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Aims The study aims to evaluate the quality of life ( QOL) and health of children with unclassified developmental delays and the impacts this had on the family. Methods In total, 60 parents of pre-school children with unclassified developmental delays and 56 parents of age and gender-matched children with typical development were recruited. We administered the Pediatric Quality of Life Inventory ( PedsQL)- Generic Core Scale and Pediatric Outcomes Data Collection Instrument to parents to evaluate the QOL and health status of their children. Parents were evaluated by World Health Organization- Quality of Life- Brief Version, PedsQL- Family Impact Module, Hospital Anxiety and Depression Scale, and PedsQL- Health satisfaction to assess the impacts of this situation on the family. Variables related to QOL and functions of children with unclassified developmental delays were analysed by stepwise regression analysis. Results Comparing children with typical development, children with unclassified developmental delays had a significantly lower QOL (including both psychosocial and physical components) and health status. Their parents had a significantly lower QOL, family function and health satisfaction, and higher psychological distress than parents of children with typical development. Gross-motor delay impacts on QOL of these children (regression coefficient: −9.59, P < 0.05), global functioning is related to cognition delay (regression coefficient: −20.22, P < 0.01) and physical health of their parents (regression coefficient: 0.87, P < 0.01). Conclusions Children with unclassified developmental delays had lower QOL and health status, and their condition had greater impacts on the family than children with typical development. Gross motor and cognition development related to the QOL and global functioning in these children. [ABSTRACT FROM AUTHOR]

Abstract Inefficient arsenic methylation capacity has been associated with developmental delay in preschool children. Selenium has antioxidant and anti-inflammatory properties that protect experimental animals from chemically induced neurotoxicity. The present study was designed to explore whether plasma selenium levels affects arsenic methylation capacity related to developmental delay in preschool children. A case-control study was conducted from August 2010 to March 2014. All participants were recruited from the Shin Kong Wu Ho-Su Memorial Teaching Hospital. In total, 178 children with a developmental delay and 88 children without a delay were recruited. High-performance liquid chromatography-linked hydride generator and atomic absorption spectrometry were used to determine urinary arsenic species, including arsenite (AsIII), arsenate (AsV), monomethylarsonic acid (MMAV), and dimethylarsinic acid (DMAV). Plasma selenium levels were measured by inductively coupled plasma mass spectrometry. As results, plasma selenium concentration was significantly inversely associated with the odds ratio (OR) of developmental delay. Plasma selenium concentration was positively associated with arsenic methylation capacity [percentage of inorganic arsenic and percentage of MMAV (MMAV%) decreased, and percentage of DMAV (DMAV%) increased]. High plasma selenium concentration and high DMA% significantly and additively interacted to decrease the OR of developmental delay; the OR and 95% confidence interval were 0.40 (0.18–0.90). This is the first study to show a combined dose-response effect of plasma selenium concentration and that efficient arsenic methylation capacity decreased the OR of developmental delay in preschool children. Highlights • Plasma selenium concentration was significantly inversely associated with the odds ratio of developmental delay. • Increases in plasma selenium concentration increased the arsenic methylation capacity. • High plasma selenium concentration and high DMA% significantly and additively interacted to decrease the OR of developmental delay. [ABSTRACT FROM AUTHOR]

