Risk Of Bladder Cancer In Men Research Articles

5α-reductase inhibitors with or without alpha-blockers and risk of incident upper tract urothelial carcinoma in men with benign prostatic hyperplasia: Analysis of US insurance claims data

BackgroundIncreasing data suggests that androgen receptor signaling may play an important role in the carcinogenesis of urothelial cancers. While the chemoprotective effect of 5-alpha reductase inhibitors (5-ARi) on bladder cancer risk in men with Benign Prostatic Hyperplasia (BPH) has been explored with conflicting results, the evidence regarding 5-ARi treatment, and the risk of incident Upper Tract Urothelial Carcinoma (UTUC) development is lacking. Therefore, our objective was to investigate the impact of the 5-ARi administration on the incidence of new UTUC cases using a large US database. MethodsThe MerativeTM Marketscan® database was used to identify men ≥ 50 years old with a diagnosis of BPH and an active 5-ARi prescription between 2007 and 2021 and were subsequently matched with paired controls. A multivariable Cox regression model was implemented to ascertain the association of 5-ARi and/or alpha-blocker (α-B) medications on the incidence of UTUC. Additional subgroup analyses were conducted based on exposure risk (with a 2-year threshold) to investigate the relationship between 5-ARi and UTUC over time. ResultsOverall, n=1,103,743 men BPH without prescriptions for BPH, n=31,142 men on 5-ARi, and n=160,049 using 5-ARi + α-B were identified. Over the follow-up period, a total of n=4,761 patients were diagnosed with UTUC. After matching, UTUC incidence ranged from 0.36% to 0.41% in men without active BPH therapy vs. 0.30% and 0.52% for the 5-ARi and 5-ARi + α-B groups, respectively. In multivariable analysis, the chemoprotective effect on UTUC risk was not observed for either 5-ARi monotherapy (adjusted hazard ratio [aHR]: 0.91, 95% CI: 0.58–1.44) or 5-ARi + α-B combination (aHR: 1.02, 95% CI: 0.87–1.19). This remained true for both short-term (≤ 2 years) and long-term (> 2 years) follow-up periods. ConclusionsThe use of 5-ARi for BPH, whether used alone or in combination with α-B, is not associated with incident UTUC.

Interaction between blood pressure and genetic risk score for bladder cancer, and risk of urothelial carcinoma in men

There is substantial genetic predisposition to bladder cancer (BC). Recently, blood pressure (BP) was positively associated with BC risk in men, but the potential interaction with genetic susceptibility for BC is unknown. We investigated a weighted genetic risk score (wGRS) of 18 BC genetic variants, BP, and their interaction, in relation to incident urothelial cancer (UC, n = 385) risk in 10,576 men. We used Cox regression, the likelihood ratio test, and the relative excess risk for interaction to calculate hazard ratios (HR) of UC, multiplicative interaction and additive interaction respectively. There was evidence of a positive additive interaction between SBP and the wGRS in relation to aggressive (P = 0.02) but not non-aggressive (P = 0.60) UC. The HR of aggressive UC was for SBP ≥ 140 mmHg and the upper 50% of the wGRS combined 1.72 (95% CI 1.03–2.87) compared to the counterpart group. Additionally, the 20-year risk of aggressive UC in 60 year-old men was 0.78% in the low SBP/low wGRS group and 1.33% in the high SBP/high wGRS group. Our findings support a potential additive interaction between the wGRS and SBP on aggressive UC among men. If replicated, the findings on interaction may provide biological and public health insight to prevent aggressive UC.

Blood pressure and bladder cancer risk in men by use of survival analysis and in interaction with NAT2 genotype, and by Mendelian randomization analysis.

The association between blood pressure (BP) and bladder cancer (BC) risk remains unclear with confounding by smoking being of particular concern. We investigated the association between BP and BC risk among men using conventional survival-analysis, and by Mendelian Randomization (MR) analysis in an attempt to disconnect the association from smoking. We additionally investigated the interaction between BP and N-acetyltransferase-2 (NAT2) rs1495741, an established BC genetic risk variant, in the association. Populations consisting of 188,167 men with 502 incident BC's in the UK-biobank and 27,107 men with 928 incident BC's in two Swedish cohorts were used for the analysis. We found a positive association between systolic BP and BC risk in Cox-regression survival analysis in the Swedish cohorts, (hazard ratio [HR] per standard deviation [SD]: 1.14 [95% confidence interval 1.05-1.22]) and MR analysis (odds ratio per SD: 2-stage least-square regression, 7.70 [1.92-30.9]; inverse-variance weighted estimate, 3.43 [1.12-10.5]), and no associations in the UK-biobank (HR systolic BP: 0.93 [0.85-1.02]; MR OR: 1.24 [0.35-4.40] and 1.37 [0.43-4.37], respectively). BP levels were positively associated with muscle-invasive BC (MIBC) (HRs: systolic BP, 1.32 [1.09-1.59]; diastolic BP, 1.27 [1.04-1.55]), but not with non-muscle invasive BC, which could be analyzed in the Swedish cohorts only. There was no interaction between BP and NAT2 in relation to BC on the additive or multiplicative scale. These results suggest that BP might be related to BC, more particularly MIBC. There was no evidence to support interaction between BP and NAT2 in relation to BC in our study.

