2,971 publications from this institution
BACKGROUND AND AIM: Global warming is increasingly affecting human populations. Occupational heat stress occurs frequently, however little is known regarding potential long-term adverse health effects of chronic occupational heat exposure. In other recent work, we examined associations of lifetime occupational heat exposure and colorectal cancer in a large Spanish multi-case-control study (MCC-Spain). We observed no clear evidence for associations with ever occupational heat exposure overall, though there were some positive associations observed among women in the highest categories of lifetime cumulative exposure and duration. Here we extend work to examine potential associations with stomach cancer. METHOD: Data from a total of 459 incident stomach cancer cases and a common set of 3,440 matched controls recruited from 10 regions from 2008-2013 in MCC-Spain were examined. The Spanish job exposure matrix, MatEmEsp, was used to assign heat exposure estimates to participant lifetime occupational history. Three exposure indices were constructed: ever vs. never, duration (years), and cumulative exposure. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) adjusting for 5-year age group, sex, education, body mass index, cigarette smoking status, and family history of stomach cancer. RESULTS: Overall, 53.9% included cases and 37.7% of controls were ever occupationally exposed to heat. There was a positive association of ever occupational heat exposure and stomach cancer overall (odds ratio (OR) 1.45; 95% CI 1.10, 1.90). ORs were also elevated in the medium (OR 1.52; 95% CI 1.06, 2.17) and highest tertiles of lifetime cumulative exposure (OR 1.62; 95% CI 1.12, 2.34) (p trend 0.05), as well as of duration of exposure (ORs 1.88; 1.24, 2.86 and 1.41; 0.98, 2.03 respectively) (p trend = 0.02). CONCLUSIONS: Preliminary findings provide some evidence for a positive association of occupational heat exposure and stomach cancer risk in MCC-Spain; findings are being extended in a pooled analysis of data from three case-control studies.
It has long been suggested that a varied diet may protect against gastric cancer, in the absence, however, of definition and quantification of the issue. Thus, we considered the relationship between diet diversity (i.e., variety of food intake computed as the total number of foods consumed at least once per week) and the risk of gastric cancer using data of a case-control study conducted between 1985 and 1993 in northern Italy on 746 gastric-cancer cases below age 75 years and 2,053 controls admitted to hospital for acute, non-neoplastic, non-digestive-tract diseases. A significant inverse association was observed between various measures of food diversity and gastric cancer risk. Compared with subjects in the lowest quartile of total diversity, the multivariate odds ratios (ORs) were 0.9 for the second, 0.9 for the third and 0.7 for the highest quartiles. The inverse association was even stronger for vegetable (OR = 0.5 for the highest level) and fruit (OR = 0.6) diversity. Our findings were not explained by allowance for total calorie intake and total number of servings, besides education as an indicator of social class, and support, therefore, the concept that a more diversified and richer diet is a relevant underlying correlate of the decline in gastric cancer rates.
The issue of diet and breast and ovarian cancers has been considered in terms of foods and nutrients, but rarely in terms of dietary patterns. We examined the associations between dietary patterns and breast and ovarian cancers in 2 Italian multicentric case-control studies. Cases were 2,569 breast cancers and 1,031 ovarian cancers hospitalized in 4 Italian areas between 1991 and 1999. Controls were 3,413 women from the same hospital network. Dietary habits were investigated through a validated food-frequency questionnaire. Dietary patterns were identified on a selected set of nutrients through principal component factor analysis. Odds ratios (OR) and 95% confidence intervals (CI) for both cancers were estimated using unconditional multiple logistic regression models on quartiles of factor scores and continuous factor scores. We identified 4 major dietary patterns named Animal products, Vitamins and fiber, Unsaturated fats and Starch-rich. The animal products pattern and the unsaturated fats pattern were inversely associated with breast cancer (OR = 0.74, 95% CI: 0.61-0.91 and OR = 0.83, 95% CI: 0.68-1.00, respectively, for the highest consumption quartile), whereas the starch-rich pattern was directly associated with it (OR = 1.34, 95% CI: 1.10-1.65). The vitamins and fiber pattern was inversely associated with ovarian cancer (OR = 0.77, 95% CI: 0.61-0.98), whereas the starch-rich pattern was directly associated with it (OR = 1.85, 95% CI: 1.37-2.48). In conclusion, the starch-rich pattern is potentially an unfavorable indicator of risk for both breast and ovarian cancers, while the animal products and the vitamins and fiber patterns may be associated with a reduced risk of breast and ovarian cancers, respectively.
