Julie Sturza1, Monica K Silver2, Lin Xu3, Mingyan Li4, Xiaoqin Mai5, Yankai Xia6, Jie Shao7, Betsy Lozoff8, John Meeker9. 1. Center for Human Growth and Development, University of Michigan, Ann Arbor, MI, USA. Electronic address: jmigrin@umich.edu. 2. Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, MI, USA. Electronic address: mksilver@umich.edu. 3. Department of Child Health Care, Children's Hospital Zhejiang University School of Medicine, Zhejiang, China. Electronic address: xlin33@163.com. 4. Department of Child Health Care, Children's Hospital Zhejiang University School of Medicine, Zhejiang, China. Electronic address: li.mingyan1984@gmail.com. 5. Department of Psychology, Renmin University of China, Beijing, China. Electronic address: maixq@ruc.edu.cn. 6. State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing, China. Electronic address: yankaixia@njmu.edu.cn. 7. Department of Child Health Care, Children's Hospital Zhejiang University School of Medicine, Zhejiang, China. Electronic address: shaojie@zju.edu.cn. 8. Center for Human Growth and Development, University of Michigan, Ann Arbor, MI, USA. Electronic address: blozoff@umich.edu. 9. Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, MI, USA. Electronic address: meekerj@umich.edu.
Abstract
BACKGROUND: Pesticides are associated with poorer neurodevelopmental outcomes, but little is known about the effects on sensory functioning. METHODS: Auditory brainstem response (ABR) and pesticide data were available for 27 healthy, full-term 9-month-old infants participating in a larger study of early iron deficiency and neurodevelopment. Cord blood was analyzed by gas chromatography-mass spectrometry for levels of 20 common pesticides. The ABR forward-masking condition consisted of a click stimulus (masker) delivered via ear canal transducers followed by an identical stimulus delayed by 8, 16, or 64 milliseconds (ms). ABR peak latencies were evaluated as a function of masker-stimulus time interval. Shorter wave latencies reflect faster neural conduction, more mature auditory pathways, and greater degree of myelination. Linear regression models were used to evaluate associations between total number of pesticides detected and ABR outcomes. We considered an additive or synergistic effect of poor iron status by stratifying our analysis by newborn ferritin (based on median split). RESULTS: Infants in the sample were highly exposed to pesticides; a mean of 4.1 pesticides were detected (range 0-9). ABR Wave V latency and central conduction time (CCT) were associated with the number of pesticides detected in cord blood for the 64ms and non-masker conditions. A similar pattern seen for CCT from the 8ms and 16ms conditions, although statistical significance was not reached. Increased pesticide exposure was associated with longer latency. The relation between number of pesticides detected in cord blood and CCT depended on the infant's cord blood ferritin level. Specifically, the relation was present in the lower cord blood ferritin group but not the higher cord blood ferritin group. CONCLUSIONS: ABR processing was slower in infants with greater prenatal pesticide exposure, indicating impaired neuromaturation. Infants with lower cord blood ferritin appeared to be more sensitive to the effects of prenatal pesticide exposure on ABR latency delay, suggesting an additive or multiplicative effect.
BACKGROUND: Pesticides are associated with poorer neurodevelopmental outcomes, but little is known about the effects on sensory functioning. METHODS: Auditory brainstem response (ABR) and pesticide data were available for 27 healthy, full-term 9-month-old infants participating in a larger study of early iron deficiency and neurodevelopment. Cord blood was analyzed by gas chromatography-mass spectrometry for levels of 20 common pesticides. The ABR forward-masking condition consisted of a click stimulus (masker) delivered via ear canal transducers followed by an identical stimulus delayed by 8, 16, or 64 milliseconds (ms). ABR peak latencies were evaluated as a function of masker-stimulus time interval. Shorter wave latencies reflect faster neural conduction, more mature auditory pathways, and greater degree of myelination. Linear regression models were used to evaluate associations between total number of pesticides detected and ABR outcomes. We considered an additive or synergistic effect of poor iron status by stratifying our analysis by newborn ferritin (based on median split). RESULTS:Infants in the sample were highly exposed to pesticides; a mean of 4.1 pesticides were detected (range 0-9). ABR Wave V latency and central conduction time (CCT) were associated with the number of pesticides detected in cord blood for the 64ms and non-masker conditions. A similar pattern seen for CCT from the 8ms and 16ms conditions, although statistical significance was not reached. Increased pesticide exposure was associated with longer latency. The relation between number of pesticides detected in cord blood and CCT depended on the infant's cord blood ferritin level. Specifically, the relation was present in the lower cord blood ferritin group but not the higher cord blood ferritin group. CONCLUSIONS: ABR processing was slower in infants with greater prenatal pesticide exposure, indicating impaired neuromaturation. Infants with lower cord blood ferritin appeared to be more sensitive to the effects of prenatal pesticide exposure on ABR latency delay, suggesting an additive or multiplicative effect.
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