EXPRESSION OF MEMBRANE-ANTIGENS ON HUMAN ALVEOLAR MACROPHAGES AFTER EXPOSURE TO NITROGEN-DIOXIDE

Evidence from both animal and human investigations suggests that expos ure to nitrogen dioxide (NO2), a common air pollutant, increases susce ptibility to respiratory infections. In animals, alveolar macrophage ( AM) antimicrobial functions are impaired following NO2 exposure. We so ught to determine whether exposure to NO2 in humans causes an influx o f less mature AM into the alveolar space and/or results in decreased e xpression of AM surface markers important in antimicrobial defense. Ei ght human volunteers underwent bronchoalveolar lavage (BAL) immediatel y following 6-h exposures to 2.0 ppm NO2 or filtered air. AM expressio n of receptors for the Fc component of immunoglobulin (Ig), complement receptor 3 (CD11b), and monocyte marker CD14 were assessed using immu nofluorescence staining and flow cytometry. The use of internal fluore scence standards reduced analytical variability by 32% and allowed det ection of relatively small changes in cell surface antigen expression. We observed an increase in AM expression of CD11b from 1.44 (SE 0.19) x 10(5) molecules oi equivalent soluble fluorochrome (MESF) after air to 1.78 (SE 0.21) x 10(5) MESE after NO2 exposure (p=.04). When corre cted for nonspecific antibody binding, the difference was no longer st atistically significant (p=.059). No significant changes were observed in cell type, size, or expression of markers of differentiation. Expo sure 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 i nto the alveolar spare immediately after exposure.