Airway inflammation in thunderstorm asthma

Summary Background Epidemics of acute asthma associated with thunderstorms occur intermittently worldwide, though airway inflammation during these acute episodes has not been characterized. The aim of this study was to characterize airway inflammation in thunderstorm asthma. Methods Cases were recru...

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Published inClinical and experimental allergy Vol. 32; no. 12; pp. 1750 - 1756
Main Authors Wark, P. A. B., Simpson, J., Hensley, M. J., Gibson, P. G.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Science Ltd 01.12.2002
Blackwell
Wiley Subscription Services, Inc
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Abstract Summary Background Epidemics of acute asthma associated with thunderstorms occur intermittently worldwide, though airway inflammation during these acute episodes has not been characterized. The aim of this study was to characterize airway inflammation in thunderstorm asthma. Methods Cases were recruited after presentation to the emergency room with acute asthma immediately following a thunderstorm (n = 6). They were compared to two control groups: a group of atopic asthmatics that had presented with acute asthma to the emergency room prior to the thunderstorm (n = 12), and a second group of corticosteroid naïve asthmatics who presented to the emergency room in the prior 12 months (n = 6). Subjects had spirometry, sputum induction and allergy skin tests acutely and at review 4 weeks later. Results Thunderstorm (TS) cases were more likely to have a history of hay fever and grass pollen allergy, and less likely to be on inhaled corticosteroids (ICS) prior to presentation. Cases and control groups had a similar degree of moderate to severe acute airway obstruction (P = 1.0). TS cases had elevated sputum eosinophils (14.8% of total cell count) compared to controls (1%, 2.6%, P < 0.01). TS cases had higher sputum eosinophil cationic protein (ECP; 11 686 ng/mL) compared to controls (1883, 3300, P = 0.02) acutely. TS cases had more cells positive for IL‐5 (30%) compared to controls (1, 1.5%, P = 0.02). When adjusted for ICS use, TS cases had a risk ratio for elevated sputum eosinophils of 2.4 (1.23–4.69). Conclusion Thunderstorm asthma is characterized by airway inflammation with IL‐5‐mediated sputum eosinophilia and eosinophil degranulation. These results are consistent with allergen exposure as the cause of the exacerbation, and are consistent with the thunderstorm‐induced grass pollen deluge as the cause of epidemic asthma after thunderstorms.
AbstractList Background Epidemics of acute asthma associated with thunderstorms occur intermittently worldwide, though airway inflammation during these acute episodes has not been characterized. The aim of this study was to characterize airway inflammation in thunderstorm asthma. Methods Cases were recruited after presentation to the emergency room with acute asthma immediately following a thunderstorm ( n  = 6). They were compared to two control groups: a group of atopic asthmatics that had presented with acute asthma to the emergency room prior to the thunderstorm ( n  = 12), and a second group of corticosteroid naïve asthmatics who presented to the emergency room in the prior 12 months ( n  = 6). Subjects had spirometry, sputum induction and allergy skin tests acutely and at review 4 weeks later. Results Thunderstorm (TS) cases were more likely to have a history of hay fever and grass pollen allergy, and less likely to be on inhaled corticosteroids (ICS) prior to presentation. Cases and control groups had a similar degree of moderate to severe acute airway obstruction ( P  = 1.0). TS cases had elevated sputum eosinophils (14.8% of total cell count) compared to controls (1%, 2.6%, P  < 0.01). TS cases had higher sputum eosinophil cationic protein (ECP; 11 686 ng/mL) compared to controls (1883, 3300, P  = 0.02) acutely. TS cases had more cells positive for IL‐5 (30%) compared to controls (1, 1.5%, P  = 0.02). When adjusted for ICS use, TS cases had a risk ratio for elevated sputum eosinophils of 2.4 (1.23–4.69). Conclusion Thunderstorm asthma is characterized by airway inflammation with IL‐5‐mediated sputum eosinophilia and eosinophil degranulation. These results are consistent with allergen exposure as the cause of the exacerbation, and are consistent with the thunderstorm‐induced grass pollen deluge as the cause of epidemic asthma after thunderstorms.
