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An Association between Fine Particles and Asthma Emergency Department
Visits for Children in Seattle

Gary Norris,1 Sharon N. YoungPong,2 Jane Q. Koenig,3 Timothy V. Larson,1
Lianne Sheppard,4 and James W. Stout5

1Department of Civil and Environmental Engineering, University of
Washington, Seattle, Washington, USA

2CH2MHill, Portland, Oregon, USA

3Department of Environmental Health; 4Department of Biostatistics; and
5Department of Pediatrics and Health Services, University of Washington,
Seattle, Washington, USA

  HYPERLINK
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l" \l "intro#intro"  Introduction

  HYPERLINK
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l" \l "met#met"  Methods

  HYPERLINK
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l" \l "res#res"  Results

  HYPERLINK
"http://www.ehponline.org/members/1999/107p489-493norris/norris-full.htm
l" \l "disc#disc"  Discussion

Abstract

Asthma is the most common chronic illness of childhood and its
prevalence is increasing, causing much concern for identification of
risk factors such as air pollution. We previously conducted a study
showing a relationship between asthma visits in all persons < 65 years
of age to emergency departments (EDs) and air pollution in Seattle,
Washington. In that study the most frequent zip codes of the visits were
in the inner city. The Seattle-King County Department of Public Health
(Seattle, WA) subsequently published a report which showed that the
hospitalization rate for children in the inner city was over
600/100,000, whereas it was < 100/100,000 for children living in the
suburbs. Therefore, we conducted the present study to evaluate whether
asthma visits to hospital emergency departments in the inner city of
Seattle were associated with outdoor air pollution levels. ED visits to
six hospitals for asthma and daily air pollution data were obtained for
15 months during 1995 and 1996. The association between air pollution
and childhood ED visits for asthma from the inner city area with high
asthma hospitalization rates were compared with those from lower
hospital utilization areas. Daily ED counts were regressed against fine
particulate matter (PM) , carbon monoxide (CO) , sulfur dioxide, and
nitrogen dioxide using a semiparametric Poisson regression model.
Significant associations were found between ED visits for asthma in
children and fine PM and CO. A change of 11 µg/m3 in fine PM was
associated with a relative rate of 1.15 [95% confidence interval (CI) ,
1.08-1.23]. There was no stronger association between ED visits for
asthma and air pollution in the higher hospital utilization area than in
the lower utilization area. These findings were seen when estimated
PM2.5 concentrations were below the newly adopted annual National
Ambient Air Quality Standard of 15 µg/m3. Key words:   HYPERLINK
"http://www.ehponline.org/tagSearch/air+pollution"  air pollution ,
HYPERLINK "http://www.ehponline.org/tagSearch/asthma"  asthma ,
HYPERLINK "http://www.ehponline.org/tagSearch/carbon+monoxide"  carbon
monoxide ,   HYPERLINK "http://www.ehponline.org/tagSearch/children"
children ,   HYPERLINK
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departments ,   HYPERLINK
"http://www.ehponline.org/tagSearch/nitrogen+dioxide"  nitrogen dioxide
,   HYPERLINK "http://www.ehponline.org/tagSearch/particulate+matter"
particulate matter . Environ Health Perspect 107:489-493 (1999) .
[Online 6 May 1999]

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http://ehpnet1.niehs.nih.gov/docs/1999/107p489-493norris/ abstract.html

Address correspondence to J.Q. Koenig, Department of Environmental
Health, 357234, University of Washington, 561A Health Sciences Building,
Room 7, PO Box 357234, Seattle, WA 98195-7234 USA. Telephone: (206)
543-2026. Fax:<PHONE_NUMBER>. E-mail:   HYPERLINK
<EMAIL_ADDRESS><EMAIL_ADDRESS>

We thank N. Maykut for providing technical advice and the Puget Sound
Air Pollution Control Agency for continuing to support air pollution
health effects research in the Puget Sound region. We also thank the
participating hospitals for their assistance, A. Park of the Seattle
King County Department of Public Health for the population data, and
D.V. Bates for helpful comments regarding the manuscript.

Funding for this research was from the Puget Sound Air Pollution Control
Agency, Seattle, Washington, and in part from NIEHS Center grant 1 P30
ES 07033.

Received 16 November 1998 ; accepted 26 February 1999.

Introduction

Asthma is the most common chronic illness in children and the cause of
most school absences (1). The rate of hospitalization for asthma has
been increasing in children < 18 years of age (2). The primary increases
in asthma morbidity are observed in minority populations in urban areas
(3). When focusing on the inner city, 8-12% of children under 18 years
of age have asthma (4). Many airborne factors can aggravate asthma,
including cigarette smoke (5), dust mites, molds, cold air, animal
dander (6), and cockroaches (7). Additionally, increases in air
pollution are associated with exacerbation of asthma as measured by
decreased lung function values and respiratory symptoms (8-10),
shortness of breath (11), emergency department (ED) visits (12-18), and
hospitalizations (19,20). Thus there is concern that air pollution is
aggravating childhood asthma (21,22).

