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This is the first pilot meta-analysis on the association of prenatal phthalate exposure with childhood cardiometabolic risks. A systematic literature search was performed in MEDLINE, Web of Science and CNKI (Chinese National Knowledge Infrastructure) until June 5, 2023. A total of seven studies with 5746 children (2646 girls and 3100 boys) were finally included. Four, three and two studies investigated the effects of maternal phthalate exposure on childhood blood pressure (BP), blood lipids and blood glucose profiles, respectively. The pilot meta-analysis suggested that di-2-ethylhexyl phthalate (DEHP) metabolite exposure was associated with a decrease in childhood z-systolic BP (SBP, β = −0.169, 95% CI = −0.338–0.001). Furthermore, the pooled results showed negative relationships of prenatal ∑DEHP exposure with z-SBP (β = −0.109, 95% CI = −0.163 to −0.055) and z-diastolic BP (DBP, β = −0.126, 95% CI = −0.182 to −0.069) in girls. In addition, MEP exposure was associated with z-SBP in girls (β = −0.227, 95% CI = −0.387 to −0.066). The pooled result showed a positive relationship between prenatal ∑DEHP exposure and triglycerides (β = 0.103, 95% CI = 0.028–0.178). The overall results revealed that exposure to ∑DEHP throughout gestation was associated with a decrease in insulin (β = −0.074, 95% CI = −0.144 to −0.004) and glucose (β = −0.129, 95% CI = −0.199 to −0.058) in boys. Interestingly, there was an inverse relationship of prenatal mono− 3 −carboxypropyl phthalate (MCPP) exposure with glucose in pubertal boys (β = −3.749, 95% CIs = −6.758 to −0.741) but not found in postpubertal children. In conclusion, prenatal phthalate exposure interfered with cardiovascular risk in children with gender-specific differences and was influenced by puberty. Overall, prenatal ∑DEHP was negatively associated with systolic blood pressure in girls and with insulin and glucose in boys but increased the level of triglycerides.

Ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, induces deficits in cognition and information processing following chronic abuse. Adolescent ketamine misuse represents a significant global public health issue; however, the neurodevelopmental mechanisms underlying this phenomenon remain largely elusive. This study investigated the long-term effects of sub-chronic ketamine (Ket) administration on the medial prefrontal cortex (mPFC) and associated behaviors. In this study, Ket administration during early adolescence displayed a reduced density of excitatory synapses on parvalbumin (PV) neurons persisting into adulthood. However, the synaptic development of excitatory pyramidal neurons was not affected by ketamine administration. Furthermore, the adult Ket group exhibited hyperexcitability and impaired socialization and working memory compared to the saline (Sal) administration group. These results strongly suggest that sub-chronic ketamine administration during adolescence results in functional deficits that persist into adulthood. Bioinformatic analysis indicated that the gene co-expression module1 (M1) decreased expression after ketamine exposure, which is crucial for synapse development in inhibitory neurons during adolescence. Collectively, these findings demonstrate that sub-chronic ketamine administration irreversibly impairs synaptic development, offering insights into potential new therapeutic strategies., Competing Interests: Declaration of competing interest The authors declare no competing interests., (Copyright © 2024 Elsevier Inc. All rights reserved.)