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Chapter: Modern Medical Toxicology: Asphyxiant Poisons: Toxic Gases

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Hydrogen Sulfide - Respiratory Irritants Asphyxiant Poison

Synonyms · Dihydrogen monosulfide, Dihydrogen sulfide, Hydrosulfide, Sulfur hydride, Hydrogen sulfuric acid, Hydrosulfuric acid, Sulfureted hydrogen.

Hydrogen Sulfide


·              Dihydrogen monosulfide, Dihydrogen sulfide, Hydrosulfide, Sulfur hydride, Hydrogen sulfuric acid, Hydrosulfuric acid, Sulfureted hydrogen.

Physical Appearance

·              Colourless gas, heavier than air, with a strong “rotten egg” odour. Because it rapidly paralyses olfactory nerve endings in high concentrations, odour is not a dependable means of detecting this gas. Natural gas containing hydrogen sulfide is termed “sour gas”. Hydrogen sulfide is a liquid at high pressures and low temperatures, and is shipped as the liquefied material under its own vapour pressure.

Uses and Sources

·      Decay of organic sulfur-containing products such as fish, manure, sewage, septic tank contents, etc. It is produced by bacterial action on sewage effluents containing sulfur compounds when oxygen has been consumed by excessive organic loading of surface water (“sewer gas”).

·      Industrial sources—pulp paper mills, leather industry, petroleum distillation and refining, vulcanising of rubber, heavy-water production, viscose-rayon production and coke manufacture from coal.

·      Natural sources—volcanoes, caves, sulfur springs, and subterranean emissions.

·      Other sources—burning of wool, hair, and hides can release hydrogen sulfide.

·      Hydrogen sulfide is used or encountered in farming (usually as agricultural disinfectants), brewing, tanning, glue making, rubber vulcanising, metal recovery processes, heavy water production (for nuclear reactors), in oil (“sour crude” refinery) and gas exploration and processing, in rayon or artificial silk manufacture, lithography and photo-engraving, fur-dressing and felt-making plants, slaughter houses, fertiliser cookers, beet sugar factories, analytical chemistry and dye production.

Usual Fatal Dose

·              Exposure to concentrations approaching 250 ppm causes irritation of mucous membranes, conjunctivitis, photo-phobia, lacrimation, corneal opacity, rhinitis, bronchitis, cyanosis, and acute lung injury.

·              At concentrations of 250 to 500 ppm, signs and symptoms include headache, nausea, vomiting, diarrhoea, vertigo, amnesia, dizziness, apnoea, palpitations, tachycardia, hypotension, muscle cramps, weakness, disorientation, and coma.

·              At concentrations of 750 to 1000 ppm, victims may expe-rience abrupt physical collapse or “knock down”. Higher concentrations may also result in respiratory paralysis, asphyxial seizures, and death. The mortality rate is in the range of six per cent.


After absorption, H2S is detoxified in the body to thiosulfate and polysulfides by enzymatic and non-enzymatic oxidation of sulfides and sulfur. This reaction is catalysed by oxyhaemo-globin. As per recent studies, hydrogen sulfide is metabolised by oxidation to sulfate, methylation, and reaction with metal-loproteins (responsible for the most serious toxic effects).

Mode of Action

·              Like cyanide (vide infra), H2S is a cellular poison and inhibits cytochrome oxidase by disrupting electron transport. In fact it is said to be a more powerful inhibitor of cytochrome oxidase than cyanide. The resulting inhibition of oxidative phosphory-lation produces cellular hypoxia and anaerobic metabolism. Anaerobic metabolism further causes lactic acidosis. H2S is also a strong respiratory irritant and reacts with the moisture on the surface of the mucous membrane to form sodium sulfide.

Clinical Features

Acute Exposure:

·              Low-level exposure: keratoconjunctivitis, corneal ulcer-ation (gas eye), rhinitis, bronchitis, pulmonary oedema. Injection of the conjunctivae, seeing coloured halos, ocular pain, corneal bullae, blurred vision and blepha-rospasm may be noted following exposure to 150 to 300 ppm. Olfactory fatigue may occur after 2 to 15 minutes of exposure at 100 ppm. Recovery of smell is slow, depends on the extent of exposure, and may require weeks to months.

·              High-level exposure: headache, vertigo, nystagmus, vomiting, dyspnoea, convulsions, sore throat, cardiac dysrhythmias, and conduction defects. Inhalation expo-sure to 500 ppm for 30 minutes produces sweating, somnolence, weakness, amnesia, malaise, confusion, delirium, hallucinations, nystagmus and coma.

