Such environmental degradation also appears to reduce treatment efficacy.
Environmental air pollution may trigger disease flares in patients with long-standing rheumatoid arthritis, and exposure is a predictor of poor response to biological therapies, according to two Italian studies.
Dr Giovanni Adami, a rheumatologist at the University of Verona, presented results from the two studies, published in Rheumatology and ACR Open Rheumatology, at the EULAR 2021 Congress in June.
Toxic air pollutants have been previously linked with an increased risk of developing rheumatoid arthritis and low-grade inflammation in lung and heart diseases. These analyses were reportedly the first to demonstrate a link between exposure to environmental air pollution and disease flares in rheumatoid arthritis patients, and a possible relationship between air pollution and poor treatment response among arthritis patients more generally.
“We found a striking association between air pollution and rheumatoid arthritis disease severity and reactivations in a cohort of patients followed over a five-year period,” Dr Adami and his colleagues wrote in the first paper, published in February.
For both studies, patient data from a University of Verona registry of biologic therapies was linked with thousands of daily public air pollution records.
Only patients living within 10km of the five air pollution monitoring sites were included in the retrospective analyses.
The first study of nearly 900 rheumatoid arthritis patients showed that exposure to high levels of air pollutants was associated with higher CRP levels, indicative of inflammation and a greater risk of experiencing a flare of arthritis, based on disease activity scores.
This excessive risk was evident at very low levels of air pollution, and for all pollutants assessed: carbon monoxide, nitrogen oxides (NOx, NO, NO2), ozone, and small and large particulate matter (PM2.5 and PM10).
“The risk of having abnormal CRP, more or equal to 5mg/L, was higher with a higher exposure to particulate matter, and [the trend] was the same for all pollutants,” Dr Adami said at EULAR.
Patients exposed to PM10 concentrations above 50g per cubic metre – the threshold for large particulate matter set by the European Union air quality directive – had a 70% higher risk of having elevated CRP levels, Dr Adami said.
As for disease flares, disease activity scores were compared in a subset of 440 patients with two or more follow-up visits, in a case-crossover design study where patients served as their own controls.
“We analysed the concentration of air pollutants in 60 days before a recorded flare, and compared it to 60 days before a low-disease activity visit,” Dr Adami explained in his presentation.
“Air pollutants concentrations were higher immediately before a flare as compared to a period of stable disease activity,” he said.
Graeme Jones, a professor of rheumatology and epidemiology at the Menzies Institute for Medical Research in Hobart, said the study shows “quite obvious associations” between air pollution and disease flares, as well as dose-response associations with CRP.
It may be “a bit more evidence for rheumatoid arthritis being mediated through lung exposures [to air pollution]”, Professor Jones said.
The second analysis, in ACR Open Rheumatology, involved a larger pool of people with rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis, from which 280 patients were selected to assess the link between air pollution and poor treatment response. Treatment failures related to adverse events or intolerance were excluded from the analysis.
“We found that air pollutants’ concentrations were higher in the 60-day period before a treatment failure and treatment switch or swap, compared with the period preceding a visit with stable bDMARD therapy for at least six months,” Dr Adami said.
“We also found that approximately 5% of switches and swaps due to drug inefficacy are due to air pollution exposure alone.”
