Search

Our aim was to review the epidemiological literature on possible cancer-preventive effects of the consumption of fruits and vegetables in humans, to quantify the effect of high versus low consumption of fruits and vegetables, and to give an overall assessment of the existing evidence. We based our work on an expert meeting conducted by the International Agency for Research on Cancer in 2003. A qualitative reading and evaluation of relevant articles on the cancer-preventive effect of the consumption of fruits and vegetables was made followed by the calculation of the mean relative risk and range for cohort and case-control studies separately. The possible population-preventable fraction for modifying diet in relation to fruit and vegetable consumption was calculated as well as an overall statement about the degree of evidence for the cancer-preventive effect of fruit and vegetable consumption for each cancer site. There is limited evidence for a cancer-preventive effect of the consumption of fruits and vegetables for cancer of the mouth and pharynx, esophagus, stomach, colon-rectum, larynx, lung, ovary (vegetables only), bladder (fruit only), and kidney. There is inadequate evidence for a cancer-preventive effect of the consumption of fruits and vegetables for all other sites. Applying this range of risk difference to the range of prevalence of low intake, the preventable fraction for low fruit and vegetable intake would fall into the range of 5-12%. It is important to recognize that this is only a crude range of estimates and that the proportion of cancers that might be preventable by increasing fruit and vegetable intake may vary beyond this range for specific cancer sites and across different regions of the world. [ABSTRACT FROM AUTHOR]

A cohort including all female workers born 1906 through 1945 (n = 413,877) in Finland was identified through the Population Census of Finland of 1970. Incident cases of cancers of the gastrointestinal tract were explored during 1971 to 1995. Job titles in census records were converted to exposures of 31 occupational agents through a job-exposure matrix. For each agent, the product of level and probability of exposures was calculated and subdivided in three categories: zero, low and medium/high. Poisson regression models estimated relative risks (RR) for each agent, standardized for birth cohort, follow-up period, and socioeconomic status. Adjustment at job title level was done for alcohol use for cancers of the esophagus and liver and smoking for pancreatic cancer. The results showing either statistically significant RR at the medium/high level of exposure (RRH) or statistically significant trend (P < 0.05) over the exposure categories were considered as positive findings. Colon cancer risk (2009 cases) was positively associated with sedentary work (RRH 1.3, 95% CI = 1.1-1.6; P trend 0.001) and negatively associated with perceived workload (P trend = 0.007). For stomach cancer (1881 cases), we observed an association with exposure to electromagnetic fields (RRH 1.44, 95% CI = 1.01-2.05) and man-made vitreous fibers (MMVF) (p trend 0.03). Rectal cancer (1323 cases) showed an association with chromium (RRH 1.9, 95% CI = 1.2-3.1) and oil mist (RR 2.0; 95% CI = 1.0-3.9). For pancreas cancer (1302 cases) we found associations with exposure to chromium (RRH 1.8; 95% CI = 1.0-3.1; P trend 0.01), electromagnetic fields (RRH 1.8; 95% CI = 1.2-2.8; P trend 0.02), and sedentary work (RRH 1.3; 95% CI = 1.0-1.7; P trend 0.05). We found no significant associations between any FINJEM agents and cancers of the esophagus (389 cases), liver (389 cases), and gallbladder (651 cases). Having examined the associations between seven cancer sites and over 30 exposures there exists the real possibility that some of the associations detected are chance findings. Therefore, the associations observed should need to be confirmed in other studies. [ABSTRACT FROM AUTHOR]

