فهرست مطالب
International Journal of Occupational and Environmental Medicine
Volume:11 Issue: 1, Jan 2020
- تاریخ انتشار: 1398/10/23
- تعداد عناوین: 9
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Pages 1-2
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Pages 3-14Background
Taking into account the differences in job requirements and conditions, it is expected that workers in some occupations are more susceptible to pain than others.
ObjectiveTo examine the prevalence of chronic pain among workers of several petrochemical and petroleum refinery plants. We also examined the predictive role of psycho-familial variables (depression, work-family conflict and job stress) in causing chronic pain when controlling for demographic and occupational factors.
MethodsThis cross-sectional study was carried out among 674 workers. Those with chronic pain were identified by affirmative answers to screening questions based on the ICD-11 criteria.
ResultsThere were 162 (24.0%; 95% CI 20.8% to 27.3%) workers meeting the ICD11 criteria for chronic pain. Headache was the most frequently reported pain (29.9%). We found a significantly (p=0.03) higher prevalence of pain among the middle age than in other age groups. Chronic pain more frequently affected divorced/widowed workers (p<0.001), and those with more work experience (p=0.04). Workers with chronic pain reported significantly higher levels of depression (p<0.001), job stress (p=0.007), and work-family conflict (p<0.001). After controlling for demographic and occupational factors, depression (p<0.001) and work-family conflict (p=0.003) were found to be independent predictors of chronic pain among studied workers.
ConclusionWorkers who experience higher levels of depression, work-family conflict and job stress might be more prone to chronic pain. The majority of these factors are modifiable, and the problem may thus be solved by establishing appropriate screening programs, and availability of proper services and education.
Keywords: Chronic pain, Prevalence, Workers, Depression, Occupational stress, Family, Work place -
Pages 15-23Background
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.
ObjectiveTo analyze the relationship between exposure to pesticides during pregnancy and low-birth weight (LBW) through the disruption of the IGF-1 hormone.
MethodsIn 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.
ResultsThere 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).
ConclusionThere was a significant relationship between pesticide exposure during pregnancy and LBW through the umbilical serum IGF-1 reduction pathway
Keywords: Pesticides, Fetal blood, Infant, low birth weight, Organophosphates, Insulinlike growth factor I -
Pages 24-32Background
Extremely low-frequency electromagnetic fields (ELF-EMFs) are abundantly produced in modern societies. In recent years, interest in the possible effects of ELF-EMFs on the immune system has progressively increased.
ObjectiveTo examine the effects of ELF-EMFs with magnetic flux densities of 1, 100, 500, and 2000 µT on the serum levels of interleukin (IL)-9, IL-10, and tumor necrosis factor-alpha (TNF-α).
Methods80 adult male rats were exposed to ELF-EMFs at a frequency of 50 Hz for 2 h/day for 60 days. The serum cytokines were measured at two phases of pre- and post-stimulation of the immune system by human serum albumin (HSA).
ResultsSerum levels of IL-9 and TNF-α, as pro-inflammatory cytokines, were decreased due to 50 Hz EMFs exposure compared with the controls in the pre- and post-stimulation phases. On the contrary, exposures to 1 and 100 µT 50 Hz EMFs increased the levels of antiinflammatory cytokine, and IL-10 only in the pre-stimulation phase. In the post-stimulation phase, the mean level of serum IL-10 was not changed in the experimental groups.
ConclusionThe magnetic flux densities of 1 and 100 µT 50 Hz EMFs had more immunological effects than EMFs with higher densities. Exposure to 50 Hz EMFs may activate anti-inflammatory effects in rats, by down-modulation of pro-inflammatory cytokines (IL-9 and TNF-α) and induction of the anti-inflammatory cytokine (IL-10).
Keywords: Interleukin-9, Interleukin-10, Tumor necrosis factor-alpha, Immunization, Electromagnetic fields -
Pages 33-40Background
Workers in cement warehouses of Kerala are enduring long-standing exposure to cement dust, which is considered genotoxic.
ObjectiveTo evaluate the extent of genotoxicity and cytotoxicity caused due to exposure of cement dust among those working in cement warehouses.
MethodsThe 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.
ResultsThe 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 [3fold 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.
ConclusionContinuous 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.
Keywords: Occupational exposure, Mutagenicity tests, Chromosome aberrations, Apoptosis, Oral mucosal absorption, Micronuclei, chromosome-defective, Micronucleus tests, Biomarkers, DNA damage -
Pages 41-52Background
Arsenic, an environmental pollutant, is a carcinogenic metalloid and also an anticancer agent.
ObjectiveTo evaluate the toxicity of arsenic nanoparticles in rat hepatocytes.
MethodsFreshly 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.
ResultsBy 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.
ConclusionExposure 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.
Keywords: Arsenic, Nanoparticles, Oxidative stress, Chemical, drug induced liver injury, Apoptosis -
Pages 53-58Background
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.
ObjectiveTo 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.
MethodsThis 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.
ResultsThere 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.
ConclusionThe GSTP1 rs1695 gene polymorphism can play a protective role in the development of toxic liver damage in petrochemical workers.
Keywords: Glutathione S-transferase, Liver diseases, Polymorphism, genetic -
Pages 59-60
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Pages 61-62