Chapter 9
Air Pollution and Health and the Role of Aerosols
9.1 Background
This chapter investigates the literature for evidence of adverse health effects associated with exposure to air pollution, and specifically to the size range of pollution particle associated with this. Specifically, we discuss the evidence linking exposure to aerosols with adverse health outcomes. Although there is significant evidence pertaining to adverse health effects in employees in certain types of industry, this chapter concentrates on effects in the general public. Presenting a comprehensive review of all papers on aerosols and health is not possible; the vast number of original papers reflects both the importance as well as challenges in this research area. We aim at giving an overview of the main findings and current understanding on the relationship of aerosols, especially ultrafine particles, and health of general populations. There may well be other papers that are not cited but which provide similar results: it would be impossible to cite all relevant publications within this chapter. The Health Effects Institute (HEI) has conducted an expert review of the state of knowledge surrounding ultrafine particles (UFPs) and health, which by its nature is more detailed than the overview presented here (HEI, 2013).
The role of particulate pollution in the air and its association with adverse health effects such as increased morbidity and mortality is well documented. The extreme pollution events in Donora, Pennsylvania in 1948 (Snyder, 1994) and in London, UK in 1952 (HMSO, 1954) were associated with many thousands of excess deaths and led to the realisation that action was needed to reduce air pollution levels. In fact, there are references throughout history to air pollution events associated with adverse health outcomes. In his excellent book on the history of air pollution, Brimblecombe (1988) refers to the documentation of adverse health effects throughout the ages, most of which are attributable to coal burning. Brimblecombe very clearly illustrates the evidence in many different countries and over the past few millennia.
Current research shows that even at low levels of pollution, adverse health effects can be detected in the general population. One key paper is that known as the ‘Harvard Six Cities Study’ (Dockery et al., 1993), which showed that life expectancy was lowest in the most polluted city and highest in the least polluted. Long exposure to particulate air pollution was associated with chronic health outcomes, while the events in London and Pennsylvania, and more recently Dublin (Kelly and Clancy, 1984), show immediate or acute health effects. Interestingly, when a pollution event occurs and the pollution then dissipates, there is evidence that the health effects of that exposure continue on (Bell and Davis, 2001; Goodman, Clancy and Dockery, 2004).
Over the past few decades, particulate air pollution was measured as the ‘blackness’ of material deposited on a filter (British Standards Institute, 1969). This system was ideally suited to measuring pollution from coal burning and from diesel emissions. It had a size cut-off of ∼4.5 µm (McFarland, Ortiz and Rodes, 1982). Although based on light refelectometry, this system produced a pollution level in micrograms per cubic metre, whereby a conversion factor was applied to the reflectometry reading. The European Union (EEC, 1980) has adopted a similar measurement system for particulate matter (PM) and sulfur dioxide.
This type of measurement has now been superseded by techniques that measure particle mass based on various size cut-offs, with air drawn through a filter and the mass of material collected and measured. The parameters measured are referred to as PM10 and PM2.5; these are both now legislated for by the European Union (EU, 2008; USEPA, 2012), and the World Health Organization (WHO) has defined guideline values for them (WHO, 1987, 2000, 2006). These limit or guideline values are set in order to protect human health.
The WHO guidelines for air quality are based on a systematic review of the scientific evidence on the association between ambient levels and health outcomes in large populations. Over the last decade, the strength of such evidence has increased, and more health end points have become associated with PM exposures in particular (WHO, 2013).
9.2 Size Fractions
In health studies, particles in the size range 2.5–10.0 µm (measured as the difference PM10 − PM2.5) are referred to as the coarse fraction, particles smaller than 2.5 µm are referred to as the fine fraction and particles smaller than 0.1 µm are termed the ultrafine fraction. It should be noted that PM10 actually also contains the PM2.5 and UFPs, and likewise PM2.5 also contains the ultrafine fraction. All these particulate-matter fractions in the atmosphere consist of aerosol.
From an environmental physics perspective, when one gets down to these very-small-size particles, particle mass may not be the most appropriate metric to use, as there may be many thousands of small particles that collectively have the same mass as one large PM2.5 particle, so particle number count or surface area might be a more relevant metric. However, as already mentioned, current air-quality legislation only specifies the use of PM2.5 and PM10 mass as approved metrics.
The availability of particle number counts for use in health studies is still quite limited, and the choice of monitoring site is very important and can show greater variability than PM measurements in a given urban area (Aalto et al., 2005). Pekkanen and Kulmala (2004) also report that central site monitoring may give a somewhat worse proxy for human exposure to UFPs than for exposure to PM2.5.
