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Air pollution exposure and auto-inflammatory and autoimmune diseases of the musculoskeletal system: a review of epidemiologic and mechanistic evidence

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ENVIRONMENTAL GEOCHEMISTRY AND HEALTH
卷 45, 期 7, 页码 4087-4105

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SPRINGER
DOI: 10.1007/s10653-023-01495-x

关键词

Air pollution; Particulate matter; Inflammation; Autoimmune diseases; Mitochondria

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Auto-inflammatory and autoimmune diseases of the musculoskeletal system are characterized by severe erosion of joints and connective tissues, leading to chronic inflammation and damage. Genetic and environmental risk factors have been identified, and recent studies suggest that air pollution exposure may play a role in the development and occurrence of these diseases. Air pollution can induce oxidative stress, inflammation, epigenetic modifications, and mitochondrial dysfunction, primarily affecting the lungs and subsequently influencing immune and inflammatory responses. This review explores the association between air pollution and specific musculoskeletal diseases, such as osteoarthritis, rheumatoid arthritis, spondyloarthritis, and juvenile idiopathic arthritis, and aims to provide a comprehensive understanding of the mechanisms involved. The findings may contribute to the formulation of effective public health policies to mitigate the adverse health effects of air pollutants.
Auto-inflammatory and autoimmune diseases of the musculoskeletal system can be perceived as a spectrum of rheumatic diseases, with the joints and connective tissues are eroded severely that progressively develop chronic inflammation and lesion. A wide range of risk factors represented by genetic and environmental factors have been uncovered by population-based surveys and experimental studies. Lately, the exposure to air pollution has been found to be potentially involved in the mechanisms of occurrence or development of such diseases, principally manifest in oxidative stress, local and systemic inflammation, and epigenetic modifications, as well as the mitochondrial dysfunction, which has been reported to participate in the intermediate links. The lungs might serve as a starting area of air pollutants, which would cause oxidative stress-induced bronchial-associated lymphoid tissue (iBALT) to further to influence T, B cells, and the secretion of pro-inflammatory cytokines. The binding of aromatic hydrocarbon receptor (AhR) to the corresponding contaminant ligands tends to regulate the reaction of Th17 and Tregs. Furthermore, air pollution components might spur on immune and inflammatory responses by damaging mitochondria that could interact with and exacerbate oxidative stress and pro-inflammatory cytokines. In this review, we focused on the association between air pollution and typical auto-inflammatory and autoimmune diseases of the musculoskeletal system, mainly including osteoarthritis (OA), rheumatoid arthritis (RA), spondyloarthritis (SpA) and juvenile idiopathic arthritis (JIA), and aim to collate the mechanisms involved and the potential channels. A complete summary and in-depth understanding of the autoimmune and inflammatory effects of air pollution exposure should hopefully contribute new perspectives on how to formulate better public health policies to alleviate the adverse health effects of air pollutants.

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