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 language | English |
|---|---|
| Pages (from-to) | 573-582 |
| Number of pages | 10 |
| Journal | Allergy, Asthma and Immunology Research |
| Volume | 7 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 2015 Jan 1 |
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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 journal › Article
}
TY - JOUR
T1 - Prenatal particulate matter/tobacco smoke increases infants' respiratory infections
T2 - COCOA study
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
PY - 2015/1/1
Y1 - 2015/1/1
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
UR - http://www.scopus.com/inward/record.url?scp=84941118325&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84941118325&partnerID=8YFLogxK
U2 - 10.4168/aair.2015.7.6.573
DO - 10.4168/aair.2015.7.6.573
M3 - Article
AN - SCOPUS:84941118325
VL - 7
SP - 573
EP - 582
JO - Allergy, Asthma and Immunology Research
JF - Allergy, Asthma and Immunology Research
SN - 2092-7355
IS - 6
ER -