Abusing the volatile organic chemicals

REGULATORY

TOXICOLOGY

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PHARMACOLOGY

5, 18-37 (1985)

Abusing the Volatile Organic Chemicals ROBERT P. GIOVACCHINI The Gillette Company, Prudential Tower Building, Boston, Massachusetts 02199

Received August 25, 1984

Intentional inhalation of volatile organic chemicals is not a new phenomenon. It has existed since ancient times. Abusing household and other commercially available products, containing volatile organic solvents, has been recognized since the early 1950s. Products containing volatile organic chemicals include everything ranging from gasoline to paints, aerosolized foods, cosmetics, and other solvent-based household products. These products are easily available, legal, and usually inexpensive when compared to the alternative, illegal substances. While inhalant abuse is small when compared to the abuse of other substances, the problem can, in some cases, be fatal to the abuser. The public sector, industry, and government all are trying to find a solution. This paper reviews the history of perverted use of commercial products, the inhalant abuser, the signs and symptoms, the pharmacotoxicology, and the various approaches t0 SOhtiOnS.

0 1985 Academic

Press, Inc.

INTRODUCTION Abusing, through intentional inhalation, the volatile organics is not a 20thcentury phenomenon. Scientific and lay literature record that it occurred among the ancient Greeks at Delphi, using an older woman who, while sniffing carbon dioxide, was able to predict the future. Columbus found West Indians inhaling various materials and, of course, all students of pharmacology know about the alcohol, ether, nitrous oxide, and chloroform intoxicant parties of the late 1800s and early 1900s. The latter situation helped create the present field of anesthesiology. However, some of the scientists were more interested in the “pleasurable effects” of the gases than in their proposed “medical uses” (Nagle, 1968). Ether was used in Ireland and the United States in the late 19th century, in an attempt to reduce alcoholism. The results, in both countries, became such a social concern that a reeducation program was instituted to return people to alcohol (Jaffe, 1975). Sniffing gasoline fumes dates from the 1930s and became a social concern in the early 1950s (Anonymous, 1964; Bartlett and Tapia, 1966; Bethell, 1965; Black, 1967; Clinger and Johnson, 195 1; Edwards, 1960; Faucett and Jensen, 1952; Grant, 1962; JaIfe, 1975; Kaufman, 1973; Law-ton and Malmquist, 1961; Nagle, 1968; Nitsche and Robinson, 1959; Nunn and Martin, 1934; Oldham, 196 1; Poklis and Burkett, 1977; Tolan and Lingl, 1964; Voegele and Dietze, 1963; Watson, 18 0273-2300/M

$3.00

Copmt 8 1985 by Academic Press, Inc. All rigJ16 of npmduction in any form -ed.

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1980). This was followed by the sniffing of glue and other forms of adhesives. The term “glue sniffing” came into vogue. By the mid-1960s the practice of “glue sniffing” had spread throughout the United States and to other countries as well (Barker and Adams, 1963; Brozovsky and Winkler, 1965; Corliss, 1965; Gellman, 1968; Glaser and Massengale, 1962; Massengale et al., 1963; Merry, 1967; Sokol, 1965; Sokol and Robinson, 1963; Watson, 1977). The chemical practice of sniffing began to involve the entire spectrum of volatile organic materials found alone or in combinations in various, assorted, commercially available products. Some of the products being abused are listed in Table 1. Thus, any material or product containing a volatile organic chemical solvent system is capable of being abused. A majority of the solvent systems, with the exception of water-based systems, contain some form of volatile chemical organic material. Why, then, not move entirely to water-based or glycol-based systems and eliminate the abuse problem? Unfortunately, many of the products we use today will not function in a waterbased system and are effective only in volatile organic chemical systems. These products do fulfill a need and are part of our daily lives. Further, they are safe under conditions of labeled use directions but are not necessarily safe when perverted use occurs, such as in “solvent sniffing.” THE

INHALANT

ABUSER

The abuser of volatile organic chemicals is young. Usually the sniffer is male, between ages 7 and 17 (Barnes, 1979; Crites and Schuckit, 1979; Medina Mora et al., 1978; Natera, 1978). Cohen has reported an increase in the number of females who sniff (Cohen, 1977). Others have reported that, following alcohol and tobacco, volatile organic chemicals are the next most-abused products. (Gossett et al., 197 1; Porter et al., 1973). However, there is some evidence that after age 15, except for the chronic sniffer, the practice appears to decrease. Mason reported that the volatile organic chemicals were not the materials of choice among most abusers-marijuana was (Mason, 1979). He found that the youngsters began experimenting with TABLE Aerosol cocktail chillers Nonstick frying pan aerosols Cold weather car starter Contact cements Dry cleaning fluids Transmission fluids Windshield washer fluids Brake fluids Fire extinguisher fluids Liquid waxes Degreasem wax strippers Lighter fluids Nail polish removers Aerosol shoe polishes

I Refrigerants Sanitizers Polishes Disinfectants Aerosol deodorants Aerosol pain relievers Aerosol fly sprays Aerosol antiperspirants Hair sprays Aerosol paints Paint lacquers & varnishes Typewriter correction fluids Anticough aerosols Room deodorizers

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cigarettes, alcohol, and marijuana at about the time they tried sniffing. Further, the choice of commercial products abused differed with the geographic areas studied: transmission fluid in Miami, aerosol shoe polish in Houston, gold paint in Louisville, and cleaning fluid or glue in New York. Press and Rubin identify two classes of sniffers (Press and Done, 1967a; Rubin and Thomas, 1968). First is the individual who tries it and uses it because there is nothing better to do. Second is the problem sniffer who uses a wide variety of volatile organic chemicals in order to survive the day. His enemy appears to be the environment. The problem sniffer appears to be unable to cope or is unwilling to try. Volatile organic chemical abusers are different from other drug users. They are younger, more likely delinquent and disruptive, usually involved with some form of the justice system, have low self-esteem and lack of motivation. They tend to do poorly academically and have a higher school-drop-out rate, They tend to be male, from a minority low-income group with family problems. They tend to be loners. Bass (1970), as well as Stephens et al. (1978), however, reported on abusers who appeared to come from a middle class background. Treating staff use the following terms in describing the inhalant abuser: psychologically maladjusted, ego weakness, personality disorganization, poor impulse control, low frustration tolerance, withdrawn, uninterested, destructive, overactive, restless, disruptive, and lacking discipline (Mason, 1979). SIGNS

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SYMPTOMS

Volatile organic chemical abusers describe the results of their sniffing as first a feeling of exhilaration, blurring of vision, tearing, numbness, weightlessness, and elation. Some feel omnipotence, have distorted space perception, and see altered colors and shapes. It appears that the feelings experienced depend to some extent on the user’s personality, expectations, the situation in which the volatile organic is used, and the past use of other volatile organics. With continued inhalation, the concentration of the volatile organic increases in the body and the subject will move to a state of stupor. If this is allowed to continue, coma eventually will follow. In this state, respirations are depressed, pupils dilate, and the heart rate increases (Cohen, 1973; Press and Done, 1967). It has been described as similar to stage I and early stage II of anesthesia. Apparently, the “high” can last for up to 1 to 2 hr, or be very brief. This allows for one to get “high” several times a day. Sniffers tend to have teary, glazed, or reddened eyes with some dilation of the pupils, giving an unfocused appearance; some may have a cough, increased salivation, unpleasant (chemical) breath, sniffling, giggling, and slurred speech with a disoriented, guarded appearance, and loss of appetite with a resultant loss of weight; tremors and unsteady gait may also appear. In “glue sniffers” a rash of the nose and mouth also has been reported (Cohen, 1973). Following intoxication, the sniffer may be subject to headaches, unpleasant taste, nausea, extremity pain, drowsiness, and possibly some temporary disorientation. This, however, does not stop the abuser from doing it again and again. Evading life’s stresses and/or being accepted by one’s peer group is more important. Depending on the volatile organic chemical whose use is being abused, a lethal consequence can occur. This unfortunate fact has been demonstrated in humans (Bass, 1970).

