Air pollution is an under-recognised global health threat linked to an increased risk of cancers and is due primarily to the burning of fossil fuels. This review provides a high-level overview of the associations between outdoor and indoor air pollution and cancer risk and outcomes. Outdoor air pollutants are largely due to the burning of fossil fuels from human activities, although there is growing data implicating outdoor pollution from wildfire smoke. Indoor air pollution is primarily caused by burning solid fuel sources such as wood, coal and charcoal for household cooking and heating. There is a growing number of pieces of evidence linking exposure to pollution and the risk of developing cancers. The strongest evidence is seen on the positive association of air pollution, particularly particulate matter 2.5 with lung cancer. Emerging data implicate exposure to pollutants in the development of breast, gastrointestinal and other cancers. The mechanisms underlying these associations include oxidative stress, inflammation and direct DNA damage facilitated by pollutant absorption and distribution in the body. References were identified through a PubMed search for articles published in 2000 to October 2024 using the terms 'air pollution' or 'pollutants' and 'carcinoma' or ''cancer'. Air pollution poses significant risks to health. Its health impacts, including cancer risks, are often underestimated. Hazardous pollutants have been studied in several epidemiological cohort studies. Despite the mounting evidence, air pollution is often overlooked in predictive cancer risk models and public health intervention.

Environmental stressors, such as air particulate matter (PM) and nutrient deficiencies, can significantly impact crucial organs involved in detoxifying xenobiotics, including lungs, liver, and kidneys, especially in vulnerable populations like children. This study investigated the effect of 4-week exposure to Residual Oil Fly Ash (ROFA) on these organs in young rats under growth-restricted nutrition (NGR). We assessed histological, histomorphometric and biochemical parameters. ROFA exposure induced histological changes and inflammation in all three organs when compared to control (C) animals. Specifically, in lungs ROFA caused a significant reduction in alveolar airspace (C: 55.8 ± 1.8% vs. ROFA: 38.7 ± 3.0%, p < 0.01) and alveolar number along with changes in alveolar size distribution, and disruption of the smooth muscle layer which may impaired respiratory function. In the liver, ROFA increased binucleated cells, macro and microvesicles and both AST and ALT serum biomarkers (AST: C = 77.7 ± 1.3 vs. ROFA = 81.6 ± 1.3, p < 0.05; ALT: C = 44.5 ± 0.9 vs. ROFA = 49.4 ± 1.3, p < 0.05). In the kidneys, a reduced Bowman's space (C: 2.15 ± 0.2 mm2 vs. ROFA: 1.74 ± 0.2 mm2, p < 0.05) was observed, indicative of glomerular filtration failure. NGR alone reduced Bowman's space (C: 2.15 ± 0.2 mm2 vs. NGR: 1.06 ± 0.1 mm2, p < 0.001). In lung and liver NGR showed higher levels of proinflammatory cytokine IL-6 (p < 0.01 and p < 0.001, respectively) when compared to C. In conclusion, both stressors negatively affected lung and excretory organs in young rats, with nutritional status further modulating the physiological response to ROFA. These findings highlight the compounded risks posed by environmental pollutants and poor nutrition in vulnerable populations.

PM2.5 is an important environmental risk factor for cardiovascular disease (CVD) and poses a threat to global health. This study combines bibliometric analysis, Mendelian randomization (MR), and Global Burden of Disease (GBD) data to comprehensively explore the relationship between PM2.5 exposure and CVD. MR analyses provided strong evidence for causality, reinforcing findings from traditional observational studies. The estimated global burden of PM2.5-related CVD indicated, that there exist significant impacts on the elderly, men, and populations in low and medium socio-demographic index (SDI) areas. This study further found that population growth and aging are the main drivers of this burden with large inequities, although medical advances have mitigated some of the effects. Overall, the opportunity to reduce the burden of CVD remains significant, particularly in medium SDI countries. Projections to 2045 suggested that the absolute burden will increase, while age-standardized rates will decline due to improvements in air quality and health care. These findings emphasized the urgent need for targeted interventions to mitigate the deleterious effects of PM2.5 on global cardiovascular health and to address health inequalities between regions.

As 3D printing has become more compact and affordable, the use of the technology has become more prevalent across household, classroom, and small business settings. The emissions of fused filament fabrication (FFF) 3D printers consist of volatile organic compounds (VOCs) and aerosolized particulate matter (PM) dependent upon the filament in use. This study investigates the hazards posed by these emissions through aerosol characterization and cell exposure. Seventeen filaments were obtained from five manufacturers, consisting of fourteen plastic filaments (polylactic acid (PLA), acrylonitrile butadiene styrene (ABS), or polycarbonate (PC) polymers) and three filaments with metal filler (copper, bronze, and steel). For 1-h trials, BEAS-2B human bronchial epithelial cells were directly exposed to aerosolized 3D printer emissions at the air-liquid interface (ALI). Particle characterization showed ABS filaments produced more PM and VOC emissions with particles in the ultrafine size range. ABS filaments also elicited a greater biological response, with significant shifts in mitochondrial activity compared to the PLA filaments. Significant changes in amounts of glutathione (GSH) were observed after ABS and PLA emission exposure. Exposure to emissions from the steel filament resulted in the lowest average amount of glutathione, though insignificant, and a significantly lower mitochondrial activity, revealing a unique cause for concern among filaments tested. 3D printer emissions and subsequent cell responses appear filament-dependent, and users should mitigate personal exposure to aerosols.

Nucleic acid (NA)-based drugs are promising therapeutics agents. Beyond efficacy, addressing safety concerns-particularly those specific to this class of drugs-is crucial. Here, we propose an in vitro approach to screen for potential adverse off-target effects of NA-based drugs. Human peripheral blood mononuclear cells (PBMCs), purified from buffy coats of healthy donors, were used to investigate the ability of NA-drugs to trigger toxicity pathways and inappropriate immune stimulation. PBMCs were selected for their ability to represent potential human responses, given their likelihood of interacting with administered drugs. As proof of concept, a small interfering RNA (siRNA) targeting Ryanodine Receptor mRNA (RyR2) identified by the Italian National Center for Gene Therapy and Drugs based on RNA Technology as a potential therapeutic target for dominant catecholaminergic polymorphic ventricular tachycardia, was selected. This compound and its scramble were formulated within a calcium phosphate nanoparticle-based delivery system. Positive controls for four toxicity pathways were identified through literature review, each associated with a specific type of cellular stress: oxidative stress (tert-butyl hydroperoxide), mitochondrial stress (rotenone), endoplasmic reticulum stress (thapsigargin), and autophagy (rapamycin). These controls were used to define specific mRNA signatures triggered in PBMCs, which were subsequently used as indicators of off-target effects. To assess immune activation, the release of pro-inflammatory cytokines (interleukin-6, interleukin-8, tumor necrosis factor-α, and interferon-γ) was measured 24 h after exposure. The proposed approach provides a rapid and effective screening method for identifying potential unintended effects in a relevant human model, which also allows to address gender effects and variability in responses.

Exposure to air pollution is thought to cause millions of deaths globally each year. According to the Who 2018, approximately 7 million deaths annually are caused predominantly by noncommunicable diseases due to air pollution. Exposure to air particulate matter 2.5 (PM2.5) has been strongly associated with increased mortality and has significant effects on brain health. Air pollution, particularly ultrafine particulate matter, has emerged as a serious environmental concern with profound implications for human health. Studies in animal models have indicated that exposure to these pollutants during gestational development impacts prenatal and postnatal brain development. In particular, air pollution has been increasingly identified as a potential causative factor, as it affects neurogenesis in the brain's hippocampal region. The hippocampus is highly vulnerable to PM exposure, and any alteration in the structure or function of this region leads to various neurodevelopmental defects and neurodegenerative disorders via oxidative stress, microglial activation, neuronal death, and differential expression of genes. The neurogenesis process involves several steps, such as proliferation, differentiation, migration, synaptogenesis, and neuritogenesis. If any step of the neurogenesis process is hampered by environmental exposure or other factors, it can lead to neurodevelopmental defects, neurodegenerative disorders, and cognitive decline. One significant contributor to these alterations is air pollution, which ranks as the leading environmental risk factor worldwide. Some of the most common effects include oxidative stress, neuroinflammation, depressive behavior, altered cognitive processes, and microglial activation. This review explores how prenatal and postnatal PM exposure affects the hippocampal regions of the brain and the defects associated with exposure.

