Case-control Study In Montreal Research Articles

Childhood body fatness and the risk of epithelial ovarian cancer: A population-based case-control study in Montreal, Canada

ObjectiveTo assess the association between childhood body fatness and epithelial ovarian cancer (EOC), and whether this association differs by type of EOC. MethodsUsing data from a population-based case-control study (497 cases and 902 controls) in Montreal, Canada conducted 2011–2016, we examined the association between childhood body fatness and EOC, overall and separately for invasive vs. borderline EOCs. A figure rating scale was used to measure body fatness at ages 5 and 10. Multivariable logistic regression was used to estimate adjusted odds ratios (aORs) and 95% confidence intervals (95% CI). Quantitative bias analyses were conducted to assess the impact of exposure misclassification and non-participation. ResultsThe aOR (95% CI) of overall EOC for high vs. low body fatness was 1.07 (0.85–1.34) at age 5 and 1.28 (0.98–1.68) at age 10. The associations were stronger for invasive EOC, specifically the endometrioid histological type. For borderline cancers, the aORs were below the null value with wide confidence intervals. Bias analyses did not reveal a strong influence of non-participation. Non-differential exposure misclassification may have biased aORs towards the null for invasive cancers but did not appear to have an appreciable influence on the aORs for borderline cancers. ConclusionsChildhood body fatness may be a risk factor for invasive EOC in later adult life. Our study highlights the potential importance of examining early life factors for a comprehensive understanding of EOC development.

Male-Pattern Vertex Baldness Trajectories, Chest Hair Patterns, and Odds of Overall and Aggressive Prostate Cancer.

The link between hormones and hair growth is well established. Inconsistent associations have been found between hair patterns and cancer of the prostate, a hormone-dependent organ. We assessed vertex baldness trajectories, chest hair amount, and their relationships with the odds of developing prostate cancer in a large case-control study in Montreal, Canada. In-person interviews were conducted with 1,931 incident prostate cancer cases and 1,994 population-based age-matched (±5 years) controls. Participants reported their hair patterns using the validated Hamilton-Norwood scale of baldness for 10-year increments starting at age 30, and their current amount of chest hair. Group-based trajectories were used to identify men sharing similar patterns of vertex baldness severity over adulthood. Multivariable logistic regression assessed associations between indicators of baldness (frontal, vertex, age at onset, severity, and trajectories), chest hair, and odds of prostate cancer. Vertex balding onset at age 30 was associated with increased odds of overall prostate cancer [Odds ratio (OR), 1.30; 95% confidence interval (CI), 1.03-1.64]. Men in the trajectory characterized by early moderate vertex baldness and developing severe baldness had increased odds of overall (OR, 1.42; 95% CI, 1.03-1.96) and especially aggressive prostate cancer (OR, 1.98; 95% CI, 1.21-3.22) compared with men without baldness. Men with little chest hair had higher odds of aggressive tumors than those with a moderate amount/a lot of chest hair. Early-onset moderate vertex baldness that progresses and having little chest hair may be useful biomarkers of aggressive prostate cancer. Integration of early-onset vertex balding patterns into risk prediction models of aggressive prostate cancer should be envisaged.

Neighbourhood social deprivation and risk of prostate cancer.

Striking geographic variations in prostate cancer incidence suggest an aetiological role for spatially-distributed factors. We assessed whether neighbourhood social deprivation, which can reflect limited social contacts, unfavourable lifestyle and environmental exposures, is associated with prostate cancer risk. In 2005-2012, we recruited 1931 incident prostate cancer cases and 1994 controls in a case-control study in Montreal, Canada. Lifetime residential addresses were linked to an area-based social deprivation index around recruitment (2006) and about 10 years earlier (1996). Logistic regression estimated adjusted odds ratios (ORs) and 95% confidence intervals (CIs). Men residing in areas characterised by greater social deprivation had elevated prostate cancer risks (ORs of 1.54 and 1.60 for recent and past exposures, respectively; highest vs lowest quintiles), independently from area- and individual-level confounders and screening patterns. The increase in risk with recent high social deprivation was particularly elevated for high-grade prostate cancer at diagnosis (OR 1.87, 95% CI 1.32-2.64). Associations were more pronounced for neighbourhoods with higher proportions of separated/divorced or widowed individuals in the past, and with higher percentages of residents living alone recently. These novel findings, suggesting that neighbourhood-level social deprivation increases the risk of prostate cancer, point out to potential targeted public health interventions.

