4
Hydrogen Sulfide1
Acute Exposure Guideline Levels

PREFACE

Under the authority of the Federal Advisory Committee Act (FACA) P.L. 92-463 of 1972, the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances (NAC/AEGL Committee) has been established to identify, review, and interpret relevant toxicologic and other scientific data and develop AEGLs for high-priority, acutely toxic chemicals.

AEGLs represent threshold exposure limits for the general public and are applicable to emergency exposure periods ranging from 10 minutes (min) to 8 hours (h). Three levels—AEGL-1, AEGL-2, and AEGL—are developed for each of five exposure periods (10 and 30 min and 1, 4, and 8 h) and are distinguished by varying degrees of severity of toxic effects. The three AEGLs have been defined as follows:


AEGL-1 is the airborne concentration (expressed as parts per million [ppm] or milligrams per cubic meter [mg/m3]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory

1

This document was prepared by the AEGL Development Team composed of Cheryl Bast (Oak Ridge National Laboratory) and Chemical Manager Steve Barbee (National Advisory Committee [NAC] on Acute Exposure Guideline Levels for Hazardous Substances). The NAC reviewed and revised the document and AEGLs as deemed necessary. Both the document and the AEGL values were then reviewed by the National Research Council (NRC) Committee on Acute Exposure Guideline Levels. The NRC committee has concluded that the AEGLs developed in this document are scientifically valid conclusions based on the data reviewed by the NRC and are consistent with the NRC guideline reports (NRC 1993, 2001).



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4 Hydrogen Sulfide1 Acute Exposure Guideline Levels PREFACE Under the authority of the Federal Advisory Committee Act (FACA) P.L. 92-463 of 1972, the National Advisory Committee for Acute Exposure Guide- line Levels for Hazardous Substances (NAC/AEGL Committee) has been estab- lished to identify, review, and interpret relevant toxicologic and other scientific data and develop AEGLs for high-priority, acutely toxic chemicals. AEGLs represent threshold exposure limits for the general public and are applicable to emergency exposure periods ranging from 10 minutes (min) to 8 hours (h). Three levels—AEGL-1, AEGL-2, and AEGL—are developed for each of five exposure periods (10 and 30 min and 1, 4, and 8 h) and are distin- guished by varying degrees of severity of toxic effects. The three AEGLs have been defined as follows: AEGL-1 is the airborne concentration (expressed as parts per million [ppm] or milligrams per cubic meter [mg/m3]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory 1 This document was prepared by the AEGL Development Team composed of Cheryl Bast (Oak Ridge National Laboratory) and Chemical Manager Steve Barbee (National Advisory Committee [NAC] on Acute Exposure Guideline Levels for Hazardous Sub- stances). The NAC reviewed and revised the document and AEGLs as deemed necessary. Both the document and the AEGL values were then reviewed by the National Research Council (NRC) Committee on Acute Exposure Guideline Levels. The NRC committee has concluded that the AEGLs developed in this document are scientifically valid conclu- sions based on the data reviewed by the NRC and are consistent with the NRC guideline reports (NRC 1993, 2001). 173

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174 Acute Exposure Guideline Levels effects. However, the effects are not disabling and are transient and reversible upon cessation of exposure. AEGL-2 is the airborne concentration (expressed as ppm or mg/m3) of a substance above which it is predicted that the general population, including sus- ceptible individuals, could experience irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape. AEGL-3 is the airborne concentration (expressed as ppm or mg/m3) of a substance above which it is predicted that the general population, including sus- ceptible individuals, could experience life-threatening health effects or death. Airborne concentrations below the AEGL-1 represent exposure levels that could produce mild and progressively increasing but transient and nondisabling odor, taste, and sensory irritation or certain asymptomatic, nonsensory effects. With increasing airborne concentrations above each AEGL, there is a progres- sive increase in the likelihood of occurrence and the severity of effects described for each corresponding AEGL. Although the AEGLs represent threshold levels for the general public, including susceptible subpopulations, such as infants, children, the elderly, persons with asthma, and those with other illnesses, it is recognized that individuals, subject to idiosyncratic responses, could experience the effects described at concentrations below the corresponding AEGL. SUMMARY Hydrogen sulfide (H2S) is a colorless, flammable gas at ambient tempera- ture and pressure. It has an odor similar to that of rotten eggs and is both an irri- tant and an asphyxiant. The air odor threshold ranges between 0.008 and 0.13 ppm, and olfactory fatigue may occur at 100 ppm. Paralysis of the olfactory nerve has been reported at 150 ppm (Beauchamp et al. 1984). Mean ambient air concentrations for H2S range between 0.00071 and 0.066 ppm. Controlled human data were used to derive AEGL-1 values. Three of 10 volunteers with asthma exposed to H2S at 2 ppm for 30 min complained of headache and 8 of 10 experienced nonsignificant increased airway resistance (Jappinen et al. 1990). As there were no clinical symptoms of respiratory diffi- culty and there were no significant changes in forced vital capacity (FVC) or forced expiratory volume in 1 second (FEV1), the AEGL-1 was based exclu- sively on increased complaints of headache in the three volunteers (Jappinen et al. 1990). A modifying factor of 3 was applied to account for the wide variabil- ity in complaints associated with the foul odor of H2S and the shallow concen- tration response at the relatively low concentrations that are consistent with definition of the AEGL-1. The 30-min experimental value was scaled to the 10- min and 1-, 4-, and 8-h time points by using the concentration-exposure duration relationship, C4.4 × t = k, where C is concentration, t is time, and k is a constant. The exponent 4.4 was derived from rat lethality data ranging from 10-min to 6-h exposures.

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175 Hydrogen Sulfide The level of distinct odor awareness (LOA) for H2S is 0.01 ppm (see Ap- pendix C for LOA derivation). The LOA represents the concentration above which it is predicted that more than half the exposed population will experience at least a distinct odor intensity, and about 10% of the population will experi- ence a strong odor intensity. The LOA should help chemical emergency re- sponders in assessing public awareness of the exposure due to odor perception. Thus, the derived AEGL-1 values are considered to have warning properties. The AEGL-2 was based on the induction of perivascular edema in rats ex- posed to H2S at 200 ppm for 4 h (Green et al. 1991; Khan et al. 1991). An uncer- tainty factor of 3 was applied as rat and mouse data suggest little interspecies variability. An intraspecies uncertainty factor of 3 was applied to account for sensitive individuals. The intraspecies uncertainty factor of 3 is considered suf- ficient because applying the default uncertainty factor of 10 would result in a total uncertainty factor of 30, which would yield AEGL-2 values inconsistent with the total database for H2S. AEGL-2 values derived with larger uncertainty factors are essentially identical to or below the 10-ppm concentration causing no adverse health effects in humans exercising to exhaustion for up to 30 min (Bhambhani and Singh 1991; Bhambhani et al. 1994, 1996a,b, 1997). Therefore, the total uncertainty factor applied in the derivation of AEGL-2 is 10. The 4-h experimental value was then scaled to the 10- and 30-min and 1- and 8-h time points, using C4.4 × t = k. The exponent 4.4 was derived from empirical rat le- thality data ranging from 10-min to 6-h exposures. The AEGL-3 was based on the highest concentration causing no mortality in the rat after a 1-h exposure (504 ppm) (MacEwen and Vernot 1972). An un- certainty factor of 3 was used to extrapolate from animals to humans as rat and mouse data suggest little interspecies variability. An uncertainty factor of 3 was applied to account for sensitive individuals. The intraspecies uncertainty factor of 3 is considered sufficient because applying the default uncertainty factor re- sults in AEGL-3 values inconsistent with the data. AEGL-3 values derived with larger uncertainty factors were equal to or less than twice the concentration that failed to produce adverse health effects in humans exercising to exhaustion for up to 30 min (Bhambhani and Singh 1991; Bhambhani et al. 1994, 1996a,b, 1997). Increased mortality or irreversible medical conditions consistent with the definition of AEGL-3 are unlikely at such concentrations. Therefore, the total uncertainty factor is 10. The value was then scaled to the 10- and 30 min and 1-, 4-, and 8-h time points, using C4.4 × t = k. The exponent 4.4 was derived from rat lethality data ranging from 10-min to 6-h exposures. The AEGL values are listed in Table 4-1. 1. INTRODUCTION Hydrogen sulfide is a colorless, flammable gas at ambient temperature and pressure (NIOSH 1977). The National Fire Protection Association (NFPA 1974) placed H2S in the highest flammability classification. Precautions against fire

