Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles
Department of Environmental Science, Aarhus University, Roskilde, Denmark
Air pollution and Autism in Denmark
Previous autism spectrum disorder (ASD) and air pollution studies focused on pregnancy exposures, but another vulnerable period is immediate postnatally. Here, we examined early life exposures to air pollution from the pre- to the postnatal period and ASD/ASD subtypes in the Danish population.
With Danish registers, we conducted a nationwide case-control study of 15,387 children with ASD born 1989-2013 and 68,139 population controls matched by birth year and sex identified from the birth registry. We generated air dispersion model (AirGIS) estimates for NO2, SO2, PM2.5 and PM10 at mothers' home from 9 months before to 9 months after pregnancy and calculated odds ratios (OR) and 95% confidence intervals (CI), adjusting for parental age, neighborhood socio-economic indicators, and maternal smoking using conditional logistic regression.
In models that included all exposure periods, we estimated adjusted ORs for ASD per interquartile range (IQR) increase for 9 month after pregnancy with NO2 of 1.08 (95% CI: 1.01, 1.15) and with PM2.5 of 1.06 (95% CI: 1.01, 1.11); associations were smaller for PM10 (1.04; 95% CI: 1.00, 1.09) and strongest for SO2 (1.21; 95% CI: 1.13, 1.29). Also, associations for pollutants were stronger in more recent years (2000-2013) and in larger cities compared with provincial towns/rural counties. For particles and NO2, associations were only specific to autism and Asperger diagnoses.
Our data suggest that air pollutant exposure in early infancy but not during pregnancy increases the risk of being diagnosed with autism and Asperger among children born in Denmark.
Institute of Health and Environment, Seoul National University, Seoul
Particulate Matter Mortality Rates and Their Modification by Spatial Synoptic Classification
Air pollution levels are highly correlated with temperature or humidity, so we investigated the relationship between PM10 and the spatial synoptic classification (SSC) scheme on daily mortality, according to age group and season. Daily death data for 2000-2014 from Seoul, Korea, were acquired, and time-series analysis was applied with respect to season and to each of seven distinct SSC types: dry moderate (DM); dry polar (DP); dry tropical (DT); moist moderate (MM); moist polar (MP); moist tropical (MT); and transition (T). Modification effects were estimated for daily, non-accidental, cardiovascular, and respiratory mortality between PM10 and SSC types. The following SSC-type-specific increased mortalities were observed, by cause of death: non-accidental mortality: DT (1.86%) and MT (1.86%); cardiovascular mortality: DT (2.83%) and MM (3.00%); respiratory mortality: MT (3.78%). Based on simplified weather types, increased PM10 effects in non-accidental mortality rates were observed in dry (1.54%) and moist (2.32%) conditions among those aged 40-59 years and were detected regardless of conditions in other age groups: 60-74 (1.11%), 75-84 (1.55%), and 85+ (1.75%). The effects of particulate air pollution, by SSC, suggest the applicability of SSC to the comparison and understanding of acute effects of daily mortality based on weather type.
Xiang Ya Nursing School, Central South University, Changsha, Hunan, China
Ambient air pollution exposure and risk of depression: A systematic review and meta-analysis of observational studies.
Recent studies have reported an association between air pollution exposure and depression, with inconsistent results. To address this controversy, we conducted a systematic review and meta-analysis of published observational studies that investigated outdoor air pollution and depression. Five electronic databases were searched, and fifteen articles were finally identified. Pooled odds risks were calculated separately based on pollutant type, exposure duration and outcome. Subgroup analyses were conducted based on design, population, important potential confounders, and pollutants levels. We found a significantly increased risk of depression with long-term exposure to PM2.5 and short-term exposure to PM10, NO2, SO2, CO. No evidence was found in the association between exposure to O3 and depression. Besides, exposure to high levels of pollutants indicates a higher risk of depression. Our results highlight the necessity of air pollution control for depression. However, further studies with standardized methods are still required to support the results due to the inconsistent results in stratified analyses and methodological limitations of the included studies.
Department of Physiology, Physiology Research Center, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Gallic acid protects particulate matter (PM10) triggers cardiac oxidative stress and inflammation causing heart adverse events in rats.
