Biodistribution of cerium dioxide and titanium dioxide nanomaterials in rats after single and repeated inhalation exposures.

BACKGROUND: Physiologically based kinetic models facilitate the safety assessment of inhaled engineered nanomaterials (ENMs). To develop these models, high quality datasets on well-characterized ENMs are needed. However, there are at present, several data gaps in the systemic availability of poorly soluble particles after inhalation. The aim of the present study was therefore to acquire two comparable datasets to parametrize a physiologically-based kinetic model. METHOD: Rats were exposed to cerium dioxide (CeO2, 28.4 ± 10.4 nm) and titanium dioxide (TiO2, 21.6 ± 1.5 nm) ENMs in a single nose-only exposure to 20 mg/m3 or a repeated exposure of 2 × 5 days to 5 mg/m3. Different dose levels were obtained by varying the exposure time for 30 min, 2 or 6 h per day. The content of cerium or titanium in three compartments of the lung (tissue, epithelial lining fluid and freely moving cells), mediastinal lymph nodes, liver, spleen, kidney, blood and excreta was measured by Inductively Coupled Plasma-Mass Spectrometry (ICP-MS) at various time points post-exposure. As biodistribution is best studied at sub-toxic dose levels, lactate dehydrogenase (LDH), total protein, total cell numbers and differential cell counts were determined in bronchoalveolar lavage fluid (BALF). RESULTS: Although similar lung deposited doses were obtained for both materials, exposure to CeO2 induced persistent inflammation indicated by neutrophil granulocytes influx and exhibited an increased lung elimination half-time, while exposure to TiO2 did not. The lavaged lung tissue contained the highest metal concentration compared to the lavage fluid and cells in the lavage fluid for both materials. Increased cerium concentrations above control levels in secondary organs such as lymph nodes, liver, spleen, kidney, urine and faeces were detected, while for titanium this was found in lymph nodes and liver after repeated exposure and in blood and faeces after a single exposure. CONCLUSION: We have provided insight in the distribution kinetics of these two ENMs based on experimental data and modelling. The study design allows extrapolation at different dose-levels and study durations. Despite equal dose levels of both ENMs, we observed different distribution patterns, that, in part may be explained by subtle differences in biological responses in the lung.

Comparison of the neurotoxic potency of different ultrafine particle fractions from diesel engine exhaust following direct and simulated inhalation exposure.

Exposure to traffic-related air pollution and ultrafine particles (<100 µm; UFP) is linked with neurodegeneration. However, the impact of the aromatic content in fuels and the contribution of different fractions of UFP, i.e., solid UFP vs SVOC UFP, on neuronal function is unknown. We therefore studied effects on neuronal activity and viability in rat primary cortical cells exposed for up to 120 h to copper oxide particles (CuO) or UFP (solid and SVOC) emitted from a heavy-duty diesel engine fueled with petroleum diesel (A20; 20 % aromatics) or Hydrotreated Vegetable Oil-type fuel (A0; 0.1 % aromatics), or solid UFP emitted from a non-road Kubota engine fueled with A20. Moreover, effects of UFP and CuO upon simulated inhalation exposure were studied by exposing an lung model (Calu-3 and THP-1 cells) for 48 h and subsequently exposing the cortical cells to the medium collected from the basal compartment of the lung model. Additionally, cell viability, cytotoxicity, barrier function, inflammation, and oxidative and cell stress were studied in the lung model after 48 h exposure to UFP and CuO. Compared to control, direct exposure to CuO and SVOC UFP decreased neuronal activity, which was partly associated with cytotoxicity. Effects on neuronal activity upon direct exposure to solid UFP were limited. A20-derived UFP (solid and SVOC) were more potent in altering neuronal function and viability than A0 counterparts. Effects on neuronal activity from simulated inhalation exposure were minor compared to direct exposures. In the lung model, CuO and A20-derived UFP increased cytokine release compared to control, whereas CuO and SVOC A20 altered gene expression indicative for oxidative stress. Our data indicate that SVOC UFP exhibit higher (neuro)toxic potency for altering neuronal activity in rat primary cortical cells than the solid fraction. Moreover, our data suggest that reducing the aromatic content in fuel decreases the (neuro)toxic potency of emitted UFP.

