Predicted 25-hydroxyvitamin D over the adult life and the risk of ovarian cancer.

The evidence from previous studies of serum 25-hydroxyvitamin D [25(OH)D] and ovarian cancer risk are not conclusive. However, 25(OH)D was generally only measured in late adulthood, which may not capture the etiologically relevant exposure periods. We investigated predicted 25(OH)D over the adult lifetime in relation to ovarian cancer risk in a population-based case-control study conducted from 2011 to 2016 in Montreal, Canada (490 cases, 896 controls). Predicted 25(OH)D was computed using previously validated regression models. Unconditional multivariable logistic regression models were used to estimate adjusted odds ratios (aOR) and 95% confidence intervals (CI) for average predicted 25(OH)D over the adult life and risk. In addition, the relative importance of different periods of past 25(OH)D exposure was explored using a weighted cumulative exposure (WCE) model. For each 20 nmol/L increase in average predicted 25(OH)D over the adult life, the aOR (95% CI) was 0.73 (0.55-0.96). In WCE analyses, the inverse association was strongest for exposures 5 to 20 years and 35 to 55 years prior to diagnosis, with aORs (95% CIs) of 0.82 (0.69-0.94) and 0.79 (0.66-1.02), respectively, for each 20 nmol/L increase in predicted 25(OH)D. These results support an inverse association between 25(OH)D in adulthood and ovarian cancer risk.

An empirical evaluation of approximate and exact regression-based causal mediation approaches for a binary outcome and a continuous or a binary mediator for case-control study designs.

BACKGROUND: In the causal mediation analysis framework, several parametric regression-based approaches have been introduced in past years for decomposing the total effect of an exposure on a binary outcome into a direct effect and an indirect effect through a target mediator. In this context, a well-known strategy involves specifying a logistic model for the outcome and invoking the rare outcome assumption (ROA) to simplify estimation. Recently, exact estimators for natural direct and indirect effects have been introduced to circumvent the challenges prompted by the ROA. As for the approximate approaches relying on the ROA, these exact approaches cannot be used as is on case-control data where the sampling mechanism depends on the outcome. METHODS: Considering a continuous or a binary mediator, we empirically compare the approximate and exact approaches using simulated data under various case-control scenarios. An illustration of these approaches on case-control data is provided, where the natural mediation effects of long-term use of oral contraceptives on ovarian cancer, with lifetime number of ovulatory cycles as the mediator, are estimated. RESULTS: In the simulations, we found few differences between the performances of the approximate and exact approaches when the outcome was rare, both marginally and conditionally on variables. However, the performance of the approximate approaches degraded as the prevalence of the outcome increased in at least one stratum of variables. Differences in behavior were also observed among the approximate approaches. In the data analysis, all studied approaches were in agreement with respect to the natural direct and indirect effects estimates. CONCLUSIONS: In the case where a violation of the ROA applies or is expected, approximate mediation approaches should be avoided or used with caution, and exact estimators favored.

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

OBJECTIVE: To assess the association between childhood body fatness and epithelial ovarian cancer (EOC), and whether this association differs by type of EOC. METHODS: Using 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. RESULTS: The 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. CONCLUSIONS: Childhood 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.

The Influence of Smoking and Occupational Risk Factors on DNA Methylation in the AHRR and F2RL3 Genes.

BACKGROUND: AHRR and F2RL3 hypomethylation has been associated with lung cancer. In this study, we investigated the cross-sectional association between smoking and occupational exposures, and AHRR and F2RL3 methylation. METHODS: A case-control study was nested in CARTaGENE to examine the association between AHRR and F2RL3 methylation and lung cancer risk (200 cases; 400 controls). A secondary analysis was conducted using the data collected from this nested study; namely, baseline information on participants' smoking behavior and longest-held job was obtained. A cumulative smoking index summarized information on the number of cigarettes smoked, duration of smoking, and time since cessation. Exposure to 13 occupational agents was estimated using the Canadian Job Exposure Matrix. In baseline blood samples, methylation ratios of 40 CpG sites in the AHRR and F2RL3 genes were measured using Sequenom EpiTYPER. Separate least squares regression models were used to estimate the associations between smoking and occupational exposures, and average AHRR and F2RL3 methylation levels, while adjusting for confounders identified from directed acyclic graphs. RESULTS: In both genes, smoking was associated with lower average methylation levels. Occupational exposure to aromatic amines, cadmium, and formaldehyde were associated with lower AHRR methylation while, only benzene was associated with F2RL3 hypomethylation; these associations were stronger among ever smokers. CONCLUSIONS: Our findings support that smoking and occupational exposures to some agents are associated with AHRR and F2RL3 hypomethylation. IMPACT: Our results inform on mechanisms underlying environmental exposures in lung cancer etiology; future studies should prioritize studying joint exposures.

