Evaluating the adverse effects and mechanisms of nanomaterial exposure on longevity of C. elegans: A literature meta-analysis and bioinformatics analysis of multi-transcriptome data.

Exposure to large-size particulate air pollution (PM2.5 or PM10) has been reported to increase risks of aging-related diseases and human death, indicating the potential pro-aging effects of airborne nanomaterials with ultra-fine particle size (which have been widely applied in various fields). However, this hypothesis remains inconclusive. Here, a meta-analysis of 99 published literatures collected from electronic databases (PubMed, EMBASE and Cochrane Library; from inception to June 2023) was performed to confirm the effects of nanomaterial exposure on aging-related indicators and molecular mechanisms in model animal C. elegans. The pooled analysis by Stata software showed that compared with the control, nanomaterial exposure significantly shortened the mean lifespan [standardized mean difference (SMD) = -2.30], reduced the survival rate (SMD = -4.57) and increased the death risk (hazard ratio = 1.36) accompanied by upregulation of ced-3, ced-4 and cep-1, while downregulation of ctl-2, ape-1, aak-2 and pmk-1. Furthermore, multi-transcriptome data associated with nanomaterial exposure were retrieved from Gene Expression Omnibus (GSE32521, GSE41486, GSE24847, GSE59470, GSE70509, GSE14932, GSE93187, GSE114881, and GSE122728) and bioinformatics analyses showed that pseudogene prg-2, mRNAs of abu, car-1, gipc-1, gsp-3, kat-1, pod-2, acdh-8, hsp-60 and egrh-2 were downregulated, while R04A9.7 was upregulated after exposure to at least two types of nanomaterials. Resveratrol (abu, hsp-60, pod-2, egrh-2, acdh-8, gsp-3, car-1, kat-1, gipc-1), naringenin (kat-1, egrh-2), coumestrol (egrh-2) or swainsonine/niacin/ferulic acid (R04A9.7) exerted therapeutic effects by reversing the expression levels of target genes. In conclusion, our study demonstrates the necessity to use phytomedicines that target hub genes to delay aging for populations with nanomaterial exposure.

Elevated ozone effects on potato leaf physiology, growth, and yield: a meta-analysis.

Potato is an important crop worldwide and threatened by various environmental stresses, including elevated ozone (e[O3]). Here, we conducted a meta-analysis to quantify the effect of e[O3] on potato plants and how it varies depending upon different experimental conditions. Regarding plant growth and biomass, e[O3] significantly decreased shoot biomass by 18% and belowground biomass by 35%, while it increased the leaf area index by 19% and total number of injured leaves by 146%. As for yield, e[O3] significantly decreased the total tuber number by 21%. A relatively pronounced effect of e[O3] on the stomatal conductance was observed when exposure lasted 31-60 days, which was significantly greater than that after exposure lasted 96-311 days. The overall quantity of leaves was mainly decreased by higher (100-150 ppb) than lower (30-80 ppb) concentrations of e[O3] compared to ambient O3. The effect of e[O3] on the total tuber number was significant mainly when exposure lasted 31-90 days and was greater in plants grown in growth chambers than those planted in open-top chambers and glasshouses. The effect of e[O3] stress on physiology, growth, and yield varied among cultivars, with some cultivars showing marked tolerance relative to other cultivars. The findings can guide strategies to manage the negative impacts of e[O3] stress on potato production.

The impact of particulate matters on apoptosis in various organs: Mechanistic and therapeutic perspectives.

Ecological air contamination is the non-homogenous suspension of insoluble particles into gas or/and liquid fluids known as particulate matter (PM). It has been discovered that exposure to PM can cause serious cellular defects, followed by tissue damage known as cellular stress. Apoptosis is a homeostatic and regulated phenomenon associated with distinguished physiological actions inclusive of organ and tissue generation, aging, and development. Moreover, it has been proposed that the deregulation of apoptotic performs an active role in the occurrence of many disorders, such as autoimmune disease, neurodegenerative, and malignant, in the human population. Recent studies have shown that PMs mainly modulate multiple signaling pathways involved in apoptosis, including MAPK, PI3K/Akt, JAK/STAT, NFκB, Endoplasmic Stress, and ATM/P53, leading to apoptosis dysregulation and apoptosis-related pathological conditions. Here, the recently published data concerning the effect of PM on the apoptosis of various organs, with a particular focus on the importance of apoptosis as a component in PM-induced toxicity and human disease development, is carefully discussed. Moreover, the review also highlighted the various therapeutic approaches, including small molecules, miRNA replacement therapy, vitamins, and PDRN, for treating diseases caused by PM toxicity. Notably, researchers have considered medicinal herbs a potential treatment for PM-induced toxicity due to their fewer side effects. So, in the final section, we analyzed the performance of some natural products for inhibition and intervention of apoptosis arising from PM-induced toxicity.

