Q J Med 2000; 93: 655-661
© 2000 Association of Physicians
Neurological deficits in solvent-exposed painters: a syndrome including impaired colour vision, cognitive defects, tremor and loss of vibration sensation
From the Department of Environmental and Occupational Medicine, University Medical School, Aberdeen
Received 9 March 2000 and in revised form 10 August 2000
 |
Summary |
|---|
 Top Summary IntroductionMethodsDiscussionReferences |
|---|
Five individuals are described who had participated in a study of former dockyard painters. All had worked between 16 years and 45 years as industrial painters, much of the time inside ships. All underwent structured neurological examination, colour vision testing (allowing calculation of a colour confusion index corrected for age and alcohol), and detailed psychometric testing. An occupational history sufficient to allow estimation of past exposure to solvents was taken. All gave a history of exposure to high concentrations of solvents at work, and several described episodes of acute narcosis. All showed neurological deficits and some had overt neurological disease, although in no case had this previously been linked to their work. The most striking features, sufficient to constitute a syndrome, were acquired blue-yellow colour vision deficits, coarse tremor, impaired vibration sensation in the legs and cognitive impairment. Their estimated cumulative exposures to solvents ranged between the equivalent of 13 and 37 calendar years working at the Occupational Exposure Standard concentration (OES years). This study for the first time gives an indication of the concentrations of solvents likely to lead to serious neurological disease in humans. It serves as a reminder to physicians to take an occupational history from patients with obscure neurological or psychological impairment.
|
Introduction |
|---|
|
TopSummaryIntroductionMethodsDiscussionReferences |
|---|
Organic solvents are widely used in industry in fuels, degreasants, adhesives and paints. The Health and Safety Executive estimates that about 2 million workers (9% of the working population) in the UK use these chemicals regularly.1 Many are narcotic and may be abused by glue sniffers, sometimes with fatal consequences. Some epidemiological studies have suggested that exposure to them may be a risk factor for a range of major neurological diseases including Parkinson's disease,2 multiple sclerosis,3,4 and motor neurone disease.5–8
We have previously reported five patients with major neurological disease in whom heavy workplace exposure to solvents seemed likely to have been an aetiological factor.9 Three of these workers had been employed as painters in a dockyard in Scotland. We followed up this observation with a questionnaire survey of the painters in this dockyard and community controls.10 The study demonstrated a significant excess of neuro-psychological symptoms among the painters, with a dose-response relationship among those with the longest exposures to solvents. A parallel study of Chinese dockyard painters showed very similar results.11
This work has now been taken further by a detailed clinical study of 120 individuals in the cohort selected on the basis of their response to the symptom questionnaire. At the conclusion of this study, it became apparent that certain features were associated with heavy solvent exposure and we here report the characteristic clinical findings in these painters.
|
Methods |
|---|
|
TopSummaryIntroductionMethodsDiscussionReferences |
|---|
Subject selection
The original dockyard painter population was 1292 men, of whom 953 were still alive and 302 had responded to the Orebro Q-16 solvent symptoms questionnaire,10 developed for screening solvent-exposed workers to identify those who might be showing symptoms of solvent neurotoxicity. Of the 302, we studied 35 painters with six or more positive symptoms recorded in their responses, 33 with two or fewer positive responses and 10 with 3–5 symptoms. We also studied 42 community controls. Among all these, we found a number of painters with strikingly similar findings on neuropsychological examination. We report five of these subjects here, together with the results of our estimates of their occupational exposures to solvents.
