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1.
Inhal Toxicol ; 30(7-8): 299-312, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30569778

RESUMO

While the impact of emissions from combustion of fossil fuel on human health has been extensively studied, current knowledge of exhaust exposure from combustion of biofuels provides limited and inconsistent information about its neurotoxicity. The objective of the present work was to compare the gene expression patterns in rat frontal cortex and hippocampus after exposure to diesel exhaust emissions (DEE) from combustion of two 1st generation fuels, 7% fatty acid methyl esters (FAME) (B7) and 20% FAME (B20), and a 2nd generation 20% FAME/hydrotreated vegetable oil (SHB20: synthetic hydrocarbon biofuel), with and without diesel particulate filter (DPF). The Fisher 344 rats (n = 7/treatment) were exposed to DEE for 7 days (6h/day), and for 28 days (6h/day, 5 days/week) in whole body exposure chambers. The controls were breathing room air. Brain histological examinations did not reveal any adverse exposure-related effects of DEE in frontal cortex or in hippocampus. Gene expression analysis showed that several genes associated with antioxidant defenses and inflammation were statistically differently expressed in DEE exposed animals versus control. In addition, the gene expression changes between the exposure groups were compared, where the observed rank order in frontal cortex was B7 > B20 > SHB20 after 7 days of exposure, and SHB20 > B7 = B20 after 28 days of exposure. In the hippocampus, the rank order was B7 > SHB20 > B20. Effect of DPF treatment was observed for Tnf only. Overall, moderate increases in bio-components in diesel blends do not appear to result in dramatic alterations in gene expression or adverse histopathological effects.


Assuntos
Biocombustíveis/toxicidade , Lobo Frontal/efeitos dos fármacos , Expressão Gênica/efeitos dos fármacos , Hipocampo/efeitos dos fármacos , Exposição por Inalação/efeitos adversos , Emissões de Veículos/toxicidade , Animais , Biocombustíveis/análise , Relação Dose-Resposta a Droga , Lobo Frontal/metabolismo , Lobo Frontal/patologia , Hipocampo/metabolismo , Hipocampo/patologia , Masculino , Ratos Endogâmicos F344 , Emissões de Veículos/análise
2.
Inhal Toxicol ; 29(5): 206-218, 2017 04.
Artigo em Inglês | MEDLINE | ID: mdl-28714748

RESUMO

Increased use of biofuels raises concerns about health effects of new emissions. We analyzed relative lung health effects, on Fisher 344 rats, of diesel engine exhausts emissions (DEE) from a Euro 5-classified diesel engine running on petrodiesel fuel containing 20% rapeseed methyl esters (B20) with and without diesel particulate filter (DPF). One group of animals was exposed to DEE for 7 days (6 h/day), and another group for 28 days (6 h/day, 5 days/week), both with and without DPF. The animals (n = 7/treatment) were exposed in whole body exposure chambers. Animals breathing clean air were used as controls. Genotoxic effects of the lungs by the Comet assay, histological examination of lung tissue, bronchoalveolar lavage fluid (BALF) markers of pulmonary injury, and mRNA markers of inflammation and oxidative stress were analyzed. Our results showed that a minor number of genes related to inflammation were slightly differently expressed in the exposed animals compared to control. Histological analysis also revealed only minor effects on inflammatory tissue markers in the lungs, and this was supported by flow cytometry and ELISA analysis of cytokines in BALF. No exposure-related indications of genotoxicity were observed. Overall, exposure to DEE with or without DPF technology produced no adverse effects in the endpoints analyzed in the rat lung tissue or the BALF. Overall, exposure to DEE from a modern Euro 5 light vehicle engine run on B20 fuel with or without DPF technology produced no adverse effects in the endpoints analyzed in the rat lung tissue or the BALF.


