The Accumulating Evidence on Passive and Active Smoking and Breast Cancer Risk

Johnson, Colin

doi:10.1097/00001648-200611001-00813

Cited by 10 publications

(19 citation statements)

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“…A recent meta-analysis of prospective studies of the association between passive smoking and breast cancer (eight studies, but not including reference 5) found an overall null association (summary relative risk: 0.99; 95% CI: 0.93, 1.05) [28]. Our study, which characterized tobacco smoke exposures in the same manner as the five studies favored by Johnson [1] in his review, agrees with the findings of most prospective cohort studies as well as a large pooled analysis [27]. …”

Section: Discussionmentioning

confidence: 50%

“…The five studies, very similar in design to this study, each showed increased odds of breast cancer among women ever passively exposed to tobacco smoke, compared with women not passively or actively exposed (summary OR: 1.9; 95% CI: 1.5, 2.4), and increased odds of breast cancer among ever-active smokers, compared to never actively, never regularly passively exposed women (summary OR: 2.1; 95% CI: 1.4, 3.0) [1]. All five of the studies highlighted in Johnson's review assessed tobacco smoke exposure retrospectively-i.e., after the breast cancer cases had occurred-and were therefore susceptible to differential exposure misclassification.…”

Section: Discussionmentioning

confidence: 60%

“…Studies of passive smoking and breast cancer risk are more evenly split between positive [2, 9, 11-13, 16, 18, 20] and null [4,5,8,10,14,17,19] associations. In a recent review, Johnson [1] identified five Lifetime passive smoking exposure (all ever actively exposed subjects excluded)…”

Section: Discussionmentioning

confidence: 99%

“…Active and passive tobacco smoke exposures are hypothesized to be modifiable risk factors for female breast cancer, a disease with few known mutable causes [1]. Several studies have assessed the tobacco smoke and breast cancer association in various populations and with varying thoroughness of exposure assessment.…”

Section: Introductionmentioning

confidence: 99%

“…Early studies showing little or no association between breast cancer risk and overall tobacco smoke exposure were criticized for inclusion of passively exposed persons in the reference group of never-active smokers, which perhaps attenuated an underlying positive association with exposure to tobacco smoke from any source [2]. Some early studies of passive tobacco smoke exposure were also criticized for failing to capture important sources of lifetime exposure (e.g., accounting for exposure at home, but not at the workplace), which might also have masked a truly elevated breast cancer risk [1]. A majority of studies have shown null associations between active tobacco smoke exposure and breast cancer [3][4][5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Lifetime tobacco smoke exposure and breast cancer incidence

Ahern

Lash

Egan

et al. 2009

Cancer Causes Control

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Section: Discussionmentioning

confidence: 50%

Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Lifetime tobacco smoke exposure and breast cancer incidence

Ahern

Lash

Egan

et al. 2009

Cancer Causes Control

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Tobacco smoking, NAT2 acetylation genotype and breast cancer risk

Lissowska

Brinton

Zatoński

et al. 2006

Intl Journal of Cancer

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The role of active and passive cigarette smoking in breast cancer etiology remains controversial. Using data from a large population-based case-control study in Poland (2386 cases, 2502 controls) conducted during 2000-2003, we examined the associations between active and passive smoking overall and for different age categories. We also evaluated differences in risk by estrogen receptor (ER) and progesterone receptor (PR) status in tumors, and the potential modification of the smoking association by N-acetyl transferase 2 (NAT2) genotype. Women ever exposed to passive smoking at home or at work had a risk of breast cancer similar to those never exposed to active or passive smoking (OR (95%CI) 5 1.11 (0.85-1.46), and no trends were observed with increasing hours/day-years of passive smoking exposure. Active smoking was associated with a significant increase in risk only among women younger than 45 years of age (OR (95%CI) 5 1.95 (1.38-2.76); 1.15 (0.93-1.40); 0.91 (0.77-1.09) for <45, 45-55 and >55 years of age, respectively; p-heterogeneity <0.001 for <45 vs. >55 years) and prevailed for both ER1 and ER2 tumors. The smoking association among women <45 years was stronger for current than former smokers, and a significant trend was observed with duration of smoking (p 5 0.04). NAT2 slow vs. rapid/intermediate acetylation genotype was not related to breast cancer risk (0.99 (0.87-1.13)), and did not significantly modify the smoking relationships. In conclusion, our data indicate that passive smoking is not associated with breast cancer risk; however, active smoking might be associated with an increased risk for early onset breast cancers. ' 2006 Wiley-Liss, Inc.

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Breast cancer prevention based on gene–environment interaction

Song

Lee

Kang

2011

Molecular Carcinogenesis

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Breast cancer, the most common cancer in women, results from combined effects of genetic and environmental factors. Although a number of preventive measures have been suggested to reduce the risk of breast cancer, only a few (e.g., regular mammogram, etc.) proved to be efficient preventive modalities. Among many potential reasons, differences in individual susceptibility factors may complicate the efficacy of the intervention. A growing body of evidence shows that the strength of association between various dietary, behavioral (exercise and obesity), and environmental exposures, and breast cancer risk may be modified by individual genetic factors. Preventive strategies against breast cancer will be discussed considering the findings of the gene-environment interaction of breast cancer. These include behavior modification for high-risk subjects (primary prevention), early detection and extensive monitoring of genetically susceptible subjects and noninvasive treatment of early stage cancer cases (secondary prevention), and finally prophylactic and therapeutic intervention to slow the progression of diseases (tertiary prevention). The accumulating evidences of the gene-environment interactions provide a better understanding of the breast cancer development and enable us to adopt individualized preventive strategies for personalized health care.

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The Accumulating Evidence on Passive and Active Smoking and Breast Cancer Risk

Cited by 10 publications

References 0 publications

Lifetime tobacco smoke exposure and breast cancer incidence

Lifetime tobacco smoke exposure and breast cancer incidence

Tobacco smoking, NAT2 acetylation genotype and breast cancer risk

Breast cancer prevention based on gene–environment interaction

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