Hydrogen sulfide skin#
Acute exposure to 50–100 ppm H 2S leads to neurological disorders (dizziness, headaches, loss of balance, lack of concentration, recent and long-term memory loss, mood unstableness, irritability, exhilaration, and sleep disturbances), behavior changes (anger, depression, tension, confusion, fatigue, and vigor), respiratory symptoms (apnea, cough, noncardiogenic pulmonary edema, and cyanosis), cardiovascular abnormalities (irregular heart beat or hypotension), eye irritations (conjunctivitis, lacrimation, and photophobia), skin symptoms (itching, dryness, and redness), and general deficits (nausea, libido decrease, gastrointestinal tract upsets, and loss of appetite). Acute exposure to H 2S causes four dose-dependent human responses: hyperpnea, unconsciousness, apnea, and death. The lethal effect of acute exposure to H 2S is at persistent high concentrations (>500 ppm). On the other hand, subchronic exposure of rats to 30 or 80 ppm H 2S results in olfactory neuron loss and basal cell hyperplasia. It was also concluded by experiment on rats that inhalation of H 2S had a severe cytotoxic effect on the nasal epithelium and a severe edematogenic effect on lung parenchyma whereas acute exposure to 400 ppm H 2S induced severe mitochondrial swelling in support cells and olfactory neurons, which progressed to olfactory epithelial necrosis and sloughing. H 2S odor was strongly associated with reports of alteration of daily activities, negative mood states, mucosal irritation, and upper respiratory symptoms. Olfactory deficits (hyposmia) with both a delayed and immediate onset have also been documented following repeated exposures to sublethal doses of H 2S in workers at a refinery construction site. This causes reversible inhibition of aerobic metabolism leading to cellular anoxia. Sulfide binds to many macromolecules, including cytochrome oxidase thereby preventing oxidative phosphorylation.
Hydrogen sulfide free#
Following inhalation, H 2S dissociates into free sulfide and hydrogen ions in the blood circulation. It was reported that exposure to higher H 2S concentration caused severe neurotoxicity, status epilepticus, bronchospasms, and delayed respiratory failure. Human exposure to the toxic effects of H 2S is characteristically dose related and most notably involves the nervous, cardiovascular, and respiratory systems. It is a by-product of numerous industrial processes, including sewage treatment, pulp and paper processing, petroleum and natural gas drilling and refining operations, and rayon textile manufacturing. Hydrogen sulfide (H 2S) is a toxic gas with a characteristic rotten egg odor. Sunlight had a significant role in reduction of ambient air H 2S level. There were no complaints of asthmatic attack upon exposure to low level of H 2S. Inhalation of H 2S produced upper respiratory tract epithelial damage that led to bleeding from nose, pharynx, gum, tongue, trachea, and bronchi. Nasal mucosa was the most vulnerable part to H 2S effect.
Other less frequent presenting symptoms were tongue bleeding, bloody sputum, headache, abdominal colic, pharyngeal soreness, fatigue, and sleepiness. This followed by pharyngeal bleeding, gum bleeding, and bloody saliva (mouth bleeding) which were encountered in five cases for each complaint (14.7 %). The most frequent presenting symptom was nasal bleeding. The presence of H 2S gas was confirmed by valid gas detector devices. Exclusion criteria were the symptoms which experienced with or without H 2S exposure. The complaints should be frequent and relapsed after each gas exposure and disappeared when there was no gas exposure. The inclusion criteria of patients were symptoms related to inhalation of H 2S gas in the oil field. The data were collected by systematic questionnaire about symptoms.
All patients were males with age range of 22–60 years (mean 37 years). Observational study included 34 patients who work at an oil field. To investigate the short-term effects of low-level hydrogen sulfide (H 2S) exposure on oil field workers.
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