DNA Damage In Children Research Articles

Assessing DNA damage in children environmentally exposed to pesticides through using the comet assay and the micronucleus test

Background Environment pesticide effects principally depend on their niche distribution and chemical stability/decomposition, according to seasonal variations. In areas of intensive pesticide use, populations are therefore more vulnerable to any detrimental effects, eg increased hypersensitivity, and may become conditioned to their short/long term actions depending on the patterns of use. Of particular concern are developmental …

Influence of genetic polymorphisms on biomarkers of exposure and effects in children living in Upper Silesia

This article is a follow-up to our previous molecular epidemiology studies on the DNA damage in children from the Upper Silesia region of Poland. It is expected that metabolic and DNA repair gene polymorphisms may modulate individual susceptibility to environmental exposure. In this study, we investigate the association between polymorphisms of metabolising (CYP2D, EPHX1, GSTM1, GSTP1, GSTT1, NAT2) and DNA repair (XPD, XRCC1, XRCC3) genes and selected biomarkers of exposure and effect such as levels of 1-hydroxypyrene (1-OHP) and urinary mutagenicity, aromatic DNA adducts, sister chromatid exchange (SCE) and micronuclei (MN) in 74 children. Both 1-OHP concentration and urinary mutagenicity tested by TA98+S9 were significantly higher in individuals with EPHX1 (exon 4) Arg/Arg genotype than in individuals with other genotype. The EPHX1 (exon 3) significantly affected urinary mutagenicity tested with strain YG1024+S9. The urinary mutagenicity in individuals with Tyr/Tyr homozygotes was lower than in individuals with Tyr/His and His/His (1057±685 vs. 1432±1003 revertants/mol creatinine). XRCC3 Met/Met genotype was associated with significantly higher levels of 1-OHP in urine compared with only The/Met genotype. The PAH-DNA adduct levels in the subgroup with GSTM1 null genotype was 2-fold higher than in individuals with GSTM1 active (7.06±5.12 vs. 13.14±9.81 adduct/10(8) nucleotides). The mean level of aromatic DNA adducts in children with deletion of the GSTT1 gene was significantly higher compared with individuals with that gene present (8.03±6.23 vs. 14.66±10.70 adduct/10(8) nucleotides). Also the carriers of the XPD Lys/Lys genotype showed higher levels of DNA adducts than heterozygotes (13.16±9.70 vs. 6.81±5.86 adducts/10(8) nucleotides). Children carrying the XRCC3-241 Met/Met genotype exhibited a higher number of SCE in peripheral blood lymphocytes than carriers of Thr/Met allele (8.15±0.86 vs. 7.62±0.79 SCE/cell). It was also observed that children with the GSTP1 slow conjugator had significantly elevated MN in peripheral blood lymphocytes compared with fast conjugator (4.23±3.49 vs. 6.56±5.00 MN/1000 cells).

DNA Damage in Children with Snoring

Objective: Learning the levels of oxidative DNA damage in children with obstructive adenotonsillar hypertrophy. We determined the 8-hydroxy 2-deoxyguanosine levels in leukocyte DNA and in urine samples as a specific marker of oxidative damage to DNA, and the plasma and urine malondialdehyde levels as an index of lipid peroxidation in children. Method: Prospective, randomized controlled study conducted between 2010 and 2011. The study consisted of 30 patients and 25 healthy controls. Patients had snoring and pauses of breathing during sleep. We obtained blood and urine samples from each child to measure 8-hydroxy 2-deoxyguanosine and malondialdehyde levels in their initial visit. Results: A significant difference was observed in leukocyte and urine 8-hydroxy 2-deoxyguanosine levels in patients with obstructive adenotonsillar hypertrophy compared to controls (P < .001 for both). Similarly, a significant difference was observed in plasma and urine malondialdehyde levels in patients with obstructive adenotonsillar hypertrophy compared to controls ( P < .001 for both). In addition, significant correlations were observed between the levels of 8-hydroxy 2-deoxyguanosine in leukocyte DNA and plasma malondialdehyde ( r = 0.648, P < .001), and between the levels of urine 8-hydroxy 2-deoxyguanosine excretion and urine malondialdehyde ( r = 0.588, P < .001). Conclusion: 8-hydroxy 2-deoxyguanosine in leukocyte DNA and urine levels in children can be useful as an indicator for obstructive adenotonsillar hypertrophy screening.

