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1.  Agents and trends in health care workers' occupational asthma 
There is a disproportionately high number of cases of work-related asthma occurring in health care occupations due to agents such as glutaraldehyde, latex and cleaning products.
To understand the causes and measure trends over time of occupational asthma (OA) in health care workers (HCWs).
We reviewed OA notifications from the Midland Thoracic Society's Surveillance Scheme of Occupational Asthma (SHIELD) database in the West Midlands, UK, from 1991 to 2011 and gathered data on occupation, causative agent and annual number of notifications.
There were 182 cases of OA in HCWs (median annual notifications = 7; interquartile range [IQR] = 5–11), representing 5–19% of annual SHIELD notifications. The modal annual notification was 20 (in 1996); notifications have declined since then, in line with total SHIELD notifications. The majority of cases (136; 75%) occurred in nursing, operating theatre, endoscopy and radiology staff. The most frequently implicated agents were glutaraldehyde (n = 69), latex (n = 47) and cleaning products (n = 27), accounting for 79% of the 182 cases. Cleaning product-related OA was an emerging cause with 22 cases after 2001 and only 5 cases between 1991 and 2000.
Control measures within the UK National Health Service have seen a decline in OA in HCWs due to latex and glutaraldehyde, though OA remains a problem amongst HCWs exposed to cleaning products. Continuing efforts are required to limit the number of cases in this employment sector.
PMCID: PMC4523129  PMID: 23933593
Cleaning agent; glutaraldehyde; health care; latex; occupational asthma
2.  Diagnostic approach in cases with suspected work-related asthma 
Work-related asthma (WRA) is a major cause of respiratory disease in modern societies. The diagnosis and consequently an opportunity for prevention are often missed in practice.
Based on recent studies and systematic reviews of the literature methods for detection of WRA and identification of specific causes of allergic WRA are discussed.
Results and Conclusions
All workers should be asked whether symptoms improve on days away from work or on holidays. Positive answers should lead to further investigation. Spirometry and non-specific bronchial responsiveness should be measured, but carefully performed and validly analysed serial peak expiratory flow or forced expiratory volume in one second (FEV1) measurements are more specific and confirm occupational asthma in about 82% of those still exposed to the causative agent. Skin prick testing or specific immunoglobulin E assays are useful to document allergy to high molecular weight allergens. Specific inhalational challenge tests come closest to a gold standard test, but lack standardisation, availability and sensitivity. Supervised workplace challenges can be used when specific challenges are unavailable or the results non-diagnostic, but methodology lacks standardisation. Finally, if the diagnosis remains unclear a follow-up with serial measurements of FEV1 and non-specific bronchial hyperresponsiveness should detect those likely to develop permanent impairment from their occupational exposures.
PMCID: PMC3716794  PMID: 23768266
Asthma; Occupational disease; Diagnosis; Work-related
3.  Bronchoalveolar neutrophilia inversely correlates with DLCO at diagnosis in asbestosis but not lung function decline at 1 year 
Journal of Thoracic Disease  2013;5(3):314-316.
The role of bronchoalveolar lavage (BAL) in the assessment of interstitial lung disease (ILD) remains controversial. Previous studies have demonstrated that BAL cell differential is useful in predicting disease progression in many forms of ILD. We wished to investigate whether BAL had a similar use in predicting disease progression in asbestosis. 21 patients who had significant asbestos exposure, findings of UIP radiologically and BAL performed as part of their investigation were reviewed. There was a significant inverse correlation between percentage BAL neutrophils and percentage predicted DLCO at diagnosis (n=21; P=0.02; r2=–0.25; CI, –0.77-0.08), but not with DLCO decline over 1 year. Unlike previous reports in IPF, BAL cell differential is not predictive of decline in classic asbestosis with a UIP pattern and its routine use in this cohort of patients provides little if any additional benefit.
PMCID: PMC3698289  PMID: 23825766
Bronchoalveolar lavage (BAL); asbestosis; neutrophilia; lung function
4.  Clinical investigation of an outbreak of alveolitis and asthma in a car engine manufacturing plant 
Thorax  2007;62(11):981-990.
