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5
Hydrogen Chloride
This chapter reviews physical and chemical properties, toxicokinetics, and toxicologic and epidemiologic data on hydrogen chloride. The Subcommittee on Submarine Escape Action Levels used this information to assess the health risk to crew members aboard a disabled submarine from exposure to hydrogen chloride and to evaluate the submarine escape action levels (SEALs) proposed to avert serious health effects and substantial degradation in crew performance from short-term exposures (up to 10 d). The subcommittee also identifies data gaps and recommends research relevant for determining the health risk attributable to exposure to hydrogen chloride.
BACKGROUND INFORMATION
Hydrogen chloride is a colorless, nonflammable gas with a pungent, suffocating odor (ACGIH 1991). It is very hygroscopic and produces fumes in moist air. The chemical and physical properties of hydrogen chloride are summarized in Table 5–1.
Hydrogen chloride is an important industrial chemical. The anhydrous form is used in making alkyl chlorides and vinyl chloride from olefins and acetylene, respectively, and in hydrochlorination, alkylation, and polymerization reactions (Sax and Lewis 1987). The hydrated form of hydrogen chloride is hydrochloric acid, which also is used in idustrial processes.
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TABLE 5–1 Physical and Chemical Properties for Hydrogen Chloride
Characteristic
Value
Synonyms
Muriatic acid, hydrochloric acid
CAS number
7647–01–1
Chemical formula
HCl
Molecular weight
36.47
Physical state
Colorless, fuming gas
Relative density
1.268 at 25°C
Boiling point/flash point
–85°C/nonflammable
Melting point
–114.22°C
Solubility
67.3 g per 100 g water at 30°C
Conversion factors in air (25°C, 1 atm)
1 mg/m3=0.67 ppm
1 ppm=1.49 mg/m3
Odor threshold
1–5 ppm
Abbreviation: CAS, Chemical Abstract Service.
Source: AIHA (1998); HDSB (2001); NRC (2000).
Hydrogen chloride can be produced from thermodegradation of chlorinated polymers (e.g., polyvinyl chloride (PVC) and chlorinated acrylics) (Coleman and Thomas 1954). When chlorinated polymers are heated to 300–900°C in air, more than 99.9% of the chlorine atoms are released as hydrogen chloride; the remaining chlorine atoms are released as carbonyl chloride. No chlorine gas is formed. Hydrogen chloride has been detected in fires involving the combustion of chlorinated polymers, most commonly PVC (Dyer and Esch 1976; Gold et al. 1978; Jankovic et al. 1991). Of hydrogen chloride released from PVC in fires, more than 2% was adsorbed to soot particles, and only about 0.8% reached the alveoli (Stone et al. 1973 as cited in the NRC 2000).
TOXICOKINETIC CONSIDERATIONS
Data on the absorption, distribution, metabolism, and excretion of hydrogen chloride are sparse. There are reports of severe nonlactic metabolic acidosis developing rapidly after ingestion of hydrochloric acid (suggesting systemic absorption from the gastrointestinal tract), but this effect has not been reported after dermal exposure to concentrated hydrochloric acid or after inhalation of hydrogen chloride vapor or aerosol. No studies were found on upper respiratory
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tract absorption of hydrogen chloride; however, it is known that two other water-soluble gases, hydrogen fluoride and formaldehyde, are readily taken up by the upper respiratory tract (Morgan and Monticello 1990). Extrapolating results from studies of those gases to hydrogen chloride is difficult because both of them have significant systemic toxicity. Liver and kidney effects have been observed in experimental animals exposed by inhalation to hydrogen chloride, which suggests that the gas is absorbed from the respiratory tract (EPA 1994). However, the effects also could be attributed to disturbance of acid-base metabolism or to decreased blood oxygen concentrations attendant to pulmonary damage. Chloride ions derived from hydrogen chloride absorbed in the upper respiratory tract should be distributed throughout the body (NRC 2000). Hydrogen chloride is not metabolized.
