We detected the lowest Σ4PBDE concentra- tion (5.5 ng/g lipid) in a pool from females > 60 years of age. Σ4PBDE concentrations in three pools of cord blood ranged from 14 to 40 ng/g lipid, with a mean of 24 ng/g lipid, similar to those in females 15–45 years of age, whose levels ranged from 8.1 to 77 ng/g lipid, with a mean of 27 ng/g lipid. The cord and female blood samples compared here were not fetus–mother pairs, and comparisons should be made with caution because both correlated (Bi et al. 2006; Mazdai et al. 2003) and noncorre- lated (Gomara et al. 2007; Meironyté Guvenius et al. 2003) PBDE concentrations in paired cord–maternal blood have been reported. The results of the present study confirm our previous findings of elevated PBDE con- centrations in children 0–4 years of age relative to adults > 16 years of age (Toms et al. 2008). Higher PBDE concentrations in children have been reported in a limited number of studies (Environmental Working Group 2008; Fischer et al. 2006; Thomsen et al. 2002). In contrast, another study found no difference in PBDE concentrations between mothers and their chil- dren 7 years of age (Fängström et al. 2005). The present study, however, is the first to use 6-month age brackets for samples ranging in age from newborn (cord blood) to 4-year-olds to determine at what age PBDEs concentra- tions peak. Increased PBDE concentrations in neonates and infants is most likely attributable to placental transfer and the consumption of human milk (e.g., Noren and Meironyté 2000; Schecter et al. 2003; Toms et al. 2007), with PBDE concentrations in sera of 4-year-olds reportedly higher in breast-fed children than in formula-fed children (Carrizo et al. 2007). In Australia, breast-feeding rates decrease from 85% at birth to 45% at 6 months, 23% at 12 months, and 1% at 24 months (Australian Bureau of Statistics 2003); con- sequently, for most infants, exposure via this pathway would not typically persist after the first year of life. Despite this pattern, PBDE 120 i)d 100 p i l g / (ng 80 n o i t tra 60 n e c n co 40 E D B P∑4 20 0 0 concentrations appear to increase past 1 year of age. Interestingly, an increasing age trend was not apparent for polychlorinated biphenyls and persistent pesticides in these same samples from birth to 15 years of age (data not shown), indicating that the routes of exposure are dif- ferent for PBDEs than for traditional persis- tent organic pollutants. However, we found an increasing trend for polychlorinated biphenyls and persistent pesticides with the subjects’ age for older subjects (data not shown). We have previously used modeled data, taking into consideration intake and half- lives, to predict the trend of elevated con- centrations in Australian infants and young children, but we did not find the magni- tude or age of peak PBDE concentrations that we found in the present study (Toms et al. 2008). Reasons for this underestimation may be related to the half-life values used, which may be inaccurate for children, and missing PBDE sources that may contribute to intake levels during early years. The half- lives of PBDEs have been calculated as 1.8, 2.9, 1.6, and 6.5 years for BDE-47, -99, -100, and -153, respectively (Geyer et al. 2004) for non-occupationally exposed adult humans and are based on daily intake and total body burden data. Dust has been sug- gested as a major source of PBDEs in young children (Jones-Otazo et al. 2005; Lorber 2008; Stapleton et al. 2005), with intake of BDE-47 via dust in Australian 2.5-year-olds estimated at 1–140 ng/day (assuming a daily dust intake rate of 50–100 mg) (Sjödin et al. 2008a). Food intake of tetra-BDEs, of which BDE-47 is the major congener, is estimated at 21 ng/day for this age group (Food Standards Australia and New Zealand 2007). However, variability in dust intake estimates (U.S. Environmental Protection Agency 1997) renders calculation of PBDE intake via this pathway less certain. In addition, BFRs have been detected in baby products such as car seats (Gearhart et al. 2007) and may result Female Male Cord blood PBDEs concentrations are high in children in exposures specific to young children. The pathways and level of exposure from such sources require further investigation. Similar to previous reports (Bradman et al. 2007; Gomara et al. 2007; Harrad and Porter 2007; Julander et al. 2005; Lee et al. 2007), we observed no apparent change in adult PBDE concentration with age. Sex. For all age groups combined, the mean ± SD Σ4PBDE concentrations in males was 26 ± 13 ng/g lipid and in females was 28 ± 20 ng/g lipid. For adults > 16 years of age, the mean ± SD Σ4PBDE concentration for males was 15 ± 11 ng/g lipid and for females was 18 ± 24 ng/g lipid. This sex difference was statistically significant (p = 0.05) for BDE-153 only. Higher PBDE concentrations in males than in females have been reported previously (Meneses et al. 1999; Schroter-Kermani et al. 2000; Takasuga et al. 2004; Thomsen et al. 2002) and appears to be attributable to placen- tal transfer and elimination during lactation. In contrast, other studies have reported either no difference or higher concentrations in females (Gomara et al. 2007; Schecter et al. 2005). Congener profile. The congener profile in all samples was dominated by BDE-47 (mean, 47%; range of contribution to Σ4PBDEs, 31–61%), followed by BDE-153 (20%; 7–47%), BDE-99 (17%; 10–33%), and BDE-100 (13%; 10–18%), whereas the remaining BDE congeners contributed < 10% to total PBDEs. Overall, the profile in these samples was similar to those found in stud- ies of human blood from Australia, New Zealand, North America, and Europe (Harrad and Porter 2007; Schecter et al. 2005; Sjödin et al. 2004a; Thomsen et al. 2002; Toms et al. 2008). In cord blood, the profile was also dom- inated by BDE-47, followed by BDE-99, -153, and -100, which is consistent with findings by Gomara et al. (2007). However, others have found BDE-153 in higher concentrations than BDE-99 (Bi et al. 2006; Meironyté Guvenius et al. 2003). We found no observable differences in pro- file by sex, except for BDE-153, which made a greater contribution to the Σ4PBDE con- centration in males than in females. The lev- els of congener contribution to the Σ4PBDE Table 1. Mean (95% confidence interval) Σ4PBDE (BDE-47, -99, -100, and -153) concentrations (ng/g lipid) by age (years), including outliers, for 2006–2007. Mean Σ4PBDE concentration Age (years) (95% CI) Newborn (cord blood) 24 (–11 to 59)a 0–2 31 (24 to 38) 2–6 41 (33 to 49) 7–12 26 (20 to 31) 13–30 20 (12 to 28) > 31 9.4 (7.9 to 11) aThree pools only. *p < 0.05. Comparison with 2- to 5-year age group (p-value) 0.047* 0.026* — 0.002* < 0.001* < 0.001* 1463 10 20 30 40 50 Mean age (years) 60 70 80 Figure 1. Σ4PBDE concentrations (ng/g lipid) by mean age (0–80 years) and sex. Each point represents a pool of up to 30 individual blood samples. Environmental Health Perspectives • volume 117 | number 9 | September 2009