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NOx and the City - Air pollution – health effects
1. Air pollution – health effects
Anthony Seaton
University of Aberdeen and Institute of
Occupational Medicine
2. The pollutants
discussed
• Particles, measured as:
– black smoke (<c4.5µm)
– total suspended particles
– PM10 or PM2.5
– numbers
• Nitrogen oxides – NO converted by
reaction with ozone to NO2
4. Increases in pollution, increases
in death rates in elderly.
• overall increase in mortality
– eg, in 29 European cities - c0.6% in relation to
rise of 10µg/m3
PM10
– with low average NO2, c0.2%
– with high average NO2, c0.8%
• less in cold than in warm climate
(Epidemiology 2001;12:521)
5. Short-term effects on people with
respiratory disease.
• overall increase in respiratory mortality
– 10 European cities - c4% increase in risk in relation to
rise of 50µg/m3
black smoke (Epidemiology
2001;12:521)
• increase in admissions for asthma
– 4 European cities - c3-7% increase in risk per 50µg/m3
rise in NO2 (Thorax 1997;52:760)
• increase in COPD admissions
– 6 European cities - c4% increase in risk per 50µg/m3
rise in black smoke (ERJ 1997;10:1064)
6. But most acute illness and death is from
cardiovascular disease (COMEAP 2004)
% increase in risk per 10µg/m3
risein:
PM10 PM2.5 Black
smoke
Cardiovascular
deaths
0.9
(0.7-1.2)
1.4
(0.7-2.2)
0.6
(0.4-0.7)
Cardiac
admissions
0.9
(0.7-1.0)
- 1.0
(0.4-1.5)
Stroke deaths 0.4
(0.0-0.8)
- -
8. Reducing pollution makes a difference: Dublin
1984-96
• Air pollution declined after
ban on coal sales by an
average 35.5µg/m3
black
smoke
• respiratory death rates fell
by 15%
• cardiac deaths fell by 10%
• c359 fewer cardio-
respiratory deaths per year
(from 5.75 to 4.94 per 1000
person-years)
9. Long-term effects: loading up the
camel
• 6% increase in cardio-pulmonary mortality in
relation to historic exposure differences of
10µg/m3
PM2.5, in US adults
(JAMA 2002;287:1132)
• 7% increase in risk of cardio-pulmonary
mortality in relation to 10µg/m3
estimated
average personal exposure to black smoke in
The Netherlands
(Lancet 2002;360:1203)
10. So, pollution is one of many factors that
lead to heart and lung disease
11. The enigma of particle toxicity
•It takes c100mg arsenic to kill someone!
•Why does a milligram or less of carbon, inhaled
over 24 hours, cause such consistent effects?
12. Not the weight but the numbers?
• Each one is a potential
invading germ, requiring an
inflammatory reaction
• the more particles above
background, the greater the
reaction,
• and thus a greater chance of
adverse effects on the
vascular system
13. And the enigma of NO2
• Short term effects – airway irritation, thus
asthma and COPD patients affected.
• Lowest level of demonstrated effects
– Healthy adults c4000µg/m3
– Asthmatics c600µg/m3
• Short term standard 200µg/m3
• but epidemiology suggests effects at much lower
concentrations, hence 40µg/m3
standard.
14. WHO, Air Quality NO2 objective.
Why 40µg/m3
?
Based on studies of children and indoor exposure
to gas cooking
“...the results cannot be readily extrapolated
quantitatively to the outdoor situation....Selecting
a well supported value based on the studies
reviewed has not been possible....”
Because the children were exposed also to fine
particles and high peaks of NO2.
17. My opinion, for what it’s worth
• We don’t all agree what in pollution harms us, but
• Air pollution adds to other risk factors in causing
loss of life, makes some ill people worse and some
well people ill.
• The main toxic agent is most likely to be fine
particles, but NO2 and ozone also play a part.
• At present NO2 is a good marker of traffic-related
pollution.
• Control is best directed at the main sources.