Fruit consumption and the risk of bladder cancer: A pooled analysis by the Bladder Cancer Epidemiology and Nutritional Determinants Study.

While the association between fruit consumption and bladder cancer risk has been extensively reported, studies have had inadequate statistical power to investigate associations between types of fruit and bladder cancer risk satisfactorily. Fruit consumption in relation to bladder cancer risk was investigated by pooling individual data from 13 cohort studies. Cox regression models with attained age as time scale were used to estimate hazard ratios (HRs) for intakes of total fruit and citrus fruits, soft fruits, stone fruits, tropical fruits, pome fruits and fruit products. Analyses were stratified by sex, smoking status and bladder cancer subtype. During on average 11.2 years of follow-up, 2836 individuals developed incident bladder cancer. Increasing fruit consumption (by 100 g/day) was inversely associated with the risk of bladder cancer in women (HR = 0.92; 95% CI 0.85-0.99). Although in women the association with fruit consumption was most evident for higher-risk nonmuscle invasive bladder cancer (NMIBC; HR = 0.72; 95% CI 0.56-0.92), the test for heterogeneity by bladder cancer subtype was nonsignificant (P-heterogeneity = .14). Increasing fruit consumption (by 100 g/day) was not associated with bladder cancer risk in men (HR = 0.99; 95% CI 0.94-1.03), never smokers (HR = 0.96; 95% CI 0.88-1.05), former smokers (HR = 0.98; 95% CI 0.92-1.05) or current smokers (HR = 0.95; 95% CI 0.89-1.01). The consumption of any type of fruit was not found to be associated with bladder cancer risk (P values > .05). Our study supports no evidence that the consumption of specific types of fruit reduces the risk of bladder cancer. However, increasing total fruit consumption may reduce bladder cancer risk in women.

Lifestyle associated factors and risk of urinary bladder cancer: A prospective cohort study from Norway.

A number of lifestyle associated factors, such as high body mass index (BMI), low physical activity, and related metabolic disorders, are associated with increased risk of cancer at several sites. For urinary bladder cancer (BC), such studies show inconsistent results, which could result from inadequate adjustment for smoking and occupational exposure. In the population‐based Janus Cohort (n = 292 851), we investigated the independent and combined impact of BMI, physical activity, blood pressure, and blood lipids on the risk of BC, by thorough adjustment for smoking and potential occupational exposure. We used cox proportional hazard regression to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) for the associations between the lifestyle associated factors and BC risk. The associations observed were dependent on smoking status and gender. Among men, diastolic blood pressure (DBP) (HR 1.07, 95% CI 1.02‐1.12) and systolic blood pressure (SBP) (HR 1.04, 95% CI 1.01‐1.07) were positively associated with BC risk. Stratification by smoking status revealed a positive association between DBP and BC risk in never smokers (HR 1.14, 95% CI 1.00‐1.30), while no association was seen for current and former smokers. A risk score, integrating information across the lifestyle factors was positively associated with BC risk in men (p trend = 0.043). In women, physical activity was associated with a decreased BC risk, but only among never smokers (HR 0.65, 95% CI 0.45‐0.94). In conclusion, relations between lifestyle associated factors and BC risk were most evident in never smokers, suggesting that smoking dominates the relation in current smokers.

Association of body mass index with bladder cancer risk in men depends on abdominal obesity.

