Polybrominated diphenyl ethers in maternal and fetal blood samples.

Abstract

Polybrominated diphenyl ethers (PBDEs) are widely used as flame retardants in consumer goods, such as plastics, electronics, textiles, and construction material. PBDEs have been found in human milk, fat, and blood samples. Rodent studies indicate that PBDEs may be detrimental to neurodevelopment, possibly by lowering thyroid hormone concentrations in blood. In the present study, we determined concentrations of PBDEs and thyroid hormones in human fetal and maternal serum. Patients presenting in labor to Indiana University and Wishard Memorial County hospitals in Indianapolis, who were older than 18 years, were recruited to participate. Twelve paired samples of maternal and cord blood were obtained and analyzed using gas chromatographic mass spectrometry; thyroid hormone concentrations were determined by radioimmunoassay. Six congeners of PBDE were measured in maternal and fetal serum samples. The concentrations of total PBDEs found in maternal sera ranged from 15 to 580 ng/g lipid, and the concentrations found in fetal samples ranged from 14 to 460 ng/g lipid. Individual fetal blood concentrations did not differ from the corresponding maternal concentrations, indicating that measurement of maternal PBDE blood levels is useful in predicting fetal exposure; similarly, other reports have shown a high correlation between PBDE in mother's milk and fetal exposure. In accord with reports on other biologic samples, the tetrabrominated PBDE congener BDE-47 accounted for 53-64% of total PBDEs in the serum. The concentrations of PBDEs found in maternal and fetal serum samples were 20-106-fold higher than the levels reported previously in a similar population of Swedish mothers and infants. In this small sample, there was no apparent correlation between serum PBDEs and thyroid hormone concentrations. Our study shows that human fetuses in the United States may be exposed to relatively high levels of PBDEs. Further investigation is required to determine if these levels are specific to central Indiana and to assess the toxic potential of these exposure levels. Key words: brominated diphenyl ethers, cord blood, human, pregnancy, serum.

Developmental neurotoxicity of polybrominated diphenyl ether (PBDE) flame retardants

“…The daily intake of PBDEs for a breastfed infant was estimated as 20.6 ng/kg/day in this study, far below the estimated exposure levels in Canada (280 mg/ kg/day; Jones-Otazo et al 2005) or in the United States (306 ng/kg/day; Schecter et al 2006a). In another study comparing maternal and fetal blood PBDE levels, no correlation was found with serum T 4 concentrations (Mazdai et al 2003). Clearly, studies investigating the relationship between body burden of PBDEs and child development are needed, in order to validate the animal findings.…”

“…It should be noted that the study by Ceccatelli et al (2006) examined effects on gene expression in the uterus, rather than alterations in the nervous system; however, upon identical exposure, changes in sexual behavior and sweet preference were also found (Lichtensteiger et al 2004;Lilienthal et al 2006). Levels in human plasma as high as 580 and 460 ng/g lipid have been reported in maternal and fetal blood, respectively (Table 6; Mazdai et al 2003). In the Fischer et al (2006) family study, the toddler was found to have plasma PBDE levels of 418 ng/lipid (651 ng/g lipid if considering also BDE-209).…”

Association of selected persistent organic pollutants in the placenta with the risk of neural tube defects

“…Those villi closest to the maternal blood supply will develop and expand into a mass of chorionic tissue that is ultimately considered to be the placenta. In addition to nutrients and oxygen, xenobiotics, especially lipophillic pollutants, can readily cross the preplacental structures and potentially impact embryonic development (16). Although much of this development has occurred after the embryo's neural tube has closed, the continuum of development from the trophoblast to the placenta proper makes this a reasonable surrogate in which environmental exposures that occurred earlier in gestation can be evaluated.…”

Exposure to DE-71 alters thyroid hormone levels and gene transcription in the hypothalamic–pituitary–thyroid axis of zebrafish larvae

“…Therefore, in the present study, zebrafish embryos/larvae were employed as models for evaluating the responses of the HPT axis to PBDE exposure and the potential mechanisms of TH disruption. To investigate the effects of DE-71 on the HPT axis, we exposed zebrafish embryos to a commercial PBDE mixture, namely, DE-71, containing most of the PBDE congeners commonly found in biota, such as BDE-47, BDE-99, BDE-153, and BDE-154 (Mazdai et al, 2003;Hites, 2004).…”