Does Air Pollution Have Anything to Do with Rheumatoid Arthritis?
Rheumatoid arthritis (RA) is an autoimmune disease with genetic and environmental origins. It is a systemic disease that affects the joints and may also involve visceral organs such as the lungs.
The pulmonary involvement is characterized by a decrease in vital capacities, the presence of bronchiectasis and/or an inflammatory lymphoplasmocytic infiltrate. The most common disorder is interstitial lung disease which leads to fibrosis during which the lung parenchyma is involved.
Lung disorders in RA patients are correlated with the serum, alveolar and histological positivity of anti-citrullinated peptide antibodies (ACPA). Parenchymal damage is found in almost 60% of patients with established RA. In addition, the role of tobacco is now well established in the pathophysiology of RA. It has also been shown that cigarette smoke in the presence of the HLA-DRB1 allele initiates the citrullination of the proteins in the presence of the ACPA.
The air pollution particles would come into contact with the lungs, which would be able to transform them and present them as antigens. These particles would therefore become precursors of autoimmunity.
Air pollution and other rheumatic diseases
Studies evaluating the impact of air pollution on RA development lead to discordant results and biases, in contrast to more robust data from systemic autoimmune rheumatic disease studies, including lupus, scleroderma, Sjögren's syndrome, dermato/polymyositis and undifferentiated connective tissue disease. In this context, a Canadian study has shown that a concentration of fine particles (smaller than 2.5 μm) greater than 5.2 mg/m 3 was associated with an increased risk of systemic autoimmune disease with OR = 2.44.
Advances at the molecular level
Studies have shown the presence of tertiary inducible bronchus-associated lymphoid tissue (iBALT). Absent healthy tissue, these develop only after prolonged exposure to one or more elements of the environment. iBALT has been linked to inflammatory lung disease and respiratory disease associated with RA. If all of the stimuli responsible for the formation of iBALT have not been identified, there is evidence that cigarette smoke, inhalation of silica, and fine particles associated with diesel combustion promote the formation of these iBALTs. Thus, these atmospheric particles would stimulate these tertiary inducible lymphoid tissues, promoting an inflammatory environment and "citrullination" in the lung, which could be responsible for the development of a specific immunity with production of ACPA. Pollution thus induces innate immunity (pro-inflammatory cytokines, reactive oxygen species) and adaptive immunity.
However, the exact relation between these cellular and molecular mechanisms and the development or maintenance of RA are not yet known. Research continues in this direction.
Reference:
Sigaux, Johanna, et al. "Air Pollution as a Determinant of Rheumatoid Arthritis." Joint Bone Spine (2018).
Tags: rheumatoid arthritis