Identification and characterization of microplastics in human nasal samples.

KEY POINTS: Human nasal cavity samples were collected, and presence of microplastics were evaluated. Microplastics were present, and major types were polyethylene, polyester, acrylic polymer, and polypropylene. Further research is needed regarding microplastics and its clinical impact on human nasal cavity.

Assessment of air quality in the Philadelphia, Pennsylvania subway.

BACKGROUND: Subways are popular and efficient modes of transportation in cities. However, people are exposed to high levels of particulate matter (PM) in subways. Subway air quality in the United States has been investigated in a few cities, but data is lacking on simultaneous measurement of several pollutants, especially ultrafine particles (UFP) and black carbon (BC), in combination with different size fractions of PM. OBJECTIVES: The goals of this study are to assess air quality in a belowground subway and compare it with outdoor ambient levels, to examine temporal variability of PM in the subway, and to analyze the correlation between PM and BC. METHODS: Particulate matter of varying sizes (PM1, PM2.5, PM10), UFP, and BC were measured using DustTrak, nanoparticle detector, and micro aethalometer, respectively. Measurements were made at the belowground subway platform and the aboveground street level at 15th Street subway station in Philadelphia during summer 2022. RESULTS: Belowground mean PM1, PM2.5, and PM10 were 112.2 ± 61.3 µg/m3, 120 ± 65.5 µg/m3, and 182.1 ± 132 µg/m3, respectively, which were 5.4, 5.7, and 7.6 times higher than the respective aboveground street levels. The UFP lung deposited surface area (LDSA) (59.4 ± 36.2 µm2/cm3) and BC (9.5 ± 5.4 µg/m3) belowground were 1.7 times and 10.7 times higher than the aboveground. The pollutant concentration varied from day-to-day on both the locations. A higher positive correlation was found between the belowground BC and PM2.5 (r = 0.51, p < 0.05) compared to the aboveground (r = 0.16, p < 0.05). IMPACT: This study showed high levels of particulate matter exposure at a belowground subway station in Philadelphia. Particulate matter levels were about 5 to 8 times higher at belowground subway station than the corresponding aboveground street level. Higher levels were also observed for UFP lung deposited surface area (LDSA), while black carbon levels showed the highest concentration at the belowground level by a factor of ten compared to the aboveground level. The study shows the need for air quality management at belowground subways to reduce particulate matter exposure for the commuters.

Comprehensive risk assessment of the inhalation of plasticizers from the use of face masks.

Disposable masks, formed mainly from polymers, often incorporate various chemical additives to enhance their performance. These additives, which include plasticizers, may be released during mask usage, presenting a novel source of human exposure to these compounds. In this study, the presence of 16 organophosphate esters (OPEs), 11 phthalates, and four alternative plasticizers, in four various types of face masks, were studied, as well as their release during simulated mask use (artificial laboratory conditions). Total plasticizer concentrations exhibited minimal variation across different mask types, with mean values of 7.27 µg/face mask for surgical, 8.61 µg/face mask for reusable, 11.0 µg/face mask for KN-95, and 13.9 µg/face mask for FFP2 masks. To explore plasticizer release behavior, inhalation experiments were conducted under different conditions. The findings revealed a significant temperature-dependent enhancement in plasticizer release from masks, subsequently increasing human inhalation exposure. The inhalation experiments showed variation in the release percentages, ranging from 0.1 to 95 %, depending on the specific compound and mask type. Notably, OPEs exhibited a mean release percentage of 1.0 %, similar to phthalates, which showed a 1.2 % release. Although alternative plasticizers were less frequently released, they still presented a notable percentage of release of 4.1 %. Daily intake estimations via inhalation ranged from 0.01 to 9.04 ng/kg body weight (bw)/day for these additives. Using these estimations, carcinogenic and non-carcinogenic risks associated with this exposure to these compounds were evaluated. All calculated values for the specific compounds studied in this paper remained below the established threshold limits. However, they do represent an additional exposure pathway that, when considered alongside other more predominant routes such as indoor/outdoor inhalation, dermal absorption, and dietary intake, makes the total exposure worthy of consideration.