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176 Acute Exposure Guideline Levels and explosion must be exercised to maintain airborne H2S below 0.43%. It has an odor similar to that of rotten eggs and it is both an irritant and an asphyxiant. The odor threshold is between 0.008 and 0.13 ppm, and olfactory fatigue, result- ing in a lack of detection of odor, may occur at 100 ppm. Paralysis of the olfac- tory nerve has been reported at 150 ppm (Beauchamp et al. 1984). Mean ambi- ent air concentrations in the United States range between 0.00071 and 0.066 ppm (NRC 1977; Graedel et al. 1986; Warneck 1988). Approximately 90% of the H2S in the atmosphere occurs from natural sources. Hydrogen sulfide arises through bacterial reduction of sulfates and or- ganic sulfur-containing compounds. It is emitted from crude oil, stagnant or pol- luted water, sewers, and manure or coal pits with low oxygen content. A small amount of H2S is emitted from volcanoes, vents, mudpots, and similar geologic formations (ATSDR 2006). Hydrogen sulfide is synthesized commercially for use in rayon manufac- turing, as an agricultural disinfectant, and as an additive in lubricants. It is also used as an intermediate in sulfuric acid and inorganic sulfide manufacturing and it is a by-product of pulp and paper manufacturing (Jaakkola et al. 1990) and geothermal operations (Kage et al. 1998); it is present in “sour” crude petroleum (NIOSH 1977; Guidotti 1994), roofing tar (Hoidal et al. 1986), natural gas, and shale oil (Ahlborg 1951; Kilburn 1993). Hydrogen sulfide has been manufac- tured in ton quantities for use in production of heavy water and as a moderator in nuclear reactors (NRC 1977). In 1997, it was manufactured in the United States by three companies at five sites (ATSDR 1999). Most H2S is made and used captively or transported by pipeline. As of 2007, total domestic commercial production in the United States exceeded 1.1 × 106 tons/year (Kroshwitz and Seidel 2007). The physicochemical properties of H2S are presented in Table 4-2. TABLE 4-1 Summary of AEGL Values for Hydrogen Sulfide End Point Classification 10 min 30 min 1h 4h 8h (Reference) AEGL-1 0.75 ppm 0.60 ppm 0.51 ppm 0.36 ppm 0.33 ppm Headache in (Nondisabling) (1.05 (0.84 (0.71 (0.50 (0.46 humans with mg/m3) mg/m3) mg/m3) mg/m3) mg/m3) asthma (Jappinen et al. 1990) AEGL-2 41 ppm 32 ppm 27 ppm 20 ppm 17 ppm Perivascular (Disabling) (59 (45 (39 (28 (24 edema in rats mg/m3) mg/m3) mg/m3) mg/m3) mg/m3) (Green et al. 1991; Khan et al. 1991) AEGL-3 76 ppm 59 ppm 50 ppm 37 ppm 31 ppm Highest (106 mg/m3)(85 (Lethality) (71 (52 (44 concentration mg/m3) mg/m3) mg/m3) mg/m3) causing no mortality in the rat after a 1-h exposure (MacEwen and Vernot 1972)

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177 Hydrogen Sulfide TABLE 4-2 Chemical and Physical Data for Hydrogen Sulfide Parameter Data Reference Common name Hydrogen sulfide ATSDR 2006 Synonyms Hydrosulfuric acid, stink damp, ATSDR 2006 sulfur hydride, sulfurated hydrogen, dihydrogen monosulfide, sewer gas, swamp gas, rotten-egg gas CAS registry number 7783-06-4 ATSDR 2006 Chemical formula H2S ATSDR 2006 Molecular weight 34.08 ATSDR 2006 Physical state Colorless gas ATSDR 2006 Melting, boiling, and −85.49°C, −60.33°C, and 26°C ATSDR 2006 flash points Density 1.5392 grams/liter at 0°C ATSDR 2006 Density in air 1.192 ATSDR 2006 Solubility 1 gram in 242 milliliters of water at 20°C; ATSDR 2006 soluble in alcohol, ether, glycerol, gasoline, kerosene, crude oil, carbon disulfide Vapor pressure 15,600 mmHg at 25°C ATSDR 2006 3 Conversion factors in air 1 ppm = 1.4 mg/m AIHA 2000 1 mg/m3 = 0.7 ppm 2. HUMAN TOXICITY DATA 2.1. Acute Lethality According to U.S. Occupational Safety and Health Administration re- cords, there were 80 fatalities in 57 H2S incidents from 1984 to 1994 (Fuller and Suruda 2000). Nineteen deaths and 36 H2S-induced injuries occurred among people attempting to rescue victims overcome by the gas. The clinical toxicology of H2S has been reviewed (Smith and Gosselin 1979; Gosselin et al. 1984; Reiffenstein et al. 1992). Literature accounts of hu- man fatalities after inhalation of H2S are abundant; however, exposure concen- trations and durations in these accidents are generally not rigorously defined. Vapor concentrations on the order of 500 to 1,000 ppm or more are usually fatal within minutes (API 1948; Ahlborg 1951; Reiffenstein et al. 1992). Most fatali- ties occur in confined spaces (sewers, animal processing plants, manure tanks) and result from respiratory failure, initially presenting with respiratory insuffi- ciency, noncardiogenic pulmonary edema, coma, or cyanosis. In many cases,