Background Epidemics of acute asthma associated with thunderstorms occur intermittently worldwide, though airway inflammation during these acute episodes has not been characterized. The aim of this study was to characterize airway inflammation in thunderstorm asthma. Methods Cases were recruited after presentation to the emergency room with acute asthma immediately following a thunderstorm (n = 6). They were compared to two control groups: a group of atopic asthmatics that had presented with acute asthma to the emergency room prior to the thunderstorm (n = 12), and a second group of corticosteroid naive asthmatics who presented to the emergency room in the prior 12 months (n = 6). Subjects had spirometry, sputum induction and allergy skin tests acutely and at review 4 weeks later. Results Thunderstorm (TS) cases were more likely to have a history of hay fever and grass pollen allergy, and less likely to be on inhaled corticosteroids (ICS) prior to presentation. Cases and control groups had a similar degree of moderate to severe acute airway obstruction (P = 1.0). TS cases had elevated sputum eosinophils (14.8% of total cell count) compared to controls (1%, 2.6%, P < 0.01). TS cases had higher sputum eosinophil cationic protein (ECP; 11 686 ng/mL) compared to controls (1883, 3300, P = 0.02) acutely. TS cases had more cells positive for IL-5 (30%) compared to controls (1, 1.5%, P = 0.02). When adjusted for ICS use, TS cases had a risk ratio for elevated sputum eosinophils of 2.4 (1.23-4.69). Conclusion Thunderstorm asthma is characterized by airway inflammation with IL-5-mediated sputum eosinophilia and eosinophil degranulation. These results are consistent with allergen exposure as the cause of the exacerbation, and are consistent with the thunderstorm-induced grass pollen deluge as the cause of epidemic asthma after thunderstorms.
Summary Background Epidemics of acute asthma associated with thunderstorms occur intermittently worldwide, though airway inflammation during these acute episodes has not been characterized. The aim of this study was to characterize airway inflammation in thunderstorm asthma. Methods Cases were recruited after presentation to the emergency room with acute asthma immediately following a thunderstorm (n = 6). They were compared to two control groups: a group of atopic asthmatics that had presented with acute asthma to the emergency room prior to the thunderstorm (n = 12), and a second group of corticosteroid naïve asthmatics who presented to the emergency room in the prior 12 months (n = 6). Subjects had spirometry, sputum induction and allergy skin tests acutely and at review 4 weeks later. Results Thunderstorm (TS) cases were more likely to have a history of hay fever and grass pollen allergy, and less likely to be on inhaled corticosteroids (ICS) prior to presentation. Cases and control groups had a similar degree of moderate to severe acute airway obstruction (P = 1.0). TS cases had elevated sputum eosinophils (14.8% of total cell count) compared to controls (1%, 2.6%, P < 0.01). TS cases had higher sputum eosinophil cationic protein (ECP; 11 686 ng/mL) compared to controls (1883, 3300, P = 0.02) acutely. TS cases had more cells positive for IL‐5 (30%) compared to controls (1, 1.5%, P = 0.02). When adjusted for ICS use, TS cases had a risk ratio for elevated sputum eosinophils of 2.4 (1.23–4.69). Conclusion Thunderstorm asthma is characterized by airway inflammation with IL‐5‐mediated sputum eosinophilia and eosinophil degranulation. These results are consistent with allergen exposure as the cause of the exacerbation, and are consistent with the thunderstorm‐induced grass pollen deluge as the cause of epidemic asthma after thunderstorms.
