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Objectives: A variable proportion of patients presenting to the emergency department (ED) with acute asthma require admission to hospital. Previous studies have identified select factors associated with admission following ED presentation; however, no review has synthesized the evidence in this regard. This systematic review summarizes the evidence regarding factors associated with hospital admission following ED presentation., Methods: Searches were conducted in seven electronic databases and common sources of grey literature. Studies reporting disposition for adults after ED presentation were included. Admission proportions and factors associated with hospitalization that remained statistically significant in multivariable analyses (p < 0.05) were reported., Results: Out of an initial 5865 identified articles, 15 articles met full inclusion criteria and 11 were included in the analyses. Female sex (n = 2) and older age (n = 2) were individual factors associated with admission. Patient vital signs and severity followed by patient attributes were the two most frequent domains associated with admission. Admission proportions were analyzed in 10 studies at an median of ∼20% with no clear change between 1996 and 2012., Conclusions: Factors such as patient demographics (e.g., female sex, older age), patient vital signs/severity, and history are associated with admission following ED presentation for acute asthma. These can be employed by ED clinicians to effectively discern patients at high risk for admission and lead to more evidence-based decision-making.

Background: Since 2001 the International Olympic Committee-Medical Commission (IOC-MC) has required athletes using inhaled beta2 agonists to provide clinical evidence of their asthmatic condition. The aim of this study was to compare the reported prevalence of asthma at the 2000 and 2004 Olympic Games in the Great British Olympic team (Team GB)., Methods: Following local ethics committee approval, 271 athletes (165 men) from the 2004 Team GB volunteered and provided written informed consent. An athlete was confirmed asthmatic if he or she had a positive bronchoprovocation or bronchodilator test as defined by the IOC-MC. Pre-Olympic medical forms from the 2000 Team GB were also examined to establish the prevalence of asthma among the members of Team GB at the 2000 Olympic Games., Results: The prevalence of asthma in the two teams at the 2000 and 2004 Olympic Games was similar (21.2% and 20.7%, respectively). In the 2004 Olympic Games 13 of 62 athletes (21.0%) with a previous diagnosis of asthma tested negative. A further seven with no previous diagnosis of asthma tested positive., Conclusions: The prevalence of asthma within Team GB remained unchanged between 2000 and 2004. The IOC-MC requirement that asthmatic athletes must submit documented evidence of asthma has highlighted that 13 (21.0%) previously diagnosed as asthmatic failed to demonstrate evidence of asthma while seven athletes with no previous history or diagnosis of asthma tested positive. Screening for asthma within elite athletic populations using bronchoprovocation challenges appears warranted to assist athletes in preparing more effectively for major sporting events.

Peak expiratory flow rate (PEFR) has been measured hourly from waking to sleeping in 29 workers with respiratory symptoms exposed to the fumes of soft soldering fluxes containing colophony (pine resin). Thirty-nine records of mean length 33 days have been analysed, and the results compared with the occupational history and bronchial provocation testing in the same workers. From plots of daily mean, maximum, and minimum PEFR, recurring physiological patterns of asthma emerge. The most common pattern is for asthma to increase with each successive working day. Some workers have an equivalent deterioration each working day. Regular recovery patterns taking one, two, and three days are described. The combination of a three-day recovery pattern and a late asthmatic reaction on Monday results in Monday being the best day of each week. Assessment of these records has shown them to be specific and sensitive, provided the worker was not taking corticosteroids or sodium cromoglycate during the period of the record and that bronchodilator usage was kept constant on days at home and at work. The results of the PEFR records correlate well with bronchial provocation testing, and provide a suitable alternative to this for the diagnosis of mild to moderate occupational asthma. The records are of particular use for screening symptomatic workers whose symptoms appear unlikely to be related to work.

