1. AIR POLLUTION AND HEALTH EFFECTS (II)

2. PARTICULATE MATTER
Since the CAA(1956) a kind of complacency set in because smoke and SO2 were very much reduced.
Some did notice an increase in fine particles
Diesel
Summer haze – secondary particles
Monitoring for PM10 rather than TSP

3. QUARG INITIALLY POSITIVE ABOUT FUTURE
Dockery et al (1993) six cities study
“An association between air pollution and mortality in six U.S. cities” New England Journal of Medicine 329,
Emissions of pollutants from vehicles looked set to decrease…

4. MORTALITY
FACTOR
SIX CITY STUDY
A long term analysis of data on air pollution and mortality undertaken by Harvard School of Public Health

5. NORTH-SOUTH DIVIDE Annual mean concentrations decrease northwards
<
35-45
<
Annual mean concentrations decrease northwards
Sahelian dust
Photochemistry
Emissions
Lack of resource and expertise in south created concern in EC

6. COMPOSITION OF DUSTS
Sardinia more than 80% of the Fe and Al come from the Sahara. Guerzoni, S et al Chemosphere (1999)
Declining emissions of fly ash from industrial plant may lower Ca and offset gains from reduced acidic emissions. Lee and Pacyna Atmos. Env. (1999)
Guerzoni, S et al
TI Role of desert aerosol in metal fluxes in the
Mediterranean area
SO CHEMOSPHERE AB The chemical composition of aerosols and
precipitation collected over Sardinia primarily reflect
Saharan and European inputs. European background
aerosols in Sardinia show a 3- to fold decrease in
EFcrust values for Cd, Zn, Pb, and Cr compared with
coastal stations in the Western Mediterranean.
Partitioning of total atmospheric deposition between soluble
and insoluble phases shows that Al, Si, Fe and Pb
originating from the atmosphere are mostly in an
insoluble form. For Ca, Cd and Cr metals, the dissolved
fraction represents 50-90% of the total input. Aerosol
dissolution experiments performed at particle
concentrations ranging from 3 to 300 mg l(-1) show that
Cd and Pb have low solubilities at high mass particle
concentrations. The solubility of Pb increases with EFcrust
values and the finest grain-size of the aerosols (<1 mu m),
and is also affected by pH. Dissolution of Al and Fe
decreases significantly from 30% (13% for Fe) at aerosol
loads lower than 5 mg l(-1) to less than 1% for both
metals at total aerosol concentrations greater than 100
mg l(-1). The fluxes (dry + wet) of metals in Sardinia
show that similar to 30% of the Cd and Pb to more than
80% of the Fe and Al come from the Sahara. (C) 1999
Elsevier Science Ltd. All rights reserved. BP 229
EP 246 PG 18
JI Chemosphere PY 1999

7. RESPIRATORY SYSTEM
Modern concerns relate more to the lung than the respiratory tract

8. PARTICULATE MATTER
Size matters – particles need to be <3 μm to get deep in lung
Immunomodulatory functions of pulmonary surfactant
Jo Rae Wright
Department of Cell Biologgy, Duke University Medical School, Durham, NC, USA
Pulmonary surfactant is a lipoprotein complex that is synthesized by the alveolar type II cells that line the airspaces. The most well established
function of surfactant is reduction of surface tension at the air-liquid interface of the lung which significantly reduces the work of breathing thus
allowing for adequate gas exchange to occur.
In addition to reducing surface tension, surfactant also participates in host defense against infection and inflammation. This somewhat
surprising function was elucidated when it was discovered that two of the surfactant proteins, surfactant protein A (SP-A) and SP-D, are
members of a family of proteins known as collectins. The name collectin was derived from the fact that the proteins all have an N-terminal
collagen-like domain and a C-terminal lectin like domain that binds avidly to carbohydrates, such as those found on the surfaces of bacteria and
viruses. In addition, SP-A and SP-D bind to immune cells such as macrophages and consequently stimulate the uptake of pathogens. In this
fashion, both SP-A and SP-D participate in what is known as the innate immune system. The innate immune system is the body’s first line of
host defense and is carried out by soluble molecules, like the collectins, complement, and acute phase proteins, and cells such as macrophages
and neutrophils. Recent studies from our and other laboratories have provided evidence that SP-A and SP-D also influence the adaptive
immune system, which is mediated by antibodies that are produced in response to antigen challenge via interactions between antigen
presenting cells, T- cells and B-cells. Thus, surfactant influences host defense by affecting both adaptive and innate immunity.

