{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T12:45:29Z","timestamp":1792673129867,"version":"4.5.0"},"reference-count":37,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2025,10,1]],"date-time":"2025-10-01T00:00:00Z","timestamp":1759276800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100001003","name":"Boehringer Ingelheim","doi-asserted-by":"publisher","award":["1199-0439"],"award-info":[{"award-number":["1199-0439"]}],"id":[{"id":"10.13039\/100001003","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001003","name":"Boehringer Ingelheim","doi-asserted-by":"publisher","award":["1199-0439"],"award-info":[{"award-number":["1199-0439"]}],"id":[{"id":"10.13039\/100001003","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.atsjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Particulate matter \u22642.5 \u03bcm (PM2.5) adversely impacts patients with fibrotic interstitial lung disease (fILD).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>We sought to determine whether PM2.5-associated epigenetic alterations contribute to the environmental pathogenesis of fILD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A retrospective two-cohort study applied satellite-derived PM2.5 and constituent exposure matching to the residential location of patients with fILD. Robust linear regressions were used to evaluate cohort-specific, epigenome-wide differential blood DNA methylation with increasing pollutant exposures (Illumina MethylationEPIC BeadChip). Cox and linear regressions were used to evaluate associations of cytosine-phosphate-guanine (CpG) loci with transplant-free survival and lung function. A Wilcoxon test was used to evaluate cartilage-associated protein (CRTAP) levels in fILD and control lungs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>The University of Pittsburgh cohort (n\u2009=\u2009306) had 5-year median PM2.5 exposures of 12.1 \u03bcg\/m3 compared with 5.1 \u03bcg\/m3 in the University of British Columbia cohort (n\u2009=\u2009170). Higher pollutant exposures in the University of Pittsburgh cohort were associated with lower methylation at cg25354716, annotated to CRTAP, a critical extracellular matrix remodeling enzyme. Higher exposures in the University of British Columbia cohort were associated with higher methylation at cg01019301, annotated to TLN2 (talin-2), a cytoskeletal protein involved in fibroblast migration. A 10% increase in cg25354716 methylation was associated with a hazard ratio of 0.81 for death or lung transplantation in the meta-analyzed cohorts (95% confidence interval\u2009=\u20090.69\u20130.96; P\u2009=\u20090.01), whereas the same change in cg01019301 was associated with a hazard ratio of 1.36 (95% confidence interval\u2009= 1.07\u20131.74; P\u2009=\u20090.01). CRTAP protein was more abundant in lungs from patients with fILD compared with those from donor controls (P\u2009&amp;lt;\u20090.001).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>PM2.5 is associated with altered blood DNA methylation in fILD. This work identifies novel pollution-sensitive targets that hold potential for therapeutic modulation in fILD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202407-1504oc","type":"journal-article","created":{"date-parts":[[2025,6,20]],"date-time":"2025-06-20T14:26:11Z","timestamp":1750429571000},"page":"1835-1845","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":10,"title":["Epigenome-Wide Analysis Identifies Pollution-Sensitive Loci in Fibrotic Interstitial Lung Disease"],"prefix":"10.1093","volume":"211","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7982-5635","authenticated-orcid":false,"given":"Gillian C.","family":"Goobie","sequence":"first","affiliation":[{"name":"Division of Respiratory Medicine, Department of Medicine, and"},{"name":"Centre for Heart Lung Innovation, St. Paul\u2019s Hospital, Vancouver, British Columbia, Canada"},{"name":"Division of Pulmonary, Allergy and Critical Care Medicine, 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