Exact analysis of aerosol deposition during steady breathing
TL;DR: In this paper, a transport equation for an aerosol breathed into and out of the human airways is derived using a trumpet lung model, and a partial differential equation is solved exactly using the method of characteristics.
About: This article is published in Powder Technology.The article was published on 1978-09-01. It has received 79 citations till now.
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TL;DR: The results suggest that the TDF of ultrafine particles increases with a decrease of particle size and with breathing patterns of longer respiratory time, a pattern that is consistent with diffusion deposition of ultra fine particles.
Abstract: Ultrafine particles (< 0.10 microm in diameter) are present in great number in polluted urban air, thus posing a potential health risk. In this study, the total deposition fraction (TDF) of ultrafine aerosols with a narrow size distribution (number median diameter NMD = 0.04-0.1 microm and geometric standard deviation sigma(g) = approximately 1.3) was measured in a group of young healthy adults (11 men and 11 women). TDF was obtained with 6 different breathing patterns: tidal volume (V(t)) of 500 ml at respiratory flow rates (Q) of 150 and 250 ml/s; V(t) = 750 ml at Q of 250 and 375 ml/s; and V(t) = 1 L at Q of 250 and 500 ml/s. Aerosols were monitored continuously by a modified condensation nuclei counter while subjects were inhaling them with prescribed breathing patterns. For a given breathing pattern, TDF increased as particle size decreased, regardless of the breathing pattern used. For example, with V(t) = 500 ml and Q = 250 ml/s, TDF (mean +/- SD) was 0.26 +/-.04, 0.30 +/-. 05, 0.35 +/-.05, and 0.44 +/-.07 for NMD = 0.10, 0.08, 0.06, and 0. 04 microm, respectively. For a given NMD, TDF increased with an increase in V(t) and a decrease in Q. TDF was greater for women than men at NMD = 0.04 microm within all breathing patterns used (p <.05), but the difference was smaller or negligible for larger sized particles. The results suggest that the TDF of ultrafine particles increases with a decrease of particle size and with breathing patterns of longer respiratory time, a pattern that is consistent with diffusion deposition of ultrafine particles. The results also suggest that there is a differential lung dose of ultrafine particles and thus there may be a differential health risk for men versus women.
268 citations
TL;DR: Data indicate that, after sensitization of mice by inhalation of antigen, the animals develop a specific IgE antibody response, expansion of PBLN lymphocyte numbers, and increased airway hyperresponsiveness in the absence of signs of airway inflammation.
Abstract: Inhalation of an antigen, ovalbumin (OVA), in the absence of adjuvant has been demonstrated to induce an immune response that is associated with increased airway responsiveness. Determination of OVA-specific serum IgE and IgG antibody responses revealed an early increase in antibody titers that were initially restricted to the IgE class. Subsequently, IgG antibody titers increased and IgE antibody plateaued. Furthermore, we observed a tenfold increase in the number of lymphocytes caused by a predominant expansion of CD3+ T cells in the peribronchial-associated lymph modes (PBLNs) of sensitized animals compared with the numbers of cells in control animals or in the gut-associated lymphoid tissue. The sensitized animals demonstrated an increase in airway responsiveness to intravenous methacholine challenge. Analysis of in vitro immunoglobulin production by spleen mononuclear cells revealed increased spontaneous IgE production that was more than fourfold enhanced in the presence of OVA, but IgG production was not increased. Spleen and PBLN lymphocytes, but not lymphocytes from gut-draining lymph nodes, demonstrated a proliferative response to OVA. Control animals exhibited no proliferative response to OVA. Histopathologic examination of the sensitized lung revealed an absence of acute inflammatory cells (e.g., neutrophils and macrophages), lymphocytes, or monocytes at the time of the increased airway hyperresponsiveness. These data indicate that, after sensitization of mice by inhalation of antigen, the animals develop a specific IgE antibody response, expansion of PBLN lymphocyte numbers, and increased airway hyperresponsiveness in the absence of signs of airway inflammation.
255 citations
TL;DR: The current literature on pulmonary exposure to CNT/CNF and associated effects is summarized; recommendations and conclusions are provided that address test guideline modifications for rodent inhalation studies that will improve dosimetric extrapolation modeling for hazard and risk characterization based on the analysis of exposure-dose-response relationships.
