Motivated by growing considerations of the scale, severity, and risks associated with human exposure to indoor particulate matter, this work reviewed existing literature to: (i) identify state-of-the-art experimental techniques used for personal exposure assessment; (ii) compare exposure levels reported for domestic/school settings in different countries (excluding exposure to environmental tobacco smoke and particulate matter from biomass cooking in developing countries); (iii) assess the contribution of outdoor background vs indoor sources to personal exposure; and (iv) examine scientific understanding of the risks posed by personal exposure to indoor aerosols. Limited studies assessing integrated daily residential exposure to just one particle size fraction, ultrafine particles, show that the contribution of indoor sources ranged from 19% to 76%. This indicates a strong dependence on resident activities, source events and site specificity, and highlights the importance of indoor sources for total personal exposure. Further, it was assessed that 10-30% of the total burden of disease from particulate matter exposure was due to indoor-generated particles, signifying that indoor environments are likely to be a dominant environmental factor affecting human health. However, due to challenges associated with conducting epidemiological assessments, the role of indoor-generated particles has not been fully acknowledged, and improved exposure/risk assessment methods are still needed, together with a serious focus on exposure control.

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A stochastic lung model is proposed for aerosol deposition calculations. Airway geometry is selected randomly to reflect intrasubject variations in the human airway system. This may also be adjusted to take intersubject variations into account. The statistical analysis of the human airway geometry used is based on morphometric data measured at the Lovelace Inhalation Toxicology Research Institute. Average values and distributions of airway diameters and lengths, distributions of branching angles and criteria for termination of the pathway (when the alveolar region is reached) are presented. Correlations between the cross sections of tubes of succeeding generations and those between diameters and lengths of the same generation are also given.

Spherical monodisperse ferromagnetic iron oxide particles of 1.9-microm geometric and 4.2-microm aerodynamic diameter were inhaled by 13 healthy nonsmoking subjects using the shallow bolus technique. The bolus width was 100 ml, and the penetration front depth was 150 +/- 27 ml. The mean flow rate during inhalation and exhalation was 250 ml/s. The Fowler dead space and the phase 1 dead space of the airways were 282 +/- 49 and 164 +/- 34 ml, respectively. Deposition was below 20% without breath holding and 51 +/- 8% after an 8-s breath-holding time. We attempted to confine the bolus deposition to the bronchial airways by limiting the bolus front depth to the phase 1 dead space volume. Particle retention was measured by the magnetopneumographic method over a period of 9 mo. Particle clearance from the airways showed a fast and a slow phase; 49 +/- 9% followed the fast phase with a mean half-time of 3.0 +/- 1.6 h and characterized the mucociliary clearance. The remaining fraction was cleared slowly with a half-time of 109 +/- 78 days. The slow clearance phase was comparable to clearance measurements from the lung periphery of healthy nonsmokers, which allowed macrophage-dependent clearance mechanisms of the slow cleared fraction to be taken into account. Despite the fact that part of the slowly cleared particles may originate from peripheral deposition, the data demonstrate that mucociliary clearance does not remove all particles deposited in the airways and that a significant fraction undergoes long-term retention mechanisms, the origin of which is still under discussion.

The apparent discrepancy between the reported preferential occurrence of bronchial carcinomas in central bronchial airways and current dose estimates for inhaled particles suggests that experimentally observed local accumulations of particles within bronchial airway bifurcations may play a crucial role in lung cancer induction. Here, we computed three-dimensional particle deposition patterns in lobar-segmental airway bifurcations and quantified the resulting inhomogeneous deposition patterns in terms of deposition enhancement factors, which are defined as the ratio of local to average deposition densities. Our results revealed that a small fraction of epithelial cells located at carinal ridges can receive massive doses that may be even a few hundred times higher than the average dose for the whole airway. This lends further credence to the hypothesis that the apparent site selectivity of neoplastic lesions may indeed be caused by the enhanced deposition of toxic particulate matter at bronchial airway bifurcations.

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