Elsevier

Revue Neurologique

Volume 172, Issue 12, December 2016, Pages 761-765
Revue Neurologique

Original article
Parkinson's disease and solvents: Is there a causal link?

https://doi.org/10.1016/j.neurol.2016.09.012Get rights and content

Abstract

We report here on chronic neurological impairment in three car painters with constant occupational exposure to organic solvents. All had a clinical presentation of Parkinson's disease and, in all cases, SPECT DaTscan brain imaging, using 123I-FP-CIT, showed bilateral reduction of tracer uptake in the basal ganglia, evidence of dysfunction at the dopaminergic terminal.

Introduction

The putative causal role of certain chemicals in disorders mimicking Parkinson's disease (PD) is based on data drawn from accidental, deliberate and occupational contamination, epidemiological studies, controlled animal studies and mechanistic investigations [1], [2], [3]. Whether prolonged exposures to individual or combinations of organic solvents result in PD remains unresolved. Nevertheless, many organic solvents have acute and chronic neurotoxic potential [4], [5], [6]. The spectrum of chronic neurological impairment in cases subjected to prolonged, repeated exposure to organic solvents is wide. The peripheral nervous system [7] as well as the central nervous system can both be targeted. Prolonged workplace exposure to organic solvents can induce a chronic solvent encephalopathy (CSE) that persists even after the exposure is terminated [8]. Organic solvent neurotoxicity can also impact the sense of smell [9], [10], sleep [10], eyesight [11] and hearing, and some solvents have a synergistic effect with noise and so induce hearing loss [12].

In the present report, we discuss three PD cases in car painters with occupational exposures to organic solvents in different workplace settings.

Section snippets

Patients and methods

The three patients had been examined and followed-up by trained neurologists at their private offices. All three had been referred to senior neurologists at PD expert centers (in Poitiers, Paris and Strasbourg), and two of them (Patients A and B) had then been further referred for consultation at the occupational medicine departments of teaching hospitals. The patients were also examined clinically and by brain dopamine transporter (DAT) single-photon emission computed tomography (SPECT), using

Results

All three patients were professional car painters (Table 1). Their jobs required the use of solvent-containing paints, thinners, glues, lacquers, adhesives and surface cleaners. Workplace products reportedly contained trichloroethylene (TCE), toluene, xylene and styrene. Only two of the patients (C and A, the latter only occasionally) used masks as personal protective equipment, and only Patient C worked in a ventilated workplace.

The patients’ personal histories revealed no regular or excessive

Discussion

With the notable exception of occupational exposures to the solvent carbon disulphide – widely used in the viscose rayon industry in France and elsewhere during the last century – with which parkinsonism has been strongly associated [16], [17], clinical reports of parkinsonism associated with chronic occupational chemical exposures are rare. The recent literature offers published cases for TCE [18], [19], [20], n-hexane [21], [22] and mixed organic solvents in cases of painters [23]. Our

Conclusion

Large-scale investigations are needed to determine whether or not chronic exposures to specific organic solvents or mixtures are associated with PD. We suggest that these be epidemiological studies in occupational settings that routinely use organic solvents (such as industrial painters). Detailed surveillance of specific chemicals in the workplace, together with assessment of personal exposures (via inhalation and skin), should be carried out longitudinally.

The question of a link between

Disclosure of interest

The authors declare that they have no competing interest.

Acknowledgments

The authors wish to thank the Solvaquest group from the Occupational health service (ASSTV86, Vienne, Poitiers, France) for patient recruitment, and neurologist Professor J.L. Houeto for these patients’ care in the neuropsychology department of the CHU of Poitiers (France). The authors also thank Dr J.M. Reiser (SNCF, Paris), Dr N. Seiller (Sarreguemines), Dr A. Anguenot (La Rochelle), Dr N. Ayrivié (La Rochelle), Dr G. Lacroix (Rochefort), Dr Prof. C. Tranchant (Strasbourg) and Dr Prof

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