when firing weapons from inside armored vehicles. It is important to note that these studies involving research on human subjects must comply with federal and other applicable regulations for the protection of human subjects of research. Protocols for research involving human subjects should receive approval by a certified Institutional Review Board.
As more data become available as a result of the committee’s recommended experiments, DOD should consider how other factors may affect the relationship between exposure and effects.
Because of the weakness of the database regarding adverse effects of small increases in body CO on brain functions, such as those involved in decision making and alertness, it is not possible at this time to make conclusions about the extent to which environmental factors, such as temperature and humidity, can confound relationships between CO exposures and performance. However, environmental factors can alter CO uptake that can potentially translate into adverse effects of CO.
The partial pressure of oxygen (O2) in the ambient air is reduced as altitude increases. This, in turn, reduces the partial pressure of O2 in the inspired air as well as the volume of O2 transported to human tissues by hemoglobin in the blood. The result is tissue hypoxia, the severity of which is determined by the absolute altitude. As described by the CFK equation, CO both competes with O2 for hemoglobin, thus reducing the amount of O2 that can be transported, and increases the affinity of hemoglobin for O2 so that O2 is released less readily in the tissues. Thus, reduced O2 transport to the tissues due to altitude may be further reduced by inhaled CO (McGrath, 2000). The resulting tissue hypoxia would be exacerbated by stress and altitude-induced hyperventilation, which would increase CO uptake and cause respiratory alkalosis, further reducing O2 transport to the tissues. Thus, possible adverse effects from CO exposure of military personnel within armored vehicles might be amplified at altitude.
CO uptake at a given inspired CO concentration might possibly decrease as a result of increased carboxyhemoglobin (COHb) in tobacco smokers or as a result of previous exposure to high inspired CO concentrations due to previous gun firings. It will be important to consider the extent to which adaptation via tobacco smoking may protect soldiers against detrimental effects of small increases in COHb due to CO uptake secondary to cannon firings.
Future computational efforts for estimating the health risks posed by exposure to combustion products in armored vehicles could include evaluation of the Toxic Gas Assessment (TGAS) model. The TGAS models (versions 1.0 and 2.0) were developed to predict the onset of death or immediate incapaci-