Neuropsychological examinations
A battery of psychometric tests, a structured neurological examination, detailed occupational histories with estimation of lifetime solvent exposures and colour vision testing using the Lanthony D-15-d test were undertaken. The psychometric tests were a mixture of pencil and paper and computerized tests. The paper and pencil tests were Trailmaking A+B, the Benton visual retention test and two measures of pre-morbid ability: the National Adult Reading Test [NFER.Nelson] and the vocabulary test of the Wechsler Adult Intelligence Test Revised [WAIS-R]. The computerized tests were all drawn from the Neurobehavioural Evaluation System 2 [NES2, Neurobehavioural Systems Inc., Atlanta, GA, USA]. Those used were the Continuous Performance Test [CPT], Symbol Digit Substitution [SDS] without paired associate learning, the Associate Learning Test [ALT] and Delayed Associate Recall [ART]. Neurological examination comprised measurement of visual acuity, temperature sensation, two-point discrimination, vibration perception, grip strength dynamometry, tendon reflexes in the legs, clonus, gait, finger-nose approximation, tremor, and recording of fasciculation or muscle wasting. Temperature sensation was assessed using PVC and copper discs applied on three occasions to the dorsum of each hand and foot. The result was scored as the number of correct responses for each limb. Two-point discrimination was measured on both index fingers with Sweet's dividers, a normal result being defined as the ability to distinguish two-points at 5 mm separation. Grip strength was measured on each hand on two occasions using a digital grip strength dynamometer (Takei Scientific Instruments). Visual acuity was tested on a 3 m Snellen chart. The Lanthony D-15-d colour vision test was used to assess acquired colour vision deficits. A McBeth Sol-Source D-65 daylight lamp was used to illuminate the chips during testing. The Lanthony D-15-d test is especially sensitive to blue-yellow colour vision deficits, and can detect sub-clinical losses. It is suitable for the detection of acquired colour vision deficits in solvent-exposed workers.12
The colour vision results were scored both qualitatively and quantitatively. The results of the Lanthony D-15-d test were charted and any transpositions compared with the axis of tritan and tetartan deficits (blue-yellow losses). These are the commonest acquired colour vision defects. They are frequently sub-clinical and are related to age and alcohol intake. The quantitative results were expressed as a Colour Confusion Index,13 and adjusted for age and alcohol consumption to produce an age- and alcohol-adjusted colour confusion index.14 A positive score equates to a worse-than-predicted performance and a negative score equates to a better-than-predicted performance.
Estimates of solvent exposures
This investigation (by SS) was independent of the clinical examination. A lifetime work history with details of job duration and work tasks was obtained from all 120 subjects. The data were refined by literature review of any measurements of solvent exposures during similar dockyard and painting work practices, by analyses of the solvent monitoring results for the dockyard between 1982 and 1992, and from data sheets. Each subject's work history was then coded into job groups for every quarter year. A total of 24 job groups was used to classify employment. Finally, these were divided into discrete job tasks that were assessed by subjective exposure modelling methods.15 This allowed estimation of exposures using logarithmic values for intrinsic emission of the substance, how it was handled, and what hygiene control measures were in place.
Each subject's exposure was calculated by marrying the job group exposure estimates with the work history database, for six marker solvents (xylene, white spirit, methylethyl ketone, 2-ethoxyethanol, dichloromethane and acetone) individually and as a total solvent score, by summating each solvent fraction relative to its UK Occupational Exposure Standard (OES). The cumulative lifetime solvent exposure estimate for all six solvents added together provided a total solvent score which was expressed in terms of OES years. For the purposes of this study, an OES year is equivalent to working at the OES for the solvent(s) 8 h a day for 365 days.
Case descriptions
Patient 1, aged 68, had worked for 45 years as a domestic painter using brush and roller and for 6 years as an industrial painter on vessels in the dockyard. His Q-16 score was 8 and total solvent score 14.6 OES years (See Table 1
for summary of key findings). When applying acoustic tiles to ships' hulls using a volatile adhesive in a tented and heated area, he recalled having felt intoxicated after short periods in spite of using a respirator. He had also stripped paint using 10–15 gallons of dichloromethane weekly and in his last 3 years had sprayed fire-retardant paint in gangways and compartments.
|
He had developed a coarse resting tremor affecting his left hand at about the time of retiral, progressing since then. He reported tingling in his feet and toes, present for 8 years, most prominent at night. Investigations for diabetes had been negative. Psychometric testing showed the verbal IQ as estimated by the National Adult Reading Test (NART) to be 103 and by the vocabulary subset of the Wechsler Adult Intelligence Scale (Revised) to be 100 IQ points. Trailmaking A and B were both poorer than predicted. Benton visual retention test score was normal at 6/10 with an error score of 6. Temperature sensation was impaired in both feet but normal in both hands. Vibration perception was diminished on the left great toe compared with the right. Grip strength was diminished in his left hand (25.5 kgf) compared with his right (34.5 kgf) in the absence of trauma or degenerative disease affecting the arm. Two-point discrimination, tendon reflexes and gait were normal, and there was no muscle wasting or fasciculation. Finger-nose approximation was normal. A left cataract had been removed several years ago and he had an early right cataract; visual acuity was 6/18 right, 6/12 left. Qualitatively colour vision showed a number of blue-yellow errors, most marked in the right eye where they may have been due to his early cataract. Quantitative scoring showed the AACCI to be 0.82, worse than predicted and supporting the qualitative impression of an acquired blue-yellow deficit.