9. PARTICULATE MATTER
Size matters – particles need to be <3 μm to get deep in lung
Alveoli
A= Alveolar
TB = Tracheobronchial
NPL = Nasal, Pharyngeal, Laryngeal
Immunomodulatory functions of pulmonary surfactant
Jo Rae Wright
Department of Cell Biologgy, Duke University Medical School, Durham, NC, USA
Pulmonary surfactant is a lipoprotein complex that is synthesized by the alveolar type II cells that line the airspaces. The most well established
function of surfactant is reduction of surface tension at the air-liquid interface of the lung which significantly reduces the work of breathing thus
allowing for adequate gas exchange to occur.
In addition to reducing surface tension, surfactant also participates in host defense against infection and inflammation. This somewhat
surprising function was elucidated when it was discovered that two of the surfactant proteins, surfactant protein A (SP-A) and SP-D, are
members of a family of proteins known as collectins. The name collectin was derived from the fact that the proteins all have an N-terminal
collagen-like domain and a C-terminal lectin like domain that binds avidly to carbohydrates, such as those found on the surfaces of bacteria and
viruses. In addition, SP-A and SP-D bind to immune cells such as macrophages and consequently stimulate the uptake of pathogens. In this
fashion, both SP-A and SP-D participate in what is known as the innate immune system. The innate immune system is the body’s first line of
host defense and is carried out by soluble molecules, like the collectins, complement, and acute phase proteins, and cells such as macrophages
and neutrophils. Recent studies from our and other laboratories have provided evidence that SP-A and SP-D also influence the adaptive
immune system, which is mediated by antibodies that are produced in response to antigen challenge via interactions between antigen
presenting cells, T- cells and B-cells. Thus, surfactant influences host defense by affecting both adaptive and innate immunity.
MSU College of Human Medicine
John Hopkins School of Medicine

10. SHORT TERM EXPOSURE RESPONSE TO PM10

11. MONTHS LOSS OF LIFE

12. PARTICLES PM10 - health effects complex... Organics and metals
Buseck et al
PARTICLES
PM10 - health effects complex...
Organics and metals
Compositional complexity and nanoscale heterogeneity [Buseck et al, Atmospheric Geochemistry No

13. PARTICULATE MATTER IN ALVOLI
Mechanisms for removal involve macrophages
ALVEOLAR
MACROPHAGES
ALVEOLI
Immunomodulatory functions of pulmonary surfactant
Jo Rae Wright
Department of Cell Biologgy, Duke University Medical School, Durham, NC, USA
Pulmonary surfactant is a lipoprotein complex that is synthesized by the alveolar type II cells that line the airspaces. The most well established
function of surfactant is reduction of surface tension at the air-liquid interface of the lung which significantly reduces the work of breathing thus
allowing for adequate gas exchange to occur.
In addition to reducing surface tension, surfactant also participates in host defense against infection and inflammation. This somewhat
surprising function was elucidated when it was discovered that two of the surfactant proteins, surfactant protein A (SP-A) and SP-D, are
members of a family of proteins known as collectins. The name collectin was derived from the fact that the proteins all have an N-terminal
collagen-like domain and a C-terminal lectin like domain that binds avidly to carbohydrates, such as those found on the surfaces of bacteria and
viruses. In addition, SP-A and SP-D bind to immune cells such as macrophages and consequently stimulate the uptake of pathogens. In this
fashion, both SP-A and SP-D participate in what is known as the innate immune system. The innate immune system is the body’s first line of
host defense and is carried out by soluble molecules, like the collectins, complement, and acute phase proteins, and cells such as macrophages
and neutrophils. Recent studies from our and other laboratories have provided evidence that SP-A and SP-D also influence the adaptive
immune system, which is mediated by antibodies that are produced in response to antigen challenge via interactions between antigen
presenting cells, T- cells and B-cells. Thus, surfactant influences host defense by affecting both adaptive and innate immunity.
MSU College of Human Medicine
John Hopkins School of Medicine

14. INJURY FROM FINE PARTICLES

15. KEY FACTORS IN EFFECTS OF PARTICULATE MATTER
Area/number
Oxidative stress
Hydroxyl radical activity –
Transition metals – Fe, V
ALVEOLI
Immunomodulatory functions of pulmonary surfactant
Jo Rae Wright
Department of Cell Biologgy, Duke University Medical School, Durham, NC, USA
Pulmonary surfactant is a lipoprotein complex that is synthesized by the alveolar type II cells that line the airspaces. The most well established
function of surfactant is reduction of surface tension at the air-liquid interface of the lung which significantly reduces the work of breathing thus
allowing for adequate gas exchange to occur.
In addition to reducing surface tension, surfactant also participates in host defense against infection and inflammation. This somewhat
surprising function was elucidated when it was discovered that two of the surfactant proteins, surfactant protein A (SP-A) and SP-D, are
members of a family of proteins known as collectins. The name collectin was derived from the fact that the proteins all have an N-terminal
collagen-like domain and a C-terminal lectin like domain that binds avidly to carbohydrates, such as those found on the surfaces of bacteria and
viruses. In addition, SP-A and SP-D bind to immune cells such as macrophages and consequently stimulate the uptake of pathogens. In this
fashion, both SP-A and SP-D participate in what is known as the innate immune system. The innate immune system is the body’s first line of
host defense and is carried out by soluble molecules, like the collectins, complement, and acute phase proteins, and cells such as macrophages
and neutrophils. Recent studies from our and other laboratories have provided evidence that SP-A and SP-D also influence the adaptive
immune system, which is mediated by antibodies that are produced in response to antigen challenge via interactions between antigen
presenting cells, T- cells and B-cells. Thus, surfactant influences host defense by affecting both adaptive and innate immunity.

