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        <identifier>oai:figshare.com:article/33412963</identifier>
        <datestamp>2026-09-23T05:41:31Z</datestamp>
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          <dc:title>Supporting data for “Berthierine-chamosite in Late Permian C1 coal and the high incidence of lung cancer in Xuan Wei, China”</dc:title>
          <dc:creator>Renyue Ji (13002972)</dc:creator>
          <dc:creator>Jie Luo (19866432)</dc:creator>
          <dc:creator>Linwei Tian (9056261)</dc:creator>
          <dc:subject>Environmental epidemiology</dc:subject>
          <dc:subject>Xuan Wei Lung Cancer Epidemic</dc:subject>
          <dc:subject>Berthierine-chamosite</dc:subject>
          <dc:subject>Chronic Lung Injury</dc:subject>
          <dc:description>&lt;p dir="ltr"&gt;Household combustion of bituminous coal has been linked to the exceptional lung cancer burden in Xuan Wei, China, but the pulmonary effects of its mineral-rich particle fraction are incompletely defined. Here, we characterized low-temperature ash (LTA) prepared from C1 coal collected in a high-incidence area and C9 coal from a lower-incidence area, and examined its effects in bronchial epithelial cells and chronic mouse exposure models. Both LTAs contained particles within the respirable size range and retained berthierine–chamosite, whereas C1 LTA contained more iron. C1 LTA elicited greater mitochondrial hyperpolarization, reactive oxygen species accumulation and FTMT induction in BEAS-2B cells. Following three months of intranasal exposure and a three-month recovery period, both LTAs persisted in the lung and were associated with inflammation, iron deposition and tissue remodeling. Bulk and single-cell RNA sequencing of independently profiled mice identified phagolysosomal, ciliary and oxidative-stress responses together with immune–vascular remodeling. Ligand–receptor inference further suggested a shift from dendritic-cell-associated Cxcl2–Cxcr2 signaling toward endothelial-cell-associated Cxcl12–Cxcr4 signaling. These findings identify persistent pulmonary responses to mineral-rich Xuan Wei coal particles and provide a framework for investigating their contribution to environmentally associated lung disease.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-23T05:41:31Z</dc:date>
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          <dc:identifier>10.25442/hku.33412963.v1</dc:identifier>
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          <dc:rights>CC BY-NC 4.0</dc:rights>
          <dc:rights>Open Access after 2028-09-03</dc:rights>
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