Air Pollution and Acute Cardio Respiratory Visits.50

ABSTRACTS
ISEE-1
SCENARIOS OF VECTOR-BORNE DISEASES AND HEAT STRESS
IN EUROPE
Michael van Liehuit, Pim Martens. ICIS
Abstract: Global climate change remains one of the biggest
environmental threats over the coming century. The impacts on human
population health are highly uncertain but are an important focus of the
policy debate regarding mitigation and adaptation. Within the cCASHhproject complex integrative approach, aims to improve our understanding
of future exposure, and adaptation possibilities and capacities to vectorborne diseases as well as heat exposure in different areas of the European
Region.
Methodology: An integrated framework, combining quantitative and
qualitative computer modelling and integrated scenario analysis has been
developed to address the future vulnerability of human health in Europe.
The existing models incorporate the dynamic global and local interaction
between the most important drivers.
Results: This work will present the results of the future risk of vectorborne diseases under a changing environment as well as future risk of
population exposure to heat stress under different adaptation scenarios.
Climate change might also affect human health directly. Most climate
scenarios show an increase in the frequency of temperature extremes,
which would entail increases in thermal stress, and consequently on
morbidity and mortality rates. The fact of a greying European population
and a scenario-dependent increase of the degree of urbanisation would
even super add to the potential morbidity and mortality rates related to
heat stress. However, depending on the populations future health status,
the ability to adapt autonomously and or social and institutional means
available, the residual mortality rates might be lower.
European Commision Grant EVK-2-2000-ENV-00070.
ISEE-2
COOKING FUELS AND INDOOR AIR POLLUTION (IAP)
Mukesh Dherani,* Astrid Fletcher,* Uma R, Kirk Smith. *London
School of Hygiene and Tropical Medicine; The Energy and Resources
Institute, New Delhi; University of California, Berkeley
Introduction: Individuals using unprocessed biomass fuels for cooking
in developing countries are exposed to very high level of particulate
matter (PM), a major component of biomass smoke. The estimated burden
of disease associated with IAP is high; 1.6 million premature deaths a
year globally according to the WHO (2002). This study focuses on the
household factors and cooking practices related to PM5 concentrations.
Method: A cross sectional survey comprising of 864 households selected
through cluster sampling in a semi-urban area, was conducted. People of
age group 50 years living there were interviewed to assess their current
and past cooking practices. In a sub-sample of 82 households PM5 levels
were measured in the kitchen during cooking, and, living room and
outdoors over a 24 hour period. Low volume air samplers (224 &endash;
PCXR7, SKC make, USA) with a cyclone (50% cut off at 5 mm) and
flow rate of 1.9 lit/min were used to measure PM5 levels.
Results: All the households (98%) reported using cattle dung and wood
as their regular fuels, mud stove without a chimney was the most common
type of stove (98%). Hara, a locally made stove that uses dung was
present in 55% of households. Liquefied Petroleum Gas (LPG) stoves
were present in more than 50% of households, however, only 5% used
them as their main stove. Almost all the women either cook currently or
used to cook in the past, while only 3% of men used to cook. The mean
PM5 level in the kitchen was 4800 3200 g/m3 (geometric mean (GM)
3800 g/m3) during cooking. The 24-hr average PM5 levels in living
room and outdoors were 450 280 g/m3 (GM 390 g/m3) and 130
Epidemiology Volume 15, Number 4, July 2004
40 g/m3, respectively. Linear regression suggested that the quantity of

each fuel (dung, wood and crop residues) was strongly associated with
PM5 level during cooking and use of Hara was the most important factor
contributing to the high PM5 levels at the cooking places. The daily
average PM5 exposure to men was 385 g/m3 h (sd 300, GM 320 g/
m3-h) and to the women was more than double, 825 g/m3 h (sd 675,
GM 590 g/m3 h). The average life time person-hour stay in the kitchen
for men was 2400 hours and for women was 36700 hours at an average
age of 61 years for both men and women.
Discussion: Kitchen levels of PM5, resulting from the excessive use of
biomass fuel specially cattle dung, were one of the highest reported.
Diseases related to IAP are expected be highly prevalent in this area. Use
of LPG was very low. Further research is needed to find out the
prevalence of related diseases, and the reasons for low LPG usage. The
analysis of the association between IAP and age-related eye diseases
(cataract and macular degeneration) is in progress.
Dr GVS Murthy, Dr Sanjeev Gupta and team of AIIMS, New Delhi, for
conductin of the survey.
ISEE-3
SHIFTING TRENDS IN INDOOR AND OUTDOOR POLLUTION IN
AN INDUSTRIALIZED URBAN AREA
Ivan Benes,* Jiri Skorkovsky, Joseph Pinto. *Public Health Institute
Usti nad Labem; Regional Hygiene Station Usti nad Labem; U.S.
EPA/NCEA
Introduction: This study investigates trends in indoor and outdoor air
pollutants in an industrial city.
Methods: Measurements of PM2.5, its elemental composition, PAHs,
VOCs, formaldehyde and mutagenicity (Ames test) were obtained in an
industrialized city in a mountainous area in central Europe. Measurements
were made for sampling periods of 12 consecutive days each in 8 indoor
and outdoor sites during winters over the past ten years. The indoor
measurements were obtained in flats, chosen on the basis of differences in
ventilation, and cooking and smoking history. Four of the flats were
occupied by smokers, half of whom could be classified as heavy smokers.
The indoor-outdoor measurements were compared to observations
collected at a central site and they were found to be typically higher
and not as highly correlated as would be the case if the sites were
affected mainly by long range transport of secondary PM.
Results: During the measurement period there have been shifts from the
use of solid fuels (e.g., lignite, wood, refuse) to cleaner burning natural
gas in home furnaces that are used for heating. This shift has been
responsible, in part for a dramatic decline in PM levels measured at the
central site. However, recent increases in the price of natural gas
compared to the more traditional solid fuels have caused shifts back to the
use of solid fuels for home heating. As a result, air quality has
deteriorated in many neighborhoods, especially in lower income areas.
Concentrations of a number of pollutants such as PM2.5, trace elements
(S, P, Cl, K, Zn, Br), PAHs (Anthracene, Chrysene, BenzoaPyrene,
DiBenzoa,hAnthracene), volatile chlorinated and aromatic hydrocarbons
and mutagenicity were generally higher in the flats occupied by smokers.
Open fireplaces installed in many homes and the transport of products of
combustion of solid fuels from nearby homes were also significant sources
of indoor mutagenicity in non smokers homes. Mutagenicity levels in the
homes of some non smokers were similar to those found in the homes of
smokers.
Discussion: Because of changes in emissions patterns in the community
over time, measurements at the central site may not accurately reflect
community exposures. There is thus the possibility of error introduced in
epidemiologic studies conducted in areas in which adequate knowledge of
the changing nature of source characteristics is lacking.
S15
Abstracts
This research was sponsored by the Czech Ministry of Health, Project NJ/
5907-3.
ISEE-4
ESTIMATING HEALTH EFFECTS FROM EXPOSURES TO
OUTDOOR AND INDOOR SOURCES OF AIR POLLUTION
Haluk Ozkaynak. EPA
Abstract: Individuals are exposed to wide variety of pollutants in various
indoor and outdoor microenvironments during the course of a typical day.
Sources of pollution in various indoor and outdoor locations produce
particulate matter (PM) and gaseous pollutants with different physical and
chemical characteristics, which may, in turn, result in different health
responses. Thus, to fully understand the relationships between exposures
to environmental pollutants and various health outcomes, personal
exposures to principal sources of toxic chemicals have to be characterized.
Proper quantification of the magnitude and timing of personal exposures
to these sources will then require identification of key microenvironments,
media, routes and pathways of exposure that contribute most to an
individuals exposure. Source apportionment techniques can provide a
useful method for determining personal exposure to PM and air toxics
from specific sources. Contributions to personal exposures from sources
that have only outdoor, indoor or both indoor and outdoor components
can be developed for generating either personal or population-level
source-specific exposure estimates, for use in epidemiologic analyses. A
number of epidemiological studies have already evaluated the relationship
between health outcomes and sources of ambient particulate matter and
co-pollutants. These studies suggest the importance of examining sources
and constituents of indoor, outdoor, and personal PM and other criteria
pollutants. However, limitations of existing measurement data on indoor,
outdoor and personal measurements to pollutants of concern (e.g., PM and
its constituents or air toxics) and longitudinal time-activity data on
susceptible population groups, hamper the investigation of health impacts
of specific air pollution sources and its components. Future community
health studies need to collect better information on indoor and outdoor
sources of personal exposures to PM, PM species and various toxics
co-pollutants.
Disclaimer: This is an abstract of a proposed presentation and does not
necessarily reflect EPA policy.
ISEE-5
RELATIONSHIP OF MULTIPLE INDOOR AIR POLLUTANTS AND
SICK BUILDING SYNDROME AT AIR-CONDITIONED OFFICE
BUILDINGS IN TAIWAN
Pei-Chih Wu,* Li Yen-Yi, Chiang Che-Ming, Su Huey-Jen,*
Lee Chun-Chang*. *Department of Environmental and Occupational
Health, Medical College, National Cheng Kung University, Taiwan, ROC;
Department of Architecture, College of Engineering, National Cheng
Kung University, Taiwan, ROC
Abstract: Exposures to various indoor factors, particularly air pollutants,
have been implicated in several health outcomes; yet most investigations
had been conducted only with measurements of selected hazards. Our
study was designed to examine associations between indoor air quality
and sick building syndrome (SBS) of employees in 8 air-conditioned
office buildings through a series of comprehensive environmental
assessments and questionnaire administration.
Airborne microbes, carbon dioxide (CO2), particulate matter (PM10),
formaldehyde, and total volatile organic compounds (TVOC) were
measured in every sampling site inside the study buildings. Frequency of
reporting symptoms and other environmental variables, such as
S16
environmental tobacco smoke exposure and air change rate, were

