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Health effects in children aged 3-6 years induced by environmental lead exposure
Yaping Jin1, Yingjun Liao, Chunwei Lu
1Department of Environmental and Occupational Health, School of Public Health, China Medical University, Shenyang, Liaoning, People's Republic of China. jinyp@mail.cmu.edu.cn
Insights
Lead exposure in young children (3-6 years) can cause oxidative damage, indicated by inhibited delta-aminolevulinic acid dehydratase (ALAD) activity and increased malondialdehyde (MDA) levels. This damage may contribute to lead-induced intellectual impairment.
Area of Science:
- Environmental Health
- Toxicology
- Pediatrics
Background:
- Lead toxicity is a significant public health concern, particularly in children.
- Oxidative stress is implicated in various toxicological mechanisms.
- Understanding the link between lead exposure and oxidative damage is crucial for early intervention.
Purpose of the Study:
- To investigate oxidative damage in children aged 3-6 years exposed to lead.
- To determine if oxidative stress indicators correlate with lead toxicity markers.
Main Methods:
- Blood samples from 408 children (3-6 years) were analyzed for blood lead levels (BLLs).
- Enzyme activities (ALAD, SOD, GSH-Px) and biochemical markers (GSH, MDA) were measured.
- Spectrophotometric and atomic absorption spectrophotometry techniques were employed.
Main Results:
- Children with BLLs ≥ 100 µg/L showed significantly lower ALAD activity.
- Elevated plasma MDA levels were observed in children with BLLs ≥ 100 µg/L.
- No significant changes in SOD, GSH-Px, or GSH were associated with elevated BLLs.
Conclusions:
- Lead exposure (BLLs ≥ 100 µg/L) induces oxidative damage in young children.
- Inhibited ALAD activity contributes to lead-induced oxidative stress.
- Oxidative damage may play a role in lead-induced intellectual impairment in preschool children.
Objectives:
To investigate the involvement of oxidative damage in lead-induced toxicity in children aged 3-6 years and to enlighten whether oxidative stress indicators are correlated with the known indices of lead toxicity.
Methods:
Blood samples were collected from 408 subjects (217 boys and 191 girls) in the urban kindergartens. The age range of the subjects was 3-6 years. Blood lead levels (BLLs) were analyzed by flameless atomic absorption spectrophotometry. Activities of delta-aminolevulinic acid dehydratase (ALAD), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and contents of glutathione (GSH) in erythrocyte and levels of plasma malondialdehyde (MDA) were analyzed spectrophotometrically in these children.
Results:
Children with BLLs >or = 100 microg/L had significantly decreased erythrocyte ALAD activities and increased plasma MDA levels compared to the children with BLLs < 100 microg/L. No significant changes were observed in erythrocyte SOD and GSH-Px activities and GSH levels associated with elevated BLLs in these children.
Conclusion:
Present data indicate that oxidative damage could be induced by lead in children with BLLs > or = 100 microg/L, and this may partly be attributed to the inhibited ALAD activities. Statistically significant changes of oxidative stress parameters in preschool children while BLLs were more than 100 microg/L could be implicated that oxidative damage might contribute to lead-induced intellectual impairment.
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