Toxic Environmental Pollutants Research Articles

Betaine-Modified Green Carbon Dot for Cr(VI) Sensing, in Vivo Cr(VI) Imaging, and Growth Promotion in the Rice Plant.

Hexavalent chromium is a toxic environmental pollutant that damages plants due to disruption of nutrient uptake, photosynthesis metabolism, and oxidative stress, which suppresses the growth and development of the plant. In this work, we have developed a betaine-modified carbon dot (BT@CD) sensor for monitoring Cr(VI) in water and plants. Fluorescent carbon dots have been synthesized using jamun juice (Syzygium cumini) as the carbon source subjected to surface modification with betaine (BT@JCD). This BT@JCD exhibits strong blue fluorescence, which significantly decreases in the presence of Cr(VI) due to the inner filter effect in a range of 5-450 nM with a detection limit of 0.033 μM. Due to its easy translocation in the vascular bundles, these fluorescence nanosensors can be applied to detect Cr(VI) in rice plants Oryza sativa) through fluorescence confocal imaging. The treatment of rice plants with BT@JCDs in the concentration range of 0.2 to 1g/mL not only triggered photophysical parameters such as carbohydrates, chlorophyll, and carotenoids but also enhanced the antioxidant enzyme activity promoting plant growth.

Sodium selenite antagonizes trimethyl tin-induced chicken hepatotoxic hepatitis through the RNS/NF-κB/NLRP3 pathway

Trimethyl tin (TMT) is a good stabilizer for plastic products but is also a toxic environmental pollutant. Selenium has good antioxidant and anti-inflammatory properties and has been widely used in the poultry industry. However, it has not been reported whether selenium enrichment can antagonize TMT-induced viral hepatitis in poultry. To fill this gap, AA broiler models exposed to TMT for 42 d were established and fed a Se-enriched diet at the same time. H&E staining showed that selenium could significantly alleviate TMT-induced liver inflammation. Further analysis of the underlying mechanism revealed that TMT induced nitrosation stress (RNS), increased NO content and iNOS expression, which in turn activated the NF-κB/NLRP3 pathway and induced pyroptosis. However, selenium enrichment can reverse this situation, that is, reduce the occurrence of RNS, reduce the degree of pyroptosis, and thus alleviate the occurrence of inflammation. In our study, we demonstrated for the first time that TMT could induce hepatotoxicity other than neurotoxicity in poultry and that selenium could antagonize TMT-induced hepatotoxic hepatitis in chickens through the RNS/NF-κB/NLRP3 pathway.

Development of a TBXT-EGFP iPS cell model for screening the early developmental toxicity of typical environmental pollutants

In our daily lives, we are inevitably exposed to a variety of environmental pollutants in numerous ways. Fortunately, recent years have witnessed significant advancements in the field of stem cell toxicology, which have provided new opportunities for research in environmental toxicology. Applying stem cell technology to environmental toxicology, overcomes some of the limitations of traditional screening methods and we can more accurately predict the toxicity of environmental pollutants. However, there are still several aspects of stem cell toxicology models that require improvement, such as increasing the throughput of detection and simplifying detection methods. Consequently, we developed an environmental pollutant toxicity detection model based on TBXT-EGFP iPS cells and screened the developmental toxicity of 38 typical environmental pollutants. Our results indicate that TBBPA-BDBPE, TBBPA-BHEE, DG, and AO2246 may interfere with the expression of TBXT, a critical marker gene for early human embryo development, implying that these environmental pollutants could lead to developmental abnormalities.

Unveiling the positive impacts of the genus Rhodococcus on plant and environmental health

Organic farming has emerged as a sustainable solution to the adverse effects (diminished nutritional value, compromised food quality, environmental contamination, and public health hazards) that are usually associated with harmful chemical pesticides. To overcome such loss, one must explore the plant-associated microbes that are the naturally occurring root commensal and could positively improve crop health. In this review, we highlight the importance of the bacterial genus Rhodococcus, a subset of Actinobacteria that carries immense potential in enhancing crop yield and is associated with bioremediation of toxic pesticides and other chemicals to improve soil health. However, it has been noticed that few species of Rhodococcus are pathogenic for the plant (R. fascians) as well as humans/animals (R. equi). But still, the majority of Rhodococcus isolates are found to be non-pathogenic and carry substantial beneficial traits. Here, we have attempted to comprise those beneficial traits of the different members of the genus Rhodococcus. The main emphasis of this review article is to explore the major areas such as enzyme production, phytohormone synthesis, growth regulation, siderophore production, bioremediation, organic compound degradation, and environmental pollution control. Opinions towards the applications of advanced methodologies for utilizing the cumulative prospective potential of the genus Rhodococcus have also been discussed in the different sections of the review. Conclusively, this article gathers the scattered information from the past and recent literature about this bacteria and provides the future direction about how it can improve plant/soil health and eliminate toxic chemicals and environmental pollutants.