Inefficient arsenic methylation capacity has been associated with developmental delay in children. The present study was designed to explore whether polymorphisms and haplotypes of arsenic methyltransferase ( AS3MT ), glutathione-S-transferase omegas ( GSTOs ), and purine nucleoside phosphorylase ( PNP ) affect arsenic methylation capacity and developmental delay. A case-control study was conducted from August 2010 to March 2014. All participants were recruited from the Shin Kong Wu Ho-Su Memorial Teaching Hospital. In total, 179 children with developmental delay and 88 children without delay were recruited. Urinary arsenic species, including arsenite (As III ), arsenate (As V ), monomethylarsonic acid (MMA V ), and dimethylarsinic acid (DMA V ) were measured using a high-performance liquid chromatography-linked hydride generator and atomic absorption spectrometry. The polymorphisms of AS3MT , GSTO , and PNP were performed using the Sequenom MassARRAY platform with iPLEX Gold chemistry. Polymorphisms of AS3MT genes were found to affect susceptibility to developmental delay in children, but GSTO and PNP polymorphisms were not. Participants with AS3MT rs3740392 A/G + G/G genotype, compared with AS3MT rs3740392 A/A genotype, had a significantly lower secondary methylation index. This may result in an increased OR for developmental delay. Participants with the AS3MT high-risk haplotype had a significantly higher OR than those with AS3MT low-risk haplotypes [OR and 95% CI, 1.59 (1.08–2.34)]. This is the first study to show a joint dose-response effect of this AS3MT high-risk haplotype and inefficient arsenic methylation capacity on developmental delay. Our data provide evidence that AS3MT genes are related to developmental delay and may partially influence arsenic methylation capacity. [ABSTRACT FROM AUTHOR]

Nucleotide-binding domain-like receptors protein 3 (NLRP3) inflammasomes are associated with neuroinflammation and multiple NLRP3 genes regulate NLRP3 expression. Our study aimed to investigate the association of NLRP3 polymorphisms with developmental delay in preschool children. We also explored whether NLRP3 polymorphisms modified the effects of total urinary arsenic and blood cadmium and lead to developmental delays. A total of 178 children with developmental delays and 88 healthy children were analyzed for urinary arsenic concentrations and red blood cell lead and cadmium concentrations. We examined the genotypes of fifteen common single-nucleotide polymorphisms in NLRP3. We observed that levels of total urinary arsenic and blood lead were significantly associated with developmental delay. The NLRP3 rs10754555 CG versus CC/GG, NLRP3 rs12048215 AG versus AA/GG, and NLRP3 rs12137901 TC/TT versus CC genotype showed a lower odds of developmental delay, with the odds ratio (OR) and 95% confidence interval (CI) = 0.38 (0.19–0.75), 0.52 (0.27–0.99), and 0.33 (0.12–0.90), respectively. Children with the NLRP3 rs10754555 CC/GG genotype and high blood lead levels had a significant multiplicative interaction with developmental delay [OR (95% CI) = 9.74 (3.59–26.45)]. This study found evidence that suggested the joint effects of NLRP3 rs10754555 CC/GG genotype and high blood lead levels on developmental delays. [Display omitted] • Increment blood lead levels significantly increased the odds of developmental delay. • NLRP3 rs10754555, rs12048215, and rs12137901 were associated with developmental delay. • NLRP3 rs10754555 interacted with blood lead levels on developmental delay. [ABSTRACT FROM AUTHOR]

Abstract: Environmental exposure to lead or mercury can cause neurodevelopmental damage. Arsenic is another neurotoxicant that can affect intellectual function in children. This study was designed to explore the difference of arsenic methylation capacity indices between with and without developmental delay in preschool children. We also aimed to identify whether blood levels of lead or mercury modify the effect of arsenic methylation capacity indices. A cross sectional study was conducted from August 2010 to March 2012. All participants recruited from the Shin Kong Wu Ho-Su Memorial Teaching Hospital. In all, 63 children with developmental delay and 35 children without developmental delay were recruited. Urinary arsenic species, including arsenite (AsIII), arsenate (AsV), monomethylarsonic acid (MMAV) and dimethylarsinic acid (DMAV) were measured with a high-performance liquid chromatography-linked hydride generator and atomic absorption spectrometry. Lead and mercury levels of red blood cells were measured by inductively coupled mass spectrometry. All participants underwent developmental assessments to confirm developmental delays, including evaluations of gross motor, fine motor, speech-language, cognition, social, and emotional domains. Urinary total arsenic and MMAV percentage were significantly positively associated and DMAV percentage was negatively associated with the risk of developmental delay in a dose-dependent manner after adjustment for blood lead or mercury levels and other risk factors. A multivariate regression analysis indicated that blood lead level and arsenic methylation capacity each independently contributed to the risk of developmental delay. This is the first study to show that arsenic methylation capacity is associated with developmental delay, even without obvious environmental arsenic exposure. [Copyright &y& Elsevier]