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.
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