Exposure to passive smoking does not appear to increase the risk of developing rheumatoid arthritis (RA), according to a population-based case-control study published in the Annals of the Rheumatic Diseases.1

RA can be divided into anti-cyclic citrullinated peptide antibodies (ACPA)-positive and ACPA-negative subsets, and smoking has been observed to induce citrullination of peptide antigens in the lungs and has been associated with an increased risk of developing RA.2-4 However, there are no studies on the risk of developing RA from exposure to environmental tobacco smoke.1

Therefore, researchers used incident cases of RA in Sweden to compare the incidence of RA among 589 never-smokers who had been exposed to passive smoking with 1764 never-smokers who had never been exposed to tobacco smoke. They collected information on current and previous smoking habits and exposure to passive smoking either at home or at work.

The researchers found no association between exposure to passive smoking and the risk of developing ACPA-positive or ACPA-negative RA. In fact, not even a trend was observed between duration of passive smoking and RA risk.

These results are consistent with a previously described threshold for exposure to smoke, where no association between risk for RA and active smoking was seen when the accumulated amount of smoking was low enough.5

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However, 1 of the limitations of this study was that the researchers only had information on the duration, not the intensity, of the exposure to passive smoking; therefore, they cannot rule out that extensive exposure to passive smoking could affect the risk of developing RA.1

“In summary, in this population-based case–control study of RA, no association was observed between exposure to passive smoking and risk of ACPA-positive or ACPA-negative RA among never-smokers,” concluded the authors.1

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References

  1. Hedström AK, Klareskog L, Alfredsson L. Exposure to passive smoking and rheumatoid arthritis risk: results from the Swedish EIRA study [published online on May 3, 2018]. Ann Rheum Dis. doi: 10.1136/annrheumdis-2018-212973
  2. Aletaha D, Neogi T, Silman AJ, et al. 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Ann Rheum Dis. 2010;69:1580-1588.
  3. Makrygiannakis D, Hermansson M, Ulfgren AK, et al. Smoking increases peptidylarginine deiminase 2 enzyme expression in human lungs and increases citrullination in BAL cells. Ann Rheum Dis. 2008;67:1488-1492.
  4. Klareskog L, Stolt P, Lundberg K, et al. A new model for an etiology of rheumatoid arthritis: smoking may trigger HLA-DR (shared epitope)-restricted immune reactions to autoantigens modified by citrullination. Arthritis Rheum. 2006;54:38-46.
  5. Hedström AK, Stawiarz L, Klareskog L, et al. Smoking and susceptibility to rheumatoid arthritis in a Swedish population-based case-control study. Eur J Epidemiol. 2018;33:415-423.