“….we are forced to conclude that the Earth system seems to be running out of resilience, losing its biophysical capacity to buffer and dampen the pressure, stress and pollution we are exposing it to.”

– Johan Rockstrom.

Prof. Dr. Sanjeev Bagai@BagaiDr Nov 18, 2024:

Many researchers have studied role of air pollutants on cognitive function, changes in brain structure, occurrence of dementia. Alzheimer’s dementia & non-Alzheimer’s dementia.

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31 studies on effect of pollutants i.e. PM10, PM2.5, NO2, O3, BC, PAHs, BTEX, FA on the occurrence of Alzheimer’s dementia. More than 80% of the studies investigated the incidence of Alzheimer’s in > 60 years. chronic exposure to air pollutants, especially (PMs), increased number of hospitalizations due to exacerbation of neurocognitive disorders by Alzheimer’s dementia or related diseases. role of exposure to air pollutants on development of this neurological disorder. air pollution is asso with atherosclerosis, increased blood inflammatory biomarkers, oxidative stress, which increases hospitalization for several neurological diseases risk of AD was asso with exposure to PM2.5 (aHR 1.10); NO2 (1.23), increased significantly so that increase of 1 µg/m3 PM2.5 is asso with a 10% increase in risk of AD. Exposure to O3reduced this risk. positive asso between exposure to O3 and NOx and dementia hosp, (O3: HR = 1.06; per 10 µg/m3; NOx: HR = 1.01; per 20 µg/m3); exposure to NOx, NO2, PM2.5, PM10, except for O3, has signif negative relationship with AD.

Air pollution: a latent key driving force of dementia by Mahdiyeh Mohammadzadeh, Amir Hossein Khoshakhlagh & Jordan Grafman, Sept 2, 2024, BMC Public Health volume 24, Article number: 2370 (2024) Cite this article

Abstract

Many researchers have studied the role of air pollutants on cognitive function, changes in brain structure, and occurrence of dementia. Due to the wide range of studies and often contradictory results, the present systematic review was conducted to try and clarify the relationship between air pollutants and dementia. To identify studies for this review, a systematic search was conducted in Scopus, PubMed, and Web of Science databases (without historical restrictions) until May 22, 2023. The PECO statement was created to clarify the research question, and articles that did not meet the criteria of this statement were excluded. In this review, animal studies, laboratory studies, books, review articles, conference papers and letters to the editors were avoided. Also, studies focused on the effect of air pollutants on cellular and biochemical changes (without investigating dementia) were also excluded. A quality assessment was done according to the type of design of each article, using the checklist developed by the Joanna Briggs Institute (JBI). Finally, selected studies were reviewed and discussed in terms of Alzheimer’s dementia and non-Alzheimer’s dementia. We identified 14,924 articles through a systematic search in databases, and after comprehensive reviews, 53 articles were found to be eligible for inclusion in the current systematic review. The results showed that chronic exposure to higher levels of air pollutants was associated with adverse effects on cognitive abilities and the presence of dementia. Studies strongly supported the negative effects of PM_2.5 and then NO₂ on the brain and the development of neurodegenerative disorders in old age. Because the onset of brain structural changes due to dementia begins decades before the onset of disease symptoms, and that exposure to air pollution is considered a modifiable risk factor, taking preventive measures to reduce air pollution and introducing behavioral interventions to reduce people’s exposure to pollutants is advisable.

Introduction

Technological development and the rapid expansion of mechanization during the last few decades have led to an increase in life expectancy in various societies, especially in developed countries [1]. An increase in the life expectancy can lead to the growth of neurological disorders [2]. According to statistics published worldwide, neurological disorders, including Parkinson’s (PD), cognitive dysfunction, Alzheimer’s (AD) and dementia, are a leading cause of disability and death [3, 4]. Cognitive function also diminishes with age [5] and therefore, elderly people are disproportionately affected by cognitive disorders and, finally, dementia [6, 7] which imposes a significant burden on health care systems. According to statistics published by the World Health Organization (WHO), approximately 55 million people worldwide suffered from dementia in 2019, which is estimated to more than double in 2050 [8]. Dementia is the cause of 2.4 million deaths and 28.8 million disability-adjusted life years (DALYs) in 2016 and is known as the third cause of neurological DALYs [3, 9].

Various factors are involved in dementia, including anthropometric parameters (for example, body mass index), the APOE Ɛ4 allele [10], lack of weight [11], inactivity [12], non-Mediterranean diet [13], and the lack of specific micronutrients and macronutrients [14].

In addition, many epidemiological studies have shown that exposure to air pollution can also contribute to neuropathology through oxidative stress, hyperactivation of microglia, disruption of the blood–brain barrier (BBB) and neuroinflammation [15, 16] and cause adverse effects on the brain, accelerate cognitive aging and even increase the occurrence of AD and other forms of dementia [17,18,19].

The 2020 Lancet Commission on dementia prevention, intervention and care, considered air pollution as a new modifiable risk factor for dementia, accounting for about 2% of cases worldwide [20]. Studies conducted in the United Kingdom showed that an increase of 1 µg/m³ PM_2.5 (particles with a diameter of 2.5 µm or less) increases the risk of dementia by 6% and the risk of AD by 10% [21]. Mortamais et al. (2021) found that an increase of 5µg/m³ in PM_2.5 level, increases 20% the risk for all-cause dementia, 20% for AD and 33% for Vascular Dementia (VaD) in elderly people over 70 years [22].

However, the adverse effects of air pollution on cognitive function are not limited to old age. Recent epidemiological studies support the hypothesis that public exposure to air pollutants can cause structural and functional changes in children’s brains [23, 24] and by causing negative effects on neuropsychological development, make them susceptible to neurological disorders in middle and old age [25, 26].

Therefore, prevention of exposure to air pollution is a potentially correctable risk factor in the occurrence of cognitive decline and dementia in the elderly. The present systematic review was conducted to critically examine the published scientific literature related to the impact of exposure to air pollution on dementia. Specifically, the objectives were: (1) to evaluate the type and concentration of air pollutants including PM₁₀ (particles with a diameter of 10 µm or less), PM_2.5, NO₂, O₃, black carbon (BC), polycyclic aromatic hydrocarbons (PAHs), benzene, toluene, ethylbenzene and xylenes (BTEX), formaldehyde (FA) in geographic areas and (2) to assess the risk of dementia in adults with chronic respiratory exposure to the mentioned pollutants.