Stage‐by‐stage exploration of normal embryonic development in the Arabian killifish, Aphanius dispar

AbstractBackgroundArabian killifish, Aphanius dispar, lives in marine coastal areas of the Middle East, as well as in streams that experience a wide range of salinities and temperatures. It has been used as a mosquito control agent and for studying the toxicities of environmental pollutants. A. dispar's eggshell (chorion) and embryos are highly transparent and are suitable for high resolution microscopic observations, offering excellent visibility of live tissues.ResultsIn this study, the staging of normal embryonic development of A. dispar was described and investigated at different temperatures. Embryonic development was then examined under different thermal environments from 26 to 34°C. Our data suggest that temperature has a significant effect on embryonic development, with accelerated development at higher temperatures.ConclusionA. dispar exhibits broad thermal tolerance and extended independent feeding capabilities, making it a promising model organism for toxicology and pathogenesis studies conducted over an extended period of time (12 days post‐fertilization).

Bioremediation of Polycyclic Aromatic Hydrocarbons by Means of Bacteria and Bacterial Enzymes.

Polycyclic aromatic hydrocarbons (PAHs) are widespread, persistent, and toxic environmental pollutants. Many anthropogenic and some natural factors contribute to the spread and accumulation of PAHs in aquatic and soil systems. The effective and environmentally friendly remediation of these chemical compounds is an important and challenging problem that has kept scientists busy over the last few decades. This review briefly summarizes data on the main sources of PAHs, their toxicity to living organisms, and physical and chemical approaches to the remediation of PAHs. The basic idea behind existing approaches to the bioremediation of PAHs is outlined with an emphasis on a detailed description of the use of bacterial strains as individual isolates, consortia, or cell-free enzymatic agents.

Subchronic Chloroform Exposure Causes Intestinal Damage and Induces Gut Microbiota Disruption and Metabolic Dysregulation in Mice.

Chloroform is a prevalent toxic environmental pollutant in urban settings, posing risks to human health through exposure via various mediums such as air and tap water. The gut microbiota plays a pivotal role in maintaining host health. However, there is a paucity of research elucidating the impact of chloroform exposure on the gut microbiota. In this investigation, 18 SPF Kunming female mice were stratified into three groups (n = 6) and subjected to oral gavage with chloroform doses equivalent to 0, 50, and 150 mg/kg of body weight over 30 days. Our findings demonstrate that subchronic chloroform exposure significantly perturbs hematological parameters in mice and induces histopathological alterations in cecal tissues, consequently engendering marked disparities in the functional composition of cecal microbiota and metabolic equilibrium of cecal contents. Ultimately, our investigation revealed a statistically robust correlation, exhibiting a high degree of significance, between the intestinal microbiome composition and the metabolites that were differentially expressed consequent to chloroform exposure.

Circadian control of polycyclic aromatic hydrocarbon-induced dysregulation of endothelial tight junctions and mitochondrial bioenergetics

The study evaluates the impact of environmental toxicants, such as polycyclic aromatic hydrocarbons (PAHs), on circadian regulations and functions of brain endothelial cells, which form the main structural element of the blood-brain barrier (BBB). PAH are lipophilic and highly toxic environmental pollutants that accumulate in human and animal tissues. Environmental factors related to climate change, such as an increase in frequency and intensity of wildfires or enhanced strength of hurricanes or tropical cyclones, may lead to redistribution of these toxicants and enhanced human exposure. These natural disasters are also associated with disruption of circadian rhythms in affected populations, linking increased exposure to environmental toxicants to alterations of circadian rhythm pathways. Several vital physiological processes are coordinated by circadian rhythms, and disruption of the circadian clock can contribute to the development of several diseases. The blood-brain barrier (BBB) is crucial for protecting the brain from blood-borne harmful substances, and its integrity is influenced by circadian rhythms. Exposure of brain endothelial cells to a human and environmentally-relevant PAH mixture resulted in dose-dependent alterations of expression of critical circadian modulators, such as Clock, Bmal1, Cry1/2, and Per1/2. Moreover, silencing of the circadian Clock gene potentiated the impact of PAHs on the expression of the main tight junction genes and proteins (namely, claudin-5, occludin, JAM-2, and ZO-2), as well as mitochondrial bioenergetics. Findings from this study contribute to a better understanding of pathological influence of PAH-induced health effects, especially those related to circadian rhythm disruption.