Abstract: Carbon nanotubes (CNT) and nanofibers (CNF) are used increasingly in a broad array of commercial products. Given current understandings, the most significant life-cycle exposures to CNT/CNF occur from inhalation when they become airborne at different stages of their life cycle, including workplace, use, and disposal. Increasing awareness of the importance of physicochemical properties as determinants of toxicity of CNT/CNF and existing difficulties in interpreting results of mostly acute rodent inhalation studies to date necessitate a reexamination of standardized inhalation testing guidelines. The current literature on pulmonary exposure to CNT/CNF and associated effects is summarized; recommendations and conclusions are provided that address test guideline modifications for rodent inhalation studies that will improve dosimetric extrapolation modeling for hazard and risk characterization based on the analysis of exposure-dose-response relationships. Several physicochemical parameters for CNT/CNF, including shape, state of agglomeration/aggregation, surface properties, impurities, and density, influence toxicity. This requires an evaluation of the correlation between structure and pulmonary responses. Inhalation, using whole-body exposures of rodents, is recommended for acute to chronic pulmonary exposure studies. Dry powder generator methods for producing CNT/CNF aerosols are preferred, and specific instrumentation to measure mass, particle size and number distribution, and morphology in the exposure chambers are identified. Methods are discussed for establishing experimental exposure concentrations that correlate with realistic human exposures, such that unrealistically high experimental concentrations need to be identified that induce effects under mechanisms that are not relevant for workplace exposures. Recommendations for anchoring data to results seen for positive and negative benchmark materials are included, as well as periods for postexposure observation. A minimum data set of specific bronchoalveolar lavage parameters is recommended. Retained lung burden data need to be gathered such that exposure-dose-response correlations may be analyzed and potency comparisons between materials and mammalian species are obtained considering dose metric parameters for interpretation of results. Finally, a list of research needs is presented to fill data gaps for further improving design, analysis, and interpretation and extrapolation of results of rodent inhalation studies to refine meaningful risk assessments for humans.
146 citations
Cites background from "Exact analysis of aerosol depositio..."
...The lung geometry also resembled a trumpet in shape when symmetric lung geometry was assumed (Scherer, Shendalman, and Greene 1972; Yu 1978)....
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TL;DR: An overview of the current status of the computational tools and approaches available for predicting respiratory-tract dosimetry of inhaled particulate matter and the progress made in each area in the last three decades is discussed along with some suggestions for future direction.
Abstract: This review article is intended to serve as an overview of the current status of the computational tools and approaches available for predicting respiratory-tract dosimetry of inhaled particulate matter. There are two groups of computational models available, depending on the intended use. The whole-lung models are designed to provide deposition prediction for the whole lung, from the oronasal cavities to the pulmonary region. The whole-lung models are generally semi-empirical and hence provide more reliable results but within the range of parameters used for empirical correlations. The local deposition or computational fluid dynamics (CFD)-based models, on the other hand, utilize comprehensive theoretical and computational approaches but are often limited to upper respiratory tracts. They are based on theoretical principles and are applicable to a wider range of parameters, but less accurate. One of the difficulties with modeling of aerosol deposition in human lung is related to the complexity of the airways geometry and the limited morphometric data available. Another difficulty corresponds to simulation of the realistic physiological conditions of lung environment. Furthermore, complex physical and chemical phenomena associated with dense and multicomponent aerosols complicate the modeling tasks. All of these issues are addressed in this review. The progress made in each area in the last three decades and the challenges ahead are discussed along with some suggestions for future direction. The following subjects are covered in this review: introduction, aerosol deposition mechanisms, elements of a computational model, respiratory-tract geometry models, whole-lung models, CFD based models, cigarette smoke deposition models, and conclusion.
121 citations
Cites methods from "Exact analysis of aerosol depositio..."
...The second approach to deposition modeling is the so-called trumpet lung model proposed by Yu (1978), which was later extended to include coagulation and hygroscopicity of particles relevant to cigarette smoke (Robinson & Yu, 2001)....
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TL;DR: A mathematical model of nanoparticle transport by airflow convection, axial diffusion, and convective mixing (dispersion) was developed in realistic stochastically generated asymmetric human lung geometries and good agreement was found between predicted depositions of ultrafine (nano) particles with measurements in the literature.
