Toxicology and Industrial Health最新文献

Organophosphate pesticides, widely used in agriculture, are effective in pest control but pose environmental and health risks through soil, water, and air contamination. Exposure to these chemicals is linked to adverse human health effects, underscoring the need for environmentally sustainable practices. This study aimed to assess urinary organophosphate metabolites and examine the relationship between GSTM1 and GSTT1 gene polymorphisms with biomarkers of oxidative stress among farmers in Himachal Pradesh exposed to pesticides. We collected urine samples (50 mL) from the exposed group to detect organophosphate metabolites using GC-MS. Blood samples (5 mL) were also obtained for GSTM1 and GSTT1 genotyping and assessment of antioxidant enzyme activities. The results showed decreased enzymatic activity of SOD (2.92 ± 1.07) and catalase (12.60 ± 3.15) in the exposed group, with increased MDA levels (4.14 ± 1.36), compared with the unexposed group (SOD: 7.04 ± 1.34, catalase: 25.75 ± 2.20, MDA: 1.15 ± 0.18). No significant associations (p > .05) were found between GSTM1 or GSTT1 genotypes and SOD, catalase, or MDA activities. The study concluded that prolonged pesticide exposure induces oxidative stress linked to specific genetic variations, suggesting directions for further research into the toxicogenetics of pesticide exposure and its health implications.

The aim of this study was to quantify VOC concentrations in different ventilation conditions, Wet Bulb Globe Temperature (WBGT), illumination and noise levels in two automobile repair shops. A cross-sectional study was conducted at two shops in Surat Thani province, Thailand. VOCs were collected by area sampling using charcoal tubes. The air samples were analyzed by GC-FID. The noise levels, illumination, and temperature were measured by using noise dosimeter, lux meter, and WBGT apparatus, respectively. Fifteen different VOCs were detected in both shops. Most of the VOCs measured had levels below the limit values suggested by ACGIH, except toluene and chloroform in shop B. The average VOCs concentrations in shop B after installation of local exhaust ventilation and opening the door for 30 minutes after finishing painting a car, was significantly lower than before and after installation of the local exhaust ventilation. The WBGT indoors varied within 26° to 31°C, TWA noise levels were within 63 to 90 dBA, and illuminations were within 250 to 988 lux. Sheet metal work task in shop A had noise levels exceeding the standard. Proper ventilation and using respirators during operator work are essential in eliminating health hazards of automobile mechanics. Hearing conservation program could prevent hearing losses.

Pesticides are applied to plants all over the world to boost food production and lower the spread of diseases carried by insects. Exposure to the pesticides may cause genotoxic effects on target and non-target organisms, including humans. In agriculture, acetamiprid (ACE), a neonicotinoid insecticide, is frequently applied either alone or in conjunction with other pesticides. A combined approach employing the micronucleus test (MNT) and chromosomal aberrations (CAs) assay was used to evaluate the genotoxic effects of acetamiprid in the bone marrow of male Swiss albino mice. Acetamiprid was administered i.p. daily at 4.6 and 2.3 mg/kg/day along with 3% gum acacia as a negative control for 30 days. ACE treatment resulted in a small dose dependent increase in the frequencies of micronuclei per cell (0.28 ± 0.04, 0.38 ± 0.03, and 0.45 ± 0.02 for the control, 2.3 and 4.6 mg/kg b.wt. groups, respectively) and chromosomal aberrations (3.67 ± 0.61, 5.00 ± 0.45, and 7.00 ± 1.43 for the control, 2.3 and 4.6 mg/kg b.wt. groups, respectively) in bone marrow cells, but no significant differences were observed between these data sets. In conclusion, daily i.p. exposure of ACE @ 2.3 and 4.6 mg/kg b.wt. for 30 days did not produce significant genotoxic effects in the somatic cells of Swiss albino male mice.