16. OXIDATIVE STRESS
Transition metals and organics on the surface of the carbon core affect the antioxidant defences within the lung lining fluid.
Consumes the protective antioxidant
Macrophages overwhelmed and more (less active particles?) can reach the surface of the lung.

17. OXIDATIVE STRESS
Ascorbate and glutathione depletion as indicators of oxidative activity.
Measured in London
HIGH TRAFFIC 17

18. PARTICLE TYPE
Impact of 10 μg/m3 increase in PM2.5 from various sources
Laden et al Association of fine particulate matter from different sources with daily mortality in six U.S. cities Environmental Health Perspectives 108, ( 2000)

19. NON CLASSICAL IMPACTS LONG TERM (20a) PM EXPOSURE AND COGNITIVE FUNCTION IN THE ELDERLY
CERAD neuropsychological test battery (Consortium to Establish a Registry for Alzheimer’s Disease)
PM translocates to the brain which causes inflammation.
Brain inflammation is promotes neurodegenerative diseases (e.g. Alzheimer's).
Ranft et al Environmental Research (2009)

20. FOREST SMOKE IN CITIES Health effects of particles
problem of size
problem of toxicity
Canadian fires affect US pollutant concentrations [Wotawa and Trainer Science 288: (5464) ]

21. Photographs
C.J. Park
YELLOW DUST
Enormous worry in Asia about dust from the Loess plateau and its potential health effects.
May incorporate organic materials and also be carcinogenic.

22. DUST CHEMISTRY
More dust perhaps with agriculatural and climate change… but pollutants in cities coat on the dust.
HNO3
H2SO4
ORGANIC
ACIDS
HULIS
NEUTRALIZATION
ORGANICS
OZONE
INTERACTIONS
SOLUBILZATION
SURFACTANTS
DUST EMISSION

23. MOONDUST NASA wories about particles less than 3m

24. LONG AND SHORT TERM EFFECTS
Need to distinguish between the effects of fine particles and oxidative stress and long term effects of carcinogenesis

25. URBAN NANOPARTICLES <1m
Health concerns over smaller and smaller particles
has driven the study of nanoparticles...
Traffic
Industry
Secondary production
… but also rapid nucleation

26. Los Angeles ULTRAFINES (50-100nm)
Most abundant
catalytic metals:
Fe, Ti, Cr,
Zn, Ce
Some 10% of primary organic
particles seem to be from cars...
Cass et al Phil. Trans. 2000

27. PULMONARY SURFACTANTS
Surfactants in alveoli aid gas exchange, but also lung defence.
Would aerosol surfactants alter these functions?
PULMONARY SURFACTANTS
ALVEOLI
Immunomodulatory functions of pulmonary surfactant
Jo Rae Wright
Department of Cell Biologgy, Duke University Medical School, Durham, NC, USA
Pulmonary surfactant is a lipoprotein complex that is synthesized by the alveolar type II cells that line the airspaces. The most well established
function of surfactant is reduction of surface tension at the air-liquid interface of the lung which significantly reduces the work of breathing thus
allowing for adequate gas exchange to occur.
In addition to reducing surface tension, surfactant also participates in host defense against infection and inflammation. This somewhat
surprising function was elucidated when it was discovered that two of the surfactant proteins, surfactant protein A (SP-A) and SP-D, are
members of a family of proteins known as collectins. The name collectin was derived from the fact that the proteins all have an N-terminal
collagen-like domain and a C-terminal lectin like domain that binds avidly to carbohydrates, such as those found on the surfaces of bacteria and
viruses. In addition, SP-A and SP-D bind to immune cells such as macrophages and consequently stimulate the uptake of pathogens. In this
fashion, both SP-A and SP-D participate in what is known as the innate immune system. The innate immune system is the body’s first line of
host defense and is carried out by soluble molecules, like the collectins, complement, and acute phase proteins, and cells such as macrophages
and neutrophils. Recent studies from our and other laboratories have provided evidence that SP-A and SP-D also influence the adaptive
immune system, which is mediated by antibodies that are produced in response to antigen challenge via interactions between antigen
presenting cells, T- cells and B-cells. Thus, surfactant influences host defense by affecting both adaptive and innate immunity.

28. REGULATION OF PM Confusion over mechanisms and measurement
Regulatory problems:
uncertainty
no-thresholds
Constitutional dilemmas TSP PM-10 PM-2.5

29. PROBLEMS WITH STANDARDS
Meeting limit values may not always reduce exposure most effectively
LIMIT
VALUE
CONCENTRATION
Meets limit
value
CURRENT
Fails to meet limit
value, but much reduced
cumulative does