Dataset Information

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

ABSTRACT:

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.

SUBMITTER: Sughis M

PROVIDER: S-EPMC3491927 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Background: The present study was designed to investigate the protective effects and mechanisms of carnosine on lipopolysaccharide (LPS)-induced injury in Caenorhabditis elegans.Methods: C. elegans individuals were stimulated for 24?h with LPS (100??g/mL), with or without carnosine (0.1, 1, 10?mM). The survival rates and behaviors were determined. The activities of superoxide dismutase (SOD), glutathione reductase (GR), and catalase (CAT) and levels of malondialdehyde (MDA) and glutathione (GSH) were determined using the respective kits. Reverse transcription polymerase chain reaction (RT-PCR) was performed to validate the differential expression of sod-1, sod-2, sod-3, daf-16, ced-3, ced-9, sek-1, and pmk-1. Western blotting was used to determine the levels of SEK1, p38 mitogen-activated protein kinase (MAPK), cleaved caspase3, and Bcl-2. C. elegans sek-1 (km2) mutants and pmk-1 (km25) mutants were used to elucidate the role of the p38 MAPK signaling pathway.Results: Carnosine improved the survival of LPS-treated C. elegans and rescued behavioral phenotypes. It also restrained oxidative stress by decreasing MDA levels and increasing SOD, GR, CAT, and GSH levels. RT-PCR results showed that carnosine treatment of wild-type C. elegans up-regulated the mRNA expression of the antioxidant-related genes sod-1, sod-2, sod-3, and daf-16. The expression of the anti-apoptosis-related gene ced-9 and apoptosis-related gene ced-3 was reversed by carnosine. In addition, carnosine treatment significantly decreased cleaved caspase3 levels and increased Bcl-2 levels in LPS-treated C. elegans. Apoptosis in the loss-of-function strains of the p38 MAPK signaling pathway was suppressed under LPS stress; however, the apoptotic effects of LPS were blocked in the sek-1 and pmk-1 mutants. The expression levels of sek-1 and pmk-1 mRNAs were up-regulated by LPS and reversed by carnosine. Finally, the expression of p-p38MAPK and SEK1 was significantly increased by LPS, which was reversed by carnosine.Conclusion: Carnosine treatment protected against LPS injury by decreasing oxidative stress and inhibiting apoptosis through the p38 MAPK pathway.