Particulate matter 2.5 accelerates aging: Exploring cellular senescence and age-related diseases

Exposure to Particulate matter 2.5 (PM2.5) accelerates aging, causing declines in tissue and organ function, and leading to diseases such as cardiovascular, neurodegenerative, and musculoskeletal disorders. PM2.5 is a major environmental pollutant and an exogenous pathogen in air pollution that is now recognized as an accelerator of human aging and a predisposing factor for several age-related diseases. In this paper, we seek to elucidate the mechanisms by which PM2.5 induces cellular senescence, such as genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, and mitochondrial dysfunction, and age-related diseases. Our goal is to increase awareness among researchers within the field of the toxicity of environmental pollutants and to advocate for personal and public health initiatives to curb their production and enhance population protection. Through these endeavors, we aim to promote longevity and health in older adults.

Enhancement of Biodegradation and Detoxification of Methylene Blue by Preformed Biofilm of Thermophilic Bacilli on Polypropylene Perforated Balls

Microbial degradation represents an eco-friendly alternative to traditional physicochemical treatments in removing persistent and toxic environmental pollutants, including synthetic dyes (i.e., methylene blue, MB) employed in different industries. The exploitation of thermophilic bacilli, such as those isolated from the shallow hydrothermal vents of the Eolian Islands (Italy), could provide valuable resources for the treatment of warm, dye-containing wastewater. In this study, we evaluated the ability of preformed biofilms on polypropylene perforated balls (BBs) of fifteen thermophilic bacilli, to decolor, degrade, and detoxify MB in aqueous solutions. Among them, BBs of Bacillus licheniformis B3-15 and Bacillus sp. s7s-1 were able to decolorize MB more than 50% in saline solution (NaCl 2%), incubated in static conditions at 45 °C for 48 h. At optimized initial conditions (10 mg L−1 MB, pH 5.2 for B3-15 or pH 4 for s7s-1), the two strains enhanced their decolorization potential, reaching 96% and 67%, respectively. As indicated by ATR-FTIR spectroscopy, the treatment with BB B3-15 was the most efficient in degrading the Cl–C and –NH groups of MB. This degraded solution was 40% less toxic than undegraded MB, and it has no impact on the bioluminescence of Vibrio harveyi, nor the growth of the marine diatom Phaeodactylum tricornutum. Biofilm formed by strain B3-15 on polypropylene perforated balls could be proposed as a component of bioreactors in the treatment of warm, dye-containing wastewater to concomitantly remediate MB pollution and simultaneously counteract harmful effects in aquatic environments.

Microscopic photoplethysmography-based evaluation of cardiotoxicity in whitefish larvae induced by acute exposure to cadmium and phenol.

Toxic environmental pollutants pose a health risk for both humans and animals. Accumulation of industrial contaminants in freshwater fish may become a significant threat to biodiversity. Comprehensive monitoring of the impact of environmental stressors on fish functional systems is important and use of non-invasive tools that can detect the presence of these toxicants in vivo is desirable. The blood circulatory system, by virtue of its sensitivity to the external stimuli, could be an informative indicator of chemical exposure. In this study, microscopic photoplethysmography-based approach was used to investigate the cardiac activity in broad whitefish larvae (Coregonus nasus) under acute exposure to cadmium and phenol. We identified contamination-induced abnormalities in the rhythms of the ventricle and atrium. Our results allow introducing additional endpoints to evaluate the cardiac dysfunction in fish larvae and contribute to the non-invasive evaluation of the toxic effects of industrial pollutants on bioaccumulation and aquatic life.

