Prenatal Particulate Matter/Tobacco Smoke Increases Infants' Respiratory Infections: COCOA Study.
10.4168/aair.2015.7.6.573
- Author:
Song I YANG
1
;
Byoung Ju KIM
;
So Yeon LEE
;
Hyo Bin KIM
;
Cheol Min LEE
;
Jinho YU
;
Mi Jin KANG
;
Ho Sung YU
;
Eun LEE
;
Young Ho JUNG
;
Hyung Young KIM
;
Ju Hee SEO
;
Ji Won KWON
;
Dae Jin SONG
;
Gwangcheon JANG
;
Woo Kyung KIM
;
Jung Yeon SHIM
;
Soo Young LEE
;
Hyeon Jong YANG
;
Dong In SUH
;
Seo Ah HONG
;
Kil Yong CHOI
;
Youn Ho SHIN
;
Kangmo AHN
;
Kyung Won KIM
;
Eun Jin KIM
;
Soo Jong HONG
Author Information
1. Department of Pediatrics, Hallym Sacred Heart Hospital, Hallym University College of Medicine, Anyang, Korea.
- Publication Type:Original Article
- Keywords:
Prenatal exposure;
particulate matter;
tobacco smoke;
respiratory tract infections;
polymorphism;
methylation
- MeSH:
Cacao*;
Cohort Studies;
Diagnosis;
Genotype;
Humans;
Infant;
Methylation;
Odds Ratio;
Oxygen;
Parents;
Particulate Matter;
Parturition;
Pregnancy;
Respiratory Tract Infections*;
Smoke*;
Tobacco
- From:Allergy, Asthma & Immunology Research
2015;7(6):573-582
- CountryRepublic of Korea
- Language:English
-
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.
