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Air Pollution Particulate Matter

3. How are we exposed to Particulate Matter?

  • 3.1 Critical sources of PM or its components responsible for health effects
  • 3.2 Relationship between ambient levels and personal exposure to PM
  • 3.3 Short-term exposure to high peak levels and exposure in hot spots for PM

3.1 Critical sources of PM or its components responsible for health effects

The source document for this Digest states:

Answer:

Short-term epidemiological studies suggest that a number of source types are associated with health effects, especially motor vehicle emissions, and also coal combustion. These sources produce primary as well as secondary particles, both of which have been associated with adverse health effects. One European cohort study focused on traffic-related air pollution specifically, and suggested the importance of this source of PM. Toxicological studies have shown that particles originating from internal combustion engines, coal burning, residual oil combustion and wood burning have strong inflammatory potential. In comparison, wind-blown dust of crustal origin seems a less critical source.

Rationale:

Some of the short-term studies suggest that a number of source-types are associated with mortality, including motor vehicle emissions, coal combustion, oil burning, and vegetative burning. Although some unresolved issues remain, the source-oriented evaluation approach, using factor analysis, seems to implicate so far that fine particles of anthropogenic origin, and especially motor vehicle emissions and fossil fuel combustion, are most important (versus crustal particles of geologic origin) in contributing to observed increased mortality risks (53). Other studies have also implicated traffic as one important source of PM related to morbidity and mortality in time series studies (155, 189, 190). The few long-term studies that have been conducted have generally not been analysed to answer the question on the relative importance of sources. The Dutch cohort study, focusing on traffic-related air pollution, has suggested that traffic is an important source of air pollution leading to premature mortality (12). Studies on genotoxicity of traffic fumes conducted in humans have produced mixed results (191, 192, 193); several studies among occupational groups exposed to traffic fumes have documented adverse effects including lung cancer and lung function changes (194, 195, 196, 197). Childhood cancers were not found to be related to traffic-related air pollution in two large studies from Copenhagen (198) and California (199).

Few studies have tried to establish the temporal variation in the contribution of specific sources to ambient PM. A study from California has suggested that on high pollution days, the contribution of mobile sources to ambient PM is disproportionately large (200).

Different kinds of combustion particles from power plants and residential heating (residual oil fly ash, coal fly ash, wood heating particles and transport/traffic-related particles) have been found to induce inflammatory/toxic responses after exposure of animals and humans both in vivo and in vitro. In addition, particles released to air from different kinds of factories have been found to have a high inflammatory/toxic potency (72, 153, 154). Windblown sand and soil erosion particles may also contribute to adverse health effects in areas such as southern Europe, but the toxicological effects of such particles have not been characterized systematically. Some of these particles may consist of quartz, known as a very potent inducer of pulmonary fibrosis. However, the potency of quartz varies between different types (201).

In some locations, a dominating source has been identified, such as in Utah Valley. In most instances, such as in urban areas, multiple sources contribute. At present, it is too early to determine the relative potency and contribution of particles from different sources in urban areas with respect to particle-induced toxic effects. The existing studies point to vehicle emissions (diesel exhaust particles) and residential heating/power plant/factory emissions (residual fly ash particles) as being important. Particles abraded from asphalt-paved roads by the use of studded tyres, have been documented to induce cytokine release in vitro and inflammatory reactions in vivo (202). The relative contribution of the different sources will, however, vary in different parts of Europe, between different cities, and between urban and rural areas. Further studies are required to address the present question.

Source & ©: WHO Regional Office for Europe  "Health Aspects of Air Pollution" (2003) Chapter 5, Particulate matter (PM) Section 5.2 Answers and rationales, Question 10

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OzoneNitrogen Dioxide

3.2 Relationship between ambient levels and personal exposure to PM

The source document for this Digest states:

Can the differences influence the results of studies?