documented by self-administrated questionnaires. Information on gender,
age of the occupant, degree of job satisfaction, recent experience of stress,
and personal history of diagnosed allergic diseases were also obtained for
adjustment in statistical analysis. Multiple logistic regression analysis was
used to identify associations between dichotomous scales of air pollutants
and health outcomes of interest, after adjusting for variables described
above.
Our data show that concentrations of indoor formaldehyde, TVOC and
airborne microbes are higher than most recommended levels quoted.
Estimates of crude odds ratios show that most air pollutants, when
analyzed by continuous scales, are associated with SBS of one or more
types. Similar relationships are seen with environmental factors of interest
and personal characteristics acquired. PM10 exposures were significantly
associated with mostly irritant outcomes, in addition to headache in
multivariate analysis. Interestingly, indoor TVOC concentrations appeared
to be protective with respect to symptom of sneezing, while exposure to
greater concentrations of indoor HCHO did not present additional adverse
effects with concurrent presence of other indoor pollutants. Most
strikingly, statistical associations were found between selected SBS and
microbial concentrations, dichotomized at 1000 CFU/m3 for its being a
reference concentrations adopted in many proposed guidelines.
The critical role of exposure to indoor microbes and PM10 is
quantitatively demonstrated in this investigation. Further work should be
designed to clarify the exact contribution of indoor TVOC exposures for
increasing use of modern compounds, like essential oils, and decoration of
synthetic materials are likely to result in rising concentrations of indoor
TVOC in future indoor environments.
ISEE-6
TOBACCO CONTROL LAWS AND SERUM COTININE LEVELS IN
NONSMOKING ADULTS, 1999-2000
Melanie Pickett,* Susan Schober,* Debra Brody,* Randy Curtin*.
*National Center for Health Statistics; Association of Teachers for
Preventive Medicine
Introduction: State and local bans or restrictions on indoor smoking are
implemented to reduce exposure to environmental tobacco smoke (ETS), a
known human carcinogen. Cotinine, a major metabolite of nicotine, is a
biomarker of exposure to ETS in nonsmokers. Data from the National
Health and Nutrition Examination Survey (NHANES) show that median
cotinine levels in nonsmokers have declined by 70% since the late 1980s.
The objective of this study is to determine the relationship between State
or local ordinances on indoor smoking and cotinine levels in the
nonsmoking adult population, taking into account racial and ethnic
differences.
Methods: NHANES is a cross-sectional survey designed to monitor the
health and nutritional status of the US population. Household interviews,
physical examinations, and cotinine level assessments were performed on
4039 adults (83% response rate), of whom 3003 were non smokers. For
each of 26 study locations, laws regulating indoor smoking (in enclosed
public spaces, workplaces, restaurants, and bars) were categorized into one
of three groups indicating minimal, moderate, or extensive regulations.
The proportion of non-smoking adults with detectable levels of serum
cotinine were compared across these three groups.
Results: Approximately 49% of nonsmoking adults had detectable levels
of cotinine. Non-Hispanic blacks had a higher proportion of detectable
levels (69%) than did non-Hispanic whites (47%) and Mexican-Americans
(44%). For Mexican Americans and non-Hispanic whites, persons living
in areas with extensive smoking regulations had a significantly smaller
proportion with detectable cotinine levels (29%) than persons living in
areas with moderate (52%) and minimal (50%) smoking regulations. The
2004 Lippincott Williams & Wilkins
difference between the moderate and minimal groups was not statistically
significant. For non-Hispanic blacks, there was no difference in the
proportion with detectable levels across the three smoking regulation
categories.
Discussion: These preliminary results suggest that at least for nonHispanic white and Mexican American adults, those living in areas with
extensive tobacco control laws have less ETS exposure compared to those
living in areas with minimal or moderate smoking regulations.
Multivariate analyses including covariates (age, gender, workplace smoke
exposure, and cigarette smoke exposure in the home) will be conducted to
further examine the relationship between tobacco control laws and ETS
exposure and the lack of variability in cotinine levels by tobacco control
laws among non-Hispanic blacks.
ISEE-7
EXPOSURE TO CARBON MONOXYDE DURING RECREATIONAL
INDOOR KARTING
Benoit
Le vesque,*
David
Bellemare,
Guy
Sanfac on,*
Jean-Franc ois Duchesne, Henri PrudHomme. *Institut national de
sante publique du Que bec; Programme sante au travail, CLSC
Haute-Ville; Unite de recherche en sante publique, Centre Hospitalier
Universitaire de Que bec; Direction re gionale de sante publique de
Que bec
Introduction: The use of motorized vehicles indoors is likely to generate
contamination from combustion products, particularly carbon monoxide
(CO). Many papers described high CO concentrations in indoor skating
rinks during their daily activities (hockey, figure skating) or during special
exhibitions events (Moto-cross, Monster truck exhibition). Karting is a
sport which increases in popularity. It is performed outdoors but also
indoors. There are no data in the literature about the body burden of CO
induced by the practice of indoor karting.
Methods: After signing a consent form, 10 male (age: 15 to 49 years
old) non smokers participated in the study. They had to race for 45
minutes, the maximum length of time for a race in the centre visited. To
evaluate the CO body burden, the alveolar CO (alvCO) was measured
within 5 minutes before and after the race. With the method used, 5.4
ppm alvCO 1% COHb. The difference between the two results
represented the body burden of CO during the race (Delta alvCO).
Ambient concentrations of CO were measured continuously from the start
to the end of the race with two detectors located at each half of the track.
Results: Mean level of ambient air concentrations was 41 ppm for the 45
minutes of exposure during the race. Mean level of alvCO for the racers
before and after the race were respectively 8.0 ppm (SD 1.6) and 24.2
ppm (SD 2.8) for a Delta alvCO of 16.2 ppm (SD 3.1).
Discussion: In evaluating the exposure of the population and the
acceptability of the results in a public health perspective, one must
consider the duration of exposure and the intensity of the activity of the
persons exposed. The World Health Organisation suggests to protect the
general population to limit exposure to CO to maintain the blood COHb
concentrations under 2.5%. When exposed to a mean of 41 ppm in
ambient air, the mean of Delta alvCO was 16.2 ppm (3% COHb) for the
subjects of this study: almost the same value predicted by the Coburn
model for a subject doing heavy physical work for the same time and the
same exposure. Therefore, based on the same model, we suggest a
reference limit of 25 ppm, an exposure that would correspond to a COHb
concentration of 2.2% for an exposure of 60 minutes for a subject doing
heavy physical work.
Abstracts
ISEE-8
AIR POLLUTION EFFECTS ON FIBRINOGEN, HIGH-SENSITIVITY
C REACTIVE PROTEIN, AND MUCOPROTEIN IN TRAFFIC
CONTROLLERS
Ubiratan P. Santos,* Luiz A.A. Pereira, Chin A. Lin, Marcos Ribeiro,*
Paulo H.N. Saldiva, Dirce M.T. Zanetta, Alfe sio L.F. Braga,
Mario Terra-Filho*. *Division of Respiratory Diseases, Heart Institute
(InCor), University of Sa o Paulo Medical School Clinics Hospital;
Laboratory of Experimental Air Pollution, University of Sa o Paulo
Medical School; Department of Epidemiology and Public Health, Sa o
Jose do Rio Preto Medical School; Environmental Pediatrics Program,
University of Santo Amaro Medical School; and Laboratory of
Experimental Air Pollution, University of Sa o Paulo Medical School,
Brazil
Abstract: Air pollutants are related with cardiovascular morbidity and
mortality.
Objective: In order to investigate the effects of urban air pollutants on
blood markers for cardiovascular risks (fibrinogen, high-sensitivity C
reactive protein -HSCRP, and mucoprotein) we carried out a panel study
with 48 traffic controllers working in high traffic avenues in Sa o Paulo
City.
Methods: All participants were males, mean age of 39.2 years ( 6.4),
non-smokers, with at least complete high school education, and healthy.
Blood samples were collected in working days, in three different periods:
August 2000 (winter), January/February 2001 (summer), and August 2001
(winter), corresponding to different mean levels of air pollutants exposure.
Linear regression models with generalized estimating equations (GEE)
were used to assess the effect of particulate matter with an aerodynamic
diameter less than 10 mm (PM10), CO, SO2, NO2, and O3 on the blood
markers, controlling for temperature, humidity, age, and body mass index.
Results: CO, SO2, PM10, and O3 where associated with changes in
blood markers. In general, the effects presented short time lags. An
interquartile range increase of CO (1.1 ppm) was associated with an
increase of 25.78 mg/dl on fibrinogen (95% CI: 8.12 43.44), increase of
1.66 mg/l on HSCRP (95% CI: 0.09 3.23), and 0.28 mg/dl on
mucoprotein (95% CI: 0.02 0.42). An interquartile range increase of SO2
(9.6 mg/m3) was associated with an increase of 0.49 mg/dl on
mucoprotein (95% CI: 0.28 0.70), increase of 1.48 mg/l on HSCRP (95%
CI: 0.222,74). An interquartile range of PM10 (33.6 mg/m3) was
associated with increases of 0.34 mg/dl on mucoprotein (95% CI:
0.01 0.67). An interquartile range increase of O3 (42.6 mg/m3) was
associated with increase of 0.25 mg/dl on mucoprotein (95% CI:
0.08 0.42).
Conclusion: In Sa o Paulo City, primary pollutants presented positively
association with, at least, one of the blood markers of cardiovascular risk.
These results are in agreement with other studies focusing the same
endpoints and with our studies that showed air pollution effects on heart
rate, blood pressure and other blood markers in the same population. Also,
they reinforce the epidemiological association between air pollution and
cardiovascular deaths reported in time-series studies.
This study was funded by: InCor, LIM05-FMUSP, and UNISA.
ISEE-9
A PANEL STUDY OF SHORT TERM VARIATION IN AIR
POLLUTION AND INFLAMMATORY MARKERS IN BLOOD
Lars Modig,* Kurt Boman,* Bertil Forsberg,* Jan-Ha kan Jansson,*
Jo rn Nielsen, Bengt Ja rvholm*. *Department of Public Health and
Clinical Medicine, Umea University; Occupational and Environmental
Medicine, Lund University
S17
Abstracts
Abstract: Studies of short term effects of air pollution have for many
years been focused on respiratory effects. Nevertheless, recent studies
have shown that a major impact on mortality caused by air pollution is
due to cardiovascular deaths.
The aim of this panel study was to investigate the relation between
fluctuations in air pollution levels and two inflammatory markers in blood;
fibrinogen and CRP, which are known risk factors for cardiovascular
disease. The study was conducted in a mid sized Swedish city (Va xjo )
during the three first moths of year 2003.
Continuous measurements of PM10, PM2.5 and NO2 were performed in
an urban background station placed in a park in the city centre. The study
panel consisted of 40 females, aged 30-65 (mean 46) years of age and all
working at the same hospital. Blood samples were taken at 5 occasions
during days with high and low predicted pollution levels. Each occasion
was chosen based on the trend in PM concentrations and temperature
observed during previous days. The participants were notified one day
before sampling, and all testing was performed by a nurse at the hospital.
Air pollution levels during the study were moderate. In total 192 blood
samples were analysed. The fibrinogene and CRP results were first
inspected by plotting the ratio between each participants level at each
occasion and the mean level of all occasions against the measured
pollution levels (two day average). For fibrinogen the results revealed a
slight increase in the ratio when plotted against NO2, but no similar trend
was found for particulates. A single pollution model, with individual
intercept and adjusted for reported infections, was used to further analyse
the relation between NO2 and fibrinogen and CRP, respectively. The
estimated beta-coefficients were 0.003 and 0.013 but insignificant.
In this study we found no significant relations between short term
exposure to air pollution and increased levels of fibrinogen or CRP in
blood. One limitation in the study so far is the use of data from only one
measuring station. A further analysis will be based on data from
dispersion models which will increase the precision in the exposure
assessment. In addition other measures of particles will be used.
ISEE-10
DOES DEATH DUO TO MYOCARDIAL INFARCTION INCREASE
AFTER 1 HOUR OF A HIGH CONCENTRATION OF SPM?
ANALYSIS OF HOURLY MEASURED AIR POLLUTION DATA
FROM TOKYO
Yoshitaka Murakami, Masaji Ono. National Institute for Environmental
Studies
Introduction:
To investigate the short-term effects of a high
concentration of suspended particulate matters (SPM) on the risk of death
from myocardial infarction (MI), we examined hourly measured air
pollution data in Tokyo from 1990-1994.
Methods: Mortality data of myocardial infarction (ICD9:410) were
obtained from the Vital Statistics of Japan. Air pollution and
meteorological data were obtained from the database of the National
Institutes for Environmental Studies and from the Japan Meteorological
Agency. In Japan, SPM is used as the criterion for pollutant particulate
matter, with a diameter less than 10 um (intermediate to that of PM10 and
PM2.5). The data of the Tokyo metropolitan area (including 23 wards and
12 cities) from 1990 to 1994 were used for the examination. To determine
the effect of 1 hour of a high concentration of SPM on MI deaths, we
defined: 1) the level of high concentration of SPM; and 2) an effect
period after the SPM high concentration. We defined a threshold value as
200 ug/m3 or 300 ug/m3 from a distribution of SPM from 1990 to 1994.
An effect period was defined as the subsequent time (3 hours to 120
hours) after SPM concentration exceeded threshold value. Deaths
occurring during the effect/non-effect period were divided by the periods
person-hours, and risk ratio (effect periods risk divided by non-effect
S18
periods risk) was calculated. A Poisson regression model was used to