These results suggest some acquired loss of intellectual function, evidence of impairment of peripheral nerve function, coarse resting tremor and blue-yellow colour vision deficit.
Patient 2, aged 67, had worked for 16 years within the dockyard. His Q-16 score was 3 and total solvent score was 16.8 OES years. He had worked for 2 years painting ships' hulls and tank cleaning with white spirits, then became a shot-blaster/painter for 7 years, blasting tanks and applying primer or chlorinated rubber to water tanks. He was proud of the ways that he and his team had been able to increase their productivity and gain extra bonuses by taking short cuts, most of which implied compromised safety. He described carrying out tank painting without airline masks, and pouring paint into tanks and spreading it around instead of brushing it. Subsequently he became a bricklayer's mate in the dockyard for 7 years, but this job still involved heavy exposure to solvents in floor adhesives and cleaning agents, and he often felt sick and high doing this task. No respiratory protective equipment was worn.
In the early 1980s he had developed a coarse tremor that got progressively worse. His workmates had teased him about this and it now interfered with rolling cigarettes and holding a mug. In 1985 he had been investigated in hospital and was advised he did not have Parkinson's disease, but no explanation was offered. His estimated verbal IQ was 100 on the NART and 106 on the WAIS-R vocabulary subset. Trailmaking A and B were abnormal. Benton visual retention test score was normal at 8/10 with an error score of 3. Temperature perception was impaired on the right hand (he had vibration white finger) but was normal in both feet. He was unable to perceive a vibrating tuning fork at or below his tibial plateaux. Two-point discrimination was normal. Grip strength was normal at 35.6 kgf in the right hand and 36.9 kgf in the left. The right knee reflex was slightly reduced compared with the left. His gait was normal. There was wasting of his right thenar eminence due to a previous injury. Finger-nose approximation was normal. Visual acuity was 6/12 right and worse than 6/60 on the left. Colour vision testing was not possible on the left eye because of cataract, but his right eye showed a marked blue-yellow defect and AACCI for the right eye was 0.81, markedly worse than predicted.
In summary, he showed blue-yellow colour vision loss, mild cognitive impairment, tremor and peripheral neuropathy. His poor performance in Trailmaking tests might have been due to mild cognitive impairment or to confounding by his tremor.
Patient 3, aged 68, had worked for 39 years as a painter, 8 years in the dockyard and a further 18 months spray-painting aircraft components. His Q-16 score was 8 and solvent exposure was 13.3 OES years. He never wore a mask in the dockyard even though he used fire-retardant, white epoxy and chlorinated rubber inside vessels. He also worked with paint stripper (dichloromethane).
Eleven years previously he had been retired on health grounds from the dockyard. In spite of his age and a lack of family history, he was diagnosed at that time as suffering from Spinal Muscular Atrophy. His attention span was poor and psychometric testing proved difficult. His IQ was low at 85 as measured by the National Adult Reading test [NART] and 89 as estimated by the WAIS-R vocabulary subset. His performance on Trailmaking A and B showed results well outwith the normal range. Benton visual retention test was 4/10 with an error score of 14, consistent with his estimated pre-morbid verbal IQ and age. A coarse tremor was found in both hands; it had been present for at least 3 years. Temperature perception was normal but two-point discrimination was impaired at 10 mm in both index fingers. Vibration was just perceived at the right tibial plateaux but not at or below the left tibial plateau. Grip strength was poor in both hands at 22.9 kgf in the right and 25 kgf in the left, non-dominant, hand. Reflexes were absent despite reinforcement. His gait was broad-based with drop-foot bilaterally. Muscle wasting without fasciculation was present in both calves. Finger-nose approximation was normal. Visual acuity was 6/9 bilaterally and colour vision testing showed a blue-yellow deficit, more marked in the right eye. However the AACCI was -0.23, slightly better than predicted for a man of his age.
It was not possible to say whether his intellectual impairment was innate or acquired, but his attention span was markedly impaired. In retrospect, his neuromuscular disorder seems unlikely to be spinal muscular atrophy, and resembles the features described in previous patients with high solvent exposures.9 The coincidence of peripheral neuropathy and tremor was similar to that of the other patients.