Exposure to metal working fluid (MWF) has been associated with outbreaks of extrinsic allergic alveolitis (EAA) in the USA, with bacterial contamination of MWF being a possible cause, but is uncommon in the UK. Twelve workers developed EAA in a car engine manufacturing plant in the UK, presenting clinically between December 2003 and May 2004. This paper reports the subsequent epidemiological investigation of the whole workforce. The study had three aims: (1) to measure the extent of the outbreak by identifying other workers who may have developed EAA or other work‐related respiratory diseases; (2) to provide case detection so that those affected could be treated; and (3) to provide epidemiological data to identify the cause of the outbreak.
The outbreak was investigated in a three‐phase cross‐sectional survey of the workforce. In phase I a respiratory screening questionnaire was completed by 808/836 workers (96.7%) in May 2004. In phase II 481 employees with at least one respiratory symptom on screening and 50 asymptomatic controls were invited for investigation at the factory in June 2004. This included a questionnaire, spirometry and clinical opinion. 454/481 (94.4%) responded and 48/50 (96%) controls. Workers were identified who needed further investigation and serial measurements of peak expiratory flow (PEF). In phase III 162 employees were seen at the Birmingham Occupational Lung Disease clinic. 198 employees returned PEF records, including 141 of the 162 who attended for clinical investigation. Case definitions for diagnoses were agreed.
87 workers (10.4% of the workforce) met case definitions for occupational lung disease, comprising EAA (n = 19), occupational asthma (n = 74) and humidifier fever (n = 7). 12 workers had more than one diagnosis. The peak onset of work‐related breathlessness was Spring 2003. The proportion of workers affected was higher for those using MWF from a large sump (27.3%) than for those working all over the manufacturing area (7.9%) (OR = 4.39, p<0.001). Two workers had positive specific provocation tests to the used but not the unused MWF solution.
Extensive investigation of the outbreak of EAA detected a large number of affected workers, not only with EAA but also occupational asthma. This is the largest reported outbreak in Europe. Mist from used MWF is the likely cause. In workplaces using MWF there is a need to carry out risk assessments, to monitor and maintain fluid quality, to control mist and to carry out respiratory health surveillance.
PMCID: PMC2117138  PMID: 17504818
5.  Defining and investigating occupational asthma: a consensus approach 
At present there is no internationally agreed definition of occupational asthma and there is a lack of guidance regarding the resources that should be readily available to physicians running specialist occupational asthma services.
To agree a working definition of occupational asthma and to develop a framework of resources necessary to run a specialist occupational asthma clinic.
A modified RAND appropriateness method was used to gain a consensus of opinion from an expert panel of clinicians running specialist occupational asthma clinics in the UK.
Consensus was reached over 10 terms defining occupational asthma including: occupational asthma is defined as asthma induced by exposure in the working environment to airborne dusts vapours or fumes, with or without pre‐existing asthma; occupational asthma encompasses the terms “sensitiser‐induced asthma” and “acute irritant‐induced asthma” (reactive airways dysfunction syndrome (RADS)); acute irritant‐induced asthma is a type of occupational asthma where there is no latency and no immunological sensitisation and should only be used when a single high exposure has occurred; and the term “work‐related asthma” can be used to include occupational asthma, acute irritant‐induced asthma (RADS) and aggravation of pre‐existing asthma. Disagreement arose on whether low dose irritant‐induced asthma existed, but the panel agreed that if it did exist they would include it in the definition of “work‐related asthma”. The panel agreed on a set of 18 resources which should be available to a specialist occupational asthma service. These included pre‐bronchodilator FEV1 and FVC (% predicted); peak flow monitoring (and plotting of results, OASYS II analysis); non‐specific provocation challenge in the laboratory and specific IgE to a wide variety of occupational agents.
It is hoped that the outcome of this process will improve uniformity of definition and investigation of occupational asthma across the UK.
PMCID: PMC2078517  PMID: 17130175
6.  FEV1 decline in occupational asthma 
Thorax  2006;61(9):751-755.
In occupational asthma continued workplace exposure to the causative agent is associated with a poor prognosis. However, there is little information available on how rapidly lung function declines in those who continue to be exposed, nor how removal from exposure affects lung function.
Forced expiratory volume in 1 second (FEV1) was studied in 156 consecutive subjects with occupational asthma (87% due to low molecular weight agents) using simple regression analyses to provide estimates of the decline in FEV1 before and after removal from exposure.
