Children Playing With Poison: Arsenic Exposure From CCA-treated Wood

Deborah L. Baptist,RN, BSN; Nan S Leslie, PhD,RN,WHNP


Journal for Nurse Practitioners. 2008;4(1):48-53. 

In This Article

Implications of Inorganic Arsenic Exposure for Young Children

In general, inorganic arsenic exposure can be classified as either acute poisoning or chronic exposure; however, evidence-based guidelines specifically addressing the care of children exposed to arsenic are currently unavailable. This is a gap in both clinical knowledge and the literature that should be addressed. If arsenic exposure is suspected in a child, the nurse practitioner may be aided in establishing a diagnosis and identifying a source of exposure by incorporating environmental history questions in the documentation of the child's health history. Environmental history questions include diet, smoking history of the child's parents or primary caregivers, location of the family's home (near smelters, other industry, a hazardous waste site), family hobbies such as gardening (exposure to pesticides and herbicides), use of wood-burning stoves and fireplaces in the home, the family's source of drinking water, home heating methods,[8] play activities of the child (outside in the dirt, in areas with CCA-treated wooden structures), and pica behavior (the gastrointestinal tract is the most common route of ingestion in children).[6] The Agency for Toxic Substances and Disease Registry and the National Institute for Occupational and Safety Health have developed an environmental history form for collection of information about exposure to environmental toxins that the nurse practitioner can modify for use when obtaining the child's medical history. This form is available at[9]

Physical manifestations of arsenic poisoning differ based on whether exposure to arsenic has been acute or chronic. Acute intoxication manifests itself within minutes to hours after exposure and includes a broad range of symptoms involving several body systems.[8] Initially, the primary signs of acute arsenic poisoning are severe hematemesis and diarrhea, which generally occur between 30 minutes to 4 hours after acute exposure. These signs may be due to the irritant effect that arsenic has on the gastric mucosa.[8,10] Other symptoms may include burning lips, abdominal pain and nausea, a garlic smell to breath, and intense thirst.[1,6,11] Hypotension, cardiac arrhythmias, acute renal failure, dizziness, delirium, seizures, and peripheral neuropathy resembling Guillain-Barré are among the symptoms that follow hematemesis and diarrhea.[1,6,10,11] Within 1 to 3 days, liver and renal damage and death can occur.[6] For those who survive the initial effects of acute poisoning, sequelae may include peripheral neuropathy, bone marrow suppression, painful dysesthesias or tactile hallucinations, nail changes such as Mees lines, new or ongoing encephalopathy, and cardiac arrhythmias.[11]

Diagnosing acute arsenic poisoning early in its course can be challenging because presenting symptoms often depend on the route of exposure, chemical form and dose of arsenic ingested, duration of exposure, age of person exposed, and nutritional status.[8,12] Furthermore, the source of arsenic exposure may not always be known.[8] Complete blood count, serum electrolytes, urinalysis, liver enzymes, and kidney function tests should be done to establish a baseline. Collection of a 24-hour urine specimen to determine urinary arsenic measurement is of great importance because this specimen is the most reliable measurement of acute arsenic exposure. It is necessary to ascertain whether the patient has ingested seafood in the 2 to 5 days before specimen collection. Seafood can contain organic arsenic, which can increase arsenic levels in the urine specimen.[8] The organic arsenicals found in seafood are not considered toxic but may contribute to high urinary arsenic levels.[1,6,8]

A documented history of exposure or an elevated concentration of arsenic in nails or hair can aid in the diagnosis of acute arsenic poisoning.[8] Hair and nail specimens may have higher arsenic concentrations because of external contamination; therefore, washing these samples before analysis is recommended.[8,12] Blood arsenic levels can also be measured to aid in the diagnosis of arsenic poisoning. However, given that the half-life in the blood of arsenic is only 1 to 2 hours, a normal level may be present even in the case of acute exposure.[8]

Initial management of acute arsenic intoxication includes fluid infusion, cardiovascular support, and gut decontamination.[8,10] Chelating agents are used in an effort to bind arsenic in an attempt to limit the full effects of arsenic toxicity.[8,10] The primary chelation agent used in the United States for acute arsenic poisoning is dimercaprol (BAL). Other chelating agents include succimer (DMSA, Chemet) and Unithiol (2,3-dimercapto-1-propanesulfonic acid, or DPMS). Both agents are water-soluble analogs of BAL that can be given orally. DPMS can also be given by intravenous infusion or intramuscular injection.[10]

Chronic exposure to inorganic arsenic (also known as arsenicosis)[13] occurs primarily in occupational and environmental settings.[1] In instances of chronic exposure symptoms may not be apparent for at least 5 years. Factors such as genetics, age, metabolism, diet, and overall health have an influence on the onset of symptoms.[6] Symptoms of chronic exposure include generalized fatigue, peripheral neuropathy, vascular and hematologic disorders, muscle tenderness, and elevated liver transaminases indicative of hepatic manifestations of arsenic toxicity such as liver cancer and fatty degeneration of the liver.[6,8,14] Skin changes such as hyperpigmentation and hyperkeratosis also occur and are the most common outward sign of chronic exposure.[13] Chronic exposure has been associated with an increased prevalence of cancer,[1] and several agencies, including the Department of Health and Human Services, have classified inorganic arsenic as a known human carcinogen.[15] Moreover, evidence suggests that patients with nonmalignant skin lesions related to arsenic exposure may be at greater risk of cancer, especially skin cancers.[13] Diagnosis for chronic exposure includes documentation of exposure, a 24-hour urine collection, and analysis of arsenic levels in hair and nails.[6,8]

Although the symptoms of both acute and chronic inorganic arsenic exposure may be similar in children and adults, children might be more susceptible to toxic effects because of their developmental and physiological differences.[1,14] Growth during childhood is a systematic process with body systems maturing at different rates and exhibiting critical periods when the child is more vulnerable to positive and negative stimuli.[16] For example, neurologic development continues for several years after a child is born, with the growth of glial cells and myelinization of axons. As a result, there are times when a child's developing brain is at increased susceptibility to toxic interference that would not affect a mature brain.[17]

Physiologically, young children are potentially at risk of increased morbidity from arsenic exposure based on differences in pharmacokinetics such as increased absorption rates and decreased efficiency in detoxification of inorganic arsenic into its metabolites. Decreased detoxification efficiency means that children are exposed to arsenic for a longer period of time after it is ingested.[18] In addition, young children may receive higher doses of toxins per unit body weight, possibly because of a higher intake by modes such as arsenic-contaminated water.[14] Consequently, "on a per-unit-body-weight basis, even if children had the same sensitivity as adults, children could have a greater prevalence of health effects because of their higher daily dose."[14](p105) Moreover, research into the biotransformation of arsenic has produced evidence of an area in arsenic metabolism found only in children whereby there is a genetic association with urinary arsenic metabolites.[19] Thus, based on the current data, one may extrapolate that prevalence among children will be greater.

A desire to better understand the effects of arsenic exposure in the context of the developmental and physiologic differences inherent between children and adults has prompted researchers to examine the relation between these variables and several health outcomes in children such as performance on intellectual function,[17] immune system integrity as a function of immunosurveillance against tumor cells,[20] and the development of peripheral neuropathy.[21] Results from each of these studies were suggestive of a link between arsenic exposure in children and the subsequent development of disease. These results point to the need for health care workers to take action to limit children's exposure to the various sources of inorganic arsenic.


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