PESTICIDE EXPOSURE AND DEMENTIA

To The Editor: A 76-year-old Caucasian male presented with a 3-year history of progressive cognitive loss and gait disturbance. Prior medical history included hypertension and mitral valve prolapse. The patient self-reported short-term memory deficit, micrographia, and paraphasias with unintended words and reversing letters. His son confirmed that the patient had required increasing help with finances and had recent and significant diminution of his work productivity. In addition, the patient had developed physical complaints; he had difficulty fastening buttons and cuff links and getting up from sitting position, and his gait had become unsteady. At the request of his children, he stopped driving. He began isolating himself, finding it difficult to socialize because he “misinterpreted what others said.” The patient had received a bachelor's degree from Dartmouth University and had become a successful real estate developer. He was an avid gardener and, for the previous 30 years, had spent at least 8 hours every day in his poorly ventilated greenhouse. He was keen on using multiple pesticides (including Sevin or Carbaryl, Sunspray oil, Proxo180SP, Orthene, Malathion, Kelthane, Dylox, Dursban, Dithane, Diaznon, Carbamate, and Chlordane) and never protected himself with use of mask, gown, or gloves, despite written warning on the containers. Indeed, his family commented on the putrid smell of the patient's clothes at dinnertime. After dinner, the patient would return to his greenhouse and refuse to bathe when he returned home at midnight. On physical examination, at the time of admission, his vital signs were within normal limits. Heart and lung examination were unremarkable. Mini-Mental State Examination score was 25 out of 30. Motor and sensory examination was normal. He had decreased rapid alternating movements bilaterally. His gait was narrow based with no arm swing. There was marked truncal instability with retropulsion. He was found to have minimal cogwheel rigidity, bradykinesia, and a stooped posture. He underwent neuropsychological testing. The performance corresponded to age-appropriate functioning. Memory recall, measured using the Bender recall, reflected the patient's impairment of short-term memory. There was evidence of memory loss for recent events such as forgetting telephone numbers, conversations, and events of the day. On the Wechsler-Adult Intelligence Scale—Revised subtests, immediate memory span was fair, as indicated using digits forward and backwards, and he had excellent abstract thinking, as indicated using similarities and interpretation of proverbs. Repeat neuropsychological evaluation, a year later, confirmed apraxia and significant errors in frontal system tasks with high levels of intrusion and perseverations; his fluency was at borderline level. The evaluation suggested dementia, with high premorbid function and education level. Laboratory tests were within normal limits. Spinal tap was negative. Magnetic resonance imaging of the brain, performed in April 1999, showed patchy increased signal intensity in mid pons. An electroencephalogram performed in June 1999 was unremarkable. A cerebral angiogram was negative. During the course of his 5-year illness, motor symptoms progressed more rapidly than cognitive losses. He became increasingly dependent, requiring assistance in activities of daily living. After the cerebral angiogram, in 1999, he suffered a grand mal seizure. Thereafter, he became increasingly lethargic and eventually virtually catatonic. On autopsy, the brain showed innumerable demyelinating foci affecting subcortical white matter and deeper layers of cerebral cortex of unknown etiology. There was no evidence of lesions characteristic of Alzheimer or Parkinson's disease or multiple sclerosis. (Figure 1) Luxol fast blue stain showing myelin pallor and lipid-laden macrophages. There was no evidence of lesions characteristic of Alzheimer's disease. More than 1,000 chemical compounds and biological agents are used around the world as insecticides. The controversy over whether neurobehavioral effects persist after recovery from organophosphate poisoning has continued for 30 years. There have been reports of deficits in memory and abstraction on test batteries. Workers who apply organophosphates but have not truly suffered poisoning episodes have shown subclinical neurobehavioral deficits.1 Little is known about the adverse effects of pesticides on the development of cognitive dysfunction. Case control data from the Canadian Study of Health and Aging show an association between occupational exposure to pesticides and dementia.2 The only other study to investigate this relationship is the Maastricht Aging Study, which showed occupational exposure to pesticides to be related to progressive worsening of cognitive testing in cross-sectional and longitudinal analyses.3 Gait impairment preceding cognitive impairment and progressing at a faster pace supports pesticide exposure as the likely etiology for the dementia in this elderly patient. As dementing illnesses receive more attention in our aging society, it would be beneficial to increase consumer awareness of the risks of pesticide use in leisure activities such as gardening.

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