Answer:

Whereas personal exposure to PM and its components is influenced by indoor sources (such as smoking) in addition to outdoor sources, there is a clear relationship on population level between ambient PM and personal PM of ambient origin over time, especially for fine combustion particles. On a population level, personal PM of ambient origin “tracks” ambient PM over time, thus measurements of PM in ambient air can serve as a reasonable “proxy” for personal exposure in time-series studies.

The relationship between long-term average ambient PM concentrations and long-term average personal PM exposure has been studied less. Contributions to personal PM exposure from smoking and occupation need to be taken into account. However, the available data suggest that imperfect relations between ambient and personal PM do not invalidate the results of the long- term studies.

Rationale:

In short-term studies, the relationship between ambient concentrations and personal PM exposures has been studied repeatedly. The relationship between ambient and personal PM varies from person to person, depending on factors such as exposure to environmental tobacco smoke. On a population average, however, the correlation between ambient and personal PM over time is fairly high, supporting the use of ambient PM measurements in time series studies as exposure surrogate (49, 128, 180, 181, 182, 183, 184, 185). Also, the correlations improve when instead of PM10, ambient and personal PM2.5, or “black smoke”, or sulphates are being correlated. This reinforces the view that variations over time in ambient fine PM are predicting variations over time in personal fine PM as well, as sulphur dioxide and “black smoke” have little or no indoor sources.

This is not to imply that the correlations between ambient PM and personal PM are universally strong. A recent study of non-smoking healthy adults (age 24 to 64) conducted in the Minneapolis-St. Paul metropolitan area found low, non-significant time series correlations between ambient PM2.5 and personal PM2.5 (186). In this study, the variation in outdoor PM2.5 was low which may have contributed to the low correlations. Also, personal PM2.5 concentrations were much higher than both home indoor (factor of 2) and outdoor PM2.5 concentrations (factor of 2.5) which is in marked contrast to studies among, e.g., elderly subjects which have found personal, indoor and outdoor PM2.5 concentrations to be similar (49). One interesting implication of these findings, if replicated in areas with higher outdoor PM2.5 variability, would be that the lack of relations between ambient PM and health endpoints in younger adults that is sometimes seen may reflect a poor exposure estimate rather than lower susceptibility.

Similar analyses have recently been made of the associations between ambient and personal levels of PM2.5 and the gaseous components O3, NO2, CO and SO2 (128). It was shown that ambient PM predicted personal PM concentrations well; however, ambient gaseous air pollution concentrations did not predict personal gaseous air pollution concentrations. Interestingly, ambient ozone concentrations predicted personal PM2.5 (positive in summer, negative in winter), ambient NO2 predicted personal PM2.5 in winter as well as summer, ambient CO predicted personal PM2.5 in winter, and ambient SO2 was negatively associated with personal PM2.5. These results suggest that ambient gaseous pollution concentrations are better surrogates for personal PM of outdoor origin than for personal exposure to the gaseous components themselves. One would expect, therefore, that ambient PM would dominate ambient gases in epidemiological time series associations between air pollution and health; this, however, is not always so, suggesting that ambient PM measurements do not fully capture the toxic potential of complex ambient air pollution mixtures.

Few studies have addressed whether ambient long-term PM concentrations predict long-term personal PM well. This is due partly to the logistical complications involved in measuring personal PM over long periods of time. Analyses conducted within the EXPOLIS study have suggested that long-term ambient PM concentrations predict the population average of a series of personal PM2.5 measurements well (187). Early work from the Six Cities Study has shown that personal sulphate measurements conducted in Watertown (low ambient sulphate) were much lower than personal sulphate measurements conducted in Steubenville (high ambient sulphate) which supports the use of outdoor measurements as exposure metric in this long-term study (188).

There are no data from toxicological studies that contribute to answering this question.

Source & ©: WHO Regional Office for Europe  "Health Aspects of Air Pollution" (2003) Chapter 5, Particulate matter (PM) Section 5.2 Answers and rationales, Question 9

3.3 Short-term exposure to high peak levels and exposure in hot spots for PM

The source document for this Digest states:

Answer:

Adverse health effects have been documented after short-term exposure to peaks, as well as long-term exposure to relatively low concentrations of PM, ozone and NO2. A direct comparison of the health relevance of short term and long-term exposures has been reported for PM, but not for ozone and NO2. For PM, long-term exposure has probably a larger impact on public health than short-term exposure to peak concentrations.