Assuntos
Poluentes Atmosféricos/química , Poluentes Atmosféricos/toxicidade , Biocombustíveis/análise , Brassica rapa/química , Filtração/instrumentação , Gasolina/análise , Animais , Lavagem Broncoalveolar , Citocinas/genética , Citocinas/metabolismo , Esquema de Medicação , Regulação da Expressão Gênica/efeitos dos fármacos , Pulmão/efeitos dos fármacos , Pulmão/patologia , Pneumopatias/induzido quimicamente , Masculino , Material Particulado , Ratos , Ratos Endogâmicos F344
3.
Environ Toxicol Pharmacol ; 67: 8-20, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30685595

RESUMO

Increased use of 1st and 2nd generation biofuels raises concerns about health effects of new emissions. We analyzed cellular and molecular lung effects in Fisher 344 rats exposed to diesel engine exhaust emissions (DEE) from a Euro 5-classified diesel engine running on B7: petrodiesel fuel containing 7% fatty acid methyl esters (FAME), or SHB20 (synthetic hydrocarbon biofuel): petrodiesel fuel containing 7% FAME and 13% hydrogenated vegetable oil. The Fisher 344 rats were exposed for 7 consecutive days (6 h/day) or 28 days (6 h/day, 5 days/week), both with and without diesel particle filter (DPF) treatment of the exhaust in whole body exposure chambers (n = 7/treatment). Histological analysis and analysis of cytokines and immune cell numbers in bronchoalveolar lavage fluid (BALF) did not reveal adverse pulmonary effects after exposure to DEE from B7 or SHB20 fuel. Significantly different gene expression levels for B7 compared to SHB20 indicate disturbed redox signaling (Cat, Hmox1), beta-adrenergic signaling (Adrb2) and xenobiotic metabolism (Cyp1a1). Exhaust filtration induced higher expression of redox genes (Cat, Gpx2) and the chemokine gene Cxcl7 compared to non-filtered exhaust. Exposure time (7 versus 28 days) also resulted in different patterns of lung gene expression. No genotoxic effects in the lungs were observed. Overall, exposure to B7 or SHB20 emissions suggests only minor effects in the lungs.


Assuntos
Poluentes Atmosféricos/toxicidade , Biocombustíveis , Pulmão/efeitos dos fármacos , Material Particulado/toxicidade , Emissões de Veículos/toxicidade , Administração por Inalação , Animais , Líquido da Lavagem Broncoalveolar , Citocinas/metabolismo , Pulmão/citologia , Pulmão/metabolismo , Pulmão/patologia , Masculino , Ratos Endogâmicos F344
4.
Environ Toxicol Pharmacol ; 52: 138-142, 2017 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-28412649

RESUMO

Biodiesel fuel fuels are introduced at an increasing extent as a more carbon-neutral alternative to reduce CO2-emissions, compared to conventional diesel fuel. In the present study we have investigated the impact of increasing the use of 1st generation fatty acid methyl ester (FAME) biodiesel from current 7% blend (B7) to 20% blend (B20), or by increasing the biodiesel content by adding 2nd generation hydrotreated vegetable oil (HVO) based biodiesel (SHB; Synthetic Hydrocarbon Biofuel) on toxicity of diesel exhaust particles (DEP) in an in vitro system. Human bronchial epithelial BEAS-2B cells were exposed for 4 and 20h to DEP from B7, B20 and SHB at different concentrations, and examined for effects on gene expression of interleukin 6 (IL-6), CXCL8 (IL-8), CYP1A1 and heme oxygenase-1 (HO-1). The results show that both B20 and SHB were more potent inducers of IL-6 expression compared to B7. Only B20 induced statistically significant increases in CXCL8 expression. By comparison the rank order of potency to induce CYP1A1 was SHB>B7>B20. No statistically significant difference were observed form HO-1 expression, suggesting that the differences in cytokine responses were not due to oxidative stress. The results show that even moderate increases in biodiesel blends, from 7% to 20%, may increase the proinflammatory potential of emitted DEP in BEAS-2B cells. This effect was observed for both addition of 1st generation FAME and 2nd generation HVO biodiesel.


Assuntos
Poluentes Atmosféricos/toxicidade , Biocombustíveis , Material Particulado/toxicidade , Emissões de Veículos/toxicidade , Brônquios/citologia , Linhagem Celular , Citocromo P-450 CYP1A1/genética , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/metabolismo , Expressão Gênica/efeitos dos fármacos , Heme Oxigenase-1/genética , Humanos , Interleucina-6/genética , Interleucina-8/genética
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