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

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. "Case Study 29: Pentachlorophenol 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

tachypneic from excess pulmonary secretions and bronchospasm; a high temperature is atypical. If necessary, a red blood cell (RBC) count and a plasma cholinesterase level can be obtained. However, even if the cholinesterase results are within normal range, tests should be repeated in a few days to determine the change in values. (See Case Studies in Environmental Medicine: Cholinesterase-Inhibiting Pesticide Toxicity.)

Dinitrophenol is present in the insecticide Dinoseb.* Like pentachlorophenol, the pathophysiology of dinitrophenol also involves the uncoupling of oxidative phosphorylation; therefore, poisoning due to these two chemicals would cause similar symptoms. A thorough and careful history would be necessary to exclude the possibility of current contact with the insecticide. Being a botanist by profession and a gardener by hobby, the patient should have an awareness of insecticides he has used, especially those used over a long period of time. Another feature that distinguishes the two chemicals is the staining property. Yellow stains appear on the skin after dermal contact with dinitrophenol; no staining occurs with pentachlorophenol.

  1. To confirm your suspicion of a PCP exposure, you could recommend that the patient’s home be tested for airborne levels of PCP. Walls in a room treated with PCP release the chemical into the air, with concentrations reaching 1 nanogram per cubic meter (ng/m3) of air on the first day after treatment and 160 ng/m3 on the fourth day. PCP is no longer used in the treatment of wood products intended for use in the interior of residences, but many log cabins and older homes were built before enforcement of regulations that restricted PCP use.

    Biologic tests on the patient could also confirm your suspicion. If the exposure is ongoing, urine and blood levels of PCP would be elevated (see Laboratory Tests, page 10).

  2. If the patient has PCP poisoning, further laboratory tests could be performed to evaluate the hepatic, renal, and hematologic systems.

  3. Phenol could easily be confused with PCP, especially because they have both been used as disinfectants and preservatives. Phenol is found in many over-the-counter and prescription medications (e.g., ointments, ear and nose drops, cold-sore lotions, mouthwashes, lozenges, gargles, toothache medications, and analgesic rubs) at concentrations of 0.5% to 1.5%. However, the action of phenol and PCP in the body is quite different. PCP primarily acts to uncouple oxidative phosphorylation with resultant hyperthermia. Phenol is primarily a caustic, causing protein denaturation and coagulation.

  4. After initiating acute care (i.e., establishing an intravenous line, administering antibiotics, and instituting cooling treatments), the priority in treating this patient is to prevent further exposure to PCP. This can be accomplished by relocating the patient or by decreasing the level of PCP inside the log cabin. Ensuring adequate ventilation indoors would help, and application of a barrier wood finish such as clear polyurethane to the indoor surfaces of the log cabin would decrease volatilization of the PCP.

*  

Use of trade names is for identification only and does not imply endorsement by the U.S. Department of Health and Human Services or the Public Health Service.

Page
557
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)