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Fuel spills in marine environments pose significant threats to aquatic ecosystems, evidencing the intricate relationship between fuel utilization and its impact on benthic species of commercial value for human consumption. This interconnectedness of human, animal and environmental welfare falls within the One Health framework. The aim of the present study was to evaluate the toxicological effects of diesel oil on the green crab Carcinus maenas, and make a parallelism between tested concentrations and petrogenic hydrocarbon levels in natural environments. Mortality, locomotion and feeding behavior, molting, somatic growth, morphological malformations, stress biomarkers, and nutritional variables were analyzed in three different bioassays. In Bioassay 1, prepuberal females were exposed to diesel oil water accommodated fraction (WAF) to determine the median lethal concentration (LC 50 ) at different periods. In Bioassay 2, prepuberal females were exposed to 168 h LC 50 and LC 25 of diesel oil WAF for 7 days, and were subsequently exposed to clean water. In Bioassay 3, prepuberal females were exposed to 168 h LC 12 and LC 6 of diesel oil WAF for 30 days. Petrogenic hydrocarbon levels in the field were quantified at a port and a nature reserve, with concentrations of aromatic hydrocarbons being 1.92 μg/g in the former and below 0.01 μg/g in the latter. In Bioassay 1, the 168 h LC 50 was estimated to be 1.04 % of diesel oil. The results obtained in Bioassays 2 (LC 50 and LC 25 ) and Bioassays 3 (LC 12 and LC 6 ) suggest that environmental exposure to petrogenic hydrocarbons produces high mortality or interferes with the molting process of crabs, leading to reduced growth and developmental abnormalities. Such malformations were observed in chelipeds, pereiopods, gills chambers and eye peduncles, and affected feeding and locomotion behaviors. Overall, this could impact on population size and health, and consequently alter the ecological role and commercial exploitation of economically important species like C. maenas., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Continental aquatic environments have undergone chemical pollution due to increased anthropogenic activities. Among those substances, petroleum hydrocarbons are a potential hazard for the aquatic animals. Additionally, alterations in the abiotic characteristics of the water, such as temperature and pH, can impose additional stress when those substances are present. We evaluate how alterations in water temperature and pH modified the acute (96 h) toxicity of the water-soluble fraction of gasoline (WSF G ) to Astyanax altiparanae through physiological analysis. We also investigated the physiological responses after the fish recovery from exposure (96 h) in clean water. Both isolated and combined exposures to WSF G resulted in significant physiological changes. Alone, WSF G altered energetic metabolism and haematopoietic functions, potentially due to metabolic hypoxia. When combined with changes in water temperature (30 °C) and pH (4.0), A. altiparanae activated additional physiological mechanisms to counterbalance osmoregulatory and acid-base imbalances, likely exacerbated by severe metabolic hypoxia. In both isolated and combined exposure scenarios, A. altiparanae maintained cellular hydration, suggesting a robust capacity to uphold homeostasis under environmental stress conditions. Following a recovery in clean water, energetic metabolism returned to control levels. Nevertheless, plasmatic Na + and Cl - levels and haematological parameters remained affected by WSF G exposure. Our findings underscore the impact of interactions between WSF G contaminants, temperature and pH, leading to additional biological damage in A. altiparanae., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: Biodiesel, a renewable diesel fuel that can be created from almost any natural fat or oil, is promoted as a greener and healthier alternative to commercial mineral diesel without the supporting experimental data to back these claims. The aim of this research was to assess the health effects of acute exposure to two types of biodiesel exhaust, or mineral diesel exhaust or air as a control in mice. Male BALB/c mice were exposed for 2-hrs to diluted exhaust obtained from a diesel engine running on mineral diesel, Tallow biodiesel or Canola biodiesel. A room air exposure group was used as a control. Twenty-four hours after exposure, a variety of respiratory related end point measurements were assessed, including lung function, responsiveness to methacholine and airway and systemic immune responses., Results: Tallow biodiesel exhaust exposure resulted in the greatest number of significant effects compared to Air controls, including increased airway hyperresponsiveness (178.1 ± 31.3% increase from saline for Tallow biodiesel exhaust exposed mice compared to 155.8 ± 19.1 for Air control), increased airway inflammation (63463 ± 13497 cells/mL in the bronchoalveolar lavage of Tallow biodiesel exhaust exposed mice compared to 40561 ± 11800 for Air exposed controls) and indications of immune dysregulation. In contrast, exposure to Canola biodiesel exhaust resulted in fewer significant effects compared to Air controls with a slight increase in airway resistance at functional residual capacity and indications of immune dysregulation. Exposure to mineral diesel exhaust resulted in significant effects between that of the two biodiesels with increased airway hyperresponsiveness and indications of immune dysregulation., Conclusion: These data show that a single, brief exposure to biodiesel exhaust can result in negative health impacts in a mouse model, and that the biological effects of exposure change depending on the feedstock used to make the biodiesel., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

The environmental impact of oil spills is a critical concern, particularly pertaining to low sulfur marine diesel (LSMD) and high sulfur fuel oil (HSFO) that are commonly involved in coastal spills. Although transcriptomic biomonitoring of sentinel animals can be a powerful tool for assessing biological effects, conventional methods utilize lethal sampling to examine the liver. As a non-lethal alternative, we have previously shown salmonid caudal fin cyp1a1 is significantly responsive to LSMD-derived toxicants. The present study further investigated the transcriptomic biomonitoring potential of coho salmon smolt caudal fin in comparison to liver tissue in the context of LSMD and HSFO seawater accommodated fraction (seaWAF) exposure in cold-water marine environments. Assessing the toxicity of these seaWAFs involved quantifying polycyclic aromatic hydrocarbon (tPAH50) concentrations and generating gene expression profiles. Initial qPCR analyses revealed significant cyp1a1 response in both liver and caudal fin tissues of both genetic sexes to all seaWAF exposures. RNA-Seq analysis, focusing on the highest LSMD and HSFO seaWAF concentrations (28.4±1.8 and 645.08±146.3 µg/L tPAH50, respectively), revealed distinct tissue-specific and genetic sex-independent transcriptomic responses with an overall enrichment of oxidative stress, cell adhesion, and morphogenesis-related pathways. Remarkably, the caudal fin tissue exhibited transcriptomic response patterns comparable to liver tissue, particularly consistent differential expression of 33 gene transcripts in the liver (independent of sex and oil type) and 44 in the caudal fin. The present work underscores the viability of using the caudal fin as a non-lethal alternative to liver sampling for assessing and tracking oil spill exposure in marine environments., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

