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

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University of Milan & IRCCS Maggiore Hospital Foundation. Milan, Italy ... Psychic and psychosomatic effects (lagoon of causative factors) ... – PowerPoint PPT presentation

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


1
THE IMPORTANCE OF OCCUPATIONAL AND ENVIRONMENTAL
EPIDEMIOLOGY FOR THE OCCUPATIONAL HEALTH PRACTICE
6 EASOM Summer School August
31st - September 2nd, 2006
  • 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
    practice Research
  • .What we have to teach to our students
    Teaching
  • .What can confer appropriateness and
    effectiveness
  • to OH practice and intervention Practice
  • .What makes evaluation possible
    Evaluation

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 gt individual level
  • Stress related disease
  • Neuro-psychological effects
  • Cost-effectiveness of occupational health
  • Risk assessment
  • Reproductive hazards

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
(Mc Lure 1991)
CASE CROSSOVER DESIGN
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
22
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23
ICMESA, the Seveso Accident plant
Dept. B Production of 2,4,5-trichlorophenol TCP
24
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25
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26
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27
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28
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29
Seveso, Italy, 1976
TCP production plant
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)
30
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31
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32
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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
  • cows milk

HUMAN EXPOSURE/ DOSE
  • personal habits and
  • activities
  • chloracne
  • biological samples

HEALTH EFFECTS
  • early and mid-term
  • long term

37
Exposure
38
The Seveso area
Bertazzi et al., Environ Health Perspect 1998
39
The Seveso area
Bertazzi et al., Environ Health Perspect 1998
40
The Seveso area
Bertazzi et al., Environ Health Perspect 1998
41
The Seveso area
Bertazzi et al., Environ Health Perspect 1998
42
TCDD plasma levels, 1976
Needham et al., Chemosphere 1998
43
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 ABR vs. REFERENCE
47
CHLORACNE CASES 1976-1977
48
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49
Incidence studies
50
Mortality (Zone AB)
Analysis adjusted for age and sex
Bertazzi et al., Am J Epidemiol 2001
 
51
Cancer incidence (Zone AB)
Analysis adjusted for age and sex
Pesatori et al., Ind Health 2003
 
52
OFFSPRING SEX RATIO AND PARENTAL TCDD LEVELS
53
Case-control retrospective study
54
Higher TCDD exposure The only determinant of
chloracne?
Chloracne Case-Control Study
  • 101 chloracne cases
  • Median age 8 years
  • 211 controls
  • Enrollment 1993-1998

Opportunity to identify susceptibility
factors!
55
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56
Mean plasma TCDD
Chloracne
Chloracne
Controls
57
Potential Susceptibility Factors
TCDDgt10 ppt
Analysis adjusted for age, sex and zone of
residence
58
Health conditions after 20 years
  • No differences between chloracne cases
    healthy controls
  • Allergic diseases
  • Gastrointestinal disorders
  • Infectious diseases
  • Endocrine disorders
  • Respiratory diseases
  • Offspring health status

Baccarelli et al., Br J Dermatol, 2005
59
Late cross-sectional studies
60
Subclinical conditions after 20 years
61
IgG plasma levels
p0.03
p0.01
Baccarelli et al., Environ Health Perspect 2002
62
Plasma TCDD vs. IgG
Baccarelli et al., Environ Health Perspect 2002
63
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64
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65
Need to rediscover population approach coupled
with high risk individual approach
  • Epidemiology has largely ceased to function as
    part of a multidisciplinary approach to
    understanding the causation of disease in
    populations and has become a set of generic
    methods for measuring associations of exposure
    and disease in individuals. .
  • (for studying) decontextualized individual risk
    factors, rather than to study population factors
    in their social and historical context.
  • We seem to be using more and more advanced
    technology to study more and more trivial issues,
    while the major causes of disease are ignored.
    Epidemiology must reintegrate itself into public
    health and must rediscover the population
    perspective.
  • (N. Pearce, Am J Public Health, 1996, 86678-683)

66
PREGNANCY LOSS RATE,1976-1977, BY TRIMESTER
67
Effect of plasma TCDD
Plasma TCDD
AhR
ARNT
AhR
EROD
DRE

_
CYP1A1
CYP1B1
Uncultured cells
TCDD stimulated Cells
Baccarelli et al., Tox Lett 2004
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