The American Journal on Addictions 10:79-94, 2001 Published by Brunner/Routledge

# 2001 American Academy of Addiction Psychiatry 1055-0496/01 $12.00 + .00

CLINICAL UPDATE

Clinical Review of Inhalants

Thomas B rouette, M .D., Raymond Anton, M .D .

While the rate of inhalant abuse continues to rise in this country, it remains
one of the least studied or discussed groups of abused substances. This review
focuses on the current knowledge of the epidemiology, pharmacology, and
sequela of inhalant abuse. We will discuss three groups of inhalants: volatile
solvents, nitrous oxide, and nitrites. We will then conclude by proposing
means by which inhalant abuse may be prevented and treated. (Am J
Addict 2001;10:79-94)

D espite its prevalence and serious

sequela, inhalant abuse remains one
of the least discussed areas in substance
treatment. As of 1996, the NIDA had only
®ve grants that focused primarily on
inhalant abuse.1 This lack of research has
led to much misinformation and confusion
about inhalant abuse. The dearth of research
on these agents may be partially attributed
to the lack of pharmacological homogeneity
among inhalants. In contrast to other classes
of substances in which one basic compound
is abused by different routes, inhalants are
de®ned solely by their route of adminis-
tration. However, not all drugs that can
be abused through inhalation are con-
sidered ``inhalants,’’ so there is an obvious
need of a de®nition of ``inhalant abuse.’’
Although authors may differ on their
speci®c de®nition of an inhalant, the three
main conventions are that the substance
is volatile at room temperature, not already
de®ned as a pharmacologically distinct class
(such as nicotine or cocaine), and is used by
snif®ng, snorting, bagging (inhaling from a
bag that contains the substance), huf®ng
(saturating a rag with the substance, placing
the rag in the mouth and inhaling), or
spraying (into the mouth) the substance
in order to alter one’s level of con-
sciousness. For the sake of this paper,
we will divide inhalants into three types
of inhalants: volatile solvents, nitrous
oxide, and nitrites.
EPIDEM IOLOG Y
Despite the lack of attention given
inhalants, both the Monitoring the Future
Study2 and the American Drug and Alcohol
Survey 3 indicate that in the 1990s, inhalants
were the second most commonly used illicit
drugs among 12- to 17-year-olds, behind
marijuana. In fact, between 1983 and 1993,
the risk of this group using inhalants has
increased threefold, from 7.2 to 21.5 per

Received July 2, 1999; accepted September 3, 1999.

From the Department of Psychiatry, Medical University of South Carolina, Charleston (Drs. Brouette and
Anton). Dr. Brouette is now with Lancaster Behavioral Health, Lancaster, Pa. Address correspondence
to Dr. Brouette, 108 Foxshire Dr., Lancaster, PA 17601. E-mail: trpbrouette@ earthlink.net.

79
Clinical Review of Inhalants
1000 persons.3 Overall, these studies ®nd
that in the United States, 6% of fourth
graders, 19.9% of eighth graders, and
17% of high school seniors had tried
inhalants at least once. Note that the
decrease between 8th and 12th grade
may be explained by the high dropout rate
among the more severe inhalant abusers.
Among all these groups, the volatile
solvents were by far abused most, with
nitrite and nitrous oxide use far less
common.
According to the National Household
Survey on Drug Abuse,3 the incidence
of inhalant abuse decreases with age. The
lifetime prevalence of inhalant abuse is 5.7%
in 12- to 17-year-olds, with 1.6% having
used within one month of the survey.
The prevalence among ages 18- 25 is 9.8%
with 0.8% currently using, and among
26- 34-year-olds the numbers decrease to
9.2% and 0.4%, respectively. Possible
reasons for the decreasing rate of use with
age will be discussed later.
Nitrous oxide and nitrite use is less
common. A 1979 study found that 20%
of dental and medical students had abused
nitrous oxide.4 The rate of nitrite use
had been high in the late 1970s, with up
to 5 million people using nitrites weekly
by 1979; however, by the early 1980s, their
use decreased substantially.5
The prevalence of inhalant use is also
in¯uenced by both community and cultural
factors. African-Americans have a low
prevalence of inhalant use, while recent
immigrants from Latin America and Native
Americans have a higher prevalence of use.6
Though some have hypothesized that
among the immigrants the rate may be
higher due to dif®culty acculturating,7
Padilla et al8 attributed the higher rate of
use among barrio Hispanics to poverty, lack
of opportunity, and social dysfunction. On
Indian Reservations, several factors may
play a role. Peters et al9 has suggested that
even small epidemic use (for example, in
a school class) will have a drastic effect
80 VOLUM E 10 N UM B ER 1
on the rate of use within a very small popu-
lation sample. Nevertheless, the lifetime
prevalence of inhalant abuse on Indian res-
ervations has been reported as 34% among
8th graders and 20% among 12th graders,10
so community and cultural in¯uences do
appear to have some impact.
More signi®cant than the prevalence of
use of inhalants is the incidence of death.
One study found that 39 people in Virginia
had died as a direct consequence of inhalant
use between 1987 and 1996.11 The majority
of these deaths were in males under age 22
and accounted for 0.3% of all deaths to
males aged 13 to 22 years. Nationwide,
the National Inhalant Prevention Coalition
reports that 240 people have died between
1996 and 1999 due to inhalant abuse.
Deaths were most frequently attributed
to the toxic effects of gas fuels or trauma
that was a consequence of an altered
sensorium.11 Clearly, the abuse of these sub-
stances can be fatal.
PSYCH OPATH OLOG Y
Although inhalant abusers, like many other
substance users, are a diverse group, those
who abuse these substances tend to be from
particularly chaotic and disrupted families.
The users often meet criteria for antisocial
personality and are frequently noted in
school to have cognitive de®cits that pre-
sumably predate their use of inhalants.6
Beauvais and Oetting12 propose that
inhalant abusers can be classi®ed into three
categories. The ®rst, inhalant-dependent
adults, have the poorest prognosis. They
predominately use inhalants, and have done
so for many years at the cost of both their
physical and psychological well-being.
The next group, polydrug users, utilizes
inhalants as an alternative when their drugs
of choice are unobtainable. This group
tends to behave like others who also abuse
their primary drug of choice. The last
group, young inhalant users, tend to be
between ages 12 and 13, and are also
WINTER 2001

