Results of Magnetic Resonance Imaging in Long-Term Manganese Dioxide-Exposed Workers

Dietz, M C; Ihrig, Andreas; Wrazidlo, W; Bader, Michael; Jansen, Olav; Triebig, Gerhard

doi:10.1006/enrs.2000.4068

Cited by 82 publications

(45 citation statements)

References 7 publications

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“…In some cases, the enhanced signal can also be observed in the globus pallidus of Mn-exposed monkeys whose neurologic deficits are absent and whose behavioral changes are subtle (Newland and Weiss, 1992;Olanow et al, 1996;Shinotoh et al, 1995). Human studies among welders, who are exposed to Mn in welding fume, have also provided strong evidence of an increased MRI signal in welders' globus pallidus (Dietz et al, 2001;Kim et al, 1999c;Nelson et al, 1993). Our data clearly showed an overall high incidence (78%) and significant increase in T1-weighted MRI among Mn-exposed workers in comparison to control workers.…”

Section: Discussionmentioning

confidence: 99%

“…An increased T1-weighted Mn signal in the globus pallidus area has been found among workers occupationally exposed to Mn (Dietz et al, 2001;Kim et al, 1999b;Lucchini et al, 2000;Nelson et al, 1993), in patients receiving long-term total parenteral nutrition (Alves et al, 1997;Ejima et al, 1992;Fell et al, 1996;Fredstrom et al, 1995;Iwase et al, 2000;Komaki et al, 1999;Nagatomo et al, 1999;Quaghebeur et al, 1996), and in clinical cases reported with hepatic failure (Butterworth et al, 1995;Chetri and Choudhuri, 2003;Hauser et al, 1994;Hazell and Butterworth, 1999;McKinney et al, 2004;Spahr et al, 2002). While in animal models the MRI intensity has been linked to external Mn exposure (Eriksson et al, 1992;Kim et al, 1999a;Misselwitz et al, 1995;Newland et al, 1989a,b;Shinotoh et al, 1995), the question as to how the change in MRI signals in humans is associated with external exposure conditions and whether this consequentially leads to alternations of the internal Mn exposure indices or the fluctuation in blood chemistry remains elusive.…”

Section: Introductionmentioning

confidence: 99%

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Brain magnetic resonance imaging and manganese concentrations in red blood cells of smelting workers: Search for biomarkers of manganese exposure

Jiang¹,

Zheng²,

Лонг³

et al. 2007

NeuroToxicology

125

128

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The MRI technique has been used in diagnosis of manganism in humans and non-human primates. This cross-sectional study was designed to explore whether the pallidal signal intensity in T1-weighted MRI correlated with Mn levels in the blood compartment among Mn-exposed workers and to understand to what extent the MRI signal could reflect Mn exposure. A group of 18 randomly selected male Mn-exposed workers of which 13 were smelting workers with high exposure (mean of airborne Mn in work place: 1.26 mg/m 3 ; range: 0.31-2.93 mg/m 3 ), and 5 power distribution control workers with low exposure (0.66 mg/m 3 and 0.23-0.77 mg/m 3 ) from a ferroalloy factory, and another group of 9 male subjects as controls from a non-smelting factory who were office or cafeteria workers (0.01 mg/m 3 and 0-0.03 mg/m 3 ) were recruited for neurological tests, MRI examination, and analysis of Mn in whole blood (MnB), plasma (MnP) or red blood cells (MnRBC). No clinical symptoms and signs of manganism were observed among these workers. MRI data showed average increases of 7.4% (p < 0.05) and 16.1% (p < 0.01) in pallidal index (PI) among low-and high-exposed workers, respectively, as compared to controls. Fourteen out of 18 Mn-exposed workers (78%) had intensified PI values, while this proportion was even higher (85%) among the high Mn-exposed workers. Among exposed workers, the PI values were significantly associated with MnRBC (r = 0.55, p = 0.02). Our data suggest that the workers exposed to airborne Mn, but without clinical symptoms, display an exposure-related, intensified MRI signal. The MRI, as well as MnRBC, may be useful in early diagnosis of Mn exposure.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Brain magnetic resonance imaging and manganese concentrations in red blood cells of smelting workers: Search for biomarkers of manganese exposure

Jiang¹,

Zheng²,

Лонг³

et al. 2007

NeuroToxicology

125

128

View full text Add to dashboard Cite

show abstract

“…Although Mn impacts multiple neurotransmitter systems (Fitsanakis et al, 2006b), the complex symptomology characteristic of Mn toxicity suggests that both the mesocorticolimbic and nigrostriatal dopamine systems might be affected. Consistent with this hypothesis, MRI studies indicate that Mn toxicity is associated with excessive Mn accumulation in the basal ganglia as well as other cortical and subcortical structures (Dietz et al, 2001;Joseph et al, 2005;Klos et al, 2006;Uchino et al, 2007).…”

Section: Introductionmentioning

confidence: 90%

Postnatal manganese exposure alters dopamine transporter function in adult rats: Potential impact on nonassociative and associative processes

