Risk of lung cancer among women in relation to lifetime history of tobacco smoking: a population-based case-control study in France (the WELCA study).

BACKGROUND: This study aims to provide new insights on the role of smoking patterns and cigarette dependence in female lung cancer, and to examine differences by histological subtype. METHODS: We conducted a population-based case-control study in the great Paris area among women including 716 incident cases diagnosed between 2014 and 2017 and 757 age-matched controls. Detailed data on smoking history was collected during in-person interviews to assess intensity and duration of tobacco smoking, time since cessation, smoking habits (depth of smoke inhalation, use of filter, type of tobacco, and type of cigarettes) and Fagerström test for cigarette dependence. The comprehensive smoking index (CSI), a score modelling the combined effects of intensity, duration and time since quitting smoking was determined for each subject. Multivariable logistic regression models were fitted to calculate odds ratios (ORs) and their confidence intervals (95%CI) of lung cancer associated with smoking variables. RESULTS: Lung cancer risk increased linearly with intensity and duration of tobacco smoking while it decreased with time since cessation, to reach the risk in never-smokers after 20 years of abstinence. The combined effect of intensity and duration of tobacco smoking was more than multiplicative (p-interaction 0.012). The OR in the highest vs the lowest quartile of CSI was 12.64 (95%CI 8.50; 18.80) (p-trend < 0.001). The risk of small cell or squamous cell carcinomas increased with the CSI more sharply than the risk of adenocarcinomas. Deep smoke inhalation, dark vs blond tobacco, conventional vs light cigarettes, and unfiltered vs filtered cigarettes, as well as having mixed smoking habits, were found to be independent risk factors. Having high cigarette addiction behaviours also increased the risk after adjusting for CSI. CONCLUSION: This study provides additional insights on the effects of tobacco smoking patterns on lung cancer risk among women.

Circadian genes polymorphisms, night work and prostate cancer risk: Findings from the EPICAP study.

Over the past two decades, several studies have attempted to understand the hypothesis that disrupting the circadian rhythm may promote the development of cancer. Some have suggested that night work and some circadian genes polymorphisms are associated with cancer, including prostate cancer. Our study aims to test the hypothesis that prostate cancer risk among night workers may be modulated by genetic polymorphisms in the circadian pathway genes based on data from the EPICAP study, a population-based case-control study including 1511 men (732 cases/779 controls) with genotyped data. We estimated odds ratio (ORs) and P values of the association between prostate cancer and circadian gene variants using logistic regression models. We tested the interaction between circadian genes variants and night work indicators that were significantly associated with prostate cancer at pathway, gene and SNP levels. Analyses were also stratified by each of these night work indicators and by cancer aggressiveness. The circadian pathway was significantly associated with aggressive prostate cancer among night workers (P = .004), particularly for men who worked at night for <20 years (P = .0002) and those who performed long night shift (>10 hours, P = .001). At the gene level, we observed among night workers significant associations between aggressive prostate cancer and ARNTL, NPAS2 and RORA. At the SNP-level, no significant association was observed. Our findings provide some clues of a potential modulating effect of circadian genes in the relationship between night work and prostate cancer. Further investigation is warranted to confirm these findings and to better elucidate the biological pathways involved.

Circadian genes and risk of prostate cancer: Findings from the EPICAP study.

Circadian rhythms regulate several physiological functions and genes controlling the circadian rhythm were found to regulate cell proliferation, cell cycle and apoptosis. Few studies have investigated the role of those circadian genes in prostate cancer occurrence. We aim to investigate the relationship between circadian genes polymorphisms and prostate cancer risk based on data from the EPICAP study, a population-based case-control study including 1,515 men (732 cases / 783 controls) with genotyped data. Odds Ratios (ORs) for association between prostate cancer and circadian gene variants were estimated for each of the 872 single nucleotide polymorphisms (SNPs) in 31 circadian clock genes. We also used a gene-based and pathway-based approach with a focus on the pathway including 9 core circadian genes. Separate analyses were conducted by prostate cancer aggressiveness. The core-circadian pathway (p = 0.0006) was significantly associated to prostate cancer, for either low (p = 0.002) or high (p = 0.01) grade tumor. At the gene level, we observed significant associations between all prostate cancer and NPAS2 and PER1 after correcting for multiple testing, while only RORA was significant for aggressive tumors. At the SNP-level, no significant association was observed. Our findings provide additional evidence of a potential link between genetic variants in circadian genes and prostate cancer risk. Further investigation is warranted to confirm these findings and to better understand the biological pathways involved.

