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Illicit drug use and its effect on the lungs

Authors Charlotte Rayner, MD, FRCP, is consultant general and respiratory physician, Parkside Hospital, London; Samantha Prigmore, MSc, BSc, RGN, is respiratory nurse consultant, St George’s Healthcare NHS Trust, London.

Abstract Rayner, C., Prigmore, S. (2008) Illicit drug use and its effect on the lungs. Nursing Times; 104: 9, 40–44. Charlotte Rayner and Samantha Prigmore describe the prevalence of illicit drug use, how these drugs are inhaled or injected and the pulmonary consequences of such drug use.

The prevalence of illicit drug use in the UK is not fully known but it is suggested that levels among young people are among the highest in the EU (Hibell et al, 2004). The 2004–2005 British Crime Survey estimated that 45.8% of 16–24-year-olds had used one or more illicit drugs in their lifetime, 26.3% had used one or more illicit drugs in the past year and 16.3% had used one or more in the past month (Roe, 2005). The survey also estimated that 15.8% of those aged 16–24 had used a class-A drug at least once, 8.1% had used at least one class-A drug in the past year and 3.7% in the past month.

The crime surveys for 2004–2005 and 2005–2006 showed cannabis was the drug most likely to be used. It is estimated that 23.5% of 16–24-year-olds had used cannabis in the previous year. Cocaine was the next most commonly used drug, with 4.9% claiming to have used it in the previous 12 months. This was closely followed by ecstasy at 4.8%. Amyl nitrite use was estimated at 3.8%, amphetamines use at 3.3% and hallucinogen use at 3.0% (Roe and Man, 2006; Roe, 2005).

A comparison of government office regions from 2003 indicated that London had the highest national level of class-A and illicit drug use. There was a strong relationship between levels of drug use and the environment, with illicit drugs highest in inner-city areas. Areas described as ‘affluent, urban’ had a higher level of class-A and illicit drug use than the national average (Condon and Smith, 2003).

Cannabis

Cannabis is the most widely used illicit drug in many developed societies, including the UK. The psychological and health effects remain the subject of much debate with polarised views for both its legal status and its potential effects.

Cannabis is derived from the female plant of Cannabis sativa. The cycloactive component of the plant is a delta-9 tetrahydrocannabinol (THC). The flowering tops of the cannabis plant have the highest content of THC. The concentration of THC is lower in the leaves, stems and seeds. Marijuana has a THC content of 0.5–5% and is prepared from the dried flowering toxin leaves. Hashish has a THC content of 2–20% and is made from compressed flowers and dried cannabis resin.

Cannabis may be smoked in a joint, which is the size of a cigarette, or in a water pipe. When smoked as a cigarette, this is normally as a roll-up without a filter. Tobacco is often added to the cannabis to assist with the burning of the leaf. To maximise absorption of cannabis, smokers inhale deeply and will often hold their breath to enable optimal and maximal absorption of THC by the lungs.

Cannabinoids act on receptors in the brain involved in coordination, pain perception, memory reward and cognition. People may have feelings of euphoria and relaxation, changes in normal perception and distortion of time. Also, sensory experiences may be intensified. Short-term memory, attention span, motor skills and reaction time are impaired. Minor cardiovascular changes occur, including increases in heart rate and blood pressure when sitting, but a slight decrease when standing.

Inhaled cannabis causes short-term bronchodilation. This peaks 10–20 minutes after inhalation and lasts for approximately an hour. This is followed by a period of bronchoconstriction.

Regular cannabis smoking will result in symptoms similar to that of COPD. Patients complain of coughing, increased mucus production and wheeze. At a mucosal level, muco-ciliary clearance will be slow. There is mucus hypersecretion and a change in the epithelium, with loss of ciliated cells, an increase in mucus-producing cells and cellular disorganisation with squamous metaplasia (benign changes in the epithelial lining).

Cannabis has a direct effect on the function of alveolar macrophages, which results in a reduction in macrophage activity. This results in an increased risk of pulmonary infections.

Cannabis leaves may be contaminated by aspergillus and there have been case reports citing cannabis as a risk factor for the development of invasive aspergillus infections. Cannabis smoking has also been cited as an independent risk factor for the development of opportunist infections in HIV, including Mycobacterium tuberculosis (Munckhof et al, 2003; Perlman et al, 1997).

The link between cannabis smoking and lung cancer is unclear. There are lines of evidence that suggest cannabis smoking may predispose people to respiratory malignancies. These include:

  • The presence of potential carcinogens in cannabis smoke and its deposition in the lungs;

  • Occurrence of pre-malignant changes in bronchial biopsies obtained from people who smoke cannabis but not tobacco;

  • Impairment of anti-tumour macrophage activity.

Physicians should advise patients of potential adverse health outcomes until further studies are performed that permit definitive conclusions.

