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Long-term exposure to fine particulate matter and ozone and the onset of systemic autoimmune rheumatic diseases: an open cohort study in Quebec, Canada
Arthritis Research & Therapy ( IF 4.9 ) Pub Date : 2022-06-23 , DOI: 10.1186/s13075-022-02843-5
Naizhuo Zhao 1 , Audrey Smargiassi 2, 3, 4 , Sonia Jean 4, 5 , Philippe Gamache 4 , Elhadji-Anassour Laouan-Sidi 4 , Hong Chen 6, 7, 8, 9 , Mark S Goldberg 1, 10 , Sasha Bernatsky 1, 10, 11, 12
Affiliation  

To estimate associations between fine particulate matter (PM2.5) and ozone and the onset of systemic autoimmune rheumatic diseases (SARDs). An open cohort of over 6 million adults was constructed from provincial physician billing and hospitalization records between 2000 and 2013. We defined incident SARD cases (SLE, Sjogren’s syndrome, scleroderma, polymyositis, dermatomyositis, polyarteritis nodosa and related conditions, polymyalgia rheumatic, other necrotizing vasculopathies, and undifferentiated connective tissue disease) based on at least two relevant billing diagnostic codes (within 2 years, with at least 1 billing from a rheumatologist), or at least one relevant hospitalization diagnostic code. Estimated PM2.5 and ozone concentrations (derived from remote sensing and/or chemical transport models) were assigned to subjects based on residential postal codes, updated throughout follow-up. Cox proportional hazards models with annual exposure levels were used to calculate hazard ratios (HRs) for SARDs incidence, adjusting for sex, age, urban-versus-rural residence, and socioeconomic status. The adjusted HR for SARDS related to one interquartile range increase in PM2.5 (3.97 µg/m3) was 1.12 (95% confidence interval 1.08–1.15), but there was no clear association with ozone. Indirectly controlling for smoking did not alter the findings. We found associations between SARDs incidence and PM2.5, but no relationships with ozone. Additional studies are needed to better understand interplays between the many constituents of air pollution and rheumatic diseases.

中文翻译:

长期暴露于细颗粒物和臭氧以及系统性自身免疫性风湿病的发病:加拿大魁北克的一项开放队列研究

估计细颗粒物 (PM2.5) 和臭氧与系统性自身免疫性风湿病 (SARD) 发病之间的关联。根据 2000 年至 2013 年间的省级医生账单和住院记录,构建了一个超过 600 万成年人的开放队列。我们定义了 SARD 事件(SLE、干燥综合征、硬皮病、多发性肌炎、皮肌炎、结节性多动脉炎和相关疾病、风湿性多肌痛、其他坏死性血管病和未分化结缔组织病)基于至少两个相关的计费诊断代码(2 年内,至少 1 次来自风湿病学家的账单),或至少一个相关的住院诊断代码。估计 PM2. 5 和臭氧浓度(来自遥感和/或化学传输模型)根据住宅邮政编码分配给受试者,并在整个随访过程中更新。使用具有年度暴露水平的 Cox 比例风险模型来计算 SARD 发病率的风险比 (HR),并根据性别、年龄、城市与农村居住地和社会经济地位进行调整。与 PM2.5 (3.97 µg/m3) 增加一个四分位数范围相关的 SARDS 的调整后 HR 为 1.12(95% 置信区间 1.08-1.15),但与臭氧没有明显关联。间接控制吸烟并没有改变研究结果。我们发现 SARD 发病率与 PM2.5 之间存在关联,但与臭氧无关。需要更多的研究来更好地了解空气污染的许多成分与风湿性疾病之间的相互作用。
更新日期:2022-06-23
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