An electron paramagnetic resonance time-course study of oxidative stress in the plasma of electronic cigarette exposed rats.

The long-term consequences of electronic cigarette (Ecig) use in humans are not yet known, but it is known that Ecig aerosols contain many toxic compounds of concern. We have recently shown that Ecig exposure impairs middle cerebral artery (MCA) endothelial function and that it takes 3 days for MCA reactivity to return to normal. However, the sources contributing to impairment of the endothelium were not investigated. We hypothesized that the increased levels of oxidative stress markers in the blood are correlated with impaired MCA reactivity. We used electron paramagnetic resonance (EPR) spectroscopy to examine plasma from 4-month-old male Sprague-Dawley rats that were exposed to either air (n = 5) or 1 h Ecig exposure, after which blood samples were collected at varying times after exposure (i.e., 1-4, 24, 48 and 72 h postexposure, n = 4 or 5 in each time group). The EPR analyses were performed using the redox-sensitive hydroxylamine spin probe 1-hydroxy-3-carboxymethyl-2,2,5,5-tetramethyl-pyrrolidine (CMH) to measure the level of reactive oxidant species in the plasma samples. We found that EPR signal intensity from the CM• radical was significantly increased in plasma at 1-4, 24 and 48 h (P < 0.05, respectively) and returned to control (air) levels by 72 h. When evaluating the EPR results with MCA reactivity, we found a significant negative correlation (Pearson's P = 0.0027). These data indicate that impaired cerebrovascular reactivity resulting from vaping is associated with the oxidative stress level (measured by EPR from plasma) and indicate that a single 1 h vaping session can negatively influence vascular health for up to 3 days after vaping. HIGHLIGHTS: What is the central question of this study? Does the time course of oxidative stress triggered by electronic cigarette exposure follow the cerebral vascular dysfunction? What is the main finding and its importance? Electron paramagnetic resonance analysis shows that the oxidative stress induced after a single 1 h exposure to electronic cigarette aerosol takes ≤72 h to return to normal, which mirrors the time course for vascular dysfunction in the middle cerebral artery that we have reported previously.

Investigation of pulmonary inflammatory responses following intratracheal instillation of and inhalation exposure to polypropylene microplastics.

BACKGROUND: Microplastics have been detected in the atmosphere as well as in the ocean, and there is concern about their biological effects in the lungs. We conducted a short-term inhalation exposure and intratracheal instillation using rats to evaluate lung disorders related to microplastics. We conducted an inhalation exposure of polypropylene fine powder at a low concentration of 2 mg/m3 and a high concentration of 10 mg/m3 on 8-week-old male Fischer 344 rats for 6 h a day, 5 days a week for 4 weeks. We also conducted an intratracheal instillation of polypropylene at a low dose of 0.2 mg/rat and a high dose of 1.0 mg/rat on 12-week-old male Fischer 344 rats. Rats were dissected from 3 days to 6 months after both exposures, and bronchoalveolar lavage fluid (BALF) and lung tissue were collected to analyze lung inflammation and lung injury. RESULTS: Both exposures to polypropylene induced a persistent influx of inflammatory cells and expression of CINC-1, CINC-2, and MPO in BALF from 1 month after exposure. Genetic analysis showed a significant increase in inflammation-related factors for up to 6 months. The low concentration in the inhalation exposure of polypropylene also induced mild lung inflammation. CONCLUSION: These findings suggest that inhaled polypropylene, which is a microplastic, induces persistent lung inflammation and has the potential for lung disorder. Exposure to 2 mg/m3 induced inflammatory changes and was thought to be the Lowest Observed Adverse Effect Level (LOAEL) for acute effects of polypropylene. However, considering the concentration of microplastics in a real general environment, the risk of environmental hazards to humans may be low.

