j 
mean level of21.7 IlgfmJ measured at two urban-center monitors in 2003 (which is used as the 

basis for the risk assessment presented in Chapter 4). This observation prompted sta:ffto further 

3 explore the comparison between PM,0•2.

5 levels monitored at Detroit and Windsor sites. This 

4 exploration has shown that in recent years, based on available Windsor and Detroit data from 

5 1999 to 2003, the Windsor monitors used in this study typically have recorded PM,0•

2.5 levels that 

6 are generally less than half the levels recorded at urban-center Detroit monitors, though the 

7 concentrations measured in Windsor are more similar to concentrations reported for suburban 

8 areas well outside the city (Ross and Langstaff, 2005). These observations lead staff to conclude 

9 that the statistically significant, generally robust association with hospital admissions in Detroit 

10 reflects popUlation exposures that may be appreciably higher than what would be estimated 

11 using data from the Windsor monitors. Taking these observations into account, staff nonetheless 

12 believes that these studies in general, and the Detroit study in particular, do provide evidence of 

13 associations between short-term exposures to PMIO•

2.S and hospital admissions. Staff does 

14 conclude, however, that the association observed in the Detroit study, which staff judges to be 

15 the strongest of these studies, likely reflects exposure levels potentially much higher in the 

central city area than those reported in that study. Based on this information, staff believes that 

alternative 24-hour PMIO•

2.5 standards appropriate for consideration in this review need not 

18 necessarily extend to levels down tll or below the ranges reported in these studies in order to 

19 provide protection from the morbidity effects related to short-term exposures to PM,0•2.

S' 

20 Staff has also looked at the evidence from U.S. and Canadian studies that report 

21 statistically significant and generally robust associations with mortality and short-term exposures 

22 to PM 10.2.5' As discussed in section 9.2.3 of the CD, the evidence associating mortality wirlr . 

23 short-term exposures to PMIO•

2.5 is too uncertain to infer a likely causal relationship, although- it 

24 is suggestive of a possible causal relationship. Staff identified two such studies, conducted in 

25 Phoenix (Mar et ai., 2000, 2003) and Coachella Valley, CA (Ostro et ai., 2000, 2003), that report 

26 981h percentile PM,0.

2.

S values of approximately 70 and 107 IlgfmJ, and 99'h percentile values of 

27 75 and 1341lgfmJ, respectively. Staff notes that these studies were conducted in areas with air 

28 quality levels that would not have met the current PM 10 standards. A staff analysis of PM 10 and 

29 estimated PMIO•

2.5 concentrations from the AQS database for 200 I to 2003 suggests that 981h 

January 2005 5-68 Draft - Do Not Quote or Cite 
particles at such a generally "equivalent" level, the evidence concerning air quality levels of 

thoracic coarse particles in the studies is not strong enough to provide a basis for revising the 

level of protection generally afforded by the current PM" standards. 

5.4.4.2 Risk-based Considerations 

Beyond looking directly at the relevant epidemiologic evidence and related air quality 

information, staff has also considered the extent to which the PM".,., risk assessment results 

discussed in Chapter 4 can help inform consideration of alternative 24-hour PM1

,.,., standards. 

While one of the goals of the PM".,., risk assessment was to provide estimates of the risk 

reductions associated with just meeting alternative PM".,., standards, staff has concluded that the 

nature and magnitude of the uncertainties and concerns associated with this portion of the risk 

assessment weigh against use of these risk estimates as a basis for recommending specific 

standard levels. These uncertainties and concerns include, but are not limited to the following: 

• as discussed above, concerns that the current PM".,., levels measured at ambient 

monitoring sites in recent years may be quite different from the levels used to 

characterize exposure in the original epidemiologic studies based on monitoring 

sites in different location, thus possibly over- or underestimating population risk 

levels; 

greater uncertainty about the reasonableness of the use of proportional rollback to 

simulate attainment of alternative PM".,., daily standards in any urban area due to 

the limited availability of PM"., , air quality data over time; 

concerns that the locations used in the risk assessment are not representative of 

urban areas in the U.S. that experience the most significant 24-hour peak PM".,., 

concentrations, and thus, observations about relative risk reductions associated 

with alternative standards may not be relevant to the areas expected to have the 

greatest health risks associated with elevated ambient PM"." levels; and 

concerns about the much smaller health effects database that supplies the 

concentration-response relationships used in the risk assessment, compared to that 

available for PM", which limits our ability to evaluate the robustness of the risk 

estimates for the same health endpoints across different locations. 

