Cellular uptake and cytotoxic potential of respirable bentonite particles with different quartz contents and chemical modifications in human lung fibroblasts

Considering the biological reactivity of pure quartz in lung cells, there is a strong interest to clarify the cellular effects of respirable siliceous dusts, like bentonites. In the present study, we investigated the cellular uptake and the cytotoxic potential of bentonite particles (Ø< 10 μm) with an α-quartz content of up to 6% and different chemical modifications (activation: alkaline, acidic, organic) in human lung fibroblasts (IMR90). Additionally, the ability of the particles to induce apoptosis in IMR90-cells and the hemolytic activity was tested. All bentonite samples were tested for endotoxins with the in vitro-Pyrogen test and were found to be negative. Cellular uptake of particles by IMR90-cells was studied by transmission electron microscopy (TEM). Cytotoxicity was analyzed in IMR90-cells by determination of viable cells using flow cytometry and by measuring of the cell respiratory activity. Induced apoptotic cells were detected by AnnexinV/Propidiumiodide-staining and gel electrophoresis. Our results demonstrate that activated bentonite particles are better taken up by IMR90-cells than untreated (native) bentonite particles. Also, activated bentonite particles with a quartz content of 5–6% were more cytotoxic than untreated bentonites or bentonites with a quartz content lower than 4%. The bentonite samples induced necrotic as well as apoptotic cell death. In general, bentonites showed a high membrane-damaging potential shown as hemolytic activity in human erythrocytes. We conclude that cellular effects of bentonite particles in human lung cells are enhanced after chemical treatment of the particles. The cytotoxic potential of the different bentonites is primarily characterized by a strong lysis of the cell membrane.     

Characterization of Gas and Particle Emission from Smoldering Incenses with Various Diameters

No abstract available.     

Emergence of unusual human rotavirus strains in Salento, Italy, during 2006–2007

Background  

In recent years, rotavirus genotyping by RT-PCR has provided valuable information about the diversity of rotaviruses (RV) circulating throughout the world.     

Air Pollution and Cardiac Arrhythmias in Patients with Implantable Cardioverter Defibrillators

Epidemiological studies have demonstrated associations between short-term increases in outdoor air pollution concentrations and adverse cardiovascular effects, including cardiac mortality and hospitalizations. One possible mechanism behind this association is that air pollution exposure increases the risk of developing a cardiac arrhythmia. To investigate this hypothesis, dates of implantable cardioverter defibrillator (ICD) discharges were abstracted from patient records in patients attending the two ICD clinics in Vancouver, BC, for the years 1997–2000. Daily outdoor air pollutant concentrations and daily meteorological data from the Vancouver region were obtained for the same 4-yr period. Generalized estimating equations were used to assess the association between short-term increases in air pollutant concentrations and ICD discharges while controlling for temporal trends, meteorology, and serial correlation in the data. Air pollution concentrations in the Vancouver region were relatively low from 1997 to 2000, as expected. In the 50 patients who resided within the Vancouver region and who experienced at least 1 ICD discharge during the period of follow-up, no significant associations between increased air pollution concentrations and increased ICD discharges were present. When the patient sample was restricted to the 16 patients who had at least 6 months of follow-up and experienced a rate of at least 2 days with ICD discharges per year, there was a statistically significant association between increased sulfur dioxide (SO₂) concentration and ICD discharge 2 days after the SO₂ increase. When stratified by season, no associations between increased air pollutant concentrations and increased risk of ICD discharge were observed in the summer, although for several pollutants, concentration increases were associated with a decrease in ICD discharges. In the winter, increased SO₂ concentrations again were seen to be associated with increased risk of ICD discharge, at both 2 and 3 days following increases in SO₂ concentrations. These findings provide no compelling evidence that short-term increases in relatively low concentrations of outdoor air pollutants have an adverse effect on individuals at risk of cardiac arrhythmias. The findings regarding SO₂ are difficult to interpret. They may be chance findings. Alternatively, given the very low concentrations of SO₂ that were present in Vancouver, SO₂ may have been serving as a surrogate measure of other environmental or meteorological factors.     

Effects of Concentrated Ambient Particles on Heart Rate,Blood Pressure,and Cardiac Contractility in Spontaneously Hypertensive Rats

Epidemiological studies have shown that particulate matter (PM) air pollution is associated with cardiovascular mortality and morbidity, especially for particles with aerodynamic diameters under 2.5 μm (PM_2.5). Recent studies have revealed an association between PM pollution and autonomic functions including heart rate (HR), blood pressure (BP), and heart-rate variability. However, the association and linking mechanisms have not been clearly demonstrated in animal studies. Utilizing a novel approach that employs a mixed-effects model to overcome the problems of variations in diseased animals and circadian cycles, we have previously demonstrated an association between concentrated PM_2.5 and changes of HR and BP in pulmonary hypertensive rats. The objective of this study is to test the plausibility of this methodology and to demonstrate the particle effects under different pathophysiology. The feasibility of cardiac contractility (measured as QA interval, QAI) as an indicator for PM toxicology was also explored. Four spontaneously hypertensive (SH) rats were repeatedly exposed to concentrated PM_2.5 during spring and summer. The mass concentration of particles during the 5 h of exposure was 202.0 ± 68.8 (mean ± SE) and 141.0 ± 54.9 μg/m³ for spring and summer experiments, respectively. During spring exposures, the maximum increase of HR and mean BP noted at the end of exposure were 51.6 bpm (p < .001) and 8.7 mm Hg (p = .002), respectively. The maximum decrease of QAI noted at the same time was 1.6 ms (p = .001). Though a similar pattern was demonstrated during summer exposures, the responses were less prominent. We conclude that concentrated PM_2.5 may increase HR and mean BP and decrease QAI in SH rats. Our results also show that QAI may be used as an indicator in PM toxicology.     

Developmental exposure to decabrominated diphenyl ether (BDE‐209): Effects on sperm oxidative stress and chromatin dna damage in mouse offspring

Polybrominated diphenyl ethers (PBDEs) are used as brominated flame retardants and have been found in human milk in recent years. This study investigates whether prenatal exposure to decabrominated diphenyl ether (BDE‐209) induces sperm dysfunction in male offspring. Pregnant CD‐1 mice were gavaged once daily with corn oil (control), 10, 500, and 1500 mg kg^?1 body weight of BDE‐209 from day 0 of gestation to day 17. The outcomes of male reproductive parameters were assessed on postnatal day 71. Anogenital distance, sperm‐head abnormalities, and testicular histopathology were significantly affected in male offspring prenatally exposed to 1500 mg kg^?1. Significant increases in the tendency for sperm DNA denaturation (αT) induction and the DNA fragmentation index (DFI) were found in those exposed to 10, 500, and 1500 mg kg^?1 (P < 0.05). We observed a significant increase of sperm hydrogen peroxide (H₂O₂) generation in the 10 and 1500 mg/kg/day groups compared to the control group (P < 0.05). Although our findings suggested that the mechanisms underlying BDE‐209‐induced sperm DNA damage and H₂O₂ generation might not be represented as a dose‐response relationship, we found that the greater the excess production of sperm H₂O₂, the greater the sperm αT (r = 0.65, P = 0.0155) and DFI (r = 0.53, P = 0.002). In conclusion, developmental exposure to BDE‐209 induced sperm‐head abnormality, oxidative stress, chromatin DNA damage, and testicular histopathological changes. These findings suggest that BDE‐209‐induced male reproductive effects might involve the formation of sperm H₂O₂ which attacks nucleic acids via H₂O₂ generation. © 2011 Wiley Periodicals, Inc. Environ Toxicol, 2013.