Emerging Areas Of Human Health Nursing Paper.

The Ottawa Charter (1986) was forged only 8 years after the historic Alma Ata meeting, which had declared Health for All by 2000. With hindsight, the goal of shaping a new and healthier world was already in jeopardy (Werner and Sanders, 1997). Perhaps, aware of this nascent weakening of the prospects for population health, the global health promotion community called for the revitalization of ambitious large-scale thinking. New strategies were devised to energize healthy individual and community behaviors, reflected in phrases such as ‘healthy choices should be easy choices’ and ‘healthy public policy’.

Nevertheless, over the ensuing two decades, the adverse social, economic and environmental trends that were already beginning to jeopardize, Health for All in 1986 have strengthened. Further, economic globalization, with increasingly powerful transnational companies shaping global consumer behaviors, has tended to make unhealthy choices the easier choices, including cigarettes, fast-food diets, high-sugar drinks, automated (no-effort) domestic technologies and others.

ORDER A PLAGIARISM-FREE PAPER HERE

These changes have occurred despite an increased understanding of the fundamental determinants of population health. Emerging Areas Of Human Health Assignment.Some of these foundations of health are at risk, and in some regions, hard-won health gains have recently been reversed. Recent attempts to re-focus attention on global public goods, such as in the Millennium Development Goals (MDGs), are weak in comparison to the scale of today's problems.

There is an urgent strategic need for health promotion to engage with the international discourse on ‘sustainability’. To date much of the discussion and policy development addressing ‘sustainable development’ has treated the economy, livelihoods, energy supplies, urban infrastructure, food-producing ecosystems, wilderness conservation and convivial communal living as if they were ends in themselves: the goals of sustainability. Clearly, those are all major assets that we value. But their value inheres in their being the foundations upon which the health and survival of populations depend. The ultimate goal of sustainability is to ensure human well-being, health and survival. If our way of living, of managing the natural environment and of organizing economic and social relations between people, groups and cultures does not maintain the flows of food and materials, freshwater supplies, environmental stability and other prerequisites for health, then that is a non-sustainable state. Emerging Areas Of Human Health Assignment.

In this paper, we discuss several of the emerging health issues. Lacking space to be comprehensive, we focus upon infectious diseases, the decline in life expectancy in several regions, the increasingly ominous challenge of large-scale environmental change and how globalization, trade and economic policy relate to indices of public health. Other emerging health issues not discussed here also reflect major recent shifts in human ecology. They too pose great environmental or social risks to health. They include urbanization, population ageing, the breakdown of traditional culture and relations and the worldwide move towards a more affluent diet and its associated environmentally damaging food production methods (McMichael, 2005).

There are two fundamental causes for the selected emerging health risks. First, most important, is the global dominance of economic policies which accord primacy to market forces, liberalized trade and the associated intensification of material throughput at the expense of other aspects of social, environmental and personal well-being. For millions in the emerging global middle class, materialism and consumerism have increased at the expense of social relations and leisure time. The gap between rich and poor, both domestically and internationally, has increased substantially in recent decades (United Nations Development Program, 2005). Inequality between countries has weakened the United Nations and other global institutions. Foreign aid has declined, replaced by claims that market forces will reduce poverty and provide public goods, including health care and environmental stability.

The second fundamental threat to the improvement and maintenance of population health is the recent advent of unprecedented global environmental changes. The scale of the human enterprise (numbers, economic intensity, waste generation) is now such that we are collectively exceeding the capacity of the planet to supply, replenish and absorb. Stocks of accessible oil appear to be declining. Meanwhile, the global emissions of carbon dioxide from fossil fuel combustion, and of other greenhouse gases from industrial and agricultural activities, are rapidly and now dangerously altering the global climate. Worldwide, land degradation, fisheries depletion, freshwater shortages and biodiversity losses are all increasing. The human population, now exceeding 6500 million, continues to increase by over 70 million persons per annum. The number of chronically undernourished people (over 800 million) is again increasing, after gradual declines in the 1980s and early 1990s (Food and Agricultural Organization, 2005). Famines in Africa remain frequent, and 300 million undernourished people live in India alone. Meanwhile, hundreds of millions of people are overnourished and, particularly via obesity, will incur an increasing burden of chronic diseases, especially diabetes and heart disease.Emerging Areas Of Human Health Nursing Paper.

The scale of these health risks is unprecedented. The global food crises of the 1960s were averted by the subsequent Green Revolution. Today, a broader-based revolution is required, not only to increase food production (again), but also to promote peace and international cooperation, slow climate change, ensure environmental protection, eliminate hunger and extreme poverty, quell resurgent infectious diseases and neutralize the obesogenic environment. This enormous population health task goes well beyond that envisaged by the MDGs.

It is, of course, difficult to get an accurate measure of these emerging risks to health. Some, such as climate change, future food sufficiency and the threat from weapons of mass destruction, may prove soluble. However, because of the inevitable time lag in understanding, evaluating and responding to these complex problems, the health promotion community should now take serious account of them. There is an expanding peer-reviewed literature on these several emerging problem, areas. To constrain health promotion by sidestepping them would be to risk being ‘penny wise but pound foolish’.

EMERGING AND RE-EMERGING INFECTIOUS DISEASES

In the early 1970s, it was widely assumed that infectious diseases would continue to decline: sanitation, vaccines and antibiotics were at hand. The subsequent generalized upturn in infectious diseases was unexpected. Worldwide, at least 30 new and re-emerging infectious diseases have been recognized since 1975 (Weiss and McMichael, 2004).Emerging Areas Of Human Health Nursing Paper. HIV/AIDS has become a serious pandemic. Several ‘old’ infectious diseases, including tuberculosis, malaria, cholera and dengue fever, have proven unexpectedly problematic, because of increased antimicrobial resistance, new ecological niches, weak public health services and activation of infectious agents (e.g. tuberculosis) in people whose immune system is weakened by AIDS. Diarrhoeal disease, acute respiratory infections and other infections continue to kill more than seven million infants and children annually (Bryce et al., 2005). Mortality rates among children are increasing in parts of sub-Saharan Africa (Horton, 2004).

The recent upturn in the range, burden and risk of infectious diseases reflects a general increase in opportunities for entry into the human species, transmission and long-distance spread, including by air travel. Although specific new infectious diseases cannot be predicted, understanding of the conditions favouring disease emergence and spread is improving. Influences include increased population density, increasingly vulnerable population age distributions and persistent poverty (Farmer, 1999). Many environmental, political and social factors contribute. These include increasing encroachment upon exotic ecosystems and disturbance of various internal biotic controls among natural ecosystems (Patz et al., 2004). There are amplified opportunities for viral mixing, such as in ‘wet animal markets’. Industrialized livestock farming also facilitates infections (such as avian influenza) emerging and spreading, and perhaps to increase in virulence. Both under- and over-nutrition and impaired immunity (including in people with poorly controlled diabetes—an obesity-associated disease now increasing globally) contribute to the persistence and spread of infectious diseases. Large-scale human-induced environmental change, including climate change, is of increasing importance.

These causes of infectious disease emergence and spread are compounded by gender, economic and structural inequities, by political ignorance and denial (particularly obvious with HIV/AIDS in parts of sub-Saharan Africa). Iatrogenesis (as with HIV in China and partial tuberculosis treatment in many developing countries), vaccine obstacles and the ‘10/90 gap’ (whereby a minority of health resources are directed towards the most severe health problems) add to this unstable picture.

We inhabit a microbially dominated world. We should therefore frame our relations with microbes primarily in ecological (not military) terms. The world's infectious agents, perhaps with the exceptions of smallpox and polio, will not be eliminated. But much can be done to reduce human population vulnerability and avert conditions conducive to the occurrence of many infectious diseases. This is an important focus for health promotion.

DECLINING REGIONAL LIFE EXPECTANCY

The upward trajectory in life expectancy forecast in the 1980s has recently been reversed in several regions, especially in Russia and sub-Saharan Africa (McMichael et al., 2004b). These could, in principle, be either temporary aberrations or unconnected to one another. However, identifiable factors appear to link these declines.

The fall in life expectancy since 1990 in Russia is unprecedented for a technologically developed country. Many proximal causes have been documented, including alcoholism, suicide, violence, accidents and cardiovascular disease. Multiple drug-resistant tuberculosis is widespread in Russian prisons. Collectively, these factors reflect social disintegration and crisis (Shkolnikov et al., 2004). Emerging Areas Of Human Health Nursing Paper.

In sub-Saharan Africa, HIV/AIDS has combined with poverty, malaria, tuberculosis, depleted soils and undernutrition (Sanchez and Swaminathan, 2005), deteriorating infrastructure, gender inequality, sexual exploitation and political taboos to foster epidemics that have reduced life expectancy, in some cases drastically. Adverse health and loss of human capital, caused by disease and the out-migration of skilled adults, have helped to ‘lock-in’ poverty. More broadly, indebtedness and ill-judged economic development policies, including charges for schooling and health services, have also impaired population health in Africa, following decades of earlier improvement. The intersectoral implications for health promotion are clear.

Conflict, most notoriously in Rwanda (André and Platteau, 1998), has also occurred on a sufficient scale to temporarily reduce life expectancy for some populations in sub-Saharan Africa. Age pyramids skewed to young adults have almost certainly played a role in this violence (Mesquida and Wiener, 1996), together with resource scarcity, pre-existing ethnic tensions, poor governance and international inactivity when crises develop.

GLOBAL ENVIRONMENTAL CHANGE

Sustainable population health depends on the viability of the planet's life-support systems (McMichael et al., 2003a). For humans, achieving and maintaining good population health is the true goal of sustainability, dependent, in turn, on achieving sustainable supportive social, economic and environmental conditions. Today, however, human-induced global environmental changes pose risks to health on unprecedented spatial and temporal scales. These environmental changes, evident at worldwide scale, include climate change, biodiversity loss, downturns in productivity of land and oceans, freshwater depletion and disruption of major elemental cycles (e.g. environmental nitrification) (McMichael, 2002). In coming decades, these long-term change processes will exact an increasing health toll via physical hazards, infectious diseases, food and water shortages, conflict and an inter-linked decline in societal capacity.

ORDER A PLAGIARISM-FREE PAPER HERE

We currently extract ‘goods and services’ from the world's natural environment about 25% faster than they can be replenished (Wackernagel et al., 2002). Our waste products are also spilling over (e.g. carbon dioxide in the atmosphere). Hence, there is now little unused global ‘biocapacity’. We are thus bequeathing an increasingly depleted and disrupted natural world to future generations. Although the resultant adverse health effects are likely to impinge unequally and, often, after time lag, this decline could eventually harm, albeit at varying levels, the entire human population.

Global climate change now attracts particular attention. Fossil fuel combustion, in particular, has caused unprecedented concentrations of atmospheric greenhouse gases. The majority expert view is that human-induced climate change is now underway (Oreskes, 2004). Emerging Areas Of Human Health Nursing Paper.The power of storms, long predicted by climate change modellers to increase (Emanuel, 2005), appears (in combination with reduced wetlands and failure to maintain infrastructure) to have contributed to the 2005 New Orleans flood. WHO has estimated that, globally, over 150 000 deaths annually result from recent change in the world's climate relative to the baseline average climate of 1961–1990 (McMichael et al., 2004a). This number will increase for at leastthe next several decades.

The most direct risks to future health from climate change are posed by heatwaves, exemplified by the estimated 25 000 extra deaths in Europe in August 2003, storms and floods. Climate-sensitive biotic systems will also be affected. This includes: (i) the vector–pathogen–host relationships involved in transmission of various infections, vector-borne and other, (ii) the production of aeroallergens and (iii) the agro-ecosystems that generate food. Recent changes in infectious disease occurrence in some locations—tickborne encephalitis in Sweden (Lindgren and Gustafson, 2001), cholera outbreaks in Bangladesh (Rodó et al., 2002) and, possibly, malaria in the east African highlands (Patz et al., 2002)—may partly reflect regional climatic changes.

Changes in the world's climate and ecosystems, biodiversity losses and other large-scale environmental stresses will, in combination, affect the productivity of local agro-ecosystems, freshwater quality and supplies and the habitability, safety and productivity of coastal zones. Such impacts will cause economic dislocation and population displacement. Conflicts and migrant flows are likely to increase, potentiating violence, injury, infectious diseases, malnutrition, mental disorders and other health problems.