The present study evaluated the protective effect of ascorbic acid (ASCB) against gasoline fumes (PET) induced testicular oxidative stress, sperm toxicity, and testosterone imbalance in Wistar rats. Twenty-four (24) male albino rats (75 ± 16 g) were randomized into three experimental groups ( N = 8). The control group: received normal saline, PET group: exposed to PET 6 h daily by inhalation in an exposure chamber and PET + 200 mg ASCB/kg body weight group: exposed to PET 6 h daily by inhalation and administered ASCB per os . Treatment of ASCB and PET exposure was done thrice and five times weekly for a period of 10 weeks respectively. ASCB co-treatment prevented PET-induced increases in the oxidative stress markers (glutathione, glutathione S -transferase, superoxide dismutase, catalase, hydrogen peroxide generation, nitric oxide, and lipid peroxidation) and serum testosterone concentration ( p < .05). Sperm quality was low and those with damaged heads and tails increased alongside histological injuries in the PET-exposed rats, which were also minimized with ASCB administration. ASCB protected against PET-induced oxidative stress, sperm, and testis damage in rats., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Gasoline station attendants are exposed to numerous chemicals that might have genotoxic and carcinogenic potential, such as benzene in fuel vapor and particulate matter and polycyclic aromatic hydrocarbons in vehicle exhaust emission. According to IARC, benzene and diesel particulates are Group 1 human carcinogens, and gasoline has been classified as Group 2A "possibly carcinogenic to humans." At gas stations, self-service is not implemented in Turkey; fuel-filling service is provided entirely by employees, and therefore they are exposed to those chemicals in the workplace during all working hours. Genetic monitoring of workers with occupational exposure to possible genotoxic agents allows early detection of cancer. We aimed to investigate the genotoxic damage due to exposures in gasoline station attendants in Turkey. Genotoxicity was evaluated by the Comet, chromosomal aberration, and cytokinesis-block micronucleus assays in peripheral blood lymphocytes. Gasoline station attendants ( n = 53) had higher tail length, tail intensity, and tail moment values than controls ( n = 61). In gasoline station attendants ( n = 46), the frequencies of chromatid gaps, chromosome gaps, and total aberrations were higher compared with controls ( n = 59). Increased frequencies of micronuclei and nucleoplasmic bridges were determined in gasoline station attendants ( n = 47) compared with controls ( n = 40). Factors such as age, duration of working, and smoking did not have any significant impact on genotoxic endpoints. Only exposure increased genotoxic damage in gasoline station attendants independently from demographic and clinical characteristics. Occupational exposure-related genotoxicity risk may increase in gasoline station attendants who are chronically exposed to gasoline and various chemicals in vehicle exhaust emissions., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Petrol vapors as important occupational and environmental pollutants can cause oxidative stress and may play a role in the development of neurodegenerative diseases along with the risk factors involved. This research is designed as a preliminary study to evaluate the protective effects of apigenin (APG) on oxidative stress caused by petrol vapors inhalation in rats. A total of 24 male Wistar rats were randomly divided into four groups inside the inhalation chamber. Body weight changes and oxidative stress markers were investigated. The average body weight of the group exposed to petrol vapors was significantly lower compared to the other groups. The level of reactive oxygen species (ROS), content of oxidized-glutathione (GSSG), and Malondialdehyde were found to be higher in the petrol-inhaled group, while the content of reduced-glutathione (GSH) was lower compared to the other groups. APG administration did result in any significant improvement in these toxicities induced by petrol vapor. APG administration may ameliorate the petrol-induced oxidative stress. In chronic exposures, in addition to personal protection and engineering control, the use of compounds of natural origin may help in reducing the side effects (such as CNS) caused by exposure to petrol vapors.

The differences in the traffic fuels have been shown to affect exhaust emissions and their toxicity. Especially, the aromatic content of diesel fuel is an important factor considering the emissions, notably particulate matter (PM) concentrations. The ultra-fine particles (UFP, particles with a diameter of <100 nm) are important components of engine emissions and connected to various health effects, such as pulmonary and systematic inflammation, and cardiovascular disorders. Studying the toxicity of the UFPs and how different fuel options can be used for mitigating the emissions and toxicity is crucial. In the present study, emissions from a heavy-duty diesel engine were used to assess the exhaust emission toxicity with a thermophoresis-based in vitro air-liquid interface (ALI) exposure system. The aim of the study was to evaluate the toxicity of engine exhaust and the potential effect of 20 % aromatic fossil diesel and 0 % aromatic renewable diesel fuel on emission toxicity. The results of the present study show that the aromatic content of the fuel increases emission toxicity, which was seen as an increase in genotoxicity, distinct inflammatory responses, and alterations in the cell cycle. The increase in genotoxicity was most likely due to the PM phase of the exhaust, as the exposures with high-efficiency particulate absorbing (HEPA)-filtered exhaust resulted in a negligible increase in genotoxicity. However, the solely gaseous exposures still elicited immunological responses. Overall, the present study shows that decreasing the aromatic content of the fuels could be a significant measure in mitigating traffic exhaust toxicity., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Exhaust emissions from gasoline vehicles are one of the major contributors to aerosol particles observed in urban areas. It is well-known that these tiny particles are associated with air pollution, climate forcing, and adverse health effects. However, their toxicity and bioreactivity after atmospheric ageing are less constrained. The aim of the present study was to investigate the chemical and toxicological properties of fresh and aged particulate matter samples derived from gasoline exhaust emissions. Chemical analyses showed that both fresh and aged PM samples were rich in organic carbon, and the dominating chemical species were n-alkane and polycyclic aromatic hydrocarbons. Comparisons between fresh and aged samples revealed that the latter contained larger amounts of oxygenated compounds. In most cases, the bioreactivity induced by the aged PM samples was significantly higher than that induced by the fresh samples. Moderate to weak correlations were identified between chemical species and the levels of biomarkers in the fresh and aged PM samples. The results of the stepwise regression analysis suggested that n-alkane and alkenoic acid were major contributors to the increase in lactate dehydrogenase (LDH) levels in the fresh samples, while polycyclic aromatic hydrocarbons (PAHs) and monocarboxylic acid were the main factors responsible for such increase in the aged samples., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Biodiesel usage is increasing steadily worldwide as the push for renewable fuel sources increases. The increased oxygen content in biodiesel fuel is believed to cause decreased particulate matter (PM) and increased nitrous oxides within its exhaust. The addition of fuel additives to further increase the oxygen content may contribute to even further benefits in exhaust composition. The aim of this study was to assess the toxicity of 10% (v/v) diethylene glycol dimethyl ether (DGDME) added as a biodiesel fuel additive. Primary human airway epithelial cells were grown at the air-liquid interface and exposed to diluted exhaust from an engine running on either grapeseed, bran, or coconut biodiesel or the same three biodiesels with 10% (v/v) DGDME added to them; mineral diesel and air were used as controls. Exhaust properties, culture permeability, epithelial cell damage, and IL-6 and IL-8 release were measured postexposure. The fuel additive DGDME caused a decrease in PM and nitrous oxide concentrations. However, exhaust exposure with DGDME also caused decreased permeability, increased epithelial cell damage, and increased release of IL-6 and IL-8 ( p < 0.05). Despite the fuel additive having beneficial effects on the exhaust properties of the biodiesel, it was found to be more toxic.

We investigated the biological response of soluble organic fraction (SOF) and water-soluble fraction (WSF) extracted from particulate matter (PM) emitted by an automotive diesel engine operating in a representative urban driving condition. The engine was fueled with ultra-low sulfur diesel (ULSD), and its binary blends by volume with 13% of butanol (Bu13), and with hydrotreated vegetable oil (HVO) at 13% (HVO13) and 20% (HVO20). Cytotoxicity, genotoxicity, oxidative DNA damage and ecotoxicity tests were carried out, and 16 polycyclic aromatic hydrocarbons (PAH) expressed as tbenzo(a)pyrene total toxicity equivalent (BaP-TEQ) were also analyzed. The Hepatocarcinoma epithelial cell line (HepG2) was exposed to SOF for 24 h and analyzed using comet assay, with the inclusion of formamidopyrimidine DNA glycosylase (FPG) and endonuclease III (Endo III) to recognize oxidized DNA bases. The WSF was evaluated through acute ecotoxicity tests with the aquatic microcrustacean Daphnia pulex (D. Pulex). Results showed that there was no cytotoxic activity for all tested SOF concentrations. Genotoxic responses by all the SOF samples were at same level, except for the HVO13 which was weaker in the absence of the enzymes. The addition of the FPG and Endo III enzymes resulted in a significant increase in the comet tail, indicating that the DNA damage from SOF for all tested fuel blends involves oxidative damage including a higher level of oxidized purines for ULSD and Bu13 in comparison with HVO blends, but the oxidized pyrimidines for HVO blends were slightly higher compared to Bu13. The WSF did not show acute ecotoxicity for any of the fuels. Unlike other samples, Bu13-derived particles significantly increase the BaP-TEQ. The contribution to the genotoxic activity and oxidative DNA from SOF was not correlated to BaP-TEQ, which means that the biological activity of PM might be affected also by other toxic compounds present in particulate phase., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Gasoline is an essential petroleum-derived product powering the automotive economy worldwide. This research focused on the Volatile Organic Component (VOC) cocktail resulting from gasoline evaporation. Petroleum fugitive VOC inhalation by petrol station attendants have been widely associated with toxicological and health risks concerns. Another unusual practice in poor nations is gasoline sniffing to get high which can lead to intoxication and organ damages. In this study, a static air/liquid interface methodology was designed to emulate acute human lung-derived cell exposure to all the gasoline-derived generated VOCs. The research investigated the cytotoxic and genotoxic end points resulting from whole gasoline fumes in vitro exposure using A549 cells. Petroleum-derived VOCs were identified and characterized by GC-MS. VOCs exposure was emulated in a controlled environment by evaporating spiked crude gasoline (1 to 100 μl) in a closed exposure chamber. In the chamber, A549 cultured cells on snapwell inserts were exposed on their apical side to various concentrations of generated vapors for one hour at 37 °C to mimic lung exposure. The results indicated that acute gasoline whole VOCs exposure reduced cell viability (IC 50  = 485 ppm immediately and IC 50  = 516 ppm 24 h post-exposure), disrupted cell membrane integrity though LDH leakage and induced DNA damages. Furthermore, VOC exposure triggered caspase-independent apoptosis in exposed cells through upregulation of apoptotic pathways. Overall, the presented findings generated by the static exposure technique showed a practical and reproducible model that can be used to assess acute crude VOCs mixture toxicity endpoints and cell death pathways., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Impacts of inhaling gasoline fumes on the lungs of adult male rats and the alleviating role of fenugreek seeds were evaluated. Twenty-four rats were divided into four groups, unexposed control and fenugreek groups, gasoline exposed groups for 6 h/6 day/week for 10 weeks with and without supplementation of fenugreek seed powder in food (5% w/w). Rats exposed to gasoline fumes showed significant elevation in lung tumor necrosis factor-α, as an inflammatory marker, and the proapoptotic marker Bax with a reduction in the antiapoptotic marker Bcl2. Moreover, remarkable elevations in transforming growth factor-β1, collagen and hydroxyproline were observed as fibrotic markers. Lung oxidative stress markers (hydrogen peroxides, malondialdehyde, and protein carbonyl) increased significantly along with marked decrease in total antioxidant capacity, superoxide dismutase, and catalase levels. Additionally, marked decreases in white and red blood cell counts, hemoglobin content, platelet count, accompanied by elevated red cell distribution width percentage were observed, supporting the inflammatory status. Histopathological changes represented by hematoxylin&eosin, immunohistochemistry staining for Bax&Bcl2, and transmission electron microscopy supported the negative impacts of gasoline fumes compared to the control group. Fenugreek seeds supplementation with gasoline exposure showed pronounced alleviation of lung biochemical and histopathological changes compared to the gasoline-exposed group., (© 2022. The Author(s).)

