Sex-specific metabolic adaptations from in utero exposure to particulate matter derived from combustion of petrodiesel and biodiesel fuels.

Maternal exposure to particulate matter derived from diesel exhaust has been shown to cause metabolic dysregulation, neurological problems, and increased susceptibility to diabetes in the offspring. Diesel exhaust is a major source of air pollution and the use of biodiesel (BD) and its blends have been progressively increasing throughout the world; however, studies on the health impact of BD vs. petrodiesel combustion-generated exhaust have been controversial in part, due to differences in the chemical and physical nature of the associated particulate matter (PM). To explore the long-term impact of prenatal exposure, pregnant mice were exposed to PM generated by combustion of petrodiesel (B0) and a 20% soy BD blend (B20) by intratracheal instillation during embryonic days 9-17 and allowed to deliver. Offspring were then followed for 52 weeks. We found that mother's exposure to B0 and B20 PM manifested in striking sex-specific phenotypes with respect to metabolic adaptation, maintenance of glucose homeostasis, and medial hypothalamic glial cell makeup in the offspring. The data suggest PM exposure limited to a narrower critical developmental window may be compensated for by the mother and/or the fetus by altered metabolic programming in a marked sex-specific and fuel-derived PM-specific manner, leading to sex-specific risk for diseases related to environmental exposure later in life.

Biodiesel exhaust particle airway toxicity and the role of polycyclic aromatic hydrocarbons.

Renewable alternatives to fossil diesel (FD) including fatty acid methyl ester (FAME) biodiesel have become more prevalent. However, toxicity of exhaust material from their combustion, relative to the fuels they are displacing has not been fully characterised. This study was carried out to examine particle toxicity within the lung epithelium and the role for polycyclic aromatic hydrocarbons (PAHs). Exhaust particles from a 20% (v/v) blend of FAME biodiesel had little impact on primary airway epithelial toxicity compared to FD derived particles but did result in an altered profile of PAHs, including an increase in particle bound carcinogenic B[a]P. Higher blends of biodiesel had significantly increased levels of more carcinogenic PAHs, which was associated with a higher level of stress response gene expression including CYP1A1, NQO1 and IL1B. Removal of semi-volatile material from particulates abolished effects on airway cells. Particle size difference and toxic metals were discounted as causative for biological effects. Finally, combustion of a single component fuel (Methyl decanoate) containing the methyl ester molecular structure found in FAME mixtures, also produced more carcinogenic PAHs at the higher fuel blend levels. These results indicate the use of FAME biodiesel at higher blends may be associated with an increased particle associated carcinogenic and toxicity risk.

Respiratory Health Effects of In Vivo Sub-Chronic Diesel and Biodiesel Exhaust Exposure.

Biodiesel, which can be made from a variety of natural oils, is currently promoted as a sustainable, healthier replacement for commercial mineral diesel despite little experimental data supporting this. The aim of our research was to investigate the health impacts of exposure to exhaust generated by the combustion of diesel and two different biodiesels. Male BALB/c mice (n = 24 per group) were exposed for 2 h/day for 8 days to diluted exhaust from a diesel engine running on ultra-low sulfur diesel (ULSD) or Tallow or Canola biodiesel, with room air exposures used as control. A variety of respiratory-related end-point measurements were assessed, including lung function, responsiveness to methacholine, airway inflammation and cytokine response, and airway morphometry. Exposure to Tallow biodiesel exhaust resulted in the most significant health impacts compared to Air controls, including increased airway hyperresponsiveness and airway inflammation. In contrast, exposure to Canola biodiesel exhaust resulted in fewer negative health effects. Exposure to ULSD resulted in health impacts between those of the two biodiesels. The health effects of biodiesel exhaust exposure vary depending on the feedstock used to make the fuel.

Biodiesel feedstock determines exhaust toxicity in 20% biodiesel: 80% mineral diesel blends.

