Toxicology and Industrial Health

Fernandes, Bruno Jose Dumêt; Couto, Ricardo David

doi: 10.1177/0748233720957816pmid: 33155520

Glycidyl methacrylate (GMA; CAS no. 106-91-2) is a chemical monomer used in the manufacture of dental resins, can coatings and polymers. GMA has demonstrated toxicity to the ocular, digestive, respiratory and dermal systems. Human exposure occurs mainly in the workplace, but it can also happen through food. Although there were no available data on carcinogenicity of GMA, carcinogenic potential in the nasal cavity is highly expected. Further studies are needed to assess GMA exposure in humans. This study provides an alert of GMA human exposure and its genotoxic and carcinogenic potential.

Fernández-Torres, J; Plata-Rodríguez, R; Zamudio-Cuevas, Y; Martínez-Nava, GA; Landa-Solís, C; Mendoza Soto, L; Olivos-Meza, A; Suárez-Ahedo, C; Barbier, OC; Narváez-Morales, J; Martínez-Flores, K

doi: 10.1177/0748233720967531pmid: 33094684

Osteoarthritis (OA) is the gradual loss of articular cartilage and involves several tissues, such as the synovial membrane, meniscus, ligaments, and adipose tissue known as Hoffa fat pad. There are largely unexplored factors that lead to OA development, such as the impact of exposure to heavy metals like cadmium (Cd) on the viability of cells in the knee joint tissue. The objective of this report was to identify the cell type with the highest susceptibility to Cd toxicity with respect to cell viability and death. Our findings showed that a concentration as low as 3 μM cadmium chloride for 12 h affects the viability of synovial cells, and a concentration of 10 μM affects Hoffa cells. Our results suggest that Cd can affect the viability of synovial and chondral cells primarily. In contrast, Hoffa cells were less susceptible, likely because Cd favors the production of pro-inflammatory cytokines before triggering their death as part of its damage mechanism at the articular level.

Xing, Zhao-Yang

doi: 10.1177/0748233720966506pmid: 33094704

Cases of abamectin poisoning have been reported previously, but cases of severe brain dysfunction after poisoning are rarely reported, and abnormal electroencephalograms (EEGs) have not been reported. We report a case of a 46-year-old female who intentionally drank 400 mL of 5% abamectin pesticide. We describe in detail the clinical and EEG characteristics of the patient. The patient was discharged in good condition after 10 days. The study indicates that serious brain dysfunction and abnormal EEG caused by abamectin poisoning are treatable. Despite poor clinical and EEG findings at the outset, recovery is still possible. This is the first report on EEG after abamectin poisoning.

Du, Xuqin; Zheng, Wei; Ye, Qiao

doi: 10.1177/0748233720958969pmid: 33094697

Background:Chronic long-term, low-dose environmental and occupational exposure to lead (Pb) has been extensively studied in large cohorts worldwide among general populations, miners, smelters, or battery workers. However, studies on severe life-threatening Pb poisoning due to accidental or chronic occupational exposure to Pb and manganese (Mn) were rarely reported.Methods:We present one case of acute severe Pb poisoning and compare it with another severe chronic occupational exposure case involving Pb and Mn. A 27-year-old woman mistakenly took a large quantity of pure Pb powder as an herbal remedy; she developed abdominal colic, severe nausea, vomiting, fatigue, and cutaneous and sclera icterus. Laboratory tests showed her blood lead level (BLL) of 173.5 µg dL−1 and urinary lead level (ULL) of 1240 µg dL−1. The patient was diagnosed with acute Pb poisoning and acute liver failure. In another chronic exposure case, a 56-year-old man worked in a Pb and Mn smelting factory for 15 years. He was brought to the emergency room with severe nausea, vomiting, and paroxysmal abdominal colic, which was intolerable during the onset of pain. His BLL was 64.8 µg dL−1 and ULL was 38 µg dL−1, but his blood and urinary Mn levels were normal. The patient was diagnosed with chronic Pb poisoning. Both patients received chelation therapy with calcium disodium ethylene-diamine-tetraacetate (CaNa2EDTA). The woman with acute severe Pb intoxication recovered well and was discharged from the hospital after treatment, and the man who survived severe Pb poisoning was diagnosed with lung cancer.Conclusion:Clinical manifestations of acute and chronic severe Pb poisoning are different. Chelation therapy with CaNa2EDTA is proven to be an effective life-saving therapy in both cases by reducing BLL. Occupational exposure to both Pb and Mn does not appear to increase Mn neurotoxicity; however, the probability that co-exposure to Mn may increase Pb toxicity in the same patient cannot be excluded.

