Trends in childhood leukemia incidence in urban countries and their relation to environmental factors, including space weather.

Leukemia is the most common cancer in children. Its incidence has been increasing worldwide since 1910th, suggesting the presence of common sources of the disease, most likely related to people's lifestyle and environment. Understanding the relationship between childhood leukemia and environmental conditions is critical to preventing the disease. This discussion article examines established potentially-carcinogenic environmental factors, such as vehicle emissions and fires, alongside space weather-related parameters like cosmic rays and the geomagnetic field. To discern the primary contributor, we analyze trends and annual variations in leukemia incidence among 0-14-year-olds in the United States, Canada, Australia, and Russia from 1990 to 2018. Comparisons are drawn with the number of vehicles (representing gasoline emissions) and fire-affected land areas (indicative of fire-related pollutants), with novel data for Russia introduced for the first time. While childhood leukemia incidence is rising in all countries under study, the rate of increase in Russia is twice that of other nations, possibly due to a delayed surge in the country's vehicle fleet compared to others. This trend in Russia may offer insights into past leukemia levels in the USA, Canada, and Australia. Our findings highlight vehicular emissions as the most substantial environmental hazard for children among the factors examined. We also advocate for the consideration of potential modulation of carcinogenic effects arising from variations in cosmic ray intensity, as well as the protective role of the geomagnetic field. To support the idea, we provide examples of potential space weather effects at both local and global scales. The additional analysis includes statistical data from 49 countries and underscores the significance of the magnetic field dip in the South Atlantic Anomaly in contributing to a peak in childhood leukemia incidence in Peru, Ecuador and Chile. We emphasize the importance of collectively assessing all potentially carcinogenic factors for the successful future predictions of childhood leukemia risk in each country.

Palliative effects of carnosol on lung-deposited pollutant particles-induced thrombogenicity and vascular injury in mice.

The toxicity of inhaled particulate air pollution perseveres even at lower concentrations than those of the existing air quality limit. Therefore, the identification of safe and effective measures against pollutant particles-induced vascular toxicity is warranted. Carnosol is a bioactive phenolic diterpene found in rosemary herb, with anti-inflammatory and antioxidant actions. However, its possible protective effect on the thrombotic and vascular injury induced by diesel exhaust particles (DEP) has not been studied before. We assessed here the potential alleviating effect of carnosol (20 mg/kg) administered intraperitoneally 1 h before intratracheal (i.t.) instillation of DEP (20 µg/mouse). Twenty-four hours after the administration of DEP, various parameters were assessed. Carnosol administration prevented the increase in the plasma concentrations of C-reactive protein, fibrinogen, and tissue factor induced by DEP exposure. Carnosol inhibited DEP-induced prothrombotic effects in pial microvessels in vivo and platelet aggregation in vitro. The shortening of activated partial thromboplastin time and prothrombin time induced by DEP was abated by carnosol administration. Carnosol inhibited the increase in pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor α) and adhesion molecules (intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, and P-selectin) in aortic tissue. Moreover, it averted the effects of DEP-induced increase of thiobarbituric acid reactive substances, depletion of antioxidants and DNA damage in the aortic tissue. Likewise, carnosol prevented the decrease in the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) caused by DEP. We conclude that carnosol alleviates DEP-induced thrombogenicity and vascular inflammation, oxidative damage, and DNA injury through Nrf2 and HO-1 activation.

Self-reported exposure to dust and diesel exhaust, respiratory symptoms, and use of respiratory protective equipment among Arctic miners.

Arctic miners face significant risks from diesel exhaust and dust exposure, potentially leading to adverse respiratory health. Employers must limit harmful exposures, using personal protective equipment (PPE) as a last line of defense. This study explored the association between reported respiratory exposure and symptoms, and PPE training and usage. Data from the MineHealth study (2012-2014) included a total of 453 Arctic open pit miners in Norway, Sweden, and Finland. Participants answered questions on exposure to dust and diesel exhaust, respiratory symptoms, and PPE use, in addition to age, gender, BMI, smoking, and self-rated health. Estimated exposure to dust was common, reported by 91%, 80%, and 82% and that of diesel exhaust by 84%, 43%, and 47% of workers in Sweden, Finland, and Norway, respectively. Reported dust exposure was significantly related to respiratory symptoms (OR 2.2, 95% CI 1.3-3.7), diesel exposure increased the occurrence of wheezing (OR 2.6, 95% CI 1.3-5.4). PPE use varied between the studied mines. Non-use was common and related to reduced visibility, wetness, skin irritation and fogging of the respiratory PPE. Future research should employ more precise exposure assessment, respiratory function as well as explore the reasons behind the non-compliance of PPE use.

