Priority Substances List Assessment Report for Respirable Particulate Matter

3.0 Assessment of "Toxic" under CEPA 1999

3.1 CEPA 1999 64(c): Human health

3.1.1 Exposure

Data on particulate matter in Canada are almost entirely from fixed-site monitoring of 24-hour concentrations in ambient air. Within the national network, long-term mean PM₁₀ concentrations during the mid-1980s to mid-1990s ranged from 11 to 42 µg/m³ at urban sites and during the mid-1990s ranged from 11 to 17 µg/m³ at rural sites. The corresponding values for PM_2.5 were 6.9-20.2 µg/m³ and 7.0-10.5 µg/m³, respectively. The values for PM₁₀ and PM_2.5 are above estimated background levels, indicating that anthropogenic activities make an important contribution to ambient particulate matter loadings. On a national scale, average particulate matter concentrations decreased approximately 2-3% annually between 1984 and 1995.

The distribution of ambient particulate matter data at a given site is typically strongly skewed, with a large number of low values and relatively few greater ones. Short-term levels can be substantially greater than mean values; for example, the 90th percentile of 24-hour concentrations from the various sites in the national network is approximately twice the mean. Typically, weekend concentrations are lower than those during the work week, and there are diurnal variations in particulate matter, with peaks occurring during the morning rush hour and late evening. There are relatively strong correlations between 24-hour concentrations of PM₁₀ and PM_2.5 at most sites in the national network, consistent with the belief that the daily variations in PM₁₀ generally reflect fluctuations in fine particles, rather than coarse particles.

There has been much discussion of the adequacy of particulate matter levels measured at fixed-area monitors as surrogates for human exposure to particulate matter. While mean personal air levels of fine particles are generally poorly correlated with ambient monitoring data collected at the same time, the correlations are stronger when individual (longitudinal) regressions of personal exposure with the nearest outdoor site are calculated and when the mean of the personal exposures from a number of studies is related to the fixed ambient monitoring. Results from studies in the United States have also indicated that outdoor air is the largest source of indoor PM₁₀ or PM_2.5, even in homes where tobacco smoking or cooking (the two main identified indoor sources of particles) took place. This should also be the case in Canada, although "tighter" building construction will lower the contribution from this source in winter. Together, these considerations suggest that ambient fine particles measured at a fixed point in the community will be related to exposure, particularly for individuals who are not exposed to important indoor sources of particles such as smoking, and that such monitoring can serve as an adequate surrogate for community (population) exposure.

3.1.2 Effects

The strongest evidence demonstrating an association between particulate matter and cardiorespiratory illness is provided by the mass of epidemiological data. These point to a "pyramid of effects" headed by increases in mortality due to cardiorespiratory diseases, increases in hospitalizations for cardiorespiratory diseases, decreases in lung function in children and in asthmatic adults, increases in respiratory symptoms, which can lead to increases in respiratory-related activity restrictions and days lost from work or school, and long-term or chronic effects, including reduced survival, reduced lung function and capacity in children, and increases in thedevelopment of chronic bronchitis and asthma in some adults (Table 10).

Table 10 Summary of adverse health effects associated with particulate matter (epidemiological studies)

Enlarge table

Although the epidemiological studies are observational rather than experimental, they have been weighted more heavily than the toxicological or controlled human exposure studies for several reasons: (1) they are the most direct way of assessing the adverse health outcomes of "real-world" complex mixtures of pollutants to which people are exposed; (2) human populations, unlike laboratory animals, are highly heterogeneous, including individuals who encompass a large range of susceptibilities, disease status and exposures and whose responses cannot be predicted from animal toxicology studies or are not available from controlled human exposure studies due to ethical reasons; and (3) no extrapolation is necessary when assessing the effects on public health of a particular concentration of air pollutant or of an ambient air objective, as measured by the ambient compliance monitoring network, despite our lack of knowledge about the exposures of each individual in the population.

The results of the time-series epidemiological studies of air pollution and health need to be interpreted within the context of mechanisms of disease pathogenesis, relevant toxicological evidence and the findings of analytical epidemiological studies such as cohort studies. The results of these investigations (i.e., the association between ambient exposure to particulate matter and cardiorespiratory mortality and morbidity) are considered, therefore, in the context of traditional criteria for causality for epidemiological studies.