Epidemics of acute asthma associated with thunderstorms occur intermittently worldwide, though airway inflammation during these acute episodes has not been characterized. The aim of this study was to characterize airway inflammation in thunderstorm asthma. Cases were recruited after presentation to the emergency room with acute asthma immediately following a thunderstorm (n = 6). They were compared to two control groups: a group of atopic asthmatics that had presented with acute asthma to the emergency room prior to the thunderstorm (n = 12), and a second group of corticosteroid naive asthmatics who presented to the emergency room in the prior 12 months (n = 6). Subjects had spirometry, sputum induction and allergy skin tests acutely and at review 4 weeks later. Thunderstorm (TS) cases were more likely to have a history of hay fever and grass pollen allergy, and less likely to be on inhaled corticosteroids (ICS) prior to presentation. Cases and control groups had a similar degree of moderate to severe acute airway obstruction (P = 1.0). TS cases had elevated sputum eosinophils (14.8% of total cell count) compared to controls (1%, 2.6%, P < 0.01). TS cases had higher sputum eosinophil cationic protein (ECP; 11,686 ng/mL) compared to controls (1,883, 3,300, P = 0.02) acutely. TS cases had more cells positive for IL-5 (30%) compared to controls (1, 1.5%, P = 0.02). When adjusted for ICS use, TS cases had a risk ratio for elevated sputum eosinophils of 2.4 (1.23-4.69). Thunderstorm asthma is characterized by airway inflammation with IL-5-mediated sputum eosinophilia and eosinophil degranulation. These results are consistent with allergen exposure as the cause of the exacerbation, and are consistent with the thunderstorm-induced grass pollen deluge as the cause of epidemic asthma after thunderstorms.
Epidemics of acute asthma associated with thunderstorms occur intermittently worldwide, though airway inflammation during these acute episodes has not been characterized. The aim of this study was to characterize airway inflammation in thunderstorm asthma.BACKGROUNDEpidemics of acute asthma associated with thunderstorms occur intermittently worldwide, though airway inflammation during these acute episodes has not been characterized. The aim of this study was to characterize airway inflammation in thunderstorm asthma.Cases were recruited after presentation to the emergency room with acute asthma immediately following a thunderstorm (n = 6). They were compared to two control groups: a group of atopic asthmatics that had presented with acute asthma to the emergency room prior to the thunderstorm (n = 12), and a second group of corticosteroid naive asthmatics who presented to the emergency room in the prior 12 months (n = 6). Subjects had spirometry, sputum induction and allergy skin tests acutely and at review 4 weeks later.METHODSCases were recruited after presentation to the emergency room with acute asthma immediately following a thunderstorm (n = 6). They were compared to two control groups: a group of atopic asthmatics that had presented with acute asthma to the emergency room prior to the thunderstorm (n = 12), and a second group of corticosteroid naive asthmatics who presented to the emergency room in the prior 12 months (n = 6). Subjects had spirometry, sputum induction and allergy skin tests acutely and at review 4 weeks later.Thunderstorm (TS) cases were more likely to have a history of hay fever and grass pollen allergy, and less likely to be on inhaled corticosteroids (ICS) prior to presentation. Cases and control groups had a similar degree of moderate to severe acute airway obstruction (P = 1.0). TS cases had elevated sputum eosinophils (14.8% of total cell count) compared to controls (1%, 2.6%, P < 0.01). TS cases had higher sputum eosinophil cationic protein (ECP; 11,686 ng/mL) compared to controls (1,883, 3,300, P = 0.02) acutely. TS cases had more cells positive for IL-5 (30%) compared to controls (1, 1.5%, P = 0.02). When adjusted for ICS use, TS cases had a risk ratio for elevated sputum eosinophils of 2.4 (1.23-4.69).RESULTSThunderstorm (TS) cases were more likely to have a history of hay fever and grass pollen allergy, and less likely to be on inhaled corticosteroids (ICS) prior to presentation. Cases and control groups had a similar degree of moderate to severe acute airway obstruction (P = 1.0). TS cases had elevated sputum eosinophils (14.8% of total cell count) compared to controls (1%, 2.6%, P < 0.01). TS cases had higher sputum eosinophil cationic protein (ECP; 11,686 ng/mL) compared to controls (1,883, 3,300, P = 0.02) acutely. TS cases had more cells positive for IL-5 (30%) compared to controls (1, 1.5%, P = 0.02). When adjusted for ICS use, TS cases had a risk ratio for elevated sputum eosinophils of 2.4 (1.23-4.69).Thunderstorm asthma is characterized by airway inflammation with IL-5-mediated sputum eosinophilia and eosinophil degranulation. These results are consistent with allergen exposure as the cause of the exacerbation, and are consistent with the thunderstorm-induced grass pollen deluge as the cause of epidemic asthma after thunderstorms.CONCLUSIONThunderstorm asthma is characterized by airway inflammation with IL-5-mediated sputum eosinophilia and eosinophil degranulation. These results are consistent with allergen exposure as the cause of the exacerbation, and are consistent with the thunderstorm-induced grass pollen deluge as the cause of epidemic asthma after thunderstorms.
