Allergy, Asthma & Immunology Research, 2015, 01, 573─582

Prenatal particulate matter/tobacco smoke increase infants’ respiratory infections: COCOA study

Song-I Yang, BJ Kim, SY Lee, HB Kim, CM Lee, JinhoYu

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.

• ISBN or ISSN: 2092-7355

• 본 연구는 질병관리본부 연구개발과제(과제번호 2013-E51011-02) 연구비를 지원받아 수행되었습니다.
• This research was supported by a fund(code 2013-E51011-02) by Research of Korea Centers for Disease Control and Prevention.