Genotoxicity by rapeseed methyl ester and hydrogenated vegetable oil combustion exhaust products in lung epithelial (A549) cells.

Biofuel is an attractive substitute for petrodiesel because of its lower environmental footprint. For instance, the polycyclic aromatic hydrocarbons (PAH) emission per fuel energy content is lower for rapeseed methyl ester (RME) than for petrodiesel. This study assesses genotoxicity by extractable organic matter (EOM) of exhaust particles from the combustion of petrodiesel, RME, and hydrogenated vegetable oil (HVO) in lung epithelial (A549) cells. Genotoxicity was assessed as DNA strand breaks by the alkaline comet assay. EOM from the combustion of petrodiesel and RME generated the same level of DNA strand breaks based on the equal concentration of total PAH (i.e. net increases of 0.13 [95% confidence interval (CI): 0.002, 0.25, and 0.12 [95% CI: 0.01, 0.24] lesions per million base pairs, respectively). In comparison, the positive control (etoposide) generated a much higher level of DNA strand breaks (i.e. 0.84, 95% CI: 0.72, 0.97) lesions per million base pairs. Relatively low concentrations of EOM from RME and HVO combustion particles (<116 ng/ml total PAH) did not cause DNA strand breaks in A549 cells, whereas benzo[a]pyrene and PAH-rich EOM from petrodiesel combusted using low oxygen inlet concentration were genotoxic. The genotoxicity was attributed to high molecular weight PAH isomers with 5-6 rings. In summary, the results show that EOM from the combustion of petrodiesel and RME generate the same level of DNA strand breaks on an equal total PAH basis. However, the genotoxic hazard of engine exhaust from on-road vehicles is lower for RME than petrodiesel because of lower PAH emission per fuel energy content.

A review of the impacts of air pollution on terrestrial birds.

Air pollution has a ubiquitous impact on ecosystem functioning through myriad processes, including the acidification and eutrophication of soil and water, deposition of heavy metals and direct (and indirect) effects on flora and fauna. Describing the impacts of air pollution on organisms in the field is difficult because levels of exposure do not occur in a uniform manner across space and time, and species responses tend to be nuanced and difficult to isolate from other environmental stressors. However, given its far-reaching effects on human and ecosystem health, the impacts of air pollution on species are expected to be substantial, and could be direct or indirect, acting via a range of mechanisms. Here, we expand on previous reviews, to evaluate the existing evidence for the impacts of air pollution on avian species in the field, and to identify knowledge gaps to guide future research. We identified 203 studies that have investigated the impacts of air pollution (including nitrogen and heavy metal deposition) on wild populations of birds, considering 231 species from ten feeding guilds. The majority of studies (82 %) document at least one species trait leading to an overall fitness value that is negatively correlated with pollution concentrations, including deleterious effects on reproductive output, molecular (DNA) damage and overall survival, and effects on foraging behaviour, plumage colouration and body size that may show adaptation. Despite this broad range of trait effects, biases in the literature towards certain species (Parus major and Ficeluda hypoleuca), geographical regions (Western Europe) and pollutants (heavy metal deposition), mean that many unknowns remain in our current understanding of the impacts of air pollution on avian species. We discuss these findings in context of future work, and propose research approaches that could help to provide a more holistic understanding of how avian species are impacted by air pollution.

Associations of fine particulate matter and its metal constituents with blood pressure: A panel study during the seventh World Military Games.

