Abstract

BackgroundShort-term exposure to ozone and nitrogen dioxide is a risk factor for acute exacerbation (AE) of idiopathic pulmonary fibrosis (AE-IPF). The comprehensive roles of exposure to fine particulate matter in AE-IPF remain unclear. We aim to investigate the association of short-term exposure to fine particulate matter with the incidence of AE-IPF and to determine the exposure-risk time window during 3 months before the diagnosis of AE-IPF.MethodsIPF patients were retrospectively identified from the nationwide registry in Japan. We conducted a case–control study to assess the correlation between AE-IPF incidence and short-term exposure to eight air pollutants, including particulate matter < 2.5 µm (PM2.5). In the time-series data, we compared monthly mean exposure concentrations between months with AE (case months) and those without AE (control months). We used multilevel mixed-effects logistic regression models to consider individual and institutional-level variables, and also adjusted these models for several covariates, including temperature and humidity. An additional analysis with different monthly lag periods was conducted to determine the risk-exposure time window for 3 months before the diagnosis of AE-IPF.ResultsOverall, 152 patients with surgically diagnosed IPF were analyzed. AE-IPF was significantly associated with an increased mean exposure level of nitric oxide (NO) and PM2.5 30 days prior to AE diagnosis. Adjusted odds ratio (OR) with a 10 unit increase in NO was 1.46 [95% confidence interval (CI) 1.11–1.93], and PM2.5 was 2.56 (95% CI 1.27–5.15). Additional analysis revealed that AE-IPF was associated with exposure to NO during the lag periods lag 1, lag 2, lag 1–2, and lag 1–3, and PM2.5 during the lag periods lag 1 and lag 1–2.ConclusionsOur results show that PM2.5 is a risk factor for AE-IPF, and the risk-exposure time window related to AE-IPF may lie within 1–2 months before the AE diagnosis. Further investigation is needed on the novel findings regarding the exposure to NO and AE-IPF.

Highlights

  • Short-term exposure to ozone and nitrogen dioxide is a risk factor for acute exacerbation (AE) of idiopathic pulmonary fibrosis (AE-Idiopathic pulmonary fibrosis (IPF))

  • Among the 465 patients included in the previous study [20], 113 were excluded for the following reasons: Multidisciplinary discussion (MDD) diagnosis was not an Idiopathic interstitial pneumonias (IIPs) (n = 21); lack of the corresponding ambient air pollution data (n = 75); AE occurred within 2 months after Surgical lung biopsy (SLB) (n = 3); follow-up period was < 2 months (n = 14) (Fig. 1)

  • Our findings showed that elevated levels of ­PM2.5, albeit lower than the P­M2.5 level of 26 μg/m3—the mean levels of ­PM2.5 established by the Japanese government in 2009— may be a risk factor for Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF)

Read more

Summary

Introduction

Short-term exposure to ozone and nitrogen dioxide is a risk factor for acute exacerbation (AE) of idiopathic pulmonary fibrosis (AE-IPF). We aim to investigate the association of short-term exposure to fine particulate matter with the incidence of AE-IPF and to determine the exposure-risk time window during 3 months before the diagnosis of AE-IPF. Regarding exposure to ambient air pollution as potential risk factors of AE-IPF, a significant association between the incidence of AE-IPF and increased mean exposure levels of ozone ­(O3) and nitrogen dioxide ­(NO2) during 0–42 days prior to AE was shown in South Korea [14]. A French study showed that short-term exposure to increased level of ­O3 was positively related to AE-IPF [4]

Objectives
Methods
Results
Discussion
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.