Identifying occupational asthma

In the second part of this respiratory health special report, Bernard Garbe looks at how serial peak expiratory flow can be used to identify occupational asthma.

The first part of the report explores the 2010 BOHRF Occupational Asthma Guidance on sensitiser-induced occupational asthma.

In occupational health, lung disease is the most common form of disease encountered after skin problems. Occupational lung diseases include byssinosis (typically cotton dust), allergic rhinitis, farmer’s lung, asbestosis, pneumoconiosis (most commonly coal dust), silicosis and chronic obstructive pulmonary disease (COPD). While COPD has the greatest mortality rate, occupational asthma (OA) has by far the greater incidence.

OA, by definition, is a lung disease caused by occupational exposures and is the cause of about 15% of adult-onset asthma. Occupational asthma often results in skilled and experienced people having to end their careers, in many cases without a confirmed diagnosis. In nearly half the diagnosed cases the diagnosis will be incorrect on the basis of history alone (Meyer et al, 2001).

The Health and Safety Executive (HSE) estimates that OA will cost the UK economy £1 billion over the next 10 years. The correct diagnosis and management of the condition is therefore vital to both workers and employers to ensure that years of productive work are not lost and that any potential medical, health and safety or compensation issues are clarified.

The British Occupational Health Research Foundation (BOHRF) range of guides for occupational asthma identification, management and prevention includes guidelines for occupational health practitioners among other groups.

Occupational health professionals often find the detection and classification of OA difficult. Patients experience a mean delay of four years for assessment in secondary care (Fishwick et al, 2007). Work-related asthma is often under-recognised and misdiagnosed (Rosenman et al, 1997). Practice often lacks the rigorous objective medical testing necessary to diagnose OA and to confirm or exclude it from a relationship with workplace exposure in an objective and documented way. Serial peak expiratory flow (PEF) measurements are a simple way to address this. The 2001 SWORD (Nicholson et al, 2005) survey showed that only 15% of OH departments were able to offer diagnostic tests complying with the new British Thoracic Society (BTS) guidelines for OA, based on the evidence-based

BOHRF guidelines. While medical history and physical examination lack both the sensitivity and specificity of diagnostic tests for occupational asthma (Malo et al, 1991), delayed diagnosis can lead to a worsened prognosis (Paggiaro et al, 1994).

In 2000, the Health and Safety Commission (HSC) announced a 10-year occupational health strategy for Great Britain. The strategy sets the ambitious target of a 30% reduction in new cases of OA by 2010. The strategy contains several components, including improved education and more research. The results are not yet published, but 2007 data from The Health and Occupation Reporting Network (THOR) seems to indicate that this will be achieved.

Work-related asthma can be divided into two general groupings: occupational asthma and work-aggravated asthma. Occupational asthma is subdivided into occupational asthma with latency and occupational asthma without latency. Latency is the interval between exposure to an asthma causing agent and the onset of asthma symptoms – the latency period can be from weeks to years and is difficult to predict. Occupational asthma without latency is also termed reactive airways dysfunction syndrome or “irritant-induced asthma”.

Agents causing OA can be subdivided into high molecular weight agents and low molecular weight agents. High molecular weight agents (for example, wheat flour) sensitise a worker via an Immunoglobin E-mediated process. Atopy is known to increase the risk of occupational asthma to high molecular weight agents. Low molecular weight agents (for example, isocyanates) often sensitise a worker via interactions with endogenous proteins inducing a physiological response (Wisnewski et al, 2003). Isocyanates, flour and grain were the most commonly cited agents for occupational asthma from 2006 to 2008 in the THOR industrial injuries and disablement benefit schemes. Occupations with high incidence rates of OA also include vehicle paint sprayers, metal making/treating process operatives, bakers and flour confectioners. The highest incidence rate of occupational asthma as reported to chest physicians was found among individuals involved in the manufacture of basic metals.

Spirometry is essential in the detection, diagnosis and management of occupational asthma in susceptible workers. Measurements of the forced expiratory volume in one second (FEV1) and the forced vital capacity (FVC) and the FEV1/FVC ratio are the essential and basic spirometric measurements. An initial assessment of whether a restrictive or obstructive pattern of impairment is present can be determined by spirometric results.

