Common Minerals That Cause Toxicity in Humans
The term mineral toxicity refers to a condition during which the concentration within the body of anybody of the minerals necessary for all times is abnormally high, and which has an adverse effect on health. The mineral nutrients are defined as all the inorganic elements or inorganic molecules that are required for all times. As far as human nutrition sustenances, the inorganic nutrients comprise water, sodium, potassium, chloride, calcium, phosphate, sulfate, magnesium, iron, fluorine, copper, zinc, chromium, manganese, iodine, selenium, and molybdenum. The last nine elements in this list are sometimes called trace minerals or micronutrients because humans need only small amounts of them in the diet. In high doses, all nine trace minerals are often toxic in humans.
Causes and Symptoms
The causes and symptoms of mineral toxicity depend upon the precise mineral in question:
Sodium:
A rise in sodium concentration within the bloodstream is often toxic. The normal concentration of sodium in human plasma is 136–145 mM, while levels over 152 mM may result in seizures and death. Increased plasma sodium, which is named hypernatremia, causes the cells in various body tissues, including those of the brain, to shrink. Shrinkage of the brain cells leads to confusion, coma, paralysis of the lung muscles, and death. Death has occurred when salt (sodium chloride) accidentally wants to feed infants rather than sugar. Death thanks to sodium toxicity has also resulted when bicarbonate of soda (sodium bicarbonate) was wont to treat excessive diarrhea or vomiting. Although the spread of processed foods contains high levels of common salt, the amount in these things isn’t enough to end in sodium toxicity.
Potassium:
The traditional level of potassium within the bloodstream is within the range of three .5–5.0 mM, while levels of 6.3–8.0 mM (severe hyperkalemia) end in cardiac arrhythmias or maybe death due to cardiac arrest. Potassium is potentially quite toxic; however, potassium poisoning is typically prevented due to the vomiting reflex. The consumption of food leads to mild increases within the concentration of potassium within the bloodstream, but these levels of potassium don't become toxic due to the uptake of potassium by various cells of the body as well as by the action of the kidneys transferring the potassium ions from the blood to the urine.
Iodine:
Iodine toxicity can result from an intake of 2.0 mg of iodide per day. Toxic levels of iodine inhibit the secretion of the hormone, leading to lower levels of the hormone within the bloodstream. As a result, the thyroid gland becomes enlarged. This condition is known as goiter or hyperthyroidism. Goiter is usually caused by iodine deficiency. In addition to goiter, iodine toxicity produces a brassy taste in the mouth, excessive production of saliva, and ulcers on the skin. This skin condition has been called kelp acne due to its association with eating kelp, an ocean plant that contains high levels of iodine. Iodine toxicity exists fairly repeatedly in Japan, where people consume huge quantities of seaweed.
Nitrite:
Nitrite poisoning should be deemed iron toxicity since nitrite produces its toxic impact by reacting with the iron atom in hemoglobin. Hemoglobin is an iron-containing protein that resides within the red blood cells. This protein is liable for transporting nearly all of the oxygen acquired from the lungs to varied tissues and organs of the body. Hemoglobin accounts for the red color of red blood cells. Per day hemoglobin spontaneously oxidizes in a very small fraction, producing a protein of a rather different structure called methemoglobin. Normally, the quantity of methemoglobin constitutes but 1 percent of the entire hemoglobin. Methemoglobin can accumulate within the blood as a result of nitrate poisoning. Infants are especially susceptible to poisoning by nitrite.
Demographics
Iron poisoning is the most prevalent type of mineral toxicity in children in the United States and is one of the top reasons for fatal poisoning in children younger than six years of age. About 20,000 children are recorded as mistakenly eating iron pills each year in the United States. However, not all of these incidents end in death. In one Indian study of 21 infants treated for iron toxicity, four of the patients died. In relation to disorders leading to mineral toxicity, around one person in ten in the United States possesses the genetic mutation that can lead to hemochromatosis. However, not everyone with this variant always gets the condition. It is believed that there are roughly 1 million individuals in the United States with hemochromatosis as of the early 2000s. About one person in 30,000 possesses the genetic abnormality that causes Wilson's illness, whereas about 1.1 percent of the overall population are bearers of the mutant gene. The incidence of Menkes disease, which mostly affects boys, is variably reported as one in 50,000 to one in 250,000 individuals. Wilson's illness and Menkes illness happen at the same rate in all races and ethnic groups.
Diagnosis
A first assessment of mineral poisoning includes collecting a comprehensive history. The doctor asks the parents of the little kid questions aimed to detect any unique characteristics of the family's diet or use of medications and chemicals. An older teenager in the workforce may be asked about probable workplace contact. The mineral content of the body may be assessed by examining samples of bodily fluids, most frequently blood plasma, red blood cells from whole blood, and urine. Diagnosis of mineral toxicities also entails monitoring the levels of certain metals in the plasma or urine. Concentrations that are above the usual range can validate the initial presumed diagnosis. Menkes disease may be detected by the unique look of the hair, skin, and facial characteristics in male babies with the ailment as well as by their developmental issues.
