This review discusses the potential hazards of exposure to micro- and nano-plastics in the workplace and its mitigation. The literature reviewed was obtained by searching the papers used in most research for the necessary data, including PubMed, specifically for the last five years. The search was performed using the key terms “microplastics”, “nano-plastics”, “toxicity”, “health”, and “workers”. Unless the plastic value chain is changed, the threats to the environment, marine ecosystems, species, human health, the economy, and communities will become intolerable. But these hazards also present special opportunities to contribute to the shift to a more sustainable world. The review underlines the need for more investigation into the intricate biological relationships and hazards associated with the buildup of MPs/NPs in the workplace, and suggests possible avenues for future research on the health of employees.

Ototoxic hearing loss can be divided into that caused by medication, and that caused by industrial chemicals. I use gene ontology analysis to focus on the functional predictions, and summarize the cochlear and vestibular distributions of functional genes. To predict and consider ototoxic changes related to gene expression, I list the ototoxic chemicals and analyze their gene expression. These include a literature to develop a list of ototoxic chemicals and related research trends; examination of the toxicogenomic changes of ototoxic chemicals and organization of an EXCEL file, etc.; examination of the metabolic pathways related to toxicogenomic changes and epigenetics related to hearing, and preparation of a plan of preventive measures for ototoxicity caused by chemical exposure. Wearing of protective gear and regular health monitoring to reduce exposure are essential to prevent hearing damage caused by ototoxic chemicals. This will contribute to creating a safe environment in the workplace by having companies and workers practice preventive measures together. I aimed to examine the toxicogenomic changes of ototoxic chemicals, and based on the results, to contribute to the establishment of preventive measures against the ototoxicity of chemicals. A literature review identifies a list of ototoxic chemicals and related research trends. Toxicogenomic changes in ototoxic chemicals are examined, and compiled in EXCEL. Metabolic pathways related to toxic genome changes are examined, and epigenetics related to hearing loss are described.

Epigenetic modifications, including miRNA regulation, have been identified as significant contributors to several disorders that include malignancies. Numerous novel compounds in epigenetic modifications have recently been receiving increasing emphasis, while the role of epigenetics in the onset and progression of illnesses has been attracting more attention. The role of miRNA and other epigenetic mechanisms in chemical toxicity needs investigation. The literature over the last decade was reviewed by searching for pertinent data in a number of reviews, using Google Scholar ( http://scholar.google.com ) and PubMed ( http://www.ncbi.nlm.nih.gov/pubmed ), together with relevant journal websites for articles published in the last five years (2019–2024). The search terms were the keywords “chemical,” “toxicity,” “microRNA,” and “epigenetics.” This review summarizes that data. MicroRNAs exhibit the characteristics due to their capacity to react to substances and their essential function in phenotypic determination. This review updates the role of miRNAs as effective instruments to elucidate the mechanisms behind the pathophysiological response to toxicants and the prognostic significance of their expression patterns linked to specific exposures. The mechanistic data related to the involvement of miRNAs in the development of occupational illnesses were examined. It is becoming increasingly evident that miRNAs serve as significant epigenetic regulators of physiological functions. Existing research concerning the impact of xenobiotics on miRNA expression patterns was also examined.

