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1.
Toxicol Lett ; 322: 20-31, 2020 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-31923465

RESUMO

Particulate matter (PM) from combustion processes has been associated with oxidative stress to DNA, whereas effects related to telomere dysfunction are less investigated. We collected air-borne PM from a passenger cabin of a diesel-propelled train and at a training facility for smoke diving exercises. Effects on oxidative stress biomarkers, genotoxicity measured by the comet assay and telomere length in PM-exposed A549 cells were compared with the genotoxicity and telomere length in peripheral blood mononuclear cells (PBMCs) from human volunteers exposed to the same aerosol source. Although elevated levels of DNA strand breaks and oxidatively damaged DNA in terms of Fpg-sensitive sites were observed in PBMCs from exposed humans, the PM collected at same locations did not cause genotoxicity in the comet assay in A549 cells. Nevertheless, A549 cells displayed telomere length shortening after four weeks exposure to PM. This is in line with slightly shorter telomere length in PBMCs from exposed humans, although it was not statistically significant. In conclusion, the results indicate that genotoxic potency measured by the comet assay of PM in A549 cells may not predict genotoxicity in exposed humans, whereas telomere length measurements may be a novel indicator of genotoxic stress in cell cultures and humans.


Assuntos
Dano ao DNA , Exposição por Inalação/efeitos adversos , Material Particulado/toxicidade , Fumaça/efeitos adversos , Homeostase do Telômero/efeitos dos fármacos , Emissões de Veículos/toxicidade , Células A549 , Poluentes Ocupacionais do Ar/toxicidade , Sobrevivência Celular/efeitos dos fármacos , Bombeiros , Humanos , Exposição por Inalação/análise , Leucócitos Mononucleares/efeitos dos fármacos , Leucócitos Mononucleares/patologia , Exposição Ocupacional/efeitos adversos , Exposição Ocupacional/análise , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/genética , Tamanho da Partícula , Homeostase do Telômero/genética
2.
Ann Otol Rhinol Laryngol ; 129(3): 245-255, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31646875

RESUMO

OBJECTIVES: Diesel exhaust particles (DEP)s are notorious ambient pollutants composed of a complex mixture of a carbon core and diverse chemical irritants. Several studies have demonstrated significant relationships between DEP exposure and serious nasal inflammatory response in vitro, but available information regarding underlying networks in terms of gene expression changes has not sufficiently explained potential mechanisms of DEP-induced nasal damage, especially in vivo. METHODS: In the present study, we identified DEP-induced gene expression profiles under short-term and long-term exposure, and identified signaling pathways based on microarray data for understanding effects of DEP exposure in the mouse nasal cavity. RESULTS: Alteration in gene expression due to DEP exposure provokes an imbalance of the immune system via dysregulated inflammatory markers, predicted to disrupt protective responses against harmful exogenous substances in the body. Several candidate markers were identified after validation using qRT-PCR, including S100A9, CAMP, IL20, and S100A8. CONCLUSIONS: Although further mechanistic studies are required for verifying the utility of the potential biomarkers suggested by the present study, our in vivo results may provide meaningful suggestions for understanding the complex cellular signaling pathways involved in DEP-induced nasal damages.


Assuntos
Expressão Gênica , Rinite/induzido quimicamente , Emissões de Veículos/toxicidade , Animais , Peptídeos Catiônicos Antimicrobianos/genética , Peptídeos Catiônicos Antimicrobianos/metabolismo , Antígeno B7-1/genética , Antígeno B7-1/metabolismo , Biomarcadores/metabolismo , Calgranulina A/genética , Calgranulina A/metabolismo , Calgranulina B/genética , Calgranulina B/metabolismo , Interleucinas/genética , Interleucinas/metabolismo , Camundongos Endogâmicos BALB C , Modelos Animais , Testes de Provocação Nasal , Análise de Sequência com Séries de Oligonucleotídeos , RNA/metabolismo , Reação em Cadeia da Polimerase em Tempo Real , Rinite/metabolismo , Transdução de Sinais , Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética , Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
3.
Ecotoxicol Environ Saf ; 189: 110053, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31862514