HUMAN TOXICITY DATA
Hydrogen chloride is a strong irritant that primarily affects the respiratory tract, resulting in coughing, pain, inflammation, edema, and desquamation (NRC 1987). Because it is soluble in water and reacts with the surface components of the upper respiratory tract, hydrogen chloride is usually retained there. At high concentrations, it is possible that the scrubbing capacity of the upper respiratory tract could be overwhelmed and penetration to the bronchioles and alveoli could occur. Other effects that can result from exposure to moderate or high concentrations include nasal lesions, pulmonary edema, retrosternal pain, and dyspnea (Ellenhorn 1997). Severe pulmonary injury can result in death. Because chloride ions are normal electrolytes in the body, prolonged exposures to low concentrations or brief exposures to high concentrations will not perturb the electrolyte homeostasis in the body enough to result in any systemic toxicity (NRC 2000). This section reviews the available human toxicity data on hydrogen chloride; some of which are summarized in Table 5–2. No epidemiology studies were found.
Experimental Studies
Stevens et al. (1992) exposed 5 men and 5 women (aged 18–25) to filtered air or to hydrogen chloride at 0.8 ppm (parts per million) or 1.8 ppm for 45 min.The 45-min exposure sessions consisted of a 15-min exercise period on a treadmill walking at 2 miles per hour at an elevation grade of 10%, followed by a 15-minute rest period and then by another 15-min exercise period. Subjects were asked to report any symptoms, such as upper respiratory effects (sore
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TABLE 5–2 Human Toxicity Data. Inhalation Exposure to Hydrogen Chloride
Subject
Concentration
(ppm)
Duration
Effect
Reference
10 asthmatics (5 men and 5 women, aged 18–25)
0.0, 0.8, or 1.8
45 min (15 min exercise, 15 min rest, 15 min exercise)
No treatment-related effects, including increase in severity of upper respiratory, lower respiratory, other symptoms; no significant differences between treated and control groups in pulmonary function tests (total respiratory resistance, thoracic gas volume at functional residual capacity, forced expiratory volume, forced vital capacity, maximal flow at 50% and 75% of expired vital capacity); no changes in nasal power data between treated and control groups.
Stevens et al. 1992
Workers
<5
NR
Apparently not harmful
Elkins 1959
Workers
≥5
NR
Immediately irritating
Elkins 1959
Workers
10–50
Several hours
Tolerable
Henderson and Haggard 1943
Workers
>10
NR
Highly irritating
Elkins 1959
Workers
35
NR
Throat irritation
Henderson and Haggard 1943
Workers
50–100
1 h
Barely tolerable
Henderson and Haggard 1943
Workers
1,000–2,000
NR
Known to be extremely dangerous even at short exposures
Henderson and Haggard 1943
Abbreviations: NR, not reported.
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throat, nasal discharge), lower respiratory effects (cough, chest pain or burning, dyspnea, wheezing), and other effects (fatigue, headache, dizziness, unusual taste or smell). Pulmonary function measurements were performed, including total respiratory resistance, thoracic gas volume at functional residual capacity, forced expiratory volume, forced vital capacity, and maximal flow at 50% and 75% of expired vital capacity. Nasal work of breathing and oral ammonia concentrations also were measured. No adverse treatment-related effects were observed.
Accidental Exposures
Three male police officers (aged 36–45) were exposed to unknown concentrations of sodium hydroxide, silicon tetrachloride, and hydrogen chloride from a roadside chemical spill (Promisloff et al. 1990). The officers developed reactive airways dysfunction syndrome (RADS), a type of bronchospastic airway disease that occurs after a single exposure to high concentrations of an irritating vapor, fume, or smoke. Subsequently episodes of bronchospasmcan be triggered by inhalation exposure to any irritant substance. A 41-yr old male (nonsmoker) with a history of asthma developed RADS after cleaning a pool with a solution containing hydrogen chloride (concentration not reported) (Boulet 1988).
No reports were found that described accidental dermal exposure to hydrogen chloride in humans. Even after dermal exposure to concentrated hydrochloric acid resulting in significant burns, there have been no reported cases suggesting systemic absorption or systemic toxicity.
Occupational Studies
Stokinger (1981) reported that repeated occupational exposure to hydrogen chloride mist at a high but not quantified concentration resulted in bleeding of the gums and nose and ulceration of the mucous membranes. Dental erosion (but not an increase in dental caries) was reported in 555 workers exposed to acids in battery, pickling, plating, and galvanizing operations (Ten Bruggen Cate 1968). These workers were exposed to various mineral acids, including hydrogen chloride.
