Transcript of "FUNCTIONAL AND OCCUPATIONAL HEALTH ASSESSMENT.doc.doc"
FUNCTIONAL AND OCCUPATIONAL HEALTH ASSESSMENT
28 Warwick Ct
Coordinator: J. Cromie
FUNCTIONAL ASSESSMENT OF THE NERVOUS SYSTEM
STRUCTURE AND FUNCTION OF THE NERVOUS SYSTEM
The nervous system is sensing, controlling and thinking system of the body.
It can be divided into 2 main sections: the central nervous system (CNS), and the peripheral nervous
The CNS comprises the brain and spinal chord, while the PNS is composed of nervous pathways to and
from the CNS.
The CNS is protected by the blood-brain-barrier (BBB) which restricts the entry of many substances
from the blood stream. Lipid – soluble substances such as organic solvents are able to cross the BBB.
The PNS is an extensive, branching network of nerves – afferent fibres carry sensory information to the
CNS, while efferent fibres transmit signals from the CNS to the peripheries. Where efferent nerves
supply skeletal muscles they are called motor nerves.
Most peripheral nerves arise from the spinal chord and are called spinal nerves. Cranial nerves, which
are also peripheral nerves, arise from the brain itself (there are 12 paired cranial nerves).
The spinal chord is continuous with the brain through an opening at the base of the skull called the
foramen magnum. It descends down the neural canal of the vertebral column.
The spinal chord consists of both grey matter -which is composed of nerve cell bodies, supportive cells
(neuroglia) and unmyelinated nerve fibres - and white matter. The white matter consists of bundles of
myelinated nerve fibres running either to or from the brain.
The 2 main functions of the spinal chord are the transmission of information between the brain and the
spinal nerves and as the centre for spinal reflexes. Spinal reflexes are involved in muscle tone, heart
rate and blood pressure, and digestive pathways.
3 major anatomical divisions of the brain succeed one another along the brain stem: the hindbrain;
midbrain; and forebrain.
The hindbrain is the centre for automatic, life-sustaining nervous control. Breathing rate, heart rate and
blood pressure regulation are among its functions. It has nerve centres that mediate muscle tone and
The cerebellum sits high on the hindbrain and is a major centre for movement coordination. Fibres run
to and from it to the cerebrum and the spinal chord. Damage to the cerebellum causes ataxic or
incordinated movements as well as loss of balance. According to Juntunen (1993), slight cerebellar
dysfunction is an early and very common symptom of neurotoxicity
The midbrain is a small area just foreward of the hindbrain. Through it runs the reticular activating
system which controls wakefulness and alertness.
Further processing of motor and sensory information as well as visual and auditory stimuli take place
in the midbrain.
The brains largest structure is the cerebrum of the forebrain. It is divided into 2 hemispheres which are
subdivided into 5 lobes.
The frontal lobes are the major centres for voluntary movement, the production of speech, personality
and higher intellectual processing (i.e. concentration, planning, decision making).
The parietal lobes responds to sensory information from the body. The parietal lobes function in the
understanding of speech.
The temporal lobes contain auditory centres and are important in memory storage.
The occipital lobes primary functions involve vision.
The insular are deep lobes that are involved in integrating cerebral activity and with memory.
The brain makes up approximately 2% of body mass and accounts for 15% of total body metabolism at
rest. Resting brain metabolism is 7.5 times higher than the rest of the body. Most of this demand is for
the pumping of electrically charged ions across its membrane to produce an action potential. The action
potential represents the electrical signal given off by the nerve.
Myelinated fibres (which appear white) are wrapped in lipid rich sheaths that act as electrical
insulators. The myelin restricts the action potential to specific sites on the nerve significantly speeding
the conduction of the signal.
All neurons or nerve cells consist of a cell body, branched dendrites for receiving signals and axons
which conduct signals away from the cell body. Axons can range in length from a few millimetres to
over a metre.
