Male patient, 30, was
picked for “Yes” answers on self-delivered questionnaire(6):
of coughing – YES
tightness – YES
dry cough, chest tightness, occasional wheezes, and breathlessness several
times a month mostly in the evening. Respiratory symptoms last >6 months.
admissions in last year, or earlier.
6 months ago – flu
(correlates with 1st episode of wheezing);
4 months ago – acute
Since then wheezes
and cough became more frequent. Last follow-up with GP: chronic bronchitis.
Antibiotics and cough syrup prescribed. Treatment had short effect and symptoms
reoccurred after treatment stopped.
Symptoms are better
on holidays and days when he does not spray coating. He felt better during
2-week vacation. Respiratory symptoms returned within few days he resumed work.
Symptoms are worse on days when he mixes chemicals and sprays in still weather.
No major changes in
procedure, or chemicals he normally used in work place, but he never had
encountered coating agents until current employment.
history: non-smoker, no alcohol consumption.
history: unremarkable. No pets.
no more cases of respiratory symptoms in crew, but several dermatological
problems registered in clinic.
Employee referred to
chest specialist with suspected occupational asthma.
Employee works as
coating sprayer operator with current employer for 1 year 3 months. Previously
worked 10 years uninterruptedly as sandblaster, manual and spray
painter-sprayer with 4 different employers. Denies work with welding and
asbestos. Sandblaster and painter for 3 years. He refuses work with coating
Current tasks: mixing
coating agent before spraying and spraying it. Work is always outdoors, 8–10
hours/day, 6 days/week.
PPE is in use while
mixing and spraying coating: gloves, overall, full face mask respirator with
He refuses hobbies
and activities outside work.
distress, breaths normally at rest, no cyanosis, no clubbing of fingers, no
involvement of auxiliary muscles in breathing, no forced posture. Sometimes dry
cough with no mucus.
Weight 76kg, height
171cm, BMI 26.
Pulse 72 BPM,
regular; BP 120/70; respirations 14RR, SpO296%.
Face: patient is not
clean shaved even he is assigned to full-face respirator.
inspection – unremarkable. Equal chest expansion on both sides. Trachea is
Chest palpation –
unremarkable, vocal fremitus – unremarkable.
Chest percussion –
Chest auscultation –
vesicular sounds with few high pitched late inspiratory wheezing spread
reduced PEF with bronchodilator is evident of airflow obstruction.
4-daily PEF was evident of fall in FEV1 on work days with short improvement on
days away from work, and diurnal variations before and after shift.
Standard laboratory –
1.3%, absolute 0.1×103/µl (normal)
U&E – unremarkable
Total serum Ig E
121 IU/ml (normal)
Chest x-ray imaging: normal.
examination – unremarkable.
Acceptable effort on
spirometry. Evidence of moderate airflow obstruction (FEV1/FVC
unlikely create respiratory distress if compliant with treatment but frequency
of attacks is difficult to predict(7,13,15).
6-minute walk test –
530 m (81% of expected 651 m). mMRC Dyspnoea Scale – Grade 0 – 1. BODE Index –
0 points (80% 4-year survival)(15).
of predicted with marked reversibility with bronchodilator suggest employee is
likely to have “sufficient pulmonary reserve” to meet OGUK fitness requirement
non-disabling episodes of respiratory symptoms,
previous or current episodes of hospital admission
do not require high dose of ICS
It is most probable
employee would be able to retain employment with minimal exposure to prevent
progress of severity, standard treatment and frequent monitoring of respiratory
function. Re-deployment to lower or no exposure environment is preferable with
consent of employee.
(mild intermittent) is intermediate probability: clinical findings, presence of
known asthmagen at work(7,13).
personalized asthma action plan with regular revision
metered aerosol as required
dose ICS trail 6 weeks (Step 2) Pulmicort Turbohaler 200 mcg BD
advice on risk of exposure and need for re-deployment
management (OH management and prevention)
As employee withdrew
consent to disclose condition to employer only result of fitness could be
communicated – restricted fitness certificate valid 1 year(8). Restriction
applied to avoid contact with potential asthmagen(1,9).
Employer should report
to HSE according to RIDDOR(10).
Equality Act 2010 is
likely to apply.
