Heavy metal toxicity is an uncommon diagnosis. With the possible exceptions of acute iron toxicity from intentional or unintentional ingestion and suspected lead toxicity, emergency physicians will rarely be alerted to the possibility of metal exposure. Yet, if unrecognized or inappropriately treated, heavy metal exposure can result in significant morbidity and mortality.
Many of the elements that can be considered heavy metals have no known benefit for human physiology. Lead, mercury, and cadmium are prime examples of such toxic metals.
The toxicity of heavy metals depends on a number of factors. Specific clinical manifestations vary according to the metal in question, the total dose absorbed, and whether the exposure was acute or chronic. The age of the person can also influence toxicity. For example, young children are more susceptible to the effects of lead exposure because they absorb several times the percent ingested compared with adults and because their brains are more plastic, and even brief exposures may influence developmental processes. The route of exposure is also important. Elemental mercury is relatively inert in the gastrointestinal tract and also poorly absorbed through intact skin, yet inhaled or injected elemental mercury may have disastrous effects.[1]
Some elements may have very different toxic profiles, depending on their chemical form. For example, barium sulfate is basically nontoxic, whereas other, more water-soluble barium salts are rapidly absorbed and cause profound, potentially fatal hypokalemia. The toxicity of radioactive metals like polonium relates more to their ability to emit particles than to their ability to bind cell proteins.
Exposure to metals may occur through the diet, from medications, from the environment, or in the course of work or play. Where heavy metal toxicity is suspected, time taken to perform a thorough dietary, occupational, and recreational history is time well spent, since identification and removal of the source of exposure is frequently the only therapy required.
A full dietary and lifestyle history may reveal hidden sources of metal exposure. Metals may be contaminants in dietary supplements, or they may leach into food and drink stores in metal containers such as lead decanters. Persons intentionally taking colloidal metals for their purported health benefits may ultimately develop toxicity. Metal toxicity may complicate some forms of drug abuse. Beer drinker’s cardiomyopathy was diagnosed in alcoholics in Quebec, and later Minnesota, during a brief period in the 1970s when cobalt was added to beer on tap to stabilize the head. A parkinsonian syndrome among Latvian injection drug users of methcathinone was linked to manganese toxicity.
Classic examples of environmental contamination include the Minamata Bay disaster and the current epidemic of arsenic poisoning in Southeast Asia. In the 1950s, industrial effluent was consistently dumped into Japan’s Minamata Bay, and methylmercury bioaccumulated to exceedingly high concentrations in local fish. Although some adults did develop signs and symptoms of toxicity, the greatest impact was on the next generation, into which many children were born with severe neurologic deficits.
Currently, millions of people living in and around Bangladesh are at risk for organ dysfunction and cancer from chronic arsenic poisoning from the water supply. In an effort to bypass water sources rife with bacterial contamination, tube wells were sunk throughout that area, deep into the water table.[2] Unfortunately, the bedrock in that part of the world is rich in arsenic, giving these deeper water stores—and the crops they irrigate—a high concentration of arsenic, and toxicity is epidemic throughout the area. Childhood lead poisoning linked to the ingestion of old paint chips in North America is another good example of environmental contamination.
In total, however, occupational exposure has probably accounted for the vast majority of heavy metal poisonings throughout human history.
The classic acute occupational heavy metal toxicity is metal fume fever (MFF), a self-limiting inhalation syndrome seen in workers exposed to metal oxide fumes. MFF, or "brass founder’s ague," "zinc shakes," or "Monday morning fever," as it is variously known, is characterized by fever, headache, fatigue, dyspnea, cough, and a metallic taste occurring within 3-10 hours after exposure. The usual culprit is zinc oxide, but MFF may occur with magnesium, cobalt, and copper oxide fumes as well.
Chronic occupational exposure to metal dusts has also been linked to the development of pneumoconioses, neuropathies, hepatorenal degeneration and a variety of cancers. These syndromes develop slowly over time and may be difficult to recognize clinically. In the United States, Occupational Safety and Health Administration (OSHA) regulations guide the surveillance of workers at risk and suggest exposure limits for metals of industrial importance.
The first antidote to heavy metal poisoning, and the basis for chelation therapy today, was British Anti-Lewisite (BAL, or dimercaprol), a large molecule with sulfhydryl groups that bind arsenic, as well as other metals, to form stable covalent bonds that can then be excreted by the body. BAL was developed by the British during World War II in anticipation of a reinitiation of chemical warfare as had been waged earlier in the century.
