TY - JOUR
T1 - Environmental toxins and breast cancer on Long Island. I. Polycyclic aromatic hydrocarbon DNA adducts
AU - Gammon, Marilie D.
AU - Santella, Regina M.
AU - Neugut, Alfred I.
AU - Eng, Sybil M.
AU - Teitelbaum, Susan L.
AU - Paykin, Andrea
AU - Levin, Bruce
AU - Terry, Mary Beth
AU - Young, Tie Lan
AU - Wang, Lian Wen
AU - Wang, Qiao
AU - Britton, Julie A.
AU - Wolff, Mary S.
AU - Stellman, Steven D.
AU - Hatch, Maureen
AU - Kabat, Geoffrey C.
AU - Senie, Ruby
AU - Garbowski, Gail
AU - Maffeo, Carla
AU - Montalvan, Pat
AU - Berkowitz, Gertrud
AU - Kemeny, Margaret
AU - Citron, Marc
AU - Schnabel, Freya
AU - Schuss, Allan
AU - Hajdu, Steven
AU - Vinceguerra, Vincent
PY - 2002
Y1 - 2002
N2 - 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.
AB - 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.
UR - https://www.scopus.com/pages/publications/0036324940
M3 - Article
C2 - 12163319
AN - SCOPUS:0036324940
SN - 1055-9965
VL - 11
SP - 677
EP - 685
JO - Cancer Epidemiology Biomarkers and Prevention
JF - Cancer Epidemiology Biomarkers and Prevention
IS - 8
ER -