Toxicology of High-Fired Beryllium Oxide Inhaled by Rodents

Sanders, C.L.; Cannon, W.C.; Powers, G.J.; Adee, R.R.; Meier, D. M.

doi:10.1080/00039896.1975.10666773

Cited by 32 publications

(8 citation statements)

References 7 publications

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“…Low urinary concentration for BeO-F was in accordance with other animal studies which have demonstrated very slow pulmonary clearance for this species (Sanders et al, 1975;Rhoads and Sanders, 1985). It is usually reported that the retention of Be in the lung can play an important role in the development of lung infl ammation (Salehi et al, 2009), but this is not obvious in our study.…”

Section: −1supporting

confidence: 92%

Urinary levels, tissue concentrations and lung inflammation after nose‐only exposure to three different chemical forms of beryllium

Müller¹,

Mazer²,

Salehi³

et al. 2010

J of Applied Toxicology

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This study aimed to determine the toxicity and toxicokinetic of three Be chemical species A total of 120 mice (four groups of 30) were nose-only exposed. The first group was used as a control while the three others were exposed to 250 microg m(-3) of fine particles of three different Be species (Be metal, Be-F; Be oxide, BeO-F; Be aluminium, BeAl-F). Exposure lasted over three consecutive weeks, five days per week and 6 h per day. Blood and several tissues were collected one week after exposure. Urines were collected before the beginning of exposure, at the end of every week of exposure and one week after exposure. Results showed that urine concentrations were different from one Be species to another and that excretion continued after the end of exposure. Except for BeO-F, where Be urine concentrations were stable during the three weeks of exposure, concentrations of Be-F and BeAl-F reached a peak after the first week. According to particle size, BeO-F obtained the highest theoretical pulmonary deposition rate, which partially led to the highest Be lung concentration. This group also presented the lowest urine concentration but that did not lead to more severe lung inflammation. Moreover, even if BeAl-F obtained the lowest percentage theoretical pulmonary deposition, it showed the highest Be urinary concentration, the lowest Be lung concentration and the lowest lung toxicity. In this specific case, a high Be concentration in urine did not reflect a high exposure or a severe toxic effect.

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Section: −1supporting

confidence: 92%

Urinary levels, tissue concentrations and lung inflammation after nose‐only exposure to three different chemical forms of beryllium

Müller¹,

Mazer²,

Salehi³

et al. 2010

J of Applied Toxicology

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“…Similar peripheral accumulations of dust have been observed in the rodent lung following exposure to beryllium oxide (Sanders and Cannon, 1975) and in rodent, dog and human lungs following exposure to plutonium oxide (Clarke and Bair, 1964;Sanders and Dagle, 1974;Voelz et al, 1976). If asbestos fibres are transported in a similar manner to the periphery of the human lung, this could be an important factor in the aetiology both of asbestosis, which generally appears to affect subpleural areas first (Becklake, 1976) and of asbestos-induced mesothelial tumours.…”

supporting

confidence: 56%

Significance of fibre length in the clearance of asbestos fibres from the lung.