Abstract: Increased production of industrial devices constructed with nanostructured materials raises the possibility of environmental and occupational human exposure with consequent adverse health effects. Ultrafine (nano) particles are suspected of having increased toxicity due to their size characteristics that serve as carrier transports. For this reason, it is critical to refine and improve existing deposition models in the nano-size range. A mathematical model of nanoparticle transport by airflow convection, axial diffusion, and convective mixing (dispersion) was developed in realistic stochastically generated asymmetric human lung geometries. The cross-sectional averaged convective-diffusion equation was solved analytically to find closed-form solutions for particle concentration and losses per lung airway. Airway losses were combined to find lobar, regional, and total lung deposition. Axial transport by diffusion and dispersion was found to have an effect on particle deposition. The primary impact was in the pulmonary region of the lung for particles larger than 10 nm in diameter. Particles below 10 nm in diameter were effectively removed from the inhaled air in the tracheobronchial region with little or no penetration into the pulmonary region. Significant variation in deposition was observed when different asymmetric lung geometries were used. Lobar deposition was found to be highest in the left lower lobe. Good agreement was found between predicted depositions of ultrafine (nano) particles with measurements in the literature. The approach used in the proposed model is recommended for more realistic assessment of regional deposition of diffusion-dominated particles in the lung, as it provides a means to more accurately relate exposure and dose to lung injury and other biological responses.
120 citations
Cites background or methods from "Exact analysis of aerosol depositio..."
...There are many deposition models available that are either empirical in nature (Rudolf et al., 1986, 1990), compartmental (ICRP, 1994; NCRP, 1997), or continuous (i.e., mechanistic), based on physics of airflow and particle transport (Yu, 1978a)....
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...In order to develop a simple and mathematically manageable theoretical model, a number of deposition modeling efforts have neglected axial diffusion and dispersion (Anjilvel & Asgharian, 1995; Asgharian et al., 2001; Hofmann & Koblinger, 1990; Yu, 1978a; and others)....
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...(2) and other similar equations have been extended to particles (Darquenne & Paiva, 1994; Hofmann et al., 1994; Taulbee & Yu, 1978) despite being specifically developed for gases....
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...…(Chang & Farhi, 1973; Davidson, 1981; Miller et al., 1985; Overton, 2001; Overton et al., 2001; Pack et al., 1977; Tawhai & Hunter, 2001; Yu, 1975) and particle deposition (Darquenne & Paiva, 1994; Hashish, 1992; Nixon & Egan, 1987; Taulbee & Yu, 1975; Taulbee et al., 1978; Yu, 1978a, b)....
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...For a uniformly expanding and contracting airway, conservation of inhaled mass yields (Yu, 1978a): ∂ A ∂t = −∂ Q ∂x [6] Expanding Eq....
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References
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841 citations
TL;DR: In this paper, the problem of steady state mass diffusion of acrosols without axial diffusion in a long cylindrical channel and for small diffusion parameter, Δ, is presented.
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TL;DR: The calculated results also give information on the amounts deposited in various regions as well as the amounts retained in different fractions of expired air.
263 citations
TL;DR: A convection-diffusion equation for the particle concentration with a loss term is used and an apparent diffusion coefficient due to the velocity dispersion in the lung is present and found to be the dominant diffusion mechanism for the cases considered here.
Abstract: The deposition of inhaled aerosol particles in the human respiratory tract is due to the mechanisms of inertia impaction, Brownian diffusion, and gravitational settling. A theory is developed to predict the particle deposition and its distribution in human respiratory tract for any breathing condition. A convection-diffusion equation for the particle concentration with a loss term is used to describe the transport and deposition of particles. In this equation, an apparent diffusion coefficient due to the velocity dispersion in the lung is present and found to be the dominant diffusion mechanism for the cases considered here. Expressions for deposition by various mechanisms are also derived. The governing equation is solved numerically with Weibel's lung model A. The particle concentration at the mouth is calculated during washin and washout and compared favorably with experimental recordings for 0.5-mum diameter di(2-ethylhexyl) sebacate particles. The total deposition in the lung for particle size ranging from 0.05 to 5 mum is also computed for a 500-cm-3 tidal volume and 15 breaths/min. The results in general agree with recent measurements of Heyder et al. However, a particle size of minimum deposition is found to exist theoretically near 0.3 mum.
151 citations
TL;DR: In this article, a simple analytical calculation method based on the analysis of limiting trajectories of particles is developed which enables the determination of the precipitation efficiency of channels of different cross-sections.
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