DNA damage in children exposed to secondhand cigarette smoke and its association with oxidative stress

To compare oxidative status, total antioxidant capacity and values of DNA damage in peripheral blood lymphocytes in children exposed to secondhand cigarette smoke with healthy controls. Analytical, Observational. 54 children without any chronic diseases, attending the healthy child monitoring polyclinic. These comprised 27 children who had been exposed to passive cigarette smoke and 27 children who had not been exposed to cigarette smoke. Urine cotinine levels by the chemiluminescent technique; DNA damage by alkaline comet assay; and total oxidant status (TOS) using a novel automated measurement method. The mean urine cotinine, TOS, Oxidative Stress Index (OSI) and DNA damage values of the group exposed to cigarette smoke were determined to be at significantly higher level compared to the group not exposed to cigarette smoke (P<0.001). No statistically significant difference was determined in the TAS level between the two groups (P=0.1) The results showed that TOS levels, OSI index and DNA damage in peripheral blood lymphocytes were significantly higher in children exposed to secondhand cigarette smoke than in those not exposed to secondhand cigarette smoke.

DNA damage in children and adolescents with cardiovascular disease risk factors

The risk of developing cardiovascular disease (CVD) is related to lifestyle (e.g. diet, physical activity and smoking) as well as to genetic factors. This study aimed at evaluating the association between CVD risk factors and DNA damage levels in children and adolescents. Anthropometry, diet and serum CVD risk factors were evaluated by standard procedures. DNA damage levels were accessed by the comet assay (Single cell gel electrophoresis; SCGE) and cytokinesis-blocked micronucleus (CBMN) assays in leukocytes. A total of 34 children and adolescents selected from a population sample were divided into three groups according to their level of CVD risk. Moderate and high CVD risk subjects showed significantly higher body fat and serum CVD risk markers than low risk subjects (P<0.05). High risk subjects also showed a significant increase in DNA damage, which was higher than that provided by low and moderate risk subjects according to SCGE, but not according to the CBMN assay. Vitamin C intake was inversely correlated with DNA damage by SCGE, and micronucleus (MN) was inversely correlated with folate intake. The present results indicate an increase in DNA damage that may be a consequence of oxidative stress in young individuals with risk factors for CVD, indicating that the DNA damage level can aid in evaluating the risk of CVD.

Adverse health effects of child labor: high exposure to chromium and oxidative DNA damage in children manufacturing surgical instruments.

Background: A considerable part of the worldwide production of surgical instruments takes place in Sialkot, Pakistan. Many children work in hazardous conditions in this industry.Objective: We investigated exposure to metals and possible health effects among children working in surgical instruments manufacturing units compared with schoolchildren from the same city.Methods: In a cross-sectional study we studied a convenience sample of 104 male children (10–14 years of age) working in surgical instruments manufacturing units and 75 male children of similar age from a school in Sialkot, Pakistan. A respiratory questionnaire was administered, spirometry was performed, and blood pressure was measured. In a spot urine sample, concentrations of metals were measured by inductively coupled plasma mass spectrometry and 8-hydroxydeoxyguanosine (8OHdG, reflecting oxidative DNA damage) by ELISA.Results: The working children reported more asthma (10% vs. 0%; p = 0.005) and dry cough at night (36% vs. 20%; p = 0.02) than did the schoolchildren, but there were no significant differences in pulmonary function or blood pressure. The urinary concentration of chromium was 35 times higher in working children [geometric mean, 23.0 µg/L; 25th–75th percentile, 8.38–58.6] than in schoolchildren [0.66 µg/L; 0.38–1.09)], and largely in excess of the occupational Biological Exposure Index for adult workers (25 µg/L). Urinary 8-OHdG concentrations were not significantly higher in working children than in schoolchildren (19.3 vs. 17.6 µg/g creatinine, p = 0.4), but were significantly correlated with urinary nickel (r = 0.41; p < 0.0001) and with a composite index of metal exposure (r = 0.46; p < 0.0001).Conclusions: Children working in the surgical instruments manufacturing industry had substantial exposure to several metals, especially chromium and nickel, which are established carcinogens. Exposure to nickel was associated with evidence of increased oxidative DNA damage.