Assessment of genotoxicity biomarkers in gasoline station attendants due to occupational exposure.

Gasoline station attendants are exposed to numerous chemicals that might have genotoxic and carcinogenic potential, such as benzene in fuel vapor and particulate matter and polycyclic aromatic hydrocarbons in vehicle exhaust emission. According to IARC, benzene and diesel particulates are Group 1 human carcinogens, and gasoline has been classified as Group 2A "possibly carcinogenic to humans." At gas stations, self-service is not implemented in Turkey; fuel-filling service is provided entirely by employees, and therefore they are exposed to those chemicals in the workplace during all working hours. Genetic monitoring of workers with occupational exposure to possible genotoxic agents allows early detection of cancer. We aimed to investigate the genotoxic damage due to exposures in gasoline station attendants in Turkey. Genotoxicity was evaluated by the Comet, chromosomal aberration, and cytokinesis-block micronucleus assays in peripheral blood lymphocytes. Gasoline station attendants (n = 53) had higher tail length, tail intensity, and tail moment values than controls (n = 61). In gasoline station attendants (n = 46), the frequencies of chromatid gaps, chromosome gaps, and total aberrations were higher compared with controls (n = 59). Increased frequencies of micronuclei and nucleoplasmic bridges were determined in gasoline station attendants (n = 47) compared with controls (n = 40). Factors such as age, duration of working, and smoking did not have any significant impact on genotoxic endpoints. Only exposure increased genotoxic damage in gasoline station attendants independently from demographic and clinical characteristics. Occupational exposure-related genotoxicity risk may increase in gasoline station attendants who are chronically exposed to gasoline and various chemicals in vehicle exhaust emissions.

Air Pollution Drives Macrophage Senescence through a Phagolysosome-15-Lipoxygenase Pathway.

Urban particulate matter (PM; uPM) poses significant health risks, particularly to the respiratory system. Fine particles, such as PM2.5, can penetrate deep into the lungs and exacerbate a range of health problems, including emphysema, asthma, and lung cancer. PM exposure is also linked to extrapulmonary disorders such as heart and neurodegenerative diseases. Moreover, prolonged exposure to elevated PM levels can reduce overall life expectancy. Senescence is a dysfunctional cell state typically associated with age but can also be precipitated by environmental stressors. This study aimed to determine whether uPM could drive senescence in macrophages, an essential cell type involved in particulate phagocytosis-mediated clearance. Although it is known that uPM exposure impairs immune function, this deficit is multifaceted and incompletely understood, partly because of the use of particulates such as diesel exhaust particles as a surrogate for true uPM. uPM was collected from several locations in the United States, including Baltimore, Houston, and Phoenix. Bone marrow-derived macrophages were stimulated with uPM or reference particulates (e.g., diesel exhaust particles) to assess senescence-related parameters. We report that uPM-exposed bone marrow-derived macrophages adopt a senescent phenotype characterized by increased IL-1α secretion, senescence-associated ß-galactosidase activity, and diminished proliferation. Exposure to allergens failed to elicit such a response, supporting a distinction between different types of environmental exposure. uPM-induced senescence was independent of key macrophage activation pathways, specifically inflammasome and scavenger receptors. However, inhibition of the phagolysosome pathway abrogated senescence markers, supporting this phenotype's attribution to uPM phagocytosis. These data suggest that uPM exposure leads to macrophage senescence, which may contribute to immunopathology.

Residential exposure to traffic pollution and mammographic density in premenopausal women.

