Effects of inhaled iron oxide particles on alveolar epithelial permeability in normal subjects

Pulmonary inflammation secondary to oxidant generation catalyzed by transit ion metals associated with inhaled particles is one factor postulated to un derlie the acute health effects of particulate air pollution. We postulated that inhaled iron oxide particles with associated amounts of soluble iron should induce mild pulmonary inflammation and lead to altered alveolar epit helial integrity and altered gas exchange. To test this hypothesis we exami ned the effects of inhaled iron oxide particles on alveolar epithelial perm eability. Sixteen healthy subjects inhaled aerosols of iron oxide particles (1.5 mum mass median aerodynamic diameter) having either high or low water -soluble iron content [3.26 +/- 0.25 (SE) and 0.14 +/- 0.04 mug soluble iro n/mg of particles, respectively] for 30 min at an average mass concentratio n of 12.7 mg/m(3). Alveolar epithelial permeability was assessed by measuri ng the pulmonary clearance of an inhaled radiolabeled tracer molecule (Tc-9 9m-DTPA, diethylene triamine pentaacetic acid) using a gamma camera at 1/2 h and 24 h post particle exposure. Carbon monoxide lung diffusing capacity (DLCO) and spirometry were also performed before and after breathing the ir on oxide. As a control, on a separate day, the procedures were duplicated e xcept that the subject breathed particle-free air. For those subjects breat hing aerosols with high soluble iron, we found no significant difference in DTPA clearance half-times after breathing particles versus particle-free a ir either at 1/2 h (97.4 +/- 15.4 vs. 116.1 +/- 15.5 min, respectively) or 24 h postinhalation (105.1 +/- 13.8 vs. 106.9 +/- 12.9 min, respectively). Likewise, for those subjects breathing aerosols with low soluble iron conte nt we found no significant difference in DTPA clearance half-times after br eathing particles versus particle-free air either at 1/2 h (108.6 +/- 31.9 vs. 95.6 +/- 10.8 min, respectively) or 24 h postinhalation (130.0 +/- 18.0 vs. 105.8 +/- 13.7 min, respectively). We found no significant differences in DLCO between particle exposures and air exposures. Minor differences in spirometric measurements were noted but were not statistically significant . We conclude that inhalation of iron oxide particles did not cause an appr eciable alteration of alveolar epithelial permeability, lung diffusing capa city, or pulmonary function in healthy subjects under the studied condition s.