Sadeghi-Yarandi, Mohsen; Karimi, Ali; Ahmadi, Vahid; Sajedian, Ali Asghar; Soltanzadeh, Ahmad; Golbabaei, Farideh

doi: 10.1177/0748233720962238pmid: 33108261

1,3-Butadiene is classified as carcinogenic to humans by inhalation. This study aimed to assess cancer and non-cancer risk following occupational exposure to 1,3-butadiene. This cross-sectional study was conducted in a petrochemical plant producing acrylonitrile butadiene styrene copolymer in Iran. Occupational exposure to 1,3-butadiene was measured according to the National Institute for Occupational Safety and Health 1024 method. Cancer and non-cancer risk assessment were performed according to the United States Environmental Protection Agency method. The average occupational exposure to 1,3-butadiene during work shifts among all participants was 560.82 ± 811.36 µg m−3. The average lifetime cancer risk (LCR) in the present study was 2.71 × 10−3; 82.2% of all exposed workers were within the definite carcinogenic risk level. Also, the mean non-cancer risk (hazard quotient (HQ)) among all participants was 10.82 ± 14.76. The highest LCR and HQ were observed in the safety and fire-fighting station workers with values of 7.75 × 10−3 and 36.57, respectively. The findings revealed that values of carcinogenic and noncarcinogenic risk in the majority of participants were within the definitive and unacceptable risk levels. Therefore, corrective measures are necessary to protect these workers from non-cancer and cancer risks from 1,3-butadiene exposure.

Lee, Seunghyun; Lee, Sang Ha; Lee, Wanhyung

doi: 10.1177/0748233720964636pmid: 33107405

Occupation-related dust exposure is common, especially with increased industrialization. While occupational dust-related health issues caused by inhalation or ingestion have been well studied, only a few studies have examined the dermatologic effects of occupational dust exposure. This study aimed to investigate the association between occupational dust exposure and dermatologic symptoms in Korean workers. Among the large-scale representative data from the fifth Korean Working Conditions Survey, 45,700 workers were selected for study. Occupational dust exposure level was categorized as none, moderate, and severe, and dermatologic symptoms were assessed using a questionnaire on health problems. We analyzed the association between occupational dust exposure and dermatologic symptoms using multivariate logistic regression. Risks of skin problems and work-related skin problems were significantly associated with the level of occupational dust exposure in a dose-dependent manner (odds ratio (95% confidence interval): moderate, 1.51 (1.14–2.01); severe, 2.39 (1.74–3.29) in general skin problems; moderate, 1.72 (1.22–2.42); severe, 3.06 (2.11–4.44) in work-related skin problems). We, thus, demonstrate an association between occupational dust exposure and skin problems. As skin absorption of dust is a major route of dust exposure at the workplace, it is necessary to determine the efficacy of continuous management of occupational dust exposure.

Obiyo, Grace E; Ogunsuyi, Opeoluwa M; Akindele O, Adeyi

doi: 10.1177/0748233720968466pmid: 33108250

Continuous occupational exposure to spent engine oil (SEO) poses physiological risks to humans, especially to automobile mechanics. This study investigated the physiological effects of SEO-contaminated soil in a male Wistar rat model. Animals were dermally exposed to soil contaminated with SEO for 120 consecutive days and compared with rats exposed to uncontaminated soil (negative control). Heavy metal (lead (Pb), nickel (Ni), zinc, and cadmium (Cd)) accumulations, hematology, biochemical (aspartate aminotransferase (AST), alanine aminotransferase, alkaline phosphatase (ALP), urea, and creatinine) parameters, sperm morphology, and histopathology (liver, kidney, lungs, brain, skin, and testis) were evaluated as end points. Results revealed that the heavy metals in SEO-contaminated soil are far greater than the World Health Organisation permissible limits, with significant (p < 0.05) increases of Pb and Ni present in the brain, and Pb and Cd in the serum compared with the uncontaminated soil for the negative control. Only significant (p < 0.05) values were observed in the lymphocytes, activities of AST and ALP, and sperm abnormalities of the exposed rats compared with those used for the negative control. Histopathological changes were not evident in the brain but lesions were observed in the liver, kidney, lungs, skin, and testis of the exposed rats. Results herein suggest that the constituents of SEO may elicit harmful physiological changes to humans who are directly exposed to them.

