. TABLE OF CONTENTS page
Introduction ...... 1-2
Section 1-Definition and Identification of Workplace Carcinogens ...... 3-43
Introduction ...... 4
Occupational Cancer...... 6 Cancer in the Work Environment .... 11
Cancer in the Workplace-Part 1...... 16
Black Workers and Cancer...... 20
OCAW Recordkeeping and Cancer ...... 23
CIP Bulletin: Ames Test ...... 29 CIP Bulletin: Animal Test...... 32
Human and Animal Carcinogens ...... 34
Common Occupational Cancers...... 42
Section 2-Risk Assessment and Policy Issues .... . 44-50
Introduction ...... 45 Estimating Potency of Carcinogens...... 46 How Safe is "Safe"'?...... 47
Risk Assessment ...... 48
Section 3-Legislative Protection...... 51-69
Introduction ...... 52 Regulation of Carcinogenic Substances...... 53 Federal California
List of Regulated Substances...... 56 Federal California Cal/OSHA Bulletin to Employers on Regulated Carcinogens. . 57 Category 1 Substance List...... 61 Additional Legislative Protection ...... 63 Toxic Substances Control Act Federal Right to Know National Labor Relations Act Cal/OSHA Fact Sheets on...... 66 Hazardous Substances Information and Training Act Access to Medical and Exposure Records
Section 4-Union Approaches to Workplace Cancer ...... 70-90 Introduction ...... 71 Union Action to Fight Workplace Cancer ...... 72 PMR Studies ...... 73 One Man Scoops the Experts...... 80 Medical Testing/Exams ...... 82 Controls and Monitoring Information ...... 84 Occupational Toxic Exposure History...... 89
References ...... 91-96 Cancer ranked in 8th place in 1900, but is currently the second most common cause of death in the United States. About one in every four people will develop cancer in their lifetime.1 More than 53 million people in the United States (more than a quarter of the population), will dIvelop some form of cancer, from which 20% of the United States population will die. The financial costs are also staggering. Treatment for one individual can range from $5,000 to $30,000; the average is in the area of $20,000 per person. 3 Total national costs from cancer were estimated to approximate $30 billion in 1978. In the past several years, various governmental and private sources have estimated that 70-90% of all cancer is environmentally induced. (This estimate includes cancer caused by cigarette smoking and by nutritional causes). In related studies, epidemiologists for the National Cancer Institute (NCI), the National Institute of Occupational Safety and Health (NIOSH), and the National Institute of Environmental Health Sciences (NIEHS), have estimated 10-38% of all cancer may be due to occupational exposures.5 Most estimates are around 10-20%. However, it is very difficult to make estimates of how much is occupationally caused or caused by any one factor. Although the estimates vary, it is agreed upon that chemicals and environmental factors are leading causes of the rising incidence of cancer in the United States today. Even more important is the fact that occupational cancers can be prevented, by controlling exposure in the workplace. It is known that sometimes cancer does not show up for 15, 20 or even 40 years after the first exposure to a cancer causing substance. Occu- pational exposures are generally involuntary and in many instances workers are never even aware of their exposure. But even brief exposures have been known to cause cancer and in too many cases, cancer cannot be cured. Therefore, the only solution is prevention, which can best be achieved by controlling workers' ex- posure to potentially carcinogenic substances. There have been various attempts at control and regulation of these substances. The issue is fraught with problems. One problem is the differing opinions as to determination and definition of what is carcinogenic (cancer causing). For example, there has been debate about the accuracy of animal vs. human studies as the basis for the determination of carcinogenicity. Once a substance has been identified as carcinogenic, there has been debate over how to incorporate substance regulation into industry. Feasibility issues (technical and economic) are raised and become enmeshed with scientific consideration so that determining a level of exposure which can be adhered to by industry becomes a political as well as a scientific and legal issue. It is in this area that decisions are made about worker exposure to occupa- tional carcinogens. The purpose of this packet is to provide information to individuals about occupational cancer. It is divided into four (4) sections. The first provides background knowledge about what occupational cancer is, what are some of its causes, and an explanation of the various tests which are used to provide evidence for labelling a substance carcinogenic. Included is a discussion of epidemiology, animal tests and short term tests. Section 2 discusses the risk assessment method used to determine the levels of risk associated with exposure to carcinogenic sub- stances. Section 3 contains information about carcinogen regulation on a federal level and in California. It also contains information about other legislative protections which can be used regarding carcinogens. Section 4 provides guidelines for union approaches to workplace cancer.
1 Each section is a complilation of articles and each section also has a list of references for further reading relevant to that section. At the end of the packet, there is a general list of references as well as agencies where infor- mation about cancer is available.
FOOTNOTES
1 Part 1 of California Deptartment of Health Services, Cancer Policy Statement, "Carcinogen Indentification Policy; A Statement of Science as a Basis of Policy", July, 1982. Page 1. Available from DHS, 714 "P" Street, Room 599? Sacramento, California 95814. 2 Ibid
3 Epstein, Samual, Politics of Cancer, Sierra Club Books, 1978, Page 8. 4 Kriebel, David, "Cancer: Some Notes for Activists", Science For The People, Vol. 12, No. 3, May/June, 1980, Page 6.
5 Loechler, Ed, "Cancer And The Workplace", Science For The People, Vol. 12, No. 3, May/June, 1980, Page 14.
2 Section 1:
Definition and Identification of Workplace Carcinogens SECTION 1
Definition And Identification Of Workplace Carcinogens
This section provides some general background information about occupational cancer: what it is, what are some of its causes, and an explanation of the various tests which are used to provide evidence for labelling a substance carcinogenic. Also included are lists of chemicals which have been categorized depending on whether they are known to cause cancer in humans or animals, or are mutagenic in short-term tests.
Articles in this section make the point that cancer is on the rise and occupational cancer is being increasingly implicated as playing an important role in the problem. One of the articles concentrates on cancer among blacks and convincingly ties this to workplace exposures. Other articles concentrate on explaining the pros and cons of human tests, animal tests and short term tests as ways of determining the potential for carcinogenicity.
Placing chemicals into certain categories based on this determination is a scientific decision. However, the decision about what regulation is demanded by each category is a political decision. IARC, EPA, and OSHA have all established various categories of substances based on test results. The way in which these results are used to decide cancer risk and to determine regulatory action will be discussed further in Sections 2 and 3.
For Additional Reading
1) Part 1 of California Department of Health Services Cancer Policy Statement "Carcinogen Identification Policy: A Statement of Science as a Basis of Policy", July, 1982.
2) Moses, Marion, "Cancer And The Workplace", American Journal of Nursing, November, 1979.
3) Goodman, Al, "Epidemic Cancer May Be The Political Issue of The 80's". 4) Polakoff, Philip, "Environmental Cancer...A Closer Look", Hazard Prevention, September/October, 1979.
5) Agran, Larry, The Cancer Connection, Houghton Mifflin Company, Boston, 1977; Chapter 2.
4 Definition and Identification of Workplace Carcinogens Section 1: Additional Reading (continued)
6) Epstein, Samuel, The Politics of Cancer, Sierra Club Books, 1978; Chapters 1, 2, and 3. 7) Association of Scientific, Technical and Managerial Staffs (ASTMS) Document No. 3, "The Prevention of Occupational Cancer", 1980. 10-26a Jamestown Road London, NW1 7DT, England Sections on Epidemiology, Animal Testing and Short Term Tests, Pages 27-32. 8) United States Department of Health, Education and Welfare, "Everything Doesn't Cause Cancer".
9) International Association of Fire Fighters, Department of Research, Health and Safety, "Occupational Cancer And The Fire Fighter", 1982. 10) Bridbord, K., M.D., Wagoner, J., and Blejer, H., M.D. "Chemical Carcinogens", Occupational Diseases: A Guide To Their Recognition, June, 1977.
5 Labor Occupational Health Program "MONITOR" Vol. 8 No. .2, March-April, 1980 Cancer A Special Report
Foundry workers, expowd to a variety ofchemicals, are at high risk ofcancer. (Photo: WorkingStel/LOHP.)
Occupational Cancer by Janet Bertinuson
Cancer is a word that is frightening to One reason more cases are seen has is, potential and known causes, test- most people. And a look at some to do with our incrased life atancy. ing of cancer suspects, regulation of statistics for this disease provides ample There is a long delay between expo- carcinogens, resources, and prevention reason for such a reaction. One out sure to a cancer causing substance of cancer. Because evidence strongly of every four Americans can expect to and appearance of the disease. Since points to occupational and environ- get cancer, and two out of every three life expectancy is greater today, more mental exposures as major causes of families will have a member who people live long enough for cancers to cancer, the article focuses on this develops some form of cancer. Although appear. But the increased rate of cancer aspect. early diagnosis and improved treatment cannot be explained solely by longer life techniques increase the chances of sur- span. We must look beyond life expect- CANCER-WHAT IS IT? vival, the rate of cancer deaths (and ancy and examine the evidence which reported cases) is rising. In 1973, points to potential occupational and The term "cancer" describes a num- 351,000 Americans died of cancer, but environmental causes. ber of different diseases with a variety by 1975 the numbers had increased to of causes. But basically, in all forms 364,000. This article will explore what cancer 6 CANCER
of cancer the body's cell division system becomes damaged, which leads to a rapid, out-of-control growth of abnormal cells. Generally cancer starts off as a disease localized in one area (often on the surface of an organ such as the skin or liver.) As growth continues, the cancer can spread deeper into the organ, and eventually spread to other parts of the body (metasta- size) by way of the blood or lymph systems. WHAT CAUSES CANCER? There are many substances in our environment that are linked to develop- ment of cancer. In fact, environmental pollutants in air, water, soil, and the workplace are now estimated to cause between 75-85% of all human cancers. The increase in manufacture and use of petrochemicals is directly connected to the proliferation of cancer-causing sub- stances in the environment. Although we often hear that "every- ronmental carcinogens have not been of people who have been exposed to a thing causes cancer," this is not the case. identified, there are numerous sub- certain substance. They compare the From human studies, about 30 sub- stances which are considered human number of cancer 'cases and deaths stances or agents have been identified as carcinogens based on results of epi- with a similar group (control group) carcinogens, and about 50 others show demiological studies as well as animal who were not exposed to the substance. evidence of carcinogenicity (ability to studies. The list in the box, above, Epidemiological studies are the best cause cancer) based on epidemiological includes some of the chemicals associ- evidence that a substance is a human evidence.* Known cancer-causers (car- ated with increased cancer risk in carcinogen. Their obvious drawback cinogens) include chemicals such as humans, as well as the type of cancer is that people continue to be exposed benzidine and other organic amines, usually associated with each chemical. while waiting for the results. So we asbestos, nickel and chromium, ben- Where the substance is regulated as a have a situation where, as Bill Lloyd zene, and arsenic, as well as ionizing carcinogen by OSHA, an "R" follows of OSHA has said, "Almost every- radiation and ultraviolet radiation. the listing. thing we know now about occupational Some cancers seem to have multiple cancer comes from counting dead causes, and exposure to more than one TRACKING DOWN bodies." carcinogen may increase risk of cancer CARCINOGENS Obviously other methods must be development. For example, both ciga- used to determine if a chemical is capa- rette smoking and asbestos are linked to Unfortunately, the majority of known ble of causing cancer. The most widely increased lung cancer risk. Asbestos carcinogens have not been discovered used tests are long-term animal studies, workers who don't smoke have an eight by any systematic method of test- although short-term tests in bacteria, times greater risk of developing lung ing chemicals before introducing them insects, or plants are being used more cancer than an unexposed population, into the workplace or general environ- frequently. while asbestos workers who do smoke ment. Instead, workers have been ex- have a 92-times greater chance when posed to substances for many years, ANIMAL TESTS compared to an unexposed population. and after increased cancer rates are seen, On the whole, however, the potential confirming tests in animals may be con- The basic aim of an animal test is for producing cancer when two chem- ducted. Because most chemical car- to measure the effects of exposing a icals interact is largely unstudied. cinogens have a long latency period particular group of animals to a spe- Although all occupational and envi- (time between initial exposure and the cific substance. Two groups of animals appearance of cancer), by the time a are used: experimental (exposed to the chemical is confirmed as a carcinogen substance) and control (unexposed). large numbers of workers may have These groups are further divided into already been exposed. subgroups, e.g., 50 animals of one sex Epidemiology is the study ofdisease occurrence Epidemiological studies are one of and species. Generally, testing is per- in a certain population. It involves comparison the major methods for determining formed in two strains of animals. Be- of disease ratos with a normal (that is, unex- that a chemical is a carcinogen. In cause of their short lifespan (about four posed) population. such a study, scientists follow a group years) rats, mice, and hamsters are the 7 common test animals. human carcinogenicity found that only The animals are normally exposed one of the chemicals, arsenic, did not in the way that most closely resembles cause cancer in test animals. human exposure (for example, inhala- Although most scientists agree that tion of asbestos fibers). Generally, chemicals which cause cancer in humans at least two doses should be used: will also cause cancer in animals, the the maximum tolerated dose, which is reverse is not true. One major reason the largest dose that will not shorten that people resist using animal test data the animal's lifespan by causing some to predict effects in humans relates to other toxic effect; and either one-half dose. The doses given to test animals or one-quarter of that dose. At the end are high, and this leads to the mis- of the test period the animals are killed conception that anything will cause and their organs examined for evidence cancer if the dose is high enough. Yet, of cancer. If the number of cancers numerous chemicals have been tested in in the exposed group is significantly animals at the normal high doses and greater than in the control group, the have not been found to be carcinogenic. substance is considered a carcinogen. High doses are used so that the pos- Animal tests are considered appro- sible effects will be easier to detect, priate in determining the cancer-causing since the group of test animals is rela- potential of a substance because evi- tively small when compared with the dence of carcinogenicity in animal tests number of potentially exposed humans. agrees with known human experience. For example, what if a low dose of a One scientist who reviewed animal test substance caused cancer in one of every data on 82 substances for which there 10,000 persons (or 10,000 tumors in was some epidemiological evidence of 100 million Americans.) If you used the Bronchogenic carcinoma in an asbestos worker. continued onp. 8 (Photo: LOHP Photo File.)
8 CANCER high, the cancers are more likely to be at least 3.5 to 4 years per test, it seen in a small group of test animals would be an impossible task not only because the cancer rate would be in- to test all the new chemicals intro- creased proportionately. And negative duced into the workplace each year, but se corresponding dose in a group of results at high doses increase the like- also to test those already in use. So 50 rats (as opposed to 10,000 rats) lihood that the substance is not a there is a great deal of interest in short- clearly the chance of cancer showing carcinogen. term tests such as the one developed up would be minimal. Reliable conclu- by Bruce Ames at the University of sons can't be drawn from such a small (OIHER TESTS California, Berkeley. The test identifies test sample. In addition, the costs of substances which are mutagens (capable using a large number of test animals Because animal tests are expensive of changing genetic material.) Ames and would be prohibitive. When doses are (up to $400,000 per test) and involve other scientists believe that most muta-
Cancer at Wor: Some Historcal Notes inary pesticide containing 1940's- A study showed chromate by Janet Bertinuson arsenic were prone to skin 50's workers had lung cancer rates cancer.) 25 to 30 times higher than Although the links between a expected. numbe 1876 Bell reported excess scrotal 'of chemicals and cancer have only been cancer rates among shale oil made in recent years, reports of occu- workers. *** ************** ******* *** ** pationally-caused cancer are not new. In fact, early reports of unusual cancer 1936 A Japanese study showed ex- rates in a variety of industries and oc- 1932 Cases of nasal sinus and lung cess lung cancer rates among cancer were cupatons should have served as a war- gas reported among ing that job exposures were causing or producer men. nickel workers. contributing to cancer incidence. And, using information which decades ago 1921-38 Death statstis from the Britsh L950's Lung cancer risk for nickel demonstrated excess cancer rates in Registrar General showed ex- workers was reported at five certain work cess lung cancer mortality for times the expected rate and groups (for example, gas producer men, chimney chimney sweeps and gas producer men), nasal cancer risk at 150 times connections could have been made to sweeps, and other gas works the expected rate. other occupations where chemical ex- employees. posures were similar (for example, coke ********** **** ************* ********** ********* ** ***** ***** oven workers.) 189S Rehn reported bladder cancer Unfortunately, this has generally not in four workers in the same been the case, and in recent years work- 1935 American and British investi- dye factory. (He suspected gators first reported observa- mers have been dying of cancers that aniline.) ould have been predicted based on tions of lung cancer among persons with asbestosis. much earlier studies. The following list 1955 Excess bladder cancers were makes it clear that ignoring earlier reported among workers ex- 1945 First cases of mesothelioma studies because numbers were not "'sta- posed to 4-aminobiphenyl. 'tistically significant," or for any other of pleura and peritoneum teason, has meant that thousands of (inings ofchest and abdominal 1955 Definitive study implicates cavities) were reported. workers have been needlessly exposed benzidine and beta natphy- to cancer causing substances. lamine as causes of bladder 1955 Sir Richard Doll made a clear cancer. (Death rates from 1775 Percival Pott, a British physi- association between asbestos bladder cancer were 19 times and lung cancer. c, described excess cases of higher than expected for ben- scrotal cancer in chimney zidine and 61 times higher sweeps: "When they get to than expected for beta napthy- puberty, (they) become partic- lamine.) ularly liable to a most noisome, 1930's Vinyl chloride was reported to painful, and fatal disease." cause in effects in animals. -i22 J.A. Paris, an English physi- 1890 First report of nasal sinus can- 1970's Italian scientists saw excess cian, reported "a cancerous cer in chromate workers. tumors in rats exposed to vinyl disease in the scrotum, similar chloride. to that which infests chimney 1911 Two cases of lung cancer were sweeps" among men exposed reported among chromate 1974 A physician at B.F. Goodrich to arsenic fumes in a copper workers. (Lung cancer was reported three cases of angio- smelter. (By 1930, scientists considered a rare disease at sarcoma (rare liver cancer) in knew that makers of a veter- that time.) workers.
