Document 8Vw56nqJ6dO8VNxReYDR78dqa

4 April 1980, Volume 208, Number 4439 SCIENCE AMERICAN ASSOCIATION FOR THE ADVANCEl\IENT OF SCIENCE Scienc~ serves its readers as a forum for the presenta tion and discussion of important lssues related to the ad~ vancement of science, including the presentation of minority or confticting points of view, rather than by pub- lishing only material on which a consensus has been reached. Accordingly, all anicles published in Scienceincluding editorials, news and comment. and book reviews-arc signed and retl..!ct the individual views of the authors and not official points of view adopted by the AAAS or the institutions with which the authors are af- filiated. Editorial Board s./9fJO: RICHARD E. BALZH!SER, WALLACE BROECK ER, CLEMENT L. MARKERT, FRANK W. PUTNAM, BRY- ANT W. ROSSITER, VERA C. RUBIN, MAXINE F. SINGER, PAUL E. WAOOONER. F. KARL WILLENBROCK 191J/: PETER BELL, BRYCE CAAWFORD, JR., E. PETER w.GEmuscHEK, EMtL HAURY, SALLY G. KoHLSTEDT, MANCUR0LSON, PETER H. RAVEN, WILLIAM P. SLICH TER, FREDERIC G. WORDEN PubUsher WILLIAM D. CARE\' Editor PHILIP H. ABELSON Editorial Stall' Managing Editor RoBERT V. ORMES Business Manager HANS NUSSBAUM A.uistant Managing Editor JoHN E. RINGLE Production Editor ELLEN E. MURPHY News Editor: BARBARA J. CULLITON News and Comment: WtLLIAM J. BROAD, LUTHER J. CARTE.R9 CoNSTANCE HoLDEN. Euor MARSHALL, DEBORAH SHAPLEY. R. JEFFREY SMITH, NICHOLAS WADE, JoHN WALSH. Editorial Assiltant, SCHERRAINE MACK Research News: BEVERLv KARPLUS HARTLINE, RICHARD A. KERR, GtNA BAR! KOLATA, JEAN L. MARX, THOMAS H. MAUGH II, ARTHUR L. ROBINSON. Editorial Assistant, FANNIE GROOM Consulting Editor: ALLEN L. HAMMOND Associate Editors: ELEANORE BuTZ, MARY DoRF- MAN, SYLVIA EBERHART, RUTH KOLSTAD Assistant Editors: CA!TtLIN GoRDON, STEPHEN KEP- PLE, LOIS SCHMITT Book Reviews: KATHERrNE LIVINGSTON. 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Membership and Subscriptions: 467-4417. Adertlslng Represenlatiwes Dirt'<tor: EARL J. SCHERAGO Prociuctimr Mana~a: GINA REILLY Ad~t'rti:tiiiK 5cllt., Mllntl_'f(r: RICHARD l . CHARLES MarAttinK Marwger: HfRDf.RT L. BURKLUND Sales: NFw YoRK, N.Y. IOOJb: Steve Hamburger. 1515 Broadway (21:!-730-1050); ScoTCH PLAINS, N.J. 07076: C. Richard Callis. 1:! Unami Lane (:!01889-4873): CHt CAGO, ILL. 60bll: Jack Ryan. Ruum :!107, '119 N. Michigan Ave. (31:!-337-4973); BE\'l'RU' Hrt.t.s, CALIF. IJO:!ll: Winn Nance, Ill N. La l'ienega Blvd. (213-657- 2772!: DtlKSil, V 1. 05251: Fred W. OielTenbach, Kent Hill Rd. !80:!-867-5581). ADVERTISING CORRESPONDENCE: Tenth Hoor, 1515 Broadway, New York, N.Y. 10036. Phone: 212730.1050. /Zero-What Does It Mean? Pollution of the environment, additives in food, exposure to radiation, hazards in the workplace, and identification of carcinogens are resulting in calls for zero discharge of pollutants. zero contamination, zero radiation, and zero risk. Congress. state and local governments, and their respective administmtive agencies have responded with a stream of new laws and regulations. Some citizens' organizations and legislators are seeking the elimination of all pollution or of what are considered contaminants. This desire to obtain zero is causing const~rnation in the minds of many engineers and scientists. When people speak of zero they apparently mean different things. And even in the case of scientific analysis. zero has changed. A few years ago analytical methods might have indicated the absence of a particular chemical in a test sample. Today, with better analytical methods, that same sample would show the particular chemical present; we no longer have the zero we had a few years ago. Analytical methods are now measuring such minute quantities of chemicals (parts per billion and even parts per trillion) that supposedly identical samples of water from the same effluent, when analyzed, show different concentrations of pollutants. The problem may be one of humans not being skilled enough to get reproducible results with sophisticated equipment (assuming the equipment is not at fault), or it may be like the four blind men trying to identify the elephant-by touching different parts of the elephant, they come up with different conclusions about what an elephant is. Concern about radioactivity's effect on health is resulting in calls for zero radiation, particularly where nuclear power plants are concerned. And yet there is naturally occurring radiation from space, from rocks. and even from our own bodies and food. Such radioactivity varies from place to place by as much as 400 to 500 percent. Knowing, then, that nowhere on earth is there zero radiation, are we talking about zero based on a particular locationand if so, which location? Or are we talking about a permissible level that is believed to be safe for human beings? With the advent of new machines, new materials and chemica]s, and new modes of living and with a greater knowledge of the things around us, we . have suddenly become aware of new ris~ ; or risks we were not previously aware of. Th~ough the years society has become used to and accepted certain risks. People learned to control fire, to build homes away from flooding rivers and volcanoes, to control the internal combustion engine. All of these things involve risks. Society has been able to reduce risks in many instances, but where natural forces are involved, risks are always present. What do we mean when we ask for zero risk? Does zero mean a standard, a limit, or perhaps a goal for each kind of risk? Will we accept {and call zero) 50,000 deaths a year from automobiles, 100 deaths from airline traffic, or 25 to 60 deaths attributable to producing electricity from coal, but refuse to accept any deaths from nuclear power plants producing electricity because we don't want to risk a possible unknown? Webster's dictionary defines zero (other than the numeral) as (i) a state of total absence or neutrality: (iii the lowest point. nadir: and (iii) something arbitrarily or conveniently designated zero. In calling for zero, people may be asking for a state of total absence. However. just as it is impossible to stop killer hurricanes and to keep people from falling out of bed, we know we are going to have accidents if we use fire to heat our homes and cook our meals or use other new things that improve the quality of life and lengthen our life-span. Knowing this, we may have to accept "something arbitrarily or conveniently designated zero" for pollutants. radiation. and risk. The costs of guessing at zero are enormous; laws and regulations must come to grips with this problem. Until they do, co~ts to society can only continue to go up. Everyone's checkbook will feel it-and there we all know what zero means.-MITCHELL H. BRADLEY, Wa.~ltin~ron Office Director. Amerinm Society of Meclwniml E11~inars, Washin~ton, D.C. 20006 FMSI 05589 . "ENVJR{]\IfvENTALLY INDUCED CANCER SEPARATING TRUTH FROM MYTH" - A Talk By Dr. Harry Demopoulos Associate Professor of Pathology, 'New York University Medical Center to the '. Synthetic Organic Chemical Manufacturers Association, Inc. October 4, 1979 Hasbrouck Heights, N.J. ------- FMSI 05590 -1- I appreciate the opportunity to come here and address you. I welcome it very much. It is probably appropriate that this meeting is being held in New Jersey because I think many problems that have beset industry with respect to regulations are founded in some of the misconceived problems that have been painted in New Jersey. When ]. came here in 1979, on a leave of absence, the Federal government had just released the National Cancer Institute (N.C.I.) mortality study by county that was conducted by looking at death certificates from 1950 to 1969; several N.C.I. epidemiologists, as well as members of the New Jersey Department of Environmental Protection, and Department of Health, concluded that after adding up the age-corrected, race- and sex-corrected death data, that New Jersey led all the other states in cancer deaths for white males, expressed per 100,000. Now, that was, indeed, a true statement. That was not a lie. The cancer rates in New Jersey were 205 white male cancer deaths per 100,000 versus the U.S. national average of 174 per 100,000. That created a big hullabaloo. It gave this state the label of "Cancer Alley". Some of the people who were in the New Jersey Department of Environmental I>rotection at that time have subsequently moved to Washington and have continuedto amplify this attitude. I must admit when I came to New Jersey, I shared the view that most New York City dwellers have, that New Jersey is a terrible place, it's horribly polluted. As a matter of fact, on February 16th of this year the New York Times published a map which was sort of the ultimate view that New York City dwellers have. It showed lung cancer rates in various parts of New York City, Staten Island, on the west side of Manhattan, and parts of Brooklyn. The New York City Department of Health blamed polluted air wafting over the river into the city as the cause of these high cancer rates. The report ignored the fact, easily seen on the map, that there (were) vast "skip" areas, and other cancer "hot spots" that wen not in the path of such air flows. The Ne"lf.T York City Department of Health report ignored rudimentary epidemiologic methods such as correcting all the data for sex and race. Further, no attempt was made to study cigarette consumption patterns. Ignored in all of these pronouncements and maps at the federal, state and city levels was the old scientific dictum of controls. This is what differentiates science from politics. When you look back at the cancer rates that were published and resulted in New Jersey being labelled "Cancer Alley", nobody mentioned the fact that Rhode Island was number two, with 203 cancer deaths per 100,000. No one mentioned that other heavily industrialize-d states did not have high cancer rates. When industry was being blamed in New Jersey, nobody looked at the cancer rates in Pennsylvania and Ohio which are remarkably similar "to New Jersey, in terms of the proportion of workers who work in "dangerous" occupations and the number of people who live in communities that are in proximity to major industrial plants that can be viewed by some as polluting. Pennsylvania, Ohio and New Jersey have several things in common. About 40 percent of the workforce is engaged in what you lo10uld call heavy, "dirty" industry. Forty percent of the population in those states lives in proximity to so-called "dirty" plants. When you look at the cancer rates, however, Pennsylvania and Ohio have cancer rates that are like the U.S. national.average. Yet, only New Jersey had higher cancer rates. The answer as to what is different about New Jersey is found very simply in the U.S. census. New Jersey has the most urbanized population; 90 percent of the population is urbanized and it also has the most dense urbanization. Only 70 percent of Ohio and Pennsylvania are urbanized. That 