Reappraisal of the Historic 1959 Cat Experiment in Minamata by the Chisso Factory.

Eto, Komyo; Yasutake, Akira; Nakano, Atsuhiro; Akagi, Hirokatsu; Tokunaga, Hidehiro; Kojima, Teruyoshi

doi:10.1620/tjem.194.197

Cited by 25 publications

(40 citation statements)

References 5 publications

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“…Most embarrassing, toxicity experiments were carried out in the late 1950s by Chisso’s company doctor, Hajime Hosokawa. Ten cats were fed standard cat food mixed with effluent from the acetaldehyde plant, where mercury was used as a catalyst (Eto et al 2001). At that time, the researchers were not aware that the effluent contained methylmercury.…”

Section: Diagnostic Difficultiesmentioning

confidence: 99%

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Adverse Effects of Methylmercury: Environmental Health Research Implications

Grandjean

Satoh

Murata

et al. 2010

Environ Health Perspect

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266

168

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BackgroundThe scientific discoveries of health risks resulting from methylmercury exposure began in 1865 describing ataxia, dysarthria, constriction of visual fields, impaired hearing, and sensory disturbance as symptoms of fatal methylmercury poisoning.ObjectiveOur aim was to examine how knowledge and consensus on methylmercury toxicity have developed in order to identify problems of wider concern in research.Data sources and extractionWe tracked key publications that reflected new insights into human methylmercury toxicity. From this evidence, we identified possible caveats of potential significance for environmental health research in general.SynthesisAt first, methylmercury research was impaired by inappropriate attention to narrow case definitions and uncertain chemical speciation. It also ignored the link between ecotoxicity and human toxicity. As a result, serious delays affected the recognition of methylmercury as a cause of serious human poisonings in Minamata, Japan. Developmental neurotoxicity was first reported in 1952, but despite accumulating evidence, the vulnerability of the developing nervous system was not taken into account in risk assessment internationally until approximately 50 years later. Imprecision in exposure assessment and other forms of uncertainty tended to cause an underestimation of methylmercury toxicity and repeatedly led to calls for more research rather than prevention.ConclusionsCoupled with legal and political rigidity that demanded convincing documentation before considering prevention and compensation, types of uncertainty that are common in environmental research delayed the scientific consensus and were used as an excuse for deferring corrective action. Symptoms of methylmercury toxicity, such as tunnel vision, forgetfulness, and lack of coordination, also seemed to affect environmental health research and its interpretation.

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Section: Diagnostic Difficultiesmentioning

confidence: 99%

“…Only in 1969 did Hosokawa reveal that the results existed and had been suppressed by his employer. A detailed scientific account was eventually published after a 40-year delay (Eto et al 2001). …”

Section: Diagnostic Difficultiesmentioning

confidence: 99%

Adverse Effects of Methylmercury: Environmental Health Research Implications

Grandjean

Satoh

Murata

et al. 2010

Environ Health Perspect

Self Cite

266

168

View full text Add to dashboard Cite

show abstract

“…If the outbreak of neurological disease in the cats had been adequately investigated at the time it occurred, many of the human cases could have been prevented (Aronson 2005;Eto et al 2001 …”

Section: Box 1 Case Example Of Shared Health Risk Between Animals Andmentioning

confidence: 99%

Animals as Sentinels: Using Comparative Medicine To Move Beyond the Laboratory

Rabinowitz¹,

Scotch²,

Conti³

2010

ILAR Journal

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The comparative medicine approach, as applied to the study of laboratory animals for the betterment of human health, has resulted in important medical and scientific progress. Much of what is known about the human health risks of many toxic and infectious hazards present in the environment derives from experimental studies in animals and observational (epidemiological) studies of exposed human populations. Yet there is a third source of "in vivo" knowledge about host-environment interactions that may be underused and -explored: the study of diseases in naturally occurring animal populations that may signal potential human health threats. Just as canaries warned coal miners of the risk of toxic gases, other nonhuman animals, due to their greater susceptibility, environmental exposure, or shorter life span, may serve as "sentinels" for human environmental health hazards. Traditionally, communication between human and animal health professionals about cross-species sentinel events has been limited, but progress in comparative genomics, animal epidemiology, and bioinformatics can now provide an enhanced forum for such communication. The "One Health" concept involves moving toward a comparative clinical approach that considers "shared risks" between humans and animals and promotes greater cooperation and collaboration between human and animal health professionals to identify and reduce such risks. In doing so, it also creates new opportunities for the field of comparative medicine that can supplement traditional laboratory animal research.

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“…At high level exposure, however, MeHg is known to induce severe brain damage including a gross loss of neurons following neuronal degeneration and death, particularly the layer IV neurons in the neocortex of humans (Hunter and Russell, 1954, Takeuchi et al, 1959, 1962; Nierenberg et al, 1998) and experimental animals (Chang and Hartmann, 1972; Shaw et al, 1975; Syversen et al, 1981; Merigan et al, 1983; O’Kusky, 1985; Wakabayashi et al, 1995; Nagashima et al, 1996; Nagashima, 1997; Eto et al, 2001a, 2001b, 2002b). Therefore, it is possible that MeHg-induced neuron loss may result in reactive gliosis and/or neuronal network rewiring and forming aberrant recurrent excitatory circuits similar to those seen in chronic epilepsy resulting from brain trauma, ischemia, tumors, infection and status epilepticus (SE) in humans (for review see Parent and Murphy, 2008; Scharfman and McCloskey, 2009) and subsequently lead to hyperexcitability.…”

Section: Introductionmentioning

confidence: 99%

Methylmercury: A potential environmental risk factor contributing to epileptogenesis

Yuan

2012

NeuroToxicology

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Epilepsy or seizure disorder is one of the most common neurological diseases in humans. Although genetic mutations in ion channels and receptors and some other risk factors such as brain injury are linked to epileptogenesis, the underlying cause for the majority of epilepsy cases remains unknown. Gene-environment interactions are thought to play a critical role in the etiology of epilepsy. Exposure to environmental chemicals is an important risk factor. Methylmercury (MeHg) is a prominent environmental neurotoxicant, which targets primarily the central nervous system (CNS). Patients or animals with acute or chronic MeHg poisoning often display epileptic seizures or show increased susceptibility to seizures, suggesting that MeHg exposure may be associated with epileptogenesis. This mini-review highlights the effects of MeHg exposure, especially developmental exposure, on the susceptibility of humans and animals to seizures, and discusses the potential role of low level MeHg exposure in epileptogenesis. This review also proposes that a preferential effect of MeHg on the inhibitory GABAergic system, leading to disinhibition of excitatory glutamatergic function, may be one of the potential mechanisms underlying MeHg-induced changes in seizure susceptibility.

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Reappraisal of the Historic 1959 Cat Experiment in Minamata by the Chisso Factory.

Cited by 25 publications

References 5 publications

Adverse Effects of Methylmercury: Environmental Health Research Implications

Adverse Effects of Methylmercury: Environmental Health Research Implications

Animals as Sentinels: Using Comparative Medicine To Move Beyond the Laboratory

Methylmercury: A potential environmental risk factor contributing to epileptogenesis

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