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Neurological and neurophysiological examinations on workers with chronic poisoning by 2,3,7,8-TCDD: follow-up 35 years after exposure
Urban P, Pelclová D, Lukás E, Kupka K, Preiss J, Fenclová Z, Smerhovský Z.
Language English Country Great Britain
NLK
Wiley Online Library (archiv)
from 1997-01-01 to 2012-12-31
- MeSH
- Cerebrovascular Disorders MeSH
- Chronic Disease MeSH
- Electroencephalography MeSH
- Financing, Organized MeSH
- Tomography, Emission-Computed, Single-Photon MeSH
- Environmental Pollutants blood poisoning MeSH
- Middle Aged MeSH
- Humans MeSH
- Follow-Up Studies MeSH
- Central Nervous System Diseases diagnosis chemically induced MeSH
- Nervous System Diseases diagnosis chemically induced MeSH
- Occupational Diseases diagnosis physiopathology psychology MeSH
- Neural Conduction MeSH
- Neurologic Examination MeSH
- Neuropsychological Tests MeSH
- Polychlorinated Dibenzodioxins blood poisoning MeSH
- Polyneuropathies diagnosis chemically induced physiopathology MeSH
- Color Vision Defects diagnosis chemically induced MeSH
- Evoked Potentials, Visual drug effects MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
Between 1965 and 1968, about 350 workers were accidentally exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in a chemical plant, which was producing herbicides based on the trichlorophenoxyacetic acid. About 80 workers developed signs of poisoning. The estimated mean concentration of TCDD at the time of exposure was about 5000 pg/g of plasma fat. Only 15 subjects from the original cohort remained available for the recent follow-up in 2004. All were men, mean age 60 years. The mean current TCDD plasma concentration was 128 pg/g. Neurological examination revealed some CNS impairment in eight subjects. Signs of polyneuropathy were found in nine subjects, confirmed by NCV studies in three cases. Electroencephalography was abnormal in three cases; Visual-evoked potential in five cases. Acquired dyschromatopsia was detected in six patients. SPECT showed focal reduction of perfusion in various brain locations in all but one patient. Two neuropsychological variables and the frequency of abnormal neurophysiological tests in individual patients correlated with TCDD plasma level. The findings support the hypothesis that TCDD can damage the nervous system. In addition to a direct neurotoxic effect of TCDD, changes secondary to vasculopathy should be considered, in the pathophysiology of the damage, because of the high frequency of lipid metabolism disorders and their complications.
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- $a Between 1965 and 1968, about 350 workers were accidentally exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in a chemical plant, which was producing herbicides based on the trichlorophenoxyacetic acid. About 80 workers developed signs of poisoning. The estimated mean concentration of TCDD at the time of exposure was about 5000 pg/g of plasma fat. Only 15 subjects from the original cohort remained available for the recent follow-up in 2004. All were men, mean age 60 years. The mean current TCDD plasma concentration was 128 pg/g. Neurological examination revealed some CNS impairment in eight subjects. Signs of polyneuropathy were found in nine subjects, confirmed by NCV studies in three cases. Electroencephalography was abnormal in three cases; Visual-evoked potential in five cases. Acquired dyschromatopsia was detected in six patients. SPECT showed focal reduction of perfusion in various brain locations in all but one patient. Two neuropsychological variables and the frequency of abnormal neurophysiological tests in individual patients correlated with TCDD plasma level. The findings support the hypothesis that TCDD can damage the nervous system. In addition to a direct neurotoxic effect of TCDD, changes secondary to vasculopathy should be considered, in the pathophysiology of the damage, because of the high frequency of lipid metabolism disorders and their complications.
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