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World Trade Center dust exposure: Ox...

Hernandez, Michelle N.

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World Trade Center dust exposure: Oxidative and nitritive stress dysfunction and injury in nasal, neurologic, and pulmonary tissues.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	World Trade Center dust exposure: Oxidative and nitritive stress dysfunction and injury in nasal, neurologic, and pulmonary tissues./
作者:	Hernandez, Michelle N.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2017,
面頁冊數:	196 p.
附註:	Source: Dissertation Abstracts International, Volume: 78-08(E), Section: B.
Contained By:	Dissertation Abstracts International78-08B(E).
標題:	Environmental health. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10244157
ISBN:	9781369630145

World Trade Center dust exposure: Oxidative and nitritive stress dysfunction and injury in nasal, neurologic, and pulmonary tissues.
Hernandez, Michelle N.

World Trade Center dust exposure: Oxidative and nitritive stress dysfunction and injury in nasal, neurologic, and pulmonary tissues. - Ann Arbor : ProQuest Dissertations & Theses, 2017 - 196 p.

Source: Dissertation Abstracts International, Volume: 78-08(E), Section: B.

Thesis (Ph.D.)--New York University, 2017.

For the last fifteen years, those who worked and resided near the World Trade Center (WTC) site at the time of the September 11, 2001 attack and thereafter, have been plagued by lower respiratory ailments. It is proposed that the myriad of respiratory ailments and illnesses that have developed since that time are caused by particulate matter (PM) exposure resulting from the WTC building collapse and cleanup (WTCPM). This study tested this hypothesis by investigating oxidative and nitritive stress outcomes, coupled with inflammatory potentials in both in vitro-cell and in vivo-mouse models, with specific emphasis on upper respiratory, lower respiratory, and CNS tissues.

ISBN: 9781369630145Subjects--Topical Terms:

543032
Environmental health.

World Trade Center dust exposure: Oxidative and nitritive stress dysfunction and injury in nasal, neurologic, and pulmonary tissues.
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245 1 0 $a World Trade Center dust exposure: Oxidative and nitritive stress dysfunction and injury in nasal, neurologic, and pulmonary tissues.
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500 $a Source: Dissertation Abstracts International, Volume: 78-08(E), Section: B.
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520 $a For the last fifteen years, those who worked and resided near the World Trade Center (WTC) site at the time of the September 11, 2001 attack and thereafter, have been plagued by lower respiratory ailments. It is proposed that the myriad of respiratory ailments and illnesses that have developed since that time are caused by particulate matter (PM) exposure resulting from the WTC building collapse and cleanup (WTCPM). This study tested this hypothesis by investigating oxidative and nitritive stress outcomes, coupled with inflammatory potentials in both in vitro-cell and in vivo-mouse models, with specific emphasis on upper respiratory, lower respiratory, and CNS tissues.
520 $a Male C57Bl/6 mice intranasally exposed to WTCPM (31microg to 4mg) revealed significant increases (11-45%) in polymorphonuclear neutrophil (PMN) influx in both nasal (NLF) and bronchoalveolar lavage fluids (BALF). Upon further investigation, pulmonary, nasal, and neurologic tissues exhibit significant oxidative stress response (increased mRNA abundance of HO1, SOD2, Txnrd2, Prdx6 genes) in conjunction with increased inflammatory markers (PMNs, total protein and cytokine/chemokine values). Concurrently, NLF, BALF, and serum nitrite (NO2-) levels were found to be significantly decreased (20-92%) in WTCPM exposed mice, and these changes were accompanied by temporal aortic dysfunction measurements over a 30 day period.
520 $a Further studies revealed acute and chronic inflammatory reactions were highly influenced, if not wholly influenced, by WTCPM alone and not by the alkaline nature of the dust. Additionally, combinations of WTCPM plus lipopolysaccharide (LPS), PM2.5, or diesel engine exhaust particles (DEP) were found to augment upper and lower respiratory oxidative/ nitritive dysfunction as well as inflammation at low concentration exposure levels. More importantly, metals associated with WTCPM, were found to persist in the lungs and whole brains of exposed mice. Thus, exposure to, and retention of WTCPM in these organs may contribute to chronic systemic effects seen in these mice and may also occur in human populations. Repetitive insults to the nasal cavity from WTCPM dust alone revealed mouse olfaction delays to be increased by 136%, with olfaction deficits still persisting 10 days post exposure. Significant changes in body weight loss (10-15%) and increased anxiety behaviors were also observed in mice experiencing olfaction loss. Collectively, these data suggest WTCPM exposure alone can result in nasal and olfactory epithelial damage, while inducing chronic stress like parameters.
520 $a Taken together, these findings are reflective of WTCPM exposure and its influence on respiratory and CNS tissues, highlighting dysfunctional pathways that precipitate inflammatory events, while altering homeostatic balances. The tight interplay between these balances, when altered, may contribute to or result in chronically diseased physical and mental states.
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