Exposure to hazardous air pollutants and risk of incident breast cancer in the nurses’ health study II

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Abstract

Background

Findings from a recent prospective cohort study in California suggested increased risk of breast cancer associated with higher exposure to certain carcinogenic and estrogen-disrupting hazardous air pollutants (HAPs). However, to date, no nationwide studies have evaluated these possible associations. Our objective was to examine the impacts of mammary carcinogen and estrogen disrupting HAPs on risk of invasive breast cancer in a nationwide cohort.

Methods

We assigned HAPs from the US Environmental Protection Agency’s 2002 National Air Toxics Assessment to 109,239 members of the nationwide, prospective Nurses’ Health Study II (NHSII). Risk of overall invasive, estrogen receptor (ER)-positive (ER+), and ER-negative (ER-) breast cancer with increasing quartiles of exposure were assessed in time-varying multivariable proportional hazards models, adjusted for traditional breast cancer risk factors.

Results

A total of 3321 invasive cases occurred (2160 ER+, 558 ER-) during follow-up 1989–2011. Overall, there was no consistent pattern of elevated risk of the HAPs with risk of breast cancer. Suggestive elevations were only seen with increasing 1,2-dibromo-3-chloropropane exposures (multivariable adjusted HR of overall breast cancer = 1.12, 95% CI: 0.98–1.29; ER+ breast cancer HR = 1.09; 95% CI: 0.92, 1.30; ER- breast cancer HR = 1.14; 95% CI: 0.81, 1.61; each in the top exposure quartile compared to the lowest).

Conclusions

Exposures to HAPs during adulthood were not consistently associated with an increased risk of overall or estrogen-receptor subtypes of invasive breast cancer in this nationwide cohort of women.

Electronic supplementary material

The online version of this article (10.1186/s12940-018-0372-3) contains supplementary material, which is available to authorized users.

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Most cited references 35

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Proportion of breast cancer cases in the United States explained by well-established risk factors.

M. P. Madigan, R G Ziegler, J Benichou … (1995)

Few estimates of the fraction of cases of breast cancer attributable to recognized risk factors have been published. All estimates are based on selected groups, making their generalizability to the U.S. population uncertain. Our goal was to estimate the fraction of breast cancer cases in the United States attributable to well-established risk factors (i.e., later age at first birth, nulliparity, higher family income, and first-degree family history of breast cancer), using data from the first National Health and Nutrition Examination Survey (NHANES I) Epidemiologic Follow-up Study (NHEFS), the survey and follow-up of a probability sample of the U.S. population. From a cohort of 7508 female participants surveyed in the early 1970s, and followed up between 1982 and 1984 and again in 1987, 193 breast cancer cases were accrued for study. We calculated incidence rates, relative risks (RRs), and population attributable risks (PARs) for breast cancer risk factors and extended our results to the U.S. female population by using sample weights from the NHANES I survey. Our PAR estimates suggest that later age at first birth and nulliparity accounted for a large fraction of U.S. breast cancer cases, 29.5% (95% confidence interval [CI] = 5.6%-53.3%); higher income contributed 18.9% (95% CI = -4.3% to 42.1%), and family history of breast cancer accounted for 9.1% (95% CI = 3.0%-15.2%). Taken together, these well-established risk factors accounted for approximately 47% (95% CI = 17%-77%) of breast cancer cases in the NHEFS cohort and about 41% (95% CI = 2%-80%) in the U.S. population. The RRs for most of these risk factors were modest, but their prevalence as a group was high, leading to estimates that suggest that a substantial proportion of breast cancer cases in the United States are explained by well-established risk factors. Elucidation of the determinants underlying recognized factors and study of other factors that may confer risk or protection are needed in efforts to advance understanding of breast cancer etiology and to aid in devising strategies for prevention.

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Comparison of molecular phenotypes of ductal carcinoma in situ and invasive breast cancer

Rulla M Tamimi, Heather J. Baer, Jonathan D. Marotti … (2008)

Introduction At least four major categories of invasive breast cancer that are associated with different clinical outcomes have been identified by gene expression profiling: luminal A, luminal B, human epidermal growth factor receptor 2 (HER2) and basal-like. However, the prevalence of these phenotypes among cases of ductal carcinoma in situ (DCIS) has not been previously evaluated in detail. The purpose of this study was to compare the prevalence of these distinct molecular subtypes among cases of DCIS and invasive breast cancer. Methods We constructed tissue microarrays (TMAs) from breast cancers that developed in 2897 women enrolled in the Nurses' Health Study (1976 to 1996). TMA slides were immunostained for oestrogen receptor (ER), progesterone receptor (PR), HER2, cytokeratin 5/6 (CK5/6) and epidermal growth factor receptor (EGFR). Using these immunostain results, cases were grouped into molecularly defined subtypes. Results The prevalence of the distinct molecular phenotypes differed significantly between DCIS (n = 272) and invasive breast cancers (n = 2249). The luminal A phenotype was significantly more frequent among invasive cancers (73.4%) than among DCIS lesions (62.5%) (p = 0.0002). In contrast, luminal B and HER2 molecular phenotypes were both more frequent among DCIS (13.2% and 13.6%, respectively) as compared with invasive tumours (5.2% and 5.7%, respectively) (p < 0.0001). The basal-like phenotype was more frequent among the invasive cancers (10.9%) than DCIS (7.7%), although this difference was not statistically significant (p = 0.15). High-grade DCIS and invasive tumours were more likely to be HER2 type and basal-like than low- or intermediate-grade lesions. Among invasive tumours, basal-like and HER2 type tumours were more likely to be more than 2 cm in size, high-grade and have nodal involvement compared with luminal A tumours. Conclusion The major molecular phenotypes previously identified among invasive breast cancers were also identified among cases of DCIS. However, the prevalence of the luminal A, luminal B and HER2 phenotypes differed significantly between DCIS and invasive breast cancers.

