Soil and water pollution represent significant threats to global health, ecosystems, and biodiversity. Healthy soils underpin terrestrial ecosystems, supporting food production, biodiversity, water retention, and carbon sequestration. However, soil degradation jeopardizes the health of 3.2 billion people, while over 2 billion live in waterstressed regions. Pollution of soil, air, and water is a leading environmental cause of disease, contributing to over 9 million premature deaths annually. Soil contamination stems from heavy metals, synthetic chemicals, pesticides, and plastics, driven by industrial activity, agriculture, and waste mismanagement. These pollutants induce oxidative stress, inflammation, and hormonal disruption, significantly increasing risks for non-communicable diseases (NCDs) such as cardiovascular disease (CVD). Emerging contaminants like micro- and nanoplastics amplify health risks through cellular damage, oxidative stress, and cardiovascular dysfunction. Urbanization and climate change exacerbate soil degradation through deforestation, overfertilization, and pollution, further threatening ecosystem sustainability and human health. Mitigation efforts, such as reducing chemical exposure, adopting sustainable land-use practices, and advancing urban planning, have shown promise in lowering pollution-related health impacts. Public health initiatives, stricter pollution controls, and lifestyle interventions, including antioxidant-rich diets, can also mitigate risks. Pollution remains preventable, as demonstrated by high-income nations implementing cost-effective solutions. Policies like the European Commission's Zero-Pollution Vision aim to reduce pollution to safe levels by 2050, promoting sustainable ecosystems and public health. Addressing soil pollution is critical to combating the global burden of NCDs, particularly CVDs, and fostering a healthier environment for future generations.

Mercury is a significant environmental pollutant and public health threat, primarily recognized for its neurotoxic effects. Increasing evidence also highlights its harmful impact on the cardiovascular system, particularly in adults. Exposure to mercury through contaminated soil, air, or water initiates a cascade of pathological events that lead to organ damage, including platelet activation, oxidative stress, enhanced inflammation, and direct injury to critical cells such as cardiomyocytes and endothelial cells. Endothelial activation triggers the upregulation of adhesion molecules, promoting the recruitment of leukocytes and platelets to vascular sites. These interactions activate both platelets and immune cells, creating a pro-inflammatory, prothrombotic environment. A key outcome is the formation of platelet-leukocyte aggregates (PLAs), which exacerbate thromboinflammation and endothelial dysfunction. These processes significantly elevate cardiovascular risks, including thrombosis and vascular inflammation. This study offers a comprehensive analysis of the mechanisms underlying mercury-induced cardiotoxicity, focusing on oxidative stress, inflammation, and cellular dysfunction. [GRAPHICS] .

Cardiovascular disease is a significant cause of morbidity and mortality among non-communicable diseases worldwide. Evidence shows that a healthy dietary pattern positively influences many risk factors of cardiometabolic health, stroke, and heart disease, supported by the effectiveness of healthy diet and lifestyles for the prevention of CVD. High quality and safety of foods are prerequisites to ensuring food security and beneficial effects. Contaminants can be present in foods mainly because of contamination from environmental sources (water, air, or soil pollution), or artificially introduced by the human. Moreover, the cross-contamination or formation during food processing, food packaging, presence or contamination by natural toxins, or use of unapproved food additives and adulterants. Numerous studies reported the association between food contaminants and cardiovascular risk by demonstrating that (1) the cross-contamination or artificial sweeteners, additives, and adulterants in food processing can be the cause of the risk for major adverse cardiovascular events and (2) environmental factors, such as heavy metals and chemical products can be also significant contributors to food contamination with a negative impact on cardiovascular systems. Furthermore, oxidative stress can be a common mechanism that mediates food contamination-associated CVDs as substantiated by studies showing impaired oxidative stress biomarkers after exposure to food contaminants.This narrative review summarizes the data suggesting how food contaminants may elicit artery injury and proposing oxidative stress as a mediator of cardiovascular damage.

The temperature state of warm permafrost is in the negative temperature near-phase-transition interval and thus is extremely sensitive to small fluctuations of the heat and stress environment. The dynamic load induced by the vehicle operation not only changes its magnitude cyclically, but also its principal stress direction (PSD) consistently changes rotationally. However, the existing conventional dynamic research methods can only simulate the cyclic stress environment with constant PSD, which is very different from the stress environment induced by locomotive operation, and thus the conventional dynamic research results are bound to be difficult to accurately reflect the influence of the stress field induced by vehicle operation on the development law of warm permafrost permanent settlement deformation. Therefore, in this paper, a series of dynamic studies were carried out for the Qinghai-Tibet silt at -2 degrees C by simulating the cardioid-shaped stress path induced during the operation of a heavy-duty locomotive using a frozen hollow cylinder apparatus. It is found that the rotational effect of the principal stress direction under the conditions of the cardioid-shaped stress path (CSSP) action accelerates the development of vertical permanent deformation in the frozen soil. The main reason that caused the axial strain increases advantage is the rotation of principal stress direction can accelerate the viscous energy dissipation during dynamic loading process. According to the law of axial strain development in the high-temperature frozen soil under the conditions of different CSSP action, an empirical model of permanent deformation development in high-temperature frozen soil considering the PSD rotation effect was established, and it was found by this model calculation that under the general condition of heavy-load locomotive operation, compared with the conventional research method without considering the PSD rotation, the axial cumulated strain in high-temperature frozen soil increased by 33.3% after considering the rotation effect in the PSD.

Atrazine (ATR), a water-soluble herbicide commonly used to control broad-leaf and monocotyledonous weeds, presents a significant risk to environmental soil and water quality. Exposure to ATR adversely affects human and animal health, frequently resulting in cardiac impairment. Curcumin (Cur), an acidic polyphenol derivative from plants acclaimed for its pronounced anti-inflammatory and antioxidant properties, has garnered interest as a potential therapeutic agent. However, whether it has the potential to ameliorate ATR-induced cardiac toxicity via modulation of endoplasmic reticulum stress (ERS) and apoptosis pathways in mice remains unclear. Our results showed that Cur supplementation attenuates ATR-induced cardiotoxicity, evidenced by decrease in creatine kinase and lactate dehydrogenase, key biochemical markers of myocardial injury, which have a more significant protecting effect in high-dose ATR induced injury. Histopathological and electron microscopy examinations further solidified these findings, demonstrating an amelioration in organellar damage, particularly in endoplasmic reticulum swelling and subsequent mitochondrial impairment. Additionally, ATR exposure augments ERS and triggers apoptotic pathways, as indicated by the upregulation of ERS-related gene expression (ATF6, CHOP, IRE1, GRP78) and pro-apoptotic markers (BAX, BAK1, Caspase3, Caspase. Intriguingly, Cur counteracts this detrimental response, significantly reducing ERS and pro-apoptotic signals at both transcriptional and translational levels. Collectively, our findings illuminate Cur's cardioprotective effect against ATRinduced injury, primarily through its anti-ERS and anti-apoptotic activities, underscoring Cur's potential as a therapeutic for ATR-induced cardiotoxicity.