Search

Background Cardiovascular toxicity as a consequence of nicotine from conventional tobacco cigarette smoking is well documented. However, little is known about the cardiovascular consequences of nicotine e-vaping. We review the literature and report a case series of three cases of major adverse cardiovascular clinical effects post nicotine e-vaping. Case summary Three patients with known peripheral arterial disease who switched from heavy cigarette smoking consumption to a high-intensity dose of nicotine e-vaping all developed further arterial complications within 6–30 months. Discussion With the recent epidemic of e-vaping in young individuals and the national outbreak of e-vaping use-associated lung injury (EVALI), the dangers of e-vaping are now coming to light. The pulmonary effects are now well described, and this paper highlights three new cases of cardiovascular toxicity associated with e-vaping. The potential role of nicotine e-vaping and the risk of coronavirus disease-2019 (COVID-19) will also be discussed.

Related the extremely transmittable abilities of SARS-CoV-2,a harmonious virus to the bat CoV, gets transmitted by three principal processes-- the inhalation of droplets from the SARS-CoV-2 infected person, contacting to the person, and by the surfaces and materials defiled with the virus. Whereupon bat Coronavirus is mostly like the pandemic causing virus SARS-CoV-2, bats are often deliberated and figured out as a possible primary host although no intermediate has not been defined yet in the wherewithal of transmission. The Spike Glycoprotein plays an important role in the case of penetration with the assistance of the ACE2 receptor and the Receptor Binding Domain. In the human body, infiltrating the nucleic acid into host cells, SARS-CoV-2 attacks one cell and one by one into the whole human body; therefore, infected cases are found symptomatic and asymptomatic considering the immune power. Patients with cardiovascular disease or diabetes proceed with their treatment with ACE2 often; therefore, there might be a high chance of getting infected. Whereas the SARS-CoV-2 infects the blood and then lungs, Antigens improvement can be better in order to avoid high-complicated effects. Currently, no vaccination or no accurate cure and treatment has not been defined. An explanation with analysis on SARS-CoV-2 has been performed from the aspect of virology, immunology and molecular biology. Several relevant figures have been included hereby in order to a better understanding of the very concept.

Lung surface is the first line of contact between inhaled carbon nanomaterials, CNMs, and the organism, so this is the place where pulmonary health effects begin. The paper analyzes the influence of several CNMs (single- and multi-walled nanotubes with various surface area: 90–1,280 m2/g and aspect ratio: 8–3,750) on the surface-active properties of the lung surfactant, LS, model (Survanta). Effects of CNM concentration (0.1–1 mg/ml) and surface oscillation rate were determined using the oscillating drop method at simulated breathing conditions (2–10 s per cycle, 37 °C). Based on the values of apparent elasticity and viscosity of the interfacial region, new parameters: Sε and Sμ were proposed to evaluate potential effect of particles on the LS at various breathing rates. Some of tested CNMs (e.g., COOH- functionalized short nanotubes) significantly influenced the surfactant dynamics, while the other had weaker effects even at high particle concentration. Analysis of changes in Sε and Sμ provides a new way to evaluate of a possible disturbance of the basic functions of LS. The results show that the expected pulmonary effects caused by inhaled CNMs at variable breathing rate depend not only on particle concentration (inhaled dose) but also on their size, structure and surface properties.

Recently, there has been a rise in the incidence of E-cigarette/Vaping-Associated Lung Injury (EVALI) in the United States, mostly involving tetrahydrocannabinol. Current treatment strategies for EVALI are aimed at controlling the inflammatory and infectious causes, in addition to supportive care. Although most patients improve with supportive measures, the long-term pulmonary effects of this illness are still not well defined. This report describes a case of EVALI resulting in progressive, irreversible destruction of the lung parenchyma that was treated with double lung transplantation.

