TY - JOUR
T1 - Exposure to PM2.5 is a risk factor for acute exacerbation of surgically diagnosed idiopathic pulmonary fibrosis
T2 - a case–control study
AU - Tahara, Masahiro
AU - Fujino, Yoshihisa
AU - Yamasaki, Kei
AU - Oda, Keishi
AU - Kido, Takashi
AU - Sakamoto, Noriho
AU - Kawanami, Toshinori
AU - Kataoka, Kensuke
AU - Egashira, Ryoko
AU - Hashisako, Mikiko
AU - Suzuki, Yuzo
AU - Fujisawa, Tomoyuki
AU - Mukae, Hiroshi
AU - Suda, Takafumi
AU - Yatera, Kazuhiro
N1 - Funding Information:
We wish to thank all members participating in the nationwide IIPs database, and our research is based on the underlying research conducted by their hard work and efforts. The underlying research reported by Fujisawa and colleagues was funded by the Practical Research Project for Rare Intractable Disease from the Japan Agency for Medical Research Group under the aegis of the Ministry of Health, Ministry of Health, Labour and Welfare, Japan. We also wish to thank Mrs. Kumiko Matsuyama for her efforts to edit the Fig. .
Funding Information:
MT received grants from GlaxoSmithKline and speakers’ fees from Boehringer Ingelheim and MSD, all outside the submitted work. YF received grants from Hitachi Systems, Ltd. and NIPPON STEEL CORPORATION and personal fees from Asahi Kasei, The Asahi Shimbun Company, AstraZeneca, CHUGAI, NTT DATA MSE CORPORATION, Pfizer, Sompo Health Support Inc., and THE LOFT CO., LTD., all outside the submitted work. KY received speakers’ fees from Novartis outside the submitted work. TK received speakers’ fees from Asahi Kasei, AstraZeneca, Boehringer Ingelheim, and TEIJIN outside the submitted work. NS received consultancy or speakers’ fees from Boehringer Ingelheim, CHUGAI, and Daiichi Sankyo outside the submitted work. TK received speakers’ fees from KYORIN outside the submitted work. KK received speakers’ fees from Boehringer Ingelheim outside the submitted work. RE received grants from the Japan Society for the Promotion of Science and speakers’ fees from AstraZeneca, Boehringer Ingelheim, Daiichi Sankyo, EISAI, KYORIN, and SHIONOGI, all outside the submitted work. YS received grants from the Japan Society for the Promotion of Science and the Ichiro Kanehara Foundation for the Promotion of Medical Sciences and Medical Care, as well as received industry-academic funding from MSD and Novartis, all outside the submitted work. HM received industry-academic funding from Asahi Kasei, Astellas, Boehringer Ingelheim, CHUGAI, Daiichi Sankyo, EISAI, Eli Lilly, Fujifilm, GlaxoSmithKline, KYORIN, Meiji Seika, MSD, Novartis, ONO PHARMACEUTICAL CO., LTD., Oxford Immunotec, Inc., Pfizer, SHIONOGI, Sumitomo Dainippon, TAIHO, TAISHO, Takeda, TEIJIN, TORAY, TORII, Toyama Chemical, and Yakult, as well as consultancy or speakers’ fees from Abbott, Asahi Kasei, Astellas, AstraZeneca, Boehringer Ingelheim, Bristol-Myers, CHUGAI, Daiichi Sankyo, Denka Seiken, Eli Lilly, Fujifilm, GlaxoSmithKline, KYORIN, Meiji Seika, MSD, Mylan, Nihon Pharmaceutical, Nikkei Radio, Novartis, ONO, Pfizer, SHIONOGI, Sumitomo Dainippon, TAIHO, TAISHO, TEIJIN, TORAY, and Toyama Chemical, all outside the submitted work. TS received industry-academic funding from Astellas, AstraZeneca, Boehringer Ingelheim, Bristol-Myers, CHUGAI, Eli Lilly, Daiichi Sankyo, KYORIN, MITSUBISHI, MSD, Novartis, ONO, Pfizer, Sanofi, SHIONOGI, TAIHO, TAISHO, Taisho Toyama, Takeda, TANABE, and TEIJIN, as well as consultancy or speakers’ fees from Astellas, AstraZeneca, Boehringer Ingelheim, CHUGAI, Eli Lilly, KYORIN, Daiichi Sankyo, SHIONOGI, MSD, Novartis, ONO, Pfizer, TAISHO, Taisho Toyama, and Tanabe Mitsubishi, all outside the submitted work. KY received industry-academic funding from Boehringer Ingelheim, GlaxoSmithKline, KYORIN, MSD, Novartis, ONO, Pfizer, TAIHO, TAISHO, and TEIJIN, as well as consultancy or speakers’ fees from Asahi Kasei, Astellas, AstraZeneca, Boehringer Ingelheim, Bristol-Myers, CHUGAI, Daiichi Sankyo, Eli Lilly, GlaxoSmithKline, KYORIN, MSD, Novartis, ONO, Pfizer, SHIONOGI, TAIHO, TAISHO, TEIJIN, and TOA EIYO LTD., all outside the submitted work. The other authors declare they have no actual or potential competing financial interests.
Publisher Copyright:
© 2021, The Author(s).
PY - 2021/12
Y1 - 2021/12
N2 - 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.
AB - 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.
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U2 - 10.1186/s12931-021-01671-6
DO - 10.1186/s12931-021-01671-6
M3 - Article
C2 - 33711988
AN - SCOPUS:85102515117
SN - 1465-9921
VL - 22
JO - Respiratory Research
JF - Respiratory Research
IS - 1
M1 - 80
ER -