Uptake, Accumulation, and Biomarkers of PM_2.5-Associated Organophosphate Flame Retardants in C57BL/6 Mice after Chronic Exposure at Real Environmental Concentrations

Abstract

Although the bioaccumulation of organophosphate flame retardants (OPFRs) in aquatic organisms has been investigated, little information is available about their bioaccumulation in mammals following chronic inhalation exposure. To address this knowledge gap, C57BL/6 mice were exposed to 7 PM 2.5 -associated OPFRs via the trachea to study their bioaccumulation, tissue distribution, and urinary metabolites. Low (corresponding to the real PM 2.5 concentrations occurring during winter in Guangzhou), medium, and high dosages were examined. After 72 days' exposure, ∑OPFR concentrations in tissues from mice in the medium dosage group decreased in the order of intestine > heart > stomach > testis > kidney > spleen > brain > liver > lung > muscle. Of the OPFRs detected in all three exposure groups, chlorinated alkyl OPFRs were most heavily accumulated in mice. We found a significant positive correlation between the bioaccumulation ratio and octanol−air partition coefficient (K OA ) in mice tissues for low log K OW OPFR congeners (log K OW ≤ 4, p < 0.05). Three urinary metabolites (di-p-cresyl phosphate: DCrP, diphenyl phosphate: DPhP, dibutyl phosphate: DnBP) were detected from the high dosage group. These results provide important insights into the bioaccumulation potential of OPFRs in mammals and emphasize the health risk of chlorinated alkyl OPFRs.

Long-Range Transport, Trophic Transfer, and Ecological Risks of Organophosphate Esters in Remote Areas

“…Chen et al investigated bioaccumulation of OPEs in C57BL/6 mice, which was chronically exposed to 7 OPEs at an environmentally relevant concentration level (PM2.5-related). 91 The result showed that chlorinated OPEs have the strongest potential of accumulation among exposed OPEs in C57BL/6 mice. 91 In addition, Greaves et al and Van den Eede et al found that biotransformation of OPEs in vitro was generally structure-specific, with the biotransformation of chlorinated OPEs slower than that of alkyl OPEs and aryl OPEs.…”

“…91 The result showed that chlorinated OPEs have the strongest potential of accumulation among exposed OPEs in C57BL/6 mice. 91 In addition, Greaves et al and Van den Eede et al found that biotransformation of OPEs in vitro was generally structure-specific, with the biotransformation of chlorinated OPEs slower than that of alkyl OPEs and aryl OPEs. 76,92 In addition to chlorinated OPEs, OPEs such as EHDPP, TNBP, and TBOEP were dominant in some biological samples.…”

“…In addition, it may also have an important influence on their fraction that chlorinated OPEs in organisms, if compared with nonchlorinated OPEs, and has higher bioaccumulation and lower biotransformation. Chen et al investigated bioaccumulation of OPEs in C57BL/6 mice, which was chronically exposed to 7 OPEs at an environmentally relevant concentration level (PM2.5-related) . The result showed that chlorinated OPEs have the strongest potential of accumulation among exposed OPEs in C57BL/6 mice .…”

“…Chen et al investigated bioaccumulation of OPEs in C57BL/6 mice, which was chronically exposed to 7 OPEs at an environmentally relevant concentration level (PM2.5-related) . The result showed that chlorinated OPEs have the strongest potential of accumulation among exposed OPEs in C57BL/6 mice . In addition, Greaves et al and Van den Eede et al found that biotransformation of OPEs in vitro was generally structure-specific, with the biotransformation of chlorinated OPEs slower than that of alkyl OPEs and aryl OPEs. , In addition to chlorinated OPEs, OPEs such as EHDPP, TNBP, and TBOEP were dominant in some biological samples. ,− Specifically, EHDPP was the most abundant OPE individual in Arctic char, polar cod, Atlantic cod liver, kittiwake liver, and common eiders from Svalbard, making up 40.1%, 30.5%, 54.5%, 53.3%, and 52.8% of the total OPEs, respectively .…”

Antagonistic role of Al3+ against PM2.5-induced neurotoxicity via suppression of NADPH oxidase-triggered oxidative stress

“…4 In recent years, the detrimental effects of PM 2.5 on the central nervous system (CNS) have received increasing attention. 5,6 Early studies have revealed that canines residing in heavily polluted cities had more obvious brain inflammation, nerve cell apoptosis and damage on blood-brain barrier compared to those living in less polluted cities. 7,8 Moreover, brain damage, memory deficits and neuroinflammation have been found in children and young adults with high exposure of PM 2.5 .…”