B3

Hydrogen Chloride

Chiu-Wing Lam, Ph.D., and King Lit Wong, Ph.D.

Johnson Space Center Toxicology Group

Medical Operations Branch

Houston, Texas

PHYSICAL AND CHEMICAL PROPERTIES

Hydrogen chloride is a colorless, nonflammable gas with a pungent odor (ACGIH 1991). It fumes in air and condenses with moisture to form hydrochloric acid (Henderson and Haggard 1943).

Formula:

HCl

CAS no.:

7647-01-1

Synonym:

Muriatic acid

Molecular weight:

36.5

Boiling point:

–85.05°C

Melting point:

–114.22°C

Vapor pressure:

>1 atm

Solubility

67.3 g per 100 g water at 30 °C

Conversion factors

1 ppm = 1.49 mg/m3;

at 25°C, 1 atm:

1 mg/m3 = 0.67 ppm

OCCURRENCE AND USE

Anhydrous hydrogen chloride is used in making alkyl chlorides and vinyl chloride from olefins and acetylene, respectively (Sax and Lewis 1987). It is also used in hydrochlorination, alkylation, and polymerization reactions. Hydrochloric acid is the hydrated form of hydrogen chloride. It is one of the most important industrial chemicals.

HCl gas is a potential thermodegradation product of chlorinated polymers, such as polyvinyl chloride (PVC) and chlorinated acrylics (Coleman and



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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 B3 Hydrogen Chloride Chiu-Wing Lam, Ph.D., and King Lit Wong, Ph.D. Johnson Space Center Toxicology Group Medical Operations Branch Houston, Texas PHYSICAL AND CHEMICAL PROPERTIES Hydrogen chloride is a colorless, nonflammable gas with a pungent odor (ACGIH 1991). It fumes in air and condenses with moisture to form hydrochloric acid (Henderson and Haggard 1943). Formula: HCl CAS no.: 7647-01-1 Synonym: Muriatic acid Molecular weight: 36.5 Boiling point: –85.05°C Melting point: –114.22°C Vapor pressure: >1 atm Solubility 67.3 g per 100 g water at 30 °C Conversion factors 1 ppm = 1.49 mg/m3; at 25°C, 1 atm: 1 mg/m3 = 0.67 ppm OCCURRENCE AND USE Anhydrous hydrogen chloride is used in making alkyl chlorides and vinyl chloride from olefins and acetylene, respectively (Sax and Lewis 1987). It is also used in hydrochlorination, alkylation, and polymerization reactions. Hydrochloric acid is the hydrated form of hydrogen chloride. It is one of the most important industrial chemicals. HCl gas is a potential thermodegradation product of chlorinated polymers, such as polyvinyl chloride (PVC) and chlorinated acrylics (Coleman and

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 Thomas 1954). When PVC or chlorinated acrylics were heated to about 300, 600, or 900°C in air, more than 99.9% of the chlorine atoms in these polymers were released in the form of HCl, and the remaining chlorine atoms were released as carbonyl chloride; no chlorine gas was formed at all. HCl has been detected in fires involving chlorinated polymers, most commonly PVC (Dyer and Esch 1976; Gold et al. 1978; Jankovic et al. 1991). Jankovic et al. detected HCl (1 to 8.5 ppm) in 2 of 22 fires or firefighters' training fires. A study by Gold et al. showed that Boston firefighters who were at the immediate location of the fire were exposed to HCl at 18, 32, 75, 128, or 150 ppm (time-weighted concentration) in 5 of 90 fires. For two of these five fires, the firefighters specifically identified ''plastics" as among the combustibles. HCl generation was suspected in an industrial incident in which a PVC extruding machine was overheated to 360°C (Froneberg et al. 1982). Sixty-three workers at this PVC plant were exposed to fumes from the overheating machine. They experienced irritation of the upper and lower respiratory tracts, headache, nausea, and fainting. The symptoms were attributed to exposure to HCl and carbon monoxide, which are known to form when PVC is heated to 300°C. During the space-shuttle mission STS-40, the electric motor of a freezer-refrigerator overheated. Postflight chemical analyses of off-gassed compounds from the motor suggested that a low concentration of HCl could have been present in the spacecraft cabin after this incident (Huntoon 1991). TOXICOKINETICS AND METABOLISM Absorption No reports on the upper-respiratory-tract (URT) absorption of HCl have been found. The uptake of two water-soluble gases, hydrogen fluoride and formaldehyde, by the URT of the rat were 100% and 93%, respectively (Morgan and Monticello 1990). Hydrogen fluoride is infinitely soluble in water (Stokinger 1981); the solubility of HCl (67.3 g/100 g at 30°C) is greater than that of formaldehyde (55 g/100 g at 25°C) (Barrow et al. 1984). Morris and Smith (1982) predicted that the URT would remove more than 99% of inhaled HCl in rats. Stone (1975) conducted a study to simulate human URT absorption of HCl. A 1-m long tube of 4-mm inside diameter (cross-sectional area 0.13 cm2) was wetted with water so as to mimic the URT. When HCl at 60, 600, or 6000 ppm in room air was introduced into the tube at about 4 L/min for 30 min, it was very well retained by the water film. The corresponding retention efficiencies were 100%, 98%, or 93%.