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THE INCIDENCE

In one U. S. survey an attempt was made to measure the prevalence of inhalant abuse (Johnson et al., 1979). It was concluded that 18.7% of the country’s 1979 high school seniors had tried inhalants at least once. From this group the period of first experience was the seventh and eighth grades, with the Northeast showing the highest prevalence. Amy1 and butyl nitrite were the inhalants of choice. In a second study, where the age ranges were 12- 17, 18-25, and 26 and older, inhalant usage was reported as 9.8% (12-17) 16.5% (18-25) and 3.9% (26 and older) (Fishbourne and Abelson, 1979). The study reported that many of the students had, during the previous 12 months, used inhalants only once or twice. Those students who had used inhalants during the study were reported at 4.6% (1217), 3.8% (18-25), and 1.0 (26 and older). A study conducted by the Maryland Department of Health and Mental Hygiene involved 35,800 students (Hamilton et al., 1981). The students were divided into three groups: young adolescents (median age 12.9), middle adolescents (median age 15.0), and late adolescents (median age 17.0). This study reported that the incidence of sniffing varied from school district to school district, but that sniffing appeared to be higher in the young adolescents. Young adolescents reported a 3.8%, while middle adolescents reported 4.0%, and late adolescents 2.3% use. The report suggests that possibly the years between 11.2 and 13.7 are the “critical age” for experimenting with solvents and that the older youngsters have “grown out” of the use of solvents. It can also be concluded that the older youngster has gone on to other substances. Fuel-type substances (7.8%) commercial solvents (7.4%), and nitrites (5.8%) are preferred by young adolescents while middle adolescents prefer nitrates (7.1%) anesthetics (4.7%), and commercial solvents (4.6%). Late adolescents prefer nitrites (5.2%) and anesthetics (3.3%), but they are the lowest users of volatile organic solvents. The report concludes that young adolescents are the major users of volatile organic solvents and that the percentage using inhalants has increased from 1978. The Maryland study also reviewed 11,683 admissions to drug abuse treatment centers where they found 1.1% of the admissions had a primary inhalant abuse problem. They found that most of the inhalant abusers were poly drug abusers who usually preferred marijuana. They have a younger first use than other drug abusers and are more likely to be readmissions to treatment because they leave the treatment programs before completion. Most are admitted through the criminal justice system as opposed to voluntary admission. The Alcoholism and Drug Addiction Research Foundation reported on substance abusers in Ontario, Canada schools. This report is the fourth in a series of studies which began in 1977. There were 5835 students involved. With respect to solvent abuse they found it reported by a small proportion of students: 3.2% for glue and 4.1% for other solvents. A greater proportion of males reported sniffing glue as compared to females. This difference was not found for other solvents being sniffed. Inhalant abuse was highest in the younger students (grade 7) (Smart et al., 1983). A survey of 4165 students from years 7 to 11 in 29 New South Wales, Australia, schools included for the first time solvent and aerosol abuse. The results demonstrated analgesics and alcohol as having the most prevalent use, with solvents and aerosols second. However, when the question was asked “in terms of having used in the last month,” marijuana was higher than solvents and aerosols. The study reported that

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sniffing was most common in adolescents ( 12- 14 years), especially girls. The result differs from findings in the United States and Canada where more males than females appear to sniff solvents. The report states that about half of the students reported having sniffed, no more than 1% reported sniffing daily which would categorize them as serious or chronic sniffers (Homel el al., 1984). PHARMACOTOXICOLOGY The variety and number of combinations of ingredients which are used in volatile consumer products are impossible to catalog fully. Animal toxicity studies of varying levels of sophistication and depth have been conducted on these agents individually. In many cases, risk assessments have been conducted on the various products under prescribed conditions of use and manufacture. While such studies provide evidence that these products are nonhazardous to the consumer who uses them properly and to the employee who works with them correctly during manufacture, these studies provide only introductory toxicology information when we examine these ingredients singly or in combinations under perverted-use conditions. An example of these problems is seen when one reviews the toxicity of volatile organic chemicals in aerosolized products. To the layman the term “aerosol,” “aerosol product,” “pressurized product,” or “pressurized aerosol” is generic for any product that has been packaged under pressure and can be dispensed from a pressurized container. Aerosol products usually contain three major components: propellants, solvents, and other formulation-aid ingredients and functional components. The propellants provide the force which discharges the other ingredients from the container. They also strongly influence the manner in which the product is dispersed, i.e., wet spray, dry spray, stream, sloppy foam, or dry foam. The solvent functions (1) to bring the concentrate into solution with the propellants, (2) to help produce a spray with an acceptable particle size for a particular application, and (3) in some products, to help reduce the vapor pressure of the propellant. Other ingredients (formulation aids) found in aerosol products are stabilizers, emollients, moisturizers, plasticizers, surfactants, and perfumes. Among the first volatile organic chemical materials to have their use perverted were the chlorofluorocarbon propellant gases. The chlorofluorocarbon propellants are saturated organic compounds which contain fluorine. The ones most generally used in the late 1960s and early 1970s and discussed here are Fluorocarbon 11 (trichloromonofluoromethane), Fluorocarbon 12 (dichlorodifluoromethane), and Fluorocarbon 114 (dichlorotetrafluoroethane). Chlorofluorocarbons originally were recommended as refrigerants and Underwriters Laboratories (UL) was among the first to report on their toxicity. Their studies evaluated the possible exposure hazard of the householder or repairman to air conditioners and refrigerators. From the basic UL studies, propellants were placed in various classes ranging from Class I (most acutely toxic) to Class VI (least acutely toxic) (Nuckolls, 1933). Refrigerants such as sulfur dioxide were placed in Class I while Fluorocarbon 11, Fluorocarbon 12, and C02, among others, were in Classes V and VI. Thus, UL had developed a comparative procedure toxicologically, ranking proposed new refrigerant propellants with then-existing refrigerant chemicals.

