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The extent to which the associations between psychosocial factors and coronary heart disease (CHD) are causal has seldom been the subject of systematic enquiry. We are updating our previous systematic review up to 2001. The objective of this study is to assess the relative strength of the epidemiological evidence for causal links between psychosocial factors and CHD incidence among healthy populations, and prognosis among CHD patients. Our methods were to systematically review prospective cohort studies identified through the Science Citation index, which met pre-specified quality criteria. We found that the proportion of etiologic studies reporting a strong or moderate association was: 6/18 for Type A behavior and hostility, 15/22 for depression, 4/8 for anxiety, 10/13 for psychosocial work characteristics and 6/9 for social support. For prognostic studies the proportions were: 2/15 for type A behavior and hostility, 18/34 for depression, 8/18 for anxiety, 2/4 for psychosocial work characteristics and 14/21 for social support. Positive studies were more likely to be cited by other papers than negative studies. We concluded that, based on prospective epidemiological data, there was evidence for an association between depression, social support and psychosocial work characteristics and CHD aetiology and prognosis. Evidence for an effect of anxiety or type A behavior was less consistent. Methods to address bias in the reporting of psychosocial data are required.

During a 4‐year period from January 1995 to December 1998, blood samples and questionnaire data were obtained from 333 incident cases of hepatocellular carcinoma (HCC), as well as from 360 controls who were hospitalized for eye, ear, nose, throat or orthopedic conditions in Athens, Greece. Coded sera were tested for hepatitis B surface antigen (HBsAg) and antibodies to hepatitis C virus (anti‐HCV) by third‐generation enzyme immunoassays, and information on smoking habits and beverage consumption was obtained. We found a significant dose‐response, positive association between smoking and HCC risk [≥ 2 packs per day, odds ratio (OR)=2.5].This association was stronger in individuals without chronic infection with either HBV or HCV (≥ 2 packs per day, OR=2.8). Consumption of alcoholic beverages above a threshold of 40 glasses per week increased the risk of HCC (OR=1.9). We also found evidence of a strong, statistically significant and apparently super‐multiplicative effect of heavy smoking and heavy drinking in the development of HCC (OR for both exposures=9.6). This interaction was particularly evident among individuals without either HBsAg or anti‐HCV (OR for both exposures=10.9). Coffee intake was not positively associated with HCC risk, but the reverse could not be excluded for the subgroup of chronically infected individuals. In conclusion, tobacco smoking and heavy alcohol consumption are associated with increased risk of HCC, especially when these 2 exposures occur together. Int. J. Cancer 85:498–502, 2000. © 2000 Wiley‐Liss, Inc.

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In the second part of our review we describe the association between tobacco use and risk of specific cancer types. There is evidence for an established association of tobacco use with cancer of the lung and larynx, head and neck, bladder, oesophagus, pancreas, stomach and kidney. In contrast, endometrial cancer is less common in women who smoke cigarettes. There are some data suggesting that tobacco use increases the risk for myeloid leukaemia, squamous cell sinonasal cancer, liver cancer, cervical cancer, colorectal cancer after an extended latency, childhood cancers and cancer of the gall bladder, adrenal gland and small intestine. Other forms of cancer, including breast, ovarian and prostate cancer, are unlikely to be linked to tobacco use.