Environmental polycyclic aromatic hydrocarbon (PAH) exposure and DNA damage in Mexican children

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous pollutants presenting a public health risk, particularly to children, a vulnerable population. PAHs have genotoxic and carcinogenic properties, which depend on their metabolism. Many enzymes involved in PAH metabolism, including CYP1A1, CYP1B1, GSTM and GSTT are polymorphic, which may modulate the activation/deactivation of these compounds. We evaluated PAH exposure and DNA damage in children living in the vicinity of the main petrochemical complex located in the Gulf of Mexico, and explored the modulation by genetic polymorphisms of PAH excretion and related DNA damage. The participants ( n = 82) were children aged 6–10 y attending schools near the industrial area. Urinary 1-hydroxypyrene (1-OHP; a biomarker of PAH exposure) was determined by reverse-phase-HPLC; DNA damage by the comet assay (Olive Tail Moment (OTM) parameter); CYP1A1*2C and CYP1B1*3 polymorphisms by real time-PCR; and GSTM1*0 and GSTT1*0 by multiplex PCR. The median value of 1-OHP was 0.37 μmol/mol creatinine; 59% of children had higher 1-OHP concentrations than those reported in environmentally exposed adults (0.24 μmol/mol creatinine). A stratified analysis showed increased DNA damage in children with 1-OHP concentrations greater than the median value. We observed higher 1-OHP concentrations in children with CYP1A1*2C or GSTM1*0 polymorphisms, and a positive influence of CYP1A1*2C on OTM values in children with the highest PAH exposure. The data indicate that children living in the surroundings of petrochemical industrial areas are exposed to high PAH levels, contributing to DNA damage and suggesting an increased health risk; furthermore, data suggest that polymorphisms affecting activation enzymes may modulate PAH metabolism and toxicity.

Malnutrition and infection influence the peripheral blood reticulocyte micronuclei frequency in children

Malnutrition is a serious public health problem that affects approximately one third of all children. Developing countries have the highest incidence of malnourished children, and approximately 60% of deaths that occur in children under five are directly related to malnutrition and associated diseases. The relationship between malnutrition and genetic damage has been widely studied in humans and animal models. The micronucleus (MN) assay is useful in detecting chromosome damage induced by several factors. The aim of this study was to evaluate the effects of infection and malnutrition on the frequency of MN in erythrocytes from the peripheral blood of well-nourished, uninfected (WN) and well-nourished, infected (WNI) children, and moderately malnourished (UNM) and severely malnourished (UNS) children, both with infection, using a flow cytometric analysis technique. The percentage of reticulocytes (RETs) was significantly higher (1.5-fold) in WNI children than well-nourished controls. In addition, the UNS group had a 2.2-fold increase in the percentage of RETs compared to the WNI group. The frequency of micronucleated reticulocytes (MN-RETs) was 2.5 times greater, in WNI group compared to the WN group. These frequencies were significantly higher (1.7- and 2.1-fold) in UNM and UNS, respectively, compared to the WNI group. The results suggest that infection and malnutrition induce DNA damage in children.

Basal damage and oxidative DNA damage in children with chronic kidney disease measured by use of the comet assay

One consequence of chronic kidney disease (CKD) is an elevated risk for cancer. There is sufficient evidence to conclude that there is an increased incidence of at least some cancers in kidney-dialysis patients. Cancer risk after kidney transplantation has mainly been attributed to immunosuppressive therapy. There are no data evaluating DNA damage in children with CKD, in dialysis patients, or following kidney transplantation. In this study, the comet assay and the enzyme-modified comet assay – with the use of endonuclease III (Endo III) and formamidopyrimidine glycosylase (FPG) enzymes – were conducted to investigate the basal damage and the oxidative DNA damage as a result of treatment in peripheral blood lymphocytes of children. Children at various stages of treatment for kidney disease, including pre-dialysis patients (PreD) (n=17), regular hemodialysis patients (HD) (n=15), and those that received kidney transplants (Tx) (n=17), comprised the study group. They were compared with age- and gender-matched healthy children (n=20) as a control group. Our results show that the %DNA intensity, a measure of basal damage, was significantly increased in children with CKD (mean±SD) (5.22±1.57) and also in each of the PreD, HD, and Tx groups [(4.92±1.23), (4.91±1.35), and (5.79±1.94), respectively, vs the healthy children (2.74±2.91) (p<0.001). Significant increases in oxidative DNA damage were only found in the FPG-sensitive sites for the PreD and Tx groups, compared with control and HD groups (p<0.05), suggesting that basal DNA damage was more evident for the PreD, HD, and Tx groups. The findings of the present study indicate a critical need for further research on genomic damage with different endpoints and also for preventive measures and improvements in treatment of pediatric patients, in order to improve their life expectancy.

