Inhalation Exposure Research Articles

Inhalation exposure to flavored electronic nicotine delivery systems (vaping) negatively impacts cardiac electrophysiology

Abstract Background Electronic nicotine delivery systems (ENDS) heat "e-liquids" to generate "e-vapor", an inhalable aerosol. E-liquids contain nicotine and flavors in a solvent of 70% vegetable glycerin, 30% propylene glycol (70VG/30PG). Flavored ENDS are very popular among teens vapers, however, the possible cardiac electrophysiological harm of inhalation exposure to flavored ENDS are not fully understood. Purpose To test if inhalation exposure to e-liquids or their constituents compromises mitochondrial integrity, increases oxidative stress, and leads to cardiac electrophysiological toxicity. Methods Gas chromatography mass spectrometry (GC/MS), and flow cytometry, in-vivo programmed electrical stimulation (PES), and transmission electron microscopy (TEM) were used in atrial like HL-1 myocytes and in mice overexpressing the antioxidant mitochondrial catalase (MCAT) which underwent inhalation exposure to e-vapor. Results We compared the toxicity of e-vapor exposure to 30 differently flavored e-liquids (70VG/30PG, with 6 mg/ml nicotine) in HL-1 cells using annexinV flow cytometry. Most e-liquids were toxic. We then quantified the concentrations of major flavoring carbonyls (cinnamaldehyde, vanillin, ethyl-vanillin, maltol, and ethyl-maltol) in the 30 e-liquids using GC/MS. Toxicity of the e-liquids in HL-1 cells correlated with their flavoring carbonyls concentration. We assessed oxidative stress (OS) via CellROX flow cytometry in HL-1 cells exposed to vanilla flavored e-vapor. OS increased in exposed cells but this was blunted by N-acetylcycteine pretreatment. In-vivo inhalation exposure to e-vapor of vanilla flavored e-liquid with 6 mg/ml nicotine increased inducible ventricular tachycardia duration in WT but not in MCAT mice versus control. In TEM, mitochondrial perimeter was unaffected, but cristae thickness decreased in exposed WT, but not in exposed MCAT hearts versus controls. We then investigated whether adverse cardiac effects of vaping are due only to nicotine. Mice were exposed to the e-vapor of 70VG/30PG base alone or base plus vanillin WITHOUT nicotine. In telemetric ECG analysis of heart rate variability, exposure to base plus vanillin decreased parasympathetic indices more than exposure to base alone. In PES, the effective refractory periods of base alone and base plus vanillin groups tended to be shortened vs air controls. While exposure to base alone and to base plus vanillin significantly increased inducible ventricular tachycardia duration compared to air controls, the increase in the base plus vanillin group was more significant compared to that of base alone. Conclusions Inhalation exposure to flavored ENDS or to their NON-NICOTINE constituents negatively affects ventricular electrophysiology, possibly via adverse mitochondrial remodeling, and increased oxidative stress.