5.4.4.3 Summary 

[n considering the relevant dosimetric, toxicologic, and epidemiologic evidence, 

associated air quality information, and related limitations and uncertainties, staff concludes that 

there is support for considering a 24-hour UPM".,., standard to replace the current PM" 

standards to provide protection against health effects associated with short-term exposures to 

thoracic coarse particles that are generally present in urban environments. [n looking at the 

evidence of associations between short-term exposure to PM".,., and morbidity and mortality, 

5-69 

JONATHAN BORAK & COMPANY, INC, 

Specialists in Occupational & Environmental Health 

August 10, 2005 

Rogene Henderson, Ph.D. 

Chair, Clean Air Scientific Advisory Committee 

Lovelace Respiratory Research Institute 

2425 Ridgecrest Drive, SE 

Albuquerque, NM 87108 

Dear Dr. Henderson: 

I am writing at the request of the National Cattlemen's Beef Association ("NCBA") 

in order to express my concerns regarding the scientific basis for the proposed 

NAAQS for coarse particulate rnatter (PM 10-2.5) that is currently under CASAC 

review. In an earlier letter (dated May 4,2005), I shared related concerns about 

the OAQPS Staff Paper (2nd draft) that was then under CASAC review. 

Since May, CASAC published its Review of the National Ambient Air Quality 

Standards for. Particulate Matter (Second Draft PM Staff Paper, January 2005) 

and thereafter EPA published a final PM Siaff Paper ("SP") (EPA-452/R-05-005, 

June 2005). As a result, the coarse particulate focus has shifted, with attention 

now directed to the regulation of "urban coarse particles" as distinguished from 

"non-urban" and "rural coarse particles". 

This standard-setting process has continued despite repeated acknowledgement 

by EPA staff that there is at best a "limited body of evidence" to support a coarse 

particulate standard. There is inadequate evidence documenting adverse health 

effects of coarse particulate: 

"a growing, but still limited, body of evidence on health effects associated 

with thoracic coarse particles from studies that use PM1o•2.5 as a measure 

of thoracic coarse particles." (SP: 5-47) (emphasis added) 

Likewise, there are sig'nificant limitations to the epidemiologic support for such a 

standard: 

234 Church Street, Suite 1100. New Haven, CT 06510 /Telephone (203) 777-6611 I Fax (203) 777-1411 
Rogene Henderson, Ph.D 

August 10, 2005 

Page 2. 

"staff recognizes that the substantial uncertainties associated with the 

limited available epidemiologic evidence present inherent difficulties in 

interpreting the evidence for setting appropriate standards ... " (SP: 5-52) 

(emphasis added) 

"The available epidemiologic evidence for effects of PM10.2.5 exposure is 

guite limited and is inherently characterized by large uncertainties, 

reflective in part of the more heterogeneous nature of the spatial 

distribution and chemical composition of thoracic coarse particles and the 

more limited and uncertain measurement methods that have generally 

been used to characterize their ambient concentrations." (SP: 5-53) 

(emphasis added) 

But even these cautionary notes and caveats are insufficient. As discussed 

below, the studies cited in the SP contain fewer relevant data and a less 

compelling "body of evidence" about coarse particulate than is claimed in the SP. 

In the following discussion, I particularly address statements made in section 5.4 

of the SP. 

ToxicologiC evidence 

The evidence presented in the SP begins with consideration of "limited 

toxicologic studies" that evaluated adverse effects of urban road dust. Two 

specific studies are cited, Kleinman et al (1) and Steerenberg et al (2). In 

addition, the SP notes that the CD presented "some very limited in vitro 

toxicologic stUdies" suggesting that coarse particulate "may elicit proinflammatory effects." 

