ABSTRACT
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⯵g/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.
Subject(s)
Animal Fins , Cytochrome P-450 CYP1A1 , Fuel Oils , Liver , Petroleum Pollution , Transcriptome , Water Pollutants, Chemical , Animals , Liver/drug effects , Liver/metabolism , Water Pollutants, Chemical/toxicity , Petroleum Pollution/adverse effects , Animal Fins/drug effects , Transcriptome/drug effects , Male , Cytochrome P-450 CYP1A1/genetics , Cytochrome P-450 CYP1A1/metabolism , Fuel Oils/toxicity , Female , Sulfur , Environmental Monitoring/methods , Oncorhynchus kisutch/genetics , Gasoline/toxicity , Polycyclic Aromatic Hydrocarbons/toxicity , Polycyclic Aromatic Hydrocarbons/analysis , Seawater/chemistryABSTRACT
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.
Subject(s)
Chromosome Aberrations , DNA Damage , Gasoline , Micronucleus Tests , Occupational Exposure , Humans , Occupational Exposure/adverse effects , Occupational Exposure/analysis , Gasoline/toxicity , Adult , Male , Turkey , Chromosome Aberrations/chemically induced , DNA Damage/drug effects , Middle Aged , Air Pollutants, Occupational/analysis , Air Pollutants, Occupational/toxicity , Comet Assay , Biomarkers , Vehicle Emissions/toxicity , Vehicle Emissions/analysis , Lymphocytes/drug effects , Female , Mutagens/toxicity , Benzene/toxicity , Benzene/analysisABSTRACT
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.
Subject(s)
Ascorbic Acid , Gasoline , Oxidative Stress , Rats, Wistar , Spermatozoa , Testis , Testosterone , Animals , Male , Gasoline/toxicity , Testosterone/blood , Oxidative Stress/drug effects , Spermatozoa/drug effects , Ascorbic Acid/pharmacology , Testis/drug effects , Rats , Antioxidants/pharmacology , Lipid Peroxidation/drug effectsABSTRACT
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.
Subject(s)
Biofuels , Mice, Inbred BALB C , Vehicle Emissions , Animals , Vehicle Emissions/toxicity , Biofuels/toxicity , Mice , Male , Gasoline/toxicity , Air Pollutants/toxicity , Lung/drug effects , Bronchoalveolar Lavage Fluid/chemistry , Inhalation ExposureABSTRACT
OBJECTIVE: Due to their toxicity, diesel emissions have been submitted to progressively more restrictive regulations in developed countries. However, in Brazil, the implementation of the Cleaner Diesel Technologies policy (Euro IV standards for vehicles produced in 2009 and low-sulfur diesel with 50 ppm of sulfur) was postponed until 2012 without a comprehensive analysis of the effect of this delay on public health parameters. We aimed to evaluate the impact of the delay in implementing the Cleaner Diesel Technologies policy on health indicators and monetary health costs in Brazil. METHODS: The primary estimator of exposure to air pollution was the concentration of ambient fine particulate matter (particles with aerodynamic diameters <2.5 μm, [PM2.5]). This parameter was measured daily in six Brazilian metropolitan areas during 2007-2008. We calculated 1) the projected reduction in the PM2.5 that would have been achieved if the Euro IV standards had been implemented in 2009 and 2) the expected reduction after implementation in 2012. The difference between these two time curves was transformed into health outcomes using previous dose-response curves. The economic valuation was performed based on the DALY (disability-adjusted life years) method. RESULTS: The delay in implementing the Cleaner Diesel Technologies policy will result in an estimated excess of 13,984 deaths up to 2040. Health expenditures are projected to be increased by nearly US$ 11.5 billion for the same period. CONCLUSIONS: The present results indicate that a significant health burden will occur because of the postponement in implementing the Cleaner Diesel Technologies policy. These results also reinforce the concept that health effects must be considered when revising fuel and emission policies.
Subject(s)
Adult , Child, Preschool , Female , Humans , Infant , Infant, Newborn , Male , Middle Aged , Air Pollutants/toxicity , Gasoline/toxicity , Health Status Indicators , Public Health , Patient Admission/statistics & numerical data , Vehicle Emissions/toxicity , Age Distribution , Air Pollutants/standards , Brazil/epidemiology , Cardiovascular Diseases/epidemiology , Environmental Policy/economics , Hospital Mortality , Particulate Matter/toxicity , Patient Admission/economics , Respiratory Tract Diseases/epidemiologyABSTRACT
OBJECTIVE: To confirm the episode of eosinophilic pneumonitis that occurred in March 2001 in Manaus, Amazon, northern Brazil, as secondary to home aerosolization with 2 percent cypermethrin diluted in diesel compared with the more conventional 1 percent cypermethrin and soybean solution used in prophylaxis of dengue. METHODS: Four groups of Swiss mice were kept in polycarbonate cages aerosolized with one of the following solutions: diesel, diesel and cypermethrin, soy oil and cypermethrin, and saline. Three and 6 days after exposure, resistance and compliance of the respiratory system and white cell kinetics in peripheral blood and lung tissue were analyzed. RESULTS: The group exposed to diesel and cypermethrin showed higher respiratory system resistance (p < 0.001), lower compliance (p = 0.03), and increased eosinophils in blood (p = 0.03) and lung tissue (p = 0.005) compared with the other groups. There was an increase of neutrophils in the blood of all experimental groups on the third day after exposure (p < 0.001). CONCLUSIONS: We concluded that diesel associated with cypermethrin induced lung hyperresponsiveness in this experimental model and was associated with increased polymorphonuclear cells (eosinophils and neutrophils) in blood and lungs. This effect is strongest on the third day after exposure. These results are similar to the episode that occurred in Manaus in 2001 and suggest that diesel plus cypermethrin home aerosolization for arbovirosis prophylaxis should be revised.