Pesticides, widely used for insect control in agriculture, public health, and veterinary medicine, are usually present as pollutants in aquatic environments. After contamination of water bodies, pesticides cause adverse effects on non-target organisms and long-term problems in the ecosystem. Lambda-cyhalothrin (LCH) is a chemical compound belonging to the family of synthetic pyrethroids (type II) and is an active ingredient in several insecticides. This study investigated the toxic effects (DNA damage) of LCH exposure on zebrafish for 24 and 72 h. After zebrafish (Danio rerio) were obtained commercially, acclimated, and adapted to laboratory conditions. They were randomly selected, transferred to the experimental aquariums (their average height is 2.51 ± 0.49 cm long, 10 L aquarium size of 10x20x35), and exposed to 0.1 mg/L LCH concentrations for 24 and 72 h. There was also a control and a solvent control group in the study, and whole body tissues of zebrafish were analyzed for 8-hydroxy-2-deoxyguanosine (8-OhdG) determination (ng/100 mg tissue), using an Agilent LC-MS/MS with electrospray ionization in positive ion mode. It was observed that the whole-body 8-OHdG tissue values were significantly increased in the group exposed to LCH for 72 h (9.82 ± 1.44) compared with the control group (6.60 ± 1.78, p = .004). These results suggest that LCH could lead to oxidative DNA damage by causing an increase in 8-OHdG activities in zebrafish, one of the aquatic ecosystem model organisms, indicating that it may also cause undesirable effects on other non-target species.

Manganese (Mn) is an essential element crucial for the proper functioning of the human body. However, excessive exposure to manganese can lead to complications, particularly neurotoxicity. Among the health issues associated with exposure to heavy metals, one of the major concerns in the adverse effect on sleep quality. A total of 189 employees from a steel factory were divided into two groups: exposed (149 people) and non-exposed (40 people). Air samples were collected using the NIOSH 7300 method, and blood samples were obtained at the end of each shift. The samples underwent analysis by ICP-OES after preparation using the acid-thermal digestion method. To gather information on sleep quality, the Petersburg Sleep Questionnaire (PSQI) was used. The data collected in this study showed abnormal conditions, leading to the inclusion of medians alongside averages. The participants had an average age of 35 and an average work experience of 6 years. The exposed group had a significantly higher median respiratory exposure to manganese (1.32 mg/m³) compared with the non-exposed group (0.20 mg/m³). The average sleep quality score in the exposed group was significantly worse (score of 7) compared with the non-exposed group (score of 4). In addition, there was a significant relationship between the quality of sleep and the level of manganese in the air, so that the quality of sleep decreases with the increase in the level of manganese in the air (p-value = .005). However, no significant relationship was observed between blood manganese level and air manganese level in the exposed group (p-value = .06).

Perfluoroalkyl chemicals are one of the most stable substances in industry and have become ubiquitous contaminants owing to their persistence in the environment. This study enrolled 1,953 participants aged ≥40 years old using data from the National Health and Nutrition Examination Survey (NHANES). We selected four perfluoroalkyl chemicals with a detection frequency of more than 80%, including perfluorohexane sulfonic acid (PFHxS), perfluorononanoic acid (PFNA), perfluorooctanoic acid (PFOA), and perfluorooctane sulfonic acid (PFOS). Multivariate logistic regression was performed to determine the relationship of serum perfluoroalkyl chemicals with COPD and airflow limitation. We evaluated the interaction between perfluoroalkyl chemicals and lung function using multivariate linear regression analyses. Our results showed that the prevalence of COPD was not significantly related to serum PFHxS, PFNA, PFOA, and PFOS. Airflow limitation was positively linked with serum PFHxS, PFOA, and PFOS. However, these significant differences were not robust after adjustment of all confounders of interest. Serum PFHxS, PFOA, and PFOS were all positively related to the forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and peak expiratory flow (PEF). However, only PFOA remained significantly linked with the FEV1 and FVC after covariate adjustment. These results indicated that there was no significant interaction between exposure to perfluoroalkyl chemicals and the prevalence of COPD. Higher levels of serum PFOA appeared to be related to higher measures of FEV1 and FVC.

