Occupational Toxins Research Articles

Lead-based paint’s impact on certain blood parameters, kidney functions and oxidative stress

Lead is added to the paint to improve its dryness, durability, and resistance to corrosion in addition to adding color. One recognized occupational toxin is lead Increased exposure to lead can have negative health impacts on the body, such as liver, kidney, and nervous system damage. Anemia, hypertension, and a host of other illnesses can also be brought on by it. Many blood indicators, antioxidants, and kidney function of lead-exposed workers were studied in this study. A control group of forty healthy individuals who were not exposed to lead at work and fifty men between the ages of 18 and 50 who work in paint-related professions were chosen. In comparison to the control group, the results indicated an increase in the number of white blood cells and a reduction in the number of red blood cells. We found no difference in the amount of creatinine in the blood of the workers and the control group, except for a rise in the percentage of urea in the blood of the workers compared to the group that was not exposed when conducting renal functions. The results also revealed a significant rise in the levels of both (MDA and CAT).

Assessing cancer in people with profound and multiple disabilities

BackgroundCancers are as common in individuals with intellectual disabilities as in the general population (GP). For the subgroup of people with profound and multiple disabilities (PMD) who present with both severe intellectual disability and major motor disorders, the frequency and distribution of cancers are currently not known, preventing proper cancer surveillance.MethodsWe carried out a systematic and synthetic review of the medical literature, including a focused search of Japanese data.ResultsThe total risk of cancer in individuals with PMD is thought to be lower than in the GP, possibly due to a shorter life expectancy. They have reduced exposure to cancer risk factors, such as alcohol, tobacco, sunlight, human papillomavirus infection, occupational toxins, and being overweight. On the other hand, individuals with PMD present a greater frequency of gastroesophageal reflux disease, Helicobacter pylori gastritis, chronic cystitis, and cryptorchidism, which increase the risk for cancer of the esophagus, stomach, urinary bladder, and testes. In addition, certain genetic disorders underlying compromised motor and cognitive functions are associated with higher risk of childhood cancers. An analysis of 135 cancers in persons with PMD in Japan suggested that they present a particular tumor profile, with certain cancers rarer than in the GP, whereas cancers of the digestive tract are frequent. Cancers of the digestive tract occurred significantly earlier than in the GP (colon: average age 48.3 years vs. 71.3 years in the GP, esophagus: 39 years vs. 72 years in the GP). An increasing number of therapeutic successes in children and adults with PMD have been reported in different countries when cancers are discovered early.ConclusionIndividuals with PMD must be appropriately monitored for cancer. Screenings for breast and colon cancer, as well as regular monitoring of the esophagus, stomach, urinary bladder, and testicles, are necessary. Population-based epidemiological studies are needed to better understand risk factors, frequency, and distribution of cancers in the PMD population.

TRPM7 restrains plasmin activity and promotes transforming growth factor-β1 signaling in primary human lung fibroblasts

Sustained exposure of the lung to various environmental or occupational toxins may eventually lead to pulmonary fibrosis, a devastating disease with no cure. Pulmonary fibrosis is characterized by excessive deposition of extracellular matrix (ECM) proteins such as fibronectin and collagens. The peptidase plasmin degrades the ECM, but protein levels of the plasmin activator inhibitor-1 (PAI-1) are increased in fibrotic lung tissue, thereby dampening plasmin activity. Transforming growth factor-β1 (TGF-β1)-induced activation of SMAD transcription factors promotes ECM deposition by enhancing collagen, fibronectin and PAI-1 levels in pulmonary fibroblasts. Hence, counteracting TGF-β1-induced signaling is a promising approach for the therapy of pulmonary fibrosis. Transient receptor potential cation channel subfamily M Member 7 (TRPM7) supports TGF-β1-promoted SMAD signaling in T-lymphocytes and the progression of fibrosis in kidney and heart. Thus, we investigated possible effects of TRPM7 on plasmin activity, ECM levels and TGF-β1 signaling in primary human pulmonary fibroblasts (pHPF). We found that two structurally unrelated TRPM7 blockers enhanced plasmin activity and reduced fibronectin or PAI-1 protein levels in pHPF under basal conditions. Further, TRPM7 blockade strongly inhibited fibronectin and collagen deposition induced by sustained TGF-β1 stimulation. In line with these data, inhibition of TRPM7 activity diminished TGF-β1-triggered phosphorylation of SMAD-2, SMAD-3/4-dependent reporter activation and PAI-1 mRNA levels. Overall, we uncover TRPM7 as a novel supporter of TGF-β1 signaling in pHPF and propose TRPM7 blockers as new candidates to control excessive ECM levels under pathophysiological conditions conducive to pulmonary fibrosis.