Occupational environment and ovarian cancer risk.

OBJECTIVES: To investigate employment in an occupation or industry and specific occupational exposures in relation to ovarian cancer risk. METHODS: In a population-based case-control study conducted in Montreal, Canada (2011-2016), lifetime occupational histories were collected for 491 cases of ovarian cancer and 897 controls. An industrial hygienist coded the occupation and industry of each participant's job. Associations with ovarian cancer risk were estimated for each of several occupations and industries. Job codes were linked to the Canadian job-exposure matrix, thereby generating exposure histories to many agents. The relationship between exposure to each of the 29 most prevalent agents and ovarian cancer risk was assessed. Odds ratios and 95% confidence intervals (OR (95% CI)) for associations with ovarian cancer risk were estimated using logistic regression and controlling for multiple covariates. RESULTS: Elevated ORs (95% CI) were observed for employment ≥10 years as Accountants (2.05 (1.10 to 3.79)); Hairdressers, Barbers, Beauticians and Related Workers (3.22 (1.25 to 8.27)); Sewers and Embroiderers (1.85 (0.77 to 4.45)); and Salespeople, Shop Assistants and Demonstrators (1.45 (0.71 to 2.96)); and in the industries of Retail Trade (1.59 (1.05 to 2.39)) and Construction (2.79 (0.52 to 4.83)). Positive associations with ORs above 1.42 were seen for high cumulative exposure versus never exposure to 18 agents: cosmetic talc, ammonia, hydrogen peroxide, hair dust, synthetic fibres, polyester fibres, organic dyes and pigments, cellulose, formaldehyde, propellant gases, aliphatic alcohols, ethanol, isopropanol, fluorocarbons, alkanes (C5-C17), mononuclear aromatic hydrocarbons, polycyclic aromatic hydrocarbons from petroleum and bleaches. CONCLUSIONS: Certain occupations, industries and specific occupational exposures may be associated with ovarian cancer risk. Further research is needed to provide a more solid grounding for any inferences in this regard.

Alcohol intake and the risk of epithelial ovarian cancer.

PURPOSE: To investigate the association between alcohol intake over the lifetime and the risk of overall, borderline, and invasive ovarian cancer. METHODS: In a population-based case-control study of 495 cases and 902 controls, conducted in Montreal, Canada, average alcohol intake over the lifetime and during specific age periods were computed from a detailed assessment of the intake of beer, red wine, white wine and spirits. Multivariable logistic regression was used to estimate odds ratios (ORs) with 95% confidence intervals (CIs) for the association between alcohol intake and ovarian cancer risk. RESULTS: For each one drink/week increment in average alcohol intake over the lifetime, the adjusted OR (95% CI) was 1.06 (1.01-1.10) for ovarian cancer overall, 1.13 (1.06-1.20) for borderline ovarian cancers and 1.02 (0.97-1.08) for invasive ovarian cancers. This pattern of association was similarly observed for alcohol intake in early (15- < 25 years), mid (25- < 40 years) and late adulthood (≥ 40 years), as well as for the intake of specific alcohol beverages over the lifetime. CONCLUSIONS: Our results support the hypothesis that a higher alcohol intake modestly increases the risk of overall ovarian cancer, and more specifically, borderline tumours.

Occupational Exposures and Lung Cancer Risk-An Analysis of the CARTaGENE Study.

OBJECTIVE: To determine the associations between prevalent occupational agents and lung cancer risk. METHODS: A case-cohort design (ncases= 147; nsub-cohort= 1,032) was nested within the CARTaGENE prospective cohort study. The Canadian Job Exposure Matrix was used to determine the probability of exposure to 27 agents in participants' longest-held jobs. Multivariable logistic regression with robust variance estimators was used to determine the associations between each agent and lung cancer risk while adjusting for established lung cancer risk factors. RESULTS: Increased lung cancer risk was observed among those exposed to ashes, calcium sulfate, formaldehyde, cooking fumes, alkanes, aliphatic aldehydes, and cleaning agents. Lower lung cancer risk was found among participants exposed to carbon monoxide and polycyclic aromatic hydrocarbons from petroleum. CONCLUSION: Our findings support the role of several occupational agents, for which we have limited knowledge, in contributing to lung cancer risk.

