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Journal of the New Zealand Medical Association, 05-May-2006, Vol 119 No 1233

Inhalant abuse in New Zealand

Michael Beasley, Laura Frampton, John Fountain

Aim To describe patterns of inhalant abuse in New Zealand and discuss management.

Methods Calls to the National Poisons Centre (NPC) from January 1 2003 to December 31 2004 were analysed. In addition, deaths following inhalational abuse were identified from the Institute of Environmental Science and Research Limited (ESR) database for 2001 and 2002 and available data for 2003.

Results Seventy calls were classified as relating to inhalational abuse incidents. In abusers whose age was known, 83% were between 11 and 20 years, and 61% were male. Over half (44/70) of the calls involved abuse of propane or butane, either alone or in combination with a synthetic pyrethroid. ESR coronial data identified 11 inhalant abuse related deaths, most commonly attributed to cardiac effects. 73% of deaths were in teenagers and all but one fatality involved propane and/or butane.

Conclusions Inhalant abuse is a persisting problem in New Zealand. NPC and ESR data demonstrate that teenagers are more likely to abuse inhalants than other age groups and butane and propane are the inhalants of choice. Acute management can be difficult, with significant mortality and morbidity. Continued education and other preventive measures are essential to help curb an extremely dangerous practice.

Inhalation of volatile compounds (including adhesives, solvents, fuels, and propellant or flammable gases) is a recognised cause of sudden death among those abusing these substances for “recreational” purposes.1 Recent Coroners’ inquests into eight deaths related to these substances have been reported by the media, along with an estimate that “...hundreds if not thousands...” may abuse these substances daily.2

This study aims to better characterise the inhalant abuse problem in New Zealand, by both reviewing the Coronial Services Office findings to identify deaths, and evaluating records maintained by the New Zealand National Poisons Centre (NZNPC) of enquiries relating to these substances. A review of the toxic mechanisms, health impacts, and management of those affected by inhalant abuse is also undertaken.

Methods

Calls to the NZNPC over the 2-year period from January 1 2003 to December 31 2004 were analysed. The NZNPC is the sole Poison Control Centre for New Zealand and serves a mixed population of urban and rural areas, covering a population of approximately 4 million people. The data were retrieved from the NZNPC calls collection database. Inclusion criteria were all inhalation exposures where the reason was recorded as intentional abuse. For the purposes of this study, carbon monoxide and nitrous oxide calls were excluded. Data included were the age and sex of the user, date and time of exposure (if acute), its location, substance involved, details of the incident, our assessment, caller background, and regional area where it occurred.

Deaths following intentional inhalational abuse were also sought. Eleven fatalities (see Table 3) were identified from the Institute of Environmental Science and Research Limited (ESR) Chemical Injury Surveillance System database (CISS), which includes data from the national Coronial Services Office.3 While all Coronial findings for 2001 and 2002 are considered available, findings for 2003 are not, as a full accounting of deaths assessed by Coroners and retrieved by ESR will typically take up to 3 years.

Results

The NZNPC received 27,020 and 28,357 calls in 2003 and 2004 respectively as shown in Table 1. Of total calls, 4.6% (2003) and 4.4% (2004) were inhalational exposures. Intentional inhalational exposures (excluding nitrous oxide and carbon monoxide) accounted for 70 cases in total over the 2-year period.

Table 1. Total calls and inhalational exposure calls to the New Zealand National Poisons Centre (NZNPC)

Variable	2003	2004
Total calls received by NZNPC Inhalational exposures Intentional inhalational exposures Intentional inhalational exposures (excluding nitrous oxide and CO): - Male - Female	27,020 1249 77 38 24 14	28,357 1241 72 32 18 14

CO=carbon monoxide.

The age of users ranged from 7 to 45 years. The age distribution of inhalant abuse calls is shown in Figure 1. The patient was classified as “adult” when the age was not known other than that they were 11 years of age or over. Where age was known, 83% percent of abusers were between the ages of 11 and 20. Forty-three (61%) were male.

