NOx and the City - Air pollution – health effects

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Presentation by Anthony Seaton, University of Aberdeen and Institute of Occupational Medicine

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  • 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.
  • NOx and the City - Air pollution – health effects

    1. 1. Air pollution – health effects Anthony Seaton University of Aberdeen and Institute of Occupational Medicine
    2. 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
    3. 3. Daily deaths in the 1952 London smog
    4. 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. 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. 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) - -
    7. 7. So pollution is usually the last straw
    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. 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. 10. So, pollution is one of many factors that lead to heart and lung disease
    11. 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. 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. 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. 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.
    15. 15. nanoparticles, NO and NO2: cooking in oven, 75 minutes (1ppb = 1.91µg/m3 )
    16. 16. Outdoor ambient air, Aberdeen; 6 months UFPs and NO2
    17. 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.
    18. 18. Thank you, ladies and gentlemen Anthony Seaton
    19. 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. 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. 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. 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. 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. 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. 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. 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. 27. Does this allow time for particles to move to interstitial space and initiate inflammation and a systemic reaction?
    28. 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....”
    29. 29. UFPs, NO and NO2: 4 rings, 15 minutes
    30. 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. 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
    32. 32. 0 25000 50000 75000 100000 Time particles/cm3 shop shop eating area shopping mall walking on Union Street Particle number count when shopping
    33. 33. Relationship between ultrafine particle number concentration and nitrogen dioxide (daily means)
    34. 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!
    35. 35. UFPs, NO and NO2 ; 4 rings 2 hours

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