These and other categories of global environmental changes, often acting in combination, pose serious health risks to current and future human societies (Figure 1). The important message here is that, increasingly, human health is influenced by socio-economic and environmental changes that originate well beyond national or local boundaries. The major, perhaps irreversible, changes to the biosphere's life-support system, including its climate system, increase the likelihood of adverse inter-generational health impacts.

Fig. 1:

Major pathways by which global and other large-scale environmental changes affect population health (based on McMichael et al., 2003b, p. 8).

View large Download slide

Major pathways by which global and other large-scale environmental changes affect population health (based on McMichael et al., 2003b, p. 8).

EMERGING HEALTH ISSUES AND THE MDGs

In 2000, UN member states agreed on eight MDGs, with targets to be achieved by 2015. Four MDGs refer explicitly to health outcomes: eradicating extreme poverty and hunger, reducing child mortality, improving maternal health and combating HIV/AIDS, malaria and other infectious diseases. Figure 2 shows how the MDG topic areas relate to the emerging health issues discussed here.

Fig. 2:

Relationships between: (i) social and environmental conditions and their underlying economic and demographic influences and (ii) the MDG topics. (Two of this paper's main issues, environmental changes and infectious diseases, are explicitly represented as boxes.)

View large Download slide

Many of the MDG targets are already in jeopardy. Although all are inter-linked, the ‘environmental sustainability’ MDG has fundamental long-term importance. Without it, the other concomitants of sustainability—economic productivity, social stability and, most importantly, population health—are unachievable. An additional reason to advance the MDGs is because that will slow population growth rates and thus reduce our collective ecological footprint (Wackernagel et al., 2002).

THE FALTERING DEMOGRAPHIC AND EPIDEMIOLOGICAL TRANSITIONS

Both the demographic and epidemiological transitions are less orderly than predicted. In some regions, declining fertility rates have overshot the rate needed for an economically and socially optimal age structure. In other countries, population growth has declined substantially because of the reduced life expectancy discussed earlier (McMichael et al., 2004b). Relatedly, the future health dividend from recent reductions in poverty may be lower than that once hoped because of the emergence of the non-communicable ‘diseases of affluence’, including those due to obesity, dietary imbalances, tobacco use and air pollution.

In the 1960s, there was widespread concern over imminent famine, affecting much of the developing world. This problem was largely averted by the ‘Green Revolution’ during the 1970s and 1980s. Meanwhile, the earlier view that unconstrained population growth had little adverse impact upon environmental amenity and other conditions needed for human wellbeing gained strength. However, in the last few years, this position has been re-evaluated (United Nations Department of Economic and Social Affairs Population Division, 2005). There is an increasing recognition of the adverse effects of rapid population growth, especially in developing countries, including from high unemployment when population increase outstrips opportunity.

Some argue that unsustainable regional population growth is characterized by age pyramids excessively skewed to young age, high levels of under- and unemployment and intense competition for limited resources. These circumstances jeopardize public health. Where there is also significant inequality and/or ethnic tension, catastrophic violence can result (André and Platteau, 1998; Butler, 2004).

Although Russia and parts of sub-Saharan Africa have vastly different demographic characteristics, there are important similarities in their recent declines in life expectancy. Both regions have a significant scarcity of public goods for health (Smith et al., 2003). In Russia, there is a lack of equality, safety and public health services. In many parts of sub-Saharan Africa, there is inadequate governance and food security as well as public safety and public health services. Viewed on an even larger scale, the miserable conditions for millions of people in these regions accord with a global class system, in which privileged groups in both developed and developing countries act (often in concert) to protect their own position at the expense of others (Butler, 2000: Navarro, 2004).

ORDER A PLAGIARISM-FREE PAPER HERE

The growth of the global population and its environmental impact means that we may now be less than a generation from exhausting the biosphere's environmental buffer, unless we can rein in our excessive demands on the natural world. If not, then the demographic and epidemiological transitions, already faltering, will be further affected. Population growth may then slow not only because of the usual development-associated fertility decrease but also because of persistently high death rates elsewhere.

Meanwhile, the growing awareness of these issues, the publicity of the MDGs, the ongoing campaigns against poverty and Third-World debt, calls for public health to address political violence and the renewed vigour of social movements for health (McCoy et al., 2004) affords new potential resources and collaborations to the global health promotion effort. These should be welcomed and acted upon.

GLOBALIZATION, TRADE, ECONOMIC POLICY AND FALTERING GLOBAL PUBLIC HEALTH: TOWARDS A UNIFYING EXPLANATION

The health benefits of the complex social, cultural, trade and economic phenomena that comprise ‘globalization’ are vigorously debated. Although differing viewpoints (Bettcher and Lee, 2002) are inevitable, the strength of this debate signifies that the net gain for population health from globalization is uncertain.

Several important health dividends often attributed to globalization have plausible alternative explanations. Many health gains in developing countries may be the time-lagged result of development policies and technologies introduced before the era of structural adjustment and partial economic liberalization, which heralded modern globalization. The accelerated demographic transition in China is a greatly under-recognized role in that country's rapidly growing wealth, as were China's earlier investments in health and education.

Proponents of gobalization assert that free trade, via ‘comparative advantage’, will benefit all populations. In reality, wealthy populations have long tilted the economic and political playing field in ways that ensure a disproportionate flow of trade benefits towards privileged populations (Mehmet, 1995). A powerful real-politic impediment to the complete removal of trade-distorting national subsidies is that this would probably entail a relatively greater loss for wealthy populations than for the poor. In contrast, the economic disadvantages incurred to date through partial market deregulation have largely been confined to relatively poor and politically weak populations in developed countries.

The pre-eminence of modern economic theory presents a major obstacle for health promoters. The narrow focus of the World Trade Organization, which largely discounts the often adverse social, environmental and public health impacts of trade, underscores the problem. Dominant economic theory evolved when environmental limits were considered remote (Daly, 1996). These theories assume that increased per capita income will offset the non-costed losses, whether these affect social welfare, environmental resources or public health. Critiques of these theories note that the harshest costs of modern economic practices fall upon ecosystems and populations with little current economic power or value, including generations not yet born.

Mobility of capital brings development, but capricious capital flight can create great hardship, including for public health. Deregulated labour conditions facilitate cheap goods, but they concentrate occupational health hazards among powerless workers. Increased labour mobility and steep economic gradients weaken family and community structures, contribute to ‘brain drain’ and promote inter-ethnic tensions. Many indices of inequality, including in health, income and environmental risk, have risen in recent decades (Butler, 2000; Parry et al., 2004).

Most critical commentary of globalization (George, 1999) is conceptual, emphasizing the adverse experiences of the disadvantaged and unborn. In contrast, the experiential feedback of the main beneficiaries of modern economic policy is largely positive. A major challenge for the promoters of health (and other forms) of justice is to adduce stronger evidence to convince policy-makers (themselves largely beneficiaries of globalization) to promote public goods, even though this may diminish the relative privilege of policy-makers and their constituencies. This is a difficult but essential task for health promotion.

EMERGING HEALTH ISSUES: THE CHALLENGES FOR HEALTH PROMOTION

In sum, global and regional inequality, narrow and outdated economic theories and an ever-nearing set of global environmental limits endanger population health. On the positive side of the ledger, there have been some gains (e.g. literacy, information sharing and food production, and new medical and public health technologies continue to confer large health benefits). Overall, though, reliance on economic, especially market-based, processes to achieve social goals and to set priorities and on technological fixes for environmental problems is poorly attuned to the long-term improvement of global human well-being and health. For that, a transformation of social institutions and norms and, hence, of public policy priorities is needed (Raskin et al., 2002). Population health can be a powerful lever in that process of social change, if health promotion can rise to this challenge.

Many of these contemporary risks to population health affect entire systems and social–cultural processes, in contrast to the continuing health risks from personal/family behaviours and localized environmental exposures. These newly recognized risks to health derive from demographic shifts, large-scale environmental changes, an economic system that emphasizes the material over other elements of well being and the cultural and behavioural changes accompanying development. Together, these emerging health risks present a huge challenge to which the wider community is not yet attuned. The risks fall outside the popular conceptual frame wherein health is viewed in relation to personal behaviours, local environmental pollutants, doctors and hospitals. In countries that promote individual choice and responsibility, there are few economic incentives for the population's health.

Health promotion must, of course, continue to deal with the many local and immediate health problems faced by individuals, families and communities. But to do so without also seeking to guide socio-economic development and the forms and policies of regional and international governance is to risk being ‘penny wise but pound foolish’. Tackling these more systemic health issues requires multi-sectoral policy coordination (Yach et al., 2005) at community, national and international levels, via an expanded repertoire of bottom-up, top-down and ‘middle-out’ approaches to health promotion.

CONCLUSION

The essential principles of the Ottawa Charter remain valid. However, today's health promotion challenge extends that foreseen in 1986 and requires work at many levels. There is need for proactive engagement with international agencies and programs that bear on the socio-economic fundamentals in disadvantaged regions/countries. Many low- and middle-income countries require financial aid from donor countries to achieve the health-related MDGs, to deal with emerging and re-emerging infectious diseases and to counter the emerging health risks from human-induced global environmental problems. Linkages between the health sector and civil society, including those struggling to promote development, human rights, human security and environmental protection, should be strengthened.

We need to understand that ‘sustainability’ is ultimately about optimizing human experience, especially well-being, health and survival. This requires changes in social and political organization and in how we design and manage our communities. We must live within the biosphere's limits. Health promotion should therefore address those emerging population health influences that transcend both national boundaries and generations. The central task is to promote sustainable environmental and social conditions that confer enduring and equitable gains in population health.

Historical perspective

Air pollution is now fully acknowledged to be a significant public health problem, responsible for a growing range of health effects that are well documented from the results of an extensive research effort conducted in many regions of the world. Whilst there is no doubt that rapid urbanisation means that we are now exposed to unhealthy concentrations and a more diverse variety of ambient air pollutants, palaeopathological research suggests the problem, in the form of smoke, plagued our oldest ancestors. Computerised tomography imaging studies on the bodies of ancient mummies have detected evidence of pneumonia, emphysema, pulmonary oedema and atherosclerosis (Zweifel et al. 2009; Thompson et al. 2013), whilst autopsies have described extensive carbon deposits in the lung (Zimmerman et al. 1971). This in turn has led to a speculative link to the daily inhalation of smoke in confined spaces from fuels used for warmth, cooking and lighting.

Leaping forward through history to Victorian London, the billowing smoke and sulphur dioxide (SO₂) from domestic and industrial coal burning, mixed with natural fog, famously caught the imagination of literary and visual artists. They regarded this meteorological phenomenon as a spectacular manifestation of turn-of-the-century life in a cosmopolitan city. Indeed, the unique style that Charles Dickens adopted in his description of the fogs meant that they became a romantic legend. For Claude Monet, the chromatic atmospheric effects created by the effects of smog on sunlight gave London magnificent breadth and became the predominant theme in his renditions of the city. As a consequence, to some, London’s notoriously toxic air became a world-famous institution rather than an appalling social evil. In December 1952, however, a vast and lethal smog, caused by cold stagnant weather conditions that trapped combustion products at ground level, brought about the worst air pollution disaster in history, resulting in an estimated 4000–12,000 deaths and an enormous increase in respiratory and cardiovascular complications (Logan 1953; Bell and Davis 2001). This crisis was also the direct incentive to pass the Clean Air Act in 1956, which successfully curtailed domestic coal burning in London and other major cities in the UK. At this point, the UK led the world in cleaning up air by implementing smokeless zones, imposing controls on industry, increasing the availability and use of natural gas and changing the industrial and economic structure of the country. The results were considerable reductions in the concentration of smoke and SO₂(Wilkins 1954; Fig. 1).

An external file that holds a picture, illustration, etc. Object name is 10653_2015_9720_Fig1_HTML.jpg

Open in a separate window

Fig. 1

Death toll and pollution concentrations during the 1952 London Smog. Source: Wilkins (1954)

Modern-day air pollution

On recounting such progress, it is especially disappointing that in recent years, improvements in air quality, not solely within the UK but in many urban areas around the world, have miserably stalled. We occasionally experience smog hanging over our cities when poor air-flow and dispersal allows pollution to build up—and it is during such episodes that susceptible individuals (e.g. those with asthma, COPD or heart disease) may undergo an acute exacerbation requiring increased medication or admission to hospital. Of greater concern, however, is the inherent, modern type of pollution in today’s urban environments, which unlike the Victorian pea-souper smog, is indiscernible at ground level but manifests in chronic health effects. This ‘invisible killer’ contains nitrogen oxides, ozone (O₃) and exceptionally small particulate matter (PM). PM₁₀ and the more abundant PM_2.5 constitute particles with diameters less than 10 and 2.5 µm, respectively—the latter being approximately 30 times less than the width of human hair. Of the modern-day air pollutants, PM has been held responsible for the majority of health effects. In urban areas, the major source is fossil fuel combustion, primarily from road transport, as well as power stations and factories. In rural and semi-urban areas of developing countries, the burning of biomass fuels on open fires or traditional stoves creates indoor concentrations of PM that far exceed those considered safe in outdoor air.