adjust for the effect of temperature, hour of death, and region (Tokyo
metropolitan ward or city). Temperature was treated as a single variable in
the model using the average temperature prior to the period that death
occurred. We determined the effect of temperature on MI deaths using
several models with temperature averaged over different time periods.
Results: The risk ratio with a SPM threshold value of 300 ug/m3 was
larger than the risk ratio with a threshold value of 200 ug/m3. The risk
ratio varied according to the duration of the effect period. When the
threshold value was 300 ug/m3, the risk ratios were 1.14 (95% CI:
0.88 1.49), 1.12 (95% CI: 0.911.38), 1.05 (95% CI: 0.89 1.23), 1.06
(95% CI: 0.931.19) and 1.07 (95% CI: 1.011.15) when the effect
periods were 3, 6, 12, 24 and 120 hours, respectively. Changing the
duration of the period over which temperature was averaged in the model
had a subtle influence on the risk ratio.
Conclusions: We showed increased risk of MI death in the short period
after a high concentration of SPM, especially 3 6 hours after a high
concentration of SPM.
ISEE-11
THE ROLE OF ULTRAFINE PARTICLES AND OTHER TRAFFICRELATED POLLUTANTS ON ISCHEMIC HEART DISEASES:
MAIN RESULTS OF THE HEAPSS PROJECT
Francesco Forastiere,* Pasi Aalto, Tom Bellander, Niklas Berglind,
Daniela dIppoliti,* Markku Kulmala, Timo Lanki, Fredrik Nyberg,
Pentti Paatero, Juha Pekkanen, Annette Peters, Sally Picciotto,*
Massimo
Stafoggia,*
Jordi
Sunyer,**
Pekka
Tiittanen,
Stephanie Von Klot, Roberto Elosua**. *Dept. Epidemiology, ASL RME;
University of Helsinki; Dept. of Occupational and Environmental
Health, Stockholm County Council; Institute of Environmental Medicine,
Karolinska Institutet; KTL-National Public Health Institute; GSFNational Research Center for Environment and Health; **IMIMMunicipal Institute for Medical Research
Background:
Health Effects of Air Pollution on Susceptible
Subpopulations (HEAPSS) is an EU-funded study of the effects of air
pollution on cardiac health in five European cities characterized by
different air quality and climates. It aimed to determine acute effects of
air pollution on: 1) fatal non-hospitalized coronary events; 2) hospitalized
acute myocardial infarctions (AMI), as well as; 3) re-hospitalizations for a
new AMI or any cardiac cause; and 4) late mortality, in AMI survivors (a
hypothesized susceptible subpopulation).
Methods: Hospital discharge records and AMI registries identified
26,888 AMI patients, 1992-2000. In one city, data on 5,144 out-ofhospital coronary deaths were collected. Mortality and hospital
readmissions (for acute myocardial infarction and other cardiac causes)
were assessed in follow-ups of 28-day survivors. PM10, CO, NO2, NO,
SO2, and O3 were collected for each city from existing networks of fixed
monitors. Particle Number Concentration (PNC) was measured for one
year (using condensation particle counters) and retrospectively estimated
for the study period. City specific time series analyses with Poisson
regression were conducted. Results were pooled using fixed or random
effects models.
Results: Estimated PNC (unit: 10,000 particles/cm3) and CO (unit: 0.2
mg/m3) at immediate lag showed the most consistent results. PNC (2.8%
increase, 95% CI 1.1-4.6%) and CO (1.0% CI 0.3-1.8%) were
strongly associated with out-of-hospital coronary events. Hospitalizations
for first AMI were weakly associated with PNC and CO. The associations
were stronger in the three cities using hospital discharge records and no
upper age limit: PNC was associated with 1.3% (CI 0.0-2.6%) and CO
with 0.7% (CI 0.1-1.2%) increase in first MI hospitalizations, and the
strongest associations were observed among persons aged 65 and over.
There was variation between cities with respect to effect modification by