In sixty-three workers exposed to toluene di-isocyanate (TDI), no overall differences in bronchial reactivity to histamine inhalation and to exercise testing were found between the total groups of positive and negative TDI reactors to provocation tests. A subgroup of TDI highly sensitive subjects reacting to very low concentrations (less than or equal to 0.001 p.p.m.) were more sensitive to both histamine and exercise than the group who were less sensitive to TDI, and who reacted to higher concentrations (0.002--0.02 p.p.m.) than the group of non-reactors. There were, however, in the last group a number of subjects with high degrees of histamine reactivity who did not react to the TDI. These findings suggest that, on the one hand, the asthmatic reactions to TDI cannot be attributed solely to non-specific mechanisms and, on the other, that in subjects with high degrees of specific sensitivity non-specific mechanisms may also be playing a part.

Occupationally related asthma developing in three patients due specifically to exposure to 1,5-naphthylene di-isocyanate (NDI), a hot curing agent used in manufacturing rubber, has been confirmed for the first time using bronchial provocation testing. This substance has been thought to be safer than toluene di-isocyanate (TDI) and diphenylmethane di-isocyanate (MDI) because of its relatively high melting point (120 degrees C). Each patient worked in the same factory and the circumstances of exposure were similar. Provocation testing was also performed with TDI in concentrations up to 0.018 parts per million (ppm) and MDI in concentrations up to 0.02 ppm, to which the patients had been exposed in the past, but no reactions were elicited. None of the patients had increased bronchial reactivity judged by histamine lability and exercise testing. Each patient was advised to give up his job, but two of the three could not find alternative employment and remained exposed. Three-year follow-up shows that airways narrowing has persisted in those who have remained exposed.

A group of twenty four workers handling di-isocyanates and with respiratory disease were investigated by occupational-type bronchial provocation tests for sensitivity to toluene di-isocyanate (TDI), to which all were exposed, and to diphenylmethane di-isocyanate (MDI) and hexamethylene di-isocyanate (HDI). Sixteen gave asthmatic reactions to TDI and eight of these also reacted to MDI. Four of the eight TDI and MDI reactors had histories of exposure only to TDI, and of them two reacted also to HDI. Of nine subjects tested with HDI, three gave asthmatic reactions, and all three also reacted to TDI and MDI. Thus reactions to MDI and HDI were elicited only in the TDI reactors. The possibility of specific sensitivity to these and other di-isocyanates requires tests in subjects exposed to them and not to TDI.

Sulphur dioxide inhaled at low concentration had no detectable effect on forced expiratory volume in one second in non-asthmatic atopic controls, but it induced asthma and increased bronchial reactivity in nine symptomless atopic and non-atopic asthmatic patients. This increased reactivity was inhibited by sodium cromoglycate (SCG) and partly inhibited by atropine. This suggests that SCG, in addition to its ability to stabilise mast cells, may also act on bronchial irritant receptors or directly on smooth muscle in asthmatic patients.

The prevalence of work-related asthma, rhinitis and urticaria was measured in a scientific establishment working with locusts. Twenty-six percent of those handling the locust in the research centre had work-related wheeze or breathlessness, and one-third had work-related rhinitis and urticaria. Work-related symptoms were uncommon in scientists exposed to locusts in the field, and in other employees at the centre. Antigens were prepared from the locusts, Schistocerca gregaria and Locusta migratoria, as well as the moth, Chilo partellus, which was also bred at the centre. Skin prick testing with the locust antigens showed positive reactions in 55% of the atopic workers at the centre, but were also present in 43% of unexposed atopic workers. In this latter group there was a correlation between positive reaction to locust and dermatophagoides antigens. Atopic workers handling the locusts developed occupational asthma more often and more quickly than similarly exposed non-atopic workers. IgG and IgE antibodies to the locust antigens were found to correlate significantly with both the degree of exposure and the presence of disease.

