Technische Universität München

The Entrepreneurial University

Acute and chronic abuse of stimulants may result in significant neurologic, cardiac, psychiatric, obstetric and respiratory complications. The severity and variability of stimulant-induced pulmonary toxic reactions appears to depend on the compound used, the dosage and the route of administration.  
Acute pulmonary symptoms of smoking cocaine include cough, black sputum, hemoptysis and pleuritic chest pain. Smokers of crack cocaine have higher carboxyhemoglobin levels and this may play a role in cocaine-related chest pain. The use of freebase cocaine has been associated with barotraumas. Pneumothorax, pneumopericardium and pneumomediastinum are the common manifestations of cocaine-induced barotraumas. Smoking of cocaine is also associated with asthma-like symptoms, exacerbation of asthma and various airway complications including sinusitis, epiglottitis, bronchitis, and bronchiolitis. In addition, hot cocaine vapours may cause thermal burns of the respiratory tract. Research has found decreased diffusion capacity of the lungs reflecting reduced alveolar-capillary interface that lasts weeks to months after cocaine exposure. The proposed mechanism of this reduction is vascular abnormalities. Crack use is associated with the syndrome of “crack-lung”, characterized by diffuse alveolar infiltrates, pulmonary and systemic eosinophilia, fever and respiratory failure. It occurs within 1 to 48 hours after heavy cocaine smoking. Pulmonary alveolar hemorrhage, hemoptysis with and without pulmonary infarction are frequently reported with cocaine abuse. Cocaine use also induces acute noncardiogenic pulmonary edema. Possible mechanisms include local cellular toxic reactions and microvascular pulmonary effects. Stimulation of the central nervous system to induce noncardiogenic or neurogenic pulmonary edema is also postulated. Stimulants generally cause respiratory stimulation, but severe overdose may lead to respiratory depression. Animal models of cocaine poisoning suggest that postictal respiratory depression or, in the absence of seizures, direct respiratory depression plays a major role in the mechanisms of cocaine-induced death.  
The effects of amphetamine intoxication on respiratory system include dyspnea, asthma exacerbation, bronchitis, and acute noncardiogenic pulmonary edema. Pulmonary hypertension has long been reported in amphetamine users.