Permissible Exposure Levels for Selected Military Fuel Vapors (1996)

The acute effects of hydrocarbons on the cardiovascular system following inhalation exposure are well known because of the historical use of hydrocarbons as anesthetics and their use as narcotics through intentional inhalation of solvent and propellant vapors. Inhalation of hydrocarbons has the potential to induce cardiac arrhythmias that can result in death. For cardiac arrhythmias to occur, however, epinephrine must be released simultaneously with inhalation (Garb and Chenoweth, 1948).

Quantitative dose-response data on the cardiovascular effects following inhalation exposure are difficult to obtain because these effects depend on both the duration of exposure and the amount of epinephrine present in blood (Chenoweth, 1946). For example, benzene and haptane were determined to be among the most potent agents in causing arrhythmias and were estimated to be effective after inhalation of 5% of the compound in air (155,000

mg/m³) (Chenoweth, 1946). It has been estimated that benzene and chlorofluorocarbon 11 are equally potent and that inhalation of about 15,500 mg/m³ is enough to cause arrhythmias (H. Trochimowicz, E.I. du Pont de Nemours, Newark, Del., personal communication, 1994). Gasoline was found to be active at approximately 8% (300,000 mg/m³) of the vapor in air (Chenoweth, 1946). A mixture like gasoline would not be expected to be potent because of the many hydrocarbons present that are weak sensitizing agents (Reinhardt et al., 1971) or that are inactive (Krantz et al., 1948).

No human studies were found in which cardiovascular effects of hydrocarbon exposure were examined. In oral studies designed to determine the LD₅₀ of JP-5 in male Sprague-Dawley rats, the hearts of deceased animals were examined (Parker et al., 1981). The authors determined that the rats died from cardiovascular collapse unrelated to myocardial necrosis. In a second study in which rats were administered 24 mL/kg (approximately 20 g/kg) by oral gavage and followed for 3 days, there was no increase in serum creatinine phosphokinase levels, an enzyme characteristic of heart-muscle damage. These data are not useful for determining PELs following inhalation exposure because the route of exposure (oral) is not relevant and the chemical composition of the total fuel differs from that of the vapors.