Exposure to toxic occupations and their association with Parkinson's disease: a systematic review with meta-analysis.

Earlier longitudinal reviews on environmental and occupational toxins and Parkinson's disease (PD) risk have limitations. This study aimed to determine the strength of association between three types of toxic occupational exposures and the occurrence of PD by diagnostic methods. A search was conducted of EMBASE, PubMed/Medline, Toxnet, LILACS, and Cochrane Library databases for longitudinal studies that assessed toxic occupational exposure, Parkinsonian, or related disorders, diagnosed by International Classification of Diseases (ICD) codes, medical records, or confirmation by a neurologist/nurse, and published in the English language from January 1990 to July 2021. Pooled risk ratios (RR) estimates were produced using random-effects models. Systematic review with meta-analysis synthesized the results. Study quality, heterogeneity, and publication bias were examined. High-quality articles that met the inclusion criteria were analyzed. Twenty-four articles were used in the analyses. The pooled RR for electromagnetic exposure and PD were (RR=1.03, 95% confidence interval [CI] 0.91-1.16) while the pooled RR between PD and metal and pesticide exposure were (RR=1.07, 95% CI 0.92-1.24) and (RR=1.41, 95% CI 1.20-1.65), respectively. Pooled RR for methods of diagnosis and their associations with PD were: confirmation by a neurologist or nurse (RR=2.17, 95% CI 1.32-3.54); ICD codes (RR=1.14, 95% CI 1.03-1.26), and medical records (RR=1.06, 95% CI 0.92-1.21). Our systematic review provides robust evidence that toxic occupational exposures are significant risk factors for PD especially those diagnosed by neurologists or nurses using standardized methods.

Association between social determinants of health and olfactory function: a scoping review

Social determinants of health (SDoH) include the socioeconomic, demographic, and social conditions that influence differences in health status among individuals and groups. The impact of these conditions on olfactory function remains poorly understood. In this scoping review, we systematically review the available literature to synthesize the association between SDoH and olfactory function. In accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Review (PRISMA-ScR) guidelines, we performed systematic search queries in PubMed, Embase, and Ovid databases and categorized articles according to themes that emerged regarding SDoH. The primary outcomes included self-reported and objective measurements of smell. We identified 722 unique references that underwent title and abstract review by two independent reviewers, with 70 articles undergoing full-text review and 57 relevant for data extraction. Six themes emerged in our review, under which we categorized the studies and synthesized respective associations with olfactory function. These include studies exploring socioeconomic status (n=19, 33%), education status (n=27, 47%), occupational exposures (n=26, 46%), racial/ethnic disparities (n=12, 21%), and lifestyle/behavioral factors (n=33, 58%). Within the context of this scoping review, olfactory dysfunction is significantly more prevalent in patients with lower socioeconomic status, exposure to environmental and occupational toxins, and of minority race/ethnicity, whereas the associations between olfactory dysfunction and education level and lifestyle factors such as smoking and drinking seem to be much more elusive. This review highlights the importance of accounting for SDoH in observational studies examining olfactory outcomes. Given the increased awareness of olfactory loss, special consideration should be given to understanding olfactory dysfunction in the context of these factors.

Exposure of Workers to Occupational Noxae

The discomfort caused by exposure in the work process to occupational hazards generates. In this regard, this paper examines how the nuisances generated by technological processes influence the activity of workers and the legislative framework for jobs in which these occupational hazards exceed the allowed limits. In order to monitor the exposure to occupational hazards, the team of the Toxicology Laboratory performed determinations for the main occupational hazards existing in the work environment to the beneficiaries, the method of determining exposure to toxins being the direct method with measuring devices with numerical display, in time respectively, taking samples and analyzing them in the laboratory. The methods of analysis are in accordance with the legal provisions in force, using devices (metrological verified) and certified methods of analysis. Following the determination of noxious substances, specific risk assessments, in accordance with the legislation in force applicable to the jobs, in order to assess their impact on the health status of the staff, respectively the employment in special / special / normal working conditions, s -drew the following conclusions: periodic determinations of occupational toxins must be widely used to confirm or refute their existence in the workplace, permanent medical monitoring performed by occupational medicine practices, in conjunction with determinations of toxins, to establish traceability of occupational diseases with exposure to the susceptibility to its occurrence.