19. Chemical components of
particles
• Large abrasion particles (>c2.5µm)
– silicates, etc
• Fine combustion/photochemical particles
(<c2.5µm)
– carbon
– ammonium sulphate and nitrate
– metals
• eg iron, zinc, vanadium
– organic compounds
• polycyclic aromatic hydrocarbons
20. Current Air Quality Standards
• Sulphur dioxide: 350µg/m3
over 1 hour (<25 pa)
125µg/m3
over 24 hours (<4 pa)
• Nitrogen dioxide: 200µg/m3
over 1 hour (<19 pa)
40µg/m3
over a year
• PM10 (Scotland): 50µg/m3
over 24 hour (<8 pa)
18µg/m3
over a year
• PM2.5 (Scotland): 12µg/m3
over a year (by Jan 2020)
• Carbon monoxide: 10mg/m3
over 8 hours
• Ozone (target): 120µg/m3
over 8 hours
(UK standard) 100µg/m3
over 8 hours
• Benzene (Scotland): 3.25µg/m3
over a year
• Benzo(a)pyrene (UK): 0.25ng/m3
over a year
21. How do we know that pollution
is harmful?
• Epidemiology – studies of populations,
measuring exposures and outcomes,
allowing calculation of risks.
• Toxicology – studies in rats, mice, cells etc,
allowing understanding of mechanisms.
• Both play their part in setting standards
22. Setting standards
• Evidence from population studies
– exposure-response relationship
– uncertainty at low end
– consider confounders, bias, chance
• Toxicological and other evidence
– consider the relevance of the model
• Judgement
– plausibility and Bradford Hill’s viewpoints
• Public health action
23. Effects on specific causes of mortality
in The Netherlands 1986-94
• per 40µg/m3
black smoke
– 8% (3-13%) increase in risk of heart failure death
– 7% (0.1-15%) for arrhythmia
– 4% (0.7-8%) for stroke
– 4% (0.9-12%) for embolism, thrombosis
• per 30µg/m3
NO2
– 2% (0.1-4%) for total cardiovascular
– 6% (2.4-11%) for heart failure
24. Short-term effects on cardiac disease
• overall increase in cardiac mortality
– 10 European cities - c2% increase in risk in
relation to rise of 50µg/m3
black smoke
(Epidemiology 2001;12:521)
• increase in cardiac admissions
– 8 European cities - 1.1% increase in association
with rise of 10µg/m3
black smoke
– 1.3% increase in over 65 year-olds
(J Epidemiol Commun Hlth 2002;56:773)
25. Usual pollution vs episode
• Normal levels
– c5000 particles/ml
– c50 billion deposited in
24hrs
– lung has 500 million
alveoli
– and c5 billion alveolar
macrophages
• ie c10 particles per
macrophage/24 hours
• Pollution episode
– 100,000 particles/ml
– c1000 billion over 24
hours for those 4
billion alveolar
macrophages
• Thus, each
macrophage may need
to deal with up to 200
particles/24 hours
26. Human targets and diseases
• The lungs - asthma and bronchitis
• The heart - heart attacks and heart failure
• The brain - stroke
• Blood vessels – thrombosis, atheroma
27. Does this allow time for particles to
move to interstitial space and initiate
inflammation and a systemic reaction?
28. WHO Air Quality Guidelines
“...However, the affected children had a pattern
of indoor exposure that included peak
exposures higher than those that occurred
typically outdoors. Thus the results cannot be
readily extrapolated quantitatively to the
outdoor situation....Selecting a well supported
value based on the studies reviewed has not
been possible....”
30. Implication - should a health-based
standard be based on particle
numbers?
0.001 0.01 0.1 1 10
Mass w eighting
Number w eighting
Diam eter (µm)
Norm alised
concent rat ion
From Kitt leson, 1998
31. And later....
We have been asked to comment on our
confidence in this guideline. Our reply is that
it remains difficult to provide solid scientific
support for the numerical value of the
guideline. There is still no robust evidence for
setting an annual average guideline value for
NO2 through a direct toxic effect.”
WHO 2005
34. What is the cause of these
associations?
• 50µg/m3
• or 1mg over 24 hours inhaled
• ie <0.5mg deposited in the lung in 24 hours
• cf arsenic - lethal dose c100mg!
The great smog caused c4000 excess deaths over a week in London.
And the majority were from heart attacks – this seems still to be the case with particulate pollution.
This slide shows the PNC while shopping. Shows the differences in exposure depending on where the person is at a certain time. Unfortunately no data available for PM2.5.
Correlation coefficient is highly significant: 0.89 This association might explain the reason why associations have been found between very low levels of NO2 and health effects, particularly cardiac effects It might be that the effects are due to exposure to UFPs rather than NO2.