An improved understanding of the mechanisms that regulate wildfire risk at local to regional scales is needed for the design of effective fire and ecosystem management. We investigated the spatial distribution of burned area in Southern California during 1960-2009 using five different data-driven methods: multiple linear regression, generalized additive models (GAMs), GAMs with spatial autocorrelation, non-linear multiplicative models, and random forest models. We used each method to separately develop burned area risk maps for Southern California's two distinct wildfire regimes: Santa Ana (SA fires), which occur during high wind events mostly in autumn, and non-Santa Ana fires (non-SA fires), which occur mostly during the hot and dry Mediterranean-climate summer. The different methods explained 38-63% of the spatial variance in burned area for SA fires and 21-48% for non-SA fires. The two fire regimes had contrasting drivers, with Fosberg fire weather index, relative humidity, minimum temperature, and distance to housing most important for SA fires, and shrub cover, road density, and distance to minor and major roads most important for non-SA fires. Our modeling framework carries implications for the strategic placement of fire suppression resources, and for prevention planning in areas facing increasing human and climate pressures.

It has been demonstrated that propylene glycol (PG), vegetable glycerin (VG), and flavoring chemicals can thermally degrade to form carbonyls during vaping, but less is known about carbonyl emissions produced by transformation of flavoring chemicals and the interactive effects among e-liquid constituents. This study characterized carbonyl composition and levels in vaping emissions of PG-VG (e-liquid base solvents) and four e-liquid formulations flavored with trans-2-hexenol, benzyl alcohol, l-(-)-menthol, or linalool. Utilizing gas chromatography (GC)- and liquid chromatography (LC)-mass spectrometry (MS) methods, 14 carbonyls were identified and quantified. PG-VG emitted highest levels of formaldehyde, acetaldehyde, and acrolein. However, flavored e-liquids contributed to the production of a wider variety of carbonyls, with some carbonyls directly corresponding to the oxidation of alcohol moieties in flavoring compounds (e.g., trans-2-hexenol and benzyl alcohol transformed into trans-2-hexenal and benzaldehyde, respectively). Detections of formaldehyde-GSH and trans-2-hexenal-GSH adducts signify interactions of carbonyls with biological nucleophiles. The global reactivity descriptors (I, A, μ, η, and ω) and condensed Fukui parameters (fk0, fk-, fk+, and dual-descriptor) were computed to elucidate site reactivities of selected simple and α,β-unsaturated carbonyls found in vaping emissions. Overall, this study highlights carbonyl emissions and reactivities and their potential health risk effects associated with vaping.

Clinical descriptions of perceptual and attentional anomalies in schizophrenia emphasize phenomena such as flooding, or inundation, by sensory stimuli. A failure of sensory "gating" mechanisms in the brain is hypothesized to account for these symptoms, and this hypothesis has led to a marked interest in their putative psychophysiological substrates. However, there are no systematic analyses of the phenomenology of these perceptual experiences, nor has the hypothesized connection between the clinical phenomena and their reported psychophysiological substrates been tested. In this investigation, a structured interview instrument was developed to measure perceptual anomalies as distinct from hallucinations and to determine their prevalence across sensory modalities in schizophrenia in 67 schizophrenia subjects and 98 normal controls. The instrument includes Likert ratings of hypersensitivity, inundation, and selective attention to external sensory stimuli. Good interrater agreement, determined from interviews, was obtained. Schizophrenia subjects had significantly higher auditory, visual, and combined scores (i.e., across all modalities) than normal controls did, indicating significantly more perceptual anomalies. For the schizophrenia group, the prevalence of auditory and visual anomalies was significantly greater than the other sensory modalities. The data indicate that the putative phenomenological correlates of sensory gating may be reliably measured and tested with the Structured Interview for Assessing Perceptual Anomalies.