experimenting with other substances, such
as cigarettes, alcohol, and marijuana. An
exception to these demographics is nitrite
abusers. This group tends to have their ®rst
exposure in their mid-20s, and are often
used more for enhancing sex than for a
``high.’’ Their use was particularly prevalent
among homosexuals until the AIDS
epidemic, which has led to signi®cant
reduction in their use.13
Though the relationship between sol-
vent inhalation and psychiatric disorders
remains controversial, there appears to be
agreement that within the population of
drug and alcohol abusers, inhalant abusers
appear to have more severe character
pathology, particularly antisocial person-
ality disorder.14 Several studies have also
found depression to be more common in
solvent abusers;15,16 however, some years
ago, Ron14 argued that solvent abuse does
not appear to cause psychiatric illness but
instead is more common among the
mentally ill. She argues that depressive-like
symptoms, such as insomnia and anorexia,
are better explained as manifestations of
withdrawal from these substances. An
opposing argument is that the apathy
and depressive mood seen in users may
be an ``amotivational syndrome’’ similar
to that suggested with marijuana use.17
At this time, all that can be said is that
inhalant abuse is assumed to be co-morbid
with severe personality disorders and
may be associated with some
depression-like syndrome.
VOLATILE SOLVEN TS
This category is the largest and most diverse
group of abused inhalants. This group con-
sists of both industrial and household prod-
ucts containing such constituents as
toluene, n-hexane, chlorohydrocarbons,
or benzene. As Table 1 illustrates, most
products are composed of several of these
compounds, plus numerous others. For
example, paint thinner contains at least
THE AM ERICAN JOURN AL ON ADDICTIONS
Brouette & Anton
200 different aromatic and aliphatic com-
pounds. In addition, inhalant abusers often
are exposed to several hundred-fold times
routine exposure.
Although snif®ng glue was the ®rst
inhalant to gain national notoriety in the
early 1960s, its popularity has been
supplanted by correction ¯uid.18 In
addition, gasoline, spray paint, and shoe
polish continue to be widely abused.
M echanism of Action
Volatile solvents quickly gain access to
the brain because of rapid absorption via the
pulmonary circulation and high lipid
solubility. This likely explains why com-
pounds composed of longer carbon chains
(and thus more lipophilic) require lower
concentrations to cause intoxication.19
For most abused solvents, 15 to 20
inhalations produces euphoria and sub-
sequent drowsiness within seconds to
minutes. Rebreathing of exhaled air (as
done in bagging) leads to hypercapnia
and hypoxia, which potentiates the
intoxicating effects of the solvent.20 The
intoxication is similar to alcohols, with
accompanying diplopia, slurred speech,
ataxia, and disorientation. At higher
exposures, visual hallucination may also
occur. The majority of substances are
excreted by a pulmonary route, but the alkyl
nitrites, aromatics, and methylene chloride
undergo metabolism in the liver to poten-
tially toxic products. Because the solvents
are highly lipid soluble, a user often has
residual intoxication, which evolves into
drowsiness and a headache over the course
of 1 to 6 hours.
The mechanism of action by which
inhalants induce intoxication is unclear.
One hypothesis involves ``¯uidization’’ of
neuronal membranes leading to slowing
of axonal ion channel transport. Perhaps
the volatile solvents resemble the
anesthetics in that the potency of anesthetics
are also proportional to their partition
81
Clinical Review of Inhalants

