Neonatal and maternal body burdens of hexachlorobenzene (HCB) in mice: gestational exposure and lactational transfer.
Hexachlorobenzene (HCB), a ubiquitous lipophilic pollutant, was readily transferred in the milk of lactating dams to their suckling neonates. Pregnant CD-1 mice were treated during gestation, and the body burdens of HCB in the neonates and the dams were determined during lactation. Also, neonates from dams treated with HCB during gestation were cross-fostered at birth to dams treated with corn oil during gestation. The body burdens of HCB were greater in the neonates exposed to HCB by lactational transfer than the neonates exposed only by gestational transfer. In many tissues, the concentration of HCB in the pups from full litter was similar to that in pups from litters reduced to two pups per litter. Lactational transfer of HCB from the dams to the pups was a major route of excretion in that 95% of HCB was depleted during 20 days of lactation. HCB depletion was similar in dams with whole litters, and those with litters reduced to two pups.
D000375:Aging; D000818:Animals; D000831:Animals, Newborn; D001724:Birth Weight / Q000187:drug effects; D001822:Body Burden; D002722:Chlorobenzenes / Q000633:toxicity*; D005260:Female; D006581:Hexachlorobenzene / Q000378:metabolism / Q000633:toxicity*; D007774:Lactation; D008099:Liver / Q000187:drug effects; D008431:Maternal-Fetal Exchange; D051379:Mice; D008892:Milk / Q000378:metabolism*; D009929:Organ Size / Q000187:drug effects; D011247:Pregnancy; D014018:Tissue Distribution
D002722:Chlorobenzenes; D006581:Hexachlorobenzene