Antioxidant enzyme activities and DNA damage in children with type 1 diabetes mellitus after 12 weeks of exercise

The objectives of this study are to assess the effects of a low-intensity exercise training which is not risky for children with type 1 diabetes mellitus (T1DM) on the antioxidant enzyme activities and oxidative stresses compared with healthy controls. We studied 10 boys with T1DM (11.21 +/- 0.97 age) and 10 age-matched healthy controls (11.90 +/- 1.85 age) during the 12 weeks of moderate intensity aerobic exercise. Measurements included peak oxygen uptake, body composition, blood lipid profiles, glycated haemoglobin (HbA1c), oxidized low density lipoprotein (ox-LDL), 8-hydroxy-2'-deoxyguanosine, superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. In T1DM patients, the baseline diastolic blood pressure and HbA1c were higher than that in controls (p < 0.05), while the GPx level was lower. The training-induced DNA damage peak was higher in T1DM patients than in controls (p < 0.05), and exercise improved both SOD and GPx levels. Although our exercise programme increase antioxidant enzyme activities, the results of the study demonstrate that low-intensity aerobic exercise training programme performed over 12 weeks may accelerate adverse effects of antioxidant defence capacity in children with T1DM. Therefore, the future studies should be performed to clarify much more the relationship to exercise and antioxidant capacity in children with T1DM.

Leukocyte DNA damage in children with iron deficiency anemia: effect of iron supplementation

Iron deficiency is frequently associated with anemia. Iron is a transition-metal ion, and it can induce free radical formation, which leads to formation of various lesions in DNA, proteins, and lipids. The aim of this study was to investigate baseline oxidative DNA damage and to clarify the role of the administration of a therapeutic dose of iron on DNA oxidation in children with iron deficiency anemia (IDA). Twenty-seven children with IDA and 20 healthy children were enrolled in the study. Leukocyte DNA damage (strand breaks and Fpg-sensitive sites) was assessed using comet assay before and after 12 weeks of daily iron administration. Before the iron administration, the frequency of DNA strand breaks in the children with IDA was found to be lower than those in the control group (P < 0.05), but there was not a significant difference for frequency of Fpg-sensitive sites. After 12 weeks of iron administration, the frequency of both DNA strand breaks and Fpg-sensitive sites were found to be increased (P < 0.01). No significant association was determined between DNA damage parameters and hemoglobin, hematocrit, serum iron, total iron binding capacity, and ferritin. In conclusion, basal level of DNA strand breaks is at a low level in children with IDA. After iron administration, DNA strand breaks and Fpg-sensitive sites, which represent oxidatively damaged DNA, increased. However, this increase was unrelated to serum level of iron and ferritin.

Assessment of DNA damage in children exposed to indoor tobacco smoke

The present study is aimed to evaluate the possible DNA damage in children who are living with smoker parents. The tests were conducted by using alkaline comet assay, measured as a percentage of DNA damage in tail (%DNA(T)). The children that participated in the study were selected from the pediatric unit of a hospital in Istanbul, Turkey. %DNA(T) was significantly higher (p<0.01) in children who were exposed to indoor tobacco smoke (10.73+/-1.38) compared to the children in the control group (8.16+/-1.29). The number of cigarettes consumed by household members did not seem to affect the severity of the DNA damage. Since children spend most of their time at home and cannot remove themselves from harmful living conditions this important genotoxic finding should be considered by smoker parents for the future health consequences of their children.

