Uncovering the link between air pollution and neurodevelopmental alterations during pregnancy and early life exposure: A systematic review.

Air pollution plays, nowadays, a huge role in human's health and in the personal economy. Moreover, there has been a rise in the prevalence of neurodevelopmental disorders like the Autism Spectrum Disorder (ASD) in recent years. Current scientific studies have established a link between prenatal or perinatal exposure to environmental pollutants and ASD. This systematic review summarizes the current literature available about the relationship between exposure to air pollutants (particulate matter [PM], Second Organic Aerosols [SOA], Diesel Exhaust [DE], and Traffic Related Air Pollution [TRAP]) and neurodevelopmental disorders in preclinical models using rats and mice. The articles were selected and filtered using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) methodology, and bias-evaluated using the SYstematic Review Centre for Laboratory animal Experimentation (SYRCLE) tool. Overall, our findings suggest that air pollutants are associated with negative developmental outcomes characterized by ASD-like behaviors, abnormal biochemical patterns, and impaired achievement of developmental milestones in rodents. However, there is not sufficient information in certain domains to establish a clear relationship. Short phrases for indexing terms: Air pollution affects neurodevelopment; PM exposure modifies glutamate system; Prenatal exposure combined with postnatal affect more to behavioral / cognitive domain; Air pollution modifies social behavior in rodents; Cognitive deficits can be detected after gestational exposure to air pollution.

Similarities between the Effects of Prenatal Chlorpyrifos and Valproic Acid on Ultrasonic Vocalization in Infant Wistar Rats.

BACKGROUND: In recent years, ultrasonic vocalizations (USV) in pups has become established as a good tool for evaluating behaviors related to communication deficits and emotional states observed in autism spectrum disorder (ASD). Prenatal valproic acid (VPA) exposure leads to impairments and social behavior deficits associated with autism, with the effects of VPA being considered as a reliable animal model of ASD. Some studies also suggest that prenatal exposure to chlorpyrifos (CPF) could enhance autistic-like behaviors. METHODS: In order to explore these similarities, in the present study we tested whether prenatal exposure to CPF at GD12.5-14.5 produces effects that are comparable to those produced by prenatal VPA exposure at GD12.5 in infant Wistar rats. Using Deep Squeek software, we evaluated total number of USVs, latency to the first call, mean call duration, principal frequency peak, high frequency peak, and type of calls. RESULTS: Consistent with our hypothesis, we found that exposure to both CPF and VPA leads to a significantly smaller number of calls along with a longer latency to produce the first call. No significant effects were found for the remaining dependent variables. CONCLUSIONS: These results suggest that prenatal exposure to CPF could produce certain behaviors that are reminiscent of those observed in ASD patients.

Adulthood dietary exposure to a common pesticide leads to an obese-like phenotype and a diabetic profile in apoE3 mice.

Increasing evidence links the widespread exposure to organophosphate (OP) pesticides to the global epidemics of type 2 diabetes and obesity. Our recent data highlighted gene×environment interactions: mice expressing the human apolipoprotein E3 (apoE3) isoform were more prone to develop obesity than those expressing apoE2 or apoE4 upon dietary challenge with chlorpyrifos (CPF), the most used OP worldwide. Thus, we aimed to further explore the contribution of the APOE3 genotype on the emergence of obesity and related metabolic dysfunctions upon subchronic exposure to CPF. Seven-month-old targeted replacement apoE3 and C57BL/6N male mice were orally exposed to CPF at 0 or 2mg/kg body weight/day for 8 consecutive weeks. We examined body weight status, food and water intake, lipid and glucose homeostasis, metabolic biomarkers concentrations, insulin levels and insulin resistance, and leptin and ghrelin profiles. CPF exposure generally increased food ingestion, glucose and total cholesterol concentrations, and tended to elevate acyl ghrelin levels. Nonetheless, excess weight gain and increased leptin levels were inherent to apoE3 mice. Moreover, the propensity towards a diabetic profile was markedly higher in these animals than in C57BL/6N, as they showed a higher homeostatic model assessment for insulin resistance index and higher insulin levels. Although both genotypes were metabolically affected by CPF, the results of the present investigation revealed that apoE3 mice were the most vulnerable to developing obesity and related disturbances following CPF administration through the diet. Since the APOE3 genotype is the most prevalent worldwide, current findings have particular implications for human health.