Prenatal particulate matter exposure and mitochondrial mutational load at the maternal-fetal interface: Effect modification by genetic ancestry.
- Resource Type
- Article
- Authors
- Brunst, Kelly J.; Hsu, Hsiao-Hsien Leon; Zhang, Li; Zhang, Xiang; Carroll, Kecia N.; Just, Allan; Coull, Brent A.; Kloog, Itai; Wright, Robert O.; Baccarelli, Andrea A.; Wright, Rosalind J.
- Source
- Mitochondrion. Jan2022, Vol. 62, p102-110. 9p.
- Subject
- *GENETIC load
*PARTICULATE matter
*ADENOSINE triphosphatase
*NADH dehydrogenase
*MITOCHONDRIA
*GENEALOGY
- Language
- ISSN
- 1567-7249
• Prenatal fine particulate matter (PM 2.5) exposure may increase placental mutational load. • PM 2.5 -related mutations may accumulate in genes coding for NADH dehydrogenase and subunits of ATP synthase. • Participants of African ancestry may represent an at-risk population. Prenatal ambient particulate matter (PM 2.5) exposure impacts infant development and alters placental mitochondrial DNA abundance. We investigated whether the timing of PM 2.5 exposure predicts placental mitochondrial mutational load using NextGen sequencing in 283 multi-ethnic mother-infant dyads. We observed increased PM 2.5 exposure, particularly during mid- to late-pregnancy and among genes coding for NADH dehydrogenase and subunits of ATP synthase, was associated with a greater amount of nonsynonymous mutations. The strongest associations were observed for participants of African ancestry. Further work is needed to tease out the role of mitochondrial genetics and its impact on offspring development and emerging disease disparities. [ABSTRACT FROM AUTHOR]