Biomonitoring the human population exposed to pollution from the oil fires in Kuwait: Analysis of placental tissue using 32P-postlabeling

Abstract

The placenta is a readily available source of material for molecular epidemiological investigations. As such, DNA damage in this tissue can be indicative of maternal exposure to environmental pollutants such as polycyclic aromatic hydrocarbons PAHs). Previous reports have demonstrated that 32P-postlabeling (PPL) is able to detect the presence of aromatic adducts in human placenta that are associated with maternal smoking during pregnancy. Using PPL we have assayed the DNA damage in placental samples from Kuwaiti mothers who were exposed to environmental pollution during pregnancy. This pollution arose in the aftermath of the Iraqi invasion of Kuwait, which left hundreds of oil wells burning. For comparison, further Kuwaiti samples were obtained approximately 1 year after the oil well fires and, as such, are from individuals unexposed to the airborne pollution from the oil well fires during pregnancy. In addition, placental samples were obtained from subjects in the United Kingdom. Adduct levels were measured in all samples using both the nuclease P1 and butanol extraction enhancement procedures. No elevation of adduct levels was observed in the placenta of mothers exposed to the oil well fires (n = 40) with either procedure (144 ± 30 attomol/μg DNA for nuclease P1 enrichment, 245 = 50 attomol/μg DNA for butanol extraction), when compared with the nonexposed Kuwaiti mothers (180 ± 32 and 281 ± 39 attomol/μg DNA, respectively, n = 24). Similar adduct levels were observed in UK mothers who smoked cigarettes (178 ± 30 and 284 ± 52 attomol/μg DNA, n = 30), which in turn were approximately twice those observed in nonsmoking mothers (90 ± 14 and 141 ± 15 attomol/μg DNA, n = 12), although there is no significant difference in the distribution of adduct levels when statistical analysis is performed. Comprehensive interpretation of the Kuwaiti data is difficult as precise information on PAH levels is unavailable, although the data do seem to indicate that exposure to PAHs was not biologically significant. © 2000 Wiley-Liss, Inc.