RESUMO

Particulate matter with an aerodynamic diameter of less than 2.5 µm (PM2.5) derived from automobile exhaust can lead to serious male spermatogenesis dysfunction, but its specific molecular mechanism is unclear. In this experiment, we focused on the blood-testis barriers (BTB) and explored the intracellular mechanisms underlying the fertility toxicity of PM2.5 originating from automobile exhaust in the primary cultured Sertoli cells(SCs) of rats. After PM2.5 exposure, excessive reactive oxygen species (ROS) and increased apoptosis of SCs were detected. The expression of the BTB related proteins including ZO-1, Occludin, N-cadherin and ß-catenin were significantly decreased and the spatial arrangement of F-actin was completely disordered through Immunofluorescence and Western blots tests. The phosphorylation of Jun N-terminal kinase (JNK), extracellular signal regulatory kinase (ERK), p38 mitogen-activated protein kinase (MAPK) were upregulated and nuclear factor (erythroid-derived 2) -like 2-related factor (Nrf2) was downregulated respectively. However, combined utilization of vitamin C and E were observed to prevent the increase of ROS generation, reduce celluar apoptosis, increase the expression of BTB related proteins, reconstructed the spatial arrangement of F-actin as well as improved the Nrf2 expression and attenuated the phosphorylation of the MAPK kinases and cleaved caspase-3 levels. Furthermore, ERK inhibitor (SCH772984), JNK inhibitor (SP600125) and p38 MAPK inhibitor (SB203580) obviously up-regulated BTB-related proteins expression as well as activated Nrf2 expression at varying degrees, indicating that ROS-MAPKs-Nrf2 is involved in the signaling pathway that leads to PM2.5-induced spermatogenesis dysfunction. These findings indicate that PM2.5 derived from automobile exhaust causes oxidative stress, which in turn causes cellular apoptosis of SCs and damage of the blood-testis barrier, resulting male spermatogenesis dysfunction, in which ROS-MAPK-Nrf-2 pathways may play a key role.


Assuntos
Barreira Hematotesticular/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Fator 2 Relacionado a NF-E2/metabolismo , Material Particulado/toxicidade , Espécies Reativas de Oxigênio/metabolismo , Células de Sertoli/efeitos dos fármacos , Emissões de Veículos/toxicidade , Animais , Apoptose/efeitos dos fármacos , Barreira Hematotesticular/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Masculino , Estresse Oxidativo/efeitos dos fármacos , Fosforilação , Ratos , Células de Sertoli/metabolismo , Células de Sertoli/patologia
4.
PLoS Genet ; 15(12): e1008528, 2019 12.
Artigo em Inglês | MEDLINE | ID: mdl-31869344

RESUMO

Asthma is a chronic inflammatory disease of the airways with contributions from genes, environmental exposures, and their interactions. While genome-wide association studies (GWAS) in humans have identified ~200 susceptibility loci, the genetic factors that modulate risk of asthma through gene-environment (GxE) interactions remain poorly understood. Using the Hybrid Mouse Diversity Panel (HMDP), we sought to identify the genetic determinants of airway hyperreactivity (AHR) in response to diesel exhaust particles (DEP), a model traffic-related air pollutant. As measured by invasive plethysmography, AHR under control and DEP-exposed conditions varied 3-4-fold in over 100 inbred strains from the HMDP. A GWAS with linear mixed models mapped two loci significantly associated with lung resistance under control exposure to chromosomes 2 (p = 3.0x10-6) and 19 (p = 5.6x10-7). The chromosome 19 locus harbors Il33 and is syntenic to asthma association signals observed at the IL33 locus in humans. A GxE GWAS for post-DEP exposure lung resistance identified a significantly associated locus on chromosome 3 (p = 2.5x10-6). Among the genes at this locus is Dapp1, an adaptor molecule expressed in immune-related and mucosal tissues, including the lung. Dapp1-deficient mice exhibited significantly lower AHR than control mice but only after DEP exposure, thus functionally validating Dapp1 as one of the genes underlying the GxE association at this locus. In summary, our results indicate that some of the genetic determinants for asthma-related phenotypes may be shared between mice and humans, as well as the existence of GxE interactions in mice that modulate lung function in response to air pollution exposures relevant to humans.


Assuntos
Proteínas Adaptadoras de Transdução de Sinal/genética , Poluentes Atmosféricos/toxicidade , Asma/genética , Hiper-Reatividade Brônquica/induzido quimicamente , Lipoproteínas/genética , Emissões de Veículos/toxicidade , Animais , Asma/induzido quimicamente , Hiper-Reatividade Brônquica/genética , Mapeamento Cromossômico , Modelos Animais de Doenças , Feminino , Interação Gene-Ambiente , Predisposição Genética para Doença , Estudo de Associação Genômica Ampla , Humanos , Masculino , Camundongos , Pletismografia
5.
Environ Pollut ; 255(Pt 1): 113366, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31668954