There is an increasing concern related to the toxic effects of the soluble portion of diesel oil on aquatic ecosystems and the organisms living in them. In this context, the aim of this study was to analyze the effects of diesel water accommodated-fraction (WAF) on behavioral and biochemical responses of mussels Perna perna. Animals were exposed to 5 and 20% of WAF for 96 h. Prior to the beginning of the experiments, Hall effect sensors and magnets were attached to the valves of the mussels. Valve gaping behavior was continuously recorded for 12 h of exposure and tissues (gills and digestive gland) were separated after 96 h of exposure. Overall, both behavior and biochemical biomarkers were altered due to WAF exposure. Animals exposed to WAF reduced the average amplitude of the valves and the fraction of time opened, and presented greater transition frequency, demonstrating avoidance behavior over the 12 h period. Furthermore, the biochemical biomarkers (GSH, GST, SOD and CAT) were altered following the 96 h of exposure to WAF. Considering the results presented, this study demonstrates the toxic potential of WAF in both shorter and longer exposure periods., (Copyright © 2022. Published by Elsevier B.V.)

Gasoline exposure has been widely reported in the literature as being toxic to human health. However, the exact underlying molecular mechanisms triggered by its inhalation have not been thoroughly investigated. We herein present a model of sub-chronic, static gasoline vapor inhalation in adult female C57BL/6 mice. Animals were exposed daily to either gasoline vapors (0.86 g/animal/90 min) or ambient air for 5 days/week over 7 consecutive weeks. At the end of the study period, toxic and molecular mechanisms underlying the inflammatory, oxidative, and apoptotic effects triggered by gasoline vapors, were examined in the lungs and liver of gasoline-exposed (GE) mice. Static gasoline exposure induced a significant increase (+21%) in lungs/body weight (BW) ratio in GE versus control (CON) mice along with a pulmonary inflammation attested by histological staining. The latter was consistent with increases in the transcript levels of proinflammatory cytokines [Interleukins (ILs) 4 and 6], respectively by ~ 6- and 4-fold in the lungs of GE mice compared to CON. Interestingly, IL-10 expression was also increased by ~ 10-fold in the lungs of GE mice suggesting an attempt to counterbalance the established inflammation. Moreover, the pulmonary expression of IL-12 and TNF-α was downregulated by 2- and 4-fold, respectively, suggesting the skewing toward Th2 phenotype. Additionally, GE mice showed a significant upregulation in Bax/Bcl-2 ratio, caspases 3, 8, and 9 with no change in JNK expression in the lungs, suggesting the activation of both intrinsic and extrinsic apoptotic pathways. Static gasoline exposure over seven consecutive weeks had a minor hepatic portal inflammation attested by H&E staining along with an increase in the hepatic expression of the mitochondrial complexes in GE mice. Therefore, tissue damage biomarkers highlight the health risks associated with vapor exposure and may present potential therapeutic targets for recovery from gasoline intoxication., (© 2022 John Wiley & Sons, Ltd.)

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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Even though petrochemical contamination frequently occurs in the form of oil spills, it is thought that a greater danger to coastal habitats is posed by chronic petrochemical toxicity associated with urban run-off, in which gasoline water-soluble-fraction (WSF) plays an important role. The hypothesis of the entrepreneurs, who were associated to the scientists uncharged of this research, was that recycled petrochemical waste may provide different gasoline formulations, having different toxic properties; the correlation between the gasoline formulations and their components’ toxicological effects might contribute to the reformulation of the products, in such a way that the gasoline generated could be less toxic and less harmful to the environment. The aim of this research was to determine the toxic effects of 14 different types of gasoline (formulated, in accordance with National Petroleum Agency standards, from petrochemical waste), on Tetraselmis chuii (microalgae culture) and Crassostrea rhizophorae (embryos). Microalgae and oyster embryos were exposed to different gasoline formulations water-soluble fractions (WSF) at a range of concentrations (0%, 4. 6%, 10. 0%, 22. 0%, 46. 0%, and 100%), for 96 and 24h, respectively. The tests were carried out under controlled conditions. End-points have been CI50-96h (concentration causing 50% growth inhibition in microalgae cultures) and EC50-24h (concentration causing abnormalities on 50% of the exposed embryos). Through these procedures, gasoline formulations, which represent the lowest environmental risk, were selected. Bioassays carried out on the 8 different gasoline components aimed to correlate gasoline toxicity with the toxic potential of its components. The analysis of principal components showed that the C9DI, a mixture of aromatic hydrocarbons of 9 carbon atoms, had the highest level of toxic potential, followed by C9S (a mixture of aromatics with 9–11 carbon atoms) and heavy naphtha. The results showed gasoline formulations 1–4 (monoaromatic hydrocarbons being the most conspicuous components) to be the least toxic, whilst formulations 12–14 (having higher content of C9DI, C9S and naphtha) were found to be the most harmful to organisms. This study led to the identification of the most toxic WSF gasoline components (C9DI and C9S), and to the possibility of developing more eco-compatible gasoline formulations. [Copyright &y& Elsevier]