Wildfires are becoming more frequent and intense on a global scale, raising concerns about their acute and long-term effects on human health. We conducted a systematic review of the current epidemiological evidence on wildfire health risks and a meta-analysis to investigate the association between wildfire smoke exposure and various health outcomes. We discovered that wildfire smoke increases the risk of premature deaths and respiratory morbidity in the general population. Meta-analysis of cause-specific mortality and morbidity revealed that wildfire smoke had the strongest associations with cardiovascular mortality (RR: 1.018, 95% CI: 1.014-1.021), asthma hospitalization (RR: 1.054, 95% CI: 1.026-1.082), and asthma emergency department visits (RR: 1.117, 95% CI: 1.035-1.204) in the general population. Subgroup analyses of age found that adults and elderly adults were more susceptible to the cardiopulmonary effects of wildfire smoke. Next, we systematically addressed the toxicological mechanisms of wildfire smoke, including direct toxicity, oxidative stress, inflammatory reactions, immune dysregulation, genotoxicity and mutations, skin allergies, inflammation, and others. We discuss wildfire smoke risk mitigation strategies including public health interventions, regulatory measures, and personal actions. We conclude by highlighting current research limitations and future directions for wildfire research, such as elucidating the complex interactions of wildfire smoke components on human health, developing personalized risk assessment tools, and improving resilience and adaptation strategies to mitigate the health effects of wildfires in changing climate.

The respiratory tract with its vast surface area and very thin air-blood tissue barrier presents an extremely large interface for potential interaction with xenobiotics such as inhaled pathogens or medicaments. To protect its large and vulnerable surface, the lung is populated with several different types of immune cells. Pulmonary epithelial cells, macrophages and dendritic cells are key players in shaping the innate and adaptive immune response. Due to their localization, they represent a frontline of cell populations that are among the first to come in contact with inhaled xenobiotics. Furthermore, depending on the lung compartment they populate, these cells show a large variety in morphology, phenotype, and function. These unique characteristics make those cell populations ideal targets for specific immunomodulators that are designed for inhalation. Depending on cell population or lung compartment targeting, a specific immune response may be triggered or modulated. The purpose of a potent carrier for pulmonary immunomodulation is, first, to efficiently target a specific immunocompetent cell and, second, to affect its role in generating an immune response. Immunomodulation may occur at different levels of immune cell-antigen interaction, i.e. antigen uptake, trafficking, processing and presentation. Inhalation of nanosized carriers for drugs or vaccines shows great potential for both prophylactic and therapeutic approaches in order to modulate immune responses locally or systemically, due to the specific deposition and targeting properties of nanoparticles. Immune responses triggered by nanosized particles may be either immunostimulatory or immunosuppressive and depending on the specific purpose, stimulation or suppression may either be desired or unwanted. Meticulous analysis of immunomodulatory potential, pharmacologic and toxicologic testing of inhalable nanocarriers is required in order to find novel and optimal approaches for prophylaxis and therapy of pulmonary diseases. The design and characterization of such nanoparticles requires well-coordinated interdisciplinary research among engineers, biologists and clinicians.

Air pollution has been recognized as a global issue, through adverse effects on environment and health. While vertical atmospheric processes substantially affect urban air pollution, traditional epidemiological research using Land-use regression (LUR) modeling usually focused on ground-level attributes without considering upper-level atmospheric conditions. This study aimed to integrate Doppler LiDAR and machine learning techniques into LUR models (LURF-LiDAR) to comprehensively evaluate urban air pollution in Hong Kong, and to assess complex interactions between vertical atmospheric processes and urban air pollution from long-term (i.e., annual) and short-term (i.e., two air pollution episodes) views in 2021. The results demonstrated significant improvements in model performance, achieving CV R2 values of 0.81 (95 % CI: 0.75-0.86) for the long-term PM2.5 prediction model and 0.90 (95 % CI: 0.87-0.91) for the short-term models. Approximately 69 % of ground-level air pollution arose from the mixing of ground- and lower-level (105 m-225 m) particles, while 21 % was associated with upper-level (825 m-945 m) atmospheric processes. The identified transboundary air pollution (TAP) layer was located at ~900 m above the ground. The identified Episode one (E1: 7 Jan-22 Jan) was induced by the accumulation of local emissions under stable atmospheric conditions, whereas Episode two (E2: 13 Dec-24 Dec) was regulated by TAP under instable and turbulent conditions. Our improved air quality prediction model is accurate and comprehensive with high interpretability for supporting urban planning and air quality policies.

The World Health Organization has declared climate change to be "the single biggest health threat facing humanity", yet there are limited studies on the impact of climate change-related air pollution on ocular health.

To explore associations between ocular surface irritation and allergy-related daily outpatient office visits with daily ambient particulate matter (PM) levels in the Denver Metropolitan Area.

Daily visit counts of ophthalmology outpatient offices were obtained from an academic health center (October 1st, 2015 to January 27th, 2023). Daily ambient average concentrations of PM ≤ 10 µm in diameter (PM10) and 2.5 micrometers or less in diameter (PM2.5) were obtained. Data were analyzed using distributed lag nonlinear models while accounting for the cumulative lagged effects of PM10 and PM2.5 for visits. Modifications due to temperature were assessed using stratified models.

There were 144,313 ocular surface irritation and allergy visits to ophthalmic clinics during the study period. Daily visit counts increased with increasing daily ambient PM10 and PM2.5 concentrations. Five-day cumulative ambient PM10 concentrations at 80, 90, 100, and 110 µg/m3 showed higher rate ratios at each level from 1.77 (95% CI: 1.71, 1.84) at concentration of 80 to 2.20 (95% CI: 2.09, 2.30) for concentration of 110 µg/m3. Similarly, the visit rate ratios increased as the daily PM2.5 concentration increased, but this gradient effect was not significantly higher as the concentration increased. The effect of PM10 was higher on days when the temperature was below the average. Temperature did not affect the association between daily visit counts and PM2.5.

This study found that ambient PM increased the rate of ophthalmology visits due to ocular surface irritation and allergies. Most importantly, this association increased in magnitude with higher ambient PM concentrations. Additional studies are required to fully understand the effects of climate change-related stressors on ocular health.

Polycyclic aromatic hydrocarbons (PAHs) are naturally occurring environmental pollutants that may contribute to obesity in the adult population. To investigate the relationship between the urinary concentrations of PAH metabolites and adult obesity among the US population, the National Health and Nutritional Examination Survey (NHANES, 2003-2016) was used as a data source for this study. As many as 4464 participants in the NHANES 2003-2016 were included in the final analyses. We used logistic regression to look at the link between urinary PAH metabolites and obesity, using odds ratios (ORs) and 95% confidence intervals (CIs). The study sample comprised 4464 individuals aged ≥18 years, 2199 were male and 2265 were female. The study characteristics for four different quartiles were analyzed, and the average ages of the four urinary PAH quartiles were 49.61 ± 20.01, 46.63 ± 20.33, 44.28 ± 19.19, and 43.27 ± 17.68 years, respectively. In the quartile analysis of all participants, the third quartile was significantly associated with an increased prevalence of obesity (OR = 1.33, 95% CI = 1.12-1.59) with p-values <.05. In addition, females, but not males, had a strong link between the second, third, and fourth quartiles of urinary PAH and a higher risk of obesity (OR = 1.27, 95% CI = 1.00-1.61; OR = 1.52, 95% CI = 1.19-1.94; and OR = 1.39, 95% CI = 1.09-1.78). In conclusion, the study observed that urinary PAH metabolites were associated with the prevalence of obesity among the US population.

Northern Thailand experiences high levels of air pollution in the dry season due to agricultural waste burning and forest fires. Some air pollutants can enter the bloodstream, and the liver has the role of detoxifying these along with other harmful substances. In this study, we assessed the effects of long-term exposure to air pollutants on liver cancer mortality in this area.

A cohort of 10,859 primary liver cancer patients diagnosed between 2003 and 2018 and followed up to the end of 2020 were included in the study. Extended time-varying covariates of the annually averaged pollutant concentrations updated each year were utilized. The associations between air pollutants and mortality risk were examined by using a Cox proportional hazard model.

