Increased lower respiratory tract iron concentrations in alkaloidal (“crack”) cocaine users

Study objective: We hypothesized that the use of inhaled alkaloidal ("crack") cocaine could increase lung content of iron, either by inducing alveolar hemorrhage or by other mechanisms. Intrapulmonary accumulation of iron could promote chronic lung diseases in crack users. The goal of this study was to determine whether iron and ferritin content of alveolar macrophages or fluid recovered by BAL was increased in subjects using crack, compared with nonsmokers. Methods: BAL was performed in 31 volunteer subjects, including healthy nonsmokers (n = 7), subjects smoking crack alone (n = 7), as well as subjects smoking both crack and cigarettes (n = 7) or cigarettes alone (n = 10). Iron content of alveolar macrophages and BAL fluid was determined by a colorimetric method and ferritin content of alveolar macrophages, and BAL fluid was measured by a two-sided immunoradiometric method. Results: Alveolar macrophages recovered from crack users contained more iron than did alveolar macrophages from nonsmokers (25.4 ± 2.9 nmol/10⁶ vs 5.5 ± 0.6 nmol/10⁶ [mean ± SE]; p < 0.01). There were similar increases in alveolar macrophage ferritin as well as BAL fluid iron and ferritin in crack users, compared with nonsmokers. BAL fluid ferritin concentrations in subjects smoking both crack and cigarettes were increased, compared with subjects smoking crack alone or cigarettes alone (p < 0.05). Conclusions: Use of crack increases intrapulmonary concentrations of iron and ferritin. Effects of crack on extracellular ferritin concentrations may be additive with effects of cigarette smoking. Although the mechanism(s) causing pulmonary iron accumulation were not identified by this study, it may be a result of occult alveolar hemorrhage or increased vascular permeability. The increase in lung iron burden in habitual crack users could promote chronic lung diseases in these subjects.