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

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. "Case Study 13: Dioxin Toxicity." Environmental Medicine: Integrating a Missing Element into Medical Education. Washington, DC: The National Academies Press, 1995.

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Environmental Medicine: Integrating a Missing Element into Medical Education
Answers to Pretest and Challenge Questions

Pretest is found on page 1. Challenge questions begin on page 4.

  1. A call to the medical director or the health and safety department of the utility company should provide the answer to the type of herbicide used and its contents. Dioxin-containing herbicides are not likely to have been used in this case since they are no longer being manufactured in the United States.

  2. The patient could be at increased risk of dioxin exposure because he is living in an area of possible soil contamination. Normal hand-to-mouth activity of children can result in ingestion of contaminated soil. Because of the child’s age, it is unlikely that he has pica (the abnormal ingestion of nonfood items, commonly found in children aged 2 to 6 years), which could significantly increase the boy’s soil intake. Children consume large quantities of milk, which can be a source of dioxins if it comes from cows grazing on contaminated vegetation. The small amount of dioxin leached from paper milk cartons is negligible.

    If the family raises its own foodstuffs and if the previous owner of the farm used contaminated herbicides that still may be present in the soil, the current root crops could contain small amounts of dioxins. (Evidence for translocation of dioxins is sparse and inconclusive.) Even though production of herbicides such as 2,4,5-T were discontinued in the United States in 1976, the half-life of dioxin in soil may be 10 years or more, depending on the type of soil. However, this source is likely to be insignificant in terms of health risk.

  3. Even if the herbicide did contain dioxins, these compounds photodegrade rapidly, resulting in a half-life on vegetation of several hours and several days in air. The half-life of dioxins in surface soil is 1 to 3 years, while dioxins beneath the soil surface could have a half-life of 10 years or more. However, dermal absorption from TCDD-contaminated soil is less than 5%. If the children do not ingest the soil, the danger is minimal.

  4. The primary human health effects of dioxin exposure are chloracne, and secondarily, hepatomegaly, elevated liver enzyme levels, and possibly peripheral neuropathy (subclinical changes in nerve conduction velocity).

  5. Although dioxins are proven carcinogens in some animals, their carcinogenic effect in humans requires further study. Even if the herbicide contained TCDD, the risk of cancer for this patient is likely to be insignificant from a one-time exposure that caused no acute effects.

  6. Some of the issues you might address in obtaining the medical history are the following: the type and extent of farming carried on by the family; their lifestyle before coming to this farm; dietary habits, including present or past pica in the child.

  7. During the physical examination, the skin should be carefully examined for evidence of rash, particularly chloracne. Chloracne is a papular, sometimes pustular, lesion located principally on the upper facial areas. The onset of chloracne is not acute, as was the rash described in the case study. In addition, an examination of the abdomen should be conducted, looking for hepatomegaly or hepatic tenderness. A neurologic examination might also be undertaken, with a mental status examination to assess more subtle CNS effects.

  8. Analytical tests for TCDD (adipose tissue, serum) are very specialized and expensive, and generally are not recommended in clinical practice, especially since interpretation in individual cases is difficult. Dioxins may be associated with hepatotoxicity, and liver function tests would be appropriate if there has been known exposure to dioxin.

  9. Symptoms associated with acute exposure to dioxin-containing substances include skin and mucous membrane irritation, headache, fatigue, abdominal pain, memory and personality changes, and insomnia. However, such symptoms are nonspecific and may have other etiologies.

  10. The cause of the child’s rash is more likely to be poison ivy, which is common in the wooded areas of the Midwest, an allergy, or exposure to some chemical other than a dioxin. This conclusion is suggested by the acute onset of the rash, its appearance, and its burning nature. Referral to a dermatologist may be warranted if standard measures of treating the rash are not efficacious. The child’s symptoms of headache and stomachache may be a result of such factors as stress, food intolerance, or viral infection. If symptoms do not resolve within a day or two, further investigation may be warranted.

Page
348
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)