso-
theliomas with gastrointestinal cancers. When the actual
numbers of mesotheliomas were given in the text, we deleted
these from “observed” deaths. One report” grouped esopha-
geal and stomach cancer deaths together for analysis. This
report was not included in the calculations for those sites.

In order to provide a quantitative summary risk index for
gastrointestinal cancers based on the studies reviewed, we
have examined a number of statistical procedures. One pro-
cedure is the combinatian of relative risks based on the vari-
ance-weighted logarithms of the relative risk.*** In this pro-
cedure, we can treat each cohort as a2 2 table and the SMR
asa special type of relative risk.*® The unexposed group in the
2x2 table would be a sample of the standard population,
whose sample size is the same as that of the exposed study
group. This procedure, however, presents some difficulties
because the number of person-years is not always presented in
every study reviewed.

Another procedure of combining the risk estimates from
these studies is the indirect standardization. We can view each
cohort as a separate stratum; within each, certain characteris-
tics are homogeneous (for example, study design, length of
follow-up and exposure). This view is similar to that in calcu-
lating SMR within a cohort, where the strata are homoge-
neous with respect to age, race, sex and so forth. In the direct
standardization only the observed and expected deaths are
needed for the calculation. The summary SMR can be calcu-
Jated as follows:

Summary SMR-=SuaLof Observed Deaths ,
Sum of Expected Deaths
In essence, the summary SMR is weighted by the number of
expected deaths, which is the reciprocal! of the variance of the
individual SMR.** Thus, this method is, to some extent, sim-
ilar to the one based on the iogarithm of the relative risks.

Needless to say, this application of the indirect standard-
i 1 SMRs from different studies is subject
to the same criticisms that are often raised in summarizing

100.

BtASBESTOS AND GASTROINTESTINAL CANCER

age-sex-race-specific rates in a single study. On the other
hand, we know of no way to overcome the bias due to the fact
that negative studies were less likely to result in published
SMRs or observed and expected values, although even studies
with negative findings in gastrointestinal cancer but with posi-
tive findings in respiratory tract cancer would still have a high
likelihood of being published.

‘We have also derived summary SMRs for three major
occupations: asbestos factory workers, insulators/shipyard
workers and miners, In the follow-up of the New York-New

Published

TABLE 1.—Summary of Siudies of Asbestos-Exposed Workers
is Date Ree >
putilished

Jersey cohort of insulation workers to 1976,? only “best evi-
dence” calculations of observed deaths are presented (Table
3). Due to the limitations of ‘best evidence’ data, summary
SMRs were also calculated after deleting observed deaths in
this cohort.

Results

Summary SMRs and confidence intervals for esophageal,
stomach, colorectal and total gastrointestinal tract cancer ap-
pear in Table 3. Significant elevations in summary SMRs

‘Cohort Description ant Comments:

1983 (48)

"Matus in patrtisns (« retence numbers,

Asbestos textile factory workers.
Follewed through 1961
-Folewed taught 1088
Followed through 1974 :
Canadian asbestos miners folawed: 1950-55
‘Multiple occupational groups studied 1954-62
Potow aeons ee
Factory workers followed 1938-60.
Same ohort oe
Asbestos shecting factory workers telowed 1986-62
~ New York-New Jersey insulators fotowed through 1962
Followed rough tae
Folowed through 1971
Folowed through 1976
Asbestos insidation viarkers, fnchuding ANNI cobiort survives,
{oloned through 1971 eee :
Folowed 10 79
Aosite factory workess through 1971
Folwes though 1877

Stipya- workers from 1967-76, 2 subtotion ot 1972a study
‘Chirysotile miners from Quebec

Asbestos products workers 1948-51. followed through Jute 1963
Asbestos products workers to 6/20/63, some fromr-peavious cabort
PMA study of asbestos workers:

Asbestos factory men

Asbestos factory women employed 1996-1942, follawed through

Follow-up of above 2 cohorts to 1970
Follow-up to 1975

170 Shij workers through 1966
Followed rou 176

Guetiec miners followed to 11/1/68

Followed through 1969 with different analysis
Followed through 1975

199 Expased.to crocidclite traced through 1975
Retirees from asbestos mtg fofowed through 1969
Retirees. presumed dense fo the ove

Reanalysis of previous two papers

Ratirees followed through on

Gase-control study of anthophyilite miners

Chrysotile factory workers 1935-54 followed through 1974
Miners fottowed through 1974

Gold miners expased to asbestitorm rock followed through: 1973
Shipyard workers followed through 1969

Gas mask workers followed through 1978

Crocidolite miners followed throught 1978.

