1 17 th epiet epidemiology course menorca, september / october 2011 environmental epidemiology...
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17th EPIET Epidemiology CourseMenorca, September / October 2011
Environmental Epidemiology(Introduction)Helen Maguire HPA London region with acknowledgement of previous work of Amandine COCHETFrench institute for public health surveillance Environmental health department and colleagues at HPA CRCE London
To provide a basic knowledge about
►Challenges and issues relating to environmental epidemiology
►Concept of low risk but large impact
►Methods of investigation
Objectives
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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
What is the environment ?
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► 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 disordersetc ...
► General environment …
High risks of adverse health outcome resulting from exposure
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December 1952 - London
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December 1952 - London
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1932-1968 - Minamata
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1932-1968 - Minamata
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December 1984 - Bhopal
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December 1984 - Bhopal
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1986 - Tchernobyl
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Thyroid cancer in children
0
20
40
60
80
100
120
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86
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87
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88
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89
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90
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91
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92
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93
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94
Years
Inci
den
ce R
ate
per
mil
lio
n
Belarus
Ukraine
Briansk
Gomel
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2003 - Paris
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2005 - Katrina
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Buncefield Explosion
• Plume stretched • for 70 miles • across southern
England
► 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
Nature of risks in general environment
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E D
The 2 most FAQ in environmental health
• 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?
?
Epidemiologicalstudies
Observational(non-intervention)
Data fromindividuals
Data from groups
Descriptive Analytic
Ecological study
Descriptive Analytic
Cross sectional study Cohort studyCase control
study
Data from groupsData fromindividuals
Experimental(intervention)
Community trialClinical trial,
individual fieldtrial
does this space time
dsitribution = a cluster?
space
1 2 3 4 5 6
time
..sometimes there is no doubt about a common exposure
Some challenges in environmental epidemiology
E D?
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Characteristics of exposure in environmental epidemiology
E D
- Multiple pollutants (RF)- Multiple routes of exposure- 1 RF n D- Low levels of exposure- Long duration of exposure- Changes over time
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Characteristics of health outcomes in environmental epidemiology
E D
- Multifactorial diseases : n RF 1 D- Rare disease- Long latent periods
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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)
0
5
10
15
20
25
30
35
40
45
4-6
6-8
8-10
10-1
212
-14
14-1
616
-18
18-2
020
-22
22-2
4 0-2
2-4
4-6
6-8
8-10
10-1
212
-14
14-1
616
-18
18-2
020
-22
22-2
4 0-2
2-4
4-6
6-8
8-10
10-1
212
-14
14-1
616
-18
18-2
020
-22
22-2
4 0-2
2-4
4-6
6-8
8-10
10-1
212
-14
14-1
616
-18
18-2
020
-22
22-2
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38697 38698 38699 38700
Date & Time
No.
Oil depot worker
Public
Em. Services
Time of explosion
… presenting complaints
Fig 2: Main presenting complaints as percentage for each group
0
10
20
30
40
50
60
70
80
90
Injuries Respiratory Anxiety Headache vomiting Cardiac
Presenting complaints
Pro
port
ion
of c
ompl
aint
s
Members of the public % of 40
Oil depot workers % of 17
Emergency workers % of 187
Characteristics of environmental risks
E D
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► High RR– benzidine / bladder cancer RR =
500– tobacco (>25cig/d) / lung cancer RR =
30
► Usually severe and often specific health outcomes
► “Well defined” populations– in space, in time, sociodemographic,
High risks
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► Urban air pollution and short-term respiratory diseases– RR = 1.1 - 1.5
► Magnetic fields and children leukaemia– RR = 1.3
► …
Low risks
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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
Small relative risks do not mean small health impacts
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example calculation of AR and AR%Phospheneexposure 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
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Heterogeneity in the population’s
sensitivity to the exposure 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
50%%
50%%
* (S) : “normal” sensitivity (s) : low sensitivity35
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
RR ref 2.0 3.0
•(D) : disease specifically related to exposure.•(d) : disease not related to exposure 36
Errors in the exposure classification
20% of non exposed (E0) are categorised E1 and 10% of non-exposedare categorised E2.
E0 E1 E2
Prevalence 50% 35% 15%
Incidence 150 214.3 250
RR ref 1.43 1.67
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Inaccuracy in the exposure categories
E0 E1
Prevalence 50% 50%
Incidence 150 225
RR Ref 1.5
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• Heterogeneity of the population
• Non specific definition of health outcome
• Errors in exposure classification
• Inaccuracy in exposure categories
E0 E1
Prevalence 50% 50%
Incidence 150 225
RR Ref 1.5
E0 E1 E2
Prevalence 80% 15% 5%
Incidence* 100 300 500
RR** ref 3.0 5.0
** RR : true Relative Risk
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 …
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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
improving assessment of exposure: biomarkers of exposure and outcome
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Ecologic studiesEcologic 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
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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 indicators44
Limits of geographical studies
• Classification biasagregated data insufficient quality of exposure and disease indicators errors of classifications (generally non differential)
• Surveillance biasif ascertainment of disease or exposure or both differs from one place to another(can be differential)
• « Ecological fallacy »
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Ecological Fallacy
population B
population C
population A
Level of exposure
Incidence rate
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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 seriesTime 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
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Epidemiologicalstudies
Observational(non-intervention)
Data fromindividuals
Data from groups
Descriptive Analytic
Ecological study
Descriptive Analytic
Cross sectional study Cohort studyCase control
study
Data from groupsData fromindividuals
Experimental(intervention)
Community trialClinical trial,
individual fieldtrial
Conclusion
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• 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, …
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 forwardchemosphere 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 epidemiologyEHP 101 (suppl 4) (1993) 49-57
Hemon D. Recherche épidémiologique sur l’environnement et la santé : quelques aspects méthodologiquesRev Epidém. et Santé Publ. 43 (1995) 395-411
References
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Thankyou
ps …I look forward to meeting you all
properly during the next 2 weeks
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