In this study, researchers examined the affects of iron oxide and sulfur dioxide from air pollution on neurotoxicity in mice and the possibility of more iron oxide leading to more neurodevelopmental disorders. They exposed mice to either particles of just iron oxide and particles of iron oxide and sulfur dioxide. The results indicated that the combination of iron and sulfur resulted in greater neurotoxic effects. Major effects occurred in the frontal cortex and in glutamatergic and dopaminergic functions. The results also indicated that females were more affected than males. 

This study looked at how early exposure to indoor air pollution affected neuropsychological development of preschoolers. They tested 300 some kids from Spain and recorded information regarding gas appliances and nitrogen dioxide levels during the first three months of life. They then assessed cognitive abilities and attention-hyperactivity behaviors at age 4. The results found that both gas appliances and nitrogen dioxide reduced cognitive function and increased odds of inattention symptoms. Neuropsychological outcomes were more pronounced in children possessing the GSTP1 Val-105 allele. This suggests that early exposure to air pollution from indoor sources might have a detrimental association with neuropsychological development among genetically susceptible children.

This study focused on how concentrated ambient particles affected fetal development of the brain. They tested this idea by exposing pregnant mice to the particles and then watching as they developed. They found that there was an enlargement of brain ventricles, abnormal increase in myelin production, and enlargement of the corpus callosum. There was also a premature shift in the number and proportion of oligodendrocytes in the corpus callosum. Many of these changes continued as the mouse matured and developed. 

The goal of this study was to see if exposure to concentrated ambient ultrafine particles lead to a susceptibility to a Parkinson's disease-like phenotype . They exposed mice to the particles and saw that the substantia nigra and striatum, regions associated with Parkinson's disease, are susceptible to components of air pollution. They appeared to target different aspects of the nigrostriatal dopamine and amino acid systems. They also increased glutamate levels, which could lead to cell damage due to over stimulation. Overall, the results showed that there was locomotor dysfunction and changes in dopaminergic and glutamatergic systems in brain regions relevant to Parkinson's disease. 

This study looked at air pollution exposure during pregnancy and childhood to see the impact on cognitive function and mental health in adolescents. They took about 500 individuals from the Neterlands and estimated air pollution exposure based on where they lived. They tested for processing speed, working memory, fluid reasoning, verbal IQ, and emotional/behavioral problems. The results indicated there was no significant association between air pollution exposure and full-scale IQ, working memory, or processing speed. Higher exposure to certain air pollutants was linked to slightly higher scores in fluid reasoning and verbal IQ. Also, increased exposure to some pollutants was associated with reduced internalizing, externalizing, and attention problems. However, they noted that this study isn't causal, meaning they believe that other variables/biases could have affected the results, so more research is needed. 

The purpose of this study was to determine how air pollution increased preference for immediate reward and impulsivity  and how concentrated ambient ultrafine particles affects the behavior of adult mice. The results indicate that the brain does have an increase preference for impulsivity and that the performance of the fixed interval was adversely affected. These behavioral changes were associated with changes in brain dopamine and glutamate systems. The results also showed that there was impaired short-term memory. Changes in amino acids in the cortex and hippocampus had the potential for excitotoxicity. Persistent glial activation was observed in the frontal cortex and corpus callosum, suggesting ongoing brain inflammation. This can lead to enduring and sex-dependent neurotoxic effects. 

This study looked to see the impacts of air pollution (specifically welding fumes) on the medial temporal lobe, which are structures that are related to Alzheimer's. They examined individual who were consistently around welding fumes and those who weren't and took scans of brain areas like the the hippocampus, entorhinal and parahippocampal cortices. They found that those exposed to welding fumes performed worse in cognitive tests related to processing/psychomotor speed, executive function, and visuospatial abilities compared to controls. This indicates they are experiencing effects similar to early-stage Alzheimer's disease. 

This study looked to see if there were potential neurodevelopmental effects of exposure to ultrafine elemental carbon. They exposed mice to the carbon element. The results indicate that carbon did not lead to significant differences in anogenital distance, body weight, or central nervous system pathological markers. Also,  locomotor activity, short-term memory, elevated plus maze (anxiety-like behavior), and tasks related to learning and impulsivity, did not show significant differences. These results indicate that carbon isn't responsible for the neurotoxic effects associated with air pollution exposure, it must be some other part of air pollution. 

The purpose of this study is to the look at the association between air pollution exposure and various neurodevelopmental disorders such as autism, attention deficit disorder, and cognitive delays. Research in mice exposed to concentrated ambient ultrafine particles during their pregnancy, demonstrated biological plausibility for these associations. The study aimed to identify the specific components of air pollution responsible for its neurotoxic effects. They recorded contamination with multiple elements, including iron and sulfur. Elevated levels of Fe and S in the brain aligned with potential mechanisms of ultrafine particle-induced neurotoxicity, such as ferroptosis, oxidative stress, and altered antioxidant capacity. This was supported by observations of increased serum oxidized glutathione and neuronal cell death in the nucleus accumbens. This needs to continue being looked at because it could lead to strategies that mitigate the detrimental effects of air pollution on neurodevelopment. 