Chapter 16 of Cassarett and Doull’s Toxicology (Klaassen, 1996) contains comprehensive lists of
neurotoxic compounds and classifies their toxicity as neuronopathic, axonopathic or myelinopathic.
SELECTED NEUROTOXIC COMPOUNDS
Organic solvents are lipid soluble and therefore able to accumulate in lipid rich tissue such as the brain
and myelin. Industries in which workers are likely to become exposed to organic solvents are auto
manufacture and repair, paint/varnish manufacture and use, electronics, industrial cleaning, dry
cleaning and metal part degreasing.
Organic solvents can enter the body through inhalation and skin contact.
Exposure to solvents typically results in CNS depression, psychomotor, and attentional deficits. Acute
low dose exposure is usually associated with temporary deficits, whereas chronic exposure can cause
permanent cognitive changes (Massaro, 2002).
A literature review by Cherry (1993) found higher rates of alcoholism among workers with solvent
exposure. Styrene and toluene slow the body’s metabolism and clearance of alcohol.
The PNS is often affected by solvent exposure with a gradual onset of tingling to numbness to muscle
A review of literature by Juntunen (1993) found that lowered performance in the neurobehavioural
tests of associated learning, digit span (memory), and block design (visuospatial ) are associated with
organic solvent exposures.
In more recent studies, Chouaniere, Wild, Fontana, Hery, Fournier, Baudin, Subra, Rousselle,
Toamain, Saurin,and Ardiot (2002) found decreased digit span (memory) performance with solvent
exposed workers. In Chouaniere’s et al 2002 study the decreased performance was associated with air
concentrations between 0 and 27 ppm of toluene at a printing press.
High levels of exposure of mixed solvents amongst shoe makers have resulted in the reporting of
headaches, irritability and tingling ( which was especially common for workers with n-hexane
exposure) (Nijem, Kristensen, Al-Khtib, Takrori, Bjertness, 2001) as well as reduced psychomotor
performance (Lee, Park, Kim, Lee, Kim, and Kang, 1998).
Carbon disulphide exposure has been associated with manic depression, parkinsonism and diffuse
encephalopathy. PNS symptoms include axonal die back and demyelination syndromes.
Cassitto, Camerino, Imbriani, Contardi, Masera and Gilioli (1993) found rayon workers exposed to
carbon disulphide to have lower performance on memory, attention and perceptive ability.
Chu, Huang, Chen and Shih (1995) compared 2 groups of rayon workers with different exposures to
carbon disulphide. Decreased amplitudes of action potentials as well as slower motor and sensory
NCV were associated with increased exposure. Of the more exposed group, 57% had signs of
The insecticidal properties of organic phosphorus (OP) compounds were discovered in the 1930s in
Germany. They were also developed as chemical weapons at that time (i.e. sarin). A less toxic OP
pesticide malathion was created in 1950 and since then a wide variety of OP pesticides have been
created and put into use. The increasing use of OP pesticides has coincided with the declining use of
organochlorine insecticides (i.e. DDT) due to environmental concerns and insect resistance. The other
main groups of pesticides are the carbamates, which are derived from calobar beans.
Both OP and carbamate insecticides work by inhibiting a neurotransmitter called acetylcholinesterase
(AChE). In humans AChE mediates neurotransmission at a number of site in the brain and PNS
In the PNS acetylcholine (ACh) is secreted from nerve endings to muscle fibre membranes which open
sodium channels allowing the stimulation to pass into the muscle. AChE deactivates ACh meaning that
inhibition of AChE will cause hyperactivity of the cholinergic pathways. Symptoms of AChE
inhibition include muscle weakness and paralysis, tremors, convulsions of limbs and diaphragm.
