Department of Epidemiology, School of Public Health, Sun Yat-sen University, China.
Department of Anesthesiology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, China.
Chemosphere. 2023 Oct;337:139362. doi: 10.1016/j.chemosphere.2023.139362. Epub 2023 Jul 4.
The association between long-term air pollution exposure and the development of idiopathic pulmonary fibrosis (IPF) has been established, but the evidence regarding the effect of low levels of air pollution, especially ambient sulfur dioxide (SO), is limited. Besides, the combined effect and interaction between genetic susceptibility and ambient SO on IPF remain uncertain.
This study retrieved data from 402,042 participants who were free of IPF at baseline in the UK Biobank. The annual mean concentration of ambient SO was estimated for each participant based on their residential addresses using a bilinear interpolation method. Cox proportional hazard models were used to examine the relationship between ambient SO and incident IPF. We further generated a polygenic risk score (PRS) for IPF and estimated the combined effects of genetic susceptibility and ambient SO on incident IPF.
After a median follow-up of 11.78 years, 2562 cases of IPF were identified. The results indicated that each 1 μg/m increase in ambient SO was associated with a hazard ratio (HR) (95% confidence interval [CI]) of 1.67 (1.58, 1.76) for incident IPF. The study found statistically significant synergistic additive interaction between genetic susceptibility and ambient SO. Individuals with high genetic risk and high ambient SO exposure had a higher risk of developing IPF (HR = 7.48, 95% CI:5.66, 9.90).
The study suggests that long-term exposure to ambient SO, even at concentrations lower than current air quality guidelines set by the Word Health Organization and European Union, may be an important risk factor for IPF. This risk is more pronounced among people with a high genetic risk. Therefore, these findings emphasize the need to consider the potential health effects of SO exposure and the necessity for stricter air quality standards.
长期暴露于空气污染与特发性肺纤维化（IPF）的发展之间存在关联，但有关低水平空气污染，特别是环境二氧化硫（SO）的影响的证据有限。此外，遗传易感性与环境 SO 对 IPF 的联合作用和相互作用仍不确定。
本研究从英国生物银行中 402042 名基线时无 IPF 的参与者中检索数据。根据参与者的居住地址，使用双线性插值法估算每个参与者的环境 SO 年平均浓度。使用 Cox 比例风险模型来研究环境 SO 与 IPF 发病之间的关系。我们进一步生成了 IPF 的多基因风险评分（PRS），并估计了遗传易感性与环境 SO 对 IPF 发病的联合作用。
在中位随访 11.78 年后，确定了 2562 例 IPF 病例。结果表明，环境 SO 每增加 1μg/m，IPF 发病的风险比（HR）（95%置信区间[CI]）为 1.67（1.58，1.76）。研究发现遗传易感性与环境 SO 之间存在统计学显著的协同附加交互作用。遗传风险高且环境 SO 暴露水平高的个体患 IPF 的风险更高（HR=7.48，95%CI：5.66，9.90）。
该研究表明，长期暴露于环境 SO，即使浓度低于世界卫生组织和欧盟设定的当前空气质量标准，也可能是 IPF 的一个重要危险因素。在遗传风险高的人群中，这种风险更为明显。因此，这些发现强调了需要考虑 SO 暴露的潜在健康影响，以及制定更严格的空气质量标准的必要性。
