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What are the adverse effects of air pollution on the cardiovascular system, and how
are these prevented by legislation?
Above image adapted from copyright free image sourced from www.morguefile.com
It was estimated that globally over 3.7m premature deaths were caused by outdoor air
pollution with roughly 80% being due to cardiovascular problems such as Ischeamic
heart disease and Myocardial Infarction. [1] Importantly research also shows that a
high percentage of these deaths can be attributed to microscopic combustion derived
nano-particules; particulate matter. [2] This comprises of various metal components
and organic matter- nitrates, ammonia, sulphate, sodium chloride, black carbon,
mineral dust and water- with the smaller the particulars being the most health
damaging. [2]
With air pollution steadily on the rise it is important to learn how it impacts upon the
body. This would give us a better understanding of the mechanisms of action allowing
effective guidelines to be produced, reducing the levels of pollution in both urban and
rural areas. By chiefly reducing particulate matter levels this would decrease the
prevalence of pollution relate diseases also reducing the strain on the health care
This word press literature review will look into the relationship between air pollution
(especially particulate matter) and cardiovascular problems. Our research question is
as follows: Does exposure, both short and long-term, to air pollution cause adverse
cardiovascular effects and what guidelines have been and could be imposed to
counteract these adverse effects.
Global Exposure to Pollution
Air pollution accounts for the most serious health effects in both the developed and
developing world, putting a burden on health services worldwide. Many studies
investigating the effects of air pollution in Western Europe and North America have
found that even low concentrations of air pollution can cause significant health
effects.3 Indoor air pollution is a preventable cause of almost 2 million deaths in
developing countries and 4% of the global burden of disease4, two-thirds of which is
accounted for by Asia.5 The continually increasing populations5 in urban areas of
Asia, Africa and South America experience considerably higher levels of air pollution
which surpass the highest levels of pollution recorded in the West.6
The source of pollutants in the developing world is very different to the developed
world. The major method of exposure in developing countries is through the use of
indoor cooking and heating fuels3,4, whereas in developed countries, it is exposure to
outdoor urban air which is the problem.7 The pollutant mix therefore consists of more
organic compounds than that of developed countries. It also gives rise to varying
exposure rates as indoor close-contact exposure to pollutants can be as high as 50
times greater than outdoor exposure to urban air.7
High socio-economic backgrounds in developing countries tend to be less severely
affected as they are able to afford cleaner fuels. Coincidentally, socio-economic class
decreases susceptibility to disease in many other respects including improving
income-related mental health and decreasing age-related illness.7 However many
studies have failed to account for this major confounding factor.4 Additionally,
although many studies have observed the above links, most of these studies have not
measured direct causal links.
Components of Air Pollution
In the developed world, air pollution is mainly the result of the combustion of
petroleum.4 In contrast, in developing countries, there is a significant problem of
indoor air pollution caused by burning of solid fuels like coal 3, 4 and biomass. Half
of the world’s population4 and 75% of people in India and China are dependent upon
such fuels for cooking and heating. It is the incomplete combustion of fuels that give
rise to pollutants.
Air pollution is a combination of a variety of compounds, namely CO, SO2, NO2, O3
and particulate matter (PM). All five individual particles have specific short and long
term effects on cardiovascular health associated to them.
Carbon Monoxide (CO) and Ozone (O3)
Increased exposure to CO is associated with an increased congenital cardiovascular
risk: an exposure-response relationship has been demonstrated in pregnant woman,
with the prevalence of ventricular septal defects (VSDs) in newborns linked to an
increase in second month maternal CO exposure8. VSDs are three times more likely
(OR 2.95) following CO exposure whereas aortic valve defects in new-borns are
increased following ozone exposure in the second month of pregnancy (OR 2.68)8. It
is important to note that these patterns are only seen if the exposure is in the second
month of pregnancy.
Sulfur Dioxide (SO2)
A significant correlation has been demonstrated between increased SO2 exposure
negative health outcomes. A 10microgram/m3 increase in SO2 concentration has been
shown to increase IHD admissions by 0.7% (95% CI 0.1-1.3),but this result was only
demonstrated in a study population that was less than 65 years old. This introduces
the concept of patient susceptibility and how certain predisposing factors can affect an
individual’s relative risk. A large American-based cohort study illustrated how age
and geographical factors are pivotal in attenuating the health risks of air pollution
exposure9. Only in Eastern and Central America, not Western, was over-exposure of
PM2.5 associated with an increased mortality risk. The oldest sub-group (patients
over 85 years old) showed no raised mortality risk with PM2.5 exposure9. This may
suggest that they have developed some form of immunity to fine PM and corresponds
with the life course model of health.
