Scope of the Problem
Inhalant abuse: a problem among kids
Picture a store manager stocking up on some of the most harmful psychoactive substances; he displays them neatly along the shelves, placing discount coupons by the colorfully packaged items. He will happily accept food stamps, and he wouldn’t even dream of placing age restrictions. Although this scenario sounds far-fetched, it actually describes the daily routine in any of your neighborhood convenience or grocery stores. Products such as spray paints, marking pens, nail polish remover, hair spray, model airplane glue, various household cleaning products, electronic dust removers, and butane lighters, to name just a few, can be used in a manner so completely dissociated from their intended purposes, that most people would not recognize their potential harmfulness or risk of abuse. Yet, because of their intoxicating effects on the nervous system and the ease with which they can be obtained, such products pose dangerous risks to young children and adolescents, who are among those most likely to abuse them and, in fact, are doing so in increasing numbers. Products that can be inhaled for a quick “high” are often among the first drugs that young kids are exposed to. Such inhalants are abused by “sniffing” or “snorting” their vapors directly from a container, by “huffing” from a substance-soaked rag stuffed in the mouth, or by inhaling from a plastic bag filled with their vapors “bagging” (APA, 2000).

Extent of the problem in the United States
Inhalant abuse, which is quite rare among the general population, is relatively common among preadolescents (Spiller, 2004). Since 1975, the National Institute on Drug Abuse (NIDA) has sponsored an annual survey of high school seniors (Monitoring the Future Study [MTF]) to document the lifetime incidence of the abuse of drugs, including inhalants. According to preliminary 2005 MTF results, 13.1 percent of 10th graders and 11.4 percent of 12th graders have abused inhalants at least once in their lives. The highest rates of inhalant abuse have been recorded at some point between seventh and ninth grades. Alarmingly, in the previous MTF survey, inhalant abuse among eighth graders was the only category of drug abuse showing a significant upward trend among all drugs assessed (Johnston et al., 2005). The percentage of eighth graders who have ever tried an inhalant, which has been creeping up steadily since 2002, appears to have stabilized at around 17 percent. This trend in such a young age group is viewed by some investigators as a possible early warning sign that the abuse of this class of drugs might be poised for a rebound in older children as well, following years of steady decline (Johnston et al., 2005).

In this regard, it is worth noting that school dropouts, who tend to be more likely to have used illicit drugs (SAMHSA, 2003b) and have a relatively higher incidence of inhalant abuse (SAMHSA, 2005), are not included in the MTF survey, which may therefore underestimate the true prevalence of pediatric inhalant abuse. This bias may explain the otherwise puzzling finding that 12th graders consistently report lower levels of lifetime inhalant use (Lorenc, 2003).

Why should we be concerned?
The persistent and growing incidence of inhalant abuse in pediatric populations is particularly worrisome when one considers the long list of serious health consequences, including death that inhalant abuse can bring (see below). Of particular concern is the robust association — discovered through ethnographic studies (i.e., scientific studies of specific human cultures) — between heavy inhalant use and a history of child and physical abuse (Fendrich et al., 1997; Pagare et al., 2004); poor school performance (Glaser & Massengale, 1962; Merry & Zachariadis, 1962); and mental illness (Wu et al., 2004). As a result, pediatric inhalant abuse may be considered not only a serious threat to a vulnerable population, but also a likely symptom of underlying social and emotional distress.

Unfortunately, a dangerous gap exists between the severity of the inhalant threat and the extent to which primary care physicians are able to effectively identify or treat this form of drug abuse among their young patients (Anderson & Loomis, 2003). Indeed, a 2000 survey of 550 treatment program directors uncovered a great deal of pessimism about treatment effectiveness, recovery rates, and availability of appropriate staff training (Beauvais et al., 2002).

Whether the current gap in addressing inhalant abuse issues is caused by historically low levels of interest (Balster, 1998), or perceived treatment challenges, it is unacceptable, and demands urgent attention from parents, educators, counselors, and clinicians. To be meaningful, however, intervention strategies must stem from a better understanding of the phenomenon itself. More research is clearly needed, but modern science can already help elucidate our understanding of pediatric inhalant abuse, the latest findings for which are summarized in this article.