Author Wark, P. A. B.
Simpson, J.
Hensley, M. J.
Gibson, P. G.
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  surname: Wark
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  surname: Simpson
  fullname: Simpson, J.
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  givenname: P. G.
  surname: Gibson
  fullname: Gibson, P. G.
  organization: Airways Research Centre John Hunter Hospital and
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Issue 12
Keywords Human
Immunopathology
Allergy
Respiratory disease
Pathogenesis
Cytokine
Granulocyte
IL-5
Inflammation
Thunderstorm
Eosinophil
Asthma
Respiratory tract
Interleukin 5
Sputum
Obstructive pulmonary disease
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Spanevello A, Confalonieri M, Sulotto F et al. Induced sputum cellularity. Reference values and distribution in normal volunteers. Am J Respir Crit Care Med 2000; 162: 1172 - 4.
Girgis ST, Marks GB, Downs SH, Kolbe A, Car GN, Paton R. Thunderstorm-associated asthma in an inland town in southeastern Australia. Who is at risk? Eur Respir J 2000; 16: 3 - 8.
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Pizzichini MMM, Pizzichini E, Efthiamiadis A et al. Asthma and natural colds inflammatory indices in induced sputum: a feasibility study. Am J Respir Crit Care Med 1998; 158: 1178 - 84.
Twaddell SH, Gibson PG, Carty K, Wolley KL, Henry RL. Assessment of airway inflammation in children with acute asthma using induced sputum. Eur Respir J 1996; 9: 2104 - 8.
Cockcroft DW, Ruffin RE, Dolovich J, Hargreave FE. Allergen-induced increase in non-allergic bronchial reactivity. Clin Allergy 1977; 7: 503 - 13.
Wark PAB, Johnston SL, Moric I, Hensley MJ, Gibson PG. Viral infection induces IL-8, eosinophil activation and neutrophil influx in acute severe asthma. Am J Respir Crit Care Med 2000; 161: A605.
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Gerschman NH, Liu H, Wong HH, Liu JT, Fahy JV. Fractional analysis of sequential induced sputum samples during sputum induction: evidence that different lung compartments are sampled at different time points. J Allergy Clin Immunol 1999; 104: 322 - 8.
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Wood LJ, Inman MD, Watson RM, Foley F, Denburg JA, O'Byrne PM. Changes in bone marrow inflammatory cell progenitors after inhaled allergen in asthmatic subjects. Am J Respir Crit Care Med 1998; 157: 99 - 105.
Holgate ST, Robinson C, Church MK. The contribution of mast cell mediators to acute allergic reactions in human skin and airways. Allergy 1988; 43 (Suppl. 5):22 - 31.
Celenza A, Fothergill J, Kupek E, Shaw RJ. Thunderstorm associated asthma: a detailed analysis of environmental factors. Br Med J 1996; 312: 604 - 7.
Norzila MZ, Fakes K, Henry RL, Simpson J, Gibson PG. Interleukin-8 secretion and neutrophil recruitment accompanies induced sputum eosinophil activation in children with acute asthma. Am J Respir Crit Care Med 2000; 161: 769 - 74.
