Recommended therapy includes nitrites, hyperbaric oxygen, and supportive care, but documentation of efficacy is lacking. Because patients with chronic neurological sequelae after acute H2S exposure continue to be reported, we suggest that any survivor of H2S poisoning who presents in coma or who manifests objectively verifiable evidence of neurotoxicity on physical examination or lab testing should undergo baseline and annual neurological and neuropsychological testing for at least five years. This approach could standardize and enhance our knowledge of, and ability to detect, the subtle but permanent alterations of central nervous system function that follow H2S exposure. The acute effects of exposure to H2S are well recognized, but accurate exposure-response data are limited to acutely lethal effects, even in animal studies. Odor followed by olfactory paralysis and keratoconjunctivitis are the characteristics effects of H2S at lower concentrations.
Knockdowns can be acutely fatal as a consequence of respiratory paralysis and cellular anoxia.
Pulmonary edema is also a well-recognized acute effect of H2S toxicity. Human studies of sublethal exposure with satisfactory exposure assessment are almost nonexistent. There are indications, poorly documented at present, of other chronic health problems associated with H2S exposure, including neurotoxicity, cardiac arrhythmia, and chronic eye irritation but apparently not cancer. Rigorous and comprehensive studies in the sour gas industry are difficult, in part because of confounding exposures and uncertain end points. It is not clear whether these processes are similar to those that occur in anoxia.