RESUMO

Air pollution is one of the leading preventable threats to public health. Emerging evidence indicates that exposure to environmental stressors is associated with abnormal foetal development. However, how prenatal exposure to diesel exhaust PM2.5 (DEP) predisposes adult offspring to the development of non-alcoholic fatty liver disease (NAFLD) remains unclear. To examine this, C57BL/6J mice were exposed to DEP or a vehicle before conception and during pregnancy and fed normal chow or a high-fat diet. Then, the hepatic fatty accumulation in the adult male offspring and possible molecular mechanisms were assessed. Our data showed that prenatal exposure to DEP on normal chow led to hepatic steatosis in adult male offspring with normal liver function. However, prenatal DEP exposure relieved the hepatic steatosis and liver function in offspring of mice fed a high-fat diet. Furthermore, prenatal exposure to DEP on normal chow increased lipogenesis and worsened fatty acid oxidation. The counteractive effect of prenatal DEP exposure on high-fat-diet-induced hepatic steatosis was produced through upregulated adenosine 5'-monophosphate-activated protein kinase, and this improved lipogenesis and fatty acid oxidation. Collectively, prenatal exposure to DEP programmed the development of NAFLD differently in the adult male offspring of mice fed normal chow and a high-fat diet, showing the pleotrophic effects of exposure to adverse environmental factors in early life.


Assuntos
Dieta Hiperlipídica , Hepatopatia Gordurosa não Alcoólica , Material Particulado/toxicidade , Emissões de Veículos/toxicidade , Crianças Adultas , Poluição do Ar , Animais , Feminino , Desenvolvimento Fetal , Metabolismo dos Lipídeos/efeitos dos fármacos , Fígado/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Material Particulado/metabolismo , Gravidez , Efeitos Tardios da Exposição Pré-Natal/metabolismo
6.
Mar Pollut Bull ; 145: 316-324, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31590793

RESUMO

In 2020, the global cap of maximum allowable sulphur content in marine fuel will be reduced from the current 3.5% to 0.5%. Another way to reduce the sulphur emissions is to install a seawater scrubber that cleans exhausts but instead release acidic water containing nutrients and contaminants back to the marine environment. In the current study, scrubber washwater was tested on a Baltic Sea microplankton community. A significant increase in chlorophyll a, particulate organic phosphorus (POP), carbon (POC) and nitrogen (PON) were observed when the community was exposed to 10% scrubber washwater for 13 days as compared to the control. A laboratory experiment with the filamentous cyanobacteria Nodularia spumigena and the chain-forming diatom Melosira cf. arctica showed negative responses in photosynthetic activity (EC10 = 8.6% for N. spumigena) and increased primary productivity (EC10 = 5.5% for M. cf. arctica), implying species-specific responses to scrubber washwater discharge.


Assuntos
Plâncton/efeitos dos fármacos , Água do Mar/microbiologia , Emissões de Veículos/prevenção & controle , Poluição da Água/prevenção & controle , Países Bálticos , Clorofila A/análise , Cianobactérias/efeitos dos fármacos , Nitrogênio/análise , Nodularia/efeitos dos fármacos , Fósforo/análise , Fotossíntese/efeitos dos fármacos , Navios , Enxofre/toxicidade , Emissões de Veículos/toxicidade
7.
Chemosphere ; 220: 993-1002, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31543100

RESUMO

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.


Assuntos
Fatores de Transcrição Hélice-Alça-Hélice Básicos/fisiologia , Biocombustíveis/toxicidade , Citocromo P-450 CYP1A1/metabolismo , Gasolina/toxicidade , Mediadores da Inflamação/metabolismo , Macrófagos/patologia , Receptores de Hidrocarboneto Arílico/fisiologia , Emissões de Veículos/toxicidade , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Animais , Biocombustíveis/análise , Gasolina/análise , Humanos , Macrófagos/efeitos dos fármacos , Macrófagos/imunologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Emissões de Veículos/análise
8.
Environ Res ; 177: 108661, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31442789

RESUMO

BACKGROUND: Ethanol vehicles release exhaust gases that contribute to the formation of secondary organic aerosols (SOA). OBJECTIVE: To determine in vivo toxicity resulting from exposure to SOA derived from vehicles using different ethanol-gasoline blends (E0, E10, E22, E85W, E85S, E100). METHODS: Exhaust emissions from vehicles using ethanol blends were delivered to a photochemical chamber and reacted to produce SOA. The aerosol samples were collected on filters, extracted, and dispersed in an aqueous solutions and intratracheally instilled into Sprague Dawley rats in doses of 700 µg/0.2 ml. After 45 min and 4 h pulmonary and cardiac chemiluminescence (CL) was measured to estimate the amount of reactive oxygen species (ROS) produced in the lungs and heart. Inflammation was measured by differential cell count in bronchoalveolar lavages (BAL). RESULTS: Statistically and biologically significant differences in response to secondary particles from the different fuel formulations were detected. Compared to the control group, animals exposed to SOA from gasoline (E0) showed a significantly higher average CL in the lungs at 45 min. The highest CL averages in the heart were observed in the groups exposed to SOA from E10 and pure ethanol (E100) at 45 min. BAL of animals exposed to SOA from E0 and E85S had a significant increased number of macrophages at 45 min. BAL neutrophil count was increased in the groups exposed to E85S (45 min) and E0 (4 h). Animals exposed to E0 and E85W had increased BAL lymphocyte count compared to the control and the other exposed groups. DISCUSSION: Our results suggest that SOA generated by gasoline (E0), followed by ethanol blends E85S and E85W, substantially induce oxidative stress measured by ROS generation and pulmonary inflammation measured by the recruitment of white blood cells in BAL.