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 Because PVC combustion releases both gaseous HCl and HCl adsorbed on soot particles, it is of interest to assess their toxicological implication in the respiratory system. As noted above, pyrolysis of PVC releases essentially all of its chlorine atoms as HCl. Stone et al. (1973) observed that flame pyrolysis of PVC at 1100°C released the bulk of HCl in the gaseous form; less than 2% of the HCl was associated with soot particles. The soot particles generated ranged from 0.03 to 0.11 µm in diameter. If these particles could penetrate deep into the lung, then the HCl in the solid particle matrix also could reach the deep lung. Yu (1978) predicted that 20-40% of the inhaled particles in that size range would be deposited in the alveolar region of the human lung. Assuming that 40% of the soot could reach the alveolar region, these data suggest that only 0.8% of the HCl generated from the PVC combustion could reach the lung. Thus, the toxicological impact of soot-associated HCl is relatively small compared with that of the gaseous HCl. Metabolism HCl is not metabolized in the body. Chloride is one of the major extracellular anions in living organisms (White et al. 1978). Chloride ions resulting from HCl adsorption in the URT should be distributed throughout the body. TOXICITY SUMMARY HCl primarily causes URT irritation. At moderate exposure concentrations, nasal lesions could also occur. At high concentrations (as in industrial accidents), in addition to causing URT irritation and lesions, HCl can reach the lung, causing pulmonary edema, retrosternal pain, and dyspnea (Ellenhorn and Barceloux 1988). 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 HCl concentrations will not perturb the electrolyte homeostasis in the body enough to result in any systemic toxicity. Acute or Short-Term Exposures Irritation to the Respiratory System Human Studies HCl is an irritant to the mucous membranes and eyes; skin irritation could occur at very high exposure concentrations (Elkins 1959; Rom and Barkman

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 1983). Hydrated HCl is less toxic than the dry gas, because the former does not have the dehydrating action of the latter (Henderson and Haggard 1943). According to a review by Henderson and Haggard (1943), HCl at 1000 to 2000 ppm is dangerous in even short exposures. An exposure to 10-50 ppm was tolerable for several hours; an exposure to 50-100 ppm was tolerable for 1 h. At 35 ppm, HCl caused throat irritation. However, Elkins (1959) reported greater HCl irritancy than that observed by others. Elkins noted that exposures to HCl above 10 ppm were highly irritating. Inhalation of HCl at 5 ppm or more was immediately irritating. Concentrations of HCl at less than 5 ppm "are apparently not harmful, although they possibly promote tooth decay." Workers developed some tolerance toward the irritant effect of HCl (Elkins 1959). Animal Studies Kaplan et al. (1986) exposed male juvenile baboons (2-3 y old, one per exposure concentration) to HCl at 190, 810, 890, 940, 2780, 11,400, 16,600, or 17,300 ppm for 5 min. Irritation signs were seen at 810-17,300 ppm but not at 190 ppm. The signs ranged from frothing at the mouth and coughing at the lower concentrations to head shaking, profuse salivation, blinking, and eye rubbing at the higher concentrations. The two baboons exposed to HCl at 16,600 or 17,300 ppm experienced severe and persistent dyspnea; pneumonia, pulmonary edema, and tracheitis were the major pathological findings in those two animals, which died at 18 or 76 d after the exposure. Kaplan et al. also exposed single rats for 5 min to 1 of 12 HCl concentrations ranging from 11,800 to 87,700 ppm. All the exposed rats showed severe irritation of the respiratory tract and eyes. Most of the rats had persistent respiratory symptoms, and some died after the exposure. The irritancy of HCl to animals exposed to high concentrations also was investigated by Darmer et al. (1974). In this study, rats were exposed to HCl at 30,000-57,000 ppm for 5 min or 2100-6700 ppm for 30 min; mice were exposed at 3200-30,000 ppm for 5 min or 410-5400 ppm for 30 min. HCl was found to be extremely irritating to the mucous membranes and exposed skin. The symptoms included excessive grooming and preening, corneal erosion and cloudiness, and rapid shallow breathing. The toxicity to exposed skin was manifested as scrotal ulceration and greenish discoloration of the fur. A similar study was conducted in rats and mice exposed for 60 min to 1800-4500 ppm and 560-2500 ppm, respectively (Wohlslagel et al. 1976). The findings were very similar to those of Darmer et al. (1974). Wohlslagel et al. reported eye and mucous membrane irritation, respiratory distress, corneal opacity, and erythema of exposed skin in these rats and mice during the exposure.

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 Machle et al. (1942) exposed groups of three rabbits and three guinea pigs to various concentrations (34-4360 ppm) of HCl for 5 min, 15 min, 1 h, 2 h, 6 h, 2 d (6 h/d), or 5 d (6 h/d). Irritation to the eyes and mucous membranes was present to various degrees in all the exposure groups. Acute distress was evident in the groups exposed at high concentrations. The irritating effect of HCl on the URT and the pulmonary region was further investigated in male guinea pigs (Burleigh-Flayer et al. 1985). Sensory irritation, characterized by a decrease in respiratory rate with lengthened expiration, results primarily from irritation of the nasal cavity; pulmonary irritation is characterized by an initial rise followed by a fall in respiratory rate, with a pause after each expiration. The guinea pigs were exposed in head-only chambers to HCl at 320 to 1380 ppm for 30 min, and respiratory patterns were monitored. Both types of irritation were detected; however, sensory irritation was seen before the onset of pulmonary irritation. That is because the majority of inhaled HCl is captured by the URT (the site where sensory irritation originated); eventually, however, enough HCl escapes scrubbing by the nose and reaches the lung to cause pulmonary irritation. Corneal opacities, a direct result of the corrosive property of HCl, were observed in animals exposed at 680 ppm or higher. The results are summarized in Table 3-1. TABLE 3-1 Time of Onset of Sensory and Pulmonary Irritation Produced by HCl HCl Exposure Concentration, ppm Sensory Irritation, Time of Onset, min Pulmonary Irritation, Time of Onset, min Animal Corneal Opacity Mortality 320 6 20 0/4 0/4 680 <1 13 1/4 0/4 1040 <1 9 4/8 2/8 1380 <1 4 5/8 3/8 Morphological Injuries to the Respiratory System In Vitro Studies The irritation/toxicity of HCl and several other irritant gases was studied in vitro. Cralley (1942) sought a gaseous concentration that would stop ciliary

