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Bladder cancer has been associated with exposure to chlorination by-products in drinking water, and experimental evidence suggests that exposure also occurs through inhalation and dermal absorption. The authors examined whether bladder cancer risk was associated with exposure to trihalomethanes (THMs) through ingestion of water and through inhalation and dermal absorption during showering, bathing, and swimming in pools. Lifetime personal information on water consumption and water-related habits was collected for 1,219 cases and 1,271 controls in a 1998-2001 case-control study in Spain and was linked with THM levels in geographic study areas. Long-term THM exposure was associated with a twofold bladder cancer risk, with an odds ratio of 2.10 (95% confidence interval: 1.09, 4.02) for average household THM levels of >49 versus < or =8 micro g/liter. Compared with subjects not drinking chlorinated water, subjects with THM exposure of >35 micro g/day through ingestion had an odds ratio of 1.35 (95% confidence interval: 0.92, 1.99). The odds ratio for duration of shower or bath weighted by residential THM level was 1.83 (95% confidence interval: 1.17, 2.87) for the highest compared with the lowest quartile. Swimming in pools was associated with an odds ratio of 1.57 (95% confidence interval: 1.18, 2.09). Bladder cancer risk was associated with long-term exposure to THMs in chlorinated water at levels regularly occurring in industrialized countries. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Studies of physical activity and colon cancer risk by anatomic site have provided inconsistent results. METHODS: We analyzed data from a population-based case-control study conducted in Iowa involving 685 colon cancer cases and 2434 control subjects. RESULTS: Among those who reported recreational activity more than twice per week, a 30% risk reduction of colon cancer was observed for all sites with a 40% risk reduction for cancer of the right colon. Occupational physical activity was also associated with a reduced risk of colon cancer. The risk was the lowest for those with both high occupational and recreational physical activity (odds ratio, 0.5; 95% confidence interval, 0.3-0.8). CONCLUSIONS: Increased physical activity was inversely associated with colon cancer risk. The inverse associations were stronger for the right than for the left colon. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Previous epidemiological studies have inconsistently linked various occupations and industries to pancreatic cancer risk. METHODS: We analyzed data from a population-based case-control study conducted in Iowa involving 376 histologically confirmed incident pancreatic cancer cases and 2434 control subjects. RESULTS: A significantly increased risk was observed among men who worked in the following industries: chemical and allied products, transportation, and elementary and secondary schools. Increased risks also were observed in men who were employed as truck drivers; railroad brake, signal, and switch operators; purchasing agents and buyers; teachers; insurance agents; and retail supervisors. Among women, a significantly increased risk of pancreatic cancer was found for employment in furniture and home furnishing stores, and a borderline significantly increased risk among textile sewing machine operators and tenders. CONCLUSIONS: Working in several occupations and industries was associated with an increased risk of pancreatic cancer in this study, and these associations warrant further investigation. [ABSTRACT FROM AUTHOR]

A case-control study involving 406 incident cases and 2,434 controls was conducted in Iowa to examine the association between occupational exposures and renal cell carcinoma risk. After adjusting for major confounders, an increased risk was observed for men among mechanics and repairers (odds ratio [OR] 1.9, 95% confidence interval [CI] = 1.2-2.9); assemblers (OR 2.5, 95% CI = 0.8-7.6); automotive dealership and service station employees (OR 1.9, 95% CI = 0.9-3.9); wholesale traders of durable goods (OR 1.5, 95% CI = 0.7-3.2); farm product vendors (OR 4.4, 95% CI = 1.3-15.5); service organization managers (OR 2.2, 95% CI = 1.0-5.1); financial specialists (OR 2.7, 95% CI = 1.0-7.6); sales occupation supervisors (OR 1.8, 95% CI = 1.0-3.3); guards (OR 5.4, 95% CI = 1.4-20.7); and general farm workers (OR 1.9, 95% CI = 1.0-3.7). Among women, an increased risk was found for employees in depository institutions (OR 3.6, 95% CI = 1.1-11.3); colleges and universities (OR 7.6-95% CI = 2.3-25.6); and retail, including those in grocery stores (OR 2.2, 95% CI = 1.0-4.7). Our results indicate that occupational exposures may increase the risk of renal cell carcinoma. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the association between alcohol consumption and the risk of non-Hodgkin's lymphoma (NHL) and to examine whether the association is modified by a family history of hematolymphoproliferative cancer (HLPC).Methods: Data on white men from two population-based case-control studies of NHL conducted in Iowa/Minnesota and Kansas were pooled for this analysis. Information on alcohol consumption, family history of HLPC, and other factors was obtained by interviewing 792 cases and 2193 controls or, if deceased, their next-of-kin. Logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs).Results: There was no clear association between NHL and the use of alcohol, beer, hard liquor, or wine. The relationship, however, may differ according to a family history of HLPC. Alcohol use was not associated with the risk of NHL in men without a family history of HLPC (ORs = 0.8 and 0.9 for men consuming alcohol < or = median and > median, respectively), the presence of a family history in the absence of alcohol use was associated with a slightly increased risk (OR = 1.4; 95% CI 0.8-2.5), whereas risks of NHL among men with a positive family history were 2.1 (CI 1.0-4.7) for men consuming alcohol < or = median (13.7 g/day) and 2.8 (1.3-5.9) for men consuming alcohol greater than median.Conclusions: The present data found no clear association between alcohol consumption and the risk of NHL among men without a family history of HLPC, whereas alcohol intake was associated an elevated risk in men with a positive family history. The finding of effect modification of the alcohol-NHL association by a family history of HLPC is novel and requires confirmation. [ABSTRACT FROM AUTHOR]

