Air Pollution and Cognition in Children

The authors examined whether air pollution at school (nitrogen dioxide) is associated with poorer child cognition and health and whether adjustment for air pollution explains or moderates previously observed associations between aircraft and road traffic noise at school and children's cognition in the 2001–2003 Road Traffic and Aircraft Noise Exposure and Children's Cognition and Health (RANCH) project. This secondary analysis of a subsample of the United Kingdom RANCH sample examined 719 children who were 9–10 years of age from 22 schools around London's Heathrow airport for whom air pollution data were available. Data were analyzed using multilevel modeling. Air pollution exposure levels at school were moderate, were not associated with a range of cognitive and health outcomes, and did not account for or moderate associations between noise exposure and cognition. Aircraft noise exposure at school was significantly associated with poorer recognition memory and conceptual recall memory after adjustment for nitrogen dioxide levels. Aircraft noise exposure was also associated with poorer reading comprehension and information recall memory after adjustment for nitrogen dioxide levels. Road traffic noise was not associated with cognition or health before or after adjustment for air pollution. Moderate levels of air pollution do not appear to confound associations of noise on cognition and health, but further studies of higher air pollution levels are needed.

Air pollution has been linked to various health problems in children, including respiratory and neurological issues. Existing research has also found that exposure to air pollution can affect children's cognitive ability and academic performance, with some studies showing a decrease in test scores and grade point averages associated with increased exposure to hazardous air pollution. This study examined the association between air pollution and children’s academic performance in Chile. This research addressed a critical gap in the literature by providing data from an understudied context and tracking children's academic performance at an individual level over time. We constructed a panel dataset that followed students from 1st to 8th grade and estimated their exposure to PM2.5, based on the distance of their school to air monitoring stations from elementary to middle school. We tracked students' academic performance using a longitudinal fixed-effects regression model to assess the relationship between their grade point average (GPA) and air pollution. The results revealed that, on average, an increase in the percentage of days exceeding different official air quality standards significantly affected students' annual GPA. The study also showed that academic performance among students from families with lower economic resources is disproportionately affected by air pollution. The findings underscore the pressing issue of environmental justice, highlighting that numerous students attend schools in the unhealthy environments of several Chilean cities that frequently bear the burden of socioeconomic disadvantage.

This study explores the adverse impact of air pollution, caused by emissions from brick kilns, on the children’s cognitive ability and physical health. A survey of children between the age of 5 and 12 years was conducted in the Peshawar district of KP province of Pakistan. The concentrations of particulate matters (PM10 and PM2.5) were found to be higher in areas within 3 km radius of brick kilns (treatment group) compared to those that are outside of this defined radius (comparison group). By employing propensity score matching method, the study found that exposure to brick kiln pollution has significant negative effect on children’s cognitive ability and physical health. These results advocate that, in addition to increasing the direct health cost, brick kiln pollution also has adverse long-term welfare consequences through indirect and unobservable effects.

BackgroundLiving 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. MethodsData 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. ResultsThe 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. ConclusionsIn 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.

Background: Natural vegetation, or "greenness," may influence cognition by increasing physical activity or buffering air pollution exposure. Early life influences of greenness on cognition, and the mediating roles of physical activity and air pollution, are not well understood. Aim: We examined associations of early childhood neighborhood greenness with mid-childhood cognition. We quantified the extent to which physical activity and air pollution explained this association.Methods: We studied 857 mother–child pairs in Project Viva, a pre-birth cohort study in Massachusetts. In early childhood (median 3.2y), we estimated residential greenness using 30m resolution Landsat satellite imagery [Normalized Difference Vegetation Index], residential particulate matter using spatiotemporal models, and number of hours/day spent in active play, reported by parents, for physical activity. In mid-childhood (7.7y), we administered standardized assessments of verbal and nonverbal intelligence, visual motor abilities (VMA), and visual memory (VM) as outcomes. Using linear regression, we examined associations of early childhood greenness with mid-childhood cognition, adjusting for demographic and socioeconomic factors. We used a causal mediation framework to determine the mediation effect through physical activity and air pollution. Results: The mean(SD) for verbal IQ was 114(14), non-verbal IQ was 107(17), VMA was 93(17), and VM was 17(4). Children living in the highest 3 greenness quartiles vs. lowest in early childhood had higher verbal intelligence (2.0 points, 95%CI: -0.06, 4.1), and higher VM (1.0 point; 95% CI: 0.3, 1.8), but lower VMA (-2.6 points, 95%CI: -5.5, 0.2). We did not observe associations of greenness with non-verbal intelligence. The associations of greenness on verbal intelligence, VM or VMA were not mediated by air pollution or physical activity (e.g.indirect effect on verbal intelligence through air pollution:-0.5, 95%CI:-1.2,0.2). Conclusions: Early childhood greenness may affect verbal intelligence, VM and VMA through other mechanisms different than air pollution or physical activity, perhaps through lowering stress levels.