Cocaine

Cocaine hydrochloride is a naturally occurring plant alkaloid derived from the coca leaf. It is refined from leaves to produce a powder. The powder can be snorted using a straw or rolled-up paper such as bank notes, smoked or rubbed directly on to mucous membranes. Patients who use cocaine regularly may exhibit the following:

  • Crack keratitis due to the local anaesthetic effect, causing the person to rub their eyes excessively;

  • Erosion of tooth enamel;

  • Hands showing crack callus of the fingers, due to repeated use of a lighter or burns consistent with handling cocaine pipes.

Cocaine causes an acute intoxication, whichis short acting and dose dependent. It is caused by an increased secretion of adrenaline. Cocaine gives rise to a feeling of euphoria and well-being, but may also result in irritability and confusion, along with hallucination and formication (sensation of insects crawling under the skin). When the effect of the cocaine wears off, depression and paranoia may occur. Physical effects of cocaine use include tachycardia, hypertension, increased respiratory rate, dilated pupils and increased mental excitement.

Crack cocaine is made by heating cocaine powder with baking soda. The crack is then smoked. Smoke from crack contains 94% cocaine particles and 6% vapour. Each particle size is roughly 2.3µm, which is able to reach the alveoli.

Cocaine has a number of effects on the respiratory tract:

  • When sniffed or snorted:
    – The nasal mucosa may become ulcerated and perforated as a result of ischaemia, necrosis
    and infection;
    – Acute and chronic sinusitis may occur along with bone destruction;

  • Crack cocaine smoking results in acute lung injury, including asthma, which may be acute, severe and occasionally fatal;

  • Barotrauma, resulting in pneumo-mediastinum and possible pneumothorax. This may occur from cocaine smoking due to forceful deep breathing or deep inhalation followed by a Valsalva manoeuvre, or from mouth-to-mouth positive pressure when sharing the drug air under pressure. This ruptures the connective tissue and dissects to the mediastinum and/or the pleura.

Crack cocaine smoke may also cause:

  • Acute non-cardiogenic pulmonary oedema;

  • Alveolar haemorrhage;

  • Interstitial infiltrates (inflammation of supporting structure making up lung parenchyma);

  • Non-specific pneumonitis;

  • Bronchiolitis obliterans (inflammation of the bronchioles and surrounding tissue in the lungs).

Crack cocaine use may cause a cough, which can produce black sputum, haemoptysis (blood in sputum), dyspnoea, wheeze and fever. Chest pain and palpitations commonly occur. Inhalation of the hot vapour can cause thermal injury to the lungs and the oesophagus and, additionally, cardiac ischaemia may be present (Kleerup et al, 2002; Meisels and Loke, 1993; Tashkin et al, 1992).

Chronic symptoms of cocaine use include: dyspnoea, with reduction in exercise tolerance; a daily cough, producing grey or black sputum; and haemoptysis. Interstitial infiltration, pulmonary hypertension, airway granulomatous change (reaction to a foreign body) and also a reduction in macrophage activity may occur.

Heroin

Heroin is a semisynthetic opiate, which acts as a central nervous system depressant and an analgesic. It is produced from morphine, which is extracted from the Asian poppy (Papaver somniferum). Heroin is the most rapidly acting opiate. It maybe sold as a white or brownish powder, or as a black sticky substance known as ‘black tar heroin’. Although pure heroin is becoming more common, most street heroin is mixed with other drugs or with substances such as sugar, starch, powdered milk and quinine.

Heroin is usually injected after being mixed with water or citric acid in a spoon and heated until it becomes a solution. The solution is filtered into
a syringe then injected. Filters used include tips from cotton buds and cigarette filters. These home-made filters remove larger particles but not bacteria, and parts of the filter material can be injected along with the drug solution.

Heroin can also be inhaled. It is placed on foil, which is heated from below, then the vapours are inhaled. This is known as ‘chasing the dragon’, ‘chinesing’ or ‘Chinese blowing’. Heroin may also be ground and mixed with a neutral substance, such as antihistamines or powdered sugar, then arranged into lines and snorted like cocaine.

Heroin acts as a respiratory depressant – an overdose causing respiratory depression may be fatal. Inhaling heroin vapour results in similar physiological changes as inhaling cocaine vapour.

Pulmonary infections associated with IV heroin misuse include:

  • More cases of community-acquired pneumonia;

  • Lung abscess formation;

  • Septic emboli with or without endocarditis;

  • M. tuberculosis and bronchitis;

  • Bronchiectasis;

  • Pleural and mediastinal infection.

Those who use heroin intravenously and have a positive HIV status are three times more likely to develop community-acquired pneumonia compared with those with a positive HIV status who do not use drugs. Lung abscess may occur due to oral pharyngeal aspiration during stupor following IV injection and this may result in a necrotising infection. This may progress to cause empyema (pus in the pleural cavity) and/or bronchopulmonary fistulas (O’Donnell, 1996).

The incidence of M. tuberculosis in those who misuse drugs and have an HIV-negative status is six times higher than in the overall population (Story et al, 2007). If those who use drugs also have an HIV-positive status, this rate is 13 times higher than for a member of the general population (Story et al, 2007). It takes longer for the sputum of those who use drugs heavily to become smear negative on commencement of anti-tuberculous therapy.

