Cardiac autonomic activity in methylmercury neurotoxicity: 14-year follow-up of a Faroese birth cohort

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

doi:10.1016/j.jpeds.2003.10.058

Cited by 197 publications

(142 citation statements)

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“…44 Neurobehavioral research has only recently begun to include cardiovascular parameters, and adverse cardiovascular effects in children are now known to occur as a result of exposures to neurotoxicants, such as lead 45 and methylmercury. 46,47 In the present study, the exposure-related increase in systolic blood pressure and the smaller, not statistically significant, increase in diastolic blood pressure were independent of stunting and other covariates. Parallel to this increase, a higher number of exposed children exceeded the expected normal range of systolic blood pressure.…”

Section: Discussioncontrasting

confidence: 46%

Pesticide Exposure and Stunting as Independent Predictors of Neurobehavioral Deficits in Ecuadorian School Children

Harari²,

et al. 2006

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OBJECTIVES. To examine possible effects on blood pressure, neurological function, and neurobehavioral tests in school-aged children with and without prenatal pesticide exposure in an area where stunting is common.METHODS. In a community of Northern Ecuador with intensive floriculture and a high female employment rate, we invited 79 children attending the 2 lowest grades of a public school for clinical examinations. In addition to a thorough physical examination, we administered simple reaction time, Santa Ana dexterity test, Stanford-Binet copying, and Wechsler Intelligence Scale for Children-Revised Digit Spans forward. Maternal interview included detailed assessment of occupational history to determine pesticide exposure during pregnancy. Recent and current pesticide exposure was assessed by erythrocyte acetylcholine esterase activity and urinary excretion of organophosphate metabolites.RESULTS. All eligible children participated in the study, but 7 children were excluded from data analysis due to other disease or age Ͼ9 years. A total of 31 of the remaining 72 children were classified as stunted based on their height for age. Maternal occupational history revealed that 37 children had been exposed to pesticides during development. After confounder adjustment, prenatal pesticide exposure was associated with a higher systolic blood pressure than in the controls. On neurological examination, 14 exposed children and 9 controls showed Ն1 abnormalities. Of 5 neurobehavioral tests, the Stanford-Binet copying test showed a lower drawing score for copying designs in exposed children than in controls. Stunting was associated with a lower score on this test only, and both risk factors remained statistically significant in a multiple regression analysis with adjustment for demographic and social confounders. Increased excretion of dimethyl and diethyl metabolites of organophosphates was associated with increased reaction time and no other outcomes.CONCLUSION. Prenatal pesticide exposure may cause lasting neurotoxic damage and add to the adverse effects of malnutrition in developing countries. The effects differ from those due to acute pesticide exposure. T HE DEVELOPING BRAIN is particularly susceptible to adverse effects of environmental toxicants and nutritional deficiencies. 1 During fetal development, the placenta offers some protection against unwanted compounds, but it is not an effective barrier against environmental neurotoxicants. 2 Furthermore, the blood-brain barrier, which protects the adult brain from many toxic agents, is not completely formed until ϳ6 months after birth 3 and, therefore, provides no protection during sensitive developmental stages. At the same time, the brain depends on appropriate supplies of essential nutrients, and malnutrition, as apparent from stunted growth, may result in delayed neurobehavioral development. [4][5][6][7][8][9] The vulnerability of the brain originates from the combination of immaturity and ongoing development. 10 For optimal brain development to occur, a numb...

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Section: Discussioncontrasting

confidence: 46%

Pesticide Exposure and Stunting as Independent Predictors of Neurobehavioral Deficits in Ecuadorian School Children

Harari²,

et al. 2006

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“…We measured 300 R-R intervals in the supine position (i.e., approximately for 3 min in preschool children or for 5 min in adults), and HRV parameters were calculated from consecutive R-R intervals with minimal deviation; i.e., the process of R-R interval data extraction for spectral analysis does not depend on observers (Murata et al 1992Grandjean et al 2004;Ishii et al 2005). Liao et al (1997) also computed LF-and HF-PSDs of HRV from 2-min beat-to-beat heart rate data in the Atherosclerosis Risk in Communities (ARIC) study.…”

Section: Discussionmentioning

confidence: 99%

“…In applying spectral analysis with fast Fourier transformation, the ARIC study used records of beat-to-beat data of 2.5 min to capture a few cycles of low-frequency heart rate fluctuation (Liao et al 1997). We employed a samplingtime of 1 msec and the autoregressive spectral model, and the model does not seem to have caused such problems (Murata et al 1992(Murata et al , 2006Grandjean et al 2004;Ishii et al 2005). Thus, it is suggested that our findings were not heavily influenced by such measurement errors.…”

Section: Discussionmentioning

confidence: 99%

“…were automatically extracted from the obtained data to reduce measurement error (Murata et al 1992;Grandjean et al 2004;Ishii et al 2005). The CV RR (%) was defined as the ratio of the S.D.…”

Section: Methodsmentioning

confidence: 99%

“…Also, it has been suggested that subjects with low HRV had an adverse cardiovascular risk profile and an elevated risk of incident CHD and death (Dekker et al 2000), and that cardiovascular autonomic function played an important role in increasing blood pressure levels associated with increased modulation of parasympathetic tone of the heart after puberty but not in preadolescents (Tanaka et al 2000). In this way, HRV is thought to be a promising and reliable tool to provide a marker of less favorable health (Grandjean et al 2004;Unalacak et al 2004;Murata et al 2006), and this approach should be applied to sleep research in children.…”

confidence: 99%

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Cardiac Autonomic Hypofunction in Preschool Children with Short Nocturnal Sleep

Sampei

Murata

Dakeishi

et al. 2006

Tohoku J. Exp. Med.

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Preschool children with sleep deficit may suffer from autonomic symptoms or hypotension. Heart rate variability, reflecting cardiac parasympathetic and sympathetic activities, and blood pressure were assessed to clarify the effects of nocturnal sleep duration on cardiac autonomic function in 134 preschool children aged 5 and 6 years. Parents reported their children's typical bedtimes and wake times for weekdays. In the children, the mean nocturnal sleep duration (± standard deviation) was 575 ± 42 min. The parasympathetic and sympathetic activities and systolic blood pressure (SBP) were significantly lower in the 80 children with short sleep (nocturnal sleep duration < 10 hrs) than in the 54 children with long sleep ( 10 hrs). Only the SBP was positively correlated with nocturnal sleep duration in the children ( p < 0.001); also, short nocturnal sleep duration was significantly related to hypotension (SBP < 100 mmHg), as judged by multiple logistic regression analysis. Among the children, inverse correlations were seen between the parasympathetic activity and SBP and between the sympathetic activity and diastolic blood pressure ( p < 0.05). These findings indicate that shortening of nocturnal sleep is associated with cardiac autonomic hypofunction and low SBP in preschool children. We suggest that sleep duration is an important predictor for autonomic development in childhood.nocturnal sleep duration; cardiac parasympathetic and sympathetic activities; blood pressure; preschool children

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