BACKGROUND: Mammographic density (MD) is the most important breast cancer biomarker. Ambient pollution is a carcinogen, and its relationship with MD is unclear. This study aims to explore the association between exposure to traffic pollution and MD in premenopausal women. METHODOLOGY: This Spanish cross-sectional study involved 769 women attending gynecological examinations in Madrid. Annual Average Daily Traffic (AADT), extracted from 1944 measurement road points provided by the City Council of Madrid, was weighted by distances (d) between road points and women's addresses to develop a Weighted Traffic Exposure Index (WTEI). Three methods were employed: method-1 (1dAADT), method-2 (1dAADT), and method-3 (e1dAADT). Multiple linear regression models, considering both log-transformed percentage of MD and untransformed MD, were used to estimate MD differences by WTEI quartiles, through two strategies: "exposed (exposure buffers between 50 and 200 m) vs. not exposed (>200 m)"; and "degree of traffic exposure". RESULTS: Results showed no association between MD and traffic pollution according to buffers of exposure to the WTEI (first strategy) for the three methods. The highest reductions in MD, although not statistically significant, were detected in the quartile with the highest traffic exposure. For instance, method-3 revealed a suggestive inverse trend (eßQ1 = 1.23, eßQ2 = 0.96, eßQ3 = 0.85, eßQ4 = 0.85, p-trend = 0.099) in the case of 75 m buffer. Similar non-statistically significant trends were observed with Methods-1 and -2. When we examined the effect of traffic exposure considering all the 1944 measurement road points in every participant (second strategy), results showed no association for any of the three methods. A slightly decreased MD, although not significant, was observed only in the quartile with the highest traffic exposure: eßQ4 = 0.98 (method-1), and eßQ4 = 0.95 (methods-2 and -3). CONCLUSIONS: Our results showed no association between exposure to traffic pollution and MD in premenopausal women. Further research is needed to validate these findings.

Highly Reactive Peroxide Species Promoted Soot Oxidation over an Ordered Macroporous Ce0.8Zr0.2O2 Integrated Catalyzed Diesel Particulate Filter.

Particulate matter, represented by soot particles, poses a significant global environmental threat, necessitating efficient control technology. Here, we innovatively designed and elaborately fabricated ordered hierarchical macroporous catalysts of Ce0.8Zr0.2O2 (OM CZO) integrated on a catalyzed diesel particulate filter (CDPF) using the self-assembly method. An oxygen-vacancy-enriched ordered macroporous Ce0.8Zr0.2O2 catalyst (VO-OM CZO) integrated CDPF was synthesized by subsequent NaBH4 reduction. The VO-OM CZO integrated CDPF exhibited a markedly enhanced soot oxidation activity compared to OM CZO and powder CZO coated CDPFs (T50: 430 vs 490 and 545 °C, respectively). The well-defined OM structure of the VO-OM CZO catalysts effectively improves the contact efficiency between soot and the catalysts. Meanwhile, oxygen vacancies trigger the formation of a large amount of highly reactive peroxide species (O22-) from molecular oxygen (O2) through electron abstraction from the three adjacent Ce3+ (3Ce3+ + Vö + O2 → 3Ce4+ + O22-), contributing to the efficient soot oxidation. This work demonstrates the fabrication of the ordered macroporous CZO integrated CDPF and reveals the importance of structure and surface engineering in soot oxidation, which sheds light on the design of highly efficient PM capture and removal devices.

Characteristics, source analysis, and health risk of PM2.5 in the urban tunnel environment associated with E10 petrol usage.

The increase in the number of motor vehicles has intensified the impact of traffic sources on air quality. Our aim was to illustrate the characteristics of PM2.5 emissions from vehicles fueled with E10 (a blend of 10% ethanol and 90% gasoline). A 21-day PM2.5 sampling in a fully enclosed urban tunnel and the component analysis were completed, and the characteristics, sources, and health risks of tunnel PM2.5 were studied. Moreover, the PM2.5 pH and its sensitivity were investigated by the thermodynamic model (ISORROPIA-II). In addition, exposure models were used to assess the health risks of different heavy metals in PM2.5 to humans through respiratory pathways. The two-point Cu/Sb ratio (entrance: 4.0 ± 1.4; exit: 4.4 ± 1.7) was close to the diagnostic criteria indicating a significant impact from brake wear. NO3-, NH4+, and SO42- constituted the main components of water-soluble ions in PM2.5 of the tunnel, accounting for 83.0-84.6% of the total concentration of inorganic ions. The organic carbon/elemental carbon ratio of the tunnel was greater than 2, indicating that the contribution of gasoline vehicle exhaust was significant. The average emission factors of PM2.5 in the fleet was 31.4 ± 16.6 mg/(veh·km). The pH value of PM2.5 in a tunnel environment (4.6 ± 0.3) was more acidic than that in an urban environment (4.9 ± 0.6). The main sensitive factors of PM2.5 pH in the urban atmosphere and tunnel environment were total ammonia (sum of gas and aerosol, NH3) and temperature, respectively. The results of the health risk assessment showed that Pb posed a potential carcinogenic risk, while As and Cd presented unacceptable risks for tunnel workers. The non-carcinogenic risk index of heavy metals of PM2.5 in the tunnel environment exceeded the safety threshold.

