Air pollution linked to increases in violent criminal behavior.
Here are two articles about this topic. The first article is very easy to understand, and the other one is formal.
The easy to understand one:
https://www.sph.umn.edu/news/air-pollution-linked-to-increases-in-violent-criminal-behavior/
The formal and academic article:
https://pubmed.ncbi.nlm.nih.gov/31430264/
Acute Air Pollution Exposure and the Risk of Violent Behavior in the United States
Background: Violence is a leading cause of death and an important public health threat, particularly among adolescents and young adults. However, the environmental causes of violent behavior are not well understood. Emerging evidence suggests exposure to air pollution may be associated with aggressive or impulsive reactions in people.
Methods: We applied a two-stage hierarchical time-series model to estimate change in risk of violent and nonviolent criminal behavior associated with short-term air pollution in U.S. counties (2000-2013). We used daily monitoring data for ozone and fine particulate matter (PM2.5) from the Environmental Protection Agency and daily crime counts from the Federal Bureau of Investigation. We evaluated the exposure-response relation and assessed differences in risk by community characteristics of poverty, urbanicity, race, and age.
Results: Our analysis spans 301 counties in 34 states, representing 86.1 million people and 721,674 days. Each 10 µg/m change in daily PM2.5 was associated with a 1.17% (95% confidence interval [CI] = 0.90, 1.43) and a 10 ppb change in ozone with a 0.59% (95% CI = 0.41, 0.78) relative risk increase (RRI) for violent crime. However, we observed no risk increase for nonviolent property crime due to PM2.5 (RRI: 0.11%; 95% CI = -0.09, 0.31) or ozone (RRI: -0.05%; 95% CI = -0.22, 0.12). Our results were robust across all community types, except rural regions. Exposure-response curves indicated increased violent crime risk at concentrations below regulatory standards.
Conclusions: Our results suggest that short-term changes in ambient air pollution may be associated with a greater risk of violent behavior, regardless of community type.
Fine particulate matter exposure during childhood relates to hemispheric-specific differences in brain structure.
Background: Emerging findings have increased concern that exposure to fine particulate matter air pollution (aerodynamic diameter ≤ 2.5 μm; PM2.5) may be neurotoxic, even at lower levels of exposure. Yet, additional studies are needed to determine if exposure to current PM2.5 levels may be linked to hemispheric and regional patterns of brain development in children across the United States.
Objectives: We examined the cross-sectional associations between geocoded measures of concurrent annual average outdoor PM2.5 exposure, regional- and hemisphere-specific differences in brain morphometry and cognition in 10,343 9- and 10- year-old children.
Methods: High-resolution structural T1-weighted brain magnetic resonance imaging (MRI) and NIH Toolbox measures of cognition were collected from children at ages 9-10 years. FreeSurfer was used to quantify cortical surface area, cortical thickness, as well as subcortical and cerebellum volumes in each hemisphere. PM2.5 concentrations were estimated using an ensemble-based model approach and assigned to each child's primary residential address collected at the study visit. We used mixed-effects models to examine regional- and hemispheric- effects of PM2.5 exposure on brain estimates and cognition after considering nesting of participants by familial relationships and study site, adjustment for socio-demographic factors and multiple comparisons.
Results: Annual residential PM2.5 exposure (7.63 ± 1.57 µg/m3) was associated with hemispheric specific differences in gray matter across cortical regions of the frontal, parietal, temporal and occipital lobes as well as subcortical and cerebellum brain regions. There were hemispheric-specific associations between PM2.5 exposures and cortical surface area in 9/31 regions; cortical thickness in 22/27 regions; and volumes of the thalamus, pallidum, and nucleus accumbens. We found neither significant associations between PM2.5 and task performance on individual measures of neurocognition nor evidence that sex moderated the observed associations.
Discussion: Even at relatively low-levels, current PM2.5 exposure across the U.S. may be an important environmental factor influencing patterns of structural brain development in childhood. Prospective follow-up of this cohort will help determine how current levels of PM2.5 exposure may affect brain development and subsequent risk for cognitive and emotional problems across adolescence.
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https://pubmed.ncbi.nlm.nih.gov/28915125/
Air pollution, aeroallergens and suicidality: a review of the effects of air pollution and aeroallergens on suicidal behavior and an exploration of possible mechanisms
Abstract
Objective: Risk factors for suicide can be broadly categorized as sociodemographic, clinical and treatment. There is interest in environmental risk and protection factors for suicide. Emerging evidence suggests a link between environmental factors in the form of air pollution and aeroallergens in relation to suicidality.
Methods: Herein, we conducted a systematic review of 15 articles which have met inclusion criteria on the aforementioned effects.
Results: The majority of the reviewed articles reported an increased suicide risk alongside increased air pollutants or aeroallergens (i.e. pollen) increase; however, not all environmental factors were explored equally. In specific, studies that were delimited to evaluating particulate matter (PM) reported a consistent association with suicidality. We also provide a brief description of putative mechanisms (e.g. inflammation and neurotransmitter dysregulation) that may mediate the association between air pollution, aeroallergens and suicidality.
