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Environmental Cancer

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Cancer is a common disease in all countries of the world. The probability that a person will develop cancer by the age of 70 years, given survival to that age, varies between about 10 and 40% in both sexes. On average, in developed countries, about one person in five will die from cancer. This proportion is about one in 15 in developing countries. In this article, environmental cancer is defined as cancer caused (or prevented) by non-genetic factors, including human behaviour, habits, lifestyle and external factors over which the individual has no control. A stricter definition of environmental cancer is sometimes used, comprising only the effect of factors such as air and water pollution, and industrial waste.

Geographical Variation

Variation between geographical areas in the rates of particular types of cancer can be much greater than that for cancer as a whole. Known variation in the incidence of the more common cancers is summarized in table 1. The incidence of nasopharyngeal carcinoma, for example, varies some 500-fold between South East Asia and Europe. This wide variation in frequency of the various cancers has led to the view that much of human cancer is caused by factors in the environment. In particular, it has been argued that the lowest rate of a cancer observed in any population is indicative of the minimum, possibly spontaneous, rate occurring in the absence of causative factors. Thus the difference between the rate of a cancer in a given population and the minimum rate observed in any population is an estimate of the rate of the cancer in the first population which is attributable to environmental factors. On this basis it has been estimated, very approximately, that some 80 to 90% of all human cancers are environmentally determined (International Agency for Research on Cancer 1990).

Table 1.  Variation between populations covered by cancer registration in the incidence of common cancers.1

Cancer (ICD9 code)

High-incidence area


Low-incidence area


Range of variation

Mouth (143-5)

France, Bas Rhin


Singapore (Malay)



Nasopharynx (147)

Hong Kong


Poland, Warsaw (rural)



Oesophagus (150)

France, Calvados


Israel (Israeli-born Jews)



Stomach (151)

Japan, Yamagata


USA, Los Angeles (Filipinos)



Colon (153)

USA, Hawaii (Japanese)


India, Madras



Rectum (154)

USA, Los Angeles (Japanese)


Kuwait (non-Kuwaiti)



Liver (155)

Thailand, Khon Khaen


Paraguay, Asuncion



Pancreas (157)

USA, Alameda County (Calif.) (Blacks)


India, Ahmedabad



Lung (162)

New Zealand (Maori)


Mali, Bamako



Melanoma of skin (172)

Australia, Capital Terr.


USA, Bay Area (Calif.)(Blacks)



Other skin cancers (173)

Australia, Tasmania


Spain, Basque Country



Breast (174)

USA, Hawaii (Hawaiian)


China, Qidong



Cervix uteri (180)

Peru, Trujillo


USA, Hawaii (Chinese)



Corpus uteri (182)

USA, Alameda County (Calif.) (Whites)


China, Qidong



Ovary (183)



Mali, Bamako



Prostate (185)

USA, Atlanta (Blacks)


China, Qidong



Bladder (188)

Italy, Florence


India, Madras



Kidney (189)

France, Bas Rhin


China, Qidong



1 Data from cancer registries included in IARC 1992. Only cancer sites with cumulative rate larger or equal to 2% in the high-incidence area are included. Rates refer to males except for breast, cervix uteri, corpus uteri and ovary cancers.
2 Cumulative rate % between 0 and 74 years of age.
Source: International Agency for Research on Cancer 1992.

There are, of course, other explanations for geographical variation in cancer rates. Under-registration of cancer in some populations may exaggerate the range of variation, but certainly cannot explain differences of the size shown in table 1. Genetic factors also may be important. It has been observed, however, that when populations migrate along a gradient of cancer incidence they often acquire a rate of cancer which is intermediate between that of their home country and that of the host country. This suggests that a change in environment, without genetic change, has changed the cancer incidence. For example, when Japanese migrate to the United States their rates of colon and breast cancer, which are low in Japan, rise, and their rate of stomach cancer, which is high in Japan, falls, both tending more closely towards United States’ rates. These changes may be delayed until the first post-migration generation but they still occur without genetic change. For some cancers, change with migration does not occur. For example, the Southern Chinese retain their high rate of cancer of the nasopharynx wherever they live, thus suggesting that genetic factors, or some cultural habit which changes little with migration, are responsible for this disease.

Time Trends

Further evidence of the role of environmental factors in cancer incidence has come from the observation of time trends. The most dramatic and well-known change has been the rise in lung cancer rates in males and females in parallel with but occurring some 20 to 30 years after the adoption of cigarette use, which has been seen in many regions of the world; more recently in a few countries, such as the United States, there has been the suggestion of a fall in rates among males following a reduction in tobacco smoking. Less well understood are the substantial falls in incidence of cancers including those of the stomach, oesophagus and cervix which have paralleled economic development in many countries. It would be difficult to explain these falls, however, except in terms of reduction in exposure to causal factors in the environment or, perhaps, increasing exposure to protective factors—again environmental.

