Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants Volume 2 (1996) / Chapter Skim
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B3 Carbon Dioxide
B3 Carbon Dioxide
Pages 105-188
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From page 105... ...
CO2 is not used in space shuttles, but it will be used as a fire extinguishant in the space station.
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06 SMACS FOR SELECTED AIRBORNE CONTAMINANTS Metabolism is a source of CO2 in spacecraft, and thermodegradation of organic materials is a potential source of CO2 (Coleman et al., 1968; Terrill et al., 1978; Wooley et al., 19791. Humans produce CO2 via oxidative metabolism of carbohydrates, fatty acids, and amino acids; the production rate is dependent on the caloric expenditure of the individual (Baggott, 1982; Diamondstone, 1982; LeBaron, 1982; Olson, 1982~.
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Tremor was produced in human subjects exposed to 6% CO2 for several hours (number of subjects unknown) (Schulte, 1964)
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reported that human subjects exposed to 2% or 3 % CO2 for several hours developed headaches on mild exertion; the
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(1970) found that mild-to-moderate frontal headaches developed in six of eight human subjects exposed to 3.9% CO2 for 30 min while doing two-thirds-maximal exercise.
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Menn et al. failed to detect intercostal muscle pain in eight human subjects exposed to 1.
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On the first day of a patrol, the plasma levels of calcium decreased, with no change in plasma phosphorus levels, but the erythrocyte level of cal .
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The hyperventilatory response is due mainly to a tidal volume increase, although the respiratory rate was found to increase in one study but not in another (Schaefer, 1963b; Glatte et al., 1967a; Guillerm and Radziszewski, 19791. The hyperventilatory response to inhaled CO2 is triggered by CO2's effect on chemoreceptors in the brain and the carotid chemoreceptors (Cotes, 1979, pp.
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CARBON DIOXIDE ~ ~ 3 TABLE 3-2 Hyperventilatory Responses to Acute CO2 Exposures Increase in Minimum Volume, % (mean + SD) Reference Concen- Exposure "ration, ~ No.
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. in some of the guinea pigs exposed to 15% CO2 in 21% 02, Schaefer's group detected subpleural atelectasis, an increase of lameliar bodies in alveolar lining cells, congestion, edema, and hemorrhage in the lungs in 1 or 6 h (Schaefer et al., 1964a)
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From page 115... ...
In another human study, a 15-30-min exposure to 5 % or 7% CO2 caused increases in blood pressure and cerebral blood flow and a decrease in cerebrovascular resistance (Kety and Schmidt, 19481. In the same study, no change in cardiac output was detected, but in another study, a 4-25-min exposure of volunteers to 7.5% CO2 increased the cardiac output and blood pressure (GrolIman, 1930~.
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postulated that the CO2-induced EKG changes were due to CO2-induced acidosis because the changes were seen with acidosis in a 45-90-min exposure of two patients at 5% CO2 in 95 % O2 and the changes disappeared within 30 min of terminating the CO2 exposure. Nervous System Exposures to CO2 at the appropriate concentrations could cause CNS depression.
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From page 117... ...
It is, therefore, possible that the CNS depression suffered by the crew was due to the relatively low oxygen concentration, carbon monoxide, or certain organic solvents instead of the 3-3.5 % CO2. Brown's test produced giddiness and headache in four human subjects exposed to 3.2% CO2 for several hours (Brown, 1930b)
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From page 118... ...
Some studies have shown that acute exposures to CO2 at high concentrations produced purely depressive signs and symptoms. For instance, unconsciousness was detected in human subjects exposed to 10% CO2 for several hours (Schulte, 1964)
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The disappearance was apparently due to sloughing of mature spermatids and Sertoli cells in the seminiferous tubules, resulting in cellular debris in the lumen. The degenerative change
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there was a report that acute exposures of guinea pigs to high concentrations of CO2 might also damage other tissues. Schaefer et al.
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As a result, the SMACs are not set based on any intestinal or splenic end point. Subchron~c and Chronic Toxicity Dyspnea and Intercostal Pain Acute CO2 exposures could cause headaches, dyspnea, and intercostal muscle pain, especially during exercise or exertion.
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TABLE 3-4 Data on CO2-Induced Headaches Concen- Exposure "ration, ~ Duration Intensity of Headache Reference 2 30 d Rare headache even during exercise Radziszewski et al., 1988 2.8 15-30 d Occasional mild transient headache Sinclair et al., during heavy exertion 1969, 1971 2.9 30 d Slight headache Radziszewski et al., 1988 3 5 d Mild-to-moderate throbbing frontal Glatte et al., 1967; headache that disappeared in 2 d Menn et al., 1968 3.8 30 d Intense and annoying headache Radziszewski et al., 1988 3.9 11 d Occasional mild transient headache Sinclair et al., during heavy exertion 1969, 1971 4 5 d Mild-to-moderate throbbing frontal Glatte et al., 1967a; headache that disappeared in 2 d Menn et al., 1968 4.3 30 d Intense and annoying headache Radziszewski et al., 1988 Nervous System As discussed in the Acute Toxicity subsection, it is questionable whether acute CO2 exposures at less than 5% cause CNS depression. Similarly, there are conflicting data on the CNS effects of subchronic CO2 exposures at 3-5%.
