Evidence From Humans
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Vehicular Traffic-Related Polycyclic Aromatic Hydrocarbon Exposure and Breast Cancer Incidence: The Long Island Breast Cancer Study Project (LIBCSP)
Mordukhovich, I., Beyea, J., Herring, A. H., Hatch, M., Stellman, S. D., Teitelbaum, S. L., Richardson, D. B., Millikan, R. C., Engel, L. S., Shantakumar, S., Steck, S. E., Neugut, A. I., Rossner, P., Jr., Santella, R. M., Gammon, M. D. Environ Health Perspect. 2016. 124:1, 30-8.
Topic area
Environmental pollutant - PAHs
Study design
Population based case-control
Funding agency
US Department of Defense NCI NIEHS Breast Cancer R
Study Participants
Number of Cases
For 1995 exposure analyses: 1,274 cases For 1960-1990 exposure analyses: 520-551 cases
Menopausal Status
The menopausal status of women included in this study is listed here.
Stratified analysis based on menopausal status
Number of Controls
For 1995 exposure analyses: 1,334 controls For 1960-1990 exposure analyses: 566-597 controls
Participant selection: Inclusion and exclusion criteria
Criteria used to select participants in the study.
Female residents of Nassau and Suffolk Counties (Long Island), NY, participating in the Long Island Breast Cancer Study Project, age 20 or older, English-speaking, newly diagnosed with in situ or invasive breast cancer in 1996-1997. Cases identified by regional hospital pathology laboratories. Controls had no breast cancer history and were matched by 5-year age group, identified by random-digit-dialing or Medicare records (for women 65 and older). Among 1,508 cases and 1,556 controls in the LIBCSP, 87% of participants provided at least one address that could be successfully geocoded to the street level.
Exposure Investigated
Exposures investigated
Geocoded self-reported residential histories in Nassau and Suffolk counties were used to model recent (1995) and long-term (1960-1990) ambient B[a]P from traffic emissions. Emissions were estimated using hourly roadway-specific traffic counts and average
How exposure was measured
GIS/Geographic location
Exposure assessment comment
Tailpipe emissions for years other than 1960, 1970, 1980 and 1990 were interpolated or extrapolated. The exposure model was validated against measurements of PAHs in soil at participant residences as well as levels of PAH-DNA adducts in blood. Limitations include not accounting for a street canyon effect, historical changes to the road network, industrial emissions, and exposure that occurred away from the home. In analysis of exposure from 1960-1990, imputation methods were used to estimate exposure for years when participants were missing residential history or for years lived outside of study area. Analyses were restricted to individuals with ≤ 20% of their cumulative exposure based on imputed values. Short-term (1995) and long-term (1960-1990) exposure estimates were strongly correlated. Most participants had lived in current homes for at least 15 years.
Breast cancer outcome investigated
Primary incident breast cancer
Confounders considered
Other breast cancer risk factors, such as family history, age at first birth, and hormone replacement therapy use, that were taken into account in the study.
Based on causal diagram: Age group, education level, annual household income, race, religion, parity, age at first birth, BMI, duration of HRT use, duration of oral contraceptive use, lifetime average alcohol intake, lifetime average physical activity, an
Genetic characterization included
If the study analyzed relationships between environmental factors and inherited genetic variations, this field will be marked Yes. No, if not.
Strength of associations reported

Recent Traffic PAH exposure estimates (1995):

All women:
≥95th percentile vs. <50th percentile: aOR 1.14 (95% CI 0.80-1.64)

Postmenopausal women:
50-75th percentile vs. <50th percentile: aOR 0.79 (95% CI 0.62-1.00)
75-95th percentile vs. <50th percentile: aOR 0.80 (95% CI 0.62-1.02)
≥95th percentile vs. <50th percentile: aOR 1.06 (95% CI 0.69-1.63)

Premenopausal women:
50-75th percentile vs. <50th percentile: aOR 0.95 (95% CI 0.68-1.32)
75-95th percentile vs. <50th percentile: aOR 1.64 (95% CI 1.13-2.38)
≥95th percentile vs. <50th percentile: aOR 1.20 (95% CI 0.58-2.47)