To address climate change concerns, and reduce the carbon footprint caused by fossil fuel use, it is likely that blend ratios of renewable biodiesel with commercial mineral diesel fuel will steadily increase, resulting in biodiesel use becoming more widespread. Exhaust toxicity of unblended biodiesels changes depending on feedstock type, however the effect of feedstock on blended fuels is less well known. The aim of this study was to assess the impact of biodiesel feedstock on exhaust toxicity of 20% blended biodiesel fuels (B20). Primary human airway epithelial cells were exposed to exhaust diluted 1/15 with air from an engine running on conventional ultra-low sulfur diesel (ULSD) or 20% blends of soy, canola, waste cooking oil (WCO), tallow, palm or cottonseed biodiesel in diesel. Physico-chemical exhaust properties were compared between fuels and the post-exposure effect of exhaust on cellular viability and media release was assessed 24 h later. Exhaust properties changed significantly between all fuels with cottonseed B20 being the most different to both ULSD and its respective unblended biodiesel. Exposure to palm B20 resulted in significantly decreased cellular viability (96.3 ± 1.7%; p < 0.01) whereas exposure to soy B20 generated the greatest number of changes in mediator release (including IL-6, IL-8 and TNF-α, p < 0.05) when compared to air exposed controls, with palm B20 and tallow B20 closely following. In contrast, canola B20 and WCO B20 were the least toxic with only mediators G-CSF and TNF-α being significantly increased. Therefore, exposure to palm B20, soy B20 and tallow B20 were found to be the most toxic and exposure to canola B20 and WCO B20 the least. The top three most toxic and the bottom three least toxic B20 fuels are consistent with their unblended counterparts, suggesting that feedstock type greatly impacts exhaust toxicity, even when biodiesel only comprises 20% of the fuel.

Understanding the environmental impacts of biogas utilization for energy production through life cycle assessment: An action towards reducing emissions.

Unlike renewable energy sources, burning fossil fuels has severe environmental impacts, such as greenhouse gas (GHG) emissions and climate change. Therefore, this study was conducted to assess and compare the environmental impacts of three biogas utilization scenarios for energy production. The life cycle assessment (LCA) method was used to compare (i) biogas combustion in combined heat and power (CHP) unit, (ii) biogas burning in a steam boiler, and (iii) biogas upgrading using pressure swing adsorption (PSA) unit to determine the most sustainable option. The results revealed that the upgrading scenario was the best option, achieving emission savings in 8 out of 10 investigated impact categories. Among them, the emission saving was the highest in the marine aquatic ecotoxicity category (-4276.97 kg 1,4-DB eq./MJ). The CHP scenario was the second-best option, followed by the boiler scenario (worst option), and both had the most beneficial performance in the ozone depletion potential category with 6.29E-08 and 9.88E-08 kg CFC-11-eq./MJ, respectively. The environmental burdens of the boiler scenario were the highest in the marine aquatic ecotoxicity category (248.92 kg 1,4-DB eq./MJ). Although the CHP and boiler scenarios contributed to environmental burdens in all impact categories, they achieved beneficial performances compared to fossil fuel-based systems.

Toxicity of different biodiesel exhausts in primary human airway epithelial cells grown at air-liquid interface.

Biodiesel is created through the transesterification of fats/oils and its usage is increasing worldwide as global warming concerns increase. Biodiesel fuel properties change depending on the feedstock used to create it. The aim of this study was to assess the different toxicological properties of biodiesel exhausts created from different feedstocks using a complex 3D air-liquid interface (ALI) model that mimics the human airway. Primary human airway epithelial cells were grown at ALI until full differentiation was achieved. Cells were then exposed to 1/20 diluted exhaust from an engine running on Diesel (ULSD), pure or 20% blended Canola biodiesel and pure or 20% blended Tallow biodiesel, or Air for control. Exhaust was analysed for various physio-chemical properties and 24-h after exposure, ALI cultures were assessed for permeability, protein release and mediator response. All measured exhaust components were within industry safety standards. ULSD contained the highest concentrations of various combustion gases. We found no differences in terms of particle characteristics for any of the tested exhausts, likely due to the high dilution used. Exposure to Tallow B100 and B20 induced increased permeability in the ALI culture and the greatest increase in mediator response in both the apical and basal compartments. In contrast, Canola B100 and B20 did not impact permeability and induced the smallest mediator response. All exhausts but Canola B20 induced increased protein release, indicating epithelial damage. Despite the concentrations of all exhausts used in this study meeting industry safety regulations, we found significant toxic effects. Tallow biodiesel was found to be the most toxic of the tested fuels and Canola the least, both for blended and pure biodiesel fuels. This suggests that the feedstock biodiesel is made from is crucial for the resulting health effects of exhaust exposure, even when not comprising the majority of fuel composition.

Physicochemical and cell toxicity properties of particulate matter (PM) from a diesel vehicle fueled with diesel, spent coffee ground biodiesel, and ethanol.