Lifetime caffeine intake and the risk of epithelial ovarian cancer

BackgroundCaffeine intake has been inconsistently associated with the risk of ovarian cancer in previous studies. The measure of caffeine in these studies has not always distinguished between caffeinated and decaffeinated sources, and the time for which intake was assessed was often for late adulthood and thus may have excluded the etiologic window. We investigated lifetime caffeine intake from caffeinated coffee, black tea, green tea and cola sodas in relation to ovarian cancer risk. MethodsAmong 497 cases and 904 controls in a population-based case-control study in Montreal, Canada, lifetime intake of caffeinated coffee, black tea, green tea and cola sodas was assessed and used to calculate lifetime total intake of caffeine. Unconditional multivariable logistic regression was used to estimate odds ratios (ORs) with 95% confidence intervals (CIs) for the association between caffeine intake and ovarian cancer risk overall, as well as by menopausal status. Multivariable polytomous logistic regression was used to estimate the associations for invasive and borderline ovarian cancers separately. ResultsAlmost all participants (98.4% of cases and 97.5% of controls) had consumed caffeine in their lifetime. The mean (standard deviation) daily consumption of caffeine over the lifetime was of 117 (89) mg/day among cases and 120 (118) mg/day among controls. The OR (95% CI) of ovarian cancer for the highest versus lowest quartile of lifetime caffeine intake was 1.17 (0.83–1.64). According to menopausal status, the OR (95% CI) was 1.56 (0.85–2.86) for premenopausal women and 0.94 (0.66–1.34) for postmenopausal women, comparing the highest to lowest tertiles of intake. Associations for invasive and borderline ovarian cancers separately were similar to that observed for ovarian cancer overall. ConclusionLifetime caffeine intake was not strongly associated with ovarian cancer risk. A difference in relationship by menopausal status is possible.

General and abdominal obesity trajectories across adulthood, and risk of prostate cancer: results from the PROtEuS study, Montreal, Canada.

Greater body fatness is a probable cause of advanced prostate cancer (PCa). Body fat distribution and timing of exposure may be relevant. We investigated associations between body size trajectories and PCa incidence in a population-based case-control study in Montreal, Canada. Cases (n = 1,931), aged ≤ 75years, were diagnosed with PCa in 2005-2009; 1,994 controls were selected from the electoral list. Interviews were conducted to assess body mass index (BMI) and Stunkard's silhouette at ages 20, 40, 50, 60years, and before interview. Current waist and hip circumferences were measured, and a predictive model estimated waist circumference in the past. BMI and waist circumference trajectories were determined to identify subgroups. Logistic regression estimated odds ratios (OR) and 95% confidence intervals (CI) for the association between anthropometric indicators and PCa. Subjects with a current BMI ≥ 30kg/m2 had a lower risk of overall PCa (OR 0.71, 95% CI 0.59-0.85). Associations with adult BMI followed similar trends for less and more aggressive tumors, with stronger inverse relationships in early adulthood. Contrastingly, current waist circumference ≥ 102cm was associated with elevated risk of high-grade PCa (OR 1.33, 95% CI 1.03-1.71). Men with increasing BMI or waist circumference adult trajectories had a lower risk of PCa, especially low-grade, than those in the normal-stable range. This was especially evident among men in the obese-increase group for BMI and waist circumference. Abdominal obesity increased the risk of aggressive PCa. The inverse relationship between body size trajectories and PCa may reflect PSA hemodilution, lower detection, and/or a true etiological effect.

Dietary Patterns Are Associated with Risk of Prostate Cancer in a Population-Based Case-Control Study in Montreal, Canada.

