Association between lifetime exposure to passive smoking and risk of breast cancer subtypes defined by hormone receptor status among non-smoking Caucasian women.
ABSTRACT: Tobacco smoking is inconsistently associated with breast cancer. Although some studies suggest that breast cancer risk is related to passive smoking, little is known about the association with breast cancer by tumor hormone receptor status. We aimed to explore the association between lifetime passive smoking and risk of breast cancer subtypes defined by estrogen receptor and progesterone receptor status among non-smoking Caucasian women. A hospital-based case-control study was performed in 585 cases and 1170 controls aged 28-90 years. Information on lifetime passive smoking and other factors was collected via a self-administered questionnaire. Logistic regression was used for analyses restricted to the 449 cases and 930 controls who had never smoked actively. All statistical tests were two-sided. Adjusted odds ratio of breast cancer was 1.01 (95% confidence interval (CI): 0.72-1.41) in women who experienced exposure to passive smoking at work, 1.88 (95% CI: 1.38-2.55) in women who had exposure at home, and 2.80 (95% CI: 1.84-4.25) in women who were exposed at home and at work, all compared with never exposed regularly. Increased risk was associated with longer exposure: women exposed ? 20 years and > 20 years had 1.27 (95% CI: 0.97-1.66) and 2.64 (95% CI: 1.87-3.74) times higher risk of breast cancer compared with never exposed (Ptrend < 0.001). The association of passive smoking with hormone receptor-positive breast cancer did not differ from that with hormone receptor-negative breast cancer (Pheterogeneity > 0.05). There was evidence of interaction between passive smoking intensity and menopausal status in both overall group (P = 0.02) and hormone receptor-positive breast cancer group (P < 0.05). In Caucasian women, lifetime exposure to passive smoking is associated with the risk of breast cancer independent of tumor hormone receptor status with the strongest association in postmenopausal women.
Project description:The relationship between passive smoking exposure (PSE) and breast cancer risk is of major interest.To evaluate the relationship between PSE from partners and breast cancer risk stratified by hormone-receptor (HR) status in Chinese urban women population.Hospital-based matched case control study.Chinese urban breast cancer patients without current or previous active smoking history in China Medical University 1st Hospital, Liaoning Province, China between Jan 2009 and Nov 2009.Each breast cancer patient was matched 1?1 with healthy controls by gender and age (±2 years) from the same hospital.The authors used unconditional logistic regression analyses to estimate odds ratio for women with PSE from partners and breast cancer risk.312 pairs were included in the study. Women who endured PSE had significantly increased risk of breast cancer (adjusted OR: 1.46; 95% CI: 1.05-2.03; P?=?0.027), comparing with unexposed women. Women who exposed to >5 cigarettes/day also had significant increased risk (adjusted OR: 1.99; 95% CI: 1.28-3.10; P?=?0.002), as were women exposed to passive smoke for 16-25 years (adjusted OR: 1.87 95% CI: 1.22-2.86; P?=?0.004), and those exposed to > 4 pack-years (adjusted OR: 1.71 95% CI: 1.17-2.50; P?=?0.004). Similar trends were significant for estrogen receptor (ER)/progesterone receptor (PR) double positive subgroup(adjusted OR: 1.71; 2.20; 1.99; 1.92, respectively), but not for ER+/PR-, ER-/PR+, or ER-/PR- subgroups.limitations of the hospital-based retrospective study, lack of information on entire lifetime PSE and low statistical power.Our findings provide further evidence that PSE from partners contributes to increased risk of breast cancer, especially for ER/PR double positive breast cancer, in Chinese urban women.
Project description:We evaluated the association between smoking and risk of breast cancer in non-Hispanic white (NHW) and Hispanic or American Indian (HAI) women living in the Southwestern United States. Data on lifetime exposure to active and passive smoke data were available from 1527 NHW cases and 1601 NHW controls; 798 HAI cases and 924 HAI controls. Interleukin 6 (IL6) and Estrogen Receptor alpha (ESR1) polymorphisms were assessed in conjunction with smoking. Pack-years of smoking (>or=15) were associated with increased risk of pre-menopausal breast cancer among NHW women (OR 1.6, 95% CI 1.1-2. 4). Passive smoke increased risk of pre-menopausal breast cancer for HAI women (OR 1.9, 95% CI 1.1-3.1 everyone; OR 2.3, 95% CI 1.2-4.5 nonsmokers). HAI pre-menopausal women who were exposed to 10+ h of passive smoke per week and had the rs2069832 IL6 GG genotype had over a fourfold increased risk of breast cancer (OR 4.4, 95% CI 1.5-12.8; P for interaction 0.01). Those with the ESR1 Xba1 AA genotype had a threefold increased risk of breast cancer if they smoked>or=15 pack-years relative to non-smokers (P interaction 0.01). These data suggest that breast cancer risk is associated with active and passive smoking.