Kleinman study (1) 

1) In this study, SO rats were exposed to resuspended "road dust" particles of 

undetermined composition with an MMAD of 4 tim: "only 4 tim MMAD particles 

were tested" (1). Neither the particle size distribution nor the proportions of 

particles <2.5 tim and >2.5 tim was reported. Accordingly, it is not possible to 

know whether observed effects were due to fine particulate, coarse particulate, or 

both. The probable confounding of the coarse fraction by fine road dust particles 

was noted by the authors: 

"there are small but significant contributions of crustal elements from road 

dust to the submicrometer particle faction of PM1Q" (1). 
Rogene Henderson, Ph.D 

August 10, 2005 

Page 3. 

Because this study could not differentiate the putative effects of PM,O•2.

5 from 

those of PM2.5, it is difficult to see its direct relevance to setting a PM1Q.2.5 

standard. 

2) Additional animals were exposed to submicrometer particles of ammonium 

sulfate or ammonium nitrate. Sulfate and nitrate were more consistent and more 

potent in their effects than was road dust: 

The "most consistent effects were observed in rats exposed to ... sulfate 

and nitrate"; their relative potency was "SO.-2 > N03' > road dust". (1) 

Thus, the authors concluded that the effects observed in the study were mainly 

due to submicrometer PM1Q components: 

"This study also supports the hypothesis that the fine fraction of PM1 0 is 

more toxic than the coarse fraction." (1). 

Because the findings attributed to resuspended road dust were relatively weak 

and inconsistent, it is difficult to see the direct relevance of this study to setting a 

PM1Q.2.5 standard. 

Steerenberg study (2) 

1) These authors evaluated the adjuvant activities of five "ambient" particulates 

(two samples of diesel exhaust, a residual oil fiy ash, and two actual ambient 

dusts) in two allergenicity models (ovalbumin in BALB/c mice and grass pollen in 

BN rats. Neither of the actual ambient dusts represented PM,0.2.5. The first 

(Ottawa dust, EHC-93) had been previously characterized (3); the count median 

diameter was 0.5-0.6 Jim and the MMAD was 3-4 Jim. The second (road tunnel 

dust) was collected by a device that can classify particulate into three size 

classes: <0.1 Jim, 0.1-2.5 Jim and 2.5-10 Jim (4), but there is no indication that 

the administered dust was other than <PM1Q. 

We can reasonably expect that diesel and fly ash samples consisted of mainly 

submicrometer particles. In addition, a SUbstantial proportion of at least one of the 

ambient dust particles was <2.5 Jim and there is no indication that the second 

ambient dust did not contain a substantial number of particles <2.5 Jim. Thus, it is 

not possible to attribute observed effects to PM,0.2.5. Because the study did not 

differentiate between fine and coarse particulate, it is difficult to see the direct 

relevance of this study to setting a PM,0.2.5 standard. 

• 
Rogene Henderson, Ph.D 

August10,2005 

Page 4. 

2) All five particle types demonstrated adjuvant activity in the ovalbumin model, 

but only one (a sample of diesel exhaust) had such activity in the pollen model. 

The authors raise various concerns about the relevance of the ovalbumin model: 

"ovalbumin might not be the most relevant antigen for respiratory allergy in 

humans to study the effects of air pollution in an animal model ... more 

realistic antigens for studying the association between air pollution and 

allergy are pollen grains or house dust mite antigens." (2) 

Because the findings attributed to ambient (i.e., road) dust were seen only in the 

model deemed less "relevant" and less "realistic", it seems inappropriate that 

staff so strongly embraced this study as directly relevant to setting a PM10-2.s 

standard. 

Epidemiologic evidence 

The SP describes three groups of epidemiologic stUdies. The first group focused 

mainly on the associations between PM exposure and morbidity. I expressed my 

concerns about those studies in my letter of May 4, 2005 and rny concerns 

persist unchanged. 

The two other groups included studies that considered "mortality associations ... 

reported ... in areas with relatively high PM10-2.S" and studies that considered 

various outcomes (e.g., hospitalizations, medical visits, mortality) "in areas where 

PM10 is typically dominated by coarse fraction particles". In the following 

discussion I present my concerns about those cited studies. 