The incidence of endometrial cancer varies up to 10-fold between high- and low-incidence regions, suggesting the importance of environmental factors, including diet, in the etiology of this disease. However, few studies have examined the role of diet in the etiology of endometrial cancer. Using unconditional logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI), we analyzed data from a large, case-control study of Swedish-born postmenopausal women aged 50-74 yr (709 cases and 2,887 controls) residing in Sweden between 1994 and 1995. We found no clear association between foods or food groups and endometrial cancer risk, although high consumption of certain foods, such as Brassica vegetables, coffee, and legumes, might be associated with small-to-moderate reduced risks of endometrial cancer, while red meat consumption might be associated with a small-to-moderate increased risk. Daily use of calcium supplements appeared to lower endometrial cancer risk (OR = 0.5, 95% CI = 0.3-0.9, P for trend = 0.04), especially among women with low calcium intake from dairy products. On the other hand, the use of iron supplements appeared to increase the risk (OR = 1.7, 95% CI = 0.9-3.3, P for trend = 0.03). The findings are discussed with respect to previous studies and the possible underlying mechanisms. [ABSTRACT FROM AUTHOR]

Objective: To investigate the association between alcoholism and risk of male breast cancer.Methods: We conducted a retrospective population-based cohort study in Sweden of men diagnosed with alcoholism between 1965 and 1995. The cohort was followed up through interlinkages with nationwide registries (the national cancer registry, immigration registry, causes of death registry, and population registry), using the national registration numbers. Standardized incidence ratios (SIRs), calculated using the Swedish national cancer incidence rate as reference, were used as estimates of relative risks.Results: A total of 145,811 men were enrolled into the cohort, contributing 1,499,504 person-years of follow-up. Sixteen incident breast cancer cases were identified, and the mean age at diagnosis was 68 years. We excluded the first year of follow-up (cases and person-years) from the analysis to avoid detection bias. The overall SIR (excluding the first year of follow-up) was 1.1 (95% CI 0.6-2.0). Although based on small numbers we found no indication of a differential SIR according to duration of follow-up, age at cohort enrolment, or age at follow-up (attained age or age at cancer diagnosis).Conclusion: The observed associations are not compatible with an increase in breast cancer risk among male alcoholics. [ABSTRACT FROM AUTHOR]

The objective of the present work is to critically summarize published studies and reassess the state of knowledge on a highly controversial topic: the potential association between prenatal exposure to passive smoking as well as maternal active smoking and postnatal exposure to environmental tobacco smoke (ETS) and enhanced incidence of childhood cancer. Elements to be considered include the substantial proportion of pregnant women who remain smokers, the widespread nature of exposure to ETS during pregnancy as well as during childhood, the known toxicology of tobacco smoke, and in particular sidestream smoke, characterized by a rich carcinogen content, the specific metabolism of foetuses and new-borns and finally the amount of epidemiologic data already available. We conducted a thorough review of the literature to identify studies either exclusively dealing with the effects of passive smoking on the occurrence of childhood cancers or more generally etiologic studies of cancer, be it overall or site-specific. We identified close to 50 publications presenting pertinent results from epidemiological investigations and about 50 more on mechanisms and metabolism, smoking in pregnancy and exposure to ETS as well as selected reviews and commentaries. Collaborative epidemiological studies were conducted in the United Kingdom (UK), USA, Sweden, Netherlands and internationally (France, Italy). In addition, other studies were also available from the USA, UK, Canada, Australia, Sweden, Italy, Denmark and People's Republic of China. The vast majority were case-control studies dealing with all cancers, leukaemia and lymphomas, central nervous system (CNS) tumours, Wilms' tumour, retinoblastoma, neuroblastoma, hepatoblastoma, rhabdomyosarcoma, bone and soft tissues tumours, germ cell tumours, as well as specific histological types of leukaemias, lymphomas or CNS tumours. No strong association between maternal smoking in pregnancy and/or exposure to ETS and childhood cancer is found. Yet, several studies found slightly increased relative risks, generally smaller than 1.5, i.e. the order of magnitude associated with some recognized hazards of exposure to ETS (1.2 to 1.3 for adult lung cancer and cardiovascular diseases). Tumours most often found associated with maternal smoking in pregnancy or ETS exposure are childhood brain tumours and leukaemia-lymphoma, with risks up to two or greater in selected studies. In a few studies, risks associated with paternal smoking are higher than the maternal ones. This evidence from human studies coupled with demonstration of genotoxic effects on the foetus of exposure to metabolites of tobacco smoke, and demonstrable presence of adducts should lead to strong recommendations aiming at fully protecting foetuses, new-borns and infants from tobacco smoke. [ABSTRACT FROM AUTHOR]