9 gens are also carcinogens. In fact, nearly CANCER identify effects of interacting sub- 900/ of those chemicals which are stances. known carcinogens test positive as mutagens in the Ames test. to these areas. Some efforts have * Tlumor registries, where all cancer Numerous other short-term tests are been made to arrive at a uniform cases would be reported, should be in use or being studied. approach, but thus far such an ap- developed throughout the country. Despite problems with short-term and proach has not been developed. Currently very few such registries animal tests, some such testing pro- * The long latency period. Because exist. gram must continue. Past experience of cancer's long latent period it's A SOCIAL DISEASE with asbestos, BCME, vinyl chloride, often difficult to identify cause and numerous other carcinogens has with effect. And regulations are The above are specific avenues for clearly shown that we cannot wait for directed toward short-term, acute dealing with the epidemic of cancer absolute proof of carcinogenicity in health effects. related to occupational and environ- humans before regulating exposure to mental exposures. But implementing potential carcinogens. PROGRAM NEEDED such programs is not enough. Cancer is not just a biological phenomenon. An effective program to prevent It is a disease with social, political, PREVENTION cancer is necessary. Such a program and economic aspects. Carcinogenic must also be aimed at those workers chemIcls are produced and used despite Because the vast majority of cancers who have already been exposed. What their effect on humans because industry are caused by agents in the envi- are some of the aspects of such a considers them necessary, and efforts ronment, it follows that they are poten- program? to control such chemicals are met tially preventable-remove the sub- with the argument that in many cases stance, remove the risk. Experience has * Workers currently p to known it is not economically feasible to do shown, however, that it is not that carcinogens must be informed of so. Controls or substitutions would simple. In fact, this country has failed their exposures and the hazards in- be costly, and increased product price abysmally in controlling exposure to volved. In addition, controls must would then be passed on to the con- carcinogens. When other countries have be instituted in those situations sumer. These arguments caused delays banned substances (for example, Italy where carcinogens are used (for in standards for substances such as and England banning benzidine and example, protective clothing, air- coke oven emissions and arsenic, and other organic amines) the U.S. has con- supplied respirators, closed systems will continue to do so as long as tinudd its quest for "safe" exposure handling carcinogens.) Education economic impact statements remain a levels. So despite knowledge of car- and training programs should be crucial issue in standard setting. cinogenicity, workers continue to be ex- developed for such workplaces. La- Cancer is also a social disease. It posed to benzene, coke oven emissions, beling requirements should also be robs the victims, their families, and asbestos, and other carcinogens. And in developed and enforced. society. And it heaps ever-increasing many cases they continue working * All carinogen use should be reported insurance and medical costs on society without being told that substances to to government agencies for enforce- as a whole. Yet we demand certain which they are exposed cause, or are ment and compliance purposes. As goods that are manufactured using suspected of causing, cancer. part of the reportng system, workers carcinogens-pesticides, hair dyes, dyes The reasons for this country's failure should receive a copy of the car- for other materials, plastics, and so on. to regulate carcinogens and adequately cinogen use report form. So we must determine how important protect workers and the general public such things are in light of their include: * Efforts must be made to find and terrible cost. Cancer is potentially pre- contact workers formerly cxposed to ventable, but all sectors of our society * Pressure from industry related to carcinogens, so that they can be must be committed to prevention if economic costs of control. This is channeled into screening programs we are to see an end to the cancer evident in industry's support of cost- aimed at early detection of cancer, epidemic. benefit analysis for new health stan- and receive medical attention if dards. But, as Samuel Epstein points necessary. out in his book, The Politics of Cancer, the benefits of using a * Research on reliable short-term tests carcinogen go to one group of to identify carcinogens should be people (corporations an,d stockhold- performed. ers) while the real costs in terms of * New chemicals introduced into in- illness, death, lost wages, medical dustry and the environment must be expenses, and so on, paid by workers tesed for carcinogenicity. Chemicals and society are dismissed or ignored. already in use should also be srnd. * Lack of a coordinated approach. A method for prioritizing chemicals The many government agencies to be tested should be developed. which have authority in terms of (The Toxic Substances Control Act research, control, prevention of can- enforced by the Environmental Pro- cer, or enforcement of carcinogen tection Agency as well as OSHA's regulations have different new cancer policy focus on this approaches aspect of carcinogen regulation.) Efforts should also be made to Coke oven worker. (Photo: Ken Light.) 10 from the B.C. Worker's Health Newsletter
Cancer in the work environment -0 by Robert Sass There is growing evidence that cancer is largely the result of carcinogenic hazards being introduced into the general environment and the workplace. Indeed, it is acknowledged by many authorities as a "man-made" disease, one of the negative side-effects of technological and industrial development. A key point to grasp is that it is only since the Second World War that pollution of the testing done in the United States has generally environment has reached globally significant been unquestionably relied upon. It has recently proportions, becoming, some ecologists fear, a been found that over 100 pesticides have been threat to the surival -of this planet's life forms. registered in Canada on the basis of fraudulent The war was the advent of the nuclear age. It or inaccurate U.S. test results. In 1980 it also brought a massive expansion of the petro- became generally known in Canada that the chemical industry, and the introduction into the validity of all studies carried out by Industrial workplace of thousands of new chemicals. The Biotest Laboratories (IBT) of Northbrook, Ulinois development of catalytic cracking made possible was in doubt. Actually the IST fraud was known a dramatic increase in hydrocarbon production before 1980, though not widely publicized. In from petroleum sources. Also, the chemical The Politics of Cancer, published in 1978, Dr. industry set to work aggressively developing Samuel Epsein wrote: "needs" for new types of products. Today, annual growth rates of 1S percent or more are common FDA and EPA investigators have established for the organic cliemical industry, while the rest that Industrial Biotest submitted falsified of the economy remains-relatively stagnant. data on potential carcinogeAs to the government. It has also been established As of November, 1977, the Chemical Abstracts that at least four unidentified major Service computer registry of chemical pesticide manufacturers were aware of this compounds contained over four million distinct fraud when they submitted the test data in entries-and it is growing at the rate of about product registration applications. 6,000 compounds per week. Of these four million chemicals, 33,000 are believed to be in common The biochemical defences of living things on this use-and relatively few have been tested for planet-including ourselves-are the product of carcinogenicity. millions of years of evolution. Ecologists warn us that these defences cannot possibly react in Although common sense would suggest that any time to protect us and the animals and plants chemical be thoroughly- tested for harmful which share our planet from this tremendous effects before being introduced into industry, onslaught of harmful new chemicals which have that has not in fact been -the pattern. Only with appeared since World War II-that is, in the last the passage of the Toxic Substances Control Act "second" of cosmic history. Ours is the first in the United States in 1976 has the philosophy of generation of man to have strontium-90 in their testing first been given a significant legislative bones and chlorinated hydrocarbons in their fat. basis. Canada's Environmental Contaminants Act of 1975 is considerably weaker than the U.S. Although it may seem a statement of the legislation, in that It merely allows the Ministers obvious, it is necessary to make clear that most of the Environment and/or Health to request of these pollutants come from industry. While information from the manufacurer. Agriculture the nonsynthetic pollutants-such as lead, Canada's Pest Controlf Products Act requires mercury, cadmium, chromium and beryllium- testing and registration of all pesticides but exist in nature, they do not there pose a grave
11 danger to large populations. The principal source nature, inferential not factual. Epidemiology is of danger is the activity of man. Thus if we wish predominantly a nonexperimental science, and to find pollutants in their most concentrated and therefore the evaluation of cause-effect lethal form-both natural substances and relationships is very difficult. Moreover, some synthetic compounds-we shall find them in the epidemiological studies on work-related cancers industrial workplace. In the workplace-the have come up with very low figures. mine, the smelter, the coke-oven plant, the steel plant, the factory, the shop, the construction One way of masking the harmful effects of site, the agricultural chemical depot-they chemicals in the workplace in an epidemiological expose workers to countless occupational health study is to ignore the "healthy worker effect". hazards. Persons hired for industrial work-predominantly young males-are more healthy, in the- first The National Cancer Institute's "cancer maps" place, than the general population; so much so, clearly indicate that the production and use of that if they end up with health problems industrial chemicals have created striking comparable to the general population, this geographic concentrations of cancer deaths. In represents a considerable deterioration of their the early 1970s, the World Health Organization health. It must be remembered that the general indicated its belief that the percentage of population includes unemployable and environmentally caused cancers ranges from 75 unemployed persons-among them being those in to 85 percent. institutions, those with congenital anomalies, those handicapped during childhood, those At least 20 percent of all cancer in the United otherwise ill at the time job seeking commences, States may be work-related, according to a 1978 and those unemployed or with unstable study from the National Cancer Institute and the employment. All these groups have a higher National Institute of Environmental Health mortality rate than the active population. A Sciences. This estimate may represent a 1975 study by E.M. Kitagawa and P.M. Hauser conservative figure in light of the fact that 17 showed that those American white males percent of all cancers detected annually are unemployed in 1950 or later (4.4 percent of the apparently caused by asbestos alone, and that population) had a standardized mortality ratio of from three to 18 percent are associated 240; that is, they were 2.4 times as likely to die exclusively with exposure to chromium, iron as the general population. oxide, nickel, and petroleum distillates. If one also considers that there are more than 2,000 Another central problem is the evaluation of other suspected industrial carcinogens, of which "negative studies." Negative studies are at least only about 20 are regulated, the relationship as important as positive ones in occupational between work and cancer becomes evident in medicine because it is extremely important to be terms of magnitude, if not detail. able to define a noneffect level for harmful exposures, Hernberg says. A clear distinction Of course, one cannot say that "at least 20 must be made between truly negative and percent of all cancers are work-related." All "nonpositivel" studies-that is,. between studies such epidemiological estimates are, by their very which actually show a noneffect and those which,
12 instead, simply fail (perhaps through defects in A Canadian example of this kind of error was a the study) to show a positive effect which may 1958 study by D.C. Braum and T.D. Truan, actually exist. entitled "An Epidemiological Study of Lung Cancer in Asbestos Miners." Knowing what we know today about asbestos and cancer, their findings appear incredible. They found no statistically significant levels of lung cancer beyond that of the general population, among 6,000 asbestos workers from the two largest mines in Quebec. The Braum and Truan study was flawed. It included some miners whose first exposure to asbestos had occurred only five years earlier. As part of the study, the miners were followed for six years, but since the latent period for lung cancer is usually more than twenty years, the inclusion of the miners with more recent exposures minimized the relative risk. This error resulted in a relative risk for lung cancer of only 1.S. Asbestos is now, of course, recognized as one of the worst industrial carcinogens, although the latency period involved may be as long as 20 to 30 years. The 1958 Braum and Truan study was not an isolated incident in the recent history of the asbestos industry in Canada and the United States. In 1978 a Toronto Globe and Mail story revealed that documents have come to light which indicate that U.S. asbestos companies and their Canadian subsidiaries may have withheld from thousands of workers evidence of the potentially deadly effects of asbestos exposure. The documents included a 1949 report by a Hernberg shows that it is extremely easy to medical officer for 3ohns.Manville Canada come up with falsely negative results in Incorporated in Asbestos, Quebec. The medical epidemiological studies in occupational health- officer who did the report for 3ohns-Manville that is, to create the impression that workplace was Kenneth Wallace Smith, now dead. In 1976, carcinogens (or other chemicals) are not Dr. Smith filed two depositions, in Louisville, Ky. contributing unduly to the incidence of cancer and Pittsburgh, Penn. His 1949 report was (or other diseases). included in one. Dr. Smith revealed he discussed the potential danger of asbestos to workers Hernberg discusses some of the most common manufacturing asbestos products with 3ohns- causes for falsely negative results in Manville executives and spoke of their reaction, epidemiological, occupational health studies. which, according to the documents, was: "We These include: inappropriate design, crude know that we are producing disease in the measuring methods, inappropriate type of employees who manufacture these products..." examination, wrong categories of exposed Dr. Smith noted in his report that the disease workers, wrong choice of reference category, asbestosis was "irreversible and permanent" and insensitive or wrong statistical methods, and added "but as long as a man is not disabled it is incorrect interpretation of data. felt he should not be told of his condition so that he can live and work in peace and the company Under "wrong categories of exposed workers" are can benefit by his many years of experience." included studies in which the follow-up time is too short. Hernberg states: "If the follow-up The conflict of interest of the industrial time is too short when diseases with a long physician who must both protect the health of latency time are studied (for example, cancer)..., workers and minimize costs to the employer is the result can...be falsely negative." well illustrated by this quotation from the 1975 13 Report of the American Association for the traditional doctor-patient relationship, whereby Advancement of Science (AAAS) Committee on the doctor sees the patient as an isolated Scientific Freedom and Responsibility: "...the individual is provided by Dr. Irving J. Selikoff's company physicians who look after the workers discovery of asbestos as a causal agent in lung sometimes join their employers in minimizing the cancer and other lung diseases. It was by chance need for more rigorous standards of health that 17 men exposed to asbestos dust in the protection. This appears to be a clear abdication factory where they worked were referred to Dr. of the prime responsibility of physicians...to Selikoff. If these 17 individuals had gone to 17 place the health of the people for whom they are different lung specialists, none of the doctors, in responsible before all other considerations. looking at an isolated case, would have placed Obviously, a doctor who is paid by a commercial much importance on the workplace as a causal enterprise will find it very difficult to act factor. In fact, Dr. Selikoff himself was contrary to the policy of the company." "unconvinced" of the relationship between asbestos and lung cancer before seeing these 17 Another reason for the prevailing climate of victims. To put the same point another way, Dr. labour distrust of the profession of occupational Selikoff was alert enough and open-minded medicine is the sense that although the company enough to see the evidence when it presented doctor may be a qualified physician, he is not itself to him. necessarily fully qualified as an industrial physician or occupational medicine practitioner. Dr. Fraser Mustard, a well known Canadian occupational health physician, has stated: "The training of doctors only provides care to the ill rather than lengthening of life by improving health gained through a better environment." There is a shortage of qualified industrial physicians even in the United States. In Canada, the situation is much worse, due to the lack of medical training in this country for the specialty of industrial medicine. The traditional doctor-patient relationship in family-physician practice, whereby the physician sees a worker in the setting of the doctor's office, divorced from the worker's place of work, But again, I must admit that the family physician is another factor in workers' distrust of the is all too often at a loss - through no fault of his medical profession - or at least their skepticism own but through a lack of training -when it of the physician's insight into the causes of comes to occupational health. Similarly, the diseases which may be contracted in the worker-as-patient is all too often caught in a workplace. In this context, then, the doctor is a dilemma. Should he rely on the plant doctor, family physician, rather than a plant doctor. who may be knowledgeable in the industrial Perhaps the patient has bronchitis or health problems but who works for the company; emphysema. The physican may attribute the or should he rely on his own family physician who patient's condition to smoking (a frequent cause, may be sympathetic but not knowledgeable in of course) and may advise the patient to quit occupational health matters? One potential smoking. The major cause- of his condition could solution to the problem which I would like to see be the smoke, dust and fumes the worker inhales employed more often would be a more open line continually at his place of work, but the family of communication between family physicians and physician may perhaps ignore this factor. government occupational health departments. A call from the family physician to a government In the seventeenth century, Bernardino occupational health physician or toxicologist Ramazzini, known as the father of industrial could provide needed information on known links medicine, always asked a patient what between certain occupations and certain occupation he followed - and advised other diseases, or between industrial chemicals and physicians to do the same. This important diseases. question is not always asked by physicians today, or if it is, the physician may not know the In conclusion, workers have many good reasons significance of the patient's reply. for concern and skepticism regarding the role of the industrial physician. Besides the problems I Another illustration of the limitations of the have already dealt with, there are a number of 14 other related concerns: the conflict in the A major part of the work of the dedicated plant United States over worker access to medical doctor, and even of the physician who may act as records; the "locating out" role of some plant a plant doctor or occupational physician only on doctors, whereby workers are weeded out on the a part-time basis, must be prevention. Perhaps basis of their health; the pre-employment in the future more prevention of occupational medical as a screening device; the "certificate of diseases will come about - but only if there is fitness" used for similar purposes; the protection more education and awareness of this aspect of of the company from raised assessments due to occupational health. Physicians as a group can Workers' Compensation claims - all of these do much to educate future doctors by calling for lead workers to believe that the plant doctor is undergraduate and graduate training in more interested in protecting the company that occupational medicine. in their health and welfare. Finally, let me say that it is my fondest wish At the same time, on the positive side - that the profession of occupational medicine will although workers will no doubt continue for some continue to develop and to become fully time to be somewhat distrustful of the medical accepted as a medical specialty, and that a profession as a whole, they will nevertheless be productive dialogue will grow between the especially grateful to and respectful towards profession, government administrators of those who have worked unstintingly on workers' occupational health legislation and regulations, behalf in the field of occupational medicine and and - most importantly - workers. the prevention of occupational disease.
Letters
-iv..-* tDear EverybodYb Your last issue was terrific! Can I get the othS Y u ho al be ost reen 04 94 IWW U SO -°gaTUa ism 0 Lprece(ieci lt7 hould-ll bew conatL byalmat mothe fner qualitY of th~[ret ntees t Marsha Love, was read wihgetitrStppobyAdvisors and Brooklyn, New York this office, both SpotSaf 1180 CWA Local Cheers, 3udith C. Lee, Workers' Adviser Compensation Advisory ServicesSrie of the Ministry of Labour, .C
You're Centre IJ.^al 01pubCE
15 "A Fact Sheet . Part I
Since the 18th century discovery of scrotal cancer among British chimney sweeps. occupational cancers have claimed an ever-increasing number of victims. So widespread is cancer today that one out of four Americans will eventually develop some form of can- cer. And one out of every five Ameri- SOME CHEMITCALS THAT CAUSE cans will die from cancer. SKIN CANCER Of course not all cancers arise from Coal tat and Petroleum oils and job exposures. There are many other derivative derivative fractions factors influencing cancer development. fraction Tar Some are peculiar to the individual Pitch Asphalt such as cigarette smoking, heredity and Aphat Carbon black diet: others are such external agents as Cresote oil Diesel oil contaminated drinking water, impure Anthracene oil Grease foods and air pollution. Soot Cutting oil, Lamp black machine oil In fact, these environmental pollu- Ugnite Wax paraffin oil tants are now thought to cause from Tar Methylated 73 to 85 percent of all human cancers. Oil naphthalene The proliferation of synthetic chemicals Wax araffins during the past few decades accounts Shale oil and Arsenic for a iarge proportion of cancer-causing wax Ultraviolet light substances in the environment. Hydrogenated Sunlight Since industry is the single largest col oil and tar X-rays contributor to environmental pollution, Froum"Wor Is anrous To Your H1a9th," S3lm.n it follows that attempts at cancer pre- vention in the workplace will help pre- vent cancer in the community. For the workplace is not an island to itself and the occupational carcinogen inevitably becomes the environmental carcinogen. This is the first of two articles deal- ing with cancer in the workplace. This month will feature a general discussion of cancer and the more common occu- pational cancers. Detection and preven- tion will be discussed next month.
FIVE YEAR CANCER SURVIVAL RATES* FOR SELECTED SITES The chart shows the cure rates for selected concers. Cancer cures are do- 0 20 40 60 80 100 fined as survival five years after diagnosis and treatment of the can- BLADDER As can 7.1% cor. be soen from the chart, oearly detection of a cancer dra. 79LARYNX matically improves one's chances of LARYNX _ survival. Regional involvemont or . ! | metastasis maakes treatment difficult LUNG 33 since the cancer has become so dif- LUNG j fue L. LOCALIZE. R(G0At. iNvOILV(YEct 'AOJUSTEO fOR NORMAL L!0F EXPfCTC?AC SOURCE tP40ESU?TS CGOl^. 'TON4AI. CAKFC£ ^,s'"'9J0540
16 What Is Cancer? A cancer or malignant tumor is a The skin, lungs, bladder and blood- group of abnormal cells that arise with- forming system are the most common out obvious cause from existing cell sites for occupational cancers to occur tissue and which have unlimited poten- since these are the places where the tial for growth, both locally and carcinogen acts most intensely. throughout the bodily system. In short, cancers are cells gone wild. Occupational cancers usually develop from prolonged exposure to a carcino- Although cancers are the second gen. However, only a few months of leading cause of death in the United exposure to such a deadly substance as States, little is known about the mech- asbestos has caused cancer deaths many anisms of cancer development years later. Cancer begins as a localized disease So there are no hard and fast rules and typically originates on the surface on length of exposure necessary for a or epithelium of tissues such as the carcinogen to become effective. Gen- skin. the lining of the bronchial tube, erally. occupational cancers undergo a intestines or bladder. After a time, the latency period which may last any- cancer cells penetrate the epitheliurn where from four to forty years with and invade underlying tissues where the average being 15 years. the growth continues. If not caught at this point. the cancer cells begin to This latency period is the time span spread from the originating site through between initial exposure to the car- the bloodstream or lymphatic system cinogen and the appearance of the can- into other parts of the body, a phenom- cer. Since there will be few, if any enon called metastasis. symptoms of the cancer during this Why some abnormal growvths remain period, the worker can easily be lulled benign (mild) while others spread, be- into a false sense of security as to his come malignant and ultimately fatal, or her health and working conditions. is largely a matter of speculation. Re- Workers should therefore make a point searchers have looked for a human of knowing any potential cancer haz- cancer virus but with no luck so far. ards they might face on the job. Others speculate that cancer is the There has been much controversy, final outcome of cell mutations that usually by industry groups, on the occur several times in a lifetime, muta- necessity of establishing a "safe" or tions that make one progressively more "acceptable" level for occupational car- susceptible to cancer development. cinogens. The evidence thus far indi- Still another theory is that the body's cates that there is no way of accurately immune system acts as a kind of stim- determining a "safe dose" for a car- ulant to the growth of cancer cells. cinogen. But until the theories become facts. the likelihood of a cancer cure remains Rather, these substances are so remote. lt seems imperative. therefore, deadly in such small quantities that a to zero tolerance level is the only way to zero in on those cancers about which insure that workers will be protected some derinitive facts are known. from the threat of cancer. Anything other than a "no detectable level" rep- Occupational Cancers recents a compromise that jeopardizes Occupational cancers are those in- the worker and negates his or her right duced by specific chemical or physical to a safe and healthful workplace. cancer-causing substances (carcino- Following are some facts about can- gens) encountered on the job as part cers that are associated with occupa- of the normal working environment tional exposures:
17 Lung Cancer Cancer of -the Skin Lung cancer, the No. 1 cause of all male cancer deaths. usually begins in the bronchial mucus Skin cancers are caused membrane or the bottom of the trachea (wind- by lengthy pipe). From there it spreads throughout the lungs exposure (20-30 years) to certain chemicals, sunlight and other sources and metastasizes to regional lymph nodes and to of distant parts of the body such as the brain and radiation. Skin cancers generally adrenal glands. start out as a wart or sore that doesn't heal. Areas likely to be affected by skin A person can have lung cancer for as long as cancers are those in immediate contact two years before noticing any symptoms. lVhen with the irritant. i.e., the hands, arms, symptoms do develop, they are often similar to legs and the scrotum in males. those of other respiratory diseases such as asthma, pneumonia and acute respiratory infections. As a While skin cancers are the most result, many people will put off seeing a doctor widespread of all cancers. they are also until the symptons have lingered for awhile. And most responsive to treatment and are when medical assistance is sought, the physician rarely fatal. may at first try to clear up the symptoms with antibiotics. So it is entirely and tragically possible In normal skin the epidermis or that three years can lapse before the epi- lung cancer thelium of the skin consists ot a sheet diagnosis is made. Tragic because once the cancer of cells five to ten cells deep which becomes symptomatic, the prospect of a cure is overlavs the dim. deeper, supporting skin layer, the dermis. The epidermis is in a One's chances of a cure also depends on the constant process of renewal. This is type of lung cancer present. Cancers are usually done through cells dividing in the oasal categorized by the type of cells involved. For in- layer of cells, those next to the aermis. stance, oat cell or small cell undifferentiated lung As the cells divide, are cancer, once thought to be associated they pushed solely with up out of the basal start to dif- cigarette smoking, divides and so layer, spreads rapidly ferentiate or change form, and. by the that it is difficult to catch it in time for a cure. time the cells reach the skin However, squamous cell surface, lung cancer, also associ- they fuse into or ated with cigarette smoking, in which the cells do flakes squames. These squames are subsequently shed from differentiate normally, offers the best chance of the skin surface. survival. One type of lung cancer, mesothelioma (cancer of the chest cavity), is caused exclusively Skin cancers disrupt this orderly by exposure to asbestos and is almost always fatal. progression of cell division and differ- entiation. two It is universally accepted that cigarette The common skin can- smoking cers are basal cell and sQuamous cell. greatly enhances one's risk of lung cancer any- In basal cell skin cancer, cells keep where from ten to 50 fold. However, some scien- and tists believe the "cigarette of dividing multiplving and do not theory" lung cancer differentiate. Rather, the cells invade overstates and oversimplifies the role of cigarettes the dermis and in lung cancer development. the sole underlyina tissues. The Placing blame result is an erosive of on cigarettes for the phenomenal rise of type ulcer but lung one which almost never cancer in the twentieth spreads or century has led to a dan- metastasizes to other ot gerous neglect of investigation into the role of parts the body. occupational and environmental respiratorv car- Squamous cell skin cancer is abnor- cinogens in lung cancer development. mal cell growth that differentiates to form For there are many squames nornally and is less in- industrial substances that vasive of cause increased incidence of lung cancer, indepen- underlying tissues than is basal cancer. dent of one's smoking habits. Among the workers cell However, squamous cell cancers at risk are those exposed to the following sub- can occasionally spread to stances: asbestos, chromates, arsenic, bis-chloro- distant sites of the body. methyl ether, coal combustion by-products, nickel, Some of the more common industrial iron oxide and certain petroleum distillates. One chemicals that can cause skin cancer study showed that uranium miners had an inci- are listed in the table. dence of oat cell lung cancer 24 times greater than the normal population. And coke oven workers are seven to ten times as likely to develop lung cancer as the general working population.
18 Bladder Cancer Occupational bladder tumors are As with lung cancers. bladder tumors caused by absorption or inhalation of may be far advanced before symptoms certain organic chemicals in the class of show up. Bladder cancers start as a aromatic amines. These chemicals are wart in the bladder lining. Initial symp- used primarily in the dyestuffs and toms are an inability or difficulty with rubber industries but cancer-causing passing urine or the presence of blood amines are also used in textile dyeing in the urine. and printing, in the manufacture of an- tioxidants and as laboratory reagents. Urinalysis to identify tumor cells which have scaled off into the urine is The carcinogenic amines are: benzi- the usual medical exam for bladder dine, 2-acetylaminofluorene, 4-amino- cancer detection. For currently exposed diphenyl, dichlorobenzidine, 4-nitro- workers as well as those exposed in the disphenyl and beta-napththylamine. All past. this urinalysis should be done on of these chemicals are covered by the a regular six-month basis. OSHA Carcinogens Standard. The stan- dard sets down strict work practices Bladder tumors are generally treated and engineering controls, but fails to by surgical removal of the tumor. After set a performance standard by which treatment, it is essential to continue the effectiveness of these controls can follow-up examinations because blad- be gauged. der tumors are prone to recur.
Adopted from an OCAIV publicatioi- DI S BY: 4'INTERNATIONAL CHEMICAL WORKRSUNION 1655 Vvest Market Street. Akron Ohio *-31-
19 LOHP Monitor Jan/Feb 1980 Epidemic Proportions Black Workers and Cancer
by Andrew Rowland Cancer rates in the Black community have been rising drastically since the 1940's. This article will examine the possibility that a significant proportion of Black cancer incidences today are related to occupational exposures of twenty or thirty years ago. THE RISE OF CANCER IN THE BLACK COMMUNITY In the early 1930's, many people thought that cancer was primarily a "white disease." At that time, the inci- dence of almost every type of cancer, including lung cancer, was very low for Black Americans. Then, sometime in (Photo: Andrew Rowland.) the late 1930's and 1940's, a dramatic These "environmental contaminants" and bricklayers before they left the reversal in these trends took place. have increased the rate of cancer South. Black Americans began to get cancer at among all Americans, including Because World War I disrupted the a faster rate than white Americans. In Blacks, during the past thirty years. flow of cheap, immigrant labor, in- a twenty-year period between 1935 and But if all of us are exposed to these dustries such as steel and auto, that 1955, Black male cancer incidence rates environmental contaminants, why has had employed White ethnic immigrants passed White male cancer rates for the incidence of cancer among Blacks to fill their hardest and dirtiest jobs, cancer amont Blacks cannot be ex- increased out of proportion to the in- now recruited Southern Blacks. In plained as genetic in origin because crease among the general American many instances, white workers who females passed White females in their population? There is evidence that the had more job opportunities available incidence rate for cancer of the answer to this question can be found to them, refused to take the hottest, esophagus, stomach, pancreas, colon, by examining the types of jobs Blacks dirtiest, most unpleasant jobs. This and lung. held when they first entered the in- caused one Black worker, interviewed Today, the overall cancer rates are dustrial workforce. in the 1930's, to say, "A Negro's job is higher among Black Americans than any job that the white man cannot among Whites. Lung cancer in partic- stand. ' ' ular has hit the Black population in But Black workers were not happy near epidemic proportions. The death BLACKS ENTER INDUSTRY with these job assignments. Some even rate from lung cancer among Blacks suspected that these jobs might be kill- today is about twenty times what it was In 1910, most Black Americans lived ing them. As one Black steelworker forty years ago. in the rural South and made their living assigned to the coke ovens in the 1930's These trends have given scientists doing some sort of agricultural work- said, "Because this work is so hard on some important information about the as field hands, tenant farmers, or men, I think that is why you find the nature of cancer itself. High rates of sharecroppers. Between 1910 and 1960, death rate among Colored so high." cancer among Blacks casnnot be ex- a major shift took place in the U.S. Many of these hot, unpleasant, dirty plaind as genetic in origin because Black population. Over 4.5 million jobs also exposed Blacks to chemicals cancer was so uncommon among Blacks left the South during these and physical agents that scientists now Blacks before 1935. So investigators years. For the most part, they settled in know or suspect cause cancer. The have had to look for other factors. the highly industrialized, urban centers combination of large numbers of Most scientists now agree that cancer is of the North. Blacks in jobs using or producing car- caused mainly by exposures to specific In the North, most of these Black cinogens plus long working hours chemicals or physical agents (such as migrants could only find employment could certainly account for the radiation) which are present in the as unskilled laborers, personal service disproportionate rise in cancer rates environment-that is, in the air, in the workers, or factory workers. This was among Blacks after 1935. (In the water, in food (for example, as addi- true even for the many Black skilled 1920's, '30's, and '40's, Blacks worked tives or pesticide residues), in certain workers who had worked as car- close to 60-hour work weeks in many medical drugs, at home, and at work. penters, blacksmiths, seamstresses, industries.)