Prevention of chronic rhinosinusitis.

Prevention of chronicity of disease and minimising its impact with individualized treatment is a fundamental tenet of precision medicine. A review of the literature has been undertaken to explore how this may apply to chronic rhinosinusitis (CRS). Prevention may be thought of across 3 main domains. Primary prevention of CRS focuses on the avoidance of exposure to environmental factors associated with increased incidence of disease. This includes avoidance of tobacco smoke and occupational toxins. Although allergic rhinitis, respiratory infections and gastro-oesophageal reflux have been shown to be risk factors, there is no evidence as yet that treatment of these conditions is associated with reduced incidence of CRS. Secondary prevention of CRS is concerned with detecting a disease in its earliest stages, intervening to achieve disease and symptom control and preventing future exacerbations. Evidence based guidelines facilitate early diagnosis and appropriate use of medical and surgical interventions. In the future the use of endotypes to direct optimal is like to allow more clinically and cost-effective use of current and emerging treatments, such as monoclonal antibodies. Tertiary prevention aims to minimise the impact of an ongoing illness or injury that has lasting effects. Anxiety and depression have been shown to be associated with symptom amplification and may require treatment. The role of disease-related factors such as the role of the microbiome and osteo-neogenesis in the development of chronicity, and the development of severe combined upper airway disease needs further research.

Ameliorative potentials of quercetin against lead-induced hematological and testicular alterations in Albino rats.

Lead is one of the oldest environmental and occupational toxins. Health hazards from increased lead exposure as a result of industrial and environmental pollution are recognized. The aim of the present study was to investigate the protective effects of quercetin as a model of an antioxidant drug against the toxic effects of lead acetate on the blood and the testis of rats. The lead concentrations were determined in blood and the testis. Testosterone (T), luteinizing hormone (LH) and follicle stimulating hormone (FSH) were assessed in serum. Hemoglobin (Hb) content, packed cell volume (PCV), white blood cell (WBC) and red blood cell (RBC) counts were evaluated in the whole blood. Our results showed that administration of lead acetate was associated with an increased lead levels in blood as well as in the testis. Lead acetate administration also caused a decrease in testicular function, Hb content, PCV and RBC count in comparison to the respective mean values of the control. In addition, lead acetate increased WBC count and induced alterations in sperm count, sperm motility and sperm abnormality and histopathology. In the contrary, administration of lead acetate along with quercetin partially restored the studied parameters to normal values. In conclusion, the treatment with quercetin may provide a partial protection against the toxic effects induced by lead acetate in blood and the testis of rats.

Cough and dyspnea in a renal transplant patient.

A 38-year-old male presented with cough and dyspnea for approximately one month. He had a past medical history of hypertension, end-stage renal disease secondary to unspecified glomerulonephritis, and living-donor renal transplant 15 years ago. He had no history of exposure to tobacco or occupational toxins. His blood tests revealed increased serum creatinine (3.0 mg/dL), normal phosphate (4.0 mg/dL) and calcium levels (9.7 mg/dL), increased parathyroid hormone (95 pg/mL), and low calcidiol (10.2 ng/mL) and calcitriol (8.1 ng/mL) levels. The patient underwent bronchioalveolar lavage, which was negative for mycobacterial or fungal infection. Chest radiograph revealed fluffy densities involving the upper and mid lobes bilaterally with sparing of the subpleural region (Fig. 1). An axial computed tomographic scan of the chest showed extensive, upper lobe predominant ground glass opacities in an acinar distribution with areas of calcification. (Fig. 2, a and b) Figure 1 Chest radiograph showing fluffy densities involving the upper lobes bilaterally with sparing of the cortex (black arrow). Figure 2 Coronal computed tomographic scan of chest in a) Mediastinal window b) lung window showing extensive, upper and middle lobe predominant ground glass opacities in an acinar distribution with areas of calcification with subpleural sparing (black arrows). ... Questions What is the diagnosis? How do you treat it? To access the full article, please complete the quiz online at www.omjournal.org Articles from Oman Medical Journal are provided here courtesy of Oman Medical Specialty Board Formats: Article | PubReader | ePub (beta) | PDF (570K) | Citation Share Facebook Twitter Google+ You are here: NCBI > Literature > PubMed Central (PMC) Write to the Help Desk External link. Please review our privacy policy. NLM NIH DHHS USA.gov Copyright | Disclaimer | Privacy | Browsers | Accessibility | Contact National Center for Biotechnology Information, U.S. National Library of Medicine 8600 Rockville Pike, Bethesda MD, 20894 USA

