No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
The Relationship Between Air Pollution and Cognitive Functions in Children and Adolescents: A Systematic Review
Abstract
Air pollution has a negative impact on one’s health and on the central nervous system. We decided to assess studies that evaluated the relationship between air pollution and cognitive functions in children and adolescents by reviewing studies that had been published between January 2009 and May 2019. We searched three major databases for original works (26 studies) and for studies using brain imaging methods based on MRI (six studies). Adverse effects of air pollutants on selected cognitive or psychomotor functions were found in all of the studies. Exposure to nitrogen dioxide, for example, was linked to impaired working memory, general cognitive functions, and psychomotor functions; particulate matter 2.5 was linked to difficulties in working memory, short-term memory, attention, processing speed, and fine motor function; black carbon was linked to poor verbal intelligence, nonverbal intelligence, and working memory; airborne copper was linked to impaired attentiveness and fine motor skills; isophorone was linked to lower mathematical skills; and polycyclic aromatic hydrocarbons in fetal life were linked to lower intelligence scores. The studies using MRI showed that high concentrations of air pollutants were linked to changes in the brain’s white matter or lower functional integration and segregation in children’s brain networks. In view of the global increase in air pollution, there is a need for further research to elucidate the relationship between air pollution and cognitive and motor development in children. According to some studies, neuroinflammation, the e4 allele of the apolipoprotein E gene, and gutathione-S-transferase gene polymorphism processes may play a role.
... PM 2.5 and road noise share similar sources, primarily motorised vehicles, while the amount of vegetation in an area (greenness) can mitigate exposure to such harmful pollutants [5,6]. Evidence suggests that some vulnerable groups, importantly children, may experience cognitive changes to the developing brain as a result of prolonged exposure to PM 2.5 , greenness, and road noise [7][8][9]. Most research in the area has considered the effects of a single environmental exposure on age-appropriate cognitive tests or educational attainment outcomes at a specified time-point during childhood or adolescence [7]. ...
... Evidence suggests that some vulnerable groups, importantly children, may experience cognitive changes to the developing brain as a result of prolonged exposure to PM 2.5 , greenness, and road noise [7][8][9]. Most research in the area has considered the effects of a single environmental exposure on age-appropriate cognitive tests or educational attainment outcomes at a specified time-point during childhood or adolescence [7]. Nevertheless, some studies recognise the importance of examining the effects of multiple exposures due to their interrelated nature and investigate diverse cognitive outcomes throughout development in order to explore nuances in the associations [2,3,10]. ...
... Although some research has quantified the relationships between major environmental factors and children's cognition, it remains an emerging research area. The evidence base lacks longitudinal studies that examine a range of cognitive assessments throughout development alongside a comprehensive set of relevant individual-, family-, school-, and area-level covariates [7,10]. The present study investigates the associations between PM 2.5 and children's cognitive performance from ages 3 to 17 years, while considering greenness and road noise, in England, in the Millennium Cohort Study (MCS). ...
Research to date suggests that air pollution may affect children’s cognitive development. This study followed 12,159 children in the Millennium Cohort Study in England for 17 years to assess the impacts of lifetime PM2.5 exposure at home and school on cognitive performance while accounting for the inter-related environmental factors of greenness and road noise. Lifetime environmental exposures were measured at home from age 9 months and at school from age 5 years. The relationships between PM2.5 and cognitive test performance at ages 3, 5, 7, 11, 14 and 17 years were investigated using multivariable linear regression models accounting for survey design and controlling for greenness, road noise, and other individual, family, school, and areal characteristics. The results suggest little evidence of observable associations between PM2.5 and cognitive performance in England, with or without adjustment for greenness and road noise, at any age in the study population. These findings also apply to greenness and road noise. This is the first study to quantify the relationship between air pollution, greenspace, noise, and children’s cognitive performance in a longitudinal cohort study in England.
... A systematic review of 32 studies from in utero to 18 years consistently showed small adverse effects of air pollutants on cognitive functions (e.g., working memory, general cognitive functions, attention and intelligence) (Lopuszanska and Samardakiewicz, 2020). However, high heterogeneity across cognitive measures prevented a meta-analysis. ...
... However, high heterogeneity across cognitive measures prevented a meta-analysis. Studies were also typically based on convenience or small samples, in high-pollution settings, and typically neglected exposure during the first 1000 days of lifea critical period of development (Lopuszanska and Samardakiewicz, 2020). Of the 32 studies, none of them considered the role of greenness. ...
... Moreover, we extend findings to a relatively low-pollution setting globally, suggesting that detrimental effects could occur at air pollution thresholds that until recently have been considered safe. Our large national population-based sample is more generalisable than previous studies that often used small or convenience samples (Lopuszanska and Samardakiewicz, 2020). ...
Unlabelled:
Exposure to ambient air pollution has been associated with reduced cognitive function in childhood and later life, with too few mid-life studies to draw conclusions. In contrast, residential greenness has been associated with enhanced cognitive function throughout the lifecourse. Here we examine the extent to which (Ritchie and Roser, 2019) ambient air pollution and residential greenness predict later cognitive function in adolescence and mid-life, and (Schraufnagel et al., 2019) greenness modifies air pollution-cognitive function associations.
Participants:
6220 adolescents (51% male) and 2623 mid-life adults (96% mothers) from the Longitudinal Study of Australian Children.
Measures:
Exposures: Annual average particulate matter <2.5 μm (PM2.5), nitrogen dioxide (NO2) and greenness (Normalised Difference Vegetation Index) for residential addresses from validated land-use regression models over a 10-13-year period.
Outcomes:
Cognitive function from CogState tests of attention, working memory and executive function, dichotomised into poorer (worst quartile) versus not poor.
Analyses:
Adjusted mixed-effects generalised linear models with residential greenness assessed as an effect modifier (high vs. low divided at median). The annual mean for PM2.5 and NO2 across exposure windows was 6.3-6.8 μg/m3, and 5.5-7.1 ppb, respectively. For adolescents, an IQR increment of NO2 was associated with 19-24% increased odds of having poorer executive function across all time windows, while associations weren't observed between air pollution and other outcomes. For adults, high NO2 predicted poorer cognitive function across all outcomes, while high PM2.5 predicted poorer attention only. There was little evidence of associations between greenness and cognitive function in adjusted models for both generations. Interactions were found between residential greenness, air pollutants and cognitive function in adolescents, but not adults. The magnitude of effects was similar across generations and exposure windows. Findings highlight the potential benefits of cognitive health associated with the regulation of air pollution and urban planning strategies for increasing green spaces and vegetation.
... Early childhood (birth to age five) and childhood (age [6][7][8][9][10][11][12] periods are critical for identifying and responding to developmental vulnerabilities and laying the foundation for later life health outcomes. Establishing and maintaining recommended levels of 24-h movement behaviours (physical activity, sedentary behaviour, and sleep) are important for optimising children's health and development. ...
... Recent systematic reviews have reported associations between air pollution and children's executive function and cognitive development [11,12]. However, few studies have considered the association between different types of pollution and children's motor development outcomes. ...
Background: Little is known about how exposure to different types of pollution is associated with motor development in children or how pollution may be related to time spent in physical activity, sedentary behaviour—including screen time, and sleep. The purpose of this study was to review the evidence on these associations, especially in light of the World Health Organization (WHO) Guidelines for these behaviours.
Methods: We searched eight electronic databases: CINAHL, Embase, ERIC, Global Health, MEDLINE, PsycINFO, Scopus, and Web of Science, from inception to May 2023. Studies that reported an association between a pollution measure (air, water, noise, or land) and at least one movement behaviour (physical activity, sleep, or sedentary time) or motor development outcome (fine or gross motor) among apparently healthy children from birth to 12 years were included. Eligibility of the studies was assessed, and extracted data was based on the study design, sample characteristics, pollution type, and type of association reported.
Results: The search returned 5358 studies, of which 18 were eligible for inclusion. Most studies were conducted in high-income countries (n=13). Studies reported measures of outdoor air (n=7), indoor air (n=4), land (n=3), and noise pollution (n=4). Findings from the review were mixed and inconsistent. Most studies reported associations between a pollution measure and motor development outcomes (n=12), followed by sleep (n=5) and physical activity and sedentary behaviour (n=1).
Conclusions: There is limited evidence regarding associations between pollution measures, 24-h movement behaviours, and motor development. Future research should pay more attention to postnatal exposure to different types of pollution and its impact on healthy levels of physical activity, sedentary behaviour, sleep, and motor development and consider confounders such as geographic location, weather conditions, and country income level.
Trial Registration: PROSPERO: CRD42022340130.
... Currently, over 100 million people in the United States live in areas with unhealthy levels of ozone (Pye, Appel, Seltzer, Ward-Caviness, & Murphy, 2022); among them, racial/ethnic minorities and lower-income groups are disproportionately affected (Jbaily et al., 2022). Ozone exposure is associated with not only physical health problems and a high mortality burden (Sun et al., 2024;Wang et al., 2025), but also neurodevelopment (Cory-Slechta, Merrill, & Sobolewski, 2023;Herting, Bottenhorn, & Cotter, 2024;Volk et al., 2021), mental health disorders (Zundel et al., 2022), and declined cognitive performance (Lopuszanska & Samardakiewicz, 2020). Psychotic-like experiences (PLEs) are among the earliest signs of psychotic disorders and are relatively common in children. ...
Background
Humans are inevitably exposed to multiple physical and social environmental risk factors, potentially contributing to psychiatric problems and cognitive deficits; however, the combined effects of prenatal air pollution and psychosocial environments on youth remain unclear. This longitudinal study aimed to examine how prenatal ozone exposure interacts with psychosocial environments at 9–10 years to affect adolescent limbic system development, cognition, and psychotic‐like experiences (PLEs) at 11–13 years.
Methods
We analyzed data from 6,778 participants in the Adolescent Brain Cognitive Development (ABCD) Study® at two time points (baseline: 9–10 years and 2‐year follow‐up). Prenatal ozone exposure was calculated as a 9‐month average of daily exposure estimates based on birth year and address. Social environmental factors included school environment and neighborhood safety at both time points. Structural MRI measures included bilateral amygdala and hippocampus volumes at both time points. Behavioral data consisted of cognition and PLEs scores at both time points. Moderation and moderated mediation models with cluster‐robust standard errors were constructed to examine the effects, controlling for covariates.
Results
Children who were prenatally exposed to greater ozone and had a more unfavorable school environment exhibited a smaller increase in left hippocampal volume, leading to poorer cognition and more PLEs. Moreover, children who were prenatally exposed to greater ozone and lived in a more unsafe neighborhood had a larger increase in right amygdala volume.
Conclusions
This longitudinal study is the first to demonstrate the combined effects of prenatal ozone pollutant and adverse social environments in childhood on youth psychotic‐like experiences and cognition, highlighting the limbic system as an important neural mechanism underlying the effects.
... On the other hand, the impact effect on cognition could be attributed to the combination of other ambiental factors such as air pollution (e.g., particulate matter, carbon monoxide (CO), nitrogen dioxide) in urban environments, creating a "double burden" of environmental stressors that may independently or synergistically impair cognitive development through mechanisms such as neuroinflammation, oxidative stress, and blood-brain barrier disruption [41,42]. Moreover, socioeconomic disparities, including parental education, socioeconomic status (SES), and home environment quality, significantly moderate the neurocognitive impacts of noise exposure. ...
Environmental noise has been repeatedly linked to negative effects on cognitive functioning among children and adolescents. This research sought to systematically assess studies investigating the relationship between noise exposure and cognitive outcomes in young individuals. Through a meta-analysis of eight primary studies published between 2001 and 2023, this study examined the effects of various noise types on cognitive performance across multiple domains in young populations. The findings reveal that noise exposure significantly impairs cognitive performance in children and adolescents, with a standardized mean difference (SMD) of –0.544 (95% CI: [−0.616, −0.472]), z = −14.85, p < 0.0001. These results underscore the profound impact of environmental noise on cognitive functioning in younger populations.
... Akibatnya, anak-anak yang terpapar polusi udara berisiko mengalami penurunan kemampuan memori, kontrol impuls, dan masalah perilaku lainnya (Ha, 2021). Selain penurunan fungsi kognitif,polusi udara juga dapat meningkatkan resiko penyakit Alzheimer, Parkinson, dan ADHD (Lopuszanska & Samardakiewicz, 2020a). Paparan polutan seperti PM2.5 dan NO2 menyebabkan penurunan fungsi memori, keterlambatan kognitif pada anak, serta perubahan struktur otak. ...
Tingginya tingkat polusi udara di Desa Laut Dendang yang berdampak negatif terhadap kesehatan masyarakat, khususnya pada anak-anak dan lansia. Polusi udara yang terus meningkat memengaruhi kualitas pernapasan dan dapat menyebabkan berbagai masalah kesehatan, terutama gangguan pernapasan kronis. Dalam upaya mengatasi masalah ini, penerapan teknologi filter udara menjadi solusi yang relevan untuk mengurangi tingkat polusi dan meningkatkan kualitas udara di daerah tersebut. Tujuan kegiatan ini adalah untuk menerapkan teknologi filter udara yang efektif dalam mengurangi polusi udara di Desa Laut Dendang, serta meningkatkan kesadaran masyarakat mengenai pentingnya kualitas udara untuk kesehatan. Metode yang digunakan dalam kegiatan ini adalah pelatihan pembuatan filter udara kepada 9 orang kepala dusun dan pegawai kantor Desa Laut Dendang. Hasil yang didapatkan bahwa kepala dusun mahir dan terampil membuat alat filter udara yang diharapkan nantinya kepala dusun tersebut dapat mengajarkan kepada warganya untuk dapat membuat sendiri alat filter udara dan dapat digunakan di rumah masing-masing sehingga kualitas udara menjadi baik yang berpengaruh terhadap kesehatan dan menurunkan angka kejadian gangguan pernapasan.
... As environmental temperature, relative humidity, and air pollution have all been shown to have varying effects on cognition, [25][26][27] and are also known to be correlated with pollen concentration, these data were collected from the Basel-Binningen monitoring station and adjusted for as potential time-varying environmental confounders. ...
Background
Prior research suggests pollen allergies may be associated with cognitive function, although the effect sizes and specific cognitive outcomes varied across studies. With pollen seasons starting earlier and intensifying due to climate change, understanding the effects of pollen exposure on cognition is increasingly relevant. This study investigated the relationship between ambient pollen exposure and cognitive performance in Swiss adults.
Methods
Four cognitive assessments were used to measure the daily performance of 392 participants (299 with pollen allergies) over a 10-day period during pollen season. We used generalized additive mixed models to assess the exposure-response relationship between individualized pollen exposure and cognitive performance, as well as allergic symptom severity and cognitive performance, adjusting for individual characteristics and time-varying environmental and individual confounders (e.g., air pollution, weather, and coffee intake).
Results
We did not find any statistically significant relationships between pollen exposure or severity of allergic symptoms and overall score or reaction time on tests of response inhibition, attention, and visual-spatial memory. We observed a 1% increase [95% confidence interval (CI) = 0.13%, 2.0%] in average reaction time on a test of grammatical reasoning for allergic participants at an exposure of 300 pollen/m ³ (12-hour average).
Conclusion
Overall, our study population did not exhibit changes in cognitive performance related to pollen exposure or perceived allergic symptoms. A marginal, but statistically significant effect on the response time of pollen-allergic individuals was observed for a test of verbal reasoning, however, this is likely to be a chance finding considering the number of exposures and outcomes evaluated.
