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Preventing Neurotoxicity at Work

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A worker not exposed to a neurotoxic substance will never develop any adverse neurotoxic health effects from that substance. Zero exposure leads to total protection against neurotoxic health effects. This is the essence of all primary prevention measures.

Toxicity Testing

New chemical compounds introduced into the workplace and in occupational settings should have already been tested for neurotoxicity. Failure to do pre-market toxicity testing can lead to workers’ contact and potentially severe adverse health effects. The introduction of methyl n-butyl ketone into a workplace in the United States is a classic example of the possible hazards of untested neurotoxicants being introduced into the workplace (Spencer and Schaumburg 1980).

Engineering Controls

Engineering controls (e.g., ventilation systems, closed production facilities) are the best means for keeping workers’ exposures below permissible exposure limits. Closed chemical processes that keep all toxicants from being released into the workplace environment are the ideal. If this is not possible, closed ventilation systems that exhaust ambient air vapours and are designed so as to pull contaminated air away from workers are useful when well designed, adequately maintained, and properly operated.

Personal Protection Equipment

In situations where engineering controls are unavailable to reduce workers’ contact with neurotoxicants, personal protective equipment must be provided. Because workplace neurotoxicants are many, and routes of exposure differ across workplaces and work conditions, the kind of personal protective equipment must be carefully selected for the situation at hand. For example, the neurotoxicant lead can exert its toxicity when lead-laden dust is breathed and when lead particles are ingested in food or water. Therefore, personal protective equipment must protect against both routes of exposure. This would mean respiratory protection equipment and adoption of personal hygiene measures to prevent consumption of lead-contaminated food or beverages. For many neurotoxicants (like industrial solvents), absorption of the substance through intact skin is a main route of exposure. Impermeable gloves, aprons and other appropriate equipment must therefore be provided to prevent skin absorption. This would be in addition to engineering controls or personal respiratory protection equipment. Considerable planning must be given to match personal protective equipment to the specific work being performed.


Administrative Controls

Administrative controls consist of managerial efforts to reduce workplace hazards through planning, training, employee rotation on job sites, changes in production processes, and product substitution (Urie 1992), as well as strict adherence to all existing regulations.
Workers’ Right-to-Know

While the employer bears the responsibility for providing a workplace or work experience that does not harm workers’ health, workers have the responsibility to follow workplace rules that are intended to protect them. Workers must be in a position to know what actions to take in protecting themselves. This means workers have the right to know about the neurotoxicity of substances with which they come into contact, and what protective measures they can take.

Worker Health Surveillance

Where conditions permit, workers should be regularly given medical examinations. A regular evaluation by occupational physicians or other medical specialists constitutes worker health surveillance. For workers known to be working with or around neurotoxicants, physicians should be knowledgeable of the effects of exposure. For example, low-level exposure to many organic solvents will produce symptoms of fatigue, sleep disorders, headaches and memory disturbances. For heavy doses of lead, wrist drop and peripheral nerve impairment would be signs of lead intoxication. Any signs and symptoms of neurotoxicant intoxication should result in reassignment of the worker to an area free of the neurotoxicant, and efforts to reduce workplace levels of the neurotoxicant.

 

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Contents

Nervous System References

Amaducci, L, C Arfaioli, D Inzitari, and M Marchi. 1982. Multiple sclerosis among shoe and leather workers: An epidemiological survey in Florence. Acta Neurol Scand 65:94-103.

Anger, KW. 1990. Worksite neurobehavioral research: Result, sensitive methods, test batteries and the transition from laboratory data to human health. Neurotoxicology 11:629-720.

Anger, WK, MG Cassitto, Y Liang, R Amador, J Hooisma, DW Chrislip, D Mergler, M Keifer, and J Hörtnagel. 1993. Comparison of performance from three continents on the WHO-recommended neurobehavioral core test battery (NCTB). Environ Res 62:125-147.

Arlien-Søborg, P. 1992. Solvent Neurotoxicity. Boca Raton: CRC Press.
Armon, C, LT Kurland, JR Daube, and PC O’Brian. 1991. Epidemiologic correlates of sporadic amyotrophic lateral sclerosis. Neurology 41:1077-1084.