Advanced malignant mesothelioma mimicking acute contained thoracic aortic rupture

In the emergent setting, patients presenting with acute interscapular pain along with haemodynamic instability require immediate evaluation. We describe the case of a patient in which computed tomographic scanning demonstrated a large hyper-dense, periaortic collection on post-contrast imaging. Urgent endovascular repair was performed for descending thoracic aortic rupture. Her postoperative course, however, was atypical with a readmission 1 week after discharge with symptoms similar to her primary presentation. Alternative pathologies were then considered in a more elective setting in which the correct diagnosis of diffuse malignant mesothelioma was ultimately discovered in a patient with no previous exposure to occupational toxins. The tumour burden was advanced and the patient opted for palliative care. Herein, we suggest a consideration for oncological thoracic pathology in patients presenting with signs and symptoms mimicking acute thoracic aortic rupture or dissection, who may demonstrate atypical symptoms.

95 Exposure to polycyclic aromatic hydrocarbons and sperm DNA integrity of coke oven workers

The objective of this study was to examine sperm DNA integrity of coke-oven workers in relation to exposure to PAHs from coke processing. A total of 72 human subjects participated...

Validation of RiskCheck Bladder Cancer ©, Version 5.0 for Risk-Adapted Screening of Bladder Cancer

Introduction: The aim of the study was to assess the strength of the online tool RiskCheck Bladder Cancer©, version 5.0 (RCBC) for early detection of bladder cancer (BC). Materials and Methods: RCBC was evaluated retrospectively based on the data of 241 patients, of which 141 were suffering from BC. Statistical analysis was performed by descriptive statistics, nonparametric group comparison, classification tree analysis and ROC analysis. Results: ROC analysis of the risk classification showed a sensitivity of 71.6%, a specificity of 56.5%, a positive predictive value of 67.8%, a negative predictive value of 52% and an accuracy of 63.5%. BC risk factors ranked by importance are time of smoking (p < 0.0001), gender (within the nonsmoking group: p < 0.009), occupational toxin exposure (within the group <35 years of smoking: p < 0.048) and amount of consumed cigarettes resulting in a 95% association with BC (within the group >35 years of smoking: p < 0.0001). Conclusions: The high predictive power of RCBC for the identification of asymptomatic patients living under risk could be demonstrated.

An elusive occupational toxin

An elusive occupational toxin

Mutational profiling of sporadic versus toxin-associated brain cancer formation: Initial findings using loss of heterozygosity profiling

The role of environmental and occupational toxin exposure as a cause of or contributing factor for cancer development and progression is incompletely understood. A unique signature of specific mutational change to discriminate toxin-exposed from sporadic cancer is generally sought but not often encountered. We report an approach to better understand cancer causality based on the measurement of the cumulative DNA damage (via loss of heterozygosity) over a defined genomic region (chromosome 3) that is applicable to archival, fixative-treated tissue and cytology specimens of cancer. Our method was applied to (1) a cohort of 10 brain tumor subjects (9 gliomas, 1 hemangioblastoma) with potential exposure to chlorinated solvents and (2) a control cohort of sporadic brain cancer controls (7 gliomas, 1 hemangioblastoma). We show that brain tumors arising in potentially toxin-exposed subjects bear a significantly higher level of passenger LOH mutations compared to sporadic cancer controls. The methodology utilized tissue microdissection, PCR amplification and capillary electrophoresis (fragment analysis for LOH determination, DNA sequencing for specific point mutations), and examined a panel of 15 microsatellite markers distributed along both arms of chromosome 3 that aimed at capturing passenger mutational change accrued during stages of clonal expansion of neoplastic cells. This proof-of-principle study using mutational profiling for passenger LOH mutational damage provides support for the utility of this approach and further studies in order to differentiate between genotoxin-associated versus sporadic (unexposed) cancer development.