Figure 1. Age of inhalant abusers

The substance(s) the NZNPC received the most calls about was propane or butane, propellants found in common household products such as air-freshener, body sprays, and fuels in gas heaters (LPG) (as shown in Table 2). Over the 2-year period (2003 and 2004) we received a total of 30 calls in regards to their abuse. In addition, there were 14 calls regarding the abuse of synthetic pyrethoids with butane (fly spray) and 8 calls about the intentional inhalation of petrol. Calls regarding toluene, kerosene, and other hydrocarbons were less frequent.

Table 2. Substance involved in inhalant abuse calls

Inhalant	Household product	2003	2004
Propane/butane Synthetic pyrethroid + butane Gasoline Hydrocarbons (various) Toluene Kerosene Trichloroethylene Mineral turpentine Methylene chloride Not specified	Air-freshener, LPG, body sprays Fly sprays Petrol Paint Adhesives Lighter fluid, kerosene Correction fluid Spray paint	15 10 5 2 2 1 1 1 0 1	15 4 3 3 2 2 0 0 1 2

Deaths from inhalant abuse (as shown in Table 3), as determined by the Coroner, were most often due to cardiac dysrhythmia. In all but one case of death, propane, butane, either alone or in combination with a synthetic pyrethroid was the inhalant involved. In 73% (8/11) of cases, the deceased was a teenager. The majority involved males.

Table 3. Substance, age of abuser, cause, and year of death due to inhalant abuse

Inhalant	Age of deceased	Sex	Mode of death	Year
Butane and fly spray Fly spray Butane Toluene Butane and Propane Butane Liquefied Petroleum Gas Butane Butane Aerosol propellants Butane	24 18 16 36 14 19 18 15 28 16 18	M F F M M M M M	Cardiac dysrhythmia Cardiac dysrhythmia Cardiac dysrhythmia Not stated Cerebral anoxia Acute cardiac failure Asphyxia Not stated Pulmonary aspiration Not stated Not stated	2001 2001 2001 2001 2002 2002 2003 2003 2003 2003 2003

Discussion

Inhalant abuse is a persisting problem in New Zealand. Coronial data suggests it may account for at least 10% of all poisoning deaths (excluding carbon monoxide), with many of these deaths occurring in teenagers. Analysis of calls received by the NZNPC supports this finding, with a large majority of calls relating to 10 to 20 year olds. Inhalant abuse in teenagers is a common phenomenon worldwide as the household products commonly abused (including air freshener and fly spray) are inexpensive to obtain, simple to hide, and provide an easy way to get ‘high’.

Our data could not provide detailed information on morbidity and outcome as we do not routinely follow up incoming enquiries (due to various reasons, including the 1993 Privacy Act). However in one prospective series in the US, ~38% of enquiries related to cases with significant effects, including loss of consciousness, seizures, metabolic acidosis, and occasionally death.4 In another review, ~ 20% of cases had either moderate effects, usually requiring treatment, or were major effects or fatalities.5

Our data indicate that some abusers can be very young, as noted elsewhere.5 They may be initially drawn by curiosity and the desire to imitate. The practice appeals because of the feelings of euphoria with loss of inhibitions. There may also be a sense of heightened powers, illusions, and hallucinations, along with mood swings and impulsive actions. However oral frothing, nausea, vomiting, light headedness, dizziness, slurred speech, ataxia, and cough with upper airway irritation can also develop. Heavier exposures can produce progressive nervous system depression. Nevertheless many subjects even with depressed levels of consciousness can have resolution of acute symptoms within one to two hours of cessation. This generally rapid recovery often means that abuse is not recognised by parents.4

Coronial data was insufficiently comprehensive to elucidate whether the apparent higher case fatality rate for males (reported elsewhere)4 applies in New Zealand. Also unclear (internationally) is the fatality risk per abuse episode. While evidence is often circumstantial, most deaths are presumed to have a primary cardiac aetiology. A significant fraction occur in association with intense sympathetic stimulation as with running,6 other exertion, auto-erotic behaviour, or agitation or startling of the abuser.

