Smoke Inhalation Research Articles

Inhalation of smoke from cooking activities in Katanga, a health burden among women users of charcoal and firewood

This study focused on the Inhalation of smoke from culinary activities in Katanga. It was carried out over a period of approximately 4 years. The study population consisted of women whose average age was 37.8 (16) years. On the one hand, 119 rural women (permanent users of coal in the Futuka village and 121 urban women (FU) in the Vallée urban district of the city of Lubumbashi were approached and selected. The fundamental question was whether prolonged or sporadic exposure to smoke from cooking activities could be an exposure factor to the risk of respiratory infections. Following the investigations made and the multiple functional explorations, we arrived at the confirmation of this hypothesis . In view of the results obtained, we found that the frequency of use of these biomasses oscillated respectively between 63.6% in town and 75% in rural areas. In the two female categories considered, the rates of cough and morning and usual sputum were, in almost all cases, higher among women from Futuka than among those from the Vallée district. Concerning the crisis of breathlessness and difficulty breathing, we noticed that for the three parameters observed (morning awakening with difficulty breathing, shortness of breath at rest during the day and shortness of breath after intense effort), the women users of the Vallée district were the more affected. For the values, apart from the Tiffnaud ratio (FEV1/FVC%), the functional exploration using the spirometer showed overall that almost all the spirometric parameters led to statistically significant differences between urban women (FU ) of the Vallée district and rural (FR) of the Futuka village. These are the forced vital capacity (FVC% pred with a p=0.034), the peak expiratory flow (PEF with a p value of 0.000) and the expiratory volume at the first second (FEV1% pred with a p value of 0.000).

Particle size matters: Discrepancies in the health risks posed by traditional cigarettes and e-cigarettes in mice and humans

Electronic cigarettes (ECs), considered a healthier alternative to traditional cigarettes (TCs), vaporize e-liquid, which may produce harmful by-products due to thermal decomposition and metal transfer. These by-products' deposition in the respiratory tract is largely determined by particle size distribution (PSD). We employ the Multiple-Path Particle Dosimetry (MPPD) model to assess particle deposition within the human and mouse respiratory tracts. Leveraging the known connection between TC smoke inhalation and atherosclerosis, we used human aortic endothelial cells (HAECs) and ApoE-/- mice to explore the potential effects of EC aerosol inhalation on atherosclerosis. Our findings reveal that TCs exhibit a highly variable PSD, with mean diameters of approximately 300 nm for mainstream (MS) smoke and 120 nm for side stream (SS) smoke. Conversely, ECs demonstrate a more stable PSD. Combined with MPPD, the deposition fraction in the human respiratory system and mice is mainly deposited in the pulmonary region and head airway. For the Apoe-/- mice exposure experiment, preliminary findings suggest a potential impact on atherosclerosis, although not statistically significant, likely due to the limited sample size and exposure duration. This study highlights the importance of considering PSD, exposure dosage, and species-specific differences in risk assessments of EC aerosols.

Intraperitoneal oxygen microbubble therapy: A novel approach to enhance systemic oxygenation in a smoke inhalation model of acute hypoxic respiratory failure

BackgroundPatients suffering from severe acute respiratory distress syndrome (ARDS) face limited therapeutic options and alarmingly high mortality rates. Refractory hypoxemia, a hallmark of ARDS, often necessitates invasive and high-risk treatments. Oxygen microbubbles (OMB) present a promising approach for extrapulmonary oxygenation, potentially augmenting systemic oxygen levels without exposing patients to significant risks. MethodsRats with severe, acute hypoxemia secondary to wood smoke inhalation (SI) received intraperitoneal (IP) bolus injections of escalating weight-by-volume (BW/V) OMB doses or normal saline to determine optimal dosage and treatment efficacy. Subsequently, a 10 % BW/V OMB bolus or saline was administered to a group of SI rats and a control group of healthy rats (SHAM). Imaging, vital signs, and laboratory studies were compared at baseline, post-smoke inhalation, and post-treatment. Histological examination and lung tissue wet/dry weight ratios were assessed at study conclusion. ResultsTreatment with various OMB doses in SI-induced acute hypoxemia revealed that a 10 % BW/V OMB dose significantly augmented systemic oxygen levels while minimizing dose volume. The second set of studies demonstrated a significant increase in partial pressure of arterial oxygen (PaO2) and normalization of heart rate with OMB treatment in the SI group compared to saline treatment or control group treatment. ConclusionsThis study highlights the successful augmentation of systemic oxygenation following OMB treatment in a small animal model of severe hypoxemia. OMB therapy emerges as a novel and promising treatment modality with immense translational potential for oxygenation support in acute care settings.