Project description:The role of passive smoking on breast cancer risk was unclear. This study aimed to evaluate the association between passive smoking and breast cancer risk among Chinese women.A hospital-based case-control study, including 877 breast cancer cases and 890 controls, frequency-matched by age and residence, was conducted. A structured questionnaire was used to collect information on passive smoking history through face-to-face interview by trained interviewers. Unconditional logistic regression models were used to estimate the association between passive smoking and breast cancer risk. A positive association between any passive smoking exposure and breast cancer risk was observed. Compared with women who were never exposed to passive smoking, women who were ever exposed had a higher breast cancer risk, with the adjusted odds ratio (OR) and 95% confidence interval (CI) of 1.35 (1.11-1.65). Similar result was found on home passive smoking exposure and breast cancer risk, but not on workplace passive smoking exposure. Women who were ever exposed to tobacco smoke at home had a higher risk of breast cancer compared with never exposed women, with the adjusted OR (95% CI) of 1.30 (1.05-1.61). Home passive smoking exposure showed significant dose-response relationships with breast cancer risk in smoker-years, cigarettes/day and total pack-years (Ptrend=0.003, 0.006 and 0.009, respectively). An increased total smoker-years of any passive exposure significantly elevated the risk of breast cancer (Ptrend<0.001). Positive associations and dose-response relationships were found among postmenopausal women and all subtypes of estrogen receptor (ER) and progesterone receptor (PR) status of breast cancer.Passive smoking was associated with an increased risk of breast cancer among non-smoking Chinese women. A stronger positive association with breast cancer risk was seen mainly among postmenopausal women.
Project description:<h4>Objective</h4>To examine the association between smoking and risk of invasive breast cancer using quantitative measures of lifetime passive and active smoking exposure among postmenopausal women.<h4>Design</h4>Prospective cohort study.<h4>Setting</h4>40 clinical centres in the United States.<h4>Participants</h4>79,990 women aged 50-79 enrolled in the Women's Health Initiative Observational Study during 1993-8.<h4>Main outcome measures</h4>Self reported active and passive smoking, pathologically confirmed invasive breast cancer.<h4>Results</h4>In total, 3520 incident cases of invasive breast cancer were identified during an average of 10.3 years of follow-up. Compared with women who had never smoked, breast cancer risk was elevated by 9% among former smokers (hazard ratio 1.09 (95% CI 1.02 to 1.17)) and by 16% among current smokers (hazard ratio 1.16 (1.00 to 1.34)). Significantly higher breast cancer risk was observed in active smokers with high intensity and duration of smoking, as well as with initiation of smoking in the teenage years. The highest breast cancer risk was found among women who had smoked for ? 50 years or more (hazard ratio 1.35 (1.03 to 1.77) compared with all lifetime non-smokers, hazard ratio 1.45 (1.06 to 1.98) compared with lifetime non-smokers with no exposure to passive smoking). An increased risk of breast cancer persisted for up to 20 years after smoking cessation. Among women who had never smoked, after adjustment for potential confounders, those with the most extensive exposure to passive smoking (? 10 years' exposure in childhood, ? 20 years' exposure as an adult at home, and ? 10 years' exposure as an adult at work) had a 32% excess risk of breast cancer compared with those who had never been exposed to passive smoking (hazard ratio 1.32 (1.04 to 1.67)). However, there was no significant association in the other groups with lower exposure and no clear dose response to cumulative passive smoking exposure.<h4>Conclusions</h4>Active smoking was associated with an increase in breast cancer risk among postmenopausal women. There was also a suggestion of an association between passive smoking and increased risk of breast cancer.
