Reappraisal of somatosensory disorders in methylmercury poisoning

Ninomiya, Tadashi; Imamura, Keiko; Kuwahata, Misako; Kindaichi, Michiaki; Susa, Mari; Ekino, Shigeo

doi:10.1016/j.ntt.2005.03.008

Cited by 54 publications

(58 citation statements)

References 21 publications

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“…In patients with fetal MD, a significant prolongation of N13-N19 interpeak latency was recorded, thus indicating a delayed central conduction time of the somatosensory pathway [Inayoshi et al, 1988]. Also, the thresholds of two-point discrimination increased at both the lip and forefingers in patients with acquired MD and the fishermen residing in nearby communities at the Shiranui Sea beyond the Minamata Bay, as compared to the age-matched controls [Ninomiya et al, 2005]. On the other hand, methylmercury-poisoned rats showed markedly decreased amplitudes, while the latencies were normal for the potentials evoked in the spinal dorsal roots [Arimura et al, 1988].…”

Section: Previous Evidence On Minamata Diseasementioning

confidence: 99%

Neurophysiological evidence of methylmercury neurotoxicity

Murata

Grandjean

Dakeishi

2007

American J Industrial Med

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Section: Previous Evidence On Minamata Diseasementioning

confidence: 99%

Neurophysiological evidence of methylmercury neurotoxicity

Murata

Grandjean

Dakeishi

2007

American J Industrial Med

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“…1). Actually, the mercury content in the hair samples of healthy Wshermen around the Shiranui Sea was about 10-20 times higher than that of Wshermen in Kumamoto city (non-polluted area) in 1960 (Doi and Matsushima 1962;Ninomiya et al 2005). As shown in Fig.…”

Section: Introductionmentioning

confidence: 92%

Age standardized cancer mortality ratios in areas heavily exposed to methyl mercury

Yorifuji

Tsuda

Kawakami

2007

Int Arch Occup Environ Health

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While the negative association between MeHg and gastric cancer might be explained by salt intake, the positive association between MeHg and leukemia could not be explained by potential confounders. Despite some limitations mainly due to its ecologic design, this study indicates the necessity of an individual-level study evaluating the association between MeHg and leukemia in regions with exposure to MeHg.

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“…The thresholds of two-point discrimination increased at both forefingers and the lip in both groups. Effects which were associated with the damage to the somatosensory cortex (apraxia limb kinetics, astereognosis and disorder of active sensation) were more frequently detected in MD patients (Ninomiya et al, 2005). Uchino et al (2005) re-examined Minamata patients with respect to neurological symptoms and signs of Minamata disease.…”

Section: Epidemiological Studies Concerning Oral Exposure To Methyl Mmentioning

confidence: 99%

Collate the literature on toxicity data on mercury in experimental animals and humans (Part I – Data on organic mercury)

Hassauer

Kaiser

Schneider

et al. 2012

EFSA Supporting Publications

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It was the scope of this project to collate, compile and summarise the scientific literature on the toxicity of methyl mercury, inorganic mercury and total mercury in humans and experimental animals published since 2002 and not evaluated in former JECFA risk assessments. Epidemiological data on MeHg toxicity confirmed former findings on an association between prenatal exposure and developmental neurotoxicity. Recent findings also support an influence of methyl mercury on the cardiovascular and immune system. Existing epidemiological data reveal several shortcomings limiting their suitability for risk assessment. Developmental neurotoxicity seems to be the most critical effect of MeHg in animals. A LOAEL of 0.01 mg/kg b.w. per day has been reported in young mice for locomotor activity exposed in utero. Rats seem to be less sensitive towards this endpoint: a NOAEL of 0.04 mg/kg b.w. per day has been reported in this species for locomotor activity. Systemic effects other than neurotoxicity have been mostly observed at higher doses than those producing neurotoxicity. No qualified epidemiological data appropriate for the evaluation of the toxicity of inorganic mercury after oral intake have been identified due to several limitations of the studies, e.g. small study group, insufficient control for confounders, inadequate exposure assessment. Toxicological studies in experimental animals widely confirmed former findings with respect to the target organs (neuro-, liver-, kidney-, immune-and reproductive toxicity, oxidative stress). The animal studies indicate that there might be relevant toxicological effects (developmental toxicity, liver toxicity) of inorganic mercury at dose levels similar or below the BMDL 10 value used for the derivation of the existing PTWI. However, due to some limitations of the studies no final conclusions can be drawn from these studies and the findings need further confirmation.

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Reappraisal of somatosensory disorders in methylmercury poisoning

Cited by 54 publications

References 21 publications

Neurophysiological evidence of methylmercury neurotoxicity

Neurophysiological evidence of methylmercury neurotoxicity

Age standardized cancer mortality ratios in areas heavily exposed to methyl mercury

Collate the literature on toxicity data on mercury in experimental animals and humans (Part I – Data on organic mercury)

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