Research suggests that breathing common workplace dust and fumes may heighten rheumatoid arthritis risk.
Rheumatoid arthritis is a long-term condition causing pain, swelling and stiffness in the joints. Several factors may increase rheumatoid arthritis risk, including genes, hormones, and smoking; however, new research published in the Annals of Rheumatic diseases illuminates how workplace dust and fumes could contribute to an increased rheumatoid arthritis risk.
The researchers also found that workplace fumes and dust may boost the effects of smoking and genetic susceptibility to the disease.
Analysing data from over 10,000 people
The researchers used data from the Swedish Epidemiological Investigation of RA, which included 4,033 people with newly diagnosed rheumatoid arthritis between 1996 and 2017 and 6,485 others matched for age and sex, but free of the disease.
Personal job histories were provided and used to estimate the amount of individual exposure to 32 airborne workplace agents, using a validated technique.
Each participant was given a Genetic Risk Score (GRS), according to whether they carried genes that could increase rheumatoid arthritis risk. The condition is characterised by the presence or absence of anti-citrullinated protein antibodies or ACPA for short. ACPA positive denotes a worse prognosis with higher rates of erosive joint damage.
Exposure to workplace fumes may increase rheumatoid arthritis risk
Nearly three-quarters of those with rheumatoid arthritis testing positive (73%) and negative (72%) for ACPA had been exposed to at least one workplace dust or fume compared with around two-thirds (67%) of people in the comparison group.
Further analysis showed that exposure to workplace agents was associated with an increased rheumatoid arthritis risk and boosted the risk further of smoking and genetic susceptibility.
Workplace fume exposure was associated with a 25% increased risk of developing ACPA-positive rheumatoid arthritis, overall. This rheumatoid arthritis risk increased to 40% in men.
More specifically, 17 out of 32 agents, including quartz, asbestos, diesel fumes, gasoline fumes, carbon monoxide, and fungicides, were strongly associated with an increased risk of developing ACPA-positive disease. Only a few agents—quartz dust (silica), asbestos, and detergents—were strongly associated with ACPA-negative disease.
The risk increased alongside the number of agents and duration of exposure, with the strongest associations for exposures lasting around eight-15 years.
It is important to note that the study is observational and cannot establish cause. Limitations include the study relying on personal recall and whilst exposure estimates were derived using a validated method, the results can be crude.
