Exposure to air pollution consisting of fine particulate matter measuring 2.5 micrometers or less in diameter (PM_2.5) is significantly associated with higher disease activity and an increased risk for flares in patients with rheumatoid arthritis (RA). This new research finding, in a large prospective, longitudinal study of patients in South Korea, provides independent confirmation of previous research from a smaller Italian study that demonstrated an association between air pollution exposure and both increased inflammatory activity and a higher risk for RA flares.

“Most of the previous studies have focused on the association between RA incidence and air pollutants,” senior study author Eun Bong Lee, MD, PhD, professor in the Division of Rheumatology at Seoul National University College of Medicine in Seoul, South Korea, told Medscape Medical News.

The new study was published on August 5, 2026, in Annals of the Rheumatic Diseases.

“[The study] identifies PM_2.5 as the pollutant most consistently associated with flares, tender and swollen joints, and higher disease activity,” Giovanni Adami, MD, PhD, rheumatologist at the University of Verona in Verona, Italy, who was not involved in the latest study, told Medscape Medical News. “It also suggests that cumulative exposure over approximately 2 weeks may be particularly relevant; that is in line with our previous study. Indeed, we found that the period at highest risk was around 15-30 days before the flare.”

Clinical and Practical Implications

The growing evidence that links air pollution to RA flares carries significant implications for clinicians and patients. “From a clinical perspective, this may offer avenues to lower the risk of RA flares by avoiding air with poor quality and provide some potential explanation for otherwise idiosyncratic RA flares,” Jeffrey A. Sparks, MD, MMSc, rheumatologist at Brigham and Women’s Hospital and Harvard Medical School, Boston, wrote in an accompanying editorial to the study.

“During prolonged periods of poor air quality, especially high PM_2.5, [patients should] reduce strenuous outdoor activity, avoid heavily trafficked areas, and consider indoor air filtration. These precautions should complement, not replace, usual treatment,” Adami said.

Clinicians should consider recent exposure to poor air quality, such as wildfire smoke, traffic pollution, or occupational dust when assessing otherwise unexplained flares, he said. “However, the evidence remains observational, so pollution should not distract from established causes such as poor adherence or inadequate treatment.

“Nonetheless, in a previous study, we found that greater air-pollution exposure was associated with poorer retention of biologic therapies, with pollutant concentrations being higher in the 60 days preceding treatment failure and a switch or swap than before periods of stable treatment,” Adami added.

These results reinforce the urgent need for policymakers to enforce stricter regulations on fine particle emissions. “Air pollution may not only cause cardiovascular and respiratory disease but also worsen chronic autoimmune conditions, increasing pain, disability, and healthcare use,” Adami said. “Policies should focus on reducing emissions at source, improving air-quality monitoring, and protecting vulnerable and highly exposed populations.”

The Study

Lee and colleagues tracked 12,583 outpatient visits from 1070 patients with RA between 2021 and 2024 at a tertiary medical center in South Korea. They evaluated monthly mean exposure levels across six major air pollutants: sulfur dioxide, nitrogen dioxide, ozone, carbon monoxide, coarse particulate matter, and PM_2.5.

Of these, PM_2.5 was the one most strongly linked to disease exacerbation. Each standard deviation increase in monthly mean PM_2.5 concentration was associated with an 11.3% increase in the risk for RA flare (adjusted odds ratio, 1.113; 95% CI, 1.017-1.218). High PM_2.5 levels were also consistently linked to measures of higher overall disease activity, including Disease Activity Score in 28 joints using C-reactive protein (DAS28-CRP) and Clinical Disease Activity Index, as well as higher tender and swollen joint counts.

Prolonged Exposure Heightens Flare Risk

The researchers conducted a case-crossover sensitivity analysis comparing daily air pollution exposure preceding flare visits with nonflare visits within the same patients.

Short-term, day-to-day spikes in PM_2.5 did not immediately trigger flares. Instead, the analysis revealed that cumulative exposure over extended periods (beyond 14 days preceding a clinic visit) was associated with a significantly increased risk for RA flare. Exposure-response modeling confirmed positive, dose-dependent associations between PM_2.5 levels and flare incidence.

Subgroup analyses showed that the association between PM_2.5 and DAS28-CRP was significantly more pronounced among women and nonsmokers. The researchers suggested that chronic smoking-related airway inflammation may mask the acute effects of ambient PM_2.5, whereas the lungs of nonsmokers remain more vulnerable to environmental oxidative stress. Patients with a higher baseline tender joint count also experienced a greater increase in disease activity with higher PM_2.5 exposure.

Unlike PM_2.5, gaseous pollutants and coarse particles were not consistently associated with RA flares.

The study controlled for various confounding factors that can affect RA disease activity, including temperature, humidity, and socioeconomic status, Lee said.

Connecting Pathogenesis to Progression

While the study was not designed to show the mechanism by which particulate matter might be associated with worsening RA disease activity, Lee suggested that the biological rationale rests on how fine particulate matter interacts with the respiratory and systemic circulatory systems.

Fine air pollution particles go deep into the lungs, causing oxidative stress on cells and releasing inflammatory cytokines. In the lungs, these particles can also alter proteins and trick the immune system into attacking the body’s own tissues, which reinforces the idea that lung problems and joint pain are directly connected, Adami explained. While air pollution can trigger the production of RA-related autoantibodies in the first place, in people who already have RA, it acts as a “second hit,” he said, further boosting inflammation throughout the body and worsening joint swelling.

According to Sparks, the study’s findings support the “mucosal origins hypothesis,” which suggests that environmental triggers first cause lung inflammation and autoantibody production years before joint pain begins. This theory may also explain why many patients with RA develop lung diseases such as interstitial lung disease or bronchiectasis.

“Pollution now links pathogenesis and progression in RA,” he wrote in the accompanying editorial. “These findings emphasize how inhalants such as pollution may drive RA and perhaps other autoimmune processes.”

“Indeed, we confirmed such association also in the so-called seronegative [rheumatoid] arthritis and other autoimmune diseases, such as psoriasis and atopic dermatitis,” Adami said.

The study was supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute, funded by the Ministry of Health & Welfare, Republic of Korea, and by the BioData Industry Professional Training Program through the Korea Institute for Advancement of Technology, funded by the Ministry of Trade, Industry, and Energy.

Lee and Adami reported having no relevant financial relationships. Sparks reported receiving support from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the National Heart, Lung, and Blood Institute, the Rheumatology Research Foundation, the Arthritis Foundation, the R. Bruce and Joan M. Mickey Research Scholar Fund, and the Llura Gund Award, funded by the Gordon and Llura Gund Foundation. He also reported having numerous financial relationships with pharmaceutical companies unrelated to the study.

Manuela Callari is an independent science journalist specializing in human and planetary health. Her work has been published in The Medical Republic, Rare Disease Advisor, New Scientist, The Guardian, MIT Technology Review, and others.