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ICE HOCKEY LUNG: NO2 POISONING
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is the largest international implant society (PO Box 2277, Grand Central Station, New York, NY 10163). 1. Editoral. Osseointegrated dental implants. Lancet 1986; ii: 26. 2. Brånemark P-I. Osseointegration and its experimental studies. J Prosthet Dentistry 1983; 50: 399-410. 3. Brånemark P-I, Zarb GA, Albrektsson T. Tissue-integrated prosthesisosseointegration in clinical dentistry. Chicago: Quintessence, 1985. 4. Lavelle C, Wedgewood D. Effect of internal irrigation on frictional heat generated from bone drilling. J Oral Surg 1985; 38: 499-503. 5. Scher ELC. An osseointegrated implant to replace a missing lateral incisor following orthodontic treatment. Br J Orthodontics 1990; 17: 147-54.
ICE HOCKEY LUNG:
NO2 POISONING
exhaust liberated in a confmed space may result in carbon monoxide poisoning. That much is well known, but it is less widely appreciated that nitrogen dioxide (NOz) may also be released. The clinical effects of emission of substantial amounts of NOz from malfunctioning iceresurfacing machines in closed arenas were first identified more than two decades ago.1 Nevertheless, there have been several outbreaks of acute respiratory illness in the past 5 years among players, cheerleaders, and spectators.Z,3 In the latest reported incident,3at least 116 individuals were affected. Cough, haemoptysis, chest pain, headache, and dyspnoea were the predominant features experienced during and within 48 hours of attending an ice hockey game. In many subjects the cough persisted for more than 2 weeks, although simple respiratory function tests revealed no persistent deficit in lung function. NOz is a largely insoluble, brown, mildly irritating gas that is usually found in association with its dimer, nitrogen tetroxide. N02occurs naturally as a result of bacterial action on nitrogenous compounds. Fermentation of silage produces high concentrations of this gas within 2 days of silo-filling. Farm workers who enter silos have experienced an acute respiratory illness and fatalities have occurred.4-6 N02 is also a by-product of many industrial processesand leaks have produced illness in firemen.8 Occupational exposure has led to respiratory symptoms in other circumstances.9-1Z Three American astronauts who were exposed to about 250 ppm of N02for 4-5 min owing to the inadvertent firing of the reaction control system in the Apollo-Soyuz spacecraft had radiological evidence of pulmonary oedema the day after splashdown.’3 The main source of atmospheric NOz is the combustion of fossil fuels as in open fires, domestic or industrial boilers, or motor vehicles. Combustion yields nitric oxide (NO), which is not itself directly hazardous, and some N02- In the air, more N02 is formed by gradual oxidation of NO by photochemical reactions that require the presence of volatile
Engine
hydrocarbons.14 The effects on lung function of chronic exposure to low concentrations (< 2 ppm) of NOz are controversial.1s Studies in patients with mild asthma suggest that short-term exposure to concentrations less than 05 ppm increases bronchial hyperreactivity to several bronchoconstrictors.16-18 The clinical features following acute exposure to higher concentrations of NOare well documented and are known to depend on the concentration of NO and the duration of exposure to the gas. Since NOz is only a mild upper respiratory tract irritant, modest acute exposure ( < 50 ppm) for a short time often produces no immediate symptoms, although throat irritation, cough, transient choking, tightness in the chest, and sweating have been observed. By contrast, exposure to a massive concentration ofNOz, such