The literature shows that information about the physical, chemical, and cell toxicity properties of particulate matter (PM) from diesel vehicles is not rich as the existence of a remarkable number of studies about the combustion, performance, and emissions of diesel vehicles using renewable liquid fuels, particularly biodiesels and alcohols. Also, the PM analyses from combustion of spent coffee ground biodiesel have not been comprehensively explored. Therefore, this research is presented. Pure diesel, 90% diesel + 10% biodiesel, and 90% diesel + 9% ethanol + 1% biodiesel, volume bases, were tested under a fast idle condition. STEM, SEM, EDS, Organic Carbon Analyzer, TGA/DSC, and Raman Spectrometer were employed for investigating the PM physical and chemical properties, and assays of cell viability, cellular reactive oxygen species, interleukin-6, and tumor necrosis factor-alpha were examined for investigating the PM cell toxicity properties. It is found that the application of both biodiesel and ethanol has the potential to change the PM properties, while the impact of ethanol is more than biodiesel on the changes. Regarding the important aspects, biodiesel can be effective for better human health (due to a decrease in cell death (-60.8%)) as well as good diesel particulate filter efficiency (due to lower activation energy (-7.6%) and frequency factor (-83.2%)). However, despite a higher impact of ethanol on the reductions in activation energy (-24.8%) and frequency factor (-99.0%), this fuel causes an increase in cell death (84.1%). Therefore, biodiesel can be an appropriate fuel to have a positive impact on human health, the environment, and emissions catalysts performance, simultaneously.

Inhalation of hydrogenated vegetable oil combustion exhaust and genotoxicity responses in humans.

Biofuels from vegetable oils or animal fats are considered to be more sustainable than petroleum-derived diesel fuel. In this study, we have assessed the effect of hydrogenated vegetable oil (HVO) exhaust on levels of DNA damage in peripheral blood mononuclear cells (PBMCs) as primary outcome, and oxidative stress and inflammation as mediators of genotoxicity. In a randomized cross-over study, healthy humans were exposed to filtered air, inorganic salt particles, exhausts from combustion of HVO in engines with aftertreatment [i.e. emission with nitrogen oxides and low amounts of particulate matter less than 2.5 µm (approximately 1 µg/m3)], or without aftertreatment (i.e. emission with nitrogen oxides and 93 ± 13 µg/m3 of PM2.5). The subjects were exposed for 3 h and blood samples were collected before, within 1 h after the exposure and 24 h after. None of the exposures caused generation of DNA strand breaks and oxidatively damaged DNA, or affected gene expression of factors related to DNA repair (Ogg1), antioxidant defense (Hmox1) or pro-inflammatory cytokines (Ccl2, Il8 and Tnfa) in PBMCs. The results from this study indicate that short-term HVO exhaust exposure is not associated with genotoxic hazard in humans.

Fuel feedstock determines biodiesel exhaust toxicity in a human airway epithelial cell exposure model.

BACKGROUND: Biodiesel is promoted as a sustainable replacement for commercial diesel. Biodiesel fuel and exhaust properties change depending on the base feedstock oil/fat used during creation. The aims of this study were, for the first time, to compare the exhaust exposure health impacts of a wide range of biodiesels made from different feedstocks and relate these effects with the corresponding exhaust characteristics. METHOD: Primary airway epithelial cells were exposed to diluted exhaust from an engine running on conventional diesel and biodiesel made from Soy, Canola, Waste Cooking Oil, Tallow, Palm and Cottonseed. Exhaust properties and cellular viability and mediator release were analysed post exposure. RESULTS: The exhaust physico-chemistry of Tallow biodiesel was the most different to diesel as well as the most toxic, with exposure resulting in significantly decreased cellular viability (95.8 ± 6.5%) and increased release of several immune mediators including IL-6 (+223.11 ± 368.83 pg/mL) and IL-8 (+1516.17 ± 2908.79 pg/mL) above Air controls. In contrast Canola biodiesel was the least toxic with exposure only increasing TNF-α (4.91 ± 8.61). CONCLUSION: This study, which investigated the toxic effects for the largest range of biodiesels, shows that exposure to different exhausts results in a spectrum of toxic effects in vitro when combusted under identical conditions.

Acute cardiovascular effects of controlled exposure to dilute Petrodiesel and biodiesel exhaust in healthy volunteers: a crossover study.

