Toms et al. concentration changed with age (Figure 2). The contributions of BDE-47 and -99 decreased with age until around 8 years of age, whereas BDE-100 and -153 increased with age until 5 and 14 years of age, respectively. The half- life of BDE-47 is reportedly shorter than that of BDE-153 (1.8 vs. 6.5 years; Geyer et al. 2004), which may explain the differences in the congener contribution with age. In addi- tion, higher brominated diphenyl ethers are reported to pass the placenta at lower rates compared with lower brominated diphenyl ethers (Bi et al. 2006; Meironyté Guvenius et al. 2003; Schecter et al. 2007), and this may explain why BDE-153 is found in lower con- centrations in the younger age groups. Qiu et al. (2009) noted that BDE-99 was more likely to be hydroxylated than are BDE-47 and BDE-100 in humans, which may explain why concentrations of BDE-99 decrease from birth compared with BDE-47 and -100. Australian comparison. We compared PBDE concentrations found in this study with those from adult samples collected and pooled in Australia in 2002–2003 and 2004–2005 [Supplemental Material, Figure 1 (doi:10.1289/ehp.0900596.S1)]. Because the age brackets for the younger age groups were different in the two collection peri- ods, we compared samples only from adults > 16 years of age. We found no difference in mean Σ4PBDE concentrations for male and female adults > 16 years of age among samples from 2002–2003 (9.9 ± 4.1 ng/g lipid), 2004– 2005 (8.1 ± 2.2 ng/g lipid), and 2006–2007 (9.9 ± 2.6 ng/g lipid). Notably, this value for 2006–2007 excluded two elevated results; when we included these, the 2006–2007 mean concentration was 16 ± 19 ng/g lipid. This indicates that despite a ban on the production of penta- and octa-BDE technical products in the European Union in 2004, a phase-out of manufacture of these products in the United States in 2004, and no imports or manufac- turing of these pure products in Australia since 2005 (National Industrial Chemicals Notification and Assessment Scheme 2007), the Australian PBDE human body burden has not yet significantly decreased. This is most likely attributable to continued import of products treated with PBDEs, the longevity of products treated with PBDEs (e.g., electrical and electronic equipment, furniture, textiles), and possible exposure after the disposal of these products (Kim et al. 2006). Another fac- tor that may have influenced these findings is the use of different analytical methods for the 2002–2003 and 2004–2005 samples [which were analyzed at Eurofins ERGO GmbH (Hamburg, Germany), as described previously] (Toms et al. 2008), versus the 2006–2007 samples, which were analyzed at the CDC. However, it should be noted that both the laboratories CDC and Eurofins ERGO par- ticipate regularly in intercalibration programs in order to certify the analytical measure- ments [see Supplemental Material for details (doi:10.1289/ehp.0900596.S1)]. International comparison. International pediatric PBDE data are limited. Where pos- sible, we matched comparisons of data from other countries to age groups in the present study. Because of different reporting practices for sum concentrations, we compared only BDE-47 concentrations. Overall, Australian BDE-47 concentrations in young children were higher than those in European countries but lower than those in the United States. The mean BDE-47 concentration in Australian children 0–4 years of age was 19 ng/g lipid, which is three times higher than results from a pooled Norwegian sam- ple (n = 14; age 0–4 years), in which BDE-47 was detected at 6.2 ng/g lipid (Thomsen et al. 2002). A Menorca Island study found mean BDE-47 concentrations in breast-fed (n = 202) and formula-fed 4-year-old subjects (n = 42) to be 3.4 and 0.73 ng/g lipid, respectively, whereas the concentration from Australian chil- dren was 5–20 times greater, at 16 ng/g lipid (Carrizo et al. 2007). Similar results were found when comparing data from 7-year-old children (n = 42) in the Faroe Islands, whose median BDE-47 concentrations were 0.87 ng/g lipid compared with approximately 15 times greater concentration for Australian children at 13 ng/g BDE-47 BDE-153 15 40 35 n30 ()to% ttirnao25 n e io nc20 tu o ib Ec15 r tn D oC PB410 ∑ 5 0 0 70 60 to tiaon 50 ) r (n% tne 40 io cn itrbu Eco 30 tonC PBD4 20 ∑ 10 0 0 1464 lipid (Fängström et al. 2005). Individual results obtained in 2004 in California (USA) from one 18-month-old toddler and a 5-year-old girl showed BDE-47 concentrations of 245 and 137 ng/g lipid, respectively (Fischer et al. 2006), whereas data from comparative age brackets in Australia were 21 ng/g lipid for 1–2 year olds and 20 ng/g lipid for 4–6 year olds. Another study from the United States of 20 children ranging in age from 1.5 to 4 years found a median BDE-47 concentration of 30.6 ng/g lipid (Environmental Working Group 2008), which is higher than that found in Australian children of this age (21 ng/g lipid) but lower than those detected in the California samples (Fischer et al. 2006). For older chil- dren, the mean BDE-47 concentrations in Australian children 6–11 years of age ranged from 7.0 to 24 ng/g lipid for males and from 5.1 to 14 ng/g lipid for females and were four to eight times lower than those collected from Mexican-American, non-Hispanic black, and non-Hispanic white children 6–11 years of age in 2001–2002 in the United States, whose BDE-47 concentrations ranged from around 60 to 105 ng/g lipid for males and from 65 to 110 ng/g lipid for females (Sjödin A, personal communication). PBDEs have been detected previously in cord blood from other countries. In the present study, the mean Σ4PBDE and BDE-47 concentrations in cord blood were 24 ng/g lipid and 12 ng/g lipid, respectively, which is almost 10 times that found in China (Bi et al. 2006) and Sweden (Meironyté Guvenius et al. 2003), around twice that found in Spain (Gomara et al. 2007), but half the concentration reported from Indiana (USA) (Mazdai et al. 2003). The mean BDE-47 concentrations in Australian adults were higher than those PBDE concentrations in human blood reported from New Zealand, Europe, the United Kingdom, and Asia (e.g., Bi et al. 2006; Harrad and Porter 2007; Schroter-Kermani et al. 2000; Thomas et al. 2006; Thomsen et al. 2002) but lower than those from samples from the United States (Anderson et al. 2008; Sandanger et al. 2007; Schecter et al. 2005; BDE-99 BDE-100 5 10 Mean age (years) 5 10 Mean age (years) 15 Figure 2. Contribution of BDE-47 and -153 (A) and BDE-99 and -100 (B) to the Σ4PBDE concentration by age (note difference of scale on y-axis). ovlume 117 | number 9 | September 2009 • Environmental Health Perspectives