Environmental toxins and breast cancer on Long Island. I. Polycyclic aromatic hydrocarbon DNA adducts.

TitleEnvironmental toxins and breast cancer on Long Island. I. Polycyclic aromatic hydrocarbon DNA adducts.
Publication TypeJournal Article
Year of Publication2002
AuthorsGammon MD, Santella RM, Neugut AI, Eng SM, Teitelbaum SL, Paykin A, Levin B, Terry MB, Young TL, Wang LW, Wang Q, Britton JA, Wolff MS, Stellman SD, Hatch M, Kabat GC, Senie R, Garbowski G, Maffeo C, Montalvan P, Berkowitz G, Kemeny M, Citron M, Schnabel F, Schuss A, Hajdu S, Vinceguerra V
JournalCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
Date Published2002 Aug
KeywordsAdult, Aged, Breast Neoplasms, Case-Control Studies, diet, DNA Adducts, DNA Damage, Environmental Exposure, Enzyme-Linked Immunosorbent Assay, Female, Humans, Middle Aged, New York City, Odds Ratio, Polycyclic Hydrocarbons, Aromatic, Risk Factors, Smoking

Polycyclic aromatic hydrocarbons (PAH) are potent mammary carcinogens in rodents, but their effect on breast cancer development in women is not clear. To examine whether currently measurable PAH damage to DNA increases breast cancer risk, a population-based case-control study was undertaken on Long Island, NY. Cases were women newly diagnosed with in situ and invasive breast cancer; controls were randomly selected women frequency matched to the age distribution of cases. Blood samples were donated by 1102 (73.0%) and 1141 (73.3%) of case and control respondents, respectively. Samples from 576 cases and 427 controls were assayed for PAH-DNA adducts using an ELISA. The geometric mean (and geometric SD) of the log-transformed levels of PAH-DNA adducts on a natural scale was slightly, but nonsignificantly, higher among cases [7.36 (7.29)] than among controls [6.21 (4.17); P = 0.51]. The age-adjusted odds ratio (OR) for breast cancer in relation to the highest quintile of adduct levels compared with the lowest was 1.51 [95% confidence interval (CI), 1.04-2.20], with little or no evidence of substantial confounding (corresponding multivariate-adjusted OR, 1.49; 95% CI, 1.00-2.21). There was no consistent elevation in risk with increasing adduct levels, nor was there a consistent association between adduct levels and two of the main sources of PAH, active or passive cigarette smoking or consumption of grilled and smoked foods. These data indicate that PAH-DNA adduct formation may influence breast cancer development, although the association does not appear to be dose dependent and may have a threshold effect.

Alternate JournalCancer Epidemiol. Biomarkers Prev.
PubMed ID12163319
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