Indoor Air Quality Assessments in 10 Long-Term Care Facilities During the COVID-19 Pandemic, California, 2021-2023.

OBJECTIVES: This study aimed to assess indoor air quality (IAQ) in long-term care facilities (LTCFs) in California during the COVID-19 pandemic and evaluate their implementation of IAQ best practices described by public health authorities to control respiratory pathogen transmission via inhalation. DESIGN: This observational study conducted IAQ assessments in a convenience sample of LTCFs to gather qualitative data on the implementation of IAQ best practices. The design included 5 pilot visits to develop a standardized method of data collection and then systematic data collection at 10 facilities. SETTING AND PARTICIPANTS: The study focused on 10 LTCFs across California, chosen from facilities that responded to flyers advertising free IAQ assessments. Some of the facilities had previously experienced COVID-19 outbreaks affecting residents and staff. METHODS: State health department industrial hygienists performed site visits to collect data on each facility's heating, ventilation, and air-conditioning (HVAC) system operation, outdoor air introduction, recirculated air filtration, use of portable air cleaners, and directional airflow in isolation areas to evaluate implementation of IAQ best practices in each of these areas. Qualitative data were obtained through visual inspections and interviews with maintenance personnel. RESULTS: Findings indicated suboptimal implementation of IAQ best practices across the assessed facilities: no facility operated HVAC systems continuously, 40% had all outdoor air dampers open, 20% used MERV-13 or higher rated filters, 20% used portable air cleaners, and 20% performed directional airflow assessment and management for isolating COVID-19 cases. CONCLUSIONS AND IMPLICATIONS: Most LTCFs assessed were not adhering to IAQ best practices, highlighting a significant opportunity for improvement. IAQ best practices described in this study are achievable with existing systems and are critical for reducing virus transmission through the air in LTCFs. The findings underscore the need for more systematic assessments and improvements in IAQ within LTCFs to protect staff and residents.

Bisphenol S and Its Chlorinated Derivatives in Indoor Dust and Human Exposure.

Bisphenol S (BPS), an environmental endocrine disruptor, has been identified in global environmental matrices. Nevertheless, limited studies have investigated the presence of chlorinated analogues of BPS (Clx-BPSs) with potential estrogenic activities in environmental matrices. In this study, the occurrence of BPS and five types of Clx-BPSs was characterized in indoor dust (n = 178) from Hangzhou City. BPS was measurable in 94% of indoor dust samples, with an average level of 0.63 µg/g (

Upregulation of Fatty Acid Synthesis Genes in the Livers of Adolescent Female Rats Caused by Inhalation Exposure to PCB52 (2,2',5,5'-Tetrachlorobiphenyl).

Elevated airborne PCB levels in older schools are concerning due to their health impacts, including cancer, metabolic dysfunction-associated steatotic liver disease (MASLD), cardiovascular issues, neurodevelopmental diseases, and diabetes. During a four-week inhalation exposure to PCB52, an air pollutant commonly found in school environments, adolescent rats exhibited notable presence of PCB52 and its hydroxylated forms in their livers, alongside changes in gene expression. Female rats exhibited more pronounced changes in gene expression compared to males, particularly in fatty acid synthesis genes regulated by the transcription factor SREBP1. In vitro studies with human liver cells showed that the hydroxylated metabolite of PCB52, 4-OH-PCB52, but not the parent compound, upregulated genes involved in fatty acid biosynthesis similar to in vivo exposure. These findings highlight the sex-specific effects of PCB52 exposure on livers, particularly in females, suggesting a potential pathway for increased MASLD susceptibility.

Organophosphate flame retardants in air from formal e-waste recycling workshops in China: Size-distribution, gas-particle partitioning and exposure assessment.

