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Chapter 3: Obstructive lung disorders 109

Incidence Pathophysiology
20% of children, 5–14% of adults, increasing in preva- The clinical picture of asthma results from mixed acute
lence. and chronic inflammation leading to bronchoconstric-
tion, mucosal oedema and secretion of mucus into the
Age lumen of the bronchi. With time this repeated stimula-
Can present at any age, predominantly in children. tion causes hyperplasia of the smooth muscle and mucus
glands within the bronchial wall as well as airway wall fi-
Sex
brosis. The pathophysiology is not yet fully understood.
M > F under 16 years, F > Mover16years.
Asthma is a complex mixture of acute and chronic in-
flammation.
Geography
Acute inflammation is largely mediated by allergen
Varies, e.g. rare in underdeveloped countries.
crosslinking of IgE on mast cells, leading to the re-
lease of mediators such as histamine, leukotrienes,
Aetiology
Asthmacanbeclassifiedasfollows,althoughthedivision prostaglandins, proteolytic enzymes and cyto-
is not always clear-cut: kines.
1 Extrinsic asthma where there is an external cause The chronic inflammation is mediated by T cells
It is allergy based and commonly presents in young
producing type 2 cytokines (TH2). IL-5 recruits
atopic individuals. eosinophils, IL-4 and IL-13 lead to IgE synthesis and
Atopy (asthma, eczema, hay fever and other aller-
mucous secretion.
gies)hasafamilialcomponent,itdescribesadisease Eosinophils are also important, secreting mediators of
manifestation related to the development of IgE acute and chronic inflammation including proteolytic
antibodies against environmental antigens. enzymes.
Neutrophils are prominent in severe and virus-
Common domestic allergens include proteins from

house-dust mites, pets and airborne fungi. induced asthma. They secrete mediators of acute and
2 Intrinsic asthma tends to present later in life. There is chronic inflammation including enzymes and oxygen
no identifiable allergic precipitant. radicals.
Epithelial cells from the bronchi are activated by al-
3 Occupational asthma is a particular type of extrinsic
asthma, which may occur in both atopic individuals lergens, viruses and air pollution and release chemo-
(who are more at risk) or non-atopic individuals. tactic factors that recruit and activate inflammatory
Some industrial trigger factors are shown in Table
cells.
3.12. Patients with occupational asthma from the All of the above cell types release mediators of chronic
listed causes are entitled to compensation under in- inflammation recruiting and activating fibroblasts
dustrial injuries legislation in the United Kingdom. leading to airway fibrosis. They also lead, through
Forall patients, non-specific irritant trigger fac-
mechanisms which are not yet clearly defined, to
tors include viral infections, cold air, exercise, bronchialhyperresponsiveness–anexaggeratedbron-
emotion, atmospheric pollution, dust, vapours, choconstrictor response to non-specific insults to the
fumes and drugs particularly nonsteroidal anti- airways.
inflammatories and β-blockers. The pattern of airway reaction following inhalation of
an allergen:
i An acute reaction occurring within minutes, peaking
Table 3.12 Industrial trigger factors for asthma
at ∼20 minutes after inhalation (the acute inflamma-
Mechanism Cause tory response).
Non IgE related Isocyanates, colophony fumes (from ii A late reaction occurring 4–8 hours after inhalation
solder), hardwood dust, complex (the chronic inflammatory response).
platinum salts iii Adual phase response incorporating both acute and
IgE related Allergens (from animals, flour, grain late phase reactions (the mixed acute and chronic in-
and mites), proteolytic enymes
flammatoryresponsethatischaracteristicofasthma).