Main Environmental Carcinogenic Agents

The importance of environmental factors as causes of human cancer has been further demonstrated by epidemiological studies relating particular agents to particular cancers. The main agents which have been identified are summarized in table 10. This table does not contain the drugs for which a causal link with human cancer has been established (such as diethylstilboestrol and several alkylating agents) or suspected (such as cyclophosphamide) (see also Table 9). In the case of these agents, the risk of cancer has to be balanced with the benefits of the treatment. Similarly, Table 10 does not contain agents that occur primarily in the occupational setting, such as chromium, nickel and aromatic amines. For a detailed discussion of these agents see the previous article “Occupational Carcinogens.” The relative importance of the agents listed in table 8 varies widely, depending on the potency of the agent and the number of people involved. The evidence of carcinogenicity of several environmental agents has been evaluated within the IARC Monographs programme (International Agency for Research on Cancer 1995) (see again “Occupational Carcinogens” for a discussion of the Monographs programme); table 10 is based mainly on the IARC Monograph evaluations. The most important agents among those listed in table 10 are those to which a substantial proportion of the population is exposed in relatively large amounts. They include particularly: ultraviolet (solar) radiation; tobacco smoking; alcohol drinking; betel quid chewing; hepatitis B; hepatitis C and human papilloma viruses; aflatoxins; possibly dietary fat, and dietary fiber and vitamin A and C deficiency; reproductive delay; and asbestos.

Attempts have been made to estimate numerically the relative contributions of these factors to the 80 or 90% of cancers which might be attributed to environmental factors. The pattern varies, of course, from population to population according to differences in exposures and possibly in the genetic susceptibility to various cancers. In many industrialized countries, however, tobacco smoking and dietary factors are likely to be responsible each for roughly one-third of environmentally determined cancers (Doll and Peto 1981); while in developing countries the role of biological agents is likely to be large and that of tobacco relatively small (but increasing, following the recent increase in the consumption of tobacco in these populations).

Interactions between Carcinogens

An additional aspect to consider is the presence of interactions between carcinogens. Thus for example, in the case of alcohol and tobacco, and cancer of the oesophagus, it has been shown that an increasing consumption of alcohol multiplies manyfold the rate of cancer produced by a given level of tobacco consumption. Alcohol by itself may facilitate transport of tobacco carcinogens, or others, into the cells of susceptible tissues. Multiplicative interaction may also be seen between initiating carcinogens, as between radon and its decay products and tobacco smoking in miners of uranium. Some environmental agents may act by promoting cancers which have been initiated by another agent—this is the most likely mechanism for an effect of dietary fat on the development of breast cancer (probably through increased production of the hormones which stimulate the breast). The reverse may also occur, as, for example, in the case of vitamin A, which probably has an anti-promoting effect on lung and possibly other cancers initiated by tobacco. Similar interactions may also occur between environmental and constitutional factors. In particular, genetic polymorphism to enzymes implicated in the metabolism of carcinogenic agents or DNA repair is probably an important requirement of individual susceptibility to the effect of environmental carcinogens.

The significance of interactions between carcinogens, from the point of view of cancer control, is that withdrawal of exposure to one of two (or more) interacting factors may give rise to a greater reduction in cancer incidence than would be predicted from consideration of the effect of the agent when acting alone. Thus, for example, withdrawal of cigarettes may eliminate almost entirely the excess rate of lung cancer in asbestos workers (although rates of mesothelioma would be unaffected).

Implications for Prevention

The realization that environmental factors are responsible for a large proportion of human cancers has laid the foundation for primary prevention of cancer by modification of exposure to the factors identified. Such modification may comprise: removal of a single major carcinogen; reduction, as discussed above, in exposure to one of several interacting carcinogens; increasing exposure to protective agents; or combinations of these approaches. While some of this may be achieved by community-wide regulation of the environment through, for example, environmental legislation, the apparent importance of lifestyle factors suggests that much of primary prevention will remain the responsibility of individuals. Governments, however, may still create a climate in which individuals find it easier to take the right decision.



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Cancer References

Aitio, A and T Kauppinen. 1991. Occupational cancer as occupational disease. In Occupational Diseases. Helsinki: Institute of Occupational Health.

Aksoy, M. 1985. Malignancies due to occupational exposure to humans. Am J Ind Med 7:395-402.

Alho, M, T Kauppinen, and E Sundquist. 1988. Use of exposure registration in the prevention of occupational cancer in Finland. Am J Ind Med 13:581-592.

Anon. Bladder tumours in industry. 1965. Lancet 2:1173.

Armitage, P and R Doll. 1961. Stochastic models for carcinogenesis. In Proceedings of the Fourth Berkeley Symposium on Mathematical Statistics and Probability, edited by J Neyman. Berkeley: Univ. of California Press.

