The rise in pollution cases globally is expected to increase in line with industrialization.
Monitoring activities for pollutants have been hampered by the astronomical costs of
instrumental-based approach. This has resulted in the intense research on low cost
biomonitoring systems using enzymes, organisms including microorganisms. Only positive
samples are sent for instrumental analysis; dramatically cutting the cost of instrumental
analysis. This review attempts to outline and give due recognition to several selected bioassay
systems that have been tested for their applicability using polluted water samples as a routine
first line-of-defense. This includes small aquatic organisms-based assays, enzymes especially
proteases and bacterial-based systems using respiratory dye or luminescence systems as a
method for toxicant detection.
Many techniques have been applied to fabricate nanostructures via top-down approach such as electron beam lithography. However, most of the techniques are very complicated and involves many process steps, high cost operation as well as the use of hazardous chemicals. Meanwhile, atomic force microscopy (AFM) lithography is a simple technique which is considered maskless and involves only an average cost and less complexity. In AFM lithography, the movement of a probe tip can be controlled to create nanoscale patterns on sample surface. For silicon nanowire (SiNW) fabrication, a conductive tip was operated in non-contact AFM mode to grow nanoscale oxide patterns on silicon-on-insulator (SOI) wafer surface based on local anodic oxidation (LAO) mechanism. The patterned structure was etched through two steps of wet etching processes. First, the TMAH was used as the etchant solution for Si removing. In the second step, diluted HF was used to remove oxide mask in order to produce a completed SiNW based devices. A SiNW based device which is formed by a nanowire channel, source and drain pads with lateral gate structures can be fabricated by well controlling the lithography process (applied tip voltage and writing speed) as well as the etching processes.
Chemical industry is one of the important industries in the world. However, incidents happened due to the release of hazardous materials, toxic and poisonous chemicals in the chemical industries can cause fatal to human and destruction of the environment. Learning from the Bhopal disaster's experience, chemical industries have developed a program - Responsible Care, aiming to regain public trust through improving the environment, health and safety performances. Malaysia has adopted Responsible Care program since 1994 under the stewardship of the Chemical Industries Council of Malaysia (CICM). Six codes of management practices have been developed by the CICM, covering distribution, community awareness and emergency response, pollution prevention, process safety, employee health & safety and product stewardship. It has been more than 20 years since its inception. However, to date, there are only 125 companies have signed the pledge to adopt Responsible Care program. The CICM has also conducted several initiatives to encourage participation of chemical companies to adopt Responsible Care program in Malaysia. Therefore, it is the aim of this paper to review the current status of Responsible Care program in Malaysia and also deliberate the way forward of this program.
Water is a vital resource supporting a broad spectrum of ecosystems and human activities. The quality of river water has declined in recent years due to the discharge of hazardous materials and toxins. Deep learning and machine learning have gained significant attention for analysing time-series data. However, these methods often suffer from high complexity and significant forecasting errors, primarily due to non-linear datasets and hyperparameter settings. To address these challenges, we have developed an innovative HDTO-DeepAR approach for predicting water quality indicators. This proposed approach is compared with standalone algorithms, including DeepAR, BiLSTM, GRU and XGBoost, using performance metrics such as MAE, MSE, MAPE, and NSE. The NSE of the hybrid approach ranges between 0.8 to 0.96. Given the value's proximity to 1, the model appears to be efficient. The PICP values (ranging from 95% to 98%) indicate that the model is highly reliable in forecasting water quality indicators. Experimental results reveal a close resemblance between the model's predictions and actual values, providing valuable insights for predicting future trends. The comparative study shows that the suggested model surpasses all existing, well-known models.
Petroleum sludge is a hazardous waste that contains various organic compounds including polycyclic aromatic hydrocarbons (PAHs) which have carcinogenic-mutagenic and toxic characteristics. This study focuses on the thermal treatment (indirect heating) of petroleum sludge cake for PAH degradation at 250, 450, and 650 degrees C using Ca(OH)2 + NaHCO3 as an additive. The treatment was conducted in a rotary drum electric heater. All experiments were carried out in triplicate. Concentrations of the 16 priority PAHs in gas (absorbed on Amberlite XAD-4 adsorbent), particulate (on quartz filter) and residue phases were determined using gas chromatography-mass spectrometry (GC-MS). The samples were extracted with acetonitrile by ultra-sonication prior to GC-MS analysis. The use of additive was beneficial and a temperature of 450 degrees C was suitable for PAH degradation. Low levels of PAH emissions, particularly carcinogenic PAH and toxic equivalent concentration (sigma TEC), were observed in gas, particulate and residue phases after treatment.
