Expression of membrane antigens on human alveolar macrophages after exposure to nitrogen dioxide

Evidence from both animal and human investigations suggests that exposure to nitrogen dioxide (NO₂,), a common air pollutant, increases susceptibility to respiratory infections. In animals, alveolar macrophage (AM) antimicrobial functions are impaired following NO₂ exposure. We sought to determine whether exposure to NO₂ in humans causes an influx of less mature AM into the alveolar space and/or results in decreased expression of AM surface markers important in antimicrobial defense. Eight human volunteers underwent bronchoalveolar lavage (BAL) immediately following 6-h exposures to 2.0 ppm NO₂ or filtered air. AM expression of receptors for the Fc component of immunoglobulin (Ig), complement receptor 3 (CD11b), and monocyte marker CD14 were assessed using imniunofluorescence staining and flow cytometry. The use of internal fluorescence standards reduced analytical variability by 32% and allowed detection of relatively small changes in cell surface antigen expression. We observed an increase in AM expression of CD 11b from 1.44 (SE 0.19) × 10⁵ molecules of equivalent soluble fluorochrome (MESF) after air to 1.78 (SE 0.21) × 10⁵ MESF after NO² exposure (p =04). When corrected for nonspecific antibody binding, the difference was no longer statistically significant (p =059). No significant changes were observed in cell type, size, or expression of markers of differentiation. Exposure to 2.0 ppm NO₂ for 6 h does not reduce AM expression of the 3 Fc receptors, CD11b, or CD14, and does not cause an influx of monocytes into the alveolar space immediately after exposure.