OBJECTIVE: To determine whether heart function in childhood is affected by exposure to methylmercury (MeHg) from seafood. STUDY DESIGN: Prospective study of a Faroese birth cohort (N=1022). Examinations at ages 7 and 14 years included blood pressure, heart rate variability (HRV) and its frequency components of autonomic origin, and brainstem auditory evoked potentials (BAEPs). Mercury concentrations were determined in cord blood and in the child's hair. RESULTS: Both low-frequency (LF) and high-frequency (HF) activities decreased by about 25% from 7 to 14 years; they correlated well with the blood pressures. A doubling of prenatal MeHg exposure was associated with a decrease in LF and HF powers of about 6.7% (P=.04) and in the coefficient of variation of the electrocardiographic R-R interval of 2.7% (P=.04) at age 14 years. No discernible effect on blood pressure was apparent. Decreased LF variability was associated with increased latency of BAEP peak III, but adjustment for MeHg exposure substantially attenuated this correlation. CONCLUSIONS: Methylmercury exposure was associated with decreased sympathetic (LF) and parasympathetic (HF) modulation of the HRV. Parallel MeHg-related delays of BAEP latencies may be caused by underlying MeHg neurotoxicity to brainstem nuclei.
OBJECTIVE: To determine whether heart function in childhood is affected by exposure to methylmercury (MeHg) from seafood. STUDY DESIGN: Prospective study of a Faroese birth cohort (N=1022). Examinations at ages 7 and 14 years included blood pressure, heart rate variability (HRV) and its frequency components of autonomic origin, and brainstem auditory evoked potentials (BAEPs). Mercury concentrations were determined in cord blood and in the child's hair. RESULTS: Both low-frequency (LF) and high-frequency (HF) activities decreased by about 25% from 7 to 14 years; they correlated well with the blood pressures. A doubling of prenatal MeHg exposure was associated with a decrease in LF and HF powers of about 6.7% (P=.04) and in the coefficient of variation of the electrocardiographic R-R interval of 2.7% (P=.04) at age 14 years. No discernible effect on blood pressure was apparent. Decreased LF variability was associated with increased latency of BAEP peak III, but adjustment for MeHg exposure substantially attenuated this correlation. CONCLUSIONS: Methylmercury exposure was associated with decreased sympathetic (LF) and parasympathetic (HF) modulation of the HRV. Parallel MeHg-related delays of BAEP latencies may be caused by underlying MeHg neurotoxicity to brainstem nuclei.
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