3.1.2.1 Consistency

The results of the time-series studies of mortality have been remarkably consistent in indicating a positive association between PM₁₀ and PM_2.5 pollution and daily mortality. These associations were seen in 43 analyses in 20 cities across North America, South America, England and Europe. The Canadian and U.S. cities included in the analyses range from large metropolitan areas, such as Toronto and New York City, to smaller cities with polluting industry, such as Steubenville and Utah Valley. The estimates of the risks have been similar, in spite of the potentials of misclassifica-tion of personal exposure to ambient particles, different combinations of co-pollutants and different health care systems. While most of the studies used the time-series analysis, widely differing analytical applications were employed, with similar results. The results of two long-term cohort studies indicated similar trends for PM₁₀-and PM_2.5-related mortality (Dockery et al.,., 1993; Pope et al.,., 1995).

With respect to studies of morbidity, diverse study designs have been used, including time-series studies, cross-sectional studies, short-term cohort or "panel" studies and longer-term cohort studies. The array of health outcomes considered in these studies is equally diverse. Significant association of PM₁₀ and PM_2.5 with respiratory hospitalizations was demonstrated in most time-series studies examined. Associations between particulate matter pollution, including PM₁₀, PM_2.5 and sulphate, and increased hospital admissions due to CVD have also been reported in Canada and the United States. Regression modelling indicates adverse effects of particle exposure on lung function in children and adults, respiratory symptoms and medication use, restricted activity days and frequency of reported chronic respiratory disease.

Thus, epidemiological studies of morbidity and mortality have provided consistent evidence of an association between exposure to particulate matter and several of these critical health outcomes, in areas with different pollutant sources, different combinations of co-pollutants and different health care systems.

3.1.2.2 Strength of association

The increased RRs for mortality and morbidity are summarized in Table 10. The magnitudes of the estimates of increased risks are seemingly small, although they represent a substantial impact on public health. Thus, the magnitude of the associations is relatively weak, but statistically significant.

3.1.2.3 Dose-response relationship

Responses increased monotonically from very low ambient concentrations of particulate matter up to much higher levels with remarkable consistency in many epidemiological studies on acute and chronic mortality (Pope et al.,., 1992, 1995; Dockery et al.,., 1993; Schwartz, 1993; Saldiva et al.,., 1995; Ostro et al.,., 1996; Pope and Kalkstein, 1996) and hospitalizations (Sunyer et al.,., 1993; Burnett et al.,., 1994, 1997; Schwartz, 1994a,b,c; Castellsague et al.,., 1995; Schwartz and Morris, 1995). The dose-response curve for mortality and morbidity versus concentrations of PM₁₀ and fine fractions (PM_2.5 and sulphate) appears to be linear in the majority of mortality and hospitalization analyses based on PM₁₀ concentration in locations including St. Louis, Missouri, six eastern and central U.S. cities, the Utah Valley and Sao Paulo, Brazil. This linear relationship is supported by studies utilizing TSP as the metric in Steubenville, Ohio, Philadelphia, Pennsylvania, and Detroit, Michigan. Non-parametric smoothing techniques applied to data from several of these locations, at least in the lower exposure range, for mortality in Philadelphia and the Utah Valley and for hospitalizations in Toronto, Ontario, Birmingham, Alabama, New Haven, Connecticut, Tacoma, Washington and Spokane, Washington, have generally confirmed the approximately monotonic dose-response.

The data from several studies are consistent with curvilinear models. In several European locations that included PM₁₀ and PM_2.5 metrics, the dose-response curve showed a steeper linear component at lower concentrations and a slight flattening (lower slope) at high concentrations. This curvilinear response was seen in mortality studies from Amsterdam, Netherlands, for both Black Smoke and PM₁₀ (Verhoeff et al.,., 1996) and from Athens, Greece, for Black Smoke (Touloumi et al.,., 1994). In the study by Burnett et al.,. (1995) on the association between sulphates and respiratory hospitalizations in southern Ontario, the decile curve appears to be slightly curvilinear and rises monotonically from 0 to 20 µg sulphate/m³ (lagged one day), with a slightly reduced slope at the higher concentrations above about 8-10 µg/m³.

In a reanalysis (by quintiles) and extension of the Utah Valley mortality data by two years, Lyon et al.,. (1995) suggested a threshold for PM₁₀ effects at a concentration of 50 µg/m³. However, this analysis was carried out by subdivision of the data by year, season, age, location and cause of death and by dichotomizing PM₁₀ data at a 50 µg/m³ cutoff, resulting in substantial losses of PM₁₀ information and statistical power.