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178 Acute Exposure Guideline Levels people lose consciousness after only one or two breaths, termed “slaughterhouse sledgehammer” (ATSDR 2006). Osbern and Crapo (1981) reported a typical, unfortunate accident involving an underground liquid manure storage pit. A farmer drained the liquid manure to a depth of 45 cm and entered the pit to re- trieve a lid that a cow had kicked into the tank. The farmer was overcome within a few minutes, as were three men who attempted to rescue him. Three of the men lapsed into unconsciousness and died before reaching the hospital. Autopsy showed massive liquid manure pulmonary aspiration in two individuals and fulminant pulmonary edema without manure aspiration in the third. “Increased heart-blood sulfide levels” indicated significant H2S exposure. The clinical course of the surviving patient was complicated by hemodynamic instability, respiratory distress syndrome, and pulmonary infection. Air samples taken a week after the accident detected H2S at 76 ppm; however, pit air concentrations were likely higher at the time of exposure because of temperature and manure concentration. Two workers collapsed and died within 45 min after entering a sewer manhole (NIOSH 1991). A concentration of 200 ppm was measured in sewer air 6 days after the accident. In another accident, a worker at a poultry-processing plant died after exposure to an estimated H2S concentration of 2,000 to 4,000 ppm for an estimated 15 to 20 min (Breysse 1961). Pulmonary, intracranial, and cerebral edema and cyanosis were observed at autopsy. Hsu et al. (1987) reported 10 cases of accidental H2S poisoning. The H2S concentration was 429 ppm 4 h after the accident. Five victims died at the site of exposure. Four lost consciousness within 2 to 20 min of the accident and fell into a deep coma for approximately 48 h, regaining consciousness only after extensive hyperbaric oxygen therapy. Electrocardiograms indicated T-wave changes in all five survivors and changes in the P-wave in the patient remaining in the coma for 2 days. By day 9 after the accident, the electroencephalograms (EEGs) were essentially normal in four victims, while the P-wave returned to normal on day 21 and the T-wave returned to normal on day 36 in the most se- verely poisoned patient. On day 3, blood urea nitrogen increased to 39.2 milli- grams per deciliter and remained above normal through day 13, while serum glutamic pyruvic transaminase activity remained increased through day 8. No pulmonary edema or long-term neurologic abnormalities were identified. Autopsy of H2S victims often reveals pulmonary edema (Adelson and Sunshine 1966; Winek et al. 1968) and petechial hemorrhage into the lungs and brain along with gray-green cyanosis or a purple-to-green cast to the cerebral cortex, viscera, and blood (Freireich 1946; Breysse 1961; Adelson and Sunshine 1966). Postmortem formation of sulfhemoglobin contributes to these discolora- tions. Pulmonary edema is not always associated with death in H2S-induced cen- tral respiratory arrest inasmuch as very high (1,000 ppm) exposures induce prompt unconsciousness, apnea, and anoxic convulsions with risus sardonicus and opisthotonos (Hurwitz and Taylor 1954). If victims are promptly evacuated, recovery can be rapid. It is at lower “but nevertheless fatal” exposure concentra-

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179 Hydrogen Sulfide tions where the development of pulmonary and other systemic signs of H2S in- toxication are permitted (Gosselin et al. 1984). 2.2. Nonlethal Toxicity 2.2.1. Case Reports Albuminuria and hematuria (Osbern and Crapo 1981), brain stem and cor- tical damage (Hurwitz and Taylor 1954), neurasthenia, amnesia, and other psy- chic disorders and difficulties with equilibrium to frank tremor can afflict survi- vors of acute H2S intoxication. People acutely exposed to lower but nonfatal concentrations commonly experience lacrimation, photophobia, corneal opacity, tachypnea, dyspnea, tracheobronchitis (with elevated risk for broncho- pneumonia), gastrointestinal distress (nausea, vomiting, diarrhea), arrhythmias, and palpitations, but these changes generally resolve promptly upon evacuation to fresh air. Patients can be left with a residual cough, hyposmia, dysosmia, or phantosmia (Kilburn and Warshaw 1995; Hirsch and Zavala 1999). At much higher concentrations, recovery from coma can be relatively rapid, and the clini- cal course is usually complete but slow in those patients who do not die. Artifi- cial respiration is appropriate in victims with depressed or absent breathing, as are supportive steps to combat development of pulmonary edema (Gosselin et al. 1984). Oxygen is indicated in those patients with acute respiratory distress syn- drome (Smith 1996). Case reports concerning nonlethal H2S effects in humans are abundant; however, exposure parameters, concentration, and duration are often either un- reported or only estimated. Symptoms of acute H2S exposure include ocular and respiratory tract irritation, nausea, headaches, loss of equilibrium, memory loss, olfactory paralysis, loss of consciousness, tremors, and convulsions (ATSDR 2006). Among tunnel, rayon, and sewer workers exposed for several hours to days, keratoconjunctivitis (“gas eye”) is commonplace (Vanhoorne et al. 1995). This condition is characterized by tearing, burning, and scratchy irritation of the cornea and conjunctivae, and the symptoms generally resolve without interven- tion or sequelae after cessation of exposure (Grant 1974). The threshold for ocu- lar irritation by H2S alone has been reported as 10 to 20 ppm (WHO 1981), but accounts of eye pain, burning, and photophobia in the presence of related sul- fides put the threshold at no more than 6 ppm (Vanhoorne et al. 1995). Parra et al. (1991) reported cases of 14 workers likely poisoned with H2S from toilet facilities. The toilets were connected to a manure pit without a si- phon. Workers complained of eye, nose, and throat irritation; nausea; dizziness; vomiting; and dyspnea. (One worker died a few hours after hospital admission. Hemorrhagic bronchitis and asphyxia were identified at autopsy.) Most workers recovered uneventfully; however, after a symptom-free period of 3 weeks, one worker reported dyspnea, chest tightness, and hemoptysis. A mild, bilateral, interstitial fibrosis was found on a chest X-ray and pulmonary function tests

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180 Acute Exposure Guideline Levels showed mild restrictive pulmonary disease. Five months after the accident, the patient was asymptomatic except for residual exertion dyspnea. Six patients were examined 5 to 10 years after accidental exposures to un- known concentrations of H2S (Tvedt et al. 1991a,b). They had been unconscious for 5 to 20 min in the H2S atmospheres. Persistent neurologic symptoms in- cluded impaired vision, memory loss, decreased motor function, tremors, ataxia, abnormal learning and retention, and slight cerebral atrophy. One patient was severely demented. In another report, 37 workers (ages 24 to 50 years) were accidentally ex- posed to an undetermined concentration of H2S while drilling a pit to lay the foundation for a municipal sewage pumping station (Snyder et al. 1995). Symp- toms included headache, dizziness, breathlessness, cough, burning discomfort in the chest, throat and eye irritation, nausea, and vomiting. Most workers recov- ered uneventfully; however, one worker died and another remained in a coma for 5 days. The comatose patient was aggressively treated with hyperbaric oxy- gen. He was discharged from the hospital on day 15 with slow speech, impaired attention span, easy distractibility, isolated retrograde amnesia, decreased ability to communicate, impaired visual memory, and poor retention of new informa- tion. His condition was unchanged at 12 and 18 months after exposure. Numer- ous other reports of permanent or persistent neurologic effects after exposure to H2S have been published (Wasch et al. 1989; Kilburn 1993; Kilburn and War- shaw 1995; Kilburn 1997). As with the other case studies, these reports lack definitive exposure parameters. In May and June 1964, a H2S emission from an industrial landfill in Terre Haute, Indiana, resulted in nearby residents complaining about odor and nausea, loss of sleep, shortness of breath, and headache (HEW 1964). Samples collected from five sites around the city indicated H2S concentrations ranging from <2 to >300 parts per billion (ppb); however, the observations are confounded by con- current exposure to other malodorous pollutants such as smoke from burning garbage and sulfurous coal tar. Data summarized and experiments carried out by the State of California Department of Health Services showed that the geometric mean of the threshold odor concentration for H2S was approximately 0.008 ppm (Amoore 1985). It was also stated that, as a provisional rule, it appears that when an unpleasant odor reaches approximately 5 times its odor threshold con- centration, the mean concentration for complaints of odor annoyance is attained. Factors responsible for odor annoyance were categorized as the unpleasant odor sensation itself, effects on social life, and instigation of headache or nausea (Amoore 1985). In another report, Ruth (1986) reported an odor threshold range of 0.0005 to 0.01 ppm and listed an irritating H2S concentration of 10 ppm. Members of the Mobile Monitoring Team, Source Sampling Team, Tech- nical Support Team, and Systems Planning and Implementation Team of the Texas Natural Resource Conservation Commission (TNRCC) conducted a mo- bile laboratory sampling trip to the Corpus Christi, Texas, area from January 31 to February 6, 1998 (TNRCC 1998). The mean H2S concentration downwind