Risk of Skin Cancer in Workers Exposed to Diesel Exhaust: A Systematic Review and Meta-Analysis of Cohort Studies.

BACKGROUND: Our objective was to study the association between occupational exposure to diesel exhaust (DE) and skin cancer. METHODS: A systematic review following STROBE guidelines and PECOS criteria was conducted to identify cohort studies describing the association between occupational DE exposure and the risk of skin cancer. We extracted 12 independent risk estimates for melanoma skin cancer (MSC), 8 for non-melanoma skin cancer (NMSC), and 3 for skin cancer not otherwise specified (SC-NOS). Random effects meta-analyses were performed, site-specific and stratified by geographic region and quality score. 95% confidence intervals (CI) were reported. Between-study heterogeneity and potential publication bias were investigated. RESULTS: There was no overall evidence of an increased risk of MSC [RR=0.90, 95% CI: 0.73-1.11; I2=92.86%, 95% CI: 82.83-97.03%], NMSC [RR=1.04, 95% CI: 0.88-1.23; I2=60.79%, 95% CI: 0-87.34%] or SC-NOS [RR=0.72, 95% CI: 0.54-0.97; I2=26.60%, 95% CI: 0-94.87%] in workers exposed to DE. No difference between low-quality and high-quality studies was found. A stratified analysis by geographical region did not reveal any significant differences. There was no evidence of publication bias. CONCLUSIONS: No evidence of an association between skin cancer and occupational DE exposure was found. Residual confounding and other sources of bias cannot be ruled out.

Subacute Exposure to Gaseous Pollutants from Diesel Engine Exhaust Attenuates Capsaicin-Induced Cardio-Pulmonary Reflex Responses Involving Oxidant Stress Mechanisms in Adult Wistar Rats.

Intravenous injection of capsaicin produces vagal-mediated protective cardio-pulmonary (CP) reflexes manifesting as tachypnea, bradycardia, and triphasic blood pressure (BP) response in anesthetized rats. Particulate matter from diesel engine exhaust has been reported to attenuate these reflexes. However, the effects of gaseous constituents of diesel exhaust are not known. Therefore, the present study was designed to investigate the effects of gaseous pollutants in diesel exhaust, on capsaicin-induced CP reflexes in rat model. Adult male rats were randomly assigned to three groups: Non-exposed (NE) group, filtered diesel exhaust-exposed (FDE) group and N-acetyl cysteine (NAC)-treated FDE group. FDE group of rats (n = 6) were exposed to filtered diesel exhaust for 5 h a day for 5 days (D1-D5), and were taken for dissection on day 6 (D6), while NE group of rats (n = 6) remained unexposed. On D6, rats were anesthetized, following which jugular vein was cannulated for injection of chemicals, and femoral artery was cannulated to record the BP. Lead II electrocardiogram and respiratory movements were also recorded. Results show that intravenous injection of capsaicin (0.1 ml; 10 µg/kg) produced immediate tachypneic, hyperventilatory, hypotensive, and bradycardiac responses in both NE and FDE groups of rats. However, these capsaicin-induced CP responses were significantly attenuated in FDE group as compared to the NE group of rats. Further, FDE-induced attenuation of capsaicin-evoked CP responses were diminished in the N-acetyl cysteine-treated FDE rats. These findings demonstrate that oxidant stress mechanisms could possibly be involved in inhibition of CP reflexes by gaseous pollutants in diesel engine exhaust.

Long-term trends of black carbon and particle number concentrations and their vehicle emission factors in Stockholm.

