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.
We reported previously that children are exposed to deltamethrin in malarious areas. In the present work we explored the levels of this insecticide in soil samples and also obtained relevant toxico-kinetic data of deltamethrin in exposed children. Results show that, after spraying, indoor levels of deltamethrin in soil samples were higher than outdoor levels. The mean half-life estimated with these data was 15.5 days for outdoor samples and 15.4 days for indoor samples. Children’s exposure to deltamethrin was assessed using as biomarkers the urinary concentrations of the metabolites 3-phenoxybenzoic acid (3-PBA) and cis-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropane-1-carboxylic acid (Br2CA). The mean level of both biomarkers reached a peak within the first 24 hr postexposure; 6 months after the initial exposure, urinary levels of 3-PBA and Br2CA were found at levels observed before exposure. Approximately 91% of the total 3-PBA or Br2CA was excreted during the first 3 days after exposure. Therefore, we estimated a half-life for this period, the values for 3-PBA and Br2CA being almost identical (13.5 vs. 14.5 hr). Finally, considering reports about the genotoxicity of deltamethrin, we assessed DNA damage in children before and 24 hr after indoor spraying of deltamethrin; we found no differences in the comet assay end points. In conclusion, we observed exposure to deltamethrin in children, but we did not find any relationship between soil concentrations of deltamethrin and urinary levels of the metabolites. At least for genotoxicity, the exposed children appeared not to be at risk.
It has been demonstrated that the human biomonitoring of susceptible populations is a valuable method for the identification of critical contaminants. Therefore, the purpose of this study was to assess the exposure profile for arsenic (As), lead (Pb), mercury (Hg), 1-hydroxypyrene (1-OHP), 1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane (DDT), 1,1-dichloro-2,2-bis(p-chlorophenyl) ethylene (DDE), polybrominated diphenyl ethers (PBDEs), and polychlorinated biphenyls (PCBs) in children living in Ciudad Juarez, Chihuahua, Mexico (a major manufacturing center in Mexico). In 2012, we evaluated a total of 135 healthy children living in Ciudad Juarez since birth. The total PBDEs levels ranged from nondetectable (< LOD) to 215 ng/g lipid, with a mean total PBDEs level of 29.5 ± 53.0 ng/g lipid (geometric mean ± standard deviation). The mean total PCBs level in the study participants was 29.0 ± 10.5 ng/g lipid (range 4.50-50.0 ng/g lipid). The mean concentration of total DDT (DDT + DDE) was 11.9 ± 6.70 ng/g lipid (range 3.00-26.0 ng/g lipid). The mean 1-OHP levels was 1.2 ± 1.1 µmol/mol creatinine (range
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