Lifetime caffeine intake and the risk of epithelial ovarian cancer.

BACKGROUND: Caffeine 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. METHODS: Among 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. RESULTS: Almost 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. CONCLUSION: Lifetime caffeine intake was not strongly associated with ovarian cancer risk. A difference in relationship by menopausal status is possible.

Vitamin D Exposure and Ovarian Cancer Risk and Prognosis.

Given the poor prognosis of ovarian cancer and limited population-level strategies for early detection and long-term treatment success, knowledge of modifiable risk factors for prevention and improved prognosis is important. Vitamin D has received wide scientific interest in cancer research as having the potential to be one such factor. We carried out a systematic narrative review of the literature on vitamin D and ovarian cancer risk and survival. We included 17 case-control and cohort studies on ovarian cancer incidence. Five analyses were of sun exposure, among which three reported an inverse association. Of 11 analyses of dietary vitamin D, two reported an inverse association. Among five studies of 25(OH)D levels, an inverse association was reported in two. Across all studies the findings were inconsistent, but some recent studies have suggested that vitamin D exposure at earlier ages may be important. Only three studies examining vitamin D exposure in relation to survival among ovarian cancer survivors were identified and the findings were inconsistent. The evidence to date supports a null influence of vitamin D on both ovarian cancer risk and survival. Future research should ensure that exposure assessment captures vitamin D exposure from all sources and for the etiologically or prognostically pertinent period.

Lifetime recreational moderate-to-vigorous physical activity and ovarian cancer risk: A case-control study.

Results of epidemiologic studies of physical activity and ovarian cancer risk are inconsistent. Few have attempted to measure physical activity over the lifetime or in specific age windows, which may better capture etiologically relevant exposures. We examined participation in moderate-to-vigorous recreational physical activity (MVPA) in relation to ovarian cancer risk. In a population-based case-control study conducted in Montreal, Canada from 2011 to 2016 (485 cases and 887 controls), information was collected on lifetime participation in various recreational physical activities, which was used to estimate MVPA for each participant. MVPA was represented as average energy expenditure over the lifetime and in specific age-periods in units of metabolic equivalents (METs)-hours per week. Odds ratios (OR) and 95% confidence intervals (CI) for the relation between average MVPA and ovarian cancer risk were estimated using multivariable logistic regression models. Confounding was assessed using directed acyclic graphs combined with a change-in-estimate approach. The adjusted OR (95% CI) for each 28.5 MET-hr/week increment of lifetime recreational MVPA was 1.11 (0.99-1.24) for ovarian cancer overall. ORs for individual age-periods were weaker. When examined by menopausal status, the OR (95% CI) for lifetime MVPA was 1.21 (1.00-1.45) for those diagnosed before menopause and 1.04 (0.89-1.21) for those diagnosed postmenopausally. The suggestive positive associations were stronger for invasive ovarian cancers and more specifically for high-grade serous carcinomas. These results do not support a reduced ovarian cancer risk associated with MVPA.

Viral load of human papillomavirus types 16/18/31/33/45 as a predictor of cervical intraepithelial neoplasia and cancer by age.