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181 Hydrogen Sulfide from an oil refinery was 0.09 ppm (30-min downwind average). The six staff members complained of persistent objectionable odors, eye and throat irritation, headache, and nausea. In most cases, the symptoms subsided within a few hours after leaving the sampling site; throat irritation persisted in two staff members through the following day. The exposure duration was about 5 h. Sulfur dioxide, benzene, methyl t-butyl ether, and toluene were also detected, and it is possible that these chemicals contributed to the complaints. Some authors hypothesize that odors, such as the rotten egg smell associ- ated with H2S, may trigger asthma attacks; however, quantitative data support- ing this premise are limited, and it is uncertain whether a toxicologic mechanism or stress-induced anxiety is involved. It is clear that objectionable odor can af- fect behavior; individuals detecting odors may stay indoors, temporarily leave the neighborhood or area, complain to officials, or consider a change of resi- dence (Shusterman 1992). Many objectionable odor sources have been impli- cated in asthma attacks, annoyance, and behavioral modifications and include municipal odors (landfills, sewage treatment plants), agricultural odors (com- posting, feed lots), industrial odors (pulp mills, refineries, hazardous waste sites) (Shusterman 1992), and household (perfumes, flowers, cleaning products, food/cooking odors) and bodily odors (Stein and Ottenberg 1958; Herbert et al. 1967). Bruvold et al. (1983) used a survey questionnaire to determine whether people living downwind of two sewage treatment plants in California (Pacifica and Novato) detected H2Sodor and experienced odor annoyance more frequently than people living in two control communities. Hydrogen sulfide concentrations in the test communities ranged from 1 to 6 ppb. Odor was reported by 49 of 54 respondents in Pacifica compared with 4 of 54 respondents in the Pacifica con- trol community and 19 of 50 respondents in Novato compared with 1 of 48 re- spondents from the Novato control community. When respondents were asked to rate odor annoyance on a scale of 0 (no annoyance) to 10 (extreme annoy- ance), the following median annoyance scores were obtained: Pacifica affected = 7.9, Pacifica control = 5.5, Novato affected = 4.3, Novato control = 1.0. One in nine respondents in the “exposed” neighborhoods also reported that they or a family member had been made sick by the odors; however, only 1% of this group sought medical attention and no odor-induced asthma was reported in these communities. Rossi et al. (1993) examined the association between emergency room vis- its for asthma attacks and weather (temperature, humidity, barometric pressure, rainfall), levels of air pollutants (nitrogen dioxide, sulfur dioxide, H2S, total sus- pended particles), and pollen counts. No association was found between pollen counts and weather conditions, except for an inverse correlation with tempera- ture. The most significant correlation was found for nitrogen dioxide, with lesser correlations for sulfur dioxide, H2S, and total suspended particles. The daily mean H2S concentration was 0.0022 ppm (range 0 to 0.02 ppm) and the daily maximum was 0.01 ppm (range 0 to 0.12 ppm). Only the relationship between nitrogen dioxide and asthma attacks held after controlling for temperature.

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182 Acute Exposure Guideline Levels Stein and Ottenberg (1958) interviewed 25 hospitalized patients with asthma to determine whether odors precipitated asthma attacks. Initially, the patients were asked what would precipitate an asthma attack. If odors were not mentioned, they were then specifically asked about odors. The responses were then analyzed for the “character of the odorous substance.” Twenty-two of the 25 subjects stated that odors precipitated attacks; of these 22, about half initially specified odor as a precipitating factor, whereas the others included odor only when prompted by the interviewer. The most common (74%) “precipitating odors” were categorized as “cleanliness/uncleanliness and included urine, sweat, feces, disinfectant, bleach, camphor, dirty/musty, smoke, sulfur, chemicals, paint, horses, and barn; followed by “romantic odors” (21%) including perfume, spring, and flowers; and foods (5%) such as bacon, onion, and garlic. In another report, Herbert et al. (1967) administered questionnaires to two groups of pa- tients with asthma, one from a psychiatric hospital and one from a general hospi- tal, to determine whether odors precipitated asthma attacks. Approximately 80% of patients reported that odor triggered asthma attacks, with the most common triggers being paint, tobacco fumes, wood smoke, household odors, and paraffin. The authors concluded that emotional distress could precipitate an asthmatic attack. There was no clear differentiation between the two groups of patients. In both the Stein and Ottenberg (1958) and Herbert et al. (1967) reports, the results are compromised by possible undefined concurrent exposures, no measure of repeatability, and the fact that neither the patient nor the interviewer was blinded to the inquiry. 2.2.2. Epidemiologic Studies Jappinen et al. (1990) studied a cohort of 26 male pulp mill workers (mean age 40.3 years, range 22 to 60 years) to assess the possible effects of H2S on respiratory function. The workers experienced daily exposure to H2S “usually below the maximum permitted concentration of 10 ppm.” Bronchial responsive- ness, FVC, and FEV1 were measured after at least 1 day off work and at the end of a workday. No significant changes in respiratory function or bronchial re- sponsiveness were observed at the end of the workday compared with control values. Studies of communities located near pulp mills have reported increased incidences of respiratory system symptoms (irritation and cough) and central nervous system symptoms (headaches, migraine) (Partti-Pellinin et al. 1996). Although H2S concentrations have been reported in these studies, the popula- tions were also exposed to relatively high concentrations of other malodorous sulfur compounds such as sulfur dioxide and mercaptans. Thus, it is difficult to define a concentration-response relationship for H2S from these reports. Hessel et al. (1997) studied a group of 175 oil and gas workers (mean age 35 years) in Alberta, Canada. Hydrogen sulfide exposure concentrations were not available; therefore, exposure groups were determined by questioning the