This article provides a brief overview of general principles in the diagnosis and management of metal toxicity. The table below reviews the typical presentation of the most commonly encountered metals and their treatment, in summary form. It is not intended to guide clinical decision-making in specific cases.[3, 4, 5, 6, 7]
Table. Typical Presentation of the Most Commonly Encountered Metals and Their Treatment
The pathophysiology of the heavy metal toxidromes remains relatively constant. For the most part, heavy metals bind to oxygen, nitrogen, and sulfhydryl groups in proteins, resulting in alterations of enzymatic activity. This affinity of metal species for sulfhydryl groups serves a protective role in heavy metal homeostasis as well.
Increased synthesis of metal-binding proteins in response to elevated levels of a number of metals is the body's primary defense against poisoning. For example, the metalloproteins are induced by many metals. These molecules are rich in thiol ligands, which allow high-affinity binding with cadmium, copper, silver, and zinc, among other elements. Other proteins involved in heavy metal transport and excretion through the formation of ligands are ferritin, transferrin, albumin, and hemoglobin.
Although ligand formation is the basis for much of the transport of heavy metals throughout the body, some metals may compete with ionized species such as calcium and zinc to move through membrane channels in the free ionic form. For example, lead follows calcium pathways in the body, so hence its deposition in bone and gingivae. Thallium is taken up into cells like potassium because of their similar ionic radii.
Nearly all organ systems are involved in heavy metal toxicity; however, the most commonly involved organ systems include the central nervous system (CNS), peripheral nervous system (PNS), and the gastrointestinal, hematopoietic, renal, and cardiovascular (CV) systems. To a lesser extent, lead toxicity involves the musculoskeletal and reproductive systems. The organ systems affected and the severity of the toxicity vary with the particular heavy metal involved, the chronicity and extent of the exposure, and the age of the individual.
A literature review by Giulioni et al indicated that heavy metal exposure is strongly associated with male infertility. According to the evidence, sperm concentration, motility, and morphology are negatively impacted by lead exposure, for the most part via oxidative stress and enzymatic inhibition. Cadmium exposure can produce sperm abnormalities through disruption of the blood-testis barrier and acrosomal function, while oxidative stress, apoptosis, and damage to sperm motility have been associated with arsenic exposure.[8]
In 2023, according to the 41st Annual Report of the National Poison Data System (NPDS) from America's Poison Centers, there were 7905 single-substance exposures to heavy metals (not including iron or arsenic-including pesticides). Of those, 2348 were reported in children aged 5 years or younger, 1013 were reported in children aged 6-19, and 3599 were reported in persons aged 20 years or older.[9]
Lead
Within the United States, lead remains the most frequently encountered toxic metal, owing to long-term exposure. In children, exposure has been shown to be a result of living in houses that contain lead paint. Between 1998 and 1999, “either an interior lead dust hazard or an interior deteriorated lead-based paint hazard” occurred in the homes of 22% of US children aged 0-5 years, with this proportion having declined to 15% in 2005-2006.[10]
Evidence has shown that lead blood levels of less than 10 μg/dL have adverse neurodevelopmental outcomes in children younger than 5 years.[11] According to the US Centers for Disease Control and Prevention (CDC), an estimated 500,000 US children aged 1-5 years have blood lead levels of 3.5 μg/dL or higher, with 3.5 μg/dL being the level at which the CDC recommends that public health actions be initiated for youngsters in this age group.[12, 13]
In children aged 1-5 years, the median blood lead level fell from 15 µg/dL in 1976-1980 to 0.6 µg/dL in 2017 to March 2020, a 96% reduction. The largest declines in blood lead levels corresponded with the US Environmental Protection Agency phasing out leaded gasoline from 1973-1995.[10]
Lead exposure in the adult population is more commonly occupational, namely in mining, manufacturing, and construction. Overall, the national prevalence rate of blood lead levels of 10 μg/dL or greater in employed adults declined from 26.6 per 100,000 in 2010 (among 37 states) to 20.4 in 2013 (among 29 reporting states). In 2013, of the 4547 adults with blood lead levels of 25 μg/dL or greater who had a known lead exposure history, 93.7% had occupational exposure[14]
In 2023, according to the NPDS, there were 2349 single-substance exposures to lead. This included 1214 reported in children aged 5 years or younger, 283 reported in children aged 6-19 years, and 653 in persons aged 20 years or older.[9]
Arsenic
Exposure to arsenic within the United States can occur through many routes. It has been used with both criminal and suicidal intent as an agent to poison individuals or groups.[15] Medications used to treat disease, such as the chemotherapeutic agent arsenic trioxide, are iatrogenic sources. Industrial exposure to the waste products of smelting plants is another potential source. Arsenic-containing pesticides are still used in some areas of the country, with its use mostly found in cotton fields.[16]
In 2023, according to the NPDS, there were 749 single-substance exposures to arsenic (excluding pesticides), including 557 reported in persons aged 20 years or older. There were also 12 single-substance exposures to arsenic-containing pesticides.[9]
Iron
Iron toxicity in the United states is largely the result of ingestion of iron tablets or multivitamins but can also be a result of blood transfusions. Iron ingestion is particularly hazardous for children who unintentionally ingest iron-containing tablets.[17] In adults, ingestion is largely intentional.