20 percent differ- FMS\ 05591 -2- ence explains the difference in th~ cancer rates among the three states. Before it became politically popular to blame industry, the National Cancer Institute epidemiologists showed unequivocally that urban crowding was a predominate factor in cancer causation. It is clearly a surrogate for something else. New Jersey has a rather small land mass and over 80 percent of the people are crowded into a rather small area in the northeast part of the state. It is, therefore, like a large city and if you compare it to similar demographic areas, with equivalent land and population density, and look at it in a controlled way, it is shocking to see that many other cities and counties and regions that do not have any industry have higher cancer rates than New Jersey. For example~an Francisco; Washington, D.C.; Nassau County, which is an eastern suburb of New York City; Westchester County; these demographic areas have rates that are equal to or greater than New Jersey's, and those areas are devoid of heavy, polluting industry. If you look at other questions beyond urbanization and ask what are the surrogate factors, the ecologists would say, well, it's urban air pollution, and it's still ultimately being derived from industry. Well, we tested that hypothesis. The hypothesis was that pollutants in the air and in the water are responsible for increasing the cancer rates by at least 25 to 30 percent. In order to test that hypothesis, we simply looked at the National Cancer Institutes own Third National Cancer Survey which surveyed 20 million people in this country, back in 1969, -70, and -71. Now, that was incidence data and as I said, it covered 20 million people. Our studies incidentally were conducted with the sole support of a grant from the National Cancer Institute when I served as the Director of the Cancer Institute of New Jersey in 1976. The diagnoses were far more accurate than the death certificates in the N.C.I.'s mortality study because these were surgical pathology specimens. The slides were all read by Board Certified pathologists. In that Third Cancer Survey, there was a wealth of information and it 'was not originally designed to answer this hypothesis, but it came out that way. There were seven cities in that survey. Four of them were what we would call "clean" cities; San Francisco, Dallas, Minneapolis and Atlanta. They are urban centres without any kind of heavy industry. In that survey also were Detroit, Pittsburgh and Birmingham, the "Pittsburgh of the South". Those seven cities encompassed 16 million people. We did not massage the data; we simply lifted it out of the tables and put the data next to each other and if the hypothesis was correct that industrial air pollution or urban air pollution were a major factor in cancer causation, we would have expected to have seen that (the) four "clean" cities had lower cancer rates than the three "dirty" cities. We looked at overall cancer rates for white males as well as for black males, age-corrected, and to our surprise, the three "dirty" cities had an overall 8 percent lower cancer rate than the four "clean" cities. I don't think the 8 percent is statistically significent, however, it invalidates the hypothesis. Furthermore, we looked at specific kinds of cancer that Blatt, who is an N.C.I. epidemiologist, and others have said are industry-types of cancers, like lung, larnyx, nasopharnyx, stomach, lymphomas, leukemias, urinary bladder, liver and skin. These are all supposed to be industry-associated types of cancer. The Third National Cancer Survey gave us site specific cancer diagnosis, i.e., by atomic site. Those supposed industry-associated cancers were not higher or greater in incidence in the three "dirty" cities compared to the four "clean" cities. In Detroit, Pittsburgh and Birmingham, 45 percent of the occupational workforce is engaged, and has been engaged for several decades, in industry that most people would say is worrisome. Further, these decades of exposure were without controls. And yet, we did not see greater cancer rates in ~ FMSI 05592 -3- these cities. A 45 percent workforce engaged in "dirty" industry translates into something like about 22 or 23 percent of the general population, which is a large enough percentage of the population to skew the data up higher if, in fact, these workers were being exP.osed to significent levels of carcinogenic hazards. ., This is the N.C.I.'s own data. We didn't manipulate it. And, curiously, in the OSHA hearings and in any discussions I have ever held with-people on the Federal level, nobody ever looks at the Third National Cancer Survey. It's almost like their unwanted child because if you examine the data, within it is contained certain answers to questions that bedevil society, government, labor and industry. For example, there are questions raised about lowdose exposures; Let's not worry just about the workers, what about the people in the communities? They are exposed to low-dose emissions. ~~at about the question of synergism, which is almost unanswerable in an experimental sense. The answers, again, to these questions, are found in the Third National Cancer Survey and the comparison of the three "dirty" cities and the four "clean" ones. Detroit, Pittsburgh and Birmingham have virtually every kind of pollutant chemical that you can imagine in the air and in the water. If synergism and chronic low-dose exposures were real hazards, and if, in fact, there were no thresholds, we should have seen higher rates in those three "dirty" cities. They have been in "business" for several decades, and the chances existed. Now, there has to be a reason why we didn't see more of any type of cancer and the reason is as follows: There are thresholds. There is a threshold for virtually every substance that is noxious to mankind. There are thresholds for deadly viruses. There are thresholds for bacteria, fungi, anything that is noxious and harmful to humans gener.ally has a threshold, and this includes carcinogens. Now, clearly the exposures, although seemingly horrendous in the three "dirty" cities, were well below the threshold levels because there was no effect. Recall, the Third National Canacer Survey showed 8% less cancer in the "dirty" cities. Another thing to keep in mind is there is a real biological reason to explain thresholds. It is not a magical thing. We have DNA repair mechanisms that are very efficient. Furthermore, most carcinogens and many toxic substances act by what we term free radical chemical mechanisms. There are endogenous anti-oxidants that we have evolved with over the eons that protect us against free radical pathology. These anti-oxidants can be overwhelmed with excessive doses of a carcinogen, such as occurs in laboratory animals, but human exposures are not at these doses, and we have not oeen overwhelmed, not even in Detroit, Pittsburgh, or Birmingham. It should be noted that the Third National Cancer Survey was conducted from 1969-1971. The cancers diagnosed at that time were starting to develop during the 1940's and 1950's. In those years, air/water pollutants were not controlled as they are now. We have therefore gone through "worst-case" conditions in our industrializedurban centers, and nothing happened. Those who beat the drums of doom, as in recent books written by non-scientists, are clearly leading a march down the wrong path in cancer prevention. Abundant controls exist now, and most of them are needed; some are not, however. Another thing that proves that there are thresholds is the experience with cigarette smoke. Cigarettes of the high-tar variety are perhaps the most c~rcinogenic substance that mankind deals with in a routine manner on a mass basis. Yet, it has been well proven through smoking dog studies; that thresholds exist; dogs, incidentially, love to smoke. Once they are trained, they jump right into the box and puff like mad. The threshold studies were FMSI 05593 -4- conducted through smoking dog studies, as well as through careful autopsies on individuals where smoking history was well recorded, and where the bron- chi were serially sectioned and examined. If you smoke 10 to 15 of the 1 mg. tar cigarettes, there are no carcinogenic hazards associated with that. We don't even see the premalignant changes in the epithelium; so that here is T the most carcinogenic substance that is massly used and there is, decidedly, a threshold. ..,. Similarly, there are thresholds with alcohol. Alcohol and cigarette smoke are synergistic and together if you smoke the high-tar cigarettes and drink excessive quantities of alcohol, you find that you can account for 35 percent of the cancer deaths. This type of synergism is rare. Most of the cancers of the mouth, larnyx, esophagus and lung are caused by these two factors and they are synergistic. But, again, it has to be with excessive quantities of distilled liquor. It's the alcohol itself, not the congeners or other substances that are found in the drink. Now, the misconceptions that have been brewing, first in New Jersey, and later in Washington, have aroused not only the ire of you fellows in industry but the ire of University medical scientists who are in the comprehensive and specialized cancer centers such as MIT, Harvard, NYU, Columbia, University of Pennsylvania, McArdle Cancer Center, and others. We are upset at what the Federal government has been doing. Our worry stems from the fact that if society is to listen to the Federal government, it will be led down yet another primrose path, blaming industry, air and water pollution for most of the cancer burden, whereas, in fact, the answers to cancer lie elsewhere and have been very well defined through a great deal of epidemologic research and extensive laboratory research. Whoever attempts to lead the nation towards less cancer had better be correct, because the selection of the wrong path is the equivalent of leading millions of Americans to certain death. There were two symposia that were held. One of February 28th, March 1st, and March 2nd, and another one, June 6th, 7th, and 8th in New York City. These twosymposia were held by the independent university scientists from the comprehensive and specialized cancer centers in this country. The symposia were under the aegis of the New York Academy of Sciences, and the American Health Foundation, with the cooperation of the American Cancer Society, as well as th~ World Health Organization's International Agency for Research on Cancer. We came up with the following predominant causes of cancer, and the word, "predominant", is important. An analogous situation is that tuberculosis is predominantly caused by the tubercle bacillus. While there are associated factors in causing tuberculosis, for example, poverty, crowding,- and malnutrition, the predominant cause is still the tubercle bacillus, and if you want to eliminate that disease, you control the tubercle bacillus. Similarly, in cancer, there are predominant causes. The University scientists decided to sponsor and attend these two sympos~a, and to continue putting on such symposia as often as is humanly possible, in order to turn around the propaganda machine that has been launched by the Federal government. This machine is leading the country down the wrong path in cancer prevention and is killing many Americans through misinformation. The University scientists just went through a 15-year period of going up a blind alley looking for cancer viruses that weren't there. That cost a billion dollars. We cannot afford, not in monetary terms or in human terms, to spend another ten years and another billion dollars or more chasing the wrong culprit in cancer causation. There will be too many lives lost, especially when we know most of tpe answers for prevention at the present time. While we are still ignorant about how exactly a normal cell becomes maligna~t, FMSI 05594 -5- we do know how to avoid situations that have such a transformation as the end result. The answers to cancer prevention.are as follows. And it's easy to keep the scorecard in mind. There are about 1,000 people a day that die of cancer in this country. 