Running may be intentional (as in avoiding apprehenders) or seem coincidental, but often appears to be caused by the inhalation, and may be due in part to vivid hallucinations, at least in cases exhibiting fearful reactions.7 The cardiac sensitising potency of inhaled hydrocarbons is greatly increased in the presence of high circulating catecholamine levels such as occurs with exercise or excitement6 (the ability of injected adrenaline to markedly increase arrhythmia risk during solvent inhalation is well demonstrated in animal studies).8

While hypoxia and hypercapnia can also enhance cardiac sensitisation,9 experimentally these do not seem such powerful influences.10 Any acidosis, hypokalaemia or hypocalcaemia can also predispose to arrhythmias.

Experimentally there is evidence that solvents can inhibit cardiac inward sodium currents,11 with risk of prolonged membrane depolarisation and slowed impulse propagation. (They “stabilise” myocardial cell membranes in ways that increase their resistance to normal trans-membrane ion currents.) Sinus bradycardia is typically the first rhythm abnormality seen in animal studies,12 followed most commonly by AV dissociation with progressively lower escape rhythms, and finally electrical asystole or ventricular fibrillation. Bradycardia and ultimately asystole may partly arise from a direct effect on the sinoatrial node.11,12 Myocardial infarction has occasionally occurred,13 the postulated mechanism being coronary artery spasm.9,14

While sudden sniffing death syndrome may occur on the 1st, 10th, or 100th time a person abuses inhalants, it appears to occur most often in naïve, first-time users. (One factor may be the difficulty in regulation or “titration” of a dose with many of the delivery methods. There is also likely substantial individual variation in susceptibility, though specific risk factors are not fully characterised.) Furthermore, the risk does not vanish immediately on cessation of inhalation, instead persisting for several hours. This is not surprising, given the high lipid solubility of solvents, which enables access into (and some persistence within) myocardial cell membranes.

Other causes of death include respiratory depression and anoxia from suffocation during the practice of inhaling substances from a plastic bag. Fatalities have also occurred due to aspiration of vomitus15 and mishaps (such as drowning or motor vehicle accidents)1 that can arise while functioning is still significantly impaired by the inhalant.

Butane and propane appear the most commonly abused inhalants which is not surprising, given they are found as propellants in a wide variety of household sprays. Both are recognised internationally as major causes of inhalant abuse fatalities.16 Indeed, one study suggested that (especially in the context of air fresheners) they may carry a disproportionately high fatality rate.5 However the data from the study, based on the toxic exposure surveillance system (TESS) database of the American Association of Poison Control Centers (AAPCC), only involved cases reported to individual PCCs, which likely represents a small proportion overall, with a potential for reporting bias.

While they are considered less narcotic and less potent cardiac sensitisers than some other propellants and solvents,17 their high volatility and rapid evaporation from compressed liquid forms can result in very high exposures during abuse, increasing the risks.8 Long term neurological sequelae may develop in surviving cases.13

Some methods of inhaling these compounds present additional hazards. Vagal inhibition may occur from a sudden freezing effect on the larynx and surrounding structures, due to the rapid expansion and cooling of gas produced from compressed liquid forms or even aerosols when sprayed directly into the mouth. For example, butane inhalation via cigarette lighter refills may involve releasing a jet of fluid cooled to ≤20°C. This can result in reflex inhibition of the heart, with bradycardia or in extreme cases, cardiac arrest.1 There is also a risk of profuse mucosal oedema, burns to the throat and airways,18 and laryngospasm with severe respiratory tract obstruction. Inhalation of burning (accidentally ignited) gas can cause adverse lung effects, including pulmonary oedema.