PM is the compound most strongly associated with cardiovascular events and is the
form of air pollution responsible for the largest financial and resource burden on the
NHS. A novel study exemplified that cardiovascular related mortality was higher than
for all other causes of death following short term elevations in daily PM levels10. In
the most polluted cities PM2.5 and sulfates have been shown to increase the mortality
rate by 15-17%, compared to the least polluted cities. The increased mortality risk is
consistent across both smokers and non-smokers but also men and women. Studies
use the association between relevant health end points and pollutant exposure to
assess the negative health impacts of air pollution. Years of life lost (YLLs) is one
such end point and it is suggested PM exposure is linked with a loss of life of 1.8-3.1
PM2.5 is the most penetrable compound and can enter into the alveolus; very small
PM (<100nms) can penetrate beyond the lungs, entering the circulation and feeding
back to the heart. In long term exposure, an elevation of 10 micrograms/m3 is
associated with an 8-18% rise in cardiovascular mortality risk11, with mortality
mostly attributable to ischaemic heart disease (IHD), dysrhythmias, and cardiac arrest.
Coronary heart disease (CHD) comprises the largest percentage of fatal
cardiovascular events: accounting for 70% of total cardiovascular events and 53% of
deaths12. This association is strongest in individuals with a raised BMI and a high
hip-to-waist ratio: therefore overweight individuals and those with underlying
cardiovascular pathologies are the most vulnerable12. In the short term, elevations in
PM2.5 exposure are linked to an increase in hospital admissions for all health
outcomes, except mechanical injury13. There is a 1.28% relative increase in
hospitalisation for heart failure per 10 micrograms/m3 increase in same day PM2.5
exposure but also increased hospital admission for other causes13 including
cerebrovascular disease (0.81% CI 0.30-1.32) and peripheral vascular disease (0.86%
CI -0.06-1.79).
The increased mortality risk of PM2.5 elevations usually persists for two years
following initial exposure and it is therefore hard to distinguish between the effect of
long and short term exposures. Decreased PM2.5 exposure is associated with
improving health outcomes, with a 10 microgram/m3 reduction in long term PM2.5
concentration is linked to an increase in mean life expectancy of 0.61 years (+/- 0.20
Although PM10 is less penetrable and possesses less health risks than PM2.5, overexposure has been associated with adverse clinical outcomes. Across all cities with air
pollution data, and accounting for all ages, a 10 microgram/m3 increase in PM10
concentration exhibits a 0.20-0.60% relative increase in all-cause mortality15. When
you compare this with the 4% relative increase in all-cause mortality rate following
PM2.5 exposure, PM10 exposure can be classified as ten fold less potent than fine
particulate matter. The daily number of cardiovascular related deaths among the
elderly population (>75 years old) also increases by 0.47% in European cities
following raised PM10 exposure15. For the study population less than 75 years old
the association was positive but not significant and this highlights how for each
individual pollutant the most susceptible demographic can change; as for PM2.5
exposure the over 85 age bracket demonstrated no increase in mortality risk9.
Importantly, there appears to be no threshold in the exposure-response relationship for
PM10 as there is no lower limit below which PM10 exposure is not related to excess
mortality rates15. The absence of a lower threshold is significant in government’s
environmental health policies. National air pollution standards that reduce PM10
concentrations to an arbitrary level expose cities that meet the standard, but could
lower the concentration further, to unnecessary cardiovascular health risks. Diabetic
individuals are also more susceptible, being twice as likely to be admitted to hospital
for heart failure following a 10 microgram/m3 increase in PM10 concentration
compared with non-diabetics (2.01% increase (95% CI 1.40-2.62%) v 0.94% increase
(95% CI 0.61-1.28%))16.
Short term exposure
‘The National Morbidity, Mortality and Air Pollution Study’ was undertaken in the
United States between 1987 and 1994.17 The aim of the investigation was to establish
the link between short term exposure to air pollution and adverse health
effects.17 The study was conducted across 20 counties, accounting for a population of
over 50 million people.17 Data surrounding the levels of air pollution in each county
was obtained from the ‘Aerometric Information Retrieval System’ (AIRS) and
included the primary constituents of air pollution; PM, ozone, carbon monoxide,
sulphur dioxide and nitrogen dioxide.17 This allows for each source of pollution and
its effects to be individually monitored on an hourly basis. The population database
was measured using the 1990 census, with daily mortality rates obtained from the
‘National Centre for Health Statistics’.17 The study accounts for confounding factors;
excluding deaths from external causes such as accidental deaths or suicides and
classifying all other deaths based on age and cause e.g. cardiovascular, respiratory or
The results of the study provide a clear indication into the relationship between the
short term exposure to increased levels of PM and for all causes of mortality as well
as for cardiovascular complications.17 The rate of death from all causes was seen to
increase by 0.51% for each 10µg/m3 rise in particulate matter on the same day (95%
posterior interval: 0.07-0.93%).17 The relative increase in the rate of death associated
with an increase of 10µg/m3 was even greater for cardiovascular causes. A 0.68%
increase was observed (95% posterior interval: 0.20-1.16%).17
Data from AIRS is available only once every six days, limiting the depth of available
data.17 The system also cannot measure the levels of PM2.5 as a separate entity from
PM10, encompassing both as one variable, which is a major limitation to the results.
