Assessing mercury contamiantion in the Amazon

3. Discussion

3.6.2. Human studies outside of the Amazon

The Minimata bay incident in the late 1950's showed for the first time that fish was an important source of methylmercury to humans (WHO, 1990). This relation has since been supported in many studies.
Furthermore, it was recognized that the fetus could be severely affected even when the mother was asymptomatic (WHO, 1990). Clinical findings in symptomatic patients with prenatal exposure were similar and included microcephaly, mental retardation, cerebral palsy, seizures and deficits of hearing and vision. The findings with postnatal exposure were similar, but the severity was often less and seemed to vary with dosage and age.
Very little data was obtained about less severe forms of prenatal exposure and none about postnatal exposure. There were many uncertainties surrounding the Minimata episode, i.e. the cause was not identified until years after exposure. Consequently, maximum exposure had to be estimated. The interpretations of exposures were further complicated by inadequate assay methods.
During the winter of 1971-1972, a widespread outbreak of methylmercury poisoning occurred in Iraq. Methylmercury treated seed grain was consumed rather than planted. There were 6530 patients of all ages admitted to the hospital and 459 known deaths (WHO, 1990 ref. to Bakir et al., 1973). Paresthesias were the first clinical symptoms reported by patients. The first clinical finding was ataxia. Furthermore, a number of children who were both prenatally and postnatally exposed, showed clinical findings similar to those from the Minimata incident (WHO, 1990 ref. to Amin-Zaki et al., 1976). Studies also showed that continued breast-feeding by mothers with elevated blood mercury levels resulted in the infants' blood mercury levels falling slower than expected. When maternal and infants blood mercury levels were compared at birth, the infants had higher blood mercury levels than those from the mothers (WHO, 1990 ref. to Amin-Zaki et al., 1976).
These studies also showed that the most severely affected offspring had been exposed to methylmercury during the second trimester and that male offspring were more severely affected than female offspring. A dose-response curve for the association between prenatal exposure and attainment of developmental milestones (walking unaided before or after 18 months of age and using two meaningful words before or after the age of 24 months) and neurological findings were determined (Cox et al., 1989). The dose-response curve suggested that prenatal exposure as low as 10 µg/g peak mercury in maternal hair might be associated with adverse fetal consequences.
This was concerning because methylmercury is naturally occurring in fish and communities relying heavily on fish are exposed to methylmercury, which easily results in hair mercury concentrations above 10 µg/g (WHO, 1990).
However, the Iraqi study had some limitations. Interviews of the mother were done through interpreters at a mean child age of 30 months. Birth dates were ascertained in relation to other events, since they are not important in Arabic culture. The background rate of neurological abnormalities in the population was unknown. Most of the positive responses (i.e. delays in onset of walking) were observed for maternal hair levels above 60 µg/g. Only 3 out of 24 children with positive responses were born to mothers with hair levels below 59 ppm. Actually, this data was used to generate the 10 µg/g guideline. It was also unclear how applicable the data from an acute seed-grain poisoning episode were to a long time low-level exposure from a dietary source (i.e. fish). Small amounts of methylmercury consumed from fish over a longer time period could alter the way the human body handles it. Interestingly, at low Methylmercury-intake rates, hair methylmercury is about 15 times daily intake, but at very high intake rates the ratio approaches 2 (Lipfert, 1997). Furthermore, selenium and amino acids in fish could also influence mercury toxicity. Selenium may decrease the toxic effects of mercury and amino acids may compete with methylmercury for transport into the brain (WHO, 1990). Long-chain polyunsaturated fatty acids are high in fish and believed to be important in brain development and may inhibit adverse effects from low-level methylmercury exposure (Myers et al., 2000).
After the Iraqi incident, studies concentrated mainly on children who were prenatally exposed to mercury. The first studies were inconclusive mainly because of inadequate procedures. An example is the New Zealand study, where a dietary survey of 11,000 women provided an oppor-tunity to study prenatal methylmercury exposure. 73 of the women had hair mercury levels above 6 µg/g with a mean hair mercury concentration of 8 µg/g. Their children were enrolled in a study when these were 4 years of age (Kjellstrom et al., 1986). It was concluded that there was a significant dose-response relationship between mean hair mercury during pregnancy and results of the Denver Developmental Screening Test. However, there was a mismatching of age and ethnicity. Pacific Island children were compared to Europeans, and controls were older and had a better chance to pass the DDST. Marsh et al. (1994) suggested that the mixing of ethnic groups and difference in age could account for the differences in DDST score. Sample size is also important when study subtle effects on populations.
Two well designed studies are the Seychelles Child developmental Study and the Faroe Island study. Both studies were initiated independently in the late 1980's.
The Seychelles study consisted of 740 children who were followed and evaluated at 6.5, 19, 29, and 66, and 96 months (Myers et al. 2000). Median maternal hair mercury concentration was 7 µg/g during pregnancy (Myers et al., 2000). The composition of test batteries was neurological, developmental and psychological. No adverse associations between prenatal or postnatal mercury exposures were found in the Seychelles study (Myers et al. 2000). However, clear relations were found between mercury concentration in the brains of stillbirths and maternal hair mercury concentrations in the Seychelles study (Cernichiari et al., 1995). The Faroese diet is high in seafood including both fish and pilot whale. Average mercury concentration in pilot whale was 3.3 µg/g (Grandjean and Weihe, 1993). The Faroe study consisted of 1000 children born during a 21-month period. The index of prenatal exposure was total mercury in umbilical cord blood and in maternal hair during pregnancy. Median mercury concentration in umbilical cord blood was 24.2 µg/l (Grandjean et al., 1994). This value corresponds to maternal hair mercury concentration of 6 µg/g (Grandjean et al., 1994).
During the early years developmental data were recorded, and at approximately 7 years of age, 917 of the children underwent detailed neurobehavioral examination (Grandjean et al., 1997). Neuro-psychological tests included Finger Tapping; Hand-Eye Coordination; reaction time on a Continuous Performance Test; Wechsler Intelligence Scale for Children-Revised Digit Spans, Similarities, and Block Designs; Bender Visual Motor Gestalt Test; Boston Naming Test; and California Verbal Learning Test (Children). Clinical examination and neurophysiological testing did not reveal any mercury-related abnormalities. However, mercury-related neuropsychological dysfunctions were most pronounced in the domains of language, attention, and memory, and to a lesser extent in visuospatial and motor functions. These associations remained after adjustment for covariates and after exclusion of children with maternal hair mercury concentrations above 10 µg/g.

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