Introduction 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.  Importantly research also shows that a high percentage of these deaths can be attributed to microscopic combustion derived nano-particules; particulate matter.  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.  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 systems. 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. Epidemiology 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 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 years10. PM2.5 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 years)14. PM10 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 other.17 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 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.  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. . 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 predisposition. 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.  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. (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 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.”  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).  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) . 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 . 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” . 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 pollutant. 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.  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). 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, 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 . 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. Legally enforced standards have been created from some of these guidelines to help control pollution. 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. 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. 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 effects. 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,. 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. 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. 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. 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. 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. 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. 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. 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. All of the WHO guidelines were supplemented by support guidelines for implementing the recommendations. 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%., 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. Conclusions 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 significantly. Limitations 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 17/11/14 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. 16/1/15 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. 22/1/15 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. 3/2/15 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. 10/2/15 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. 17/2/15 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. 20/2 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. 3/3 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. 6/3 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. 11/3 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. 16/3 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. 17/3 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. 19/3 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. Contributions 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 conclusions. 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. 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