OBJECTIVE: We assessed whether human papillomavirus (HPV) viral load is an independent predictor of underlying cervical disease and its diagnostic accuracy by age. METHODS: The Biomarkers of Cervical Cancer Risk study was a case-control study from 2001 to 2010 in Montréal, Canada. Cases were histologically-confirmed cervical intraepithelial neoplasia (CIN), adenocarcinoma in situ (AIS), or cervical cancer cases. Controls were women presenting for routine screening with normal cytology results. We quantified HPV16/18/31/33/45 viral load from exfoliated cervical cells using a real-time PCR assay. Diagnostic accuracy of viral load was assessed using the area under the receiver operating characteristic curve (AUC). We restricted the analysis to the 632 cases and controls who were HPV16/18/31/33/45 positive. RESULTS: Geometric mean HPV16/18/31/33/45 viral load increased with severity of lesion grade, ranging from 0.7, 3.1, 4.8, 7.2, and 12.4 copies/cell in normal, CIN1, CIN2, CIN3&AIS, and cervical cancer respectively. The adjusted odds ratio of CIN1+ and CIN2+ increased respectively by 1.3 (95%CI 1.1-1.4) and 1.2 (95%CI 1.1-1.3) per log-transformed viral copy/cell increase of HPV16/18/31/33/45. This association was mainly driven by HPV16, 18, and 31 viral loads. The AUC of HPV16/18/31/33/45 viral load for discriminating between normal and CIN1+ women was 0.70 (95%CI 0.64-0.76) in HPV-positive women, and was 0.76 (95%CI 0.66-0.86) for women ≥30 years and 0.66 (95%CI 0.58-0.74) for women under 30 years. CONCLUSIONS: HPV viral load has lower diagnostic accuracy than has been reported for other HPV screening triage tests. However, it may be useful for triaging HPV tests in settings without cytology results such as HPV self-sampling.

Shift Work Patterns, Chronotype, and Epithelial Ovarian Cancer Risk.

BACKGROUND: Shift work causing circadian disruption is classified as a "probable carcinogen" and may contribute to the pathogenesis of hormone-sensitive cancers. This study investigated shift work exposure in relation to epithelial ovarian cancer (EOC) risk. METHODS: In a population-based case-control study with 496 EOC cases and 906 controls, lifetime occupational histories were collected and used to calculate cumulative years of shift work exposure, average number of night shifts per month, and average number of consecutive night shifts per month. ORs and 95% confidence intervals (CI) for associations with EOC risk were estimated using logistic regression. Associations were also examined according to chronotype and menopausal status. RESULTS: More than half of the cases (53.4%) and controls (51.7%) worked evening and/or night shifts. There was no clear pattern of increasing EOC risk with increasing years of shift work; the adjusted OR of EOC comparing the highest shift work category versus never working shift work was 1.20 (95% CI, 0.89-1.63). This association was more pronounced among those self-identified as having a "morning" chronotype (OR, 1.64; 95% CI, 1.01-2.65). Associations did not greatly differ by menopausal status. CONCLUSIONS: These results do not strongly demonstrate a relationship between shift work and EOC risk. IMPACT: This study collected detailed shift work information and examined shift work patterns according to shift times and schedules. The findings highlight that chronotype should be considered in studies of shift work as an exposure.

Alcohol consumption and lung cancer risk: A pooled analysis from the International Lung Cancer Consortium and the SYNERGY study.

BACKGROUND: There is inadequate evidence to determine whether there is an effect of alcohol consumption on lung cancer risk. We conducted a pooled analysis of data from the International Lung Cancer Consortium and the SYNERGY study to investigate this possible association by type of beverage with adjustment for other potential confounders. METHODS: Twenty one case-control studies and one cohort study with alcohol-intake data obtained from questionnaires were included in this pooled analysis (19,149 cases and 362,340 controls). Adjusted odds ratios (OR) or hazard ratios (HR) with corresponding 95% confidence intervals (CI) were estimated for each measure of alcohol consumption. Effect estimates were combined using random or fixed-effects models where appropriate. Associations were examined for overall lung cancer and by histological type. RESULTS: We observed an inverse association between overall risk of lung cancer and consumption of alcoholic beverages compared to non-drinkers, but the association was not monotonic. The lowest risk was observed for persons who consumed 10-19.9 g/day ethanol (OR vs. non-drinkers = 0.78; 95% CI: 0.67, 0.91), where 1 drink is approximately 12-15 g. This J-shaped association was most prominent for squamous cell carcinoma (SCC). The association with all lung cancer varied little by type of alcoholic beverage, but there were notable differences for SCC. We observed an association with beer intake (OR for ≥20 g/day vs nondrinker = 1.42; 95% CI: 1.06, 1.90). CONCLUSIONS: Whether the non-monotonic associations we observed or the positive association between beer drinking and squamous cell carcinoma reflect real effects await future analyses and insights about possible biological mechanisms.

Genetic Data from Nearly 63,000 Women of European Descent Predicts DNA Methylation Biomarkers and Epithelial Ovarian Cancer Risk.