Improving approaches to hygienic rationing of antimicrobial drugs

Introduction. Currently, the production of medicines, including those with antimicrobial properties, is expanding at chemical and pharmaceutical enterprises. However, scientific approaches to hygienic regulation of the content of specific antimicrobials in the air of the work area are not yet available. The study aims to substantiate approaches to predicting approximate safe levels of exposure (ASLE) to substances with a specific antimicrobial effect. Materials and methods. The scientists have carried out the research in two stages. The first stage is an experimental study of the single inhalation effect of an antibiotic clarithromycin at concentrations of 54.2; 25.4; 15.3; 9.1; 2.8 and 0.9 mg/m3 on mongrel female rats weighing 230–250 g. The authors have evaluated the indicators of toxic (morphological and functional parameters of the nervous, cardiovascular and respiratory systems, biochemical parameters of the liver and kidneys, as well as the composition of peripheral blood) and specific effects (qualitative and quantitative composition of the microbiota of the large intestine of rats). The second stage was the analysis of the database on hygienic rationing of chemicals, which consisted in searching for hygienic standards (ASLE, MPC), threshold concentrations for the general toxic (Limint) and specific (Limbact) effects of antimicrobials. Results. During the experiment, experts have established the threshold of acute inhalation exposure (Limac int) of clarithromycin at a concentration of 25.4 mg/m3 according to the total toxic effects (peripheral blood counts, liver and kidney function). When exposed to an antibiotic at a concentration of 2.8 mg/m3, there was an imbalance of the intestinal microflora in the absence of a general toxic effect, which indicated a specific and selective antimicrobial effect of the drug. Based on the analysis of literature data, the parameters of toxicometry of 21 substances with antimicrobial effect were determined, their representative sample was justified and its regression analysis was carried out. Conclusion. Based on experimental and literary data, the authors established a significantly strong correlation (r=0.729) between the values of MPC (ASLE) and the threshold of antimicrobial action (Limbact). They also developed a mathematical equation to predict safe levels of antimicrobials based on their specific and selective activity.

A mouse model of wildfire smoke-induced health effects: sex differences in acute and sustained effects of inhalation exposures

Due to climate change, wildfires have increased in intensity and duration. While wildfires threaten lives directly, the smoke has more far-reaching adverse health impacts. During an extreme 2017 wildfire event, residents of Seeley Lake, Montana were exposed to unusually high levels of wood smoke (WS) causing sustained effects on lung function (decreased FEV1/FVC). Objective: The present study utilized an animal model of WS exposure to research cellular and molecular mechanisms of the resulting health effects. Methods: Mice were exposed to inhaled WS utilizing locally harvested wood to recapitulate community exposures. WS was generated at a rate resulting in a 5 mg/m3 PM2.5 exposure for five days. Results: This exposure resulted in a similar 0.28 mg/m2 particle deposition (lung surface area) in mice that was calculated for human exposure. As with the community observations, there was a significant effect on lung function, increased resistance, and decreased compliance, that was more pronounced in males at an extended (2 months) timepoint and males were more affected than females: ex vivo assays illustrated changes to alveolar macrophage functions (increased TNFα secretion and decreased efferocytosis). Female mice had significantly elevated IL-33 levels in lungs, however, pretreatment of male mice with IL-33 resulted in an abrogation of the observed WS effects, suggesting a dose-dependent role of IL-33. Additionally, there were greater immunotoxic effects in male mice. Discussion: These findings replicated the outcomes in humans and suggest that IL-33 is involved in a mechanism of the adverse effects of WS exposures that inform on potential sex differences.

A novel approach to assess the health risk of aryl hydrocarbon receptor-bound contaminants via inhalation exposure using CYP1A1 expression as a biomarker

Polycyclic aromatic hydrocarbons (PAHs) and dioxins are potential causes of multiple diseases by activating the aryl hydrocarbon receptor (AhR) pathway. Health risk assessment of chemicals primarily relies on the relative potency factor (RPF), although its accuracy may be limited when solely using EC50 values. The induction of cytochrome P4501A1 (CYP1A1) serves as a biomarker for AhR activation and is an integrator of dioxin-like toxicity. Here, we present a method for evaluating the risks associated with AhR activation using mathematical models of dose-CYP1A1 induction. The dose-effect curves for certain PAHs and dioxins, including Ant, BghiP, 1,2,3,4,7,8-HxCDD, and others, exhibited a non-classical S-shaped form. The toxic equivalent factor (TEF) profiles revealed a broad range of toxic equivalent factor values. The TEFs for PAHs ranged from approximately 0.01 to 6, with higher values being observed when the concentration was less than 10−10 M, with the exceptions of Ace, Phe, and BghiP. Most congeners of dioxins got the lowest TEF value at around 10−10 M, ranging from 0.04 to 1.00. The binding affinity of AhR to ligands did not display a strong correlation with the EC50 of CYP1A1 expression, suggesting that the AhR-mediated effects of PAHs and dioxins are not fixed but instead fluctuate with the dose. Air samples acquired from a parking area were used to compare the proficiency of RPF and our current approach. In the current method, naphthalene and chrysene were the primary contributors of PAHs to AhR-mediated risks in parking lots air samples, respectively. However, the contributions of naphthalene and chrysene could be disregarded in the RPF approach.