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Criteria of entering and extracting studies

In this review, we excluded studies focused on the effects of exposure to air pollutants on neurological and biochemical changes (without examining dementia) and studies that investigated exposure to air pollutants as a dependent variable. Animal studies, laboratory studies, books, review articles, conference papers, and letters to the editors were also excluded. In this systematic review, only original peer-reviewed articles in English were reviewed.

Finally, the following information was extracted from the selected articles:

Authors, the year of publication, study design, country, the number of sample people, the age range of people, gender, the type of pollutant, the mean concentration of pollutant, diagnosis tool, and the type of dementia.

…

Results and Discussion

Selection process and characteristics of articles

In this review, 14,924 articles were obtained through a systematic search in databases, of which 4532 studies were retrieved from PubMed, 5878 from Scopus, and 4514 from Web of Science. After entering the articles into EndNote X20 software, 6546 duplicates were removed and 8378 studies were screened for title and abstract. At this stage, 8289 articles were excluded and the entry and exit criteria and quality assessment were done for 88 full texts. Finally, after conducting additional reviews, 36 studies were excluded for the following reasons:

Nine studies were review articles, two studies only investigated brain volume, in twelve articles the type of air pollutant was not specified, five studies investigated the effect of other pollutants on dementia, five studies were excluded due to the high risk of bias and access to three full texts was not possible.

In addition, hand searching and systematic search of the selected articles’ reference lists were also conducted to identify additional studies eligible for inclusion, which led to the identification of two studies through reference checking. Therefore, the total number of studies included in this systematic review increased to 53 articles (Fig. 2).

The studies in this systematic review included 6 case–control [29,30,31,32,33,34], 7 cross-sectional [19, 35,36,37,38,39,40], and 40 cohort studies [1, 2, 18, 21, 22, 41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75]. Specifically, selected studies have been conducted in 17 countries around the world:

19 in the United States of America, 7 in Sweden, 7 in Taiwan, 4 in Canada, 3 in France, 2 in Australia, 2 in Germany, 2 in Hong Kong, 2 in Mexico, 2 in the United Kingdom, 1 in each country of Netherlands, Spain, China, Denmark, England, Italy, and the Republic of Korea.

In total, 173,698,774 subjects were contained in the studies examined in this systematic review. The characteristics of the reviewed studies are shown in Table 2.

