Transcript Diapositive 1 - European Centre for Disease Prevention and

17th EPIET Epidemiology Course
Menorca, September / October 2011
Environmental Epidemiology
(Introduction)
Helen Maguire
HPA London region
with acknowledgement of previous work of
Amandine COCHET
French institute for public health surveillance
Environmental health department
and colleagues at HPA CRCE London
1
Objectives
To provide a basic knowledge about
►Challenges and issues relating to environmental epidemiology
►Concept of low risk but large impact
►Methods of investigation
2
What is the environment ?
Restrictive definition: environment = air + water + soil
► all the physical, chemical and biological factors external
to a person, and all the related behaviours (WHO)
► the sum of all external conditions affecting the life,
development and survival of an organism (US-EPA)
► everything that is not me (Einstein)
► Involuntary exposure
3
High risks of adverse health outcome
resulting from exposure
► Occupational environment
- aromatic amines and bladder cancer
- asbestos fibres and mesothelioma
- cadmium and kidney diseases
- benzene and leukaemia
- pesticides and infertility
- organic solvents and neurological disorders
etc ...
► General environment …
4
December 1952 - London
5
December 1952 - London
6
1932-1968 - Minamata
7
1932-1968 - Minamata
8
December 1984 - Bhopal
9
December 1984 - Bhopal
10
1986 - Tchernobyl
11
Thyroid cancer in children
Incidence Rate per million
120
100
80
Belarus
Ukraine
Briansk
Gomel
60
40
20
0
1994
1993
1992
1991
1990
1989
1988
1987
1986
Years
12
2003 - Paris
13
2005 - Katrina
14
Buncefield Explosion
• Plume stretched
• for 70 miles
• across southern
England
Nature of risks in general environment
► Anthropogenic activities
– London fog 1952, Minamata 1953, Bhopal 1984,
Tchernobyl 1986, Buncefield fire England 2005,
► Natural origin
– Heat waves,
– Hurricanes…
► Mixed origin
– UV and melanoma
18
The 2 most FAQ in environmental health
?
E
D
• What is the environment’s Health impact =
Considering environmental factor E, how many cases of
disease D is it expected to generate?
• What is the Burden of disease attributable to the
environment = Considering disease D, what percentage is
due to environmental factor E?
Epidemiological
studies
Experimental
(intervention)
Observational
(non-intervention)
Data from groups
Descriptive
Analytic
Ecological study
Data from
individuals
Descriptive
Cross sectional study
Analytic
Cohort study
Data from groups
Data from
individuals
Community trial
Clinical trial,
individual field
trial
Case control
study
does this
space time
dsitribution =
a cluster?
space
1
2
3
time
4
5
6
..sometimes there is no doubt about a
common exposure
Some challenges in environmental
epidemiology
E
?
D
23
Characteristics of exposure in
environmental epidemiology
E
-
D
Multiple pollutants (RF)
Multiple routes of exposure
1 RF
nD
Low levels of exposure
Long duration of exposure
Changes over time
24
Characteristics of health outcomes in
environmental epidemiology
E
- Multifactorial diseases : n RF
- Rare disease
- Long latent periods
D
1D
25
Buncefiled oil depot explosion and fire East of England
2005
attendance at A&E after the fire
Fig 1: Distribution of attendances in Hemel Hempstead and Watford A&E
between 11/12/05 and 14/12/05, by date and time. (N=244)
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Time of
explosion
40
35
30
Oil depot worker
25
20
Public
15
Em. Services
10
5
4-6
6-8
8-10
10-12
12-14
14-16
16-18
18-20
20-22
22-24
0-2
2-4
4-6
6-8
8-10
10-12
12-14
14-16
16-18
18-20
20-22
22-24
0-2
2-4
4-6
6-8
8-10
10-12
12-14
14-16
16-18
18-20
20-22
22-24
0-2
2-4
4-6
6-8
8-10
10-12
12-14
14-16
16-18
18-20
20-22
22-24
No.
0
38697
38698
38699
Date & Time
38700
… presenting complaints
90
Fig 2: Main presenting complaints as percentage for
each group
Proportion of complaints
80
Members of the public % of 40
70
Oil depot workers % of 17
60
Emergency workers % of 187
50
40
30
20
10
0
Injuries
Respiratory
Anxiety
Headache
Presenting complaints
vomiting
Cardiac
Characteristics of environmental risks
E
D
28
High risks
► High RR
– benzidine / bladder cancer
– tobacco (>25cig/d) / lung cancer
RR = 500
RR = 30
► Usually severe and often specific health
outcomes
► “Well defined” populations
– in space, in time, sociodemographic,
29
Low risks
► Urban air pollution and short-term respiratory
diseases
– RR = 1.1 - 1.5
► Magnetic fields and children leukaemia
– RR = 1.3
►…
30
Small relative risks do not mean
small health impacts
Relative risk
ratio measure
Attributable risk (AR) %
100 * (Incidence in exposed – Incidence unexposed)
______________________________
Incidence in exposed
• PAR% = p * ( RR -1) / [ 1+ p * ( RR - 1) ]
if the relation is causal, it estimates the proportion
(amount) of disease that we can attribute to the
exposure
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example calculation of AR and AR%
Phosphene
exposure
incidence genetic mutation
exposed
0.71
unexposed
0.14
RR
0.71/0.14 =
5.1
attributable risk
0.71-0.14=
0.57
AR%
0.57/0.71*100=
80%
attributable risk for smoking and lung cancer
death (Doll and Hill 1956)
exposure
lung cancer death/100,000
heavy smokers
166
non smokers
7
RR
166/7=
23.7
attributable risk
166-7=
159
AR%
159/166*100=
95.7%
Further challenges: misclassification
Theoretical baseline situation
E0
E1
E2
Prevalence
80%
15%
5%
Incidence*
100
300
500
RR**
ref
3.0
5.0
E0 = non exposed, E1=low exposure, E2=high exposure
* Incidence : x /100.000, ** RR : true Relative Risk
34
Heterogeneity in the population’s
sensitivity to the exposure
50%
50%
E0
E1
E2
Prevalence
80%
15%
5%
Incidence (S)
100
300
500
Incidence (s)
100
200
300
Incidence (mean)
100
250
400
RR
ref
2.5
4.0
* (S) : “normal” sensitivity
(s) : low sensitivity
35
Non specific definition of the health outcome
E0
E1
E2
Prevalence
80%
15%
5%
Incidence (D)
100
250
400
Incidence (d)
50
50
50
150
300
450
ref
2.0
3.0
RR
•(D) : disease specifically related to exposure.
•(d) : disease not related to exposure
36
Errors in the exposure classification
E0
E1
E2
Prevalence
50%
35%
15%
Incidence
150
214.3
250
RR
ref
1.43
1.67
20% of non exposed (E0) are categorised E1 and 10% of non-exposed
are categorised E2.
37
Inaccuracy in the exposure categories
E0
E1
Prevalence
50%
50%
Incidence
150
225
RR
Ref
1.5
38
• Heterogeneity of
the population
• Non specific
definition of health
outcome
E0
E1
E2
Prevalence
80%
15%
5%
Incidence*
100
300
500
RR**
ref
3.0
5.0
• Errors in
exposure
classification
• Inaccuracy in
exposure
categories
** RR : true Relative Risk
E0
E1
Prevalence
50%
50%
Incidence
150
225
RR
Ref
1.5
RR : estimated Relative Risk
methods to improve epidemiological study
where there are low risks
• Improve data quality
• confounders, diagnosis
• Improve statistical power
• meta analysis, large studies, pool data
• Take careful account of
• critical periods of exposure
• individual history of exposure
• behaviour, space-time activities …
40
improving assessment of exposure:
biomarkers of exposure and outcome
Biomonitoring
assessment of human exposure to chemicals
by measuring the chemicals or their metabolites
in human specimens (blood, urine, hair,…)
 biomarkers of exposure and outcome
41
Ecologic studies
Unit of observation is group, not individual
Ecological studies: objectives
 To generate or to test etiologic hypotheses
To evaluate the impact of intervention
programs or policies
43
Ecological studies: methods
• Aggregated data
• Statistical unit = « group » (time/space)
– Group exposure
• Mean exposure, environmental proxy
– Group effect
• Frequency of disease in the statistical unit
• Research of an association between:
–
Variations of exposure levels
– Variation of health indicators
44
Limits of geographical studies
• Classification bias
agregated data  insufficient quality of exposure and
disease indicators  errors of classifications
(generally non differential)
• Surveillance bias
if ascertainment of disease or exposure or both differs
from one place to another
(can be differential)
• « Ecological fallacy »
45
Ecological Fallacy
Incidence
rate
population C
 