The previous epidemiological studies about the associations between obesity and bladder cancer risk have reported inconsistent results. Therefore, we analyzed whether the abdominal obesity effected on the risk of developing bladder cancer according to body mass index (BMI) using nationally representative data from the National Health Insurance System (NHIS). Among people who underwent at least one health examination from 2009 to 2012 in Korea, 11,823,876 men without a previous diagnosis of bladder cancer were followed up until December 2015. Multiple Cox regression analysis was conducted to determine the hazard ratio (HR) and 95% confidence interval (CI) for the association between bladder cancer and BMI or waist circumference (WC). Significant upward trends in the risk of bladder cancer were observed with increasing BMI or WC according to the multivariate-adjusted model. However, the association between BMI and bladder cancer is influenced by the presence of abdominal obesity. In the group with WC < 90cm, there was no significant change in the HRs for bladder cancer development beyond the reference BMI. In contrast, the HRs for bladder cancer showed statistically significant increase as the BMI increased beyond the reference BMI in the group with WC ≥ 90cm. This population-based study showed that increasing BMI and increasing WC were risk factors for developing bladder cancer in men, independent of confounding variables. However, there was a discrepancy in the trend of bladder cancer development according to BMI between the groups with abdominal obesity and without abdominal obesity.

Diabetes mellitus and the risk of bladder cancer: A PRISMA-compliant meta-analysis of cohort studies.

Epidemiologic studies have reported inconsistent results regarding the relationship between diabetes mellitus (DM) and the incidence of bladder cancer. This comprehensive systematic review and meta-analysis explored and evaluated this relationship in participants with different characteristics. Studies indexed in the PubMed, Embase, and the Cochrane Library databases that compared bladder cancer incidence mortality between DM and non-DM participants were included in the present study. The relative risks (RRs) of a random-effects model were used to assess these associations. The final analysis included 21 cohort studies, involving a total of 13,505,643 participants. Overall, DM was associated with an increased risk of bladder cancer or cancer mortality when compared with non-DM participants (RR: 1.23; 95% confidence interval [CI]: 1.12-1.35; P < .001). Furthermore, DM had a harmful impact on subsequent bladder cancer risk in men compared with those without DM (RR: 1.23; 95% CI: 1.06-1.42; P = .005), whereas no significant relationship was observed between DM and bladder cancer in women (RR: 1.24; 95% CI: 0.95-1.61; P = .119). There was no significant gender difference for this relationship (ratio of RR: 0.99; 95% CI: 0.73-1.34; P = .958). In addition, cancer incidence (RR: 1.21; 95% CI: 1.09-1.35; P < .001) and cancer mortality (RR: 1.25; 1.17-1.35; P < .001) both increased in DM patients. Finally, smoking status and follow-up duration might also affect this relationship in men and women. The findings of this study indicated that DM was associated with elevated bladder cancer or cancer mortality risk, especially in men. This relationship in women requires further exploration.

Occupational Exposure to Diesel and Gasoline Engine Emissions and Bladder Cancer Risk in Men: a Canadian Population-Based Case-Control Study

Background: The International Agency for Research on Cancer has classified diesel exhaust as a carcinogen and gasoline exhaust as a possible carcinogen based on evidence for lung cancer. Our goal was to determine whether a positive association exists between occupational exposure to diesel or gasoline exhaust and bladder cancer. Methods: A population-based design was used to recruit 670 cases and 2547 frequency-matched controls from eight Canadian provinces between 1994 and 1997. Lifetime occupational history, including job title, status and duties, and information on possible risk factors was obtained by self-reported questionnaire. Concentration and frequency of occupational exposure to diesel and gasoline exhaust, and a measure of the reliability of exposure assessment, was assigned for each job using a job-exposure matrix supplemented by expert review. Exposure metrics were modeled as ever-never, highest attained concentration, duration, and cumulative exposure. Unconditional logistic regression was used to calculate odds ratios and their 95% confidence intervals. Analyses were restricted to estimates with high reliability and adjustment was made for proxy respondent, province, age, smoking, alcohol, occupational silica and aromatic amine exposure. Results: Relative to unexposed men, elevated odds of bladder cancer were observed for men whose highest attained diesel exhaust exposure concentration was high (1.97, 1.08-3.58) and who spent more than 30% of time at work exposed to diesel (1.80, 1.02-3.15). A statistically significant trend in increased risk of bladder cancer was observed with increasing duration of exposure to medium/high concentrations of diesel exhaust (&gt;20 years, 1.82, 1.07-3.10, p-trend=0.002). We found no association between exposure to gasoline exhaust and bladder cancer. Conclusions: Our results suggest that occupational exposure to diesel exhaust increases bladder cancer risk in men, independent of smoking and other occupational exposures.

Anthropometric measures and bladder cancer risk: a prospective study in the EPIC cohort.