20 In addition, the reversal in White Chemical. Black workers were often The extent of exposures faced by and Black cancer incidence rates began hired as laborers in the chemical in- Black workers between 1910 and 1960 about twenty years after Black workers dustry. In some parts of the country, is, at present, unknown. Therefore the first entered the urban labor market at the chemical industry relied almost en- extent to which the Black cancer the end of World War I. For most tirely on nonwhite workers for these epidemic is due to work exposures is forms of cancer, there is a twenty- to jobs. For example, in 1940 almost also impossible to assess. Although thirty-year "lag" period between ex- three-fourths of all laborer jobs in many of these jobs have improved, and posure to cancer-causing agents and Southern chemical plants were held by the average American work week is onset of the disease. This is exactly Blacks. Because the chemical industry shorter (thereby reducing exposure what happened! has always been so diversified, it is dif- risks), Blacks continue to fill a fi'cult to determine what types of ex- disproportionate number of the dirt- posures these workers incurred. Never- iest, lowest paying, and most danger- INDUSTRY CASE theless, recent studies linking organic ous jobs in American industry today. EXAMPLES solvents such as benzene and certain And, in spite of government regula- agricultural pesticides with cancer tions, potentially cancer-causing chemicals are still introduced in- The following industry case ex- underscore the importance of deter- being mining chIcals to the workplace in ever-increasing amples probably touch on only a smail exactly which these workers were exposed to. numbers each year. percentage of the carcinogens to which Blacks were habitually exposed during the 1920's, '30's, and '40's. But they Tobacco. The tobacco industry, IMPLICATIONS FOR vividly illustrate the potential cause which is very old in this country, has RESEARCH AND and effect relationship between occu- depended almost entirely on Black OTHER ACTION pational exosure and rising cancer in- labor for many parts of the production cidence among Blacks after 1935 and process. Even today, it employs a This article presents a hypothesis into the present. higher percentage of Black workers that the increase in cancer in the Black Auto. So many Black automobile than any other American industry. community is based to a significant ex- workers were hired in the foundry that During the '30's and '40's, Black tent on Blacks' exposures to carcin- it became known as the "Black Depart- workers, mostly women, worked in the ogens on the job when they first ment." One author describing the auto very dusty stemming areas where entered the industrial workforce in industry in the 1940's wrote, "One can tobacco leaves were separated from the large numbers. Until research is done be quite certain that an automobile stems. Until the mid-1940's, tobacco that proves whether the number of plant employing a sizeable proportion leaves were treated regularly with workers exposed to carcinogens during of Negro laborers includes a foundry arseic- now proven to be a powerful this period was as large as this article department." A recent foundry study skin and lung carcinogen. suggests, the hypothesis will remain reported sharp increases in cancer unproven. Conclusive proof can only deaths for workers employed in the Wood products. Blacks have tradi- come through a large-scale research 1930's: those employed for five years tionally been hired in logging (a project that documents how many prior to 1938 had two times the ex- notoriously dangerous occupation), as Black workers were exposed to carcin- pected number of deaths due to operatives in lumber mills, and to some ogens on the job during these years and digestive and respiratory (lung) extent as laborers and operatives in the how extensive their exposures were. cancers. furniture industry, particularly in the Until that research is done, the pos- South. Recent studies of these occupa- sibility that there is such a connection Steel. During these years, the most tions have caused researchers to sus- carries with it the foilowing implications common job for Black workers was as pect that wood dust in itself may cause for the occupational health community: a laborer in the coke oven department. cancer. In addition, lumber that is used community: A recent study shows that coke oven outside is often treated with arsenic, workers have a risk of developing lung exposing Black workers in wood preserv- Scientists: Scientists are now in a cancer of between 2.5 and ten times ing plants as well as in construction. position to find out more about the that of other steel workers, depending Laundry and dry cleaning. Laundry nature of cancer itself by exploring the on the amount of coke oven emissions work is another occupation where con- extent to which Black cancer rates re- to which they were exposed. ditions are hot and damp. In the flect occupational exposures. If further 1940's, many Black workers were hired research confirms a close relationship, Shipyards. For most of the years be- into dry cleaning jobs during a period the now accepted belief that occupa- tween World Wars I and II, Black of rapid growth. A recent study of tional cancers make up only a few per- workers were excluded from working laundry and dry cleaning workers cent of all cancers will be disproved. in the shipbuilding and repair indus- showed increased rates of cancer of the tries. But when a labor shortage lung, cervix, blood, and liver, possibly Government. Despite large amounts developed in World War II shipyards, due to exposure to dry cleaning of government money poured into Blacks were hired in record numbers. solvents such as tetrachloroethylene the"War on Cancer," very little Recently, researchers have proven con- ("perc"), carbon tetrachloride (used research has been done to determine clusively that all World War II extensively until recently, when it was the causes of increased cancer in- shipyard workers are at serious risk of banned due to its severe liver effects cidences among Blacks. Our govern- developing lung and other cancers and cancer-causing potential), and ment has a responsibility to the Black from asbestos exposure. trichloroethylene. 21 BLACK WORKERS workers who are identified can then be Management. The rise in cancer continued from P.15 encouraged to seek regular medical among Black workers should cause examinations in order to catch any management to re-evaluate whether community to pay more attention to cancers as they develop. Additionally, they have done everything possible to this problem and to back it with these workers need to be counseled on protect workers from exposure to car- research dollars. In addition, should a their right to receive disability and cinogens on the job. Particular atten- close connection between Black work workers' compensation benefits. tion needs to be paid to those tradi- exposures and increased cancer inci- tionally "hot, dirty, and unpleasant dences be confirmed, this poses a clear Labor Unions. As new links are jobs" that have changed very little in requirement for more emphatic en- made between cancer and the jobs the last fifty years, especially in indus- forcement and regulation of envi- traditionally held by Blacks, labor tries that are not unionized. In most ronmental (including occupational) unions might want to consider whether cases, the technology now exists to pro- carcinogens. minority workers they represent are tect workers from exposure to cancer- Medical Personnel, Health still working in the most dangerous causing substances. Educators, Community Workers. A jobs. If so, an assessment of the rela- major problem is identifying and tionship between job assignment and In summary, the rise in Black cancer informing workers who have been ex- discriminatory employment practices deaths can alert the occupational posed to carcinogens. The fact that would also be necessary. This type of heatlh community to the serious health many Black workers were often the last evaluation may disclose a need for tar- hazards Black and other minority hired and first fired (or laid off) means geting minority worker training pro- workers face. And the changes neces- that Black workers are likely to have grams, as well as special organizing sary to reduce Black worker exposure had more jobs (and more exposures to approaches to reach groups of un- to carcinogens on the job may be a step carcinogens) during their lifetimes than protected or uninformed minority toward cleaning up the workplace for other workers. Medical personnel, workers. all workers. health educators, and community workers need to become sensitized to these issues. They also need to be train- ed to take extensive work histories that will enable them to identify workers at risk of developing cancer. Exposed
0 1,0t
l l @O Industrial Relations, Nonprofit Org. U rty of CaUlofrnia U.S. Postage C _ter for Labor Rearch and Educatin P A I D 2521 Channing Way Berkeley, Calif. SWkeley. CA 94720 Permit No. 1 1 J~~~~~~~~~~~~~~
Addfess Correction Requested
22 '"Occupational Epidemiology"OIl, CiemicaI and Atomic Workers International Union
RECORDKEEPING A-MD CANCvR
Cancer is now one of the leading causes of death in the United States, killing close to 400,000 neople every year. It is common to hear that most cases of cancer are due to personal lifestyle factors, such as cigarette smoking or diet. But we know that there are literally hundreds of cancer-causing sub- stances in wQrkplaces around the country. Asbestos workers, uranium miners, dye-makers, coke-oven workers -- all have been proven to have higher rates of cancer than they should, were it not for their exoosure to knowr! carcinogens at work. Refinery workers also have a higher percentage of deaths due to cancer than is found in the general population, but it is not known exactly what the cause of this increase is. How have w > learned of these relationships between occupation and cancer? Generally, this knowledge has been gained through the use of enidemiology - the study of epidemics. Basically, epidemiology is the fancy name for comparing diseases in different grouns of people, and looking for clues about why the rates of disease in the two groups might be different. In some cases, the answers seem fairly clear: suppose your local union hosted a barbecue. The next day, half of the people get a stomach illness. Your investigation indicates that all of the people who got ill had eaten the chicken salad at the barbecue. No one who stayed well had eaten the chicken salad. Common sense tells you there might have been something wrong with the chicken salad that made people get sick. Most of the time the relationship between different ty_pes of exposure and illness is more complicated. An epidemiologic study requires piecing together many bits of evidence ant. znalyzing them carefully. Keep in mind that an epidemiologic study talks about why grours of people are at increased risk for aetting a disease. Which doesn't mean that everyone with the same exposure will necessarily get the same disease. For example, those who do smoke
23 cigarettes are more likely to develop heart disease. But as you've observed, not everyone who smokes more than a pack a day gets heart disease. But, it is still true that if everyone stopped smoking, there would be less heart disease. The same is true of asbestos exposure and lung cancer. The study of cancer in the workplace is difficult for several reasons. First, cancer is a chronic disease. Unlike food poisoning, it takes many, many years for a cancer to show up after exposures to the factor that initiates the cancer process. This time, called the latency period, averages from 15 to 40 years. Wlhat this means is that it is hard to look backward in time to identify the various types of exposures of a worker that may have been responsible for causing the cancer. Or, if you decide to look at a group of workers who have certain kn4own exposures, it means you'd have to wait a very long time before you would see- cancer cases develop. Another problem in occupational epidemiology is that most workers have exposures to more than one chemical. Therefore, it may be very difficult to sort out which narticular substance is in fact responsible for a higher rate of disease in a particular worksite. On the other hand, the same disease may have more than one chemical cause. Lung cancer mav be caused by asbestos, BCME, cigarette smoke, radon gas, or many other substances. And to make things even more complicated, exposure to two cancer-causing chemicals at the same time may greatly increase the risk of getting cancer - asbestos and smoking .being the best known examples. How do epidemiologists try to sort all of this out? There are essentially two different kinds of epidemiological studies. The "nrospective" study starts with a group of exposed workers and follows them over time to see what types of ilness they develop. The biggest advantage of this sort of study is that it allows the scientist to keep good track of the types of exposures. The dis- advantage is that prospective studies take years and years before the results are in, and people may continue to be exposed toxic substances in the meantime. A retrospective study, on the other hand, starts with a groun of people who have a particular disease and then analyzes the past histories of thq.ese people to see if there are differences in their casts from individuals who do not have the disease. This type of study is easier and quicker, but, as mentioned above, it may he very hard to figure out wl-%= the exposures really were so long ago. One basic proble;t. v ith epidemiology is that it looks at disease after it has happened. Some have called it the "body in the morgue" approach. Unions and workers' scientific friends have
24 been pushing to base stronger regulations of cancer causing substances on the results of animal and short term laboratory testing. That way we won't have to wait for the "proof" in human suffering. Until this happens, and even when it does, it will still be important to keep records and analyze them for other in- dication of relationships of work to disease. Some chemicals will not show their ability to cause cancer in laboratory testing, for example arsenic. Epidemiology then is one important way to demonstrate human occupationally caused illness. It may be useful in pushing for changes that at least will protect future generations of workers, or may help in fighting for adequate compensation for those who have already become ill. Sometimes epidemiology is frustrating because it give us only partial answers. For example the OCAW narticipated in a study that showed that more refinery workers do have cancer than others in the same communities, but we don't know exactly what exposure is causing this. Therefore, it is hard to know what changes need to be made to protect workers. At least, we helped start the process that will keep looking at this situation, instead of allowing the scientific world to shut its eyes to this concern. Also, sometimes an effect of a chemical can't be seen unless we look at a large group of exposed workers. In these cases our continuing suspicions may lead to several groups pooling information before it is possible to prove or disprove our fears. All types of epidemiologic studies rely on exactly the same types of information. Because companies have not been overly anxious to open their records to research, many of these studies have been based on union records of death benefits, bibles. etc. Usually too, it has been workers who have noticed the first clues of relationships between the job and their health. These clues then stimulated the interest of researchers to begin an occupational epidemiology study. With thousand of chemicals in use in US industry, and hundreds of different occupations, epidemiologists will have to rely on the workers for the clues to which chemicals, which work situations to look at first. These are the reasons that it is important that Local Unions begin to keep records. The more information you have, the more may be learned from them. The arnidemiology study will attempt to document your suspicions and answer WHY. Your local need to collect the information on WHO?, WHAT?, WHENM?, and WH?ERE?RE fol.lovoing is an explanation of the details of what you need to rp"ord. Each year you should send in your records for the Health ai4 oafety Department to review for any trends that might exist. It may be easiest to record this information only for active members of the local. But your recordkeeping will be much more
25 valuable if you also include retirees - after all, cancer is a disease of older people, and many people with work-related cancer do not learn of their illness until after retirement. Keep in touch through your retirees club, or look at pension records, or watch the obituary column of your local newspaper for news of deaths in retirees. WHO? Obviously, the first step is to identify the group of people you are interested in. Name Date of Birth Sex.. Race These items are all important because the expected rates of cancer vary in different age, sex, and racial groups. Since eoidemiology relies on comparisons between groups, it is necessary to control for these factors. Social Security : Important not only as a positive identifier, but also in obtaining a death certificate.
WHAT? Next, it helps to narrow down the type of disease. A group of workers may have an average rate of cancers if you lump all types of cancer together, but an unusually high rate of a particular type of cancer - for example, leukemia resulting from exposure to benzene. Location of cancer: breast? brain? lungs? etc. Type of cancer: most people will be told a specific type of cancer by their doctor: CEX: malignant melanoma, small-cell, lymphocytic leukemia, etc.)
WSHEN? Date of diagnosis: rates of disease are usually calculated on the basis of a particular time period, so it is. important to know when cancer was diagnosed. Date of death (if applicable): you should also make a note of place of death in order to make it easier to obtain a death certificate. Date of employment: tai.? is very important, because it tells us how long someone -has been exposed to various substances; in some cases, it tells us that a worker may have had exposure to a substance no
26 longer used in the plant.
WHERE?. This information may help identify a particular group of workers with a problem - for example, lung cancer may be showing up at a high rate in maintenance workers with a lot of asbestos exposure. Job classification (welder, pipefitter, operator, lab worker) Plant department (cat cracker, warehouse. etc) Many people change jobs several times during the course of their work for one company. If you can, you should write down not only the current or last job for each person on your list, but also expand this section to include a complete job history, listing nuer of years spent at each location. This section will also be much more valuable if your local keeps a separate file on exposures, with records of all information you have obtained from the company on the type of exposures in different parts of the plant. For each entry in your "'Cancer registry", you should make a note of the source of your information, so that if it is determined that a more in-depth investigation needs to be done, the Health and Safety Department will have a head start on finding more detailed information. Because cancer is not a common disease (even though it is a leading cause of death), it is unlikely that you will be adding names to your registry very quickly. If you are concerned that there have been more cancer deaths than there should be over the past several years, you may want to go backward in time and try to expand your list to previous years, using pension records, disability logs, etc. There is some other basic information that will be very helpful in trving to analyze the data in your cancer registry. You should try to collect this information about once a year, and send it in to the Health and Safety Department with your list: How many people in your local? How many people in each bargaining unit? In each department? What is the general breakdown of your local by age? sex? race? Again, this information is helpful in tryinasco determine rates of disease that would be expected in a ncr.al population without the type of exposures you have in the workplace.
27 Name Date of Birth (if this is unavailable, age) Race (this is important because cancer rates sometimes vary in different racial groups) Sex ( n ) Social Security Number (if available) Job Classification Job Department Date of Employment Location of Cancer (breast, brain, etc.) Type of Cancer (small cell, melanoma, etc.) Date of diagnosis Date of death (if applicable) Place of death Source of Information
The form above is oriented toward keeping track of cancer in your shop. You can use the same principles to look at any disease or symptoms, any group of workers, or any one part of your plant that may concern you. If you want more help on adapting recordkeeping for problems other than cancer, ask the Health and Safety Department for advise.
28 "CIp 3ulletin #3 September, 1978
THE AMES SALMONELLA MUTAGENESIS TEST
The Cancer Problem Nearly 700,000 Americans will find out in the next year that they have cancer. At present rates of incidence one in four Americans will develop cancer during their lifetime. Someone in two out of every three families is expected to be affected. The causes of cancer are varied and not well understood, but the World Health Organization estimates that between 75 and 85 percent of all cacners are brought on by environmental factors. The most important of these factors are chemical compounds, most or them organic, that is, containing the element carbon. About 63,000 distinct chemical compounds are in common use. Twenty-five of these have been shown to cause cancer, or are suspected of causing cancer, in people. Several hundred have been shown, in laboratory tests, to cause cancer in animals, raising the possibility that they might be dangerous to human beings. Thousands of chemicals remain to be tested, mainly because such animal tests are very costly and time-consuming. A comprehensive animal test of a single chemical costs $100,000 to $300,000 and takes from one to two years. Even in the face of a public outcry for more testing, it's doubtful that government or business has the money or could find the trained scientists and facilities to perform tests on all the chemicals now in use. For the past 20 years scientists have been looking for a quick, cheap way to detect cancer-causing substances. Animal tests are slow and expensive because large numbers of animals must be observed long enough to see whether they develop cancer. Fast tests are indirect. They look for some easily observed property which is well correlated with the substance's cancer-causing capability. The Ames Test Several short-term tests are based on the expectation that carcinogens are likely to induce inherent changes -- mutations -- in living cells. The most promising of these mutation tests was developed over the past 12 years by Dr. Bruce N. Ames and his colleagues at the University of California, Berkeley. This test measures the capability of a chemical substance to cause mutations in special strains of the bacterium Salmonella (best known as a cause of food poisoning). In the Ames test bacteria and the chemical being studied are placed in a conventional bacterial growth plate, provided with special nutrients and incubated. If the chemical is a mutagen, it will cause some of the bacteria to mutate and become genetically different from the original bacteria. Normally, it would be hard to detect such mutations, because they would get lost in the general bacterial growth. Ames developed forms of the bacteria which are genetically incapable of growing unless they are supplied with the amino acid histidine. The bacteria are applied to a plate which contains all their growth requirements except histidine. So, the bacteria do not grow. However, if the substance being tested mutates the bacteria, some of the mutated cells will be able to make their own histidine. These mutant bacteria then multiply, producing millions of cells which form a visible, round colony. Each such colony means that one of the original cells has mutated and has become capable of growing. In the test, after 48 hours of
29 incubation, the mutated colonies on each plate are counted and compared to control plates which did not receive any of the test chemical. If the plate which contains the chemical has significantly more bacterial colonies than the control plate, the chemical is mutagenic. Not only is the test quick, but it only costs a few hundred dollars per chemical tested. Reliability
Several hundred organic chemicals known to cause cancer in animals and a similar number which are known not to cause cancer have been studied with the Ames test. These studies show that if an organic chemical is positive in the Ames test, there is about a 90% probability that it also causes cancer in animals. With a slightly lower probability, it is found that a substance which is negative in the Ames test does not cause cancer in animals. Thus the test is an effective way to determine rapidly and at minimum cost whether or not a previously untested substance is likely to cause cancer. Hundreds of such tests of specific chemicals and complex environ- mental samples such as dust, water and food have been carried out in recent years, greatly expanding the list of suspected carcinogens. The idea that the Ames test can identify chemicals likely to cause cancer is not accepted by all scientists. Some argue that the process leading to a mutation in bacteria is not the same as that leading to cancer in humans. It is true that this theoretical relationship between mutagenesis and carcinogenesis is far from proven. However, the usefulness of the Ames test is not based on such a theoretical relationship but on its successful experimental record in identifying as mutagens chemicals which are already known to cause cancer in laboratory animals. The value of the Ames test was recently recognized by the Occupational Safety and Health Administration, when it proposed that evidence of cancer activity in one- species of animals and a positive result in the Ames test, when taken together, be grounds to initiate emergency action to reduce workplace exposures. The Ames test has already provided rapid warnings that a substance may cause cancer. For example, Japanese investigators showed that a substance widely used there to preserve foods was mutagenic in the Ames test. The Japanese government was urged to ban the use of the chemical (called AF-2) in foods. The government refused, but did carry out tests on laboratory animals. Two years later, it was established that the chemical causes cancer in laboratory animals and it was banned. In the same way, Ames' discovery that several hair dye constitutents are mutagenic was followed by the later discovery that at least one of these substances causes cancer in laboratory animals. Short term tests, like the Ames test, can therefore go a long way toward assessing the hazard from thousands of as yet untested substances. For More Information "Mutagenesis: A Probe for Carcinogenicity," Barry Commoner, Hospital Practice, March 1975, P. 43.
"Carcinogens are Mutagens: A Simple Test System Combining Liver Homogenates for Activation and Bacteria for Detection," Bruce N. Ames, et al, Proceedings of the National Academy of Sciences, U.S.A., Vol. 70, no. 8, PP. 2281-2285, August 1973.
30 "!Reliability of Bacterial Mutagenesis Techniques to Distinguish Carcinogenic and Noncarcinogenic Chemicals," Barry Commoner, et al, EPA Report No. EPA-600/ 1-76-022, available from the National Technical Information Service, 1976. "Detection of Carcinogens as Mutagens in the Salmonella/Microsome Test: Assay of 300 Chemicals," Joyce McCann, et al, Proceedings of the National Academy of Sciences, U.S.A., Vol. 72, no 12, p. 5135, 1975.
The aim of the Carcinogen Information Program is to provide the public with reliable, understandable information about the carcinogen problem. For a complete list of available bulletins, write to the Carcinogen Information Program at the address given below.
