Outdoor Air Pollution and Childhood Respiratory Disease: The Role of Oxidative Stress

Abstract

The leading mechanisms through which air pollutants exert their damaging effects are the promotion of oxidative stress, the induction of an inflammatory response, and the deregulation of the immune system by reducing its ability to limit infectious agents’ spreading. This influence starts in the prenatal age and continues during childhood, the most susceptible period of life, due to a lower efficiency of oxidative damage detoxification, a higher metabolic and breathing rate, and enhanced oxygen consumption per unit of body mass. Air pollution is involved in acute disorders like asthma exacerbations and upper and lower respiratory infections, including bronchiolitis, tuberculosis, and pneumoniae. Pollutants can also contribute to the onset of chronic asthma, and they can lead to a deficit in lung function and growth, long-term respiratory damage, and eventually chronic respiratory illness. Air pollution abatement policies, applied in the last decades, are contributing to mitigating air quality issues, but more efforts should be encouraged to improve acute childhood respiratory disease with possible positive long-term effects on lung function. This narrative review aims to summarize the most recent studies on the links between air pollution and childhood respiratory illness.

Exposure to outdoor air pollution and risk of hospitalization for bronchiolitis in an urban environment: A 9‐year observational study

“…This suggests that exposure to the same mass concentrations (meaning the same value of PM 2.5 or PM 10 ) can be associated with extremely different toxicological properties and substantially different health outcomes 35 . As pointed out by several authors, a possible recommendation for future studies could be to use alternative metrics to focus on air pollution data for specific types of PM 20 (e.g., Black/Elemental Carbon, Ultrafine PM, ROS species) and/or specific types of sources 36 (e.g., traffic, biomass burning, secondary PM) to be related to specific health/biological outcomes (in vivo or in vitro) 34 . On the other hand, some factors other than outdoor air pollutants and pre‐existing personal determinants have been shown to influence the course of bronchiolitis.…”

“…Indeed, PM is generally identified as the key indicator of air quality brought into the air by a variety of natural and human activities and as the main driver of health effects. However, at the center of the scientific debates, there is a growing awareness that most studies are based on PM mass, a metric that is now recognized to be not ideal for representing the toxicologically active dose of PM, 34 because health impacts can vary significantly depending on the blend of particles and gaseous compounds, as well as additional factors such as the mixing state of PM populations, weather conditions, atmospheric dilution, and processing, and so forth. Indeed, PM 2.5 physicochemical properties vary in space and time and can be affected by a myriad of emission sources.…”

“…35 As pointed out by several authors, a possible recommendation for future studies could be to use alternative metrics to focus on air pollution data for specific types of PM 20 (e.g., Black/Elemental Carbon, Ultrafine PM, ROS species) and/or specific types of sources 36 (e.g., traffic, biomass burning, secondary PM) to be related to specific health/biological outcomes (in vivo or in vitro). 34 On the other hand, some factors other than outdoor air pollutants and pre-existing personal determinants have been shown to influence the course of bronchiolitis. Maternal asthma, maternal smoking during pregnancy, postnatal exposure to cigarette passive smoking, living in a crowded home, and having older siblings have been shown to be important factors in determining the severity of bronchiolitis.…”

Short‐term effects of air pollution on hospitalization of children with acute upper respiratory infections: A time series analysis in Lanzhou, China

“…Gaseous pollutants like SO 2 and NO 2 are capable of producing reactive oxides (ROS), which can initiate oxidative stress. This oxidative stress, in turn, can cause inflammation and damage to the tissues of the respiratory tract, thereby increasing the susceptibility of children to AURI 25 …”

“…On the other hand, PM 2.5 and SO 2 had a more pronounced impact on children aged 0–1 years. This could be attributed to the incomplete development of the respiratory tract in infants and young children, as well as their comparatively weaker immune system 25,29 …”