Search

Respiratory aerosols with diameters smaller than 100 μ m have been confirmed as important vectors for the spread of diseases such as SARS-CoV-2. While disposable and cloth masks afford some protection, they are typically inefficient at filtering these aerosols and require specialized fabrication devices to produce. We describe a fabrication technique that makes use of a folding procedure (origami) to transform any filtration material into a mask. These origami masks can be fabricated by non-experts at minimal cost and effort, provide adequate filtration efficiencies, and are easily scaled to different facial sizes. Using a mannequin fit test simulator, we demonstrate that these masks can provide filtration efficiencies of over 90% while simultaneously providing greater comfort as demonstrated by pressure drops of <20 Pa. We also quantify mask leakage by measuring the variations in filtration efficiency and pressure drop when masks are sealed to the mannequin face compared to when the mask is unsealed but positioned to achieve the best fit. While leakage generally trended with pressure drop, some of the best performing mask media achieved <10% reduction in filtration efficiency due to leakage. Because this mask can provide high filtration efficiencies at low pressure drop compared to commercial alternatives, it is likely to promote greater mask wearing tolerance and acceptance. [ABSTRACT FROM AUTHOR]

Background: Alzheimer's Disease (AD) impacts brain regions associated with memory and executive function in early stages. The Stroop task is used to evaluate inhibition, a common factor for executive functioning. Alpha Event‐Related Desynchronization (ERD) from electroencephalogram (EEG) analysis evaluates brain activation during a task. Also of interest is cardiovascular function such as heart rate (HR) and blood pressure (BP) as it relates to cognitive functioning in AD progression. However, the combined analysis of functional EEG with HR and BP have not been thoroughly reported in a Cognitively Healthy (CH) cohort. To fill this gap, we studied these measurements in CH participants who underwent a Stroop task. Method: We previously reported Stroop alpha ERD of CH participants when their cerebrospinal fluid amyloid/tau ratio were normal (≥2.71, CH‐NATs) or pathological (<2.71, CH‐PATs). Their heart rate (HRmax, HRmin, and HRmax‐HRmin) were analyzed from 5‐minute electrocardiogram (ECG) during resting or Stroop testing. Using a second cohort, including 22 CH‐NATs and 15 CH‐PATs, we analyzed alpha ERD while participants completed a Stroop task on a computer wearing a dry electroencephalogram (EEG) headset with 19 head sensors, which were correlated with HR and BP collected pre‐ and post‐task using an automatic blood pressure monitor. Result: HRmax and HRmax‐HRmin from rest to task were significantly increased in CH‐PATs but not CH‐NATs, while HRmin significantly increased in CH‐NATs (Fig. 1). Frontal alpha ERD during incongruent trials were positively correlated with pre‐(R2 = 0.43, p = 0.008) and post‐(R2 = 0.42, p = 0.009) task HR in CH‐PATs but not CH‐NATs. Pre‐test diastolic BP correlated positively with central alpha ERD during congruent trials in CH‐NATs (R2 = 0.20, p = 0.039) but not CH‐PATs (Fig. 2). Conclusion: These pilot results suggest 1) from resting to task, CH‐NATs presented greater HRmin, while CH‐PATs presented greater HRmax and HRmax‐HRmin; 2) HR is positively correlated with alpha ERD in CH‐PATs such that higher HR related to less brain activation (less negative alpha ERD). Higher pre‐task diastolic BP related to less brain activation in CH‐NATs. Although a larger sample is needed, these results support a potential application of non‐invasive EEG and ECG to identify those at higher risk of cognitive decline. [ABSTRACT FROM AUTHOR]

Introduction: Somatic mutations in myeloid growth factor pathway genes, such as JAK2, and genes involved in epigenetic regulation, such as TET2, in hematopoietic stem cells (HSCs) leads to clonal hematopoiesis of indeterminate potential (CHIP) which presents a risk factor for hematologic malignancy and cardiovascular disease. Smoking behavior has been repeatedly associated with the occurrence of CHIP but whether smoking is an environmental inflammatory stressor in promoting clonal expansion has not been investigated. Methods: We performed in vivo smoke exposures in both wildtype (WT) mice and transplanted mice carrying Jak2V617F mutant and Tet2 knockout (Tet-/-) cells to determine the impact of cigarette smoke (CS) in the HSC compartment as well as favoring mutant cell expansion. Results: WTmiceexposedtosmokedisplayed increasedoxidative stress in long-term HSCs and suppression of the hematopoietic stem and progenitor compartment but smokeexposuredid not translate to impaired hematopoietic reconstitutioninprimary bonemarrowtransplants. Geneexpression analysisofhematopoietic cells inthebone marrow identified an imbalance between Th17 and Treg immune cells suggesting a local inflammatory environment. We also observed enhanced survival of Jak2V617F cellsexposed toCSin vivoand cigarettesmokeextract (CSE) invitro. WTbonemarrow hematopoietic cells fromWT/Jak2V617F chimeric mice exposed toCSdemonstrated an increase in neutrophil abundance and distinct overexpression of bone marrow stromal antigen 2 (Bst2) and retinoic acid early transcript 1 (Raet1) targets. Bst2 and Raet1 are indicative of increased interferon signaling and cellular stress including oxidative stress and DNA damage, respectively. In chimericmice containing bothWT and Tet2-/-cells, we observed an increased percentage of circulatingmutant cells in peripheral blood post-cigarette smoke exposure when compared to pre-exposure levels while this difference was absent in air-exposed controls. Conclusion: Altogether, these findings demonstrate that CS results in an inflamed bone marrow environment that provides a selection pressure for existing CHIP mutations such as Jak2V617F and Tet2 loss-of-function. [ABSTRACT FROM AUTHOR]

