Vectorization by nanoparticles decreases the overall toxicity of airborne pollutants.
Ontology highlight
ABSTRACT:
SUBMITTER: Carpentier R
PROVIDER: S-EPMC5557588 | biostudies-other | 2017
REPOSITORIES: biostudies-other
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Project description:Mitochondria have small mitochondrial DNA (mtDNA) molecules independent from the nuclear DNA, a separate epigenetic machinery that generates mtDNA methylation, and are primary sources of oxidative-stress generation in response to exogenous environments. However, no study has yet investigated whether mitochondrial DNA methylation is sensitive to pro-oxidant environmental exposures.We sampled 40 male participants (20 high-, 20 low-exposure) from each of three studies on airborne pollutants, including investigations of steel workers exposed to metal-rich particulate matter (measured as PM1) in Brescia, Italy (Study 1); gas-station attendants exposed to air benzene in Milan, Italy (Study 2); and truck drivers exposed to traffic-derived Elemental Carbon (EC) in Beijing, China (Study 3). We have measured DNA methylation from buffy coats of the participants. We measured methylation by bisulfite-Pyrosequencing in three mtDNA regions, i.e., the transfer RNA phenylalanine (MT-TF), 12S ribosomal RNA (MT-RNR1) gene and "D-loop" control region. All analyses were adjusted for age and smoking.In Study 1, participants with high metal-rich PM1 exposure showed higher MT-TF and MT-RNR1 methylation than low-exposed controls (difference = 1.41, P = 0.002); MT-TF and MT-RNR1 methylation was significantly associated with PM1 exposure (beta = 1.35, P = 0.025); and MT-RNR1 methylation was positively correlated with mtDNA copy number (r = 0.36; P = 0.02). D-loop methylation was not associated with PM1 exposure. We found no effects on mtDNA methylation from air benzene (Study 2) and traffic-derived EC exposure (Study 3).Mitochondrial MT-TF and MT-RNR1 DNA methylation was associated with metal-rich PM1 exposure and mtDNA copy number. Our results suggest that locus-specific mtDNA methylation is correlated to selected exposures and mtDNA damage. Larger studies are needed to validate our observations.
| S-EPMC3660297 | biostudies-literature
Project description:Mercury is an important global toxic contaminant of concern that causes cognitive and neuromuscular damage in humans. It is ubiquitous in the environment and can travel in the air, in water, or adsorb to soils, snow, ice and sediment. Two significant factors that influence the fate of atmospheric mercury, its introduction to aquatic and terrestrial environments, and its bioaccumulation and biomagnification in biotic systems are the chemical species or forms that mercury exists as (elemental, oxidized or organic) and its physical phase (solid, liquid/aqueous, or gaseous). In this work, we show that previously unknown mercury-containing nanoparticles exist in the air using high-resolution scanning transmission electron microscopy imaging (HR-STEM). Deploying an urban-air field campaign near a mercury point source, we provide further evidence for mercury nanoparticles and determine the extent to which these particles contain two long suspected forms of oxidized mercury (mercuric bromide and mercuric chloride) using mercury mass spectrometry (Hg-MS). Using optical particle sizers, we also conclude that the conventional method of measuring gaseous oxidized mercury worldwide can trap up to 95% of nanoparticulate mercuric halides leading to erroneous measurements. Finally, we estimate airborne mercury aerosols may contribute to half of the oxidized mercury measured in wintertime Montréal urban air using Hg-MS. These emerging mercury-containing nanoparticle contaminants will influence mercury deposition, speciation and other atmospheric and aquatic biogeochemical mercury processes including the bioavailability of oxidized mercury to biota and its transformation to neurotoxic organic mercury.
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Project description:Repetitive elements take up >40% of the human genome and can change distribution through transposition, thus generating subfamilies. Repetitive element DNA methylation has associated with several diseases and environmental exposures, including exposure to airborne pollutants. No systematic analysis has yet been conducted to examine the effects of exposures across different repetitive element subfamilies. The purpose of the study is to evaluate sensitivity of DNA methylation in differentially?evolved LINE, Alu, and HERV subfamilies to different types of airborne pollutants.We sampled a total of 120 male participants from three studies (20 high-, 20 low-exposure in each study) of steel workers exposed to metal-rich particulate matter (measured as PM10) (Study 1); gas-station attendants exposed to air benzene (Study 2); and truck drivers exposed to traffic-derived elemental carbon (Study 3). We measured methylation by bisulfite-PCR-pyrosequencing in 10 differentially?evolved repetitive element subfamilies.High-exposure groups exhibited subfamily-specific methylation differences compared to low-exposure groups: L1PA2 showed lower DNA methylation in steel workers (P=0.04) and gas station attendants (P=0.03); L1Ta showed lower DNA methylation in steel workers (P=0.02); AluYb8 showed higher DNA methylation in truck drivers (P=0.05). Within each study, dose-response analyses showed subfamily-specific correlations of methylation with exposure levels. Interaction models showed that the effects of the exposures on DNA methylation were dependent on the subfamily evolutionary age, with stronger effects on older LINEs from PM10 (p?interaction=0.003) and benzene (p?interaction=0.04), and on younger Alus from PM10 (p-interaction=0.02).The evolutionary age of repetitive element subfamilies determines differential susceptibility of DNA methylation to airborne pollutants.
