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Does early life exposure to exogenous sources of reactive oxygen species (ROS) increase the risk of respiratory and allergic diseases in children? A longitudinal cohort study
BACKGROUND: Excess reactive oxygen species (ROS) can cause oxidative stress damaging cells and tissues, leading to adverse health effects in the respiratory tract. Yet, few human epidemiological studies have quantified the adverse effect of early life exposure to ROS on child health. Thus, this stud...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9528154/ https://www.ncbi.nlm.nih.gov/pubmed/36184638 http://dx.doi.org/10.1186/s12940-022-00902-7 |
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author | To, Teresa Terebessy, Emilie Zhu, Jingqin Zhang, Kimball Lakey, Pascale SJ Shiraiwa, Manabu Hatzopoulou, Marianne Minet, Laura Weichenthal, Scott Dell, Sharon Stieb, Dave |
author_facet | To, Teresa Terebessy, Emilie Zhu, Jingqin Zhang, Kimball Lakey, Pascale SJ Shiraiwa, Manabu Hatzopoulou, Marianne Minet, Laura Weichenthal, Scott Dell, Sharon Stieb, Dave |
author_sort | To, Teresa |
collection | PubMed |
description | BACKGROUND: Excess reactive oxygen species (ROS) can cause oxidative stress damaging cells and tissues, leading to adverse health effects in the respiratory tract. Yet, few human epidemiological studies have quantified the adverse effect of early life exposure to ROS on child health. Thus, this study aimed to examine the association of levels of ROS exposure at birth and the subsequent risk of developing common respiratory and allergic diseases in children. METHODS: 1,284 Toronto Child Health Evaluation Questionnaire (T-CHEQ) participants were followed from birth (born between 1996 and 2000) until outcome, March 31, 2016 or loss-to-follow-up. Using ROS data from air monitoring campaigns and land use data in Toronto, ROS concentrations generated in the human respiratory tract in response to inhaled pollutants were estimated using a kinetic multi-layer model. These ROS values were assigned to participants’ postal codes at birth. Cox proportional hazards regression models, adjusted for confounders, were then used to estimate hazard ratios (HR) with 95% confidence intervals (CI) per unit increase in interquartile range (IQR). RESULTS: After adjusting for confounders, iron (Fe) and copper (Cu) were not significantly associated with the risk of asthma, allergic rhinitis, nor eczema. However, ROS, a measure of the combined impacts of Fe and Cu in PM(2.5), was associated with an increased risk of asthma (HR = 1.11, 95% CI: 1.02–1.21, p < 0.02) per IQR. There were no statistically significant associations of ROS with allergic rhinitis (HR = 0.96, 95% CI: 0.88–1.04, p = 0.35) and eczema (HR = 1.03, 95% CI: 0.98–1.09, p = 0.24). CONCLUSION: These findings showed that ROS exposure in early life significantly increased the childhood risk of asthma, but not allergic rhinitis and eczema. |
format | Online Article Text |
id | pubmed-9528154 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-95281542022-10-04 Does early life exposure to exogenous sources of reactive oxygen species (ROS) increase the risk of respiratory and allergic diseases in children? A longitudinal cohort study To, Teresa Terebessy, Emilie Zhu, Jingqin Zhang, Kimball Lakey, Pascale SJ Shiraiwa, Manabu Hatzopoulou, Marianne Minet, Laura Weichenthal, Scott Dell, Sharon Stieb, Dave Environ Health Research BACKGROUND: Excess reactive oxygen species (ROS) can cause oxidative stress damaging cells and tissues, leading to adverse health effects in the respiratory tract. Yet, few human epidemiological studies have quantified the adverse effect of early life exposure to ROS on child health. Thus, this study aimed to examine the association of levels of ROS exposure at birth and the subsequent risk of developing common respiratory and allergic diseases in children. METHODS: 1,284 Toronto Child Health Evaluation Questionnaire (T-CHEQ) participants were followed from birth (born between 1996 and 2000) until outcome, March 31, 2016 or loss-to-follow-up. Using ROS data from air monitoring campaigns and land use data in Toronto, ROS concentrations generated in the human respiratory tract in response to inhaled pollutants were estimated using a kinetic multi-layer model. These ROS values were assigned to participants’ postal codes at birth. Cox proportional hazards regression models, adjusted for confounders, were then used to estimate hazard ratios (HR) with 95% confidence intervals (CI) per unit increase in interquartile range (IQR). RESULTS: After adjusting for confounders, iron (Fe) and copper (Cu) were not significantly associated with the risk of asthma, allergic rhinitis, nor eczema. However, ROS, a measure of the combined impacts of Fe and Cu in PM(2.5), was associated with an increased risk of asthma (HR = 1.11, 95% CI: 1.02–1.21, p < 0.02) per IQR. There were no statistically significant associations of ROS with allergic rhinitis (HR = 0.96, 95% CI: 0.88–1.04, p = 0.35) and eczema (HR = 1.03, 95% CI: 0.98–1.09, p = 0.24). CONCLUSION: These findings showed that ROS exposure in early life significantly increased the childhood risk of asthma, but not allergic rhinitis and eczema. BioMed Central 2022-10-03 /pmc/articles/PMC9528154/ /pubmed/36184638 http://dx.doi.org/10.1186/s12940-022-00902-7 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research To, Teresa Terebessy, Emilie Zhu, Jingqin Zhang, Kimball Lakey, Pascale SJ Shiraiwa, Manabu Hatzopoulou, Marianne Minet, Laura Weichenthal, Scott Dell, Sharon Stieb, Dave Does early life exposure to exogenous sources of reactive oxygen species (ROS) increase the risk of respiratory and allergic diseases in children? A longitudinal cohort study |
title | Does early life exposure to exogenous sources of reactive oxygen species (ROS) increase the risk of respiratory and allergic diseases in children? A longitudinal cohort study |
title_full | Does early life exposure to exogenous sources of reactive oxygen species (ROS) increase the risk of respiratory and allergic diseases in children? A longitudinal cohort study |
title_fullStr | Does early life exposure to exogenous sources of reactive oxygen species (ROS) increase the risk of respiratory and allergic diseases in children? A longitudinal cohort study |
title_full_unstemmed | Does early life exposure to exogenous sources of reactive oxygen species (ROS) increase the risk of respiratory and allergic diseases in children? A longitudinal cohort study |
title_short | Does early life exposure to exogenous sources of reactive oxygen species (ROS) increase the risk of respiratory and allergic diseases in children? A longitudinal cohort study |
title_sort | does early life exposure to exogenous sources of reactive oxygen species (ros) increase the risk of respiratory and allergic diseases in children? a longitudinal cohort study |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9528154/ https://www.ncbi.nlm.nih.gov/pubmed/36184638 http://dx.doi.org/10.1186/s12940-022-00902-7 |
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