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The data available indicate that a subchronic CO2 exposure at less than 2% definitely has no CNS impairment effect. In a summary report of a 42-d study of 23 human volunteers exposed to ~ .5 % CO2 in a submarine, Schaefer (1961)
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(1967a) found that an exposure of seven humans to CO2 at 21 mm Hg (equivalent to 2.~% at sealevel)
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(1964) showed that the time course of arterial pH changes in guinea pigs exposed to 15% CO2 followed that of pCO2 quite closely.
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(1963b) found that, in 20 human subjects exposed to 1.5 % CO2 for 42 6, the plasma calcium levels were lowered in the first 3 w of the exposure, but they returned to the pre-exposure levels in the last 3 w.
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(1979b) with guinea pigs exposed to 0.5% CO2 for ~ w, no change in plasma calcium levels was detected in w 4 and an increase was detected in w S
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They found no changes in the daily urine volume and the urinary and fecal excretions of calcium. There were two studies in which the amounts of urinary calcium excretion were reported, but the investigators were silent about the daily urine volume.
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Bones and Kidneys The changes in plasma calcium levels discovered by Schaefer et al.
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An S-w exposure of guinea pigs to 0.5% CO2 resulted in an increase in the plasma calcium level and a larger than 25 % rise in the renal calcium levels with no change in bone calcium levels in w ~ (but not in w 4-6) (Schaefer et al., 1979b)
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The question is whether the larger number of workdays lost to ureteral calculi in 1963-1967 was due to the higher CO2 concentrations onboard. In other words, could subchronic CO2 exposures cause ureteral calculi in humans?
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From page 132... ...
Urinary stones are usually formed when calcium salts become supersaturated in the urine (Coe and Favus, 19871. Since CO2 exposures have been shown to either lower or not change urinary calcium excretion (Schaefer et al., 1963b; Glatte et al., 1967a; Davies et al., 197Sa)
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hypothesized that the increase in plasma calcium levels was due to CO2 binding to the bone and releasing calcium from the bone in guinea pigs. As a result of this hypothesis, several scientists in NASA raised their concerns on the potential of CO2 in releasing calcium from the bone of astronauts in the space station and causing kidney stones.
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From page 134... ...
The plasma calcium levels reached a plateau at about 5 6, and the urinary calcium excretion reached a plateau in about 20 d. To prove that CO2 exposures in spacecraft play no important role in calcium changes in astronauts, calcium data from a space mission with CO2 concentrations at much less than 5.3 mm Hg, but of a similar duration as Skylab missions, is needed as control data.
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. ~ 1 1 1 ~ 10 20 30 40 50 60 70 80 90 Days _- n = B -a- n = 6 - -n =4 -X-n =3 FIGURE 3-1 Inflight calcium data from Skylab and Spacelab 2 .
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From page 136... ...
Table 3-8 shows the amounts of ventilatory increase attained, after a plateau has been reached, in human subjects exposed to CO2 for more than a day. The sum of the data shows that it takes at least ~ % CO2 to increase, with statistical significance, the minute volume after the hyperventilatory response reaches a plateau after the first few hours in a subchronic exposure.
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An Air Force study showed that a 5-d exposure of seven human volunteers to 3 % CO2 resulted in no changes in maximum breathing capacity, vital capacity, and 1-s vital capacity (Glatte et al., 1967a)
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Due to the fact that there was no difference between the arterial PO2 in the guinea pigs with CO2-induced type II pneumocyte changes and the control guinea pigs (Douglas et al., 1979) , the proliferation of type lI pneumocytes caused by 1 % CO2 in guinea pigs did not impair gas exchanges.
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However, However, Douglas et al., 1979 showed that exposure to l% CO2 increased the number and size of lamellar bodies by only 30-50% in type T} pneumocytes of guinea pigs. Assuming that the amount of lung surfactants secreted by type IT pneumocytes in these guinea pigs was also increased by 30-50%, increases of such magnitude are not expected to have any harmful effect in the lung because any resultant decreases in surface tension would be of little clinical significance.
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From page 140... ...
According to the investigators, the experiment "failed to demonstrate any signs of myocardial damage in guinea pigs exposed for periods up to 7 days to 15% CO2" (Schaefer et al., 19711. The fat deposition probably represents only a metabolic change in the heart and not any serious damage.
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From page 141... ...
(1971) reported that the testes of the guinea pigs and rats exposed to 3% CO2 for 42 ~ or to 1.5% CO2 for 6 mo appeared normal histologically, it can be concluded that a subchronic exposure to 3 % CO2 is not toxic to the testis.
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From page 142... ...
In these workers, exposed to 1.1% CO2 TWA with 3-min excursions up to ~ %, the blood HCO3- levels did not differ from the control values (Riley and Barnea-Bromberger, 1976~. Genetic Toxicity No genotoxic data of CO2 have been found.
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A subcutaneous injection of naloxone at 5 mg/kg has been shown to increase the hyperventilatory response to CO2 in rats because naloxone displaced endogenous endorphins from central opioid receptors (Tsom and Elshowihy, 19821. In addition to interacting with CO, CO2 is known to interact with NO2.
