Reduced mitochondrial DNA copy number in occupational workers from brominated flame retardants manufacturing plants
Tian Chen1, Xueting Wang1, Jiaxin Jia1
1School of Public Health and Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China.
Abstract:
Decabrominated diphenyl ether (BDE-209) and its substitute decabromodiphenyl ethane (DBDPE) are two flame retardants that have similar structure and are widely used in various industrial products. The accumulation and potential toxicity of them to human health have already aroused attention, and some research showed that they may affect mitochondrial function. Therefore, this study focused on the population with high exposure to brominated flame retardants (BFRs) and the related changes in mtDNA copy number (mtDNAcn) in whole blood. 334 blood samples were collected from three groups of people in Shandong Province, including 42 BDE-209 occupational exposure workers from the BDE-209 manufacturing plant, 131 DBDPE occupational exposure workers from the DBDPE manufacturing plant, and 161 non-BFRs occupational exposure residents from the BFRs contaminated area. We measured the levels of BDE-209, DBDPE in serum sample, and the mtDNAcn in whole blood sample and analyzed these data by multiple linear regression. The average concentrations of BDE-209, DBDPE and ∑(BDE-209 + DBDPE) in BDE-209 occupational workers were 3510, 639 and 4600 ng/g lw, respectively; the average concentrations of BDE-209, DBDPE and ∑(BDE-209 + DBDPE) in DBDPE occupational workers were 229, 4040 and 4470 ng/g lw, respectively; the average concentrations of BDE-209, DBDPE and ∑(BDE-209 + DBDPE) in non-BFRs occupational exposure residents were 66.3, 45.7 and 137 ng/g lw, respectively. The relative mtDNAcn was 0.823 in BDE-209 occupational workers, 0.845 in DBDPE occupational workers and 0.989 in non-BFRs occupational exposure residents. A 10-fold increase in BDE-209, DBDPE concentrations was separately associated with a 0.068 and 0.063 decrease in mtDNAcn. Therefore, our study implied that BFRs may affect mitochondrial function. As increasing BFRs exposure has emerged in recent years, the relationship between BFRs exposure and mitochondrial function needs further study.
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