Posted By Adrian Watson
Hydrogen sulphide is an irritant gas, and exposure to concentrations between 70 and 700 ppm may irritate the mucous membranes of the eyes and the respiratory tract. Pulmonary oedema or bronchial pneumonia is likely to follow prolonged exposure to concentrations of the order of 250 to 600 ppm. These levels of exposure may cause such symptoms as headache, dizziness, excitement, nausea or GI disturbances, dryness and sensation of pain in the nose, throat, and chest, and coughing.
Among the subacute and chronic effects of exposure to hydrogen sulphide, eye irritation that results in conjunctivitis or “gas eyes” is the most common and, ranging from mild to severe with extent and intensity of exposure, may include itching and smarting, a feeling of sand in the eyes, marked inflammation and swelling, cloudy cornea, and destruction of the epithelial layer and scaling that results in blurring of vision. Exposure to light may increase the painful effect. Atmospheric concentrations above 50 ppm and up to 300 ppm are conducive to this condition.
By far the greatest danger of inhaling of hydrogen sulphide is its acute effects. Whether the effects are acute or subacute and chronic depends on the concentration of the gas in the atmosphere. Death or permanent injury may also occur after very short exposure to small quantities of hydrogen sulphide. It acts directly upon the nervous system and results in paralyzing of respiratory centers. Contact with eyes causes painful conjunctivitis, sensitivity to light, tearing, and clouding of vision. Inhalation of low concentrations causes a runny nose with a sense of smell loss, laboured breathing, and shortness of breath. Direct contact with skin causes pain and redness. Other symptoms of exposure include profuse salivation, nausea, vomiting, diarrhoea, giddiness, headache, dizziness, confusion, rapid breathing, rapid heart beat, sweating, weakness, sudden collapse, unconsciousness, and death due to respiratory paralysis. Deaths occur rapidly on the site. Patients who have vital signs at hospital arrival usually survive, if severe hypoxic encephalopathy is absent. Histopathological evaluation most often reveals changes in the lung, brain, and heart. The thyroid and heart may also be target organs.
Concentrations of 700 ppm and above may result in acute poisoning, and although the gas is an irritant, the systemic effects from absorption of hydrogen sulphide into the bloodstream overshadow the irritant effects. These acute systemic effects result from the action of free hydrogen sulphide in the blood stream and occur whenever the gas is absorbed faster than it can be oxidized to pharmacologically inert compounds, such as thiosulfate or sulphate. Such oxidation occurs rapidly in humans or animals, and even following inhalation exposure to concentrations up to 700 ppm of hydrogen sulphide in the atmosphere, hydrogen sulphide does not appear in the exhaled breath. Relatively massive doses are required to overcome this protective activity of the body. Sodium sulphydrate, (NaHS), solution injected intravenously into dogs rapidly disappears from the circulating blood when a rate equivalent to 0.1 to 0.2 mg of hydrogen sulphide per kilogram of body weight per minute is not exceeded. When the amount absorbed into the bloodstream exceeds that which is readily oxidized, systemic poisoning results. There is a general action on the nervous system, hyperpnoea occurs shortly; and respiratory paralysis may follow immediately. This condition may be reached almost without warning because the originally detected odour of hydrogen sulphide may have disappeared as a result of olfactory fatigue. Unless the victim is removed to fresh air within a very few minutes and breathing is stimulated or induced by artificial respiration, death occurs. Unconsciousness and collapse occur within seconds in high concentrations; for that reason many persons have lost their lives attempting to save victims who collapsed from exposure. In such a case, holding the breath permits a brief stay in the atmosphere, whereas inhaling would cause almost immediate collapse.
Hydrogen sulphide is acutely toxic to humans as evidenced by the numerous reports of individuals fatally poisoned by accidental exposure. According to NIOSH, hydrogen sulphide is a leading cause of sudden death in the workplace. The odour threshold is reported as 25 ppb (0.035 mg/m3). Levels in the 3 to 5 ppm range cause an offensive odour. At levels around 100 ppm, no odour is detectable, because olfactory sensation is lost, which results in loss of warning properties at lethal levels. In reports of acute poisoning, systemic intoxication can result from a single (one to two breaths) massive exposure to concentrations usually greater than 1000 ppm. High levels of hydrogen sulphide inhaled act directly on the respiratory centre, causing respiratory paralysis with consequent asphyxia and subsequent death. At levels between 500 and 1000 ppm, acute effects include symptoms of sudden fatigue, headache, dizziness, intense anxiety, loss of olfactory function, nausea, abrupt loss of consciousness, disturbances of the optic nerves, hypertension, insomnia, mental disturbances, pulmonary oedema, coma, and convulsions and respiratory arrest, followed by cardiac failure and, often, death. Levels estimated at 250 ppm resulted in unconsciousness in three workers after several minutes of exposure. Cardiac effects in acute hydrogen sulphide intoxication have been reported in humans and animals. If exposure is terminated promptly, recovery occurs quickly. However, neurological effects have reportedly persisted in survivors of high-level exposure.
Two case studies noted neuropsychological dysfunction characterized by cognitive impairment, deficits of verbal fluency, disorders of written language, and impairment of various memory, psychomotor, and perceptual abilities in individuals acutely exposed to hydrogen sulphide. The persistent damage that has been observed after hydrogen sulphide exposure is not distinguishable from the effects of systemic anoxia or ischemia of the brain or heart, and no specific hydrogen sulphide chronic systemic toxicity has been defined.