... No encontramos evidencia de impactos amplios o severos; sin embargo, los niños cuyas familias se vieron dañadas de modo desproporcionado por el Covid 19 pueden necesitar apoyo específico en la escuela y en el hogar para evitar que aumenten las diferencias educativas y de salud antes de la pandemia (Silva de Paula & Navas, 2018). Así mismo, se adiciona un factor más que afectan los procesos cognitivos en el ser humano, estos mencionan que la exposición al dióxido de nitrógeno, por ejemplo, se relacionó con problemas de memoria de trabajo, funciones cognitivas generales y funciones psicomotoras; el material particulado 2,5 se vinculó con problemas en la atención, memoria de trabajo, pensamiento, motricidad fina y velocidad de procesamiento; el carbón se relacionó con la memoria de trabajo, inteligencia verbal y no verbal deficientes; el cobre en el aire se vinculó con problemas de atención y habilidades motoras finas (Lopuszanska & Samardakiewicz, 2020). ...
La investigación bibliométrica analiza la literatura científica sobre atención y concentración en niños preescolares entre 2018 y junio de 2023. Utilizando operadores booleanos y el diagrama Prisma, se seleccionaron 22 artículos de bases de datos como Scopus, BASE, IEEE Xplore, entre otras. Estados Unidos lidera en publicaciones, seguido por Chile, China, Brasil y Turquía. El año con más publicaciones fue 2020. Se destaca la importancia de actividades que mejoran la fatiga atencional y rapidez mental, abogando por estrategias de estudio y descanso efectivas en entornos escolares y laborales. La investigación subraya la relevancia de la etapa preescolar para el desarrollo cognitivo, resaltando la importancia de actividades físicas y lúdicas para estimular la atención, concentración, resolución de problemas y regulación emocional en los niños. En resumen, el desarrollo de habilidades cognitivas está intrínsecamente ligado al fortalecimiento de la atención y la concentración en la infancia
... The neurotoxic effects of these pollutants become very crucial for the progression of neurological diseases. Similar results have also discovered by the research study of Lopuszanska and Samardakiewicz, 2020. On the same note, the study has revealed that the percentage of risk that is associated with the development of ADHD, Autism has been found to increase due to impacts of environmental pollutants. ...
The development of neurological disorders such as Parkinson’s disease, Alzheimer’s disease, ADHD, Autism become and the presence of environmental pollutants. In this particular study, the impact of neurotoxicity of the environmental pollutants on a child’s brain development are described. This study includes the formation of a literature review which was used for gathering concepts regarding the environmental pollutants, their relationship with neurological disorders, and the cognitive development of children. The method of this research holds the use of secondary data. The results have shown that high levels of pollution exposure ultimately decreases the cognitive characteristics of a child.
... Finally, we were unable to include some other air pollutants such as polycyclic aromatic hydrocarbons, black carbon and O 3 , which have been found particularly harmful to neurodevelopment in children. 56 Although we have accounted for most of the important confounders in this study, unfortunately, we did not collect information on the feeding patterns of infants. This may undermine the validity and reliability of our findings. ...
Objectives
To investigate the associations of traffic-related air pollution exposures in early pregnancy with birth outcomes and infant neurocognitive development.
Design
Cohort study.
Setting
Eligible women attended six visits in the maternity clinics of two centres, the First Affiliated Hospital of Chongqing Medical University and Chongqing Health Centre for Women and Children.
Participants
Women who were between 20 and 40 years of age and were at 11–14 weeks gestation with a singleton pregnancy were eligible for participation. Women were excluded if they had a history of premature delivery before 32 weeks of gestation, maternal milk allergy or aversion or severe lactose intolerance. 1273 pregnant women enrolled in 2015–2016 and 1174 live births were included in this analysis.
Exposures
Air pollution concentrations at their home addresses, including particulate matter with diameter ≤2.5 µm (PM2.5) and nitrogen dioxide (NO2), during pre-conception and each trimester period were estimated using land-use regression models.
Outcome measures
Birth outcomes (ie, birth weight, birth length, preterm birth, low birth weight, large for gestational age and small for gestational age (SGA) status) and neurodevelopment outcomes measured by the Chinese version of Bayley Scales of Infant Development.
Results
An association between SGA and per-IQR increases in NO2 was found in the first trimester (OR: 1.57, 95% CI: 1.06 to 2.32) and during the whole pregnancy (OR: 1.33, 99% CI: 1.01 to 1.75). Both PM2.5 and NO2 exposure in the 90 days prior to conception were associated with lower Psychomotor Development Index scores (β: −6.15, 95% CI: −8.84 to –3.46; β: −2.83, 95% CI: −4.27 to –1.39, respectively). Increased NO2 exposure was associated with an increased risk of psychomotor development delay during different trimesters of pregnancy.
Conclusions
Increased exposures to NO2 during pregnancy were associated with increased risks of SGA and psychomotor development delay, while increased exposures to both PM2.5 and NO2 pre-conception were associated with adverse psychomotor development outcomes at 12 months of age.
Trial registration number
ChiCTR-IOR-16007700
... Jadi menangkap bola bisa diawali dengan bola kain atau bola plastik, pantulannya lebih sedikit dan baru setelah anak sudah menguasai dalam menangkap benda tersebut barulah anak dapat dilatih menangkap bola dengan ukuran yang berbeda-beda (Disorder et al., 2015;Kakebeeke et al., 2018;Rivilis et al., 2011;Wang et al., 2022). Perkembangan motorik kasar anak akan optimal apabila lingkungan tumbuh kembang anak memungkinkan anak untuk bergerak bebas (Binter et al., 2022;Houwen et al., 2021;Lopuszanska & Samardakiewicz, 2020). Motorik anak dapat berkembang dengan baik dan sempurna namun perlu dilakukan stimulasi yang terarah dan terpadu salah satunya dalam bentuk permainan (Dapp et al., 2021;Haugen & Johansen, 2018;Houwen et al., 2021;Park et al., 2023;Poole et al., 2018). ...
Aktif secara fisik memainkan peran dalam perkembangan fisik anak. Meskipun ada banyak bukti hubungan positif antara aktivitas fisik dan keterampilan motorik pada anak. Bagaimana aktivitas fisik yang seharusnya dilaksanakan untuk meningkatkan perkembangan keterampilan motorik kasar secara optimal masih kurang jelas. Penelitian ini bertujuan untuk melihat efektivitas permainan lempar tangkap bola kecil terhadap perkembangan motorik kasar anak prasekolah. Desain penelitian pre eksperimen dengan the one group pre test-post test, sampel penelitian anak prasekolah usia 4-6 tahun. Pengumpulan data dilakukan melalui observasi dan uji coba dengan analisis data menggunakan statistik deskriptif dan inferensial. Hasil penelitian menujukan, terdapat peningkatan perkembangan keterampilan motorik kasar antara sebelum dan sesudah diberikan perlakuan. Kesimpulannya, pemberian permainan lempar tangkap bola kecil secara rutin melalui pembelajaran memberikan pengaruh terhadap perkembangan motorik kasar anak prasekolah. Hasil penelitian ini menambah pengetahuan guru dan orang tua murid akan pentingnya permainan lempar tangkap bola kecil terhadap peningkatan kemampuan motorik kasar anak prasekolah.
... It is plausible that toxic air contributes to age-related disorders through first influencing development and health in childhood. Early life air pollution exposure has been associated with change in BMI (Kim et al., 2018), lung development (Bettiol et al., 2021;Hsu et al., 2023;Yu et al., 2023), and brain development and cognition (Lubczyńska et al., 2021;Lopuszanska and Samardakiewicz, 2020), as well as cardiometabolic health (Johnson et al., 2021) in childhood; key determinants for later life health and longevity (e.g. (Calvin et al., 2011)). ...
... Lopuszanska et al 23 reported that air pollution hurts the central nervous system, and exposure to NO 2 was related to impaired working memory, general cognitive functions, and psychomotor functions. Moreover, PM2.5 was linked with working memory problems, short-term memory, attention, processing speed, and fine motor function. ...
Objective:
Environmental pollution is an emerging global public health problem across the world and causes serious threats to ecosystems, human health, and the planet. This study is designed to explore the impact of environmental pollution particulate matter PM2.5, PM10, carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3) on cognitive functions in students from schools located in or away from air-polluted areas.
Subjects and methods:
In this study, two schools were selected: one was located near a traffic-polluted area (school #1), and the second was in an area away from the traffic-polluted area (school #2). In this study, a total of 300 students were recruited: 150 (75 male and 75 female) students from school #1 located in a traffic-polluted area, and 150 students (75 male and 75 female) from school #2 located away from a traffic polluted area. The overall average age of students was 13.53±1.20 years. The students were selected based on age, gender, health status, height, weight, BMI, ethnicity, and homogenous socio-economic and educational status. The pollutants PM2.5, PM10, CO, NO2, O3, and SO2 were recorded in the surrounding environment. The overall mean concentration of environmental pollutants in school #1 was 35.00±0.65 and in school #2 was 29.95±0.32. The levels of airborne particles were measured, and the cognitive functions were recorded using the Cambridge Neuropsychological Test Automated Battery (CANTAB). The students performed the cognitive functions tasks, including the attention switching task (AST), choice reaction time (CRT), and motor screening task (MOT).
Results:
The results revealed that the AST-Mean 928.34±182.23 vs. 483.79±146.73 (p=0.001), AST-mean congruent 889.12±197.12 vs. 473.30±120.11 (p=0.001), AST-mean in-congruent 988.98±201.27 vs. 483.87±144.57 (p=0.001), CRT-Mean 721.36±251.72 vs. 418.17±89.71 (p=0.001), and MOT-Mean 995.07±394.37 vs. 526.03±57.83 (p=0.001) were significantly delayed among the students who studied in school located in the traffic polluted area compared to students who studied in school which was located away from the traffic-polluted area.
Conclusions:
Environmental pollution was significantly higher in motor vehicle-congested areas. Cognitive functions were impaired among the students who were studying in a school located in a polluted area. The results further revealed that the students studying in schools located in environmentally polluted areas have attention, thinking, and decision-making abilities related to cognitive function impairment.
... As an example, working memory, a key part of the equation in learning from screen media, is significantly impacted by external factors-like sleep (e.g., Frenda & Fenn, 2016), poverty (e.g., Evans & Schamberg, 2009), and even pollution (Lopuszanska & Samardakiewicz, 2020). Thus, these same external factors will likely impact how children learn from digital media-just like they impact how young children learn at school (e.g., Buckhalt, 2011;Hair et al., 2015;Margolis et al., 2021). ...
Barr and Kirkorian (2023) provide a much-needed comprehensive framework for studying children’s learning and memory in the context of screen-based digital media. By integrating decades of research about what is known about children’s abilities and limitations in learning and memory in early childhood, both generally and via digital experiences, they offer a framework offering testable hypotheses and a potential path forward for parents, educators, and policy makers. This commentary suggests that this is an important step forward for the study of children’s increasing digital world, but we also push forward an argument that an even wider lens view is necessary when the world’s children are facing a number of community and societal challenges coupled with a period of rapid technological advancement.
... Furthermore, it is crucial to acknowledge that other environmental stressors have firmly established their negative influence on cognitive health. Air pollution (Lopuszanska and Samardakiewicz, 2020;Gao et al., 2021) and heavy metal exposure (Wang and Matsushita, 2021) have both been associated with cognitive impairments. In a comprehensive review by Singh et al. (2019), it was highlighted that ROS, stemming from exposure to environmental stressors such as ultraviolet and ionizing radiation, as well as chemical pollution, play a central role in neurodegeneration and neurological disorders. ...
With rapid industrialization, urbanization, and climate change, the impact of environmental factors on human health is becoming increasingly evident and understanding the complex mechanisms involved is vital from a healthcare perspective. Nevertheless, the relationship between physiological stress resulting from environmental stressors and environmental disease is complex and not well understood. Chronic exposure to environmental stressors, such as air and water contaminants, pesticides, and toxic metals, has been recognized as a potent elicitor of physiological responses ranging from systemic inflammation to immune system dysregulation causing or progressing environmental diseases. Conversely, physiological stress can exacerbate susceptibility to environmental diseases. Stress-induced alterations in immune function and hormonal balance may impair the ability to detoxify harmful substances and combat pathogens. Additionally, prolonged stress can impact lifestyle choices, leading to harmful behaviors. Understanding the link between physiological stress and environmental disease requires a systematic, multidisciplinary approach. Addressing this complex relationship necessitates the establishment of a global research network. This perspective discusses the intricate interplay between physiological stress and environmental disease, focusing on common environmental diseases, cancer, diabetes, and cognitive degeneration. Furthermore, we highlight the intricate and reciprocal nature of the connection between physiological stress and these environmental diseases giving a perspective on the current state of knowledge as well as identifying where further information is necessary. Recognizing the role of physiological stress in environmental health outcomes will aid in the development of comprehensive strategies to safeguard public health and promote ecological balance.
... Due to the repeated measurements (same participant under different chamber conditions), univariable linear mixed-effect models were used to assess the association between cognitive test results (response times and error rates) and CO 2 concentrations (600, 1500 and 2100 ppm). Potential confounding factors (Table S5, Supplementary Material) that were considered in this analysis were: gender [53][54][55][56][57], age [54,55,[57][58][59][60], education [53,57], first language [61], weekday [62,63], test time durations (41.5 ± 4.6 min), meal [64], caffeine drink [65], exercise [66], sleep hours [67], thermal sensation [68], perceived air quality [69], perceived lighting quality [70], perceived noise level [70,71], acute health symptoms [72][73][74][75], personal impacts, menstrual period [76], clothing level, perceived difficulty level [77], exit, TVOC concentration [15,78] and PM levels [79]. Factors that were significantly associated (p-value <0.05) with at least five cognitive performance outcomes (response times and error rates of BARS tests) across the three conditions were then included in multivariable mixed-effect models to correct for confounding. ...
Educational buildings frequently experience elevated CO2 concentrations with inadequate ventilation and high
occupancy, sometimes exceeding building guideline levels. Some studies reported detrimental impacts on
cognitive performance of indoor CO2 levels, while others did not. To generate further evidence, we conducted an
experiment in an environmentally controlled chamber. Sixty-nine healthy university students were exposed
individually for 70 min, in three separate sessions, to three CO2 conditions of 600, 1500 and 2100 ppm (crossover
design). With fixed ventilation rates, pure CO2 was injected to achieve different exposure levels. A validated
neurobehavioral BARS test battery was used to assess participants’ cognitive performance. Participants gave
subjective ratings of indoor environment and reported any health symptom through questionnaires. Comparing
elevated CO2 levels to 600 ppm, after adjusting for potential confounders, results showed significant improved
performance, that is, responses were quicker in two out of ten tests, and no significant differences in accuracy for
any test. Under 1500 ppm, participants rated the air quality significantly higher than at 600 ppm, but there were
no differences at 2100 ppm. Differences were not significant on thermal sensation, perceived lighting quality,
perceived noise level, or health symptoms for comparisons between conditions. Results indicate no clear link
between pure CO2 levels below 2100 ppm and cognitive performance, perceived indoor environment quality and
health symptoms. The findings are consistent with some prior studies, indicating that pure CO2 below 2100 ppm
implies no harm in adults and should not be treated as a potential indoor pollutant in higher educational
environments.