Gauvreau GM, Watson RM, O'Byrne PM. Kinetics of allergen-induced airway eosinophilic cytokine production and airway inflammation. Am J Respir Crit Care Med 1999; 160: 640 - 7.
Sur S, Kita H, Gleich GJ, Chenier TC, Hunt LW. Eosinophil recruitment is associated with IL-5, but not with RANTES, twenty four hours after allergen challenge. J Allergy Clin Immunol 1996; 97: 1272 - 8.
Wark PAB, Johnston SL, Moric I, Simpson JL, Hensley MJ, Gibson PG. Neutrophil degranulation and cell lysis is associated with clinical severity in virus-induced asthma. Eur Respir J 2002; 19: 55 - 68 .
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References_xml – reference: Suphioglu C, Singh MB, Taylor P et al. Mechanism of grass-pollen induced asthma. Lancet 1992; 339: 569 - 72.
– reference: Popov TA, Pizzichinini MMM, Pizzichini E et al. Some technical factors influencing the induction of sputum for cell analysis. Eur Respir J 1995; 8: 559 - 65.
– reference: Wood LJ, Inman MD, Watson RM, Foley F, Denburg JA, O'Byrne PM. Changes in bone marrow inflammatory cell progenitors after inhaled allergen in asthmatic subjects. Am J Respir Crit Care Med 1998; 157: 99 - 105.
– reference: Aas K. Heterogeneity of bronchial asthma. Allergy 1981; 36: 3 - 14.
– reference: Fahy JV, Kim KW, Liu J, Boushey HA. Prominent neutrophilic inflammation in sputum from subjects with asthma exacerbation. J Allergy Clin Immunol 1995; 95: 843 - 52.
– reference: Cockcroft DW, Ruffin RE, Dolovich J, Hargreave FE. Allergen-induced increase in non-allergic bronchial reactivity. Clin Allergy 1977; 7: 503 - 13.
– reference: Packe GE, Ayres JG. Asthma outbreak during a thunderstorm. Lancet 1985; 2: 199 - 203.
– reference: DeMonchy JGRHF, Kauffmann P, Venge GH et al. Bronchoalveolar eosinophilia during allergen-induced late asthmatic reactions. Am Rev Respir Dis 1985; 131: 373 - 6.
– reference: Gerschman NH, Liu H, Wong HH, Liu JT, Fahy JV. Fractional analysis of sequential induced sputum samples during sputum induction: evidence that different lung compartments are sampled at different time points. J Allergy Clin Immunol 1999; 104: 322 - 8.
– reference: Twaddell SH, Gibson PG, Carty K, Wolley KL, Henry RL. Assessment of airway inflammation in children with acute asthma using induced sputum. Eur Respir J 1996; 9: 2104 - 8.
– reference: Wark PAB, Johnston SL, Moric I, Hensley MJ, Gibson PG. Viral infection induces IL-8, eosinophil activation and neutrophil influx in acute severe asthma. Am J Respir Crit Care Med 2000; 161: A605.
– reference: Bellomo R, Gigliotti P, Treloar A et al. Two consecutive thunderstorm associated epidemics of asthma in the city of Melbourne: the possible role of rye grass pollen. Med J Aust 1992; 156: 834 - 7.
– reference: Sur S, Kita H, Gleich GJ, Chenier TC, Hunt LW. Eosinophil recruitment is associated with IL-5, but not with RANTES, twenty four hours after allergen challenge. J Allergy Clin Immunol 1996; 97: 1272 - 8.
– reference: Newson R, Strachan D, Archibald E, Emberlin J, Hardaker P, Collier C. Effect of thunderstorms and airborne grass pollen on the incidence of acute asthma in England 1990-94. Thorax 1997; 52: 680 - 5.
– reference: Girgis ST, Marks GB, Downs SH, Kolbe A, Car GN, Paton R. Thunderstorm-associated asthma in an inland town in southeastern Australia. Who is at risk? Eur Respir J 2000; 16: 3 - 8.