Table 2 Characteristics of selected studies

From: Air pollution: a latent key driving force of dementia

First Author	Title	study design	Country (city)	N
Walter A. Kukull(1995) [29]	Solvent Exposure as a Risk Factor for Alzheimer’s Disease: A Case Control Study	Case–Control	USA(Seattle)	Case: 193Control: 243Total: 436
Ulrich Ranft(2009) [41]	Long-term exposure to traffic-related particulate matter impairs cognitive function in the elderly	Cohort	Germany(Ruhr)	402
Kuang-Hsi Chang(2014) [42]	Increased Risk of Dementia in Patients Exposed to Nitrogen Dioxide and Carbon Monoxide: A Population-Based Retrospective Cohort Study	Cohort	Taiwan(Taichung)	29,547
Yun-Chun Wu(2015) [30]	Association between air pollutants and dementia risk in the elderly	Case–control	Taiwan(Taipei)	Case: 374Control: 497Total: 871
Chau-Ren Jung(2015) [43]	Ozone, Particulate Matter, and Newly Diagnosed Alzheimer’s Disease: A Population-Based Cohort Study in Taiwan	Cohort	Taiwan(National)	95,690
Anna Oudin(2016) [44]	Traffic-Related Air Pollution and Dementia Incidence in Northern Sweden: A Longitudinal Study	Cohort	Sweden(Umeå)	1,806
Hong Chen(2017) [45]	Exposure to ambient air pollution and the incidence of dementia: A population-based cohort study	Cohort	Canada(Ontario)	2,066,639
Dante Roger Culqui(2017) [46]	Association between environmental factors and emergency hospital admissions due to Alzheimer’s disease in Madrid	Cohort	Spain(Madrid)	3,287
Jiu-Chiuan Chen(2017) [47]	Particulate Air Pollutants, Brain Structure, and Neurocognitive Disorders in Older Women	Cohort	USA(National)	1,403
John Andersson(2018) [48)	Road traffic noise, air pollution, and risk of dementia – results from the Betula project	Cohort	Sweden(Umeå)	1,721
Anna Oudin(2018) [49]	Association between air pollution from residential wood burning and dementia incidence in a longitudinal study in Northern Sweden	Cohort	Sweden(Umeå)	1,806
Iain M Carey(2018) [21]	Are noise and air pollution related to the incidence of dementia? A cohort study in London, England	Cohort	England(London)	130,978
Chung-Yi Li(2019) [31]	Association between air pollution and risk of vascular dementia: A multipollutant analysis in Taiwan	Case–control	Taiwan(National)	Case: 831Control: 3,324Total: 4,155
Hyewon Lee(2019) [50]	Exposure to ambient fine particles and neuropsychiatric symptoms in cognitive disorder: A repeated measure analysis from the CREDOS (Clinical Research Center for Dementia of South Korea) study	Cohort	Republic of Korea(Seoul)	645
Ruo-Ling Li(2019) [51]	Influence of PM_2.5 Exposure Level on the Association between Alzheimer’s Disease and Allergic Rhinitis: A National Population-Based Cohort Study	Cohort	Taiwan(National)	2,384
Francesco Cerza(2019) [52]	Long-term exposure to air pollution and hospitalization for dementia in the Rome longitudinal study	Cohort	Italy(Rome)	350,844
Anna Oudin(2019) [53]	Traffic-Related Air Pollution as a Risk Factor for Dementia: No Clear Modifying Effects of APOE 4 in the Betula Cohort	Cohort	Sweden(Umea)	1,567
Han-Wei Zhang(2019) [54]	Long-Term Exposure to Ambient Hydrocarbons Increases Dementia Risk in People Aged 50 Years and above in Taiwan	Cohort	Taiwan(National)	178,085
Marta Crous-Bou(2020) [1]	Impact of urban environmental exposures on cognitive performance and brain structure of healthy individuals at risk for Alzheimer’s dementia	Cohort	Spain(Barcelona)	958
Liuhua Shi(2020) [2]	Long-term effects of PM_2.5 on neurological disorders in the American Medicare population: a longitudinal cohort study	Cohort	USA(National)	63,038,019
Audrey Smargiassi(2020) [55]	Exposure to ambient air pollutants and the onset of dementia in Quebec, Canada	Cohort	Canada(Quebec)	1,807,133
Sindana D Ilango(2020) [56]	The role of cardiovascular disease in the relationship between air pollution and incident dementia: a population-based cohort study	Cohort	Canada(Ontario)	34,391
Kimberly C. Paul(2020) [57]	Traffic-Related Air Pollution and Incident Dementia: Direct and Indirect Pathways Through Metabolic Dysfunction	Cohort	USA(National)	1,564
Weiran Yuchi(2020) [32]	Road proximity, air pollution, noise, green space and neurologic disease incidence: a population-based cohort study	Case–control	Canada(Metro Vancouver)	678,000
Marion Mortamais(2021) [22]	Long-term exposure to ambient air pollution and risk of dementia: Results of the prospective Three-City Study	Cohort	France(Dijon, Bordeaux, and Montpellier)	7,066
Jiping Tan(2021) [35]	Associations of particulate matter with dementia and mild cognitive impairment in China: A multicenter cross-sectional study	Cross-sectional	China(National)	7,040
Jinjun Ran(2021) [58]	Long-term exposure to fine particulate matter and dementia incidence: A cohort study in Hong Kong	Cohort	Hong Kong	59,349
Andrew J. Petkus(2021) [36]	Associations Between Air Pollution Exposure and Empirically Derived Profiles of Cognitive Performance in Older Women	Cross-sectional	USA	2,142
Rachel M.Shaffer(2021) [59]	Fine Particulate Matte rand Dementia Incidence in the Adult Changes in Thought Study	Cohort	USA(Seattle)	4,166
Sung Han Rhew(2021) [33]	Exposure to low-dose ambient fine particulate matter PM_2.5 and Alzheimer’s disease, non-Alzheimer’s dementia, and Parkinson’s disease in North Carolina	Case–control	USA(North Carolina)	Case: 1,665,073Control: 357,574Total: 2,022,647
Diana Younan(2021) [60]	PM_2.5 Associated With Gray Matter Atrophy Reflecting Increased Alzheimer Risk in Older Women	Cohort	USA(48 states)	1,365
Maayan Yitshak-Sade(2021) [61]	PM_2.5 and Hospital Admissions Among Medicare Enrollees with Chronic Debilitating Brain Disorders	Cohort	USA(National)	30,079,287
Rachel M. Shaffer(2021) [62]	Fine Particulate Matter and Markers of Alzheimer’s Disease Neuropathology at Autopsy in a Community-Based Cohort	Cohort	USA(National)	5,546
Kevin J Sullivan(2021) [63]	Ambient Fine Particulate Matter (PM_2.5) Exposure and Incident Mild Cognitive Impairment and Dementia	Cohort	USA(National)	2,735
Hedi Katre Kriit(2021) [64]	Annual dementia incidence and monetary burden attributable to fine particulate matter (PM_2.5) exposure in Sweden	Cohort	Sweden(National)	820
Liuhua Shi(2021) [65]	A national cohort study (2000–2018) of long-term air pollution exposure and incident dementia in older adults in the United States	Cohort	USA(National)	24,689,818
Feng Cheng Lin(2021) [34]	Air Pollution Is Associated with Cognitive Deterioration of Alzheimer’s Disease	Case–control	Taiwan(Kaohsiung,Pingtung)	704
Jing Wu(2022) [66]	Air pollution as a risk factor for Cognitive Impairment no Dementia (CIND) and its progression to dementia: A longitudinal study	Cohort	Sweden(Stockholm)	1,987
Zorana J. Andersen(2022) [67]	Long-term exposure to air pollution and mortality from dementia, psychiatric disorders, and suicide in a large pooled European cohort: ELAPSE study	Cohort	Sweden, Denmark, France, Netherlands, Germany, Austria	271,720
ErinO. Semmens(2022) [37]	Air pollution and dementia in older adults in the Ginkgo Evaluation of Memory Study	Cross-sectional	USA(Winston, Hagerstown, Sacramento, Pittsburgh)	2,564
Lilian Calderón-Garcidueñas(2022) [38]	Metals, Nanoparticles, Particulate Matter, and Cognitive Decline	Cross-sectional	Mexico(Mexico City)	336
Diana Younan(2022) [68]	Racial/Ethnic Disparities in Alzheimer’s Disease Risk: Role of Exposure to Ambient Fine Particles	Cohort	USA(24 states)	6485
Fan He(2022) [69]	Impact of air pollution exposure on the risk of Alzheimer’s disease in China: A community-based cohort study	Cohort	China(Changshan, Haishu, Jingning, Tongxiang, Yuecheng, Yuhuan)	6,115
Dylan Wood(2022) [70]	Exposure to Ambient Air Pollution and the Incidence of Dementia in the Elderly of England: The ELSA Cohort	Cohort	UK(National)	8,525
Lilian Calderón-Garcidueñas(2022) [39]	Hemispheric Cortical, Cerebellar and Caudate Atrophy Associated to Cognitive Impairment in Metropolitan Mexico City Young Adults Exposed to Fine Particulate Matter Air Pollution	Cross-sectional	Mexico(Mexico City)	302
Cheng Chen(2022) [71]	B vitamin intakes modify the association between particulate air pollutants and incidence of all-cause dementia: Findings from the Women’s Health Initiative Memory Study	Cohort	USA(National)	7,183
Noémie Letellier(2022) [72]	Air quality improvement and incident dementia: Effects of observed and hypothetical reductions in air pollutant using parametric g computation	Cohort	France(Bordeaux, Dijon, andMontpellier)	7,051
Zhenjiang Li(2022) [19]	Neighborhood characteristics as confounders and effect modifiers for the association between air pollution exposure and subjective cognitive functioning	Cross-sectional	USA(Atlanta)	12,058
Kimberly L. Parra(2022) [73]	Exposure to air pollution and risk of incident dementia in the UK Biobank	Cohort	UK(National)	187,194
Michelle L. Trevenen(2022) [74]	Ambient air pollution and risk of incident dementia in older men living in a region with relatively low concentrations of pollutants: The Health in Men Study	Cohort	Australia(Perth)	11,243
Daniel Mork(2023) [18]	Time-lagged relationships between a decade of air pollution exposure and first hospitalization with Alzheimer’s disease and related dementias	Cohort	USA(National)	8,507,437
Liuhua Shi(2023) [75]	Incident dementia and long-term exposure to constituents of fine particle air pollution: A national cohort study in the United States	Cohort	USA(National)	37.7 million
Haisu Zhang(2023) [40]	Short-term associations between ambient air pollution and emergency department visits for Alzheimer’s disease and related dementias	Cross-sectional	USA(California, Missouri, North Carolina, New Jersey, and New York)	1,595,783