Cumulative patient effective dose and acute radiation-induced chromosomal DNA damage in children with congenital heart disease

BackgroundThe seventh Committee on “Biological Effects of Ionizing Radiation” (BEIR VII, 2006) underlines “the need of studies of infants who are exposed to diagnostic radiation because catheters have been placed...

DNA damage in children with asthma bronchiale and its association with oxidative and antioxidative measurements

Increased production of reactive oxygen species leading to an imbalance between the oxidative forces and the antioxidant defense systems favoring an oxidative injury has been implicated in the pathogenesis of asthma. The aim of the study was to investigate the peripheral DNA damage, and its association with oxidative and antioxidative measurements in children with asthma bronchiale. The study population contained 42 children with asthma bronchiale and 32 healthy controls. DNA damage was assessed by alkaline comet assay in peripheral lymphocytes. Plasma levels of total antioxidant status (TAS), total peroxide concentration (LOOHs), and total oxidant status (TOS) were determined. In asthma bronchiale patients, DNA damage was significantly higher than in controls (17.9 +/- 11.8 AU vs. 1.2 +/- 2.0 AU, p < 0.001). Plasma TOS and LOOHs were higher in patients than in healthy controls (13.4 +/- 7.0 vs. 9.0 +/- 3.5, p = 0.002; 9.9 +/- 3.4 vs. 4.4 +/- 1.5, p < 0.001, respectively). Plasma TAS level in patients was higher than in healthy controls (5.5 +/- 2.5 vs. 1.0 +/- 0.6, p < 0.001). DNA damage was correlated with TOS (r = 0,616, p < 0.001). The findings indicated that lymphocyte DNA damage level increases in children with asthma bronchiale. Elevated DNA damage may be related to increased oxidative stress. However, the mechanism of this association, and whether it is direct or indirect, remains to be explored.

The Effects of Aerobic Exercise Program Participation on Antioxidant Related Gene Expression and Lipid, DNA Damage in Children with IDDM

The Effects of Aerobic Exercise Program Participation on Antioxidant Related Gene Expression and Lipid, DNA Damage in Children with IDDM

The evaluation of oxidative DNA damage in children with brain damage using 8-hydroxydeoxyguanosine levels

Urinary and cerebrospinal fluid (CSF) levels of 8-hydroxydeoxyguanosine (8-OHdG) were examined to estimate the relevance of oxidative stress in children with brain damage. Urinary 8-OHdG levels were measured in 51 children with various forms of central nervous system (CNS) disorders (status epilepticus [SE], hypoxic–ischemic encephalopathy [HIE], CNS infections and chronic epilepsy) and these levels were compared with those in 51 healthy children. CSF 8-OHdG levels were measured in 25 children with brain damage and in 19 control subjects. In addition, urinary and CSF levels of 8-OHdG were compared between the children with brain damage and healthy children. Finally, the relationship between urinary and CSF levels of 8-OHdG was determined in 12 children that provided both urinary and CSF samples. Our results showed that urinary 8-OHdG levels in children with HIE and CNS infections were higher than those of controls (Steel test; p < 0.05 and p < 0.05, respectively) and that CSF 8-OHdG levels were higher in children with SE, HIE, and CNS infections than in control subjects (Steel test; p < 0.01, 0.05 and 0.05, respectively). In addition, a positive correlation between the levels of urinary and CSF 8-OHdG was noted in the 12 children that provided both CSF and urinary samples (Spearman’s rank correlation; ρ = 0.82, p < 0.01). Further, we observed changes in the urinary 8-OHdG in a patient with HHV-6 encephalopathy, and found that the changes correlated well with the patient’s clinical condition. These results suggest that oxidative stress is strongly related to acute brain damage in children, and that 8-OHdG is a useful marker of brain damage. Therefore, repeated measurements of urinary 8-OHdG may be helpful in estimating the extent of brain damage.