T A BLE 1. Chemicals in Commonly Abused Inhalants

Inhalant Chemical

Adhesives:
Airplane glue Toluene; ethyl acetate
Rubber cement Hexane; toluene; methyl chloride; acetone; methyl ethyl ketone
PVC cement Trichloroethylene
Aerosols:
Spray paint Butane; propane; ¯uorocarbons; toluene; hydrocarbons
Hair spray Butane; propane; ¯uorocarbons
Deodorants Butane; propane; ¯uorocarbons
Room freshener Butane; propane; ¯uorocarbons
Analgesic spray Fluorocarbons
Asthma spray Fluorocarbons
Cleaning agents:
Dry cleaning Tetrachloroethylene; trichloroethane
Spot remover Tetrachloroethylene; trichloroethane; trichloroethylene
Degreaser Tetrachloroethylene; trichloroethane; trichloroethylene
Solvent:
Nail polish remover Acetone; ethyl acetate; toluene
Paint thinner Toluene; methylene chloride; methanol
Correction ¯uid Trichloroethylene; trichloroethane
Fuel gas Butane
Lighter Butane; isopropane
Fire extinguisher Bromochlorodi¯uromethane
Gasoline Aliphatic and aromatic hydrocarbons; organic (and possibly
inorganic) lead; benzene; methylcyclopentadienyl manganese
tricarbonyl; ethanol; methanol; methyl tertiary butyl ether
Adapted from Sharp CW, Rosenberg NL. Inhalants. In: Lowinson JH, Ruiz P, Millman RB, Langrod JG, eds.
Substance Abuse: A Comprehensive Textbook. 3rd ed. Baltimore, Md.: Williams & Wilkins; 1997: 246- 264.
Copyright 1997 Williams & Wilkins. Reprinted with permission.

coef®cient.19 Another theory proposes that
volatile solvents potentiate hyperpolariza-
tion of GABA receptors and interact at
glutamate receptors.21 This theory is
supported by several animal studies that
have found a cross-tolerance between
1,1,1-trichloroehtane, toluene, ethanol, bar-
biturates, and benzodiazepines.22 Hence,
although no mechanism of action has been
yet discerned, volatile solvents may exert
their effect by interactions with neuronal
membranes as well as GABA and glutamate
receptors.
Tolerance and Withdrawal
Both tolerance and withdrawal may
develop to volatile solvents. Tolerance
has been demonstrated in humans, and
may develop to toluene within three
months of regular use.14 Inhalant with-
drawal, although not included in DSM-IV,
has been demonstrated in several studies.
Two studies propose that the sleep dis-
turbances, nausea, tremor, and irritability
that last 2 to 5 days after last use are mani-
festations of a withdrawal syndrome and
not just residual intoxication.23,24 An earlier
study proposed a syndrome resembling
delirium tremors that may develop in
chronic abusers.25 However, more research
is still required in order to demarcate
residual effects of solvent inhalation from
withdrawal symptoms.
M edical Sequela
Considering the diversity of compo-
unds, it is not surprising that there is a long
list of possible medical sequela from abus-

82 VOLUM E 10 N UM B ER 1 WINTER 2001


ing these compounds (see Table 2).
Therefore, this section will focus on several
of the most signi®cant complications and
then discuss disorders that are associated
with particular agents.
Acute Use. After the acute use of these
inhalants, the user has sneezing, coughing,
excess salivation, and conjunctival
erythema. As the dose increases, slurred
speech, diplopia, ataxia, disorientation,
and visual hallucinations become apparent.
Further use may lead to severe CNS
depression with coma, seizure, or death.
Inhalation can also be quite irritating to
the respiratory system, and dyspnea,
wheezes, or rales are common for up to
2 hours after use. Noting these signs and
symptoms, as well as noting a characteristic
perioral ``huffer’s rash,’’ are useful cues to
prompt clinicians to question a patient
about inhalant abuse.
Chronic Abuse. The liver and the heart are
two organs that are commonly effected in
volatile solvent abusers. Hepatotoxicity is
associated with carbon tetrachloride,
chloroform, chloroethylene, and possibly
toluene abuse; fortunately, even in chronic
abusers, the elevated liver functions often
improve within 2 weeks of abstinence.26
The cardiac system is less forgiving. Rapid
cooling of the larynx, as frequently occurs
when abusing aerosol inhalants such as
spray paint, causes re¯ex vagal inhibition,
which can precipitate a cardiac arrhythmia
and sudden death.27 The solvents them-
selves are also arrhythmogenic in that both
aliphatic compounds and halogenated
hydrocarbons sensitize the myocardium
to catecholamines. 28 Therefore, the inhalant
sensitizes the heart to the stress reaction
caused by substance-associated hypoxia,
leading to an increased risk of arrhythmia.
These compounds can also have direct
effects on the heart by inducing sinus
bradycardia, myocarditis, and ®brosis,
and an indirect effect by causing a
THE AM ERICAN JOURN AL ON ADDICTIONS
Brouette & Anton
hypoxia-induced heart block.29,30 Hence,
cardiac complications are probably the
most serious medical complication in vol-
atile solvent abusers and may have lethal
consequences.
The lethality of these substances is not
just limited to their effects on speci®c organ
systems. Accidents play a signi®cant role in
the death of many of inhalant abusers.31 The
impaired judgment and ataxia that
accompany intoxication can make the user
susceptible to a variety of accidental
injuries. The glue sniffers are at a particu-
larly high risk of accidental death because
of the increased risk of losing consciousness
and subsequent adherence of the glue ®lled
bag to their face and mouth. Asphyxia
or aspiration, often interpreted as a suicide
attempt, may ensue.
Neuropsychiatric Effects. Inhalant abuse
can also precipitate a broad variety of
neurological sequela, most of which will
be discussed along with the associated com-
pound. However, the group as a whole
demonstrates similar changes in
neuroimaging studies. MRI demonstrates
that chronic abuse leads to generalized cer-
ebral and cerebellar atrophy, particularly
along the corpus callosum and the
hippocampus.32 In addition, other studies
have noted hypointensity of the thalamus,
which is presumed to be secondary to iron
deposition.31 These ®ndings do appear to
be clinically signi®cant in that the severity
of the damage correlates with both
duration of abuse and degree of neurologi-
cal impairment.32,33 Most neurological
sequela do not tend to develop until the
person is using two to three times a week
for at least six months.14 Solvent
inhalation, however, may lead to clinically
relevant white matter degeneration, and
any degree of abuse in a patient should
prompt a physician to be diligent about
assessing for any subtle neurological
de®cits.
The neuropsychiatric consequences are
83
Clinical Review of Inhalants