A CROSS-SECTIONAL STUDY OF SURGICAL SMOKE INHALATION, ITS HAZARDS AND PREVENTION AMONG PAEDIATRIC SURGICAL RESIDENTS IN PAKISTAN

Background: For thousands of years human beings have been using heat as a source of ligature and to treat the wound either it’s from the trauma or fought in the wars. In 1854 an imminent surgeon Albrecht Theodor Middendorf published a paper on the application of electrocautery in surgical operations. The objective of the study was to analyze the hazards of surgical smoke inhalation in Paediatric Surgery residents and to create awareness of its signs and symptoms, risk factors and utilizing preventive measures. Methods: A Cross-sectional study was conducted involving all the Paediatric Surgery residents enrolled on a supervised training program in Pakistan between 1st July 2022 to 30th June 2023 at all the tertiary care hospitals in Pakistan. Their socio-demographic, academic data, signs and symptoms and risk factors were calculated. Data was analyzed with descriptive and comparative analysis using SPSS. A Pearson contingency coefficient is used to determine the association between categorical variables. Results: Our study included all the Paediatric Surgery residents in Pakistan n=155 over a span of one year starting from July 1st 2022 to June 30th 2023. N=75 (48.4%) were males and n=80 (52.6%) were female residents. Their mean age was 29.5 years±4 (SD). 41% of the residents were from Khyber Teaching Hospital, 32% from Children’s Hospital, 14% from National Institute of Child Health Karachi, 9.8% from Children’s Hospital Islamabad (PIMS) and 5.2% from Lady Reading Hospital Peshawar. N=135 (87.1%) of the residents used electrocautery while performing the surgery (p=0.006). N=121 (78.1%) were aware of its hazards (p=0.341). 90% think they are at an increased risk (p=0.032). Most of them (84.6%) wear a surgical mask while only (64%) wear protective equipment (p=0.321). Think they are at an increased risk of cancers (83.9%) (p=0.002) and should be screened (93.7%) (p=0.343). Conclusion: Paediatric surgery residents are at an increased risk of surgical smoke inhalation, pointing to the emerging need to adopt protective measures by creating awareness, and utilizing health safety checklists and smoke evacuation mechanisms in operation rooms. All residents should seek knowledge on the subject and use personal protective equipment for less harmful effects on their health.

Intravenous Autologous Bone Marrow-derived Mesenchymal Stromal Cells Delay Acute Respiratory Distress Syndrome in Swine.

Rationale: Early post injury mitigation strategies in ARDS are in short supply. Treatments with allogeneic stromal cells are administered after ARDS develops, require specialized expertise and equipment, and to date have shown limited benefit. Objectives: Assess the efficacy of immediate post injury intravenous administration of autologous or allogeneic bone marrow-derived mesenchymal stromal cells (MSCs) for the treatment of acute respiratory distress syndrome (ARDS) due to smoke inhalation and burns. Methods: Yorkshire swine (n = 32, 44.3 ± 0.5 kg) underwent intravenous anesthesia, placement of lines, severe smoke inhalation, and 40% total body surface area flame burns, followed by 72 hours of around-the-clock ICU care. Mechanical ventilation, fluids, pressors, bronchoscopic cast removal, daily lung computed tomography scans, and arterial blood assays were performed. After injury and 24 and 48 hours later, animals were randomized to receive autologous concentrated bone marrow aspirate (n = 10; 3 × 106 white blood cells and a mean of 56.6 × 106 platelets per dose), allogeneic MSCs (n = 10; 6.1 × 106 MSCs per dose) harvested from healthy donor swine, or no treatment in injured control animals (n = 12). Measurements and Main Results: The intravenous administration of MSCs after injury and at 24 and 48 hours delayed the onset of ARDS in swine treated with autologous MSCs (48 ± 10 h) versus control animals (14 ± 2 h) (P = 0.004), reduced ARDS severity at 24 (P < 0.001) and 48 (P = 0.003) hours, and demonstrated visibly diminished consolidation on computed tomography (not significant). Mortality at 72 hours was 1 in 10 (10%) in the autologous group, 5 in 10 (50%) in the allogeneic group, and 6 in 12 (50%) in injured control animals (not significant). Both autologous and allogeneic MSCs suppressed systemic concentrations of TNF-α (tumor necrosis factor-α). Conclusions: The intravenous administration of three doses of freshly processed autologous bone marrow-derived MSCs delays ARDS development and reduces its severity in swine. Bedside retrieval and administration of autologous MSCs in swine is feasible and may be a viable injury mitigation strategy for ARDS.

