Workplace hydrogen sulphide intoxication – What an occupational physician should know

Hydrogen sulphide poisoning remains a recognized but rare cause of morbidity and mortality in the UK and is typically associated with specific high-risk occupational settings such as sewage, waste management, and certain industrial environments. Although exposure is very rare, it is important for physicians – particularly those who work within these industries where the potential for exposure is high – to be aware of potential symptoms, treatments, and the need for workplace monitoring. This article explores the symptoms, pathophysiology, and treatment options available.

Hydrogen sulphide poisoning typically occurs in confined or poorly ventilated environments where the gas is generated or accumulates. Common settings include sewers, wastewater treatment facilities, manure storage tanks, fishing boat cabins, and other sites where organic material decays under anaerobic conditions, such as in the petroleum, maritime, and farming industries. Occupational exposures are most frequently reported, but domestic incidents can also occur because of faulty plumbing or stagnant wastewater in residential settings (Shen et al., 2024).

Acute poisoning events are often associated with maintenance or cleaning activities in these environments, particularly when agitation or disturbance of organic waste leads to sudden gas release. Fatalities have also been reported in open spaces when large volumes of hydrogen sulphide are rapidly released, such as from tanker trucks containing leachate water (Haouzi et al., 2020). Additionally, hydrogen sulphide has been used in suicide attempts, posing a significant risk to first responders.

The impact upon health has been shown to be influenced directly by exposure levels (Austigard, 2024). Research noted that during exposure, short peaks (of less than 1 minute duration) can reach 100 ppm, posing an immediate danger to life and health (IDLH). At levels of 0.13 ppm an odour is detectable; however, this odour warning fails above 100 ppm. While the effects of long-term low-level exposure (<5 ppm) are debated in the literature, it has been noted that at 2 ppm physiological changes occur (increased muscle lactate during exercise) even though this is well below the ceiling value (10 ppm) and the Occupational Exposure Limit (OEL) of 5 ppm (Austigard, 2024). This could indicate that biological effects start at concentrations traditionally considered ‘safe’, reinforcing the need for peak-sensitive monitoring rather than relying solely on Time-Weighted Averages (TWA). The Norwegian Occupational Exposure Limit to hydrogen sulphide is currently 5 ppm (8-hour TWA) with a ceiling value of 10 ppm.

Hydrogen sulphide poisoning occurs primarily through inhalation of hydrogen sulphide (H₂S) gas, which is rapidly absorbed via the lungs. Once in the bloodstream, H₂S dissociates into free sulphide ions that bind with high affinity to metalloproteins, most notably mitochondrial cytochrome c oxidase (complex IV), thereby inhibiting oxidative phosphorylation and cellular aerobic metabolism (Haouzi et al., 2016). This results in cellular hypoxia despite adequate oxygen delivery, leading to lactic acidosis, rapid loss of consciousness, respiratory failure, and potentially death within minutes at high concentrations (Quist and Johnston, 2024).

Hydrogen sulphide intoxication can present with a spectrum of symptoms and signs depending on the concentration and duration of exposure. Knowledge of the exposure history is key in determining early treatment. Early symptoms can include headache, dizziness, nausea, vomiting, fatigue, and a characteristic rotten-egg odour – although olfactory fatigue can rapidly occur at high concentrations, making the odour undetectable (Henretig et al., 2019).

At lower concentrations, H₂S acts as a mucous membrane irritant, causing upper airway irritation and pulmonary injury. Respiratory tract irritation is common, with cough, dyspnoea, chest tightness, and sore throat (Quist and Johnston, 2024). Severe exposures can cause acute lung injury, non-cardiogenic pulmonary oedema, and hypoxemia. At higher concentrations, olfactory paralysis occurs, eliminating the warning odour and increasing the risk of exposure.

Ocular exposure may result in conjunctivitis and corneal ulceration (‘gas eye’). Acute severe poisoning is characterized by sudden collapse (‘knockdown’), coma, seizures, apnoea, and cardiovascular collapse because of electromechanical dissociation of the heart. In severe cases, cardiac arrest may ensue (Oesterhelweg and Püschel, 2008). Survivors may develop long-term neurological sequelae because of direct neuronal toxicity and secondary hypoxic injury, which may include persistent cognitive, motor, or behavioural deficits (Shen et al., 2024).

The diagnosis is largely clinical, based on a history of exposure and characteristic symptoms (sudden loss of consciousness, respiratory distress, mucous membrane irritation, and ‘gas eye’ corneal ulcerations). However, several investigations can be useful to assist in diagnosis and exclude other causes:

• Biological monitoring (blood or urinary thiosulfate): Measurement of blood or urinary thiosulfate is the most reliable biomarker of acute exposure, especially if samples are collected within hours of exposure. Blood or urine hydrogen sulphide is less reliable because of rapid clearance and post-mortem production, but thiosulfate levels can help confirm exposure in both clinical and forensic settings (Wang et al., 2022). Blood thiosulfate concentrations above approximately 4–10 mg/L (0.025–0.648 μmol/mL) and urine thiosulfate concentrations above approximately 0.12–137 mg/L (0.12–2.669 μmol/mL) are considered indicative of hydrogen sulphide poisoning, based on case series and forensic investigations (Kage et al., 1997). In non-fatal cases, urine thiosulfate is typically elevated, with values at least 4–14 times higher than those found in healthy individuals (normal urine thiosulfate is generally <0.03–0.1 μmol/mL, or <2–20 μM). In fatal cases, blood thiosulfate is markedly increased, often exceeding 4 mg/L, and may reach up to 10 mg/L or higher.