Mortality Studies in Areas with Relatively High PM10-2.S 

The SP cites three studies (six reports) in support of their statement that 

statistically significant mortality associations were reported in areas with 

"relatively high PM 1O•2.S concentrations". I note that the SP does not define or 

explain the term "relatively high ... concentrations." 

Phoenix study 

1) The Phoenix study, published originally in 1997 (5) and after statistical 

reanalysis in 2000 (6), found "marginally significant (p<0.1 0)" associations 

between PM1o-2.s (referred to as PMCF) and total mortality, but there was no 

significant association between total mortality and PM2.S. PM measures were 

statistically associated with cardiovascular mortality, but that association was 
Rogene Henderson, Ph.D 

August 10, 2005 

Page 5. 

weakest for PM10-2.5. In the statistical reanalysis, the strength of marginally 

significant associations was reduced. 

A great number of statistical analyses were performed on a large number of 

variables under a variety of lag conditions. The scope of these analyses (but not 

their actual number) is indicated by the authors in the following statement: 

"Summaries of the RR between the exposure variables and both total and 

cardiovascular mortality are presented in Table 6 and 7, respectively. 

Because of space limitations, we only present statistically significant 

(p<0.05) and marginally significant (p<0.10) results in the tables, although 

models were run using all of the pollutants listed in Table 5. We evaluated 

the associations ... using single-pollutant models." (5) 

Because Table 5 lists 17 pollutants and because there were at least 5 lag 

conditions and two mortality categories, I infer that at least 170 analyses were 

performed. The authors describe no adjustments and express no concerns 

about the statistical complexity caused by such multiple comparisons (7). 

In such a context, even when authors can justify not adjusting for multiple 

comparisons, it is difficult to support the assumption that "marginal" and "weak" 

associations (i.e., p<0.1 0) have much statistical meaning. Such concerns are 

heightened when "marginal" findings are internally inconsistent (i.e., sporadic 

findings within a data set) and externally inconsistent (i.e., not supported by most 

other studies and therefore unexpected). This is the case for the Phoenix coarse 

particulate data. 

2) The lack of significant association between PM2.5 and total rnortality is 

surprising and difficult to reconcile with the robust associations documented in 

most studies (and described in the CD). That finding does not seem adequately 

explained by merely observing that Phoenix PM2.5 represented only a minority of 

total PMlO. In other cities where PM10.2.5 > PM2.5 (e.g., Topeka in the Harvard Six 

Cities study (8)), the expected positive association between PM2.5 and mortality 

was observed. 

Thus, the lack of an association between PM2.5 and total mortality in Phoenix 

raises concerns about the integrity of the database and whether it is appropriate 

as the basis for generalization. 

3) A negative association was found between soil and total mortality, although 

soil was well correlated with PM10.2.5 (r=0.66). Similar findings derive from the 

Factor Analysis, which reported a significant negative association between "fine 
Rogene Henderson, Ph.D 

August 10, 2005 

Page 6. 

soil" and total mortality; there was no significant association between "fine soil" 

and cardiovascular mortality. 

While it is unlikely that exposure to crustal particulate is protective, these findings 

support the results of other studies (e.g., (9)) that found few or no adverse health 

effects attributable to coarse crustal particulate. 

4) It is unfortunate that this study used only single-pollutant models: 

"We evaluated the associations between total and cardiovascular mortality 

and the gaseous pollutants, PM mass metrics, and PM composition 

metrics using single-pollutant models." (5) 

In my earlier letter, I discussed (with respect to the Toronto (10) and Detroit (11) 

studies) the limitations that stem from use of such models. Based on their study, 

which found that apparent associations with particulates disappeared after 

adjustment for co-pollutants, Burnett and colleagues recommended that: 

"all available air pollution measures be considered in assessing the effects 

of any single pollutant on health". (10) 

Likewise, the HEI Health Research Committee echoed that recommendation in 

its comments on the Detroit study: 

"I n order to determine the relative effects of several risk factors on a health 

outcome, ideally all variables under considerations would be included in a 

single model." HEI Synopsis: 80 in (11) 

The use of single-pollutant models limits the meaningfulness of the conclusions 

drawn fram the Phoenix study. 