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Project description:The outbreak of COVID-19, caused by SARS-CoV-2, has spread across many countries globally. Greatly, there are limited studies concerned with the effect of airborne pollutants on COVID-19 infection, while exposure to airborne pollutants may harm human health. This paper aimed to examine the associations of acute exposure to ambient atmospheric pollutants to daily newly COVID-19 confirmed cases in 41 Chinese cities. Using a generalized additive model with Poisson distribution controlling for temperature and relative humidity, we evaluated the association between pollutant concentrations and daily COVID-19 confirmation at single-city level and multicity levels. We observed a 10-μg/m3 rise in levels of PM2.5 (lag 0-14), O3 (lag 0-1), SO2 (lag 0), and NO2 (lag 0-14) were positively associated with relative risks of 1.050 (95% CI: 1.028, 1.073), 1.011 (1.007, 1.015), 1.052 (1.022, 1.083), and 1.094 (1.028, 1.164) of daily newly confirmed cases, respectively. Further adjustment for other pollutants did not change the associations materially (excepting in the model for SO2). Our results indicated that COVID-19 incidence may be susceptible to airborne pollutants such as PM2.5, O3, SO2, and NO2, and mitigation strategies of environmental factors are required to prevent spreading.
| S-EPMC8105699 | biostudies-literature
Project description:BackgroundExposure to ambient air pollution is widespread and may be detrimental to human brain development and a potential risk factor for Autism Spectrum Disorder (ASD). We conducted a systematic review of the human evidence on the relationship between ASD and exposure to all airborne pollutants, including particulate matter air pollutants and others (e.g. pesticides and metals).ObjectiveTo answer the question: "is developmental exposure to air pollution associated with ASD?"MethodsWe conducted a comprehensive search of the literature, identified relevant studies using inclusion/exclusion criteria pre-specified in our protocol (registered in PROSPERO, CRD # 42015017890), evaluated the potential risk of bias for each included study and identified an appropriate subset of studies to combine in a meta-analysis. We then rated the overall quality and strength of the evidence collectively across all air pollutants.ResultsOf 1,158 total references identified, 23 human studies met our inclusion criteria (17 case-control, 4 ecological, 2 cohort). Risk of bias was generally low across studies for most domains; study limitations were related to potential confounding and accuracy of exposure assessment methods. We rated the quality of the body of evidence across all air pollutants as "moderate." From our meta-analysis, we found statistically significant summary odds ratios (ORs) of 1.07 (95% CI: 1.06, 1.08) per 10-μg/m3 increase in PM10 exposure (n = 6 studies) and 2.32 (95% CI: 2.15, 2.51) per 10-μg/m3 increase in PM2.5 exposure (n = 3 studies). For pollutants not included in a meta-analysis, we collectively evaluated evidence from each study in rating the strength and quality of overall evidence considering factors such as inconsistency, imprecision, and evidence of dose-response. All included studies generally showed increased risk of ASD with increasing exposure to air pollution, although not consistently across all chemical components.ConclusionAfter considering strengths and limitations of the body of research, we concluded that there is "limited evidence of toxicity" for the association between early life exposure to air pollution as a whole and diagnosis of ASD. The strongest evidence was between prenatal exposure to particulate matter and ASD. However, the small number of studies in the meta-analysis and unexplained statistical heterogeneity across the individual study estimates means that the effect could be larger or smaller (including not significant) than these studies estimate. Our research supports the need for health protective public policy to reduce exposures to harmful airborne contaminants among pregnant women and children and suggests opportunities for optimizing future research.