Anthropometric measures have been related to risk of several cancers. For bladder cancer, however, evidence is sparse. Comparability of existing studies is hampered by use of different obesity-measures, inadequate control for smoking, and few female cases. This study examined associations between height, weight, waist and hip circumference, waist-hip ratio, waist-height ratio, body mass index (BMI), recalled weight at age 20 and bladder cancer, and investigated effect modification by age, tumor aggressiveness and smoking. The study was conducted in the European Prospective Investigation into Cancer and Nutrition cohort, in 390,878 participants. Associations were calculated using Cox Proportional Hazards Models. During follow-up, 1,391 bladder cancers (1,018 male; 373 female) occurred. Height was unrelated to bladder cancer in both genders. We found a small but significant positive association with weight [1.04 (1.01-1.07) per 5 kilo], BMI [1.05 (1.02-1.08) per 2 units], waist circumference [1.04 (1.01-1.08) per 5 cm], waist-hip ratio (1.07 (1.02-1.13) per 0.05 unit] and waist-height ratio [1.07 (1.01-1.13) per 0.05 unit] in men. Stratification by smoking status confined associations in men to former smokers. In never smokers, we found no significant associations, suggesting residual confounding by smoking. Results did not differ with tumor aggressiveness and age. Residual analyses on BMI/waist circumference showed a significantly higher disease risk with BMI in men (p = 0.01), but no association with waist circumference. In conclusion, in this large study, height was unrelated to bladder cancer, whereas overweight was associated with a slightly higher bladder cancer risk in men. This association may, however, be distorted by residual confounding by smoking.

62 Occupational exposure to aromatic amines and polycyclic aromatic hydrocarbons and bladder cancer: Results from the EPIC cohort

ObjectivesExposure to aromatic amines (AA) has been strongly linked to bladder cancer. Also polycyclic aromatic hydrocarbons (PAH) have been associated with bladder cancer. Here we investigate the bladder cancer risk...

Understanding the Gender Disparity in Bladder Cancer Risk: The Impact of Sex Hormones and Liver on Bladder Susceptibility to Carcinogens

It has long been known that bladder cancer (BC) incidence is approximately four-fold higher in men than in women in the United States, and a similar disparity also exists in other countries. The reason for this phenomenon is not known, which impedes progress in BC prevention. However, BC incidence is also significantly higher in male animals than in their female counterparts after treatment with aromatic amines, which are principal human bladder carcinogens. These animal studies and related studies in the context of available human data provide significant insight into what may drive the excessive BC risk in men, which is the focus of this article. The carcinogenicity and biotransformation of bladder carcinogens as well as the impact of sex hormones on these processes are discussed, highlighting the novel concept that the gender disparity in BC risk may result primarily from the interplay of androgen, estrogen, and liver, with the liver functioning via its metabolic enzymes as the main decider of bladder exposure to carcinogens in the urine and the male and female hormones exerting opposing effects on carcinogenesis in the bladder and likely also on liver enzymes handling bladder carcinogens. The findings may facilitate further investigation into the mechanism of gender disparity in BC risk and may also have important implications for BC prevention.

Coffee, green tea, and caffeine consumption and subsequent risk of bladder cancer in relation to smoking status: a prospective study in Japan

Coffee and caffeine consumption are thought to increase the risk of bladder cancer. However, few studies have stratified this risk by smoking status, which is a potential confounder. Here, we investigated the association between coffee, green tea (another major source of caffeine), and caffeine, and bladder cancer incidence in relation to smoking status. We conducted a population-based prospective study in a cohort of Japanese, comprising a total of 49 566 men and 54 874 women aged 40–69 years who reported their coffee and green tea consumption at baseline. During follow-up from 1990 through 2005, 164 men and 42 women were newly diagnosed with bladder cancer. Cigarette smoking was associated with an increased risk of bladder cancer, with a strong dose–response relationship. Coffee was positively associated with bladder cancer risk in men, without statistical significance. When stratified by smoking status, coffee and caffeine consumption were associated with an increased risk of bladder cancer in never- or former-smoking men, with hazard ratios (95% confidence interval) in the highest categories of coffee (one or more cups per day) and caffeine consumption compared with the lowest of 2.24 (95% CI = 1.21–4.16) and 2.05 (95% CI = 1.15–3.66), respectively. In conclusion, cigarette smoking was confirmed as a risk factor for bladder cancer. Coffee and caffeine may be associated with an increased bladder cancer risk in never or former smokers among Japanese men.