9.3 Which Pollution Particle Sizes Are Important?
Air pollution can comprise a complex mix of gases and particles (i.e. complex aerosols), with the mix very much depending on the sources, be they industrial, traffic or domestic. The mixture of particles in the air can range in size over a number of orders of magnitude, typically from a few nanometres to tens of micrometres in aerodynamic diameter, 3–4 orders of magnitude in diameter and thus 9–12 orders of magnitude in volume and mass. This raises the question as to which particle sizes are most strongly associated with adverse health outcomes: the smaller aerosol particles or the coarse fraction? The fact that particle pollution is currently controlled in terms of mass concentration is based on the abundant evidence for the association of mass concentration and health. However, the associations between different size fractions in the particulate pollution mix can vary quite significantly; for example, Boogaard et al. (2010) report that mean concentrations of UFP (number concentration) are poorly associated with PM10 and soot. In their extensive review, Pope and Dockery (2006) report that the vast majority of the literature suggests that it is the fine and potentially also UFPs that are most associated with adverse health effects. They report that people more exposed to ambient air pollution experience more respiratory and cardiovascular health outcomes.
9.4 What Health Outcomes Are Associated with Exposure to Air Pollution?
Initially it was assumed that respiratory problems would be found to be the major health of effect of air pollution, and while this is true, there is significant evidence in the literature that exposure to air pollution is also associated with adverse cardiovascular health outcomes, such as stroke, heart attacks and so on. There is also some evidence that cardiovascular effects are more immediate, occurring within hours to days, while respiratory effects follow longer exposures of days to weeks. The literature also suggests that those who already have health conditions are more susceptible to exposure to pollution. Brook et al. (2010) provide a detailed review of some of the health effects associated with exposure to particulate pollution. As we progress through this chapter, we will consider both the respiratory and cardiovascular evidence from exposure to aerosols in the air and the different response times associated with each health outcome.
9.5 Sources of Atmospheric Aerosols
The production of aerosols is often from combustions processes, be they in motor vehicles, domestic heating and cooking or even natural sources.
Particles can be released into the atmosphere directly (e.g., soot emissions from combustion processes, desert sandstorms) but a substantial fraction of the ambient mass concentration is formed in the atmosphere from gaseous precursors in photo- and other chemical reactions. The three most abundant components affecting these processes are sulfates, nitrates and ammonia, although volatile organic compounds play a significant role in the formation of secondary organic aerosols.
Most of our routine measurement techniques cannot distinguish between the sources of aerosols, so the majority of health-related studies have focussed on reporting aerosol mass and number concentrations. Franck et al. (2006) report that in urban areas, UFPs originate primarily from rapidly increasing traffic, which is the dominating source at many urban sites.
9.6 Particle Deposition in the Lungs
If we take the example of tobacco smoke, we know that the smoke is predominantly in the aerosol size range, and it is well known that people who smoke tobacco and other illegal substances rapidly experience a ‘high’, indicating that these aerosols have passed through the lungs and into the bloodstream.
A lot of the early aerosol research was conducted in Dublin, where Nolan and Pollak (Nolan, 1972) developed the condensation nucleus counter (CNC). Burke and Nolan (1955) reported that the number of aerosols exhaled by a person is lower than the number they inhale; some of this difference is accounted for by coagulation processes but some aerosols remain ‘trapped’ in the body.1
Some researchers have studied the deposition of aerosols in the healthy and diseased lung. For example, Wiebert et al. (2006) report a high retention of UFPs, with little difference between healthy and diseased lungs. Moller et al. (2008) showed negligible clearance of UFP 24 hours after exposure; that is, the particles are retained in the body. There is some evidence that UFP can translocate or travel to other organs via the blood (Geiser and Kreyling, 2010), but this has not been observed for larger particles, although the mechanisms are not currently well understood.
If we focus on the area of tobacco smoking as an example of aerosol exposure, we now know that this is a major cause of disease and death across the world, with 95% of lung cancers attributable to it and tobacco smokers having a significantly greater risk of many aspects of cardiovascular disease as compared to nonsmokers (US Surgeon General, 2006). This illustrates that the inhalation of aerosols—in this case the products of tobacco smoke combustion—leads to the deposition of a fraction of their number in the lungs and bloodstream, where over time they give rise to adverse health effects. Certainly not all aerosols will be associated with such adverse health outcomes, but this illustrates the efficiency of aerosols to enter deep into the human body.
There is also significant evidence in the research literature to show that nonsmokers exposed to environmental tobacco smoke (ETS) also show adverse health effects that are greater than those found in people not so exposed (US Surgeon General, 2006).
