فهرست مطالب

Occupational and Environmental Medicine - Volume:11 Issue:1, 2020
  • Volume:11 Issue:1, 2020
  • تاریخ انتشار: 1398/10/23
  • تعداد عناوین: 9
|
  • Farrokh Habibzadeh Pages 1-2
  • Maryam Shaygan*, Maryam Yazdanpanah Pages 3-14
    Background

    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.

    Objective

    To 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.

    Methods

    This 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.

    Results

    There 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.

    Conclusion

    Workers 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
  • Sigit Ambar Widyawati, Suhartono Suhartono*, Maria Mexitalia, Ariawan Soejoenoes Pages 15-23
    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

    Keywords: Pesticides, Fetal blood, Infant, low birth weight, Organophosphates, Insulinlike growth factor I
  • Hanie Mahaki, Naghi Jabarivasal, Khosro Sardarian, Alireza Zamani* Pages 24-32
    Background

    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.

    Objective

    To 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).

    Methods

    80 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).

    Results

    Serum 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.

    Conclusion

    The 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
  • Lalu Krishna, Ursula Sampson, Panthapulaykal Theru Annamala, Kumudam M Unni, Bhaskarapillai Binukumar, Alex George, Ranjith Sreedharan* Pages 33-40
    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 [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.

    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.

    Keywords: Occupational exposure, Mutagenicity tests, Chromosome aberrations, Apoptosis, Oral mucosal absorption, Micronuclei, chromosome-defective, Micronucleus tests, Biomarkers, DNA damage
  • Jahangirnejad, Mehdi Goudarzi, Heibatullah Kalantari, Hossein Najafzadeh, Mohsen Rezaei* Pages 41-52
    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.

    Keywords: Arsenic, Nanoparticles, Oxidative stress, Chemical, drug induced liver injury, Apoptosis
  • Elvira Timeryanovna Valeeva, Guzel Fanisovna Mukhammadiyeva*, Akhat Barievich Bakirov Pages 53-58
    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.

    Keywords: Glutathione S-transferase, Liver diseases, Polymorphism, genetic
  • Ramin Mehrdad* Pages 59-60
  • Pages 61-62