The effect of of glucocorticoids on grain dust-induced airway disease.
OBJECTIVE
To determine the effect of glucocorticoids on grain dust-induced airflow obstruction and airway inflammation.


METHODS
Randomized controlled trial.


METHODS
University hospital.


METHODS
Health volunteers.


METHODS
Two randomized, placebo-controlled trials, each studying 10 healthy volunteers who were pretreated with either triamcinolone acetonide (Azmacort) oral inhaler 4 puffs twice daily (800 microg daily) for 7 consecutive days or IV hydrocortisone (3 microg/kg/min) as a 14-h continuous infusion, then subjected to a controlled inhalation exposure to corn dust extract (CDE) (endotoxin exposure dose of 3 microg/kg). A single-blind, crossover study design was performed for each trial enrolling 10 healthy, lifetime nonsmokers, with no history of lung disease or environmental exposure to grain dust.


RESULTS
Following each inhalation exposure to CDE, spirometry was performed at regular intervals and BAL was performed at 4 h. Both treatment and placebo groups demonstrated significant decrements in spirometry and increments in BAL cellularity following CDE inhalation compared with placebo. Inhaled steroid treatment resulted in a significantly higher FEV1 only at the 2-h time point following CDE inhalation with no significant differences observed in the BAL total cell concentration or cellular differential compared with placebo. IV hydrocortisone treatment resulted in a significantly higher FEV1 and FVC between 2 and 4 h after CDE inhalation, as well as significant reductions in the BAL total cell, macrophage, and eosinophil concentrations. Interestingly, the concentration of tumor necrosis factor-alpha and interleukin-8 in the BAL fluid was also decreased following treatment with IV glucocorticoids.


CONCLUSIONS
These results demonstrate that glucocorticoids, administered IV and perhaps by inhalation, have a mildly protective effect on airflow obstruction and airway inflammation induced by inhalation of grain dust.
Trapp
J F
JF
Department of Internal Medicine, The University of Iowa College of Medicine, Iowa City 52242-1081, USA.
Watt
J L
JL
Frees
K L
KL
Quinn
T J
TJ
Nonnenmann
M W
MW
Schwartz
D A
DA
D000280:Administration, Inhalation; D000328:Adult; D000402:Airway Obstruction / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D002452:Cell Count; D018592:Cross-Over Studies; D004391:Dust / Q000009:adverse effects*; D004804:Eosinophils / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D005541:Forced Expiratory Volume / Q000187:drug effects; D005938:Glucocorticoids / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D006854:Hydrocortisone / Q000008:administration & dosage / Q000627:therapeutic use*; D007262:Infusions, Intravenous; D016209:Interleukin-8 / Q000032:analysis; D007958:Leukocyte Count; D016676:Macrophages, Alveolar / Q000473:pathology; D008297:Male; D010919:Placebos; D011014:Pneumonia / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D011292:Premedication; D016037:Single-Blind Method; D013147:Spirometry; D014222:Triamcinolone Acetonide / Q000008:administration & dosage / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014797:Vital Capacity / Q000187:drug effects; D003313:Zea mays
D000893:Anti-Inflammatory Agents; D004391:Dust; D005938:Glucocorticoids; D016209:Interleukin-8; D010919:Placebos; D014409:Tumor Necrosis Factor-alpha; D014222:Triamcinolone Acetonide; D006854:Hydrocortisone