In their recent review of smoking bans, Goodman et al. (2009) showed that the health of the general population improved very soon after implementation of the bans, mostly in association with reduced cardiovascular health events. This review looked at bans across many continents and found consistent results, suggesting that the smoking bans removed the exposure of the general population when they were out socialising. Goodman et al. (2009) also reported that a number of studies observed improved health among workers.
When a person inhales air containing aerosols, a number of things must happen for these aerosols to be associated with adverse health effects: the aerosols must be able to enter into the lungs, and once in there they must either be deposited or else be absorbed into the bloodstream. Significant work has been done by the International Commission on Radiation Protection (ICRP) on the deposition of aerosols in the human lung, and in fact the deposition models it has developed are considered the definitive models in this regard. Although the ICRP was initially interested in the deposition of radioactive particles, the results are directly transferrable to any type of aerosol.
The ICRP model for particle-size-dependent uptake was first published in 1994. This model divides the human respiratory tract into three regions (extrathoracic, thoracic and alveolar) and five subregions (Figure 9.1). As demonstrated in Figures 9.2–9.4, coarser particles have higher probabilities of depositing in the nasal region and UFPs in the alveolar region. However, even supermicron particles have substantial deposition efficiencies in the alveolar region and, due to their huge masses in comparison with ultrafines, easily dominate mass-based particle uptake even in the alveolar region. (The mass of a 1 µm particle is a million times greater than that of a 10 nm particle, assuming the same density. Often the UFPs have lower densities due to their fractal shapes.) UFPs dominate the particle numbers, as well as the deposited fractions in all respiratory tract regions.
Figure 9.1 Illustration of the major anatomical regions of the human respiratory tract (ICRP, 1994). ET1, anterior nasal passages; ET2, posterior nasal passages, naso-oropharynx and larynx; BB, bronchial region, including trachea and bronchi; bb, bronchiolar region, consisting of bronchioles and terminal bronchioles; AI, alveolar–interstitial region, consisting of respiratory bronchioles and alveolar ducts and sacs surrounded by alveoli. Reprinted from Hofmann (2011). Copyright © 2011, with permission from Elsevier.
Figure 9.2 Comparison of five mainstream modelling approaches for estimation of the respiratory tract uptake of particles as a function of particle size. Reprinted from Hofmann (2011). Copyright © 2011, with permission from Elsevier.
Figure 9.3 Comparison of the alveolar and broncheoliar deposition efficiencies for subjects of different ages according to the ICRP (1994) model.
Figure 9.4 Dependence of the alveolar and bronchiolar deposition efficiency of aerosol particles by size on the physical activity level, as estimated by the ICRP (1994) model. Aerosol density: 1.5 g cm−3 corresponding ambient aerosols (Sorjamaa and Hänninen, 2011). See plate section for colour version.
This preferential deposition by particle size also has beneficial applications in the delivery of medications, as covered later in this chapter.
Werner Hofmann (2011) reviewed different models developed to characterise the uptake of particles in the human respiratory tract and showed that despite major differences in model formulation, the differences between them are relatively modest in comparison with the overall variability in particle-size-specific deposition efficiency.
9.7 Aerosol Interaction Mechanisms in the Human Body
The mechanisms by which aerosol particles interact and give rise to adverse health effects are not clearly understood. Brown et al. (2001) report that low-toxicity particles such as polystyrene give rise to proinflammatory activity as a consequence of their large surface area, and they suggest that this is one of the ways in which particles cause adverse health effects. Araujo et al. (2008) report that in animal studies, UFPs result in the inhibition of the antiinflammatory capacity of high-density lipoprotein and in greater systemic oxidative stress, as evidenced by a significant increase in hepatic malondialdehyde levels and upregulation of Nrf2-regulated antioxidant genes, from which they conclude that UFPs concentrate the proatherogenic effects of ambient PM and may constitute a significant cardiovascular risk factor.
Song et al. (2011) report significant associations between concentrations of UFP and itchiness symptoms in children with atopic dermatitis. Sannolo, Lamberti and Pedata (2010), in their review of the literature relating to UFP and cellular interactions, report that in vitro toxicological research has shown that UFPs induces several types of adverse cellular effect, including cytotoxicity, mutagenicity, DNA oxidative damage and stimulation of proinflammatory cytokine production. Eder et al. (2009) also suggest some mechanisms that might account for some of the effects of inhaled particles, such as their activation and/or the detoxification capabilities of inhaled toxic compounds. Alessandrini et al. (2006), having conducted exposure studies, report that allergen-sensitised individuals may be more susceptible to the detrimental effects of UFPs. Pope (2000) summarises the evidence as follows: particle-induced pulmonary inflammation, cytokine release and altered cardiac autonomic function may be part of the pathophysiological mechanisms or pathways linking particulate pollution with cardiopulmonary disease.