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 activity in 10 min. Such concentrations were found to stop the ciliary activity in rabbit tracheal explants for the following: HCl at 60 ppm, chlorine at 30 ppm, sulfur dioxide at 30 ppm, NO2 at 60 ppm, formaldehyde at 30-60 ppm, and ammonia at 600 ppm. In reacting with water, 30-ppm chlorine is converted to roughly 60-ppm HCl, 30-ppm SO2 is converted to 30-ppm H2SO3, and 60-ppm NO2 is converted to 60-ppm HNO3. Interestingly, all of those acid species, including HCl, at their effective concentrations generated roughly 60-ppm H +. The data suggest that the toxicity of those acidic species on the ciliary cells in this in vitro system is due primarily to the hydrogen ions formed in the mucosal surface. Human Data Doub (1933) reported a case involving a man occupationally exposed to HCl fumes of an unknown concentration for about 10 min. The man started to cough at the end of the exposure. He then coughed up some blood; that continued for a day. On the second day, he was hospitalized and given a chest X-ray, which revealed a dense, hazy mottled shadow spanning both lungs together with areas of consolidation. Coarse, bubbling rales were also heard over both lungs. He was diagnosed with acute bronchitis and bronchopneumonia, and recovered fully 9 d after the exposure. Inhalation exposures to respiratory irritants, such as HCl, are known to trigger asthmatic attacks in people with asthma (Boulet 1988). A nonatopic, nonsmoking man with a 6-y history of mild asthma developed a rapidly progressive and severe bronchospasm after cleaning a pool for about an hour with a product containing hydrochloric acid. After the incident, his asthma changed from mild to severe. However, it is not known whether the cleaning product contained any other offending ingredients or whether any volatile reaction products were formed during the cleaning. Animal Data According to Machle et al. (1942), HCl injures primarily the respiratory tract at concentrations higher than 34 ppm. Repeated exposures to HCl at 67 ppm for 5 d (6 h/d) induced mild bronchitis with some peribronchial fibrosis in guinea pigs but did not cause severe lesions. However, in rabbits, lobular pneumonia and pulmonary abscesses were commonly detected after repetitive exposures at 67 ppm. Machle et al. (1942) concluded that "high concentrations produce necrosis of the tracheal, bronchial and alveolar epithelium, accompa-

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 nied by extensive pulmonary edema, atelectasis, and emphysema." However, the exact concentrations that produced those toxicities were not reported. Edema and necrosis of the intima and media of the pulmonary blood vessels, accompanied by thrombi and pulmonary infarcts, were also found. Unfortunately, the reported results of this large-scale study, which consisted of 37 experiments with varying exposure times and concentrations, lacked details. Morphological changes induced by HCl were investigated in male guinea pigs exposed to the compound at 1040 ppm for 30 min (Burleigh-Flayer et al. 1985). When examined by light microscopy 2 d after the exposure, the larger conducting airways showed squamous metaplasia with a loss of cilia and acute submucosal inflammation. Multifocal acute inflammation with congestion and mild hemorrhage were found in the alveoli. Fifteen days after the HCl exposure, goblet-cell hyperplasia and mild inflammation in the larger conducting airways were observed; mild lymphoid hyperplasia in the parenchyma and interstitial inflammation in the lung also were noted. These data demonstrated that HCl exposures at 1040 ppm led to tissue damage in the airways and the alveolar regions. Morphological insults from HCl in the respiratory tract were also studied in mice and rats (Darmer et al. 1974). In this study, rats were exposed to HCl at 2100 to 57,000 ppm, and mice were exposed to 410 to 30,000 ppm, for 5 or 30 min. Darmer et al. reported observing badly damaged nasal and tracheal epithelium, moderate-to-severe alveolar emphysema, pulmonary edema, atelectasis, and occasional spotting of the lung; however, the exposure concentrations that produced those toxicities were not specified. The survivors of exposures to high concentrations showed a clicking breathing noise, breathing difficulty, and bloody discharge from the nares. Buckley et al. (1984) reported that 5-d exposures (6 h/d) of mice to HCl at 310 ppm resulted in necrosis, exfoliation, erosion, and ulceration of the respiratory epithelium in the nose, but no histopathological changes in the lung. Because HCl gas is well absorbed in the nasal cavity, the toxicity of HCl depends in part on whether the exposure is via breathing through the nose or the mouth. Stavert et al. (1991) fitted male rats with mouthpieces coupled with endotracheal tubes to simulate mouth breathing. They exposed the "mouth-breathing" rats and the normal (i.e., nose-breathing) rats to HCl at 1300 ppm for 30 min. About 46% of the mouth-breathing rats died versus only 6% of the nose-breathing rats. The survivors were killed 24 h after the HCl exposure. The mouth-breathing rats had epithelial and submucosal necrosis in the trachea with fibrinous and neutrophilic exudates. The nose-breathing rats developed necrosis of the epithelium, submucosa, and bone, with fibrinous and neutrophilic exudates, but showed no tracheal injury. The dry and wet weights of the lungs of the mouth-breathing rats were increased, compared with controls, but

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 those weights in the nose-breathing rats were unchanged. In summary, the toxicity of HCl is confined primarily to the nose in normal breathing. Mouth breathing allows HCl to reach deep into the lung to produce injury. Functional Injuries to the Respiratory System Hartzell et al. (1985) reported that respiratory minute volume (RMV) decreased by 30% in rats exposed to HCl at 200 or 300 ppm for 30 min. Concentrations of 780 to 1500 ppm reduced the RMV further to about 60%. The logarithm of the exposure concentrations was linearly related to the percentage decrease in RMV or respiratory rate. The drops in RMV paralleled the decreases in respiratory rate; that finding indicates that tidal volume was probably not affected. In rats exposed to HCl at 780 ppm, the decrease in RMV began almost as soon as the HCl exposure started and reached a maximum 3 min into the 30-min exposure. The decreases in the respiratory rate and minute volume of these rats were typical of the respiratory responses to sensory irritants (Alarie 1981). In contrast to rats, HCl increased the RMV in baboons. A 30-min exposure of baboons of HCl at 500, 5000, or 10,000 ppm increased the respiratory rate in a concentration-dependent fashion, with no significant changes in tidal volume (Kaplan et al. 1988). However, analyses conducted on blood samples collected during the exposure and within 10 min of the exposure showed a drop in arterial pO2 by about 45% in the baboons exposed at 5000 or 10,000 ppm. Arterial pH and pCO2 showed no changes. The finding on hypoxemia is not consistent with an increased RMV, which should increase arterial pO2. Pulmonary edema or small airway constriction was suspected in the exposed baboons. Because chest X-rays taken within 1 h of exposure were negative, the investigators believed that pulmonary edema, even if present, could not have been severe. Blood analyses conducted 3 d and 3 mo after the exposure showed no hypoxemia. Results of pulmonary function tests conducted at those times showed no changes in functional residual capacity, vital capacity, inspiratory capacity, diffusing capacity of the lungs for carbon monoxide, the diffusing capacity per unit lung volume, pulmonary blood flow, and pulmonary static compliance. Systemic Injuries outside the Respiratory system Darmer et al. (1974) found that acute HCl exposures of rats and mice failed to produce any gross or histological injuries to tissues other than the respiratory