In order to understand the organophosphate flame retardants (OPFRs) pollution and evaluate the inhalation exposure risk in formal e-waste recycling facilities, the air concentrations, particle size distribution and gas-particle partitioning of OPFRs in four typical workshops were investigated. The total Σ15OPFR concentrations inside workshops were in the range of 64.7-682 ng/m3, with 5.80-23.4 ng/m3 in gas phase and 58.8-658 ng/m3 in particle phase. Triphenyl phosphate (TPHP) and tris(2-chloroisopropyl) phosphate (TCIPP) were main analogs, both of which contributed to 49.0-85.7% of total OPFRs. In the waste printed circuit boards thermal treatment workshop, the OPFRs concentration was the highest, and particle-bound OPFRs mainly distributed in 0.7-1.1 µm particles. The proportions of TPHP in different size particles increased as the decrease of particle size, while TCIPP presented an opposite trend. The gas-particle partitioning of OPFR analogs was dominated by absorption process, and did not reach equilibrium state due to continuous emission of OPFRs from the recycling activities. The deposition fluxes of OPFRs in respiratory tract were 65.7-639 ng/h, and the estimated daily intake doses of OPFRs were 8.52-76.9 ng/(kg·day) in four workshops. Inhalation exposure was an important exposure pathway for e-waste recycling workers, and deposition fluxes of size-segregated OPFRs were mainly in head airways region.

Characterization of Wildland Firefighters' Exposure to Coarse, Fine, and Ultrafine Particles; Polycyclic Aromatic Hydrocarbons; and Metal(loid)s, and Estimation of Associated Health Risks.

Firefighters' occupational activity causes cancer, and the characterization of exposure during firefighting activities remains limited. This work characterizes, for the first time, firefighters' exposure to (coarse/fine/ultrafine) particulate matter (PM) bound polycyclic aromatic hydrocarbons (PAHs) and metal(loid)s during prescribed fires, Fire 1 and Fire 2 (210 min). An impactor collected 14 PM fractions, the PM levels were determined by gravimetry, and the PM-bound PAHs and metal(loid)s were determined by chromatographic and spectroscopic methodologies, respectively. Firefighters were exposed to a total PM level of 1408.3 and 342.5 µg/m3 in Fire 1 and Fire 2, respectively; fine/ultrafine PM represented more than 90% of total PM. Total PM-bound PAHs (3260.2 ng/m3 in Fire 1; 412.1 ng/m3 in Fire 2) and metal(loid)s (660.8 ng/m3 versus 262.2 ng/m3), distributed between fine/ultrafine PM, contained 4.57-24.5% and 11.7-12.6% of (possible/probable) carcinogenic PAHs and metal(loid)s, respectively. Firefighters' exposure to PM, PAHs, and metal(loid)s were below available occupational limits. The estimated carcinogenic risks associated with the inhalation of PM-bound PAHs (3.78 × 10-9 - 1.74 × 10-6) and metal(loid)s (1.50 × 10-2 - 2.37 × 10-2) were, respectively, below and 150-237 times higher than the acceptable risk level defined by the USEPA during 210 min of firefighting activity and assuming a 40-year career as a firefighter. Additional studies need to (1) explore exposure to (coarse/fine/ultrafine) PM, (2) assess health risks, (3) identify intervention needs, and (4) support regulatory agencies recommending mitigation procedures to reduce the impact of fire effluents on firefighters.

[A ssociations of short-term ambient particulate matter exposure and MTNR1B gene with triglyceride-glucose index: A family-based study].