EXPERIMENTAL ANIMAL TOXICITY DATA
Numerous experimental animal studies have examined the toxicity of hydrogen chloride. They are summarized below; the experimental details are presented in Table 5–3.
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Acute Exposure
Several laboratories examined lethality as a result of inhalation exposure to hydrogen chloride. Rat LC50 (the concentration that causes death in 50% of test animals) ranges from 31,000 to 41,000 ppm for a 5-min exposure (Darmer et al. 1974; Higgins et al. 1972). Rat LC50 values for a 30-min exposure are 4,700 ppm for hydrogen chloride vapor and 5,600 ppm for aerosol (Darmer et al. 1974). The LC50 for a 60-min exposure is 3,124 ppm (Wohlslagel et al. 1976). Guinea pigs exposed at 586 ppm for 3 min died (Malek and Alarie 1989), but no deaths were reported in guinea pigs exposed at 162 ppm for 30 min (Malek and Alarie 1989). Two of eight guinea pigs exposed at 1,040 or 1,380 ppm for 30 min died, but no deaths were reported in guinea pigs exposed at 320 or 680 ppm for 30 min (Burleigh-Flayer et al. 1985).
Nonlethal toxicity studies demonstrate that hydrogen chloride is a sensory and respiratory irritant. At relatively low concentrations and short exposure times, hydrogen chloride can cause changes to the upper respiratory tract. Rats exposed at 200–1,500 ppm for 30 min showed a decrease in respiratory rate and minute volume, and nasal pathology (Hartzell et al. 1985; Stavert et al. 1991). Respiratory tract irritation was observed in rats exposed at 1,800–4,500 ppm for 60 min (Wohlslagel et al. 1976) and at 11,800–57,000 for 5 minutes (Kaplan et al. 1986; Darmer et al. 1974).
Mice showed extreme respiratory irritation when exposed at 410–5400 ppm for 60 min, 560–2,500 ppm for 30 min, or 3,200–30,000 ppm for 5 min (Darmer et al. 1974; Doub 1933; Wohlslagel et al. 1976). Guinea pigs exposed at 107 ppm for 30 min showed only mild sensory irritation, but guinea pigs exposed at 140– 1,040 ppm for 30 min showed more severe sensory irritation or incapacitation (Burleigh-Flayer et al. 1985; Malek and Alarie 1989). Exposure at 190 ppm for 5 min did not cause adverse effects in a baboon, but exposure at 500 or 5,000 ppm for 30 min caused increased respiratory rate and minute volume (Kaplan et al. 1988). Baboons exposed at 16,600–17,300 ppm for 5 min showed pulmonary edema, pneumonia, and bacterial infections; the animals died weeks after the exposure (Kaplan et al. 1988).
Although some reports state that vapor is more toxic at a given concentration than is aerosol because of the lack of desiccating activity with aerosols, hydrogen chloride is so water reactive that the emergency exposure guidance level documentation (NRC 1987) states that published reports are assumed to deal with hydrogen chloride aerosol unless specifically stated otherwise. Because of the predicted cold and humid atmosphere in a disabled submarine, exposures would likely be to aerosol rather than vapor. In rats and mice, there was no significant difference in toxicity between vapor and aerosol exposure at various concentrations.
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TABLE 5–3 Experimental Animal Toxicity Data, Exposure to Hydrogen Chloride
Species
Exposure
Route
Exposure
Concentration, ppm
Exposure
Duration
Effects
Reference
ACUTE TOXICITY (LETHALITY)
Rat
Inhalation
41,000 (vapor)
31,000 (aerosol)
5 min
LC50
Darmer et al. 1974
Rat
Inhalation
4,700 (vapor)
5,600 (aerosol)
30 min
LC50
Darmer et al. 1974
Rat
Inhalation
1,813
60 min
0 of 10 died
Wohlslagel et al. 1976
Rat
Inhalation
2,585
60 min
2 of 10 died
Wohlslagel et al. 1976
Rat
Inhalation
3,274
60 min
6 of 10 died
Wohlslagel at al. 1976
Rat
Inhalation
3,941
60 min
8 of 10 died
Wohlslagel at al. 1976
Rat
Inhalation
4,455
60 min
10 of 10 died
Wohlslagel at al. 1976
Rat
Inhalation
30,000
5 min
0 of 10 died
Higgins et al. 1972
Rat
Inhalation
32,000
5 min
1 of 10 died
Higgins et al. 1972
Rat
Inhalation
39,800
5 min
6 of 10 died
Higgins et al. 1972
Rat
Inhalation
45,200
5 min
7 of 10 died
Higgins et al. 1972
Rat
Inhalation
57,290
5 min
9 of 10 died
Higgins et al. 1972
Mouse
Inhalation
13,700 (vapor)
11,200 (aerosol)
5 min
LC50
Darmer et al. 1974
Mouse
Inhalation
2,600 (vapor)
2,100 (aerosol)
30 min
LC50
Darmer et al. 1974
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Mouse
Inhalation
557
60 min
2 of 10 died
Wohlslagel et al. 1976
Mouse
Inhalation
985
60 min
3 of 10 died.
