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

The placenta is a readily available source of material for molecular epidem iological investigations. As such, DNA damage in this tissue can be indicat ive of maternal exposure to environmental pollutants such as polycyclic aro matic hydrocarbons (PAHs). Previous reports have demonstrated that P-32-pos tlabeling (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 mothe rs who were exposed to environmental pollution during pregnancy. This pollu tion arose in the aftermath of the Iraqi invasion of Kuwait, which left hun dreds of oil wells burning. For comparison, further Kuwaiti samples were ob tained approximate year after the oil well fires and, as such, ore individu als unexposed to the airborne pollution From the oil well fires during preg nancy. In addition, placental samples were obtained From subjects in the Un ited Kingdom. Adduct levels were measured in all samples using both the nuc lease P1 and butanol extraction enhancement procedures. No elevation of add uct levels was observed in the placenta of mothers exposed to the oil well fires (n = 40) with either procedure (144 +/- 30 atto-mol/mug DNA for nucle ase P1 enrichment 245 +/- 50 attomol/mug DNA for butanol extraction), when compared with the nonexposed Kuwaiti mothers (180 +/- 32 and 281 +/- 39 att omol/mug DNA, respectively, n = 24). Similar adduct levels were observed in UK mothers who smoked cigarettes (178 +/- 30 and 284 +/- 52 attomol/mug DN A, n = 30), which in turn were approximately twice those observed in nonsmo king mothers (90 +/- 14 and 141 +/- 15 attomol/mug DNA, n = 12), although t here is no significant difference in the distribution of adduct levels when statistical analysis is performed. Comprehensive interpretation of the Kuw aiti data is difficult as precise information on PAH levels is unavailable, although the data do seem to indicate that exposure to PAHs was not biolog ically significant. Environ. Mel. Mutagen. 36: 274-282, 2000. (C) 2000 Wile y-Liss, Inc.