In the present study, the suitability and sensitivity of different in vitro toxicity endpoints were determined to evaluate and distinguish the specific contributions of polycyclic aromatic carbon (PAC) mixtures from various sites in Toronto (Canada), to pulmonary toxicity. Air samples were collected for two-month periods from April 2014 to March 2015 from one location, and from August 2016 to August 2017 from multiple locations reflecting different geographical areas in Toronto, and the Greater Toronto Area, with varying source emissions including background, traffic, urban, industrial and residential sites. Relative concentrations of PACs and their derivatives in these air samples were characterised. In vitro cytotoxicity, pro-inflammatory, and oxidative stress assays were employed to assess the acute pulmonary effects of urban-air-derived air pollutants. In addition, global transcriptional profiling was utilized to understand how these chemical mixtures exert their harmful effects. Lastly, the transcriptomic data and the chemical profiles for each site and season were used to relate the biological response back to individual constituents. Site-specific responses could not be derived; however, the Spring season was identified as the most responsive through benchmark concentration analysis. A combination of correlational analysis and principal component analysis revealed that nitrated and oxygenated polycyclic aromatic hydrocarbons (PAHs) drive the response at lower concentrations while specific PAHs drive the response at the highest concentration tested. Unsubstituted PAHs are the current targets for analysis as priority pollutants. The present study highlights the importance of by-products of PAH degradation in the assessment of risk. The study also demonstrates the usefulness of in vitro toxicity assays to derive meaningful data in support of risk assessment.

Remote ischemic preconditioning (RIP) has been demonstrated to protect against ischemia-reperfusion-injury in different target organs. The mechanisms that eventually lead to these protective effects have been investigated in depth but are not yet fully elucidated. Although the effects of RIP seem to be promising in animal experiments and smaller clinical studies, they failed to achieve clinical significance in multicenter trials. These trials have mainly focused on the heart, the brain, and the kidneys, but only little is known concerning the effects of RIP on the lungs. This review will provide an overview on what is already published on RIP and its effects on the respiratory system. Different modes of RIP action have been assessed, like systemic, humoral, and neural responses. As mechanical ventilation, and especially one-lung ventilation, is harmful to the lungs, it is of great interest to find ways of protecting the respiratory system in clinical practice. Therefore, experimental as well as clinical trials have been performed to seek for protective devices. RIP is easy to perform and cheap to apply and is therefore a promising and interesting tool that might find its way into clinical practice in order to attenuate the detrimental effects of mechanical ventilation to the lungs. The present review will highlight and discuss recent experimental data especially on pulmonary effects of RIP.

Physical inactivity has caused serious effects on the health of the population, having an impact on the quality of life and the cost of healthcare for many countries. This has motivated government and private institutions to promote regular physical activity, which, paradoxically, can involve health risks when it is carried out in areas with poor air quality. This review collects information from studies conducted on healthy humans related to the pulmonary effects caused by the practice of physical activity when there is poor air quality. In addition, several challenges related to the technological and educational areas, as well as to applied and basic research, have been identified to facilitate the rational practice of exercise in poor air quality conditions.

Exposure to wildfire smoke continues to be a growing threat to public health, yet the chemical components in wildfire smoke that primarily drive toxicity and associated disease are largely unknown. This study utilized a suite of computational approaches to identify groups of chemicals induced by variable biomass burn conditions that were associated with biological responses in the mouse lung, including pulmonary immune response and injury markers. Smoke condensate samples were collected and characterized, resulting in chemical distribution information for 86 constituents across ten different exposures. Mixtures-relevant statistical methods included (i) a chemical clustering and data-reduction method, weighted chemical co-expression network analysis (WCCNA), (ii) a quantile g-computation approach to address the joint effect of multiple chemicals in different groupings, and (iii) a correlation analysis to compare mixtures modeling results against individual chemical relationships. Seven chemical groups were identified using WCCNA based on co-occurrence showing both positive and negative relationships with biological responses. A group containing methoxyphenols (e.g., coniferyl aldehyde, eugenol, guaiacol, and vanillin) displayed highly significant, negative relationships with several biological esponses, including cytokines and lung injury markers. This group was further shown through quantile g-computation methods to associate with reduced biological responses. Specifically, mixtures modeling based on all chemicals excluding those in the methoxyphenol group demonstrated more significant, positive relationships with several biological responses; whereas mixtures modeling based on just those in the methoxyphenol group demonstrated significant negative relationships with several biological responses, suggesting potential protective effects. Mixtures-based analyses also identified other groups consisting of inorganic elements and ionic constituents showing positive relationships with several biological responses, including markers of inflammation. Many of the effects identified through mixtures modeling in this analysis were not captured through individual chemical analyses. Together, this study demonstrates the utility of mixtures-based approaches to identify potential drivers and inhibitors of toxicity relevant to wildfire exposures., Graphical Abstract

