How can mercury enter the body

Like oxidized elemental mercury, mercuric salts are more water soluble and toxic than elemental mercury. Mercuric salts are also easily absorbed by the gastrointestinal tract [ 10 ].

The average whole body half-life of inorganic mercury is about 40 days [ 11 ]. The most common form of organic mercury is methylmercury MeHg , which is the major source of organic mercury found in the ecosystems [ 12 ].

MeHg is readily transported by water into the aquatic ecosystems. Because of its low water solubility it is considered to be relatively lipid soluble. MeHg is easily taken up by lower organisms, tends to work its way up the food chain and exhibits a proclivity to bioaccumulate in fish [ 13 ].

Fish appear to be the primary source of MeHg poisoning in humans. Through mechanisms which are not yet known, various species of fish tend to have higher rates of MeHg bioaccumulation Table 1 [ 14 ]. The gastrointestinal tract absorbs approximately ninety five percent of ingested MeHg where it can then enter the red blood cells and the brain by binding covalently to glutathione and cysteine protein groups [ 15 , 16 ].

The biological half-life of MeHg is 39 to 70 days depending on body burden. Potential sources of organic mercury included exposure to fossil fuel emissions, the incineration of medical waste, dental amalgam, and various commercial products including skin creams, germicidal soaps, various medications, teething powders, analgesics, diaper treatments, vaccinations, thermometers, sphygmomanometer, barometers, incandescent lights, and batteries [ 5 , 7 ].

Other sources for organic mercury include phenyl mercury compounds and ethyl mercury compounds, which were components of latex paints that were used before s [ 12 ] and thimerosal which has been used as a preservative in vaccines [ 7 ]. Among the most dangerous mercury compound is dimethylmercury CH 3 2Hg which is toxic enough to cause death if only a few microliters is spilled on the skin, or even latex gloves [ 17 ]. Mercury poisoning can result in death, mental retardation, dysarthria, blindness, neurological deficits, loss of hearing, developmental defects, and abnormal muscle tone [ 7 ].

Table 2 presents a helpful mnemonic that practitioners can use when examining possible MeHg toxicity. Mercury content of different seafoods [ 14 ].

Mercury exposure has been associated with the induction of over symptoms which can complicate accurate diagnosis. Differential diagnosis begins with a patient history and physical examination consistent with mercury exposure.

Laboratory testing typically includes 1 blood analysis; 2 urinalysis, with a hour urine analysis, and a urine challenge test with a "chelating" agent; 3 hair analysis; and d tissue biopsy if warranted [ 10 , 18 ]. Because mercury can be quickly removed from the blood, redistributed and sequestered into different tissues it is important to note that there may not be a direct correlation between blood mercury concentration and the severity of mercury poisoning.

Indeed, it is thought that shortly after entering the body that mercury quickly becomes tightly bound in the brain, spinal cord, ganglia, autonomic ganglia, and peripheral motor neurons.

Nonetheless although the nervous system is the primary repository for mercury exposure, the transient and residual systemic distribution of mercury has the potential to cause symptoms in a number of different organ systems. In addition reports indicate that individual genetic background may play a role in mercury toxicokinetics [ 19 ].

At the cellular level mercury exposure is associated with alterations in membrane permeability, changes in macromolecular structure due to its affinity for sulfhydryl and thiol groups, and DNA damage [ 20 , 21 , 22 ]. Mercury has also been shown to induce oxidative stress and mitochondrial dysfunction [ 23 ] which can result in alterations in calcium homeostasis and increased lipid peroxidation [ 24 ].

In addition, mercury may also increase radical oxygen species levels because of its ability to act as a catalyst for Fenton-type reactions [ 24 ]. Mercury accumulation in the heart is thought to contribute to cardiomyopathy. Indeed, mercury levels in the heart tissue of individuals who died from idiopathic dilated cardiomyopathy were found to be on average 22 times higher than in individuals who died of other forms of heart disease [ 25 , 26 ].

Mercury poisoning may also cause chest pain or angina, especially in individuals under age 45 [ 26 ]. In vitro studies have indicated that MeHg can inhibit the cardioprotective activity of paraoxonase 1 [ 27 ]. There is also good evidence linking mercury with anemia including hemolytic anemia and aplastic anemia as mercury is thought to compete with iron for binding to hemoglobin which can result in impaired hemoglobin formation [ 28 ].

In addition to anemia, additional data has also suggested that mercury may be a causative factor in mononucleosis and involved in leukemia, and Hodgkin's disease [ 29 , 30 , 31 ]. Case control studies have demonstrated that the chronic inhalation of even low concentrations of mercury 0.

