BackgroundPopulation pharmacokinetic models combined with multiple sets of age–concentration biomonitoring data facilitate back-calculation of chemical uptake rates from biomonitoring data.ObjectivesWe back-calculated uptake rates of PBDEs for the Australian population from multiple biomonitoring surveys (top-down) and compared them with uptake rates calculated from dietary intake estimates of PBDEs and PBDE concentrations in dust (bottom-up).MethodsUsing three sets of PBDE elimination half-lives, we applied a population pharmacokinetic model to the PBDE biomonitoring data measured between 2002–2003 and 2010–2011 to derive the top-down uptake rates of four key PBDE congeners and six age groups. For the bottom-up approach, we used PBDE concentrations measured around 2005.ResultsTop-down uptake rates of Σ4BDE (the sum of BDEs 47, 99, 100, and 153) varied from 7.9 to 19 ng/kg/day for toddlers and from 1.2 to 3.0 ng/kg/day for adults; in most cases, they were—for all age groups—higher than the bottom-up uptake rates. The discrepancy was largest for toddlers with factors up to 7–15 depending on the congener. Despite different elimination half-lives of the four congeners, the age–concentration trends showed no increase in concentration with age and were similar for all congeners.ConclusionsIn the bottom-up approach, PBDE uptake is underestimated; currently known pathways are not sufficient to explain measured PBDE concentrations, especially in young children. Although PBDE exposure of toddlers has declined in the past years, pre- and postnatal exposure to PBDEs has remained almost constant because the mothers’ PBDE body burden has not yet decreased substantially.CitationGyalpo T, Toms LM, Mueller JF, Harden FA, Scheringer M, Hungerbühler K. 2015. Insights into PBDE uptake, body burden, and elimination gained from Australian age–concentration trends observed shortly after peak exposure. Environ Health Perspect 123:978–984; http://dx.doi.org/10.1289/ehp.1408960

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Blood and breast milk samples from inhabitants living in dwellings treated with DDT in indoor residual spraying show high DDT levels. This is of concern since mothers transfer lipid-soluble contaminants such as DDT via breastfeeding to their children. We focused on DDT use in South Africa and used a pharmacokinetic model to identify the dominant DDT uptake routes (food vs. inhalation), to estimate DDT levels in human lipid tissue over the full lifetime of an individual, and to determine the amount of DDT transferred to children during pregnancy and breastfeeding. In particular, the effects of breastfeeding duration, parity, and the mother's age on the DDT concentrations of mother and infant were estimated. The model results suggest that primiparous mothers have greater DDT concentrations than multiparous mothers which lead to higher DDT exposure for their first-born children. Furthermore, DDT in the body mainly originates from diet (92-95%). Our modeled DDT levels reproduce the levels found in South African biomonitoring data within a factor of five or less.