The smaller aerodynamic diameter of PM2.5 allows it to penetrate deeper into the
lungs, resulting in a greater adverse effect on the cardiovascular system than PM10.
The study doesn’t account for the socioeconomic differences within the population
and the effect that this has cardiovascular events.17
As part of ‘The Air Pollution and Health: A European Approach’ (APHEA) project,
the short term effects of particulate air pollution on cardiovascular events were
presented in 2002.18 The study investigated the direct association between airborne
particles and hospital admissions for cardiac causes in 8 European cities.18 PM10 and
sulphur dioxide data was available and measured on a 24 hour basis, with other
pollutants e.g. ozone, nitrogen dioxide, and carbon monoxide measured on an hourly
basis.18 Measuring stations were chosen based on location, mimicking inner city
pollution levels.18 Therefore stations located proximally to motorways were excluded
from the data, preventing misrepresentative values. Emergency admissions data for
cardiovascular events was, however three cities were only able to provide general
admissions data.18
In all cities an average increase in PM10 of 10µg/m3 resulted in a 0.5% increase in
hospital admissions for general cardiovascular events (95% confidence interval: 0.2 to
0.8).18 This value rose in the over 65 population alone with an increase 0f 0.7% in
cardiac admission being associated with an increase of 10µg/m3 of PM10 in urban
pollution (95% confidence interval: 0.4-1.0).18 The effects of ‘black smoke’ on
cardiac admissions is also significant, relating to a 1% increase in cardiac admissions
with every 10µg/m3 rise (95% confidence interval: 0.4-2.2).18
A 0.7% increase in admissions for ischaemic heart disease in people over the age of
65 correlated with a 10µg/m3 increases in PM10 (95% confidence
interval).18 Results for ischaemic heart disease were inconclusive in the under 65
population.18 Data gathered on admissions with stroke in either age group were
insignificant and inconclusive.18
The study is primarily limited by data collection methods. Two of the cities provided
data on TSP (total suspended particles) rather than particulate matter.18 A conversion
factor for TSP was applied allowing comparability of the results, however this
increases heterogeneity in the results, decreasing reliability.18 Despite such
discrepancies, the underlying theme that an increase in air pollution results in adverse
cardiac effects is apparent.18
Using a time-stratified case-crossover design, over 400 000 myocardial infarction
(MI) events from the Myocardial Ischaemia National Audit Project (MINAP)
database, over 2 million CVD emergency hospital admissions and over 600 000 CVD
deaths were linked with daily mean concentrations of carbon monoxide (CO),
nitrogen dioxide (NO2), particulate matter less than 10 μm in aerodynamic diameter
(PM10), particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5) and
sulphur dioxide (SO2).19 Pollutant effects were modelled using lags up to 4 days and
adjusted for ambient temperature and day of week.19 A major strength of this study is
the national coverage of a wide range of CVD outcomes.19
Mechanisms suggested to explain how air pollution effects the cardiovascular system
mainly centre on disruption of the autonomic nervous system and/or an inflammatory
response.19 Evidence suggests specific biological mechanisms trigger cardiovascular
events including: vascular dysfunction, vasoconstriction, thrombosis, elevated arterial
pressure, and atherosclerosis.19 Although it is likely that air pollution affects
cardiovascular health via multiple mechanisms, the stronger associations with non-MI
outcomes in the current study, suggests that pollution effects on cardiovascular health
may in part be mediated by non-thrombotic pathways.19 However, thrombogenic
mechanisms may still operate and are the most likely explanation for the observed
associations with pulmonary embolism as mentioned later on.19
There are some limitations.19 First, the consistency of results on MI using MINAP
and HES data is to be expected as there will be considerable overlap between the two
databases.19 Also, no information is available on those MIs that result in death before
admission to hospital. Second, fixed monitoring sites were used to represent air
pollution and so may not accurately reflect personal exposure.19 Exclusion of
roadside monitors and correlations between other stations were generally high within
50 km of each other.19 A 50 km limit ensured that a high number of CVD events
were successfully linked to exposure (over 80% for all pollutants except
PM2.5).19 Some exposure misclassification may have contributed to the largely null
results and restricting analyses to events substantially nearer the monitoring sites may
have revealed stronger associations.19 Third, most of the national PM2.5 monitoring
sites are mainly located in urban residential areas.19 Thus, our PM2.5 effects may not
be representative of those living in other settings. Ultrafine particles, black carbon or
NOx may be better indicators of primary combustion particles compared with PM10
and PM2.5 from urban background stations, which also reflect secondary PM and
road dust.19 However, there is no such national monitoring network in the UK.