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The toxicological studies were all acute (short term, one to several hours) exposures. While the objective of these studies was to evaluate the acute inhalation hazard, subsequent studies and experience have confirmed the low order of toxicity for these chemical entities by various routes of administration (Clayton, 1967, 1970; Downing and Madinabertia, 1960; Sayers et al., 1930). From the above data it was generally presumed that the propellant systems were, for practical purposes, pharmacologically inert. In late 1967, seven deaths occurred due to the intentional inhalation of Fluorocarbon 12 from cocktail glass-chiller products. The procedure involved concentrating the propellant by spraying the product into a balloon and then inhaling the contents of the balloon. Scientists were not only surprised but also perplexed. After studying the chemical structure of these gases and reviewing the literature, several theories were proposed as to the cause of death. They were (1) anoxia and narcosis, (2) displacement of air in the lungs, (3) laryngeal spasm or edema, (4) propellant competition in the red blood cell with oxygen, as seen in carbon monoxide poisoning, and (5) the propellant gases acting directly on the cardiac conduction system producing cardiac sensitization to epinephrine. While these volatile organic chemicals were being deliberately concentrated and inhaled, it was reasonable to assume that anoxia and narcosis, with their accompanying symptoms, could occur. Laryngeal edema could result from aspiration of yet unvaporized droplets of the aerosol propellant causing shock to or freezing of the larynx. The autopsy findings, however, did not support these theories. Further, the fact that some of the individuals were walking or running immediately before death, coupled with the lack of autopsy findings, suggested possible cardiac involvement in the clinical picture. It was then postulated that the inhalation of high concentrations of propellant, in conjunction with increased blood levels of epinephrine, could induce cardiac arrhythmias. Of course, this phenomenon termed “cardiac sensitization” was not new. It had been known for some time that the inhalation of certain volatile anesthetics, for example, cyclopropane and chloroform, could make the mammalian heart abnormally reactive or sensitive to epinephrine, resulting in cardiac arrhythmias (Bass, 1970; Levy, 19 11, 19 12- 19 13, 19 13- 19 14). In 1970 Bass reported an epidemic of 110 sudden sniffing deaths apparently due to the “perverted use” of volatile halocarbons (Bass, 1970). He reported that the chemicals most frequently involved were trichloroethane and fluorinated hydrocarbons. He also noted that the pathophysiology of sudden sniffing death exhibited many features that resembled anesthetic deaths and postulated that the mechanism of action might be sensitization of the cardiac conduction system with sudden, severe arrhythmia and ventricular fibrillation. Later that year, Taylor and Harris (1970) reported that the fluorocarbon propellant gases were toxic to the hearts of mice, as demonstrated by asphyxia-induced sinus bradycardia, atrioventricular block, and T-wave depression. They reported that cardiac sensitization was rapid, long-lasting, and lethal. The authors concluded that the propellant gases possessed a spectrum of cardiotoxic effects capable, in various species, of causing bradyarrhythmias, tachyarrhythmias, or myocardial depression. In 197 1, Reinhardt and co-workers reported on experiments which indicated that all of the volatile organic chemical propellants he studied were capable of sensitizing the mammalian heart to epinephrine, resulting in serious cardiac arrhythmias (Reinhardt et al., 1971a). The fright experiments in particular were significant in

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that cardiac arrhythmias developed without the administration of exogenous epinephrine. Reinhardt et al. cited such factors as hypoxia and hypercardia as potential contributing elements to cardiac sensitization. Azar (1972), studying the acute toxicity of Fluorocarbon 12, exposed two human volunteers to concentrations of 1000 to 10,000 ppm of Fluorocarbon 12 for 2.5 hr. The subjects were exposed twice to both concentrations. Clinical observations, laboratory tests, subjective impressions, continuous electrocardiogram monitoring, and tests of psychomotor performance did not reveal any adverse effects resulting from exposure to 1000 ppm of Fluorocarbon 12. Exposure to 10,000 ppm resulted in a 7% reduction in the standardized psychomotor test score. These findings, they concluded, suggested that exposure to 10,000 ppm of Fluorocarbon 12 to 2.5 hr would not pose a serious threat to an individual’s health. In addition, measurements of the subject’s tidal air for Fluorocarbon 12, made immediately postexposure and periodically thereafter, showed that the compound was rapidly eliminated from the lungs. Reinhardt et al. (197 la) exposed human volunteers to Fluorocarbon 113 at concentrations of 500 to 5000 ppm for five days, three hours in the morning and three hours in the afternoon at each concentration, to determine the effect of repeated exposure of this fluorocarbon. Clinical observations, laboratory tests, subjective impressions, and measurement of psychomotor performance were used to determine possible compound effects. The test results did not reveal evidence of any adverse effects resulting from the exposure. Analysis of blood samples did not indicate a significant body buildup for Fluorocarbon 113. Morgan studied the absorption and retention of inhaled fluorocarbon gases. Radioactive tracer techniques were used to measure the partition coefficients of the fluorocarbon gases (Fluorocarbons 11, 12, 113, and 114) which had been administered to volunteers in a single breath, to simulate propellant administration from pressurized bronchodilator aerosols in which they were used (Morgan et al., 1972). Measurements were made of (1) the change in concentration in alveolar air with breathholding time and (2) the elimination in breath during normal breathing over a period of 30 min. Because of the low lipid solubility, much of the inhaled fluorocarbon vapor was exhaled without being absorbed. After 30 min, the fraction of administered material retained varied from about 10% for Fluorocarbon 114 to 23% for Fluorocarbon 11. A few measurements were made of fluorocarbon levels in venous blood and revealed that, after 5 minutes, only a small fraction of the retained material was present in the bloodstream. The rate of transfer to other compartments was less rapid for Fluorocarbon 11 than for Fluorocarbons 12 and 114. Aviado and others studied the toxicity of aerosol propellants on the respiratory and circulatory system in a variety of animals (Aviado and Belej, 1974; Brody et al., 1974; Friedman et al., 1973). The propellants studied were grouped by Aviado into four classes. They were Class I, low-pressure propellants of high toxicity; Class II, low-pressure propellants of intermediate toxicity; Class III, high-pressure propellants of intermediate toxicity; and Class IV, high-pressure propellants of low toxicity. Of the 15 gases studied, Aviado stated that Fluorocarbons 11, 113, and 21, methylene chloride, and I, I, I -trichlorethane were in Class I; Fluorocarbons 114 and 142b, C3 18, and isobutane were in Class II; Fluorocarbons 12 and 22, propane, and vinyl chloride were in Class 111; and, Fluorocarbons 115 and 152a were in Class IV.

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Aviado noted that the propellant having the greatest propensity for induction of cardiac arrhythmia was Fluorocarbon 11. These studies, along with the other reported earlier, began to allow one to place safety factors on the propellants. Propellants tested by Aviado were tested at 10 ~01% in air. Research reported earlier had demonstrated that patients and/or consumers are exposed to between 0.01 and 0.02 ~01% of these propellants for periods of 1 to 2 min. Thus, a more-thansufficient safety factor could be demonstrated. These studies conclude that the propellant concentrations necessary to produce serious cardiac conduction and respiratory problems appear to be extremely high when compared to that reached by the normal consumer. However, the studies demonstrated that the perverted use of aerosols to obtain a “high” is fraught with hazard, the possibility of cardiac failure, and death. Hoffman (1974) studied the airborne concentration of selective volatile vapors in a modem, professionally operated beauty salon. His study demonstrated that, based on safe inhalation exposure, i.e., threshold limit values (TLVs) adopted by the Occupational Safety and Health Administration (OSHA), the 12 beauticians employed in the particular salon study were not exposed to hazardous propellant concentrations. Normal inhalation exposure and exposure during the hair spray application did not exceed the TLV established for any measured compound. The gases studied included Fluorocarbons 11 and 12, methylene chloride, isobutane, propane, ethanol, carbon dioxide, carbon monoxide, and methane. Background concentrations of propellant measured at the salon did not exceed 50 ppm by volume in air. Peak samples taken after a beautician completed spraying the hair showed that, for brief periods of 1 to 2 min, the beautician’s position vis-i-vis the customer affected the peak-exposure situations. Peak sample air-quality data ranged between 1 and 3 10 ppm per propellant. Three l-week-duration air-quality studies demonstrated the level of propellant to be less than 50 ppm and the level of solvent to be less than 150 ppm during inhalation exposure. Air samples analyzed for carbon monoxide and methane contained fewer than 10 ppm for these gases and air samples analyzed for carbon dioxide contained from 300 to 3700 ppm which is below the TLV of 5000 ppm. Others studied the effect of propellant gases on the respiratory system, on the cardiac-conduction system, and on the defense mechanism of the body (Adir et al., 1975; Bohning et al., 1975; Disher and Hall, 1979; Flowers et al., 1975; Giovacchini, 1975; Guarneri et al., 1976; Stewart et al., 1973). These studies also demonstrated that the gases are safe when products containing them are used following label directions. Similar scientific findings also have been reported for the aliphatic and aromatic hydrocarbons. Hydrocarbon gases have played a significant role in both aerosol and nonaerosol products. Examples of these materials are propane, butane, and their various blends. They are from the lower homologs of the paraffin series (CjHs, C4HIO). These gases have been used in fuels and as refrigerants. Straight-chain hydrocarbons with four carbon atoms or fewer are gases, while those with more carbon atoms (pentane, octane) are volatile solvents. Their odor detection and toxicity appear to increase with the molecular weight of the material (National Air Pollution Control Administration, 1970; Patty and Yant, 1929). Methane (CHJ appears to have no pharmacological action except to create a condition of “oxygen want.”

