Recent climate change-induced wildfires and nuclear energy phasing-out policies have fostered atmospheric emissions of polycyclic aromatic hydrocarbons (PAHs). PAHs are pollutants produced by natural and anthropic processes under thermal treatment of organic matter, e.g. in fires and sedimentary rocks (Henner et al. 1997, Lichtfouse et al. 1997). They occur widely in the environment from trace levels, e.g. in polar ice, to high concentrations in oil spills. They have been found in aerosols, soils, sediments, waters, meterorites, coal, petroleum, bitumen and living organisms. Surprisingly, out of the 16 polycyclic aromatic hydrocarbons defined as 'priority' polluants for toxicity evaluation, ten light homologues have been poorly investigated because they did not show obvious carcinogenic effects. Here, we argue that the toxicity of light PAHs has been overlooked (Fig. 1).

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is a chronic liver disease affecting 25% of the European population, with rising global incidence. Liver damage includes ballooning, steatosis, inflammation and fibrosis. Associated brain disorders include sleep, cognitive issues, anxiety, and depression. While neurological complications in advanced MASLD are well documented, early cerebral manifestations remain largely unexplored. This study aimed at developing an MASLD rat model to assess the onset of early brain damage, focusing on impairments of the circadian cycle rhythm and associated neuroinflammation. Sprague Dawley rats were divided into two groups: one received a high-fat, high-cholesterol (HFHC) diet for 90 days, while the other received a standard diet. Histological analysis showed significant hepatic steatosis, ballooning, and inflammation in the HFHC group (p < 0.01). These lesions correlated with elevated hepatic triglycerides (p < 0.01), increased Alanine Aminotransferase, Aspartate Aminotransferase, total cholesterol, and low-density lipoprotein, alongside decreased plasma high-density lipoprotein. Behavioural analysis using activity wheels revealed that the HFHC rats steadily maintained their activity level during the rest periods when compared with controls (p < 0.05). This behavioural alteration occurred alongside neuroinflammation, demonstrated by changes in the expression of 36 and 17 inflammatory mediators in the cerebellum and frontal cortex respectively. These changes were associated with an increase in the expression of glial cell markers (Aif1 and Gfap genes) and an increase in the number of microglial cells, affecting the frontal cortex and cerebellum differently. This rat model of early MASLD shows circadian rhythm disturbances, which could reflect sleep disorders in humans. These early brain disturbances specific to MASLD, which occur before the symptoms of liver disease become clinically apparent, could therefore be used as an early diagnosis marker for MASLD patients.

Evidence is now growing that exposure to environmental pollutants during the critical early-life period of brain development may contribute to the emergence of Autism Spectrum Disorders (ASD). This study seeks to compare the developmental neurotoxicity of the α-isomer of hexabromocyclododecane (α-HBCDD), a persistent brominated flame retardant, to the valproic acid (VPA) model of ASD in rodents. Pregnant Wistar rats were divided into three groups: control, α-HBCDD (100 ng/kg/day p.o., GD0-PND21) and VPA (600 mg/kg i.p., GD12). Male offspring were tested for their neuromotor development from PND2-21. At PND21, brain functionality was assessed by measuring cytochrome oxidase activity (CO). Modifications in neuroglia and synaptic plasticity were evaluated in the cortex. Similar subtle behavioural changes related to neuromotor maturation and noise reaction were observed in both treated groups. At PND21, a reduction in CO activity was measured in the VPA group only, in specific areas including auditory nuclei, visual cortex, cingulate and frontal cortices. At the same age, α-HBCDD pointed out significant overexpression of cortical markers of synaptic plasticity while both treated groups showed a significant under expression of astrocyte proteins (S100-β and GFAP). Early-life exposure to a low dose of α-HBCDD may trigger neurobehavioural alterations in line with ASD.