Diagnostic methods in the types of dementia

When we examined the 53 selected studies, 39 diagnostic tools and methods for AD and other types of dementia had been used (Appendix A2 and A3); of these, 21 diagnostic tools were used for Alzheimer’s dementia and 28 methods for non-Alzheimer’s dementia. According to the investigations carried out in studies related to Alzheimer’s dementia, the methods of medical records (N = 11) and Mini-Mental Status Examination (MMSE) (N = 8) were the most prevalent. Five studies also used medical imaging (such as MRI and CT scan) to investigate the changes made in brain structures, which indicate the onset of Alzheimer’s disease. In addition, the most common diagnostic tools for non-Alzheimer’s dementia were included medical reports (N = 4), MMSE (N = 10), Medical imaging (N = 4), Clinical Dementia Rating Sum of Box (CDR-SB) (N = 4), and the Montreal Cognitive Assessment (MoCA) (N = 3).

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In our systematic review, the main neuroimaging technique used was MRI. This tool can measure brain atrophy, especially in the mesial-temporal structures, and detect it even before appearing the first clinical symptoms [97, 98]. This method is included in both the diagnostic criteria presented by Dubois [99] and NIA-AA [100] and has been used as a reliable diagnostic tool by many researchers [101,102,103]. The sensitivity of this method as an AD marker has been reported to be more than 85% [97], which is more than PiB-PET (70%) [104] and FDG-PET (80%) [105, 106].

Atrophy in the medial temporal lobe, especially the hippocampus, and a decrease in the thickness of the cerebral cortex in vulnerable areas of AD are among the first signs detectable by MRI in the early stages of the disease [107,108,109]. This tool can show hippocampal volume reduction 2 to 3 years before the onset of dementia in asymptomatic carriers of APP mutations [110] and in elderly people up to 6 years before that [103, 107]. In addition, entorhinal cortex volume reduction, which progresses up to four years before cognitive decline, can be detected by MRI up to 90% [107].

Alzheimer’s dementia

The characteristics and results extracted from the articles related to Alzheimer’s dementia are shown in Appendix A2. Thirty-one studies investigated the effect of pollutants i.e. PM₁₀, PM_2.5, NO₂, O₃, BC, PAHs, BTEX, and FA on the occurrence of Alzheimer’s dementia. These studies were published from 1995–2023, and most were since 2018, indicating the novelty of the subject under discussion. More than 80% of the studies investigated the incidence of Alzheimer’s in people over 60 years old, but some studies included younger people, comprising Haisu Zhang (2023) [40], Lilian Calderón-Garcidueñas (2022) [38, 39], Marta Crous-Bou (2020) [1], Anna Oudin (2019 and 2016) [44, 53], and Ruo-Ling Li (2019) [51].

The results showed that chronic exposure to air pollutants, especially particulate matter (PMs), increases the number of hospitalizations due to the exacerbation of neurocognitive disorders caused by Alzheimer’s dementia or related diseases. This finding is compatible with previous studies on the role of exposure to air pollutants on the development of this neurological disorder [18, 74, 75]. Results from human and animal studies have shown that air pollution is associated with atherosclerosis, increased blood inflammatory biomarkers, and oxidative stress, which may accelerate hospitalization for several neurological diseases [111, 112]. In the United Kingdom, the results of a population-based cohort study showed that the risk of AD was associated with exposure to PM_2.5 (adjusted hazard ratio—HR 1.10, 95% CI 1.02–1.18) and NO₂ (1.23, 1.07–1.43) increases significantly so that an increase of 1 µg/m³ PM_2.5 is associated with a 10% increase in the risk of AD. Exposure to O₃ reduced this risk [21]. Also Cerza et al. (2019) in a cohort study in Italy concluded that a positive association between exposure to O₃ and NO_x and dementia hospitalizations, (O₃: HR = 1.06; 95% CI: 1.04–1.09 per 10 μg/m³; NO_x: HR = 1.01; 95% CI: 1.00–1.02 per 20 μg/m³) [52]. This study showed that exposure to NO_x, NO₂, PM_2.5, and PM₁₀, except for O₃, has a significant negative relationship with AD [52].

He et al. (2022) also demonstrated in a population-based cohort study in China that exposure to PM_2.5, PM₁₀, and CO pollutants was significantly associated with an increased risk of AD, but there is no significant relationship between exposure to NO and SO₂ with the occurrence of this disorder. This study also showed an inverse relationship between O₃ exposure and AD [69]. Meanwhile, Jung et al. (2015) concluded that for an increase of 9.63 ppb in O₃ concentration, the risk of AD increases 1.06 times in the elderly ≥ 65 years (adjusted HR 1.06, 1.00–1.12) [43]. The difference between the results of these studies can be caused by different characteristics in the study population, study design, sample size, setting, and different measurements of exposure to air pollutants.

In addition, the researchers found evidence of the adverse effect of exposure to air pollutants on episodic memory. Several animal studies showed that exposure to inhaled PM_2.5 can impair neural systems that underlie episodic memory processes [113,114,115]. So far, limited longitudinal epidemiological studies have been conducted about PM_2.5 and episodic memory in humans [116,117,118]. The results of a prospective study on 998 elderly women aged 73 to 87 years old in the US showed that chronic exposure to PM_2.5 in residential environments was associated with a rapid decline in episodic memory, especially in measures of immediate recall and learning of new material [68]. A decrease in verbal episodic memory (such as the ability to remember details, with context, from daily and distant experiences) is prominent in AD and can be detected in the preclinical stage [119, 120]. For example, impaired episodic memory is one of the main criteria for the classic diagnosis of AD by Dubois et al. (2007), which appears early in the course of the disease [99]. Studies have proven that the rapid decline of this memory is somewhat associated with an increase in the Alzheimer’s disease pattern similarity (AD-PS) score [68]. AD-PS is a brain MRI-based structural biomarker that reflects high-dimensional gray matter atrophies in brain regions vulnerable to AD neuropathology [68]. In addition to exposure to environmental factors, natural aging can also lead to a decrease in episodic memory, which is related to the decrease in the volume of the hippocampus and other structures of the medial temporal lobe [121]. The medial temporal lobe and its structural components, especially the hippocampus, play an important role in encoding (learning, recalling) and retrieving (recalling) the details of events that make up episodic memories [121].