Long-term exposure to organic solvents is known to affect human health posing serious occupational hazards. Organic solvents are genotoxic, and they can cause genetic changes in the exposed employees' somatic or germ cells. Chemicals such as benzene, toluene, and gasoline induce an excessive amount of genotoxicity results either in genetic polymorphism or culminates in deleterious mutations when concentration crosses the threshold limits. The impact of genotoxicity is directly related to the time of exposure, types, and quantum of solvent. Genotoxicity affects almost all the physiological systems, but the most vulnerable ones are the nervous system, reproductive system, and blood circulatory system. Based on the available literature report, we propose to evaluate the outcomes of such chemicals on the exposed humans at the workplace. Attempts would be made to ascertain if the long-term exposure makes a person resistant to such chemicals. This may seem to be a far-fetched idea but has not been studied. The health prospect of this study is envisaged to complement the already existing data facilitating a deeper understanding of the genotoxicity across the population. This would also demonstrate if it correlates with the demographic profile of the population and contributes to comorbidity and epidemiology., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Exhaust fumes from petrol/diesel-powered electric generators contribute significantly to air pollution in many developing countries, constituting health hazards to both humans and animals. This study evaluated the serum concentrations of Troponin I (TnI), C-reactive protein (CRP) and serum levels/activities of oxidative stress markers: catalase (CAT), reduced glutathione (GSH), malondialdehyde (MDA), nitric oxide (NO) and superoxide dismutase (SOD) in dogs experimentally exposed to graded levels of petrol generator exhaust fume (PGEF). Sixteen (16) healthy and adult male Basenji dogs were randomly assigned into four groups (A-D). Group A was the unexposed control while groups B, C and D were exposed to PGEF for 1, 2 and 3 h per day, respectively, for 90 days. Repeated analysis were performed at the baseline, and every thirty days, for a total of 90 days. There was a significant interaction (p < 0.05) between the effects of PGEF exposure level (in h/day) and duration of exposure (in months) on all the tested serum parameters. There was a significant main effect (p < 0.05) for PGEF exposure level on the serum parameters. As the level of PGEF exposure was increased, the serum concentrations of TnI, CRP, CAT, MDA and NO increased, GSH decreased, whereas SOD activity increased by day 30 but declined at the end. Moreover, there was a significant simple main effect (p < 0.05) for duration of PGEF exposure. All the parameters increased as the duration of PGEF exposure was increased to 90 days except GSH concentration which decreased, whereas SOD activity increased initially but declined at the end of the study. Thus, there was increased serum concentrations of TnI, CRP and increased oxidative stress in the PGEF-exposed dogs. These findings are instructive and could be grounds for further studies on air pollutants-induced cardiovascular disease given the widespread use of electricity generators in many low-resource countries., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Emissions from road traffic are among the major contributors to air pollution worldwide and represent a serious environmental health risk. Although traffic-related pollution has been most commonly associated with diesel engines, increasing evidence suggests that gasoline engines also produce a considerable amount of potentially hazardous particulate matter (PM). The primary objective of this study was to compare the intrinsic toxic properties of the organic components of PM, generated by a conventional gasoline engine fueled with neat gasoline (E0), or gasoline-ethanol blend (15 % ethanol, v/v, E15). Our results showed that while E15 has produced, compared to gasoline and per kg of fuel, comparable particle mass (μg PM/kg fuel) and slightly more particles by number, the organic extract from the particulate matter produced by E15 contained a larger amount of harmful polycyclic aromatic hydrocarbons (PAHs), as determined by the chemical analysis. To examine the toxicity, we monitored genome-wide gene expression changes in human lung BEAS-2B cells, exposed for 4 h and 24 h to a subtoxic dose of each PM extract. After 4 h exposure, numerous dysregulated genes and processes such as oxidative stress, lipid and steroid metabolism, PPARα signaling and immune response, were found to be common for both extract treatments. On the other hand, 24 h exposure resulted in more distinctive gene expression patterns. Although we identified several common modulated processes indicating the metabolism of PAHs and activation of aryl hydrocarbon receptor (AhR), E15 specifically dysregulated a variety of other genes and pathways related to cancer promotion and progression. Overall, our findings suggest that the ethanol addition to gasoline changed the intrinsic properties of PM emissions and increased the PAH content in PM organic extract, thus contributing to a more extensive toxic response particularly after 24 h exposure in BEAS-2B cells., (Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.)

Road traffic emissions consist of gaseous components, particles of various sizes, and chemical compounds that are bound to them. Exposure to vehicle emissions is implicated in the etiology of inflammatory respiratory disorders. We investigated the inflammation-related markers in human bronchial epithelial cells (BEAS-2B) and a 3D model of the human airways (MucilAir™), after exposure to complete emissions and extractable organic matter (EOM) from particles generated by ordinary gasoline (E5), and a gasoline-ethanol blend (E20; ethanol content 20% v/v). The production of 22 lipid oxidation products (derivatives of linoleic and arachidonic acid, AA) and 45 inflammatory molecules (cytokines, chemokines, growth factors) was assessed after days 1 and 5 of exposure, using LC-MS/MS and a multiplex immunoassay, respectively. The response observed in MucilAir™ exposed to E5 gasoline emissions, characterized by elevated levels of pro-inflammatory AA metabolites (prostaglandins) and inflammatory markers, was the most pronounced. E20 EOM exposure was associated with increased levels of AA metabolites with anti-inflammatory effects in this cell model. The exposure of BEAS-2B cells to complete emissions reduced lipid oxidation, while E20 EOM tended to increase concentrations of AA metabolite and chemokine production; the impacts on other inflammatory markers were limited. In summary, complete E5 emission exposure of MucilAir™ induces the processes associated with the pro-inflammatory response. This observation highlights the potential negative health impacts of ordinary gasoline, while the effects of alternative fuel are relatively weak., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Outdoor air pollution is classified as carcinogenic to humans and exposure to it contributes to increased incidence of various diseases, including cardiovascular, neurological or pulmonary disorders. Vehicle engine emissions represent a significant part of outdoor air pollutants, particularly in large cities with high population density. Considering the potentially negative health impacts of engine emissions exposure, the application of reliable test systems allowing assessment of the biological effects of these pollutants is crucial. The exposure systems should use relevant, preferably multicellular, cell models that are treated with the complete engine exhaust (i.e. a realistic mixture of particles, chemical compounds bound to them and gaseous phase) at the air-liquid interface. The controlled delivery and characterization of chemical and/or particle composition of the exhaust should be possible. In this mini-review we report on such exposure systems that have been developed to date. We focus on a brief description and technical characterization of the systems, and discuss the biological parameters detected following exposure to a gasoline/diesel exhaust. Finally, we summarize and compare findings from the individual systems, including their advantages/limitations., (Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.)

Although cancer is traditionally considered a genetic disease, the epigenetic abnormalities, including DNA hypermethylation, histone deacetylation, and/or microRNA dysregulation, have been demonstrated as a hallmark of cancer. Compared with gene mutations, aberrant epigenetic changes occur more frequently, and cellular epigenome is more susceptible to change by environmental factors. Excess cancer risks are positively associated with exposure to occupational and environmental chemical carcinogens, including those from gasoline combustion exhausted in vehicles. Of note, previous studies proposed particulate matter index (PMI) as a measure for gasoline sooting tendency, and showed that, compared with the other molecules in gasoline, 1,2,4-Trimethylbenzene, 2-methylnaphthalene and toluene significantly contribute to PMI of the gasoline blends. Mechanistically, both epigenome and genome are important in carcinogenicity, and the genotoxicity of chemical agents has been thoroughly studied. However, less effort has been put into studying the epigenotoxicity. Moreover, as the blending of ethanol into gasoline substitutes for carcinogens, like benzene, toluene, xylene, butadiene, and polycyclic aromatic hydrocarbons, etc., a reduction of secondary aromatics has been achieved in the atmosphere. This may lead to diminished cancer initiation and progression through altered cellular epigenetic landscape. The present review summarizes the most important findings in the literature on the association between exposures to carcinogens from gasoline combustion, cancer epigenetics and the potential epigenetic impacts of biofuels.

Petroleum product fumes (PPFs) containing toxic organic components are pervasive in the environment, emanating from anthropogenic activities, including petroleum exploration and utilization by end-user activities from petrol-gasoline stations. Petrol station attendants are exposed to PPF through inhalation and dermal contact with consequent toxicological implications. We investigated the effects of chronic exposure (60 and 90 days) to petrol (P), kerosene (K) and diesel (D) alone and combined exposure to petrol, kerosene and diesel (PKD) fumes on hepatotoxicity, haematological function and oxidative stress in rats. Following sacrifice, we evaluated hepatic damage biomarkers, blood glucose, oxidative stress and haematological function. Chronic exposure to PPF significantly increased organo-somatic indices, blood glucose, biomarkers of hepatic toxicity and oxidative stress in an exposure duration-dependent manner. There was a simultaneous decrease in the protective capacity of antioxidants. Furthermore, exposure to PPF increased pro-inflammatory biomarkers in rats (90 > 60 days). Regardless of exposure duration, plateletcrit, mean platelet volume, platelet distribution width and red cell distribution width in the coefficient of variation increased, whereas red blood cell count, haemoglobin, packed cell volume, mean corpuscular volume, mean corpuscular haemoglobin, mean corpuscular haemoglobin concentration, white blood cell, lymphocyte, monocyte-basophil-eosinophil mixed counts and platelet count decreased after 60 and 90 days exposure. Microscopic examination of the liver demonstrated hepatic pathological changes paralleling the duration of exposure to PKD fumes. However, the injury observed was lesser to that of rats treated with the diethylnitrosamine - positive control. Our results expanded previous findings and further demonstrated the probable adverse effect on populations' health occasioned by persistent exposure to PPF. Individuals chronically exposed by occupation to PPF may be at greater risk of developing disorders promoted by continuous oxido-inflammatory perturbation and suboptimal haematological-immunologic function - thereby enabling a permissive environment for pathogenesis notwithstanding the limitation of quantifying PPF absolute values in our model system.

