Visualization of Combustion Phases of Biomass Particles: Effects of Fuel Properties
Ontology highlight
ABSTRACT:
SUBMITTER: Jia Y
PROVIDER: S-EPMC8552231 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:The physicochemical properties of combustion particles that promote lung toxicity are not fully understood, hindered by the fact that combustion particles vary based on the fuel and combustion conditions. Real-world combustion-particle properties also continually change as new fuels are implemented, engines age, and engine technologies evolve. This work used laboratory-generated particles produced under controlled combustion conditions in an effort to understand the relationship between different particle properties and the activation of established toxicological outcomes in human lung cells (H441 and THP-1). Particles were generated from controlled combustion of two simple biofuel/diesel surrogates (methyl decanoate and dodecane/biofuel-blended diesel (BD), and butanol and dodecane/alcohol-blended diesel (AD)) and compared to a widely studied reference diesel (RD) particle (NIST SRM2975/RD). BD, AD, and RD particles exhibited differences in size, surface area, extractable chemical mass, and the content of individual polycyclic aromatic hydrocarbons (PAHs). Some of these differences were directly associated with different effects on biological responses. BD particles had the greatest surface area, amount of extractable material, and oxidizing potential. These particles and extracts induced cytochrome P450 1A1 and 1B1 enzyme mRNA in lung cells. AD particles and extracts had the greatest total PAH content and also caused CYP1A1 and 1B1 mRNA induction. The RD extract contained the highest relative concentration of 2-ring PAHs and stimulated the greatest level of interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNFα) cytokine secretion. Finally, AD and RD were more potent activators of TRPA1 than BD, and while neither the TRPA1 antagonist HC-030031 nor the antioxidant N-acetylcysteine (NAC) affected CYP1A1 or 1B1 mRNA induction, both inhibitors reduced IL-8 secretion and mRNA induction. These results highlight that differences in fuel and combustion conditions affect the physicochemical properties of particles, and these differences, in turn, affect commonly studied biological/toxicological responses.
| S-EPMC5815945 | biostudies-literature
Project description:BackgroundExposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles' physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season. The overall aim of this study was therefore to investigate cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures.ResultsWSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved.ConclusionThe toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs.
| S-EPMC3544657 | biostudies-literature
Project description:The dataset presented in this article is related to the uncertainty quantification of fuel variability effect on high hydrogen content syngas combustion physicochemical properties. The 1D flame data included in this dataset are collected using PREMIX module available in Chemkin-Pro. Inputs to and outputs collected from the PREMIX module are generated and post-processed using UQTk-3.0.4, an open-access uncertainty quantification (UQ) toolkit developed at Sandia National Laboratories. The 1D flame data here refers to the calculation of flame speed, flame temperature, NO emission, etc. using three detailed chemical mechanisms: the GRI-Mech 3.0, the San Diego, and the NUI Galway Mechanism. The main analysis performed using UQTk-3.0.4 focuses on obtaining main and joint sensitivity effects (Sobol Indices) of uniformly distributed fuel uncertainty on 1D premixed physicochemical property. Other parameters such as the resulted probability density function or fluctuation of these properties are also explored. This new and original dataset is suitable for further analyzing fuel variability effect on other significant flame controlling parameters such as Karlovitz number, flame thickness, etc. in the discipline of turbulent combustion simulation.
| S-EPMC6992945 | biostudies-literature
Project description:Combustion-derived particles (CDPs), due to the presence in their composition of several toxic and carcinogenic chemical compounds, such as polycyclic aromatic hydrocarbons (PAHs) and metals, are linked to several respiratory diseases, including lung cancer. Epithelial-to-mesenchymal transition (EMT) is a crucial step in lung cancer progression, involving several morphological and phenotypical changes. The study aims to investigate how exposure to CDPs from different biomass sources might be involved in cancer development, focusing mainly on the effects linked to EMT and invasion on human A549 lung cells. Biomass combustion-derived particles (BCDPs) were collected from a stove fuelled with pellet, charcoal or wood, respectively. A time course and dose response evaluation on cell viability and pro-inflammatory response was performed to select the optimal conditions for EMT-related studies. A significant release of IL-8 was found after 72 h of exposure to 2.5 μg/cm2 BCDPs. The EMT activation was then examined by evaluating the expression of some typical markers, such as E-cadherin and N-cadherin, and the possible enhanced migration and invasiveness. Sub-acute exposure revealed that BCDPs differentially modulated cell viability, migration and invasion, as well as the expression of proteins linked to EMT. Results showed a reduction in the epithelial marker E-cadherin and a parallel increase in the mesenchymal markers N-cadherin, mainly after exposure to charcoal and wood. Migration and invasion were also increased. In conclusion, our results suggest that BCDPs with a higher content of organic compounds (e.g. PAHs) in their chemical composition might play a crucial role in inducing pro-carcinogenic effects on epithelial cells.
