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

Page
515
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Environmental Medicine: Integrating a Missing Element into Medical Education

diovascular stress in the patient with coronary heart disease to be dangerous.912

The elevated COHb level resulting from CH2Cl2 exposure has a biological half-life twice that of COHb produced from exposure to CO. This occurs because the absorbed CH2Cl2 is released slowly from storage in body tissues and then is metabolized to CO over a protracted period of time. Thus, because it is so sustained following exposure, the cardiovascular stress produced by elevated COHb levels, derived from CH2Cl2 metabolism, is greater than that resulting from equally high COHb levels derived from CO. The addition of methanol to paint-remover formulations extends the biologic half-life of COHb derived from CH2Cl2 (Figure), further prolonging the period of cardiovascular stress.

The ethical responsibility for informing the public about the potential hazard of CH2Cl2 in paint removers lies with the manufacturer who is obliged to market a product that can be used safely. This is the purpose of the label. It should warn the susceptible segment of the population of the CO hazard. The manufacturers of paint removers have been cognizant of the problem since 1972, yet product labels make no mention of CO. Only one manufacturer of paint removers has acted positively. This Racine, Wis, firm has withdrawn its product from the market.

The legal responsibility for protecting the public currently rests with the Consumer Product Safety Commission. It has remained mute, as did the governmental agency originally responsible, the Environmental Protection Agency, when in 1971 the CH2Cl2 hazard was formally called to its attention.

The medical responsibility for protecting patients unable to tolerate the cardiovascular stress of elevated COHb levels must rest with the physician until the general public is made aware of the CH2Cl2 hazard and all paint-remover formulations are appropriately labeled. This is a critical duty because one sixth of the 180 million kg of CH2Cl2 produced in the United States is being consumed in the rapidly expanding paint-remover market.13

This investigation was supported in part by contract HSM-99–72–84 from the National Institute of Occupational Safety and Health.

Anthony Wu, PhD, and Sally A.Graff provided technical assistance.

References

1. Stewart RD, Fisher TN, Hosko MJ, et al: Carboxyhemoglobin elevation after exposure to dichloromethane. Science 176:295–296, 1972.

2. Stewart RD, Fisher TN, Hosko MJ, et al: Experimental human exposure to methylene chloride. Arch Environ Health 25:324–348, 1972.

3. Kubic VL, Anders MW, Engel RR, et al: Metabolism of dihalomethanes to carbon monoxide. Drug Metabolism and Disposition. 2:53–57, 1974.

4. Ratney RS, Wegman DH, Elkins HB: In vivo conversion of methylene chloride to carbon monoxide. Arch Environ Health 28:223–226, 1974.

5. Fodor GG, Prajsnar D, Schlipkoter H: Endogenous CO formation by incorporated halogenated hydrocarbons of the methane series. Staub Reinhaltung der Luft 33:260–261, 1973.

6. DiVincenzo GD, Hamilton ML: Fate and disposition of methylene chloride in the rat. Toxicol Appl Pharmacol 32:385–393, 1975.

7. Stewart RD, Hake CL, Forster HV, et al: Methylene chloride: development of a biologic standard for the industrial worker by breath analysis, report No. NIOSH-MCOW-ENVM-MC-74–9. Cincinnati, National Institute of Occupational Safety and Health, 1974.

8. Stewart RD, Baretta ED, Platte LR, et al: Carboxyhemoglobin levels in american blood donors. JAMA 229:1187–1195, 1974.

9. Aronow WS, Harris CN, Isbell MW, et al: Effect of freeway travel on angina pectoris. Ann Intern Med 77:669–676, 1972.

10. Aronow WS, Isbell MW: Carbon monoxide effect on exercise-induced angina pectoris . Ann Intern Med 79:392–395, 1973.

11. Anderson EW, Andelman RJ, Strauch JM, et al: Effect of low-level carbon monoxide exposure on onset and duration of angina pectoris: A study in ten patients with ischemic heart disease. Ann Intern Med 79:46–50, 1973.

12. Scharf SM, Thames MD, Sargent RK: Transmural myocardial infarction after exposure to carbon monoxide in coronary artery disease: Report of a case. N Engl J Med 291:85–86, 1974.

13. Paint-remover sales take off. Chemical Week 65–66, Oct 20, 1971.

Page
515
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)