Four studies included subjects with RA (two case-control studies [18, 19] and two cohort studies [17, 20]) and examined associations with exposure to NO2, SO2, PM2.5, and PM10 (Table 2). In Hart et al., 2013, using data from the Nurses' Health Study and land use regression models, there was no definite evidence for increased RA risk related to a cumulative average exposure to NO2, SO2, PM10, or PM2.5 after adjustment for covariates . In Hart et al., 2013, using data from the Swedish Epidemiological Investigation of Rheumatoid Arthritis study and land use regression models, the investigators were unable to demonstrate any increased risk for the development of RA with exposure to NO2, PM10, or SO2 . In the study by De Roos et al., RA definitions were based on physician billing and prescription data; land use regression was used in the estimates for PM2.5 and NO2 as well as additional pollutants, black carbon and NO, and the inverse distance weighting method was used for PM10 and SO2 estimates as well as for NO, ozone, and CO . When the RA definition required a specialist-confirmed diagnosis, air pollutant exposure effect estimates were all inversely associated with the development of RA. In this study, residence proximity to roadway was additionally studied as a proxy for air pollutant exposure, with a significantly higher risk for RA for those within 50 metres from a highway compared to those over 150 metres away (OR: 1.37; 95% CI: 1.11 to 1.68). In the study by Chang et al., data from monitoring sites were linked to administrative health data and incident RA cases were studied . No association was found for PM2.5 exposure, but a significantly higher risk of incident RA was found in those exposed to the highest NO2 levels (adjusted HR for 3rd quartile: 1.53; 95% CI: 1.12 to 2.09; adjusted HR for 4th quartile: 1.52; 95% CI: 1.11 to 2.08).