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

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. "Case Study 15: Formalin Asthma in Hospital Staff." 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

MEDICAL MEMORANDA

Formalin Asthma in Hospital Staff

D.J.HENDRICK, D.J.LANE

British Medical Journal, 1975, 1, 607–608

Few cases of airways obstruction attributable to inhaled formaldehyde have been reported, though it has been suggested that the presence of formaldehyde contributes to the aggravation of chest diseases caused by air pollution (Kotin and Falk, 1964). Occupational “formalin asthma” has been described in a worker in a match factory (Vaughan, 1939) and in workers employed in the tanning and rubber industries (Popa et al., 1969). We report here the use of inhalation provocation tests to investigate the relevance of inhaled formalin fumes to airways obstruction in two hospital staff members continually exposed to this substance in the course of their work.

Case 1

This patient was a 41-year-old nursing sister who began working with formalin in a renal dialysis unit in 1969. She developed a persistent dry cough and episodic attacks of wheezing within a few months which were not improved when she stopped smoking. On two occasions wheezing began four to five hours after exposure for five to 20 minutes to spilled undiluted formalin B.P.C. (34–38% solution of formaldehyde in water w/w). There were no other obvious provoking factors. In 1973 her wheezing, accompanied by increasing breathlessness and rhinitis, became persistent and her cough became productive. Treatment with antibiotics and bronchodilators brought little relief and in June 1973 she was obliged to take sick leave, during

FIG. 1—Case 1. Results of inhalation provocation tests. Values in parentheses are readings obtained immediately before each exposure.

   

Chest Clinic, Churchill Hospital, Oxford OX3 7LJ

D.J.HENDRICK, M.B., M.R.C.P., Senior Registrar

D.J.LANE, D.M., M.R.C.P., Consultant Physician

which she slowly recovered. A chest x-ray film showed inflammatory changes in the apical segment of the right lower lobe. The haemoglobin was 13·4 g/dl and the W.B.C. was 13·1×109/1 (13 100/mm3), of which 2·1×109/1 (2100/mm3) were eosinophils. Routine skin prick tests with 12 common allergens proved negative.

Inhalation provocation tests were begun one month later, when she was receiving no medication. She simulated occupational exposure by “painting” formalin on identical cardboard pieces on different mornings within a confined space. A nose clip prevented her recognizing 25% but not 100% formalin. Ventilatory function was monitored by measurement of forced expiratory volume in one second (FEV1) using a dry spirometer (Vitalograph) or peak expiratory flow (PEF) using a Wright’s meter. The results, expressed as % change, are shown in fig. 1. The late asthmatic reaction seen in test 1 persisted for some days and like that of test 3 showed little objective response to inhaled salbutamol. It was inhibited by prior inhalation of betamethasone 17-valerate 200 µg (test 4). There was no febrile response or significant change in W.B.C. or eosinophil count after any of these tests.

After these studies extractor fans were fitted to the dialysis unit, and undiluted formalin was handled more carefully. The nurse avoided unnecessary exposure and, in particular, no longer cleared up spilled undiluted formalin herself. With these measures her symptoms were completely relieved and she needed no medication.

Case 2

A 59-year-old pathologist had suffered mild asthma as a child and hay fever from the age of 19. Airways obstruction had recurred in 1970 and been slowly progressive ever since. He smoked a pipe and had worked with formalin continually for 17 years. He thought that prolonged exposures worsened his symptoms during the evening after. Routine investigations showed an eosinophilia of 1·19×109/1 (1188/mm3), and a skin-prick test produced a positive reaction to grass pollen. There was no other abnormality.

Inhalation provocation tests were conducted as in case 1. Increasing exposures to formalin produced no febrile or haematological response and no significant change in the pattern of ventilatory function from that shown on a control day (fig. 2). The exposure of test 4 was thought to have exceeded the daily maximum encountered naturally in the course of his work. He may consequently be regarded as a control to case 1.

FIG. 2—Case 2. Results of inhalation provocation tests. Values in parentheses are readings obtained immediately before each exposure.

Reprinted with permission from Hendrick and Lane, BMJ 1(5958):607–8, Copyright 1975, BMJ Publishing Group.

Page
372
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)

