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TitleAsthma 4th ed - T. Clark (Arnold, 2000) WW
File Size33.0 MB
Total Pages493
Table of Contents
Preface to the fourth edition
Preface to the third edition
1 The definition of asthma: its relationship to other chronic obstructive lung diseases
2 Lung function and bronchial hyperresponsiveness: physiological aspects
3 Exercise and environmentally-induced asthma
4 Bronchial challenge by pharmacological agents
5 The autonomic nervous system in asthma
6 Inflammatory mediators and cytokines in asthma
7 Genetics of asthma
8 Pathology of asthma
9 Epidemiology
10 Occupational asthma
11 β-Agonists: mode of action and place in management
12 Non-steroidal prophylactic agents: mode of action and place in management
13 Corticosteroids: mode of action and place in management
14 Devices for inhaling medications
15 Management of asthma in adults
16 Childhood asthma
17 Health professional and patient education
18 Allergy and asthma: control and treatment
Document Text Contents
Page 2

4th edition

Page 246

Diagnosis of occupational asthma 229

work. Improvement on holidays is more complicated. Holidays away from home need to be
differentiated from holidays at home as domestic allergens, such as animals, birds and moulds,
may be avoided on holidays away from home.

About two-thirds of the workers with occupational asthma complain of cough, sputum and
chest pain which frequently leads to the initial diagnosis of bronchitis (Burge, 1984). Some
workers also have other organs affected and complain of rhinitis, eye irritation, dermatitis or,
occasionally, bowel symptoms. A few workers have fever and joint aches and pains, which are
more often the feature of alveolitis. Indeed some workers have symptoms of both diseases.
However, systemic symptoms can be seen in workers without changes in gas transfer in whom
the predominant part of the disease is in the airways (Paisley, 1969; Lemiere et al., 1996).

Other helpful items to identify in the history are the latent intervals between first exposure
to the possible cause and the onset of disease. Many workers attribute their symptoms to
materials that have recently been introduced and also to materials with strong smells, such as
solvents, but even though these may be responsible, the offending agents may have been in the
workplace for some time. If there is no latent interval the causative agent is likely to be acting
as a direct irritant, such as sulphur dioxide (irritant-induced occupational asthma). Some
occupational allergens, such as laboratory animals or complex salts of platinum, are associated
with short latent intervals averaging a few months. Some, such as isocyanates, have a latent
interval averaging 2 years, and longer in those exposed to colophony, which has a mean latent
interval of 4 years. In bakers, sensitization may occur for the first time more than 20 years after
first exposure. It is likely that the latent interval is longer when exposures are lower.
Occupational asthma is not usually associated with catastrophic attacks of asthma on minimal
exposure at work, although there are a few well publicized cases where this has happened (and
indeed a few deaths due to unexpected exposures). Those with the most extreme sensitivity
are frequently exposed to platinum salts, antibiotics and laboratory animals. In these
circumstances workers may bring home sufficient allergen on their hair or clothing to induce
attacks in an individual with whom they have contact only outside the workplace (Newman
Taylor et al., 1989). The majority of workers, however, show much less sensitivity than this and
can tolerate 8-hour exposures to materials to which they are sensitized day-by-day (much in
the same way as individuals sensitized to house dust mites and grass pollens).

Although the diagnosis can often be made with a reasonable degree of certainty on history
alone, further confirmation should be obtained before decisions are made about change of
work practices, change of employment, or improvements at work are suggested. Few
employers are prepared to spend money on their process solely after a diagnosis made from
the account of an individual worker. Objective confirmation of a diagnosis is much easier at
the early stage of the disease when treatment is minimal and the political situation unclouded.
The best way of proceeding to make an objective diagnosis of occupational asthma is with
serial measurements of peak flow, as described below (Burge, 1982; Bright and Burge, 1996;
Gannon et al., 1996). These do not usually identify the precise cause of the occupational
asthma for which immunological techniques, bronchial provocation testing or
epidemiological studies are required. Nevertheless, there is often enough information from
serial measurements of peak flow on which to base clinical decisions.

Serial measurements of peak flow

International guidelines are available (Moscato et al., 1995). Workers with extreme sensitivity,
who can easily be identified from their history, are not suitable for unsupervised re-exposure
at work, which is a necessary part of serial peak flow measurements. In these patients the
diagnosis can often be confirmed by skin-prick tests or specific IgE measurements, or,

Page 247

230 Occupational asthma

occasionally, by bronchial provocation testing by skilled and experienced investigators, the
levels and duration of exposure being carefully controlled.