Effects of cigarette smoke inhalation on the immune-inflammatory profile of experimental apical periodontitis in rats.

To evaluate the effects of cigarette smoke inhalation on the immune-inflammatory profile of experimental apical periodontitis in rats. In total, 32 male Wistar rats were divided into four groups (n = 8): AP-induced apical periodontitis; S-cigarette smoke inhalation; APS-induced AP and cigarette smoke inhalation; and C (control)-neither AP nor cigarette smoke inhalation. To induce cigarette smoke inhalation, the animals were kept in a chamber filled with tobacco smoke for 8 min thrice a day for 50 days. AP was induced 20 days after inhalation initiation by exposing their coronary pulp to their oral environment for 30 days. After animals were euthanized, their right hemimaxillae were removed for histopathological, semi-quantitative and immunohistochemical (F4/80, CD206 and iNOS) analyses. Quantitative data showed a moderate number of inflammatory infiltrates in AP and an intense number in APS (p < .05). Comparing F4/80+ cells showed no statistically significant differences among groups, but we found more CD206+ cells in AP than in C and S (p > .05). INOS+ immunostaining showed a significant increase in AP and APS, when compared with C and S (p < .05). APS had more iNOS+ cells than AP (p < .05). Cigarette smoke inhalation worsened AP, leading to a predominantly pro- inflammatory profile in our experimental model.

The social justice issues of smoke im/mobilities

ABSTRACT In 2014, the Hazelwood mine fire burned for 45 days. Local communities were impacted by smoke and ash, and there were reports of raised carbon monoxide levels. Local news and social media reported residents experiencing numerous physical symptoms of smoke inhalation, including bleeding noses, coughing, wheezing and chest tightness. Paper masks to filter particulate matter were made available to residents to wear outside. The dust and ash constantly seeped into homes and offices, which required cleaning daily and sometimes multiple times during the day. Smoke was free to move across physical and bodily boundaries while those most vulnerable were hampered by lack of movement: pregnant women, the elderly and children were advised to leave the area. However, this suggestion to ‘simply’ move ignored the context of a community disproportionately impacted through years of economic decline and societal change. This paper explores the unequal mobilities of smoke and people that arose as a result of this event and draws on concepts of mobility justice (Sheller 2018) and emergency mobilities (Adey 2016) to reflect on the political dimensions of uneven mobility in times of crisis.

Vardenafil alleviates cigarette smoke-induced chronic obstructive pulmonary disease by activating autophagy via the AMPK/mTOR signalling pathway: an in vitro and in vivo study.

