The migratory and phagocytic capabilities of pulmonary macrophages are important elements in lung defense against particles and pathogens deposited on alveolar surfaces. Both functions rely on macrophage cytoplasmic movements. We examined how a common respiratory exposure, cigarette smoking, affects intracellular motions in human pulmonary macrophages (HPM phi). We observed that HPM phi isolated by bronchoalveolar lavage from human volunteers and cultured in vitro were capable of ingesting unopsonized magnetic iron oxide particles localized within phagosomes and phagolysosomes. Upon magnetization, the particles collectively produced a remanent magnetic field (RMF). Motions of particle-containing organelles caused a decay of the RMF, or "relaxation." We applied this technique, which is an alternative to optical microscopy, for evaluating both movement and viscosity of macrophage cytoplasm. In our in vitro studies, we found that HPM phi isolated from smokers exhibited more rapid RMF decay than did HPM phi isolated from nonsmokers. Rotating the intracellular magnetic particles with external fields showed that the HPM phi cytosol was highly viscous in both smoker and nonsmoker cells. In both cell groups, resistance to particle rotation was increased by 2.6 ng/ml phorbol myristate acetate. Our in vitro magnetometric quantification of intracellular particle movement in isolated HPM phi suggests that lung macrophage cell organelle motions are increased in smokers; this may be the mechanism for the enhanced in vivo magnetic-particle motion reported previously in magnetometric studies of human subjects who are smokers.