7 Effects of Military Fuel Vapors on the Central Nervous System All volatile hydrocarbons are central-nervous-system (CNS) depressants and can produce anesthesia or asphyxia at sufficiently high concentrations (Andrews and Snyder, 1986; Marshall and Wollman, 1985). The extent to which vapors from JP-5, JP-8, and DFM are effective as CNS depressants depends on the volatility of their component hydrocarbons. The vapors from these fuels contain a mixture of volatile hydrocarbons.

The achievable depth of anesthesia and the rate at which anesthesia occurs are related to the minimum alveolar concentration (MAC). MAC, expressed as percent of air in the alveolus, is the concentration necessary to produce anesthesia for the components of the vapor and their blood/air partition coefficients. If the MAC is low (e.g., halothane = 0.75% and methoxyflurane = 0.16%), the chemical is a highly potent anesthetic. If the MAC is high (e.g., nitrous oxide = 105%), the chemical is not a potent anesthetic.

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However, if the blood/gas partition ratio is high (e.g., methoxyflu. Rane = 12), the rate of anesthesia is slow; if the blood/gas partition ratio is low (e.g., halothane = 2.3 and nitrous oxide = 0.47), the rate of anesthesia is rapid.

Volatility also remains a key factor among the fuels. The maximum vapor concentration achievable with methoxyflurane is only 3%, whereas halothane can achieve a concentration of 32%. Thus, the degree to which the components of the fuel can volatilize, their potency as CNS depressants, and their blood/air partition coefficients are the determining factors in their ability to depress the CNS. These values have not been reported for JP-5, JP-8, and DFM. NEUROPHYSIOLOGICAL AND PSYCHOLOGICAL EFFECTS OF FUEL VAPORS Many organic solvents, including those that are components of military fuels, have the potential to cause narcosis and death after acute exposure.

Workers acutely exposed to high concentrations of solvents typically show signs of CNS disturbance. Effects of acute high-level exposure include disorientation, euphoria, giddiness, confusion, tremor, and convulsions. Recovery from CNS effects is rapid and complete in the majority of subjects following removal from exposure. For example, Davies (1964) described a jet pilot who experienced exposure to JP-4 from a fuel leak in the cockpit during flight.

It was estimated that the vapor concentration to which he was exposed reached 3,000-7,000 ppm (24,000-56,000 mg/m 3). He reported feeling groggy and weak and was forced to land his aircraft.

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Upon landing, he demonstrated a staggering gait, slurring of speech, and a number of signs indicative of early anesthesia. Physical examination revealed an odor of fuel on his flying suit; a slight stagger to his gait; slurring of speech; peripheral sensory loss (positive Romberg); generalized, mild muscular weak. Ness; and possible decreased sensation to pain on the surface of his arm. The pilot had previous experience with hypoxia and denied that it resembled the present episode.

He reported that he did not feel 'normal' for 36 hr after exposure but appeared in good condition during the next few days and 5 months later. Porter (1990) described the effects experienced by two aviators after acute exposure to JP-5 fuel vapor. Symptoms included headache, nausea, euphoria, memory defects, wobbly gait, impaired hand-eye coordination, runny nose, sneezing, anorexia, and excessive fatigue. The examination of blood and urine from both aviators was negative for aromatic hydrocarbons and carbon monoxide (. Workers (n = 16).

The heavily exposed group (group A) had exposure described as “continuous exposure for several hours daily to high concentrations of jet fuel fumes in the fuel rig or the test cells or intermittent exposure to high concentrations for at least 20-30 min each time with an average frequency of at least every second or third week.” Exposure of the less heavily exposed group (group B) was characterized as “less frequent intermittent exposure that group A.” A multicomponent evaluation of neurological and psychiatric factors was made. The workers were questioned about personal history and the occurrence of symptoms of neurasthenia and polyneuropathy. They were given neurological examinations designed to evaluate peripheral nerve function.