Currently, the association between sources of atmospheric pollution and RA has been investigated in three large epidemiological studies: the Nurses’ Health Study (NHS) in the United States [
8,
9], the British Colombian (BC) study in Canada[
10], and the Swedish Epidemiological Investigation of Rheumatoid Arthritis (EIRA) [
11,
12]. In the NHS, association of distance to road-a marker of traffic pollution exposure- and incidence of RA was studied in 90297 women. After adjustment for multiple confounders (age, calendar year, race, cigarette smoking, parity, lactation, menopausal status and hormone use, oral contraceptive use, body mass index, physical activity, and census-tract-level median income and house value), women living within 50 m of a road had an incremented risk of RA compared with those living 200 m or farther away (hazard ratio [HR] = 1.31; 95 % CI 0.98–1.74) [
8]. This finding was more consistent among nonsmokers (HR = 1.62; 95 % CI, 1.04–2.52). Similarly, the BC study assessed the effects of proximity to traffic, ambient air pollution, and community noise on the risk of developing RA using health records of 640041 subjects at risk of developing RA in the Border Air Quality Study cohort. Residential proximity to traffic five years prior to RA diagnosis, but consistently not noise, was associated with an increased risk of RA; with highest risks noted for highways and with greater proximity. Since health service records did not contain informations on low socioeconomic status, nonwhite race, and smoking which are all risk factors for RA highly prevalent close to roadways, the authors did not adjust for these factors in statistical analyses. Nevertheless, there was little confounding due to neighborhood-level income, and smoking was unlikely to be an important confounder according to sensitivity analyses [
10]. Additionally, Sigari et al. [
13] recently found significantly elevated anticyclic citrullinated protein/peptide antibody (ACPA) levels in 56 wood smoke-induced COPD patients compared to 56 tobacco-induced COPD patients, and to 56 healthy controls. It is noteworthy that ACPA (the most specific biological markers with predictive and prognostic value in RA patients) are elevated in patients’ sera five to 10 years prior to diagnosis with RA [
4,
11,
12,
14], suggesting that factors initiating autoimmunity in RA may act before appearance of symptoms and signs characteristic of clinical disease. In this sense, wood smoke might be a risk factor for RA. However, tropospheric pollutants including PM
10, PM
2.5, SO
2, and NO
2 were associated with RA neither in the NHS [
9], nor in the BC study [
10]. In the same way, the EIRA Swedish population-based study of 1497 incident RA patients compared with 2536 age and sex matched controls investigated the impact of an interquartile range increase (2 μg/m
3 for PM
10, 8 μg/m
3 for SO
2, and 9 μg/m
3 for NO
2) in each pollutant from traffic and home heating sources in the 5th, 10th, and 20th years prior to symptom onset (considering increment of ACPA titers five to 10 years before occurrence of clinical signs and symptoms of RA) and average exposure on the risk of all RA and the risk of RA serologic features. Total RA risks were increased for exposure to the gaseous pollutants (NO
2 and SO
2) in the 10th year before onset, but were no more statistically significant after adjustment for smoking and education (odds ratio [OR] =1.18, 95 % CI 0.97–1.43] and OR = 1.09, 95 % CI: 0.99–1.19) for SO
2 and NO
2 respectively). Stronger elevated risks at the same time point were noted for ACPA-negative RA cases even after adjustment for smoking and education (OR = 1.48, 95 % CI 1.13–1.95 and OR = 1.22, 95 % CI 1.07–1.40 for SO
2 and NO
2 respectively) [
12]. Discrepant results about NO
2 and SO
2 between studies indicate the necessity to better clarify their role in the pathogenesis of RA [
8,
10,
12], as well as that of PM which can be formed from these gases by enucleation in the air [
7], and considering the high correlation between NO
2 and PM
10 [
12]. Furthermore, results have not been verified across populations including different age groups, especially the ageing population which is more at risk of developing RA [
1], and mixed ancestries. Moreover, a major shortcoming of the study by Hart el al. [
9] which examined the association between specific pollutants and incident RA within the NHS was the lack of informations necessary for assessment of the impact of each nurses’ total air pollution exposure experience on the incidence of RA (amount of time spent at each home address, exposure to pollutants at locations other than the residence, exposure models that can perfectly predict personal exposures) [
9]. In addition, the follow up period of the BC cohort was probably shorter than the induction period of tropospheric pollutants [
10]. Taken together, sources of air pollution including traffic and probably solid fuels are associated with RA, but smoking may attenuate this association. Yet, inconclusiveness persists regarding the role of tropospheric pollutants including NO
2, SO
2 and PM. Indirect arguments can help support the role of these pollutants in the pathogenesis of RA.