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 in | Clinical and experimental allergy Vol. 32; no. 12; pp. 1750 - 1756 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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. |
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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. |
Author_xml | – sequence: 1 givenname: P. A. B. surname: Wark fullname: Wark, P. A. B. organization: Respiratory Cell and Molecular Biology, Research Division, Southampton General Hospital, Southampton, UK – sequence: 2 givenname: J. surname: Simpson fullname: Simpson, J. organization: Airways Research Centre John Hunter Hospital and – sequence: 3 givenname: M. J. surname: Hensley fullname: Hensley, M. J. organization: Faculty of Medicine and Health Sciences, University of Newcastle, Australia – sequence: 4 givenname: P. G. surname: Gibson fullname: Gibson, P. G. organization: Airways Research Centre John Hunter Hospital and |
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Keywords | Human Immunopathology Allergy Respiratory disease Pathogenesis Cytokine Granulocyte IL-5 Inflammation Thunderstorm Eosinophil Asthma Respiratory tract Interleukin 5 Sputum Obstructive pulmonary disease Aggravation |
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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. 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Allergy 1988; 43 (Suppl. 5):22 - 31. – volume: 131 start-page: 373 year: 1985 end-page: 6 article-title: Bronchoalveolar eosinophilia during allergen‐induced late asthmatic reactions publication-title: Am Rev Respir Dis – volume: 162 start-page: 2139 year: 2000 end-page: 44 article-title: The effects of inhaled budesonide on circulating eosinophil progenitors and their expression of cytokines after allergen challenge in subjects with atopic asthma publication-title: Am J Respir Crit Care Med – volume: 312 start-page: 604 year: 1996 end-page: 7 article-title: Thunderstorm associated asthma: a detailed analysis of environmental factors publication-title: Br Med J – volume: 95 start-page: 843 year: 1995 end-page: 52 article-title: Prominent neutrophilic inflammation in sputum from subjects with asthma exacerbation publication-title: J Allergy Clin Immunol – volume: 2 start-page: 199 year: 1985 end-page: 203 article-title: Asthma outbreak during a thunderstorm publication-title: Lancet – volume: 4 start-page: 100 year: 1992 end-page: 1 article-title: Epidemic asthma surveillance in the New England region 1990–92 publication-title: Public Health Bull – volume: 156 start-page: 834 year: 1992 end-page: 7 article-title: Two consecutive thunderstorm associated epidemics of asthma in the city of Melbourne: the possible role of rye grass pollen publication-title: Med J Aust – volume: 52 start-page: 680 year: 1997 end-page: 5 article-title: Effect of thunderstorms and airborne grass pollen on the incidence of acute asthma in England 1990–94 publication-title: Thorax – volume: 8 start-page: 559 year: 1995 end-page: 65 article-title: Some technical factors influencing the induction of sputum for cell analysis publication-title: Eur Respir J – volume: 158 start-page: 1178 year: 1998 end-page: 84 article-title: Asthma and natural colds inflammatory indices in induced sputum: a feasibility study publication-title: Am J Respir Crit Care Med – volume: 9 start-page: 2104 year: 1996 end-page: 8 article-title: Assessment of airway inflammation in children with acute asthma using induced sputum publication-title: Eur Respir J – volume: 104 start-page: 322 year: 1999 end-page: 8 article-title: Fractional analysis of sequential induced sputum samples during sputum induction: evidence that different lung compartments are sampled at different time points publication-title: J Allergy Clin Immunol – volume: 7 start-page: 503 year: 1977 end-page: 13 article-title: Allergen‐induced increase in non‐allergic bronchial reactivity publication-title: Clin Allergy – volume: 43 start-page: 22 issue: Suppl. 