GAPDH inhibition mediated by thiol oxidation in human airway epithelial cells exposed to an environmental peroxide

Intracellular redox homeostasis in the airway epithelium is closely regulated through adaptive signaling and metabolic pathways. However, inhalational exposure to xenobiotic stressors such as secondary organic aerosols (SOA) can alter intracellular redox homeostasis. Isoprene hydroxy hydroperoxide (ISOPOOH), a ubiquitous volatile organic compound derived from the atmospheric photooxidation of biogenic isoprene, is a major contributor to SOA. We have previously demonstrated that exposure of human airway epithelial cells (HAEC) to ISOPOOH induces oxidative stress through multiple mechanisms including lipid peroxidation, glutathione oxidation, and alterations of glycolytic metabolism. Using dimedone-based reagents and copper catalyzed azo-alkynyl cycloaddition to tag intracellular protein thiol oxidation, we demonstrate that exposure of HAEC to micromolar levels of ISOPOOH induces reversible oxidation of cysteinyl thiols in multiple intracellular proteins, including GAPDH, that was accompanied by a dose-dependent loss of GAPDH enzymatic activity. These results demonstrate that ISOPOOH induces an oxidative modification of intracellular proteins that results in loss of GAPDH activity, which ultimately impacts the dynamic regulation of the intracellular redox homeostatic landscape in HAEC.

Carcinogenicity and non-carcinogenicity health risks due to PM2.5 bound trace metals at a sub urban site in Northwest Indo-Gangetic Plain.

This study investigates the PM2.5 bound metals using yearlong measurements at a regionally representative suburban site in the Northwest Indo-Gangetic Plain (NWIGP). The order of the measured annual average concentrations of PM2.5 bound metals is Fe > Zn > Ba > Sn > Pb > Cd > Ni > Mn > Cr > Li. Lithium bound to airborne PM2.5 has been reported for the first time in NWIGP. Ni (72.4 ng m-3) and Cd (36.9 ng m-3) have exceeded the acceptable limits set by NAAQS, India. Estimated the hazard quotient (HQ > 1) of Mn and hazard index (HI > 1) of measured metals exceeded the threshold limits indicating the potential non-carcinogenic health risk due to inhalation exposure of PM2.5 bound trace metals. Further, excessive lifetime cancer risk due to inhalation exposure to Cd, Ni and Cr was estimated and found to exceed the threshold limit set by the USEPA for adults and children.

Safety evaluation of synthesized magnesium carbonate hydrate particles following inhalation exposure

Numerous fine particles or mist from environmental substances significantly contribute to human beings, affecting health issues for both humans and the environment by irritating the respiratory system. To achieve scarcity of information regarding exposure routes and the relationship between substance and health effects needs to be investigated more. Here, we investigated flame retardants (FRs): magnesium carbonate was synthesized, and its inhalation toxicity was examined for the first time by applying it to Sprague-Dawley rats using a mist aerosol-supplying chamber condition. The synthesized magnesium carbonate was fully physiochemically characterized, exhibiting a mesoporous sheet-like morphology, size distribution of 4.971 ± 2.363 μm, the dypingite phase, a surface area of 10.718 m² g−1, and a pore volume of 0.051 cm³ g−1. As a result of the inhalation toxicity study, the 50% lethal concentration (LC50) of magnesium carbonate was determined to be equal to or greater than 1.91 mg m−3. Microscopic examination for assessing pulmonary residue levels of magnesium carbonate reveals the presence of residues in the lungs up to 3 days post-administration. However, over time, there is a gradual decrease of pulmonary residues, and by the 14th day of administration, it is regarded that no residual presence is observable within the pulmonary system.