BACKGROUND: Air pollution derived from combustion is associated with considerable cardiorespiratory morbidity and mortality in addition to environmental effects. Replacing petrodiesel with biodiesel may have ecological benefits, but impacts on human health remain unquantified. The objective was to compare acute cardiovascular effects of blended and pure biodiesel exhaust exposure against known adverse effects of petrodiesel exhaust (PDE) exposure in human subjects. In two randomized controlled double-blind crossover studies, healthy volunteers were exposed to PDE or biodiesel exhaust for one hour. In study one, 16 subjects were exposed, on separate occasions, to PDE and 30% rapeseed methyl ester biodiesel blend (RME30) exhaust, aiming at PM10 300 µg/m3. In study two, 19 male subjects were separately exposed to PDE and exhaust from a 100% RME fuel (RME100) using similar engine load and exhaust dilution. Generated exhaust was analyzed for physicochemical composition and oxidative potential. Following exposure, vascular endothelial function was assessed using forearm venous occlusion plethysmography and ex vivo thrombus formation was assessed using a Badimon chamber model of acute arterial injury. Biomarkers of inflammation, platelet activation and fibrinolysis were measured in the blood. RESULTS: In study 1, PDE and RME30 exposures were at comparable PM levels (314 ± 27 µg/m3; (PM10 ± SD) and 309 ± 30 µg/m3 respectively), whereas in study 2, the PDE exposure concentrations remained similar (310 ± 34 µg/m3), but RME100 levels were lower in PM (165 ± 16 µg/m3) and PAHs, but higher in particle number concentration. Compared to PDE, PM from RME had less oxidative potential. Forearm infusion of the vasodilators acetylcholine, bradykinin, sodium nitroprusside and verapamil resulted in dose-dependent increases in blood flow after all exposures. Vasodilatation and ex vivo thrombus formation were similar following exposure to exhaust from petrodiesel and the two biodiesel formulations (RME30 and RME100). There were no significant differences in blood biomarkers or exhaled nitric oxide levels between exposures. CONCLUSIONS: Despite differences in PM composition and particle reactivity, controlled exposure to biodiesel exhaust was associated with similar cardiovascular effects to PDE. We suggest that the potential adverse health effects of biodiesel fuel emissions should be taken into account when evaluating future fuel policies. TRIAL REGISTRATION: ClinicalTrials.gov, NCT01337882 /NCT01883466. Date of first enrollment March 11, 2011, registered April 19, 2011, i.e. retrospectively registered.

Green toxicological investigation for biofuel candidates.

To avoid potential risks of biofuels on the environment and human, ecotoxicity investigation should be integrated into the early design stage for promising biofuel candidates. In the present study, a green toxicology testing strategy combining experimental bioassays with in silico tools was established to investigate the potential ecotoxicity of biofuel candidates. Experimental results obtained from the acute immobilisation test, the fish embryo acute toxicity test and the in vitro micronucleus assay (Chinese hamster lung fibroblast cell line V79) were compared with model prediction results by ECOSAR and OECD QSAR Toolbox. Both our experimental and model prediction results showed that 1-Octanol (1-Oct) and Di-n-butyl ether (DNBE) were the most toxic to Daphnia magna and zebrafish among all the biofuel candidates we investigated, while Methyl ethyl ketone (MEK), Dimethoxymethane (DMM) and Diethoxymethane (DEM) were the least toxic. Moreover, both in vitro micronucleus assay and OECD QSAR Toolbox evaluation suggested that the metabolites present higher genotoxicity than biofuel candidates themselves. Overall, our results proved that this green toxicology testing strategy is a useful tool for assessing ecotoxicity of biofuel candidates.

Palm oil biodiesel: An assessment of PAH emissions, oxidative potential and ecotoxicity of particulate matter.

This work assessed the impact of fuelling an automotive engine with palm biodiesel (pure, and two blends of 10% and 20% with diesel, B100, B10 and B20, respectively) operating under representative urban driving conditions on 17 priority polycyclic aromatic hydrocarbon (PAH) compounds, oxidative potential of ascorbic acid (OPAA), and ecotoxicity through Daphnia pulex mortality test. PM diluted with filtered fresh air (WD) gathered in a minitunel, and particulate matter (PM) collected directly from the exhaust gas stream (W/oD) were used for comparison. Results showed that PM collecting method significantly impact PAH concentration. Although all PAH appeared in both, WD and W/oD, higher concentrations were obtained in the last case. Increasing biodiesel concentration in the fuel blend decreased all PAH compounds, and those with 3 and 5 aromatic rings were the most abundant. Palm biodiesel affected both OPAA and ecotoxicity. While B10 and B20 exhibited the same rate of ascorbic acid (AA) depletion, B100 showed significant faster oxidation rate during the first four minutes and oxidized 10% more AA at the end of the test. B100 and B20 were significantly more ecotoxic than B10. The lethal concentration LC50 for B10 was 6.13 mg/L. It was concluded that palm biodiesel decreased PAH compounds, but increased the oxidative potential and ecotoxicity.