The most well-known health effects of environmental degradation are related to air pollution, water quality, diet, poor sanitation, and hazardous chemicals. Air pollution is the biggest environmental health risk today. It affects the most vulnerable populations and is linked to heart diseases, strokes, lung diseases, lung cancer, and other organ diseases. Also, it affects neurodevelopment and cognitive abilities in children, can trigger childhood asthma and cancer, and can lead to chronic diseases such as heart attacks later in their lives. Indoor air pollution and the combustion of solid fuelsleadto a large number of premature deaths from diseases caused by dangerousinhaled particles, especially in children. In addition, improper collection of wastethat pollutes the soil, water, and atmosphere has been shown to be directly linked to public health, so the development and implementation of new waste management methods are imperative. With this work, we emphasize that children, in particular, have lifelong impacts on their health, educational prospects, and quality of life from air pollution and environmental degradation, and therefore monitoring, evaluation, and special planning for their health and well-being are required. The information gap needs to be immediately filled by raising awareness in society through educational programs in schools, the community, and the media, as well as by immediately implementingcorresponding policies to achieve these goals.

OPINION article Front. Psychol., 09 July 2012Sec. Developmental Psychology https://doi.org/10.3389/fpsyg.2012.00217

The research exploring the association between the built environment and children's mental health and cognitive abilities has produced mixed results. This may be due to the inconsistency in the approach taken to describe the built environment. This study, using data from the Millennium Cohort Study (MCS), a large general-population birth cohort, considered simultaneously several measures to describe it when the participant child was 3 years old, including neighbourhood disorder (assessed by an MCS interviewer by direct observation of several physical and social aspects of the immediate neighbourhood), area green space, air pollution, urbanicity and neighbourhood socio-economic disadvantage. It then explored its role in the trajectory of mental health (measured with the Strengths and Difficulties Questionnaire-SDQ) and cognitive ability (measured with the British Ability Scales-BAS) across ages 3–11 years in 4454 children of stayer families in England. Using growth curve modelling we found that neighbourhood disorder was associated with emotional symptoms and conduct problems at age 3 and with the trajectory of cognitive ability from ages 3 to 11. These associations were robust to controls for quality of the indoor housing environment and parental mental health and socio-economic status. Neither green space nor air pollution had any effect on our outcomes. Our findings shed light on the importance of specific aspects of the built environment for mental health and cognition during childhood. They also highlight the value of using direct observation of the immediate neighbourhood.

In-utero exposure to air pollution and early-life neural development and cognition

Nutrition and epigenetic changes is the emerging topic of interest in the present scenario to understand the effects of increased supplementation of micronutrients like Folic Acid (FA). The study is taken up in the public health interest, to evaluate the importance of balancing the different micronutrients in the diet to avoid unbalanced nutritional disorders and other health complications later in life. It has been hypothesized that disease risks after birth or later in life can be determined by paternal or maternal diet. This raised an interest to study in-utero effects of environmental exposures like air pollution, toxins, nutrition, etc. It had been assumed that during embryonic period most of the dividing tissues get exposed to the environmental insults and that change results in predisposition of cancer or other health outcomes. There could be the possibility of maternal exposures like nutrition may alter the intrauterine one-carbon metabolism or the precursor milieu and may be involved in the disruption of one-carbon metabolism in developing offspring. Modification in methyl me of offspring with subsequent changes in phenotypes has been noted in the preliminary studies with increased folic acid (FA) supplementation during pregnancy. Maternal folate deficiency has been implicated as a cause of prematurity and both folate deficiency and cobalamin deficiency have been implicated in recurrent fetal loss and neural tube defects. Folic acid supplementation at the time of conception and in the first 12 weeks of pregnancy is expected to reduce by 70% the incidence of neural tube defects (NTDs) (meningomyelocele, encephalocele and spina bifida) in the fetus. Most of the protective effect can be achieved by taking folic acid, 0.4 mg daily at the time of conception. However there is no clear relationship between maternal folatestatus and the fetal abnormalities. It has been observed that, the lower the maternal folate, the greater the risk to the fetus. On the other hand maternal cobalamin status is a strong predictor of vitamin B12 in breastfed infants up to at least 6 months of age. Because of the transfer from mother to offspring during pregnancy and lactation, maternal requirements during this period are increased and deficiency may occur. The influence of low vitamin B12 during pregnancy may have cognitive ability of children later in life. Hypothyroidism is caused by insufficient production of thyroid hormones by the thyroid gland. In females, hypothyroidism is associated mainly with oligomenorrhea.