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Project description:Aromatic compounds contribute significantly to the budget of atmospheric pollutants and represent considerable hazard to living organisms. However, they are only rarely included into atmospheric models which deviate substantially from field measurements. A powerful experimental-simulation tool for the assessment of the impact of low- and semi-volatile aromatic pollutants on the environment due to their atmospheric aqueous phase aging has been developed and introduced for the first time. The case study herein reveals that remote biotopes might be the most damaged by wet urban guaiacol-containing biomass burning aerosols. It is shown that only after the primary pollutant guaiacol has been consumed, its probably most toxic nitroaromatic product is largely formed. Revising the recent understanding of atmospheric aqueous phase chemistry, which is mostly concerned with the radical nitration mechanisms, the observed phenomenon is mainly attributed to the electrophilic nitrogen-containing reactive species. Here, their intriguing role is closely inspected and discussed from the ecological perspective.
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Project description:In 2012 air pollutants were responsible of seven million human death worldwide, and among them particulate matter with an aerodynamic diameter of 2.5 micrometers or less (PM2.5) are the most hazardous because they are small enough to invade even the smallest airways and penetrate to the lungs. During the last decade the size, shape, composition, sources and effect of these particles on human health have been studied. However, the noxiousness of these particles not only relies on their chemical toxicity, but particle morphology and mechanical properties affect their thermodynamic behavior, which has notable impact on their biological activity. Therefore, correlating the physical, mechanical and chemical properties of PM2.5 airborne pollutants should be the first step to characterize their interaction with other bodies but, unfortunately, such analysis has never been reported before. In this work, we present the first nanomechanical characterization of the most abundant and universal groups of PM2.5 airborne pollutants and, by means of atomic force microscope (AFM) combined with other characterization tools, we observe that fluffy soot aggregates are the most sticky and unstable. Our experiments demonstrate that such particles show strong adhesiveness and aggregation, leading to a more diverse composition and compiling all possible toxic chemicals.
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Project description:Recent investigations have associated airborne particulate matter (PM) with increased coagulation and thrombosis, but underlying biological mechanisms are still incompletely characterised. DNA methylation is an environmentally sensitive mechanism of gene regulation that could potentially contribute to PM-induced hypercoagulability. We aimed to test whether altered methylation mediates environmental effects on coagulation.We investigated 63 steel workers exposed to a wide range of PM levels, as a work-related condition with well-characterised prothrombotic exposure. We measured personal PM10 (PM?10 µm in aerodynamic diameter), PM1 (?1 µm) and air metal components. We determined leukocyte DNA methylation of NOS3 (nitric-oxide-synthase-3) and EDN1 (endothelin-1) through bisulfite-pyrosequencing and we measured ETP as a global coagulation-activation test after standardised triggers.ETP increased in association with PM10 (?=20.0, 95% CI 3.0 to 37.0), PM1 (?=80.8 95% CI 14.9 to 146.7) and zinc (?=51.3, 95% CI 0.01 to 111.1) exposures. NOS3 methylation was negatively associated with PM10 (?=-0.2, 95% CI -0.4 to -0.03), PM1 (?=-0.8, 95% CI -1.4 to -0.1), zinc (?=-0.9, 95% CI -1.4 to -0.3) and iron (?=-0.7, 95% CI -1.4 to -0.01) exposures. Zinc exposure was negatively associated with EDN1 (?=-0.3, 95% CI -0.8 to -0.1) methylation. Lower NOS3 (?=-42.3; p<0.001) and EDN1 (?=-14.5; p=0.05) were associated with higher ETP. Statistical mediation analysis formally confirmed NOS3 and EDN1 hypomethylation as intermediate mechanisms for PM-related coagulation effects.Our study showed for the first time, that gene hypomethylation contributes to environmentally induced hypercoagulability.
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Project description:Veterinary antiparasitic pharmaceuticals as well as pesticides have been detected in surface waters, and they may cause several toxic effects in this environmental compartment. In the present study, we evaluated the toxicity after exposure of different concentration of ivermectin (IVM; 50, 100, and 200 μg L-1) and cypermethrin (CYP; 5, 10, and 25 μg L-1) and the combination of these two compounds at non-toxic concentration (IVM 100 + CYP 5 μg L-1) in zebrafish embryos. Combination of IVM at 100 μg L-1 with CYP at 5 μg L-1 exposure induced hatching delay and malformations at 96 hpf in zebrafish larvae as well as significant induction of cell death in zebrafish larvae. At the same time, the two single concentrations of IVM and CYP did not show a toxic effect on zebrafish development. In conclusion, our study suggests that IVM and CYP show a synergistic effect at common, ineffective concentrations, promoting malformation and cell death in fish development.
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