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 tract. However, the exposures were short (up to 30 min). HCl can produce systemic toxicity if the exposure period is long and the concentration is high enough. When 111 rabbits and 111 guinea pigs were exposed in 37 experiments to HCl at 34 to 4360 ppm for durations of 5 min to 4 w (6 h/d), 51 rabbits and 57 guinea pigs died shortly or several months after the exposures (Machle et al. 1942). Death attributed to hepatic damage was observed in 12 rabbits and 23 guinea pigs; pathological findings included extensive parenchymal edema, congestion, necrosis, hemorrhage, fatty changes, cirrhotic sclerosis, or other degenerative changes. Liver lesions were also seen in animals that died of other causes. The kidneys in some animals showed hyaline thickening of the glomerular tufts, glomerular sclerosis, tubular atrophy and degeneration, and chronic cellular infiltration of the interstitium. In the heart, HCl exposures produced myocardial degeneration, hyaline necrosis with fibrous replacement, and chronic cellular infiltrations of the myocardial bundles and interstitium. The comparative toxicity of HCl and hydrogen fluoride (HF) was investigated by Machle's group (1934, 1935, and 1942). Repetitive exposures of guinea pigs and rabbits to HF at 20 ppm for 10 w (6 h/d, 5 d/w) led to injuries in the respiratory tract and liver (Machle and Kitzmiller 1935); the exposed rabbits also showed kidney damage. Comparing those results with the toxicity results for HCl described above, Machle et al. (1942) concluded that the acute irritant effects of HCl and HF were similar. However, HF is more systemically toxic than HCl because the pathological changes were more severe and frequent. Notably, chloride ion is a normal electrolyte in the body, and fluoride ion is not. Machle et al. (1942) further concluded that in prolonged exposures, the safe concentration of HF is lower than that of HCl. Death As discussed above, high concentrations of HCl can cause pulmonary injury. Severe pulmonary injury can lead to death. Machle et al. (1942) reported that an acute exposure to HCl at 1000 mg/m3 (670 ppm) for 2 h killed all three rabbits and all three guinea pigs exposed; an exposure at 6500 mg/m3 (4400 ppm) took only 30 min to kill all the exposed rabbits and guinea pigs. Guinea pigs tended to succumb faster than rabbits; 30% of the guinea-pig deaths occurred within 48 h of the start of the exposure compared with only 6% of the rabbit deaths. These early deaths were primarily caused by acute respiratory damage. Animals that did not die immediately after exposure succumbed later to pulmonary and nasal infections. Longer exposures to moderately high concentrations can cause death from hepatic damage (Machle et al. 1942). However, some animals survived a single 5-min exposure to 5500 mg/m3 (3700

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 ppm). Five days (6 h/d) of exposure to a relatively low concentration of HCl (67 ppm) did not kill any exposed animal (Machle et al. 1942). The acute toxicity of HCl was also studied in mice and rats (Darmer et al. 1974). Rats were more tolerant of HCl than mice; the 5-min and 30-min LC50s (lethal concentrations for 50% of the animals) for rats were two to three times those for mice. More delayed deaths were noted in mice than in rats. A similar study by Wohlslagel et al. (1976) also showed that rats were more tolerant of HCl than mice. The LC50 values reported by Darmer et al. (1974) and Wohlslagel et al. (1976) are listed in Table 3-2. Using those data to calculate the C × T values for exposures that produced 50% mortality in rats exposed for 5 min, 30 min, or 60 min yielded 205,000, 141,000, and 186,000 ppm-min, respectively. The corresponding values in mice were 70,000, 78,000, and 66,000 ppm-min. Thus, for HCl exposures of 60 min or less, the C × T values that produce 50% mortality are relatively constant for rats and mice. The mortality response curves of HCl in rats and mice are both quite steep. Data from Wohlslagel et al. (1976) showed that to reduce the mortality of a 60-min HCl exposure from 80% to 20%, the exposure concentration would need to be reduced by only 34% for rats and by 70% for mice. Species sensitivity to the acute toxicity of HCl was further investigated by Kaplan et al. (1988). Three groups of baboons (three per group) were each exposed to HCl at either 500, 5000, or 10,000 ppm for 15 min and were observed for 3 mo afterward. None of the animals died, and all gained weight normally. When six mice were exposed at 2550 ppm for the same length of time, five died. Kaplan et al. (1988) concluded that primates are less sensitive to HCl than rodents, and "baboons can survive exposure to concentrations of HCl that are at least five times greater than those that are lethal to the mouse." TABLE 3-2 LC50 Values Reported by Darmer et al.(1974) and Wohlslagel et al. (1976) Species 5-min LC50, ppm 30-min LC50, ppm 60-min LC50, ppm Rat 41,000a 4700 3100   (35,000-48,000)b (4100-5400) (2800-3500) Mouse 14,000 2600 1100   (10,000-18,000) (2300-3100) (870-1400) a Maximum likelihood estimate. b The concentration range predicted with 95% confidence.

