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The source document for this Digest states:
Answer:
Positive impacts of reductions in ambient PM concentrations on public health have been shown in the past, after the introduction of clean air legislation. Such positive impacts have also been reported more recently in a limited number of studies. Toxicological findings also suggest that qualitative changes in PM composition could be of importance for the reduction of PM-induced adverse health effects.
Rationale:
Some studies have addressed directly the question whether public health benefits can be shown as a result of planned or unplanned downward changes in air pollution concentrations. A recent study from Dublin has documented health benefits of the ban on the use of coal for domestic heating enforced in 1990 (203). In the Utah Valley, PM air pollution concentrations decreased strongly during a 14-month strike in a local steel factory in the 1980s, and mortality as well as respiratory morbidity was found to be reduced during this period (204, 205). Studies from the former German Democratic Republic have documented a reduction in childhood bronchitis and improved lung function along with sharp reductions in SO2 and PM concentrations after the German reunification (90, 91, 92, 206).
On balance, these studies suggest that reduction in ambient PM concentrations brings about benefits to public health. However, available epidemiological intervention studies do not give direct, quantitative evidence as to the relative health benefits that would result from selective reduction of specific PM size fractions. Also, these studies do not yet provide firm grounds for quantitative prediction of the relative health benefits of single-pollutant reduction strategies vs. multi-pollutant reduction strategies. In the discussed “natural experiments”, potentially confounding factors other than ambient PM concentrations also may have changed and thus may have modified the size of the changes in health effects.
In the Children’s Health Study in Southern California, the effects of reductions and increases in ambient air pollution concentrations on longitudinal lung function growth have been investigated (24). Follow-up lung function tests were administered to children who had moved away from the study area after the baseline lung function test, which was administered while the children lived within the area. Moving to a community with lower ambient PM10 concentration was associated with increasing lung function growth rates, and moving to a community with higher PM10 concentrations was associated with decreased growth. Corresponding associations with community levels of NO2 and O3 were weaker. This study suggests that reduction in long-term ambient PM10 levels is indeed associated with improvement of children’s lung growth, and that increase in these levels is associated with retardation of lung growth.
A reduction in adverse particle-induced health effects could be expected following a decrease in ambient PM concentrations and/or by qualitative changes in the PM types and their physical properties and chemical composition. The magnitude of a possible favourable effect for public health will depend on the concentrations of the ambient PM in relation to the shape of the dose- response curve for the adverse effects, such as the existence of threshold concentrations and/or a levelling off of the adverse effects at high exposure concentrations. Exposure studies with sensitive human individuals at a relevant concentration range for ambient PM are rare, and exposure periods are usually very short e.g., from Swedish tunnel experiments (207).
Toxicological studies have been performed to examine whether a change in the concentration of inert vs. active components in the PM fraction could reduce the inflammatory/toxic potential of ambient PM. Both controlled human exposures (154, 208) and animal studies (153) using Utah Valley PM10 sampled before, during and after closing of the steel factory, showed considerable coherence of inflammatory outcomes in the lung and changes in airway hyper-responsiveness compared to the epidemiological findings. The change of toxicity potential was attributed to a change in metal concentrations in the PM (167). However, to establish the causal relationship between qualitative changes in ambient PM and time-dependent reduction in toxic/inflammatory potential, further studies are required in other settings with different PM profiles.
Source & ©: WHO Regional Office for Europe
The source document for this Digest states:
Answer:
As effects have been observed from both short-term and long-term ambient PM exposures, short-term (24 hours) as well as long-term (annual average) guidelines are recommended.
Rationale:
A large number of studies have linked PM concentrations averaged over one to a few days to health endpoints such as daily mortality and hospital admissions. A 24-hour guideline value should be developed because using a one-day averaging time allows transparent linking of the chosen value to the exposure-response relationships that can be derived from the time-series studies. With the advent of instruments that measure ambient PM with high time resolution, studies are now being published which suggest that short-term peak exposures may also be important for events such as triggering myocardial infarctions and attacks of asthma (39, 209). However, the data are yet insufficient to recommend development of guideline values for averaging times of less than 24 hours.
There is now also a substantial body of evidence linking long-term average ambient PM to health effects. Therefore, it is also recommended to develop guideline values for long-term average concentrations of ambient PM. In practice, an annual average will be sufficient to fulfil this need.