This article is a reprint The Carcinogen Information Program, Inc. from: P.O. Box 6057 St. Louis, Missouri 63139 CIP Bulletin, #3, September 1978
31 #6, March 1979
CARCINOGEN INFORMATION PROGRAM, INC. 0 CIP Bulletin P.O. BOX 6057, ST. LOUIS, MISSOURI 63139
ANIMAL TESTS
The Cancer Problem example, carcinogens often cause obvious genetic changes in bacteria, insects and Animal tests play an important role in plants. (For a description of one short- deciding whether a substance can cause term test, see CIP Bulletin #3, The Ames cancer in people. More than three-fourths Salmonella Mutagenesis test.) of all cancers are caused by environmental factors, like smoking, diet and occupa- Epidemiological surveys are the best evi- tional hazards. So scientists are using dence that a substance causes cancer in animal tests to assess the role of many people, but they are not perfect. Because chemicals in environmental cancer. cancer develops over a person's lifetime, exposure may go on for 20-30 years before Yet the validity of animal tests is often any effect is observpd in an epidemiological questioned. Critics argue that the high survey. Short-term tests are quick and doses used in animal tests are unrealistic. cheap, but they are also indirect, whereas (In the debate over saccharin critics claimed animal tests show directly that a substance that a person would have to drink 800 cans can cause cancer. of diet soft drink a day to get adose equiv- alent to the one received by animals.) Some- The Animal Test people even say that "everything" causes cancer, if the dose is large enough. Some The aim of an animal test is to determine critics complain that animals are different the effect of exposing the animal to a than people and that if one species of particular substance. So, the animals are animals gets cancer and one doesn't, scien- divided into two groups: one group is ex- tists worry about the animals that get posed to the substance (the "experimental" cancer. Critics also complain that anl group) and one isn't (the "control" group). tests are unrealistic because they do not Both groups live in the same environment. resemble human exposure to a substance. For statistical reasons about 500 animals Carcinogen Testing - are needed for a typical test. Mice, rats and hamsters are the most common test ani- Epidemiological studies and short-term mals. Not only are they easy to breed and tests, as well as animal tests, are used handle, but they are inexpensive and easy to detect carcinogens. An epidemiological to care for. Their lifespans are relatively study looks at a specific group of people short, and so it is possible to expose them who have been exposed to a substance, com- to the substance for most of their lives. pares those people to another group who Two,species of animals and both sexes are were not exposed to the-substance, and usually used to test a substance. Groups compares the number of cancer cases in each of at least 50 animals of one sex and group. Short-term -tests rely on specific species are used in both the experimental biological changes, other than cancer in- and control groups. The test animals are duction, but correlated with it. For normally exposed to the substance in a way
The aim of the Carcinogen Information Program is to provide the public with reliable, understandable information about the carcinogen problem. For a complete list of available bulletins, write to the Carcinogen Information Program at the address given above. 32 that most closely resbles human exposure: of the population. Yet cancer is thE second by feeding, inhalation or skin painting. leading cause of death. An increase in this At least two doses are used, the maximum incidence to two or three percent would be tolerated dose (the largest amount the catastrophic. And yet, it would be impos- animals can be exposed to without large sible for an animal test to detect an increase numbers of them dying) and either one-half in cancer incidence from one-half to three or one-quarter of the maximum tolerated dose. percent, unless thousands of animals were used. Instead, high doses of the substance Animals which die during the experiment are are used, causing cancer in 50 to 100 per- thoroughly examined for evidence of cancer. cint of the animals, instead of one or two At the end of the experiment the remaining percent. animals are killed and examed for signs of cancer. An animal test on a single sub- It is simply untrue that "everything" causes stance usually takes three and one-half cancer when taken in large enough doses. years and costs more than $250,000. If a substance cannot produce cancer, no dose-no matter how large--will produce can-' Interpreting Animal Tests cer in animalS. However, the most logical route of exposure may not allow enough of If the nuer of cancers in the experimental the substance to get into the animal's group is substantially greater the num- system. So scientists sometimes decide to ber in the control group, then the test sub- feed a substance to animals rather than stance is designated a carcinogen. If the apply it to their skin, or inject it rather nuer of cancers is greatest in the group than feed it. that received the highest dose, and smallest in the group exposed ta the smallest dose, The argument against the use of high doses this increases confidence in the conclusion often assumes that the human body can that the substance is a carcinogen. detoxify small amounts of a carcinogen. Yet small amounts of some well-studied One reason animal tests are used to decide carcinogens, asbestos and radiation, for whether a substance can cause cancer in example, do cause cancer. Until other evi- people is high correlation between the car- dence appears, exposure to small amounts of cinogenic effect of different chemicals on a carcinogen must be as a risk to people regarded and animals. One study reviewed 82 human health. Large doses also .compensate chemicals for which there is some evidence for the many different of human carcinogens the carcinogenicity. With one excep- average person is exposed to. While an tion, arsenic, all 82 have been shown to animal is exposed to one carcinogen, many cause cancer in aniimals. Moreover, at people face the cumulative, combined effects least six chemicals were shown to cause of many carcinogens. cancer in animals before epidemiological studies showed they cause cancer in people. Conclusion
The biological characteristics of human If a substance causes poputions are much more cancer in any labora- variable than tory animal it should be treated as a those of laboratory animals. One of these human carcinogen. biological characteristics is the amount of certain enzymes which convert carcinogens For More Information into their active forms. For example, rats have certain enzymes capable of converting Samuel S. 2-acetylaminofluorene Epstein, ThePnlitics of Cancer, (WAAF) into a carcino- San Francisco: Sierra Club Books, 1978, gen. So rats fed AAF develop cancer. Chapter 3, "The Animal Guinea pigs do not possess these enzymes. Experiment." So they are not affected-by AAF. Because the huma Thomas H. Maugh II, "Chemical Carcinogens: population is so variable, it The Scientific Basis- for Regulation," will probably contain some individuals Science., 1978. who react like one species, some who react Sept. 29, like the other and many who occupy the whole range in between. Barry Comner, "Saccharin and Cancer," The Washington Post, March 27, 1977. The incidence of cancer (the number of new @ CBNS, 1979. cases reported per year) in the United States is less than one-half of one percent 33 Adapted from IARC Monographs and HESIS Carcinogen Policy Statement
HUMAN AND ANIMAL CARCINOGENS
The following are lists of chemicals and industrial processes that have been found to have substantial evidence of carcinogenicity. Various agencies evaluate the avail- able evidence of carcinogenicity and make judgments on the "adequacy" of that evidence. The following lists of human and animal carcinogens have been compiled from two sources: the International Agency for Research on Cancer (IARC) and the National Cancer Institute (NCI). The Environmental Protection Agency (EPA) and OSHA lists can be found in other sections of this packet (Section 3). I. List 1: IARC- Summary Evaluation of Carcinogenic Risk to Humans from Chemicals The following list of chemicals have been evaluated as to their carcinogenic risk to humans, based on consideration of both the existing epidemiological and experimental evidence. The chemicals, groups of chemicals, industrial, process or occupational exposures were put into one of three groups:
Group 1 The chemical, group of chemicals, industrial process or occupational exposure is carcinogenic to humans. This category was used only when there was sufficient evidence from epidemiological studies to support a causal association between the exposure and cancer.
Group 2
The chemical, group of chemicals, industrial process or occupational exposure is probably carcinogenic to humans. This category includes exposures for which,at one extreme, the evidence of human carcinogenicity is almost sufficient, as well as exposures for which, at the other extreme, it is in- adequate. To reflect this range, the cate"ory was divided into higher (Group A) and lower (Group B) degrees of evidence. Usually, category 2A was re- served for exposures for which there was at least limited evidence of car- cinogenicity to humans. The data from studies in experimental animals played an important role in assigning studies to category 2, and particularly those in Group B; thus the combination of sufficient evidence in animals and inade- quate data in humans usually resulted in a classification of 2B. In some cases, the Working Group considered that the known chemical proper- ties of a compound and the results from short-term tests allowed its transfer from Group 3 to 2B or from Group 2B to 2A.
Group 3
The chemical, group of chemicals, industrial process or occupational ex- posure cannot be classified as to its carcinogenicity to humans.
34 List - 1: Summary Evaluation of Carcinogenic Risk to Humans From Chemicals, Industrial Processes, and Industries Based on Evidence for Carcinogenicity to Human and to Animals and for Activity in Short-term Tests. (from IARC Monographs, Vol. 1-29, Supplement 4, October 1982.)
Chemical, process Evidence for Evidence for Evidence for Summary or industry carcinogenicity carcinogenicity activity in evaluation in humans. in animals short-term of carcino- tests. genic risk to humans
Acrylonitrile limited sufficient sufficient 2A Actinomycin D inadequate limited sufficient 2B Adriamycin inadequate sufficient sufficient 2B Aflatoxins limited sufficient sufficient 2A Aldrin inadequate limited inadequate 3 4-Aminobiphenyl sufficient sufficient sufficient 1 Amitrcle inadequate sufficient inadequate 2B Anaesthetics, volatile inadequate inadequate inadequate 3 Analgesic mixtures containing phenacetin sufficient limited no data 1 Phenacetin limited sufficient limited 2A Aniline inadequate limited inadequate 3 Arsenic & certain arsenic compounds sufficient inadequate limited 1 Asbestos sufficient sufficient inadequate 1 Auramine (technical grade) limited limited sufficient 2B Manufacture of auramine sufficient 1 Azathioprine sufficient limited sufficient 1 Benzene sufficient limited limited 1 Benzidine sufficient sufficient sufficient Benzidine-based dyes 12 Direct Black 38 (technical grade) inadequate sufficient inadequate 2B Direct Blue 6 (technical grade) inadequate sufficient no data 2B Direct Brown 95 (technical grade) inadequate limited no data 2B Beryllium and beryllium compounds limited sufficient inadequate 2A N,N-Bis (2-chloro- ethyl)-2-naphtylamine (Chlomaphazine) sufficient limited limited 1 Bischloroethyl nitrosourea (BCNU) inadequate sufficient sufficient 2B Bis (chloromethyl) ether and technical- grade chloromethyl- methyl ether sufficient sufficient limited 1 Bleomycins inadequate inadequate sufficient 3 1, 4-Butanediol dimethanesulphonate (Myleran) sufficient limited sufficient 1
35 Chemical, process Evidence for Evidence for Evidence for Summary or industry carcinogenicity carcinogenicity activity in evaluation in humans in animals short-term of carcino- tests genic risk to humans
Cadmium and cadmium compounds limited sufficient inadequate 2B Carbon tetrachloride inadequate sufficient inadequate 2B Certain combined chemotherapy for lymphomas (including MOPP) sufficient inadequate 1 Chlorambucil sufficient sufficient sufficient 1 Chloramphenicol limited inadequate inadequate 2B Chlordane/Heptachlor inadequate limited inadequate 3 1-(2-Chloroethyl)- 3-cyclohexyl- 1-nitrosourea (CCNU) inadequate sufficient sufficient 2B Chlorinated toluenes (production of): Benzyl chloride inadequate limited sufficient 3 Benzol chloride inadequate inadequate inadequate 3 Benzal chloride inadequate limited limited 3 Benzotrichloride inadequate sufficient limited 2B Chloroform inadequate sufficient inadequate 2B Chlorophenols (occupational exposure to) limited 2B Chloroprene inadequate inadequate sufficient 3 Chromium and certain chromium compounds sufficient sufficient sufficient 1 (Cr V1) inadequate (Cr 111) Cisplatin inadequate limited sufficient 2B Clofibrate inadequate limited inadequate 3 Clomiphene inadequate inadequate no data 3 Cyclamates inadequate limited inadequate 3 Cyclophosphamide sufficient sufficient sufficient 1 2,4-D and esters (See also Phenoxy- acetic acid herbi- cides, occupational exposure to) inadequate inadequate inadequate 3 Dacarbazine inadequate sufficient limited 2B Dapsone inadequate limited inadequate 3 DDT inadequate sufficient inadequate 2B ortho-Dichloro- benzene and para- Dichlorobenzene inadequate inadequate inadequate 3 3,3-Dichlorobenzidine inadequate sufficient sufficient 2B Dichloromethane inadequate inadequate limited 3 Dieldrin inadequate limited inadequate 3 Diethyl sulphate limited sufficient sufficient 2A 3,3-Dimethoxy- benzidine (ortho- Dianisidine) inadequate sufficient limited 2B
36 Chemical, process Evidence for Evidence for Evidence for Summary or industry carcinogenicity carcinogenicity activity in evaluation in humans in animals short-term of carcino- tests genic risk to humans
Dimethylcarbamoyl chloride inadequate sufficient sufficient 2B Dimethyl sulphate inadequate sufficient sufficient 2A 1,4-Dioxane inadequate sufficient inadequate 2B Epichlorohydrin inadequate sufficient sufficient 2B Ethylene dibromide inadequate sufficient sufficient 2B Ethylene oxide inadequate limited sufficient 2B Ethylene thiourea inadequate sufficient limited 2B 5 -FluQrouracil inadequate inadequate limited 3 Formaldehyde (gas) inadequate sufficient sufficient 2B Hexachlorocyclohexane inadequate limited inadequate 3 Hydralazine inadequate limited sufficient 3 Hydrazine inadequate sufficient sufficient 2B Industries Boot & Shoe Manufacture and repair (certain occupations) sufficient 1 Carpentry & joinery (certain exposures) inadequate 3 Furniture manufacture sufficient 1 Leather goods manufact. inadequate 3 Leather tanning inadequate 3 Lumber & sawmill indus. inadequate 3 Pulp & paper manufact. (certain exposures) inadequate 3 Rubber industry (certain occupations) sufficient 1 Iron dextran complex inadequate sufficient inadequate Isonicotinic acid 3 hydrazide inadequate limited limited 3 Lead & lead compounds inadequate sufficient inadequate 3 (for some salts) Manufacture of isopropyl alcohol (strong-acid process) sufficient 1 Isopropyl oils inadequate inadequate no data 3 Manufacture of magenta limited 2A Magenta (technical grade) inadequate inadequate inadequate 3 Melphalan sufficient sufficient sufficient 1 6-Mercaptopurine inadequate inadequate sufficient 3 Methotrexate inadequate inadequate sufficient 3 Methoxsalen with ultraviolet A therapy (PUVA) sufficient sufficient sufficient 1 Metroindazole inadequate sufficient limited 2B Mustard gas sufficient limited sufficient 1 .1-Naphthylamine inadequate inadequate sufficient 3 2-Naphthylamine sufficient sufficient sufficient 1 Nickel refining sufficient 1 Nickel & certain nickel compounds limited sufficient inadequate 2A
37 Chemical, process Evidence for Evidence for Evidence for Summary or industry carcinogenicity carcinogenicity activity in evaluation in humans in animals short-term of carcino- tests genic risk to humans
Nitrogen mustard (See also Certain combined chemotherapy for lymphomas) i nadequate sufficient sufficient 2A Osterogens:and progestins, Combined oral contraceptives 1 imited inadequate 2A Sequential oral contraceptives 1;imited 2B Other oestrogen- progestin combinations i£nadequate 3 Conjugated oestrogens Siufficient inadequate inadequate 1 Oestrogens: Dienoestrol limited inadequate inadequate 2B Diethylstilboestrol sufficient sufficient inadequate 1 Ethinyloestradiol inadequate sufficient inadequate 2B Mestranol inadequate sufficient inadequate 2B Oestradiol-17B inadequate sufficient inadequate 2B Oestrone inadequate sufficient inadequate 2B Progestins: Chlormadinone acetate inadequate limited inadequate 3 Dimethisterone inadequate inadequate inadequate 3 Ethynodiol diacetate inadequate limited inadequate 3 17a-Hydroxyproges- terone caproate inadequate inadequate no data 3 Lynoestrenol inadequate inadequate inadequate 3 Medroxyprogesterone acetate inadequate limited inadequate 3 Megestrol acetate inadequate limited inadequate 3 Norethisterone inadequate sufficient inadequate 2B Norethynodrel inadequate limited inadequate 3 Norgestrel inadequate inadequate no data 3 Progesterone inadequate sufficient inadequate 2B Oxymetholone limited no data no data 2A Pentachlorophenol (See also Chlorophenols, occupational exposure to) inadequate inadequate inadequate 3 Phenazopyricine inadequate sufficient no data 2B Phenelzine inadequate limited inadequate 3 Phenobarbital inadequate limited inadequate 3 Phenoxyacetic acid herbicides (occupational exposure to) limited 2B Phenylbutazone inadequate no data inadequate 3 N-Phenyl-2-naphthylamine inadequate inadequate inadequate 3 Phenytoin limited limited inadequate 2B Polychlorinated biphenyls inadequate sufficient inadequate 2B
38 Chemical, process Evidence for Evidence for Evidence for Summary or industry Carcinogenicity carcinogenicity activity in evaluation in humans in animals short-term of carcino- tests genic risk to humans
Prednisone (See also Certain combined chemotherapy: for lymphomas) inadequate inadequate inadequate 3 Procarbazine (See also Certain combined chemotherapy for lymphomas) inadequate sufficient sufficient 2A Propylthiouracil inadequate sufficient no data 2B Reserpine inadequate limited inadequate 3 Saccharin inadequate limited inadequate 3 Soots, tars & oils sufficient sufficient 1 Benzo(a)pryene inadequate sufficient sufficient 2A Spironolactone inadequate limited no data 3 Styrene inadequate limited sufficient 3 Styrene oxide inadequate limited sufficient 3 Sulfafurazole inadequate inadequate inadequate 3 Sulfamethoxazole inadequate limited inadequate 3 2,4,5-T and esters (See also Phenoxyacetic acid herbicides, occu- pational exposure to) inadequate inadequate inadequate 3 Tetrachlorodibenzo-para- dioxin (TCDD) inadequate sufficient inadequate 2B Tetrachloroethylene inadequate limited inadequate 3 ortho-Toluidine inadequate sufficient sufficient 2A Treosulphan sufficient no data inadequate 1 Trichloroethylene inadequate limited inadequate 3 2,4,5-Trichlorophenol (See also Chlorophenols, occupational exposure to) inadequate inadequate no data 3 2,4,6-Trichlorophenol (See also Chlorophenols, occupational exposure to) inadequate sufficient no data 2B Tris (aziridinyl) -para- benzoquone (Triaziquone)inadequate limited sufficient 2B Tris(l-aziridinyl)pho- sphine sulphide (Thiotepa) inadequate sufficient sufficient 2B Underground haematite mining (with exposure to radon) sufficient 1 Haematite inadequate inadequate inadequate 3 Uracil mustard inadequate sufficient sufficient 2B Vinblastine inadequate inadequate inadequate 3 Vincristine (See also Certain com ined chemo- therapy for lymphomas) inadequate inadequate inadequate 3 Vinyl chloride sufficient sufficient sufficient 1 Vinylidene chloride inadequate limited sufficient 3
39 II. Lists 2A-2D: NCI Lists of Chemicals with Evidence of Carcinogenicity
2A. Chemicals With Very Strong Evidence (to an Unusual Degree and/or in Multiple Experiments) for Carcinogenicity in Two Animal Species 3-Amino-9-ethylcarbazole hydrochloride 1,5-Naphthalenediamine ortho-Anisidine hydrochloride 5-Nitroacenaphthene Chlordecone Nitrilotriacetic acid, Chloroform trisodium salt 4-Chloro-ortho-phenylenediamine Nitrilotriacetic acid para-Cresidine Phenazopyridine hydrochloride Cupferron Phenoxybenzamine hydrochloride 2,4-Diaminoanisole sulfate Procarbazine 2,4-Diaminotoluene Reserpine Dibromochloropropane Selenium Sulfide 1,2-Dibromoethane Sulfallate 1,2-Dichloroethane 4,4'-Thiodianiline 1,4-Dioxane Thio-TEPA Hydrazobenzene ortho-Toluidine hydrochloride 4,4'-Methylene-bis (N,N-dimethyl 2,4,5-Trimethylaniline benzenamine Tris(2,3-dibromapropyl)-phosphate Michler's ketone 2B. Chemicals with Very Strong Evidence for Carcinogenicity in One Species and Sufficient Evidence in a Second Species 2-Aminoanthraquinone I-Amino-2-methyl-anthraquinone 5-Nitro-ortho-anisidine Nitrofen para-Nitrosodiphenylamine Phenestrin 2,4,6-Trichlorophenol Trimethylprosphate
2C. Chemicals with Very Strong Evidence for Carcinogenicity in One Species and No Evidence in a Second Species
Acronycine Direct dye, blue 6 4-Amino-2-nitrophenol Direct dye, black 38 Aniline hydrochloride Direct dye, brown 95 Azobenzene Heptachlor Chlordane Hexachloroethane Chlorobenzilate Lasiocarpine 3-(Chloromethyl)pyridine hydrochloride 2-Methyl-l-nitroanthraquinone 5-Chloro-ortho-toluidine 6-Nitrobenzimidazole 4-Chloro-ortho-toluidine hydrochloride N-Nitrosodiphenylamine Chlorothanonil 6-Nitro-ortho-toluidine Cinnamyla-anthranilate Oestradiol mustard meta-Cresidine Pivalolactone Dapsone para-Quinone dioxime pare, para'-DDE 1,1,2,2-Tetrachloroethane N,N'-Diethylthiourea Tetrachloroethylene 3,3'-Dimethoxybenzidine-4,4'-diiso- Toxaphene cyanate 1,1,2-Trichloroethane- Trifluralin Trichloroethylene *NCI data as evaluated by R.A. Griesemer and C. Cueto, Jr.
10 2D. Chemicals with Sufficient Evidence for Carcinogenicity in Two Species 4-Chloro-meta-phenylenediamine ICRF-159 Isophosphamide Nithiazide
41 from LOHP Files
Common Occupational Carcinogens
Agent Organ Affected Occupation Wood Nasal cavity and sinuses Woodworkers Leather Nasal cavity and sinuses; Leather and shoe workers urinary bladder Iron Oxide Lung; larynx Iron ore miners; metal grinders and polishers; silver finishers; iron foundry workers. Nickel Nasal sinuses; lung Nickel smelters, mixers, and roasters; electrolysis workers. Arsenic Skin; lung; liver Miners; smelters; insecti- cide makers and sprayers; tanners; chemical workers; oil refiners; vintners. Chromium Nasal cavity and Chromium producers, pro- sinuses; lung; larynx cessors, and users; ace- tylene and aniline work- ers; bleachers; glass, pottery, and linoleum workers; battery makers. Asbestos Lung (pleural and Miners; millers; textile, peritoneal mesothe- insulation, and shipyard lioma) workers. Petroleum, petroleum Nasal cavity; larynx; Contact with lubricating, coke, wax, creosote, lung; skin; scootum cooling, paraffin or wax anthracene, paraffin, fuel oils or coke; rubber shale, and mineral oils fillers; retort workers; textile weavers; diesel jet testers.
Mustard gas Larynx; lung; trachea; Mustard gas workers. bronchi Vinyl chloride Liver; brain Plastic workers. Bis-chloromethyl ether, Lung Chemical workers. chloromethyl methyl ether
Isopropyl oil Nasal cavity Isopropyl oil producers.
42 Common Occupational Carcinogens (continued)
Agent Organ Affected Occupation Coal soot, coal tar, Lung; larynx; skin; Gashouse workers, stokers, other products of coal scrotum; urinary and producers; asphalt, coal combustion bladder tar; and pitch workers; coke oven workers; miners; still cleaners.
Benzene Bone marrow Explosives, benzene, or rubber cement workers; dis- tillers; dye users; painters; shoemakers.
Auramine, benzidine, Urinary bladder Dyestuffs manufacturers and alpha-Naphthylamine, users; rubber workers (press- beta-Naphthylamine, men, laborers, filtermen); magenta, 4-Aminodiphenyl, textile dyers; paint manu- 4-Nitrodiphenyl facturers.
43 Section 2:
Risk Assessment and Policy Issues SECTION 2 Risk Assessment and Policy Issues
This section discusses some of the methods used to help translate scientific information into public policy.
Deciding how to set standards and regulate chemicals known to cause cancer in humans can be a difficult problem and involves the weighing of both scientific and political criteria. Deciding what levels of chemicals are dangerous to humans based on the results of animal studies can be an even greater problem. Quantitative risk assessment involves using mathematical models to extrapolate the animal test results to obtain a prediction of risk to humans. There are several models which can be used - each with its own benefits and disadvantages. Also, the science of this extrapolation is imprecise and therefore opens the issue to debate no matter what results are obtained. However, some basis of risk must be determined and applied to decision making about regulation. How this decision is made is a poli- tical issue and is the fuel for policy debate over carcinogen regulation.
Additional Reading
Parts 2 and 3 of California Department of Health Services' Cancer Policy Statement, "Carcinogen Identification Policy: A Statement of Science as a Basis of Policy": Part 2: Methods for Estimating Cancer Risk from Exposure to Carcinogens. Part 3: A Policy for Reducing the Risk of Cancer.