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183 Hydrogen Sulfide workers about “exposures strong enough to cause symptoms,” “exposures that resulted in loss of consciousness (knockdown),” or no exposure. Exposures strong enough to cause symptoms were reported by 51 workers, “knockdown” was reported by 14 workers, and 110 workers reported no exposure. Exposures strong enough to cause symptoms were not associated with lower spirometric values. Knockdowns were not associated with lower spirometric values but were associated with shortness of breath while hurrying on the level or up a slight hill, wheezing with chest tightness, and wheezing attacks. In another study, 21 swine confinement facility owner-operators were tested by spirometry immediately before and after a 4-h work period (Donham et al. 1984). The confinement workers had statistically significant (p < 0.05) reduc- tions in pulmonary flow rates ranging from 3.3% to 11.9% mean forced expira- tory flow (FEF) after the 4-h work period. The report states that the work envi- ronment was sampled for particulates and gases during the exposure period and that evidence suggested a concentration-response relationship between carbon dioxide and H2S exposure and lung function decrements. However, these moni- toring data were not presented in the study report. 2.2.3. Experimental Studies Jappinen et al. (1990) exposed a group of 10 people with asthma (3 men age 33 to 50 years and 7 women age 31 to 61 years) to H2S at 2 ppm for 30 min. The subjects had been diagnosed with bronchial asthma for 1 to 13 years and were under medical supervision. Severe asthma patients were excluded from the protocol. Two volunteers were exposed simultaneously in a 10-m3 sealed tile- walled exposure chamber with an oxygen flow of 2 liters (L)/min. Hydrogen sulfide concentration was monitored continuously with a sulfur dioxide analyzer connected to a converter that transformed H2S into sulfur dioxide at 840°C. The H2S was supplied to the chamber from laminated plastic bags through plastic tubing. All asthma subjects complained of an unpleasant odor and nasal and pharyngeal dryness at the initiation of exposure. Three of the 10 complained of headache after exposure. There were no significant effects on FVC, FEV1, or FEF values after exposure to H2S. Airway resistance (Raw) value was slightly decreased in two and increased in eight subjects. The range of Raw differences was –5.95% to +137.78%, with an average increase of 26.3%; no accompanying clinical symptoms were observed. The range of specific airway conductance (SGaw) differences was –57.7% to +30%, with an average decrease of 8.4%. These effects were not statistically significant; however, in two subjects, changes were greater than 30% in both Raw and SGaw. Bhambhani and Singh (1991) exposed 16 healthy male volunteers (age 25.2 ± 5.5 years) to H2S at 0, 0.5, 2.0, or 5.0 ppm during graded cycle exercise performed to exhaustion (up to 16 min). Filtered air from a pressurized cylinder was passed through a stainless steel humidifying chamber at a flow rate of 50 L/min. After humidification, the air was mixed with H2S at 1,000 ppm in nitro-

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208 Acute Exposure Guideline Levels Jaakkola, J.J., V. Vilkka, O. Marttila, P. Jappinen, and T. Haahtela. 1990. The South Karelia Air Pollution Study. The effects of malodorous sulfur compounds from pulp mills on respiratory and other symptoms. Am. Rev. Respir. Dis. 142(6 Pt 1):1344-1350. Jappinen, P., V. Vilkka, O. Marttila, and T. Haahtela. 1990. Exposure to hydrogen sulfide and respiratory function. Br. J. Ind. Med. 47(12):824-828. Kage, S., T. Nagata, K. Takekawa, K. Kimura, K. Kudo, and T. Imamura. 1992. The usefulness of thiosulfate as an indicator of hydrogen sulfide poisoning in forensic toxicological examination: A study with animal experiments. Jpn. J. Forensic Toxicol. 10(3):223-227. Kage, S., S. Ito, T. Kishida, K. Kudo, and N. Ikeda. 1998. A fatal case of hydrogen sul- fide poisoning in a geothermal power plant. J. Forensic Sci. 43(4):908-910. Khan, A.A., M.M. Schuler, M.G. Prior, S. Yong, R.W. Coppock, L.Z. Florence, and L.E. Lillie. 1990. Effects of hydrogen sulfide exposure on lung mitochondrial respira- tory chain enzymes in rats. Toxicol. Appl. Pharmacol. 103(3):482-490. Khan, A.A., S. Yong, M.G. Prior, and L.E. Lillie. 1991. Cytotoxic effects of hydrogen sulfide on pulmonary alveolar macrophages in rats. J. Toxicol. Environ. Health 33(1):57-64. Khan, A.A., R.W. Coppock, M.M. Schuler, and M.G. Prior. 1998. Biochemical effects of repeated exposures to low and moderate concentrations of hydrogen sulfide in Fischer 344 rats. Inhal. Toxicol. 10(11):1037-1044. Kilburn, K.H. 1993. Case report: Profound neurobehavioral deficits in an oil field worker overcome by hydrogen sulfide. Am. J. Med. Sci. 306(5):301-305. Kilburn, K.H. 1997. Exposure to reduced sulfur gases impairs neurobehavioral function. South. Med. J. 90(10):997-1006. Kilburn, K.H., and R.H. Warshaw. 1995. Hydrogen sulfide and reduced-sulfur gases adversely affect neurophysiological functions. Toxicol. Ind. Health 11(2):185-197. Kimura, H. 2000. Hydrogen sulfide induces cyclic AMP and modulates NMDA receptor. Biochem. Biophys. Res. Commun. 267(1):129-133. Kohno, M., E. Tanaka, T. Nakamura, N. Shimojo, and S. Misawa. 1991. Influence of the short-term inhalation of hydrogen sulfide in rats [in Japanese]. Eisei Kagaku 37(2):103-106. Kośmider, S., E. Rogala, and A. Pacholek. 1966. Studies on the toxic action mechanism of hydrogen sulfide [in German]. Int. Arch. Arbeitsmed. 22(1):60-76. Kroshwitz, J.I., and A. Seidel. 2007. Sulfur compounds. Pp. 621-701 in Kirk-Othmer Encyclopedia of Chemical Technology, 5th Ed., Vol. 23, A. Seidel, ed. Hoboken, NJ: Wiley-Interscience. Lefebvre, M., D. Yee, D. Fritz, and M.G. Prior. 1991. Objective measures of ocular irrita- tion as a consequence of hydrogen sulfide exposure. Vet. Hum. Toxicol. 33(6):564-566. Lopez, A., M. Prior, S. Yong, M. Albassam, and L.E. Lillie. 1987. Biochemical and cy- tologic alterations in the respiratory tract of rats exposed for 4 hours to hydrogen sulfide. Fundam. Appl. Toxicol. 9(4):753-762. Lopez, A., M. Prior, S. Yong, L. Lillie, and M. Lefebvre. 1988. Nasal lesions in rats ex- posed to hydrogen sulfide for 4 hours. Am. J. Vet. Res. 49(7):1107-1111. Lopez, A., M.G. Prior, R.J. Reiffenstein, and L.R. Goodwin. 1989. Peracute toxic effects of inhaled hydrogen sulfide and injected sodium hydrosulfide on the lungs of rats. Fundam. Appl. Toxicol. 12(2):367-373.