Thus, a dose-response relationship has consistently been observed, with risks increased even at very low ambient concentrations of particulate matter.

3.1.2.4 Coherence

A "pyramid of effects" of varying severity of outcome has been observed in the epidemiological studies. Particulate matter has been associated in many studies with cardiorespiratory mortality. One would expect that hospital admissions would also be elevated, and to a greater degree than mortality, since not all affected people would die. Similarly, emergency department and doctors' visits, respiratory symptoms, lung function, respiratory-related reduced activity and days absent from work or school due to respiratory illnesses would be expected to be elevated. All of these have in fact been observed, providing a strongly coherent picture (Table 10). The slopes of the response curves also tend to increase as the effects go down the scale of seriousness on the "pyramid of effects," which adds to the evidence for coherence.

A strong pattern of coherence between endpoints is hence provided both qualitatively and quantitatively by the associations shown between particulate matter and a broad range of endpoints from the least to the most serious, i.e., mortality.

3.1.2.5 Temporal relationship

In many epidemiological studies, the lag time between pollution peaks and onset of effects was investigated. In some, "reverse lag," or effects several days prior to the episode, were analysed to ensure that the time sequence was correct. Daily peaks of particulate matter were followed within 24 hours to several days by mortality, hospitalizations, lung function changes and respiratory symptoms. Thus, the criterion of temporality was satisfied by the study results. However, for mortality, this lag period was surprisingly short, being less than 24 hours in a number of studies. This has created some difficulties in trying to explain what mechanism could be responsible for these sudden deaths, since not enough time would have elapsed for sufficient tissue damage to occur to account for mortality or for infections to have progressed to this stage so rapidly, unless there was an acute coronary artery spasm and a subsequent massive myocardial infarction or a malignant arrhythmia. Alternatively, this short lag time might be due to the susceptibility of certain subpopulations whose health had already been compromised by cardiorespiratory diseases and who were particularly vulnerable to environmental changes.

The time pattern of exposure and effect adds to the weight of evidence for causality, with the exception of the rapidity of the effects on mortality.

3.1.2.6 Specificity

Evidence shows that particulate pollution-related increases in mortality and hospitalizations were associated with cardiorespiratory causes, but not with other diseases (Thurston et al.,., 1994; Burnett et al.,., 1995; Schwartz and Morris, 1995).

With respect to specificity of the agent, possible confounders such as temperature, weather, season and (in some studies) epidemics of influenza were controlled for in the analyses, and it seems unlikely that such factors could be responsible for the associations of particulate matter and mortality in such a wide range of locales. The evidence for particulate matter as opposed to certain gaseous pollutants is strong in the majority of studies, although a broad range of air pollutants has been examined in only a few studies. On the other hand, the associations have been observed in a wide range of locations with differing mixtures of air pollutants and have been quite consistently positive for particulate matter. In analyses designed to help separate out effects of one pollutant from another, such as bivariate or multivariate regressions, the associations of PM₁₀, PM_2.5 and sulphate with adverse health outcomes were remarkably robust to inclusion (one at a time) of all four gaseous air pollutants (sulphur dioxide, nitrogen dioxide, carbon monoxide and ozone). Moreover, the magnitude of this association was often (but not always) greater than that for any of the gaseous pollutants individually or combined.

The evidence is considered to be strong regarding the specificity of effect for respiratory and cardiac outcomes. With respect to specificity of cause, the evidence is harder to judge, but, where possible confounding factors have been examined, they have not explained the observed excesses of adverse health outcomes.

3.1.2.7 Biological plausibility

When evaluating the effects of low-level ambient particles, acute adverse effects - i.e., mortality and morbidity - correlated with daily changes in ambient levels need to be clearly distinguished from chronic effects that are associated with long-term levels of particulate pollution. The association of mortality with daily variations in particulate air pollution presents difficulties in establishing a plausible mechanism that could explain these associations, because of the very short lag period, or in some cases no lag, between recording of elevated particle concentrations and the occurrence of increased mortality. Several hypotheses have been proposed for acute particle-related mortality, including: (1) exacerbation of severe asthma or COPD; (2) progression of an acute respiratory infection; (3) worsening of pulmonary edema, due perhaps to either a permeability defect or left ventricular dysfunction; and (4) malignant cardiac arrhythmias.

