title: Evidence of chronic damage to the pulmonary microcirculation in habitual users of alkaloidal ("crack") cocaine.
abstract: OBJECTIVE
  To evaluate BAL cells obtained from habitual users of alkaloidal ("crack") cocaine alone or in combination with tobacco, for evidence of cocaine-associated alveolar injury.
  
  
  METHODS
  Prospective cohort study.
  
  
  METHODS
  A total of 36 healthy men and women (mean age [SD], 37.5 [7.5] years), including 10 cocaine-only smokers (CS), 6 cocaine-plus-tobacco smokers (CTS), 10 tobacco smokers (TS), and 10 nonsmokers (NS), underwent fiberoptic bronchoscopy and BAL.
  
  
  METHODS
  Cytospins were prepared from BAL cells and stained with Wright-Giemsa for cell differentials and Gomori's stain for detection of hemosiderin. Endothelin (ET)-1 levels were determined from lavage fluid by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  None of the cocaine users reported episodes of hemoptysis or respiratory distress, and routine spirometry findings were within normal limits in all subjects. While there was little effect on total cell numbers or differential counts, the percentages of hemosiderin-positive alveolar macrophages (AMs) were markedly increased in CS (33.8 +/- 8.7% [SEM]) compared to TS and NS (< 2%; p < 0.05). The percentages of hemosiderin-laden AMs were also numerically increased in CTS (11.8 +/- 7.8%), but this value was not statistically significant from that of TS or NS. ET-1 levels were significantly increased in the fluid recovered from CS (6.2 +/- 0.8 pg/mL) when compared to NS (1.2 +/- 0.4 pg/mL) and TS (1.3 +/- 0.2 pg/mL) [p < 0.05], while ET-1 levels were elevated to a lesser extent in CTS (2.5 +/- 0.6 pg/mL). ET-1 levels correlated with the percentage of hemosiderin-positive AMs when CS were analyzed in conjunction with CTS (r = 0.64; p = 0.0004).
  
  
  CONCLUSIONS
  Clinically inapparent alveolar hemorrhage occurs frequently in otherwise healthy crack cocaine smokers and is associated with elevated levels of ET-1, indicative of cocaine-induced pulmonary microvascular injury.
authors.affiliation: Division of Hematology, UCLA School of Medicine, Los Angeles, CA 90095-1678, USA. gbaldwin@mednet.ucla.edu
authors.forename: Gayle Cocita
authors.initials: GC
authors.lastname: Baldwin
authors.forename: Ruth
authors.initials: R
authors.lastname: Choi
authors.forename: Michael D
authors.initials: MD
authors.lastname: Roth
authors.forename: Angela H
authors.initials: AH
authors.lastname: Shay
authors.forename: Eric C
authors.initials: EC
authors.lastname: Kleerup
authors.forename: Michael S
authors.initials: MS
authors.lastname: Simmons
authors.forename: Donald P
authors.initials: DP
authors.lastname: Tashkin
mesh_terms: D000328:Adult; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D002452:Cell Count; D019970:Cocaine-Related Disorders / Q000503:physiopathology*; D016578:Crack Cocaine / Q000009:adverse effects*; D005260:Female; D006470:Hemorrhage / Q000139:chemically induced / Q000503:physiopathology; D006485:Hemosiderin / Q000378:metabolism; D006801:Humans; D008168:Lung / Q000098:blood supply*; D016676:Macrophages, Alveolar / Q000166:cytology; D008297:Male; D008833:Microcirculation / Q000187:drug effects / Q000503:physiopathology; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000139:chemically induced* / Q000503:physiopathology; D012307:Risk Factors
chemical_list: D016578:Crack Cocaine; D006485:Hemosiderin