Case-control study of the effects of trihalomethanes on urinary bladder cancer risk

In this research, the authors examined the relation between the estimated concentrations in drinking water of disinfectant byproduct (DBP) trihalomethanes (THMs) and the risk for urinary bladder cancer in a case-control study of 567 white men aged 35 to 90 years, in western New York State. They used logistic regression to estimate odds ratios (ORS) and to assess the effects of THM consumption on cancer risk. Higher levels of consumption of THMs led to increased risk for cancer of the urinary bladder (total 551, a composite measure of THMs based upon method 551 developed by the US Environmental Protection Agency: OR = 2.34; 95% confidence interval [CI] = 1.01-3.66). Results were most significant for bromoform (OR = 3.05; 95% CI = 1.51-5.69), and risk was highest (OR = 5.85; 95% CI = 1.93-17.46) for those who consumed the greatest amount of water at points within the distribution system with the oldest postdisinfected tap water.     

Trihalomethanes in public water supplies and risk of stillbirth

BACKGROUND: The chlorine used to disinfect public drinking water supplies reacts with naturally occurring organic matter to form a number of chemical byproducts. Recent studies have implicated exposure to chlorination byproducts in drinking water, trihalomethanes (THMs), in particular, with intrauterine death. METHODS: We conducted a population-based case-control study in Nova Scotia and Eastern Ontario, Canada, to examine the effect of exposure to THMs on stillbirth risk. Cases were women who had a stillborn infant, and controls were a random sample of women with live births. Subjects were interviewed, and women with a public water source provided a residential water sample. Risks were examined according to residential THM level in tap water and to a total exposure metric incorporating tap water ingestion, showering, and bathing. RESULTS: We enrolled 112 stillbirth cases and 398 live birth controls. Women with a residential total THM level of 80 or more microg/L had twice the risk of a stillbirth compared with women with no exposure to THMs (adjusted odds ratio [OR] = 2.2; 95% confidence interval [CI] = 1.1-4.4). The highest quintile of total THM exposure using the total exposure metric was associated with an adjusted odds ratio of 2.4 (95% CI = 1.2-4.6) compared with women not exposed to THMs. Similar results were seen for specific THM compounds. A monotonic dose-response relationship was not seen. CONCLUSIONS: Our results provide evidence for an increased risk of stillbirth associated with exposure to chlorination byproducts through ingestion and showering and bathing, although there was not a clear dose-response relationship.     

Maternal exposure to nitrate from drinking water and diet and risk for neural tube defects

In this population-based case-control study conducted in California between June 1989 and May 1991, the authors investigated the association between maternal periconceptional exposure to nitrate from drinking water and diet and risk for neural tube defects. The mothers of 538 cases and 539 nonmalformed controls were interviewed regarding residential history, consumption of tap water at home, and dietary intake during the periconceptional period. Dietary nitrate exposure was not associated with increased risk for neural tube defects. Exposure to nitrate in drinking water at concentrations above the 45 mg/liter maximum contaminant level was associated with increased risk for anencephaly (odds ratio (OR) = 4.0, 95% confidence interval (CI): 1.0, 15.4), but not for spina bifida. Increased risks for anencephaly were observed at nitrate levels below the maximum contaminant level among groundwater drinkers only (OR = 2.1, 95% CI: 1.1,4.1 for 5-15 mg/liter; OR = 2.3, 95% CI: 1.1, 4.5 for 16-35 mg/liter; and OR = 6.9, 95% CI: 1.9, 24.9 for 36-67 mg/liter compared with <5 mg/liter). Adjustment for identified risk factors for anencephaly did not substantially alter these associations, nor did control for maternal dietary nitrate, total vitamin C intake, and quantity of tap water consumed. The lack of an observed elevation in risk for anencephaly in association with exposure to mixed water containing nitrate at levels comparable with the concentration in groundwater may indicate that something other than nitrate accounts for these findings.     

