American Journal of Industrial Medicine 2 2 M 3 - 4 4 6 (1992)

COMMENTARY

How Are We Going to Change Our Attitudes and Opinions Regarding Asbestos and Cancer in the Next 20 Years? Jean Bignon, MD

Key words: history of medicine, asbestos regulation, scientific debate

INTRODUCTION The review by Professor Enterline on “Changing attitudes and opinions regarding asbestos and cancer 1934-65” [ 19911 incites me to make some personal remarks with the intention of justifying why the asbestos problem was raised in France with a two decades’ delay, by comparison with the USA and UK. I will also comment on the difficulties we are going to encounter for changing some controversial opinions regarding the relationships between asbestos and cancer. The solidly documented paper is a brilliant illustration of the common behavior of medical scientists when they have to discuss a new etiological factor of cancer in the field of occupational medicine. As noted by Enterline, there were several reasons which delayed the international consensus on what appears now as evident, i.e., the relationship of occupational exposure to asbestos with lung cancer and mesothelioma. First, the priority given by a country to public health. In France after World War 11, there was good organization of clinical occupational medicine in the workplace. However, epidemiological and experimental occupational toxicology were underdeveloped, except at CERCHAR (Research Laboratories of Coalwork of France) where a well known biologist, Professor Policard, conducted an advanced international toxicology research program in the field of coal dust pneumoconiosis. As in many other countries until the 1960s, the relationship between lung cancer and occupational exposure to asbestos was only anecdotally reported. This was the case in the 1962 paper of Champeix et al., cited in the 1991 article. Indeed, at that time in France, the young Epidemiology School headed by Professor Schwartz, gave priority to the study of tobacco-related disease. By contrast, there was practically no occupational epidemiology, particularly on asbestos exposed workers. Pulmonary Research Unit, University of Pans, Paris, France. Address reprint requests to Dr. Jean Bignon, Pulmonary Research Unit, University of Paris-Valde-Marne, CHU Henri Mondor, 51, Ave. du Markchal de Lahre de Tassigny, 94010 Crkteil Ctdex, France. Accepted for publication February 24, 1992.

0 1992 Wiley-Liss, Inc.

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As stressed by Enterline, economic reasons were probably another important factor in the delay. Indeed, when in the 1970s, 1 was calling attention to the serious health hazards of asbestos workers in our country, there was no legislation regulating asbestos exposure [Bignon et al., 19751. It was only in 1977 that French legislation for the control of fiber concentrations in asbestos plants was promulgated. One year later, legislation prohibiting the spraying of asbestos inside buildings was also enacted. Nowadays, although the use of asbestos is strictly controlled in France, there is still a clean and apparently prosperous asbestos industry. To the closing of the Enterline paper “Nevertheless, health effects like those resulting from asbestos are not likely to be missed for long in the future,” my question is: “Are we sure that we are now able to avoid such long delays before discovering the scientific evidence, particularly concerning environmental exposures?” I will illustrate with four areas of divergent opinions concerning our present knowledge in the field of asbestos-related diseases. In my view, it will take one or possibly two more decades to resolve the controversies. 1. The first problem is illustrated by the common assertion that the development of asbestos-related lung cancer is always preceded by pulmonary fibrosis [Bignon and Brochard, 19901. This means that some factors mediated by lung fibrosis may be able to facilitate carcinogenesis. This issue remains unsolved. Nevertheless, it could be elucidated in animal experiments specifically designed to answer this question. This point is particularly relevant for compensation rejection for the numerous lung cancers presently observed in persons with a long history of smoking, yet having also been occupationally exposed to asbestos in previous work. 2. The second issue concerns contradictions concerning mesothelioma and fiber types. Indeed, numerous epidemiological and mineralogical studies have provided some evidence suggesting that asbestos-related mesotheliomas were more often associated with amphiboles, including tremolite as a contaminant, than with chrysotile [McDonald and McDonald, 19871. However, some authors disagree with this statement, considering that long-term amphibole retention in the lung is not necessarily the only causal factor responsible for pleural mesothelioma. Actually, most experimental data do not bring satisfactory answers to this human evidence. In fact, all types of asbestos, either amphiboles or chrysotile, are capable of inducing mesothelioma at the same rate in rodents, even by inhalation [Wagner et al., 1974; Davis et al., 19781 and are similarly prone to transform rat pleural mesothelial cells in vitro [Jaurand et al., in press]. Thus, the only hypothesis for explaining such discrepancies is the much longer biopersistence of amphibole fibers in human than in rodent lung, due to the long duration of life in man. Nevertheless, other interpretations are possible and there is a risk that the resolution of this controversy will take time. 3. The third issue is presently the most important one. Indeed, most epidemiological studies (registries, case-control studies) indicate that about 20-30% of mesothelioma cases observed are without characterized exposure to asbestos [Hirsch et al., 1982; Peterson et al., 19841. Are those cases due to environmental exposure to low doses of asbestos or are they related to other unsuspected causal factors (chemicals, metals)? This question will probably take more than 20 years to be resolved. 4. This last point is strongly related to another issue: what are the health effects of exposure to low doses of asbestos? It was the topic of a recent Workshop held in

