Suppression of rat and mouse lymphocyte function by urban air particulates(Ottawa dust) is reversed by N-acetylcysteine

Epidemiology studies have demonstrated increased pulmonary morbidity such a s allergy and infection with episodes of high particulate air pollution (si ze range 0.1-10 mu m diameter, PM10), but the mechanism(s) for this associa tion is not yet well defined. The present study was undertaken to evaluate the effects of EHC-93 urban particles (Ottawa dust) on immune functions of peripheral blood mononuclear cells (PBMCs) and splenocytes from male Fische r 344 rats and C57Bl/6 mice. Immune function endpoints evaluated included c ell viability, lymphocyte blastogenesis stimulated by T-cell mitogen (conca navalin A, Con A) or B-cell mitogens [lipopolysaccharide (LPS) or LPS/dextr an sulfate], intracellular Ca2+ concentration, interleukin 2 (IL-21 product ion, and expression of receptors for transferrin (TfR) and IL-2 (IL-2R). In addition, the effect of N-acetylcysteine (NAC), an antioxidant, on the tox icity of EHC-93 particles was evaluated Total EHC-93 particles, water leach ate of EHC-93, and washed EHC-93 suppressed proliferation of PBMCs and sple nocytes to T- and B-cell mitogens. Treatment of splenocytes with EHC-93 par ticles did nor alter intracellular Ca2+ concentration or mitogen-induced ex pression of TfR and IL-2R expression, bur increased IL-2 production assayed by enzyme-linked immunosorbent assay (ELISA). in spire of an increase in I L-2 production, exogenous IL-2 when added to cultures was able to reverse t he suppression of Con A-induced lymphocyte proliferation by EHC-93 particle s. Furthermore, the suppressive effect of EHC-93 particles on mitogen-induc ed lymphocyte proliferation was completely abolished by addition of the ant ioxidant NAC to cultures, suggesting a possible role of oxidative factors f or the toxicity Of EHC-93 particles.