Conclusion: Available evidence suggests that exposure to harmful air quality may be associated with suicidality. There are significant public health implications which are amplified in regions and countries with greater levels of air pollution and aeroallergens. In addition, those with atopic sensitivity may represent a specific subgroup that is at risk.
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https://pubmed.ncbi.nlm.nih.gov/25522338/
The association between maternal exposure to particulate matter (PM) air pollution and odds of ASD in her child.
Autism spectrum disorder and particulate matter air pollution before, during, and after pregnancy: a nested case-control analysis within the Nurses' Health Study II Cohort
Background: Autism spectrum disorder (ASD) is a developmental disorder with increasing prevalence worldwide, yet has unclear etiology.
Objective: We explored the association between maternal exposure to particulate matter (PM) air pollution and odds of ASD in her child.
Methods: We conducted a nested case-control study of participants in the Nurses' Health Study II (NHS II), a prospective cohort of 116,430 U.S. female nurses recruited in 1989, followed by biennial mailed questionnaires. Subjects were NHS II participants' children born 1990-2002 with ASD (n = 245), and children without ASD (n = 1,522) randomly selected using frequency matching for birth years. Diagnosis of ASD was based on maternal report, which was validated against the Autism Diagnostic Interview-Revised in a subset. Monthly averages of PM with diameters ≤ 2.5 μm (PM2.5) and 2.5-10 μm (PM10-2.5) were predicted from a spatiotemporal model for the continental United States and linked to residential addresses.
Results: PM2.5 exposure during pregnancy was associated with increased odds of ASD, with an adjusted odds ratio (OR) for ASD per interquartile range (IQR) higher PM2.5 (4.42 μg/m3) of 1.57 (95% CI: 1.22, 2.03) among women with the same address before and after pregnancy (160 cases, 986 controls). Associations with PM2.5 exposure 9 months before or after the pregnancy were weaker in independent models and null when all three time periods were included, whereas the association with the 9 months of pregnancy remained (OR = 1.63; 95% CI: 1.08, 2.47). The association between ASD and PM2.5 was stronger for exposure during the third trimester (OR = 1.42 per IQR increase in PM2.5; 95% CI: 1.09, 1.86) than during the first two trimesters (ORs = 1.06 and 1.00) when mutually adjusted. There was little association between PM10-2.5 and ASD.
Conclusions: Higher maternal exposure to PM2.5 during pregnancy, particularly the third trimester, was associated with greater odds of a child having ASD.
Notes from the website owner: PM2.5 are tiny particles found in pollution. ASD is autism spectrum disorder.
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5003346/
The Novel Relationship between Urban Air Pollution and Epilepsy.
The data concerning the association between environmental pollution and epilepsy attacks are limited. The aim of this study was to explore the association between acute air pollution exposure and epilepsy attack.
Methods
A hospital record-based study was carried out in Xi’an, a heavily-polluted metropolis in China. Daily baseline data were obtained. Time-series Poisson regression models were applied to analyze the association between air pollution and epilepsy.
Results
A 10 μg/m3 increase of NO2, SO2, and O3 concentrations corresponded to 3.17% (95%Cl: 1.41%, 4.93%), 3.55% (95%Cl: 1.93%, 5.18%), and -0.84% (95%Cl: -1.58%, 0.09%) increase in outpatient-visits for epilepsy on the concurrent days, which were significantly influenced by sex and age. The effects of NO2 and SO2 would be stronger when adjusted for PM2.5. As for O3, a -1.14% (95%Cl: -1.90%, -0.39%) decrease was evidenced when adjusted for NO2. The lag models showed that the most significant effects were evidenced on concurrent days.
Conclusions
We discovered previously undocumented relationships between short-term air pollution exposure and epilepsy: while NO2 and SO2 were positively associated with outpatient-visits of epilepsy, O3 might be associated with reduced risk.
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Pollution negatively influences working memory, executive function, and academic achievement.
https://pubmed.ncbi.nlm.nih.gov/35055570/
Note from the website owner: PM10, PM2.5, and NO2 are all chemicals found in pollution.
The Effects of Traffic Air Pollution in and around Schools on Executive Function and Academic Performance in Children:
This review summarises the extant literature investigating the relation between traffic-related air pollution levels in and around schools and executive functioning in primary-school-aged children. An electronic search was conducted using Web of Science, Scopus, and Education Literature Datasets databases (February 2020). Review articles were also searched, and forwards and backwards searches of identified studies were performed. Included papers were assessed for quality. We included 9 separate studies (published in 13 papers). Findings suggest that indoor and outdoor particulate matter with a diameter of 2.5 μm or less (PM2.5) negatively influences executive function and academic achievement and that indoor and outdoor nitrogen dioxide (NO2) adversely affects working memory. Evidence for the effects of particulate matter with a diameter of 10 μm or less (PM10) is limited but suggests potential wide-ranging negative effects on attention, reasoning, and academic test scores. Air pollution in and around schools influences executive function and appears to impede the developmental trajectory of working memory. Further research is required to establish the extent of these effects, reproducibility, consequences for future attainment, and place within the wider context of cognitive development.
