210). Visual inspection of empirical

cross-sectional data in 2003 and 2009 shows no obvious decreasing trend between 2003 and 2009, and especially in cross-sectional data of 2009, no significant difference for the human body burdens in pools of different age groups, except for the youngest cohort that is likely exposed by breastfeeding (see Supplementary material, Fig. S1-n). The modeled intrinsic elimination half-life for p,p′-DDT is about 115 years, which is much longer than that estimated by Ritter et al. (2009). However, the intrinsic elimination half-life could be unresolvable by our model fitting procedure because of ongoing low-level exposure to fresh DDT, which was also indicated by our modeled intake trend of p,p′-DDT showing an almost unchanged intake levels (see Supplementary material, Fig. S1-n). Mueller et al. (2008) speculated that the decline in DDT contamination in human milk in Australia slowed after the 1980s due Pexidartinib to new GSK1349572 mw input via long range transport or via consumption of food imported from more polluted countries. A significant increase of the intake of total DDT in 1990s was also observed in the total dietary studies in Australia ( Connell et al., 2007). However, a declining trend over the past decade in estuarine urban water measured using passive samplers in Australia

was observed by Mueller et al. (2011). Therefore, an ongoing exposure to fresh DDT may be due to changing exposure pathways as the use pattern changed ( Ritter et al., 2011a). The modeled adult reference intakes in 1975 for PCB congeners ranged from 0.89 to 24.5 ng/kg bw/day, which were slightly lower than the daily intakes for p,p′-DDE and much lower than those for HCB ( Table 2 and Table 3). After the bans of PCBs and OCPs, a sharp decline of the total human intake was expected. The modeled reduction half-lives of intake range from 1.1 to 1.3 years with the exception

of PCB-74 and PCB-99, which are declining more slowly than other congeners. The reduction of intake of OCPs is comparable to PCBs, with the reduction half-lives of 0.83–0.97 years. The PCB congeners considered in this study are generally eliminated more slowly from the human body than the OCPs considered Wilson disease protein here. The shortest intrinsic human elimination half-life is 6.4 years for HCB, and the longest is 30 years for PCB-74. Fig. 1 illustrates the modeled age–concentration structures at different sampling years for PCB-156 and TNONA, with empirical cross-sectional data available at 2003 and 2009. Graphical results for the other PCBs and OCPs are shown in SI-3 (see Supplementary material). Similar age–concentration trends were observed for PCB-156 and TNONA at different sampling years. The difference between human body burdens of PCB-156 and TNONA becomes smaller as the post-ban period increases, which is because TNONA has a shorter elimination half-life (9.7 years) than PCB-156 (18 years).