Patient 4, aged 50, had worked for 26 years as a dockyard painter. His Q-16 score was 2 and total solvent score was 36.7 OES years, the third highest we have recorded. He had spent all his working life in the dockyard, particularly in the spray-booth area. He rarely used respiratory protective equipment, even when spraying. He described using a bucket of thinners (white spirit) each day to wash down electrical equipment prior to spraying. He also used large quantities of dichloromethane on board certain ships.
He admitted taking more than 60 units alcohol/week for 
5 years. After he developed grand mal epilepsy (which was attributed to his alcohol abuse), he reduced but did not cease his drinking. His grand mal convulsions only occurred while asleep. Estimated verbal IQ was 95 on the National Adult Reading Test and 91 on the WAIS-R. Trailmaking A was 38 s and Trailmaking B was prolonged at 146 s. Benton visual retention test score was reduced at 5/10 with six errors, raising the question of cognitive impairment. Neurological examination showed finger-nose approximation to be abnormal on both sides. He did not have a tremor. He had impaired temperature perception on the right hand only. Two-point discrimination was normal. He had reduced vibration perception to the mid-shin on the right leg and to the ankle on the left. Grip strength was 33.4 kgf in the right hand and 32.1 kgf in the left. Tendon reflexes were present with reinforcement in the lower limbs with the exception of an absent left ankle reflex. There was no clonus, muscle wasting or fasciculation. Visual acuity was 6/9 right and 6/12 left, and colour vision testing showed, qualitatively, a blue-yellow deficit in both eyes with multiple transpositions. The AACCI at 2.1 confirmed impaired blue-yellow vision.
The evidence of impaired colour vision, cognitive impairment, grand mal epilepsy, mild peripheral neuropathy and incoordination suggests multi-focal impairment related to both alcohol and solvent exposure.
Patient 5, aged 60, had worked for 34 years as a painter, 17 in the dockyard. His Q-16 score was 9 and total solvent score was 20.1 OES years. He was involved in a large amount of painting in very confined spaces using highly volatile paints and chlorinated rubber, and rarely felt able to wear the mask provided. He recalled an occasion when he and five colleagues using a new epoxy paint in cabins ended up in the dockyard hospital after 1 h work suffering from burning throats and eyes. He dated his history of 10 years' recurring light-headedness to that acute exposure. He had initially complained of light-headedness, poor balance and staggering, sore throat and eyes. Investigations at a teaching hospital had led to him being diagnosed as suffering from ‘myalgic encephalomyelitis’. His symptoms had persisted, tending to fluctuate in severity.
He had an estimated verbal IQ on the NART of 108 and on the WAIS-R of 104. Trailmaking A and B were both prolonged. Benton visual retention test score was 5/10 (predicted 6/10) with eight errors (predicted five), raising the question of acquired cognitive impairment. He had a coarse resting tremor, worse in the left arm. Temperature perception was impaired in the left foot only. Two-point discrimination was normal. Vibration perception was absent below the tibial plateaux. The hand grip at 22.8 kgf on the right and 8.0 kgf on the left was poor, more on the left where he had osteoarthritis of the shoulder. Reflexes in the legs were normal and there was no muscle wasting or fasciculation. He walked with a limp on the left due to sciatica. He reported reduced power in his lower legs and altered sensation over the lateral border of his left foot that he related to his sciatica. Finger-nose approximation was impaired bilaterally. Visual acuity was 6/9 bilaterally. Colour vision testing showed a blue-yellow deficit in the right eye, but his AACCI was better than predicted at -0.44.
He thus showed a combination of cognitive impairment, tremor and loss of vibration perception. His peripheral sensory deficits may have been due to his back problems. His mild colour vision deficit does not seem to be linked to his solvent exposure.
|
Discussion |
|---|
|
TopSummaryIntroductionMethodsDiscussionReferences |
|---|
Our investigation of solvent-related neurological disease started with the clinical referral of a number of patients with obscure disease to one of the authors, leading to a report in this journal suggesting that heavy exposures could cause serious neurological impairment.9 Three of those reported had worked as painters in the same dockyard, leading us to carry out a study of the entire cohort of 1292 dockyard painters of whom 239 had died (two of motor neurone disease).10 That study used a neuropsychological questionnaire and was duplicated in a Chinese dockyard;11 both showed substantial differences between painters and controls in symptom prevalence.