The study looked to see if inhaled manganese oxide ultrafine particles can translocate through the olfactory nerve to the brain, and if this translocation leads to potential health effects in rats. The rats were then exposed to the manganese particles through both nostrels, or with one open and the other closed. The results indicate that with both nostrils open, increased concentrations of manganese were found in the olfactory bulb, lung, striatum, frontal cortex, and cerebellum. Inflammatory changes were observed in the olfactory bulb, and to a lesser extent, in other brain regions with increased manganese levels. When the right nostril was closed, manganese accumulated only in the left olfactory bulb. The findings suggest that inhaled manganese oxide UFPs can efficiently translocate through the olfactory pathway to the central nervous system in rats, leading to inflammatory changes.

This study looked to see if postnatal exposure to ultrafine particles on social behavior in adult mice and the change in hormone levels. Previous studies have linked air pollution exposure to various neurodevelopmental disorders, including autism spectrum disorder, attention deficit disorder, and schizophrenia, which are more common in males. There were male-biased neuropathological changes, cognitive deficits, and impulsivity. The results showed a decrease in serum testosterone. There was also a reduced social nose-to-nose sniff rates when interacting with unfamiliar males, indicating social communication deficits. These results demonstrate a connection between hormonal changes and behavioral changes due to air pollution. 

This study examined the effects of ultrafine concentrated ambient particles on the central nervous system by exposing mice to the various particles. The results showed that lateral ventricle dilation was observed in male mice. There were also decreases in the CNS cytokines , while females exposed to CAPs had a neuroinflammatory response with increased CNS cytokines. Changes in neurotransmitters and glial activation were seen in multiple brain regions. Male mice also showed increased levels of glutamate in the hippocampus. The lateral ventricle dilation suggests a potential link to poor neurodevelopmental outcomes, autism, and schizophrenia. 

The study looked to see how cognitive funtion was affected by exposure to ambient ultrafine particles, specifically in context to Alzheimer's disease. They exposed older mice that had an AD background and those that didn't have an AD background to the particles. The results show that locomotor activity wasn't affected, but that there was cognitive defects in learning and memory. They had reduced spatial learning abilities and impaired short-term memory. Mice with an AD background experienced worse memory issues and appetitive motivation and olfactory discrimination were negatively impacted. Overall, even short-term inhalation exposure to UFPs resulted in lasting adverse effects on multiple memory areas, independent of AD background.  

This study looked to see if exposure to concentrated ambient particles during the first two weeks of life, would impact the preference for immediate rewards in mice. The results showed that the young mice displayed an enhanced bias towards immediate rewards, as indicated by increased response rates in spite of the added response cost. This suggests a preference for immediate gratification/rewards. This preference for immediate gratification is linked to various central nervous system and psychiatric disorders like obesity, addiction, and attention deficit. 

This study looked to see how the exposure of concentrated ambient ultrafine particles impacted the central nervous system of mice. The mice were exposed to two levels of ultrafine particles and were then examined. The results indicated signs of abnormal immune activation in the brains of exposed mice. Elevated levels of glial fibrillary acidic protein were also found, suggesting glial cell activation. There were no significant changes in the active forms of MAP kinases. However, the fraction of active JNK was increased in animals exposed to the lower concentrations of ultrafine particles. This suggests that the activation of JNK might be involved in the signaling pathway leading to the activation of these transcription factors. 

This study looks to examine the link between a diagnosis of autism spectrum disorder and maternal exposure to aircraft ultrafine particles. The researchers obtained the health data of over 300,000 kids from 5 and under, who were diagnosed with ASD and then estimated aircraft ultrafine particle exposure based on the data obtained. The study found that there was an increased risk of ASD diagnosis in children when they were exposed to aircraft ultrafine particles during pregnancy. For every incremental increase of 0.02 μg/m3 in exposure to aircraft ultrafine particles, there was a 2% higher hazard ratio for ASD diagnosis. 

The purpose of this study was to see the potential influence traffic-related air pollution has on the development of autism. They used data from air monitoring stations and land use regression models to determine exposure levels. The study found that there was a 12-15% increase in the odds of autism for ozone and particulate matter and a 3–9% increase in the odds of autism in exposure levels for nitric oxide and nitrogen dioxide. This suggests that higher exposure to these pollutants was associated with an increased risk of autism.

This study looked at the neurotoxic effects of concentrated ultrafine particles on wildtype mice and mice modeled for Alzheimer's disease at different stages of development. They exposed the mice to particles for 12 weeks and found that diseased mice had significant memory impairment without changes in amyloid-β pathology, synaptic degeneration, or neuroinflammation. In aged mice, both groups exposed showed marked memory impairment and neuronal loss. In the diseased mice, increased amyloid-β buildup and glial activation, including ferritin-positive microglia and C3-positive astrocytes, were observed. This glial activation could contribute to the progression of degenerative changes in the brain. The findings indicate that exposure to particles impaired cognitive function in mice at both early and later stages of life.

