Genotoxicity caused by tobacco smoke was assessed in peripheral blood lymphocytes of smokers living in Mexico City by determining sister chromatid exchange (SCE), cell proliferation kinetics (CPK), replication index (RI) and mitotic index (MI). Nicotine levels, and its major metabolite cotinine, were also estimated in urine samples using gas-chromatography-mass spectrometry to quantify smoking intensity. The outcome of the analysis and the comparison of the 77-smoker group with a non-smoking control group showed that moderate and heavy smokers exhibited significant differences ( P < 0.001 and P < 0.05, respectively) in CPK, with an underlying delay in the cellular cycle; similarly, RI was significantly different in these groups ( P < 0.001 and P < 0.0001, respectively). There were significant correlations ( P < 0.05) between age and number of years the subject had been smoking, as well as between RI and nicotine and cotinine levels and between CPK (M1, M2 and M3) and nicotine and cotinine levels. Smokers were classified for the analysis according to the nicotine levels (it is in relation to number of cigarettes smoked per day) found in urine (ng/mL) as: light (10—250), moderate (251—850) and heavy (851—4110). Significant differences in CPK were found ( P < 0.05) between moderate and heavy smokers and non-smokers. Significant differences in RI were found between moderate ( P < 0.001) and heavy smokers ( P < 0.0001) and non-smokers, but not for the light smoking group. MI was determined in 57 of the smokers, whereas SCE frequency was only recorded in 34 smokers. Both parameters yielded no significant differences, nor correlations with any of the assessed variables. In conclusion, cytokinetic and cytostatic effects were mainly detected in heavy and moderate smokers. Cell cycle delay and RI decrease were found in all `healthy' smokers. The nicotine and cotinine exposure (causing oxidative damage to DNA) may have implications in the decrease in cell replication due to direct damage to DNA and/or a decrease in the DNA repair mechanisms. Alternatively, nicotine and cotinine may possibly induce apoptosis. Human & Experimental Toxicology (2007) 26, 715—722

Se evaluaron invertebrados del suelo, en particular los colémbolos, como bioindicadores de la calidad de suelos contaminados con hidrocarburos en el sureste de México. Se realizaron 2 muestreos en verano-otoño del 2004, en 4 parcelas de 2 hectáreas, denominadas zona 1, 2, 3 y control. De cada unidad se tomaron 8 muestras que fueron procesadas por medio del embudo de Berlese-Tullgren y 4 por el método de fl otación. Para colémbolos se determinaron los siguientes índices ecológicos: abundancia, riqueza, índice de Shannon (H'), dominancia (λ), equidad(J') e índice de similitud (S). Se realizaron análisis fi sicoquímicos del suelo: hidrocarburos totales del petróleo (HTP) e hidrocarburos aromáticos policíclicos (HAP), porosidad, pH, CE, MO, N, P, K, CIC y textura. Los HTP, en las zonas contaminadas, sobrepasan los límites de las normas mexicanas ambientales. En todas las zonas de estudio se observaron colémbolos, ácaros y larvas de dípteros, por lo que su abundancia y diversidad pueden ser utilizadas como bioindicadores del grado de contaminación y calidad del suelo. En las zonas contaminadas se registraron abundancias muy bajas de Crustacea, Formicidae, Araneae, Diptera, Pseudoscorpionida, y Diplopoda. Las familias de los colémbolos más ampliamente distribuidas fueron Sminthurididae e Isotomidae. De acuerdo con el análisis de correlación, su diversidad de colémbolos es afectada por la presencia de HAP (fl ouranteno, naftaleno, pireno, criseno y fenantreno) Palabras clave: Collembola, suelos contaminados, hidrocarburos, mesofauna.

Airborne lead has been considered for many years one of the main pollutants adversely affecting the health of human beings. Moreover, this problem becomes remarkably important in large urban areas such as Mexico City. In order to assess the influence of atmospheric airborne lead in a children population, a biological blood sampling was carried out from September 1992 to June 1993 taking 698 samples in children with ages ranging from a few weeks to thirteen years old. Lead contents in whole blood were determined using anode stripping voltammetry as analytical technique. At the same time, aerosol lead contents were determined by PIXE from samples taken twice a week (two samples per day) in a neighbour area. In 58 % of the samples, lead contents in blood was found over the maximum permissible level established by the Center for Disease Control (CDC) of the U.S.A. The biological sampling was correlated to levels of airborne lead as well as children age and date of sampling. General results of these comparisons are presented.

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