Cardiovascular function is also affected. The cause of death from acute poisoning is usually respiratory
Exposure to some OP compounds has been linked to myelin and axonal degeneration called
oganophosphate induced delayed neurotoxicity (OPIDN). OPIDN affects long myelinated fibres of
spinal nerves and within the spinal chord. Symptoms of OPIDN, loss of sensation progressing to
muscle weakness of the hands and feet, do not appear for weeks after exposure, are progressive and
largely irreversible ( Massaro, 2002).
Peiris-John, Ruberu, Wickremasinghe, Smit and Hoek (2002) studied farmers who had been exposed to
OP pesticides for an average of 13.8 years. During the cultivation season, when they sprayed for
approximately 20 hours they had a reduction in blood AChE levels and reduced motor and sensory
NCV. Interestingly in between seasons the farmers had significantly higher sensory NCV speeds than
the controls leading the authors to speculate that abnormal spreading of electrical impulses between
nerve fibres (ephatic conduction) might be occurring.
Occupational lead exposure typically results in peripheral neuropathy from axonopathy (Klaassen,
1996). Lead can also interfere with calcium in neurotransmission. Electromyographic abnormalities
were found in lead workers at a battery recycling plant (Yeh, Chang, Wang, 1995)
Workers in lead smelters with blood lead concentrations of .43 to 3.24 micromol/l and average 4 years
duration have demonstrated CNS deficits in mood states, memory, perceptual speed and manual
dexterity (Maizlish, Parra and Feo, 1995).
Manganese readily crosses the BBB and chronic inhalation exposure can result in mood disorders,
speech disorders, and difficulty walking. If the condition persists it can result in a Parkinson –like
syndrome (Klaassen, 1996). The first phase of manganese encephalopathy is characterised by
subjective symptoms such as headaches, anorexia and sexual dysfunction (Deschamps, Guillaumot and
Inorganic mercury compounds have been associated with lower NCV speeds in the PNS. Chronic
exposure to metallic mercury vapour can cause CNS dysfunction. Fluorescent lamp workers with
raised urinary mercury levels had deficits in short term memory while dentists exposed to mercury
vapour have been found to have deficits in memory, visual reproduction, psychomotor performance
and attention tests.( Echeverria, Heyer, Martin, Naleway, Woods and Bittner, 1994).
There are three main types of functional assessment for occupational neurological assessment:
subjective questionnaires; behavioural assessment, and electrophysiological studies.
SUBJECTIVE SYMPTOMS QUESTIONNAIRE
Subjective questionnaires are relatively inexpensive and can be routinely administered as a screening
process. The first stages of neurological disease may be undetectable to formal neurologic or
psychiatric testing. Many human studies of neurotoxicy have found correlations between subjective
symptoms and neurotoxin exposure. As well as subjective symptoms, family/personal history of
neurological diseases, alcohol, recreational and medical drug use patterns have relevance to
neurological sensitivity and symptomology.
Work history is important, as previous occupational exposures to neurotoxic substances are a potential
source of symptoms.
Below is an example of a subjective symptoms questionnaire taken from the WHO publication
‘Prevention of Neurotoxic Illness in Working Populations’, (Johnson, B, 1987).
1.Have you tired more easily than expected for the amount of activity you do?
2.Have you felt lightheaded or dizzy?
3.Have you had difficulty concentrating?
4.Have you been confused or disorientated?
5.Have you had trouble remembering things?
6.Have your relatives noticed that you have trouble remembering things?
7.Have you had to make notes to remember things?
8.Have you found it hard to understand the meaning of newspapers, magazines and books you have
9.Have you felt irritable?
10.Have you felt depressed?
11.Have you had heart palpitations when not exerting yourself?
12.Have you had a seizure?
13.Have you been sleeping more than is normal for you?
14.Have you had difficulty falling asleep?
15.Have you been bothered by incoordination or loss of balance.
16.Have you had any loss of muscle strength in your legs or feet?
17.Have you had any loss of muscle strength in your arms or hands?
18.Have you had difficulty moving your fingers or grasping things?