Black carbon (BC) and particle number (PN) concentrations are usually high in cities due to traffic emissions. European mitigation policies, including Euro emission standards, have been implemented to curb these emissions. We analyzed BC and PN (particle diameter Dp > 4 nm) concentrations in Stockholm spanning the years 2013-2019 (BC) and 2009-2019 (PN) measured at street canyon and rooftop sites to assess the effectiveness of the implemented policies. Combining these data with inverse dispersion modeling, we estimated BC and PN emission factors (EFBC and EFPN) for the mixed fleet, reflecting real-world driving conditions. The pollutants showed decreasing trends at both sites, but PN concentrations remained high at the canyon site considering the World Health Organization (WHO) recommendations. BC concentrations declined more rapidly than PN concentrations, showing a -9.4% and -4.9% annual decrease at the canyon and -7.2% and -0.5% at the rooftop site in the years 2013-2019. The EFBC and EFPN trends showed that the mitigation strategies for reducing particulate emissions for on-road vehicles were successful over the study period. However, the introduction of biofuels in the vehicle fleet -ethanol and later rapeseed methyl ester (RME)- increased the concentrations of particles with Dp < 10 nm before the adoption of particulate filters in the exhausts. Stricter Euro emission regulations, especially with diesel particulate filters (DPF) in Euro 5, 6, and VI vehicles, led to 66% decrease in EFBC and 55% in EFPN. Real-world EFBC surpassed HBEFA (Handbook Emission Factors for Road Transport) database values by 2.4-4.8 times; however, direct comparisons between real-world and HBEFA EFPN are difficult due to differences in lower cut-off sizes and measurement techniques. Our results underscore the necessity for revising the HBEFA database, updating laboratory testing methods and portable emission measuring systems (PEMS) measurements to account for liquid condensate contributions to PN measurements.

Lichen biomonitoring to assess spatial variability, potential sources and human health risks of polycyclic aromatic hydrocarbons (PAHs) and airborne metal concentrations in Manchester (UK).

Airborne metals and organic pollutants are linked to severe human health impacts, i.e. affecting the nervous system and being associated with cancer. Airborne metals and polycyclic aromatic hydrocarbons (PAHs) in urban environments are derived from diverse sources, including combustion and industrial and vehicular emissions, posing a threat to air quality and subsequently human health. A lichen biomonitoring approach was used to assess spatial variability of airborne metals and PAHs, identify potential pollution sources and assess human health risks across the City of Manchester (UK). Metal concentrations recorded in lichen samples were highest within the city centre area and along the major road network, and lichen PAH profiles were dominated by 4-ring PAHs (189.82 ng g-1 in Xanthoria parietina), with 5- and 6-ring PAHs also contributing to the overall PAH profile. Cluster analysis and pollution index factor (PIF) calculations for lichen-derived metal concentrations suggested deteriorated air quality being primarily linked to vehicular emissions. Comparably, PAH diagnostic ratios identified vehicular sources as a primary cause of PAH pollution across Manchester. However, local more complex sources (e.g. industrial emissions) were further identified. Human health risk assessment found a "moderate" risk for adults and children by airborne potential harmful element (PHEs) concentrations, whereas PAH exposure in Manchester is potentially linked to 1455 (ILCR = 1.45 × 10-3) cancer cases (in 1,000,000). Findings of this study indicate that an easy-to-use lichen biomonitoring approach can aid to identify hotspots of impaired air quality and potential human health impacts by airborne metals and PAHs across an urban environment, particularly at locations that are not continuously covered by (non-)automated air quality measurement programmes.

Assessing emission-driven changes in health risk of source-specific PM2.5-bound heavy metals by adjusting meteorological covariates.

Heavy metals (HMs) in PM2.5 gain much attention for their toxicity and carcinogenic risk. This study evaluates the health risks of PM2.5-bound HMs, focusing on how meteorological conditions affect these risks against the backdrop of PM2.5 reduction trends in China. By applying a receptor model with a meteorological normalization technique, followed by health risk assessment, this work reveals emission-driven changes in health risk of source-specific HMs in the outskirt of Tianjin during the implementation of China' second Clean Air Action (2018-2020). Sources of PM2.5-bound HMs were identified, with significant contributions from vehicular emissions (on average, 33.4 %), coal combustion (26.3 %), biomass burning (14.1 %), dust (11.7 %), industrial boilers (9.7 %), and shipping emission and sea salt (4.7 %). The source-specific emission-driven health risk can be enlarged or dwarfed by the changing meteorological conditions over time, demonstrating that the actual risks from these source emissions for a given time period may be higher or smaller than those estimated by traditional assessments. Meteorology contributed on average 56.1 % to the interannual changes in source-specific carcinogenic risk of HMs from 2018 to 2019, and 5.6 % from 2019 to 2020. For the source-specific noncarcinogenic risk changes, the contributions were 38.3 % and 46.4 % for the respective periods. Meteorology exerts a more profound impact on daily risk (short-term trends) than on annual risk (long-term trends). Such meteorological impacts differ among emission sources in both sign and magnitude. Reduced health risks of HMs were largely from targeted regulatory measures on sources. Therefore, the meteorological covariates should be considered to better evaluate the health benefits attributable to pollution control measures in health risk assessment frameworks.

