scholarly journals Growing evidence links air pollution exposure to risk of Alzheimer’s disease and related dementia

Brain ◽  
2019 ◽  
Vol 143 (1) ◽  
pp. 8-10
Author(s):  
Melinda C Power
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Air Pollution ◽  
Particulate Matter ◽  
Episodic Memory ◽  
Memory Decline ◽  
Air Pollution Exposure ◽  
Pollution Exposure

This scientific commentary refers to ‘Particulate matter and episodic memory decline mediated by early neuroanatomic biomarkers of Alzheimer’s disease’, by Younan et al. (doi: 10.1093/brain/awz348).

Ozone Atmospheric Pollution and Alzheimer’s Disease: From Epidemiological Facts to Molecular Mechanisms

2021 ◽  
Author(s):  
Marine L. Croze ◽  
Luc Zimmer
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Air Pollution ◽  
Atmospheric Pollution ◽  
Molecular Mechanisms ◽  
Ozone Pollution ◽  
Adverse Health Outcomes ◽  
Air Pollution Exposure ◽  
Airborne Pollutant ◽  
Pollution Exposure

Atmospheric pollution is a well-known environmental hazard, especially in developing countries where millions of people are exposed to airborne pollutant levels above safety standards. Accordingly, several epidemiological and animal studies confirmed its role in respiratory and cardiovascular pathologies and identified a strong link between ambient air pollution exposure and adverse health outcomes such as hospitalization and mortality. More recently, the potential deleterious effect of air pollution inhalation on the central nervous system was also investigated and mounting evidence supports a link between air pollution exposure and neurodegenerative pathologies, especially Alzheimer’s disease (AD). The focus of this review is to highlight the possible link between ozone air pollution exposure and AD incidence. This review’s approach will go from observational and epidemiological facts to the proposal of molecular mechanisms. First, epidemiological and postmortem human study data concerning residents of ozone-severely polluted megacities will be presented and discussed. Then, the more particular role of ozone air pollution in AD pathology will be described and evidenced by toxicological studies in rat or mouse with ozone pollution exposure only. The experimental paradigms used to reproduce in rodent the human exposure to ozone air pollution will be described. Finally, current insights into the molecular mechanisms through which ozone inhalation can affect the brain and play a role in AD development or progression will be recapitulated.

scholarly journals O4-13-04: THE ASSOCIATION BETWEEN PARTICULATE MATTER AND EPISODIC MEMORY DECLINE IS PARTIALLY MEDIATED BY EARLY NEUROANATOMIC BIOMARKERS OF ALZHEIMER'S DISEASE

2019 ◽  
Vol 15 ◽  
pp. P1271-P1272
Author(s):  
Andrew J. Petkus ◽  
Diana Younan ◽  
Keith F. Widaman ◽  
Xinhui Wang ◽  
Ramon Casanova ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Particulate Matter ◽  
Episodic Memory ◽  
Memory Decline

Air Pollution, Combustion and Friction Derived Nanoparticles, and Alzheimer’s Disease in Urban Children and Young Adults

2021 ◽  
Author(s):  
Lilian Calderón-Garcidueñas ◽  
Angélica González-Maciel ◽  
Randy J. Kulesza ◽  
Luis Oscar González-González ◽  
Rafael Reynoso-Robles ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Air Pollution ◽  
Young Adults ◽  
Particulate Matter ◽  
Mexico City ◽  
Neurofibrillary Tangle ◽  
Rapid Progression ◽  
Us Epa ◽  
Children And Young Adults

Exposures to fine particulate matter (PM2.5) and ozone (O3)≥US EPA standards are associated with Alzheimer’s disease (AD) risk. The projection of 13.8 million AD cases in the US by the year 2050 obligate us to explore early environmental exposures as contributors to AD risk and pathogenesis. Metropolitan Mexico City children and young adults have lifetime exposures to PM2.5 and O3, and AD starting in the brainstem and olfactory bulb is relentlessly progressing in the first two decades of life. Magnetite combustion and friction-derived nanoparticles reach the brain and are associated with early and progressive damage to the neurovascular unit and to brain cells. In this review: 1) we highlight the interplay environment/genetics in the AD development in young populations; 2) comment upon ApoE ε4 and the rapid progression of neurofibrillary tangle stages and higher suicide risk in youth; and 3) discuss the role of combustion-derived nanoparticles and brain damage. A key aspect of this review is to show the reader that air pollution is complex and that profiles change from city to city with common denominators across countries. We explore and compare particulate matter profiles in Mexico City, Paris, and Santiago in Chile and make the point of why we should invest in decreasing PM2.5 to at least our current US EPA standard. Multidisciplinary intervention strategies are critical for prevention or amelioration of cognitive deficits and AD progression and risk of suicide in young individuals. AD pathology evolving from childhood is threating the wellbeing of future generations.