Finally the effects of black carbon may not be dissimilar to PM2.5 or PM10.19
Although many studies have investigated the association between air pollution and
myocardial infarction, only three studies20,21,22 have used information on the time
of onset of myocardial infarction to be able to study the immediate temporal
relationship between air pollution, exposure and onset of myocardial
infarction.25 Although this study showed no evidence of increased risk of myocardial
infarction, a summary of four other studies conducted20,21,22,23 appears to show a
weak support of a rapid effect of air pollution in triggering the onset of myocardial
infarction. A meta-analysis of 19 time-series studies showed a 0.8% increased risk
(95% CI 0.6, 1.1) of hospital admissions for ischemic heart disease with a 10
μg/m3 short-term increase of PM10.24
Long term exposure
Manifestations of the long-term harmful effects of particulate matter are seen in the
cardiovascular system and can cause problems such as atherosclerosis, heart failure
(HF) and arrhythmias. In this section the long-term effects of exposure to pollution
will be explored, in particular the effects of combustion-derived nanoparticles.
Atherosclerosis is a potentially serious clinical condition, in which there is a change
in the blood vessels causing plaques and various other factors to clog the arteries. [25]
A large prospective cohort study investigated the relationship between long term
exposure to air pollution and the number of cardiovascular incidences related to
atherosclerosis in woman. The study included data from 350, 000 patient years of
follow up and concluded that air pollution increases the number of fatal
cardiovascular related deaths by 76% (hazard ratio 1.76, CI 1.25-2.47) for every 10
g/m3 increase in PM2.5. [26]. Thus, efforts to limit microscopic particular matter
exposure are justified. However, no pollution threshold was identified as being a
marker for the start of progression of disease so it would be impossible to know
definitively if all cardiovascular problems were a result of the PM, instead of an initial
Another study focused upon determining the atherosclerotic potential of pollution
through mice. It found that prolonged exposure (5 hours a day for 1 and a half
months) to PM with an aerodynamic diameter of <2.5 (PM2.5) caused the composite
plaque area in the arteries to increase to 41.5% (p<0.001) compared to a plaque area
of 19.2% (p=0.15) in the control group. [27] This indicates that PM has a critical role
in the progression of the plaque resulting in atherothrombosis and various other
ischemic events. A weakness of the study is that the phrase ”long term exposure” can
be ambiguous, in the sense 1 and a half months may not be considered as long term.
Also a further study looked at carotid media thickness in nearlu 800 residents in Los
Angeles and found that for every 10 micro g/m3 increase in PM2.5 in the air, there
was an increase of 5.9% of carotid- intima media thickness.[28] (95% confidence
interval, 1-11%). Adjustment for confounding factors including age and further
adjustment for covariates indicated an increase of 3.9-4.3% increase (p values, 0.050.1).
Atherothrombosis is the disruption of an atherosclerotic plaque and consequent
thrombus formation. As a result of these physiological changes many acute coronary
problems can occur along with cardiovascular death. Therefore environmental
pollution can drive alterations in the vessel wall or in thrombus formation.
An interesting human cohort study focused on the chronic effects of exposure to
biomass smoke determining whether this had an effect on the activation of leukocytes
and the formation of leukocyte aggregation. Leukocyte aggregation was classified as
“CD11b-postive polymorphonuclear leukocytes and monocytes co-expressing
platelet-specific markers CD41 or CD62P.” [29] 165 women from eastern India who
cook solely with dirty fuels such as wood and dung were selected, along with a
control group who cook with cleaner fuels (liquefied petroleum). [29] Quantitatively,
an increase in CD62P expression on platelets was found in women who cooked with
biomass which indicates an increase in the stimulation of platelet activity. This shows
that pollution levels have a large effect on atherothrombosis as it can increase the
chance of a smooth atherosclerotic cap becoming unstable and rupturing due to the
increased activity of platelets.
Furthermore among the biomass user group there was a 15.1% incidence of chest pain
or chest tightness (p<0.001) and a 6% incidence of hypertension (p<0.05), compared
to the control group who showed only a 2.5% incidence of chest pain or chest
tightness (p<0.001) and 3.2% of hypertension. (p<0.05) [29]. This highlights that
because of increased rates of atherosclerosis women cooking with biomass fuels can
be more prone to other cardiovascular problems such as angina and myocardial
infarction. Despite this a definite weakness of the study is that the exposure to
biomass fuels may not have been the sole cause of the increase in platelet aggregation
as tobacco chewing may also have been a factor. Moreover the term “chronic” is not
defined but rather based on the assumption that the woman have always been using
biomass fuels and petroleum fuels.