Metastatic cancer stage had the highest adjusted hazard ratio (aHR) of 3.57 (95% confidence interval (CI):3.23-3.95). Being male (aHR = 1.10; 95% CI: 1.04-1.15), over 60 years old (aHR = 1.16; 95% CI: 1.11-1.21), having a history of smoking (aHR = 1.16; 95%CI: 1.11-1.22), and being exposed to a time-updated local concentration of PM2.5 of 40 μg/m3 (aHR = 1.10; 95% CI: 1.05-1.15) increased the mortality risk.

We found that air pollution is one of several detrimental factors on the mortality risk of liver cancer.

Military burn pits, used for waste disposal in combat zones, involve the open-air burning of waste materials, including plastics, metals, chemicals, and medical waste. The pits release a complex mixture of occupational toxic substances, including particulate matter (PM), volatile organic compounds (VOCs), heavy metals, dioxins, and polycyclic aromatic hydrocarbons (PAHs). Air pollution significantly impacts brain health through mechanisms involving neuroinflammation. Pollutants penetrate the respiratory system, enter the bloodstream, and cross the blood-brain barrier (BBB), triggering inflammatory responses in the central nervous system (CNS). Chronic environmental exposures result in sustained inflammation, oxidative stress, and neuronal damage, contributing to neurodegenerative diseases and cognitive impairment. Veterans exposed to burn pit toxins are particularly at risk, reporting higher rates of respiratory issues, neurological conditions, cognitive impairments, and mental health disorders. Studies demonstrate that Veterans exposed to these toxins have higher rates of neuroinflammatory markers, accelerated cognitive decline, and increased risks of neurodegenerative diseases. This narrative review synthesizes the research linking airborne pollutants such as PM, VOCs, and heavy metals to neuroinflammatory processes and cognitive effects. There is a need for targeted interventions to mitigate the harmful and escalating effects of environmental air pollution exposures on the CNS, improving public health outcomes for vulnerable populations, especially for Veterans exposed to military burn pit toxins.

Unpredictable emergency department (ED) admissions challenge healthcare systems, causing resource allocation inefficiencies. This study analyses associations between air pollutants, meteorological factors, and 2,655,861 cause-specific ED admissions from 2014 to 2018 across 12 categories. Generalized additive models were used to assess non-linear associations for each exposure, yielding Incidence Rate Ratios (IRR), while the population attributable fraction (PAF) calculated each exposure's contribution to cause-specific ED admissions. IRRs revealed increased risks of ED admissions for respiratory infections (IRR: 1.06, 95% CI: 1.01-1.11) and infectious and parasitic diseases (IRR: 1.09, 95% CI: 1.03-1.15) during increased rainfall (13.21-16.97 mm). Wind speeds >12.73 km/hr corresponded to increased risks of ED admissions for respiratory infections (IRR: 1.12, 95% CI: 1.03-1.21) and oral diseases (IRR: 1.58, 95% CI: 1.31-1.91). Higher concentrations of air pollutants were associated with elevated risks of cardiovascular disease (IRR: 1.16, 95% CI: 1.05-1.27 for PM10) and respiratory infection-related ED admissions (IRR: 2.78, 95% CI: 1.69-4.56 for CO). Wind speeds >12.5 km/hr were predicted to contribute toward 10% of respiratory infection ED admissions, while mean temperatures >28°C corresponded to increases in the PAF up to 5% for genitourinary disorders and digestive diseases. PM10 concentrations >60 μg/m3 were highly attributable toward cardiovascular disease (PAF: 10%), digestive disease (PAF: 15%) and musculoskeletal disease (PAF: 10%) ED admissions. CO concentrations >0.6 ppm were highly attributable to respiratory infections (PAF: 20%) and diabetes mellitus (PAF: 20%) ED admissions. This study underscores protective effects of meteorological variables and deleterious impacts of air pollutant exposures across the ED admission categories considered.

Air pollution is recognized as a risk factor for cardiovascular diseases; however, the precise underlying mechanisms remain unclear. This study investigated the impact of occupational air pollution exposure on endothelial function in workers within the steel industry. Specifically, we examined male employees in the coke-making division of the Isfahan Steel Company in Iran, as well as those in administrative roles with no known history of cardiovascular risk. Data on age, body mass index, duration of employment, blood pressure, fasting blood sugar, and lipid profile were collected. To assess endothelial function, flow-mediated dilation (FMD) was measured. The baseline brachial artery diameter was greater (mean difference [95% CI] = 0.068 mm [0.008 to 0.128]), while the FMD was lower (mean difference [95% CI] = -0.908 % [-1.740 to -0.075]) in the coke-making group than in the control group. After controlling for potential confounding variables, it was observed that working in the coke-making sector of the industry was associated with lower FMD (F = 3.954, p = .049). These findings indicated that occupational air pollution exposure among workers in the steel industry is linked to impaired endothelium-dependent vasodilation.

This study investigated particle and volatile organic compound (VOC) emission rates (ER) from 3D pens, which are increasingly popular in children's toys. Nine filaments and two 3D pens were evaluated using a flow tunnel, a scanning mobility particle sizer, a proton-transfer-reaction time-of-flight mass spectrometer for particles, and a thermal desorption-gas chromatography-mass spectrometer for VOCs. Results showed that the ERs varied with the pen type, filament, and brand. The particle ER was highest for acrylonitrile butadiene styrene (ABS), followed by polylactic acid (PLA) and polycaprolactone (PCL). Notably, ERs of 83 % and 33 % of ABS and PLA filaments exceeded the maximum allowable particle ER (MAER; 5 × 109 particles/min) for 3D printers but were lower than the VOC MAER (173 μg/min in the office). Different filaments emitted diverse VOCs; ABS emitted styrene and benzene, PLA emitted lactide, and PCL emitted phenol. While particle ERs from 3D pens were comparable to those from printers, the total VOC ERs from 3D pens were slightly lower. Caution is warranted when using 3D pens because of potential health risks, especially their prolonged use, proximity to the breathing zone, and usage by children. This study highlights the need for considering particles and VOCs when assessing the safety of 3D pens, emphasizing awareness of potential hazards, particularly in child-oriented settings.

Environmental stresses are increasingly recognized as significant risk factors for adverse health outcomes. In particular, various forms of pollution and climate change are playing a growing role in promoting noncommunicable diseases, especially cardiovascular disease. Given recent trends, global warming and air pollution are now associated with substantial cardiovascular morbidity and mortality. As a vicious cycle, global warming increases the occurrence, size, and severity of wildfires, which are significant sources of airborne particulate matter. Exposure to wildfire smoke is associated with cardiovascular disease, and these effects are underpinned by mechanisms that include oxidative stress, inflammation, impaired cardiac function, and proatherosclerotic effects in the circulation. In the first part of a 2-part series on pollution and cardiovascular disease, this review provides an overview of the impact of global warming and air pollution, and because of recent events and emerging trends specific attention is paid to air pollution caused by wildfires.

Strategies to reach out-of-hospital cardiac arrests (called cardiac arrest) in residential areas and reduce disparities in care and outcomes are warranted. This study investigated incidences of cardiac arrests in public housing areas.

This register-based cohort study included cardiac arrest patients from Amsterdam (the Netherlands) from 2016 to 2021, Copenhagen (Denmark) from 2016 to 2021, and Vienna (Austria) from 2018 to 2021. Using Poisson regression adjusted for spatial correlation and city, we compared cardiac arrest incidence rates (number per square kilometer per year and number per 100 000 inhabitants per year) in public housing and other residential areas and examined the proportion of cardiac arrests within public housing and adjacent areas (100-m radius).

Overall, 9152 patients were included of which 3038 (33.2%) cardiac arrests occurred in public housing areas and 2685 (29.3%) in adjacent areas. In Amsterdam, 635/1801 (35.3%) cardiac arrests occurred in public housing areas; in Copenhagen, 1036/3077 (33.7%); and in Vienna, 1367/4274 (32.0%). Public housing areas covered 42.4 (12.6%) of 336.7 km2 and 1 024 470 (24.6%) of 4 164 700 inhabitants. Across the capitals, we observed a lower probability of 30-day survival in public housing versus other residential areas (244/2803 [8.7%] versus 783/5532 [14.2%]). The incidence rates and rate ratio of cardiac arrest in public housing versus other residential areas were incidence rate, 16.5 versus 4.1 n/km2 per year; rate ratio, 3.46 (95% CI, 3.31-3.62) and incidence rate, 56.1 versus 36.8 n/100 000 inhabitants per year; rate ratio, 1.48 (95% CI, 1.42-1.55). The incidence rates and rate ratios in public housing versus other residential areas were consistent across the 3 capitals.