The clinical data lend only limited support to the results of the epidemiological studies. Controlled human exposure studies have shown that asthmatic individuals, especially asthmatic children and adolescents, are responsive to acidic aerosols at concentrations close to ambient levels (~35 µg sulphuric acid/m³ for 40 minutes ) (Koenig et al.,., 1989, 1992; Hanley et al.,., 1992). However, there is no conclusive evidence of enhanced responsiveness in other susceptible groups identified in the epidemiological studies (the elderly or individuals with COPD) and little or no support for the observation that daily fluctuations of ambient particulate concentrations are associated with mortality within hours or a few days at most. The discrepancy between clinical and epidemiological findings may be due to one or more of the following: for practical and ethical reasons, the experimental subjects can be exposed to the tested air pollutants only for shorter durations than pollution episodes, and the studies cannot include those people most likely to be affected by air pollutants, such as cardiovascular patients; the pulmonary function parameters that are most often used in clinical studies may not be sensitive enough to indicate particulate matter-induced adverse health effects; artificial particles used in exposure chambers may not reflect the potential synergistic effects of ambient particulate matter and aerosol mixtures; and in most human studies, the sizes of aerosols used are above 0.5 µm, whereas nanometre-sized ultrafine particles have been found in animal studies to induce acute pulmonary inflammation and death at very low concentrations (Oberdörster et al.,., 1994a).

Experimental animal studies thus far have not corroborated the epidemiological findings of an association between 24-hour ambient levels of PM₁₀ and PM_2.5 below 100 µg/m³ and mortality, but this may be the result of dosimetric differences between animals and humans. The lowest concentration of PM_2.5 reported that caused death in rats with acute pulmonary inflammation or chronic bronchitis was 250 µg/m³ (three days, six hours per day) (Godleski et al.,., 1996). Based on a recent comparative dosimetric analysis conducted by Miller et al.,. (1995), it was estimated that humans receive approximately a 10-fold higher number of ultrafine particles than do rats exposed to the same mass concentration, when calculated per ventilatory unit or per alveolus. This difference has been observed to be even more pronounced for individuals with compromised lungs (smokers and patients with respiratory diseases) than for normal subjects (Kim and Kang, 1997). Based on this analysis, the results of studies of animals exposed to several hundred µg particulate matter/m³ appear relevant to ambient exposures for the general population.

Several studies have shown that bronchial hypersensitivity to non-specific stimuli, morbidity and mortality are most likely to occur in animals with pre-existing cardiorespiratory diseases (Slauson et al.,., 1989; Raabe et al.,., 1994; Gilmour et al.,., 1997; Killingsworth et al.,., 1997), providing further support for the epidemiological findings.

Based on data from toxicological studies in animals, the epidemiological observations of rapid effects of low ambient particle concentrations in cardiorespiratory disease may be attributable to ultrafine particles. The urban particulate cloud may contain up to millions of nanometre-sized particles per millilitre, with a gravimetric concentration of only 100-200 µg/m³. The particle surface area is therefore greatly enlarged and has been shown to be capable of carrying adsorbed metals, acids and toxic organic molecules down to the deep recesses of the lung. Pulmonary inflammation and mortality in animals have been observed at near-ambient concentrations of ultrafine particles -i.e., 9-60 µg/m³ (Warheit et al.,., 1990; Chen et al.,., 1992b; Oberdörster et al.,., 1995).

The available data from animal toxicological and controlled human clinical studies have implied a mechanistic basis for PM₁₀- and PM_2.5-induced cardiorespiratory injury - namely, by altering the airway immune system and/or causing epithelial cell damage, resulting in respiratory diseases. The mechanism for the cardiovascular effects is not clear but may be the result of lipoprotein peroxidation and modifying blood coagulation, resulting in cardiovascular abnormalities. The effects are most frequently observed in individuals with a compromised cardiorespiratory system.

In summary, available data provide some, although weak, support to satisfy the criterion of biological plausibility.