Effect of diesel exhaust particles on RANK/RANKL expression in in vivo and in vitro models of middle ear inflammation.

OBJECTIVE: Increasing evidence suggests a link between middle ear inflammation and the development of diesel exhaust particles (DEPs). Chronic middle ear inflammation can lead to bone damage and remodeling. This study aimed to explore the impact of DEPs on the expression of interleukin (IL)-6 and RANKL under conditions of middle ear inflammation. METHODS: DEPs were collected by burning fuel in a diesel engine at the Gwangju Institute of Science and Technology. Human middle ear epithelial cells were cultured to 70-80% confluence in culture plates and then treated with DEPs at concentrations of 0, 5, 10, 20, 40, and 80 µg/mL for 24 h. Cell viability was assessed manually. B6.SJL mice, aged 9 weeks, were exposed to DEPs at a concentration of 200 µg/m3 for 1 h daily over a period of 28 days. The expression levels of IL-6, tumor necrosis factor α, RANKL, and RANK were evaluated using hematoxylin and eosin staining and western blot analysis of the harvested middle ear samples. RESULTS: The viability of human middle ear epithelial cells was found to decrease in a dose-dependent manner after 24 h. The mRNA expression level of IL-6 exhibited the most significant increase at the 48-h mark. In contrast, the mRNA expression levels of RANKL and RANK showed a marked increase as early as 6 h post-exposure, with both genes subsequently displaying a time-dependent decrease. Histological analysis revealed that the middle ear mucosa was thicker in the group exposed to DEPs compared to the control group. Additionally, the protein expression levels of IL-6 and RANKL were elevated in the DEP-exposed group relative to the normal control group. CONCLUSIONS: We confirmed the expression of osteoclast-related proteins in the mouse middle ear. These results imply that air pollutants might affect RANKL/RANK signaling, which is associated with bone remodeling.

High spatial-resolved source-specific exposure and risk in the city scale: Influence of spatial interrelationship between PM2.5 sources and population on exposure.

Research on High Spatial-Resolved Source-Specific Exposure and Risk (HSRSSER) was conducted based on multiple-year, multiple-site synchronous measurement of PM2.5-bound (particulate matter with aerodynamic diameter<2.5 µm) toxic components in a Chinese megacity. The developed HSRSSER model combined the Positive Matrix Factorization (PMF) and Land Use Regression (LUR) to predict high spatial-resolved source contributions, and estimated the source-specific exposure and risk by personal activity time- and population-weighting. A total of 287 PM2.5 samples were collected at ten sites in 2018-2020, and toxic species including heavy metals (HMs), polycyclic aromatic hydrocarbons (PAHs) and organophosphate esters (OPEs) were analyzed. The percentage non-cancer risk were in the order of traffic emission (48 %) > industrial emission (22 %) > coal combustion (12 %) > waste incineration (11 %) > resuspend dust (7 %) > OPE-related products (0 %) ≈ secondary particles (0 %). Similar orders were observed in cancer risk. For traffic emission, due to its higher source contributions and large population in central area, non-cancer and cancer risk fraction increased from 23 % to 48 % and 20 % to 46 % after exposure estimation; while for industrial emission, higher source contributions but small population in suburb area decreased the percentage non-cancer and cancer risk from 38 % to 22 % and 39 % to 24 %, respectively.

Evaluation of neural reflex activation as a potential mode of action for respiratory and cardiovascular effects of fine particulate matter.