5 year: 1988 end-page: 31 article-title: The contribution of mast cell mediators to acute allergic reactions in human skin and airways publication-title: Allergy – volume: 36 start-page: 3 year: 1981 end-page: 14 article-title: Heterogeneity of bronchial asthma publication-title: Allergy – volume: 158 start-page: 36 year: 1998 end-page: 41 article-title: Epidemiological association of airway inflammation with asthma symptoms and airway hyperresponsiveness in childhood publication-title: Am J Respir Crit Care Med – volume: 161 start-page: 769 year: 2000 end-page: 74 article-title: Interleukin‐8 secretion and neutrophil recruitment accompanies induced sputum eosinophil activation in children with acute asthma publication-title: Am J Respir Crit Care Med – volume: 161 start-page: A605 year: 2000 article-title: Viral infection induces IL‐8, eosinophil activation and neutrophil influx in acute severe asthma publication-title: Am J Respir Crit Care Med – volume: 339 start-page: 569 year: 1992 end-page: 72 article-title: Mechanism of grass‐pollen induced asthma publication-title: Lancet – volume: 19 start-page: 55 year: 2002 end-page: 68 article-title: Neutrophil degranulation and cell lysis is associated with clinical severity in virus‐induced asthma publication-title: Eur Respir J – volume: 162 start-page: 1172 year: 2000 end-page: 4 article-title: Induced sputum cellularity. Reference values and distribution in normal volunteers publication-title: Am J Respir Crit Care Med – volume: 160 start-page: 640 year: 1999 end-page: 7 article-title: Kinetics of allergen‐induced airway eosinophilic cytokine production and airway inflammation publication-title: Am J Respir Crit Care Med – volume: 16 start-page: 3 year: 2000 end-page: 8 article-title: Thunderstorm‐associated asthma in an inland town in southeastern Australia. Who is at risk? publication-title: Eur Respir J – volume: 157 start-page: 99 year: 1998 end-page: 105 article-title: Changes in bone marrow inflammatory cell progenitors after inhaled allergen in asthmatic subjects publication-title: Am J Respir Crit Care Med – volume: 97 start-page: 1272 year: 1996 end-page: 8 article-title: Eosinophil recruitment is associated with IL‐5, but not with RANTES, twenty four hours after allergen challenge publication-title: J Allergy Clin Immunol – ident: e_1_2_6_21_2 doi: 10.1016/S0091-6749(96)70195-1 – volume: 19 start-page: 55 year: 2002 ident: e_1_2_6_13_2 article-title: Neutrophil degranulation and cell lysis is associated with clinical severity in virus‐induced asthma publication-title: Eur Respir J – ident: e_1_2_6_18_2 doi: 10.1111/j.1365-2222.1977.tb01481.x – ident: e_1_2_6_8_2 doi: 10.1016/0140-6736(92)90864-Y – ident: e_1_2_6_15_2 doi: 10.1164/ajrccm.158.1.9705031 – ident: e_1_2_6_22_2 doi: 10.1164/ajrccm.157.1.9704125 – ident: e_1_2_6_25_2 doi: 10.1016/S0091-6749(99)70374-X – volume: 131 start-page: 373 year: 1985 ident: e_1_2_6_9_2 article-title: Bronchoalveolar eosinophilia during allergen‐induced late asthmatic reactions publication-title: Am Rev Respir Dis – volume: 161 start-page: A605 year: 2000 ident: e_1_2_6_12_2 article-title: Viral infection induces IL‐8, eosinophil activation and neutrophil influx in acute severe asthma publication-title: Am J Respir Crit Care Med – ident: e_1_2_6_20_2 doi: 10.1046/j.1365-2249.1998.00688.x – ident: e_1_2_6_23_2 doi: 10.1164/ajrccm.158.4.9712082 – ident: e_1_2_6_7_2 doi: 10.1136/bmj.312.7031.604 – ident: e_1_2_6_6_2 doi: 10.1034/j.1399-3003.2000.16a02.x – ident: e_1_2_6_2_2 doi: 10.1016/S0140-6736(85)91510-7 – ident: e_1_2_6_5_2 doi: 10.1136/thx.52.8.680 – ident: e_1_2_6_11_2 doi: 10.1164/ajrccm.161.3.9809071 – ident: e_1_2_6_17_2 doi: 10.1164/ajrccm.162.3.9908057 – volume: 8 start-page: 559 year: 1995 ident: e_1_2_6_24_2 article-title: Some technical factors influencing the induction of sputum for cell analysis publication-title: Eur Respir J doi: 10.1183/09031936.95.08040559 – ident: e_1_2_6_26_2 doi: 10.1164/ajrccm.162.6.2001120 – ident: e_1_2_6_14_2 doi: 10.1111/j.1398-9995.1981.tb01818.x – ident: e_1_2_6_10_2 doi: 10.1016/S0091-6749(95)70128-1 – ident: e_1_2_6_3_2 doi: 10.5694/j.1326-5377.1992.tb136994.x – ident: e_1_2_6_19_2 doi: 10.1111/j.1398-9995.1988.tb05044.x – ident: e_1_2_6_4_2 doi: 10.1071/NB93049 – ident: e_1_2_6_16_2 doi: 10.1183/09031936.96.09102104 |
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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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