What are inhalants?
Inhalants are a widely diverse group of volatile substances whose chemical vapors can be inhaled to induce mind-altering effects. While other abused substances can be inhaled, the term “inhalants” is used to describe substances that are rarely, if ever, taken by any route other than inhalation. While their heterogeneity would make an exhaustive cataloguing impossible, three major classes of inhalants are relevant in the context of pediatric populations:

Volatile solvents are liquids that vaporize at room temperature. They are found in numerous common household products. Toluene or acetone, for example, are typical ingredients in paint thinners and removers, model airplane glues, spray paints, nail polish remover, marking pens, and shoe polish.

Aerosols are sprays that contain propellants and solvents. They include deodorants and hair sprays, vegetable oil sprays for cooking, and fabric protector sprays. Butane, a common gas is also found as a propellant in sprays.

Gases can be used for medical anesthetics as well as propellants in household or commercial products. Medical anesthetic gases include ether, chloroform, halothane, and nitrous oxide. Nitrous oxide is the most abused of these gases and can be found in whipped cream dispensers and products that boost octane levels in racing cars. Abusable gases are also found in propane tanks and refrigerants (e.g., Freon ®). Butane is most typically found in cigarette lighters. Increasingly common is the abuse of the propellant gases difluoro- and tetrafluoroethane, which produce the cleaning blast of electronic dust removers (also referred to as “dusters” or “canned air”).

These three classes of abusable inhalants encompass an extremely broad range of chemicals found in virtually hundreds of existing (and certainly, future) products displaying a similarly broad array of negative drug effects. Consequently, the ability to affect the phenomenon of pediatric inhalant abuse presents a complex challenge to the scientific, health care, and policy making communities.

Brain and psychoactive effects: the neurobiology of inhalants
Acute effects on brain physiology and cognition
It is difficult to understand why anyone would stuff a solvent-soaked rag in their mouth, and begin huffing the concentrated vapors. Perhaps part of the lure of inhalants is the fact that intoxication usually lasts only a few minutes, making their abuse easier to conceal than alcohol or marijuana abuse. Inhalant intoxication is quick and transient because of the substances’ high lipophilicity (i.e., rapid entry from the lungs into the bloodstream and into lipid-rich brain and liver tissues), and is consistent with experiments in non-human primates showing that inhalants’ transit through the brain has a half life of approximately 20 minutes (Gerasimov et al., 2002a). Because of this rapid turnover, many children abuse inhalants hoping for a quick high resembling alcohol inebriation, which is characterized by similar mild stimulation, loss of inhibition, and distorted perceptions.

Because inhalants generally target the same areas of the brain that are affected by alcohol (and other drugs of addiction) (Gerasimov et al., 2002a; Gerasimov et al., 2002b), it is not surprising that, in addition to the inhalant-produced intoxication, abusers experience nausea, vomiting, slurred speech, and loss of coordination. And while we cannot yet fully characterize inhalant abuse intoxication, it is generally understood that most inhalants typically used by children produce pleasurable effects by depressing the central nervous system (CNS), a conclusion supported by a large number of animal studies (Evans & Balster, 1991). Evidence has been accumulating, for example, that both alcohol and many inhalants affect the transmission among neurons by modulating brain receptors for certain neurotransmitters (Balster, 2003).

The striking similarities between alcohol and inhalant abuse have led to the potentially useful suggestion that preadolescent children seek out inhalants as an easily obtainable substitute for alcohol (Volkow, 2005). Moreover, the existence of shared and similarly affected neural pathways, suggests significant commonalities in the underlying biological causes and environmental risk factors that may predispose people to both inhalant and alcohol abuse (Kipke et al., 1997). Still, other effects of inhalants, such as hallucinations, tremors, and seizures, do not lend to such a simple classification. Also, while many of the known acute neurologic effects are reversible with abstinence, some of the more pervasive consequences of chronic abuse, like dementia, may prove long-lasting.

