Apr 27, 1987 - because of breathlessness and bird watching because of his cough. He had worked for the last 28 years in the same foundry core shop, with ...
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Journal of the Royal Society of Medicine Volume 81 May 1988
Papers read to joint meeting of Sections of Measurement in Medicine and Occupational Medicine, 27 April 1987
Occupational asthma and alveolitis
Occupational asthma- does it exist? P Sherwood Burge MD FRCP Department of Occupational Chest Diseases, East Birmingham Hospital, Bordesley Green East, B9 Keywords: occupational asthma; foundry; isocyanates; peak flow measurements; diagnosis
To make the diagnosis of occupational asthma you need time and enthusiasm. The following case history demonstrates some of the points to make and pitfalls to avoid.
0141-0768/88/ 050252-03/$02.00/0 1988 The Royal Society of Medicine
Case history A 48-year-old foundry core shop trouble shooter developed cough, chest tightness and wheeze, which was diagnosed as bronchitis. He was a life-long nonsmoker and had three such episodes over the next 6 months. After waking with shortness of breath, cough and wheeze at night, asthma was diagnosed. He was treated with inhalers and made an improvement. He then started to become breathless at work, starting at mid-morning and worsening after work at night, and becoming progressively worse as the week progressed. Initially, he was better on weekends away from work and on holidays, but later was not noticeably better at weekends and had become breathless on arriving at work in the morning. He had 3 further episodes of 'bronchitis' with improvement following antibiotics and a 2-4 week period off work. He also became severely breathless on exercise. He was then referred for further investigation. At that time his airways obstruction was also provoked by cold air, exercise, infection, paint fumes, cigarette smoke and hair sprays. He had had to give up gardening and fishing because of breathlessness and bird watching because of his cough. He had worked for the last 28 years in the same foundry core shop, with cores made by different processes; for at least 28 years, some had been made with linseed oil binding; for the last 20 years the shell box system using furanes and phenol-formaldehyde was used; in addition, for the last two years, a cold box system, using phenol-formaldehyde and MDI (diphenyl methane di-isocyanate) had been introduced. On examination, he was wheezy and skin tests to common environmental antigens showed borderline positives to house dust mite and horse hair. Chest X-ray and ECG were normal. Simple lung function tests showed an FEV, of 1.64 (55% of predicted) and an FVC of 3.25 (93% of predicted) and an FEV, and FVC ratio of 50%. Following salbutamol, the FEV, increased by 13% to 1.85 1. Measurements of gas transfer and lung volumes were normal. Comment Asthma in general, and occupational asthma in particular, is frequently misdiagnosed as bronchitis.
Repeated episodes of bronchitis, particularly in the same year, should raise the possibility of asthma. The presence ofcough and sputum maybe apart of asthma. Questions on rest day and holiday improvement are critical to the diagnosis of occupational asthma. Many people with occupational asthma are not worse at work, but are worse after work as in this patient. Once occupational asthma has developed, many nonspecific stimuli frequently induce the asthma, even though the whole cause was related to work. Exercise and infection are the two most common nonspecific provokers of asthma. The diagnosis of occupational asthma may be made on history alone. However, few managers are prepared to alter industrial processes on such evidence. Objective confirmation of the diagnosis can be made from serial measurements of peak flow, provided that the worker is still at work. These records can confirm the workplace as the cause of the asthma, but are often insufficient to pinpoint the exact cause. The detail needed to obtain the most out of serial peak flow measurements is important'. The best method requires 2 hourly measurements of peak expiratory flow rate on days at home and days at work. In patients with marked symptoms, as in this patient, a decision has to be made whether to improve symptoms first, or to obtain records of peak flow at work. It is almost impossible to disentangle the effects
520 500 480 460
r-
440
420 400 380 Peak
Flow l Itres/ min
360 340 320
300 280 260 240
240 1
4
1
II
18
25
Days
Figure 1. Daily maximum (top line), mean (middle line) and minimum (bottom line) peak flow. Workdays have a shaded background, days away from work a clear background. The dose of Becotide was increased from 300 to 800 mg/day at the start of the record. There is sustained improvement throughout the record with no clear work related effect. Such records do not allow the effect of work to be evaluated, for which further recordings are necessary once improvement (or deterioration) has levelled out
Journal of the Royal Society of Medicine Volume 81 May 1988 520 500 480
2.6
2.4
-
460
2.2
440
-
420
-
400
-
380
-
2.0
1.8
-
1.6
Peak
1.4 _
Flow
360
3
340
-
320
-
300
-
Figure 3. Bronchial methane
280
260
-
240
-
................ .
220
1
a
30
min
7 5 6 Hours after challeow
provocation testing
di-isocyanate)
following
,...............
-
4
showing
a
late
8
10
9
to MDI
11
(diphenyl
asthmatic
reaction
exposure to 0.01 ppm
substantial commitment both from the worker and the
~~~medical
..............testing is started, materials used at work, the circumstances of exposure, including the concentration ... ........... ....reached
I
I
330
t-
1
19
be determined so that suitable tests can be carried out. Behind the simple figures (Figure 3) demonstrating
days
that this worker has occupational asthma related to
Figure 2. The next 3 workweeks in the sam e worker. There is deterioration during each workweek, wit)h at least 3 days required for recovery (often making the first day off work the worst each week)
MDI lies a
tests carried out in this worker starting with control exposures which, in this case, were complicated by a late
of work from the effects of treatment change when they both occur together (see Figure 1). Figures 1 and 2 show some of thE Bproblems in evaluated serial peak flow measurement bs. If consistent deterioration at work is seen with Lout weekend recovery, more prolonged periods offwork are required. The occupational history identified three possible causes of occupational asthma (formald ehyde, furanes and MDI). Occupational asthma had not previously been diagnosed in this foundry, making it particularly important to come to the correct diagnoE3is. The precise cause can sometimes be elucidated by fiinding specific IgE antibodies to the offending materrial. However, specific IgE antibodies are not of diagnlOStiC use with furanes, formaldehyde or isocyanates. The only other way of making a precise aetiological dieagnosis is from bronchial provocation testing, which involves a
substantial amount of work.
Table 1 shows the series of bronchial provocation
fall
in FEy1
in the evening.
Workers
days after leaving work, sometimes necessitating several weeks off work before challenge testing is possible.
Our
patient
had
no
reaction
Concentration
(ppm)
did he react to low concentrations of MDI. However when the concentration of MDI was increased, he had a significant late asthmatic reaction and also became hyper-responsive to histamine. Finally, following a further controlled exposure, his sensitivity to MDI was confirmed.
It is interesting that he did not
improve when he stopped working with the cold box system. He was presumably sufficiently exposed to the MDI fumes from this process as a bystander to
maintain his symptoms. Following diagnosis the only job available to him was as a cleaner in the factory yard and a repairer
Max reaction (%) Exposure time Late Starting FEV1 Immediate (min)
Test material
23.11.82 24.11.82 26.11.82 30.11.82 1.12.82 2.12.82 20.1.83 21.1.83 22.1.83 23.1.83 24.1.83 7.2.83 8.2.83 9.2.83 9.2.83
Control Formaldehyde 1%-
-
MDI MDI foam Control Furane resin Cold box MDI Control MDI
< 0.002
