The Rheumatic Dangers of Wildfire Smoke

As wildfires become more common, the smoke pollution they cause may be contributing to the risk of rheumatoid arthritis (RA) and RA-associated interstitial lung disease (ILD), recent research suggests.¹

The study in Arthritis & Rheumatology adds to a growing body of research that points to an association between air pollutants and RA and RA-ILD.

The researchers’ case-control analysis using healthcare data from the U.S. Veterans Affairs, as well as federal air pollution data, found that exposure to fire smoke particulate matter smaller than 2.5 microns (PM_2.5) is associated with RA-ILD. Exposure to nitrogen oxides (NO_x), ozone and particulate matter smaller than 10 microns (PM₁₀) is associated with incident RA risk, the paper notes.

“We were able to study almost 80,000 veterans across the U.S., and we found that increased fire smoke exposure was associated with both RA and RA-ILD, and other pollutants may also be associated with RA. These pollutants come from either the wildfires or fossil fuel combustion,” says lead author Vanessa L. Kronzer, MD, first author and assistant professor of medicine in the Division of Rheumatology, Mayo Clinic, Rochester, Minn.

The Study

Dr. Kronzer

Dr. Kronzer says the study arose from her involvement in Mayo Clinic’s long-established Rochester Epidemiology Project, which focuses on Olmsted County and a family vacation in an area affected by wildfire smoke. Dr. Kronzer and lead author Bryan England, MD—who also vacationed amid wildfire smoke—knew that respiratory inflammation is associated with RA in many forms. Inflammation triggers include military burn pits, smoking and occupational exposures. “It occurred to us that this smoke [may be] another inhaled irritant that could be associated with RA,” says Dr. Kronzer.

In their study, the researchers aimed to determine whether substances in fire smoke are associated with RA and RA-ILD. The researchers analyzed more than nine years of Veterans Affairs (VA) healthcare data on 9,701 patients with RA, including 531 with ILD, and 68,582 controls matched for age, sex and VA enrollment year. The researchers analyzed exposures to fire smoke PM_2.5, plus other pollutants. These included NO_x, ozone, overall PM_2.5, PM₁₀, and sulfur dioxide (SO₂). The researchers chose these pollutants because they are included in Environmental Protection Agency (EPA) air quality system ground pollutant monitoring data. Preliminary data suggested many of these pollutants may have an association, Dr. Kronzer explains.

The researchers determined fire smoke exposure from combining these EPA data with satellite-based smoke plume imagery from the National Oceanic and Atmospheric Administration Hazard Mapping System. The researchers overlapped these data sources to produce daily grids of smoke-related PM_2.5, non-smoke PM_2.5 and overall total PM_2.5 over the contiguous U.S. The researchers’ analysis also involved assigning daily concentrations of each pollutant to ZIP codes.

Fire smoke PM_2.5 was not associated with overall RA risk, but was significantly associated with RA-ILD. Post hoc analyses showed that fire smoke PM_2.5 concentrations of 0.28 μg/m3 and higher seemed to drive this elevated risk.

Higher levels of NO_x were associated with an increased risk for incident RA at the highest exposure quartiles, versus the lowest ones. Ozone and PM₁₀ levels were associated with an elevated risk for incident RA without specific antibodies like rheumatoid factor or anti-cyclic citrullinated peptide antibodies, the paper says.

Timing of pollutant exposure may be important. The researchers found that fire smoke PM_2.5 exposure was most associated with RA in the one to three and three to five years prior to RA diagnosis. NO_x showed the strongest point estimates in the three to five years and five years before RA onset. PM₁₀ exposure was most strongly associated with RA in the three to five years before RA onset.

ZIP codes—known to be a source of misclassification—is a study limitation, notes Dr. Kronzer. “I think if we truly had correct pollutant exposure data for each patient, the associations would be stronger,” she adds. Other limitations include selection bias due to missing data in controls and individuals from rural areas, over-representation of male sex and smoking history in the VA population, and sparse pollution monitoring in rural areas.

Growing Awareness of Environmental Factors in RA

A recent review paper points to growing evidence that autoimmune disease results from multiple exposures that alter susceptible genomes over time. Those exposures include a variety of pollutants, xenobiotics, infections, occupational exposures, medications, smoking, psychosocial stressors, changes in diet, obesity, exercise and sleep patterns, as well as wildfire and other climate change effects.²

Dr. Kronzer’s study adds to a growing body of research linking pollution specifically to poorer rheumatology outcomes. She points to other studies that suggest pollution plays a role in RA. For example, a Swedish study suggests RA incidence increases as NO₂ from local traffic and SO₂ from home heating sources increase, with stronger associations for patients who are negative for anti-citrullinated protein antibody.³

Korean researchers have found associations between high PM₁₀ exposure and mortality in RA-ILD patients.⁴

Researchers in Sweden and Korea had access to their nations’ detailed pollution monitoring systems, Dr. Kronzer says.

Dr. Kronzer is part of the Rheumatology Engaged in Action for Environmental Health initiative, which raises awareness of environmental changes’ potential impact on rheumatic diseases and suggests practical, cost‐effective and sustainable solutions. In addition to wildfires, the initiative focuses on extreme weather events, heat waves, extreme cold, ultra­violet light, pathogens, sea level rise, food insecurity and environmental toxins.

Dr. Kronzer would also like to explore how microplastic exposure affects patients with RA.

Implications

Dr. Kronzer suggests rheumatologists delve into patients’ histories to see who is at risk for RA or RA-related diseases on the basis of environmental risk factors. She recalls working with a resident who thought a patient with new joint pain did not have RA. However, she was able to diagnose the patient with it, knowing that, like many military veterans, the patient had been exposed to burn pits.

“We need to be counseling patients that environmental exposures can increase their risk for the [RA] lung disease complication, as well as [disease] flares. It may be more important for them than other people to avoid pollution exposures. And we also need to be aware of the higher likelihood of having a flare—as opposed to other things that mimic flares—during times of high pollutant burden,” she adds.

Patients already diagnosed with RA should consider staying indoors if they are in areas with high levels of pollution and wearing a mask if they must go out, she advises.

Deborah Levenson is a writer and editor based in College Park, Md.

References

1. Kronzer VL, Yang Y, Roul P, et al. Associations of fire smoke and other pollutants with incident rheumatoid arthritis and rheumatoid arthritis-associated interstitial lung disease. Arthritis Rheumatol. 2025 July;77(7):808–816.
2. Miller F. Environment, lifestyles, and climate change: The many nongenetic contributors to the long and winding road to autoimmune diseases. Arthritis Care Res (Hoboken). 2025 Jan;77(1):3–11.
3. Hart JE, Källberg H, Laden F, et al. Ambient air pollution exposures and risk of rheumatoid arthritis: Results from the Swedish EIRA case-control study. Ann Rheum Dis. 2013 Jun;72(6):888–894.
4. Park JS, Cho S, Kim K, et al. Association of particulate matter with autoimmune rheumatic diseases among adults in South Korea. Rheumatology (Oxford). Nov 3;60(11):5117–5126.