These facts speak to a strong need for more research on all aspects of the inhalant abuse phenomenon. Confronting this need for more knowledge, NIDA in 2001 launched an aggressive inhalant research agenda that today includes a diverse portfolio of projects designed to better understand, prevent, and, even reverse the neurocognitive effects of inhalant abuse.

Long-term brain effects
In contrast to our incomplete understanding of the cellular mechanisms underlying inhalant abuse, a wealth of information describes the nature and severity of the many overall deleterious health effects brought on by inhaling various chemical mixtures. The neurotoxic profiles of some of the components found in abused volatile products, for example, have been well documented as part of the standard procedures put in place to report material safety information. In addition, numerous case reports (Doring et al., 2002; Korobkin et al., 1975; Oh & Kim, 1976; Shirabe et al., 1974) and imaging studies (Kamran & Bakshi, 1998; Kornfeld et al., 1994; Sharp & Rosenberg, 1997) have clearly shown the toxic effects of chronic inhalant exposure on the human brain and other parts of the nervous system. Animal and human research further corroborates that most inhalants are neurotoxic.

Still, significant differences emerge when comparing the harmful effects of various volatile solvents (Bowen et al., 2005). For instance, the chronic abuse of toluene that can lead to dementia, has been linked to destruction of nerve fibers in the brain and peripheral nervous system damage (Rosenberg & Sharp, 1992), while gasoline sniffing is likely to produce neurological and cognitive abnormalities in the absence of acute toxic brain diseases (Maruff et al., 1998). Nevertheless, while effects of particular solvents may differ, similar clinical pictures will likely emerge as a result of exposure to equivalent doses for equivalent periods of time (Rosenberg & Sharp, 1992).

Observations made in Emergency Departments provide further evidence of the wide range of possible neurotoxic effects brought on by inhalant abuse. Upon admission, long-term inhalant abusers may display an array of neuropsychiatric signs and symptoms — that is, disorders with both neurological and psychiatric features. Complaints of memory loss, delusions, or hallucinations are typical, as is slurred speech, staggering or stumbling, visual changes, and loss of hearing or sense of smell (Meadows & Verghese, 1996). Most commonly, however, inhalant abusers arrive unconscious or dead. Unfortunately, there is no specific set of symptoms that the clinician can use to confirm or reject a suspicion of inhalant abuse.

Addiction liability
Similar to addictive illicit drugs, inhalants can be euphorigenic, or mood altering (Balster, 1998). Consequently, inhalants can trigger levels of “liking” and drug seeking that are almost equivalent to those induced by nicotine or methamphetamine (Miyata et al., 2004). Further, users report that they abuse inhalants in spite of known negative consequences (Kono et al., 2001). Interestingly, while many inhalant abusers expose themselves to a wide variety of volatile substances, a subset restricts themselves largely or exclusively to inhalation of specific product (Filley et al., 2004). In light of these facts, scientists began to wonder whether inhalants might have the potential to cause addiction.

More is known about the addictive liability of toluene than any other inhalant, the inhalation of paint fumes being one of the most popular forms of inhalant abuse, particularly among young users (SAMHSA, 2005). Considerable scientific evidence suggests common neural substrates for inhalants and other drugs of abuse. In a recent study, for example, the brains of rats exposed to toluene displayed significantly increased levels of dopamine in the same regions that respond to other drugs of addiction (Gerasimov et al., 2002b). Other evidence supports a tendency for organic solvents to target dopamine centers in the brain, as seen in the case of a patient that developed parkinsonism, or nervous disorders similar to Parkinson’s disease (e.g., muscular rigidity, tremor, and impaired motor control) following heavy abuse of lacquer thinner (Uitti et al., 1994). The affected circuits in these and additional (Balster, 2003; Zacny et al., 1999) examples point to the same dopamine centers that have been shown repeatedly to play a major role in the rewarding effects of many drugs of abuse. Finally, when inhalants are used heavily, typical signs of physical dependence like tolerance and withdrawal symptoms may develop within several hours to a few days after use (Kono et al., 2001). These symptoms may include sweating, rapid pulse, hand tremors, insomnia, nausea, vomiting, physical agitation, anxiety, hallucinations, and grand mal seizures (NIDA, 2005).

