Lung-depositing surface area (LDSA) of particles in office spaces around Europe : Size distributions, I/O-ratios and infiltration

Air pollution, and specifically particulate matter pollution, is one of the greatest dangers to human health. Outdoor air pollution ranks third in causes for premature death. Improving indoor air quality is of immense importance, as the time spent indoors is often much greater than the time spent outdoors. In this experimental study, we evaluate the levels of particle pollution in indoor air in four offices across Europe, compare the indoor particles to outdoor particles and assess where the particles originate from. The measurements were conducted with an Electrical Low-Pressure Impactor (ELPI+) for particles between 6 nm and 1 μm. The chosen metric, lung-deposited particle surface area (LDSA), targets the health impacts of particle pollution. Based on the measurements, we determined that most of the indoor air particles infiltrated from outdoor air, although two of the offices had very limited indoor activity during the measurement campaigns and may not represent typical use. The highest median indoor LDSA concentration during daytime hours was 27.2 μm2/cm3, whereas the lowest was 2.8 μm2/cm3. Indoor air in general had lower LDSA concentrations than outdoor air, the corresponding outdoor LDSA concentrations being 35.8 μm2/cm3 and 9.8 μm2/cm3. The particle size ranges which contributed to the highest concentrations were 50–100 nm and 300–500 nm. These size ranges correspond to soot mode and accumulation mode particles, which represent local and regional sources, respectively. Based on this study, limiting particle infiltration is the key factor in keeping indoor air in offices free of lung-depositing particles.Peer reviewe

Off-cycle, Real-World Emissions of Modern Light Duty Diesel Vehicles

Copyright © 2009 SAE International This paper investigates the emissions performance of modern European light-duty passenger vehicles with turbodiesel engines during real-world driving, notably during two extreme but not uncommon operating regimes: congested urban traffic and high-speed and performance driving. Four cars and one van were tested on a chassis dynamometer and/or on the road with a portable, on-board emissions monitoring system capable of online measurements of particulate and gaseous emissions. On all cars, operation at speeds and acceleration rates in excess to those within the applicable certification NEDC cycle resulted in higher concentrations of nitrogen oxide (NO) and particulate matter (PM). High-speed driving in excess of 120 km/h resulted in a marked increase in NO and PM concentrations, with further increases past 130-140 km/h. In urban driving, highest PM concentrations occurred at the onset of and during accelerations from low rpm. Aggressive, performance driving resulted in substantial increase in NO and PM emissions per kg of fuel compared to normal driving. No marked increases outside of NEDC regimes were, however, observed on the van. The results support the arguments against increase in 130 km/h freeway speed limits and for augmenting the EU certification tests for light diesel vehicles with supplemental cycles or tests

Immunohistochemical Detection of Cancer Stem Cell Related Markers CD44 and CD133 in Metastatic Colorectal Cancer Patients

Aim. The goal of this study was to semiquantitatively detect presence of cancer stem cells markers CD44 and CD133 in immunohistochemically stained paired samples of colorectal cancer (CRC) and colorectal liver metastases (CLM). Level of staining intensity was compared to clinical and pathological characteristics of tumors with the aim to identify impact of CD44 or CD133 expression on tumor behavior. Patients and Methods. Formalin fixed paraffin embedded samples from 94 patients with colorectal tumor and liver metastases were collected at Sikl’s Department of Pathology. Samples were stained by antibodies against CD44 and CD133. Presence and intensity of staining was assessed semiquantitatively by three trained researchers. Results. Patients with higher level of CD133 staining in CRC had longer disease free interval (Cox-Mantel P=0.0244), whereas we found no relation between CD44 expression and overall survival or disease free interval. CD133 expression in CRC and CLM differed based on CRC grading; in case of CD44 we found differences in staining intensity in individual stages of tumor lymph node invasion. Conclusion. Effect of cancer stem cell markers on prognosis of colorectal cancer can vary depending on pathological classification of tumor, and we have shown that CD133, generally considered to be a negative marker, can bear also clinically positive prognostic information in group of patients with colorectal liver metastases

Ordinary Gasoline Emissions Induce a Toxic Response in Bronchial Cells Grown at Air-Liquid Interface

Gasoline engine emissions have been classified as possibly carcinogenic to humans and represent a significant health risk. In this study, we used MucilAir™, a three-dimensional (3D) model of the human airway, and BEAS-2B, cells originating from the human bronchial epithelium, grown at the air-liquid interface to assess the toxicity of ordinary gasoline exhaust produced by a direct injection spark ignition engine. The transepithelial electrical resistance (TEER), production of mucin, and lactate dehydrogenase (LDH) and adenylate kinase (AK) activities were analyzed after one day and five days of exposure. The induction of double-stranded DNA breaks was measured by the detection of histone H2AX phosphorylation. Next-generation sequencing was used to analyze the modulation of expression of the relevant 370 genes. The exposure to gasoline emissions affected the integrity, as well as LDH and AK leakage in the 3D model, particularly after longer exposure periods. Mucin production was mostly decreased with the exception of longer BEAS-2B treatment, for which a significant increase was detected. DNA damage was detected after five days of exposure in the 3D model, but not in BEAS-2B cells. The expression of CYP1A1 and GSTA3 was modulated in MucilAir™ tissues after 5 days of treatment. In BEAS-2B cells, the expression of 39 mRNAs was affected after short exposure, most of them were upregulated. The five days of exposure modulated the expression of 11 genes in this cell line. In conclusion, the ordinary gasoline emissions induced a toxic response in MucilAir™. In BEAS-2B cells, the biological response was less pronounced, mostly limited to gene expression changes