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Hydrogen sulfide (H2S) is responsible for many incidents of occupational toxic exposure, especially in the petroleum industry. The clinical effects of H2S depend on its concentration and the duration of exposure. H2S is immediately fatal when concentrations are over 500-1000 parts per million (ppm) but exposure to lower concentrations, such as 10-500 ppm, can cause various respiratory symptoms that range from rhinitis to acute respiratory failure. H2S may also affect multiple organs, causing temporary or permanent derangements in the nervous, cardiovascular, renal, hepatic, and hematological systems. We present a case of occupational exposure to H2S leading to multi-organ involvement, acute respiratory failure, organizing pneumonia, and shock resembling acute sepsis. The patient also developed mild obstructive and restrictive pulmonary disease and peripheral neuropathy.
Hydrogen sulfide (H2S) is responsible for many incidents of occupational toxic exposure, especially in the petroleum industry. The clinical effects of H2S depend on its concentration and the duration of exposure. H2S is immediately fatal when concentrations are over 500-1000 parts per million (ppm).
Hence, H2S has been referred to as the “knock down gas” because inhalation of high concentrations can cause immediate loss of consciousness and death.2,3 However, prolonged exposure to lower concentrations, such as 10-500 ppm, can cause various respiratory symptoms that range from rhinitis to acute respiratory failure.
There are many cases of H2S exposure in the agricultural industry4 and their prevalence has increased markedly with the development of porcine confinement facilities.1,5 H2S is the primary chemical hazard of natural gas production.6 We report a severe case of hydrogen sulfide (H2S) intoxication. The patient survived long enough to observe the sequelae of this entity, which can include neuropsychiatric morbidity.
The patient was a 31-year-old male who worked in an oil refinery. He was brought to the emergency department with fever (a temperature of 39.3°C) and respiratory symptoms. He was hypotensive with a blood pressure of 68/40 mm Hg. He reported that he had been welding in a large container used for the storage of sulfur compounds in an open space before the onset of symptoms. No other chemical compounds were used and the container was clean at that time, but there were some unknown fluid residues on the floor. At the beginning of the welding process, white fumes with a “rotten egg” odor emanating from the container. The patient immediately felt dizzy and developed rhinorrhea, teary eyes, nausea, and shortness of breath, chest tightness and cough. These symptoms increased over the following hours followed by hemoptysis. He was seen by first aid providers and was removed from the scene, given oxygen, and was transported to the emergency room. There were no other workers in the same place during the event of the poisoning. He was using his personal protective equipment, including gowns and a mask.
Subsequently, the patient was admitted to the intensive care unit. On examination, he was found to be hypotensive (BP 68/40 mm Hg) and tachypneic (respiratory rate of 26/min). The neck was supple without any lymphadenopathy. A chest examination revealed bilateral rhonchi, but examination of the heart and abdomen found no abnormalities. Neurologically, he was combative and confused initially and became lethargic and obtunded later. There were no skin lesions. Shortly after admission, the patient developed acute respiratory failure requiring mechanical ventilation. Chest radiography (CXR) showed right pleural effusion and consolidation ( ). Initial and subsequent laboratory ( ) revealed signs of ischemic cardiac injury, abnormal coagulation profile, renal insufficiency, and slight leukocytosis. Arterial blood gas showed a pH of 7.34; PCO2: 44 mm Hg; PO2: 77 mm Hg; and oxygen saturation: 95% on an inspired oxygen of 35%. Other laboratory data were as follows: BUN 43 mEq/L, creatinine 2.6 mg/dL, Na 135 mEq/L, K 4.8 mEq/L, Cl− 105 mEq/L, and CO2 19 mEq/L.
Open in a separate windowAs the patient was hypotensive, he was resuscitated with intravenous fluid and vasopressors. Intravenous hydrocortisone was started for chemical pneumonitis, but it was stopped after four days because there were no signs of improvement. Infections were ruled out and empirical broad-spectrum antibiotics were subsequently discontinued. All serological studies were negative, including Mycoplasma, Legionella, and HIV. A thoracentesis revealed an exudative pleural fluid. The gram stain showed many cells, 90% neutrophils, no organisms, and the cultures were negative. Cytology on bronchoalveolar lavage showed a few cells consistent with herpes simplex infection, thought to be a contamination from an upper airway and nasal infection. After several days of supportive care, the patient became hemodynamically stable with improved cardiac function and was extubated successfully.