The genetic material of all organisms exists within the context of a regulatory network that governs gene expression that is collectively known as the epigenome. While epigenetics plays a central role in the study of diseases such as cancer, diabetes, and neurodegeneration, its integration with the field of toxicology is still in its infancy. After investigating the characteristics of small RNA (miRNA, siRNA), lncRNA, etc. through the literature and the expression and regulation of miRNA genes and proteins according to chemicals, we review the expression and regulation of miRNA genes and proteins in specific cancers, organize the target substances and related substances for each organ in rat, and examine the expression and regulation of miRNA genes and proteins according to chemicals in specific cancers. This study examines the relationship between the expression of miRNA, an epigenetic indicator, and the regulation of the carcinogenic process due to chemical exposure in the discovery of carcinogenic chemicals, and uses it as a basic study to select carcinogenic candidates, contributing to the examination of the carcinogenic mechanism of lung cancer such as cooking fume exposure, and the establishment of countermeasures. Common miRNAs, such as miR-21, miR-33a, miR-155, and miR-181a, were found to be suppressor genes related to SIRT6, PTEN, Nrf2, and TGIF2 cell apoptosis (programmed cell death), proliferation, invasion, and metastasis. Oncoprotective miRNAs, such as let-7a, miR-22, miR-266, miR-466, and miR-499a, were found to be regulated by genes associated with the expression of mutated oncogenes as their main targets. To select efficient inhalation carcinogenic priority substances, a new attempt is made to select carcinogenic substances using miRNA, an epigenetic technique, and the relationship between miRNA expression, an epigenetic indicator, and the regulation of the carcinogenic process due to chemical exposure in the discovery of carcinogenic chemicals. This is intended to provide a basic study to select carcinogenic candidate substances. The carcinogenicity exhibited by (inhalation) exposure to benzo(a)pyrene in cooking fumes was used to predict the following epigenetic regulatory process. First, the expression of the let-7 family suppresses the expression of the Kras oncogene protein, which leads to EGF up-regulation and the resulting increase in Kras expression by the Pten tumor suppressor protein, which is suppressed by the expression of a different pathway, miR-21 and miR-494. Meanwhile, the expression of another pathway, miR-30d and miR-34c, affects cell growth and proliferation; we consider that their multi-step action can lead to carcinogenicity.

While differences in cancer incidence between the two sexes/genders are often explained by differences in environmental exposure or the influence of sex hormones, there is little research on intrinsic differences in sensitivity to chemical carcinogens. This review summarizes the literature obtained by searching the papers used in most research for the necessary data, including PubMed, specifically for the last 5 years 2019–2023. The search was performed using the key terms “chemical”, “toxicity”, “gender”, and “sex differences”, and “cancer” or “disease”. Based on the literature data, over 80 potential articles were found. A total of 28 papers that satisfied the inclusion criteria were selected for detailed analysis. While some sex differences in cancer occur through the action of circulating sex hormones, other sex differences are unrelated to estrogen, testosterone, or progesterone levels. Globally, sex differences in tumor incidence and mortality are evident across a wide range of age groups.

Objectives Differences in cancer incidence between men and women are often explained by differences in environmental exposure, or the influence of sex hormones. However, there is little research on the intrinsic differences in sensitivity to chemical carcinogens. Methods To predict and consider related in vivo carcinogenicity tests, changes in gene expression were examined in rats and mice (by gender and organ) due to exposure to carcinogenic chemicals such as phenyl compounds, which among chemicals are the main cause of carcinogenesis. Results In the case of male SD rats, the genes IL1B, TNF, NOS2, IL6, and NGF were related, and the probability of carcinogenesis in the urinary bladder, kidney, and oral cavity was high. In female SD rats, the genes ADRB2, TNF, HMOX1, CYP1A1, PTGS2, ILB1, CASP3, POR, PRL, TSC22D1, ATEG, REG1, HRH2, NFE2L2, AKR1C2, ADRB2, NR3C1, IL6, ADRB1, ADRB3, and LPO showed high probability of carcinogenesis in the stomach, liver, and nasal cavity. In the male F344 rat, the genes ACACA, ACSL1, ALB, ALCAM, CYP19A1, PPARA, CYP4A1, ACAA1, and ACOX1 were related, and showed a high probability of carcinogenesis in the liver, kidney, stomach, and urinary bladder. In the female F344 rat, no related genes were found, but a high probability of carcinogenesis was shown in the kidney, ear, Zymbal’s gland, stomach, and liver. In male ICR mice, no related genes and organs with a high probability of carcinogenesis were found, while in female ICR mice, genes for KRAS, ACHE, CAT, CYP3A4, and GPT were involved, and carcinogenesis occurred in the stomach, thyroid gland, ovary, liver, etc. The probability was shown to be high. In BALBc mice, no related genes and organs with a high probability of carcinogenesis were found, while in female BALBc mice, the genes NR1I2, CYP3A4, ABCB1, CYP2B6, PRKDC, CYP2C9, and NCOA1 were related, and the liver, etc., had a high probability of carcinogenesis. Conclusion Differences in the epigenetics of each sex begin at the moment of fertilization due to differences in sex chromosome gene expression and metabolic profiles between XX and XY embryos. These fundamental sex differences in nutrient utilization and mitochondrial activity may contribute to sex differences in the metabolic reprogramming of cancer cells, which is important during cancer development, cancer progression, and response to anticancer treatment. Purpose of review In this study, I compared and considered the degree of toxicity and genome expression in each male and female gender and organ due to exposure to phenyl compounds (PAH, etc.), which are the basis of benzene toxicity as aromatic hydrocarbons, and conducted future inhalation toxicity tests and related carcinogenicity tests. Recent findings Differences in the epigenetics of each sex begin at the moment of fertilization due to differences in sex chromosome gene expression and metabolic profiles between XX and XY embryos. Throughout development, additional processes, such as X-chromosome inactivation and gonadal steroid exposure, further distinguish the sexes.

