Our current understanding of the transport and deposition of aerosols (viruses, bacteria, air pollutants, aerosolized drugs) deep in the lung has been grounded in dispersive theories based on untested assumptions about the nature of acinar airflow fields. Traditionally, these have been taken to be simple and kinematically reversible. In this article, we apply the recently discovered fluid mechanical phenomenon of irreversible low-Reynolds number flow to the lung. We demonstrate, through flow visualization studies in rhythmically ventilated rat lungs, that such a foundation is false, and that chaotic mixing may be key to aerosol transport. We found substantial alveolar flow irreversibility with stretched and folded fractal patterns, which lead to a sudden increase in mixing. These findings support our theory that chaotic alveolar flow-characterized by stagnation saddle points associated with alveolar vortices-governs gas kinematics in the lung periphery, and hence the transport, mixing, and ultimately the deposition of fine aerosols. This mechanism calls for a rethinking of the relationship of exposure and deposition of fine inhaled particles.P athogenic aerosols play a major role in causing or exacerbating many pulmonary diseases such as lung cancer, bronchitis, emphysema, and asthma (1-4) and in spreading infectious diseases such as influenza, anthrax, and tuberculosis (5-8). The long-term effects of particulate air pollution on public health are striking; they have been shown to be equivalent to a shortening of life expectancy of approximately 2 years in the United States (9, 10). The magnitude of this effect is comparable to the deaths caused by all cancers (11). Fine particles-less than a few micrometers in diameter-are of great concern because they can penetrate deep into the pulmonary acinus (i.e., the gas exchange region of the lung). The critical factor that determines the fate of inhaled fine particles-whether deposited deep in the lung or exhaled in the next breath-is the kinematic interaction of inhaled and residual alveolar gas, but the underlying mechanism of this interaction is still not well understood.Because gas flow in the alveolar region occurs at very low Reynolds number (12) and the wall motion of the lung during breathing is essentially reversible (13-16), it has long been assumed that flow patterns deep in the lung are well described as a kinematically reversible Stokes flow (17-21). This means that, apart from the effects of molecular diffusion, a fluid ''particle'' that is transported by Stokes flow returns [by reversing the flow (22)] to its original position at the completion of one breathing cycle. This assumption implies that there is negligible flow-induced mixing between inhaled particles and the alveolar residual gas (17-21) and consequently little deposition of fine particles (18, 21). Experimental studies, however, consistently demonstrate appreciable aerosol mixing (23, 24) and deposition (25) deep in the lung, which cannot be accounted for by any known mechanism such as inerti...