Letter from the British Occupational Health
Research Foundation
We do not have any research relating to non-occupational
allergies and their impact on work and attendance. However, we
are able to provide evidence pertaining to a specific allergy
ie; occupational asthma from: Newman Taylor AJ, Nicholson PJ (Editors).
Guidelines for the prevention, identification and management of
occupational asthma: Evidence review and recommendations. British
Occupational Health Research Foundation. London 2004.
The strength of evidence is identified as:
*** Strong evidence—provided
by generally consistent findings in multiple, high quality scientific
studies.
** Moderate evidence—provided
by generally consistent findings in fewer, smaller or lower quality
scientific studies.
* Limited or contradictory evidence—provided
by one scientific study or inconsistent findings in multiple scientific
studies.
We note that your letter refers to "The
Provision of Allergy Services" Department of Health July
2006. One of the editors of the BOHRF Evidence Review was a member
of the National Allergy Advisory Group associated with that review.
DEFINING THE
PROBLEM:
What is asthma?
Asthma is a condition of chronic inflammation
of the airways, characterised by widespread airflow limitation
that is reversible, either spontaneously or with treatment over
short periods of time. The inflammation results in hyper-responsiveness
of the airways to many stimuli eg cold air, cigarette smoke, exercise,
etc and in the clinical setting to methacholine and histamine.
Symptoms include wheeze, cough, shortness of breath and chest
tightness and are often worse at night or in the early morning.
Work-related asthma occurs when there
is an association between symptoms and work. The two different
types of work-related asthma are:
— work aggravated asthma, ie pre-existing
or coincidental new onset adult asthma which is made worse by
non-specific factors in the workplace, and
— occupational asthma ie adult asthma
caused by workplace exposure and not by factors outside of the
workplace.
Occupational asthma is subdivided into:
— allergic occupational asthma characterised
by a latency period between first exposure to a respiratory sensitiser
at work and the development of hypersensitivity symptoms, and
— irritant-induced occupational
asthma that occurs typically within a few hours of a high
concentration exposure to an irritant gas, fume or vapour at work.
The evidence provided hereafter relates exclusively
to allergic occupational asthma.
What is and what is not known about the origins
and progression of occupational asthma?
Four risk factors have been identified including
the predisposing factors of atopy and genetic predisposition,
the causative factor of exposure to an agent at work and the contributing
factor of cigarette smoking.
Atopy is a state characterised by the
propensity to produce specific immunoglobulin IgE on ordinary
exposure to common allergens in the subject's environment.
*** Atopy increases the risk of developing
occupational asthma caused by exposure to many high molecular
weight agents that induce the production of specific IgE antibodies.
** Some genes may predispose to occupational
asthma for some agents.
Several hundred workplace agents are reported
to cause occupational asthma. Those that induce allergic occupational
asthma can be divided into those of high and low molecular weight.
The former are usually proteins and appear to act through a type
I, IgE associated hypersensitivity. Whilst some low molecular
weight chemicals are associated with specific IgE antibodies,
this is not the case for the majority.
*** The risk of sensitisation and occupational
asthma is increased by higher exposures to many workplace agents.
*** The most frequently reported agents include
isocyanates, flour and grain dust, colophony and fluxes, latex,
animals, aldehydes and wood dust.
*** The workers most commonly reported to
surveillance schemes of occupational asthma include paint sprayers,
bakers and pastry makers, nurses, chemical workers, animal handlers,
welders, food processing workers and timber workers.
** The workers reported from population studies
to be at increased risk of developing asthma include bakers, food
processors, forestry workers, chemical workers, plastics and rubber
workers, metal workers, welders, textile workers, electrical and
electronic production workers, storage workers, farm workers,
waiters, cleaners, painters, plastic workers, dental workers and
laboratory technicians.
** Cigarette smoking can increase the risk
of developing occupational asthma with some sensitising agents.
** Occupational rhinitis and occupational
asthma frequently occur as co-morbid conditions in IgE associated
occupational asthma.
Occupational rhinitis is a risk factor for the
development of occupational asthma, especially for high-molecular-weight
sensitisers:
** Rhino-conjunctivitis is more likely to
appear before the onset of IgE associated occupational asthma.
* The risk of developing occupational asthma
is highest in the year after the onset of occupational rhinitis.
Generally, occupational asthma is reported to
have a poor prognosis and to be likely to persist and deteriorate
unless identified early and managed effectively.
*** The symptoms and functional impairment
of occupational asthma caused by various agents may persist for
many years after avoidance of further exposure to the causative
agent.