BackgroundThis study seeks to estimate whether a chemical has carcinogenic potential; and if it has carcinogenic activity, its carcinogenic efficacy in humans and experimental animals in terms of oral and inhalation slope factors.ObjectiveTarget chemicals were selected by literature search using Google Scholar, PubMed, ScienceDirect, etc., among the chemicals set by the Ministry of Employment and Labor in Korea as existing chemicals, and the CSF of each chemical was determined using various sites and programs, including EPA Comptox Dashboard and VEGA Hub QSAR (ver. 1.2.3). The CSF value of each chemical obtained using the Comparative Toxicogenomics Database (CTD) was subjected to gene expression analysis for inhalation carcinogenicity according to CSF value priority estimation, and a database (chemical list) was made possible.ResultsBased on KOSHA-MSDS, GHS classification, and reference values for the CSF of each chemical, they were classified and organized using the OncoLogic 9.0 program. The priority of inhalation carcinogenicity was estimated by comparison with gene expression and CSF values, especially those with large inhalation-related values, and carcinogenesis of priority chemicals for inhalation. All the contents were organized and presented in an Excel file, and the priority of inhalation carcinogenicity was estimated through comparison with gene expression, focusing on CSFs, especially those with large inhalation-related values.ConclusionBased on the obtained CSF value, the gene expression analysis of each chemical and toxic gene expression analysis of the CTD, inhalation carcinogenicity priority was estimated and a DB (chemical list) was prepared according to the CSF value.

Exposure to mixtures has already become a daily reality, as we are exposed to numerous chemicals throughout our lives from a variety of environmental sources. However, although humans are exposed to several mixtures, rather than a single chemical, most of the existing toxicity data are from exposure to a single chemical. This is to conduct a comprehensive review of scientific evaluation and risk assessment of exposure to mixtures in the workplace for the prevention of occupational diseases. This review responds to social issues by scientifically explaining the mixed harmfulness and toxic pathological mechanisms caused by exposure to mixtures for each process, which have become social issues, and is intended to be based on the development of inhalation toxicity testing. The interaction mechanism between chemicals and the research results related to biological reactions, toxic genome expression analysis using differential gene expression analysis and the Comparative Toxicogenomics Database, and data retrieved from the Kyoto Encyclopedia of Genes and Genomes DB, etc., were analyzed. The specific genes related to mixtures, genes on specific pathways related to proteins, etc., and protein–protein interactions were considered. The major hazardous chemicals that workers can be exposed to in the semiconductor process, gravure printing, and construction industry are combined into a matrix, focusing on carcinogenicity, germ cell mutagenicity, and reproductive toxicity (CMR), which among various hazards are the most important toxicity indicators. The main adverse outcome pathways (AOPs) that can occur when major toxic chemicals are co-exposed in the form of mixtures are illustrated, and a schematic of the AOPs provided by AOP − Wiki is shown. Gene expression and related pathway diseases by exposure to mixtures are summarized and presented. The mechanism pathway provided by the KEGG sites is shown, and additional research is considered about exposure to mixtures in each industry. In the case of semiconductor manufacturing, among various chemical combinations showing major toxicity, catechol and dimethyl sulfoxide are the main toxic potentials. In the gravure printing process, among the mixtures of various chemicals showing major toxicity, the mixture with ethanol is suspected as having the most toxic potential. In the painting process in the construction industry, among the mixtures of various chemicals that show major toxicity, a mixture of 10 chemicals, such as benzene, toluene, and xylene, along with the components of Portland cement, are suspected of inducing toxic potential. Verification studies on these should be conducted in the future.