Checkoway, H, NE Pearce, and DJ Crawford-Brown. 1989. Research Methods in Occupational Epidemiology. New York: Oxford Univ. Press.

Decoufle, P. 1982. Occupation. In Cancer Epidemiology and Prevention, edited by D Schottenfeld and JF Fraumenti. Philadelphia: WB Saunders.

Doll, R and R Peto. 1981. The causes of cancer. J Natl Cancer Inst 66:1191-1308.

Ennever, FK. 1993. Biologically based mathematical models of lung cancer risk. Epidemiology 4:193-194.

Frumkin, H and BS Levy. 1988. Carcinogens. In Occupational Health, edited by BS Levy and DH Wegman. Boston: Little, Brown & Co.

Higginson, J. 1969. Present trends in cancer epidemiology. Proc Canadian Cancer Res Conf 8:40-75.

Higginson, J and CS Muir. 1976. The role of epidemiology in elucidating the importance of environmental factors in human cancer. Cancer Detec Prev 1:79-105.

—. 1979. Environmental carcinogenesis: Misconceptions and limitations to cancer control. J Natl Cancer Inst 63:1291-1298.

Hogan, MD and DG Hoel. 1981. Estimated cancer risk associated with occupational asbestos exposure. Risk Anal 1:67-76.

International Agency for Research on Cancer (IARC). 1972-1995. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Vol. 1-63. Lyon: IARC.

—. 1990. Cancer: Causes, Occurrence and Control. IARC Scientific Publication, No. 100. Lyon: IARC.

—. 1992. Cancer Incidence in Five Continents. Vol. VI. IARC Scientific Publications, No. 120. Lyon: IARC.

Jeyaratnam, J. 1994. Transfer of hazardous industries. In Occupational Cancer in Developing Countries, edited by NE Pearce, E Matos, H Vainio, P Boffetta, and M Kogevinas. Lyon: IARC.

Kerva, A and T Partanen. 1981. Computerizing occupational carcinogenic data in Finland. Am Ind Hyg Assoc J 42:529-533.

Kogevinas, M, P Boffetta, and N Pearce. 1994. Occupational exposure to carcinogens in developing countries. In Occupational Cancer in Developing Countries, edited by NE Pearce, E Matos, H Vainio, P Boffetta, and M Kogevinas. Lyon: International Agency for Research on Cancer (IARC).

Moolgavkar, S. 1978. The multistage theory of carcinogenesis and the age distribution of cancer in man. J Natl Cancer Inst 61:49-52.

Moolgavkar, SH, EG Luebeck, D Krewski, and JM Zielinski. 1993. Radon, cigarette smoke and lung cancer: A re-analysis of the Colorado Plateau uranium miners’ data. Epidemiology 4:204-217.

Pearce, NE and E Matos. 1994. Strategies for prevention of occupational cancer in developing countries. In Occupational Cancer in Developing Countries, edited by NE Pearce, E Matos, H Vainio, P Boffetta, and M Kogevinas. Lyon: International Agency for Research on Cancer (IARC).

Pearce, NE, E Matos, M Koivusalo, and S Wing. 1994. Industrialization and health. In Occupational Cancer in Developing Countries, edited by NE Pearce, E Matos, H Vainio, P Boffetta, and M Kogevinas. Lyon: International  Agency  for  Research  on  Cancer (IARC).

Pisani, P and M Parkin. 1994. Burden of cancer in developing countries. In Occupational Cancer in Developing Countries, edited by NE Pearce, E Matos, H Vainio, P Boffetta, and M Kogevinas. Lyon: International Agency for Research on Cancer (IARC).

Pott, P. 1775. Chirugical Observations. London: Hawes, Clarke and Collins.

Siemiatycki, J. 1991. Risk Factors for Cancer in the Workplace. London: CRC Press.

Swerdlow, AJ. 1990. Effectiveness of primary prevention of occupational exposures on cancer risk. In Evaluating Effectiveness of Primary Prevention of Cancer, edited by M Hakama, V Veral, JW Cullen, and DM Parkin. IARC Scientific Publications, No. 103. Lyon: International Agency for Research on Cancer (IARC).

Vineis, P and L Simonato. 1991. Proportion of lung and bladder cancers in males resulting from occupation: A systematic approach. Arch Environ Health 46:6-15.

Waldron, HA. 1983. A brief history of scrotal cancer. Br J Ind Med 40:390-401.

World Health Organization (WHO). 1978. International Classification of Diseases. Geneva: WHO.

—. 1992. International Classification of Diseases and Related Health Problems. Geneva: WHO.

Wynder, EJ and GB Gori. 1977. Contribution of the environment to cancer incidence: An epidemiologic exercise. J Natl Cancer Inst 58:825-832.