Bladder cancer and exposure to water disinfection by-products through ingestion, bathing, showering, and swimming in pools

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.     

Case control study of the geographic variability of exposure to disinfectant byproducts and risk for rectal cancer

Background  

Levels of byproducts that result from the disinfection of drinking water vary within a water distribution system. This prompted us to question whether the risk for rectal cancer also varies, depending upon one's long term geographic location within the system. Such a geographic distribution in rectal cancer risk would follow naturally from an association between level of byproduct and rectal cancer risk. We assess the effects of estimated geographic variability in exposure to some of the components of the trihalomethane group of disinfectant byproducts (DBPs) on the odds ratios and probabilities for rectal cancer in white males in a case control study of 128 cases and 253 controls, conducted in Monroe County, Western New York State, U.S.A. The study was designed around health data initially collected at the University at Buffalo (Department of Social and Preventative Medicine) as part of the Upstate New York Diet Study, and trihalomethane (THM) data collected from a separate independent study of THMs conducted by Monroe County Department of Health. Case participants were chosen from hospital pathology records. The controls are disease-free white males between 35–90 years old, living in Monroe County, and chosen from control groups for studies from cancer of five other (unrelated) sites. Using a combination of case control methodology and spatial analysis, the spatial patterns of THMs and individual measures of tap water consumption provide estimates of the effects of ingestion of specific amounts of some DBPs on rectal cancer risk. Trihalomethane (THM) data were used to spatially interpolate levels at the taps of cases and controls, and odds ratios were estimated using logistic regression to assess the effects of estimated THM exposure dose on cancer risk, adjusting for alcohol, dietary beta carotene intake, tap water intake, and total caloric intake.     

Milk consumption and bladder cancer risk: a meta-analysis of published epidemiological studies

Studies investigating the association of milk consumption with bladder cancer risk have reported inconsistent findings. We conducted a meta-analysis of published cohort and case-control studies to pool the risk estimates of the association between milk intake and bladder cancer. We quantified associations with bladder cancer using meta-analysis of odds ratio (OR) associated with the highest vs. the lowest category of milk intake using fixed- or random-effect models depending on the heterogeneity of effects among studies. Nineteen cohort and case-control studies were eligible for inclusion. High milk intake was significantly associated with decreased risk of bladder cancer (OR, 0.84; 95% CI, 0.71-0.97) when comparing the highest with the lowest category of milk intake. The inverse association was stronger in Asia (OR, 0.60; 95% CI, 0.40-0.81) than North America (OR, 0.89; 95% CI, 0.76-1.03), and no association was observed in Europe (OR, 1.05; 95% CI, 0.85-1.26). This relationship also varied significantly by specific dairy products. Our results suggest that milk may be related to the reduction of bladder cancer risk. Further studies need to clarify the biological mechanisms.     

Water disinfection by-products and bladder cancer: is there a European specificity? A pooled and meta-analysis of European case-control studies

Several epidemiological studies suggested an association between the risk of bladder cancer and the exposure to trihalomethanes (THMs), the main disinfection by-products (DBPs) of chlorinated water. A previous pooled analysis of case-control studies from North America and Europe estimated a summarized dose-response relation. For policy guidance of drinking water disinfection in Europe and because major differences exist in water disinfection practices and DBPs occurrence between both continents, specific risk estimates for bladder cancer in relation to DBPs exposure for European populations were needed. We conducted a pooled and a two-stage random-effect meta-analyses of three European case-control studies from France, Finland, and Spain (5467 individuals: 2381 cases and 3086 controls). Individual exposure to THMs was calculated combining information on residential history, estimates of the average total THMs (TTHM) level in tap water at the successive residences and personal water consumption. A significant odds-ratio was observed for men exposed to an average residential TTHM level > 50 μg/l (OR = 1.47 (1.05; 2.05)) when compared to men exposed to levels ≤ 5 μg/l. The linear trend of the exposure-risk association was significant (p = 0.01). Risks increased significantly for exposure levels above 25 μg/l and with more than 30 years of exposure to chlorinated water, but were mainly driven by the level rather than the duration of exposure. No significant association was found among women or with cumulative exposure through ingestion. There was no evidence of a differential exposure-response relation for TTHM and bladder cancer in Europe and North America. Consequently, a global exposure-risk relation based on 4351 cases and 7055 controls is now available.     

