Abstract
In our previous study of 3-year-old children in a dioxin contamination hot spot in Vietnam, the high total dioxin toxic equivalent (TEQ-PCDDs/Fs)-exposed group during the perinatal period displayed lower Bayley III neurodevelopmental scores, whereas the high 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-exposed group displayed increased autistic traits. In autistic children, urinary amino acid profiles have revealed metabolic alterations in the amino acids that serve as neurotransmitters in the developing brain. Therefore, our present study aimed to investigate the use of alterations in urinary amino acid excretion as biomarkers of dioxin exposure-induced neurodevelopmental deficits in highly exposed 3-year-old children in Vietnam. A nested case-control study of urinary analyses was performed for 26 children who were selected from 111 3-year-old children whose perinatal dioxin exposure levels and neurodevelopmental status were examined in follow-up surveys conducted in a dioxin contaminated hot spot. We compared urinary amino acid levels between the following 4 groups: (1) a high TEQ-PCDDs/Fs and high TCDD-exposed group; (2) a high TEQ-PCDDs/Fs but low TCDD-exposed group; (3) a low TEQ-PCDDs/Fs exposed and poorly developed group; and (4) a low TEQ-PCDDs/Fs exposed and well-developed group. Urinary levels of histidine and tryptophan were significantly decreased in the high TEQ-PCDDs/Fs and high TCDD group, as well as in the high TEQ-PCDDs/Fs but low TCDD group, compared with the low TEQ-PCDDs/Fs and well-developed group. However, the ratio of histidine to glycine was significantly lower only in the high TEQ-PCDDs/Fs and high TCDD group. Furthermore, urinary histidine levels and the ratio of histidine to glycine were significantly correlated with neurodevelopmental scores, particularly for language and fine motor skills. These results indicate that urinary histidine is specifically associated with dioxin exposure-induced neurodevelopmental deficits, suggesting that urinary histidine may be a useful marker of dioxin-induced neurodevelopmental deficits and that histaminergic neurotransmission may be an important pathological contributor to dioxin-mediated neurotoxicity.
Highlights
We previously followed up on infant cohorts in dioxin contamination hot spots in Vietnam and reported considerable neurodevelopmental impacts of perinatal dioxin exposure including postnatal exposure by breast feeding, which were examined using the Bayley Scales of Infant and Toddler Development, Version 3 (Bayley III) when the infants were 4 months old [1,2,3]
We extended the follow-up period to 3 years of age in this infant cohort in Vietnamese hot spots of dioxin contamination and reported that increases in autistic traits were associated with perinatal 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure [4]
In the present study, we investigated possible differences in urinary amino acid levels in 3-year-old children with high perinatal dioxin exposure and lower neurodevelopmental scores compared to well-developed children with low exposure levels, which were estimated based on dioxin concentrations in the breast milk of mothers residing in the most highly polluted areas of Vietnam
Summary
We previously followed up on infant cohorts in dioxin contamination hot spots in Vietnam and reported considerable neurodevelopmental impacts of perinatal dioxin exposure including postnatal exposure by breast feeding, which were examined using the Bayley Scales of Infant and Toddler Development, Version 3 (Bayley III) when the infants were 4 months old [1,2,3]. In the present study, we investigated possible differences in urinary amino acid levels in 3-year-old children with high perinatal dioxin exposure and lower neurodevelopmental scores compared to well-developed children with low exposure levels, which were estimated based on dioxin concentrations in the breast milk of mothers residing in the most highly polluted areas of Vietnam. We performed dietary surveys and compared amino acid levels between the high—and low-exposure groups after adjusting for food intake
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