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A. Acute Toxicity 1. Oral. Propane, on ingestion, appears to have no effect on the body (Fiero and Johnson, 1969). Both propane and butane are accepted by the Food and Drug Administration (FDA) as generally recognized as safe (GRAS) food-contact materials (Food and Drug Administration, 1983; National Air Pollution Control Administration, 1970). While, due to the extremely rapid vaporization, these materials would not be considered a source of systemic toxicity, they may cause irritation of the mucous membranes of the oral cavity if the gases are willfully concentrated. The higher molecular weight hydrocarbons (C,-C,) are liquids and while their oral toxicity also is low, their effects on the lungs, following aspiration, are pneumonitis, pulmonary edema, and hemorrhage (Gerarde, 1963). 2. Skin and MUCOUS membranes. These gases are fat solvents and due to their rapid vaporization they can cause not only defatting of the skin but also localized burning and frost bite. Vapor concentrations of 10% ( 100,000 ppm) propane are not irritating to the skin (Patty and Yant, 1929). 3. Ophthalmic. Vapor concentrations of 10% (100,000 ppm) propane are not irritating to the eyes (Patty and Yant, 1929). Acute concentrated vapor exposure can cause localized burning and chilling of the ophthalmic tissues due to the rapid vaporization rate of the gases. 4. Inhalation. (a) Drowsiness and dizziness are the first symptoms noted on highconcentration exposure. As the concentration is increased, these first symptoms are followed by analgesia and narcosis. Increasing the chain length appears to augment the pharmacological effects while branching appears to decrease these findings. (Aviado, 1975a; Patty and Yant, 1929; Shugaev, 1969; Stoughton and Lamson, 1936). The LCso for butane, in mice with 2 hr exposure, is greater than 25%. In rats, with 4 hr exposure, it is reported at both 28 and 0.28% (Aviado et al., 1977; National Institute for Occupational Safety and Health, 1982; Shugaev, 1969; Stoughton and Lamson, 1936). Propane, at 1% with 10 min exposure in man, does not produce drowsiness. At 10% in man it will produce dizziness within minutes. Sixty percent propane mixed with forty percent oxygen, in cats, produces analgesia. Ninety-three percent propane produces anesthesia (Brown and Henderson, 1926). Butane, at 1% with 10 min exposure in man, will produce drowsiness and dizziness. n-Butane, at 13% and 25 min exposure in man, produces slight anesthesia. Concentrations of 45% isobutane and 25% butane will produce anesthesia in dogs (Stoughton and Lamson, 1936). (b) Cardiorespiratory. In dogs, sensitization of the myocardium will occur following inhalation of 10% or more propane, butane, or isobutane if exogenous epinephrine does not demonstrate “cardiac sensitization.” Under the same conditions isobutane at 2.5% did not demonstrate “cardiac sensitization” (Reinhardt et al., 197 1a). Aviado examined the effects of certain chlorofluorocarbon and hydrocarbon propellant gases on the respiratory and cardiac systems of the mouse, dog, and monkey (Aviado and Belej, 1974; Aviado et al., 1977; Belej et al., 1974; Brown and Henderson, 1926; National Institute for Occupational Safety and Health, 1982). He concluded that Fluorocarbon 11 produces cardiac arrhythmia at concentrations of 0.25% while isobutane and butane produced no effects at concentrations of up to

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10% and propane up to 25% (Aviado, 1975a,b). In addition, he noted that the hydrocarbons examined had less potential for effecting depression of the cardiac function as compared with Fluorocarbon 11 (Aviado et al., 1977). B. Chronic Toxicity 1. The literature reports neurological findings in humans with hydrocarbons containing more than six carbon atoms, specifically n-hexane. It is reported that the effects may be due to the metabolic breakdown of hexane to 2,5hexanedione (Cianchetti et al,, 1976; DiVincenzo and Krasavage, 1974; DiVincenzo et al., 1976; Herskowitz et al., 197 1; Prockop, 1979). In addition, there is some evidence, in mice and rats, posing the possibility of liver injury following chronic exposure to nhexane (Bohlen et al., 1973; DiVincenzo and Krasavage, 1974). There is no literature evidence reporting such adverse effects with the lower homologs (propane, the butanes) of the aliphatic hydrocarbons. 2. Mutagenicity. Propane, butane, and isobutane were found nonmutagenic when evaluated by microbiological testing techniques (Simon, 1977; Simon and Wiest, 1977). 3. Occupational exposure. The TLV set by OSHA for propane is 1000 ppm. The TLV for butane, set by the American Conference of Governmental Industrial Hygienists (ACGIH), is 600 ppm. All TLVs (the time-weighted average concentration for a normal 8-hr work day or 40-hr work week, to which nearly all workers may repeatedly be exposed, day after day, without adverse effect) have safety factors “built” into the allowable exposure. For example, Stewart et al. (1973) exposed humans for up to 8 hr to 1000 ppm propane and to 1000 ppm isobutane without adverse effect. It would appear from the present scientific literature that the hydrocarbon propellant gases, propane, the butanes, and their blends are safe for use as propellant gases in products under conditions of consumer use and safe, from a toxicological standpoint, under conditions of manufacture. Further, these gases appear to be relatively less toxic to the cardiac system than some chlorofluorocarbon gases. However, under abuse conditions, they are also hazardous and can be fatal. In addition, amyl and butyl nitrites are being abused. While amyl nitrite is a prescription drug, butyl nitrite is found in some so-called “room deodorants.” In homosexuals who were studied, no adverse effects were noted following exposure up to four times weekly (Israelstam et al., 1978; Sigell et al., 1978). Other volatile organic chemicals found in commercial products and subject to abuse are xylene, toluene, acetone, trichloroethylene, perchloroethylene, methylene chloride, and 1, 1,l -trichloroethane. Xylene is used in such commercial products as paint thinner and as a solvent for inks, rubber, gums, resins, adhesives, lacquers, and paint removers. There is a question as to which material is more toxic-xylene or toluene. At low doses, toluene may be more toxic than xylene, whereas at high doses, xylene may be more toxic than toluene (Clayton and Clayton, 1978). Xylene in contact with the eyes can cause comeal bums and conjunctivitis. Skin contact produces defatting which leads to cracking, dryness, blistering, or dermatitis. Inhalation of concentrations in the area of 10,000 ppm can cause reddening of