BackgroundDecreased 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...

<b>Study question:</b> Decreased adult lung function predicts 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 hypothesised that childhood lung function would longitudinally predict cognitive ability. <b>Methods:</b> Lung function was measured at age 8 (Forced Expiratory Volume [FEV1], Forced Vital Capacity [FVC]; % predicted), and cognitive ability at 8 (Wechsler Intelligence Scale for Children, 3rd edition) and 15 (Wechsler Abbreviated Scale of Intelligence), in the Avon Longitudinal Study of Parents and Children. Potential confounders were identified as preterm birth, birthweight, breastfeeding duration, prenatal maternal smoking, childhood environmental tobacco smoke exposure, socioeconomic status, and prenatal/childhood air pollution exposure. Uni- and multivariable linear models (n range=2,332-6,672) were fitted to assess the effect of lung function on cognitive scores, and longitudinal change relative to peers. <b>Results:</b> In univariate analyses, FEV1 and FVC at age 8 were associated with cognitive ability at both ages, but after adjustment, only FVC affected full-scale IQ (FSIQ) at ages 8 (β=0.09 [95% CI 0.05, 0.12; p&lt;0.001]), and 15 (β=0.06 [0.03, 0.10; p=0.001]). We found little evidence that lung function influenced change in FSIQ percentile ranking. <b>Interpretation:</b> Reduced FVC is associated with decreased cognitive ability in children. This low-magnitude effect attenuates between ages 8 and 15, and no impact is evident on change in FSIQ relative to peers. Our results support an association between FVC and cognition across the life course.

“Air pollution is bad for my health”: Hungarian children's knowledge of the role of environment in health and disease

Introduction: Prenatal environmental exposures have been associated with children’s cognitive, behavioral, and mental health problems, and alterations in DNA methylation have been hypothesized as an underlying biological mechanism. However, when testing this hypothesis, it is often difficult to overcome the problem of multiple comparisons in statistical testing when evaluating a large number of developmental outcomes and DNA methylation sites as potential mediators. The objective of this study is to implement a ‘meet-in-the-middle’ approach with a sequential roadmap to address this concern. Methods: In the Columbia Center for Children’s Environmental Health birth cohort study, we implemented a 5-step sequential process for identifying CpG sites that mediate associations between prenatal environmental exposures and cognitive, behavioral, and mental health problems as measured by the Wechsler Intelligence Scale for Children-Fourth Edition (WISC-IV) and the Child Behavior Checklist (CBCL). These steps include 1) the identification of biological pathways that are relevant to each outcome of interest; 2) selection of a set of genes and CpGs on genes that are significantly associated with the outcomes; 3) identification of exposures that are significantly associated with selected CpGs; 4) examination of exposure-outcome relationships among those where significant CpGs were identified; and 5) mediation analysis of the selected exposures and corresponding outcomes. In this study, we considered a spectrum of environmental exposure classes including environmental phenols, pesticides, phthalates, flame retardants and air pollutants. Results: Among all considered exposures and outcomes, we found one CpG site (cg27510182) on gene (DAB1) that potentially mediates the effect of exposure to PAH on CBCL social problems at children aged 7. Conclusion: This ‘meet-in-the-middle’ approach attenuates concerns regarding multiple comparisons by focusing on genes and pathways that are biologically relevant for the hypothesis.

Commentary: Height and intelligence