INTRODUCTION

Hydrogen sulfide and sulfur dioxide are two sulfur-based gases that exhibit entirely different toxicological characteristics. Litigation issues involving these two gases are as different as are their disparate toxic effects in humans.

HYDROGEN SULFIDE

Toxicology

Hydrogen sulfide is a highly toxic gas that has caused many fatalities. It exerts its significant toxic effects primarily in two ways: 1. As a central nervous system toxin (neurotoxin), and 2. As a local irritant. Although not considered a toxic effect, very low concentrations of hydrogen sulfide in the air can create a very significant odor nuisance. More than 1000 cases of acute hydrogen sulfide poisoning have been reported over the past five decades. Case fatality rates approximate 5% (Aves, 1929; Ahlborg, 1951; Kleinfeld, et al., 1964; Burnett, et al., 1977; Arnold, et al. 1984; Gregorakos, et al., 1995). Inhaled hydrogen sulfide is very rapidly destroyed by normal detoxification mechanisms and does not accumulate in the body (Haggard, 1921; Evans, 1967).

1. Central nervous system toxicity

When inhaled, hydrogen sulfide is quickly and effectively absorbed into the blood through the lung and immediately transported to the brain where it acts as an inhibitor of a critical respiratory enzyme, cytochrome oxidase (Smith and Gosselin, 1979). This enzyme is necessary for cellular respiration, and when it is inhibited, the brain is deprived of molecular oxygen required for its normal functioning. Cerebral hypoxia is the result.

At air concentrations of about 750 ppm, inhalation of hydrogen sulfide gas can cause immediate collapse and unconsciousness. If exposure is very brief, for example, transitory envelopment by a passing gas cloud, the victim may awaken promptly and experience no adverse effects at all (Beauchamp, et al., 1984; Guidotti, 1994). In industries where hydrogen sulfide exposure is commonplace, for example oil field work, employees often refer to this phenomenon as "knockdown" (Guidotti, 1994). If exposure is prolonged, or air concentrations are high (above 1000-1500 ppm), the unconscious victim may cease breathing (apnea), and will die unless promptly moved to fresh air and given immediate artificial respiration (Haggard and Henderson, 1922). Overall, however, most victims of hydrogen sulfide-induced collapse recover completely (Milby and Baselt, 1999a; Beauchamp, et al., 1984). In a small percentage of victims, primarily those who are very severely poisoned or who are not promptly rescued, prolonged apnea can lead to hypoxic encephalopathy and sequelae ranging from mild neurological deficits to hypoxia-related dementias or death (Freireich, 1946; Hurwitz and Taylor, 1954; Larson, 1964; Kemper, 1966; Matuso, et al., 1979; Adelson and Sunshine, 1986; Deng and Chang, 1987; Tvedt, et al., 1991).

The preponderance of scientific evidence indicates that hydrogen sulfide- induced central neurotoxicity results primarily as a consequence of the ability of blood-borne sulfide to inhibit cytochrome oxidase and interfere with, or diminish, cellular respiration in the brain (Smith and Gosselin, 1979; Riffenstein, et al., 1992). Understanding this mechanism of action is important to both the treating physician and the forensic toxicologist. To the clinician, the critical need for prompt treatment aimed at re-oxygenating the brain becomes undisputable. The forensic toxicologist should be aware that there is no reliable evidence that poisoning by this gas leads to neurotoxic sequelae such as memory loss, concentration problems, ataxia, headaches, or other chronic effects in the absence of clinically significant cerebral hypoxia occurring as a direct consequence of one or more of the following events: unambiguous unconsciousness with apnea, respiratory insufficiency induced by pulmonary edema, or significant airway obstruction (Milby, 1962; Beauchamp, et al., 1984; Milby and Baselt, 1999b).

2. Local irritation

A. Eye irritation.

After several hours of exposure to hydrogen sulfide gas in concentrations of about 50 ppm, or after only a few minutes at higher, neurotoxic air levels, conjunctivitis and keratoconjunctivitis may become clinically apparent (Milby, 1962; Beauchamp, et al.1984). In older literature, this was called "gas eye" (Yant, 1930). The current OSHA PEL of 20 ppm was established to protection against eye irritation in most workers.

B. Pulmonary edema

Unlike sulfur dioxide, hydrogen sulfide is not very soluble in water. For this reason, it is not efficiently removed from the inhaled air by the moist mucous membranes of the upper respiratory tract and is free to penetrate deeply into the lungs. Here it encounters the most sensitive tissues of the lung causing irritation, which may give way to pulmonary edema (Burnett, et al., 1977; Arnold, et al., 1985, Tanaka, et al., 1999). On a practical basis, the more dramatic, life-threatening neurotoxic effects associate with hydrogen sulfide toxicity often overshadow its irritative effects, although occasionally, pulmonary edema can cause serious complications, even death (Kleinfeld, et al., 1964). In consideration of the potential danger for developing pulmonary edema, a person significantly exposed to hydrogen sulfide gas should be under medical observation, preferably under hospital conditions, for at least 24 hours after exposure (Milby, 1962).

3. Odor nuisance

Most people can detect the characteristic rotten-egg smell of hydrogen sulfide gas at very low air concentrations, usually well under 0.1 ppm (Beauchamp, et al., 1984). Short-lived exposures to air levels of this magnitude do not cause physical injury, nor is there any reliable evidence that such exposures induce sensitivity to the gas or to other chemicals. However, under some conditions, especially if exposure is intense or prolonged, the pervasive, foul, rotten-egg odor of hydrogen sulfide can cause transitory headache and sleep disturbances at air concentrations at low as 0.250 -0.300 ppm (Milby and Baselt, 1999a; Haahtela, et al., 1992; PHS, 1964).