DNA methylation is instrumental for gene regulation. Global changes in the epigenetic landscape have been recognized as a hallmark of cancer. However, the role of DNA methylation in epithelial ovarian cancer (EOC) remains unclear. In this study, high-density genetic and DNA methylation data in white blood cells from the Framingham Heart Study (N = 1,595) were used to build genetic models to predict DNA methylation levels. These prediction models were then applied to the summary statistics of a genome-wide association study (GWAS) of ovarian cancer including 22,406 EOC cases and 40,941 controls to investigate genetically predicted DNA methylation levels in association with EOC risk. Among 62,938 CpG sites investigated, genetically predicted methylation levels at 89 CpG were significantly associated with EOC risk at a Bonferroni-corrected threshold of P < 7.94 × 10-7. Of them, 87 were located at GWAS-identified EOC susceptibility regions and two resided in a genomic region not previously reported to be associated with EOC risk. Integrative analyses of genetic, methylation, and gene expression data identified consistent directions of associations across 12 CpG, five genes, and EOC risk, suggesting that methylation at these 12 CpG may influence EOC risk by regulating expression of these five genes, namely MAPT, HOXB3, ABHD8, ARHGAP27, and SKAP1. We identified novel DNA methylation markers associated with EOC risk and propose that methylation at multiple CpG may affect EOC risk via regulation of gene expression. SIGNIFICANCE: Identification of novel DNA methylation markers associated with EOC risk suggests that methylation at multiple CpG may affect EOC risk through regulation of gene expression.

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.

Addition of food group equivalents to the Canadian Diet History Questionnaire II for the estimation of the Canadian Healthy Eating Index-2005. / Ajout d'équivalents des groupes alimentaires au Questionnaire canadien de fréquence alimentaire II pour estimer l'Indice canadien de saine alimentation-2005.

INTRODUCTION: Poor diet quality has been shown to increase the risk of common chronic diseases that can negatively impact quality of life and burden the healthcare system. Canada's Food Guide evidence-based recommendations provide dietary guidance aimed at increasing diet quality. Compliance with Canada's Food Guide can be assessed with the Canadian Healthy Eating Index (C-HEI), a diet quality score. The recently designed Canadian Diet History Questionnaire II (C-DHQ II), a comprehensive food frequency questionnaire could be used to estimate the C-HEI in Canadian populations with the addition of food group equivalents (representing Canada's Food Guide servings) to the C-DHQ II nutrient database. We describe methods developed to augment the C-DHQ II nutrient database to estimate the C-HEI. METHODS: Food group equivalents were created using food and nutrient data from existing published food and nutrient databases (e.g. the Canadian Community Health Survey - Cycle 2.2 Nutrition [2004]). The variables were then added to the C-DHQ II companion nutrient database. C-HEI scores were determined and descriptive analyses conducted for participants who completed the C-DHQ II in a cross-sectional Canadian study. RESULTS: The mean (standard deviation) C-HEI score in this sample of 446 adults aged 20 to 83 was 64.4 (10.8). Women, non-smokers, and those with more than high school education had statistically significant higher C-HEI scores than men, smokers and those with high school diplomas or less. CONCLUSION: The ability to assess C-HEI using the C-DHQ II facilitates the study of diet quality and health outcomes in Canada.

INTRODUCTION: Il a été prouvé qu'un régime alimentaire de piètre qualité augmente le risque de maladies chroniques courantes susceptibles de nuire à la qualité de vie et d'alourdir le fardeau qui pèse sur le système de santé. Les recommandations fondées sur des données probantes du Guide alimentaire canadien (GAC) fournissent des conseils nutritionnels destinés à améliorer la qualité du régime alimentaire. L'Indice canadien de saine alimentation (ICSA), un outil de mesure de la qualité du régime alimentaire, permet d'évaluer la conformité au GAC. Le Questionnaire canadien de fréquence alimentaire II (QFA-C II) [Canadian Diet History Questionnaire II, C-DHQ II], mis au point récemment, pourrait quant à lui servir à estimer l'ICSA au sein de la population canadienne si on pouvait ajouter à sa base de données sur les éléments nutritifs les équivalents des groupes alimentaires (correspondant aux portions du GAC). Nous décrivons dans cet article des méthodes destinées à enrichir cette base de données sur les éléments nutritifs du QFA-C II en vue d'estimer l'ICSA. MÉTHODOLOGIE: Nous avons créé des équivalents des groupes alimentaires à partir de données provenant de diverses bases de données sur les aliments et les éléments nutritifs, en particulier l'Enquête sur la santé dans les collectivités canadiennes, cycle 2.2 Nutrition de 2004. Nous avons ajouté ces variables à la base de données sur les éléments nutritifs du QFA-C II. Nous avons déterminé les scores de l'ICSA et avons effectué des analyses descriptives pour les participants qui ont répondu au QFA-C II dans le cadre d'une étude transversale canadienne. RÉSULTATS: Le score moyen de l'ICSA dans notre échantillon de 446 adultes de 20 à 83 ans était de 64,4 (écart-type : 10,8). Les femmes, les non-fumeurs et les personnes ayant un niveau de scolarité supérieur au secondaire ont obtenu de manière statistiquement significative des notes plus élevées que les hommes, les fumeurs et les personnes détenant un diplôme d'études secondaires ou moins. CONCLUSION: La possibilité d'évaluer l'ICSA à l'aide du QFA-C II facilite l'étude de la qualité du régime alimentaire et de l'état de santé de la population canadienne.