Across 3 European capitals, one-third of cardiac arrests occurred in public housing areas, with an additional third in adjacent areas. Public housing areas exhibited consistently higher cardiac arrest incidences per square kilometer and 100 000 inhabitants and lower survival than other residential areas. Public housing areas could be a key target to improve cardiac arrest survival in countries with a public housing sector.

Exposure to ambient PM2.5 is associated with neurodegenerative disorders, in which microglia activation plays a critical role. Thus far, the underlying mechanisms for PM2.5-induced microglia activation have not been well elucidated. In this study, a human microglial cell line (HMC3) was used as the in vitro model to examine the inflammatory effect (hall marker of microglia activation) of PM2.5 and regulatory pathways. The expression of inflammatory mediators including interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2) as well as the brain derived neurotrophic factor (BDNF) were determined by ELISA and/or real-time PCR, respectively. Flow cytometry was used to measure the production of intracellular reactive oxygen species (ROS). Western blot was used to measure protein levels of Toll-like receptor 4 (TLR4), NF-κB inhibitor α (IκBα) and COX-2. It was shown that PM2.5 stimulation increased IL-6 and COX-2 expression but decreased BDNF expression in a dose-dependent manner. Further studies showed that PM2.5 triggered the formation of ROS and pre-treatment with the ROS scavenger acetylcysteine (NAC) significantly suppressed PM2.5-induced IL-6 and COX-2 expression. Moreover, the nuclear factor kappa B (NF-κB) inhibitor BAY11-7085 or the TLR4 neutralizing antibody markedly blocked PM2.5-induced IL-6 and COX-2 expression. However, NAC or BAY11-7085 exhibited minimal effect on PM2.5-induced BDNF down-regulation. In addition, pre-treatment with BAY11-7085 or TLR4 neutralizing antibody reduced ROS production induced by PM2.5, and NAC pre-treatment inhibited TLR4 expression and NF-κB activation induced by PM2.5. Collectively, PM2.5 treatment induced IL-6 and COX-2 but suppressed BDNF expression. PM2.5-induced IL-6 and COX-2 expression was mediated by interactive oxidative stress and TLR4/NF-κB pathway.

The increasing application of nanotechnology has resulted in a growing number of nano-enabled consumer products, and they could be important contributors to indoor particulate matter, with potential adverse health effects. This study investigated the exposure of adults and children to the released and resuspended manufactured particles from seven nano-enabled consumer sprays. Sedimentation and resuspension of released particles were investigated in a newly constructed 2.8 × 1.6 × 2.4 m3 chamber. The resuspension of deposited particles was investigated as a function of product type, flooring material (e.g., carpet and vinyl), resuspension force (e.g., walking by an adult and motion of a robotic sampler that simulated a child), and measurement height. The concentration of released and resuspended particles in the air was determined using Button Aerosol Samplers (SKC Inc.) with 25-mm 2 μm-pore PTFE filters. Samplers were positioned in the experimenter's breathing zone (e.g., 1.5 m for adults and 0.3 m for a child-simulating robot) and at fixed stations of 0.3 m and 1.1 m heights. Resuspended particle mass concentrations ranged from 28 to 905 μg/m3, and the resuspension rates of deposited spray particles for the same variable combinations varied from 10-4 to 10-1 h-1, depending on product type, flooring material, sampling height, and resuspension force. Particle resuspension rates from carpet were up to 320 % higher than resuspension rates from vinyl flooring, resuspension rates measured at 0.3 m were up to 195 % higher than the rates measured with a 1.1 m stationary sampler, and resuspension rates due to a walking adult were up to 243 % higher than resuspension rates caused to a moving robot that simulated a child. Overall, these data on the resuspension of particles from nano-enabled consumer sprays could help us understand the resulting exposures and support future studies on human exposure reduction.

Study on fine aerosols composition can help understand the particles formation and is crucial for improving the accuracy of model simulations. Based on field data measured by a Q-ACSM (Quadrupole-Aerosol Chemical Speciation Monitor), we have comprehensively compared the characteristics, evolution, and potential formation mechanisms of the components in NR-PM2.5 during wintertime at two megacities (Beijing and Guangzhou) of southern and northern China. We show that as PM pollution intensifies, the mass fraction of the primary aerosols (e.g., COA, HOA) in PM2.5 in Guangzhou increased, along with a slight decline in proportion of both the secondary organic (SOA) and inorganic (SIA) aerosols; In contrast, in Beijing, the proportion of the SIA ramped up from 28 % to 53 % with the pollution evolution; and the fraction of SOA in total OA also increased due to a substantial increment in the proportion of MO-OOA (from 29 % to 48 %), suggesting a significance of the secondary processes in worsening aerosols pollution in Beijing. Our further analysis demonstrates a leading role of aqueous pathway in the secondary formation of aerosols at the Beijing site, presenting an exponential rising of SIA and SOA with the relative humidity (RH) increase. Compared to Beijing, however, we find that the photochemical oxidation other than aqueous process in Guangzhou plays a more critical role in those secondary aerosols formation. Combined with the Hysplit trajectory model, we identify the high humid conditions in Guangzhou are typically affected by clean marine air masses, explaining the slower response of secondary components to the RH changes. Moreover, the particles in Guangzhou were observed less hygroscopic that is adverse to the aerosol aqueous chemistry. The results provide basis for the precise control of PM pollution in different regions across China and would be helpful in improving model simulations.

Pollution is ubiquitous, and much of it is anthropogenic in nature, which is a severe risk factor not only for respiratory infections or asthma sufferers but also for Alzheimer's disease, which has received a lot of attention recently. This Review aims to investigate the primary environmental risk factors and their profound impact on Alzheimer's disease. It underscores the pivotal role of multidimensional imaging in early disease identification and prevention. Conducting a comprehensive review, we delved into a plethora of literature sources available through esteemed databases, including Science Direct, Google Scholar, Scopus, Cochrane, and PubMed. Our search strategy incorporated keywords such as "Alzheimer Disease", "Alzheimer's", "Dementia", "Oxidative Stress", and "Phytotherapy" in conjunction with "Criteria Pollutants", "Imaging", "Pathology", and "Particulate Matter". Alzheimer's disease is not only a result of complex biological factors but is exacerbated by the infiltration of airborne particles and gases that surreptitiously breach the nasal defenses to traverse the brain, akin to a Trojan horse. Various imaging modalities and noninvasive techniques have been harnessed to identify disease progression in its incipient stages. However, each imaging approach possesses inherent limitations, prompting exploration of a unified technique under a single umbrella. Multidimensional imaging stands as the linchpin for detecting and forestalling the relentless march of Alzheimer's disease. Given the intricate etiology of the condition, identifying a prospective candidate for Alzheimer's disease may take decades, rendering the development of a multimodal imaging technique an imperative. This research underscores the pressing need to recognize the chronic ramifications of invisible particulate matter and to advance our understanding of the insidious environmental factors that contribute to Alzheimer's disease.

Airborne environmental and engineered nanoparticles (NPs) are inhaled and deposited in the respiratory system. The inhaled dose of such NPs and their deposition location in the lung determines their impact on health. When calculating NP deposition using particle inhalation models, a common approach is to use the bulk material density, ρb, rather than the effective density, ρeff. This neglects though the porous agglomerate structure of NPs and may result in a significant error of their lung-deposited dose and location.

Here, the deposition of various environmental NPs (aircraft and diesel black carbon, wood smoke) and engineered NPs (silica, zirconia) in the respiratory system of humans and mice is calculated using the Multiple-Path Particle Dosimetry model accounting for their realistic structure and effective density. This is done by measuring the NP ρeff which was found to be up to one order of magnitude smaller than ρb. Accounting for the realistic ρeff of NPs reduces their deposited mass in the pulmonary region of the respiratory system up to a factor of two in both human and mouse models. Neglecting the ρeff of NPs does not alter significantly the distribution of the deposited mass fractions in the human or mouse respiratory tract that are obtained by normalizing the mass deposited at the head, tracheobronchial and pulmonary regions by the total deposited mass. Finally, the total deposited mass fraction derived this way is in excellent agreement with those measured in human studies for diesel black carbon.

