Dataset Information

Lack of an association between passive smoking and incidence of female breast cancer in non-smokers: evidence from 10 prospective cohort studies.

ABSTRACT:

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.

SUBMITTER: Yang Y

PROVIDER: S-EPMC3800073 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Lack of an association between passive smoking and incidence of female breast cancer in non-smokers: evidence from 10 prospective cohort studies.

Yang Yuan Y Zhang Fan F Skrip Laura L Wang Yang Y Liu Shengchun S

PloS one 20131018 10

<h4>Background</h4>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.<h4>Methods</h4>Relevant articles published before August 2012 were identified by searching the electronic dat ...[more]

PMID: 24204725

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Project description:INTRODUCTION The number of cessation clinics in China have been increasing ever since the Chinese government supported the establishment of smoking cessation clinics (SCCs) in each province in 2014. Many studies have examined smoking cessation behaviors among male smokers, but few of female smokers. This study aimed to understand female smokers’ quitting behaviors in SCCs and identify predictors of successful cessation. METHODS This study used data of the SCCs Platform in China from 2018 to 2020. The self-reported 7-day point prevalence of abstinence rate (PPAR) at 1 month and at 3 months follow-up and the continuous abstinence rate (CAR) at 3 months follow-up are reported based on smokers’ characteristics and intention to treat analysis. A multiple logistic regression model was used to identify predictors of continuous abstinence at 3 months follow-up. RESULTS The 7-day PPAR of female outpatients in SCCs was 29.20% at 1 month follow-up and 28.36% at 3 months follow-up. The CAR at 3 months follow-up was 19.88%. Female smokers who were prepared to quit within 7 days (AOR=2.86; 95% CI: 1.53–5.32), today (AOR=4.01; 95% CI: 2.35–6.85), had started to quit (AOR=7.11; 95% CI: 4.12–12.27), and used a combination of counseling and drugs (AOR=2.41; 95% CI: 1.73–3.35) were more likely to quit smoking. Associated with lower quitting rates were: living in the central region of China (AOR=0.47; 95% CI: 0.31–0.73) and the west region (AOR=0.48; 95% CI: 0.31–0.73); being aged 30–39 years (AOR=0.39; 95% CI: 0.23–0.64), and 40–49 years (AOR=0.41; 95% CI:0.24–0.69); being unemployed (AOR=0.64; 95% CI: 0.45–0.91); having a fair perceived health status at the first visit (AOR=0.65; 95% CI: 0.47–0.91) and a poor one (AOR=0.37; 95% CI: 0.21–0.64); having a moderate nicotine dependence (AOR=0.64; 95% CI: 0.44–0.92) and a severe one (AOR=0.50; 95% CI: 0.34–0.72). CONCLUSIONS In our study, the region of residence, age, employment, perceived health status, Fagerström test for nicotine dependence (FTND), readiness to quit, and intervention model were independent predictors of quitting for female smokers. Improving the motivation to quit, providing intensive psychological interventions and equipping SCCs with cessation medication would assist female smokers to quit.

Project description:BackgroundLung cancer is the leading cause of worldwide cancer deaths. While smoking is its leading risk factor, few prospective cohort studies have reported on the association of lung cancer with both active and passive smoking. This study aimed to determine the relationship between lung cancer incidence with both active and passive smoking (childhood, adult at home, and at work).Patients and methodsThe Women's Health Initiative Observational Study (WHI-OS) was a prospective cohort study conducted at 40 US centers that enrolled postmenopausal women from 1993 to 1999. Among 93 676 multiethnic participants aged 50-79, 76 304 women with complete smoking and covariate data comprised the analytic cohort. Lung cancer incidence was calculated by Cox proportional hazards models, stratified by smoking status.ResultsOver 10.5 mean follow-up years, 901 lung cancer cases were identified. Compared with never smokers (NS), lung cancer incidence was much higher in current [hazard ratio (HR) 13.44, 95% confidence interval (CI) 10.80-16.75] and former smokers (FS; HR 4.20, 95% CI 3.48-5.08) in a dose-dependent manner. Current and FS had significantly increased risk for all lung cancer subtypes, particularly small-cell and squamous cell carcinoma. Among NS, any passive smoking exposure did not significantly increase lung cancer risk (HR 0.88, 95% CI 0.52-1.49). However, risk tended to be increased in NS with adult home passive smoking exposure ≥30 years, compared with NS with no adult home exposure (HR 1.61, 95% CI 1.00-2.58).ConclusionsIn this prospective cohort of postmenopausal women, active smoking significantly increased risk of all lung cancer subtypes; current smokers had significantly increased risk compared with FS. Among NS, prolonged passive adult home exposure tended to increase lung cancer risk. These data support continued need for smoking prevention and cessation interventions, passive smoking research, and further study of lung cancer risk factors in addition to smoking. CLINICALTRIALS.GOV: NCT00000611.

Project description:CHRNA5-A3-B4 variants, rs16969968, rs588765 and rs578776, are consistently associated with tobacco consumption among smokers, but the association with smoking cessation is less consistent. Among the studies that reported significant associations with cessation, the effects were observed in smokers treated with placebo treatment in some studies and conversely in those receiving active pharmacological therapy (bupropion and nicotine replacement therapies) in others. Thus, it remains unclear whether CHRNA5-A3-B4 is a useful marker for optimizing smoking cessation. Using data from 654 Caucasian smokers treated with placebo, nicotine patch or varenicline, we investigated whether CHRNA5-A3-B4 variants were associated with smoking cessation outcomes, and whether there were significant genotype-by-treatment or haplotype-by-treatment interactions. We observed no significant associations between CHRNA5-A3-B4 variants and smoking cessation, despite replicating previous associations with baseline tobacco consumption. At end of treatment the effect size on smoking cessation in the placebo, patch and varenicline groups for rs16969968 [GG vs. GA+AA] was OR = 0.66 (P = 0.23), OR = 1.01 (P = 0.99), and OR = 1.30 (P = 0.36) respectively, of rs588765 [CC vs. CT+TT] was OR = 0.96 (P = 0.90), OR = 0.84 (P = 0.58), and OR = 0.74 (P = 0.29) respectively, and for rs578776 [GG vs. GA+AA] on smoking cessation was OR = 1.02 (P = 0.95), OR = 0.75 (P = 0.35), and OR = 1.20 (P = 0.51) respectively. Furthermore, we observed no associations with cessation using the CHRNA5-A3-B4 haplotype (constructed using rs16969968 and rs588765), nor did we observe any significant genotype-by-treatment interactions, with or without adjusting for the rate of nicotine metabolism (all P>0.05). We also observed no significant genetic associations with 6 month or 12 month smoking abstinence. In conclusion, we found no association between CHRNA5-A3-B4 variants and smoking cessation rates in this clinical trial; however, as expected, significant associations with baseline tobacco consumption were replicated. Our data suggest that CHRNA5-A3-B4 gene variants do not exhibit a robust association with smoking cessation and are unlikely to be useful for clinically optimizing smoking cessation pharmacotherapy for Caucasian smokers.

Dataset Information

Lack of an association between passive smoking and incidence of female breast cancer in non-smokers: evidence from 10 prospective cohort studies.

Background

Methods

Results

Conclusion

Publications

Lack of an association between passive smoking and incidence of female breast cancer in non-smokers: evidence from 10 prospective cohort studies.

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