When ambient PM is primarily of secondary origin, concentrations tend to be similar over large regions, and annual average concentrations are highly correlated with 24-hour means. On the basis of such relations, a ratio of annual average and expected maximum 24-hour average concentrations can be estimated which may be region specific. On the basis of such ratios, an evaluation is possible of which guideline value (short term or long term) will be the more stringent in a specific area. It is recommended that guideline values be developed for long term and short term averaging times independently, on the basis of the exposure-response relationships, as they exist for long-term and short-term exposures. The evaluation of expected ratios can then be used as a tool for policy makers to decide whether they should focus primarily on reducing long-term average or short-term average ambient PM concentrations.
Source & ©: WHO Regional Office for Europe
The source document for this Digest states:
Answer:
The current WHO Air quality guidelines (AQC) provide exposure-response relationships describing the relation between ambient PM and various health endpoints. No specific guideline value was proposed as it was felt that a threshold could not be identified below which no adverse effects on health occurred. In recent years, a large body of new scientific evidence has emerged that has strengthened the link between ambient PM exposure and health effects (especially cardiovascular effects), justifying reconsideration of the current WHO PM Air quality guidelines and the underlying exposure-response relationships.
The present information shows that fine particles (commonly measured as PM2.5) are strongly associated with mortality and other endpoints such as hospitalization for cardio-pulmonary disease, so that it is recommended that Air quality guidelines for PM2.5 be further developed. Revision of the NO10 WHO AQGs and continuation of NO10 measurement is indicated for public health protection. A smaller body of evidence suggests that coarse mass (particles between 2.5 and 10 µm) also has some effects on health, so a separate guideline for coarse mass may be warranted. The value of black smoke as an indicator for traffic-related air pollution should also be re-evaluated.
Rationale:
In 1996, the last US air quality criteria document on particulate matter was published and in the same year the reviews of the literature for the revised version of the WHO Air quality guidelines for Europe were finished, although the document was published only recently, in the year 2000 (3). At the time, WHO decided not to propose an AQG for PM as it was not possible to identify maximum long-term and/or short-term average concentrations protecting public health through exposure-response relationships based on the notion that a threshold below which no effect on health was expected.
Since then a large number of new epidemiological studies on nearly all aspects of exposure and health effects of PM have been completed. These have added greatly to the available knowledge, and therefore reconsideration of the current WHO AQG (3) is justified. The United States Environment Protection Agency has compiled the recent literature in a new Criteria Document that is currently still being reviewed and finalized (8).
Specifically, the database on long-term effects of PM on mortality has been expanded by three new cohort studies, an extension of the American Cancer Society (ACS) cohort study, and a thorough re-analysis of the original Six Cities and ACS cohort study papers by the Health Effects Institute (HEI) (9, 10, 11, 12, 13). In view of the extensive scrutiny that was applied in the HEI reanalysis to the Harvard Six Cities Study and the ACS study, it is reasonable to attach most weight to these two. The HEI re-analysis has largely corroborated the findings of the original two US cohort studies, which both showed an increase in mortality with an increase in fine PM and sulfate. The increase in mortality was mostly related to increased cardiovascular mortality. A major concern remaining was that spatial clustering of air pollution and health data in the ACS study made it difficult to disentangle air pollution effects from those of spatial auto-correlation of health data per se. The extension of the ACS study found for all causes, cardiopulmonary and lung cancer deaths statistically significant increases of relative risks for PM2.5. TSP and coarse particles (PM15 – PM2.5) were not significantly associated with mortality (13). The effect estimates remained largely unchanged even after taking spatial auto-correlation into account.
Another concern was about the role of SO2. Inclusion of SO2 in multi-pollutant models decreased PM effect estimates considerably in the re-analysis, suggesting that there was an additional role for SO2 or for pollutants spatially co-varying with it. This issue was not further addressed in the extension of the ACS study. The HEI re-analysis report concluded that the spatial adjustment might have over-adjusted the estimated effect for regional pollutants such as fine particles and sulphate compared to effect estimates for more local pollutants such as SO2.