This study looked at the deposition, uptake, and transport of inhaled ultrafine iron-soot particles in the nasal cavities of mice. They examined whether combustion-generated nanoparticles can access the olfactory bulb through the olfactory pathway. Adult female mice were exposed to iron-soot combustion particles at a concentration of 200 μg/m³ for 6 hours a day, 5 days a week, over 5 consecutive weeks. The results show that the inhaled ultrafine iron-soot particles reached the brain via the olfactory nerves. Additionally, the presence of these particles in the olfactory system was associated with indicators of neural inflammation. This study highlighted the potential for combustion-generated nanoparticles to access the brain through the olfactory pathway, indicating a possible route for particulate exposure to contribute to neural inflammation.

This study looks at the impact concentrated ambient ultrafine particle exposure on amyloid-β, tau, and microglial morphology in two cohorts of aged mice. They exposed the mice to either filtered air or air with the ultrafine particles. The results showed a significant genotype by exposure interactions in microglia and amyloid-β markers. Specifically, ultrafine particle-exposed mice showed lower levels of microglia and amyloid-β markers compared to the air-exposed group. Also, Ultrafine particle exposure led to significant elevations in phosphorylated tau in mice. These results highlight that exposure to ultrafine particulates induced changes in tau phosphorylation and microglial morphology, which is indicative of Alzheimer's disease. 

This study looked to see if there was an association between ambient ultrafine particle exposure and brain tumors in adults. The researchers gathered data on 1.9 million adults in Canada from 1991-2006. Level of ultrafine particle exposure was based on where they lived at that time. The results indicate there is a positive association between brain tumors and ultrafine particle exposure. For every 10,000 particles per cubic centimeter increase in ultrafine particle concentration, there was a corresponding increase in brain tumor incidence. The study found that PM2.5 and NO2 were not linked to an increased incidence of brain tumors and they adjusted for things like smoking and body mass index. Conclusively, the findings suggest that ambient ultrafine particle could potentially represent a previously unidentified risk factor for brain tumors among adults. 

This study looked at the impact of exposure to ultrafine particles during forced exercise on the expression of genes related to inflammation, oxidative stress, and Brain-Derived Neurotrophic Factor in rats. Four groups of Wistar rats: UFP with exercise, UFP without exercise, ambient air with exercise, and ambient air without exercise. The results showed that in the condition of ambient air with exercise, there was an up-regulation of BDNF and NFE2L2 expression in the hippocampus. Also, the expression of certain inflammatory genes (IL1α and NOS3) in the prefrontal cortex and olfactory bulb was down-regulated compared to the control. However, in the condition of UFP exposure with exercise, there were no differences in gene expression compared to the control. This indicates that UFP exposure negated the exercise-induced up-regulation of BDNF gene expression in the hippocampus of rats. In the UFP exposure without exercise condition, the hippocampal expression of NFE2L2 was down-regulated, and there was a trend towards reduced BDNF expression compared to the control. The study suggests a detrimental effect of UFP exposure on the beneficial impact of exercise on BDNF gene expression in the rat hippocampus.

This study looked to see if there was an association between ambient pollution particles and blood sex hormone levels. They took a group of men aged 20-55 to study in this research. They measured testosterone, follicle stimulating hormone, luteinizing hormone, estradiol, and prolactin in each participant and collected data on daily ambient levels of various pollutants. The results indicated a connection between immediate and short-term cumulative exposure to particulate matter. It altered serum sex hormone levels, particularly testosterone, in men. An increase of 10 μg/m3 on the current day correlated with a 1.6% and 1.1% decrease in testosterone, respectively. This shows we need to limit ambient particle pollution in order to mitigate the effect it will have on men's reproductive help.

This study looked to see if short-term ambient ultrafine particle exposure impacted stroke type. They distinguished between ischemic and hemorrhagic strokes, mild and severe strokes, and ischemic strokes with or without atrial fibrillation. They then took health data from roughly 7,000 stroke patients from 2003 to 2006 and also used that to determine exposure. The results indicated there was a significant positive association observed between UFPs and ischemic strokes. The study found a 21% increase in hospital admissions for mild ischemic strokes of likely thrombotic origin (without AF) following UFP exposure. The results suggest potential effects of traffic-related air pollution, notably UFPs, on hospital admissions for ischemic stroke, particularly for mild ischemic strokes without AF, highlighting the importance of understanding the impact of air pollution on stroke severity and origin. 

This study looked to see the impact of fine and ultrafine particles on dopaminergic transmission. Using rat striatal isolated nerve terminals (synaptosomes), exposure to FP and UFP occurred by collecting from the air of Mexico City, which resulted in inhibition of dopamine uptake and increased depolarization-evoked dopamine release. The particles also heightened the affinity of dopamine receptors for dopamine, both in rat striatum and in cells transfected with the human D2R. Also, FP and UFP increased the effectiveness of dopamine or the D2R agonist quinpirole in inhibiting cAMP formation in cells or striatal slices, showing a concentration-dependent effect, with UFP having a more pronounced impact. These findings indicate a direct influence of FP and UFP on dopaminergic transmission.