Metal fume fever: a case report and review of the literature

Kaye, Philip; Young, Holly; O’Sullivan, I

doi:10.1136/emj.19.3.268

Cited by 31 publications

(16 citation statements)

References 3 publications

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“…It has been shown that ZnO increases the production of oxygen radicals from human neutrophils (Lindahl et al 1998), which may contribute to the pathogenesis of zinc fume fever (Kaye et al 2002). ZnO nanoparticles have also been shown to increase TNF-α, IL-6 and IL-8 production, which can lead to metal fume fever in welders (Xia et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Transport of metal oxide nanoparticles and single-walled carbon nanotubes in human mucus

et al. 2011

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Whether mucus layers lining entrance points into the body, including the lung airways, provide protection against the penetration of engineered nanoparticles remains poorly understood. We measured the diffusion coefficients of hundreds of individual nanoparticles of three different metal oxides (nMeOs) and two types of single-walled carbon nanotubes (SWCNTs) in undiluted human mucus. We found that the vast majority of these nanoparticles are efficiently trapped in human mucus and, further, that the mechanism of trapping is adhesive interactions as opposed to steric obstruction. However, a small fraction of zinc oxide (ZnO) nanoparticles moved at rates fast enough to penetrate airway mucus layers. We conclude that human mucus layers probably provide considerable protection for mucosal tissues from the penetration of most nMeOs and SWCNTs, and suggest that further investigation of the potential health risks of exposure to ZnO nanoparticles is warranted.

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Section: Discussionmentioning

confidence: 99%

Transport of metal oxide nanoparticles and single-walled carbon nanotubes in human mucus

et al. 2011

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“…Although a high level of suspicion for arsenic poisoning must be maintained because of its role in poisoning, it is rarely seen clinically. [27][28][29][30][31] Physical findings in arsenic toxicity vary with age and dose. Any combination of GI complaints, neurologic dysfunction, and anemia should prompt a search for arsenic toxicity.…”

Section: Disposal Considerationsmentioning

confidence: 99%

“…Generally, children are more susceptible to the toxic effects of the heavy metals and are more prone to accidental exposures. [27][28][29][30][31] Arsenic is a naturally occurring element widely distributed in the earth's crust. It combines with oxygen and other elements to form inorganic arsenic compounds.…”

Section: Disposal Considerationsmentioning

confidence: 99%

Physico-chemical properties and toxic effect of fruit-ripening agent calcium carbide

Asif¹

2012

Ann Trop Med Public Health

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Ripening is the final stage of the maturation process, when the fruit changes color, softens and develops the flavor, texture and aroma that constitute optimum eating quality. This study was conducted to discuss the use of unsatisfactory calcium carbide to ripen fruits for domestic markets as well as their toxic effects on human health. The commonly used ripening agents are calcium carbide, acetylene, ethylene, propylene, ethrel (2-chloroethyl phosphonic acid), glycol, ethanol and some other agents. The calcium carbide is one of the most commonly used ripening agent for fruits, while other calcium salts like calcium ammonium nitrate, calcium chloride and calcium sulfate are used to delay fruit ripening agents for local fruit industries. The use of calcium carbide is being discouraged worldwide, due to associated health hazards. Calcium carbide treatment of food is extremely hazardous because it contains traces of arsenic and phosphorous, and once dissolved in water, it produces acetylene gas. Arsenic, phosphorous and acetylene gas may affect the different body organs and causes various health problems like headache, dizziness, mood disturbances, sleepiness, mental confusion, memory loss, cerebral edema, seizures and prolonged hypoxia. Asif: Toxic effect of calcium carbide Cite this article as: Asif M. Physico-chemical properties and toxic effect of fruit-ripening agent calcium carbide. Ann Trop Med Public Health 2012;5:150-6.

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“…ZnO particles are toxic within several different cell types; In vitro , they have been shown to cause oxidative stress [30-33], to trigger an anti-oxidative response [30,34], to promote inflammation [30,35-37] and to elicit cytotoxic effects [13,30-32,38]. Furthermore, occupational medicine has long - standing experience with “metal fume fever”, a classical flu like inflammatory disease among workers exposed to metal oxide, mainly ZnO, aerosols (“fumes”) released during such processes as welding, heating and cutting of galvanized metals [29,39-41]. …”

Section: Introductionmentioning

confidence: 99%

Effects of flame made zinc oxide particles in human lung cells - a comparison of aerosol and suspension exposures

et al. 2012

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BackgroundPredominantly, studies of nanoparticle (NPs) toxicology in vitro are based upon the exposure of submerged cell cultures to particle suspensions. Such an approach however, does not reflect particle inhalation. As a more realistic simulation of such a scenario, efforts were made towards direct delivery of aerosols to air-liquid-interface cultivated cell cultures by the use of aerosol exposure systems.This study aims to provide a direct comparison of the effects of zinc oxide (ZnO) NPs when delivered as either an aerosol, or in suspension to a triple cell co-culture model of the epithelial airway barrier. To ensure dose–equivalence, ZnO-deposition was determined in each exposure scenario by atomic absorption spectroscopy. Biological endpoints being investigated after 4 or 24h incubation include cytotoxicity, total reduced glutathione, induction of antioxidative genes such as heme-oxygenase 1 (HO–1) as well as the release of the (pro)-inflammatory cytokine TNFα.ResultsOff-gases released as by-product of flame ZnO synthesis caused a significant decrease of total reduced GSH and induced further the release of the cytokine TNFα, demonstrating the influence of the gas phase on aerosol toxicology. No direct effects could be attributed to ZnO particles. By performing suspension exposure to avoid the factor “flame-gases”, particle specific effects become apparent. Other parameters such as LDH and HO–1 were not influenced by gaseous compounds: Following aerosol exposure, LDH levels appeared elevated at both timepoints and the HO–1 transcript correlated positively with deposited ZnO-dose. Under submerged conditions, the HO–1 induction scheme deviated for 4 and 24h and increased extracellular LDH was found following 24h exposure.ConclusionIn the current study, aerosol and suspension-exposure has been compared by exposing cell cultures to equivalent amounts of ZnO. Both exposure strategies differ fundamentally in their dose–response pattern. Additional differences can be found for the factor time: In the aerosol scenario, parameters tend to their maximum already after 4h of exposure, whereas under submerged conditions, effects appear most pronounced mainly after 24h. Aerosol exposure provides information about the synergistic interplay of gaseous and particulate phase of an aerosol in the context of inhalation toxicology. Exposure to suspensions represents a valuable complementary method and allows investigations on particle-associated toxicity by excluding all gas–derived effects.

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Metal fume fever: a case report and review of the literature

Cited by 31 publications

References 3 publications

Transport of metal oxide nanoparticles and single-walled carbon nanotubes in human mucus

Transport of metal oxide nanoparticles and single-walled carbon nanotubes in human mucus

Physico-chemical properties and toxic effect of fruit-ripening agent calcium carbide

Effects of flame made zinc oxide particles in human lung cells - a comparison of aerosol and suspension exposures

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