Mercury poisoning is associated with several different pulmonary conditions including Young's syndrome [ 34 ], bronchitis and pulmonary fibrosis [ 35 , 36 ]. Mercury is absorbed through the epithelial cells when ingested. This absorbed mercury can cause various digestive disturbances as it can inhibit the production of the digestive trypsin, chymotrypsin, and pepsin along with the function of xanthine oxidase and dipeptyl peptidase IV [ 37 ].

The effects of mercury on the gastrointestinal system typically present as abdominal pain, indigestion, inflammatory bowel disease, ulcers and bloody diarrhea. Mercury ingestion has also been associated with the destruction of intestinal flora which can increase the amount of undigested food products in the blood stream causing immune mediated reactions and reduced resistance to pathogenic infection [ 38 ].

Mercury can cause kidney damage and evidence suggests a linkage between mercury exposure and acute tubular necrosis, glomerulonephritis, chronic renal disease, renal cancer and nephrotic syndrome [ 35 , 39 , 40 , 41 ]. Various reports have shown mercury exposure can lead to various kidney injuries including: subacute-onset nephrotic syndrome, tubular dysfunction, secondary focal segmental glomerulosclerosis, syncreticatic nephrotic syndrome, nephritic syndrome, nephrotic-range proteinuria, glomerular disease, and membranous glomerulonephritis [ 42 ].

Klinghardt's axiom states that "Most, if not all, chronic infectious diseases are not caused by a failure of the immune system, but are a conscious adaptation of the immune system to an otherwise lethal heavy metal environment". It has been known for many years that mercury impairs immune system function most likely via its deleterious effects on the polymorphonuclear leukocytes PMNs. Mercury through suppression of adrenocorticosteroids production prevents normal stimulation of PMNs production and also affects PMN function by inhibiting their ability to destroy foreign substances [ 43 ].

Mercury-sensitive individuals are more likely to have allergies, asthma, and autoimmune-like symptoms, especially rheumatoid-like ones. Mercury can produce an immune response in the central nervous system, induce alterations in immune cell production and function, and modulate the production of interferon gamma and interleukin-2 [ 44 ].

With impairment comes a chronically susceptible to infections, if not chronic sickness. Interestingly, the ingestion of mercury is oftentimes associated with increased levels of yeasts, bacteria, and molds which are thought to function in a protective manner to absorb excess mercury from the body. Indiscriminant and rapid destruction of the Candida albicans and other pathogens by antibiotics in adults with a significant body burden of toxic metals, including mercury, may cause the sudden release of large amounts of toxic metals contained within them and be potentially very dangerous.

It is clear that mercury is accumulated in nervous tissues all through the body [ 52 ]. The most devastating effect of mercury in the nervous system is interference with the production of energy which can impair cellular detoxification processes causing the cell to either die or live in a state of chronic malnutrition.

It is thought that mercury causes neuronal problems through blockage of the P enzymatic process [ 26 ]. Mercury is associated with increased tissue oxidative damage, and children with autism had significantly higher urinary levels of lipid peroxidation when compared to controls. In the peripheral nervous system, circulating inorganic mercury can be taken up into the nerve terminals where it can impair the synthesis of tubulin and actin which are important constituents of neuronal cell structure and detoxification processes [ 53 ].

Primary sensory neuropathy is a hallmark of MeHg poisoning. In the central nervous system mercury can damage the blood brain barrier and it facilitates penetration of the brain by other toxic metals and substances. The effects of mercury poisoning effects in the central nervous system include depression, paranoia, extreme irritability, hallucinations, an inability to concentrate, memory loss, tremors of the hands, head, lips, tongue, jaw and eyelids, weight loss, perpetually low body temperature, drowsiness, headaches, insomnia, and fatigue.

Along with nervous system effects, mercury has also shown to have various effects on other special sensory systems including blindness, retinopathy, optic neuropathy, hearing loss, a reduced sense of smell, and abnormal touch sensation [ 54 ]. Autism is a syndrome characterized by impairments in social relatedness, language and communication, a need for routine and sameness, abnormal movements, and sensory dysfunction [ 55 ]. Mercury can cause immune, sensory, neurological, motor, and behavioral dysfunctions similar to traits defining or associated with autism [ 56 ] leading some to suggest that many cases of autism may be a form of mercury poisoning [ 55 ].

Low exposure levels of mercury may affect the endocrine system in animals and people by disruption of the pituitary, thyroid, adrenal glands and pancreas [ 57 ].

