Overall, exposure was linked to a 25% increased risk of developing rheumatoid arthritis. And in males, this risk increased to 40%.

And if you are a smoker or have a high Genetic Risk Score, it was associated with a very high risk of ACPA-positive disease, ranging from 16 to 68 times higher, compared with ‘triple non-exposure’.

According to a study that was just published in the Annals of Rheumatic Diseases, breathing in common occupational dust and fumes from agents such as vapours, gases, and solvents could increase the risk of developing rheumatoid arthritis.

In addition, they seem to exacerbate the negative effects of smoking and genetic vulnerability to the illness, according to the study.

Rheumatoid arthritis or RA in short is a chronic inflammatory illness that affects the joints and is characterized by severe inflammation that may make movement difficult or impossible. It affects around 1% of the global population.

Even though it is known that smoking cigarettes raises the risk of rheumatoid arthritis, no one knows what effect breathing in dust and fumes at work might have.

In order to determine this, the researchers used data from the Swedish Epidemiological Investigation of Rheumatoid Arthritis. This includes 4033 patients newly diagnosed between 1996 and 2017 and 6485 others matched for age and sex who were disease-free (comparison group).

Using a proven method, personal employment histories were used to estimate individual exposure to 32 airborne occupational chemicals.

According to whether they had genes that potentially raise their risk of developing rheumatoid arthritis, each participant was given a Genetic Risk Score (GRS).

Anti-citrullinated protein antibodies, or simply ACPA, are used to describe rheumatoid arthritis and determine if they are present or absent. Positive ACPA results in increased rates of erosive joint injury and a poorer prognosis.

Nearly three-quarters of individuals with rheumatoid arthritis who tested positive (73%) or negative (72%) for ACPA had been exposed to at least one occupational dust or fume, compared to around two-thirds (67%) of the control group.

Data analysis revealed that occupational exposure was not only linked to an increased chance of developing rheumatoid arthritis but also appeared to increase that risk by interacting with smoking and genetic vulnerability.

Overall, exposure to any occupational agent was linked to a 25% increased chance of developing ACPA-positive rheumatoid arthritis. And in males, this risk jumped to 40%.

In particular, 17 of 32 agents studied, including quartz, asbestos, diesel fumes, gasoline fumes, carbon monoxide, and fungicides, were significantly linked to an elevated chance of having ACPA-positive illness. Few substances, including quartz dust (silica), asbestos, and detergents, were highly linked to ACPA-negative illness.

The risk rose proportionally with the number of agents and period of exposure, with the highest correlations seen for exposures lasting between 8 and 15 years. Men were often exposed to more agents and for longer durations than women.

When compared to ‘triple non-exposure,’ ‘triple exposure’ to a workplace agent, plus smoking, plus a high GRS, was linked to a very high probability of ACPA-positive illness, ranging from 16 to 68 times greater.

The probability of developing ACPA-positive rheumatoid arthritis was 45 times greater for the threefold exposure to gasoline engine exhaust fumes, 28 times higher for diesel exhaust, 68 times higher for pesticides, and 32 times higher for quartz dust (silica). There was no significant difference in the same range for ACPA-negative illness.

Due to its observational nature, this research cannot determine the cause. The researchers also note a number of limitations in their findings: the study depended on personal recall, and although the exposure estimates were calculated using a validated approach, the results may be somewhat inaccurate.

And because there are often many agents in the air at the same time at work, it is hard to figure out which ones might be the cause.

Still, the researchers came to the following conclusion: “Occupational inhalable agents could act as important environmental triggers in RA development and interact with smoking and RA-risk genes, leading to an excessive risk for ACPA-positive RA.

“Our study emphasises the importance of occupational respiratory protections, particularly for individuals who are genetically predisposed to RA.” 

In a linked editorial, Dr. Jeffrey Sparks of Brigham and Women’s Hospital in Boston, USA, says that the study’s results have several important implications for how diseases develop and how they can be stopped.

“First, each occupational inhalable agent had a unique profile of the way it interacted with RA risk genes and with smoking….

These unique interactions suggest that if the relationship between inhalable agents and RA is indeed causal, they may do so via distinct pathways.”

Dr. Sparks, alluding to the greater connections discovered for ACPA positivity, notes that the data lend more credence to the notion that ACPA-positive rheumatoid arthritis may be quite different from ACPA-negative rheumatoid arthritis.

He comes to the conclusion that more has to be done in the field of public health to reduce the likelihood of rheumatoid arthritis.

“First, environmental health initiatives should reduce public exposure to ambient pollutants, including carbon monoxide and gasoline exhaust. Second, occupational health initiatives should mitigate occupational hazards, including detergents and asbestos. Third, public health initiatives should continue to reduce cigarette smoking,” he adds. 

Source: 10.1136/ard-2022-223286

Image Credit: Getty


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