Metal Fume Fever

Fine, Jonathan; Gordon, Terry; Chen, Lung Chi; Kinney, Patrick; Falcone, Gary; Beckett, William S.

doi:10.1097/00043764-199708000-00006

Cited by 140 publications

(32 citation statements)

References 12 publications

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“…Zinc is a metal with remarkable procoagulant effect (Gilmour et al, 2006; Sangani et al, 2010; Tarantini et al, 2013). Zinc is a common constituent of ambient PM and a workplace toxin that can lead to functional changes in the lung and subsequent systemic inflammation and cardiovascular alterations in humans (Fine et al, 1997). Animal rat models have demonstrated systemic inflammation and procoagulant effects following pulmonary zinc exposure (Gilmour et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Extracellular histones mediate the effects of metal-rich air particles on blood coagulation

Cantone

Angelici

Bollati

et al. 2014

Environmental Research

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Background Epidemiological studies have shown associations of particulate matter (PM) exposure with hypercoagulability and thrombosis. Extracellular circulating histones have recently been identified as novel mediators of inflammatory and procoagulant responses. The potential roles of extracellular histones in PM-related hypercoagulability have yet not been investigated. Objectives In 63 steel workers, we evaluated the effects of exposure to PM and PM metal components on two extracellular histone modifications (H3K4me3 and H3K9ac); and the association of H3K4me3 and H3K9ac with coagulation markers. Methods Extracellular H3K4me3 and H3K9ac were determined in plasma through enzyme-linked immunosorbent assays. Coagulation markers included endogenous thrombin potentials (ETPs), tissue-type plasminogen activator antigen (t-PA) and d-dimer. Exposure to PM with aerodynamic diameters <1 µm (PM1) or <10 µm (PM10) and PM10 metal components were estimated for each participant. Results The coagulation marker ETP, measured in the presence of soluble thrombomodulin (ETP TM+), showed significant positive associations with PM1 (β=107.84, p=0.03), PM10 (β=83.06, p=0.02), and zinc (β=75.14, p=0.03); and a marginal association with iron (β=122.58, p=0.07). Additional PM effects were observed on t-PA, D-dimer, and ETP TM+. PM1 exposure was associated with increased plasma H3K4me3 and H3K9ac (β=0.20, p=0.02; β=0.16, p=0.05, respectively). H3K4me3, but not H3K9ac, was associated with zinc (β=0.13, p=0.03) and iron (β=0.32, p=0.01) contained in PM. ETP TM+ was increased in association with higher plasma H3K4me3 (β=0.50, p=0.05) and H3K9ac (β=0.54, p=0.05). Conclusions This observational study suggests potential roles of extracellular histones in PM-induced hypercoagulability. Experimental studies are warranted to further characterize these findings.

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Section: Discussionmentioning

confidence: 99%

Extracellular histones mediate the effects of metal-rich air particles on blood coagulation

Cantone

Angelici

Bollati

et al. 2014

Environmental Research

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“…96 Pulmonary exposure to ZnO NP generated as a by-product of welding could lead to transient acute lung inflammation, a disease called metal fume fever. 97, 98 Xia et al showed that the toxicity of ZnO was dependent on particle dissolution and shedding of toxic Zn ions. 99 …”

Section: Biological Effectsmentioning

confidence: 99%

A work group report on ultrafine particles (American Academy of Allergy, Asthma & Immunology): Why ambient ultrafine and engineered nanoparticles should receive special attention for possible adverse health outcomes in human subjects

Georas

Alexis

et al. 2016

Journal of Allergy and Clinical Immunology

217

136

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Ultrafine particles are airborne particulates of less than 100 nm in aerodynamic diameter. Examples of ultrafine particles are diesel exhaust particles, products of cooking, heating and wood burning in indoor environments, and more recently, products generated through the use of nanotechnology. Studies have shown that ambient ultrafine particles have detrimental effects on both the cardiovascular and respiratory systems, including a higher incidence of atherosclerosis and the exacerbation rate of asthma. Ultrafine particles have been found to alter in vitro and in vivo responses of the immune system to allergens and may also play a role in allergen sensitization. The inflammatory properties of ultrafine particles may be mediated by a number of different mechanisms, including the ability to produce reactive oxygen species, leading to the generation of pro-inflammatory cytokines and airway inflammation. In addition, because of their small size, ultrafine particles also have unique distribution characteristics in the respiratory tree and circulation and may be able to alter cellular function in ways that circumvent normal signaling pathways. Additionally, ultrafine particles can penetrate intracellularly and potentially cause DNA damage. The recent advances in nanotechnology, while opening up new opportunities for the advancement of technology and medicine, could also lead to unforeseen adverse health effects in exposed humans. Further research is needed to clarify the safety of nanoscale particles, as well as the elucidation of the possible beneficial use of these particulates to treat disease.

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“…[10-14]). However, there are no known long-term effects of ZnO fume inhalation, and there is some evidence that, whilst initial exposures can induce a pulmonary inflammatory response [15-17], humans may develop tolerance to inhaled ZnO fumes upon repeated exposure [18]. …”

Section: Introductionmentioning

confidence: 99%

Surface coatings of ZnO nanoparticles mitigate differentially a host of transcriptional, protein and signalling responses in primary human olfactory cells

Osmond

Oytam

et al. 2013

Part Fibre Toxicol

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BackgroundInhaled nanoparticles have been reported in some instances to translocate from the nostril to the olfactory bulb in exposed rats. In close proximity to the olfactory bulb is the olfactory mucosa, within which resides a niche of multipotent cells. Cells isolated from this area may provide a relevant in vitro system to investigate potential effects of workplace exposure to inhaled zinc oxide nanoparticles.MethodsFour types of commercially-available zinc oxide (ZnO) nanoparticles, two coated and two uncoated, were examined for their effects on primary human cells cultured from the olfactory mucosa. Human olfactory neurosphere-derived (hONS) cells from healthy adult donors were analyzed for modulation of cytokine levels, activation of intracellular signalling pathways, changes in gene-expression patterns across the whole genome, and compromised cellular function over a 24 h period following exposure to the nanoparticles suspended in cell culture medium.ResultsZnO nanoparticle toxicity in hONS cells was mediated through a battery of mechanisms largely related to cell stress, inflammatory response and apoptosis, but not activation of mechanisms that repair damaged DNA. Surface coatings on the ZnO nanoparticles mitigated these cellular responses to varying degrees.ConclusionsThe results indicate that care should be taken in the workplace to minimize generation of, and exposure to, aerosols of uncoated ZnO nanoparticles, given the adverse responses reported here using multipotent cells derived from the olfactory mucosa.

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Metal Fume Fever

Cited by 140 publications

References 12 publications

Extracellular histones mediate the effects of metal-rich air particles on blood coagulation

Extracellular histones mediate the effects of metal-rich air particles on blood coagulation

A work group report on ultrafine particles (American Academy of Allergy, Asthma & Immunology): Why ambient ultrafine and engineered nanoparticles should receive special attention for possible adverse health outcomes in human subjects

Surface coatings of ZnO nanoparticles mitigate differentially a host of transcriptional, protein and signalling responses in primary human olfactory cells

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