Hormones that appear to be the most affected by mercury are insulin, estrogen, testosterone, and adrenaline. Mercury can also inhibit catecholamine degradation through inactivation of S-adenosyl-methionine which can cause the accumulation of epinephrine and hyperhidrosis, tachycardia, ptyalism hyper salivation and hypertension [ 1 ].

In the adrenal cortex, mercury exposure has been found to be associated with lowered plasma levels of corticosterone [ 58 ]. Reduced cortisol production causes a compensatory rise in adrenocorticotropic hormone leading to adrenal hyperplasia. Mercury-induced adrenal hyperplasia may eventually stress the adrenal to a point at which there is adrenal atrophy and may be a causative factor in the development of Addison's disease [ 43 ]. Autopsy studies in revealed that the thyroid and pituitary retain and accumulate more inorganic mercury than the kidneys [ 59 ].

Mercury levels in the pituitary gland ranged from 6. Low levels of pituitary function are associated with depression and suicidal thoughts, and appear to be a major factor in suicide of teenagers and other vulnerable groups. Because of its effect on the pituitary, mercury is known to cause frequent urination as well as high blood pressure [ 61 ]. The thyroid is one of the largest endocrine glands in the body. The thyroid controls how quickly the body burns energy, makes proteins, and how sensitive the body should be to other hormones.

Like the pituitary, the thyroid displays an affinity for accumulating mercury. Mercury blocks thyroid hormone production by occupying iodine-binding sites and inhibiting or altering hormone action leading to the impairment of body temperature control, hypothyroidism, thyroid inflammation and depression [ 43 , 61 ].

Like the thyroid, the pancreas is also susceptible to the toxic effects of mercury. Insulin, the molecule involved in diabetes, has three sulfur-binding sites which can be bound by mercury causing the interference with normal biological function and a dysregulation of blood glucose levels [ 62 ]. Mercury can precipitate pathophysiological changes along the hypothalamus-pituitary-adrenal and gonadal axis that may affect reproductive function by altering the circulating of levels of follicle-stimulating hormone FSH , luteinizing hormone LH , inhibin, estrogen, progesterone, and the androgens [ 63 , 64 ].

Reduced fertility among dental assistants with occupational exposure to mercury has been noted [ 65 , 66 ]. Studies in Hong Kong demonstrated that increased mercury levels were associated with infertility in both men and women [ 67 ]. In males, mercury can have adverse effects on spermatogenesis [ 68 ], epididymal sperm count, and testicular weight. Evidence also exists linking mercury with erectile dysfunction [ 64 ].

In females, mercury has been shown to inhibit the release of FSH and LH from the anterior pituitary which in turn can effect estrogen and progesterone levels leading to ovarial dysfunction, painful or irregular menstruation, premature menopause, and tipped uterus [ 62 ]. There is good evidence linking mercury with menstrual disorders including abnormal bleeding, short, long, irregular cycles, and painful periods [ 63 ]. In addition to reproductive issues, mercury is also associated with the fetotoxicity which can present as miscarriage, spontaneous abortions, stillbirth, and low birth weights [ 69 ].

In the neonate, mercury exposure during pregnancy has been linked to neural tube defects, craniofacial malformations, delayed growth, and others [ 69 ]. Mercury is known to cross the placenta where it can inhibit fetal brain development resulting in cerebral palsy and psychomotor retardation in the latter stages of development [ 70 , 71 ]. In primates maternal MeHg blood levels were moderatelyrelated to increased abortion rates and decreased oregnancy rates [ 72 ]. Embryopathic effects of MeHg in humans have also been reported.

Fetal autopsies indicated a generalized hypoplasia of the cerebellum, decreased number of nerve cells in the cerebral cortex, marked decrease in total brain weight, abnormal neuron migration, and brain centers and layer deranged organization [ 73 , 74 , 75 , 76 ].

MeHg easily enters through the placenta and damages the brain of the fetus. Many exposed feti go on to develop infantile cerebral palsy and there may be a relation with the development of Minamata disease. Babies may be born with a variety of birth defects.

Mercury inhibits the trans membrane transport of nutrients including selenium in the placenta. In animal experiments it has also been shown that there is a much higher accumulation of mercury in the fetal brain tissue than in the maternal brain tissue [ 77 ]. It is evident by the number of organ systems and cellular functions affected by mercury that exposure to the various form of mercury is detrimental to public health.