Heart Failure
Another adverse effect of PM exposure is heart failure (HF); defined as a reflection of
the inability of the heart to perfuse peripheral tissues adequately.HF was found to
account for 10% of general cardiovascular deaths, and 30% of those related to air
pollution by C. Arden-Pope et al. in their study into the relationship between
cardiovascular mortality and long term exposure to particulate air pollution [30]. This
study concludes that, although HF related deaths contribute a numerically smaller
proportion of cardiovascular disease-related deaths, there is a stronger association
between air pollution and HF than there is between air pollution and total
cardiovascular mortality.
In 2000, the American Heart Journal published a study by DR Gold et al. entitled
“Ambient Pollution and Heart Rate Variability” [31]. This study aimed to investigate
the relationship between changes in multiple air pollutants and changes in Heart Rate
Variability (HRV). The researchers mention two previous studies in which
associations between ambient particle levels and decreased HRV were suggested
[32,33], but noted that these studies did not investigate the effect of other types of
For this study, Gold et al. recruited 21 volunteers between the ages of 53 and 87. The
small sample size of this study is a significant weakness, although the wide range of
health status of the participants counteracts this somewhat to make the study
population more representative of the wider population. [31] Exclusion criteria
included unstable angina, atrial flutter, atrial fibrillation, paced rhythm or left bundlebranch block. Each participant was then examined once per week for four months.
These examinations consisted of continuous Holter ECG monitoring for 23 minutes
which was broken down into five sections including resting, exercise and slow
breathing. This final slow breathing section was included to determine whether the
effects of pollution on HRV were independent of respiratory rate, which may also be
influenced by pollution levels. Heart rate was then calculated by counting
milliseconds (ms) between beats. To eliminate any confounding factors, time
invariate and time varying factors were adjusted for by the use of multivariate
regression models.
The study found that heart rate (HR) rose and HRV fell during exercise, when
sympathetic stimuli take over from vagal tone, and vice versa during periods of slow
breathing. The strongest association between reduced HR and PM2.5 was found to be
with mean 24-hour PM2.5, where an interquartile increase in PM2.5 (14.35 μg/m3)
correlated with a reduction in HR of 4ms/beat for the first rest period and 6ms/beat
during slow breathing (P=0.006). The largest reductions in HR were seen in smokers
(3.8 vs 1.5ms/beat; P=0.08) and persons in moderate-to-poor health (3.9 vs
1.3ms/beat; P=0.02)[2]. With regards to other pollutants, NO2 and SO2 were
associated with reduced HR, but not altered HRV. O3 had similar effects to PM2.5 on
reducing HRV, but had no effect on HR. Neither coarse PM nor CO had any
graphically plausible association.
Gold et al. theorize that PM2.5 and ozone cause a decrease in vagal tone, resulting in
a decrease in HRV[31], although it is unknown whether this plays a part in
contributing to mortality as a contributing factor or if it is merely a marker for poor
health. This aside, there is evidence for changes in autonomic function related to
extremes in either sympathetic or parasympathetic output being linked to increased
cardiac morbidity. Since there is correlation between altered HRV and
sympathetic/parasympathetic output abnormality, it would follow that there is a strong
case for altered HRV being an etiological factor in cardiovascular mortality,
specifically in HF.
If decreased HRV were a causative factor in mortality, then it is hypothesized that its
mechanism of action would be through sympathetic predominance and/or diminished
parasympathetic tone. Gold et al. describe two pathways to explain this dysregulation
of function [31]. One suggestion is that pollution-related pulmonary inflammation
may lead to systemic autonomic dysfunction through stimulation of vagal receptors in
the lung. This systemic dysfunction could manifest itself in the cardiovascular system
by disrupting autonomic control of heart rate and contractility, leading to HF. It is
also suggested that the cause could be derangements in cardiac neural conduction
caused by inflammatory mediators. This localised derangement of conduction would
lead to loss of sinus rhythm, affecting the heart’s ability to export blood with
sufficient force to perfuse peripheral tissues, also leading to HF.
Air Pollution Guidelines
Since the mid-20th century ambient urban air pollution has been identified as a health
risk and from 1958 the World Health Organisation (WHO) has aimed to introduce
preventative measures to reduce the harmful effects on human health. Based upon
health related assessments, over several decades the WHO has developed guidelines
which recommend safe levels of exposure to different pollutants. Using these
threshold values, the WHO Air Quality Guidelines were constructed for Europe in
1987 and have been more recently revised in 2005[34]. Legally enforced standards
have been created from some of these guidelines to help control pollution[35].
