Effects of SO₂Exposure on Canine Pulmonary Epithelial Functions

Abstract

We examined the effects of a single exposure of high concentrations of sulfur dioxide (SO2) on the pulmonary epithelium in adult dogs over a period of several weeks. Mucociliary tracheal transport rates and alveolar clearance of 99mTc-labeled diethylene triamine pentacetate (99mTcO4-) were measured in vivo, before and immediately after inhalation of 100 ppm or 500 ppm SO2, and then weekly for 3-5 weeks. At the completion of the in vivo studies, tracheal epithelium was studied in Ussing chambers for bioelectric properties (short-circuited current, transepithelial potential difference), nonelectrolyte permeability for calculation of pore sizes, and changes in bioelectric properties following pharmacological manipulations. These tissues were then fixed for scanning electron microscopy studies. Additional dogs were sacrificed for microscopy studies at several time intervals to provide a histological basis for the altered mucociliary transport. We found that despite marked derangement of mucociliary transport caused by damage to the ciliated cells, recovery occurred over a period of several weeks, and alveolar permeability as assessed by the radioaerosol technique did not change. We concluded that the solubility of SO2 and perhaps a more severe damaging effect of SO2 specific on the ciliated cells might be the explanation for the observations.

Interactions of Oxygen Radicals with Airway Epithelium

“…Ciliated epithelial cell necrosis has been observed after 03 exposure in rats (57). Sulfur dioxide causes airway hyperreactivity (58) and has been reported to damage ciliated airway epithelial cells and decrease mucociliary transport in dogs (59). Nitrogen dioxide decreases mucociliary transport and functional residual capacity in dogs (60).…”

“…Decreased epithelial barrier function causes edema that may contribute to hypersecretion of mucus by exposing airway secretory cells to plasma secretagogues (55). Increased epithelial cell paracellular permeability (decreased barrier function) has been reported in a) pulmonary epithelium of dogs exposed to sulfur dioxide (59) and nitrogen dioxide (60); b) Madin Darby canine kidney (MDCK) epithelial cells exposed to H202, glucose/glucose oxidase, and xanthine/XO (66); c) ferret tracheal epithelium exposed to xanthine/XO (67); and d) rat alveolar epithelium exposed to H202 (15). P/XO also induces permeability edema in isolated perfused rabbit lungs (68 pulmonary endothelial cells (70).…”

Signature current of SO2-induced bronchitis in rabbit.

“…The significant hypoxia and increase in A-aDO 2 in the present results may reflect a local shunt blood flow at the distal alveolar region due to bronchiolitis and/or mucus plugging, because the SO 2 -induced bronchitis is reversible both in function and morphology (6,15), and the alveoli is reported to be histologically intact during SO 2 exposure (8). The rabbit pathological trachea shares common morphological characteristics with other animal models of SO 2 -exposed bronchitis (6)(7)(8) except that mucus gland hypertrophy or the mucus gland itself is absent in the rabbit model. Although a quantitative study was not performed, one of the most prominent features noted in the SO 2 -exposed rabbit was a thickening of the airway epithelium (Fig.…”

Effect of Air Pollution on Exacerbations of Bronchiectasis in Badalona, Spain, 2008–2016

“…In chronically exposed animals, it has been seen to cause mucus gland hypersecretion and replacement of ciliated cells by nonciliated cells [23]. Several authors have described dysfunction of mucociliary clearance in animals exposed to SO 2 [24-26]. This functional impairment can be reversible [24] and might occur at concentrations which yield no detectable morphological alterations, such as widening of intercellular spaces [25].…”

“…Several authors have described dysfunction of mucociliary clearance in animals exposed to SO 2 [24-26]. This functional impairment can be reversible [24] and might occur at concentrations which yield no detectable morphological alterations, such as widening of intercellular spaces [25]. When the barrier function of the airway mucosa and/or the mucociliary function are impaired, the contact of bacteria with the mucosa could be increased and the invasion of inhaled pathogens could be eased [25], thus predisposing to exacerbations.…”