Evidence From Humans
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Aromatic DNA adducts in adjacent tissues of breast cancer patients: clues to breast cancer etiology
Li, D., Wang, M., Dhingra, K., Hittelman, W. N. Cancer Research. 1996. 56:2, 287-93.
Topic area
Environmental pollutant - Pharmaceutical hormones
Study design
Case-control study
Funding agency
University of Texas M.D. Anderson Cancer Center Ph
Study Participants
Menopausal Status
The menopausal status of women included in this study is listed here.
Pre menopausal
Post menopausal
Number of Controls
Controls: 29
Participant selection: Inclusion and exclusion criteria
Criteria used to select participants in the study.
Breast cancer patients compared with reduction mammoplasty noncancer patients
Comment about participation selection
Reduction mammoplasty patients are not representative of the populations from which the breast cancers arose. Controls were much younger (mean 32 years) than cases (mean 54 years). 15 patients received treatment, which damages DNA (though authors state only cyclophosphamide might be expected to induce DNA adducts), prior to surgery. Adduct levels integrate information about exposure and individual metabolic processes, which may improve ability to detect impact on breast cancer risk.
Exposures investigated
DNA adducts in extracted histologically normal breast tissue adjacent to tumor or in reduction mammoplasty. Adducts categorized as (a) Benzo(a)pyrene-like adduct -- "single bulky adduct near the origin," (b) smoking-related (DRZ), and (c) unidentified. 3
Statistical Analysis
Ethnic groups with separate analysis
If this study provided a separate analysis by ethnic or racial group, the groups are listed here.
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.
Age, menopausal status, smoking history
Genetic characterization included
If the study analyzed relationships between environmental factors and inherited genetic variations, this field will be marked “Yes.” “No”, if not.
Description of major analysis
Comparisons between means: Student's t test, Mann-Whitney test, Wilcoxon signed rank test. Regression analysis for age-dependency and dose-response for smoking-related adducts.
Strength of associations reported
Total adducts
cases mean level higher than controls p < 0.01
Benzo(a)pyrene-like adduct
detected in 36 (41%) of cases and no controls. Majority with BP-like adduct were nonsmokers. 46% of nonsmokers, 47% of smokers had BP-like adduct.
Smoking-related adducts
Identified in cases: 17 of 17 current smokers, 5 of 8 former smokers, 4 of 52 nonsmokers
Controls: 2 of 10, smoking status unknown
Detected in former smoker who quit 18 years ago
No dose-response among current smokers
Unidentified adducts
cases mean level higher than controls p < 0.001

Adduct levels not correlated with age
Results Comments
Supports the hypothesis that smoking is not the primary source of benzo(a)pyrene exposure. Authors state food accounts for vastly largest source. (Note that air pollution is one source of BP in food). Supports the hypothesis that environmental carcinogens, specifically PAH, contribute to breast cancer risk; however, this study is small and controls are not representative of a general population. This study contributes primarily to much-needed methods development for exposure assessment by suggesting strategies for separating smoking- and non-smoking PAH exposure and suggesting that PAH adducts may measure exposure as long as 18 years in the past.
Author address
Department of Clinical Investigations, University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.
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