PRINCIPLES OF TOXICOLOGY

106 HEMATOTOXICITY: CHEMICALLY INDUCED TOXICITY OF THE BLOOD
of workers who collapse and died within minutes of entering silos storing silage. Table 4.6 lists
increasing air concentrations of hydrogen sulfide and the effects that may result from exposure at each
level.
The current OSHA acceptable ceiling concentration for hydrogen sulfide is 20 ppm, with maximum
10-min peak concentrations of 50 ppm allowed over an 8 h workshift (29 CFR, Part 1910). The
American Conference of Governmental and Industrial Hygienists recommend a time-weighted average
(TWA) exposure of 10 ppm.
Once absorbed from the lungs, hydrogen sulfide is rapidly metabolized in the blood and liver. A
series of enzymatic and non-enzymatic pathways convert hydrogen sulfide (the sulfide anion) to
thiosulfate and then sulfate, which is eliminated from the body. If a blood sample is drawn shortly after
exposure, elevated blood concentrations of sulfide can be detected. However, in general, blood sulfide
determinations are usually forgotten during an emergency since the immediate concern is to treat the
patient. The delay between exposure and blood sampling is usually too long to determine the blood
sulfide concentration that was responsible for the observed acute effects. Furthermore, blood sulfide
determination is usually considered a specialty analysis that must be conducted by laboratories outside
the hospital.
The term sulfhemoglobin has been used to describe hemoglobin with unique spectral characteristics
distinguishable from simple methemoglobin. Sulfhemoglobin spectral changes were
originally observed when hydrogen sulfide was bubbled through whole blood. The observation
between high concentrations of hydrogen sulfide in the test tube and sulfhemoglobin formation
has led to the misconception that hydrogen sulfide poisoning also produces measurable sulfhemoglobin
(often used as a biomarker of hydrogen sulfide poisoning). However, this is an erroneous
concept since sulfhemoglobin formation requires concentrations of hydrogen sulfide that far
exceed those required to completely shut down oxidative phosphorylation. Thus, sulfhemoglobin
determinations are not useful in verifying toxicity or lethality caused by hydrogen sulfide
exposure.
TABLE 4.6 Dose-Response Relationship for Hydrogen Sulfide
Air Concentrations of Hydrogen
Sulfide (parts per million) Effect
0.022 No odor.
0.025–0.13 Noticeable to minimally detectable odor.
0.3 Distinct odor.
0.77 Generally perceptible.
3–6 Quite noticeable, offensive, moderately intense.
20 OSHA acceptable ceiling level.
20–30 Strong intense odor but not intolerable.
150 Olfactory nerve paralysis and mucous membrane irritation.
200 Less intense odor due to eventual sensory fatigue.
250 Prolonged exposure may cause pulmonary edema. Increasing mucous
membrane irritation.
500 Dizziness over a few minutes to severe central nervous system impairment
and unconsciousness if inhaled for more than a few minutes. Increasing
mucous membrane irritation.
700–1000 Unconsciousness may develop rapidly followed by respiratory paralysis and
death within minutes. Increasing mucous membrane irritation.
5,000 Imminent death.