Increased DNA damage in children caused by passive smoking as assessed by comet assay and oxidative stress

The present study aimed to evaluate the association between the environmental tobacco smoke (ETS) and DNA damage in relation to oxidative stress (OS) in children. Sixty-four children of age 1–8 years, selected from the outpatient clinic of Mansoura University Children Hospital were divided into two groups (23 children/group) based on high (>20 cigarettes/day) or low (<20 cigarettes/day) exposure to ETS at home. Twenty symptom-free children with normal cotinine level and with no exposure to ETS were recruited as controls. The comet assay was used to quantify the level of DNA damage in lymphocytes isolated from all children. Spectrophotometric methods were used to assess the serum level of malondialdehyde (MDA) and activity of glutathione peroxidase (GSH-Px) in erythrocytes. Also, serum level of tocopherol fractions (α, γ, δ) was assessed by high performance liquid chromatography (HPLC). Children exposed to ETS exhibited retarded growth, more chest problems, and gastroenteritis than the control. A significant increase in mean comet tail length indicating DNA damage was observed in ETS-exposed children ( P < 0.001) compared to controls. ETS-exposed children had significantly ( P < 0.001) higher MDA level paralleled with significant ( P < 0.001) decrease in the level of GSH-Px and tocopherol fractions compared with controls. The GSH-Px activity and tocopherol levels were inversely correlated with the increase of ETS exposure. These results show that inhalation of ETS is associated with an increase in the level of oxidants and a simultaneous decrease in the level of antioxidants in the children's blood. This status of oxidant–antioxidant imbalance (OS) may be one of the mechanisms leading to DNA damage detected in lymphocytes of ETS-exposed children. In conclusion, the present study gives an indication of an association between DNA damage and ETS exposure in children.

Evaluation of systemic oxidative status and mononuclear leukocytes Dna damage in children with caustic esophageal stricture

Esophageal stricture (ES) due to accidentally caustic digestions is a common problem in children. Mucosal damage and repeated dilatations lead to chronic inflammation and finally ES. We investigated the oxidative status and DNA damage of children with ES. Five children with ES were compared with the same age- and sex-matched healthy subjects. Oxidative status of plasma was evaluated by measuring myeloperoxidase (MPO) activity, and total peroxide (TP) level. Anti-oxidative status of the plasma was evaluated by measuring catalase (CAT) activity, and total antioxidant response (TAR). We used the Single Cell Gel Electrophoresis (also called Comet Assay) to measure DNA strand break in peripheral blood mononuclear leukocytes. Mean MPO activity and TP levels in the ES group were significantly higher than the control group (0.83 +/- 0.35, 0.09 +/- 0.03 and 0.98 +/- 0.38, 0.34 +/- 0.20, P = 0.009 and P = 0.047 respectively). There was no significant difference in CAT activity and TAR levels between the two groups (P = 0.347). DNA damage in patients with ES was increased compared to control subjects (108.8 +/- 51.2 and 57.6 +/- 31.2 arbitrary units, respectively), but this difference was not significant statistically (P= 0.09). This study shows that systemic oxidative stress and alteration at the nuclear level occur in patients with ES, as a result of multiple dilatations and tissue injury. On the other hand, these results support that patients with ES may benefit from antioxidant treatment.

Environmental Health Assessment of Deltamethrin in a Malarious Area of Mexico: Environmental Persistence, Toxicokinetics, and Genotoxicity in Exposed Children

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.

DNA damage in blood cells from children exposed to arsenic and lead in a mining area

In this work, we studied the frequency of DNA damage in children living in Villa de la Paz, Mexico, a mining site contaminated with arsenic and lead. DNA damage in blood cells was assessed using the Comet assay, and the results were compared to those found in children living in a less exposed town (Matehuala). In Villa de la Paz, high concentrations of arsenic and lead in surface soil and household dust were found. All of the soil samples had concentrations above 100 mg/kg of arsenic, and 58% of the samples were higher than 400 mg/kg of lead (these concentrations are used as intervention guidelines by the United States Environmental Protection Agency). In agreement with the environmental results, urinary arsenic in children living in Villa de la Paz (geometric mean 136 μg/g creatinine) was significantly higher than that found in children living in Matehuala (34 μg/g creatinine). Blood lead levels were also significantly higher in children from Villa de la Paz (11.6 μg/dL) than in children from Matehuala (8.3 μg/dL). The results of the Comet assay showed that the tail length and the tail moment in children living in Villa de la Paz were higher than those observed for children in Matehuala ( P<0.05). Taking all the data into account, our study has shown increased DNA damage in children exposed to arsenic and lead in the mining site of Villa de la Paz.