Chronic exposure to benzene is a risk factor for hematological malignancies. Gasoline-station workers are exposed to benzene in gasoline, via both inhalation and dermal contact (attendants and managers) or inhalation (workers in the on-site convenience stores and offices). We have studied the exposure of these workers to benzene and the resulting genotoxic and immunotoxic effects. Levels of urinary trans, trans-muconic acid were higher among gasoline-station workers than among office workers with no known exposure to benzene (comparison group). Among the exposed workers, we observed statistically significant biological effects, including elevated DNA damage (comet assay); higher frequencies of micronuclei and nuclear buds (CBMN assay); lower levels of T-helper lymphocytes and naive Th lymphocytes; lower CD4 / CD8 ratio; and higher levels of NK cells and memory Th lymphocytes. Both groups of exposed workers (inhalation and inhalation + dermal routes) showed similar genotoxic and immunotoxic effects., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Global demand for energy is rapidly increasing, and resources for the production of petroleum-based fuels are running out. For this, renewable fuels like biodiesel and hydrotreated vegetable oil biofuel are considered important alternatives to replace such fuels. In this study, we evaluated the in vitro genotoxicity effect on HepG2 cells of organic material extracted from particulate matter emissions of an engine fueled with conventional diesel or mixtures of diesel with 10% of biomass. The emissions were collected in two operational modes, 2410 rpm (slope simulation) and 1890 rpm (plane). Genotoxicity was evaluated through two methods, chromosomal aberration test and the alkaline comet assay. The former did not show any genotoxic effect, but the latter exhibited a statistically significant effect despite the operational mode of the engine and the concentration organic material extracted. In conclusion, regardless of the concentration of organic material extracted from particulate matter, the operational mode of the engine, or the fuel used, a significant damage of the DNA was found. In general, at the physicochemical level, a decrease in the amount of emissions of the used fuels is not directly related to a decrease in the genotoxicity potential.

Fire suppression agents are recommended for extinguishing fires by flammable liquids and frequently end in water bodies, combined with the fuels. There is a lack of toxicity information on these commercial formulations and the effects of mixtures of fire suppression agents and fuels. The aim of the present study was to evaluate the toxic effects of different fire suppression agents, the gasoline water-soluble fraction (GWSF), and mixtures of each fire suppression agent and GWSF. Individual tests were performed with Daphnia similis and Artemia sp.; the most toxic fire suppression agents to D. similis and Artemia sp. were F-500®, Cold Fire®, Agefoam®, and Kidde Sintex® 1%; the GWSF was the least toxic. The concentration addition model was used to predict the mixture effects and evaluate synergism/antagonism, dose ratio dependence, and dose level dependence. Cold Fire with GWSF showed dose level deviation to D. similis, marked mainly by synergism; for Artemia sp., the dose ratio pattern was predicted, with a synergistic response mainly by Cold Fire. Agefoam and GWSF behaved additively for D. similis and dose ratio for Artemia sp., with synergism being caused by Agefoam. Kidde Sintex 1% with GWSF were dose ratio for both organisms, with Kidde Sintex 1% being responsible for synergism. Our results show that some mixtures of fire suppression agents and GWSF may cause toxicity to aquatic organisms, posing risk in a real environmental scenario, such as a major fire combat. Environ Toxicol Chem 2021;40:767-779. © 2020 SETAC., (© 2020 SETAC.)

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 (OP AA ), 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 OP AA 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., (Copyright © 2020. Published by Elsevier B.V.)

As an ecotoxicological tool, bioassays are an effective screening tool to eliminate plants sensitive to the contaminant of interest, and thereby reduce the number of plant species requiring further study. We conducted a bioassay analysis of fifteen plant species to determine their tolerance to diesel fuel toxicity. Dose-response analysis revealed that increasing diesel fuel concentrations in the soil generally led to a monotonically decreasing biomass in 13 species (P < 0.001), with EC10 values (±SE) ranging from 0.36 ± 0.18 g/kg to 12.67 ± 2.13 g/kg. On the other hand, hydrocarbons had a statistically significant hormetic influence on Medicago sativa (f = 3.90 ± 1.08; P < 0.01). The EC10 and EC50 values (±SE) from the fitted hormetic model were 15.33 ± 1.47 g/kg and 26.89 ± 2.00 g/kg, respectively. While previous studies have shown M. sativa's tolerance of hydrocarbon toxicity, this is the first attempt to describe diesel fuel-induced hormesis in M. sativa using the Cedergreen-Ritz-Streibig model. This study thus shows that hormesis cannot be ignored in plant toxicology research, and that when present, an appropriate statistical model is necessary to avoid drawing wrong conclusions., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Objective: This study assessed the health risk of benzene exposure among Thai gasoline station workers through biomarker detection and experience of adverse symptoms., Methods: Trans, trans-muconic acid (tt-MA) metabolites of benzene were analyzed from spot urine sampled among gasoline station workers after shift work using HPLC-UV. Air benzene monitoring was done with an active sampler connected to a charcoal sorbent tube, and analyzed by GC-FID. The health risk was calculated by using the biomatrix of the likelihood of benzene exposure and the severity of adverse symptoms., Results: The tt-MA concentration, among 235 workers, ranged from less than 10-2159 µg/g Cr, which corresponded to the air benzene concentration range of <0.1 to 65.8 ppb. In total, 32.3% of workers had a higher than acceptable risk level and there was a significant association between gasoline station work zones and the likelihood of benzene exposure as well as the health risk of workers. The health risk levels estimated from the biomarker monitoring were consistent with the risk matrix of air benzene monitoring., Conclusion: This tt-MA biomarker monitoring and biomatrix of health risk assessment is suggested as useful for health surveillance of gasoline station workers exposed to benzene., (© 2021 The Authors. Journal of Occupational Health published by John Wiley & Sons Australia, Ltd on behalf of The Japan Society for Occupational Health.)

Air pollution has become one of the most serious issues for human health and has been shown to be particularly concerning for neural and cognitive health. Recent studies suggest that fine particulate matter of less than 2.5 (PM2.5), common in air pollution, can reach the brain, potentially resulting in the development and acceleration of various neurological disorders including Alzheimer's disease, Parkinson's disease, and other forms of dementia, but the underlying pathological mechanisms are not clear. Astaxanthin is a red-colored phytonutrient carotenoid that has been known for anti-inflammatory and neuroprotective effects. In this study, we demonstrated that exposure to PM2.5 increases the neuroinflammation, the expression of proinflammatory M1, and disease-associated microglia (DAM) signature markers in microglial cells, and that treatment with astaxanthin can prevent the neurotoxic effects of this exposure through anti-inflammatory properties. Diesel particulate matter (Sigma-Aldrich) was used as a fine particulate matter 2.5 in the present study. Cultured rat glial cells and BV-2 microglial cells were treated with various concentrations of PM2.5, and then the expression of various inflammatory mediators and signaling pathways were measured using qRT-PCR and Western blot. Astaxanthin was then added and assayed as above to evaluate its effects on microglial changes, inflammation, and toxicity induced by PM2.5. PM2.5 increased the production of nitric oxide and reactive oxygen species and upregulated the transcription of various proinflammatory markers including Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Tumor necrosis factor α (TNFα), inducible nitric oxide synthase (iNOS), triggering receptor expressed on myeloid cells 2 (TREM2), Toll-like receptor 2/4 (TLR2/4), and cyclooxygenase-2 (COX-2) in BV-2 microglial cells. However, the mRNA expression of IL-10 and arginase-1 decreased following PM2.5 treatment. PM2.5 treatment increased c-Jun N-terminal kinases (JNK) phosphorylation and decreased Akt phosphorylation. Astaxanthin attenuated these PM2.5-induced responses, reducing transcription of the proinflammatory markers iNOS and heme oxygenase-1 (HO-1), which prevented neuronal cell death. Our results indicate that PM2.5 exposure reformulates microglia via proinflammatory M1 and DAM phenotype, leading to neurotoxicity, and the fact that astaxanthin treatment can prevent neurotoxicity by inhibiting transition to the proinflammatory M1 and DAM phenotypes. These results demonstrate that PM2.5 exposure can induce brain damage through the change of proinflammatory M1 and DAM signatures in the microglial cells, as well as the fact that astaxanthin can have a potential beneficial effect on PM2.5 exposure of the brain.