This study describes the association between dietary patterns and prostate cancer (PCa) risk in a population-based case-control study conducted in Montreal, Canada (2005–2012). Cases (n = 1919) were histologically confirmed, aged ≤75 years. Concomitantly, controls (n = 1991) were randomly selected from the electoral list and frequency-matched to cases by age (±5 years). During face-to-face interviews, a 63-item food frequency questionnaire focusing on the two years before diagnosis/interview was administered. Three dietary patterns were identified from principal component analysis. Unconditional logistic regression estimated the association between dietary patterns and PCa, adjusting for age, ethnicity, education, family history, and timing of last PCa screening. When comparing scores in the highest vs. lowest quartiles, the Healthy Eating pattern was associated with a decreased risk of overall PCa (Odds ratio (OR) = 0.76, 95% confidence interval (CI) = 0.61, 0.93); this association was stronger for high-grade cancers (OR = 0.66, 95% CI = 0.48, 0.89). By contrast, the Western Sweet and Beverages pattern was associated with an elevated risk of overall PCa (OR = 1.35, 95% CI = 1.10, 1.66). The Western Salty and Alcohol pattern was not associated with PCa risk. These findings suggest that some dietary patterns influence PCa development.

Risk of lung cancer in relation to various metrics of smoking history: a case-control study in Montreal

BackgroundFew epidemiologic findings are as well established as the association between smoking and lung cancer. It is therefore somewhat surprising that there is not yet a clear consensus about the exposure-response relationships between various metrics of smoking and lung cancer risk. In part this is due to heterogeneity of how exposure-response results have been presented and the relative paucity of published results using any particular metric of exposure. The purposes of this study are: to provide new data on smoking-lung cancer associations and to explore the relative impact of different dimensions of smoking history on lung cancer risk.MethodsBased on a large lung cancer case-control study (1203 cases and 1513 controls) conducted in Montreal in 1996–2000, we estimated the lifetime prevalence of smoking and odds ratios in relation to several smoking metrics, both categorical and continuous based on multivariable unconditional logistic regression.ResultsOdds ratios (ORs) for ever vs never smoking were 7.82 among males and 11.76 among females. ORs increased sharply with every metric of smoking examined, more so for duration than for daily intensity. In models using continuous smoking variables, all metrics had strong effects on OR and mutual adjustment among smoking metrics did not noticeably attenuate the OR estimates, indicating that each metric carries some independent risk-related information. Among all the models tested, the one based on a smoking index that integrates several smoking dimensions, provided the best fitting model. Similar patterns were observed for the different histologic types of lung cancer.ConclusionsThis study provides many estimates of exposure-response relationships between smoking and lung cancer; these can be used in future meta-analyses. Irrespective of the histologic type of lung cancer and the smoking metric examined, high levels of smoking led to high levels of risk, for both men and women.

Investigating the effects of multiple exposure measures to traffic-related air pollution on the risk of breast and prostate cancer

Traffic-related nitrogen dioxide (NO2) has been traditionally estimated using surfaces generated through land-use regression (LUR). Recently, air pollution dispersion has been used to derive NO2 exposures in urban areas. There is evidence that data collection protocols and modelling assumptions can have a large effect on the resulting NO2 spatial distribution. This study investigates the effects of various NO2 surfaces on the risk estimates of postmenopausal breast cancer (BC) and prostate cancer (PC), both of which have already been associated with traffic-related air pollution. We derived exposures for individuals in two case control studies in Montreal, Canada using four different surfaces for NO2. Two of the surfaces were developed using LUR but employed different data collection protocols (LUR-1 and LUR-2), and the other two surfaces were generated using dispersion modelling; one with a regional model (dispersion-1) and another with a street canyon model (dispersion-2). Also, we estimated separate odds ratios (ORs) using concentrations of NO2 as measures of exposure for both cancers. While the range of NO2 concentrations from dispersion (4–26 ppb) was lower than the range from LUR (4–36 ppb), the four surfaces were found to be moderately correlated, with Spearman correlation coefficients ranging from 0.76 to 0.88. The ORs for BC were estimated to be 1.26, 1.10, 1.07, and 1.05 based on LUR-1, LUR-2, dispersion-1, and dispersion-2. In contrast, the ORs for PC were estimated to be 1.39, 1.30, 1.13, and 1.04 based on LUR-1, LUR-2, dispersion-1, and dispersion-2. The four exposure measures indicated positive associations but we observed higher mean ORs based on the LUR surfaces albeit with overlapping CIs. Since LUR models capture all sources of NO2 and dispersion models only capture traffic emissions, it is possible that this difference is due to the fact that non-road sources also contribute to the spatial distribution in NO2 concentrations.