3.1.3 Human health risk characterization

Based on the weight of evidence presented in this section, the epidemiological evidence for mortality and morbidity in response to current levels of particulate air pollution meets a number of the criteria for causality, including consistency, dose-response relationship, coherence, temporal relationship and specificity (of both outcome and agent). With respect to the biological plausibility of the association, the results of animal studies and, to a lesser extent, controlled human studies provide support for the target tissues and susceptible populations and preliminary indications of possible mechanisms. Although ambient levels of particulate matter in Canada have been decreasing over time, there are clear indications of adverse health effects based on the results of very recent studies in Canada and in other countries at ambient levels similar to those currently occurring in Canada. The database supports, therefore, a causal relation between current ambient PM₁₀ and PM_2.5 exposure and adverse health effects and provides a reasonable basis for preventive action.

The epidemiological evidence is suggestive that adverse health effects occur only in a susceptible subset of the general population. This group appears to include those with pre-existing respiratory or cardiovascular conditions, a group that forms a substantial fraction of the general population. That this group comprises the responders to particulate matter is supported by the results of recent laboratory experiments using appropriate animal models such as bronchitic rats.

There is no clear evidence of a level below which the positive associations between PM₁₀ (and probably PM_2.5 too) and both daily mortality and hospitalization rates are not observed. That is, any increase in ambient particulate matter is associated with a statistical increase in mortality and hospitalization rates. While mortality and hospitalization rates have been emphasized owing to their adequacy as a basis for a quantitative measure of risk, other adverse health effects have also been observed, including exacerbation of respiratory symptoms such as bronchitis and asthma, reduced lung function, restricted activity due to illness, loss of work-days or school-days and increased costs for medication. Effects of particulate matter on respiratory health (lung function, symptoms and absenteeism), although much less serious than hospitalizations and mortality, have the potential to affect much more of the population.

These particulate matter-related adverse health effects are observed at concentrations currently occurring in Canada. The results were highly consistent under the widely varying climatic exposure conditions and pollutant mixtures encountered in the different locations. While the increases in RR are of small magnitude, they signify substantial numbers of deaths due to the very large size of the populations that are impacted by air pollution.

3.1.4 Uncertainties and degree of confidence in the human health risk characterization

There is a fair degree of uncertainty in the exposure assessment for particulate matter. Even though the monitoring data are extensive and national in scope and have been collected using appropriate methods, virtually all of the data are for 24-hour ambient concentrations of particulate matter collected at fixed sites. Hence, there is a lack of individual exposure data; this may be particularly important, since it is likely that the susceptible subpopulations (i.e., those with pre-existing cardiorespiratory diseases) are relatively inactive and spend more time indoors than average. In addition, the ambient monitoring network does not provide information on diurnal fluctuations in particulate matter, and it is possible that the health effects observed may be the result of peak exposures, rather than those averaged over the monitoring period. There are also no monitoring data for ultrafine particles in Canada, and the results of some studies in animals and humans have suggested that this fraction of the fine particles is extremely toxic. The overall degree of confidence in the exposure assessment is, therefore, moderate, owing principally to the lack of information on personal exposure to particulate matter.

There is more certainty in the effects characterization for particulate matter. As outlined in Section 3.1.2, statistically significant and concentration-related associations between ambient concentrations of particulate matter and a "pyramid" of related cardiorespiratory health effects, including mortality, have been remarkably consistently observed in the available epidemiological studies. These have been observed at ambient concentrations similar to those currently occurring in Canada, obviating the need to extrapolate the results of these studies in assessing the health risks posed by particulate matter. The results of controlled exposures of humans and animals to particulate matter have provided support, albeit limited, for the epidemiological findings in terms of target tissues, susceptible populations and plausible mechanisms of action.

However, there are still some important uncertainties in the available effects-related data. There is concern for possible confounding from exposure to other co-occurring (and often highly correlated) pollutants, in which case the increased risk could be ascribed to the wrong agent (although, as discussed in Section 3.1.2, the weight of evidence suggests that particulate matter is the best indicator for effects of air pollution on health outcomes, and measures to reduce exposure to particulate matter, particularly PM_2.5, would also reduce exposure to these other pollutants). The strength of the association is also weak, although fairly consistent, particularly with respect to mortality. There are no epidemiological studies that have investigated health outcomes in relation to exposure to ultrafine particles or to personal exposures, and there are few epidemiological data on the health effects of long-term exposure to particulate matter. The available controlled studies of humans exposed to particulate matter are quite limited; there are no studies of cardiovascular outcomes, and sensitive biomarkers of effect have not been identified. With respect to studies in animals, there are few dosimetric data to account for differences in responses observed in animals and humans, and the modes of action for particulate matter-related health effects have still not been elucidated, although there are emerging data from both areas that support the biological plausibility of the epidemiological observations. Overall, the degree of confidence in the effects characterization is considered to be moderate to high, owing principally to the limitations in the available epidemiological studies, although it is noted that this database is far more extensive than is generally the case for environmental pollutants.