An investigation into the potential toxicological effects of fracking sand dust (FSD), collected from unconventional gas drilling sites, has been undertaken, along with characterization of their chemical and biophysical properties. Using intratracheal instillation of nine FSDs in rats and a whole body 4-d inhalation model for one of the FSDs, i.e., FSD 8, and related in vivo and in vitro experiments, the effects of nine FSDs on the respiratory, cardiovascular and immune systems, brain and kidney were reported in the preceding eight tandem papers. Here, a summary is given of the key observations made in the organ systems reported in the individual studies. The major finding that inhaled FSD 8 elicits responses in extra-pulmonary organ systems is unexpected, as is the observation that the pulmonary effects of inhaled FSD 8 are attenuated relative to forms of crystalline silica more frequently used in animal studies, i.e., MIN-U-SIL® 5. An attempt is made to understand the basis for the extra-pulmonary toxicity and comparatively attenuated pulmonary toxicity of FSD 8.

The release of catecholamines is preceded by glucocorticoids during a stress response. We have shown that ozone-induced pulmonary responses are mediated through the activation of stress hormone receptors. To examine the interdependence of beta-adrenergic (βAR) and glucocorticoid receptors (GR), we inhibited βAR while inducing GR or inhibited GR while inducing βAR and examined ozone-induced stress-response. Twelve-week-old male Wistar-Kyoto rats were pretreated daily with saline or propranolol (PROP; βAR-antagonist; 10 mg/kg-i.p.; starting 7-days prior to exposure) followed-by saline or dexamethasone sulfate (DEX; GR-agonist; 0.02 mg/kg-i.p.; starting 1-day prior to exposure) and exposed to air or 0.8-ppm ozone (4hr/dayx2-days). In a second experiment, rats were similarly pretreated with corn-oil or mifepristone (MIFE; GR-antagonist, 30 mg/kg-s.c.) followed by saline or clenbuterol (CLEN; β(2)AR-agonist; 0.02 mg/kg-i.p.) and exposed. DEX and PROP+DEX decreased adrenal, spleen and thymus weights in all rats. DEX and MIFE decreased and increased corticosterone, respectively. Ozone-induced protein leakage, inflammation and IL-6 increases were inhibited by PROP or PROP+DEX and exacerbated by CLEN or CLEN+MIFE. DEX and ozone induced while MIFE reversed lymphopenia (MIFE>CLEN+MIFE). DEX exacerbated while PROP, MIFE or CLEN+MIFE inhibited ozone-induced hyperglycemia and glucose intolerance. Ozone inhibited glucose-mediated insulin release. In summary, 1) activating βAR, even with GR inhibition, exacerbated and inhibiting βAR, even with GR activation, attenuated ozone-induced pulmonary effects; and 2) activating GR exacerbated ozone systemic effects, but with βAR inhibition, this exacerbation was less remarkable. These data suggest the independent roles of βAR in pulmonary and dependent roles of βAR and GR in systemic effects of ozone.

Purpose This experimental sepsis model created with Escherichia coli aimed to investigate the histopathological effects of two different doses of ozone combined with antibiotherapy on lung tissue. Methods Rats were divided into 5 groups. Then sepsis was induced intraperitoneally in the first 4 groups. The 1st group was treated with cefepime, the 2nd and 3rd groups were treated with cefepime combined with ozone at a dose of 0.6 mg/kg and 1.1 mg/kg. Lung tissue sections were stained with hematoxylin-eosin and assessed under light microscope and scored between 0-4 in terms of histopathological findings. Results In the comparisons between Group 1 and Group 4 in terms of cellular damage (p=0.030), inflammation (p=0.000) and overall score (p=0.007), statistically significant positive effects were observed in favor of Group 1. In the comparisons of Groups 2 and 3 with Group 4, only positive effects were observed in terms of inflammation (p=0.020, p=0.012, respectively). Conclusion Although negative histopathological effects of ozone on tissue injury were detected, it was noteworthy that the increase in the ozone dose reduced the number of damaged parameters.