– reference: Wark PAB, Johnston SL, Moric I, Simpson JL, Hensley MJ, Gibson PG. Neutrophil degranulation and cell lysis is associated with clinical severity in virus-induced asthma. Eur Respir J 2002; 19: 55 - 68 .
– reference: Waters J, Corbett S, Gibson PG, Hensley MJ. Epidemic asthma surveillance in the New England region 1990-92. Public Health Bull 1992; 4: 100 - 1.
– reference: Gauvreau GMLJ, Wood R, Sehmi RM et al. The effects of inhaled budesonide on circulating eosinophil progenitors and their expression of cytokines after allergen challenge in subjects with atopic asthma. Am J Respir Crit Care Med 2000; 162: 2139 - 44.
– reference: Pizzichini MMM, Pizzichini E, Efthiamiadis A et al. Asthma and natural colds inflammatory indices in induced sputum: a feasibility study. Am J Respir Crit Care Med 1998; 158: 1178 - 84.
– reference: Gauvreau GM, Watson RM, O'Byrne PM. Kinetics of allergen-induced airway eosinophilic cytokine production and airway inflammation. Am J Respir Crit Care Med 1999; 160: 640 - 7.
– reference: Gibson PG, Wlodarczyk J, Hensley MJ et al. Epidemiological association of airway inflammation with asthma symptoms and airway hyperresponsiveness in childhood. Am J Respir Crit Care Med 1998; 158: 36 - 41.
– reference: Spanevello A, Confalonieri M, Sulotto F et al. Induced sputum cellularity. Reference values and distribution in normal volunteers. Am J Respir Crit Care Med 2000; 162: 1172 - 4.
– reference: Celenza A, Fothergill J, Kupek E, Shaw RJ. Thunderstorm associated asthma: a detailed analysis of environmental factors. Br Med J 1996; 312: 604 - 7.
– reference: Norzila MZ, Fakes K, Henry RL, Simpson J, Gibson PG. Interleukin-8 secretion and neutrophil recruitment accompanies induced sputum eosinophil activation in children with acute asthma. Am J Respir Crit Care Med 2000; 161: 769 - 74.
– reference: Holgate ST, Robinson C, Church MK. The contribution of mast cell mediators to acute allergic reactions in human skin and airways. Allergy 1988; 43 (Suppl. 5):22 - 31.
– volume: 131
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  year: 1985
  end-page: 6
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Snippet Summary Background Epidemics of acute asthma associated with thunderstorms occur intermittently worldwide, though airway inflammation during these acute...
Background Epidemics of acute asthma associated with thunderstorms occur intermittently worldwide, though airway inflammation during these acute episodes has...
Epidemics of acute asthma associated with thunderstorms occur intermittently worldwide, though airway inflammation during these acute episodes has not been...
Background Epidemics of acute asthma associated with thunderstorms occur intermittently worldwide, though airway inflammation during these acute episodes has...
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SubjectTerms Acute Disease
Adult
Airway Obstruction - complications
Allergens - adverse effects
Allergic diseases
asthma
Asthma - etiology
Asthma - immunology
Biological and medical sciences
Case-Control Studies
Cell Degranulation
eosinophil
Eosinophils - pathology
Female
Humans
Hypersensitivity, Immediate - complications
IL-5
Immunopathology
Interleukin-5 - analysis
Logistic Models
Male
Medical sciences
Middle Aged
Pulmonary Eosinophilia - complications
Respiratory and ent allergic diseases
Rhinitis, Allergic, Seasonal - complications
Risk Factors
Skin Tests - methods
sputum
Sputum - cytology
thunderstorm
Weather
Title Airway inflammation in thunderstorm asthma
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https://www.ncbi.nlm.nih.gov/pubmed/12653167
https://www.proquest.com/docview/199897405
https://www.proquest.com/docview/18723305
https://www.proquest.com/docview/72869633
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