OBJECTIVE: To explore the effects of short-term particulate matter (PM) exposure and the melatonin receptor 1B (MTNR1B) gene on triglyceride-glucose (TyG) index utilizing data from Fang-shan Family-based Ischemic Stroke Study in China (FISSIC). METHODS: Probands and their relatives from 9 rural areas in Fangshan District, Beijing, were included in the study. PM data were obtained from fixed monitoring stations of the National Air Pollution Monitoring System. TyG index was calculated by fasting triglyceride and glucose concentrations. The associations of short-term PM exposure and rs10830963 polymorphism of the MTNR1B gene with the TyG index were assessed using mixed linear models, in which covariates such as age, sex, and lifestyles were adjusted for. Gene-environment inter-action analysis was furtherly performed using the maximum likelihood methods to explore the potential effect modifier role of rs10830963 polymorphism in the association of PM with TyG index. RESULTS: A total of 4 395 participants from 2 084 families were included in the study, and the mean age of the study participants was (58.98±8.68) years, with 53. 90% females. The results of association analyses showed that for every 10 µg/m3 increase in PM2.5 concentration, TyG index increased by 0.017 (95%CI: 0.007-0.027), while for per 10 µg/m3 increment in PM10, TyG index increased by 0.010 (95%CI: 0.003-0.017). And the associations all had lagged effects. In addition, there was a positive association between the rs10830963 polymorphism and the TyG index. For per increase in risk allele G, TyG index was elevated by 0.040 (95%CI: 0.004-0.076). The TyG index was 0.079 (95%CI: 0.005-0.152) higher in carriers of the GG genotype compared with carriers of the CC genotype. The interaction of rs10830963 polymorphism with PM exposure had not been found to be statistically significant in the present study. CONCLUSION: Short-term exposure to PM2.5 and PM10 were associated with higher TyG index. The G allele of rs10830963 polymorphism in the MTNR1B gene was associated with the elevated TyG index.

Exposure to structurally unique ß-d-glucans differentially affects inflammatory responses in male mouse lungs.

Pro-inflammatory fungal ß-d-glucan (BDG) polysaccharides cause respiratory pathology. However, specific immunological effects of unique BDG structures on pulmonary inflammation are understudied. We characterized the effect of four unique fungal BDGs with unique branching patterns, solubility, and molecular weights in murine airways. Scleroglucan (1 → 3)(1 → 6)-highly branched BDG, laminarin (1 → 3)(1 → 6)-branched BDG, curdlan (1 → 3)-linear BDG, and pustulan (1 → 6)-linear BDG were assessed by nuclear magnetic resonance spectroscopy. Each BDG was tested by inhalation model with C3HeB/FeJ mice and compared to saline-exposed control mice and unexposed sentinels (n = 3-19). Studies were performed ±heat-inactivation (1 h autoclave) to increase BDG solubility. Outcomes included bronchoalveolar lavage (BAL) differential cell counts (macrophages, neutrophils, lymphocytes, eosinophils), cytokines, serum IgE, and IgG2a (multiplex and ELISA). Ex vivo primary cells removed from lungs and plated at monolayer were stimulated (BDG, lipopolysaccharide (LPS), anti-CD3), and cytokines compared to unstimulated cells. Right lung histology was performed. Inhalation of BDGs with distinct branching patterns exhibited varying inflammatory potency and immunogenicity. Lichen-derived (1 → 6)-linear pustulan was the most pro-inflammatory BDG, increasing inflammatory infiltrate (BAL), serum IgE and IgG2a, and cytokine production. Primed lung cells responded to secondary LPS stimulation with a T-cell-specific response to pustulan. Glucan source and solubility should be considered in exposure and toxicological studies.

Inhaled polystyrene microplastics impaired lung function through pulmonary flora/TLR4-mediated iron homeostasis imbalance.

Microplastics (MPs) have been found in the air, human nasal cavity, and lung, suggesting that the respiratory tract is one of the important exposure routes for MPs. The lung is a direct target organ for injury from inhaled MPs, but data on lung injury from longer-term exposure to environmental doses of MPs are limited, and the mechanisms remain unclear. Here, C57BL/6 J mice were treated with 5 µm polystyrene (PS)-MPs by intratracheal instillation (0.6, 3, and 15 mg/kg) for 60 days to establish MPs exposure model. We found that PS-MPs lead to increased collagen fibers and decreased lung barrier permeability and lung function in lung tissue. Mechanistically, the abundance of gram-negative bacteria in the pulmonary flora increased after inhalation of PS-MPs, causing lipopolysaccharide (LPS) release. The expression of Toll-like receptor 4 (TLR4), the key receptor of LPS, was increased, and ferroptosis occurred in lung tissue cells. Further in vitro intervention experiments were performed, pulmonary flora/TLR4-induced imbalance of lung iron homeostasis is an important mechanism of PS-MPs-induced lung injury. Our study provides new evidence for lung injury caused by environmental doses of MPs and strategies to prevent it through longer-term dynamic observation.