45 Estimating Potency of Carcinogens Is an Inexact Science If the balance between risks and benefits is to be consid- balance of the animals; and by stressing the animals in ered in regulation of carcinogens, it is important to have various ways, such as by increasing the number in a cage. some estimate of their potency. Potential benefits of a Significant differences in potency can also be observed in chemical would have to be very high to justify the risks different animals. Aflatoxin, for example, is a very potent associated with a potent carcinogen, for example, whereas carcinogen in rats. but is not a carcinogen in adult mice; 2- less substantial benefits might justify use of a weak carcino- fluorenylacetamide is a very potent carcinogen in one gen. Unfortunately, the scientific basis for estimating the strain of rats, buit is not a carcinogen in another strain; and potency in humans of chemicals shown to be carcinogenic 2-naphthylamine is a potent carcinogen in humans, but is in animals is very limited. not a carcinogen in rats. Great caution must thus be used in Chemical carcinogens exhibit a wide range of potency in extrapolation of potency estimates between species. laboratory animals. The accompanying diagram, compiled The problem is further complicated when estimates of from the literature by Bruce Ames and his colleagues at the carcinogenic potency are made from results of short-term University of California at San Francisco, illustrates the mutagenicity assays such as the Ames test. Ames has ob- daily dose of a carcinogen (per kilogram of body weight) served an approximately linear correlation between the that is required to induce tumors in 50 percent of a group of mutagenic potency of a chemical in the Salitiewlfa test and rats or mice over the course of their lifetimes. The diagram its carcinogenic potency in animals. Other scientists, how- clearly shows that there is a millionfold difference in po- ever, have reservations about such correlations. particular- tency between aflatoxin B 1, one of the most potent car- ly since other studies have shown that the correlation does cinogens known, and saccharin, one not hold for polycyclic aromatic of the weakest. Miost scientists as- hydrocarbons and nitrosamines. Some sume that potency in rodents is a - Sac:charsn of the problems may. arise. say John rough indicator of potency in humans, Ashby and J. A. Styles of Imperial but evidence to support this assump- -Trichloiroethylene Chemical Industries Ltd. in England. tion is limited because of the diffi- because of the variations in the prep- culties of obtaining dose information 1 sin t aration of rat liver homogenates in humans exposed to carcinogens. used to activate mutagens in the Estimates of dose levels for sub- Ames and other short-term tests. stances that have caused cancer in Metroanedazote ~ They recently demonstrated that the humans are available from epidemio- E observed mutagenic potency of benz- logical studies for only six substances (alpyrene can vary by more than a -benzidine, chlornaphazin, diethyl- - mUMethyl me thanesulfonate factor of 100 depending on how the stilbestrol, afRatoxin BI. vinyl chlo- cC Carbon t >etrachiorideq liver homogenate is prepared. Since ride, and cigarette smoke. For each Unrathaie the Ames test, in their laboratory. is of these chemicals, according to Mat- valid only over a thousandfold range thew Meselson of Harvard Univer- DIbenz (a.h) antihracene*8enzidene of potency, they conc.tide that accep- sity. there is a rough correlation Tres 12.3 d,brorn toropyl) phosphate tance of a linear correlation is pre- 2AcetyIaiminofluorene between potency in rodents and in gt 1 mg r- mature. humans. This correlation is the justi- bromochloropropane The bottom line, at least for the r fication for most estimates of potency kpropylen ne-Dimethyinstrosamene_ present. is that it is very difficult to a in humans. 0 estimate the potency of carcinogens But potency is the result of a com- in humans-except in a few cases 3-methyl4 plex series of biological events and 0 where the carcinogen is patently verv can be altered by many external potent or very weak. Until it is pos- factors. Significant differences in the .0 SterugtMatocystln sible to make such estimations acci- observed potency of carcinogens in rately, any balancing of risks and laboratory animals can be obtained, la& benefits will neqessarily be error- for example, by exposing the animals prone. In most cases, then, it seemv to chemical agents that stimulate or likely that regulatory agencies will depress drug-metabolizing enzyme ban carcinogens outright rather than Ak1 a toxin systems; by modification of the an- I. S1 take -a chance of underestimating imals' diet; by changing the hormonaF their hazards.-T.H.M.
from: SCIENCE, 6 October 1978
46 How Safe Is "Safe"? Carcinogenesis studies carried out with reasonable numbers of animals are statistically significant only when the observed incidence of induced tu- mors is greater than 5 percent. A nlegative result in an animal bioassay for carcinogenicity, therefore, does not necessarily mean that the chemical is safe. Consider an animal test in which 100 rodents are fed a chemical. If none of the rodents develop a tumor, then we are 99 percent confident that the actual incidence of tumors that might be caused by the chemical is less than 4.5 percent. If the substance had been fed to the rodents at a dosage of I percent of the diet, we can, by direct extrapolation, estimate the risk of cancer in humans at an exposure level of 10 parts per million (ppm) to be less than S x I0-$. That appears to be rather a small risk, but multiplying it by the population of the United States (2 x 10') yields a value of 104. Thus, a negative result with 100 animals tells us merely that less than 10.000 people might contract cancer if everyone in this country were exposed to the chemical at a concentration of 10 ppm. More conclusive proof of safety would require larger numbers of animals. A negative result with 1000 animals, for example, would indicate that the actual incidence is less than 0.45 percent, and so on. Obviously, it is never possible to show compiete safety with animal assays. Current testing pro- grams at the National Cancer Institute (NC!) use about 400 laboratory ani- mals. No one has calculated the actual incidence of tumors that could result even if no animals develop tumors, but it is obviously between I and 4 percent. (NCI has, however, calculated the probability that a carcinogen may slip through the tests undetected; that probability is about 4 to 5 per- cent.) Since there is a finite possibility that a chemical may be a carcinogen even though it tests negative, how does one estimate a ""safe" dose? At one ex- treme, the common practice has been arbitrarily to divide the highest dose tested in animals (D) by 100 and consider that a "safe" dose. This approach leaves much to be desired, particularly if the chemical has been tested in only a small number of animals. At the other extreme, a linear extrapolation based on the "one-hit" principle of carcinogenesis would require the dose to be reduced by a factor of 10 for every tenfold decrease in risk. If the risk were to be reduced from I percent (I in 102) to I in 102, the "safe" level would be D/10. The danger in this approach is that it will in most instances lead to such low "safe" levels that, in practice, the chemical could not be used. A reasonable alternative, suggested by Nathan Mantel of George Wash- ington University and Mtarvin A. Schneiderman of NCI, would be to assume that the risk decreases by one standard deviation (or probit) for every factor of 10 decrease in the dose. If it were determined that an acceptable risk might be one cancer per 100 million exposed individuals, and no tumors were observed in 100 laboratory animals, the '"safe" dose can be calculated to be D/8300. This approach would have the advantage of rewardin$g good testing. The higher the dose tested, the highe-rwould be the-"safe"' dose. Use of more animals would also increase the "'safe" dose. If only 50 animals were tested, the "safe" dose would be D/18,000. but if 1000 animals were used, the "'safe" dose would be D/1000.-T.H.M.
from: SCIENCE, 6 October 1978
47 Linda Rudolph, M.D. for LOHP files
Risk Assessment
Risk assessment refers to the evaluation of the likelihood that adverse huran health effects may occur as a result of exposure to various hazards. It is a method for piecing together the results from epidemiological, animal and short-term studies (see Section 1) with information about exposures, in order to systematically characterize the magnitude of risk facing a particular popu- lation. There are literally tens of thousands of substances that could be regulated, and there is often uncertainty about just how hazardous each substance is. Risk assessment offers one potential method for bridging the gap between scientific data and regulatory action. Regulatory agencies are turning to this process with increasing frequency as a basis for both determining priorities for action, and selecting among different regulatory options. The Supreme Court encouraged the use of risk assessment by regulatory agencies with its 1980 decision in the benzene case. The Court ruled that OSHA needed to demonstrate "more likely than not", the existence of "significant" health risk in order to regulate a substance in the work- place. However, the science of risk assessment is still in its infancy. Also, workers may be exposed to literally dozens of substances. Different chemicals may have additive effects or they may interact synergistically to increase risk by many times that of each chemical alone. Risk assessment is usually only performed for 1 chemical separately. It is the total cancer risk from exposures in the real work- place that workers need to be concerned about. There are so many uncertainties in the risk assessment process that, for now, the results of risk assessment can only be regarded as rough guides to tell us which of the many hazards faced are the most serious. Basically, there are four (4) steps in risk assessment: hazard identification; dose-response assessment; exposure assessment; and risk characterization. Hazard Identification Hazard Identification is the process of deciding whether or not a particular agent is carcinogenic, and whether exposure will cause an increase in the occurrence of cancer. Generally, this determination is based on epidemiology, animal cancer bioassays, short-term tests, and comparison of the chemical structure of different substances. There has been a tremendous amount of debate on the significance of each of these types of studies. Many scientists feel that any substance which causes cancer in animals must be considered a potential human carcinogen, and that positive short-term test results should increase the significance of positive animal test results. Industry representatives, on the other hand, have often argued that negative epidemiological studies should outweigh positive animal studies. Unfor- tunately, most epidemiological studies have studied populations that are too small, or the follow-up period is inadequate to allow for the long latency period of most cancers.
The International Agency for Research on Cancer (IARC) is engaged in an on- going review of available evidence to determine if substances are carcinogenic. IARC publishes a list of those chemicals and industrial processes which may state either definetly cause cancer in humans, probably cause cancer in humans, or have sufficient evidence for carcinogenicity in test animals. The U.S. National Toxi- cology Program (NTP) also tests substances for carcinogenicity in test animals.
48 In the final section of the California Department of Health Services draft of the Carcinogen Policy, the Department proposed using the IARC and NTP classi- fications as the basis for Hazard Identification for carcinogens. Dose Response Assessment
Dose Response Assessment is the process for describing the relationship that exists between the amount of a substance that is taken into the body and the degree to which the risk of cancer is increased. Some chemicals are very potent, and can produce a great increase in the risk of cancer at very low doses - as low as a millionth of a gram. Other substances are weaker carcinogens that require much larger doses to produce a comparable increase in risk. Most animal cancer tests are done at dose levels much higher than the levels to which humans are exposed. Therefore, dose-response assessments must include an extrapolation from the risks at the high doses used in animal bioassay to the risks at the lowest doses which may occur in the workplace. There are several different mathematical models available to make this extrapolation. At high doses each model describes the experimental data reasonably well, but at low doses the estimates of risk vary widely (sometimes by several orders of magnitude) depending upon the model used. At present, there is no practical way to scientifically determine which of these low dose extrapolation models is the best one. Choosing the most conservative model would tend to overestimate risk and therefore err on the side of protecting the public health. Other models might underestimate risks, leading to less protective policies. Clearly, the choice of such a model is a POLICY decision, and can be in- fluenced by a variety of issues. The next step in the dose-response assessment involves extrapolation from estimates of risk in animals to estimates for humans. Many factors should be considered here, including differences in size and metabolism, sensitivity to the effects of the chemicals, and pharmacokinetics (the rate and pathway by which the substance is broken down in the body). There is sufficient knowledge about all of these areas for only a very few chemicals, and in most cases there is almost no in- formation available that allows scientists to address these issues with any certainty. So, once again, policy decisions must be made in deciding whether risk calculations should be based on the assumption that humans resemble the most sensitive animals, or on other assumptions which are less protective of worker health. Exposure Assessment Exposure Assessment is the process of estimating human exposure to a particular substance. This involves evaluation of the potential sources and routes of exposure, the levels, duration and frequency of anticipated exposure, and the characteristics of the population, including an estimate of how many people might be exposed, their ages, etc. Because use reporting data and industrial hygiene monitoring are frequently not available, exposure assessment as with other aspects of risk assessment, often requires the use of estimates that are based on little hard data.
49 Risk Characterization The final step in the risk assessment process, risk characterization, is the preparation of a summary statement reflecting a judgement about the overall magnitude of the risk to human health that is associated with human exposure to a substance. This step draws on the information and evaluation from each of the preceeding steps. Clearly, the final risk characterization is only as certain as the information upon which hazard identification, dose-response assessment, and exposure is based. This is the fundamental problem with risk assessment: the information available at this time is glaringly inadequate. Of the 70,000 chemicals in industrial use, there are extremely few for which we know most of the data which are needed in the risk assessment process. Given the lack of decisive evidence on which to base decisions, even the most informed "scientific" choices (of dose-response model, of valid test data, or of estimates of exposure), represents a complex mix of scientific conjecture and ethical values. For this reason, it is very important that members of the public (workers, consumers) whose lives will be affected by regulatory decisions be involved in basic decisions about how risk assessments are to be made. With such involvement, risk assessments should be based on assumptions that are amply protective of worker and public health.
50 Section 3:
Legisla1tive Protection SECTION 3 Legislative Protections
This section starts with a brief summary of the history and current status of the carcinogen regulations on a Federal level and in California. It also provides information about which substances are regulated under California and Federal law.
Each of these regulated carcinogens have established standards of allowable worker exposure and specific guidelines for use, storage, worker training and worker protection. A copy of the general requirements for carcinogen use under CAL/OSHA standards is also included. The specific guidelines for particular chemicals are contained in Sections 5208-5215 of Title 8 of the California Admin- istrative Code (for California) and Title 29, Code of Federal Register 1910 (for Federal).
This section also contains information on additional legislative protections regarding carcinogens. These laws can be used by workers to guarantee their basic rights to know about chemicals they are working with and to have access to medical and monitoring records. The right to refuse hazardous work is also discussed.
Additional Reading
1) Sections 5208 - 5215, Title 8 of California Code - California Regulated Substances. 2) Feds CFR 1910, Title 29 - Federal Regulated Substances. 3) Fact sheets on substances regulated as carcinogens. 4) Federal Register - January 1980 for Federal generic cancer policy. 5) California generic cancer policy, Parts 1, 2, and 3 - available from California Department of Health Services
52 from LOHP Files
Regulation of Carcinogenic Substances
Despite the fact that there are hundreds of substances suspected of causing cancer (because they have produced tumors in at least one animal), there are only 21 substances regulated as carcinogens in California and 17 substances regulated on a Federal level. The reasons for this are varied. The complex nature of es- tablishing carcinogenicity, determining risk and setting standards for "safe" exposure by extrapolating from animals to humans, ensuring that the standards can be adhered to and that workplaces can be monitored and the slow process of establishing regulations have all contributed to so few regulations being enacted.
Federal Regulation - History and Current In the past, regulation has been approached substance by substance. There has always been considerable labor/industry debate over each regulation and most standards have taken several years to pass through the whole process. This is the way 17 of the substances have been regulated by the Federal government. It was through labor initiative that the first 14 regulations were passed. The Health Research Group and OCAW petitioned for regulation of 14 substances in 1973. It was not until 1974 that they were actually regulated. One of these was eventually challenged and removed from regulation and four (4) other substances have been regulated since. As early as 1977, a proposal was made by OSHA under Eula Bingham, for a generic cancer policy. Finally in January 1980, a new Cancer Standard was proposed which was designed to streamline the process of regulating carcinogens. It sought to establish policy guidelines and to eliminate debate on some of the same issues over and over again with each substance. Specifically, it established positive animal tests as an acceptable basis for determining potential human carcinogenicity and outlined a process to be followed for regulation of substances. The policy stated that there would be 2 categories for classifying potential carcinogens based on the evidence available about them. Category I. Potential carcinogens would be substances that show carcinogenicity in humans or a single animal species with results backed up by other evidence including tests in the same or other species, short term tests or results of tumors at injection or im- plantation site. Category II. Potential carcinogens would be those substances in which Category I type evidence is available but is only "suggestive" or for which there is no positive evidence in an animal species. for Category I substances, proposed regulation would set exposure levels at "as low as feasible through engineering and/or work practice controls." If a substance was found for Category I substances, no occupational exposure would be allowed. Category II carcinogens would be less tightly controlled.
53 OSHA stated that it would publish a candidate list of substances to be considered for Category I or Category II. This policy also contained provisions for medical surveillance and training programs for employees. Several months after this policy was announced (August 1980), the first candidate list of 107 substances was released and work was begun on assigning the substances to Category I or Category II. There was considerable industry opposition which stopped the process and in January 1981 the Reagan administration proposed a total review of the whole policy. In September of 1981, OSHA announced that it would negotiate with industry regarding carcinogenic substances rather than publishing lists. In January of 1982, OSHA announced a stay on the policy while it took some time to reassess the policy that had been in effect for 20 months. In May 1982, a stay on the candidate and priority lists was also announced. In addition, the Reagan administration is currently (first proposed in October 1982) encouraging inserting provisions for cost effectiveness, cost benefit, and/ or risk assessment analysis. This would mean each proposed standard would be assessed for its economic impact on industry. This is the current status of the Federal cancer policy, (November 1983). Essentially, the 17 regulated carcinogens are the same as before the proposed generic policy and no new standards have been established since October 1978. The generic policy has never really been im- plemented, though it is on record.
54 from LOHP Files
California Regulation - History and Current
California regulation has consistently gone beyond federal regulation, starting with the Occupational Carcinogens Control Act of 1974 (SB 1678). This bill contained all the same substances as the initial Federal regulation with the addition of asbestos. All substances regulated as carcinogens on a Federal level have subsequently been regulated in California as well. However, California also has the ability and authority to establish regulations which go beyond the Federal regulations. They have a separate standards board that en- tertains petitions for standards, does research into the petition and decides whether or not a standard will be promulgated. This is under CAL/OSHA. Thus, there are four (4) substances regulated as carcinogens in California which are not regulated as such on a Federal level. However, regulation in California has also been substance by substance and thus has been slow. On August 4, 1982, the California Department of Health Services announced a new carcinogen identification policy: "Carcinogen Identification Policy: A Statement of Science as a Basis of Policy". This policy was developed over a three (3) year period.
The presentation of this policy was in three (3) parts starting in October 1982. Public hearings were held on the first part in October. This part provides background on the characteristics of carcinogens, considerations in the use of human, animal and short term tests for identifying carcinogens and lists of chemicals that are carcinogenic in humans and animals. The second part, "Methods for Estimating Cancer Risks from Exposures to Carcinogens," deals with the technicalities involved in estimating risk and with the controversy surrounding these issues. Public hearings were held on Section 2 in December, 1982. Part 3, "A Policy for Reducing the Risk of Cancer," was introduced at this time and hearings were held in September, 1983. The purpose of Part 3 is to articulate a policy framework that will consider the latest scientific information to identify carcinogens and to develop priorities for intervention and, where appropriate, regulation. The DHS Carcinogen Policy would not have regulatory impact per se, but could serve as a guide for other state agencies in the promulgation of carcinogen regulations. As on a Federal level, regulation remains substance by substance, and though an idea for a generic policy has been introduced, it has not been implemented.
55 LIST OF REGULATED CARCINOGENS
Federally Regulated Carcinogens Substance GISO Date Regulated 2-Acetylaminoflourene 1910.1014 6/27/74 4-Aminodiphenyl 1910.1011 6/27/74 Benzidine (+ salts) 1910.1010 6/27/74 3,3'-Dichlorobenzidine 1910.1007 6/27/74 4-Dimethylaminoazobenzene 1910. 1015 6/27/74 alpha--Naphthylamine 1910.1004 6/27/74 beta-Naphthylamine 1910.1009 6/27/74 4-Nitrobiphenyl 1910. 1003 6/27/74 beta-Propiolactone 1910. 1013 6/27/74 4-Nitrosodimethylamine 1010. 1016 6/27/74 Bis-Chloromethyl ether 1910.1008 6/27/74 Methyl chloromethyl ether 1910. 1006 6/27/74 Ethyleneimine 1910.1012 6/26/74 Acrylonitrile 1910.1045 10/03/78 Vinyl chloride 1910.1017 10/04/74 Coke ovenremissions 1910. 1029 10/22/76 Inorganic arsenic 1910. 1018 5/05/78 Asbestos (1910.1001) and DBCP (1910.1044) are known carcinogens but are not controlled Federally for their carcinogenic properties. Asbestos is regulated to protect workers from the lung disease asbestosis. DBCP is regulated for its reproductive effects. California Regulated Substances
Substance Title 8 Section Numbers 2-Acetylaminoflourene 5209 4-Aminodiphenyl 5209 Benzidine (+ salts) 5209 3,3'-Dichlorobenzidine 5209 4-Dimethylaminoazobenzene 5209 alpha-Naphthylamine 5209 beta-Naphthylamine 5209 4-Nitrobiphenyl 5209 4-Nitrosodimethylamine 5209 beta--Propiolactone 5209 bis-Chloromethyl ether 5209 Methyl Chlormethyl ether 5209 Ethyleneimine 5209 Asbestos 5208 Vinyl chloride 5210 4,4'-Methylene (bis) 2-chloraniline (MOCA) 5215 Coke oven emissions 5211 Acrylonitrile 5213 Inorganic arsenic 5214 DBCP 5212 EDB 5219 56 II s X fX i m @ State of California 1A~~~~ ~Department of Industrial Relations FJ~~~~ DIVISION OF OCCUPATIONALGolden Gate SAFETY-AND HEALTH W n ^2i1t) E)L]n IL ~San~~~525Francisco, CaliforniaAvenuel94102
DATE: 7-8-81
TO: ALL EMPLOYERS USING REGULATED CARCINOGENS FROM: DR. RICHARD WADE, DEPUTY CHIEF - HEALTH RE: REQUIREMENTS FOR CARCINOGEN USE UNDER CAL/OSHA STANDARDS REGISTRATION This is to advise you that Sections 5208-521q of Title 8 of the California Administrative Code require that every employer who manufactures, processes, uses, repackages, stores, releases or otherwise handles any of the 20 carcinogens listed below and currently regulated by California law, MUST REPORT, IN WRITING to the Chief of the Division of Occupational Safety and Health, P.O. Box 603, San Francisco, CA 94101 the following information,in general (see specific standards for exact requirements): 1. The name of the employer and the address of each place of employment where a carcinogen is present. 2. A brief description and in-plant location of each regulated area. 3. The name(s) and other identifying information as to the presence of carcinogen(s) in each place of employment. 4. The number of employees in each regulated area during normal operations including maintenance activities. 5. The manner in which each carcinogen is present in each place of employment: e.g., whether it is manufactured, processed, used, repackaged, released, stored or otherwise handled including the approximate quantity of each carcinogen. 6. The names and addresses of any collective bargaining or other representative of the affected employees. Any change in the information above must be reported to the Chief of the Division of Occupational Safety and Health in writing within 15 calendar days of such change. REGULATED CARCINOGENS (and the section of Title 8 under which they are regulated) j 2-Acetylaminoflourene (5209) bis-Chloromethyl ether (5209) 4-Aminodiphenyl (5209) Methyl chloromethyl ether (5209) Benzidine (and its salts) (5209) Ethyleneimine (5209) 3,3'-Dichlorobenzidine (and its salts) (5209) Asbestos (5208) 4-Dimethylaminoazobenzene (5209) Vinyl Chloride (5210) alpha-Naphthylamine (5209) Ccke Oven Emissions (5211) beta-Naphthylamine (5209) DBCP (5212) 4-Nitrobi.phenyl (5209) Acrylonitrile (5213) N-Nitrosoaimethylamine (5209) 4,4'-Methylenebis (2-chloroaniline) (522 beta-Propiolactone (5209) Inorganic Arsenic (5Z14) (over) 57 V 5s) REPORTING | Incidents which result in the release of a carcinogen 'into any area where employeesC may be potentially exposed shall be reported sin general (see also specific standards) 1) A report of the occurrence of the incident and the facts obtainable at that time including a report on any medical treatment of affected employees is to be made within 24 hours to the Chief of the Division of Occupational Safety and Health. 2) A written report is to be filed with the Chief within 15 calendar days after an incident and must include: * a specification of the amount of the material released, the amount of time involved, and an explanation of the procedure used in determining this figure; o a description of the area involved and the extent of known and possible employee exposure and area contamination; * a report of any medical treatment of affected employees and any medical surveillance program implemented; and * an analysis of the circumstances of the incident and measures taken or to be taken, with specific completion dates, to avoid further similar releases. OTHER REQUIREMENTS Detailed specific requirements for use of particular carcinogens, employee training, medical surveillance, labeling, and establishment of regulated areas are outlined i Sections 5208-5215 of Title 8 (General Industry Safety Orders). You may purchase the General Industry Safety Orders from: Office of Procurement - Publications Section P.O. Box 1015 North Highlands, CA 95660. When new substances become regulated carcinogens, that information will be available from the CAL/OSHA Standards Board or the Division of Occupational Safety and Health. If you need assistance in interpreting or applying the requirements for carcinogens outlined in Title 8, contact the nearest office of the CAL/OSHA Consultation Service (see back page). GISO 3204 General Industry Safety Order 3204 was recently adopted and will affect carcinogen users in that it requires employers to make available to their employees: * the employee's medical records and records of exposure to toxic substances * records of exposure to toxic substances of all employees with past or present similar job duties or working conditions * Material Safety Data Sheets, which the employer currently has on hand, or other information that the employer has for chemicals or substances used in the workplace (or to which employees may be exposed). A copy of GISO 3204 is available from the CAL/OSHA Standards Board,1006 Fourth St., Sacramento, CA 95814. Additional information and assistance is available from the K. CAL/OSHA Consultation Service. (continued) 58 CAL/OSHA INFORMATION BULLETIN - CARCINOGEN REQUI,REMENTS -3 HAZARDOUS SUBSTANCES INFORMATION AND TRAINING ACT This new law (California Labor Code sections 6380-6399) and the standard CAL/OSHA is adopting to implement this law will become effective approximately 180 days after the Director of the Department of Industrial Relations establishes a List of Hazardous Substances (which will include carcinogens); the List is expected to be adopted in late 1981. CAL/OSHA standards implementing the provisions of this law will be available from the CAL/OSHA Standards Board. Both the Hazardous Substances Information and Training Act and the CAL/OSHA standards related to it, will affect carcinogen users. Briefly, they will require employers to: * provide employees who use or may be exposed to hazardous materials with information, including the Material Safety Data Sheets, for those materials. Note: The information which must be contained in a Material Safety Data Sheet is specified in Labor Code section 6391. In general, information which will be required will be: - chemical name, common name, and CAS number of the hazardous substance - the potential for fire, explosion, and reactivity - the acute and chronic health effects or risks from exposure, the potential routes of exposure, and symptoms of overexposure - proper precautions, handling practices, necessary personal protective equipment, and other safety precautions in the use of or exposure to the hazardous substance. - emergency procedures for spills, fire, disposal, and first aid - a description in lay terms of the specific potential health risks posed by the substance * provide employees with training for working safely with these materials. Note: Refer to current carcinogen standards for specific employer responsibilities for providing information and training to workers. DISPOSAL Employers who now have carcinogenic substances on hand, but wish to dispose of them should contact one of the following offices of the Department of Health Services - Hazardous Waste Unit:
Berkeley...... 2151 Berkeley Way 94704 415-540-2356 Los Angeles...... P.O. Box 31327 Terminal Annex 90030 213-620-2380 Sacramento...... 714 P Street 95814 916-322-2337
OFFICES OF THE DIVISION OF OCCUPATIONAL SAFETY AtND HEALTH AND THE CAL/OSHA CONSULTATION SERVICE ARE LISTED ON THE BACK OF THIS SHEET.