Over the last 10 years, there has been a substantial increase in findings from many research disciplines (e.g. population exposure, observational epidemiology, controlled exposure studies, animal toxicology and in vitro mechanistic work) that these modern-day ambient pollutants are not only exerting a greater impact on established health endpoints, but are also associated with a broader number of disease outcomes. The aim of this brief review article is to summarise the increased health hazards to emerge from PM air pollution research in recent years, drawing upon findings published in international projects (WHO 2012, 2013a), Health Effects Institute (HEI) research reports (HEI 2010, 2013a, b), authoritative reviews (Brook et al. 2010) and important individual publications. We will also discuss how the increased evidence base of risk relates to current public awareness and understanding of the problem. Indeed, focused education and continued evolution of sophisticated information systems have the potential to achieve a durable change in public attitude and behaviour, in a way that improves people’s health as well as the quality of the air they breathe.

Health effects of PM air pollution

Mortality

The ultimate effect of air pollution on public health is to bring about premature death. Epidemiological evidence first emerged from American research, which arguably began as a consequence of the 1952 air pollution episode in London. The reported associations between increased respiratory and cardiovascular mortality and acute and chronic exposures to particulate air pollution (Schwartz and Dockery 1992; Dockery et al. 1993) were subsequently confirmed outside of the USA, in many cities around the world (Katsouyanni et al. 2001; Hoek et al. 2002; Filleul et al. 2005). Of particular note, recent long-term studies show associations between PM and mortality at levels well below the current annual World health Organisation (WHO) air quality guideline level for PM_2.5. Several updates to the Havard Six Cities Study and the study of the American Cancer Society cohort continue to cite consistent and significant associations between long-term exposure to PM_2.5 and mortality (Lepeule et al. 2012; Krewski et al. 2009). In addition, new prospective cohorts provide additional evidence of this association, including effects observed at lower concentrations (mean 8.7 μg/m³; interquartile range 6.2 μg/m³), whilst the emerging multicity cities have confirmed previously reported increases in daily mortality (Ostro et al. 2006; Naess et al. 2007; Crouse et al. 2012; Meister et al. 2012).

We now understand that air pollution has overtaken poor sanitation and a lack of drinking water to become the main environmental cause of premature death (OECD 2014). The latest estimate from the WHO reported that in 2012, approximately 3.7 million people died from outdoor urban and rural sources (WHO 2014). The cause of deaths was broken down as follows: ischaemic heart disease (40 %), stroke (40 %); chronic obstructive pulmonary disease (COPD) (11 %), lung cancer (6 %) and acute lower respiratory infections in children (3 %). These figures are based not only on a greater understanding of the diseases caused by poor air quality, but also more accurate exposure assessment that utilises sophisticated measurement and modelling technology. Of note, the overall mortality estimate more than doubles previous ones and reveals that the vast majority of deaths stem from cardiovascular disease.

By region, the largest outdoor air pollution burden is found in the low- and middle-income countries of the Western Pacific and South-East Asia, with 2.6 million linked deaths in 2012 (WHO 2014), reflecting the heavy industry and air pollution hotspots within the developing nations of these areas. However, the problem is very much a global one. Focusing on Europe, air pollution is again the biggest environment risk factor behind premature death (EEA 2014). In 2012, mortality numbers related to outdoor air pollution in the low- to middle-income, and high-income countries were estimated at 203,000 and 280,000, respectively (WHO 2014). In recent years (2010–2012) the proportion of the urban population in the 28 European Union (EU) Member States who live in areas where the EU daily limit value for PM₁₀ and PM_2.5concentrations exceeded that was 21 and 10 %, respectively (EEA 2014). The percentage of the EU urban population exposure to PM concentrations above the WHO AQG (WHO 2006) is significantly higher, reaching 64 and 92 % for PM₁₀ and PM_2.5, respectively (EEA 2014). Life expectancy of Europeans is reduced, on average, by about 8.6 months owing to PM_2.5 pollution (WHO 2013b), whilst traditional health impact assessment methods used in the project Improving Knowledge and Communication for Decision-making on Air Pollution and Health in Europe (Aphekom 2011), estimates that potential exists to increase average life expectancy in the most polluted cities by approximately 22 months if PM_2.5concentrations were reduced to the WHO AQG annual level (Fig. 2).

An external file that holds a picture, illustration, etc. Object name is 10653_2015_9720_Fig2_HTML.jpg

Fig. 2

Predicted average gain in life expectancy (months) for persons 30 years of age and older in 25 Aphekom cities for a decrease in average annual level of PM_2.5 to 10 µg/m³. Source: Aphekom project, InVS (Aphekom 2011)

In the UK, outdoor air pollution also makes a significant contribution to mortality. Current (2008) data estimate that if the effect of PM_2.5 air pollution is considered by itself, it is responsible for at least 29,000 premature deaths, alternatively represented as an average loss of life expectancy from birth of approximately 6 months (COMEAP 2010). A more recent activity by Public Health England (PHE) has investigated the burden at a more local level in the UK, with mortality rate estimates from long-term PM_2.5pollution ranging from around 2.5 % in some in rural areas of Scotland and Northern Ireland, between 3 and 5 % in Wales, to over 8 % in certain London boroughs (PHE 2014). Upon comparing commonly acknowledged mortality risks, it has been estimated that a 10 µg/m³ reduction in ambient PM_2.5 pollution (roughly equivalent to eradicating all anthropogenic particles) would have a larger impact on life expectancy in England and Wales than eliminating road traffic accidents or passive smoking (IOM 2006).

Cardiopulmonary morbidity

The impact of particulate air pollution on morbidity endpoints has been subject to intense study, resulting in strong scientific consensus on the independent associations of airborne PM_2.5 and PM₁₀, with negative impacts on respiratory and cardiovascular health following both short-term and chronic exposures. Furthermore, data strongly suggest that effects have no threshold within the studied range of ambient concentrations, can occur at levels close to PM_2.5 background concentrations and that they follow a mostly linear concentration–response function (WHO 2013a). Evidence is now well-established and particularly strong for reduced lung function, heightened severity of symptoms in individuals with asthmatics, COPD and ischaemic heart disease which includes heart attacks. We refer to previous reviews on cardiovascular effects (Brook et al. 2010) and respiratory disease (Kelly and Fussell 2011).

More recent evidence to emerge has now linked long-term exposure to PM_2.5 to atherosclerosis—a condition that underlies many cardiovascular diseases. Indeed, the promotion and vulnerability of atherosclerotic plaques is a potential mechanism by which PM air pollution could trigger cardiovascular mortality and morbidity. In support of this, long-term exposure to PM_2.5 concentrations, as well as proximity to traffic, is associated with preclinical markers (carotid intima media thickness [CIMT] and coronary artery calcification) of atherosclerosis (Künzli et al. 2005; Hoffmann et al. 2007; Bauer et al. 2010) and also with progression of this pathology (Künzli et al. 2010).

Emerging respiratory data now link long-term exposure to PM to childhood respiratory disease. Birth cohort studies have suggested associations between PM during pregnancy and higher respiratory need, airway inflammation and an increased susceptibility to respiratory infections (Latzin et al. 2009; Jedrychowski et al. 2013). The latest meta-analysis of 10 European birth cohorts from the ESCAPE project also provides robust evidence that post-natal PM₁₀ (but notably not PM_2.5), and traffic exposure is associated with an increased risk of pneumonia in early childhood as well as some evidence for an association with otitis media (MacIntyre et al. 2013). In a birth cohort in the Netherlands, further associations have been reported between long-term exposure to traffic-related air pollution at the birth address and both symptoms of asthma and low lung function in young children (Gehring et al. 2010; Eenhuizen et al. 2013; Molter et al. 2013). Another interesting epidemiological observation includes a possible link between chronic PM exposure during childhood and vulnerability to COPD in adulthood (Grigg 2009).

New health outcomes

Other than the well-documented effects on respiratory and cardiovascular health, an increasing number of studies have investigated the potential of PM air pollution to negatively influence several new health outcomes. We now have evidence linking long-term exposure to PM_2.5 with adverse birth outcomes, whilst emerging data suggest possible effects of long-term PM_2.5 exposure on diabetes, neurodevelopment, cognitive function. The number of studies linking maternal exposure to air pollutants, including particulates, during pregnancy to various birth outcomes is steadily increasing and is of particular interest owing to the crucial time span of biological development and as such, the potential to have long-term consequences on overall health. Harmful effects have been shown for low birth weight, small for gestational age and preterm birth (Ritz and Wilhelm 2008; Sapkota et al. 2012; Proietti et al. 2013). A small number of studies have investigated traffic-related air pollution exposure at participants’ residential address as a novel risk factor for type 2 diabetes mellitus (T2DM). Although not conclusive, results suggest an association between risk of T2DM and exposure to PM (Kramer et al. 2010; Puett et al. 2011a; Coogan et al. 2012); however, evidence is stronger for NO₂ and distance to road (Raaschou-Nielsen et al. 2013). That the deleterious effects of PM air pollution may extend to the brain have only recently been discovered and research in this area is currently limited and results inconclusive (Guxens and Sunyer 2012). For example, a study of women (68–79 years old) who lived for more than 20 years in the same residence showed a significant reduction in mild cognitive function (associated with a high risk of progression to Alzheimer’s Disease) in those who were 74 years old or younger and lived within 50 m to the next busy road with a traffic density of more than 10,000 cars per day (Ranft et al. 2009). However, no effect in cognitive function was found for PM₁₀ concentrations.Improved air quality and improved health

We now also have consistent evidence that a reduction in the level of particulate pollution following a sustained intervention (mainly regulatory actions) is associated with improvements in public health. In the USA, Pope et al. (2009) used data from the 51 cities from the American Cancer Society study for which long-term PM_2.5 data are available. It was reported that after adjustment for changes in other risk factors, the reduction in PM_2.5 concentration between 1980 and 2000 was strongly associated with 2.7 year overall increases in life expectancy that occurred during that period (Fig. 3). Evidence has also been demonstrated in the Swiss Study on Air Pollution and Lung Diseases in Adults (SAPALIDIA) that assessed lung diseases in adults in eight communities in 1991 and again in 2002—a period when the annual average PM₁₀concentration decreased by 5–6 µg/m³. This reduction in particle levels was associated with attenuation in the annual rate of decline of lung function (Downs et al. 2007). Using the same cohort, Schindler et al. (2009) reported that fewer reports of regular cough, chronic cough or phlegm, and wheezing and breathlessness could also be attributed to the observed decrease in PM₁₀. In a separate Swiss investigation following children from nine Swiss communities between 1992 and 2001, declining concentrations in ambient PM₁₀ was associated with improved respiratory health (reduced incidence of chronic cough, bronchitis, common cold, nocturnal dry cough and conjunctivitis symptoms; Bayer-Oglesby et al. 2005). The results suggest that health improvements can be expected to appear almost immediately and can be seen following almost any decrease in the concentration of PM (for example, the observed beneficial effects in respiratory health of the Swiss children occurred following relatively small changes of rather moderate air pollution levels) enormously strengthens the argument for optimal air quality management.

ORDER A PLAGIARISM-FREE PAPER HERE

An external file that holds a picture, illustration, etc. Object name is 10653_2015_9720_Fig3_HTML.jpg

Open in a separate window

Fig. 3

Changes in life expectancy for the 1980s–1990s plotted against reductions in PM_2.5 concentrations for 1980–2000. Dots and circles labelled with numbers represent changes in population-weighted mean life expectancies at the county level and metropolitan area level, respectively. The solid and broken lines represent regression lines with the use of county-level and metropolitan-area-level observations, respectively. Reproduced with permission from Pope et al. (2009)

Go to:

Differential toxicity of PM

Epidemiological and toxicological research findings have shown that PM mass (PM_2.5 and PM₁₀) comprises fractions and sources with varying types and degrees of health effects (Kelly and Fussell 2012). The subject of relative toxicity represents one of the most challenging areas of environmental health research in that PM is not a single entity. It is a complex, heterogeneous mixture that can exist as solids or liquids. These particles vary not only in chemical composition, mass, size (few nanometres to tens of micrometres), number, shape and surface area, but also source, reactivity, solubility and reactivity. In London, particulate pollution is predominantly diesel exhaust particles (DEPs) mixed with resuspended particles of tyre rubber and brake dust (Yanosky et al. 2012). This compares with combinations of traffic-derived PM and desert sand in parts of Ghana, biomass smoke Ethiopia and soot from coal fired power stations in the eastern provinces of China. All of the many characteristics of PM have the potential to influence the toxicity of ambient PM. Current knowledge does not, however, allow individual characteristics or sources to be definitely identified as being closely related to specific health effects and likewise, no specific source, component or size category can be excluded as having no adverse effects (EPA 2009; WHO 2013a; HEI 2013a). Rather, the capability of PM to induce disease may be the result of multiple components acting on different physiological mechanisms.

