Vanadium concentrations in lung tissue were determined by atomic absorption spectrometry from autopsy specimens taken from residents of Mexico City during the 1960s and 1990s (20 males and 19 females, and 30 males and 18 females, respectively). Samples from the 1990s had significantly increased mean vanadium concentrations (mean +/- standard deviation: 1.36 +/- 0.08), compared with those from the 1960s (1.04 +/- 0.05). Concentrations were not correlated with gender, smoking habit, age, cause of death, or occupation. These findings suggest that vanadium in ambient air is increasing and it represents a potential health hazard for Mexico City residents. Air pollution monitoring efforts should include vanadium concentrations in suspended particles to follow-up the findings reported herein. Researchers need to acquire a better knowledge of the levels of airborne vanadium exposure at which risk to human health occurs.
Air pollution is an important health problem in some countries. For Mexico City, repeatedly high levels of some metals including lead (Pb) have been reported. Since there is no relevant information, we used an inhalation model to identify the possible lung cell damage after exposure of animals to Pb. We used thirty CD-1 male mice that were inhaling (for 1 hour) aerosolized lead acetate 0.1M, three times per week during two weeks. Mice were sacrificed by cervical dislocation on days 1, 3, 5, 7, 10 and 15 after the last Pb exposure. Their lungs were fixed by intratracheal instillation of glutaraldehyde. Lung tissue for morphological observation and metal concentration was sampled. In the exposed mice, on days 3 and 5 changes in the nonciliated bronchiolar cells appeared. Whorl-like structures were present in the cell apex. These structures compressed other organelles. On day 5 after the final inhalation, the structures increased in size, and by day 10 they disappeared. After the last inhalation, the metal concentration in the lung tissue continuously decreased until day 7 when no more metal was detected. It was evident that the contact of the NCBC with Pb produces changes in the morphology of these cells. The metal concentrations in the lung decreased when the exposure ended. This finding supports the assumption that Pb is not accumulated in lung tissue. As a consequence, the cellular modifications decreased and began their way to morphological recovery.
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