The findings add to evidence that environmental exposures may play a role in worsening established rheumatoid arthritis.
Fine particulate air pollution has been linked to increased rheumatoid arthritis disease activity and a higher risk of flares in a large prospective cohort study.
The South Korean study, published in the Annals of the Rheumatic Diseases, analysed 12,583 outpatient visits from 1070 people with RA between 2021 and 2024.
The researchers found PM2.5 (airborne particulate matter measuring 2.5µm or less) had the strongest and most consistent association with worsening disease.
“Previous epidemiologic studies have shown an association between air pollution and an increased risk of developing rheumatoid arthritis,” the researchers wrote.
“However, the effects of air pollution on disease activity and flare occurrence in patients with established RA remain unclear, and the underlying mechanisms have not been fully elucidated.”
They examined exposure to six pollutants, including sulphur dioxide, nitrogen dioxide, ozone, carbon monoxide, PM10, and PM2.5, using monthly concentrations matched to patients’ residential regions.
RA flares were defined as an increase in DAS28-CRP of more than 1.2 from the previous visit, or more than 0.6 where the current DAS28-CRP was at least 3.2. The researchers also assessed tender and swollen joint counts, CDAI, and DAS28-CRP.
During more than 3200 person-years of follow-up, 1278 flares occurred among 604 patients, equivalent to 39.5 flares per 100 person-years.
Of the six individual pollutants, PM2.5 was significantly associated with flare risk after adjustment for factors including age, sex, smoking, serological status, RA medications, socioeconomic factors, temperature, and humidity.
Each one-standard-deviation increase in monthly PM2.5 concentration was associated with an adjusted 11.3% increase in the odds of an RA flare (OR 1.113, 95% CI 1.017-1.218). PM10 and ozone showed positive but non-significant associations with flare risk.
PM2.5 was also the only pollutant significantly associated with all four measures of disease activity examined: DAS28-CRP, CDAI, tender joint count, and swollen joint count. Disease activity generally increased as PM2.5 exposure rose.
The association between PM2.5 and DAS28-CRP was more pronounced among women and non-smokers, although clinical characteristics did not significantly modify the association between PM2.5 and the occurrence of flares.
A case-crossover sensitivity analysis involving 603 patients who experienced at least one flare produced similar findings.
Longer cumulative exposure to PM2.5 was associated with greater flare risk, with the relationship becoming more pronounced when exposure extended beyond about 14 days. The analysis also showed a positive dose-response relationship between PM2.5 concentrations and flare risk.
The researchers said oxidative stress offered one possible biological explanation. Fine particles could penetrate deeply into the respiratory tract and trigger production of reactive oxygen species, potentially promoting systemic and synovial inflammation.
Writing in an accompanying editorial in the Annals of the Rheumatic Diseases, US rheumatologist Dr Jeffrey Sparks said the study was one of the largest to use robust methods to investigate the relationship between air pollution and RA disease activity.
“Considering rising levels of air pollutants, these results have significant clinical, biologic, and public health implications,” Dr Sparks wrote.
“They also further reinforce that inhalants may have broad implications for risk and progression of RA and perhaps other autoimmune diseases.
“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.”
Dr Sparks noted that PM2.5 may be particularly relevant to RA, while PM10 had not been consistently associated with RA outcomes in either the current study or previous research.
However, both the researchers and editorial cautioned against assuming causation. Pollution exposure was estimated geographically rather than measured at an individual level, meaning actual exposure could vary according to factors such as time spent away from home and use of air purification.
The cohort was also drawn from a single tertiary medical centre in South Korea, potentially limiting the generalisability of the findings, and residual confounding could not be ruled out.
Dr Sparks said intervention studies were now needed to determine whether measures such as reducing exposure during periods of high PM2.5 or using air purification could translate the observational findings into improved outcomes for people with RA.
The researchers similarly concluded that further research was needed to determine whether improving air quality could reduce disease activity in patients with RA.
“This study provides real-world evidence that higher levels of air pollution, particularly PM2.5, are related to worsened RA disease activity and a higher risk of flare,” the researchers wrote.
“Although further external validation is needed, these findings have important clinical and public health implications.
“Physicians should encourage patients with RA to minimise exposure to poor air quality, and policymakers should prioritise air quality improvement to reduce the burden of chronic illnesses, including RA flares and elevated disease activity.”
Annals of the Rheumatic Diseases, August 2026 (research)
Annals of the Rheumatic Diseases, August 2026 (editorial)