Protocol sC-II of subClinical investigations for the presence of occupational environmental toxins, engineered nanoparticles, irritants and allergens as triggers and causative agents of toxic, allergic and immune responses in individuals within human habitations

Protocol sC-II of subClinical investigations for the presence of occupational environmental toxins, engineered nanoparticles, irritants and allergens as triggers and causative agents of toxic, allergic and immune responses in individuals within human habitations

Validating the Genetic Regulation of Liver Carcinogenesis under Environmental Stress

Purpose: Inadvertent exposure to environmental and industrial contaminants on human health is now a serious concern. However, liver work as a first line of defence against environmental as well as occupational toxins. Isocyanates, an important chemical entity with diverse industrial usage have drawn significant attention in the recent past as they react with DNA to produce toxicogenomic insults due to high degree of reactivity and low molecular weight having functional group -N=C=O. Moreover, health complications resulting from occupational and accidental exposures of these compounds are yet too elusive.This study was to explicate the role of different cellular proteins in cultured mouse liver epithelial cells after environmental stress using isocyanates. Methods: The present study was carried in NCTC clone 1469 (liver epithelial cell line) to assess cellular response of methyl isocyanate (MIC) using 0.005 μM of N-succinimidyl N-methylcarbamate, a surrogate chemical substitute to MIC. Studies were conducted in different time intervals to evaluate different cellular responses through addressing the role of different DNA damage responsive proteins; ATM, ATR & γH2AX; cell cycle regulatory proteins: cyclin A and E & cdk2; tumor suppressor proteins: p53, p21& Gadd45 and repair proteins: Mre11, Nbs1 & Rad50 through immuno-blotting and immunofluorescence. Results: Analysis of different cellular modulators through Western blot and immunofluorescence reveals interesting results. With initial activation of DNA damage sensors, different tumor suppressor proteins viz. p53, p21 and Gadd45 and repair proteins- Mre11, Rad50 & Nbs1 showed distress expression in N-succinimidyl N-methylcarbamate treated cells during different time intervals denoting their incompetence to regulate cell cycle due to profuse genetic alteration in comparison to controls cells. On the other hand, over-expression cyclins (cyclin A & cyclin E) and Cdk2 proteins were observed in different progressive time intervals in contrast to controls implicating their role in tumorigenesis due to inactivation of cell cycle checkpoints that, in turn, resulting abnormal cell proliferation. Conclusion: In conclusion, our investigation enlightens the tumorigenic proficiency of MIC with increased phosphorylation of DNA damage responsive proteins, impaired DNA repair process, deregulation of cyclins and decreased expression of different tumor suppressor proteins. The toxicant may affect the cascade of signaling mechanism of p53 and p21 proteins expression involved in cell cycle arrest with perturbation of GADD45 expression. Over-expression of cyclins and cdk2 expression further substantiated the progression of liver carcinogenesis.

The Specialty of Medical Toxicology: Beyond Poisonous Arrows and Activated Charcoal

Medical toxicology is a subspecialty focusing on the diagnosis, management and prevention of poisoning effects due to medications, occupational and environmental toxins and xenobiotics, radiological and biological agents. This subspecialty provides an array of opportunities for physicians to care for patients in different settings: medication overdoses, substance abuse management, adverse drug events, exposures to industrial chemical products, and envenomations. Many medical toxicologists work in the pharmaceutical industry and in many government agencies such as as the Centers for Disease Control and Prevention (CDC), the Environmental Protection Agency (EPA), the US Food and Drug Administration (FDA), and the Department of Homeland Security.

