Introduction & Objectives
Rheumatoid arthritis (RA) is one of the most common autoimmune diseases, affecting nearly one in 100 individuals. Researchers have hypothesized that seropositive RA originates from inflammation in the respiratory tract, resulting in autoantibody formation that later leads to disease. However, questions remain.
Several studies have shown an association between asthma and RA, which may be explained by a shared immunologic mechanism. However, a major limitation of previous studies is the lack of adjustment for allergic disease. Moreover, none included adjustment for secondhand cigarette smoke or urban pollution, which are known contributors to RA and asthma. It is unclear whether asthma is associated with RA after adjustment for these important confounders.
The association between personal smoking and RA has been well-established, but a limited number of studies have investigated the association between passive smoke exposure and RA. The results of these studies conflict, with two suggesting an association between passive smoking and RA and the other showing no association. None characterized workplace smoke exposure alone or contained information about both the duration and intensity to allow a dose-response analysis. Earlier age of smoking may also be important, but has not yet been studied in patients with RA.
Kronzer et al. set out to narrow the knowledge gaps related to the oral-respiratory factors that may mediate RA pathogenesis. Specifically, they wanted to determine the association of RA with asthma after controlling for allergic disease, urban environment, passive smoke exposure (at home and work) and the age when people start smoking. They hypothesized the association with asthma would be attenuated after adjustment for allergy and environmental pollutants, that passive smoke at higher doses would be associated with RA and that earlier age at the start of smoking would be associated with an increased risk of RA.
For this case-control study, the researchers identified 1,023 cases of RA (175 incident) within a single-center biobank population, using a rules-based algorithm that combined self-report with two diagnostic codes. Exposures were self-reported on biobank questionnaires. Logistic regression models were used to calculate the association of exposures with RA, adjusting for potential confounders. Odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated.
After adjustment for allergies, urban environment and passive smoke exposure, asthma was associated with RA in the full cohort (OR 1.28 [95% CI 1.04–1.58; P=0.02]), but not in the incident RA cohort (OR 1.17 [95% CI 0.66–2.06; P=0.60]).
History of allergic disease was associated with RA in both the full cohort (OR 1.30 [95% CI 1.12–1.51; P<0.001]) and the incident RA cohort (OR 1.61 [95% CI 1.11–2.33; P=0.01]), especially food allergy, which was significantly associated with RA in the full cohort (OR 1.38 [95% CI 1.08–1.75; P=0.01]) and showed a trend toward significance in the incident RA cohort (OR 1.83 [95% CI 0.97–3.45; P=0.06]).