Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation.

Smoking is the major cause of cardiovascular diseases and cancer. It induces oxidative stress, leading to DNA damage and cellular senescence. Senescent cells increase the expression and release of pro-inflammatory molecules and matrix metalloproteinase, which are known to play a vital role in the initiation and progression of cardiovascular diseases and metastasis in cancer. The current study investigated the smoking induced cellular senescence and employed colchicine that blocked senescence in endothelial cells exposed to tobacco smoke condensate. Colchicine prevented oxidative stress and DNA damage in tobacco smoke-condensate-treated endothelial cells. Colchicin reduced ß-gal activity, improved Lamin B1, and attenuated cell growth arrest markers P21 and P53. Colchicine also ameliorated the expression of SASP factors and inhibited the activation of NF-kB and MAPKs P38 and ERK. In summary, colchicine inhibited tobacco smoke condensate-induced senescence in endothelial cells by blocking the activation of NF-kB and MAPKs P38 and ERK.

Exploring the adverse effect of fine particulate matter (PM2.5) on wildland firefighters' pulmonary function and DNA damage.

Chiang Mai encounters severe pollution during the wildfire season. Wildland firefighters encounter various hazards while engaged in fire suppression operations, which encompass significant exposure to elevated concentrations of air pollutants resulting from combustion, especially particulate matter. The adverse effects of wildfire smoke on respiratory health are a significant concern. The objective of this study was to examine the potential adverse effects of PM2.5 exposure on the respiratory function and DNA damage of wildland firefighters. This prospective cohort study conducted in Chiang Mai from January to May 2022 planned to evaluate the health status of wildland firefighters during the pre-peak, peak, and post-peak ambient air pollution seasons. The measurement of PM2.5 was done at every forest fire station, as well as utilizing data from the Pollution Control Department. Participants received general health examinations, spirometry evaluations, and blood tests for DNA damage analysis. Pair t-tests and multiple regression models were used to examine the connection between pulmonary function parameters (FVC, FEV1) and PM2.5 concentration, with a significance level of P < 0.05. Thirty-three peak-season and twenty-one post-peak-season participants were enrolled. Four pre-peak-season wildland firefighters had FVC and FEV1 declines of > 15%. Multiple regression analysis showed a negative association between PM2.5 exposure and FVC% predicted (- 2.81%, 95% CI - 5.27 to - 0.34%, P = 0.027) and a marginally significant negative correlation with FVC (- 114.38 ml, 95% CI - 230.36 to 1.59 ml, P = 0.053). The remaining pulmonary measures showed a statistically insignificant decline. There were no significant changes in DNA damage detected. Wildland firefighters suffered a significant decline in pulmonary function associated with PM2.5 exposure. Spirometry is crucial for monitoring and promptly identifying respiratory issues that occur during wildfire seasons. Further research is recommended to explore DNA damage alterations and their potential association with PM2.5.

Seasonal extreme temperatures and short-term fine particulate matter increases pediatric respiratory healthcare encounters in a sparsely populated region of the intermountain western United States.

BACKGROUND: Western Montana, USA, experiences complex air pollution patterns with predominant exposure sources from summer wildfire smoke and winter wood smoke. In addition, climate change related temperatures events are becoming more extreme and expected to contribute to increases in hospital admissions for a range of health outcomes. Evaluating while accounting for these exposures (air pollution and temperature) that often occur simultaneously and may act synergistically on health is becoming more important. METHODS: We explored short-term exposure to air pollution on children's respiratory health outcomes and how extreme temperature or seasonal period modify the risk of air pollution-associated healthcare events. The main outcome measure included individual-based address located respiratory-related healthcare visits for three categories: asthma, lower respiratory tract infections (LRTI), and upper respiratory tract infections (URTI) across western Montana for ages 0-17 from 2017-2020. We used a time-stratified, case-crossover analysis with distributed lag models to identify sensitive exposure windows of fine particulate matter (PM2.5) lagged from 0 (same-day) to 14 prior-days modified by temperature or season. RESULTS: For asthma, increases of 1 µg/m3 in PM2.5 exposure 7-13 days prior a healthcare visit date was associated with increased odds that were magnified during median to colder temperatures and winter periods. For LRTIs, 1 µg/m3 increases during 12 days of cumulative PM2.5 with peak exposure periods between 6-12 days before healthcare visit date was associated with elevated LRTI events, also heightened in median to colder temperatures but no seasonal effect was observed. For URTIs, 1 unit increases during 13 days of cumulative PM2.5 with peak exposure periods between 4-10 days prior event date was associated with greater risk for URTIs visits that were intensified during median to hotter temperatures and spring to summer periods. CONCLUSIONS: Delayed, short-term exposure increases of PM2.5 were associated with elevated odds of all three pediatric respiratory healthcare visit categories in a sparsely population area of the inter-Rocky Mountains, USA. PM2.5 in colder temperatures tended to increase instances of asthma and LRTIs, while PM2.5 during hotter periods increased URTIs.