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0 . 0 0 F 0 U : LI. 0 c UI. cn I= CI,) In, I C cn 60 "Category 1 List of Carcinogenic Substances" CURRENT REPORT EPA CARCINOGEN ASSESSMENT GROUP CARCINOGENS LIST REFERENCED IN CANCER POLICY CANDIDATES NOTICE
CHEMICALS HAVING SUBSTANTIAL EVIDENCE Diepoxybutane OF CARCINOGENICITY' 1,2-Diethylhydrazine Diethylstilbestrol (DES) 2-Acetylaminofluorene Dihydrosafrole Acrylonitrile 3.3'-Dimethoxybenzidine (o-Dianisidine) Aflatoxins' I)-Dimethylaminoazobenzene Aldrin 7.1 2-Dimethylbenz(a )anthracene 4-Aminobiphenyl 3.3'-Dimethylbenzidine (o-Tolidine) Amitrole Dimethylcarbamoyl Chloride Aramite 1,1-Dimethylhydrazine Arsenic and Arsenic Compounds 1,2-Dimethylhydrazine Asbestos Dimethyl Sulfate Auramine and the manufacture of Auramine 2,4-Dinitrotoluene Azaserine 2 1,4-Dioxane Benz(c)acridine' 1.2-Diphenylhydrazine Benz(a)anthracene Epichlorohydrin Benzene Ethylenebisdithiocarbamate (EBDC) Benzidine Ethyleneimine (Aziridine)' Benzo(a)pyrene Ethylene Oxide Benzo(b)fluoranthene Ethylenethiourea Benzo(j)fluoranthene 4 Ethyl Methanesulfonate Beryllium and Beryllium Compounds Formaldehyde N,N-Bis ( 2-Chloroethyl )-2- Naphthylamine (Chlor- Glycidaldehyde naphazine) 3 Heptachlor Cadmium and Cadmium Compounds Hexachlorobenzene Carbon Tetrachloride Hexachlorobutadiene Chlorambucil I Hexachlorocyclohexane (HCH) Chloroalkyl Ethers Hydrazine Bis(2-chloroethyl) ether (BCEE) 4 Indeno( 1,2,3-cd)pyrene Bis(chloromethyl) ether (BCME) Iron Dextran Chloromethyl methyl ether (CMME), technical grade Chlordane Isosafrole Chlorinated Ethanes Kepone (Chlordecone). 1,2-Dichloroethane [Ethylene Chloride, Ethylene Lasiocarpine Dichloride (EDC)J Melphalan 3 Hexachloroethane Methapyrilene 1,1,2,2-Tetrachloroethane 3-Methylcholanthrene 1,1,2-Trichloroethane' 4.4'-Methylenebis(2-Chloroaniline) (MOCA) Chlorobenzilate Methyl Iodide Chloroform Methyl Methanesulfonate Chromium Compounds, Hexavalent N-Mtethyl-N'-nitro-N-nitrosoguanidine Chrysene ' Methylthiouracil 3 Citrus Red No. 2 Mitomycin C Coal Tar and Soot Mustard Gas Coke Oven Emissions (Polycyclic Organic Matter (POM)J l-Naphthylamine, technical grade Creosote 2-Naphthylamine Cycasin Nickel and Nickel Compounds Cyclophosphamide 3 Nitrogen Mustard and its hydrochloride Daunomycin ' Nitrogen Mustard N-oxide and its hydrochloride DDT (Dichlorodiphenyltrichloroethane) 5-Nitro-o-toluidine Diallate' 4-iNitroquinoline-l-oxide Dibenz(a,h)acridine Nitrosamines Dibenz(a,j)acridine Nl;-Nitrosodiethanolamine Dibenz(a,h)anthracene N-Nitrosodiethylamine (DENA) 7H-Dibenzo(c,g)carbazole N-Nitrosodimethylamine (DM2NA) Dibenzo(a,e)pyrene N-Nitrosodi-n-butylamine Dibenzo(a,h)pyrene N-Nitrosodi-n-propylamine Dibenzo(a,i )pyrene iN-Nitrosomethylethylamine 1,2-Dibromo-3-chloropropane (DBCP) N-Nitrosomethylvinylamine 1,2-Dibromoethane [Ethylene N-Nitroso-N-Ethylurea (NEU) Bromide, Ethylene N-Nitroso-N-Methylurea (NMU) Dibromide (EDB) I N-Nitroso-N-methylurethane 3,3' Dichlorobenzidine (DCB) N-Nitrosomorpholine Dieldrin 61 N-Nitrosonornicotine
8-1480 Published bV THE BUREAU OF NA*6ONAL AFFAIRS INC WASHINGTON D C 20037 OCCUPATIONAL SAFETY & HEALTH REPORTER Nitrosamines (continued) N-Nitrosopiperidine Saccharin N-Nitrosopyrrolidine Safrole I N-Nitrososarcosine Selenium Sulfide Pentachloronitrobenzene Streptozotocin ' Phenacetin ' 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Polychlorinated Biphenyls (PCBs) Tetrachloroethylene (Perchloroethylene) Pronamide Thioacetamide 1,3Propane Sultone Thiourea B-Propiolactone o-Toluidine Hydrochloride Propylthiouracill Toxaphene Reserpine' Trichloroethylene 2,4,6-Trichlorophenol This is not a comprehensive list of all chenicals having sbstan- Tris (1-aziridinyl)phosphine sulfide (Thio-TEPA)3 tial evidence of carcinogenicity. Other chemicals wil be added. No )phosphate attempt has been made to select chemicals based upon ap- Tris( 2,3-dibromopropyl propnatenes for regulation by EPA. The list is intended to be a Tris( 2,3-dibromopropyl)phosphate oass fcr selection by the various proam offices according to their Trypan Blue, commercial grade specific needs. Uracil Mustard I 'Fungul toxin, not an industrially manufactured product. 'Used as a drug. Urethane (Ethyl carbamate; ethyl ester of carbamic acid) *Evaluated by IARC as not having sufficient evidence of car- Vinyl Chloride anogenicity. Vinylidene Chloride 'Used as a food.
62 LOHP Files
ADDITIONAL LEGISLATIVE PROTECTIONS
The legal responsibilities of industry and the rights and protections for workers regarding cancer causing substances are contained in several pieces of legislation in addition to the California and Federal cancer policies and standards which were discussed in Section 4. These additional pieces of leg- islation include the following: A. Toxic Substances Control Act B. Federal Right To Know and Access to Records (CFR 1910.20) This also includes OSHA 200 Forms (CFR 1904.7). C. California Right to Know (GISO 5194) and Access To Records (GISO 3204) D. National Labor Relations Act
Although no one of these relates exclusively to carcinogens, each of them can be used to obtain information and as additional protections when the issue is one of working with or being exposed to a cancer causing substance in the workplace. Toxic Substances Control Act
This act was signed into law in October 1976. While it contains no specific provisions regarding notification of employees by their employers about toxic substances, it is important in that it requires that the manufacturers of toxic substances inform the government of the possible health effects of substances they are manufacturing. Manufacturers must give this information to the EPA within 90 days of manufacture. The manufacturers can be required to conduct tests on the chemicals at their expense. EPA may prohibit or limit the manufacture, processing, distribution in commerce, use or disposal of a chemical substance or mixture if these activities present an unreasonable risk to health or the environment. Labelling may be required for a chemical or any article containing the chemical. This act set the precedent for the responsibility of manufacturers to supply information about the chemicals that they manufacture. Federal Right To Know and Access To Records (CFR 1910.20), OSHA Log 200 Forms (CFR 1904.7).
The Federal Right to Know Standard includes rules on access to medical records and exposure records. The original standard was issued August 21, 1980 and went into effect January, 1981. It gave workers the right to examine and copy the following records. A. Exposure Records 1. Records of workers own past and present exposure to toxic substances or harmful physical agents. 2. Records of the exposure of other workers who have similar working conditions.
63 A. Exposure Records: (continued) 3. MSDS and other similar records of a non-specific nature which pertain to the workplace. 4. Exposure records of workplaces or working conditions to which a worker is being transferred or assigned B. Medical Records:
1. Medical and employment questionnaires and histories. 2. Results of medical exams and lab tests. 3. Medical opinions and diagnosis. 4. Description of treatments.
Union representatives have full access to these records with a release of information from the employee. Access to records must be granted within 15 days of an employee or union's request. Also, all records were required to be kept for 30 years.
Within several weeks of Reagan taking office, this Federal Access Rule was withdrawn and on March 19, 1982, a new "Hazards Communication" standard was proposed. The major substantive differences between the new standard and the one issued in 1981 are as follows: - Fewer employees are covered; retail construction, maritime, agriculture services and research industries are excluded entirely.
- The determination of what chemicals are hazardous is left to the manufacturer; information must only be supplied on those chemicals. This potentially reduces the number of chemicals covered from 39,000 to 3,500. - MSDS sheets are accessible only to employees and designated represent- atives Mxpeeed;MSDS must only be kept until replaced by another or until the substance is no longer in the workplace (1981 standard mandated they would be kept for 30 years). - Trade secret provisions are very broad. Hearings were held in summer of 1982 on this new standard and in November, 1982 the rule was upheld in its entirety. The Federal Hazard Communication Rule was published in November, 1983. Several unions filed suit against the ruling. A major concern of many unions and environmental groups is that the new rule may preempt more protective local and state right to know laws. C. OSHA Log 200 Forms: These forms contain a record of all work related illnesses and injuries. Employers are required by law to keep these records and to post the cumulative account once a year in February. These OSHA logs are not very detailed and will not be helpful in most cancer investigations. However, they can be a first clue that something unusual is going on.
64 California Right To Know (SB 1874) and Access to Records (GISO 3204).
The California Right To Know law provides workers rights of access to medical and exposure records similar to the original federal standard. In addition, the California SB 1874 strengthens the access rule by mandating that MSDS will be developed on all chemicals on the list adopted by the Director of DIR. This list of substances (GISO 5194) is available from CAL/OSHA Communications Unit, 520 Golden Gate Ave., Third Floor, San Francisco, CA 94102. The list contains approximately 700 chemicals. National Labor Relations Act (NLRA)
This act covers a variety of labor relations issues. The one of most importance to the issues of access toinformation, which would include information about carcinogenic substances, has been decided in a series of landmark cases. The NLRB's decisions in Minnesota Mining and Manufacturing Company, Borden Chemical and Colgate Palmolive Company require that requests for lists of chemicals to which workers are exposed, together with other health, safety and medical in- formation must be honored by the employer. The NLRB held that the companies involved violated federal labor law by refusing to comply with the unions' request. This right was recently upheld in the Federal Appeals Court. The decisions provide another legal means by which unions can seek company held data. OSHA regulations provide for individual and union access to exposure data, hazard information and medical records. In addition, state and local laws provide workers with a "right to know" about workplace hazards. The NLRB decisions complement these requirements to form a more comprehensive access to information right for workers and unions.
Another protection that the NLRB provides is the right to refuse hazardous work. This protection is contained in Section 7. "Employees shall have the right to self-organization, to form, join, or assist labor organizations, to bargain collectively through representatives of their own choosing, and to engage in other concerted activities for the purpose of collective bargaining or other mutual aid or protection..." Various court interpretations of this section (including the Supreme Court) have validated the employee's right to refuse hazardous work. However, there are several stipulations to, and interpretations of, Section 7 which must be examined if a worker is to be protected if they do refuse. One of these is that employees must be acting out a genuine fear that the work is unsafe. (This is slightly different than OSHAct which stipulates that the person who refuses must see the situation as any other reasonable person would.) Also, NLRA protects other workers who might join in the refusal even though they are not immediately affected. In order to be protected, the action must constitute concerted activity which tends to advance group interests. However, employees covered under an explicit or implicit no-strike clause cannot engage in refusal if this would constitute a strike as defined by the NLRA. In extremely dangerous situations, there is Section 502 of the Labor-Management Relations Act which would afford protection anyway but the interpretation is confined to "abnormally dangerous work" and is therefore more subjective. Since there are a variety of stipulations and interpretations, it is best to consult with your union or someone who is clear on both OSHA and NLRA protections before you exercise your right to refuse hazardous work.
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GISO 3204 assess the absorption of a substance or provides workers with the right to see agent by body systems and copy: Material Safety Data Sheets, or if these 1) their own medical records and are not available, any other information records of exposure to toxic which reveals the identity (chemical, substances common or trade names) of a toxic 2) records of exposure to toxic substance or harmful physical agent. substances of employees with similar past or present jobs or working Unless otherwise specified by a CAL/OSHA standard, employee exposure conditions must 3) Material Safety Data Sheets or other records be preserved and information that the employer has for maintained-with certain exceptions-for chemicals or substances used in the at least 30 years. workplace (or to which employees In addition to the provisions of GISO may be exposed) which are listed in 3204, Labor Code Section 6408 the latest National Institute for requires employers to notify any Occupational Safety and Health employee who has been or is being (NIOSH) Registry of Toxic Effects of exposed to harmful substances in excess Chemical Substances (RTECS). of exposure limits set by CAL/OSHA, This article contains only a general and to tell the employee what is being summary of some of the provisions of done to correct the problem. In addition, GISO 3204 and is printed here primarily the employer must allow workers ortheir to inform workers and employers of the representatives access to accurate adoption of the standard. A copy of records of worker exposures to GISO 3204 is available from the potentially harmful substances. CAL/OSHA Standards Board, 1006 4th Street, 3rd Floor, Sacramento, CA Information considered under GISO 95814; it will automatically be mailed to 3204 to be pertinent to an employee you if you subscribe to the General medical record made or maintained by a Industry Safety Orders. physician, nurse, or other health care professional or technician is: GISO 3204 will apply to each employer who makes, maintains, contracts for, or * medical and employment question- has access to employee exposure or naires or histories medical records, or analyses of these results of medical examinations and to records, which pertain employees laboratory and other diagnostic tests exposed to toxic substances or harmful physical agents; whether or not these * medical opinions, diagnoses, progress records are related to specific CAL/OSHA notes, and recommendations standards. over 68 , s * descriptions of treatments and has produced positive evidence of an prescriptions acute or chronic health hazard in human, animal, or other biological * employee medical complaints testing conducted by, or known to, the Exceptions to these requirements will be employer or is described by a Material I- outlined in GISO 3204 (c)(6)(B). Unless Safety Data Sheet (available to the otherwise specified, these records must employer) which states that the be kept at least for the duration of material may pose a hazard to human employment plus 30 years. health. For the purposes ofthis standard, a toxic Notwithstanding any trade secret substance or harmful physical agent is any claims, whenever access to records is chemical substance, biological agent requested, the employer must provide (bacteria, virus, fungus, etc.), or physical access to chemical or physical agent stress (noise, heat, cold, vibration, identities including chemical names, repetitive motion, ionizing and non- levels of exposure, and employee health ionizing radiation, hypo- or hyperbaric status data contained in the requested pressure, etc.) which: records. - is regulated by any California or When an employer ceases to do business, Federal law or rule because it is the employer must either transfer exposure harmful or potentially harmful to and medical records to the next employer to health be maintained or, if there will be no successor employer, notify affected - is listed in the latest printed edition of employees and make arrangements to the National Institute for Occupational transfer the records to NIOSH according to Safety and Health (NIOSH) Registry of GISO 3204 requirements. Toxic Effects of Chemical Substances (RTECS) Workers can get answers to their questions about their rights under GISO 3204 from any office of the Division of Occupational Safety and Health or the Division's Employee Education Unit. Employers can get information and assistance from any office of the CAL/OSHA Consultation Service. o DIVISION OF OCCUPATIONAL SAFETY 4.t AND HEALTH (DOSH) DISTRICT OFFICES Bakersfid ...... 225A Chester Ave. 93301 (805) 395-2718 Berkeley ...... 1625 Shattuck Ave. 94709 (415) 540-3030 Concord 1070 Concord Ave. 94520 (415) 676-5333 Monte ...... 3415 Fletcher Ave. 91731 (213) 572-9003 Freno ...... 2550 Maripos St. 93721 (209) 445-5302 Long Beach ...... 2828 Junipero Ave. 90806 (213) 595-8477 Los Angeles...-..... 3460 Wilshire Blvd. 90010 (213) 736-3041 Modesto ...... 1800 Coffee Rd. 95355 (209) 576-6260 Panorama City.... 8155 Van Nuys Blvd. 91402 (213) 782-1800 Redding ...... 421 Court St. 96001 (916) 246-6571 CAL/OSHA CONSULTATION SERVICE Sacramento ...... 2422 Arden Way 95825 (916) 920-6123 San Bernardino ...... 303 W. Third St. 92401 (714) 383-4321 Toll-Free telephone ...... 800-652-1476 San Diego ...... 7807 Convoy Court 921 11 (714) 237-7325 San Francisco .. 455 Golden Gate Ave. 94102 (415) 557-1677 San Jose N...... 888 First St. 95112 (408) 277-1260 HEADQUARTERS Santa Ana ...... 28 Civic Center Plaza 92701 (714) 5584141 Santa Barba ...... 3704 State St. 93105 (805) 682-2578 San Francisco . 525 Golden Gate Ave. 94102 (415) 557-2870 Santa Fe Springs 14111 E. Freeway Dr. 90670 (213)802-1711 Santa Rosa ...... 725 Farmers Lane 95405 (707) 542-8802 FlELD OFFICES Vernon ...... 2833 Leonis Blvd. 90058 (213) 589-5848 FIELD OFFICES Downey ...... 8535 E. Florence Ave. 90240 (213) 861.9993 Fresno ...... 3374 E. Shields Ave. 93726 (209) 445-5072 Chico ..... 555 Rio Ave. 95926 Panorama LUndo (916) 345-7131 City ...... 14547 Titus St. 91402 (213) 786-3870 Eureka .. ... 619 Second St. 95501 (707) 442-6232 Sacramento ...... 2424 Arden Way 95825 (916) 920-6131 Salinas .. ... 21 W. Laurel Dr. 93902 (408) 443-3050 San Bernardino ...... 303 W. Third St. 92401 (714) 383-4567 Stockton ... .. 31 E. Channel St. 95202 (209) 948-7762 San Diego 6151 Fairmount Ext 92120 (714) 280-5304 Ukih ..... 776 S. State St. 95482 (707) 462-8850 San Francisco 455 Golden Gate Ave 94102 (415) 557-1034 Ventura ...... 5740 Ralston St. 93003 (805) 654-4581 HEALTHWOFFICES Berkeley ...... 625 Shattuck Ave. 94709 (415) 540-2673 Los Angeles ...... 1449 W Temple St. 90026 (213) 620-4290 Los Angeles ...... 3460 Wlishire Blvd. 90010 (213) 381-1382 Sacramento ...... 2422 Arden Way 95825 (916) 920-6804 San Francisco .. 455 Golden Gate Ave. 94102 (415) 557-1710 Santa Ana ...... 28 Civic Center Plaza 92701 (714) 558-4904 EMPLOYEE EDUCATION PROGRAM 415-557-8149 APRIL 21, 1981 69 Section 4: Union Approachs to Workplace Cancer SECTION 4 Union Approaches to Workplace Cancer This last section provides guidelines for ways in which individuals and/ or unions could approach investigating their own workplaces. One approach involves surveying for symptoms of disease or monitoring for workplace ex- posures. The second approach involves doing mortality studies to investigate if there is an excess of cancer deaths at a particular workplace. The latter approach is one which was used by a UAW union local president in Flint, Michigan. Some pages in this section are xeroxed from a booklet they put out on investi- gating your own workplace called "The Case of the Workplace Killers." (The address is listed in the general reference section at the end of the packet.) The ideas they propose are adaptable to any workplace. The next part of this section is on medical exams and tests and the last is on controls. One part of gathering evidence and protecting worker health can be identification of disease or potential disease. Surveys are one way to do this. Medical exams and tests are another, although exams are not, in most cases, helpful in identifying occupational cancer. Since few physicians are trained in occupational medicine, it is important for workers to provide in- formation to doctors about potential exposures. In this way, they can be advised about what kinds of tests to order, (if any) and if there is an abnormal result, they may be helped in making a possible connection to an occupational exposure. Also, some medical screening can help insure that workers aren't getting other illnesses from their jobs. The last section on controls covers the basic methods of preventing exposures to carcinogenic substances. This is the only way to avoid occupational cancer. Additional Reading "Case of the Workplace Killers" -- UAW publication. Address is reference section. 71 Adapted from UAW publications Union Action to Fight Workplace Cancer 1) List substances in the plant which are known or suspected hazards. Locations where cancer agents may be found should be noted and workers informed. 2) Arm yourself with accurate information. Know your rights and exercise them. 3) Make sure workers who have been exposed to potential carcinogenic substances are informed. 4) Collect information about exposures and symptoms through surveys or other means. 5) Insist on medical programs for workers who have had exposures to workplace hazards. (This will be more useful for substances causing other illnesses than cancer, but may help detect cancer due to occupational origin). 6) Press for strict controls even if minimum government standards are being met. Remember, there is no safe exposure to a cancer agent. 7) Remeber the basic control techniques: substitution, process changes, enclosure, local exhaust ventilation, strict housekeeping and protective equipment. 8) Develop political action to support strong regulations for the control of workplace cancer. Fight for a generic cancer policy or other similar legislation. 72 From "Case of the Workplace Killers", UAW, November 1980. PROPIIORTIONAL MORTALITY RATIO LOMJTHINO THE UNiON CAN DO A PMR study is a comparison of deaths between two groups of people. All the deaths among workers and retirees from a plant are listed. The percentage and number of these deaths due to specific causes is calculated. This is compared with a similar number of deaths among people not from the plant. Differences in sex, age or race between the two groups must be taken into account. PMR studies can be done for the whole plant or they can focus on specific departments or jobs. A study can look at all cancers combined, specific types of cancer or other illnesses. The results of a PMR study look something like the following: PMR DEATH CERTIFICATE STUDY Cause of Death Actual Number Expected Number of Ratio of Actual of Deaths Deaths Based on U.S. to Expected National Average (PMR) Cancer 75 50 Heart Disease 100 120 0.83 Other 25 30 0.83 These results show that 75 cancer deaths occurred in the plant. Only 50 were expected* according to national figures. Thus, cancer deaths in the plant occur 1.5 times as often as expected. Does this prove that the cancer rate is high or that something in the workplace is responsible? No. It's strong evidence, not final proof. PMRs give useful, but preliminary findings. In some situations they will not hold up when more comprehensive follow-up studies are done: Incomplete data: If people know you are searching for cases of cancer deaths, they will be likely to remember these and tell you about them. They may not bring deaths from other causes like heart disease to your attention. If this happens the percentage of cancer deaths can be artificially high and misleading. *The "expected number" of deaths in the plant is based on mortality statistics for the general population outside the plant. For instance, if 60% of all deaths in the country are due to heart disease, and there were 100 deaths in the plant, we would expect 60% of these, or 60, to be from heart disease-that is unless something unusual was going on in the plant. Most studies use na- tional statistics for comparison, but state or county figures are even better. 