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particulate
237 studies tagged particulate, dated 1994-07-01 to 2026-10-11. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Carbonaceous Components Underlying Wildfire Smoke PM 2.5 -Associated Alzheimer’s Disease and Related Dementias in Older US Adults 2026-10-11
- Micro- and nanoplastics alter electrophysiological brain patterns and reshape human neurodevelopmental trajectories 2026-09-24
- Neuroexposomics to Prevent Neurodegenerative Disease: Challenges, Next Steps, and Recommendations 2026-08-31
Studies
237 studies carry this tag.
Date range
1994 to 2026
Top journals
- Journal of Alzheimer's disease : JAD 24
- Environmental research 21
- Environment international 8
- Environmental health perspectives 8
- medRxiv 7
130 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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The adjusted hazard ratio (HR) of dementia for a 5-μg/m3 increase in NO2 was 1.09 (95% CI, 1.05-1.14); the adjusted HR of dementia for a 1-μg/m3 increase in PM2.5 was 1.10 (1.04-1.17).
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In 2017, the Lancet Commission on Dementia Prevention, Intervention, and Care included air pollution in its list of potential risk factors for dementia; in 2018, the Lancet Commission on Pollution concluded that the evidence for a causal relationship between fine particulate matter (PM) and dementia is encouraging.
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Higher chronic exposure to SO2 was associated with a faster decline in memory score, whereas chronic exposure to CO, NO2 , and PM10 were not associated with the rate of cognitive decline.
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71/100
During the follow-up period, we identified a total of 617 incident neurodegenerative diseases, 301 PD and 182 AD.
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68/100
This study included 5646 participants (mean age 76 years, 65% female).
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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 to neurodevelopmental disorders, such as autism spectrum disorders, neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, and mental disorders, such as schizophrenia, depression, and bipolar disorder.
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46/100
In total, 104 incident dementia and 159 incident dementia/CIND cases were identified during the 10 years of follow-up.
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70/100
Evidence on the association between air pollution and dementia is accumulating but still inconclusive, and the potential effect modification by genetics is unclear.
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With recent findings connecting the Epstein-Barr virus to an increased risk of multiple sclerosis and growing concerns regarding the neurological impact of the coronavirus pandemic, we examined potential links between viral exposures and neurodegenerative disease risk.
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Of the 7,511 non-demented participants at baseline, 545 developed dementia during a median follow-up of 7 years.
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Temperature extremes and variability both associated with stroke incidence and severity, migraine headaches, hospitalization in patients with dementia, and multiple sclerosis exacerbations.
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55/100
Ambient 2-year averaged exposure of PM2.5 was associated with changes of neuroinflammatory markers, that is, CSF sTREM2 (β = -0.116, p = 0.0002).
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A total of 20 studies were included in the systematic review, and 17 provided data for the meta-analysis.
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70/100
In total, 20 articles were selected for review; 18 included results on the long-term effects of PM2.5 on dementia, 13 on AD, and eight on VaD.
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Traffic-related air pollution (TRAP) has been a common public health problem, which is associated with central nervous system dysfunction according to large-scale epidemiological studies.
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Respirable fine particulate matter (PM 2.5 ) has been one of the most widely publicized indicators of pollution in recent years.
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The environmental role in disease progression has been appreciated for decades; however, understanding how airborne toxicant exposure can affect organs beyond the lungs is an underappreciated area of scientific inquiry.
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Long-term exposure to PM 2.5 contributed to the development of cognitive decline, which may be partly explained by brain amyloid accumulation indicative of increased AD risk.
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Neurodegeneration leads to the loss of structural and functioning components of neurons over time.
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An interquartile range increase in 20-year PM2.5 was associated with a 20% higher risk of dementia (95% confidence interval [CI]: 5%, 37%) and an increased risk of mixed VaD/AD but not AD alone.
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Exposure to particulate matter (PM) pollution damages the human brain.
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The increasing amount of particulate matter (PM) in the ambient air is a pressing public health issue globally.
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Exposure to metals is ubiquitous and emission sources include gasoline, diesel, smoke from wildfires, contaminated soil, water and food, medical implants, waste recycling facilities, subway exposures, and occupational environments.
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Parkinson's disease, as well as other neurodegenerative disorders, are primarily characterized by pathological accumulation of proteins, inflammation, and neuron loss.