Chronic obstructive pulmonary disease (COPD) has always attracted global attention with its high prevalence, incidence rate, and mortality. Exposure to cigarette smoke is one of main causes of COPD. Therefore, it is still necessary to study its pathogenesis and find new therapeutic strategies for early COPD prevention and treatment. Vardenafil, a type 5 phosphodiesterase (PDE5) inhibitor, is known to have an efficient therapy in some cardiovascular, pulmonary, and vascular diseases, which is an important mechanism for COPD. However, it still loss relevant research on whether vardenafil is effective in COPD and its mechanism. In this study, the cigarette smoke inhalation was performed to establish cigarette smoke-induced COPD model using C57BL/6 mice and 16HBE cells were treated with cigarette smoke extract (CSE). Mice were treated with vardenafil for 30 d. Then condition of lung injury was evaluated using histological analysis. The content of cytokines and the number of inflammatory cells in lung tissues or bronchoalveolar lavage fluid were measured. Additionally, western blot analysis was employed to evaluate the activation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR)-mediated autophagy in vitro. The results showed that vardenafil abolished CSE's effect by activating autophagy via the AMPK/mTOR signalling pathway in vitro. Vardenafil attenuated cigarette smoke-induced lung injury and inflammation response by activating autophagy via the AMPK/mTOR signalling pathway in vivo. These results provide valuable insights into the molecular mechanisms underlying vardenafil's beneficial effects in cigarette smoke-induced COPD treatment. In conclusion, vardenafil alleviates cigarette smoke-induced experimental COPD by activating autophagy via the AMPK/mTOR signalling pathway.

Tobacco Cessation Centres: Vital Cog in the Fight against Tobacco Epidemic Preparedness towards a future pandemic

The tobacco crisis, which claims more than 8 million lives yearly and adds 1.2 million more from secondhand smoke inhalation, is a serious concern for world health. The detrimental impact of tobacco usage on health is projected to have an annual economic cost of 1.4 trillion US dollars (health costs plus lost productivity) or 1.8% of the world's GDP. Both smokers and users of smokeless tobacco can profit greatly from quitting. Quitting smoking lowers the likelihood of developing respiratory problems, delays their beginning, and slows the progression of chronic lung diseases. Therefore, the "World Health Organisation (WHO)" and the "Ministry of Health &amp; Family Welfare", Government of India, worked together to open official tobacco cessation clinics throughout India. The goal of tobacco cessation centers was to offer to counsel people trying to stop smoking. This includes monitoring the patient's progress and providing counseling, either by itself or in conjunction with medication.

Acute kidney injury in patients with burns.

Burn injury is associated with a high risk of acute kidney injury (AKI) with a prevalence of AKI among patients with burns of 9-50%. Despite an improvement in burn injury survival in the past decade, AKI in patients with burns is associated with an extremely poor short-term and long-term prognosis, with a mortality of >80% among those with severe AKI. Factors that contribute to the development of AKI in patients with burns include haemodynamic alterations, burn-induced systemic inflammation and apoptosis, haemolysis, rhabdomyolysis, smoke inhalation injury, drug nephrotoxicity and sepsis. Early and late AKI after burn injury differ in their aetiologies and outcomes. Sepsis is the main driver of late AKI in patients with burns and late AKI has been associated with higher mortality than early AKI. Prevention of early AKI involves correction of hypovolaemia and avoidance of nephrotoxic drugs (for example, hydroxocobalamin), whereas prevention of late AKI involves prevention and early recognition of sepsis as well as avoidance of nephrotoxins. Treatment of AKI in patients with burns remains supportive, including prevention of fluid overload, treatment of electrolyte disturbance and use of kidney replacement therapy when indicated.

Antioxidant Activity of Fermented Red Bean Extract on Sperm Quality of Mice Exposed to Cigarette Smoke

Smoking has a negative effect on fertilization as it decreases sperm quality. The current research aimed to investigate the effect of fermented red bean (Phaseolus vulgaris L.) extract on sperm motility, viability, and plasma membrane integrity of white mice (Mus musculus) exposed to cigarette smoke. The red beans were subjected to a 36-hour fermentation process using Rhizopus spp. Then, methanol was extracted by maceration method for 24 hours until maceration was obtained. In this study, 25 male white mice aged 3 months were randomly divided into 5 groups of 5 mice. Group C (negative control) was given 0.5 mL of carboxymethyl cellulose natrium (CMC Na) 1% solution orally without unfiltered cigarette smoke exposure, and group C+ (positive control) was given 0.5 mL of CMC Na 1% solution orally and unfiltered cigarette smoke exposure. Treatment groups T1, T2, and T3 were orally given fermented red bean extract at doses of 26 mg/kg Body weight (BW), 52 mg/kg BW, and 104 mg/kg BW, respectively, and then were exposed to unfiltered cigarette smoke. For 36 days, treatment groups (except the negative control) were subjected to the inhalation of smoke from an unfiltered cigarette containing a nicotine dose of 2.2 mg. The exposure period lasted for 20 minutes each day. Each group was put into a cigarette smoke-exposing box. The sperm motility (observing the forward movement of spermatozoa), the sperm viability (examining the color of the sperm head), and the sperm plasma membrane integrity (observing the tail shape using the hypoosmotic swelling test) were then evaluated. The findings indicated significant differences in sperm motility, viability, and plasma membrane integrity of each group with positive control. A dose of 104 mg/kg BW of fermented red bean extract had the best potential to maintain sperm motility (70%), viability (82.13%), and plasma membrane integrity (61.93%) of mice exposed to unfiltered cigarette smoke.