Assuntos
Poluentes Atmosféricos/toxicidade , Pneumonia/induzido quimicamente , Espécies Reativas de Oxigênio/metabolismo , Emissões de Veículos/toxicidade , Animais , Etanol , Gasolina , Coração/efeitos dos fármacos , Contagem de Leucócitos , Pulmão/efeitos dos fármacos , Macrófagos/citologia , Neutrófilos/citologia , Estresse Oxidativo , Ratos , Ratos Sprague-Dawley
9.
Ecotoxicol Environ Saf ; 183: 109552, 2019 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-31442804

RESUMO

To study source-specific carcinogenicity and mutagenicity of polycyclic aromatic hydrocarbons (PAHs) under diverse anthropogenic activities, PM2.5-bound PAHs were detected in Beijing in four periods. PAHs in Asia-Pacific Economic Cooperation meeting (APEC) was much lower than that in after-APEC period. The highest PAHs concentration was in heating period (303 ng/m3). Sources were quantified by Positive Matrix Factorization (PMF). In heating period, due to high emissions, weak diffusion, low degradation and evaporation, high contributions of all sources were observed, and both absolute and relative contributions of coal combustion increased. Changed contributions in during-APEC and after-APEC periods implied effectiveness of reinforced emission control, especially for coal combustion and vehicles. Furthermore, variations of sources-specific carcinogenicity and mutagenicity were investigated. In non-heating period, contributions of gasoline exhaust (38.4% TEQ: Toxic Equivalent Quantity, 33.7% MEQ: Mutagenic Equivalent Quantity) and diesel exhaust (53.8% TEQ, 57.9% MEQ) dominated both carcinogenic and mutagenic risks. Coal combustion sharply increased in heating period, attributing 27.5% TEQ and 21.7% MEQ. In during-APEC period, all contributions to carcinogenicity and mutagenicity were lower than those in after-APEC period, but "others" linked with regional transport contributed increased fractions (above 20%). Sources-specific carcinogenicity and mutagenicity under diverse anthropogenic activities, especially for APEC meeting with reinforced control, gave a new insight into assessment of control measures based on health risks.


Assuntos
Poluentes Atmosféricos/análise , Carcinógenos/análise , Monitoramento Ambiental/métodos , Mutagênicos/análise , Material Particulado/análise , Hidrocarbonetos Policíclicos Aromáticos/análise , Poluentes Atmosféricos/toxicidade , Pequim , Carcinógenos/toxicidade , China , Carvão Mineral/análise , Carvão Mineral/toxicidade , Calefação , Atividades Humanas , Mutagênicos/toxicidade , Tamanho da Partícula , Material Particulado/toxicidade , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Emissões de Veículos/análise , Emissões de Veículos/toxicidade
10.
Toxicol Lett ; 315: 47-54, 2019 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-31449845

RESUMO

Particulate matter with a diameter of less than 2.5 µm (PM2.5) easily deposits on lung alveoli and degrades human health. Surfactant protein A (SP-A) is the most abundant pulmonary surfactant protein stored in lamellar bodies (LBs) of alveolar epithelial type II cells. The impacts of PM2.5 on SP-A are multifaceted and intractable, and the underlying mechanism remains unclear. In this study, the expression and distribution of SP-A in Balb/c mice and A549 cells under PM2.5 exposure were investigated. The results showed that the low and medium concentration of PM2.5 gradually enhanced SP-A protein and mRNA expression, whereas the high concentration of PM2.5 conspicuously decreased SP-A protein but not its mRNA compared with the control. The trafficking of SP-A to LBs was gradually disturbed, and concomitantly, the lesions of LBs responsible for the transport and storage of SP-A protein were exacerbated with increased PM2.5 concentration. Reactive oxygen species production abundantly increased upon PM2.5 exposure, and it was antagonized by the oxidant inhibitor N-acetylcysteine. Subsequently, the injured LBs and the decrease in SP-A expression under exposure to the high concentration of PM2.5 were well rescued. The present study provides a new perspective to investigate the adverse effects of PM2.5 or diesel exhaust particles on other proteins transported to and stored in LBs.


