People living with rheumatoid arthritis may have another reason to pay attention to air quality.
A large study from South Korea found that exposure to air pollution, especially very small particles known as PM2.5, was linked to more active disease and a greater chance of painful flare-ups.
The research was led by Eun Bong Lee and colleagues at Seoul National University. The findings were published in Annals of the Rheumatic Diseases, together with an editorial discussing their possible importance for patients and public health.
Rheumatoid arthritis, or RA, is a long-term disease in which the immune system mistakenly attacks the body’s own tissues. It mainly causes swelling, stiffness and pain in the joints, but inflammation can also affect the lungs, heart, blood vessels and other parts of the body.
RA affects about 0.5% to 1% of adults worldwide. Medicines can often control it, but many patients still experience flares, periods when pain, swelling, stiffness and other symptoms suddenly become worse.
Researchers have long known that both genes and the environment influence RA. Cigarette smoking is one of the clearest environmental risk factors, while exposure to substances such as silica dust has also been connected with the disease.
Air pollution has become another concern. Earlier studies suggested that people exposed to more pollution may be more likely to develop RA, but scientists knew less about whether polluted air can worsen symptoms in people who already have the condition.
To investigate, the South Korean researchers followed 1,070 people with RA over four years, from 2021 through 2024. Together, the patients made 12,583 outpatient visits, giving the team repeated information about changes in their disease.
The researchers compared each visit with levels of six common air pollutants, including sulfur dioxide, nitrogen dioxide, ozone, carbon monoxide, PM10 and PM2.5. They also considered factors such as medication use, patient characteristics, blood markers, socioeconomic conditions and weather.
PM2.5 stood out most clearly. Higher concentrations were associated with greater RA disease activity and a higher likelihood of a flare, particularly when elevated exposure continued for more than two weeks.
PM2.5 means airborne particles no more than 2.5 micrometers across. They can come from vehicle exhaust, fires, power generation and industrial activity, and their tiny size allows them to travel deep into the lungs.
Scientists think these particles can trigger harmful changes that extend beyond the lungs. Pollution can increase unstable molecules that place cells under stress, damage DNA and encourage inflammatory signals throughout the body.
For someone with rheumatoid arthritis, whose immune system is already producing too much inflammation, this extra stress could potentially contribute to worsening disease. However, the study did not directly prove that this biological process caused the flares that researchers observed.
The investigators also performed a second analysis using daily pollution concentrations before clinic visits. By comparing different exposure periods within the same patients, they tried to reduce the chance that fixed differences between individuals were responsible for the results.
An accompanying editorial by Jeffrey Sparks of Mass General Brigham, Brigham and Women’s Hospital and Harvard Medical School described the research as one of the largest studies using strong methods to connect air pollution with RA activity. The editorial noted that inhaled substances may have wider effects on autoimmune disease than previously recognized.
The findings could eventually have practical value. If future research confirms that pollution contributes to RA flares, air-quality information might help patients identify periods when limiting prolonged exposure to polluted outdoor air could be useful.
Still, the research cannot prove that PM2.5 directly caused patients’ symptoms to worsen. It was observational, so other environmental or personal factors may have influenced the association despite the researchers’ efforts to account for them.
Another limitation is that all participants came from a South Korean population. Genetics, climate, pollution sources, housing and daily patterns of exposure differ around the world, so researchers need to determine whether the same pattern appears in other countries.
The study also estimated pollution exposure from environmental measurements rather than measuring exactly how much pollution each person inhaled. People spend different amounts of time indoors, outdoors and in traffic, meaning their true exposure may differ from local pollution readings.
Even with these limits, the research has important strengths. It followed more than a thousand patients across thousands of real clinical visits, repeatedly measured disease activity and used several methods to test whether the pollution link remained.
Overall, the results make PM2.5 a plausible but not yet proven contributor to rheumatoid arthritis flares. The next important step is to test whether reducing exposure or improving community air quality actually leads to better disease control, which would turn an observed association into something more useful for patient care.
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Source: Seoul National University.