BACKGROUND: Our aim in this study was to compare the blood gas changes, the malondialdehyde (MDA) and endogenous antiox-idant glutathione (GSH) levels in blood and lung tissues after ischemia/reperfusion, the histopathological damage in lung tissue in rats provided respiratory support with mechanical ventilation after translaryngeal intubation and tracheostomy. METHODS: Group 1 rats were provided mechanical ventilator support after translaryngeal intubation, Group 2 mechanical ventilator support after tracheostomy, and Group 3 was the control group where rats were only anesthetized. Three groups were compared for blood gas changes, MDA, GSH, and histopathological changes. RESULTS: Blood gas evaluation showed a more marked increase in pO2 values and decline in pCO2 values in Group 2 than Group 1 (p0.05). In terms of histopathological scoring, the damage score in Group 1 was higher than in Group 2 (p

A wealth of literature exists regarding the pulmonary effects of ozone, a photochemical pollutant produced by the reaction of nitrogen oxide and volatile organic precursors in the presence of sunlight. This paper focuses on epidemiological panel studies and human clinical studies of ozone exposure, and discusses issues specific to this pollutant that may influence study design and interpretation as well as other, broader considerations relevant to ozone-health research. The issues are discussed using examples drawn from the wider literature. The recent panel and clinical literature is also reviewed. Health outcomes considered include lung function, symptoms, and pulmonary inflammation. Issues discussed include adversity, reversibility, adaptation, variability in ozone exposure metric used and health outcomes evaluated, co-pollutants in panel studies, influence of temperature in panel studies, and multiple comparisons. Improvements in and standardization of panel study approaches are recommended to facilitate comparisons between studies as well as meta-analyses. Additional clinical studies at or near the current National Ambient Air Quality Standard (NAAQS) of 70 ppb are recommended, as are clinical studies in sensitive subpopulations such as asthmatics.The pulmonary health impacts of ozone exposure have been well documented using both epidemiological and chamber study designs. However, there are a number of specific methodological and related issues that should be considered when interpreting the results of these studies and planning additional research, including the standardization of exposure and health metrics to facilitate comparisons among studies.

Carbon nanotubes (CNTs) are widely used in the aerospace, automotive, and electronics industries because of their stability, enhanced metallic, and electrical properties. CNTs are also being investigated for biomedical applications such as drug delivery systems and biosensors. However, the toxic potential of CNTs was reported in various cell lines and animal models. The toxicity depends on diverse properties of the CNTs, such as length, aspect ratio, surface area, degree of aggregation, purity, concentration, and dose. In addition, CNTs and/or associated contaminants were well known for oxidative stress, inflammation, apoptosis, pulmonary inflammation, fibrosis, and granuloma in lungs. The increased production of CNTs likely enhanced the possibility of its exposure in people. Studies on the toxicity of CNTs are mainly focused on the pulmonary effects after intratracheal administration, and only a few studies are reported about the toxicity of CNTs via other routes of exposure. So, it is essential to consider the chronic toxicity of CNTs before using them for various biomedical applications. This review focuses on the potential toxicities of CNTs.

Background: Being exposed to cooking fumes, kitchen workers are occupationally at risk of multiple respiratory hazards. No conclusive evidence exists as to whether occupational exposure to these fumes is associated with acute and chronic pulmonary effects and symptoms of respiratory diseases. Objective: To quantify the exposure levels and evaluate possible chronic and acute pulmonary effects associated with exposure to cooking fumes. Methods: In this cross-sectional study, 60 kitchen workers exposed to cooking fumes and 60 unexposed employees were investigated. The prevalence of respiratory symptoms among these groups was determined through completion of a standard questionnaire. Pulmonary function parameters were also measured before and after participants' work shift. Moreover, air samples were collected and analyzed to quantify their aldehyde, particle, and volatile organic contents. Results: The mean airborne concentrations of formaldehyde, acetaldehyde, and acrolein was 0.45 (SD 0.41), 0.13 (0.1), and 1.56 (0.41) mg/m 3 , respectively. The mean atmospheric concentrations of PM 1 , PM 2.5 , PM 7 , PM 10 , and total volatile organic compounds (TVOCs) was 3.31 (2.6), 12.21 (5.9), 44.16 (16.6), 57 (21.55) μg/m 3 , and 1.31 (1.11) mg/m 3 , respectively. All respiratory symptoms were significantly (p