Background: Cigarette smoking is a well-established risk factor for bladder cancer. The effects of smoking duration, intensity (cigarettes per day), and total exposure (pack-years); smoking cessation; exposure to environmental tobacco smoke; and changes in the composition of tobacco and cigarette design over time on risk of bladder cancer are unclear.Methods: We examined bladder cancer risk in relation to smoking practices based on interview data from a large, population-based case-control study conducted in Maine, New Hampshire, and Vermont from 2001 to 2004 (N = 1170 urothelial carcinoma case patients and 1413 control subjects). We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using unconditional logistic regression. To examine changes in smoking-induced bladder cancer risk over time, we compared odds ratios from New Hampshire residents in this study (305 case patients and 335 control subjects) with those from two case-control studies conducted in New Hampshire in 1994-1998 and in 1998-2001 (843 case patients and 1183 control subjects).Results: Regular and current cigarette smokers had higher risks of bladder cancer than never-smokers (for regular smokers, OR = 3.0, 95% CI = 2.4 to 3.6; for current smokers, OR = 5.2, 95% CI = 4.0 to 6.6). In New Hampshire, there was a statistically significant increasing trend in smoking-related bladder cancer risk over three consecutive periods (1994-1998, 1998-2001, and 2002-2004) among former smokers (OR = 1.4, 95% CI = 1.0 to 2.0; OR = 2.0, 95% CI = 1.4 to 2.9; and OR = 2.6, 95% CI = 1.7 to 4.0, respectively) and current smokers (OR = 2.9, 95% CI = 2.0 to 4.2; OR = 4.2, 95% CI = 2.8 to 6.3; OR = 5.5, 95% CI = 3.5 to 8.9, respectively) (P for homogeneity of trends over time periods = .04). We also observed that within categories of intensity, odds ratios increased approximately linearly with increasing pack-years smoked, but the slope of the increasing trend declined with increasing intensity.Conclusions: Smoking-related risks of bladder cancer appear to have increased in New Hampshire since the mid-1990s. Based on our modeling of pack-years and intensity, smoking fewer cigarettes over a long time appears more harmful than smoking more cigarettes over a shorter time, for equal total pack-years of cigarettes smoked. [ABSTRACT FROM AUTHOR]

Purpose: The magnitude and timing of the reported decrease in risk of renal cell carcinoma (RCC) attributed to smoking cessation is not well characterized. Furthermore, conclusions from previous investigations have been hampered by unstable risk estimates, broad exposure categories and/or insufficient adjustment for the inverse correlation of cessation years with lifetime smoking exposure.Methods: To address these issues, we report data from a population-based case-control study conducted in Iowa from 1986 to 1989. RCC cases (n = 387) were identified through the Iowa Cancer Registry, while controls (n = 2,333) were randomly selected from the general population, frequency-matched on age and sex. Subjects provided detailed information on a mailed questionnaire regarding their smoking history as well as other anthropometric, lifestyle, dietary and medical history risk factors.Results: Smoothing spline regression analysis provided evidence of a consistent inverse linear trend between years of cessation and risk of RCC. In categorical analysis, compared with current smokers, those quitting > or =30 years ago experienced a 50% reduction in risk of RCC (OR = 0.5; 95% CI 0.3 to 0.8) after adjustment for age, sex, BMI, hypertension and pack-years of smoking. Risk among long-term quitters was similar to risk among never smokers (OR = 0.6; 95% CI 0.4 to 0.8). In contrast, cessation of <10 years, 10 to 19 years and 20 to 29 years all resulted in a less pronounced reduction in RCC risk ( approximately 20% to 30%).Conclusions: Our findings suggest that while cessation of smoking is indeed associated with a linear decrease in RCC risk even after adjustment for potential confounders, this benefit may not be sizeable until more than 20 years following cessation. [ABSTRACT FROM AUTHOR]