Some studies have documented that subjects living close to busy roads experience more short- term and long-term effects of air pollution than subjects living further away. In urban areas, up to 10% of the population may be living at such “hot spots”. The public health burden of such exposures is therefore significant. Unequal distribution of health risks over the population also raises concerns of environmental justice and equity.

Rationale:

Particulate matter: Short-term versus long-term
Effects of long-term exposure to PM on mortality are of prime concern, as discussed previously (WHO, 2003). It has been estimated that long-term exposure to moderate levels of fine PM can be associated with a reduction in life expectancy of up to several months.

Effects of short-term exposure to PM have been documented in numerous time series studies on mortality and morbidity endpoints. Again, the evidence has been discussed before (WHO, 2003).

Consequently, both short-term and long-term effects of exposure to PM are of concern. In contrast to ozone and NO2, there have been analyses published on the relative public health significance of short-term and long-term exposures to PM. “Disability Adjusted Life Years” (DALYs) have been estimated for both types of effect, and the analysis suggests that the public health significance of the long-term effects clearly outweighs the public health significance of the short term effects (de Hollander et al., 1999). This obviously does not diminish the significance of the short-term effects of PM, which consist of very large numbers of attributable deaths and cardiovascular and respiratory hospital admissions in Europe.

Particulate matter and nitrogen dioxide: Hot spots versus background
This question of “hot spots” relates to the relevance of spatial differences in exposures, i.e. the importance of location and proximity to emission sources. This issue is of relevance for NO2 and PM (also for other pollutants such as CO which are not being further discussed here). NO2 can be significantly elevated near sources of NOx, especially near busy roads. The same is true for PM, and then especially PM components such as elemental carbon and ultrafine particles which are considerably elevated near traffic sources. Recent evidence has shown that subjects living near busy roads (the best investigated type of hot spot) are insufficiently characterized by air pollution measurements obtained from urban background locations, and that they are also at increased risk of adverse health effects (Roemer and van Wijnen 2001; Venn et al., 2001; Hoek et al., 2002; Garshick et al., 2003; Janssen et al., 2003; Nicolai et al., 2003). It is worth noting that a significant part of the urban population may be affected. Roemer and van Wijnen (2001) estimated that 10 % of the population of Amsterdam was living along roads with more than 10 000 vehicles a day. Increased risks at hot spots raises concerns about an unequal distribution of risks connected to involuntary environmental exposures. This may affect in particular socially disadvantaged groups; a California study has shown that socially disadvantaged children have a higher chance of living close to major roads (Gunier et al., 2003).

In addition, the vast majority of epidemiological studies characterize exposure with measurements that describe urban background concentrations rather than concentrations at locations influenced by sources in the immediate vicinity. Thus, the effect estimates may not sufficiently include effects due to local hot spots. Even when measurements would be conducted near hot spots, especially busy roads, there are good indications that these hot spots are insufficiently characterized by measurement of the currently regulated PM10 metrics, not even by the contemplated PM2.5 metric. For that reason, WHO recommended already in response to the previous set of CAFE questions to give further consideration to black carbon or other measures of traffic “soot” (WHO, 2003). Also, further investigations are needed on effects of ultrafine particles (particles with a diameter smaller than 100 nm). Ultrafine particles have been shown to be greatly elevated near busy roads (e.g. Hitchins et al., 2000). Some studies have suggested adverse health effects of ultrafine particles at ambient concentrations (e.g. Peters et al., 1997); consequently, there is a need to address exposure to ultrafine particles as one of the possible PM characteristics important for the adverse effects observed at roadside “hot spots”.

Source & ©: WHO Regional Office for Europe  "Health Aspects of Air Pollution - answers to follow-up questions from CAFE (2004), Question 4


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