19.Have you had numbness or tingling in your fingers lasting more than a day or two?
20.Have you had any numbness or tingling in your toes lasting more than a day or two?
21.Have you had headaches at least once a week?
22.Have you had difficulty driving home from work because you felt dizzy or tired, even though you’d
23.Have you felt high from chemicals you use at work?
24.Have you had a lower tolerance for alcohol (takes less to get drunk)?
Acute symptoms during the workday
During the last month that you have worked have you noticed that you felt or experienced any of the
following symptoms during the workday:
3.Lightheaded or ‘high’
6.Difficulty remembering things
9.Loss of muscle strength
If you have answered yes to any of the symptoms above, do these symptoms come on when you are
using a specific substance? Please explain.
Answers to all 33 questions are graded: not at all; a little; moderately; quite a bit; or extremely.
Neurobehavioural tests are important to establish the objective impact of neurotoxic exposure on
behaviour. Behavioural changes may have an effect on accident rates. Suspicion that significant
neurotoxic exposure has occurred can come from hazard identification or from complaints or
observations of changes in the worker.
There are a wide variety of neurobehavioural tests and set batteries of tests available and
neurotoxilogical research utilises many different combinations of these. Lezaks’ textbook,
“Neuropsycological Assessment” (1995), contains an extensive compendium of tests with reference to
the cognitive functions being assessed, associations with known brain injury and normative data.
Fiedler, Feldman, Jacobson, Rahill and Wetherell (1996), in their review of neurobehavioural
assessment state that to adequately establish the effects of neurotoxicity on behaviour the test battery
must contain test for: overall cognitive ability; attention/concentration; motor skills; visuomotor
coordination; visuospatial relations; memory; and affect/personality.
The Neurobehavioral Core Test Battery (NCTB), recommended by the WHO has been found to be
sensitive for workers exposed to neurotoxic compounds (Anger, Cassitto, Liang, Amador, Hooisma,
Chrislip, Mergler, Keifer, Hortnagl, Fournier, Dudek, and Zsogon, (1993)). This reference contains a
description of the seven tests contained in the NCTB.
Electrophysiological tests are conducted by neurologists to diagnose injuries to the PNS (Gilman and
Winans-Newman,2001) Nerve conduction velocities (NCV) measure the speed of the impulse along
the nerve fibre. Demyelination injuries typically result in lower NCV than axonopathies ( Gilman and
Electromyography studies the electrical activity of the muscle by the insertion of a needle electrode
into muscle. The pattern of recruitment of motor units during muscle contraction are indicative of
pathology to either the nerve or the muscle (Gilman and Winins-Newman, 2001).
PROTECTION FROM NEUROLOGICAL INJURY
Below is a very brief summary of control remedies that may be applied once a thorough risk
assessment has been done.
Substitution/elimination: Can a less toxic substance be used instead? (i.e. non lipid soluble solvents)
Engineering controls: Wet grinding techniques to reduce atmospheric dust.
Isolation to reduce the number of workers exposed (i.e. spray painting booths)
Ventilation. Exhaust ventilation traps and removes contaminated air. General
ventilation dilutes the concentration of the substance in the environment.
Administrative controls: Job rotation to decrease the duration of exposure. Provide education and
training to supplement engineering controls.
Personal protective equipment: When exposure is unavoidable. Australian standards exist for the
selection and maintenance of respiratory devices (AS/NZS 1715 and 1716),
protective gloves (AS/NZS 2161), footwear (AS 2210) and protective clothing
Anger, W, Cassitto, M, Liang, Y, Amador, R, Hooisma, J, Chrislip, D, Mergler, D, Keifer, M,
Hortnagl, J, Fournier, L, Dudek, B, Zsogon, E (1993). Comparison of Performance from Three
Continents on the WHO-Recommended Neurobehavioural Core Test Battery. Environmental Research.
