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Pulmonary Manifestations of Inhaled Arsenic Trioxide Following an Acute Accidental Exposure
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A2974 - Pulmonary Manifestations of Inhaled Arsenic Trioxide Following an Acute Accidental Exposure
Author Block: N. Mariappan1, I. Zafar1, M. Husain1, M. Vaid1, R. Surolia2, M. P. Kashyap3, R. Srivastava3, S. Ahmad1, A. Agarwal4, M. Athar3, V. B. Antony2, A. Aftab1; 1Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, AL, United States, 2Pulmonary, Allergy and Critical care Medicine, University of Alabama at Birmingham, Birmingham, AL, United States, 3Department of Dermatology, University of Alabama at Birmingham, Birmingham, AL, United States, 4Division of Nephrology, University of Alabama at Birmingham, Birmingham, AL, United States.
Aim: Arsenic trioxide (ATO) is a common industrial chemical. Significant public health risk exists for exposure due to intentional, terrorism related or accidental release, as ATO is extensively imported into the United States for manufacturing wood preservatives, insecticides, herbicides, growth stimulants, and electrical goods. Multi-organ failure combined with acute respiratory distress syndrome has been reported in individuals poisoned with ATO. The goal of our current studies is to determine mechanisms by which ATO causes respiratory distress and failure. Methods: Arsenic trioxide was administered intranasally. Twenty-four and 48 h post exposure mice were sacrificed and arterial blood gas measurements along with complete blood counts were performed. Lung tissues were fixed and analyzed for histological changes. Lung function was also carried out using flexiVent. Differential cell counts were performed in the bronchoalveolar fluid (BALF). BALF was also analyzed for protein and IgM. Results: ATO exposure caused increases in respiratory system elastance (Ers), tissue elastance (H) and tissue damping (G) when compared to the saline controls. There was however a decrease in respiratory resistance (Rrs) and no change in the Newtonian airway resistance (Rn). Arterial blood gas measurements showed respiratory acidosis. Lung histology showed increased airway wall thickening in ATO exposed animals when compared to saline control. There was also a marked increase in neutrophil influx in the bronchoalveolar lavage fluid (BALF) of ATO exposed group when compared to the saline controls. Mechanistic in vitro studies with air-liquid interface cultures of human airway epithelial cells and studies with electrical cell impedance of primary human lung microvascular endothelial cells demonstrated disruption of cell monolayers following exposure to ATO. Conclusions: Taken together, these results demonstrate that ATO exposure results in increased airway wall thickening and inflammation along with significant impairment of pulmonary function.
Author Block: N. Mariappan1, I. Zafar1, M. Husain1, M. Vaid1, R. Surolia2, M. P. Kashyap3, R. Srivastava3, S. Ahmad1, A. Agarwal4, M. Athar3, V. B. Antony2, A. Aftab1; 1Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, AL, United States, 2Pulmonary, Allergy and Critical care Medicine, University of Alabama at Birmingham, Birmingham, AL, United States, 3Department of Dermatology, University of Alabama at Birmingham, Birmingham, AL, United States, 4Division of Nephrology, University of Alabama at Birmingham, Birmingham, AL, United States.
Aim: Arsenic trioxide (ATO) is a common industrial chemical. Significant public health risk exists for exposure due to intentional, terrorism related or accidental release, as ATO is extensively imported into the United States for manufacturing wood preservatives, insecticides, herbicides, growth stimulants, and electrical goods. Multi-organ failure combined with acute respiratory distress syndrome has been reported in individuals poisoned with ATO. The goal of our current studies is to determine mechanisms by which ATO causes respiratory distress and failure. Methods: Arsenic trioxide was administered intranasally. Twenty-four and 48 h post exposure mice were sacrificed and arterial blood gas measurements along with complete blood counts were performed. Lung tissues were fixed and analyzed for histological changes. Lung function was also carried out using flexiVent. Differential cell counts were performed in the bronchoalveolar fluid (BALF). BALF was also analyzed for protein and IgM. Results: ATO exposure caused increases in respiratory system elastance (Ers), tissue elastance (H) and tissue damping (G) when compared to the saline controls. There was however a decrease in respiratory resistance (Rrs) and no change in the Newtonian airway resistance (Rn). Arterial blood gas measurements showed respiratory acidosis. Lung histology showed increased airway wall thickening in ATO exposed animals when compared to saline control. There was also a marked increase in neutrophil influx in the bronchoalveolar lavage fluid (BALF) of ATO exposed group when compared to the saline controls. Mechanistic in vitro studies with air-liquid interface cultures of human airway epithelial cells and studies with electrical cell impedance of primary human lung microvascular endothelial cells demonstrated disruption of cell monolayers following exposure to ATO. Conclusions: Taken together, these results demonstrate that ATO exposure results in increased airway wall thickening and inflammation along with significant impairment of pulmonary function.
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