 2.5 µm in aerodynamic diameter (PM2.5), and the coarse fraction
PM10-PM2.5] (20). Sources of PM in Seattle include wood smoke, gasoline
and diesel vehicles, resuspended road dust, and industry (23). A source
apportionment study of PM10 in Seattle in 1991-1992 found that during
the heating season, 80% of PM in residential areas originated from
wood-burning devices (24). Concentrations of all measured air pollutants
have been decreasing in Seattle over the last decade (25).

The Seattle-King County Health Department (Seattle, WA) carried out a
survey from 1987 to 1996 on asthma hospitalization rates for children in
Seattle and surrounding areas using the Comprehensive Hospital Abstract
Reporting System and found > 50% higher hospitalization rates in central
and southeast Seattle (the inner city) as compared to other districts
around Seattle (26). The present study examined whether there was a
stronger association between air pollution and ED visits for asthma for
children in the inner city area than for other children in Seattle using
the same hospitals and found that there was not.

Methods

Health data. Daily ED visits for asthma were obtained from six hospitals
in central and southeast Seattle from 1 September 1995 to 31 December
1996. Permission for use of the hospital data was obtained from the
University of Washington Human Subjects Office in Seattle. Four of the
six hospitals were downtown; the other two were located within 12 km of
central Seattle (Figure 1). The total number of daily visits were
compiled based on the International Classification of Disease, Ninth
Revision (World Health Organization, Geneva) codes for asthma
(493.01-493.99). Only data for patients under the age of 18 who lived in
a 36-zip code region were used. The zip code region contained the six
hospitals and was limited to an area between the air monitoring stations
to the north and south of the central area identified in the
hospitalization survey (Figure 1). The 36 zip codes in that region were
divided into a high and low utilization density based on the childhood
ED visits for asthma. The top 20th percentile zip codes were designated
as the high ED asthma utilization areas (seven zip codes). The rest of
the zip codes were designated as the low ED asthma utilization areas (29
zip codes). The association between air pollution and ED asthma visits
was evaluated for the entire study region (36 zip codes), as well as
separately for the high and low ED utilization regions (Figure 1).

 sp, dry light scattering.

*Additional station that operated from February 1996 to January 1997.

  sp) were available at three sites--north, central, and south Seattle.
Dry light scattering coefficient obtained from an integrating
nephelometer most efficiently measures particles between 0.2 and 0.9 µm
(27), which makes it a measure of the concentration of PM < 1 µm.
Carbon monoxide (CO) values were obtained from four sites within the
Seattle study region. Sulfur dioxide (SO2) concentrations were measured
at one site in central Seattle. Nitrogen dioxide (NO2) and ozone data
were obtained from the WDOE for a site in central Seattle and at a site
20 km east of Seattle, respectively. Because the health data collected
for this study only covered one ozone season (April-October) there were
sufficient ozone data for our model. In addition, the photochemical belt
where ozone concentrations are measured is 20 km east of the area where
children in this study resided.

For pollutants measured at multiple sites, a daily arithmetic average
was calculated and used in the time-series analyses. The appropriate
averaging time for each pollutant was based on national and state air
quality standards. A 24-hr average was used for measures of PM. A 1-hr
average was used for SO2 to reflect the WDOE 1-hr standard of 400 ppb
for SO2. Because there is only an annual National Ambient Air Quality
Standard (NAAQS) for NO2, we selected the daily maximum 1 hr and daily
average concentration for this pollutant. A number of studies have used
the daily maximum 1 hr NO2 concentration for time-series analyses
(14,15,28). We assumed that CO was a general indicator of the build up
of air pollution and we used an averaging time that matched the PM
measurements (24 hr). Dew point temperature and average daily
temperature data were collected from the Seattle Tacoma International
Airport by the National Oceanic and Atmospheric Administration National
Climatic Data Center (Figure 1); 24-hr averages were used for these
meteorologic variables.

Statistical analysis. The ED visits for asthma were regressed on
predictor and confounding variables using a semiparametric Poisson
regression model, a method of choice in recent studies (20,29). All
analyses were conducted with the S-PLUS statistical package (StatSci,
Seattle, WA) using a generalized additive model (30). Base models were
first constructed that adjusted for potential confounding factors using
day-of-week indicator variables, smooth functions for time trends,
temperature, and dew point temperature. The smooth function for time
trends used a smoothing spline (31) that was approximately equivalent to
a 2-month moving average. The degrees of freedom for the smoothing
splines for temperature and dew point temperature were selected based on
minimizing the degree of freedom adjusted deviance (32). After the base
models were created for each of the three utilization areas (high, low,
and entire area), the air pollution exposure variables were evaluated by
adding them individually into the model. The final models were evaluated
for overdispersion and autocorrelation. Additionally, the assumption of
a linear dose response was evaluated using a smooth function.