Evaluation of the epidemiological consequences of mercury toxicity over the years has added greatly to the understanding of mercury toxicity and its human impact. All of these events have left us with an indelible account of the detrimental effects of mercury on human health. In light of these historic events and the toxicological evidence presenting in this review regarding the systemic effects of mercury on cellular, cardiovascular, hematological, pulmonary, renal, immunological, neurological, endocrine, reproductive, and embryonic development, efforts should be made to insure adequate steps are taken in public health and prevention to reduce the occurrence of mercury exposure and raise public awareness.

The authors have no conflicts of interest with the material presented in this paper. National Center for Biotechnology Information , U.

J Prev Med Public Health. Published online Mar Kevin M. Rice , 1 Ernest M. Blough 1, 2, 4. Find articles by Kevin M. Ernest M. Find articles by Ernest M. Walker, Jr. Find articles by Miaozong Wu. Find articles by Chris Gillette. Eric R. The most common way people in the U. Other exposures may result from using or breaking products containing mercury. If you are concerned for your health or your family's health as a result of a potential exposure to mercury, get in touch with your physician or other health care provider.

They will be able to tell you if the degree of mercury exposure is a concern, and what to do about it. Methylmercury, a highly toxic organic compound, is the form of mercury people in the United States encounter most frequently. Almost all people in the world have at least trace amounts of methylmercury in their bodies, reflecting its prevalence in the environment. However, most people have mercury levels in their bodies below the level associated with possible health effects.

Nearly all methylmercury exposures in the United States occur through eating fish and shellfish that contain higher levels of methylmercury. In a given water body, the highest concentrations of methylmercury are generally found in large fish that eat other fish.

Fish is a beneficial part of people's diet, and we encourage people to eat fish low in methylmercury. Some communities eat significantly more quantities of fish than the general population. As a result, they may be exposed to much greater mercury contamination than the general population. In past outbreaks of methylmercury poisoning, mothers with no symptoms of nervous system damage gave birth to infants with severe disabilities.

This presented evidence that the nervous system of a developing infant may be more vulnerable to methylmercury exposures than an adult nervous system.

Mothers who are exposed to methylmercury and breast-feed may also expose their infant children through their milk. Mercury poisoning also poses a risk to the reproductive system. It may cause reduced sperm count or decreased fertility and may also cause problems with the fetus. Possible effects of mercury poisoning include deformity and a decreased survival rate of the fetus, and reduced growth and size of the newborn at birth.

Mercury helps promote the accumulation of free radicals in the body, which puts the cells at risk for damage. This may lead to an increased risk of heart problems, including heart attack and coronary heart disease. The most common cause of mercury poisoning is from eating seafood, but people can get mercury poisoning from industrial processing, thermometers and blood pressure machines, dental work, and old paints.

Eating seafood that has been tainted with mercury is one of the most common ways humans accumulate mercury in their bodies. The mercury in seafood is a highly poisonous form of the metal called methylmercury, which forms when mercury dissolves into the water. Methylmercury can be absorbed from the water by all sea creatures, but it also continues through the food chain. Small sea creatures, such as shrimp, often ingest methylmercury and are then eaten by other fish. These fish will now have more methylmercury in them than the original shrimp.

This process continues all the way up the food chain, so that a large fish may contain much more mercury than the fish it has eaten. This does not necessarily make it better to eat smaller fish, however. It is always essential for a person to check the source of their seafood to avoid contaminated fish and shellfish. People worried about their exposure to mercury may want to limit their seafood intake, particularly of fish that are high on the food chain, such as swordfish, shark, white tuna, pike, walleye, and bass.

Pregnant or breast-feeding women may want to avoid or restrict their intake of fish and shellfish, as any mercury they contain can pass to the fetus or infant through the umbilical cord or breast milk. Amalgam fillings, commonly called silver fillings, contain approximately 40 to 50 percent mercury.

Amalgam fillings are not often used now, as there are newer and safer alternatives. Some people choose to replace their amalgam fillings to reduce their long-term exposure to mercury. Mercury poisoning may also be due to direct or environmental exposure. Mercury exposure may come from one or more of the following sources:. Doctors can usually diagnose mercury poisoning through a physical exam and blood tests.

Doctors may ask about any symptoms the person is having, as well as for a general breakdown of their diet. They may also ask questions about the environment the person lives or works in, including whether they live near any factories or work in an industrial plant.

If the doctor suspects mercury poisoning, a blood and or urine mercury test can gauge the levels of mercury in the body. Treatment of mercury poisoning involves eliminating any and all exposure to the metal.