that found in a silo, can produce severe and immediate hypoxaemia, which may be fatal. Methaemoglobinaemia’9 may also be induced in these circumstances and compound the pre-existing hypoxaemia. In less severe cases, the onset of symptoms may be delayed for a few hours (typically 3-36) and the patient then gets dyspnoea, chest pain (which may be pleuritic), haemoptysis, tachycardia, headache, conjunctivitis, generalised weakness, and dizziness (which
as
hypotension). Most of these patients will make an uneventful recovery with bronchodilator and corticosteroid therapy but a few will become acutely ill with cough, wheeze, frothy bloodstained sputum, increasing dyspnoea, restlessness, and fever. Pulmonary oedema, which may also occur in those who were previously symptom-free, is due to extravasation of fluid from a vascular space of compromised integrity. 1-4 The oedema responds poorly to diuretics; corticosteroids and mechanical ventilation with positive end-expiratory pressure offer the best hope of reducing the mortality, which may be as high as 40% in severe cases.14 Patients may relapse after recovery, and this is more likely if corticosteroids are discontinued prematurely. Not only may a second episode of pulmonary oedema occur but also bronchiolitis obliterans may develop within 2-6 weeks.lO,2O When extensive and untreated, this complication may be fatal, but corticosteroids are highly effective if continued for at least 2 months.20 may be due to
1. Anderson DE. Problems created for ice arenas by engine exhaust. Am Ind Hyg Assoc J 1971; 32: 790-801. 2. Dewailly E, Allaire S, Nantel A. Nitrogen dioxide poisoning at a skating rink—Québec. Can Dis Weekly Rep 1988; 14: 61-62. 3. Hedberg K, Hedberg CW, Iber C, et al. An outbreak of nitrogen dioxide-induced respiratory illness among ice hockey players. JAMA 1989; 262: 3014-17. 4. Grayson RR. Silage gas poisoning: nitrogen dioxide pneumonia, a new disease in agricultural workers. Ann Intern Med 1956;45: 393-408. 5. Ramirez-R J, Dowell AR. Silo-filler’s disease: nitrogen dioxide-induced lung injury. Ann Intern Med 1971; 74: 569-76. 6. Moskowitz RL, Lyons HA, Cottle HR. Silo filler’s disease. Am J Med
1964; 36: 457-62. 7. WHO Environmental Health Criteria Document: oxides of nitrogen. Geneva: WHO, 1977. 8. Tse RL, Bockman AA. Nitrogen dioxide toxicity: report of four cases in firemen. JAMA 1970; 212: 1341-44. 9. Norwood WD, Wisehart DE, Earl CA, Adley FE, Anderson DE. Nitrogen dioxide poisoning due to metal-cutting with oxyacetylene torch. J Occup Med 1966; 8: 301-06. 10. Milne JEH. Nitrogen dioxide inhalation and bronchiolitis obliterans. J Occup Med 1969; 11: 538-47. 11. Muller B. Nitrogen dioxide intoxication after a mining accident. Respiration 1969; 26: 249-61. 12. Genovesi MG, Tashkin DP, Chopra S, Morgan M. McElroy C. Transient hypoxemia in firemen following inhalation of smoke. Chest 1977; 71: 441-44. 13. Hatton DV, Leach CS, Nicogossian AE, Di Ferrante N. Collagen breakdown and nitrogen dioxide inhalation. Arch Environ Hlth 1977; 32: 33-36. 14. Guidotti TL. The higher oxides of nitrogen: inhalation toxicology. Environ Res 1978; 15: 443-72. 15.WHO. Air quality guidelines for Europe. WHO regional publications, European series no. 23. Copenhagen: WHO, 1987: 297-314. 16. Orehek J, Massari JP, Gayrard P, Grimaud C, Charpin J. Effect of short-term, low-level nitrogen dioxide exposure on bronchial sensitivity of asthmatic patients. J Clin Invest 1976; 57: 301-07. 17. Bylin G, Lindvall T, Rehn T, Sundin B. Effects of short-term exposure to ambient nitrogen dioxide concentrations on human bronchial reactivity and lung function. Eur J Respir Dis 1985; 66: 205-17. 18. Kleinman MT, Bailey RM, Linn WS, et al. Effects of 0·2 ppm nitrogen dioxide on pulmonary function and response to bronchoprovocation in asthmatics. J Toxicol Environ Hlth 1983; 12: 815-26. 19. Fleetham JA, Tunnicliffe BW, Munt PW. Methemoglobinemia and the oxides of nitrogen. N Engl J Med 1978; 298: 1150. 20. Horvath EP, doPico GA, Barbee RA, Dickie HA. Nitrogen dioxideinduced pulmonary disease. J Occup Med 1978: 20: 103-10.
