Air pollution may be linked to heightened autoimmune disease risk, scientists say

Exposure to traffic and industrial pollutants associated with 40% higher risk of rheumatoid arthritis, and 20% higher risk of inflammatory bowel disease

‘Misfiring’ adaptive response to pollutants from vehicles and industry can cause inflammation and tissue damage leading to autoimmune diseases, study warns (Getty )

Long term exposure to air pollution may be linked to a range of autoimmune diseases including rheumatoid arthritis, multiple sclerosis and bowel inflammation diseases such as Crohn’s and ulcerative colitis, new research has found.

Researchers in Italy warned the most common forms of environmental air pollution, such as vehicle exhaust fumes and industrial emissions can trigger adaptive immunity, a process in which the body reacts to a specific disease-causing entity, but in cases where this adaptive response "misfires", it can prompt systemic inflammation, tissue damage, and ultimately autoimmune disease.

The number of people suffering from these conditions, which also include connective tissue diseases such as osteoarthritis, have steadily increased over the past decade.

Scientists have said the reasons for which aren’t entirely clear, and whether air pollution is linked to a heightened risk of autoimmune disease has remained a matter of debate.

To try and shed some light on the issues, the researchers examined the national Italian fracture risk database, which holds medical information on 81,363 men and women submitted by more than 3500 doctors between June 2016 and November 2020.

Most were women (92 per cent) with an average age of 65, and 17,866 (22 per cent) had at least one co-existing health condition.

Each participant was linked to the nearest air quality monitoring station run by the Italian Institute of Environment Protection and Research via their residential postcode.

The researchers were particularly interested in the potential impact of particulate matter (PM10) and fine particulate matter (PM2.5).

Some 9,723 people, 12 per cent of the group studied, were diagnosed with an autoimmune disease between 2016 and 2020.

Information on air quality was obtained from 617 monitoring stations in 110 Italian provinces. Average long term exposure between 2013 and 2019 for both PM10 and PM2.5 were both just under the levels deemed "harmful".

The researchers found different impacts depending on the types of pollution and the concentrations people were exposed to.

"Long-term exposure to air pollution was associated with higher risk of developing autoimmune diseases," the researchers said.

"In particular rheumatoid arthritis, connective tissue diseases (CDTs) and inflammatory bowel diseases (IBDs). Chronic exposure to levels above the threshold for human protection was associated with a 10 per cent higher risk of developing immune-mediated diseases."

"In particular, we witnessed an association with rheumatoid arthritis, CTDs and IBDs in patients exposed to high levels of PM2.5."

They added: "The biological rationale supporting our results is strong. Our study has been inspired by numerous preclinical studies and several clinical observational studies.

Long term exposure to PM10 was specifically associated with a heightened risk of rheumatoid arthritis, while long term exposure to PM2.5 was associated with a heightened risk of rheumatoid arthritis, connective tissue diseases, and inflammatory bowel diseases.

Overall, long term exposure to traffic and industrial air pollutants was associated with an approximately 40 per cent higher risk of rheumatoid arthritis, a 20 per cent higher risk of inflammatory bowel disease, and a 15 per cent higher risk of connective tissue diseases.

The team cautioned that this was an observational study, and as such, can’t establish cause.

But they said "air pollution has already been linked to immune system abnormalities, and smoking, which shares some toxins with fossil fuel emissions, is a predisposing factor for rheumatoid arthritis".

The research is published in the journal RMD Open.