Cadmium is one of the most toxic heavy metal elements that seriously threaten food safety and agricultural production worldwide. Because of its high solubility, cadmium can easily enter plants, inhibiting plant growth and reducing crop yield. Therefore, finding a way to alleviate the inhibitory effects of cadmium on plant growth is critical. Silicon, the second most abundant element in the Earth\'s crust, has been widely reported to promote plant growth and alleviate cadmium toxicity. This review summarizes the recent progress made to elucidate how silicon mitigates cadmium toxicity in plants. We describe the role of silicon in reducing cadmium uptake and transport, improving plant mineral nutrient supply, regulating antioxidant systems and optimizing plant architecture. We also summarize in detail the regulation of plant water balance by silicon, and the role of this phenomenon in enhancing plant resistance to cadmium toxicity. An in-depth analysis of literature has been conducted to identify the current problems related to cadmium toxicity and to propose future research directions.

To support a mixture risk assessment with a focus on developmental neurotoxicity we evaluated the strength of evidence for associations of cadmium exposures with declines in IQ by conducting a systematic review and confidence rating. We searched peer-reviewed studies published in English between 2012 and July 2021 and identified 15 eligible studies (11 prospective cohort studies, and 4 cross-sectional studies). Of the 10 studies that observed associations of cadmium exposure with child IQ declines, two achieved an overall \"High (H)\" confidence rating, five a \"Medium to High (M/H)\", one a \"Medium (M)\" and two a \"Low (L)\" confidence rating. Five studies did not detect significant associations between cadmium exposure and reduced cognitive ability; of these, two received a \"High (H)\" confidence rating, two an overall rating of \"Medium to High (M/H)\" and one a \"Medium (M)\" rating. The null findings reported by the \"High (H)\" and Medium to High (M/H)\" studies could partly be explained by low exposures to cadmium or confounding with high levels of lead. By using a one-compartment toxicokinetic model in a reverse dosimetry approach, we estimated that a daily intake of 0.2 μg/kg body weight/day corresponds to urinary cadmium levels no longer associated with cognitive declines observed in a \"High (H)\"-confidence study. This estimate is 1.8-fold lower than the current health-based guidance value (HBGV) for kidney toxicity of 0.36 μg/kg bodyweight/day established by the European Food Safety Authority (EFSA). Our value does not have the normative character associated with health-based guidance values and is intended only as a reasonable estimate for the purpose of mixture risk assessments. However, with cadmium exposures in Europe between 0.28 (middle bound) and up to 0.52 μg/kg bodyweight/day (95th percentile), our review suggests that pregnant women and children are poorly protected against neurodevelopmental effects. This warrants a revision of the current HBGV.

More than one and a half centuries ago, adverse human health effects were reported after use of a cadmium-containing silver polishing agent. Long-term cadmium exposure gives rise to kidney or bone disease, reproductive toxicity and cancer in animals and humans. At present, high human exposures to cadmium occur in small-scale mining, underlining the need for preventive measures. This is particularly urgent in view of the growing demand for minerals and metals in global climate change mitigation. This review deals with a specific part of cadmium toxicology that is important for understanding when toxic effects appear and, thus, is crucial for risk assessment. The discovery of the low-molecular-weight protein metallothionein (MT) in 1957 was an important milestone because, when this protein binds cadmium, it modifies cellular cadmium toxicity. The present authors contributed evidence in the 1970s concerning cadmium binding to MT and synthesis of the protein in tissues. We showed that binding of cadmium to metallothionein in tissues prevented some toxic effects, but that metallothionein can increase the transport of cadmium to the kidneys. Special studies showed the importance of the Cd/Zn ratio in MT for expression of toxicity in the kidneys. We also developed models of cadmium toxicokinetics based on our MT-related findings. This model combined with estimates of tissue levels giving rise to toxicity, made it possible to calculate expected risks in relation to exposure. Other scientists developed these models further and international organizations have successfully used these amended models in recent publications. Our contributions in recent decades included studies in humans of MT-related biomarkers showing the importance of MT gene expression in lymphocytes and MT autoantibodies for risks of Cd-related adverse effects in cadmium-exposed population groups. In a study of the impact of zinc status on the risk of kidney dysfunction in a cadmium-exposed group, the risks were low when zinc status was good and high when zinc status was poor. The present review summarizes this evidence in a risk assessment context and calls for its application in order to improve preventive measures against adverse effects of cadmium exposures in humans and animals.

Cadmium (Cd) has been recognized as one of the most toxic heavy metals, which is continuously discharged into environments through anthropogenic (industrial activities, fertilizer production, and waste disposal) and natural sources with anthropogenic sources contributing greater than the natural sources. Therefore, Cd concentration sometimes increases in feeds, fodders, water bodies, and tissues of livestock including poultry in the vicinity of the industrial areas, which causes metabolic, structural, and functional changes of different organs of all animals. In poultry, bioaccumulation of Cd occurs in several organs mainly in the liver, kidney, lung, and reproductive organs due to its continuous exposure. Intake of Cd reduces growth and egg laying performance and feed conversion efficiency in poultry. Chronic exposure of Cd at low doses can also alter the microscopic structures of tissues, particularly in the liver, kidney, brain, pancreas, intestine, and reproductive organs due to increased content of Cd in these tissues. Continuous Cd exposure causes increased oxidative stress at cellular levels due to over-production of reactive oxygen species, exhausting antioxidant defense mechanisms. This leads to disruption of biologically relevant molecules, particularly nucleic acid, protein and lipid, and subsequently apoptosis, cell damage, and necrotic cell death. The histopatholocal changes in the liver, kidneys, and other organs are adversely reflected in hemogram and serum biochemical and enzyme activities. The present review discusses about Cd bioaccumulation and histopathological alterations in different tissues, pathogenesis of Cd toxicity, blood-biochemical changes, and its different ameliorative measures in poultry.

Cadmium (Cd) is a heavy and toxic metal and easily absorbed by animals and plants; subsequently, it is an environmental risk factor with several toxic effects in humans and animals. The main pathway of human or animal exposure to Cd is through its ingestion by water or food and by particles or fume inhalation during industrial processes. With continuous exposure to small levels of cadmium, it is being deposited in different tissues day after day, causing toxic effects on the liver, kidney, and testes. Long-term exposure to this toxic metal resulted in inflammatory infiltration, necrosis of hepatocytes, degenerative changes in testis tissues, reduction in spermatocytes, degeneration in renal tubules, and hypertrophy of renal epithelium. Therefore, we need an effective treatment to overcome cadmium poisoning. Thus, in the current review, we try to provide compiled reports and summarize information about the toxicological effects of Cd in human, animals, and poultry. This review also provides updated information about the protective actions of herbs and herbal extracts and their role as an effective strategy in reducing or preventing serious health problems and tissue damage in response to Cd toxicity.