OBJECTIVES: Mortality from respiratory and cardiovascular health conditions contributes largely to the total mortality that has been associated with exposure to PM2.5 in epidemiology studies. A mode of action (MoA) for these underlying morbidities has not been established, but it has been proposed that some effects of PM2.5 occur through activation of neural reflexes. MATERIALS AND METHODS: We critically reviewed the experimental studies of PM2.5 (including ambient PM2.5, diesel exhaust particles, concentrated ambient particles, diesel exhaust, and cigarette smoke) and neural reflex activation, and applied the principles of the International Programme on Chemical Safety (IPCS) MoA/human relevance framework to assess whether they support a biologically plausible and human-relevant MoA by which PM2.5 could contribute to cardiovascular and respiratory causes of death. We also considered whether the evidence from these studies supports a non-threshold MoA that operates at low, human-relevant PM2.5 exposure concentrations. RESULTS AND DISCUSSION: We found that the proposed MoA of neural reflex activation is biologically plausible for PM2.5-induced respiratory effects at high exposure levels used in experimental studies, but further studies are needed to fill important data gaps regarding the relevance of this MoA to humans at lower PM2.5 exposure levels. A role for the proposed MoA in PM2.5-induced cardiovascular effects is plausible for some effects but not others. CONCLUSIONS: Further studies are needed to determine whether neural reflex activation is the MoA by which PM2.5 could cause either respiratory or cardiovascular morbidities in humans, particularly at the ambient concentrations associated with total mortality in epidemiology studies.

Epithelial MAPK signaling directs endothelial NRF2 signaling and IL-8 secretion in a tri-culture model of the alveolar-microvascular interface following diesel exhaust particulate (DEP) exposure.

BACKGROUND: Particulate matter 2.5 (PM2.5) deposition in the lung's alveolar capillary region (ACR) is significantly associated with respiratory disease development, yet the molecular mechanisms are not completely understood. Adverse responses that promote respiratory disease development involve orchestrated, intercellular signaling between multiple cell types within the ACR. We investigated the molecular mechanisms elicited in response to PM2.5 deposition in the ACR, in an in vitro model that enables intercellular communication between multiple resident cell types of the ACR. METHODS: An in vitro, tri-culture model of the ACR, incorporating alveolar-like epithelial cells (NCI-H441), pulmonary fibroblasts (IMR90), and pulmonary microvascular endothelial cells (HULEC) was developed to investigate cell type-specific molecular responses to a PM2.5 exposure in an in-vivo-like model. This tri-culture in vitro model was termed the alveolar capillary region exposure (ACRE) model. Alveolar epithelial cells in the ACRE model were exposed to a suspension of diesel exhaust particulates (DEP) (20 µg/cm2) with an average diameter of 2.5 µm. Alveolar epithelial barrier formation, and transcriptional and protein expression alterations in the directly exposed alveolar epithelial and the underlying endothelial cells were investigated over a 24 h DEP exposure. RESULTS: Alveolar epithelial barrier formation was not perturbed by the 24 h DEP exposure. Despite no alteration in barrier formation, we demonstrate that alveolar epithelial DEP exposure induces transcriptional and protein changes in both the alveolar epithelial cells and the underlying microvascular endothelial cells. Specifically, we show that the underlying microvascular endothelial cells develop redox dysfunction and increase proinflammatory cytokine secretion. Furthermore, we demonstrate that alveolar epithelial MAPK signaling modulates the activation of NRF2 and IL-8 secretion in the underlying microvascular endothelial cells. CONCLUSIONS: Endothelial redox dysfunction and increased proinflammatory cytokine secretion are two common events in respiratory disease development. These findings highlight new, cell-type specific roles of the alveolar epithelium and microvascular endothelium in the ACR in respiratory disease development following PM2.5 exposure. Ultimately, these data expand our current understanding of respiratory disease development following particle exposures and illustrate the utility of multicellular in vitro systems for investigating respiratory tract health.

Electrification of Transit Buses in the United States Reduces Greenhouse Gas Emissions.

The transportation sector is the largest emitter of greenhouse gas emissions (GHGs) in the United States. Increased use of public transit and electrification of public transit could help reduce these emissions. The electrification of public transit systems could also reduce air pollutant emissions in densely populated areas, where air pollution disproportionally burdens vulnerable communities with high health impacts and associated social costs. We analyze the life cycle emissions of transit buses powered by electricity, diesel, gasoline, and compressed natural gas and model GHGs and air pollutants mitigated for a transition to a fully electric U.S. public transit bus fleet using transit agency-level data. The electrification of the U.S. bus fleet would reduce several conventional air pollutants and has the potential to reduce transit bus GHGs by 33-65% within the next 14 years depending on how quickly the transition is made and how quickly the electricity grid decarbonizes. A levelized cost of driving analysis shows that with falling capital costs and an increase in annual passenger-kilometers of battery electric buses, the technology could reach levelized cost parity with diesel buses when electric bus capital costs fall below about $670 000 per bus.

