Search

We assessed the association of processed meat intake with the risk of renal cell carcinoma (RCC) and bladder cancer. We used data from two Italian hospital-based case-control studies, including 1,115 RCC cases and 2,582 controls, and 1,417 bladder cancer cases and 1,732 controls. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) with unconditional logistic regression models, adjusted for major confounders. The median consumption of processed meat in cases and controls was around 2 portions/week (50 g/portion). The ORs for a daily 10 g increment of processed meat was 0.89 (95% CI 0.84-0.94) for RCC and 1.00 (95% CI 0.94-1.06) for bladder cancer. The OR for the highest vs. the lowest consumption was 0.80 (95% CI 0.66-0.96) for RCC and 0.98 (95% CI 0.80-1.21) for bladder cancer. The ORs were consistent in strata of various covariates. For bladder cancer, however, a significant 23% excess risk was found in women (95% CI 1.03-1.47) for a daily increase of 10 g, significantly heterogeneous from the risk recorded in men (OR 0.96, 95% CI 0.90-1.02). The inconsistent results between men and women and the absence of association in both sexes combined indicate that the apparent association between processed meat and bladder cancer in women is unlikely to be causal.

Introduction: Recent findings reported an inverse relationship between solar ultraviolet-B (UV-B) exposure and mortality from various types of cancers, including renal cancer., Methods: We reviewed the literature concerning the relationship between sun exposure and incidence of kidney cancer. We performed a case-control study, evaluating recreational sun exposure in 50 kidney cancer patients and 50 controls.A questionnaire concerning sun exposure habits during childhood, adult life and in the previous 2 years was filled in by every patient. The questionnaire focused on: hours/day spent in the sun during summer; hours/day spent sunbathing (considering as well which kind of UV protection was used); sunburns; holidays in tropical countries., Results: We found and analyzed few articles concerning the relationship between kidney cancer and sunlight exposure. The two cohorts of patients we evaluated were homogeneous for age, phototype, origin and living area.We found no statistically significant differences between sun exposure in patients affected by kidney cancer and controls, both during childhood and adult life; no differences were found in the use of sunscreens either., Conclusions: Recreational sunlight exposure does not differ in our cohorts of patients and controls; studies on greater cohorts are needed to evaluate the effect of recreational sun exposure in the development of kidney cancer.

Aspirin and nonsteroidal anti-inflammatory drugs have been related to decreased risk of several cancers, but studies on the relation with the risk of renal cell cancer (RCC) are inconsistent. A case-control study of RCC was conducted in Italy between 1992 and 2004. Cases were 755 patients with incident, histologically confirmed RCC, and controls were 1297 patients in hospital for acute non-neoplastic conditions. Odds ratios (OR) and 95% confidence intervals (CI) for RCC were conditioned on center, sex, age, and year of interview, and adjusted for education, smoking, alcohol consumption, diabetes, and hypertension. Regular use of aspirin for at least 6 months was reported by 67 cases and 99 controls, corresponding to an OR of 0.98 (95% CI 0.69-1.38). The ORs were 0.91 (95% CI 0.55-1.50) in regular users for less than 3 years, and 1.04 (95% CI 0.67-1.63) in users for 3 years or longer; 0.47 (95% CI 0.20-1.12) when aspirin was used as analgesic and 1.10 (95% CI 0.75-1.62) when it was used for cardiovascular disease prevention. No significant heterogeneity was found for regular use of aspirin across strata of age and sex. This study, based on a large dataset, suggests that regular use of aspirin did not increase RCC risk.

The relation between coffee, decaffeinated coffee, and tea intake and renal cell carcinoma (RCC) risk was analyzed in a case-control study conducted in Italy between 1992 and 2004. Cases were 767 subjects with incident histologically confirmed RCC and controls were 1,534 patients in hospital for acute non neoplastic conditions. Odds ratios (OR) and 95% confidence intervals (CI) for RCC were computed by multiple logistic regression models, conditioned on study center, sex, and age. Coffee intake (mostly espresso and mocha) was not associated with RCC risk, with an OR of 1.02 (95% CI 0.73-1.43) in drinkers of > or = 4 cups/day compared with drinkers of < 1 cup/day. The corresponding ORs were 1.34 (95% CI 0.87-2.07) in men and 0.67 (95% CI 0.38-1.18) in women, 1.91 (95% CI 0.85-4.31) in current smokers and 0.74 (95% CI 0.41-1.31) in never smokers, with no trend in risk with dose. No relation was observed with decaffeinated coffee (OR = 1.38, 95% CI 0.94-2.03 for drinkers compared with nondrinkers) and tea intake (OR = 0.78, 95% CI 0.59-1.05 for drinkers of > or = 1 cup/day compared with nondrinkers). No significant heterogeneity was found for coffee intake across strata of age, education, body mass index, and consumption of sugar. This study, based on a large dataset, provides further evidence that coffee, decaffeinated coffee, and tea consumption are not related to RCC risk.

