Faculty Bibliography

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. The nature of these ailments is proposed to be induced by inhalation exposure to WTC particulate matter (WTC_PM), released during the collapse of the buildings and subsequent resuspension during cleanup. We investigated this hypothesis using both an in vitro and an in vivo mouse intranasal (IN) exposure model to identify the inflammatory potential of WTC_PM with specific emphasis on respiratory and endothelial tissue responses. In vitro studies identified WTC_PM exposure to be positively correlated with cytotoxicity and increased NO₂^- production in both BEAS-2B pulmonary epithelial cells and THP-1 macrophage cells. In vivo C57BL/6 mouse studies exhibited 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 total protein and cytokine/chemokines levels. Concurrently, NLF, BALF, and serum NO₂^- levels exhibited significant homeostatic temporal deviations with evidence of temporal aortic dysfunction in myography studies. Respiratory exposure to- and evidence -based retention of- WTC_PM may contribute to chronic systemic effects seen in mice, with resemblance to observed effects in WTC_PM-exposed human populations. Collectively, findings reported herein are reflective of WTC_PM 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.