Inhalant abuse

First Nations and Inuit Health Committee, Canadian Paediatric Society (CPS)

Paediatr Child Health 1998;3(2):123-6
Reference No. II97-01

Revision in progress February 2009

Parent handout: About inhalants 

Index of position statements from the First Nations, Inuit and Métis Health Committee

Contents

• Epidemiology
• Types of chemicals and products abused
• Causes of inhalant abuse
• Mechanism of abuse and immediate effects of inhalants
• Morbidity and mortality
• Detection of inhalant abuse
• Prevention of inhalant abuse
• Conclusion and recommendations
• References

Inhalant abuse is the intentional inhalation of a volatile substance for the purpose of achieving a euphoric state. It is also known as solvent abuse, volatile substance abuse, glue sniffing, sniffing and huffing. Beginning with children as young as six years of age, it is an under-recognized form of substance abuse with a significant morbidity and mortality. This statement reviews important aspects of inhalant abuse and makes several recommendations involving prevention and education strategies to address this problem.

Epidemiology

As with other types of substance abuse, precise epidemiological data on inhalant abuse are not available. Peak age of inhalant abuse is 14 to 15 years, with onset occurring in those as young as six to eight years of age. Use typically declines by age 17 to 19 years; however, some users may continue into adulthood.

Although there is significant Canadian contribution to the inhalant abuse literature (1-18), systematic national prevalence and mortality data are unavailable. Since 1975 in the United States, the National Institute on Drug Abuse annual survey of high school seniors (Monitoring the Future Study) has documented a lifetime incidence of inhalant abuse of 15% to 20%, with 5% to 10% of seniors using inhalants during the previous year (19). This survey underestimates the true prevalence because school dropouts, who have a relatively higher incidence of substance abuse, are not included. The United Kingdom is the only major country in the Western world that tracks inhalant abuse fatalities, where an incidence of two deaths per week has been documented (20).

Patterns of inhalant use are similar to patterns of abuse of other types of substances. There are experimenters, intermittent users and chronic inhalant abusers. Experimentation is ubiquitous, occurring in urban, suburban, rural and remote communities of Canada. However, chronic use tends to be endemic in inner city areas and remote communities (4), coincident with unemployment, poverty, substance abuse and dysfunctional families. It is noteworthy that inhalant abuse is epidemic in some remote communities and virtually absent in others. Although morbidity and mortality are associated with frequency of use, the ‘sudden sniffing death syndrome’ (21), which is the most common cause of death in inhalant abuse, can occur in first-time users.

Types of chemicals and products abused

Products selected by inhalant abusers are volatile, capable of rapidly producing a pleasurable sensory experience, available, convenient and inexpensive. The latter three qualities are important because children have less sophisticated resources for acquiring substances of abuse.

Virtually any hydrocarbon can have mind-altering effects when inhaled in large doses. The most commonly abused inhalants are aliphatic, aromatic or halogenated hydrocarbons. Chemicals from these groups are found in thousands of commonly used and readily available consumer products (Table 1). Furthermore, almost all pressurized aerosol products can be abused because their propellants are volatile hydrocarbons.

TABLE 1: Commonly abused products

Causes of inhalant abuse

Important factors that contribute to the initial experimentation and continued use of inhalants include peer pressure and dysfunctional families. Peer pressure is a powerful force contributing to initial experimentation. Children of dysfunctional families who accept violence and substance abuse as a part of their lives are more likely to engage in drug experimentation that escalates to chronic abuse. Although inhalant abuse is more prevalent among the poor, it crosses all socioeconomic boundaries. While seen in all ethnic groups in Canada, it is especially prevalent among native Canadian children and adolescents (7), perhaps because of an increased likelihood of membership in drug-using peer clusters and a perception of a lack of opportunities.

Mechanism of abuse and immediate effects of inhalants

The fumes of the product may be directly inhaled from a container, plastic bag or saturated rag. Inhalation is usually through the mouth, with several deep inspirations required to produce euphoria.