The doses of inhaled NPs are overestimated by inhalation particle deposition models when the ρb is used instead of the real-world effective density which can vary significantly due to the porous agglomerate structure of NPs. So the use of realistic ρeff, which can be measured as described here, is essential to determine the lung deposition and dosimetry of inhaled NPs and their impact on public health.

Air pollutants may contribute to the development of Parkinson's disease (PD), but empirical evidence is limited and inconsistent.

This study aimed to prospectively investigate the associations of PD with ambient exposures to fine particulate matter with aerodynamic diameter ≤ 2.5 μ m (PM 2.5 ) and nitrogen dioxide (NO 2 ).

We analyzed data from 47,108 US women from the Sister Study, enrolled from 2003-2009 (35-80 years of age) and followed through 2018. Exposures of interest included address-level ambient PM 2.5 and NO 2 in 2009 and their cumulative averages from 2009 to PD diagnosis with varying lag-years. The primary outcome was PD diagnosis between 2009 and 2018 (n = 163 ). We used multivariable Cox proportional hazards and time-varying Cox models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs).

NO 2 exposure in 2009 was associated with PD risk in a dose-response manner. The HR and 95% CI were 1.22 (95% CI: 1.03, 1.46) for one interquartile [4.8 parts per billion (ppb)] increment in NO 2 , adjusting for age, race and ethnicity, education, smoking status, alcohol drinking, caffeine intake, body mass index, physical activity, census region, residential area type, area deprivation index (ADI), and self-reported health status. The association was confirmed in secondary analyses with time-varying averaged cumulative exposures. For example, the multivariable adjusted HR for PD per 4.8   ppb increment in NO 2 was 1.25 (95% CI: 1.05, 1.50) in the 2-year lag analysis using cumulative average exposure. Post hoc subgroup analyses overall confirmed the association. However, statistical interaction analyses found that the positive association of NO 2 with PD risk was limited to women in urban, rural, and small town areas and women with ≥ 50 th percentile ADI but not among women from suburban areas or areas with < 50 th percentile ADI. In contrast, PM 2.5 exposure was not associated with PD risk with the possible exception for women from the Midwest region of the US (HR interquartile -range = 2.49 , 95% CI: 1.20, 5.14) but not in other census regions.

In this nationwide cohort of US women, higher level exposure to ambient NO 2 is associated with a greater risk of PD. This finding needs to be independently confirmed and the underlying mechanisms warrant further investigation. https://doi.org/10.1289/EHP13009.

Air pollution is a universal issue and has significant deleterious effects on both human health and also environment. The important indicators of air pollution include ozone (O3), particulate matter (PM), nitrogen dioxide (NO2), and sulfur dioxide (SO2). This research aims to investigate the impacts of ambient air pollution (AAP), SO2, and O3 on oxidative stress parameters, liver tissue histopathology, and expression of some carcinogenesis-related genes in the hepatic tissue of rats.

32 Wistar rats were randomly allocated to four groups: the control group, the AAP group, the SO2 group (10 ppm), and the ozone group (0.6 ppm). Over a period of five consecutive weeks, the rats were exposed to the specified pollutants for 3 h daily; liver tissues were harvested and instantly fixed with formalin. Pathological changes were assessed in the tissue samples. Additionally, the RT-qPCR technique was utilized to investigate Expression alterations of BAX, p-53, BCL2, caspase-3, caspase-8 and caspase-9. Furthermore, 30 milligrams of hepatic tissues were extracted to assess the activities of oxidative stress enzymes.

The liver catalase and MDA activity were elevated in the air pollution (p < .05). Also, liver GPx activity in air pollution and ozone groups was significant in comparison to the control group (p < .05). The SO2 group exhibited severe lesions in histopathology examinations.

The findings revealed an alteration in liver histopathology, an induction of oxidative stress, and the expression of some apoptosis-related genes in hepatic tissues after exposure to AAP, SO2, and O3.

Nanoporous materials are categorized as microporous (pore sizes 0.2-2 nm), mesoporous (pore sizes 2-50 nm), and macroporous (pore sizes 50-1000 nm). Mesoporous silica (MS) has gained a significant interest due to its notable characteristics, including organized pore networks, specific surface areas, and the ability to be integrated in a variety of morphologies. Recently, MS has been widely accepted by range of manufacturer and as drug carrier. Moreover, silica nanoparticles containing mesopores, also known as mesoporous silica nanoparticles (MSNs), have attracted widespread attention in additive manufacturing (AM). AM commonly known as three-dimensional printing is the formalized rapid prototyping (RP) technology. AM techniques, in comparison to conventional methods, aid in reducing the necessity for tooling and allow versatility in product and design customization. There are generally several types of AM processes reported including VAT polymerization (VP), powder bed fusion (PBF), sheet lamination (SL), material extrusion (ME), binder jetting (BJ), direct energy deposition (DED), and material jetting (MJ). Furthermore, AM techniques are utilized in fabrication of various classified fields such as architectural modeling, fuel cell manufacturing, lightweight machines, medical, and fabrication of drug delivery systems. The review concisely elaborates on applications of mesoporous silica as versatile material in fabrication of various AM-based pharmaceutical products with an elaboration on various AM techniques to reduce the knowledge gap.

Diesel exhaust (DE) induces neutrophilia and lymphocytosis in experimentally exposed humans. These responses occur in parallel to nuclear migration of NF-κB and c-Jun, activation of mitogen activated protein kinases and increased production of inflammatory mediators. There remains uncertainty regarding the impact of DE on endogenous antioxidant and xenobiotic defences, mediated by nuclear factor erythroid 2-related factor 2 (Nrf2) and the aryl hydrocarbon receptor (AhR) respectively, and the extent to which cellular antioxidant adaptations protect against the adverse effects of DE.

Using immunohistochemistry we investigated the nuclear localization of Nrf2 and AhR in the epithelium of endobronchial mucosal biopsies from healthy subjects six-hours post exposure to DE (PM10, 300 µg/m3) versus post-filtered air in a randomized double blind study, as a marker of activation. Cytoplasmic expression of cytochrome P450s, family 1, subfamily A, polypeptide 1 (CYP1A1) and subfamily B, Polypeptide 1 (CYP1B1) were examined to confirm AhR activation; with the expression of aldo-keto reductases (AKR1A1, AKR1C1 and AKR1C3), epoxide hydrolase and NAD(P)H dehydrogenase quinone 1 (NQO1) also quantified. Inflammatory and oxidative stress markers were examined to contextualize the responses observed.

DE exposure caused an influx of neutrophils to the bronchial airway surface (p = 0.013), as well as increased bronchial submucosal neutrophil (p < 0.001), lymphocyte (p = 0.007) and mast cell (p = 0.002) numbers. In addition, DE exposure enhanced the nuclear translocation of the AhR and increased the CYP1A1 expression in the bronchial epithelium (p = 0.001 and p = 0.028, respectively). Nuclear translocation of AhR was also increased in the submucosal leukocytes (p < 0.001). Epithelial nuclear AhR expression was negatively associated with bronchial submucosal CD3 numbers post DE (r = -0.706, p = 0.002). In contrast, DE did not increase nuclear translocation of Nrf2 and was associated with decreased NQO1 in bronchial epithelial cells (p = 0.02), without affecting CYP1B1, aldo-keto reductases, or epoxide hydrolase protein expression.

These in vivo human data confirm earlier cell and animal-based observations of the induction of the AhR and CYP1A1 by diesel exhaust. The induction of phase I xenobiotic response occurred in the absence of the induction of antioxidant or phase II xenobiotic defences at the investigated time point 6 h post-exposures. This suggests DE-associated compounds, such as polycyclic aromatic hydrocarbons (PAHs), may induce acute inflammation and alter detoxification enzymes without concomitant protective cellular adaptations in human airways.