McDougall¹,

Reichel²,

Farley³

et al. 2008

Neuroscience

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In the present study, we examined whether exposing rats to a high-dose regimen of manganese chloride (Mn) during the postnatal period would depress presynaptic dopamine functioning and alter nonassociative and associative behaviors. To this end, rats were given oral supplements of Mn (750 μg/day) on postnatal days (PD) 1-21. On PD 90, dopamine transporter (DAT) immunoreactivity and [ 3 H]dopamine uptake were assayed in the striatum and nucleus accumbens, while in vivo microdialysis was used to measure dopamine efflux in the same brain regions. The effects of postnatal Mn exposure on nigrostriatal functioning were evaluated by assessing rotorod performance and amphetamine-induced stereotypy in adulthood. In terms of associative processes, both cocaineinduced conditioned place preference (CPP) and sucrose-reinforced operant responding were examined. Results showed that postnatal Mn exposure caused persistent declines in DAT protein expression and [ 3 H]dopamine uptake in the striatum and nucleus accumbens, as well as long-term reductions in striatal dopamine efflux. Rotorod performance did not differ according to exposure condition, however Mn-exposed rats did exhibit substantially more amphetamine-induced stereotypy than vehicle controls. Mn exposure did not alter performance on any aspect of the CPP task (preference, extinction, or reinstatement testing), nor did Mn affect progressive ratio responding (a measure of motivation). Interestingly, acquisition of a fixed ratio task was impaired in Mn-exposed rats, suggesting a deficit in procedural learning. In sum, these results indicate that postnatal Mn exposure causes persistent declines in various indices of presynaptic dopaminergic functioning. Mninduced alterations in striatal functioning may have long-term impact on associative and nonassociative behavior.

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“…Some investigators suggest that manganese concentrations in blood seem to be fairly stable over long periods of time in humans exposed to this metal in mining and industrial environments, and thus can be used to reflect the manganese body burden. 40,41 Others, mainly based on the animal studies, [42][43][44] point out that manganese is rapidly eliminated from the blood circulation and possesses a rather short blood t 1/2 , but a prolonged tissue t 1/2 , after exposure. The discrepancy between blood and tissue t 1/2 and possibly a predominant tissue accumulation of manganese may render the blood manganese level less relevant as an indicator of total body burden of manganese.…”

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confidence: 99%

Occupational Exposure to Welding Fume among Welders: Alterations of Manganese, Iron, Zinc, Copper, and Lead in Body Fluids and the Oxidative Stress Status

Zhang

et al. 2004

Journal of Occupational and Environmental Medicine

144

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Welders in this study were selected from a vehicle manufacturer; control subjects were from a nearby food factory. Airborne manganese levels in the breathing zones of welders and controls were 1.45 ± SD1.08 mg/m 3 and 0.11 ± 0.07 μg/m 3 , respectively. Serum levels of manganese and iron in welders were 4.3-fold and 1.9-fold, respectively, higher than those of controls. Blood lead concentrations in welders increased 2.5-fold, whereas serum zinc levels decreased 1.2-fold, in comparison with controls. Linear regression revealed the lack of associations between blood levels of five metals and welder's age. Furthermore, welders had erythrocytic superoxide dismutase activity and serum malondialdehyde levels 24% less and 78% higher, respectively, than those of controls. These findings suggest that occupational exposure to welding fumes among welders disturbs the homeostasis of trace elements in systemic circulation and induces oxidative stress.The welding fume generated during the welding process possesses at least 13 metals, including manganese (Mn), beryllium (Be), cadmium (Cd), chromium (Cr), cobalt (Co), copper (Cu), iron (Fe), lead (Pb), mercury (Hg), molybdenum (Mo), nickel (Ni), zinc (Zn), antimony (Sb), and vanadium (V). 1 Welders are known to be at risk, particularly for chronic exposure to airborne manganese, which is one of the major coating materials in welding products (eg, bars and wires). [2][3][4][5][6] A recent study even suggests that exposure to manganese during welding may be a risk factor for the etiology of Parkinson's disease among the career welders. 7 Although limited studies have documented airborne manganese levels during welding, the question as to how low-level, long-term exposure to manganese or welding fume may affect blood levels of trace metals is unanswered. However, altered systemic homeostasis of iron and manganese is known to be associated with neurodegenerative disorders. 8 Manganese-induced neurological lesions are reportedly located in the globus pallidus and striatum of the basal ganglia. The pallidus and striatum display a marked decrease in myelinated nerve fibers, accompanied by depletion of striatal dopamine. [11][12][13][14] The mechanism whereby manganese induces neurodegenerative damage remains elusive. Nonetheless, several recent reports have suggested that manganese neurotoxicity may be associated with its interaction with other essential trace elements, including iron, 10,13,15,16 zinc, 17 copper, 17 and aluminum. 13,15,18 Particularly regarding manganese-induced neurotoxicity, studies have shown that chronic exposure to manganese appears to be associated with altered iron concentrations in blood as well as in the cerebrospinal fluid, presumably the result of Mn-Fe interaction at certain [Fe-S]-containing proteins, which regulate the homeostasis of iron. 10,16,[19][20][21] The excess accumulation of iron in neurons may consequently produce cellular oxidative stress, leading to neuronal damage.Superoxide dismutase (SOD), a cytoplasmic enzyme, catalyzes the react...

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Results of Magnetic Resonance Imaging in Long-Term Manganese Dioxide-Exposed Workers

Cited by 82 publications

References 7 publications

Brain magnetic resonance imaging and manganese concentrations in red blood cells of smelting workers: Search for biomarkers of manganese exposure

Brain magnetic resonance imaging and manganese concentrations in red blood cells of smelting workers: Search for biomarkers of manganese exposure

Postnatal manganese exposure alters dopamine transporter function in adult rats: Potential impact on nonassociative and associative processes

Occupational Exposure to Welding Fume among Welders: Alterations of Manganese, Iron, Zinc, Copper, and Lead in Body Fluids and the Oxidative Stress Status

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