Air, water, and soil pollution is estimated to account for only 1%-4% of all cancers. A small percentage of lung cancer (less than 5%) may be due to chronic inhalation of outdoor air pollutants such as industrial or engine exhaust chemicals. Indoor air pollutants such as secondhand smoke and radon are thought to be contributors, but this risk is most likely exaggerated (see below). In China and some other Asian countries, chronic inhalation of cooking oil smoke may be a causative agent of lung cancer.90 The contamination of the atmosphere by chlorofluorocar-bons (whose production is now banned in developed countries) in refrigerant and propellants has been implicated in destruction of the ozone layer and a resultant increase in skin cancer due to a lower filtering of UV irradiation from the sun. Occupational exposure to inhaled asbestos, such as occurred in Liberty Ship building in World War II, has been clearly linked to me-sothelioma.
Regarding water pollution, high exposure to arsenic in drinking water in certain countries (e.g., Bangladesh) and areas of the United States (Alaska) and South America (Argentina, Chile) appears to be related to an increased risk of bladder and skin cancers.90 A number of other groups of water pollutants have been investigated as possible sources of cancer risk, but the data are not conclusive, even though a popular myth is that the contents of our drinking water are causing cancer.
Evidence that potential carcinogens in the air or water might cause cancer is based on several assumptions as well as on epidemiologic data. One of the assumptions is that there is a linear, nonthreshold dose-response relationship between the given dose of carcinogen and the number of cases of cancer. This assumption is based primarily on dose-response studies in experimental animals. Such a dose-response relationship carries the implication that there is no such thing as a safe level of exposure to a carcinogen (discussed in Chapter 2). Taking the nonthreshold approach to evaluation of exposure to environmental agents is, of course, the most conservative policy; it tends to predict the largest response (i.e., the largest number of cancers) for any given level of low-dose exposure. Since the possible consequences of exposure to carcinogens in the general environment are so enormous, a number of investigators think that it is appropriate to use this approach. Although this approach seems reasonable to environmentalists, currently only limited evidence supports it. Evidence from air pollution studies, for example, indicates that estimates of cancer risk by extrapolation of dose-response relationships may be an oversimplification of the problem. Large metropolitan areas have a substantially higher level of atmospheric carcinogens, such as benzo[a]pyrene, resulting from combustion of fossil fuels, than rural areas, yet some studies91 show that nonsmokers in urban areas do not have a significantly higher risk of lung cancer than that of rural nonsmokers. However, urban smokers do have a significantly higher incidence of lung cancer than comparably heavy smokers in rural areas. These observations and others, such as the potentiation of lung cancer in uranium miners92 and asbestos workers93,94 who smoke, support the idea that a combination of urban air pollution and smoking is the most carcinogenic.
Numerous potential carcinogens have been found in air and water, particularly in areas near or downstream from large industrial complexes. For example, nitrosamines, a class of chemicals that are amongthe mostpotentcarcinogens known from experimental animal studies, are present in the environment, albeit usually at very low concentrations.
In addition to industrial sources, domestic sewage treatment plant effluents may contain carcinogenic substances that may find their way into drinking water supplies. More than 50 chlorinated hydrocarbons have been identified in domestic sewage effluents.95 This same study estimated that over 1000 tons of chlorinated organic compounds are discharged by sewage treatment plants into the nation's waterways annually. Chlorinated hydrocarbons result from the chlo-rination of water heavily polluted with organic chemicals.96 Some of these chlorinated compounds are known to be carcinogenic in animals.
Although discharges from industrial and municipal waste treatment plants may be continuous sources of pollution, spills resulting from industrial operations, transportation accidents, or dumping of chemical wastes on or near bodies of water can contribute significant levels of hazardous substances to public water supplies.