Zhao et al. (2019) showed in a human imaging study that atrophy in hippocampal subfields can impose a wide range of effects on measures of episodic memory (immediate recalls, delayed-recalls, and recognition) [122]. Although so far the relative roles of hippocampal subfields (e.g. cornu ammonis (CA, CA2-3), CA4-denate gyrus, presubiculum, subiculum) have not been determined in the processes related to encoding and retrieval, animal studies have proven the adverse effects of PMs on the morphology and functional changes in hippocampal subfields. Also, we can mention the decrease in apical dendritic spine density and dendritic branches in the CA1 and CA3 regions [123], decrease in synaptic function in CA1 neurons [114, 124], decrease in basic protein in white matter, and increase in atrophy of neurites in the CA1 region [125]. Based on the studies, encoding is done by CA2, CA3, and dentate gyrus, while CA1 and subiculum are involved in retrieval [126]. According to the results obtained by Younan et al. (2020), it seems that the significant reduction of episodic memory processes (immediate recall/new learning) caused by exposure to PM_2.5 is more due to the adverse effects of this pollutant on hippocampal subfields associated with encoding, such as CA2, CA3, and dentate gyrus [68]. These neurotoxicological results indicate that some hippocampal subfields may be more sensitive to the adverse effects of particulate matter than other subfields.

So far, many studies have proven the existence of an inverse relationship between exposure to air pollutants and white matter volume, gray matter volume, and cerebral cortex thickness in brain areas affected by AD [127,128,129,130]. Wilker et al. (2015) showed in a study that with increasing PM_2.5 concentration, brain volume decreases by 0.32% [131], which was consistent with the results obtained by Chen et al. (2015) regarding the reduction of white matter volume and the volume of the whole brain due to exposure to high concentrations of this pollutant [128]. The results of the study by Crous-Bou et al. (2020) showed that chronic exposure to air pollutants, especially NO₂ and PM₁₀, is associated with a decrease in the thickness of the cerebral cortex in brain areas affected by AD [1], which is consistent with the results of study done by Casanova et al. (2016) [127]. In a voxel-based morphometry study, they examined the local brain structure related to PMs in elderly women and concluded that exposure to PM_2.5 has an inverse relationship with the reduction of the frontal cortex [127]. Furthermore, Cho et al. (2023) showed that a 10 µg/m³ increase in (…) NO₂ are significantly associated with decreasing MoCA score. Also, these two pollutants were significantly associated with an increase in AD-like cortical atrophy scores and a decrease in the thickness of the cerebral cortex [129].

PET ligand studies indicate that gray matter atrophy of the brain can be caused by tau neuropathological processes, which can lead to cognitive decline in patients [132,133,134]. Several plausible biological mechanisms explain the rapid development or onset of neurological diseases caused by exposure to air pollution. After inhalation, air pollutants can pass through the BBB and enter the brain through the olfactory bulb or systemic circulation [135] causing oxidative stress and systemic inflammatory responses, disruption of the blood–brain barrier, deposition of peptides beta-amyloid (Aβ) and activation of microglia and as a result may exacerbate the disease progression of AD [136, 137]. In addition, it has been reported that NO₂ is associated with inflammatory responses and markers such as increased serum concentration of systemic interleukin IL-6 [138]. Recent studies have shown that exposure to air pollutants can be effective in causing neurological and cognitive disorders by contributing to AD pathologies such as brain Aβ and tau burden [139, 140]. Researchers use the levels of Aβ, total tau (t-tau) and phospho-tau (p-tau) in CSF as specific biomarkers for the clinical diagnosis of probable AD [99]. Some studies have proven that CSF Aβ, as the first marker of AD, shows abnormal levels several years before the appearance of impaired memory [141, 142]. Diagnosis of early AD in patients with mild cognitive impairment (MCI) can be done by detecting low levels of Aβ and high levels of p-tau and t-tau in CSF [143].

Reports show that living in areas with high air pollution can lead to the accumulation of Aβ in neurons and astrocytes [144]. Also, the results obtained from the study of Fu et al. (2022) indicate that the increase in the concentration of each unit of ln-transformed Ʃ-OH PAHs in the urine of coke oven workers was associated with an increase of 9.416 units of P-Tau231 in plasma and a decrease of 0.281 in visuospatial/executive function [145]. Tau is a microtubule-associated protein that contributes to the stability of axonal microtubules in the brain [146]. The presence of hyperphosphorylated tau leads to the formation of neurofibrillary tangles, which is considered a pathological characteristic of AD [147]. Some researchers have reported changes in the concentration of phosphorylated tau as a possible sign of the progression of some neurological diseases [148, 149]. This is consistent with the results of Nie et al.’s (2013) study, which showed that benzo[a]pyrene (B[a]P) leads to tau 231 hyperphosphorylation [150].

Non-Alzheimer’s dementia

Among the 53 selected articles, 41 studies investigated the effect of air pollutants on the incidence of non-Alzheimer’s dementia (Appendix A3), which were published during the years 2014–2023. Except for the studies of Anna Oudin (2016) [44], Anna Oudin (2018) [49], Iain M Carey (2018) [21], Anna Oudin (2019) [53], Han-Wei Zhang (2019) [54], Zorana J. Andersen (2022) [67], Lilian Calderón-Garcidueñas (2022) [38, 39], and Haisu Zhang (2023) [40], the rest of the articles included people over the age of 60 years old.

Non-Alzheimer’s dementia accounts for almost half of dementia cases [151]. The most common non-Alzheimer’s neurological disorders include vascular dementia (VaD) [152, 153], Parkinson’s disease (PD) [154], Fronto-Temporal Dementia (FTD) [155] and Dementia with Lewy Bodies (DLB) [92], which are characterized by the accumulation of natural proteins in the CNS, as proteinopathies [156].

Vascular Dementia

The present study showed that exposure to air pollutants may have a direct effect on the incidence and progression of VaD. In a longitudinal study, Oudin et al. (2016) concluded that the probability of VaD diagnosis, with HR = 1.43, was higher among citizens with the highest exposure to traffic-related air pollution than those with low exposure [44]. These results were consistent with the study conducted by Cerza et al. (2019) [52]. In a longitudinal study on elderly men and women in Italy, they reported that chronic exposure to NO_x, NO₂, PM₁₀ and PM_2.5 has a positive relationship with VaD. In addition, a direct relationship between exposure to O₃ and NO_x with dementia hospitalization was also observed (O₃: HR = 1.06 per 10 μg/m³; NO_x: HR = 1.01; per 20 μg/m³) [52].

