Air pollutants may be environmental risk factors in chronic rhinosinusitis disease progression
Air pollutants may be environmental risk factors in chronic rhinosinusitis disease progression
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DOI：
10.1002/alr.22052
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发表时间：
2018-03-01
影响因子：
6.4
通讯作者：
Lee, Stella E.
中科院分区：
文献类型：
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作者：
Mady, Leila J.;Schwarzbach, Hannah L.;Lee, Stella E.
背景环境暴露在慢性鼻-鼻窦炎(CRS)病理生理学中的作用知之甚少。在这项研究中，我们测量了空气污染物(颗粒物2.5[PM2.5]和黑碳[BC])对鼻息肉病CRS(CRSwNP)和非鼻息肉CRS(CRSsNP)的影响。方法使用污染物监测点的空间模拟来估计符合纳入标准的患者居住环境的暴露(总患者234例；CRSsNP，96例；CRSwNP，n=138)。疾病严重程度结果测量包括改良Lund-Mackay评分(LMS)、全身类固醇激素、功能性内窥镜鼻窦手术次数(FESS)和22项鼻-鼻结果测试(SNOT-22)评分。结果CRSwNP患者和CRSsNP患者以及有哮喘和无哮喘的患者之间PM2.5和BC的平均结果没有显著差异。在CRSsNP患者中，PM2.5与FESS显著相关。PM2.5值每增加一个单位，需要进一步手术的CRSsNP患者的风险增加1.89倍(p=0.015)。在CRSwNP患者中未发现这种关联(p=0.445)。在CRSsNP组中，BC也与SNOT-22评分显著相关。BC每增加0.1U，Snot-22就增加7.97U(p=0.008)。结论空气污染物与慢性阻塞性肺疾病症状严重程度相关，可能受暴露水平的影响，对慢性阻塞性肺疾病患者的影响更为明显。这项研究首次证明了吸入性污染物在CRS表型中的可能作用，解决了导致疾病进展的环境风险因素的关键知识差距。
BackgroundLittle is known about the role of environmental exposures in the pathophysiology of chronic rhinosinusitis (CRS). In this study, we measured the impact of air pollutants (particulate matter 2.5 [PM2.5] and black carbon [BC]) on CRS with nasal polyposis (CRSwNP) and CRS without nasal polyposis (CRSsNP).MethodsSpatial modeling from pollutant monitoring sites was used to estimate exposures surrounding residences for patients meeting inclusion criteria (total patients, n = 234; CRSsNP, n = 96; CRSwNP, n = 138). Disease severity outcome measures included modified Lund-Mackay score (LMS), systemic steroids, number of functional endoscopic sinus surgeries (FESS), and 22-item Sino-Nasal Outcome Test (SNOT-22) score. PM2.5 and BC exposures were correlated with outcome measures.ResultsMean PM2.5 and BC findings were not significantly different between CRSwNP and CRSsNP patients or patients with and without asthma. Among those with CRSsNP, PM2.5 was significantly associated with undergoing FESS. For each unit increase in PM2.5, there was a 1.89-fold increased risk in the proportion of CRSsNP patients who required further surgery (p = 0.015). This association was not identified in CRSwNP patients (p = 0.445). BC was also significantly associated with SNOT-22 score in the CRSsNP group. For each 0.1-unit increase in BC, there was a 7.97-unit increase in SNOT-22 (p = 0.008). A similar, although not significant, increase in SNOT-22 was found with increasing BC in the CRSwNP group (p = 0.728).ConclusionAir pollutants correlate with CRS symptom severity that may be influenced by exposure levels, with a more pronounced impact on CRSsNP patients. This study is the first to demonstrate the possible role of inhalant pollutants in CRS phenotypes, addressing a critical knowledge gap in environmental risk factors for disease progression.