Peak expiratory flow rate (PEFR) has been recorded hourly or two-hourly from waking to sleeping in workers with respiratory symptoms who were exposed to isocyanate fumes at work. Twenty-three recordings averaging 33 days duration were recorded in 20 workers. Each worker was also admitted for bronchial provocation testing to toluene di-isocyanate (TDI) or diphenylmethane di-isocyanate (MDI) fumes or both. A final assessment of work-related asthma made from subsequent work exposure was compared with the results of bronchial provocation testing and a subjective assessment of the peak flow records. Both techniques were specific and sensitive. Physiological patterns of occupational asthma were defined from the records of PEFR. The most striking finding was the slow recovery from work-induced asthma. This commonly took several days to start and in one worker took 70 days to complete after leaving work. Several workers developed a pattern resembling fixed airways obstruction after repeated exposure at work. The consequences of these findings for the recording of symptoms of occupational asthma are discussed and recommendations are made for the recording of PEFR in workers in general.

A teacher with breathlessness of insidious onset developed acute symptoms on return home following his discharge from hospital. His flat was found to have extensive dry rot (Merulius lacrymans). Precipitins and specific IgE and IgG antibody against M. lacrymans were present and intracutaneous testing gave a typical dual skin reaction. Pulmonary physiology demonstrated airflow obstruction with a low DLCO and KCO, and a chest X-ray showed diffuse micronodular shadowing, maximal in the mid-zones. Inhalation challenge testing provoked a combined asthmatic reaction without a change in DLCO. Rapid clinical recovery and more gradual radiographic and physiological improvement followed cessation of exposure to the antigen.

A group of forty-two steroid-dependent perennial asthmatics was studied over a 13-week period incuding the 8 weeks of a double-blind controlled trial of oral sodium cromoglycate. Given at a dose of 200 mg four times per day the drug provided no significant benefit to the patients when compared with results for those on placebo. Blood from eleven patients consistently failed to release more than 25% of the total cellular histamine when challenged with a range of concentrations of antibody to IgE. All six of the cryptogenic (intrinsic) asthmatics in the trial fell within this group, together with 2/12 asthmatics with negative skin tests but suggestive clinical histories implicating common alergens, and 3/24 extrinsic asthmastics with positive skin prick tests. There was no correlation between drug usage and histamine release in response to challenge with antibody to IgE.

4 patients in whom Didymella exitialis seemed to be an important cause of their asthma were investigated. All 4 patients had immediate skinprick test reactions and specific IgE antibody to D exitialis and Alternaria alternata. Inhalation of a soluble extract of D exitialis provoked immediate asthmatic reactions in these 4, but not in a skin-prick-test-negative volunteer. Radioallergosorbent inhibition studies with D exitialis and A alternata showed self and cross inhibition, which suggested shared antigens. During summer, 1983, 1 of the 4 recorded peak expiratory flow rate (PEFR) twice a day. Spore counts of D exitialis and A alternata were made during this time. Falls in PEFR occurred when D exitialis spore counts increased, usually after a rainfall. Of 34 allergy clinic patients, 6 had skin-prick test reaction to both fungi, but 2 had reactions to A alternata only and 3 to D exitialis only, which suggests the existence of specific antigens. D exitialis seems to be a cause of late summer asthma. Its importance is not known, but allergy to it may contribute to asthma following thunderstorms.

Two patients are described with occupational asthma due to carmine, a natural dye extracted from the insect Coccus cactus. Both had dual asthmatic reactons after carmine inhalation. Oral challenge provoked gastrointestinal symptoms in one patient, and asthma in them both, perhaps accounting for their continuing symptoms. One patient worked extracting carmine from the insects and the other used carmine as a cosmetic colouring agent.

Thirty-seven patients with asthma or alveolitis thought to result from exposure to materials commonly encountered at their work were tested by inhalation of an aerosol of these materials. Twenty-four (65%) developed an immediate asthmatic reaction, which was followed by a non-immediate reaction in 10, of whom six developed the signs and symptoms of alveolitis. Eighteen (76%) patients with asthmatic reactions to test material were prick test positive to that material while only two our of 13 with a negative inhalation test were prick test positive (15%). Precipitating antibody to test material was measured in 23 and was present in nine (39%) of those with positive inhalation tests, and one (12%) of those with negative tests. It was present in five of the six with a reaction in the gas exchanging portions of the lung.