OBJETIVO: Confirmar el episodio de neumonía eosinofílica ocurrido en marzo de 2001 en Manaus, Amazonas, en el norte de Brasil, secundario al uso de aerosol de cipermetrina diluida al 2 por ciento en aceite diésel en las viviendas en comparación con la profilaxis más convencional contra el dengue, basada en cipermetrina al 1 por ciento con aceite de soya. MÉTODOS: Se mantuvieron cuatro grupos de ratones suizos en jaulas de policarbonato y se aplicó aerosol con una de las siguientes soluciones: aceite diésel, aceite diésel y cipermetrina, aceite de soya y cipermetrina, y solución salina. Se analizaron la resistencia y el funcionamiento del sistema respiratorio y la cinética de leucocitos en sangre periférica y tejido pulmonar a los tres y seis días después de la exposición. RESULTADOS: El grupo expuesto a aceite diésel y cipermetrina mostró mayor resistencia del sistema respiratorio (P < 0,001), peor funcionamiento (P = 0,03) y más eosinófilos en sangre (P = 0,03) y tejido pulmonar (P = 0,005) que los otros grupos. Se observó un aumento de neutrófilos en sangre en todos los grupos experimentales al tercer día después de la exposición (P < 0,001). CONCLUSIONES: El aceite diésel con cipermetrina indujo una hiperrespuesta pulmonar en este modelo experimental y se asoció con un aumento en las células polimorfonucleares (eosinófilos y neutrófilos) en sangre y tejido pulmonar. Este efecto es mayor al tercer día después de la exposición. Estos efectos son similares a los observados en el episodio ocurrido en Manaus en 2001 e indican que se debe reevaluar el uso de aerosol de aceite diésel con cipermetrina para la profilaxis de arbovirus en las viviendas.
Subject(s)
Animals , Male , Mice , Gasoline/toxicity , Insecticides/toxicity , Pulmonary Eosinophilia/chemically induced , Pyrethrins/toxicity , AerosolsABSTRACT
In the present study, the micronucleus test was applied in exfoliated cells of buccal mucosa to assess the mutagenicity risk associated with occupational exposure for gas station attendants. For each individual, 2000 exfoliated buccal cells were analyzed for micronucleus frequency. A highly significant difference was found between exposed and control groups. Likewise, a significant difference was found between these groups regarding the frequency of binucleated and broken egg cells. To determine whether smoking, alcohol habit, age, gender, or working time could exert any additional effect, we determined the frequency of micronuclei and binucleated and broken egg cells amongst exposed and control individuals. The results allowed us to conclude that the individuals studied belong to a risk group and should periodically undergo biological monitoring and appropriate care.
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Occupational Exposure/adverse effects , Gasoline/toxicity , Air Pollutants, Occupational/adverse effects , Micronucleus Tests/methods , Case-Control Studies , Risk Factors , Mouth Mucosa/drug effects , Mouth Mucosa/pathologyABSTRACT
Para estudiar la relación en sangre, en madres y sus recién nacidos, se determinó la plumbemia a 51 parturientas y sus hijos en el Hospital Central de Maracay. Las determinaciones de plomo se hicieron por espectrofotometría de absorción atómica de llama, encontrándose un promedio de 11,8 µg/dl en las madres y 10,5 µg/dl en los recién nacidos, no existiendo diferencias estadísticamente significativas (p<0,05) y una correlación positiva (r Pearson = o,75). Se evidenció un incremento sustancial del plomo en sangre de los niños cuyas madres trabajan fuera del hogar, y un 63 por ciento de los recién nacidos presentó plubemias superiores a 10 µg/dl, que sobrepasan los límites establecidos en países industrializados. No se encontró asociación entre plubemia y el resto de las variables estudiadas, que incluyen edad y ocupación de la madre, edad gestacional, sexo, talla y peso del recién nacido. Surge la necesidad de nuevas investigaciones para evaluar el efecto neurotóxico del plomo en el desarrollo psicomotor de niños expuestos a concentraciones superiores a 10 µg/dl, y de tomar medidas para reducir o eliminar la principal fuente de contaminación atmosférica por plomo, representada por la utilización de gasolina con derivados alquílicos de ese metal