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Reactive Airways Dysfunction Syndrome 

(RADS)


Definition.

There has been some debate as to whether RADS is a type of  "Occupational asthma" (OA) but the balance of agreement seems to be shifting to the conclusion that it should be considered to be such. However it has features which are different from the original classical description of OA. 

RADS can therefore be considered as a category of occupational asthma developing without a period of latency and often associated with exposure to high concentrations of irritants. Its symptoms may be somewhat different from that of asthma that follows a latent period. The airways irritability tends to persist for a variable period after the causal exposure and is provoked by a range of occupational and non-occupational irritants or other provoking factors (e.g. cold). This is thus referred to as Reactive Airways Dysfunction Syndrome. 

Zinc exposure and aluminium refining have been associated with RADS/OA although usually in contexts of high exposure to irritant fume. However it is not yet possible to draw specific conclusions as to which agents (elemental metals, their salts or gaseous irritants) in these occupations are specific asthmagens and why. They might be included within a category of inorganic asthmagens which is much less clearly defined both as regards mechanistic inferences and in the nature of their associated adverse outcome. Often  these substances tend to be relatively water soluble gases which result in a   low pH such as sulphur dioxide and/or which have a high oxidant capacity, such as is the case with chlorine. Other causal exposures which have been  described have included high concentrations of diesel fume from locomotives. 

The mechanism of their action is still unclear, but oxidation or other cell surface reactions are probably important in inflicting severe damage to the mucosal epithelium and setting off a cascade resulting in asthma. Additionally there are exposures which do not, as far as is known, generally cause asthma on their own but which increase risk of occupational asthma.  The most notable and ubiquitous of these is tobacco smoking. Further study is needed to determine the chemical reactions associated with intermediary biological effects such as increased epithelial permeability which may then increase the risk of developing occupational asthma. 

Classical immune sensitisation is probably not a significant factor in RADS. 

There is anecdotal evidence that the risk of developing RADS is related to the exposure level. In other words - the higher the concentration of inhaled agent, the greater the likelihood of   of experiencing symptoms of asthma. However it is difficult to set exposure limits below which exposures can be regarded as 'safe' in an absolute sense. Moreover it is likely that once RADS develops the airborne concentrations at which symptoms could be provoked might be significantly lower than the concentrations responsible for the illness in the first place. 

Good health and safety management and work practice should prevent RADS. In one of the cases seen by the author the condition developed after mixing of acid and bleaching solution resulted in a massive release of chlorine. In another, a substantial release of sulphur dioxide from a film developing machine in a poorly ventilated area was responsible. They should have been easily preventable. Personal protection, albeit the last line of defence, may play an important role in situations where control at source is clearly impracticable. Similarly, personal protective equipment would clearly be appropriate if a process plant was undergoing maintenance or being upgraded. 

RADS is being increasingly recognised as a contributor of work-related ill-health, although if distinguished from the main bulk of occupational asthma it is a small component of  occupational lung disease in general. 
 
 


Conclusion

RADS will undoubtedly be the subject of further research and will hopefully become more easily defined and explained and prevented in due course. The number of recognised occupational hazards is likely to increase. Many are probably already in existence but have not yet been recognised. Our capability to predict these hazards should improve, and better control methods should be more universally applied. In those lamentable instances where prevention or early detection fail, affected workers must hope that the paths to rehabilitation and to compensation will become smoother. 
 
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References

(This section is not yet complete) 
    In: Banks DE and Mei-lin W. (Eds). Occupational Asthma. State of the Art Review: Occupational Medicine. Hanley & Belfus Inc, Philadelphia 2000; Volume 15, (No 2). 
  • Agius RM.  Why are some low molecular weight agents asthmagenic? In: Banks DE and Mei-lin W. (Eds). Occupational Asthma. State of the Art Review: Occupational Medicine. Hanley & Belfus Inc, Philadelphia 2000; Volume 15, (No 2).369-383.
  • Bernstein IL, Chan-Yeung M, Malo J-L, Bernstein DI.Asthma in the Workplace. Marcel Dekker, New York, 


 
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