Search

"Minamata disease" (methylmercury poisoning), originally found in Minamata, Japan 3 decades ago, still poses a medico-socio-legal problem mostly resulting from difficulty in drawing diagnostic demarcation. To examine the efficacy of urinary beta-2-microglobulin (BMG) in identifying patients with Minamata disease, the authors studied 115 patients (63 males and 52 females) who were officially registered for compensation (registered patients); 114 patients (54 males, 60 females) currently undergoing medical evaluations for compensation (unregistered patients); and 82 control subjects (40 males, 42 females) matched for sex and age. There was no significant difference with regard to urinary BMG (corrected by creatinine) among the above three groups, although there was a parallel increase in urinary BMG and neurological scores of male patients which suggested the presence of a dose-effect relationship. Although renal tubular dysfunction manifesting hyper-beta-2-microglobulinuria has been reported in patients with Minamata disease, our findings indicate that excessive excretion of BMG is not a satisfactory diagnostic parameter for Minamata disease.

Nerve conduction velocity (NCV) of the median motor, median sensory, and sural nerves was assessed in 16 workers chronically exposed to various inorganic mercury compounds. Exposed workers were compared with an unexposed control group using t test analyses. Slowing of the median motor nerve NCV was found, which was correlated with both increased levels of mercury in blood and urine, and with increased number of neurologic symptoms. Sensitive evaluation of neural function was found to be practical and informative for investigating mercury toxicity. Such evaluation can help determine safe mercury levels at the workplace.

Forty-two workers from a chemical plant producing inorganic mercury compounds were evaluated for neurologic, nephrotic, and ophthalmologic toxicity. Despite elevated blood and urinary mercury levels, routine clinical testing such as physical examination, blood chemistries, and urinalysis were generally normal. These findings from the routine examination are in contrast to the complaints of neuropsychological symptoms, elevated urinary n-acetyl B-D-glucosaminidase (NAG) levels, decreased motor nerve conduction velocities, and the presence of lenticular opacities on slit-lamp examination that were found, when organ systems known to be affected by mercury were targeted. More sensitive but objective indicators of toxicity need to be included in routine medical screening so as to help diagnose the etiology of neuropsychological symptoms and prevent long-term sequelae in workers exposed to mercury.

Data suggestive of a neuromuscular disorder responsive to neostigmine was uncovered in the course of electrophysiological testing of Iraqi patients poisoned by methylmercury. Subsequent neostigmine therapy produced a remarkable clinical improvement of the patients. Placebo substitution resulted in a substantial loss of testable strength that was restored when drug therapy was resumed.

Renal function indicated by urinary albumin and N-acetyl-beta-glucosaminidase was studied among a group of male chlorine-alkali workers (N = 60) and their matched referents (N = 60). Exposure to mercury vapor had occurred at least 5 y (mean 13.7 y; SD 5.5 y). The estimated long-term exposure level calculated from the time-weighted average blood concentrations of mercury had been approximately 25 micrograms/m3 of air. Neither glomerular nor tubular effects were shown in the exposed workers.