Table IV.
Summary of studies assessing the effects of criteria air pollutants on oxidative stress and endothelial dysfunction among children and young adults
Reference | Location | Population studied | Aims | Findings |
---|---|---|---|---|
Oxidative stress | ||||
Kelishadi et al., 2009 [29] | Isfahan, Iran | A population-based sample of children aged 10-18 years (n=374) | To determine the association of air pollution as well as dietary and physical activity habits with markers of inflammation, oxidative stress and insulin resistance | The Pollutant Standard Index (PSI) and the level of fine particulate matter had a significant independent association with all biomarkers studied |
Yang, Omaye, 2009 [74] | Review | Review of studies on air pollution and chronic obstructive pulmonary diseases, cardiovascular diseases, asthma, and cancer | To provide some insight into the health problems associated with various air pollutants and their relationship in promoting chronic diseases through changes in oxidative stress and modulation of gene expression | By-products of oxidative stress found in air pollutants are common initiators or promoters of the damage produced in chronic diseases |
Chuang et al., 2007 [75] | Taipei, Taiwan | Young healthy university students (n=76) | To investigate whether biological mechanisms linking air pollution to cardiovascular events occurred concurrently in human subjects exposed to urban air pollutants | Air pollution is associated with inflammation, oxidative stress and blood coagulation in healthy young humans |
Endothelial dysfunction | ||||
Brook, 2008 [76] | Review | Review of studies on air pollution and cardiovascular diseases | To address the cardiovascular effects of air pollution and related mechanisms | Air particle exposure may both trigger acute events as well as prompt the chronic development of cardiovascular diseases. One of the mechanisms is by triggering acute endothelial dysfunction |
Nadadur et al., 2008 [77] | USA | Differential gene expression and transcription factor activation profiles in human vascular endothelial cells exposed to a non-cytotoxic dose of fly ash or V following semi-global gene expression profiling of approximately 8000 genes | To explore potential biomarkers for PM-induced endothelial dysfunction | Cardiovascular effects associated with exposure to PM may be mediated by perturbations in endothelial cell permeability, membrane integrity, and ultimately endothelial dysfunction |