In 90 subjects in whom FEV1 measurements had been performed for at least 1 year before removal from exposure (median 2.9 years), the mean (SE) rate of decline in FEV1 was 100.9 (17.7) ml/year. One year after removal from exposure FEV1 had improved by a mean (SE) of 12.3 (31.6) ml. The mean (SE) decline in FEV1 was 26.6 (18.0) ml/year in 86 subjects in whom measurements were made for at least 1 year (median 2.6 years) following removal from exposure. The decline in FEV1 was not significantly worse in current smokers than in never smokers, nor was it affected by the use of inhaled corticosteroids.
FEV1 declines rapidly in exposed workers with occupational asthma. Following removal from exposure, FEV1 continued to decline but at a slower rate, similar to the rate of decline in healthy adults.
PMCID: PMC2117105  PMID: 16670172
occupational health; asthma; lung function; exposure
7.  Inhaled corticosteroids and mortality in chronic obstructive pulmonary disease 
Thorax  2005;60(12):992-997.
Background: Clinical studies suggest that inhaled corticosteroids reduce exacerbations and improve health status in chronic obstructive pulmonary disease (COPD). However, their effect on mortality is unknown.
Methods: A pooled analysis, based on intention to treat, of individual patient data from seven randomised trials (involving 5085 patients) was performed in which the effects of inhaled corticosteroids and placebo were compared over at least 12 months in patients with stable COPD. The end point was all-cause mortality.
Results: Overall, 4% of the participants died during a mean follow up period of 26 months. Inhaled corticosteroids reduced all-cause mortality by about 25% relative to placebo. Stratification by individual trials and adjustments for age, sex, baseline post-bronchodilator percentage predicted forced expiratory volume in 1 second, smoking status, and body mass index did not materially change the results (adjusted hazard ratio (HR) 0.73; 95% confidence interval (CI) 0.55 to 0.96). Although there was considerable overlap between subgroups in terms of effect sizes, the beneficial effect was especially noticeable in women (adjusted HR 0.46; 95% CI 0.24 to 0.91) and former smokers (adjusted HR 0.60; 95% CI 0.39 to 0.93).
Conclusions: Inhaled corticosteroids reduce all-cause mortality in COPD. Further studies are required to determine whether the survival benefits persist beyond 2–3 years.
PMCID: PMC1747271  PMID: 16227327
8.  BOHRF guidelines for occupational asthma 
Thorax  2005;60(5):364-366.
PMCID: PMC1758914  PMID: 15860710
9.  Evidence based guidelines for the prevention, identification, and management of occupational asthma 
Background: Occupational asthma is the most frequently reported work related respiratory disease in many countries. This work was commissioned by the British Occupational Health Research Foundation to assist the Health and Safety Executive in achieving its target of reducing the incidence of occupational asthma in Great Britain by 30% by 2010.
Aim: The guidelines aim to improve the prevention, identification, and management of occupational asthma by providing evidence based recommendations on which future practice can be based.
Methods: The literature was searched systematically using Medline and Embase for articles published in all languages up to the end of June 2004. Evidence based statements and recommendations were graded according to the Royal College of General Practitioner's star system and the revised Scottish Intercollegiate Guidelines Network grading system.
Results: A total of 474 original studies were selected for appraisal from over 2500 abstracts. The systematic review produced 52 graded evidence statements and 22 recommendations based on 223 studies.
Discussion: Evidence based guidelines have become benchmarks for practice in healthcare and the process used to prepare them is well established. This evidence review and its recommendations focus on interventions and outcomes to provide a robust approach to the prevention, identification, and management of occupational asthma, based on and using the best available medical evidence. The most important action to prevent cases of occupational asthma is to reduce exposure at source. Thereafter surveillance should be performed for the early identification of symptoms, including occupational rhinitis, with additional functional and immunological tests where appropriate. Effective management of workers suspected to have occupational asthma involves the identification and investigation of symptoms suggestive of asthma immediately they occur. Those workers who are confirmed to have occupational asthma should be advised to avoid further exposure completely and early in the course of their disease to offer the best chance of recovery.
PMCID: PMC1741012  PMID: 15837849
10.  Ethics of placebo controlled studies of inhaled steroids for COPD 
Thorax  2004;59(6):539-540.
