Prenatal and postnatal droughts interact in shaping cognitive development.

Associations between prenatal and postnatal substance exposure and salivary C-reactive protein in early childhood

Considering Prenatal Alcohol Exposure in a Developmental Origins of Health and Disease Framework.

Background:Prenatal exposure to organophosphorous (OP) pesticides has been found to be associated with adverse effects on child neurodevelopment, but evidence on potential effects induced by both prenatal and postnatal OP exposure in infants is limited.Objectives:Our aim was to investigate the associations of both prenatal and postnatal OP exposure with birth outcomes and infant neurodevelopment.Methods:Exposure to OP in 310 mother–infant pairs was assessed by measuring dimethylphosphate (DM), diethylphosphate (DE), and total dialkylphosphate (DAP) metabolites in urines from pregnant women and their children at 2 years of age. The Gesell Developmental Schedules was administered to examine neurodevelopment of 2-year-old children.Results:Based on the Gesell Developmental Schedules, the proportions of children with developmental delays were < 6%. Adverse associations between head circumference at birth and prenatal OP exposure were demonstrated. Both prenatal and postnatal OP exposure was significantly associated with increased risk of being developmentally delayed. Specifically, odds ratio (OR) value for prenatal DEs was 9.75 (95% CI: 1.28, 73.98, p = 0.028) in the adaptive area, whereas in the social area, OR values for postnatal DEs and DAPs were 9.56 (95% CI: 1.59, 57.57, p = 0.014) and 12.00 (95% CI: 1.23, 117.37, p = 0.033), respectively. Adverse associations were observed only in boys, not in girls.Conclusions:Both prenatal and postnatal OP exposure may adversely affect the neurodevelopment of infants living in the agricultural area. The present study adds to the accumulating evidence on associations of prenatal and postnatal OP exposure with infant neurodevelopment.Citation:Liu P, Wu C, Chang X, Qi X, Zheng M, Zhou Z. 2016. Adverse associations of both prenatal and postnatal exposure to organophosphorous pesticides with infant neurodevelopment in an agricultural area of Jiangsu Province, China. Environ Health Perspect 124:1637–1643; http://dx.doi.org/10.1289/EHP196

To study the effects of prenatal and postnatal perfluorooctane sulfonate (PFOS) exposure on spatial learning and memory, N-methyl-D-aspartate receptor 2B (NR2B) mRNA and protein level in frontal cortex and hippocampus of rat pups and to explore the mechanism of developmental neurotoxicity induced by PFOS. Twenty-eight pregnant rats were randomly divided into three groups in proportion of 3:2:2, including control group (C), low dose group (L) and high dose group (H) by means of randomized number table, which respectively received 0, 7.2, 14.4 mg/kg PFOS feed from pregnancy day 0 to postnatal day (PND) 30 by free feedings. The animal models of prenatal and postnatal non-exposure (CC), prenatal exposure (LC and HC), postnatal exposure (CL and CH), and prenatal and postnatal exposure (LL and HH) to PFOS were established by cross-fostering method. The spatial learning and memory were measured by water maze experiment,the NR2B mRNA levels in frontal cortex of rat pups was determined with semi-quantitative RT-PCR, NR2B protein express in cerebral cortex (frontal and temporal cortex) and hippocampus (CA1, CA3, CA4 and DG regions) of rat pups was detected by immunohistochemistry. The escape latency of CL, CH, LL and HH groups pups in water maze experiment were (99.83 +/- 25.77) s, (111.30 +/- 17.82) s, (106.40 +/- 18.71) s, (107.70 +/- 16.85) s, and longer as compared with CC group [(54.90 +/- 26.69) s] (q value were 4.349, 4.773, 6.026 and 5.641, respectively, P <0.01). The number of errors of HH group rat pups entering dead end was (22.30 +/- 7.56) at the training day 4, and it was significantly higher than that of CC group (9.80 +/- 4.64) (q = 5.173, P < 0.01). The NR2B mRNA levels of frontal cortex of pups in HC group at PND1, and LC group, HC group and HH group at PND14 were (0.167 +/- 0.008), (0.364 +/- 0.035), (0.341 +/- 0.030) and (0.328 +/- 0.045) respectively,which were significantly lower than CC group (0.271 +/- 0.060) and (0.465 +/- 0.067) (q values were 3.547, 3.739, 4.597 and 5.006, respectively, P< 0.05 ). The results of immunohistochemistry indicated that NR2B protein express of the hippocampus CA1 region of pups in LC group was (0.091 +/- 0.005), and showed significant lower than CC group which was (0.123 +/- 0.009) at PND1 (q = 5.209, P <0.05). At PND14, the effect of PFOS extended to cerebral cortex and hippocampus regions. At PND28, the effects of PFOS were showed in hippocampus CA1, CA3 and temporal cortex regions. Prenatal and postnatal exposure to PFOS should result in the spatial learning and memory damage,and the mechanism might be possibly involved in the decrease of NR2B level in cerebral cortex and hippocampal formation regions.

