Sequelae of fume exposure in confined space welding: A neurological and neuropsychological case series

Abstract

Welding fume contains manganese (Mn) which is known to be bio-available to and neurotoxic for the central nervous system. Although an essential metal, Mn overexposure may cause manganism, a parkinsonian syndrome. The present welder study sought to improve the clinical portrait of manganism and to determine dose–effect relationships. The welders were employed in the construction of the new Bay Bridge (San Francisco) and welded in confined spaces for up to 2 years with minimal protection and poor ventilation. Neurological, neuropsychological, neurophysiological, and pulmonary examinations were given to 49 welders. Clinical cases were selected on the basis of apriori defined criteria pertaining to welding history and neurological/neuropsychological features. Among the 43 eligible welders, 11 cases of manganism were identified presenting with the following symptoms: sleep disturbance, mood changes, bradykinesia, headaches, sexual dysfunction, olfaction loss, muscular rigidity, tremors, hallucinations, slurred speech, postural instability, monotonous voice, and facial masking. Significant associations between outcome variables and cumulative exposure index (CEI) or blood Mn (MnB) were obtained with CEI for variables implicating attention and concentration, working and immediate memory, cognitive flexibility, and verbal learning; and with MnB for executive function, cognitive flexibility, visuo-spatial construction ability, and visual contrast sensitivity. This study strongly suggests that neuropsychological features contribute in a dose–effect related way to the portrait of manganism usually characterized by tremor, loss in balance, diminished cognitive performance, and signs and symptoms of parkinsonism.

Introduction

Manganese intoxication was first described in 1837 by John Couper (UK) in pyrolusite ore grinding workers who were observed with signs and symptoms which presently would prompt diagnosis of manganism. Reports of health effects from manganese (Mn) in welding fume exposures have been relatively recent (Racette et al., 2005). Table 1 summarizes our review of the literature of health effects of Mn exposure in the domains of tremor, motor, neurocognitive, memory, vision, sleep, sexual function, and mood for the period of 1955–2006. Apart from the study by Mergler et al. (1999) on environmental Mn exposure, these occupational Mn exposure studies, other than the relatively few in welders (highlighted in bold), deal with exposures from mining and smelter activities, ferroalloy and dry battery production, and pesticide (Maneb) manipulation.

Manganese has been shown to cause a parkinsonian syndrome sometimes referred to as manganism which is often misdiagnosed as Parkinson's disease (PD). Similarities between symptoms of PD and manganism include tremor, masked facies, generalized bradykinesia (abnormal slowed movement associated with movement initiation difficulties) and cogwheel rigidity (Feldman, 1999). Differences may include more frequent dystonia (slow, involuntary, arrhythmic muscle contractions) in manganism and a tendency to fall backward in PD and falling forward in manganism. Magnetic resonance imaging (MRI) can be used to reveal Mn²⁺ deposition in the brain, exhibiting a T1-weighted signal hyperintensity, especially in the globus pallidus and striatum, in both animals (Shinotoh et al., 1995) and humans exposed to manganese (Nelson et al., 1993, Kim et al., 1994, Kim et al., 1998, Kim et al., 1999a, Kim et al., 1999b, Lucchini et al., 2000, Dietz et al., 2001, Gasparotti et al., 2002). PD is associated with lesions in the substantia nigra pars compacta and does not produce similar MRI abnormality as manganism (Kim, 2006). Other differentiating features between manganism and PD are younger age of onset and little or no response to l-dopa among the manganism cases (Lu et al., 1994, Feldman, 1999, Koller et al., 2004). Case reports of neurological findings in career welders exposed to Mn have revealed dystonia bilaterally in the shoulders and distal four limbs, as well as other parkinsonian features (Sato et al., 2000, Koller et al., 2004, Bowler et al., 2006b).

In patients who have had manganese intoxication, the MRI can have diagnostic value provided the scans are done within less than 6 months of cessation of exposure (Lucchini et al., 2000), whereas blood, serum or urine Mn concentrations are not very useful for neurotoxic risk assessment. Nevertheless, increased manganese levels in blood were often found in groups of workers exposed to Mn dust and fumes (Roels et al., 1987, Roels et al., 1992, Wang et al., 1989, Lucchini et al., 1995, Lucchini et al., 1997, Lucchini et al., 1999, Sjögren et al., 1996, Deschamps et al., 2001, Chia et al., 1993, Mergler et al., 1994, Yim et al., 1998, Moon et al., 1999). Herrero et al. (2006) described findings of markedly elevated urinary manganese levels after administration of a chelating agent (CaEDTA) to seven patients, one of whom was a welder affected by Mn-induced parkinsonism, but urinary Mn is not frequently used as an exclusive biomarker for Mn exposure because the kidney is not a major excretion route.

Neuropsychological testing procedures developed over the past two decades have been shown to be successful tools to differentiate Mn-exposed welders from controls (Sjögren et al., 1996, Bowler et al., 2003a, Bowler et al., 2006a, Bowler et al., 2006b). Recently, we conducted a study in a group of 49 welders working on the new San Francisco Bay Bridge using neurological and neuropsychological methods (Bowler et al., 2006c). A neurological risk assessment of this welder group estimated an excess lifetime risk for disabling or fatal health outcome (Park et al., 2006). The present investigation builds on this initial health study and its objectives are (1) to select clinical cases based on neurological and neuropsychological signs and symptoms; (2) to determine if in this group of cases dose–effect relationships exist between neurological, neuropsychological, and neurophysiological functions and Mn concentration in whole blood or the cumulative exposure index (CEI); and (3) to improve knowledge on a neurological/neuropsychological portrait of manganism.