Urine proteome profile of firefighters with exposure to emergency fire-induced smoke: A pilot study to identify potential carcinogenic effects.

Firefighters are frequently exposed to a variety of chemicals formed from smoke, which pose a risk for numerous diseases, including cancer. Comparative urine proteome profiling could significantly improve our understanding of the early detection of potential cancer biomarkers. In this study, for the first time, we conducted a comparative protein profile analysis of 20 urine samples collected from ten real-life firefighters prior to and following emergency fire-induced smoke. Using a label-free quantitative proteomics platform, we identified and quantified 1325 unique protein groups, of which 45 proteins showed differential expressions in abundance in response to fire-smoke exposure (post) compared to the control (pre). Pathway analysis showed proteins associated with epithelium development (e.g., RHCG, HEG1, ADAMTSL2) and Alzheimer's disease (SORL1) were significantly increased in response to smoke exposure samples. A protein-protein-network study showed a possible link between these differentially abundant proteins and the known cancer gene (TP53). Moreover, a cross-comparison analysis revealed that seven proteins-ALDH1A1, APCS, POMC, COL2A1, RDX, DDAH2, and SDC4 overlapped with the previously published urine cancer proteome datasets, suggesting a potential cancer risk. Our findings demonstrated that the discovery proteomic platform is a promising analytical technique for identifying potential non-invasive biomarkers associated with fire-smoke exposure in firefighters that may be related to cancer.

Assessment of Left Lung Remodeling With Magnetic Resonance Imaging in a Murine Model Following Exposure to Douglas Fir Smoke.

Wildland firefighters (WLFFs) experience lung function decline due to occupational exposure to fire smoke. WLFFs typically do not wear respiratory personal protective equipment, and if they do, it is a simple bandana, which is not effective at filtering smoke. To pinpoint the biological underpinnings of abnormal respiratory function following 3-7 years of WLFF service, we exposed mice to Douglas fir smoke (DFS) over 8 weeks. Following exposure, we assessed changes in lung structure through Magnetic Resonance Imaging (MRI) and histological analysis, which was supported by immunohistochemistry staining. With MRI, we found that the signal decay time, T2*, from ultrashort echo time (UTE) images was significantly shorter in mice exposed to DFS compared to air controls. In addition, the variation in T2* was more heterogeneously distributed throughout the left lung in DFS-exposed mice, compared to air controls. As confirmed by histological analysis, shorter T2* was caused by larger parenchyma airspace sizes and not fibrotic remodeling. Destruction of the alveolar spaces was likely due to inflammation, as measured by an influx of CD68+ macrophages and destruction due to enhanced neutrophil elastase. In addition, measurements of airspace dimensions from histology were more heterogeneously distributed throughout the lung, corroborating the enhanced relative dispersion of T2*. Findings from this study suggest that the decline in lung function observed in WLFFs may be due to emphysema-like changes in the lung, which can be quantified with MRI.

Climate change and health: rethinking public health messaging for wildfire smoke and extreme heat co-exposures.

With the growing climate change crisis, public health agencies and practitioners must increasingly develop guidance documents addressing the public health risks and protective measures associated with multi-hazard events. Our Policy and Practice Review aims to assess current public health guidance and related messaging about co-exposure to wildfire smoke and extreme heat and recommend strengthened messaging to better protect people from these climate-sensitive hazards. We reviewed public health messaging published by governmental agencies between January 2013 and May 2023 in Canada and the United States. Publicly available resources were eligible if they discussed the co-occurrence of wildfire smoke and extreme heat and mentioned personal interventions (protective measures) to prevent exposure to either hazard. We reviewed local, regional, and national governmental agency messaging resources, such as online fact sheets and guidance documents. We assessed these resources according to four public health messaging themes, including (1) discussions around vulnerable groups and risk factors, (2) symptoms associated with these exposures, (3) health risks of each exposure individually, and (4) health risks from combined exposure. Additionally, we conducted a detailed assessment of current messaging about measures to mitigate exposure. We found 15 online public-facing resources that provided health messaging about co-exposure; however, only one discussed all four themes. We identified 21 distinct protective measures mentioned across the 15 resources. There is considerable variability and inconsistency regarding the types and level of detail across described protective measures. Of the identified 21 protective measures, nine may protect against both hazards simultaneously, suggesting opportunities to emphasize these particular messages to address both hazards together. More precise, complete, and coordinated public health messaging would protect against climate-sensitive health outcomes attributable to wildfire smoke and extreme heat co-exposures.