السموم البيئية وتأثيراتها على الأعضاء: مراجعة شاملة لتعرض الإنسان وتراكمها

Environmental pollutants lead to problems in ecosystems differently depending on the extent of their toxicity, and thus their arrival to humans leads to health problems at different levels. The danger of any substance introduced into the environment can be determined depending on its quantity (dose). In addition, based on the overdose, it can be considered (whether it is alien or original) is toxic. Poisoning is the harmful effect that occurs as a result of ingestion, inhalation, or contact with a toxic substance. Potential toxic substances include chemical, biological, and physical toxins, fungi, plants, and animal toxins. Environmental pollutants are heavy metals (lead, cadmium, mercury, etc.), pesticides, organic materials, food additives, etc. The severity of the toxic effect depends primarily on the concentration and persistence of the final toxic substance. The final toxic substance is often the original chemical to which the organism is exposed. In other cases, the final toxic substance is a metabolite of the original compound, reactive oxygen species, or nitrogen (ROS, RNS) generated during Transformation into a toxic substance. Exposure to lead can affect proteins that interfere with their enzymatic functions or ability to bind other cellular components, leading to DNA damage and induction of oxidative stress. Asbestos can also damage DNA and affect gene expression. Exposure to acrolein irritates the bronchi, while mercury causes neurological symptoms. This review deals with understanding toxic environmental pollutants that affect humans, the extent of accumulation of toxic substances in organs, and methods of exposure to them.

MERCURY EXPOSURE AND HUMAN REPRODUCTIVE HEALTH (LITERATURE REVIEW)

Mercury (Hg), a highly toxic environmental pollutant, which hazards for human health, including to reproductive system, fertility and pregnancy outcome. Research has shown that Hg could induce impairments in the reproductive function due to cellular deformation of the Leydig cells and the seminiferous tubules, testicular degeneration and degenerative atresia of primordial and primary follicles as well as diminishes the steroidogenesis and synthesis of sex hormones. Some studies investigated miscarriage, spontaneous abortions, stillbirth, and low birth weight due to occupational Hg exposure. This review evaluates the hypothesis that exposure to Hg may. This review evaluates the hypothesis that chronic exposure to mercury can increase the risk of reduced fertility, spontaneous abortion and congenital deficits or abnormalities.

Transcriptome-wide m6A methylation profile reveals tissue specific regulatory networks in switchgrass (Panicum virgatum L.) under cadmium stress

The heavy metal cadmium (Cd), known for its high toxicity, poses a grave threat to human health through the food chain. N6-methyladenosine (m6A), the most abundant internal modification, regulates plant adaptation to various adversities, yet the panorama of m6A modifications in switchgrass under cadmium stress remains elusive. This study examines the physiological responses of switchgrass roots and shoots exposed to 50 μM CdCl2, alongside an overview of transcriptome-wide m6A methylation patterns. After cadmium treatment, methylation modifications are primarily enriched near stop codons and the 3′UTR region, with a negative correlation between m6A modification and gene expression levels. In shoots, approximately 58 % of DEGs with m6A modifications show upregulation in expression and decrease in m6A peaks, including zinc transporter 4-like (ZIP4). In roots, about 43 % of DEGs with m6A modifications exhibit downregulation in expression and increase in m6A peaks, such as the ABC transporter family member (ABCG25). We further validate the m6A enrichment, gene expression and mRNA stability of ZIP4 in response to Cd treatment. The results suggest that the negative correlation of m6A enrichment and gene expression is due to altered mRNA stability. Our study establishes an m6A regulatory network governing cadmium transport in switchgrass roots and shoots, offering new avenues for candidate gene manipulation in phytoremediation applications of heavy metal pollution.

Melatonin prevents cadmium-induced osteoporosis by affecting the osteoblast and osteoclast differentiation and pyroptosis in duck

Cadmium (Cd), is a highly toxic environmental pollutant, which seriously threatens the health of poultry and humans. The occurrence of osteoporosis is the main manifestation of cadmium toxicity. Pyroptosis plays an important role in the development of osteoporosis. Melatonin has been shown to affect preserving bone health. However, the underlying mechanism has not been elucidated. In the present study, these functions of melatonin have been investigated in duck bone tissue and osteoblast during cadmium exposure. In vivo, the studies suggest that melatonin protects against cadmium-induced duck osteoporosis by improving the osteogenesis function, inhibiting bone resorption, and suppressing the occurrence of pyroptosis. In vitro, the findings demonstrated that melatonin alleviated the inhibition effect of cadmium on duck bone marrow-derived mesenchymal stem cells (BMSC) osteogenic differentiation, and suppressed the cadmium-induced osteoclast differentiation. In addition, we also found that melatonin prevents cytokines release of lactate dehydrogenase (LDH), interleukin-18 (IL-18), and interleukin-1β (IL-1β) by cadmium-induced, and reduces the expression of n-terminal Gasdermin D (N-GSDMD), alleviates the osteoblast death rate. In short, melatonin as a potential therapeutic agent has bright prospects in cadmium-induced bone toxicity.

