Background: There are increasing concerns over adverse effects of prenatal phthalate exposure on the neurodevelopment of infants.Objectives: Our goal was to explore the association between prenatal di(2-ethylhexyl) phthalate and dibutyl phthalate exposure and the Mental and Psychomotor Developmental Indices (MDI and PDI, respectively) of the Bayley Scales of Infant Development at 6 months, as part of the Mothers and Children’s Environmental Health Study.Methods: Between 2006 and 2009, 460 mother–infant pairs from Seoul, Cheonan, and Ulsan, Korea, participated. Prenatal mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono-n-butyl phthalate (MBP) were measured in one urine sample acquired from each mother during the third trimester of pregnancy. Associations with log-transformed creatinine-corrected phthalate concentrations were estimated using linear regression models adjusted for potential confounders.Results: MDI was inversely associated with the natural log concentrations (micrograms per gram creatinine) of MEHHP [β = –0.97; confidence interval (CI), –1.85 to –0.08] and MEOHP (β = –0.95; CI, –1.87 to –0.03), and PDI was inversely associated with MEHHP (β = –1.20; CI, –2.33 to –0.08). In males, MDI was inversely associated with MEHHP (β = –1.46; CI, –2.70 to –0.22), MEOHP (β = –1.57; CI, –2.87 to –0.28), and MBP (β = –0.93; CI, –1.82 to –0.05); PDI was inversely associated with MEHHP (β = –2.36; CI, –3.94 to –0.79), MEOHP (β = –2.05; CI, –3.71 to –0.39), and MBP (β = –1.25; CI, –2.40 to –0.11). No significant linear associations were observed for females.Conclusions: The results suggest that prenatal exposure to phthalates may be inversely associated with the MDI and PDI of infants, particularly males, at 6 months.

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BackgroundSubstance use among Korean adolescents has been increasing, but little is known about the correlates of substance use in this population. Identification of the correlates is required for development of preventive approaches that aim to reduce or eliminate risk. Therefore, we examined the prevalence and correlates of substance use including psychological problems in a nationwide sample of Korean adolescents.MethodsData from the 2014 Korean Youth Risk Behavior Web-Based Survey, collected from 72,060 adolescents aged 12–18 years (mean age 14.94 ± 1.75 years), were analyzed. Participants’ lifetime experiences with substances (alcohol, tobacco, and illicit drugs) were assessed. Participants’ perceived stress, depressive mood, and suicidality during the previous 12 months were also investigated.ResultsThe lifetime prevalence estimates of alcohol, tobacco, and illicit drug use were 43.0, 19.9, and 0.4 % of the participants, respectively. The most commonly used illicit drugs were inhalants. Older age, male gender, non-residence with family, low parental educational level and socio-economic status, and low academic achievement were positively and significantly associated with substance use. Substance (alcohol, tobacco, and illicit drug) use was positively and significantly associated with severe stress, depressive mood, and suicidality during the previous 12 months, with the highest odds ratios obtained from illicit drug use.ConclusionsThese results indicate that the use of substances (alcohol, tobacco, and illicit drugs) among Korean adolescents is associated with socially disadvantaged families, psychological problems, and risky behavior. Health education including dependency prevention programs is needed for these high-risk groups.

Our current knowledge of the pathophysiology and molecular mechanisms causing psychiatric disorders is modest, but genetic susceptibility and environmental factors are central to the etiology of these conditions. Autism, schizophrenia, bipolar disorder and major depressive disorder show genetic gene risk overlap and share symptoms and metabolic comorbidities. The identification of such common features may provide insights into the development of these disorders. Multiple pieces of evidence suggest that brain energy metabolism, mitochondrial functions and redox balance are impaired to various degrees in psychiatric disorders. Since mitochondrial metabolism and redox signaling can integrate genetic and environmental environmental factors affecting the brain, it is possible that they are implicated in the etiology and progression of psychiatric disorders. However, evidence for direct links between cellular mitochondrial dysfunction and disease features are missing. A better understanding of the mitochondrial biology and its intracellular connections to the nuclear genome, the endoplasmic reticulum and signaling pathways, as well as its role in intercellular communication in the organism, is still needed. This review focuses on the findings that implicate mitochondrial dysfunction, the resultant metabolic changes and oxidative stress as important etiological factors in the context of psychiatric disorders. We also propose a model where specific pathophysiologies of psychiatric disorders depend on circuit-specific impairments of mitochondrial dysfunction and redox signaling at specific developmental stages.