Inhalants are depressants and are pharmacologically related to anaesthetic gases. In fact, some anaesthetic gases, such as ether and nitrous oxide, are also abused. The immediate effects of inhalant abuse are similar to the early classic stages of anesthesia. The user is initially stimulated and disinhibited and prone to impulsive behaviour. Speech becomes slurred and gait becomes staggered. Euphoria, frequently with hallucinations, is followed by drowsiness and sleep, particularly after repeated cycles of inhalations. Coma is unusual because as the user becomes drowsy, exposure to the inhalant is terminated before large enough doses are absorbed.

Morbidity and mortality

Significant morbidity and mortality are associated with inhalant abuse. Morbidity is psychosocial as well as organic. Ongoing inhalant abuse is associated with failure in school, delinquency and an inability to achieve societal adjustment (22,23). There is evidence that withdrawal symptoms can occur (24) and that inhalant abuse can lead to the abuse of other substances (25-27).

The chief organic morbidity, a consequence of chronic abuse, is central nervous system damage resulting in dementia and cerebellar dysfunction (9,28,29). Typically, there is a loss of cognitive and other higher functions, gait disturbance and loss of coordination. Computed tomography demonstrates a loss of brain mass (9) and magnetic resonance imaging shows white matter degeneration (28,29). Inhalants are commonly used both in industry and by consumers as fat solvents. Thus, because the brain is a lipid-rich organ, chronic solvent abuse dissolves brain cells.

Chronic use of any inhalant risks brain injury. Other organic effects are related to specific chemicals found in some but not all products. The strength of the association ranges from definite through likely to speculative. Definite associations include peripheral neuropathy (hexane) (30), deafness (toluene) (31,32) and metabolic acidosis (toluene) (33,34). Likely morbidities include embryopathy (toluene) (35,36), neonatal withdrawal (multiple agents) (18) and lung damage (paint pigments) (37). Speculative morbidities include cardiomyopathy (38), toxic hepatitis (chlorinated hydrocarbons) (38,40), decreased visual acuity (toluene) (32,41), aplastic anemia (benzene) (42,43), and leukemia (benzene) (42). Because the latter complications are hypothetical, routine laboratory testing for their presence is not indicated.

Death due to inhalant abuse can occur by several mechanisms including asphyxia, suffocation, dangerous behaviour, aspiration and sudden sniffing death syndrome. Asphyxia is probably of only theoretic concern because it requires the partial pressure of the inhalant to be so high that oxygen is displaced. In British experience, suffocation, dangerous behaviour and aspiration each account for approximately 15% of fatalities caused by inhalant abuse, whereas sudden sniffing death syndrome is responsible for the remaining 55% (44). Suffocation occurs when the mode of use involves inhalation through the nose and mouth from a plastic bag, which may occlude the airway if the user loses consciousness. Disinhibition while under the influence of inhalants may cause dangerous behaviour and result in risks such as drowning, jumps or falls from heights, hypothermia, and, particularly, fire-associated deaths because of the flammability of most inhalants. The risk for death caused by aspiration is similar to that for alcohol or other depressants and is related to the combination of decreased level of consciousness and loss of protective airway reflexes.

Sudden sniffing death syndrome was originally described by Bass (21). Death occurs suddenly after the user is startled during inhalation (usually as a consequence of being discovered by an authority figure or from a particularly stimulating hallucination). The pathophysiology of sudden sniffing death has been elucidated (21). The hydrocarbons of inhalants sensitize the myocardium to adrenaline, and the sudden surge of this hormone produced by the startle reflex results in a fatal cardiac arrhythmia. No cause of death is found at autopsy. Sudden sniffing death can result during the initial experimentation or from any episode of inhalant abuse. In one study of death from inhalant abuse, there was no history of previous inhalant abuse in 22% of the victims (44).