350 of them, or 35 percent, are going to die today from having smoked high-tar cigarettes and having consumed excessive quantities of distilled liquor and they will die of cancer of the mouth, larnyx, esopnagus and lung. Another 45 percent are attributable to diet, and this figure was courageously stated by Dr. Arthur Upton, the Director of the National Cancer Institute on Tuesday, before a Subcommittee on Nutrition. He has confirmed what the University scientists have been saying for the past few years. No other government scientist has had the integrity to state what Dr. Upton stated; he further and strongly recommended major decreases in fat consumption, with increases in fresh fruit and vegetable consumption. 45 percent of cancer deaths are related to disordered nutrition. Under the category of disordered nutrition, there are four subcategories: excess calories; excess fat ingestion; obesity, carrying around an extra 30 or 40 pounds; and nutritional deficiencies such as fiber deficiency and Vitamin A deficiency. Now, with Vitamin A you have to be careful. There is an optimum dose which happens to be the Recommended Daily Allowance. Too much Vitamin A will ' also cause cancer in addition to being toxic. Too little Vitamin A will also cause cancer. There is evidence that the 5 percent of cancer deaths that are due to occupational exposures may have plateaued and may be on the way down. If you look at hemangio sarcomas that are caused by vinyl chloride monomer exposure, the latency periods and the ages of the patients are longer and older, respectively. It means they are developing at slower rates. Similarly, we did a study at NYU showing that mesotheliomas, which are caused by asbestos exposures, are at a plateau. We do not see an increasing incidence of mesotheliomas, despite the fact that most of the people we see at the NYU Cancer Center, where we treat 4,000 new cancer patients a year, are drawn from places like the Veteran's Administration and Bellevue Hospital, and includes a fair number of construction workers, and Brooklyn Navy Shipyard workers. Our Cancer Center is a general one, and does not have a specialized referral component for mesothiomes, as at Mt. Sinai Hospital; therefore, our rates are indictative of the general rates. We have not been seeing an increasing incidence in mesothelioma over the past 12 to 15 years. It's at a plateau. So that I think if controls are kept over the very dangerous chemicals and physical processes that you use in industry, I think we can continue to see what looks like a decline in occupational cancer, which we think is currently around 5 percent. Sir Richard Doll and others think it's much lower, but I would caution you that you cannot relax. The chemicals that you deal with in ever increasing quantities to meet "consumer demands and to try to remain competitive in a ferocious world market are dangerous, and I think there are elements of truth to what the government regulators say; we can see a major explosion in industrially caused cancer if we do not have sensible controls. The question is, how rigid should the controls be? I think that we can be less rigid than what OSHA and EPA have proposed recently since there is clear evidence that there is no need for that kind of rigidity. Occupational carcinogens are under control, and new chemicals are receiving close scrutiny; air and water pollution are blameless in carcinogenesis. A few other points that I would like to make in closing are that in addition to determining that cigarettes and alcohol, disordered nutrition, and occupational exposures cause 85 percent of cancer deaths, t~.,:,o:e is anoth<'.!t" 3 FMSI 05595 ---------------------------------- -6- percent that are caused by exposure to radiation which is largely background, not nuclear plants, but background radiation. We have enough radioactive potassium in our bodies, for example, to cause 4,000 radioactive decays per minute. That adds up. Another 2 percent of the cancer deaths are caused by pre-existing medical disorders, like chronic ulcerative colitis, chronic gastritis and th.ings I like that. And about 1 percent are caused by prescription drugs for the ! treatment of serious medical disorders. The symposium held in June also determined, and this was brought forth by Dr. Cuyler Hammond of the American Cancer Society, that almost zero percent of ~ancer deaths, it's something like .00001 percent, are caused by air pollution. Water pollution is in the same category of zero percent. Other studies have shown that nuclear power plant accidents, asbestos in hair dryers, asbestos in school rooms, and saccharin/cyclamates can not cause cancer as presently used. And yet, those things that are listed as being zero percent are uppermost in the public's mind. This is due to the propaganda machines. We are treated to outrageous remarks by individuals like Wolfe from Ralph Nader's group that asbestos is the second leading cause of cancer deaths in males in this country. It's an absolutely unfounded statement that, by no stret~h of even Sellikoff's imagination, could that be true. And yet, individuals like this are placed politically on the National Cancer Advisory Board and govern, and help to govern the National Cancer Institute's policy. It is terrifying because our nation can be led down the wrong path in prevention. So you have an uphill fight in terms of public relations but I think that, if controls are kept, truth and reason are on your side and I think that you can win this battle that you are in. Thank you. QUESTION: I assume that the reason for the higher cancer rates in the cities is due to the factors you describe, more smoking, and so on. DR. DEMOPOULOS: And they may have far more disordered nutrition. The urban crowding is a surrogate for all of the factors that we know to cause cancer and it is proven too, with animal studies. The reason is ultimately the kinds of stress that you get when you start crowding any living organisms together. This has been well-defined with rat behavioral studies where if you take a room of a given size and keep putting more and more rats in there, even though you provide them with enough food and water, and places to sleep and rest, you will see back biting, tail biting, homosexuality, fighting and all the other things we see in urban settings. In medical school we are taught that certain diseases are urban diseases, i.e., they occur more frequently in urban areas. For example. obesity, hypertension, chronic ulcerative diseases of the GI tract (the gastrointesliinal tract), heart disease, suicide, hom~cide, drug addiction, are all far more common in urban settings. This includes the cities and their surrounding suburbs. Now, I think to that list should be added cancer. And I don't think it's stress per se, but rather it's the way humans choose to relieve their stress, through gorging themselves, drinking themselves into oblivion, and surrounding themselves with smoke, that cause cancer. QUESTION: I understood that in other parts of the world that different types of cancers occur. DR. DEMOPOULOS: Well, there are some interesting reports that have come from China recently. There are regions of China that have extraordinary rates of esopha~('al cancer, for example. r.ven their chickens have esop":.ageal cancer. FMSI 05596 -7- But, that has been traced to the particular kind of food that these individuals make. They apparently take various .kinds of vegetables and peel them and let them sit around for months and months and finally they eat them and their chickens eat the same scraps. There are other situations, where there has been a good deal of epidemiologic research done on the nutritional habits of the people in correlating it with diseases, and it keeps coming back to what we eat that causes cancer. And, this is true also for atherosclerosis as well as premature aging. For example, there are tribes in Africa that make a habit of eating raw meat and blood together with milk and this is all they eat. They don't eat any fruits and vegetables. Their life expectancy is about 30 to 35 years of age. They die of heart disease, strokes, hypertension and cancer. And it's the worldwide studies that have been the strongest implicators of d.iet as a predominant cause of cancer. QUESTION: In your listing of causes, it seems to me that you came up with about 91 percent. Where is the other 9 percent? DR. DEMOPOULOS: God. I think that we are not immortal and that we have to accept certain things. I think it's part of the aging process. Almost every male over the age of 85, at autopsy, has cancer of the prostate gland, if the prostate gland is adequately examined. These cancers are microscopic and produce no symptoms. Similarly, urinary bladder cancer is a cancer of the aged. It keeps climbing as you get into the 80 and 90 year old brackets. I think it's an accompaniment to age and Dr. Handler, President of the National Academy of Sciences, has offered the hypothesis that oxygen, one of the most toxic gases known is responsible. ,oxygen happens to be diradical. It oxidizes everything, including our lipids and I am sort of surprised, as a free radical pathologist, that we can exist with oxygen. I wouldn't have chosen it. Methane would have been better. But, Dr. Handler has proposed that simply existing in an aerobic atmosphere is cause enough to give us cancer, and were it not for the major antioxidants that we have, we would have even more diseases. The decline in cancer of the stomach is appropriate to mention at this point in that regard. Cancer of the stomach used to be the commonest cancer killer in this country 40 and 50 years ago. Nowadays, it's a rare disease. In medical centers, we keep these cases extra days as teaching cases because medical students will