Pregnancy exposure to PM2.5 from wildland fire smoke and preterm birth in California.

BACKGROUND: Wildfires in the Western United States are a growing and significant source of air pollution that is eroding decades of progress in air pollution reduction. The effects on preterm birth during critical periods of pregnancy are unknown. METHODS: We assessed associations between prenatal exposure to wildland fire smoke and risk of preterm birth (gestational age < 37 weeks). We assigned smoke exposure to geocoded residence at birth for all live singleton births in California conceived 2007-2018, using weekly average concentrations of particulate matter ≤ 2.5 µm (PM2.5) attributable to wildland fires from United States Environmental Protection Agency's Community Multiscale Air Quality Model. Logistic regression yielded odds ratio (OR) for preterm birth in relation to increases in average exposure across the whole pregnancy, each trimester, and each week of pregnancy. Models adjusted for season, age, education, race/ethnicity, medical insurance, and smoking of the birthing parent. RESULTS: For the 5,155,026 births, higher wildland fire PM2.5 exposure averaged across pregnancy, or any trimester, was associated with higher odds of preterm birth. The OR for an increase of 1 µg/m3 of average wildland fire PM2.5 during pregnancy was 1.013 (95 % CI:1.008,1.017). Wildland fire PM2.5 during most weeks of pregnancy was associated with higher odds. Strongest estimates were observed in weeks in the second and third trimesters. A 10 µg/m3 increase in average wildland fire PM2·5 in gestational week 23 was associated with OR = 1.034; 95 % CI: 1.019, 1.049 for preterm birth. CONCLUSIONS: Preterm birth is sensitive to wildland fire PM2.5; therefore, we must reduce exposure during pregnancy.

Monitoring redox stress in human airway epithelial cells exposed to woodsmoke at an air-liquid interface.

Wildland fires contribute significantly to the ambient air pollution burden worldwide, causing a range of adverse health effects in exposed populations. The toxicity of woodsmoke, a complex mixture of gases, volatile organic compounds, and particulate matter, is commonly studied in vitro using isolated exposures of conventionally cultured lung cells to either resuspended particulate matter or organic solvent extracts of smoke, leading to incomplete toxicity evaluations. This study aimed to improve our understanding of the effects of woodsmoke inhalation by building an advanced in vitro exposure system that emulates human exposure of the airway epithelium. We report the development and characterization of an innovative system that permits live-cell monitoring of the intracellular redox status of differentiated primary human bronchial epithelial cells cultured at an air-liquid interface (pHBEC-ALI) as they are exposed to unfractionated woodsmoke generated in a tube furnace in real time. pHBEC-ALI exposed to freshly generated woodsmoke showed oxidative changes that were dose-dependent and reversible, and not attributable to carbon monoxide exposure. These findings show the utility of this novel system for studying the molecular initiating events underlying woodsmoke-induced toxicity in a physiologically relevant in vitro model, and its potential to provide biological plausibility for risk assessment and public health measures.

Quantitative modeling of in vitro data using an adverse outcome pathway for the risk assessment of decreased lung function in humans.

In the absence of epidemiological data, there is a need to develop computational models that convert in vitro findings to human disease risk predictions following toxicant exposure. In such efforts, in vitro data can be evaluated in the context of adverse outcome pathways (AOPs) that organize mechanistic knowledge based on empirical evidence into a sequence of molecular-, cellular-, tissue-, and organ-level key events that precede an adverse outcome (AO). Here we combined data from advanced in vitro organotypic airway models exposed to combustible cigarette (CC) smoke or Tobacco Heating System (THS) aerosol with an AOP for increased oxidative stress leads to decreased lung function. The mathematical modeling predicted reduced risk of decreased ciliary beating frequency (CBF) based on oxidative stress measurements and reduced risk of decreased mucociliary clearance (MCC) based on CBF measurements in THS aerosol- compared with CC smoke-exposed cultures. To extend the predictions to the AO of decreased lung function, we leveraged human MCC data from current smokers, nonsmokers, former smokers, and users of heated tobacco products. This approach provided a plausible prediction of diminished reduction in lung function in response to THS use compared with continued smoking. The current approach may also present a basis for an integrated approach to testing and assessment of tobacco products for future regulatory decision-making.

