Determinants of prenatal exposure to polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) in an urban population.

Use of polybrominated diphenyl ethers (PBDEs) as flame retardants (FRs) in plastics, including electronic enclosures and poly-urethane used in upholstery cushioning and carpet pads, has increased steadily in the past 30 years (Alaee et al. 2003; de Wit 2002; Hardy 2002b). PBDEs used as additive FRs are more likely to leach over time than reactive FRs, which are chemically bonded to the plastic polymer (Alaee and Wenning 2002; Eriksson et al. 2001; Sjodin et al. 2001a). PBDEs are similar to polychlorinated biphenyls (PCBs) in structure, lipophilicity, persistence, and ability to bioaccumulate (Hardy 2002a; McDonald 2002). Since the 1970s, environmental concentrations of PCBs and other persistent organic pollutants (POPs) have fallen whereas levels of PBDEs have increased exponentially (Alaee and Wenning 2002; Eriksson et al. 2001; Meironyte et al. 1999; Sjodin et al. 2001b). Currently, human PBDE levels are of a magnitude similar to PCB concentrations in some regions (Hites 2004; Petreas et al. 2004). Human levels of PBDEs are higher in North America than in Europe and within a given population, a small fraction (5–10%) of individuals have concentrations far exceeding average levels (Betts 2003; Hites 2004; Schecter et al. 2005; Sjodin et al. 2003; Wilford et al. 2005). Although there have been no studies investigating the health effects associated with PBDEs in humans, there are reports of human exposure levels that may be on par with levels eliciting harmful effects in laboratory animals (McDonald 2005). Animal studies have shown evidence of the disruption of normal endocrine function and neurodevelopmental, hepatic, and reproductive toxicity (Betts 2004, 2005; Johnson-Restrepo et al. 2005). Currently, there is an incomplete understanding of how humans are exposed to PBDEs. It is reasonable to posit that among those with high concentrations, occupational exposures may be involved in some cases (Sjodin et al. 1999; Thuresson et al. 2005). In the general population, several potential routes of PBDE exposure have been identified: a) direct contact with treated products; b) dietary, as these lipophilic compounds are stored in the fat of meats, fish, and dairy products (Harrad et al. 2004; Schecter et al. 2004, 2006; Wilford et al. 2005); and c) ingestion and to a lesser degree inhalation of PBDE-containing house dust (Jones-Otazo et al. 2005; Stapleton et al. 2005; Wilford et al. 2005; Wu et al. 2007) Only a few studies have been able to explore individual determinants of PBDE body burdens in much detail (Morland et al. 2005; Wu et al. 2007). Levels of PBDEs (as well as PCBs and organochlorine pesticides) measured in adipose tissue, blood, or milk can be used to assess exposures (Sjodin et al. 2003). Infants and fetuses are sensitive subpopulations to consider, because these stages of development may be especially susceptible to effects of chemical exposures (Howdeshell 2002). Toxicologic models have indicated that immature animals have slower metabolism and excretion of PBDEs; approximately 50% of the administered 2,2′,4,4′-tetraBDE (BDE-47) dose is excreted in the first 24 hr in adult animals compared with 31% and 41% in animals dosed at 10 and 22 days after birth (Staskal et al. 2006). Measuring PBDEs in cord blood serum is noninvasive, using a blood sample that is otherwise usually discarded, and is a direct measure of prenatal exposure. The estimated half-lives of these compounds in humans are long enough—BDE-47 1.8–3.0 years, 2,2′,4,4′,5-pentaBDE (BDE-99) 2.9–5.4 years, and 2,2′,4,4′,5,5′-hexaBDE (BDE-153) 6.5–11.7 years (Geyer et al. 2004)—that cord blood concentrations reflect exposure through the course of pregnancy. Such levels also provide a reasonable estimate of maternal serum concentrations (Mazdai et al. 2003). The principal objective of this investigation was to characterize fetal exposure to PBDEs and selected PCBs among newborns from Baltimore, Maryland, via the assessment of concentrations in umbilical cord serum. We explored demographic characteristics and attributes to identify determinants and to explain variations in exposure levels and patterns within this largely urban and African-American population.