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

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  Gammon, M. D., Santella, R. M., Neugut, A. I., Eng, S. M.,   Teitelbaum, S. L., Paykin, A., Levin, B., Terry, M. B., Young, T.   L., Wang, L. W., Wang, Q., Britton, J. A., Wolff, M. S.,   Stellman, S. D., Hatch, M., Kabat, G. C., Senie, R., Garbowski,   G., Maffeo, C., Montalvan, P., Berkowitz, G., Kemeny, M., Citron,   M., Schnabel, F., Schuss, A., Hajdu, S., Vinceguerra, V.   11 (8) 677-85-

  Abstract: 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.

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