3.2 Conclusion

Based principally on the sufficient weight of evidence of mortality and morbidity in the general population exposed to ambient concentrations of PM₁₀ and PM_2.5 examined in recent extensive epidemiological analyses in Canada and in other countries (at ambient concentrations currently occurring in Canada), as well as on some limited supporting data in experimental animal and controlled human exposure studies, PM₁₀ and particularly PM_2.5 are considered to be entering the environment in a quantity or concentration or under conditions that constitute a danger in Canada to human life or health. On this basis, PM₁₀ and particularly PM_2.5 are considered to be "toxic" as defined in Section 64 of CEPA 1999.

3.3 Considerations for follow-up (further action)

The robustness and consistency of the association between respirable particulate matter and adverse health effects across so many locations with differing air pollutant mixtures support the position that PM₁₀, PM_2.5 and sulphate are the best indicators for the effects of air pollution on adverse health outcomes. In the available time-series analyses, the fine fraction of particulate matter (PM_2.5) was consistently associated with adverse health effects; moreover, the association was usually of greater magnitude than those with other particle metrics, including PM₁₀, in studies that included several measures of exposure. In a few studies (Dockery et al.,., 1992; Schwartz et al.,., 1996; Burnett et al.,., 1997) in which associations with the coarse fraction of PM₁₀ in addition to PM₁₀ and/or PM_2.5 were examined, the coarse fraction was often not associated with adverse health outcomes, while the fine fraction and often the total PM₁₀ fraction were. Moreover, approximately 25-60% of PM_2.5 can be deposited in the human alveolar region, compared with <5% of larger particles (~10 µm) (Lippmann, 1977), which may render the fine fraction more harmful in causing lung injury.

While sulphate has been used as a surrogate for PM_2.5 in locations where data on concentrations of PM_2.5 were not available, the magnitude of the sulphate-related association was not as great as that of total PM_2.5 when both were available in the same location. In addition, sulphate appears to be too area-specific to be used as a general metric for regulatory purposes.

Thus, based on available data on health effects of particulate matter, investigations of options to reduce exposure to particulate matter should be focussed on the fine fraction (PM_2.5). (However, it is noted that coarse particles [PM_10-2.5] have not yet been eliminated from consideration, as there is some indication that they may play a role in respiratory and/or cardiovascular disease.) The investigation of management options should also be designed to reduce mid-range (24-hour average) rather than peak exposures (i.e., <24-hour periods), since, on the basis of available data, 24-hour average exposure is associated with increases in mortality and morbidity.

The fine fraction of particulate matter (which can remain in the atmosphere for days to weeks) is composed of organic compounds and secondary sulphates and nitrates. In urban areas, these compounds and their precursor gases (sulphur oxides, nitrogen oxides and VOCs) originate typically from combustion processes -motor vehicles, industrial processes and vegetative burning; 30-82% of PM_2.5 is estimated to be generated locally. In contrast, the coarse fraction of PM₁₀ (particles >2.5 µm but ≤10 µm) is typically associated with mechanical processes, such as wind erosion, breaking ocean waves and grinding operations. These coarse particles, which are efficiently removed by gravitational settling, remain in the atmosphere for shorter periods of a few hours to a few days. Further detail is available in Appendix G of the National Ambient Air Quality Objectives for Particulate Matter, Addendum to the Science Assessment Document (WGAQOG, 1999).

The available data clearly indicate that relative source contributions to PM₁₀ and PM_2.5 vary by province/territory and by region, and there are ongoing initiatives in risk management designed to accommodate these regional variations. Under the Canada-wide Standards subagreement of the Harmonization Accord signed by the Environment Ministers in January 1998, federal and provincial/territorial governments will develop numerical air quality standards for PM₁₀ and PM_2.5, with each jurisdiction developing a plan of action to achieve the standards in a specific time frame. Any investigations of options to reduce exposure as a result of the assessment of particulate matter as a Priority Substance under CEPA 1999 will complement those for this ongoing initiative.