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 The comparative acute toxicity of HCl and HF also was studied by Wohlslaget et al. (1976). On the basis of LC50 values, HF was more deadly than HCl in rats and mice. The 60-min LC50 values of HF for rats and mice were only 30-45% of the LC50 values of HCl, with no overlap of the respective 95% confidence limits. Effect on Exercise Ability HCl is generated in household fires that involve burning of chlorinated polymers. In an effort to study the potential escape ability of fire victims who might be exposed to HCl, Malek and Alarie (1989) studied the effect of a 30-min HCl exposure on the ability of guinea pigs to run on a wheel. The guinea pigs were allowed to run on the wheel for 10 min while breathing air before the HCl exposure began. When exposed to HCl at 107 ppm, three guinea pigs were able to run for the entire 30-min exposure. However, at 140, 160, or 590 ppm, all the guinea pigs were incapacitated after 17, 1.3, or 0.7 min (on the average), respectively, into the HCl exposure. When the guinea pigs reached the incapacitation stage, they stopped running abruptly and were "severely compromised." Signs of mild irritation were observed at 107 ppm, and severe irritation was detected at 590 ppm with lacrimation, frothing at the mouth, coughing, and cyanosis. The six guinea pigs in the 107-ppm and 140-ppm groups (three per group) survived the 30-min exposure. The two guinea pigs in the 160-ppm group also survived the 30-min exposure, but all four guinea pigs exposed at 590 ppm died in about 3 min. Those data show that an acute HCl exposure that is only mildly irritating is not incapacitating at least in guinea pigs, but a severely irritating acute HCl exposure can be incapacitating. However, the data are of little value for assessing the ability of HCl to prevent fire victims from running for their lives. Subchronic and Chronic Exposures Toxicity of HCl in the Respiratory Tract Similar to acute and short-term repetitive exposures, subchronic and chronic exposures to HCl produce primarily mucosal irritation and possibly injuries to the upper respiratory system.

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 Concentration, ppm Exposure Duration Species Effects Reference 100 50 d (6 h/d) Rabbit, guinea pig All animals showed signs of agitation; guinea pigs had nasal discharge and mild lacrimation in the first hour of each day of exposure; no changes in RBC count, hemoglobin concentration, body-weight gain, bactericidal capacity of lungs, or susceptibility to pulmonary challenges with bacteria; guinea pigs developed slight emphysema Ronzani 1909 107 30 min Guinea pig No incapacitation: able to run on a wheel but showed signs of mild sensory irritation Malek and Alarie 1989 140 30 min Guinea pig Unable to run on a wheel by 17 min into exposure Malek and Alarie 1989 160 30 min Guinea pig Unable to run on a wheel by 1.3 min into exposure Malek and Alarie 1989 190 5 min Baboon (n=1) No signs of irritation Kaplan et al. 1986 200 or 300 30 min Rat 30% decrease in respiratory rate and minute volume Hartzell et al. 1985 310 5 d (6 h/d) Mouse Necrosis, exfoliation, erosion, and ulceration of respiratory epithelium in the nose; no lung injury Buckley et al. 1984 320 30 min Guinea pig Sensory irritation began in 6 min; lung irritation began in 20 min Burleigh-Flayer et al. 1985 410-5400 30 min Mouse Extreme irritation of mucous membranes and some irritation of exposed skin Doub 1933 500 30 min Baboon (n=3) 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 the exposure Kaplan et al. 1988 560 60 min Mouse 2 of 10 mice died Wohlslagel et al. 1976 560-2500 60 min Mouse Eye and mucous membrane irritation, respiratory distress, corneal opacity, and erythema of exposed skin Wohlslagel et al. 1976

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 Concentration, ppm Exposure Duration Species Effects Reference 590 30 min Guinea pig Incapacitated at 0.7 min into exposure; lacrimation, frothing at the mouth, coughing, cyanosis, and death in about 3 min Malek and Alarie 1989 670 2-6 h Rabbit, guinea pig All died; guinea pigs died faster than rabbits; the early deaths due to respiratory damage; hepatic damage was the most common cause of death in 2 to 7 d after the exposure; lung infection was the most common cause of death after 7 d Machle et al. 1942 680 30 min Guinea pig Sensory irritation began in < 1 min; lung irritation began in 13 min; corneal opacities in 1 of 4 guinea pigs Burleigh-Flayer et al. 1985 780-1500 30 min Rat 60% reduction in respiratory rate and minute volume Hartzell et al. 1985 810-940 5 min Baboon (n=3) Frothing at the mouth and coughing Kaplan et al. 1988 1040 30 min Guinea pig Sensory irritation began in < 1 min; lung irritation began in 9 min; corneal opacities in 4 of 8 guinea pigs; 2 of 8 died; 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 1100 60 min Mouse Half died Wohlslagel et al. 1976 1300 30 min Nose-breathing rat, "mouth-breathing" rat 6% of nose-breathing rats died vs. 46% of "mouth-breathing" rats; necrosis of the mucosa, submucosa, bone, and submucosal gland in the nose-breathing rats; necrosis of the tracheal mucosa and submucosa of the mouth-breathing rats; the dry and wet lung weights were elevated in the mouth-breathing rats but not in normal rats Stavert et al. 1991 1380 30 min Guinea pig Sensory irritation began in < 1 min; lung irritation began in 4 min; corneal opacities in 5 of 8 guinea pigs; 3 out of 8 died Burleigh-Flayer et al. 1985 1800 60 min Rat None of the 10 died Wohlslagel et al. 1976

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 Concentration, ppm Exposure Duration Species Effects Reference 1800-4500 60 min Rat Eye and mucous-membrane irritation, respiratory distress, corneal opacity, and erythema of exposed skin Wohlslagel et al. 1976 1900 60 min Mouse 8 of 10 died Wohlslagel et al. 1976 2100-6700 30 min Rat Extreme irritation of mucous membranes and some irritation to exposed skin Darmer et al. 1974 2600 60 min Rat 2 of 10 died Wohlslagel et al. 1976 2600 30 min Mouse Half died Wohlslagel et al. 1976 3100 60 min Rat Half died Wohlslagel et al. 1976 3200-30,000 5 min Mouse Extreme irritation of mucous membranes and some irritation to exposed skin Darmer et al. 1974 3690 5 min Rabbit, guinea pig No deaths Machle et al. 1942 3900 60 min Rat 8 of 10 died Wohlslagel et al. 1976 4360 30 min Rabbit, guinea pig All died Machle et al. 1942 4700 30 min Rat Half died Wohlslagel et al. 1976 5000 30 min Baboon (n=3) 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 11,800-18,400 5 min Rat Severe irritation of the respiratory tract and eyes Kaplan et al. 1986 14,000 5 min Mouse Half died Wohlslagel et al. 1976

