Issues in neurological risk assessment for occupational exposures: The Bay Bridge welders

Park, Robert M.; Bowler, Rosemarie M.; Eggerth, Donald E.; Diamond, Emily; Spencer, Katie J.; Smith, Donald R.; Gwiazda, R.

doi:10.1016/j.neuro.2005.10.010

Cited by 38 publications

(35 citation statements)

References 25 publications

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“…5,7,8 In a recent study of 351 welders, more than half had "taste" problems, although no chemosensory testing was performed and no distinction was made between flavor sensations dependent on the sense of smell and those dependent on the sense of taste. 3 In the present study, a component of the San Francisco/Oakland Bay Bridge Welder Study, 9,10,11 we quantitatively evaluated the olfactory function of professional welders who worked in confined spaces on the Bay Bridge, and compared their test scores with those of matched normal controls. These scores were also correlated with those from a number of neurologic, neuropsychological, and physiologic (e.g., blood levels of Mn, Fe, Cu, and Pb) measures.…”

mentioning

confidence: 99%

San Francisco/Oakland Bay Bridge Welder Study

Antunes

Bowler²,

Doty³

2007

Neurology

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mentioning

confidence: 99%

San Francisco/Oakland Bay Bridge Welder Study

Antunes

Bowler²,

Doty³

2007

Neurology

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“…In other words, the lack of an FIGURE 2. Association between cumulative air Mn exposure index (CEI) and blood (A), plasma (B), and urine (C) Mn levels in Bay Bridge welders (see Park et al [2006] and Bowler et al [2007] association between air and blood Mn in the high exposure group may reflect both the variable nature of the exposure, and the fact that there may be a contribution from endogenous Mn accumulated from past exposures.…”

Section: Occupational Studiesmentioning

confidence: 99%

Biomarkers of Mn exposure in humans

Smith

Gwiazda

Bowler

et al. 2007

American J Industrial Med

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153

133

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These data suggest a complex and limited relationship between exposure and blood Mn levels that may depend upon exposure attributes and the latency of blood sampling relative to exposure; plasma and urine Mn appear to be of little utility as exposure biomarkers. This underscores the need to fully characterize and validate these or other biomarkers for use in constructing appropriate exposure metrics and determining exposure-effect relationships.

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“…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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Issues in neurological risk assessment for occupational exposures: The Bay Bridge welders

Cited by 38 publications

References 25 publications

San Francisco/Oakland Bay Bridge Welder Study

San Francisco/Oakland Bay Bridge Welder Study

Biomarkers of Mn exposure in humans

Are There Common Biochemical and Molecular Mechanisms Controlling Manganism and Parkisonism

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