Coachella 

1) The SP cites three reports by Ostra and colleagues that evaluated mortality in 

the Coachella Valley (12-14). The first report considered only PM10, while the 

subsequent reports considered PMlO, PM2.5 and PMlO.2.5. PM10 data were 

available for a 10-year period, but PM2.5 data were available for only 2.5 years. 

Accordingly, the missing PM2.5 and PM 10.2.5 were "estimated" using a predictive 

function that estimated PM10.2.5 as a cubic function of PM10· 

I 
Rogene Henderson, Ph.D 

August 10, 2005 

Page 7. 

Since PM'O-2.5 was estimated from PM,o by means of a formula fitted to the 

existing data by ordinary least squares, it is not surprising that a high correlation 

was found between PM10 and PM'O-2.5. But there was such poor fit for PM2.5 data 

that the authors concluded that "predictive models could not be successfully 

estimated" (14). 

It is disturbing that this study relied on estimated data that could not fit the 

expected simple relationship: PM'O-2.5 = PM,o - PM2.5. I presume that this reflects 

a decision to derive a best fit equation for only the relationship between PM'O-2.5 

and PM1O, rather than finding the best fit to simultaneously predict both PM'O-2.5 

and PM2.5. Regardless of the correlation reported, it is difficult to accept that the 

predictive equation truthfully reflects the nature of PM in the Coachella Valley. 

In turn, inferences drawn from these estimated data should be viewed with 

skepticism. 

2) The above concerns about the estimated coarse particulate data also raise 

concerns about the precision of the Coachella Valley effects data and their 

appropriateness for quantitative risk assessment. The SP established a criterion 

("rough indicator of '" precision") for deciding whether studies effects data were 

sufficiently precise to be used in quantitative estimates of exposure-response 

relationships: 

. "The natural logarithm of the mortality-days (a product of each city's daily 

mortality rate and the number of days for which PM data were available) 

can be used as a rough indicator of the degree of precision of effect 

estimates ... staff chose to consider only those urban areas in which 

studies with relatively greater precision were conducted, specifically 

including studies that have a natural log of mortality-days greater than or 

equal to 9.0 (i.e., approximately 8,000 deaths) for total non-accidental 

mortality." (SP, p. 4-6) 

Because the Coachella study contained only 2.5 years of PM2.5 data and deaths 

averaged 5.8 per day, the SP excluded this study from quantitative analyses. 

Likewise, because there were only 2.5 years of 'real' data for coarse particulate 

(i.e., measures of PM'O-2.5 determined literally as the difference between PM'0 

and PM2.

5), there were too few mortality-days to use the Coachella study for 

quantitative assessment of exposure-response relationships for coarse 

particulate. 

I 
Rogene Henderson, Ph.D 

August 10, 2005 

Page 8. 

Six Cities Study 

1) The SP cites Steubenville, one of the cities included in the Harvard Six Cities 

study, as supporting the view that statistically significant mortality associations 

were reported in areas with "relatively high PM1o-2.5 concentrations". The study 

data were originally published in 1996 (8); a statistical reanalysis was published 

in 2003 (15). The staff view differs from the conclusions of the study authors: 

"The particle associations were specifically with fine particle mass 

concentrations, with little additional contributions from the coarse particle 

mass fraction ... For the coarse particle mass fraction, the combined effect 

estimate was weaker, not statistically significant, and inconsistent in the 

city-specific associations." . 

2) It is curious that staff put such emphasis on Steubenville, because in the 

context of estimating exposure-response relationships for PM2.5, the SP had 

earlier discounted the Steubenville data as imprecise: 

"The natural logarithm of the mortality-days (a product of each city's daily 

mortality rate and the number of days for which PM data were available) 

can be used as a rough indicator of the degree of precision of effect 

estimates ... staff chose to consider only those urban areas in which 

studies with relatively greater precision were conducted, specifically 

including studies that have a natural log of mortality-days greater than or 

equal to 9.0 (i.e., approximately 8,000 deaths) for total non-accidental 

mortality." (SP, p. 4-6) 

On the basis of this criterion, Steubenville was excluded from the quantitative 

analysis. 

3) Besides possible imprecision, it is likely that the Steubenville PM1O-2.5 data 

were confounded by PM2.5. 