The Effect of Two Siderophore-Producing Bacillus Strains on the Growth Promotion of Perennial Ryegrass under Cadmium Stress.

Cadmium (Cd) is a highly toxic and cumulative environmental pollutant. Siderophores are heavy metal chelators with high affinity to heavy metals, such as Cd. Ryegrass (Lolium perenne L.) has a potential remediation capacity for soils contaminated by heavy metals. Consequently, using ryegrass alongside beneficial soil microorganisms that produce siderophores may be an effective means to remediate soils contaminated with Cd. In this study, the Bacillus strains WL1210 and CD303, which were previously isolated from the rhizospheres of Nitraria tangutorum in Wulan and Peganum harmala L. in Dachaidan, Qinghai, China, respectively, both arid and sandy environments, were evaluated for heavy metal pollution mitigation. Our quantitative analyses have discerned that the two bacterial strains possess commendable attributes of phosphorus (P) solubilization and potassium (K) dissolution, coupled with the capacity to produce phytohormones. To assess the heavy metal stress resilience of these strains, they were subjected to a cadmium concentration gradient, revealing their incremental growth despite cadmium presence, indicative of a pronounced tolerance threshold. The subsequent phylogenetic analysis, bolstered by robust genomic data from conserved housekeeping genes, including 16S rDNA, gyr B gene sequencing, as well as dnaK and recA, delineated a species-level phylogenetic tree, thereby confirming the strains as Bacillus atrophaeus. Additionally, we identified the types of iron-carrier-producing strains as catechol (WL1210) and carboxylic acid ferrophilin (CD303). A genomic analysis uncovered functional genes in strain CD303 associated with plant growth and iron carrier biosynthesis, such as fnr and iscA. Ryegrass seed germination assays, alongside morphological and physiological evaluations under diverse heavy metal stress, underscored the strains' potential to enhance ryegrass growth under high cadmium stress when treated with bacterial suspensions. This insight probes the strains' utility in leveraging alpine microbial resources and promoting ryegrass proliferation.

Molecular mechanisms of environmental pollutant-induced cartilage damage: from developmental disorders to osteoarthritis.

The objective of the present study was to review the molecular mechanisms of the adverse effects of environmental pollutants on chondrocytes and extracellular matrix (ECM). Existing data demonstrate that both heavy metals, including cadmium (Cd), lead (Pb), and arsenic (As), as well as organic pollutants, including polychlorinated dioxins and furans (PCDD/Fs) and polychlorinated biphenyls (PCB), bisphenol A, phthalates, polycyclic aromatic hydrocarbons (PAH), pesticides, and certain other organic pollutants that target cartilage ontogeny and functioning. Overall, environmental pollutants reduce chondrocyte viability through the induction apoptosis, senescence, and inflammatory response, resulting in cell death and impaired ECM production. The effects of organic pollutants on chondrocyte development and viability were shown to be mediated by binding to the aryl hydrocarbon receptor (AhR) signaling and modulation of non-coding RNA expression. Adverse effects of pollutant exposures were observed in articular and growth plate chondrocytes. These mechanisms also damage chondrocyte precursors and subsequently hinder cartilage development. In addition, pollutant exposure was shown to impair chondrogenesis by inhibiting the expression of Sox9 and other regulators. Along with altered Runx2 signaling, these effects also contribute to impaired chondrocyte hypertrophy and chondrocyte-to-osteoblast trans-differentiation, resulting in altered endochondral ossification. Several organic pollutants including PCDD/Fs, PCBs and PAHs, were shown to induce transgenerational adverse effects on cartilage development and the resulting skeletal deformities. Despite of epidemiological evidence linking human environmental pollutant exposure to osteoarthritis or other cartilage pathologies, the data on the molecular mechanisms of adverse effects of environmental pollutant exposure on cartilage tissue were obtained from studies in laboratory rodents, fish, or cell cultures and should be carefully extrapolated to humans, although they clearly demonstrate that cartilage should be considered a putative target for environmental pollutant toxicity.