Detection of inhalant abuse

Chronic heavy inhalant abusers may be identifiable because of poor hygiene and grooming, frequent obvious episodes of intoxication, weight loss from decreased caloric intake and, most importantly, the conspicuous odour of the inhalant (45). This odour is often present because a significant proportion of the absorbed dose exits the body by the same route that it enters (via the lungs) so the odour can persist on the breath for many hours (45). The product may also be spilled onto clothing during use, resulting in another source of the odour. Additional clues include stained clothing, flecks of paint or glitter on the face and perioral pyodermas (45) related to inhalants drying the skin and resulting in small cracks which serve as portals of entry for bacteria. Finding products of abuse stored in unusual locations, such as a can of gasoline under the child’s bed or a large cache of a potential inhalant, often suggests inhalant abuse. Finally, deviation from normal behaviour can be an indicator of potential dysfunction in the adolescent and can be a sign of inhalant abuse. Urine drug screens do not detect these chemicals; laboratory testing for organ dysfunction should only be considered in chronic abusers.

Prevention of inhalant abuse

As with other types of substance abuse, the most effective way to curtail use is through prevention. While chronic users must not be ignored, their treatment is very difficult, expensive and not highly effective.

There are many potential preventive strategies; however, most of these are impractical and are known to have failed. Limiting the availability of inhalants is impractical because they comprise a large group of products that are universally available and licit, and have legitimate uses. Restricting the availability of some of these products merely results in a shift to the use of other products or creates a black market for the restricted products (46). Adding a noxious chemical to the product to prevent misuse is also ineffective (46,47) because there are multiple products that would require such adulterants and the result is often unacceptable to the legitimate consumer. Reformulating the product by replacing the hydrocarbon with other chemicals is not practical because this usually results in a less effective product. Warning labels on packages may be counterproductive because they allow children to identify sniffable substances easily (46,48). Criminalization of the user is not a meaningful deterrent for the prevention of inhalant abuse either for the experienced user or for the initial experimenter. One only has to consider the experience with tobacco and alcohol. Criminalization of the vendor is ineffective again because of the issue of dealing with multiple products with legitimate uses. In the United States where annual inhalant abuse prevalence data are collected, these supply side and demand side laws have had no significant impact. However, criminalization of the vendor is a popular approach because it is perceived as an effective strategy, and it makes the point that society condemns inhalant abuse.

Education is considered as the most effective preventive strategy (46), particularly if it is initiated before the usual age of experimentation. A progressive school-based inhalant abuse curriculum beginning in kindergarten with developmentally appropriate modules throughout elementary school is seen as the most efficient strategy and should be implemented particularly in areas where inhalant abuse is prevalent. The provision of alternate activities such as recreational facilities and the promotion of traditional cultural values encourage positive lifestyles thereby diminishing the risk for inhalant abuse and other destructive behaviours. Prevention workers are especially effective if they are from the local community. However, they must be appropriately trained and have access to ongoing support.

The treatment of inhalant users is difficult because of the many pharmacological, clinical, cultural and demographic factors that make this type of substance abuse unique. Such treatment requires specific rather than generic substance abuse treatment approaches and may be most effective when conducted by reformed inhalant abusers.

Conclusion and recommendations

The Canadian Paediatric Society is extremely concerned with the practice of inhalant abuse among children and adolescents and wishes to draw attention to this under-recognized and dangerous practice.

• Paediatricians are encouraged to increase their awareness of the unique clinical aspects and complications of inhalant abuse, particularly central nervous system damage and sudden sniffing death syndrome.
• Paediatricians need to promote education about the health hazards posed by substance abuse to children, adolescents, parents, teachers, media representatives and vendors of volatile substances.
• Inhalant abuse should be included in all substance abuse prevention curricula in the primary grades and emphasized especially in areas where inhalant abuse is endemic.
• Research efforts to identify and evaluate prevention and treatment approaches that are specific for this type of substance abuse should be increased.
• There is a need for focused prevention, intervention and treatment in communities where inhalant abuse is endemic.

References

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2. Musclow CE, Awen CF. Glue sniffing: report of a fatal case. Can Med Assoc J 1971;104:315-9.