Milk Consumption and Bladder Cancer Risk: A Meta-Analysis of Published Epidemiological Studies

Studies investigating the association of milk consumption with bladder cancer risk have reported inconsistent findings. We conducted a meta-analysis of published cohort and case-control studies to pool the risk estimates of the association between milk intake and bladder cancer. We quantified associations with bladder cancer using meta-analysis of odds ratio (OR) associated with the highest vs. the lowest category of milk intake using fixed- or random-effect models depending on the heterogeneity of effects among studies. Nineteen cohort and case-control studies were eligible for inclusion. High milk intake was significantly associated with decreased risk of bladder cancer (OR, 0.84; 95% CI, 0.71–0.97) when comparing the highest with the lowest category of milk intake. The inverse association was stronger in Asia (OR, 0.60; 95% CI, 0.40–0.81) than North America (OR, 0.89; 95% CI, 0.76–1.03), and no association was observed in Europe (OR, 1.05; 95% CI, 0.85–1.26). This relationship also varied significantly by specific dairy products. Our results suggest that milk may be related to the reduction of bladder cancer risk. Further studies need to clarify the biological mechanisms.     

Nitrate intake does not influence bladder cancer risk: the Netherlands cohort study

OBJECTIVES: N-nitroso compounds, endogenously formed from nitrate-derived nitrite, are suspected to be important bladder carcinogens. However, the association between nitrate exposure from food or drinking water and bladder cancer has not been substantially investigated in epidemiologic studies. METHODS: We evaluated the associations between nitrate exposure and bladder cancer in the Netherlands Cohort Study, conducted among 120,852 men and women, 55-69 years of age at entry. Information on nitrate from diet was collected via a food frequency questionnaire in 1986 and a database on nitrate content of foods. Individual nitrate exposures from beverages prepared with tap water were calculated by linking the postal code of individual residence at baseline to water company data. After 9.3 years of follow-up and after excluding subjects with incomplete or inconsistent dietary data, 889 cases and 4,441 subcohort members were available for multivariate analyses. We calculated incidence rate ratios (RR) and corresponding 95% confidence intervals (CIs) using Cox regression analyses. We also evaluated possible effect modification of dietary intake of vitamins C and E (low/high) and cigarette smoking (never/ever). RESULTS: The multivariate RRs for nitrate exposure from food, drinking water, and estimated total nitrate exposure were 1.06 (95% CI, 0.81-1.31), 1.06 (95% CI, 0.82-1.37), and 1.09 (95% CI, 0.84-1.42), respectively, comparing the highest to the lowest quintiles of intake. Dietary intake of vitamins C and E (low/high) and cigarette smoking (never/ever) had no significant impact on these results. CONCLUSION: Although the association between nitrate exposure and bladder cancer risk is biologically plausible, our results in this study do not support an association between nitrate exposure and bladder cancer risk.     

Effect modification of the association between trihalomethanes and pancreatic cancer by drinking water hardness: Evidence from an ecological study

