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Allergy Asthma Immunol Res.  2015 Nov;7(6):573-582. 10.4168/aair.2015.7.6.573.

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

Affiliations
  • 1Department of Pediatrics, Hallym Sacred Heart Hospital, Hallym University College of Medicine, Anyang, Korea.
  • 2Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
  • 3Department of Pediatrics, Inje University Sanggye Paik Hospital, Seoul, Korea.
  • 4Institute of Environmental and Industrial Medicine, Hanyang University, Seoul, Korea.
  • 5Department of Pediatrics, Childhood Asthma Atopy Center, Environmental Health Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. sjhong@amc.seoul.kr
  • 6Asan Institute for Life Science, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
  • 7Department of Pediatrics, Bundang CHA Medical Center, CHA University School of Medicine, Seongnam, Korea.
  • 8Department of Pediatrics, Pusan National University Yangsan Hospital, Yangsan, Korea.
  • 9Department of Pediatrics, Korea Cancer Center Hospital, Seoul, Korea.
  • 10Department of Pediatrics, Seoul National University Bundang Hospital, Seungnam, Korea.
  • 11Department of Pediatrics, College of Medicine, Korea University, Seoul, Korea.
  • 12Department of Pediatrics, National Health Insurance Corporation Ilsan Hospital, Goyang, Korea.
  • 13Department of Pediatrics and the Allergy and Respiratory Research Laboratory, Inje University Seoul Paik Hospital, Seoul, Korea.
  • 14Department of Pediatrics, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea.
  • 15Department of Pediatrics, Ajou University School of Medicine, Suwon, Korea.
  • 16Department of Pediatrics, Soonchunhyang University College of Medicine, Seoul, Korea.
  • 17Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea.
  • 18Department of Pediatrics, Gangnam CHA Medical Center, CHA University College of Medicine, Seoul, Korea.
  • 19Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
  • 20Department of Pediatrics, Yonsei University College of Medicine, Seoul, Korea.
  • 21Division of Allergy and Chronic Respiratory diseases, Center for of Biomedical Sciences, Korea National Institute of Health, Korea Centers for Disease Control and Prevention, Osong, Korea.

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.

Keyword

Prenatal exposure; particulate matter; tobacco smoke; respiratory tract infections; polymorphism; methylation

MeSH Terms

Cacao*
Cohort Studies
Diagnosis
Genotype
Humans
Infant
Methylation
Odds Ratio
Oxygen
Parents
Particulate Matter
Parturition
Pregnancy
Respiratory Tract Infections*
Smoke*
Tobacco
Oxygen
Particulate Matter
Smoke

Figure

  • Fig. 1 Flow chart of the study population. Of infants with prenatal indoor PM2.5 measurements (n=608), 14 met the exclusion criteria, 72 were withdrawn from the study, and 11 were lost to follow-up. An additional 204 infants were then excluded because the RTIs, prenatal ETS exposure, or genotype data were missing. ETS, environmental tobacco smoke; PM2.5, fine particulate matter; RTIs, respiratory tract infections.

  • Fig. 2 Effect of combined exposure to both PM2.5 and ETS according to exposure time on susceptibility to (A) lower and (B) upper respiratory tract infections in infancy. The groups were stratified by exposure time: (a) prenatal PM2.5/prenatal ETS; (b) prenatal PM2.5/postnatal ETS; (c) postnatal PM2.5/prenatal ETS; and (d) postnatal PM2.5/postnatal ETS. Prenatal high indoor PM2.5 and ETS exposure acted additively to increase the risk of lower respiratory tract infections. *Adjustments for maternal age at delivery, maternal body mass index, maternal educational degree, gestational age, delivery mode, infant sex, and family history of allergy. ETS, environmental tobacco smoke; PM2.5, fine particulate matter.


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