T A BLE 2. Sequelae of Volatile Solvent Use

Organ System Sequelae

Neurological Diplopia
Headache
Ataxia
Slurred speech
Depressed re¯exes
Nystagmus
Tremor
Cerebellar degeneration (toluene)
Sensorineuronal hearing loss (toluene)
Optic neuropathy (toluene)
EEG slowing (n-hexane)
Peripheral neuropathy (n-hexane)
Trigeminal neuralgia (trichloroethylene)
Parkinsonism (inorganic manganese)
Sensorimotor polyneuropathy (methyl butyl ketone)
Neuropsychiatric Subcortical-like dementia
Decreased IQ
Memory loss
Poor attention
Insomnia
Depression
Apathy
Psychosis (lead)
Renal Renal tubular acidosis (toluene)
Goodpasture’s syndrome (toluene; n-hexane)
Electrolyte imbalance
Cardiovascular Arrhythmia
Sinus bradycardia
Decreased myocardial contractility
Hypoxia-induced heart block
Myocardidtis
Pulmonary Cough
Dyspnea
Wheezing
Chemical pneumonitis
Emphysema (toluene)
Digestive Nausea
Vomiting
Hepatotoxicity
Induce CYT P-450 (toluene)
Anorexia (lead)
Dermatological Perioral eczema
Contact dermatitis
Burns
Hematological Bone marrow suppression
Leukemia (benzene)
Aplastic anemia (benzene)

