OBJECTIVETo examine the effect of parents' occupational and life exposure during six months before pregnancy on executive function of preschool children.

METHODSPregnant women involved in the study came from the Ma'anshan Birth Cohort Study,a part of the China-Anhui Birth Cohort Study. Between October 2008 and October 2010, pregnant women who accepted pregnancy care in four municipal medical and health institutions in Ma'anshan city were recruited as study objects. A total of 5,084 pregnant women and 4,669 singleton live births entered in this cohort. Between April 2014 and April 2015, a total of 3,803 pre-school children were followed up. Finally, except 32 preschool children did not have EF evaluation result, there were 3,771 children included in this study. By using self-designed " Maternal health handbook", we researched parents' general demographic characteristics, and life and occupational exposure during six months before pregnancy. To research preschool children's executive function, we used the Behavior Rating Inventory of Executive Function-Preschool Version (BRIEF-P). Univariate and multivariate statistical method was used to analyze the association of parents' life and occupational exposure during six months before pregnancy and preschool children's EF.

RESULTS3,771 preschool children's detected rate of inhibitory self-control index (ISCI), flexibility index (FI), emergent metacognition index (EMI) and global executive composite (GEC) dysplasia were 4.8% (182), 2.3% (88), 16.5% (623) and 8.6% (324) respectively. During six months before pregnancy, children whose parents were lived in a noise environment (OR=1.86, 95% CI: 1.36-2.54), whose maternal were exposed to pesticides were the risk of ISCI dysplasia(OR=3.60, 95% CI: 1.45-8.95). During six months before pregnancy, children whose maternal were exposed to pesticides (OR=6.72, 95% CI: 2.50-18.07) and whose father were exposed to occupational lead (OR=2.10, 95% CI: 1.25-3.54) were the risk of FI dysplasia. During six months before pregnancy, children whose parents were lived in a noise environment (OR=1.42, 95%CI: 1.18-1.71) and whose father were exposed to occupational lead (OR=1.30, 95%CI: 1.02-1.65) were the risk of EMI dysplasia. During six months before pregnancy, children whose parents were lived in a noise environment (OR=1.58, 95% CI: 1.24-2.01) and whose maternal were exposed to pesticides (OR=2.39, 95% CI: 1.02-5.58) were the risk of GEC dysplasia.

CONCLUSIONThe development of executive function is worse among preschool children whose parents live in noise environment, mother exposed to pesticides, and father exposed to occupational lead during six months before pregnancy.

Child ; Child, Preschool ; China ; Cohort Studies ; Environmental Exposure ; adverse effects ; Executive Function ; Family Characteristics ; Female ; Humans ; Lead ; adverse effects ; Male ; Occupational Exposure ; adverse effects ; Parents ; Pesticides ; adverse effects ; Pregnancy ; Prenatal Exposure Delayed Effects ; epidemiology ; psychology

Animals ; Female ; Hippocampus ; physiology ; Learning ; Long-Term Potentiation ; Male ; Memory ; Mice ; Mice, Inbred Strains ; Pregnancy ; Prenatal Exposure Delayed Effects ; psychology ; Tobacco Smoke Pollution

BACKGROUND: Arsenic is a developmental neurotoxicant. It means that its neurotoxic effect could occur in offspring by maternal arsenic exposure. Our previous study showed that developmental arsenic exposure impaired social behavior and serotonergic system in C3H adult male mice. These effects might affect the next generation with no direct exposure to arsenic. This study aimed to detect the social behavior and related gene expression changes in F2 male mice born to gestationally arsenite-exposed F1 mice. METHODS: Pregnant C3H/HeN mice (F0) were given free access to tap water (control mice) or tap water containing 85 ppm sodium arsenite from days 8 to 18 of gestation. Arsenite was not given to F1 or F2 mice. The F2 mice were generated by mating among control F1 males and females, and arsenite-F1 males and females at the age of 10 weeks. At 41 weeks and 74 weeks of age respectively, F2 males were used for the assessment of social behavior by a three-chamber social behavior apparatus. Histological features of the prefrontal cortex were studied by ordinary light microscope. Social behavior-related gene expressions were determined in the prefrontal cortex by real time RT-PCR method. RESULTS: The arsenite-F2 male mice showed significantly poor sociability and social novelty preference in both 41-week-old group and 74-week-old group. There was no significant histological difference between the control mice and the arsenite-F2 mice. Regarding gene expression, serotonin receptor 5B (5-HT 5B) mRNA expression was significantly decreased (p < 0.05) in the arsenite-F2 male mice compared to the control F2 male mice in both groups. Brain-derived neurotrophic factor (BDNF) and dopamine receptor D1a (Drd1a) gene expressions were significantly decreased (p < 0.05) only in the arsenite-F2 male mice of the 74-week-old group. Heme oxygenase-1 (HO-1) gene expression was significantly increased (p < 0.001) in the arsenite-F2 male mice of both groups, but plasma 8-hydroxy-2'-deoxyguanosine (8-OHdG) and cyclooxygenase-2 (COX-2) gene expression were not significantly different. Interleukin-1β (IL-1β) mRNA expression was significantly increased only in 41-week-old arsenite-F2 mice. CONCLUSIONS These findings suggest that maternal arsenic exposure affects social behavior in F2 male mice via serotonergic system in the prefrontal cortex. In this study, COX-2 were not increased although oxidative stress marker (HO-1) was increased significantly in arsnite-F2 male mice.
Animals ; Arsenic/toxicity* ; Arsenites/toxicity* ; Behavior, Animal/drug effects* ; Environmental Pollutants/toxicity* ; Female ; Gene Expression/drug effects* ; Genetic Markers ; Male ; Maternal Exposure/adverse effects* ; Mice ; Mice, Inbred C3H ; Oxidative Stress/genetics* ; Prefrontal Cortex/drug effects* ; Pregnancy ; Prenatal Exposure Delayed Effects/psychology* ; Reverse Transcriptase Polymerase Chain Reaction ; Serotonin/metabolism* ; Social Behavior ; Sodium Compounds/toxicity*

