Exposure to arsenic and lead in children from Salamanca México, effects on telomeric lengthening and mitochondrial DNA

Levels of urinary arsenic and levels of lead in blood were measured in children attending elementary schools located in an industrial zone in Salamanca, México. Its possible effects using telomere length and mitochondrial DNA copy number as biomarkers of genomic disequilibrium by oxidative stress were studied. Eighty-eight children (6–15 years old) were included and urine samples were collected for quantification of arsenic, while lead was measured in blood samples using inductively coupled plasma mass spectrometry (ICP-MS). DNA was isolated from peripheral blood and relative telomere length and the mitochondrial DNA copy number were determined by real-time PCR. The geometric mean of urinary arsenic was 54.16 μg/L (11.7–141.1 μg/L). Ninety-eight percent of the children were above 15 μg/L (biomonitoring equivalent value). With respect to the concentration of lead in blood, the mean was 3.78 μg/dL (LOD-22.61), where 24.5% of the participants had equal or above the reference value (5 μg/dL; Mexican Official Norm NOM-199-SSA1–2000, 2017). A positive association between urinary arsenic and telomere length was found (β = 0.161; 95% CI: 0.12; 0.301; P = 0.034), while lead blood concentrations were negatively associated with mitochondrial DNA copy number (β = − 0.198; 95% CI: − 2.81; − 0.17; P = 0.019), after adjusting by age, sex, and total white blood cell count. Differences in the mitochondrial DNA content were observed in children with lead blood levels from 2.5 μg/dL, (P ≤ 0.001), suggesting an effect at lead exposure levels considered acceptable (< 5 μg/dL). In conclusion, children living in an industrial area in Salamanca showed an exposure to arsenic and lead and an impact on telomere length and mitochondrial DNA content associated with arsenic and lead exposure, respectively.