Saline fish wastewater in biogas plants - Biomethanation toxicity and safe use.

Increasing marine land-based recirculating aquaculture systems (RAS) and stricter environmental regulations, pose new challenges to the aquaculture industry on how to treat and dispose saline fish wastewater. The fish wastewater could be incorporated into biogas reactors, but currently, the effects of salinity on the biomethanation process are poorly known. This study aimed to assess the toxicity of fish wastewater with different salinities on the biomethanation process and to propose optimum co-digestion scenarios for maximal methane potential and safe use in biogas plants. Results showed that, depending on salinity and organic content, it is possible to efficiently co-digest from 3.22 to 61.85% fish wastewater (v/v, wastewater/manure) and improve the maximum methane production rate from 2.72 to 61.85%, respectively compared to cow manure mono-digestion. Additionally, salinity was identified as the main inhibitor of biomethanation process with a half-maximal inhibitory concentration (IC50) of 4.37 g L-1, while sulphate reduction was identified as a secondary inhibitor.

Inflammation, oxidative stress and genotoxicity responses to biodiesel emissions in cultured mammalian cells and animals.

Biodiesel fuels are alternatives to petrodiesel, especially in the transport sector where they have lower carbon footprint. Notwithstanding the environmental benefit, biodiesel fuels may have other toxicological properties than petrodiesel. Particulate matter (PM) from petrodiesel causes cancer in the lung as a consequence of delivery of genotoxic polycyclic aromatic hydrocarbons, oxidative stress and inflammation. We have reviewed articles from 2002 to 2019 (50% of the articles since 2015) that have described toxicological effects in terms of genotoxicity, oxidative stress and inflammation of biodiesel exhaust exposure in humans, animals and cell cultures. The studies have assessed first generation biodiesel from different feedstock (e.g. rapeseed and soy), certain second generation fuels (e.g. waste oil), and hydrogenated vegetable oil. It is not possible to rank the potency of toxicological effects of specific biodiesel fuels. However, exposure to biodiesel exhaust causes oxidative stress, inflammation and genotoxicity in cell cultures. Three studies in animals have not indicated genotoxicity in lung tissue. The database on oxidative stress and inflammation in animal studies is larger (13 studies); ten studies have reported increased levels of oxidative stress biomarkers or inflammation, although the effects have been modest in most studies. The cell culture and animal studies have not consistently shown a different potency in effect between biodiesel and petrodiesel exhausts. Both increased and decreased potency have been reported, which might be due to differences in feedstock or combustion conditions. In conclusion, combustion products from biodiesel and petrodiesel fuel may evoke similar toxicological effects on genotoxicity, oxidative stress and inflammation.

Mutagenicity emission factors of canola oil and waste vegetable oil biodiesel: Comparison to soy biodiesel.

Canola (or rapeseed) oil and waste vegetable oil (WVO) are used commonly to make biodiesel fuels composed completely from these oils (B100) or as blends with petroleum diesel (B0). However, no studies have reported the mutagenic potencies of the particulate matter with diameter ≤2.5 µm (PM2.5) or the mutagenicity emission factors, such as revertants/MJthermal (rev/MJth) for these biodiesel emissions. Using strains TA98 and TA100 with the Salmonella (Ames) mutagenicity assay, we determined these metrics for organic extracts of PM2.5 of emissions from biodiesel containing 5% soy oil (soy B5); 5, 20, 50, and 100% canola (canola B5, B20, B50, B100), and 100% waste vegetable oil (WVO B100). The mutagenic potencies (rev/mg PM2.5) of the canola B100 and WVO B100 emissions were generally greater than those of B0, whereas the mutagenicity emission factors (rev/MJth, rev/kg fuel, and rev/m3) were less, reflecting the lower PM emissions of the biodiesels relative to B0. Nearly all the rev/mg PM2.5 and rev/MJth values were greater in TA98 with S9 than without S9, indicating a relatively greater role for polycyclic aromatic hydrocarbons, which require S9, than nitroarenes, which do not. In TA100 -S9, the rev/mg PM2.5 and rev/MJth for the biodiesels were generally ≥ to those of B0, indicating that most of these biodiesels produced more direct-acting, base-substitution mutagenic activity than did B0. For B100 biodiesels and petroleum diesel, the rev/MJth in TA98 + S9 ranked: petroleum diesel > canola > WVO > soy. The diesel emissions generally had rev/MJth values orders of magnitude higher than those of large utility-scale combustors (natural gas, coal, oil, or wood) but orders of magnitude lower than those of inefficient open burning (e.g., residential wood fireplaces). These comparative data of the potential health effects of a variety of biodiesel fuels will help inform the life-cycle assessment and use of biodiesel fuels.

