Cancer Risk Factors

Epidemiology shows that, because different world populations show different types of levels of disease, much human cancer may be avoidable. For example, immigrants take on the cancer pattern of their new home, as immigrants to Australia have within decades, or Japanese immigrants experience higher breast cancer rates after a few decades in the United States than in comparative populations in Japan. Further, groups with unique and differentiating cultural or lifestyle characteristics such as Seventh Day Adventists, Mormons, or African-Americans in parts of the United States have cancer patterns distinct from those of the general community. Comparisons support the generally agreed-upon estimate that upward of 80% to 90% of cancer may be attributable to environmental factors such as dietary, social, and cultural practices.19

However, such factors have not been clearly delineated, nor has it been made clear how individuals are affected by combination or accretion of factors. Cancer prevention efforts have focused on efforts to reduce exposures or behaviors suspect in incidence, such as smoking, and to promote those with protective effects, such as physical exercise, and, as well, to reduce concerns over exposures or acts that may have trivial or no impact on cancer, such as cell phone use. Cancer control studies thus embrace a variety of elements and approaches and aim to reduce the incidence of cancer, and failing which, to reduce mortality, either by finding disease at an early and curable stage or by improving survival rates stage-for-stage by therapeutic improvements. Cancer prevention, control, and education programs bring epidemiologists into contact and cooperation with several other disciplines including clinical science, behavioral science, and health education and communication.


Tobacco smoking, the single most lethal human carcinogen, remains the largest single avoidable cause of premature death worldwide.20 Estimates connect at least 16% of all cancers in developed countries to tobacco use, with a higher proportion of tobacco-related cancers among men (25%) than women (4%). Tobacco-related cancers include those of the oral cavity, pharynx, larynx, lung, bladder, pancreas, kidney, renal pelvis, and endometrium. However, in the last case, reduced rather than increased risk is thought to result from antiestrogenic effects of tobacco use rather than exposure to the more than 55 carcinogenic compounds identified by the International Agency for Research on Cancer.21 For more than 40 years, it has been clear that prevention of smoking would lead to substantial reductions in death associated with lung and other cancers and heart disease, bronchitis, emphysema, and other conditions. Nonetheless, tobacco-related disease has increased in many parts of the world, especially in developing countries where tobacco use has started within the past 30 years and involves 80% of the world's daily smokers, now estimated at 1.1 billion.

Tobacco addiction mechanisms are complex. As suggested by reports of associations between smoking quit-rates and specific polymorphisms in the dopamine receptor gene (DRD2),22 a key receptor in the mesolimbic dopaminergic reward system, the genetic susceptibility of individuals to tobacco addiction varies considerably. Just as multiple factors affect behavior, multiple factors likely influence susceptibility to tobacco-related cancers, which helps explain why not all tobacco users get cancer.

Important smoking outcomes appear to be related to gender, ethnicity, and life experiences. Women, relative to men, and African-Americans, compared to white Americans, appear to have higher risk of bladder cancer associated with tobacco use. Age is also an important factor because smokers usually begin during their teens or early adult years. Early-start smokers persist and smoke higher amounts than late starters, increasing their risks over time. Synergistic effects with tobacco use have been observed with asbestos and crystalline silica in occupational settings, and with alcohol acting as a solvent, probably facilitating absorption of smoking byproducts, whereas a diet high in intake of fruits and vegetables may impede the formation of smoking-related DNA adducts, reduce the DNA damage from tobacco carcinogens, and promote other mechanisms that prevent cellular damage and reduce risk.

Recent tobacco research includes the evaluation of exposure to environmental tobacco smoke and outcomes of exposure-related adverse health events, including lung cancer. Based on 30 epidemiologic studies, the United States Environmental Protection Agency (EPA) concluded that environmental tobacco smoke was a human lung carcinogen and that nonsmokers who are exposed to environmental tobacco smoke faced increased risk of lung cancer.23 Although diluted with ambient air, environmental tobacco smoke tends to have more carcinogens than smoke inhaled through filters. However, the current emphasis of research and health policy in Western countries on passive smoke inhalation should not divert attention from the major public health issue of active cigarette smoking: smokers are at much higher risk of cancer than others involuntarily inhaling cigarette smoke. Therefore, any program of cancer control should put control of smoking first; such control is likely to have greater impact on reducing cancer incidence and cancer mortality than any other current strategy.

Viruses and Infection

The contribution of viruses to the public health burden of cancer incidence is greatest in young to middle-aged individuals, the age-incidence curve peaking before middle age.24 The estimated attributable risk associated with viruses and cancer is about 15% worldwide.25 However, to date, only five viruses have been firmly established associated with increased cancer risk: human papilloma virus (HPV), with an increased risk of cervix cancer in women; Epstein-Barr virus (EBV) with an increased risk of nasopharyngeal cancer and Burkitt's and Hodgkin's lymphoma; human T-lymphotropic virus type 1 (HTLV-1), with adult T-cell leukemia and some types of non-Hodgkin's lymphoma; hepatitis B and C with an increased risk of primary liver cancer; and human herpesvirus 8 (HHV-8) infection with Kaposi's sarcoma and some forms of non-Hodgkin's lymphoma (Table 22.1).24 Advances in technology and laboratory techniques, such as polymerase chain reaction (PCR) have facilitated research, but because the mechanisms by which viruses cause cancer may leave little evidence of infection and because some viruses can remain latent for many years, definitive implication of specific viruses in carcinogenesis has been difficult.

Long latency periods between infection and cancer diagnosis, and the fact that only a portion of people who are infected develop cancer, suggest that although viral agents may increase the risk of individuals for developing cancer they are not the sole determinant for developing the disease.

TABLE 22.1. Known viral risk factors for selected human cancers.

Viral risk factor

Cancer type

Other factors that influence risk

Epstein-Barr virus (EBV)

Burkitt's lymphoma Nasopharyngeal carcinoma B-cell lymphoma Hodgkin's disease Breast cancera

Malaria Nitrosamines

Immunodeficiency, human immunodeficiency virus (HIV)-1

Hepatitis B virus (HBV)

Liver cancer

Aflatoxin, alcohol

Hepatitis C virus (HCV)

Liver cancer Splenic lymphoma

Aflatoxin, alcohol

Human herpesvirus-8 (HHV-8)

Kaposi's sarcoma

Primary effusion lymphoma

Multicentric Castleman disease


Human papillomavirus (HPV)

Cancer of the cervix, vulva, vagina, penis, anus, skin, and oropharyngeal region

Smoking, oral contraceptive use, multiparity, other sexually transmitted diseases

Human T-cell lymphotrophic virus type 1 (HTLV-1)

Adult T-cell leukemia/lymphoma (ATL)

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