Wohlslagel et al. 1976
Mouse
Inhalation
1,387
60 min
6 of 10 died
Wohlslagel et al. 1976
Mouse
Inhalation
1,902
60 min
8 of 10 died
Wohlslagel et al. 1976
Mouse
Inhalation
2,476
60 min
10 of 10 died
Wohlslagel et al. 1976
Mouse
Inhalation
3,200
5 min
1 of 15 died
Higgins et al. 1972
Mouse
Inhalation
5,060
5 min
1 of 15 died
Higgins et al. 1972
Mouse
Inhalation
6,145
5 min
2 of 15 died
Higgins et al. 1972
Mouse
Inhalation
6,410
5 min
0 of 15 died
Higgins et al. 1972
Mouse
Inhalation
7,525
5 min
6 of 15 died
Higgins et al. 1972
Mouse
Inhalation
8,065
5 min
2 of 15 died
Higgins et al. 1972
Mouse
Inhalation
9,276
5 min
5 of 15 died
Higgins et al. 1972
Mouse
Inhalation
13,655
5 min
6 of 15 died
Higgins et al. 1972
Mouse
Inhalation
26,485
5 min
13 of 15 died
Higgins et al. 1972
Mouse
Inhalation
30,000
5 min
13 of 15 died
Higgins et al. 1972
Guinea pig
Inhalation
586
3 min
100% mortality
Malek and Alarie 1989
Guinea pig
Inhalation
162
30 min
No deaths
Malek and Alarie 1989
Guinea pig
Inhalation
320
680
1,040
1,380
30 min
0 of 8 died
0 of 8 died
2 of 8 died
3 of 8 died
Burleigh-Flayer et al. 1985
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Species
Exposure
Route
Exposure
Concentration, ppm
Exposure
Duration
Effects
Reference
ACUTE EXPOSURE (NONLETHAL TOXICITY)
Rat
Inhalation
200–300
30 min
30% decrease in respiratory rate and minute volume. 60% decrease in respiratory rate and minute volume.
Hartzell et al. 1985
780–1,500
Rat
Inhalation “nose-breathing rats” and “mouth-breathing rats”
1,300
30 min
6% of nose-breathing rats died versus 46% of mouth-breathing rats; necrosis of the mucosa, submucosa, bone, submucosal gland in the nose-breathing rats; necrosis of the tracheal mucosa and submucosa of the mouth-breathing rats; dry and wet lung weights elevated in the mouth-breathing rats but not the nose-breathing rats.
Stavert et al. 1991
Rat
Inhalation
1,800–4,500
60 min
Eye and mucous membrane irritation, respiratory distress, corneal opacity, erythema of exposed skin.
Wohlslagel et al. 1976
Inhalation
11,800–18,400
5 min
Severe irritation of the respiratory tract and eyes.
Kaplan et al. 1986
Rat
Inhalation
30,000–57,000
5 min
Extreme irritation to mucous
Darmer et al. 1974
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membranes and some irritation to exposed skin.
Mouse
Inhalation
410–5,400
30 min
Extreme irritation of mucous membranes and some irritation of exposed skin.
Doub 1933
Mouse
Inhalation
560–2,500
60 min
Eye and mucous membrane irritation, respiratory distress, corneal opacity, and erythema of exposed skin.
Wohlslagel et al. 1976
Mouse
Inhalation
3,200–30,000
5 min
Extreme irritation of mucous membranes and some irritation to exposed skin.
Darmer et al. 1974
Guinea pig
Inhalation
107
30 min
No incapacitation; animals able to run on a wheel but showed signs of mild sensory irritation.