Measuring long-term exposure to wildfire PM2.5 in California: Time-varying inequities in environmental burden.

Wildfires have become more frequent and intense due to climate change and outdoor wildfire fine particulate matter (PM2.5) concentrations differ from relatively smoothly varying total PM2.5. Thus, we introduced a conceptual model for computing long-term wildfire PM2.5 and assessed disproportionate exposures among marginalized communities. We used monitoring data and statistical techniques to characterize annual wildfire PM2.5 exposure based on intermittent and extreme daily wildfire PM2.5 concentrations in California census tracts (2006 to 2020). Metrics included: 1) weeks with wildfire PM2.5 < 5 µg/m3; 2) days with non-zero wildfire PM2.5; 3) mean wildfire PM2.5 during peak exposure week; 4) smoke waves (≥2 consecutive days with <15 µg/m3 wildfire PM2.5); and 5) mean annual wildfire PM2.5 concentration. We classified tracts by their racial/ethnic composition and CalEnviroScreen (CES) score, an environmental and social vulnerability composite measure. We examined associations of CES and racial/ethnic composition with the wildfire PM2.5 metrics using mixed-effects models. Averaged 2006 to 2020, we detected little difference in exposure by CES score or racial/ethnic composition, except for non-Hispanic American Indian and Alaska Native populations, where a 1-SD increase was associated with higher exposure for 4/5 metrics. CES or racial/ethnic × year interaction term models revealed exposure disparities in some years. Compared to their California-wide representation, the exposed populations of non-Hispanic American Indian and Alaska Native (1.68×, 95% CI: 1.01 to 2.81), white (1.13×, 95% CI: 0.99 to 1.32), and multiracial (1.06×, 95% CI: 0.97 to 1.23) people were over-represented from 2006 to 2020. In conclusion, during our study period in California, we detected disproportionate long-term wildfire PM2.5 exposure for several racial/ethnic groups.

Excess prenatal loss and respiratory illnesses of infant macaques living outdoors and exposed to wildfire smoke.

Global climate change has transformed predictions of fire seasons in the near future, and record-breaking wildfire events have had catastrophic consequences in recent years. In September 2020, multiple wildfires subjected Oregon to hazardous air quality for several days. In this retrospective cohort study, we aimed to examine prenatal loss, morbidity, and mortality of rhesus (Macaca mulatta) and Japanese macaques (Macaca fuscata) exposed to poor air quality from the nearby wildfires. Detailed medical records from 2014 to 2020 of 580 macaques housed outdoors at a research facility in Beaverton, Oregon were used to evaluate the association between these health outcomes and wildfire smoke exposure. Logistic regression models estimated excess prenatal loss, hospitalization rates, respiratory problems, and mortality during and following the wildfire event, and Kruskal-Wallis statistics were used to determine if infant growth was affected by wildfire smoke exposure. Risk of pregnancy loss (relative risk = 4.1; p < 0.001) and odds of diagnosis with a respiratory problem (odds ratio = 4.47; p = 0.003) were higher in exposed infant macaques compared to nonexposed infants. Infant growth was not affected by poor air quality exposure. Our findings suggest wildfire smoke exposure poses a risk to the health of infants and pregnant individuals and should be monitored more closely in the future.

High-frequency electric knife smoke particles: An experimental study on factors influencing emission characteristics.

