Hazard ratios and 95% confidence intervals for risk of breast cancer in relation to number of nevi, stratified by menopausal status, E3N cohort (<i>n = </i>89,802).

a<p>Adjusted for age (timescale), education, age at menopause (in postmenopausal women), use of MHT (in postmenopausal women), and use of premenopausal progestogens, and stratified according to year of birth in 5-y categories (Model 2).</p>b<p>Additionally adjusted for personal history of BBD and family history of breast cancer (model used for homogeneity test) (Model 4).</p

Hazard ratios and 95% confidence intervals for risk of breast cancer in relation to number of nevi, stratified by hormonal receptor status, E3N cohort (<i>n = </i>88,387).

<p>Women with missing information on hormone receptor status were excluded from this analysis (<i>n = </i>1,415).</p>b<p>Adjusted for age (timescale), education, menopausal status, age at menopause (in postmenopausal women), use of MHT (in postmenopausal women), and use of premenopausal progestogens, and stratified according to year of birth in 5-y categories (Model 2).</p>c<p>Additionally adjusted for personal history of BBD and family history of breast cancer (model used for homogeneity test) (Model 4).</p

Hazard ratios and 95% confidence intervals for risk of breast cancer in relation to number of nevi, stratified by histological type of breast cancer, E3N cohort (<i>n</i> = 89,429).

a<p>Adjusted for age (timescale), education, menopausal status, age at menopause (in postmenopausal women), use of MHT (in postmenopausal women), and use of premenopausal progestogens, and stratified according to year of birth in 5-y categories (Model 2).</p>b<p>Additionally adjusted for personal history of BBD and family history of breast cancer (model used for homogeneity test) (Model 4).</p

Odds ratios and 95% confidence intervals for number of nevi in relation to family history of breast cancer, E3N cohort.

a<p>Adjusted for education and age at inclusion.</p

Hazard ratios and 95% confidence intervals for risk of breast cancer in relation to number of nevi, E3N cohort (<i>n = </i>89,802).

a<p>Adjusted for age (timescale), education, menopausal status, age at menopause (in postmenopausal women), use of MHT (in postmenopausal women), and use of premenopausal progestogens, and stratified according to year of birth in 5-y categories.</p>b<p>Model 2 additionally adjusted for personal history of BBD.</p>c<p>Model 3 additionally adjusted for personal history of BBD and family history of breast cancer.</p>d<p>Model 4 additionally adjusted for BMI, height, physical activity, age at menarche, age at first full-term pregnancy, parity, breastfeeding, use of OCs, history of mammographic exam, UV dose in county of birth, and UV dose in county of residence at inclusion.</p

Odds ratios and 95% confidence intervals for number of nevi in relation to history of benign breast disease, E3N cohort.

a<p>Adjusted for age at cohort inclusion, age at last returned questionnaire, education, menopausal status, age at menopause (in postmenopausal women), use of MHT (in postmenopausal women), use of premenopausal progestogens, and family history of breast cancer.</p

Hazard ratios and 95% confidence intervals for risk of breast cancer in relation to number of nevi, stratified by hormonal receptor status, E3N cohort (<i>n = </i>88,387).

<p>Women with missing information on hormone receptor status were excluded from this analysis (<i>n = </i>1,415).</p>b<p>Adjusted for age (timescale), education, menopausal status, age at menopause (in postmenopausal women), use of MHT (in postmenopausal women), and use of premenopausal progestogens, and stratified according to year of birth in 5-y categories (Model 2).</p>c<p>Additionally adjusted for personal history of BBD and family history of breast cancer (model used for homogeneity test) (Model 4).</p

Additional file 1: of Validity and reproducibility of a short food frequency questionnaire among patients with chronic kidney disease

Flow diagram. (DOCX 85 kb

Additional file 2: of Validity and reproducibility of a short food frequency questionnaire among patients with chronic kidney disease

SFFQ items used to obtain nutritional data (n = 49). (DOCX 20 kb

Long-term exposure to ambient air pollution and bladder cancer incidence in a pooled European cohort: the ELAPSE project

Background: The evidence linking ambient air pollution to bladder cancer is limited and mixed. Methods: We assessed the associations of bladder cancer incidence with residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight PM2.5 elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in a pooled cohort (N = 302,493). Exposures were primarily assessed based on 2010 measurements and back-extrapolated to the baseline years. We applied Cox proportional hazard models adjusting for individual- and area-level potential confounders. Results: During an average of 18.2 years follow-up, 967 bladder cancer cases occurred. We observed a positive though statistically non-significant association between PM2.5 and bladder cancer incidence. Hazard Ratios (HR) were 1.09 (95% confidence interval (CI): 0.93–1.27) per 5 µg/m3 for 2010 exposure and 1.06 (95% CI: 0.99–1.14) for baseline exposure. Effect estimates for NO2, BC and O3 were close to unity. A positive association was observed with PM2.5 zinc (HR 1.08; 95% CI: 1.00–1.16 per 10 ng/m3). Conclusions: We found suggestive evidence of an association between long-term PM2.5 mass exposure and bladder cancer, strengthening the evidence from the few previous studies. The association with zinc in PM2.5 suggests the importance of industrial emissions