Air pollution and mortality: Historical perspectives

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Air pollution and mortality Historical
perspectives

• Ross Anderson
• St Georges, University of London
• SAHSU Jubilee Scientific Meeting
• Imperial College, December 2007

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Outline

• Brief review of what we know about outdoor air
  pollution and mortality and how we got there
• Reflection on some of the most influential
  conceptual developments
• Focus on concepts of causality and mechanisms

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Outdoor air pollutants

• Gases
• Oxides of nitrogen
• Ozone
• Sulphur dioxide
• Carbon monoxide
• Air Toxics
• 1,3-butadiene
• Polycyclic organic matter e.g. PAHs.
• Benzene
• Aldehydes, e.g. formaldehyde

• Inhalable Particulates(PM10)
• Fine (PM2.5) Ultrafine (PM0.1)
• Created from Combustion
• Primary carbonaceous
• Secondary sulphates, nitrates
• Lead
• Coarse (PM2.5-10)
• Mechanically generated
• Crustal source silicaceous
• Non combustion mobile sources eg Tyre and brake
  wear
• Sea spray (coastal areas)
• Biological
• Pollen fragments, fungal spores

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Outdoor air pollution and mortality Short-term
exposure (temporal) studies

• Episodes
• Increase in mortality
• Daily mortality studies
• Short-term associations with daily mortality
• Mainly cardiovascular and respiratory diagnoses
  affected
• Little specificity for specific diagnoses
• Not explained by short-term mortality
  displacement alone
• No threshold identified
• Cannot estimate life years lost
• Intervention studies
• Step reductions in air pollution are associated
  with short-term and long term reductions in
  mortality.
• What source or component of pollution?
• Some evidence that particles are most important
• But generally low specificity for specific
  components or sources of pollution.
• Some coherence with temporal studies of morbidity
  and pathophysiological effects

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Outdoor air pollution and mortalityLong-term
exposure (spatial) studies

• Spatial variations in chronic exposure to air
  pollution are associated with increased risk of
  mortality even after controlling for individual
  risk factors
• Cardiovascular and respiratory causes are both
  affected
• Emerging evidence of effects on infant mortality
• No threshold has been identified
• Relative risks of mortality are greater than for
  time-series studies
• Life years lost can be calculated
• What source or component of pollution?
• Some evidence that particles are most important
• But generally low specificity for specific
  components or sources of pollution.

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Air pollution and mortalitySome uncertainties

• Roles of specific pollutants and sources
• Relationship between ambient concentrations and
  dose to putative target organs
• Causality of epidemiological associations
• How air pollution actually increases mortality

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Outdoor Air pollution and mortalityEvolution of
epidemiology

• Pre 1850s
• Urban fogs associated with increased mortality
• Increased mortality in low lying urban areas
  attributed to miasma
• Pre 1930s
• Mortality in winter episodes attributed mainly to
  cold
• 1930/50s
• Formal investigation of major episodes.
• 1960s
• Spatial ecological studies
• 1970/80s
• Spatial studies with individual level confounder
  control
• 1980s
• Temporal studies of daily mortality

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Underlying trends affecting the development of
air pollution science

• Trends in methods and concepts
• Trends in the culture of science and the role of
  scientists in society
• Trends in societal attitudes and priorities
  relating to the environment and the causation of
  disease
• Trends in public administration

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How does knowledge evolve?

• Paradigm shifts

Thomas Kuhn (1962). The structure of scientific
revolutions.
Origin of humankind creation gtgtgtgt
evolution Physics Newtonian gtgtgtgt
Einsteinian Pathophysiology Galenic gtgtgtgt
modern Disease causation miasma gtgtgtgt germ theory
Concepts
Methods
Registration of deaths Environmental measurements
and modelling Biomedical measurements Statistical
theory Data processing
Causality Mechanisms
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Weighing the evidence of observational studies

• Is there any other way of explaining the set of
  facts before us, is there any other answer
  equally, or more, likely than cause and effect?
  Bradford Hill (1965)

Temporality Size of effect Dose response
Specificity Consistency Coherence Plausibili
ty Analogy
Legal weight of evidence Balance of
probabilities ? public health action Beyond
all reasonable doubt ? scientific acceptance
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EVIDENCE FROM POPULATIONS
ASSOCIATIONS Air pollution and health
EXCLUDE Chance, Bias Confounding
OTHER EVIDENCE (TOXICOLOGY)
APPLY Scientific reasoning
JUDGEMENT Causality
Hills viewpoints
POLICY
Precautionary principle
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Mechanistic theories