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Growing evidence has linked long-term fine particulate matter (PM 2.5 ) exposure to neurological disorders.
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DEP exposure at 100μg/m3 for 5 h, but not lower doses, caused oxidative damage, complement and microglia activation in cerebral cortex and corpus callosum.
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The adverse effects of air pollutants on the respiratory and cardiovascular systems are unquestionable.
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Air pollution may increase risk of Alzheimer's disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear.
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Cerebrovascular pathologies are commonly associated with dementia.
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Particulate matter with a diameter of less than 2.5 μm or PM2.5 is recognized worldwide as a cause of public health problems, mainly associated with respiratory and cardiovascular diseases.
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43/100
Fine particulate matter (PM2.5), a major component among air pollutants, highlights as a global health concern.
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Strong conclusions remain elusive, although the weight of the evidence suggests an adverse association between PM2.5 and cognitive decline.
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In a population of cognitively unimpaired adults with increased risk of AD, long-term exposure to air pollution was associated with higher levels in biomarkers of AD pathology.
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Asthma participants had widespread and large-magnitude differences in several dMRI metrics, which were indicative of neuroinflammation and neurodegeneration, and which were robustly associated with GFAP and, to a lesser extent, NfL.
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45/100
The scientific literature is scarce when referring to the influence of atmospheric pollutants on neurodegenerative diseases for present and future climate change scenarios.
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We report 1,136 cases of incident dementia among 4,166 individuals with nonmissing APOE status.
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The risk of dementia and Alzheimer's disease in Latin America and the Caribbean (LAC) rises with increasing age and polluted air.
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Alzheimer's disease (AD), non-AD dementia, and Parkinson's disease (PD) are increasingly common in older adults, yet all risk factors for their onset are not fully understood.
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Air pollution is regarded as an important risk factor for many diseases that affect a large proportion of the human population.
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These data demonstrate that chronic exposure to ambient TRAP promoted AD phenotypes in wildtype and genetically susceptible rats.
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PubMed, Embase and Web of Science Core Collection were searched for articles meeting the criteria published on/before 13 February 2020.
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Modeling estimated single-year exposure, each 1 μg/m3 higher ambient PM2.5 was associated with 67% higher adjusted risk of incident dementia (hazard ratio [HR] = 1.669, 95% credible interval [CI]: 1.298, 2.136) and 75% higher adjusted risk of incident MCI (HR = 1.746, 95% CI: 1.518, 2.032).
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The PSI was higher in Kaohsiung and compared with Pingtung patients, Kaohsiung patients were exposed to higher average annual concentrations of CO, NO2, PM10, and SO2.
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PM2.5 can enter the central nervous system through 2 main pathways, the blood-brain barrier and olfactory neurons.
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10-year average (SD) PM2.5 from death across the autopsy cohort was 8.2 (1.9) μg/m3.
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41/100
The Aβ plaque load was significantly increased in the hippocampus of PM2.5-exposed APP/PS1 mice compared to their respective FA controls.
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Five older nPM batches (2009-2017) and four recent nPM batches (2018, 2019) for NF-κB and Nrf2 induction showed declines in nPM potency after 2017 that paralleled declines of in vivo activity from independent exposures in different years.
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61/100
Recent studies suggested that long-term exposure to fine particulate matter (PM2.5) was related to a higher risk of dementia incidence or hospitalizations in western populations, but the evidence is limited in Asian cities.
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Bans on persistent organic pollutants (POPs) have reduced pollution by PCBs and DDT.
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39/100
During the follow-up, we identified 159 incident dementia or CIND cases in total.
From across this tag
7 of the 237 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 7. The same 7 appear here every time.
- PM2.5 exposure aggravates oligomeric amyloid beta-induced neuronal injury and promotes NLRP3 inflammasome activation in an in vitro model of Alzheimer's disease
- Traffic-Related Air Pollution and Parkinson's Disease in Denmark: A Case-Control Study
- Diesel engine exhaust accelerates plaque formation in a mouse model of Alzheimer's disease
- Environmental exposures and gene regulation in disease etiology
- Microglia-derived extracellular vesicles mediate fine particulate matter-induced Alzheimer's disease-like behaviors through the miR-34a-5p/DUSP10/p-p38 MAPK pathway
- Effects of air pollution on human health and practical measures for prevention in Iran
- Ambient air pollution and neurotoxicity on brain structure: Evidence from women's health initiative memory study