never see one like it in their career. The reason for the decline in stomach cancer is the increased consumption of fresh fruits and vegetables and the antioxidants therein. BHT has probably helped. Dr. Arthur Upton concurs in this view, as do many University scientists. QUESTION: Does a significent segment of the scientific community, people working in cancer causation, feel the same way you do about the problem? From your point od view, why is it that these scientific arguments about what industry is doing are presented by people like Wolfe, Epstein and Barry Commoner? Why don't we ever hear f~om those people who have spent their lives actually doing research? DR. DEMOPOULOS: A good reason is that University medical scientists do not have a PR or propaganda machine, nor do they have a policy that they are trying to advocate. It's one of the defects of science, in general, that unless there is an organized effort to get the truth out of the medical journals wherein it is buried, you are going to have misconceptions, as we have now. I think the reasons for the origins of the misconceptions lie in the fact that as we prove the lack of validity of the virus hypothesis, there was a void. Everybody asked, well, if it's not viruses, what is it? Unfortunately, the term "environmental cancer" came into being. That was seized as meaning the general community enviror~ent rat4er than the personal env~con- FMSI 05597 -8- ment created by our habits, diet and lifestyle. There was a void, a gap, before the nutr~tional data was gathered epidemiologically and from animal studies. We now know what the predominant causes of cancer are but, at the time the time the virus theory was shown to be invalid, the "greenies" and the ecology people came into the picture and stole center stage and they are still at it and they are holding onto it come hell or high water. They seem oblivious to the consequences of leading a march of cancer prevention down the wrong path. ~ QUESTION: As a taxpayer who was able to pay for tearing the asbestos out of all the schools and other public buildings, I am gratified that you don't seem to think tha~'s a terribly important factor. DR. DEMOPOULOS: I think it's a tragic misconception and it's the height of hypocracy and stupidity to see classrooms being torn apart. This recently happened in New York City where pretty close to half a million dollars were spent redoing the whole school because of the asbestos scare. Somebody had gone in and sampled the air only in the classrooms and found asbestos there. The conclusion was that it was coming from the ceiling. They tore everything down and they went back and they sampled the air again. They found just as much asbestos. Then, and only then, did they go out and do what is called the control. They went to the outside air and sampled it several blocks away and they found even more asbestos in the outside air. The point is, asbestos is a natural product, it's all over the place. We use it extensively in urban settings; brake linings, construction, everything. The point is that the doses we get in school rooms and, office buildings are far below any kind of danger level, yet within these classrooms we have smoking lounges. As the NYU study has shown, we are not seeing an epidemic of mesotheliomas. If you go in~o the cafeterias and watch what the kids eat, it's garbage, as far as I am concerned. Loaded with fat. No fresh fruits and vegetables, and these are wrong. It's as stupid as when a cigarette company used to advertise high-tar cigarettes as being good for your "T-zone". QUESTION: Is there any really definitive data on the effect of the so-called social drugs like marijuana? DR. DEMOPOULOS: They haven't been used long enough nor in any good epidemiologic studies but just looking at tetrahydrocannabinol, that's a toxic substance. That will damage cell membranes and will damage DNA, so will LSD; so will most of these so-called recreational drugs. I think they are fearsome and they really should be controlled for a variety of reasons, including their carcinogenic and mutagenic potential as well as the fact that they ab- solutely destroy nerve cells. The reason for producing a "high" is a lot of nerve cells are just getting disconnected. The synapses are missing so that you no longer have the major inhibitions that are inherent in the electrical circuits in .the brain that keep us under control. I don't mean moral inhibitions, I mean the ability to focus ~n one thing at a time, to concentrate. The brain functions by blotting out everything else except what you are supposed to pay attention to. The reason you get a "high" and start seeing visions with LSD amd mescaline is that a lot of circuits are disconnected and you can no longer focus on any one thing; virtually every circuit in your brain has been turned on and is short circuiting. These drugs are very dangerous. Whenever you start damaging cell membranes like that, you damage a lot of cell control mechanisms and open the way to birth defects, cancer and every other chronic disease, including aging. rl... 1 FMSI 05598  -9QUESTION: In our community we have had some questions about asbestos cement water pipes. Is there any problem? DR. DEMOPOULOS: I think in specific instances, you would have to sample water like that. You would have to look at it. I don't doubt that in occasional circumstances it is quite possible to carry carcinogenic loads of a chemical substance through the air and through the water, but I think they are unusual; where there are questions, I think you should take a look and see wha~.the concentration is. The dose is all important, for sure. If it's a low dose, I wouldn't worry about it. QUESTION: There are numerous problems that you have mentioned in your discussion relati~e to society's view of the cancer situation. Number one, you have the terror factor, the fact that people are more afraid of cancer than they are of heart disease. What, in your opinion, can communities, can we as concerned people, many of us, do to offset that view? DR. DEMOPOULOS: Well, I think you have already done one thing as industry groups, and that is, I think, coordinated programs as AIHC has carried out on behalf of industry are very important. You must be unswerving in the pursuit of truth, it's good business. I was shocked and amazed back in 1976 when I came here to direct the Cancer Institute in New Jersey~ The press and the Department of Environmental Protection in Trenton were literally tearing industry apart. I always thought that you fellows were really hot stuff and would have answered back and I was surprised that,industry was just laying back being beaten up. There was no response. I couldn't understand it. I think AIHC is one way to respond. I think that if you tap the angry potential that I assure you is there in large numbers in the academic university community, you will have a very firm ally provided you seek to serve truth and society. We have had no problems getting topnotch university scientists to stand up and be counted and speak the truth even at the risk of angering the National Cancer Institute from whence their grants come. Our peers judge our grant application; thank God the politicians and "greenies" do not. FMSI 05599 '{,''c:;} l. "'~pccupational Health & Safl'ty Letter. Dl'ccmber 8. 1979 F/'1S/ 5 "The Commission will notify all parties whethl'r the case will proceed under simplified or l'omentional rules. Prior to the conference-hearing. the parties will get together to determine what is being disputed and the issues to be resolved. The Judge will then schedule a conference and a hearing. At the Conference the Judge will list in the record all agreements reached and defenses raised. The parties and the Judge will then attempt to resolve the disputed issues. "If any issue remains in dispute. the Judge will hold a hearing. At the end of the hearing each party can present oral argument. If any party wishes to file a written argument. the Judge should be infom1ed so that a date for filing can be set. A transcript will be taken of the hearing. The Judge will then file a written decision with the Commission. It shall become final 30 days thereafter unless it is called for review by any of the Commission members. The Commission will then issue an order affirming, modifying or vacating the Judge's decision." DR. WEILL'S SUi\t:\lARY REFLECTS YALt;E OF LYON 1\JEETI:\G ON :\UNERAL FIBERS: Dr. Hans Weill of the pulmonary diseases section of Tulane University's Department of Medicine was charged with summarizing the Symposium on Biological Effects of Mineral Fibers sponsored by the Inter- national Agency for Research on Cancer Sept. 25-27 in Lyon. France. His report discussed what was new. what was controversial. where additional research was needed and. in general. reflected the previously reported view of other participants that the meeting was valuable (OCCUPA TIOSAL HEALTH & SAFETY LETTER. Oct. 22, 1979). He said that considerable progress has been made in the identification and quantification of asbestos fibers in tissue, although some reservations were expressed about differences in tissue mineral fiber counts between labs. "Questions remained concerning the effect of high temperatures on the physical integrity of asbestos fibers. with a prominent example being the fate of asbestos in brake-lining during use," Dr. Weill's summary Jsaid. "Is there consequent altered crystalline structure with the production of unstable fibers? The defini- \ tive answer seemed not vet available." Th;re~medto b~ agreement among conference participants that carcinogenic potential of asbestos is importantly related to fiber length, he said. Asbestos exposure in the asbestos-cement industry was con- sidered by some to differ from other sources of asbestos exposure. perhaps related in part to altered surface properties, or possibly because asbestos fibers may be coated with small calcium-containing particles. "There appeared to be little new information on the relationship of fibrogenesis and carcinogenesis associated with asbestos exposure," Dr. Weill's report said. "Animal invesr:gations seem not to have been helpful in resolving this important question. Some participants continue to ask whether an excess carcino- genic risk (lung cancer) is associated with asbestos exposure in the absence of pulmonary fibrosis (asbes- tosis). Jt was agreed that we will probably never be able to make the determination in an individual case, but preliminary epidemiologic data suggest that the carcinogenic and fibrogenic dose in some aspects of the industry may be similar or indeed that the fibrogenic dose could even be lower. "On the relationships between asbestos exposure and smoking in detennining the relative lung cancer risk, it should be pointed out that non-smokers have been shown to be at greater risk than non-smoking workers who have not been exposed to asbestos. Data from New York and Quebec suggest that asbestos exposure alone (without cigarette smoking) carries such an increased risk, although the number of excess cases is far smaller than for smoking asbestos workers. J sensed disappointment (which I share) in the expression by some conference participants of contin- uing difficulty in diagnosing mesothelioma, in spite of the use of electron microscopic and histochemical techniques. There did not seem to be general agreement that all mesothelioma panels have uniformly helped to increase the precision with which the diagnosis of mesothelioma can be established. Some panels appeared to be more successful than others. ( ... Jt was suggested that perhaps p:.athologists should borrow some principles and approaches from the developers of the ILO U/C R:Hiiographic Classification, with greater emph:~sis on standardization, quanti- tation of inter- and intra-observer variability and similar considerations. Discussants generally felt that there still were inadequate data on dose-response rebtionships for mesothelioma but the important contri- ~ 1 \ Yl f\ .bution of Dr. Whitwell was noted as a convincing demonstration of dose relatedness for this tumor." v;.. r~ ?) FMS\ 05600 -------,---~----------------------------------------------- Occupational Health & Safety Letter, December 8. 