Why study occupational asthma? Public health importance Distribution Determinants Interventions Model for ‘garden’ asthma Genetics Induction Outcome

Public health importance Distribution Surveillance Community studies Causes Agents Occupations Why the difference? PAR estimates Cleaners Incidencev prevalence 1 o cause v aggravation Physicianv self reported

Public health importance Determinants Exposure-response relationships: Hypersensitivity induced Enzymes Flour Laboratory animals Acid anhydrides Irritant induced Acute toxic inhalation (acetic acid) Does < ac. Inhalation injury  ch. asthma

Public health importance Interventions (to reduce incidence of occupational asthma) Efficacy – exposure control + surveillance Enzymes (detergent industry) Latex (health care) Laboratory animals Isocyanates How to intervene effectively in small industries Regulation enforcement not feasible ? Economic incentives We know what to do Not how to do it

Occupational asthma as a model Well characterised exposure Well defined population at risk Well defined phenotype – often of high importance - within short interval Genetics Genetic associations Gene-environment interactions Gene-gene interactions Induction Immunological response to novel Ag Outcome Chronic asthma / resolution Ag and irritant

Beyond occupational (induced) asthma Work aggravated asthma Work limited by asthma frequency Importance severity Causes and consequences

Asthma at work Inducers (initiate) Physical demands Sensitisersof work Irritants Provokers Social work structure (aggravate) Autonomy Flexibility (i.e. adapting to chronic illness) ASTHMA Low Socio-econ status Educational attainment initiate asthma aggravate asthma physical demands autonomy & flexibility JOBS After Blanc