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

Abstract

PurposeTo investigate whether prenatal exposure to indoor fine particulate matter (PM2.5) and environmental tobacco smoke (ETS) affects susceptibility to respiratory tract infections (RTIs) in infancy, to compare their effects between prenatal and postnatal exposure, and to determine whether genetic factors modify these environmental effects.MethodsThe study population consisted of 307 birth cohort infants. A diagnosis of RTIs was based on parental report of a physician's diagnosis. Indoor PM2.5 and ETS levels were measured during pregnancy and infancy. TaqMan was used for genotyping of nuclear factor erythroid 2-related factor (Nrf2) (rs6726395), glutathione-S-transferase-pi (GSTP) 1 (rs1695), and glutathione-S-transferase-mu (GSTM) 1. Microarrays were used for genome-wide methylation analysis.ResultsPrenatal exposure to indoor PM2.5 increased the susceptibility of lower RTIs (LRTIs) in infancy (adjusted odds ratio [aOR]=2.11). In terms of combined exposure to both indoor PM2.5 and ETS, prenatal exposure to both pollutants increased susceptibility to LRTIs (aOR=6.56); however, this association was not found for postnatal exposure. The Nrf2 GG (aOR=23.69), GSTM1 null (aOR=8.18), and GSTP1 AG or GG (aOR=7.37) genotypes increased the combined LRTIs-promoting effects of prenatal exposure to the 2 indoor pollutants. Such effects of prenatal indoor PM2.5 and ETS exposure were not found for upper RTIs.ConclusionsPrenatal exposure to both indoor PM2.5 and ETS may increase susceptibility to LRTIs. This effect can be modified by polymorphisms in reactive oxygen species-related genes.

In utero ultrafine particulate matter exposure causes offspring pulmonary immunosuppression

“…Disruption of Nrf2 has been shown to enhance susceptibility to allergic airway inflammatory responses induced by chronic exposure DEPM (43). Previous findings from a birth cohort in Korea demonstrating increased susceptibility to lower respiratory tract infections in infants exposed in utero to PM 2.5 were significantly modified by polymorphisms in maternal genes related to oxidative stress response pathways, especially Nrf2 (44). Likewise, in inbred strains of mice, including C57BL/6 mice, Nrf2 polymorphisms have been shown to influence hyperoxia susceptibility (42), indicating that the differences in Nrf2 response across strains underscore differences in host response to oxidative stress.…”

Contrasting The Effects of Intra-Uterine Smoking and One-Carbon Micronutrient Exposures on Offspring DNA Methylation

“…One study investigated promoter-based CpG sites using the Affymetrix Human Promoter 1.0R array [ 26 ] and another investigated whole-genome bisulfite sequencing [ 10 ]. Sample sizes for the 24 studies varied from just nine mother–offspring pairs [ 31 ] to 6685 mother–offspring pairs in a meta-analysis across 13 cohorts [ 5 ]. Measures of smoke exposure varied from retrospective report, prospective report and objective measures of cotinine, with a few studies using a combination of cotinine and self-report [ 9–10 , 14–16 , 23 ].…”

The effect of exposure to particulate matter during pregnancy on lower respiratory tract infection hospitalizations during first year of life

“…Nevertheless, relatively few studies examined the effect of intrauterine exposure to pollution and early life respiratory infections [ 1 , 20 ]. Some have found an association between prenatal exposure to PM and respiratory infections in children [ 1 , 21 , 22 ] while others did not find any association between the two, specifically for exposure to nitrogen dioxide (NO 2 ) during pregnancy [ 23 ].…”