1979 On the key question of dose-response relationship, Or. Weill's summary stated: "In regard to carcinogenic effects, there appeared to be a consensus that the shape of the curve is linear and that no threshold exists. While in no way refuting these hypotheses, I would only raise the question as to whether we have come to this consensus by genuine agreement or submission. There can be little doubt that cancer risks at low doses over a working lifetime have not to date been estimated by obsenations at these low levels of exposure but rather by extrapolation via the mechanism of statistical modeling. "In the absence of observations, this is certainly the correct approach to risk assessment. However. the advantages of obtaining biological response data at long-tenn low-level exposure with adequate followup of exposed working populations are undeniable. "Additional but incomplete data have emerged in recent years suggesting the probability that dose response curves differ for various phases of the industry, but how and whether this should influence public policy decisions is certainly not clear. Further, as regards the dose relatedness of these diseases, one might ask if Mr. Peto has surrendered on his 'no dose relationship' position. If he is right, what are the control implications? They seem both obvious and dismal. "Happily, the great majority of the participants of this conference are convinced by the evidence which leads to the conclusion that the lower the dose of asbestos exposure, the lesser the risk of malignant and non-malignant disease. "Finally, since the validity of dose-response relationships depends critically on measurement of exposure, it is appropriate to ask: are we now measuring airborne asbestos dust with adequate precision and sensitivity? Alternatives to the now widely applied optical microscopic counting of asbestos fibers are El\1 techniques and mass measurements. There seemed little discussion on this point by the participants of this symposium, which may suggest that these alternatives are not practical for wide use or that their biologic validity or relevance has not been established." SHELL STUDY SAYS CHEMICAL WORKERS ARE LESS WORRIED TBAI'I PUBLIC: Workers in the chemical industry are less concerned about workplace exposures than is the general public, according to a study by Rene D. Zentner, manager of opinion research at Shell Oil Co., and presented to the American Institute of Chemical Engineers meeting in San Francisco. "Despite public apprehension over exposure to carcinogens in the workplace, statistics show that chemical workers, the group most directly affected by it, are less concerned," he said. The study also used data from Cambridge Reports, Inc., whose partner is Pat Caddell, President Carter's pollster. "For many years, the U.S. chemical industry has enjoyed a good re"~utation," the report said. ..Recently, because of a number of well-publicized industry bad practices, public confidence in it has declined. The public increasingly sees the chemical industry as contributing to air and water pollution, and are beginning to blame workplace exposure to chemicals as a key cause of cancer. Nevertheless, there is general agreement that the safety and health of the workplace have been increasing recently. Chemical workers are significantly more supportive of industry practices than is the general public." Drawing on a series of tables from the Cambridge Reports national public opinion surveys to support his conclusion that chemical industry workers often support positions taken by industry management in regard to such matters as zero-risk, costs, etc., Zentner said that several trends and conclusions can be drawn: ..The first trend is the well-established national apprehension over the disease cancer. The second trend is the increasing identification by Americans with the American chemical industry as a source of carcinogenic substances. So long as these trends continue to converge, it can reasonably be expected that the public will support legislative policies restricting exposure to chemicals, both of consumers and of workers in the chemical industry. ..It should be kept in mind that the apprehension over widespread exposure to carcinogenic chemicals is a perception not necessarily exact. Indeed, the federal government agency responsible for national environmental policy, the Council on Environmental Quality, stresses the small proportion of chemicals that may cause cancer... ..Whatever the underlying phenomena, however, the public increasingly is concerned about its exposure to carcinogenic chemicals, both on and off the job. "Despite public apprehension over exposure to carcinogens in the workplace, however, chemical ------------ FMSI 05601 . 0 '. ~re probably transported by macrophages to the muco- Asbestos-related disease, portals ciliary escalator ofthe respiratory passages and cleared from the lung to be subsequently swallowed. The fate of entry and types of exposure of the remaining fibres is thought to depend upondiameter, 67 Asbestosis, which may be defined as fibrosis of the length and possibly straightness. Animal experiments lungs caused by asbestos dusts which may or may not be show that, for reasons not fully understood, much less associated with fibrosis of the parietal (outer) or pul- chrysotile than amphibole fibre remains in lung tissue monary (inner) layer of the pleura, lung cancer (carci- after inhalation has ceased. noma of the bronchus), and mesothelioma ofthe pleura 65 Fibres ofa wide range ofchemical st~tureM-. eluding substances as diverse as glass and aluminium oxide as well as asbestos) have been shown to produce and peritoneum are universally accepted as diseases with a causal relationship to the inhalation of asbestos fibre. Benign pleural effusion (fluid developing in the space between lung and chest wall) may occur acutely in mesothelioma after injection into the pleural or peritoneal association with other asbestos-related lung diseases cavities in animals ifthe configuration ofthe fibres falls or as the only or most prominent disease process. It may within a certain range. Experiments shciwed that for be discovered by accident or associated with pain, fever asbestos, glass fibre and aluminium oxide the degree of ~rcinogenicity is related to the proportion of fibres with diameters between 0.5 and 2.5f.Lm and lengths l0-80f.tm. In later experiments using glass fibre only the highest and malaise. Thickening ofthe pleura may occur, alone or in association with fibrosis ofthe lung, and may be symptomless or associated with chest discomfort and restriction of breathing. incidence oftumours occurred with fibres up to l.5fl.m in 68 Asbestosis, which by definition is specifically related diameter, including very thin fibres ofdiameter less than to asbestos, is difficult to diagnose because its onset is 0.25f.tni and oflength greater than 8f.tm. It is important to point out that 0.5f.tm represents the approximate limit oflight microscopy in respect of fibre diameter. gradual, and because the symptoms and signs may occur in other diseases and are often difficult to detect. Minor changes in x-ray pictures attributable to asbe~tos may exist for many years without symptoms or progression. 66 So although the doses administered were very large indeed and the results of intrapleural implantation of fibres in rats cannot be used as a reliable predictor of risk to manthrough inhalation, theseexperimentsstrongly suggest with the current optical methods the total number of respirable fibres will have been under-estimated but to a similar degree in different types ofexposure, so that our conclusions about relative risks are not significantly affected. However there must remain uncertainty about 69 Lung cancer is easier to diagnose than asbestosis but the tumours which occur in relation to asbestos have no special diagnostic feature. As tobacco-related lung cancer is common and the effects ortobacco and asbestos are known to interact synergistically in smokers exposed to asbestos, it may be impossible to determine in a particular case whether or to what extent a bronchial tumour is related to asbestos. this. The development ofmethods which measure the 70 In the case ofmesothelioma, although there are also whole range ofrespirable fibres is urgently needed. diagnostic problems, the position at present is that the Table 10 (see Vol 2 Table 3a) Cancer of the .JIIStlo-intestinal tract and peritoneal mesothelioma in 8 surveys (includina 2 studyina two different sub-populations) in which an excess of the former hu been reported. . ReferentY Population fErctMCnu11 Coull Obserml (0) 0/E 0-E Pl'rl.mes. Fibre Type Selikoff" Insulators 43 13.6 3.1S 29.4(S)f 2S C&A Elmes & Simpsoa' Shipyard workers 1S S.2 2.91 9.8(S) 0 Cr,C,A Selikotr Amosite workers 26 12.S 2.07 13.S(S) 6 A Enterline' Maintenance workers 22 13.3 1.6S 8.7(S) ot C.A&Cr Seliltoff Insulators 61 37.8 1.61 23.2(S) 63 C&A Newhouse' Insulation manufacturers 31 20.4 I.S2 10.6(S} IS C.A&Cr Mancuso' McDonald e1 111 Enterlinel McDonald et aP Petoet al Production workers Thetford minen and millen Production worlten Asbestos mlnen and millers Textile worken 16 10.6 Ul 16S I<M.B 1.14 37 32.5 1.14 J2S 150.4 0.83 16 15.7 1.03 A - Amosite; C - Cltylotlle; Cr - C'roddollte. fit Is knowD tht many cal of'IIIIIOibelloma occ:uned Ia JOUIIIII' llllllln thlll'lctorJ. S(S)- ...,...ac_(P<O.os)(NI) ......... .,..(P>G.OS). I S.4(NS) 20.2(NS) 4.S(NS) -2S.4(NS) 0.4(NS) 6? 