Cognitive Development and Prenatal Air Pollution Exposure in the CHAMACOS Cohort DOI Creative Commons
Stephanie M. Holm, John R. Balmes, Robert B. Gunier

et al.

Environmental Health Perspectives, Journal Year: 2023, Volume and Issue: 131(3)

Published: March 1, 2023

Background: Because fine particulate matter [PM, with aerodynamic diameter ≤2.5μm (PM2.5)] is a ubiquitous environmental exposure, small changes in cognition associated PM2.5 exposure could have great societal costs. Prior studies demonstrated relationship between utero and cognitive development urban populations, but it not known whether these effects are similar rural populations they persist into late childhood. Objectives: In this study, we tested for associations prenatal both full-scale subscale measures of IQ among longitudinal cohort at age 10.5 y. Methods: This analysis used data from 568 children enrolled the Center Health Assessment Mothers Children Salinas (CHAMACOS), birth study California's agricultural Valley. Exposures were estimated residential addresses during pregnancy using state art, modeled surfaces. testing was performed by bilingual psychometricians dominant language child. Results: A 3-μg/m3 higher average over −1.79 points [95% confidence interval (CI): −2.98, −0.58], decrements specifically Working Memory (WMIQ) Processing Speed (PSIQ) subscales [WMIQ −1.72 (95% CI: −0.45) PSIQ −1.19 −2.54, 0.16)]. Flexible modeling course illustrated mid-to-late (months 5–7) as particularly susceptible times, sex differences timing windows which most affected [Verbal Comprehension (VCIQ) WMIQ males; females]. Discussion: We found that increases outdoor slightly lower childhood, robust to many sensitivity analyses. there larger effect on childhood than has previously been observed, perhaps due PM composition or because developmental disruption alter trajectory thus appear more pronounced get older. https://doi.org/10.1289/EHP10812

Language: Английский

Air Pollution and Central Nervous System Disease: A Review of the Impact of Fine Particulate Matter on Neurological Disorders DOI Creative Commons
Hyun‐Young Kim, Won‐Ho Kim,

Young-Youl Kim

et al.

Frontiers in Public Health, Journal Year: 2020, Volume and Issue: 8

Published: Dec. 16, 2020

Background: It is widely known that the harmful effects of fine dust can cause various diseases. Research on correlation between and health has been mainly focused lung cardiovascular By contrast, air pollution central nervous system (CNS) are not broadly recognized. Findings: Air diverse neurological disorders as result inflammation system, oxidative stress, activation microglial cells, protein condensation, cerebral vascular-barrier disorders, but uncertainty remains concerning biological mechanisms by which produces disease. Neuronal cell damage caused dust, especially in fetuses infants, permanent brain or lead to disease adulthood. Conclusion: necessary study pollution–CNS connection with particular care commitment. Moreover, epidemiological experimental association exposure CNS critical public quality life. Here, we summarize correlations reported so far make suggestions direction future research should take.

Language: Английский

Citations

148
Toxicological Effects of Fine Particulate Matter (PM2.5): Health Risks and Associated Systemic Injuries—Systematic Review DOI Open Access

Amanda Garcia,

Eduarda Santa-Helena, Anna De Falco

et al.

Water Air & Soil Pollution, Journal Year: 2023, Volume and Issue: 234(6)

Published: May 24, 2023

Language: Английский

Citations

73
Genetics and epigenetics of autism: A Review DOI Open Access
Mary Miu Yee Waye, Ho Yu Cheng

Psychiatry and Clinical Neurosciences, Journal Year: 2017, Volume and Issue: 72(4), P. 228 - 244

Published: Sept. 23, 2017

Autism is a developmental disorder that starts before age 3 years, and children with autism have impairment in both social interaction communication, restricted, repetitive, stereotyped patterns of behavior, interests, activities. There strong heritable component spectrum (ASD) as studies shown parents who child ASD 2–18% chance having second ASD. The prevalence been increasing during the last decades much research has carried out to understand etiology, so develop novel preventive treatment strategies. This review aims at summarizing latest related ASD, focusing not only on genetics but also some epigenetic findings autism/ASD. Some promising areas using transgenic/knockout animals ideas potential prevention strategies will be discussed.

Language: Английский

Citations

136
NF-κB-regulated microRNA-574-5p underlies synaptic and cognitive impairment in response to atmospheric PM2.5 aspiration DOI Creative Commons
Tingting Ku, Ben Li, Rui Gao

et al.

Particle and Fibre Toxicology, Journal Year: 2017, Volume and Issue: 14(1)