Below is a brief overview of current evidence on the contribution to adverse health effects played by chemical constituents (black carbon [BC], organic carbon [OC], inorganic secondary aerosols), size (coarse PM, ultrafine particles [UFP) and source (road transport). The findings discussed have arisen from the WHO REVIHAAP Project (Review of Evidence on Health Aspects of Air Pollution) (WHO 2013a), together with other recent critical reviews and systematic research efforts on the subject (WHO 2012; HEI 2010, 2013a, b).

Black carbon

In addition to the WHO REVIHAAP project (WHO 2013a), the health effects of BC particles have also undergone a recent systematic review by the WHO Regional Office for Europe (WHO 2012). These initiatives have confirmed that sufficient epidemiological evidence exists to link short-term (daily) variations in BC particles with all-cause and cardiovascular mortality and cardiopulmonary hospital admissions. Evidence is also conclusive that long-term (annual) BC exposure is associated with all-cause and cardiopulmonary mortality. Although distinct mechanistic effects have not been identified from toxicological studies, suggesting that BC may not be a direct toxic component of fine PM, it is hypothesised that these particles may operate as a universal carrier of combustion-derived chemicals (semi-volatile organic fractions, transition metals) of varying toxicity to not only the lungs, but to systemic circulation and beyond. Furthermore, in that short-term studies show that health effect associations with BC were more robust than those with PM_2.5 or PM₁₀, although BC particles may not constitute a causal agent, it is the opinion that they may well serve as a better indicator of harmful particulate substances (e.g. organics) from primary traffic-related combustion particles compared to undifferentiated PM mass (WHO 2012).

Organic carbon

OC is a very complex and heterogenous mixture of primary and secondary organic aerosols and owing to the common combustion source, can co-exist with BC. As a consequence, it is a huge challenge to identify the potential toxicity of specific OC constituents and in fact evidence is currently insufficient to distinguish between the toxicity of primary and secondary organic aerosols. Studies are, however, generating increasing amounts of data on associations between total organic carbon and a variety of health effects including short-term perturbations in both respiratory (Kim et al. 2008; Hildebrandt et al. 2009) and cardiovascular (Delfino et al. 2010; Ito et al. 2011; Kim et al. 2012; Son et al. 2012; Zanobetti and Schwartz 2009) endpoints. Ostro et al. (2010) has also observed associations between long-term exposure to organic carbon and both ischaemic heart disease and pulmonary mortality.

Inorganic secondary aerosols

Epidemiological evidence continues to accumulate on the short-term effects of sulphate on cardiovascular mortality as well as both respiratory and cardiovascular hospital admissions (Ito et al. 2011; Kim et al. 2012). Data have also emerged on associations between daily increments in ambient sulphate and physiological changes to the cardiovasculature, namely ventricular arrhythmias (Anderson et al. 2010) and markets of endothelial dysfunction (Bind et al. 2012). The HEI’s comprehensive National Particle Component (NPACT) initiative also identified significant associations in the epidemiological studies between secondary inorganic sulphate and health effects and moreover, these were backed up by complimentary findings in the toxicological element of the project (HEI 2013a). Historically, toxicological evidence has been seemingly consistent that the components of inorganic secondary aerosols (ammonium, sulphates or nitrates) pose little threat, but uncertainties do exist. For example, the cations (metals, hydrogen) associated with sulphates/nitrates and/or other absorbed components (metals, organic particles) may have an underlying toxic role or else secondary inorganic components may influence bioavailability and as a consequence, toxicity of other particulate components (Oakes et al. 2012).

Coarse PM

Accumulating epidemiological evidence suggests that short-term exposures to coarse particles (between 2.5 and 10 μm) are associated with effects on adverse cardiovascular health, respiratory endpoints health, including premature mortality (Peng et al. 2008; Atkinson et al. 2010; Mann et al. 2010; Meister et al. 2012; Qiu et al. 2012). Overall opinions made by various systematic reviews and assessments are variable as to whether such effect estimates are higher or lower than those for fine PM (Brunekreef and Forsberg 2005; EPA 2009). Investigations into long-term effects of coarse PM are fewer and have reported no or limited evidence that this size fraction has an effect on mortality or cardiovascular health (Puett et al. 2009, 2011b). Toxicological studies comparing coarse and fine PM have reported that coarse particles can be as toxic as PM_2.5 on a mass basis (Graff et al. 2009; Wegesser et al. 2009). Data, however, are not only scarce, but also difficult to interpret owing differences in the inhalability and deposition efficiency of these size fractions.

Ultrafine particles

UFPs (smaller than 0.1 μm) have many unique properties that have led scientists to hypothesise that this size fraction may have specific or enhanced toxicity relative to fine (PM_2.5) or coarse PM. Apart from the relationship between particle diameter and penetration within the lung and to extrapulmonary sites, on a mass basis, smaller particles have a much greater surface area and with that, a high capacity to adsorb toxic chemicals. In addition, the finer the particles, the greater the likelihood of penetration to indoor environments, being suspended in the atmosphere for longer periods and being transported over large distances. As a consequence, a substantial body of literature has now been published on the mechanisms of UFP toxicity and adverse effects in animals and in humans, including a recent HEI review (HEI 2013b). Epidemiological data, however, are still limited and provide suggestive rather than strong and consistent evidence of adverse effects of UFPs [reviewed by Rückerl et al. (2011), Weichenthal (2012)]. The HEI review noted that “The current evidence does not support a conclusion that exposure to UFPs alone can account in substantial ways for the adverse effects of PM_2.5” (HEI 2013b). Toxicological studies have certainly advanced our understanding of the action of UFPs, showing the potential of this size fraction to adopt differential patterns of deposition, clearance and translocation (Kreyling et al. 2010). Emerging Areas Of Human Health Assignment.

Source

Many PM pollution sources, namely coal combustion, shipping, power generation, the metal industry, biomass combustion, desert dust episodes and road transport have been associated with different types of health effects (EPA 2009; WHO 2013a). Of these, the main source of urban pollution—road transport—is also the source associated with the most serious health outcomes. A critical review of the literature on the health effects of traffic-related air pollution concluded that sufficient evidence had accumulated to support a causal relationship between exposure to traffic-related air pollution and exacerbation of asthma. Further evidence was found to be suggestive of a causal relationship with onset of childhood asthma, non-asthma respiratory symptoms, impaired lung function, total and cardiovascular mortality, and cardiovascular morbidity (HEI 2010).

The PM components from road traffic include engine emissions, comprising largely of EC and OC, plus non-exhaust sources that are often characterised by elevated concentrations of transition metals (brake wear [copper, antimony], tyre abrasion [zinc], dust from road surfaces [iron]). The largest single source is derived from diesel exhaust (DE). Indeed, owing to the increased domestic market penetration of diesel engines, the fuel powering the majority of our buses and taxis in many industrialised countries and the fact that they generate up to 100 times more particles than comparable gasoline engines with 3-way catalytic convertors (Quality of urban air review group 1996), diesel exhaust particles (DEPs) contribute significantly to the air shed in many of the world’s largest cities. DEPs have also been shown to have substantial toxicological capacity, facilitated by the size (80 % of DEPs have an aerodynamic diameter of <1 µm) of such particles as well as their surface chemistry characteristics. For instance, DEPs have a highly adsorptive carbon core that act as a vector for the delivery, deep into the lung, of redox active metals, polyaromatic hydrocarbons and quinones. In addition to traffic density per se, it is not surprising therefore that the greatest health impacts appear to be associated with proximity to roads carrying a high proportion of diesel powered heavy and light good vehicles (Janssen et al. 2003; Gowers et al. 2012). In 2012, the International Agency for Research on Cancer (IARC) classified particulates in diesel fumes as carcinogenic to humans based on sufficient evidence that it is linked to an increased risk of lung cancer, as well as limited evidence linking it to an increased risk of bladder cancer (IARC 2012). Although most studies into the toxicity and health consequences of roadside PM have focused on DEPs, the non-exhaust sources are attracting interest and deservedly so (van der Gon et al. 2013). Emerging Areas Of Human Health Assignment.Whilst contributions from brake/tyre wear and road surface abrasion in the wake of passing traffic will become more important with progressive reductions in exhaust emissions, their potential to elicit health effects is largely ignored at the regulatory level despite links with cardiopulmonary toxicity (Gasser et al. 2009; Gottipolu et al. 2008; Mantecca et al. 2009; Riediker et al. 2004).

Go to:

Mechanisms of PM toxicity

The well-established evidence that PM pollution contributes to an array of health outcomes has resulted in an enormous research effort to understand the underlying biological basis of toxicity by identifying mechanistic pathways. Although there remains much to be understood, our appreciation of the physiological effects and plausible biological mechanisms that link short- and long-term PM_2.5 exposure with mortality and morbidity has evolved rapidly and continues to do so. For example, in investigating subclinical physiological changes, epidemiological research has reported variations in cardiovascular biomarkers of systemic inflammation such as C-reactive protein and fibrinogen—subtle responses that have been consistently linked to subsequent cardiovascular disease and death (Brook et al. 2010). A particularly powerful tool to study mechanistic pathways and physiological endpoints related to adverse effects following DEP exposure is the use of controlled exposure studies in healthy volunteers (Salvi et al. 1999, 2000; Mudway et al. 2004; Pourazar et al. 2004, 2005; Mills et al. 2005; Behndig et al. 2006; Peretz et al. 2007; Tornqvist et al. 2007; Lucking et al. 2008; Lundback et al. 2009) as well as mild asthmatics (Stenfors et al. 2004) and individuals with stable coronary heart disease (Mills et al. 2007). Carefully characterised and environmentally relevant DE exposure experiments, combined with cardiovascular measurements, BAL and bronchial biopsy have revealed well-defined systemic, pulmonary and cardiac responses involving a variety of cellular and molecular perturbations. It is probable that associations between the various constituents of PM and health effects are the result of multiple, complex and interdependent mechanistic pathways acting on different physiological mechanisms. Current evidence does, however, support a chain of events involving pollution-induced pulmonary and systemic oxidative stress and inflammation, translocation of particle constituents and an associated risk of vascular dysfunction, atherosclerosis, altered cardiac autonomic function and ischaemic cardiovascular and obstructive pulmonary diseases (Kelly and Fussell 2015; Fig. 4).

An external file that holds a picture, illustration, etc. Object name is 10653_2015_9720_Fig4_HTML.jpg

Fig. 4

Biological pathways linking PM exposure with oxidative and inflammatory pathways in the lung and cardiovasculature

Since oxidative stress is widely believed to play a key role in the harmful effects of a range of particles at the cellular level, the oxidative potential (OP) of PM (their capacity to cause damaging oxidative reactions) is regarded as an attractive exposure metric in our bid to identify the toxic components and sources within an ambient PM mix (Ayres et al. 2008; HEI 2010). The OP of ambient PM collected at busy roadside sites is clearly enhanced relative to urban background and rural sites, and this appears to be associated with an enrichment of metals (copper, barium) linked with abrasion and brake wear processes (Godri et al. 2011; Kelly et al. 2011; Boogaard et al. 2012). Concern surrounding these findings is well founded in that they highlight a toxic contribution by non-exhaust pollutants and as such, by a currently unregulated source. Oxidative stress is linked to several DNA lesions and the formation of bulky adducts—mechanisms by which traffic-related pollution could elicit mutagenesis and in turn cause cancer (Loeb 2001). Of the biomarkers of oxidatively damaged DNA, urinary excretion of 8-oxo-7,8-dihydro-2-deoxyguanosine (8oxodG) has now been validated to evaluate the pro-oxidant effects of vehicle exhaust emissions on the DNA of exposed subjects (Barbato et al. 2010). DNA adduct levels in non-smoking workers have been found to reflect average levels of exposure to PM₁₀ in high-traffic urban areas (Palli et al. 2008) and were also reported to be increased in cord blood after maternal exposures to traffic-related air pollution (Pedersen et al. 2009)—the latter demonstrating the potential for transplacental environmental exposures to induce DNA damage early in newborns and with that, increased risk for adverse effects later in life.

