Gewerbehygienische Kontrolle bei Herstellung von Alkylquecksilberverbindungen

Franke, Elk; Lundgren, K. D.

doi:10.1007/bf00334056

Cited by 4 publications

(3 citation statements)

References 4 publications

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“…Not surprisingly, the experimental treatments resulted in severe side effects in the patients ( Hepp 1887 ); therefore, this approach was not further pursued. However, the microbial toxicity was used in applications of methylmercury as a fungicide, which became important commercially starting around 1914, initially with few published records of adverse effects ( Franke and Lundgren 1956 ; Hunter and Russell 1954 ). This application of mercury became widely used in developing countries as part of the “green revolution,” without any monitoring of dissemination of mercury in the environment or of associated adverse effects.…”

Section: Early Evidence Of Human Toxicitymentioning

confidence: 99%

“…Despite the characteristic features of severe methylmercury poisoning, linkage to a causative exposure could be complicated by the latency period of several weeks to months between the exposure and the development of clinical symptoms ( Edwards 1865 ; Franke and Lundgren 1956 ). In addition, early symptoms, as seen in farmers and factory workers, were hard to recognize.…”

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

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: Early Evidence Of Human Toxicitymentioning

confidence: 99%

Section: Diagnostic Difficultiesmentioning

confidence: 99%

Adverse Effects of Methylmercury: Environmental Health Research Implications

Grandjean

Satoh

Murata

et al. 2010

Environ Health Perspect

266

168

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“…Methylmercury neurotoxicity was first demonstrated in adults, with extensive evidence accumulated from poisoning episodes 4. However, adverse effects proved to be difficult to diagnose due to the latency period of several weeks to months between exposure and development of clinical symptoms 5. Thus, in regard to routine health examinations of exposed workers, Ahlmark stated, “Such symptoms [of MeHg poisoning] scarcely differ from those generally found in neurasthenics when they think that they have been exposed to toxic risks.”6 Not surprisingly, therefore, the vulnerability of the developing human brain to MeHg was only discovered later on, as children in fishing populations experienced lasting adverse effects on brain function due to MeHg crossing the placental barrier 7.…”

Section: Introductionmentioning

confidence: 99%

Methylmercury and Brain Development: Imprecision and Underestimation of Developmental Neurotoxicity in Humans

Grandjean

Herz

2011

Mount Sinai J Medicine

105

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Methylmercury is now recognized as an important developmental neurotoxicant, though this insight developed slowly over many decades. Developmental neurotoxicity was first reported in a Swedish case report in 1952, and from a serious outbreak in Minamata, Japan a few years later. While the infant suffered congenital poisoning, the mother was barely harmed, thus reflecting a unique vulnerability of the developing nervous system. Nonetheless, exposure limits for this environmental chemical were based solely on adult toxicity until 50 years after the first report on developmental neurotoxicity. Even current evidence is affected by uncertainty, most importantly by imprecision of the exposure assessment in epidemiological studies. Detailed calculations suggest that the relative imprecision may be as much as 50%, or greater, thereby substantially biasing the results toward the null. In addition, as methylmercury exposure usually originates from fish and seafood that also contains essential nutrients, so-called negative confounding may occur. Thus, the beneficial effects of the nutrients may appear to dampen the toxicity, unless proper adjustment is included in the analysis to reveal the true extent of adverse effects. These problems delayed the recognition of low-level methylmercury neurotoxicity. However, such problems are not unique, and many other industrial compounds are thought to cause developmental neurotoxicity, mostly with less epidemiological support than methylmercury. The experience obtained with methylmercury should therefore be taken into account when evaluating the evidence for other substances suspected of being neurotoxic.

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