Taken together, these and similar observations, strongly suggest that inhalant abuse can progress into the chronic and relapsing disease of addiction. Furthermore, the addictive effects of inhalants on the still developing brain of young adolescents may render early onset of inhalant abuse a significant risk factor for other drug abuse later in life (Davies et al., 1985; Oetting et al., 1988). Consistent with this hypothesis, an epidemiologic analysis conducted in 1994 found that, even after adjusting for sex, age, race, socioeconomic status, and use of marijuana, inhalant users were at least five times as likely as nonusers to have injected drugs (Schutz et al., 1994).

The strength of this cumulative evidence notwithstanding, it is extremely difficult to arrive at a reliable estimate of the prevalence of inhalant addiction among our youth. Most inhalant abusers seem to either outgrow this behavior or move on to other drugs. Close examination of MTF results for the 1975-1982 period, for example, suggest that only 1.5 percent of adolescent inhalant users may abuse volatile substances to the point of possible addiction (using over 40 times per year) (Johnston et al., 1982). This figure stands in sharp contrast with the estimated 6.4 percent and 20 percent who become frequent users of marijuana and alcohol, respectively. More recently, a study that attempted to cast some light on this issue by reanalyzing the 2000-2001 National Household Survey dataset using established criteria for abuse and dependence, found that among adolescents aged 12 to 17 who used inhalants in the previous year, 11 percent met the DSM-IV criteria for abuse or dependence in that year, while 4 percent of past-year users met DSM-IV criteria for past-year inhalant dependence (Wu et al., 2004).

Whatever the precise number of youngsters addicted to inhalants might be, we must always remember that at the individual level, even infrequent or single episodes of inhalant abuse can have catastrophic consequences. From a population perspective, it is clear that the behavior represents a likely vulnerability marker that could be harnessed to design better addiction intervention strategies.

Other health effects
While it is obvious that abuse of inhalants can have long-lasting consequences on brain physiology and behavior, particularly in children, the most serious health consequence is death itself, stemming from aspiration, accidental trauma, or asphyxia (Bowen et al., 1999). Death can also occur as a result of cardiac arrhythmias, anoxia, respiratory depression, burns from accidental flash fires, hypothermic injuries from propellants, and the triggering of underlying asthma or allergic reactions. As many as 50 percent of inhalant-related deaths are caused by sudden-sniffing death syndrome (Bass, 1970), which occurs when the acutely intoxicated inhalant abuser is startled, prompting a burst of catecholamines, or adrenal hormones, that can trigger ventricular fibrillation, an often fatal form of heart arrhythmia (Anderson & Loomis, 2003).

In addition to brain damage, addiction, or death, inhalant abuse can also cause chronic and serious damage to whole body systems, including nervous, cardiovascular, respiratory, and renal. Neurologic toxicity has been observed as a side effect of inhaling toxic vapors. In addition to CNS findings, peripheral neuropathies may cause local or generalized muscle weakness, muscle wasting, and absent or decreased tendon reflexes.

Finally, we need to recognize that early exposure to inhalants may happen even before birth. Inhalant abuse by women who are pregnant can increase the risks of spontaneous abortion or result in fetal solvent syndrome, which causes low birth weight, small head size, facial malformations, and muscle tone abnormalities similar to the effects of fetal alcohol syndrome (Jones & Balster, 1998).

Diagnosis, treatment, and prevention
Criteria for intoxication
General indicators of inhalant abuse include paint or stains on the body or clothing, spots or sores around the mouth, red or runny eyes and nose, a drunken or dazed appearance, loss of appetite, excitability, and/or irritability. However, the detection of a chemical odor in the breath or on the clothing remains one the most reliable signs of inhalant abuse. More formal criteria that need to be fulfilled before an abused inhalant can be implicated in an intoxication event are defined in the diagnostic and statistical manual of mental disorders (APA, 2000).