is the largest international implant society (PO Box 2277, Grand Central Station, New York, NY 10163). 1. Editoral. Osseointegrated dental implants. Lancet 1986; ii: 26. 2. Brånemark P-I. Osseointegration and its experimental studies. J Prosthet Dentistry 1983; 50: 399-410. 3. Brånemark P-I, Zarb GA, Albrektsson T. Tissue-integrated prosthesisosseointegration in clinical dentistry. Chicago: Quintessence, 1985. 4. Lavelle C, Wedgewood D. Effect of internal irrigation on frictional heat generated from bone drilling. J Oral Surg 1985; 38: 499-503. 5. Scher ELC. An osseointegrated implant to replace a missing lateral incisor following orthodontic treatment. Br J Orthodontics 1990; 17: 147-54.
ICE HOCKEY LUNG:
NO2 POISONING
exhaust liberated in a confmed space may result in carbon monoxide poisoning. That much is well known, but it is less widely appreciated that nitrogen dioxide (NOz) may also be released. The clinical effects of emission of substantial amounts of NOz from malfunctioning iceresurfacing machines in closed arenas were first identified more than two decades ago.1 Nevertheless, there have been several outbreaks of acute respiratory illness in the past 5 years among players, cheerleaders, and spectators.Z,3 In the latest reported incident,3at least 116 individuals were affected. Cough, haemoptysis, chest pain, headache, and dyspnoea were the predominant features experienced during and within 48 hours of attending an ice hockey game. In many subjects the cough persisted for more than 2 weeks, although simple respiratory function tests revealed no persistent deficit in lung function. NOz is a largely insoluble, brown, mildly irritating gas that is usually found in association with its dimer, nitrogen tetroxide. N02occurs naturally as a result of bacterial action on nitrogenous compounds. Fermentation of silage produces high concentrations of this gas within 2 days of silo-filling. Farm workers who enter silos have experienced an acute respiratory illness and fatalities have occurred.4-6 N02 is also a by-product of many industrial processesand leaks have produced illness in firemen.8 Occupational exposure has led to respiratory symptoms in other circumstances.9-1Z Three American astronauts who were exposed to about 250 ppm of N02for 4-5 min owing to the inadvertent firing of the reaction control system in the Apollo-Soyuz spacecraft had radiological evidence of pulmonary oedema the day after splashdown.’3 The main source of atmospheric NOz is the combustion of fossil fuels as in open fires, domestic or industrial boilers, or motor vehicles. Combustion yields nitric oxide (NO), which is not itself directly hazardous, and some N02- In the air, more N02 is formed by gradual oxidation of NO by photochemical reactions that require the presence of volatile
Engine
hydrocarbons.14 The effects on lung function of chronic exposure to low concentrations (< 2 ppm) of NOz are controversial.1s Studies in patients with mild asthma suggest that short-term exposure to concentrations less than 05 ppm increases bronchial hyperreactivity to several bronchoconstrictors.16-18 The clinical features following acute exposure to higher concentrations of NOare well documented and are known to depend on the concentration of NO and the duration of exposure to the gas. Since NOz is only a mild upper respiratory tract irritant, modest acute exposure ( < 50 ppm) for a short time often produces no immediate symptoms, although throat irritation, cough, transient choking, tightness in the chest, and sweating have been observed. By contrast, exposure to a massive concentration ofNOz, such
that found in a silo, can produce severe and immediate hypoxaemia, which may be fatal. Methaemoglobinaemia’9 may also be induced in these circumstances and compound the pre-existing hypoxaemia. In less severe cases, the onset of symptoms may be delayed for a few hours (typically 3-36) and the patient then gets dyspnoea, chest pain (which may be pleuritic), haemoptysis, tachycardia, headache, conjunctivitis, generalised weakness, and dizziness (which