The aims of serial measurements of peak flow are to investigate the effects of work on peak
flow. They are substantially more difficult to interpret in those who are changing their
treatment at the same time, and they are less sensitive in workers who are on inhaled steroids
or cromoglycate when the records are made (Burge et al., 1979a,b). It is therefore preferable to
carry out these recordings before treatment is instituted. If prophylactic treatment is being
taken it is important to keep the treatment the same on days at and away from work. It is also
best to make pre-bronchodilator measurements and to keep bronchodilator treatment the
same on work and rest days. The records are more suited to those who are exposed regularly at
work rather than those who have intermittent and irregular exposures.

The best records are obtained by measuring peak expiratory flow two-hourly from waking
to sleeping over several weeks, and to include similar records on days at and away from work
(Gannon et al., 1998). Individuals should be taught to make reproducible measurements of
their peak flow, making at least three readings on each occasion, the best two to be within
20 L/min of each other or else further readings should be made. The best is recorded. It is also
important to record the times of arriving at and leaving work, and any unusual exposures.
Workers who change shifts will also need to record waking and sleeping times, as the diurnal
variation in airway calibre is superimposed upon that related to occupational exposure. These
records are by their nature unsupervised and are potentially liable to falsification. Logging
meters have allowed assessment of incorrectly recorded and prefabricated measurements.
Inaccuracies in time are more common than completely prefabricated readings, which have
been measured between 7% (Gannon et al., 1993) and 24% (Quirce et al., 1995).


When these records are plotted sequentially as a traditional treatment record they are more
difficult to interpret than after replotting, as shown in Figs 10.1-10.3; plotting the daily
maximum, minimum and mean peak flow. The 'day' should start with the first reading at work
and continue until the last reading before work the next day (or equivalent). OASYS is a
commercially available computer-assisted diagnostic aid for the plotting and interpretation of
occupation peak expiratory flow records which includes the ability to plot 'days' as above,
linearize non-linear meters and provided summary plots and an assessment of the likelihood
of an occupational effect (Gannon et al., 1996). The format of the plot is shown in Fig. 10.2.
Visual inspection of these records has been shown to lead to more sensitive and specific
diagnoses than statistical analysis, principally because of the varying interval between
stopping work and the onset of improvement, and between starting work and the onset of
deterioration (Burge, 1982). If it takes several days to improve away from work and several
days to deteriorate at work it may be that the first day or two of work exposure are better than
the first day or two away from work. This substantially complicates statistical analysis. The

Figure 10.1 (opposite) Serial plot of peak expiratory flow (PEF) in an injection moulder with isocyanate

(MDI) exposure. The periods of work have a shaded background, the vertical lines denote waking and

sleeping. The workday is from 6 a. m. to 2 p. m. in the upper panel; the PEF improves over the working

period, and declines during sleep. The workday is from 2 p.m. to 10 p.m. in the lower panel, when PEF

declines, with little change while sleeping. The PEF improves during the days off work at the start of the

lower panel.

Page 492

Index 475

remission related to age, 21-2
in diagnosis and definition, 20-1,199
self-management plans based on, 439
in severity assessment, 359-60

Systemic effects
P-agonists, 257, 260-1,272

tolerance, 262
steroids, 320-3, 364-5

Systemic route
[3-agonists, 273-4
steroids see Corticosteroids

T cells/lymphocytes, 129
chemotactic factors for, 136,138-9
COPDvs asthma, 10-12, 186
helper, 185

allergy and, 446
steroid effects, 311

inflammatory mediators released from, 129
receptor genes, 167

Tachycardia, b-agonist-induced, 260

airway contraction and, 111
in pathophysiology of asthma, 118
receptors see NK receptors

Taifun DPI, 339, 340
drug delivery characteristics, 342

Temperature, air, and exercise- and hyperventilation-
induced asthma, 68-9, 72

Temporal aspects see Time
Terbutaline, 367-8

compared with other agents, 265
pharmacokinetics, 257
prodrug (=bambuterol), 273, 365
subcutaneous, 274

Tetrafluoroethane propellant, 331
Th1 cells, development, 140
Th2 cells

allergy/allergens and, 446
fetus and, 452

cytokines derived from, 139^40
development, 140
steroid effects, 311

Theophylline, 297-8, 366-7
adults, 366-7

step 3 use (moderate-to-severe asthma), 407
step 4/5 use (severe asthma), 407

chronic use, 298
dose/administration, 298, 362
side-effects, 366-7
withdrawal, 297-8