In 2023, according to the NPDS, there were 5780 single-substance exposures to iron and iron salts (not including iron-supplemented multivitamins). Of those, 2380 were reported in children aged 5 years or younger, 1017 were reported in children aged 6-19 years, and 2105 were reported in persons aged 20 years or older.[9]
Mercury
Mercury toxicity can occur through exposure to mercury in its pure elemental form, as an inorganic salt, or through organic mercury compounds. Toxicity to the pure elemental form stems largely from inhalation of mercury vapor as a result of occupational exposure, for example melting mercury-containing dental amalgam. Another common route is vacuuming spilled mercury from a broken thermometer. Exposure to the inorganic salts and organic compounds stems largely from ingestion.[18]
Industrial emissions of mercury have polluted fresh and coastal waters, leading to contamination of fish. This has raised public concerns about long-term exposure to mercury through the consumption of wild fish.[19]
In 2023, according to the NPDS, there were 872 single-substance exposures to elemental mercury (excluding thermometers). This included 49 reported in children aged 5 years or younger, 109 reported in children aged 6-19 years, and 530 reported in persons aged 20 years or older. Also that year there were 793 single-substance exposures to mercury-containing thermometers, including 117 reported in children aged 5 years or younger, 90 reported in children aged 6-19 years, and 390 reported in persons aged 20 years or older. In addition, there were 275 other single-substance mercury exposures in 2023, including 201 reported in persons aged 20 years or older.[9]
International
Heavy metal toxicity has emerged as a significant occupational hazard associated with electronics recycling in China and Southeast Asia. Much of the recycling industry there takes place within the informal sector, and the use of personal protective equipment (eg, respirators) is poorly regulated and uncommon.
Large-scale epidemics of lead poisoning were reported in China in 2009, involving more than 2000 children living near smelting plants and sparking riots.[20, 21] The true prevalence of lead poisoning in childhood worldwide is not well understood. Availability of leaded gasoline, paint, cosmetics, and piping in many lower income countries suggests that there is a significant if under-recognized burden of toxicity.
Studies of street dust in Chinese cities have found elevated levels of heavy metals in street dust. These have included cadmium, chromium, and arsenic posing potential risk of carcinogenicity.[22]
Chronic arsenic toxicity is epidemic in Bangladesh and contiguous areas of the Indian subcontinent, where arsenic is an important component of bedrock. As previously discussed, deep tube wells constructed to provide an alternative water source to bacteriologically suspect surface deposits frequently supply water with a high arsenic content, with major public health consequences for the region.
Race- and sex-related demographics
In the United States, a higher incidence of lead toxicity occurs in the African-American population because of delays in removing lead sources from the environment in lower socioeconomic areas.
Little or no difference in prevalence exists between the sexes. Occupations with heavy metal exposure that predominantly involve a particular sex are associated with higher rates of exposure in that sex.
Age
Several points are of concern in heavy metal toxicity with respect to age. Generally, children are more susceptible to the toxic effects of the heavy metals and are more prone to unintentional exposures.
Inorganic lead salts enter the body by way of ingestion or inhalation. For adults, only about 10% of the ingested dose is absorbed. In contrast, children may absorb as much as 50% of an ingested dose.
