ARYL-HYDROCARBON HYDROXYLASE-ACTIVITY IN HUMAN PLACENTA AND THREATENED PRETERM DELIVERY

Citation
G. Huel et al., ARYL-HYDROCARBON HYDROXYLASE-ACTIVITY IN HUMAN PLACENTA AND THREATENED PRETERM DELIVERY, Journal of exposure analysis and environmental epidemiology, 3, 1993, pp. 187-199
Citations number
NO
Categorie Soggetti
Environmental Sciences","Public, Environmental & Occupation Heath",Toxicology
ISSN journal
10534245
Volume
3
Year of publication
1993
Supplement
1
Pages
187 - 199
Database
ISI
SICI code
1053-4245(1993)3:<187:AHIHPA>2.0.ZU;2-4
Abstract
Induction of aryl hydrocarbon hydroxylase (AHH) activity in the placen ta has been well documented. This enzyme may be induced by a variety o f Polycyclic Aromatic Hydrocarbons (PAHs) and the AHH inducibility is associated with harmful effects of environmental chemicals. Toxic effe cts of PAHs in tissues such as placenta have been demonstrated to be d ue to their metabolites, epoxides, which interact with DNA. Thus, envi ronmental PAHs may be related to its alterations in fetal development. Founded on these findings the PAH metabolites could interfere with th e normal course of the pregnancy and may be an aborticide, a teratogen or a carcinogen. We hypothesize that low increased activity of placen tal Aryl Hydrocarbon Hydroxylase (AHH) may be an important determinant of human fetotoxicity. The present investigation was designed to exam ine the possible implications of PAH exposure at environmental exposur e levels on the normal course of the pregnancy using AHH induction as an indicator of PAH exposure. Threatened Preterm Delivery (TPD) was us ed as an index of problems in the normal course of pregnancy. A group of forty pregnancies at term with TPD was compared with eighty control s for placental AHH induction. Macroscopic placental examination was a lso performed. A significant increase in prevalence of placental AHH i nduction with TPD was shown (Odds-Ratio = 2.8; 95% confidence bounds [ 1.3 - 6.2]; chi2 = 6.7 p < 0.01). No such increases were found associa ted with placental pathology. When taking into account the group of pl acenta without basal plate calcifications, the significant increase in prevalence of placental AHH induction with TPD above mentioned was gr eatly increased (Odds-Ratio = 8.9; 95% confidence bounds [2.4 - 32.9], chi2 = 11.1 p < 0. 001) controlling for gestational age. The increase in prevalence of placental AHH induction with TPD disappeared when ta king into account the subgroup with basal plate or parenchyma calcific ations. It is hypothesized that the high estrogen and progesterone at term may explain these associations.