Assuntos
Células Epiteliais Alveolares/metabolismo , Material Particulado/toxicidade , Alvéolos Pulmonares/fisiopatologia , Proteína A Associada a Surfactante Pulmonar/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Emissões de Veículos/toxicidade , Animais , Feminino , Humanos , Camundongos , Camundongos Endogâmicos BALB C , Tamanho da Partícula
11.
Ecotoxicol Environ Saf ; 183: 109500, 2019 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-31450033

RESUMO

Exposure to diesel engine exhaust (DEE) impairs lung function. But the underlying mechanisms are still not fully understood. The aim of this study was to investigate the effects of long-term DEE exposure on lung inflammation and the underlying mechanisms. Sprague-Dawley male rats were exposed to DEE with 3 mg/m3 of diesel exhaust particles (DEP) for 12 weeks. Then urine, blood, bronchoalveolar lavage fluid (BALF), and lung tissue were collected for the determination of biochemistry indexes, DNA methylation status, and histological changes in the lung. The results showed that the metabolites of polycyclic aromatic hydrocarbons (PAHs) 2-hydroxyphenanthrene (2-OHPh) and 9-OHPh, and 8-hydroxy-2'-deoxyguanosine (8-OHdG), and malondialdehyde (MDA) level were higher in urine of DEE-exposed rats than control group. The level of proinflammatory cytokines IL-8, IL-6, and TNF-α was significantly higher in serum (1.8, 3.5, and nearly 1.0-fold increase, respectively), BALF (2.2, 3.8, and 2.0-fold increase, respectively) and lung tissues (3.5, 4.3, and 2.4-fold increase, respectively) of DEE-exposed rats than control group. While the level of clara cell secretory protein (CC16) and pulmonary surfactant protein D (SP-D) with anti-inflammatory property was obviously lower in serum (reduction of 29% and 38%, respectively), BALF (reduction of 50% and 46%, respectively) and lung tissues (reduction of 50% and 55%, respectively) of DEE-exposed rats than control group. Exposure to DEE also resulted in significant increases in total white blood cell (WBC), neutrophil, eosinophil, and lymphocyte number in BALF. Airway inflammation and remolding were apparent in DEE group. The methylation level of CCAAT/enhancer-binding protein alpha (C/EBPα) promoter was markedly increased (about 3.2-fold increase), and its mRNA and protein expression were significantly decreased (about 62% and 68% decrease, respectively) in the lungs of DEE-exposed rats compared with the group. Further, cell experiments were performed to investigate the relationship between C/EBPα and CC16, and CC16 function under DEP conditions. The results showed that DEP inhibited CC16 expression via methylation of C/EBPα promoter, and the increase of CC16 level significantly relieved the proinflammatory effects caused by DEP exposure. In conclusion, our data indicated that long-term exposure to DEE can cause lung inflammation, at least in part via methylation of C/EBPα promoter, and inhibition of CC16 expression.


Assuntos
Proteína alfa Estimuladora de Ligação a CCAAT/genética , Exposição por Inalação/efeitos adversos , Pneumonia/induzido quimicamente , Emissões de Veículos/toxicidade , Animais , Citocinas/metabolismo , Metilação de DNA/efeitos dos fármacos , Masculino , Pneumonia/metabolismo , Pneumonia/patologia , Hidrocarbonetos Policíclicos Aromáticos/urina , Regiões Promotoras Genéticas , RNA Mensageiro/metabolismo , Ratos Sprague-Dawley , Uteroglobina/genética , Uteroglobina/metabolismo
12.
BMC Public Health ; 19(1): 877, 2019 Jul 04.
Artigo em Inglês | MEDLINE | ID: mdl-31272504

RESUMO

BACKGROUND: This study uses bibliometric analysis to describe the state of research about the association of NO2, PM2.5 and noise exposures - three traffic-related pollutants - with cardiometabolic disorders. METHODS: We retrieved references published 1994-2017 from Scopus and classified references with respect to exposure, health outcome and study design using index keywords. Temporal trend, top cited references, used index keywords and the number of hypothesis testing and non-hypothesis testing study design for each group were identified. RESULTS: Results show PM2.5 is the most frequently studied exposure (47%), followed by both NO2 and PM2.5 exposure (29%). Only 3% of references considered multiple exposures between NO2 and/or PM2.5 and noise, and these were published after 2008. While we observed a growing trend in studies with NO2 and/or PM2.5 and noise and diabetes in the last decade, there is a diminishing trend in studies with noise and diabetes. Different patterns of study designs were found through H/NH ratio, the number of references classified as having a hypothesis (H)-testing design relative to the number of references classified as having a non-hypothesis (NH)-testing design. Studies with NO2 and/or PM2.5 exposure are more likely to have a H-testing design, while those with noise exposure are more likely to have a NH-testing design, such as cross-sectional study design. CONCLUSIONS: We conclude with three themes about research trends. First, the study of simultaneous exposures to multiple pollutants is a current trend, and likely to continue. Second, the association between traffic-related pollutants and diabetes and metabolic symptoms is an area for growth in research. Third, the transition to the use of H-testing study designs to explore associations between noise and cardiometabolic outcomes may be supported by improved understanding of the mechanism of action, and/or improvements to the accuracy and precision of air pollution and noise exposure assessments for environmental health research.