The ED visits for asthma were assumed to be precipitated by either the
same-day air pollution or air pollution levels up to 4 days before the
visit (0- to 4-day lags). These lag times are consistent with that
reported by Canny and colleagues (33) who found 84% of the asthmatic
children had symptoms for 72 hr or less prior to arrival to the ED.

Results

Table 1 shows a summary of pollutant concentrations in this study. Table
2 summarizes the correlations between the exposure variables that were
used. The PM10 and light-scattering measurements were highly correlated
(r = 0.82). CO was also correlated with these PM measurements, but not
with NO2 or SO2. An additional nephelometer was placed in south Seattle
prior to this study to determine whether the inner city area fine PM
values correlated with the other fixed PM monitors (Figure 1). The
light-scattering measurements from the inner city monitor were highly
correlated with the other monitors in the network, with a correlation
coefficients ranging from 0.75 to 0.85.

The average number of ED visits for asthma in our study for children <
18 years of age was 1.8 per day, with a maximum of nine visits on any
day. This number is low because we restricted the study area to the
inner city and surrounding areas. The age distribution of the ED visits
for asthma in children < 18 years of age is shown in Table 3. The
majority of the ED visits were for children younger than 5 years of age.
This age group accounted for 55 and 54% of the asthma visits for the
high and low utilization regions, respectively. When comparing asthma ED
visits between the two study areas, the high utilization area accounted
for 41% of all the asthma ED visits (seven zip codes).

  sp) were significantly associated with increased ED asthma visits in
children from all three zip code areas with relative rate increases
ranging from 1.13 to 1.16 across the study regions. PM10 and CO had
similar relative rates over the study regions and were significantly
associated with ED visits for asthma in the low utilization area and in
the total study area. The daily 1-hr maximum SO2 and NO2 were not
significantly associated with an increase in ED visits for asthma for
any of the study areas. The association between ED visits for asthma and
ozone was only determined for the entire study area because of the large
number of missing data (45% of the days). Ozone was not significantly
associated with ED visits for asthma; the relative rate was 1.02 [95%
confidence interval (CI), 0.98-1.05] for an IQR of 4.6 ppb in the
maximum daily running 8-hr average.

Multipollutant models containing either PM measurement (light scattering
or PM10), SO2, and NO2 were also analyzed for the entire study region
using a 1-day lag. CO was excluded from the multipollutant model because
it was assumed to be a surrogate for stagnant conditions. The relative
rate for light scattering and PM10 remained significant with relative
rates of 1.17 (CI, 1.08-1.26) and 1.14 (CI, 1.04-1.26), whereas the SO2
and NO2 terms were not significantly associated with an increase in ED
visits for asthma (data not shown).

The highest PM concentrations were observed during the winter heating
season, as was seen in three earlier studies in Seattle (8,12,20)
(Figure 2). Initial analyses showed that 24 and 25 December 1995 were
influential data points in the regression because of the high measured
PM concentrations. To assess the impact of these data, we repeated the
analyses with and without these 2 days to evaluate the effect of these
atypically high PM concentrations (Figure 2). The relative rates for
increased ED visits for asthma in the entire study area including and
excluding 24 and 25 December were 1.11 (CI, 1.02-1.20) and 1.14 (CI,
1.05-1.24), respectively, for an 11.5-µg/m3 increase in PM10. Relative
rates for inclusion and exclusion of those dates for associations with
light scattering were 1.10 (CI, 1.04-1.17) and 1.15 (CI, 1.07-1.23) for
an IQR increase. These results show the relative rates remained
significant with the inclusion of the influential dates, but the
relative rate for light scattering decreased 5% with the inclusion of
the two high concentration points. Additionally, the inclusion of 24 and
25 December 1995 caused the dose-response relationships for light
scattering to show nonlinear behavior above values approximately equal
to 40 µg/m3 PM2.5. Because these 2 days were holidays, the use of the
ED visits for asthma may have been different from other days in the
study. Based on the high influence and a potential holiday effect, these
2 days were not included in our primary analysis.

 10 µm in aerodynamic diameter.

aEstimated from light-scattering data.

Discussion

We found significant associations between ED visits for asthma in
children and PM10, light-scattering measurement of fine PM, and CO.
Light scattering, which is a measure of fine PM primarily < 1.0 µm in
diameter, was significantly associated with ED visits for asthma in all
the analyses. Additionally, PM10 and CO were significant predictors of
ED asthma visits in the low utilization and for the combined utilization
areas. The higher relative risk in this study as compared to the earlier
results by Schwartz and colleagues (12) may be due to the fact that our
population was restricted to individuals under the age of 18, a more
susceptible group than the population at large.

