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Respiratory particulates deposition

The ICRP (1994b, 1995) developed a Human Respiratory Tract Model for Radiological Protection, which contains respiratory tract deposition and clearance compartmental models for inhalation exposure that may be applied to particulate aerosols of americium compounds. The ICRP (1986, 1989) has a biokinetic model for human oral exposure that applies to americium. The National Council on Radiation Protection and Measurement (NCRP) has also developed a respiratory tract model for inhaled radionuclides (NCRP 1997). At this time, the NCRP recommends the use of the ICRP model for calculating exposures for radiation workers and the general public. Readers interested in this topic are referred to NCRP Report No. 125 Deposition, Retention and Dosimetry of Inhaled Radioactive Substances (NCRP 1997). In the appendix to the report, NCRP provides the animal testing clearance data and equations fitting the data that supported the development of the human mode for americium. [Pg.76]

The size of the fibrous particles that appear to induce disease in the animal models is compatible with the measured respiratory range in humans (Lipp-man, 1977). Most particulate deposition takes place not in the upper or conducting portion of the airways but in the alveolar region of the pulmonary tree (the respiratory unit). Some surface deposition may occur at bifurcations in the bronchial tree, but the actual amount at each location is influenced by anatomy, specific to the species—probably to an individual—as well as the variety of fiber. A large proportion of airborne particulates are rejected as part of the normal clearance mechanisms in animals, but in humans clearance mechanisms may be compromised by smoking, for example. We are unaware of any experiments on fiber toxicity using smoking rats ... [Pg.143]

Respiratory effects typically associated with inhalation of particulates and lung overload have been observed in animals. The pulmonary toxicity of alchlor (a propylene glycol complex of aluminum chlorhydrate), a common component of antiperspirants, was examined in hamsters in a series of studies conducted by Drew et al. (1974). A 3-day exposure to 31 or 33 mg Al/m3 resulted in moderate-to-marked thickening of the alveolar walls due to neutrophil and macrophage infiltration and small granulomatous foci at the bronchioloalveolar junction (a likely site of particulate deposition). A decrease in the severity of the pulmonary effects was observed in animals killed 3, 6, 10, or 27 days after exposure termination. Similar pulmonary effects were observed in rabbits exposed to 43 mg Al/m3 for 5 days (Drew et al. [Pg.42]

Uncertainty of Iodine Particulate Deposition in the Respiratory Tract... [Pg.259]

Particulate deposition s influence on radiation dose to the respiratory tract... [Pg.265]

Other investigators have experimentally or theoretically estimated particulate deposition in the respiratory tract using various experimental techniques (ICRP, 1994 Miller et al., 1988 Stahlhofen et ai, 1983 Yu and Diu, 1982 Yeh and Schum, 1980 Hansen and Ampaya, 1975 Heyder et ai, 1975 Olson et al., 1970 Weibel, 1963). Fractional deposition estimates will be compared by breathing pattern for adult males and females. [Pg.268]

For radionuclides inhaled by workers in particulate form, it is assumed that entry into and regional deposition in the respiratory tract are governed only by the size distribution of the aerosol particles. The situation is different for gases and vapours, for which respiratory tract deposition is material specific. Almost all inhaled... [Pg.35]

The likelihood that materials will produce local effects in the respiratory tract depends on their physical and chemical properties, solubiHty, reactivity with fluid-lining layers of the respiratory tract, reactivity with local tissue components, and (in the case of particulates) the site of deposition. Depending on the nature of the material, and the conditions of the exposure, the types of local response produced include acute inflammation and damage, chronic... [Pg.229]