age. PNC (2.6%, CI 0.5-4.8) and CO (1.4%, CI 0.1-2.6%) were
associated with cardiac readmissions among myocardial infarction
survivors in the five cities. Air pollution was weakly associated with allcause mortality in AMI survivors, with considerable heterogeneity
between cities. In the two centers using AMI register data, an association
was found for both PNC (7.0%, CI 2.0-12%) and CO (6.0%, CI 012) at lag 0-1.
Conclusions: Air pollution from traffic is associated with out-of-hospital
coronary deaths, hospitalizations for myocardial infarction, and subsequent
cardiac readmissions among AMI survivors. Weak and inconsistent results
were found for total mortality. Differences in air pollution levels, age and
sex structure, and treatment practices among centers might explain the
heterogeneity of the results and require further analysis.
Funded by EU (QLK4-2000-00708).
Abstracts
analyses will examine pollution associations with the counts of

arrhythmias within each visit, and will examine confounding and synergy
among pollutants.
This work is supported by funding from the NIH/NIEHS (ES-09825), U.S.
EPA
(R826780-01-0,
R827353-01-0)
and
the
U.S.
DOE
(EP-P4464/C2166).
ISEE-13
CARDIOVASCULAR DISEASE HOSPITALIZATIONS AMONG
MEDICARE ELDERLY AND PARTICULATE MATTER AIR
POLLUTION IN 6 U.S. CITIES
Lynn Disney, Case Western University, OH
ISEE-12
ASSOCIATIONS BETWEEN CARDIAC ARRHYTHMIA AND
AMBIENT AIR POLLUTANTS IN AN ELDERLY POPULATION
Stefanie T. Ebelt,* Helen H. Suh,* Brent A. Coull,* Joel Schwartz,*
Peter H. Stone, Diane R. Gold. *Harvard School of Public Health;
Cardiovascular Division, Brigham and Womens Hospital, Harvard
Medical School; The Channing Laboratory, Brigham and Womens
Hospital, Harvard Medical School
Introduction: Cardiovascular mortality and morbidity has been strongly
associated with ambient air pollutant concentrations in numerous
epidemiological studies. A proposed mechanism by which particles exert
their effects involves autonomic nervous system dysfunction, which may
lead to arrhythmia. Here we examine air pollution-induced cardiac
arrhythmia in an elderly population.
Methods: 32 non-smoking older adults (mean age 70.8 years, 3 male,
29 female) participated in a repeated measures study during the summer
and fall of 2000. The cardiovascular health of each participant was
assessed weekly for 24 weeks following a standardized protocol that
included continuous EKG measurements through 5-minute intervals of
supine baseline rest, standing, exercise outdoors, supine second rest and
deep breathing. For each part of the protocol, EKG data were analyzed for
counts of supraventricular ectopy (SVE) and ventricular ectopy (VE).
Ambient hourly PM2.5, gases and meteorological parameters were
collected at a central site within one mile from participant residences and
clinic rooms. Logistic mixed effects regressions predicting the presence of
arrhythmia were performed for the entire protocol and for each interval,
controlling for subject, apparent temperature and time trend, for pollutant
lags up to 24-hours and moving averages up to 120-hours prior to the
health assessment. Results were scaled to interquartile range (IQR)
differences in pollution.
Results: Over the 24-week study period, a total of 645 participant visits
were conducted. Mean counts for SVE (2787) and VE (2892) over the
protocol varied strongly by subject, with subject-specific means between
0-363 for SVE and 0-350 for VE. The odds of having an arrhythmia were
most strongly associated with PM2.5, O3 and NO2, and were weaker for
CO, NO and SO2. For SVE, both short- and long-term exposures appeared
important. For example, while standing, significant O3 odds ratios (OR) of
up to 3.80 (95% CI: 1.89-7.61, IQR38.5 ppb) were observed in the 1421 hours prior to the health assessment, as well as for the mean 48-hours
prior (OR3.50, 95% CI: 1.62-7.55, IQR21.7 ppb). For VE, long-term
exposures appeared the most important, with an OR of 1.72 (95% CI:
1.02-2.92, IQR11.2 ug/m3) for 96-hour PM2.5 and an OR of 5.68 (95%
CI: 1.78-18.12, IQR21.4 ppb) for 96-hour O3.
Discussion: Results suggest that there is an increased risk of cardiac
arrhythmia with elevated ambient PM2.5 and O3 concentrations. Future
Introduction: The Harvard Six Cities study was seminal in establishing