Go to:

Public awareness and education

That poor air quality can have such a significant impact on human health is undisputed, and the previous sections have drawn upon research conducted over recent years that supports the notion that risks are increasing as new hazards emerge. How then does this translate to public awareness of the problem? The general consensus is that society would benefit from being better engaged and educated about the complex relationship between air quality and ill health (Kelly et al. 2012). If people are aware of variations in the quality of the air they breathe, the effect of pollutants on health as well as concentrations likely to cause adverse effects and actions to curtail pollution, there follows a greater likelihood of motivating changes in both individual behavior and public policy. In turn, such awareness has the potential to create a cleaner environment and a healthier population.

Studies and initiatives examining public awareness and understanding in this area have yielded mixed results, with some acknowledging a significant amount of concern within the public over poor air quality, an awareness of air quality warnings, and a positive relationship between alerts and a change in outdoor activities (DEFRA 2002; Wen et al. 2009; McDermott et al. 2006). In fact, following findings that air quality warnings associated with ground level O₃ do have a significant impact on attendance at outdoor facilities in Southern California, Neidell and Kinney (2010) suggested that ambient air quality measurements from monitors may not reflect personal exposure if individuals intentionally limit their exposure in response poor air quality. Bell et al. (2004) have also hypothesised that deliberate avoidance in time spent outdoors could contribute to the considerable heterogeneity in O₃-induced mortality observed across US communities. Other research has concluded that both awareness of the links between air pollution and ill health and an understanding of air quality information are lacking amongst the public (Bickerstaff and Walker 2001; Semenza et al. 2008; COMEAP 2011). In 2013, the European Commission (EC) conducted a flash Euro barometer to gain a greater insight into the views of the European public on matters of air quality and air pollution (EC 2013). Six out of ten Europeans responded that they did not feel informed about air quality issues in their country. When asked how serious they considered a range of air quality related problems to be in their country, responses for respiratory disorders, cardiovascular diseases and asthma/allergy were 87, 92 and 87 % respectively. Emerging Areas Of Human Health Assignment.

Factors determining awareness

Other than the availability of sufficient information that will be covered in the following section, factors governing how aware individuals are about the quality of their air and potential repercussions for their health are likely to include understanding, perception and a vested interest. Individuals may choose not to concern themselves about air quality owing to a poor understanding of what is undoubtedly a complex science. Unlike other environmental risks that are routinely communicated such as UV and heat, overall air quality encompasses several primary pollutants as well as secondary products owing to atmospheric transformation. Rural areas for example are very often considered safe places to escape from pollution. However, at times, O₃ concentrations can be as high or greater than urban locations owing to the presence of lower concentrations of nitrogen oxides to sequester rural O₃. A lack of vested interest in the topic is also possible amongst ‘healthy’ people, less likely to have any personal experience of the benefits that lessoning pollution and/or increasing medication may bring. Indeed, where research has indicated that individuals are aware of air quality warnings and take responsive actions, larger responses were observed for more susceptible groups or carers thereof (McDermott et al. 2006; Wen et al. 2009). Within a cross-sectional study of 33,888 adults participating in the 2005 Behavioral Risk Factor Surveillance System, 31 % with asthma versus 16 % without changed outdoor activity in response to media alerts (Wen et al. 2009). Perception is another factor influencing the public understanding of the importance of healthy air, as attitudes and behavior can be driven by a person’s immediate locality and own understanding rather than accurate data generated by monitoring sites and communicated via an advisory service (Shooter and Brimblecombe 2009). Emerging Areas Of Human Health Assignment.Several studies have investigated the relationship between perceived and measured outdoor air quality provided by monitoring stations and whilst some studies found a significant association between the perception of air quality and specific air pollutants (Atari et al. 2009), others have found little or no association (Rotko et al. 2002). Of relevance, Semenza et al. (2008) not only reported a low (10–15 %) level of behavioural change during an air pollution episode, but that the personal perception of poor air quality rather than the advisory service, drove the response. Some epidemiological researchers have also indicated that self-reported health status is associated with perceived air pollution rather than measured air pollution (Lercher et al. 1995; Yen et al. 2006; Piro et al. 2008). Emerging Areas Of Human Health Assignment.

Information services

Public awareness is fundamentally dependent upon optimal air pollution monitoring, forecasting and reporting. Many countries have air quality monitoring networks that are structured around a particular country’s regulatory obligation to report monitored air quality data and modelled predictions (Kelly et al. 2012). Output from measured concentrations of pollutants, air quality modelling systems and meteorological data are also processed to create a national air quality index (AQI). Again in line with national legislation, an AQI communicates pollution levels and health effects likely to be experienced on the day described by the index or days soon afterwards (i.e. the short term; Table 1). These data are used by the public and organisations (health services and governments) to reduce the health impacts of predicted air pollution. For example, people susceptible to high levels of pollution may be prompted to take actions (reduce exposure and/or increase use of inhaled reliever medication) to reduce their symptoms, and the general public may be encouraged to use public rather than private transport during periods of poor air quality. Another information tool is provided by accessible air pollution alert services that provide real-time data and proactively alert registered users of impending pollution events via a computer/tablet (websites, email, social media) or phone (texts, apps) (London Air Quality Network; City of London). These are becoming increasingly informative and engaging, allowing people to sign up to specific user groups (e.g. cyclist, jogger, business, at risk) and receive notifications when pollution exceeds concentrations at a site(s) of their choice. These services also offer tailored advice on how specific groups can reduce emissions by for example, providing low pollution journey planners to reduce exposure (Fig. 5). Emerging Areas Of Human Health Assignment.

Table 1

Health advice for the general population to accompany the UK AQI

Air pollution banding	Value	Accompanying health messages for at-risk groups and the general population
Air pollution banding	Value	At-risk individuals^a	General population
Low	1–3	Enjoy your usual outdoor activities	Enjoy your usual outdoor activities
Moderate	4–6	Adults and children with lung problems, and adults with heart problems, who experience symptoms, should consider reducingstrenuous physical activity, particularly outdoors	Enjoy your usual outdoor activities
High	7–9	Adults and children with lung problems, and adults with heart problems, should reduce strenuous physical exertion, particularly outdoors, and particularly if they experience symptoms. People with asthma may find they need to use their reliever inhaler more often. Older people should also reduce physical exertion	Anyone experiencing discomfort such as sore eyes, cough or sore throat should consider reducing activity, particularly outdoors
Very high	10	Adults and children with lung problems, adults with heart problems, and older people, should avoid strenuous physical activity. People with asthma may find they need to use their reliever inhaler more often	Reduce physical exertion, particularly outdoors, especially if you experience symptoms such as cough or sore throat

Open in a separate window

^aAdults and children with heart or lung problems are at greater risk of symptoms

An external file that holds a picture, illustration, etc. Object name is 10653_2015_9720_Fig5_HTML.jpg

Fig. 5

City Air iPhone app. a Advice tailored to specific user groups. b Notification alert when pollution levels change. c 3-D low pollution journey planners

New developments

Whilst monitoring, forecasting and reporting of air quality have become increasingly sophisticated and accurate, the future use of more individualised exposure measurements holds a great deal more potential. Air pollution levels can vary dramatically over short distances and time scales and in addition people’s daily mobility and activities will result in variability in exposure and inhalation. Emerging Areas Of Human Health Assignment.As such, AQIs and alert systems sourced by fixed site monitoring stations are always going to be limited by location, spacing and density. Up until recently, the use of personal pollution monitors was primarily limited to industries associated with high occupational exposures and researchers assessing individual exposures in vulnerable groups such as cyclists (Nwokoro et al. 2012) and asthmatic children (Spira-Cohen et al. 2011). Now we are witnessing an emerging role for inexpensive, portable, easy-to-use personal monitoring devices (Austen 2015). Although the quality of information generated by such sensors is not currently robust enough to compliment data for official monitoring networks, there is undoubtedly a need for more dynamic measures of time-activity patterns in relation to exposures. In an initiative to better understand in real time the impacts of harmful air pollutants, the US Environmental Protection Agency awarded a $100,000 prize to designers of a low-cost wearable breathing analysis tool that calculates the amount of polluted air a person breathes and transmits the data to any Bluetooth-enabled device such as a mobile phone (EPA 2013). Smart phone technology, integrated with low-cost air quality sensors, also has the potential to produce dynamic, temporally and spatially more precise exposure measures for the mass population. Emerging Areas Of Human Health Assignment.Added to their ubiquitous technology, the penetration of these phones is unrivalled in demographics, geographic coverage, acceptance and presence in everyday life (Pratt et al. 2012). This opens up new possibilities in the communication of individual exposure and activity data, tailored to locations where people commute and reside. In the environmental research setting, novel smartphone-based software that records people’s movements and physical activity levels in the urban environment and is integrated with spatial–temporal maps of air pollution is already being developed to enhance large-scale air pollution exposure data collection in a cost-effective, accurate unobtrusive way (de Nazelle et al. 2013).

ORDER A PLAGIARISM-FREE PAPER HERE

Discussion

Despite past improvements in air quality, very large parts of the population in urban areas breathe air that does not meet European standards let alone WHO Air Quality Guidelines. It should not be surprising therefore that health effects of PM—one of the pollutants deemed most dangerous to health—are well documented. Airborne PM has been the focus of extensive research and debate around the world for several decades and as a consequence, the evidence base for the association between short- and long-term exposure to PM and cardiopulmonary mortality and morbidity has become much larger and broader. DEPs are now classified as carcinogenic, and an increasing number of studies are investigating the potential for particulate air pollution to negatively influence birth outcomes, diabetes, neuro development and cognitive function. We now also appreciate that there is no evidence of a safe level of exposure or a threshold below which no adverse health effects occur, with recent long-term studies are showing associations between PM and mortality at levels well below the current annual WHO air quality guideline level for PM_2.5. Emerging Areas Of Human Health Assignment.Correspondingly, reductions in population exposure to air pollution expressed as annual average PM_2.5 or PM₁₀ have appreciable benefits in terms of increased life expectancy and improvements to respiratory health.

Having firmly established associations between ambient PM and adverse health effects, there has been an enormous effort to identify what it is in ambient PM that affects health—information that in turn will inform policy makers how best to legislate for cleaner air. The topic of relative toxicity has been the subject of several critical reviews over recent years but despite this the general conclusion remains that the current database of experimental and epidemiologic studies precludes individual characteristics or sources to be definitely identified as critical for toxicity. A better understanding of exposure and health effects plus further progress in comparing and synthesising data from existing studies is therefore needed before concluding that additional indicators (be they BC or UFPs) have a role in protecting public health more effectively than the targeting total PM mass. Another challenge has been to unravel the underlying biological basis of toxicity by identifying pathways that ultimately link pollution-induced pulmonary and systemic oxidative stress with an associated risk of cardiovascular and obstructive pulmonary diseases. Emerging Areas Of Human Health Assignment.

Evidence has emerged that (a) the burden of ambient PM pollution on health is significant at relatively low concentrations, (b) there is no safe lower limit and (c) effects follow a mostly linear concentration–response function, suggesting that public health benefits will result from any reduction in concentrations. As has been advocated many times before, interventions to reduce levels of particulate pollution require a concerted action by a host of sectors with a vested interest in air quality management (environment, transport, energy, health, housing) at regional, national and international levels. The significant toll of ill health brought about by traffic-related particulates means that forward-looking and integrated transport policies are critical for the improvement of urban environments.Emerging Areas Of Human Health Assignment. Traffic must be reduced and we must ensure a cleaner and greener element to what remains on the road. This can be achieved through an expansion of low emission zones, investment in clean and affordable public transport and incentives for its use, a move back from diesel to petrol or at least a ban on all highly polluting diesel vehicles, lowering speed limits and enhancing cycle routes.

Another intervention in moving towards a cleaner and healthier environment necessitates behavioural changes by the public, which in turn requires continued education and optimal communication. Engagement must be blatant and put in the context of other public health risks such as passive smoking, it must also utilise compelling messages such as premature death. In an ideal world, people, and especially susceptible individuals, should be aware of their air quality by regularly checking the AQI or targeted notifications for real-time data before going to work, school or to pursue leisure activities, enabling them to take action in the event of increased pollution. Improving air quality is a considerable but not an intractable challenge. Translating the correct scientific evidence into bold, realistic and effective policies undisputedly has the potential to reduce air pollution so that it no longer poses a damaging and costly toll on public health.

