Research | Children’s Health Serum Polybrominated Diphenyl Ether (PBDE) Levels Are Higher in Children (2–5 Years of Age) than in Infants and Adults Leisa-Maree L. Toms,1 Andreas Sjödin,2 Fiona Harden,3 Peter Hobson,4 Richard Jones,2 Emily Edenfield,2 and Jochen F. Mueller 1 1University of Queensland, National Research Centre for Environmental Toxicology, Coopers Plains, Queensland, Australia; 2Centers for Disease Control and Prevention, Atlanta, Georgia, USA; 3School of Life Science, Queensland University of Technology, Gardens Point, Queensland, Australia; 4Sullivan Nicolaides Pathology, Taringa, Queensland, Australia Background : Polybrominated diphenyl ethers (PBDEs) are used as flame retardants in many products and have been detected in human samples worldwide. Limited data show that concentra- tions are elevated in young children. o Bjectivs : We investigated the association between PBDEs and age with an emphasis on young children from Australia in 2006–2007. Methods : We collected human blood serum samples (n = 2,420), which we stratified by age and sex and pooled for analysis of PBDEs. r tluse : The sum of BDE-47, -99, -100, and -153 concentrations (Σ4PBDE) increased from 0–0.5 years (mean ± SD, 14 ± 3.4 ng/g lipid) to peak at 2.6–3 years (51 ± 36 ng/g lipid; p < 0.001) and then decreased until 31–45 years (9.9 ± 1.6 ng/g lipid). We observed no further significant decrease among ages 31–45, 45–60 (p = 0.964), or > 60 years (p = 0.894). The mean Σ4PBDE concentration in cord blood (24 ± 14 ng/g lipid) did not differ significantly from that in adult serum at ages 15–30 (p = 0.198) or 31–45 years (p = 0.140). We found no temporal trend when we compared the present results with Australian PBDE data from 2002–2005. PBDE concentrations were higher in males than in females; however, this difference reached statistical significance only for BDE-153 (p = 0.05). c onclusi : The observed peak concentration at 2.6–3 years of age is later than the period when breast-feeding is typically ceased. This suggests that in addition to the exposure via human milk, young children have higher exposure to these chemicals and/or a lower capacity to eliminate them. k ey words : Australia, children, cord blood, human blood serum, PBDEs, polybrominated diphenyl ethers. Environ Health Perspect 117:1461–1465 (2009). doi:10.1289/ehp.0900596 avail- able via http://dx.doi.org/ [Online 6 May 2009] Polybrominated diphenyl ethers (PBDEs) are a class of brominated flame retardants (BFRs) used to reduce the flammability of a multitude of products, including electrical and electronic equipment, plastics, textiles, and furniture. PBDEs are additive chemicals that can leach from products over time and have a tendency to bioaccumulate and bioconcentrate (Martin et al. 2004; McDonald 2002). Their use over the last 30 years has resulted in worldwide con- tamination of biological and environmental samples (Hites 2004). Data on adverse health effects due to human exposure to PBDEs are limited. Recent studies, however, have shown PBDE concen- trations in human milk to be associated with congenital cryptorchidism (Main et al. 2007) or with lower birth weight, length, and chest circumference (Chao et al. 2007). Thyroid hormone homeostasis in children may be dis- rupted because of exposure to PBDEs and other contaminants via house dust (Suzuki et al. 2007). Developmental, reproductive, and neurotoxic effects, as well as permanent effects on learning, activity, and behaviors after PBDE exposure have been reported in animals (Birnbaum 2007), with reproduc- tive and developmental toxicity studies show- ing that fetuses are more sensitive to PBDEs than are adults (Darnerud et al. 2001). Costa and Giordano (2007) state that there is accumulating evidence showing that PBDE exposure in animals causes developmental neurotoxicity at doses similar to those reported in the North American human population. Data suggest that human exposure to PBDEs occurs in a variety of ways: dietary sources (e.g., Darnerud et al. 2006; Domingo et al. 2008), inhalation in indoor and outdoor environments as well as in cars (e.g., Allen et al. 2007; Mandalakis et al. 2008; Wilford et al. 2005), and dust ingestion (e.g., Sjödin et al. 2008a; Stapleton et al. 2005). Infants and young children receive additional exposure via placental transfer (Bi et al. 2006; Gomara et al. 2007; Mazdai et al. 2003; Schecter et al. 2007), consumption of human milk (Carrizo et al. 2007), and child-specific behaviors, including mouthing of hands and objects possibly con- taminated with PBDEs (Stapleton et al. 2008). PBDEs have been detected in human blood of adults from many countries (e.g., Gomara et al. 2007; Harrad and Porter 2007; Lee et al. 2007; Sandanger et al. 2007; Sjödin et al. 2008b). However, despite the limited scientific evidence suggesting PBDE concen- trations in young children are elevated com- pared with adults (Fischer et al. 2006; Sjödin et al. 2008b; Thomsen et al. 2002), few stud- ies have focused on PBDE concentrations in infants and children. Previously, we observed PBDE concentrations in children 0–4 years of Environmental Health Perspectives • volume 117 | number 9 | September 2009 age in Australia to be four to five times higher than concentrations in adults > 16 years of age (Toms et al. 2008), although the use of wide age brackets for pooled samples resulted in an inability to accurately assess the age at which the levels peaked. The aim of this study was to investigate the age and level of peak PBDE concentrations in the Australian population, with an emphasis on infants and children. Human blood samples were collected from 17 age groups [ranging from newborn (cord blood) to > 60 years] to assess PBDE concentrations. From newborn to 4 years of age, the age brackets covered 6-month periods, followed by 3-year periods for ages 4–15 years and 15-year periods for ages 16 to > 60 years. In addition to samples from chil- dren, we collected adult samples in 2006–2007 for temporal comparison with data collected in Australia in 2002–2003 and 2004–2005. Materials and Methods Samples. We obtained deidentified serum samples from Sullivan Nicolaides Pathology (Taringa, Queensland, Australia) from surplus stored sera that had been collected as part of routine pathology testing. All samples were col- lected from South East Queensland because previous studies found no geographic differences among pooled samples collected from different regions of Australia (Toms et al. 2008). Before pooling, we stratified all samples according to age and sex. The age groups were as follows: newborn (cord blood), 0–0.5, 0.6–1, 1.1–1.5, 1.6–2, 2.1–2.5, 2.6–3, 3.1–3.5, 3.6–4, 4.1–6, 6.1–9, 9.1–12, 12.1–15, 16–30, 31–45, 46–60, and > 60 years. Age, sex, and date of collection were available for each sample. We calculated Address correspondence to L.-M.L. Toms, National Research Centre for Environmental Toxicology, University of Queensland, 39 Kessels Rd., Coopers Plains, Queensland, 4108 Australia. Telephone: 617- 3274-9060. Fax: 617-3274-9003. E-mail: l.toms@ uq.edu.au Supplemental Material is available online (doi:10.1289/ehp.0900596.S1 via http://dx.doi.org/). We thank the staff at Sullivan Nicolaides Pathology, Eurofins ERGO GmbH, and Centers for Disease Control and Prevention. Special thanks to N. Leontjew for assistance with sample collection. The National Research Centre for Environmental Toxicology is a partnership between Queensland Health and the University of Queensland. The authors declare they have no competing financial interests. Received 20 January 2009; accepted 6 May 2009. 1461