Manganese exposure in foundry furnacemen and scrap recycling workers

Lander, Flemming; Kristiansen, Jesper; Lauritsen, Jens

doi:10.1007/s004200050414

Cited by 38 publications

(23 citation statements)

References 16 publications

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“…Researchers have pointed out that the consequences of exposure to manganese in the workplace and uptake of this element in the body will bring about the central nervous system disorder, which would be called manganism, as the complications; there are many similarities with Parkinson's disease [5][6][7][8][9][10][11][12]. One of the most important scientific methods, particularly to determine the exposure to pollutants, is biological monitoring of workplaces [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Correlation between airborne manganese concentration at the workstations in the iron foundry and manganese concentration in workers’ blood

Mirmohammadi¹,

Moghaddasi²,

Yazdani³

et al. 2017

Med Pr

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Background: Manganese (Mn) used as raw material for melting process in the ferrous foundry is considered as hazardous neurotoxic substance because it accumulates in the central nervous system and may cause neurological disorders. The furnace-men and melting department workers are potentially exposed to manganese particles or fume in the workplace. The objective of the research has been to investigate the sources and levels of manganese exposure in the foundry by correlation of blood-manganese (B-Mn) and air-manganese (air-Mn) measurement. Material and Methods: Air-Mn and Mn of blood serum were measured involving workers who worked in a big-sized foundry during 1 year. The standard method of the Occupational Safety and Health Administration (OSHA) ID-121 was used for air and blood assessment and atomic absorption spectroscopy (AAS) was carried out for air and blood sample analysis. Results: The air sampling results have revealed that there is a high exposure to manganese (4.5 mg/m 3 ) in the workplace as compared to the National Institute for Occupational Safety and Health's (NIOSH) time weighted average (the reference time-weighted average (TWA) = 1 mg/m 3 ). The average blood serum Mn concentration was 2.745 μg/l for subjects working for shorter than 3 months and 274.85 μg/l for subjects working 3-12 months. Conclusions: Against the research hypothesis there was no correlation between the air-Mn concentration and the B-Mn (serum) level of manganese in the serum of the exposed subjects. It may be due to short time of air sampling of manganese airborne particles, and a real-time monitoring of airborne manganese particles is suggested for any future study. Med Pr 2017;68(4): [449][450][451][452][453][454][455][456][457][458]

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Section: Introductionmentioning

confidence: 99%

Correlation between airborne manganese concentration at the workstations in the iron foundry and manganese concentration in workers’ blood

Mirmohammadi¹,

Moghaddasi²,

Yazdani³

et al. 2017

Med Pr

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“…29 Manganese levels in urine and feces my be used as a marker for exposure to manganese within the previous few hours, whereas manganese can be detected in blood for days to weeks after exposure ceases. 30 Although present occupational standards for exposure levels for manganese in total dust causing neurologic effects have been estimated to be approximately 0.2 mg/m 3 , this threshold limit value (TLV) has never been validated by well-designed scientific studies. 31 Manganeseinduced neurotoxicity has been reported to occur only after chronic exposure to high levels of manganese, 26 usually above the permissible exposure limit ceiling at 5 mg/m 3 set by the Occupational Safety and Health Administration.…”

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confidence: 99%

Searching for a relationship between manganese and welding and Parkinson’s disease

Jankovic

2005

Neurology

153

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Abstract-Research into the causes of Parkinson disease (PD) has accelerated recently with the discovery of novel gene mutations. The majority of PD cases, however, remain idiopathic and in those cases environmental causes should be considered. Several recent reports have focused on welding and manganese toxicity as potential risk factors for parkinsonism and some have even proposed that welding is a risk factor for PD. The controversy has stimulated this review, the primary aim of which is to critically and objectively examine the evidence or lack of evidence for a relationship among welding, manganese, parkinsonism, and PD. NEUROLOGY 2005;64:2021-2028 Parkinson disease (PD) is one of the most common neurodegenerative disorders, affecting approximately 1 million Americans and 1 to 2% of those over age 60 worldwide.1-3 With the lifetime risk of 2% and an increasing incidence with age, coupled with aging of the population, the prevalence of PD is expected to triple over the next 50 years.Despite the growing number of newly identified genetic causes of parkinsonism, 4,5 in the majority of cases the cause is unknown, hence the enormous interest in the role of environmental factors in various parkinsonian disorders.6,7 While numerous toxins have been found to produce nigrostriatal degeneration in experimental animals, 8 there is no evidence that any environmental toxin causes PD. A variety of environmental and occupational exposures, however, have been implicated in the etiology of PD. These include exposure to well water, pesticides, herbicides, rural living, certain metals, fuel oil, magnetic fields, and employment in the steel/alloy industry, wood/pulp plants, farming, carpentry, cleaning, orchards, planer mill, forestry, logging, mining, as well as certain occupations such as body and fender repairmen, auto painters, railroad and car shop mechanics, and workers in oil and gas fields. [9][10][11][12][13][14][15][16][17] In the recent past, several reports have also suggested that welders may be at a higher risk for developing parkinsonism, and some have even proposed that welding is a risk factor for PD.18,19 These claims have entered the legal system and numerous lawsuits have been filed on behalf of welders alleging that toxic fumes generated by the welding rods have caused not only parkinsonism, but also PD. In this review, we intend to examine the evidence for and against a relationship among welding, manganese, parkinsonism, and PD.With the discovery of new causes of parkinsonism and with the recognition that the same etiology (e.g., a single gene mutation) can be associated with markedly diverse pathology, the traditional view that pathologic examination is the gold standard in the diagnosis of PD has been recently challenged. 20,21 In this review, unless a specific etiologic cause is identified, we will define PD based on clinical-pathologic criteria.22 This approach is supported by several studies demonstrating that when PD is diagnosed clinically by expert parkinsonologists, the autopsy confirms the diagn...