Project description:BACKGROUND:The role of passive smoking on cervical carcinogenesis remains controversial. We investigated the association of passive smoking with the risk of cervical intraepithelial neoplasia (CIN) and cervical cancer. METHODS:The study recruited 1,322 women, aged 18-65 with normal cytology (n = 592), CIN1 (n = 420), CIN2/3 (n = 165), and cervical cancer (n = 145) from 2006 to 2009. This study is a cross-sectional analysis using the baseline data from the Korean human papillomavirus (HPV) cohort study. Detailed information on smoking behaviors and lifestyles were collected using questionnaires. Multinomial logistic regression analysis was performed to estimate multivariable-adjusted odds ratios (ORs). RESULTS:Passive smoking was not statistically related to the risk of CINs and cervical cancer. However, passive smoking among non-smokers was associated with higher CIN 1 risk (OR 1.53; 95% confidence interval [CI], 1.07-2.18), compared to not passive smoking, after adjusting for demographic factors, lifestyles, and oncogenic-HPV infection status. CIN 1 risk increased with longer time exposed to passive smoking (P for trend <0.0003). Multivariate odds of <2 hours/day of passive smoking and that of ?2 hours/day of passive smoking were 2.48 (95% CI, 1.49-4.14) and 2.28 (95% CI, 1.21-4.26) for CIN 1, compared to not passive smoking. CONCLUSIONS:This study found that passive smoking among non-smoking women is associated with the risk of CIN 1.
Project description:Alcohol intake has been associated to breast cancer in pre and postmenopausal women; however results are inconclusive regarding tumor hormonal receptor status, and potential modifying factors like age at start drinking. Therefore, we investigated the relation between alcohol intake and the risk of breast cancer using prospective observational data from the European Prospective Investigation into Cancer and Nutrition (EPIC). Up to 334,850 women, aged 35-70 years at baseline, were recruited in ten European countries and followed up an average of 11 years. Alcohol intake at baseline and average lifetime alcohol intake were calculated from country-specific dietary and lifestyle questionnaires. The study outcomes were the Hazard ratios (HR) of developing breast cancer according to hormonal receptor status. During 3,670,439 person-years, 11,576 incident breast cancer cases were diagnosed. Alcohol intake was significantly related to breast cancer risk, for each 10 g/day increase in alcohol intake the HR increased by 4.2% (95% CI: 2.7-5.8%). Taking 0 to 5 g/day as reference, alcohol intake of >5 to 15 g/day was related to a 5.9% increase in breast cancer risk (95% CI: 1-11%). Significant increasing trends were observed between alcohol intake and ER+/PR+, ER-/PR-, HER2- and ER-/PR-HER2- tumors. Breast cancer risk was stronger among women who started drinking prior to first full-time pregnancy. Overall, our results confirm the association between alcohol intake and both hormone receptor positive and hormone receptor negative breast tumors, suggesting that timing of exposure to alcohol drinking may affect the risk. Therefore, women should be advised to control their alcohol consumption.
Project description:Breast cancer is the most common female cancer, affecting approximately one in eight women during their lifetime in North America and Europe. Receptor Activator of NF-kB Ligand (RANKL), its receptor RANK and the natural antagonist osteoprotegerin (OPG) are essential regulators of bone resorption. We have initially shown that RANKL/RANK are essential for hormone-driven mammary epithelial proliferation in pregnancy and RANKL/RANK have been implicated in mammary stem cell biology. Using genetic mouse-models, we and others identified the RANKL/RANK system as a key regulator of sex hormone, BRCA1-mutation, and oncogene-driven breast cancer and we proposed that RANKL/RANK might be involved in the initiation of breast tumors. We now report that in postmenopausal women without known genetic predisposition, high RANKL and progesterone serum levels stratify a subpopulation of women at high risk of developing breast cancer 12-24 months before diagnosis (5.33-fold risk, 95%CI 1.5-25.4; P=0.02). In women with established breast cancer, we demonstrate that RANKL/OPG ratios change dependent on the presence of circulating tumor cells (CTCs). Finally, we show in a prospective human breast cancer cohort that alterations in RANKL/OPG ratios are significantly associated with breast cancer manifestation. These data indicate that the RANKL/RANK/OPG system is deregulated in post-menopausal women at high risk for breast cancer and in women with circulating tumor cells. Thus, serum levels of RANKL/OPG are potentially indicative of predisposition and progression of breast cancer in humans. Advancement of our findings towards clinical application awaits prior validation in independent patient cohorts.