Why does the UK in particular have such a high
prevalence of occupational asthma?
The reported prevalence of occupational asthma
in the UK is similar to other westernised countries.
*** Occupational factors are estimated to
account for 9-15 per cent of cases of asthma in adults of working
age, including new onset or recurrent disease.
*** The annual population incidence of occupationally
related asthma ranges from an estimated 12 to 170 cases per million
workers with an estimated mean of 47 cases per million workers.
What gaps exist in establishing the overall disease
burden of occupational asthma and what are the barriers to filling
the gaps?
One of the two reporting schemes (SWORD) is
voluntary and the other (RIDDOR) requires patient consent. This
leads to under-reporting in both.
* The population incidence of occupational
asthma may be underestimated by as much as 50 per cent.
TREATMENT AND
MANAGEMENT
What is the effect of current treatments on the
natural history of occupational asthma?
The pharmacological management of occupational
asthma is no different to that of any case of adult asthma. What
differs is the occupational health management.
A single small randomised-controlled trial has
examined the effect of inhaled corticosteroids on the recovery
from occupational asthma after cessation of exposure. Small but
statistically significant improvements in some symptoms, peak
flow and quality of life were reported.
Workers who remain in the same job and continue
to be exposed to the same causative agent after diagnosis are
unlikely to improve and symptoms may worsen.
What is the evidence base for pharmacological
and non-pharmacological management strategies?
Complete avoidance of exposure may or may not
improve symptoms and bronchial hyper-responsiveness. Both the
duration of continued exposure following the onset of symptoms
and the severity of asthma at diagnosis may be important determinants
of outcome. Early diagnosis and early avoidance of further exposure
either by relocation of the worker or substitution of the hazard
offer the best chance of complete recovery.
*** The likelihood of improvement or resolution
of symptoms or of preventing deterioration is greater in workers
who have no further exposure to the causative agent.
** The likelihood of improvement or resolution
of symptoms or of preventing deterioration is greater in workers
who have relatively normal lung function at the time of diagnosis.
** The likelihood of improvement or resolution
of symptoms or of preventing deterioration is greater in workers
who have shorter duration of symptoms prior to diagnosis.
** The likelihood of improvement or resolution
of symptoms or of preventing deterioration is greater in workers
who have shorter duration of symptoms prior to avoidance of exposure.
Is the level of UK research into occupational
asthma adequate?
BOHRF produced the world's first evidence based
guidelines for occupational asthma hence the UK is seen as a world
leader in this area along with Canada, France and Spain. More
research has been identified by the Health & Safety Executive
examining in particular worker behaviour. Further research should
be undertaken to assess the impact of evidence based guidelines
and how their impact might be improved, and the most suitable
components and frequency of health surveillance.
GOVERNMENT POLICIES
How effective have existing Government policy
and advice been in addressing the rise in occupational asthma?
The Health and Safety Executive (HSE) estimate
that 1,500 to 3,000 people develop occupational asthma each year.
HSE estimates that the costs to society of new cases of occupational
asthma are up to £1.1 billion over 10 years. HSE set up an
Asthma Project Board in 2000 to help it reduce the incidence of
occupational asthma by 30 per cent over 10 years. Data suggests
that the incidence has reduced in the last three years.
PATIENT AND
CONSUMER ISSUES
What impact does occupational asthma have on quality
of life of patients and their families?
There is consistent evidence that:
** Approximately one third of workers with
occupational asthma are unemployed up to six years after diagnosis.
** Workers with occupational asthma suffer
financially.
What can be done to better educate the public
and to improve the quality of information that is available to
patients and undiagnosed sufferers?
We believe that the BOHRF reviews and their
practical lay guidance for the public, managers and safety professionals
serve as a good model for communicating important messages as
both hard copy and on the internet. Furthermore leaflets and internet
based advice aimed at primary care staff serves to increase awareness
to lead to earlier identification of cases.
Only one in eight of the UK workforce has access
to comprehensive occupational health support. Making access more
available is a key opportunity. As well as increasing the numbers
of competent human resource, it would be useful to provide access
to better online support, eg by making respiratory questionnaires
accessible online.
Are current regulatory arrangements for private
clinics satisfactory?
Any clinician may open and offer an occupational
health service. Competence should be better defined and relate
to qualifications and revalidation of providers.
Since many cases of occupational asthma first
report to primary care, there is a need for better training in
occupational medicine for GPs.
31 October 2006
| 
