scholarly journals Fine Particulate Matter and Markers of Alzheimer’s Disease Neuropathology at Autopsy in a Community-Based Cohort

2021 ◽  
Vol 79 (4) ◽  
pp. 1761-1773
Author(s):  
Rachel M. Shaffer ◽  
Ge Li ◽  
Sara D. Adar ◽  
C. Dirk Keene ◽  
Caitlin S. Latimer ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Particulate Matter ◽  
Fine Particulate Matter ◽  
Braak Stage ◽  
Community Based ◽  
Spatiotemporal Model ◽  
Fine Particulate ◽  
Autopsy Specimens

Background: Evidence links fine particulate matter (PM2.5) to Alzheimer’s disease (AD), but no community-based prospective cohort studies in older adults have evaluated the association between long-term exposure to PM2.5 and markers of AD neuropathology at autopsy. Objective: Using a well-established autopsy cohort and new spatiotemporal predictions of air pollution, we evaluated associations of 10-year PM2.5 exposure prior to death with Braak stage, Consortium to Establish a Registry for AD (CERAD) score, and combined AD neuropathologic change (ABC score). Methods: We used autopsy specimens (N = 832) from the Adult Changes in Thought (ACT) study, with enrollment ongoing since 1994. We assigned long-term exposure at residential address based on two-week average concentrations from a newly developed spatiotemporal model. To account for potential selection bias, we conducted inverse probability weighting. Adjusting for covariates with tiered models, we performed ordinal regression for Braak and CERAD and logistic regression for dichotomized ABC score. Results: 10-year average (SD) PM2.5 from death across the autopsy cohort was 8.2 (1.9) μg/m3. Average age (SD) at death was 89 (7) years. Each 1μg/m3 increase in 10-year average PM2.5 prior to death was associated with a suggestive increase in the odds of worse neuropathology as indicated by CERAD score (OR: 1.35 (0.90, 1.90)) but a suggestive decreased odds of neuropathology as defined by the ABC score (OR: 0.79 (0.49, 1.19)). There was no association with Braak stage (OR: 0.99 (0.64, 1.47)). Conclusion: We report inconclusive associations between PM2.5 and AD neuropathology at autopsy among a cohort where 94% of individuals experienced 10-year exposures below the current EPA standard. Prior studies of AD risk factors and AD neuropathology are similarly inconclusive, suggesting alternative mechanistic pathways for disease or residual confounding.

Fine particulate matter is a potential determinant of Alzheimer's disease: A systemic review and meta-analysis

2019 ◽  
Vol 177 ◽  
pp. 108638 ◽  
Author(s):  
Tsung-Lin Tsai ◽  
Yu-Ting Lin ◽  
Bing-Fang Hwang ◽  
Shoji F. Nakayama ◽  
Chon-Haw Tsai ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Particulate Matter ◽  
Meta Analysis ◽  
Fine Particulate Matter ◽  
Systemic Review ◽  
Fine Particulate ◽  
Potential Determinant

NLRP3 Inflammasome: A Potential Therapeutic Target in Fine Particulate Matter-Induced Neuroinflammation in Alzheimer’s Disease

2021 ◽  
Author(s):  
Jian-Quan Shi ◽  
Bian-Rong Wang ◽  
Teng Jiang ◽  
Li Gao ◽  
Ying-Dong Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Particulate Matter ◽  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Fine Particulate Matter ◽  
Transport Pathway ◽  
Critical Gap ◽  
Fine Particulate ◽  
Pm2.5 Exposure

As one of the most harmful air pollutants, fine particulate matter (PM2.5) has been implicated as a risk factor for multiple diseases, which has generated widespread public concern. Accordingly, a growing literature links PM2.5 exposure with Alzheimer’s disease (AD). A critical gap in our understanding of the adverse effects of PM2.5 on AD is the mechanism triggered by PM2.5 that contributes to disease progression. Recent evidence has demonstrated that PM2.5 can activate NLRP3 inflammasome-mediated neuroinflammation. In this review, we highlight the novel evidence between PM2.5 exposure and AD incidence, which is collected and summarized from neuropathological, epidemiological, and neuroimaging studies to in-depth deciphering molecular mechanisms. First, neuropathological, epidemiological, and neuroimaging studies will be summarized. Then, the transport pathway for central nervous system delivery of PM2.5 will be presented. Finally, the role of NLRP3 inflammasome-mediated neuroinflammation in PM2.5 induced-effects on AD will be recapitulated.