Modulation of cigarette smoke induced alterations by aqueous Ocimum sanctum leaf extract in pulmonary tissue of rodents

Smoking has been associated with an increased risk of asthma, lung cancer, cardiovascular diseases, chronic bronchitis, and a massive amount of oxidative stress. The present study was undertaken to determine the modulatory effects of Holi Basil/Tulsi, (Ocimum sanctum) leaf extract on cigarette smoke-induced pulmonary damage in mice. Cigarette smoke (CS) inhalation increased the levels of pulmonary lipid peroxidation, and reactive oxygen species and decreased the levels of glutathione. Histoarchitectural alterations and enhanced tissue lactate dehydrogenase (LDH) activity in pulmonary tissue was distinctly indicative of damage. Enhanced mucin production was also observed through mucicarmine and Alcian Blue-Periodic Acid Schiff (PAS) staining. Increased expression of MUC5AC was also observed. Alterations in the lung were also evident through FTIR studies. Administration of Ocimum sanctum leaf extract (80 mg/kg b.w) to CS exposed mice ameliorated these alterations to a greater extent. These findings are suggestive of the fact that Ocimum sanctum leaf extract effectively modulated CS-induced deleterious effects on pulmonary tissue.

Testicular tissue response following a 90-day subchronic exposure to HTP aerosols and cigarette smoke in rats.

Researches have shown that chronic inhalation of cigarette smoke (CS) disrupts male reproductive system, but it is unclear about the mechanisms behind reproductive damages by tobacco toxicants in male rats. This study was designed to explore the effects of heated tobacco products (HTP) aerosols and CS exposure on the testicular health of rats. Experiments were performed on male SD rats exposed to filtered air, HTP aerosols at 10 μg/L, 23 μg/L, and 50 μg/L nicotine-equivalent contents, and also CS at 23 μg/L nicotine-equivalent content for 90 days in five exposure groups (coded as sham, HTP_10, HTP_23, HTP_50 and Cig_23). The expression of serum testosterone, testicular tissue inflammatory cytokines (IL-1β, IL-6, IL-10, TNF-α), reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA), NLRP3 inflammasome-related mRNAs and proteins (NLRP3, ASC, and Caspase-1), the degree of pyroptosis and histopathology were investigated. The results demonstrated that HTP_50 and Cig_23 caused varying degrees of oxidative damage to rat testis, resulting in a decrease of sperm quantity and serum testosterone contents, an increase in the deformity rate, expression levels of proinflammatory cytokines, and NLRP3 inflammasome-related mRNA, and an increase in the NLRP3, ASC, and Caspase-1-immunopositive cells, pyroptosis cell indices, and histopathological damage in the testes of rats. Responses from the HTP_10 and HTP_23 groups were less than those found in the above two exposure groups. These findings indicate that HTP_50 and Cig_23 induced oxidative stress in rat testes, induced inflammation and pyroptosis through the ROS/NLRP3/Caspase-1 pathway, and destroyed the integrity of thetesticular tissue structure.