Non-infectious complications of IV heroin misuse include emphysema, bullous lung
disease, pulmonary vascular disease, pulmonary hypertension and talcosis.

Talc may be mixed with heroin before the heroin is sold and, when injected, the particles of talc become lodged in pulmonary vessels before migrating into the interstitium of the lung. This results in a foreign-body reaction, which can progress to interstitial fibrosis. Patients presenting with talcosis experience increasing dyspnoea, reduction in exercise tolerance and cough.

In addition to the interstitial disease, patients may also develop pulmonary hypertension. A chest X-ray will demonstrate widespread nodules that coalesce over a period of time. This change mimics the massive fibrosis seen in silicosis or
coal workers with pneumoconiosis. Diaphragmatic calcification can also be seen, which also occurs following an individual’s exposure to asbestos. A high-resolution CT (HRCT) scan of the lungs will demonstrate a typical diffuse fine micronodular pattern or ground-glass attenuation (McCarroll and Roszler, 1991).

Patients with bullous lung disease and emphysema present with dyspnoea and pneumothorax (Wolff and O’Donnell, 2004). An HRCT scan will show severe diffuse emphysema with bullae. This can be difficult to distinguish radiologically from emphysema and bullous change linked with tobacco smoking, although, on lung biopsy, talc granulomas may be seen (McCarroll and Roszler, 1991).

Volatile substance misuse

Between 3% and 10% of adolescents have experimented with volatile substances at some point, but fewer than 1% are regular users.

The acute toxic effect of all commonly misused solvents are similar and a result of central nervous system depressant effects, which resemble alcohol intoxication. Acute toxic effects include a feeling of well-being, with euphoria due to disinhibition. High levels of inhalation result in hallucinations and changes in perception, and may also result in impaired coordination with ataxia and confusion. This may be followed by aggression and risk-taking behaviour (Meadows and Verghese, 1996).

Pulmonary complications include hypoxia with airway obstruction, and potential central respiratory depression with respiratory failure. Individuals may then aspirate and experience significant vagal inhibition and cardiac arrhythmias (Anderson and Loomis, 2003).

Conclusion

Illicit drug misuse is rising and the lungs are at risk of injury from inhaled, smoked and injected drugs. In our experience patients will volunteer information about drug use when asked and are often unaware, particularly if smoking cannabis or cocaine, that the smoke can cause lung damage. Patients are often receptive to advice on prevention of further injury.

References:

Anderson, C.E., Loomis, G.A. (2003) Recognition and prevention of inhalant abuse. American Family Physician; 68: 5, 869–874.

Condon, J., Smith, N. (2003) Prevalence of Drug Use: Key Findings from the 2002/2003 British Crime Survey. www.homeoffice.gov.uk/rds/pdfs2/r229.pdf

Hibell, B. et al (2004) The ESPAD Report 2003. Alcohol and Other Drug Use Among Students in 35 Countries. Stockholm: The Swedish Council for Information on Alcohol and Other Drugs, the Pompidou Group at the Council of Europe.

Kleerup, E.C. et al (2002) Chronic and acute effects of ‘crack’ cocaine on diffusing capacity, membrane diffusion, and pulmonary capillary blood volume in the lung. Chest; 22: 2, 629–638.

McCarroll, K.A., Roszler, M.H. (1991) Lung disorders due to drug abuse. Journal of Thoracic Imaging; 6: 1, 30–35.

Meadows, R., Verghese, A. (1996) Medical complications of glue sniffing. Southern Medical Journal; 89: 5, 455–462.

Meisels, I.S., Loke, J. (1993) The pulmonary effects of free-base cocaine: a review. Clinical Journal of Medicine; 60: 4, 325–329.

Munckhof, W.J. et al (2003) A cluster of tuberculosis associated with use of a marijuana water pipe. International Journal of Tuberculosis and Lung Disease; 7: 9, 860–865.

O’Donnell A.E. (1996) HIV in illicit drug users. Clinics in Chest Medicine; 17: 4, 797–807.

Perlman, D.C. et al (1997) ‘Shotgunning’ as an illicit drug smoking practice. Journal of Substance Abuse Treatment; 14: 1, 3–9.

Roe, S. (2005) Drug Misuse Declared: Findings from the 2004/05 British Crime Survey. Home Office statistical bulletin. www.homeoffice.gov.uk/rds/pdfs05/hosb1605.pdf

Roe, S., Man, L. (2006) Drug Misuse Declared: Findings from the 2005/06 British Crime Survey. Home Office statistical bulletin.

Story, A. et al (2007) Tuberculosis in London: the importance of homelessness, problem drug use and prison. Thorax; 62: 8, 667–671.

Tashkin, D.P. et al (1992) Respiratory effects of cocaine freebasing among habitual cocaine users. Journal of Addictive Disease; 11: 4, 59–70.

Wolff, A.J., O’Donnell, A.E. (2004) Pulmonary effects of illicit drug use. Clinics in Chest Medicine; 25: 1, 203–216.

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