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the face, disturbed vision, dizziness, tremors, salivation, cardiac stress, respiratory difficulties, central nervous system (CNS) depression, confusion, and coma. Xylene is classified as a solvent which can sensitize the cardiac muscle to epinephrine and cause death. Chronic exposure presents more systemic problems which include CNS excitation than depression, with paresthesia, tremors, apprehension, impaired memory, weakness, nervous irritation, vertigo, headache, anorexia, nausea, anemia, and mucosal hemorrhage. Bone marrow hyperplasia, liver enlargement, necrosis, and nephrosis have been reported (Clayton and Clayton, 1978). Toluene is used as a solvent in the chemical, rubber, paint, and drug industries, as a thinner for inks, perfumes, and dyes. Toluene resembles benzene in its toxicological properties without benzene’s hematopoietic effects. Toluene is readily absorbed by inhalation and ingestion, the most rapid route being inhalation. In humans, psychological effects and transient irritation were seen at 100 ppm; CNS effects were seen at 200 ppm; eye irritation, lacrimation, and hilarity at 400 ppm; lassitude and slight nausea at 600 ppm; metallic taste, headache, nausea, and impaired balance at 800 ppm. High concentrations produce paresthesia, visual disturbance, dizziness, narcosis, and collapse. Toluene is considered a cardiac sensitizer, causes hepatomegaly, and has hepatotoxic and nephrotoxic characteristics. Several reports reviewing chronic “glue sniffing” suggest organic liver and renal changes as well as cerebellar dystrophy (Clayton and Clayton, 1978; Grabski, 196 1; Knox and Nelson, 1966; Verhulst and Crotty, 1964). While considered one of the least toxic solvents, acetone, in high concentrations, can cause CNS depression and narcosis. Exposure to 1000 ppm in humans for 3 hr/day for from 7 to 15 years produced respiratory tract irritation, dizziness, and loss of strength. Trichloroethylene is used in metal degreasing and extraction processes. It has also been used as an anesthetic agent (trilene). High concentrations of exposure produce visual disturbances, mental confusion, fatigue, and CNS depression. Sensitization of the heart is reported. A “degreaser’s flush” occurs where workers have been exposed to trichloroethylene and then drink ethyl alcohol. Centrilobular hepatic necrosis and acute renal failure have been reported in “solvent sniffers.” (Baerg and Kimberg, 1970). Abusing the material by deliberately concentrating the fumes can cause death. Perchloroethylene (tetrachloroethylene) is used in the dry-cleaning industry and also as a degreaser. At high concentrations of exposure in humans, it also is a CNS depressant producing nausea, headache, anorexia, vertigo, and dizziness. Liver injury has also been reported in a human following exposure to 400 ppm for 3‘hr. The patient was in a semicomatose state (Stewart et al., 1970). Methylene chloride is an industrial solvent used in aerosol formulations, as a blowing agent for foams, and in paint-stripping formulations. It is a CNS depressant causing dizziness, nausea, tingling or numbness of the extremities, sense of fullness in the head, sense of heat, stupor, dullness, lethargy, and drunkenness. Stewart demonstrated that human exposure to methylene chloride vapors, in concentrations of 500 to 1000 ppm for 1 to 2 hr, increased carboxyhemoglobin levels, suggesting that carbon monoxide is a metabolite (Stewart et al., 1972). High concentration exposure can lead to unconsciousness and death. Myocardial arrhythmia has been reported with methylene chloride.

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1, 1,l -Trichloroethane is a widely used industrial solvent. It is considered one of the safest of the chlorinated aliphatic hydrocarbon solvents. It is rapidly absorbed into the body by ingestion or inhalation. Following absorption, most of the material is removed from the body via the lungs, as small amounts can be metabolized in the body to trichloroethanol. Exposure to l,l, 1-trichloroethane at levels of 9001000 ppm produces transient eye irritation and some impairment of coordination. At levels of 1700 ppm equilibrium control is visibly disturbed. The chemical is a CNS depressant and can sensitize the heart to epinephrine. Deaths have been reported due to high concentrations in industrial situations as well as under abuse conditions (Greer, 1984; Pointer, 1982). Transient hepatic and renal damage has also been reported with an increase in urinary urobilinogen (Halevy et al., 1980; Steward, 1968). Before concluding this discussion, it should be noted that volatile organic chemicals used as anesthetic agents also are being abused. Nitrous oxide is the agent most commonly abused. It can be found in many commercial aerosol products where it is used as a propellant system. Medical and health-care personnel have used other anesthetic agents to achieve a high. Spencer reported on three hospital technicians who died following inhalation of stolen halothane (Spencer et al., 1976). THE ATTEMPTED

SOLUTIONS

When industry first became aware of the situation, the issue appeared to be incomprehensible and seemingly impossible to deal with. Why would anyone want to “sniff’ gasoline, lighter fluid, dry-cleaning fluid, nail-polish remover, correction fluids, or any of the hundreds of commercially available products? The problem appeared to have a variety of solutions. These products are legal, easily available anywhere, and relatively inexpensive or easily shoplifted; “that is why they are abused.” Short-term solutions ranged from banning all sniffable products to putting such products behind the sales counter, as well as allowing only adults the right to purchase. “This will stop ‘sniffing.’ ” As various types of banning measures (or restricting the sale of products) have gone into effect, the response of the sniffer has been simply to change the product he sniffs. Another solution was to add deterrents to sniffable products. Thus, it has become clear that the products, in and of themselves, are not the cause of the problem; rather, it is the individual. The Federal Trade Commission (FTC) in 1968 took the approach of labeling cocktail chillers with a warning label. Examples of warning statements were: “Warning: use as directed-inhalation of the concentrated vapors of this product is harmful and may cause death” and “Warning: Use only as directed-misuse of this product by inhaling its concentrated vapors is harmful and may cause death” (Federal Trade Commission, 1969). The Consumer Product Safety Commission (CPSC) held hearings in an attempt to determine if the ingredients in commercial products were safe under conditions of label directions and to determine the scope of the “sniffing” problem (Consumer Product Safety Commission, 1974). Some members of industry looked for deterrents (ginger, pepper, oil of mustard) which could be added to a product and act as an olfactory stimulant to the abuser but have no effect on the 99.9% of the population that used the product correctly. In 1973 FDA also moved toward labeling certain chlorofluorocarbon aerosol products under its jurisdiction (Food and Drug Administration, 1973). Industry also tested

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the deterrent value of labeling and from these studies a warning label was proposed (Daniel Yankelovich, Inc., 1977). The FDA’s proposed label stated: “Do not inhale directly; deliberate inhalation of contents can cause death.” Industry’s proposed label stated: “Use only as directed, intentional misuse by deliberately concentrating and inhaling the contents can be harmful or fatal.” Industry’s label was approved for use (Food and Drug Administration, 1975). Thus, the first attempts at trying to control “sniffing” included warning labels, use of a chemical deterrent-where stability was not a problem-and attempts at reformulating products, where possible. Obviously products could be and were labeled. However, not all products could have a chemical deterrent added. In some cases the solvent system was such that the deterrent was unstable and did not stay in the product. In other types of product such as deodorants and whipped-cream aerosols, adding a deterrent completely destroyed the product’s usefulness to the consumer. In other products, reformulation was impossible. Industry also developed an education program and founded the Aerosol Education Bureau (Aerosol Education Bureau, 1970). The program was to work with the government’s campaign of the 1960s and 1970s which utilized a public-information and a school-program approach alerting the public to the harmful effects of substance abuse. Many in industry, government, and the public sector were opposed to these approaches stating that they would increase, rather than decrease, the problems of substance abuse. One such theory held, for example, that labeling notified the “sniffer” of which commercial products were abusable. Others argued that the use of a chemical deterrent just added another chemical to the formula and might even affect the performance of the product, giving the legitimate consumer a less-thanacceptable product. Some said all of these approaches were of no value because the “sniffer” is a “sniffer.” “ Sniffing” is a social problem, not a product problem, and none of the approaches would have any impact. While it was agreed that “sniffing” was part of the substance-abuse problem, no alternative program, other than the above approaches, seemed acceptable to the majority of those involved. Unfortunately, the solvent-abuse phenomenon has not abated, which raises the issue of whether some or all of the above approaches are effective in any substantive way. The literature in the field tends to demonstrate a divergence of opinion. Some impressions are that substance-abuse information curricula in the schools have little or no recognizable effect on decreasing substance abuse (Goodstadt, 1974; Kinder et al., 1980; Schaps, 1981; Smart and Fejer, 1974; Tennant et al., 1973). Thus, the development of a public-information campaign along with school drug-information and education programs appears not to have met all the initial goals, but has been of some value (National Institute on Drug Abuse, 1983). Another approach during the 1970s was called the generic prevention program @chaps et al., 1975). These effective and alternative education programs focused in on youth problems in general and not specifically on substance abuse. Here again, there is a difference of opinion as to their success in producing changes in substanceabuse attitudes or usage. During the late 1970s two similar approaches began to show promise. One method develops a community effort to effect a climate of no substance abuse. The program utilizes community leaders, parents, media, and schools. There appears to be evidence that this program has, over a 3-year period, reduced substance abuse (Manatt, 1979). The second approach utilizes positive peer pressure and has been

