Department of Global Health, The Peking University School of Public Health, Beijing, China.
Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Sci Total Environ. 2024 Aug 25;940:173526. doi: 10.1016/j.scitotenv.2024.173526. Epub 2024 May 31.
Chronic rhinosinusitis (CRS) is a prevalent upper respiratory condition that manifests in two primary subtypes: CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). While previous studies indicate a correlation between air pollution and CRS, the role of genetic predisposition in this relationship remains largely unexplored. We hypothesized that higher air pollution exposure would lead to the development of CRS, and that genetic susceptibility might modify this association.
This cohort study involving 367,298 adult participants from the UK Biobank, followed from March 2006 to October 2021. Air pollution metrics were estimated at residential locations using land-use regression models. Cox proportional hazard models were employed to explore the associations between air pollution exposure and CRS, CRSwNP, and CRSsNP. A polygenic risk score (PRS) was constructed to evaluate the joint effect of air pollution and genetic predisposition on the development of CRS.
We found that the risk of CRS increased under long-term exposure to PM [the hazard ratios (HRs) with 95 % CIs: 1.59 (1.26-2.01)], PM [1.64 (1.26-2.12)], NO [1.11 (1.04-1.17)], and NO [1.18 (1.12-1.25)], respectively. These effects were more pronounced among participants with CRSwNP, although the differences were not statistically significant. Additionally, we found that the risks for CRS and CRSwNP increased in a graded manner among participants with higher PRS or higher exposure to PM, PM, or NO concentrations. However, no multiplicative or additive interactions were observed.
Long-term exposure to air pollution increases the risk of CRS, particularly CRSwNP underscoring the need to prioritize clean air initiatives and environmental regulations.
慢性鼻-鼻窦炎（CRS）是一种常见的上呼吸道疾病，表现为两种主要亚型：伴有鼻息肉的 CRS（CRSwNP）和不伴有鼻息肉的 CRS（CRSsNP）。尽管先前的研究表明空气污染与 CRS 之间存在相关性，但遗传易感性在这种关系中的作用在很大程度上仍未得到探索。我们假设更高的空气污染暴露会导致 CRS 的发生，而遗传易感性可能会改变这种关联。
这项涉及来自英国生物库的 367298 名成年参与者的队列研究，从 2006 年 3 月至 2021 年 10 月进行随访。使用基于土地利用的回归模型在居住地点估算空气污染指标。采用 Cox 比例风险模型探讨空气污染暴露与 CRS、CRSwNP 和 CRSsNP 之间的关联。构建多基因风险评分（PRS）来评估空气污染和遗传易感性对 CRS 发生的联合影响。
我们发现，长期暴露于 PM[风险比（HR）及其 95%置信区间：1.59（1.26-2.01）]、PM[1.64（1.26-2.12）]、NO[1.11（1.04-1.17）]和 NO[1.18（1.12-1.25）]会增加 CRS 的风险。在 CRSwNP 患者中，这些影响更为明显，尽管差异无统计学意义。此外，我们发现，在 PRS 较高或 PM、PM 或 NO 浓度较高的参与者中，CRS 和 CRSwNP 的风险呈递增方式增加。然而，未观察到乘法或加法交互作用。
长期暴露于空气污染会增加 CRS 的风险，特别是 CRSwNP，这突显了优先实施清洁空气倡议和环境法规的必要性。