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Breast cancer risk prediction using a clinical risk model and polygenic risk score

Elad Ziv, Karla Kerlikowske, Steven R Cummings … (2016)

Breast cancer risk assessment can inform the use of screening and prevention modalities. We investigated the performance of the Breast Cancer Surveillance Consortium (BCSC) risk model in combination with a polygenic risk score (PRS) comprised of 83 single nucleotide polymorphisms identified from genome-wide association studies. We conducted a nested case-control study of 486 cases and 495 matched controls within a screening cohort. The PRS was calculated using a Bayesian approach. The contributions of the PRS and variables in the BCSC model to breast cancer risk were tested using conditional logistic regression. Discriminatory accuracy of the models was compared using the area under the receiver operating characteristic curve (AUROC). Increasing quartiles of the PRS were positively associated with breast cancer risk, with OR 2.54 (95 % CI 1.69-3.82) for breast cancer in the highest versus lowest quartile. In a multivariable model, the PRS, family history, and breast density remained strong risk factors. The AUROC of the PRS was 0.60 (95 % CI 0.57-0.64), and an Asian-specific PRS had AUROC 0.64 (95 % CI 0.53-0.74). A combined model including the BCSC risk factors and PRS had better discrimination than the BCSC model (AUROC 0.65 versus 0.62, p = 0.01). The BCSC-PRS model classified 18 % of cases as high-risk (5-year risk ≥3 %), compared with 7 % using the BCSC model. The PRS improved discrimination of the BCSC risk model and classified more cases as high-risk. Further consideration of the PRS's role in decision-making around screening and prevention strategies is merited.

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Author and article information

Contributors

Jaime E. Hart: 617-525-2289 , Jaime.hart@channing.harvard.edu

Kimberly A. Bertrand: kab15@bu.edu

Natalie DuPre: ncd121@mail.harvard.edu

Peter James: pjames@hsph.harvard.edu

Verónica M. Vieira: vvieira@uci.edu

Trang VoPham: tvopham@hsph.harvard.edu

Maggie R. Mittleman: mmittlem@wellesley.edu

Rulla M. Tamimi: rulla.tamimi@channing.harvard.edu

Francine Laden: francine.laden@channing.harvard.edu

Journal

Journal ID (nlm-ta): Environ Health

Journal ID (iso-abbrev): Environ Health

Title: Environmental Health

Publisher: BioMed Central (London )

ISSN (Electronic): 1476-069X

Publication date (Electronic): 27 March 2018

Publication date PMC-release: 27 March 2018

Publication date Collection: 2018

Volume: 17

Electronic Location Identifier: 28

Affiliations

[1 ]ISNI 0000 0004 0378 8294, GRID grid.62560.37, Channing Division of Network Medicine, Department of Medicine, , Brigham and Women’s Hospital and Harvard Medical School, ; 401 Park Dr, Landmark Center, 3rd Floor West (BWH/HSPH), Boston, MA 02215 USA

[2 ]ISNI 000000041936754X, GRID grid.38142.3c, Exposure, Epidemiology, and Risk Program, Department of Environmental Health, Harvard T.H. Chan School of Public Health, ; Boston, MA USA

[3 ]ISNI 0000 0004 1936 7558, GRID grid.189504.1, Slone Epidemiology Center at Boston University, ; Boston, MA USA

[4 ]ISNI 000000041936754X, GRID grid.38142.3c, Department of Epidemiology, Harvard T.H. Chan School of Public Health, ; Boston, MA USA

[5 ]Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA USA

[6 ]ISNI 0000 0001 0668 7243, GRID grid.266093.8, Program in Public Health, , University of California, ; Irvine, CA USA

Article

Publisher ID: 372

DOI: 10.1186/s12940-018-0372-3

PMC ID: 5870204

PubMed ID: 29587753

SO-VID: 7fa91074-ad44-4a07-8071-edfa53aebade

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 23 August 2017

Date accepted : 13 March 2018

Funding

Funded by: FundRef http://dx.doi.org/10.13039/100000869, Susan G. Komen for the Cure;

Award ID: IIR13264020

Award Recipient : Rulla M. Tamimi

Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;

Award ID: T32 CA009001

Funded by: FundRef http://dx.doi.org/10.13039/100000054, National Cancer Institute;

Award ID: K99 CA201542

Award ID: UM1 CA176726

Award Recipient : Peter James

Funded by: FundRef http://dx.doi.org/10.13039/100000066, National Institute of Environmental Health Sciences;

Award ID: R01 ES017017

Award ID: P30 ES000002

Award Recipient : Francine Laden

Custom metadata

ScienceOpen disciplines: Public health

Keywords: air pollution,hazardous air pollutants,breast cancer

Data availability:

ScienceOpen disciplines: Public health

Keywords: air pollution, hazardous air pollutants, breast cancer

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Exposure to hazardous air pollutants and risk of incident breast cancer in the nurses’ health study II

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Abstract

Background

Methods

Results

Conclusions

Electronic supplementary material

Related collections

Pneumonia, sex, and the environment

Most cited references 35

Proportion of breast cancer cases in the United States explained by well-established risk factors.

Comparison of molecular phenotypes of ductal carcinoma in situ and invasive breast cancer

Breast cancer risk prediction using a clinical risk model and polygenic risk score

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Cited by 12

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