The genotoxicity of organic extracts from particulate truck emissions produced at various engine operating modes using diesel or biodiesel (B100) fuel: A pilot study.

An analysis of the toxic effects of emissions should reflect real traffic conditions. The exhaust emissions of particulate matter from diesel engines strongly depend on their operating conditions, with low-speed, low-load "urban creep" conditions, common for truck traffic in heavily congested urban areas, being one of the worst. We aimed to detect the genotoxicity of organic extracts from particulate matter in the exhaust of the diesel engine Zetor 1505 running on diesel and biodiesel (B100) fuels at characteristic modes of extended "urban creep", typical for transit truck traffic in Prague, comparing the first 5 min of idling with extended (20-80 min) idling, full load after idle, "stabilized" full load, and 30% load. The diluted exhaust was sampled with high volume samplers on glass fiber fluorocarbon coated filters. The filters were extracted with dichloromethane and DNA damage was analyzed in A549 cells using comet assay, with the inclusion of formamidopyrimidine DNA glycosylase (FPG) and endonuclease III (ENDOIII) to recognize oxidized DNA bases. The cells were exposed to extractable organic matter (EOM) for 4 and 24 h at non-cytotoxic dose corresponding to 0.001 m3 of undiluted exhaust gas per ml cell media. At the 4 h exposure interval, all samples from B100 and diesel emissions induced DNA damage. EOM from the extended idle engine mode exerted the strongest genotoxic effect for both fuels. Twenty hours later, the cells exposed to diesel EOM exhibited a further increase of DNA strand breaks compared to the preceding interval. In contrast, DNA damage seemed to be fully repaired in cells treated with EOM derived from biodiesel B100. The preliminary results suggest that (i) diesel emissions are more genotoxic than the emissions from B100, (ii) biodiesel induced DNA lesions are repaired within 24 h.

Inflammatory marker and aryl hydrocarbon receptor-dependent responses in human macrophages exposed to emissions from biodiesel fuels.

Biodiesel or renewable diesel fuels are alternative fuels produced from vegetable oil and animal tallow that are being considered to help reduce the use of petroleum-based fuels and emissions of air pollutants including greenhouse gases. Here, we analyzed the gene expression of inflammatory marker responses and the cytochrome P450 1A1 (CYP1A1) enzyme after exposure to diesel and biodiesel emission samples generated from an in-use heavy-duty diesel vehicle. Particulate emission samples from petroleum-based California Air Resource Board (CARB)-certified ultralow sulfur diesel (CARB ULSD), biodiesel, and renewable hydro-treated diesel all induced inflammatory markers such as cyclooxygenase-2 (COX)-2 and interleukin (IL)-8 in human U937-derived macrophages and the expression of the xenobiotic metabolizing enzyme CYP1A1. Furthermore, the results indicate that the particle emissions from CARB ULSD and the alternative diesel fuel blends activate the aryl hydrocarbon receptor (AhR) and induce CYP1A1 in a dose- and AhR-dependent manner which was supported by the AhR luciferase reporter assay and gel shift analysis. Based on a per mile emissions with the model year 2000 heavy duty vehicle tested, the effects of the alternative diesel fuel blends emissions on the expression on inflammatory markers like IL-8 and COX-2 tend to be lower than emission samples derived from CARB ULSD fuel. The results will help to assess the potential benefits and toxicity from biofuel use as alternative fuels in modern technology diesel engines.

