Veterinarians are most likely to encounter hydrogen sulfide emanating from concentrated decaying organic matter (eg, septic/sewage ponds/manure handling facilities in intensive animal production facilities, rotting feed stores, carcasses pits, etc). When near sewage ponds, it is particularly important not to disturb the surface of the pond or to cause mixing of the contents, because this will trigger degassing of dissolved hydrogen sulfide.
Hydrogen sulfide is a colorless, flammable, and very rapidly toxic gas. Hydrogen sulfide is slightly heavier than air, tends to accumulate in low-lying, poorly ventilated spaces, and is highly flammable and explosive. It has a characteristic rotten-egg odor that can be sensed at concentrations as low as 0.5 ppb. However, the sensitivity to hydrogen sulfide odor is genetically determined, and a significant proportion of the human population has poor odor detection ability to this gas; additionally, extended exposure (2–15 min at 100 ppm) to hydrogen sulfide results in paralysis of the olfactory nerve, resulting in a loss of ability to detect the gas. Therefore, odor is not a reliable indicator of the presence of hydrogen sulfide and cannot be relied on to provide a warning of hazardous concentrations. The use of hydrogen sulfide monitors and/or testing of breathing air with a Drӓger tube apparatus or similar test method are strongly recommended before entry into any environment where hydrogen sulfide might be present.
Veterinarians are typically exposed to hydrogen sulfide via inhalation. Children are more susceptible because of their high minute volume to weight ratio and higher lung surface area to body weight ratio. Prolonged exposure to hydrogen sulfide is notably irritating to the skin and eyes. Hydrogen sulfide is also a notable mucous membrane and respiratory tract irritant, and the acute and/or delayed (up to 72 hr after exposure) respiratory distress syndromes are common sequela of prolonged inhalation exposure to nonacutely fatal levels of hydrogen sulfide.
Hydrogen sulfide acts by inactivating mitochondrial cytochrome oxidase, resulting in the failure of oxidative metabolism, histotoxic hypoxia, and acute anion-gap metabolic acidosis. Its mode of action resembles that of cyanide. Acute exposure to high concentrations of hydrogen sulfide will result in sudden collapse and death due to central respiratory failure (hydrogen sulfide knock-down effect) caused by its peracute effects on the brain. Signs and symptoms of acute exposure include initial CNS stimulation, nausea, headaches, impaired gait, dizziness, disturbed equilibrium, tremors, convulsions, skin and eye irritation, coma, respiratory paralysis, and death. Many survivors of acute hydrogen sulfide poisoning have hypoxic brain and cardiac injuries. Hypoxic brain damage can be associated with personality changes, memory deficits, disturbances in voluntary muscle movements, and appearance of involuntary movements (extrapyramidal syndromes).
Low concentrations of hydrogen sulfide (~50 ppm) rapidly produce upper respiratory tract irritation, and prolonged exposure can result in pulmonary irritation (cough, shortness of breath, and bronchial or lung hemorrhage, bronchitis, and immediate or delayed pulmonary edema). Cyanosis may be present. Hydrogen sulfide inhalation is associated with cardiac arrhythmias. Nausea and vomiting are also common.
Chronic, repeated, lower-level hydrogen sulfide exposure is associated with hypotension, headache, nausea, loss of appetite, weight loss, ataxia, conjunctivitis, chronic cough, and neuropsychological disorders.
Ill-advised and poorly equipped attempts at rescuing victims from hydrogen sulfide–contaminated hot zones have resulted in large numbers of hydrogen sulfide–associated human casualties. There is currently no effective antidote for hydrogen sulfide poisoning. Resuscitation combined with oxygen is the only known effective approach to treatment. Rescue and treatment of individuals with hydrogen sulfide poisoning is a matter for properly equipped and trained professionals.
Last full review/revision December 2014 by Rhian B. Cope, BVSC, PhD, DABT, ERT, FACTRA