Association between Occupational Exposure to Textile Fibre Dusts and Lung Cancer in a Population-Based Case-Control Study in Montreal: A Preliminary Analysis Comparing Results from Three Analytical Methods

Objectives: To compare results estimated using two causal inference methods, inverse probability of exposure weighting (IPEW) and G-computation, to that estimated using the conventional multivariable logistic regression, on the association between occupational exposure to textile fibre dusts and lung cancer risk.Methods: A population-based case-control study on lung cancer was conducted from 1996 to 2001 in Montreal, Canada. Cases were individuals diagnosed with incident lung cancer and population controls were randomly selected from electoral lists and frequency-matched to cases by age, sex and electoral district. Questionnaires on lifetime occupational history, smoking and demographic characteristics were collected during in-person interview. Experts reviewed subjects’ work history and assessed exposure to 294 agents, including textile fibre dusts. Odds ratios (OR) and their 95% confidence intervals (CIs) for the association between ever exposure to textile fibre dusts and lung cancer risk were estimated using three different methods: 1) IPEW, 2) G-computation, and 3) conventional multivariable regression.Results: The two causal inference methods produced higher point estimates (ORIPEW=1.17, 95% CI=0.86-1.57; ORG-computation=1.11, 95% CI=0.80-1.49) compared to that estimated using the conventional multivariable logistic regression (OR=0.87, 95% CI=0.68-1.11). However, all three sets of OR results were close to the null value.Conclusion: The different methods provided rather similar results, albeit not identical. They are compatible with a null association between occupational exposure to textile fibre dusts and lung cancer.

Predicting serum vitamin D concentrations based on self-reported lifestyle factors and personal attributes.

Evidence supports the role of vitamin D in various conditions of development and ageing. Serum 25-hydroxyvitamin D (25(OH)D) is the best indicator for current vitamin D status. However, the cost of its measurement can be prohibitive in epidemiological research. We developed and validated multivariable regression models that quantified the relationships between vitamin D determinants, measured through an in-person interview, and serum 25(OH)D concentrations. A total of 200 controls participating in a population-based case-control study in Montreal, Canada, provided a blood specimen and completed an in-person interview on socio-demographic, reproductive, medical and lifestyle characteristics and personal attributes. Serum 25(OH)D concentrations were quantified by liquid chromatography-tandem MS. Multivariable least squares regression was used to build models that predict 25(OH)D concentrations from interview responses. We assessed high-order effects, performed sensitivity analysis using the lasso method and conducted cross-validation of the prediction models. Prediction models were built for users and non-users of vitamin D supplements separately. Among users, alcohol intake, outdoor time, sun protection, dose of supplement use, menopausal status and recent vacation were predictive of 25(OH)D concentrations. Among non-users, BMI, sun sensitivity, season and recent vacation were predictive of 25(OH)D concentrations. In cross-validation, 46-47 % of the variation in 25(OH)D concentrations were explained by these predictors. In the absence of 25(OH)D measures, our study supports that predicted 25(OH)D scores may be used to assign exposure in epidemiological studies that examine vitamin D exposure.

Physical activity and lung cancer risk in men and women.

