Anita Koushik

Occupational environment and ovarian cancer risk

ObjectivesTo investigate employment in an occupation or industry and specific occupational exposures in relation to ovarian cancer risk.MethodsIn 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.ResultsElevated 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.ConclusionsCertain 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.

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.

Lifetime caffeine intake and the risk of epithelial ovarian cancer

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. 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. 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. Lifetime caffeine intake was not strongly associated with ovarian cancer risk. A difference in relationship by menopausal status is possible.

Sleep duration and the risk of epithelial ovarian cancer

Variations in sleep duration have been linked to biological mechanisms that may affect cancer risk. We investigated the association between sleep duration during adult life and the risk of epithelial ovarian cancer overall, and according to tumor behavior and invasive cancer type, in a population-based case-control study. Among 465 cases and 855 controls, sleep duration during life periods starting at age 20 years was assessed, with which average sleep during adult life was calculated. Unconditional multivariable logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI). Polytomous logistic regression was used to estimate associations by tumor behavior (invasive vs. borderline) and invasive cancer type (Type I vs. II). Compared to an average sleep duration during adult life of the recommended 7-9 h/night, the ORs (95% CI) for ovarian cancer overall were 1.04 (0.74-1.46) and 1.78 (1.15-2.75) for  9 h/night, respectively. An increased risk with > 9 h/night was also observed for invasive and borderline tumors and among Type I and Type II invasive cancer types. The results suggest that sleep durations longer than the recommended 7-9 h/night during adulthood may be associated with an increased ovarian cancer risk.

Trajectories of body fatness in adulthood and the risk of ovarian cancer.

While excess body fatness in older adulthood has been linked to ovarian cancer, the influence of changes in body fatness over time is unclear. This study examined the association between adulthood trajectories of body mass index (BMI), a proxy for body fatness, and ovarian cancer. In a population-based case-control study (440 cases, 820 controls), we used a group-based trajectory approach to identify BMI trajectories from age 20-70. Using unconditional logistic regression, we estimated adjusted odds ratios (aOR) and 95 % confidence intervals (95 % CI) for the associations between the estimated trajectories and ovarian cancer. We identified three distinct BMI trajectories: a normal-stable trajectory, a normal-to-overweight trajectory and an overweight-to-obese trajectory, which included 63.2 %, 31.0 % and 6.8 % of the population, respectively. Multivariable aORs suggested that participants with normal weight at the onset of adulthood who became overweight over their adulthood time did not differ in their risk of ovarian cancer compared to those who maintained a normal weight throughout adulthood (aOR (95 %CI): 0.89 (0.69-1.16)). Among those in the overweight-to-obese trajectory, the aOR (95 %CI) was 1.45 (0.87-2.43), and thus in the direction of an increased ovarian cancer risk compared to those who maintained a normal weight. Our findings underscore the need for further research to clarify the role of body fatness across the lifetime in the etiology of ovarian cancer.