Occupational exposure to wood dust and risk of lung cancer: the ICARE study.

OBJECTIVES: In a previous analysis of data from a French population-based case-control study (the Investigation of occupational and environmental CAuses of REspiratory cancers (ICARE) study), 'having ever worked' in wood-related occupations was associated with excess lung cancer risk after adjusting for smoking but not for occupational factors. The present study aimed to investigate the relationship between lung cancer risk and wood dust exposure after adjusting for occupational exposures. METHODS: Data were obtained from 2276 cases and 2780 controls on smoking habits and lifelong occupational history, using a standardised questionnaire with a job-specific questionnaire for wood dust exposure. Logistic regression models were used to calculate ORs and 95% CIs adjusted for age, area of residence, tobacco smoking, the number of job periods and exposure to silica, asbestos and diesel motor exhaust (DME). RESULTS: No significant association was found between lung cancer and wood dust exposure after adjustment for smoking, asbestos, silica and DME exposures. The risk of lung cancer was slightly increased among those who were exposed to wood dust more than 10 years, and had over 40 years since the first exposure. CONCLUSION: Our findings do not provide a strong support to the hypothesis that wood dust exposure is a risk factor for lung cancer. This study showed the importance of taking into account smoking and occupational coexposures in studies on lung cancer and wood dust exposure. Further studies evaluating the level and frequency of exposure during various tasks in woodwork are needed.

Prostatitis, other genitourinary infections and prostate cancer risk: Influence of non-steroidal anti-inflammatory drugs? Results from the EPICAP study.

Epidemiological studies have suggested that prostatitis may increase the risk of prostate cancer due to chronic inflammation. We studied the association between several genitourinary infections and the risk of prostate cancer based on data from the EPICAP study. EPICAP is a population-based case-control study conducted in the département of Hérault, France, between 2012 and 2014. A total of 819 incident cases and 879 controls have been face to face interviewed using a standardized questionnaire gathering information on known or suspected risk factors of prostate cancer, and personal history of genitourinary infections: prostatitis, urethritis, orchi-epididymitis, and acute pyelonephritis. Odds Ratios (OR) and their 95% confidence interval were estimated using multivariate unconditional logistic regression. Overall, 139 (18%) cases and 98 (12%) controls reported having at least one personal history of genitourinary infections (OR = 1.64 [1.23-2.20]). The risk increased with the number of infections (p-trend < 0.05). The association was specifically observed with personal history of chronic prostatitis and acute pyelonephritis (OR = 2.95 [1.26-6.92] and OR = 2.66 [1.29-5.51], respectively) and in men who did not use any non-steroidal anti-inflammatory drugs (OR = 2.00 [1.37-2.91]). Our results reinforce the hypothesis that chronic inflammation, generated by a personal history of genitourinary infections, may play a role in prostate carcinogenesis.

Night work and prostate cancer risk: results from the EPICAP Study.

OBJECTIVE: To investigate the role of night work in prostate cancer based on data from the EPICAP Study. METHODS: EPICAP is a French population-based case-control study including 818 incident prostate cancer cases and 875 frequency-matched controls that have been interviewed face to face on several potential risk factors including lifetime occupational history. Detailed information on work schedules for each job (permanent or rotating night work, duration, total number of nights, length of the shift, number of consecutive nights) as well as sleep duration and chronotype, was gathered. Prostate cancer aggressiveness was assessed by Gleason Score. RESULTS: Night work was not associated with prostate cancer, whatever the aggressiveness of prostate cancer, while we observed an overall increased risk among men with an evening chronotype (OR=1.83, 95% CI 1.05 to 3.19). A long duration of at least 20 years of permanent night work was associated with aggressive prostate cancer (OR=1.76, 95% CI 1.13 to 2.75), even more pronounced in combination with a shift length >10 hours or ≥ 6 consecutive nights (OR=4.64, 95% CI 1.78 to 12.13; OR=2.43, 95% CI 1.32 to 4.47, respectively). CONCLUSION: Overall, ever night work, either permanent or rotating, was not associated to prostate cancer. Nevertheless, our results suggest that a long duration of permanent night work in combination with a long shift length or at least six consecutive nights may be associated with prostate cancer, particularly with aggressive prostate cancer. Further studies are needed to confirm those findings.