84 VOLUM E 10 N UM B ER 1 WINTER 2001


particularly striking. Several studies of
chronic inhalant abusers have found de®cits
in memory, attention, auditory dis-
crimination, and visual-motor function.34,35
However, a methodological limitation of
these and similar studies is that most do
not adequately demonstrate that these de®-
cits did not precede inhalant use.36 As pre-
viously discussed, inhalant abusers often
come from deprived backgrounds and have
poor school performance that may result
from premorbid neuropsychiatric de®cits.
Yamanouchi et al37 attempted to correct
for this bias by selecting volatile solvent
abusers and comparing those with and
without characteristic white matter changes.
They found that de®cits in the patient’s
verbal IQ correlated with the severity of
pontine atrophy and ventricular hyper-
trophy. Consistent with this ®nding,
chronic volatile solvent abusers, particularly
those using materials rich in toluene, may
develop a subcorticol dementia character-
ized by attention dysfunction, psychomotor
dysfunction, insomnia, depression,
irritability, and tremor.31 Those who abuse
both alcohol and solvents are particularly
susceptible to this dementia.38 Most of
the acute neurological and neuropsychiatric
sequela of volatile solvent abuse is
reversible unless there was signi®cant cer-
ebral hypoxia or metabolic acidosis. After
chronic use, however, resolution of these
symptoms is slower and less complete.7
Thus, solvent abusersö a group often
already cognitively compromisedö may
suffer further signi®cant damage from con-
tinued abuse.
Congenital Effects. Nearly all volatile
solvents cross the placenta; thus, abuse in
the mother may affect the developing fetus.
In a study of pregnant workers exposed to
these compounds, no growth or behavioral
abnormalities were noted in their
offspring.39 However, as previously noted,
solvent abusers inhale several hundred
times those encountered in industry.
THE AM ERICAN JOURN AL ON ADDICTIONS
Brouette & Anton
Studies of children born to solvent abusers,
particularly to those who abuse solvents
containing toluene, have found a syndrome
that resembles fetal alcohol syndrome.40
The children have small midfaces, short
palpebral ®ssure, deep set eyes, low set ears,
micrognathia, mild limb abnormalities,
intrauterine growth retardation, and devel-
opmental delays. In addition, other studies
have noted offspring of solvent abusers
may show signs of withdrawal if the
mother had used within a few days of
delivery.41 Thus, maternal solvent abuse
can have a devastating effect on the fetus.
Toluene. Toluene is one of the most com-
mon constituents of abused inhalants, par-
ticularly glues, and is implicated in
several of the medical complications noted
in users. The most signi®cant of these
derangements is renal toxicity with associ-
ated distal renal tubular acidosis and result-
ing hypophosphatemia and hypokalemia.
Toluene might also promote numerous
other renal dyscrasias, such as Fanconi’s
syndrome and glomerulonephritis (see
Table 2). Toluene can also cause a
reversible hepatorenal failure and induce
the liver’s P450 system.42,43 In chronic
abusers, this compound also causes
thinning and ruptures of the alveolar wall
with resulting emphysema.44 Neurol-
ogically, toluene has been linked to white
matter changes in the cerebellar peduncles
and regions adjacent to the dentate
nucleus.32 Ataxia is one of the conse-
quences of these changes. Other more rare
but worrisome effects of toluene use are
sensorimotor deafness and optic neuro-
pathy. Chronic abuse of toluene, thus,
may impart severe medical consequences.
N-hexane. N-hexane, a common constitu-
ent of glue, primarily damages the nervous
system. This hydrocarbon causes a periph-
eral neuropathy, likely via its neurotoxic
metabolite 2,5-hexanedione.45 This poly-
neuropathy causes markedly decreased
85
Clinical Review of Inhalants
nerve conduction on EMG, is usually
sensorimotor, symmetrical, and pro-
gressive, and may be associated with cranial
nerves. Centrally, n-hexane has been associ-
ated with generalized focal slow wave
changes on an EEG that may re¯ect
decreased cerebral function.46 Hence,
n-hexane appears to affect both the central
and peripheral nervous system.
Trichloroethylene. This widely used indus-
trial solvent contributes to a slowly
reversible trigeminal neuralgia. This
syndrome is unlikely caused by the
chemical, but instead by its breakdown
product dichloroacetylene. 7
Methylene Chloride. This constituent of
aerosol propellants and industrial products
is metabolized to carbon monoxide. Thus,
hypoxia and elevated carboxyhemoglobin
are a concern. If a patient is suspected of
being exposed to this chemical, obtain a
carboxyhemoglobin level and give them
100% oxygen by a rebreather mask.
Methyl Butyl Ketone. This compound is
associated with an initially painless
sensorimotor polyneuropathy that primar-
ily affects the small ®bers (light touch,
pinprick, and temperature) in the distal
limbs after several months of continued
exposure.
Gasoline. As previously mentioned, gaso-
line remains one of the more frequently
abused substances by inhalant users. In
contrast to the previous sub-categories,
gasoline is a mixture of many different con-
stituents. Its composition can vary widely
based on octane level, brand, and in what
country the gasoline is obtained. In the
United States, leaded gasoline is scarce,
but it continues to be available in many
other parts of the world. Although individ-
uals with inorganic lead poisoning present
with anorexia, mood disturbances, and epi-
sodic vomiting, organic lead poisoning
86 VOLUM E 10 N UM B ER 1
more typically presents with psychosis.
Even if the person has been abusing
unleaded gasoline, they may be exposed
to lead from tanks or containers. Chelation
therapy can be very bene®cial to those
who have been exposed to lead, and so lead
levels should be obtained on anyone who is
suspected of inhaling gasoline.
An additional concern is the additives
in gasoline. Benzene, which had been
removed from many previously abused
industrial products, was added to gasoline
after lead was removed. Benzene can cause
aplastic anemia and leukemia. Manganese-
containing constituents can also be
problematic in that organic manganese
can be toxic to the pulmonary system.
Chronic inorganic manganese exposure
has been associated with Parkinsonism.47
Lastly, gasoline can cause signi®cant chemi-
cal burns. Thus, the abuse of this substance
requires particular care to ensure the user
receives a thorough medical evaluation.
N ITROU S OXIDE
Nitrous oxide, also known as ``laughing
gas,’’ has multiple medical and industrial
uses. Aside from being an anesthetic, sev-
eral studies have demonstrated its utility
in the treatment of withdrawal from
alcohol, cannabis, nicotine, and opiates.48,49
The gas is also available to non-medical per-
sonal due to its use as a propellant in
whipped cream.
Although many persons experience
nitrous oxide intoxication as uneventful
or unpleasant, others ®nd the experience
euphorogenic. The high is often described
as a dissociative experience with accom-
panying body tingling, numbness,
dizziness, auditory hallucinations, stiffness,
and warmth. Polysubstance abusers
indicate intoxication closely resembles that
of the psychedelics.50 Because of this drug’s
rapid elimination, this euphoria ceases
within minutes of ending use. Aside from
one case report, no withdrawal syndrome
WINTER 2001