Evidence is needed to elucidate the association of blood pressure (BP) changes with metal constituents in fine particulate matter (PM2.5). Therefore, we designed a longitudinal panel study enrolling 70 healthy students from Wuhan University in the context of the seventh World Military Games (the 7th WMG) from September 2019 to January 2020. A total of eight visits were conducted before, during, and after the 7th WMG. During every visit, each participant was asked to carry a personal PM2.5 monitor to measure hourly PM2.5 levels for three consecutive days. Questionnaire investigation and physical examination were completed on the fourth day. We analyzed ten metal constituents of ambient PM2.5 collected from the fixed station, and blood pressure was recorded during each visit. The linear mixed-effects models were performed to evaluate associations of metal constituents and blood pressure measurements. We observed a dramatic variation of PM2.5 concentration ranging from 7.38 to 132.04 µg/m3. A 10 µg/m3 increment of PM2.5 was associated with an increase of 0.64 mmHg (95% CI: 0.44, 0.84) in systolic BP (SBP), 0.40 mmHg (0.26, 0.54) in diastolic BP (DBP), 0.31 mmHg (0.15, 0.47) in pulse pressure (PP) and 0.44 mmHg (0.26, 0.62) in mean artery pressure (MAP), respectively. For metal constituents in PM2.5, robust positive associations were observed between BP and selenium, manganese, arsenic, cadmium, and thallium. For example, for an IQR (0.93 ng/m3) increment of selenium, SBP and MAP elevated by 0.98 mmHg (0.09, 1.87) and 0.71 mmHg (0.03, 1.39), respectively. Aluminum was found to be robustly associated with decreased SBP, DBP, and MAP. The study indicated that exposure to PM2.5 total mass and metal constituents including selenium, manganese, arsenic, cadmium, and thallium were associated with the elevated BP.

Solid fuel derived PM2.5 induced oxidative stress and according cytotoxicity in A549 cells: The evidence and potential neutralization by green tea.

PM2.5 (particulate matter with aerodynamic diameter ≤ 2.5 µm) is a well-known cytotoxic pollutant that capable to induce severe intracellular oxidative stress while the underlying mechanisms remain unclear. Herein, 4 types of PM2.5 derived from solid fuel burning were selected as stimuli in A549 cells exposure model to evaluate their effects on oxidative stress and inflammatory responses. Although resulting in different responses in cell viability, all PM2.5 exhibited over 50 % higher oxidative stress than control group, expression as intracellular reactive oxygen species, malondialdehyde and superoxide dismutase levels. The Pearson's correlation results indicated that cations (e.g., Ca2+), heavy metals (e.g., Cr and Pb), nPAHs (nitro-polycyclic aromatic hydrocarbons, e.g., 6-nitrochrysene) and oPAHs (oxygenated PAHs, e.g., 9-fluorenone) were the main functioning toxics (r > 0.6). A key finding was the dual-directional regulation function of ECG (epicatechin gallate), that is, it could either increase the low A549 cell viabilities in coal combustion PM2.5 group or reduce them in charcoal PM2.5 group (P < 0.05). The dual-directional effects were likely because ECG can activate Nrf2 oxidation signaling pathway then inhibit the inflammatory signaling pathway NF-κB accordingly. Therefore, evidences indicated cytotoxicity of solid fuel derived PM2.5 were mainly caused by oxidative stress, which was proved to be reversed by green tea, providing a potential therapy method to PM2.5 and other hazards.

Preventive Effect of Epigallocatechin Gallate, the Main Component of Green Tea, on Acute Lung Injury Caused by Air Pollutants.

Reducing the health hazards caused by air pollution is a global challenge and is included in the Sustainable Development Goals. Air pollutants, such as PM2.5, induce respiratory and cardiovascular disorders by causing various inflammatory responses via oxidative stress. Catechins and polyphenols, which are components of green tea, have various protective effects, owing to their antioxidant ability. The main catechin in green tea, epigallocatechin gallate (EGCG), is potentially effective against respiratory diseases, such as idiopathic pulmonary fibrosis and asthma, but its effectiveness against air-pollution-dependent lung injury has not yet been investigated. In this study, we examined the effect of EGCG on urban aerosol-induced acute lung injury in mice. Urban aerosol treatment caused increases in inflammatory cell counts, protein levels, and inflammatory cytokine expression in the lungs of ICR mice, but pretreatment with EGCG markedly suppressed these responses. Analyses of oxidative stress revealed that urban aerosol exposure enhanced reactive oxygen species (ROS) production and the formation of ROS-activated neutrophil extracellular traps (NETs) in the lungs of mice. However, ROS production and NETs formation were markedly suppressed by pretreating the mice with EGCG. Gallocatechin gallate (GCG), a heat-epimerized form of EGCG, also markedly suppressed urban aerosol-dependent inflammatory responses and ROS production in vivo and in vitro. These findings suggest that EGCG and GCG prevent acute lung injury caused by urban aerosols through their inhibitory effects on ROS production. Thus, we believe that foods and medications containing EGCG or GCG may be candidates to prevent the onset and progression of acute lung injury caused by air pollutants.

