Prenatal exposure to particulate matter and ozone: Bulky DNA adducts, plasma isoprostanes, allele risk variants, and neonate susceptibility in the Mexico City Metropolitan Area

Environ Mol Mutagen. 2019 Jun;60(5):428-442. doi: 10.1002/em.22276. Epub 2019 Feb 25.

Abstract

Mexico City's Metropolitan Area (MCMA) includes Mexico City and 60 municipalities of the neighbor states. Inhabitants are exposed to emissions from over five million vehicles and stationary sources of air pollutants such as particulate matter (PM) and ozone. MCMA PM contains elemental carbon and organic carbon (OC). OCs include polycyclic aromatic hydrocarbons (PAHs), many of which induce mutagenic and carcinogenic DNA adducts. Gestational exposure to air pollution has been associated with increased risk of intrauterine growth restriction, preterm birth or low birth weight risk, and PAH-DNA adducts. These effects also depend on the presence of risk alleles. We investigated the presence of bulky PAH-DNA adducts, plasma 8-iso-PGF (8-iso-prostaglandin F ) and risk allele variants in neonates cord blood and their non-smoking mothers' leucocytes from families that were living in a highly polluted area during 2014-2015. The presence of adducts was significantly associated with both PM2.5 and PM10 levels, mainly during the last trimester of gestation in both neonates and mothers, while the last month of pregnancy was significant for the association between ozone levels and maternal plasma 8-iso-PGF . Fetal CYP1B1*3 risk allele was associated with increased adduct levels in neonates while the presence of the maternal allele significantly reduced the levels of fetal adducts. Maternal NQO1*2 was associated with lower maternal levels of adducts. Our findings suggest the need to reduce actual PM limits in MCMA. We did not observe a clear association between PM and/or adduct levels and neonate weight, length, body mass index, Apgar or Capurro score. Environ. Mol. Mutagen. 60:428-442, 2019. © 2019 Wiley Periodicals, Inc.

Keywords: PAH-DNA adducts; air pollution; allelic variants of risk; gestational exposure; particulate matter.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Air Pollution / analysis
  • Cytochrome P-450 CYP1B1 / genetics
  • DNA Adducts / analysis*
  • DNA Adducts / genetics
  • Female
  • Fetal Blood / chemistry
  • Humans
  • Infant, Newborn
  • Isoprostanes / blood
  • Maternal Exposure*
  • Maternal-Fetal Exchange / physiology*
  • Mexico
  • NAD(P)H Dehydrogenase (Quinone) / genetics
  • Ozone / toxicity*
  • Particulate Matter / toxicity*
  • Polycyclic Aromatic Hydrocarbons / analysis*
  • Pregnancy
  • Prenatal Exposure Delayed Effects / pathology*
  • Vehicle Emissions / analysis
  • Young Adult

Substances

  • DNA Adducts
  • Isoprostanes
  • Particulate Matter
  • Polycyclic Aromatic Hydrocarbons
  • Vehicle Emissions
  • polycyclic aromatic hydrocarbons-DNA adduct
  • Ozone
  • CYP1B1 protein, human
  • Cytochrome P-450 CYP1B1
  • NAD(P)H Dehydrogenase (Quinone)
  • NQO1 protein, human