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  • 标题:Long-term personal air pollution exposure and risk for acute exacerbation of idiopathic pulmonary fibrosis
  • 本地全文:下载
  • 作者:Ioannis Tomos ; Konstantina Dimakopoulou ; Effrosyni D. Manali
  • 期刊名称:Environmental Health - a Global Access Science Source
  • 印刷版ISSN:1476-069X
  • 电子版ISSN:1476-069X
  • 出版年度:2021
  • 卷号:20
  • DOI:10.1186/s12940-021-00786-z
  • 语种:English
  • 出版社:BioMed Central
  • 摘要:Urban air pollution is involved in the progress of idiopathic pulmonary fibrosis (IPF). Its potential role on the devastating event of Acute Exacerbation of IPF (AE-IPF) needs to be clarified. This study examined the association between long-term personal air pollution exposure and AE- IPF risk taking into consideration inflammatory mediators and telomere length (TL). Methods All consecutive IPF-patients referred to our Hospital from October 2013-June 2019 were included. AE-IPF events were recorded and inflammatory mediators and TL measured. Long-term personal air pollution exposures were assigned to each patient retrospectively, for O 3, NO 2, PM 2.5 [and PM 10, based on geo-coded residential addresses. Logistic regression models assessed the association of air pollutants’ levels with AE-IPF and inflammatory mediators adjusting for potential confounders. Results 118 IPF patients (mean age 72 ± 8.3 years) were analyzed. We detected positive significant associations between AE-IPF and a 10 μg/m 3 increase in previous-year mean level of NO 2 (OR = 1.52, 95%CI:1.15–2.0, p  = 0.003), PM 2.5 (OR = 2.21, 95%CI:1.16–4.20, p  = 0.016) and PM 10 (OR = 2.18, 95%CI:1.15–4.15, p  = 0.017) independent of age, gender, smoking, lung function and antifibrotic treatment. Introduction of TL in all models of a subgroup of 36 patients did not change the direction of the observed associations. Finally, O 3 was positively associated with %change of IL-4 ( p  = 0.014) whilst PM 2.5, PM 10 and NO 2 were inversely associated with %changes of IL-4 ( p  = 0.003, p  = 0.003, p  = 0.032) and osteopontin ( p  = 0.013, p  = 0.013, p  = 0.085) respectively. Conclusions Long-term personal exposure to increased concentrations of air pollutants is an independent risk factor of AE-IPF. Inflammatory mediators implicated in lung repair mechanisms are involved. Supplementary Information The online version contains supplementary material available at 10.1186/s12940-021-00786-z.
  • 关键词:Idiopathic pulmonary fibrosis; Air pollution; Acute exacerbation of idiopathic pulmonary fibrosis; Ozone; PM; Personal exposure
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