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It is established that higher pre-diagnostic circulating androgen and estrogen levels are associated with increased breast cancer risk in premenopausal and postmenopausal women. Pooled analyses in postmenopausal women report higher androgen and estrogen levels in current heavy cigarette smokers compared to nonsmokers. However, evidence among premenopausal women has been inconsistent. We conducted a systematic review and meta-analysis to estimate differences in standardized mean hormone levels among current premenopausal smokers compared to nonsmokers. We reviewed and collated publications with sex hormone levels by smoking status among healthy, premenopausal women who were nonusers of exogenous hormones, including oral contraceptives, using PubMed through December 2019. A random effects meta-analysis was conducted to combine the standardized mean differences (SMD) and 95% confidence intervals (CIs) for estradiol, progesterone, testosterone, dehydroepiandrosterone, dehydroepiandrosterone-sulfate, and sex hormone-binding globulin by smoking status. Findings were summarized by menstrual cycle phase and overall. Nineteen published peer-reviewed articles were included. Significantly increased testosterone levels among smokers compared to nonsmokers were identified from cross-sectional studies with varied menstrual phase timing (SMD 0.14; 95% CI 0.0005, 0.29) and significantly increased dehydroepiandrosterone-sulfate levels were found over all phases (SMD 0.12; 95% CI 0.01, 0.22). However, substantial heterogeneity existed in these studies. This meta-analysis suggests that smoking may increase blood androgen levels in healthy premenopausal women which may increase breast cancer risk; however, the differences were modest. Larger and covariate-adjusted studies with standardized collection over the menstrual cycle are needed to better understand this relationship and to reduce heterogeneity. Implications: Existing research has described associations between high pre-diagnost

IntroductionIt is established that higher prediagnostic circulating androgen and estrogen levels are associated with increased breast cancer risk in premenopausal and postmenopausal women. Pooled analyses in postmenopausal women report higher androgen and estrogen levels in current heavy cigarette smokers compared to nonsmokers. However, evidence among premenopausal women has been inconsistent.Aims and methodsWe conducted a systematic review and meta-analysis to estimate differences in standardized mean hormone levels among current premenopausal smokers compared to nonsmokers. We reviewed and collated publications with sex hormone levels by smoking status among healthy, premenopausal women who were nonusers of exogenous hormones, including oral contraceptives, using PubMed through December 2019. A random effects meta-analysis was conducted to combine the standardized mean differences (SMD) and 95% confidence intervals (CIs) for estradiol, progesterone, testosterone, dehydroepiandrosterone, dehydroepiandrosterone-sulfate, and sex hormone-binding globulin by smoking status. Findings were summarized by menstrual cycle phase and overall.ResultsNineteen published peer-reviewed articles were included. Significantly increased testosterone levels among smokers compared to nonsmokers were identified from cross-sectional studies with varied menstrual phase timing (SMD 0.14; 95% CI 0.0005, 0.29) and significantly increased dehydroepiandrosterone-sulfate levels were found over all phases (SMD 0.12; 95% CI 0.01, 0.22). However, substantial heterogeneity existed in these studies.ConclusionsThis meta-analysis suggests that smoking may increase blood androgen levels in healthy premenopausal women which may increase breast cancer risk; however, the differences were modest. Larger and covariate-adjusted studies with standardized collection over the menstrual cycle are needed to better understand this relationship and to reduce heterogeneity.ImplicationsExisting research has described

PurposeTo evaluate the association between lifetime personal cigarette smoking and young-onset breast cancer (YOBC; diagnosed <50 years of age) risk overall and by breast cancer (BC) subtype, and whether risk varies by race or socioeconomic position (SEP).MethodsData are from the Young Women's Health History Study (YWHHS), a population-based case-control study of non-Hispanic Black (NHB) and White (NHW) women, ages 20-49 years (n = 1812 cases, n = 1381 controls) in the Los Angeles County and Metropolitan Detroit Surveillance, Epidemiology, and End Results (SEER) registry areas, 2010-2015. Lifetime personal cigarette smoking characteristics and YOBC risk by subtype were examined using sample-weighted, multivariable-adjusted polytomous logistic regression.ResultsYOBC risk associated with ever versus never smoking differed by subtype (Pheterogeneity = 0.01) with risk significantly increased for Luminal A (adjusted odds ratio [aOR] 1.34; 95% confidence interval [CI] 1.06-1.68) and HER2-type (aOR 1.97; 95% CI 1.23-3.16), and no association with Luminal B or Triple Negative subtypes. Additionally, ≥30 years since smoking initiation (versus never) was statistically significantly associated with an increased risk of Luminal A (aOR 1.55; 95% CI 1.07-2.26) and HER2-type YOBC (aOR 2.77; 95% CI 1.32-5.79), but not other subtypes. In addition, among parous women, smoking initiated before first full-term pregnancy (versus never) was significantly associated with an increased risk of Luminal A YOBC (aOR 1.45; 95% CI 1.11-1.89). We observed little evidence for interactions by race and SEP.ConclusionFindings confirm prior reports of a positive association between cigarette smoking and Luminal A YOBC and identify a novel association between smoking and HER2-type YOBC.