Mefenamic acid (Mfe) is one of the most frequently detected nonsteroidal anti-inflammatory drugs in the environment. This study investigated the kinetics and the transformation by-products of Mfe during aqueous chlorination. The potential ecotoxicity of the transformation by-products was also evaluated. In the kinetic study, the second-order rate constant (kapp) for the reaction between Mfe and free available chlorine (FAC) was determined at 25 ± 0.1 °C. The result indicated that the degradation of Mfe by FAC is highly pH-dependent. When the pH was increased from 6 to 8, it was found that the kapp for the reaction between Mfe and FAC was decreased from 16.44 to 4.4 M(-1) s(-1). Characterization of the transformation by-products formed during the chlorination of Mfe was carried out using liquid chromatography-quadrupole time-of-flight accurate mass spectrometry. Four major transformation by-products were identified. These transformation by-products were mainly formed through hydroxylation, chlorination and oxidation reactions. Ecotoxicity assessment revealed that transformation by-products, particularly monohydroxylated Mfe which is more toxic than Mfe, can be formed during aqueous chlorination.
Cell death is a process of dying within biological cells that are ceasing to function. This process is essential in regulating organism development, tissue homeostasis, and to eliminate cells in the body that are irreparably damaged. In general, dysfunction in normal cellular death is tightly linked to cancer progression. Specifically, the up-regulation of pro-survival factors, including oncogenic factors and antiapoptotic signaling pathways, and the down-regulation of pro-apoptotic factors, including tumor suppressive factors, confers resistance to cell death in tumor cells, which supports the emergence of a fully immortalized cellular phenotype. This review considers the potential relevance of ubiquitous environmental chemical exposures that have been shown to disrupt key pathways and mechanisms associated with this sort of dysfunction. Specifically, bisphenol A, chlorothalonil, dibutyl phthalate, dichlorvos, lindane, linuron, methoxychlor and oxyfluorfen are discussed as prototypical chemical disruptors; as their effects relate to resistance to cell death, as constituents within environmental mixtures and as potential contributors to environmental carcinogenesis.
Genome instability is a prerequisite for the development of cancer. It occurs when genome maintenance systems fail to safeguard the genome's integrity, whether as a consequence of inherited defects or induced via exposure to environmental agents (chemicals, biological agents and radiation). Thus, genome instability can be defined as an enhanced tendency for the genome to acquire mutations; ranging from changes to the nucleotide sequence to chromosomal gain, rearrangements or loss. This review raises the hypothesis that in addition to known human carcinogens, exposure to low dose of other chemicals present in our modern society could contribute to carcinogenesis by indirectly affecting genome stability. The selected chemicals with their mechanisms of action proposed to indirectly contribute to genome instability are: heavy metals (DNA repair, epigenetic modification, DNA damage signaling, telomere length), acrylamide (DNA repair, chromosome segregation), bisphenol A (epigenetic modification, DNA damage signaling, mitochondrial function, chromosome segregation), benomyl (chromosome segregation), quinones (epigenetic modification) and nano-sized particles (epigenetic pathways, mitochondrial function, chromosome segregation, telomere length). The purpose of this review is to describe the crucial aspects of genome instability, to outline the ways in which environmental chemicals can affect this cancer hallmark and to identify candidate chemicals for further study. The overall aim is to make scientists aware of the increasing need to unravel the underlying mechanisms via which chemicals at low doses can induce genome instability and thus promote carcinogenesis.
One of the important 'hallmarks' of cancer is angiogenesis, which is the process of formation of new blood vessels that are necessary for tumor expansion, invasion and metastasis. Under normal physiological conditions, angiogenesis is well balanced and controlled by endogenous proangiogenic factors and antiangiogenic factors. However, factors produced by cancer cells, cancer stem cells and other cell types in the tumor stroma can disrupt the balance so that the tumor microenvironment favors tumor angiogenesis. These factors include vascular endothelial growth factor, endothelial tissue factor and other membrane bound receptors that mediate multiple intracellular signaling pathways that contribute to tumor angiogenesis. Though environmental exposures to certain chemicals have been found to initiate and promote tumor development, the role of these exposures (particularly to low doses of multiple substances), is largely unknown in relation to tumor angiogenesis. This review summarizes the evidence of the role of environmental chemical bioactivity and exposure in tumor angiogenesis and carcinogenesis. We identify a number of ubiquitous (prototypical) chemicals with disruptive potential that may warrant further investigation given their selectivity for high-throughput screening assay targets associated with proangiogenic pathways. We also consider the cross-hallmark relationships of a number of important angiogenic pathway targets with other cancer hallmarks and we make recommendations for future research. Understanding of the role of low-dose exposure of chemicals with disruptive potential could help us refine our approach to cancer risk assessment, and may ultimately aid in preventing cancer by reducing or eliminating exposures to synergistic mixtures of chemicals with carcinogenic potential.