Background: Diesel exhaust is carcinogenic and exposure to diesel particles cause health effects. We investigated the toxicity of diesel exhaust particles designed to have varying physicochemical properties in order to attribute health effects to specific particle characteristics. Particles from three fuel types were compared at 13% engine intake O 2 concentration: MK1 ultra low sulfur diesel (DEP13) and the two renewable diesel fuels hydrotreated vegetable oil (HVO13) and rapeseed methyl ester (RME13). Additionally, diesel particles from MK1 ultra low sulfur diesel were generated at 9.7% (DEP9.7) and 17% (DEP17) intake O 2 concentration. We evaluated physicochemical properties and histopathological, inflammatory and genotoxic responses on day 1, 28, and 90 after single intratracheal instillation in mice compared to reference diesel particles and carbon black., Results: Moderate variations were seen in physical properties for the five particles: primary particle diameter: 15-22 nm, specific surface area: 152-222 m 2 /g, and count median mobility diameter: 55-103 nm. Larger differences were found in chemical composition: organic carbon/total carbon ratio (0.12-0.60), polycyclic aromatic hydrocarbon content (1-27 μg/mg) and acid-extractable metal content (0.9-16 μg/mg). Intratracheal exposure to all five particles induced similar toxicological responses, with different potency. Lung particle retention was observed in DEP13 and HVO13 exposed mice on day 28 post-exposure, with less retention for the other fuel types. RME exposure induced limited response whereas the remaining particles induced dose-dependent inflammation and acute phase response on day 1. DEP13 induced acute phase response on day 28 and inflammation on day 90. DNA strand break levels were not increased as compared to vehicle, but were increased in lung and liver compared to blank filter extraction control. Neutrophil influx on day 1 correlated best with estimated deposited surface area, but also with elemental carbon, organic carbon and PAHs. DNA strand break levels in lung on day 28 and in liver on day 90 correlated with acellular particle-induced ROS., Conclusions: We studied diesel exhaust particles designed to differ in physicochemical properties. Our study highlights specific surface area, elemental carbon content, PAHs and ROS-generating potential as physicochemical predictors of diesel particle toxicity.

Lubricant oils are among oil-based products that are not fully consumed during its use, thereby producing non-biodegradable residues which can cause contamination of natural systems. This study evaluated the toxicity of new and used lubricating oil (0.01 and 0.1 mL L -1 ) in adult Nile tilapia (Oreochromis niloticus), by assessing the effects on oxidative stress, biotransformation enzymes (liver and gills), and histopathological alterations on hepatic and pancreatic tissues after 3 and 7 days of exposure. Results showed that 3-days exposure to 0.1 mL L -1 of used and new lubricating oil increased the activity of superoxide dismutase (SOD) and malondialdehyde (MDA) levels in liver of O. niloticus, respectively. In gills, catalase (CAT) was decreased in fish exposed to 0.1 mL L -1 of non-used oil after 3 days, but pronounced increases in CAT was detected after 7 days-exposure to both new and used oil. Shorter exposure to both concentrations of new and used oil also raised glutathione-S-transferase activity (GST) in gills. Ethoxyresorufin-O-deethylase (EROD) was induced in liver of fish exposed to 0.1 mL L -1 of used oil after 3 and 7 days, however a reduced response of this enzyme was detected in gills of animals from both oil treatments. In vitro analysis showed that hepatic EROD was inhibited by lubricating oil exposures, with more pronounced responses in treatments containing used oil. Hepatic lesions, such as cytoplasmic vacuolization, nuclei abnormally, changes in hepatocytes shape, steatosis, cholestasis, eosinophilic inclusions and necrosis were mainly increased by 7 days exposure to used lubricating oil at higher concentration., Competing Interests: Declaration of competing interest The authors declare no competing financial or other relationship with other people or organizations interests., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Background: Emissions from road traffic are under constant discussion since they pose a major threat to human health despite the increasingly strict emission targets and regulations. Although the new passenger car regulations have been very effective in reducing the particulate matter (PM) emissions, the aged car fleet in some EU countries remains a substantial source of PM emissions. Moreover, toxicity of PM emissions from multiple new types of bio-based fuels remain uncertain and different driving conditions such as the sub-zero running temperature has been shown to affect the emissions. Overall, the current literature and experimental knowledge on the toxicology of these PM emissions and conditions is scarce., Methods: In the present study, we show that exhaust gas PM from newly regulated passenger cars fueled by different fuels at sub-zero temperatures, induce toxicological responses in vitro. We used exhaust gas volume-based PM doses to give us better insight on the real-life exposure and included one older diesel car to estimate the effect of the new emissions regulations., Results: In cars compliant with the new regulations, gasoline (E10) displayed the highest PM concentrations and toxicological responses, while the higher ethanol blend (E85) resulted in slightly lower exhaust gas PM concentrations and notably lower toxicological responses in comparison. Engines powered by modern diesel and compressed natural gas (CNG) yielded the lowest PM concentrations and toxicological responses., Conclusions: The present study shows that toxicity of the exhaust gas PM varies depending on the fuels used. Additionally, concentration and toxicity of PM from an older diesel car were vastly higher, compared to contemporary vehicles, indicating the beneficial effects of the new emissions regulations.

Increased malondialdehyde (MDA) levels are commonly considered an indicator of lipid peroxidation derived from oxidative stress insults promoted by exposure of fish to pollutants. However, a decrease in MDA levels after xenobiotic exposure has been also reported, an effect that is mostly attributed to enhanced antioxidant defenses. In this study, we assessed whether pollutant-mediated MDA decrease would be associated with antioxidant enhancement or with its metabolism by aldehyde dehydrogenase (ALDH) in the liver and gills of lambari (Astyanax altiparanae) exposed to diesel oil (0.001, 0.01, and 0.1 mL/L). MDA levels were decreased in the liver of lambari exposed to diesel. The activities of the antioxidant enzymes, catalase (CAT) and glutathione peroxidase (GPx), were unchanged in the liver, while that of glucose-6-phosphate dehydrogenase (G6PDH) was decreased. In contrast, levels of total glutathione (tGSH) and the activity of glutathione S-transferase (GST) were increased in the liver, which partly support antioxidant protection against lipid peroxidation. More importantly, ALDH activity increased in a concentration-dependent manner, being negatively correlated with MDA levels, indicating MDA metabolism by ALDH. In the gills, diesel exposure increased MDA and lipid hydroperoxide levels, and promoted increases in antioxidant defenses, indicating oxidative stress. Curiously, ALDH activity was undetectable in the gills, supporting the possibility of direct MDA excretion in the water by the gills. Analyses of MDA in the water revealed increased levels of MDA in the aquaria in which the fish were exposed to diesel, compared to control aquaria. A second experiment was carried out in which the fish were intraperitoneally injected with MDA (10 mg/kg) and analyzed after 1, 6, and 12 h. MDA injection caused a time-dependent decrease in hepatic MDA levels, did not alter ALDH, CAT, GPx, and GST activities, and decreased G6PDH activity and tGSH levels. In the gills, MDA injection caused a slight increase in MDA levels after 1 h, but did not alter GPx, G6PDH, and GST activities. MDA injection also enhanced CAT activity and tGSH levels in the gills. MDA concentration in water increased progressively after 1, 6, and 12 h, supporting the hypothesis of direct MDA excretion as an alternative route for MDA elimination in fish. Our results suggest that the decreased MDA levels after exposure of lambari to diesel oil pollutant probably reflects an association between enhanced antioxidant protection, MDA metabolism, and MDA excretion in water., (Copyright © 2019 Elsevier Inc. All rights reserved.)

