Manganese cumulative exposure and symptoms: A follow-up study of alloy workers

Bouchard, Maryse F.; Mergler, Donna; Baldwin, Mary; Panisset, Michel

doi:10.1016/j.neuro.2008.04.013

Cited by 57 publications

(31 citation statements)

References 29 publications

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“…21 Higher means were reported in alloy-production workers (12 mg/l). 26,29,30 A receiver operating characteristic analysis determined 10 mg/l as 95 th % percentile in a group of unexposed South African workers in comparison to smelters. 26 Every other welder in our study was above that value.…”

Section: Discussionmentioning

confidence: 99%

Levels and predictors of airborne and internal exposure to manganese and iron among welders

Pesch

Weiß

Kendzia

et al. 2012

J Expo Sci Environ Epidemiol

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ning 11 and The Weldox GroupWe investigated airborne and internal exposure to manganese (Mn) and iron (Fe) among welders. Personal sampling of welding fumes was carried out in 241 welders during a shift. Metals were determined by inductively coupled plasma mass spectrometry. Mn in blood (MnB) was analyzed by graphite furnace atom absorption spectrometry. Determinants of exposure levels were estimated with multiple regression models. Respirable Mn was measured with a median of 62 (inter-quartile range (IQR) 8.4 --320) mg/m 3 and correlated with Fe (r ¼ 0.92, 95% CI 0.90 --0.94). Inhalable Mn was measured with similar concentrations (IQR 10 --340 mg/m 3 ). About 70% of the variance of Mn and Fe could be explained, mainly by the welding process. Ventilation decreased exposure to Fe and Mn significantly. Median concentrations of MnB and serum ferritin (SF) were 10.30 mg/l (IQR 8.33 --13.15 mg/l) and 131 mg/l (IQR 76 --240 mg/l), respectively. Few welders were presented with low iron stores, and MnB and SF were not correlated (r ¼ 0.07, 95% CI À0.05 to 0.20). Regression models revealed a significant association of the parent metal with MnB and SF, but a low fraction of variance was explained by exposure-related factors. Mn is mainly respirable in welding fumes. Airborne Mn and Fe influenced MnB and SF, respectively, in welders. This indicates an effect on the biological regulation of both metals. Mn and Fe were strongly correlated, whereas MnB and SF were not, likely due to higher iron stores among welders.

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Section: Discussionmentioning

confidence: 99%

Levels and predictors of airborne and internal exposure to manganese and iron among welders

Pesch

Weiß

Kendzia

et al. 2012

J Expo Sci Environ Epidemiol

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“…As noted above, manganism is also associated with a unique cock-like walk and loss of balance which is distinguishable from that of Parkinsonism. As will be described below, many of the initial extrapyramidal symptoms associated with Mn toxicity most likely reflect differences in the primary lesioned site within the CNS for the two disorders, although manganism like Parkinsonism, is a progressive disorder producing continued impairment even after exposure to Mn has ceased (Sadek et al 2003;Kessler et al 2003;Kenangil et al 2006;Huang 2007;Huang et al 2007;Bouchard et al 2008). A recent study has confirmed persistent and even enhanced neurological deficits in subjects with manganism over a 10-year period after the initial diagnosis (Huang 2007).…”

Section: Symptoms Of Manganism and The Relationship To Parkinsonismmentioning

confidence: 99%

“…For example, chronic exposure to Mn can lead to increased susceptibility toward developing pulmonary infections including pneumonia and bronchitis (Baader 1932;Davies and Harding 1949;Rodier 1955;Maigetter et al 1976;Bencko and Cikrt 1984;Roels et al 1987;Saric 1992;Saric and Piasek 2000;Jafari and Assari 2004;Bowler et al 2007;Antonini et al 2009). Similarly, hearing deficits have also been reported in occupations in which individuals are exposed to chronic high levels of Mn (Nikolov 1974;Khalkova and Kostadinova 1986;Korczynski 2000;Josephs et al 2005;Park et al 2006;Da Silva et al 2007;Vezér et al 2007;Bouchard et al 2008). Although Mn readily accumulates in both the lung and inner ear (Kalliomäki et al 1983;Park et al 2007;Ma et al 2008), few studies have actually attempted to characterize the specific biochemical and molecular mechanisms leading to malfunction in these organs.…”

Section: Introductionmentioning

confidence: 98%

Are There Common Biochemical and Molecular Mechanisms Controlling Manganism and Parkisonism

Roth

2009

Neuromol Med

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Over the past several decades there has been considerable progress in our basic knowledge as to the mechanisms and factors regulating Mn toxicity. The disorder known as manganism is associated with the preferential accumulation of Mn in the globus pallidus of the basal ganglia which is generally considered to be the major and initial site of injury. Because the area of the CNS comprising the basal ganglia is very complex and dependent on the precise function and balance of several neurotransmitters, it is not surprising that symptoms of manganism often overlap with that of Parkinson's disease. The fact that neurological symptoms and onset of Mn toxicity are quite broad and can vary unpredictably probably reflects specific genetic variance of the physiological and biochemical makeup within the basal ganglia in any individual. Differences in response to Mn overexposure are, thus, likely due to underlying genetic variability which ultimately presents in deviations in both susceptibility as well as the characteristics of the neurological lesions and symptoms expressed. Although chronic exposure to Mn is not the initial causative agent provoking Parkinsonism, there is evidence suggesting that persistent exposure can predispose an individual to acquire dystonic movements associated with Parkinson's disease. As noted in this review, there appears to be common threads between the two disorders, as mutations in the genes, parkin and ATP13A2, associated with early onset of Parkinsonism, may also predispose an individual to develop Mn toxicity. Mutations in both genes appear to effect transport of Mn into the cell. These genetic difference coupled with additional environmental or nutritional factors must also be considered as contributing to the severity and onset of manganism.

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“…It was subsequently recognised that doses one hundred times less than this could also induce overt manganism, and that early or preclinical neurological effects can occur in generally asymptomatic workers at much lower concentrations still (IPCS 1981(IPCS , 1999WHO 2001;Rodríguez-Agudelo et al 2006). Furthermore, the most recent epidemiological studies indicate that health effects due to chronic Mn inhalation can continue many years after exposure has ceased (Lucchini et al 2007;Bouchard et al 2008). Consequently, guideline concentration limits have been defined for both workplace and outside ambient air, and in several cases have lowered as more health information becomes available (e.g.…”

Section: Introductionmentioning

confidence: 99%

Manganese in the urban atmosphere: identifying anomalous concentrations and sources

Moreno

Pandolfi

Querol

et al. 2010

Environ Sci Pollut Res

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We demonstrate the anomalous nature of such concentrations by comparing them with >2,500 PM(10) chemical analyses of ambient PM(10) from other sites in Spain which show how current background Mn levels in urban air typically average only 10 ng/m(3), rising to 20-25 ng/m(3) in city traffic sites. Daily levels of atmospheric Mn PM(10) only rarely exceed 50 ng/m(3), usually during desert dust intrusions which, in extreme cases (such as Canary Islands "calima" events from Africa) can produce Mn concentrations of 100-125 ng/m(3).

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Manganese cumulative exposure and symptoms: A follow-up study of alloy workers

Cited by 57 publications

References 29 publications

Levels and predictors of airborne and internal exposure to manganese and iron among welders

Levels and predictors of airborne and internal exposure to manganese and iron among welders

Are There Common Biochemical and Molecular Mechanisms Controlling Manganism and Parkisonism

Manganese in the urban atmosphere: identifying anomalous concentrations and sources

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