has been identi®ed with nitrous oxide use.49
M echanism of Action
Nitrous oxide exerts its effects primarily
via the opiate system. The compound
mediates the release of beta-endorphins,
and directly binds to mu, delta, and kappa
opiate receptors. In addition, it is also an
NMDA antagonist. These multiple binding
properties likely explain its use as an
anesthesia, its utility in easing withdrawal
of several different drug classes, and its
psychogenic properties. Furthermore,
nitrous oxide appears to affect different
brain regions preferentially. Inhalation
has been demonstrated to activate the
anterior cingulate cortex and deactivate
regions of the posterior cingulate,
hippocampus, parahippocampus, and visual
association cortices in both hemispheres.51
This potentially explains the cognitive alter-
ations noted, as well as the memory de®cits
that will be discussed later.
M edical Sequela
Acutely, the inhalation of nitrous oxide
may cause transient hypoxia, nausea, or
claustrophobia. As use intensi®es, users
may have both medical and neuro-
psychiatric sequela (see Table 3), the most
prominent being a peripheral neuropathy
or short-term memory loss. The peripheral
neuropathy resembles pernicious anemia
and is characterized by loss of vibration
and position senses, ataxia, and broad-based
gait, which may progress to upper motor
signs (see Pema et al52 for more detailed
discussion). Nitrous oxide oxidizes vitamin
B12, and the addition of dietary sources of
methionine may be helpful in reversing
these effects. Cognitively, the most
prominent ®nding is a de®cit in short-term
memory. Glutamate binding to the NMDA
receptor is necessary for long-term
potentiation and memory consolidation.53
Because nitrous oxide blocks the NMDA
THE AM ERICAN JOURN AL ON ADDICTIONS
Brouette & Anton
receptor, this could lead to memory de®cits.
Gyulai et al51 proposed another
neurobiological explanation for this effect.
They proposed that activation of the
anterior cingulate and deactivation of the
posterior cingulate, visual association
cortices, hippocampus, and parahippocamal
regions may explain the learning and mem-
ory de®cits noted in nitrous oxide abusers.
Regardless, all of these medical and
neuropsychiatric effects subside when the
patient stops abusing nitrous oxide.
N ITRITES
This category includes amyl, butyl, and
isobutyl nitrite, which are readily available
in room odorizers and for sale in sex
and head shops. Nitrites are unique in
the unusual impact history has had on their
use. Nitrite abuse was common in the
1970s, particularly in the homosexual
community, until the dawn of AIDS.
Because nitrite inhalation was so common
among the earliest AIDS patient, these
agents were presumed to be the etiology
of this disorder before HIV was discovered.
Consequently, nitrite use quickly dimin-
ished and never resumed its early
popularity.
M echanism of Action
Nitrites are used both to induce
euphoria and enhance the sexual experience.
Upon inhalation, the desired effects are
achieved within 10 seconds, but rapidly
diminish within 5 minutes. For this reason,
some users may inhale 20 or more times
over several hours.54 Nitrites initially pro-
mote a ¯oating sensation and increased skin
perception, which is followed by reduced
social and sexual inhibitions, heightened
sexual arousal, relaxation of the anal
sphincter, and prolonged orgasm.5 The pre-
sumed mechanism of these effects is
vasodilation and relaxation of smooth
muscles. Vasodilation of cerebral arteries
87
Clinical Review of Inhalants

T A BLE 3. Sequelae of Nitrous Oxide Abuse

Sequelae Presentation

Neuropsychiatric Recent memory loss

Visual hallucinations
Depression
Psychosis
Dysphasia
Claustrophobia
Neurological Peripheral neuropathy (likely secondary to vitamin B12 de®ciency)
Reduced knee and ankle re¯ex
Impaired vibration sense
Hyperactive re¯exes
Babinski’s sign
Myeloneuropathy
Hematological Bone marrow suppression

likely produces the mental component of
nitrite intoxication, and neuroimaging
studies have shown that there are no
regional differences in cerebral blood
¯ow.55
M edical Sequela
Acute. After inhalation, many users
report a mild headache, dizziness,
palpitations and, feeling faint. Some may
even complain of a more persistent pulsatile
headache, nausea, vomiting, weakness,
syncope, restlessness, a cold chill, or invol-
untary emptying of their bowel and
bladder. These effects, though unpleasant,
are not as concerning as some as the other
effects of nitrite use. The user can have
a sharp drop in both their systolic and
diastolic blood pressure, with resulting
tachycardia.56 These rapid ¯uctuations
can lead to transient effects that are mani-
fest by inverted T waves and depressed
ST segments on an ECG.5 These com-
pounds can also be quite caustic. Patients
may complain of sinusitis, naso-tracheal
irritation, and dermatitis. The dermatitis
can be a nonspeci®c hypersensitivity reac-
tion, or be characterized by a yellow
crustation, which is possibly the result of
nitric acid promoting an xanthroprotein
reaction.57 Thus, these agents can affect
several systems.
Chronic. Despite the importance of the
above problems, the most profound effect
of nitrite use is on the hematological and
immune system. Inhaling amyl nitrite leads
to increased methemoglobin and a resulting
hemolytic anemia. 58 Nitrites also affect
lymphocyte number and function. Inha-
lation can suppress natural killer cell
activity, reduce monocyte adherence, and
can severely compromise T-dependent anti-
body induction, cytotoxic T cell induc-
tion, and the tumoricidal activity of
macrophage.59,60 This latter effect is note-
worthy because nitrite use can produce car-
cinogenic nitrosamines. Perhaps these
effects play a role in the association
between nitrite use and AIDS. As discussed
above, nitrites were one of the early
suspects for the etiology of AIDS because
of the high prevalence of nitrite users
who presented with Kaposi’s sarcoma.
Aside from accelerating the decline in T cell
function, nitrite-induced vasodilation may
increase the availability of the HIV and a
herpes virus that promote the develop-
ment of Kaposi’s sarcoma.61 The combi-
nation of the HIV infection and nitrite
use is thus a lethal combination since it