Go to:

Acknowledgments

This work was supported by the UK’s cross-research council Environmental Exposures and Health Initiative (NE/I007806/1) and the National Institute for Health Research Health Protection Research Unit (NIHR HPRU) in Health Impact of Environmental Hazards at King’s College London in partnership with Public Health England (PHE). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR, the Department of Health or Public Health England.

References

Anderson HR, Armstrong B, Hajat S, Harrison R, Monk V, Poloniecki J, et al. Air pollution and activation of implantable cardioverter defibrillators in London. Epidemiology. 2010;21(3):405–413.[PubMed] [Google Scholar]
Aphekom. (2011). Improving knowledge and communication for decision making on air pollution and health in Europe. Summary report of the Aphekom project 2008–2011. http://www.endseurope.com/docs/110302b.pdf. Accessed 11 February 2015.
Atari DO, Luginaah IN, Fung K. The relationship between odour annoyance scores and modelled ambient air pollution in Sarnia, “Chemical Valley”, Ontario. International Journal of Environmental Research and Public Health. 2009;6(10):2655–2675. [PMC free article] [PubMed] [Google Scholar]
Atkinson RW, Fuller GW, Anderson HR, Harrison RM, Armstrong B. Urban ambient particle metrics and health: A time-series analysis. Epidemiology. 2010;21(4):501–511. [PubMed] [Google Scholar]
Austen K. Environmental science. Pollution patrol. Nature. 2015;517:136–138. [PubMed] [Google Scholar] Emerging Areas Of Human Health Assignment.
Ayres JG, Borm P, Cassee FR, Castranova V, Donaldson K, Ghio A, et al. Evaluating the toxicity of airborne particulate matter and nanoparticles by measuring oxidative stress potential-a workshop report and consensus statement. Inhalation Toxicology. 2008;20(1):75–99. [PubMed] [Google Scholar]
Barbato DL, Tomei G, Tomei F, Sancini A. Traffic air pollution and oxidatively generated DNA damage: can urinary 8-oxo-7,8-dihydro-2-deoxyguanosine be considered a good biomarker? A meta-analysis. Biomarkers. 2010;15(6):538–545. [PubMed] [Google Scholar]
Bauer M, Moebus S, Möhlenkamp S, Dragano N, Nonnemacher M, Fuchsluger M, et al. Urban particulate matter air pollution is associated with subclinical atherosclerosis. Results from the HNR (Heinz Nixdorf Recall) Study. Journal of the American College of Cardiology. 2010;56(22):1803–1808. [PubMed] [Google Scholar]
Bayer-Oglesby L, Grize L, Gassner M, Takken-Sahli K, Sennhauser FH, Neu U, et al. Decline of ambient air pollution levels and improved respiratory health in Swiss children. Environmental Health Perspectives. 2005;113(11):1632–1637. [PMC free article] [PubMed] [Google Scholar]
Behndig AF, Mudway IS, Brown JL, Stenfors N, Heleday R, Duggan ST, et al. Airway antioxidant and inflammatory responses to diesel exhaust exposure in healthy humans. European Respiratory Journal. 2006;27(2):359–365. [PubMed] [Google Scholar]
Bell ML, Davis DL. Reassessment of the lethal London fog of 1952: Novel indicators of acute and chronic consequences of acute exposure to air pollution. Environmental Health Perspectives. 2001;109(Suppl 3):389–394. [PMC free article] [PubMed] [Google Scholar]
Bell ML, McDermott A, Zeger SL, Samet JM, Dominici F, et al. Ozone and short-term mortality in 95 US urban communities, 1987–2000. Journal of the American Medical Association. 2004;292(19):2372–2378. [PMC free article] [PubMed] [Google Scholar]
Bickerstaff K, Walker G. Public understandings of air pollution: The ‘localisation’ of environmental risk. Global Environmental Change. 2001;11(2):133–145. [Google Scholar]
Bind MA, Baccarelli A, Zanobetti A, Tarantini L, Suh H, Vokonas P, et al. Air pollution and markers of coagulation, inflammation, and endothelial function: Associations and epigene-environment interactions in an elderly cohort. Epidemiology. 2012;23(2):332–340. [PMC free article] [PubMed] [Google Scholar]
Boogaard H, Janssen NA, Fischer PH, Kos GP, Weijers EP, Cassee FR, et al. Contrasts in oxidative potential and other particulate matter characteristics collected near major streets and background locations. Environmental Health Perspectives. 2012;120(2):185–191. [PMC free article] [PubMed] [Google Scholar] Emerging Areas Of Human Health Assignment.
Brook RD, Rajagopalan S, Pope CA, III, Brook JR, Bhatnagar A, Diez-Roux AV, et al. Particulate matter air pollution and cardiovascular disease. An update to the Scientific Statement from the American Heart Association. Circulation. 2010;121(21):2331–2378. [PubMed] [Google Scholar]
Brunekreef B, Forsberg B. Epidemiological evidence of effects of coarse airborne particles on health. European Respiratory Journal. 2005;26(2):309–318. [PubMed] [Google Scholar]
CityAir. http://cityairapp.com/. Accessed 13 February 2015.
Committee on the Medical Effects of Air Pollutants (COMEAP). (2010). The mortality effects of long-term exposure to particulate air pollution in the United Kingdom. https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/304641/COMEAP_mortality_effects_of_long_term_exposure.pdf. Accessed 10 February 2010.
Committee on the Medical Effects of Air Pollutants (COMEAP). (2011). Review of the UK Air Quality Index. https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/304633/COMEAP_review_of_the_uk_air_quality_index.pdf. Accessed 21 February 2015.
Coogan PF, White LF, Jerrett M, Brook RD, Su JG, Seto E, et al. Air pollution and incidence of hypertension and diabetes mellitus in black women living in Los Angeles. Circulation. 2012;125(6):767–772. [PMC free article] [PubMed] [Google Scholar]
Crouse DL, Peters PA, van Donkelaar A, Goldberg MS, Villeneuve PJ, Brion O, et al. Risk of nonaccidental and cardiovascular mortality in relation to long-term exposure to low concentrations of fine particulate matter: A Canadian national-level cohort study. Environmental Health Perspectives. 2012;120(5):708–714. [PMC free article] [PubMed] [Google Scholar]
De Nazelle A, Seto E, Donaire-Gonzalez D. Improving estimates of air pollution exposure through ubiquitous sensing technologies. Environmental Pollution. 2013;176:92–99. [PMC free article][PubMed] [Google Scholar]
Delfino RJ, Tjoa T, Gillen DL, Staimer N, Polidori A, Arhami M, et al. Traffic-related air pollution and blood pressure in elderly subjects with coronary artery disease. Epidemiology. 2010;21(3):396–404. [PMC free article] [PubMed] [Google Scholar]
Department for Environment, Food and Rural Affairs (DEFRA). (2002). Survey of public attitudes to quality of life and to the environment. http://archive.defra.gov.uk/evidence/statistics/environment/pubatt/download/survey2001.pdf. Accessed 21 February 2015.
Dockery DW, Pope CA, Xu X, Spengler JD, Ware JH, Fay ME, et al. An association between air pollution and mortality in six U.S. cities. New England Journal of Medicine. 1993;329(24):1753–1759. [PubMed] [Google Scholar] Emerging Areas Of Human Health Assignment.
Downs SH, Schindler C, Liu LJ, Keidel D, Bayer-Oglesby L, Brutsche MH, et al. Reduced exposure to PM₁₀ and attenuated age-related decline in lung function. New England Journal of Medicine. 2007;357(23):2338–2347. [PubMed] [Google Scholar]
Eenhuizen E, Gehring U, Wijga AH, Smit HA, Fischer PH, Brauer M, et al. Traffic related air pollution is related to interrupter resistance in four-year old children. European Respiratory Journal. 2013;41:1257–1263. [PubMed] [Google Scholar]
Environmental Protection Agency (EPA). (2009). Integrated science assessment for particulate matter (final report). Washington, DC: United States Environmental Protection Agency. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=216546#Download. Accessed 15 February 2015.
Environmental Protection Agency (EPA). (2013). EPA and NIH announce the winning team in my air, my health challenge/winners developed a low cost, real time personal digital device that measures health effects of harmful air pollution. http://blog.epa.gov/science/2013/06/visualizing-the-invisible-with-the-my-air-my-health-challenge-winners/. Accessed 12 February 2015.
European Commission (EC). (2013). Attitudes of Europeans towards air quality. http://ec.europa.eu/public_opinion/flash/fl_360_en.pdf. Accessed 17 February 2015.
European Environment Agency (EEA). (2014). Air quality in Europe. http://www.eea.europa.eu/publications/air-quality-in-europe-2014. Accessed 9 February 2015.
Filleul L, Rondeau V, Vandentorren S, Le Moual N, Cantagrel A, Annesi-Maesano I, et al. Twenty five year mortality and air pollution: Results from the French PAARC survey. Occupational and Environmental Medicine. 2005;62(7):453–460. [PMC free article] [PubMed] [Google Scholar]
Gasser M, Riediker M, Mueller L, Perrenoud A, Blank F, Gehr P, et al. Toxic effects of brake wear particles on epithelial lung cells in vitro. Particle and Fibre Toxicology. 2009;6:30.[PMC free article] [PubMed] [Google Scholar]
Gehring U, Wijga AH, Brauer M, Fischer P, de Jongste JC, Kerkhof M, et al. Traffic-related air pollution and the development of asthma and allergies during the first 8 years of life. American Journal of Respiratory and Critical Care Medicine. 2010;181(6):596–603. [PubMed] [Google Scholar]
Godri KJ, Harrison RM, Evans T, Baker T, Dunster C, Mudway IS, et al. Increased oxidative burden associated with traffic component of ambient particulate matter at roadside and urban background school sites in London. RM, Evans T, Baker T, Dunster C, Mudway IS et al. 2011. PLoS ONE. 2011;6:e21961. [PMC free article] [PubMed] [Google Scholar]
Gottipolu RR, Landa ER, Schladweiler MC, McGee JK, Ledbetter AD, Richards JH, et al. Cardiopulmonary responses of intratracheally instilled tire particles and constituent metal components. Inhalation Toxicology. 2008;20(5):473–484. [PubMed] [Google Scholar]
Gowers AM, Cullinan P, Ayres JG, Anderson HR, Strachan DP, Holgate ST, et al. Does outdoor air pollution induce new cases of asthma? Biological plausibility and evidence. Respirology. 2012;17(6):887–898. [PubMed] [Google Scholar]
Graff DW, Cascio WE, Rappold A, Zhou H, Huang YC, Devlin RB, et al. Exposure to concentrated coarse air pollution particles causes mild cardiopulmonary effects in healthy young adults. Environmental Health Perspectives. 2009;117(7):1089–1094. [PMC free article] [PubMed] [Google Scholar] Emerging Areas Of Human Health Assignment.
Grigg J. Particulate matter exposure in children. Relevance to chronic obstructive pulmonary disease. Proceedings of the American Thoracic Society. 2009;6(7):564–569. [PubMed] [Google Scholar]
Guxens M, Sunyer J. A review of epidemiological studies on neuropsychological effects of air pollution. Swiss Medical Weekly. 2012;141:w13322. [PubMed] [Google Scholar]
Health Effects Institute (HEI) National Particle Component Toxicity (NPACT) Review Panel. (2013a). NPACT Initiative. http://pubs.healtheffects.org/getfile.php?u=934. Accessed 16 February 2015.
Health Effects Institute (HEI) Panel on the Health Effects of Traffic-Related Air Pollution. Special Report 17. (2010). Traffic-related air pollution: a critical review of the literature on emissions, exposure and health effects. http://pubs.healtheffects.org/getfile.php?u=553. Accessed 21 February 2015.
Health Effects Institute (HEI) Review Panel on Ultrafine Particles. (2013b). Understanding the health effects of ambient ultrafine particles. http://pubs.healtheffects.org/getfile.php?u=893. Accessed 16 February 2015.
Hildebrandt K, Rückerl R, Koenig W, Schneider A, Pitz M, Heinrich J, et al. Short-term effects of air pollution: A panel study of blood markers in patients with chronic pulmonary disease. Particle and Fibre Toxicology. 2009;6:25. [PMC free article] [PubMed] [Google Scholar]
Hoek G, Brunekreef B, Goldbohm S, Fischer P, van den Brandt PA. Association between mortality and indicators of traffic-related air pollution in the Netherlands: A cohort study. The Lancet. 2002;360(9341):1203–1209. [PubMed] [Google Scholar]
Hoffmann B, Moebus S, Möhlenkamp S, Stang A, Lehmann N, Dragano N, et al. Residential exposure to traffic is associated with coronary atherosclerosis. Circulation. 2007;116(5):489–496.[PubMed] [Google Scholar]
International Agency for Research on Cancer (IARC). (2012). Diesel engine exhaust carcinogenic. http://www.iarc.fr/en/media-centre/pr/2012/pdfs/pr213_E.pdf. Accessed 10 February 2015.