Treatment
In the year 2003, inhalants were mentioned in about 1,600 substance abuse related admissions to emergency departments (SAMHSA, 2003a). Data from prior years show that people admitted for inhalant abuse were generally under age 18 (44 percent), male (72 percent), and non-Hispanic White (66 percent). Twenty-eight percent of those admitted reported daily use of inhalants, and almost 26 percent admitted using inhalants by age 12.
More than a decade ago, it was considered that volatile solvent abusers were among the most difficult and refractory people to treat (Jumper-Thurman & Beauvais, 1992). Indeed, the field of inhalant abuse intervention has been characterized by the absence of even a rudimentary treatment model. The daunting nature of studying inhalant abuse, particularly in children, is likely to have discouraged intense research in this area for a long time, leaving us with a less than adequate palliative response to this problem. For example, there is no specific agent that can currently reverse or alleviate acute solvent intoxication, addiction, nor the rare cases which present with withdrawal symptoms.

One of the likely obstacles to faster progress in this area may be that volatile substance abusers do not fit well within existing treatment regimes, perhaps because young inhalant users appear to be categorically different from other drug users (Mackesy-Amiti & Fendrich, 1999). Many young adolescents with inhalant disorders, for example, also report coexisting mental health treatment (Wu et al., 2004), while adults who initiated inhalant use at or before age 13 were about five times more likely than those who never used, to report substance abuse or addiction, as well as dropping out of school and lifetime arrests (SAMHSA, 2005). In fact, pediatric inhalant abuse may exemplify the increasingly well documented high prevalence of dually diagnosed mental and substance use disorders (Crowley & Riggs, 1995; Kandel et al., 1999; Whitmore et al., 1997). The existence of such a robust medical link in the general population has been a driving force for NIDA in setting priorities over the past decade, and the underlying reason for including the integrated treatment of comorbid psychiatric disorders as one of our 13 core treatment principles (NIDA, 2000). Disappointingly, these empirically supported guidelines are being adopted at an exceedingly slow pace, mainly because of the stigma that still surrounds mental illnesses and substance abuse, and the unfair regulations placed on mental health care benefits and service delivery system (DHHS, 2003). Faster implementation of NIDA’s integrated treatment principles would jumpstart a long overdue focus on the problems associated with pediatric inhalant abuse.

Prevention
Banning those colorfully displayed products containing abusable volatile solvents from the supermarket shelves is clearly not an option. A solution to this problem must enter from a different angle, one that aims to educate children and others about the dangers and risks involved. Nationwide surveys of drug abuse–related behaviors consistently show a close inverse relationship between substance abuse and perception of harm (Johnston et al., 2005; Volkow & Li, 2005). We must then affect this perception by increasing knowledge of potential harm. Children and adolescents who abuse inhalants put themselves at substantial risk of illness and death, a fact that needs to be clearly explained to them and their parents as the best way to curb this type of abuse (AAP, 1996). It follows that the best hope for effective intervention hinges on the targeted dissemination of accurate information based on the best scientific data available. At the same time, it is critical for educators, physicians, and counselors to thoughtfully consider how to best use informational vehicles describing the dangers of widely available inhalants, an inherently tricky enterprise that ought to be approached carefully (Burk, 2001).

Preventing the onset and establishment of inhalant abuse should become a critical goal of pediatric care, with special attention focused on young adolescent populations displaying recognized risk factors. As mentioned, NIDA-supported research clearly shows that young people who have been treated for mental health problems; have a history of foster care; or who already abuse other drugs, have an increased risk of abusing or becoming addicted to inhalants. In addition, adolescents who first begin using inhalants at an early age are more likely to become addicted to them (Wu et al., 2004). When filling out a clinical history, specific questions about “huffing”, “snorting”, and “bagging” should be asked, in addition to questions about drinking alcohol or smoking cigarettes and marijuana, and the answers considered in the context of risk factors associated with inhalant abuse.