According to the studies, chronic exposure to air pollutants can cause vascular damage caused by large vessel atherosclerosis and small vessel arteriosclerosis and cause cortical and subcortical infarcts, sub-infarct ischemic lesions, and large and small cerebral hemorrhages [153, 157]. Researchers identify these factors as responsible for the initiation of VaD [153]. Moreover, dysfunction and degeneration of the neurovascular unit, which consists of a network of pericytes, myocytes, astrocytes, neurons, oligodendrocytes, endothelial cells and cerebral microvessels, aggravate the pathogenesis of VaD by disrupting the BBB [158]; which require hospital care to treat and prevent further side effects.

Also, the results obtained from a case–control study in Taiwan indicate that exposure to high levels of NO₂ significantly increases the risk of developing VaD [31]. According to the studies, some researchers showed that for an increase of 5 μg/m³ NO₂, the risk of VaD increases by 1.62 [74]. However, some studies have reached contradictory results. A cohort study conducted in England estimated the prevalence of VaD among men and women aged 50–79 years old at 29%, but found little evidence of the effect of air pollution on this neurological disorder [21]. Differences in results could be due to differences in instruments used, study design, and sample population characteristics.

VaD is a pathological condition in the elderly characterized by progressive cognitive dysfunction and is the second most common form of dementia, after AD [159]. This disorder is manifested by the loss of rationality, judgment skills, and especially cognitive functions and memory, and patients usually survive only 5–7 years after its onset [160]. Multifactorial etiopathology, diverse clinical manifestations, and numerous clinical subgroups are among the characteristics of VaD [152]. Chronic reduction in cerebral blood flow is one of the main characteristics of this neurological disorder [161], which results in the departure of brain blood vessels from regulation. This causes functional damage to capillaries, arteries and venules and damage to myelinated axons, and by creating a lesion in the white matter, it starts the pathophysiological process of VaD [162]. Small vessel disease (leukoaraiosis and lacunar infarcts), microinfarcts, microhemorrhages, cerebral amyloid angiopathy, and mixed vascular lesions are among the most important debilitating lesions of VaD [163, 164]. In addition, chronic cerebral hypoperfusion (CCH) has been reported as the main cause of this type of dementia [163, 165]. The results obtained from the studies indicate that CCH is associated with both neurodegeneration and dementia [166, 167]. Studies have shown that exposure to PMs can increase CCH-induced white matter neurotoxicity by enhancing pathophysiology [168, 169]. In a recent epidemiological study, Chen et al. (2015) showed that exposure to PM_2.5 was associated with a decrease in regional white matter volume in the corpus callosum and frontal/temporal lobes of elderly women [128], which is consistent with the results of the study by Erickson et al. (2020) was matched [170]. In addition, experimental data obtained from animal studies showed that exposure to air pollutants, especially PMs, causes changes in myelin in the CA1 area of the hippocampus in rodents [171], which can increase the risk of developing neurological disorders and types of dementia.

Dementia due to Parkinson’s disease

The results of the studies retrieved in this systematic review showed that dementia due to PD, a dementia that begins 1 year or more after well-established Parkinson’s disease [92], can be considered as one of the adverse effects of exposure to air pollutants, especially PMs. Shi et al. (2020) in a national cohort study in the USA showed that for an annual increase of 5 µg/m³ PM_2.5, the probability of the first hospital admission due to PD and other related dementias will increase by 1.13 times for the American Medicare population (HR = 1.13) [75]. In this regard, Yuchi et al. (2020) also obtained similar results [32]. In a population-based cohort study in Canada, they proved that exposure to air pollutants increases the risk of PD (HR for PMs = 1.09, HR for BC = 1.03, HR for NO₂ = 1.12), but no relationship was observed on the occurrence of AD [32]. These results were consistent with those obtained from the studies of Rhew et al. (2021) [33], Yitshak-Sade et al. (2021) [61] and Calderón-Garcidueñas et al. [39].

The studies have demonstrated that over 80% of individuals with Parkinson’s disease develop dementia [172]. Generally, the point prevalence of dementia in patients with Parkinson’s has been determined to be approximately 25%, which has a higher prevalence in men than in women [173]. Researchers have proven that the risk of dementia increased as the duration of the disease increased, so that this probability reached 50% 10 years after the diagnosis of Parkinson’s [91]. Research indicates that dementia occurs in patients who survive for more than 10 years [93].

PD, containing Lewy bodies and Lewy neurites, is one of the common brain disorders associated with aging and is characterized by the accumulation of α-synuclein in intracellular inclusions [154]. The main pathological characteristic of PD is the progressive loss of nigrostriatal dopaminergic neurons in the substantia nigra pars compacta, which causes Parkinsonism in PD patients [174]. Parkinsonism is a clinical syndrome characterized by rest tremor, rigidity, bradykinesia and gait dysfunction with postural instability [174]. Neurological disorders such as progressive supranuclear palsy (PSP), corticobasal syndrome (CBS), or FTD may overlap in their symptoms with PD [156]. Reports show that a significant number of people with PD suffer from cognitive impairment and PD dementia during their disease [172, 175]. In some cases, co-existing pathology of TDP-43 can also be detected in PD patients [176]. TDP-43 is a protein biomarker whose accumulation can diagnose and classify neurological disorders [177]. The available evidence indicates that exposure to air pollutants plays a role in the accumulation of this protein [178]. Neuropathological examination of 44 children (average age 12.89 ± 4.9 years old) and 159 young adults (average age 29.2 ± 6.8 years old) living in Mexico City showed that exposure to PM_2.5 and O₃ pollutants can cause AD and PD in 23% of people. Furthermore, it causes TDP-43 pathology in 18.7% of cases [179, 180], which is in line with the results of the present systematic review.

Fronto-Temporal Dementia

FTD is a group of neurodegenerative disorders and although clinically and pathologically heterogeneous, they mainly affect the frontal and/or temporal lobes of the brain [156, 181]. This type of dementia is usually characterized by predominant frontal or temporal atrophy, and atrophy in the fronto-polar region is considered a special symptom of FTD [182]. The main clinical manifestations of FTD include two types of behavioral variant (bvFTD) and primary progressive aphasia (PPA). BvFTD mainly leads to personality changes and behavioral problems; While PPA causes gradual deterioration in speech/language and has a lower prevalence than bvFTD [183]. Primary Parkinsonism is observed in more than 20% of patients with FTD, mostly in bvFTD patients, and then non-fluent variant primary progressive aphasia occurs [184]. Each of the mentioned stages can have an effective role in reducing people’s lives and increasing the economic burden for health systems by creating FTD.