In five of the six study cities (but not Steubenville), correlations between PM2.5 

and PM 1O-2.5 were relatively low (0.23-0.45). In Steubenville, however, the 

correlation was "quite high (0.7)" (8). Furthermore, in ancillary analyses, it was 

shown that the estimated association with PM 1O-2.5 was explained by PM2.5 and 

that the estimated effect of a given increase in PM 1o-2.5 increased "proportionately 

with the correlation between PM1Q.2.5 and PM2.5" (8). 

, 
Rogene Henderson, Ph.D 

August 10, 2005 

Page 9. 

Thus it seems very likely that the apparent association of mortality and coarse 

particulate in Steubenville was due to unresolved confounding. 

4) It is also noteworthy that in one of the six cities (Topeka) there was a negative 

association between mortality and PM10-2.5 (but not PM2.5). Topeka was also the 

only city for which PM10.2.5 levels> PM2.5 levels. These findings suggest that in 

Topeka, a city "subject to windblown dust", coarse particulate was predominantly 

crustal and therefore associated with a negative exposure-effect relationship. 

This observation was noted above with reference to the negative mortality 

association between mortality and soil seen in Phoenix. 

Outcomes in Areas where PM10 is Dominated by Coarse Particles 

The SP cites four studies (five reports) in support of their statement that 

statistically significant associations were reported for various other health 

outcomes "in areas where PM 10 is dominated by coarse particles". I note that the 

SP does not define or explain the term "dominated by coarse particles." 

Tucson study 

1) The SP cites a 1997 study of cardiovascular hospitalizations (16) as evidence 

of adverse health outcomes "in areas where PM10 is dominated by coarse 

particles". However, the study contains no data on ambient levels of PM2.5: 

"Unfortunately, no PM2.5 data are available in Tucson ... " (16). 

2) The author notes that in western cities such as Tucson, PM2.5 represents a 

smaller proportion of PM10 than in northeast cities: 

"in general, PM2.5 is about 50% of PM10 in such western locations, vs. 

about 62% in the northeast." (16) 

But in this study the proportion of PM2.5 was probably greater than that otherwise 

expected because the source of PM data was a monitoring station, Garden 

Grove, that had been selected in part because it was less likely to measure wind 

blown crustal dust: 

"Several monitoring stations were available in Tucson ... most of them 

were more subject to windblown dust than the Garden Grove station." 

(17) 

• 
Rogene Henderson, Ph.D 

August 10, 2005 

Page 10. 

3) In addition, the Garden Grove station was "located in a neighborhood site 

likely to be representative of population exposure" (17). From that, I infer that 

the station was located in a residential area where PM from domestic and 

vehicular sources was more likely and crustal coarse PM, as might be associated 

with arid western dust, less likely. The statement quoted above implies that such 

exposures are more representative of the sorts of "population exposures" that 

might be associated with the adverse health outcomes evaluated in the study. 

Accordingly, I am cautious to accept the SP conclusion that this study represents 

an area "where PMlO is dominated by coarse particles." 

Reno/Sparks study 

1) The SP cites a study of hospital admissions for COPD in Reno/Sparks, 

Nevada (18). But there is no evidence in the study that PM,o was "dominated" by 

PM1O-2.5. To the contrary, the report contains the following relevant observations: 

a) During the time span of this study, data for PM2.5 were not available in 

this area. Thus, one cannot determine objectively that PM,o was 

"dominated by coarse particles". 

b) Higher PM10 peaks occurred during the winter season, an observation 

that the authors propose to be the result of "increased residential 

combustion due to cold weather in the study area" (18). 

c) A negative correlation was found between wind speed and levels of 

PMlO, which suggests that wind blown dust crustal dust was not an 

important determinant of coarse particulate levels. 

d) Levels of PM lO were highest on weekdays and lowest on weekends. 

The authors attribute this difference to reduced weekend vehicular traffic, 

but they did not differentiate the relative contributions of reentrained road 

dust vs. vehicular exhaust. 

There is apparently no objective evidence in this study that PM10 was "dominated" 

by PMlO-2.5. Accordingly, it is difficult to see the direct relevance of this study to 

setting a PM 1O-2.5 standard. 