Cassitto, M, Camerino, D, Imbriani, M, Contardi, T, Masera, L, Gilioli, R (1993). Carbon Disulphide
and the Central Nervous System: A 15-Year Neurobehavioral Surveillance of an Exposed Population.
Environmental Research 63, 252-263
Cherry, N (1993). Neurobehavioural Effects of Solvents: The Role of Alcohol. Environmental
Research 62, 155-158
Chouaniere, D, Wild, P, Fontana, J-M, Hery, M, Fournier, M, Baudin, V, Subra, I, Rousselle, D,
Toamain, J-P, Saurin, S, Ardiot, M-R (2002). Neurobehavioral Disturbances Arising from
Occupational Toluene Exposure. American Journal of Industrial Medicine 41(2), 77-88
Chu, C-C, Huaang, C-C, Chen, R-S, Shih, T-S (1995). Polyneuropathy Induced by Carbon Disulphide
in Viscose Rayon Workers. Occupational and Environmental Medicine 52, 404-407
Deschamps, F, Guillaumot, M, Raux, S (2001). Neurological Effects in Workers Exposed to
Manganese. Journal of Occupational and Environmental Medicine 43(2), 127-132
Echeverria, D, Heyer, N, Martin, M, Naleway, C, Woods, J, Bittner, A (1995). Behavioral Effects of
Low-Level Exposure to Hg Among Dentists. Neurotoxicology and Teratology 17(2), 161-168
Feidler, N, Feldman, R, Jacobsen, J, Rahill, A, Wetherell, A (1996). The Assessment of
Neurobehavioral Toxicity: SGOMSEC Joint Report. Environmental Health Perspectives 104, (suppl.
Gilman, S, Winnans-Newman, S (2001). Manter and Gantz’ Essentials of Clinical Neuroanatomy and
Neurophysiology (7th ed) F.A. Davis Philadelphia
Klaassen, C (ed) (1996). Casserett and Doull’s Toxicology: The Basic Science of Poisons 5th ed.
MaGraw-Hill, New York.
Johnson, B (ed) (1987). Prevention of Neurotoxic Illness in Working Populations. World Health
Juntunen, J (1993). Neurotoxic Syndromes and Occupational Exposure to Solvents. Environmental
Research 60, 98-111
Lee, D, Park, I, Kim, J, Lee, Y, Kim, D, Kang, S-K (1998). Neurobehavioral Changes in Shoe
Manufacturing Workers. Neurotoxicology and Teratology 20(3), 259-263
Lezak, M (1995). Neuropsycological Assessment 3rd ed. Oxford University Press, New York.
Lindgren, K, Masten, V, Ford, D, Bleecker, M (1996). Relation of Cummulative Exposure to Inorganic
Lead and Neuropsycological Test Performance. Occupational and Environmental Medicine 53,
Maizlish, N, Parra, G, Feo, O (1995). Neurobehavioural Evaluation of Venezuelan Workers Exposed to
Inorganic Lead. Occupational and Environmental Medicine 52,408-414
Massaro, E (ed) (2002). Handbook of Neurotoxicology (vol 1) Humana Press, New Jersey
Nijem, K, Kristensen, P, Al-Khatib, A, Takhori, F, Bjertness, E (2001). Prevalence of Neuropsychiatric
and Mucous Membrane Irritation Complaints Among Palestinian Shoe Factory Workers Exposed to
Organic Solvents and Plastic Compounds. American Journal of Industrial Medicine 40(2), 192-198
Peiris-John, R, Ruberu, D, Wickremasinghe, A, Smit, L, Hoek, W (2002). Effects of Occupational
Exposure to Organophosphate Pesticides on Nerve and Neuromuscular Function. Journal of
Occupational and Environmental Medicine 44, 352-357
Yeh, J-H, Chang, Y-C, Wang, J-D (1995). Combined Electroneurographic and Electromyographic
Studies in Lead Workers. Occupational and Environmental Medicine 52, 415-419