Although evidence has accumulated that recreational physical activities (PA) may reduce lung cancer risk, there is little evidence concerning the possible role of a potentially more important source of PA, namely occupational PA. We investigated both recreational and lifetime occupational PA in relation to lung cancer risk in a population-based case-control study in Montreal, Canada (NCASES = 727; NCONTROLS = 1,351). Unconditional logistic regression was used to estimate odds ratios (OR), separately for men and women, adjusting for smoking, exposure to occupational carcinogens, and sociodemographic and lifestyle factors. In both sexes, increasing recreational PA was associated with a lower lung cancer risk (ORMEN = 0.66, 95% confidence interval (CI) 0.47-0.92; ORWOMEN = 0.55, 95% CI 0.34-0.88, comparing the highest versus lowest tertiles). For occupational PA, no association was observed among women, while increasing occupational PA was associated with increased risk among men (ORMEN = 1.96, 95% CI 1.27-3.01). ORs were not modified by occupational lung carcinogen exposure, body mass index, and smoking level; results were similar across lung cancer histological types. Our results support the previous findings for recreational PA and lung cancer risk. Unexpectedly, our findings suggest a positive association for occupational PA; this requires replication and more detailed investigation.

Lifetime report of perceived stress at work and cancer among men: A case-control study in Montreal, Canada

BackgroundThe association between perceived workplace psychological stress, over the entire work career, and cancer among men has never been assessed. This was explored in the context of a population-based case-control study conducted in Montreal, Canada. Methods3103 incident cancer cases (11 types) diagnosed in 1979–1985 and 512 population controls were interviewed. Subjects described in detail each job held during their lifetime, including the occurrence of stress, and its reason. Logistic regression estimated odds ratios (OR) and 95% confidence intervals (CI) for the association between perceived workplace stress and its duration, and each cancer site, adjusting for lifestyle and occupational factors. ResultsEmployment in at least one stressful job was associated with increased odds of cancers of the lung (OR=1.33, 95% CI: 1.01–1.75), colon (OR=1.51, 95% CI: 1.15–1.98), bladder (OR=1.37, 95% CI: 1.03–1.81), rectal (OR=1.52, 95% CI: 1.10–2.10), and stomach (OR=1.53, 95% CI: 1.08–2.15). A duration-response trend was found for cancers of the lung, colon, rectum, stomach, and for NHL. Subjects reported changes in stress level over their career. Perceived stress was ascribed to several sources, including high demand and time pressure, financial issues, job insecurity, and hazardous conditions. ConclusionProlonged exposure to perceived stress at work was associated with greater odds of cancer at 5 out of 11 sites. While over reporting of stress by cases cannot be fully ruled out, these associations, if substantiated, would bear important public health significance. Prospective studies building on detailed stress assessment protocols considering all sources and changes over the career are necessary.

Residential greenness and risk of prostate cancer: A case-control study in Montreal, Canada

BackgroundRecent studies suggest that exposure to greenness favors several health outcomes. We assessed whether living in the proximity of greener areas was related to prostate cancer incidence in a population-based case-control study in Montreal, Canada. Materials and methodsInterviews eliciting lifetime addresses were conducted with 1933 prostate cancer cases diagnosed in 2005–2009 and 1994 population controls. Odds ratios (OR) and 95% confidence intervals (CI) estimated the association between residential greenness, both at recruitment (2005–2009) and about ten years prior (1996), defined by the normalized difference vegetation index (NDVI) around the home, and prostate cancer risk. Three models were developed adjusting for age, individual characteristics, and individual and ecological characteristics, estimating relative risk in relation to an interquartile range (IQR) increase of the NDVI. ResultsWe observed inverse associations between greenness measured within home buffers of 150m, 300m, 500m and 1000m, at both time points, and risk of prostate cancer, independently of individual and ecological characteristics. For instance, using a buffer of 300m, the OR for an IQR increase of 0.11 in NDVI at the time of recruitment was 0.82 (95%CI 0.74–0.92). The corresponding OR for an IQR increase of 0.15 in NDVI in 1996 was 0.86 (95%CI 0.74–1.00). There were little differences in risks according to buffer size, the time point of exposure, when considering prostate cancer aggressiveness, or when restricting controls to men recently screened for prostate cancer to reduce the likelihood of undiagnosed cancer among them. ConclusionMen living in greener areas, either recently or about a decade earlier, had lower risks of prostate cancer, independently of socio-demographic and lifestyle factors. These observations are novel and require confirmation.