2) It is also notable that this was a relatively small study. The study included 

1814 days, but hospital admissions for COPD averaged only 1.72 per day. 

Applying the "rough indicator of the degree of precision of effect estimates" 

, 
Rogene Henderson, Ph.D 

August 10, 2005 

Page 11. 

described in the SP (p. 4-6) and discussed above, we find that this study does 

not meet the test. Thus, using staff criteria this study should .be regarded as too 

imprecise to be used for quantitative analyses. 

Utah Valley study 

1) The SP cites three reports by Pope and colleagues that evaluated respiratory 

disease and mortality in the Utah Valley (19-21). But there is no evidence in the 

study that PM10 was "dominated" by PM10-2.5. To the contrary, the report 

contains the following relevant observations: 

a) Levels of TSP and PM10, but not PM2.5 were measured and reported in 

this study. Thus, one cannot determine objectively that PM10 was 

"dominated by coarse particles". 

b) The major sources of PM10 in the Utah Valley were combustion-related. 

Those sources and their proportionate contributions were: steel mill (47-

80%); wood burning (-16%); road dust (-11%); diesel fuel and oil 

combustion (-7%) (19). Accordingly, one would expect that PM2.5, not 

PM10 would predominate in the area. 

Discussion 

The studies cited in the CD and SP raise important concerns about the public 

health risks of ambient coarse particulates and a number of them lend significant 

support to a weight-of-evidence assessment of the hazard. Unfortunately, they 

do not sustain quantitative risk assessment. 

For example, even if crustal coarse PM were shown to be inherently harmless, it 

would be reasonable to suppose that sufficiently high contamination levels could 

render that particulate toxic. Thus, it is not unreasonable to suggest that urban 

road dust could be more toxic than wind blown crustal PM. On the other hand, 

such weight-ot-evidence is not sufficient to establish and justify specific exposure 

standards. 

Important data deficiencies currently obstruct the setting of such a standard. It is 

insufficient to argue on the basis of fine PM studies (e.g., (22)) that significant 

levels of toxic contaminants can be found in urban coarse PM. It is necessary 

instead to determine whether and when toxic contaminants achieve levels such 

that their hazards are more than theoretical. For example, the surface area of a 

given particulate mass declines exponentially as particle size increases. Thus, 

for any given mass of PM: one can expect that the dose of adsorbed toxicant 

, 
Rogene Henderson, Ph.D 

August 10,2005 

Page 12. 

received via inhalation from contaminated particulate will decline rapidly as 

particulate size increased. 

In other words, if crustal coarse particulate is essentially harmless but urban 

coarse proves harmful at relevant ambient concentrations, then any necessary 

coarse PM exposure standard developed in response should be focused on 

those components that.make the urban dust harmful (e.g., transition metals; 

PAHs; latex particles). Whether such standards are set specifically or 

categorically, they should be derived from toxicologic and epidemiologic studies 

that consider appropriately sized PM contaminated by well-characterized 

toxicants. One would also hope that future epidemiologic studies would be of 

sufficient size and rigor to be acceptable as the basis of quantitative risk 

assessment. I urge CASAC to lend its full weight to ensure adequate funding is 

available to support the gathering of further data, and sound research and 

analysis of the potential health risks from coarse PM that are of concern to it. 

Such data and research are necessary to determine whether there is a need for 

a coarse PM to address public health risks at ambient concentrations, and to 

characterize the indicator and concentration. 

ours truly, 

, DABT, FACP, FACOEM 
Rogene Henderson, Ph.D 

August 10, 2005 

Page 13. 

References 

1. Kleinman MT, Bhalla OK, Mautz WJ, et al: Cellular and immunological 

injury with PM-1 0 inhalation. Inhal Toxicol 7:589-602, 1995. 

2. Steerenberg PA, Withagen CE, Dormans JAMA, et al: Adjuvant activity of 

various diesel exhaust and ambient particle in two allergic models. ,[ 

Toxicol Environ Health A 66:1421-1439,2003. 