Incense smoke (IS) inhalation exposure system: Physicochemical characterization, IS particle deposition and clearance in human airway using MPPD model

Incense smoke (IS) is source of indoor air pollution and key risk for diverse human diseases. Less information is available regarding controlled IS rodent inhalation exposure system and IS particulate matter (PM) deposition in human airways. Study aimed to demonstrate stable ISPM physicochemical parameters of 10 incense products inside the customized whole body inhalation exposure chamber (without animal) connected to smoke generation unit via aerosol mixing device. IS analyzed for size segregated PM emission, ISPM in vitro aerodynamics (MMAD and GSD determination), fine and ultrafine particle's SEM, SEM-EDX and PAH analysis. Using real life exposure scenario by utilizing MMAD, GSD and PM concentration after Tier 1 exposure assessment as key input parameters, ISPM dosimetry in infant (3 months) and adult (21 years male and female) human airways was calculated using multiple-path particle dosimetry (MPPD 3.04) modeling. Mass median aerodynamic diameter (MMAD) and geometric standard deviation (GSD) ranged between 0.55 and 2.10 μm and 1.22 to 1.77 (polydisperse) respectively. PM1.0 and PM0.1 showed multiple morphology and presence of heavy and trace elements. PAH like acenaphthylene, anthracene, fluorene, naphthalene and phenanthrene were detected (0.84–143.17 μg/g). MPPD results showed higher ISPM deposition in pulmonary region and lowest in trachea bronchial region. ISPM deposition in tissue was higher in lower, peripheral lung as compared to upper and central lung tissue. Whole body inhalation exposure system showed stable IS atmosphere (physicochemical parameters) indicating the device suitability in future inhalation studies. MPPD ISPM deposition fraction and clearance data showed deep lung penetrating and retention behavior with higher risk in infant followed by female and then male. These modeled particle deposition and clearance data may be useful in risk assessment analysis of IS.

Evaluation of hydroxocobalamin use for the treatment of suspected cyanide toxicity secondary to smoke inhalation

Hydroxocobalamin is used for cyanide toxicity after smoke inhalation, but diagnosis is challenging. Retrospective studies have associated hydroxocobalamin with acute kidney injury (AKI). This is a retrospective analysis of patients receiving hydroxocobalamin for suspected cyanide toxicity. The primary outcome was the proportion of patients meeting predefined appropriate use criteria defined as ≥1 of the following: serum lactate ≥8 mmol/L, systolic blood pressure (SBP) <90 mmHg, new-onset seizure, cardiac arrest, or respiratory arrest. Secondary outcomes included incidence of AKI, pneumonia, resolution of initial neurologic symptoms, and in-hospital mortality. Forty-six patients were included; 35 (76%) met the primary outcome. All met appropriate use criteria due to respiratory arrest, 15 (43%) for lactate, 14 (40%) for SBP, 12 (34%) for cardiac arrest. AKI, pneumonia, and resolution of neurologic symptoms occurred in 30%, 21%, and 49% of patients, respectively. In-hospital mortality was higher in patients meeting criteria, 49% vs. 9% (95% CI 0.16, 0.64). When appropriate use criteria were modified to exclude respiratory arrest in a post-hoc analysis, differences were maintained, suggesting respiratory arrest alone is not a critical component to determine hydroxocobalamin administration. Predefined appropriate use criteria identify severely ill smoke inhalation victims and provides hydroxocobalamin treatment guidance.

Epidemiology and mortality in patients hospitalized for burns in Catalonia, Spain

Burn injuries are one of the leading causes of morbidity worldwide. Although the overall incidence of burns and burn-related mortality is declining, these factors have not been analysed in our population for 25 years. The aim of this study has been to determine whether the epidemiological profile of patients hospitalized for burns has changed over the past 25 years. We performed a retrospective cohort study of patients hospitalised between 1 January 2011 and 31 December 2018 with a primary diagnosis of burns. The incidence of burns in our setting was 3.68/105 population. Most patients admitted for burns were men (61%), aged between 35 and 45 years (16.8%), followed by children aged between 0 and 4 years (12.4%). Scalding was the most prevalent mechanism of injury, and the region most frequently affected was the hands. The mean burned total body surface (TBSA) area was 8.3%, and the proportion of severely burned patients was 9.7%. Obesity was the most prevalent comorbidity (39.5%). The median length of stay was 1.8 days. The most frequent in-hospital complications were sepsis (16.6%), acute kidney injury (7.9%), and cardiovascular complications (5.9%). Risk factors for mortality were advanced age, high abbreviated burn severity index score, smoke inhalation, existing cardiovascular disease full-thickness burn, and high percentage of burned TBSA. Overall mortality was 4.3%. Multi-organ failure was the most frequent cause of death, with an incidence of 49.5%. The population has aged over the 25 years since the previous study, and the number of comorbidities has increased. The incidence and severity of burns, and the percentage of burned TBSA have all decreased, with scalding being the most prevalent mechanism of injury. The clinical presentation and evolution of burns differs between children and adults. Risk factors for mortality were advanced age, smoke inhalation, existing cardiovascular disease, full-thickness burn, and high percentage of burned TBSA.