Despite this, however, a rapidly rising global population coupled with the increased
combustion of fuels has made air pollution an increasing health burden. Expert
analysis has identified the principal sources of air pollution emissions as particulate
matter, ozone, nitrogen dioxide and sulfur dioxide[36]. Current guidelines are focused
on improving the cardiovascular related morbidity which is associated with exposure
to these substances.
The WHO has explained that it is extremely difficult to establish guideline values at
which there is absolutely no risk to human health for a number of reasons. There is
limited data about the short-term human toxicity of pollutants at particular
concentrations but less still is known about the long-term health impact of exposure to
air pollution. Nonetheless, it is suggested that there is a range of concentrations that
make humans vulnerable to an acceptable risk of harm. This ‘acceptable risk’ can
vary between countries depending upon socioeconomic priorities and other risks to
population health in that geographical region. The use of expert consensus
accompanied with evaluation of available scientific evidence must therefore be
applied in order to produce a meaningful guideline[34].
Currently the UK complies with WHO Air Quality Guidelines (2005) and the
European Air Quality Directive (2008). The European Air Quality Directive governs
the emissions of air pollutants for member states by determining annual permitted
concentrations. The guidelines were produced with the intention of reducing exposure
to harmful levels of air pollutants but it is clearly stated that operating within these
guideline values does not necessarily protect you from adverse or undesired
The responsibility for air quality control in the UK is delegated from central
government to regional areas. For this reason Scotland can determine its own air
quality standards and accompanying legislation to enforce this. In Scotland, the
government works in partnership with other regulatory bodies to ensure that
international and European legislation is implemented. Alongside this, there is a
commitment to following the UK Air Quality Strategy Objectives published in 1997
which focus on reducing eight priority pollutants: carbon monoxide, nitrogen dioxide,
particulate matter, sulphur dioxide, lead, benzene, 1,3-butadiene and tropospheric
ozone. The objectives aim to reduce levels of these pollutants according to standards
set by the Environmental Act of 1995 based on the adverse effects and the likelihood
of targets being met. They look to continually update the objectives and due to a
recent review in 2007, particulate matter of the PM2.5 fraction is now included in this
strategy. This new addition was made in light of recent research recognising its
increased negative health effects in comparison to the PM10 fraction which was
previously included. The Air Quality Strategy has links to the Committee on the
Medical Effects of Air Pollutants (COMEAP) and Air Quality Experts Group, which
provide guidance on climate change, and therefore makes best use of expert opinion
and reliable scientific evidence to manage the objectives[38],[39].
It is extremely important to enforce certain legal standards so that the regional
government can monitor and control pollution. By analysing the current data and
comparing it to the standards, progress can be monitored and if the data has exceeded
the standards, certain measures can be put into place. On an even smaller scale, the
Local Air Quality Management (LAQM) regime attempts to focus on particularly
polluted areas within Scotland[40]. Diffusion tubes are used to analyse the nitrogen
dioxide levels in the area to review and highlight these local areas where special
measures may be required. However, these tubes can overestimate nitrogen dioxide
pollution levels suggesting that the identification of these areas may be
inaccurate[41]. Once an area has been recognised, the local authority must produce a
plan to restore the environment back to an appropriate state according to the air
quality standards. It is a legal requirement to report these highly polluted areas but
local authorities are not obliged to achieve the set standards as this may bee affected
by factors out with their control.
Continuous evaluation of current legislation is pivotal to planning the most effective
future policies. In 2004 an Air Quality Strategy Evaluation Report was published. The
report assessed road transport and electricity generation air quality policies by
analysing their cost effectiveness and success between 1990 and 2001. Success was
measured by comparing air pollution levels under existing policies with levels as
estimated in the absence of these policies. The report evaluated policies adopted to
reduce road transport and electricity generation emissions produced by national,
European and international bodies. The study concluded that significant progress
towards air quality targets had been reached. In road transport emissions, there was an
almost complete removal of lead as well as significant reductions in NO2. In
electricity generation policies, there was a significant reduction in SO2 in the
evaluation period. Furthermore, both sectors showed large reductions in PM10. The
study emphasised how each sector aided the other in the overall reduction of
pollution. The cost benefit ratio was positive in both sectors with it being slightly
higher in electricity generation policies. The study found the Euro I framework
standards was the most successful road transport policy. In electricity generation,
there were a number of successful initiatives including UNECE sulfur protocols, IPC
licensing, “Dash for Gas” initiative and NFFO orders[42].