3. Bouthillier L, Vincent R, Goegan P, et al: Acute effects of inhaled urban 

particles and ozone. Lung morphology, macrophage activity, and plasma 

endothelin-1. Am J Pathol 153:1873-1884,1998. 

4. Chang M, Sioutas C, Cassee FR, et al: Field evaluation of a mobile highcapacity particle size classifier (HCPSC) for separate collection of coarse, 

fine and ultrafine particles. Aerosol Science 32:139-156,2001. 

5. Mar TF, Norris GA, Koenig JQ, et al: Association between air pollution 

and mortality in Phoenix, 1995-1997. Environ Health Perspect 108:347-

353,2000. 

6. Mar TF, Norris GA, Larson TV, et al. Air Pollution and Cardiovascular 

Mortality in Phoenix, 1995-1997. In: Revised Analyses oftime-series 

studies of air pollution and health, Health Effects Institute (ed). Boston: 

Health Effects Istitute, pp. 177-182,2003. 

7. Borak J, Bidulescu A: Some thoughts on multiple comparisons and their 

correction. OEM Rep 14:65-68, 2005. 

8. Schwartz J, Dockery OW, Neas LM: Is daily mortality associated 

specifically with fine particles? J Air Waste Manage Assoc 46:927-939, 

1996. 

9. Schwartz J, Norris G, Larson T, et al: Episodes of high coarse particle 

concentrations are not associated with increased mortality. Environ 

Health Perspect 107:339-342,1999. 

10. Burnett RT, Cakmak S, Brook JR, et al: The role of particulate size and 

chemistry in the association between summertime ambient air pollution 

and hospitalization for cardiorespiratory. Environ Health Perspect 

105:614-620,1997. 

11. Lipprnann M, Ito K, Nadas A, et al: Association of particulate matter 

components with daily rnortality and morbidity in Urban populations. In: 

Carnbridge: Health Effects Institute, 2000. 
Rogene Henderson, Ph.D 

August 10, 2005 

Page 14. 

12. Ostro BO, Hurley S, Lipsett MJ: Air pollution and daily mortality in the 

Coachella Valley, California: A study of PM1 0 dominated by coarse 

particles. Environ Res 81 :231-238, 1999. 

13. Ostro BO, Broadwin R, Lipsett MJ: Coarse and fine particles and daily 

mortality in the Coachella Valley, California: A follow-up study. J Exp 

Analysis Environ Epidemiol 10:412-419,2000. 

14. Ostro BO, Broadwin R, Lipsett MJ. Coarse particles and daily mortality in 

Coachella Valley, California. In: Revised analyses of time-series studies 

of air pollution and health, Health Effects Institute (ed). Boston: Health 

Effects Institute, pp. 199-204,2003. 

15. Klemm RJ, Mason R. Replication of reanalysis of Harvard Six-City 

Mortality Study. In: Revised analyses of time-series studies of air pollution 

and health, Health Effects Institute (ed). Boston: Health Effects Institute, 

2003. 

16. Schwartz J: Air pollution and hospital admissions for cardiovascular 

disease in Tucson. Epidemiol 8:371-377,1997. 

17. Choudbury AH, Gordian ME, Morris 88: Associations between respiratory 

illness and PM10 air pollution. Arch Environ Health 52:113-117,1997. 

18. Chen L, Yang W, Jennison BL, et al: Air particulate pollution and hospital 

admissions for chronic obstructive pulmonary disease in Reno, Nevada. 

Inhal Toxicol 12:281-298,2000. 

19. Pope CA, III: Respiratory disease associated with community air pollution 

and a steel mill, Utah Valley. Am J Public Health 79:623-628,1989. 

20. Pope CA, III: Respiratory hospital admissions associated with PM10 

pollution in Utah, Salt Lake, and Cache Valleys. Arch Environ Health 

46:90-97, 1991. 

21. Pope CA, Schwartz J, Ransom MR: Oaily mortality and PM10 pollution in 

Utah Valley. Arch Environ Health 47:211-217,1992. 

22. Batalha JRF, 8aldiva PHN, Clarke RW, et al: Concentrated ambient air 

particles induce vasoconstriction of small pulmonary arteries in rats. 

Environ Health Perspect 110:1191-1197, 2002.