We recognize that ED data from hospitals contain some misdiagnoses.
Delfino and associates (34) found a good association between hospital
summary data and chart review. The majority of cases in our study came
from a single children's hospital specializing in diagnoses for
childhood diseases.

The number of visits for the high utilization region (371) was less than
the low utilization area (529) and likely did not achieve statistical
significance for PM10 and CO because of the reduced number of events.
Otherwise, the high and low utilization areas did not appear to have
different associations between air pollution and increased ED visits for
asthma. The estimated numbers of children under 18 years of age in the
high utilization area and in the rest of Seattle were 6,921 and 100,895,
respectively. However, we cannot compare the absolute number of visits
for the two utilization areas because a given relative rate increase in
ED visits in the high utilization area caused more absolute visits than
in the low utilization area.

In this study, relative rates for light scattering in the low and high
utilization areas were 13 and 16% for an IQR increase of approximately
10 µg/m3 of fine PM. The light-scattering IQR was converted to
represent PM2.5 gravimetric mass based on colocated nephelometer and
PM2.5 monitors at the southernmost PM monitoring site (224 days, r =
0.86). The average concentration for the 15-month period of this study
was approximately 12 µg/m3 PM2.5, a concentration below the new EPA
annual standard (15 µg/m3). PM10 was associated with a 14% increase in
ED asthma visits for an increase of 12 µg/m3 PM10.

 The association between increased asthma visits and CO was investigated
in Anchorage, Alaska (35), Reno, Nevada (36), and Seattle (20). The
Anchorage and Reno studies did not find a significant association
between ED visits for asthma and CO; however, CO was associated with
hospital admissions in Seattle (20). The Reno study used the highest
hourly maximum level in their local air pollution network, and the
Anchorage study used the daily average 8-hr maximum concentration during
winter months. The Seattle hospital admission study (20) used the daily
average of four monitoring stations. In the present study, we used a
24-hr average of four sites in our study region for the entire 15
months. Because CO has no biologically plausible mechanism for the
exacerbation of asthma (37) we interpret it as a general indicator of
air pollution. The significant association between increased ED visits
for asthma and CO found in this analysis could result from the high
correlation between CO and PM10 (0.74) as well as light scattering
(0.74). To explore this possibility, a factor analysis of the physical
and chemical nature of air pollution in Seattle was conducted on both
the CO and particulate composition data collected previously (38) at the
southernmost PM site in this study. Factor analysis with a varimax
rotation has been used to both examine the colinearity among the various
air pollutant variables and to identify important features of the
variability in these pollutants (Table 5) (39,40). Main et al. (38)
measured the composition of PM2.5 or fine soil and coarse PM
(PM10-PM2.5). Coarse and fine soil mass were reconstructed by adding the
mass of the oxides of soil species (Si, Ca, Fe, and Ti) (41). Using
these data we derived three factors which explained 95% of the variance
and show that the variability in PM2.5 composition is influenced by
three factors: a) incomplete combustion products consisting of CO,
elemental carbon, organic carbon, and soluble potassium (wood smoke
marker); b) secondary aerosols consisting of ammonium and sulfate; and
c) fine and coarse soil (Table 5). The light scattering and PM10 data
are correlated with the first factor scores, with correlation
coefficients of 0.81 and 0.77, respectively. Note that CO is associated
with the buildup of incomplete combustion-derived products including
particulate organic carbon and particulate elemental carbon.

This study did not find a significant association between NO2, SO2, or
ozone and increased ED asthma visits. The NO2, SO2, and ozone
measurements are only taken at one site in the network and may be
subject to a greater degree of exposure misclassification than the CO
and PM pollutant measures that represent averages of three to four sites
in the study area. In addition, the SO2 concentrations were low, with a
mean daily 1-hr maximum concentration of 6 ppb. Other investigators have
reported that the peak hourly NO2 concentration was significantly
associated with increased ED visits for asthma during winter months in
Northern California (15) and with increased ED visits and respiratory
admissions in Athens, Greece (28). Peak hourly NO2 was also associated
with increased ED visits for asthma during both the winter and summer
months in Barcelona, Spain (14). The average peak NO2 concentrations in
the Northern California, Athens, and Barcelona studies were 69 ppb, 50
ppb, and 58 ppb, respectively. These concentrations are significantly
higher than the average peak hourly NO2 concentration of 35 ppb observed
in this study. Our finding of no significant association between ED
asthma visits and maximum hourly SO2 is consistent with the earlier
Seattle study (12) and the study in Barcelona (14). The lack of a
significant association between ED visits for asthma and ozone in this
study may be due to the large number of missing measurements.

In summary, this study found a small but significant association between
air pollution and increased ED visits for asthma in children in Seattle.
PM and CO concentrations in this study were associated with increased
childhood ED visits for asthma and represent the daily variation in
incomplete combustion products including elemental carbon and organic
carbon. Results from this study of a susceptible subpopulation show
significant increases of ED asthma visits for children with daily PM2.5
concentrations substantially below the newly adopted National Ambient
Air Quality Standard of 15 µg/m annually (42).

