Metal fume fever: A case report and literature review

Merchant, John; Webby, Rosalind

doi:10.1046/j.1035-6851.2001.00243.x

Cited by 8 publications

(5 citation statements)

References 11 publications

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“…The latter is seen in workers chronically exposed to high levels of airborne Zn (e.g. during galvanization of iron, welding and manufacture of brass) [220]. Interestingly, instillation of Zn salts into the mouse lung induced necrosis of Type 1 alveolar epithelial cells followed by inflammation and elevation of protein levels in BALF over a 2-week period [221].…”

Section: Zinc Supplementationmentioning

confidence: 97%

Zinc and its Specific Transporters as Potential Targets in Airway Disease

Murgia

Lang

Truong-Tran

et al. 2006

CDT

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The dietary group IIb metal zinc (Zn) plays essential housekeeping roles in cellular metabolism and gene expression. It regulates a number of cellular processes including mitosis, apoptosis, secretion and signal transduction as well as critical events in physiological processes as diverse as insulin release, T cell cytokine production, wound healing, vision and neurotransmission. Critical to these processes are the mechanisms that regulate Zn homeostasis in cells and tissues. The proteins that control Zn uptake and compartmentalization are rapidly being identified and characterized. Recently, the first images of sub-cellular pools of Zn in airway epithelium have been obtained. This review discusses what we currently know about Zn in the airways, both in the normal and inflamed states, and then considers how we might target Zn metabolism by developing strategies to monitor and manipulate airway Zn levels in airway disease.

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Section: Zinc Supplementationmentioning

confidence: 97%

Zinc and its Specific Transporters as Potential Targets in Airway Disease

Murgia

Lang

Truong-Tran

et al. 2006

CDT

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“…In the absence of intact epithelial barrier, the airway lumen may contain harmful substances, which could initiate inflammatory reactions in the submucosa (1)(2)(3). Exposure to high concentration of zinc in the air may cause significant health risk (4). Zinc toxicity can cause acute respiratory tract inflammation together with bronchial hyper-responsiveness.…”

Section: Introductionmentioning

confidence: 99%

Suppression of Gadd45 Alleviates the G2/M Blockage and the Enhanced Phosphorylation of p53 and p38 in Zinc Supplemented Normal Human Bronchial Epithelial Cells

Shih

Wong

Schoene

et al. 2008

Exp Biol Med (Maywood)

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An adequate zinc status is essential for optimal cellular functions and growth. Yet, excessive zinc supplementation can be cytotoxic and can impair cell growth. Gadd45 plays a vital role as cellular stress sensor in the modulation of cell signal transduction in response to stress. The present study was designed to determine the influence of zinc status on Gadd45 expression and cell cycle progression in zinc deficient and supplemented normal human bronchial epithelial (NHBE) cells, and to decipher the molecular mechanism(s) exerted by the suppression of Gadd45 expression on cell growth and cell cycle progression in this cell type. Cells were cultured for one passage in different concentration of zinc: <0.4 muM (ZD) as severe zinc deficient; 4 muM as normal zinc level in culture medium; 16 microM (ZA) as normal human plasma zinc level; and 32 muM (ZS) as the high end of plasma zinc attainable by oral supplementation. Inhibition of cell growth, upregulation of Gadd45 mRNA and protein expression, and blockage of G2/M cell cycle progression were observed in ZS cells. In contrast, little or no changes in these parameters were seen in ZD cells. The siRNA-mediated knocking down of Gadd45 was found to relieve G2/M blockage in ZS cells, which indicated that the blockage was Gadd45 dependent. Moreover, the enhanced phosphorylation of p38 and p53 (ser15) in ZS cells was normalized after suppression of Gadd45 by siRNA, implicating that the enhanced phosphorylation of these proteins was Gadd45 dependent. Thus, we demonstrated for the first time that an elevated zinc status modulated signal transduction to produce a delay at G2/M during cell cycle progression in NHBE cells.

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“…Metal fume fever is a flu-like occupational disease caused by the inhalation of metal fumes, which contain such metals as Zn, Mn, Cu, Cd, Ni, and Al, and which leads to respiratory and systemic syndromes that often occur in workers exposed to metal fumes when welding galvanized metal and melting metal 2 3 4 . Metal fume fever is considered to be a reversible symptom after exposure; however, increasing clinical evidence has found that exposure to metal fumes results in adverse health effects 5 6 . For example, workers using an acetylene torch to dismantle galvanized steel in a poorly ventilated area were diagnosed with diffuse alveolar damage to the lungs 5 .…”

mentioning

confidence: 99%

Physicochemistry and cardiovascular toxicity of metal fume PM2.5: a study of human coronary artery endothelial cells and welding workers

Lai

Chuang

et al. 2016

Sci Rep

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Occupational exposure to welding fumes causes a higher incidence of cardiovascular disease; however, the association remains unclear. To clarify the possible association, exposure assessment of metal fumes with an aerodynamic diameter of <2.5 μm (PM2.5) in welding and office areas was characterized in a shipyard in Taiwan. Cardiovascular toxicity caused by PM2.5 was determined in workers (in both the welding and office areas). Significant amounts of bimodal metal fume particles with count median diameters (CMDs) of 14.1~15.1 and 126.3~135.8 nm were produced in the shipyard. Metal fume PM2.5 resulted in decreased cell viability and increased levels of 8-hydroxy-2’-deoxyguanosine (8-OHdG), interleukin (IL)-6, and nitric oxide (NO) in human coronary artery epithelial cells (HCAECs). We recruited 118 welding workers and 45 office workers for a personal PM2.5 exposure assessment and determination of urinary levels of 8-OHdG, 8-iso-prostaglandin F2α (8-iso-PGF2α), and various metals. We observed that a 10-μg/m3 increase in the mean PM2.5 concentration was associated with a 2.15% increase in 8-OHdG and an 8.43% increase in 8-iso-PGF2α in welding workers. Both 8-OHdG and 8-iso-PGF2α were associated with Fe and Zn in the urine. In conclusion, metal fume PM2.5 could increase the risk of cardiovascular toxicity after inhalation.

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Metal fume fever: A case report and literature review

Cited by 8 publications

References 11 publications

Zinc and its Specific Transporters as Potential Targets in Airway Disease

Zinc and its Specific Transporters as Potential Targets in Airway Disease

Suppression of Gadd45 Alleviates the G2/M Blockage and the Enhanced Phosphorylation of p53 and p38 in Zinc Supplemented Normal Human Bronchial Epithelial Cells

Physicochemistry and cardiovascular toxicity of metal fume PM2.5: a study of human coronary artery endothelial cells and welding workers

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