Why study occupational asthma?Why study occupational asthma?

Public health importance

Distribution

Determinants

Interventions

Model for ‘garden’ asthma

Genetics

Induction

Outcome

Public health importancePublic health importance

DistributionSurveillanceCommunity studies

CausesAgentsOccupations

Why the difference?PAR estimatesCleaners

Incidence v prevalence 1o cause v aggravation Physician v self reported

Public health importancePublic health importance

DeterminantsExposure-response relationships:Hypersensitivity induced

EnzymesFlourLaboratory animalsAcid anhydrides

Irritant inducedAcute toxic inhalation (acetic acid)

Does < ac. Inhalation injury ch. asthma

Public health importancePublic health importance

Interventions (to reduce incidence of occupational asthma)

Efficacy – exposure control + surveillance

Enzymes (detergent industry)Latex (health care)Laboratory animalsIsocyanates

How to intervene effectively in small industriesRegulation enforcement not feasible? Economic incentives

We know what to doNot how to do it

Occupational asthma as a Occupational asthma as a modelmodelWell characterised exposure

Well defined population at riskWell defined phenotype – often of high importance

- within short intervalGenetics

Genetic associationsGene-environment interactionsGene-gene interactions

InductionImmunological response to novel Ag

OutcomeChronic asthma / resolutionAg and irritant

Beyond occupational (induced) asthmaBeyond occupational (induced) asthma

Work aggravated asthma

Work limited by asthma

frequencyImportance

severity

Causes and consequences

Asthma at workAsthma at work

Inducers (initiate) Physical demandsSensitisers of workIrritants

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