The percentage of absorbed lead is increased with deficiencies of iron, calcium, and zinc. It is also increased with a predominantly milk diet, possibly due to the high lipid content.
Children and infants are prone to developmental delays secondary to lead toxicity. One study found that blood lead concentrations obtained in children aged 6 years are more strongly associated with cognitive and behavior development than are blood lead concentrations measured in children aged 2 years.[23]
Metal toxicity is rarely encountered clinically and may be challenging to recognize. If untreated, acute exposures may progress to multiorgan failure and death or permanent organ damage. Chronic exposure to metals may present with nonspecific symptoms, but if it is not identified and the exposure is allowed to continue, permanent neurologic damage, organ failure, or cancer may develop.
Studies of a possible association of toxic metals and autism have yielded inconsistent results. Adams et al reported significantly higher average excretion levels of lead, tin, thallium, and antimony in 67 patients with autism spectrum disorder, compared with 50 neurotypical controls.[24]
Encephalopathy is a leading cause of mortality in patients with either acute or chronic heavy metal toxicity.
A history of exposure is the most critical aspect of diagnosing heavy metal toxicity. A complete history includes questions about potential occupational exposures, hobbies, recreational activities, and potential environmental exposure.
A complete dietary history should be taken, especially with regard to the ingestion of fish, seafood, and seaweed products, since these will frequently be implicated as dietary sources of organic (and relatively nontoxic) mercury, arsenic, or both. The timing of ingestion relative to the collection of urine samples is critical to interpreting the results.
Herbal medications and dietary supplements are also potential sources of heavy metal exposure. Many Ayurvedic and Chinese patent medicines contain heavy metals.
Most acute presentations of heavy metal toxicity involve industrial exposure.
The ingestion of nonfood items such as paint chips, toys, and ballistic devices has also been implicated as the source of metal exposure in several cases.
Retained lead shot may ultimately lead to toxicity as well, although generally the shot must be bathed in relatively acidic body fluid, such as peritoneal fluid, pleural fluid, cerebrospinal fluid, or synovial fluid, for significant absorption of metal ions to occur.
Argyria results from prolonged contact with or ingestion of silver salts. Argyria is characterized by gray to gray-black staining of the skin and mucous membranes produced by silver deposition. Silver may be deposited in the skin either from industrial exposure or as a result of medications containing silver salts.
The physical examination of patients with suspected metal toxicity should focus on the most commonly involved organ systems: the nervous, gastrointestinal, hematologic,[25] renal, and integumentary systems.
Nausea, persistent vomiting, diarrhea, and abdominal pain are the hallmark of most acute metal ingestions. Dehydration is common. Metal salts are generally corrosive.
Encephalopathy, cardiomyopathy, dysrhythmias, acute tubular necrosis, and metabolic acidosis are also commonly seen with acute, high-dose exposures to most metals.
Patients with chronic metal toxicity tend to have more prominent involvement of the central and peripheral nervous systems. However, encephalopathy and peripheral neuropathies may occur within a few hours to days of acute high-dose exposure.
A classic presentation of chronic metal exposure includes anemia, Mees lines (horizontal hypopigmented lines across all nails), and subtle neurologic findings. These findings should prompt suspicion of heavy metal toxicity in any patient regardless of the chief complaint.
Because lead toxicity is relatively common, any combination of gastrointestinal complaints, neurologic dysfunction, and anemia should prompt a search for lead toxicity.
The first priority in managing any patient with detectable serum lead is to determine the source of exposure and to remove the person from it. The finding of any elevated serum or urine metal concentration in an asymptomatic person should prompt a thorough dietary, occupational, and recreational history, and radiographs should be used where indicated to identify any source of ongoing exposure. Occupational or recreational histories in parents can also reveal a source of exposure for children.
Specific laboratory testing for metals should be undertaken when the likelihood of toxicity is significant, based on a history and/or symptoms consistent with excessive exposure. See the relevant articles, as follow, for more detailed recommendations regarding the most reliable testing measures for individual metal toxicity:
Lead Toxicity
Mercury Toxicity
Arsenic Toxicity
Iron Toxicity
When specific testing is indicated, samples should be sent in metal-free containers.
Hair analysis is not generally reliable and rarely indicated.