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 Concentration, ppm Exposure Species Effects Reference 16,600-17,300 5 min Baboon (n=2) Head shaking, profuse salivation, blinking, and eye rubbing during exposure; severe dyspnea persisted after exposure; died of pneumonia, lung edema with tracheitis 18 or 76 d after exposure Kaplan et al. 1986 30,000-57,000 5 min Rat Extreme irritation to mucous membranes and some irritation to exposed skin Darmer et al. 1974 41,000 5 min Rat Half died Wohlslagel et al. 1976

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 RATIONALE FOR ACCEPTABLE CONCENTRATIONS Table 3-6 presents exposure limits for hydrogen chloride set by other organizations and Table 3-7 presents the SMACs established by NASA. SMACs are derived in accordance with guidelines developed by the SMAC subcommittee of the Committee on Toxicology (NRC 1992). The SMACs are set by choosing the lowest values among the acceptable concentrations (Acs) TABLE 3-6 Exposure Limits Set or Recommended by Other Organizations Organization Exposure Limit, ppm Reference ACGIH's TLV 5 (ceiling) ACGIH 1991 OSHA's PEL 5 (ceiling) NIOSH 1990 NIOSH's REL 5 (ceiling) NIOSH 1990 NIOSH's IDLH 100 NIOSH 1990 NRC's 90-d CEGL 0.5 NRC 1987 NRC's 24-h SPEGL 1 NRC 1987 NRC's 1-h SPEGL 1 NRC 1987 NRC's 24-h EEGL 20 NRC 1987 NRC's 1-h EEGL 20 NRC 1987 NRC's 10-min EEGL 100 NRC 1987 TLV, Theshold Limit Value; PEL, permissible exposure limit; REL, recommended exposure limit; IDLH, immediately dangerous to life and health; CEGL, continuous exposure guidance level; SPEGL, short-term public emergency guidance level; EEGL, emergency exposure guidance level. TABLE 3-7 Spacecraft Maximum Allowable Concentrations Duration Concentration, ppm Concentration, mg/m3 Target Toxicity 1 h 5 7.5 URT irritation 24 h 2.5 3.8 URT irritation 7 da 1 1.5 URT irritation, lesions 30 d 1 1.5 URT irritation, lesions 180 d 1 1.5 URT irritation, lesions a Previous 7-d SMAC = 1 ppm (1.5 mg/m3).

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 (see Table 3-8). HCl primarily produces URT irritation, lesions, or both. The ACs of HCl, therefore, are set on the basis of sensory irritation or pathological changes of the URT found in humans and rodents. Toxicity of HCl in the liver and kidney of rabbits and guinea pigs was reported by Machle et al. (1942). However, these systemic toxicities were observed in animals exposed to high HCl concentrations for prolonged periods. A 90-d exposure to HCl at up to 50 ppm in mice and in two strains of rats produced no systemic toxicity, including hepatotoxicity or renotoxicity (Toxigenics 1983); life-time exposures of rats (128 w) to HCl at 10 ppm also produced no systemic toxicity (Sellakumar et al. 1985). Liver and kidney lesions were found only in animals exposed to conditions that would not be encountered by humans; thus, lesions in these organs are not considered in setting the SMAC values. 1-h and 24-h ACs Henderson and Haggard (1943), in their review of HCl data gathered from human exposures, stated that exposure to HCl at 10-50 ppm is tolerable for several hours. However, Elkins (1959) noted that exposures at more than 10 ppm are highly irritating in humans, exposures at 5 ppm or more are immediately irritating, and exposures at less than 5 ppm apparently are not harmful. Unfortunately, Elkins did not specify the degree of sensory irritation caused by HCl at 5 ppm. Judging by Henderson and Haggard's finding that HCl at 10-50 ppm is tolerable for several hours and Bond's finding that some workers in chemical plants were routinely exposed to an average HCl concentration of 3.75 ppm (Bond et al. 1991), it seems that HCl at 5 ppm would be likely to cause only mild or, at most, moderate irritation. Therefore, the 1-h AC is set at 5 ppm. Because the possibility of moderate irritation would not be acceptable for a 24-h exposure, the concentration is reduced by a factor of 2 to reach a concentration that would cause only slight-to-mild irritation. The AC of 2.5 ppm for a 24-h exposure is derived as follows: 24-h AC = 5 ppm × ½ = 2.5 ppm. 7-d, 30-d, and 180-d ACs AC Based on Human Exposure Data Because irritation is not a time-dependent clinical toxic sign, a given HCl concentration will produce the same magnitude of irritation regardless of the duration of exposure. HCl is a very water-soluble compound and is not ac-