population B

 
population A


 
Level of exposure
46
Ecological Fallacy
Incidence
rate
Level of exposure
The Ecological Fallacy is
the inability to generalize information
gathered at the group level
to specific individuals.

Time series
• A type of ecological study
• Looks at the (short-term) temporal association
between health events and pollution
• Less subject to confounding than many study
designs
• Time-varying confounders: temperature,
humidity, influenza, day of the week, public
holidays
Time series
mortality and mean temperature in Paris
1999-2002 versus 2003
50
Epidemiological
studies
Observational
(non-intervention)
Data from groups
Descriptive
Analytic
Ecological study
Experimental
(intervention)
Data from
individuals
Descriptive
Cross sectional study
Analytic
Cohort study
Data from groups
Data from
individuals
Community trial
Clinical trial,
individual field
trial
Case control
study
Conclusion
• Critical aspects and challenges in
environmental epidemiology
• Difficulties in exposure measurements, outcomes
assessments
• Low risk can have large / important public health
impact
• Question of causality is crucial
• Epidemiology is one of the tools
• Risk assessment,
• Cluster investigation, …
52
References
 H. Morgenstern, Uses of ecologic analysis in epidemiologic research.
American Journal of Public Health, Vol. 72, Issue 12 1336-1344, 1982.
Talbott E. An Introduction to Environmental Epidemiology
CRC Press, 1995
Bertollini R. Environmental epidemiology. Exposure and disease
CRC Press, 1996
Aldrich T.E. Environmental epidemiology forward
chemosphere 41 (2000) 59-67
Morgenstern H. Principles of study design in environmental epidemiology
EHP 101 (suppl 4) (1993) 23-38
Hatch M. Measurement issues in environmental epidemiology
EHP 101 (suppl 4) (1993) 49-57
Hemon D. Recherche épidémiologique sur l’environnement et la santé :
quelques aspects méthodologiques
Rev Epidém. et Santé Publ. 43 (1995) 395-411
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Thankyou
ps …I look forward to
meeting you all properly
during the next 2 weeks

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