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References and Notes

1. Hill RA, Standen PJ, Tattersfield AE. Asthma, wheezing, and school
absence in primary schools. Arch Dis Child 644:246-251 (1989).

2. Gergen PJ, Weiss KB. Changing patterns of asthma hospitalization
among children: 1979 to 1987. J Am Med Assoc 264:1688-1692 (1990).

3. Moore CM, Ahmed I, Mouallem R, May W, Ehlayel M, Sorensen RU. Care of
asthma: allergy clinic versus emergency room. Ann Allergy Asthma Immunol
78:373-380 (1997).

4. Crain EF, Weiss KB, Bijur PE, Hersh M, Westbrook, Stein REK. An
estimate of the prevalence of asthma and wheezing among inner-city
children. Pediatrics 94:356-364 (1994).

5. Azizi BHO, Zulkifli HI, Kasim MS. Indoor air pollution and asthma in
hospitalized children in a tropical environment. J Asthma 32:413-418
(1995).

6. Burr ML, Limb ES, Andrae S, Barry DM, Nagel F. Childhood asthma in
four countries: a comparative survey. Int J Epidemiol 23:341-347 (1994).

7. Rosenstreich DL, Eggleston P, Kattan M, Baker D, Slavin RG, Gergen P,
Mitchell H, McNiff-Mortimer K, Lynn H, Ownby D, et al. The role of
cockroach allergy and exposure to cockroach allergen in causing
morbidity among inner city children with asthma. N Engl J Med
336:1356-1363 (1997).

8. Koenig JQ, Larson TV, Hanley QS, Robelledo V, Dumler K, Checkoway H,
Wang SZ, Lin D, Pierson WE. Pulmonary function changes in children
associated with fine particulate matter. Environ Res 63:26-38 (1993).

9. Romieu I, Meneses F, Ruiz S, Sienra JJ, Huerta J, White MC, Etzel RA.
Effects of air pollution on the respiratory health of asthmatic children
living in Mexico City. Am J Respir Crit Care Med 154: 300-307 (1996).

10. Peters A, Dockery DW, Heinrich J, Wichmann HE. Short-term effects of
particulate air pollution on respiratory morbidity in asthmatic
children. Eur Respir J 10: 872-879 (1997).

11. Ostro B, Lipsett MJ, Mann JK, Braxton-Owens H, White MC. Air
pollution and asthma exacerbations among African-American children in
Los Angeles. Inhal Toxicol 7: 711-722 (1995).

12. Schwartz J, Slater D, Larson TV, Pierson WE, Koenig JQ. Particulate
air pollution and hospital emergency room visits for asthma in Seattle.
Am Rev Respir Dis 147:826-831 (1993).

13. Bates DV, Baker-Anderson M, Sizto R. Asthma attack periodicity: a
study of hospital emergency visits in Vancouver. Environ Res 51:51-70
(1990).

14. Castellsague J, Sunyer J, Saez M, Anto JM. Short-term association
between air pollution and emergency room visits for asthma in Barcelona.
Thorax 50:1051-1056 (1995).

15. Lipsett M, Hurley SB, Ostro B. Air pollution and emergency room
visits for asthma in Santa Clara County, California. Environ Health
Perspect 105:216-222 (1997).

16. Delfino RJ, Murphy-Moulton AM, Burnett RT, Brook JR, Becklane MR.
Effects of air pollution on emergency room visits for respiratory
illnesses in Montreal, Quebec. Am J Respir Crit Care Med 155:568-576
(1997).

17. Steib DM, Burnett RT, Beveridge RC, Brook JR. Association between
ozone and asthma emergency department visits in Saint John, New
Brunswick, Canada. Environ Health Perspect 104:1354-1360 (1996).

18. Sunyer J, Spix C, Quenel P, Ponce-de-Leon A, Ponka A, Barumandzadeh
T, Touloumi G, Backarova L, Wojtyniak B, Vonk J, et al. Urban air
pollution and emergency admissions for asthma in four European cities:
the APHEA Project. Thorax 52: 760-765 (1997).

19. Pope CA III. Respiratory hospital admissions associated with PM10
pollution in Utah, Salt Lake, and Cache valleys. Arch Environ Health
46:90-97 (1991).

20. Sheppard L, Levy D, Norris G, Larson TV, Koenig JQ. Effects of
ambient air pollution on non-elderly asthma hospital admissions in
Seattle, 1987-1994. Epidemiology 10:23-30.

21. Bates DV. Observations on asthma. Environ Health Perspect 103(suppl
6):243-247 (1995).

22. Etzel RA. Indoor air pollution and childhood asthma: effective
environmental interventions. Environ Health Perspect 103(suppl 6):55-58
(1995).