73 onso.ccupational risks: It is no secret that cigarette smoking is a major cause of lung cancer deaths. Let's say that a greater percentage of the workers in a plant smoke cigarettes than people in the community. If the plant group has more lung cancer than the communi- ty group, we'd have a hard time knowing whether it was cigarettes, a chemical in the plant, or a combination of factors which was responsible. "Healthy Worker Effect": A PMR study may show an increased proportion of cancer deaths for two different reasons. Either people are really dying from cancer at a higher rate than expected, or people are dying fronm other causes at low rates and cancer only seems high in comparison. This may happen mathematically if workers with chronic heart and lung clisease leave employment and only "healthy" workers remain on the job. If these "healthy workers" eventually die of cancer the PMR result can look abnormal even though there is no cancer-causing chemical on the job. PMR studies are, therefore, a good first step. They are relatively simple and can provide useful information. They usually don't point conclusively to a specific cancer agent in the plant. But if the results are suspicious, other studies can be organized and interim protec- tive action can be taken. WHIEN TO DO A STUDY In certain situations a cancer study should be one of your main priorities. This will be the case when you suspect there are too many cancer cases but: *The chemicals in the plant are not thought to be dangerous. *Measurements show chemicals at levels supposed to be "safe". *You don't know what chemicals are being used. In these situations you won't know exactly how to protect workers unless a study points you in the right direction. What should make you suspicious in the first place? The "Tricks of the Trade" section of this manual goes into this in detail (p. 23). But basically, if you've had questions about any of the following, you deserve to have them answered: *High numbers of cancer deaths or cancer cases among living workers. *Cancer deaths among young workers, especially those with more than 10 years' seniority. *Cancer cases which are clustered within a specific department or job classification. *SUnusual types of cancer among workers. Not every occupational health and safety problem calls for an im. mediate cancer mortality study. Studies are not the first order of business: *When an OSHA standard has been violated. *When health and safety protections in your contract are being violated. *When there is exposure to a known cancer-causing chemical. *When measurements show a possibly dangerous level of a chemical to be present. In these situations the priority is to reduce the exposure. Once immediate protective measures have been taken, it may still be a good idea to get a study under way. But the UAW opposes the "wait and see" attitude which postpones all action until studies are com- pleted. By that time it may be too late to do anything except bury the dead. 74 The International UAW can often help prised if it takes a year or more. It will go Local Unions decide if a cancer study is a lot more quickly if you have easy local needed and how to conduct it. The Inter- access to death certificates. national Union has health and safety ex- perts to help along the way, but once a STEP I: SIZINC THING;S UP study is started, the Local Union will have The first step is to decide if things look to play an active, involved role. The Local suspicious enough to undertake a study Union will have three tasks: and whether you have access to the *Compiling a complete list of active necessary records. You should discuss and retired members who have died over things with your International Represen- a period of five to ten years. tative who can consult with the UAW *Gathering death certificates for each Health and Safety Staff. Prepare yourself to person on the list. talk about these five things: *Putting together information on the 1. How many deaths do you know about seniority and past jobs of everyone on the among active and retired workers in the list. past five years? When did they die? How If you can get this information, the UAW old were they? What was their sex and can do a Proportional Mortality Ratio race? When were they hired and where (PMR) death certificate study. If you can did they work? only get some of this material, it may still It will be important to have some infor- be possible to do a smaller scale study. mation about the causes of death. The The whole process is slow-don't be sur- more precise you can be, the better. The 75 more information you can get from written documents (death certificates, insurance records) instead of word of mouth, the bet- ter. It is not necessary at this early stage to have a complete list. 2. How many cancer cases do you know about among active and retired workers who are still alive? What type of cancer? Age, race, and sex? When were they hired and where did they work? 3. Gather whatever information the Local Union has about chemical exposures in the plant. Lists of chemicals. Air sampling results. OSHA citations. Were there any major plant changes in the past 20 years that you can recall (e.g. foundry shut down in 1958; complete new ventilation system in 1962)? 4. Make a search of the Local Union's files to see what kind of records have been stored away. Dust off old boxes of records you may have piled up in the attic, base- ment, or storerooms. Does the Local Union have a file of death certificates for retiree deaths? Does the Local Union receive written notices of death from the company? Have old seniority lists been kept on file? Do seniority lists include Social Security numbers? Do the dues checkoff cards or other records include listings of job assignments and classifica- tions over the years? 5. How many current active workers and retirees are there? How many were there 10 years ago and 20 years ago? Determine this for the plant as a whole and, if you can, for any suspicious departments or jobs. After going over this information, you and your Servicing Representative will have to make a judgment. Is there enough evidence of a possible problem to make it worth going on? Your rule of thumb will be: When in doubt, go on to Step 11. 76 STEP IIo: DIGGING DEEPER gaps in your information. For example, 1. Complete the roster of deceased were you able to include workers who left workers. the plant with less than ten years' seniori- a. Decide exactly what is going to be ty and then died? studied: For example, all deaths occurring 2. Begin to get copies of death certificates in a specified five-year period, or only from state and county health departments. deaths among workers in certain depart- See page 17 ("How to Get Your Hands on ments or particular job classifications. It is the Evidence") for details. best (but not essential) to have at least 50 3. A plant walk-through by a UAW Health to 100 deaths included-this will often and Safety Staff member and International determine how long a period of time to Servicing Representative to see the plant use and whether the study should be layout and operations may be helpful at plant-wide or departmental. this point. This would include an evalua- b. Expand the list of deceased workers tion of potential chemical exposures and you started in Step 1. Your goal now is all the status of industrial hygiene controls. the active and retired workers who died during the time period you're studying. STEP III: COMPLETING This will not be easy. See page 17 ("How THE PMR STUDY to Get Your Hands on the Evidence") for 1. This step begins when you have obtain- some hints. ed all or most of the death certificates. You For each person you should include as can now do some calculations. Add up the much of the following as possible: total number of deaths and figure out the *Name percentage due to various causes. You can *Race and Sex compare these with the national figures on *Social Security Number pages 25-27 for a rough estimate of how *Date of Birth urgent this situation is.* *Date of Hire It may be appropriate to go to the com- *Date of Death and Age at Death pany at this stage to talk about voluntary *Active Worker or Retiree medical examinations or industrial hygiene *Place of Death (State and County) control even before the entire PMR study *Job History (See below) is completed. Or you may decide to wait. c. The more information you can gather Discuss this with your International Servic- on job histories, the better the study will ing Representative. be. What classifications and departments 2. Computer analysis of death certificates: were people in? During which years? You The Health and Safety Staff of the Interna- may not be able to get this information tional UAW is capable of doing this. It in- from Local Union records. But don't get cludes these steps: discouraged and don't stop your investiga- a. Dividing these certificates into more tion. The PMR study does not depend on detailed categories according to cause of this. Later, once you have some figures on death using an international coding the cancer deaths, it may be easier to get system. some job history information from the company. *This is rough because cancer varies with age, sex, race, d. Estimate how complete the list is. It's and year of death-you haven't considered these yet. important to know if there are any major 77 b. Obtaining mortality statistics on a comparison group (national or local death data; sometimes groups within the plant can be compared with each other.) c. Calculating the number of deaths ex- pected to occur among the workers. This is done separately for each cause of death and for different age, race, and sex groups. d. Comparing the expected number of deaths with the actual number that occur- red. This gives the type of PMR results described on page 1 1. STEP IV: PLANNING FOR FOLLOW.UP The International UAW will help you analyze and interpret the PMR results. If the PMR study shows that there are cancer excesses, it may be possible to link the problem to a particular chemical or type of work. But it's more likely that you won't be able to pin this down specifically without additional work. Possible Further Studies "Case control" studies involve a com- parison of job histories of workers who died of cancer with those who died of other causes. Detailed employment records are the key to this. "Industry-wide" PMR studies combine records from more than one plant and more than one company. "SMR or Standardized Mortality Ratio" studies involve tracing everyone who worked in the plant over the past 20 to 40 years, even those who only had short seniority. In most cases these follow-up studies will require outside help and company cooperation. Whether or not these studies are undertaken, the PMR results by themselves-will often help you decide whether to push for specific industrial hygiene controls and medical examina- tions. 78 CANCXER MORTALITY RATES 1 9751977 VARIRES (Deaths per year per 100,000 people) WITH IRACE I -144 Rates are greater among Whites than Blacks for: Breast Ovary Uterus (excluding the cervix) Bladder & Kidney Source: U.S. National Center for Health Statistics 79 I N rl*S6 7M5 .AAAl4 8'3L 91 -^ Before the OcMueona Sday an Hc&.th Adminstuon eablishas s5tn' HEALTHeANDiSAFE jLet requlaons tor v sulauon in 1971. iundreas o die casn macnina used to opate without any vniago at aiL S 'caMicnaeBnnt. who ha worked at ex\_t _ _1 , One Coidwater byRoad since 196w, says tht man scoops tL somaim sd-afterson the work ar would fill with smoke and fume so For this reasn the stry of .Miuchl tuck that woeras' coud aot r=ognize Benett's worple cancer Uvegation each other as Little as 'O ft awey. is apsecay ssgiicant It is a vivid exam. Exposu to mats from chrome and pie of wht a local union can aceom. nickel platg was aiso common. Fumaes pbsh-even when o L heath * from hot acids and plag soluuons issu are as complicatd as the cancer causd shorts of bmr and a cnog Lam is. UAW indusal hygiei Dm feeling Ventilation systema or the .McLmod deeba aBnet's work as a chrom tanka were poriy ed. mo for "barfoot di " It is And the huge oum nickel.piang an al-Iman rst stepti the Lon tan cancer is vented'dsrry into the March -si the wrkplac Thank tO OSHA reguiaon and yig. Geral Motor' Codw Rodfacdity orona union activty to, ensure Laur en. .... JA.11.19..TH .,TRr is a ma've. windowlan on'eor buhid. foM , working co u a Cold. ingatching over Idof squa fan and peched on 2.0 ar in * " in the la- 10 year Bennt the induitial suburhe nonrt of Film, S~~~~~~~~~~sav An as .ca mag i hav wn. Michigan. At the dime of its u A the ewiy 1950h, th pat was ooe of 80 of the die - Iy paint g the large die ca and a -J at the plast has beo pnad Ou Indus. facda in the world. kd wow am By Raober Howr Die ca B_'s fJdigs trial hygene ma indicate chat is:an induaSnl pamm in coXAfed by pfersinei sn & eore to me haa also ban sun. P L N4 r. E.I ( i. which molten me, usualy muc or suatl mdnX. But for the workes- aluinum, is injectd inwo wr-coold m:_red nor adaquaeby studied for at Coidvw Road sma wno worked un the i*Nw announced the wtin. met die a farned it Pae thur crnec effect. For yaz.- '50 and '60a-end who war Ue suc. mnOf is third annual such as door binge and handle, window workm at Coldwasr Rod wee expod je of!Michal Bent's t_dy.-(ha aank handles body tm and moldng. to m I fUMe and orgn too and auwbody items. comnouston change cam at. awrsiI"outstanding gal deo Afte prodm cased when hydaulic ois and Whe aked to expain how he con- men and women who"e accompilshments the rough edge on the pansMr ground die lubrcants ca m conta with the ad and c outd his workplaeacanu in.' and contributions have enricnled the smooth the pat are clened rinsed and hot mea used in the die castng proces. Contnued oa page 15 Ilva the platd in solutor ot coppr nickel of the stat's 9.2 millon residents." and chrome. Among the morw predictable luman-. While th chromat and The ari of the Great Lake SLata-tucta as nik com- cance study Bennett designed for DrOmt Lions footoal star Bly Sims pounds isai th platng prom ar Detfoit'v Catholic Cardinal. ;ohn known hum r the spc his own local is aimodel for other eand Reagan Admis o REAd. Di= b boy.onder. David Slocknan-wa the hav.i n unions of "barefoot epideiologyr." siame of -Michael Bennett a 37.Year.old journyma ppeflitter at the G-enr Motors Fisher Body plane on C;oldwatgr Roa in Fint. Mlcnigan. In 1977,Bent becme suspkicous about what sinned to be an unusually high numtbr of his fellow worker who wer sufering.and dyi.g from caner. So wnen he was ekacedom,identvof the UnAited Auto Workers Local 326 in 1978, Bennett dainded to do somnetning abu it. Ova the next tw yewr. Bnnet documented rate of cancer among Cald. water Road woreers two and thre tane the normal te in a comparable popula. dion. sett int motion a major ncr alem at the C.M-Fisher Bodyv plant. According to the Deuroit Vews, "Ben- ntt's work has drawn atetion to the oheath hannd that aeisn the autmo- uive indtust and paved the way ror rutur inveisusations." Bennett's rindings. since confimed by UAW health and safety profeasonals, the Michigan Department of P.blIc Helth.and the Sloa-Ceterng Founa'a- tion (under contract to General Motors), ae an important additon to the mount. ing evidence that occupational cuane is a sarous Proolem in American industry in generl ad the automoole industy in particlar The -Natina Canc Institute and4 toe NanionailInstitute for Occupa. tionsa Sasety and Heauth have cmm&Wne that betwm 20 and 38 M=9~Of ail can. Udathuar reated to epoure on the job. In the auto indusy alone, reiminu- ary studiet save identified abnormally high number of an rhated eAt among netal worKers, foundr wcr.ers, and W oo ro0nel and P 3trMaK19. Then lng latecy period aof mo can- cm and the wide varety of potentaly caroogenc c±sernucasi used in Industry mage0oth tho cent of ccupalona cwncr and its secric causa notoiously difficut to determie. -ut even "if only a fraction of the retorts sre eventually sun. itatiateo." .id jAW -,,resident Doug. ias Frae in an aadress to the Amercan Olccupationas 4e2ith Conference .ast !ear. '-e will fact a suotic .'scestn mroo- .emuo maior 1i.nsions.' EdUo,'s nstoe 7h&S a thesecond of infee sric,as oy Rooe? Hot-era on. worsen' '?eaatth and sal e:v. Like mne 'In:f O7let in the :eners in thn times. ofarrs 'i. a aPof7ler a successfl /inoofloo, efmfounr: -fdIC' wO,xdp,he 11ta:ara. A 'mat i- Cie wtead he pa'osnuecfrni,cn 'nOK. wa.Ad e mlat,voV n nAetAt Reagan Ocnn. SO is rTht TWO hAO4 &Af - of has submt' lat known addrn. he poputon to 23L. Union cxo an cn' of the lung," says Dr. Ro bepan a massiv seamrc of ptsdic rsrws made a few muno tedincal cnsangat-for W i.eek, dirtor of occunataonni aiery for the deah metifltt -MOt we cumple. redaing the ceona for su heathforGe ral Motors. "'s it due found in Ge_ume Couty we th caus of deth so tha they corupona to iwtoram eptosur? Sura it could Cancer vpl is l But som come from to the In--aol Clarficuo of Dis. be But it could alo be somethng els. stae a fr ay as A=n and an svstm d adjustng the .com. We mUli do't kow enot shout the Contunid /mm pep 7 FloIda. pso n_Benet's sway for ag. sm. poble to sy. The imtaon an ther: wauion Micne Bent cam it 0m be had the deah etificaL, r. ad ver of dea. When ue rear. the IS no Gaun about Lta But weCneed was "m a matr of comm si i.'" Sam s AM a fl yw on wha ganasd as wae plugg in to an elan-t more time." UAW inouwi hygen Dan .MCUso he mil "th l dIfscu powtl of ha ora c omputer pro Union offiia say tht dapse dis- ha a bew on te matof Be dydev-opeag c na for fthe deveope a th Havad Sdood of Pub. sumena betwem compay and uni lt's iin nL dfe. hes ca. "mie o(dth" bst eanthedmfm Bc Healh ai runly. added to the ove the cua sgficnm of Bennet's Smu "veted" _spdlog fram and compam tbm w nauona ns- UAW com,put. staffas not only coo- flnins, thei vy et n to t. "We did it al amallwy." he as. frmd s rndMp but wfe able inaon the aeo ney have re. _udmologyE is th studyof themu- "We dId't bae a compu or san. to trmtt the" Wpoersm cmvdb- force the c n to of diseas by wgit anhum Popeibe- thing' tn"-tht u, th nube of yasM acL So far. GM hat arm sto an why mom The clnc fathe of epedeiiol og When he finell complaud he study inwre workA in thd la'.'a dMmhy warning cancar dwAmon systm.at the w Londoo phyusoa John snow WmIImi Mardi. 19, Bennet bad uncovaud relatd to thmw ofve mm The pat and an indusIa hypene surveyqto 1855ia_m epudme of choi tot th drMme fldne Blghty.wo of his =S lun c rcn meR= punter as inmre Cmor pamuar levels la fit _mWV drinkin wat p- by suibem ded of ci-36.4 puinama yws of wor b th pln inauud. a step b the dscion abo new ae one of Loudon'as m prive we W sudy popuama fwfora pinn solid "inion tha the camms a Cl- -in cootrobLs A prprinlmortal- compamW Any eFfwive enidnelsM. mwt_enu mono m Them acm. wow Rou wawwrk-aia ky mo study is also uneway as a sit ca stisy of o o db_ nMm a dam"e Wm Wsha tomy inunsud Uni on eat and sdafey pofaniouds plautof te Fint fac ity. AndSlan .. ak th_m M uic LS tmm a for by Imp r. Th et e twn w on s. fute. By lmean of a terig ha b enr toconduw a Mha probho mongasmfl gong of may blg mm des as nano fg "em Crol stuy" i te job more thorough " isad mortaiy worm? If so is i wk.rieud? And lIf woul Mm o to mpmm And for hadoeh-of th_ worikea n sd man" uyof Catelodwor . it i Wo u who is Xt a or the owh wosan ho stdy. S 'spoput_noop who had died fm cm= "We wl do eveytig we cm to WY to P sX in th pn ta s to be finim wa Wpedaiy The with the of work.. who hd nm thy fid dhe sa ufi reason for thi" saida cmu_ th prolm? lsungmm reo on M A.mp.m.haf ed to dcovr whom work a any GM spokeaman. "Aftr al, ty am ou On big owe Mich a_Sm _wred urnI the hek tin. ler job or dn - pea- thefisof tb_mquunoa Heedevelogud The UAW's bInt a safty sff plsta . BnuaIeof the S0M p~v ifo_nm on th "hoOth hwond of Momens stuady at the imoi du& availble, says MI4WM Silverman. The h lin of defe. stat" of Coi Ro work bY tarn Cs W Motoe and the pens the rmb of the camcommoi study wow The _oo of Coidw Road for UAW coming the men 'o duo ibe he "We Wm plany fflppe out whee we "slsve, cmsn finey amugh Mm bhah ad saferty profrnas is that sudy popuslhoa to the u_oos goer. sw at. Seomea vmmsogood." san On for thepupoa mvm an" wke sm like Mche Sm's m o- -MacLeAd. "ft mat a very pM ed At thie point, no oude knowI.- for sme betheopiggwedg negoio wh_ su.bWe kegp MM *''o thd what musudthe ofC e the ao o cum Snaftrhe?waWmIIcm lcianon iy?' lod but un_. oomr have thw via. polcy. "Cokdmat Road is a mil. SmenM _-t inbe IV1V8,Sm~ ftwmean Dra.MlM MvrI.aap mioB.pao S d knoa craog such th soma."' says uno inusua hygei fie of 1mw from _mpen oofyuig gOn on the uONs health Nd St a mom ad mud, the key sspect Du MLeaod "It sort of glied ow th local nc am a for Codwain. carefuly wm Somer's Ap. is abm of d-mah known -pofygy ida about dog ths art of thig On L Rawdemloye dia TheletmetWI- "Imdimely. it bmuotappunmo the dile sunsuiP hy aroaroa or PAkILS the of a wider bMmi ma agom wa C1M 'MOM had thoAS thioughtIthpIm PSm wmaerw igorgrnawo =Oh For nmeivy them years the UIAW Mmkh an the UAW thaooelV hd mealag is pMOMy SUeNeI waY tho an 011kmb- ..in:som or oal iL bwaned. thet are to do wIs and safety rnff has Mm dituomig hsow beath andsfety. The o ea wul hv bougtit theough me I.Mcbinlb to PAH fMmy. ben to amile the ammr Isse. "'We've Pa WmorSao -ocl mo VW AS - t I saw Mhe "Wy he tidged the. Bern of tfMmoWe _mgeis -oweur it pay out a beneit the Mm alking about 'hiow do we do re- nuder cingniN tMI I how it we sek.g W- be C- One PA a. ha smedi? What's our wategy?'" Michae - apsmlw ths M I fabolm ry 4ly" Mm idtoldat abm for.IOnerM i_m ho'eis'o f_ of Sm'as study demostratmed that tbe ia= t MeBu wabe Sm :e apdydhoydam. uwok.a, Worm m colm then own datawith.-. m oe collo Pro an homed of cow UAW bhIth Mm safey poeMI dwtsbeomn.Smmonmin n oum having. to deend onm manaens gt o VMU Mm wok-rMm? apIme tho'the anoa fohm ad and pId a mast "All of a sudden Mike prvi ananm aof=25 Cldwewload How. the UAW's healt ad eafety mi fghiaa in" in the dwie MpomR s waMerwhothd ov a pe swe." aptlunei Mced"T is the Alvew.er ad both velidao and comm the oripgia may b aveeao workerwsto wmar=b. way we can go. It involve our loca pmc. frm Janry 1. 1974 to Ds _ 3H1. fd. Rnhdsflmt heL e mn t But PAHM r be. a the Thm. working from - pie and gin us a way to cod= informs. *I9M. JmWo oni's pinoa mso sadild "VOTud ameig operaumnlaatmo Mm adaguase lion without having to go to the coal- Iv studied. and diacoluring ftem Pen. we've fo"undths realy ipnai * PAH Mi fMS is t caly dfflual so be able to say to the helos, 'here are ;"We he rio, omonv abou PANs mu= thing that you man do.'"" 1:1 tok nunmy" saysM Silversim "Cam. To enemeem this kand of rankand. crs backd up by a subtim a ut file snitisoe and axperuns. fth UAW has ,oi 4 _n B t thra to developed aco"-Pmprmieve owmuetiona this p_rom po, we doat av the amm progaE m.thpsd to provide an dam to peor thefsm at PAHs a op.- ineio alunionsppr sysum for -oo to ot her immie", promp s, hos-im-m epdeiolgc in- vsauOm f potential hazards. Th Thu ou_ -'l,*X u kmohopublIshd a handbook for loca Thes hawing unemy hatshpd the offiials enoled "th cor of fAt Work- negumiomh Mhe UAW adCGm. p1wv xman A MeaWfaador Lmmwe D- am Moms about wha to do a Coidwa- to&tWinkomstssacatanepuysow the Jo. It aplain how tw oud adotoam p iComm workers can aom peemoogu data ib geneaL The UAW ha ad_opd a pr*. on then own and whe they should come vme approm* tha midkn ay in to the ineraiona for hap. The uno diao howwer prellunnery. of hig ame hat an arrasnaenit with the stat Of m tun atpunds for "Ipruumouve Muchign making it cner for loMm to mon." Whie comidona at Coidwae get deWat cerl'mzea dirmity from the Rood ha ilmmvkn co rbly ove state thus avoiding tumecoeamig the ls 10 yins, uon meus say thr countLy-by-countmy searhat. AnwMe am sIl chan to be Wma. Momvr. tedeathub fcs havethem toMmogo, new Mmrds ae p-ong Xmexous fth nmoms coompute is available to ad alon wish theto=auhsanm used Mn analys the dat compeled by the locale. *-tho dplic _edcu. "gWe do't Slmc Mmdg and safety reglaton has mm mowa what the nsm asn wsh thme bemme a prime targe for the Reama no ae" ealleSlst Admlmmion- (and Mmisel Smut's For tm ama the a is sei. fello Mlha Of the Yew. buidg gw GM for'am be shiWNW dirnor David Stockniani thisrank-end. -nsed m-m uv r of the fie labor appreond to Wmorkpli cmm Coldwater Road wokfoe. liududig is all the more nomery. OSHA's nww woker eumnon progi sbout oa. Cmm policY. laumndied. simont a-e meoa_: fute eplImo ago, ho alreadytbeen hobbled bythe Su- mi anmd a om preme Court's beazene decision of las summer, whicm challenged te regulatory Says Sivussein. "'We want to aie the princile of "lowMea famsbie uponae." step today that am oig t avod havung And one of the rims acts of Raymiond another MIhds Sm rport 10 yer Donovan's Labor Departmen was to dow the rod." camml public hemntp on a proposed In coaa to the unons preuiv OSHA standard to give workers the ngnt apwrt however. Generai Moors ha emphasized the cautious search for scam- ae unng in the workpam. tific ceaiy-hard proof linkg high So whit corporauons wat for scientif- Cance atm to spcfic substancn in tme ic ewuwny. an ue foaa governmnmt woraplac. While rWognsnn what one bacs sway from mu commiLmnt to corporate spoaesman termed "the worm helth and saiuy aLogteie. it begistend concen about caner among wil be Uo to ianor to sero tne oraia- " wa, er at Coidwatr Road tte cormo - onancm isu alive. Ths. anyway. is ao a stil unwillig to aat tha tnae Mchael bnntt's nop. What w UAW c wws 1otc o the job. C's Progam wlU mea, ie Says. is "The OSY nss we is tha it a tha "*hr ar going to be a la mo pars Uw is ean devaid omM of sunam like my own." a * ~~~81 LOHP Files Medical Testing/Exams and Cancer Since few physicians are trained in occupational medicine, it is important that whenyou visit the doctor you supply a good work history that includes any exposures that you might have had to any cancer causing substance. This will shed light on the possible causes if any abnormal results show up on the exam or lab tests. Some cancers can be detected early and are more likely to be able to be cured. These include skin, breast, cervix, larynx and some oral cavity cancers. In terms of detecting cancers at an early stage, it is important to keep in mind the seven warning sighs of cancer: 1) Change in bowel or bladder habits 2) A sore that does not heal 3) Unusual bleeding or discharge 4) Thickening or a lump in the breast or elsewhere 5) Indigestion or difficulty swallowing 6) Obvious change in a wart of mole 7) Nagging cough or hoarseness The primary sites for occupational cancer are lung, skin and bladder. Other sites which are also affected include nasal cavity (nickel) liver (vinyl chloride, carbon tetrachloride), blood (benzene), stomach (asbestos), and bone (radiation). Currently, there are no really good medical tests for revealing cancer. Checking bladder by cystoscopy is used for bladder cancer detection in some cases. (Sputum cytoloty has been used to detect lung cancer, but to date there is nM evidence of its value). Also, these are not practical on a large scale and are not totally reliable. Many workplaces have medical surveillance programs. In fact, OSHA regulations require companies to offer exams to workers exposed to the following regulated carcinogenic substances: Asbestos Vinyl Chloride 4-Nitrobiphenyl 4,4-Methylenebis (2-Chloraniline) alpha-Naphthylamine methyl chloromethyl ether 3, 3-Dichlorobenzidine (and its salts) beta-Napthylamine 4-Aminodiphenyl beta-Propiolactone 2-Acetylaminoflourene 4-Nitrosodmethylamine bis-Chloromethyl ether Benzidine (and its salts) Ethyleneimine Coke oven emission Arsenic Acrylonitrile 4-Dimethylaminoazobenzene 82 The particulars of what tests should be offered for each substance are contained in the regulations and should be checked when a surveillance program is being offered. Also, even though companies are required to offer the tests, workers are not required to take them. If they do take them and problems are uncovered, there are protections from total job loss and provisions for con- tinuing medical care which should be offered to the employee. 83 Adapted from WIOES/LOHP files & fact sheets Monitoring and Controlling Carcinogens in the Workplace' I. Monitoring the Occupational Environment The general principles involved in evaluating and monitoring the oc- cupational environment include the following: recognition of poten- tial hazards, preparation for and conducting of field studies, and interpretation of results. A. Recognition In order to discover what potential hazards need to be monitored, one must do the following: 1. Become familiar with the exact work processes. 2. Obtain an inventory of all chemical and physical agents present. 3. Periodically review the various work processes for changes. 