The present work aimed to investigate the effects of acute (12, 24, 48 and 96 h) and subchronic (168 and 336 h) exposure of seahorse, Hippocampus reidi to water-accommodated fraction (WAF) of diesel fuel on biotransformation parameters, antioxidant defenses and DNA integrity. In addition, a recovery experiment was performed, where the organisms remained in absence of the contaminant for 336 h, after WAF exposure for 168 h (totaling 504 h). At the end of each experimental protocol, the concentration of pyrene-, benzo(a)pyrene- and naphthalene-type metabolites in bile, hepatic activity of glutathione-S-transferase (GST), superoxide dismutase (SOD), and catalase (CAT), as well as lipid peroxidation (LPO) levels in hepatocytes, were analyzed, in addition to the DNA damage and the micronucleus (MN) test in the peripheral blood. It was observed that both acute and subchronic WAF exposure affected the investigated parameters in different ways. In general, the exposed groups presented higher mean values for the investigated parameters if compared with their respective controls. After the recovery experiment, the mean values of PAH metabolites, LPO, DNA damage and MN frequency were significantly lower than those of animals exposed for 168 h, indicating that the recovery period was appropriately long for the evaluated biomarkers return to the control levels. The results indicated that the selected H. reidi biomarkers proved to be adequate and complementary tools in determining the first impacts of acute and subchronic exposure caused by WAF of diesel fuel in fish, as well as their recovery in clean water., (Copyright © 2019. Published by Elsevier B.V.)

Contamination of aquatic environments by petroleum and its products (e.g. gasoline) is a hazard for aquatic organisms as a result of the potential toxicity of monocyclic aromatic hydrocarbons (BTEX) and polycyclic aromatic hydrocarbons (PAH). Our goal was to evaluate the acute effects of the water-soluble fraction of gasoline (WSF G ) on nitrogen excretion, osmoregulation, and metabolism of goldfish Carassius auratus. We first chemically characterized the WSF G and then tested its effects on these physiological aspects of C. auratus, in several different exposure scenarios (0, 0.25, 5, 10 and 25% of WSF G ). The WSF G contained high concentrations BTEX (toluene 70% and benzene 17%) relative to PAH (<1%), and low levels of several metals (Al, Fe, Zn, Sr). Routine O 2 uptake rate (MO 2 ) of goldfish was inhibited by exposure to 5% WSF G , and during post-exposure recovery, MO 2 increased in a dose-dependent fashion. Ammonia excretion was not affected by exposure to WSF G , but urea-N excretion increased progressively with the WSF G concentration. The same pattern of dose/response was observed for net Mg 2+ loss rates and steadily increasing plasma lactate concentrations. Loss rates of Na + , Ca 2+ , K + and Cl - , and plasma concentrations of Mg 2+ and urea-N were not significantly altered. We propose that acute exposure to WSF G inhibits aerobic metabolism and activates anaerobic metabolism, breaking down ATP such that bound Mg 2+ is liberated and the purine ring component is metabolized to urea-N, both of which are subsequently excreted., (Copyright © 2019 Elsevier Inc. All rights reserved.)

This study aimed to assess the carcinogenic and non-carcinogenic risks of in-vehicle exposure in Tehran, Iran to formaldehyde and acetaldehyde for different models of taxis, and to explore the effects of city zone, taxi vehicle type, the taxi's age (<1, 1-5, 5-10), fuel type (gasoline, CNG, and LPG), and refueling activities on the estimated health risks based on previously measured concentrations. The overall and age-specific carcinogenic and non-carcinogenic risks of these compounds for taxi drivers and passengers were estimated separately using Monte Carlo simulations. Three scenarios of exposure frequency were defined for taxis commuting in different zones of city: Restricted Traffic Zone (RTZ) and Odd-Even Zone (OEZ) as two plans to reduce air pollution, and no-restriction zone (NRZ). The carcinogenic risks for drivers and passengers, the average risks of formaldehyde and acetaldehyde for most cases were above the 1 × 10 -4 . The health risks were greater in Restricted Traffic Zone (RTZ) and Odd-Even Zone (OEZ) in comparison to no-restriction zone (NRZ). The carcinogenic risk from formaldehyde exposures were higher than those for acetaldehyde in all cases. Taxis fueled with LPG showed lower cancer risks for both acetaldehyde and formaldehyde. Refueling increased the carcinogenic risk from both compounds. For non-carcinogenic risks from acetaldehyde, the average hazard ratios for both drivers and passengers were >1, indicating a non-negligible risk. Cancer and non-cancer risks for the taxi drivers were greater than the passengers given the higher time of occupancy. The present study showed that transportation in taxis can impose significant long-term health risks to both passengers and drivers. Development and investment in cleaner choices for public transportations are required., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

In this study, we compared the expression of CYP153, sodA, sodC, and recA genes and ROS generation in hydrocarbon-degrading Rhodococcus erythropolis in the presence of cyclohexane, naphthalene, and diesel fuel. The expression of cytochrome P450, sodA (encoding Fe/Mn superoxide dismutase), recA, and superoxide anion radical generation rate increased after the addition of all studied hydrocarbons. The peak of CYP153, sodA, and recA gene expression was registered in the presence of naphthalene. The same substrate upregulated the Cu/Zn superoxide dismutase gene, sodC. Cyclohexane generated the highest level of superoxide anion radical production. Hydrogen peroxide accumulated in the medium enriched with diesel fuel. Taken together, hydrocarbon biotransformation leads to oxidative stress and upregulation of antioxidant enzymes and CYP153 genes, and increases DNA reparation levels in R. erythropolis cells., (© 2019 The Authors. MicrobiologyOpen published by John Wiley & Sons Ltd.)

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 m 3 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., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Diesel emissions contain high levels of particulate matter (PM) which can have a severe effect on the airways. Diesel PM can be effectively reduced with the substitution of diesel fuel with a biofuel such as vegetable oil. Unfortunately, very little is known about the cellular effects of these alternative diesel emissions on the airways. The aim of this study was to test whether coconut oil substitution in diesel fuel reduces the adverse effect of diesel emission exposure on human bronchial epithelial cells. Human bronchial epithelial cells were cultured at air-liquid interface for 7 days and exposed to diesel engine emissions from conventional diesel fuel or diesel fuel blended with raw coconut oil at low (10%), moderate (15%) and high (20%) proportions. Cell viability, inflammation, antioxidant production and xenobiotic metabolism were measured. Compared to conventional diesel, low fractional coconut oil substitution (10% and 15%) reduced inflammation and increased antioxidant expression, whereas higher fractional coconut oil (20%) reduced cell viability and increased inflammation. Therefore, cellular responses after exposure to alternative diesel emission are dependent on fuel composition.

Grass Elymus elongatus has a potential in phytoremediation and was used in this study in a potted experiment, which was performed to determine the effect of polluting soil (Eutric Cambisol) with diesel oil (DO) and unleaded petroleum (P) on the diversity of soil microorganisms, activity of soil enzymes, physicochemical properties of soil, and on the resistance of Elymus elongatus to DO and P, which altogether allowed evaluating soil health. Both petroleum products were administered in doses of 0 and 7 cm 3 kg -1 soil d.m. Vegetation of Elymus elongatus spanned for 105 days. Grasses were harvested three times, i.e., on day 45, 75, and 105 of the experiment. The study results demonstrated a stronger toxic effect of DO than of P on the growth and development of Elymus elongatus . Diesel oil caused greater changes in soil microbiome compared to unleaded petroleum. This hypothesis was additionally confirmed by Shannon and Simpson indices computed based on operational taxonomic unit (OTU) abundance, whose values were the lowest in the DO-polluted soil. Soil pollution with DO reduced the counts of all bacterial taxa and stimulated the activity of soil enzymes, whereas soil pollution with P diminished the diversity of bacteria only at the phylum, class, order, and family levels, but significantly suppressed the enzymatic activity. More polycyclic aromatic hydrocarbons (PAHs) were degraded in the soil polluted with P compared to DO, which may be attributed to the stimulating effect of Elymus elongatus on this process, as it grew better in the soil polluted with P than in that polluted with DO.