Polluting characteristics, sources, cancer risk, and cellular toxicity of PAHs bound in atmospheric particulates sampled from an economic transformation demonstration area of Dongguan in the Pearl River Delta, China.

The Songshan Lake Science and Technology Industrial Park is a national economic transition demonstration area, which centers at a traditional industrial region, in Dongguan, China. We were interested in the involved atmospheric particulates-bound PAHs regarding their sources, cancer risk, and related cellular toxicity for those in other areas under comparable conditions. In this study, the daily concentrations of TSP, PM10, and PM2.5 were averaged 127.95, 95.91, and 67.62 µg/m3, and the bound PAHs were averaged 1.31, 1.22, and 0.77 ng/m3 in summer and 12.72, 20.51 and 40.27 ng/m3 in winter, respectively. The dominant PAHs were those with 5-6 rings, and 4-6 rings in summer and winter, respectively. The incremental lifetime cancer risk (ILCR) (90th percentile probability) of total PAHs was above 1.00E-06 in each age group, particularly high in adolescents. Sensitivity analysis indicated that slope factor and body weight had greater impact than exposure duration and inhalation rate on the ILCR. Moreover, treatment of human bronchial epithelial BEAS-2B cells with mixed five indicative PAHs increased the formation of ROS, DNA damage (elevation in γ-H2AX), and protein levels of CAR, PXR, CYP1A1, 1A2, 1B1, while reduced the AhR protein, with the winter mixture more potent than summer. For the sources of PAHs, the stable carbon isotope ratio analysis and diagnostic ratios consistently pointed to petroleum and fossil fuel combustion as major sources. In conclusion, our findings suggest that particulates-bound PAHs deserve serious concerns for a cancer risk in such environment, and the development of new power sources for reducing fossil fuel combustion is highly encouraged.

Inhalation risk to PAHs and BTEX during barbecuing: The role of fuel/food type and route of exposure.

The manuscript presents an innovative and holistic approach to quantifying PAHs and BTEX emissions from the grilling process and indicates a novel driven-toxicity-based solution to recognize health effects related to BBQ emissions. The exposure scenario includes the type of grilling device, food type, and individual attitudes, but also a keen understanding of the broad health implications related to the gaseous/particulate PAHs emission, or age-related effects. The calculated incremental lifetime cancer risk (ILCR) associated with the exposure to PAH congeners and BTEX indicates an unacceptable level in the case of charcoal and briquette grilling with the highest values for professional cooks. The sum of 15 PAH concentrations in grilled foods was highest for meat grilling over charcoal briquettes - 382,020.39 ng/m3 and lowest for meat grilling on a gas grill - 1442.16 ng/m3. The emissions of BTEX from lump charcoal grilling were 130 times higher compared to the gaseous grill. In all considered scenarios lump-charcoal and charcoal briquettes grilling derive the ILCR above the 10-4, indicating negative effects of traditional grills on human health. The paper completes knowledge of wide-ranging health implications associated with BBQs, a topic that is almost completely unaddressed among the scientific community and policymakers.

Acute cytotoxicity, genotoxicity, and apoptosis induced by petroleum VOC emissions in A549 cell line.