| S-EPMC8032642 | biostudies-literature
Project description:BackgroundFine-particulate-matter (i.e. with an aerodynamic diameter of ≤2.5 µm, PM2.5) air pollution is commonly treated as if it had 'equivalent toxicity', irrespective of the source and composition. We investigate the respective roles of fossil-fuel- and biomass-combustion particles in the PM2.5 relationship with cardiovascular morbidity and mortality using tracers of sources in Dhaka, Bangladesh. Results provide insight into the often observed levelling of the PM2.5 exposure-response curve at high-pollution levels.MethodsA time-series regression model, adjusted for potentially confounding influences, was applied to 340 758 cardiovascular disease (CVD) emergency-department visits (EDVs) during January 2014 to December 2017, 253 407 hospital admissions during September 2013 to December 2017 and 16 858 CVD deaths during January 2014 to October 2017.ResultsSignificant associations were confirmed between PM2.5-mass exposures and increased risk of cardiovascular EDV [0.27%, (0.07% to 0.47%)] at lag-0, hospitalizations [0.32% (0.08% to 0.55%)] at lag-0 and deaths [0.87%, (0.27% to 1.47%)] at lag-1 per 10-μg/m3 increase in PM2.5. However, the relationship of PM2.5 with morbidity and mortality effect slopes was less steep and non-significant at higher PM2.5 concentrations (during crop-burning-dominated exposures) and varied with PM2.5 source. Fossil-fuel-combustion PM2.5 had roughly a four times greater effect on CVD mortality and double the effect on CVD hospital admissions on a per-µg/m3 basis than did biomass-combustion PM2.5.ConclusionBiomass burning was responsible for most PM2.5 air pollution in Dhaka, but fossil-fuel-combustion PM2.5 dominated the CVD adverse health impacts. Such by-source variations in the health impacts of PM2.5 should be considered in conducting ambient particulate-matter risk assessments, as well as in prioritizing air-pollution-mitigation measures and clinical advice.
| S-EPMC8633660 | biostudies-literature
Project description:BACKGROUND: Residential wood combustion is now recognized as a major particle source in many developed countries, and the number of studies investigating the negative health effects associated with wood smoke exposure is currently increasing. The combustion appliances in use today provide highly variable combustion conditions resulting in large variations in the physicochemical characteristics of the emitted particles. These differences in physicochemical properties are likely to influence the biological effects induced by the wood smoke particles. OUTLINE: The focus of this review is to discuss the present knowledge on physicochemical properties of wood smoke particles from different combustion conditions in relation to wood smoke-induced health effects. In addition, the human wood smoke exposure in developed countries is explored in order to identify the particle characteristics that are relevant for experimental studies of wood smoke-induced health effects. Finally, recent experimental studies regarding wood smoke exposure are discussed with respect to the applied combustion conditions and particle properties. CONCLUSION: Overall, the reviewed literature regarding the physicochemical properties of wood smoke particles provides a relatively clear picture of how these properties vary with the combustion conditions, whereas particle emissions from specific classes of combustion appliances are less well characterised. The major gaps in knowledge concern; (i) characterisation of the atmospheric transformations of wood smoke particles, (ii) characterisation of the physicochemical properties of wood smoke particles in ambient and indoor environments, and (iii) identification of the physicochemical properties that influence the biological effects of wood smoke particles.
| S-EPMC2777846 | biostudies-other
Project description:Available evidence concerning the association between indoor air pollution (IAP) from biomass and solid fuel combustion and preeclampsia/eclampsia is not available in developing countries. We investigated the association between exposure to IAP from biomass and solid fuel combustion and symptoms of preeclampsia/eclampsia in Indian women by analyzing cross-sectional data from India's third National Family Health Survey (NFHS-3, 2005-2006). Self-reported symptoms of preeclampsia/eclampsia during pregnancy such as convulsions (not from fever), swelling of legs, body or face, excessive fatigue or vision difficulty during daylight, were obtained from 39,657 women aged 15-49 years who had a live birth in the previous 5 years. Effects of exposure to cooking smoke, ascertained by type of fuel used for cooking on preeclampsia/eclampsia risk, were estimated using logistic regression after adjusting for various confounders. Results indicate that women living in households using biomass and solid fuels have two times higher likelihood of reporting preeclampsia/eclampsia symptoms than do those living in households using cleaner fuels (OR = 2.21; 95%: 1.26-3.87; P = 0.006), even after controlling for the effects of a number of potentially confounding factors. This study is the first to empirically estimate the associations of IAP from biomass and solid fuel combustion and reported symptoms suggestive of preeclampsia/eclampsia in a large nationally representative sample of Indian women and we observed increased risk. These findings have important program and policy implications for countries such as India, where large proportions of the population rely on polluting biomass fuels for cooking and space heating. More epidemiological research with detailed exposure assessments and clinical measures of preeclampsia/eclampsia is needed in a developing country setting to validate these findings.
