RESUMEN
OBJECTIVES: To investigate (1) whether working in cold environment (WCE) is associated with an increased risk of developing rheumatoid arthritis (RA) (overall), anticitrullinated protein antibody (ACPA)-positive RA and ACPA-negative RA and (2) whether WCE interacts with occupational physical workload in conferring RA risk. METHODS: Data from the Swedish population-based case-control study Epidemiological Investigation of Rheumatoid Arthritis involving 3659 incident cases and 5925 controls were analysed. Study participants were asked whether they had ever worked in cold/outdoor environment along with their exposure duration and frequency. Occurrence of RA among exposed and unexposed subjects were compared by calculating ORs with 95% CI using logistic regression. Additive interactions between WCE and six types of physical workload were assessed using the principle of departure from additivity by calculating attributable proportion due to interaction (AP). RESULTS: The OR associated with having ever worked in cold environment was 1.5 (95% CI 1.4 to 1.7) for RA (overall), 1.6 (95% CI 1.4 to 1.8) for ACPA-positive RA and 1.4 (95% CI 1.2 to 1.6) for ACPA-negative RA. The risk of developing RA increased with increasing cumulative dose of working in cold indoor environment (p value <0.001), but not working in cold outdoor environment. Positive additive interaction was observed between WCE and repetitive hand/finger movements (AP 0.3 (95% CI 0.1 to 0.5)). CONCLUSIONS: WCE is associated with increased risk of developing both ACPA-positive and ACPA-negative RA. A dose-response relationship was found between working in cold indoor environment and risk of developing RA. Moderate additive interaction was observed between exposure to cold environment and exposure to repetitive hand/finger movements.
RESUMEN
OBJECTIVES: This study investigated: (1) the association of physical workload (PW) and risk of rheumatoid arthritis (RA); (2) the potential interactions between PW and the genes in the human leucocyte antigen (HLA) region. METHODS: A population-based case-control study involving incident cases of RA (3150 cases and 5130 controls) was performed using data from the Swedish Epidemiological Investigation of Rheumatoid Arthritis. Information on 7 types of self-reported PW exposure and HLA-DRB1 genotypes of cases and controls were gathered. Anticitrullinated protein antibody (ACPA) status of cases was identified. For each PW exposures, exposed participants were compared with unexposed participants. ORs with 95% CIs of RA (overall), ACPA-positive RA and ACPA-negative RA associated with different PWs were estimated using logistic regression. HLA-PW interactions were estimated using the principle of departure from additivity of effects by calculating attributable proportion (AP) due to interaction. RESULTS: ORs of developing RA associated with 6 various PW exposures ranging from 1.3 (95% CI 1.1 to 1.4) to 1.8 (95% CI 1.6 to 2.0) were observed. Exposure to more types of PW was associated with increasing risk for RA (p<0.0001). No major difference in the ORs between ACPA-positive and ACPA-negative RA was found. For some exposures, we found evidence of interactions between PW and the HLA-DRB1 shared epitope genes, regarding risk of ACPA-positive RA (AP: from 0.3 (95% CI 0.1 to 0.5) to 0.4 (95% CI 0.2 to 0.6)). CONCLUSIONS: PW is associated with the risk of ACPA-positive and ACPA-negative RA. Interactions between PW and the HLA-DRB1 shared epitope were found in ACPA-positive RA.