The objective of this study was to examine the relationship between total trihalomethanes (TTHM) levels in public water supplies and risk of pancreatic cancer and to determine whether calcium (Ca) and magnesium (Mg) levels in drinking water modify the effects of TTHM on risk to develop pancreatic cancer. A matched case-control study was used to investigate the relationship between the risk of death attributed to pancreatic cancer and exposure to TTHM in drinking water in 53 municipalities in Taiwan. All pancreatic cancer deaths in the 53 municipalities from 1998 through 2007 were obtained from the Bureau of Vital Statistics of the Taiwan Provincial Department of Health. Controls were deaths from other causes and were pair matched to the cancer cases by gender, year of birth, and year of death. Each matched control was selected randomly from the set of possible controls for each cancer case. Data on TTHM levels in drinking water were collected from Taiwan Environmental Protection Administration. Information on the levels of Ca and Mg in drinking water was obtained from the Taiwan Water Supply Corporation. The municipality of residence for cancer cases and controls was presumed to be the source of the subject's TTHM, Ca, and Mg exposure via drinking water. Relative to individuals whose TTHM exposure level<4.9 ppb, the adjusted OR (95% CI) for pancreatic cancer was 1.01 (0.85-1.21) for individuals who resided in municipalities served by drinking water with a TTHM exposure>4.9 ppb. There was no evidence of an interaction of drinking water TTHM levels with low Ca intake via drinking water. However, we observed evidence of an interaction between drinking water TTHM concentrations and Mg intake via drinking water. Our findings showed that the correlation between TTHM exposure and risk of pancreatic cancer is influenced by Mg in drinking water. Increased knowledge of the interaction between Mg and TTHM in reducing pancreatic cancer risk will aid in public policy making and standard setting.     

Association of fluids from beverages with risk of rectal cancer

Little information is available about how fluid intake from beverages and sources of fluid intake influence risk of rectal cancer. We examined these associations with risk of incident rectal cancer in a population-based case-control study of 952 cases and 1,205 controls living in northern California and Utah. We also determined if intake of fiber (soluble and insoluble), physical activity, and nonsteroidal anti-inflammatory medications (NSAIDs) or aspirin modified the associations between fluid intake and rectal cancer. We identified a modest inverse association of water intake (odds ratio, OR = 0.70; 95% confidence interval, CI = 0.48, 1.02) and total fluid intake (high vs. low OR = 0.70; 95% CI = 0.46, 1.06) with risk of rectal cancer in men and a positive association with juice among women (high vs. low OR = 1.56; 95% CI = 1.00, 2.41). Risk of rectal cancer increased nonsignificantly among men with beer consumption, among women with high white wine use, and among men and women with high long-term alcohol use. NSAIDs modified the association of alcohol consumption with rectal cancer: 1) risk associated with beer increased among men who did not take NSAIDs and had a high beer intake (OR = 1.60; 95% CI = 1.08, 2.39) and 2) risk associated with long-term alcohol intake increased in a linear fashion in women who did not use NSAIDs (OR = 1.98; 95% CI = 1.15, 3.40). Risk of rectal cancer increased among estrogen-negative women if they consumed any beer or white wine but decreased among estrogen-positive women with beer. In men, low intake of water and low insoluble fiber intake were associated with increased risk of rectal cancer beyond that of either factor alone (OR = 1.82; 95% CI = 1.11, 3.00). The interactions of fiber with water intake suggest that bowel motility may be the mechanism responsible for modification of rectal cancer risk for water. Associations of alcohol to risk for rectal cancer may be related to cellular hyperproliferation and may be modified by NSAID use.     

Haloacetic acids in drinking water and risk for stillbirth

Aims: To investigate the effects of haloacetic acid (HAA) compounds in drinking water on stillbirth risk.

Methods: A population based case-control study was conducted in Nova Scotia and Eastern Ontario, Canada. Estimates of daily exposure to total and specific HAAs were based on household water samples and questionnaire information on water consumption at home and work.

Results: The analysis included 112 stillbirth cases and 398 live birth controls. In analysis without adjustment for total THM exposure, a relative risk greater than 2 was observed for an intermediate exposure category for total HAA and dichloroacetic acid measures. After adjustment for total THM exposure, the risk estimates for intermediate exposure categories were diminished, the relative risk associated with the highest category was in the direction of a protective effect, and all confidence intervals included the null value.