Exposure to traffic-related air pollution consisting of particulate matter (PM) is associated with cognitive decline leading to Alzheimer's disease (AD). In this study, we sought to examine the neurotoxic effects of exposure to ultrafine PM and how it exacerbates neuronal loss and AD-like neuropathology in wildtype (WT) mice and a knock-in mouse model of AD (AppNL-G-F/+ -KI) when the exposure occurs at a prepathologic stage or at a later age with the presence of neuropathology. AppNL-G-F/+ -KI and WT mice were exposed to concentrated ultrafine PM from local ambient air in Irvine, California, for 12 weeks, starting at 3 or 9 months of age. Particulate matter-exposed animals received concentrated ultrafine PM up to 8 times above the ambient levels, whereas control animals were exposed to purified air. Particulate matter exposure resulted in a marked impairment of memory tasks in prepathologic AppNL-G-F/+ -KI mice without measurable changes in amyloid-β pathology, synaptic degeneration, and neuroinflammation. At aged, both WT and AppNL-G-F/+ -KI mice exposed to PM showed a significant memory impairment along with neuronal loss. In AppNL-G-F/+ -KI mice, we also detected an increased amyloid-β buildup and potentially harmful glial activation including ferritin-positive microglia and C3-positive astrocytes. Such glial activation could promote the cascade of degenerative consequences in the brain. Our results suggest that exposure to PM impairs cognitive function at both ages while exacerbation of AD-related pathology and neuronal loss may depend on the stage of pathology, aging, and/or state of glial activation. Further studies will be required to unveil the neurotoxic role of glial activation activated by PM exposure. [ABSTRACT FROM AUTHOR]

The heart and brain have bi-directional influences on each other, including autonomic regulation and hemodynamic connections. Heart rate variability (HRV) measures variation in beat-to-beat intervals. New findings about disorganized sinus rhythm (erratic rhythm, quantified as heart rate fragmentation, HRF) are discussed and suggest overestimation of autonomic activities in HRV changes, especially during aging or cardiovascular events. When excluding HRF, HRV is regulated via the central autonomic network (CAN). HRV acts as a proxy of autonomic activity and is associated with executive functions, decision-making, and emotional regulation in our health and wellbeing. Abnormal changes of HRV (e.g., decreased vagal functioning) are observed in various neurological conditions including mild cognitive impairments, dementia, mild traumatic brain injury, migraine, COVID-19, stroke, epilepsy, and psychological conditions (e.g., anxiety, stress, and schizophrenia). Efforts are needed to improve the dynamic and intriguing heart-brain interactions. [ABSTRACT FROM AUTHOR]

Purpose: We investigated the effects of exposure to electronic cigarettes (E-cig) vapor on the sizes of the no-reflow and myocardial infarction regions, and cardiovascular function compared to exposure to purified air and standard cigarette smoke. Methods and Results: Sprague Dawley rats (both male and female, 6 weeks old) were successfully exposed to filtered air (n = 32), E-cig with nicotine (E-cig Nic-, n = 26), E-cig without nicotine (E-cig Nic+, n = 26), or standard cigarette smoke (1R6F reference, n = 31). All rats were exposed to inhalation exposure for 8 weeks, prior to being subjected to 30 minutes of left coronary artery occlusion followed by 3 hours of reperfusion. Exposure to E-cig vapor with or without nicotine or exposure to standard cigarettes did not increase myocardial infarct size or worsen the no-reflow phenomenon. Exposure to E-cig Nic- reduced the body weight gain, and increased the LV weight normalized to body weight and LV wall thickness and enhanced the collagen deposition within the LV wall. E-cig exposure led to cardiovascular dysfunction, such as reductions in cardiac output, LV positive and negative dp/dt, suggesting a reduction in contractility and relaxation, and increased systemic arterial resistance after coronary artery occlusion and reperfusion in rats compared to air or cigarette exposure. Conclusions: E-cig exposure did not increase myocardial infarct size or worsen the no-reflow phenomenon, but induced deleterious changes in LV structure leading to cardiovascular dysfunction and increased systemic arterial resistance after coronary artery occlusion followed by reperfusion. [ABSTRACT FROM AUTHOR]

