Prenatal particulate matter/tobacco smoke increases infants' respiratory infections

COCOA study

The COCOA Study Group

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Purpose: To 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. Methods: The 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. Results: Prenatal 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. Conclusions: Prenatal 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.

Original languageEnglish
Pages (from-to)573-582
Number of pages10
JournalAllergy, Asthma and Immunology Research
Volume7
Issue number6
DOIs
Publication statusPublished - 2015 Jan 1

Fingerprint

Particulate Matter
Smoke
Respiratory Tract Infections
Tobacco
Odds Ratio
Glutathione Transferase
Glutathione S-Transferase pi
Methylation
Reactive Oxygen Species
Genotype
Parturition
Genome
Physicians
Pregnancy
Population
Genes

Keywords

  • Methylation
  • Particulate matter
  • Polymorphism
  • Prenatal exposure
  • Respiratory tract infections
  • Tobacco smoke

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Pulmonary and Respiratory Medicine

Cite this

Prenatal particulate matter/tobacco smoke increases infants' respiratory infections : COCOA study. / The COCOA Study Group.

In: Allergy, Asthma and Immunology Research, Vol. 7, No. 6, 01.01.2015, p. 573-582.

Research output: Contribution to journalArticle

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abstract = "Purpose: To 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. Methods: The 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. Results: Prenatal 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. Conclusions: Prenatal 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.",
keywords = "Methylation, Particulate matter, Polymorphism, Prenatal exposure, Respiratory tract infections, Tobacco smoke",
author = "{The COCOA Study Group} and Yang, {Song I.} and Kim, {Byoung Ju} and Lee, {So Yeon} and Kim, {Hyo Bin} and Lee, {Cheol Min} and Jinho Yu and Kang, {Mi Jin} and Yu, {Ho Sung} and Eun Lee and Jung, {Young Ho} and Kim, {Hyung Young} and Seo, {Ju Hee} and Kwon, {Ji Won} and Dae-Jin Song and Jang, {Gwang Cheon} and Kim, {Woo Kyung} and Shim, {Jung Yeon} and Lee, {Soo Young} and Yang, {Hyeon Jong} and Suh, {Dong In} and Hong, {Seo Ah} and Choi, {Kil Yong} and Shin, {Youn Ho} and Kangmo Ahn and Kim, {Kyung Won} and Kim, {Eun Jin} and Hong, {Soo Jong}",
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AU - The COCOA Study Group

AU - Yang, Song I.

AU - Kim, Byoung Ju

AU - Lee, So Yeon

AU - Kim, Hyo Bin

AU - Lee, Cheol Min

AU - Yu, Jinho

AU - Kang, Mi Jin

AU - Yu, Ho Sung

AU - Lee, Eun

AU - Jung, Young Ho

AU - Kim, Hyung Young

AU - Seo, Ju Hee

AU - Kwon, Ji Won

AU - Song, Dae-Jin

AU - Jang, Gwang Cheon

AU - Kim, Woo Kyung

AU - Shim, Jung Yeon

AU - Lee, Soo Young

AU - Yang, Hyeon Jong

AU - Suh, Dong In

AU - Hong, Seo Ah

AU - Choi, Kil Yong

AU - Shin, Youn Ho

AU - Ahn, Kangmo

AU - Kim, Kyung Won

AU - Kim, Eun Jin

AU - Hong, Soo Jong

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N2 - Purpose: To 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. Methods: The 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. Results: Prenatal 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. Conclusions: Prenatal 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.

AB - Purpose: To 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. Methods: The 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. Results: Prenatal 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. Conclusions: Prenatal 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.

KW - Methylation

KW - Particulate matter

KW - Polymorphism

KW - Prenatal exposure

KW - Respiratory tract infections

KW - Tobacco smoke

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