However, he continued to have a right lower lobe consolidation ( and ) despite appropriate antimicrobial therapy, including acyclovir. Lung biopsy via video-assisted thoracoscopic surgery was performed and showed diffuse alveolar damage with organizing pneumonia. Special stains for herpes viruses were negative. Sections of the lung showed the presence of numerous alveolar spaces lined by reactive pneumocytes type II. Many of the alveolar spaces were filled with an admixture of macrophages, scattered eosinophils, and neutrophils. In addition, several alveoli showed clumps of proliferating fibroblasts admixed with histiocytes and other inflammatory cells, denoting the presence of organizing pneumonia. He was restarted on intravenous hydrocortisone and showed a remarkable response with significant improvement in respiratory symptoms and radiographic findings ( ).
Open in a separate windowOpen in a separate windowOpen in a separate windowAbout 40 days after the incident, spirometery revealed a mild obstruction with an insignificant response to bronchodilators. Lung volume showed mild restriction and the diffusion capacity was at low-normal levels after correction for alveolar volume. The findings were consistent with mixed restrictive and obstructive pulmonary disease. He developed grayish nail-bed discoloration, suggestive of an exposure to a sulfur compound. Neurological evaluation, including an electromyography, revealed evidence of peripheral neuropathy. A follow-up chest x-ray after discharge showed complete resolution of his pulmonary infiltrate.
Hydrogen sulfide (H2S) is the primary chemical hazard of natural gas production.6,7 In a retrospective review from oil and gas industry in Canada revealed 221 cases of H2S exposure from 1969 to 1973, and 173 patients were transported to the hospital; 14 victims (6%) were dead on arrival.8
The findings in this case are consistent with exposure to H2S. There was a history of an odor of rotten eggs emanating from residues in the work site that was suggestive of H2S with related symptoms and clinical findings, as described previously.9–11 H2S is a colorless gas with a characteristic odor.12 However, persistent exposure to air concentrations above 100 ppm produces olfactory fatigue, which impairs the ability to detect the characteristic odor of rotten eggs.12
Following the inhalation accident, the patient developed multi-organ involvement simulating sepsis: acute respiratory failure, obtundation, leucopenia, neutrophilia, abnormal coagulation profile, renal insufficiency, shock, cardiac injury, and reduced cardiac output (an ejection fraction of 30%).9,13 A persistent pulmonary infiltrate proved to be an organizing pneumonia. Organizing pneumonia is characterized by the presence of granulation tissue in the distal air spaces consisting of fibroblasts–myofibroblasts embedded in connective tissue.14 When organizing pneumonia is an associated feature, the term, “bronchiolitis obliterans” is added. Bronchiolitis obliterans organizing pneumonia (BOOP) may follow pulmonary infection, drug toxicity, or may appear in the context of connective tissue diseases or after lung or bone marrow transplantation.15 Cryptogenic organizing pneumonia (COP), the idiopathic form of organizing pneumonia (also known as idiopathic BOOP), is a distinct clinical entity. COP has the predominant features of pneumonia, rather than a primary airway disorder.14 The mainstay of treatment of BOOP is with a corticosteroid resulting in a rapid clinical improvement and clearing of the opacities on chest imaging without significant sequelae.14,16
Injury due to H2S exposure occurs primarily by inhalation. Once absorbed, the compound is distributed in the blood and taken up by the brain, liver, kidney, pancreas, and small intestines. Sulfur compounds are severely irritating to the respiratory tract, leading to rhinorrhea, sneezing, sore throat, wheezing, shortness of breath, chest tightness, hemoptysis, and a feeling of suffocation.1 Sulfur compounds can cause leucopenia and neutropenia,9,13 as well as cardiac injury with elevation of troponin I and creatine kinase.9,10 The mechanism of H2S toxicity is related to inhibition of oxidative phosphorylation, which causes a decrease in the available cellular energy. A phenomenon referred to as “knockdown” was reported in oil field workers to describe a sudden, brief loss of consciousness associated with amnesia, followed by immediate full recovery. This phenomenon usually occurs after short-term exposure to very high concentrations of H2S.17