Assuntos
Doenças Cardiovasculares/epidemiologia , Doenças Metabólicas/epidemiologia , Emissões de Veículos/toxicidade , Bibliometria , Diabetes Mellitus/epidemiologia , Humanos , Dióxido de Nitrogênio/efeitos adversos , Ruído/efeitos adversos , Material Particulado/efeitos adversos
13.
Environ Pollut ; 253: 667-679, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31330358

RESUMO

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


Assuntos
Biocombustíveis/toxicidade , Emissões de Veículos/toxicidade , Alérgenos , Animais , Asma/induzido quimicamente , Biocombustíveis/análise , Líquido da Lavagem Broncoalveolar , Citocinas , Modelos Animais de Doenças , Humanos , Inflamação/induzido quimicamente , Interleucina-17 , Pulmão/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Neutrófilos , Material Particulado/efeitos adversos , Testes de Toxicidade , Emissões de Veículos/análise
14.
Chem Biol Interact ; 311: 108762, 2019 Sep 25.
Artigo em Inglês | MEDLINE | ID: mdl-31348917

RESUMO

Neurotoxicity caused by particulate matter (PM) has been highlighted as being a potential risk factor for neurodegenerative diseases. However, the effects of brain inflammation in response to traffic-related PM remain unclear. The objective of this study was to investigate the effects of traffic-related PM on microglial responses. We determined the cytotoxicity, oxidative stress, lipid peroxidation, inflammation, activation, autophagy, and apoptosis due to exposure to carbon black (CB) and diesel exhaust particles (DEPs) in Bv2 microglial cells. Additionally, cells were pretreated with corticosteroid to determine alterations in microglial activation and inflammation. For in vivo confirmation, Sprague Dawley (SD) rats were whole-body exposed to traffic-related PM1 (PM with an aerodynamic diameter of <1 µm) for 3 and 6 months. We observed that a decrease in cell viability and increases in dichlorodihydrofluorescein (DCFH), lactate dehydrogenase (LDH), and thiobarbituric acid-reactive substances (TBARSs) occurred due to CB and DEP. Production of interleukin (IL)-6 and soluble tumor necrosis factor (TNF)-α was significantly stimulated by CB and DEP, whereas production of cellular TNF-α was significantly stimulated by CB. Iba1 and prostaglandin E2 (PGE2) significantly increased due to CB and DEP. Consistently, we observed significant increases in Iba1 in the hippocampus of rats after 3 and 6 months of exposure to traffic-related PM1. We found that the light chain 3II (LC3II)/LC3I ratio and caspase-3 activity increased due to CB and DEP exposure. Subsequently, LDH, TBARS, LC3II/I, and caspase-3 activities did not clearly respond to corticosteroid pretreatment followed by DEP exposure in BV2 cells. Results of the present study suggested that traffic-related PM induced cytotoxicity, lipid peroxidation, microglial activation, and inflammation as well as autophagy and caspase-3 regulation in microglia. We demonstrated that microglial activation and inflammation may play important roles in the response of the brain to traffic-related PM.


Assuntos
Inflamação/etiologia , Microglia/efeitos dos fármacos , Material Particulado/toxicidade , Animais , Autofagia/efeitos dos fármacos , Encéfalo/patologia , Proteínas de Ligação ao Cálcio/análise , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Dinoprostona/análise , Interleucina-6/metabolismo , L-Lactato Desidrogenase/metabolismo , Masculino , Proteínas dos Microfilamentos/análise , Microglia/metabolismo , Proteínas Associadas aos Microtúbulos/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Fator de Necrose Tumoral alfa/metabolismo , Regulação para Cima/efeitos dos fármacos , Emissões de Veículos/toxicidade
16.
Part Fibre Toxicol ; 16(1): 21, 2019 06 11.
Artigo em Inglês | MEDLINE | ID: mdl-31182122

