UK PM10: PollenUK PM10: Pollen

biogenic

BéruBé & Jones (2006), APR

UK PM10: Insect Material UK PM10: Insect Material

biogenic

BéruBé & Jones (2006), APR

UK PM10: SulphatesUK PM10: Sulphates

secondary

BéruBé & Jones (2006), APR

UK PM10: ChloridesUK PM10: Chlorides

secondary

BéruBé & Jones (2006), APR

UK PM10: SootUK PM10: Soot

BéruBé & Jones (2006), APR

anthropogenic

Diameter of human hair (for scale): 60 µm

PM10

(≤ 10 µm)

PM2.5

(≤ 2.5

µm)

PM0.1

(≤ 0.1

µm)

Typical Weekday Diurnal Plot (Mon-Fri)

Pm10 24 Hour mean over 2009

No of times per year when 24 hour average of PM10 exceeds the annual average by at least 10 microgrammes per cubic metre = 34 for 2009

Time Series Studies of Mortality

APHEA – 2 Study – 43 million people in European cities monitored in the 1990’s

All – cause daily mortality increased by 0.6% for each 10 ugm-3 increase in Pm10 (24 hour mean)

NMMAPS – 50 million inhabitants of metropolitan areas between 1987-94

All cause mortality increased by 0.5% for each 10 ugm-3 increase in PM10 (24 hour mean)

Hospital Admissions -Time Series Studies

APHEA2 – Hospital admissions for cardiovascular disease admissions in people >65 were increased by 0.5% per 10 ugm-3

increase in PM10

Ten cities in USA – CVD admissions in people >65 were increased by 1.1% per 10 ugm-3 increase in PM10

The Six Cities StudyCohort study measured mortality in 8,000 adults

living in six U.S cities in relation to PM2.5

pollution. Followed up between 1974-1991

Mortality rate was 30% different between most and least polluted cities

Associations only with deaths from heart disease, respiratory disease and lung cancer

The American Cancer StudyCohort of >500,000 adults across the USA

followed from 1982-1989

There was a 20% difference in mortality rate between most and least polluted (PM2.5) areas.

Effects on lung development

3,677 children, mean age 10 years in Californian communities followed for 8 years beginning in mid 1990s.

Pulmonary function measured annually.

Effects on lung development

Substantial deficits in 8 year lung development for children living within 500m of a motorway compared to those living further than 1500m.

Regional air PM2.5 had independent effect on lung function development

RESPIRATORY EFFECTS OF EXPOSURE TO DIESEL TRAFFIC IN PERSONS WITH ASTHMAThe New England Journal of Medicine – 2007

Walking for 3 hours on Oxford Street induced asymptomatic but consistent reductions in the forced expiratory volume in 1 second (FEV) (up to 6.1%) that were significantly larger than the reductions in FEV1 after exposure in Hyde Park.

How are particles causing adverse health effects?

Size Matters

How are particles causing adverse health effects?

High surface reactivity and the ability to cross cell membranes may have negative impacts on health

Inflammation/accelerated atherosclerosis

Increased concentrations of inflammatory markers are associated with increased risk of cardiovascular events

Elevated levels of C-reactive protein

Production of proinflammatory cytokines

Endothelial dysfunction

Autonomic functionElevated PM exposure is associated with

changes in HRV (humans and animals).

Cardiac patients with implanted cardioverter defibrillators had higher rates of discharges when PM10 increased.

Location of urban particulate collection in a Swansea Street

Dekati ELPI sampling system

Exposure to in vitro Model

Human Derived Respiratory Epithelium

NHBE cells

Elvidge T, Matthews IP, Gregory C, Hoogendoorn B. (2013) Feasibility of using biomarkers in blood serum as markers of effect following exposure of the lungs to particulate matter air pollution. Journal of Environmental Science and Health, Part C. 31:1-44.Abstract:For this review, research investigating association of blood serum biomarkers and exposure to PM was identified, finding 26 different biomarkers that were significantly associated with exposure. Recent evidence links different effects to different components of PM. Future research on biomarkers of effect will need to address exposure by all PM size fractions.

Clark J, Gregory C, Matthews IP, Hoogendoorn B. (2013) The biological effects upon the cardiovascular system consequent to exposure to particulates of less than 500 nm in size. Manuscript in preparation for Circulation Research.Abstract: Rationale. There is a scientific consensus that PM2.5 exposure presents a causal risk for cardiovascular disease. The relative contribution to this risk from the smallest size fractions is not known and these are not specifically subject to regulation. Combustion sources, notably traffic in urban areas, are a primary source. There are high numbers of these in urban air up to approximately 500 nm in size and further human alveolar deposition of inhaled particles is significant up to approximately the same size. Objective. This review will examine the biological outcomes detected beyond the alveolar barrier within the body or on in vitro tissues such as the vascular endothelium subsequent to exposure to particles less than 500 nm in size. Conclusion. Limited strong evidence describes effects upon heart rate modulation, vasoactivity changes, atherosclerotic advancement and oxidative stress. Weaker evidence describes coagulability and inflammatory changes within the circulation. .