Introduction Year after year, we spend an increasing amount of time in a sitting position. Often, we sit with poor posture, as indicated by numerous pain syndromes within the musculoskeletal system. Several reports confirm that body posture and the amount of time spent in a seated position have extensive implications for our health. Previous studies and a literature review suggest there is limited knowledge regarding an ergonomic sitting position. Objective The aim of the study was to analyze the research relating to a proper sitting position and the consequences of incorrect sitting posture. A database search was conducted in Science Direct, Scopus, PubMed, Medline, and Google Scholar. Selection was made on the basis of titles, the abstracts and full texts of the studies. No limits were applied to the date of publication. Conclusions Incorrect sitting posture contributes to many disorders, especially in the cervical and lumbar spine. It also determines the work of the respiratory system. Most authors suggest that maintenance of the physiological curvature of the spine is crucial for the biomechanics of the sitting position, as well as the location of the head and position of the pelvis. It raises awareness of work-related hazards and the introduction of education on the principles of proper seating. It is necessary to draw attention to the risks associated with work performed in a sitting posture, and education on the principles of ergonomical sitting.

Background: Ozone increases IL-33 in the lungs, and obesity augments the pulmonary effects of acute ozone exposure. Objectives: We assessed the role of IL-33 in the augmented effects of ozone observed in obese mice. Methods: Lean wildtype and obese db/db mice were pretreated with antibodies blocking the IL-33 receptor, ST2, and then exposed to ozone (2 ppm for 3 hr). Airway responsiveness was assessed, bronchoalveolar lavage (BAL) was performed, and lung cells harvested for flow cytometry 24 hr later. Effects of ozone were also assessed in obese and lean mice deficient in γδ T cells and their wildtype controls. Results and Discussion: Ozone caused greater increases in BAL IL-33, neutrophils, and airway responsiveness in obese than lean mice. Anti-ST2 reduced ozone-induced airway hyperresponsiveness and inflammation in obese mice but had no effect in lean mice. Obesity also augmented ozone-induced increases in BAL CXCL1 and IL-6, and in BAL type 2 cytokines, whereas anti-ST2 treatment reduced these cytokines. In obese mice, ozone increased lung IL-13+ innate lymphoid cells type 2 (ILC2) and IL-13+ γδ T cells. Ozone increased ST2+ γδ T cells, indicating that these cells can be targets of IL-33, and γδ T cell deficiency reduced obesity-related increases in the response to ozone, including increases in type 2 cytokines. Conclusions: Our data indicate that IL-33 contributes to augmented responses to ozone in obese mice. Obesity and ozone also interacted to promote type 2 cytokine production in γδ T cells and ILC2 in the lungs, which may contribute to the observed effects of IL-33. Citation: Mathews JA, Krishnamoorthy N, Kasahara DI, Cho Y, Wurmbrand AP, Ribeiro L, Smith D, Umetsu D, Levy BD, Shore SA. 2017. IL-33 drives augmented responses to ozone in obese mice. Environ Health Perspect 125:246–253; http://dx.doi.org/10.1289/EHP272

Background: Inhaled crystalline silica may cause lung function decline. However, biological mechanisms associated with pulmonary effects in exposed workers have not been completely elucidated. Objectives: We aimed to investigate if crystalline silica exposed rock drillers had induced systemic inflammation compared to a group of referents. Methods: Serum samples were collected in 121 male rock drillers and 48 male referents after examination with spirometry in a cross-sectional study. Air samples were collected in a sub-sample of the drillers. Cumulative exposure to crystalline silica was calculated based on the measured air concentration of α-quartz and their occupational history. The interleukins IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-13, TNF and IFN(interferon)γ were measured. Results: Geometric mean current and cumulative exposure to crystalline silica were 36 µg/m3 and 234 µg/m3, respectively. The rock drillers had been exposed for 10.4 years on average. None of the cytokine concentrations differed significantly between the groups, but multiple linear regression analysis showed that IL-6 and IL-8 were negatively associated with being exposed. When stratifying the non-smoking exposed subjects into three equally large groups according to cumulative exposure, the highest exposed subjects had significantly lower concentrations of IL-12 and IL-6. IL-12 was also significantly associated with FEV1/FVC, suggesting lower concentrations by lower ratio. Conclusions: Surprisingly, there was a tendency towards lower pro-inflammatory cytokine concentrations in exposed workers. Whether these observations may be related to polarization towards M2 pulmonary macrophages remains to be elucidated.