Gasoline is an essential petroleum-derived product powering the automotive economy worldwide. This research focused on the Volatile Organic Component (VOC) cocktail resulting from gasoline evaporation. Petroleum fugitive VOC inhalation by petrol station attendants have been widely associated with toxicological and health risks concerns. Another unusual practice in poor nations is gasoline sniffing to get high which can lead to intoxication and organ damages. In this study, a static air/liquid interface methodology was designed to emulate acute human lung-derived cell exposure to all the gasoline-derived generated VOCs. The research investigated the cytotoxic and genotoxic end points resulting from whole gasoline fumes in vitro exposure using A549 cells. Petroleum-derived VOCs were identified and characterized by GC-MS. VOCs exposure was emulated in a controlled environment by evaporating spiked crude gasoline (1 to 100 µl) in a closed exposure chamber. In the chamber, A549 cultured cells on snapwell inserts were exposed on their apical side to various concentrations of generated vapors for one hour at 37 °C to mimic lung exposure. The results indicated that acute gasoline whole VOCs exposure reduced cell viability (IC50 = 485 ppm immediately and IC50 = 516 ppm 24 h post-exposure), disrupted cell membrane integrity though LDH leakage and induced DNA damages. Furthermore, VOC exposure triggered caspase-independent apoptosis in exposed cells through upregulation of apoptotic pathways. Overall, the presented findings generated by the static exposure technique showed a practical and reproducible model that can be used to assess acute crude VOCs mixture toxicity endpoints and cell death pathways.

Autism-like symptoms by exposure to air pollution and valproic acid-induced in male rats.

Exposure to air pollution during prenatal or neonatal periods is associated with autism spectrum disorder (ASD) according to epidemiology studies. Furthermore, prenatal exposure to valproic acid (VPA) has also been found to be associated with an increased prevalence of ASD. To assess the association between simultaneous exposure to VPA and air pollutants, seven exposure groups of rats were included in current study (PM2.5 and gaseous pollutants exposed - high dose of VPA (PGE-high); PM2.5 and gaseous pollutants exposed - low dose of VPA (PGE-low); gaseous pollutants only exposed - high dose of VPA (GE-high); gaseous pollutants only exposed - low dose of VPA (GE-low); clean air exposed - high dose of VPA (CAE-high); clean air exposed - low dose of VPA (CAE-low) and clean air exposed (CAE)). The pollution-exposed rats were exposed to air pollutants from embryonic day (E0) to postnatal day 42 (PND42). In all the induced groups, decreased oxidative stress biomarkers, decreased oxytocin receptor (OXTR) levels, and increased the expression of interleukin 6 (IL-6), interleukin 1ß (IL-1ß), and tumor necrosis factor alpha (TNF-α) were found. The volumes of the cerebellum, hippocampus, striatum, and prefrontal decreased in all induced groups in comparison to CAE. Additionally, increased numerical density of glial cells and decreased of numerical density of neurons were found in all induced groups. Results show that simultaneous exposure to air pollution and VPA can cause ASD-related behavioral deficits and air pollution reinforced the mechanism of inducing ASD ̉s in VPA-induced rat model of autism.

Physicochemical and cell toxicity properties of particulate matter (PM) from a diesel vehicle fueled with diesel, spent coffee ground biodiesel, and ethanol.

The literature shows that information about the physical, chemical, and cell toxicity properties of particulate matter (PM) from diesel vehicles is not rich as the existence of a remarkable number of studies about the combustion, performance, and emissions of diesel vehicles using renewable liquid fuels, particularly biodiesels and alcohols. Also, the PM analyses from combustion of spent coffee ground biodiesel have not been comprehensively explored. Therefore, this research is presented. Pure diesel, 90% diesel + 10% biodiesel, and 90% diesel + 9% ethanol + 1% biodiesel, volume bases, were tested under a fast idle condition. STEM, SEM, EDS, Organic Carbon Analyzer, TGA/DSC, and Raman Spectrometer were employed for investigating the PM physical and chemical properties, and assays of cell viability, cellular reactive oxygen species, interleukin-6, and tumor necrosis factor-alpha were examined for investigating the PM cell toxicity properties. It is found that the application of both biodiesel and ethanol has the potential to change the PM properties, while the impact of ethanol is more than biodiesel on the changes. Regarding the important aspects, biodiesel can be effective for better human health (due to a decrease in cell death (-60.8%)) as well as good diesel particulate filter efficiency (due to lower activation energy (-7.6%) and frequency factor (-83.2%)). However, despite a higher impact of ethanol on the reductions in activation energy (-24.8%) and frequency factor (-99.0%), this fuel causes an increase in cell death (84.1%). Therefore, biodiesel can be an appropriate fuel to have a positive impact on human health, the environment, and emissions catalysts performance, simultaneously.

Ambient air pollution and COVID-19 incidence during four 2020-2021 case surges.

