National Academies Press: OpenBook
« Previous: B2 C3 to C8 Aliphatic Saturated Aldehydes
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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%.

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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.

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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-

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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.

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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.

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Human Studies

One case-control study was conducted with workers exposed to HCl gas in chemical plants (Bond et al. 1991). However, no data were gathered on whether the exposures led to the irritation in the workers, and no data were gathered on the exposure concentrations that might have led to complaints of an irritant. Those data were not collected because this retrospective epidemiological study was carried out after most of the subjects had left their jobs (Bond, G., Dow Chemical Co., personal commun., 1993).

Animal Studies

Ronzani (1909) exposed 15 rabbits and 20 guinea pigs to HCl at 100 ppm for 50 d (6 h/d). The animals showed signs of agitation, nasal discharge, and mild lacrimation in the first hour of each day of exposure. No significant changes were found in red-blood-cell count; hemoglobin concentration; body-weight gain; bactericidal capacity of the lung; or susceptibility to a pulmonary challenge of anthrax, diplococcal bacteria, typhus, and tuberculosis. However, numerous guinea pigs, but not rabbits, developed slight emphysema.

In a study sponsored by the Chemical Industry Institute of Toxicology (CIIT), four groups of rodents were exposed to HCl (Toxigenics 1983). Each group consisted of 52 Fischer 344 (F344) rats, 52 Sprague-Dawley (SD) rats, and 52 B3C3F1 mice (31 males and 21 females of each strain). The groups were exposed to HCl at 0, 10, 20, or 50 ppm for 90 d (6 h/d, 5 d/w). Interim killings of 10 animals per sex-species-strain-exposure group exposed for 5 d showed that the effects of HCl were confined to the URT. The rats of the 20-ppm group showed minimal-to-mild rhinitis, and rhinitis in the 50-ppm group was mild. Similar results were observed in the rats killed after 90 d of HCl exposure (i.e., both strains of rats exposed to either 20 ppm or 50 ppm showed minimal-to-mild rhinitis). A 90-d exposure to HCl at 10 ppm caused minimal rhinitis in some of the exposed F344 rats and in none of the SD rats. However, rhinitis was not present in all exposed mice. Instead, mice exposed to HCl at 20 or 50 ppm for 90 d showed minimal-to-mild eosinophilic globules in the nose. In addition, the 50-ppm mouse group had varying degrees of cheilitis (inflammation of the lip) characterized by the presence of hemosiderin-laden macrophages (Toxigenics 1983). The incidence of nasal lesions is summarized in Table 3-3.

Sellakumar et al. (1985) found that chronic exposure of rats to HCl at 10 ppm for 128 w (6 h/d, 5 d/w) produced a nonstatistically significant increase

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

TABLE 3-3 Incidence of Nasal Lesions in Male and Female Animals

Exposure Concentration, ppm

F344 Rat Rhinitis Incidence

SD Rat Rhinitis Incidence

B6C3F1 Mouse Eosinophilic Globules

5 d

90 d

5 d

90 d

5 d

90 d

0

0/20

0/20

0/20a

5/20a

0/20

0/20

10

0/20

6/20a,b

0/20

8/20a

0/20

3/20c

20

5,20a,b

12/20b,c

4/20a

13/20b,c

0/20

6/20a,b

50

13/20b,c

5/20b,c

9/20b,c

13/20a,b

0/20

8/20b,c

a The responders were affected minimally.

b Statistically significant compared with the controls according to Fisher's exact probability test (p < 0.05).

c The responders were affected either minimally or mildly.

in rhinitis, epithelial hyperplasia, or squamous metaplasia in the nose. They concluded that at 10 ppm ''HCl did not induce any serious irritating effects in the nasal epithelium." The HCl exposure, however, increased the incidence of hyperplasia in the laryngeal and tracheal epithelium (21% and 26%, respectively, in the test rats vs. 2% and 6%, respectively, in control rats). The authors did not specify the degree of severity of the hyperplastic change observed in the exposed rats. Because the HCl exposure did not produce any mucosal injury in the nose and because HCl is believed to affect the nasal cavity more than other parts of the respiratory tract, the laryngeal and tracheal hyperplasia seen in 20% of the exposed rats was most likely only mild. Hyperplasia is an increase in the number of normal cells in response to stimuli without any loss of the normal cellular arrangement in a tissue (Robbins et al. 1984; Anderson et al. 1988). Mild laryngeal and tracheal hyperplasia should be viewed as adaptive changes without any significant functional decrement. Moreover, exposure of rats and mice to HCl at 10, 20 or 50 ppm in the CIIT-sponsored study revealed no lesions outside the nasal cavity (Toxigenics 1983). Therefore, laryngeal and tracheal hyperplasia will not be considered in setting the human exposure limits.