Potentially carcinogenic compounds may cause cancer through direct DNA damage or through indirect cellular or physiological effects. To study possible carcinogens, the fields of endocrinology, genetics, epigenetics, medicine, environmental health, toxicology, pharmacology and oncology must be considered. Disruptive chemicals may also contribute to multiple stages of tumor development through effects on the tumor microenvironment. In turn, the tumor microenvironment consists of a complex interaction among blood vessels that feed the tumor, the extracellular matrix that provides structural and biochemical support, signaling molecules that send messages and soluble factors such as cytokines. The tumor microenvironment also consists of many host cellular effectors including multipotent stromal cells/mesenchymal stem cells, fibroblasts, endothelial cell precursors, antigen-presenting cells, lymphocytes and innate immune cells. Carcinogens can influence the tumor microenvironment through effects on epithelial cells, the most common origin of cancer, as well as on stromal cells, extracellular matrix components and immune cells. Here, we review how environmental exposures can perturb the tumor microenvironment. We suggest a role for disrupting chemicals such as nickel chloride, Bisphenol A, butyltins, methylmercury and paraquat as well as more traditional carcinogens, such as radiation, and pharmaceuticals, such as diabetes medications, in the disruption of the tumor microenvironment. Further studies interrogating the role of chemicals and their mixtures in dose-dependent effects on the tumor microenvironment could have important general mechanistic implications for the etiology and prevention of tumorigenesis.
As part of the Halifax Project, this review brings attention to the potential effects of environmental chemicals on important molecular and cellular regulators of the cancer hallmark of evading growth suppression. Specifically, we review the mechanisms by which cancer cells escape the growth-inhibitory signals of p53, retinoblastoma protein, transforming growth factor-beta, gap junctions and contact inhibition. We discuss the effects of selected environmental chemicals on these mechanisms of growth inhibition and cross-reference the effects of these chemicals in other classical cancer hallmarks.
The aim of this work is to review current knowledge relating the established cancer hallmark, sustained cell proliferation to the existence of chemicals present as low dose mixtures in the environment. Normal cell proliferation is under tight control, i.e. cells respond to a signal to proliferate, and although most cells continue to proliferate into adult life, the multiplication ceases once the stimulatory signal disappears or if the cells are exposed to growth inhibitory signals. Under such circumstances, normal cells remain quiescent until they are stimulated to resume further proliferation. In contrast, tumour cells are unable to halt proliferation, either when subjected to growth inhibitory signals or in the absence of growth stimulatory signals. Environmental chemicals with carcinogenic potential may cause sustained cell proliferation by interfering with some cell proliferation control mechanisms committing cells to an indefinite proliferative span.
Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology.
The present paper studies a predator-prey fishery model which incorporates the independent harvesting strategies and nonlinear impact of an anthropogenic toxicant. Both fish populations are harvested with different harvesting efforts, and the cases for the presence and non-presence of harvesting effort are discussed. The prey fish population is assumed to be infected by the toxicant directly which causes indirect infection to predator fish population through the feeding process. Each equilibrium of the proposed system is examined by analyzing the respective local stability properties. Dynamical behavior and bifurcations are studied with the assistance of threshold conditions influencing the persistence and extinction of both predator and prey. Bionomic equilibrium solutions for three possible cases are investigated with certain restrictions. Optimal harvesting policy is explored by utilizing the Pontryagin's Maximum Principle to optimize the profit while maintaining the sustainability of the marine ecosystem. Bifurcation analysis showed that the harvesting parameters are the key elements causing fishery extinction. Numerical simulations of bionomic and optimal equilibrium solutions showed that the presence of toxicant has a detrimental effect on the fish populations.
In Malaysia exposures in the workplace are regulated under the Factories and Machinery Act (FMA), 1967 and also under the more comprehensive Occupational Safety and Health Act (OSHA) enacted in 1994. With OSHA 1994 the philosophy of legislating safety and health in the workplace changed from one that was very prescriptive and containing detailed technical provisions under FMA, 1967 to one that is more flexible and encourages self-regulation under OSHA 1994. OSHA 1994 is supported by regulations, codes of practices and guidelines to further clarify the provisions in the Act. Under the FMA 1967 emphasis was on safety while with OSHA 1994 there has been equal emphasis on addressing health hazards in the workplace. Regulations for occupational exposures are developed by the Department of Occupational Safety and Health with tripartite and stakeholder consultation. When developing these regulations International Labor Organization Conventions, laws of other countries and occupational exposure standards adopted internationally are reviewed. The government also conducts surveys to collect information on both exposures and health effects in workplaces to have better understanding on specific occupational health problems. Effective law enforcement is crucial in ensuring compliance to safety and health law. The challenge at the moment is to ensure all employers and employees, particularly those in the small and medium enterprises, understand and comply with the provisions stipulated in the legislation.
