The Lung in Metal Fume Fever

Blanc, Paul D.; Boushey, Homer A.

doi:10.1055/s-2007-1006321

Cited by 13 publications

(2 citation statements)

References 49 publications

(78 reference statements)

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“…Exposure to fly ash, which occurs in a variety of occupational and environmental settings, has been linked with lung function decline including obstructive lung disease (13) and interstitial fibrosis (14). Further, inhalation of zinc oxide fume in high concentration is a wellestablished cause of the occupational flulike syndrome metal fume fever (15)(16)(17). We have previously reported a pulmonary inflammatory cellular response in healthy humans following experimental inhalational exposure to zinc oxide fume (18)(19)(20).…”

mentioning

confidence: 99%

Human Pulmonary Responses to Experimental Inhalation of High Concentration Fine and Ultrafine Magnesium Oxide Particles

Kuschner¹,

Wong²,

D’Alessandro³

et al. 1997

Environmental Health Perspectives

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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.Exposure to air polluted with particles less than 2.5 pm in size is associated epidemiologically with adverse cardiopulmonary health consequences in humans. The goal of this study was to characterize human pulmonary responses to controlled experimental high-dose exposure to fine and ultrafine magnesium oxide particles. We quantified bronchoalveolar lavage (BAL) cell and cytokine concentrations, pulmonary function, and peripheral blood neutrophil concentrations in six healthy volunteers 18 to 20 hr after inhalation of fine and ultrafine magnesium oxide particles produced from a furnace system model. We compared postexposure studies with control studies from the same six subjects. Mean ? standard deviation (SD) cumulative magnesium dose was 4,138 ? 2,163 min x mg/m3. By weight, 28% of fume particles were ultrafine (<0.1 pm in diameter) and over 98% of fume particles were fine (<2.5 pm in diameter). There were no significant differences in BAL inflammatory cell concentrations, BAL interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor, pulmonary function, or peripheral blood neutrophil concentrations postexposure compared with control. Our findings suggest that high-dose fine and ultrafine magnesium oxide particle exposure does not produce a measurable pulmonary inflammatory response. These findings are in marked contrast with the well-described pulmonary inflammatory response following zinc oxide particle inhalation. We conclude that fine and ultrafine particle inhalation does not result in toxicity in a generic manner independent of particle composition. Our findings support the concept that particle chemical composition, in addition to particle size, is an important determinant of respiratory effects.

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mentioning

confidence: 99%

Human Pulmonary Responses to Experimental Inhalation of High Concentration Fine and Ultrafine Magnesium Oxide Particles

Kuschner¹,

Wong²,

D’Alessandro³

et al. 1997

Environmental Health Perspectives

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“…5.1.2.1. Fièvre des métaux La fièvre des métaux est une entité faisant partie intégrante des fièvres d'inhalation.Cette pathologie est également connue sous les noms de « fièvre du lundi » et « fièvre des fondeurs ou des soudeurs », ces deux professions étant les plus exposées aux fumées d'oxydes métalliques[39][40][41]. Elle peut survenir lors de l'inhalation de fumées d'oxydes métalliques, notamment de fumées d'oxyde de zinc, qui reste la mieux documentée.…”

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Intoxication aiguë et chronique au cadmium

Andujar

Bensefa‐Colas

Descatha

2010

La Revue de Médecine Interne

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Cadmium is a metallic impurity in various minerals. The two main cadmium exposure sources in general population are food and tobacco smoking. Its industrial exploitation has grown in the early twentieth century. Cadmium is used in accumulators or alkaline batteries (80%) and in pigments for paints or plastics (10%), in electrolytic process by deposit or by cadmium plating on metals or to reduce melting points (welding rods...). Cadmium is a cumulative toxic substance whose half-time for elimination is about 20 to 40 years and it is mainly stored in the liver and kidneys. Inhalation of cadmium oxide fumes may cause inhalation fevers or chemical pneumonitis. Cadmium chronic poisoning causes mainly renal tubulopathy and could be the cause of osteomalacia and diffuse osteoporosis. Cadmium is classified as certain carcinogen agent for humans by International Agency for Research on Cancer (IARC). The most relevant biological index exposure is the urinary cadmium. According to literature, no chelating agent can be still used in human cadmium poisonings. In France, some diseases caused by occupational exposure to cadmium may be compensated.

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