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

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Abstract

Purpose

To investigate whether prenatal exposure to indoor fine particulate matter (PM _2.5) 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 PM _2.5 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 PM _2.5 increased the susceptibility of lower RTIs (LRTIs) in infancy (adjusted odds ratio [aOR]=2.11). In terms of combined exposure to both indoor PM _2.5 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 PM _2.5 and ETS exposure were not found for upper RTIs.

Conclusions

Prenatal exposure to both indoor PM _2.5 and ETS may increase susceptibility to LRTIs. This effect can be modified by polymorphisms in reactive oxygen species-related genes.

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Most cited references 43

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Asthma and allergy patterns over 18 years after severe RSV bronchiolitis in the first year of life.

Nele Sigurs, Fatma Aljassim, Bengt Kjellman … (2010)

An increased prevalence of asthma/recurrent wheeze (RW), clinical allergy and allergic sensitisation up to age 13 years has previously been reported in subjects hospitalised with respiratory syncytial virus (RSV) bronchiolitis in their first year of life compared with matched controls. A study was undertaken to examine whether these features persist into early adulthood, to report longitudinal wheeze and allergy patterns, and to see how large and small airway function relates to RSV infection and asthma. Follow-up at age 18 years was performed in 46 of 47 subjects with RSV and 92 of 93 controls. Assessments included questionnaire, clinical examination, skin prick tests, serum IgE antibodies to inhaled allergens, blood eosinophils, fraction of exhaled nitric oxide (FeNO), spirometry, multiple breath washout (lung clearance index, LCI) and dry air hyperventilation challenge. Increased prevalence of asthma/RW (39% vs 9%), clinical allergy (43% vs 17%) and sensitisation to perennial allergens (41% vs 14%) were present at age 18 in the RSV cohort compared with controls. Persistent/relapsing wheeze associated with early allergic sensitisation predominated in the RSV cohort compared with controls (30% vs 1%). Spirometric function was reduced in subjects with RSV with or without current asthma, but not in asthmatic controls. LCI was linked only to current asthma, airway hyperresponsiveness and FeNO. Severe early RSV bronchiolitis is associated with an increased prevalence of allergic asthma persisting into early adulthood. Small airway dysfunction (LCI) is related to current asthma and airway inflammation but not to RSV bronchiolitis. Reduced spirometry after RSV may reflect airway remodelling.

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Oxidative stress: its role in air pollution and adverse health effects.

F. J. KELLY (2003)

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Oxidants and the pathogenesis of lung diseases.

Jonathan Ciencewicki, Shweta Trivedi, Steven Kleeberger (2008)

The increasing number of population-based and epidemiologic associations between oxidant pollutant exposures and cardiopulmonary disease exacerbation, decrements in pulmonary function, and mortality underscores the important detrimental effects of oxidants on public health. Because inhaled oxidants initiate a number of pathologic processes, including inflammation of the airways, which may contribute to the pathogenesis and/or exacerbation of airways disease, it is critical to understand the mechanisms through which exogenous and endogenous oxidants interact with molecules in the cells, tissues, and epithelial lining fluid of the lung. Furthermore, it is clear that interindividual variation in response to a given exposure also exists across an individual lifetime. Because of the potential impact that oxidant exposures may have on reproductive outcomes and infant, child, and adult health, identification of the intrinsic and extrinsic factors that may influence susceptibility to oxidants remains an important issue. In this review, we discuss mechanisms of oxidant stress in the lung, the role of oxidants in lung disease pathogenesis and exacerbation (eg, asthma, chronic obstructive pulmonary disease, and acute respiratory distress syndrome), and the potential risk factors (eg, age, genetics) for enhanced susceptibility to oxidant-induced disease.

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Author and article information

Journal

Journal ID (nlm-ta): Allergy Asthma Immunol Res

Journal ID (iso-abbrev): Allergy Asthma Immunol Res

Journal ID (publisher-id): AAIR

Title: Allergy, Asthma & Immunology Research

Publisher: The Korean Academy of Asthma, Allergy and Clinical Immunology; The Korean Academy of Pediatric Allergy and Respiratory Disease

ISSN (Print): 2092-7355

ISSN (Electronic): 2092-7363

Publication date (Print): November 2015

Publication date (Electronic): 25 June 2015

Volume: 7

Issue: 6

Pages: 573-582

Affiliations

[1 ]Department of Pediatrics, Hallym Sacred Heart Hospital, Hallym University College of Medicine, Anyang, Korea.

[2 ]Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.

[3 ]Department of Pediatrics, Inje University Sanggye Paik Hospital, Seoul, Korea.

[4 ]Institute of Environmental and Industrial Medicine, Hanyang University, Seoul, Korea.

[5 ]Department of Pediatrics, Childhood Asthma Atopy Center, Environmental Health Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.

[6 ]Asan Institute for Life Science, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.

[7 ]Department of Pediatrics, Bundang CHA Medical Center, CHA University School of Medicine, Seongnam, Korea.

[8 ]Department of Pediatrics, Pusan National University Yangsan Hospital, Yangsan, Korea.

[9 ]Department of Pediatrics, Korea Cancer Center Hospital, Seoul, Korea.

[10 ]Department of Pediatrics, Seoul National University Bundang Hospital, Seungnam, Korea.

[11 ]Department of Pediatrics, College of Medicine, Korea University, Seoul, Korea.

[12 ]Department of Pediatrics, National Health Insurance Corporation Ilsan Hospital, Goyang, Korea.

[13 ]Department of Pediatrics and the Allergy and Respiratory Research Laboratory, Inje University Seoul Paik Hospital, Seoul, Korea.

[14 ]Department of Pediatrics, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea.

[15 ]Department of Pediatrics, Ajou University School of Medicine, Suwon, Korea.

[16 ]Department of Pediatrics, Soonchunhyang University College of Medicine, Seoul, Korea.

[17 ]Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea.

[18 ]Department of Pediatrics, Gangnam CHA Medical Center, CHA University College of Medicine, Seoul, Korea.

[19 ]Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.

[20 ]Department of Pediatrics, Yonsei University College of Medicine, Seoul, Korea.

[21 ]Division 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.

Author notes

Correspondence to: Soo-Jong Hong, MD, PhD, Department of Pediatrics, Childhood Asthma Atopy Center, Environmental health Center, Asan Medical Center, 86 Asanbyeongwon-gil, Songpa-gu, Seoul 138-736, Korea. Tel: +82-2-3010-3379; Fax: +82-2-473-3725; sjhong@ 123456amc.seoul.kr

Article

DOI: 10.4168/aair.2015.7.6.573

PMC ID: 4605930

PubMed ID: 26333704

SO-VID: c6be585d-e7c7-4cc7-bf44-393831ba01f5

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 13 December 2014

Date revision received : 23 April 2015

Date accepted : 04 May 2015

Funding

Funded by: Korea Centers for Disease Control & Prevention

Award ID: 2008-E33030-00

Award ID: 2009-E33033-00

Award ID: 2011-E33021-00

Award ID: 2012-E33012-00

Award ID: 2013-E51011-00

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

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Abstract

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Most cited references 43

Asthma and allergy patterns over 18 years after severe RSV bronchiolitis in the first year of life.

Oxidative stress: its role in air pollution and adverse health effects.

Oxidants and the pathogenesis of lung diseases.

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Cited by 11

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