Cross-shift changes in pulmonary function and occupational exposure to particulate matter among e-waste workers in Ghana.

Little is known on the association between cross-shift changes in pulmonary function and personal inhalation exposure to particulate matter (PM) among informal electronic-waste (e-waste) recovery workers who have substantial occupational exposure to airborne pollutants from burning e-waste. Using a cross-shift design, pre- and post-shift pulmonary function assessments and accompanying personal inhalation exposure to PM (sizes <1, <2.5 μm, and the coarse fraction, 2.5-10 μm in aerodynamic diameter) were measured among e-waste workers (n = 142) at the Agbogbloshie e-waste site and a comparison population (n = 65) in Accra, Ghana during 2017 and 2018. Linear mixed models estimated associations between percent changes in pulmonary function and personal PM. Declines in forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) per hour were not significantly associated with increases in PM (all sizes) among either study population, despite breathing zone concentrations of PM (all sizes) that exceeded health-based guidelines in both populations. E-waste workers who worked "yesterday" did, however, have larger cross-shift declines in FVC [-2.4% (95%CI: -4.04%, -0.81%)] in comparison to those who did not work "yesterday," suggesting a possible role of cumulative exposure. Overall, short-term respiratory-related health effects related to PM exposure among e-waste workers were not seen in this sample. Selection bias due to the "healthy worker" effect, short shift duration, and inability to capture a true "pre-shift" pulmonary function test among workers who live at the worksite may explain results and suggest the need to adapt cross-shift studies for informal settings.

Benzo[a]pyrene evokes epithelial-mesenchymal transition and pulmonary fibrosis through AhR-mediated Nrf2-p62 signaling

Benzo[a]pyrene (BaP) and its metabolic end product benzo(a)pyren-7,8-dihydrodiol-9,10-epoxide (BPDE), are known toxic environmental pollutants. This study aimed to analyze whether sub-chronic BPDE exposure initiated pulmonary fibrosis and the potential mechanisms. In this work, male C57BL6/J mice were exposed to BPDE by dynamic inhalation exposure for 8 weeks. Our results indicated that sub-chronic BPDE exposure evoked pulmonary fibrosis and epithelial-mesenchymal transition (EMT) in mice. Both in vivo and in vitro, BPDE exposure promoted nuclear translocation of Snail. Further experiments indicated that nuclear factor erythroid 2-related factor 2 (Nrf2) and p62 were upregulated in BPDE-exposed alveolar epithelial cells. Moreover, Nrf2 siRNA transfection evidently attenuated BPDE-induced p62 upregulation. Besides, p62 shRNA inhibited BPDE-incurred Snail nuclear translocation and EMT. Mechanically, BPDE facilitated physical interaction between p62 and Snail in the nucleus, then repressed Snail protein degradation by p62-dependent autophagy-lysosome pathway, and finally upregulated transcriptional activity of Snail. Additionally, aryl hydrocarbon receptor (AhR) was activated in BPDE-treated alveolar epithelial cells. Dual-luciferase assay indicated activating AhR could bind to Nrf2 gene promoter. Moreover, pretreatment with CH223191 or α-naphthoflavone (α-NF), AhR antagonists, inhibited BPDE-activated Nrf2-p62 signaling, and alleviated BPDE-induced EMT and pulmonary fibrosis in mice. Taken together, AhR-mediated Nrf2-p62 signaling contributes to BaP-induced EMT and pulmonary fibrosis.

Proposals for new spray drift exposure values in orchards and vineyards for residents and bystanders

In the EU, predicted exposure to spray drift for residents and bystanders from applications in orchards and vineyards is based on data from one study published in 1987, where one downwind distance (8 m) was considered. CropLife Europe conducted sixteen new GLP compliant studies in 4 EU countries, 8 in orchards, 8 in vineyards with early and late season applications, using adult and child mannequins located 5, 10 and 15 m downwind from the last row to measure dermal and inhalation exposures. The resulting “Bystander Resident Orchard Vineyard (BROV)” database comprises 288 observations and offers a more comprehensive option for exposure prediction.There were differences between adult and child, crop type, leaf cover and distance from the sprayer, supporting the derivation of mean, median, 75th and 95th percentile exposures for each subset. Exposures did not generally correlate with wind speed, wind direction, sprayer type, spray quality, spray concentration or amount applied. Dermal and inhalation exposure were lower in vineyards than in orchards and further analysis is required to understand why.