Patients should be instructed to abstain from seafood and seaweed products prior to testing for metals such as arsenic and mercury, since elevated concentrations in patients who have not abstained for at least several days to 1-2 weeks may simply reflect nontoxic organic forms ingested in the diet. Samples with elevated concentrations may also be sent for speciation for either of these metals to determine the relative contributions of organic forms versus inorganic forms.
The following standard laboratory determinations may help to make the diagnosis of heavy metal toxicity or help to gauge its severity:
Complete blood cell count (CBC) with peripheral smear - Findings may include basophilic stippling of the red blood cells (RBCs) on peripheral blood smears; basophilic stippling is not specific for lead toxicity and may be observed in arsenic toxicity, sideroblastic anemia, and thalassemia; the anemia of lead toxicity may be normocytic or microcytic
Abdominal radiographs are indicated in acute ingestions. Radio-opacities demonstrable in the gastrointestinal tract should be cleared by whole-bowel irrigation prior to instituting chelation therapy. Large, retained gastric foreign bodies (eg, bullets, shotgun cartridges, fishing sinkers, curtain weights) may cause lead toxicity and should be removed endoscopically if they do not pass, if serum lead concentrations are concerning or increasing, or if the patient becomes symptomatic.
Several reported cases of patients who have injected elemental mercury subcutaneously and developed mercury toxicity have been documented. Radiographs of the suspect areas showing large subcutaneous deposits of radio-opaque material were helpful in confirming the diagnosis and need for surgical intervention to limit the exposure.
A majority of asymptomatic children and adults with elevated lead levels can be safely managed solely by removing the source of exposure. Contact a medical toxicologist or the local poison control center for specific recommendations.
All cases of significantly elevated lead levels should be reported to the local health department. Report any industry- or workplace-related heavy metal toxicities to OSHA. Symptomatic patients with elevated metal concentrations should be treated more aggressively.
Arsenic is frequently used for homicidal or suicidal purposes. Thoroughly scrutinize all arsenic toxicity cases for evidence of such activity. Report all cases with possible homicidal association to the proper legal authorities before discharge. Patients with suspected suicidal intent should undergo psychiatric evaluation before discharge from the hospital.
Please refer to the relevant articles (see Arsenic Toxicity, Lead Toxicity, Mercury Toxicity, Iron Toxicity) or contact a medical toxicologist, for more specific recommendations.
Removal of the patient from the source of exposure is critical to limiting dose.
Treatment may include whole-bowel irrigation with polyethylene glycol electrolyte solution if radiographic studies show evidence of retained metal (toys, coins, paint chips) in the gastrointestinal tract.
Resuscitation
Good supportive care is critical. Ensure airway patency and protection, provide mechanical ventilation where necessary, correct dysrhythmias, replace fluid and electrolytes (significant fluid losses generally occur and require aggressive rehydration), and monitor and treat the sequelae of organ dysfunction.
Chelation
Chelation is rarely indicated in the emergent setting. A possible exception is lead encephalopathy. Consideration of chelation therapy for patients with suspected or confirmed metal exposures should be made in conjunction with a medical toxicologist or the local poison control center.
Contact a certified poison control center or medical toxicologist. Consult a gastroenterologist if the possibility of corrosive gastrointestinal effects is present.
If intentional ingestion or overdose is suspected, place the patient in a closely monitored unit, screen for co-ingestion of acetaminophen, and consult a medical toxicologist and psychiatrist.
Even small elemental mercury spills can result in extensive contamination. Thermostats should be turned to low settings in buildings where such spills have occurred, as heat increases elemental mercury volatilization. Vaporization occurs when spills are vacuumed or swept in an enclosed space, leading to further contamination and inhalation exposure. The proper authorities should be called to handle any spill with the appropriate mercury decontamination kits and procedures.[26]
The most important therapeutic maneuver in many cases of metal toxicity is to remove the source of exposure.
Chelation regimens have been shown to enhance elimination of some metals and thereby decrease the total body burden. See the table for a list of accepted chelation agents for specific metals.
There is evidence of no benefit from chelation therapy for several metals, and evidence of increased toxicity after chelation of several others (eg, selenium). Therefore, routine chelation of patients with heavy metal exposure cannot be recommended, and the decision to chelate should be made in conjunction with a medical toxicologist or local poison control center.
