BackgroundPolybrominated diphenyl ethers (PBDEs) are used as flame retardants in many products and have been detected in human samples worldwide. Limited data show that concentrations are elevated in young children.ObjectivesWe investigated the association between PBDEs and age with an emphasis on young children from Australia in 2006–2007.MethodsWe collected human blood serum samples (n = 2,420), which we stratified by age and sex and pooled for analysis of PBDEs.ResultsThe sum of BDE-47, -99, -100, and -153 concentrations (∑4PBDE) 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 ∑4PBDE 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).ConclusionsThe 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.

Polyfluoroalkyl chemicals (PFCs) have been used worldwide for more than 50 years in a wide variety of industrial and consumer products. Limited data exist on human exposure to PFCs in the Southern Hemisphere. Human blood serum collected in southeast Queensland, Australia, in 2006-2007 from 2420 donors was pooled according to age (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) and gender and was analyzed for eight PFCs. Across all pools, perfluorooctane sulfonate (PFOS) was detected at the highest mean concentration (15.2 ng/mL) followed by perfluorooctanoate (PFOA, 6.4 ng/mL), perfluorohexane sulfonate (PFHxS, 3.1 ng/mL), perfluorononanoate (PFNA, 0.8 ng/mL), 2-(N-methylperfluorooctance sulfonamide) acetate (Me-PFOSA-AcOH, 0.66 ng/mL), and perfluorodecanoate (PFDeA, 0.29 ng/mL). Perfluorooctane sulfonamide was detected in only 24% of the pools, and 2-(N-ethylperfluorooctane sulfonamide) acetate was detected in only one. PFOS concentrations were significantly higher in pools from adult males than from adult females (p = 0.002); no gender differences were apparent in the pools from children (< 12 years old). The highest mean concentrations of PFOA, PFHxS, PFNA, PFDeA, and Me-PFOSA-AcOH were found in children < 15 years, while PFOS was highest in adults > 60 years. Investigation into the sources and exposure pathways in Australia, in particular for children, is necessary as well as continued biomonitoring to determine the potential effects on human concentrations as a result of changes in the PFC manufacturing practices, including the cessation of production of several PFCs.

Although there is suggestive evidence that exposure to BFRs is harmful to health, further epidemiological investigations particularly among children, and long-term monitoring and surveillance of chemical impacts on humans are required to confirm these relationships.

Pooled serum samples from 3802 Australian residents were analyzed for four perfluoroalkylsulfonates, seven perfluoroalkylcarboxylates, and perfluorooctanesulfonamide (PFOSA). Serum was collected from men and women of five different age groups and from rural and urban regions in Australia. The highest mean concentration was obtained for perfluorooctane sulfonate (PFOS, 20.8 ng/mL) followed by perfluorooctanoic acid (PFOA, 7.6 ng/mL), perfluorohexane sulfonate (PFHxS, 6.2 ng/mL), perfluorononanoic acid (PFNA, 1.1 ng/mL), and PFOSA (0.71 ng/mL). Additional four PFCs were detected in 5−18% of the samples at concentrations near the detection limits (0.1−0.5 ng/mL). An increase in PFOS concentration with increasing age in both regions and genders was observed. The male pool levels of some of the age groups compared to females were higher for PFOS, PFOA, and PFHxS. In contrast, PFNA concentrations were higher in the female pools. No substantial difference was found in levels of PFCs between the urban and rural regions. The levels are equal or higher than previously reported serum levels in Europe and Asia but lower compared to the U.S.A. These results suggest that emissions from production in the Northern Hemisphere are of less importance for human exposure.

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Polybrominated diphenyl ethers (PBDEs) are lipophilic, persistent pollutants found worldwide in environmental and human samples. Exposure pathways for PBDEs remain unclear but may include food, air and dust. The aim of this study was to conduct an integrated assessment of PBDE exposure and human body burden using 10 matched samples of human milk, indoor air and dust collected in 2007-2008 in Brisbane, Australia. In addition, temporal analysis was investigated comparing the results of the current study with PBDE concentrations in human milk collected in 2002-2003 from the same region. PBDEs were detected in all matrices and the median concentrations of BDEs -47 and -209 in human milk, air and dust were: 4.2 and 0.3 ng/g lipid; 25 and 7.8 pg/m(3); and 56 and 291 ng/g dust, respectively. Significant correlations were observed between the concentrations of BDE-99 in air and human milk (r=0.661, p=0.038) and BDE-153 in dust and BDE-183 in human milk (r=0.697, p=0.025). These correlations do not suggest causal relationships - there is no hypothesis that can be offered to explain why BDE-153 in dust and BDE-183 in milk are correlated. The fact that so few correlations were found in the data could be a function of the small sample size, or because additional factors, such as sources of exposure not considered or measured in the study, might be important in explaining exposure to PBDEs. There was a slight decrease in PBDE concentrations from 2002-2003 to 2007-2008 but this may be due to sampling and analytical differences. Overall, average PBDE concentrations from these individual samples were similar to results from pooled human milk collected in Brisbane in 2002-2003 indicating that pooling may be an efficient, cost-effective strategy of assessing PBDE concentrations on a population basis. The results of this study were used to estimate an infant's daily PBDE intake via inhalation, dust ingestion and human milk consumption. Differences in PBDE intake of individual congeners from the different matrices were observed. Specifically, as the level of bromination increased, the contribution of PBDE intake decreased via human milk and increased via dust. As the impacts of the ban of the lower brominated (penta- and octa-BDE) products become evident, an increased use of the higher brominated deca-BDE product may result in dust making a greater contribution to infant exposure than it does currently. To better understand human body burden, further research is required into the sources and exposure pathways of PBDEs and metabolic differences influencing an individual's response to exposure. In addition, temporal trend analysis is necessary with continued monitoring of PBDEs in the human population as well as in the suggested exposure matrices of food, dust and air.

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Pooled serum samples collected from 8132 residents in 2002/ 03 and 2004/05 were analyzed to assess human polybrominated diphenyl ether (PBDE) concentrations from specified strata of the Australian population. The strata were defined by age (0-4 years, 5-15 years, < 16 years, 16-30 years, 31-45 years, 46-60 years, and > 60 years); region; and gender. For both time periods, infants and older children had substantially higher PBDE concentrations than adults. For samples collected in 2004/ 05, the mean +/- standard deviation sigmaPBDE (sum of the homologue groups for the mono-, di-, tri-, tetra-, penta-, hexa-, hepta-, octa-, nona-, and deca-BDEs) concentrations for 0-4 and 5-15 years were 73 +/- 7 and 29 +/- 7 ng g(-1) lipid, respectively, while for all adults > 16 years, the mean concentration was lower at 18 +/- 5 ng g(-1) lipid. A similar trend was observed for the samples collected in 2002/03, with the mean sigmaPBDE concentration for children < 16 years being 28 +/- 8 ng g(-1) lipid and for the adults >16 years, 15 +/- 5 ng g(-1) lipid. No regional or gender specific differences were observed. Measured data were compared with a model that we developed to incorporate the primary known exposure pathways (food, air, dust, breast milk) and clearance (half-life) data. The model was used to predict PBDE concentration trends and indicated that the elevated concentrations in infants were primarily due to maternal transfer and breast milk consumption with inhalation and ingestion of dust making a comparatively lower contribution.