Chronic Obstructive Pulmonary Disease

Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable and treatable lung disease. It is characterized by chronic respiratory symptoms and airflow limitation due to abnormalities of the airways caused by continuous exposure to noxious particles or gases. COPD occupies the third position for the cause of death worldwide. The major risk factor for the development of COPD is tobacco smoking. The inhalation of toxic particles, biomass exposure and outdoor air pollution along with other host factors including abnormal lung development and accelerated lung aging can also contribute. Spirometry characterized by non-fully reversible airflow limitation i.e., FEV1/FVC &lt; 0.7 post bronchodilation, confirms the diagnosis of COPD. The major goals of management are to reduce risk factors, manage stable COPD, prevent and treat acute exacerbations, and manage associated illnesses. The conservative management comprising of antibiotics, inhaled corticosteroids, mucolytics etc. offer promising results in this condition. But tachycardia, glossitis, glaucoma, nausea are some of the common adverse reactions noticed on chronic use of these group of drugs. The contemporary health scenario demands more contribution in this regard from the indigenous system of medicine. In Āyurvedic view, COPD can be considered under the spectrum of Prāṇavaha srotodushti vikaras. The clinical features and etiology mentioned for diseases mentioned in Ayurveda such as Kāsa, Tamaka śvāsa, Rajayakshma etc has similarity with that of COPD. Though COPD cannot be correlated to any single condition of Prāṇavaha sroto duṣti, Tamaka śvāsa can be considered as includes most of the clinical features including cough. When the etiological factors favour, the vitiated and aggravated Kapha dosha blocks the channels of Prāna and Udāna vāta causing the onset and symptoms of the disease.

PM2.5-induced cellular senescence drives brown adipose tissue impairment in middle-aged mice

Airborne fine particulate matter (PM2.5) exposure is closely associated with metabolic disturbance, in which brown adipose tissue (BAT) is one of the main contributing organs. However, knowledge of the phenotype and mechanism of PM2.5 exposure-impaired BAT is quite limited. In the study, male C57BL/6 mice at three different life phases (young, adult, and middle-aged) were simultaneously exposed to concentrated ambient PM2.5 or filtered air for 8 weeks using a whole-body inhalational exposure system. H&E staining and high-resolution respirometry were used to assess the size of adipocytes and mitochondrial function. Transcriptomics was performed to determine the differentially expressed genes in BAT. Quantitative RT-PCR, immunohistochemistry staining, and immunoblots were performed to verify the transcriptomics and explore the mechanism for BAT mitochondrial dysfunction. Firstly, PM2.5 exposure caused altered BAT morphology and mitochondrial dysfunction in middle-aged but not young or adult mice. Furthermore, PM2.5 exposure increased cellular senescence in BAT of middle-aged mice, accompanied by cell cycle arrest, impaired DNA replication, and inhibited AKT signaling pathway. Moreover, PM2.5 exposure disrupted apoptosis and autophagy homeostasis in BAT of middle-aged mice. Therefore, BAT in middle-aged mice was more vulnerable to PM2.5 exposure, and the cellular senescence-initiated apoptosis, autophagy, and mitochondrial dysfunction may be the mechanism of PM2.5 exposure-induced BAT impairment.

Biomarkers of Organophosphate and Polybrominated Diphenyl Ether (PBDE) Flame Retardants of American Workers and Associations with Inhalation and Dermal Exposures.