We can significantly reduce the impact of inhalant abuse on future generations of Americans if we recognize and remove the systemic and economic barriers to integrated treatment (Libby & Riggs, 2005), and if health care providers, counselors, and parents become more aware of the risks and more familiar with the facts related to pediatric inhalant abuse.

Nora D. Volkow, MD, has served as the director of NIDA since 2003. Dr. Volkow came to NIDA from Brookhaven National Laboratory, where she held concurrent positions as associate director for life sciences, director of nuclear medicine, and director of the NIDA-Department of Energy Regional Neuroimaging Center.

References
AAP. (1996). Inhalant abuse. American academy of pediatrics, committee on substance abuse and committee on Native American child health. Pediatrics, 97(3), 420-423.
Anderson, C. E., & Loomis, G. A. (2003). Recognition and prevention of inhalant abuse. Am Fam Physician, 68(5), 869-874.
APA. (2000). American psychiatric association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, d.C.: American psychiatric association.
(Vol. 239).
Balster, R. L. (1998). Neural basis of inhalant abuse. Drug Alcohol Depend, 51(1-2), 207-214.
Balster, R. L. (2003). The pharmacology of inhalants. Chevy Chase, MD: American Society of Addiction medicine.
Bass, M. (1970). Sudden sniffing death. Jama, 212(12), 2075-2079.
Beauvais, F., Jumper-Thurman, P., Plested, B., & Helm, H. (2002). A survey of attitudes among drug user treatment providers toward the treatment of inhalant users. Subst Use Misuse, 37(11), 1391-1410.
Bowen, S. E., Batis, J. C., Mohammadi, M. H., & Hannigan, J. H. (2005). Abuse pattern of gestational toluene exposure and early postnatal development in rats. Neurotoxicol Teratol, 27(1), 105-116.
Bowen, S. E., Daniel, J., & Balster, R. L. (1999). Deaths associated with inhalant abuse in Virginia from 1987 to 1996. Drug Alcohol Depend, 53(3), 239-245.
Burk, I. (2001). Inhalant prevention resource guide. Richmond, VA: Virginia Department of Education.
Crowley, T., & Riggs, P. (1995). Adolescent substance use disorder with conduct disorder and comorbid conditions. Rockville, MD: US Department of Health and Human Services.
Davies, B., Thorley, A., & O’Connor, D. (1985). Progression of addiction careers in young adult solvent misusers. Br Med J (Clin Res Ed), 290(6462), 109-110.
DHHS. (2003). President’s new freedom commission on mental health. Achieving the promise: Transforming mental health care in America. In M. Department of Health and Human Services. Rockville (Ed.): DHHS.
Doring, G., Baumeister, F. A., Peters, J., & von der Beek, J. (2002). Butane abuse associated encephalopathy. Klin Pediatr, 214(5), 295-298.
Evans, E. B., & Balster, R. L. (1991). CNS depressant effects of volatile organic solvents. Neurosci Biobehav Rev, 15(2), 233-241.
Fendrich, M., Mackesy-Amiti, M. E., Wislar, J. S., & Goldstein, P. J. (1997). Childhood abuse and the use of inhalants: Differences by degree of use. Am J Public Health, 87(5), 765-769.
Filley, C. M., Halliday, W., & Kleinschmidt-DeMasters, B. K. (2004). The effects of toluene on the central nervous system. J Neuropathol Exp Neurol, 63(1), 1-12.
Gerasimov, M. R., Ferrieri, R. A., Schiffer, W. K., Logan, J., Gatley, S. J., Gifford, A. N., et al. (2002a). Study of brain uptake and biodistribution of [11c]toluene in non-human primates and mice. Life Sci, 70(23), 2811-2828.
