Abstract：
BACKGROUND: 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.
METHODS: 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.
RESULTS: We found that the risk of CRS increased under long-term exposure to PM2.5 [the hazard ratios (HRs) with 95 % CIs: 1.59 (1.26-2.01)], PM10 [1.64 (1.26-2.12)], NO2 [1.11 (1.04-1.17)], and NOx [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 PM2.5, PM10, or NOx concentrations. However, no multiplicative or additive interactions were observed.
CONCLUSIONS: Long-term exposure to air pollution increases the risk of CRS, particularly CRSwNP underscoring the need to prioritize clean air initiatives and environmental regulations.
METHODS: 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.
RESULTS: We found that the risk of CRS increased under long-term exposure to PM2.5 [the hazard ratios (HRs) with 95 % CIs: 1.59 (1.26-2.01)], PM10 [1.64 (1.26-2.12)], NO2 [1.11 (1.04-1.17)], and NOx [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 PM2.5, PM10, or NOx concentrations. However, no multiplicative or additive interactions were observed.
CONCLUSIONS: Long-term exposure to air pollution increases the risk of CRS, particularly CRSwNP underscoring the need to prioritize clean air initiatives and environmental regulations.
摘要：
背景：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：伴鼻息肉的CRS（CRSwNP）和不伴鼻息肉的CRS（CRSsNP）。虽然以前的研究表明空气污染和CRS之间存在相关性，遗传易感性在这种关系中的作用仍未被探索。我们假设更高的空气污染暴露会导致CRS的发展，遗传易感性可能会改变这种联系。
方法：这项队列研究涉及来自英国生物库的367,298名成年参与者，从2006年3月到2021年10月。使用土地使用回归模型估算了居民点的空气污染指标。Cox比例风险模型用于探索空气污染暴露与CRS之间的关系。CRSwNP,和CRSsNP。构建了多基因风险评分（PRS），以评估空气污染和遗传易感性对CRS发展的联合影响。
结果：我们发现，在长期暴露于PM2.5的情况下，CRS的风险增加[95％CIs的风险比（HR）：1.59（1.26-2.01）]，PM10[1.64(1.26-2.12)],NO2[1.11(1.04-1.17)],和NOx[1.18(1.12-1.25)]，分别。这些影响在CRSwNP参与者中更为明显，尽管差异无统计学意义。此外,我们发现,在PRS较高或PM2.5,PM10或NOx浓度较高的参与者中,CRS和CRSwNP的风险呈分级增加.然而,没有观察到乘法或加性相互作用。
结论：长期暴露于空气污染会增加CRS的风险，特别是CRSwNP强调需要优先考虑清洁空气倡议和环境法规。
方法：这项队列研究涉及来自英国生物库的367,298名成年参与者，从2006年3月到2021年10月。使用土地使用回归模型估算了居民点的空气污染指标。Cox比例风险模型用于探索空气污染暴露与CRS之间的关系。CRSwNP,和CRSsNP。构建了多基因风险评分（PRS），以评估空气污染和遗传易感性对CRS发展的联合影响。
结果：我们发现，在长期暴露于PM2.5的情况下，CRS的风险增加[95％CIs的风险比（HR）：1.59（1.26-2.01）]，PM10[1.64(1.26-2.12)],NO2[1.11(1.04-1.17)],和NOx[1.18(1.12-1.25)]，分别。这些影响在CRSwNP参与者中更为明显，尽管差异无统计学意义。此外,我们发现,在PRS较高或PM2.5,PM10或NOx浓度较高的参与者中,CRS和CRSwNP的风险呈分级增加.然而,没有观察到乘法或加性相互作用。
结论：长期暴露于空气污染会增加CRS的风险，特别是CRSwNP强调需要优先考虑清洁空气倡议和环境法规。
