PDF(Pubmed)
Abstract：
UNASSIGNED: There is a growing body of evidence suggesting a causal relationship between interstitial lung disease (ILD) and air pollution, both for the development of the disease, and driving disease progression. We aim to provide a comprehensive literature review of the association between air pollution, and ILD, including idiopathic pulmonary fibrosis (IPF).
UNASSIGNED: We systematically searched from six online database. Two independent authors (DL and CF) selected studies and critically appraised the risk of bias using the Newcastle-Ottawa Scale (NOS). Findings are presented through a narrative synthesis and meta-analysis. Meta-analyses were performed exclusively when there was a minimum of three studies examining identical pollutant-health outcome pairs, all evaluating equivalent increments in pollutant concentration, using a random effects model.
UNASSIGNED: 24 observational studies conducted in 13 countries or regions were identified. Pollutants under investigation encompassed ozone (O3), nitrogen dioxide (NO2), Particulate matter with diameters of 10 micrometers or less (PM10) and 2.5 micrometers or less (PM2.5), sulfur dioxide (SO2), carbon monoxide (CO), nitric oxide (NO) and nitrogen oxides (NOx). We conducted meta-analyses to assess the estimated Risk Ratios (RRs) for acute exacerbations (AE)-IPF in relation to exposure to every 10 μg/m3 increment in air pollutant concentrations, including O3, NO2, PM10, and PM2.5. The meta-analysis revealed a significant association between the increased risk of AE-IPF in PM2.5, yielding RR 1.94 (95% CI 1.30-2.90; p = 0.001). Findings across all the included studies suggest that increased exposure to air pollutants may be linked to a range of health issues in individuals with ILDs.
UNASSIGNED: A scarcity of available studies on the air pollutants and ILD relationship underscores the imperative for further comprehensive research in this domain. The available data suggest that reducing levels of PM2.5 in the atmosphere could potentially reduce AE frequency and severity in ILD patients.
UNASSIGNED: We systematically searched from six online database. Two independent authors (DL and CF) selected studies and critically appraised the risk of bias using the Newcastle-Ottawa Scale (NOS). Findings are presented through a narrative synthesis and meta-analysis. Meta-analyses were performed exclusively when there was a minimum of three studies examining identical pollutant-health outcome pairs, all evaluating equivalent increments in pollutant concentration, using a random effects model.
UNASSIGNED: 24 observational studies conducted in 13 countries or regions were identified. Pollutants under investigation encompassed ozone (O3), nitrogen dioxide (NO2), Particulate matter with diameters of 10 micrometers or less (PM10) and 2.5 micrometers or less (PM2.5), sulfur dioxide (SO2), carbon monoxide (CO), nitric oxide (NO) and nitrogen oxides (NOx). We conducted meta-analyses to assess the estimated Risk Ratios (RRs) for acute exacerbations (AE)-IPF in relation to exposure to every 10 μg/m3 increment in air pollutant concentrations, including O3, NO2, PM10, and PM2.5. The meta-analysis revealed a significant association between the increased risk of AE-IPF in PM2.5, yielding RR 1.94 (95% CI 1.30-2.90; p = 0.001). Findings across all the included studies suggest that increased exposure to air pollutants may be linked to a range of health issues in individuals with ILDs.
UNASSIGNED: A scarcity of available studies on the air pollutants and ILD relationship underscores the imperative for further comprehensive research in this domain. The available data suggest that reducing levels of PM2.5 in the atmosphere could potentially reduce AE frequency and severity in ILD patients.
摘要：
■越来越多的证据表明间质性肺病（ILD）与空气污染之间存在因果关系，都是为了疾病的发展，并推动疾病进展。我们的目标是提供关于空气污染之间关联的全面文献综述，ILD,包括特发性肺纤维化（IPF）。
■我们从六个在线数据库中进行了系统搜索。两名独立作者（DL和CF）选择了研究，并使用纽卡斯尔-渥太华量表（NOS）严格评估了偏倚的风险。研究结果通过叙事综合和荟萃分析呈现。当至少有三项研究检查相同的污染物-健康结果对时，仅进行荟萃分析。所有评估污染物浓度的等效增量，使用随机效应模型。
■确定了在13个国家或地区进行的24项观察性研究。正在调查的污染物包括臭氧(O3)，二氧化氮(NO2),直径为10微米或更小（PM10）和2.5微米或更小（PM2.5）的颗粒物，二氧化硫(SO2),一氧化碳(CO),一氧化氮（NO）和氮氧化物（NOx）。我们进行了荟萃分析，以评估急性加重（AE）-IPF的估计风险比（RR）与暴露于空气污染物浓度每增加10μg/m3有关。包括O3、NO2、PM10和PM2.5。荟萃分析显示，PM2.5中AE-IPF的风险增加之间存在显着关联，RR为1.94（95％CI1.30-2.90；p=0.001）。所有纳入研究的结果表明，暴露于空气污染物的增加可能与ILD患者的一系列健康问题有关。
■关于空气污染物和ILD关系的现有研究的匮乏强调了在该领域进行进一步全面研究的必要性。现有数据表明，降低大气中PM2.5的水平可能会降低ILD患者的AE频率和严重程度。
■我们从六个在线数据库中进行了系统搜索。两名独立作者（DL和CF）选择了研究，并使用纽卡斯尔-渥太华量表（NOS）严格评估了偏倚的风险。研究结果通过叙事综合和荟萃分析呈现。当至少有三项研究检查相同的污染物-健康结果对时，仅进行荟萃分析。所有评估污染物浓度的等效增量，使用随机效应模型。
■确定了在13个国家或地区进行的24项观察性研究。正在调查的污染物包括臭氧(O3)，二氧化氮(NO2),直径为10微米或更小（PM10）和2.5微米或更小（PM2.5）的颗粒物，二氧化硫(SO2),一氧化碳(CO),一氧化氮（NO）和氮氧化物（NOx）。我们进行了荟萃分析，以评估急性加重（AE）-IPF的估计风险比（RR）与暴露于空气污染物浓度每增加10μg/m3有关。包括O3、NO2、PM10和PM2.5。荟萃分析显示，PM2.5中AE-IPF的风险增加之间存在显着关联，RR为1.94（95％CI1.30-2.90；p=0.001）。所有纳入研究的结果表明，暴露于空气污染物的增加可能与ILD患者的一系列健康问题有关。
■关于空气污染物和ILD关系的现有研究的匮乏强调了在该领域进行进一步全面研究的必要性。现有数据表明，降低大气中PM2.5的水平可能会降低ILD患者的AE频率和严重程度。