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210 Acute Exposure Guideline Levels NRC (National Research Council). 2001. Standing Operating Procedures for Developing Acute Exposure Guideline Levels for Hazardous Chemicals. Washington, DC: Na- tional Academy Press. NRC (National Research Council). 2002. Review of Submarine Escape Action Levels for Selected Chemicals. Washington, DC: National Academy Press. Osbern, L.N., and R.O. Crapo. 1981. Dung lung: A report of toxic exposure to liquid manure. Ann. Intern. Med. 95(3):312-314. Parra, O., E. Monso, M. Gallego, and J. Morera. 1991. Inhalation of hydrogen sulfide: A case of subacute manifestations and long term sequelae. Br. J. Ind. Med. 48(4):286-287. Partti-Pellinen, K., O. Marttilla, V. Vilkka, J.J. Jaakkola, P. Jäppinen, and T. Haahtela. 1996. The South Karelia Air Pollution Study: Effects of low-level exposure to malodorous sulfur compounds on symptoms. Arch. Environ. Health 51(4):315- 320. Poda, G.A. 1966. Hydrogen sulfide can be handled safely. Arch. Environ. Health 12(6):795-800. Prior, M.G., A.K. Sharma, S. Yong, and A. Lopez. 1988. Concentration-time interactions in hydrogen sulfide toxicity in rats. Can. J. Vet. Res. 52(3):375-379. Reiffenstein, R.J., W.C. Hulbert, and S.H. Roth. 1992. Toxicology of hydrogen sulfide. Ann. Rev. Pharmacol. Toxicol. 32:109-134. Rossi, O.V., V.L. Kinnula, J. Tienari, and E. Huhti. 1993. Association of severe asthma attacks with weather, pollen, and air pollutants. Thorax 48(3):244-248. Ruijten, M.W.M.M., R. van Doorn, and A.P. van Harreveld. 2009. Assessment of Odour Annoyance in Chemical Emergency Management. RIVM Report 609200001/2009. RIVM, Bithoven, The Netherlands: RIVM [online]. Available: http://www.rivm.nl/ bibliotheek/rapporten/609200001.pdf [accessed April 12, 2010]. Ruth, J.H. 1986. Odor thresholds and irritation levels of several chemical substances: A review. Am. Ind. Hyg. Assoc. J. 47(3):A142-A151. Saillenfait, A.M., P. Bonnet, and J. de Ceaurriz. 1989. Effects of inhalation exposure to carbon disulfide and its combination with hydrogen sulfide on embryonal and fetal development in rats. Toxicol. Lett. 48(1):57-66. Shusterman, D. 1992. Critical review: The health significance of environmental odor pollution. Arch. Environ. Health 47(1):76-87. Skrajny, B., R.S. Hannah, and S.H. Roth. 1992. Low concentrations of hydrogen sulfide alter monoamine levels in the developing rat central nervous system. Can. J. Physiol. Pharmacol. 70(11):1515-1518. Skrajny, B., R.J. Reiffenstein, R.S. Sainsbury, and S.H. Roth. 1996. Effects of repeated exposures of hydrogen sulfide on rat hippocampal EEG. Toxicol. Lett. 84(1):43- 53. Smith, L., H. Kruszyna, and R.P. Smith. 1977. The effect of methemoglobin on the inhi- bition of cytochrome c oxidase by cyanide, sulfide or azide. Biochem. Pharmacol. 26(23):2247-2250. Smith, R.P. 1996. Toxic responses of the blood. Pp. 335-354 in Cassarett and Doull’s Toxicology: The Basic Science of Poisons, 5th Ed., C.D. Klaassen, ed. New York: Macmillan. Smith, R.P., and R.E. Gosselin. 1979. Hydrogen sulfide poisoning. J. Occup. Med. 21(2):93-97. Snyder, J.W., E.F. Safir, G.P. Summerville, and R.A. Middleberg. 1995. Occupational fatality and persistent neurological sequelae after mass exposure to hydrogen sul- fide. Am. J. Emerg. Med. 13(2):199-203.

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211 Hydrogen Sulfide Stein, M., and P. Ottenberg. 1958. Role of odors in asthma. Psychosom. Med. 20(1):60- 65. Swedish Work Environment Authority. 2005. Occupational Exposure Limit Value and Measures against Air Contaminants. AFS 2005:17 [online]. Available: http://ww w.av.se/dokument/inenglish/legislations/eng0517.pdf [accessed Apr. 6, 2010]. Tansy, M.F., F.M. Kendall, J. Fantasia, W.E. Landin, R. Oberly, and W. Sherman. 1981. Acute and subchronic toxicity studies of rats exposed to vapors of methyl mercap- tan and other reduced-sulfur compounds. J. Toxicol. Environ. Health 8(1-2):71-88. ten Berge, W.F., A. Zwart, and L.M. Appelman. 1986. Concentration-time mortality response relationship of irritant and systemically acting vapors and gases. J. Haz- ard. Mater. 13(3):301-309. TNRCC (Texas Natural Resources Conservation Commission). 1998. Real-Time Gas Chromatography and Composite Sampling, Sulfur Dioxide, Hydrogen Sulfide, and Impinger Sampling, Corpus Christi Mobile Laboratory Trip, January 31- February 6, 1998. Memorandum from Tim Doty to JoAnn Wiersma. April 20, 1998. Tvedt, B., K. Skyberg, O. Aaserud, A. Hobbesland, and T. Mathiesen. 1991a. Brain dam- age caused by hydrogen sulfide: A follow-up study of six patients. Am. J. Ind. Med. 20(1):91-101. Tvedt, B., A. Edlund, K. Skyberg, and O. Forberg. 1991b. Delayed neuropsychiatric se- quelae after acute hydrogen sulfide poisoning: Affection of motor function, mem- ory, vision, and hearing. Acta. Neurol. Scand. 84(4):348-351. Vanhoorne, M., A. de Rouck, and D. de Bacquer. 1995. Epidemiological study of eye irritation by hydrogen sulfide and/or carbon disulphide exposure in viscose rayon workers. Ann. Occup. Hyg. 39(3):307-315. Warenycia, M.W., L.R. Goodwin, D.M. Francom, F.P. Dieken, S.B. Kombian, and R.J. Reiffenstein. 1990. Dithiothreitol liberates non-acid labile sulfide from brain tissue of H2S-poisoned animals. Arch. Toxicol. 64(8):650-655. Warneck, P. 1988. Chemistry of the Natural Atmosphere. San Diego: Academic Press. Wasch, H.H., W.J. Estrin, P. Yip, R. Bowler, and J.E. Cone. 1989. Prolongation of the P- 300 latency associated with hydrogen sulfide exposure. Arch. Neurol. 46(8):902- 904. Wever, R., B.F. van Gelder, and D.V. Dervartanian. 1975. Biochemical and biophysical studies on cytochrome c oxidase. XX. Reaction with sulphide. Biochim. Biophys. Acta 387(2):189-193. WHO (World Health Organization). 1981. Hydrogen Sulfide. Environmental Health Cri- teria 19. Geneva: WHO [online]. Available: http://www.inchem.org/documents/eh c/ehc/ehc019.htm [accessed Apr. 15, 2010]. Williams, V.R., and H.B. Williams. 1967. Pp. 138 in Basic Physical Chemistry for the Life Sciences. San Francisco: W.H. Freeman. Winek, C.L., W.D. Collom, and C.H. Wecht. 1968. Death from hydrogen sulfide fumes. Lancet 1(7551):1096. Xu, X., S.I. Cho, M. Sammel, L. You, S. Cui, Y. Huang, G. Ma, C. Padungtod, L. Poth- ier, T. Niu, D. Christiani, T. Smith, L. Ryan, and L. Wang. 1998. Association of petrochemical exposure with spontaneous abortion. Occup. Environ. Med. 55(1): 31-36. Zwart, A., J.H.E. Arts, J.M. Klokman-Houweling, and E.D. Schoen. 1990. Determination of concentration-time-mortality relationships to replace LC50 values. Inhal. Toxi- col. 2(2):105-117.