Previous studies have shown that exposure to particulate matter (PM) increased variety of health problems, particularly cardiovascular diseases leading to premature mortality. The cardiac effects of particulate matter containing PM10 include increased infarct size, decreased heart function, and increased arrhythmias in experimental ischemia-reperfusion models in rats. The aim of this study was to evaluate the effects of particles with an aerodynamic diameter smaller than 10 μm (PM10) on isolated-rat heart and also to determine the efficacy of gallic acid (GA) as a preventive agent in oxidative damage. The healthy rats were divided into 8 equal groups which served as, control, GA, PM10 (0.5, 2.5, and 5 mg/kg), and PM10+GA groups. PM10 administered into the lungs via the trachea in two stages with 48-h interval. After all experiments, the electrocardiogram was recorded. Then, the hemodynamic parameters and ventricular arrhythmias in rat isolated-hearts were assessed using Langendorff apparatus and according to the Lambeth conventions. In addition, the inflammation and oxidative stress factors in cardiac tissues were evaluated in all groups. The obtained results showed that the exposure to PM caused to decrease in cardiac hemodynamic and electrocardiogram parameters. Also, in PM10 rat groups, the IL-6, TNF-α, and oxidative stress parameters were increased. Gallic acid preserved the value of cardiac parameters and inflammation in rat hearts. In summary, we added a novel therapeutic effect of gallic acid for cardiac dysfunction induced by particulate matter. These findings could be related to antioxidant and antiinflammation properties and the obtained results suggest that natural antioxidant like gallic acid could be a therapeutic agent in prevention and management of health issues in the polluted areas of the world.
Faculty of Medicine, Department of Physiology , Persian Gulf Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences , Ahvaz , Iran
In vivo and in vitro evidence for the involvement of Nrf2-antioxidant response element signaling pathway in the inflammation and oxidative stress induced by particulate matter (PM10): the effective role of gallic acid.
Environmental pollution is one of the risk factors for respiratory diseases. The nuclear factor erythroid 2-related factor 2 (Nrf2) is the major mechanisms contributing to cellular defense against oxidative damage. Gallic acid (GA) is regarded as potent anti-inflammatory and antioxidant agents. The aim was to evaluate the role of Nrf2 pathway in particulate matter (PM10) exposure on lung and epithelial cells with an emphasis on the role of GA. In in vivo part, the rats were divided as control, GA (30 mg/kg), particulate matter (PM) (0.5, 2.5, and 5 mg/kg), and PM + GA. In in vitro study, the cells were divided as control, PM10 (100, 250, and 500 µg/ml), GA (50 µmol/L) and PM10+GA. Inflammation, oxidative stress and Nrf2-pathway factors were assessed. PM10 groups showed a considerable increase in the epithelial permeability and inflammatory parameters. We also found a significant decrease in the expression of Nrf2 and its up-stream regulators genes. Accordingly, the biosynthesis of glutathione (GSH) and other antioxidant activities significantly decreased. Gallic acid was identified to restore the antioxidant status to the normal levels. Our findings approved that Nrf2 is involved in PM10-induced oxidative damages and showed that Nrf2 activation by natural agents could ameliorate respiratory injuries induced by PM10.
Department of Toxicogenomics, GROW School for Oncology and Developmental Biology, Maastricht University, Maastricht, the Netherlands
Short-term exposure to traffic-related air pollution reveals a compound-specific circulating miRNA profile indicating multiple disease risks
Traffic-related air pollution (TRAP) is a complex mixture of compounds that contributes to the pathogenesis of many diseases including several types of cancer, pulmonary, cardiovascular and neurodegenerative diseases, and more recently also diabetes mellitus. In search of an early diagnostic biomarker for improved environmental health risk assessment, recent human studies have shown that certain extracellular miRNAs are altered upon exposure to TRAP. Here, we present a global circulating miRNA analysis in a human population exposed to different levels of TRAP. The cross-over study, with sampling taking place during resting and physical activity in two different exposure scenarios, included for each subject personal exposure measurements of PM10,PM2.5, NO, NO2, CO, CO2, BC and UFP. Next-generation sequencing technology was used to identify global circulating miRNA levels across all subjects. We identified 8 miRNAs to be associated with the mixture of TRAP and 27 miRNAs that were associated with the individual pollutants NO, NO2, CO, CO2, BC and UFP. We did not find significant associations between miRNA levels and PM10 or PM2.5. Integrated network analysis revealed that these circulating miRNAs are potentially involved in processes that are implicated in the development of air pollution-induced diseases. Altogether, this study demonstrates that signatures consisting of circulating miRNAs present a potential novel biomarker to be used in health risk assessment.
National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands; Institute for Risk Assessment Sciences (IRAS), Utrecht University, Utrecht, the Netherlands
Associations of combined exposures to surrounding green, air pollution and traffic noise on mental health.