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used in the United States and Australia. Again, the early evidence seems to be very positive (Botvin, 1983; Campbell, 1982; Durell and Bukoski, 1984). According to Polich, “illicit drug use is widespread among both adolescents and adults. Programs to control it have employed three principal methods: (1) enforcement of drug laws; (2) treatment of chronic abusers; and (3) prevention of initial drug use.” In 1982 the federal government spent over $1 billion on drug programs, the majority of them related to law enforcement projects. These include stopping the production, importing, distribution, and consumer sales of drugs. These programs, while having some impact, have not been highly successful (Polich et al., 1984). In 1982, more than $500 million was spent at the federal, state, and local level in more than 3000 treatment facilities for drug users. There is considerable disagreement on how effective these programs were and whether they were properly structured for the adolescent. Polich suggested that while enforcement and treatment programs should not be stopped, drug-prevention programs, such as the antismoking programs, should be used in the schools beginning at about the seventh grade (ages 12-l 3). Recently, several governments, with the voluntary support of industry, have prepared a Retail Merchant’s Information Program on Solvent Abuse. In Canada, the products covered are contact cement, cleaner and thinner, lacquer thinner, lighter fluid, hobby cement for plastic or wood, nail-polish remover, typewriter correction fluid, felt-tip marking pens, pure organic solvents, and aerosol cooking sprays in package sizes of 250 ml or less. The program consists of inserting a “Your Help is Needed” leaflet in each shipping container of product. In the United Kingdom, a similar program has been instituted. The Department of Health and Special Security has distributed a leaflet and poster which is sent to retailers telling them how to identify sniffers and advising retailers that they do not have to sell abusable products to anyone who, they may suspect, is abusing the product (Department of Health and Social Security, U. K., 1984). Also, the Victoria Police, Melbourne, Australia, have developed a pamphlet for retailers (Victoria Police, 1984). The Public Health Department of Western Australia has developed a booklet for community workers and teachers (Public Health Department, 1983). In the United States, the Aerosol Education Bureau recently has developed a new brochure called “Fighting Back.” It covers substances abused, the sniffer’s profile, the toxicological effects, how to identify the sniffer, and what can be done (Aerosol Education Bureau, 1984). Industry currently also is looking at primary-prevention techniques at the local level (Young, 1984). The Solvent Abuse Foundation for Education (SAFE), an industry coalition, is currently funding a 25-school prevention program in Texas. The Center for Educational Development of San Antonio, Texas, is conducting this program. It is called “The School Team Approach.” CONCLUSIONS Perverting the use of commercially available volatile organic chemicals is an international problem. The aberration occurs in the home, in the school, on the street, and in the factory. It can occur anywhere and, apparently, in all age groups. Further, the literature demonstrates that this is not a new phenomenon. We today are living in a sophisticated world and the youngsters are able to obtain

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information on abusable products very rapidly. The abusers “underground’ can, if impelled, adroitly find abusable products with the skills of a graduate pharmacologist. The abuser is young, usually a male; however, more female users are being reported. Sniffers appear to be different from other substance abusers and will not use volatile organics to reach a high if other products (alcohol, marijuana) are readily available. The sniffer suffers from lack of self-esteem and motivation and generally comes from a problem-home condition. In the United States, industry has, through various trade associations, tried, since the 1970s to decrease the number of youngsters who attempt this dangerous procedure. Not everyone believes that the industry program attempted to date can be effective and, in fact, some believe that the program will increase the incidence of solvent abuse. Industry developed a program of (1) labeling products, (2) attempting to add deterrents where feasible, and (3) an education program in the schools. In certain specific products, where possible, a deterrent, oil of mustard, was added to the products. It is believed that these actions have discouraged the phenomenon because they have alerted the younger generation, as well as adults, to the hazards of abusing and perverting the use of commercial products. Local governments and community groups have taken, in many cases, a more narrow approach. They, usually, have concluded that products that can be abused should either be banned or their sale restricted. They have requested that government (state and/or federal) initiate appropriate regulations to stop, curtail, or restrict distribution and sale of such products. Further, they are requesting the establishment of rehabilitation centers to treat “sniffers” as opposed to the current thinking of educating youngsters on not starting at all. The regulators have been faced with the public sector demanding an immediate answer, elected respresentatives questioning why a quick answer is not forthcoming, and the current thinking of those involved in the drug-abuse solution. It would appear that the regulators, at least at the federal level, see the solution as labeling in the short term and education in the long term (Reagan, 1984). Possibly a concentrated effort to reduce the problem is beginning. The medical and toxicological literature demonstrates that almost everything, if abused, is hazardous to one’s health. It is obvious that banning or restricting the sale of “sniffable” products does not stop the “sniffer.” In fact, if all the sniffable products were controlled it would just bring our present modem society to a complete halt. Products and chemicals do not cause sniffing per se. We must face up to the fact that we have a social psychological problem on our hands. The only solution apparent at this time is education. REFERENCES I., BLAKE, D. A., AND MERGNEN, G. M. (1975). Pharmacokinetics of fluorocarbon 11 and 12 in dogs and humans. J. Clin.Phannacol. 15,760-770. Aerosol Education Bureau ( 1970). R4P ON,An Encounter ontheProblemofAerosolSn@ing. Washington, D. C. Aerosol Education Bureau (1984). FightingBack,Washington, D. C. ANONYMOUS (1970). Addiction to petrol vapour. Luncet1,707. AVIADO, D. M. (1975a). Toxicity of aerosols. J. Clin.Phumacol.15,86-104. ADIR,