Pathophysiologic effects of waterpipe (shisha) smoke inhalation on liver morphology and function in mice

AimsThe global prevalence of waterpipe tobacco smoking is increasing. Although the cardiorespiratory, renal, and reproductive effects of waterpipe smoking (WPS) are well-documented, there is limited knowledge regarding its adverse impact on the liver. Therefore, our study aimed to assess the effects and potential mechanisms of WPS inhalation for one or four weeks on the liver. Main methodsMice were exposed to WPS for 30 min per day, five days per week, while control mice were exposed to clean air. Key findingsAnalysis using light microscopy revealed the infiltration of immune cells (neutrophils and lymphocytes) accompanied by vacuolar hepatic degeneration upon WPS inhalation. At the four-week timepoint, electron microscopy analysis demonstrated an increased number of mitochondria with a concomitant pinching-off of hepatocyte plasma membranes. WPS exposure led to a significant rise in the activities of liver enzymes alanine aminotransferase and aspartate aminotransferase in the bloodstream. Additionally, WPS inhalation elevated lipid peroxidation and reactive oxygen species levels and disrupted the levels of the antioxidant glutathione in liver tissue homogenates. The concentration of proinflammatory cytokines, including tumor necrosis factor α, interleukin (IL)-6, and IL-1β, was significantly increased in the WPS-exposed group. Furthermore, WPS inhalation induced DNA damage and a significant increase in the levels of cleaved caspase-3, cytochrome C and hypoxia-inducible factor 1α along with alterations in the activity of mitochondrial complexes I, II, III and IV. SignificanceOur findings provide evidence that WPS inhalation triggers changes in liver morphology, oxidative stress, inflammation, DNA damage, apoptosis, and alterations in mitochondrial activity.

ASSESSMENT OF INDOOR SECOND-HAND CIGARETTE SMOKE ON THE RESPIRATORY MECHANICS AND PREVENTIVE BENEFITS OF EUCALYPTOL: A MURINE MODEL

Second-hand smokers, in various settings such as recreational areas, schools, workplaces, homes and other enclosed public spaces also experience the detrimental effects of exposure to cigarette smoke (CS). Out of the 8 million deaths attributed to smoking, 1.2 million are a result of non-smokers being exposed to second-hand smoke. As a preventive strategy to these damages, Eucalyptol has been shown to be effective in the treatment of lung lesions caused by smoking. This study aimed to assess the effects of indoor second-hand cigarette smoke on respiratory mechanics and lung tissue, in addition to investigating the potential benefit of Eucalyptol against lung damage caused by this type of aggression. The experiments were conducted for 14 days with 40 BALB/c mice, divided into 5 groups: a control group, two groups nebulized with saline solution, divided into active and passive (second-hand) exposure to CS, two groups pre-treated with eucalyptol (10 mg/mL by nebulization) divided into active and passive exposure to CS. Lung mechanics data were collected on a flexiVent® small animal mechanical ventilator. In addition, ex vivo analysis of lung tissue micromechanics, morphometric analyzes and qualitative analyzes of lung tissue were performed. The results showed that 14 days of second-hand exposure generated significant tissue damage, causing infiltration of inflammatory cells and altering respiratory mechanics. However, pre-treatment with eucalyptol was able to prevent all changes caused by CS in both exposure protocols. We conclude that indoor second-hand smoke is capable of causing damage similar to active tobacco consumption and that Eucalyptol can be used as a preventive or nutritional resource against the changes caused by the inhalation of cigarette smoke.