Pilot study exploring the acute effects of exposure to vehicle emissions on serum inflammatory markers.

HumanProInflammatory 9-PlexAssayIL-2, IL-8, IL-12p70, IL-1beta, GM-CSF, IFN-gamma, IL-6, IL-10, TNF-alpha

Vascular Injury Panel I Assaythrombomodulin, intercellular adhesion molecule-3 (ICAM-3), E-selectin and P-selectin

Vascular Injury Panel II Assayserum amyloid A (SAA), C-reactive protein (CRP), vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1)

Residential proximity to traffic and hospital admissions

Geocode all Cardiff addresses and link to PEDW data

Categorise roads

Network analysis of traffic flow

Perform logistic

Gareth John HSW, Quentin Cooper CPLAC, Sarah Jones PHW

Road traffic noise and Cardiovascular health

Percentage of persons highly annoyed by aircraft, road, and rail traffic noises.

Münzel T et al. Eur Heart J 2014;35:829-836

© The Author 2014. Published by Oxford University Press on behalf of the European Society of Cardiology.

There is some evidence from laboratory studies that noise is a non-specific stressor that arouses the autonomic nervous system and endocrine system ,which in turn affects risk factors for cardiovascular disease e.g blood pressure.

There is habituation of this effect in community subjects

Approx. 40 % of the population in European countries is exposed to road traffic noise at levels greater than 55dBLdn.

WHO estimates that in Western Europe there are 61000 disability adjusted life years lost to noise induced cardiovascular disease

WHO considers that average nocturnal noise levels L A eqoutside 55 dB as an interim goal when 40 dB is not feasible.

CROSS- SECTIONAL STUDIES

Meta-analysis of 24 X –sectional studies gave an odds ratio of 1.07(C.I. 1.02-1.12) for prevalence of hypertension per 10 dB increase of the 16 h day time average road traffic noise level in the range<50 to > 75 dB

COHORT STUDIES

Copenhagen cohort of Incident Stroke between 1997-2006.For those over 64 years of age the Incidence Rate Ratio= 1.27(CI 1.13-1.43) per 10 dB higher level of road traffic noise (L den)

Copenhagen cohort of Incident M.I. gave IRR= 1.12 per 10 dB (CI 1.02-1.22)

HEINZ- NIXDORF COHORT

Population of 4800 randomly selsected people.

Long-term exposure to pm 2.5 and night time traffic noise are both independently associated with sub-clinical atherosclerosis.

Are air pollution and traffic noise independently associated with atherosclerosis: the Heinz Nixdorf Recall Study Table 3 Estimated % change in thoracic aortic calcification per change in particulate matter air pollutant by interquartile range, for exposure to high traffic per 100 m decrease in distance and for traffic-noise in 5dB(A) categories compared with the reference category

Exposure % change estimate (95%-CI) in TAC Score

Crude Maina Main+city Main+Lnight

b or main+PM2.5

c

PM2.5 (per 2.4 µg/m3) 26.5 (12.8; 41.8)

19.5 (7.9; 32.4)

15.7 (0.3; 33.5)

18.1 (6.6; 30.9)b

PM10 (per 4.0 µg/m3) 19.6 (6.2; 34.7)

11.6 (0.4; 24.1)

0.4 (−13.6; 16.7)

9.4 (−1.8; 21.9)b

Distance to highly trafficked road (per reduction by 50%)

12.9 (−0.4; 24.5)

12.1 (0.1; 22.7)

12.3 (0.3; 22.8)

8.8 (−4.2; 20.3)b

Lden (per 5dB with a cut point at 45 dB) 2.5 (−3.9; 9.4)

2.5 (−3.3; 8.6)

2.1 (−3.6; 8.2) 1.9 (−3.8; 8.0)c

Lnight (per 5 dB with a cut point of 35 dB) 5.5 (1.0; 10.1) 4.6 (0.7; 8.7) 4.1 (0.1; 8.2) 3.9 (0.0; 8.0)c Lden, weighted 24 h mean of road traffic noise; Lnight, weighted mean of night-time noise(22–6 h); PM, particulate matter; TAC,

thoracic aortic calcification.

amain: sex, age, unemployment rate in neighbourhood, smoking status, packyears of smoking, ETS, physical activity, BMI , alcohol intake.

bPlus Lnight.

PSYCHOLOGICAL MORBIDITY

In the Caerphilly cohort there was no association between road traffic noise and psychological morbidity.

Noise sensitivity is an intervening variable.