THE IMPORTANCE OF OCCUPATIONAL AND ENVIRONMENTAL EPIDEMIOLOGY FOR THE OCCUPATIONAL HEALTH PRACTICE

1. 6° EASOM Summer School August 31st - September 2nd, 2006 THE IMPORTANCE OF OCCUPATIONAL AND ENVIRONMENTAL EPIDEMIOLOGY FOR THE OCCUPATIONAL HEALTH PRACTICE Pier Alberto Bertazzi University of Milan & IRCCS Maggiore Hospital Foundation Milan, Italy

2. Outline • Challenges ahead • Epid. designs to address them • Seveso as a case in point

3. OH Practice • Traditionally, the recognition, diagnosis and control of occupational risks and diseases have been following well specified and standardized procedures (regulated sometimes not just by medical and scientific competence but even by law). The OH practice was essentially called to comply with those regulations.

4. Occup/envir. epidemiology • Occup/envir epidemiology has mainly been serving OH practice by addressing particular, specific issues, in particular occupational cancer hazards identification.

5. Changes at the workplace Today, things have changed and still are changing at work, in science and in medicine. • Workplace hazards are less obvious to identify and to measure. • Occupational factors increase the risk of “common” diseases (a-specific effects) • Specific effects are vague, psychological, subjective (distress, discomfort). • Genetics and behaviour are becoming more and more relevant. • Working population is changing in terms of age structure, sex composition, and ethnicity.

6. Change in hazards Workplace hazards are less obvious to identify and measure (and hence to control) • Population vs. sick individual approach • Longitudinal observation of exposed (exposure-dose-early effect-disease)

7. Change in effects I Occupational factors increase the risk of common diseases (a-specific effects). • Populations comparison (exposed vs. reference) • Small increase in risk visible only in relative terms (vs. background) • Need to observe large groups.

8. Change in effects II Specific effects are vague in nature, mainly psychological, subjective (distress and discomfort). • Accuracy and validity of diagnostic means and procedures • Surveillance of healthy population not of sick individuals • Need to observe large groups.

9. Novel causative components Genetic and behavioural components are becoming more and more relevant. • Gene – environment interaction as population effect • Psychic and psychosomatic effects (lagoon of causative factors) • Avoid bias, control confounding, consider interactions.

10. Working population change Working population is changing in terms of age structure, sex composition, and ethnicity. • Relevance of inherited and acquired susceptibility. • Multi-component causative web • Targeted interventions including re-training and health promotion

11. The core type of activity needed in such a changing context: OBSERVATIONAL STUDY OF EXPOSED POPULATION OVER TIME This is…… ….What we ought to contribute to, when we practiceResearch ….What we have to teach to our studentsTeaching ….What can confer appropriateness and effectiveness to OH practice and intervention Practice ….What makes evaluation possibleEvaluation

12. PRIORITIES IN OCCUPATIONAL HEALTH RESEARCH - UK • Natural history of work related ill health • Musculoskeletal disorders (back & upper limb) • Asthma • Accidents • Skin disease • Vibration induced disease • Suicide • Depression • Hearing loss • Audit in occupational health screening procedures • Environmental impact of industrial activity • Community > individual level • Stress related disease • Neuro-psychological effects • Cost-effectiveness of occupational health • Risk assessment • Reproductive hazards • Effects of pharmacological agents • Development of biomarkers as early evidence of an exposure effect

13. Need to answering new questions about safety and health at the workplace: Which study design? Depends on the exposure and nature of health outcome of interest, and on feasibility

14. Cohort Follow up of an exposed population and determination of subsequent incidence of health outcomes • Historical - long induction and latency period • Prospective – short temporal relation between exposure and subsequent risk

15. Cross sectional Comparison of disease prevalence among groups classified according to exposure. • Study of persistent conditions (rather than transient and reversible) • Repeated measurement study

16. Case-control Exposure comparison between an index case group and a reference group of persons free of the disease at the time of case definition • Nested within a cohort • Community based

17. Case-cohort Multiple case groups and a common comparison group, “reference sub-cohort”, random sample of the source population (cohort) • Efficient in testing associations with multiple health outcomes

18. Case-crossover Comparison of cases’ exposure immediately before their events with exposure that occur at other typical times. Each case serves as his/her matched control. • Suitable for risk factors of health outcomes that occur in close temporal sequence to exposure (disease triggers). • Full control of time invariant confounders (genetics)

19. CASE CROSSOVER DESIGN (Mc Lure 1991)

20. In the light of the specific issues we are facing today in OSH….. • Strategy of choice appears to often be a combination of epidemiologic studies. • The best way to illustrate and to teach this is through examples (hypothetical, at least) of complex multi-causal effects and given workplace exposure or case studies of complex exposures related to multiple effects (e.g., the Seveso accident).

21. Lombardy Region

23. ICMESA, the Seveso Accident plant Dept. B: Production of 2,4,5-trichlorophenol TCP

29. Seveso, Italy, 1976 TCP production plant 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)

33. Seveso, Italy, 1976

34. DESIGN and CONDUCT ISSUES • Exposure: type, entity, duration. • Exposed/Pop. at risk: definition, identification. • Effects: type, latency, diagnosis. • Follow-up: contact, observation, means and procedures. • Study: type of design, study population (sample), duration. • Reference population: control of confounding. • Information: validity and quality. • Analyses and interpretation. • Communication: scientific and social.

35. OBJECTIVES ADDRESSED AFTER THE ACCIDENT • Ascertaining the exposure, its nature and characteristics, the extent of contamination and number of people involved • Managing the risk with preventive measures for people and their environment • Planning and conducting health surveillance programs

36. EXPOSURE ASSESSMENT EMISSION SOURCE ECOLOGICAL AND ENVIRONMENTAL MEASUREMENTS • pollutant type • amount released • surface soil • deeper soil layers • water • airborne dust • vegetation • animals • cow’s milk HUMAN EXPOSURE/ DOSE • personal habits and • activities • chloracne • biological samples HEALTH EFFECTS • early and mid-term • long term

37. Exposure

38. Accident Zone A Zone A Population: 804 Reference zone Zone B Soil TCDD (1976):15.5-580.4 µg/m2 Zone R The Seveso area Bertazzi et al., Environ Health Perspect 1998

39. Accident Zone A Zone B Population: 5,941 Reference zone Zone B Soil TCDD (1976):1.7-4.3 µg/m2 Zone R The Seveso area Bertazzi et al., Environ Health Perspect 1998

40. Accident Zone A Zone R Population: 38,624 Reference zone Zone B Soil TCDD (1976):0.9-1.4 µg/m2 Zone R The Seveso area Bertazzi et al., Environ Health Perspect 1998

41. Accident Zone A Reference Population: 232,745 Reference zone Zone B Soil TCDD (1976):NA Zone R The Seveso area Bertazzi et al., Environ Health Perspect 1998

42. 100,000 10,000 1,000 Plasma TCDD (ppt) 100 10 } Background Zone A Zone B Zone R Zone A Zone B Zone R TCDD plasma levels, 1976 Needham et al., Chemosphere 1998

43. Zone A Zone B Reference Plasma TCDD after 20 years TCDD Range: 1.0-89.9 ppt, lipid adjusted Landi et al., Lancet 1997

44. Early cross-sectional studies

45. CHROMOSOMAL ABERRATIONSIN LYMPHOCYTES, 1977

46. CONGENITAL MALFORMATIONSZONES A+B+R vs. REFERENCE

47. CHLORACNE CASES 1976-1977

49. Incidence studies

50. Mortality (Zone A+B) *Analysis adjusted for age and sex Bertazzi et al., Am J Epidemiol 2001