Smoking as an Environmental Risk Factor for Rheumatoid Arthritis

Countering scientific myths has been one of the themes of PSIO 495 this semester. In the arthritis section we discussed how the myth that osteoarthritis does not have an inflammatory component is now generally discredited. In fact both osteoarthritis and rheumatoid arthritis have inflammatory components. There are also myths about the origins of these diseases. Many consider rheumatoid arthritis to be a purely genetic disorder while others consider osteoarthritis to be a disorder due to environment and old age. Both of these ideas have been shown to be false. There are genetic components for osteoarthritis and there are also environmental risk factors for rheumatoid arthritis. Klareskog et al¹ elaborated on the current evidence that indicates smoking as a current environmental risk factor for rheumatoid arthritis.

This article found that cigarette smoking, but not nicotine patches, is a risk factor for rheumatoid factor positive types of rheumatoid arthritis. Surprisingly pure nicotine actually suppressed inflammation but smoking itself is incredibly pro-inflammatory. They also found that RA risk due to smoking was greatly increased in people with some specific forms of the major histocompatibility antigens. These specific human leukocyte antigens included HLA-DRB1 and HLA-DRB SE.

Currently auto antibodies against the alpha amino acid citrullin are considered to be to be present in 60% of RA patients.¹ Thus the authors also wanted to see if smoking could induce these auto-antibodies in the lungs. Klareskog et al² showed that smoking does indeed induce the circulation of these auto-antibodies.

In the future more clinical studies will be conducted to see if smoking does actually cause rheumatoid arthritis. In the mean time scientists will have to be content with knowing that smoking elevates the number one risk factor of rheumatoid arthritis which is elevated auto-antibodies against citrullin.

1. Curr Opin Rheumatol. 2007 Jan;19(1):49-54. Smoking as a trigger for inflammatory rheumatic diseases. Klareskog L, Padyukov L, Alfredsson L. Rheumatology Unit, Department of Medicine, Karolinska Institutet at Karolinska University Hospital Solna, Stockholm, Sweden http://www.ncbi.nlm.nih.gov/pubmed/17143096

2. 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; 54:38–4633.

http://onlinelibrary.wiley.com/doi/10.1002/art.21575/pdf