Vanadium inhalation in a mouse model for the understanding of air-suspended particle systemic repercussion.

There is an increased concern about the health effects that air-suspended particles have on human health which have been dissected in animal models. Using CD-1 mouse, we explore the effects that vanadium inhalation produce in different tissues and organs. Our findings support the systemic effects of air pollution. In this paper, we describe our findings in different organs in our conditions and contrast our results with the literature.

Endogenous antioxidants and nasal human epithelium response to air pollutants: genotoxic and inmmuno-cytochemical evaluation.

Nasal epithelium is a source for identifying atmospheric pollution impact. Antioxidants play a relevant role in the protection of the cells from environmental injury, but scarce information is available about the interaction of endogenous antioxidants and genotoxic damage in nasal epithelium from urban populations highly exposed to traffic-generated air pollutants. An immunocytochemical and genotoxic evaluation was implemented in nasal cell epithelium in a population chronically exposed to atmospheric pollution from autumn 2004 to autumn 2005. Superoxide dismutase (SOD) and Catalase (CAT) were evaluated in nasal scrapings by morphometry and genotoxicity by comet assay. An increase in DNA damage correlates with a decrease in SOD and CAT in nasal cells during autumn and the inverse result was observed during summer (R = 0.88). Not only should exogenous antioxidant supplements be encouraged, but also a healthy diet to strengthen intracellular defenses against oxidative stress induced by exposure to air pollutants.

Overview of environmental and occupational vanadium exposure and associated health outcomes: an article based on a presentation at the 8th International Symposium on Vanadium Chemistry, Biological Chemistry, and Toxicology, Washington DC, August 15-18, 2012.

Vanadium (V) has a variety of applications that make it suitable for use in ceramic production and decoration, production of pigments for a variety of products, an accelerator for drying paint, production of aniline black dye, and as a mordant in coloring textiles. Taking advantage of its hardness, resilience, ability to form alloys, and its resistance to corrosion, V is also used in the production of tools, steel, machinery, and surgical implants. V is employed in producing photographic developers, batteries, and semi-conductors, and in catalyst-based recycling processes. As technologies have evolved, the use of V has increased in jet aircraft and space technology, as well as in manufacture of ultraviolet filter glass to prevent radiation injury. Due to these myriad uses, the potential for occupational exposure to V is ever-evident. Similarly, there is an increased risk for environmental contamination by V agents themselves or as components of by-products released into the environment. For example, the use of V in sulfuric acid production results in the release of soot and/or fly ash rich in vanadium pentoxide. Petroleum refinery, smelting, welding, and cutting of V-rich steel alloy, the cleaning and repair of oil-fired boilers, and catalysis of chemical productions are other sources of increased airborne V-bearing particles in local/distant environments. Exposure of non-workers to V is an increasing health concern. Studies have demonstrated associations between exposure to airborne V-bearing particles (as part of air pollution) and increased risks of a variety of pathologies like hypertension, dysrhythmia, systemic inflammation, hyper-coagulation, cancers, and bronchial hyper-reactivity. This paper will provide a review of the history of V usage in occupational settings, documented exposure levels, environmental levels of V associated with pollution, epidemiologic data relating V exposure(s) to adverse health outcomes, and governmental responses to protect both workers and non-workers from exposure to this metal.

Vanadium pentoxide inhalation provokes germinal center hyperplasia and suppressed humoral immune responses.