Erdem, Johanna Samulin; Arnoldussen, Yke Jildouw; Tajik, Sepideh; Ellingsen, Dag G; Zienolddiny, Shanbeh

doi: 10.1177/0748233720962685pmid: 33025859

Welders have an increased risk for cardiovascular disease (CVD) following exposure to welding fumes. The underlying mechanisms are largely unknown; however, oxidative stress, systemic inflammation, and endothelial dysfunction have been suggested as contributing factors to particle-induced CVD. We investigated effects of mild steel welding fume (MSWF) on three target cell types: macrophages, pulmonary epithelial, and vascular endothelial cells. Cells were exposed to MSWF at nontoxic doses for 6 h/day, for five consecutive days. The expression of 40 genes involved in inflammation, fibrosis, and endothelial activation was analyzed. Moreover, changes in the reactive oxygen species production and migration capacity of cells were assessed. The expression of matrix metallopeptidase 1 (MMP1) was induced in both epithelial and endothelial cells following repeated exposure to MSWF. Although MMP1 is important in inflammatory responses in vivo, this effect was not concurrent with changes in the inflammatory status, cell proliferation, and migration capacities, nor did it induce oxidative stress in the cells. Thus, repeated exposure with low doses of MSWF was sufficient neither for inducing inflammatory stress in epithelial cells and macrophages nor for endothelial activation, and higher concentrations of MSWF or the nonparticle fraction of MSWF may be critical in causing the increased risk of CVD observed among welders.

Gao, Ke; Zhang, Chengfei; Tian, Yihong; Naeem, Sajid; Zhang, Yingmei; Qi, Yongmei

doi: 10.1177/0748233720971882pmid: 33169630

It is well-documented that lead (Pb) toxicity can affect almost all systems in living organisms. It can induce selective autophagy of mitochondria (mitophagy) by triggering reactive oxygen species production. Emerging evidence has suggested that Pb-induced autophagy can also be activated by the endoplasmic reticulum (ER) stress pathway. However, the interplay between ER stress and mitophagy remains to be elucidated. In this study, human embryonic kidney HEK293 cells were employed to investigate the role of ER stress in Pb-induced mitophagy. The results showed that the cell viability was decreased and cell damage was induced after exposure to Pb (0, 0.5, 1, 2, and 4 mM) for 24 h in a dose-dependent manner. Moreover, the expression of LC3-Ⅱ was significantly increased, and the expression of HSP60 was dramatically decreased after exposure to 1 mM and 2 mM Pb, indicating the induction of mitophagy following Pb exposure. Meanwhile, the expressions of activating transcription factor 6, inositol-requiring protein-1α, CCAAT/enhancer binding protein homologous protein, and glucose-regulated protein 78 were dramatically increased after Pb treatment, signifying the initiation of ER stress. Notably, the mitophagic effect was significantly compromised when ER stress was inhibited by 0.5 mM 4-phenylbutyrate, which was evidenced by lesser decreases in HSP60 expression and level of LC3-Ⅱ, suggesting Pb-induced mitophagy may be activated by the ER stress. Taken together, these findings provide a better understanding of Pb toxicity and suggest that Pb-induced ER stress may play a regulatory role in the upstream of mitophagy.

Burcu, Acikgoz; Nevin, Ersoy; Ilkay, Aksu; Amac, Kiray; Alper, Bagriyanik Husnu; Muge, Kiray

doi: 10.1177/0748233720973136pmid: 33190593

Exposure to an electromagnetic field (EMF) can have adverse effects on many organs and tissues, including the reproductive system. This study aimed to investigate the effects of EMF exposure during prenatal and postnatal periods on ovarian development in rat offspring. In this study, rat pups born from eight pregnant rats were used. EMF exposure was initiated on the first day of pregnancy and continued until the 42nd postnatal day. The blood and ovarian tissue samples of female offspring in sham and EMF groups were collected when they reached the age of 42 days. Follicle-stimulating hormone levels were significantly higher in the EMF group than in the sham group. Estradiol levels were significantly lower in the EMF group than in the sham group. Tissue-inducible nitric oxide synthase (iNOS) levels and expression were significantly greater in the EMF group than in the sham group. In the EMF group, congestion, bleeding areas, and degeneration of follicle structures were observed in ovarian tissue. The findings suggest that exposure to 50-Hz, 3-mT EMF used in this study during prenatal and postnatal periods may lead to impaired ovarian structure and function in female offspring. EMF may affect ovarian physiology by increasing iNOS levels and may lead to fertility disorders.