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 cumulated in the URT; thus, an exposure concentration that does not produce irritation in 7 d also will not produce irritation in 180 d. Therefore, the same AC value is set for 7 d, 30 d, and 180 d. Mild irritation is acceptable for up to 24 h of exposure but is not acceptable for longer exposures. The 24-h AC is further reduced from the 1-h AC by a factor of 2 to 1 ppm for the longer exposure periods. AC Based on Animal Data The nasal cavity is the primary target of HCl. A CIIT-sponsored study in which rodents were exposed to HCl at 10, 20, or 50 ppm for 5 d or 90 d revealed no histopathological changes in any organs, except for very minimal-to-mild inflammation (rhinitis) of the nasal cavity in the rats but not in the mice (Toxigenics 1983). In the 10-ppm exposed groups, mild rhinitis was seen in 6 of the 20 exposed F344 rats, but the incidence of rhinitis was not statistically increased in SD rats. An increase in mild rhinitis in SD rats exposed to HCl at 10 ppm for 128 w (6 h/d, 5 d/w) in another study also was not statistically significant (Sellakumar et al. 1985). Therefore, 10 ppm was the overall lowest-observed-adverse-effect level (LOAEL) of HCl. Because the rhinitis was mild and was only statistically increased in the F344 rats, but not in mice or SD rats, an extrapolation factor of 3 instead of 10 is applied to the LOAEL to obtain the no-observed-adverse-effect level (NOAEL) of 3 ppm. Rhinitis in these animals was due to superficial irritation by HCl. Tissue responses to irritation would not differ greatly among animal species. Therefore, a species factor of 3 instead of 10 is used for extrapolation from animal to human. Increasing the exposure time from 5 d to 90 d increased the incidence of minimal or mild rhinitis in rats exposed at 10 or 20 ppm but not at 50 ppm. In fact, for the F344 rats exposed at 50 ppm, the incidence of mild rhinitis was actually lower when the exposure time increased (12 of 20 rats exposed for 5 d vs. 5 of 20 rats exposed for 90 d). Furthermore, exposing SD rats to HCl at 10 ppm for 90 d or 128 w produced an insignificant increase in mild rhinitis. Since no strong correlation was found between rhinitis and exposure length, no time adjustment factor is applied. Therefore, the AC for 5-d, 30-d, or 180-d exposure is derived as follows: AC = 10 ppm ÷ 3 ÷ 3 = 1 ppm (rounded from 1.3). AC Summary Table The ACs derived from various toxicity end points are summarized in Table 3-8. The SMACs are set by choosing the lowest values among these ACs.

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 TABLE 3-8 Acceptable Concentrations End point, Exposure Data, Reference   Safety Factors     Acceptable Concentrations, ppm Species NOAEL Time Species 1 h 24 h 7 d 30 d 180 d Nasal irritation Human 1 to 5 1 1 5 2.5 1 1 1 LOAEL, 5 ppm (Elkin 1959) Minimal rhinitis Rats 3 1 3     1 1 1 LOAEL, 10 ppm for 90 d (Toxigenics 1983) SMACs         5 2.5 1 1 1

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 REFERENCES ACGIH. 1991. Hydrogen chloride. Pp.773-774. in Documentation of the Threshold Limit Values and Biological Exposure Indexes. Vol II. 6th Ed. American Conference of Governmental Industrial Hygienists, Cincinnati, Ohio. Alarie, Y. 1981. Toxicological evaluation of airborne chemical irritants and allergens using respiratory reflex reactions. Pp. 207-231 in Symposium on Inhalation Toxicology and Technology, B.K.J. Leong, ed. Ann Arbor, Mich.: Ann Arbor Science. Albert, R.E., A.R. Sellakumar, S. Laskin, M. Kuschner, N. Nelson, and C.A. Snyder. 1982. Gaseous formaldehyde and hydrogen chloride induction of nasal cancer in the rat. J. Natl. Cancer Inst. 68:597-603. Anderson, D.M., J.M. Patwell, K. Plaut, and K. McCullough. 1988. Dorland's Illustrated Medical Dictionary, 27th Ed. Philadelphia: W.B. Saunders. Barrow, C.S., L.A. Buckley, R.A. James, W.H. Steinhagen, and J. Chang. 1984. Sensory irritation: Studies on correlation to pathology, structure-activity, tolerance development, and prediction of species differences to nasal injury. Pp. 101-122 in Toxicology of the Nasal Passages, C.S. Barrow, ed. Washington, D.C.: Hemisphere. Bond, G.G., G.H. Flores, B.A. Stafford, and G.W. Olsen. 1991. Lung cancer and hydrogen chloride exposure: Results from a nested case-control study of chemical workers. J. Occup. Med. 33:958-961. Boulet, L.P. 1988. Increase in airway responsiveness following acute exposure to respiratory irritants. Reactive airway dysfunction syndrome or occupational asthma? Chest 94:476-481. Buckley, L.A., X.Z. Jiang, R.A. James, K.T. Morgan, and C.S. Barrow. 1984. Respiratory tract lesions induced by sensory irritants at the RD50 concentration. Toxicol. Appl. Pharmacol. 74:417-429. Burleigh-Flayer, H., K.L. Wong, and Y. Alarie. 1985. Evaluation of the pulmonary effects of HCl using CO2 challenges in guinea pigs. Fundam. Appl. Toxicol. 5:978-985. Coleman, E.H., and C.H. Thomas. 1954. The products of combustion of chlorinated plastics. J. App. Chem. 4:379-383. Cralley, L.V. 1942. The effect of irritant gases upon the rate of ciliary activity. J. Ind. Hyg. Toxicol. 24:193-198. Darmer, K.I., E.R. Kinkead, and L.C. DiPasquale. 1974. Acute toxicity in rats and mice exposed to hydrogen chloride gas and aerosols. Am. Ind. Hyg. Assoc. J. 35:623-631. Doub, H.P. 1933. Pulmonary changes from inhalation of noxious gases. Radiology 21:105-113. Dyer, R.F., and V.H. Esch. 1976. Polyvinyl chloride toxicity in fires. Hydrogen chloride toxicity in fire fighters. J. Am. Med. Assoc. 235:393-397. Elkins, H.B. 1959. Pp. 79-80 in The Chemistry of Industrial Toxicology, 2nd Ed. New York: John Wiley & Sons.

