Aim: The present review is aimed to assess the role of inflammatory mediators in the initiation and progression of the disorders, related to air pollution, with a special focus on cytokines.
Background: Air pollution adversely affects human health. The outdoor and indoor pollution accounts for approximately 4 million deaths every year. The major pollutants include gaseous compounds, polycyclic aromatic hydrocarbons (PAH) and particulate matter (PM). Epidemiologic data shows the increase in the incidence of cardiopulmonary and central nervous system disorders on exposure of the pollutants and how do they aggravate the pre-existing disease conditions. Also, it contributes to the higher rate in cancer prevalence also.
Review results: Numerous studies were carried out in delineating the underlying pathological changes of these diseases due to pollution. The suggestive mechanisms include the local and systemic inflammatory response and bone marrow stimulation elicited as a result of the entry of the toxic compounds. The oxidative stress developed also is said to be a contributing factor. The multiple interactions of a broad range of compounds like, cytokines, growth factors, adhesion molecules, reactive oxygen species, and acute phase proteins are also involved in the reactions.
Conclusion: Multiple interrelated molecular pathways of inflammation are stimulated as a result of air pollution and which in turn leads to the secretion of the mediators and effector molecules. Cytokines are significant intermediaries of both the innate and the adaptive immune responses. These compounds take a m ajor position in the events in pathogenesis.
Clinical significance: The concentrations of cytokines are seen altered in circulation and tissues. Hence, these may have the potential in considering as markers for evaluating adverse effects of air pollution.
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