Project description:Previous studies investigating the relationship between passive maternal smoking and preterm birth reveal inconsistent results. We conducted the current meta-analysis of observational studies to evaluate the relationship between passive maternal smoking and preterm birth. We identified relevant studies by searching PubMed, EMBASE, and ISI Web of Science databases. We used random-effects models to estimate summary odds ratios (SORs) and 95% confidence intervals (CIs) for aforementioned association. For the analysis, we included 24 studies that involved a total of 5607 women who experienced preterm birth. Overall, the SORs of preterm birth for women who were ever exposed to passive smoking versus women who had never been exposed to passive smoking at any place and at home were 1.20 (95%CI = 1.07-1.34,I(2) = 36.1%) and 1.16 (95%CI = 1.04-1.30,I(2) = 4.4%), respectively. When we conducted a stratified analysis according to study design, the risk estimate was slightly weaker in cohort studies (SOR = 1.10, 95%CI = 1.00-1.21,n = 16) than in cross-sectional studies (SOR = 1.47, 95%CI = 1.23-1.74,n = 5). Additionally, the associations between passive maternal smoking and preterm birth were statistically significant for studies conducted in Asia (SOR = 1.26, 95%CI = 1.05-1.52), for studies including more than 100 cases of preterm birth (SOR = 1.22, 95%CI = 1.05-1.41), and for studies adjusted for maternal age (SOR = 1.27,95%CI = 1.09-1.47), socioeconomic status and/or education (SOR = 1.28, 95%CI = 1.10-1.49), body mass index (SOR = 1.33, 95%CI = 1.04-1.71), and parity (SOR = 1.27, 95%CI = 1.13-1.43). Our findings demonstrate that passive maternal smoking is associated with an increased risk of preterm birth. Future prospective cohort studies are warranted to provide more detailed results stratified by passive maternal smoking during different trimesters of pregnancy and by different types and causes of preterm birth.
Project description:BACKGROUND: Several case-control studies have suggested that passive smoking may increase the incidence of female breast cancer. However, the results of cohort studies have been inconsistent in establishing an association. The present study evaluated the association between passive smoking and incidence of female breast cancer through a meta-analysis of prospective cohort studies. METHODS: Relevant articles published before August 2012 were identified by searching the electronic databases PubMed, Embase, and Web of Science. Pooled relative risks (RRs) were determined with either a fixed or random effects model and were used to assess the strength of the association. Sensitivity and subgroup analyses according to ethnicity, menopausal status, and the period and place of exposure to passive smoking were also performed. RESULTS: Ten prospective cohort studies involving 782 534 female non-smokers were included in the meta-analysis and 14 831 breast cancer cases were detected. Compared with the women without exposure to passive smoking, the overall combined RR of breast cancer was 1.01 (95% confidence interval: 0.96 to 1.06, P = 0.73) among women with exposure to passive smoking. Similar results were achieved through the subgroup analyses. No evidence of publication bias was observed. CONCLUSION: The results suggest that passive smoking may not be associated with increased incidence of breast cancer. However, the present conclusion should be considered carefully and confirmed with further studies.
Project description:INTRODUCTION:Previous investigations found elevated mortality after breast cancer in association with biomarkers of persistent organochlorine pesticides in non-occupationally exposed women. We hypothesized that lifetime residential pesticide use, which includes persistent and non-persistent pesticides, would also be associated with increased mortality after breast cancer. METHODS:A population-based cohort of 1505 women with invasive or in situ breast cancer was interviewed in 1996-1997, shortly after diagnosis, about pre-diagnostic lifetime residential pesticide use. Participants were followed for mortality through 2014 (595 deaths from any cause and 236 from breast cancer, after 17.6 years of follow-up). Pesticides were examined as 15 individual categories; a group of seven used for lawn and garden purposes; a group of eight used for nuisance-pest purposes; and all combined. Cox regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and breast cancer-specific mortality. Modification by estrogen receptor (ER) status, body mass index, and long-term residence was examined. RESULTS:Ever use (HR?=?0.77, 95%CI?=?0.63-0.95) and higher lifetime applications (4th quartile: HR?=?0.62, 95%CI?=?0.47-0.81, ptrend?=?0.3) of the lawn and garden group of pesticides were inversely associated with all-cause mortality, compared to never use. The inverse association for lawn and garden pesticide use was limited to ER positive (vs. negative) tumors (pinteraction?=?0.05). Nuisance-pest pesticides, and all groups combined, were not associated with all-cause or breast cancer-specific mortality. CONCLUSIONS:Contrary to our hypothesis, lifetime residential use of lawn and garden pesticides, but not all combined or nuisance-pest pesticides, was inversely associated with all-cause mortality after breast cancer.