We studied if the pulmonary and systemic toxicity of nanofibrillated celluloses can be reduced by carboxylation. Nanofibrillated celluloses administered at 6 or 18 mu g to mice by intratracheal instillation were: 1) FINE NFC, 2-20 mu m in length, 2-15 nm in width, 2) AS (-COOH), carboxylated, 0.5-10 mu m in length, 4-10 nm in width, containing the biocide BIM MC4901 and 3) BIOCID FINE NFC: as (1) but containing BIM MC4901. FINE NFC administration increased neutrophil influx in BAL and induced SAA3 in plasma. AS (-COOH) produced lower neutrophil influx and systemic SAA3 levels than FINE NFC. Results obtained with BIOCID FINE NFC suggested that BIM MC4901 biocide did not explain the lowered response. Increased DNA damage levels were observed across materials, doses and time points. In conclusion, carboxylation of nanofibrillated cellulose was associated with reduced pulmonary and systemic toxicity, suggesting involvement of OH groups in the inflammatory and acute phase responses.

Background The provision of guidance in ventilator therapy by continuous monitoring of regional lung ventilation, aeration and respiratory system mechanics is the main clinical benefit of electrical impedance tomography (EIT). A new application was recently described in critically ill patients undergoing diagnostic bronchoalveolar lavage (BAL) with the intention of using EIT to identify the region where sampling was performed. Increased electrical bioimpedance was reported after fluid instillation. To verify the accuracy of these findings, contradicting the current EIT knowledge, we have systematically analysed chest EIT data acquired under controlled experimental conditions in animals undergoing a large number of BAL procedures. Methods One hundred thirteen BAL procedures were performed in 13 newborn piglets positioned both supine and prone. EIT data was obtained at 13 images before, during and after each BAL. The data was analysed at three time points: (1) after disconnection from the ventilator before the fluid instillation and by the ends of fluid (2) instillation and (3) recovery by suction and compared with the baseline measurements before the procedure. Functional EIT images were generated, and changes in pixel electrical bioimpedance were calculated relative to baseline. The data was examined in the whole image and in three (ventral, middle, dorsal) regions-of-interest per lung. Results Compared with the baseline phase, chest electrical bioimpedance fell after the disconnection from the ventilator in all animals in both postures during all procedures. The fluid instillation further decreased electrical bioimpedance. During fluid recovery, electrical bioimpedance increased, but not to baseline values. All effects were highly significant (p

Hydraulic fracturing (“fracking”) is used in unconventional gas drilling to allow for the free flow of natural gas from rock. Sand in fracking fluid is pumped into the well bore under high pressure to enter and stabilize fissures in the rock. In the process of manipulating the sand on site, respirable dust (fracking sand dust, FSD) is generated. Inhalation of FSD is a potential hazard to workers inasmuch as respirable crystalline silica causes silicosis, and levels of FSD at drilling work sites have exceeded occupational exposure limits set by OSHA. In the absence of any information about its potential toxicity, a comprehensive rat animal model was designed to investigate the bioactivities of several FSDs in comparison to MIN-U-SIL® 5, a respirable α-quartz reference dust used in previous animal models of silicosis, in several organ systems (Fedan, J.S., Toxicol Appl Pharmacol. 00, 000–000, 2020). The present report, part of the larger investigation, describes: 1) a comparison of the physico-chemical properties of nine FSDs, collected at drilling sites, and MIN-U-SIL® 5, a reference silica dust, and 2) a comparison of the pulmonary inflammatory responses to intratracheal instillation of the nine FSDs and MIN-U-SIL® 5. Our findings indicate that, in many respects, the physico-chemical characteristics, and the biological effects of the FSDs and MIN-U-SIL® 5 after intratracheal instillation, have distinct differences.