| S-EPMC4431462 | biostudies-literature
Project description:The characteristics of wildland fire smoke exposures which initiate or exacerbate cardiopulmonary conditions are unclear. We previously reported that, on a mass basis, lung toxicity associated with particulate matter (PM) from flaming smoke aspirated into mouse lungs is greater than smoldering PM. In this study, we developed a computer-controlled inhalation system which can precisely control complex biomass smoke emissions from different combustion conditions. This system was used to examine the toxicity of inhaled biomass smoke from peat, eucalyptus, and oak fuels generated under smoldering and flaming phases with emissions set to the same approximate concentration of carbon monoxide (CO) for each exposure (60-110 ppm), resulting in PM levels of ~ 4 mg/m3 for flaming and ~ 40 mg/m3 for smoldering conditions. Mice were exposed by inhalation 1 h/day for 2 days, and assessed for lung toxicity at 4 and 24 h after the final exposure. Peat (flaming and smoldering) and eucalyptus (smoldering) smoke elicited significant inflammation (neutrophil influx) in mouse lungs at 4 h with the peat (flaming) smoke causing even greater lung inflammation at 24-h post-exposure. A significant alteration in ventilatory timing was also observed in mice exposed to the peat (flaming) and eucalyptus (flaming and smoldering) smoke immediately after each day of exposure. No responses were seen for exposures to similar concentrations of flaming or smoldering oak smoke. The lung toxicity potencies (neutrophil influx per PM mass) agreed well between the inhalation and previously reported aspiration studies, demonstrating that although flaming smoke contains much less PM mass than smoldering smoke, it is more toxic on a mass basis than smoldering smoke exposure, and that fuel type is also a controlling factor.
| S-EPMC6991149 | biostudies-literature
Project description:Exposure to fine particulate matter (PM2.5) is associated with an increased risk of morbidity and mortality. In Europe, residential fuel combustion and road transport emissions contribute significantly to PM2.5. Toxicological studies indicate that PM2.5 from these sources is relatively more hazardous, owing to its high content of black and organic carbon. Here, we study the contribution of the emissions from these sectors to long-term exposure and excess mortality in Europe. We quantified the impact of anthropogenic carbonaceous aerosols on excess mortality and performed a sensitivity analysis assuming that they are twice as toxic as inorganic particles. We find that total PM2.5 from residential combustion leads to 72,000 (95% confidence interval: 48,000-99,000) excess deaths per year, with about 40% attributed to carbonaceous aerosols. Similarly, road transport leads to about 35,000 (CI 23,000-47,000) excess deaths per year, with 6000 (CI 4000-9000) due to carbonaceous particles. Assuming that carbonaceous aerosols are twice as toxic as other PM2.5 components, they contribute 80% and 37%, respectively, to residential fuel combustion and road transport-related deaths. We uncover robust national variations in the contribution of each sector to excess mortality and emphasize the importance of country-specific emission reduction policies based on national characteristics and sectoral shares.
| S-EPMC10794246 | biostudies-literature
Project description:BackgroundExposure to indoor air pollution from solid fuel combustion is associated with lung diseases and cancer. This study investigated the cytotoxicity and molecular mechanisms of biomass combustion-derived particles in human pulmonary alveolar epithelial cells (HPAEpiC) using a platform that combines air-liquid interface (ALI) and dynamic culture (DC) systems.MethodsHPAEpiC were cultured on the surface of polycarbonate (PC) membranes on the ALI-DC platform. The cells were sprayed with an aerosolized solution of biomass combustion soluble constituents (BCSCs) and simultaneously nourished with culture medium flowing beneath the permeable PC membranes. The ALI-DC method was compared with the traditional submerged culture approach. BCSC particle morphology and dosages deposited on the chip were determined for particle characterization. Flow cytometry, scanning electron microscopy, and transmission electron microscopy were used to investigate the apoptosis rate of HPAEpiC and changes in the cell ultrastructure induced by BCSCs. Additionally, the underlying apoptotic pathway was examined by determining the protein expression levels by western blotting.ResultsScanning electron microscope images demonstrated that the sample processing and delivering approach of the ALI-DC platform were suitable for pollutant exposure. Compared with the submerged culture method, a significant decline in cell viability and increase in apoptosis rate was observed after BCSC exposure on the ALI-DC platform, indicating that the ALI-DC platform is a more sensitive system for investigating cytotoxicity of indoor air pollutants in lung cells. The morphology and ultrastructure of the cells were damaged after exposure to BCSCs, and the p53 pathway was activated. The Bcl-2/Bax ratio was reduced, upregulating caspase-9 and caspase-3 expression and subsequently inducing apoptosis of HPAEpiC. The addition of N-acetyl cysteine antioxidant significantly alleviated the cytotoxicity induced by BCSCs.ConclusionA novel ALI-DC platform was developed to study the cytotoxicity of air pollutants on lung cells. Using the platform, we demonstrated that BCSCs could damage the mitochondria, produce reactive oxygen species, and activate p53 in HPAEpiC, ultimately inducing apoptosis.
| S-EPMC8379799 | biostudies-literature