·              Pure gas exposure: Death can result in seconds due to respiratory failure if the gas is inhaled in its pure form. Characteristics of a fatal exposure are rapid collapse, respiratory depression, tremors, blurred vision, cyanosis, seizures and tachycardia.

·              Skin exposure: may result in severe pain, itching, burning, and erythema, especially in moist areas. Cyanosis may be noted.

·              Recovery may be associated with neurological sequelae such as memory failure ( amnestic syndrome), disorientation, delirium, and dementia. There may also be impairment of hearing, vision, and olfaction. Basal ganglia damage results in tremor, ataxia, and muscle rigidity. Some of these effects are irreversible.

Chronic Exposure:

·              Results in headache, weakness, nausea, and weight loss.

·              One report suggests basal ganglia abnormalities— ataxia, dystonia and choreoathetosis.

·              An epidemiological study of Chinese female workers found an increased risk of spontaneous abortions associ-ated with exposure to benzene, gasoline and hydrogen sulfide.


·      Rotten egg odour in the vicinity of the patient.

·      Blackening of copper and silver coins in the patient’s pockets, or darkening of jewellery.

·              Measurement of sulfide ion level in the blood by ion-selec-tive electrode in combination with Conway microdiffusion cells. Levels higher than 0.05 mg/L are associated with toxic effects. Reliable results are obtained only if the analysis is done within 2 hours of exposure, and the sample had been tested without delay, because sulfide concentrations rise with tissue decomposition.

·      Presence of H2S in the air at a scene of poisoning can be detected by exposing a strip of filter paper moistened with lead acetate. It will get blackened.

·      Monitor vital signs. Monitor pulse oximetry and/or arterial blood gases and chest radiograph in patients with respiratory signs or symptoms.

·      Measuring blood sulfide and thiosulfate levels or urinary thio-sulfate levels may be performed to document the exposure but are not useful for emergency treatment. Whole blood sulfide concentration in normal subjects is less than 0.05 mg/L.

·      In fatal cases, confirmation of hydrogen sulfide poisoning can be done by measuring both sulfide and thiosulfate levels in blood.

Clinical (Toxic) Features

·      Respiratory arrest can occur.

·      Mydriasis, urinary retention, and seizures may occur, espe-cially following large doses of mecamylamine. Tremor, hallucinations, and confusion may also follow high dose mecamylamine.


·              Immediate removal of victim from contaminated area to fresh-air area. Rescuers must use self-contained breathing apparatus. Immediate supportive care should be given as most fatalities occur at the scene. Maximum oxygen flow and supportive care may be sufficient treatment without the need to use nitrites. Seizures may have to be controlled with muscle relaxants (i.e. succinylcholine) to complete intubation. Symptomatic patients must be kept under observation for an average of 48 hours, and monitored closely for acute lung injury, dysrhythmias, peripheral neuritis, or some degree of neurological disturbance.

·      High-flow oxygen. Hyperbaric oxygen is said to be benefi-cial.

·      Nitrites are antidotal in action in H2S poisoning. They induce methaemoglobinaemia. Since H2S has greater affinity for methaemoglobin than for cytochrome oxidase, it dissociates from the latter and binds preferentially to the former resulting in the formation of sulfmethaemoglobin. Dose:

o     An amyl nitrite perle is broken and inhaled for 30 seconds every minute until intravenous sodium nitrite can be begun.

o     Sodium nitrite, 10 ml of 3% solution (amounting to 300 mg), is given IV over 4 minutes.

o     Unlike in the case of cyanide poisoning, sodium thio-sulfate is not necessary in hydrogen sulfide poisoning because the body spontaneously detoxifies sulfmethae-moglobin.

·              Many cases of H2S poisoning have been treated success-fully with supportive care and oxygen, without resorting to nitrites.

o     Use maximum oxygen flow.

o     Monitor fluid and electrolyte balance.

o     Watch for development of aspiration pneumonia and pulmonary oedema.

o     Treat convulsions with conventional anticonvulsants. Refractory seizures may have to be managed by succi-nylcholine (with ventilatory support).

o     Treat metabolic acidosis in the usual way.

Autopsy Features

·              Greenish discolouration of grey matter of brain, viscera, and bronchial secretions.

·              Characteristic odour.

·              Pulmonary oedema.

·              Generalised visceral congestion with scattered petechiae.

·              Decomposition is said to be faster in hydrogen sulfide- related death.

Forensic Issues

·              Most cases of poisoning are accidental in nature arising out of industrial or occupational mishaps. Cleaning out sewers replete sometimes be potentially life-threatening.


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