Gerasimov, M. R., Schiffer, W. K., Marstellar, D., Ferrieri, R., Alexoff, D., & Dewey, S. L. (2002b). Toluene inhalation produces regionally specific changes in extracellular dopamine. Drug Alcohol Depend, 65(3), 243-251.
Glaser, H. H., & Massengale, O. N. (1962). Glue-sniffing in children. Deliberate inhalation of vaporized plastic cements. JAMA, 181, 300-303.
Johnston, Bachman, J. G., & O’Malley, P. M. (1982). Student drug use, attitudes, and beliefs: National trends, 1975-1982. (dhhs publication no. [adm] 83-1260). Rockville, md: National institute on drug abuse, 134 pp.
Johnston, O’Malley, P., Bachman, J., & Schulenberg, J. (2005). Monitoring the future national results on adolescent drug use: Overview of key findings, 2004. NIH publication 05-5726.
Jones, H. E., & Balster, R. L. (1998). Inhalant abuse in pregnancy. Obstet Gynecol Clin North Am, 25(1), 153-167.
Jumper-Thurman, P., & Beauvais, F. (1992). Solvent toxicity: A neurological focus. In Sharp, C.W.; Beauvais, F. And Spence, R. Inhalant abuse: A volatile research agenda (p. 203). Rockville MD, National Institute on Drug Abuse. Research monograph series 129.
Kamran, S., & Bakshi, R. (1998). Mri in chronic toluene abuse: Low signal in the cerebral cortex on t2-weighted images. Neuroradiology, 40(8), 519-521.
Kandel, D. B., Johnson, J. G., Bird, H. R., Weissman, M. M., Goodman, S. H., Lahey, B. B., et al. (1999). Psychiatric comorbidity among adolescents with substance use disorders: Findings from the meca study. J Am Acad Child Adolesc Psychiatry, 38(6), 693-699.
Kipke, M. D., Montgomery, S. B., Simon, T. R., & Iverson, E. F. (1997). “Substance abuse” disorders among runaway and homeless youth. Subst Use Misuse, 32(7-8), 969-986.
Kono, J., Miyata, H., Ushijima, S., Yanagita, T., Miyasato, K., Ikawa, G., et al. (2001). Nicotine, alcohol, methamphetamine, and inhalant dependence: A comparison of clinical features with the use of a new clinical evaluation form. Alcohol, 24(2), 99-106.
Kornfeld, M., Moser, A. B., Moser, H. W., Kleinschmidt-DeMasters, B., Nolte, K., & Phelps, A. (1994). Solvent vapor abuse leukoencephalopathy. Comparison to adreno-leukodystrophy. J Neuropathol Exp Neurol, 53(4), 389-398.
Korobkin, R., Asbury, A. K., Sumner, A. J., & Nielsen, S. L. (1975). Glue-sniffing neuropathy. Arch Neurol, 32(3), 158-162.
Libby, A. M., & Riggs, P. D. (2005). Integrated substance use and mental health treatment for adolescents: Aligning organizational and financial incentives. J Child Adolesc Psychopharmacol, 15(5), 826-834.
Lorenc, J. D. (2003). Inhalant abuse in the pediatric population: A persistent challenge. Curr Opin Pediatr, 15(2), 204-209.
Mackesy-Amiti, M. E., & Fendrich, M. (1999). Inhalant use and delinquent behavior among adolescents: A comparison of inhalant users and other drug users. Addiction, 94(4), 555-564.
Maruff, P., Burns, C. B., Tyler, P., Currie, B. J., & Currie, J. (1998). Neurological and cognitive abnormalities associated with chronic petrol sniffing. Brain, 121 (Pt 10), 1903-1917.
Meadows, R., & Verghese, A. (1996). Medical complications of glue sniffing. South Med J, 89(5), 455-462.
Merry, J., & Zachariadis, N. (1962). Addiction to glue sniffing. Br Med J, 5317, 1448.
Miyata, H., Kono, J., Ushijima, S., Yanagita, T., Miyasato, K., & Fukui, K. (2004). Clinical features of nicotine dependence compared with those of alcohol, methamphetamine, and inhalant dependence. Ann N Y Acad Sci, 1025, 481-488.
NIDA. (2000). National institute on drug abuse: Principles of drug addiction treatment: A reserach-based guide. NIDA publication no 00-4180. Rockville, md. In D. o. H. a. H. Services (Ed.).
