Objective Airborne agents including cigarette smoke associate with an increased risk of rheumatoid arthritis (RA). We analysed to which extent occupational exposure to asbestos and silica confers an increased risk of developing serologically defined subsets of RA.
Methods This Swedish population-based case-control study enrolled incident RA cases between 1996 and 2013 (n=11 285), identified through national public authority and quality registers, as well as from the Epidemiological Investigation of Rheumatoid Arthritis (EIRA) Study. Controls (n=1 15 249) were randomly selected from Sweden’s population register and matched on sex, age, index year and county. Occupational histories were obtained from national censuses. Exposure to asbestos and silica was assessed by job-exposure matrices. Logistic regression was used to calculate ORs adjusted for age, sex, county, index year, alcohol use and smoking.
Results Results showed that male workers exposed to asbestos had higher risk of seropositive RA (OR=1.2, 95% CI 1.0 to 1.4) and seronegative RA (OR=1.2, 95% CI 1.0 to 1.5) compared with unexposed workers. The risk was highest among workers exposed to asbestos from 1970, before a national ban was introduced. Male workers exposed to silica also had higher risk of RA (seropositive RA: OR=1.4, 95% CI 1.2 to 1.6; seronegative RA: OR=1.3, 95% CI 1.0 to 1.5). For the largest subset, seropositive RA, the OR increased with the number of years exposed to silica, up to OR=2.3 (95% CI 1.4 to 3.8, p for trend <0.0001). Women overall had lower ORs than men, but the duration and intensity of their exposure were lower.
Conclusions In conclusion, we observed an association between asbestos exposure and risk of developing RA and extended previous findings of an association between silica exposure and RA risk, where a dose-response relationship was observed.
- rheumatoid arthritis
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Contributors AI had full access to all of the data used for the analysis in this study and takes full responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: AI, LA and PG.Acquisition of data: JA, LA, LK, AI and PW.Statistical analysis: AI. Analysis and interpretation of data: all authors. Drafting of manuscript: AI. Critical revision of manuscript and final approval given: all authors.
Funding The present study was supported by grants from the Swedish Research Council for Health, Working Life and Welfare [grant number 2013–0194] and AFA Insurance [grant number 120 299].
Competing interests LK and LA have been supported by research grants for the EIRA study from the Swedish Medical Research Council, the Swedish Council for Health, Working life and Welfare, King Gustaf V:s 80-year foundation, the Swedish Rheumatism Foundation, Stockholm County Council, the insurance company AFA, and the IMI-supported RTCure projects, unrelated to the submitted work. SS is a part-time employee of deCODE Genetics, unrelated to the submitted work. PW has received research grants from AFA Insurance, unrelated to the submitted work. JA has or has had research agreements with Abbvie, BMS, MSD, Eli Lilly, Novartis, Pfizer, Roche, Samsung Bioepis and UCB outside the submitted work, mainly in the context of safety monitoring of biologics via ARTIS/Swedish Biologics Register. Karolinska Institutet has received remuneration for JA participating in advisory boards arranged by Pfizer and Lilly. PG has received research grants from the Swedish Research Council for Health, Working Life and Welfare, unrelated to the submitted work. LA received grants from the Swedish Research Council for Health, Working Life and Welfare (grant number 2013-0194) and AFA Insurance (grant number 120299) to support the present study.
Patient consent for publication Not required.
Ethics approval Regional Stockholm ethics committee.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement No data are available.
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