Various misconceptions about the relationship between environmental pollution and human disease, particularly cancer, drive regulatory policy. In this paper, we highlight 10 such misconceptions and briefly present the scientific evidence that undermines each.

Cancer death rates overall in the U.S. (excluding lung cancer due to smoking) have declined 16 percent since 1950. 1 If lung cancer is included, mortality rates have increased over time, but recently have declined in men due to decreased smoking.

• The types of cancer deaths that have decreased are primarily stomach, cervical, uterine and colorectal.

• The types that have increased are primarily lung cancer (90 percent is due to smoking, as are 35 percent of all cancer deaths in the U.S.), melanoma (probably due to sunburns) and non-Hodgkin's lymphoma.

The rise in incidence rates in older age groups for some cancers, e.g., prostate, can be explained by known factors such as improved screening. 2 As one study noted, "The reason for not focusing on the reported incidence of cancer is that the scope and precision of diagnostic information, practices in screening and early detection, and criteria for reporting cancer have changed so much over time that trends in incidence are not reliable." 3 Life expectancy has continued to rise since 1950.

Neither the study of patterns of disease in humans (epidemiology) nor experimental studies on laboratory animals (toxicology) support this idea. 4 Epidemiological studies have identified the factors that are likely to have a major effect on lowering rates of cancer: reduction of smoking, improving diet (e.g., increased consumption of fruits and vegetables), hormonal factors and control of infections. Although some epidemiologic studies find an association between cancer and low levels of industrial pollutants, the associations are usually weak, the results are usually conflicting and the studies do not correct for potentially large confounding factors like diet. Moreover, exposures to synthetic pollutants are tiny and rarely seem toxicologically plausible as a causal factor, particularly when compared to the background of natural chemicals that are rodent carcinogens. 5

Even assuming that worst-case risk estimates for synthetic pollutants are true risks, the proportion of cancer that the Environmental Protection Agency (EPA) could prevent by regulation would be tiny. 6 Occupational exposures to some carcinogens cause cancer, though how much has been a controversial issue: a few percent seems a reasonable estimate, 7 much of this from asbestos in smokers. Exposures to substances in the workplace can be high in comparison with other chemical exposures in food, air or water. Past occupational exposures have sometimes been high and therefore comparatively little quantitative extrapolation may be required for risk assessment from high-dose rodent tests to high-dose occupational exposures. Since occupational cancer is concentrated among small groups exposed at high levels, there is an opportunity to control or eliminate risks once they are identified; however, current permitted workplace exposures are sometimes close to the carcinogenic dose in rodents. 8

Cancer is due in part to normal aging and increases exponentially with age in both rodents and humans. 9 To the extent that the major external risk factors for cancer are diminished, cancer will occur at a later age, and the proportion of cancer caused by normal metabolic processes will increase. Aging and its degenerative diseases appear to be due in good part to oxidative damage to DNA and other macromolecules. 10 Oxidant by-products of normal metabolism - superoxide, hydrogen peroxide and hydroxyl radical - are the same mutagens (agents that alter DNA) produced by radiation. Mitochondria from old animals leak oxidants; 11 old rats have about 66,000 oxidative DNA lesions per cell. 12 DNA is oxidized in normal metabolism because antioxidant defenses, though numerous, are not perfect. Antioxidant defenses against oxidative damage include Vitamins C and E and perhaps carotenoids, 13 most of which come from dietary fruits and vegetables.

Smoking contributes to about 35 percent of U.S. cancer, about one-quarter of heart disease and about 400,000 premature deaths per year in the United States. 14 Tobacco is a known cause of cancer of the lung, bladder, mouth, pharynx, pancreas, stomach, larynx, esophagus and possibly colon. Tobacco causes even more deaths by diseases other than cancer. Smoke contains a wide variety of mutagens and rodent carcinogens. Smoking is also a severe oxidative stress and causes inflammation in the lung. The oxidants in cigarette smoke - mainly nitrogen oxides - deplete the body's antioxidants. Thus, smokers must ingest two to three times more Vitamin C than non-smokers to achieve the same level in blood, but they rarely do. Inadequate concentration of Vitamin C in plasma is more common among the poor and smokers.

Men with inadequate diets or who smoke may damage the DNA of their sperm as well as the DNA in the rest of their cells. When the level of dietary Vitamin C is insufficient to keep seminal fluid Vitamin C at an adequate level, the oxidative lesions in sperm DNA are increased 250 percent. 15 Male smokers, compared to non-smokers, have more oxidative lesions in sperm DNA16 and more chromosomal abnormalities in sperm. 17 Smoking by fathers, therefore, may plausibly increase the risk of birth defects and childhood cancer in offspring. 18 A new epidemiological study suggests that the rate of childhood cancers is increased in offspring of male smokers, e.g., acute lymphocytic leukemia, lymphoma, and brain tumors are increased three to four times. 19

The authors estimate that unbalanced diets (e.g., low intake of fruits and vegetables) account for about one-third of cancer risk, in agreement with the earlier estimate of researchers R. Doll and R. Peto. 20 [See Misconception #3.] There has been considerable interest in calories (and dietary fat) as a risk factor for cancer, in part because caloric restriction markedly lowers the cancer rate and increases life span in rodents. 21

Chronic inflammation from chronic infection, a major contributor to cancer, 22 results in release from white cells of oxidants that are mutagens. White cells and other phagocytic cells of the immune system combat bacteria, parasites and virus-infected cells by destroying them with potent, mutagenic oxidizing agents. The oxidants protect humans from immediate death from infection, but they also cause oxidative damage to DNA, chronic cell killing with compensatory cell division, and mutation23 and thus contribute to the carcinogenic process. Antioxidants appear to inhibit some of the pathology of chronic inflammation. Chronic infections cause about 21 percent of new cancer cases in developing countries and 9 percent in developed countries. 24

Reproductive hormones play a large role in cancer, including breast, prostate, ovary and endometrium (the inner lining of the uterus), 25 contributing to as much as 20 percent of all cancer. Many lifestyle factors such as reproductive history, lack of exercise, obesity and alcohol intake influence hormone levels and therefore increase risk. 26

Other causal factors in human cancer are excessive alcohol consumption, excessive sun exposure, and viruses. Genetic factors also play a significant role and interact with lifestyle and other risk factors. Biomedical research is uncovering important genetic variation in humans.