We have previously demonstrated that intranasal administration of ambient ultrafine particles (UFP) acts as an adjuvant for primary allergic sensitization to ovalbumin (OVA) in Balb/c mice. It is important to find out whether inhaled UFP exert the same effect on the secondary immune response as a way of explaining asthma flares in already-sensitized individuals due to traffic exposure near a freeway. The objective of this study is to determine whether inhalation exposure to ambient UFP near an urban freeway could enhance the secondary immune response to OVA in already-sensitized mice. Prior OVA-sensitized animals were exposed to concentrated ambient UFP at the time of secondary OVA challenge in our mobile animal laboratory in Los Angeles. OVA-specific antibody production, airway morphometry, allergic airway inflammation, cytokine gene expression, and oxidative stress marker were assessed. As few as five ambient UFP exposures were sufficient to promote the OVA recall immune response, including generating allergic airway inflammation in smaller and more distal airways compared with the adjuvant effect of intranasally instilled UFP on the primary immune response. The secondary immune response was characterized by the T helper 2 and IL-17 cytokine gene expression in the lung. In summary, our results demonstrated that inhalation of prooxidative ambient UFP could effectively boost the secondary immune response to an experimental allergen, indicating that vehicular traffic exposure could exacerbate allergic inflammation in already-sensitized subjects. allergic inflammation; oxidative stress; distal lung doi: 10.1152/ajplung.00115.2010.

ABSTRACT The goal of this study was to test the following hypotheses: (1) exposure to mobile emissions from mobile sources close to a heavily trafficked roadway will exacerbate airway inflammation [...]

ABSTRACT This study tested the hypothesis that exposure to mixtures containing fine particles and ozone ([O.sub.3]) would cause pulmonary injury and decrements in functions of immunological cells in exposed rats [...]

Background: Fine particulate matter (PM2.5) exposure accelerates atherosclerosis and contains known ovotoxic chemicals. However, effects of exposure to PM2.5 on the finite ovarian follicle pool have hardly been investigated, nor have interactions between ovarian and cardiovascular effects. We hypothesized that subchronic inhalation exposure to human-relevant concentrations of PM2.5 results in destruction of ovarian follicles via apoptosis induction, as well as accelerated recruitment of primordial follicles into the growing pool. Further, we hypothesized that destruction of ovarian follicles enhances the adverse cardiovascular effects of PM2.5 in females. Results: Hyperlipidemic apolipoprotein E (Apoe) null ovary-intact or ovariectomized female mice and testis-intact male mice were exposed to concentrated ambient PM2.5 or filtered air for 12 weeks, 5 days/week for 4 h/day using a versatile aerosol concentration enrichment system. Primordial, primary, and secondary ovarian follicle numbers were decreased by 45%, 40%, and 17%, respectively, in PM2.5-exposed ovary-intact mice compared to controls (P < 0.05). The percentage of primary follicles with granulosa cells positive for the mitosis marker Ki67 was increased in the ovaries from PM2.5-exposed females versus controls (P < 0.05), consistent with increased recruitment of primordial follicles into the growing pool. Exposure to PM2.5 increased the percentages of primary and secondary follicles with DNA damage, assessed by γH2AX immunostaining (P < 0.05). Exposure to PM2.5 increased the percentages of apoptotic antral follicles, determined by TUNEL and activated caspase 3 immunostaining (P < 0.05). Removal of the ovaries and PM2.5-exposure exacerbated the atherosclerotic effects of hyperlipidemia in females (P < 0.05). While there were statistically significant changes in blood pressure and heart rate variability in PM2.5-compared to Air-exposed gonad-intact males and females and ovariectomized females, the changes were not consistent between exposure years and assessment methods. Conclusions: These results demonstrate that subchronic PM2.5 exposure depletes the ovarian reserve by increasing recruitment of primordial follicles into the growing pool and increasing apoptosis of growing follicles. Further, PM2.5 exposure and removal of the ovaries each increase atherosclerosis progression in Apoe-/- females. Premature loss of ovarian function is associated with increased risk of osteoporosis, cardiovascular disease and Alzheimer's disease in women. Our results thus support possible links between PM2.5 exposure and other adverse health outcomes in women. [ABSTRACT FROM AUTHOR]

With more than 4,000 individual PFAS compounds present in a variety of industrial or consumer products, we are at stage where our ability to measure these compounds far exceeds our understanding of the potential health impacts and our ability to communicate human health risks when the compounds are found in the environment. In a collaboration between North Carolina State and Oregon State Universities, we are currently measuring PFAS in landfill gas from about 25 landfills across the U.S. Michael A. Abraczinskas: PFAS challenges for environmental regulatory agencies This critical review of PFAS exposures in humans is timely and deserves considerable attention due to concerns over toxicity and persistence in the environment. Michael Kleinman: PFOA and PFAS: toxicology and mechanistic considerations Perfluorooctanoic acid (PFOA) and Perfluoroalkyl substances (PFAS), which are used in many commercial applications, are persistent in the environment, do not readily undergo chemical degradation or biotransformation, bioaccumulate and are found, not only in the serum of occupationally exposed workers, but also the blood and tissues of the general population (Kudo and Kawashima [48]; Sanchez Garcia et al. [63]) including children and adolescents (Duffek et al. [25]). Many PFAS and PFOA compounds degrade to acid forms (PFAAs), environmental exposures are often to mixtures of compounds and toxic potential (potency) can vary across the family of compounds. [Extracted from the article]