Conclusions: No association was observed between HAA exposures and stillbirth risk after controlling for THM exposures.

     

Cigarette smoking and risk of bladder, pancreas, kidney, and colorectal cancers in Iowa

PURPOSE: Although there are numerous reports on the effects of cigarette smoking and cancer, they have infrequently compared risks at more than one cancer site after multivariate adjustment. We analyzed data from a population-based case-control study that included five anatomic sites to evaluate the association between cigarette smoking and each cancer site and to rank the associations by site. METHODS: Study respondents included 1452 bladder, 406 kidney, 376 pancreatic, 685 colon, and 655 rectal cancer cases, as well as 2434 population controls. A self-administered questionnaire was used to collect information on cigarette smoking and other potential confounders including occupation, drinking water source, and dietary practices. Logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs), after adjustment for age, total energy intake, and other site- and sex-specific confounders. RESULTS: In both sexes, cigarette smoking (ever vs. never) was associated with risk of bladder cancer (OR = 2.5; 95% CI, 2.0-3.1 for males; OR = 2.7; 2.0-3.6 for females) and pancreatic cancer (OR = 1.8; 1.2-2.8 for males; OR = 2.1; 1.4-3.1 for females). Cigarette smoking also increased the risk of kidney cancer among males (OR = 1.8; 1.3-2.7), and to a lesser degree, among females (OR = 1.2; 0.8-1.8). No association was found for colon or rectal cancer in either sex. CONCLUSIONS: Cigarette smoking increased the risk of bladder, kidney, and pancreatic cancer in men and women. The rankings of multivariate-adjusted ORs from highest to lowest were bladder, pancreas, kidney, and colorectum, with little difference between men and women.     

Disinfection byproducts and bladder cancer: a pooled analysis

BACKGROUND: Exposure to disinfection byproducts in drinking water has been associated with an increased risk of bladder cancer. We pooled the primary data from 6 case-control studies of bladder cancer that used trihalomethanes as a marker of disinfection byproducts. METHODS: Two studies were included from the United States and one each from Canada, France, Italy, and Finland. Inclusion criteria were availability of detailed data on trihalomethane exposure and individual water consumption. The analysis included 2806 cases and 5254 controls, all of whom had measures of known exposure for at least 70% of the exposure window of 40 years before the interview. Cumulative exposure to trihalomethanes was estimated by combining individual year-by-year average trihalomethane level and daily tap water consumption. RESULTS: There was an adjusted odds ratio (OR) of 1.24 in men exposed to an average of more than 1 microg/L (ppb) trihalomethanes compared with those who had lower or no exposure (95% confidence interval [CI] = 1.09-1.41). Estimated relative risks increased with increasing exposure, with an OR of 1.44 (1.20-1.73) for exposure higher than 50 microg/L (ppb). Similar results were found with other indices of trihalomethane exposure. Among women, trihalomethane exposure was not associated with bladder cancer risk (0.95; 0.76-1.20). CONCLUSIONS: These findings strengthen the hypothesis that the risk of bladder cancer is increased with long-term exposure to disinfection byproducts at levels currently observed in many industrialized countries.     

Nitrate in public water supplies and risk of bladder cancer

BACKGROUND: Nitrate is a precursor compound in the formation of N-nitroso compounds, most of which are potent animal carcinogens. N-nitroso compounds and their precursors have not been extensively evaluated as bladder cancer risk factors. METHODS: We conducted a population-based case-control study of bladder cancer in Iowa. Cases were men and women newly diagnosed with bladder cancer in 1986-1989. Nitrate data for Iowa public water supplies were sparse before the 1960s. To reduce misclassification by unknown nitrate levels, we included only those who used public supplies with nitrate data for 70% or more of their person-years since 1960 (808 cases, 1259 controls). RESULTS: Among controls, the median average nitrate level for their Iowa residences with public water supplies was 1.3 mg/liter nitrate-nitrogen (interquartile range = 0.6-3.0). After adjustment for confounders, we found no increased risk of bladder cancer with increasing average nitrate levels in drinking water; the highest quartile odds ratio for women was 0.8 (95% confidence interval = 0.4-0.8), and for men 0.5 (0.4-0.8). We observed no association among those with high water nitrate exposure (>median) and low (相似文献   

Does ozonation of drinking water reduce the risk of bladder cancer?

