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World Trade Center Dust Induces Airway Inflammation while Promoting Aortic Endothelial Dysfunction
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8 01 2020
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Source: Toxicol Appl Pharmacol. 400:115041
[PDF-1012.01 KB]
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Alternative Title:Toxicol Appl Pharmacol
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Description:Respiratory ailments have plagued occupational and public health communities exposed to World Trade Center (WTC) dust since the September 11, 2001 attack on the Twin Towers in Lower Manhattan. We proposed that these ailments were proposed to be induced by inhalation exposure to WTC particulate matter (WTC|), that was released during the collapse of the buildings and its subsequent resuspension during cleanup. We investigated this hypothesis using both an in vitro and an in vivo mouse intranasal (IN) exposure models to identify the inflammatory potential of WTC| with specific emphasis on respiratory and endothelial tissue responses. The in vitro exposure studies found WTC| exposure to be positively correlated with cytotoxicity and increased NO| production in both BEAS-2B pulmonary epithelial cells and THP-1 macrophage cells. The in vivo C57BL/6 mouse studies found significant increases in inflammatory markers including increases in polymorphonuclear neutrophil (PMN) influx into nasal and bronchoalveolar lavage fluids (NLF and BALF), as well as increased levels of total protein and cytokine/chemokines levels. Concurrently, NLF, BALF, and serum NO| levels exhibited significant homeostatic temporal deviations as well as temporal myograohic aortic dysfunction in myography studies. Respiratory exposure to- and evidence -based retention of- WTC| may have contributed to chronic systemic effects in exposed mice that r resembled to observed effects in WTC|-exposed human populations. Collectively, these findings are reflective of WTC| exposure and its effect(s) on respiratory and aortic tissues, highlighting potential dysfunctional pathways that may precipitate inflammatory events, while simultaneously altering homeostatic balances. The tight interplay between these balances, when chronically altered, may contribute to- or result in- chronically diseased pathological states.
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Pubmed ID:32428593
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Pubmed Central ID:PMC7370403
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Volume:400
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