ORDER A PLAGIARISM-FREE PAPER HERE

IOM. (2006). Comparing estimated risks for air pollution with risks for other health effects. http://www.iom-world.org/pubs/IOM_TM0601.pdf. Accessed 10 February 2015.
Ito K, Mathes R, Ross Z, Nádas A, Thurston G, Matte T. Fine particulate matter constituents associated with cardiovascular hospitalizations and mortality in New York City. Environmental Health Perspectives. 2011;119(4):467–473. [PMC free article] [PubMed] [Google Scholar]
Janssen NA, Brunekreef B, van Vliet P, Aarts F, Meliefste K, Harssema H, et al. The relationship between air pollution from heavy traffic and allergic sensitization, bronchial hyperresponsiveness, and respiratory symptoms in Dutch schoolchildren. Environmental Health Perspectives. 2003;111(12):1512–1518. [PMC free article] [PubMed] [Google Scholar]
Jedrychowski WA, Perera FP, Spengler JD, Mroz E, Stigter L, Flak E, et al. Intrauterine exposure to fine particulate matter as a risk factor for increased susceptibility to acute bronchopulmonary infections in early childhood. International Journal of Hygiene and Environmental Health. 2013;216(4):395–401. [PMC free article] [PubMed] [Google Scholar]
Katsouyanni K, Touloumi G, Samoli E, Gryparis A, Le Tertre A, Monopolis Y, et al. Confounding and effect modification in the short-term effects of ambient particles on total mortality: results from 29 European cities within the APHEA2 project. Epidemiology. 2001;12(5):521–531. [PubMed] [Google Scholar]
Kelly FJ, Anderson HR, Armstrong B, Atkinson R, Barratt B, Beevers S, et al. Impact of the congestion charging scheme on air quality in London. Part 2. Analysis of the oxidative potential of particulate matter. Research Report. (Health Effects Institute) 2011;155:73–144. [PubMed] [Google Scholar]
Kelly FJ, Fuller GW, Walton HA, Fussell JC. Monitoring air pollution: Use of early warning systems for public health. Respirology. 2012;17(1):7–19. [PubMed] [Google Scholar]
Kelly FJ, Fussell JC. Air pollution and airway disease. Clinical and Exerimental Allergy. 2011;41(8):1059–1071. [PubMed] [Google Scholar]
Kelly FJ, Fussell JC. Size, source and chemical composition as determinants of toxicity attributable to ambient particular matter. Atmospheric Environment. 2012;60:504–526. [Google Scholar]
Kelly, F. J., & Fussell, J. C. (2015). Linking ambient particulate matter pollution effects with oxidative biology and immune responses. Annals of the New York Academy of Science, 1340, 84–94. [PubMed]
Kim JJ, Huen K, Adams S, Smorodinsky S, Hoats A, Malig B, et al. Residential traffic and children’s respiratory health. Environmental Health Perspectives. 2008;116(9):1274–1279.[PMC free article] [PubMed] [Google Scholar] Emerging Areas Of Human Health Assignment.
Kim SY, Peel JL, Hannigan MP, Dutton SJ, Sheppard L, Clark ML, et al. The temporal lag structure of short-term associations of fine particulate matter chemical constituents and cardiovascular and respiratory hospitalizations. Environmental Health Perspectives. 2012;120(8):1094–1099.[PMC free article] [PubMed] [Google Scholar]
Kramer U, Herder C, Sugiri D, Strassburger K, Schikowski T, Ranft U, et al. Traffic-related air pollution and incident type 2 diabetes: Results from the SALIA cohort study. Environmental Health Perspectives. 2010;118(9):1273–1279. [PMC free article] [PubMed] [Google Scholar]
Krewski D, Jerrett M, Burnett RT, Ma R, Hughes E, Shi Y, et al. Extended follow-up and spatial analysis of the American Cancer Society study linking particulate air pollution and mortality. Research Report. (Health Effects Institute) 2009;140:5–114. [PubMed] [Google Scholar]
Kreyling WG, Hirn S, Schleh C. Nanoparticles in the lung. Nature Biotechnology. 2010;28(12):1275–1276. [PubMed] [Google Scholar]
Künzli N, Jerrett M, Garcia-Esteban R, Basagaña X, Beckermann B, Gilliland F, et al. Ambient air pollution and the progression of atherosclerosis in adults. PLoS ONE. 2010;5(2):e9096.[PMC free article] [PubMed] [Google Scholar]
Künzli N, Jerrett M, Mack WJ, Beckerman B, LaBree L, Gilliland F, et al. Ambient air pollution and atherosclerosis in Los Angeles. Environmental Health Perspectives. 2005;113(2):201–206.[PMC free article] [PubMed] [Google Scholar]
Latzin P, Röösli M, Huss A, Kuehni CE, Frey U. Air pollution during pregnancy and lung function in newborns: A birth cohort study. European Respiratory Journal. 2009;33(3):594–603. [PubMed] [Google Scholar]
Lepeule J, Laden F, Dockery D, Schwartz J. Chronic exposure to fine particles and mortality: An extended follow-up of the Harvard Six Cities study from 1974 to 2009. Environmental Health Perspectives. 2012;120(7):965–970. [PMC free article] [PubMed] [Google Scholar]
Lercher P, Schmitzberger R, Kofler W. Perceived traffic air pollution, associated behaviour and health in an alpine area. Science of the Total Environment. 1995;169(1–3):71–74. [PubMed] [Google Scholar]
Loeb LA. A mutator phenotype in cancer. Cancer Research. 2001;61(8):3230–3239. [PubMed] [Google Scholar]
Logan WP. Mortality in the London fog incident, 1952. The Lancet. 1953;1(6755):336–338.[PubMed] [Google Scholar]
London Air Quality Network (LAQN). London air applications. http://www.londonair.org.uk/LondonAir/MobileApps/. Accessed 13 February 2015.
Lucking AJ, Lundback M, Mills NL, Faratian D, Barath SL, Pourazar J, et al. Diesel exhaust inhalation increases thrombus formation in man. European Heart Journal. 2008;29(24):3043–3051.[PubMed] [Google Scholar]
Lundback M, Mills NL, Lucking A, Barath S, Donaldson K, Newby DE, et al. Experimental exposure to diesel exhaust increases arterial stiffness in man. Particle and Fibre Toxicology. 2009;6:7. [PMC free article] [PubMed] [Google Scholar]
Macintyre EA, Gehring U, Molter A, Fuertes E, Klümper C, Krämer U, et al. Air pollution and respiratory infections during early childhood: An analysis of 10 European birth cohorts within the escape project. Environmental Health Perspectives. 2013;122(1):107–113. [PMC free article][PubMed] [Google Scholar]
Mann JK, Balmes JR, Bruckner TA, Mortimer KM, Margolis HG, Pratt B, et al. Short-term effects of air pollution on wheeze in asthmatic children in Fresno, California. Environmental Health Perspectives. 2010;118(10):1497–1502. [PMC free article] [PubMed] [Google Scholar]
Mantecca P, Sancini G, Moschini E, Farina F, Gualtieri M, Rohr A, et al. Lung toxicity induced by intratracheal instillation of size-fractionated tire particles. Toxicology Letters. 2009;189(3):206–214.[PubMed] [Google Scholar]
McDermott M, Srivastava R, Croskell S. Awareness of and compliance with air pollution advisories: A comparison of parents of asthmatics with other parents. Journal of Asthma. 2006;43(3):235–239.[PubMed] [Google Scholar]
Meister K, Johansson C, Forsberg B. Estimated short-term effects of coarse particles on daily mortality in Stockholm, Sweden. Environmental Health Perspectives. 2012;120(3):431–436.[PMC free article] [PubMed] [Google Scholar]
Mills NL, Tornqvist H, Gonzalez MC, Vink E, Robinson SD, Söderberg S, et al. Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease. New England Journal of Medicine. 2007;357(11):1075–1082. [PubMed] [Google Scholar]
Mills NL, Tornqvist H, Robinson SD, Gonzalez M, Darnley K, MacNee W, et al. Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis. Circulation. 2005;112(25):3930–3936. [PubMed] [Google Scholar]
Molter A, Agius RM, de Vocht F, Lindley S, Gerrard W, Lowe L, et al. Long-term Exposure to PM₁₀and NO₂ in association with lung volume and airway resistance in the MAAS birth cohort. Environmental Health Perspectives. 2013;121(10):1232–1238. [PMC free article] [PubMed] [Google Scholar]
Mudway IS, Stenfors N, Duggan ST, Roxborough H, Zielinski H, Marklund SL, et al. An in vitro and in vivo investigation of the effects of diesel exhaust on human airway lining fluid antioxidants. Archives of Biochemistry and Biophysics. 2004;423(1):200–212. [PubMed] [Google Scholar]
Naess Ø, Nafstad P, Aamodt G, Claussen B, Rosland P. Relation between concentration of air pollution and cause-specific mortality: Four-year exposures to nitrogen dioxide and particulate matter pollutants in 470 neighborhoods in Oslo, Norway. American Journal of Epidemiology. 2007;165(4):435–443. [PubMed] [Google Scholar]
Neidell M, Kinney PL. Estimates of the association between ozone and asthma hospitalizations that account for behavioural responses to air quality information. Environmental Science & Policy. 2010;13(2):97–103. [Google Scholar]
Nwokoro C, Ewin C, Harrison C, Ibrahim M, Dundas I, Dickson I. Cycling to work in London and inhaled dose of black carbon. European Respiratory Journal. 2012;40(5):1091–1097. [PubMed] [Google Scholar]
Oakes M, Ingall ED, Lai B, Shafer MM, Hays MD, Liu ZG, et al. Iron solubility related to particle sulfur content in source emission and ambient fine particles. Environmental Science and Technology. 2012;46(12):6637–6644. [PubMed] [Google Scholar] Emerging Areas Of Human Health Assignment.
OECD (Organisation for Economic Co-operation and development). (2014). The cost of air pollution. Health impacts of road transport. http://www.keepeek.com/Digital-Asset-Management/oecd/environment/the-cost-of-air-pollution_9789264210448-en#page1. Accessed 9 February 2015.
Ostro B, Broadwin R, Green S, Feng WY, Lipsett M. Fine particulate air pollution and mortality in nine California counties: Results from CALFINE. Environmental Health Perspectives. 2006;114(1):29–33. [PMC free article] [PubMed] [Google Scholar]
Ostro B, Lipsett M, Reynolds P, Goldberg D, Hertz A, Garcia C, et al. Long-term exposure to constituents of fine particulate air pollution and mortality: Results from the California Teachers Study. Environmental Health Perspectives. 2010;118(3):363–369. [PMC free article] [PubMed] [Google Scholar]
Palli D, Saieva C, Munnia A, Peluso M, Grechi D, Zanna I, et al. DNA adducts and PM(10) exposure in traffic-exposed workers and urban residents from the EPIC-Florence City study. Science of the Total Environment. 2008;403(1–3):105–112. [PubMed] [Google Scholar]
Pedersen M, Wichmann J, Autrup H, Dang DA, Decordier I, Hvidberg M, et al. Increased micronuclei and bulky DNA adducts in cord blood after maternal exposures to traffic-related air pollution. Environmental Research. 2009;109(8):1012–1020. [PubMed] [Google Scholar]
Peng RD, Chang HH, Bell ML, McDermott A, Zeger SL, Samet JM, et al. Coarse particulate matter air pollution and hospital admissions for cardiovascular and respiratory diseases among Medicare patients. Journal of the American Medical Association. 2008;299(18):2172–2179. [PMC free article][PubMed] [Google Scholar]
Peretz A, Peck EC, Bammler TK, Beyer RP, Sullivan JH, Trenga CA, et al. Diesel exhaust inhalation and assessment of peripheral blood mononuclear cell gene transcription effects: An exploratory study of healthy human volunteers. Inhalation Toxicology. 2007;19(14):1107–1119. [PubMed] [Google Scholar]
Piro FN, Madsen C, Naess O, Nafstad P, Claussen B. A comparison of self reported air pollution problems and GIS-modeled levels of air pollution in people with and without chronic diseases. Environmental Health. 2008;7:9. [PMC free article] [PubMed] [Google Scholar]
Pope CA, III, Ezzati M, Dockery DW. Fine-particulate air pollution and life expectancy in the United States. New England Journal of Medicine. 2009;360(4):376–386. [PMC free article] [PubMed] [Google Scholar]
Pourazar J, Frew AJ, Blomberg A, Helleday R, Kelly FJ, Wilson S, et al. Diesel exhaust exposure enhances the expression of IL-13 in the bronchial epithelium of healthy subjects. Respiratory Medicine. 2004;98(9):821–825. [PubMed] [Google Scholar]
Pourazar J, Mudway IS, Samet JM, Helleday R, Blomberg A, Wilson SJ, et al. Diesel exhaust activates redox-sensitive transcription factors and kinases in human airways. American Journal of Physiology. Lung Cellular and Molecular Physiology. 2005;289(5):L724–L730. [PubMed] [Google Scholar]
Pratt, M., Sarmiento, O. L., Montes, F., Ogilvie, D., Marcus, B. H., Perez, L. G., et al. for the Lancet Physical Activity Series Working Group. (2012). The implications of megatrends in information and communication technology and transportation for changes in global physical activity. Lancet, 380(9838), 282–293. [PMC free article] [PubMed]
Proietti E, Röösli M, Frey U, Latzin P. Air pollution during pregnancy and neonatal outcome: A review. Journal of Aerosol Medicine and Pulmonary Drug Delivery. 2013;26(1):9–23. [PubMed] [Google Scholar]
Public Health England (PHE). (2014). Estimating local mortality burdens associated with particulate air pollution. https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/332854/PHE_CRCE_010.pdf. Accessed 10 February 2015. Emerging Areas Of Human Health Assignment.
Puett RC, Hart JE, Schwartz J, Hu FB, Liese AD, Laden F. Are particulate matter exposures associated with risk of type 2 diabetes? Environmental Health Perspectives. 2011;119(3):384–389.[PMC free article] [PubMed] [Google Scholar]