The Adventist Health and Smog (AHSMOG) study (9) found significant effects of NO10 on non- malignant respiratory deaths in men and women, and on lung cancer mortality in men in a relatively small sample of non-smoking Seventh-Day Adventists. Results for NO10 were insensitive to adjustment for co-pollutants. In contrast to the Six Cities and ACS studies, no association with cardiovascular deaths was found. For the first 10 years of the 15-year follow-up period, NO10 was estimated from TSP measurements which were much less related to mortality in the other two cohorts also. A later analysis of the AHSMOG study suggested that effects became stronger when analysed in relation to PM2.5 estimated from airport visibility data (14), which further reduces the degree of discrepancy with the other two cohort studies. The US- EPRI-Washington University Veterans’ Cohort Mortality Study used a prospective cohort of up to 70 000 middle-aged men (51 +/-12 years) assembled by the Veterans Administration (VA) (11). No consistent effects of PM on mortality were found; however, statistical models included up to 230 terms, and effects of active smoking on mortality in this cohort were clearly smaller than in other studies, calling into question the modelling approach that was used. Also, data on total mortality only were reported, precluding conclusions with respect to cause-specific deaths. The VA database has been described by the “VA’s Seattle Epidemiologic Research and Information Centre” as being less suitable for etiological research of this kind (15). The first European cohort study was reported from the Netherlands (12), suggesting that exposure to traffic-related air pollution including PM was associated with increased cardio-pulmonary mortality in subjects living close to main roads.
Answer:
The relationship between air pollution and lung cancer has also been addressed in several case- control studies (16, 17). A study from Sweden found a relationship with motor vehicle emissions, estimated as the NO2 contribution from road traffic, using retrospective dispersion modelling (18, 19). Diesel exhaust may be involved in this (20, 21) but so far, diesel exhaust has not been classified by the International Agency for Research on Cancer (IARC) as a proven human carcinogen. However, new evaluations are underway both in the United States and at the IARC, as new studies and reviews have appeared since IARC last evaluated diesel exhaust in 1989.
Studies focusing on morbidity endpoints of long-term exposure have been published as well. Notably, work from Southern California has shown that lung function growth in children is reduced in areas with high PM concentrations (22, 23) and that the lung function growth rate changes in step with relocation of children to areas with higher or lower PM concentrations that before (24).
Short-term studies
The database on short-term effects of PM on mortality and morbidity has been augmented by numerous new studies. Two large multi-centre studies from the United States of America (National Morbidity, Mortality, and Air Pollution study, NMMAPS) and Europe (Air Pollution and Health: a European Approach, APHEA) have produced effect estimates that are more precise than those available six years ago. They are also different in magnitude (generally smaller), so that estimates of health impact based on current exposure-response relationships will be different from estimates based on the relationships published in the previous WHO AQG report. The new studies have also addressed issues such as thresholds and extent of mortality displacement (25, 26, 27, 28, 29, 30). Published effect estimates from APHEA and NMMAPS are presented in Table 1. In spring 2003, St. George’s Medical School in London is conducting a systematic meta-analysis including APHEA and NMMAPS. Recently, questions have been raised as to the optimal statistical methodology to analyse time series data (31, 32, 33, 34), and it has been shown that in the NMMAPS data, effect estimates were considerably reduced when alternative models were applied to the data. A peer-reviewed report is being prepared for publication in the spring of 2003 by HEI to discuss to what extent published effect estimates for a series of other studies should change because of this.
It has become clear that not all methodological questions surrounding the modelling of time series data on air pollution and mortality and morbidity will be resolved in the near future. In the interests of public health, the best currently available effect estimates need to be used to update the exposure-response relationshipss for PM published in the previous WHO AQG. As a result of the meta-analysis of St. George’s Medical School in London, and the HEI report mentioned above that will be available before the summer of 2003, revised exposure-response relationships will be adopted. Preliminary results of the meta-analysis of St. George’s Medical School suggest that after adjustment for publication bias, 26 studies that have not used the potentially flawed GAM methods result in an estimate of a 0.4% increase in daily mortality per 10 g/m3 PM10, an estimate very close to the uncorrected NMMAPS and APHEA estimates mentioned in Table 1 (35).
The mortality and morbidity time series studies have shown, much more clearly than before, that cardiovascular deaths and morbidity indicators are related to ambient PM (36, 37, 38, 39, 40, 41, 42, 43). The quoted references are just a small selection of key papers on the link between PM and cardiovascular endpoints that have appeared in recent years. Understanding of the mechanistic background of relations between ambient PM and cardiovascular endpoints has increased (see below). Compared to when the previous WHO AQG were developed, insights into cardiovascular disease (CVD) effects of ambient PM have increased multifold. The new work on relations between PM and arteriosclerosis provides an interesting background to observed relations between PM and mortality in the cohort studies (41, 43). Possibly, ultrafine particles (smaller than 100 nm) play a role here, as these may be relocated from the respiratory system into systemic circulation (44, 45) where they may lead to thrombosis (46). The epidemiological database is still small, which is in part related to the technical difficulties in performing exposure assessment for ultrafine particles in the field. Further discussion of the possible role of ultrafines can be found in the rationale for the answer to question 7.
