Cocaine is a potent central nervous system stimulant derived from the Erythroxylon coca plant. It acts primarily as a strong vasoconstrictor, causing blood vessels throughout the body to narrow. Cocaine definitively affects the lungs, causing a wide range of acute and chronic respiratory complications regardless of the administration method. Its toxicity and stimulant properties can rapidly lead to life-threatening pulmonary issues, often resulting in emergency department visits.
Mechanisms of Pulmonary Injury
Cocaine causes severe pulmonary vasoconstriction, narrowing the lung’s blood vessels. This constriction reduces blood flow, potentially leading to ischemia and damage to the delicate capillary walls. Damaged capillaries become more permeable, allowing fluid to leak from the bloodstream into the alveolar air sacs.
The drug and its metabolites also directly damage alveolar and bronchial cells, triggering a powerful inflammatory response known as pneumonitis. This cellular injury recruits immune cells, which further damage the lung parenchyma. When cocaine is smoked, the inhalation of superheated vapors and combustion products adds thermal injury to the airways, burning the lining of the bronchi and alveoli.
Acute Cocaine-Related Respiratory Syndromes
“Crack lung” is a recognized immediate complication, typically developing within 48 hours of smoking freebase cocaine. This acute pulmonary syndrome involves diffuse alveolar damage and hemorrhagic alveolitis, causing the air sacs to become inflamed and bleed. Patients often present with severe shortness of breath, fever, chest pain, and hemoptysis (coughing up blood).
Acute pulmonary edema can also occur, resulting from either direct toxic injury to the alveolar-capillary membrane or from heart failure induced by cocaine’s cardiovascular effects. The damaged capillaries become leaky, causing non-cardiogenic fluid accumulation in the lungs that impairs gas exchange. Another serious acute risk is barotrauma, which includes pneumothorax (collapsed lung) and pneumomediastinum (air in the chest cavity). Barotrauma results from intense coughing or the Valsalva maneuver (forcibly holding the breath) used to maximize the drug’s effect, which suddenly increases intrabronchial pressure and ruptures the alveoli.
Long-Term Structural Damage and Chronic Disease
Chronic cocaine use promotes persistent inflammation and structural changes, leading to long-term respiratory impairment. This chronic irritation can result in pulmonary fibrosis (scar tissue formation), which decreases the elasticity and capacity of the lungs to exchange oxygen. Interstitial pneumonitis, a chronic inflammation of the tissue around the air sacs, often precedes fibrosis and contributes to progressive respiratory insufficiency.
Persistent vasoconstriction of the pulmonary arteries can evolve into pulmonary hypertension, characterized by high blood pressure in the lung arteries. This sustained pressure forces the right side of the heart to work harder, potentially leading to heart failure. Chronic use also exacerbates pre-existing obstructive lung diseases like asthma or contributes to chronic obstructive pulmonary disease (COPD) and bullous emphysema. Damage to the lung’s defense mechanisms and altered mental status increase the risk of infectious diseases, including aspiration pneumonia and tuberculosis.
How Administration Method Influences Risk
The specific route of cocaine administration significantly alters the type and severity of pulmonary risk. Smoking freebase or crack cocaine carries the highest risk for acute lower respiratory syndromes, such as “crack lung” and thermal airway injuries. This is because the drug and its combustion products are delivered directly to the deepest parts of the lungs. Smoking also increases the likelihood of barotrauma due to the specific inhalation techniques used.
Intranasal use (snorting) primarily affects the upper respiratory tract, causing chronic inflammation, ischemia, and potential necrosis of the nasal septum and sinuses due to vasoconstriction. Although less likely to cause acute lower lung syndromes than smoking, some drug still reaches the lower airways, contributing to irritation and bronchospasm. Intravenous injection introduces risks from insoluble fillers like talc, silica, or lactose, which are often used to cut the drug. These foreign materials travel to the lungs, causing foreign-body granulomas and potentially leading to pulmonary embolism or progressive pulmonary fibrosis.