... Similarly, to tobacco, air pollutants [e.g., nitrogen oxides, sulfur dioxide and carbon dioxide, and particulate matter (PM)] are considered as other important factors that can adversely impact brain formation, due to increased emissions caused by anthropogenic activity. It is estimated that over 90% of people breathe the air that does not meet the WHO standards [36]. Early life exposure to air pollutants has been shown to lead to impaired neurodevelopment and has been linked with neurological dysfunctions [37], such as functional impairment of the CNS [38] or ASD, which has been positively linked to exposure to air pollution [39]. ...
Brain development, a complex process, consisting of several phases, starting as early as two weeks after conception, and continuing through childhood till early adolescence, is crucial for the development of properly functioning body systems, behavioral traits, and neurocognitive abilities. Infancy and childhood are recognized as important periods for initial brain formation, however in later stages of life, such as childhood and adulthood, experiences, together with environmental exposures, can still influence brain physiology. The developing brain is particularly susceptible to epigenetic changes with many factors being proposed as modifiers by directly impacting DNA methylation as well as histone and chromatin modifications within genes implicated in development. These factors include: maternal stress and diet, exposure to pollutants, sleep quality, as well as dietary habits. Evidence indicates exposures to environmental threats can lead to inappropriate neurological, metabolic, and endocrine functioning often mediated by epigenetic mechanisms with symptoms manifesting themselves as early as childhood or in later stages of life. Therefore, the main aim of this review is to evaluate the current studies focused on negative environmental exposures and their consequences on the developing brain directed by epigenetic mechanisms.
... Air pollution in early life may also affect brain development: maternal air pollution exposure from the 25th gestational week onwards is associated with head growth (Clemens et al., 2017) but being exposed postnatal PM 2.5 concentration is also linked to poorer cognitive performance in childhood (Ni et al., 2022;Chiu et al., 2016;Lopuszanska and Samardakiewicz, 2020). The human brain undergoes rapid developments in the early years which continues well into childhood with the differentiation and maturation of neurons and myelination of axons (Hedman et al., 2012;Stiles and Jernigan, 2010). ...
Background:
Living in areas with high air pollution concentrations is associated with all-cause and cause-specific mortality. Exposure in sensitive developmental periods might be long-lasting but studies with very long follow-up are rare, and mediating pathways between early life exposure and life-course mortality are not fully understood.
Methods:
Data were drawn from the Scottish Longitudinal Study Birth Cohort of 1936, a representative record-linkage study comprising 5% of the Scottish population born in 1936. Participants had valid age 11 cognitive ability test scores along with linked mortality data until age 86. Fine particle (PM2.5) concentrations estimated with the EMEP4UK atmospheric chemistry transport model were linked to participants' residential address derived from the National Identity Register in 1939 (age 3). Confounder-adjusted Cox regression estimated associations between PM2.5 and mortality; regression-based causal mediation analysis explored mediation through childhood cognitive ability.
Results:
The final sample consisted of 2734 individuals with 1608 deaths registered during the 1,833,517 person-months at risk follow-up time. Higher early life PM2.5 exposure increased the risk of all-cause mortality (HR = 1.03, 95% CI: 1.01-1.04 per 10 μg m-3 increment), associations were stronger for mortality between age 65 and 86. PM2.5 increased the risk of cancer-related mortality (HR = 1.05, 95% CI: 1.02-1.08), especially for lung cancer among females (HR = 1.11, 95% CI: 1.02-1.21), but not for cardiovascular and respiratory diseases. Higher PM2.5 in early life (≥50 μg m-3) was associated with lower childhood cognitive ability, which, in turn, increased the risk of all-cause mortality and mediated 25% of the total associations.
Conclusions:
In our life-course study with 75-year of continuous mortality records, we found that exposure to air pollution in early life was associated with higher mortality in late adulthood, and that childhood cognitive ability partly mediated this relationship. Findings suggest that past air pollution concentrations will likely impact health and longevity for decades to come.
... 17 Studies have specifically linked traffic-related NO 2 exposure to reduced EFs in children and adolescents. 18,19 Additionally, short-term exposure to PM 2.5 has been associated with executive dysfunction and slower cognitive processing times in healthy young adults. 20,21,22 However, due to the challenge of J o u r n a l P r e -p r o o f generalizing the decline in cognitive function to a population known for their exceptional EF abilities compared to the general population, 23 further research in this area is warranted. ...
Introduction:
Air pollution is a global issue known to effect on human health and performance. In the context of highly skilled athletes, the influence of air pollution on players' physical and technical abilities are established, yet its effects on cognitive performance have received little consideration. This study aims to address this research gap by comprehensively examining the influence of air pollution on the performance of highly skilled athletes using a holistic approach, including both the athlete's brain and body.
Methods:
Between 2016 and 2022, a total of 799 soccer players (578 males, 221 females) belonging to a German professional first division club were measured on a battery of performance assessments, including physical, technical, and cognitive tests. The performance data were combined with the average daily concentration of three pollutants: PM10, O3 and NO2.
Results:
Increased levels of PM10 and O3 were primarily associated with decreased physical and technical performance, including slower sprinting times, impaired change of direction and worse speed and accuracy in the technical assessment. For instance, if the assessment test was held when PM10 levels were at 20 μg/m3, players ran an average 22 ms slower on the 30 m sprint test, 36 ms slower on the change of direction test and showed a 1 % decrease in accuracy on the technical assessment (p < .001). Furthermore, higher concentrations of NO2 negatively impacted cognitive performance across four separate tests of athletes' executive functions (p < .05).
Conclusion:
By encompassing physical, technical, and cognitive assessments, this study highlights the multifaceted nature of performance impairments resulting from air pollution exposure in a population characterized by have exceptional abilities across all three domains. These findings underscore the widespread impact of pollution on a diverse sample of athletes and emphasize the need to consider air pollution in the broader context of its effects on human health and the environment.
... 19 Open access maternal smoking 22 23 and air pollution exposure, 24 25 preterm birth, 26 27 birth weight, 22 28 duration of breast feeding, 29 30 childhood environmental tobacco smoke 31 32 and air pollution exposure. 24 25 The relationships identified by the DAG determined what would be adjusted for in our multivariable analysis. Age, height, sex and ethnicity were not included in our models due to the use of GLI % predicted values for lung function, which are preadjusted for these. ...
Background
Decreased adult lung function is associated with subsequent impairment in cognition. A similar relationship in early life could be of great policy importance, since childhood cognitive ability determines key adult outcomes, including socioeconomic status and mortality. We aimed to expand the very limited data available on this relationship in children, and hypothesised that reduced lung function would be longitudinally associated with decreased cognitive ability.
Methods
Lung function was measured at age 8 (forced expiratory volume in one second (FEV1), forced vital capacity (FVC); % predicted), and cognitive ability was measured at ages 8 (Wechsler Intelligence Scale for Children, third edition) and 15 (Wechsler Abbreviated Scale of Intelligence), in the Avon Longitudinal Study of Parents and Children. Potential confounders were identified as preterm birth, birth weight, breastfeeding duration, prenatal maternal smoking, childhood environmental tobacco smoke exposure, socioeconomic status and prenatal/childhood air pollution exposure. Univariable and multivariable linear models (n range=2332–6672) were fitted to assess the cross-sectional and longitudinal associations of lung function with cognitive ability, and change in cognitive ability between ages 8 and 15.
Results
In univariate analyses, both FEV1 and FVC at age 8 were associated with cognitive ability at both ages, but after adjustment, only FVC was associated with full-scale IQ (FSIQ) at ages 8 (β=0.09 (95% CI 0.05 to 0.12; p<0.001)) and 15 (β=0.06 (0.03 to 0.10; p=0.001)). We did not find evidence of an association between either lung function parameter and interval change in standardised FSIQ.
Discussion
Reduced FVC, but not FEV1, is independently associated with decreased cognitive ability in children. This low-magnitude association attenuates between ages 8 and 15, while no association is evident with longitudinal change in cognitive ability. Our results support a link between FVC and cognition across the life course, possibly due to shared genetic or environmental risk, rather than causation.
... Third, we show that PM 2.5 could impact multiple language skills, particularly writing. Lastly, our estimates suggest that the impacts of PM 2.5 could differ between the CET4 and CET6, implying that air pollution could be more harmful to more complex tasks.Research has shown that short-term exposure to PM 2.5 could cause a decline in processing speed and difficulties in reasoning and logical thinking (Bedi et al. 2021;Shehab and Pope 2019;Lopuszanska and Samardakiewicz 2020). Our analysis has important policy implications. ...
This paper investigates the impact of air pollution on students’ cognitive performance in a high-stakes exam: China’s College English Test (CET). We match exams taken from 2013 to 2017 at 22 universities across China with hourly air pollution measures from the nearest monitoring stations. Identification leverages a student fixed effects model, which alleviates the concern of omitted variables, such as students’ ability. Our estimates indicate a statistically significant negative impact of fine particulate matters (PM2.5) exposure during exam windows on cognitive performance. By focusing on a single language exam, instead of comparing performance across different test subjects, we are able to paint a more accurate picture of the cognitive impact of air pollution. We highlight the importance of short-term air pollution exposure for high-stakes cognitive performance. Our results suggest that temporary defensive measures could be important in mitigating the negative consequences of air pollution.
INTRODUCCIÓN. La contaminación del aire de naturaleza química es un problema que se presenta diariamente por la constante exposición crónica y prolongada a factores externos, como la congestión vehicular y la existencia de zonas industriales, superando en muchas ocasiones el índice de contaminación permitida, normada por los estándares de calidad ambiental. El estudio tuvo como fin mostrar la influencia del nivel de contaminación química del aire en las capacidades cognitivas de los escolares. Se evaluaron los contaminantes del aire más importantes, a través de las ocho estaciones de monitoreo, a nivel de Lima Metropolitana. Entre estos contaminantes figuran el monóxido de carbono (CO), dióxido de nitrógeno (NO2), dióxido de azufre (SO2) y material particulado (PM2,5 y PM10). MÉTODO. La investigación es de tipo cuantitativa, no experimental y es ex post facto. La muestra fue de 350 estudiantes de ambos sexos, de 10 a 12 años de edad, en niñas había un 47% y en niños un 53%. La edad promedio era de 10,88 años y una desviación estándar típica de 0,824, del 6.º grado de primaria de colegios privados, distribuidos en ocho puntos de monitoreo a nivel de Lima Metropolitana. Se aplicó un test neuropsicológico conocido como test de percepción de diferencias: CARAS-R, donde se evaluaron las capacidades perceptivas y atencionales, validados por baremos nacionales e internacionales. RESULTADOS. La concentración PM10 presentó una correlación negativa y significativamente fuerte con R = - 0,98, con un IC: 95% para las capacidades perceptivas y atencionales. El CO y el PM2,5 tuvieron una relación negativa moderada con un valor promedio de R = - 0,72 (IC: 95%). El NO2 presentó una correlación débil y poco significativa, para la percepción y atención, con un factor de correlación R = 0,44. DISCUSIÓN. Los niños en edad escolar de 10 a 12 años que cursan el 6.º grado de primaria, expuestos de manera crónica y prolongada a la contaminación química del aire, experimentan menor capacidad cognitiva tanto perceptivas como atencionales.
The widespread use of plastics has revolutionized modern life, but also led to environmental pollution. Although microplastics (MPs) have been detected in various environments, their presence in the atmosphere, particularly in Brazil, is poorly studied. This research investigated atmospheric MP concentrations at Alvaro Guiao School in Sao Carlos, Brazil, from 2021 to 2022. Outdoor MP concentrations ranged from the limit of detection (LOD) to 168.03 items m− 2 day− 1, and indoor concentrations ranged from LOD to 60.16 items m− 2 day− 1. Predominantly, these MPs were fragments, even in the indoor environment, suggesting abundant sources, such as resuspension. Seasonal variations were not observed for outdoor fragments and fibers, nor for indoor fragments. However, indoor fiber concentrations were higher during the dry season (p > 0.05), likely due to winter clothing and
reduced ventilation. Fragment sizes were mainly <60 μm, while fibers ranged from <60 μm to 3000–5000 μm. Polyester was the primary MP component (83–100% outdoors and 29–100% indoors), followed by ethylene vinyl acetate (EVA, 0–17% outdoors and 0–57% indoors), common in synthetic clothing and school supplies, respectively. Other plastics, found in packaging and bottles, like polyethylene (0–14%) and polyethylene terephthalate (0–6%), were also identified indoors. This study not only enhances the current understanding, but also pioneers analyses within a school environment. Despite being a work in progress, this study has already shown the presence of plastic particles in nvironments where children, one of the most susceptible groups to air ollution, spend a significant portion of their time. Furthermore, it can assist in developing an assessment of acceptable levels and guidelines.
Objective:
This article aims to assess the impact of climate change, a reality already presents in the environment, on the neurodevelopment of both neurotypical and atypical children.
Data sources:
A narrative review of the literature was carried out based on articles available in the PubMed database, published in the last five years using the keywords neurodevelopment and climate change, as well as websites of organizations dedicated to childhood such as UNICEF, the American Academy of Pediatrics and the Center for Developing Childhood at Harvard University.
Summary of findings:
Children and adolescents are more directly affected by the effects of climate change due to their developmental stage and greater vulnerability. Prolonged exposure to air pollutants can affect brain development, resulting in cognitive and behavioral problems. Extreme weather events, such as floods, cyclones, and heat waves, can destroy essential infrastructure such as schools and hospitals, interrupting the educational process and access to health care. Changes in rainfall patterns and extreme droughts can affect food production, leading to malnutrition and food insecurity. Direct experience of natural disasters can cause stress and psychological trauma, affecting children's emotional and mental well-being.
Conclusions:
Studies clearly demonstrate the potential impact of climate change on the neurodevelopment and mental health of children and adolescents. This topic should be part of the current agenda of pediatricians, not only treating the resulting illnesses but mainly acting on the front line and supporting proposals to attenuate the environmental disaster that has already occurred.
Background:
Emerging literature suggests that fine particulate matter [with aerodynamic diameter ≤2.5μm (PM2.5)] air pollution and its components are linked to various neurodevelopmental outcomes. However, few studies have evaluated how PM2.5 component mixtures from distinct sources relate to cognitive outcomes in children.
Objectives:
This cross-sectional study investigated how ambient concentrations of PM2.5 component mixtures relate to neurocognitive performance in 9- to 10-year-old children, as well as explored potential source-specific effects of these associations, across the US.
Methods:
Using spatiotemporal hybrid models, annual concentrations of 15 chemical components of PM2.5 were estimated based on the residential address of child participants from the Adolescent Brain Cognitive Development (ABCD) Study. General cognitive ability, executive function, and learning/memory scores were derived from the NIH Toolbox. We applied positive matrix factorization to identify six major PM2.5 sources based on the 15 components, which included crustal, ammonium sulfate, biomass burning, traffic, ammonium nitrate, and industrial/residual fuel burning. We then utilized weighted quantile sum (WQS) and linear regression models to investigate associations between PM2.5 components' mixture, their potential sources, and children's cognitive scores.
Results:
Mixture modeling revealed associations between cumulative exposure and worse cognitive performance across all three outcome domains, including shared overlap in detrimental effects driven by ammonium nitrates, silicon, and calcium. Using the identified six sources of exposure, source-specific negative associations were identified between ammonium nitrates and learning & memory, traffic and executive function, and crustal and industrial mixtures and general cognitive ability. Unexpected positive associations were also seen between traffic and general ability as well as biomass burning and executive function.
Discussion:
This work suggests nuanced associations between outdoor PM2.5 exposure and childhood cognitive performance, including important differences in cognition related both to individual chemicals as well as to specific sources of these exposures. https://doi.org/10.1289/EHP14418.