Malek and Alarie 1989
Guinea pig
Inhalation
140
30 min
Animals unable to run on a wheel by 17 min into exposure.
Malek and Alarie 1989
Guinea pig
Inhalation
160
30 min
Animals unable to run a wheel by 1.3 min into exposure.
Malek and Alarie 1989
Guinea pig
Inhalation
320
30 min
Sensory irritation began at 6 min; lung irritation began at 20 min.
Burleigh-Flayer et al. 1985
Guinea pig
Inhalation
590
30 min
Incapacitated at 0.7 min into exposure; lacrimation, frothing at the mouth, coughing, cyanosis, death in about 3 min.
Malek and Alarie 1989
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Species
Exposure
Route
Exposure
Concentration, ppm
Exposure
Duration
Effects
Reference
Guinea pig
Inhalation
680
30 min
Sensory irritation at <1 min; lung irritation at 13 min; corneal opacities in 1 of 4 animals.
Burleigh-Flayer et al. 1985
Guinea pig
Inhalation
1,040
30 min
Sensory irritation at <1 min; lung irritation at 9 min; corneal opacities in 4 of 8 animals; squamous metaplasia with ciliary loss and submucosal inflammation in large airways and multifocal acute alveolitis 2 d after exposure; goblet-cell hyperplasia and mild inflammation in large airways, mild lymphoid hyperplasia and interstitial inflammation in the lung 15 d after exposure.
Burleigh-Flayer et al. 1985
Guinea pig
Inhalation
1,380
30 min
Sensory irritation at <1 min; lung irritation at 4 min; corneal opacities in 5 of 8 animals.
Burleigh-Flayer et al. 1985
Baboon (n=1)
Inhalation
190
5 min
No sign of irritation.
Kaplan et al. 1988
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Baboon (n=3)
Inhalation
500
30 min
Increased respiratory rate and minute volume during exposure; no changes in lung function, arterial pH, pO2, or pCO2 at 3 d or 3 mo after exposure.
Kaplan et al. 1988
Baboon (n=3)
Inhalation
810–940
5 min
Frothing at the mouth and coughing.
Kaplan et al. 1988
Baboon (n=3)
Inhalation
5,000
30 min
Increased respiratory rate and minute volume during exposure; hypoxemia; normal chest X-ray 1 h after exposure; normal lung function 3 d or 3 mo after exposure.
Kaplan et al. 1988
Baboon (n=2)
Inhalation
16,600–17,300
5 min
Head shaking, profuse salivation, blinking, eye rubbing during exposure; severe dyspnea after exposure; lung edema with tracheitis 18 or 76 d after exposure; died of pneumonia.
Kaplan et al. 1988
REPEATED EXPOSURE
Rat
Inhalation
10
6 h/d, 5 d/wk for 90 d
Significant increase in incidence of minimal rhinitis in F344 rats, but not in Sprague-
Toxigenics 1983
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Species
Exposure
Route
Exposure
Concentration, ppm
Exposure
Duration
Effects
Reference
Dawley rats; no changes in urinalysis, serum chemistry, hematology.
Rat
Inhalation
10
6 h/d, 5 d/wk for 128 wk
Incidence of mucosal hyperplasia increased in the larynx and trachea, not in the nose. No increase in tumor incidence.
Sellakumar et al. 1985
Rat
Inhalation
20
6 h/d, 5 d/wk for 90 d
Mild rhinitis, but no histopathology in other tissues. No changes in urinalysis, serum chemistry, hematology.
Toxigenics 1983
Rat
Inhalation
50
6 h/d, 5 d/wk for 90 d
Depressed body weight gain in wk 3–8 exposure in males; minimal to mild rhinitis. No change in urinalysis, serum chemistry, hematology. No histopathology in tissues other than nose.
Toxigenics 1983
Mouse
Inhalation
10
6 h/d, 5 d/wk for 90 d
No significant changes in histopathology, no changes in urinalysis, serum chemistry, or hematology.
Toxigenics 1983
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Mouse
Inhalation
20
6 h/d, 5 d/wk for 90 d
Minimal increase in eosinophilic globules in nose. No histopathology in other tissues; no changes in urinalysis, serum chemistry, hematology.