This study evaluated workers' exposures to flame retardants, including polybrominated diphenyl ethers (PBDEs), organophosphate esters (OPEs), and other brominated flame retardants (BFRs), in various industries. The study aimed to characterize OPE metabolite urinary concentrations and PBDE serum concentrations among workers from different industries, compare these concentrations between industries and the general population, and evaluate the likely route of exposure (dermal or inhalation). The results showed that workers from chemical manufacturing had significantly higher (p <0.05) urinary concentrations of OPE metabolites compared to other industries. Spray polyurethane foam workers had significantly higher (p <0.05) urinary concentrations of bis(1-chloro-2-propyl) phosphate (BCPP) compared to other industries. Electronic scrap workers had higher serum concentrations of certain PBDE congeners compared to the general population. Correlations were observed between hand wipe samples and air samples containing specific flame-retardant parent chemicals and urinary metabolite concentrations for some industries, suggesting both dermal absorption and inhalation as primary routes of exposure for OPEs. Overall, this study provides insights into occupational exposure to flame retardants in different industries and highlights the need for further research on emerging flame retardants and exposure reduction interventions.

Opening windows as a supplementary ventilation strategy for large classrooms in a pandemic situation: Field measurements and simulation

The coronavirus disease 2019 (COVID-19) has led to significant global health emergencies in recent years, prompting widespread recommendations across various regions for opening windows in building codes. However, official guidelines have not adequately addressed the details of window opening arrangements related to the supporting evidence from existing literature. This study investigated the risk of disease outbreaks via respiratory transmission in large university studio classrooms. It examined the effectiveness of window-door opening strategies combined with mechanical ventilation in mitigating the infection risk of respiratory diseases in such spaces. A full-scale school ventilation performance test bed was used to measure indoor airflow and CO2 distribution patterns. Comparisons were made with the numerical simulation of exhaled viral emissions. A modified Wells-Riley equation was employed to calculate inhalation exposure and disease infection risks at the room level. Measurements showed that fresh air ventilation from the mechanical system was relatively low compared to existing standards, especially in pandemic situations. The results show that opening windows can lead to a decrease to low probabilities (below 5 %) of infection risk in 85.02 % area of a classroom over an 8-h period, which demonstrates that window-opening behavior is an effective supplementary strategy for large educational spaces with mechanically ventilated systems during emergencies when active measures are insufficient for diluting diseases. Furthermore, the study reveals that maximizing outdoor air rates by opening all windows may occasionally result in adverse indoor airflow redistribution, increasing virus load from 0.0382 to 0.8926 quanta/m3 near the virus source locations.

Probabilistic Reference and 10% Effect Concentrations for Characterizing Inhalation Non-cancer and Developmental/Reproductive Effects for 2,160 Substances.

Chemicals assessment and management frameworks rely on regulatory toxicity values, which are based on points of departure (POD) identified following rigorous dose-response assessments. Yet, regulatory PODs and toxicity values for inhalation exposure (i.e., reference concentrations [RfCs]) are available for only ∼200 chemicals. To address this gap, we applied a workflow to determine surrogate inhalation route PODs and corresponding toxicity values, where regulatory assessments are lacking. We curated and selected inhalation in vivo data from the U.S. EPA's ToxValDB and adjusted reported effect values to chronic human equivalent benchmark concentrations (BMCh) following the WHO/IPCS framework. Using ToxValDB chemicals with existing PODs associated with regulatory toxicity values, we found that the 25th %-ile of a chemical's BMCh distribution () could serve as a suitable surrogate for regulatory PODs (Q2 ≥ 0.76, RSE ≤ 0.82 log10 units). We applied this approach to derive for 2,095 substances with general non-cancer toxicity effects and 638 substances with reproductive/developmental toxicity effects, yielding a total coverage of 2,160 substances. From these , we derived probabilistic RfCs and human population effect concentrations. With this work, we have expanded the number of chemicals with toxicity values available, thereby enabling a much broader coverage for inhalation risk and impact assessment.