Occupational exposure to textile dust and lung cancer risk: Results from the ICARE Study.

BACKGROUND: To investigate the association of lung cancer with occupational exposure to textile dust and specifically to cotton dust in the population-based case-control study ICARE. METHODS: Lifelong occupational history of 2926 cases and 3555 controls was collected using standardized questionnaires, with specific questions for textile dust exposure. Odds ratios (ORs) and 95% confidence intervals (CI) were estimated using unconditional logistic regression models controlling for confounding factors including smoking and asbestos exposure. RESULTS: An inverse association between textile dust exposure and lung cancer was found among workers exposed ≥5% of their work time (OR = 0.80, 95%CI = 0.58-1.09), more pronounced for distant exposures (40+ years; up to a 56% reduced risk, statistically significant). The OR of lung cancer was significantly decreased among workers exposed to cotton fibers (OR = 0.70, 95%CI = 0.48-0.97). CONCLUSIONS: Our results provide some evidence of a decreased risk of lung cancer associated with exposure to textile dust, particularly cotton.

Occupational exposure to endotoxins and lung cancer risk: results of the ICARE Study.

OBJECTIVES: To investigate the role of occupational exposure to endotoxins in lung cancer in a French population-based case-control study (ICARE (Investigation of occupational and environmental causes of respiratory cancers)). METHODS: Detailed information was collected on the occupational history and smoking habits from 2926 patients with histologically confirmed lung cancer and 3555 matched controls. We evaluated each subject's endotoxin exposure after cross referencing International Standard Classification of Occupations (ISCO) codes (for job tasks) and Nomenclature d'Activités Françaises (NAF) codes (for activity sectors). Endotoxin exposure levels were attributed to each work environment based on literature reports. ORs and 95% CIs were estimated using unconditional logistic regression models and controlled for main confounding factors. RESULTS: An inverse association between exposure to endotoxins and lung cancer was found (OR=0.80, 95% CI 0.66 to 0.95). Negative trends were shown with duration and cumulative exposure, and the risk was decreased decades after exposure cessation (all statistically significant). Lung cancer risk was particularly reduced among workers highly exposed (eg, in dairy, cattle, poultry, pig farms), but also in those weakly exposed (eg, in waste treatment). Statistically significant interactions were shown with smoking, and never/light smokers were more sensitive to an endotoxin effect than heavy smokers (eg, OR=0.14, 95% CI 0.06 to 0.32 and OR=0.80, 95% CI 0.45 to 1.40, respectively, for the quartiles with the highest cumulative exposure, compared with those never exposed). Pronounced inverse associations were shown with adenocarcinoma histological subtype (OR=0.37, 95% CI 0.25 to 0.55 in the highly exposed). CONCLUSIONS: Our findings suggest that exposure to endotoxins, even at a low level, reduces the risk of lung cancer.

The joint effect of asbestos exposure, tobacco smoking and alcohol drinking on laryngeal cancer risk: evidence from the French population-based case-control study, ICARE.

