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Environmental Medicine: Integrating a Missing Element into Medical Education (1995)
Institute of Medicine (IOM)

Page
446
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Environmental Medicine: Integrating a Missing Element into Medical Education

FIGURE 1. Typical Changes in the Skin of the Hands. The skin is scaly and has a pink color.

New Hampshire. A urinary level of 0.09 mg. of mercury per liter, with a urinary specific gravity of 1.004, confirmed the clinical diagnosis. (Normally, no mercury is found in the urine; the hazard level for industrial workers is 0.20 mg. of mercury per liter, with a specific gravity of 1.024.) The patient was referred to the Massachusetts General Hospital for further evaluation and treatment.

Upon admission he had the typical symptoms and signs of acrodynia. These included complaints of pain in the abdomen, extremities and joints, irritability, swinging changes of mood, a marked degree of photophobia, increased perspiration, desquamation and pink color of the hands (Fig. 1), hypertension, hypotonia, salaam positioning (Fig. 2), anorexia and insomnia. His weight was 17 kg., and the body-surface area 0.7 square meter.

Laboratory studies included a normal hemogram and normal electrolytes, blood urea nitrogen, albumin, globulin, serum glutamic oxalacetic transaminase and alkaline phosphatase. An L.E.-cell preparation was negative.

Lumbar puncture revealed a normal spinal-fluid pressure, protein, sugar and colloidal-gold curve. An electroencephalogram was interpreted as being a moderately abnormal waking record because of asymmetry of the 2 sides. There was poor driving and response to strobe on the left. A repeat electroencephalogram 3 days later revealed no marked change.

X-ray films of the skull, knees, shoulders and an intravenous urogram* were normal. X-ray study of the teeth revealed extensive caries involving the deciduous teeth, and several permanent teeth were loose.

Urinalysis was within normal limits. The urine contained trace amounts of lead, but no protein or arsenic. The creatinine clearances were 53 and 54 liters per day. The 24-hour urinary coproporphyrin excretion was normal. Catechol amine studies, done because of clinical signs of increased sympathetic activity, showed a urinary excretion of 3 microgm. of epinephrine and 79 microgm. of norepinephrine per 24 hours. The vanilmandelic acid excretion was 3.5 mg. per 24 hours.

FIGURE 2. Typical Posture Assumed by the Patient. He is burrowing his head into the pillow to blot out the light.

FIGURE 3. Response to N-acetyl-D,L-penicillamine (0= Normal, +=Slightly Abnormal, ++=Mildly Abnormal, +++=Moderately Abnormal, and ++++=Severely Abnormal, as Seen in Acrodynia).

Aliquots of twenty-four-hour urine collections were used for the mercury determinations. The average twenty-four-hour volume range was 500 to 800 ml.

Urine specimens were quantitatively analyzed for mercury throughout the course of the patient’s illness with the use of a modification of the Monkmon method.22 Samples of urine were cold digested with potassium permanganate and sulfuric acid to destroy the organic material. The excess potassium permanganate was bleached with hydroxylamine hydrochloride, and after adjustment to a pH of 6, the solution of the soluble divalent mercury was passed through a glass filter impregnated with cadmium sulfide. The mercury in solution was retained on the pad as a sulfide. The sulfide was then placed in a flask and heated. Evolved mercury was drawn through a General Electric Mercury Vapor Detector, and the readings plotted at 10-second intervals. Standard urines containing known amounts of mercury were treated in a similar manner, and the readings compared with that of the unknown solutions. (The method is very sensitive and is reproducible to less than 0.1 microgm. of mercury per aliquot.)

The patient was treated with N-acetyl-D,L-penicillamine,* 0.125 gm. given 4 times a day (30 mg. per kilogram of body weight per day). The urinary excretion of mercury is shown in Figure 3. The mercury levels of the urine samples rose with treatment, diminished upon discontinuation and were again elevated with the reinstitution of treatment. The daily clinical course, emphasizing change in blood pressure, frequency of abnormal posturing, photophobia and redness and desquamation of the hands, is charted in Figure 3. There was some increase of pain, a slight increase of erythema of the palms, more frequent salaam posturing and greater fluctuation of mood when therapy was discontinued.

With N-acetyl-D,L-penicillamine therapy the patient showed general improvement except for his behavior. This became progressively worse as evidenced by refusal to eat, lying on the floor, throwing away urine specimens and great fluctuation in mood. However, when he was informed of his impending discharge, his behavior became much improved. A follow-up electroencephalogram had reverted to normal.

At home his behavior again became a problem, necessitating readmission 11 days after discharge. He was given a 6-day course of N-acetyl-D,L-penicillamine. His behavior markedly improved although there was no significant increase in the urinary mercury excretion. After 8 days in the hospital he was discharged, and since this last discharge he has maintained his clinical improvement. Ten months later a urine sample contained 0.016 mg. of mercury per liter.

*  

Obtained from Dr. Alfred Bader, Aldrich Chemical Company, Milwaukee, Wisconsin.