RESUMO

BACKGROUND: Short-term controlled exposure to diesel exhaust (DE) in chamber studies have shown mixed results on lung and systemic effects. There is a paucity of studies on well-characterized real-life DE exposure in humans. In the present study, 29 healthy volunteers were exposed to DE while sitting as passengers in diesel-powered trains. Exposure in electric trains was used as control scenario. Each train scenario consisted of three consecutive days (6 h/day) ending with biomarker samplings. RESULTS: Combustion-derived air pollutants were considerably higher in the passenger carriages of diesel trains compared with electric trains. The concentrations of black carbon and ultrafine particles were 8.5 µg/m3 and 1.2-1.8 × 105 particles/cm3 higher, respectively, in diesel as compared to electric trains. Net increases of NOx and NO2 concentrations were 317 µg/m3 and 36 µg/m3. Exposure to DE was associated with reduced lung function and increased levels of DNA strand breaks in peripheral blood mononuclear cells (PBMCs), whereas there were unaltered levels of oxidatively damaged DNA, soluble cell adhesion molecules, acute phase proteins in blood and urinary excretion of metabolites of polycyclic aromatic hydrocarbons. Also the microvascular function was unaltered. An increase in the low frequency of heart rate variability measures was observed, whereas time-domain measures were unaltered. CONCLUSION: Exposure to DE inside diesel-powered trains for 3 days was associated with reduced lung function and systemic effects in terms of altered heart rate variability and increased levels of DNA strand breaks in PBMCs compared with electric trains. TRIAL REGISTRATION: ClinicalTrials.Gov ( NCT03104387 ). Registered on March 23rd 2017.


Assuntos
Poluentes Atmosféricos/análise , Sistema Cardiovascular/efeitos dos fármacos , Dano ao DNA , Pulmão/efeitos dos fármacos , Material Particulado/análise , Emissões de Veículos/análise , Poluentes Atmosféricos/toxicidade , Biomarcadores/sangue , Biomarcadores/urina , Sistema Cardiovascular/fisiopatologia , Monitoramento Ambiental , Gasolina , Voluntários Saudáveis , Humanos , Pulmão/fisiopatologia , Material Particulado/toxicidade , Ferrovias , Emissões de Veículos/toxicidade
17.
Toxicol Mech Methods ; 29(8): 616-622, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31237464

RESUMO

The exposure to exhaust emissions from fuels as diesel and pyrolysis oil may result in adverse effects on human lungs. This study investigated the effects of exposing mice to the exhaust emissions from diesel, biodiesel or pyrolysis oil, for 1 hour/day for 3 days, on lung oxidative stress and whether selenium administration into these mice affects the oxidative stress. The levels of lung malondialdehyde and nitric oxide were increased after exposure to pyrolysis oil exhaust. The intraperitoneal injection of 1.78 µg selenium/kg body weight 15 minutes before the exposure to the pyrolysis oil exhaust (pyrolysis oil + selenium group) restored the normal levels of malondialdehyde and nitric oxide. The catalase and SOD activities were decreased in the groups of the mice exposed to the exhaust emissions from pyrolysis oil, biodiesel or diesel. Selenium pretreatment of these groups showed no significant change in the activities of both enzymes. In conclusion, the increased lung levels of malondialdehyde and nitric oxide after the exposure to the exhaust emission from pyrolysis oil were restored to normal by selenium administration.


Assuntos
Poluentes Atmosféricos/toxicidade , Óleos Combustíveis , Pulmão/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Selenito de Sódio/farmacologia , Emissões de Veículos/toxicidade , Animais , Biocombustíveis , Suplementos Nutricionais , Gasolina , Exposição por Inalação/efeitos adversos , Exposição por Inalação/análise , Pulmão/metabolismo , Masculino , Malondialdeído/sangue , Camundongos , Óxido Nítrico/sangue , Pirólise
18.
Int J Mol Sci ; 20(11)2019 Jun 08.
Artigo em Inglês | MEDLINE | ID: mdl-31181746

RESUMO

Exposure to ultrafine particles (UFPs) leads to adverse effects on health caused by an unbalanced ratio between UFPs deposition and clearance efficacy. Since air pollution toxicity is first direct to cardiorespiratory system, we compared the acute and sub-acute effects of diesel exhaust particles (DEP) and biomass burning-derived particles (BB) on bronchoalveolar Lavage Fluid (BALf), lung and heart parenchyma. Markers of cytotoxicity, oxidative stress and inflammation were analysed in male BALB/c mice submitted to single and repeated intra-tracheal instillations of 50 µg UFPs. This in-vivo study showed the activation of inflammatory response (COX-2 and MPO) after exposure to UFPs, both in respiratory and cardiovascular systems. Exposure to DEP results also in pro- and anti-oxidant (HO-1, iNOS, Cyp1b1, Hsp70) protein levels increase, although, stress persist only in cardiac tissue under repeated instillations. Statistical correlations suggest that stress marker variation was probably due to soluble components and/or mediators translocation of from first deposition site. This mechanism, appears more important after repeated instillations, since inflammation and oxidative stress endure only in heart. In summary, chemical composition of UFPs influenced the activation of different responses mediated by their components or pro-inflammatory and pro-oxidative molecules, indicating DEP as the most damaging pollutant in the comparison.