Published: Aug. 29, 2017

PM2.5 (particulate matter ≤ 2.5 μm) is one of the leading environmental risk factors for global burden disease. Whereas increasing evidence has linked adverse roles with cardiovascular and respiratory diseases, limited but growing emerging suggests that exposure can affect nervous system, causing neuroinflammation, synaptic dysfunction cognitive deterioration. However, molecular mechanisms underlying deficits elicited by are largely unknown. C57BL/6 mice received oropharyngeal aspiration (1 5 mg/kg bw) every other day 4 weeks. The were also stereotaxically injected β-site amyloid precursor protein cleaving enzyme 1 (β-secretase, BACE1) shRNA or LV-miR-574-5p lentiviral constructs in absence presence at bw Spatial learning memory assessed Morris water maze test, function integrity was evaluated electrophysiological recordings long-term potentiation (LTP) immunoblot analyses glutamate receptor subunit expression. expression α-secretase (ADAM10), BACE1, γ-secretase (nicastrin) synthesis accumulation β (Aβ) measured enzyme-linked immunosorbent assay (ELISA). MicroRNA (miRNA) screened a microRNA microarray analysis confirmed real-time quantitative reverse transcription PCR (qRT-PCR) analysis. Dual-luciferase reporter gene chromatin immunoprecipitation (ChIP) used to detect binding miR-574-5p 3'UTR BACE1 NF-κB p65 promoter miR-574-5p, respectively. caused neuroinflammation deteriorated spatial memory, effects associated induction BACE1. action mediated p65-regulated downregulation which targets Overexpression hippocampal region decreased expression, restored function, improved following exposure. Taken together, our findings reveal novel mechanism impaired PM2.5, suggesting potential intervention target prevention treatment PM2.5-induced neurological disorders.

Language: Английский

Citations

129
Air pollution associated epigenetic modifications: Transgenerational inheritance and underlying molecular mechanisms DOI

Anushi Shukla,

Neha Bunkar, Rajat Kumar

et al.

The Science of The Total Environment, Journal Year: 2018, Volume and Issue: 656, P. 760 - 777

Published: Nov. 28, 2018

Language: Английский

Citations

127
Fine particulate matter induces mitochondrial dysfunction and oxidative stress in human SH-SY5Y cells DOI
Ying Wáng, Mei Zhang,

Zhiping Li

et al.

Chemosphere, Journal Year: 2018, Volume and Issue: 218, P. 577 - 588

Published: Nov. 23, 2018

Language: Английский

Citations

109
Environmental pollution and mental health: a narrative review of literature DOI
Antonio Ventriglio, Antonello Bellomo,

Ilaria Di Gioia

et al.

CNS Spectrums, Journal Year: 2020, Volume and Issue: 26(1), P. 51 - 61

Published: April 14, 2020

Abstract Pollutant agents are exponentially increasing in modern society since industrialization processes and technology being developed worldwide. Impact of pollution on public health is well known but little has been described the association between environmental pollutants mental health. A literature search PubMed EMBASE conducted 134 articles published issue have included, cited, reviewed, summarized. Emerging evidences collected major ( air , heavy metals ionizing radiation [IR] organophosphate pesticides light noise catastrophes ) various disorders including anxiety, mood, psychotic syndromes. Underlying pathogenesis includes direct indirect effects these brain, respectively, due to their biological effect human Central Nervous System or related some levels stress generated by exposure pollutant over time. Most emerging still nonconclusive. Further studies should clarify how industrial production, exploitation certain resources, proximity waste energy residues, noise, change lifestyles connected with psychological distress problems for affected populations.

Language: Английский

Citations

100
DNA methylation: a potential mediator between air pollution and metabolic syndrome DOI Creative Commons
Parinaz Poursafa, Zoha Kamali, Eliza Fraszczyk

et al.

Clinical Epigenetics, Journal Year: 2022, Volume and Issue: 14(1)

Published: June 30, 2022

Given the global increase in air pollution and its crucial role human health, as well steep rise prevalence of metabolic syndrome (MetS), a better understanding underlying mechanisms by which environmental may influence MetS is imperative. Exposure to known impact DNA methylation, turn affect health. This paper comprehensively reviews evidence for hypothesis that effect on mediated methylation blood. First, we present summary dysregulation, including components MetS, i.e., disorders blood glucose, lipid profile, pressure, obesity. Then, provide relation between endothelial dysfunction one possible mechanism MetS. Subsequently, review (PM, ozone, NO

Language: Английский

Citations

41
Neurodevelopmental toxicity induced by PM2.5 Exposure and its possible role in Neurodegenerative and mental disorders DOI Creative Commons
X. Liu, Jia Huang, Chao Song

et al.

Human & Experimental Toxicology, Journal Year: 2023, Volume and Issue: 42

Published: March 1, 2023

Recent extensive evidence suggests that ambient fine particulate matter (PM2.5, with an aerodynamic diameter ≤2.5 μm) may be neurotoxic to the brain and cause central nervous system damage, contributing neurodevelopmental disorders, such as autism spectrum neurodegenerative diseases, Alzheimer's disease Parkinson's disease, mental schizophrenia, depression, bipolar disorder. PM2.5 can enter via various pathways, including blood-brain barrier, olfactory system, gut-brain axis, leading adverse effects on CNS. Studies in humans animals have revealed PM2.5-mediated mechanisms, neuroinflammation, oxidative stress, systemic inflammation, gut flora dysbiosis, play a crucial role CNS damage. Additionally, exposure induce epigenetic alterations, hypomethylation of DNA, which contribute pathogenesis some Through literature analysis, we suggest promising therapeutic targets for alleviating PM2.5-induced neurological damage include inhibiting microglia overactivation, regulating microbiota antibiotics, targeting signaling PKA/CREB/BDNF WNT/β-catenin. several studies observed association between changes neuropsychiatric disorders. This review summarizes discusses possible mechanisms by causes neurotoxicity.

Language: Английский

Citations

29
Neurotoxicity of the air-borne particles: From molecular events to human diseases DOI
Fang Liu, Chunyan Liu, Yin Liu

et al.

Journal of Hazardous Materials, Journal Year: 2023, Volume and Issue: 457, P. 131827 - 131827

Published: June 10, 2023

Language: Английский

Citations

26