Health effects attributed to sulfur oxides are likely due to exposure to sulfur dioxide, sulfate aerosols, and sulfur dioxide adsorbed onto particulate matter. Alone, sulfur dioxide will dissolve in the watery fluids of the upper respiratory system and be absorbed into the bloodstream. Sulfur dioxide reacts with other substances in the atmosphere to form sulfate aerosols. Since most sulfate aerosols are part of PMj 5, they may have an important role in the health impacts associated with fine particulates. However, sulfate aerosols can be transported long distances through the atmosphere before deposition actually occurs. Average sulfate aerosol concentrations are about 40% of average fine particulate levels in regions where fuels with high sulfur content are commonly used. Sulfur dioxide adsorbed on particles can be carried deep into the pulmonary system. Therefore, reducing concentrations of particulate matter may also reduce the health impacts of sulfur dioxide. Acid aerosols affect respiratory and sensory functions. [Pg.39]

During occupational exposure, respiratory absorption of soluble and insoluble nickel compounds is the major route of entry, with gastrointestinal absorption secondary (WHO 1991). Inhalation exposure studies of nickel in humans and test animals show that nickel localizes in the lungs, with much lower levels in liver and kidneys (USPHS 1993). About half the inhaled nickel is deposited on bronchial mucosa and swept upward in mucous to be swallowed about 25% of the inhaled nickel is deposited in the pulmonary parenchyma (NAS 1975). The relative amount of inhaled nickel absorbed from the pulmonary tract is dependent on the chemical and physical properties of the nickel compound (USEPA 1986). Pulmonary absorption into the blood is greatest for nickel carbonyl vapor about half the inhaled amount is absorbed (USEPA 1980). Nickel in particulate matter is absorbed from the pulmonary tract to a lesser degree than nickel carbonyl however, smaller particles are absorbed more readily than larger ones (USEPA 1980). Large nickel particles (>2 pm in diameter) are deposited in the upper respiratory tract smaller particles tend to enter the lower respiratory tract. In humans, 35% of the inhaled nickel is absorbed into the blood from the respiratory tract the remainder is either swallowed or expectorated. Soluble nickel compounds... [Pg.450]

The importance of tobacco includes both those constituents in smoke that may interact with nicotine directly, as well as those that indirectly influence a smoker s perception and behaviors. For example, some tobacco smoke constituents may alter the site of absorption of nicotine, such as bronchodilators (e.g., cocoa, licorice), which allow deeper inhalation and subsequent deposition of constituents in more highly permeable areas of the respiratory tract. Likewise, product changes to alter or control particle size, or to provide particulate carriers for vapor-phase smoke constituents, also could facilitate changes at the site of absorption (Ingebrethsen 1993). This would also include the use of acids or bases to alter the form of nicotine and basicity of smoke. Again, a wide range of relevant findings is indicated by internal documents (Ferris Wayne et al. 2006 Keithly et al. 2005 Pankow 2001). [Pg.462]

Particle deposition in the respiratory tract can initiate inflammatory responses. With repeated deposition, inflammation becomes chronic, and the site or sites of deposition beeome laden, not only with the particulates, but with several types of cells—fibroblasts, macrophages, leukocytes, and lymphocytes. These cells are normal constituents of the lung, an organ composed predominantly of connective tissue. Lung connective tissue forms the thin membrane that defines the functional alveolar-capillary unit. Inside this air sac and on the membrane are specialized eells required for gas exchange, maintenance, and repair (Fig. 3.6). [Pg.121]

Respiratory Effects. No studies were located regarding respiratory effects in humans after inhalation exposure to 1,3,5-TNB. One retrospective study (Okubo and Shigeta 1982) of acute occupational exposure to 1,3-DNB dust particles was located. Six workers were removing crystallized 1,3-DNB from a tank and were protected with gauze masks and rubber gloves. Exposure occurred over a period of 6 days. By the end of the exposure period, some of the workers complained of slight dyspnea upon exertion. Inhalation was considered to be a primary route of exposure because a relatively small skin area (face and neck) was exposed. Limitations of this study include lack of information on the concentration of 1,3-DNB in the air, the amount of particulate 1,3-DNB deposited on workers skin, and the exact duration of exposure. [Pg.18]

The chief factor that determines the site of deposition of particulate matter in the respiratory tract is its size. Particles having an aerodynamic diameter of 5-30 pm are primarily... [Pg.6]


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