Exposure to persistent organic pollutants (POPs) and DNA damage as an indicator of environmental stress in fish of different feeding habits of Coatzacoalcos, Veracruz, Mexico.

The region of Coatzacoalcos, Veracruz hosts one of the largest and most important industrial areas of Mexico and Latin America. Industrial development and rapid population growth, have triggered a severe impact on aquatic ecosystems of the region. The aim of this study was to determine the levels of POPs in sediment and in muscle tissue of five fish species from different trophic levels in downstream residents of the Coatzacoalcos River, and their integration with DNA damage in the fish, evaluated with the comet assay in whole blood as a biological indicator of stress, in order to obtain a baseline of the ecological condition of the region. The compounds detected in sediment and in muscle tissue were hexachlorobenzene (HCB), α-, ß-, γ-hexachlorocyclohexane (HCH), dichlorodiphenyltrichloroethane (DDT), dichlorodiphenyldichloroethylene (DDE), mirex and polychlorinated biphenyls (PCBs). Sediment concentrations of these pollutants (except for mirex) exceeded the values of protection provided by international guidelines, suggesting a potential risk to aquatic life in the region. DNA damage recorded in the fish species is evidence of exposure to a mix of genotoxic pollutants, which combined with exposure to POPs, reflects the degree of environmental stress of aquatic organisms in the region. The results of this study show the importance of determining the presence of contaminants in the environment, the bioaccumulation in tissues and their effects on exposed organisms, providing an integrated approach in assessing the health of aquatic ecosystems.

Exposure assessment of persistent organic pollutants and metals in Mexican children.

Environmental policies in Mexico have contributed to the reduction in the production or use of some persistent organic pollutants (POPs) and metals. However, monitoring of POPs concentrations in humans living in hot spots is lacking. Therefore, the objective of this study was to conduct a screening for POPs and metals first in Mexican children living in high-risk areas. During the year 2004, we analyzed a total of 229 healthy children (aged 6-12 years old) who resided in communities located in nine Mexican states. Organochlorine insecticides, PCBs and metals were quantified in plasma and urine samples. We detected p'p-DDE in all the children; moreover, p'p-DDT, lindane and hexachlorobenzene were detected respectively in 14%, 85% and 10% of the children studied. Measurable levels of PCBs were recorded in only one community, where six of 14 PCB congeners assayed were detected (numbers 52, 118, 138, 153, 170 and 180). All the children had detectable levels of lead in their blood (mean level, 4.6 microg dL(-1)); furthermore, 57% of the children studied had levels higher than 5.0 microg/dL. The mean level of urinary arsenic (UAs) for all the children was 22.35 microg g(-1) creatinine and 15% of those children had concentrations of UAs above 50 microg g(-1) creatinine. For cadmium, the mean urinary level was 0.78 microg g(-1) creatinine, and only one percent of the children had values above 2.0 microg g(-1) creatinine. The results cannot be generalized since the communities selected are not representative of the Mexican population; however, they indicate that Mexican children are exposed to chemicals and some at risk levels.

Lipoprotein(a) and cardiovascular risk in adult Mexicans

De 1991 a 1992 se realizó un estudio epidemiológico transversal en una muestra aleatoria de la población adulta de la ciuda de México en la que se analizaron los factores de riesgo de enfermedad arterial coronaria (EAC). La concentración plasmática de lipoproteína(A) (Lp(a)) se midió por ELISA en 404 hombres y 311 mujeres de 20 a 90 años de edad. La mediana de Lp(a) fue de 6.9 mg/dL y la prevalencia de valores elevados (> 30 mg/dL) de 14 por ciento. El nivel de Lp(a) correlacionó positivamente con el de colesterol total (rs = 0.16) y con el colesterol de lipoproteína de baja densidad (C-LDL) (rs = 0.21), y en forma negativa con la insulina (rs = 0.13). La insulina y el C-LDL fueron las variables que mejoro explicaron las concentraciones de Lp(a) en la población. La distribución de Lp(a) en la ciudad de México es similar a la descrita para otras poblaciones y nuestros resultados sugieren, aunque sin alcanzar significancia estadística, que las cifras elevadas de Lp(a) pudieran estar asociadas con la EAC en nuestra población

Lipoproteína(a) en hipercolesterolemia familiar heterocigota / Lipoprotein (a) in heterozygous familial hypercholesterolemia

La hipercolesterolemia familiar es el trastorno genérico que más se asocia a cardiopatía aterosclerosa. Existe sin embargo, variabilidad en los heterocigotos en edad de presentación y gravedad de la aterosclerosis. En los últimos años se han informado concentraciones elevadas de Lp(a) en la hipercolesterolemia familiar, y se propone que ésto contribuya al desarrollo de la cardiopatía. Realizamos este estudio para valorar la relación entre concentraciones de Lp(a), y presencia de CAE en hipercolesterolemia familiar. Se estudiaron 38 pacientes con HF heterocigota: 13 con enfermedad coronaria y sin cardiopatía, y un grupo control. En comparación con el grupo control, los pacientes con HF tuvieron concentraciones mayores de Lp(a) (mediana 8.1 vs 16) y prevalencia mayor de niveles elevados de Lp(a) tomando como corte 30 mg/dl (11.4 vs 25.7 por ciento). Los cardiopatas tuvieron concentraciones más altas de Lp(a) (22.8 vs 14.4) que los no cardiópatas. Se encontró una correlación negativa, en las mujeres, entre la edad de aparición de la cardiopatía y las concentraciones de Lp(a). El grupo de cardiópatas mostró preponderancia de sexo masculino, edad más avanzada, frecuencia más alta de HTA y relación cintura/cadera mayor, valores medidos de Tg y prevalencia de hipertrigliceridemia más altos. Nuestros hallazgos sugieren que la Lp(a) puede constituir un factor de riesgo adicional para el desarrollo de aterosclerosis en la hipercolesterolemia familiar.