Various pulmonary complications may follow inhalation injury. In a study of 203 patients with first- to third-degree burns, lung complications developed in 7.8%, leading to adult respiratory distress syndrome (ARDS) in 5.4%.18 Organizing pneumonia may occur following inhalation of toxic fumes and chemicals. These pathological changes are relatively well-known for patients who have been exposed to relatively high concentrations of any slightly water-soluble, toxic, inhaled compound (not unique to H2S) and may represent a spectrum of inhalation concentrations and severity. It is interesting to note that unilateral pulmonary abnormalities occurred in the present case. Similarly, in the study cited above, 36% of the patients had only right lung involvement.18 The presence of leucopenia and neutropenia in the present case is also interesting. In a study of chronic exposure to H2S, the absolute mean numbers of white blood cells, lymphocytes, and neutrophils were seen to be significantly decreased in the exposed group compared with the control.19
The patient showed evidence of neuropathy on follow-up visits. Annual neurological and neuropsychological testing for at least five years is recommended for patients with H2S exposure because of the potential chronic neurological sequelae.20 Other reports suggest that temporary memory loss, attention deficits, blunted affect, permanent retrograde amnesia, executive function deficits, slowing in central information processing, and planning deficits may occur in such patients.17
The mainstay of therapy is supportive care. There are reports that suggest early administration of hyperbaric oxygen, amyl nitrite, and sodium nitrite may be beneficial.2,21 Amyl nitrite-induced methemoglobinemia is due to competitive binding of the hydrosulfide anion. This effect presumably reactivates and protects cytochrome oxidase.22 However, one of the toxic effects of H2S is the inhibition of cytochrome oxidase. Nitrites produce methemoglobin which has a higher affinity for H2S than for cytochrome oxidase. The resulting sulfmethemoglobin eventually returns to hemoglobin. Hyperbaric oxygen in a few case reports and animal studies may work as an adjuvant treatment in patients with persistent neurological injury or oxygenation defects.23 Therapeutic red cell exchange may also be used to treat H2S toxicity similar to the treatment of aniline, arsine, chloramines, carbon monoxide, cyanide, and, methemoglobinemia.24
As H2S is a potential problem in the transport and storage of crude oil, preventive measures are extremely important in preventing lethal exposure to hydrogen sulfide toxicity. Personal protective equipment should include safety glasses, respiratory protection or equipment, and long-sleeved shirts.25 In addition, limiting exposure at the work place and the use of a personal safety gas detector may aid in the protection of employees working with potential gas exposure. In a retrospective analysis, 77 of the 80 deaths were thought to be potentially preventable with the use of an H2S alarm or portable meters.26
In conclusion, we report a case of an occupational exposure to H2S leading to acute respiratory failure, multi-organ involvement simulating sepsis, and organizing pneumonia. The diagnosis of hydrogen sulfide poisoning relies mainly on the clinical presentation and exposure. H2S poisoning may lead to persistent neuropsychiatric morbidity. The treatment remains generally supportive and amyl nitrites may be beneficial.
The authors wish to acknowledge the use of Saudi Aramco Medical Services Organization (SAMSO) facilities for the data and study, which resulted in this paper. Opinions expressed in this article are those of the authors and not necessarily of SAMSO.
CAS number: 7783–06–4
NIOSH REL: 10 ppm (15 mg/m3) 10-minute CEILING
Current OSHA PEL: 20 ppm CEILING, 50 ppm 10-minute MAXIMUM PEAK
1989 OSHA PEL: 10 ppm (14 mg/m3) TWA, 15 ppm (21 mg/m3) STEL
1993-1994 ACGIH TLV: 10 ppm (14 mg/m3) TWA, 15 ppm (21 mg/m3) STEL
Description of Substance: Colorless gas with a strong odor of rotten eggs.
LEL: 4.0% (10% LEL, 4,000 ppm)
Original (SCP) IDLH: 300 ppm
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Basis for original (SCP) IDLH: The chosen IDLH is based on the statements by Patty [1963] that 170 to 300 ppm is the maximum concentration that can be endured for 1 hour without serious consequences; 400 to 700 ppm is dangerous after exposure of 0.5 to 1 hour [Henderson and Haggard 1943]. AIHA [1963] reported that 400 to 700 ppm caused loss of consciousness and possible death in 0.5 to 1 hour [MCA 1950].