The Air Quality Strategy Evaluation Report (2004) also concluded with proposals for
future reductions in air pollution with the key proposal being an emphasis on more
local rather than national strategies. This is based upon the highest concentrations of
pollution, especially NO2, being in urban areas and the potential for this to be
significantly reduced[42]. Since 1950, the number of motor vehicles has increased by
a factor of 10 there is no sign that this trend is going to reverse. Additionally, industry
and global energy consumption has also increased by a very large factor.[43] It is now
recognised that pollution from urban environments can travel very long distances and
affect areas much larger than the urban area itself. This makes urban environments a
key area to control.[34]
As previously mentioned, indoor air pollution from household fuel combustion also
has significant detrimental health consequences and lead to 4.3 million premature
deaths globally in 2012. The WHO has responded to these concerns by producing
recommendations for domestic emissions from the use of coal and kerosene. The
WHO also emphasise the importance of adequate ventilation, stressing that
conditioning systems and appropriate building design be used.[44] Lastly, it is
important that building materials with reduced emission of volatile organic
compounds (VOC) be used. These substances can be released for long periods of
times after construction and make adequate ventilation hugely important.[34] All of
the WHO guidelines were supplemented by support guidelines for implementing the
In countries with particularly high air pollution, additional protective equipment such
as personal facemasks may be an important tool in limiting harmful exposure. These
masks act by removing dangerous particles such as dust, soot and smoke from the air
and their use is currently highest in city centre areas where visibility is reduced due to
increased particulate matter. One study demonstrated a high efficacy of personal
facemasks by reducing exposure to particulate matter by 96.6%.[45],[46]
To conclude, various standards have been enforced to control pollution thus reducing
its adverse effects. By considering the sources of the pollutants, every attempt should
be made to prevent emission at the source in order to best achieve guideline levels.
Given the resounding link between pollution and ill-health the government needs to
create clear goals and provide widespread information on how these can be achieved.
We set ourselves the task of determining if pollution has adverse effects on the
cardiovascular system. By appraising medical literature we have been able to come to
the following conclusions:
Our primary finding was that there is a positive exposure-response relationship
between increasing air pollution and negative cardiovascular health outcomes.
This demonstrates that longer exposure is associated with a worsening
prognosis, including diseases such as IHD, HF, PVD and atherothrombosis.
Importantly, it was found that PM2.5 was the most penetrable pollutants;
causing the most adverse cardiovascular effects and representing the biggest
burden on the NHS. It has become evident that pollution has to be reduced at the
source in order for this to have a significant effect on improving the
cardiovascular health of the population. Lastly, clear guidelines have to be adhered
to on a local and national level.
Major at risk groups are:
 pregnant women
 diabetics
 elderly patients
 individuals with underlying cardiovascular pathologies
 populations in developing countries
 those in more industrialized, urban areas.
By enforcing the previously mentioned guidelines to lower national pollution levels,
pressure on the NHS would be relieved since less government funding would be
needed to treat pollution related cardiovascular problems. Any future strategies would
be cost effective in the long term as hospital admission rates should decrease
One weakness was a lack of a universal definition for short and long term exposure
periods. A lot of studies were done in developed countries making the results less
representative of the global population. This is important as pollution is a bigger
problem in over crowded, developing countries meaning that there will be more
cardiovascular incidents, causing the health care systems more money. Furthermore
despite the existence of guidelines, these can vary vastly on a national and local level,
therefore making it difficult to impose and track progress.
In summation more research is required to determine whether a pollution threshold
exists below which there are minimal affects on cardiovascular health. The absence of
a lower threshold is significant in government’s environmental health policies.
Certain cities are meeting national air pollution standards but could reduce particulate
matter levels further thereby reducing unnecessary cardiovascular health risks.
Weekly Diary
The group was formed and mutually it was decided that we wanted to undertake an
SSC project focusing on the cardiovascular system. Giles said he knew a cardiologist
at the Royal Infirmary and approached him to ask if he would be willing to be the
tutor for the project. The cardiologist, Tim Cartilidge, agreed to tutor the project and a
topic of the effects of pollution of the cardiovascular system was decided. A group
name list, title of the project and contact details of the tutor was sent to the Year 2
Medicine programme coordinator and the project was approved.
The group met to discuss where to begin the project. We all thought it necessary to
arrange a meeting with Tim for as soon as possible. It was decided that we should all
do some background reading and scoping of literature relevant to the project title prior
to meeting Tim.
The group met Tim for the first time. We discussed our findings from our research
prior to the meeting and agreed on a final project title – “Is pollution to our
cardiovascular system?” From this we sub-divided the project into four main headings
and two people were assigned as a pair to each sub-division. Tim gave the group a
literature article to read which was a good starting point for everyone. Before the next
meeting it was decided each pair was to begin researching their heading and report
their main findings back to the group in the next meeting.
