Accumulation of endocrine disrupting compounds in sheep fetal and maternal liver tissue following exposure to pastures treated with sewage sludge.
Fetal tissue concentrations of endocrine disrupting compounds (EDCs), and their relationship to maternal tissue concentrations, are largely unknown, in any species. In particular, the patterns of accumulation in the respective tissues following increased rates of environmental exposure are little known. This study was designed to determine fetal and maternal tissue concentrations of selected EDCs in sheep exposed to background, environmental concentrations of EDCs (pastures treated with inorganic fertiliser; Control; C) or to elevated, environmental concentrations (sludge-treated pastures; Treated; T). Mean log concentrations of diethylhexyl phthalate (DEHP) were similar in adult and fetal livers but there was a significant interaction between stage of development (maternal or fetal) and treatment reflecting the fact that mean concentrations were lower (P < 0.05) in C than T fetuses but not adults. Relative concentrations of polychlorinated biphenyls (PCB) in maternal and fetal tissue differed with congener; concentrations of congener 101 were higher (P < 0.05) in fetal tissue. Neither maternal nor fetal liver concentrations of any of the PCB congeners differed significantly with treatment. Polybrominated diphenyl ethers (PBDE) in the tissue were represented primarily by congeners 47 and 99. PBDE 99 concentrations were higher in maternal than fetal tissue (P = 0.01). None differed with treatment in either maternal or fetal tissues. Concentrations of many polycyclic aromatic hydrocarbons (PAH) were higher in maternal tissue but none differed with treatment in either adult or fetuses. It is concluded that sheep fetal liver EDC concentrations are variably related to those of their dams and in some cases appear to be selectively accumulated in fetuses. Differential accumulation of individual pollutants may have important implications for the assessment of risk from exposure.
Rhind
S M
SM
Macaulay Institute, Craigiebuckler, Aberdeen, UK. s.rhind@macaulay.ac.uk
Kyle
C E
CE
Mackie
C
C
McDonald
L
L
D000818:Animals; D004051:Diethylhexyl Phthalate / Q000378:metabolism / Q000633:toxicity; D052244:Endocrine Disruptors / Q000032:analysis / Q000378:metabolism* / Q000633:toxicity; D005260:Female; D005308:Fertilizers / Q000633:toxicity; D005333:Fetus / Q000378:metabolism; D055768:Halogenated Diphenyl Ethers / Q000378:metabolism / Q000633:toxicity; D008099:Liver / Q000196:embryology / Q000378:metabolism*; D008297:Male; D018811:Maternal Exposure; D006109:Poaceae / Q000737:chemistry; D011078:Polychlorinated Biphenyls / Q000378:metabolism / Q000633:toxicity; D011084:Polycyclic Aromatic Hydrocarbons / Q000378:metabolism / Q000633:toxicity; D012722:Sewage / Q000737:chemistry*; D012756:Sheep
D052244:Endocrine Disruptors; D005308:Fertilizers; D055768:Halogenated Diphenyl Ethers; D011084:Polycyclic Aromatic Hydrocarbons; D012722:Sewage; D004051:Diethylhexyl Phthalate; D011078:Polychlorinated Biphenyls