Black smoke
Black smoke” (BS) refers to a measurement method that uses the light reflectance of particles collected in filters to assess the “blackness” of the collected material. The method was originally developed to measure smoke from coal combustion, and a calibration curve exists, developed in the 1960s, that translates the reflectance units into a mass number. That translation is no longer valid as was shown in a Europe-wide study conducted in the winter of 1993/1994 (47, 48). However, the measurement of light reflectance of PM filters has been shown to be highly correlated with elemental carbon in some recent studies (49, 50). In several recent European studies, BS was found to be at least as predictive of negative health outcomes as PM10 or PM2.5 (51, 52). The Dutch cohort study reported that traffic-related pollution, as indexed by NO2 was strongly associated with long-term mortality rates, while Laden et al. (53) indicated, based on source-apportionment, that excess daily mortality was more closely associated with traffic pollution than any other source category analysed. These findings indicate that black smoke, which is closely-related in the modern urban setting with diesel engine exhaust, could serve as a useful marker in epidemiological studies, perhaps even retrospective analyses using the historic data available in many European urban areas.
Since routine monitoring methods for the coarse fraction PM(10-2.5) and ultrafine particle number concentration are not yet established, it is prudent to maintain established PM10 monitoring programme for a number of additional years. While estimates of PM(10-2.5) from the algebraic difference of PM2.5 and PM10 measurements have an unfortunately high degree of imprecision, especially when PM2.5 is a major fraction of the PM10 concentration, the resulting estimates of PM(10-2.5) can still be informative about the need in future for more direct measurements of the mass concentration of PM(10-2.5). They can also be useful for refinement of new methods that can provide future monitoring data simultaneously on PM2.5, PM(10-2.5), and black smoke. The working group recommends that consideration for this option be given to an optimized dichotomous sampler, with photometric analysis of black smoke on the PM2.5 filter.
For these reasons, and because BS concentrations are much more directly influenced by local traffic sources, it is recommended to re-evaluate BS as part of the reconsideration of the WHO Air quality guidelines.
Toxicological studies
Concentrations of PM that are somewhat higher than those common in ambient air in cities, are necessary to induce toxic effects in very short-term clinical experimental studies. Exposure to concentrated ambient air particles (23–311 g/m3) for 2 hours induced transient, mild pulmonary inflammatory reactions in healthy human volunteers exposed to the highest concentrations, with an average of 200 µg/m3 PM2.5 (54). However, no other indicators of pulmonary injury, respiratory symptoms or decrements in pulmonary function were observed in association with exposure. In another study, exposure to ambient air particles (23–124 g/m3) for 2 hours did not induce any observed inflammation in healthy volunteers (55). Although technical difficulties still affect comparison with ambient air conditions, these studies have made it possible to explore possible effects at somewhat higher concentrations leading to a more comprehensive understanding of the processes involved. The effects measured in healthy individuals in these studies appear to be mild. Also studies with diesel exhaust show mild effects in individuals with compromised health (56). Controlled human exposure studies with diesel engine exhaust showed clear inflammatory effects locally in the respiratory tract, as well as systemically (56, 57, 58, 59, 60, 61, 62).
Animal exposure studies have generally supported many of the findings reported in human studies and have provided additional information about mechanisms of toxicity. However, the limited toxicological data and knowledge of the mechanisms of PM effects and of the characteristics of PM that produce effects constrains the interpretation of these data. Furthermore, there are many unresolved issues when attempting to extrapolate findings in animal studies to humans, including the appropriateness of the various animal models, the particular kinds of particles used, and the health-related endpoints being assessed. A number of in vivo and in vitro studies demonstrate that ambient urban particulates may be more toxic than some surrogate particles such as iron oxide or carbon particles (63, 64). For animal models of chronic bronchitis, cardiac impairment, or lung injury, increased susceptibility to PM has been established (63, 65, 66, 67). Animal studies have also shown that fine particulate matter recovered from cities can cause lung inflammation and injury (63). Changes in cardiac function have also been replicated in animals exposed to PM collected from cities and provide insights on the mechanisms of PM toxicity (68, 69, 70, 71).
Several toxicological studies with different types of particles have been conducted during the last few years, pointing to different particle characteristics as being of importance for toxic effects. Among the parameters that play an important role for eliciting health effects are the size and surface of particles, their number and their composition, e.g. their content of soluble transition metals (72).
Source & ©: WHO Regional Office for Europe
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