Toxicgenics 1983
Mouse
Inhalation
50
6 h/d, 5 d/wk for 90 d
Pigmented macrophages in lips; minimal ulcerative cheilitis; minimal to mild eosinophilic globules in nose. No changes in urinalysis, serum chemistry, hematology. No histopathology changes in tissues other than lip or nose. Depressed body weight gain.
Toxicogenics 1983
Mouse
Inhalation
310
6 h/d for 5 d
Necrosis, exfoliation, erosion, ulceration of respiratory epithelium in the nose. No lung injury.
Buckley et al. 1984
Guinea pig
Inhalation
34
6 h/d, 5 d/wk for 4 4 wk
No histopathology
Machle et al. 1942
Guinea pig
Inhalation
67
6 h/d for 5 d
Mild bronchitis with some peribronchial fibrosis. No deaths.
Machle et al. 1942
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Species
Exposure
Route
Exposure
Concentration, ppm
Exposure
Duration
Effects
Reference
Guinea pig
Inhalation
100
6 h/d for 50 d
Signs of agitation; nasal discharge and mild lacrimation in the first hour of each day of exposure. No changes in red blood cell count, hemoglobin concentration, body-weight gain, bactericidal capacity of lungs, or susceptibility to pulmonary challenges with bacteria. Slight emphysema.
Ronzani 1909, as cited in NRC 2000
Abbreviations: LC50, median lethal concentration; ppm, parts per million.
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Repeated Exposure
Rats and mice exposed by inhalation at 10–50 ppm for 6 h/d, 5 d/wk for 90 d exhibited no significant histopathology, although the rats exposed at 50 ppm did show mild rhinitis (Toxigenics 1983). Mice exposed at 310 ppm for 6 h/d for 5 d showed necrosis, exfoliation, erosion, and ulceration of the respiratory epithelium in the nose (Buckley et al. 1984). No effects were observed in guinea pigs exposed at 34 ppm for 6 h/d, 5 d/wk for 4 wk (Machle et al. 1942). Respiratory effects were observed in guinea pigs exposed at 67 ppm for 6 h/d for 5 d and at 100 ppm for 6 h/d for 50 d (Machle et al. 1942; Ronzani 1909, as cited in NRC 2000).
NAVY’S RECOMMENDED SEALS
The Navy proposes to set a SEAL 1 of 2.5 ppm and a SEAL 2 of 25 ppm for exposure to hydrogen chloride. Those values appear to be based on the Short-Term Public Limits and the Public Emergency Limits (NRC 1987).
ADDITIONAL RECOMMENDATIONS FROM THE NRC AND OTHER ORGANIZATIONS
Recommended exposure guidance levels for hydrogen chloride from other organizations are summarized in Table 5–4. The 24-h emergency exposure guidance level (EEGL) is the most relevant guidance level to compare to the SEALs (NRC 1987). EEGLs were developed for healthy military personnel for emergency situations. An important difference between EEGLs and SEALs is that EEGLs allow mild, reversible health effects, whereas SEALs allow moderate, reversible health effects. That is, SEALs allow effects that are somewhat more intense or potent than those for EEGLs. Therefore, the SEALs are higher than the corresponding EEGLs.
SUBCOMMITTEE ANALYSIS AND RECOMMENDATIONS
Submarine Escape Action Level 1
On the basis of its review of human and experimental animal health-effects and related data, the subcommittee concludes that the Navy’s proposed SEAL 1 of 2.5 ppm for hydrogen chloride is too conservative. The subcommittee
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TABLE 5–4 Recommendations from Other Organizations for Hydrogen Chloride
Organization
Type of Exposure Level
Recommended Exposure Level
Reference
ACGIH
TLV-C
5 ppm
ACGIH 1998
AIHA
ERPG-1
3 ppm
AIHA 1998
ERPG-2
20 ppm
ERPG-3
150 ppm
DFG
MAK (8 h/d during a 40-h workweek)
5 ppm
DFG 1997
Peak Limit (5 min maximum duration, 8 times per shift)
10 ppm
NAC
Proposed AEGL-1
1.8 ppm
Federal Register, June 23, 2000, 65(122):39263–39277.