• Arterial blood gas analysis: To assess for hypoxemia and metabolic acidosis, which are common in severe poisoning due to inhibition of cellular respiration and resultant lactic acidosis. A normal result does not exclude poisoning.

• Serum lactate: Elevated levels indicate impaired oxidative phosphorylation and are a marker of severity. While higher serum lactate is a marker of more severe hypoxic injury in H2S poisoning, it does not directly quantify the degree of H2S exposure or poisoning severity (Shen et al., 2024).

• Chest imaging (chest X-ray or CT): To evaluate for acute lung injury or pulmonary oedema, which are frequent complications (Shen et al., 2024). A normal result does not exclude poisoning as a diagnosis.

• Neurological imaging (CT or MRI of the brain): In cases with altered mental status or coma, to assess for cerebral oedema or basal ganglia injury, which correlate with severity and prognosis (Tang et al., 2022).

• Electrocardiogram (ECG): To detect arrhythmias or cardiac dysfunction, as hydrogen sulphide can cause direct myocardial depression (Shen et al., 2024).

• Routine laboratory tests: Complete blood count, renal and liver function tests to assess for multi-organ involvement – again a normal result does not exclude poisoning as a diagnosis but is associated with favourable prognostic outcomes.

Direct measurement of hydrogen sulphide in blood is not recommended owing to its volatility and rapid disappearance post-exposure (Wang et al., 2022).

Treatment for hydrogen sulphide poisoning is largely supportive. Key principles are targeted at immediate removal from exposure and aggressive supportive care with airway protection and the administration of 100% oxygen. For severe poisoning with coma, respiratory failure or cardiovascular collapse, nitrite-induced methemoglobinemia (using sodium nitrite) has been used to bind hydrogen sulphide and protect cytochrome oxidase (Stine, 1976). The sodium nitrite converts haemoglobin into methemoglobin, which can bind sulphide ions. This reduces the amount of free sulphide available to inhibit cytochrome c oxidase in mitochondria – the main mechanism of H₂S toxicity. Whilst Sodium Nitrite has been used as an antidote candidate by inducing methemoglobinemia, some centres use Sodium Carbonate/Bicarbonate to correct any metabolic acidosis caused by H₂S toxicity. This is a widely accepted in general management of metabolic acidosis beyond Hydrogen Sulphide poisoning however does not counteract the Hydrogen Sulphide toxicity directly. Both substances operate via different means.

Other therapies remain investigational. Methylene blue has shown benefit in animal models and in some clinical case series for reversing cardiac and neurological toxicity, but its use in humans remains investigational (Shen et al., 2024). Hyperbaric oxygen therapy has been used in some severe cases, but again evidence is limited and it is not standard of care (Shen et al., 2024). Hydroxocobalamin, which can bind hydrogen sulphide, has also been used in severe cases, and may be considered, especially if cyanide poisoning is also suspected (Fujita et al., 2011; Shen et al., 2024). These may be considered in severe poisoning under the care of a hospital physician, but their efficacy remains not well established. Research has found that cobinamide (Brenner, 2010) showed strong potential as a targeted antidote for H₂S poisoning by concurrently reversing mitochondrial inhibition and reducing oxidative damage with superior potency when compared to hydroxocobalamin (Jiang et al., 2016).

In view of the potential exposures and symptoms, workplace areas where exposure is considered to be sufficiently high should have workplace monitoring performed.

Personal alarm equipment should be capable of detecting low concentrations (as low as 1.6 ppm) and providing immediate alerts to workers when hazardous levels are reached. Modern portable monitors and real-time detection systems are effective for this purpose, and their use is considered standard practice for workplace safety surveillance. In addition, biological monitoring (e.g., urinary thiosulfate) may be used in incident investigations but is not routinely recommended for ongoing workplace surveillance (Jones, 2014). Personal alarm equipment should be capable of detecting low concentrations (as low as 1.6 ppm) and providing immediate alerts to workers when hazardous levels are reached. Modern portable monitors and real-time detection systems are effective for this purpose, and their use is considered standard practice for workplace safety surveillance. In addition, biological monitoring (e.g., urinary thiosulfate) may be used in incident investigations but is not routinely recommended for ongoing workplace surveillance (Jones, 2014).

Primary prevention involves engineering controls such as adequate ventilation, gas detection, alarm systems and process modifications to minimize H₂S release. Administrative controls include worker education, training on H₂S hazards, and strict adherence to entry procedures for confined spaces. The use of appropriate PPE, such as self-contained breathing apparatus (SCBA), is essential when entering areas where H₂S may be present.

In summary, physicians should be aware that hydrogen sulphide poisoning is a life-threatening occupational hazard characterized by rapid onset of central nervous system and respiratory depression, often leading to sudden loss of consciousness (‘knockdown’), respiratory arrest, and potentially death. High-risk environments include sewage systems, manure pits, fishing cabins, and any setting with decaying organic matter or industrial processes producing H₂S. Although a rarity within the United Kingdom, this is something that all physicians who work in these industries with exposure should be aware of – extending to the awareness of symptoms and supportive initial treatments.