Prevention
When mineral poisoning arises from the heavy intake of mineral supplements. Toxicity can be averted by reducing the use of dietary supplements and keeping iron pills in particular out of the reach of children. Zinc poisoning may be averted by not keeping food or beverages in zinc containers. In the case of iodine, poisoning can be minimized by avoiding overconsumption of seaweed or kelp. In the case of selenium poisoning originating from high-selenium soils, toxicity can be averted by depending on food and water purchased from a low-selenium zone.
Did You Know?
An increase in the concentrations of sodium in the bloodstream can be toxic. The normal concentration of sodium within the plasma is 136 - 145 mM, while levels over 152 mM may result in seizures and death. Increased plasma sodium, which is named hypernatremia, causes various cells of the body, including those of the brain, to shrink. Shrinkage of the brain cells leads to confusion, coma, paralysis of the lung muscles, and death. Death has occurred where salt (sodium chloride) was accidentally used, rather than sugar, for feeding infants. Death thanks to sodium toxicity has also resulted when bicarbonate of soda (sodium bicarbonate) was used during attempted therapy of excessive diarrhea or vomiting. Although the spread of processed foods contains high levels of common salt, the amount used isn’t enough to end in sodium toxicity.
Potassium is potentially quite toxic, however toxicity or death thanks to potassium poisoning is typically prevented due to the vomiting reflex.
FAQs on Mineral Toxicity: Causes, Effects, and Prevention
1. What is the definition of mineral toxicity in plants?
Mineral toxicity is a condition that occurs when a mineral element accumulates in plant tissues to a concentration high enough to be harmful. Any mineral ion concentration in tissues that reduces the dry weight of the tissues by about 10 per cent is considered toxic. This excess disrupts the plant's normal metabolism, physiology, and growth, often leading to visible symptoms and reduced vitality.
2. What are the common causes of mineral toxicity in agricultural soils?
Mineral toxicity in plants is primarily caused by several factors, including:
- Over-fertilisation: Applying excessive amounts of mineral fertilisers can lead to their accumulation in the soil.
- Industrial Pollution: Contamination of soil and water with heavy metals from industrial waste is a major cause.
- Soil pH: Acidic soils can increase the solubility and availability of certain minerals like manganese and aluminium to toxic levels.
- Irrigation Water: Using water with a high concentration of dissolved salts or specific minerals can also lead to toxicity over time.
3. Can you provide a specific example of mineral toxicity and its effects on a plant?
A classic example is manganese (Mn) toxicity. When manganese is present in excess, it competes with other essential minerals for uptake. Specifically, it competes with iron and magnesium for absorption and with magnesium for binding to enzymes. It also inhibits the translocation of calcium to the shoot apex. As a result, symptoms of manganese toxicity often appear as the deficiency symptoms of iron, magnesium, and calcium, such as brown spots surrounded by chlorotic (yellowed) veins.
4. What are the general symptoms that indicate a plant may be suffering from mineral toxicity?
While symptoms are specific to the mineral, common signs of toxicity include stunted growth, chlorosis (yellowing of leaves), and necrosis (death of plant tissue). A prominent symptom of manganese toxicity, for instance, is the appearance of brown spots surrounded by chlorotic veins. Identifying the specific toxic mineral often requires a soil or plant tissue analysis, as symptoms can be misleading.
5. How is mineral toxicity fundamentally different from mineral deficiency?
The fundamental difference lies in the concentration of the mineral. Mineral deficiency occurs when an essential nutrient is available in a concentration so low that it limits plant growth. In contrast, mineral toxicity occurs when a mineral is present in a concentration so high that it becomes harmful and impairs metabolic functions. In simple terms, deficiency is a case of 'too little', while toxicity is a case of 'too much'.
6. How can an excess of one mineral element induce the deficiency of another?
This happens due to a process called competitive inhibition or antagonism. Different mineral ions with similar chemical properties (like size and charge) compete for the same uptake transporters in the plant's root cells. For example, an excess of manganese (Mn²⁺) can competitively inhibit the uptake of iron (Fe²⁺) and magnesium (Mg²⁺). Even if iron and magnesium are present in adequate amounts in the soil, the plant cannot absorb them efficiently, leading to their deficiency symptoms.
7. Why is it often difficult for a student to identify mineral toxicity based on visual symptoms alone?
It is difficult because the symptoms of toxicity for one mineral can often mimic the deficiency symptoms of another. As seen with manganese toxicity causing symptoms of iron and magnesium deficiency, the visible signs are not a direct indication of the excess mineral. This overlap makes accurate visual diagnosis unreliable without a proper soil test or plant tissue analysis to confirm the actual mineral concentrations within the plant and soil.