Objective and methods Three-dimensional (3D) printing is providing new tools. However, the feedstocks use synthetic polymers, such as acrylonitrile, butadiene, styrene, polylactic acid, nylon, and some metals; and while 3D printing, volatile organic compounds and nanoparticles can be released. The literature search was performed using the key terms "3D printing", "chemicals", "toxicity", "health", and "workers". This review examines the search responses for their related experimental results, as well as adverse effects or toxicities, to gain more understanding of their health effects, and help prevent the occupational diseases of workers from the 3D printing process. Results and conclusion Additive manufacturing or "3D-printing" is a ground-breaking technology that enables the production of complex 3D parts. Its rapid growth calls for immediate toxicological investigations of possible human exposure to estimate occupational health risks. General management measures for hazardous chemicals or harmful factors include substitution, isolation, and ventilation as engineering measures, and the wearing of protective equipment and education as administrative measures. Environmental management measures may be applied.

Objective and methods Information on chemicals was not disclosed due to the lack of technology protection in the semiconductor industry. As semiconductor technology advances, the amount of chemicals used has (sometimes) changed. This report summarizes a literature review that was undertaken by searching the major websites used in most reviews for the necessary data, including Google Scholar, ScienceDirect, and Scopus, specifically for the last five years. The search was performed using the key terms "chemicals", "effect", "health", "semiconductor", and "workers". This review examines the chemicals in the semiconductor industry, the prevention of occupational diseases of workers, and future prospects for occupational health. Results and conclusion Based on the characteristics of the semiconductor industry and social issues of worker health, I address worker safety and discuss the perspectives of occupational health toward chemicals in the semiconductor manufacturing industries. Continuous occupational disease prevention activities must be carried out, and the development of advanced technologies such as AOP-KBs is also required. I'd like to give information on toxic chemicals such as their exposure routes, related genes, and gene interactions, target organs, symptoms, and health hazards as well as diseases or outcomes for improving future studies to prevent the occupational diseases of workers.

Objective and methods While lung cancer is the main cause of cancer death worldwide because of cigarette smoking, cooking oil fume is one of the major sources of aerial volatile organic compounds. This review summarizes the literature that was obtained by searching the papers used in most research for the necessary data, including PubMed, specifically for the last 20 years. The search was performed using the key terms “cooking oil fumes,” “effect,” “toxicity,” “health,” and “workers.” This review examines the literature on their related experimental results, as well as adverse effects or toxicities, to gain more understanding of health effects and prevent the occupational diseases of workers. Results and conclusion Based on the development of the catering and cafeteria industry, cooking oil fume is one of the major air pollution sources, and many types of research into cooking oil fume have been conducted for their high threat to human, especially workers’, health. It is limited, in that national emission inventory data specific to the catering service industry, occupational cooking oil fume exposure, and family heredity history were also feasible risk factors that indicated a complex disease, and the correlation of environmental and heredity factors played a major role in occupational disease from cooking oil fumes.

