Distribution of Inhaled Metal Oxide Particles in Pulmonary Alveoli

Sanders, C.L.

doi:10.1001/archinte.1971.00310180101014

Cited by 14 publications

(3 citation statements)

References 9 publications

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“…Kaolinite, silica, and other silicates in the particles were present. 137 Though extensive large aluminum silicate inclusions in alveolar macrophages of smokers were described in earlier citations, [103][104][105][106] Becker et al stated that neutrophils exhibited a stronger oxidative response to silicate exposure, whereas alveolar macrophages exhibited stronger response to oil fly ash particulate (higher in transition metals, lower in silicate, 138 and consistent with the data from Sanders et al 122 and suggested that wide variation in macrophage response to metal oxide or silica was likely associated with particle composition. They concluded that reactive oxidant activation as a consequence of various sources of particulate matter is cell specific, and that the inflamed lung is more susceptible to harm from a broader range of particulate size and composition because of the oxidant stress posed.…”

Section: Toxicological Consequences Of Metallo-particle Inhalation Spsupporting

confidence: 75%

“…The authors pointed out that neutrophils were rarely observed in alveolar lumens of hamsters exposed to only NiO, and that observed vacuolization was a more common finding in macrophages from animals which were also exposed to cigarette smoke. 122 Gilmour et al demonstrated that intratracheal exposure of rats to either high transition metal-containing residual oil fly ash particulate or its major constituent metals alone (nickel or vanadium) caused significant pulmonary inflammation. Increased protein levels and TNF-α, monocyte and granulocyte migration to the site were observed.…”

Section: Immune Cells and Metallo-particles: Mixed Immunological Actimentioning

confidence: 99%

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Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

2011

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Biochemically and pathologically, there is strong evidence for both atopic and nonatopic airway sensitization, hyperresponsiveness, and inflammation as a consequence of exposure to tobacco mainstream or sidestream smoke particulate. There is growing evidence for the relation between exposure to mainstream and sidestream smoke and diseases resulting from reactive oxidant challenge and inflammation directly as a consequence of the combined activity of neutrophils, macrophages, dendritic cells, eosinophils, basophils, as a humoral immunological consequence of sensitization, and that the metal components of the particulate play a role in adjuvant effects. As an end consequence, carcinogenicity is a known outcome of chronic inflammation.Smokeless tobacco has been evaluated by the IARC as a group 1 carcinogen. Of the many harmful constituents in smokeless tobacco, oral tissue metallothionein gradients suggest that metals contribute to the toxicity from smokeless tobacco use and possibly sensitization.This work reviews and examines work on probable contributions of toxic metals from tobacco and smoke to pathology observed as a consequence of smoking and the use of smokeless tobacco. Metals and metalloids in tobaccoThough exposure to substances from tobacco use is obviously a complex exposure, the carcinogens in tobacco smoke have been classified for health risk determinations into five major chemical classes. 1 Some of these have been carefully studied, contributing to a strong weight of evidence for associated health risks. 2 Toxic metals and metalloids constitute one of the more understudied major carcinogenic chemical classes in smokeless tobacco products and tobacco smoke. Eight of the top forty substances in the Fowles and Dybing table of cancer risk indices are metals or metalloid compounds. 1 In their table of non-cancer risk indices for individual chemical constituents of mainstream cigarette smoke based on a single cigarette per day, three of the top eight listed for respiratory effect health risk, cadmium, hexavalent chromium, and nickel, were metals. Another metalloid, silicon in the form of silicates, poses serious health risks by inhalation, but limited data is available, likely due to analytical difficulties.Metals and metalloids in smoke from biomass combustion including tobacco are generally considered to be present in ionic form, but may also occur in a gaseous elemental form, as is the case for mercury. 3 Whether a tobacco product is consumed by smoking or in a smokeless form, the exposure to toxic metals is directly related to the concentration in the tobacco leaf, assuming no metal containing additives are included during manufacture. [4][5][6] The soil (including any amendments to the soil such as sludge, fertilizers, or irrigation with

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Section: Toxicological Consequences Of Metallo-particle Inhalation Spsupporting

confidence: 75%

Section: Immune Cells and Metallo-particles: Mixed Immunological Actimentioning

confidence: 99%

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

2011

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“…Acute exposure to cigarette smoke has been shown to inhibit the bactericidal activity of alveolar macrophages cultured in vitro (6, 7) and the ability of mouse alveolar macrophages to phagocytose inhaled particles (22). However, the effect of chronic inhalation of cigarette smoke on phagocytic and bactericidal activities is not clear.…”

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confidence: 99%

Cigarette smoke and phagocyte function: effect of chronic exposure in vivo and acute exposure in vitro

Thomas¹,

Holt²,

Keast³

1978

Infect Immun

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Phagocytic function was studied in mice chronically exposed to cigarette smoke, and the effects of in vitro exposure to cigarette smoke on macrophage activity were also assessed. Cultures of radiolabeled Pseudomonas aeruginosa were employed to investigate phagocyte activity in vivo and in vitro. Mice were exposed on weekdays to fresh cigarette smoke for periods up to 37 weeks and the bactericidal and clearance activity of their lungs was measured. Both pulmonary clearance and bactericidal activity was impaired. The clearance of intravenously injected bacteria from the blood of smoke-exposed mice occurred at the same rate as in control mice, but the accumulation of radiolabel by the liver was decreased. In addition, the rate of elimination of radiolabel from the liver was less than the controls. Macrophages exposed to cigarette smoke in vitro initially had a depressed phagocytic rate, but if phagocytosis over a prolonged period was measured it was eventually enhanced over the rate of control macrophages. The vapor phase of cigarette smoke could also transiently inhibit and then enhance the phagocytic activity.

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Alveolar Clearance of Aerosols

Morrow¹

1973

Arch Intern Med

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The alveolar region of the lungs is endowed with several "cleansing" mechanisms whereby nongaseous substances of intrinsic and extrinsic origins are continuously removed. Collectively, the clearance mechanisms and pathways can be categorized into those effecting the removal of the readily transportable materials, eg, dissolved or monomeric substances, by passive and active absorption processes; and of the more persistent, less easily transportable materials, eg, "insoluble" dusts, by endocytosis and dissolution. The author critically assesses various clearance concepts and reviews the salient physiological and anatomical considerations that underly these concepts.

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Distribution of Inhaled Metal Oxide Particles in Pulmonary Alveoli

Cited by 14 publications

References 9 publications

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

Cigarette smoke and phagocyte function: effect of chronic exposure in vivo and acute exposure in vitro

Alveolar Clearance of Aerosols

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