PMCID: PMC1747042  PMID: 15170046
11.  Prednisolone response in patients with COPD 
Thorax  2004;59(2):179.
PMCID: PMC1746940  PMID: 14760166
12.  Sick building syndrome 
PMCID: PMC1740708  PMID: 14739390
13.  So inhaled steroids slow the rate of decline of FEV1 in patients with COPD after all? 
Thorax  2003;58(11):911-913.
PMCID: PMC1746502  PMID: 14586036
14.  Bronchodilator reversibility testing in chronic obstructive pulmonary disease 
Thorax  2003;58(8):659-664.
Background: A limited or absent bronchodilator response is used to classify chronic obstructive pulmonary disease (COPD) and can determine the treatment offered. The reliability of the recommended response criteria and their relationship to disease progression has not been established.
Methods: 660 patients meeting European Respiratory Society (ERS) diagnostic criteria for irreversible COPD were studied. Spirometric parameters were measured on three occasions before and after salbutamol and ipratropium bromide sequentially or in combination over 2 months. Responses were classified using the American Thoracic Society/GOLD (ATS) and ERS criteria. Patients were followed for 3 years with post-bronchodilator FEV1 and exacerbation history recorded 3 monthly and health status 6 monthly.
Results: FEV1 increased significantly with each bronchodilator, a response that was normally distributed. Mean post-bronchodilator FEV1 was reproducible between visits (intraclass correlation 0.93). The absolute change in FEV1 was independent of the pre-bronchodilator value but the percentage change correlated with pre-bronchodilator FEV1 (r=-0.44; p<0.0001). Using ATS criteria, 52.1% of patients changed responder status between visits compared with 38.2% using ERS criteria. Smoking status, atopy, and withdrawing inhaled corticosteroids were unrelated to bronchodilator response, as was the rate of decline in FEV1, decline in health status, and exacerbation rate.
Conclusion: In moderate to severe COPD bronchodilator responsiveness is a continuous variable. Classifying patients as "responders" and "non-responders" can be misleading and does not predict disease progression.
PMCID: PMC1746778  PMID: 12885978
15.  Prednisolone response in patients with chronic obstructive pulmonary disease: results from the ISOLDE study 
Thorax  2003;58(8):654-658.
Background: A trial of corticosteroids has been recommended for all patients with chronic obstructive pulmonary disease (COPD), with the subsequent "response" determining the treatment selected. This approach assumes that patients can be reliably divided into responder and non-responder groups. We have assessed whether such a separation is statistically valid, which factors influence the change in forced expiratory volume in 1 second (FEV1) after prednisolone, and whether the prednisolone response predicts 3 year changes in FEV1, health status, or number of exacerbations during placebo or fluticasone propionate treatment.
Methods: Oral prednisolone 0.6 mg/kg was given for 14 days to 524 patients with COPD before randomised treatment for 3 years with fluticasone propionate or placebo. Factors relating to change in FEV1 after prednisolone were investigated using multiple regression. The response to prednisolone was entered into separate mixed effects models of decline in FEV1 and health status during the 3 years of the study.
Results: The post-bronchodilator FEV1 increased by a mean 60 ml (CI 46 to 74) after prednisolone with a wide unimodal distribution. Current smoking was the factor most strongly associated with the change in FEV1 after prednisolone, with an increase of 35 ml in current smokers and 74 ml in confirmed ex-smokers (p<0.001). There was no relationship between the change in FEV1 after prednisolone and the response to inhaled bronchodilators, baseline FEV1, atopic status, age, or sex. The response to prednisolone, however expressed, was unrelated to the subsequent change in FEV1 over the following 3 years on either placebo or fluticasone propionate. Regression to the mean effects explained much of the apparent prednisolone response. The significant effect of treatment on decline in health status was not predicted by the prednisolone response.
Conclusion: Patients with COPD cannot be separated into discrete groups of corticosteroid responders and non-responders. Current smoking reduces the FEV1 response to prednisolone. Prednisolone testing is an unreliable predictor of the benefit from inhaled fluticasone propionate in individual patients.
PMCID: PMC1746769  PMID: 12885977
16.  Occupational asthma evaluation 
Thorax  2003;58(5):461.