The increased awareness about possible health effects arising from micro- and nanoplastics (MNPs) pollution is driving a huge amount of studies. Many international efforts are in place to better understand and characterize the hazard of MNPs present in the environment. The literature search was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) methodology in two different databases (PubMed and Embase). The selection of articles was carried out blind, screening titles and abstracts according to inclusion and exclusion criteria. In general, these studies rely on the methodology already in use for assessing hazard from nanomaterials and particles of concern. However, only a limited number of studies have so far directly measured human exposure to MNPs and examined the relationship between such exposure and its impact on human health. This review aims to provide an overview of the current state of research on biomarkers of oxidative stress, inflammation, and genotoxicity that have been explored in relation to MNPs exposure, using human, cellular, animal, and plant models. Both in-vitro and in-vivo models suggest an increased level of oxidative stress and inflammation as the main mechanism of action (MOA) leading to adverse effects such as chronic inflammation, immunotoxicity and genotoxicity. With the identification of such biological endpoints, representing critical key initiating events (KIEs) towards adaptive or adverse outcomes, it is possible to identify a panel of surrogate biomarkers to be applied and validated especially in occupational settings, where higher levels of exposure may occur.

Nanoparticles (NPs) released from engineered materials or combustion processes as well as persistent herpesvirus infection are omnipresent and are associated with chronic lung diseases. Previously, we showed that pulmonary exposure of a single dose of soot-like carbonaceous NPs (CNPs) or fiber-shaped double-walled carbon nanotubes (DWCNTs) induced an increase of lytic virus protein expression in mouse lungs latently infected with murine γ-herpesvirus 68 (MHV-68), with a similar pattern to acute infection suggesting virus reactivation. Here we investigate the effects of a more relevant repeated NP exposure on lung disease development as well as herpesvirus reactivation mechanistically and suggest an avenue for therapeutic prevention. In the MHV-68 mouse model, progressive lung inflammation and emphysema-like injury were detected 1 week after repetitive CNP and DWCNT exposure. NPs reactivated the latent herpesvirus mainly in CD11b+ macrophages in the lungs. In vitro, in persistently MHV-68 infected bone marrow-derived macrophages, ERK1/2, JNK, and p38 MAPK were rapidly activated after CNP and DWCNT exposure, followed by viral gene expression and increased viral titer but without generating a pro-inflammatory signature. Pharmacological inhibition of p38 activation abrogated CNP- but not DWCNT-triggered virus reactivation in vitro, and inhibitor pretreatment of latently infected mice attenuated CNP-exposure-induced pulmonary MHV-68 reactivation. Our findings suggest a crucial contribution of particle-exposure-triggered herpesvirus reactivation for nanomaterial exposure or air pollution related lung emphysema development, and pharmacological p38 inhibition might serve as a protective target to alleviate air pollution related chronic lung disease exacerbations. Because of the required precondition of latent infection described here, the use of single hit models might have severe limitations when assessing the respiratory toxicity of nanoparticle exposure.

Approximately 5 million fatalities occur annually due to stroke, along with its substantial effects on patient well-being and functional impairment. Research has established a connection between extended exposure to air pollutants and ischemic stroke. However, the link between short-term exposure to air pollutants and stroke remains less definitive.

A comprehensive search was conducted on MEDLINE, Scopus, the Cochrane Central Register of Controlled Trials (CENTRAL), and Web of Sciences databases up until February 2023, without any language restrictions. The inclusion criteria encompassed observational or interventional studies that examined the correlation between short-term exposure to air pollutants (carbon monoxide [CO], sulfur dioxide [SO2], nitrogen dioxide [NO2], ozone [O3]) and particulate matter with diameters of less than 1 µm, less than 2.5 µm, or less than 10 µm (PM1, PM2.5, and PM10), with the incidence and mortality of ischemic stroke. Short-term exposure was defined as exposure occurring within 5 days of the onset of stroke.

A total of 18,035,408 cases of ischemic stroke were included in the analysis, derived from 110 observational studies. Asia accounted for most included studies, representing 58.8% of the total. By contrast, Europe and the Americas contributed 24.6% and 16.7% of the studies, respectively. Notably, none of the included studies were conducted in Africa. Stroke incidence was significantly associated with an increase in the concentration of NO2 (RR = 1.28; 95% CI 1.21-1.36), O3 (RR = 1.05; 95% CI 1.03-1.07), CO (RR = 1.26; 95% CI 1.21-1.32), SO2 (RR = 1.15; 95% CI 1.11-1.19), PM1 (RR = 1.09; 95% CI 1.06-1.12), PM2.5 (RR = 1.15; 95% CI 1.13-1.17), and PM10 (RR = 1.14; 95% CI 1.12-1.16). Moreover, an increase in the concentration of NO2 (RR = 1.33; 95% CI 1.07-1.65), SO2 (RR = 1.60; 95% CI 1.05-2.44), PM2.5 (RR = 1.09; 95% CI 1.04-1.15), and PM10 (RR = 1.02; 95% CI 1.00-1.04) was associated with an increase in stroke mortality.

There is a strong and significant correlation between gaseous and particulate air pollutants and the occurrence and mortality rates of stroke. This close temporal association underscores the importance of implementing global initiatives to develop policies aimed at reducing air pollution. By doing so, alleviate the burden of ischemic stroke and its consequences.

This work aimed to investigate the impact of PM2.5 exposure on acute liver injury METHODS: C57BL/6 mice were used to examine the hepatic histopathological changes in PM2.5-exposed mice, as well as in CCl4-mediated acute liver injury mice after long-term exposure to PM2.5. During in vitro experiments, Kupffer cells were detected for M1 polarization level after treating with PM2.5, and the activation level of NLRP3 inflammasomes were assessed.

According to our findings, PM2.5 can induce M1 polarization of Kupffer cells in the liver to create an inflammatory microenvironment. Long-term exposure to PM2.5 can aggravate acute liver injury in mice. Treatment with MCC950, an NLRP3 inhibitor, can inhibit the effect of PM2.5. As demonstrated by in vitro analysis, PM2.5 can promote M1 polarization of Kupffer cells.

As suggested by our results, long-term exposure to PM2.5 can create an inflammatory microenvironment to aggravate mouse acute liver injury. The effect is related to NLRP3-mediated M1 polarization in Kupffer cells.

Air pollution remains a great challenge for public health, with the detrimental effects of air pollution on cardiovascular, rhinosinusitis, and pulmonary health increasingly well understood. Recent epidemiological associations point to the adverse effects of air pollution on cognitive decline and neurodegenerative diseases. Mouse models of subchronic exposure to PM 2.5 (ambient air particulate matter < 2.5 µm) provide an opportunity to demonstrate the causality of target diseases. Here, we subchronically exposed mice to concentrated ambient PM 2.5 for 7 weeks (5 days/week; 8h/day) and assessed its effect on behavior using standard tests measuring cognition or anxiety-like behaviors. Average daily PM 2.5 concentration was 200 µg/m 3 in the PM 2.5 group and 10 µg/m 3 in the filtered air group. The novel object recognition (NOR) test was used to assess the effect of PM 2.5 exposure on recognition memory. The increase in exploration time for a novel object versus a familiarized object was lower for PM 2.5 -exposed mice (42% increase) compared to the filtered air (FA) control group (110% increase). In addition, the calculated discrimination index for novel object recognition was significantly higher in FA mice (67 %) compared to PM 2.5 exposed mice (57.3%). The object location test (OLT) was used to examine the effect of PM 2.5 exposure on spatial memory. In contrast to the FA-exposed control mice, the PM 2.5 exposed mice exhibited no significant increase in their exploration time between novel location versus familiarized location indicating their deficit in spatial memory. Furthermore, the discrimination index for novel location was significantly higher in FA mice (62.6%) compared to PM 2.5 exposed mice (51%). Overall, our results demonstrate that subchronic exposure to higher levels of PM 2.5 in mice causes impairment of novelty recognition and spatial memory.