  • When both the FEV1 and the FEV1/FVC values are below reference values, an obstructive pattern of respiratory impairment is considered present.
  • A restrictive pattern of respiratoryimpairment is indicated when the FVC is below reference values and the FEV1/FVC is normal.

Asthma is characterised by reversible airflow obstruction. To document reversibility from a depressed baseline examination spirometry is performed before and after a dose of a short-acting bronchodilator. Reversibility of airflow obstruction is indicated by a 12% increase in FEV1, typically with a minimum volume increase of 200ml. Occasionally, obstruction is present that is not initially reversible. Two- to four-week trials of a corticosteroid may be necessary to mitigate the inflammatory component of the asthma such that reversibility may be demonstrated (comparing pre- and post-steroid FEV1).

A normal spirometric result does not exclude a diagnosis of asthma. An asthmatic may have normal FEV1 during asymptomatic periods and between asthma episodes. There is little diagnostic value in assessing bronchodilator response when the spirometric values are normal and the patient is asymptomatic.

Peak expiratory flow (PEF) readings can assess large airways obstruction in OA, and PEF is useful in assessing changes related to workplace activities. Supportive evidence of asthma is provided by documenting variability in peak flow readings over the course of the day or after inhaled bronchodilators.

Opinion is divided about whether peak flow or FEV1 is of most value in OA assessment but, whichever value is used, appropriate instruction, coaching and monitoring of technique are essential to avoid variability due to poor effort or technique.

An effective peak flow test is performed as follows:

  • Fit a mouthpiece or bacterial viral filter to the peak flow meter.
  • Ask the subject to inhale as deeply as possible and without exhaling form an airtight seal around the mouthpiece.
  • Exhort the subject to exhale, with as much force as possible, for at least a second.

It is important when measuring only PEF that the expiration is the same as the beginning of a spirometry test manoeuvre, “spitting” into the peak flow meter produces falsely high results.

  • Repeat the test three times and take the highest reading from the three tests as the result.

Workplace challenge testing through serial PEF monitoring is commonly used to demonstrate a workplace association to asthma. Such challenge testing can take three forms:

  • serial PEF both within the workplace and outside the workplace;
  • EF measurements pre- and post- workplace exposure (cross-shift); and
  • stop/resume workplace testing with appropriate clinical and PEF monitoring.

Serial PEF monitoring is simple, inexpensive and usually acceptable to the worker and employer. The worker is instructed to measure his/her PEF every two to four hours, during waking hours, for two weeks while still at work and for two weeks while not at work. A typical protocol may be PEF reading on waking, at noon, following work and at bedtime. Each measurement should consist of three attempts. The worker should be instructed to record the best measurement. Any medications should be used after the PEF measurement.

The worker is typically asked to record times of starting and ending work, waking and bedtime, medication use, time periods of workplace exposures, the types of chemical exposures and asthma symptoms.

A potential limitation to serial PEF is the ability to measure and record peak flow accurately and worker adherence in taking measurements. The use of a hand-held automated respiratory monitor is optimal for recording collection of PEF measurements and documentation of compliance. In one study, data collected on computerised peak flow devices in workers not informed of the automated data collection revealed that only 55% of manually recorded measurements were completely accurate relative to electronic documentation and 23% were complete fabrications (Quirce et al, 1995). While eight recordings per day is optimal, four measures per day has good sensitivity and specificity (Anees et al, 2004).

Devices, such as the Vitalograph e-diary, can record PEF and the events as well as incorporating questionnaires. Data from this e-diary can be sent in real time to a web server if required. Whether manual, semi-automated or fully automated, a graph of the maximum PEF rate is documented for each set of measurements during the worker’s waking hours.

PEF records can be difficult to interpret. Patients with asthma usually have their lowest PEF in the early morning. The physician looks for a pattern of lower peak flow following workplace exposure. This may be cumulative through the week. The “diurnal variation” of PEFs – the difference of the maximum PEF and the minimum during the course of a day – is also used. This difference is expressed as a percentage of the maximum PEF rate, termed the “diurnal variation percentage”.

A big diurnal variation is a clear indicator for asthma, but is it work related? Increased diurnal variation percentages or reductions in the maximum peak expiratory flow rate during work exposures relative to non-work periods are indicative of work-related asthma (Chan-Yeung et al, 1995). But this factor is helpful only in a regular working week. Many workers with exposure to potential OA-causing agents work a rotating shift pattern.