PMCID: PMC1746676  PMID: 12728180
17.  Interpretation of occupational peak flow records: level of agreement between expert clinicians and Oasys-2 
Thorax  2002;57(10):860-864.
Background: Oasys-2 is a validated diagnostic aid for occupational asthma that interprets peak expiratory flow (PEF) records as well as generating summary plots. The system removes inconsistency in interpretation, which is important if there is limited agreement between experts. A study was undertaken to assess the level of agreement between expert clinicians interpreting serial PEF measurements in relation to work exposure and to compare the responses given by Oasys-2.
Method: 35 PEF records from workers under investigation for suspected occupational asthma were available for review. Records included details of nature of work, intercurrent illness, drug therapy, predicted PEF, rest periods, and holidays. Simple plots of PEF and the Oasys-2 generated plots were available. Experts were advised that approximately 1 hour was available to review the records. They were asked to score each work-rest-work (WRW) period and each rest-work-rest (RWR) period for evidence of occupational effect. At the end of each record scores of 0–100% were given for evidence of "asthma" and "occupational effect" for the whole record. Kappa values were calculated for each scored period and for the opinions on the whole record. The scores were converted into four groups (0–25%, 26–50%, 51–75%, 76–100%) and two groups (0–50% and 51–100%) for analysis. This is relevant to scores produced by Oasys-2. Agreement between Oasys-2 scores and each expert was calculated.
Results: 24 of 35 records were analysed by seven experts in the allotted time. For whole record occupational effect, median kappa values were 0.83 (range 0.56–0.94) for two groups and 0.62 (0.11–0.83) for four groups. For asthma, median kappa values were 0.58 (0–0.67) and 0.42 (0.15–0.70) for two and four groups respectively. For all WRW and RWR periods kappa values were 0.84 (0.42–0.94) and 0.70 (0.46–0.87) respectively. Agreement between Oasys-2 and individual experts showed a median kappa value of 0.75 (0.50–0.92) for two groups and 0.50 (0.39–0.70) for four groups. Kappa values for the median expert score v Oasys-2 were 0.75 for two groups and 0.67 for four groups. Agreement was poor for records with intermediate probability, as defined by Oasys-2.
Conclusion: Considerable variation in agreement was seen in expert interpretation of occupational PEF records which may lead to inconsistencies in diagnosis of occupational asthma. There is a need for an objective scoring system which removes human variability, such as that provided by Oasys-2.
PMCID: PMC1746200  PMID: 12324671
18.  Occupational asthma due to low molecular weight agents: eosinophilic and non-eosinophilic variants 
Thorax  2002;57(3):231-236.
Background: Despite having a work related deterioration in peak expiratory flow (PEF), many workers with occupational asthma show a low degree of within day diurnal variability atypical of non-occupational asthma. It was hypothesised that these workers would have a neutrophilic rather than an eosinophilic airway inflammatory response.
Methods: Thirty eight consecutive workers with occupational asthma induced by low molecular weight agents underwent sputum induction and assessment of airway physiology while still exposed at work.
Results: Only 14 (36.8%) of the 38 workers had sputum eosinophilia (>2.2%). Both eosinophilic and non-eosinophilic groups had sputum neutrophilia (mean (SD) 59.5 (19.6)% and 55.1 (18.8)%, respectively). The diurnal variation and magnitude of fall in PEF during work periods was not significantly different between workers with and without sputum eosinophilia. Those with eosinophilia had a lower forced expiratory volume in 1 second (FEV1; 61.4% v 83% predicted, mean difference 21.6, 95% confidence interval (CI) 9.2 to 34.1, p=0.001) and greater methacholine reactivity (geometric mean PD20 253 µg v 1401 µg, p=0.007). They also had greater bronchodilator reversibility (397 ml v 161 ml, mean difference 236, 95% CI of difference 84 to 389, p=0.003) which was unrelated to differences in baseline FEV1. The presence of sputum eosinophilia did not relate to the causative agent, duration of exposure, atopy, or lack of treatment.
Conclusions: Asthma caused by low molecular weight agents can be separated into eosinophilic and non-eosinophilic pathophysiological variants with the latter predominating. Both groups had evidence of sputum neutrophilia. Sputum eosinophilia was associated with more severe disease and greater bronchodilator reversibility but no difference in PEF response to work exposure.
