Polybrominated diphenyl ether (PBDE) levels in livers of U.S. human fetuses and newborns.

Polybrominated diphenyl ether (PBDE) brominated flame retardants have recently been found to contaminate humans in the United States and other countries. U.S. human breast milk and blood levels of PBDEs are presently the highest in the world. U.S. cord blood samples tested positive for PBDEs, but until now there have been no peer-reviewed published data concerning levels of PBDEs in human tissue prior to and immediately after birth. Liver tissues were obtained from 4 stillborn fetuses and 7 liveborn infants, ranging from 20.5 to 39 wk gestational age; only 2 of the liveborn infants lived longer than 4 h and none were formula-fed or nursed, so tissue levels reflect intrauterine PBDE intake only. All samples were contaminated with PBDEs. Levels varied from 4 to 98 ppb, lipid. The mean level was 23.1 and the median 15.2 ppb, lipid. PBDE levels did not increase with gestational age. These data document the transfer of PBDEs from maternal to fetal tissue. PBDE concentrations are somewhat lower than those reported in adult blood or breast milk. The health consequences of prenatal contamination are not clear at present.

Polybrominated diphenyl ethers (PBDEs) in U.S. mothers' milk.

No previous reports exist on polybrominated diphenyl ether (PBDE) congeners in human milk from individual U.S. mothers. This article on PBDEs is an extension of our previous studies on concentrations of dioxins, dibenzofurans, polychlorinated biphenyls, and other chlorinated organic compounds in human milk in a number of countries. PBDE commercial products are used as flame retardants in flexible polyurethane foam (penta-BDE), in acrylonitrile-butadiene-styrene resins (octa-BDE), and in high-impact polystyrene resins (deca-BDE). Their use is permitted in the United States but is banned in some European countries because of presumed toxicity, demonstrated persistence, and bioaccumulation. Different commercial products can be found in various consumer products such as television sets, computers, computer monitors and printers, carpets, and upholstery. Analyses of human levels of these compounds suggest low but rising levels in European human milk, which may have peaked, at least in Sweden, in the late 1990s. Very few data exist on levels of PBDEs in humans in the United States, and none from milk from individual nursing mothers. To address this issue, we analyzed 47 individual milk samples from nursing mothers, 20-41 years of age, from a milk bank in Austin, Texas, and a community women's health clinic in Dallas, Texas. Up to 13 PBDE congeners were measured. The concentrations of the sum of PBDE congeners varied from 6.2 to 419 ng/g (or parts per billion) lipid, with a median of 34 ng/g and a mean of 73.9 ng/g lipid. The PBDE levels in breast milk from Texas were similar to levels found in U.S. blood and adipose tissue lipid from California and Indiana and are 10-100 times greater than human tissue levels in Europe. Their detection in breast milk raises concern for potential toxicity to nursing infants, given the persistence and bioaccumulative nature of some of the PBDE congeners. These results indicate a need for more detailed investigation of the levels of PBDE in people and food, as well as determining if animal fat in food is the major route of exposure of the general U.S. population. Other routes of intake may also be significant.