Therapy see Management
Thromboxane, 133^1

synthesis inhibitors, 296
Thrush, oropharyngeal, steroid-related, 319, 364
Tidal breathing, 39, 43
Tidal breathing method (bronchial challenge), 401

mortality trends over, 214-15, 428
in occupational agent reactions, 233-7

Tone, airway/bronchial smooth muscle
autonomic nervous system and, 33,105-6,111
exercise effects on, in asthmatic person, 74
in health, 33,105-6

Total lung capacity, 43
in bronchial challenge tests, 97

Total respiratory system resistance, measurement in
bronchial challenge tests, 98

Trace elements, 211
Tracheal disorders, children, 394-5
Tracheomalacia, 394

of health professionals, 431-3
physical, exercise-induced asthma and effects of, 83

cyclic AMP response element binding protein and,

steroid effects, 305-6, 327

inflammatory and anti-inflammatory genes,

Transcription factor-steroid interactions, 306, 307,

Transfer factor, CO, 47
Transmission disequilibrium test, 156-7
Treadmill test, 64-6
Treatment see Management
Triamcinolone acetonide, 324
Triggering/provoking factors

avoidance, 371
children, 415
see also Prophylaxis

exercise-induced asthma, 71-2
least and most likely, 82

hyperventilation-induced asthmas, 71-2
occupational asthma, 245-6, 447-8

osmotically-induced asthmas, 71-2
Troleandomycin, 317
Tube spacers, 336
Tumour, paediatric airway, 395
Tumour necrosis factor-a gene polymorphisms, 166-7
Turbuhaler, 339, 340, 341

drug delivery characteristics, 341, 342
steroids in, systemic effects, 320

Twin studies, 151,152

Ultrahaler, 339, 340, 341
Ultrasonic nebulizers, 345-6
Upper airway disease in paediatric differential

diagnosis, 394

Vagus nerve, 105
airway smooth muscle and, 33
airway vasodilation and, 113

Vagus reflex mechanisms, 40

alterations in asthma, 119,182-3
permeability, P-agonists reducing, 260

Page 493

476 Index

Vasculature - contd
airway/pulmonary - contd

smooth muscle, autonomic nervous system and,

rings (surrounding trachea), 394-5
Vasoactive intestinal peptide (VIP), 108

airway epithelium and, 114
in pathophysiology of asthma, 117
smooth muscle and

bronchial, 111-12
vascular, 112-13

Ventilation, b-agonist-related increase, 261
Ventilation-perfusion (V/Q) ratios, 44-5
Ventilatory control and acid-base status, 47-8
Ventricular failure, left, diagnosis, 50
Ventstream, 344
Venturi nebulizers, 343, 344
VIP see Vasoactive intestinal peptide
Viral infections, 209

allergy and, 206
paediatric, 206, 209, 389-90

in differential diagnosis, 394, 395
wheezing and, 209, 297-8, 395

Vital capacity (VC)
in bronchial challenge tests, 97
bronchodilator response assessed via, 51
forced see Forced vital capacity

Vitamins, 211
Vocal cord dysfunction, children, 394
Voice hoarseness (dysphonia), steroid-induced, 319,

Volumatic, 336, 337, 338
Voluntary surveillance schemes, 226-8

Wall, airway
innervation see Autonomic nervous system
structural change/thickening, 39, 42

BHRand, 16, 41,187-8
COPD vs asthma, 12-15, 16

Wall, chest, mechanics, 43-4
Weather see Climatic/weather conditions

Weekly patterns, occupational asthma, 235

child's, as sign of chronicity, 399
excess, 372

in defining of asthma phenotype, 149
diagnostic importance, 2
early onset/childhood, 385, 396-8

infants see Infants
post-bronchiolitic see Bronchiolitis
prognosis, 213

epidemiological aspects, 201
functional, 50
genetic factors, 203
viral infections and, 209, 297-8, 395

Whooping cough (pertussis) and its vaccine, 206
Wood dusts, 242-3
Workplace see Occupational asthma
Wright nebulizer, 94
Written action plan, 372, 437-9

X-ray, chest, child, 401-2

Zafirlukast, 288, 370
adverse effects, 294, 370
clinical studies

baseline lung function, 291
bronchoconstrictor response attenuated by, 290
comparison with add-on therapies, 293
comparison with inhaled steroids, 293
comparison with inhaled steroids plus P-

agonists, 370
mild-to-moderate asthma, 292, 293

mode of action, 289, 290
Zileuton, 288, 369

adverse effects, 293-4
clinical studies, 291, 292

baseline lung function, 291
bronchoconstrictor response attenuation, 290

mode of action, 289, 290

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