Toxicity of hydrogen sulfide

However, since the latter reaction is an equilibrium process the Claus sulfur still contains traces of H2S (200-350 ppm, mostly in the form of polysulfanes) which causes serious problems since the H2S partly escapes on cooling or solidification of the sulfur. Obviously, the H2S content needs to be controlled because of the extreme toxicity of hydrogen sulfide and its ability... 

Higuchi Y and Fukamachi M. 1977. [Behavioral studies on toxicity of hydrogen sulfide by means of conditioned avoidance responses in rats.] Folia Pharmacologica Japonica 73 307-319. (Japanese)... 

There is a fairly large body of animal data characterizing the toxicity of hydrogen sulfide. Studies have been conducted in monkeys, dogs, rabbits, mice, rats, and guinea pigs in which animals have been exposed via both inhalation and dermal contact. Inhalation studies have documented responses at different atmospheric concentrations over varying periods of time. Both local and systemic effects have been observed. 

Hydrochloric acid can be used to dissolve calcium carbonate and iron sulfide scales. However, iron sulfide chemically reacts with hydrochloric acid and produces hydrogen sulfide, a highly toxic gas having the odor of rotten eggs. Due to the high toxicity of hydrogen sulfide, safety provisions need to be implemented. 

If hydrogen sulfide is present in the produced reservoir fluid, or if sulfate reducing bacteria are a problem in the reservoir or production equipment, hydrogen sulfide will likewise be present in the produced water stream. Hydrogen sulfide is corrosive, can cause iron sulfide scaling, and is extremely toxic if inhaled. The toxicity of hydrogen sulfide hinders operation and maintenance of equipment, particularly when the vessels must be opened for adjustments, as in the case when weir adjustments are required in gas flotation cells. Special training... 

Arsenic is another element with different bioavailabiUty in its different redox states. Arsenic is not known to be an essential nutrient for eukaryotes, but arsenate (As(V)) and arsenite (As(III)) are toxic, with the latter being rather more so, at least to mammals. Nevertheless, some microorganisms grow at the expense of reducing arsenate to arsenite (81), while others are able to reduce these species to more reduced forms. In this case it is known that the element can be immobilized as an insoluble polymetallic sulfide by sulfate reducing bacteria, presumably adventitiously due to the production of hydrogen sulfide (82). Indeed many contaminant metal and metalloid ions can be immobilized as metal sulfides by sulfate reducing bacteria. 

Organisms also evolved powerful detoxifying mechanisms that remove toxic materials or convert them to non-toxic forms or nutrients. Examples of alterations to non-toxic forms are the conversions of hydrogen sulfide to sulfate and nitrite to nitrate. The prime example of development of the ability to use a toxic substance is the evolution of aerobic metabolism, which converted a serious and widespread toxin, oxygen, into a major resource. This development, as we have seen, greatly increased the productivity of the biosphere and generated the oxygen-rich atmosphere of today s Earth. 

The primary purpose of this chapter is to provide public health officials, physicians, toxicologists, and other interested individuals and groups with an overall perspective of the toxicology of hydrogen sulfide. It contains descriptions and evaluations of toxicological studies and epidemiological investigations and provides conclusions, where possible, on the relevance of toxicity and toxicokinetic data to public health. 

The mechanism of hydrogen sulfide toxicity is in part similar to that of cyanide. Like cyanide, hydrogen sulfide can inhibit the enzyme cytochrome oxidase resulting in tissue hypoxia. Specific health effects are discussed in greater detail below. 

The usefulness of urinary thiosulfate as an indicator of nonfatal hydrogen sulfide toxicity has been studied (Kangas and Savolainen 1987). Urinary samples for thiosulfate were obtained from volunteers exposed by inhalation to 8, 18, or 30 ppm of hydrogen sulfide for 30-45 minutes (the occupational exposure limit of 10 ppm for 8 hours was never exceeded). Excretion of urinary thiosulfate increased linearly up to 15 hours postexposure. Beyond 15 hours, the urinary thiosulfate concentration remained low, possibly indicating that most of the absorbed hydrogen sulfide was metabolized or excreted within 15 hours. 

Alterations in blood heme metabolism have been proposed as a possible indicator of the biological effects of hydrogen sulfide (Jappinen and Tenhunen 1990), but this does not relate to the mechanism of toxicity in humans. The activities of the enzymes of heme synthesis, i.e., delta-aminolevulinic acid synthase (ALA-S) and heme synthase (Haem-S), were examined in 21 cases of acute hydrogen sulfide toxicity in Finnish pulp mill and oil refinery workers. Subjects were exposed to hydrogen sulfide for periods ranging from approximately 1 minute to up to 3.5 hours. Hydrogen sulfide concentrations were considered to be in the range of 20-200 ppm. Several subjects lost consciousness for up to 3 minutes. 

There appears to be some evidence that ethanol can increase the effects of hydrogen sulfide. In 6 cases, less hydrogen sulfide was needed for toxic effects to be observed when workers had consumed alcohol 16-24 hours earlier (Poda 1966). 

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