BACKGROUND: Air pollution exposure may make people more vulnerable to COVID-19 infection. However, previous studies in this area mostly focused on infection before May 2020 and long-term exposure. OBJECTIVE: To assess both long-term and short-term exposure to air pollution and COVID-19 incidence across four case surges from 03/1/2020 to 02/28/2021. METHODS: The cohort included 4.6 million members from a large integrated health care system in southern California with comprehensive electronic medical records (EMR). COVID-19 cases were identified from EMR. Incidence of COVID-19 was computed at the census tract-level among members. Prior 1-month and 1-year averaged air pollutant levels (PM2.5, NO2, and O3) at the census tract-level were estimated based on hourly and daily air quality data. Data analyses were conducted by each wave: 3/1/2020-5/31/2020, 6/1/202-9/30/2020, 10/1/2020-12/31/2020, and 1/1/2021-2/28/2021 and pooled across waves using meta-analysis. Generalized linear mixed effects models with Poisson distribution and spatial autocorrelation were used with adjustment for meteorological factors and census tract-level social and health characteristics. Results were expressed as relative risk (RR) per 1 standard deviation. RESULTS: The cohort included 446,440 COVID-19 cases covering 4609 census tracts. The pooled RRs (95% CI) of COVID-19 incidence associated with 1-year exposures to PM2.5, NO2, and O3 were 1.11 (1.04, 1.18) per 2.3 µg/m3,1.09 (1.02, 1.17) per 3.2 ppb, and 1.06 (1.00, 1.12) per 5.5 ppb respectively. The corresponding RRs (95% CI) associated with prior 1-month exposures were 1.11 (1.03, 1.20) per 5.2 µg/m3 for PM2.5, 1.09 (1.01, 1.17) per 6.0 ppb for NO2 and 0.96 (0.85, 1.08) per 12.0 ppb for O3. CONCLUSION: Long-term PM2.5 and NO2 exposures were associated with increased risk of COVID-19 incidence across all case surges before February 2021. Short-term PM2.5 and NO2 exposures were also associated. Our findings suggest that air pollution may play a role in increasing the risk of COVID-19 infection.

The exposome in practice: an exploratory panel study of biomarkers of air pollutant exposure in Chinese people aged 60-69 years (China BAPE Study).

The exposome overhauls conventional environmental health impact research paradigms and provides a novel methodological framework that comprehensively addresses the complex, highly dynamic interplays of exogenous exposures, endogenous exposures, and modifiable factors in humans. Holistic assessments of the adverse health effects and systematic elucidation of the mechanisms underlying environmental exposures are major scientific challenges with widespread societal implications. However, to date, few studies have comprehensively and simultaneously measured airborne pollutant exposures and explored the associated biomarkers in susceptible healthy elderly subjects, potentially resulting in the suboptimal assessment and management of health risks. To demonstrate the exposome paradigm, we describe the rationale and design of a comprehensive biomarker and biomonitoring panel study to systematically explore the association between individual airborne exposure and adverse health outcomes. We used a combination of personal monitoring for airborne pollutants, extensive human biomonitoring, advanced omics analysis, confounding information, and statistical methods. We established an exploratory panel study of Biomarkers of Air Pollutant Exposure in Chinese people aged 60-69 years (China BAPE), which included 76 healthy residents from a representative community in Jinan City, Shandong Province. During the period between September 2018 and January 2019, we conducted prospective longitudinal monitoring with a 3-day assessment every month. This project: (1) leveraged advanced tools for personal airborne exposure monitoring (external exposures); (2) comprehensively characterized biological samples for exogenous and endogenous compounds (e.g., targeted and untargeted monitoring) and multi-omics scale measurements to explore potential biomarkers and putative toxicity pathways; and (3) systematically evaluated the relationships between personal exposure to air pollutants, and novel biomarkers of exposures and effects using exposome-wide association study approaches. These findings will contribute to our understanding of the mechanisms underlying the adverse health impacts of air pollution exposures and identify potential adverse clinical outcomes that can facilitate the development of effective prevention and targeted intervention techniques.

Toxic effect of cooking oil fume (COF) on lungs: Evidence of endoplasmic reticulum stress in rat.