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D. M. (1975b). Toxicity of aerosol propellants in the respiratory and circulatory systems. IX. Summary of the most toxic: Trichlorofluoromethane (FC- 11). ~oxico&y 3, 3 1l-3 19. AVIADO, D. M., AND BELEJ, M. A. (1974). Toxicity of aerosol propellants on the respiratory and circulatory systems. I. Cardiac arrhythmia in the mouse. Toxicology 2, 3 l-42. AVIADO, D. M., ZAKHARI, S., AND WRITANABE, T. (1977). Non-fluorinated Propellants and Solvents for Aerosols. CRC Press, Cleveland, Ohio. AZAR, A., REINHARDT, C. F., MAXFIELD, M. E., SMITH, P. E., AND MULLIN, L. S. (1972). Experimental human exposure to fluorocarbon-12. Amer. Ind. Hyg. Assoc. J. 33, 207-2 16. BAERG, R. D., AND KIMBERG, D. V. (1970). CentriIobular hepatic necrosis and acute renal failure in “Solvent Sniffers.” Ann. Intern. Med. 73, 713-720. BARKER, G. H., AND ADAMS, W. T. (1963). Glue sniffing. Social. Social Res. 47, 298-310. BARNES, G. E. (1979). Solvent abuse: A review. Int. J. Addict. 14, l-26. BARTLETT, S., AND TAPIA, F. (1966). Glue and gasoline “Sniffing,” the addiction of youth. MO. Med. 63, 270-272. BASS, M. (1970). Sudden sniffing death. Amer. Med. Assoc. 212,2075-2079. BELEJ, M. A., SMITH, D. G., AND AVIADO, D. M. (1974). Toxicity of aerosol propellants in the respiratory and circulatory systems. IV. Cardiotoxicity in the monkey. Toxicology 2, 381-395. BETHELL, M. F. (1965). Toxic psychosis caused by inhalation of petrol fumes. Bit. Med. J 2(5456), 276-277. BLACK, P. D. (1967). Mental illness due to the voluntary inhalation of petrol vapour. Med. J. Aust. 2, 70-7 1. BOHLEN, P., SCHLUNEGGER, U. P., AND LAUPPI, E. (1973). Uptake and distribution of hexane in rat tissues. Toxicol. Appl. Pharmacol. 25, 242-249. BOHNING, D. E., ALBERT, R. E., LIPPMANN, M., AND COHEN, V. R. (1975). Effects of Fluorocarbons 11 and 12 on tracheobronchial particle deposition and clearance in donkeys. Amer. Ind. Hyg. Assoc. 36, 902-908. BOTVIN, G. (1983). Prevention of adolescent substance abuse through the development of personal and social competence. In Preventing Adolescent Drug Abuse: Intervention Strategies (T. Glynn and C. Leukefeld, eds.), Publication No. (ADM) 83-1280. Department of Health and Human Services, Washington, D. C. BRODY, R. S., WATANABE, T., AND AVIADO, D. M. (1974). Toxicity of aerosol propellants on the respiratory and circulatory systems. III. IntIuence of bronchopulmonary lesion on cardiopulmonary toxicity in the mouse. Toxicology 2, 173-184. BROWN, W. E., AND HENDERSON, V. E. (1926). Experiments with anesthetic gases. J. Pharmacol. 27, l-8. BROZOVSKY, M., AND WINKLER, E. G. (1965). Glue sniffing in children and adolescents. N. Y. State J. Med. 65, 1984-1989. CAMPBELL, E. ( 1982). The Peer Support Program: A Personal Development Course for Secondary Schools. The Peer Support Foundation Limited, Manly, Australia. CIANCHETTI, C., ABBRITTI, G., PERTICONI, G., SIRACUSA, A., AND CURRANDI, F. (1976). Toxic polyneuropathy of shoe industry workers. A study of 122 cases, J. Neural. Neurosurg. Psychiat. 39, 1151-1161. CLAYTON, G. D., AND CLAYTON, F. E. (eds.) (1978). Patty’s Industrial Hygiene and Toxicology, 3rd rev. ed. Wiley, New York. CLAYTON, J. W. (1967). Fluorocarbon toxicity and biological action. Fluorine Chem. Rev. 1, 197-252. CLAYTON, J. W. (1970). Toxicity. In Principles of Aerosol Technology (P. A. Sanders, ed.), pp. 372-390, Van Nostrand Reinhold, New York. CLINGER, O., AND JOHNSON, H. (1951). Purposeful inhalation of gasoline vapors. Psychoanal. Q. 25, 557-567. COHEN, S. (1973). The volatile solvents. Public Health Rev. 2, 185-214. COHEN, S. (1977). Inhalant abuse: An overview of the problem. In Review of Inhalants: Euphoria to Dysfunction (C. W. Sharp and M. L. Brehm, eds.), pp. 2-11, National Institute on Drug Abuse, Rockville, Md. Consumer Product Safety Commission (Feb. 20-21, March 1 I, 1974). Public Hearing on a Petition to Issue Regulations for the Safety and Packaging of AI/ UnreguIated Aerosol Spray Products. Washington. D. C. CORLISS,L. M. (1965). A review of the evidence on glue sniffing-A persistent problem. J. School Health 35,442-449. AVIADO,

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CRITFS, J., AND %HUCKIT, M. A. (1979). Solvent misuse in adolescents at a community alcohol center. J. Clin. Psychiat. 40, 39-43. Department of Health and social Security, U. K. (1984). Solvent Abuse-Nail Polish Remover, IICCI Bulletin No. 4, p. 8. DISHER,D. P., AND HALL, C. E. (June 1979). Prevalence of Cardiorespiratory Disease among Cosmetologists. University of Washington and San Jose Medical Research Foundation. DIVINCENZO, G. D., KAPLAN, C. J., AND DEDINAS, J. (1976). Characterization of the metabolites of methyl n-butyl ketone, methyl iso-butyl ketone, and methyl ethyl ketone in guinea pig serum and their clearance. Toxicol. Appl. Pharmacol. 36, 51 l-522. DIVINCENZO, G. D., AND KRASAVAGE, W. J. (1974). Serum omithine carbamyl transferase as a liver response test for exposure to organic solvents. Amer. Ind. Hyg. Assoc. J. 35, 21-29. DOWNING, R. C., AND MADINABERTIA, D. (1960). The toxicity of fluorinated hydrocarbon aerosol propellants. Aerosol Age 5, (9)27, 74-76. DURELL, J., AND BUKOSKI, W. (1984). Preventing substance abuse: The state of the art. Public Health Rep. 99, 23-31. EDWARDS, R. V. (1960). A case report of gasoline sniffing. Amer. J. Psychiat. 117, 555-557. FAUCET, R. I., AND JENSEN, R. A. (1952). Addiction to gasoline fumes in a child. J. Pediat. 41, 364368. Federal Trade Commission (Feb. 20, 1969). Failure to Disclose the Lethal Effects of Inhaling QuickFreeze Aerosol Spray Products Used for Frosting Cocktail Glasses, 34FR2417. FIERO, G. W., AND JOHNSON, M. A. (1969). Safety of petroleum hydrocarbons in household aerosols: Part 1. Aerosol Age 14(9), 22-33. FISHBOURNE,P. M., AND ABELSON, H. I. (1979). National Survey on Drug Abuse: Main Findings, 1979. National Institute on Drug Abuse, Rockville, Md. FLOWERS, N. C., HAND, R. C., AND HORAN, L. E. (1975). Concentrations of fluoroalkanes associated with cardiac conduction systems toxicity. Arch. Environ. Health 30, 353-360. Food and Drug Administration (Mar. 7, 1973). Labeling Aerosolized Products, Food, Drug and Cosmetics Warnings Proposal, 38FR6 19 1. Food and Drug Administration (Mar. 3, 1975). Food, Drug, Cosmetic Products Warning Statements, 4OFR89 12. Food and Drug Administration (Dec. 29, 1983). GRAS Status of Carbon Dioxide, Nitrogen, Helium, Propane, n-Butane, Iso-butane, and Nitrous Oxide, 48FR57269, 21CFR184.1165 21CFR184.1655. FRIEDMAN, S. A., CAMMARATO, M., AND AVIAW, D. M. (1973). Toxicity of aerosol propellants on the respiratory and circulatory systems. II. Respiratory and bronchopulmonary effectsin the rat. Toxicology 1,345-355.