OBJECTIVE: The objective of the study was to investigate the joint effect of occupational exposure to asbestos, and tobacco and alcohol consumption, on the risk of laryngeal cancer among men. METHODS: We used data from a large population-based case-control study conducted in France. We estimated two-way and three-way interactions between asbestos exposure (never vs ever exposed), tobacco consumption (<20 vs. ≥20 pack-years) and alcohol consumption (<5 vs. ≥5 drinks per day). The interaction on an additive scale was assessed by estimating the relative excess risk due to interaction (RERI) and the attributable proportion due to interaction, and the interaction on a multiplicative scale was assessed by estimating the multiplicative interaction parameter (ψ). Multiplicative interactions were also assessed using fractional polynomials for alcohol drinking, tobacco smoking and asbestos exposure. RESULTS: When compared with light-to-moderate smokers and drinkers never exposed to asbestos, the increase in laryngeal cancer risk was smallest among light-to-moderate drinkers and smokers exposed to asbestos (OR=2.23 (1.08 to 4.60)), and highest among heavy smokers and drinkers ever exposed to asbestos (OR=69.39 (35.54 to 135.5)). We found an additive joint effect between asbestos exposure and alcohol consumption (RERI=4.75 (-4.29 to 11.12)), whereas we observed a more than additive joint effect between asbestos exposure and tobacco consumption (RERI=8.50 (0.71 to 23.81)), as well as between asbestos exposure, and tobacco and alcohol consumption (RERI=26.57 (11.52 to 67.88)). However, our results did not suggest any interaction on a multiplicative scale. CONCLUSIONS: Our results suggest that asbestos exposure, in combination with tobacco and alcohol exposure, accounted for a substantial number of laryngeal cancer cases. Our findings therefore highlight the need for prevention in activities, such as construction work, where exposure to asbestos-containing materials remains.

Multidimensional analysis of the effect of occupational exposure to organic solvents on lung cancer risk: the ICARE study.

BACKGROUND: The association between lung cancer and occupational exposure to organic solvents is discussed. Since different solvents are often used simultaneously, it is difficult to assess the role of individual substances. OBJECTIVES: The present study is focused on an in-depth investigation of the potential association between lung cancer risk and occupational exposure to a large group of organic solvents, taking into account the well-known risk factors for lung cancer, tobacco smoking and occupational exposure to asbestos. METHODS: We analysed data from the Investigation of occupational and environmental causes of respiratory cancers (ICARE) study, a large French population-based case-control study, set up between 2001 and 2007. A total of 2276 male cases and 2780 male controls were interviewed, and long-life occupational history was collected. In order to overcome the analytical difficulties created by multiple correlated exposures, we carried out a novel type of analysis based on Bayesian profile regression. RESULTS: After analysis with conventional logistic regression methods, none of the 11 solvents examined were associated with lung cancer risk. Through a profile regression approach, we did not observe any significant association between solvent exposure and lung cancer. However, we identified clusters at high risk that are related to occupations known to be at risk of developing lung cancer, such as painters. CONCLUSIONS: Organic solvents do not appear to be substantial contributors to the occupational risk of lung cancer for the occupations known to be at risk.

Welding, a risk factor of lung cancer: the ICARE study.

OBJECTIVES: We investigated the relationship between lung cancer and occupational exposure to welding activity in ICARE, a population-based case-control study. METHODS: Analyses were restricted to men (2276 cases, 2780 controls). Welding exposure was assessed through detailed questionnaires, including lifelong occupational history. ORs were computed using unconditional logistic regression, adjusted for lifelong cigarette smoking and occupational exposure to asbestos. RESULTS: Among the regular welders, welding was associated with a risk of lung cancer (OR=1.7, 95% CI 1.1 to 2.5), which increased with the duration (OR=2.0, 95% CI 1.0 to 3.9 when duration >10 years), and was maximum 10-20 years since last welding. The risk was more pronounced in case of gas welding (OR=2.0, 95% CI 1.2 to 3.3), when the workpiece was covered by paint, grease, or other substances (OR=2.0, 95% CI 1.2 to 3.4) and when it was cleaned with chemical substances before welding. No statistically significant increase in lung cancer risk was observed among occasional welders. CONCLUSIONS: Although these results should be confirmed, we showed that type of welding and mode of workpiece preparation are important determinants of the lung cancer risk in regular welders.

Exposure to chlorinated solvents and lung cancer: results of the ICARE study.

OBJECTIVE: To investigate the role of occupational exposure to chlorinated solvents in lung cancer aetiology. METHODS: ICARE (Investigation of occupational and environmental CAuses of REspiratory cancers) is a French, multicentre, population-based, case-control study. Information on the lifelong work history of 2926 cases and 3555 controls was collected using standardised questionnaires. Occupational exposures were assessed using job-exposure matrices for five chlorinated solvents. Solvents were studied separately and in combinations. ORs were computed using unconditional logistic regression models adjusted for classic risk factors, including a history of cigarette smoking and exposure to asbestos. Adjustment for socioeconomic status (SES) was also made. RESULTS: After adjustment for exposure to asbestos, we observed a positive, statistically significant association with lung cancer for men and women exposed to a combination of perchloroethylene (PCE), trichloroethylene and dichloromethane (DCM). Further adjustment for SES slightly decreased this association. In contrast, no statistically significant associations were found for other solvent combinations. CONCLUSIONS: These results suggest that exposure to PCE may constitute a risk factor for lung cancer, especially among women, who seem to have a higher prevalence of exposure than men.

