Environmental air pollution and rheumatoid arthritis flares



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Environmental air pollution and rheumatoid arthritis flares

Rheumatoid arthritis is a chronic, ankylosing and progressive inflammatory polyarthritis with autoimmune pathogenesis and unknown etiology, mainly affecting the synovial joints. It can cause deformation and pain that can lead to loss of joint function.

The condition can also present with signs and symptoms in different organs. It differs from osteoarthritis because it initially affects the synovial membrane and not the cartilage, it affects less frequently and at a younger age than osteoarthritis.

The onset is mainly observed at the end of adolescence or between the 4th and 5th decade of life; a second peak is observed between the ages of 60 and 70. It is the most widespread systemic disease of autoimmune origin, affecting between 0.5 and 1 percent of the world adult population as of 2016.

The cause of onset is not fully known. There is an inflammatory response of the synovium with swelling of the synovial cells, excess synovial fluid and development of fibrous tissue in the synovium. It also affects the underlying bone and cartilage, with thinning and destruction.

The condition can also manifest itself with widespread inflammation in the lungs, pericardium, pleura, sclera of the eye, and with diffuse nodular lesions in the subcutaneous tissue. Diagnosis is mainly made on the basis of symptoms and with x-rays.

Treatment includes both prescription drugs and other measures to control joint inflammation and prevent joint damage and subsequent disability. The study: Association between environmental air pollution and rheumatoid arthritis flares, published on the Rheumatology magazine, explained: "Environmental air pollution has been linked to the pathogenesis of RA.

Nevertheless, evidence linking higher concentrations of air pollutants with the risk of RA reactivations is missing. The objective of the present study was to determine the association between RA flares and air pollution. We collected longitudinal data of patients affected by RA and of the daily concentration of air pollutants in the Verona area.

We designed a case-crossover study. We compared the exposure to pollutants in the 30-day and 60-day periods preceding an arthritic flare referent to the 30-day and 60-day preceding a low-disease activity visit. The study included 888 patients with RA with 3396 follow-up visits; 13 636 daily air pollution records were retrieved.

We found an exposure-response relationship between the concentration of air pollutants and the risk of having abnormal CRP levels. Patients exposed to greater concentrations of air pollutants were at higher risk of having CRP levels ≥5 mg / l.

Concentrations of CO, NO, NO2, NOx, PM10, PM2.5 and O3 were higher in the 60-day period preceding a flare. We found a striking association between air pollution and RA disease severity and reactivations in a cohort of patients followed over a 5-year period.

The exposure to high levels of air pollutants was associated with increased CRP levels and a higher risk of experiencing a flare of arthritis. This excessive risk was evident at very low levels of exposure."