Proposed AEGL-2
2.7 ppm
Proposed AEGL-3
13 ppm
NASA
SMAC:
NRC 2000
1 h
5 ppm
24 h
2.5 ppm
7 d
1.0 ppm
30 d
1.0 ppm
180 d
1.0 ppm
NIOSH
Ceiling Concentration
5 ppm
NIOSH 1990
NIOSH
IDLH
50 ppm
NIOSH 1997
NRC
90 d CEGL
0.5 ppm
NRC 1987
NRC
SPEGL:
NRC 1987
1 h
1 ppm
24 h
1 ppm
NRC
EEGL:
NRC 1987
10 min
100 ppm
1 h
20 ppm
24 h
20 ppm
OSHA
PEL-C
5 ppm
NIOSH 1990
Abbreviations: ACGIH, American Conference on Governmental Industrial Hygienists; AEGL, acute exposure guideline level; AIHA, American Industrial Hygiene Association; CEGL, continuous exposure guidance level; DFG, Deutsche Forschungsgemeinschaft; EEGL, emergency exposure guidance level; ERPG, emergency response planning guideline; IDLH, immediately dangerous to life and health; MAK, maximum concentration value in the workplace; NIOSH, National Institute for Occupational Safety and Health; NRC, National Research Council; OSHA, Occupational Safety and Health Administration; PEL-C, permissible exposure level—ceiling; ppm, parts per million; SMAC, spacecraft maximum allowable concentration; SPEGL, short-term public emergency guidance level; TLV-C, Threshold Limit Value-ceiling.
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recommends a SEAL 1 of 20 ppm. No relevant human data are available on hydrogen chloride for deriving SEALs. The subcommittee’s recommended SEAL 1 is based on a study in which the RD50 (50% decrease in respiratory rate) for hydrogen chloride was found to be 309 ppm in mice (Kane et al. 1979). Applying an uncertainty factor of 10 to account for interspecies differences, the SEAL 1 would be 31 ppm. Because of the paucity of human and animal data and the longer duration of exposure (up to 10 d), the subcommittee recommends a SEAL 1 of 20 ppm. At low concentrations (such as 20 ppm), the toxicity of hydrogen chloride depends on concentration, rather than dose (i.e., Haber’s Rule is not applicable) (NRC 1987). The subcommittee concludes that healthy submariners should be able to tolerate irritative effects associated with exposures to less than 20 ppm for up to 10 d. The subcommittee’s recommended SEAL 1 of 20 ppm is also supported by studies in which rats, mice, and guinea pigs were exposed to hydrogen chloride at 10–50 ppm for 6 h/d, 5 d/wk, for 90 d (rats and mice) or 28 d (guinea pigs) and no significant irritation or systemic effects were observed (Toxigenics 1983; Machle et al. 1942).
Submarine Escape Action Level 2
On the basis of its review of human and experimental animal health-effects and related data, the subcommittee concludes that the Navy’s proposed SEAL 2 of 25 ppm for hydrogen chloride is too conservative. The subcommittee recommends a SEAL 2 of 35 ppm. The subcommittee’s recommendation is based on a study in which a baboon exposed at a concentration of 190 ppm hydrogen chloride for 5 min showed no signs of irritation and baboons exposed at a concentration of 500 ppm for 30 min had only minor, transient respiratory effects (Kaplan et al. 1988). The recommended SEAL 2 is further supported by a study in which guinea pigs exposed to hydrogen chloride at a concentration of 107 ppm for 30 min showed only mild sensory irritation and no incapacitation (Malek and Alarie 1989). Since the toxicity of hydrogen chloride depends on concentration, rather than dose, and Haber’s rule is not applicable to hydrogen chloride (NRC 1987), the subcommittee concludes that exposure of healthy submariners at 35 ppm for 24 h would produce moderate irritative effects that would be tolerable and would not produce irreversible health effects.
DATA GAPS AND RESEARCH NEEDS
The subcommittee recommends that the Navy consider conducting the following studies:
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Healthy volunteers—people with no asthma or other respiratory sensitivities—be studied to determine the actual NOAEL and LOAEL for hydrogen chloride;
The absorption (if any) of hydrogen chloride vapor and aerosol through intact human skin in vitro should be studied;
Additional information on the interaction of hydrogen chloride and the other irritant gases should be obtained;
Finally, the potential effects of hyperbaric atmospheres under the conditions found in a disabled submarine should be studied as they obtain in the case of hydrogen chloride exposures.
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Representative terms from entire chapter:
guinea pigs