Nicotine is a highly addictive principal component of both tobacco and electronic cigarette that is readily absorbed in blood. Nicotine-containing electronic cigarettes are promoted as a safe alternative to cigarette smoking. However, the isolated effects of inhaled nicotine are largely unknown. Here we report a novel rat model of aerosolized nicotine with a particle size (~1 μm) in the respirable diameter range. Acute nicotine inhalation caused increased pulmonary edema and lung injury as measured by enhanced bronchoalveolar lavage fluid protein, IgM, lung wet-to-dry weight ratio, and high-mobility group box 1 (HMGB1) protein and decreased lung E-cadherin protein. Immunohistochemical analysis revealed congested blood vessels and increased neutrophil infiltration. Lung myeloperoxidase mRNA and protein increased in the nicotine-exposed rats. Complete blood counts also showed an increase in neutrophils, white blood cells, eosinophils, and basophils. Arterial blood gas measurements showed an increase in lactate. Lungs of nicotine-inhaling animals revealed increased mRNA levels of IL-1A and CXCL1. There was also an increase in IL-1α protein. In in vitro air-liquid interface cultures of airway epithelial cells, there was a dose dependent increase in HMGB1 release with nicotine treatment. Air-liquid cultures exposed to nicotine also resulted in a dose-dependent loss of barrier as measured by transepithelial electrical resistance and a decrease in E-cadherin expression. Nicotine also caused a dose-dependent increase in epithelial cell death and an increase in caspase-3/7 activities. These results show that the nicotine content of electronic cigarettes may have adverse pulmonary and systemic effects.

Background Cigarette smoke exposure can affect pulmonary lipid homeostasis and cause a progressive increase in pulmonary antibodies against oxidized low-density lipoproteins (OxLDL). Similarly, increased anti-OxLDL antibodies are observed in atherosclerosis, a pathology also tightly associated with smoking and lipid homeostasis disruption. Several immunization strategies against oxidized lipid species to help with their clearance have been shown to reduce the formation of atherosclerotic lesions. Since oxidized lipids are generated during cigarette smoke exposure, we investigated the impact of a prophylactic immunization protocol against OxLDL on the pulmonary effects of cigarette smoke exposure in mice. Methods Mice were immunized systemically with a mixture of human OxLDL (antigen source) and AddaVax (adjuvant) or PBS alone prior to the initiation of acute (2 week) or sub-chronic (8 weeks) cigarette smoke exposure protocols. Anti-OxLDL antibodies were measured in the bronchoalveolar lavage (BAL) fluid and serum by direct ELISA. Pulmonary impacts of cigarette smoke exposure and OxLDL immunization were assessed by measuring BAL inflammatory cells, lung functions, and changes in lung structure and gene levels of matrix/matrix-related genes. Results Immunization to OxLDL led to a marked increase in circulating and pulmonary antibodies against OxLDL that persisted during cigarette smoke exposure. OxLDL immunization did not exacerbate or reduce the inflammatory response following acute or sub-chronic exposure to cigarette smoke. OxLDL immunization alone had effects similar to cigarette smoke exposure on lung functions but OxLDL immunization and cigarette smoke exposure had no additive effects on these parameters. No obvious changes in lung histology, airspace or levels of matrix and matrix-related genes were caused by OxLDL immunization compared to vehicle treatment. Conclusions Overall, this study shows for the first time that a prophylactic immunization protocol against OxLDL can potentially have detrimental effects lung functions, without having additive effects over cigarette smoke exposure. This work sheds light on a complex dynamic between anti-OxLDL antibodies and the pulmonary response to cigarette smoke exposure.

The postoperative diagnosis and management of complications related to bariatric surgery requires a high degree of clinical suspicion in conjunction with swift implementation of diagnostic and therapeutic strategies. The most common medical complications related to bariatric surgery include venous thromboembolic events, cardiac complications, and nutritional deficiencies. These have all been observed in bariatric patients regardless of the type of surgery. The most common surgical complication related to the gastric band is band slippage, which requires take back to the operating room. The most common surgical complication related to the sleeve gastrectomy is staple line leak. Marginal ulcer, anastomotic leak, and bowel obstruction are all possible complications related to the gastric bypass. Lastly, critical care management of the bariatric patient requires particular attention to the cardiac and pulmonary effects of obesity toward respective physiologic functioning.