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 Ellenhorn, M. J., and D.G. Barceloux. 1988. Medical Toxicology: Diagnosis and Treatment of Human Poisoning. New York: Elsevier. Froneberg, B., P.L. Johnson, and P.J. Landrigan. 1982. Respiratory illness caused by overheating of polyvinyl chloride . Br. J. Ind. Med. 39:239-243. Gold, A., W.A. Burgess, and E.V. Clougherty. 1978. Exposure of firefighters to toxic air contaminants. Am. Ind. Hyg. Assoc. J. 39:534-539. Guyton, A.C. 1986. Pp. 405-407 in Textbook of Medical Physiology, 7th Ed. Philadelphia: W.B. Saunders. Hartzell, G.E., A.F. Grand, and W.G. Switzer. 1987. Modeling of toxicological effects of fire gases. VI. Further studies on the toxicity of smoke containing hydrogen chloride. J. Fire Sci. 5:368-391. Hartzell, G.E., H.W. Stacy, W.G. Switzer, D.N. Priest, and S.C. Packham. 1985. Modeling of toxicological effects of fire gases. IV. Intoxication of rats by carbon monoxide in the presence of an irritant. J. Fire Sci. 3:263-279. Henderson, Y., and H.W. Haggard. 1943. Pp. 126-127 in Noxious Gases and the Principles of Respiration Influencing Their Action. 2nd Ed. New York: Van Nostrand Reinhold. Huntoon, C.L. 1991. Toxicological Analysis of STS-40 Atmosphere. Rep. Memo. No. SD4/91-362. National Aeronautics and Space Administration, Lyndon B. Johnson Space Center, Houston, Tex. Jankovic, J., W. Jones, J. Burkhart, and G. Noonan. 1991. Environmental study of firefighters. Ann. Occup. Hyg. 35:581-602. Kaplan, H.L., A. Anzueto, W.G. Switzer, and R.K. Hinderer. 1988. Effects of hydrogen chloride on respiratory response and pulmonary function of the baboon. J. Toxicol. Environ. Health 23:473-493. Kaplan, H.L., A.F. Grand, W.G. Switzer, D.S. Mitchell, W.R. Rogers, and G.E. Hartzell. 1986. Effects of combustion gases on escape performance of the baboon and the rat. Danger. Prop. Ind. Mat. Rep. July/Aug.:2-12. Machle, W., and K. Kitzmiller. 1935. The effects of the inhalation of hydrogen fluoride. II. The response following exposure to low concentrations. J. Ind. Hyg. Toxicol. 17:223-229. Machle, W., F. Thamann, K. Kitzmiller, and J. Cholak. 1934. The effects of the inhalation of hydrogen fluoride. I. The response following exposure to high concentrations. J. Ind. Hyg. Toxicol. 16:129-145. Machle, W., K. V. Kitzmiller, E. W. Scott, and J.F. Treon. 1942. The effect of the inhalation of hydrogen chloride. J. Ind. Hyg. Toxicol. 24:222-225. Malek, D.E., and Y. Alarie. 1989. Ergometer within a whole-body plethysmograph to evaluate performance of guinea pigs under toxic atmospheres. Toxicol. Appl. Pharmacol. 101:340-355. Morgan, K.T., and T.M. Monticello. 1990. Airflow, gas deposition, and lesion distribution in the nasal passages. Environ. Health Perspect. 88:209-218. Morris, J.B., and F.A. Smith. 1982. Regional deposition and absorption of inhaled hydrogen fluoride in the rat. Toxicol. Appl. Pharmacol. 62:81-89. NIOSH. 1990. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publ.

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Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 No. 90-117. U.S. Department of Health and Human Services, National Institute for Occupational Safety and Health, Cincinnati, Ohio. NRC (National Research Council). 1987. Pp. 17-30 in Emergency and Continuous Exposure Guidance Levels for Selected Airborne Contaminants. Vol. 7. Washington, D.C.: National Academy Press. NRC (National Research Council). 1992. Guidelines for Developing Spacecraft Maximum Allowable Concentrations for Space Station Contaminants. Washington, D.C.: National Academy Press. Pavlova, T.E. 1976. Disturbance of development of the progeny of rats exposed to hydrogen chloride. Bull. Exp. Biol. Med. 82:1078-1081. Robbins, S.L., R.S. Cotran, and V. Kumar. 1984. Pp. 32-33 in Pathologic Basis of Disease, 3rd Ed. Philadelphia: W.B. Saunders. Rom, W.N., and H. Barkman. 1983. Respiratory irritants. P. 275 in Environmental and Occupational Medicine, W.N. Rom, ed. Boston: Little Brown. Ronzani, E. 1909. [Concerning the influence of inhaling irritating industrial gases on the strength of the body's defenses against infectious disease]. Arch. F. Hyg. 70:217-269. Sax, N.I., and R.J. Lewis Sr. 1987. P. 615 in Hawley's Condensed Chemical Dictionary. 11th Ed. New York: Van Nostrand Reinhold. Sellakumar, A.R., C.A. Snyder, J.J. Solomon, and R.E. Albert. 1985. Carcinogenicity of formaldehyde and hydrogen chloride in rats. Toxicol. Appl. Pharmacol. 81:401-406. Stavert, D.M., D.C. Archuleta, M.J. Behr, and B.E. Lehnert. 1991. Relative acute toxicities of hydrogen fluoride, hydrogen chloride, and hydrogen bromide in nose-and pseudo-mouth-breathing rats. Fundam. Appl. Toxicol. 16:636-655. Stokinger, H.E. 1981. The halogens and nonmetals boron and silicon. Pp. 2937-3043. in Patty's Industrial Hygiene and Toxicology, Vol IIB., 3rd. Ed., G.D. Clayton and F.E. Clayton, eds. New York: John Wiley & Sohn. Stone, J.P. 1975. Transport of hydrogen chloride by water aerosol in simulated fires. J. Fire Flam./Combust. Toxicol. 2:127-138. Stone, J.P., R.N. Hazlett, J.E. Johnson, and H.W. Carhart. 1973. The transport of hydrogen chloride by soot burning polyvinyl chloride. J. Fire Flam. 4:42-51. Toxigenics. 1983. 90-Day Inhalation Toxicity Study of Hydrogen Chloride Gas in B6C3F1 Mice, Sprague-Dawley Rats, and Fischer-344 Rats. Pp. 1-68 in Rep. No. 420-1087, CIIT Docket No. 20915. Toxigenics, Decatur, Ill. White, A., P. Handler, E.L. Smith, R.L. Hill, and I.R. Lehman. 1978. Pp. 1013-1015 in Principles of Biochemistry, 6th Ed. New York: McGraw-Hill. Wohlslagel, J., L.C. DiPasquale, and E.H. Vernot. 1976. Toxicity of solid rocket motor exhaust: effects of HCl, HF, and alumina on rodents. J. Combust. Toxicol. 3:61-70. Yu, C.P. 1978. A two-component theory of aerosol depostion in lung airways. Bull. Math. Biol. 40:693-706.