88 VOLUM E 10 N UM B ER 1 WINTER 2001


hastens the decline of the immune system
and possibly predisposes users to cancer.
The nitrites, though much less com-
monly abused than in the past, remain a
concern. With their easy accessibility and
potentially lethal effects (see Table 4), they
are a category of inhalants that clinicians
should continue to be aware of and include
in their evaluations of inhalant abuse.
TREATM EN T
As discussed in the introduction, little
research has been done on speci®c
modalities for the treatment of inhalant
abuse. When treating a patient with an
inhalant use disorder, clinicians must rely
on principles used in the treatment of other
substances use disorders and apply strat-
egies that have been effective for some com-
munities in curbing inhalant use.
Like any other substance use disorder,
the ®rst step in treatment is performing
a detailed history (including which products
are used, how often, and via what medium
the substances are inhaled) and physical
examination. In chronic inhalant abusers,
pay particular attention to the neurological
examination and the laboratory work-up.
Because of the heterogeneity of inhaled
compounds, the patient should be screened
for damage to the liver, kidney, and heart.
Initial labs should include electrolytes,
BUN, creatine, liver functions, and an
ECG. Further work-up can then be
performed as needed.
Patients who had been abusing volatile
solvents may be at risk for withdrawal.
Although inhalant abusers rarely experience
signi®cant withdrawal symptoms22 (and
some authors even suggest there is no role
for medication in inhalant abuse
treatment),6 we recommend that the patient
be closely monitored as if they were being
treated for alcohol withdrawal. If symptoms
develop, the limited literature suggests
benzodiazepines should be the ®rst line
of drug used to treat these symptoms;
THE AM ERICAN JOURN AL ON ADDICTIONS
Brouette & Anton
however, a great deal more studies need
to be performed before this could be stated
as the de®nitive treatment.
The absence of studies about the exclu-
sive treatment of inhalant abuse lends itself
to applying principles that have worked
in other areas of addiction. Patients rarely
present primarily for the treatment of
inhalant use 62 and other substance abuse
and psychiatric co-morbidity are high
within this patient group; therefore, the
treatment of co-morbid illness should be
a priority. In cases in which the patient
is a child, adolescent, or is retarded, a family
assessment should be performed with par-
ticular concern for parental substance use
and mental disorders.63 This evaluation
can offer an inroad to addressing dif®culties
within the family, help identify stressors
within the patient’s life, and begin the pro-
cess of teaching alternative methods to
dealing with these stressors. Increasing per-
sonal and ethnic self-identity has also been
helpful for inhalant abusers.64- 66 In adults,
methods such as cognitive-behavioral
therapy, twelve-step facilitation, or moti-
vational enhancement may be of bene®t.
Consider, however, that many inhalant
users have neurocognitive de®cits. In these
cases, formal neuropsychiatric testing
may be needed to better characterize the
de®cits and alter the treatment plan
accordingly.
Outside the clinical setting, communi-
ties that have dealt with epidemic inhalant
use have found several interventions
helpful. Some Native American tribes,
when faced with increasing inhalant use
by their young, formed ``parent patrols.’’6,7
These parents were able to prevent inhalant
use by ®nding out the places where
inhalants were being abused and then
monitoring that place frequently. Reducing
the inhalant user’s free time via recreation or
other structured programs may also be of
bene®t.63 Hence, often the issue of
inhalant abuse is better dealt with as a public
health issue than as a disorder of a single
89
Clinical Review of Inhalants

T A BLE 4. Sequelae of Nitrite Abuse

Sequelae Presentation

Nervous system Headache (mild or pulsating)

