Epidemic of asthma possibly related to thunderstorms

Murray, Virginia; Venables, K M; Laing-Morton, T; Thurston, M. P. J.; Williams, Deborah

doi:10.1136/bmj.309.6947.131c

Cited by 42 publications

(29 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because of their very small size, starch granules can penetrate the lower airways and induce the appearance of bronchial allergic symptoms. Other thunderstorm-associated asthma outbreaks occurred in London, UK, on the night between June 24-25 1944 [133][134][135] and in Wagga Wagga, Australia on October 30, 1997 [136]. The asthma outbreak of London was the largest episode; there werey100 emergency visits of several hospitals of London and southwest England.…”

Section: Plant-derived Allergensmentioning

confidence: 99%

“…This phenomenon was also followed by a rapid increase in hospital or general practitioner visits for asthma. No unusual levels of air pollution were noted at the time of these epidemics but there was a strong association with rye grass pollen [35,[133][134][135][136]. Rye grass pollens, after rupture by osmotic shock during thunderstorms, release large amounts of paucimicronic allergenic particles, i.e.…”

Section: Plant-derived Allergensmentioning

confidence: 99%

See 1 more Smart Citation

Outdoor air pollution, climatic changes and allergic bronchial asthma

D’Amato¹,

Liccardi²,

D’Amato³

et al. 2002

European Respiratory Journal

222

158

View full text Add to dashboard Cite

Both the prevalence and severity of respiratory allergic diseases such as bronchial asthma have increased in recent years. Among the factors implicated in this "epidemic" are indoor and outdoor airborne pollutants. Urbanisation with its high levels of vehicle emissions and Westernised lifestyle parallels the increase in respiratory allergy in most industrialised countries, and people who live in urban areas tend to be more affected by the disease than those of rural areas. In atopic subjects, exposure to air pollution increases airway responsiveness to aeroallergens. Pollen is a good model with which to study the interrelationship between air pollution and respiratory allergic diseases. Biological aerosols carrying antigenic proteins, such as pollen grains or plantderived paucimicronic components, can produce allergic symptoms. By adhering to the surface of these airborne allergenic agents, air pollutants could modify their antigenic properties. Several factors influence this interaction, i.e., type of air pollutant, plant species, nutrient balance, climatic factors, degree of airway sensitisation and hyperresponsiveness of exposed subjects. However, the airway mucosal damage and the impaired mucociliary clearance induced by air pollution may facilitate the penetration and the access of inhaled allergens to the cells of the immune system, and so promote airway sensitisation. As a consequence, an enhanced immunoglobulin E-mediated response to aeroallergens and enhanced airway inflammation favoured by air pollution could account for the increasing prevalence of allergic respiratory diseases in urban areas.

show abstract

Section: Plant-derived Allergensmentioning

confidence: 99%

Section: Plant-derived Allergensmentioning

confidence: 99%

Outdoor air pollution, climatic changes and allergic bronchial asthma

D’Amato¹,

Liccardi²,

D’Amato³

et al. 2002

European Respiratory Journal

222

158

View full text Add to dashboard Cite

show abstract

“…Epidemic asthma outbreaks have been described in many cities: New Orleans [15], New York [16], Melbourne [17], Birmingham [18], London [19], Barcelona [20], Naples [21], Cartagena (Spain) [22], and Toledo (USA) [23]. Soybean [20][21][22] and castor bean [23] are wellestablished causes of asthma outbreaks.…”

Section: Sporadic and Epidemic Sudden Onset Severe Asthma Exacerbationsmentioning

confidence: 99%

Classification of severe asthma exacerbations: a proposal

Picado

1996

Eur Respir J

View full text Add to dashboard Cite

C Cl la as ss si if fi ic ca at ti io on n o of f s se ev ve er re e a as st th hm ma a e ex xa ac ce er rb ba at ti io on ns s: : a a p pr ro op po os sa al l C. PicadoClassification of severe asthma exacerbations: a proposal. C. Picado. ERS Journals Ltd 1996. ABSTRACT: The intensity of asthma exacerbations may vary from mild to severe. Many studies have demonstrated that the speed at which severe asthma exacerbation (SAE) develops varies among patients. In some asthmatics, the exacerbation comes on very quickly, whereas in others there is a progressive deterioration of clinical, functional and blood gas parameters.Sudden SAE are characterised by their explosive presentation and quick recovery. This evolution contrasts with that of patients with a slow onset SAE, who often need prolonged hospitalization. Absence of secretions suctioned from the airways during mechanical ventilation has been reported in sudden SAE, whereas large amounts of viscid mucus are found in patients with the slow onset SAE. The lungs of patients who died during a sudden onset SAE often show empty airways and a predominant neutrophilic infiltration in the bronchial epithelium, in contrast to the presence of abundant eosinophils in patients who died during a slow onset SAE.Sudden onset SAE may occur as sporadic cases or in outbreaks. Sporadic cases may result from the ingestion of nonsteroidal anti-inflammatory drugs (NSAID) in patients with intolerance to these products, massive exposure to common allergens and ingestion of foods containing sulphites. Asthma outbreaks have been described in many cities. In contrast to sudden onset SAE, slow onset SAE is characterized by a progressive deterioration, accompanied by an increase in the use of bronchodilators. Lack of appropriate monitoring of function by peak expiratory flow (PEF) recording, failure of patients to recognize worsening symptoms and underusage of inhaled and oral steroid treatment have been repeatedly identified as factors which are likely to be associated with slow onset SAE. The contribution of psychosocial problems, depression, denial of asthma severity and nonadherence with the treatment should not be overlooked in patients with slow onset SAE.Classification of severe asthma exacerbations into two types (sudden onset and slow onset) could help to reveal the aetiology of the attack and may also be relevant to the management of the patient.

show abstract

“…This condition may be caused either by massive inhalation of airborne soybean dust [9] or thunderstorm activity [10], or associated with sensitivity and exposure to other allergens, such as Alternaria alternata [11], or a stressful event, with a higher incidence of respiratory arrest but a more rapid remission, with a shorter duration of mechanical ventilation. These fulminant, calamitous, dismal presentations of ASA have been categorized by SUR et al [12] as "sudden-onset" fatal asthma, as opposed to the more common "slow-onset" form, to highlight a different aetiopathogenic mechanism and, possibly, a specific underlying structural derangement of the airway.…”

Section: Clinical Frameworkmentioning

confidence: 99%