We have now taken this work further by detailed clinical studies of a sample of 78 of these men and 42 community controls. Because of the complex and time-consuming nature of the studies, only a limited number of individuals were prepared to take part, and they do not represent a random sample. Further analyses are underway, to relate solvent exposure estimates to clinical findings, but we were impressed by the combination of certain signs in many subjects. On subsequent investigation of their exposures, we found all to have been exceedingly high, and believe this to be a syndrome worth drawing to the attention of physicians. Taken together with the three patients reported previously and the two diagnosed as having died from motor neurone disease among this cohort of 1292 men,9 even in the unlikely event that we found all subjects with neurological disease, there must be a strong suspicion that work as a painter in this particular dockyard was in part responsible. Indeed, at least five other subjects in this study (not reported here) showed a similar but incomplete pattern of abnormalities.
We have used a new and sophisticated method of estimating solvent exposures. Prior to making these assessments, the occupational hygienist undertook a comprehensive training program in the subjective exposure modelling technique, comparing estimated exposures with measured results for a variety of exposure scenarios. A mean log (estimated): log (measured) ratio of 1.08 was achieved with a correlation coefficient of 0.89 between measured and estimated results. A proportion of the exposure estimates was also validated against measured results from dockyard records. It was apparent from the workers' own reports that they had very substantial solvent exposures, often sufficient to cause narcosis, and it seems likely that there were technical difficulties in achieving adequate ventilation during painting in confined spaces in the ships. We are aware that the performance of the ventilation and airlines was variable. Moreover, respiratory protective equipment may not be effective and in confined spaces may make a difficult job impossible. The use of bonus systems can lead to shortcuts being taken to achieve productivity targets, and supervisors may turn a blind eye to such practices as deadlines loom.
In 1985 a description of neuro-behavioural disorders associated with exposure to solvents was agreed.16 A Type 2B deficit was described as follows: ‘Impairment in intellectual function. There is difficulty in concentration, impairment of memory and a decrease in learning capacity. These symptoms are accompanied by objective evidence of impairment. There may also be minor neurological signs. The complete reversibility of Type 2-B is questionable.’ Most of the patients described here would meet this case definition. In terms of intellectual impairment, some of the subjects described here showed poor performance on Trailmaking A and B but normal Benton visual retention tests. It may be that Trailmaking tests are more sensitive to subtle cognitive impairment in solvent-exposed workers than is the Benton visual retention test, but it is possible that poor performance on Trailmaking may reflect tremor and not cognitive impairment. Alternatively, the Benton visual retention test may provide an overestimate, since results are expressed with reference to expected performance after adjusting for age and IQ. Pre-morbid IQ is estimated by a vocabulary test, on the basis that vocabulary tests show ‘hold’ properties, at least in the presence of mild cognitive impairment, and this may not be true in solvent-exposed workers.17,18 To date, no study has examined the performance of either the NART or WAIS-R in a solvent-exposed cohort. If vocabulary tests do not hold in solvent-exposed workers, then the painters' estimated pre-morbid IQ would be lower than their true ability, and thus the IQ-corrected Benton test may fail to detect a true deficit.
There have now been several studies apart from ours that suggest an excess of major neurological disease in solvent-exposed workers.2–8 As well as an excess of conditions such as motor neurone disease, there have been case reports of atypical neurological illnesses in solvent-exposed workers and solvent abusers.9,19 Others have described panic attacks in association with solvent exposure,20 as did our first patient. Solvent exposure has also been linked to epilepsy, as in our patient 4, in a number of workers and abusers.21,22 There have also been studies that have implicated solvent exposure in the development of poor balance,23,24 as in our patient 5.
A recent report described sensory polyneuropathy consistent with an axonopathy in two of three former painters.25 These painters had impaired vibration perception in the feet, and all three had a tremor. It is well known that certain solvents, such as n-hexane, may cause peripheral neuropathy. There is now evidence from epidemiological studies and case reports that other solvent mixtures may be associated with peripheral neuropathy. Two of three studies have found evidence of peripheral neurological abnormalities in the legs of exposed workers.26,27 The third study, using nerve conduction studies in the arms only, did not find neuropathy.28
Whether solvent exposure can cause cognitive impairment remains controversial in the UK.28–30 A number of carefully conducted studies have suggested that solvent exposures are linked to mild cognitive impairment.31–33 While there have been well-conducted negative studies, these have been in workers with relatively low-level exposure.34 Our findings suggest that high workplace exposures have such adverse effects, but they may be subtle and go undiagnosed or, if identified, may not be recognised as work-related. It is important to take an occupational history when assessing patients with vague neuropsychological complaints, especially when the clinical picture is unusual.