In the current review, only two studies investigated FTD. Parra et al. (2022) concluded in a national cohort in the UK that there was a strong association between exposure to PM_2.5, NO₂, and NO_x with the incidence of AD and VaD but not with FTD [73]. Meanwhile, Calderón-Garcidueñas et al. (2022) obtained completely contradictory results in the study of neurological disorders caused by exposure to PM_2.5 in young adults living in the metropolis of Mexico City [39]. They showed that chronic exposure to PM_2.5 higher than the values recommended by US-EPA causes a significant reduction of gray matter in higher-order cortical areas, which is usually associated with AD, PD and FTD in educated Mexicans [39]. The discrepancy in the results of these two studies can be explained by the difference in the number of cases, the age range of the cases, and the country under study.

Strengths and limitations of the study

Although several review studies related to exposure to air pollutants and the incidence of dementia have been published in recent years [135, 185,186,187], the present systematic review has several notable strengths that distinguish our study from other review studies. First, this study is the most up-to-date systematic review published related to the role of chronic exposure to air pollutants on dementia (Alzheimer’s/Non-Alzheimer’s).

Second, unlike other studies, we did not impose any restrictions on publication time [135], study design [185,186,187], and geographic scope [185] in the systematic search, which allowed us to find more studies and more comprehensive results. In addition, we tried to perform a systematic search in the largest and the most reliable databases to ensure the inclusion of all eligible studies. This resulted in the extraction of 53 related studies that met the inclusion criteria for the present review. However, our investigations showed that none of the recent review articles discussed the current number of studies [135, 185,186,187].

Third, due to the inclusion of an acceptable number of articles in the present systematic review, the results obtained from examining a substantial population of subjects, 173,698,774 people, were presented, which indicates the comprehensiveness and generalizability of the results of the present study.

Fourth, our study included types of dementia, such as Alzheimer’s and non-Alzheimer’s, and related dementias. This will help researchers to understand the impact of air pollution on each type of dementia and the action mechanism of pollutants in creating structural changes in the brain.

Fifth, in this study, in addition to criterion pollutants, other common and dangerous air pollutants, including FA, BTEX, and PAHs, were also investigated; these pollutants were not investigated in any of the published reviews.

However, the lack of access to the full texts of some studies and the examination of a limited number of pollutants were among the inevitable limitations of this systematic review.

Gaps and Recommendations

An in-depth review of published studies indicates the existence of some gaps in this important health field, including the lack of sufficient studies related to the role of air pollutants on FTD. As mentioned earlier, we could find only two studies related to the effect of exposure to PM_2.5, PM₁₀, NO₂, and NO_x on FTD [39, 73], which makes it impossible to compare the results with each other. Therefore, it is recommended that more researchers investigate the impact of exposure to different pollutants in diverse populations on FTD, to cover this important gap.

Moreover, the presence of various confounding factors can also be effective in achieving contradictory results in studies. Researchers believe that factors such as aging, early retirement, smoking, body mass index (BMI), alcohol consumption, and physical inactivity are among the confounding factors that can accelerate the process of dementia [66].

Also, studies have proven that co-morbidities, such as cardiovascular diseases, cerebrovascular disease, diabetes and mental health, environmental tobacco smoke (ETS), chronic exposure to noiseFrac’ing not only invades communities with toxic air and intentionally contaminates drinking water, it abuses humans and other species with extreme levels of relentless noise 24/7, with no escape resulting in disrupted sleep, stress eating and other harmful coping behaviours. Encana’s years of frac noises drove song birds away from my property and disrupted my dogs so much they often paced instead of slept and when let out raced towards the company’s non compliant compressors barking – a behaviour they did not engage in pre-frac’ing, insufficient sleep, and unhealthy diet can also play an effective role in occurring or developing dementia at an older age [188].

Research has identified several potential socioeconomic factors that can influence the relationship between air pollution exposure and neurological outcomes at the individual and regional levels. Based on this, living in deprived neighborhoods and on the outskirts of cities increases the possibility of exposure to high levels of air pollution [189]. Studies have also shown that lower levels of education, and poor access to socioeconomic benefits, such as health care, are associated with an increased risk of dementia in the future [190, 191]. Therefore, it is necessary to consider strategies to control the impact of confounding factors to achieve more accurate results.

Also, due to the limited number of studies related to occupational exposure to pollutants in dementia, it is recommended to conduct more research to investigate occupational exposure in workers of different occupations and compare and analyze their results.

Since it has been proven that prenatal exposure is effective in the occurrence of some diseases in the future; therefore, it is recommended that cohort studies be designed and implemented to investigate the role of prenatal exposure to air pollutants and dementia at older ages.

Conclusion

The results of this systematic review showed that chronic exposure to air pollutants, especially PM_2.5 and NO₂, could have a potential role in the development and progression of AD and non-Alzheimer’s dementia in old age. The review of selected studies indicates that the relationship between exposure to PM_2.5 and then NO₂ and O₃ and suffering from dementia has been the focus of researchers in the last 5 years. No study was found that investigated the effect of FA on dementia and met the inclusion criteria for this study. In addition, BTEX and PAHs have been neglected by researchers, which is surprising due to the widespread presence of these pollutants in the environment and industries. Therefore, conducting more studies on the impact of other air pollutants, including FA, BTEX and PAHs, on the incidence of dementia and cognitive disorders is highly recommended. We believe that the identification and prevention of modifiable risk factors, such as exposure to toxic air in conjunction with behavioral interventions, can help prevent or delay the progression of neurodegenerative disorders and significantly reduce the burden of those disorders on society.

***

Humans projected to be functionally extinct by 2045 (and not from climate): “Falling human fertility can’t be reversed by cheerleading for motherhood… [this] cannot overcome the relentless chemical assault on human fertility.” Don’t just collapse, #JustCollapse.www.resilience.org/stories/2024…
— Just Collapse (@justcollapse.bsky.social) 2024-11-19T07:02:39.495Z

@justcollapse.bsky.social‬:

Humans projected to be functionally extinct by 2045 (and not from climate): “Falling human fertility can’t be reversed by cheerleading for motherhood… [this] cannot overcome the relentless chemical assault on human fertility.”