Effect of transfluthrin on fertility and pregnancy outcome after inhalation and oral exposure in rats

Effect of transfluthrin on fertility and pregnancy outcome after inhalation and oral exposure in rats

Occurrence, seasonal variations, and spatial distributions of current-use organoamine pesticides in the atmosphere of Shanghai, China

An increasing trend in pesticide usage requires a better understanding of the occurrence, fate, and exposure risk of current-use organoamine pesticides (CUOAPs) in the atmosphere as the population grows and climate changes. 33 target CUOAPs were measured in 89 atmospheric samples collected in different seasons from Shanghai, including gaseous and particulate phases. The total concentrations of gaseous phase CUOAPs ranged from 407 to 2980 pg/m3, with an average value of 887 ± 426 pg/m3. Conversely, the total concentrations of particulate CUOAPs were found to be one to two orders of magnitude lower than those in the gas phase, with low detection frequencies. Diphenylamine and Molinate were ubiquitous and predominant in the gaseous CUOAPs. The average total concentrations of gaseous CUOAPs were significantly higher in spring than those in winter and autumn seasons. Gaseous CUOAPs concentrations increased from rural to downtown areas during spring, showing different spatial distribution from winter and autumn. A significant correlation was observed between temperature and the presence of Dicloran, Pirimicarb, Diphenylamine, and Acetochlor. Agricultural activities and city pest control may be the main sources of CUOAPs, while meteorological factors including temperature and wind speed also impact the dispersal of these chemicals in the atmosphere. The increased risk of exposure was observed to be higher during the spring season compared to the autumn and winter seasons, aligning with the pattern of heightened utilization of CUOAPs during the planting and growing phases. The daily inhalation exposure of CUOAPs did not exceed the current oral reference dose.

Impact of COVID-19 Lockdown on Inhaled Toxic Elements in PM2.5 in Beijing: Composition Characterization and Source-Specific Health Risks Assessment

In early 2020, China experienced a mass outbreak of a novel coronavirus disease (COVID-19). With an aim to evaluate the impact of emission variations on toxic element species in PM2.5 and the health risks associated with inhalation exposure during COVID-19, we collected PM2.5 filter samples in Beijing from January 1 to February 28, 2020. Positive matrix factorization (PMF) and a health risk (HR) assessment model were used to assess the health risks of the toxic elements and critical risk sources. The total concentration of eight toxic elements (Se, Cd, Pb, Zn, As, Cu, Ni, and Cr) in Beijing showed a trend of first increasing and then decreasing: full lockdown (322.9 ng m−3) &gt; pre-lockdown (264.2 ng m−3) &gt; partial lockdown (245.3 ng m−3). During the lockdown period, stringent control measures resulted in significant reductions (6−20%) in Zn, Pb, Cd, and Ni levels, while concentrations of Se, As, Cu, and Cr were unexpectedly elevated (14−348%). A total of five sources was identified: traffic emission, coal combustion, dust emission, industrial emission and mixed source of biomass burning and firework combustion. Total carcinogenic risk (TCR) of the selected toxic elements exceeded the US EPA limits for children and adults. As and Cr (IV) were the main contributors to non-carcinogenic and carcinogenic risks, respectively. For source-resolved risks, coal combustion was the main contributor to HI (43%), while industrial emissions were the main cause of TCR (45%). Additionally, increased contributions from coal combustion, biomass burning, and firework combustion during the full lockdown elevated the HI and TCR values.

Chemical characterization of road dust during diwali festival in Guwahati city of Assam, Northeast India.