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“…Under physiological conditions, Mn(II) has been shown to exhibit catalase-like activity (13,14) and is capable of protecting endothelial cells from H 2 O 2 toxicity and from reactive oxygen species (ROS) generated during oxidative burst of neutrophils (15,16). We have shown that in the 0.5-2 mM range Mn(II) induced mitochondria-independent apoptosis in HeLa cells, and it also caused an elevation of ROS and Mn(II)-superoxide dismutase (17).…”

mentioning

confidence: 99%

Manganese(II) Induces Apoptotic Cell Death in NIH3T3 Cells via a Caspase-12-dependent Pathway

Oubrahim

Chock

Stadtman

2002

Journal of Biological Chemistry

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Under physiological conditions, manganese(II) exhibits catalase-like activity. However, at elevated concentrations, it induces apoptosis via a non-mitochondriamediated mechanism (Oubrahim, H., Stadtman, E. R., and Chock, P. B. (2001) Proc. Natl. Acad. Sci. U. S. A. 98, 9505-9510). In this study, we show that the Mn(II)-induced apoptosis, as monitored by caspase-3-like activity, in NIH3T3 cells was inhibited by calpain inhibitors I and II or the p38 MAP kinase inhibitor, SB202190. The control experiments showed that each of these inhibitors in the concentration ranges used exerted no effect on activated caspase-3-like activity. Furthermore, caspase-12 was cleaved in Mn(II)-treated cells, suggesting that the Mn(II)-induced apoptosis is mediated by caspase-12. This notion is confirmed by the observations that pretreatment of NIH3T3 cells with either caspase-12 antisense RNA or dsRNA corresponding to the full-length caspase-12 led to a dramatic decrease in caspase-3-like activity induced by Mn(II). The precise mechanism by which Mn(II) induced the apoptosis is not clear. Nevertheless, Mn(II), in part, exerts its effect via its ability to replace Ca(II) in the activation of m-calpain, which in turn activates caspase-12 and degrades Bcl-xL. In addition, the dsRNA i method serves as an effective technique for knocking out caspase-12 in NIH3T3 cells without causing apoptosis.Apoptosis is the physiological form of programmed cell death that serves to remove damaged and unwanted cells and to maintain tissue homeostasis. It is characterized by a series of distinct morphological and biochemical changes (1, 2). Proteases, particularly the family of cysteine proteases called caspases, have been shown to play critical roles in cellular execution of apoptosis (3-6). To date, 14 caspases have been identified. Most are located in the cytosol as zymogens, where they are activated by apoptotic stimuli-mediated signaling cascades (3, 4, 6). Caspase-8 mediates apoptotic signals from death receptors on plasma membranes (7, 8), caspase-9 plays a key role in mitochondria-mediated apoptosis (9), and caspase-12, which can be activated in cells by ␤ amyloid peptide and respiratory syncythial virus, mediates endoplasmic reticulum (ER) 1 -specific apoptosis (10). ER regulates a number of cellular functions, including cellular responses to stress and intracellular Ca(II) levels. Elevation of intracellular Ca(II) and oxidants have been shown to cause ER stress and ultimately lead to apoptosis (11,12).Under physiological conditions, Mn(II) has been shown to exhibit catalase-like activity (13,14) and is capable of protecting endothelial cells from H 2 O 2 toxicity and from reactive oxygen species (ROS) generated during oxidative burst of neutrophils (15, 16). We have shown that in the 0.5-2 mM range Mn(II) induced mitochondria-independent apoptosis in HeLa cells, and it also caused an elevation of ROS and Mn(II)-superoxide dismutase (17). Here we show by the dsRNA i and antisense RNA methods that the observed Mn(II)-induced apoptosis is mediated...

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Manganese exposure in foundry furnacemen and scrap recycling workers

Cited by 38 publications

References 16 publications

Correlation between airborne manganese concentration at the workstations in the iron foundry and manganese concentration in workers’ blood

Correlation between airborne manganese concentration at the workstations in the iron foundry and manganese concentration in workers’ blood

Searching for a relationship between manganese and welding and Parkinson’s disease

Manganese(II) Induces Apoptotic Cell Death in NIH3T3 Cells via a Caspase-12-dependent Pathway

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