IL1B rs1143634 Polymorphism, Cigarette Smoking, Alcohol Use, and Lung Cancer Risk in a Japanese Population

Interleukin 1B (IL1B) is involved in pulmonary inflammation induced by environmental or occupational toxins. Chronic inflammation has been implicated in the development of lung cancer. We evaluated the role of IL1B (rs1143634, 3954C>T) in a case-control study comprised of 462 lung cancer cases and 379 controls in a Japanese population. Logistic regression was used to assess the adjusted odds ratios (OR) and 95% confidence intervals (95% CI). Individuals with a history of smoking and at least one T allele (adjusted OR = 5.45, 95% CI = 2.75-4.42, p < 0.01) presented a higher risk of lung cancer than those with the CC genotype (adjusted OR = 2.86, 95% CI = 2.02-4.05, p < 0.01) as compared with never smokers with the CC genotype (reference). The adjusted attributable proportion because of interaction between the IL1B rs1143634 genotypes and smoking was estimated to be 0.45 (95% CI = 0.08-0.83, p = 0.02), indicating that 45% of the excess risk for lung cancer in ever smokers with at least one T allele was due to additive interaction. Subjects with excessive alcohol intake and at least one T allele had a significantly higher risk (OR = 2.48, 95% CI =1.36-4.54, p < 0.01) than drinkers with appropriate intake and the CC genotype. There was no interaction between the polymorphism and alcohol intake. Our findings indicate the possible association of the T allele carriers of the IL1B rs1143634 polymorphism with higher risk of lung cancer especially among smokers. Additional studies are warranted to confirm the IL1B rs1143634-smoking interaction suggested in this study.

Potential for diffuse parenchymal lung disease after exposures at World Trade Center Disaster site

The diffuse parenchymal lung diseases (DPLDs) are a heterogeneous group of disorders that result from damage to the lung parenchyma. While the cause of most DPLDs remains unknown, extensive epidemiological and experimental evidence has linked exposure to environmental toxins to the pathogenesis of some of those diseases. The purpose of this review is to examine the potential relation between exposure to toxins released from the World Trade Center (WTC) collapse on September 11th, 2001 and the development of DPLD based on published evidence up to date. We examine such evidence from two points of view, (1) exposure, and (2) histopathogenesis. Analyses of WTC-dust and particle size demonstrate that some portion of the dust was composed of particles small enough to penetrate deep into the lungs, reaching distal airways and alveoli. The presence of such particles has been confirmed in studies of induced sputum and bronchoalveolar lavage in WTC-exposed firefighters. Histopathogenesis: In vitro and animal experiments and patient evidence suggest that WTC dust is capable of inducing a pulmonary interstitial inflammatory response. To date, there have been limited clinical reports documenting the development of diffuse parenchymal responses following exposure to WTC dust. No single common pathologic response has been described. The one common denominator in the reports is that the individuals who developed disease were heavily exposed either during the disaster or during the initial 2-to-3 days following the disaster. DLPDs are probably associated with heavy or extended exposure to the toxins released at the WTC disaster site. Coupled with the historical experience with exposures to occupational toxins this mandates continued long-term clinical observation of this cohort.

Application of Oligonucleotide Microarray Technology to Toxic Occupational Exposures

Microarray technology has advanced toward analysis of toxic occupational exposures in biological systems. Microarray analysis is an ideal way to search for biomarkers of exposure, even if no specific gene or pathway has been identified. Analysis may now be performed on thousands of genes simultaneously, as opposed to small numbers of genes as in the past. This ability has been put to use to analyze gene expression profiles of a variety of occupational toxins in animal models to classify toxins into specific categories based on response. Analysis of normal human cell strains allows an extension of this analysis to investigate the role of interindividual variation in response to various toxins. This methodology was used to analyze four occupationally related toxins in our lab: oxythioquinox (OTQ), a quinoxaline pesticide; malathion, an organophosphate pesticide; di-n-butyl phthalate (DBP), a chemical commonly found in personal care and cosmetic items; and benzo[a]pyrene (BaP), an environmental and occupational carcinogen. The results for each exposure highlighted signaling pathways involved in response to these occupational exposures. Both pesticides showed increase in metabolic enzymes, while DBP showed alterations in genes related to fertility. BaP exposure showed alterations in two cytochrome P450s related to carcinogenicity. When used with occupational exposure information, these data may be used to augment risk assessment to make the workplace safer for a greater proportion of the workforce, including individuals susceptible to disease related to exposures.