Differential pulmonary toxicity and autoantibody formation in genetically distinct mouse strains following combined exposure to silica and diesel exhaust particles.

BACKGROUND: Inhalation of airborne particulate matter, such as silica and diesel exhaust particles, poses serious long-term respiratory and systemic health risks. Silica exposure can lead to silicosis and systemic autoimmune diseases, while DEP exposure is linked to asthma and cancer. Combined exposure to silica and DEP, common in mining, may have more severe effects. This study investigates the separate and combined effects of occupational-level silica and ambient-level DEP on lung injury, inflammation, and autoantibody formation in two genetically distinct mouse strains, thereby aiming at understanding the interplay between genetic susceptibility, particulate exposure, and disease outcomes. Silica and diesel exhaust particles were administered to mice via oropharyngeal aspiration. Assessments of lung injury and host response included in vivo lung micro-computed tomography, lung function tests, bronchoalveolar lavage fluid analysis including inflammatory cytokines and antinuclear antibodies, and histopathology with particle colocalization. RESULTS: The findings highlight the distinct effects of silica and diesel exhaust particles (DEP) on lung injury, inflammation, and autoantibody formation in C57BL/6J and NOD/ShiLtJ mice. Silica exposure elicited a well-established inflammatory response marked by inflammatory infiltrates, release of cytokines, and chemokines, alongside mild fibrosis, indicated by collagen deposition in the lungs of both C57BL/6J and NOD/ShilLtJ mice. Notably, these strains exhibited divergent responses in terms of respiratory function and lung volumes, as assessed through micro-computed tomography. Additionally, silica exposure induced airway hyperreactivity and elevated antinuclear antibody levels in bronchoalveolar lavage fluid, particularly prominent in NOD/ShiLtJ mice. Moreover, antinuclear antibodies correlated with extent of lung inflammation in NOD/ShiLTJ mice. Lung tissue analysis revealed DEP loaded macrophages and co-localization of silica and DEP particles. However, aside from contributing to airway hyperreactivity specifically in NOD/ShiLtJ mice, the ambient-level DEP did not significantly amplify the effects induced by silica. There was no evidence of synergistic or additive interaction between these specific doses of silica and DEP in inducing lung damage or inflammation in either of the mouse strains. CONCLUSION: Mouse strain variations exerted a substantial influence on the development of silica induced lung alterations. Furthermore, the additional impact of ambient-level DEP on these silica-induced effects was minimal.

Fine particle trace elements at a mountain site in southern China: Source identification, transport, and health risks.

Trace elements in atmospheric particulate matter play a significant role in air quality, human health, and biogeochemical cycles. In this study, the trace elements (Ca, Al, K, Fe, Na, Mg, Zn, Pb, Mn, Ti, Cu, Cr, Sr, Ni) in PM2.5 samples collected at the summit of Mt. Lushan were analyzed to quantify their abundance, source, transport, and health risks. During the whole sampling period, the major trace elements was Ca, Al, and K. While the trace metals with the lowest concentrations were Sr, Ni, Rb, and Cd. The trace elements were influenced by air mass transport routes, exhibiting an increasing trend of crustal elements in the northwesterly airmass and anthropogenic elements (Zn, Mn, Cu, and Ni) in the easterly air masses. Construction dust, coal + biomass burning, vehicle emission, urban nitrate-rich + urban waste incineration emissions, and soil dust + industry emissions were common sources of PM2.5 on Mt. Lushan. Different air mass transport routes had various source contribution patterns. These results indicate that trace elements at Mt. Lushan are influenced by regional anthropogenic emissions and monsoon-dominated trace element transport. The total resulting cancer risk value that these elements posed were below the acceptable risk value of 1 × 10-6, while the non-carcinogenic risk value (1.72) was higher than the safety level, suggesting that non-carcinogenic effects due to these trace elements inhalation were likely to occur. Vehicle emission and coal + biomass burning were the common dominant sources of non-cancer risks posed by trace elements at Mt. Lushan.