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 (PODp25BMCh) could serve as a suitable surrogate for regulatory PODs (Q2 ≥ 0.76, RSE ≤ 0.82 log10 units). We applied this approach to derive PODp25BMCh 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 PODp25BMCh, 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.

The application of PTR-MS and non-targeted analysis to characterize VOCs emitted from a plastic recycling facility fire.

BACKGROUND: On April 11th, 2023, the My Way Trading (MWT) recycling facility in Richmond, Indiana caught fire, mandating the evacuation of local residents and necessitating the U.S. Environmental Protection Agency (EPA) to conduct air monitoring. The EPA detected elevated levels of plastic combustion-related air pollutants, including hydrogen cyanide and benzene. OBJECTIVE: We aimed to identify these and other volatile organic compounds (VOCs) present as well as to identify the potential hazard of each compound for various human health effects. METHODS: To identify the VOCs, we conducted air monitoring at sites within and bordering the evacuation zone using proton transfer reaction mass spectrometry (PTR-MS) and non-targeted analysis (NTA). To facilitate risk assessment of the emitted VOCs, we used the EPA Hazard Comparison Dashboard. RESULTS: We identified 46 VOCs, within and outside the evacuation zone, with average detection levels above local background levels measured in Middletown, OH. Levels of hydrogen cyanide and 4 other VOCs were at least 1.8-fold higher near the incidence site in comparison to background levels and displayed unique temporal and spatial patterns. The 46 VOCs identified had the highest hazardous potential for eye and skin irritation, with approximately 45% and 39%, respectively, of the VOCs classified as high and very high hazards for these endpoints. Notably, all detected VOC levels were below the hazard thresholds set for single VOC exposures; however, hazard thresholds for exposure to VOC mixtures are currently unclear. IMPACT: This study serves as a proof-of-concept that PTR-MS coupled with NTA can facilitate rapid identification and hazard assessment of VOCs emitted following anthropogenic disasters. Furthermore, it demonstrates that this approach may augment future disaster responses to quantify additional VOCs present in complex combustion mixtures.

The role of membrane transporters in the absorption of atrazine following nasal exposure.

OBJECTIVE: The purpose of these studies was to investigate the uptake of atrazine across the nasal mucosa to determine whether direct transport to the brain through the olfactory epithelium is likely to occur. These studies were undertaken to provide important new information about the potential for the enhanced neurotoxicity of herbicides following nasal inhalation. MATERIALS AND METHODS: Transport of atrazine from aqueous solution and from commercial atrazine-containing herbicide products was assessed using excised nasal mucosal tissues. The permeation rate and the role of membrane transporters in the uptake of atrazine across the nasal mucosa were also investigated. Histological examination of the nasal tissues was conducted to assess the effects of commercial atrazine-containing products on nasal tissue morphology. RESULTS: Atrazine showed high flux across both nasal respiratory and olfactory tissues, and efflux transporters were found to play an essential role in limiting its uptake at low exposure concentrations. Commercial atrazine-containing herbicide products showed remarkably high transfer across the nasal tissues, and histological evaluation showed significant changes in the morphology of the nasal epithelium following exposure to the herbicide products. DISCUSSION: Lipophilic herbicides such as atrazine can freely permeate across the nasal mucosa despite the activity of efflux transporters. The adjuvant compounds in commercial herbicide products disrupt the nasal mucosa's epithelial barrier, resulting in even greater atrazine permeation across the tissues. The properties of the herbicide itself and those of the formulated products play crucial roles in the potential for the enhanced neurotoxicity of herbicides following nasal inhalation.