Dizziness
Ataxia
Syncope
Sedation
Weakness
Loss of bowel or bladder control
Gastrointestinal system Nausea
Vomiting
Hepatotoxicity (in rats)
Cardiovascular system Acute hypotension (both systolic and diastolic)
Rebound tachycardia
Coronary vasodilation
Hematological Methemoglobinemia
Heinz-body positive anemia
Reduced lymphocyte production
Reduced cell-mediated cytotoxicity
Reduced monocyte adherence
Mucocutaneous Naso-tracheal irritation
``Huåer’s rash’’
Contact dermatitis
Immune system Decreased immunity
Inhibits production of a and b interferon
Potentiates progression of AIDS
Ocular Increased intraocular pressure
Cancers Produces nitrosamine (a carcinogen)
Increased susceptibility to Kaposi’s sarcoma in HIV positive patients

patient or family. common among future users and how that

Unique to these groups of inhalants,
nitrites are often used more for enhancing
the sexual experience than for achieving
intoxication. Hence, within this subgroup
of inhalant users, patient education and
teaching alternative ways of enhancing
the sexual experience may be bene®cial in
curbing use. Certainly the rapid decline
in nitrite use following their association
with AIDS demonstrates the potential
effectiveness of this approach.
Although studies have demonstrated
inhalant use as a reliable predictor of later
substance use, little research has focused
on the prevention or treatment of inhalant
abuse. Areas that seem particularly rich
for study are understanding what
pre-morbid neurocognitive de®cits are
information can be used to prevent and
treat future substance use. Another
intriguing area of study is the apparently
similar neurobiological mechanisms of vol-
atile solvents and ethanol. Perhaps this
similarity will translate into comparable
responses to treatment modalities for
alcohol dependence. Certainly a great deal
more needs to be learned about the
neurobiology of the inhalants before treat-
ment strategies, particularly pharma-
cological, unique to inhalants will be
developed.
SUM M ARY
Despite the prevalence and recent escalation
in the abuse of solvents, solvent abuse

90 VOLUM E 10 N UM B ER 1 WINTER 2001


remains one of the least discussed and
studied areas of substance abuse. A poten-
tial reason for this void is the absence of
an agreed upon de®nition of inhalants.
Despite the lack of attention given to
inhalants, they are the second most abused
illicit substances among 12- to 17-year-olds,
and their use appears to be increasing. By
eighth grade, approximately 19.9% of
American children have tried inhalants at
least once. In addition, 240 deaths in the
United States were attributed to inhalant
use between 1996 and 1999.
The prevalence of inhalant use appears
to be in¯uenced by community and cultural
factors, with recent immigrants from Latin
America and Native Americans particularly
vulnerable; however, this observation
might be explained by poverty, social
dysfunction, and lack of opportunity within
these groups. The ``typical’’ inhalant user is
from a chaotic family, has compromised
cognitive skills, and has friends whom also
abuse inhalants.
The largest and most diverse group of
inhalants are the volatile solvents found in
both household and industrial products.
This group causes an intoxication similar
to ethanol, and may cause this effect via
a similar mechanism. Volatile solvent
abuse acutely causes sneezing, coughing,
confusion, and respiratory mucosa
irritation. Chronic solvent use is associated
with a variety of medical sequela, including
damage to the brain, kidney, liver, and
heart. Chronic volatile solvent abuse
may also contribute to substantial
neurocognitive changes. In addition, since
all the volatile solvents cross the placenta,
the abuse of volatile solvents can lead
to congenital defects and possibly a fetal
alcohol-like syndrome.
The next group of inhalants, nitrous
oxide or ``laughing gas,’’ is used as both
THE AM ERICAN JOURN AL ON ADDICTIONS
Brouette & Anton
an anesthetic and as a propellant for
whipped cream, and is readily available
in industry. Nitrous oxide intoxication
produces a dissociative-like experience that
has been compared to hallucinogen intoxi-
cation. Nitrous oxide potentially works via
binding opiate receptors and acting as a
NMDA antagonist. Acutely, nitrous oxide
use can lead to transient hypoxia, nausea,
and claustrophobia. After prolonged
abuse, users may develop a peripheral
neuropathy and short-term memory loss.
The last group, nitrites, are abused pri-
marily for their effect on enhancing the
sexual experience, are available in room
deodorizers, and are for sale in sex and
head shops. Amyl, butyl, and isobutyl
nitrite are all thought to induce their
intoxicating effects via vasodilation and
relaxation of smooth muscle. After acute
inhalation, the user may complain of
headache, dizziness, palpitations, and feel-
ing faint. Chronic use can have such a pro-
found effect on the hematological and
immune systems that it was initially
hypothesized to be the etiology of AIDS.
The abuse of nitrites continues to be a con-
cern in patients at risk for AIDS since
nitrite use may hasten the immune system’s
decline and predispose users to Kaposi’s
sarcoma.
The treatment of inhalant abuse has
not been thoroughly studied; however,
the principle of ®rst obtaining a detailed
history and physical examination certainly
applies. After the patient’s medical needs
have been addressed, models of substance
treatment that have been effective for other
substances should be applied in the treat-
ment of the inhalant abuser. However, a
great deal more research needs to be done
before any conclusions can be drawn about
the ef®cacy of any of these models for the
treatment of inhalant abusers.
91
Clinical Review of Inhalants
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