0 0 0 0 ? c c c c&?er c\ (X f\,q/\\ 49 \ ) FMSI 05602 phyllite alone (Table 15). However, as important gaps in our knowledge ofthis aspect of the field remain unanswered, the weight which can be attached to this conclusion at present is limited. The high relative risks oflung cancer reported in a single study ofworkers making insulation material containing amosite even after very short exposure is worrying in view ofthe increase in utilisation ofthis material in the United Kingdom since the War (Table 16). There is no reliable information from South African amosite miners to help us on this point. We conclude that a firm judgment on the question whether amosite has been more dangerous than chrysotile in respect oflung cancer is not possible at present and that further work should be commissioned urgently. 300 200 Number of deaths from maothellome leccordlng to duth Cll'tlfiCitll} 0 0 0 0 0 00 ASBESTOSIS IN MAN 80 Quantitative evidence about impairment oflung function in man in relation to fibre type is limited to one study which suggests that crocidolite may have been more harmful than chrysotile. Information from the same amosite insulation manufacturers as were mentioned in connection with lung cancer, and their families, shows that radiological changes suggestive ofasbestosis occurred after relatively short exposures. Evidence for a difference in risk of asbestosis with fibre type is at present slight. 100 0 MESOTHELIOMA IN MAN 1968 '70 '12 '74 '78 Year of death 0 81 As far as mesothelioma is concerned, evidence from miners; from process workers exposed to a single fibre Pia 3 (see Vol2 Fig 17) Death certifi~tes mcntionins meso- type; from the distribution of neighbourhood and dom- theliome. Great Britain, 1967-76 by year. . estic cases; and from the geography ofmesothelioma, when combined, presents a powerful case from four ~ure to chrysotile alone has increased the risk of gastro- different sources that crocidolite has been more dangerous intestinal tract cancer is less consistent {see Table 10). than chrysotile and anthophyllite. The position of amosite may be intermediate between crocidolite and chrysotile. CHANGES IN INDUSTRIAL PRACTICE There is no doubt that some crocidolite was used at Rochdale, but the significance ofthis as a cause ofthe mesothelioma cases there is not certain. It can be conclud _ed that exposure to chrysotile alone has'rarely been shown to cause mesothelioma. 84 Inhalation experiments in animals show that all fibre types ofasbestos have the potential to produce similar amounts ofthe main types of asbestos related disease ifthe physical configuration of the fibres in the dust is appropriate. Intrapleural injection experiments also 82 The death rate from mesothelioma as certified on show that finely divided chrysotile can be prepared in death certificates in Britain, although small in absolute such a way that it produces a similar number of meso- terms, has doubled in the decade 1967-76, (Table 14 theliomas to crocidolite. It follows that any change in and Fig 3). Although this trend may be affected by a industrial practice in the direction of the production of recent tendency to diagnose mesothelioma more readily. more finely divided chrysotile fibre is likely to increase the evidence concerning occupational dust exposure the health risk. conditions in earlier years (to which deaths occurring at present are mainly due) suggests that the number of deaths from mesothelioma may be expected to increase Dose-response relationships further before the peak is reached. 85 The incidence and severity ofthe pathological CANCER OF THE OASTRQ.INTESTINAL TRAer INMAN response to increasing doses of asbestos in man is crucial to framing a rational policy about an acceptable level of exposure. Thus, iftl1ere were a level ofdose below which 83 Significant excesses ofcancer ascribed to these sites no risk ofsickness or death is incurred (ie a threshold) have occurred in most populations ofindustrial worken at least such a level would be acceptable. In contrast, ifit heavily exposed in the past to mixtures oramphiboles could be shown that the largest increments in risk per with chrysotile and in one population thought to be exposed exclusively to amosite. The evdenc:e that expo- unit ofexposure occurred at the lower end ofthe range of dose. a policy ofwry strictcontrol miaht be indicated. 53 FMSI 05603 Standardilld Mortality R1tlo IS.M.R.J 1200 1!. Maintenance-Service Workel'l x Prlductlon Workal'l o OUibec Mlnera and Mill Workll'l 1!. Table 18 (see Vol2 Table 31) Mesothelioma deaths In asbestos factory worken in Barkina. Ty~ ofexposure Duration of toasbeltos en,rployment Detlllu Ratepn 100000 subjret years Malel Low to moderate Severe Under2yean More than 2 years Undcr2yean More than 2 years 3 5 10 13 31 83 77 195 Totel (males) 31 88 800 Femalel Low to moderate Undcr2years 0 More than l years 0 600 Severe Under2yean More than 2 yean 9 5 106 126 Totel (females) 14 97 Can be rcprdcd as 'rate per 100 000 per aMum' Source: Abstracted from Newhouse and Berry (1976)" 200 100 o~--~~20-0 ---~40-0 ---~6-00---~--- Flaf(aeeVoi2Plall) hebandna.drawa. Cumulative 0011 lmp/cf-vl ~foriUDicaDCII'wltb Relative Risk the exact relationship is uncertain and may be less than multiplicative. One consequence ofthis synergism is that any future diminution in the tobacco habit in pei'SODI exposed to asbestos will have a greater beneficial effect than in persons not so exposed. MESOTHELIOMA 99 As far as mesothelioma is concerned the data so far available in man strongly suggest that the risk of this tumour increases with increasing dose. This is suggested by a study of 10 000 wQrkers at a Barking factory by Newhouse and Berry" (Table 18); Jaggers were found to fare worse than process workers. The occurrence ofcases due to domesticcontact with people occupationally exposed and in the neighbourhood of factories and mines also suggests that relatively low doses may be followed by the development ofcancer. However, information about the precise relationship between dose and response is lacking at present. 0 1000 2000 3000 Cumulative D011 (mp/cf-yl Pla7(aee Voi2Fia IZ) l..uDICIIDal'~reladoalhlp Cor Quebec mlnen llld millen. IDtemal CCJIIIIIUIIOD:.-....rllbc.lculated......10 tHiow taiPCIIUN fJOIIP.. 56 OTHER ASBESTOS RELATED DISEASE 100 As far as cancer of the gastro-intestinal tract is concerned, information about response to dose is limited to two studies reporting small excesses ofthese cancers, and the relationships are on the whole irregular and weak compared with lung cancer (Figs 9 and 10). It is worth noting, however, that a significant relationship ~tween increasins dose and increasi~llSC in statistical terms is present for cancer ofthe gastr~ intestinal tract for maintenance workers (exposed to chrysotile and amphiboles) but not for factory workers ~npged in thC manufacture ofasbestOs textiles, building products and friction materials ex osed to otile , Not ns definite can be said about the shape ofthe dose response curve or the existence or otherwise ofathreshold. 101 For calcified pleural plaques an irregular increase in prevalence with increasing dose is observed in fisures from the single study available (Fig 11) but in Quebec this phenomenon may be due to substances other thaD ubeltol. No information ia available on the doeorupollll reladcmaJUp ofcancer oftbe larynx. 0 FMSI 05604 Extrapolation and the public health alone in respect ofmesothelioma and perhaps more .dangerous tn respect of lung cancer; 102 The view taken in this section depends upon firsdy a number of the conclusions reached in the previous sections (recapitulated in summary form below); secondly certain assumptions about extrapolation of data derived from industry to situations where large numbers ofpersons are exposed to very low doses; thirdly, the evidence about the size ofthe population exposed and the severity and duration ofthe exposure outside the workplace. 103 The conclusions already reached relevant to this section are as follows: (1) that asbestos fibres, principally comprising chrysotile and amosite, arc continuing to accumulate in a wide variety ofmaterials in the UK while, although raw crocidolite imports have ceased, a substantial amount ofthis material remains; (2) that amphiboles and mixtures ofchrY8otile rich in tyn2hibolea are certaioly more danmoue than chrysotile (3) that where quantitative data from industrialexperience are available there is generally evidence for the existence ofan increasing biological response to increasing dose; within the industry we have found no convincing evidence for the existence ofa threshold below which no increment of risk takes place for lung cancer or mesothelioma and where sufficient data are available (as in the case ofchrysotilc and lung cancer, and mixtures of chrysotile and amphiboles and lung cancer) they are consistent with the linear hypqthesis. For the other fibres in relation to lung cancer and for mesothelioma in relation to all three fibre types the precise shape ofthe dose-response curves is unknown. For gastro-intestinal cancer the question ofthe existence of a threshold is unsettled. (4) The significance ofminor clinical and radiological changes is in so much doubt that extrapolation from industrial experience in respect ofasbestosis to the general Relatiw Risk 8 6 4 0 2 0 1- Death Rete Per ThouAnd 0 30 20 - Ali Respiratory ~----o Ali Gastro-Intestinal &---6 Oesophagaaand Stomech o----o Intestine and Rec:tum ---.,.. ........... ,,'J' ,I ,I _______ .:. / ' A----- 10 0 2 0~----2~00----~40-0 ---6~00----~80-0 ---~1000 Durltion of hpo1ure IYeen) I Cumulative Dos9 Imp/el-y) Fll I (lee Voll Pia 13) lleladw rlalt orcleach from IUDJ CIIIOII' In a . ...9 (Voll Pial5) Mortality from 01 cancer and dust In Quebec arouP orIIDOIIte IIIIUiadoft worbn b)' duration ottllpOIUN ' . mlnen and millen. (After 8lldmu ec al.)'l ' loanll: McDoaald JC and McDonald AD (1977).11i 51 FMSI 05605 Tabie 19 (~~ee Vol 2 Table 33) Asbestos dust concentrations in UK bulldinp accordin1 to (a) materials used, (b) type of buildin1 (Byrom and colleaaues. 