During surgery, the use of a high-frequency electric knife produces smoke, which can be harmful to the health of indoor medical staff and patients. The quantity and particle size distribution of smoke particles produced by different tissues may vary. Understanding the release characteristics of these smoke particles is necessary to clarify their impact on the surgical environment and to seek effective smoke control methods. A previous comparative analysis of human and pig tissues revealed that they share similar water and fat compositions in certain anatomical regions. In this study, we investigated the emission characteristics of smoke particles from various tissues of pigs (skeletal muscle, liver, kidney, skin, and subcutaneous fat) under different operating powers of an electric knife. We measured the indoor particle number concentration (particle concentration), and estimated the PM2.5 mass concentration (PM2.5 concentration), particle size distribution, and emission rate of the smoke particles. The study obtained the particle emission rates of different tissues under different electric knife operating powers, results of which showed that (1) during the operation of the electric knife, mainly small particles below 1 µm are produced. Among them, particles of 0.3 µm were the most abundant, with a particle concentration level of up to 109 particles/m3, accounting for 85.17-97.64% of the total particle number, and as the particle size increased, the particle concentration and percentage decreased significantly. (2) The water and fat compositions of different tissues influenced the indoor particle concentration and emission rate of the smoke emitted by the electric knife. Among different tissues, subcutaneous fat tissue had the lowest particle concentration and emission rate. (3) The electric knife operating power mainly affected particles below 1 µm, and except for kidney tissue, the indoor concentration and emission rate of these particle sizes were positively correlated with the power. The experimental results can provide data reference for the use of high-frequency electric knives in surgeries involving different human tissues in the operating room.

The firestorm within: A narrative review of extreme heat and wildfire smoke effects on brain health.

Climate change is generating increased heatwaves and wildfires across much of the world. With these escalating environmental changes comes greater impacts on human health leading to increased numbers of people suffering from heat- and wildfire smoke-associated respiratory and cardiovascular impairment. One area of health impact of climate change that has received far less attention is the effects of extreme heat and wildfire smoke exposure on human brain health. As elevated temperatures, and wildfire-associated smoke, are increasingly experienced simultaneously over summer periods, understanding this combined impact is critical to management of human health especially in the elderly, and people with dementia, and other neurological disorders. Both extreme heat and wildfire smoke air pollution (especially particulate matter, PM) induce neuroinflammatory and cerebrovascular effects, oxidative stress, and cognitive impairment, however the combined effect of these impacts are not well understood. In this narrative review, a comprehensive examination of extreme heat and wildfire smoke impact on human brain health is presented, with a focus on how these factors contribute to cognitive impairment, and dementia, one of the leading health issues today. Also discussed is the potential impact of combined heat and wildfire smoke on brain health, and where future efforts should be applied to help advance knowledge in this rapidly growing and critical field of health research.

Personal strategies to reduce the effects of landscape fire smoke on asthma-related outcomes: a protocol for systematic review and meta-analysis.

INTRODUCTION: Landscape fire smoke (LFS) contains several hazardous air pollutants that are known to be detrimental to human health. People with asthma are more vulnerable to the health impact of LFS than general populations. The aim of this review is to investigate the effectiveness of personal strategies to reduce the effect of LFS on asthma-related outcomes. METHODS AND ANALYSIS: We will electronically search databases such as Medline, Embase, CINAHL and Cochrane Clinical Trials Register to identify eligible articles for the review. Screening of search results and data extraction from included studies will be completed by two independent reviewers. The risk of bias (RoB 2) will be assessed using the Risk of Bias Assessment Tool for Non-Randomised Studies for observational studies, the Cochrane Collaboration tool for assessing the RoB 2 for randomised controlled trials (RCTs) and the Risk Of Bias In Nonrandomized Studies of Interventions tool for non-RCTs. A random-effect meta-analysis will be performed to determine the pooled summary of findings of the included studies. If meta-analysis is not possible, we will conduct a narrative synthesis. Findings will be reported according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement. ETHICS AND DISSEMINATION: This study will synthesise the available evidence obtained from published studies and as such, no ethical approval is required. The review will be disseminated through peer-reviewed publications and conference presentations. PROSPERO REGISTRATION NUMBER: CRD42022341120.

Exploring spatial heterogeneity in synergistic effects of compound climate hazards: Extreme heat and wildfire smoke on cardiorespiratory hospitalizations in California.

Extreme heat and wildfire smoke events are increasingly co-occurring in the context of climate change, especially in California. Extreme heat and wildfire smoke may have synergistic effects on population health that vary over space. We leveraged high-resolution satellite and monitoring data to quantify spatially varying compound exposures to extreme heat and wildfire smoke in California (2006-2019) at ZIP Code Tabulation Area (ZCTA) level. We found synergistic effects between extreme heat and wildfire smoke on daily cardiorespiratory hospitalizations at the state level. We also found spatial heterogeneity in such synergistic effects across ZCTAs. Communities with lower education attainment, lower health insurance coverage, lower income, lower proportion of automobile ownership, lower tree canopy coverage, higher population density, and higher proportions of racial/ethnic minorities experienced higher synergistic effects. This study highlights the need to incorporate compound hazards and environmental justice considerations into evidence-based policy development to protect populations from increasingly prevalent compound hazards.