To solve current issues using big data, solve current issues related to the semiconductor and electronics industry, I tried to establish the data for each toxicity mechanism for adverse outcome pathway (AOP) for the exposure. I planned to increase the efficiency of human hazard assessment by searching, analyzing, and linking test data on the relationship between key events occurred at each level, which are the biological targets of chemicals in semiconductor manufacturing. It was found that 48 kinds of chemicals had 11 AOPs, while 103 chemicals had multiple AOPs, and 26 had case evidence. As a result of AOP analysis, it was found that a total of 320 chemicals had 42 AOPs, and 190 major chemicals corresponded to 11 AOPs. It was found necessary to develop a complex AOP and secure an (inhalation or dermal) exposure scenario for combined exposure at work. As a comparative search (41 out of 190 chemicals) of biomarkers specific to occupational diseases, 12 biomarkers were found to be related to breast cancer. The AOPs for 50 specific chemicals were presented, together with occupational disease-specific AOPs and key events relationship from 50 chemicals, and taxonomic classification for each AOP analysis could be found. With a comparative search, 41 out of 190 chemicals were associated with specific biomarkers for occupational diseases, and 12 mRNA or protein biomarkers were found to be related to breast cancer by cross-validation with the attached Table 24 of the Enforcement Regulations of the OSHAct and the CTD. The mechanism of occupational diseases caused by chemicals was presented, together with pathological preventions. I believe that a strategy is needed to expand the target organization for each chemical by linking with activities, such as work environment measurement, and cooperating with screening items and methods suitable for toxic chemicals, like AOP tools.

Objective and methods This report is intended to present a comprehensive review of the scientific evaluation of mixture exposure and risk assessment at work, in order to prevent occupational disease. The report summarizes the literature review that was undertaken by searching the major websites used in most reviews for the necessary data, addresses worker safety and discusses the future perspectives of occupational health issues from chemical mixtures. Results and conclusion Many workers are known to be potentially exposed to complex mixtures with high exposure levels, with the potential for toxic damage from those chemical mixtures. Although many chemicals are regulated, the exposure to occupational mixtures can cause significant health problems, such exposure is still very present in the working environment and worker exposure to this mixture still presents a threat to occupational health. However, the future of mixture research is very bright, as not only are efforts being made to find more than just the combining of chemicals, interactions are being predicted between chemicals and non-chemical factors targeting adverse outcome pathways, based on the latest understanding of biological systems. Much progress has been made in predicting the concomitant effects using the concept of mixed chemicals and more sophisticated big data analysis methods as well as tools that can be used to test hypotheses such as in vitro, in silico and alternatives to animal testing. Since the information to be utilized is also available, exposure information with a high-throughput can be suggested, which will help to detect related diseases.

Objective and methods This study examines the protection of workers from the "COVID-19" pandemic, especially healthcare workers, disinfection workers, and future prospects in occupational health. To summarize this concept, I searched the major websites using the key terms "COVID-19," "coronavirus," "pandemic," "workers' health," and "quarantine" or "disinfection." Results and conclusion The use of disinfectants is recognized to be effective in preventing viruses, but this is also increasing the need to solve problems, such as the side effects caused by the increase in disinfectant use. This paper presents the precautions for safer use of chemicals handled by workers during quarantine and disinfection and proposes policy suggestions. The COVID-19 pandemic will have long-lasting effects on workers. Syndromic methods for monitoring illness outside of healthcare settings can be useful adjuncts to conventional disease reporting. From these results, it is important that the precautions for chemicals' safety handled by workers during quarantine and disinfection as well as policy suggestions for quarantine and disinfection workers are very important to protect workers.

Objective and methods This study reviewed the concept of in silico prediction of chemical toxicity for prevention of occupational cancer and future prospects in workers’ health. In this review, a new approach to determine the credibility of in silico predictions with raw data is explored, and the method of determining the confidence level of evaluation based on the credibility of data is discussed. I searched various papers and books related to the in silico prediction of chemical toxicity and carcinogenicity. The intention was to utilize the most recent reports after 2015 regarding in silico prediction. Results and conclusion The application of in silico methods is increasing with the prediction of toxic risks to human and the environment. The various toxic effects of industrial chemicals have triggered the recognition of the importance of using a combination of in silico models in the risk assessments. In silico occupational exposure models, industrial accidents, and occupational cancers are effectively managed and chemicals evaluated. It is important to identify and manage hazardous substances proactively through the rigorous evaluation of chemicals.