BACKGROUND: Cooking oil fumes (COF) is one of the primary sources of indoor air pollution in China, which is associated with respiratory diseases such as acute lung injury and lung cancer. However, evidence of COF toxic effect was few. OBJECTIVES: The research was aimed to investigate the toxic effect and the underlying mechanisms induced by COF. METHODS: The female Wistar rats were randomly divided into several groups, including control group, COF exposure group and VE protection group, and instilled intratracheally with different COF suspensions (0.2, 2, 20 mg/kg) or saline once every 3 days for 30 days. After 24 h of final exposure, all rat were anesthetic euthanasia to draw materials. The alveolar lavage fluid (BALF) was for inflammatory cell count. The lung homogenate was to determine the biochemical indexes such as oxidative stress, apoptosis factors, carcinogenic toxicity and endoplasmic reticulum (ER) stress. The left lung was made for immunohistochemical and histopathological analysis. RESULTS: The results showed that the levels of oxidative stress (ROS), apoptosis factors (NF-κB), carcinogenic toxicity (P53 and 8-OhdG), ER stress (IRE-1α and Caspase-12) in 2 mg/kg and 20 mg/kg COF exposure groups were significantly increased compared with the saline groups. The above pathological changes were improved after vitamin E (VE) supplementation. In addition, the immunohistochemical and histopathological analysis found the same trend. CONCLUSION: The COF had health risk of heredity and potential carcinogenicity. Besides, COFs can not only induce oxidative stress, but also induce ER stress in lung and airway epithelial cells of female rats through the unfolded protein reaction (UPR) pathway. It revealed that the oxidative stress and ER stress interacted in aggravating lung injury. VE could effectively alleviate the lung injury causing by COF exposure.

Prenatal PM2.5 exposure in the second and third trimesters predicts neurocognitive performance at age 9-10 years: A cohort study of Mexico City children.

INTRODUCTION: Prenatal exposure to fine particulate matter air pollution (PM2.5) is an important, under-studied risk factor for neurodevelopmental dysfunction. We describe the relationships between prenatal PM2.5 exposure and vigilance and inhibitory control, executive functions related to multiple health outcomes in Mexico City children. METHODS: We studied 320 children enrolled in Programming Research in Obesity, GRowth, Environment and Social Stressors, a longitudinal birth cohort study in Mexico City. We used a spatio-temporal model to estimate daily prenatal PM2.5 exposure at each participant's residential address. At age 9-10 years, children performed three Go/No-Go tasks, which measure vigilance and inhibitory control ability. We used Latent class analysis (LCA) to classify performance into subgroups that reflected neurocognitive performance and applied multivariate regression and distributed lag regression modeling (DLM) to test overall and time-dependent associations between prenatal PM2.5 exposure and Go/No-Go performance. RESULTS: LCA detected two Go/No-Go phenotypes: high performers (Class 1) and low performers (Class 2). Predicting odds of Class 1 vs Class 2 membership based on prenatal PM2.5 exposure timing, logistic regression modeling showed that average prenatal PM2.5 exposure in the second and third trimesters correlated with increased odds of membership in low-performance Class 2 (OR = 1.59 (1.16, 2.17), p = 0.004). Additionally, DLM analysis identified a critical window consisting of gestational days 103-268 (second and third trimesters) in which prenatal PM2.5 exposure predicted poorer Go/No-Go performance. DISCUSSION: Increased prenatal PM2.5 exposure predicted decreased vigilance and inhibitory control at age 9-10 years. These findings highlight the second and third trimesters of gestation as critical windows of PM2.5 exposure for the development of vigilance and inhibitory control in preadolescent children. Because childhood development of vigilance and inhibitory control informs behavior, academic performance, and self-regulation into adulthood, these results may help to describe the relationship of prenatal PM2.5 exposure to long-term health and psychosocial outcomes. The integrative methodology of this study also contributes to a shift towards more holistic analysis.

Characterising non-linear associations between airborne pollen counts and respiratory symptoms from the AirRater smartphone app in Tasmania, Australia: A case time series approach.

