Questions? Call 888-624-8373

HARDBACK + PDF
your price: $63.50
add to cart

HARDBACK
list:$54.00
Web:$48.60
add to cart

PDF BOOK
your price: $41.50
add to cart

PDF CHAPTERS
your price: $1.00
select

Rights & Permissions

topleft topright

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

Page
448
bottomleft bottomright

The following HTML text is provided to enhance online readability. Many aspects of typography translate only awkwardly to HTML. Please use the page image as the authoritative form to ensure accuracy.


Environmental Medicine: Integrating a Missing Element into Medical Education

dilatation of the hands, which normally follows heating of the trunk and legs, was absent. This capacity was regained with the use of tolazoline hydrochloride (Priscoline) and tetraethylammonium bromide. Farquhar et al.32 described increased urinary sympathin in 3 of 4 cases of acrodynia as compared with normal children. Cheek and his associates33,34 demonstrated that calomel potentiates the effect of epinephrine in the rat, and suggested that mercury potentiates sympathetic activity in acrodynia. Peterson and Laughmiller35 reported the relief of symptoms in 6 of 7 cases of acrodynia treated with tolazoline. Bower36 noted relief of all symptoms except for photophobia with sympatholytic drugs such as hexamethonium tartrate and pentolinium bromide; he confirmed the relief of arteriolar spasm in patients with acrodynia by these drugs. Ritzel, Berger and Roulet37 recently observed increased catechol amine excretion in a case of acrodynia. Now that better methods for the determinaton of urinary catechol amines are available, sympathetic activity in acrodynia should offer a field for fruitful investigation.

Another interesting and unique finding in this case is the apparent source of mercury in the house paint. The demonstration that potentially harmful levels of mercury could result from vaporization of these paints supports this conclusion. The patient’s home, household contents and surrounding areas were examined by both the New Hampshire Department of Health and ourselves. The only source of mercury that could be detected was found in the paint. The amount of mercury in the urine and the length of time during which it was excreted implies that the inhalation of mercury vapor by the patient occurred over a long period. The discovery of mercury in the paint and our studies of the continuing emission of mercury into the air surrounding the painted surfaces present a new and potentially common cause for mercury poisoning. One wonders if there may be patients with some of the more subtle signs and symptoms of acrodynia in whom this diagnosis is not being considered. The paint manufacturer’s responsibility is a matter of public-health interest. Mercury-containing paint should be labeled properly and should indicate the possible danger to children upon ingestion or exposure to the toxic vapors. These mercury-containing paints should be limited to outdoor use.

SUMMARY AND CONCLUSIONS

A case of acrodynia in a patient who had increased urinary excretion of mercury is presented. New methods for mercury analysis are described. The source of mercury was found in house paint, and the epidemiologic implications of this finding are discussed.

The patient was treated with N-acetyl-D,L-penicillamine, which markedly increased the urinary output of mercury.

The rationale for this form of therapy in acrodynia is presented and compared with previously reported therapeutic methods.

Increased excretion of catechol amines was found in the urine. The relation of this finding to theories of the pathogenesis of acrodynia is considered.

We are indebted to Dr. Douglas W.Walker of Laconia, New Hampshire, for referring this patient to our service and for assistance in the collection of essential data, to Drs. Harriet L.Hardy and John D.Crawford, of the Massachusetts General Hospital, for inspiration and guidance, to the New Hampshire State Department of Health for help and interest, to Mr. Frederick Viles, Jr., and Mr. Richard Chamberlin, of Massachusetts Institute of Technology, for aid in the mercury determinations and to Dr. Nathan B.Talbot, chief of the Children’s Service, Massachusetts General Hospital, for guidance and helpful suggestions in the preparation of the manuscript.

REFERENCES

1. Warkany, J., and Hubbard, D.M. Mercury in urine of children with acrodynia. Lancet 1:829, 1948.

2. Fanconi, G., and Botsztein, A. Die Feersche Krankheit (Akrodynie) und Quecksilbermedikation. Helvet. paediat. acta 3:264–271, 1948.

