Division of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital.
Harvard Medical School, Boston, Massachusetts, USA.
Curr Opin Rheumatol. 2020 May;32(3):279-288. doi: 10.1097/BOR.0000000000000705.
The current review summarizes the current evidence on inhalants other than personal cigarette smoking and risk for developing rheumatoid arthritis (RA).
Personal 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.
Several 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.
本文总结了除个人吸烟以外的吸入物与类风湿关节炎（RA）发病风险的现有证据。
个人吸烟已被认为是血清阳性 RA 的环境风险因素，这可能是通过在肺黏膜诱导自身免疫。由于许多 RA 患者不吸烟，因此正在研究其他吸入物作为潜在的 RA 危险因素。最近的病例对照和队列研究调查了被动吸烟、空气污染、与吸入物相关的职业、二氧化硅、杀虫剂、家庭环境和变应性吸入物作为 RA 风险的吸入物暴露。与吸入物相关的职业和二氧化硅吸入物与 RA 风险增加的关联最具一致性证据。然而，大多数研究依赖于回顾性设计，调整个人吸烟的能力有限，并且无法调查非吸烟者之间的关联。
除个人吸烟以外的几种吸入物可能与 RA 发病风险增加相关。这些结果支持这样一种假说，即吸入物、肺黏膜炎症和 RA 发病机制可能存在关联。未来的研究需要确定这些发现与个人吸烟的独立性，并确定与 RA 发病机制相关的特定吸入物和生物学机制。