Pollen is a well-established trigger of asthma and allergic rhinitis, yet concentration-response relationships, lagged effects, and interactions with other environmental factors remain poorly understood. Smartphone technology offers an opportunity to address these challenges using large, multi-year datasets that capture individual symptoms and exposures in real time. We aimed to characterise associations between six pollen types and respiratory symptoms logged by users of the AirRater smartphone app in Tasmania, Australia. We analyzed 44,820 symptom reports logged by 2272 AirRater app users in Tasmania over four years (2015-2019). With these data we evaluated associations between daily respiratory symptoms and atmospheric pollen concentrations. We implemented Poisson regression models, using the case time series approach designed for app-sourced data. We assessed potentially non-linear and lagged associations with (a) total pollen and (b) six individual pollen taxa. We adjusted for seasonality and meteorology and tested for interactions with particulate air pollution (PM2.5). We found evidence of non-linear associations between total pollen and respiratory symptoms for up to three days following exposure. For total pollen, the same-day relative risk (RR) increased to 1.31 (95% CI: 1.26-1.37) at a concentration of 50 grains/m3 before plateauing. Associations with individual pollen taxa were also non-linear with some diversity in shapes. For all pollen taxa the same-day RR was highest. The interaction between total pollen and PM2.5 was positive, with risks associated with pollen significantly higher in the presence of high concentrations of PM2.5. Our results support a non-linear response between airborne pollen and respiratory symptoms. The association was strongest on the day of exposure and synergistic with particulate air pollution. The associations found with Dodonaea and Myrtaceae highlight the need to further investigate the role of Australian native pollen types in allergic respiratory disease.

Particulate matter air pollutants and cardiovascular disease: Strategies for intervention.

Air pollution is consistently linked with elevations in cardiovascular disease (CVD) and CVD-related mortality. Particulate matter (PM) is a critical factor in air pollution-associated CVD. PM forms in the air during the combustion of fuels as solid particles and liquid droplets and the sources of airborne PM range from dust and dirt to soot and smoke. The health impacts of PM inhalation are well documented. In the US, where CVD is already the leading cause of death, it is estimated that PM2.5 (PM < 2.5 µm in size) is responsible for nearly 200,000 premature deaths annually. Despite the public health data, definitive mechanisms underlying PM-associated CVD are elusive. However, evidence to-date implicates mechanisms involving oxidative stress, inflammation, metabolic dysfunction and dyslipidemia, contributing to vascular dysfunction and atherosclerosis, along with autonomic dysfunction and hypertension. For the benefit of susceptible individuals and individuals who live in areas where PM levels exceed the National Ambient Air Quality Standard, interventional strategies for mitigating PM-associated CVD are necessary. This review will highlight current state of knowledge with respect to mechanisms for PM-dependent CVD. Based upon these mechanisms, strategies for intervention will be outlined. Citing data from animal models and human subjects, these highlighted strategies include: 1) antioxidants, such as vitamins E and C, carnosine, sulforaphane and resveratrol, to reduce oxidative stress and systemic inflammation; 2) omega-3 fatty acids, to inhibit inflammation and autonomic dysfunction; 3) statins, to decrease cholesterol accumulation and inflammation; 4) melatonin, to regulate the immune-pineal axis and 5) metformin, to address PM-associated metabolic dysfunction. Each of these will be discussed with respect to its potential role in limiting PM-associated CVD.

Effects of short-term personal exposure to air pollution on platelet mitochondrial DNA methylation levels and the potential mitigation by L-arginine supplementation.

The potential effect of short-term exposure to air pollution on mitochondrial DNA (mtDNA) methylation remains to be explored. This study adopted an experimental exposure protocol nested with an intervention study on L-arginine (L-Arg) supplementation among 118 participants. Participants walked along a traffic road for 2 hours in the last day of a 14-day intervention to investigate the effects of short-term personal exposure to air pollution on platelet mtDNA methylation and the possible modifying effects of L-Arg supplementation. Results showed that short-term personal exposure to air pollutants was associated with hypomethylation in platelet mtDNA in 110 participants who completed the study protocol. Specifically, 2-h fine particulate matter (PM2.5) exposure during the outdoor walk was significantly associated with hypomethylation in mt12sRNA; 24-h PM2.5 and black carbon (BC) exposures from the start of the walk till next morning were both significantly associated with hypomethylation in the D-loop region; 24-h BC exposure was also significantly associated with hypomethylation in ATP8_P1. Supplementation with L-Arg could mitigate the air pollution effects on platelet mtDNA methylation, especially the D-loop region. These findings suggest that platelet mtDNA methylation may be sensitive effect biomarker for short-term exposure to air pollution and may help deepen the understanding of the epigenetic mechanisms of adverse cardiovascular effects of air pollution.