No abstract

The aim of this study was to evaluate DNA damage and the capacity for DNA repair in children exposed to arsenic and lead. During 2006, we studied a total of 85 healthy children (aged 4-11 years) who were residents of Villa de la Paz (community A), Matehuala (community B), and Soledad de Graciano Sanchez (community C) in San Luis Potosi, Mexico. The quantification of arsenic in urine (AsU) and lead in blood (PbB) was performed by atomic absorption spectrophotometry. The alkaline comet assay was used to evaluate DNA damage and DNA repair. The highest levels of AsU and PbB in children were found in community A (44.5 μg/g creatinine for arsenic and 11.4 μg/dL for lead), followed by community B (16.8 μg/g creatinine for arsenic and 7.3 μg/dL for lead) and finally by children living in community C (12.8 μg/g creatinine for arsenic and 5.3 μg/dL for lead). When DNA damage was assessed, children living in community A had the highest DNA damage. Analysis of these same cells 1 h after a challenge with H(2)O(2) 10 μM showed a dramatic increase in DNA damage in the cells of children living in community B and community C, but not in the cells of children living in community A. Moreover, significantly higher levels of DNA damage were observed 3 h after the challenge ended (repair period) in cells from individuals living in community A. Our results show that children exposed to metals might be more susceptible to DNA alterations.

No abstract

In order to test the value of an integrated approach for the analysis of health risks at contaminated sites, an integrated health risk assessment in a mining area was performed following 3 steps: 1) Environmental monitoring of surface soil, 2) assessment of exposure to metals in children and native rodents, and 3) DNA damage evaluation (comet assay) in children and rodents. These aspects also were studied in less exposed populations. Our results in humans showed that children living in the most polluted area (Villa de la Paz, Mexico) had higher lead blood concentrations (geometric mean of 13.8 microg/dL) and urinary arsenic levels (geometric mean of 52.1 microg/g creatinine) compared to children living in a control area (Matehuala, Mexico; blood lead of 7.3 microg/dL; urinary arsenic of 16.8 microg/g creatinine). Furthermore, the exposed children also had increased DNA damage (tail moment mean in Villa de la Paz of 4.8 vs 3.9 in Matehuala; p < 0.05). Results in rodents were identical. Animals captured in the polluted area had higher levels of arsenic (geometric mean of 1.3 microg/g in liver and 1.8 microg/g in kidney), lead (0.2 microg/g in liver and 0.9 microg/g in kidney), and cadmium (0.8 microg/g in liver and 2.2 microg/g in kidney), and increased DNA damage (tail moment mean of 18.2) when compared to control animals (arsenic in liver of 0.08 microg/g and kidney of 0.1 microg/g; lead in liver of 0.06 microg/g and kidney of 0.3 microg/g; cadmium in liver of 0.06 microg/g and kidney of 0.6 microg/g; and tail moment of 14.2). With the data in children and rodents, the weight-of-evidence for health risks (in this case DNA damage) associated with metal exposure in Villa de la Paz was strengthened. Therefore, a remediation program was easier to justify, and a feasibility study at this site is under way.

Exposure to organochlorine pesticides was studied in a group of mother-infant pairs living in a rural area where agriculture is the main economic activity. Fumigation in this zone is performed with airplanes, thus affecting the inhabited areas around them, including schools. Heparinized venous blood of mothers and umbilical cords was used to evaluate the olive tail moment in the comet assay, and micronuclei, chromatin buds, and nucleoplasmic bridges in peripheral blood lymphocytes. Cord blood samples were taken at the moment of birth only from natural and normal parturitions. Determinations of hexachlorobenzene, aldrin, heptachlor epoxide, oxichlordane, t and c-chlordane, cis-nonachlor, mirex, alpha and beta-endosulfan, alpha, beta and gamma hexachlorocyclohexane, and p'p'-DDT, p'p'-DDE were conducted to establish the differential distribution of the toxicants between compartments, i.e., mother and umbilical cord. Significantly higher pesticide levels were found in umbilical cord plasma than in mothers' plasma for almost all compounds tested, except DDE and oxychlordane. Significantly higher olive tail moments were found in umbilical cords than in mothers, whereas micronuclei frequencies were higher in mothers than in umbilical cords. However, neither the levels of micronuclei nor the olive tail moment were correlated with pesticide levels. Given that no other exposure to toxic compounds has been identified in this region, the lack of correlation between genotoxicity biomarkers and pesticide levels may be due to the variability of the exposure and to endogenous processes related to lipid mobility during pregnancy, the metabolism of the compounds, and individual susceptibilities.