Adverse health effects in humans exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

The environmental contaminant 2,3,7,8-tetrachlordibenzo-p-dioxin (TCDD) belongs to the category of highly toxic, persistent organic pollutants that accumulate in animal fat and plant tissues. Today, background TCDD levels in human fat are showing a decreasing trend. The food chain is the main source of exposure in the human population. TCDD regulates the expression of a wide range of drug-metabolizing enzymes and has an impact on a large number of biological systems. The most pronounced effects have occurred in occupational settings following the uncontrolled formation of TCDD after industrial accidents, as well as in rare intentional intoxications. Although the acute effects of TCDD exposure are well described in the literature, the long-term consequences have been underevaluated. The most well-known symptoms of severe acute intoxication are chloracne, porphyria, transient hepatotoxicity, and peripheral and central neurotoxicity. Because of the long-term persistence of TCDD in the human body, atherosclerosis, hypertension, diabetes, vascular ocular changes, and signs of neural system damage, including neuropsychological impairment, can be present several decades after massive exposure. Such chronic effects are nonspecific, multifactorial, and may be causally linked to TCDD only in heavily intoxicated subjects. This opinion is supported by the dose-dependent effect of TCDD found in exposed workers and by experimental animal studies.

Color discrimination impairment in workers exposed to mercury vapor.

OBJECTIVE: To study color discrimination impairment in workers exposed to elemental mercury (Hg) vapor. SUBJECTS: Twenty-four male workers from a chloralkali plant exposed to Hg vapor, aged 42+/-9.8 years, duration of exposure 14.7+/-9.7 years, were examined. The 8h TWA air-borne Hg concentration in workplace was 59 microg/m(3); mean Hg urinary excretion (HgU) was 20.5+/-19.3 microg/g creatinine; mean Hg urinary excretion after the administration of a chelating agent, sodium 2,3-dimercapto-1-propane-sulfonate (DMPS), was 751.9+/-648 microg/48h. Twenty-four age- and gender-matched control subjects were compared. Visual acuity, alcohol intake, smoking habits, and history of diseases or drugs potentially influencing color vision were registered. METHODS: The Lanthony 15-Hue desaturated test (L-D15-d) was used to assess color vision. The results were expressed quantitatively as Bowman's Color Confusion Index (CCI), and qualitatively according to Verriest's classification of acquired dyschromatopsias. RESULTS: The CCI was significantly higher in the exposed group than in the control (mean CCI 1.15 versus 1.04; P=0.04). The proportion of subjects with errorless performance on the Lanthony test was significantly lower in the Hg exposed group compared to referents (52% versus 73%; P=0.035). The exposed group showed higher frequency of type III dyschromatopsias (blue-yellow confusion axis) in comparison with the control group (12.5% versus 8.3%), however, the difference did not reach statistical significance. Multiple regression did not show any significant relationship between the CCI, and age, alcohol consumption, or measures of exposure. CONCLUSION: In agreement with previous studies by Cavalleri et al. [Toxicol. Lett. 77 (1995) 351; Environ. Res. Sec. A 77 (1998) 173], the results of this study support the hypothesis that exposure to mercury vapor can induce sub-clinical color vision impairment. This effect was observed at an exposure level below the current biological limit for occupational exposure to mercury. This raises doubts on the actual protection afforded by this limit concerning the effect of mercury on color vision.

EEG photic driving in workers exposed to mercury vapors.

OBJECTIVE: To assess the potential of EEG photic driving (PD) as an indicator of an early neurotoxic effect of long-term, low-level exposure to mercury vapors. SUBJECTS AND METHODS: Twenty-four chloralkali workers exposed to mercury vapors; twenty-four age- and gender-matched control subjects. Level of exposure was determined by urinary mercury excreted both spontaneously and after administration of a chelating agent, sodium 2,3-dimercapto-1-propane sulfonate. A computerized method for quantitative evaluation of PD was developed. Five parameters describing PD were compared. RESULTS: The number of stimulation frequencies eliciting PD was higher in the exposed group, with a median of 17 frequencies, as compared to 10 frequencies in the control group (P < 0.001). The maximum value of PD was higher in the exposed group, with a median of 24.6 z-units as compared to 9.4 in the control group (P < 0.001). The median of the stimulation frequency with maximum PD was shifted from 15 Hz in the control group to 20 Hz in the exposed group (P < 0.01). The median of the sum of PD and the median of the index of PD were significantly higher in the exposed than in the control group (P < 0.001). The increased PD was particularly prominent at high stimulation frequencies in the beta range. There was no significant association between the measures of PD and the measures of exposure. CONCLUSIONS: In comparison with a control group, significantly increased photic driving was observed in a group of workers exposed to mercury vapors. The issue of whether or nor the intergroup differences in PD are mercury related, could not be determined on the basis of our results. Should the enhanced PD be caused by mercury, then this electrophysiological phenomenon might be regarded as a marker of the CNS hyperexcitability due to an early neurotoxic effect of mercury, the clinical expression of which is erethism.