The Toxicity of Hydrogen Sulphide and Other Sulphides

Abstract

1. Hydrogen sulphide inhaled, or sulphide or H,S injected in solution into the circulation, is carried for a time in the plasma in the form of an equilibrium mixture of sulphide and H2S. It only slowly penetrates into the red cells, where it is destroyed in reactions in which oxyhaemoglobin is reduced. The lethal dose of H2S will therefore vary according to the rate and site of its administration.2. The physiological effects of hydrogen sulphide and other sulphides are similar to those of hydrocyanic acid, probably for the reason that both fix the iron in cytochrome A3, so reducing the oxygen intake of cells, and especially of nerve cells.3. The most conspicuous actions of sulphides are on the nerve centres, which are first stimulated and then paralysed. The actions are reversible.4. Because of the slow penetration of the red cells by H2S, or by the HS ion, the removal of sulphides from the plasma and their subsequent destruction is relatively slow, so that injections into the blood stream at sites from which the nerve centres are soon reached are more potent than those made at more remote places.5. The reduction of oxyhaemoglobin resulting from the action of sulphides is reversible, and this is probably true also for the cytochrome A ,. The action is therefore reversible, and the main treatment indicated is the application of artificial respiration.

The avian respiratory system: a unique model for studies of respiratory toxicosis and for monitoring air quality.

“…Hydrogen sulfide (H2S) is a toxic gas that inhibits enzyme systems in animals (91), and a single inhalation of 1,800 ppm can produce death in mammals (dog and humans) (92). Inhaling 500-1,500 ppm for long periods can lead to respiratory failure and death (93)(94)(95) …”

Behavioural response of three nereid polychaetes to injection of sulfide inside burrows

“…The inhibitory effects of sulfide on respiration are reversible once sulfide dissipates or is chemically oxidized (Evans 1967). Results from the present study indicate that sulfide is most probably removed from the burrow environment by ventilation processes.…”

“…The discrepancy between the ventilation patterns obtained during sulfide exposure in this study and those observed by Kristensen (1983a) during hypoxia probably illustrated toxic effects of HS-, particularly at high concentrations. Toxicity to sulfide results from the blockage of the respiratory electron transport chain (Torrans & Clemens 1982) which in turn inhibits key enzymes (Evans 1967). The pronounced rightsided tail of the HS-efflux curve especially for N. virens (Fig.…”

“…Survival is usually consid-'Present address: GIROQ, Departement de Biologie, Universite Laval, Quebec,Canada G1K 7P4 erably reduced by the presence of high concentrations of hydrogen sulfide (HS-) in the environment (Swanson & Sindermann 1979, Jsrgensen 1980, Llanso 1991. Sulfide is known to be toxic to aerobic organisms at low concentrations, often causing the inhibition of metalloenzymes, cytochrome oxydase and blood pigments (Evans 1967). Physiological and biochemical adaptations may improve tolerance and survival in the presence of HS- (Warren 1984), and studies have shown that Nereis diversicolor is capable of active HSdetoxification (Vismann 1990).…”

Diagnosing hydrogen sulfide toxicosis with a silver/sulfide ion-selective electrode

“…'^'^ Swine exposed to 1000 ppm H^S, can recover immediately upon termination of the gas, and appear clinically normal.^®® Torrans and Clemens^'^^ reported that catfish cytochrome oxidase activity inhibited 50% of normal returned to control levels in six hours. Cows continuously exposed for three weeks at 20 ppm did not develop alterations in heart rate, feed Table Nervous system Fatalities associated with hydrogen sulfide are generally due to irreversible cellular changes in the nervous system that result in acute respiratory paralysis., 74,96,253,268 Depression of cytochrome oxidase has long been considered the mechanism of systemic toxicosis, although alternate or additional routes causing respiratory distress have recently been proposed. At <200 ppm the gas depresses the central nervous system, >200 ppm can stimulate the CMS, and >700 ppm results in paralysis (Table 5) Reduced capacity for potential conduction is suggested.…”