BACKGROUND: There have been inconsistent findings reported on maternal passive smoking during pregnancy and child risk of ADHD. In this study, ADHD symptoms at pre-school age children in association with prenatal passive and active tobacco smoke exposure determined by maternal plasma cotinine levels in the third trimester were investigated. METHODS: This was a follow-up study of the birth cohort: the Hokkaido Study on Environment and Children's Health. Children whose parents answered Strengths and Difficulties Questionnaire (SDQ) to identify child ADHD symptoms (hyperactivity/inattention and conduct problems) and total difficulties at age 5 years with available maternal plasma cotinine level at the third trimester were included (n = 3216). Cotinine levels were categorized into 4 groups; ≦ 0.21 ng/ml (non-smoker), 0.22-0.51 ng/ml (low-passive smoker), 0.52-11.48 ng/ml (high-passive smoker), and ≧ 11.49 ng/ml (active smoker). RESULTS: Maternal cotinine levels of active smokers were significantly associated with an increased risk of total difficulties (OR = 1.67) and maternal low- and high-passive smoking also increased the risk (OR = 1.11, 1.25, respectively) without statistical significance. Similarly, maternal cotinine levels of active smokers were associated with an increased risk of hyperactivity/inattention (OR = 1.49). Maternal low- and high-passive smoking and active smoking increased the risk of hyperactivity/inattention (OR = 1.45, 1.43, and OR = 1.59, respectively) only in boys. CONCLUSION Our findings suggested that maternal active smoking during pregnancy may contribute to the increased risk of child total difficulties and hyperactivity/inattention at pre-school age. Pregnant women should be encouraged to quit smoking and avoid exposure to tobacco smoke.
Adult ; Attention Deficit Disorder with Hyperactivity ; epidemiology ; etiology ; physiopathology ; psychology ; Child, Preschool ; Cotinine ; blood ; Female ; Follow-Up Studies ; Humans ; Japan ; epidemiology ; Male ; Maternal Exposure ; adverse effects ; Mothers ; Pregnancy ; Pregnancy Trimester, Third ; Prenatal Exposure Delayed Effects ; epidemiology ; etiology ; Risk ; Sex Factors ; Tobacco Smoking ; adverse effects ; epidemiology

BACKGROUND: Prenatal stress can cause neurobiological and behavioral defects in offspring; environmental factors play a crucial role in regulating the development of brain and behavioral; this study was designed to test and verify whether an enriched environment can repair learning and memory impairment in offspring rats induced by prenatal stress and to explore its mechanism involving the expression of insulin-like growth factor-2 (IGF-2) and activity-regulated cytoskeletal-associated protein (Arc) in the hippocampus of the offspring. METHODS: Rats were selected to establish a chronic unpredictable mild stress (CUMS) model during pregnancy. Offspring were weaned on 21st day and housed under either standard or an enriched environment. The learning and memory ability were tested using Morris water maze and Y-maze. The expression of IGF-2 and Arc mRNA and protein were respectively measured by using RT-PCR and Western blotting. RESULTS: There was an elevation in the plasma corticosterone level of rat model of maternal chronic stress during pregnancy. Maternal stress's offspring exposed to an enriched environment could decrease their plasma corticosterone level and improve their weight. The offspring of maternal stress during pregnancy exhibited abnormalities in Morris water maze and Y-maze, which were improved in an enriched environment. The expression of IGF-2, Arc mRNA, and protein in offspring of maternal stress during pregnancy was boosted and some relationships existed between these parameters after being exposed enriched environment. CONCLUSIONS The learning and memory impairment in offspring of prenatal stress can be rectified by the enriched environment, the mechanism of which is related to the decreasing plasma corticosterone and increasing hippocampal IGF-2 and Arc of offspring rats following maternal chronic stress during pregnancy.
Animals ; Cytoskeletal Proteins/metabolism* ; Female ; Gene Expression Regulation ; Hippocampus/metabolism* ; Insulin-Like Growth Factor II/metabolism* ; Learning ; Learning Disabilities/psychology* ; Male ; Memory Disorders/psychology* ; Nerve Tissue Proteins/metabolism* ; Pregnancy ; Prenatal Exposure Delayed Effects/psychology* ; Random Allocation ; Rats ; Rats, Wistar ; Social Environment ; Stress, Psychological/genetics*