4. Ascertain what controls (if any) are present. For carcinogens regulated by either Federal or CAL/OSHA, em- ployers are required to register their use with these agencies, as well as post signs that these carcinogens are present in the workplace. For materials which are not regulated as carcinogens by Federal or CAL/OSHA, but are listed by various agencies as suspect car- cinogens, the posting of signs is- not required. Employees should be able to obtain MSDS's for the materials that are used in their place of employment and should check to see if they are listed as suspect carcinogens. B. Preparations for Conducting Field Studies Once the processes have been evaluated, the chemical and physical agents have been identified, and a check of controls has been made, monitoring of exposure levels can then take place. Monitoring is important for both workers and employers: workers be- cause they may be exposed to dangerous materials; employers be- cause, under OSHA, they are responsible for controlling worker's exposure to toxic materials. There are quite a few instruments available to monitor the envir- onment. They are generally classified by: 1) direct reading in- struments; 2) those which remove the contaminant from a measured amount of air; and 3) those which collect a known volume of air for later analysis. The type of instrument used usually depends on: 1) how portable it is; 2) its reliability under field use; 3) the accuracy of the equipment; 4) the type of analysis re- quired; and 5) the availability of the instrument. 84 There are also continuous monitoring devices to evaluate the workplace. Examples include monitors for chlorinated hydrocarbons, used in the production of carbon tetrachloride and monitors for hydrogen sulfide gas. The number of samples and length of sampling times depend on a number of factors including: 1. the type of hazard (acute vs. chronic); 2. the sampling rate of the instrument used; and 3. the sensitivity of the method employed. Substances with very low Permissable Exposure Limits (PELs) may require long sampling times. In preparing for monitoring, one should also determine the best time and location in which to sample. Sampling should take place during the greatest potential exposure period, if this can be determined prior to monitoring. In terms of where to sample, there are three general locations: (1) the personal monitoring device placed on the worker, (2) the device held in the worker's breathing zone, and (3) a general room sample (area sample). In assessing worker exposure levels, personal monitoring provides the best overall estimate of the exposure to the worker. For certain carcinogens (asbestos, vinyl chloride, EDB, DBCP, acrylonitrile, MBOCA, inorganic arsenic, and coke oven emissions) specific requirements for monitoring are spelled out in the federal and Cal-OSHA regulations. For other substances which are not specif- ically regulated as carcinogens but have established PELs, NIOSH certifies specific sampling and analytical methods for specific sub- stances. For the 14 materials regulated as carcinogens (4-aminodiphenyl, etc.) there are no monitoring requirements specified as there is no allowable exposure limit for these substances. Rather, the employer is required to report the use of these substances to OSHA and is also required to file an incident report if any worker by accident comes in contact with these substances. C. Interpreting the Results Interpretation of results is the final step in the evaluation of the work environment. Workers have the right to request these results from their employers. Once obtained, the results should be compared against the applicable state of local standards. Permissible Exposure Limits (PELs) (for cancer-causing substances (see List I) which have established exposure levels can be found in various sections of the federal OSHA and Cal/OSHA regulations. As stated earlier, for certain carcinogens (see List 2) there is no established PEL as it is felt that no level of exposure is acceptable. Also, it is important to remember that existing PELs may not represent safe levels. 85 In addition to comparing the monitoring results with PELs, workers may want to check other sources for comparison as well. In some cases, the Threshold Limit Values (T.L.V.'s) established by the American Conference of Government Industrial Hygienists (ACGIH) may be lower than the OSHA PELs. NIOSH also has recom- mended lower exposure levels for certain substances. One example is asbestos, a known carcinogen. The OSHA P.E.L. for asbestos is currently Q5 fibers/cc; whereas a NIOSH/OSHA workgroup recommended a level of 0.1 fibers/cc in 1980. Finally, the many occupational health specialists believe there is no safe exposure level for asbestos, or for any other known carcinogen. List 1. Substances Regulated as Carcinogens* Which Have Permissible Exposure Limits Acrylonitrile Inorganic arsenic Asbestos Coke oven emissions Dibromochloropropane (DBCP) Ethylene dibromide (EDB) Vinyl chloride *Fed OSHA does not regulate DBCP or asbestos as carcinogens, but Cal/OSHA does. List 2. Regulated Carcinogens for Which There is No P.E.L. n-Nitrosodimethylamine 4-Dimethylaminoazobenzene altha Naphthylamine(1-NA) alpha Naphtylamine (1-NA) 4,4'-methylene Bis (2-chloroaniline, MBOCA) methyl chloromethyl ether (ClIIE) 3,3' dichlorobenzidine (and its salts) bis-Chloromethyl ether (BCME) beta-Naphthylamine (2-NA) Benzidine (and its salts) 4-Aminodiphenyl 2-Acetylaminoflourine Ethyleneimine beta-Propiolactone II. Controlling Exposure to Known and Suspected Carcinogens Controlling exposures to known and suspect carcinogens follow the same principles as controlling exposures to other substances, i.e., engineering controls, work practice (administrative) controls, and personal protective equipment. A. Engineering Controls The most effective and permanent way to control health hazards is through the use of engineering controls. There are three main engineering control techniques: substitution, isolation, and ventila- tion. 86 1. Substitution Substitution of materials, processes or equipment, is the most positive form of engineering control. One example of material sub- stitution involves the carcinogen vinyl chloride. After discovering that vinyl chloride caused liver cancer, it was replaced by carbon dioxide (CO2) as a propellant in certain aerosol cans. An example of process substitution is the substitution of dipping instead of spray painting to coat metal parts. This substitution of one process for another greatly reduces potential exposure to hazardous substances. 2. Isolation Isolation means installing a barrier between a potential hazard and the people who may be affected by it. The best example of isolation to control exposure to carcinogens is the establishment of a fully en- closed structure (such as a glove box), which is impervious to the passage of carcinogens into the work area. Specific procedures for isolation of carcinogens are spelled out in the OSHA regulations cover- ing carcinogens. 3. Ventilation Ventilation is the movement of air to keep contamination from reaching the breathing zone of workers in the area. There are two main types of ventilation: general or dilution ventilation, and local exhaust ventilation. The first type (dilution or general ventiation) dilutes contaminants in a room by providing constant air exchanges. Local exhaust ventilation removes contaminants at their source of generation. Of the two, only local exhaust ventilation can be used to control exposure to known or suspect carcinogens or any other toxic substances. Specific regulations concerning ventilation for use in controlling exposure to regulated carcinogens can be found in the OSHA regulations. B. Administrative Controls Administrative controls consist of measures such as rotation of workers in hazardous areas, job training and education, written work procedures, and posting of warning signs-. In some cases administrative controls (such as training and education) may be combined with other control measures. In general, the use of administrative controls is less desireable than the use of engineering controls. For exposure to regulated carcinogens, specifics for education, training, labeling, and posting of signs are spelled out in the OSHA regulations. C. Personal Protective Equipment The third and least desireable way to control exposure is through the use of personal protective equipment (PPE). This is the principle of isolating the worker from the environment. For the most part PPE should only be used for emergencies or while administrative and engineering controls are being instituted. PPE may include respiratory protection, protective clothing, and protective eyewear. 87 1. Respiratory Protection. There are two main classes of respir- ators: air-purifying and air-supplied. Air-purifying clean the air that is inhaled while air-supplied provide workers with their own source of air. Cal and Fed/OSHA specify the particular type for a particular exposure level or for particular substances. In general, air-supplied respirators are required (by law) or recommended for exposure to cancer-causing substances. However, for certain car- cinogens OSHA does allow air-purifying respirators for exposure to very low levels of the substance (e.g., high-efficiency air-purify- ing particulate (HEPA) filter respirator for exposure to asbestos). In addition to the regulated carcinogens, OSHA requires employers to provide respirators "when workers are required to work in areas where chemical and radiological hazards, or irritants, may impair their health." These regulations mandate that the employer must establish a respiratory protection program which includes written operating procedures, a training program for work, provisions for proper cleaning, inspection, maintenance and storage of respirators, individual assignment of respirator (when feasible) and, routine monitoring of the area to assess exposure levels. 2. Protective Clothing. In addition to respiratory protection, protective clothing is also required to protect workers from exposure to cancer-causing substances. The type of protective clothing necessary depends on where contact with the substance is made and its route(s) of entry into the body. Protective clothing may include gloves, hair covers, face shields, goggles, smocks, arm covers, pants, and/or full impermeable body suits. If the entire body is exposed, the proper type of clothing would normally include a jump suit with a hood. For exposure to known or suspect carcinogens, separate clothing (including full-body protective clothing, shoe covers and gloves) is usually required to prevent exposure. OSHA has specific require- ments as to the proper protective clothing to be used when working with regulated cancer-causing substances. In addition to providing the proper type of clothing, it is the employer's responsibility to provide separate lockers for workers and to provide for decontamination and cleaning of this clothing. In summary, personal protective equipment (PPE) should only be used in emergency situations or while instituting other types of controls. There are numerous limitations associated with personal protective equipment, including: inability to obtain a correct fit of the respirator or the clothing; breaking of the seal on the respirator while talking and working; breakthrough of toxic substances through the protective clothing; inability to communicate with other workers while wearing PPE; increased breath stress for the worker; and potential difficulty in breathing while wearing air-purifying, negative pressure respirators. 88 OCCUPATIONAL TOXIC EXPOSURE HISTORY I -Mm m C) CA C) (D -J -a- -J. -J m 0) OJW --A a. o (< Tl - 0 C- -J . I > CD C3 0 a 0 CD 5) M=3 = £ CD I CD c)I -3 I-,3mC-i -0> 0CD -J. CD = CD -< Z CD 3 ,.<'. mm CD -J. * OD 0 ; S. m C CD -4-) CD (D r 0 0 -- 0.0 £ X CD:=- --a. 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Cm 0 M'C (ICD .A -5 00C (0 CfD- M U) m 0 CD (D:~~~a - Dl 0 - r~~~~~~C {D' 0-' O00 0 -. (0- -:.0-' 0_. 0 =-0 0(0~~~~~~(CD '-a) 0 en0 =-- gwo ox *-. =0 A- = 70-0-C+1 m 0-5 S- 0 SCD 0 0 < . U) =. O0t< CD .CD .3 -n QCO 0 0 -U) 5-CD CD *CfD Or'._U)- = _: Q~~ _O- 0-_ -5 _ f~~~~~~D -4 0 30 90 References REFERENCES WRITTEN MATERIALS: Asbestos Dust: Everybody's Problem, by Robert A. Fowler, Western Institute for Occupational/Environmental Sciences, Inc. 1977. Contains much useful information about asbestos hazards, occupational lung cancer, industries where asbestos is used, and the responsibilities of workers, unions, employers, and government in combating job hazards. Basic Concepts of Occupational Cancer, Gordon Atherly and Robert Whiting. The Canadian Labor Congress on Cancer in the Workplace, February, 1981. Montreal, Quebec, Canada. Biological Abstracts and Chemical Abstracts. Subject index gives a reference number for technical reviews and original research articles. Good for a quick review of available literature. Cancer and Chemicals. Corbett, Thomas, Nelson-Hall publisher. Cancer and White Lung - The Plight of North Carolina's Asbestos Workers, North Carolina Occupational Safety and Health Project and the North Carolina Public Interest Research Group, 1979. 70-Pages. Available from: NCCSH, Institute for Southern Studies, P.O. Box 230, Chapel-Hills, North Carolina 27514. Cancer: What To Know, What To Do About It, NCI. NIH Publication number 82-211. Pamphlet. Available from: Cancer Information Service. (800) 638-6694. Cancer and the Worker. Tehmann, Phyllis, New York Academy of Sciences, 1977. 2 East 63rd St., New York 10021. Cancer and Your Industrial Workplace. Occupational Cancer Task Force of Suburban Cook-DuPage County Health Systems Agency, October 1982. The Cancer Connection. Agran, Larry, Houghton Mifflin Co., 1977 Carcinogens. NIOSH publication, DHEW 77-206, Public Health Service, Center for Disease Control Case of Workplace Killers, A Manual for Cancer Detectives on the Job. UAW, 1980 Chemicals, Work and Cancer. Le Serve, Vose, Wigley & Bennett, 1980; Nelson Canada Ltd., 81 Curlew Drive, Don Mills, Ontario M3A 2R1. CIP Bulletins available from the Carcinogen Information Program, Webster College, 470 E. Lockwood, St. Louis, MO 63119. Bulletins providing reliable, understandable information on selected carcinogens. Fifteen bulletins are now available. Write for more information. Consumers Sourcebook, Vol 1 and 2, by Paul Wasserman and Jean Morgan, Ed. Gale Research Co., Detroit, MI, 1978. A directory and guide to government, media, health and legal organizations, consumer groups, newspapers and trade and professional organizations 92 Corporate Causes of Cancer in California, Paul Blanc. Los Angeles: CED, 1978. Prepared for the Campaign for Economic Democracy (CED) and the Public Policy Center. Available from: Campaign for Economic Democracy, 304 South Broadway, Suite 501, Los Angeles, California 90013. Crisis in the Workplace: Occupational Disease and Injury. Ashford, Nicholas, MIT Press, 1976. A look at the major issues surrounding occupational health and safety. Discusses the effectiveness of OSHA standards and provides information about inspection activity and penalties levied against employers who violate the law. Dangerous Properties of Industrial Materials. Sax, Irving. Section 12 lists chemical substances and gives a "Hazard Analysis" of each compound. Information on toxicity is given in clear, easy to understand language. Will indicate if a sub- stance is carcinogenic. Covers a large number of industrial materials which are not found in other places. Death on the Job. Berman, Daniel M., Monthly Review Press, 1978. An interesting historical look at the growing awareness of occupational illness and how workers, unions, and government have responded. Covers, for example, the enactment of the Coal Mine Health and Safety Act of 1969, including the union and political struggles that brought about the legislation. Also discusses the difficulty of obtaining compensation for occupational diseases. Environmental Cancer: Causes, Victims, Solutions. Available for $1.50 from: Urban Environment Conference, Inc., 666 11th St., N.W., Washington, DC 20001. General overview of the cancer problem by many experts. Everything Doesn't Cause Cancer. National Cancer Institute, 1979. Pamphlet. Available from: Cancer Information Service. (800) 638-6694. Free. Finding Your Way Through EPA, Available free from the U.S. Environmental Protection Agency, Office of Public Awareness (A-107), Washington, DC 20460. Guide to the different branches and personnel in EPA. A Handbook-of Key Federal Regulations and Criteria for Multimedia Environmental Control, by D. R. Greenwood, G.L. Kingsbury and J.G. Cleland for the U.S. Environmental Protection Agency, August 1979 (EPA-600/7-79-175). An overview of federal environmental regulatory laws such as the Clean Air Act, Safe Drinking Water Act, Occupational Safety and Health Act and Federal Insecticide, Fungicide and Rodenticide Act. Good for background information on which federal regulations cover what specific problems. Help for the Working Wounded. Mancuso, Thomas F., International Association of Machinists and Aerospace Workers, 1976. Provides details about the hazards represented by various industrial substances and processes and discusses problems workers face in receiving adequate treatment and compensation for occupational illnesses. The International Agency for Research on Cancer (IARC) Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Vol 1-23. Monograph reviews on hundreds of chemicals include all current animal tests and description and background information on a chemical substance. One of a kind in bringing international research information together in one place. May be slow reading for the general public. 93 Job Related Cancer - How You Can Help Prevent It. Employee Rights under the Occupational Carcinogens Control Act. California Department of Industrial Relations. Available from CAL/JSHA Communications, 525 Golden Gate Avenue, Third Floor, San Francisco, California 94102. (415) 557-2237. Malignant Neglect, by the Environmental Defense Fund and Robert H. Boyle, Vintage Books, NY 1980. Up-to-date report on cancer-causing chemicals in the environment. Clear and easy to read. The Merck Index: An Encyclopedia of Chemicals and Drugs. Gives synonyms, chemical data, references for original papers on the chemical, drawings of the compound structures and most common uses. The Merck Index usually does not mention toxicity or carcinogenicity and is useful mostly as a guide for chemical information only. National Toxicology Program's Second Annual Report on Carcinogens. From National Technical Information Service, Springfield, VA 22161, (Report No. PB 82-229-808.) NTIS Government Reports: Announcements and Index. The National Technical Infor- mation Service (NTIS) is a central source for public sale of government-sponsored technical publications. Includes subject, author and report number catalogues. Occupational Cancer and the Fire Fighter. Department of Research, Health and Safety Division, Int'l Association of Fire Fighters, AFL-CIO, 1982. Occupational Diseases: A Guide to Their Recognition. U.S. Department of Health, Education and Welfare, 1977. A rather technical volume intended for health professionals, but contains several good detailed articles about occupational lung diseases. The Politics of Cancer. Epstein, Samuel S., Anchor Books, NY, 1979. Reviews government policy in controlling carcinogens, health effects of many chemical sub- stances and agencies responsible for regulation. Clear, accurate and very powerful. This Rat Died In A Cancer Lab To Save Lives: Animal Tests Find Most Chemicals Aren't Killers. Washington, U.S. EPA, 1980. Pamphlet. Available from EPA, Washington, D.C. 20460. (Order number EOA 15/80.) Free. The Readers Guide to Periodical Literature. Lists articles found in popular magazines according to subject and author on a monthly/yearly basis. Registry of Toxic Effects of Chemical Substances, by the National Institute for Occupational Safety and Health. Available for sale by the Superintendent of Documents, U.S. Government Printing Office, Washington, D.C. 20402. For thousands of chemicals, gives toxicity, dosage, species tested, manner tested, references, regulation standards, other chemical names and data. Report of The UEF-NCI Workgroup on Environmental and Occupational Cancer Information/Education. Urban Environment Foundation, 1979. Under grant from NCI, Office of Cancer Communications. Available from: UEF-NCI Workgroup Report, National Cancer Institute, Building 31, Room 4B39, Bethesda, ND 20205. A Retrospective Survey of Cancer In Relation To Occupation. P. Decoufle, et al. NIOSH #77-178. Research Report. Available from GPO. (Order No. 017-003-00230-4) Limited free copies available from NIOSH. $3.75. Science and Cancer. NCI. NIH Publication number 80-568. Pamphlet. Available from: Cancer Information Service. (800) 638-6694. 94 Science Citation Index. A listing of scientific literature on various subjects. tHas a subject, source and citation index. Very useful but may be difficult for a beginner to use. A Toxic Primer. by the League of Women Voters, 1730 M. St., N.W., Washington, DC 20036. Explains the difference between carcinogenicity, mutagenicity and teratogenicity. Copies are 40, each. Ask for Publication No. 545. The Toxic Substances Dilemma: A Plan for Citizen Action, available free from The National Wildlife Federation, 1412 Sixteenth St., N.W., Dept. T.D., Washington DC 20036. Excellent review of toxic problem. Explains toxics, toxic effects, government regulations and actions citizens can take. United States Government Manual, for sale by the Superintendent of Documents, U.S. Government Printing Office, Washington, DC 20402. Stock No. 022-003-00982-5. An excellent overview of government agencies. Each branch, agency, commission, etc., is reviewed with an explanation of purpose, function and jurisdiction. United States Government Publications: Monthly Catalogue. Lists of government documents on a monthly basis. Indexed by subject, title and author. Government depository libraries have many of the publications in the catalogue. Ordering information is given. What Every Black American Should Know About Cancer. USDHHS, NIH Publication No. 82-1635. What You Need To Know About Cancer, NCI. NIH Publication number 83-1828. Bi-lingual pamphlet. Available from: Cancer Information Service. (800) 638-6694. Work and Health, Inseparable in the '80s, by Howard P. Greenwald, Ph.D., 1980, WIOES, 2520 Milvia, Berkeley, CA 94704. AGENCIES: Citizen Organizations (*indicates major areas of interest; ** indicates newsletter, magazine or other publication). (C.enter for Scienre in The Public Interest (CSPI), 1757 S. Street, N.W., Washington, DC 20UU9 (202/322-4250). * Consumer issues, food additives and nutrition. **Nutrition Action. Consumer Union of the United States, Inc., 256 Washington St., Mount Vernon, NY 10550 (914/664-6400). * Consumer products including many food and household products. ** Consumer Reports. Environmental Defense Fund, 1525 18th St., N.W., Washington, DC 20036 (202/833-1484). *Toxic chemicals, pesticides, air and water pollution, cosmetics and consumer products. **Individual reports. Health Policy Advisory Center (HEALTH/PAC), 17 Murray St., New York, NY 10007 (212/287-8890). *Occupational and environmental health. ** Health-Pac Bulletin. Health Research Group, 2000 P. St., N.W., Suite 708, Washington, DC 20036 (202/872-0320). * Toxic substances, food and drugs, health care, occupational safety. **Individual reports. National Resources Defense Council, 15 West 44th St., New York, NY 10036 (212-869-0150). *Carcinogenic food contamination and air and water pollution. Toxic Project Clearinghouse, Environmental Action Foundation, 724 Dupont Circle Bldg., Washington, DC 20036 (202/b59-9682). *Toxic substances. **Ex osure. Government Agencies (*indicates areas regulated by this agency). U.S. Food and Drug Administration (FDA), 5600 Fishers Lane, Rockville, MD 20857. *Foods, cosmetics, food additives, drugs, tobacco and illegal levels of pesticides and chemicals in food. Address inquiries to the Office of Public Affairs HF1-40; complaints to the Commissioner. U.S. Environmental Protection Agency (EPA), 401 M St. S.W. (A-107), Washington, DC 20460. *Pollution or air, water and land and the setting of allowable levels of pesticide residues on food products enforced by the EPA. Address inquiries to the Office of Public Awareness; complaints to the appropriate branch (see Finding Your Way Through the EPA above). U.S. Occupational Safety and Health Administration (OSHA), Department of Labor, 200 Constitution Avenue, N.W., Washington, DC 20210. *Workplace safety. Address inquiries to the Office of Public Information. Consumer Product Safety Commission (CPSC), 1111 18th St., N.W., Washington, DC 20207. *Consumer products not regulated by other government agencies such as micro- wave overns, formaldehyde home insulation, etc. Address inquiries to the Office of Communications. National Institute for Occupational Safety and Health (NIOSH), 5600 Fishers Lane, Rockville, MD 20857. Investigates all areas of occupational safety and health and provides a basis for standards set by OSHA. Government Information Services (to obtain a toll-free number for hotline services listed below, call the toll-free information operator 1-800-555-1212). Cancer Information Service. Free hotline service providing information on cancer. For a listing of toll-free numbers write: U.S. Department of Health, Education and Welfare, Public Health Service, National Institute of Health, 200 Independence Ave., S.W., Washington, DC 20201. Ask for Publ No. (NIH)79-1488. Occupational Safety and Health Administration, U.S. Dept. of Labor 200 Constitution Ave., N.W., Washington, DC 20210. Free hotline providing information about OSHA. Workers can report work-related accidents and obtain information. Consumer Information Center, Pueblo, CO 81009. Offers many publications free or at low cost on such topics as food, health and medical problems. For a free catalogue of publications write to the above address. Consumer Product Safety Commission, 1111 18th St., N.W., Room 303, Washington, DC 20207. 1-800-638-8326 (Maryland only). Free hotline providing information on harmful chemicals the agency has had experience with. Also provides free news releases "News from CPSC" upon request. U.S. Environmental Protection Agency. Toll-free hotline for information on environmental pollution and reporting pollution episodes. U.S. Office of Consumer Affairs, 621 Reporters Building, Washington, DC 20021. Publishes a monthly newsletter, Consumer Action Update, which is available free by writing to the above address. 96