Dataset Information

Pooled analysis of active cigarette smoking and invasive breast cancer risk in 14 cohort studies.

ABSTRACT:

Background

The 2014?US Surgeon General's report noted research gaps necessary to determine a causal relationship between active cigarette smoking and invasive breast cancer risk, including the role of alcohol consumption, timing of exposure, modification by menopausal status and heterogeneity by oestrogen receptor (ER) status.

Methods

To address these issues, we pooled data from 14 cohort studies contributing 934 681 participants (36 060 invasive breast cancer cases). Cox proportional hazard regression models were used to calculate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs).

Results

Smoking duration before first birth was positively associated with risk ( P -value for trend = 2 × 10 -7 ) with the highest HR for initiation >10 years before first birth (HR?=?1.18, CI 1.12-1.24). Effect modification by current alcohol consumption was evident for the association with smoking duration before first birth ( P -value=2×10 -4 ); compared with never-smoking non-drinkers, initiation >10 years before first birth was associated with risk in every category of alcohol intake, including non-drinkers (HR?=?1.15, CI 1.04-1.28) and those who consumed at least three drinks per day (1.85, 1.55-2.21). Associations with smoking before first birth were limited to risk of ER+ breast cancer ( P -value for homogeneity=3×10 -3 ). Other smoking timing and duration characteristics were associated with risk even after controlling for alcohol, but were not associated with risk in non-drinkers. Effect modification by menopause was not evident.

Conclusions

Smoking, particularly if initiated before first birth, was modestly associated with ER+ breast cancer risk that was not confounded by amount of adult alcohol intake. Possible links with breast cancer provide additional motivation for young women to not initiate smoking.

SUBMITTER: Gaudet MM

PROVIDER: S-EPMC5837778 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature

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Publications

Pooled analysis of active cigarette smoking and invasive breast cancer risk in 14 cohort studies.

Gaudet Mia M MM Carter Brian D BD Brinton Louise A LA Falk Roni T RT Gram Inger T IT Luo Juhua J Milne Roger L RL Nyante Sarah J SJ Weiderpass Elisabete E Beane Freeman Laura E LE Sandler Dale P DP Robien Kim K Anderson Kristin E KE Giles Graham G GG Chen Wendy Y WY Feskanich Diane D Braaten Tonje T Isaacs Claudine C Butler Lesley M LM Koh Woon-Puay WP Wolk Alicja A Adami Hans-Olov HO White Emily E Margolis Karen L KL Thun Michael J MJ Gapstur Susan M SM

International journal of epidemiology 20170601 3

<h4>Background</h4>The 2014 US Surgeon General's report noted research gaps necessary to determine a causal relationship between active cigarette smoking and invasive breast cancer risk, including the role of alcohol consumption, timing of exposure, modification by menopausal status and heterogeneity by oestrogen receptor (ER) status.<h4>Methods</h4>To address these issues, we pooled data from 14 cohort studies contributing 934 681 participants (36 060 invasive breast cancer cases). Cox proporti ...[more]

PMID: 28031315

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Project description:BACKGROUND:Alcohol consumption and cigarette smoking are associated with an increased risk of breast cancer (BC), but it is unclear whether these associations vary by a woman's familial BC risk. METHODS:Using the Prospective Family Study Cohort, we evaluated associations between alcohol consumption, cigarette smoking, and BC risk. We used multivariable Cox proportional hazard models to estimate hazard ratios (HR) and 95% confidence intervals (CI). We examined whether associations were modified by familial risk profile (FRP), defined as the 1-year incidence of BC predicted by Breast Ovarian Analysis of Disease Incidence and Carrier Estimation Algorithm (BOADICEA), a pedigree-based algorithm. RESULTS:We observed 1009 incident BC cases in 17,435 women during a median follow-up of 10.4 years. We found no overall association of smoking or alcohol consumption with BC risk (current smokers compared with never smokers HR 1.02, 95% CI 0.85-1.23; consuming ≥ 7 drinks/week compared with non-regular drinkers HR 1.10, 95% CI 0.92-1.32), but we did observe differences in associations based on FRP and by estrogen receptor (ER) status. Women with lower FRP had an increased risk of ER-positive BC associated with consuming ≥ 7 drinks/week (compared to non-regular drinkers), whereas there was no association for women with higher FRP. For example, women at the 10th percentile of FRP (5-year BOADICEA = 0.15%) had an estimated HR of 1.46 (95% CI 1.07-1.99), whereas there was no association for women at the 90th percentile (5-year BOADICEA = 4.2%) (HR 1.07, 95% CI 0.80-1.44). While the associations with smoking were not modified by FRP, we observed a positive multiplicative interaction by FRP (pinteraction = 0.01) for smoking status in women who also consumed alcohol, but not in women who were non-regular drinkers. CONCLUSIONS:Moderate alcohol intake was associated with increased BC risk, particularly for women with ER-positive BC, but only for those at lower predicted familial BC risk (5-year BOADICEA < 1.25). For women with a high FRP (5-year BOADICEA ≥ 6.5%) who also consumed alcohol, being a current smoker was associated with increased BC risk.

Project description:BACKGROUND:Observational studies suggested that tobacco smoking was associated with diabetic nephropathy (DN). However, the results were conflicting and inconsistent. In the study, we performed a meta-analysis to assess the relationship between tobacco smoking and the development of DN. MATERIALS AND METHODS:We searched in PubMed, Embase, Web of Science and the Cochrane Library (CENTRAL) from database inception until Mar 8, 2018, and updated our search on May 1, 2018. We screened the reference lists of the retrieved articles. Only original prospective cohort studies which have investigated the association between smoking and DN incidence or its progression were included. Pooled HRs and 95% confidence intervals (CIs) were calculated using a random effects model. RESULTS:A total of 9 prospective cohort studies were identified, including more than 203337 participants. Compared with those of no smoking, smoking participants increased the risk of developing DN (HR = 1.07, 95% CI: 1.01-1.13, P = 0.01). The subgroup analysis showed that the current and total smoking may increase the risk of DN, but these results did not reach statistical significance (current: HR = 1.69, 95% CI = 0.79-3.64, p = 0.17; total: HR = 1.17, 95% CI = 0.97-1.41, p = 0.10), whereas former smoking significantly increased the risk of DN (HR = 1.04, 95% CI = 1.03-1.05, p<0.001). Compared with no-smokers, smokers showed an elevated risk of developing DN (HR = 1.05; 95% CI, 1.00-1.11, P = 0.05). In patients with T2DM, those who smoked were at an increased risk of developing DN, as compared to those who had never smoked (HR = 1.05; 95% CI, 1.00-1.11, P = 0.05). However, compared to no smoking, smoking did not increase the risk of DN development in patients with T2DM (HR = 1.15; 95% CI, 0.9-1.47, P = 0.25). Univariate and multivariate meta-regression did not find any confounding factors. No publication bias was found in the meta-analysis. CONCLUSIONS:The present study highlighted that smoking was an independent risk factor for DN, especially in patients with T1DM. This is the first meta-analysis of prospective cohort studies to discuss the relationship between smoking and DN.

Dataset Information

Pooled analysis of active cigarette smoking and invasive breast cancer risk in 14 cohort studies.

Background

Methods

Results

Conclusions

Publications

Pooled analysis of active cigarette smoking and invasive breast cancer risk in 14 cohort studies.

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