During the week beginning 3/2/15 each pair met up separately to discuss their
individual findings and collate information to report back to the group.
During this week halfway feedback was submitted and the general consensus was that
the group was working very well and excellent progress has been made to-date.
Each pair reported back to the rest of the group the research they had found. Any
problems found whilst researching were raised and addressed as a group. It was
decided that the pairs were to meet up separately again and produce a more finalised
version of their section.
During the week beginning 17/2/15 each pair met up, and using peer feedback from
the previous meeting, created a more finalised version of their sections.
The group had a meeting to discuss some techniques of writing the sub-sections. We
mostly focussed on how to perform continual critical appraisals throughout the
literature review. Techniques from SSC2a were focal to the group discussion and
everyone in the group really benefitted from listening to the perspective of peers.
This meeting was in preparation for the meeting with Tim later on in the week. Each
pair had produced a final first draft of their sub-section. The group split into two
smaller groups to read over subsections.
Anita, Giles, Fraser and Alasdair collated their sections on short and long term
pathophysiology and read over the combined section as a whole and noted any
amendments to make.
Hannah, James, Bhavya and Simon took a slightly different approach and simply
allowed the other pair to read over their subsection and vice versa. This allowed a
different perspective to offer constructive advice.
It was decided that all amendments suggested from the meeting were made to each
subsection and the entirety of the work done to-date was sent to Tim for him to read
prior to the meeting.
Anita, Hannah, Bhavya and Fraser met with Tim to discuss the work to-date. Tim
offered many suggestions and improvements to make to each subsection. The meeting
also offered the opportunity for us to ask Tim questions or uncertainties we have with
the content of the project and for him to best guide us in the right direction. It was
decided that following Tim’s suggestions the sub sections should be amended and any
improvements made. We then planned to meet Tim again on 11/3 to discuss the
changes made and what exactly needs to be done in the final week.
Bhavya, Simon, Fraser, James and Giles met Tim for a brief meeting that allowed the
chance to discuss any problems reached with research and writing of sub sections. It
was agreed the project was still on course to easily meet the deadline.
The group met to produce final drafts to send to Tim for him to read over for the final
time. Any issues that had arisen recently were discussed and everybody got involved
with providing constructive advice on other sub sections. The group wrote the
conclusion together and that was also sent over to Tim for him to look over.
Tim provided feedback on each sub section and each pair met up to finalise their subsection and finish referencing the document ready for upload on the 19/3. Hannah and
Anita wrote the information search report and uploaded that to the wordpress site.
This was the final group meeting for the project. Each final section was uploaded to
the wordpress site and a word document with all the site contents was created.
Everyone re-read the project as a whole from start to finish and any final amendments
were made. As each section had been individually referenced, during this meeting the
wordpress site was referenced as a whole. The final weekly diary entry was written
and the weekly diary uploaded. Peer feedback was due for 20/3, in which each group
member had the opportunity to provide comments and marks for each group member
and Tim.
Simon Robson: Co-wrote the section on epidemiology. Co-wrote the conclusions.
Hannah Pulford: Co-wrote the section on air pollution guidelines and co-wrote the
information search report. Wrote the weekly diary.
Bhavya Rajagopalan: Co-wrote the section on epidemiology. Co-wrote the
Fraser Barbour: Co-wrote the section on short term exposure.
James Lucocq: Co-wrote the section on air pollution guidelines.
Anita Balaji: Co-wrote the section on long term exposure, co-wrote the information
search report and wrote the introduction. Co-wrote the conclusions.
Giles Lewis-Morgan: Co-wrote the section on long term exposure.
Alasdair Carmichael: Co-wrote the section on short term exposure.
Information Search Report
At the beginning of our SSC 2b project our tutor provided us with an initial paper
entitled “Adverse cardiovascular effects of air pollution”. From reading this, we
gained an introductory insight into the topic and it provided us with a base point to
which we could scope literature further. The group all individually used online search
engines such as PubMed, Web of Science, Google Scholar and EMBASE to find
more relevant articles for background reading prior to finalising the project title.
With a defined title the group was sub-divided into pairs and each pair given a more
specific focus. With a sub-title had been assigned the searches could be narrowed. We
used the aforementioned search engines to perform literature searches that involved
skills we have acquired previously such as using Boolean logic (‘AND’ and ‘OR’) to
retrieve relevant articles. As the project focused on critically appraising articles used,
where possible, we searched for controlled studies to gain access to primary sources.
Initially it was useful to use review articles and the studies referenced in those articles
to gain a better overview of the cardiovascular affects of pollution.
Being part of the University of Edinburgh allowed us to gain full access to all articles
we came across.
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