The solution to this complexity is OASYS (occupational asthma expert system), (Moore et al, 2010), a free-to-use web-based software package. OASYS is a sensitive tool for detecting work-related changes in PEF readings. It has advanced graphing to aid visual analysis and three methods of computer scoring for non-experts.

Oasys score and probabilityof OA

  1. <1% probability of OA
  2. 1%-49% probability of OA
  3. 50%-99% probability of OA
  4. >99% probability of OA

The OASYS program scores each rest-work-rest or work-rest-work complex in a serial peak flow record between 1 and 4 (see box right).

It is common for a person no longer working in the job role associated with his/her symptoms to be diagnosed with OA (Friedman-Jiménez et al, 2000). In such instances, referral to an asthma specialist is advisable. If return to the job role of exposure is feasible, and there are no medical contraindications, a diagnostic trial of return to work is attempted.

Following return to the workplace, clinical symptoms, medication use and serial PEF are monitored for a determination of how much they are work related.

In conclusion, serial PEF recording with an electronic device is a part of the proper objective evaluation of a worker with OA and is essential for appropriate diagnosis and management. Diagnostic testing for OA can be undertaken by the non-expert, but post-employment occupational asthma requires the services of an OA specialist.

Bernard Garbe is managing director of Vitalograph.

References

Meyer JD, Holt DL, Chen Y, Cherry NM, McDonald J C, SWORD 99: Surveillance of Work-Related and Occupational Respiratory Disease in the UK, Occup Med (London), 2001; 51:204-208.

British Occupational Health Research Foundation (BOHRF).

Fishwick D, Bradshaw L, Davies J, Henson M, Stenton C, Burge S, Niven R, Warburton CJ, Hendrick D, Rogers T, Rawbone R, Curran AD. Are we failing workers with symptoms suggestive of occupational asthma?

Prim Care Respir J. 2007 Oct; 16(5):304-10.

Rosenman KD, Reilly MJ, Kalinowski DJ. A state-based surveillance system for work-related asthma. J Occup Env Med. 1997; 39(5):415-425.

Nicholson PJ, Cullinan P, Newman Taylor AJ, Burge PS, Boyle C. Evidence based guidelines for the prevention, identification, and management of occupational asthma, Occup Environ Med, 2005; 62:290-299.

British Thoracic Society; Scottish Intercollegiate Guidelines Network. British guideline on the management of asthma. Thorax 2003: 58 Suppl 1:i1-94.

Malo JL, Ghezzo H, L’Archeveque J, Lagier F, Perrin B, Cartier A. Is the clinical history a satisfactory means of diagnosing occupational asthma? Am Rev Respir Dis. 1991; 143:528-532.

Paggiaro PL, Vagaggini B, Bacci E, Bancalari L, Carrara M, Di Franco A, Giannini D, Dente FL, Giuntini C. Prognosis of occupational asthma. Eur Respir J. 1994; 7:761-767.

THOR publications Papers published from the occupational disease reporting schemes.

Wisnewski AV, Herrick CA, Liu Q, Chen L, Bottomly K, Redlich CA. Human gamma/delta T-cell proliferation and IFN-gamma production induced by hexamethylene diisocyanate. J Allergy Clin Immunol. 2003; 113:538-546.

Health and Safety Executive Table THORR07.

Quirce S, Contreras G, Dybuncio A, Chan-Yeung M. Peak expiratory flow monitoring is not a reliable method for establishing the diagnosis of occupational asthma. Am Rev Respir Dis. 1995; 152:1100-1102.

Anees W, Gannon PF, Huggins V, Pantin CFA, Burge PS. Effect of peak expiratory flow data quantity on diagnostic sensitivity and specificity in occupational asthma. Eur Respir J. 2004; 23:730-734.

Chan-Yeung M. Assessment of asthma in the Workplace. Chest. 1995; 108(3):1084-1117.

Moore VC, Jaakkola MS, Burge PS, A Systematic Review of Serial Peak Expiratory Flow Measurements in the Diagnosis of Occupational Asthma, Annals of Respiratory Medicine, 2010; 1:31-44.

Friedman-Jiménez G, Beckett WS, Szeinuk J, Petsonk EL. Clinical evaluation, management, and prevention of work-related asthma. AJIM. 2000; 37:121-141.

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