Page
446
Front Matter (R1-R12)
Executive Summary (1-4)
1 Introduction (5-13)
2 Curriculum Content (14-21)
3 Implementation Strategies (22-43)
4 Changing Medical Education (44-51)
5 Concluding Remarks (52-53)
References (54-58)
Appendixes (59-60)
A: Taking an Exposure History (61-96)
B: Medical School Courses and Clerkships: Access Points for Integrating Environmental Medicine (97-120)
C: Case Studies in Environmental Medicine (121-138)
Case Study 1: Arsenic Toxicity (139-163)
Case Study 2: Seasonal Arsenic Exposure from Burning Chromium-Copper-Arsenate-Treated Wood (164-167)
Case Study 3: Asbestos Toxicity (168-188)
Case Study 4: Benzene Toxicity (189-207)
Case Study 5: Beryllium Toxicity (208-223)
Case Study 6: Cadmium Toxicity (224-243)
Case Study 7: Fetal Death Due to Nonlethal Maternal Carbon Monoxide Poisoning (244-248)
Case Study 8: Carbon Tetrachloride Toxicity (249-266)
Case Study 9: Chlordane Toxicity (267-288)
Case Study 10: Chronic Reactive Airway Disease Following Acute Chlorine Gas Exposure in an Asymptomatic Atopic Patient (289-290)
Case Study 11: Chromium Toxicity (291-311)
Case Study 12: Cyanide Toxicity (312-331)
Case Study 13: Dioxin Toxicity (332-348)
Case Study 14: Ethylene/Propylene Glycol Toxicity (349-371)
Case Study 15: Formalin Asthma in Hospital Staff (372-373)
Case Study 16: Gasoline Toxicity (374-394)
Case Study 17: Hantavirus Pulmonary Syndrome: A Clinical Description of 17 Patients with a Newly Recognized Disease (395-401)
Case Study 18: Lead Poisoning from Mobilization of Bone Stores During Thyrotoxicosis (402-409)
Case Study 19: Lead Toxicity (410-435)
Case Study 20: Legionaires' Disease: Description of an Epidemic of Pneumonia (436-444)
Case Study 21: Mercury in House Paint as a Cause of Acrodynia: Effect of Therapy with N-Acetyl-D, L-Penixillamine (445-449)
Case Study 22: Mercury Toxicity (450-472)
Case Study 23: Methanol Toxicity (473-492)
Case Study 24: Methylene Chloride Toxicity (493-511)
Case Study 25: Paint Remover Hazard (512-515)
Case Study 26: Fatal Outcome of Methemoglobinemia in an Infant (516-517)
Case Study 27: Nitrate/Nitrite Toxicity (518-537)
Case Study 28: An Outbreak of Nitrogen Dioxide-Induced Respiratory Illness Among Ice Hockey Players (538-541)
Case Study 29: Pentachlorophenol Toxicity (542-557)
Case Study 30: Aldicarb Poisoning: A Case Report with Prolonged Cholinesterase Inhibition and Improvement After Pralidoxime Therapy (558-561)
Case Study 31: Cholinesterase-Inhibiting Pesticide Toxicity (562-584)
Case Study 32: Infertility in Male Pesticide Workers (585-587)
Case Study 33: Pesticide Food Poisoning from Contaminated Watermelons in California, 1985 (588-595)
Case Study 34: Poisoning of an Urban Family Due to Misapplication of Household Organophosphate and Carbamate Pesticides (596-604)
Case Study 35: Polynuclear Aromatic Hydrocarbon (PAH) Toxicity (605-621)
Case Study 36: Polychlorinated Biphenyl (PCB) Toxicity (622-638)
Case Study 37: Ionizing Radiation (639-673)
Case Study 38: Radon Toxicity (674-694)
Case Study 39: Residential Radon Exposure and Lung Cancer in Sweden (695-700)
Case Study 40: Community Oubreaks of Asthma Associated with Inhalation of Soybean Dust (701-706)
Case Study 41: Tetrachloroethylene Toxicity (707-726)
Case Study 42: Toluene Toxicity (727-743)
Case Study 43: Occupational Asthma Due to Toluene Diisocyanate Among Velcro-like Tape Manufacturers (744-749)
Case Study 44: 1,1,1-Trichloroethane (750-766)
Case Study 45: Trimethyltin Encephalopathy (767-771)
Case Study 46: Trichloroethylene Toxicity (772-792)
Case Study 47: Vinyl Chloride Toxicity (793-811)
Case Study 48: Work-Related Disorders of the Neck and Upper Extremity (812-813)
Case Study 49: Contact Dermatitis in Surgeons from Methylmethacrylate Bone Cement (814-816)
Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions (817-861)
Case Study 51: Acoustic Trauma Caused by the Telephone: A Report of Two Cases (862-867)
Case Study 52: Behavioral and Audiologic Manifestations of Noise-Induced Hearing Loss (868-871)
Case Study 53: Reproductive and Developmental Hazards (872-892)
Case Study 54: Childhood Asthma and Indoor Enviromental Risk Factors (893-903)
Case Study 55: Populations at Risk From Particulate Air Pollution - United States, 1992 (904-908)
D: Resources: Agencies, Organizations, Services, REferences, and Tables of Environmental Health Hazards (909-970)
E: Committee and Staff Biographies (971-975)