Causation: An Overview for Occupational & Environmental Medicine

1. Causation: An Overview for Occupational & Environmental Medicine Tee L. Guidotti The George Washington University Washington DC

2. Causation • Causation, as normally used in occupational medicine, is the determination of the probable cause of the worker’s condition or disability. • Not the same as diagnosis. • Primary goal is assessment of relationship to work.

3. Causation is not so simple. The fence was broken, so the cow got out, walked down the road, into the house, up the stairs, fell through the floor, and destroyed the house. Thus was “causation” born in Anglo-American law.

4. Causation The medical approach to the worker with suspected occupational disease must reflect two realities: • medical diagnosis and treatment, with which physicians are universally familiar. • the requirements of social mechanisms for handling disease due to occupation.

5. Documentation is critical - it drives the system. • Comprehensive • Accurate • Neutral • Detailed on critical issues • Omit superfluous personal detail • Accessible language

6. Who documents what? • Treating physician • what happened • diagnosis • care given • Medical expert • causation • work relationship • impairment, FTW

7. Who are the medical experts and what do they do? • Medical advisors • Medical expert witnesses • Independent medical examiners • Agreed medical examiners

8. Medical experts do not treat - they interpret • Review documentation • Formulate an opinion • Test the opinion against the facts • Test alternative opinions • Use accessible terminology • Preparereport

9. Documentation is required to determine... • eligibility for insured medical services or benefits • eligibility for entitlement programs that provide income support • whether impairment is temporary or permanent • violations of standards and regulations • trends in the industry

10. Documentation must address... • level of causation, • work relationship, • apportionment, • explanation of the causal circumstances, • assessment of impairment, • prediction of future impairment, • surveillance for sentinel event monitoring.

11. Levels of Causation • direct, • proximate, • precipitating, • underlying, • aggravational. It is quite possible to have multiple causes for the same outcome in the same case.

12. Establish these relationships: • disorder and workplace exposure, • workplace exposure and specific employment, • impairment due to the disorder, • proportion of impairment attributable, • whether impairment is stable or changing, • are others exposed or at risk.

13. The Five Basic Questions on First Encounter • What is the nature of the process? • What exposure is responsible? • What is the natural history and what level of impairment can be predicted? • What can be done to control or to limit the disease process? • Are other people in the workplace affected?

14. Why These Questions are Important • identifying the process by determining structure, function, and malignant potential • identifying proximate causation, the exposure that led to the disorder • prognosis and stability of impairment • treatment and other interventions • prevention

15. Why One Needs to Identify the Responsible Exposure • to establish responsibility on the part of the employer or manufacturer • to establish the work-relationship of a condition for purposes of compensation • to counsel the worker to avoid future exposure • to prevent the exposure of others, where possible

16. Attributing to Causes • Attribution (on population basis) • Apportionment (on individual basis) • Presumption (usually rebuttable) • Substantial contribution (significant) • Sufficient cause (may/not be “necessary”) • Aggravational or “exacerbating” • Interaction

17. Using Scientific Evidence • Epidemiology must be interpreted • Empirical data trumphs mechanistic arguments • “more likely than not” is usualcriteria • Benefitof doubt to claimant in WC

18. Strong criteria Strength of association Dose-response relationships Consistency of findings across studies Biological plausibility (or experimental evidence) Temporal cogency Control of confounding and bias Weak criteria Specificity Coherence Analogy Combines Hill criteria, U.S. Surgeon General and individual authors including Lilienfeld and Stolley. Accepted criteria for causation on epidemiological evidence

19. Applying Literature to the Individual Case • Profile of the case: age, latency, level of exposure, individual characteristics • Principle of “thin skull” (susceptibility) • Principle of “take the worker(s) as they come” • Empirical evidence trumphs mechanistic theorizing, which trumphs personal opinion

20. Care in the Use of Language • Know the act and regulations in the jurisdiction where you practice • Know what “and” and “or” mean • Keep it civil • Do not question or challenge the system in your report • Be very careful in using words like “aggravate”, “possible” and “substantial”

21. CAUSATION CASE STUDIES

22. Case #1 - Presentation • 52 yo woman with wheezing on job associated with dust, searching for goods in military warehouse with good housekeeping • history since childhood of multiple allergies, confirmed to many common allergens (molds, housedust) • diagnosis by practitioner of “multiple chemicalsensitivities”

23. Case #1 - Framework for Analysis • Diagnosis • Causation • Work relationship • Prognosis • Return to work

24. Case #1 - Analysis • Reactive airways associated with allergic rhinitis, not arising from work • Minor aggravation by nonspecific irritant (dust) and exposure to common allergens • Exposed at workplace • Prognosis for further problems in a warehouse • Advise alternateduty

25. Case #2 - Presentation • 43 yo nonsmoking male firefighter  14 y • adenoCa presenting as sz disorder • History of: • intense FF activity in early years • ETS at home as child, minimized by mother • early COPD in father, with modest smoking Hx

26. Case #2 - Analysis • Causation: • apportionment - possible • work as FF remains most likely association • literature on FF • Associated issues: • latency • relative risk estimate • tissue type

27. Case #3 - Presentation • 60 yo male ex-smoker, FF  35 y, newly retired • astrocytoma Grade II, one year after retirement • no industrial exposure to vinyl chloride, etc. • exposure to smoke, combustion products of unusual fires (pesticides, treated wood)

28. Case #3 - Analysis • No special aspects of this case on which to base a modification of risk estimate • Rel risk for brain Ca among FF’s is about 1.5 in positive studies • Falls short of presumption, or “more likely than not”

29. Case #4 - Presentation • Dozen claims for Ca from workers in a mine that was decommissioned in 1988 • Ca’s  prostate, stomach, kidney, nHL • Cr: Water supply in bathhouse exceeds drinking water standards (50 g/l) at 85 g/l • Cr associated with lung cancer • Mine produced asbestos

30. Case #4 -Analysis • This is not a true Ca cluster • not a consistent cancer type • Exposure opportunity not documented: how many miners drank the water? • Asbestos is not claimed to be an issue: irrelevant or confounding exposure?

31. Case #4 - Causation • Speciation: Cr VI is carcinogen. Cr III is essentially nontoxic. • Cr III predominates in freshwater and Cr VI  Cr III in stomach due to pH, redox • None of the Ca’s reflect known associations of Cr VI; few consistent with asbestos exp • Most Cr III intake (c. 50%) is from food: Cr IV III reduced by gastric pH