1969)." TJpe ofmaUrial Total Fibres per em' lrualallort board Albestos Sprayed cement sheeting asbestos OtMP- No. % 0-0.00S >O.OOS-0.01 17 2 7 8 83 s 0 34 46 16 22 >0.01-0.02 62 2 0 10 14 >0.02-0.03 2 30 68 >0.03-0.04 20 0 0 23 >0.04-0.0S 20 0 0 23 >0.05-0.08 20 0 34 compressed flat shtett, partition board and low density panels. C, Fibres per em' O-O.OOS >O.OOS-0.01 >0.01-0.02 >0.02-0.03 >0.03-0.04 >0.04-0.05 >0.05-0.08 Hospital 4 2 0 0 0 Factory or Education ltorap 15 3 32 04 02 0 00 00 Of/ice 6 2 0 0 2 Slwp 4 0 0 0 0 Ploceof assembly Reslderrce Ml&c. 2 30 2 2 020 000 00 00 Total No. 34 16 10 6 2 2 3 % 46 22 14 8 3 3 4 I %of the present standard for chrysotile. We conclude _characteristics ofwater supplies for households and the that, in view ofthe presence in certain buildings of manufacture offood and drink. asbestos products, some ofwhich contain crocidolite or amosite which may be subject to abrasion or damage during normal use, larger samples of buildings The public health risk should be studied, particularly where amphiboles have been sprayed or used in insulation board. AIR 109 We conclude that the presence of chrysotile con- 107 Studies oflung tissue taken in samples ofpersons taining small quantities of amphiboles is unlikely to have subjected to autopsy have shown that the prevalence ofembedded asbestos fibre may be as high as SO%, that produced any material increase in the risk oflung cancer in the general population or any appreciable number of the prevalence is increasing and that it varies geographi eases or mesothelioma. The same is certainly true of cally. The component ofthis prevalence which is OCCU asbestosis. Pleural changes similar to those associated pational, or non-occupational in origin, is not clear with occupational exposure occur in circumstances from the published work. Many of the fibres found are where occupationally related exposure is unlikely. The extremely short. relationship of these to environmental asbestos or other I08 There is no published information about the presence or otherwise ofasbestos fibres in water in the u K. There is evidence from abroad which suggests that fibres may be leached from asbestos-containing pressure minerals is not proven. Cases ofpleural thickening and calcification have been reported in thoSe presumed to have. been exposed to asbestos dust non-occupationally in the neighbourhood of mines and factories. piping under certain circumstances. Fibres from asbestos 110 As far as the amphiboles crocidolite and amosite deposits in other rocks and ores and from industrial and mixtures rich in them are concerned, the position is contamination of water supplies have also been found. less certain because ofthe lack ofquantitative data Following on from the report of the FACC alld the results about the relationship of response to dose. Such data as of investiptions by the 0011, we believe that it would be advisable to study this phenomenon withi.n the ranae rorencountAn'ecl the UK ofacidity aad odllr cbemical ' exist suggest that the risk oflung cancer associated with amphiboles may be sreater than for chrysotile. An exceu luna cancer risk canaot be completely excluded, at 59 FMSI 05606 .. ca-Table 10 A comparison of the number ofdeaths from mesothelioma Ia the UK during 19~ and Types of asbestos: implications all cancers lung cancer me5othelioma J39,899}uK 37,152 256 for public policy I14 Following the lines laid down in the terms of Source: Annual Abstract ofStatisticsl976. Mesothelioma Register present, in those who have been exposed only to amphi boles in buildings. But the number ofcases, if any, is probably very small. reference of the report each type ofasbestos fibre is dealt with separately in this section. However it is important to repeat here a point made in earlier sections. This is that the conclusions reached about the effects of the different fibre types on man relate to past Ill While the majority of reported mesotheliomas are attributable to occupational and indirect OCCUJ:!ational exposure to amphiboles, some cases have been reported industrial practices, and ttult any.change in industrial practice in the direction of the production ofmore finely divided fibre is likely to increase the health risk. where the exposure his arisen as a result of domestic contact or neighbourhood exposure. Other mesothelio- CROCIDOLITE mas cannot be convincingly attributed to asbestos 115 There is strong evidence from a number ofsources exposure but some ofthese in other countries a arto that inhalation ofcrocidolite can cause mesothelioma, have n cause y o er brous minerals. A marked and that although the risk increases with increasing dose feature ofthe asbestos-related mesotheliomas has been it is possible for mesothelioma to occur after relatively the geographical clustering of cases in areas where large briefexposure to this amphibole. A substantial propor- quantities ofamphiboles were handled. The absolute tion of the deaths from mesothelioma which have number of mesotheliomas registered in comparison occurred and are occurring in Britain have probably with other causes of death is low (see Table 20), but been due to the inhalation ofamphiboles including despite the improvement of industrial practice in the crocidolite. Although the available evidence is incon- last twenty years and a number ofother favourable points clusive it is consistent with'the view that crocidolite may which have been mentioned above which give grounds for also have been more dangerous than chrysotile as far as optimism, an important area ofuncertainty remains. the causation of lung cancer is concerned. Crocidolite is one ofthe amphiboles associated with the excesses of THE RISK TO CHILDREN cancers ofthe gastro-intestinal tract (ifthese are in I 1.2 Although published instances ofasbestos related disease due to the exposure to asbestos ofchildren at home, in schools and in the vicinity ofdumps attract reality not misdiagnosed peritoneal mesotheliomas) and may also be concerned in a small number ofcases of laryngeal cancer. Evidence from the only study in man attention, they are rare. However, further surveys of school buildings containing asbestos and ofdumps in the vicinity ofasbestos factories on which children might play are desirable for two reasons. The first is that in which quantitative comparisons between crocidolite and chrysotile are possible suggests that crocidolite may cause more asbestosis than chrysotile. The animal work on this point is conflicting. susceptibility to cancer is known to vary with age, the very young being especially at risk in relation to certain stimuli. The second is that as children can be expected to live longer than adults they have more chance of being affected by carcinogens with long latent periods. 116 We believe that contact between man and crocidolite should be limited to the minimum practicable and stringent regulations for the protection ofworkers and of the public should continue to be applied in respect ofcrocidolite-containing materials still present WATER, FOOD AND BEVERAGES in buildings, vehicles, ships, dumps and other locations. 113 The scale ofconsumption ofdrinking water ' ~ . AMOSITE supplied through asbestos-containing pipes is such that 117 The importance of reaching a correct judgment even a very small increase in risk of abdominal tumours, about the amphibole ainosite is underlined by the should it be found to exist, might cause an appreciable number ofcases in absolute terms. It would also be extremely difficult to detect. There is however no evidence of the existence of risk in animals associated with the ingestion of asbestos. Industrial experience import trends to the UK since World War II which show a sevenfold increase in tonnage imported compared to a twofold increase in chrysotile. The tonnage of amosite imported in 1975 (19 200 tonrl.es} was almost three times the largest import figure for crocidolite since suggests that any risk in man may be limited to persons exposed to high doses, and the quantities ofasbestos ,, 1945 (6800 tonnes); (see Table 3 of Chapter 1}. fibres in water have been found in other countries to be 118 The principal difficulty about the evidence on the extremely low. It is understood, however, that further effects ofamosite upon health is that very few definable studies on the ingestion ofasbestos are being carried out. groups ofmen have been exposed to amosite who have Following on from the FACC report, we believe that .' not also been ex~sed to crocidolite, particularly in the astudies of the leaching ofasbestos fibres from presaure . United Kingdom. As cause ofmesothelioma, we take pipes in the range ofacidity encountered in UK public r, the view that the risk from amosite may be intermediate water uppliellhould be undertaken. , ' between chrylotile and crocidoliee. For reuona aqued 60 () 0 0 FMSI 05607 i28 n t e ot r an 1t IS essent1al to restate the proven . capacity ofchrysotile to produce mesotheliomas in animals ifthe fibre is of the appropriate configuration, and to emphasise once again that chrysotile is probably becoming increasingly finely divided and respirable. made ofthem a transformation must be carried out. This at best introduces additional uncertainties. Our approach has been to show the effect of three possible conversion factors. For the Rochdale lung cancer study we show the effect of taking the dust levels as measured and of increasing them by factors of 2 and S to take account respectively of the effect of modem instruments, and of the combined effect of modern instruments and personal samplers (see Table 17). 129 In the case oflung cancer there are two studies from North American and one from Britain which provide data which can be used to help us arrive at a standard. In the North American studies (Quebec miners and Enterline's process workers) the doses ofdust are recorded in particles per cubic foot. It follows that if use is to be 130 The array of figures in Table 21 sets out the excess mortality from lung cancer which would occur to work- yearsmen exposed to various chrysolite levels over SO from calculations based on the various studies. A range ofexcesses is allowed for from 2% (i.e. that 2% more of the men exposed at the given level would die of lung 0 Table 11 (sec Vol2 Table 35) Dust concentrations in fibres/a: that would produce shown excess mortality rrom luna cancer after 50 yean exposure aa:brdina to linear dose-responae models. Study Quebec Enterline (production worken) Enterline (IIWntenanc:e workers) Fibre type c c C,A,Cr Converllon /actorf s 2 1 s 2 1 s 1 1 Dust /enlr/or statedexceu mortaUty from IUIII t:tlllr 0.1 ~~ o.s 0.2 0.1 0.3 0.1 0.1 0.5% 3 I 0.5 1 0.5 0.3 1% 5 2 1 3 1 0.5 2% 11 4 2 s 2 1 0.1 0.4 0.8 0.04 0.2 0.3 0.02 0.1 0.2 2 0.6 0.3 Rochdale C,?Cr 1 5 0.04 0.2 0.08 0.4 0.2 1 0.4 0.8 2 0.8 ].6 4 c = Chrysotile, A = Amosite, Cr = Crocidollte. fFor Quebec"' and Enterline' studies ftaures are ratios or fibres per a: to million particles per cubic foOt. For Rochdale convenion facton are the Jowat and hlahest shown In Table 17 to convert to modem techniques with personal samplina. 