Inhalants other than personal cigarette smoking and risk for developing rheumatoid arthritis

• Published in: Current opinion in rheumatology Vol. 32; no. 3; pp. 279 - 288
• Main Authors: Prisco, Lauren C., Martin, Lily W., Sparks, Jeffrey A.
• Format: Journal Article
• Language: English
• Published: United States Wolters Kluwer Health, Inc. All rights reserved 01-05-2020; Copyright Wolters Kluwer Health, Inc. All rights reserved
• Subjects: Air Pollutants - adverse effects; Air Pollution - adverse effects; Arthritis, Rheumatoid - etiology; Environmental Exposure - adverse effects; Humans; Risk Factors; Tobacco Smoke Pollution - adverse effects
• ISSN: 1040-8711; 1531-6963
• DOI: 10.1097/BOR.0000000000000705

PURPOSE OF REVIEWThe current review summarizes the current evidence on inhalants other than personal cigarette smoking and risk for developing rheumatoid arthritis (RA).
RECENT FINDINGSPersonal cigarette smoking has been implicated as an environmental risk factor for seropositive RA, perhaps by inducing autoimmunity at pulmonary mucosa. Since many patients with RA are nonsmokers, other inhalants are being investigated as potential RA risk factors. Recent case–control and cohort studies have investigated passive cigarette smoking, air pollution, inhalant-related occupations, silica, pesticides, household environment, and allergic inhalants as inhalant exposures for RA risk. Inhalant-related occupations and silica inhalants have the most consistent evidence for associations with increased RA risk. However, most studies relied on retrospective designs and had limited ability to adjust for personal cigarette smoking or investigate associations among nonsmokers.
SUMMARYSeveral inhalants other than personal cigarette smoking may be associated with increased risk for developing RA. These results support the hypothesis that inhalants, pulmonary mucosal inflammation, and RA pathogenesis may be linked. Future studies are needed to firmly establish the independence of these findings from personal cigarette smoking and to determine the specific inhalants and biologic mechanisms related to RA pathogenesis.