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
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.