Systemic Toxicity of HCl

In the CIIT-sponsored study in which rats and mice were exposed to HCl at 0, 10, 20, or 50 ppm for 90 d (Toxigenics 1983), results of interim killings revealed no systemic macroscopic and microscopic lesions after 5 d of exposure. Clinical observations showed that the males and the females in the 50-

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

ppm group had depressed body-weight gain starting the third week of exposure. Male rats in the 50-ppm group also had depressed body-weight gain in the third to eighth weeks of exposure. After 90 d of exposure, no changes were found on urinalysis (volume, specific gravity, pH, protein, ketone, glucose, appearance, or presence of blood), hematology (erythrocyte count, hemoglobin, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin, total and differential white-blood-cell counts, or platelet and thrombocyte counts), or serum chemistry (glutamic pyruvic transaminase, urea nitrogen, total bilirubin, glucose, alkaline phosphatase, inorganic phosphorus, or calcium). Histopathological results of the 10 animals killed in each sex-species-strain-exposure group at the end of 90 d revealed no lesions in trachea, lungs, liver, kidneys, or other tissues.

Machle et al. (1942) reported that systemic histopathological changes were not seen in three rabbits and three guinea pigs exposed to HCl at 34 ppm for 4 w (6 h/d, 5 d/w). Sellakumar et al. (1985) also found no systemic toxicity in rats exposed to HCl at 10 ppm for 128 w.

Lack of Carcinogenic Response
Human Studies

Reports in the literature have failed to associate HCl exposure with tumors. Bond et al. (1991) did a case-control study with workers exposed to HCl gas in chemical plants to determine the correlation, if any, between cancer and HCl exposures. The workers were classified on the basis of HCl exposure concentrations (0, 0.25, 1.5, and 3.75 ppm [time-weighted average], as estimated by an industrial hygienist) and length of occupational HCl exposure (less than l y, 1-4.9 y, or 5 y or more). They studied a group of 308 workers who died of cancer of the lungs, bronchus, and trachea. The 95% confidence intervals of adjusted relative risk associated with cumulative exposure among the lung-cancer cases and controls were as follows: cumulative exposure of 0.1-3.0 ppm-y, 0.6-1.3; 4.0-12.4 ppm-y, 0.8-1.9; and at least 12.5 ppm-y, 0.6-1.8. Bond et al. (1991) concluded that there was "no evidence of an association between HCl exposure and lung cancer."

Animal Studies

Albert et al. (1982) exposed rats to HCl at 10 ppm for 84 w (6 h/d, 5 d/w) and found no carcinogenic response. A lifetime cancer bioassay conducted by the

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

same laboratory on rats exposed to the same concentration of HCl for 128 w showed no increase in tumor incidence in the nasal cavity or any organs (Sellakumar et al. 1985). A reported increase in nasal squamous metaplasia was not statistically significant. A co-exposure of rats to HCl at 10 ppm and formaldehyde at 14 ppm for 128 w did not affect formaldehyde carcinogenesis in the nasal cavity.

Genotoxicity

No genotoxicity data for HCl were found in the literature.

Developmental Toxicity

Only one report was found regarding possible developmental effects of HCl (Pavlova 1976). A 1-h exposure of an unspecified number of female rats to HCl at 300 ppm (450 mg/m3) on d 9 of gestation resulted in severe dyspnea and cyanosis. One-third of the dams died; autopsy revealed lung congestion, edema, and hemorrhage. Hypoxemia was detected in the surviving dams 5 d after the HCl exposure. These findings indicate that the exposure caused maternal toxicity. The surviving dams were allowed to deliver; more progeny of dams in the exposure group died than in the control group. In utero HCl exposure also might affect renal function. Diuresis was seen in the progeny of the HCl-exposed dams when they reached 2 mo of age, but it disappeared at 3 mo of age. However, it is not known that the renal-function impairment was due to HCl-induced maternal toxicity or the direct action of HCl on the embryoes. The severe maternal toxicity found by Pavlova (1976) renders any findings of the developmental toxicity of HCl questionable.