3. Wyse DG. Deliberate inhalation of volatile hydrocarbons: a review. Can Med Assoc J 1973;108:71-4.

4. Boeckx RL, Postl B, Coodin FJ. Gasoline sniffing and tetraethyl lead poisoning in children. Pediatrics 1977:60:140-5.

5. Israelstam S, Lambert S, Oki G. Poppers, a recreational drug craze. Can Psychiatr Assoc J 1978;23:493-5.

6. Hunter AG, Thompson D, Evans JA. Is there a fetal gasoline syndrome? Teratology 1979;20:75-9.

7. Barnes GE. Solvent abuse: a review. Int J Addict 1979;14:11-26.

8. Hindmarsh KW, Hensman LR, Fulgerud DH. Solvent and aerosol abuse. Can Pharm J 1980;113:99-102.

9. Fornazzari L, Wilkinson DA, Kapur BM, Carlen PL. Cerebellar cortical and functional impairment in toluene abusers. Acta Neurol Scand 1983;67:319-29.

10. Hindmarsh KW, Hensman LR, Kolbinson CL, Mucha AM. Solvent abuse – attitudes and knowledge among Saskatchewan retailers.
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11. Tenenbein M, deGroot W, Rajani KR. Peripheral neuropathy following intentional inhalation of naphtha fumes. Can Med Assoc J 1984;131:1077-9.

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13. Smart RG, Goodstadt MS, Adlaf EM, et al. Trends in the prevalence of alcohol and other drug use among Ontario students: 1977-1983. Can J Public Health 1985;76:157-62.

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17. Gfellner BM, Hundleby JD. Patterns of drug use among native and white adolescents: 1990-1993. Can J Public Health 1995;86:95-7.

18. Tenenbein M, Casiro OG, Seshia MMK, Debooy VD. Neonatal withdrawal from maternal volatile substance abuse. Arch Dis Child 1996;74:F204-7.

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33. Taher SM, Anderson RJ, McCartney R, et al. Renal tubular acidosis associated with toluene “sniffing”. N Engl J Med 1974;290:765-8.

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41. Keane JR. Toluene optic neuropathy. Ann Neurol 1978;4:390.

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First Nations and Inuit Health Committee (1996-97)

Members: Drs Fred Baker (chair); Sioux Lookout Program, University of Toronto, Toronto, Ontario; Garth Andrew Bruce, Department of Paediatrics, Royal University Hospital, Saskatoon, Saskatchewan; Nicole Lise M Chatal, Stanton Yellowknife Hospital, Yellowknife Northwest Territories; Gerrit W De Groot, Winnipeg, Manitoba; Frank Friesen (director responsible), Manitoba Clinic, Winnipeg, Manitoba; Johanne Morel, Montreal, Quebec; Brian David Postl, Children’s Hospital, Winnipeg, Manitoba
Consultants: Drs John C Godel, Royal Alexandra Hospital, Edmonton, Alberta; Michael EK Moffatt, Department of Community Health Sciences, University of Manitoba, Winnipeg, Manitoba; Ms Margaret Moyston Cumming, Epidemiology and Community Health Specialties, Health Canada, Ottawa, Ontario; Drs Gary Sean Pekeles, Montreal Children’s Hospital, Montreal Quebec; Margaret Jane Stockwell, Medical Services Branch, Health Canada, Ottawa, Ontario.
Liaisons: Dr Lance Chilton, Albuquerque NM (American Academy of Pediatrics, Committee on Native American Child Health); Ms Marilyn Sark, Lennox Island, Prince Edward Island (Aboriginal Nurses Association of Canada); Ms Brenda Thomas, Ottawa, Ontario (Assembly of First Nations); Ms Margaret Horn, Kahnawake, Quebec (National Indian Inuit Community Health Representative); Ms Roda Grey, Ottawa, Ontario (Inuit Women’s Association); Vincent Tookenay, Ottawa, Ontario (Native Physician Association in Canada)

This statement was adapted with permission from the American Academy of Pediatrics (AAP), and modified by Dr Milton Tenenbein, Children’s Hospital, Winnipeg, Manitoba. Inhalant Abuse, a policy statement of the AAP, was written by the Committee on Substance Abuse and Committee on Native American Child Health, and first appeared in Pediatrics 1996;97:420-3.

Dr Tenenbein was the principal author of the AAP statement.