Temporal variations of PM2.5-bound organophosphate flame retardants in different microenvironments in Beijing, China, and implications for human exposure

Abstract

In the present study, the temporal distribution of PM2.5-bound organophosphate flame retardants (OPFRs) was comprehensively investigated in various indoor environments as well as outdoor air in Beijing, China over a one-year period. The mean concentrations of Σ9OPFRs were 22.7 ng m−3 and 1.40 ng m−3 in paired indoor and outdoor PM2.5, respectively. The concentrations of tri-n-butyl phosphate (TNBP), tris (2-chloroethyl) phosphate (TCEP) and tris (2-chloroisopropyl) phosphate (TCIPP) in indoor PM2.5 were significantly correlated with those in outdoor PM2.5. For different indoor microenvironments, mean concentrations of Σ9OPFRs were in the order of office (29.0 ± 11.7 ng m−3) > home (24.0 ± 9.4 ng m−3) > dormitory (19.4 ± 4.9 ng m−3) > activity room (14.4 ± 3.1 ng m−3). TCIPP was the most abundant compound in the indoor PM2.5, followed by TCEP. Significantly higher concentrations of OPFRs were observed in indoor environments with more furnishing, electronics or other materials (p < 0.05). Moreover, lower levels of OPFRs in indoor air were observed at well-ventilated (with higher air exchange rate) indoor sampling sites. Concentrations of Σ9OPFRs in the activity room, dormitory, homes and outdoor sites generally increased in summer and heating seasons (November 2016 to February 2017). Significant correlations (p < 0.05) were observed between temperatures and mass concentrations of OPFRs with higher vapor pressures, i.e. TNBP, TCEP and TCIPP in all indoor and outdoor samples. Seasonal differences in human exposure were observed and the highest daily exposure dose occurred in summer. Toddlers may suffer the highest exposure risk of PM2.5-bound OPFRs via inhalation among all age groups. This is one of the very few studies that have revealed the seasonal variation and human exposure of PM2.5-bound OPFRs in different microenvironments, which shed light on emission sources and fate of OPFRs and potential human exposure pathway.