Air pollution exposure has been associated with adverse cognitive and mental health outcomes in children, adolescents, and adults, although youth may be particularly susceptible given ongoing brain development. However, the neurodevelopmental mechanisms underlying the associations among air pollution, cognition, and mental health remain unclear. We examined the impact of particulate matter (PM2.5) on resting-state functional connectivity (rsFC) of the default mode network (DMN) and three key attention networks: dorsal attention, ventral attention, and cingulo-opercular. Longitudinal changes in rsFC within/between networks were assessed from baseline (9-10 years) to the two-year follow-up (11-12 years) in 10,072 youth (M+SD=9.93+0.63 years; 49% female) from the Adolescent Brain Cognitive Development (ABCD®) study. Annual ambient PM2.5 concentrations from the 2016 calendar year were estimated using hybrid ensemble spatiotemporal models. RsFC was estimated using functional neuroimaging. Linear mixed models were used to test associations between PM2.5 and change in rsFC over time while adjusting for relevant covariates (e.g., age, sex, race/ethnicity, parental education, family income) and other air pollutants (O3, NO2). A PM2.5 x time interaction was significant for within-network rsFC of the DMN such that higher PM2.5 concentrations were associated with a smaller increase in rsFC over time. Further, significant PM2.5 x time interactions were observed for between-network rsFC of the DMN and all three attention networks, with varied directionality. PM2.5 exposure was associated with alterations in the development and equilibrium of the DMN-a network implicated in self-referential processing-and anti-correlated attention networks, which may impact trajectories of cognitive and mental health symptoms across adolescence.
Purpose of Review
This review summarizes the current knowledge (definition, source, formation, structure, chemical composition, and health effects) about atmospheric soot particles and aims to analyze their health effects combined with their structural characteristics.
Recent Findings
The new understanding of soot microstructure (analogous to reduced graphene oxide (RGO)) suggests the presence of oxygen-containing functional groups (OFGs) in carbonaceous core (CC) of soot, which may enhance its health effects. Toxicological studies have proved that the two major components (CC and outer coating) both contribute to soot toxicity, but there is still controversy over who is playing the main role. Recently, there are many studies questioning the past experimental results. The bioavailability of the outer coating bound on CC is particularly pointed out to be taken into account for soot toxicity. Existing epidemiological studies on black carbon (BC), a near-synonym of soot in atmospheric science, have prompted the adverse health effects especially for cardiovascular system. A stronger association between short term BC exposure and health endpoints is lately found than fine particulate matter (PM2.5), but still needs more consistent evidence. Therefore, the health effects of soot need more attention as well as comprehensive and in-depth research.
Summary
It is evident from the review that soot is a responsible agent for adverse health effects, which may exceed PM2.5. The CC and outer coating have been proved to exert toxicity separately, of which oxidative stress, inflammation, and DNA damage are most important toxicity mechanisms. However, their antagonistic interaction may weaken the toxicity of the whole soot particle.
The main objective of this review is to provide a brief overview of some new directions and trends in the field of atmospheric particulate matter detection by laser-induced breakdown spectroscopy...
Little is known about the impact of long-term ambient air pollution (AP) and noise exposure on change in cognitive function over years in the elderly. In this study, we wanted to examine the association between long-term exposure to AP and noise with the rate of cognitive decline in a population aged 50 and older and susceptible groups with mild cognitive impairment or at a genetically higher risk of Alzheimer's disease (Apolipoprotein E ε4 positive). Participants in the German population-based Heinz Nixdorf Recall study carried out five neuropsychological tests. Individual tests scores at the first (T1 = 2006-2008) and second (T2 = 2011-2015) follow-up for each test were used as outcomes after standardization using predicted means adjusted for age and education. Global cognitive score (GCS) was defined as sum of five standardized scores of individual tests. Long-term exposures to particulate matter (PM2.5, PM10, PM2.5 absorbance), accumulation mode particle number (PNacc), a proxy of ultrafine particles, and nitrogen dioxide were estimated by the land-use regression and chemistry transport models. Noise exposures were assessed as outdoor weighted nighttime road traffic noise (Lnight) means. We performed linear regression analyses adjusted for sex, age, individual and neighborhood socio-economic status, and lifestyle variables. Effect modification in vulnerable groups was estimated using multiplicative interaction terms between exposure and a modifier. Overall, 2554 participants (49.5% men, median age is 63 (IQR = 12)) were included. We found weak associations between higher exposure to PM10 and PM2.5 with faster decline in the immediate verbal memory test. Adjustment for potential confounders and for co-exposures did not change the results. We saw no effects on GCS, and no effect of noise exposure. In susceptible groups, higher AP and noise exposure were tended to be associated with faster decline in GCS. Our results suggest that AP exposure may accelerate cognitive decline in older ages, particularly in susceptible groups.
Background: Living in areas with high air pollution concentrations is associated with all-cause and cause-specific mortality. Exposure in sensitive developmental periods might be long-lasting but studies with very long follow-up are rare, and mediating pathways between early life exposure and life-course mortality are not fully understood.
Methods: Data were drawn from the Scottish Longitudinal Study Birth Cohort of 1936, a representative record-linkage study comprising 5% of the Scottish population born in 1936. Participants had valid age 11 cognitive ability test scores along with linked mortality data until age 86. Fine particle (PM2.5) concentrations estimated with the EMEP4UK atmospheric chemistry transport model were linked to participants' residential address from the National Identity Register in 1939 (age 3). Confounder-adjusted Cox regression estimated associations between PM2.5 and mortality; regression-based causal mediation analysis explored mediation through childhood cognitive ability.
Results: The final sample consisted of 2734 individuals with 1608 deaths registered during the 1,833,517 person-months at risk follow-up time. Higher early life PM2.5 exposure increased the risk of all-cause mortality (HR=1.03, 95% CI: 1.01-1.04 per 10ug m-3 increment), associations were stronger for mortality between age 65 and 86. PM2.5 increased the risk of cancer-related mortality (HR=1.05, 95% CI: 1.02-1.08), especially for lung cancer among females (HR=1.11, 95% CI: 1.02-1.21), but not for cardiovascular and respiratory diseases. Higher PM2.5 in early life (≥50ug m-3) was associated with lower childhood cognitive ability, which, in turn, increased the risk of all-cause mortality and mediated 25% of the total associations.
Conclusions: In our life-course study with 75-year of continuous mortality records, we found that exposure to air pollution in early life was associated with higher mortality in late adulthood, and that childhood cognitive ability partly mediated this relationship. Findings suggest that past air pollution concentrations will likely impact health and longevity for decades to come.
An increasing number of studies have shown that particulate matter (PM) exposure can produce damaging effects on respiratory and cardiovascular systems, however, whether PM can enter the brain and produce neurotoxicity has been an important research question for PM health effects in recent years. In this review, we discuss the health risks of PM (mainly PM2.5) on the central nervous system (CNS) in age-specific cohorts, exposure pathways and molecular mechanisms by reviewing the latest in vivo and in vitro evidence from relevant experimental and epidemiological studies. The sensitivity and vulnerability to PM2.5 exposure varied across different cohorts, especially in the children, the elderly groups and occupational populations working in dusty environments. PM2.5 may affect the CNS directly or indirectly through the blood–brain barrier, olfactory nerve, optic nerve, microbiota-gut-brain axis, and nasal microbes. They exert neurotoxicological effects by inducing oxidative stress, inflammation, mitochondrial dysfunction, neuronal apoptosis, synaptic damage, DNA methylation, cellular autophagy, blood homeostasis imbalance and metabolic disturbance. This review presents the requirements for further research on the neurotoxicological effects of PM2.5 exposure, points out future research orientations in this field and provides a theoretical basis and prevention strategies for alleviating the adverse effects of PM2.5 exposure to the CNS.
Allergic symptoms are quite common, but some underlying pathological mechanisms may not follow the traditional allergy pathways, and therefore treatment may be difficult. Urban air pollution, closed spaces and buildings with poor air quality may contribute greatly to the development and sometimes worsening of those symptoms. Occupational exposure to toxins and sick-building syndrome symptoms may be improved by air filtration and ventilation. Noise and sound pollution interfere with sleep and can further impair physical and mental wellbeing. In addition to those external physical factors, stress in the work environment causes mental health illnesses, burnout, and pre-existing medical ailments may be exacerbated. Raising awareness of toxic places and situations, the development of safety protocols and coping strategies should be implemented in every work environment.
Neuroimaging studies showing the adverse effects of air pollution on neurodevelopment have largely focused on smaller samples from limited geographical locations and have implemented univariant approaches to assess exposure and brain macrostructure. Herein, we implement restriction spectrum imaging and a multivariate approach to examine how one year of annual exposure to daily fine particulate matter (PM2.5), daily nitrogen dioxide (NO2), and 8-h maximum ozone (O3) at ages 9-10 years relates to subcortical gray matter microarchitecture in a geographically diverse subsample of children from the Adolescent Brain Cognitive Development (ABCD) Study℠. Adjusting for confounders, we identified a latent variable representing 66% of the variance between one year of air pollution and subcortical gray matter microarchitecture. PM2.5 was related to greater isotropic intracellular diffusion in the thalamus, brainstem, and accumbens, which related to cognition and internalizing symptoms. These findings may be indicative of previously identified air pollution-related risk for neuroinflammation and early neurodegenerative pathologies.
Exposure to ambient air pollution may affect cognitive functioning and development in children. Unfortunately, there is little evidence available for low- and middle-income countries (LMICs), where air pollution levels are highest. We analysed the association between exposure to ambient fine particulate matter (≤2.5 μm [PM2.5]) and cognitive development indicators in a cross-sectional analysis of children (aged 3-4 years) in 12 LMICs. We linked Demographic and Health Survey data, conducted between 2011 and 2018, with global estimates of PM2.5 mass concentrations to examine annual average exposure to PM2.5 and cognitive development (literacy-numeracy and learning domains) in children. Cognitive development was assessed using the United Nations Children's Fund's early child development indicators administered to each child's mother. We used multivariable logistic regression models, adjusted for individual- and area-level covariates, and multi-pollutant models (including nitrogen dioxide and surface-level ozone). We assessed if sex and urban/rural status modified the association of PM2.5 with the outcome. We included 57,647 children, of whom, 9613 (13.3%) had indicators of cognitive delay. In the adjusted model, a 5 μg/m3 increase in annual all composition PM2.5 was associated with greater odds of cognitive delay (OR = 1.17; 95% CI: 1.13, 1.22). A 5 μg/m3 increase in anthropogenic PM2.5 was also associated with greater odds of cognitive delay (OR = 1.05; 95% CI: 1.00, 1.10). These results were robust to several sensitivity analyses, including multi-pollutant models. Interaction terms showed that urban-dwelling children had greater odds of cognitive delay than rural-dwelling children, while there was no significant difference by sex. Our findings suggest that annual average exposure to PM2.5 in young children was associated with adverse effects on cognitive development, which may have long-term consequences for educational attainment and health.
Background
Environmental resources are related to childhood obesity risk and altered brain development, but whether these relationships are stable or if they have sustained impact is unknown. Here, we utilized a multidimensional index of childhood neighborhood conditions to compare the influence of various social and environmental disparities (SED) on body mass index (BMI)-brain relationships over a 2-year period in early adolescence.
Methods
Data were gathered the Adolescent Brain Cognitive Development Study® (n = 2,970, 49.8% female, 69.1% White, no siblings). Structure magnetic resonance imaging (sMRI), anthropometrics, and demographic information were collected at baseline (9/10-years-old) and the 2-year-follow-up (11/12-years-old). Region of interest (ROIs; 68 cortical, 18 subcortical) estimates of cortical thickness and subcortical volume were extracted from sMRI T1w images using the Desikan atlas. Residential addresses at baseline were used to obtain geocoded estimates of SEDs from 3 domains of childhood opportunity index (COI): healthy environment (COIHE), social/economic (COISE), and education (COIED). Nested, random-effects mixed models were conducted to evaluate relationships of BMI with (1) ROI * COI[domain] and (2) ROI * COI[domain] * Time. Models controlled for sex, race, ethnicity, puberty, and the other two COI domains of non-interest, allowing us to estimate the unique variance explained by each domain and its interaction with ROI and time.
Results
Youth living in areas with lower COISE and COIED scores were heavier at the 2-year follow-up than baseline and exhibited greater thinning in the bilateral occipital cortex between visits. Lower COISE scores corresponded with larger volume of the bilateral caudate and greater BMI at the 2-year follow-up. COIHE scores showed the greatest associations (n = 20 ROIs) with brain-BMI relationships: youth living in areas with lower COIHE had thinner cortices in prefrontal regions and larger volumes of the left pallidum and Ventral DC. Time did not moderate the COIHE x ROI interaction for any brain region during the examined 2-year period. Findings were independent of family income (i.e., income-to-needs).
Conclusion
Collectively our findings demonstrate that neighborhood SEDs for health-promoting resources play a particularly important role in moderating relationships between brain and BMI in early adolescence regardless of family-level financial resources.
Outdoor air pollution has been recognized as a novel environmental neurotoxin. Studies have begun to use brain Magnetic Resonance Imaging (MRI) to investigate how air pollution may adversely impact developing brains. A systematic review was conducted to evaluate and synthesize the reported evidence from MRI studies on how early-life exposure to outdoor air pollution affects neurodevelopment. Using PubMed and Web of Knowledge, we conducted a systematic search, followed by structural review of original articles with individual-level exposure data and that met other inclusion criteria. Six studies were identified, each sampled from 3 cohorts of children in Spain, The Netherlands, and the United States. All studies included a one-time assessment of brain MRI when children were 6–12 years old. Air pollutants from traffic and/or regional sources, including polycyclic aromatic hydrocarbons (PAHs), nitrogen dioxide, elemental carbon, particulate matter (<2.5 or <10 μm), and copper, were estimated prenatally (n = 1), during childhood (n = 3), or both (n = 2), using personal monitoring and urinary biomarkers (n = 1), air sampling at schools (n = 4), or a land-use regression (LUR) modeling based on residences (n = 2). Associations between exposure and brain were noted, including: smaller white matter surface area (n = 1) and microstructure (n = 1); region-specific patterns of cortical thinness (n = 1) and smaller volumes and/or less density within the caudate (n = 3); altered resting-state functional connectivity (n = 2) and brain activity to sensory stimuli (n = 1). Preliminary findings suggest that outdoor air pollutants may impact MRI brain structure and function, but limitations highlight that the design of future air pollution-neuroimaging studies needs to incorporate a developmental neurosciences perspective, considering the exposure timing, age of study population, and the most appropriate neurodevelopmental milestones.
The aim of this study was to investigate the associations between ambient air pollutants and cognitive impairment in Korean older adults. The cognitive function of 2,896 participants aged 70 to 84 years was measured using the Korean version of the mini-mental state examination, the digit span test, the word list learning test, and the frontal assessment battery. After matching the average concentrations of particulate matter (PM) <10 μm in size (PM10) and <2.5 μm (PM2.5), NO2, CO, SO2, and O3 between 2013 and 2017, the association between air pollutants and cognitive scales was analyzed using a linear mixed regression and a multiple logistic regression analysis (after adjusting for age, sex, health related behaviors, socioeconomic status, comorbidity, and meteorological data). Exposure to PM2.5, PM10, NO2, SO2, and CO was associated with cognitive impairment above and beyond age or education level effects. Specifically, PM2.5 was negatively associated with most components of the cognitive scales (interquartile range for PM2.5: 2.0 μg/m3, odds ratio for poor global cognition: 2.28, 95% confidence interval: 1.60–3.26). These associations may be affected by sex, residence area, or alcohol intake. Conclusively, air pollutants, especially PM2.5, were associated with cognitive impairment, including global cognition, attention, memory, and executive function in Korean older adults aged ≥70 years.