PMCID: PMC1746281  PMID: 11867827
19.  Reliability of PEF diaries 
Thorax  2001;56(9):742.
PMCID: PMC1746145  PMID: 11563363
20.  Glutaraldehyde induced asthma in endoscopy nursing staff 
PMCID: PMC1740178  PMID: 11452052
21.  Sensitisation to natural rubber latex: an epidemiological study of workers exposed during tapping and glove manufacture in Thailand 
OBJECTIVES—To estimate the prevalence of sensitisation to natural rubber latex in latex tappers and latex glove factory workers, and to relate this to airborne exposure to latex.
METHODS—Five hundred workers employed in three latex glove factories, 314 tappers, and 144 college students (control group) were studied. The workers in the glove factories were classified into three exposure groups; high, moderate, and low. Personal exposures to natural rubber latex aeroallergens were measured by immunoassay. Symptom questionnaires and skin prick tests with latex allergens (Stallergènes 1:200 w/v) and other common environmental allergens were performed. The criterion for positivity was a wheal reaction at least 3 mm in diameter greater than that to a diluent control.
RESULTS—The geometric mean (GM) concentration of latex in air was 15.4 µg/m3 for those employed in glove stripping, glove inspections, and packing of powdered gloves. The moderate exposure glove manufacturing group and the tappers had GM concentrations of 2.3 and 2.4 µg/m3 respectively, compared with United Kingdom users of latex powdered gloves,who had GM concentrations of 0.5 µg/m3. The prevalence of sensitisation to latex in the tappers and latex glove factory workers was 1.3% and 1.7% respectively. No positive cases were found among the college students. Workers who showed a positive skin prick test to latex were more likely to be atopic. Work related respiratory and dermatological symptoms were found in about 20% of each population studied, but were not related to the presence of positive latex prick tests.
CONCLUSIONS—This study suggests that in the Thai latex industries, latex sensitisation is rare despite high concentrations of airborne exposure and is less prevalent than in the healthcare sector in Europe where skin exposure is greater. 

Keywords: natural rubber; latex; allergy; glove factory; healthcare
PMCID: PMC1740139  PMID: 11351054
22.  Prevalence and risk factors for latex allergy 
PMCID: PMC1739991  PMID: 10917715
23.  Development of an expert system for the interpretation of serial peak expiratory flow measurements in the diagnosis of occupational asthma. Midlands Thoracic Society Research Group 
If asthma is due to work exposures there must be a relation between these exposures and the asthma. Asthma causes airway hyperresponsiveness and obstruction; the obstruction can be measured with portable meters, which usually measure peak expiratory flow, or sometimes forced expiratory volume in 1 second (FEV1). These can be measured serially (for instance 2 hourly) over several weeks at and away from work. Once occupational asthma develops, the asthma will be induced by many non-specific triggers common to non-occupational asthma. The challenge is to identify changes in peak expiratory flow due to work among other non-occupational causes. Standard statistical tests have been found to be insensitive or non-specific, principally because of the variable period for deterioration to occur after exposure, and the sometimes prolonged time for recovery to occur, such that days away from work may initially have lower measurements than days at work. A computer assisted diagnostic aid (Oasys) has been developed to separate occupational from non-occupational causes of airflow obstruction. Oasys-2 is based on a discriminant analysis, and achieved a sensitivity of 75% and a specificity of at least 94%; therefore peak expiratory flow monitoring combined with Oasys-2 analysis is better to confirm than to exclude occupational asthma. A neural network version in development has improved on this. Both have been based on expert interpretation of peak flow measurements plotted as daily maximum, mean, and minimum, with the first reading at work taken as the first reading of the day. Oasys has been evaluated with independent criteria against measurements made in a wide range of occupational situations. Oasys is sufficiently developed to be the initial method for the confirmation, although less so for exclusion of occupational asthma.
PMCID: PMC1757688  PMID: 10658562
24.  Inhaled corticosteroids in COPD 
Thorax  1999;54(7):655-656.
PMCID: PMC1745528  PMID: 10438305
25.  EUROSCOP, ISOLDE and the Copenhagen City Lung Study 
Thorax  1999;54(4):287-288.
PMCID: PMC1745471  PMID: 10092687

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