The mineral fibres in the lung tissue samples of 54 Finnish lung cancer patients were analysed using both scanning (SEM) and transmission (TEM) electron microscopy. The fibre concentrations ranged from < 0.1 to about 60 million fibres per g dry tissue with both methods. In general, the results obtained with TEM were higher than the ones with SEM. When the limits of 1 million fibres per g with SEM and 3 million fibres per g with TEM were considered to indicate occupational exposure to asbestos, consistent results were achieved in 93% of the patients. Anthophyllite was the predominant fibre type detected, followed by amosite–crocidolite and chrysotile. Anthophyllite fibres were on average longer and thicker than amosite–crocidolite and chrysotile fibres. [ABSTRACT FROM PUBLISHER]

Hemminki K [Institute of Occupational Health, Haartmaninkatu 1, 00290 Helsinki 29, Finland] Niemi M-L, Saloniemi I, Vainio Hand Hemminki E. Spontaneous abortions by occupation and social class in Finland. 1980, 9: 149–153. A hospital discharge registry covering all general hospitals in Finland was used in the study of spontaneous abortions. Spontaneous abortions were analysed by the women's occupation and socio-economic class for 1973–75 inclusive. The risk of spontaneous abortion increased from social class 1 to 4 by about 50%. The occupational groups with an increased frequency of spontaneous abortions included industrial and construction work, agriculture, forestry and fishing, sales, transport and communication, services, and students and trainees. Decreased frequency of spontaneous abortions was noted among housewives, and in managerial and clerical occupations. The results suggest that socio-economic factors contribute to the rate of spontaneous abortions analogous to their known adverse effects on pre-term birth, birth weight and perinatal mortality. [ABSTRACT FROM PUBLISHER]

Only the results of epidemiological studies can be used to establish a causal relationship between an exposure to an agent and human cancer; however, such studies often cannot be carried out due to limitations of population or latent period or to the presence of mixed exposures. It is essential, therefore, that the validity be established of extrapolating to humans the results obtained from long-term carcinogenicity tests in animals. The responses of experimental animals to known and suspected human carcinogens, as evaluated in the series, were analysed as an indication of the sensitivity of animal tests for predicting human carcinogens. Although the response was high - 84% - it would have been even higher had all the compounds been adequately tested experimentally. An additional finding was that for many exposures causally related to human cancer, there is a target organ in common between humans and at least one animal species, despite many inherent physiological differences. These findings show clearly the importance of experimental carcinogenicity studies in the primary prevention of cancer. [ABSTRACT FROM PUBLISHER]

Data were extracted from volumes 1–38 on chemicals and exposures for which some data on carcinogenicity in humans, or sufficient evidence of carcinogenicity in experimental animals existed. In all, 288 chemicals, industrial processes and complex mixtures fulfilled these criteria. For 30 chemicals or mixtures of chemicals, and nine industrial processes, there was sufficient evidence of carcinogenicity in humans; and for 63 chemicals and mixtures of chemicals and for five industrial processes, there was evidence that these exposures were probably carcinogenic to humans. For 61 chemicals or groups of chemicals and six industrial processes or occupations, no evaluation of carcinogenicity to humans could be made. For 115 chemicals there is sufficient evidence of carcinogenicity to experimental animals, but no epidemiological data are available. Publications not earlier referred to on the carcinogenicity of these chemicals and exposures were found for ∼70. A call is made for further information on these exposures with a view to updating the . [ABSTRACT FROM PUBLISHER]

Both styrene and its presumed active metabolite styrene oxide show dose response as potent inducers of sister chromatid exchanges (SCEs) in human lymphocyte cultures. The SCE inducing and clastogenic capacity of styrene in lymphocytes can be explained by gas chromatographically measurable increase of styrene oxide in styrene treated cultures. [ABSTRACT FROM PUBLISHER]