Air pollution is a risk factor for cardiovascular and respiratory morbidity and mortality. A growing literature also links exposure to diverse air pollutants (e.g., nanoparticles, particulate matter, ozone, traffic-related air pollution) with brain health, including increased incidence of neurological and psychiatric disorders such as cognitive decline, dementia (including Alzheimer’s disease), anxiety, depression, and suicide. A critical gap in our understanding of adverse impacts of pollutants on the central nervous system (CNS) is the early initiating events triggered by pollutant inhalation that contribute to disease progression. Recent experimental evidence has shown that particulate matter and ozone, two common pollutants with differing characteristics and reactivity, can activate the hypothalamic-pituitary-adrenal (HPA) axis and release glucocorticoid stress hormones (cortisol in humans, corticosterone in rodents) as part of a neuroendocrine stress response. The brain is highly sensitive to stress: stress hormones affect cognition and mental health, and chronic stress can produce profound biochemical and structural changes in the brain. Chronic activation and/or dysfunction of the HPA axis also increases the burden on physiological stress response systems, conceptualized as allostatic load, and is a common pathway implicated in many diseases. The present paper provides an overview of how systemic stress-dependent biological responses common to particulate matter and ozone may provide insight into early CNS effects of pollutants, including links with oxidative, inflammatory, and metabolic processes. Evidence of pollutant effect modification by non-chemical stressors (e.g., socioeconomic position, psychosocial, noise), age (prenatal to elderly), and sex will also be reviewed in the context of susceptibility across the lifespan.
Objective
To investigate whether the incidence of dementia is related to residential levels of air and noise pollution in London.
Design
Retrospective cohort study using primary care data.
Setting
75 Greater London practices.
Participants
130 978 adults aged 50–79 years registered with their general practices on 1 January 2005, with no recorded history of dementia or care home residence.
Primary and secondary outcome measures
A first recorded diagnosis of dementia and, where specified, subgroups of Alzheimer’s disease and vascular dementia during 2005–2013. The average annual concentrations during 2004 of nitrogen dioxide (NO 2 ), particulate matter with a median aerodynamic diameter ≤2.5 µm (PM 2.5 ) and ozone (O 3 ) were estimated at 20×20 m resolution from dispersion models. Traffic intensity, distance from major road and night-time noise levels (L night ) were estimated at the postcode level. All exposure measures were linked anonymously to clinical data via residential postcode. HRs from Cox models were adjusted for age, sex, ethnicity, smoking and body mass index, with further adjustments explored for area deprivation and comorbidity.
Results
2181 subjects (1.7%) received an incident diagnosis of dementia (39% mentioning Alzheimer’s disease, 29% vascular dementia). There was a positive exposure response relationship between dementia and all measures of air pollution except O 3 , which was not readily explained by further adjustment. Adults living in areas with the highest fifth of NO 2 concentration (>41.5 µg/m ³ ) versus the lowest fifth (<31.9 µg/m ³ ) were at a higher risk of dementia (HR=1.40, 95% CI 1.12 to 1.74). Increases in dementia risk were also observed with PM 2.5 , PM 2.5 specifically from primary traffic sources only and L night , but only NO 2 and PM 2.5 remained statistically significant in multipollutant models. Associations were more consistent for Alzheimer’s disease than vascular dementia.
Conclusions
We have found evidence of a positive association between residential levels of air pollution across London and being diagnosed with dementia, which is unexplained by known confounding factors.
Significance
Most of the population in developing countries live in places with unsafe air. Utilizing variations in transitory and cumulative air pollution exposures for the same individuals over time in China, we provide evidence that polluted air may impede cognitive ability as people become older, especially for less educated men. Cutting annual mean concentration of particulate matter smaller than 10 μm (PM10) in China to the Environmental Protection Agency’s standard (50 μg/m ³ ) would move people from the median to the 63rd percentile (verbal test scores) and the 58th percentile (math test scores), respectively. The damage on the aging brain by air pollution likely imposes substantial health and economic costs, considering that cognitive functioning is critical for the elderly for both running daily errands and making high-stake decisions.
Background:
Traffic-related air pollution is emerging as a risk factor for Alzheimer's disease (AD) and impaired brain development. Individual differences in vulnerability to air pollution may involve the allele of Apolipoprotein E (APOE) gene, the primary genetic risk factor for AD.
Objective:
We analyzed whether the association between traffic air pollution and neurodevelopmental outcomes is modified by APOE ε4 status in children.
Methods:
Data on parent-reported behavior problems (total difficulties scores, Strengths and Difficulties Questionnaire), teacher-reported attention-deficit hyperactivity disorder (ADHD) symptom scores, cognitive performance trajectories (computerized tests of inattentiveness and working memory repeated 2-4 times during January 2012-March 2013), and APOE genotypes were obtained for 1,667 children age 7-11 y attending 39 schools in or near Barcelona. Basal ganglia volume (putamen, caudate, and globus pallidum) was measured in 163 of the children by MRI (October 2012-April 2014.) Average annual outdoor polycyclic aromatic hydrocarbons (PAHs), elemental carbon (EC), and nitrogen dioxide (NO2) concentrations were estimated based on measurements at each school (two 1-wk campaigns conducted 6 months apart in 2012).
Results:
APOE ε4 allele carriers had significantly higher behavior problem scores than noncarriers, and adverse associations with PAHs and NO2 were stronger or limited to carriers for behavior problem scores (P-interaction 0.03 and 0.04), caudate volume (P-interaction 0.04 and 0.03), and inattentiveness trajectories (P-interaction 0.15 and 0.08, respectively). Patterns of associations with the same outcomes were similar for EC.
Conclusion:
PAHs, EC, and were associated with higher behavior problem scores, smaller reductions in inattentiveness over time, and smaller caudate volume in APOE ε4 allele carriers in our study population, and corresponding associations were weak or absent among noncarriers. These findings support a potential role of APOE in biological mechanisms that may contribute to associations between air pollution and neurobehavioral outcomes in children. https://doi.org/10.1289/EHP2246.
In this issue of the Biomedical Journal, we learn how air pollution may contribute to cognitive decline and even increase risk for Alzheimer's disease. We also highlight original research documenting the body's response to infection with a common oral pathogen. Finally, we learn how a cellular antioxidant protein protects against mitochondrial dysfunction in Parkinson's disease.
As incidence of Alzheimer's disease (AD) and other neurodegenerative diseases rise, there is increasing interest in environmental factors which may contribute to disease onset and progression. Air pollution has been known as a major health hazard for decades. While its effects on cardiopulmonary morbidity and mortality have been extensively studied, growing evidence has emerged that exposure to polluted air is associated with impaired cognitive functions at all ages and increased risk of AD and other dementias in later life; this association is particularly notable with traffic related pollutants such as nitrogen dioxide, nitrous oxide, black carbon, and small diameter airborne solids and liquids known as particulate matter. The exact mechanisms by which air pollutants mediate neurotoxicity in the central nervous system (CNS) and lead to cognitive decline and AD remain largely unknown. Studies using animal and cell culture models indicate that amyloid-beta processing, anti-oxidant defense, and inflammation are altered following the exposure to constituents of polluted air. In this review, we summarize recent evidence supporting exposure to air pollution as a risk for cognitive decline at all ages and AD at later lifetime. Additionally, we review the current body of work investigating the molecular mechanisms by which air pollutants mediate damage in the CNS. Understanding of the neurotoxic effects of air pollution and its constituents is still limited, and further studies will be essential to better understand the cellular and molecular mechanisms linking air pollution and cognitive decline.
Purpose of review:
An emerging body of evidence has raised concern regarding the potentially harmful effects of inhaled pollutants on the central nervous system during the last decade. In the general population, traffic-related air pollution (TRAP) exposure has been associated with adverse effects on cognitive, behavior, and psychomotor development in children, and with cognitive decline and higher risk of dementia in the elderly. Recently, studies have interfaced environmental epidemiology with magnetic resonance imaging to investigate in vivo the effects of TRAP on the human brain. The aim of this systematic review was to describe and synthesize the findings from these studies. The bibliographic search was carried out in PubMed with ad hoc keywords.
Recent findings:
The selected studies revealed that cerebral white matter, cortical gray matter, and basal ganglia might be the targets of TRAP. The detected brain damages could be involved in cognition changes. The effect of TRAP on cognition appears to be biologically plausible. Interfacing environmental epidemiology and neuroimaging is an emerging field with room for improvement. Future studies, together with inputs from experimental findings, should provide more relevant and detailed knowledge about the nature of the relationship between TRAP exposure and cognitive, behavior, and psychomotor disorders observed in the general population.
Background:
Exposure to air pollution during pregnancy may increase attention-deficit/ hyperactivity disorder (ADHD) symptoms in children, but findings have been inconsistent. We aimed to study this association in a collaborative study of eight European population-based birth/child cohorts, including 29,127 mother-child pairs.
Methods:
Air pollution concentrations [nitrogen dioxide (NO2) and particulate matter (PM)] were estimated at the birth address by land-use regression models based on monitoring campaigns performed between 2008 and 2011. We extrapolated concentrations back in time to exact pregnancy periods. Teachers or parents assessed ADHD symptoms at 3-10 years of age. We classified children as having ADHD symptoms within the borderline/clinical range and within the clinical range using validated cut-offs. We combined all adjusted area-specific effect estimates using random-effects meta-analysis and multiple imputation and applied inverse probability weighting methods to correct for loss to follow-up.
Results:
We classified a total of 2,801 children as having ADHD symptoms within the borderline/clinical range, and 1,590 within the clinical range. Exposure to air pollution during pregnancy was not associated with a higher odds of ADHD symptoms within the borderline/clinical range (e.g., adjusted odds ratio (OR) for ADHD symptoms of 0.95, 95% confidence interval (CI) 0.89-1.01 per 10µg/m increase in NO2 and 0.98, 95%CI 0.80-1.19 per 5µg/m increase in PM2.5). We observed similar associations for ADHD within the clinical range.
Conclusions:
There was no evidence for an increase in risk of ADHD symptoms with increasing prenatal air pollution levels in children aged 3 to 10 years.
Air pollution is a global health threat and causes millions of human deaths annually. The late onset of respiratory diseases in children and adults due to prenatal or perinatal exposure to air pollutants is emerging as a critical concern in human health. Pregnancy and fetal development stages are highly susceptible to environmental exposure and tend to develop a long-term impact in later life. In this review, we briefly glance at the direct impact of outdoor and indoor air pollutants on lung diseases and pregnancy disorders. We further focus on lung complications in later life with early exposure to air pollutants. Epidemiological evidence is provided to show the association of prenatal or perinatal exposure to air pollutants with various adverse birth outcomes, such as preterm birth, lower birth weight, and lung developmental defects, which further associate with respiratory diseases and reduced lung function in children and adults. Mechanistic evidence is also discussed to support that air pollutants impact various cellular and molecular targets at early life, which link to the pathogenesis and altered immune responses related to abnormal respiratory functions and lung diseases in later life. Keywords: Air pollutants, Polycyclic aromatic hydrocarbon, Particulate matter, Early disease origin, Respiratory diseases
Background
Prenatal exposure to environmental pollutants such as mold, lead, pesticides, tobacco, and air pollutants has been suggested to impair cognitive development. Evidence is needed from longitudinal studies to understand their joint impact on child development across time.
Objective
To study associations between exposure to indoor environmental pollutants or outdoor air pollution during pregnancy and offspring cognitive development trajectories through 7 years.
Methods
We included 718 Mexican mother-child pairs. Prenatal exposure to indoor environmental pollutants (mold, ventilation, pesticides, tobacco smoke, and use of vidiartred clay pots) was self-reported by the mothers and integrated into an index, or objectively measured in the case of outdoor air pollutants (nitrogen oxides, benzene, toluene, and xylene). Child global cognitive development was measured at 12, 18, 60, or 84 months. Using Latent Class Growth Analysis, we identified three developmental trajectories (positive = 108, average = 362, low = 248). We used multinomial logistic models to test associations between environmental pollutant score (EPS) or outdoor air pollutants, and cognitive development trajectories.
Results
After adjustment for sociodemographic covariates, EPS was associated with the average (OR = 1.26 95%CI = 1.01, 1.55) and low (OR = 1.41 95%CI = 1.11, 1.79) trajectories compared to positive; where a unit increase in EPS means an additional prenatal exposure to a pollutant. There was no association between outdoor air pollutants and cognitive development trajectories.
Conclusion
Children of women who reported higher exposure to indoor environmental pollutants during pregnancy were more likely to follow worse developmental trajectories through 7 years. These results support the development and testing of interventions to reduce exposure to environmental pollutants during pregnancy and early childhood as a potential strategy to improve long-term cognitive development.
METHODS: We performed a series of analyses using data from a subcohort of 253 Barcelona schoolchildren from the Brain Development and Air Pollution Ultrafine Particles in School Children (BREATHE) project. We averaged satellite-based normalized difference vegetation index (NDVI) across 100-m buffers around all residential addresses since birth to estimate each participant's lifelong exposure to residential surrounding greenness, and we used high-resolution 3D MRIs of brain anatomy to identify regional differences in voxel-wise brain volume associated with greenness exposure. In addition, we performed a supporting substudy to identify regional differences in brain volume associated with measures of working memory (d' from computerized n-back tests) and inattentiveness (hit reaction time standard error from the Attentional Network Task instrument) that were repeated four times over one year. We also performed a second supporting substudy to determine whether peak voxel tissue volumes in brain regions associated with residential greenness predicted cognitive function test scores.
Air pollution exposure and HIV infection can each cause neurocognitive insult in children. The purpose of this study was to test whether children with combined high air pollution exposure and perinatal HIV infection have even greater risk of neurocognitive impairment. This was a cross-sectional study of HIV-uninfected unexposed (HUU) and HIV-infected children and their caregivers in Nairobi, Kenya. We used a detailed neuropsychological battery to evaluate neurocognitive functioning in several domains. We measured caregiver 24-h personal CO exposure as a proxy for child CO exposure and child urinary 1-hydroxypyrene (1-OHP), a biomarker for exposure to polycyclic aromatic hydrocarbons (PAHs). Median 24-h caregiver CO exposure was 6.1 and 3.7 ppm for 45 HIV-infected (mean age 6.6 years) and 49 HUU (mean age 6.7 years), respectively; 48.5% of HIV-infected and 38.6% of HUU had caregiver 24-h CO levels exceeding the WHO recommended level. Median 1-OHP exposure was 0.6 and 0.7 µmol/mol creatinine among HIV-infected and HUU children, respectively. HIV-infected children with high urinary 1-OHP (exceeding 0.68 µmol/mol creatinine) had significantly lower global cognition (p = 0.04), delayed memory (p = 0.01), and attention scores (p = 0.003). Among HUU children, urinary 1-OHP and caregiver 24-h caregiver CO were not significantly associated with neurocognitive function. Our findings suggest that combined chronic exposure to air pollutants and perinatal HIV infection may be associated with poorer neurocognitive outcomes. High prevalence of air pollution exposure highlights the need to reduce these exposures.