≥95th percentile vs. <50th percentile from polytomous regression:
ER+/PR+ cancers vs all other subtypes: Ratio of aORs 0.74 (95% CI 0.40-1.38)
ER-/PR- cancers vs all other subtypes: Ratio of aORs 2.09 (95% CI 1.08-4.06)

≥75th percentile vs. <50th percentile from polytomous regression:
In situ vs invasive: Ratio of aORs 1.46 (95% CI 1.02-2.09)

Long-term Traffic PAH exposure estimates (1960-1990):

All women:
≥95th percentile vs. <50th percentile: aOR 1.47 (95% CI 0.70-3.08)

Postmenopausal women:
50-75th percentile vs. <50th percentile: aOR 1.00 (95% CI 0.70-1.42)
≥75th percentile vs. <50th percentile: aOR 0.91 (95% CI 0.64-1.29)

Premenopausal women:
50-75th percentile vs. <50th percentile: aOR 0.84 (95% CI 0.42-1.66)
≥75th percentile vs. <50th percentile: aOR 1.31 (95% CI 0.63-2.71)

≥75th percentile vs. <50th percentile from polytomous regression:
In situ vs invasive: Ratio of aORs 1.64 (95% CI 0.87-3.89)
Results Comments
There was evidence that the traffic-PAH association was modified by fruit/vegetable intake (stronger associations among those with low fruit/veg intake, p for interaction = 0.01 for 1995 estimates and p for interaction = 0.04 for 1960-1990 estimates). There was no evidence for effect modification of vehicular traffic PAH exposure by tumor p53 mutation status. 1995 exposure estimates: The analysis for 1995 was restricted to 1,274 cases and 1,334 cases with complete exposure information. OR for association with traffic PAH exposure ≥ 95th vs <50th percentile was significantly higher for ER-/PR- breast cancer than for all other sub-types. OR for ≥ 95th vs
BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants, known human lung carcinogens, and potent mammary carcinogens in laboratory animals. However, the association between PAHs and breast cancer in women is unclear. Vehicular traffic is a major ambient source of PAH exposure. OBJECTIVES: Our study aim was to evaluate the association between residential exposure to vehicular traffic and breast cancer incidence. METHODS: Residential histories of 1,508 participants with breast cancer (case participants) and 1,556 particpants with no breast cancer (control participants) were assessed in a population-based investigation conducted in 1996-1997. Traffic exposure estimates of benzo[a]pyrene (B[a]P), as a proxy for traffic-related PAHs, for the years 1960-1995 were reconstructed using a model previously shown to generate estimates consistent with measured soil PAHs, PAH-DNA adducts, and CO readings. Associations between vehicular traffic exposure estimates and breast cancer incidence were evaluated using unconditional logistic regression. RESULTS: The odds ratio (95% CI) was modestly elevated by 1.44 (0.78, 2.68) for the association between breast cancer and long-term 1960-1990 vehicular traffic estimates in the top 5%, compared with below the median. The association with recent 1995 traffic exposure was elevated by 1.14 (0.80, 1.64) for the top 5%, compared with below the median, which was stronger among women with low fruit/vegetable intake [1.46 (0.89, 2.40)], but not among those with high fruit/vegetable intake [0.92 (0.53, 1.60)]. Among the subset of women with information regarding traffic exposure and tumor hormone receptor subtype, the traffic-breast cancer association was higher for those with estrogen/progesterone-negative tumors [1.67 (0.91, 3.05) relative to control participants], but lower among all other tumor subtypes [0.80 (0.50, 1.27) compared with control participants]. CONCLUSIONS: In our population-based study, we observed positive associations between vehicular traffic-related B[a]P exposure and breast cancer incidence among women with comparatively high long-term traffic B[a]P exposures, although effect estimates were imprecise.
Author address
Department of Epidemiology, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, USA.