NLRP3 Inflammasome: A Potential Therapeutic Target in Fine Particulate Matter-Induced Neuroinflammation in Alzheimer’s Disease

2020 ◽  
Vol 77 (3) ◽  
pp. 923-934
Author(s):  
Jian-Quan Shi ◽  
Bian-Rong Wang ◽  
Teng Jiang ◽  
Li Gao ◽  
Ying-Dong Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Particulate Matter ◽  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Fine Particulate Matter ◽  
Transport Pathway ◽  
Critical Gap ◽  
Fine Particulate ◽  
Pm2.5 Exposure

As one of the most harmful air pollutants, fine particulate matter (PM2.5) has been implicated as a risk factor for multiple diseases, which has generated widespread public concern. Accordingly, a growing literature links PM2.5 exposure with Alzheimer’s disease (AD). A critical gap in our understanding of the adverse effects of PM2.5 on AD is the mechanism triggered by PM2.5 that contributes to disease progression. Recent evidence has demonstrated that PM2.5 can activate NLRP3 inflammasome-mediated neuroinflammation. In this review, we highlight the novel evidence between PM2.5 exposure and AD incidence, which is collected and summarized from neuropathological, epidemiological, and neuroimaging studies to in-depth deciphering molecular mechanisms. First, neuropathological, epidemiological, and neuroimaging studies will be summarized. Then, the transport pathway for central nervous system delivery of PM2.5 will be presented. Finally, the role of NLRP3 inflammasome-mediated neuroinflammation in PM2.5 induced-effects on AD will be recapitulated.

scholarly journals Long-Term Fine Particulate Matter Exposure and Major Depressive Disorder in a Community-Based Urban Cohort

2016 ◽  
Vol 124 (10) ◽  
pp. 1547-1553 ◽  
Author(s):  
Kyoung-Nam Kim ◽  
Youn-Hee Lim ◽  
Hyun Joo Bae ◽  
Myounghee Kim ◽  
Kweon Jung ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Particulate Matter ◽  
Depressive Disorder ◽  
Fine Particulate Matter ◽  
Community Based ◽  
Major Depressive ◽  
Fine Particulate ◽  
Particulate Matter Exposure

P1-030: ENVIRONMENTAL DETERMINANTS OF NEUROANATOMIC RISK FOR ALZHEIMER'S DISEASE IN OLDER WOMEN: ROLE OF FINE PARTICULATE MATTER

2006 ◽  
Vol 14 (7S_Part_4) ◽  
pp. P278-P278
Author(s):  
Diana Younan ◽  
Xinhui Wang ◽  
Andrew J. Petkus ◽  
Ramon Casanova ◽  
Ryan Barnard ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Particulate Matter ◽  
Older Women ◽  
Fine Particulate Matter ◽  
Environmental Determinants ◽  
Fine Particulate

Short-term and long-term exposures to fine particulate matter constituents and health: A systematic review and meta-analysis

2019 ◽  
Vol 247 ◽  
pp. 874-882 ◽  
Author(s):  
Yang Yang ◽  
Zengliang Ruan ◽  
Xiaojie Wang ◽  
Yin Yang ◽  
Tonya G. Mason ◽  
...  
Keyword(s):  
Systematic Review ◽  
Particulate Matter ◽  
Meta Analysis ◽  
Fine Particulate Matter ◽  
Short Term ◽  
Fine Particulate

scholarly journals Long‐Term Exposure to Particulate Air Pollution Is Associated With 30‐Day Readmissions and Hospital Visits Among Patients With Heart Failure

