Prenatal Particulate Matter/Tobacco Smoke Increases Infants' Respiratory Infections: COCOA Study
Open accessAbstract
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.
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Findings from a birth cohort in Korea demonstrated increased susceptibility of lower respiratory tract infections in infants prenatally exposed to PM2.5 was significantly modified by polymorphisms in the maternal Nrf2 gene.
“Findings from a birth cohort in Korea demonstrating increased susceptibility of lower respiratory tract infections in infants prenatally exposed to PM2.5 was significantly modified by polymorphisms in the maternal Nrf2 gene [145].”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [145]
The Abstract Results and Results section report increased infant LRTI risk after prenatal indoor PM2.5 exposure, with a stronger association for the Nrf2 GG genotype when exposure included both PM2.5 and environmental tobacco smoke. But the Genotyping methods say DNA came from newborn umbilical cord blood, not mothers; the reported Nrf2 finding also concerns combined exposure, rather than PM2.5 alone. (LLM, conf=0.91)
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Johnson, N. M., Hoffmann, A. R., Behlen, J. C., Lau, C., Pendleton, D., Harvey, N., Shore, R., Li, Y., Chen, J., Tian, Y., et al. (2021) · Environmental Health and Preventive Medicine · doi:10.1186/s12199-021-00995-5 · Cited by 339 · see citing works
“5 was significantly modified by polymorphisms in the maternal Nrf2 gene [145].”
BackgroundIn utero ultrafine particulate matter exposure causes offspring pulmonary immunosuppression
Rychlik, K. A., Secrest, J. R., Lau, C., Pulczinski, J., Zamora, M. L., Leal, J., Langley, R., Myatt, L. G., Raju, M., Chang, R. C.-A., et al. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1816103116 · Cited by 98 · see citing works
- Authors
- Yang, S.-I., Kim, B.-J., Lee, S.-Y., Kim, H.-B., Lee, C. M., Yu, J., Kang, M.-J., Yu, H.-S., Lee, E., Jung, Y.-H., Kim, H. Y., Seo, J.-H., Kwon, J.-W., Song, D. J., Jang, G., Kim, W.-K., Shim, J. Y., Lee, S.-Y., Yang, H. J., Suh, D. I., Hong, S. A., Choi, K.-Y., Shin, Y. H., Ahn, K., Kim, K. W., Kim, E.-J., Hong, S.-J., & COCOA Study Group
- Affiliations
- Hallym University (KR)
- University of Cincinnati (US)
- Inje University Sanggye Paik Hospital (KR)
- Hanyang University (KR)
- Asan Medical Center (KR)
- CHA University Bundang Medical Center (KR)
- Department of Pediatrics, Korea Cancer Center Hospital, Seoul, Korea.
- Seoul National University Bundang Hospital (KR)
- Korea University (KR)
- Department of Pediatrics, National Health Insurance Corporation Ilsan Hospital, Goyang, Korea.
- Inje University Seoul Paik Hospital (KR)
- Kangbuk Samsung Hospital (KR)
- Department of Pediatrics, Ajou University School of Medicine, Suwon, Korea.
- Soonchunhyang University (KR)
- Seoul National University (KR)
- Asan Institute for Life Science, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
- CHA University (KR)
- Samsung Medical Center (KR)
- Yonsei University (KR)
- Korea National Institute of Health (KR)
- Corresponding author
- Hong, Soo-Jong
- ORCID
- Venue
- Allergy, Asthma & Immunology Research
- Publisher
- XMLink
- Published
- 2015
- Volume
- 7
- Issue
- 6
- Pages
- 573
- ISSN
- 2092-7355 (ISSN-L)
- 2092-7363
- PMC
- PMC4605930
- OpenAlex
- W2168097233
- Cited by
- 29
- References
- 2
- Citations by year
- 2026: 2 · 2024: 3 · 2023: 4 · 2022: 4 · 2021: 6 · 2020: 3 · 2019: 3 · 2018: 1 · 2017: 2 · 2016: 1
- FWCI
- 0.84
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Allergy Asthma and Immunology Research (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- AJOU Open Repository (Ajou University) (submittedVersion, cc-by-nc)
- YUHSpace (Yonsei University Medical Library) (submittedVersion, cc-by-nc-nd)
- Funders
- Korea Centers for Disease Control & Prevention (2008-E33030-00, 2009-E33033-00, 2011-E33021-00, 2012-E33012-00, 2013-E51011-00)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Indoor Air Quality and Microbial Exposure
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Keywords
- prenatal exposure, PM2.5, environmental tobacco smoke, respiratory infections, lower respiratory tract infection, infant susceptibility, gene-environment interaction, Nrf2, GSTP1, GSTM1, DNA methylation, reactive oxygen species
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