3. Andersen, D. Acrodynia caused by exposure to mercury. Acta paediat. 40(Supp. 83):123, 1951.

4. James, G.A. Mercury as cause of pink disease. Great Ormond St. J. 1:48–51, 1951.

5. Laplane, R., Fabiani, P., and Desarmenien, H. Acrodynie et mercure: à propos de neuf observations. Nourrison 39:235–247, 1951.

6. Warkany, J., and Hubbard, D.M. Adverse mercurial reactions in form of acrodynia and related conditions. Am. J. Dis. Child. 81: 335–373, 1951.

7. Holzel, A., and James, T. Mercury and pink disease. Lancet 1: 441–443, 1952.

8. Speirs, A.L. Further evidence of association between mercury and pink disease. Brit. M. J. 2:142, 1959.

9. Bivings, L., and Lewis, G. Acrodynia, new treatment with BAL. J. Pediat. 32:63–65, 1948.

10. Elmore, S.E. Ingestion of mercury as probable cause of acrodynia and its treatment with dimercaprol (BAL): report of 2 cases. Pediatrics 1:643–647, 1948.

11. Bivings, L. Acrodynia: summary of BAL therapy reports and case report of calomel disease. J. Pediat. 34:322–324, 1949.

12. Carithers. H.A. Mercury poisoning from calomel producing subacute acrodynia and its treatment with dimercaprol: report of case. Pediatrics 4:820–824, 1949.

13. Denys, P. Acrodynie, mercure et B.A.L. Acta paediat. belg. 4: 16–25, 1950.

14. Fischer, A.E., and Hodes, H.L. Subacute mercury poisoning (acrodynia) caused by protiodide of mercury: successful treatment with BAL . J. Pediat. 40:143–151, 1952.

15. Debre, R., Schapira, G., and Royer, S. Acrodynie et hydrargyrurie. Arch, franç. pédiat. 9:443–446, 1952.

16. McCoy, J.E., Carre, I.J., and Freeman, M. Controlled trial of edathamil calcium disodium in acrodynia. Pediatrics 25:304–308, 1960.

17. Launay, C., Fabiani, P., Grenet, P., Hadengue, A., and Radzievsky. Absorption massive et prolongée de calomel chez un enfant: etude de l’élimination urinaire du mercure. Arch, franç. pédiat. 7:75–79, 1950.

18. Bouineau, M. Quatre cas d’acrodynie traités par la pénicilline. Arch, franç. pédiat. 8:785, 1951.

19. Aposhian, H.V., and Aposhian, M.M. N-acetyl-DL-penicillamine, new oral protective agent against lethal effects of mercuric chloride. J. Pharmacol. & Exper. Therap. 126:131–135, 1959.

20. Aposhian, H.V. Penicillamine and its analogues: metabolic properties and oral activities against lethal effects of mercuric chloride. In Metal-Binding in Medicine. Edited by M.J.Seven. 400 pp. New York: Lippincott, 1960. Pp. 290–295.

21. Smith, A.D.M., and Miller, J.W. Treatment of inorganic mercury poisoning with N-acetyl-D,L-penicillamine. Lancet 1:640–642, 1961.

22. Monkmon, J.L., Maffett, P.A., and Doherty, T.F. Determination of mercury in air samples and biological materials. Am. Indust. Hyg. A. Quart. 17:418–420, 1956.

23. Zellweiger, H., and Wehrli, S. Der Quecksilbernachweis im Urin und seine Bedeutung für die Diagnose der Akrodynie. Helvet. paediat. acta 6:397–405, 1951.

24. Helmick, A.G. Symptomatology of acrodynia as basis for new line of investigation as to its etiology. Arch. Pediat. 44:405–410, 1927.

25. Warkany, J., and Hubbard, D.M. Acrodynia and mercury. J. Pediat. 42:365–386, 1953.

26. Feer, E. Eine eigenartige Neurose des vegetativen Systems beim Kleinkinde (Acrodynie, Erythrödem, Pink disease). Jahrb. f. Kinderh. 108:267–281, 1925.

27. Stolz, S. Cited in Woringer, P. L’acrodynie infantile. Rev. franç. de pédiat. 2:440–462, 1926.

28. Blackfan, K.D., and McKhann, C.F. Acrodynia, note on pathologic physiology. J. Pediat. 3:45–54, 1933.

Page
448
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)