Interaction with Other Chemicals

No literature reports on the synergistic effects of HCl and other chemicals have been found, but there are reports of HCl interacting with other chemicals. Because the combustion of chlorinated plastics is known to produce both HCl and carbon monoxide (CO) (Coleman and Thomas 1954), the potential interaction of HCl and CO has been of toxicological interest (Hartzell et al. 1985, 1987). These authors showed that a co-exposure of rats to HCl at 400-1000 ppm lengthened the time CO took to incapacitate the rats by means of depressing of respiration. High concentrations of HCl have been shown to cause

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

pulmonary edema. Edema might slow the diffusion of CO across the pulmonary lining, thereby delaying the toxic action of CO.

Hartzell et al. (1987) also compared the lethality in rats of pure HCl, HCl in smoke generated by flaming thermodegradation of PVC, or HCl in smoke generated by flaming thermodegradation of PVC. The authors observed that HCl in smoke generated by flaming thermodegradation of PVC (30-min LC50 = 2141 ppm, 95% confidence limit [CL] = 1584 and 2505 ppm) was slightly more lethal than HCl with smoke generated by nonflaming thermodegradation (LC50 = 2924 ppm, 95% CL = 2171 and 3662 ppm), which in turn was slightly more lethal than pure HCl (LC 50 = 3817 ppm, 95% CL = 3051 and 4830 ppm).

Summary

Summaries of inhalation toxicity for humans and for animals are shown in Tables 3-4 and 3-5, respectively. The data are arranged in ascending order according to inhalation exposure concentrations.

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

TABLE 3-4 Toxicity Summary of Human Inhalation Exposure

Concentration, ppm

Exposure Duration

Species

Effects

Reference

<5

NS

Human

Apparently not harmful

Elkins 1959

≥5

NS

Human

Immediately irritating

Elkins 1959

10-50

Several h

Human

Tolerable

Henderson and Haggard 1943

>10

NS

Human

Highly irritating

Elkins 1959

35

NS

Human

Throat irritation

Henderson and Haggard 1943

50-100

1 h

Human

Tolerable

Henderson and Haggard 1943

1000-2000

NS

Human

Known to be extremely dangerous for even short exposures

Henderson and Haggard 1943

NS, not specified.

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

TABLE 3-5 Toxicity Summary of Animal Inhalation Exposure

Concentration, ppm

Exposure Duration

Species

Effects

Reference

10

90 d (6 h/d, 5 d/w)

Mouse

No significant changes in histopathology; no changes in urinalysis, serum chemistry, or hematology

Toxigenics 1983

10

90 d (6 h/d, 5 d/w)

Rat

Significant increase in incidence of minimal rhinitis in F344 rats, but not in Sprague-Dawley rats; no changes in urinalysis, serum chemistry, or hematology

Toxigenics 1983

10

128 w (6 h/d, 5 d/w)

Rat

Incidence of mucosal hyperplasia was increased in the larynx and trachea but not in the nose; no increase in tumor incidence

Sellakumar et al. 1985

20

90 d (6 h/d, 5 d/w)

Mouse

Minimal increase in eosinophilic globules in nose; no histopathology in other tissues; no changes in urinalysis, serum chemistry, or hematology

Toxigenics 1983

20

90 d (6 h/d, 5 d/w)

Rat

Minimal-to-mild rhinitis, but no histopathology in other tissues; no changes in urinalysis, serum chemistry, or hematology

Toxigenics 1983

34

4 w (6 h/d, 5 d/w)

Rabbit, guinea pig

No histopathology

Machle et al. 1942

50

90 d (6 h/d, 5 d/w)

Mice

Pigmented macrophages in lips; minimal ulcerative cheilitis; minimal-to-mild eosinophilic globules in nose; but no changes in urinalysis, serum chemistry, or hematology, and no histopathology in tissues other than the lip or nose; depressed body weight gain

Toxigenics 1983

50

90 d (6 h/d, 5 d/w)

Rat

Depressed body weight gain in the w 3 to 8 of exposure in males; minimal-to-mild rhinitis; no changes in urinalysis, serum chemistry, and hematology, as well as no histopathology in tissues other than the nose

 

67

5 d (6 h/d)

Guinea pig

Mild bronchitis with some peribronchial fibrosis; no deaths

Machle et al. 1942

67

5 d (6 h/d)

Rabbit

Lobular pneumonia and lung abscesses; no deaths

Machle et al. 1942

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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).