GELLMAN, V. (1968). Glue-sniffing among Winnipeg school children. Canad. Med. Assoc. J. 98, 41 l413. GERARDE, H. W. (1963). The ahphatic (open chain, acyclic) hydrocarbons. In Industrial Hygiene and Toxicology (F. A. Patty, ed.), 2nd ed., Vol. II, pp. 1195-1206. Interscience, New York. GIOVACCHINI, R. P. (1975). Aerosols: The safety issues reviewed. CTFA Cosmet. J. 7 (4), 4-16. GLASER, H. H., AND MASSENGALE, 0. H. (1962). Glue sniffing in children: Deliberate inhalation of vaporized plastic cements. J. Amer. Med. Assoc. 181, 300-303. GOODSTADT, M. (ed.) (1974). Research on Methods and Programs of Drug Education Addiction Research Foundation, Toronto. GOSSE~, J. T., LEWIS, J. M., AND PHILLIPS, V. A. (1971). Extent and prevalence of illicit drug use as reported by 56,745 students. J. Amer. Med. Assoc. 216, 1464-1470. GRABSKI, D. A. (1961). Toluene sniffing producing cerebcllar degeneration. Amer. J. Psychiat. 118,461462. GRANT, W. B. (1962). Inhalation of gasoline fumes by a child. Psychiat. Q. 36, 555-557. GREER, J. E. (1984). Adolescent abuse of typewriter correction fluid. South. Med. J. 77, 297-301. GUARNERI, J. J., LAURENZI, G. A., AND SIERRA, M. F. (1976). Influence of trichlorofluoromethane and dichloroditluoromethane on the clearance of Staphylococcus aureus from lungs of mice. Dev. Ind. Microbial. 17, 43 l-44 1. HAL-EW, J., PITLIK, S., AND ROSENFELD, J. (1980). “l,l,l-Tricbloroethane intoxication: A case report with transient liver and renal damage. Review of the literature. C&z. Toxicol. 16,467-472. HAMILTON, R. L., FARRELL, E. V., AND MARTIN, R. M. (1981). Report on Inhalant Abuse in Maryland. Maryland Department of Health and Mental Hygiene, Drug Abuse Administration, Baltimore.

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HERSKOWITZ, A., ISHII, N., AND SCHAUMBURG, H. (1971). n-Hexane neuropathy. N. Engl. J. Med. 285, 82-85. HOFFMAN, C. S. (1974). Beauty salon air quality measurements. CTFA Cosmet. J. 5, 16-2 1. HOMEL, P., FLAHERTY, B., TREBILCO, P., AND DUNOON, D. (1984). Highlights of the 1983 Survey of Drug Use by Secondary School Students in New South Wales. New South Wales Drug and Alcohol Authority, In-House Report Series, Sydney. ISRAELSTAM, S., LAMBERT, S., AND OKI, G. (1978). Use of isobutyl nitrite as a recreational drug. &it. J Addict. 73, 3 19-320. JAFFE, J. H. (1975). Drug addiction and drug abuse. In The Pharmacological Basis of Therapeutics, (L. S. Goodman and A. Gillman, eds.), 5th ed., pp. 284-324. MacMillan Company, New York. JOHNSON, L. D., BACHMAN, J. G., AND O’MALLEY, P. M. (1979). Drugs and the Nation’s High School Students: Five Year Trends, 1979 Highlights. National Institute on Drug Abuse, Rockvihe, Md. KAUFMAN, A. (1973). Gasoline sniffing among children in a Pueblo Indian village. Pediatrics 51, 10601064. KINDER, B., PAPE, H., AND WALFISH, S. (1980). Drug and alcohol education programs: A review of outcome studies. Int. J Addict. 15, 1035-1054. KNOX, J., AND NELSON, J. (I 966). Permanent encephalopathy from toluene inhalation. N. Engl. J. Med. 275, 1494-1496. LAWTON, J. J., AND MALMQUIST, C. P. (1961). Gasoline addiction in children. Psychiat. Q. 35, 555-561. LEVY, A. G. (191 I). Sudden death under light chloroform anesthesia. J. Physiol. 42,3-7. LEW, A. G. ( 19 I2- 19 13). The exciting causes of ventricular fibrillation in animals under chloroform anesthesia. Heart 4, 319-378. LEVY, A. G. ( 19 13- 19 14). The genesis of ventricular extra systoles under chloroform with special reference to consecutive ventricular fibrillation. Heart 5, 299-334. MANA~, M. (1979). Parents, Peers and Pot, II. National Institute on Drug Abuse, RockviUe, Md. MASON, T. (1979). Inhalant Use and Treatment. National Institute on Drug Abuse, Rockville, Md. MASSENGALE, 0. H., GLASER, H. H., LELIEVRE, R. E., DODD& J. B., AND KOOK, M. E. (1963). Physical and psychologic factors in glue sni5ng. N. Engl. J. Med. 269, 1340-l 344. MEDINA MORA, M. E., SCHNAAS, L., TERROBA, G., ISOARD, Y., AND SUAREZ, C. (1978). Epidemiology of inhalant use in Mexico. In Voluntary Inhalation of Industrial Solvents, (C. W. Sharp and L. T. Carroll, eds.), National Institute on Drug Abuse, Rockville, Md. MERRY, J. (1967). Glue sniffing and heroin abuse. Brit. Med. J. 2, 360. MORGAN, A., BLACK, A., WALSH, M., AND BELCHER, D. R. (1972). The absorption and retention of inhaled fluorinated hydrocarbon vapours. Int. J. Appl Radiat. Isotopes 23,285-291. NAGLE, D. (1968). Anesthetic addiction and drunkenness: A contemporary and historical survey. Int. J. Addict. 3(I), 25-40. NATERA, G. (1978). Study on the incidence of use of volatile solvents in 27 centers in Mexico. In Voluntary Inhalation of Industrial Solvents (C. W. Sharp and L. T. Carroll, eds.), National Institute on Drug Abuse, Rockville, Md. National Air Pollution Control Administration (1970). Air Quality Criteria Jar Hydrocarbons, pp. 7-l 1. U. S. Dept. of Health, Education, and Welfare, Washington, D. C. National Institute for Occupational Safety and Health (1982). Registry of Toxic Eficts of Chemical Substances, Butane (EJ42OOOOO). National Institute on Drug Abuse (1983). Highlights from Student Drug Use in America, 1975-1982, Publication No. (ADM) 83-1260. Department of Health and Human Services, Washington, D. C. NEAL, C. D., AND THOMAS, M. I. (1974). “Petrol sniffing: A case study. Brit. J. Addiction, 69, 357-360. NITSCHE, C. J., AND ROBINSON, J. F. (1959). A case of gasoline addiction. Amer. J. Orthopsychiat. 29, 417-419. NUCKOLLS, A. H. (Nov. 13, 1933). The Comparative Life. Fire and ExpIosion Hazards of Common Refrigerants, Miscellaneous Hazard No. 2375. Underwriters Laboratories, Chicago. NUNN, J. A., AND MARTIN, F. M. (1934). Gasoline and kerosene poisoning in children. J. Amer. Med. Assoc. 103,474-484. OLDHAM, W. (1961). Deliberate self-intoxication with petrol vapour. &it. Med. J. 2(5268), 1687-1688. PASTY, F. A., AND YANT, W. A. (1929). Report of Investigations. Report No. 2979, U. S. Bureau of Mines. POINTER, J. (1982). Typewriter correction fluid inhalation: A new substance of abuse. J. Toxicol. Clin. Toxicol. 19(5), 493-499. POKLIS, A., AND BURKE~, C. D. (1977). Gasoline sniffing: A review. C’lin. Toxicol. 11, 35-41.

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Strategies for Controlling

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