Toxics

Cement production exerts a significant negative impact on the environment through the emission of greenhouse gases, particulate matter (PM), heavy metals, and other toxic substances into the atmosphere, soil, and bodies of water, degrading the environment and affecting the population’s health. This study reviews different solutions to reduce pollution and mitigate its effects. Particular attention is given to Carbon Capture, Utilization, and Storage (CCUS) technologies and their ability to significantly reduce CO₂. Biomass and waste-derived fuels were identified as viable substitutes for fossil fuels, although challenges related to supply chain reliability and secondary environmental impacts remain. The study further examined mitigation strategies for non-gaseous pollutants, including noise pollution control measures such as sound barriers and vibration isolation systems, soil remediation techniques such as phytoremediation and the recycling of cement kiln dust (CKD), and water pollution control technologies, including filtration, chemical precipitation, biological treatment, and Zero Liquid Discharge (ZLD) systems. Key research gaps were identified, particularly concerning the long-term durability, scalability, and cost-effectiveness of these mitigation approaches. Overall, the review emphasizes the need for integrated pollution control strategies to support the transition toward a more sustainable cement industry and recommends future research focused on developing mitigation technologies that are efficient, economically viable, and adaptable to large-scale industrial applications.

Procambarus clarkii (red swamp crayfish) exhibits physiological plasticity that enables adaptation to variable freshwater conditions, such as those in Lake Trasimeno. This study examined whether fluctuations in hydrometric level and associated physicochemical parameters affect oxidative stress responses in the hepatopancreas and abdominal muscle of male and female individuals. Superoxide dismutase, catalase, glutathione peroxidase, and metallothionein reveal tissue, sex, and season-specific differences that indicate adaptive physiological adjustments. Temporal trends were evaluated, and multivariate analyses summarised environmental and metal gradients. Generalised Additive Models (GAMs) were used to explore relationships between oxidative responses and these gradients, with sex as a categorical factor. Associations were identified with hydrometric level, temperature, conductivity, transparency, pH, dissolved oxygen, and metals of biological relevance. These results highlight the remarkable physiological plasticity of P. clarkii, which underpins its success as an invasive species in fluctuating freshwater ecosystems.

As a typical halogenated hydrocarbon environmental pollutant, 1,2-dichloroethane (1,2-DCE) exhibits clinically confirmed hepatotoxicity with incompletely understood mechanisms. This study integrated network toxicology, molecular docking, and in vitro experiments to investigate necroptosis in 1,2-DCE-induced liver injury. Computational analysis predicted involvement of the aryl hydrocarbon receptor (AHR)/cytochrome P450 1A1 (CYP1A1) pathway, and molecular docking suggested potential binding between 1,2-DCE and AHR (−6.5 kcal/mol). CCK-8 assays showed that 1,2-DCE reduced THLE-2 hepatocyte viability in a concentration-dependent manner. Notably, 1,2-DCE triggered rapid AHR nuclear translocation within 1 h and transiently upregulated CYP1A1 at both the transcriptional and protein levels (3–6 h). Further studies revealed elevated intracellular reactive oxygen species (ROS) at 24 h. After 48 h exposure, CYP1A1 expression was significantly suppressed, accompanied by activation of necroptosis markers, including increased lactate dehydrogenase (LDH) release, enhanced propidium iodide (PI) staining, and elevated phosphorylation of receptor-interacting protein kinase 3 (RIPK3) and mixed lineage kinase domain-like protein (MLKL). These findings reveal a dual-phase mechanism: an early adaptive stress response via the AHR-CYP1A1 axis, followed by pathway dysfunction and transition to necroptosis, suggesting AHR as a potential target for intervening in 1,2-DCE-induced hepatotoxicity.