Dockyard workers 1947-78

Factory workers followed through 1974

Ashestos (mma file) fr i 1 1942-7
Fate satay choot) iéton material workers, 1942-79
Female gas'mask workers, 40-year. follow-up’

62

—l

THE WESTERN JGUANAL OF MEDICINEASBESTOS AND GASTROINTESTINAL CANCER

were found for esophageal (SMR=214) and gastric
{SMR=183) cancer. Although summary SMRs for these
sites were based on data from four studies, numbers were
small and the 95% confidence intervals were wide. The slight
excess in SMR for colorectal cancer (SMR= 113) was not
statistically significant. The SMR for total gastrointestinal
tract cancer (SMR = 108) was minimally but significantly ele-
vated.

‘fable 4 presents site-specific summary SMRs after “best
evidence” data are deleted. Esophageal cancer remains ele-
vated (SMR =238, P<.05).

‘Total gastrointestinal tract cancer deaths and summary

SMRs for three exposure categories are presented in Table 5.
Of the three occupational groups, only insulators/shipyard
workers had a significant elevation in total gastrointestinal
tract cancer (SMR = }32), Total gastrointestinal tract cancer
was not significantly elevated in insulators when “best evi-
dence” data were removed.

Discussion

The strongest evidence linking asbestos to esophageal and
gastric cancer is a series of studies of the New York-New
Jersey (NY-NJ) and US-Canadian insulation workers.*:*"*
‘The summary SMR for esophageal cancer was significantly

TABLE 2.—Summary of SMR3 from Various Cohort Studies
Cohort Person Standard _f=oahageal Cancer Slomech Cancer Colorectal Cncar
Author (DateComments (Ref. No) Sze Years‘ Popuialion “SHR Obs Exe “SHR Obs &xp SMR Obs Bp SMA Obs Exe
Peto et al (1977) 22.22... (12) 4,106 16.072 BritNath W216 157
Asbestos factory workers
Selikotf et al {F 79), vere (3 832 13.925 us 1 i 14 352 19" «G4 277 23" BS 285 43" 15.4
NY-NJ insulators to 1976
(“best evidence” used)
Sete etal Se O78 ices sete eee (2) 17,800 166.853 us 23318 71 127) 18 14.2 152 58 38.1 158 94 59-4
soc etal ee sees -(22 582 6,317 New Jersey 1250 1 98 2000 4 20 212 11 52 200 16 8.0
Amosite factory workers: .
‘Seltkoff et al (79 peeee eee (7 388 ae US vw 8 Bf
‘Shipyard worker ~
Nicholson ot a 87 beens ( 8} 844 7,408 Canada Natt 10510 95
Chrysotile mining .
miling
‘MeDonaid et al (1980) . 0... (33) 11,379 Quebec «= 127-130" 102.0 127 130° 102.0 78 79 101.0 103 209 202.9
ysotile miners, 20 or
more years after ist em-
ployment; stomach
deaths.
together
Newhouse and Bery (1979) . . (28) 5,522 ves Bit ee +
Rates exclude 8) 136 60" 44.2
Enteriine and Kendrick wen (24) 24,758 cee UW kee ees 106 8378.2
‘exposures {t
frictionextile products}
sate includes malignant
mesotheliomas
Henderson and Enterline (1979) (38) 1,248 cae US
sen (1978) (38) 138-110 79.7
mesotheliomas
Meurman etal (1974) 02... (39) 1,002 Finland ee ee
v8 . @ 7 149
Viet seeee (4 264 ee us .
Ciysotl mine 5 4 38
stomach & colorectal
cancers combined to
calculate GI cancer SMR
Fe ane al 1879) wees eeee 1} 952 21,459 italy 8 19 18.4
Jones et at <7 wees (44) 954 cee Bt, ee ee ee
Gas mask workers @ 1 aa4
Sipe - (46) 6,292 EngiWates 83 638 75.9
Hughes a and Weill (1980)... (13) 5,645 ve US
Factory workers 50 25 50.0
eat wen Coulter (1963) .. (17) 1,495 23,257 us 20004 05 107 2 191458 5 35 135 8 5.9
and Newhouse (1989) 1,
“e ta tas (88) 11.182 163,009 Engi/Wates 98 192 1348
‘chrysi
workers:
‘tergastrabesinal, SMRe standardized mertalty rao
Sen coment in Auth (OeCommers coke