2021 ◽  
Author(s):  
Cavin K. Ward‐Caviness, ◽  
Mahdieh Danesh Yazdi, ◽  
Joshua Moyer, ◽  
Anne M. Weaver, ◽  
Wayne E. Cascio, ◽  
...  
Keyword(s):  
Heart Failure ◽  
Air Pollution ◽  
Particulate Matter ◽  
Fine Particulate Matter ◽  
Total Hospital ◽  
Fine Particulate ◽  
Patients With Heart Failure ◽  
Hospital Visits ◽  
Pollution Exposure

Background Long‐term air pollution exposure is a significant risk factor for inpatient hospital admissions in the general population. However, we lack information on whether long‐term air pollution exposure is a risk factor for hospital readmissions, particularly in individuals with elevated readmission rates. Methods and Results We determined the number of readmissions and total hospital visits (outpatient visits+emergency room visits+inpatient admissions) for 20 920 individuals with heart failure. We used quasi‐Poisson regression models to associate annual average fine particulate matter at the date of heart failure diagnosis with the number of hospital visits and 30‐day readmissions. We used inverse probability weights to balance the distribution of confounders and adjust for the competing risk of death. Models were adjusted for age, race, sex, smoking status, urbanicity, year of diagnosis, short‐term fine particulate matter exposure, comorbid disease, and socioeconomic status. A 1‐µg/m 3 increase in fine particulate matter was associated with a 9.31% increase (95% CI, 7.85%–10.8%) in total hospital visits, a 4.35% increase (95% CI, 1.12%–7.68%) in inpatient admissions, and a 14.2% increase (95% CI, 8.41%–20.2%) in 30‐day readmissions. Associations were robust to different modeling approaches. Conclusions These results highlight the potential for air pollution to play a role in hospital use, particularly hospital visits and readmissions. Given the elevated frequency of hospitalizations and readmissions among patients with heart failure, these results also represent an important insight into modifiable environmental risk factors that may improve outcomes and reduce hospital use among patients with heart failure.

scholarly journals Exposure to low-dose ambient fine particulate matter PM2.5 and Alzheimer’s disease, non-Alzheimer’s dementia, and Parkinson’s disease in North Carolina

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0253253
Author(s):  
Sung Han Rhew ◽  
Julia Kravchenko ◽  
H. Kim Lyerly
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
North Carolina ◽  
Particulate Matter ◽  
Hospital Admissions ◽  
Study Group ◽  
Air Particulate Matter ◽  
Air Particulate

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. Consequently, environmental exposures, including air pollution, have been hypothesized to contribute to the etiology of neurodegeneration. Because persistently elevated rates of AD mortality in the southern Piedmont area of North Carolina (NC) have been documented, we studied mortality and hospital admissions for AD, non-AD dementia, and PD in residential populations aged 65+ with long-term exposures to elevated levels of ambient air particulate matter 2.5 (PM2.5) exceeding the World Health Organization (WHO) air quality standards (≥10μg/m3). Health data were obtained from the State Center for Health Statistics and the Healthcare Cost and Utilization Project. PM2.5 levels were obtained from the MODIS/MISR and SeaWiFS datafiles. Residents in the Study group of elevated air particulate matter (87 zip codes with PM2.5≥10μg/m3) were compared to the residents in the Control group with low levels of air particulate matter (81 zip codes with PM2.5≤7.61μg/m3), and were found to have higher age-adjusted rates of mortality and hospital admissions for AD, non-AD dementia, and PD, including a most pronounced increase in AD mortality (323/100,000 vs. 257/100,000, respectively). After adjustment for multiple co-factors, the risk of death (odds ratio, or OR) from AD in the Study group (OR = 1.35, 95%CI[1.24–1.48]) was significantly higher than ORs of non-AD dementia or PD (OR = 0.97, 95%CI[0.90–1.04] and OR = 1.13, 95%CI[0.92–1.31]). The OR of hospital admissions was significantly increased only for AD as a primary case of hospitalization (OR = 1.54, 95%CI[1.31–1.82]). Conclusion: NC residents aged 65+ with long-term exposures to ambient PM2.5 levels exceeding the WHO standard had significantly increased risks of death and hospital admissions for AD. The effects for non-AD dementia and PD were less pronounced.

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