Theoretical models of respiratory tract deposition of inhaled particles are compared to experimental studies of deposition patterns in humans and animals, as determined principally by particle size, density, respiratory rate and flow parameters. Various models of inhaled particle deposition make use of convenient approximations of the respiratory tract to predict tractional deposition according to fundamental physical processes of impaction, sedimentation, and difussion. These theoretical models for both total deposition and regional Inasopharyngeal, tracheobronchial, and pulmonary) deposition are compared with experimental studies of inhaled dusts in humans or experimental animals that have been performed in many laboratories over several decades. Reasonable correlation has been obtained between theoretical and experimental studies, but the behavior of very fine (<0.01 inn) particles requires further refinement. Properties of particle shape, charge, and hygroscopicity as well as the degree of respiratory tract pathology also influence deposition patterns and further experimental work is urgently needed in these areas. The influence upon deposition patterns of dynamic alterations in inspiratory flow profiles caused by a variety of breathing patterns also requires further study, and the use of such techniques with selected inhaled particle size holds promise in possible diagnostic aid in diagnosis of normal versus disease conditions. Mechanisms of conducting airway and alveolar clearance processes involving mucociliary clearance, dissolution, transport to systemic circulation, and translocation via regional lymphatic clearance are discussed. The roles of the pulmonary macrophage in airway and alveolar clearance are described, and the applicability of recent solubility models for translocation or deposited materials to liver, skeleton, or other systemic organs is discussed.

No abstract

The development of theoretical models and the experimental studies that have been done describe the deposition of aerosols in the respiratory tract as a function of particle size and respiration patterns. Descriptions of the anatomical structure of the respiratory tract, air flows, and the physical behavior of airborne particles illustrate the basis of the various models of inhaled particle deposition. Particle density, shape, hygroscopicity, and pathology influence particle deposition, and the particle size distribution and deposition site of the inhaled aerosol influence the resultant biological response.The possible cause-and-effect rela¬ tionships between inhalation of airborne particles and pulmonary or systemic disease have been recog¬ nized for several hundred years. In 1556, Agricola described the condi¬ tions of mining in the region of Sax¬ ony and the pathological effects re¬ sulting from such work.1 In 1865, Siegle reported experiments indicat¬ ing penetration of airborne materials deep into the lungs.2 Zenker, in 1867, proposed the term "pneumonokoniosis" to describe the severe pulmo¬ nary diseases prevalent in dusty trades, including silicatosis, anthracosis, siderosis, and byssinosis.1 Shortly after the discovery of bac¬ teria a century ago, associations were suggested between the inhalation of airborne microorganisms and subse¬ quent development of tuberculosis4 and anthrax.5 At the beginning of the 20th century, the increased levels of pulmonary disease among miners of silica-bearing ores were ascribed to fine, hard particles of rock dust in the mine atmosphere.6 The critical role of particle size in the development of silicosis was indicated by the studies of Watkins-Pitchford and Moir, who found 80% of the particles in silicotic lungs to be less than 2ju.7 In 1923, Mavrogordato stated that phthisis was caused by free silica particles of 0.5]ii to 5|ii diameter.8 It is currently believed that the effective dose of quartz-bearing material needed to produce silicosis may be less than 1% of the total dust inhaled over many years. Exposure to aerosols of fresh, finely divided zinc oxide (< 0.6ju) pro¬ duces "metal-fume fever," but expo¬ sure for equal times to equal air con¬ centrations of zinc oxide particulates generated from a bulk volume may produce no detectable effect." Thus, it became increasingly evident that knowledge of the concentration of an airborne contaminant and the total inhaled air volume involved was not sufficient to reliably predict the physi¬ ological or pathological results of in¬ halation exposure. Further informa¬ tion was urgently needed concerning the depth of penetration and frac¬ tional removal of specific sized par¬ ticles to determine the critical sites of action, related clearance mechanisms, probability of infection by inhaled pathogens, and translocation and ex¬ cretion patterns of inhaled particu¬ late materials. This review begins with brief de¬ scriptions of the anatomical and physiological aspects of the lung that regulate airflow, and the basic physi¬ cal proces...

No abstract

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) and Brogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.Theoretical models of respiratory tract deposition of inhaled particles are compared to experimental studies of deposition patterns in humans and animals, as determined principally by particle size, density, respiratory rate and flow parameters. Various models of inhaled particle deposition make use of convenient approximations of the respiratory tract to predict tractional deposition according to fundamental physical processes of impaction, sedimentation, and difussion. These theoretical models for both total deposition and regional nasopharyngeal, tracheobronchial, and pulmonary t deposition are compared with experimental studies of inhaled dusts in humans or experimental animals that have been performed in many laboratories over several decades. Reasonable correlation has been obtained between theoretical and experimental studies, but the behavior of very fine 4<0.01 1lm} particles requires further refinement. Properties of particle shape, charge, and hygroscopicity as well as the degree of respiratory tract pathology also influence deposition patterns and further experimental work is urgently needed in these areas. The influence upon deposition patterns of dynamic alterations in inspiratory flow profiles caused by a variety of breathing patterns also requires further study, and the use of such techniques with selected inhaled particle size holds promise in possible diagnostic aid in diagnosis of normal versus disease conditions. Mechanisms of conducting airway and alveolar clearance processes involving mucociliary clearance, dissolution, transport to systemic circulation, and translocation via regional Iymphatic clearance are discussed. The roles of the pulmonary macrophage in airway and alveolar clearance are described, and the applicability of recent solubility models for translocation or deposited materials to liver, skeleton, or other systemic organs is discussed. reliabley to predict the physiological or pathological results of inhalation exposure. Additional information is urgently needed concerning the depth of penetration and fractional removal of inhaled particles to determine their critical sites of action and their related clearance mechanisms. Clarification is also needed of interrelated roles of aerosol parameters such as size, shape, density, hydroscopicity and electric charge as these determine the sites of deposition of particles in the respiratory tract. In addition the physiological parameters that affect dsposition of aerosols need further definition. These may involve...