Delayed brainstem auditory evoked potential latencies in 14-year-old children exposed to methylmercury

Murata, Katsuyuki; Weihe, Pál; Budtz‐Jørgensen, Esben; Jørgensen, Poul J.; Grandjean, Philippe

doi:10.1016/j.jpeds.2003.10.059

Cited by 218 publications

(148 citation statements)

References 20 publications

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“…Even given these provisos, the confluent finding of effects on tasks assessing attention, manual motor speed, and language/semantic memory suggests that the effects of MeHg at these levels of brain development are multi-focal or diffuse, affecting widely divergent brain structures. The existence of sustained neurotoxic effects in adolescents is also supported by the neurophysiological examinations that were carried out in parallel [26]. Thus, auditory evoked potential latencies at age 14 years increased at higher prenatal MeHg exposures, and the heart rate variability decreased.…”

Section: Discussionmentioning

confidence: 83%

“…Exposure levels at age 14 years averaged about one-fifth of those experienced prenatally, although exposures at age 7 years were slightly higher [26]. Table 3 shows associations with potential confounders.…”

Section: Resultsmentioning

confidence: 99%

“…A disadvantage of these supplementary analyses was that information was missing from several participants, thus affecting the statistical power of regression analyses that rely on complete cases. Additional analyses also incorporated the PCB exposure [16] and postnatal MeHg exposure parameters [26] as explanatory variables.…”

Section: Discussionmentioning

confidence: 99%

“…Blood specimens and hair samples were again obtained, and the proximal 2-cm hair segment was used for mercury analysis [26]. Detailed quality assurance data showed acceptable analyses for both exposure biomarkers.…”

Section: Methodsmentioning

confidence: 99%

“…In choosing feasible effect parameters, an important consideration includes suitability for the age group and culture. As confounderindependent outcomes, neurophysiological measurements have provided evidence that developmental MeHg neurotoxicity is detectable through age 14 years [26]. Clinical neurological tests have shown mercury-related adverse effects neonatally [29], but such tests may not be sensitive enough at school age [18].…”

Section: Introductionmentioning

confidence: 99%

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Impact of prenatal methylmercury exposure on neurobehavioral function at age 14 years

Debes

Budtz‐Jørgensen

Weihe

et al. 2006

Neurotoxicology and Teratology

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249

167

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A cohort of 1022 consecutive singleton births was generated during [1987][1988] in the Faroe Islands, where increased methylmercury exposure occurs from traditional seafood diets that include pilot whale meat. The prenatal exposure level was determined from mercury analyses of cord blood, cord tissue, and maternal hair. At age 14 years, 878 of 1010 living cohort members underwent detailed neurobehavioral examination. Eighteen participants with neurological disorders were excluded. Blood and hair samples obtained from the participants were analyzed for mercury. The neuropsychological test battery was designed based on the same criteria as applied at the examination at age 7 years. Multiple regression analysis was carried out and included adjustment for confounders. Indicators of prenatal methylmercury exposure were significantly associated with deficits in finger tapping speed, reaction time on a continued performance task, and cued naming. Postnatal methylmercury exposure had no discernible effect. These findings are similar to those obtained at age 7 years, and the relative contribution of mercury exposure to the predictive power of the multiple regression models was also similar. An analysis of the test score difference between results at 7 and 14 years suggested that mercury-associated deficits had not changed between the two examinations. In structural equation model analyses, the neuropsychological tests were separated into five groups; methylmercury exposure was significantly associated with deficits in motor, attention, and verbal tests. These findings are supported by independent assessment of neurophysiological outcomes. The effects on brain function associated with prenatal methylmercury exposure therefore appear to be multi-focal and permanent.

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Section: Discussionmentioning

confidence: 83%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Impact of prenatal methylmercury exposure on neurobehavioral function at age 14 years

Debes

Budtz‐Jørgensen

Weihe

et al. 2006

Neurotoxicology and Teratology

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249

167

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Heavy Metals Exposure and Hearing Loss in US Adolescents

Shargorodsky¹,

Curhan²,

Henderson³

et al. 2011

Arch Otolaryngol Head Neck Surg

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Methylmercury

Bellinger¹

2008

Encyclopedia of Quantitative Risk Analysis and Assessment

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Methylmercury (MeHg) is a heavy metal that is dispersed into the environment as the result of both natural and anthropogenic processes. The primary pathway of human exposure is the consumption of seafood from contaminated waters. Because of biomagnification and bioaccumulation as MeHg ascends the aquatic food chain, MeHg levels are highest in the muscles of long‐lived predatory fish. MeHg is actively transported to the brain and across the placenta. The devastating effects of high‐dose MeHg exposures were revealed by poisoning episodes in Japan and Iraq. These episodes resulted in the recognition that fetal exposure is particularly deleterious. They also provided motivation for the conduct of many epidemiological studies seeking to determine whether adverse effects result from chronic low‐dose MeHg exposure as the result of frequent consumption of seafood. For risk assessment purposes, the most important of these studies, some of which are ongoing, were conducted in New Zealand, the Faroe Islands, and the Seychelles Islands. The findings have been mixed, and different governmental agencies have made different choices in selecting the data on which to base MeHg risk assessments. The benchmark dose modeling approach used by the US Environmental Protection Agency to establish a MeHg reference dose (RfD) is described. The sensitivity of the RfD to the underlying assumptions is illustrated. All MeHg risk assessments are complicated by the fact that the consumption of seafood also provides beneficial nutrients whose health effects can be antagonistic to those of MeHg.

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Delayed brainstem auditory evoked potential latencies in 14-year-old children exposed to methylmercury

Cited by 218 publications

References 20 publications

Impact of prenatal methylmercury exposure on neurobehavioral function at age 14 years

Impact of prenatal methylmercury exposure on neurobehavioral function at age 14 years

Heavy Metals Exposure and Hearing Loss in US Adolescents

Methylmercury

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