Vanadium, an important air pollutant derived from fuel product combustion, aggravates respiratory diseases and impairs cardiovascular function. In contrast, its effects on immune response are conflicting. The aim of our work was to determine if spleens of vanadium-exposed CD1 mice showed histological lesions that might result in immune response malfunction. One hundred and twelve CD-1 male mice were placed in an acrylic box and inhaled 0.02 M vanadium pentoxide (V2O5); actual concentration in chamber approximately 1.4 mg V2O5/m(3)) for 1 hr/d, twice a week, for 12 wk. Control mice inhaled only vehicle. Eight mice were sacrificed prior to the exposures. Eight control and eight V2O5-exposed mice were sacrificed 24 hr after the second exposure of each week until the 12-wk study was over. Another 8 mice that completed the 12-wk regimen were immunized with recombinant Hepatitis B surface antigen (HBsAg; three times over an 8-wk period) before sacrifice and analyses of their levels of anti-HBsAg antibody (HBSAb) using ELISA. In all studies, at sacrifice, blood samples were obtained by direct heart puncture and the spleen was removed, weighed and processed for H-E staining and quantitation of CD19 cells. The results indicated that the spleen weight of V2O5-exposed animals peaked at 9 wk (546 +/- 45 vs. 274 +/- 27 mg, p < 0.0001) and thereafter progressively decreased (321 +/- 39 mg at 12 wk, p < 0.001; control spleen = 298 +/- 35 mg). Spleens of V2O5-exposed animals showed an increased number of very large and non-clearly delimited germinal centers (that contained more lymphocytes and megakaryocytes) compared to those of control mice. In addition, their red pulp was poorly delimited and had an increase in CD19+ cells within hyperplasic germinal nodes. The mean HBsAb levels in immunized control mice were greater than that in the exposed hosts (i.e., OD = 0.39 +/- 0.03 vs. 0.11 +/- 0.05, p < 0.01). HBsAb avidity dropped to a value of 40 in V2O5-exposed animals vs. 86 in controls (p < 0.0001). We conclude that the chronic inhalation of V2O5, a frequent particle (PM(2.5)) component, induces histological changes and functional damage to the spleen, each of which appear to result in severe effects on the humoral immune response.

Matrix metalloproteinases 2 and 9 in central nervous system and their modification after vanadium inhalation.

Vanadium (V) derivatives are well-known environmental pollutants and its toxicity has been related with oxidative stress. Toxicity after vanadium inhalation on the substantia nigra, corpus striatum, hippocampus and ependymal epithelium was reported previously. The purpose of this study was to analyse the role of matrix metalloproteinases 2 (MMP-2) and 9 (MMP-9) in the changes observed in brain tissue after chronic V inhalation. Mice were exposed to vaporized, vanadium pentoxide 0.02 m in deionized water for 1 h twice a week, and killed at 1 h, 1, 2 and 4 weeks after exposure. The brain was removed and the olfactory bulb, prefrontal cortex, striatum and hippocampus were dissected and the MMP content was obtained by zymography. The results showed that MMP-9 increased in all the structures at the end of the exposure, although in the hippocampus this increment was evident after 1 week of exposure. When MMP-2 was analysed in the olfactory bulb and prefrontal cortex it remained unchanged throughout the whole exposure, while in the hippocampus it increased at week 4, while in the striatum MMP-2 increased from the second week only, through the whole experiment. These results demonstrate that V increased MMPs in different structures of the CNS and this change might be associated with the previously reported modifications, such as dendritic spine loss and neuronal cell death. The modifications in MMPs could be related with blood-brain barrier (BBB) disruption which was reported previously. Oxidative stress might also be involved in the activation of these gelatinases as part of the different mechanisms which take place in V toxicity in the CNS.

DNA damage as an early biomarker of effect in human health.

In the last few decades the need for new approaches to assess DNA damage has been increasing due to the implications that different insults on genetic material may have on human health. In this context, the identification of how chemical agents with different mechanisms of action (i.e., antineoplastic drugs) damage DNA provides a good model to investigate some cellular and molecular mechanisms underlying the basis of genetic toxicology. The nasal epithelium is the first barrier with which environmental pollutants interact, and for this reason this epithelium can be useful as a sentinel in order to assess the interactions between the environment and the living organisms. Taking these phenomena into account and using a simple, sensitive and rapid method such as the single cell gel electrophoresis, we could obtain information and an initial approach on the DNA status. This assay in combination with other techniques that provide more information about other molecular parameters could give us a better view of the biological status of the living cell.