Existing short-term exposure guidelines: 1991 American Industrial Hygiene Association (AIHA) Emergency Response Planning Guidelines (ERPGs):
ERPG-1: 0.1 ppm (60-minute)
ERPG-2: 30 ppm (60-minute)
ERPG-3: 100 ppm (60-minute)
National Research Council [NRC 1985] Emergency Exposure Guidance Levels (EEGLs):
10-minute EEGL: 50 ppm
24-hour EEGL: 10 ppm
ACUTE TOXICITY DATA:
Lethal concentration data:
Species Reference LC50(ppm)
LCLo(ppm)
Time Adjusted 0.5-hrLC (CF*)
Derived value Rat Back et al. 1972 713 ----- 1 hr 977 ppm (1.37) 98 ppm Mouse Back et al. 1972 673 ----- 1 hr 922 ppm (1.37) 92 ppm Human Lefaux 1968 ----- 600 30 min 600 ppm (1.0) 60 ppm Mouse MacEwen and Vernot 1972 634 ----- 1 hr 869 ppm (1.37) 87 ppm Human Tab Biol Per 1933 ----- 800 5 min 354 ppm (0.44) 35 ppm Rat Tansey et al. 1981 444 ----- 4 hr 1,141 ppm (2.57) 114 ppm*Note: Conversion factor (CF) was determined with "n" = 2.2 [ten Berge et al. 1986].
Other human data: It has been reported that 170 to 300 ppm is the maximum concentration that can be endured for 1 hour without serious consequences [Henderson and Haggard 1943] and that olfactory fatigue occurs at 100 ppm [Poda 1966]. It has also been reported that 50 to 100 ppm causes mild conjunctivitis and respiratory irritation after 1 hour; 500 to 700 ppm may be dangerous in 0.5 to 1 hour; 700 to 1,000 ppm results in rapid unconsciousness, cessation of respiration, and death; and 1,000 to 2,000 ppm results in unconsciousness, cessation of respiration, and death in a few minutes [Yant 1930].
Revised IDLH: 100 ppm
Basis for revised IDLH: The revised IDLH for hydrogen sulfide is 100 ppm based on acute inhalation toxicity data in humans [Henderson and Haggard 1943; Poda 1966; Yant 1930] and animals [Back et al. 1972; MacEwen and Vernot 1972; Tansey et al. 1981].
REFERENCES:
1. AIHA [1963]. Hydrogen sulfide. In: Hygienic guide series. Am Ind Hyg Assoc J 24:92-94.
2. Back KC, Thomas AA, MacEwen JD [1972]. Reclassification of materials listed as transportation health hazards. Wright-Patterson Air Force Base, OH: 6570th Aerospace Medical Research Laboratory, Report No. TSA-20-72-3, pp. A-220 to A-221.
3. Henderson Y, Haggard HW [1943]. Noxious gases. 2nd ed. New York, NY: Reinhold Publishing Corporation, p. 245.
4. Lefaux R [1968]. Practical toxicology of plastics. Cleveland, OH: Chemical Rubber Co., p. 207.
5. MacEwen JD, Vernot EH [1972]. Toxic Hazards Research Unit annual report: 1972. Wright-Patterson Air Force Base, OH: Air Force Systems Command, Aerospace Medical Division, Aerospace Medical Research Laboratory Report, AMRL-TR-72-62.
6. MCA [1968]. Chemical safety data sheet SD-36: properties and essential information for safe handling and use of hydrogen sulfide. Washington, DC: Manufacturing Chemists Association, pp. 1-13.
7. NRC [1985]. Emergency and continuous exposure guidance levels for selected airborne contaminants. Vol. 4. Washington, DC: National Academy Press, Committee on Toxicology, Board on Toxicology and Environmental Health Hazards, Commission on Life Sciences, National Research Council, pp. 55-68.
8. Patty FA, ed. [1963]. Industrial hygiene and toxicology. 2nd rev. ed. Vol. II. Toxicology. New York, NY: Interscience Publishers, Inc., p. 899.
9. Poda GA [1966]. Hydrogen sulfide can be handled safety. Arch Environ Health 12:795-800.
10. Tab Biol Per [1933]; 3:231 (in German).
11. Tansey MF, Kendall FM, Fantasia J, Landin WE, Oberly R [1981]. Acute and subchronic toxicity studies of rats exposed to vapors of methyl mercaptan and other reduced sulfur compounds. J Toxicol Environ Health 8:71-88.
12. ten Berge WF, Zwart A, Appelman LM [1986]. Concentration-time mortality response relationship of irritant and systematically acting vapours and gases. J Haz Mat 13:301-309.
13. Yant WP [1930]. Hydrogen sulfide in industry: occurrence, effects and treatment. Am J Public Health 20:598-608.
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