Lung cancer is the leading cause of cancer occurrence around the world. When exploring the geographic distribution in lung cancer incidence in Poland, we found that PM10-bound benzo(a)pyrene (B(a)P) emission from domestic heating contributes to lung cancer risk mostly in areas outside the cities and agglomerations (so-called remaining areas). When averaging B(a)P concentrations within provinces, the B(a)P exposure accounts for even 31% to the total lung cancer cases. To check to which extent the concentration of B(a)P could contribute to an increase probability of lung cancer occurrence, the analysis of health risk was performed. The B(a)P concentration data were downloaded from the Polish Chief Inspectorate of Environmental Protection (CIEP) database. Those concerned the period between 2010 and 2015 and included cities, agglomerations, typically rural sites, and the remaining areas. It was found that the mean concentration of B(a)P in the mentioned period, averaged within specific geographic areas, varied from 1.39 ng/m³ at the rural sites to 4.86 ng/m³ in the remaining areas. The inhalation lung cancer risk resulting from the life-long exposure to B(a)P in most conservative (pessimistic) scenario was above the acceptable limits, i.e., E−06. On average, the highest lung cancer risk was found in Opolskie (7.33E−04) and the lowest one in Lubelskie province (1.02E−04), while in the rural areas one order of magnitude lower and amounted to (E−05). Presented results indicate the need for further research on geographic patterns of lung cancer incidence in Poland due to regional differences in air pollution. Such information could be further used for planning long-term strategies to reduce the ambient concentrations of B(a)P.
Cognitive skills are one component of school readiness that reflect a child’s neurodevelopment and are influenced by environmental and social factors. Most studies assess the impact of these factors individually, without taking into consideration the complex interactions of multiple factors. The objective of this study was to examine the joint association of markers of environmental pollution and of social factors on early cognitive skills in an urban cohort of children. For this, we chose isophorone in ambient air as a marker of industrial air pollution. Low quality home learning environments was chosen as a marker of the social factors contributing to cognitive development. Using a subpopulation from the Early Childhood Longitudinal Study, Birth Cohort (N = 4050), isophorone exposure was assigned using the 2002 National Air Toxics Assessment. Home learning environment was assessed with a modified version of the Home Observation for Measurement of the Environment (HOME) Inventory, and standardized math assessment scores were used as a measure of early cognitive skills. Multiple linear regression was used to estimate the effect of both exposures on math scores. After adjustment for confounders, children living in areas with ambient isophorone in the upper quintile of exposure (>0.49 ng/m3) had math scores that were 1.63 points lower than their less exposed peers [95% CI: −2.91, −0.34], and children with lower HOME scores (at or below 9 out of 12) had math scores that were 1.20 points lower than children with better HOME scores [95% CI: −2.30, −0.10]. In adjusted models accounting for identified confounders and both exposures of interest, both high isophorone exposure and low HOME score remained independently associated with math scores [−1.48, 95% CI: −2.79, −0.18; −1.05, 95% CI: −2.15, 0.05, respectively]. There was no statistical evidence of interaction between the two exposures, although children with both higher isophorone exposure and a low HOME score had a decrement in math scale score beyond the additive effect of each exposure. This was primarily observed among male children. These findings suggest that aspects of both the physical and social environments are independently associated with children’s early cognitive skills. Future research aiming to improve children’s early cognitive skills and subsequent school readiness should address both domains.
Prenatal exposure to air pollution has been associated with autism spectrum disorder (ASD) risk but no study has examined associations with ASD severity or functioning. Cognitive ability, adaptive functioning, and ASD severity were assessed in 327 children with ASD from the Childhood Autism Risks from Genetics and the Environment study using the Mullen Scales of Early Learning (MSEL), the Vineland Adaptive Behavior Scales (VABS), and the Autism Diagnostic Observation Schedule calibrated severity score. Estimates of nitrogen dioxide (NO2), particulate matter (PM2.5 and PM10), ozone, and near-roadway air pollution were assigned to each trimester of pregnancy and first year of life. Increasing prenatal and first year NO2 exposures were associated with decreased MSEL and VABS scores. Increasing PM10 exposure in the third trimester was paradoxically associated with improved performance on the VABS. ASD severity was not associated with air pollution exposure.
Purpose of review:
Epidemiological and animal studies suggest that air pollution may negatively affect the central nervous system (CNS) and contribute to CNS diseases. Traffic-related air pollution is a major contributor to global air pollution, and diesel exhaust (DE) is its most important component.
Recent findings:
Several studies suggest that young individuals may be particularly susceptible to air pollution-induced neurotoxicity and that perinatal exposure may cause or contribute to developmental disabilities and behavioral abnormalities. In particular, a number of recent studies have found associations between exposures to traffic-related air pollution and autism spectrum disorders (ASD), which are characterized by impairment in socialization and in communication and by the presence of repetitive and unusual behaviors. The cause(s) of ASD are unknown, and while it may have a hereditary component, environmental factors are increasingly suspected as playing a pivotal role in its etiology, particularly in genetically susceptible individuals. Autistic children present higher levels of neuroinflammation and systemic inflammation, which are also hallmarks of exposure to traffic-related air pollution. Gene-environment interactions may play a relevant role in determining individual susceptibility to air pollution developmental neurotoxicity. Given the worldwide presence of elevated air pollution, studies on its effects and mechanisms on the developing brain, genetic susceptibility, role in neurodevelopmental disorders, and possible therapeutic interventions are certainly warranted.
Objective To investigate associations between exposure to air pollution and child and adolescent mental health.
Design Observational study.
Setting Swedish National Register data on dispensed medications for a broad range of psychiatric disorders, including sedative medications, sleeping pills and antipsychotic medications, together with socioeconomic and demographic data and a national land use regression model for air pollution concentrations for NO2, PM10 and PM2.5.
Participants The entire population under 18 years of age in 4 major counties. We excluded cohort members whose parents had dispensed a medication in the same medication group since the start date of the register. The cohort size was 552 221.
Main outcome measures Cox proportional hazards models to estimate HRs and their 95% CIs for the outcomes, adjusted for individual-level and group-level characteristics.
Results The average length of follow-up was 3.5 years, with an average number of events per 1000 cohort members of ∼21. The mean annual level of NO2 was 9.8 µg/m3. Children and adolescents living in areas with higher air pollution concentrations were more likely to have a dispensed medication for a psychiatric disorder during follow-up (HR=1.09, 95% CI 1.06 to 1.12, associated with a 10 µg/m3 increase in NO2). The association with NO2 was clearly present in 3 out of 4 counties in the study area; however, no statistically significant heterogeneity was detected.
Conclusion There may be a link between exposure to air pollution and dispensed medications for certain psychiatric disorders in children and adolescents even at the relatively low levels of air pollution in the study regions. The findings should be corroborated by others.
The present review synthesizes lines of emerging evidence showing how several samples of children populations living in large cities around the world suffer to some degree neural, behavioral and cognitive changes associated with air pollution exposure. The breakdown of natural barriers warding against the entry of toxic particles, including the nasal, gut and lung epithelial barriers, as well as widespread breakdown of the blood-brain barrier facilitatethe passage of airborne pollutants into the body of young urban residents. Extensive neuroinflammation contributes to cell loss within the central nervous system, and likely is a crucial mechanism by which cognitive deficits may arise. Although subtle, neurocognitive effects of air pollution are substantial, apparent across all populations, and potentially clinically relevant as early evidence of evolving neurodegenerative changes. The diffuse nature of the neuroinflammation risk suggests an integrated neuroscientific approach incorporating current clinical, cognitive, neurophysiological, radiological and epidemiologic research. Neuropediatric air pollution research requires extensive multidisciplinary collaborations to accomplish the goal of protecting exposed children through multidimensional interventions having both broad impact and reach. While intervening by improving environmental quality at a global scale is imperative, we also need to devise efficient strategies on how the neurocognitive effects on local pediatric populations should be monitored.
Systematic reviews and meta-analyses have become increasingly important in health care. Clinicians read them to keep up to date with their field [1],[2], and they are often used as a starting point for developing clinical practice guidelines. Granting agencies may require a systematic review to ensure there is justification for further research [3], and some health care journals are moving in this direction [4]. As with all research, the value of a systematic review depends on what was done, what was found, and the clarity of reporting. As with other publications, the reporting quality of systematic reviews varies, limiting readers' ability to assess the strengths and weaknesses of those reviews.
Several early studies evaluated the quality of review reports. In 1987, Mulrow examined 50 review articles published in four leading medical journals in 1985 and 1986 and found that none met all eight explicit scientific criteria, such as a quality assessment of included studies [5]. In 1987, Sacks and colleagues [6] evaluated the adequacy of reporting of 83 meta-analyses on 23 characteristics in six domains. Reporting was generally poor; between one and 14 characteristics were adequately reported (mean = 7.7; standard deviation = 2.7). A 1996 update of this study found little improvement [7].
In 1996, to address the suboptimal reporting of meta-analyses, an international group developed a guidance called the QUOROM Statement (QUality Of Reporting Of Meta-analyses), which focused on the reporting of meta-analyses of randomized controlled trials [8]. In this article, we summarize a revision of these guidelines, renamed PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses), which have been updated to address several conceptual and practical advances in the science of systematic reviews (Box 1).
Box 1: Conceptual Issues in the Evolution from QUOROM to PRISMA
Completing a Systematic Review Is an Iterative Process
The conduct of a systematic review depends heavily on the scope and quality of included studies: thus systematic reviewers may need to modify their original review protocol during its conduct. Any systematic review reporting guideline should recommend that such changes can be reported and explained without suggesting that they are inappropriate. The PRISMA Statement (Items 5, 11, 16, and 23) acknowledges this iterative process. Aside from Cochrane reviews, all of which should have a protocol, only about 10% of systematic reviewers report working from a protocol [22]. Without a protocol that is publicly accessible, it is difficult to judge between appropriate and inappropriate modifications.
Influences of prenatal and early life exposures to air pollution on cognition are not well-understood.
Examine associations of gestational and childhood exposure to traffic-related pollution with childhood cognition.
We studied 1,109 mother-child pairs in Project Viva, a prospective birth cohort study in Eastern Massachusetts (USA). In mid-childhood (mean age 8.0 years), we measured verbal and non-verbal intelligence, visual motor abilities, and visual memory. For periods in late pregnancy and childhood we estimated spatially and temporally resolved black carbon (BC) and fine particulate matter (PM2.5) exposures, residential proximity to major roadways, and near-residence traffic density. We used linear regression models to examine associations of exposures with cognitive assessment scores, adjusted for potential confounders.
Compared to children living ≥200 m from a major roadway at birth, those living <50 m away had lower non-verbal IQ (-7.5 points; 95% confidence interval (CI): -13.1, -1.9), and somewhat lower verbal IQ (-3.8 points; 95% CI: -8.2, 0.6) and visual motor abilities (-5.3 points; 95% CI: -11.0, 0.4). Cross-sectional associations of major roadway proximity and cognition at mid-childhood were weaker. Prenatal and childhood exposure to traffic density and PM2.5 did not appear associated with poorer cognitive performance. Third trimester and childhood BC exposures were associated with lower verbal IQ in minimally adjusted models, but after adjustment for socioeconomic covariates, associations were attenuated or reversed.
Residential proximity to major roadways during gestation and early-life may affect cognitive development. Influences of pollutants and socioeconomic conditions on cognition may be difficult to disentangle.
Air pollution is a suspected developmental neurotoxicant. Many schools are located in close proximity to busy roads, and traffic air pollution peaks when children are at school. We aimed to assess whether exposure of children in primary school to traffic-related air pollutants is associated with impaired cognitive development.
We conducted a prospective study of children (n = 2,715, aged 7 to 10 y) from 39 schools in Barcelona (Catalonia, Spain) exposed to high and low traffic-related air pollution, paired by school socioeconomic index; children were tested four times (i.e., to assess the 12-mo developmental trajectories) via computerized tests (n = 10,112). Chronic traffic air pollution (elemental carbon [EC], nitrogen dioxide [NO2], and ultrafine particle number [UFP; 10-700 nm]) was measured twice during 1-wk campaigns both in the courtyard (outdoor) and inside the classroom (indoor) simultaneously in each school pair. Cognitive development was assessed with the n-back and the attentional network tests, in particular, working memory (two-back detectability), superior working memory (three-back detectability), and inattentiveness (hit reaction time standard error). Linear mixed effects models were adjusted for age, sex, maternal education, socioeconomic status, and air pollution exposure at home. Children from highly polluted schools had a smaller growth in cognitive development than children from the paired lowly polluted schools, both in crude and adjusted models (e.g., 7.4% [95% CI 5.6%-8.8%] versus 11.5% [95% CI 8.9%-12.5%] improvement in working memory, p = 0.0024). Cogently, children attending schools with higher levels of EC, NO2, and UFP both indoors and outdoors experienced substantially smaller growth in all the cognitive measurements; for example, a change from the first to the fourth quartile in indoor EC reduced the gain in working memory by 13.0% (95% CI 4.2%-23.1%). Residual confounding for social class could not be discarded completely; however, the associations remained in stratified analyses (e.g., for type of school or high-/low-polluted area) and after additional adjustments (e.g., for commuting, educational quality, or smoking at home), contradicting a potential residual confounding explanation.
Children attending schools with higher traffic-related air pollution had a smaller improvement in cognitive development.
Children's urban air pollution exposures result in systemic and brain inflammation and the early hallmarks of Alzheimer's disease (AD). The apolipoprotein E (APOE) ε4 allele is the most prevalent genetic risk for AD. We assessed whether APOE in healthy children modulates cognition, olfaction, and metabolic brain indices. The Wechsler Intelligence Scale for Children (WISC-R) and the University of Pennsylvania Smell Identification Test were administered to 50 Mexico City Metropolitan Area children (13.4 ± 4.8 years, 28 APOE ε3 and 22 APOE ε4). N-acetylaspartate (NAA)/creatine (Cr), choline (Cho)/Cr, myo-inositol (mI)/Cr, and NAA/mI were calculated using proton magnetic resonance spectroscopy in the white matter of the frontal and parietal lobes, hippocampus, and pons. APOE ε4 versus ε3 children had a reduced NAA/Cr ratio in the right frontal white matter and decrements on attention, short-term memory, and below-average scores in Verbal and Full Scale IQ (>10 points). APOE modulated the group effects between WISC-R and left frontal and parietal white matter, and hippocampus metabolites. Soap was the predominantly failed odor in urban children and, in APOE ε4 versus ε3 carriers, strongly correlated with left hippocampus mI/Cr ratio. APOE modulates responses to air pollution in the developing brain. APOE ε4 carriers could have a higher risk of developing early AD if they reside in a polluted environment. APOE, cognition, and olfaction testing and targeted magnetic resonance spectroscopy may contribute to the assessment of urban children and their results could provide new paths toward the unprecedented opportunity for early neuroprotection and AD prevention.
Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants produced by combustion of fossil fuel and other organic materials. Both experimental animal and human studies have reported the harmful impacts of PAH compounds on fetal growth and neurodevelopment, including verbal IQ of children. Here, we have assessed the association between cognitive function of children and prenatal PAH exposures. The study is part of an ongoing, longitudinal investigation of the health effects of prenatal exposure to air pollution on infants and children in Krakow, Poland. The subjects in this report included 170 children whose mothers were enrolled to the study in the first or second trimester of pregnancy whose cord blood were tested for PAH-DNA adducts and who were assessed at age 7 using the Wechsler Intelligence Scale for Children-Revised (WISC-R). The outcome of a priori interest was depressed verbal IQ index (DepVIQ), which is the difference between WISC-R performance and verbal IQ scores. Prenatal PAH exposure was measured by cord blood PAH-DNA adducts, an individual dosimeter, integrating exposure from various sources of exposure over the gestational period. The estimated effect of prenatal PAH exposure on cognitive function was adjusted in multivariable regression for a set of potential confounders (child's gender, parity, maternal education, breastfeeding practice, environmental tobacco smoke (ETS), and postnatal PAH exposure). The prevalence of DepVIQ was significantly higher in children with detectable PAH-DNA adducts compared to those with undetectable adducts (13.7 vs. 4.4 %,). Binary multivariable regression documented that the relative risk of DepVIQ increased threefold with a ln-unit increase in cord blood adducts (relative risk (RR) = 3.0, 95 % confidence interval (CI) 1.3-6.8). Postnatal PAH exposure also increased the risk of DepVIQ (RR = 1.6, 95 % CI 1.1-2.5). Long-term exclusive breastfeeding (at least 6 months) showed a protective effect (RR = 0.3, 95 % CI 0.1-0.9). In conclusion, these results provide further evidence that PAHs are harmful to the developing fetal brain with effects extending through childhood, with implications for the academic success of the children.
Background
The hippocampus is important for memory processing. Several neuropsychiatric diseases including Alzheimer’s disease are associated with reduced hippocampal volume, and further the hippocampus appears vulnerable to environmental insult. Air pollution has been associated with cardiovascular disease, abnormal brain structure, and cognitive deficits.
Objective
Because of hippocampal vulnerability to environmental insults and based on the association between exposure to air pollution and cognitive function and brain structure, we evaluated the association between exposure to toxins in air pollution and left and right hippocampal volume using brain-imaging and air-pollution data from the UK Biobank, a large community-based dataset.
Methods
We used regression modelling to evaluate the association between exposure to nitrogen dioxide, nitrogen oxides, PM2.5, PM2.5-10, and PM10. and left and right hippocampal volume controlling for age, sex, body-mass index, overall health, alcohol use, smoking, educational attainment, socioeconomic status, inverse distance from the nearest major road, and a measure of total brain volume.
Results
In these models, PM2.5 concentration was associated with smaller left hippocampal volume. None of the other measures of air pollution was associated with either left or right hippocampal volume, although interaction models provided some evidence that sex might moderate the relationship between air pollution and hippocampal volume. In adjusted models, age, sex, educational attainment, income, overall health, current smoking, alcohol intake, and body-mass index were associated with hippocampal volume.
Conclusions
PM2.5 at levels found in the United Kingdom was associated with smaller left hippocampal volume. Additional associations between several covariates and hippocampal volumes indicate that hippocampal volume might be associated with several potentially modifiable variables.
Introduction: Fine particle pollution, including diesel exhaust particles (DEP), is a well-recognized and significant threat to public health. Cerebrovascular disease has been shown to be among the pathologies produced by fine particle exposure, and is thought to arise in this context through oxidative and inflammatory mechanisms. The manner by which these mechanisms interface with normal cerebral metabolism in their promotion of cerebrovascular pathogenesis, however, remains to be elucidated. Recent evidence has emerged that implicates a new pathway in post-stroke oxidative injury: gluconeogenesis. Therefore, we investigated whether diesel exhaust particle (DEP)-mediated oxidative injury to brain cells was associated with upregulation of the gluconeogenic pathway.
Methods: Human neuroblastoma SH-SY5Y cells were maintained in complete Dulbecco’s Modified Eagle’s Medium (DMEM)/F12 at 37°C. Cells were exposed to freshly dispersed DEP preparations at 0, 6.25, 12.5, 25, 50, 100, or 200 µg/ml for either 3 or 24 h. Cell survival was then gauged by MTT assay, intracellular oxidative stress was quantified by fluorescence, and expression of gluconeogenic enzymes was assayed by quantitative RT-PCR.
Results: Exposure to increasing concentrations of DEP yielded proportional, significant decreases in cell viability in conjunction with proportional, significant increases in intracellular ROS generation. These findings occurred in the context of DEP-induced reactive gluconeogenesis, as demonstrated by significant transcriptional upregulation of the key regulatory gluconeogenic enzymes PEPCK, PC, G6PC, and FBP.
Conclusion: Gluconeogenesis was induced in human neural cells exposed to fine particles (DEP), in association with cell damage and oxidative stress. These findings suggest that the pathogenesis of cerebrovascular injury due to fine particle pollutant exposure may proceed through derangements in gluconeogenic metabolism.
Abbreviations: DEP: diesel exhaust particles, ICA: intracranial atherosclerosis, ROS: reactive oxygen species
Importance: The etiology of autism spectrum disorder (ASD) is poorly understood, but prior studies suggest associations with airborne pollutants.
Objective: To evaluate the association between prenatal exposures to airborne pollutants and ASD in a large population-based cohort.
Design, Setting, and Participants: This population-based cohort encompassed nearly all births in Metro Vancouver, British Columbia, Canada, from 2004 through 2009, with follow-up through 2014. Children were diagnosed with ASD using a standardized assessment with the Autism Diagnostic Interview–Revised and Autism Diagnostic Observation Schedule. Monthly mean exposures to particulate matter with a diameter less than 2.5 µm (PM2.5), nitric oxide (NO), and nitrogen dioxide (NO2) at the maternal residence during pregnancy were estimated with temporally adjusted, high-resolution land use regression models. The association between prenatal air pollution exposures and the odds of developing ASD was evaluated using logistic regression adjusted for child sex, birth month, birth year, maternal age, maternal birthplace, and neighborhood-level urbanicity and income band. Data analysis occurred from June 2016 to May 2018.
Exposures: Mean monthly concentrations of ambient PM2.5, NO, and NO2 at the maternal residence during pregnancy, calculated retrospectively using temporally adjusted, high-resolution land use regression models.
Main Outcomes and Measures: Autism spectrum disorder diagnoses based on standardized assessment of the Autism Diagnostic Interview–Revised and Autism Diagnostic Observation Schedule. The hypothesis being tested was formulated during data collection.
Results: In a cohort of 132 256 births, 1307 children (1.0%) were diagnosed with ASD by the age of 5 years. The final sample size for the PM2.5-adjusted model was 129 439 children, and for NO and NO2, it was 129 436 children; of these, 1276 (1.0%) were diagnosed with ASD. Adjusted odds ratios for ASD per interquartile range (IQR) were not significant for exposure to PM2.5 during pregnancy (1.04 [95% CI, 0.98-1.10] per 1.5 μg/m3 increase [IQR] in PM2.5) or NO2 (1.06 [95% CI, 0.99-1.12] per 4.8 ppb [IQR] increase in NO2) but the odds ratio was significant for NO (1.07 [95% CI, 1.01-1.13] per 10.7 ppb [IQR] increase in NO). Odds ratios for male children were 1.04 (95% CI, 0.98-1.10) for PM2.5; 1.09 (95% CI, 1.02-1.15) for NO; and 1.07 (95% CI, 1.00-1.13) for NO2. For female children, they were for 1.03 (95% CI, 0.90-1.18) for PM2.5; 0.98 (95% CI, 0.83-1.13) for NO; and 1.00 (95% CI, 0.86-1.16) for NO2.
Conclusions and Relevance: In a population-based birth cohort, we detected an association between exposure to NO and ASD but no significant association with PM2.5 and NO2.
Some recent human and animal studies have suggested that air pollution may affect the central nervous system and contribute to neurodevelopmental outcomes, such as autism spectrum disorder (ASD). We aimed to investigate the association between long-term exposure to ambient air pollution and increased odds of ASD among 2 to 10-year-old children. We conducted a case-control study in Tehran, Iran. Cases were 134 children born between 2004 and 2012 diagnosed with ASD whose mothers were resident in Tehran during their pregnancy, and controls were 388 children without ASD randomly selected from public schools and kindergartens. Land-use regression models were used to estimate their annual mean exposure to ambient particulate matter with aerodynamic diameter ≤10 μm (PM 10), sulfur dioxide (SO 2), benzene, toluene, ethylbenzene, p-xylene, o-xylene, m-xylene (BTEX), and total BTEX. Logistic regression was used for the analyses and adjusted for possible confounding variables. The odds ratios per 1 unit increase in pollutants in the adjusted models were 1.00 (95% CI: 0.99, 1.01) for PM 10 , 0.99 (95% CI: 0.99, 1.00) for SO 2 , 0.96 (0.83, 1.11) for benzene, 1.00 (0.96, 1.04) for toluene, 0.95 (0.79, 1.16) for ethylbenzene, 1.00 (0.78, 1.27) for p-xylene, 1.09 (0.94, 1.27) for o-xylene, 1.01 (0.92, 1.12) for m-xylene, and 0.99 (0.97, 1.01) for total BTEX. We did not find the evidence of association between estimated annual mean exposure to abovementioned ambient air pollutants and increased odds of ASD in children. However, our findings might be due to some important limitations. Further research with better control of confounding variables, improved spatiotemporal exposure estimates, and inclusion of other important markers of air pollution is recommended.
Background
Attention deficit hyperactivity disorder (ADHD) is a frequently occurring neurodevelopmental disorder, symptoms of which first appear in early childhood. Etiology of ADHD is not well understood. We investigated whether outdoor air pollution and greenspace affect ADHD incidence in children residing in Saxony.
Methods
66,823 children, all beneficiaries of the statutory health insurance company AOK PLUS and born between 2000 and 2004, were followed until 2014. We considered any child with at least one ICD-10-GM F90 diagnosis by a child/adolescent psychiatrist, neuropaediatrician, or psychotherapist an ADHD case. Children's home addresses were known up to their four-digit postal code area. Population-weighted mean values of particulate matter with diameter of < 10 μm (PM10), nitrogen dioxide (NO2), and MODIS Normalized Difference Vegetation Index (NDVI) were calculated for 186 postal code areas. Associations with each exposure were assessed by two-level adjusted Poisson regression models.
Results
2044 children (3.06%) were diagnosed with ADHD within the observation period. An increase of PM10 and NO2 by 10 μg/m3 raised the relative risk of ADHD by a factor of 1.97 [95% CI: 1.35–2.86] and 1.32 [1.10–1.58], respectively. A 0.1-unit increase in NDVI decreased the relative risk of ADHD by a factor of 0.82 [0.68–0.98]. Better access to child/adolescent psychiatrists was the most important confounder that increased ADHD risk across all models.
Conclusion
Our results provide some evidence that air pollution might affect ADHD. Future studies with more detailed address information and better control for confounders, in particular socioeconomic status and parental psychopathology, should replicate the observed associations.
Epidemiological studies have demonstrated that air pollution particulate matter (PM) and adsorbed toxicants (organic compounds and trace metals) may affect child development already in utero. Recent studies have also indicated that PM may be a risk factor for neurodevelopmental disorders (NDDs). A pattern of increasing prevalence of attention deficit/hyperactivity disorder (ADHD) has been suggested to partly be linked to environmental pollutants exposure, including PM. Epidemiological studies suggest associations between pre- or postnatal exposure to air pollution components and ADHD symptoms. However, many studies are cross-sectional without possibility to reveal causality. Cohort studies are often small with poor exposure characterization, and confounded by traffic noise and socioeconomic factors, possibly overestimating the study associations. Furthermore, the mechanistic knowledge how exposure to PM during early brain development may contribute to increased risk of ADHD symptoms or cognitive deficits is limited. The closure of this knowledge gap requires the combined use of well-designed longitudinal cohort studies, supported by mechanistic in vitro studies. As ADHD has profound consequences for the children affected and their families, the identification of preventable risk factors such as air pollution exposure should be of high priority.
Suicide is a major public health problem. Previous studies have reported a significant association between acute exposure to air pollution and suicide; little attention has been paid to the long-term effects of air pollution on risk of suicide. We investigated whether long-term exposure to particulate matter of ≤10μm in diameter (PM10), nitrogen dioxide (NO2), and sulfur dioxide (SO2) would be associated with a greater risk of death by suicide. The study sample comprised 265,749 adults enrolled in the National Health Insurance Service-National Sample Cohort (2002-2013) in South Korea. Suicide death was defined as per ICD-10 code. Data on air pollution exposure used nationwide monitoring data, and individual exposure levels were assigned using geographic information systems. Air pollution exposure was categorized as the interquartile range (IQR) and quartiles. Hazards ratios (HRs) were calculated for the occurrence of suicide death after adjusting for potential covariates. During the study period, 564 (0.2%) subjects died from suicide. Increases in IQR pollutants (7.5μg/m3for PM10, 11.8ppb for NO2, and 0.8ppb for SO2) significantly increased HR for suicide death [PM10: HR=3.09 (95% CI: 2.63-3.63); NO2: HR=1.33 (95% CI: 1.09-1.64); and SO2: HR=1.15 (95% CI: 1.07-1.24)]. Compared with the lowest level of air pollutants (Quartile 1), the risk of suicide significantly increased in the highest quartile level (Quartile 4) for PM10(HR=4.03; 95% CI: 2.97-5.47) and SO2(HR=1.65; 95% CI: 1.29-2.11) and in the third quartile for NO2(HR=1.52; 95% CI: 1.17-1.96). HRs for subjects with a physical or mental disorder were higher than that those for subjects without the disorder. Subjects living in metropolitan areas were more vulnerable to long-term PM10exposure than those living in non-metropolitan areas. Long-term exposure to air pollution was associated with a significantly increased risk of suicide death. People having underlying diseases or living in metropolitan areas may be more susceptible to high air pollution exposure.
Background:
Little is known about developmental neurotoxicity of particulate matter composition. We aimed to investigate associations between exposure to elemental composition of outdoor PM2.5 at birth and cognitive and psychomotor functions in childhood.
Methods:
We analyzed data from 4 European population-based birth cohorts in the Netherlands, Germany, Italy and Spain, with recruitment in 2000-2006. Elemental composition of PM2.5 measurements were performed in each region in 2008-2011 and land use regression models were used to predict concentrations at participants' residential addresses at birth. We selected 8 elements (copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc) and used principal component analysis to combine elements from the same sources. Cognitive (general, verbal, and non-verbal) and psychomotor (fine and gross) functions were assessed between 1 and 9years of age. Adjusted cohort-specific effect estimates were combined using random-effects meta-analysis.
Results:
7246 children were included in this analysis. Single element analysis resulted in negative association between estimated airborne iron and fine motor function (-1.25 points [95% CI -2.45 to -0.06] per 100ng/m(3) increase of iron). Association between the motorized traffic component, derived from principal component analysis, and fine motor function was not significant (-0.29 points [95% CI -0.64 to 0.06] per unit increase). None of the elements were associated with gross motor function or cognitive function, although the latter estimates were predominantly negative.
Conclusion:
Our results suggest that iron, a highly prevalent element in motorized traffic pollution, may be a neurotoxic compound. This raises concern given the ubiquity of motorized traffic air pollution.
A few studies have found associations between the exposure to traffic-related air pollution at school and/or home and cognitive development. The impact on cognitive development of the exposure to air pollutants during commuting has not been explored. We aimed to assess the role of the exposure to traffic-related air pollutants during walking commute to school on cognitive development of children. We performed a longitudinal study of children (n = 1,234, aged 7-10 y) from 39 schools in Barcelona (Catalonia, Spain) who commuted by foot to school. Children were tested four times during a 12-month follow-up to characterize their developmental trajectories of working memory (d' of the three-back numbers test) and inattentiveness (hit reaction time standard error of the Attention Network Test). Average particulate matter ≤2.5 μm (PM2.5), Black Carbon (BC) and NO2 concentrations were estimated using Land Use Regression for the shortest walking route to school. Differences in cognitive growth were evaluated by linear mixed effects models with age-by-pollutant interaction terms. Exposure to PM2.5 and BC from the commutes by foot was associated with a reduction in the growth of working memory (an interquartile range increase in PM2.5 and BC concentrations decreased the annual growth of working memory by 5.4 (95% CI [-10.2, -0.6]) and 4.6 (95% CI [-9.0, -0.1]) points, respectively). The findings for NO2 were not conclusive and none of the pollutants were associated with inattentiveness. Efforts should be made to implement pedestrian school pathways through low traffic streets in order to increase security and minimize children's exposure to air pollutants.