23. Puget Sound Air Pollution Control Agency. Unpublished data, 1988.

24. Larson TV, Yuen P, Maykut N. Weekly composite sampling of PM2.5 for
total mass and trace elements analysis. In: Transactions of the Air and
Waste Management Association Specialty Conference on PM10 Standards and
Nontraditional Particulate Source Controls (Chow JC, Ono DM, eds).
Pittsburgh, PA:Air and Waste Management Association, 1992;39-52.

25. PSAPCA. Data Summary, 1996. Seattle, WA:Puget Sound Air Pollution
Control Agency, 1997.

26. The Public Health Data Watch. Seattle, WA:The Seattle-King County
Department of Public Health, 1998.

27. National Research Council. Airborne Particles. Washington,
DC:National Academy of Sciences, 1977.

28. Pantazopoulou A, Katsouyanni K, Kourea-Kremastinou J, Trichopoulos
D. Short-term effects of air pollution on hospital emergency outpatient
visits and admissions in the greater Athens, and Greece area. Environ
Res 69: 31-36 (1995).

29. Kelsall JE, Samet JM, Zeger SL, Xu J. Air pollution and mortality in
Philadelphia, 1974-1988. Am J Epidemiol 146:750-62 (1997).

30. StatSci. S-PLUS. Seattle, WA:StatSci, 1993.

31. Hastie T, Tibshirani R. Generalized Additive Models. London:Chapman
and Hall, 1990.

32. Akiake H. Statistical predictor identification. Ann Inst Math
22:203-207 (1970).

33. Canny GJ, Reisman J, Healy R, Schwartz C, Petrou C, Rebuck AS,
Levison H. Acute asthma: observations regarding the management of a
pediatric emergency room. Pediatrics 83:507-512 (1989).

34. Delfino RJ, Becklake MR, Hanley JA. Reliability of hospital data for
population-based studies of air pollution. Arch Environ Health
48:140-146 (1993).

35. Gordian ME, Özkaynak H, Xue J, Morris SS, Spengler JD. Particulate
air pollution and respiratory disease in Anchorage, Alaska. Environ
Health Perspect 104:290-297 (1996).

36. Yang W, Jennison BL, Omaye ST. Air pollution and asthma emergency
room visits in Reno, Nevada. Inhal Toxicol 9:15-29 (1997).

37. Committee of the Environmental and Occupational Health Assembly of
the American Thoracic Society. Health effects of outdoor air pollution.
Am J Respir Crit Care Med 153:3-50 (1996).

38. Main HH, Richards LW, Chinkin LR, Evans VA, Chow JC, Divita F. PM10
Chemical Analysis and Source Receptor Modeling Study for the
Seattle-Tacoma Area. STI-93140-1444-FR. Santa Rosa, CA:Sonoma
Technology, Inc., 1995.

39. Gatz GF. Identification of aerosol sources in the St Louis area
using factor analysis. J Appl Meteor 17:600-608 (1978).

40. Biegalski SR, Landsberger S, Hoff RM. Source-receptor modeling using
trace metals in aerosols collected at three rural Canadian Great Lakes
sampling stations. J Am Med Assoc 48: 227-237 (1998).

41. Malm WC, Sisler JF, Huffman D, Eldred RA, Cahill TA. Spatial and
seasonal trends in particle concentration and optical extinction in the
United States. J Geophys Res 99:1347-1370 (1994).

42. U.S. Environmental Protection Agency. National Ambient Air Quality
Standards for particulate matter; final rule. Fed Reg
62(138):38651-38701 (1997).


[Federal Register: February 13, 2007 (Volume 72, Number 29)]
[Notices]
[Page 6799-6801]
[DOCID:fr13fe07-80]

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SECURITIES AND EXCHANGE COMMISSION

[Release No. 34-55244; File No. SR-NYSE-2007-11]

Self-Regulatory Organizations; New York Stock Exchange LLC;
Notice of Filing and Immediate Effectiveness of Proposed Rule Change
Relating to Rule 122 (Orders With More Than One Broker) Until the
Availability of Full d-Quote Functions in a Particular Security or
March 5, 2007, Whichever Comes First

February 5, 2007.
    Pursuant to Section 19(b)(1) of the Securities Exchange Act of 1934
(``Act'') \1\ and Rule 19b-4 thereunder,\2\ notice is hereby given that
on February 5, 2007, the New York Stock Exchange LLC (``NYSE'' or
``Exchange'') filed with the Securities and Exchange Commission
(``Commission'') the proposed rule change as described in Items I and
II below, which Items have been substantially prepared by the self-
regulatory organization. NYSE filed the proposed rule change pursuant
to Section 19(b)(3) of the Act \3\ and Rule 19b-4(f)(6) thereunder,\4\
which renders the proposed rule change effective upon filing with the
Commission. The Commission is publishing this notice to solicit
comments on the proposed rule change from interested persons.
---------------------------------------------------------------------------