The increasing abuse of fly sprays is also concerning due to the presence of synthetic pyrethroids as the active constituent. Comparatively little is known about the effects of pyrethroids on the heart (as opposed to neurons). However, some experimental evidence suggests “type II” pyrethroids possess considerable mammalian cardiac arrhythmogenic potential.19 Pyrethroids can also produce marked adrenal stimulation, with increased circulating catecholamines.20 While severe allergic respiratory reactions are described with natural pyrethrum, and even its purified pyrethrin extracts,21 they appear less of a risk with synthetic pyrethroids. In one case of a fly-spray abuse related death discussed with the NZNPC, lack of sputum eosinophils argued against an allergic basis. However allergic asthma has been attributed to tetramethrin.22 While the role of pyrethroids as opposed to propane/butane in fly spray abuse-related deaths remains uncertain, they could be expected to increase the risk.

Acute management of abusers can be difficult, as there may be rapid onset of life-threatening effects, yet limited opportunity for early intervention, as abuse may take place in unobserved and/or remote situations. Most deaths occur outside hospital.23

All cases of acute abuse should be observed (even if without initially obvious clinical abnormalities), as a risk of sudden arrhythmia may remain for some hours after inhalation.24 It is important to calm conscious victims to reduce further release of endogenous catecholamines.7 Symptomatic cases should be medically observed until 8 to 12 hours post-exposure, while asymptomatic cases remaining so and without ECG abnormalities can probably be discharged safely after four hours.

Oxygen should be administered to all symptomatic patients. Severe respiratory depression requires assisted ventilation, and early airway protection has been recommended, particularly in unconscious patients, as vomiting is common.23 However, intubation in the presence of laryngospasm (or for agents known to cause it) must be cautious, as this may cause excessive vagal stimulation, exacerbating bradycardia, and is not advised in patients with impending cardiac arrest.9 Instead Ambu bag ventilation using an oropharyngeal airway has been successful in this situation.7,9 With improvement in cardiac rhythm, endotracheal intubation, assisted by neuromuscular paralysis if necessary, can be instituted. Bronchoscopy may be required to remove aspirated material. In the event of bronchospasm, use of inhaled beta 2 adrenergic receptor agonists must be cautious, to minimise any additional risk of arrhythmia.

Resuscitation from cardiac arrhythmias has not often been successful, partly due to their rapidity of onset. It is generally not advised to administer catecholamines, as they can increase the risk of arrhythmias including ventricular fibrillation.9 Standard electrical methods and early use of antiarrhythmic agents should be considered, particularly with recurrent ventricular arrhythmias.25 Agents used in association with occasional successful outcomes have included amiodarone, lignocaine, and mexiletine.9,14 Amiodarone has the advantage of causing little or no myocardial depression; initial doses of 300 mg IV have been used,25 the same as recommended for ventricular fibrillation in other contexts.

Hypotension is largely secondary to cardiac arrhythmia or impaired contractility. It may respond to fluid replacement or management of any underlying cardiac rhythm disturbance. Careful use of an agent with inotropic (and/or chronotropic) properties may be required. Noradrenaline25 and dopamine26 (with additional vasopressor effects) have sometimes been used with success, despite concerns regarding arrhythmia risks. While a non-catecholamine might be theoretically preferable, there appears no reported experience with other inotropes such as glucagon. Myocardial infarction can occasionally be a factor in severe hypotension or arrhythmia, including recurrence of ventricular fibrillation.25 In some cases it appears as a complication,26 but might also occur as a primary event. Treatment with catecholamines may require extra caution in this situation.

The effectiveness of atropine for persistent, haemodynamically significant bradycardia appears unclear. Glucagon might be useful, and would be theoretically preferable to catecholamines in terms of safety. It directly increases automaticity at the sinoatrial and atrioventricular nodes,27 and is known to have potent chronotropic as well as inotropic actions. However there is no guidance on doses. It can also stimulate release of endogenous catecholamines.28

Beta-adrenergic blockers have been recommended to protect the catecholamine sensitised heart,9 but should be used with care given their negative inotropic and chronotropic effects,25 with risk of hypotension,26 particularly in the presence of bradycardia. There are few reports of their use, (though a short acting compound appeared beneficial for junctional rhythm in one case).29