Introduction:
Recently, we showed that exposure to traffic-related air pollutants (TRAPs) at school was negatively associated with cognitive development, specifically working memory and inattentiveness, in primary schoolchildren during a course of 12 months. The persistence of such associations over longer periods remains as an open question.
Objective:
To study the longitudinal association between TRAPs at school and cognitive development over a period of 3.5 years.
Methods:
Indoor and outdoor levels of TRAPs (elemental carbon (EC), dioxide nitrogen (NO2), particulate matter (PM2.5) from traffic sources and ultrafine particles (UFP)) were measured at 39 schools across Barcelona during 2012/2013. Working memory, as a measure of cognitive development, was evaluated 4 times in 2012/2013 assessment and was re-evaluated one more time in 2015 using computerized n-back test (3-back d' as main outcome). Linear mixed effects models were used to test the association between TRAPs and 3-back d', adding child and school as random effects to account for the multilevel nature of the data, and school air pollutants levels (one at a time) as predictor.
Results:
We found detrimental associations between all TRAPs and annual change in 3-back d' (working memory) (i.e. slower development of working memory in children attending schools with higher levels of air pollution). The associations (per one interquartile range increase in exposure) were strongest for outdoor NO2 (Coefficient (Coef) = - 4.22, 95% confidence interval (CI), - 6.22, - 2.22) and indoor UFP (Coef = - 4.12, 95%CI, - 5.68, - 1.83). These reductions were equivalent to - 20% (95%CI, - 30.1, - 10.7) and - 19.9% (95%CI, - 31.5, - 8.4) change in annual working memory development associated with one interquartile range increase in outdoor NO2 and indoor UFP, respectively.
Conclusion:
Our findings suggest the persistence of the negative association between TRAPs exposure at school and cognitive trajectory measured by n-back test over a period of 3.5 years.
Data-driven machine learning methods present an opportunity to simultaneously assess the impact of multiple air pollutants on health outcomes. The goal of this study was to apply a two-stage, data-driven approach to identify associations between air pollutant exposure profiles and children's cognitive skills. Data from 6900 children enrolled in the Early Childhood Longitudinal Study, Birth Cohort, a national study of children born in 2001 and followed through kindergarten, were linked to estimated concentrations of 104 ambient air toxics in the 2002 National Air Toxics Assessment using ZIP code of residence at age 9 months. In the first-stage, 100 regression trees were learned to identify ambient air pollutant exposure profiles most closely associated with scores on a standardized mathematics test administered to children in kindergarten. In the second-stage, the exposure profiles frequently predicting lower math scores were included within linear regression models and adjusted for confounders in order to estimate the magnitude of their effect on math scores. This approach was applied to the full population, and then to the populations living in urban and highly-populated urban areas. Our first-stage results in the full population suggested children with low trichloroethylene exposure had significantly lower math scores. This association was not observed for children living in urban communities, suggesting that confounding related to urbanicity needs to be considered within the first-stage. When restricting our analysis to populations living in urban and highly-populated urban areas, high isophorone levels were found to predict lower math scores. Within adjusted regression models of children in highly-populated urban areas, the estimated effect of higher isophorone exposure on math scores was −1.19 points (95% CI −1.94, −0.44). Similar results were observed for the overall population of urban children. This data-driven, two-stage approach can be applied to other populations, exposures and outcomes to generate hypotheses within high-dimensional exposure data.
Background:
Prenatal and postnatal exposure to air pollution has been linked to cognitive impairment in children, but very few studies have assessed its association with attentional function.
Objectives:
To evaluate the association between prenatal and postnatal exposure to nitrogen dioxide (NO2) and attentional function in children at 4-5years of age.
Methods:
We used data from four regions of the Spanish INMA-Environment and Childhood-Project, a population-based birth cohort. Using land-use regression models (LUR), we estimated prenatal and postnatal NO2 levels in all of these regions at the participants' residential addresses. We assessed attentional function using the Kiddie-Conners Continuous Performance Test (K-CPT). We combined the region-specific adjusted effect estimates using random-effects meta-analysis.
Results:
We included 1298 children with complete data. Prenatal exposure to NO2 was associated with an impaired standard error of the hit reaction time (HRT(SE)) (increase of 1.12ms [95% CI; 0.22 a 2.02] per 10μg/m(3) increase in prenatal NO2) and increased omission errors (6% [95% CI; 1.01 to 1.11] per 10μg/m(3) increase in prenatal NO2). Postnatal exposure to NO2 resulted in a similar but borderline significant increase of omission errors (5% [95% CI; =0.99 to 1.11] per 10μg/m(3) increase in postnatal NO2). These associations did not vary markedly between regions, and were mainly observed in girls. Commission errors and lower detectability were associated with prenatal and postnatal exposure to NO2 only in some regions.
Conclusions:
This study indicates that higher exposure to ambient NO2, mainly during pregnancy and to a lesser extent postnatally, is associated with impaired attentional function in children at 4-5years of age.
Background:
Epidemiological studies have implicated air pollution in the causation of neurodevelopmental disorders, including attention-deficit hyperactivity disorder (ADHD), but definitive evidence of this linkage is lacking.
Objectives:
We examined the association between cumulative exposure to air pollutants from birth to diagnosis, particularly particulate matter of <10μm (PM10) and nitric dioxide (NO2), and childhood ADHD.
Methods:
We used the National Health Insurance Service-National Sample Cohort (2002-2012), a population-wide health insurance claims dataset. A total of 8936 infants (age 0) born between January 2002 and December 2002 were followed-up for a 10-year period (2003-2012). ADHD was defined as per ICD-10 code F90.0. Exposure levels of PM10 and NO2 were extrapolated using geographic information systems and collated with the subjects' administrative district code, and individual exposure levels assigned. Hazard ratios (HRs) were calculated for the development of ADHD, after adjusting for gender, metropolitan area, income, and history of diseases.
Results:
During the study period, ADHD occurred in 314 subjects (3.5%). With the increase in 1μg/m(3) of air pollutants, the HRs of childhood ADHD were 1.18 (95% CI: 1.15-1.21) in case of PM10 and 1.03 (95% CI: 1.02-1.04) in case of NO2. Compared with infants with the lowest tertile of PM10 or NO2 exposure, those with the highest tertile of PM10 (HR=3.88; 95% CI: 2.87-5.23) or NO2 (HR=2.10; 95% CI, 1.54-2.85) exposure had a 2 to 3 fold increased risk for ADHD.
Conclusion:
Exposure to PM10 and NO2 was associated with the incidence of ADHD in childhood.
Recent research indicates that airborne copper exposure in scholar children negatively affects brain functioning. These effects are likely to be influenced by the efficiency of copper metabolism, which is partly regulated by the ATPase copper transporting beta (ATP7B) gene. We investigated whether indoor and outdoor airborne copper exposure is differentially associated with child inattentiveness depending on genetic variation within the ATP7B gene in 1645 scholar children from the BREATHE project. Outdoor (courtyard) and indoor (classroom) air pollution levels were measured during class hours in each school. Inattentiveness was assessed through a follow-up with four measurements via the Attentional Network Test (4475 observations). Linear mixed models considering repeated measures were conducted to assess genetic and exposure main and interaction effects. Two interactions were detected indicating that ATP7B-rs1061472 (P for interaction 0.016) and ATP7B-rs1801243 (P for interaction 0.003) polymorphisms modified the association between indoor copper exposure and inattentiveness. Stratified analysis by genotypes revealed that both outdoor and indoor copper exposure increased inattentiveness in rs1061472-CC and rs1801243-CC carriers. These findings suggest that the genetic background promotes the association between airborne copper exposure at school with inattentiveness in children.
Children's air pollution exposures are associated with systemic and brain inflammation and the early hallmarks of Alzheimer's disease (AD). The Apolipoprotein E (APOE) 4 allele is the most prevalent genetic risk for AD, with higher risk for women. We assessed whether gender, BMI, APOE and metabolic variables in healthy children with high exposures to ozone and fine particulate matter (PM2.5) influence cognition. The Wechsler Intelligence Scale for Children (WISC-R) was administered to 105 Mexico City children (12.32±5.4 years, 69 APOE 3/3 and 36 APOE 3/4). APOE 4v 3 children showed decrements on attention and short-term memory subscales, and below-average scores in Verbal, Performance and Full Scale IQ. APOE 4 females had higher BMI and females with normal BMI between 75-94% percentiles had the highest deficits in Total IQ, Performance IQ, Digit Span, Picture Arrangement, Block Design and Object Assembly. Fasting glucose was significantly higher in APOE 4 children p=0.006, while Gender was the main variable accounting for the difference in insulin, HOMA-IR and leptin (p<.05). Gender, BMI and APOE influence children's cognitive responses to air pollution and glucose is likely a key player. APOE 4 heterozygous females with >75% to <94% BMI percentiles are at the highest risk of severe cognitive deficits (1.5-2SD from average IQ). Young female results highlight the urgent need for gender-targeted health programmes to improve cognitive responses. Multidisciplinary intervention strategies could provide paths for prevention or amelioration of female air pollution targeted cognitive deficits and possible long-term AD progression.
Children are more vulnerable to the effects of environmental elements due to their active developmental processes. Exposure to urban air pollution has been associated with poorer cognitive performance, which is thought to be a result of direct interference with brain maturation. We aimed to assess the extent of such potential effects of urban pollution on child brain maturation using general indicators of vehicle exhaust measured in the school environment and a comprehensive imaging evaluation. A group of 263 children, aged 8 to 12 years, underwent MRI to quantify regional brain volumes, tissue composition, myelination, cortical thickness, neural tract architecture, membrane metabolites, functional connectivity in major neural networks and activation/deactivation dynamics during a sensory task. A combined measurement of elemental carbon and NO2 was used as a putative marker of vehicle exhaust. Air pollution exposure was associated with brain changes of a functional nature, with no evident effect on brain anatomy, structure or membrane metabolites. Specifically, a higher content of pollutants was associated with lower functional integration and segregation in key brain networks relevant to both inner mental processes (the default mode network) and stimulus-driven mental operations. Age and performance (motor response speed) both showed the opposite effect to that of pollution, thus indicating that higher exposure is associated with slower brain maturation. In conclusion, urban air pollution appears to adversely affect brain maturation in a critical age with changes specifically concerning the functional domain.
Background:
Early life exposure to air pollution has been linked with cognitive impairment in children, but the results have not been conclusive. We analyzed the association between traffic-related air pollution and cognitive function in a prospective birth cohort in Rome.
Methods:
A cohort of 719 newborns was enrolled in 2003-2004 as part of the GASPII project. At 7 years of age, 474 children took the Wechsler Intelligence Scale for Children-III to assess their cognitive development in terms of IQ composite scores. Exposure to air pollutants (NO2, PMcoarse, PM2.5, PM2.5 absorbance) at birth was assessed using land use regression models. We also considered variables indicating traffic intensity. The effect of environmental pollution on IQ was evaluated performing a linear regression model for each outcome, adjusting for gender, child age at cognitive test, maternal age at delivery, parental educational level, siblings, socio-economic status, maternal smoking during pregnancy, tester. To account for selection bias at enrolment and during follow-up, the regression models were weighted for the inverse probabilities of participation and follow-up.
Results:
A 10 µg/m higher NO2 exposure during pregnancy was associated with 1.4 fewer points (95%CI:-2.6 to -0.20) of Verbal IQ, and 1.4 fewer points (95%CI:-2.7 to -0.20) of Verbal Comprehension IQ. Similar associations were found for traffic intensity in a 100mt buffer around home. Other pollutantsshowed negative associationswith larger confidence intervals.
Conclusions:
Consistent with previous evidence, this study suggests an association of exposure to NO2 and traffic intensity with the verbal area of cognitive development.
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous and neurotoxic environmental contaminants. Prenatal PAH exposure is associated with subsequent cognitive and behavioral disturbances in childhood.
To identify the effects of prenatal PAH exposure on brain structure and to assess the cognitive and behavioral correlates of those abnormalities in school-age children.
Cross-sectional imaging study in a representative community-based cohort followed up prospectively from the fetal period to ages 7 to 9 years. The setting was urban community residences and an academic imaging center. Participants included a sample of 40 minority urban youth born to Latina (Dominican) or African American women. They were recruited between February 2, 1998, and March 17, 2006.
Morphological measures that index local volumes of the surface of the brain and of the white matter surface after cortical gray matter was removed.
We detected a dose-response relationship between increased prenatal PAH exposure (measured in the third trimester but thought to index exposure for all of gestation) and reductions of the white matter surface in later childhood that were confined almost exclusively to the left hemisphere of the brain and that involved almost its entire surface. Reduced left hemisphere white matter was associated with slower information processing speed during intelligence testing and with more severe externalizing behavioral problems, including attention-deficit/hyperactivity disorder symptoms and conduct disorder problems. The magnitude of left hemisphere white matter disturbances mediated the significant association of PAH exposure with slower processing speed. In addition, measures of postnatal PAH exposure correlated with white matter surface measures in dorsal prefrontal regions bilaterally when controlling for prenatal PAH.
Our findings suggest that prenatal exposure to PAH air pollutants contributes to slower processing speed, attention-deficit/hyperactivity disorder symptoms, and externalizing problems in urban youth by disrupting the development of left hemisphere white matter, whereas postnatal PAH exposure contributes to additional disturbances in the development of white matter in dorsal prefrontal regions.
Background:
Accumulating evidence from laboratory animal and human studies suggests that air pollution exposure during pregnancy affects cognitive and psychomotor development in childhood.
Methods:
We analyzed data from 6 European population-based birth cohorts-GENERATION R (The Netherlands), DUISBURG (Germany), EDEN (France), GASPII (Italy), RHEA (Greece), and INMA (Spain)-that recruited mother-infant pairs from 1997 to 2008. Air pollution levels-nitrogen oxides (NO2, NOx) in all regions and particulate matter (PM) with diameters of <2.5, <10, and 2.5-10 μm (PM2.5, PM10, and PMcoarse, respectively) and PM2.5 absorbance in a subgroup-at birth addresses were estimated by land-use regression models, based on monitoring campaigns performed primarily between 2008 and 2011. Levels were back-extrapolated to exact pregnancy periods using background monitoring sites. Cognitive and psychomotor development was assessed between 1 and 6 years of age. Adjusted region-specific effect estimates were combined using random-effects meta-analysis.
Results:
A total of 9482 children were included. Air pollution exposure during pregnancy, particularly NO2, was associated with reduced psychomotor development (global psychomotor development score decreased by 0.68 points [95% confidence interval = -1.25 to -0.11] per increase of 10 μg/m in NO2). Similar trends were observed in most regions. No associations were found between any air pollutant and cognitive development.
Conclusions:
Air pollution exposure during pregnancy, particularly NO2 (for which motorized traffic is a major source), was associated with delayed psychomotor development during childhood. Due to the widespread nature of air pollution exposure, the public health impact of the small changes observed at an individual level could be considerable.