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212 Acute Exposure Guideline Levels APPENDIX A TIME-SCALING CALCULATIONS FOR HYDROGEN SULFIDE Derivation of AEGL-1 Key study: Jappinen et al. 1990 Toxicity end point: Headache in human asthma subjects C4.4 × t = k Scaling: (2 ppm)4.4 × 0.5 h = 10.27 ppm-h Modifying factor: 3, wide variability in complaints associated with the foul odor of H2S and the shallow concentration response at the relatively low concentrations that are consistent with definition of the AEGL-1 Calculations: C4.4 × 0.167 h = 10.27 ppm-h 10-min AEGL-1: C4.4 = 61.5 ppm C = 2.6 ppm 10-min AEGL-1 = 2.6/3 = 0.75 ppm C4.4 × 0.5 h = 10.27 ppm-h 30-min AEGL-1: C4.4 = 20.54 ppm C = 2.00 ppm 30-min AEGL-1 = 2.0/3 = 0.60 ppm C4.4 × 1 h = 10.27 ppm-h 1-h AEGL-1: C4.4 = 10.27 ppm C = 1.71 ppm 1-h AEGL-1 = 1.7/3 = 0.51 ppm C4.4 × 4 h = 10.27 ppm-h 4-h AEGL-1: C4.4 = 2.57 ppm C = 1.28 ppm 4-h AEGL-1 =1.28/3 = 0.36 ppm C4.4 × 8 h = 10.27 ppm-h 8-h AEGL-1: C4.4 = 1.28 ppm C = 1.06 ppm 8-h AEGL-1 = 1.06/3 = 0.33 ppm

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213 Hydrogen Sulfide Derivation of AEGL-2 Key studies: Green et al. 1991; Khan et al. 1991 Toxicity end points: Minor perivascular edema present and significant increase in protein and LDH in lung lavage fluid. C4.4 × t = k Scaling: (200 ppm)4.4 × 4 h =4.31 × 1010 ppm-h Uncertainty factors: 3 for interspecies variability 3 for intraspecies variability Calculations: C4.4 × 0.167 h = 4.31 × 1010 ppm-h 10-min AEGL-2: C4.4 = 2.58 × 1011 ppm C = 414.4 ppm 10-min AEGL-2 = 414.4/10 = 41.4 ppm C4.4 × 0.5 h = 4.31 × 1010 ppm-h 30-min AEGL-2: C4.4 = 8.62 × 1010 ppm C = 322.2 ppm 30-min AEGL-2 = 322.2/10 = 32.2 ppm C4.4 × 1 hr = 4.31 ×1010 ppm-h 1-h AEGL-2: C4.4 =4.31 × 1010 ppm C = 274 ppm 1-h AEGL-2 =274/10 = 27.4 ppm C4.4 × 4 hr = 4.31 × 1010 ppm-h 4-h AEGL-2: C4.4 = 1.08 ×1010 ppm C = 199.9 ppm 4-h AEGL-2 =199.9/10 = 19.9 ppm C4.4 × 8 h =4.31 × 1010 ppm-h 8-h AEGL-2: C4.4 = 5.39 × 109 ppm C = 170.6 ppm 8-h AEGL-2 =170.6/10 = 17.1 ppm

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214 Acute Exposure Guideline Levels Derivation of AEGL-3 Key study: MacEwen and Vernot 1972 Toxicity end point: Highest concentration causing no death after a 1-h exposure in rats C4.4 × t = k Scaling: (504 ppm)4.4 × 1 h = 6.06 × 1011 ppm-h Uncertainty factors: 3 for interspecies variability 3 for intraspecies variability Calculations: C4.4 × 0.167 h = 6.06 × 1011 ppm-h 10-min AEGL-3: C4.4 = 3.63 × 1012 ppm C = 759.8 ppm 10-min AEGL-3 = 759.8/10 = 75.9 ppm C4.4 × 0.5 h = 6.06 ×1011 ppm-h 30-min AEGL-3: C4.4 = 1.21 × 1012 ppm C = 590.8 ppm 30-min AEGL-3 = 590.8/10 = 59.1 ppm C4.4 × 1 h = 6.06 × 1011 ppm-h 1-h AEGL-3: C4.4 = 6.06 × 1011 ppm C = 503.9 ppm 1-h AEGL-3 =503.9/10 = 50.4 ppm C4.4 × 4 h = 6.06 × 1011 ppm-h 4-h AEGL-3: C4.4 = 1.52 × 1011 ppm C = 366.7 ppm 4-h AEGL-3 =366.7/10 = 36.7 ppm C4.4 × 8 hr = 6.06 × 1011 ppm-h 8-h AEGL-3: C4.4 = 7.58 × 1010 ppm C = 312.8 ppm 8-h AEGL-3 = 312.8/10 = 31.3 ppm

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215 Hydrogen Sulfide APPENDIX B ACUTE EXPOSURE GUIDELINES FOR HYDROGEN SULFIDE Derivation Summary for Hydrogen Sulfide AEGL-1 VALUES 10 min 30 min 1h 4h 8h 0.75 ppm 0.60 ppm 0.51 ppm 0.36 ppm 0.33 ppm Key Reference: Jappinen, P., V. Vilkka, O. Marttila, P. Jappinen, and T. Haahtela. 1990. Exposure to hydrogen sulfide and respiratory function. Br. J. Ind. Med. 47(12):824-828. Test Species/Strain/Number: Human/10 asthma patients Exposure Route/Concentrations/Durations: Inhalation/2 ppm /30 min Effects: Odor and pharyngeal dryness at the beginning of exposure; headache (3/10); increased Raw (significant in 2/10) with no accompanying clinical signs or lung function effects End Point/Concentration/Rationale: headache/2 ppm Uncertainty Factors/Rationale: Interspecies 1: subjects were human Modifying Factor: 3 to account for the wide variability in complaints associated with the foul odor of H2S and the shallow concentration response at the relatively low concentrations that are consistent with definition of the AEGL-1 Animal to Human Dosimetric Adjustment: NA Time-Scaling: Cn × t = k, where n = 4.4; value derived from rat lethality data ranging from 10 min to 6 h. Data point used for AEGL-1 derivation was 30 min. Other time points were based on extrapolation. Data Quality and Research Needs: These values are supported by the fact that no adverse effects were observed in healthy humans exposed to H2S at 5 ppm for 30 min or 10 ppm for 15 min while exercising to exhaustion (Bhambhani and Singh 1991; Bhambhani et al. 1994, 1996a,b). Using these concentrations and applying an uncertainty factor of 10 for sensitive human subpopulations, the following AEGL-1 values would be obtained: 0.64, 0.50, 0.43, 0.31, and 0.26 ppm for the 10- and 30-min and 1-, 4-, and 8-h time points, respectively, for the 5-ppm exposure for 30 min; and 1.1, 0.85, 0.73, 0.53, and 0.45 ppm for the 10- and 30-min and 1-, 4-, and 8-h time points, respectively, for the 10-ppm exposure for 15 min. These values suggest that the proposed AEGL-1 values are protective.

