The effects of smoking on military readiness was extensively reviewed in a 1986 report from the US Army Aeromedical Research Laboratory (Dyer, 1986); the sections below summarize that report’s major findings and update the literature with additional information from the few new studies available on the subject. The committee was surprised and dismayed by the lack of recent research on the effects of tobacco use on military readiness, given the number of tobacco users in the military and the need for military readiness during the last decade.
Smoking may impair performance both through direct exposures to nicotine, carbon monoxide (CO), and other tobacco-smoke toxicants and through nicotine withdrawal. Nicotine withdrawal refers to the effects of being unable to take in nicotine when a smoker would usually do so because of lack of tobacco or restrictions on its use. Regular intake of nicotine produces changes in brain chemistry and function, as described in detail in Chapter 3, causing the brain to become dependent on nicotine for normal functioning. In the absence of nicotine, brain function becomes abnormal, leading to withdrawal symptoms, which may include irritability; restlessness; anger; difficulty in concentrating; anxiety; depressed mood; and impaired performance in a variety of attentional, reaction-time, and other cognitive tasks (Sommese and Patterson, 1995). The potential adverse consequences of nicotine withdrawal on military performance, specifically cognitive functions and activities, is discussed below. Although most research indicates that nicotine acts as a stimulant to improve or maintain performance in simple perceptual and reaction-time tasks, there is evidence that smoking results in short-term impairment of performance in complex information-processing tasks (Spilich et al., 1992).
Smoking impairs strength and physical endurance in part by exposing the smoker to CO, which reduces the oxygen-carrying capacity of blood. Smoking also causes chronic pulmonary inflammation and impairs blood-vessel endothelial function, reducing the vascular dilation associated with physical activity. In most studies, maximal oxygen consumption, reflecting aerobic capacity, is generally similar in young (18–24 years old) smokers and nonsmokers (Chevalier et al., 1963; Knapik et al., 2001; Krumholz et al., 1965; Maksud and Baron, 1980; Montoye et al., 1980). Older smokers have lower aerobic capacity than older nonsmokers (Raven et al., 1974). Among younger smokers, the immediate effects of smoking are reduced maximal oxygen consumption