A review of pulmonary pathology and mechanisms associated with inhalation of freebase cocaine ("crack")

Abstract

The use of cocaine in the United States has reached near epidemic proportions. A major factor responsible for the dramatic increase in cocaine use is the ability to freebase cocaine and extract essentially pure drug to be smoked as crack. As a result, a variety of respiratory problems temporally associated with crack inhalation have been reported. Cocaine may cause changes in the respiratory tract as a result of its pharmacologic effects exerted either locally or systemically, its method of administration (smoking, sniffing, injecting), or its alteration of central nervous system neuroregulation of pulmonary function. These changes include such diverse disorders as thermal airway injury, pulmonary edema and hemorrhage, hypersensitivity reactions, and interstitial lung disease. However, a review of the pulmonary pathology and dysfunction associated with crack and/or cocaine use indicates that the reported changes are most likely multifactorial, even idiosyncratic, and fails to reveal common features diagnostic of cocaine use. It is likely that the spectrum of cocaine-induced pulmonary disease will continue to enlarge.