Don’t just collapse, JustCollapse.

Falling human fertility can’t be reversed by cheerleading for motherhood

Refer also to:

2024: EPA’s 2023 emissions data: Oil & gas pollution keeps rising as other economic sectors decarbonize.

2024: New study: Air pollution, namely nitrogen dioxide (NO2 – from tailpipes, gas stoves, drilling, frac’ing, flaring, production, compressors, gas plants, etc.), linked to uterine cancer. LNG means more toxic frac’ing, more cancers, more deaths.

2024: Global warming: Human pollution caused temperature extremes linked to brain damage in kids (before they’re even born).

2024: New research: Fossil fuel pollution irreversibly harms kids’ brains, including causing cancer. Imagine babies born into and growing up in bitumen, H2S and or frac fields (rampant in Alberta) where crews spew clouds of diesel fumes and facilities blast out mystery chemicals 24/7 for years on end as they frac and refrac and refrac. No wonder Albertans vote so stupidly.

Dr. Robert Howarth @howarth_cornell:

And most air pollution comes from burning fossil fuels.

Above photos in Alberta frac fields.

The last one is spewing brain-eating pollution just NW of Calgary.

Above photos in NEBC frac fields, all near homes and farms.

Much of the deadly pollution belongs to Encana/Ovintiv.

2023 05 15: Rapid response to: Air pollution is the largest environmental risk to public health and children are especially vulnerable BMJ 2023; 381 doi: https://doi.org/10.1136/bmj.p1037 (Published 15 May 2023) Cite this as: BMJ 2023;381:p1037

Rapid Response:

Re: Air pollution is the largest environmental risk to public health and children are especially vulnerable

Dear Editor

The Royal College of Physicians of Edinburgh, Air Pollution Working group, read with interest Dr Camilla Kingdon’s article entitled ‘Air pollution is the largest environmental risk to public health and children are especially vulnerable’ [1]. This resonates with this Working Group. Our children are our future, but yet we do not know if they are protected against transport emissions when at school.

Scotland has some of the cleanest air globally, and some of the more stringent air quality objectives in Europe (2) striving to limit annual average levels of nitrogen dioxide (NO2) to below 40 µg/m3, particulate matter 10 (PM10, having a diameter of less than 10 µm or less) to 18 µg/m3, and PM2.5 (diameter of less than 2.5 µm or less) to 10 µg/m3.

Achieving levels below these targets is key to maximise health gains. Areas of significant transport-derived air pollution still exist around our city streets. Furthermore, harmful effects of air pollution are seen below the target Scottish levels, leading the World Health Organisation to recommended far more stringent air quality guidelines (WHO Global Air Quality Guidelines 2021) [3].

Children are among the most susceptible to air pollution (1,4). Gestation, infancy, and early childhood are vulnerable times because the young body is developing rapidly and has immature immune systems. Children spend a higher proportion of time outdoors and are therefore at greater risk of exposure to ambient air pollutants. There is a correlation between areas of high deprivation and poor air quality in both children (5) and adults, exacerbating prexisting health inequalities.

Not infrequently, schools are sited near sour oil and gas wells/facilities and incessantly repetitive frac jobs busy roads and traffic junctions, and air quality is worsened by the ‘school run’ and idling engines (6). It is essential our schoolchildren are protected from air pollution in playgrounds and on the roads surrounding the school, with considerable health and other benefits to be gained, including educational attainment.

In schoolchildren, we know that the brain (7, 8, 9), lung (10, 11) heart (12, 13), hormone systems and immunity can all be harmed by air pollution. On days where air pollution was above guideline levels, hospital admissions for children rose significantly in Tayside, Scotland, with around 1000 excess admissions on high pollution days per year (14).

Because of the serious and long-term effects of air pollution on children, The Royal College of Physicians of Edinburgh’s Working Group on Air Pollution determined to evaluate air quality around Scottish Schools. We sought published data on air pollution from the Scottish Government and local Council published levels of air pollution in Edinburgh, Glasgow, Aberdeen, Dundee, and Perth. We were surprised to discover that very few schools were near enough to a networked air quality monitor to provide accurate local readings. We were thus unable to draw any conclusions about the safety of our school children at school in Scottish Cities, many are on busy city streets.

It is imperative to establish these levels as often the introduction of small changes in traffic movement round schools can effect improvement in air pollution and thus health (15. 16, 17). Targeted ‘greening’ can reduce playground pollution levels (18. 19) and within classrooms, air purifiers can be used to reduce particles where levels are persistently high (20, 21).

In conclusion, there is overwhelming evidence that air pollution harms the health of school children. What is missing in the UK is data on air pollutant levels at near-school areas and whether pollutants are present at levels above those recommended. As mitigation can produce significant health benefits, we recommend, and are campaigning for, the introduction of air quality monitors round all city schools as a matter of priority.But, data is unwanted by our corrupt politicians owned by polluters especially those in Alberta, BC, SK and Ontario. If brain-damaging contamination is monitored around schools, hospitals and senior facilities, companies might be required to mitigate their deadly fumes which would render frac’ing econmically impossible, or worse, prohibited entirely from engaging in their poisoning activities.

2016: Map of more than 700 Andadarko now Fleur de Lis energy wells around Midwest School in Salt Creek Field, Wyoming. There are many more wells now.

2013: Map of NEBC showing sour gas wells surrounding schools leaving kids learning in life-threatening danger and breathing brain-damaging air. There are many more wells now.

References:
1. Kingdon C. Air pollution is the largest environmental risk to public health and children are especially vulnerable. BMJ 2023;381;1037
2. Air Quality Standards and Objectives. Air Quality in Scotland. [Internet]. [cited March 2023].
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6. Ryan PH, Reponen T, Simmons M, Yermakov M, Sharkey K, Garland-Porter D, et al. The impact of an anti-idling campaign on outdoor air quality at four urban schools. Environmental Science: Processes & Impacts. 2013;15(11):2030-7.
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13. Calderón-Garcidueñas L, Vincent R, Mora-Tiscareño A, Franco-Lira M, Henríquez-Roldán C, Barragán-Mejía G, et al. Elevated plasma endothelin-1 and pulmonary arterial pressure in children exposed to air pollution. Environmental health perspectives. 2007;115(8):1248-53.
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20. Kumar P, Rawat N, Tiwari A. Micro-characteristics of a naturally ventilated classroom air quality under varying air purifier placements. Environmental Research. 2023;217:114849.
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