the link between particulate air pollution and premature mortality. It has
been reviewed and reanalyzed numerous times finding similar results. In
this study, the same cities were studied examining hospitalization rates
among the Medicare elderly ( 65).
Methods: Zip codes corresponding to the 6 cities (Watertown, MA;
Topeka, KS; Portage, WI; Harriman, TN; Steubenville, OH and St. Louis,
MO) were identified from the U.S. Postal Service. Medicare eligible
beneficiaries who resided in the six Harvard cities were selected from the
1989 denominator files. The cohort was restricted to white residents over
age 65 who were not enrolled in an HMO in 1989. Hospitalization data
(Part A) were merged by HCFA claim number. CVD (ICD-9 400.0-440.0)
admissions were then identified among these beneficiaries for 9 years after
cohort year (1989-1997). The first identified hospitalization with ICD-9 in
the specified range was coded as a CVD admission. CVD admission
compared to no CVD admission was analyzed using logistic regression
analysis. Age at baseline in 1989, sex and high school graduation rates
were all measured confounders. High school graduation rates were
obtained from zip code level census data.
Results: 149,634 white residents over age 65 were identified. The
demographic distribution of the study population is displayed below.
Table 1. Demographics of Study Population
Number
%Female
%Not HS graduate
MA
5,015
65.3
16.2
TN
3,811
58.5
32.0
OH
5,792
61.1
27.9
WI
2,036
58.1
21.6
KS
15,421
63.0
14.7
MO
117,559
64.0
23.4
In all, 90,360 hospitalizations were identified for CVD from 1989-1997.
The logistic regression results are shown graphically in Figure 1.
Discussion: The observed results showing the association between
cardiovascular diseases and fine particulate matter are very similar to
those observed by Dockery et al. The area with the highest levels of
particulate matter also had the highest probability of admission for CVD.
Similarly, residence in Portage, WI and Topeka, KS are at the lowest risk
of CVD admission. This study supports that of others that fine particulate
matter may contribute to the prevalence of CVD. The main disadvantage
of this study is the lack of direct measurement of confounding variables.
Key to this analysis is lack of information on places of residence and
personal risk factors such as cigarette smoking, obesity and occupational
exposures. These results show that claims data can be used to support
population based studies of environmental risks.
S19
Abstracts
Discussion: Our findings suggested that exposures to traffic-related air

pollutants in urban environment, such as NO2 or CO, are associated with
decreased HRV in susceptible population.
FIGURE 1. Odds Ratios from Logistic Regression Model v. Fine

Particulate
ISEE-14
EFFECTS OF NITROGEN DIOXIDE ON HEART RATE
VARIABILITY
Chang-Chuan Chan,* Kai-Jen Chuang,* Ta-Chen Su, Lian-Yu Lin.
*Institute of Occupational Medicine and Industrial Hygiene, College of
Public Health, National Taiwan University; Department of Internal
Medicine (Cardiology Section), National Taiwan University Hospital
Introduction: Although many studies have shown decrease in heart rate
variability (HRV) was associated with particulate air pollutants, relatively
few studies have investigated its association with gaseous air pollutants.
Objective: This study was to examine the relationship between nitrogen
dioxide (NO2) and HRV in the elderly population.
Methods: We used a panel study to investigate short-term effects of air
pollution on HRV. Our study subjects are 83 patients (mean age 61) from
the cardiology section, Department of Internal medicine, National Taiwan
University Hospital in Taipei. Continuous ambulatory electrocardiographic
(ECG) monitoring was performed on each study subject, which measured
time and frequency domains of HRV, such as standard deviation of
normal-to-normal (NN) intervals (SDNN) and the square root of the mean
of the squared differences between adjacent NN intervals (r-MSSD), high
frequency (HF, 0.15-0.40 Hz) low frequency (LF, 0.04-0.15 Hz). NO2 and
other co-pollutants, such as sulfur dioxide (SO2), carbon monoxide (CO),
ozone, PM10 (particulate matter less than 10 um in diameter) and PM2.5
(particulate matter less than 2.5 um in diameter) measured at each
subjects close-by monitoring stations were used to represent personal
exposure. We used linear mixed-effects models in single pollutant and
multiple pollutant models to estimate the relationship between air
pollution and log10-transformed HRV. Potential confounders, such as
subjects age, sex, body mass index (BMI), disease status of coronary
heart diseases, smoking status, and ambient temperature were also
adjusted in all models.
Results: Single pollutant models showed that NO2 is the most consistent
air pollutants responsible for both time and frequency domains of HRV
decreases among all air pollutants. Such effects occurred at 1 to 4-hour
moving averages. CO is also responsible for decreases in SDNN, r-MSSD,
LF, and HF at 1-hour moving CO average. By contrast, we found no
associations between HRV and PM2.5, PM10, SO2, or ozone. Multiple
pollutant models with NO2 and CO further showed that NO2 was
responsible for SDNN decreases at 1 to 4-hour moving NO2 average after
controlling confounders. The models showed a 1ppb increase in NO2
exposure with 1-4 hour moving averages was associated 0.08-0.17%
decreases in SDNN.
S20
ISEE-15
CAN THE PM2.5-INDUCED HEART RATE VARIABILITY
CHANGES BE PREVENTED? RESULTS FROM A RANDOMIZED
STUDY OF FISH AND SOY OIL SUPPLEMENTATION
Fernando
Holguin,*
Mara
Tellez-Rojo,
Mariana
Lazo,
Abigail
Manzano,
Marlene
Cortez,
Mauricio
Hernandez,
David Mannino, Stephen Redd, Pierre Julien, Marie-Claire Belanger,
Isabelle Romieu. *Emory University Department of Medicine and
Centers for Disease Control; Instituto Nacional de Salud Publica;
Centers for Disease Control; Laval University, Lipid Research Center,
Quebec
Introduction: Supplementation with omega-3 fatty acids is associated
with increased heart rate variability. However, it is unknown whether
omega-3 fatty acids can prevent or lessen the reductions in heart rate
variability associated with environmental exposure to PM2.5.
Methods: Nursing home residents in Mexico City were followed for 5
months with alternate 6-min heart rate variability (HRV) measurements
and simultaneous monitoring of daily indoor and outdoor 24-h average
levels of PM2.5. After 1 month of follow up, participants were
randomized to receive 2 gr/day of fish oil (85% Eicosopentanoic acid and
Docosahexaenoic acid) in divided doses vs 2 gr/day of soy oil (6.78%
alpha-Linolenic acid). We used a mixed effects model to estimate the
effect of the same-day PM2.5 on HRV parameters, and adjusted the
model for age, gender and HR and an interaction term for fish and soy
oil.
Results: A total of 50 subjects were enrolled in the study. The average
age was 81 years (65-95), and 35% were male. During the study, the
levels of PM2.5 were: 19.18 g/m3 (SD 10.46) (5.09 106.6). A total of
1610 HRV measurements were done during follow up. The concentration
of omega-3 (in red cell membranes) increased from 6.4 to 13.5% in the
fish oil group (p0.01) and from 7 to 8.8% (p0.04) in the soy oil
group. Pre-randomization, exposure to same-day PM2.5 was associated
with a significant reduction in the high frequency (HF) HRV component
coef 0.034 (p0.01) and SDNN (standard deviation of normal to
normal heart beats) coef 0.013 (p0.01). Fish oil supplementation
prevented the reduction associated with same exposure to PM2.5 in the
HF-HRV (coef 0.0021; p0.5) and SDNN (coef 0.0005; p0.6)
parameters. Soy oil supplementation did not prevent reductions in HFHRV (coef 0.008; p0.01); however, it prevented the reduction in
SDNN (coef 0.0025; p0.11).
Conclusions: This is the first study to show that the cardiac autonomic
response to ambient PM2.5 in the elderly can be prevented by
supplementation with omega-3 fatty acids, and to a lesser extent with
alpha-Linolenic acid (which is partially metabolized to omega-3 fatty
acids) in soy oil.
ISEE-16
ARRHYTHMOGENESIS
IN
HUMAN
RESPONSE
TO
PARTICULATE AIR POLLUTANTS
Jiu-Chiuan Chen,* Peter H. Stone, Joel Schwartz,* Jee-Young Kim,*
Robert F. Herrick,* David C. Christiani*. *Department of Environmental
Health, Harvard School of Public Health; Cardiovascular Division,
Brigham and Womens Hospital
Introduction: Epidemiologic studies have shown that exposure to
particulate matter (PM) increased arrhythmia-related mortality and
morbidity. Patients with arrhythmia are also found to be more sensitive to
the PM-mediated acute cardiac effects. Although these epidemiologic