Evidence is emerging that poor mental health is associated with the environmental exposures of surrounding green, air pollution and traffic noise. Most studies have evaluated only associations of single exposures with poor mental health.
To evaluate associations of combined exposure to surrounding green, air pollution and traffic noise with poor mental health.
In this cross-sectional study, we linked data from a Dutch national health survey among 387,195 adults including questions about psychological distress, based on the Kessler 10 scale, to an external database on registered prescriptions of anxiolytics, hypnotics & sedatives and antidepressants. We added data on residential surrounding green in a 300 m and a 1000 m buffer based on the Normalized Difference Vegetation Index (NDVI) and a land-use database (TOP10NL), modeled annual average air pollutant concentrations (including particulate matter (PM10, PM2.5), and nitrogen dioxide (NO2)) and modeled road- and rail-traffic noise (Lden and Lnight) to the survey. We used logistic regression to analyze associations of surrounding green, air pollution and traffic noise exposure with poor mental health.
In single exposure models, surrounding green was inversely associated with poor mental health. Air pollution was positively associated with poor mental health. Road-traffic noise was only positively associated with prescription of anxiolytics, while rail-traffic noise was only positively associated with psychological distress. For prescription of anxiolytics, we found an odds ratio [OR] of 0.88 (95% CI: 0.85, 0.92) per interquartile range [IQR] increase in NDVI within 300 m, an OR of 1.14 (95% CI: 1.10, 1.19) per IQR increase in NO2 and an OR of 1.07 (95% CI: 1.03, 1.11) per IQR increase in road-traffic noise. In multi exposure analyses, associations with surrounding green and air pollution generally remained but attenuated. Joint odds ratios [JOR], based on the Cumulative Risk Index (CRI) method, of combined exposure to air pollution, traffic noise and decreased surrounding green were higher than the ORs of single exposure models. Associations of environmental exposures with poor mental health differed somewhat by age.
Studies including only one of these three correlated exposures may overestimate the influence of poor mental health attributed to the studied exposure, while underestimating the influence of combined environmental exposures.
Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill
Institute of Epidemiology, Helmholtz Zentrum München, Ingolstaedter Landstrasse 1, Neuherberg, Germany
Methylome-wide association study provides evidence of particulate matter air pollution-associated DNA methylation
DNA methylation (DNAm) may contribute to processes that underlie associations between air pollution and poor health. Therefore, our objective was to evaluate associations between DNAm and ambient concentrations of particulate matter (PM) ≤2.5, ≤10, and 2.5-10 μm in diameter (PM2.5; PM10; PM2.5-10).
We conducted a methylome-wide association study among twelve cohort- and race/ethnicity-stratified subpopulations from the Women's Health Initiative and the Atherosclerosis Risk in Communities study (n = 8397; mean age: 61.5 years; 83% female; 45% African American; 9% Hispanic/Latino American). We averaged geocoded address-specific estimates of daily and monthly mean PM concentrations over 2, 7, 28, and 365 days and 1 and 12 months before exams at which we measured leukocyte DNAm in whole blood. We estimated subpopulation-specific, DNAm-PM associations at approximately 485,000 Cytosine-phosphate-Guanine (CpG) sites in multi-level, linear, mixed-effects models. We combined subpopulation- and site-specific estimates in fixed-effects, inverse variance-weighted meta-analyses, then for associations that exceeded methylome-wide significance and were not heterogeneous across subpopulations (P < 1.0 × 10-7; PCochran's Q > 0.10), we characterized associations using publicly accessible genomic databases and attempted replication in the Cooperative Health Research in the Region of Augsburg (KORA) study.
Analyses identified significant DNAm-PM associations at three CpG sites. Twenty-eight-day mean PM10 was positively associated with DNAm at cg19004594 (chromosome 20; MATN4; P = 3.33 × 10-8). One-month mean PM10 and PM2.5-10 were positively associated with DNAm at cg24102420 (chromosome 10; ARPP21; P = 5.84 × 10-8) and inversely associated with DNAm at cg12124767 (chromosome 7; CFTR; P = 9.86 × 10-8). The PM-sensitive CpG sites mapped to neurological, pulmonary, endocrine, and cardiovascular disease-related genes, but DNAm at those sites was not associated with gene expression in blood cells and did not replicate in KORA.
