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Reproductive ecology is defined as "the study of causes and mechanisms of the effects of environmental risk factors on reproductive health and the methods of their prevention and management." Major areas of concern, within the purview of this paper, relate to adverse pregnancy outcomes, effects on target tissues in the male and the female, and alterations in the control and regulatory mechanisms of reproductive processes. Teratogenic potential of chemicals, released as a result of accidents and catastrophes, is of critical significance. Congenital Minamata disease is due to transplacental fetal toxicity caused by accidental ingestion of methyl mercury. Generalized disorders of ectodermal tissue following prenatal exposure to polychlorinated biphenyls have been reported in Taiwan and Japan. The Bhopal gas disaster, a catastrophic industrial accident, was due to a leak of toxic gas, methyl isocyanate (MIC), in the pesticide manufacturing process. The outcome of pregnancy was studied in female survivors of MIC exposure. The spontaneous abortion rate was nearly four times more common in the affected areas as compared to the control area (24.2% versus 5.6%; p < 0.0001). Furthermore, while stillbirth rate was found to be similar in the affected and control areas, the perinatal and neonatal mortality rates were observed to be higher in the affected area. The rate of congenital malformations in the affected and control areas did not show any significant difference. Chromosomal aberrations and sister chromatid exchange (SCE) frequencies were investigated in human survivors of exposure. The observed SCE frequencies in control and exposed groups indicated that mutagenesis has been induced. Strategies for the management, prediction, and preventability of such disasters are outlined.

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The objective of the present study was to determine the toxic trace element status of 51 healthy Austrian women and their newborn babies. Lead, mercury and cadmium content of early breast milk, blood and urine were measured post partum by atomic absorption spectrophotometry. None of the toxic trace elements could be found in elevated concentrations; the content of mercury and cadmium in milk was below limits of detection. Mean lead concentration in breast milk was 35.8 (SD:15.0) micrograms/l. Whole blood content of lead was 37.0 (SD:12.7) micrograms/l in mothers and 26.3 (SD:11.6) in newborns. High blood concentrations of mercury were found both in mothers (4.46 micrograms/l, SD:1.95) and in umbilical cord blood (5.58 micrograms/l, SD:2.33). The corresponding values for cadmium were 0.44 (SD:0.4) micrograms/l and 0.08 (SD:0.16) micrograms/l. Urine excretion of the elements assayed was normal. Significant correlations between maternal and neonatal blood toxic mineral levels could be demonstrated in lead (p < 0.001).

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A case of slight renal tubular dysfunction associated with cataract and anaemia was diagnosed in a 3-month-old black boy in whom high levels of mercury were found in blood and urine. Several arguments suggest that the renal, ocular and haematological defects may have resulted from exposure to mercury during foetal life and the 1-month lactation period due to the extensive use of inorganic mercury containing cosmetics by the mother.

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Minamata disease is a relatively new disease entity secondary to an environmental pollution, methyl mercury poisoning. The pathogenesis and pathology are described. The disease is a preventable one and precautionary steps through more stringent environmental policies are currently under way.

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A male, born on December 8, 1956, during the period when many Minamata diseases broke out in a district. His parents who ate much fish and shell fish taken in Minamata Bay suffered from the light, incomplete Minamata disease showing sensory disturbance, the constriction of the visual field, muscular weakness, etc. He weighed 3,225 gr. upon the normal birth given 10 months after pregnancy. His abnormalities were noted since his head was not stabilized on the neck even six months after the birth. Because of the delay in the development of the motor function, he became barely able to sit, stand up and begin walking at the ages of 3, 5 and 6 respectively. In 1962 (at the age of 6), his congenital Minamata disease was diagnosed in view of his clinical symptoms and epidemiological conditions. The mercury value in the hair and blood upon the birth is not known because a considerable time had elapsed after the birth when his mercury poisoning was discovered. However, the clinical symptoms included intelligence disturbance, character change, dysarthria, primitive reflexes, strabismus, hypersalivation, ataxia and hyperkinesia, indicating a typical congenital Minamata disease. Until he became 13 years old (1969) or so, his mental and motor function developed, both gradually. In the same year, he was admitted to a special class for the handicapped. EEG examination revealed that there was a slow alpha activity in the basic pattern and that 6 Hz positive spike was found in the sleep EEG. The constriction of the visual field was classified through examination.2+

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Extensive use of mercury in various economic branches and its toxic properties as well as increasing number of exposed population make it necessary to elaborate the data on the relatively little known aspects of hazardous effects of this compound. Basing on the data from literature and our own studies we analysed the effects of mercury on the sex cycle in humans and animals, penetration of mercury from mother's blood to fetus, embryotoxic and teratogenic effects of mercury and influence of prenatal intoxication on postnatal development of progeny. Toxic effects of organic and inorganic effects of mercuric compounds, especially mercury vapours, were compared. A need was pointed out to decrease the value of the maximum allowable concentration of mercury vapour to 0.01 mg/m3 in case of women's occupational exposure to that element.

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The EEGs of four siblings with organic mercury poisoning were recorded. The series of EEGs spanned two to eight years. Additional EEGs were obtained from an asymptomatic family member (the mother) who initially had elevated mercury levels. Various types of abnormalities were noted in the tracings of the siblings, including epileptiform features and disturbances of background rhythms. The mother's EEGs were normal. The degree of EEG change reflected the clinical state. In the two cases in which seizures were present, epileptiform activity was seen. Both clinical severity and EEG abnormalities may correlate with age.

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Detailed clinical and neuropathological studies have been made in two fullterm newborn human infants who were exposed to methylmercury in utero as a result of maternal ingestion of methylmercury-contaminated bread in early phases of pregnancy. High levels of mercury were detected in various regions of the brain at autopsy. Study of the brains revealed a disturbance in the development in both cases, consisting essentially of an incomplete or abnormal migration of neurons to the cerebellar and cerebral cortices, and deranged cortical organization of the cerebrum. There were numerous heterotopic neurons, both isolated and in groups, in the white matter of cerebrum and cerebellum and the laminar cortical pattern of the laminar cortical pattern of the cerebrum was disturbed in many regions as was shown by the irregular groupings and the deranged alignment of cortical. Prominent in the white matter of the cerebrum and the cerebellum was diffuse gemistocytic astrocytosis accompanied by an accumulation of mercury grains in their cytoplasm. These findings indicate a high degree of vulnerability of human fetal brain to maternal intoxication by methylmercury. A major effect appears to be related to faulty development and not to destructive focal neuronal damage as has been observed in mercury intoxicaiton in adults and children exposed postnatally.

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Methylmercury poisoning occurred in four cases after passage of methylmercury through the food chain. The neurological damage in all four cases was severe. The damage was greater at younger ages with maximum involvement in the case of transplacental poisoning. Significant recovery occurred in two cases, but on six-year follow-up two cases remained severely impaired. Clinical and electrophysiological evidence suggests that damage to peripheral sensory nerves may not be the cause of the late sensory symptomatology.

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