Separate and joint effects of tranplacental and postnatal inhalatory exposure to polycyclic aromatic hydrocarbons: Prospective birth cohort study on wheezing events

How can sensory-motor skills developed as a fetus transfer to postnatal life? We investigate a simulated reaching task by training controllers under prenatal conditions (i.e. confined space) and evaluating them based on postnatal conditions (i.e. targets outside of the confined training space). One possible solution is to identify a sensory representation that is easy to extrapolate over. We compared two kinds of sensory representations: world-centered sensory representation based on Cartesian coordinates and agent-centered sensory representation based on polar coordinates. Despite similar performance under prenatal conditions, controllers using agent-centered sensory representation had significantly better performance than controllers using world-centered sensory representation under postnatal conditions. It turns out that the success of the agent-centered sensory representation is (in part) due to being complementary to the action encodings. Further analysis shows that the action encodings (i.e. changes in joint angles) were highly predictive of the change in state when agent-centered sensory representation was used (but not world-centered). This suggests that a powerful strategy for transferring sensory-motor skills to postnatal life involves selecting a sensory representation that complements the action encodings used by an agent.

High stability, the quality that made polychlorinated biphenyls (PCBs) so useful in hundreds of industrial and commercial applications during the mid-1900s, has ensured the compounds’ continuing presence in the environment despite decades of banned and restricted use.1 This class of more than 200 structurally related chemicals has been linked to both cancer and noncancer outcomes,1 and some studies suggest prenatal or early-life exposure to PCBs may adversely affect the auditory system.2,3 A new study reported in EHP specifically links postnatal—but not prenatal—PCB exposure with impaired cochlear function.2 Clusters of hair cells populate the cochlea and detect sounds transmitted to the inner ear. The cochlea, an extremely sensitive organ in the inner ear, converts soundwave vibrations to nerve impulses transmitted to the brain. Cochlear damage can impair hearing and is a well-known side effect of certain antibiotics and chemotherapeutic drugs.4 Rodent studies have shown that PCBs, too, can affect the cochlea, leading to hearing loss.5 Some human studies have reported associations between PCB exposure and hearing impairment, particularly in children,6,7 although others have found no such association.8 The current study focused on mother–infant pairs from an ongoing birth cohort study in eastern Slovakia. Study participants enrolled during hospital stays for childbirth in 2002–2004. Maternal and cord blood samples were collected for PCB and lipid measurements, and children underwent blood tests at 6, 16, and 45 months of age. At 45 months, the children also underwent otological and auditory testing, including an assessment of distortion product otoacoustic emissions (DPOAEs), a measure of cochlear function. Health records provided information on the children’s births and subsequent medical visits. Mothers completed questionnaires at study enrollment and at the 16- and 45-month followup visits, providing sociodemographic information and data on lifestyle, diet, medical history, and other factors that could affect their children’s health and hearing. A total of 351 children were included in the study. Blood tests measured 15 PCB congeners, but analyses focused on PCB-153, which was detected in nearly all samples and closely correlated with total PCB concentrations. An inverse relationship existed between decreased DPOAE amplitude (a marker of diminished cochlear function) and postnatal serum PCB concentrations, with the strongest association observed for cumulative levels of PCBs. The authors suggest this could indicate that duration of exposure, rather than timing, is most important for cochlear development. No association was observed between prenatal PCB exposure and decreased DPOAE amplitude.2 The PCB-associated decrease in DPOAE amplitude was not large.2 “Certainly, the hearing impairment would be subclinical,” says study coauthor Tomas Trnovec, a professor of environmental medicine at Slovak Medical University in Bratislava. However, the cochlea is vulnerable to any number of environmental insults, including noise, organochlorine pesticides, and drugs, among others, Trnovec says. “The combined effect of these factors is completely unknown,” he says, adding that “under different settings and other data treatment … a prenatal exposure effect cannot be excluded.” It’s also unknown whether effects persist and whether continued exposure (combined with other stressors) builds on early damage. “In my opinion, PCB ototoxicity may be involved in the pathogenesis of hearing impairment in the adult population,” says Kyoung-Bok Min, an assistant professor in occupational and environmental medicine at South Korea’s Ajou University School of Medicine, who was not involved in the study. Min and colleagues recently reported an association between PCB serum levels and increased prevalence of hearing impairment in adults who participated in the National Health and Nutrition Examination Survey.9 “Further epidemiologic studies are needed in terms of whether the impact of exposure to PCBs on cochlear function changes throughout the life span of the human,” he says. In addition, Susan Schantz, a professor of veterinary biosciences and psychology at the University of Illinois at Urbana–Champaign, raises the possibility of potential impacts beyond hearing. “One of the things that really interests me—and that I don’t know the answer to—is what does that kind of a decrease [in DPOAE amplitude] mean? Would it be enough to have subtle impacts on language acquisition in children?” asks Schantz, who was not involved in the study. Previous PCB cohort studies have shown an adverse impact on cognitive function, including verbal abilities.10 “I’ve always wondered whether subtle changes in hearing could be affecting language development, and then that could be affecting verbal abilities,” Schantz says. The new study features a particularly strong design based on multiple PCB measurements in a well-characterized population. However, it did not account for potential effects of co-contaminants, which may produce damage when combined with other exposures.11 “I think it’s very interesting that they’re seeing reductions to amplitudes related to postnatal exposure,” says Schantz. “That’s not what I would have predicted based on the animal research, but I think it’s very interesting and potentially important.”

