Introduction
Many locations throughout the world have recorded cases of cadmium iodide poisoning. In some cases, it is a widespread health issue that can lead to yearly fatalities. Cadmium iodide poisoning affects several organs. Cancer and organ system toxicity, including damage to the skeletal, urinary, reproductive, cardiovascular, central and peripheral nervous, and respiratory systems, are caused by prolonged exposure to cadmium through the air, water, soil, and food. The amount of cadmium can be determined by samples of blood, urine, hair, nails, and saliva. With the proper novel chelating agents and nanoparticle-based antidotes, patients with cadmium toxicity require gastrointestinal tract irrigation, supportive care, and chemical decontamination in traditional chelation therapy. To prevent cadmium poisoning, it has also been advised to assess the extent of food contamination and consider awareness initiatives for those affected.
What Is the Epidemiology of Cadmium Exposure and Poisoning?
Despite the massive global production, consumption, and release of cadmium (Cd) compounds into the environment, there are no effective means to recycle them. As a result, exposure to Cd compounds by humans could have adverse health effects. For example, cadmium has been used to create polyvinyl chloride plastic, nickel-cadmium batteries, paint pigments, and electroplating. Additionally, depending on dietary preferences, cadmium is a mineral found in varying amounts in most foods.
Due to human activities like burning garbage and using fossil fuels, cadmium is present in the environment in significant amounts. In addition, sludge from sewage systems that have leaked into agricultural soil may contain cadmium compounds absorbed by plants and may be transferred to humans through various organ systems. Cigarette smoke is another significant source of cadmium exposure. When cadmium levels in blood samples from smokers and non-smokers were compared, it was shown that the smokers' levels were 4 to 5 times greater.
There have been numerous reports of cadmium exposure during the past century. Lung damage in cadmium-exposed employees has been documented going back to the 1930s. Additionally, specific incidences of cadmium exposure-related bone and renal toxicity were reported during the ensuing decades. Japanese citizens experienced various amounts of pollution throughout the 1960s and 1970s following World War II. One of these ailments caused by persistent cadmium contamination in rice fields was the Itai-itai illness. Between 1910 and 2007, there were thought to have been 400 people with the condition.
Although cadmium exposure has recently been reduced in many nations, its biological half-life is still relatively lengthy (10 years to 30 years). Therefore, human activities involving it should be kept to a minimum or at no dangerous level.
To significantly lower the occurrence of cadmium toxicity, it is required to prepare the fundamental facts about cadmium poisoning and create an educational and preventative plan. Therefore, the present review may be instructive and beneficial to manage all facets of cadmium compound toxicity.
What Are the Adverse Health Effects of Cadmium Iodine Toxicity?
The adverse health effects of cadmium iodine toxicity are as follows:
1. Renal Damage in Cadmium Toxicity:
Although it can be found in other tissues, including bone and the placenta, cadmium tends to collect most heavily in the kidney and liver. Renal impairment has reportedly been linked to cadmium exposure in the workplace and environment. Kidney injury, proteinuria, calcium loss, and tubular lesions can all be symptoms of cadmium exposure. Analyzing urine may be able to show early indications of kidney impairment. The glomerular filtration rate (GFR) and reserve filtration capacity are often reduced, and severe cadmium toxicity may cause nephrotoxicity with consequences such as glucosuria (excess sugar in urine), aminoaciduria (abnormal amount of amino acid in the urine), hyperphosphaturia, hypercalciuria, polyuria, and reduced buffering capacity. In addition, calcium, amino acids, enzymes, and a rise in proteins are also lost due to cellular damage and functional integrity in the proximal tubules.
2. Cadmium and Reproductive System:
Cadmium has the potential to impact reproduction and development in a variety of mammalian species, according to several earlier research, and more recent investigations have supported similar findings. It is asserted that cadmium increases immature sperm formation while decreasing sperm density, volume, and number compared to animal research. Issues with spermatogenesis, sperm quality, and accessory gland secretory processes are frequently reported. Additionally, it lowers serum testosterone levels as well as libido (sex drive) and fertility. The growth of oocytes and the function of the ovary in the female reproductive system may also be affected. Ovarian bleeding and necrosis can co-occur due to cadmium poisoning, which eventually reduces steroidogenesis. According to reports, the frequency of spontaneous abortions and the length of pregnancies are rising while the frequency of live births is falling due to cadmium poisoning.
3. Cadmium and Cardiovascular System:
Cadmium may contribute to endothelial dysfunction, according to in vitro studies. Additionally, in vivo, atherosclerotic plaque development was reported. Endothelial dysfunction at the onset of cardiovascular disease (CVD), loss of endothelial cell structure leading to cell death, and thrombogenic events are possible after cadmium poisoning. These findings are consistent with the theory that cadmium has a role in heart disease and myocardial infarction. In addition, studies in epidemiology have linked exposure to cadmium to a higher chance of developing high blood pressure (systolic and diastolic blood pressure).
Cadmium may prevent acetylcholine-induced arterial relaxation and reduce endothelial nitric oxide synthase, which results in hypertension. Moreover, endothelial damage and cytokine production may both be stimulated by cadmium poisoning.
4. Cadmium and Other Systems:
Recently, cadmium's acute central and peripheral neurotoxicity has been documented. In the brain, cadmium may cause lipid peroxidation and cellular damage. The oxidative deamination of monoamine neurotransmitters is caused by their impact on monoaminoxidase (MAO). Cadmium lessens cellular defense against oxidation and boosts the generation of free radicals in the central nervous system. The effects of this pathway include memory impairment, attention deficits, psychomotor activity disorders, and olfactory abnormalities. Neurodegenerative illnesses, including Parkinson's, Alzheimer's, and Huntington's, accompanied by memory loss and behavioral problems, can also occur due to cadmium poisoning.
According to recent research, cadmium may play a role in respiratory conditions like chronic obstructive pulmonary disease and emphysema. In animal experiments, cadmium chloride has been shown to reduce vital lung capacity and increase the alveolar wall thickness. Emphysema and lung inflammation may arise from inhaling cadmium as vapor without antioxidants and under oxidative stress conditions. In addition, cadmium may cause lung cancer in humans, according to the Agency for Toxic Substances and Disease Registry.
5. Cadmium and Carcinogenicity:
The International Agency for Research on Cancer classified cadmium compounds as human carcinogens (IARC). It could be classified as a lung carcinogen and a prostatic or renal cancer inducer. The crucial aspect is that cadmium can disrupt testosterone synthesis and cause hyperplasia of testicular interstitial cells. According to some research, cadmium may be related to cancers of the liver, hematopoietic system, bladder, and stomach. Cadmium may also pose a danger for developing breast cancer. Another study hypothesized that cadmium exposure might contribute to pancreatic cancer.
The disruption of cell adhesion, activation of proto-oncogenes, inactivation of tumor suppressor genes, and inhibition of DNA repair are some of the cellular and molecular processes implicating cadmium carcinogenicity. In addition, DNA strand breakage or malfunctioning in the DNA-protein crosslinks can stop cell growth. In conclusion, it is hypothesized that exposure to cadmium can influence cell signaling, apoptosis, differentiation, and other biological processes. These actions may have an indirect or direct impact on carcinogenesis.
Conclusion
High cadmium exposure affects people's lungs and can be fatal. Over time, exposure to low quantities of cadmium in the environment—through tobacco smoke can increase the risk of renal disease and brittle bones. Moreover, cadmium is also a potential cancer-causing agent.