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

(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-

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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.

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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.

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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.

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×

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.

Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 60
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 61
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 62
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 63
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 64
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 65
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 66
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 67
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 68
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 69
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 70
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 71
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 72
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 73
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 74
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 75
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 76
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 77
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 78
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 79
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 80
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 81
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 82
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 83
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 84
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 85
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 86
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 87
Suggested Citation:"B3 Hydrogen Chloride." National Research Council. 2000. Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4. Washington, DC: The National Academies Press. doi: 10.17226/9786.
×
Page 88
Next: B4 Isoprene »
Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 Get This Book
×
Buy Paperback | $77.00 Buy Ebook | $59.99
MyNAP members save 10% online.
Login or Register to save!
Download Free PDF

The National Aeronautics and Space Administration (NASA) is aware of the potential toxicological hazards to crew members that might be associated with prolonged spacecraft missions. Despite major engineering advances in controlling the atmosphere within spacecraft, some contamination of the air appears inevitable. NASA has measured numerous airborne contaminants during space missions. As the missions increase in duration and complexity, ensuring the health and well-being of astronauts traveling and working in this unique environment becomes increasingly difficult.

As part of its efforts to promote safe conditions aboard spacecraft, NASA requested the National Research Council (NRC) to develop guidelines for establishing spacecraft maximum allowable concentrations (SMACs) for contaminants, and to review SMACs for various spacecraft contaminants to determine whether NASA's recommended exposure limits are consistent with the guidelines recommended by the subcommittee. In response to this request, the NRC first developed criteria and methods for preparing SMACs for spacecraft contaminants, published in its 1992 report Guidelines for Developing Spacecraft Maximum Allowable Concentrations for Space Station Contaminants. Since then, the NRC's Subcommittee on Spacecraft Maximum Allowable Concentrations has been reviewing NASA's documentation of chemical-specific SMACs. This report is the fourth volume in the series Spacecraft Maximum Allowable Concentrations for Space Station Contaminants. The first volume was published in 1994 and the second and third in 1996.

Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants: Volume 4 has been reviewed in draft form by individuals chosen for their technical expertise and diverse perspectives in accordance with procedures approved by the NRC's Report Review Committee for reviewing NRC and Institute of Medicine reports. The purpose of that Independent review was to provide candid and critical comments to assist the NRC in making the published report as sound as possible and to ensure that the report meets institutional standards for objectivity, evidence, and responsiveness to the study charge. The review comments and draft manuscript remain confidential to protect the integrity of the deliberative process.

  1. ×

    Welcome to OpenBook!

    You're looking at OpenBook, NAP.edu's online reading room since 1999. Based on feedback from you, our users, we've made some improvements that make it easier than ever to read thousands of publications on our website.

    Do you want to take a quick tour of the OpenBook's features?

    No Thanks Take a Tour »
  2. ×

    Show this book's table of contents, where you can jump to any chapter by name.

    « Back Next »
  3. ×

    ...or use these buttons to go back to the previous chapter or skip to the next one.

    « Back Next »
  4. ×

    Jump up to the previous page or down to the next one. Also, you can type in a page number and press Enter to go directly to that page in the book.

    « Back Next »
  5. ×

    Switch between the Original Pages, where you can read the report as it appeared in print, and Text Pages for the web version, where you can highlight and search the text.

    « Back Next »
  6. ×

    To search the entire text of this book, type in your search term here and press Enter.

    « Back Next »
  7. ×

    Share a link to this book page on your preferred social network or via email.

    « Back Next »
  8. ×

    View our suggested citation for this chapter.

    « Back Next »
  9. ×

    Ready to take your reading offline? Click here to buy this book in print or download it as a free PDF, if available.

    « Back Next »
Stay Connected!