(E)-1,1,1,2,2,5,5,6,6,6-Decafluoro-3-hexene (HFO-153-10mczz-E) (CASRN 1256353-26-0) is a volatile liquid proposed for use as a new low global-warming potential dielectric fluid in cooling applications. Workplace exposures are expected to be by inhalation exposure. The substance has low acute inhalation toxicity as indicated by a 4-h inhalation LC₅₀ value of approximately 8000 ppm. A suite of in vitro assays was negative for skin and eye irritation as well as for skin sensitization potential. The chemical did not induce cardiac sensitization up to 5000 ppm. Repeated inhalation exposure in rats for 4 or 13 weeks did not produce any effects attributable to the substance at 3000 ppm, the maximum tested concentration. No indications of developmental or reproductive toxicity were observed in studies in rats, also conducted with a maximum concentration of 3000 ppm. There was no indication of genotoxicity in the Ames assay, an assay with human TK cells, chromosome aberration in cultured human lymphocytes, or an in vivo rat micronucleus assay. The critical study for the development of the 8-hour TWA WEEL is the 13-week inhalation toxicity study with a NOAEC of 3000 ppm (32,400) mg/m³). This inhalation NOAEC was adjusted by application of appropriate uncertainty factors to account for interindividual variability, subchronic to chronic exposure extrapolation and other sources of uncertainty. A WEEL value of 200 ppm (2160 mg/m³) is expected to provide an acceptable margin of safety for potential adverse health effects in workers.

Di-2-(ethylhexyl)phthalate (DEHP) is a phthalate derivative used extensively in a wide range of materials, such as medical devices, toys, cosmetics, and personal care products. Many mechanisms, including epigenetics, may be involved in the effects of phthalates on brain development. In this study, Sprague-Dawley male rats were obtained 21-23 days after their birth (post-weaning) and were exposed to DEHP during the prepubertal period with low-dose DEHP (DEHP-L, 30 mg/kg/day) and high-dose DEHP (DEHP-H, 60 mg/kg/day, 37 days) until the end of adolescence (PND 60). The rats in the study groups were sacrificed during adulthood, and histopathological changes, epigenetic changes, and oxidative stress parameters were evaluated in brain tissues. Histopathological findings indicating the presence of deterioration in brain tissue morphology were obtained, more prominently in the DEHP-H group. Examining the hippocampus under the light microscope, pyramidal neuron loss was detected only in CA1 of the DEHP-L group, while in DEHP-H rats, pyramidal neuron losses were detected in the CA1, CA2, and CA3 regions. No significant change was observed in brain lipid peroxidation levels with DEHP compared to control. Significant increases in total glutathione (GSH) in both dose groups were considered to be an adaptive response to DEHP-induced oxidative stress. The decrease in DNA methylation in the brain, although not statistically significant, and the increase in histone modification showed that exposure to DEHP may cause epigenetic changes in the brain and these epigenetic changes may also take place as one of the mechanisms underlying the damage observed in the brain. The results suggest that DEHP exposure during early development may have a significant effect on brain development.

This study investigated the etiology, clinical features, and management of acute hydrogen sulfide (H₂S) poisoning in Zhoushan. A retrospective analysis was conducted on 10 patients admitted to our hospital between August and September 2023 due to two incidents of acute H₂S poisoning. The first incident involved fishermen working in a fishing cabin (6 patients), while the second involved sanitation workers during sewer maintenance (4 patients). Among the patients, 4 had severe poisoning, 3 had moderate poisoning, and 3 had mild poisoning. Corneal chemical injuries were observed in 4 severe patients, and chest CT scans showed bilateral infiltrative changes in 7 patients. Elevated lactate concentrations, and low oxygenation indices were noted in all severe patients. Severe cases received intensive care, including tracheal intubation, mechanical ventilation, corticosteroids, methylene blue, ulinastatin, and hyperbaric oxygen therapy. Patients with mild to moderate symptoms received supportive treatments, including oxygen therapy and hyperbaric oxygen therapy. With the exception of one fatality, all other patients were discharged after successful treatment. Fishing boat cabins and decomposed sewage channels in island areas are common sites for acute H₂S poisoning. Rapid identification of H₂S poisoning and evaluation are crucial. Early airway management is essential for severe cases to prevent vital organ hypoxia.