The importance of the major risk factors for endometrial cancer in women of different ages was evaluated with the use of data from a hospital-based case-control study conducted in Milan, Italy, on 283 women with endometrial cancer and 566 age-matched controls. Current weight was related strongly to the risk of endometrial cancer both in younger (premenopausal) and in older women (with risk estimates for the heaviest categories of 20.3 and 7.7, respectively), thus confirming that obesity is the major cause of endometrial cancer in Northern Italy. Endometrial cancer risk appeared to be approximately proportional to the second power of body mass index. Early menarche and nulliparity were associated with an increased risk of endometrial cancer in premenopausal women, the point estimate for nulliparity rising to 35.1 (with lower confidence limit of 10.2) after adjustment for marital status. However, no association with these factors was evident in postmenopausal women. Combination oral contraceptives were used by 2 cases and 19 controls only [relative risk (RR) = 0.2, with 95% confidence interval = 0.1-0.8]. The use of noncontraceptive estrogens was associated with an elevated risk, which was greater in perimenopausal women (RR = 5.1 for greater than 2 yr of use), and decreased progressively with increasing time after menopause. Late menopause was also related to endometrial cancer. However, the risk estimates for late menopause apparently were more elevated in older women (greater than or equal to 65 yr) than in perimenopausal women. Most of the risk factors identified (excluding late menopause) apparently act on one of the later stages of the process of carcinogenesis, because the excess risk drops after cessation of exposure.
Hysterectomy approximately halves the risk of ovarian cancer, possibly because of altered ovarian blood flow or the opportunity that hysterectomy provides for examining the ovaries.
The relationship between self-reported height and cancer risk was investigated in an integrated series of case-control studies including 273 cases of cancer of the oesophagus, 474 of the stomach, 558 of the colon, 352 of the rectum, 227 of the liver, 267 of the pancreas, 110 of the larynx, 2,388 of the breast, 545 of the cervix uteri, 563 of the endometrium, 688 of the ovary, 80 of the prostate, 263 of the bladder, 105 of the kidney, 43 Hodgkin's disease, 152 non-Hodgkin's lymphomas, 109 multiple myelomas, and a total of 5,574 controls admitted to hospital for acute, non-neoplastic conditions. No significant positive trend in risk was observed for any of the cancer sites considered, and some suggestion of elevated risks for the upper quintile of height was observed only for prostate (relative risk, RR = 1.4), kidney (RR = 2.7) and colon (RR = 1.2) in males (but not in females). For breast cancer, all the RRs for subsequent quintiles of height were close to unity. Four neoplasms showed significant inverse trends with height: oesophagus (RR = 0.7 for highest vs. lowest quintile), cervix (RR = 0.4), endometrium (RR = 0.7) and ovary (RR = 0.6). For oesophagus and cervix the trends could be explained, at least in part, in terms of social class correlates (multivariate RR 0.8 and 0.5, respectively), while for endometrium they could possibly be related to an inverse correlation between height and body mass (multivariate RR 0.9). Thus, our study did not support the hypothesis that nutrition in childhood and adolescence (which in this population is a determinant of adult height) is directly related to the subsequent risk of cancer at several major cancer sites. A number of inverse associations emerged, which may be either spurious and incidental, or suggest that poorer nutrition early in life may be an unfavourable indicator of the subsequent risk of selected neoplasms.
Colorectal cancer is the leading cancer in non-smokers in Western countries, and over the last decades its trends have been generally more favourable for women than for men. Possible explanations of the sex differentials in colorectal cancer relate to different exposure to exogenous hormones and to other risk factors including diet, physical activity and alcohol drinking. The objective of this investigation was to systematically analyse the trends in colorectal cancer mortality sex ratios in major European countries over the last four decades. Trends in death certification rates from colorectal cancer over the period 1955-1996 were analysed for 20 European countries (excluding the former Soviet Union and a few of the smaller countries). In all countries, the mortality sex ratios (M/F) were around or slightly above unity in the 1950s, and systematically increased to approach 1.5 in the 1990s. The extent of the rises varied across countries, ranging between + 0.8% in Germany, + 9.7% in Sweden, and + 12.1% in Denmark (the lowest increases) to + 65.3% in Spain, + 56.2% in Portugal, and + 50.4% in Hungary (the highest ones). Mortality sex ratios in Europe show more favourable trends for females, which may be attributable, in part, to the introduction of exogenous hormones in the late 1950s and 1960s, and, in part, to differential sex exposure to major environmental risk factors.