Carcinogenesis is thought to be a multistep process, with clonal evolution playing a central role in the process. Clonal evolution involves the repeated 'selection and succession' of rare variant cells that acquire a growth advantage over the remaining cell population through the acquisition of 'driver mutations' enabling a selective advantage in a particular micro-environment. Clonal selection is the driving force behind tumorigenesis and possesses three basic requirements: (i) effective competitive proliferation of the variant clone when compared with its neighboring cells, (ii) acquisition of an indefinite capacity for self-renewal, and (iii) establishment of sufficiently high levels of genetic and epigenetic variability to permit the emergence of rare variants. However, several questions regarding the process of clonal evolution remain. Which cellular processes initiate carcinogenesis in the first place? To what extent are environmental carcinogens responsible for the initiation of clonal evolution? What are the roles of genotoxic and non-genotoxic carcinogens in carcinogenesis? What are the underlying mechanisms responsible for chemical carcinogen-induced cellular immortality? Here, we explore the possible mechanisms of cellular immortalization, the contribution of immortalization to tumorigenesis and the mechanisms by which chemical carcinogens may contribute to these processes.
Organophosphorus (OP) compounds are one of the most hazardous chemicals used as insecticides/pesticide in agricultural practices. A large variety of OP compounds are hydrolyzed by organophosphorus hydrolases (OPH; EC 3.1.8.1). Therefore, OPHs are among the most suitable candidates which could be used in designing enzyme-based sensors for detecting OP compounds. In the present work, a novel nanobiosensor for the detection of paraoxon was designed and fabricated. More specifically, OPH was covalently embedded onto chitosan and the enzyme-chitosan bioconjugate was then immobilized on negatively charged gold nanoparticles (AuNPs) electrostatically. The enzyme was immobilized on AuNPs without chitosan as well to compare the two systems in terms of detection limit and enzyme stability under different pH and temperature conditions. Coumarin 1, a competitive inhibitor of the enzyme, was used as a fluorogenic probe. The emission of coumarin 1 was effectively quenched by the immobilized Au-NPs when bound to the developed nanobioconjugates. However, in the presence of paraoxon, coumarin 1 left the nanobioconjugate leading to enhanced fluorescence intensity. Moreover, compared to the immobilized enzyme without chitosan, the chitosan-immobilized enzyme was found to possess decreased Km value by over 50%, increased Vmax and Kcat values by around 15% and 74%, respectively. Higher stability within a wider range of pH (2-12) and temperature (25-90°C) was also achieved. The method worked in the 0 to 1050 nM concentration ranges, and had a detection limit as low as 5 × 10(-11) M.
The Department of Occupational Safety and Health Malaysia (DOSH) is the authority responsible to safeguard the occupational safety, health and welfare of workers in Malaysia. Occupational noise-related hearing disorders are the leading type of occupational diseases recorded by DOSH every year. Occupational Health Doctor (OHD) is a competency recognized by DOSH and their scope of duties in industries is currently confined to conduct medical surveillance for workers with hazardous chemical exposure and confined space medical fitness examination. The duties of OHD are good to be expanded by empowering more of their roles in industrial activities involving other legislations under DOSH. The noise exposure regulation under the Factories and Machinery Act (FMA) 1967 has been governing the worker’s exposure to hazardous industrial noise and preventing noise-induced hearing loss (NIHL) since 1989. However, the provisions of the regulation need to be strengthened in some essential medical elements of the Hearing Conservation Programme (HCP) for a comprehensive prevention of NIHL at the workplace. Recently enacted Occupational Safety and Health (Noise Exposure) Regulations 2019 offer a wider coverage of workers in ten sectors of industries applicable under the Occupational Safety and Health Act (OSHA) 1994. The current regulatory requirements for management of workplace noise have many improvements compared to the existing law. Enhancement in the medical requirements of industrial audiometry is made prominent by involving OHDs to interpret audiograms and conduct medical examination for workers. The reporting of occupational noise-related hearing disorders to DOSH is outlined better in the new regulation. The occurrence of NIHL and other related hearing disorders are expected to reduce eventually after the introduction of Occupational Safety and Health (Noise Exposure) Regulations 2019. The OHDs will play a pivotal role in industrial audiometry and prevention of hearing disorders among the working population.