observations are supported by results of many animal studies, direct
human data so far have only provided evidence supporting the
contribution of arrhythmia to population susceptibility.
Methods:
We investigated whether particulate pollutants result in
arrhythmogenesis in a short-term prospective study of 10 male
boilermakers (age 34.38.1 years) with no overt cardiac diseases. They
were exposed to high levels of metal particulates in their workplace.
Episodes of extrasystoles within each 5-minute epoch were determined by
validated algorithms across 24-hour Holter recordings. The PM2.5 (PM
with aerodynamic diameter 2.5 um) levels were monitored concurrently
using personal air samplers. Information on the time profile of daily
activities was retrieved from detailed diary records. We used
autoregressive logistic regression to model the probability of extrasystoles,
and employed autoregressive Poisson regression to estimate the average
counts of premature complexes. Supraventricular and ventricular
extrasystoles were analyzed separately.
Results: The cross-shift average PM2.5 level was 1.78 1.25 mg/m3.
Of all the recorded 5-min epochs, 7.6% (95% CI: 6.3, 9.1) had
supraventricular extrasystoles and 23% (95% CI: 19, 28) had ventricular
extrasystoles. Within each positive recording, the average number of
extrasystoles was 1.6 (ranging from 1.3-1.9) per 5-min for
supraventricular beats and 5 (ranging from 4.0 to 6.5) per 5-min for
ventricular beats. We found a statistically significant association between
exposures to PM2.5 and the increased extrasystole frequency. For each
1-mg/m3 increase in the preceding 4-hour average concentration of
PM2.5, the associated OR was 1.82 (95% confidence interval CI: 1.52,
2.17) for having supraventricular extrasystoles, and the frequency of
supraventricular premature beats increased by 72% (95% CI: 52, 94). For
each 1-mg/m3 increase in the preceding 6-hour average concentration of
PM2.5, the associated OR was 1.58 (95% CI: 1.18, 2.12) for having
ventricular extrasystoles, and the frequency of ventricular premature beats
increased by 21% (95% CI: 10, 32). After adjusting for circadian rhythm
(morning, afternoon, evening, night), sleeping, smoking, alcohol use,
coffee drinking, 5-min average heart rate, and personal coronary risk
profiles, we observed a consistently positive association between PM2.5
and supraventricular extrasystoles. The adjusted analyses revealed a
slightly stronger association between PM2.5 and the probability and
frequency of ventricular premature complexes.
Discussion: These results provide significant evidence indicating that
high levels of metal particulates may induce extrasystoles in healthy
working men without overt heart diseases.
This abstract is funded by the NIH grant (ES 09860). Dr. J.C. Chen was
supported by the Liberty Mutual-Harvard Program for Occupational
Safety and Health.
ISEE-17
CARDIOVASCULAR EFFECTS OF AIR POLLUTION IN ADULTS
O, SA
O PAULO, BRAZIL
IN CUBATA
Luiz Alberto Amador Pereira,* Gleice Margarete de Sousa Conceic a o,
Alfesio L.F.Braga. *Catholic University of Santos; Brazil; Department
of Internal Medicine, Federal University of Sa o Paulo School of
Medicine; Program of Community Health, Catholic University of Santos;
and Environmental Pediatrics Program University of Santo Amaro School
of Medicine
Abstract: Cubata o is a southeast seaboard Brazilian city that has a very
important industrial center with a steel mill, several petrochemical and
chemical industries, surrounded on three sides by mountains that interfere
in air pollution dispersion. Because of that, the region was called in the
80s of the XX Century the Valley of Death. Since then, some air
Abstracts
pollution control policies were adopted in order to decrease air pollution

level.
Objective: A time-series study was conducted to estimate air pollution
effects on cardiovascular (CVD) hospital admissions using records from
Brazilian public health system for people older than 30 years of age, in
the city of Cubata o, from 1997 to 2000, and air pollution and weather
data provided by Sa o Paulo State Environmental Agency.
Methods: We performed analysis for the whole group and for two
sub-groups: people from 30 to 64 years and older than 64 years of age.
We adopted generalized linear Poisson regression single-pollutant models
to assess the effects of PM10, CO, NO2, SO2, and O3 on CVD
controlling for seasonality (long and short-term trends) and weather
variables using a semi-parametric smoother (loess). We adopted more
stringent convergence parameters than the S-PLUS software default. The
eight days cumulative effects of air pollutants were assessed using thirddegree polynomial distributed lag models.
Results: PM10 was positively associated with cardiovascular diseases for
two age groups: 30 to 64 years of age and older than 64 years of age. An
interquartile range increase on PM10 concentration (40g/m3) was
associated with increases of 16% (95% CI &endash; 1;30) and 21% (95%
CI&endash;3;38) in CVD admissions for the younger and the older age
groups, respectively. The associations of the other studied pollutants with
CVD were also positive but not statistically significant.
Conclusion: Despite of the polices adopted to reduce air pollution in the
City of Cubata o in the last two decades, this study showed that air
pollution has a remarkable impact on cardiovascular morbidity and
reinforces the necessity of additional air pollutant emission-controlling
polices in that area.
This study was funded by: UNISANTOS, CEACL-UNIFESP, LIM05FMUSP, and UNISA.
ISEE-18
THE EFFECT OF PARTICULATE AIR POLLUTION ON THE RISK
OF MYOCARDIAL INFARCTION IN ELDERLY: A MULTI-CITY
CASE-CROSSOVER ANALYSIS
Antonella Zanobetti, Gregory A. Wellenius, Ariana Zeka, Joel Schwartz.
Harvard School of Public Health
Abstract: Few studies have examined the acute effects of air pollution on
the occurrence of hospital admissions for myocardial infarctions (MI),
pneumonia, and chronic obstructive pulmonary disease (COPD), and these
have mostly been single cities studies. We conducted a multi-city casecrossover study of the acute effect of PM10 on the increased risk of being
admitted to the hospital among the elderly in twenty-four US cities.
We examined the association between daily particulate matter (PM10) and
Medicare data (age GE 65) on hospital admissions from the emergency
room with a primary diagnosis of MI (ICD-9: 410), COPD (ICD-9: 490496, except 493) and pneumonia (ICD-9: 480-487), in those cities for the
years 1985-1998. In the first stage of the analysis, we applied a casecrossover design in each city with referent exposure days chosen using the
time-stratified approach such that exposures on the case day were
compared to exposures occurring every third day of the same month as
the case day. We controlled for apparent temperature and day-of-week in
the model. In the second stage of the analysis we combined the cityspecific estimates using a random effect approach.
We found that a 10 g/m3 increase in PM10 was associated with a 0.72%
increase (95% CI: 0.3, 1.1) in risk of admissions for MI on the same day.
When we analyzed COPD we found a 0.6% increase (95% CI: 0.1, 1.2)
for 10 g/m3 increase in PM10, while we found a 0.69% increase (95%
S21
Abstracts
CI: 0.4, 1.0) in risk of admissions for pneumonia and PM10 on the same
day.
We conclude that our analysis showed an increased risk of hospitalization
for MI, COPD and pneumonia associated with PM10. More studies are
needed to understand the biological mechanism and to examine effect
modification.
Founded by: EPA R82735301 and NIEHS ES00002
ISEE-19
AIR POLLUTION AND MARKERS OF CARDIOVASCULAR RISK
Antonella Zanobetti,* Joel Schwartz,* Paul M. Ridker. *Harvard School
of Public Health; Brigham and Womens Hospital
Abstract: Air pollution has been associated with increased risk of death
and hospital admissions all over the world. Many of those associations are
from cardiovascular disease, however the mechanism by which airborne
particles increases the risk of cardiovascular deaths is still being explored.
We looked at the effects of medium term and long term (annual mean) of
particulate air pollution (PM2.5), ozone (O3), carbon monoxide (CO), and
nitrogen dioxide (NO2), and changes in blood markers of cardiovascular
risk, including HDL cholesterol, triglycerides and C-reactive protein, in
the PRINCE study, a large, national randomized trial of the use of statins
to lower such risk factors. A total of 5778 participants were matched to
exposure from monitors in their county of resident.
We controlled for subject, trend, season, age, gender, race, body mass
index, education, smoking history, hormone replacement therapy, exercise,
and whether receiving a statin or a placebo.
We found a medium term (mean of the two previous months) effect
between C-reactive protein and PM2.5, CO, NO2, with an increase of
7.7% (95% CI: 0.96-14.96) for 10 mg/m3 of PM2.5, an increase of 3.8%
(95% CI: 0.3-7.3) for 5 ppm of NO2, an increase of 2.1% (95% CI: 0.14.1) for 0.5 ppm of CO. When we examined interactions with statin use
we found a higher increase in subjects on placebo.
We found a significant association between triglycerides and the mean of
the three previous months of ozone with an increase of 0.95% (95% CI:
0.1-1.8) for 5 ppm of O3. For the same time period for PM2.5, we found
that the association was almost entirely in the subjects not receiving
statins. In those subjects we found for the mean of the three previous
months an increase of 8.3% (95% CI: 1.2-15.8).
For HDL cholesterol we fund an association with a longer averaging
period (annual mean) of pollution, with a 3% increase (95% CI:-5.7- 0.3) for 10 mg/m3 of PM2.5 and a 1% increase (95% CI:-1.7- -0.3) for 5
ppm of O3.
These results present new the evidence of possible mechanism for the
association between air pollution and cardiac events, and the cancellation
of the effect by statins points to mechanistic pathways effected by statins.
Founded by: EPA R82735301 and NIEHS ES00002.
ISEE-20
EFFECTS OF PARTICULATE AIR POLLUTION ON MEAN
DECELERATION MAGNITUDE IN PATIENTS WITH CORONARY
HEART DISEASE: A NOVEL APPROACH TO ASSESS HEART
RATE FLUCTUATIONS
Angela Ibald-Mulli,* Regina Ru ckerl, Raphael Schneider, Axel Bauer,
Georg Schmidt, Josef Cyrys,* H.-Erich Wichmann,* Wojciech Zareba,
Annette Peters. *GSF-Insitute of Epidemiology and IBE Department of
Epidemiology, Ludwig-Maximilians-University Munich; GSF-Insitute of
Epidemiology; Working Group of Biological Signal Analysis, 1.
Medizinische Klinik, Technical University, Munich; Working Group of
S22
Biological Signal Analysis, Deutsches Herzzentrum Mu nchen, Department