Telomere Length, Cigarette Smoking, and Bladder Cancer Risk in Men and Women

Truncated telomeres are among the defining characteristics of most carcinomas. Given the role of telomeres in tumorigenesis, we reasoned that constitutionally short telomeres might be associated with an increased risk of bladder cancer. Using quantitative real-time PCR, we measured relative telomere length in bladder cancer cases and healthy controls and evaluated the association between telomere length, cigarette smoking, and bladder cancer risk in a case-control study nested within the Health Professionals Follow-up Study and a case-control study nested within the Nurses' Health Study. Telomeres were significantly shorter in bladder cancer cases (n = 184) than in controls (n = 192). The mean relative telomere length in cases was 0.23 (SD, 0.16) versus 0.27 (SD, 0.15) in controls (P = 0.001). The adjusted odds ratio for bladder cancer was 1.88 (95% confidence interval, 1.05, 3.36) for individuals in the quartile with the shortest telomeres as compared with individuals in the quartile with the longest telomeres (P(trend) = 0.006). We observed a statistically significant difference in telomere length among men and women (P < 0.001); however, the interaction between gender, telomere length, and bladder cancer risk was not significant. We also observed a significant difference in telomere length across categories of pack-years of smoking (P = 0.01). These findings suggest that truncated telomeres are associated with an increased risk of bladder cancer.

Polymorphisms in GSTT1, GSTM1, NAT1 and NAT2genes and bladder cancer risk in men and women

BackgroundCigarette smoking is an established risk factor for bladder cancer. Epidemiological and biological data suggest that genetic polymorphisms in activating and detoxifying enzymes may play a role in determining an individual's susceptibility to bladder cancer in particular when in combination with specific environmental exposures such as cigarette smoking. N-acetyltransferase (NAT) enzymes, NAT1 and NAT2, are involved in the activation and detoxification of tobacco smoke constituents. Polymorphisms in these genes alter the ability of these enzymes to metabolize carcinogens, as certain allelic combinations result in a slow or rapid acetylation phenotype. Glutathione S-transferases (GSTs) also detoxify tobacco smoke constituents, and polymorphisms within the GSTM1 and GSTT1 genes can result in a complete lack of enzyme activity.MethodsWe assessed the association between common polymorphisms identified in the GSTM1, GSTT1, NAT1, and NAT2 genes and the risk of bladder cancer in two nested case-control studies within the Nurses' Health Study (n = 78 female cases, 234 female controls) and the Health Professionals' Follow-up Study (n = 139 male cases, 293 male controls). We also evaluated whether cigarette smoking modified the associations of the genotypes and bladder cancer risk in men and women.ResultsOverall, we observed no statistically significant associations between the polymorphisms and bladder cancer risk among men and women, although given our sample size, we had limited power to detect small to moderate effects. There was however the suggestion of an increased risk among female ever smokers with the NAT2 slow genotype and an increased risk in male never smokers with the GSTM1 null genotype.ConclusionIn summary, these prospective results are consistent with previous literature supporting associations between bladder cancer and the NAT2 slow acetylation and the GSTM1 null genotypes.

The association between smoking, beverage consumption, diet and bladder cancer: a systematic literature review.

In this paper the association between smoking history, beverage consumption, diet and bladder cancer incidence is systematically reviewed. A rating system has been used to summarise the level of scientific evidence (i.e. convincing, probable, possible, and no evidence) and the level of association (i.e. substantially increased, (RR> or =2.5), moderately increased (1.5< or =RR<2.5), slightly increased (1.2< or =RR<1.5), no association (0.8< or =RR<1.2), slightly decreased (0.7< or =RR<0.8), moderately decreased (0.4< or =RR<0.7), and substantially decreased (RR<0.4)). There is convincing evidence that cigarette smoking status, frequency and duration substantially increase the risk of bladder cancer. However, the evidence is not clear for other forms of smoking. A small increased risk for cigar, pipe, and environmental smoking is only possible. There is possible evidence that total fluid intake is not associated with bladder cancer. Although there is convincing evidence for a positive association between alcohol consumption and bladder cancer risk in men, the risk is small and not clinically relevant. Coffee and tea consumption are probably not associated with bladder cancer. The authors conclude that total fruit consumption is probably associated with a small decrease in risk. There is probably no association between total vegetable intake, vitamin A intake, vitamin C intake and bladder cancer and a possibly moderate inverse association with vitamin E intake. Folate is possibly not associated with bladder cancer. There probably is a moderate inverse association between selenium intake and bladder cancer risk.