Celluloid, the predecessor to plastic, was synthesized in 1869, and due to technological advancements, plastic products appear to be ubiquitous in daily life. The massive production, rampant usage, and inadequate disposal of plastic products have led to severe environmental pollution. Consequently, reducing the employment of plastic has emerged as a pressing concern for governments globally. This review explores microplastics, including their origins, absorption, and harmful effects on the environment and humans. Several methods exist for breaking down plastics, including thermal, mechanical, light, catalytic, and biological processes. Despite these methods, microplastics (MPs, between 1 and 5 mm in size) continue to be produced during degradation. Acknowledging the significant threat that MPs pose to the environment and human health is imperative. This form of pollution is pervasive in the air and food and infiltrates our bodies through ingestion, inhalation, or skin contact. It is essential to assess the potential hazards that MPs can introduce. There is evidence suggesting that MPs may have negative impacts on different areas of human health. These include the respiratory, gastrointestinal, immune, nervous, and reproductive systems, the liver and organs, the skin, and even the placenta and placental barrier. It is encouraging to see that most of the countries have taken steps to regulate plastic particles. These measures aim to reduce plastic usage, which is essential today. At the same time, this review summarizes the degradation mechanism of plastics, their impact on human health, and plastic reduction policies worldwide. It provides valuable information for future research on MPs and regulatory development.

Although chronic low-level exposure to Hg²⁺ and Cd²⁺ causes human nephrotoxicity, the bioinorganic processes that deliver them to their target organs are poorly understood. Since the plasma protein human serum albumin (HSA) has distinct binding sites for these metal ions, we wanted to gain insight into these translocation processes and have employed size-exclusion chromatography coupled on-line to an inductively coupled plasma atomic emission spectrometer using phosphate-buffered saline mobile phases. When HSA 'labeled' with Hg²⁺ and Cd²⁺ (1:0.1:0.1) using 300 μM of L-methionine was analyzed, the co-elution of a single C, S, Cd, and Hg peak was observed, which implied the intact bis-metalated HSA complex. Since human plasma contains small molecular weight thiols and sulfur-containing metabolites, we analyzed the bis-metalated HSA complex with mobile phases containing 50-200 µM of L-cysteine (Cys), D,L-homocysteine (hCys), or glutathione (GSH), which provided insight into the comparative mobilization of each metal from their respective binding sites on HSA. Interestingly, 50 µM Cys, hCys, or GSH mobilized Hg²⁺ from its HSA binding site but only partially mobilized Cd²⁺ from its binding site. Since these findings were obtained at conditions simulating near-physiological conditions of plasma, they provide a feasible explanation for the higher 'mobility' of Hg²⁺ and its concomitant interaction with mammalian target organs compared to Cd²⁺. Furthermore, 50 µM Cys resulted in the co-elution of similar-sized Hg and Cd species, which provides a biomolecular explanation for the nephrotoxicity of Hg²⁺ and Cd²⁺.

Air pollutants have a significant impact on public health. The aim of the study was to find out the relationship between ambulatory blood pressure measured by 24-h ambulatory blood pressure monitoring (ABPM) and the atmospheric pollutants that are measured regularly (PM10, PM2.5, NO2 and SO2). An observational study of temporal and geographic measurements of individual patients (case-time series design) was carried out in Primary Care Centres and Hypertension Units in the Barcelona metropolitan area. We included 2888 hypertensive patients≥18 years old, untreated, with a first valid ABPM performed between 2005 and 2014 and with at least one air pollution station within a radius of <3km.

The mean age was 54.3 (SD 14.6) years. 50.1% were women and 16.9% of the sample were smokers. Mean 24-h blood pressure (BP) was 128.0 (12.7)/77.4 (9.7) mmHg. After adjusting for mean ambient temperature and different risk factors, a significant association was found between ambulatory diastolic BP (DBP) and PM10 concentrations the day before ABPM. For each increase of 10μg/m3 of PM10, an increase of 1.37mmHg 24-h DBP and 1.48mmHg daytime DBP was observed. No relationship was found between PM2.5, NO2 and SO2 and ambulatory BP, nor between any pollutant and clinical BP. The concentration of PM10 the day before the ABPM is significantly associated with an increase in 24-h DBP and daytime DBP.

Air pollution is acknowledged as a determinant of blood pressure (BP), supporting the hypothesis that air pollution, via hypertension and other mechanisms, has detrimental effects on human health. Previous studies evaluating the associations between air pollution exposure and BP did not consider the effect that air pollutant mixtures may have on BP. We investigated the effect of exposure to single species or their synergistic effects as air pollution mixture on ambulatory BP. Using portable sensors, we measured personal concentrations of black carbon (BC), nitrogen dioxide (NO2), nitrogen monoxide (NO), carbon monoxide (CO), ozone (O3), and particles with aerodynamic diameters below 2.5 μm (PM2.5). We simultaneously collected ambulatory BP measurements (30-min intervals, N = 3319) of 221 participants over one day of their lives. Air pollution concentrations were averaged over 5 min to 1 h before each BP measurement, and inhaled doses were estimated across the same exposure windows using estimated ventilation rates. Fixed-effect linear models as well as quantile G-computation techniques were applied to associate air pollutants' individual and combined effects with BP, adjusting for potential confounders. In mixture models, a quartile increase in air pollutant concentrations (BC, NO2, NO, CO, and O3) in the previous 5 min was associated with a 1.92 mmHg (95% CI: 0.63, 3.20) higher systolic BP (SBP), while 30-min and 1-h exposures were not associated with SBP. However, the effects on diastolic BP (DBP) were inconsistent across exposure windows. Unlike concentration mixtures, inhalation mixtures in the previous 5 min to 1 h were associated with increased SBP. Out-of-home BC and O3 concentrations were more strongly associated with ambulatory BP outcomes than in-home concentrations. In contrast, only the in-home concentration of CO reduced DBP in stratified analyses. This study shows that exposure to a mixture of air pollutants (concentration and inhalation) was associated with elevated SBP.

Some studies have investigated the effects of PM_2.5 on cardiovascular diseases based on the population-average exposure data from several monitoring stations. No one has explored the short-term effect of PM_2.5 on cardiovascular hospitalizations using individual-level exposure data. We assessed the short-term effects of individual exposure to PM_2.5 on hospitalizations for myocardial infarction (MI) and stroke in Guangzhou, China, during 2014-2019. The population-based data on cardio-cerebrovascular events were provided by Guangzhou Center for Disease Control and Prevention. Average annual percent changes (AAPCs) were used to describe trends in the hospitalization rates of MI and stroke. The conditional logistic regression model with a time-stratified case-crossover design was applied to estimate the effects of satellite-retrieved PM_2.5 with 1-km resolution as individual-level exposure. Furthermore, we performed stratified analyses by demographic characteristics and season. There were 28,346 cases of MI, 188,611, and 36,850 cases of ischemic stroke (IS) and hemorrhagic stroke (HS), respectively, with an annual average hospitalization rate of 37.2, 247, and 48.4 per 100,000 people. Over the six-year study period, significant increasing trends in the hospitalization rates were observed with AAPCs of 12.3% (95% confidence interval [CI]: 7.24%, 17.6%), 13.1% (95% CI: 9.54%, 16.7%), and 9.57% (95% CI: 6.27%, 13.0%) for MI, IS, and HS, respectively. A 10 μg/m³ increase in PM_2.5 was associated with an increase of 1.15% (95% CI: 0.308%, 1.99%) in MI hospitalization and 1.29% (95% CI: 0.882%, 1.70%) in IS hospitalization. A PM_2.5-associated reduction of 1.17% (95% CI: 0.298%, 2.03%) was found for HS hospitalization. The impact of PM_2.5 was greater in males than in females for MI hospitalization, and greater effects were observed in the elderly (≥ 65 years) and in cold seasons for IS hospitalization. Our study added important evidence on the adverse effect of PM_2.5 based on satellite-retrieved individual-level exposure data.