NIDA. (2005). NIDA community alert drug bulletins: Inhalants. NIH publication number 05-5623. In M. Department of Health and Human Services. Rockville (Ed.): DHHS.
Oetting, E. R., Edwards, R. W., & Beauvais, F. (1988). Social and psychological factors underlying inhalant abuse. NIDA Res Monogr, 85, 172-203.
Oh, S. J., & Kim, J. M. (1976). Giant axonal swelling in “huffer’s” neuropathy. Arch Neurol, 33(8), 583-586.
Pagare, D., Meena, G. S., Singh, M. M., & Sahu, R. (2004). Risk factors of substance use among street children from delhi. Indian Pediatr, 41(3), 221-225.
Rosenberg, N. L., & Sharp, C. W. (1992). Solvent toxicity: A neurological focus. In Sharp, C.W.; Beauvais, F. And Spence, R. Inhalant abuse: A volatile research agenda (pp. 119-120). Rockville md, national institute on drug abuse. Research monograph series 129.
SAMHSA. (2003a). Drug abuse warning network, 2003: Interim national estimates of drug-related emergency department visits.
SAMHSA. (2003b). The NSDUH report: Substance use among school dropouts. In DHHS (Ed.): Office of Applied Studies, Substance Abuse and Mental Health Services Administration.
SAMHSA. (2005). The NSDUH report: Inhalant use and delinquent behaviors among young adolescents. In DHHS (Ed.): Office of Applied Studies, Substance Abuse and Mental Health Services Administration.
Schutz, C. G., Chilcoat, H. D., & Anthony, J. C. (1994). The association between sniffing inhalants and injecting drugs. Compr Psychiatry, 35(2), 99-105.
Sharp, C., & Rosenberg, N. (1997). Inhalant-related disorders. In: Tasman, psychiatry, vol. 1. 835-852, Philadelphia: W.B. Saunders.
Shirabe, T., Tsuda, T., Terao, A., & Araki, S. (1974). Toxic polyneuropathy due to glue-sniffing. Report of two cases with a light and electron-microscopic study of the peripheral nerves and muscles. J Neurol Sci, 21(1), 101-113.
Spiller, H. A. (2004). Epidemiology of volatile substance abuse (vsa) cases reported to us poison centers. Am J Drug Alcohol Abuse, 30(1), 155-165.
Uitti, R. J., Snow, B. J., Shinotoh, H., Vingerhoets, F. J., Hayward, M., Hashimoto, S., et al. (1994). Parkinsonism induced by solvent abuse. Ann Neurol, 35(5), 616-619.
Volkow, N. D. (2005). Inhalant abuse: Danger under the kitchen sink (Vol. 20, pp. 3): NIDA Notes. National Institute on Drug Abuse.
Volkow, N. D., & Li, T. K. (2005). Drugs and alcohol: Treating and preventing abuse, addiction and their medical consequences. Pharmacol Ther, 108(1), 3-17.
Whitmore, E. A., Mikulich, S. K., Thompson, L. L., Riggs, P. D., Aarons, G. A., & Crowley, T. J. (1997). Influences on adolescent substance dependence: Conduct disorder, depression, attention deficit hyperactivity disorder, and gender. Drug Alcohol Depend, 47(2), 87-97.
Wu, L. T., Pilowsky, D. J., & Schlenger, W. E. (2004). Inhalant abuse and dependence among adolescents in the united states. J Am Acad Child Adolesc Psychiatry, 43(10), 1206-1214.
Zacny, J. P., Janiszewski, D., Sadeghi, P., & Black, M. L. (1999). Reinforcing, subjective, and psychomotor effects of sevoflurane and nitrous oxide in moderate-drinking healthy volunteers. Addiction, 94(12), 1817-1828.

This article is published in Counselor,The Magazine for Addiction Professionals, April 2006, v.7, n.2, pp.12-24.

No one has commented on this article.

Please keep your comments brief and on topic, and remember that this is not a discussion thread.
Name :
Comment(s) :

J! Reactions 1.09.00 • Professional Site License
Copyright © 2006 S. A. DeCaro

---