Background Roasted coffee beans are broadly consumed in nearly all classes of the population. 2,3-Butanedione is a food flavor that causes obstructive bronchiolitis in microwave popcorn manufacturing workers. It can be naturally produced when coffee is roasted. Objective To determine effects of 2,3-butanedione (diacetyl) and 2,3-pentanedione on workers’ health during the coffee roasting process, we performed a toxicogenomics study for differentially expressed genes in lung cells after exposure to the two chemicals. Results Gene selection was performed by clustering, gene ontology/pathway, and data mining using microarray data. Target microRNAs and genes were selected based on the expression of microRNAs and correlation analysis of genes and microRNAs. As a result of expression analysis of target gene miRNAs affected by the two chemicals, it was evaluated that Fosl1 , Rb1 , Aspn , Dusp1 , Rnf19b , Jun , and Hbegf were over-regulated by targeting down-regulated miRNAs mutated by two chemicals. Using OMIM database and KEGG pathway, we found that Terc and Bmpr2 were two changed genes by matching with the KEGG disease pathway database. Conclusion Dosage, duration, exposure, and extrapolations are necessary to reflect effects of diacetyl and 2,3-pentanedione on workers in the coffee roasting process. This study focuses on early biochemical changes, mechanisms, and early biomarker discovery when normal lung cells are exposed to these two chemicals.

Objective and methods:Various papers related to the application of adverse outcome pathways (AOPs) for the prevention of occupational disease were reviewed. The Internet was used as the primary tool to search for the necessary research data and information, using such online resources as Google Scholar, ScienceDirect, Scopus, NDSL, and PubMed. The key search terms were "adverse outcome pathway," "toxicology," "risk assessment," "human," "worker," "occupational safety and health," and so on.Results and conclusion:The aim of this paper is to explain the use of AOP for the understanding of chemical toxicity as a conceptual means and to predict the toxic mechanism. The tools of AOP have emerged as a forward-looking alternative to the existing chemical risk assessment paradigm. AOP is being applied to the assessment of acute toxicity and to chronic toxic chemicals in the workplace. Not only can it lead to breakthroughs in occupational and environmental cancer prevention, it is also widely used in chemical risk assessment and has led to breakthroughs in the prevention of occupational disease in the workplace.

Since it has been considered acceptable to expose animal to conditions and procedures that would not be considered acceptable for human, animals have long been used as surrogates for human beings for in vivo toxicology. This has focused mainly on gaining a better understanding of how the body’s cells, organs, and systems function and are controlled, which failures could lead to pathological conditions. However, attitudes that rely on this approach are changing as the know ledge gained from animal studies is not directly related to humans, and there is a growing perception that it can also have dangerous consequences. In this re view, I collected the references about not only in vitro models for chemical toxicity, but also their applications and prospects focused on chemical hazard evaluations. In this review, I try to gather the issues and considerations that are considered necessary to develop a viable and reliable testing strategy to replace animals in toxicity testing. Most of the authors of the papers cited here share the opinion that animals will no longer be used for safety assessment, but that a more predictable human-derived in vitro system and in silico approach will be developed step-by-step. I collected information from peer-reviewed literature on the in vitro models for toxicological investigation of chemicals that may impact environmental or occupational diseases.

Objective and Methods Because of its characteristic sensory properties and physiological properties, coffee is one of the most popular beverages in the world. Roasted coffee beans are broadly consumed in nearly all classes of the population. The literature search used a lot of sites, including PubMed, Google Scholar, and ScienceDirect, and was further refined by reviewing titles, abstracts, and references in the bibliography to confirm additional missing reports. In this review, I collected the references for not only coffee intake and its related diseases, but also its beneficial effects on health, and investigated the toxic effects on workers, focusing on occupational lung diseases in the coffee roasting process, such as obstructive bronchiolitis. Results and Conclusion With respect to respiratory health for diacetyl and 2,3-pentanedione, air exposure was assessed in coffee packaging and roasting processes, and alpha-diketones were the most exposed during bean processing in the production process. OSHA recommended regular monitoring of diacetyl in related processes, providing respiratory protection to workers, and active medical surveillance, including health screening for all workers.