International Journal of Occupational and Environmental Medicine最新文献

Background: Workers in cement warehouses of Kerala are enduring long-standing exposure to cement dust, which is considered genotoxic.

Objective: To evaluate the extent of genotoxicity and cytotoxicity caused due to exposure of cement dust among those working in cement warehouses.

Methods: The study included 82 cement warehouse workers and 82 age-matched individuals with no exposure to cement dust. Exfoliated buccal micronucleus cytome assay (BMCyt) was performed to analyze the genotoxic and cytotoxic effects caused by inhalation of cement dust.

Results: The frequency of various genotoxic and cytotoxic end markers (micronucleated cells [2-fold increase, p<0.001], nuclear buds [4-fold increase, p<0.001], binucleated cells [4-fold increase, p<0.001], karyorrhectic cells [2-fold increase, p<0.001], pyknotic cells [3-fold increase, p<0.001], and karyolytic cells [2-fold increase, p<0.001]) were higher in the exposed workers compared with unexposed group. Increase of these parameters represented an increased level of chromosomal damage, nuclear disintegration and increased cell death among exposed group compared with unexposed group.

Conclusion: Continuous exposure to cement dust results in increased frequency of nuclear aberrations and cellular apoptosis. This may lead to defects in genome maintenance, accelerated ageing, increased chance of oral cancer and neurodegenerative disorders in those occupationally exposed to cement dust.

Background: Arsenic, an environmental pollutant, is a carcinogenic metalloid and also an anticancer agent.

Objective: To evaluate the toxicity of arsenic nanoparticles in rat hepatocytes.

Methods: Freshly isolated rat hepatocytes were exposed to 0, 20, 40, and 100 μM of arsenic nanoparticles and its bulk counterpart. Their viability, reactive oxygen species level, glutathione depletion, mitochondrial and lysosomal damage, and apoptosis were evaluated.

Results: By all concentrations, lysosomal damage and apoptosis were clearly evident in hepatocytes exposed to arsenic nanoparticles. Evaluation of mitochondria and lysosomes revealed that lysosomes were highly damaged.

Conclusion: Exposure to arsenic nanoparticles causes apoptosis and organelle impairment. The nanoparticles have potentially higher toxicity than the bulk arsenic. Lysosomes are highly affected. It seems that, instead of mitochondria, lysosomes are the first target organelles involved in the toxicity induced by arsenic nanoparticles.

Background: Exposure to numerous chemicals, including industrial ones, may result in liver damage. The body susceptibility to the environmental hazards largely depends on the activity of the enzymes in the xenobiotic detoxification system. Function abnormalities of such enzymes due to genetic variations would increase the risk of developing various diseases.

Objective: To elucidate the relationship between polymorphism in glutathione S-transferase genes (GSTM1, GSTT1 and GSTP1) and the risk of toxic liver damage in a group of petrochemical workers.

Methods: This study was conducted on 72 workers with toxic liver injury, 156 healthy workers, and 322 healthy individuals without history of occupational exposure to chemicals. Genotyping of the GSTP1 rs1695 gene polymorphism was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Polymerase chain reaction (PCR) was used to perform genotyping of the GSTM1 and GSTT1 genes polymorphism.

Results: There was a significant difference in genotype frequencies of the GSTP1 rs1695 gene polymorphism among the groups studied. The distribution of Val/Val genotype of the GSTP1 rs1695 gene polymorphism had a higher incidence in healthy workers compared with patients with toxic liver damage (p=0.036). No significant association was found between the GSTM1 and GSTT1 polymorphisms and toxic liver damage.

Conclusion: The GSTP1 rs1695 gene polymorphism can play a protective role in the development of toxic liver damage in petrochemical workers.

Background: Birth weight is very important for long-term physical, mental, health, and brain development. Pesticide exposure is thought to interfere with fetal growth, among others, through disruption of the function of the insulin-like growth hormone-1 (IGF-1) hormone.

Objective: To analyze the relationship between exposure to pesticides during pregnancy and low-birth weight (LBW) through the disruption of the IGF-1 hormone.

Methods: In a case-control study, babies born with LBW (birth weight <2500 g) and those born later with normal birth weight (=2500 g) at 2 hospitals in Brebes were chosen as cases and controls, respectively. Maternal pesticide exposure was measured by interview using a questionnaire. Umbilical serum IGF-I level was tested using the ELISA method.

Results: There was a significant relationship between pesticide exposure during pregnancy and LBW (OR 6.8; 95% CI 2.0 to 22.9) and low umbilical serum IGF-1 levels (OR 3.6; 95% CI 1.2 to 11.1). There was a significant relationship between low umbilical serum IGF-1 levels and LBW (OR 8.9; 95% CI 2.4 to 32.1).

Conclusion: There was a significant relationship between pesticide exposure during pregnancy and LBW through the umbilical serum IGF-1 reduction pathway.