Ozone, Particulate Matter, and Newly Diagnosed Alzheimer’s Disease: A Population-Based Cohort Study in Taiwan

2021 ◽  
Author(s):  
Chau-Ren Jung ◽  
Yu-Ting Lin ◽  
Bing-Fang Hwang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Air Pollution ◽  
Cohort Study ◽  
Particulate Matter ◽  
Proportional Hazards ◽  
Newly Diagnosed ◽  
Hazards Model

Several studies with animal research associate air pollution in Alzheimer’s disease (AD) neuropathology, but the actual impact of air pollution on the risk of AD is unknown. Here, this study investigates the association between long-term exposure to ozone (O3) and particulate matter (PM) with an aerodynamic diameter equal to or less than 2.5 μm (PM2.5), and newly diagnosed AD in Taiwan. We conducted a cohort study of 95,690 individuals’ age ≥ 65 during 2001–2010. We obtained PM10 and O3 data from Taiwan Environmental Protection Agency during 2000–2010. Since PM2.5 data is only accessible entirely after 2006, we used the mean ratio between PM2.5 and PM10 during 2006–2010 (0.57) to estimate the PM2.5 concentrations from 2000 to 2005. A Cox proportional hazards model was used to evaluate the associations between O3 and PM2.5 at baseline and changes of O3 and PM2.5 during the follow-up period and AD. The adjusted HR for AD was weakly associated with a raised concentration in O3 at baseline per increase of 9.63 ppb (adjusted HR 1.06, 95% confidence interval (CI) 1.00–1.12). Further, we estimated a 211% risk of increase of AD per increase of 10.91 ppb in O3 over the follow-up period (95% CI 2.92–3.33). We found a 138% risk of increase of AD per increase of 4.34 μg/m3 in PM2.5 over the follow-up period (95% CI 2.21–2.56). These findings suggest long-term exposure to O3 and PM2.5 above the current US EPA standards are associated with increased the risk of AD.

scholarly journals Air pollution and the development of asthma from birth until young adulthood

2020 ◽  
Vol 56 (1) ◽  
pp. 2000147 ◽  
Author(s):  
Ulrike Gehring ◽  
Alet H. Wijga ◽  
Gerard H. Koppelman ◽  
Judith M. Vonk ◽  
Henriette A. Smit ◽  
...  
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Early Adulthood ◽  
Childhood And Adolescence ◽  
Asthma Incidence ◽  
Mite Allergy ◽  
Increased Risk ◽  
Air Pollution Exposure ◽  
Pollution Exposure ◽  
The Impact

BackgroundAir pollution is associated with asthma development in children and adults, but the impact on asthma development during the transition from adolescence to adulthood is unclear. Adult studies lack historical exposures and consequently cannot assess the relevance of exposure during different periods of life. We assessed the relevance of early-life and more recent air pollution exposure for asthma development from birth until early adulthood.MethodsWe used data of 3687 participants of the prospective Dutch PIAMA (Prevention and Incidence of Asthma and Mite Allergy) birth cohort and linked asthma incidence until age 20 years to estimated concentrations of nitrogen dioxide (NO2), particulate matter with a diameter <2.5 μm (PM2.5), <10 μm (PM10), and 2.5–10 μm, and PM2.5 absorbance (“soot”) at the residential address. We assessed overall and age-specific associations with air pollution exposure with discrete time-hazard models, adjusting for potential confounders.ResultsOverall, we found higher incidence of asthma until the age of 20 years with higher exposure to all pollutants at the birth address (adjusted odds ratio (95% CI) ranging from 1.09 (1.01–1.18) for PM10 to 1.20 (1.10–1.32) for NO2) per interquartile range increase) that were rather persistent with age. Similar associations were observed with more recent exposure defined as exposure at the current home address. In two-pollutant models with particulate matter, associations with NO2 persisted.ConclusionsExposure to air pollution, especially from motorised traffic, early in life may have long-term consequences for asthma development, as it is associated with an increased risk of developing asthma through childhood and adolescence into early adulthood.

scholarly journals Air pollution interventions and respiratory health: a systematic review

2020 ◽  
Vol 24 (2) ◽  
pp. 150-164 ◽  
Author(s):  
S. Saleh ◽  
W. Shepherd ◽  
C. Jewell ◽  
N. L. Lam ◽  
J. Balmes ◽  
...  
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Respiratory Health ◽  
Grey Literature ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Potential Health ◽  
Exposure Reduction ◽  
Air Pollution Exposure ◽  
Pollution Exposure

BACKGROUND: Indoor and ambient air pollution exposure is a major risk to respiratory health worldwide, particularly in low- and middle-income countries (LMICs). Interventional trials have mainly focused on alternatives to cooking stoves, with mixed results. Beyond cooking, additional sources of particulate matter also contribute to the burden of air pollution exposure. This review explores evidence from current randomised controlled trials (RCTs) on the clinical effectiveness of interventions to reduce particulate matter in LMICs.METHODS: Twelve databases and the grey literature (e.g., Government reports and policy papers) were searched. Eligible studies were RCTs conducted in LMICs aiming to reduce particulate exposure from any source and reporting on at least one clinical respiratory outcome (respiratory symptoms, lung function or clinical diagnoses). Data from relevant studies were systematically extracted, the risk of bias assessed and narrative synthesis provided.RESULTS: Of the 14 included studies, 12 tested ‘improved' cookstoves, most using biomass, but solar and bioethanol cookers were also included. One trial used solar lamps and another was an integrated intervention incorporating behavioural and environmental components for the treatment and prevention of chronic obstructive pulmonary disease. Of the six studies reporting child pneumonia outcomes, none demonstrated significant benefit in intention-to-treat analysis. Ten studies reported respiratory symptom outcomes with some improvements seen, but self-reporting made these outcomes highly vulnerable to bias. Substantial inter-study clinical and methodological heterogeneity precluded calculation of pooled effect estimates.CONCLUSION: Evidence from the RCTs performed to date suggests that individual household-level interventions for air pollution exposure reduction have limited benefits for respiratory health. More comprehensive approaches to air pollution exposure reduction must be developed so their potential health benefits can be assessed.

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