BACKGROUND: Epidemiologic studies of drinking water disinfection byproducts have focused primarily on the carcinogenic potential of chlorination byproducts. Because drinking water has been ozonated in France for decades, we were able to assess the carcinogenic risk of the disinfection byproducts generated by both ozonation and chlorination. METHODS: We used data from a case-control study of bladder cancer conducted between 1985 and 1987 in 7 French hospitals. We compared 281 cases and 272 controls for whom we could reconstruct at least 70% of the residential exposure to drinking water contaminants over a 30-year period. RESULTS: When we took potential confounders and exposure to chlorination byproducts into account, the risk of bladder cancer decreased as duration of exposure to ozonated water increased (OR = 0.60 [95% CI = 0.3-1.3] for 1-9 years; OR = 0.31 [0.1-0.7] for 10 years or more). Simultaneously, the risk of bladder cancer increased with duration of exposure to chlorinated surface water and with the estimated trihalomethane content of the water. Our data suggest that ozonation reduces the risk associated with the chlorination of surface water and that ozonation alone could have an independent beneficial effect on bladder cancer risk. CONCLUSIONS: Our results are consistent with experimental evidence that ozonation in combination with chlorination decreases the concentration of trihalomethane in treated water and eliminates some of the mutagenicity of raw water.     

Trihalomethane exposures from municipal water supplies and selected congenital malformations

BACKGROUND: Concerns about potential health effects of trihalomethanes (THMs) have prompted investigations on whether infants whose mothers were periconceptionally exposed to drinking water containing THMs are at greater risk of congenital malformations. METHODS: We used two large case-control maternal interview studies that were conducted among California deliveries from 1987 through 1991. One study comprised 538 infants/fetuses with neural tube defects (NTDs) and 539 nonmalformed control infants. The second study included an additional 265 infants with NTDs, 207 infants with conotruncal heart defects, 409 infants with orofacial clefts, and 481 control infants. Expert personnel from municipal water companies estimated THM levels for a particular residence and specific periconceptional time period using quarterly monitoring measurements. Estimates were also made for four individual THM levels and for the total THM level. RESULTS: NTD risk in the first study was inversely associated with total THM exposure. Although the second study did not show the same inverse relationship for NTDs, there were no positive associations of NTDs or the other malformations with total THM as estimated from continuous models. Elevated risks were observed for the lowest category of exposure (1-24 ppb), but risks were either not substantially elevated or were imprecise for higher exposure levels. Thus no evidence was observed for an exposure-response relation. CONCLUSIONS: Our results do not provide a clear pattern of association between THM exposure and risks of specific congenital malformations. Imprecise exposure measures coupled with a lack of information about other possible sources of THM exposure may have caused associations to be underestimated.     