as
hypotension). Most of these patients will make an uneventful recovery with bronchodilator and corticosteroid therapy but a few will become acutely ill with cough, wheeze, frothy bloodstained sputum, increasing dyspnoea, restlessness, and fever. Pulmonary oedema, which may also occur in those who were previously symptom-free, is due to extravasation of fluid from a vascular space of compromised integrity. 1-4 The oedema responds poorly to diuretics; corticosteroids and mechanical ventilation with positive end-expiratory pressure offer the best hope of reducing the mortality, which may be as high as 40% in severe cases.14 Patients may relapse after recovery, and this is more likely if corticosteroids are discontinued prematurely. Not only may a second episode of pulmonary oedema occur but also bronchiolitis obliterans may develop within 2-6 weeks.lO,2O When extensive and untreated, this complication may be fatal, but corticosteroids are highly effective if continued for at least 2 months.20 may be due to
1. Anderson DE. Problems created for ice arenas by engine exhaust. Am Ind Hyg Assoc J 1971; 32: 790-801. 2. Dewailly E, Allaire S, Nantel A. Nitrogen dioxide poisoning at a skating rink—Québec. Can Dis Weekly Rep 1988; 14: 61-62. 3. Hedberg K, Hedberg CW, Iber C, et al. An outbreak of nitrogen dioxide-induced respiratory illness among ice hockey players. JAMA 1989; 262: 3014-17. 4. Grayson RR. Silage gas poisoning: nitrogen dioxide pneumonia, a new disease in agricultural workers. Ann Intern Med 1956;45: 393-408. 5. Ramirez-R J, Dowell AR. Silo-filler’s disease: nitrogen dioxide-induced lung injury. Ann Intern Med 1971; 74: 569-76. 6. Moskowitz RL, Lyons HA, Cottle HR. Silo filler’s disease. Am J Med
1964; 36: 457-62. 7. WHO Environmental Health Criteria Document: oxides of nitrogen. Geneva: WHO, 1977. 8. Tse RL, Bockman AA. Nitrogen dioxide toxicity: report of four cases in firemen. JAMA 1970; 212: 1341-44. 9. Norwood WD, Wisehart DE, Earl CA, Adley FE, Anderson DE. Nitrogen dioxide poisoning due to metal-cutting with oxyacetylene torch. J Occup Med 1966; 8: 301-06. 10. Milne JEH. Nitrogen dioxide inhalation and bronchiolitis obliterans. J Occup Med 1969; 11: 538-47. 11. Muller B. Nitrogen dioxide intoxication after a mining accident. Respiration 1969; 26: 249-61. 12. Genovesi MG, Tashkin DP, Chopra S, Morgan M. McElroy C. Transient hypoxemia in firemen following inhalation of smoke. Chest 1977; 71: 441-44. 13. Hatton DV, Leach CS, Nicogossian AE, Di Ferrante N. Collagen breakdown and nitrogen dioxide inhalation. Arch Environ Hlth 1977; 32: 33-36. 14. Guidotti TL. The higher oxides of nitrogen: inhalation toxicology. Environ Res 1978; 15: 443-72. 15.WHO. Air quality guidelines for Europe. WHO regional publications, European series no. 23. Copenhagen: WHO, 1987: 297-314. 16. Orehek J, Massari JP, Gayrard P, Grimaud C, Charpin J. Effect of short-term, low-level nitrogen dioxide exposure on bronchial sensitivity of asthmatic patients. J Clin Invest 1976; 57: 301-07. 17. Bylin G, Lindvall T, Rehn T, Sundin B. Effects of short-term exposure to ambient nitrogen dioxide concentrations on human bronchial reactivity and lung function. Eur J Respir Dis 1985; 66: 205-17. 18. Kleinman MT, Bailey RM, Linn WS, et al. Effects of 0·2 ppm nitrogen dioxide on pulmonary function and response to bronchoprovocation in asthmatics. J Toxicol Environ Hlth 1983; 12: 815-26. 19. Fleetham JA, Tunnicliffe BW, Munt PW. Methemoglobinemia and the oxides of nitrogen. N Engl J Med 1978; 298: 1150. 20. Horvath EP, doPico GA, Barbee RA, Dickie HA. Nitrogen dioxideinduced pulmonary disease. J Occup Med 1978: 20: 103-10.