This study cannot prove a causal link between solvent exposure and neuropsychological deficits, but we believe that such a link is likely given the high exposures. We recognize that the working conditions in this dockyard have improved greatly over the last 30 years and that work as a painter now is unlikely to pose the same risk as it did in the 1960s; however, there is little room for complacency. Confined spaces are still painted, and great care is needed to prevent high solvent exposures.
|
Notes |
|---|
Address correspondence to Professor A. Seaton, DEOM, Medical School, Foresterhill, Aberdeen AB25 2ZD. e-mail: a.seaton{at}abdn.ac.uk
|
References |
|---|
|
TopSummaryIntroductionMethodsDiscussionReferences |
|---|
1. HSE. Health risks management: a guide to working with solvents. HSG188, 1st edn. Sudbury, HSE Books, 1999;1.
2. Smargiassi A, Mutti A, De Rosa A, De Palma G, Negrotti A, Calzetti S. A case-control study of occupational and environmental risk factors for Parkinson's disease in the Emilia-Romagna region of Italy. Neurotoxicology1998; 19:709–12.[ISI][Medline]
3. Amaducci L, Arfaioli C, Inzitari D, Marchi M. Multiple sclerosis among shoe and leather workers: An epidemiological survey in Florence. Acta Neurol Scand1982; 65:94–103.[ISI][Medline]
4. Flodin U, Söderfeldt B, Noorlind-Brage H, Fredriksson M, Axelson O. Multiple sclerosis, solvents and pets. A case referent study. Arch Neurol1988; 45:620–3.[Abstract]
5. Gunnarsson L-G, Bodin L, Söderfeldt B, Axelson O. A case-control study of motor neurone disease: its relation to heritability, and occupational exposures, particularly to solvents. Br J Ind Med1992; 49:791–8.[ISI][Medline]
6. Chancellor AM, Slattery JM, Fraser H, Warlow CP. Risk factors for motor neuron disease: a case-control study based on patients from the Scottish Motor Neuron Disease Register. Neurol Neurosurg Psychiatry1993; 56:1200–6.
7.
Schulte PA, Burnett CA, Boeniger MF, Johnson J. Neurodegenerative diseases: occupational occurrence and potential risk factors, 1982 through 1991. Am J Public Health1996; 86:1281–8.
8. Graham AJ, Macdonald AM, Hawkes CH. British motor neuron disease twin study. Neurol Neurosurg Psychiatry1997; 62:562–9.
9.
Seaton A, Jellinek EH, Kennedy P. Major neurological disease and occupational exposure to organic solvents. Q J Med1992; 84:707–12.
10. Chen R, Dick F, Seaton A. Health effects of solvent exposure among dockyard painters: mortality and neuropsychological symptoms. Occup Environ Med1999; 56:383–7.[Abstract]
11. Chen R, Wei L, Seaton A. Neuropsychological symptoms in Chinese male and female painters: an epidemiological study in dockyard workers. Occup Environ Med1999; 56:388–90.[Abstract]
12. Mergler D, Blain L. Assessing colour vision loss among solvent-exposed workers. Am J Ind Med1987; 12:195–203.[ISI][Medline]
13. Bowman KJ. A method for quantitative scoring of the Farnsworth Panel D-15. Acta Opthalmol1982; 60:907–16.
14.
Semple S, Dick F, Osborne A, Cherrie JW, Seaton A, Haites N. Impairment of colour vision in workers exposed to organic solvents. Occup Environ Med2000; 57, 582–87.
15. Cherrie JW, Schneider T, Spankie S, Quinn M. A new method for structured, subjective assessments of past concentrations. Occupational Hygiene1996; 3:75–83.
16. Cranmer JM, Golberg L. Proceedings of the workshop on neurobehavioural effects of solvents. Neurotoxicology1987; 7:45–56.
17. Michélsen H, Lundberg I. Neuropsychological verbal tests may lack ‘hold’ properties in occupational studies of neurotoxic effects. Occup Environ Med1996; 53:478–83.[Abstract]
18. Viaene M, Veulemans H, Masschelein R. Experience with a vocabulary test for workers previously and still exposed to styrene. Scand J Work Environ Health1998; 24:308–11.[ISI][Medline]
19. Poungvarin N. Multifocal brain damage due to lacquer sniffing: the first case report from Thailand. J Med Assoc Thai1991; 74:296–300.[Medline]
20.