Menstrual and reproductive factors and lung cancer risk: A pooled analysis from the international lung cancer consortium.

Many clinical features of lung cancer are different in women and men. Sex steroid hormones exert effects in nonreproductive organs, such as the lungs. The association between menstrual and childbearing factors and the risk of lung cancer among women is still debated. We performed a pooled analysis of eight studies contributing to the International Lung Cancer Consortium (4,386 cases and 4,177 controls). Pooled associations between menstrual or reproductive factors and lung cancer were estimated using multivariable unconditional logistic regression. Subgroup analyses were done for menopause status, smoking habits and histology. We found no strong support for an association of age at menarche and at menopause with lung cancer, but peri/postmenopausal women were at higher risk compared to premenopausal (OR 1.47, 95% CI 1.11-1.93). Premenopausal women showed increased risks associated with parity (OR 1.74, 95% CI 1.03-2.93) and number of children (OR 2.88, 95% CI 1.21-6.93 for more than 3 children; p for trend 0.01) and decreased with breastfeeding (OR 0.54, 95% CI 0.30-0.98). In contrast, peri/postmenopausal subjects had ORs around unity for the same exposures. No major effect modification was exerted by smoking status or cancer histology. Menstrual and reproductive factors may play a role in the genesis of lung cancer, yet the mechanisms are unclear, and smoking remains the most important modifiable risk factor. More investigations in large well-designed studies are needed to confirm these findings and to clarify the underlying mechanisms of gender differences in lung cancer risk.

Physical activity and lung cancer risk in men and women.

PURPOSE: 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). METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Inverse Association between Dietary Intake of Selected Carotenoids and Vitamin C and Risk of Lung Cancer.

While diets rich in fruit and vegetables appear to reduce lung cancer risk, the evidence for individual carotenoid and vitamin intakes has been judged too limited to reach firm conclusions. Data from a case-control study of lung cancer (Montreal, QC, Canada, 1996-2002) were used to investigate the role of dietary intakes of ß-carotene, α-carotene, ß-cryptoxanthin, lutein/zeaxanthin, lycopene, and vitamin C in lung cancer risk. In-person interviews elicited dietary information from 1,105 incident cases and 1,449 population controls. Usual frequency of consumption of 49 fruits and vegetables 2 years prior to diagnosis/interview was collected. Odds ratios (ORs) and 95% confidence intervals (CIs) between intake variables and lung cancer were estimated using logistic or polytomous regression, adjusting for potential confounding factors including a detailed smoking history. ORs associated with upper versus lower tertiles of intake were 0.66 (95% CI = 0.51-0.84) for ß-carotene, 0.70 (95% CI = 0.55-0.90) for α-carotene, 0.65 (95% CI = 0.51-0.84) for ß-cryptoxanthin, 0.75 (95% CI = 0.59-0.95) for lycopene, and 0.74 (95% CI = 0.58-0.96) for vitamin C. ORs suggestive of a protective effect were found for elevated intakes of ß-carotene, α-carotene, ß-cryptoxanthin, and lycopene in male heavy smokers and of vitamin C in female heavy smokers. Selected antioxidants were also associated with a lower risk of lung cancer in female moderate smokers, and of squamous cell carcinoma, adenocarcinoma, and small cell carcinoma. These results suggest that several dietary antioxidants found in common food sources may protect against lung cancer, even among heavy smokers.