by Glen Swartwout
Hydrogen sulfide (H2S) is a flammable, colorless gas with a characteristic odor of rotten eggs at concentrations of 0.1 ppm. It is one of the most common air pollutants. It is found in volcanic gasses around fumaroles and around geothermal power plants as well as numerous industrial sources1, especially those involving petrochemicals. Normally, ambient levels are very low, less than 1 ppb. However, workplace exposure to levels over 800 ppm is a leading cause of sudden death. At night, ambient levels are much higher due to cooler air, with studies showing undetectable levels below 200 pptv after 10 or 11 AM, yet 1 to 5 ppbv at night (Tarver, 1997).
The toxicity of H2S is similar to that of cyanide. It blocks the blood’s oxygen carrying capacity, inhibits the respiratory center in the brain and blocks the aerobic metabolism in the cells.
Chronic low level exposure to hydrogen sulfide(H2S) gas from Puna Geothermal here in Hawai’i has recently been linked to neurotoxicity symptoms in 86% of cases, with 71% reporting eye symptoms. A control group in Hilo, 20 miles away, showed only 26% (Morris, 1996, Legator, 1997 and Morris, 1997). The most common CNS symptoms are fatigue, anxiety and sensory effects. ENT symptoms are equally prevalent, affecting 91% of those exposed, with the most common symptom being burning eyes (Legator, 1999).
A panel on H2S at the American Public Health Association meeting in 1997 presented data that show exposure to extremely low concentrations can cause long-term damage to the central nervous system. This damage is considered to be irreversible (Legator, 1997, and Borda, 1997). Symptoms can include deficits in balance, reaction time, dizziness, insomnia and severe fatigue. Other symptoms linked to chronic hydrogen sulfide exposure are altered moods and states of depression and tension as well as changes in brain density, headache, memory loss and decreased smell (Morris, 1996).
H2S can be absorbed through the skin directly from the air, or through the gastrointestinal mucosa from contaminated water. While the main route of absorption of H2S systemically is through the lungs, the corneal and conjunctival epithelium of the eyes recieves the highest concentration exposure. H2S is dispersed widely in the body (Nagata, 1990 and Voight, 1955), with high concentrations distributed to the brain stem (Warenycia, 1989).
The body has three ways to metabolize H2S: (Beauchamp, 1984)
• Oxidation to sulfate (enhanced environmentally with Oxozone or Ozone and physiologically with Ginkgo, Cell Silver, Energessence, Chelation, etc.)
• Methylation (can be enhanced with TMG and SAMe)
• Reaction with metallo- or disulfide- containing proteins (can be competitively inhibited with organic sulfur: MSM, NAC, Reduced Glutathione, Cysteine or Methionine)
The primary toxicity pathway is via deactivation of enzymes. Disulfide bridges are responsible for maintaining the 3-dimensional conformation of enzymes, which is essential to their function of holding a substrate in a specific spatial relationship with the enzymes active site. In particular, H2S interferes with the cytochrome oxidase enzyme which is necessary for cells to utilize oxygen (Smith, 1979).
H2S is excreted via the lungs (Kleinfeld, 1964), but only if the individual is moved to an area with lower concentrations of H2S in the air, or if the ambient level is reduced by oxidation with oxozone or ozone generators. Elimination of sulfates has been shown to take place via the kidneys (Kangas, 1987).
Increased sensitivity and risk with H2S exposure include fetuses and children (Dales, 1989), people with heart disease (Jappinen and Tola, 1990) or asthma (Jappinen et al, 1990), people drinking alcohol (Beck, 1979, and Poda, 1966) and anyone with difficulty metabolizing organosulfides (Mitchell, 1984 and Harris, 1986). H2S toxicity may be additive with mercury, which also binds to disulfide groups. Cataracts were reported among a population chronically exposed to H2S (Legator, 1999), and the crystalline lens of the eye has been found to retain mercury longer than any other tissue. Both of these facts may be due to the lens containing the highest concentration of protein of any body tissue, and thus a high level of disulfide groups.
Beauchamp RO Jr et al, 1984, CRC Crit Rev Toxicol 13:25-96
Beck JF et al, 1979, Toxicol Lett #:311-13
Borda B, 1997, Panel on Hydrogen Sulfide, APHA Annual Meeting, Indianapolis, Indiana
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Harris CM et al, 1986, Lancet I:492-3
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Jappinen P et al, 1990, Br J Ind Med 47:824-8
Kangas J and Savolainen H, 1987, Clin Chim Acta 164:7-10
Kleinfeld M et al, 1964, Ind Med Surg 33:656-600
Legator MS and Singleton C, 1997, Panel on Hydrogen Sulfide, APHA Annual Meeting, Indianapolis, Indiana
Legator, 1999 in peer review
Mitchell SC et al, 1984, Br J Clin Pharm 18:507-21
Morris DL and Legator MS, Hydrogen Sulfide, October 1996, privately circulated draft presentation
Morris J, New alarm over hydrogen sulfide; Researchers document lasting damage to human nervous system. A three-part investigative report, Houston Chronicle, Nov. 1997
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Electrophysiological biofeedback measurements can be utilized to select the most biocompatible approach(es) for your unique physiology.
1 Sources include:
Oil and natural gas production, processing, refining and handling facilities
Pulp and paper mills and paper production facilities
Sewage treatment plants
Hog & livestock operations, slaughterhouses and rendering plants; animal fat and oil processing
Portland cement kilns
Coke ovens and blast furnaces
Coal gassification plants
Geothermal power plants
Sulfur, sulfur products and sulfide production (e.g. carbon disulfide)
Asphalt storage facilities
Breweries and fermentation processes
Metal processing (gold ore, lead ore, lead removal, copper ore sulfidizing and metallurgy)
Barium carbonate and barium salt production
Hydrochloric acid purification
Polysulfide caulking production
Bromide and bromine
Artificial flavor production
Sugar cane and sugar beet processing