CURRENT PERSPECTIVES ON AEROSOL TOXICITY 275 erant action of the propellants (12), which may cause reflex airway obstruc- tion, especially of the larynx, and tissue damage to the delicate mucous mem- branes of the vulva (7) and eye (29) decomposition into phosgene when the vapors come into contact with an open flame (30) and finally, systemic toxicity, chiefly referrable to the cardiovascular system (9,1, 9,2). It is this lat- ter type of toxicity which has been accorded so much unwarranted publicity by the press. The problem of teen-age abuse of aerosols is one over which the aerosol industry has little control, other than to update the warnings printed on the aerosol cans. The Inter-Industry Committee on Aerosol Use has established the Aerosol Education Bureau (31) to administer a safety campaign which is designed to warn teen-agers of the potential lethal consequences of abusing aerosolized products. Soon after the controversy regarding the deaths from aerosol "sniffing" began, Taylor and Harris (21) reported that the exposure of mice to several propellants, followed by asphyxia in a plastic bag, produced sensitization of the myocardium to hypoxia, resulting in arrhythmias such as sinus brady- cardia, atrioventricular block, and T wave depression. They used these ex- periments to postulate that the sudden deaths that followed aerosol abuse by teen-agers could be the result of a toxic action of the propellants used in al- most all aerosol packages, as well as to provide a basis for warning against the possible hazards to frequent users of a variety of aerosol products. It is well known, and has been for some time, that high concentrations of many pro- pellants frequently used by aerosol manufacturers can produce a wide variety of toxic effects. Ataxia, tremors, liver, and kidney damage are among some of the more common findings (32, 33). But these experimental results in animals, especially at the high concentrations studied, bear little or no relationship to the lower concentrations to which the consumer of aerosol products is ex- posed (9,8). Also, there is lack of general agreement as to the accuracy of the data on aerosol toxicity when it is extrapolated from animal studies to humans (22, 34). Following several reports by Taylor and Harris on the cardiac toxicity of aerosol propellants, other investigators attempted to reproduce their findings, with little success. McClure, in 1972, failed to produce significant changes in the heart rate or electrocardiogram of anesthetized mice after the administra- tion of several propellants in aerosol form, followed by asphyxia (35). In general, he found that the cardiovascular effects produced by propellant ex- posure were similar to the cardiovascular effects of asphyxia alone. McClure was also unable to confirm similar findings reported by Taylor and Harris in dogs (21). Egle et al. (23) also attempted to repeat the results of Taylor and Harris. They exposed mice to several propellants, either alone or with nitro- gen-induced asphyxia, and reported no augmentation of the asphyxia-induced bradycardia or atrioventricular block by the several fiuorocarbon propellants

276 JOURNAL OF THE SOCIETY OF COSMETIC CHEMISTS studied. In all, four groups of investigators have failed to repeat the findings reported by Taylor and Harris (22). On the other hand, many investigators have reported the safety of the fiuoroearbon propellants in concentrations generally produced following nor- mal use. McClure (35) reported no effect on heart rate, blood pressure, and eleetroeardiogram in dogs following the intratraeheal administration of an epinephrine aerosol. Azar eta[. (36) were unable to produce arrhythmias in anoxie and hypcreapnie dogs following repeated exposure to several com- mercial aerosols. Others were unable to produce significant eleetroeardio- graphic changes in several patients, ill with a variety of bronchopulmonary disorders, following the repeated inhalation of Propellant 11 and Propellant 12 (27). There is little question that the various propellants can, when administered in high concentrations over a prolonged exposure period, produce cardiac arrhythmias. Flowers and Horan (37) exposed anesthetized dogs to several commercial aerosols in high concentrations their data showed bradycardia and ventricular arrhythmias in many of the dogs thus treated. Reinhardt et al., in 1971, reported that the inhalation of high concentrations did, in fact, sensi- tize dogs to catecholamine-induced cardiac arrhythmias (28). In addition, the propellants also produced questionable sensitization to endogenous]y-re- leased catecholamines resulting from audiogenic stimuli (28). The conditions described in these experiments, as well as many others, do postulate a mech- anism for the sudden deaths resulting from aerosol abuse, but in no way per- tain to the safety of the thousands of commercially available aerosol products currently in use today, assuming reasonable use of such products. TOxICiTY OF COSMETIC AND PERSONAL PRODUCT AEROSOLS Antiperspirants and Deodorants These have been reported to cause granulomas of the axilla (38), which are probably linked to a hypersensitivity to the zirconium, aluminum, or other heavy metal salts used in these preparations (12). While the few reported cases to date have resulted from using either lotion or stick deodorants, sim- ilar reactions may possibly occur in allergic individuals using aerosol deodor- ants or antiperspirants containing these chemicals. Other toxic reactions reported to be associated with the use of antiperspir- ant/deodorant aerosols include: pulmonary granulomatosis (1), epithelial keratinization of the eye (9), and clogging of the sweat glands with subse- quent infection (18). There have not been enough reported cases in any of these incidents to establish a definite cause-effect relationship. Aerosol deodorants have been reported to produce "flashback" reac- tions in users of hallucinogenie drugs, such as mescaline and LSD. Two such