Occupation and head and neck cancer in women-Results of the ICARE study.

BACKGROUND: Few occupational studies have addressed head and neck cancer, and these studies have been predominantly conducted in men. Accordingly, our objective was to investigate the association between head and neck cancer and occupation in women. METHODS: ICARE, a French population-based case-control study, included 296 squamous cell carcinomas of the head and neck in women and 775 controls. Lifelong occupational history was collected. Odds ratios (ORs) and 95% confidence intervals (CI), adjusted for smoking, alcohol drinking and education level, were estimated for occupations and industries. RESULTS: An elevated OR was observed for working proprietors working for 10 years or more (OR = 3.83, 95% CI: 1.12-13.0) with a significant trend with duration of employment (P = 0.047). Elevated but non-significant ORs were observed for street vendors (OR = 3.76, 95% CI: 0.99-14.3, P for trend = 0.13), bakers (OR = 4.19, 95% CI: 0.63-27.9, P for trend = 0.06), and welders and flame cutters (OR = 2.18, 95% CI: 0.33-14.4, P for trend = 0.05). CONCLUSIONS: This exploratory study suggests a role of occupational exposures in the development of HN cancer in women. Further investigations of exposures to specific agents are needed.

Body mass index, body mass change, and risk of oral cavity cancer: results of a large population-based case-control study, the ICARE study.

OBJECTIVE: The association between body mass index (BMI) and the risk of oral cavity cancer, suggested by the few available studies, is controversial because of weight loss preceding cancer diagnosis and possible confounding by tobacco and alcohol consumption. The aim of this study was to evaluate in France, a high-incidence country, the association between the risk of oral cavity cancer and body mass index at interview, 2 years before the interview and at age 30, as well as BMI change. METHODS: We used data from a population-based case-control study, the Investigation of occupational and environmental CAuses of REspiratory cancers study, with personal interviews and standardized questionnaires including 689 cases of oral cavity squamous cell carcinoma and 3,481 controls. Odds ratios (ORs) and 95% confidence intervals (95% CI) were estimated by unconditional logistic regression and were adjusted for gender, age, area of residence, education, tobacco smoking, and alcohol drinking. RESULTS: ORs were increased in underweight subjects at interview (OR 6.25, 95% CI 3.74-10.45). No association with underweight 2 years before the interview and at age 30 was found. Overweight and obesity at interview, 2 years before the interview and at age 30 were associated with decreased ORs (ranging from 0.13 to 0.60). BMI gain greater than 5% between age 30 and 2 years before the interview was inversely associated with oral cavity cancer (OR 0.42, 95% CI 0.33-0.54). These associations were stronger in men, and in smokers and drinkers. CONCLUSION: These results add further support to the existence of a reduced risk of oral cavity cancer among overweight and obese people or among people who increased their BMI in adulthood. The underlying mechanisms remain to be clarified.

Family history of cancer, personal history of medical conditions and risk of oral cavity cancer in France: the ICARE study.

BACKGROUND: The aim of this study was to evaluate the role of family history of cancer and personal history of other medical conditions in the aetiology of the oral cavity cancer in France. METHODS: We used data from 689 cases of oral cavity squamous cell carcinoma and 3481 controls included in a population-based case-control study, the ICARE study. Odds-ratios (ORs) associated with family history of cancer and personal medical conditions and their 95% confidence intervals (95% CI) were estimated by unconditional logistic regression and were adjusted for age, gender, area of residence, education, body mass index, tobacco smoking and alcohol drinking. RESULTS: Personal history of oral candidiasis was related to a significantly increased risk of oral cavity cancer (OR 5.0, 95% CI 2.1-12.1). History of head and neck cancers among the first-degree relatives was associated with an OR of 1.9 (95% CI 1.2-2.8). The risk increased with the number of first-degree relatives with head and neck cancer. CONCLUSION: A family history of head and neck cancer is a marker of an increased risk of oral cavity cancer and should be taken into account to target prevention efforts and screening. Further studies are needed to clarify the association between oral cavity cancer and personal history of candidiasis.