Table of contents Ujjwala 2. 0 from access to sustained usage

By September 2019, some 80 million poor households will have been connected to LPG since 2015 through the national programme, Pradhan Mantri Ujjwala Yojana (Ujjwala). This is in addition to "normal" growth in LPG connections amounting to approximately 40 million households. By any account, this is a remarkable achievement, bringing total households with LPG connections from about 60% of the country early this decade to some 95% by the beginning of the next. Connection, however, does not mean full usage and many new Ujjwala households and others continue to use significant amounts of biomass fuel, with consequent impacts on the health of village populations from the smoke. In addition, it is now well established that smoke from household biomass use is the largest single source of outdoor air pollution in the country, although of course not the only one.3 Its continued use thus is a problem for all Indians. How to continue to fulfill the promise of Ujjwala in its second phase, here called Ujjwala 2.0, is an important policy discussion in the country.

Identification and validation of SNP markers linked to seed toxicity in Jatropha curcas L.

Edible/non-toxic varieties of Jatropha curcas L. are gaining increasing attention, providing both oil as biofuel feedstock or even as edible oil and the seed kernel meal as animal feed ingredient. They are a viable alternative to the limitation posed by the presence of phorbol esters in toxic varieties. Accurate genotyping of toxic/non-toxic accessions is critical to breeding management. The aim of this study was to identify SNP markers linked to seed toxicity in J. curcas. For SNP discovery, NGS technology was used to sequence the whole genomes of a toxic and non-toxic parent along with a bulk of 51 toxic and 30 non-toxic F2 plants. To ascertain the association between SNP markers and seed toxicity trait, candidate SNPs were genotyped on 672 individuals segregating for seed toxicity and two collections of J. curcas composed of 96 individuals each. In silico SNP discovery approaches led to the identification of 64 candidate SNPs discriminating non-toxic and toxic samples. These SNPs were mapped on Chromosome 8 within the Linkage Group 8 previously identified as a genomic region important for phorbol ester biosynthesis. The association study identified two new SNPs, SNP_J22 and SNP_J24 significantly linked to low toxicity with R2 values of 0.75 and 0.54, respectively. Our study released two valuable SNP markers for high-throughput, marker-assisted breeding of seed toxicity in J. curcas.

Inflammatory and functional responses after (bio)diesel exhaust exposure in allergic sensitized mice. A comparison between diesel and biodiesel.

Many cities fail to meet air quality standards, which results in increased risk for pulmonary disorders, including asthma. Human and experimental studies have shown that diesel exhaust (DE) particles are associated with worsening of allergic asthma. Biodiesel (BD), a cleaner fuel from renewable sources, was introduced in the eighties. Because of the reduction in particulate matter (PM) emissions, BD was expected to cause fewer adverse pulmonary effects. However, only limited data on the effect of BD emissions in asthma are available. OBJECTIVE: Determine whether BD exhaust exposure in allergic sensitized mice leads to different effects on inflammatory and functional responses compared to DE exposure. METHODS: Balb/C mice were orotracheally sensitized with House Dust Mite (HDM) or a saline solution with 3 weekly instillations. From day 9 until day 17 after sensitization, they were exposed daily to filtered air (FA), DE and BD exhaust (concentration: 600 µg/m3 PM2.5). Lung function, bronchoalveolar lavage fluid (BALF) cell counts, cytokine levels (IL-2, IL-4, IL-5, IL-17, TNF-α, TSLP) in the BALF, peribronchiolar eosinophils and parenchymal macrophages were measured. RESULTS: HDM-sensitized animals presented increased lung elastance (p = 0.046), IgG1 serum levels (p = 0.029), peribronchiolar eosinophils (p = 0.028), BALF levels of total cells (p = 0.020), eosinophils (p = 0.028), IL-5 levels (p = 0.002) and TSLP levels (p = 0.046) in BALF. DE exposure alone increased lung elastance (p = 0.000) and BALF IL-4 levels (p = 0.045), whereas BD exposure alone increased BALF TSLP levels (p = 0.004). BD exposure did not influence any parameters after HDM challenge, while DE exposed animals presented increased BALF levels of total cells (p = 0.019), lymphocytes (p = 0.000), neutrophils (p = 0.040), macrophages (p = 0.034), BALF IL-4 levels (p = 0.028), and macrophagic inflammation in the lung tissue (p = 0.037), as well as decreased IgG1 (p = 0.046) and IgG2 (p = 0.043) levels when compared to the HDM group. CONCLUSION: The results indicate more adverse pulmonary effects of DE compared to BD exposure in allergic sensitized animals.