9.8 Human Respiratory Outcomes and Aerosol Exposure
In this section we investigate the literature relating to the evidence or otherwise of respiratory effects caused by exposure to aerosol particles. Oberdorster et al. (1995) conclude based on animal studies that since UFPs are always present in the urban atmosphere, they play a role in causing acute lung injury in sensitive subgroups of the population. However, in contrast, Pekkanen et al. (1997) found UFPs to be no different to PM10 or black smoke in their effects on respiratory function in asthmatic children, while Peters et al. (1997) reported that UFPs were more strongly associated with adverse changes in pulmonary function in asthmatic adults.
Another study providing contradictory evidence comes from Iskandar et al. (2012), who report that coarse and fine particles, but not UFPs, are a trigger for hospital admissions for asthma in children.
In a multicity study, Karakatsani et al. (2012) reported that no consistent association was observed between fine-particle concentrations and respiratory health effects.
Overall, the evidence for respiratory health effects from aerosol exposure in relation to pulmonary function is inconsistent. It may be that there is no effect, or if there is an effect, that the current studies have not been able to detect it. Another factor in some of these studies is that a significant percentage of the study populations may have been taking respiratory medications for their asthma.
9.9 Cardiovascular Outcomes and Aerosol Exposure
In a study of hypertensive crisis, Franck et al. (2011) reported that significant effects were detected for UFP, with two days' lag after exposure, but that no consistent effects were detected for PM2.5 and PM10. Weichenthal (2012) reports that the evidence to date suggests that UFPs have a measurable impact on physiological measures known to be altered in cases of acute cardiovascular morbidity.
Amatullah et al. (2012) report that their findings ‘indicate that coarse and fine PM influence lung function and airways responsiveness, while ultrafine PM can perturb cardiac function. This study supports the hypothesis that coarse and fine PM exerts its predominant physiologic effects at the site of deposition in the airways, whereas ultrafine PM likely crosses the alveolar epithelial barrier into the systemic circulation to affect cardiovascular function.’
In a study in Bejing, Breitner et al. (2011) reported an increase in cardiovascular mortality associated with UFP concentrations, with a 2 day lag, and that unlike the other particle measures, the association with UFP number count was not modified by air mass origin. It is most likely that UFP number count is a better indicator of local sources. Cho et al. (2008) found similar results for cardiovascular and respiratory mortality in a study in Seoul, especially in the elderly population.
Stolzel et al. (2007) found an association between UFP number concentration and increases in cardiorespiratory mortality in Eufurt; the lag in this case was 4 days. They did not observe any effect for UFP mass.
9.10 Conclusions and Recommendations
The evidence shows that exposure to ambient UFPs and aerosols are associated with adverse health effects. These effects are more pronounced in those with preexisting respiratory and cardiovascular disease.
In the case of cardiovascular outcomes, the evidence suggests that acute adverse effects are detected within 2 days of exposure. There is a large body of evidence in the literature on the adverse health effects associated with long term exposure to air pollution, which are too extensive to present here. The Dockery et al paper from 1993 is one of the key indicators that living in a location with higher air pollution reduces life expectancy. Recently in Europe, Hannien and Knol (2011) suggest that exposure to airborne particles are the dominant source of environmental health risk to the european population. For respirator health outcomes, the evidence is less clear. The exposure metric that seems to be most relevant when considering adverse health effects is the particle number concentration.
Because there is currently no legislative requirement to measure UFP/aerosol number concentrations in the ambient air, the number of health-related studies is somewhat limited, with none available for large population groups, particularly compared to the number of studies available in relation to both PM2.5 and PM10.
Currently neither EU nor USEPA air quality guidelines cover exposure to UFPs/aerosols, and neither gives guideline values or any requirements for the measurement of such particles in the ambient air.
We recommend that monitoring of the number concentrations of aerosols in ambient air be undertaken, ideally at the same time as other measurements. This would allow the development of a database on the concentrations of aerosols in ambient air, and would facilitate future research into the health effects of such exposures. It would also allow the development of guideline limit values.
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1 While mentioning the Dublin group, it is also interesting to note that they developed the ionisation ‘smoke alarm’, which responds to aerosols in the air: clearly a positive health outcome that has saved countless lives.