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From page 162... ...
TABLE 3-11 Spacecraft Maximum Allowable Concentrations Duration ppm mg/m3 Target Toxicity 1 h 13,000 23,400 CNS depression, visual disturbance 24 h 13,000 23,400 CNS depression, visual disturbance 7 da 7000 12,600 Hyperventilation 30 d 7000 12,600 Hyperventilation 180 d 7000 12,600 Hyperventilation aThere was no 7-d SMAC. Space-shuttle flight rules require mission termination at 2% or above and flight surgeon's evaluation at 1-2% (NASA, 1988~.
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From page 163... ...
Visual Impa~nnents, Tremors, and CNS Depression An exposure of human subjects to 6% CO2 for several hours produced visual disturbances and tremors (Schulte, 1964~. Similarly, visual intensity discrimination was also found to be reduced in a 1-2 min exposure of human subjects to 6% CO2 (Gelihorn, 1936~.
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From page 164... ...
(1988) did not find any visual problems or tremors in six human subjects exposed to 2.9% CO2 for 30 d.
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From page 165... ...
These individuals performed a 45-min continuous steady state exercise at low, moderate, or heavy load once during the 1-h exposure and twice daily during the 15-20 d of CO2 exposure. Radziszewski and his colleagues reported no dyspnea or intercostal pain in six human subjects exposed to 2.9% CO2 and who exercised at a 150-watt workload for 10 min twice a week (Radziszewski et al., 19881.
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From page 166... ...
should also be a NOAEL for these six subjects. 7-d, 30-d, and 180-d ACs for dyspnea and intercostal pain = 15-20 d NOAEL x 1/small n factor 15-20 d NOAEL x (square root of n)
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From page 167... ...
In a French study, there was no report of any symptoms or complaints in six human volunteers exposed for 30 d to 2% CO2, which increased the minute volume by 45% in d 8-30 (Radziszewski et al., 1988; Guillerm end Radziszewski; 19791. So the Air Force and French studies indicate that humans can tolerate 2-3.9% CO2; the low end of the range, 2%, appears to be a prudent choice as the NOAEL based on tolerability.
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From page 168... ...
(1967a) Air Force study showed that six out of seven human volunteers easily tolerated daily 1-h moderate exercises at a 100watt workload during a S-d exposure to 3 % CO2.
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From page 169... ...
Theoretically, increased total lung resistance could be caused by an increase in tissue resistance in the lung or airway resistance. Although an increased tissue resistance could be produced by CO2 because CO2 is known to raise the surface tension of the alveolar extract (Schaefer et
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From page 170... ...
and Widdicombe (1962) that an acute exposure to ~ % CO2 increased the total lung resistance without changing the lung compliance supports the notion that CO2 increases the total lung resistance by increasing the airway resistance.
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From page 171... ...
(1971) was not adequately controlled, the absence of testicular damage in guinea pigs and rats exposed to 3% CO2 for 42 d suggests that 3% could be treated as a NOAEL for subchronic exposures.
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From page 172... ...
, CO2's SMACs need not be adjusted for hypercalciuria because CO2 exposures are not known to increase urinary calcium excretion in human subjects (in fact CO2 exposures decreased urinary calcium excretion in human subjects) (Messier et al., 1976; Schaefer et al., 1963b)
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From page 173... ...
no on' v)
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From page 174... ...
1988. Relationship of animal protein-rich diet to kidney stone formation and calcium metabolism.
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From page 175... ...
No. 55-357, WrightPatterson Air Force Base, Dayton, Ohio.
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From page 176... ...
1936. Effect of O2 lack, variations in CO ~content of inspired air, and hyperpnea on visual intensity discrimination.
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From page 177... ...
1969. The Effects on Respiratory Dead Space of Prolonged Exposure to a Submarine Environment.
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From page 178... ...
1948. The effects of altered arterial tensions of carbon dioxide and oxygen on cerebral blood flow and cerebral oxygen co-nsumption of normal young men.
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1987. Toxicological interactions between carbon monoxide and carbon dioxide.
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From page 180... ...
1962. Effect of changes in blood as tensions and carotid sinus pressure on tracheal volume and total lung resistance to airflow.
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From page 181... ...
1962. Development of hyaline membranes and atelectasis in experimental chronic respiratory acidosis.
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From page 182... ...
1949b. [Respiratory and acid-base balance during prolonged exposure to a 3 % CO2 atmosphere.]
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From page 183... ...
656. Naval Submarine Medical Research Laboratory, Groton, Conn.
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From page 184... ...
1979b. Effect of prolonged exposure to 0.5% CO2 on kidney calcification and ultrastructure of lungs.
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From page 185... ...
1991. The influence of diet on urinary risk factors for stones in healthy subjects and idiopathic renal calcium stone formers.
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From page 186... ...
1979. Effect of prolonged exposure to elevated carbon monoxide and carbon dioxide levels on red blood cell parameters during submarine patrols.
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From page 187... ...
1975. Carbon dioxide poisoning after prolonged exposure.
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