Axelson, O. 1996. Where do we go in occupational neuroepidemiology? Scand J Work Environ Health 22: 81-83.

Axelson, O, M Hane, and C Hogstedt. 1976. A case-referent study on neuropsychiatric disorders among workers exposed to solvents. Scand J Work Environ Health 2:14-20.

Bowler, R, D Mergler, S Rauch, R Harrison, and J Cone. 1991. Affective and personality disturbance among women former microelectronics workers. J Clin Psychiatry 47:41-52.

Brackbill, RM, N Maizlish, and T Fischbach. 1990. Risk of neuropsychiatric disability among painters in the United States. Scand J Work Environ Health 16:182-188.

Campbell, AMG, ER Williams, and D Barltrop. 1970. Motor neuron disease and exposure to lead. J Neurol Neurosurg Psychiatry 33:877-885.

Cherry, NM, FP Labrèche, and JC McDonald. 1992. Organic brain damage and occupational solvent exposure. Br J Ind Med 49:776-781.

Chio, A, A Tribolo, and D Schiffer. 1989. Motorneuron disease and glue exposure. Lancet 2:921.

Cooper, JR, FE Bloom, and RT Roth. 1986. The Biochemical Basis of Neuropharmacology. New York: Oxford Univ. Press.

Dehart, RL. 1992. Multiple chemical sensitivity—What is it? Multiple chemical sensitivities. Addendum to: Biologic markers in immunotoxicology. Washington, DC: National Academy Press.

Feldman, RG. 1990. Effects of toxins and physical agents on the nervous system. In Neurology in Clinical Practice, edited by WG Bradley, RB Daroff, GM Fenichel, and CD Marsden. Stoneham, Mass: Butterworth.

Feldman, RG and LD Quenzer. 1984. Fundamentals of Neuropsychopharmacology. Sunderland, Mass: Sinauer Associates.

Flodin, U, B Söderfeldt, H Noorlind-Brage, M Fredriksson, and O Axelson. 1988. Multiple sclerosis, solvents and pets: A case-referent study. Arch Neurol 45:620-623.

Fratiglioni L, A Ahlbom, M Viitanen and B Winblad. 1993. Risk factors for late-onset Alzheimer’s disease: a population-based case-control study. Ann Neurol 33:258-66.

Goldsmith, JR, Y Herishanu, JM Abarbanel, and Z Weinbaum. 1990. Clustering of Parkinson’s disease points to environmental etiology. Arch Environ Health 45:88-94.

Graves, AB, CM van Duijn, V Chandra, L Fratiglioni, A Heyman, AF Jorm, et al. 1991. Occupational exposure to solvents and lead as risk factors for Alzheimer’s disease: A collaborative re-analysis of case-control studies. Int J Epidemiol 20 Suppl. 2:58-61.

Grönning, M, G Albrektsen, G Kvåle, B Moen, JA Aarli, and H Nyland. 1993. Organic solvents and multiple sclerosis. Acta Neurol Scand 88:247-250.

Gunnarsson, L-G, L Bodin, B Söderfeldt, and O Axelson. 1992. A case-control study of motor neuron disease: Its relation to heritability and occupational exposures, particularly solvents. Br J Ind Med 49:791-798.

Hänninen, H and K Lindstrom. 1979. Neurobehavioral Test Battery of the Institute of Occupational Health. Helsinki: Institute of Occupational Health.

Hagberg, M, H Morgenstem, and M Kelsh. 1992. Impact of occupations and job tasks on the prevalence of carpal tunnel syndrome. Scand J Work Environ Health 18:337-345.

Hart, DE. 1988. Neuropsychological Toxicology: Identification and Assessment of Human Neurotoxic Syndromes. New York: Pergamon Press.

Hawkes, CH, JB Cavanagh, and AJ Fox. 1989. Motorneuron disease: A disorder secondary to solvent exposure? Lancet 1:73-76.

Howard, JK. 1979. A clinical survey of paraquat formulation workers. Br J Ind Med 36:220-223.

