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Combined Exposures to Hydrogen Cyanide and Carbon Monoxide in Army Operations: Final Report (2008)
Board on Environmental Studies and Toxicology (BEST)

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. "6 Are There Other Deleterious Effects of Varying Exposures to Carbon Monoxide and Hydrogen Cyanide?." Combined Exposures to Hydrogen Cyanide and Carbon Monoxide in Army Operations: Final Report. Washington, DC: The National Academies Press, 2008.

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Combined Exposures to Hydrogen Cyanide and Carbon Monoxide in Army Operations: Final Report

6
Are There Other Deleterious Effects of Varying Exposures to Carbon Monoxide and Hydrogen Cyanide?

We have considered the direct effects of carbon monoxide (CO) and hydrogen cyanide (HCN) on both physical and neuropsychological and neurophysiologic performance. It is clear from the medical literature that there are other direct and indirect effects of both CO and HCN in humans that might be relevant to human performance, either acutely or chronically. For example, CO may play a role in normal neurotransmission and vasomotor control; however, the pathophysiologic effect of low-level exposures is not yet well understood (EPA 2000).

Perhaps the best studied is the effect of CO inhalation on cardiac function. Several studies have looked at risks of cardiac dysrhythmia in patients with coronary artery disease (CAD) exposed to CO (Hinderliter et al. 1989; Sheps et al. 1990, 1991; Chaitman et al. 1992; Dahms et al. 1993). Carboxyhemoglobin COHb levels below 6% did not appear to exert significant effects on rhythm. However, 6% COHb resulted in an increased frequency of complex premature ventricular beats in the CAD patients (Chaitman et al. 1992; Dahms et al. 1993). Effects were more pronounced with advancing age. Another group of studies looked at exercise tolerance in CAD patients during CO exposure (Sheps et al. 1987; Adams et al. 1988; Allred et al. 1989a,b; Allred 1991; Kleinman et al. 1989; Chaitman et al. 1992; Dahms et al. 1993). Most of these studies have shown decreased exercise tolerance in CAD patients at COHb levels in the 3-4% range, a range commonly found in smokers. Although not specifically studied, other cardiac diseases, such as congenital heart disease and congestive heart failure, with the potential for hypoxia would probably show similar effects. At least one human study has suggested that chronic CO exposure in the occupational setting may contribute to the development of arteriosclerotic heart disease with aging (Stern et al. 1988). Although no similar studies have been done on HCN, it probably would have similar effects at concentrations capable of producing mild tissue hypoxia. These effects should be considered, given the existing data on CO and HCN concentrations within armored vehicles and the uncertainty about comprehensive screening of crew members.

There are few data in the medical literature relating to the effects of chronic or frequent intermittent exposure to either CO or HCN. Epidemiologic studies, primarily in the occupational literature, have suggested that chronic exposure to HCN may result in the formation of enlarged thyroid glands and hypothyroidism (El Ghawabi et al. 1975; Blanc et al. 1985). Chronic headaches, tremors, chronic fatigue, and changes in smell and taste have also been reported (Radojicic 1973; El-Ghawabi et al. 1975; Blanc et al. 1985). The incidence of these effects and the magnitude of exposure required to produce them are unknown. It is also not known whether these effects have occurred or may occur under the conditions of interest to this study.

Similar data from the literature on CO suggest that chronic occupational exposure can result in chronic headaches, chronic fatigue, sleep and memory problems, vertigo, and emotional problems (Beck

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Combined Exposures to Hydrogen Cyanide and Carbon Monoxide in Army Operations: Final Report 6 Are There Other Deleterious Effects of Varying Exposures to Carbon Monoxide and Hydrogen Cyanide? We have considered the direct effects of carbon monoxide (CO) and hydrogen cyanide (HCN) on both physical and neuropsychological and neurophysiologic performance. It is clear from the medical literature that there are other direct and indirect effects of both CO and HCN in humans that might be relevant to human performance, either acutely or chronically. For example, CO may play a role in normal neurotransmission and vasomotor control; however, the pathophysiologic effect of low-level exposures is not yet well understood (EPA 2000). Perhaps the best studied is the effect of CO inhalation on cardiac function. Several studies have looked at risks of cardiac dysrhythmia in patients with coronary artery disease (CAD) exposed to CO (Hinderliter et al. 1989; Sheps et al. 1990, 1991; Chaitman et al. 1992; Dahms et al. 1993). Carboxyhemoglobin COHb levels below 6% did not appear to exert significant effects on rhythm. However, 6% COHb resulted in an increased frequency of complex premature ventricular beats in the CAD patients (Chaitman et al. 1992; Dahms et al. 1993). Effects were more pronounced with advancing age. Another group of studies looked at exercise tolerance in CAD patients during CO exposure (Sheps et al. 1987; Adams et al. 1988; Allred et al. 1989a,b; Allred 1991; Kleinman et al. 1989; Chaitman et al. 1992; Dahms et al. 1993). Most of these studies have shown decreased exercise tolerance in CAD patients at COHb levels in the 3-4% range, a range commonly found in smokers. Although not specifically studied, other cardiac diseases, such as congenital heart disease and congestive heart failure, with the potential for hypoxia would probably show similar effects. At least one human study has suggested that chronic CO exposure in the occupational setting may contribute to the development of arteriosclerotic heart disease with aging (Stern et al. 1988). Although no similar studies have been done on HCN, it probably would have similar effects at concentrations capable of producing mild tissue hypoxia. These effects should be considered, given the existing data on CO and HCN concentrations within armored vehicles and the uncertainty about comprehensive screening of crew members. There are few data in the medical literature relating to the effects of chronic or frequent intermittent exposure to either CO or HCN. Epidemiologic studies, primarily in the occupational literature, have suggested that chronic exposure to HCN may result in the formation of enlarged thyroid glands and hypothyroidism (El Ghawabi et al. 1975; Blanc et al. 1985). Chronic headaches, tremors, chronic fatigue, and changes in smell and taste have also been reported (Radojicic 1973; El-Ghawabi et al. 1975; Blanc et al. 1985). The incidence of these effects and the magnitude of exposure required to produce them are unknown. It is also not known whether these effects have occurred or may occur under the conditions of interest to this study. Similar data from the literature on CO suggest that chronic occupational exposure can result in chronic headaches, chronic fatigue, sleep and memory problems, vertigo, and emotional problems (Beck

OCR for page 21
Combined Exposures to Hydrogen Cyanide and Carbon Monoxide in Army Operations: Final Report 1936; Alistair et al. 2000; Penney 2000). Again, the incidence of these effects and the conditions necessary for their occurrence are not known. It is also not known whether these effects have occurred or may occur under the conditions of interest to this study. CO and HCN are the major toxic gases considered in this report; however, the committee recognizes that other gases, such as oxides of nitrogen and sulfur dioxide, are produced during the combustion process and from other sources within armored vehicles. Both CO2 and HCN are known to affect respiratory rates (Peterson and Stewart 1975; Purser et al. 1984), and the presence of these agents could result in an increased uptake of CO and other toxic gases. Data on such complex mixtures are insufficient to ascertain whether any such effects are functionally relevant to the questions the committee has been asked to address. Recommendation The Army should consider close and systematic surveillance of vehicle crews with the intent of identifying any increased risk of sudden death, myocardial infarction, or other significant medical problems.