Morgan¹,

Talbot²,

Holmes³

1978

Occupational and Environmental Medicine

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Rats were exposed by inhalation to radioactive anthophyllite asbestos. Animals were then killed serially over a period of 205 days and the fibre content of the lungs measured radiometrically. The lungs were subjected to selective bronchopulmonary lavage and the mean fibre content determined of free cells recovered from the alveolar spaces. The length distributions of fibres recovered from the lungs by lavage, and of those remaining in the lungs following lavage, were measured. Short (less than 5 ,um) fibres are cleared from the lung via the conducting airways more efficiently than longer fibres and fibres exceeding 50 ,m in length are not removed from the lungs by this route. Although fibres of about 200 jum in length were present in all the lungs examined, the longest which could be recovered by lavage, once fibre deposited in the airways had been cleared, was only about 100 ,tm decreasing to 60-70 ,um after 205 days. It is suggested that long fibres are more liable than short to penetrate the alveolar wall as they tend to bridge the alveolar ducts and alveoli.It has been shown by Morgan et al. (1977a) using autoradiographic techniques that when small amounts of asbestos are deposited in the rat lung the fibres tend, in the course of time, to accumulate not only in the tracheobronchial lymph nodes but also in subpleural foci. Similar peripheral accumulations of dust have been observed in the rodent lung following exposure to beryllium oxide (Sanders and Cannon, 1975) and in rodent, dog and human lungs following exposure to plutonium oxide (Clarke and Bair, 1964;Sanders and Dagle, 1974;Voelz et al., 1976). If asbestos fibres are transported in a similar manner to the periphery of the human lung, this could be an important factor in the aetiology both of asbestosis, which generally appears to affect subpleural areas first (Becklake, 1976) and of asbestos-induced mesothelial tumours. If, as seems likely, this movement occurs within or through the alveolar wall rather than over its surface, then it is important to know how the dimensions of asbestos fibres affect their penetration into the interstitium.To investigate the fate of asbestos fibres deposited in the rat lung, the selective bronchopulmonary lavage procedure of Brain and Frank (1973) applied by Morgan et al. (1977b) to the lungs of animals killed serially following exposure to radioactive asbestos by inhalation. In this technique the initial washings are with a balanced salt solution containing calcium and magnesium. Under these circumstances relatively few cells (only those which are loosely attached) are washed out of the lung. These include alveolar macrophages which are present on the mucous layer in the conducting airways and which are in the process of being removed from the lung. On subsequent washing with physiological saline, in the absence of divalent cations, alveolar macrophages detach themselves from the alveolar wall and are recovered in large numbers. To determine the length distribution of fibres present in the various washes, a ...

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“…These data are similar to those reported by others (55,56,58) in which foreign-body type granulomatous inflammation of the lung occured after inhalation exposure of rats to Be materials. In these previous reports, lymphocytes were not a significant component of the lesions, and granuloma formation either did not occur or was limited to that associated with cholesterol cleft formation, an indicator of cell necrosis.…”

Section: Chronic Beryllium Diseasesupporting

confidence: 93%

Mechanisms of Granulomatous Lung Disease from Inhaled Beryllium: The Role of Antigenicity in Granuloma Formation*1

Haley

1991

Toxicologic Pathology

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Granulomatous lung disease is a debilitating and sometimes fatal condition encountered in humans, for which the cellular and molecular mechanisms are poorly understood. Two patterns of granulomatous lung disease are recognized; foreign-body reactions and immune-mediated granulomas. Beryllium inhalation by humans results, in a small number of exposed individuals, in a chronic, granulomatous, immune-mediated pulmonary disease (chronic beryllium lung disease, CBD). Animal models used to study CBD have demonstrated significant species differences in the pathologic response to beryllium. While rats exposed to beryllium appear to develop a chronic, foreign-body response within the lung, dogs so exposed develop beryllium-specific immune responses within the lung and blood, accompanied by immune granulomas within the lung. At the heart of this difference appears to be the ability of the dog, but not the rat, to immunologically recognize the antigenicity of beryllium. This important difference further underscores the need to understand the mechanistic differences among similar disease syndromes, particularly if therapeutic regimens are to be used.

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Toxicology of High-Fired Beryllium Oxide Inhaled by Rodents

Cited by 32 publications

References 7 publications

Urinary levels, tissue concentrations and lung inflammation after nose‐only exposure to three different chemical forms of beryllium

Urinary levels, tissue concentrations and lung inflammation after nose‐only exposure to three different chemical forms of beryllium

Significance of fibre length in the clearance of asbestos fibres from the lung.

Mechanisms of Granulomatous Lung Disease from Inhaled Beryllium: The Role of Antigenicity in Granuloma Formation*1

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