Common workplace fumes and dust may heighten rheumatoid arthritis risk. 

A new study has found that breathing in common workplace dusts and fumes from agents such as vapours, gases, and solvents, may heighten the risk of developing rheumatoid arthritis.

The Swedish study also found that the substances seem to boost the detrimental impact of smoking and genetic susceptibility to the disease.

While it is known that cigarette smoking increases the risk of developing rheumatoid arthritis, it has not been clear what impact breathing in workplace dusts and fumes might have.

In a bid to find out, researchers drew on data from the Swedish Epidemiological Investigation of RA. This comprises 4,033 people newly diagnosed between 1996 and 2017 and 6485 others matched for age and sex, but free of the disease (comparison group).

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 assigned a Genetic Risk Score (GRS), according to whether they carried genes that could increase their chances of developing rheumatoid arthritis.

Rheumatoid arthritis is characterised by the presence or absence of anti-citrullinated protein antibodies or ACPA for short. ACPA positivity denotes a worse prognosis with higher rates of erosive joint damage.

Nearly three quarters of those with rheumatoid arthritis testing positive (73 pe cent) and negative (72 per cent) for ACPA had been exposed to at least one workplace dust or fume compared with around two thirds (67 per cent) of people in the comparison group.

Analysis of the data showed that exposure to workplace agents was not only associated with a heightened risk of developing rheumatoid arthritis, but also seemed to boost that risk further by interacting with smoking and genetic susceptibility.

Exposure to any workplace agent was associated with a 25 per cent heightened risk of developing  ACPA positive rheumatoid arthritis, overall. This risk increased to 40 per cent in men.

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 in tandem with the number of agents and duration of exposure, with the strongest associations seen for exposures lasting around 8 to 15 years. Men tended to have been exposed to more agents, and for longer, than women.

‘Triple exposure’ to a workplace agent, plus smoking, plus a high GRS, was associated with a very high risk of ACPA positive disease, ranging from 16 to 68 times higher, compared with ‘triple non-exposure’.

In particular, the risk of developing ACPA positive rheumatoid arthritis for the triple exposed was 45 times higher for gasoline engine exhaust fumes, 28 times for diesel exhaust, 68 times higher for insecticides and 32 times higher for quartz dust (silica). The corresponding range for ACPA negative disease was not significant.

This is an observational study, and as such, cannot establish cause. The researchers also acknowledge several limitations to their findings: the study relied on personal recall; and while the exposure estimates were derived using a validated method, the results can be relatively crude.

Also, given that there are often several workplace agents in the air at any one time, it is difficult to pinpoint which ones might be the potential triggers.

Nevertheless, the researchers conclude: “Occupational inhalable agents could act as important environmental triggers in RA development and interact with smoking and RA-risk genes, leading to excessive risk for ACPA-positive RA.”

The full study is accessible here.