Association between lifetime alcohol consumption and prostate cancer risk: A case-control study in Montreal, Canada

BackgroundAlcohol intake may increase the risk of prostate cancer (PCa). Many previous studies harbored important methodological limitations. MethodsWe conducted a population-based case-control study of PCa comprising 1933 cases and 1994 controls in Montreal, Canada. Lifetime alcohol consumption was elicited, by type of beverage, during in-person interviews. Odds ratios (OR) and 95% confidence intervals (CI) assessed the association between alcohol intake and PCa risk, adjusting for potential confounders and considering the subjects’ PCa screening history. ResultsWe observed a weak, non-significant positive association between high consumption of total alcohol over the lifetime and risk of high-grade PCa (OR=1.18, 95% CI 0.81–1.73). Risk estimates were more pronounced among current drinkers (OR=1.40, 95%CI 1.00–1.97), particularly after adjusting for the timing of last PCa screening (OR=1.52, 95%CI 1.07–2.16). These associations were largely driven by beer consumption. The OR for high-grade PCa associated with high beer intake was 1.37 (95%CI 1.00–1.89); it was 1.49 (95%CI 0.99–2.23) among current drinkers and 1.68 (95% CI 1.10–2.57) after adjusting for screening recency. High cumulative consumption of spirits was associated with a lower risk of low-grade PCa (OR=0.75, 95%CI 0.60–0.94) but the risk estimate no longer achieved statistical significance when restricting to current users. No association was found for wine consumption. ConclusionFindings add to the accumulating evidence that high alcohol consumption increases the risk of high-grade PCa. This association largely reflected beer intake in our population, and was strengthened when taking into account PCa screening history.

Metabolic syndrome and prostate cancer risk in a population-based case-control study in Montreal, Canada.

BackgroundThe role of metabolic syndrome (MetS) in prostate cancer risk is still debated. We investigated it in a large population-based case–control study.MethodsCases were 1937 men with incident prostate cancer, aged ≤75 years, diagnosed across French hospitals in the Montreal area between 2005 and 2009. Concurrently, 1995 population controls from the same residential area and age distribution were randomly selected from electoral list of French-speaking men. Detailed lifestyle and medical histories, and anthropometric measures, were collected during in-person interviews. Prevalence of MetS components (type 2 diabetes, high blood pressure, dyslipidemia and abdominal obesity) was estimated at 2 years before diagnosis for cases/ interview for controls, and at ages 20, 40, 50 and 60. Logistic regression was used to estimate odds ratios (OR) and 95 % confidence intervals for the association between MetS and prostate cancer risk.ResultsA history of MetS (≥3 components vs <3) was associated with a reduced risk of prostate cancer (OR = 0.70 [0.60, 0.82]) after considering potential confounders. The negative association was particularly pronounced with a young age (≤40 years) at MetS onset (OR = 0.38 [0.16-0.89]), did not vary according to prostate cancer aggressiveness, and was only partly explained by the presence of type 2 diabetes. A risk decrease was observed with the number of MetS components, suggesting a synergistic interaction of the components.DiscussionThe observed negative association, consistent with results from other North American populations undergoing regular prostate cancer screening, underlines the importance of considering PSA-testing when studying the MetS-prostate cancer association.ConclusionsFindings from this study are consistent with an inverse association between MetS and prostate cancer risk.

Occupational exposure to wood dust and risk of lung cancer in two population-based case-control studies in Montreal, Canada.

BackgroundWood dust is one of the oldest and one of the most common occupational exposures in the world. The present analyses examine the effect of lifetime exposure to wood dust in diverse occupational settings on lung cancer risk.MethodsWe conducted two population-based case–control studies in Montreal: Study I (1979–1986) included 857 cases and two sets of controls (533 population and 1349 cancer controls), and Study II (1996–2001) comprised 736 cases and 894 population controls. Detailed job histories were obtained by interview and each job was evaluated by expert chemist–hygienists to estimate the likelihood and level of exposure to many substances, one of which was wood dust. Odds ratios (ORs) were computed in relation to different indices of exposure to wood dust, adjusting for several covariates including smoking. Three datasets were analysed: Study I with population controls, Study I with cancer controls, and Study II.ResultsThe most frequently exposed occupations in our study population were in construction, timber and furniture making industries. We found increased risks of lung cancer for substantial cumulative exposure to wood dust in Study I with cancer controls, (OR = 1.4: 95% confidence interval 1.0;-2.0) and in Study II (OR = 1.7: 95% confidence interval 1.1-2.7). There were no excess risks of lung cancer in any of the three datasets among workers whose cumulative exposure was not substantial. These tendencies held equally within strata of low smokers and heavy smokers.ConclusionThere was evidence of increased risk of lung cancer among workers with substantial cumulative exposure to wood dust.Electronic supplementary materialThe online version of this article (doi:10.1186/1476-069X-14-1) contains supplementary material, which is available to authorized users.