Bronchial provocation studies on 15 workers occupationally exposed to formaldehyde are described. The results show that formaldehyde exposure can cause asthmatic reactions, and suggest that these are sometimes due to hypersensitivity and sometimes to a direct irritant effect. Three workers had classical occupational asthma caused by formaldehyde fumes, which was likely to be due to hypersensitivity, with late asthmatic reactions following formaldehyde exposure. Six workers developed immediate asthmatic reactions, which were likely to be due to a direct irritant effect as the reactions were shorter in duration than those seen after soluble allergen exposure and were closely related to histamine reactivity. The breathing zone concentrations of formaldehyde required to elicit these irritant reactions (mean 4.8 mg/m3) were higher than those encountered in buildings recently insulated with urea formaldehyde foam, but within levels sometimes found in industry.

Twenty-one patients are described who developed asthma, or evidence of a peripheral airways reaction, while working in the electronics industry and exposed to solder flux fumes containing colophony (pine resin). This selected group contained five patients with pre-existing asthma. Fourteen patients had never smoked. Prick-testing with common environmental antigens gave one or more positive reactions in nine patients. The diagnosis was confirmed by occupational-type provocation tests in all workers with colophony-based cored solder, and reproduced by exposure to the fumes of heated colophony alone. Control subjects did not react to the test with colophony. The clinical findings and provocation test reactins have features of a hypersensitivity reaction, although so far specific antibodies have not been found.

Out of twenty patients with a history of asthma or urticaria attributed to food substances, ten reacted on oral challenge: seven with asthma, one with asthma and urticaria and two with urticaria alone. In five of the eight asthmatic reactors, the symptoms developed within a few sec and there was no associated rise in free venous plasma histamine. In those remaining, two with asthma, two with urticaria and one with both, the symptoms developed only after 20-30 min. A rise in free plasma histamine occurred only in the two subjects with urticaria alone. The third with urticaria and asthma did not have blood estimations performed. Sodium cromoglycate in a dosage of 800 mg a day for 1 week, or a single dose of 1.0 g by mouth, did not block any of the reactions. By inhalation it blocked the asthmatic reactions which developed within a few sec of challenge.

Flux cored solder commonly used in the electronics industry is a metal alloy, based on tin and lead, and a flux consisting of colophony with a small concentration of an activator. Thirty-four electronics workers with occupational asthma and seventeen with respiratory symptoms, probably from other causes, have been investigated by occupational type bronchial provocation testing. All the sensitized workers had a significant fall in FEV1 after exposure to colophony fumes for 15 min or less. The non-sensitized workers had no significant reactivity to this test. There was little correlation between the reaction to colophony fumes and the non specific reactivity to histamine, suggesting that colophony fumes were causing specific sensitization. In sensitized workers Portuguese Y colophony was found to cause slightly larger reactions than similar exposures to American WW colophony. In the six workers tested reactions followed exposure to abietic acid alone, the principal resin acid in colophony. Methylation of the carboxyl group of colophony was associated with decreased reactivity. Workers with non-specific bronchial hyperreactivity also sometimes reacted after exposure to fumes from the flux activators alone, but even this reaction could show specificity for the specific activator to which the workers was exposed. Finally two non-colophony substitute materials were evaluated.

Dose-response curves for atropine and ipratropium bromide were made in nine asthmatics unresponsive to salbutamol. Conventional doses of ipratropium resulted in significantly less bronchodilatation than large doses of atropine, suggesting that larger doses of ipratropium should be used.

Histamine has been measured in whole blood and in the plasma of twenty-three subjects following exercise testing of seventeen asthmatics and six normal controls. Whole blood histamine rose in both asthmatics and controls and was associated with a concomitant rise in the basophil count. Plasma histamine in the peripheral venous blood only rose in one patient who developed urticaria after exercise.

The article highlights the studies presented during the meeting about the advances in allergic disease of the skin and lungs. Bruce Mitchell of the Clinical Research Center, described studies on the pathology of delayed hypersensitivity skin reactions elicited by patch testing. John Price examined the immediate and late reactions in skin, lungs, and nose of selected children with perennial asthma. Meanwhile, David Atherton reviewed several studies on the dietary treatment of atopic eczema.