JULY 1985 © 143 6 4

63ASBESTOS AND GASTROINTESTINAL CANCER

elevated even after “best evidence” data on observed deaths
in the New York-New Jersey cohort were removed, Gastric
cancer in the NY-NJ cohort contributed 19 observed deaths of
43 deaths in the calculation of the summary SMR. For the
NY-NJ cohort, unfortunately, causes of death used in analysis
were obtained not only from death certificates but from “best
evidence.” The authors did not present the number of ob-
served deaths derived solely from death certificate informa-
tion. The gastric cancer summary SMR was not significantly
elevated when “best evidence’’ data were deleted. The same
researchers found no excess of gastrointestinal cancer in ei-
ther shipyard workers’ or chrysotile miners.* One of the best-
performed and longest-term cohort studies*"*? has found no
increase of gastrointestinal cancers of any type after more
than 50 years of meticulous follow-up from first exposure,
Most of the evidence favoring an association between as-
bestos and gastrointestinal cancer comes from a series of
studies by one group of investigators; these results must with-
stand critical review if a causal relationship is to be accepted.
The fallacy of using ‘best evidence” for the cause of death
has been discussed above, as a bias that inflates SMRs. In
addition, repeated publishing of the same results may have

created the illusion of more positive evidence than actually
exists. Four cohorts have resulted in at least 14 publications
{see Table 1). The original table describing the original New
York-New Jersey cohort, first published in 1964, was repub-
lished in 1979 without incorporating the follow-up that had
been accomplished and published in the interim. The 1976
follow-up was published in both 1979 and 1981. The 1976
follow-up of the US-Canadian cohort was published twice in
1979 and the amosite cohort follow-up of 1977 was published
in 1979, 1980 and 1981. The negative studies’* have not been
republished.

In an earlier review, Miller came to the conclusion that
asbestos and gastrointestinal malignant conditions were caus-
ally related, although he did not attempt to calculate a sum-
mary risk estimate. Most of his conclusions were based upon
the work of Selikoff and the review did not have the later
negative studies coming from Peto,'? Hughes"? and Selikoff's
associates,”* Miller also failed to appreciate the error in-
volved in the practice of using “best evidence” rather than the
certificated cause of death for comparison with national statis-
tics. Finally, although the review paper acknowledges the
work by Newhouse in showing the extent of cause-of-death

TABLE 3.—Summary SMPs

95% Can’

‘SMR= standarzed mortally catio

“Reference 54.
$e 5.
-PRY-NY conart and US-Canadian cohort

Observed Expected SMA __dence intervat* References
a 08 aia 132.6-327.8 24.17.22
a 235 183 132.4-246.5 24,1722
176 186.4 NS 96.5-130.4  24.17,22,33
12 840.9 108¢ 1015-115.7 — 24,7,8,12,19,17,22,24.28,
33,38,41,44,46,48

TABLE 4.—Summary SMRs Deleting ‘Best Evidence’ Data

‘95% Conk.
Sie of Cancer Observed Expected — SMR dence Interval" References
20 84 238t 145-368 24,17,22
. 24 18.1 133 85-197 Ah 17,22
153 148.1 103 88-121 24,17 ,22,33
Total gastrointestinal tract... 869 825.8 105t 98-113 24,7,8,12, 13,17, 22.24.28,
SUR santana arab rl 35,38-41.44.48,
P<.
+1US-Canadian cohort; NYAS cohort excluded.

TABLE 5.—Summary SMRs By Occupation for Yotal Gastrointestinal Tract Cancer

95% Conk.

Ooewipation Observed Expected SMR_—_denve Interval” References
Asbestos factory workers... . ABC 436.9 105 95.9-115.4 12,13, 47,22,24,28 38,44,48
insulators/shipyard workers. _ + 208 153.5, 132t 118.7-181.7, 23,7,46
Insuiators/shipyard workers deleting “hest evidence” data . Ee 138.4 M16 98.0-135.0 287,46
Asbestos MINES oer eee 249 250.5 ag 87.4-412.5 8,33,39,40,41
‘SMReestuntarized mostly ric

*Roferonee 5.

Pe 05,

ENVAD coon ang

oho NY-R cabot tun.

THE WESTERN JGUANAL OF MEDICINEASBESTOS AND GASTROINTESTINAL CANCER

misclassification, there was little attention paid to its potential
impact on study results,

Conclusion

Malignant lesions of the lung, pleura and peritoneum have
been clearly linked with exposure to asbestos. Some studies of
cohorts occupationally exposed to asbestos have also found
elevations in incidence of gastrointestinal cancer, while other
reports have not found excesses after years of follow-up.

in an effort to summarize the available studies of gastroin-
testinal cancers in asbestos-exposed workers, we have calcu-
lated summary SMRs for esophageal, gastric, colorectal and
total gastrointestinal tract cancer. In addition, we have de-
rived total gastrointestinal tract cancer summary SMRs for
workers exposed to asbestos in three specific capacities: fac-
tory work, shipyard/insulation work and mining.

Although there are statistically significant elevations of
SMR for esophageal and gastric cancer for all groups and for
total gastrointestinal tract cancer for insulators and shipyard
workers, we are not convinced of the relationship to asbestos
exposure, especially for stomach cancer, where the finding is
inconsistent and possibly erroneous in the largest positive
study, For colorectal cancer, at this time there is no discern-
ible relationship to asbestos exposure. We hope that the occu-
pationally exposed cohorts now under study will provide more
conclusive evidence soon~-refuting or supporting such an
association.

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