Previous studies have found that tobacco exposure is associated with an increased risk of premenopausal breast cancer (BC) overall and some studies suggest that risk is only increased for Luminal A BC. Few studies have described the association between tobacco exposure and BC risk with characterization of the human epidermal growth factor receptor 2 (HER2) subtype. This analysis explored associations between smoking over the life course and BC risk overall and by BC subtype among a socioeconomically diverse population of young non-Hispanic (NH) Black and White women. Data were examined from a population-based case-control study in women under 50 years of age, the Young Women’s Health History Study. In total, 1,812 women with invasive BC (1,130 NH White, 682 NH Black) and an area-based sample of 1,381 (716 NH White, 665 NH Black) control women, frequency matched to cases by five-year age group, study site and self-reported race were identified from the Los Angeles County and Metropolitan Detroit SEER registry areas. Lifetime smoking histories were collected from in-person interviews. Sample-weighted logistic regression analysis was conducted to estimate the association between lifetime cigarette smoking status (never versus ever smoker) and BC risk adjusted for known BC risk factors and study site. Multinomial logistic regression analysis was conducted for analyses by BC subtype. Heterogeneity in the odds ratio (OR) estimates by BC subtype and cross-product interaction terms of smoking status by race and by household percent poverty (HHP) were evaluated by the Wald test. In adjusted models, BC risk overall was not significantly associated with ever smoking at least 1 cigarette a day for 6 months or more (OR 1.18; 95% confidence interval (CI) 0.97- 1.43). By BC subtype, ever smokers displayed a statistically significant 30% increase in Luminal A BC risk compared to never smokers (OR 1.30; 95% CI 1.03-1.64) and a 90% increased risk of HER2-type BC (OR 1.90; 95

The etiology of breast cancer (BC) among young women is not well understood. Recent studies have suggested that tobacco exposure is associated with an increased risk of BC but few studies have evaluated risk among women under age 50 or racial and socioeconomic disparities in risk. We hypothesized that racial and socioeconomic differences in age at smoking initiation and lifetime cigarette smoking contribute to disparities in BC risk among young women. Data were examined from a population-based case-control study in women under 50 years of age, the Young Women’s Health History Study. In total, 1,812 women with invasive BC (1,130 Non-Hispanic (NH) White, 682 NH Black) and an area-based sample of 1,381 control women (716 NH White, 665 NH Black), frequency matched to cases by five-year age group, study site and race were identified and interviewed from the Los Angeles County and Metropolitan Detroit SEER registry areas. Lifetime smoking history (including age at initiation, duration, and frequency) were collected from structured in-person interviews. Survey-weighted multivariable logistic regression was used to evaluate the association between lifetime cigarette smoking and BC risk adjusted for matching and known BC risk factors. Additionally, cross-product interaction terms of smoking exposure by race and by socioeconomic position (SEP; based on household percent poverty) were evaluated by Wald’s test. Among controls, 36.5% reported ever smoking at least 1 cigarette a day for at least 6 months in their lifetime with White women compared to Black women (38.3% vs. 32.3%) and women of lower SEP (<150% of poverty) compared to higher SEP (≥150% of poverty) (50.4% vs. 31.5%) being more likely to have ever smoked. In adjusted models, those who ever vs. never smoked were 1.20 times as likely to develop BC; findings were marginally significant (95% confidence interval (CI): 0.99-1.46, p=0.07). No differences were found by race or SEP, nor was there a consistent asso

The US Food and Drug Administration (FDA) applies the Population Health Standard in tobacco product review processes by weighing anticipated health benefits against risks associated with a given commercial tobacco product at the population level. However, systemic racism (ie, discriminatory policies and practices) contributes to an inequitable distribution of tobacco-related health benefits and risks between white and Black/African Americans at the population level. Therefore, Black-centered, antiracist data standards for tobacco product review processes are needed to achieve racial equity and social justice in US tobacco control policy. Regardless of whether FDA implements such data standards, non-industry tobacco scientists should prioritise producing and disseminating Black-centred data relevant to FDA's regulatory authority. We describe how systemic racism contributes to disparities in tobacco-related outcomes and why these disparities are relevant for population-level risk assessments, then discuss four possible options for Black-centred data standards relevant to tobacco product review processes.

The US Food and Drug Administration (FDA) applies the Population Health Standard in tobacco product review processes by weighing anticipated health benefits against risks associated with a given commercial tobacco product at the population level. However, systemic racism (ie, discriminatory policies and practices) contributes to an inequitable distribution of tobacco-related health benefits and risks between white and Black/African Americans at the population level. Therefore, Black-centered, antiracist data standards for tobacco product review processes are needed to achieve racial equity and social justice in US tobacco control policy. Regardless of whether FDA implements such data standards, non-industry tobacco scientists should prioritise producing and disseminating Black-centred data relevant to FDA's regulatory authority. We describe how systemic racism contributes to disparities in tobacco-related outcomes and why these disparities are relevant for population-level risk assessments, then discuss four possible options for Black-centred data standards relevant to tobacco product review processes.

The US Food and Drug Administration (FDA) applies the Population Health Standard in tobacco product review processes by weighing anticipated health benefits against risks associated with a given commercial tobacco product at the population level. However, systemic racism (ie, discriminatory policies and practices) contributes to an inequitable distribution of tobacco-related health benefits and risks between white and Black/African Americans at the population level. Therefore, Black-centered, antiracist data standards for tobacco product review processes are needed to achieve racial equity and social justice in US tobacco control policy. Regardless of whether FDA implements such data standards, non-industry tobacco scientists should prioritise producing and disseminating Black-centred data relevant to FDA's regulatory authority. We describe how systemic racism contributes to disparities in tobacco-related outcomes and why these disparities are relevant for population-level risk assessments, then discuss four possible options for Black-centred data standards relevant to tobacco product review processes.