Gamma glutamyl transferase (GGT) is related to oxidative stress and an indicator for liver damage. We investigated the association between air pollution and GGT in a large Austrian cohort (N = 116,109) to better understand how air pollution affects human health. Data come from voluntary prevention visits that were routinely collected within the Vorarlberg Health Monitoring and Prevention Program (VHM&PP). Recruitment was ongoing from 1985 to 2005. Blood was drawn and GGT measured centralized in two laboratories. Land use regression models were applied to estimate individuals' exposure at their home address for particulate matter (PM) with a diameter of <2.5 μm (PM2.5), <10 μm (PM10), fraction between 10 μm and 2.5 μm (PMcoarse), as well as PM2.5 absorbance (PM2.5abs), NO₂, NO_x and eight components of PM. Linear regression models, adjusting for relevant individual and community-level confounders were calculated. The study population was 56 % female with a mean age of 42 years and mean GGT was 19.0 units. Individual PM2.5 and NO₂ exposures were essentially below European limit values of 25 and 40 μg/m³, respectively, with means of 13.58 μg/m³ for PM2.5 and 19.93 μg/m³ for NO₂. Positive associations were observed for PM2.5, PM10, PM2.5abs, NO₂, NO_x, and Cu, K, S in PM2.5 and PM10 fractions and Zn mainly in PM2.5 fraction. The strongest association per interquartile range observed was an increase of serum GGT concentration by 1.40 % (95 %-CI: 0.85 %; 1.95 %) per 45.7 ng/m³ S in PM2.5. Associations were robust to adjustments for other biomarkers, in two-pollutant models and the subset with a stable residential history. We found that long-term exposure to air pollution (PM2.5, PM10, PM2.5abs, NO₂, NO_x) as well as certain elements, were positively associated with baseline GGT levels. The elements associated suggest a role of traffic emissions, long range transport and wood burning.

Exposure to micro- and nanoplastic particles (MNPs) in humans is being identified in both the indoor and outdoor environment. Detection of these materials in the air has made inhalation exposure to MNPs a major cause for concern. One type of plastic polymer found in indoor and outdoor settings is polyamide, often referred to as nylon. Inhalation of combustion-derived, metallic, and carbonaceous aerosols generate pulmonary inflammation, cardiovascular dysfunction, and systemic inflammation. Additionally, due to the additives present in plastics, MNPs may act as endocrine disruptors. Currently there is limited knowledge on potential health effects caused by polyamide or general MNP inhalation.

The purpose of this study is to assess the toxicological consequences of a single inhalation exposure of female rats to polyamide MNP during estrus by means of aerosolization of MNP.

Bulk polyamide powder (i.e., nylon) served as a representative MNP. Polyamide aerosolization was characterized using particle sizers, cascade impactors, and aerosol samplers. Multiple-Path Particle Dosimetry (MPPD) modeling was used to evaluate pulmonary deposition of MNPs. Pulmonary inflammation was assessed by bronchoalveolar lavage (BAL) cell content and H&E-stained tissue sections. Mean arterial pressure (MAP), wire myography of the aorta and uterine artery, and pressure myography of the radial artery was used to assess cardiovascular function. Systemic inflammation and endocrine disruption were quantified by measurement of proinflammatory cytokines and reproductive hormones.

Our aerosolization exposure platform was found to generate particles within the micro- and nano-size ranges (thereby constituting MNPs). Inhaled particles were predicted to deposit in all regions of the lung; no overt pulmonary inflammation was observed. Conversely, increased blood pressure and impaired dilation in the uterine vasculature was noted while aortic vascular reactivity was unaffected. Inhalation of MNPs resulted in systemic inflammation as measured by increased plasma levels of IL-6. Decreased levels of 17β-estradiol were also observed suggesting that MNPs have endocrine disrupting activity.

These data demonstrate aerosolization of MNPs in our inhalation exposure platform. Inhaled MNP aerosols were found to alter inflammatory, cardiovascular, and endocrine activity. These novel findings will contribute to a better understanding of inhaled plastic particle toxicity.

The prevalence of age-related neurodegenerative diseases has risen in conjunction with an increase in life expectancy. Although there is emerging evidence that air pollution might accelerate or worsen dementia progression, studies on Asian regions remains limited. This study aimed to investigate the relationship between long-term exposure to PM₁₀ and the risk of developing Alzheimer's disease and vascular dementia in the elderly population in South Korea.

The baseline population was 1.4 million people aged 65 years and above who participated in at least one national health checkup program from the National Health Insurance Service between 2008 and 2009. A nationwide retrospective cohort study was designed, and patients were followed from the date of cohort entry (January 1, 2008) to the date of dementia occurrence, death, moving residence, or the end of the study period (December 31, 2019), whichever came first. Long-term average PM₁₀ exposure variable was constructed from national monitoring data considering time-dependent exposure. Extended Cox proportional hazard models with time-varying exposure were used to estimate hazard ratios (HR) for Alzheimer's disease and vascular dementia.

A total of 1,436,361 participants were selected, of whom 167,988 were newly diagnosed with dementia (134,811 with Alzheimer's disease and 12,215 with vascular dementia). The results show that for every 10 µg/m³ increase in PM₁₀, the HR was 0.99 (95% CI 0.98-1.00) for Alzheimer's disease and 1.05 (95% CI 1.02-1.08) for vascular dementia. Stratified analysis according to sex and age group showed that the risk of vascular dementia was higher in men and in those under 75 years of age.

The results found that long-term PM₁₀ exposure was significantly associated with the risk of developing vascular dementia but not with Alzheimer's disease. These findings suggest that the mechanism behind the PM₁₀-dementia relationship could be linked to vascular damage.

To analyze whether the high levels of air pollutants are related to a greater severity of decompensated heart failure (HF).

Patients diagnosed with decompensated HF in the emergency department of 4 hospitals in Barcelona and 3 in Madrid were included. Clinical data (age, sex, comorbidities, baseline functional status), atmospheric (temperature, atmospheric pressure) and pollutant data (SO₂, NO₂, CO, O₃, PM₁₀, PM_2.5) were collected in the city on the day of emergency care. The severity of decompensation was estimated using 7-day mortality (primary indicator) and the need for hospitalization, in-hospital mortality, and prolonged hospitalization (secondary indicators). The association adjusted for clinical, atmospheric and city data between pollutant concentration and severity was investigated using linear regression (linearity assumption) and restricted cubic spline curves (no linearity assumption).

A total of 5292 decompensations were included, with a median age of 83 years (IQR=76-88) and 56% women. The medians (IQR) of the daily pollutant averages were: SO₂=2.5μg/m³ (1.4-7.0), NO₂=43μg/m³ (34-57), CO=0.48mg/m³ (0.35-0.63), O₃=35μg/m³ (25-48), PM₁₀=22μg/m³ (15-31) and PM_2.5=12μg/m³ (8-17). Mortality at 7 days was 3.9%, and hospitalization, in-hospital mortality, and prolonged hospitalization were 78.9, 6.9, and 47.5%, respectively. SO₂ was the only pollutant that showed a linear association with the severity of decompensation, since each unit of increase implied an OR for the need for hospitalization of 1.04 (95% CI 1.01-1.08). The restricted cubic spline curves study also did not show clear associations between pollutants and severity, except for SO₂ and hospitalization, with OR of 1.55 (95% CI 1.01-2.36) and 2.71 (95% CI 1.13-6.49) for concentrations of 15 and 24μg/m³, respectively, in relation to a reference concentration of 5μg/m³.

Exposure to ambient air pollutants, in a medium to low concentration range, is generally not related to the severity of HF decompensations, and only NO₂ may be associated with an increased need for hospitalization.

The World Health Organization (WHO) has identified air pollution as one of the greatest environmental risks to public health. High levels of ambient air pollution are known to have adverse health effects, but the relationship between exposure to air pollutants and migraine attack has not been established.

This study aims to systematically review the effects of short-term exposure to fine and coarse particulate matter (PM), ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide on migraine attack.

The systematic review and meta-analysis will follow the WHO handbook for guideline development. Our protocol will comply with the guidelines of the Preferred Reporting Items for Systematic Review and meta-Analysis Protocols.

Original peer-reviewed studies conducted in the general population regardless of age and sex to investigate the association between short-term exposure to ambient air pollutants and migraine will be eligible for inclusion. Only time-series, case-crossover, and panel studies will be included.

We will search the electronic databases MEDLINE, Embase, Web of Science, Global Health, Cumulative Index to Nursing and Allied Health Literature in accordance with the pre-established search strategy. We will also check the reference list of included papers and previous reviews for supplementary search.

We will perform data extraction in accordance with the predesigned table. Using random-effects meta-analysis, we will present summary statistics (RRs and corresponding 95% CIs) associated with standardized increases in each pollutant level. Heterogeneity between studies will be assessed using 80% prediction intervals (PI). Subgroup analyzes will be performed to explore sources of heterogeneity, if any. The main findings will be presented in summary of finding table, visual display and narrative synthesis. We will review the impact of each air pollutant exposure separately.

We will employ the adaption of Grading of Recommendations, Assessment, Development, and Evaluations tool to assess the confidence in the body of evidence.