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Year : 2015  |  Volume : 4  |  Issue : 5  |  Page : 59

Effects of air pollution on respiratory health

Department of Chest Diseases, School of Medicine, University of Gaziantep, Gaziantep 27310, Turkey

Correspondence Address:
Hasan Bayram
Department of Chest Diseases, School of Medicine, University of Gaziantep, Gaziantep 27310
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Source of Support: None, Conflict of Interest: None

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Epidemiological studies have demonstrated that there is an association between increases in air pollution and cardiopulmonary mortality and morbidity. Multi-center studies in North America and Western European countries reported that an increase in the levels of particulate matter (PM), ozone, nitrogen oxides (NOx) and sulphur dioxide (SO2) leads to increases in prevalence, emergency room visits and hospitalization due to chronic respiratory diseases such as asthma and chronic obstructive disease (COPD). Furthermore, it has been shown that increased levels of air pollutants are associated with increased prevalence of respiratory infections, including pneumonia. Although studies of indoor air pollution clearly showed a significant association with tuberculosis (TB), studies investigating the role of outdoor air pollution are lacking. However, it has recently been reported that increased ambient levels of air pollutants such as PM≤2.5 μm and SO2 were associated with increased risk of TB. In vivo human studies demonstrated that exposure to ozone, NO2 and diesel exhaust (DE) leads to irritation in the mouth and nose, dyspnoea, wheezing, chest tightness, decreases in lung function tests, and increased airway hyper-responsiveness. There were also increased levels of neutrophils, lymphocytes and inflammatory mediators in bronchial lavage and bronchial biopsies of subjects exposed to ozone and DE. Furthermore, SO2 and NO2 increased airway response of allergic asthmatic subjects to allergens, such as house dust mite allergen. In vitro studies reported that DE particles (DEP) induce inflammatory mediator expression and synthesis of IgE specific to allergens in human B cells. Studies of human macrophages demonstrated that fine carbon black (CB) induced inflammatory cytokines and impaired phagocytosis of pneumococci and mycobacteria TB with a reduction in the oxidative burst capacity of these cells. This study has demonstrated that DEP, which constitute an important fraction of PM pollution, can decrease ciliary beat frequency (CBF), and induce the release of inflammatory mediators such as interleukin (IL)-8, granulocyte macrophage-colony stimulating factor (GM-CSF), normal T-cell expressed and secreted (RANTES) and soluble intercellular adhesion molecule (sICAM)-1 from primary bronchial epithelial cells (BECs). More recently, this study found that DEP can decrease airway epithelial cell viability and modify the cell cycle progression and apoptosis by inducing oxidative stress-related pathways, such as activator protein (AP)-1 and nuclear factor (NF)-κB, and an increased expression of apoptosis and cell cycle regulating proteins such as p21, p27, p53, cyclin E, c-myc, and cyclin-dependant kinase 2 (CDK2). Interestingly, serum, as can be seen in the inflamed airways of patients with chronic airway diseases such as asthma and COPD because of extravasation, enhanced the detrimental effects of DEP. Furthermore, these studies showed that gaseous air pollutants such as ozone and NO2 induce permeability of BEC cultures with an increase in the release of inflammatory mediators. More importantly, this study demonstrated that BECs from patients with chronic airway diseases such as asthma and COPD are more susceptible to deleterious effects of air pollutants. In conclusion, air pollutants can induce respiratory mortality and morbidity by leading to airway and lung inflammation and impairing the airway defence system against noxious agents and microorganisms such as mycobacteria TB.

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