of Adult Cardiology; Department of Medicine, University of Rochester
Abstract: Epidemiological studies on air pollution and cardiovascular
function showed adverse effects of particulate air pollution on
conventional parameters of heart rate variability (HRV). Between October
2000 and April 2001 a panel study with 58 coronary heart disease patients
was conducted in Erfurt, Germany to assess the association between
cardiac function and daily variations in particulate air pollution. In the
present analysis the mean deceleration magnitude (MDM), a new
parameter to characterise fluctuations in heart rate, was applied to assess
alterations in cardiac function associated with exposure to elevated levels
of particulate air pollution. MDM was calculated from 24 hour HolterECG recordings that were conducted once every four weeks in each
participant. Ambient exposure to particulate air pollution was measured at
a central site using an aerosol spectrometer covering the size range from
10 nm to 2.5 m. Elemental (EC) and organic carbon (OC) were
determined hourly from an ambient carbon monitor. Random effect linear
regression was used to model the association between individual 24-h
mean concentrations of particle mass and number concentrations and
MDM in a total of 254 recordings. Effects were adjusted for trend,
weekday, temperature, and relative humidity. Preliminary results based on
% change of mean MDM show a significant decrease in MDM in
association with fine (PM2.5, 2.5 m) and ultrafine particles (UFP,
0.1 m) as well as EC and OC. MDM decreased by 14.6% (95% CI:
6.2%, 23.0%) and 12.2% (95% CI: 4.2%, 20.1%) in association
with concurrent concentrations of EC and OC per increase in interquartile
range pollutant. In contrast to EC and OC, PM2.5 and number
concentrations of UFP showed larger effects on MDM with the
cumulative mean of particle concentrations measured from the end of the
recording up to 4 days prior to the recording (14.6% (95% CI:
5.0%,24.3%) and 12.3% (95% CI: 0.3%, 24.9%)). Previous
analyses on conventional HRV parameters such as SDNN or RMSSD in
the same study population observed smaller and less significant effects of
particles in particular with respect to ultrafine particles. Most recently a
decrease in MDM has been identified as a more powerful predictor of
mortality after myocardial infarction than predictors such as HRV or left
ventricular ejection fraction. The results indicate that MDM might be a
more sensitive parameter to assess adverse effects of particulate air
pollution on cardiac function than conventionally used parameters to
assess changes in heart rate fluctuations.
We would like to acknowledge the EPA Particulate Matter Center at the
University of Rochester, which is funded by the Environmental Protection
Agency (US-EPA STAR (Science To Achieve Results) Center Grant R827354) for funding the study.
ISEE-21
AMBIENT AIR POLLUTION AND ARRHYTHMIC EVENTS IN
PATIENTS
WITH
IMPLANTED
CARDIOVERTER
DEFIBRILLATORS, 1993-2002
Kristina B. Metzger,* Paige E. Tolbert,* Mitch Klein,* Jennifer L. Peel,*
W. Dana Flanders,* James A. Mulholland. *Rollins School of Public
Health, Emory University, Atlanta, GA; Georgia Institute of Technology,
Atlanta, GA
Abstract: To better understand specific cardiac responses to air pollution
and roles of various pollutants, the relationship of ambient pollutant levels
and tachyarrhythmic events was studied in patients with implanted
cardioverter defibrillators (ICDs). ICDs are electronic devices implanted in
patients at high risk for sudden cardiac death, ventricular tachycardia, and
ventricular fibrillation. The device continuously monitors the heart rate for
tachyarrhythmias, emits electrical pulses or shocks to convert the heart
back to normal sinus rhythm as needed, and records and saves data on
each tachyarrhythmic event, including the date and time of the event and
the type of therapy delivered. The medical records of ICD patients at
three electrophysiology clinics in a major U.S. city were examined to
collect patient and event information for the study period, January 1,
1993, to December 31, 2002. We studied the occurrence of
tachyarrhythmic events in these patients in relation to speciated PM data
from August 1, 1998, to December 31, 2002, and in relation to other air
quality data for the period 1993 through 2002. In preliminary analyses
through 2000, there were 570 patients, 335 of whom experienced at least
one tachyarrhythmic event, contributing 3677 event-days in almost
300,000 total follow-up days. We used repeated-measures unconditional
logistic regression, controlling for temporal trends, meteorologic
conditions, and the occurrence of recent events. For this period, a
statistically significant association was observed between tachyarrhythmic
events and ambient levels of carbon monoxide, coarse particles, and
PM2.5 organic carbon on the same day. Abstracting of event data for the
period through December 2002 is nearly complete. We estimate that there
will be 855 patients for the full study period, with approximately 5500
event-days. Results through 2002 will be presented.
ISEE-22
AIR POLLUTION AND INFLAMMATORY MARKERS IN BLOOD
Sara D. Dubowsky,* Diane R. Gold, Joel Schwartz,* Brent Coull,*
Helen Suh*. *Harvard School of Public Health; Channing Laboratory,
Harvard Medical School
Introduction: The adverse cardiovascular health effects of air pollution
may be caused in part by systemic inflammation triggered by oxidative
stress to the lungs. Recent studies have suggested that these associations
may be strongest for traffic-related particles. In order to examine the
associations between traffic-related particles and systemic inflammation,
we conducted a study in which a panel of senior citizens was exposed to
elevated traffic-related pollutant exposures through a series of bus trips.
Methods: Repeated blood samples were collected from forty-four nonsmoking participants living at one of four suburban independent senior
living facilities. Blood samples were obtained between April and June of
2002, approximately 18-hours after study subjects participated in a field
trip that included two hours aboard a diesel bus. Each subject participated
in approximately four field trips, about once every 3-weeks. Blood
samples were analyzed for red and white cell parameters using a CBC
with differential analyses. Samples were also tested for interleukin-6, creactive protein, intracellular adhesion molecule1, fibrinogen, and von
willebrands factor. Particulate exposures of the participants were assessed
using two mobile carts that followed the subjects throughout each field
trip. Micro-environmental exposure measurements included continuous
readings of fine particle mass (PM2.5), ultra-fine, fine, and coarse particle
counts, and black carbon. Carbon monoxide and nitric oxide
concentrations were also measured continuously during the bus rides.
These exposure measures were supplemented with ambient air
concentrations of gases, particle mass and number, and meteorological
parameters measured at a local USEPA-funded Supersite.
Results: Among the 138 blood samples analyzed, levels of circulating
inflammatory markers were found to be comparable to the values reported
by previous studies. Evaluation of the air monitoring data indicates that
the bus trips successfully elevated hourly exposures above levels observed
at the residence facilities and central site. The mean hourly black carbon
concentration during the bus trip periods was 3,400 (SD: 1,200) ng/m3 as
compared to mean hourly concentrations of 350 (SD: 450) ng/m3 during
facility periods and 750 (SD: 370) ng/m3 at the Supersite during times
concurrent with the bus trip. Measures of PM2.5 and particle counts were
also substantially elevated during periods when subjects were aboard the
bus. The impacts of these micro-environmental changes on circulating
Abstracts
inflammatory markers will be presented using the results of longitudinal