Cessation of further
exposure to asthmagen is required(1,3,4,9). Employee declined change
of employment or re-deployment, refused consent to disclose condition to
employer. Modification of work place to minimize exposure was required: covered
container for chemicals, hood with constant air flow (airline breathing
Further exposure has
risk of progress of asthma. Standard treatment is required. Frequent monitoring
with series of PEF is required(3,4,9,12).
Employee may be
legible for disability benefit (IIDB D7 Occupational Asthma)(5).
Employee did not
require rehabilitation and resumed full capacity. Treatment prescribed and
continued with good adherence and compliance.
chest doctor for follow up and treatment regularly with frequent monitoring of
spirometry. Respiratory function did not decline and admissions to hospital or
absenteeism not occurred.
Employee returned to
work without interruption. Functional capacity of employee retained with
implemented work changes (advanced respiratory protection, enclosed container
to reduce evaporation of chemicals) and continued treatment.
Management and HSE
department took information of asthma case at work seriously. Recommended
changes for the whole crew implemented as advised in new risk assessment.
Employee resigned in
1 year after diagnosis with completion of project.
Asthma presents as reversible
widespread airflow limitation due to airways exaggerated response to offensive
agent as consequence of airways inflammation. Clinical presentation includes
respiratory symptoms, cough, wheezes, chest tightness, breath shortness.
Symptoms of occupational asthma (OA) are associated with workplace exposure(9,12).
asthma pre-exists or coincidentally occurs as new onset, and workplace makes
symptoms worse. OA is result of workplace exposures(3,9,12).
Allergic OA involves
immunologic mechanisms with manifestation after latent period, usually within
first year of exposure to sensitizer(3,4,9,12). Irritant induced OA produces
symptoms within hours after exposure to high concentration of airborne
Most common OA
causative agents: isocyanates, colophony, aldehydes, wood dust, other
occupational agents(9), which are responsible for 9-15% of asthma
cases in working age population(9).
~200-300 new cases of
OA are reported annually, which is most probably underestimated incidence of OA(9).
Diagnosis of OA is
based on thorough medical history and detailed symptoms collection, clinical
examination, variability of clinical symptoms in relation to days on and off
workplace and evidence of casual relation between exposure and symptoms,
symptoms severity and temporal relation(3,4,7,9,12).
occupational exposure is important for diagnosis. Air-sampling in workplace may
be helpful in exposure assessment and identification of offensive agent(1,9,12).
Serial measurement of
respiratory function during work and period away from exposure may reveal reversibility
of airways obstruction to confirm diagnosis of OA(3,4,9,12). Diurnal
PEF variability 20% would strongly suggest asthma(7,9). Serial PEF
requires patient cooperation and compliance(3,4,7,9,12).
Airflow limitation with
reversibility (improvement of FEV1>12%) after bronchodilator are sensitive
and specific indicators, but insufficient to confirm OA if used alone(3,4,9,12).
hyperresponsiveness test is helpful to evaluate degree of bronchial response to
pharmacological agent, particularly in absence of airflow limitation(3,4,7,9,12).
would be helpful for OA induced by HMW allergens, but does not have value for
LMW allergens and irritant induced OA. Skin testing and IgE measurements for
agents responsible for immunological mechanism of OA are useful to confirm
challenge is “gold standard”, but must be administered in specialized centers
and for unclear diagnosis(9,12).
Treatment of OA is
multidisciplinary and patient-centred and of the same step-wise approach as for
treatment of non-occupational asthma(7,13).
Prevention of OA is
required by COSHH(1). Confirmed OA is reportable under RIDDOR(10).
Primary prevention of
OA grounds on workplace risk assessment with identification of asthmagens,
assessment of exposure to them and control of exposure to minimize it(1,3,4,9,12).
is key component of prevention. High level surveillance program should exist
where risk exposure is evident. It encompasses pre-placement and ongoing
respiratory questionnaires, respiratory functions testing, immunology tests if
appropriate, industrial hygiene air monitoring(1,3,4,9,12).
Employee with confirmed
OA is subject to disability protection law, and could be legible for industrial
injury benefits as OA is prescribed occupational disease(5).
Confirmed OA in
workplace should attract revision of health risk assessment followed by
correction and enhancement of existing control measures to prevent further
is crucial, ideally during the first year of symptoms. Redeployment to low or
no exposure location is the best modification to achieve improvement or
resolution of symptoms(1,3,4,9,12). However, continuous low level exposure
is not always effective in those developed OA. Symptoms may persist years after
OH interventions to
be focused on prevention of long term disability and unemployment(1,12).