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216 Acute Exposure Guideline Levels AEGL-2 VALUES 10 min 30 min 1h 4h 8h 41 ppm 32 ppm 27 ppm 20 ppm 17 ppm Key References: Green, F.H., S. Schurch, G.T. DeSanctis, J.A. Wallace, S. Cheng, and M. Prior. 1991. Effects of hydrogen sulfide exposure on surface properties of lung surfactant. J. Appl. Physiol. 70(5):1943-1949. Khan, A.A., S. Yong, M.G. Prior, and L.E. Lillie. 1991. Cytotoxic effects of hydrogen sulfide on pulmonary alveolar macrophages in rats. J. Toxicol. Environ. Health 33(1):57-64. Test Species/Strain/Number: (1) Rat/F344/6 males; (2) Rat/F344/6 males Exposure Route/Concentrations/Durations: Inhalation/0, 200, or 300 ppm/4 h; Inhalation/0, 50, 200, or 400 ppm/4 h Effects: 200 ppm: No adverse clinical signs or gross lung pathology, increased protein and LDH in lavage fluid 300 ppm: Clinical signs during exposure, increased protein and LDH in lavage fluid, lung atelectasis, and edema 50 and 200 ppm: No effect on viability of pulmonary alveolar macrophages 300 ppm: Decreased viability of pulmonary alveolar macrophages (200 ppm for 4 h was determinant for AEGL-2) End Point/Concentration/Rationale: (1) No-effect level for gross lung pathology, minor perivascular edema, increased protein and LDH in lung lavage fluid. (2) No-effect level for pulmonary alveolar macrophage viability/200 ppm Uncertainty Factors/Rationale: Interspecies 3: rat and mouse data suggest little interspecies variability Intraspecies 3: The intraspecies uncertainty factor of 3 is considered sufficient because application of the default uncertainty factor of 10 would result in a total uncertainty factor of 30, which would yield AEGL-2 values inconsistent with the total database. AEGL-2 values derived with a total uncertainty factor of 30 would be 14 ppm for 10 min, 11 ppm for 30 min, 9.0 ppm for 1 h, 6.7 ppm for 4 h, and 5.7 ppm for 8 h, values essentially identical to or below the 10-ppm concentration causing no effects in humans exercising to exhaustion (Bhambhani and Singh 1991; Bhambhani et al. 1994, 1996a,b, 1997). Total Uncertainty Factor: 10. The total adjustment is 10 because each of the factors of 3 represents a logarithmic mean (3.16) of 10; therefore, 3.16 × 3.16 = 10. Modifying Factor: NA Animal to Human Dosimetric Adjustment: NA Time-Scaling: Cn × t = k, where n = 4.4; value derived from rat lethality data ranging from 10 min to 6 h. Data point used for AEGL-2 derivation was 4 h. Other time points were based on extrapolation. Data quality and research needs: Two well-conducted studies in rats support one another.

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217 Hydrogen Sulfide AEGL-3 VALUES 10 min 30 min 1h 4h 8h 76 ppm 59 ppm 50 ppm 37 ppm 31 ppm Key Reference: MacEwen, J.D., and E.H. Vernot. 1972. Acute toxicity of hydrogen sulfide. Pp. 66-70 in Toxic Hazards Research Unit Annual Report: 1972. Report No. ARML-TR-72-62. Aerospace Medical Research Laboratory, Air Force Systems Command, Wright-Patterson Air Force Base, OH. Test Species/Strain/Sex/Number: Sprague-Dawley rats/10 males/concentration Exposure Route/Concentrations/Durations: Rats/inhalation: 400, 504, 635, or 800 ppm/1 h (Highest concentration causing no death in rats after a 1-h exposure (504 ppm) was determinant for AEGL-3.) End Point/Concentration/Rationale: Highest concentration causing no death in rats after a 1 h-exposure/504 ppm/threshold for death for 1-h exposure in rats. Effects: Concentration Mortality 400 ppm 0/10 504 ppm 0/10 635 ppm 1/10 800 ppm 9/10 Uncertainty Factors/Rationale: Total uncertainty factor: 10 Interspecies: 3 for rat and mouse data suggest little interspecies variability Intraspecies: 3 is considered sufficient because application of the default uncertainty factor of 10 would result in a total uncertainty factor of 30, which would yield AEGL-3 values inconsistent with the total database. AEGL-3 values derived with a total uncertainty factor of 30 would be 25 ppm for 10 min, 20 ppm for 30 min, 17 ppm for 1 h, 12 ppm for 4 h, and 10 ppm for 8 h, values equal to or less than 2-fold the concentration causing no effects in humans exercising to exhaustion (Bhambhani and Singh 1991; Bhambhani et al. 1994, 1996a,b, 1997). Effects consistent with the definition of AEGL-3 would be unlikely to occur at such concentrations. Total Uncertainty Factor: 10. The total adjustment is 10 because each of the factors of 3 represents a logarithmic mean (3.16) of 10; therefore, 3.16 × 3.16 = 10. Modifying Factor: NA Animal to Human Dosimetric Adjustment: Insufficient data Time-Scaling: Cn × t = k, where n = 4.4, value derived from rat lethality data ranging from 10 min to 6 h. Data point used for AEGL-3 derivation was 1 h. Other time points were based on extrapolation. Data Quality and Research Needs: Well-conducted study with appropriate end point for AEGL-3.

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218 Acute Exposure Guideline Levels APPENDIX C Derivation of the Level of Distinct Odor Awareness for Hydrogen Sulfide The level of distinct odor awareness (LOA) represents the concentration above which it is predicted that more than half of the exposed population will experience at least a distinct odor intensity, and about 10% of the population will experience a strong odor intensity. The LOA should help chemical emer- gency responders in assessing public awareness of the exposure due to odor per- ception. The LOA derivation follows the guidance given by Ruijten et al. (2009). The odor detection threshold (concentration at which 50% of people detect an odor; OT50) for H2S was calculated to be 0.0006 ppm (Ruijten et al. 2009). The concentration (C) leading to an odor intensity (I) of distinct odor de- tection (I = 3) is derived with the Fechner function: I = kw × log(C/OT50) + 0.5. For the Fechner coefficient, the default of kw = 2.33 is used because of a lack of chemical-specific data: 3 = 2.33 × log(C /0.0006) + 0.5, which can be rearranged to log(C /0.0006) = (3 - 0.5)/2.33 = 1.07 and results in C = (101.07) × 0.0006 = 0.0071 ppm. The resulting concentration is multiplied by an empirical field correction factor. It takes into account that in everyday life factors such as sex, age, sleep, smoking, upper airway infections, and allergy as well as distraction increase the OT50 by a factor of 4. In addition, it takes into account that odor perception is very fast (about 5 seconds) which leads to the perception of concentration peaks. On the basis of current knowledge, a factor of 1/3 is applied to adjust for peak exposure. Adjustment for distraction and peak exposure lead to a correction fac- tor of 4/3 = 1.33. LOA = C × 1.33 = 0.0071 ppm × 1.33 = 0.01 ppm. The LOA for H2S is 0.01 ppm.