Λεξικό .. Occupational asthma

Occupational asthma is an important disorder, both for the affected individual and for society. The diagnosis of this condition is not easy and it, therefore, often happens that the occupational origin of asthma is overlooked by physicians. In most instances occupational asthma is due to immunological sensitization to an agent present in the workplace. The numerous possible causes of occupational asthma can be classified in high molecular weight compounds of biologic origin and low molecular weight chemicals. Occupational asthma can also follow from airway irritation, either after an acute inhalational injury, or after chronic or repeated peak exposures to irritants. From a medicolegal point of view, occupational asthma presents problems with regard to establishing a causal relationship between work and asthma and in relation to the generally inadequate compensation of victims. To prevent occupational asthma the best policy is to avoid and minimize exposure to sensitizers at work. Occupational asthma offers interesting models for the study of asthma in general[1] .

About 4% to 9% of adult asthmatics may have occupational asthma. The condition is still under-diagnosed and under-reported. Asking an adult asthma patient whether his or her symptoms improve when away from work and worsen during periods at work is important in detecting potential cases of occupational asthma. Serial peak expiratory flow rate (PEFR) monitoring during periods at work and away from work is useful for providing objective documentation of work-relatedness. Specific challenge testing is carried out to confirm a specific causative agent where a new agent is suspected, where there are multiple agents involved and it is important to establish the exact agent, and when it is not possible to carry out serial PEFR monitoring. Early diagnosis and removal from further exposure to the causative agent in the workplace will benefit the patient with occupational asthma. Preventive measures are important to protect other workers at risk.[3]

.Occupational asthma has been defined as asthma (symptomatic variable airflow limitation associated with airway hyperresponsiveness) caused by exposure to dusts, gases, vapors or fumes in the workplace.  Occupational asthma has been limited to those conditions in which asthma is caused by a sensitizing agent, either an IgE-mediated inhalant allergen or a low molecular weight sensitizing chemical.  The causes of occupational asthma can be classified as following.  The high and low molecular weight chemicals, the former being protein containing antigens which stimulate IgE production.[4]  The low molecular weight chemicals can be further divided into those which have been documented to form haptenes and stimulate IgE production, and those low molecular weight chemical sensitizers whose immunopathogenesis is uncertain. There is an increasing number of airborne noxious agents at work leading to the development of bronchial asthma. Among these are: 

1) (Glyco)-proteins of animal (animal hair, dander, feather bloom, protein dust, insect debris). 

2) Plant: (Flour, grain dust, soya, rastor and green coffee beans, henna, colophony, papain). 

3) Microbial: Isolated enzymes (e.g. a-amylase, glucoamylase, bac, subt. protease, molds, antibiotics). 

4) Chemicals: Isocyanates, anhydrides, formaldehyde, persulfate salts, paraphenylene diamine, azo dyes, platinum salts, cobalt, chloramine T. Occupational asthma has complex pathomechanisms and may involved IgE-mediated responses, irritating effects, toxic lessions and inflammatory reactions. Several studies have indicated that inflammation of the bronchial mucosa is associated with late asthmatic responses and bronchial hyperreactivity. Most important in cases of occupational asthma is a consequent avoidance of the causative materials. Symptomatic treatment is similar to that for bronchial asthma. In occupations with a high prevalence of asthma such as bakers, platinum refiners, isocyanate, anhydride and wood workers, pre-employment investigations and medical surveilance programs ought to be mandatory and regularly performed during employment.. Patients with occupational asthma usually have markedly increased non-allergic bronchial responsiveness. This hyperresponsiveness decreases slowly after removal from exposure months before a normal level is reached. Some patients remain hyper-responsive even after complete cessation of the occupational exposure for several years (Lam et al 1979).

The paucity of available literature indicates that the study of psychological factors associated with occupational asthma is still in its infancy. Though preliminary and in need of replication, the only published study to date suggests that patients with occupational asthma may be highly anxious and many are chronically depressed, a finding that is consistent with previous studies with nonoccupational asthmatics. The established link between psychological factors (e.g., depression and anxiety) and nonoccupational asthma suggests that future studies are desperately needed to more comprehensively assess the scope and severity of the psychological burden of this disease.[2]

References

1. Nemery B. Occupational asthmaVerh K Acad Geneeskd Belg. 1999;61(5):629-42

2. Lavoie KL, Joseph M, Bacon SL. Psychological distress and occupational asthma. Curr Opin Allergy Clin Immunol. 2009 Apr;9(2):103-9.

3. Lee HS, Chee CB. Clinical update on occupational asthma. Ann Acad Med Singapore. 2001 Sep;30(5):546-50; quiz 551

4. Maestrelli P, Boschetto P, Fabbri LM, Mapp CE. Mechanisms of occupational asthma. J Allergy Clin Immunol. 2009 Mar;123(3):531-42; quiz 543-4.