Exposure to PM2.5 is a risk factor for acute exacerbation of surgically diagnosed idiopathic pulmonary fibrosis: a case–control study

Abstract

Background Short-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. Methods IPF 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. Results Overall, 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. Conclusions Our 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.

Air pollution and hospitalization of patients with idiopathic pulmonary fibrosis in Beijing: a time-series study

“…Previously, Johannson et al only analysed O 3 concentrations in summer months and reported a significant positive association with acute exacerbation of IPF [ 5 ] whilst Sesé et al also reported a significant positive association, but without stratifying the risk by season [ 9 ]. The studies in Chile [ 10 ] and Japan [ 11 ] did not report an association with O 3 . As ours is the only study to date that reported seasonal variations of O 3 associations with IPF hospitalization, these patterns remain to be determined in future studies.…”

“…The exact exposure time window during which IPF patients develop an episode of worsening symptoms remains debated, although by convention the onset should be within one month prior to diagnosis [ 21 ]. Exposure time windows of some recent studies on confirmed IPF acute exacerbation cases were generally between the preceding 0–42 days [ 5 , 11 ].…”

“…Increased exposure to Ozone (O 3 ) were found to be associated with acute exacerbation of IPF six weeks after exposure in 436 and 192 patients in South Korea [ 5 ] and France [ 9 ] respectively, while number of hospitalizations was significantly higher following the days when levels of air pollutants including nitrogen dioxide (NO 2 ), Particulate Matter with a diameter less than or equal to 10 μm (PM 10 ) or 2.5 μm (PM 2.5 ) were high in Santiago, Chile [ 10 ]. A more recent study of 152 patients in Japan concluded that exposure to PM 2.5 and nitric oxide in the previous 30 days were significantly associated with IPF acute exacerbation [ 11 ]. Two studies in the United States found that higher air pollution exposure was associated with a lower level [ 12 ], or a faster decline [ 13 ], of forced vital capacity (FVC) among a small group of IPF patients.…”

Pharmacological Management of Idiopathic Pulmonary Fibrosis

“…Acute exacerbations (AE) are defined as an acute downturn in blood oxygenation, increased lung attenuation per computed tomography scan, and acute worsening of dyspnea [33]. Common causes include exposure to particulate matter (PM) ≥ 2.5 μm or crocin peptide released by S. nepalensis, bronchoscopy or lung biopsy, and inhalation of water repellant [33][34][35][36]. Sources of PM include tobacco smoke, candles, forest fires, and dust [33,37].…”

“…Common causes include exposure to particulate matter (PM) ≥ 2.5 μm or crocin peptide released by S. nepalensis, bronchoscopy or lung biopsy, and inhalation of water repellant [33][34][35][36]. Sources of PM include tobacco smoke, candles, forest fires, and dust [33,37]. The exact incidence of exacerbations is unknown but is estimated to vary between 5 and 20% [36,38].…”