    \1\ 15 U.S.C. 78s(b)(1).
    \2\ 17 CFR 240.19b-4.
    \3\ 15 U.S.C. 78s(b)(3)(A).
    \4\ 17 CFR 240.19b-4(f)(6).
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I. Self-Regulatory Organization's Statement of the Terms of Substance
of the Proposed Rule Change

    The Exchange proposes to continue the Floor brokers' ability to
maintain discretionary e-Quotes (``d-Quotes'') \5\ and CAP-DI orders
\6\ in a security on the same side of the market for the same order
that are capable of trading at the same price until the completion of
Phase IV implementation of the HYBRID MARKETSM (``Hybrid
Market'') in the relevant security or until March 5, 2007, whichever
comes first. The text of the proposed rule change is available on the
Exchange's Web site (http://www.nyse.com), at the Exchange's Office of the

Secretary, and at the Commission's Public Reference Room.
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    \5\ See Securities Exchange Act Release No. 54577 (October 5,
2006), 71 FR 60208 (October 12, 2006) (SR-NYSE-2006-36).
    \6\ See Exchange Rules 13 and 123A.30(a). Exchange Rule
123A.30(a) describes a CAP-DI order as: ``The elected or converted
portion of a `percentage order that is convertible on a
destabilizing tick and designated immediate execution or cancel
election' (``CAP-DI order'') may be automatically executed and may
participate in a sweep.''
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II. Self-Regulatory Organization's Statement of the Purpose of, and
Statutory Basis for, the Proposed Rule Change

    In its filing with the Commission, the self-regulatory organization
included statements concerning the purpose of and basis for the
proposed rule change. The text of these statements may be examined at
the places specified in Item IV below. The self-regulatory organization
has prepared summaries, set forth in sections A, B, and C below, of the
most significant aspects of such statements.

A. Self-Regulatory Organization's Statement of the Purpose of, and
Statutory Basis for, the Proposed Rule Change

1. Purpose
    On October 25, 2006, the Exchange filed with the Commission an
amendment to Rule 122 to permit Floor brokers to enter d-Quotes and
CAP-DI orders in a security on the same side of the market for the same
underlying order that are capable of trading at the same price until
the implementation of full d-Quoting functionality in the relevant
security or until February 5, 2007, whichever came first.\7\
---------------------------------------------------------------------------

    \7\ See Securities Exchange Act Release No. 54653 (October 26,
2006), 71 FR 64594 (November 2, 2006) (SR-NYSE-2006-94).
---------------------------------------------------------------------------

    On January 25, 2007, the Exchange commenced the implementation of
Phase IV of the Hybrid Market, which includes the remaining d-Quote
functions: (i) The ability to trade against non-marketable interest
within a Floor broker's discretionary range and (ii) routing control
for Floor brokers with respect to d-Quotes.\8\
---------------------------------------------------------------------------

    \8\ Other d-Quote functions were implemented in Phase III.
---------------------------------------------------------------------------

    The Exchange anticipates that the implementation of Phase IV will
not be completed as originally anticipated by February 5, 2007. Through
this filing the Exchange therefore requests to extend Floor brokers'
ability to enter d-Quotes and CAP-DI orders in a security on the same
side of the market for the same orders that are capable of trading at
the same price until the implementation of

full d-Quoting functionality in the relevant security or until March 5,
2007 whichever comes first.
    The Exchange believes that extending the time period in which Floor
brokers have this capability is necessary in order to ensure that Floor
brokers remain competitive. Currently, the specialist can send
electronically a ``hit bid'' or ``take offer'' message based on an
incoming order that would create a new best bid or best offer; thus
allowing the specialist to trade electronically with the newly
published bid or offer. Without complete d-Quote functionality, a Floor
broker only has the ability to interact manually with such new bid or
offer. As a result, the speed disparity between a manual action and an
electronic one places the Floor broker at a competitive disadvantage.
    While a Floor broker can seek to trade at the bid or offer price by
manually ``hitting the bid'' or ``taking the offer'' the Floor broker
can also send a CAP-DI order to the specialist for conversion or
election at that price. Marketable CAP-DI orders are automatically
converted and trade along with specialist proprietary executions.
Accordingly, by allowing Floor brokers to have CAP-DI orders and d-
Quotes, they retain the ability to compete with specialist algorithmic
trading for executions involving marketable incoming orders via
discretionary pricing instructions, but do not miss participating in
executions when specialists algorithmically hit a bid or take an offer.
2. Statutory Basis
    The basis under the Act for this proposed rule change is the
requirement under Section 6(b)(5) of the Act \9\ that an Exchange have
rules that are designed to promote just and equitable principles of
trade, to remove impediments to and perfect the mechanism of a free and
open market and a national market system and, in general, to protect
investors and the public interest. The proposed rule change also is
designed to support the principles of Section 11A(a)(1) of the Act \10\
in that it seeks to assure economically efficient execution of
securities transactions, make it practicable for brokers to execute
investors' orders in the best market and provide an opportunity for
investors' orders to be executed without the participation of a dealer.
---------------------------------------------------------------------------

    \9\ 15 U.S.C. 78f(b)(5).
    \10\ 15 U.S.C. 78k-1(a)(1).
---------------------------------------------------------------------------

B. Self-Regulatory Organization's Statement on Burden on Competition

    The Exchange does not believe that the proposed rule change will
impose any burden on competition that is not necessary or appropriate
in furtherance of the purposes of the Act.

