Suspected Chronic Organochlorine Pesticide Poisoning

Abstract

Background. A woman presented with complaints of fatigue and a history of childhood pesticide exposure. Problem. A diagnosis of chronic pesticide poisoning is challenging, given its nonspecific presentation and lack of reliable laboratory confirmation. Demographic facts. A 42-yr-old Caucasian woman presented to her physician with complaints of anxiety, fatigue, and depression. Medical history included idiopathic thrombocytic purpura (ITP) and cholelithiasis. Surgical history included a splenectomy for ITP and a cholecystectomy. There had been a high incidence of cancer in her family. No history of acute pesticide poisoning by the patient or other family members was reported. Setting/exposure location. As a child, the patient had routinely played in basins used for mixing pesticides on her family’s farm. Type of chemical. The patient had experienced chronic childhood dermal exposure to organochlorine pesticides. Results. The results of physical examination were within normal limits. Objective measurements. Serum electrolytes, hematologic parameters, and liver and kidney profiles were within normal limits. Laboratory findings were negative for systemic lupus erythematosus. A serum pesticide panel demonstrated trace amounts (i.e., greater than laboratory reference level) of 1, l -dichloro-2,2-bis-(p dichlorodipheny1)-ethylene (p,pDDE). Imaging. Normal chest and pelvic radiographs were obtained. Summary. The use of pesticides for agriculture contributes its share to pesticide exposures. Although much is known about acute exposure, little is known about chronic Both dichlorodiphenyltrichloroethane (DDT) and DDE are bound extensively to plasma proteins. The primary sites of toxicity are the central and peripheral nervous systems, with particular toxicity to the cerebellum and motor cortex. Although its chronic toxicity is not understood completely, DDT prolongs neuronal repolarization by disrupting sodium, potassium, and calcium-adenosine triphosphatases-in addition to calmodulin-thus resulting in prolonged depolarization. Symptoms from organochlorine exposure are often nonspecific and include nausea, vomiting, fatigue, anorexia, tremor, parasthesias, and other neurotoxic effect^.^ Organochlorine pesticides are noted for their long half-li~es.~ DDT is transformed slowly in mammalian systems. Furthermore, DDT and its metabolites are not very soluble in water and are highly soluble in Once absorbed, the metabolites are stored in adipose tissue and are transformed slowly by cytochrome P450dependent monooxygenases into bis(dichlorodipheny1) acetic acid and are subsequently excreted in urine. Storage in adipose tissue may be protective because pesticide levels in the brain are minimized.8 Concentrations of DDT and its metabolites within adipose tissue may exist at levels that are several hundred times those that exist in blood, perhaps calling into question the usefulness of serum pesticide panels for the detection of chronic poisoning.’ Analysis of organochlorine concentrations in tissue may be more accurate on a lipid-weight basis inasmuch as serum analysis may not be indicative of adipose ~on ten t .~ The presence of such pesticides within adipose tissue may set the stage for a cycle of acute increases in the serum level of pesticide resulting from breakdown of adipose tissue and subsequent pesticide release into the blood. This fact is supported by studies in which starvation of DDT-poisoned