Traffic-related particulate matter (PM) is a major source of outdoor air pollution worldwide. It has been recently hypothesized to cause cardiometabolic syndrome, including cardiovascular dysfunction, obesity, and diabetes. The environmental and toxicological factors involved in the processes, and the detailed mechanisms remain to be explored. The objective of this study is to assess the current scientific evidence of traffic-related PM-induced cardiometabolic syndrome. We conducted a literature review by searching the keywords of "traffic related air pollution", "particulate matter", "human health", and "metabolic syndrome" from 1980 to 2018. This resulted in 25 independent research studies for the final review. Both epidemiological and toxicological findings reveal consistent correlations between traffic-related PM exposure and the measured cardiometabolic health endpoints. Smaller sizes of PM, particularly ultrafine particles, are shown to be more harmful due to their greater concentrations, reactive compositions, longer lung retention, and bioavailability. The active components in traffic-related PM could be attributed to metals, black carbon, elemental carbon, polyaromatic hydrocarbons, and diesel exhaust particles. Existing evidence points out that the development of cardiometabolic symptoms can occur through chronic systemic inflammation and increased oxidative stress. The elderly (especially for women), children, genetically susceptible individuals, and people with pre-existing conditions are identified as vulnerable groups. To advance the characterization of the potential health risks of traffic-related PM, additional research is needed to investigate the detailed chemical compositions of PM constituents, atmospheric transformations, and the mode of action to induce adverse health effects. Furthermore, we recommend that future studies could explore the roles of genetic and epigenetic factors in influencing cardiometabolic health outcomes by integrating multi-omics approaches (e.g., genomics, epigenomics, and transcriptomics) to provide a comprehensive assessment of biological perturbations caused by traffic-related PM.

Background

Existing studies on the health effects of e-cigarettes focused on e-cigarette users themselves. To study the corresponding effects on passive vapers, it is crucial to quantify e-cigarette chemicals deposited in their airways.

Objective

This study proposed an innovative approach to estimate the deposited dose of e-cigarette chemicals in the passive vapers' airways. The effect of the distance between active and passive vapers on the deposited dose was also examined.

Methods

The chemical constituent analysis was conducted to detect Nicotine and flavoring agents in e-cigarette aerosol. The Mobile Aerosol Lung Deposition Apparatus (MALDA) was employed to conduct aerosol respiratory deposition experiments in real-life settings to generate real-time data.

Results

For e-cigarette aerosol in the ultrafine particle regime, the deposited doses in the alveolar region were on average 3.2 times higher than those in the head-to-TB airways, and the deposited dose in the passive vaper's airways increased when being closer to the active vaper.

Significance

With prolonged exposure and close proximity to active vapers, passive vapers may be at risk for potential health effects of harmful e-cigarette chemicals. The methodology developed in this study has laid the groundwork for future research on exposure assessment and health risk analysis for passive vaping.

In late 2019, the outbreak of e-cigarette or vaping-associated lung injuries (EVALIs) in the United States demonstrated to the public the potential health risks of vaping. While studies since the outbreak have identified vitamin E acetate (VEA), a diluent of tetrahydrocannabinol (THC) in vape cartridges, as a potential contributor to lung injuries, the molecular mechanisms through which VEA may cause damage are still unclear. Recent studies have found that the thermal degradation of e-liquids during vaping can result in the formation of products that are more toxic than the parent compounds. In this study, we assessed the role of duroquinone (DQ) in VEA vaping emissions that may act as a mechanism through which VEA vaping causes lung damage. VEA vaping emissions were collected and analyzed for their potential to generate reactive oxygen species (ROS) and induce oxidative stress-associated gene expression in human bronchial epithelial cells (BEAS-2B). Significant ROS generation by VEA vaping emissions was observed in both acellular and cellular systems. Furthermore, exposure to vaping emissions resulted in significant upregulation of NQO1 and HMOX-1 genes in BEAS-2B cells, indicating a strong potential for vaped VEA to cause oxidative damage and acute lung injury; the effects are more profound than exposure to equivalent concentrations of DQ alone. Our findings suggest that there may be synergistic interactions between thermal decomposition products of VEA, highlighting the multifaceted nature of vaping toxicity.