The present study focuses on the elemental analysis of road dust in Guwahati, the largest city of Assam and the largest metropolis of Northeast India during the Diwali festival. Road dust samples were collected on pre-Diwali (PD), the Day after Diwali (DaD), and one week after Diwali (WaD) from two sites (Lankeshwar; LKW and Patharquarry; PTQ). Three composite samples were collected from 3 points at each site. The elemental concentration was analyzed using inductively coupled plasma mass spectrometry (ICP-MS). The concentrations of Ba and Sr increased by 1.6 and 1.7 times, respectively, after Diwali. Among other firework-related elements (FREs), Mg, Al, K, and Cu increased at LKW following Diwali (both DaD and WaD), whereas Mg, Al, and K increased in DaD dust at PTQ. The average concentration of Traffic Related Elements (TREs) at PTQ was significantly higher than at LKW (p < 0.05; 75.40mg/kg vs 63.96mg/kg). Cd had the highest enrichment (EF), followed by Ni and Zn. EF for Cd, Ni, and Zn ranged from high to extremely high enrichment. Ni and Cd exhibited moderate contamination (CF). The ecological risk (ER) values for Cd at LKW and PTQ were 54.32 and 56.71, respectively, indicating a moderate ER. Pearson's correlation was performed to study the relationship between elements, while PCA analysis was used to identify the main sources of these elements. Although the health hazard indices presently do not suggest any immediate danger, hazard quotient (HQ) values for ingestion, inhalation, and dermal exposure were higher for children than adults. In children, the contribution of HQing to HI (total risk) was the highest, accounting for more than 65% of all elements. There is no apparent lifetime cancer risk due to road dust exposure through inhalation.

Evaluation of antihypoxic effects of therapeutic breathing mixtures with high argon content on the example of acute blood loss in laboratory animals: a preclinical randomized experimental study

Background. According to the hypothesis of the study, the therapeutic efficacy of measures to treat hypoxic (ischemic) emergencies can be significantly increased by using an artificial gas mixture with normal or increased oxygen content and a high content of argon, being bioactive despite its chemical inertness.Objective. To experimentally evaluate the antihypoxic effects of argon on the example of acute massive blood loss in experimental animals.Methods. The study was carried out on 72 albino male gray rats with a baseline body weight of 220–250 g. The experiments were performed at the premises of the Konstantinov St. Petersburg Nuclear Physics Institute of the Kurchatov Institute and the Smorodintsev Research Institute of Influenza (Russia). Prior to the experiment, the animals were quarantined for 2 weeks in the vivariums of the performing organizations. Acute massive blood loss in rats was formed by taking blood (12 ± 1% of body weight on average) using syringe method by transcutaneous cardiac puncture. Rats were randomized into 3 groups (24 individuals each) depending on the gaseous medium where the animal was placed after artificial blood loss. Composition of the applied gaseous medium in the comparison groups: medium No. 1 — oxygen 21% vol.; argon — 30% vol.; nitrogen — the rest; medium No. 2 — oxygen 21% vol.; argon — the rest; medium No. 3 (control) — air. The postoperative follow-up (post-conditioning) for 8 hours involved assessing and recording the following indicators: survival/lethality rates; recovery rates (anesthesia recovery, somatic mobilization); clinical symptoms of possible intoxication with the gas mixture during inhalation exposure. The surviving animals were then monitored for 4 days to evaluate their health and behavioral performance. Upon completing the observation period, the animals were euthanized.Results. After artificially-induced blood loss, all the non-survivors died within 1.5–8 hours after the operation. In group 1 (post-conditioning in medium No. 1), the lethality of laboratory animals amounted to 4 individuals out of 24 (16%); in group 2 (post-conditioning in medium No. 2) — 2 individuals out of 24 (8%). In the control group, the lethality rate was significantly higher — 10 animals out of 24 (42%). The surviving animals demonstrated no lethality or morbidity within 4 days after the exposure. Analysis of outcomes between experimental groups and controls revealed that the significance of differences in the lethality index between group 1 and control (by Fisher’s two-sided criterion) comprised p = 0.06; between group 2 and control — p = 0.017. When the statistical “power” of the experimental group was increased (by combining samples 1 and 2), the significance of differences in outcomes in this group compared to the control accounted for p &lt; 0.001.Conclusion. The conducted studies confirmed the hypothesis about the pronounced antihypoxic effect of argon, which significantly increased the survival rate of experimental animals after massive artificially-induced blood loss.