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Environ Int. 2016 Apr-May;89-90:185-92. doi: 10.1016/j.envint.2016.02.009. Epub 2016 Feb 13.

Exposure to multiple sources of polycyclic aromatic hydrocarbons and breast cancer incidence.

Author information

1
Department of Epidemiology, University of North Carolina, Chapel Hill, NC, USA. Electronic address: whitea@unc.edu.
2
Department of Nutrition, University of North Carolina, Chapel Hill, NC, USA.
3
Department of Biostatistics, University of North Carolina, Chapel Hill, NC, USA.
4
Department of Preventive Medicine, Ichan School of Medicine at Mt. Sinai, New York, NY, USA.
5
Consulting in the Public Interest (CIPI), Lambertville, NJ, USA.
6
Department of Epidemiology, Columbia University, USA.
7
Department of Epidemiology and Biostatistics, University of South Carolina, Columbia, SC, USA.
8
Department of Epidemiology, University of North Carolina, Chapel Hill, NC, USA.
9
Division of Cancer Epidemiology and Genetics, Radiation Epidemiology Branch, National Cancer Institute, Bethesda, MD, USA.
10
Department of Epidemiology, Columbia University, USA; Department of Medicine, Columbia University, USA.
11
Department of Environmental Health Sciences, Columbia University, USA.

Abstract

BACKGROUND:

Despite studies having consistently linked exposure to single-source polycyclic aromatic hydrocarbons (PAHs) to breast cancer, it is unclear whether single sources or specific groups of PAH sources should be targeted for breast cancer risk reduction.

OBJECTIVES:

This study considers the impact on breast cancer incidence from multiple PAH exposure sources in a single model, which better reflects exposure to these complex mixtures.

METHODS:

In a population-based case-control study conducted on Long Island, New York (N=1508 breast cancer cases/1556 controls), a Bayesian hierarchical regression approach was used to estimate adjusted posterior means and credible intervals (CrI) for the adjusted odds ratios (ORs) for PAH exposure sources, considered singly and as groups: active smoking; residential environmental tobacco smoke (ETS); indoor and outdoor air pollution; and grilled/smoked meat intake.

RESULTS:

Most women were exposed to PAHs from multiple sources, and the most common included active/passive smoking and grilled/smoked food intake. In multiple-PAH source models, breast cancer incidence was associated with residential ETS from a spouse (OR=1.20, 95%CrI=1.03, 1.40) and synthetic firelog burning (OR=1.29, 95%CrI=1.06, 1.57); these estimates are similar, but slightly attenuated, to those from single-source models. Additionally when we considered PAH exposure groups, the most pronounced significant associations included total indoor sources (active smoking, ETS from spouse, grilled/smoked meat intake, stove/fireplace use, OR=1.45, 95%CrI=1.02, 2.04).

CONCLUSIONS:

Groups of PAH sources, particularly indoor sources, were associated with a 30-50% increase in breast cancer incidence. PAH exposure is ubiquitous and a potentially modifiable breast cancer risk factor.

KEYWORDS:

Breast cancer; Environmental tobacco smoke; Grilled meat; Indoor air; Outdoor air; Polycyclic aromatic hydrocarbons; Smoking

PMID:
26878284
PMCID:
PMC4818720
DOI:
10.1016/j.envint.2016.02.009
[Indexed for MEDLINE]
Free PMC Article

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