Body mass index and lung cancer risk: results from the ICARE study, a large, population-based case-control study.

BACKGROUND: The association between body mass index (BMI) and lung cancer is still disputed because of possible residual confounding by smoking and preclinical weight loss in case-control studies. We examined this association using data from the multicenter ICARE study in France, a large, population-based case-control study. METHODS: A total of 2,625 incident lung cancer cases and 3,381 controls were included. Weight was collected at interview, 2 years before the interview, and at age 30. Lifetime smoking exposure was calculated using the comprehensive smoking index (CSI). Adjusted odds ratios (aORs) and 95 % confidence intervals were estimated by unconditional logistic regression and controlled for age, area, education, CSI, occupational exposure, previous chronic bronchitis, and parental history of lung cancer. We also examined the role of weight change. Analyses were stratified by smoking status and sex. RESULTS: When compared with that of men with normal BMI 2 years before the interview, lung cancer aORs (95 % CI) among men with BMIs of <18.5, 25-29.9, 30-32.4, and ≥32.5 kg/m(2) were 2.7 (95 % CI 1.2-6.2), 0.9 (95 % CI 0.7-1.1), 0.8 (95 % CI 0.6-1.1), and 0.8 (95 % CI 0.6-1.0), respectively (p(trend) = 0.02). Results were more pronounced among current smokers and were similar in men and women. Weight gain over time was associated with a significant decreased risk of lung cancer. CONCLUSIONS: We found an inverse dose-dependent association between lung cancer risk and BMI 2 years prior to interview in current smokers. IMPACT STATEMENT: BMI might be an individual factor impacting the risk of lung cancer related to smoking's carcinogen-induced DNA damage.

Diabetes, metabolic syndrome and prostate cancer risk: Results from the EPICAP case-control study.

BACKGROUND: Diabetes may be associated with decreased prostate cancer (PCa) risk. However, previous studies have not always accounted for time since diabetes diagnosis or antidiabetic drug use. Futhermore, the role of metabolic syndrome (MetS) in PCa risk is still debated. We investigated the role of diabetes and MetS in PCa risk based on data from the Epidemiological study of PCa (EPICAP). METHODS: EPICAP is a population-based case-control study that included 819 incident PCa cases in 2012-2013 and 879 controls frequency matched by age. MetS was characterized according to National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III). Logistic regression models adjusted for age, family history of PCa and ethnicity, were used to assess odds ratios (ORs) and their 95%conficence intervals (CIs) for the associations between diabetes, MetS and PCa risk. RESULTS: Whereas we did not observed an association between diabetes and PCa, a decreased risk of PCa has been highlighted with an increasing treated diabetes duration (p-trend=0.008). No association has been observed between MetS, the number of MetS criteria and the risk of PCa. However, we suggested that NSAIDs use could modify the association between MetS and PCa risk. CONCLUSION: Our results suggest an inverse association between the duration of diabetes and PCa risk. The role of metabolic factors, such as MetS and its components, in PCa risk remains unclear and requires further investigations.

Occupation and prostate Cancer risk: results from the epidemiological study of prostate cancer (EPICAP).

BACKGROUND: Although prostate cancer (PCa) is the most frequent male cancer in industrialized countries, little is known about its aetiology. The literature has suggested an influence of the environment, including occupational exposures, but results are inconsistent. In this context, we investigated PCa risk associated to employment among several occupations using data from EPICAP study. METHODS: EPICAP is a French population-based case-control study including 819 PCa incident cases and 879 controls frequency-matched on age. In-person interviews gathered data on potential risk factors and lifetime occupational histories for each job held at least 6 months. Then, occupations were coded using ISCO 68. Unconditional logistic regressions were performed to assess the association between occupations (ever occupied and by duration) and PCa risk, whether all and aggressive, after adjusting for potential confounders. RESULTS: For ≥10 years of employment, we found positive associations with PCa, whether overall and aggressive, among Medical, Dental and Veterinary workers (OR (odds ratios) =5.01 [95% confidence interval] [1.27; 19.77]), Members of the armed forces (OR = 5.14 [0.99; 26.71]) and Fishermen, hunters and related workers (OR = 4.58 [1.33; 15.78]); whether overall and non-aggressive PCa, among Legislative officials and Government administrators (OR = 3.30 [1.10; 9.84]) or Managers (OR = 1.68 [1.18; 2.41]); however a negative association, whether overall and non-aggressive PCa, among Material-Handling and Related Equipment Operators, Dockers and Freight Handlers (OR = 0.40 [0.17; 0.97]). CONCLUSION: Excess PCa risks were observed in the EPICAP study mostly among white collar workers exposed to several factors in their work environment. These emerging associations can be used to lead future research investigating specific occupational exposures.