Background: An increased risk of renal cell cancer (RCC) has been reported in subjects with hypertension. Whether this association may vary according to sex, smoking, obesity, or RCC clinical presentation is unclear. Results on the link between diabetes mellitus and RCC are inconclusive., Patients and Methods: We conducted an Italian multicenter case-control study, including 767 (494 men, 273 women) incident cases of RCC, under 80 years of age, and 1534 hospital controls, frequency-matched to cases. Multiple logistic regression models, conditioned to center, sex, and age, and adjusted for period of interview, education, smoking, and body mass were used to estimate odds ratios (OR)., Results: Compared with subjects never treated, patients with a history of treated hypertension [OR = 1.7, 95% confidence interval (CI) 1.4-2.1] reported an excess risk of RCC. This pattern was confirmed in different strata of sex, education, smoking habits, body mass, tumor histological type, stage, or grade. The attributable risk of RCC for treated hypertension in this population was 16%. A slight, nonsignificant increased risk was found for history of diabetes mellitus (OR = 1.3, 95% CI 0.9-1.7)., Conclusion: A possible causal role of hypertension in renal cell carcinogenesis is supported by the consistency of the direct association.

The percent population attributable risk (AR) for kidney cancer was estimated in relation to smoking habits, beta-carotene intake, history of cystitis and family history of kidney cancer, using data from a case-control study conducted between 1985 and 1989 in Milan, northern Italy. The data comprised 133 histologically confirmed cases of incident kidney cancer and 392 controls, admitted to hospital for a wide range of acute, non-neoplastic, non-smoking-related diseases. On the basis of multivariate odds ratios (ORs), smoking habits accounted for about 26% of cases, a low beta-carotene intake for 18%, a history of cystitis for 7%, and a family history of kidney cancer in first-degree relatives for 3% of cases. Ever smoking and low beta-carotene intake combined explained 38% of all kidney cancers, and the combination of these two factors plus a history of cystitis and a family history of kidney cancer explained 45% of the incidence of the disease. Thus, even if available, dietary information was limited and the AR estimates were based on somewhat arbitrary assumptions. A considerable proportion of kidney cancers could be avoided simply by eliminating smoking and increasing consumption of fruit and vegetables in this Italian population. This would mean that about 1,500 kidney cancer deaths every year in the whole of Italy could be avoided.

A hospital-based case-control study of renal cell cancer was conducted in northern Italy between 1986 and 1989, with 240 cases of renal cell cancer (150 males and 90 females), and 665 controls (445 males and 220 females) chosen on the basis of age, sex, and area of residence. No associations were found between renal cell cancer and: body mass index (BMI); number of cigarettes smoked; age at starting to smoke; years of smoking; consumption of wine, beer, spirits, coffee, decaffeinated coffee; tea; intake of animal protein, fruits, and vegetables; various reproductive factors; hormonal use; sexual habits; sexually transmitted diseases; or selected occupational exposures. The odds ratio (OR) was above unity in smokers (OR = 1.34 for greater than or equal to 15 cigarettes/day), but the trends in risk with dose or duration were not statistically significant. Significant positive associations were found between renal cell cancer and sources of fat intake, especially margarine (OR for highest vs lowest intake = 1.71), and oils (OR = 1.89) whereas carrot intake showed a negative association (OR = 0.62). Also, a history of nephrolithiasis and multiple episodes of cystitis showed weak positive associations (OR = 2.00, 95 percent confidence interval (CI) 1.07-3.73; and OR = 1.60, 95 percent CI 0.95-2.70, respectively).

The role of asbestos in the etiology of lung cancer and of mesothelioma of the pleura and peritoneum has been well documented. The evidence for a causal association between asbestos and other human cancers is not as extensive but suggests that asbestos may be carcinogenic at several different sites. This paper is concerned specifically with a possible causal association between asbestos and human kidney cancer. A review of the evidence to date indicates that only three human studies have sufficient statistical power to detect an excess mortality from kidney cancer among workers exposed to asbestos. All three were occupational cohort studies, and two of these gave strong direct evidence for such an excess; a study of U.S. insulators (kidney cancer SMR = 2.22, 90% CI 1.44-3.30), and a study of U.S. asbestos products company workers (kidney cancer SMR = 2.76, 90% CI 1.29-5.18). The third study, of Italian shipyard workers, reported excess mortality from "cancers of the kidney, urinary bladder, and other urinary organs" (SMR = 1.98, 90% CI 1.42-2.70). Further support for a causal association includes studies finding asbestos fibers in human kidneys and urine, as well as reports of kidney tumors in two animal bioassays. It is concluded that asbestos should be regarded as a probable cause of human kidney cancer.

The mortality experience of 1595 male workers employed in one of the largest Italian refineries in the period from 1949-1982 was examined. From the comparison with national and local death rates, increases in mortality owing to lung and kidney cancers, brain tumors, and leukemias emerged. No definite trends according to duration of exposure and years since first exposure were apparent. The increases regarding cancer of the lung, kidney and brain appeared to be associated with the early period of operations. Analysis by exposure category suggested an association of the increased mortality from leukemias with working in production (observed = 2; expected = 0.61). Kidney cancer mortality was elevated among maintenance workers (obs. = 2; exp. = 0.18). Small numbers prevented firmer conclusions. Workers in the moving department had a significantly increased mortality from all cancers (obs. = 22; exp. = 11.7), and lung cancer (obs. = 11; exp. = 3.6). Confounding by smoking could be excluded as sufficient explanation of the three-fold increase in lung cancer deaths. It was in moving that highest airborne levels of polynuclear aromatic hydrocarbons had been discovered in an independent environmental investigation.