ORDER A PLAGIARISM-FREE PAPER HERE

Puett RC, Hart JE, Suh H, Mittleman M, Laden F, et al. Particulate matter exposures, mortality, and cardiovascular disease in the health professionals follow-up study. Environmental Health Perspectives. 2011;119(8):1130–1135. [PMC free article] [PubMed] [Google Scholar]
Puett RC, Hart JE, Yanosky JD, Paciorek C, Schwartz J, Suh H, et al. Chronic fine and coarse particulate exposure, mortality, and coronary heart disease in the Nurses’ Health Study. Environmental Health Perspectives. 2009;117(11):1697–1701. [PMC free article] [PubMed] [Google Scholar]
Qiu H, Yu IT, Tian L, Wang X, Tse LA, Tam W, et al. Effects of coarse particulate matter on emergency hospital admissions for respiratory diseases: A time-series analysis in Hong Kong. Environmental Health Perspectives. 2012;120(4):572–576. [PMC free article] [PubMed] [Google Scholar]
Quality of urban air review group. (1996). Airborne particulate matter in the UK. http://uk-air.defra.gov.uk/assets/documents/reports/empire/quarg/quarg_11.pdf. Accessed 18 February 2015.
Raaschou-Nielsen O, Sørensen M, Ketzel M, Hertel O, Loft S, Tjønneland A, et al. Long-term exposure to traffic-related air pollution and diabetes-associated mortality: A cohort study. Diabetologia. 2013;56(1):36–46. [PubMed] [Google Scholar]
Ranft U, Schikowski T, Sugiri D, Krutmann J, Krämer U, et al. Long-term exposure to traffic-related particulate matter impairs cognitive function in the elderly. Environmental Research. 2009;109(8):1004–1011. [PubMed] [Google Scholar]
Riediker M, Devlin RB, Griggs TR, Herbst MC, Bromberg PA, Williams RW, et al. Cardiovascular effects in patrol officers are associated with fine particulate matter from brake wear and engine emissions. Particle and Fibre Toxicology. 2004;1:2. [PMC free article] [PubMed] [Google Scholar]
Ritz B, Wilhelm M. Ambient air pollution and adverse birth outcomes: methodologic issues in an emerging field. Basic & Clinical Pharmacology & Toxicology. 2008;102(2):182–190.[PMC free article] [PubMed] [Google Scholar]
Rotko T, Oglesby L, Künzli N, Carrer P, Nieuwenhuijsen MJ, Jantunen M. Determinants of perceived air pollution annoyance and association between annoyance scores and air pollution (PM_2.5, NO₂) concentrations in the European EXPOLIS study. Atmospheric Environment. 2002;36(29):4593–4602. [Google Scholar]
Rückerl R, Schneider A, Breitner S, Cyrys J, Peters A, et al. Health effects of particulate air pollution: A review of epidemiological evidence. Inhalation Toxicology. 2011;23(10):555–592.[PubMed] [Google Scholar]
Salvi SS, Blomberg A, Rudell B, Kelly F, Sandström T, Holgate ST, Frew A, et al. Acute inflammatory responses in the airways and peripheral blood after short-term exposure to diesel exhaust in healthy human volunteers. American Journal of Respiratory and Critical Care Medicine. 1999;159(3):702–709. [PubMed] [Google Scholar]
Salvi SS, Nordenhall C, Blomberg A, Rudell B, Pourazar J, Kelly FJ, et al. Acute exposure to diesel exhaust increases IL-8 and GRO-α production in healthy human airways. American Journal of Respiratory and Critical Care Medicine. 2000;161((2 pt1)):550–557. [PubMed] [Google Scholar]
Sapkota A, Chelikowsky AP, Nachman KE, Cohen AJ, Ritz B, et al. Exposure to particulate matter and adverse birth outcomes: A comprehensive review and meta-analysis. Air Quality, Atmosphere and Health. 2012;5(4):369–381. [Google Scholar]
Schindler C, Keidel D, Gerbase MW, Zemp E, Bettschart R, Brändli O, et al. Improvements in PM₁₀exposure and reduced rates of respiratory symptoms in a cohort of Swiss adults (SAPALDIA) American Journal of Respiratory and Critical Care Medicine. 2009;179(7):579–587. [PubMed] [Google Scholar]
Schwartz J, Dockery DW. Increased mortality in Philadelphia associated with daily air pollution concentrations. American Review of Respiratory Diseases. 1992;145(3):600–604. [PubMed] [Google Scholar]
Semenza JC, Wilson DJ, Parra J, Bontempo BD, Sailor DJ, George LA. Public perception and behaviour change in relationship to hot weather and air pollution. Environmental Research. 2008;107(3):401–411. [PubMed] [Google Scholar]
Shooter D, Brimblecombe P. Air quality indexing. International Journal of Environmental Pollution. 2009;36(1–3):305–323. [Google Scholar]
Son JY, Lee JT, Kim KH, Jung K, Bell ML. Characterization of fine particulate matter and associations between particulate chemical constituents and mortality in Seoul, Korea. Environmental Health Perspectives. 2012;120(6):872–878. [PMC free article] [PubMed] [Google Scholar]
Spira-Cohen A, Chen LC, Kendall M, Lall R, Thurston GD. Personal exposures to traffic-related air pollution and acute respiratory health among bronx school-children with asthma. Environmental Health Perspectives. 2011;119(4):559–565. [PMC free article] [PubMed] [Google Scholar]
Stenfors N, Nordenhall C, Salvi SS, Mudway I, Söderberg M, Blomberg A, et al. Different airway inflammatory responses in asthmatic and healthy humans exposed to diesel. European Respiratory Journal. 2004;23(1):82–86. [PubMed] [Google Scholar]
Thompson RC, Allam AH, Lombardi GP, Wann LS, Sutherland ML, Sutherland JD, et al. Atherosclerosis across 4000 years of human history: The Horus study of four ancient populations. The Lancet. 2013;381(9873):1211–1222. [PubMed] [Google Scholar]
Tornqvist H, Mills NL, Gonzalez M, Miller MR, Robinson SD, Megson IL, et al. Persistent endothelial dysfunction in humans after diesel exhaust inhalation. American Journal of Respiratory and Critical Care Medicine. 2007;176(4):395–400. [PubMed] [Google Scholar]
van der Gon HA, Gerlofs-Nijland ME, Gehrig R, Gustafsson M, Janssen N, Harrison RM, et al. The policy relevance of wear emissions from road transport, now and in the future—an international workshop report and consensus statement. Journal of the Air and Waste Management Association. 2013;63(2):136–149. [PubMed] [Google Scholar] Emerging Areas Of Human Health Assignment.
Wegesser TC, Pinkerton KE, Last JA. California wildfires of 2008: Coarse and fine particulate matter toxicity. Environmental Health Perspectives. 2009;117(6):893–897. [PMC free article][PubMed] [Google Scholar]
Weichenthal S. Selected physiological effects of ultrafine particles in acute cardiovascular morbidity. Environmental Research. 2012;115:26–36. [PubMed] [Google Scholar]
Wen X-J, Balluz L, Mokdad A. Association between media alerts of air quality index and change of outdoor activity among adult asthma in six states, BRFSS, 2005. Journal of Community Health. 2009;34(1):40–46. [PubMed] [Google Scholar]
Wilkins ET. Air pollution aspects of the London fog of December 1952. Quarterly Journal of the Royal Meteorological Society. 1954;80(344):267–271. [Google Scholar]
World Health Organisation (WHO). (2014). Burden of disease from air pollution. http://www.who.int/phe/health_topics/outdoorair/databases/FINAL_HAP_AAP_BoD_24March2014.pdf?ua=1. Accessed 9 February 2015.
World Health Organisation (WHO) Regional Office for Europe. (2006). Air quality guidelines global update 2005: Particulate matter, ozone, nitrogen dioxide and sulfur dioxide. Copenhagen. http://www.euro.who.int/__data/assets/pdf_file/0005/78638/E90038.pdf. Accessed 9 February 2015.
World Health Organisation (WHO) Regional Office for Europe. (2012). Health effects of black carbon. http://www.euro.who.int/__data/assets/pdf_file/0004/162535/e96541.pdf?ua=1. Accessed 16 February 2015.
World Health Organisation (WHO) Regional Office for Europe. (2013a). Review of evidence on health aspects of air pollution—REVIHAAP project, technical report. http://www.euro.who.int/__data/assets/pdf_file/0004/193108/REVIHAAP-Final-technical-report-final-version.pdf?ua=1. Accessed 16 February 2015.

ORDER A PLAGIARISM-FREE PAPER HERE

World Health Organisation (WHO) Regional Office for Europe. (2013b). Health effects of particulate matter: Policy implications for countries in Eastern Europe, Caucasus and central Asia. http://www.euro.who.int/__data/assets/pdf_file/0006/189051/Health-effects-of-particulate-matter-final-Eng.pdf. Accessed 9 February 2015.
Yanosky JD, Tonne CC, Beevers SD, Wilkinson P, Kelly FJ. Modeling exposures to the oxidative potential of PM10. Environmental Science and Technology. 2012;46(14):7612–7620.[PMC free article] [PubMed] [Google Scholar]
Yen IH, Yelin EH, Katz P, Eisner MD, Blanc PD. Perceived neighborhood problems and quality of life, physical functioning, and depressive symptoms among adults with asthma. American Journal of Public Health. 2006;96(5):873–879. [PMC free article] [PubMed] [Google Scholar]
Zanobetti A, Schwartz J. The effect of fine and coarse particulate air pollution on mortality: A national analysis. Environmental Health Perspectives. 2009;117(6):898–903. [PMC free article][PubMed] [Google Scholar]
Zimmerman MR, Yeatman GW, Spinz H. Examination of an Aleutian mummy. Bulletin of the New York Academy of Medicine. 1971;47(1):80–103. [PMC free article] [PubMed] [Google Scholar]
Zweifel L, Böni T, Ruhli FJ. Evidence-based palaeopathology: Meta-analysis of PubMed-listed scientific studies on ancient Egyptian mummies. Journal of Comparative Human Biology. 2009;60(5):405–427. [PubMed] [Google Scholar] Emerging Areas Of Human Health Assignment.