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Daria Pereg,^1,2 Éric Dewailly,² Guy G. Poirier,¹ and Pierre Ayotte²

¹Département de Biologie Médicale, Faculté de Médecine, Université Laval et Unité de recherche en santé et environnement, Ste-Foy, Québec, Canada; ²Département de Médecine Sociale et Préventive, Faculté de Médecine, Université Laval et Unité de recherche en santé publique, Beauport, Québec, Canada

Abstract

Some polychlorinated biphenyl (PCB) congeners are CYP1A1 inducers, and induction of this enzyme in the placenta has been linked to adverse effects on fetal development. The objective of this study was to determine if the body burden of PCBs is related to placental CYP1A1 activity in Inuit women from Nunavik (northern Québec) , a population highly exposed to organochlorines. Placenta and cord blood samples were obtained from 35 Inuit women and 30 women from a southern Québec community exposed to background levels of organochlorines. We measured PCB concentrations in all cord plasma samples and in a subset of placenta samples from the Nunavik group and assessed CYP1A1 activity (ethoxyresorufin-O-deethylase ; EROD) in placental microsomes from all participants. Concentrations of PCBs in cord plasma were strongly correlated to those in placenta (Pearson's r = 0.77-0.97, p < 0.001) and were on average 4-fold higher in Inuit women than in southern Québec women [for PCB 153, the geometric means (geometric SDs) were 83.3 (1.9) ng/g lipid vs. 16.9 (1.6) ng/g lipid, respectively]. Despite this difference in PCB body burden, both study groups had similar EROD activities when data were stratified according to tobacco smoking. Although simple correlation analysis first showed that placental EROD activity was correlated with PCB 153 plasma concentration in the Nunavik group, a multivariate analysis failed to demonstrate a significant contribution of PCBs to EROD activity when tobacco smoking was included in the analysis. We conclude that dietary exposure to PCBs in Inuit women from Nunavik does not significantly influence EROD activity in the placenta, implicating tobacco smoking as the major modulating factor. Key words: CYP1A1, Inuit, placenta, polychlorinated biphenyl, tobacco smoke. Environ Health Perspect 110:607-612 (2002) . [Online 29 April 2002]

http://ehpnet1.niehs.nih.gov/docs/2002/110p607-612pereg/ abstract.html

Address correspondence to P. Ayotte, Unité de recherche en santé publique, CHUL-CHUQ, 2400, d'Estimauville, Beauport, Québec, G1E 7G9 Canada. Telephone: (418) 666-7000 ext. 245. Fax: (418) 666-2776. E-mail: pierre.ayotte@crchul.ulaval.ca

We thank A. Leblanc, L. Ferron, and M. Lefebvre from the Institut national de Santé Publique du Québec for PCB and cotinine analyses.

This study was funded by Indian and Northern Affairs Canada (Northern Contaminants Program) , the Tri-Council Secretariat of the Eco-Research Program (922-94-0021) , and FCAR and MRC fellowships.

Received 31 July 2001 ; accepted 10 December 2001.