Clinical Context:
DOC in the treatment of lead, arsenic, and mercury toxicity. Administered via deep IM injection only, q4h, mixed in a peanut oil base. Chelates intracellular and extracellular lead and is excreted in urine and bile. First choice for patients with lead encephalopathy, in conjunction with EDTA. May be given to patients with renal failure.
Clinical Context:
Second-line for lead toxicity. Most effective when given early in the course of acute poisoning. Chelates only extracellular lead and may induce CNS toxicity if BAL therapy not initiated first. Begin therapy 4 h after BAL is given. Only given IV, and continuous infusion is recommended.
Not recommended with renal failure. Because of potential for renal toxicity, patient should be well hydrated. To prevent hypocalcemia, use only calcium disodium salt of EDTA for chelation in heavy metal toxicity.
What is heavy metal toxicity?How does exposure to heavy metal occur?What are the signs and symptoms of heavy metal toxicity?What is the pathophysiology of heavy metal toxicity?What is the US prevalence of heavy metal toxicity?What is the prevalence of lead toxicity in the US?What is the prevalence of arsenic toxicity in the US?What is the prevalence of iron toxicity in the US?What is the prevalence of mercury toxicity in the US?What is the global prevalence of heavy metal toxicity?What are the racial predilections of heavy metal toxicity?What are the sexual predilections of heavy metal toxicity?How does the prevalence of heavy metal toxicity vary by age?What is the prognosis for heavy metal toxicity?Which clinical history findings suggest heavy metal toxicity?Which physical findings are characteristic of heavy metal toxicity?Which conditions should be included in the differential diagnoses of heavy metal toxicity?What are the differential diagnoses for Heavy Metal Toxicity?How is the source of heavy metal toxicity identified?What is the role of lab testing in the diagnosis of heavy metal toxicity?Which standard lab tests are performed in the workup of heavy metal toxicity?What is the role of imaging studies in the workup of heavy metal toxicity?What is the role of ECG in the workup of heavy metal toxicity?How is heavy metal toxicity treated?When should intentional poisoning or suicide be suspected in heavy metal toxicity?What is included in the emergency department (ED) treatment of heavy metal toxicity?What is the role of chelation in the treatment of heavy metal toxicity?Which specialist consultations are beneficial to patients with heavy metal toxicity?Which medications are indicated in the treatment of heavy metal toxicity?
Adefris Adal, MD, MS, Clinical Assistant Instructor, Resident Physician, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center
Disclosure: Nothing to disclose.
Coauthor(s)
Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center
Disclosure: Nothing to disclose.
Specialty Editors
John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals
Disclosure: Nothing to disclose.
John G Benitez, MD, MPH, Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center
Disclosure: Nothing to disclose.
Chief Editor
Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center
Disclosure: Nothing to disclose.
Additional Contributors
Kamila K Padlewska, MD, PhD, Professor, Warsaw Academy of Cosmetics and Health Care; Chief Executive, Cosmetic-Medical Cooperative Izis, Poland
Disclosure: Nothing to disclose.
Mark Louden, MD, Assistant Professor of Clinical Medicine, Division of Emergency Medicine, Department of Medicine, University of Miami, Leonard M Miller School of Medicine
Disclosure: Nothing to disclose.
Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School
Disclosure: Nothing to disclose.
Acknowledgements
Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Samara Soghoian, MD, MA Clinical Assistant Professor of Emergency Medicine, New York University School of Medicine, Bellevue Hospital Center
Samara Soghoian, MD, MA is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
References
Sue YJ. Mercury. In: Hoffman RS, Howland MA, Lewin NA, Nelson LS, Goldfrank LR, eds. Goldfrank's Toxicologic Emergencies. 10th ed. New York, NY: McGraw-Hill Education; 2015. 1334-1344.
US Environmental Protection Agency. Key Findings of America’s Children and the Environment. EPA. Available at https://www.epa.gov/americaschildrenenvironment/key-findings-americas-children-and-environment. Accessed: April 21, 2025.
US Centers for Disease Control and Prevention. About Childhood Lead Poisoning Prevention. CDC. Available at https://www.cdc.gov/lead-prevention/about/index.html. March 13, 2025; Accessed: April 21, 2025.
Sharp D. In Maine, pains linger for arsenic poisoning survivors. LA Times. June 15, 2008. Available at http://articles.latimes.com/2008/jun/15/news/adna-arsenic15