• Specific factors (e.g. Known carcinogens)
• Acute respiratory inflammation
• Secondary effects of respiratory inflammation on
  cardiovascular system
• Chronic irritation
• Induction of asthmatic inflammation
• Systemic (i.e. beyond the respiratory tract)
• chemical mediator release
• neural stimulation

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Mechanisms of PM effects
Pope and Dockery 2006
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London 1952 smog ratio of deaths in episode week
to previous week, by age
Ministry of Health 1954
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Numbers of deaths certified as due to
cardiovascular and respiratory disease
London, December 1952 (MOH 1954)
Numbers of deaths certified as due to myocardial
(mainly IHD) disease. Coroners death
certificates.
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Paracelsus 1493 1541)
All things are poison and nothing is without
poison, only the dose permits something not to be
poisonous
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The single cause threshold concept of disease
causation does not explain the findings of
epidemiology

• Why small exposures can have clinically important
  effects, including death
• Why there is a lack of threshold in exposure
  response relationships
• Why effects vary between individuals and
  populations

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Multifactorial causation of disease

• Diseases or health states occur because of the
  combined influences of a number of different
  factors, none of which are, alone, necessary or
  sufficient to cause the condition.
• In a multifactorial situation, causes are
  insufficient but necessary components of
  unnecessary but sufficient causes (Mackie 1965)
• The cause of a disease event is an antecedent
  event, condition or characteristic that was
  necessary (given that all other conditions are
  fixed) for the occurrence of the disease at the
  moment it occurred. (Rothman and Greenland 2002)

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Contribution of acute and chronic disease to
loss of reserve (vulnerability)
Causal field
Causal field
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Added contribution of air pollution to acute and
chronic disease to loss of reserve (vulnerability)
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Event brought forward
Added event
No event
Threshold for change in clinical state.
Reserve
Vulnerablity
Vulnerability
Time
Interaction between air pollution and clinical
vulnerability
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Role of air pollution in chronic disease
Death
Symptoms and disability
Reserve
Vulnerability
Birth Childhood Middle age Old age Very old
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Policy implications of multifactorial causation

• Prevention of adverse effects should also
  consider other factors affecting vulnerability.
• Public education is made difficult because the
  increased risks are statistical. It is not
  possible to identify which individuals died due
  to air pollution (unlike a car crash in which the
  proximal cause is clear)

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PM and mortality Exposure response relationships
from spatial studies
From Pope and Dockery 2006
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PM10 and daily mortality 22 European cities.
Samoli et al 2005
Ozone and daily mortality 21 European cities.
Gryparis et al 2004
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Policy implications of a low or absent threshold
of effect

• Exposure reduction across the whole population is
  likely to have greater benefits than regulating
  high exposures using standards.

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BLOOD CHOLESTEROL REDUCTION TO PREVENT CORONARY
HEART DISEASE - WHICH STRATEGY?
CHD death rate (per 1000 in 6 yrs)

Total cholesterol (mmol/L)
Derived from MRFIT Study (Martin et al 1986)
Slide courtesy of Peter Whincup
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Public health benefits of limit value vs exposure
reduction approach (Defra 2007)
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Comparison of exposure reduction approach and
current objective (standard/limit) approachUK
National Air Quality Strategy for 2020
(consultation)
1 Cohort evidence Pope et al. 6 hazard rate
per 10µg/m3 2 Combined measures (EURO V, VI
standards, penetration of low emission vehicles,
small plant combustion
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The concept of multifactorial causation

• Offers an explanation as to why small exposures
  may have big effects
• Why do we not observe clear evidence of a
  threshold in epidemiological studies
• Draws attention to the importance of other causal
  factors increasing vulnerability
• Has profound implications for abatement
  strategies
• Leads to difficulties in risk communication

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Concluding remarks

• As in any other scientific field, knowledge of
  the health effects of air pollution has increased
  as a result of advances in methods and concepts.
• However, there are many things we are uncertain
  about
• Pathophysiological and clinical mechanisms
• Relative toxicity of constituents
• The relationship between exposure measures and
  actual dose to the target organ
• The possibility of residual confounding
• Do we need a paradigm shift? What could it be?

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Congratulations SAHSUHappy Christmas everyone