Gasoline station attendants spend a great deal of their time in the direct exposure to noxious substances such as benzene and byproducts of gasoline combustion. Such occupational exposure increases the risk of oxidative stress. This study aimed to evaluate hematological and biochemical alterations among petrol station workers. Forty gas station attendants and 39 non-attendants were recruited as exposed and control subjects, respectively. Plasma samples were evaluated for hemoglobin, hematocrit, and red blood cell count via the Sysmex KX-21 analyzer. Then, oxidized hemoglobin, methemoglobin, and hemichrome were measured spectrophotometrically. Moreover, serum antioxidant capacity and protein oxidation were evaluated. The means ± SD of hemoglobin (16.76 ± 0.14 g/dl vs 15.25 ± 0.14 g/dl), hematocrit (49.11 ± 0.36% vs 45.37 ± 0.31%), RBC count (5.85 ± 0.06 mil/μl vs 5.33 ± 0.06 mil/μl), Met-HB (1.07 ± 0.07 g/dl vs 0.39 ± 0.04 g/dl), and hemichrome (0.80 ± 0.07 g/dl vs 0.37 ± 0.02 g/dl) in the exposed group were significantly greater than the control group (P < 0.001). The results of the independent-sample t test illustrated that the FRAP test value in the exposed group (0.23 ± 0.01 mM) was significantly lower than the control group (0.34 ± 0.01 mM), while the value of the plasma protein carbonyl test in the exposed group (7.47 ± 0.33 mmol/mg protein) was meaningfully greater than the control group (5.81 ± 0.19 mmol/mg protein) (P < 0.001). In conclusion, gas station attendants suffer from higher levels of oxidative stress, and they need to take antioxidants in order to minimize the effects of oxidative stress.

Introduction: Diesel emissions have a high level of particulate matter which can cause inflammation and oxidative stress in the airways. A strategy to reduce diesel particulate matter and the associated adverse effects is the use of biodiesels and fuel additives. However, very little is known about the biological effects of these alternative emissions. The aim of this study is to compare the effect of biodiesel and triacetin/biodiesel emissions on primary human bronchial epithelial cells (pHBECs) compared to diesel emissions., Methods: pHBECs were exposed to diesel, biodiesel (20%, 50% and 100% biodiesel derived from coconut oil) and triacetin/biodiesel (4% and 10% triacetin) emissions for 30 min at air-liquid interface. Cell viability (cellular metabolism, cell death, CASP3 mRNA expression and BCL2 mRNA expression), inflammation (IL-8 and IL-6 secretion), antioxidant production (HO-1 mRNA expression) and xenobiotic metabolism (CYP1a1 mRNA expression) were measured., Results: Biodiesel emissions (B50) reduced cell viability, and increased oxidative stress. Triacetin/biodiesel emissions (B90) decreased cell viability and increased antioxidant production, inflammation and xenobiotic metabolism. Biodiesel emissions (B100) reduced cell viability, and increased IL-8 secretion and xenobiotic metabolism., Conclusions: Biodiesel substitution in diesel fuel and triacetin substitution in biodiesel can increase the adverse effects of diesel emissions of pHBECs. Further studies of the effect of these diesel fuel alternatives on pHBECs are required., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

The worldwide spillage of fossil fuels causes an ever-increasing environmental concern due to their resistance to biodegradation and toxicity. The diesel fuel is one of the derivative forms of petroleum that is widely used in the world. Its composition has many aromatic compounds and long hydrocarbons chains, both persistent and hazardous, thus requiring complex microbial dynamics to achieve full biodegradation. At this point, biodiesel has advantages because it is produced from renewable sources. It also has a relatively fast biodegradation. Biodiesel formulation chemically varies according to the raw material used for its production. While vegetable oils tend to have homogeneous proportions of linoleic and oleic fatty acids, animal fats have an heterogeneous distribution of stearic, palmitic and oleic fatty acids. As some studies have already detected the toxic potential of biodiesel from vegetable oil, this study sought information on the phytotoxic and genotoxic potential of animal fat-based biodiesel and compare it with fossil fuel as diesel fuel and crude petroleum. The impacts on the microbial activity of soils contaminated with biodiesel, diesel fuel and crude petroleum were performed by the dehydrogenase activity. Phytotoxicity tests were performed with Eruca sativa seeds and genotoxicity bioassays with Allium cepa seeds. The results showed a rapid assimilation of biodiesel by the autochthonous soil microorganisms. Soil contaminated with either diesel or crude petroleum inhibited the root and hypocotyl elongation of E. sativa. Overall, petroleum contaminated soils showed higher genotoxic potential. Biodiesel from animal fat was rapidly assimilated by soil microorganisms and did not present significant phytotoxic or genotoxic potential, but significantly reduced the mitotic index of A. cepa roots. Our results showed that biodiesel from animal fat have rapid biodegradability. Biodiesel also led to less impacts during seed development and lower genotoxic potential when compared to crude petroleum and diesel fuel. In addition, biodiesel from animal fat does not present the same toxicity demonstrated by biodiesel from soybean-based biodiesel described in current literature.

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., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Objective: To examine the association between occupational exposure to petroleum-based and oxygenated solvents and the risk of oral and oropharyngeal cancer., Methods: The ICARE study is a large population-based case-control study conducted in France between 2001 and 2007. This present analysis was restricted to men and included 350 and 543 cases of squamous cell-carcinoma of the oral cavity and oropharynx, respectively, and 2780 controls. Lifetime tobacco, alcohol consumption and complete occupational history were assessed through detailed questionnaires. Job-exposure matrices allowed us to assess occupational exposure to five petroleum-based solvents (white spirits; diesel/fuel oils/kerosene; gasoline; benzene; special petroleum products) and five oxygenated solvents (diethyl ether; tetrahydrofuran; ketones and esters; alcohols; ethylene glycol). Odds-ratios (ORs), adjusted for age, smoking, alcohol consumption and socioeconomic status, and 95% confidence intervals (CI) were estimated using unconditional logistic models., Results: Associations between oral cancer risk and exposure to white spirits and diesel/fuel oils/kerosene were suggested, but there was no exposure-response trend. Concerning exposure to oxygenated solvents, participants with the highest levels of cumulative exposure to diethyl ether had a significant excess risk of oropharyngeal cancer (OR = 7.78, 95%CI 1.42 to 42.59; p for trend = 0.04). Ever exposure to tetrahydrofuran was associated with a borderline significant increased risk of oral cancer (OR = 1.87, 95%CI 0.97 to 3.61), but no exposure-response trend was observed. Additional adjustments for exposure to other solvents did not substantially change the results., Conclusion: Our results do not provide evidence for a major role of petroleum-based and oxygenated solvents in the occurrence of oral and oropharyngeal cancers in men., (Copyright © 2019. Published by Elsevier Ltd.)

The widespread use of diesel as a transportation fuel and the introduction of biodiesel into the world energy matrix increase the likelihood of aquatic contamination with these fuels. In this case, it is important to know the environmental impacts caused by water-soluble fraction (WSF) of these fuels, since it is the portion that can result in long-term impacts and affect regions far away from the location of a spill. Therefore, we evaluated and compared the aquatic ecotoxicity of the WSF of biodiesel and diesel through acute ecotoxicity tests with the aquatic microcrustacean Daphnia magna and the marine bacteria Aliivibrio fischeri, as well as chronic ecotoxicity tests with D. magna. The WSF of diesel was 2.5-4 folds more toxic than the WSF of biodiesel in acute ecotoxicity tests. Similarly, a comparison of the chronic ecotoxicity demonstrated that the WSF of diesel was more toxic than the WSF of biodiesel. WSF of diesel causes chronic effects on reproduction, longevity and growth of D. magna (NOEC was 12.5, 12.5, 6.25%, respectively), while WSF of biodiesel did not present significantly different results compared to the control for any of the parameters evaluated in any of the dilutions tested (NOEC> 25%). To the best of our knowledge, this is the first study that compares the chronic ecotoxicity of WSF of diesel and biodiesel on D. magna., (Copyright © 2019 Elsevier Ltd. All rights reserved.)