Hutchinson, LJ, RW Amsler, JA Lybarger, and W Chappell. 1992. Neurobehavioral Test Batteries for Use in Environmental Health Field Studies. Atlanta: Agency for Toxic Substances and Disease Registry (ATSDR).

Johnson, BL. 1987. Prevention of Neurotoxic Illness in Working Populations. Chichester: Wiley.

Kandel, ER, HH Schwartz, and TM Kessel. 1991. Principles of Neural Sciences. New York: Elsevier.

Kukull, WA, EB Larson, JD Bowen, WC McCormick, L Teri, ML Pfanschmidt, et al. 1995. Solvent exposure as a risk factor for Alzheimer’s disease: A case-control study. Am J Epidemiol 141:1059-1071.

Landtblom, A-M, U Flodin, M Karlsson, S Pålhagen, O Axelson, and B Söderfeldt. 1993. Multiple sclerosis and exposure to solvents, ionizing radiation and animals. Scand J Work Environ Health 19:399-404.

Landtblom, A-M, U Flodin, B Söderfeldt, C Wolfson and O Axelson. 1996. Organic solvents and multiple sclerosis: A synthesis of the cement evidence. Epidemiology 7: 429-433.

Maizlish, D and O Feo. 1994. Alteraciones neuropsicológicas en trabajadores expuestos a neurotóxicos. Salud de los Trabajadores 2:5-34.

Mergler, D. 1995. Behavioral neurophysiology: Quantitative measures of sensory toxicity. In Neurotoxicology: Approaches and Methods, edited by L Chang and W Slikker. New York: Academic Press.

O’Donoghue, JL. 1985. Neurotoxicity of Industrial and Commercial Chemicals. Vol. I & II. Boca Raton: CRC Press.

Sassine, MP, D Mergler, F Larribe, and S Bélanger. 1996. Détérioration de la santé mentale chez des travailleurs exposés au styrène. Rev epidmiol med soc santé publ 44:14-24.

Semchuk, KM, EJ Love, and RG Lee. 1992. Parkinson’s disease and exposure to agricultural work and pesticide chemicals. Neurology 42:1328-1335.

Seppäläinen, AMH. 1988. Neurophysiological approaches to the detection of early neurotoxicity in humans. Crit Rev Toxicol 14:245-297.

Sienko, DG, JD Davis, JA Taylor, and BR Brooks. 1990. Amyotrophic lateral sclerosis: A case-control study following detection of a cluster in a small Wisconsin community. Arch Neurol 47:38-41.

Simonsen, L, H Johnsen, SP Lund, E Matikainen, U Midtgård, and A Wennberg. 1994. Evaluation of neurotoxicity data: A methodological approach to classification of neurotoxic chemicals. Scand J Work Environ Health 20:1-12.

Sobel, E, Z Davanipour, R Sulkava, T Erkinjuntti, J Wikström, VW Henderson, et al. 1995. Occupations with exposure to electromagnetic fields: A possible risk factor for Alzheimer’s disease. Am J Epidemiol 142:515-524.

Spencer, PS and HH Schaumburg. 1980. Experimental and Clinical Neurotoxicology. Baltimore: Williams & Wilkins.

Tanner, CM. 1989. The role of environmental toxins in the etiology of Parkinson’s disease. Trends Neurosci 12:49-54.

Urie, RL. 1992. Personal protection from hazardous materials exposures. In Hazardous Materials Toxicology: Clinical Principles of Environmental Health, edited by JB Sullivan and GR Krieger. Baltimore: Williams & Wilkins.

World Health Organization (WHO). 1978. Principles and Methods of Evaluating the Toxicity of Chemicals, Part 1 and 2. EHC, No. 6, Part 1 and 2. Geneva: WHO.

World Health Organization and Nordic Council of Ministers. 1985. Chronic Effects of Organic Solvents On the Central Nervous System and Diagnostic Criteria. EHC, No. 5. Geneva: WHO.

Zayed, J, G Ducic, G Campanella, JC Panisset, P André, H Masson, et al. 1990. Facteurs environnementaux dans l’étiologie de la maladie de Parkinson. Can J Neurol Sci 17:286-291.