Dager SR, Holland JP, Cowley DS, Dunner DL. Panic disorder precipitated by exposure to organic solvents in the work place. Am J Psych1987; 144:1056–8.
21. Byrne A, Kirby B, Zibin T, Ensminger S. Psychiatric and neurological effects of chronic solvent abuse. Can J Psych1991; 36:735–8.
22. Jacobsen M, Baelum J, Bonde JP. Temporal epileptic seizures and occupational exposure to solvents. Occ Environ Med1994; 51:429–30.[Abstract]
23. Niklasson M, Möller C, Üdkvist LM, Ekberg K, Flodin U, Dige N, Sköldestig Å. Are deficits in the equilibrium system relevant to the clinical investigation of solvent-induced neurotoxicity? Scand J Work Environ Health1997; 23:206–13.[ISI][Medline]
24. Smith LB, Bhattacharya A, Lemasters G, Succop P, Puhala II E, Medvedovic M, Joyce J. Effect of chronic low-level exposure to jet fuel on postural balance of US Air Force personnel. J Occ Environ Med1997; 39:623–32.[ISI][Medline]
25. Hageman G, van der Hoek J, van Hout M, van Der Laan G, Steur EJ, de Bruin W, Herholz K. Parkinsonism, pyramidal signs, polyneuropathy, and cognitive decline after long-term occupational solvent exposure. J Neurol1999; 246:198–206.[ISI][Medline]
26. Halonen P, Halonen J-P, Lang HA, Karskela V. Vibratory perception thresholds in shipyard workers exposed to solvents. Acta Neurol Scand1986; 73:561–5.[ISI][Medline]
27. Ruitjen MWMM, Hooisma J, Brons JT, Habets CEP, Emmen HH, Muijser H. Neurobehavioural effects of long-term exposure to xylene and mixed organic solvents in shipyard spray painters. Neurotoxicology1994; 15:613–20.[ISI][Medline]
28. Cherry N, Hutchins H, Pace T, Waldron HA. Neurobehavioural effects of repeated occupational exposure to toluene and paint solvents. Br J Ind Med1985; 42:291–300.[ISI][Medline]
29. Grasso P, Sharratt M, Davies DM, Irvine D. Neuropsychological and psychological disorders and occupational exposure to organic solvents. Food Chem Toxicol1984; 22:819–52.[ISI][Medline]
30. Waldron HA. Solvents and the brain (editorial). Br J Ind Med1986; 43:73–4.[ISI][Medline]
31. Lundberg I, Michélsen H, Nise G, Hogstedt C, Högberg M, Alfredsson L, Almkvist O,Gustavsson A, Hagman M, Herlofson J, Hindmarsh T, Wennberg A. Neuropsychiatric function of housepainters with previous long-term heavy exposure to organic solvents. Scand J Work Environ Health1995; 21(suppl 1):3–44.[ISI][Medline]
32. Morrow LA, Steinhauer SR, Condray R, Hodgson M. Neuropsychological performance of journeymen painters under acute solvent exposure and exposure-free conditions. J Int Neuropsychol Soc1997; 3:269–75.[Medline]
33. Daniell WE, Claypoole KH, Checkoway H, Smith-Weller T, Dager SR, Townes BD, Rosenstock L. Neuropsychological function in retired workers with previous long term occupational exposure to solvents. Occup Environ Med1999; 56:93–105.[Abstract]
34. Spurgeon A, Glass DC, Calvert IA, Cunningham-Hill M, Harrington JM. Investigation of dose-related neurobehavioural effects in paint makers exposed to low levels of solvents. Occup Environ Med1994; 51:626–30.[Abstract]
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  F. Dick, S. Semple, A. Osborne, A. Soutar, A. Seaton, J.W. Cherrie, L.G. Walker, and N. Haites Organic solvent exposure, genes, and risk of neuropsychological impairment QJM, June 1, 2002; 95(6): 379 - 387. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R Chen, S Semple, F Dick, and A Seaton Nasal, eye, and skin irritation in dockyard painters Occup. Environ. Med., August 1, 2001; 58(8): 542 - 543. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||