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Paris, June 10-12, 1991 [Valleron and Bignon, in press]. This question is currently of import because of the long persistence of asbestos-containing materials in public and commercial buildings. Only the risk assessment methodology, consisting in extrapolation of the dose-response curves, acquired from mortality studies conducted in several cohorts of asbestos workers, to persons potentially exposed to low doses, can allow prediction of the extrapulmonary cancers that might be attributed to an exposure at the low doses [Hughes and Weill 19861. For the optimists who aim at the most reasonable social behavior, the tendency is to consider that this problem is not a real health concern. But what about the pessimists? We do not know who is right. Actually, the dose-response relationship for lung cancer and mesothelioma for exposure at very low concentrations of asbestos, e.g., 0.001 f/ml or less (0.0001 f/ml) as measured in buildings with asbestoscontaining materials, cannot be assessed by the classic epidemiological methods, even when using meta-analysis. It will take probably more than two decades to obtain the answer to this critical point, presently responsible for litigations in Western countries.

I will not enter into the debate of asbestos substitutes. I only wish to indicate that it is possible that some of them may not be as safe as expected. The concerned industries are well aware of this problem and are trying to design the best methodology for selecting the safest fibers. However, in the future, the task will be difficult for clinicians and epidemiologists to ascertain the fibers really responsible for disease, because workers during their lifetimes will have been exposed to more than one type of fiber (asbestos, natural fibers, synthetic fibers). Although environmental sciences have advanced very quickly during the last 20 years, we are often faced with unsolvable issues. The simultaneous advance in education and information of the general population of the Western World has led to these people always asking for more sophisticated methodologies but also for more safety regarding the industrial products. We may hope that better knowledge of the cellular and molecular events in toxicology will help to shorten such delays. But, already, we must admit our limitations and express the wish that scientists, industrialists, politicians, and consumers will endeavor to work together in order to reach a consensus on acceptable risk. REFERENCES Bignon J , SCbastien P, Bonnaud G (1975): Le risque asbestosique actuel. Med Hyg 33:674-677. Bignon J , Brochard P (1990): lnconsistencies and limitations. In Miller K , Lidell FDK (Eds): “Mineral Fibers and Health.” Boca Raton, FL: CRC Press, pp 198-206. Charnpeix J , De Laguillaumie B, Jacquemet L, Mory F, Geille A (1962): Cancer bronchique et exposition aux poussieres d’amiante. Arch Ma1 Prof 23:267-271. Davis JMG, Beckett S, Bolton RE, Collings P, Middelton AP (1978): Mass and number of fibres in the pathogenesis of asbestos-relatedlung disease in rats. Br J Cancer 37:673-688. Enterline PE (1991): Changing attitudes and opinions regarding asbestos and cancer 1934-1965. Am J Ind Med 20:685-700. Hirsch A, Brochard P, De Crernoux H, Erkan L, SCbastien P, Di Menza L, Bignon J (1982):Features of asbestos-exposed and unexposed mesothelioma. Am J Ind Med 3:413-422. Hughes JM, Weill H (1986): Asbestos exposure, quantitative assessment of risk. Am Rev Respir Dis I33:5-15. Jaurand MC, Saint-Etienne L, Van der Meeren A, Endo-Capron S, Renier A, Bignon J (in press):

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“Neoplastic Transformation of Rodent Cells. Cellular and Molecular Aspects of Fiber Carcinogenesis. Current Communication in Molecular Biology, No. 2.” New York: Cold Spring Harbor. McDonald AD, McDonald JC (1987): Epidemiology of malignant mesothelioma. In Antman K, Aisner MJ (eds): “Asbestos Related Malignancy.” New York: Grune and Stratton, pp 31-55. Peterson JT, Greenberg SD, Buffler PA (1984): Non asbestos related malignant mesothelioma. A Review. Cancer 54:951-960. Valleron AJ, Bignon J. Low exposure to natural and manmade fibres and the risk of cancer: towards a collaborative European epidemiology. Workshop, Paris, June 10-12. BJ Indust Med in press. Wagner JC, Berry G, Skidmore JW, Timbrel1 V (1974):The effects of the inhalation of asbestos in rats. Br J Cancer 29:252-269.

How are we going to change our attitudes and opinions regarding asbestos and cancer in the next 20 years?

American Journal of Industrial Medicine 2 2 M 3 - 4 4 6 (1992) COMMENTARY How Are We Going to Change Our Attitudes and Opinions Regarding Asbestos a...
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