Sleep Patterns and Risk of Prostate Cancer: A Population-Based Case Control Study in France (EPICAP).

BACKGROUND: Sleep disturbances have been singled out for their implication in the risk of several cancer sites. However, results for prostate cancer are still inconsistent. METHODS: We used data from the EPICAP study, a French population-based case-control study including 819 incident prostate cancer cases and 879 controls frequency matched by age. Detailed information on sleep duration on work/free days, and sleep medication over lifetime was collected. RESULTS: Sleep duration and sleep deprivation were not associated with prostate cancer, whatever the aggressiveness of prostate cancer. However, sleep deprivation was associated with an increased prostate cancer risk among men with an evening chronotype [OR, 1.96; 95% confidence interval (CI), 1.04-3.70]. We also observed an increased risk of prostate cancer with higher duration of sleep medication use (Ptrend = 0.008). This association with long duration of sleep medication use (≥10 years) was more pronounced among men who worked at night 15 years or more (OR, 3.84; 95% CI, 1.30-11.4) and among nonusers of NSAID (OR, 2.08; 95% CI, 1.15-3.75). CONCLUSIONS: Our results suggested that chronotype, night work, or NSAID use could modify the association between sleep disorders and prostate cancer occurrence needing further investigations to go further. IMPACT: EPICAP is the first study, which investigates several sleep indicators taking into account potential effect modifiers. If our findings were confirmed, we could identify subgroups of men at higher risk of prostate cancer that may be accessible to preventive measures.

Breast cancer risk in relation to ambient concentrations of nitrogen dioxide and particulate matter: results of a population-based case-control study corrected for potential selection bias (the CECILE study).

BACKGROUND: There is only scant evidence that air pollution increases the risk of breast cancer. OBJECTIVES: We investigated this relationship for three air pollutants: nitrogen dioxide (NO2) and particulate matter with an aerodynamical diameter below 10 µm (PM10) and 2.5 µm (PM2.5). METHODS: We conducted a population-based case-control study on breast cancer in two French départements, including 1,229 women diagnosed with breast cancer in 2005-2007 and 1,316 control women frequency-matched on age. Concentrations of NO2, PM10 and PM2.5 at participants' addresses occupied during the last 10 years were assessed using a chemistry transport model. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using multivariable logistic regression models where each woman was assigned a weight depending on her probability of selection into the study. RESULTS: The OR for breast cancer per 10-µg/m3 increase in NO2 was 1.11 (95% CI, 0.98, 1.26), and 1.41 (95% CI 1.07, 1.86) in the highest exposure quintile (Q5), compared to the first. The ORs per 10-µg/m3 NO2 did not markedly differ between pre- (OR 1.09, 95% CI 0.89, 1.35)) and post-menopausal women (OR 1.14, 95% CI 0.97, 1.33)), but the OR was substantially higher for hormone-receptor positive (ER+/PR+) breast tumor subtypes (OR 1.15, 95% CI 1.00, 1.31) than for ER-/PR- tumors (OR 0.95, 95% CI 0.72, 1.26). Breast cancer risk was not associated with either PM10 (OR per 1 µg/m3 1.01, 95% CI, 0.96, 1.06) or PM2.5 (OR per 1 µg/m3 1.02, 95% CI 0.95, 1.08), regardless of the menopausal status or of the breast tumor subtype. DISCUSSION: Our study provides evidence that NO2 exposure, a marker of traffic-related air pollutants, may be associated with an increased risk of breast cancer, particularly ER+/PR+ tumors.