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OCR for page 372
Environmental Medicine: Integrating a Missing Element into Medical Education MEDICAL MEMORANDA Formalin Asthma in Hospital Staff D.J.HENDRICK, D.J.LANE British Medical Journal, 1975, 1, 607–608 Few cases of airways obstruction attributable to inhaled formaldehyde have been reported, though it has been suggested that the presence of formaldehyde contributes to the aggravation of chest diseases caused by air pollution (Kotin and Falk, 1964). Occupational “formalin asthma” has been described in a worker in a match factory (Vaughan, 1939) and in workers employed in the tanning and rubber industries (Popa et al., 1969). We report here the use of inhalation provocation tests to investigate the relevance of inhaled formalin fumes to airways obstruction in two hospital staff members continually exposed to this substance in the course of their work. Case 1 This patient was a 41-year-old nursing sister who began working with formalin in a renal dialysis unit in 1969. She developed a persistent dry cough and episodic attacks of wheezing within a few months which were not improved when she stopped smoking. On two occasions wheezing began four to five hours after exposure for five to 20 minutes to spilled undiluted formalin B.P.C. (34–38% solution of formaldehyde in water w/w). There were no other obvious provoking factors. In 1973 her wheezing, accompanied by increasing breathlessness and rhinitis, became persistent and her cough became productive. Treatment with antibiotics and bronchodilators brought little relief and in June 1973 she was obliged to take sick leave, during FIG. 1—Case 1. Results of inhalation provocation tests. Values in parentheses are readings obtained immediately before each exposure.     Chest Clinic, Churchill Hospital, Oxford OX3 7LJ D.J.HENDRICK, M.B., M.R.C.P., Senior Registrar D.J.LANE, D.M., M.R.C.P., Consultant Physician which she slowly recovered. A chest x-ray film showed inflammatory changes in the apical segment of the right lower lobe. The haemoglobin was 13·4 g/dl and the W.B.C. was 13·1×109/1 (13 100/mm3), of which 2·1×109/1 (2100/mm3) were eosinophils. Routine skin prick tests with 12 common allergens proved negative. Inhalation provocation tests were begun one month later, when she was receiving no medication. She simulated occupational exposure by “painting” formalin on identical cardboard pieces on different mornings within a confined space. A nose clip prevented her recognizing 25% but not 100% formalin. Ventilatory function was monitored by measurement of forced expiratory volume in one second (FEV1) using a dry spirometer (Vitalograph) or peak expiratory flow (PEF) using a Wright’s meter. The results, expressed as % change, are shown in fig. 1. The late asthmatic reaction seen in test 1 persisted for some days and like that of test 3 showed little objective response to inhaled salbutamol. It was inhibited by prior inhalation of betamethasone 17-valerate 200 µg (test 4). There was no febrile response or significant change in W.B.C. or eosinophil count after any of these tests. After these studies extractor fans were fitted to the dialysis unit, and undiluted formalin was handled more carefully. The nurse avoided unnecessary exposure and, in particular, no longer cleared up spilled undiluted formalin herself. With these measures her symptoms were completely relieved and she needed no medication. Case 2 A 59-year-old pathologist had suffered mild asthma as a child and hay fever from the age of 19. Airways obstruction had recurred in 1970 and been slowly progressive ever since. He smoked a pipe and had worked with formalin continually for 17 years. He thought that prolonged exposures worsened his symptoms during the evening after. Routine investigations showed an eosinophilia of 1·19×109/1 (1188/mm3), and a skin-prick test produced a positive reaction to grass pollen. There was no other abnormality. Inhalation provocation tests were conducted as in case 1. Increasing exposures to formalin produced no febrile or haematological response and no significant change in the pattern of ventilatory function from that shown on a control day (fig. 2). The exposure of test 4 was thought to have exceeded the daily maximum encountered naturally in the course of his work. He may consequently be regarded as a control to case 1. FIG. 2—Case 2. Results of inhalation provocation tests. Values in parentheses are readings obtained immediately before each exposure. Reprinted with permission from Hendrick and Lane, BMJ 1(5958):607–8, Copyright 1975, BMJ Publishing Group.

OCR for page 373
Environmental Medicine: Integrating a Missing Element into Medical Education Comment The value of inhalation provocation tests as an adjunct to a carefully taken occupational history in the investigation of airways obstruction is well illustrated by these two cases. The suspected aetiological role of formalin was confirmed in one patient but excluded in the other. As a result measures of environmental control were introduced where appropriate, with good effect. The responses observed in case 1 seemed to be specific asthmatic reactions to formalin fumes. They began between two and four hours after exposure was begun. The greater the exposure the longer the reaction persisted, though the maximum percentage fall in ventilatory function was similar, provided exposure was sufficiently prolonged to provoke a positive response. Similar late asthmatic reactions have been described after the inhalation of fumes of other chemicals, including tolylene di-isocyanate (Pepys et al., 1972) and aminoethyl ethanolamine (Sterling, 1967; Pepys and Pickering, 1972). Such reactions may be inhibited by the prior inhalation of corticosteroid aerosols (Pepys et al., 1974), and this was confirmed in our patient though subsequent treatment did not in the event prove We thank the medical illustration department, Radcliffe Infirmary, for the illustrations. References Kotin, P., and Falk, H.L. (1964). Annual Review of Medicine, 15, 233. Pepys, J., et al. (1972). Clinical Allergy, 2, 225. Pepys, J., and Pickering, C.A.C. (1972). Clinical Allergy, 2, 197. Pepys, J., et al. (1974). Clinical Allergy, 4, 13. Popa, V., et al. (1969). Diseases of the Chest, 56, 395. Sterling, G.M. (1967). Thorax, 22, 533. Vaughan, W.T. (1939). The Practice of Allergy, p. 677. St. Louis, Mosby.

Representative terms from entire chapter:

inhalation provocation