The Environmental Protection Agency and other groups have undertaken studies of several large metropolitan areas to evaluate the level of contamination of public drinking water supplies and to assess the carcinogenic risk associated with this contamination. In a survey of 80 cities, a number of potentially dangerous trihalometh-anes, including chloroform, bromodichloro-methane, dibromochloromethane, and bromo-form, were detected.97 Chloroform, a known carcinogen in animals, was found in the drinking water of 80 cities. Carbon tetrachloride, also a known carcinogen, was found in the drinking water of 10 cities. In one survey98, 325 organic chemicals were identified in the drinking water of various cities. Only about 10% of these have been adequately tested for carcinogenicity. Among the known or suspected carcinogens identified in drinking water are benzene, bis(chloro-methyl) ether, carbon tetrachloride, chloroform, dieldrin, polychlorinated biphenyls, 1,1,2-trichloroethylene, and vinyl chloride. Thus, it is evident that the general public is exposed to a wide variety of environmental chemical carcinogens. Since there is a 20- to 30-year latent period between exposure to certain carcinogenic agents and the development of clinically detectable cancer, it will probably take several decades to fully evaluate the impact of our contaminated environment. It should be pointed out, however, that the expected correlations between exposure to a given carcinogen in the drinking water and the type of cancer expected to result from such exposure have not been established. For example, even though chloroform, a hepatocarcino-gen, is the predominant organic contaminant in the drinking water of certain communities in Louisiana that take their water from the Mississippi, there is no increased mortality from hepatic cancers in those communities.99
Nevertheless, a considerable debate over the role of environmental pollutants in human cancer continues. On the basis of studies of cancer incidence in various regions in Africa, Higginson and Oettle100 provided some definitive data on the impact of environmental factors in the causation of human cancer. The work of Higginson and colleagues has generally been credited with establishing the fact that about two-thirds of all human cancers have an environmental cause and thus, theoretically at least, are preventable. This has led many people to believe that the environmental agents responsible for cancer are chemicals that we inhale or ingest. However, as Hig-ginson himself has reiterated,101,102 what he meant by "the environment" is the total milieu in which people live, including cultural habits, diet, exposure to various infectious agents, average age of menarche, number of children a woman bears, age of menopause—in short, the cultural as well as the chemical environment.
Although we have seen that clear correlations between excess occupational exposure to carcinogenic chemicals and some cancers can be made, the contribution of these occupationally related cancers to the total incidence of cancer in industrialized nations is small. Furthermore, although urban-rural differences in cancer incidence have been reported in several countries, these differences tend to disappear when homogeneous populations with a similar lifestyle, for example, the Mormons, are studied.103 And, although in England and Wales, certain occupations have been associated with a different risk of cancer from that of the general population, nearly 90% of such variation is eliminated if individual groups of similar social class and habits are compared.104 Other inconsistencies also occur. For example, bladder cancer is linked to certain chemical and allied industries in United States, but no clear industrial association has been found in Japan. Prostate cancer is higher in blacks than in whites living in the same counties in the United States, and both black and white males in the United States have a higher incidence of prostate cancer than men in the industrialized United Kingdom and Japan. However, the differences in incidence between the United States and the United Kingdom may be mainly due to PSA screening because PSA screening is not widely used in the United Kingdom. Interestingly, the mortality rates are similar between the two countries.32
Thus, the overall distribution patterns of cancer observed in North America and Western Europe, with high frequencies of lung, colon, breast, and uterine cancer, suggest some common factors in the environment of these regions in comparison with regions in Africa in which there is a much lower incidence of these malignant diseases. At present, however, it is unjustified to link these differences in incidence directly to recent food additives or chemical pollutants. Lifestyle differences appear to play a large role in the causation of these and other cancers.101 For example, the varying incidence of cancer of the breast, ovary, and uterus can be related at least partly to differences in average age at onset of menarche, sexual behavior, and reproductive patterns among different population groups. Taken together, all the data accumulated to date suggest that cancer distribution patterns represent a variety of differences in lifestyle, with exposure to chemical pollutants in the ambient environment of industrialized societies contributing to some but an as-yet unclear percent of the total number of cancer deaths.
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