Assuntos
Exposição por Inalação/efeitos adversos , Material Particulado/toxicidade , Emissões de Veículos/toxicidade , Animais , Biomarcadores/análise , Líquido da Lavagem Broncoalveolar/química , Ciclo-Oxigenase 2/análise , Citocromo P-450 CYP1B1/análise , Proteínas de Choque Térmico HSP70/análise , Heme Oxigenase-1/análise , Inflamação/etiologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Óxido Nítrico Sintase Tipo II/análise
19.
Chemosphere ; 230: 424-431, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31112865

RESUMO

The atmospheric fine particulate matters (PM2.5) induce significant negative effects on human health, such as in the form of oxidative stress and pro-inflammatory response. Organic pollutants are important harmful and toxic compositions in PM2.5, risks of which usually show temporal and spatial variations. To investigate the toxic effects of airborne organic pollutants on human lung epithelial cells A549, the PM2.5 samples were collected monthly from both urban and industrial areas during a whole year in Nanjing, eastern China. After exposure to organic components extracted from these PM2.5, the cell viability, lactate dehydrogenase content, oxidative stress index level and inflammatory factor expression level were measured. Supported by the concentrations of polycyclic aromatic hydrocarbons (PAHs) and n-alkanes, results showed that, organic components of PM2.5 from cold season (winter and spring) typically influenced cell membrane, cell oxidation and inflammatory damage, while the urban samples of warm season (summer and autumn) impacted cell viability more prominently. Spatially, the toxicity of samples from industrial sources was generally stronger than that from urban source, but urban samples induced much stronger damage to cell membranes than industrial one. The correlations between the PAHs, n-alkanes contents and toxicity parameters indicated that, the airborne organic components derived from motor vehicle exhaust and coal combustion were possibly the key toxic sources.


Assuntos
Poluentes Atmosféricos/toxicidade , Alcanos/toxicidade , Monitoramento Ambiental/métodos , Material Particulado/toxicidade , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Emissões de Veículos/toxicidade , Células A549 , Poluentes Atmosféricos/análise , Alcanos/análise , Sobrevivência Celular/efeitos dos fármacos , China , Cidades , Clima , Humanos , Indústrias , Material Particulado/análise , Hidrocarbonetos Policíclicos Aromáticos/análise , Estações do Ano , Emissões de Veículos/análise
20.
Ecotoxicol Environ Saf ; 180: 679-685, 2019 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-31146154

RESUMO

Two lichen species, Usnea aciculifera and Usnea luridorufa, were used as biomonitors for the deposition of traffic-related metals in China's Shennongjia National Nature Reserve. The suitability of the two lichen species for use as biomonitors was compared. The health threat to the Sichuan snub-nosed (aka golden) monkey (Rhinopithecus roxellana) from consuming lichen with elevated metal concentrations due to vehicular traffic was then assessed. Lichens, with large surface areas and neither roots nor stomata, efficiently absorb both particulate and gaseous air pollutants. The resulting data was used to assess the effect of heavy metal accumulation on the lichens as well as the health risk imposed on the monkeys as lichen is a primary food source. Lichen samples were collected in the core area of the reserve at three locations of varying traffic intensity. A forth site in the reserve, with no proximate traffic, was used as the control. Results show: (1) lichen from high traffic sites has significantly higher concentrations of Fe, Cd, Pb Zn, and Cr than lichen collected from the control site; (2) vehicular traffic is the primary source of metals in lichen; (3) U. luridorufa collected at high traffic sites displayed decreased photosynthetic efficiency, an indication of stress; (4) intake of Cd and Pb from vehicle emissions in the Shennongjia National Nature Reserve could adversely affect snub-nosed monkey health. This research advances the science of biomonitoring, contributes to environmental protection efforts in China's nature reserves and helps improve food safety for Sichuan snub-nosed monkey, a national treasure of China.


Assuntos
Colobinae/fisiologia , Biomarcadores Ambientais/efeitos dos fármacos , Líquens/efeitos dos fármacos , Metais Pesados/toxicidade , Emissões de Veículos/toxicidade , Poluentes Atmosféricos/metabolismo , Poluentes Atmosféricos/toxicidade , Animais , China , Conservação dos Recursos Naturais , Líquens/metabolismo , Metais Pesados/metabolismo , Medição de Risco
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