Seizures should be treated aggressively with benzodiazepines as their contribution to hypoxia, acidosis, and catecholamine stimulation can increase risk of arrhythmias. Rhabdomyolysis may develop, especially in cases involving seizures, prolonged immobilisation, or severe hypokalaemia. It may be a factor in cases of renal failure unexplained by circulatory impairment. Acidosis if severe requires treatment (an added advantage being this reduces risk of myoglobinuria induced renal tubular damage). Electrolyte disturbances may require correction, under close monitoring. Haemodialysis has occasionally been required for renal failure.

Chronic symptoms of inhalant abuse may include a chemical smell on the breath, poor attention to hygiene, obvious intoxication where alcohol is not a factor, personality changes, alterations in sleeping and eating behaviour and a persistently runny nose or eye irritations. A rash or acne around the nose/mouth may also be present but could be easily confused for what is a common complaint in many teenagers.

Toluene has been widely abused in the past and carries significant acute cardiac risk.30 However in chronic abusers, neuropsychiatric disorders, gastro-intestinal complaints, and muscle weakness often feature.31 Effects on short term memory, concentration, visuo-spatial and other executive or abstract thinking functions can be marked. Psychotic episodes may be precipitated or even initiated by high exposures.32 Temporal lobe epilepsy, cranial nerve dysfunction, and peripheral neuropathy are reported (though co-exposure to other solvents can also be a factor).33 Neurological effects are not always reversible. Imaging techniques have demonstrated decreased perfusion and atrophy of cerebral, cerebellar, thalamic and brainstem structures.34 Jaundice is reported and abnormal liver function tests may take up to six months to normalise.35 Chronic myocardial36 effects have been reported, and adverse pulmonary effects may also occur.37

It can also produce renal tubular acidosis (RTA), with impaired ability to acidify the urine and thus increased risk of acidosis. Distal or less commonly proximal tubular acidosis or a mixed form can occur.38 The tubular dysfunction can also result in electrolyte disturbances, including hypokalaemia, hypocalcaemia, hypophosphataemia, and hyperchloraemia.31 Hypokalaemia (a risk factor for rhabdomyolysis) is more common than hyperkalaemia, especially in acute-on-chronic abuse, but the latter can occur acutely, generally as a result of rhabdomyolysis, which itself may result in acute tubular damage.39 However renal insufficiency is often rapidly reversible, with reduced urine output for two or three days only after sniffing episodes.35 Metabolic acidosis can be marked; when present as an acute effect38 there is often an elevated anion gap component due to accumulation of toluene metabolites,40 while with regular abusers, RTA is a common contributor. Maternal abuse has been associated with a foetal solvent syndrome,41 postnatal persistence of growth deficiency, and electrolyte abnormalities in the newborn.42

Given the difficulties in acute management and the significant chronic morbidity, preventive measures are critical. Following acute treatment, all patients should be referred to an appropriate substance abuse program. Youthful users motivated primarily by curiosity and peer pressure may be responsive to educational campaigns,43 however the best approach may be to also provide family and community counselling, residential care, and alternative recreational activities.44,45 Fortunately it appears that most users ultimately abandon the practice, often before they develop physical complications, such as neurological or renal damage. However, it appears to be a gateway phenomenon among younger adolescents where children who abuse inhalants early in life are more likely later to use other illicit drugs.46 Continued efforts to optimise prevention are required, while recognising that complete control of supply of all inhalants with abuse potential is not possible.

Author information: Michael Beasley, Medical Toxicologist; Laura E Frampton, Poisons Information Officer; John S Fountain, Medical Toxicologist; National Poisons Centre, Dunedin School of Medicine, University of Otago, Dunedin

Correspondence: Michael Beasley, National Poisons Centre, Dunedin School of Medicine, University of Otago, P O Box 913, Dunedin. Fax (03) 477 0509; email: michael.beasley@stonebow.otago.ac.nz

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