Abstract

Background: Associations between prenatal household air pollution (HAP) exposure or cookstove intervention to reduce HAP and cord blood mononuclear cell (CBMC) mitochondrial deoxyribonucleic acid copy number (mtDNAcn), an oxidative stress biomarker, are unknown. Materials and Methods: Pregnant women were recruited and randomized to one of two cookstove interventions, including a clean-burning liquefied petroleum gas (LPG) stove, or control. Prenatal HAP exposure was determined by serial, personal carbon monoxide (CO) measurements. CBMC mtDNAcn was measured by quantitative polymerase chain reaction. Multivariable linear regression determined associations between prenatal CO and cookstove arm on mtDNAcn. Associations between mtDNAcn and birth outcomes and effect modification by infant sex were explored. Results: LPG users had the lowest CO exposures (p = 0.02 by ANOVA). In boys only, average prenatal CO was inversely associated with mtDNAcn (β = -14.84, SE = 6.41, p = 0.03, per 1ppm increase in CO). When examined by study arm, LPG cookstove had the opposite effect in all children (LPG β = 19.34, SE = 9.72, p = 0.049), but especially boys (β = 30.65, SE = 14.46, p = 0.04), as compared to Control. Increased mtDNAcn was associated with improved birth outcomes. Conclusions: Increased prenatal HAP exposure reduces CBMC mtDNAcn, suggesting cumulative prenatal oxidative stress injury. An LPG stove intervention may reverse this effect. Boys appear most susceptible.

Highlights

  • 3 billion people worldwide are exposed daily to household air pollution (HAP)secondary to the burning of solid fuels in combustion-inefficient cookstoves [1]

  • Rural Ghanaian birth cohort derived from a cookstove intervention trial, we examined the impact of prenatal HAP exposure, as indexed by personal prenatal carbon monoxide (CO) exposure assessments, and a cookstove intervention on cord blood mononuclear cell (CBMC) mitochondrial DNA copy number (mtDNAcn)

  • Cord blood mononuclear cell DNA was extracted in n = 162 samples

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Summary

Introduction

3 billion people worldwide are exposed daily to household air pollution (HAP)secondary to the burning of solid fuels in combustion-inefficient cookstoves [1]. Emerging evidence suggests that early life HAP exposure may explain a large proportion of the risks associated with HAP. Prenatal HAP exposure has been linked to adverse birth outcomes (i.e., low birth weight, stillbirth, and preterm delivery [10,11]), which may increase the risk of neonatal mortality [12], acute lower respiratory infection (ALRI) in childhood [13], and cardiorespiratory [14,15] disease later in life. Associations between prenatal household air pollution (HAP) exposure or cookstove intervention to reduce HAP and cord blood mononuclear cell (CBMC) mitochondrial deoxyribonucleic acid copy number (mtDNAcn), an oxidative stress biomarker, are unknown

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