Minamata disease

Abstract

Minamata disease (methylmercury poisoning) was first discovered in 1956 around Minamata Bay, Kumamoto Prefecture, Japan. A second epidemic in Japan occurred in 1965 along the Agano River, Niigata Prefecture. This paper presents a brief review of Minamata disease with an emphasis on the cases found in Kumamoto Prefecture. At autopsy, the most conspicuous destructive lesion in the cerebrum was found in the anterior portions of the calcarine cortex. Less severe but similar lesions may be found in the post-central, pre-central and temporal transverse cortices. Secondary degeneration from primary lesions may be seen in cases with long survival. In the cerebellum, pathological changes occur deep in the hemisphere. The granule cell population was more affected, compared with Purkinje cells. Among peripheral nerves, sensory nerves were more affected than motor nerves. Our recent experimental studies that reveal knowledge of the pathogenesis of methylmercury poisoning will be discussed.

High diversity of bacterial mercuric reductase genes from surface and sub-surface floodplain soil (Oak Ridge, USA)

“…However, severe mercury contamination of natural environments can often be attributed to inappropriate human activities. Examples include the Minamata Bay in Japan, where the local fish-consuming villagers were exposed and poisoned by high levels of methylmercury in their seafood due to contamination by a nearby acetaldehyde production facility (Eto, 2000;Tomiyasu et al, 2006). The Y12 nuclear weapons plant facility at Oak Ridge (TN, USA) used mercury for lithium isotope separation during the 1950s and 1960s, and this resulted in an estimated 75-150 tonnes of mercury inadvertently being released to the local environment, including the East Fork Poplar Creek (Han et al, 2006).…”

A Review on the Cognitive Neuroscience of Autism

“…Another related theory is autism induced by neurotoxic levels of mercury, or from the presence of ethylmercury in the vaccine preservative thimerosal. Associational evidence for this theory exists in well-documented regional reports of prenatal methylmercury exposure resulting in developmental disorders and neuropsychological effects often similar to those in autism (Eto, 2000;Grandjean et al, 1997). However, some studies have not shown significant adverse effects from methylmercury exposure (Marsh, Turner, Smith, Allen, & Richdale, 1995;McKeown-Eyssen, Ruedy, & Neims, 1983;Myers et al, 2003).…”

Thimerosal and Autism?

“…5,6 These signs, along with tremor, muscle pains, and weakness, are noted on relatively high-dose exposure, acute or chronic. In 3 Romanian children accidentally exposed to ethyl mercury in a fungicide, these same symptoms were prominent.…”

“…5,6,9 With lesser exposure there may be compromise of contrast sensitivity. 10,11 In addition, there may be paresthesias or, in infants, erythema and pain in hands and feet because of peripheral neuropathy.…”

“…Heavy prenatal exposure resulted in low birth weight, microcephaly, profound developmental delay, cerebral palsy, deafness, blindness, and seizures. 6,46 Affected adults experienced impairments of speech, constriction of visual fields, ataxia, sensory disturbance, and tremor.…”