An association between NQO1 genetic polymorphism and risk of bladder cancer

NAD(P)H:quinone oxidoreductase (NQO1) is a detoxification enzyme that plays a critical role in protecting cells against chemically induced oxidative stress, cytotoxicity, mutagenicity, and carcinogenicity. NQO1 protects cells from oxidative damage by preventing the generation of reactive oxygen species and reducing certain environmental carcinogens, such as nitroaromatic compounds, heterocyclic amines, and possible cigarette smoke condensate. A C→T single nucleotide polymorphism in exon 6 was shown to reduce NQO1 enzyme activity, which may diminish the protection provided by NQO1. Therefore, we hypothesized that people with the variant allele genotypes of NQO1 are at higher risk for bladder cancer. In an ongoing case-control study, the NQO1 genotypes were successfully identified by polymerase chain reaction restriction fragment length polymorphism in 265 bladder cancer patients and 261 control subjects matched for age, sex, and ethnicity. The frequency of the variant NQO1 allele was 18% for controls and 21% for cases. The variant allele genotypes of NQO1 were associated with a higher risk of bladder cancer in Caucasians (odds ratio (OR)=1.51; 95% confidence interval (CI)=1.01–2.25). Further analysis in Caucasians showed an elevated bladder cancer risk in men (OR=1.75; 95% CI=1.08–2.85) but not in women (OR=1.16; 95% CI=0.57–2.37). In addition, the variant allele genotypes were associated with higher bladder cancer risk in ever smokers (OR=1.78; 95% CI=1.06–3.00), but not in never smokers (OR=1.19; 95% CI=0.65–2.20). These results suggest that the NQO1 genetic polymorphism modulates bladder cancer risk, especially in men and ever smokers.

Are coffee, tea, and total fluid consumption associated with bladder cancer risk? Results from the Netherlands Cohort Study.

Coffee, tea, and fluid consumption have been thought to influence bladder cancer incidence. In a large prospective study, these associations were investigated. In 1986, cohort members (55-69 years) completed a questionnaire on cancer risk factors. Follow-up was established by linkage to cancer registries until 1992. The multivariable case-cohort analysis was based on 569 bladder cancer cases and 3,123 subcohort members. The incidence rate ratios (RR) for men consuming <2 cups of coffee/day was 0.89 (95% CI 0.51-1.5) using the median consumption category (4-<5 cups/day) as reference. This RR increased to 1.3 (95% CI 0.94-1.9) for men consuming >7 cups/day, although no clear dose response association was found. The RRs decreased from 1.2 (95% CI 0.56-2.7) for women consuming <2 cups of coffee/day to 0.36 (95% CI 0.18-0.72) for women consuming >5 cups/day compared to the median consumption category (3-<4 cups/day). Men and women who abstained from drinking tea had a RR of 1.3 (95% Cl 0.97-1.8) compared to those consuming 2-<3 cups of tea per day (median consumption category). The RR for men and women comparing highest to lowest quintile of total fluid consumption was 0.87 (95% CI 0.63 1.2). The data suggest a possible positive association between coffee consumption and bladder cancer risk in men and a probable inverse association in women. Tea consumption was inversely associated with bladder cancer. Total fluid consumption did not appear to be associated with bladder cancer.

Foods and Nutrients in Relation to Bladder Cancer Risk: A Case-Control Study in Aichi Prefecture, Central Japan

To elucidate the role of diet in the etiology of bladder cancer, we conducted a case-control study from 1996 to 1999 in Aichi Prefecture, Central Japan. Cases were patients newly diagnosed with bladder cancer, and one hospital control was selected for each case, matching gender, age, and hospital. A well-validated food frequency questionnaire was adopted to estimate intakes of nutrients and food groups. Odds ratios (ORs) adjusted for smoking and occupational history were computed using conditional logistic models. The analyses based on 297 cases and 295 controls revealed the following. 1) The more the intake of milk and dairy products, the lower the OR; the ORs across quartiles in all subjects were 1.02, 0.73, and 0.52. Fruit intake was negatively associated with the risk, particularly in men (ORs across quartiles = 0.76, 0.77, and 0.52). Green-yellow vegetables were associated with a decreased risk in the highest quartile of consumption in men (OR = 0.57). 2) Dietary intakes of retinol and saturated fatty acids were related to a reduced risk in all subjects (ORs across quartiles = 0.75, 0.54, and 0.66 and 0.55, 0.54, and 0.60, respectively). Monounsaturated fatty acids had an inverse association with bladder cancer risk in men.