C. Self-Regulatory Organization's Statement on Comments on the Proposed
Rule Change Received From Members, Participants or Others

    The Exchange has neither solicited nor received written comments on
the proposed rule change.

III. Date of Effectiveness of the Proposed Rule Change and Timing for
Commission Action

    Because the foregoing proposed rule change does not: (i)
Significantly affect the protection of investors or the public
interest; (ii) impose any significant burden on competition; and (iii)
by its terms, become operative for 30 days from the date on which it
was filed, or such shorter time as the Commission may designate if
consistent with the protection of investors and the public interest, it
has become effective pursuant to Section 19(b)(3)(A) of the Act \11\
and Rule 19b-4(f)(6) thereunder.\12\
---------------------------------------------------------------------------

    \11\ 15 U.S.C. 78s(b)(3)(A).
    \12\ 17 CFR 240.19b-4(f)(6).
---------------------------------------------------------------------------

    A proposed rule change filed under Rule 19b-4(f)(6) normally may
not become operative prior to 30 days after the date of filing.
However, Rule 19b-4(f)(6)(iii) \13\ permits the Commission to designate
a shorter time if such action is consistent with the protection of
investors and the public interest. The Exchange has requested that the
Commission waive the 30-day operative delay and designate the proposed
rule change immediately operative upon filing. The Commission believes
that waiver of the 30-day operative delay is consistent with the
protection of investors and the public interest. Specifically, the
Commission believes that the proposal would enable floor brokers to
continue to compete with specialists in certain trades on behalf of
their customers, while the Exchange is in the process of implementing
the d-Quote functions. Accordingly, the Commission designates the
proposal to be effective and operative upon filing with the Commission
until the availability of full d-Quote functions in a particular
security or March 5, 2007, whichever comes first.\14\
---------------------------------------------------------------------------

    \13\ 17 CFR 240.19b-4(f)(6)(iii).
    \14\ For purposes only of waiving the operative delay for this
proposal, the Commission has considered the proposed rule's impact
on efficiency, competition, and capital formation. See 15 U.S.C.
78c(f).
---------------------------------------------------------------------------

    At any time within 60 days of the filing of the proposed rule
change, the Commission may summarily abrogate such proposed rule change
if it appears to the Commission that such action is necessary or
appropriate in the public interest, for the protection of investors, or
otherwise in furtherance of the purposes of the Act.

IV. Solicitation of Comments

    Interested persons are invited to submit written data, views and
arguments concerning the foregoing, including whether the proposed rule
change is consistent with the Act. Comments may be submitted by any of
the following methods:

Electronic Comments

     Use the Commission's Internet comment form (http://www.sec.gov/rules/sro.shtml.
); or     Send an e-mail to<EMAIL_ADDRESS>Please include

File Number SR-NYSE-2007-11 on the subject line.

Paper Comments

     Send paper comments in triplicate to Nancy M. Morris,
Secretary, Securities and Exchange Commission, 100 F Street, NE,
Washington, DC 20549-1090.
    All submissions should refer to File Number SR-NYSE-2007-11. This
file number should be included on the subject line if e-mail is used.
To help the Commission process and review your comments more
efficiently, please use only one method. The Commission will post all
comments on the Commission's Internet Web site (http://www.sec.gov/rules/sro.shtml
). Copies of the submission, all subsequent amendments,

all written statements with respect to the proposed rule change that
are filed with the Commission, and all written communications relating
to the proposed rule change between the Commission and any person,
other than those that may be withheld from the public in accordance
with the provisions of 5 U.S.C. 552, will be available for inspection
and copying in the Commission's Public Reference Room. Copies of such
filing also will be available for inspection and copying at the
principal office of the Exchange. All comments received will be posted
without change; the Commission does not edit personal identifying
information from submissions. You should submit only information that
you wish to make available publicly. All

submissions should refer to File Number SR-NYSE-2007-11 and should be
submitted on or before March 6, 2007.

    For the Commission, by the Division of Market Regulation,
pursuant to delegated authority.\15\
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    \15\ 17 CFR 200.30-3(a)(12).
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Florence E. Harmon,
Deputy Secretary.
[FR Doc. E7-2406 Filed 2-12-07; 8:45 am]

BILLING CODE 8010-01-P