Cristina Monteiro

Emission of trace gases and organic components in smoke particles from a wildfire in a mixed-evergreen forest in Portugal

On May 2009, both the gas and particulate fractions of smoke from a wildfire in Sever do Vouga, central Portugal, were sampled. Total hydrocarbons and carbon oxides (CO(2) and CO) were measured using automatic analysers with flame ionisation and non-dispersive infrared detectors, respectively. Fine (PM(2.5)) and coarse (PM(2.5-10)) particles from the smoke plume were analysed by a thermal-optical transmission technique to determine the elemental and organic carbon (EC and OC) content. Subsequently, the particle samples were solvent extracted and fractionated by vacuum flash chromatography into different classes of organic compounds. The detailed organic speciation was performed by gas chromatography-mass spectrometry. The CO, CO(2) and total hydrocarbon emission factors (g kg(-1) dry fuel) were 170 ± 83, 1485 ± 147, and 9.8 ± 0.90, respectively. It was observed that the particulate matter and OC emissions are significantly enhanced under smouldering fire conditions. The aerosol emissions were dominated by fine particles whose mass was mainly composed of organic constituents, such as degradation products from biopolymers (e.g. levoglucosan from cellulose, methoxyphenols from lignin). The compound classes also included homologous series (n-alkanes, n-alkenes, n-alkanoic acids and n-alkanols), monosaccharide derivatives from cellulose, steroid and terpenoid biomarkers, and polycyclic aromatic hydrocarbons (PAHs). The most abundant PAH was retene. Even carbon number homologs of monoglycerides were identified for the first time as biomarkers in biomass burning aerosols.

Cadmium-induced genotoxicity in human osteoblast-like cells.

Cadmium (Cd) is a widespread heavy metal used in numerous industrial processes. Cd exerts toxicological effects mostly in kidney and liver. Bone is also an important target of Cd, however, the cellular mechanisms of Cd toxicological effects in the bone cells are still poorly understood. Therefore, the present work aimed to investigate the putative cytotoxic and genotoxic effects of Cd to human bone cells. For that, the osteoblast-like MG-63 cells were exposed to 20 and 50μM Cd for 24 and 48h. Results showed a dose-dependent increase in Cd accumulation in cells and a decrease in cell viability, especially after 48h. Cell cycle analysis showed a delay at S phase concomitant with a decrease in cells at G0/G1 phase. After 24h, Cd treatment downregulated the expression of CHEK1, CHEK2 and CDK2 genes and upregulated the expression of CCNE1 gene. After 48h, the expression of ATM and CCNB1 genes were downregulated. Also, a 3.3 fold increase on the expression of gene CCNE1 was detected. Both Cd doses induced DNA fragmentation at 48h, while an increase in micronuclei (MN) and nucleoplasmic bridges (NPBs) together with an increase in the percentage of apoptotic/necrotic cells was detected for both time periods. Overall, our results demonstrate the cytotoxicity and genotoxicity of Cd in human bone cells. Also, the cytokinesis-block micronucleus (CBMN) assay parameters (MN, NPBs and the percentage of cells under apoptosis or necrosis) together with the cell cycle appear as the most sensitive to Cd cyto- and genotoxicity, being early affected even with the lowest Cd dose. Therefore, these cyto-/genotoxic techniques may be selected for early detection of Cd-induced toxicity.

Hydrocarbons in particulate samples from wildfire events in central Portugal in summer 2010