0238 Lung cancer and exposure to benzene, toluene and xylene: results from two case-control studies in Montreal

ObjectivesWe aimed to evaluate the risks of lung cancer associated with exposure to benzene, to toluene and to xylene.MethodTwo population-based case-control studies conducted in Montreal included 1896 lung cancer cases...

Occupational exposure to lead and lung cancer: results from two case-control studies in Montreal, Canada

ObjectivesWe investigated the association between workplace lead exposure and lung cancer risk, separately for organic lead and for inorganic lead, from either engine emissions or from other sources.MethodsTwo population-based case-control...

The Risk of Lung Cancer Related to Dietary Intake of Flavonoids

It has been hypothesized that flavonoids in foods and beverages may reduce cancer risk through antioxidation, inhibition of inflammation, and other antimutagenic and antiproliferative properties. We examined associations between intake of 5 flavonoid subclasses (anthocyanidins, flavan-3-ols, flavones, flavonols, and flavanones) and lung cancer risk in a population-based case-control study in Montreal, Canada (1061 cases and 1425 controls). Flavonoid intake was estimated from a food frequency questionnaire that assessed diet 2 yr prior to diagnosis (cases) or interview (controls). Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression. Overall, total flavonoid intake was not associated with lung cancer risk, the effect being similar regardless of sex and smoking level. However, low flavonoid intake from food, but not from beverages, was associated with an increased risk. The adjusted ORs (95% CIs) comparing the highest vs. the lowest quartiles of intake were 0.63 (0.47–0.85) for total flavonoids, 0.82 (0.61–1.11) for anthocyanidins, 0.67 (0.50–0.90) for flavan-3-ols, 0.68 (0.50–0.93) for flavones, 0.62 (0.45–0.84) for flavonols, and 0.70 (0.53–0.94) for flavanones. An inverse association with total flavone and flavanone intake was observed for squamous cell carcinoma but not adenocarcinoma. In conclusion, low flavonoid intake from food may increase lung cancer risk.

Exposure to welding fumes increases lung cancer risk among light smokers but not among heavy smokers: evidence from two case-control studies in Montreal.

We investigated relationships between occupational exposure to gas and arc welding fumes and the risk of lung cancer among workers exposed to these agents throughout the spectrum of industries. Two population-based case–control studies were conducted in Montreal. Study I (1979–1986) included 857 cases and 1066 controls, and Study II (1996–2001) comprised 736 cases and 894 controls. Detailed job histories were obtained by interview and evaluated by an expert team of chemist–hygienists to estimate degree of exposure to approximately 300 substances for each job. Gas and arc welding fumes were among the agents evaluated. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) of lung cancer using logistic regression, adjusting for smoking history and other covariates. The two studies provided similar results, so a pooled analysis was conducted. Among all subjects, no significant association was found between lung cancer and gas welding fumes (OR = 1.1; 95% CI = 0.9–1.4) or arc welding fumes (OR = 1.0; 95% CI = 0.8–1.2). However, when restricting attention to light smokers, there was an increased risk of lung cancer in relation to gas welding fumes (OR = 2.9; 95% CI = 1.7–4.8) and arc welding fumes (OR = 2.3; 95% CI = 1.3–3.8), with even higher OR estimates among workers with the highest cumulative exposures. In conclusion, there was no detectable excess risk of lung cancer due to welding fumes among moderate to heavy smokers; but among light smokers we found an excess risk related to both types of welding fumes.