User Questions

These are questions that users of this website want evidence based answers for. Users can associate references with these questions and leave comments.

They will be considered at the next review of the BOHRF occupational asthma guidelines in 2007.

This is not a part of the BOHRF occupational asthma guidelines.

What resources are needed in referral centres for workers with suspected occupational asthma?

burgeps Barber 2007 not really on topic, but a paper showing how little investigation is considered in a patient with possible occupational asthma seen by general consultant respiratory physicians in the UK

How big a difference between mean PEF on workdays and restdays is required to diagnose occupational asthma

Can occupational asthma exist with a diurnal variation in PEF consistently below 15%

What is the benefit of substitution of a sensitising agent in the control of occupational asthma

burgeps Linnett 1999 A good example of controlling sensitisation by substituting ammonium hexachlorplatinate with tetraammine platinum dichloride in catalytic car exhaust manufacture

What is the effect of omalizumab on occupational asthma?

burgeps Olivieri 2008

What is the role of exhaled breath Nitric Oxide in the diagnosis and management of occupational asthma.

Cedd Burge Smit 2009 Gives a good estimate of the effect of current smoking on the reduction of exhaled breath nitric oxide, which also appears lower in females than in men.
burgeps Baur 2005 eNO measured at 1 and 22 hours following specific challenge with powdered latex gloves and powdered vinyl gloves as control. eNO increased at 1 hour in challenge positive and negative workers (39% challenge positive and 71% challenge negative). At 22 hours an increase >50 in eno had a sensitivity of 69% for astma and 35% for rhinitis. Specificity (no rhinitis or asthma) 100%. eNO reduced in smokers, sensitivity >50% at 22 hrs smoking asthmatics 50% and non-smokers 100%. Supports eNO at 22 hours only in latex asthma, does not separate occupational asthma from occupational rhinitis, but increase >50 at 22 hours seems specific
burgeps Lemiere 2010 The effects of inhaled corticosteroids on FeNO levels appeared to be gone 72 hours after the last dose. There was no increase 7 hours post challenge, an increase >10ppb seen in 6/16 challenge positive workers at 24 hours. FeNO did not contribute to the interpretation of the challenge in this post hoc analysis
burgeps Bohadana 2011 FeNO measured during surveillance of baker and hairdresser apprentices. Raised levels identified a separate group from those with airflow obstruction. No investigation for occupational asthma so utility in diagnosisg occupational asthma not clarified
burgeps Fell 2011

What is the use of induced sputum eosinophilia in the diagnosis of occupational asthma

burgeps Vandenplas 2009 6 of 35 workers with an initial negative specific challenge had a positive challenge on a separate day with higher exposures. 4/6 had an increase in sputum eosinophils >3% after the first negative challenge. 2/29 without occupational asthma also had a >3% increase in sputum eosinophilia after a negative challenge. In this retrospective analysis an increase in sputum eosinophils >3% had a sensitivity of 67% and specificity 97%. Most were exposed to HMW agents. (the paper quotes specificity of 97% but table 2 suggests 2 controls had an increase of at least 3%). NSBR not so sensitive
burgeps Moscato 2010 occupational asthma present with and without sputum eosinophlia. Eosinophilia present in occupational rhinitis
burgeps Lemiere 2010 A 2.2% increase in sputum eosinohils post challenge was seen in 16/20 challenge positive workers and 3/16 challenge negatives. Not affected by maintenance inhaled corticosteroids. This was a post hoc analysis
burgeps Malo 2011 This is an interesting paper, but all the analysis is retrospective and requires prospective validation. Although there was a relationship between sputum eosinophilia, NSBR and occupatiuonal asthma both together and separately, the negative combination is not enough to exclude occupational asthma (negative predictive value 58% when compared with non-occupational asthma. There is no particular reason why NSBR or sputum eosinophilia should be diffeent in occupational and non-occupational asthma. If non-asthmatics are include the negative predictive value is higher. It shows that there are workers with challenge positive occupational asthma where both the NSBR and sputum eosinophils are normal when investigated a median 76 days after last exposure (Interquartile range 1 to 173, showing at least 25% were currently exposed at the time of the challenge). Sputum eosinophils <1% in 65/129 challenge positive OA

What is the benefit of surveillance for occupational asthma and how should it be achieved

burgeps Allan 2010
burgeps Nicholson 2010 Despite its title the recommendations lack evidence as none was found. Baseline questionnaire, face-to-face assessment, and spirometry are recommended. Specific IgE to domestic and laboratory animals MAY be used. Surveillance questionnaires should be used at increased frequency in the first few years, frequency being determined by risk assessment. Surveillance failures should have multidiciplinary investigation.
burgeps Meijster 2011 The authors estimate that the break even point for 3-yearly health surveillance and relocation of workers with nasal or respiratory symptoms, and/or a positive IgE to baking antigens needs to remain below Euro 10,000 per intervention for there to be a net benefit. If the interventions are fully paid for by the employers, the average cost must remain below Euro 4,650 per individual intervention so as not to exceed the employer’s benefits. However, it should be acknowledged that in many cases workplace changes are likely to affect more than one worker and changes will also impact on future workers, which further complicates the assessment of intervention costs at an individual level.
burgeps Suojalehto 2017 At first glance this paper finds that surveillance only detect 11/60 new cases cases of occupational asthma in workers exposed to sensitising agents in Finland, and also states that no cases were detected by spirometry who were asymptomatic. However we are also told that the median time from first symptom to diagnosis was 2.1 years is those detected by surveillance and 2.2 years in those detected (?by their occupational health services) outside formal surveillance visits, and that spirometry was abnormal in 8/15 in whom it was performed at the time investigation was initiated. An alternative explanation would be that symptoms of asthma or rhinitis, or abnormal spirometry, identified at surveillance, did not trigger an evaluation for occupational asthma, or that surveillance was being carried out too infrequently (we have no information on this).

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