0 Table 11 (see Vol 2 Table 36) Number of excea cleaths from tuna cancer amona one million people that mllht be caused by the hilhest observed environmental ubestoa dull levels in ambient air and the median or hlahest levels encountered by Byrom in buildinp if they were exposed continuously for 50 yean. Study Flbrltw-t Conwrlitm/fiCtatf f:LNumber ofextra deaths/rom ct~~U:er amo~~~JD" birtlu/rom 1tat.Jexposur to 1to.r infib,-, )'Hrl ....percc 0.01* O.l5tf Quebec c5 2 1 o0..s2 5 81 12.5 203 1.0 2S 405 Enterline (production workers) c s 2 1 0.4 10 162 1.0 25 405 2.0 50 810 Enterline (maintenance worken) Rochdale C,A,Cr c. ?Cr 5 2 I 2 5 1.4 35 540 3.4 BS 1 350 6.8 170 2700 2.7 68 I 080 1.4 34 540 0.5 14 216 f See Table 21. JO nano1fBD11 per cubic metre for 50 yean taken to be equiVIIent to O.Olllbn yean per cc, o.OB ftbr per co for 50 yean 11 equlwalent to 4 flbn yean perco. o.oos ftbrel perce for 50 ,..,.llequlftllnt to o.2S llbte,..,. perco. ' 0 62 FMSI 05608 245 This proposal would be appropriate for the scheduled processes discussed in para 243 above and possibly for some other operations in specified circumstances. We believe, however, that it could not be applied generally. Oearly, any such new requirement on measuring would need to be designed so as to be compatible with local authorities' powers under the Control of Pollution Act. The appropriate Inspectorate in liaison with other parties in HSB and after consultations with the industry, could help in the provision ofguidance O!! the best practicable means oftaking and assessing the samples. Recommendation 33: we recommend that ifrecommendation 32 is implemented, designated and especially scheduled works which emit asbestos dust into the atmosphere should measure such emissions regularly and systematically and keep appropriate records. Asbestos in the general atmosphere 246 On the basis of the evidence currently available, we concluded in Chapter 3 that, unless contaminated buildings are very much commoner than seems likely, no appreciable mortality from lung cancer can be associated with any degree ofcontamination by chrysotile likely to be en~untered in the UK in the air or in buildings not under active construction or repair. Even so, we recommend in our second report ttiara programme of work should be prepared to evaluate asbestos exposure in the non-occupational environment. We advised that resources would be most usefully directed initially to places where contamination with asbestos dust was likely to be highest and where information was most quickly needed. We are glad to hear that the Department Table 15 Current lepland administratiw controls for tho aenera1 public Rt!levont legi&IDtion t!IC Public Health Act 1936 and 1961 Public Health {Scotland) Act 1897 Clean Air Acts 1956 and 1968 Control of Pollution Act 1974 Merchant Shippina (Dangerous Gooda) Ru1es1965 Merchant ShippiiiJ Act 1970 Deposit of PoiSODOUI Waste Act 1972 Rivers Prevention of Pollution Acts 1951 and 1961 Consumer Safety Act 1978 J Food Drup Act 1955 Enaland aiKS Wales Water Act 1973 Health & Satety at Work etc IvA 1974 Grwral rt!mtll'lc.r Summary oftht! relt!vant provisions -St-at-ut-o-ry-n-ui-sa-nc-e-p-ro-vl-si-on-a-o-f ~ 1 Local Authorities (LA's) responsible for the control orasbestos Act may apply emissions. 2 Use of asbestos in the construction of buildings is covered by the Buildina Regs 1976 made under the Public Health Acts. These Regs apply in whole ofEnaland and Wales except inner London where the London Building (Constructional) Bye Laws apply. Similar Regs apply in Scotland and Northern Ireland. 816 (General nuisances) LA'a have a responsibility for (1) any accumulation or deposit of mineral refuse which is noxious, or injurious, or dangerous to health; (2) any work etc inJurious to the health of the neiahbourhood or so conducted as to be injunous or dangeroua to health; (3) LA's haveil duty to inspect their area from time to time to identify nuisances. Emissions ofdust from furnaces covered Any asbestos In dust from a furnace can be subject to some element of duat control. Act provide~! framework for a systematic and co-ordinated approach to waste collection and disposal I LA's have powen to require information from any works about emissions to air at intervals of 3 months or more. 2 A waste disposal site liunsina reaime now operates. The carriaae ofdangerous aoods and substances as car110 on UJt reaistered shipa is reaulated and controlled under these rules Specific advice on carriafC: and packina of individual substances is aiven in the International Mantime Danaerous Goods Code. Powers are availablo under S19 to make resull\tions to secure safo worldnt condldons and practices 1 The Dept ofTrade's recommendation made in the 'Code of Safe Workins practices for the Safety of Merchant Seamen'. 2 The Department ofTrade have issued Merchant Shippina Notices on asbestos. 1 Disposers of most types ofasbestos waste should notify the responsible authority. 2 Jt is an offence to deposit poisonous noxious or polluting waste on land in such a way that it is liable to aive rise to an environmental hazard. Tbere Ia alimilar Act Ia Scotlalld Any discharge of liquid effluence to controlled waten from asbestos works requires the consent of the relevant Water Authority in Enaland or Wales or River Purification Board in Scotland. There is no leaislation dealina specifically with the use ofasbestos in consumer products but there is power to introduce such leaislation in tho Act. There are similar Acts in Scotland and Northern Ireland; while there are no specific statutoryJimitslaid down in UJt for the levels of asbestos in food, this Act will apply to any question ofcontamination. Water Authorities supply water and LA'sshould see the water is wholesome. 53 obllps employers and self-employed persons to conduct their undertaldDJSln IUch a way u to ensure, so far u Ia reasonably practicable. that penons not Ia their employment who IDa)' be atrected thereby are not tbenby aPQIId to rlab to thelrsafoty, 0 0 FMSI 05609 sample from which this can be ascertained and whether within the scope of the improvements to the Asbesto!l all the precautions taken for large scale work on Regulations that we arc now proposing. Nevertheless crocidolite should also apply to minor repair and similar we feel that something more is needed than a mere work. tightening ofmeasures to protect workers exposed to Recommenclatloa 2: we recommend that the term - asbestos dust in the workplace, or a more rigorous containing crocidolite' should be defined and that the enforcement of these matters. Where a substance such u definition should specify the technique or techniques of asbestos has no clearly defined threshold concentration analysis to be used and the criteria for deciding whether below which the health risk is non-existent there arc crocidolite is present. obvious advantages in replacing it with an alternative material, provided that alternative is significantly less 14S One approach would be to require analysis ofall hazardous. such materials containing or suspected to contain asbestos to determine the asbestos type. This requirement is 147 While the evidence so far available indicates that already implicit in Regulation 6 ofthe Asbeatos the most commonly used man-made mineral fibres are Regulations 1969, inasmuch as notice has to be given to !,css harmful to man than asbestos, animal experiments HMFI ofall work involving crocidolite. Many responsible building and demolition contractors already carry out suggest that any ill effects from such fibres are related inore to the size and shape ofthe fibre than its chemical bulk sampling before they start work involving materials composition. It follows therefore ifthCSlzeandshapc- known or suspected to contain asbestos, and either notify offibrcs of materials used as substitutes for asbestos arc HMFJ or not according to whether crocidolite is found. similar to those ofasbestos there may be a tentialrisk. The main practical problem ariSes withjobs where the s ts ere ore an area tn w tc one should proceed quantity of the suspect material is so small that to treat with caution. it as containing crocidolite (that is, to usc more stringent safety precautions) is cheaper than to have the material sampled and analysed. We understand that some firms already choose the cheaper alternative in such cases: that is, when in doubt, they treat thematerialascrocidoUte and notify HMFI. For smallscale jobs, we consider this approach sensible. 148 We have been advised that it is doubtful how far Section 2 of the HSW Act can be taken to require an employer to use a less hazardous substance in place of asbestos even if it is reasonably practicable for him to do so. Because ofthis doubt, we concentrate here on the principles ofpossible requirements onsubstitutionwithout considering in detail how they might be fitted into the Recommenclatlon 3: we recommend that, if as at present framework ofexisting health and safety legislation or, an employer chooses to treat a given substance as indeed, to what extent they are already implicit in that containing crocidolite, he should continue to be under legislation. We urge, however, that our recommendations no obligation to carry out tests to determine whether should be implemented in such a way as not to weaken crocidolite is in fact present. any such implicit requirement. We also emphasise that On the other hand, we believe that the obligation implicit none ofour recommendations should be implemented in Regulation 6 should be strengthened. in such a way as to require the precipitate substitution of Recommendation 4: we recommend that, ifan employer does not treat a substance as containing crocidolite, asbestos or products containing it by alternative materials whose safetyis itselfunknown or in serious doubt. the onus should be on him to show that crocidolite is not present ifhis action is challenged. Currently the only satisfactory way ofdischarging that obligation in respect of old lagging or sprayed coatings is by bulk sampling and laboratory analysis. In future years, when Recommendations 1 and 2 ofour First Report are implemented so that asbestos is banned in insulation and sprayed coatings, it may be sufficient for an employer to show proofthat the material was installed after the ban came into effect. Meanwhile the Code of Practice also recommended in our First Report wiU give practical guidance on work in those arcu. 149 We have considered carefully two possible approaches, which are not mutually exclusive. The first approach would be to adopt a system ofgradual compulsory substitution. This would mean that the whole range ofasbestos products would need to be examined periodically by a central authority (HSE) to identify appropriate candidates for substitution. This examination would involve considering factors such as the health risk associated with each product in both manufacture and subsequent use, its economic import ance, the availability ofsubstitutes, their relative performance and cost and the health risk associated with them. Such a scheme would, in effect, amount to a Substitution gradual extension ofprohibition. It would be substan 146 We now tum to those types ofasbestos and products containing it for which we consider that the ultimate sanction ofprohibition is not justified by tbe evidence at present. All processes involving the use of these fibres and products at work are subject to the tially similar to the programme for substitution suggested in the roc's written evidence to the committee and would in our view only be aCceptable where the criteria set out in para 142 above applied. ISO The second approach would be to require Health and Safety at Work etc Act 1974 and moat are subject to tbe Asbestos Replatioaal969.'All would be manuftlcturers, specifiers and users ofproducts con tainiaa asbestos to weighcarefUUy tbe risb incumd 0 0 70 FMSI 05610