Sub-acute Inhalation Exposure to Aluminum Oxide Nanoparticles and its Effects on Wistar Rats as Opposed to the Micro-sized Chemical Analog.

INTRODUCTION: Aluminum oxide nanoparticles (Al2O3 NPs) are widely used in various productions. Simultaneously, many research works report the toxic effects of this nanomaterial. Given that, there is a growing risk of negative effects produced by Al2O3 NPs on public health. AIMS: This study aims to investigate the toxic effects of Al2O3 NPs as opposed to the micro-sized chemical analogue under sub-acute inhalation exposure. MATERIALS AND METHODS: We identified the physical properties of Al2O3 NPs as opposed to the micro- sized chemical analogue, including size, specific surface area, and total pore volume. Inhalation exposure to Al2O3 NPs was simulated on Wistar rats in a chamber for whole-body. The animals were exposed for 4 hours each day for 28 days. NPs and MPs concentrations in the chamber were kept at ~ 1/4000 from LC50. Rats' behavior was examined prior to the exposure period and after it; after the last daily exposure, we examined biochemical and hematological blood indicators, NPs and MPs bioaccumulation, and pathomorphological changes in organ tissues. RESULTS: The tested Al2O3 sample is a nanomaterial according to its analyzed physical properties. Rats' behavior changed more apparently under exposure to NPs compared to MPs. Aluminum levels, which were 1.62-55.20 times higher than the control, were identified in the lungs, liver, brain, and blood under exposure to NPs. These levels were also 1.55-7.65 times higher than the control under exposure to MPs. Biochemical indicators of rats' blood also changed under exposure to NPs against the control. We identified more active ALT, AST, ALP, and LDH, elevated levels of GABA, MDA, and conjugated bilirubin, and a lower level of Glu. As opposed to exposure to MPs, ALT, AST, and ALP were more active; GABA and MDA levels were higher; Glu level was lower. Under exposure to NPs, the number of platelets grew, whereas no similar effect occurred under exposure to MPs. We established pathomorphological changes in tissues of the lungs, brain, heart, and liver under exposure to Al2O3 NPs; similar changes occurred only in the lungs under exposure to MPs. Exposure to NPs induced changes in tissue structures in a wider range of various organs, and these changes were more apparent than under exposure to MPs. CONCLUSION: Greater toxicity of Al2O3 NPs as opposed to MPs is evidenced by a wider range of organs where their bioaccumulation occurs, more apparent pathomorphological and pathological functional changes. Established peculiarities of toxic effects produced by the analyzed nanomaterial should be considered when developing hygienic recommendations aimed at preventing and mitigating adverse impacts of Al2O3 NPs on human health under inhalation exposure.

Veno-venous extracorporeal membrane oxygenation for acute respiratory distress syndrome caused by nitrogen dioxide inhalation: A case report.

Background: Nitrogen dioxide (NO2) is known to cause lung injury, but there is no established treatment for acute respiratory distress syndrome (ARDS) caused by NO2 inhalation. Case Presentation: A 35-year-old man was accidentally exposed to NO2 fumes and presented to the emergency department. On admission, his oxygen saturation was 87% on ambient air and he was diagnosed with ARDS caused by NO2 inhalation and immediately intubated; however, hypoxemia and hypercapnia were not ameliorated. Hence, veno-venous extracorporeal membrane oxygenation (V-V ECMO) was introduced and the ventilator settings were set for lung-protective ventilation. Methylprednisolone was also administered. After the initiation of these treatments, oxygenation gradually improved. Therefore, ECMO was weaned off on day 11 and he was extubated on day 12. Conclusion: Lung injury caused by NO2 inhalation can cause ARDS, and lung-protective ventilation with V-V ECMO induction, as well as glucocorticoid administration, may be effective for this condition.