Pancreatic cancer and drinking water and dietary sources of nitrate and nitrite

N-Nitroso compounds, known animal carcinogens, are formed endogenously from drinking water and dietary sources of nitrate and nitrite. The authors conducted a population-based case-control study of pancreatic cancer in Iowa to determine whether increased consumption of nitrate and nitrite from drinking water and dietary sources was associated with risk. They linked detailed water source histories to nitrate measurements for Iowa community water supplies. After exclusions for insufficient data, 1,244 controls and 189 pancreatic cancer cases were available for analysis. Among controls, the median average nitrate level (1960-1987) was 1.27 (interquartile range, 0.6-2.8) mg of nitrate nitrogen per liter of water. No association was observed between pancreatic cancer risk and increasing quartiles of the community water supplies' nitrate level. Increasing intake of dietary nitrite from animal sources was associated with an elevated risk of pancreatic cancer among men and women (highest quartile odds ratios = 2.3, 95% confidence interval: 1.1, 5.1, for men and 3.2, 95% confidence interval: 1.6, 6.4, for women). In contrast, dietary nitrate intake showed an inverse association with risk among women and no association among men. This study suggests that long-term exposure to drinking water nitrate at levels below the maximum contaminant level of nitrate nitrogen (10 mg/liter) is not associated with pancreatic cancer; however, the consumption of dietary nitrite from animal products may increase risk.     

Dietary carotenoids and genetic instability modify bladder cancer risk

In vitro and in vivo studies have shown that carotenoid supplementation is associated with decreased DNA damage, but the role of dietary carotenoids in cancer risk remains controversial because epidemiologic studies have yielded conflicting results. Limited data exist regarding the role of dietary carotenoids in the context of constitutional genetic instability in cancer risk. This case-control study estimated dietary carotenoid intake [microg/(kJ . d)] from a FFQ for 423 patients with bladder cancer and 467 healthy controls, and quantified baseline and benzo[a]pyrene diol epoxide (BPDE)- and gamma-radiation-induced DNA damage in the peripheral blood lymphocytes using the comet assay. Overall, intake of total carotenoids was lower (P < 0.01) for bladder cancer cases (mean +/- SD: 1273.4 +/- 688.9) compared with healthy controls (1501.3 +/- 791.5). When categorized into quartiles, there was an inverse association between increasing levels of carotenoid intake and bladder cancer risk with greatest protective effect [odds ratio (OR) = 0.56, 95% CI, 0.37-0.85] in the quartile with the highest level of intake. Baseline and mutagen-induced DNA damage was significantly higher in cases than in controls; when analyzed jointly with carotenoid intake, high DNA damage and low carotenoid intake were associated with the highest risk. For example, with high baseline DNA damage and low total carotenoid intake, the OR was 3.08 (95% CI, 1.64-5.77); with high baseline DNA damage and high total carotenoid intake, the risk was somewhat attenuated (OR = 2.49, 95% CI, 1.28-4.84). The risk was decreased further for low baseline DNA damage and low total carotenoid intake (OR = 2.18; 95% CI, 1.13-4.22). This study provides evidence of a preventive role for carotenoids in bladder cancer, and these data may have important implications for cancer prevention, especially for individuals susceptible to DNA damage.     

Tea consumption and risk of bladder and kidney cancers in a population-based case-control study

Recent epidemiologic studies have suggested that tea may be protective against cancers of the urinary tract. The authors examined the association between usual adult tea consumption and risk of bladder and kidney cancers in a population-based case-control study that included 1,452 bladder cancer cases, 406 kidney cancer cases, and 2,434 controls. For bladder cancer, the age- and sex-adjusted odds ratios (OR) (95% confidence intervals (CI)) referent to nonusers of tea were 0.9 (0.7, 1.1) for <1.0 cup/day, 1.0 (0.8, 1.2) for 1.0-2.6 cups/day, and 0.9 (0.7, 1.1) for >2.6 cups/day (cutpoints for users based on the tertile distribution among controls). When more extreme cutpoints were used, persons who consumed >5 cups/day (>90th percentile) had a suggestive decreased risk (OR = 0.7; 95% CI 0.5, 1.0), but there was no evidence of a dose-response relation. In analyses stratified by median total beverage intake (2.6 liters/day), there was an inverse association with tea use among persons who consumed less than the median (OR = 0.5; 95% CI 0.3, 0.8) but no association for persons who consumed at or above the median. In contrast, for kidney cancer, there was no association with tea use. Adjustment for site-specific risk factors did not alter these results. This study offers only minimal support for an inverse association between tea consumption and bladder or kidney cancer risk.