1990•Fundamental and Applied ToxicologyOpen access

Modulation of pulmonary eicosanoid metabolism following exposure to sulfuric acid

Richard Schlesinger

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Abstract

Eicosanoids (arachidonic acid metabolites) are potent biological mediators. Modulation of their metabolism by air pollutants may be a possible factor in the pathogenesis of environmentally related lung disease. Sulfuric acid (H2SO4) aerosols are components of ambient air in many areas. Rabbits were exposed to H2SO4 (0.3 microns) at 250, 500, or 1000 micrograms/m3 for 1 hr/day for 5 days. They were then euthanized, the lungs lavaged, and eicosanoid analyses performed by radioimmunoassay of acellular lavage fluid. An exposure-concentration-dependent decrease in levels of prostaglandins E2 and F2 alpha and thromboxane B2 was found; no change in leukotriene B4 was observed. Tracheal explants exposed to acidic environments in vitro also showed reduced production of PGE2, PGF2 alpha, and TxB2. Incubation with sodium sulfate (Na2SO4) showed no effect of the sulfate ion (SO4(2-)). This study, the first to examine eicosanoid production after in vivo exposure to pure H2SO4 droplets, indicates that such exposure can modulate arachidonic acid metabolism, and that this is likely due to the deposition of hydrogen ion (H+) on target tissue.

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What this paper is about

Eicosanoids (arachidonic acid metabolites) are potent biological mediators. Modulation of their metabolism by air pollutants may be a possible factor in the pathogenesis of environmentally related lung disease. Sulfuric acid (H2SO4) aerosols are components of ambient air in many areas. Rabbits were exposed to H2SO4 (0.3 microns) at 250, 500, or 1000 micrograms/m3 for 1 hr/day for 5 days. They were then euthanized, the lungs lavaged, and eicosanoid analyses performed by radioimmunoassay of acellular lavage fluid. An exposure-concentration-dependent decrease in levels of prostaglandins E2 and F2 alpha and thromboxane B2 was found; no change in leukotriene B4 was observed. Tracheal explants exposed to acidic environments in vitro also showed reduced production of PGE2, PGF2 alpha, and TxB2. Incubation with sodium sulfate (Na2SO4) showed no effect of the sulfate ion (SO4(2-)). This study, the first to examine eicosanoid production after in vivo exposure to pure H2SO4 droplets, indicates that such exposure can modulate arachidonic acid metabolism, and that this is likely due to the deposition of hydrogen ion (H+) on target tissue.

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Available abstract

Eicosanoids (arachidonic acid metabolites) are potent biological mediators. Modulation of their metabolism by air pollutants may be a possible factor in the pathogenesis of environmentally related lung disease. Sulfuric acid (H2SO4) aerosols are components of ambient air in many areas. Rabbits were exposed to H2SO4 (0.3 microns) at 250, 500, or 1000 micrograms/m3 for 1 hr/day for 5 days. They were then euthanized, the lungs lavaged, and eicosanoid analyses performed by radioimmunoassay of acellular lavage fluid. An exposure-concentration-dependent decrease in levels of prostaglandins E2 and F2 alpha and thromboxane B2 was found; no change in leukotriene B4 was observed. Tracheal explants exposed to acidic environments in vitro also showed reduced production of PGE2, PGF2 alpha, and TxB2. Incubation with sodium sulfate (Na2SO4) showed no effect of the sulfate ion (SO4(2-)). This study, the first to examine eicosanoid production after in vivo exposure to pure H2SO4 droplets, indicates that such exposure can modulate arachidonic acid metabolism, and that this is likely due to the deposition of hydrogen ion (H+) on target tissue.

Key concepts: Eicosanoid, Eicosanoid metabolism, Arachidonic acid, Chemistry, Thromboxane B2, Metabolism, Thromboxane A2, Sulfuric acid

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