Ambient PM concentrations were associated with DNAm at genomic regions potentially related to poor health among racially, ethnically and environmentally diverse populations of U.S. women and men. Further investigation is warranted to uncover mechanisms through which PM-induced epigenomic changes may cause disease.
18 August 2017
DNA methylation in demyelinated multiple sclerosis hippocampus
Demyelination correlates with changes in DNA methylation and de-methylation enzymes in MS hippocampus
Free full text.Petr75 wrote: ↑Sat Aug 10, 2019 11:22 am18 August 2017
DNA methylation in demyelinated multiple sclerosis hippocampus
Demyelination correlates with changes in DNA methylation and de-methylation enzymes in MS hippocampus
If I've interpreted this paper correctly, then these authors appear to be saying that demyelination leads to changes in gene methylation and not that the methylation changes precede demyelination.
Department of Medical and Surgical Specialties, Radiological Science and Public Health, University of Brescia, 11 viale Europa, Brescia, Italy
"Risk is in the air": Polycyclic aromatic hydrocarbons, metals and mutagenicity of atmospheric particulate matter in a town of Northern Italy (Respira study).
Air pollution has well-known harmful effects on human beings, causing both acute and chronic diseases. Some data suggest that genetic damage occurring early in life may influence the risk of having cancer and other chronic diseases in adulthood. Therefore, there is a growing interest in studying the genotoxic activity of air pollution, and especially particulate matter. The aim of this study was to analyze airborne particulate matter (PM10) collected in an industrialized town of Northern Italy. PM10 was sampled in six areas of the town, divided in three distinct dimensional classes (<0.5 μm; 0.5-3 μm and 3-10 μm), and analyzed for the quantification of polynuclear aromatic hydrocarbons and metals contents. A model-based approach using diagnostic ratios and toxic equivalency factor was also followed. Concurrently, biological assays were performed for the assessment of mutagenicity and genotoxicity in bacteria, human and plant cells. Mutagenicity was observed in bacteria and human cells, with a clear dose-response relationship, induced above all by the finest PM samples (PM0.5 and PM0.5-3), which contained the largest number of polycyclic aromatic hydrocarbons. DNA damage, such as chromosomal aberrations and micronuclei, was also found in Allium cepa root cells, but without a clear relationship with the tested doses. The in-vitro models utilized showed to be good indicators of air quality for mutagenicity. Chemical analyses evidenced high content of polycyclic aromatic hydrocarbons, metals and semi-metals in PM extracts. Polycyclic aromatic hydrocarbons, metals and mutagenicity can be ascribed mainly to vehicular traffic (in terms of both exhausted gases emission and mechanical losses), which represents a constant and ubiquitous source of human exposure, and to steel working, carried out within the urban area.
Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, USA
Air pollution, particulate matter composition and methylation-based biologic age
Epigenetic age, as defined by DNA methylation, may be influenced by air pollution exposure.
To evaluate the relationship between NO2, particulate matter (PM), PM components and accelerated epigenetic age.
In a sample of non-Hispanic white women living in the contiguous U.S. (n = 2747), we estimated residential exposure to PM2.5, PM10 and NO2 using a model incorporating land-use regression and kriging. Predictive k-means was used to assign participants to clusters representing different PM2.5 component profiles. We measured DNA methylation (DNAm) in blood using the Illumina's Infinium HumanMethylation450 BeadChip and calculated DNAm age using the Hannum, Horvath and Levine epigenetic clocks. Age acceleration was defined based on residuals after regressing DNAm age on chronological age. We estimated associations between interquartile range (IQR) increases in pollutants and age acceleration using linear regression. For PM2.5, we stratified by cluster membership. We examined epigenome-wide associations using robust linear regression models corrected with false discovery rate q-values.
NO2 was inversely associated with age acceleration using the Hannum clock (β = -0.24, 95% CI: -0.47, -0.02). No associations were observed for PM10. For PM2.5, the association with age acceleration varied by PM2.5 component cluster. For example, with the Levine clock, an IQR increase in PM2.5 was associated with an over 6-year age acceleration in a cluster that has relatively high fractions of crustal elements relative to overall PM2.5 (β = 6.57, 95% CI: 2.68, 10.47), and an almost 2-year acceleration in a cluster characterized by relatively low sulfur fractions (β = 1.88, 95% CI: 0.51, 3.25). In a cluster distinguished by lower relative nitrate concentrations, PM2.5 was inversely associated with age acceleration (β = -1.33, 95% CI: -2.43, -0.23). Across the epigenome, NO2 was associated with methylation at 2 CpG sites.