[Bibliometric and visual analysis of neurological damage caused by electrical welding operations].

Objective: To analyze and summarize the trends and hot spots in the field of neurological damage caused by electric welding operations, and to provide ideas for new researches by searching the domestic and international literature. Methods: In December 2022, using Web of Science Citation Index (Web of Science), China Journal Full-Text Database (CNKI) and Wanfang Database as search databases, literature search was conducted on the Chinese and English search terms related to eletrical welding operations and neurological damage. The bibliometric analysis software VOSviewer 1.6.18 and CiteSpace 6.1.6 were used to visualize the publication year, publication quantity, country, research institution and key words of the literature. Results: A total of 309 articles (112 in Chinese and 197 in English) were included in this study. The first domestic and international papers were published in 1976 and 1994 respectively, and the number of papers reached the peak in 2006 and 2018, and then showed a downward trend to varying degrees. In China, Shandong First Medical University (including Shandong Institute of Occupational Health and Occupational Disease Prevention and Shandong Academy of Medical Sciences) and Wuhan University of Science and Technology had the largest number of publications. The 309 articles were from 52 Chinese journals and 86 English journals. The co-occurrence analysis of key words showed that the domestic research mainly focused on eletrical welding operation, welding workers, neurobehavioral function and manganese, and the nervous system damage caused by manganese in welding smoke was the field of international attention. Long term exposure, risk, and performance were key buzzwords in the field. Conclusion: The research focus in the field of nervous system damage caused by electric welding operation has an obvious trend of time evolution, gradually transiting from clinical manifestations to its toxic mechanism and early biomarkers.

The mortality burden attributable to wood heater smoke particulate matter (PM2.5) in Australia.

Air pollution is the leading environmental risk factor for mortality worldwide. In Australia, residential wood heating is the single largest source of pollution in many regions of the country. Estimates around the world and in some limited locations across Australia have shown that the health burden attributable to wood heating PM2.5 is considerable, and that there is great potential to reduce this burden. Here, we aimed to calculate the mortality burden attributable to wood heating emissions (WHE)-related PM2.5 throughout Australia and estimate the potential health benefits of reducing WHE-related air pollution, by replacing wood heaters with cleaner heating technologies. In summary, we used a four-stage process to (1) compile a nationwide WHE inventory, (2) generate annual exposure estimates of WHE-PM2.5, (3) estimate the annual mortality burden attributable to wood heater use across Australia for the year 2015, and (4) assess the potential health benefits of replacing existing wood heaters with cleaner heating technologies. We estimated that population weighted WHE-PM2.5 exposure across Australia for 2015 ranged between 0.62 µg/m3 and 1.35 µg/m3, with differing exposures across State/Territories. We estimated a considerable mortality burden attributable to WHE-PM2.5 ranging between 558 (95 % CI, 364-738) and 1555 (95 % CI, 1180-1740) deaths annually, depending on the scenario assessed. We calculated that replacing 50 % of the current wood heater stock, with zero or lower emission technologies could produce relevant health benefits, of between $AUD 1.61 and $AUD 1.93 billion per year (303-364 attributable deaths). These findings provide a preliminary and likely conservative assessment of the health burden of wood heater smoke across Australia, and an estimation of the potential benefits from replacing the current wood heater stock with cleaner technologies. The results presented here underscore the magnitude of the health burden attributable to wood heating in Australia.

Surgical smoke and its components, effects, and mitigation: a contemporary review.

Energy-based surgical instruments produce surgical smoke, which contains harmful byproducts, such as polycyclic aromatic hydrocarbons, volatile organic compounds, particulate matter, and viable microorganisms. The research setting has shifted from the laboratory to the operating room. However, significant heterogeneity in the methods of detection and placement of samplers, diversity in the tissue operated on, and types of surgeries tested has resulted in variability in detected levels and composition of surgical smoke. State regulation limiting surgical smoke exposure through local evacuators is expanding but has yet to reach the national regulatory level. However, most studies have not shown levels above standard established limits but relatively short bursts of high concentrations of these harmful by-products. This review highlights the limitations of the current research and unsupported conclusions while also suggesting further areas of interest that need more focus to improve Occupational Safety and Health Administration guidelines.