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https://pubmed.ncbi.nlm.nih.gov/26610921/
The central nervous system is emerging as an important target for adverse health effects of air pollution, where it may contribute to neurodevelopmental and neurodegenerative disorders. Air pollution comprises several components, including particulate matter (PM) and ultrafine particulate matter (UFPM), gases, organic compounds, and metals. An important source of ambient PM and UFPM is represented by traffic-related air pollution, primarily diesel exhaust (DE). Human epidemiological studies and controlled animal studies have shown that exposure to air pollution, and to traffic-related air pollution or DE (diesel exhaust) in particular, may lead to neurotoxicity. In particular, air pollution is emerging as a possible etiological factor in neurodevelopmental (e.g. autism spectrum disorders) and neurodegenerative (e.g. Alzheimer's disease) disorders. The most prominent effects caused by air pollution in both humans and animals are oxidative stress and neuro-inflammation. Studies in mice acutely exposed to DE (diesel exhaust) (250-300μg/m3 for 6h) have shown microglia activation, increased lipid peroxidation, and neuro-inflammation in various brain regions, particularly the hippocampus and the olfactory bulb. An impairment of adult neurogenesis was also found. In most cases, the effects of DE were more pronounced in male mice, possibly because of lower antioxidant abilities due to lower expression of paraoxonase 2.
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https://pubmed.ncbi.nlm.nih.gov/30916743/
Association of Air Pollution Exposure With Psychotic Experiences During Adolescence
Importance: Urbanicity is a well-established risk factor for clinical (eg, schizophrenia) and subclinical (eg, hearing voices and paranoia) expressions of psychosis. To our knowledge, no studies have examined the association of air pollution with adolescent psychotic experiences, despite air pollution being a major environmental problem in cities.
Objectives: To examine the association between exposure to air pollution and adolescent psychotic experiences and test whether exposure mediates the association between urban residency and adolescent psychotic experiences.
Design, setting, and participants: The Environmental-Risk Longitudinal Twin Study is a population-based cohort study of 2232 children born during the period from January 1, 1994, through December 4, 1995, in England and Wales and followed up from birth through 18 years of age. The cohort represents the geographic and socioeconomic composition of UK households. Of the original cohort, 2066 (92.6%) participated in assessments at 18 years of age, of whom 2063 (99.9%) provided data on psychotic experiences. Generation of the pollution data was completed on October 4, 2017, and data were analyzed from May 4 to November 21, 2018.
Exposures: High-resolution annualized estimates of exposure to 4 air pollutants-nitrogen dioxide (NO2), nitrogen oxides (NOx), and particulate matter with aerodynamic diameters of less than 2.5 (PM2.5) and less than 10 μm (PM10)-were modeled for 2012 and linked to the home addresses of the sample plus 2 commonly visited locations when the participants were 18 years old.
Main outcomes and measures: At 18 years of age, participants were privately interviewed regarding adolescent psychotic experiences. Urbanicity was estimated using 2011 census data.
Results: Among the 2063 participants who provided data on psychotic experiences, sex was evenly distributed (52.5% female). Six hundred twenty-three participants (30.2%) had at least 1 psychotic experience from 12 to 18 years of age. Psychotic experiences were significantly more common among adolescents with the highest (top quartile) level of annual exposure to NO2 (odds ratio [OR], 1.71; 95% CI, 1.28-2.28), NOx (OR, 1.72; 95% CI, 1.30-2.29), and PM2.5 (OR, 1.45; 95% CI, 1.11-1.90). Together NO2 and NOx statistically explained 60% of the association between urbanicity and adolescent psychotic experiences. No evidence of confounding by family socioeconomic status, family psychiatric history, maternal psychosis, childhood psychotic symptoms, adolescent smoking and substance dependence, or neighborhood socioeconomic status, crime, and social conditions occurred.
Conclusions and relevance: In this study, air pollution exposure-particularly NO2 and NOx-was associated with increased odds of adolescent psychotic experiences, which partly explained the association between urban residency and adolescent psychotic experiences. Biological (eg, neuroinflammation) and psychosocial (eg, stress) mechanisms are plausible.
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Association between air pollution exposure and mental health service use among individuals with first presentations of psychotic and mood disorders: retrospective cohort study
Joanne B. Newbury, Robert Stewart, Helen L. Fisher, Sean Beevers, David Dajnak, Matthew Broadbent, Megan Pritchard, Narushige Shiode, Margaret Heslin, Ryan Hammoud, Matthew Hotopf, Stephani L. Hatch, Ian S. Mudway,* and Ioannis Bakolis*
Abstract
Background
Growing evidence suggests that air pollution exposure may adversely affect the brain and increase risk for psychiatric disorders such as schizophrenia and depression. However, little is known about the potential role of air pollution in severity and relapse following illness onset.