Camera traps link population-level activity patterns with wildfire smoke events for mammals in Eastern Washington State

BackgroundDue to anthropogenic climate change and historic fire suppression, wildfire frequency and severity are increasing across the western United States. Whereas the indirect effects of fire on wildlife via habitat change are well studied, less is known about the impacts of wildfire smoke on animal health and behavior. In this study, we explore the effects of wildfire smoke on the behavior of eight medium- to large-bodied mammalian species in a heterogenous study area in Washington, USA. We linked population-level activity metrics derived from camera trap data to concentrations of fire-specific fine particulate matter (PM2.5). We hypothesized that mammalian activity would decline during smoke events, as animals attempt to reduce potential health impacts of smoke inhalation. We used occupancy models and Poisson regression models to test the effect of fire-specific PM2.5 levels on daily detection probability and the number of detections per day, respectively, for each study species.ResultsWhile we did not observe any significant responses to daily mean concentrations of PM2.5 in the occupancy models, we found three species with significant responses in their rates of detections per day in the Poisson regression. Specifically, for each standard deviation increase in the daily mean concentration of PM2.5, there was a 12.9% decrease in the number of bobcat detections per day, an 11.2% decrease in the number of moose detections per day, and a 5.8% increase in the number of mule deer detections per day. In general, the effects of PM2.5 were small compared to other relevant covariates.ConclusionsWe generally found little evidence to support our hypothesis that animals would reduce their activity in response to wildfire smoke. However, our study demonstrated that mammals exhibited species-specific behavioral responses to smoke, which are possibly adaptive responses to reduce health impacts from smoke inhalation. Though we found only a few immediate behavioral responses to smoke exposure, we note that longer-term health consequences of smoke exposure for wildlife are also likely and generally unknown. Our study shows how camera traps, which are already widely used to study wildlife, can also be used to investigate the impacts of wildfire smoke on animal behavior and provides a step towards developing methods to better understand this increasing source of environmental stress on wildlife.

Biomass smoke inhalation promotes neuroinflammatory and metabolomic temporal changes in the hippocampus of female mice

Smoke from wildland fires has been shown to produce neuroinflammation in preclinical models, characterized by neural infiltrations of neutrophils and monocytes, as well as altered neurovascular endothelial phenotypes. To address the longevity of such outcomes, the present study examined the temporal dynamics of neuroinflammation and metabolomics after inhalation exposures from biomass-derived smoke. 2-month-old female C57BL/6 J mice were exposed to wood smoke every other day for 2 weeks at an average exposure concentration of 0.5 mg/m3. Subsequent serial euthanasia occurred at 1-, 3-, 7-, 14-, and 28-day post-exposure. Flow cytometry of right hemispheres revealed two endothelial populations of CD31Hi and CD31Med expressors, with wood smoke inhalation causing an increased proportion of CD31Hi. These populations of CD31Hi and CD31Med were associated with an anti-inflammatory and pro-inflammatory response, respectively, and their inflammatory profiles were largely resolved by the 28-day mark. However, activated microglial populations (CD11b+/CD45low) remained higher in wood smoke-exposed mice than controls at day 28. Infiltrating neutrophil populations decreased to levels below controls by day 28. However, the MHC-II expression of the peripheral immune infiltrate remained high, and the population of neutrophils retained an increased expression of CD45, Ly6C, and MHC-II. Utilizing an unbiased approach examining the metabolomic alterations, we observed notable hippocampal perturbations in neurotransmitter and signaling molecules, such as glutamate, quinolinic acid, and 5-α-dihydroprogesterone. Utilizing a targeted panel designed to explore the aging-associated NAD+ metabolic pathway, wood smoke exposure drove fluctuations and compensations across the 28-day time course, ending with decreased hippocampal NAD+ abundance on day 28. Summarily, these results indicate a highly dynamic neuroinflammatory environment, with potential resolution extending past 28 days, the implications of which may include long-term behavioral changes, systemic and neurological sequalae directly associated with wildfire smoke exposure.