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Prenatal Particulate Matter/Tobacco Smoke Increases Infants' Respiratory Infections: COCOA Study

Song I Yang1, Byoung Ju Kim2, So Yeon Lee1

  • 1Department of Pediatrics, Hallym Sacred Heart Hospital, Hallym University College of Medicine, Anyang, Korea.

Allergy, Asthma & Immunology Research
|September 4, 2015
PubMed

Insights

Prenatal exposure to indoor fine particulate matter (PM₂.₅) and environmental tobacco smoke (ETS) increases infant susceptibility to lower respiratory tract infections (LRTIs). Genetic factors can modify these effects, highlighting the impact of early-life environmental exposures.

Area of Science:

  • Environmental Health
  • Pediatric Respiratory Medicine
  • Genetic Epidemiology

Background:

  • Infant respiratory tract infections (RTIs) pose a significant health burden.
  • Indoor air pollutants, including fine particulate matter (PM₂.₅) and environmental tobacco smoke (ETS), are common exposures during pregnancy and infancy.
  • The impact of these exposures on RTI susceptibility and potential genetic modifications requires further investigation.

Purpose of the Study:

  • To assess the association between prenatal exposure to indoor PM₂.₅ and ETS and infant susceptibility to RTIs.
  • To compare the effects of prenatal versus postnatal exposure to these pollutants.
  • To determine if genetic polymorphisms modify the relationship between environmental exposures and RTI risk.

Main Methods:

  • A cohort of 307 infants was studied.
  • Indoor PM₂.₅ and ETS levels were measured during pregnancy and infancy.
  • Genotyping for Nrf2, GSTP1, and GSTM1, along with genome-wide methylation analysis, was performed.

Main Results:

  • Prenatal PM₂.₅ exposure significantly increased the risk of lower RTIs (LRTIs) in infancy (aOR=2.11).
  • Combined prenatal exposure to PM₂.₅ and ETS showed a strong association with increased LRTIs (aOR=6.56), an effect not observed with postnatal exposure.
  • Specific genotypes (Nrf2 GG, GSTM1 null, GSTP1 AG/GG) amplified the LRTIs risk associated with combined prenatal exposure to PM₂.₅ and ETS.

Conclusions:

  • Prenatal exposure to both indoor PM₂.₅ and ETS may elevate infant susceptibility to LRTIs.
  • Genetic variations in reactive oxygen species-related genes can modulate the impact of these prenatal exposures on LRTIs.
Abstract

Keywords:
Prenatal exposuremethylationparticulate matterpolymorphismrespiratory tract infectionstobacco smoke

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