Benzo[a]pyrene evokes epithelial-mesenchymal transition and pulmonary fibrosis through AhR-mediated Nrf2-p62 signaling

Benzo[a]pyrene (BaP) and its metabolic end product benzo(a)pyren-7,8-dihydrodiol-9,10-epoxide (BPDE), are known toxic environmental pollutants. This study aimed to analyze whether sub-chronic BPDE exposure initiated pulmonary fibrosis and the potential mechanisms. In this work, male C57BL6/J mice were exposed to BPDE by dynamic inhalation exposure for 8 weeks. Our results indicated that sub-chronic BPDE exposure evoked pulmonary fibrosis and epithelial-mesenchymal transition (EMT) in mice. Both in vivo and in vitro, BPDE exposure promoted nuclear translocation of Snail. Further experiments indicated that nuclear factor erythroid 2-related factor 2 (Nrf2) and p62 were upregulated in BPDE-exposed alveolar epithelial cells. Moreover, Nrf2 siRNA transfection evidently attenuated BPDE-induced p62 upregulation. Besides, p62 shRNA inhibited BPDE-incurred Snail nuclear translocation and EMT. Mechanically, BPDE facilitated physical interaction between p62 and Snail in the nucleus, then repressed Snail protein degradation by p62-dependent autophagy-lysosome pathway, and finally upregulated transcriptional activity of Snail. Additionally, aryl hydrocarbon receptor (AhR) was activated in BPDE-treated alveolar epithelial cells. Dual-luciferase assay indicated activating AhR could bind to Nrf2 gene promoter. Moreover, pretreatment with CH223191 or α-naphthoflavone (α-NF), AhR antagonists, inhibited BPDE-activated Nrf2-p62 signaling, and alleviated BPDE-induced EMT and pulmonary fibrosis in mice. Taken together, AhR-mediated Nrf2-p62 signaling contributes to BaP-induced EMT and pulmonary fibrosis.

Long-term tributyltin exposure alters behavior, oocyte maturation, and histomorphology of the ovary due to oxidative stress in adult zebrafish

Tributyltin (TBT), an organotin endocrine-disrupting substance, is recognized as one of the important toxic environmental pollutants. The present study was carried out to investigate the toxic effects of TBT on behavior and the ovary of adult zebrafish with a focus on oxidative stress markers and oocyte maturation. Adult zebrafish were exposed to three different concentrations (125, 250, and 500 ng/L of water) of TBT for 28 days. TBT exposure produced a concentration-dependent negative effect on the body weight and behavior (anxiety-like symptoms) of adult zebrafish. Alterations in the activity of superoxide dismutase (SOD) and catalase (CAT), the total antioxidant capacity of ovarian tissue by the highest exposure level of TBT resulted in lipid peroxidation as indicated by increased malondialdehyde (MDA) level. The numbers of early-vitellogenic oocytes were significantly increased in zebrafish exposed to TBT as low as 125 ng/L. However, the numbers and size of fully-grown (mature) oocytes were significantly reduced in the highest exposure group only. Correlation between the MDA level and pre-vitellogenic oocytes in the 500 ng/L group indicated that lipid peroxidation prevented the maturation of pre-vitellogenic oocytes. TBT exposure produced significant histological changes in the ovary as evidenced by disturbed maturation of oocytes. In conclusion, TBT adversely affected the maturation of oocytes in zebrafish ovary through oxidative stress-mediated mechanisms.

Chemical health hazards and toxicity of environmental pollutants on humans, animals and others: An overview

Toxicology, rooted in ancient civilizations and evolving through pivotal historical figures like Paracelsus and Alice Hamilton, has become a multidisciplinary field encompassing various branches such as pharmacology, medical, forensic, and environmental toxicology. This exploration embarks on a journey through time and science, unravelling the intricate interplay between chemicals, pollutants, and their profound impacts on human, animal, and environmental well-being. Spanning from ancient practices like the use of hemlock in Greek capital punishment to modern-day concerns surrounding industrial chemicals and pesticides, the review delves into the mechanisms by which toxins disrupt biochemical pathways and induce organ dysfunctions. From heavy metals and pesticides persistent effects on the nervous and reproductive systems to the carcinogenic properties of polychlorinated biphenyls (PCBs), hydrocarbons, polycyclic aromatic hydrocarbons (PAHs), and volatile organic compounds (VOCs). The review highlights the diverse range of toxicants and their widespread impact on human health. Additionally, the review underscores the importance of proactive measures to mitigate exposure to harmful substances, advocating for the development of antidotes, bioremediation techniques, and stricter environmental regulations. By addressing the urgent need for comprehensive strategies to combat toxicological hazards, this review aims to contribute to ongoing efforts to safeguard public health and environmental sustainability in the face of evolving chemical threats.