Pre- and postnatal antibiotic exposure and risk of developing attention deficit hyperactivity disorder–A systematic review and meta-analysis combining evidence from human and animal studies

Caesarean sections, prenatal and postnatal conditions and childhood acute lymphoblastic leukaemia: A case-control study in the State of São Paulo, Brazil

Several studies mention that early consumption of cannabis, alcohol, or even cocaine is related to an increase in the prevalence of daily consumption of tobacco in adulthood. However, other factors, such as genetic comorbidity, social influences, and even molecular, neurochemical, and behavioral alterations induced by prenatal and postnatal cocaine exposure, could also explain these observations, since these factors together increase the vulnerability of the offspring to the reinforcing effects of nicotine. The objective of this study was to determine the effect of prenatal and postnatal exposure to cocaine on nicotine-induced locomotor sensitization in young and adult rats. The study was divided into two stages: prenatal and postnatal. In the prenatal stage, a group of pregnant female Wistar rats was administered cocaine daily from day GD0 to GD21 (cocaine preexposure group), and another group of pregnant female rats was administered saline daily (saline preexposure group). Of the litters resulting from the cocaine preexposed and saline preexposed pregnant female groups, in the postnatal stage, only the male rats were used for the recording of the locomotor activity induced by different doses of nicotine (0.2, 0.4, and 0.6 mg/kg) during the induction and expression of locomotor sensitization at different postnatal ages (30, 60, 90, and 120 days). Prenatal and postnatal cocaine exposure enhanced nicotine-induced locomotor activity and locomotor sensitization. This suggests that prenatal and postnatal cocaine exposure can result in increased vulnerability to other drugs of abuse, such as nicotine, in humans. Several studies have shown that the abuse of a drug, such as cannabis, alcohol, or even cocaine, at an early age can progress to more severe levels of use of other drugs, such as nicotine, to adulthood. Our data are consistent with this hypothesis, since prenatal and postnatal cocaine exposure enhanced the nicotine-induced increase in locomotor activity and locomotor sensitization. This suggests that prenatal and postnatal exposure to cocaine enhances the drug's salience.

Early postnatal alcohol exposure reduced the size of vibrissal barrel field in rat somatosensory cortex (SI) but did not disrupt barrel field organization

Pre- and post-natal exposure of children to organophosphate flame retardants: A nationwide survey in France.

Data from 10 years of ASER (Annual Status of Education Report) surveys in India reveal two clear trends. First, a steady increase in private school enrollment is visible across rural India. Second, children’s ability to read simple text and do basic arithmetic is extremely poor and has not improved over time. ASER data show that the learning gap is widening between government and private schools but that a larger proportion of this gap is attributable to household factors rather than to private schools themselves. This means that the most disadvantaged children, those who study in government schools, are falling further behind. Data from the India Early Childhood Education Impact (IECEI) study also suggests that although the majority of children in the IECEI study spent between 1 and 2 years in an early childhood education program prior to entering primary school, the impact of this participation on their school readiness and subsequent early grade learning is attributable more to their family background than to the institutions that they attended, which varied very little within a given state in terms of quality. However, variations across states suggest that uptake of developmentally appropriate policies and programs at the state level is likely to influence not only government but also private providers of early childhood services.

Prenatal and early life air pollution exposure has been linked with several adverse health outcomes. However, the mechanisms underlying these relationships are not yet fully understood. Therefore, this study utilizes fecal metabolomics to determine if pre- and postnatal exposure to ambient air pollutants (i.e., PM10, PM2.5, and NO2) is associated with the fecal metabolome in the first 2 years of life in a Latino cohort from Southern California. The aims of this analysis were to estimate associations between (1) prenatal air pollution exposure with fecal metabolic features at 1-month of age, (2) prior month postnatal air pollution exposure with fecal metabolites from 1-month to 2 years of age, and (3) how postnatal air pollution exposure impacts the change over time of fecal metabolites in the first 2 years of life. Prenatal exposure to air pollutants was associated with several Level-1 metabolites, including those involved in vitamin B6 and tyrosine metabolism. Prior month air pollution exposure in the postnatal period was associated with Level-1 metabolites involved in histidine metabolism. Lastly, we found that pre- and postnatal ambient air pollution exposure was associated with changes in metabolic features involved in metabolic pathways including amino acid metabolism, histidine metabolism, and fatty acid metabolism.

Prenatal and postnatal exposure to organophosphate pesticides and child neurodevelopment in an agricultural area of Jiangsu province, China: a cohort study