Page 671 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

636 SECTION | IX Gases, Solvents and Other Industrial Toxicants

VetBooks.ir TABLE 48.2 Dose Thresholds for Hydrogen Sulfide (H 2 S)

Concentration (ppm)
Effect
0.02 Human odor threshold
10 Obvious unpleasant odor 1 mild eye irritation
20 US OSHA PEL 15-min ceiling limit
50 Definite conjuctival irritation
50 100 Mild respiratory irritation
100 Olfactory fatigue
150 200 Olfactory nerve paralysis
250 Prolonged exposure results in pulmonary edema
300 500 Imminent threat to life plus pulmonary edema plus potentially apnea
500 30- to 60-min exposure results in excitement, staggering, unconsciousness, apnea, and respiratory failure
500 1000 Acts primarily as a systemic poison producing unconsciousness and death due to respiratory paralysis
700 Rapid unconsciousness and death if not rescued immediately
5000 Sudden death
Source: Data from Beauchamp, R.O. Jr., Bus, J.S., Popp, J.A., et al., 1984. A critical review of the literature on hydrogen sulfide toxicity. Crit. Rev. Toxicol.
13:25 97.

Toxicokinetics and Toxicodynamics et al., 1984). This results in the classical H 2 S knockdown
H 2 S is rapidly absorbed through the lungs, although effects in humans. Death from H 2 S poisoning is usually
respiratory excretion is minimal (Caravati, 2004; Chou due to respiratory arrest and hypoxia (Caravati, 2004).
et al., 2006). Metabolic detoxification to sulfate within Individuals who survive the initial exposure may subse-
erythrocytes and hepatocyte mitochondria occurs rela- quently die from the effects of pulmonary edema/acute
tively rapidly. Sulfate is primarily eliminated in urine. respiratory distress syndromes.
Approximately 85% of an acutely lethal dose is elimi-
nated per hour. Vulnerable Populations
Fetuses and neonates are assumed to be more vulnerable
Pathophysiology than adults (Caravati, 2004).
The classical pathophysiology is essentially the same as
Clinical Presentation
that for cyanide poisoning, i.e., it produces histotoxic
anoxia (Reiffenstein et al., 1992; Smith, 1997; Milby and The H 2 S knockdown or “one breath means death” phe-
Baselt, 1999; Albin, 2000; Caravati, 2004; Woodall et al., nomenon occurs with exposures greater than 750 ppm and
2005; Chou et al., 2006; Khoshniat, 2008; Oesterhelweg is characterized by apnea, sudden collapse, loss of con-
and Puschel, 2008; Ballerino-Regan and Longmire, 2010). sciousness and death (Reiffenstein et al., 1992; Smith,
H 2 S binds to the ferric moiety of cytochrome c oxidase, 1997; Milby and Baselt, 1999; Albin, 2000; Caravati,
thus disrupting the mitochondrial electron transport chain 2004; Woodall et al., 2005; Chou et al., 2006; Khoshniat,
and blocking of cellular aerobic energy generation. 2008; Oesterhelweg and Puschel, 2008; Ballerino-Regan
Anaerobic metabolism then predominates, resulting in and Longmire, 2010). Individuals may occasionally
lactate accumulation and metabolic acidosis. At lower recover from H 2 S knockdown if exposure ceases,
concentrations, H 2 S is an eye, mucous membrane, and although permanent neurological damage is the usual
respiratory irritant (Caravati, 2004). The respiratory sequel. Acute respiratory distress due to pulmonary edema
effects of H 2 S (initial respiratory stimulation followed by occurs following prolonged exposures to greater than
apnea) are produced by direct central respiratory effects 250 ppm (Caravati, 2004). At lower levels of exposure,
and/or by sulfide stimulation of the chemoreceptors of the upper respiratory and ocular irritation (“gas eye”) effects
carotid body, which results in initial respiratory hypocap- may dominate the clinical picture. Sulfur deposits may be
nia followed by reflex apnea that may be sustained and/or detectable on the eye lashes. Reactive airway disease,
lethal if significant hypocapnia is present (Beauchamp bronchiolitis obliterans, and pulmonary interstitial fibrosis