In summer 2010, twenty eight (14 PM2.5 samples plus 14 samples PM2.5-10) smoke samples were collected during wildfires that occurred in central Portugal. A portable high-volume sampler was used to perform the sampling, on quartz fibre filters of coarse (PM2.5-10) and fine (PM2.5) smoke samples. The carbonaceous content (elemental and organic carbon) of particulate matter was analysed by a thermal-optical technique. Subsequently, the particulate samples were solvent extracted and fractionated by vacuum flash chromatography into three different classes of organic compounds (aliphatics, polycyclic aromatic hydrocarbons (PAHs) and carbonyl compounds). The organic speciation was performed by gas chromatography-mass spectrometry (GC-MS). Emissions were dominated by the fine particles, which represented around 92% of the PM10. A clear predominance of carbonaceous constituents was observed, with organic to elemental carbon (OC/EC) ratios ranging between 1.69 and 245 in both size fractions. The isoprenoid ketone 6,10,14-trimethyl-2-pentadecanone, a tracer for secondary organic aerosol formation, was one of the dominant constituents in both fine and coarse particles. Retene was the most abundant compound in all samples. Good correlations were obtained between OC and both aliphatic and PAH compounds. Pyrogenic processes, thermal release of biogenic compounds and secondary processing accounted for 97% of the apportioned PM2.5 levels.

Biochemical and transcriptional analyses of cadmium-induced mitochondrial dysfunction and oxidative stress in human osteoblasts

ABSTRACT Cadmium (Cd) accumulation is known to occur predominantly in kidney and liver; however, low-level long-term exposure to Cd may also result in bone damage. Few studies have addressed Cd-induced toxicity in osteoblasts, particularly upon cell mitochondrial energy processing and putative associations with oxidative stress in bone. To assess the influence of Cd treatment on mitochondrial function and oxidative status in osteoblast cells, human MG-63 cells were treated with Cd (up to 65 μM) for 24 or 48 h. Intracellular reactive oxygen species (ROS), lipid and protein oxidation and antioxidant defense mechanisms such as total antioxidant activity (TAA) and gene expression of antioxidant enzymes were analyzed. In addition, Cd-induced effects on mitochondrial function were assessed by analyzing the activity of enzymes involved in mitochondrial respiration, membrane potential (ΔΨm), mitochondrial morphology and adenylate energy charge. Treatment with Cd increased oxidative stress, concomitantly with lipid and protein oxidation. Real-time polymerase chain reaction (qRT-PCR) analyses of antioxidant genes catalase (CAT), glutathione peroxidase 1 (GPX1), glutathione S-reductase (GSR), and superoxide dismutase (SOD1 and SOD2) exhibited a trend toward decrease in transcripts in Cd-stressed cells, particularly a downregulation of GSR. Longer treatment with Cd (48 h) resulted in energy charge states significantly below those commonly observed in living cells. Mitochondrial function was affected by ΔΨm reduction. Inhibition of mitochondrial respiratory chain enzymes and citrate synthase also occurred following Cd treatment. In conclusion, Cd induced mitochondrial dysfunction which appeared to be associated with oxidative stress in human osteoblasts.

Bridging a Gap between Cr(VI)-Induced Oxidative Stress and Genotoxicity in Lettuce Organs after a Long-Term Exposure

Chromium (Cr) contamination in arable soils and irrigating water remains a priority, particularly due to the challenges posed to crop production and food safety. Long-term Cr(VI) effects remain less addressed than short-term ones, particularly regarding organ-specific genotoxic profiles. Here we used the crop Lactuca sativa growing in a protected horticultural system and irrigated for 21 days with Cr(VI) (up to 200 mg/L). Besides the oxidative stress, the genotoxicity was evaluated. Shoots and roots showed distinctive oxidative stress status and genotoxic effects, in a dose-dependent manner. While 50 mg/L stimulated antioxidant activities and no major genotoxic effects were found, plants exposed to ≥150 showed an increase of oxidative disorders, together with cytostatic and DNA damage effects, and some mitotic impairment. Leaves showed less oxidative signs at 50 mg/L, while at 150/200 mg/L the antioxidant battery was stimulated. In Cr treated plants, the highest dose increased the DNA damage, reinforcing the idea that DNA breaks were related to mitotic disorders in higher doses. In conclusion, long-term exposure data show a highly responsive root, with a quadratic response meaning higher defenses at lower Cr doses, and higher oxidative and DNA damage and cytostatic effect at a higher dose.