mixed models.
This work is supported by funding from the NIEHS (1P01E-ES09825-01),
USEPA (R827353-01-0), and EPRI (W09207-02).
ISEE-23
SHORT-TERM COMMUNITY AIR POLLUTION EXPOSURES
RELATED TO LEVELS OF CLOTTING FACTOR VIII INDICATIVE
OF ALTERED HEMOSTASIS IN AN ELDERLY COHORT
Helene Margolis,* Paul Enright, Dane Westerdahl,* John Robbins.
*California Air Resources Board; University of Arizona; University of
California, Davis School of Medicine
Introduction: The biological mechanisms that underlie the reported air
pollution-related excess risk of cardiovascular morbidity/mortality are
unknown; hypotheses include oxidative stress, altered hemostasis and/or
changes in autonomic function. The National Heart, Lung, Blood
Institutes Cardiovascular Health Study (CHS) is a population-based
longitudinal study of coronary heart disease and stroke among older
women and men. We initiated a CHS Ancillary Study in 1999 to evaluate
the subclinical and clinical effects of air pollution.
Objective: Evaluate relationship between short-term exposures to O3,
NO2, CO, SO2, PM10, PM2.5, PM10 2.5 and clotting factor VII (FVII) and
VIII (FVIII) levels.
Methods: Continuous enrollment of the main cohort between June 1989
and May 1990, and temporal variation in day-to-day pollutant levels
allows evaluation of short-term exposure effects. Baseline data were
obtained from the CHS for participants in Allegheny County, PA
(n1275), Forsyth County, NC (n1305), and Sacramento County, CA
(n1318). Air quality and meteorological data were obtained from the
U.S. EPA, CA Air Resources Board or U.S. National Climatic Data
Center. Various strategies were used to estimate exposures on days with
missing data. Gender-specific single-pollutant linear regression models
were used to evaluate effects of 24-hour average pollutant concentrations
averaged over exposure periods (EAP) of 2- days (day of exam and
previous day (L01)) or 7-days (day of exam and previous 6 days). Natural
log transformations of FVII and FVIII were required to meet model
assumptions. Final models were adjusted for age-at-exam, Community,
24-hour average temperature (L01), and (in FVII model only) 24-hour
average dew point (L01).
Results: Across the range of pollutant exposures experienced by the
cohort over the 1-year baseline period, small significant effects on
population mean levels of FVIII, but not FVII, were observed. A
3
10-g/m higher level of PM10 (7-day EAP) was associated with higher
FVIII levels among women (1.3% (95% CI: 0.12%, 2.6%)) and men
(1.5% (95% CI: 0.14%, 2.8%)). PM2.5 was also positively associated with
FVIII (women: 2.1% (95% CI: 0.6%, 3.7%); men 2.1% (95% CI: 0.5%,
3.8%)). Perhaps reflecting different mechanism(s)/kinetics of response,
among women, mean FVIII levels were inversely related to the 2-day
EAP for O3 (2.3% (95% CI: 4.3%, 0.23%) and PM10 2.5 (2.3%
(95% CI: 4.6%, 0.01%). PM10 2.5 (2d-EAP) was also inversely related
to FVIII among men (2.1% (95% CI: 4.9%, 0.73%). These results will
be discussed in the context of specific mechanistic hypotheses.
ISEE-24
ASSOCIATION OF SUBCLINICAL ATHEROSCLEROSIS (CAROTID
INTIMA MEDIA THICKNESS) WITH RESIDENTIAL AMBIENT
PM2.5 IN HEALTHY ADULTS
Nino Kuenzli,* Mike Jerrett, Bernie Beckerman, Wendy Mack,
Frank Gilliland, Duncan Thomas, John Peters. *University of
Southern California; USC
S23
Abstracts
Abstract: Long-term exposure to fine ambient particulate matter (PM2.5)

is associated with mortality due to cardiovascular disease (CVD) in
prospective cohort studies. The largest study (1) observed a 12% (8 15%)
increase in CVD death per 10 g/m3 PM2.5. The pathophysiologic
mechanisms that might underlie these associations are currently unknown,
but limited experimental evidence suggests that inhalation of PM leads to
pulmonary and systemic inflammatory responses. In a rabbit model, PM
inhalation was associated with the progression of atherosclerotic lesions.
Moreover, carotid artery intima-media thickness (IMT) in humans steadily
increases from childhood to death, and correlates well with all of the
major cardiovascular risk factors (smoking, LDL, blood pressure etc.), and
with coronary artery atherosclerosis. Studies also show a 5% higher
IMT to be associated with 510% higher rates of CVD events. We
hypothesize that exposure to ambient PM leads to increases in IMT and
may contribute thereby to increased mortality from CVD.
We used the baseline IMT measurements from two trials conducted in
healthy adults to investigate effects of Vitamin E and B on IMT. Between
1996 and 2003, carotid IMT was measured among 445 men and 356
women (age 40 89; mean: 59 yrs). Participants live across Southern
California. Residential zip codes were geo-coded to assign the zip code
centroid levels (1999) of ambient PM2.5, derived from a predictive PM2.5
surface (geostatistical kriging model; assigned exposures were mostly
within / 3 g/m3 of monitored values). We determined the crosssectional association of log-IMT with the individually assigned residential
PM2.5, with/without adjustment (age, sex, blood pressure, LDL, smoking,
estrogen replacement, education, prescriptions).
The average (SD) IMT was 0.755 mm (0.147). Individually assigned
ambient PM2.5 estimates ranged from 5.2 to 26.9 g/m3 (mean: 20.3).
For each 10 g/m3 increase in PM2.5, IMT increased by 5.6% (95% CI:
0.710.6%) unadjusted and by 3.8 to 4.6% in various multivariate
models (p-values 0.02 0.07).
This cross-sectional assessment, which considers only recent exposure
provides a first test of our hypothesis. These findings require corroboration
in larger samples, taking further potential confounders and effect modifiers
into account. Information on long-term, time-varying exposure to PM on
various spatial scales (region, neighborhood, residence, work place,
commute) and from various sources needs to be developed. Most
importantly, the association of air pollution and IMT progression also
needs to be investigated using longitudinal data.
(1) Pope et al., Circulation 2004; 109:719.
ISEE-25
DO SHORT-TERM INCREASES IN AMBIENT AIR POLLUTANTS
TRIGGER ARRHYTHMIA? A POPULATION-BASED STUDY
Yinkang Duan,* Duanping Liao,* Gerardo Heiss, Hung-mo Lin,*
Zhi-jie Zheng, Megan Darnell,* Xuejuan Jin*. *Penn State University
College of Medicine; University of North Carolina at Chapel Hill;
Center for Disease Control and Prevention
Abstract: An association between air pollution and cardiovascular disease
(CVD) mortality has been reported. One of the hypothesized
arrhythmogenic mechanisms is the impairment of cardiac autonomic
control by pollutants. We examined the short-term associations of ambient
pollutants (particulate matter 10 m in diameter PM10, O3, CO, NO2,
and SO2) with cardiac arrhythmias using data from the baseline
examination (19871989) of the population-based Atherosclerosis Risk in
Communities study. We calculated the following pollutant exposures oneday prior to each participants randomly assigned examination date: PM10,
CO, NO2, and SO2 as 24-hour averages, and O3 as an 8-hour average of
the hourly measures, from the EPAs Aerometric Information Retrieval
System (AIRS). We assessed the presence, frequency, and complexity of
arrhythmias from standardized 2-minutes EKG rhythm strips recorded
S24
during the baseline clinical examination. After excluding missing data on

the ambient exposure measurements, the effective sample sizes for PM10,
SO2, NO2, CO, and O3) were 4,001, 7,404, 7,427, 10,699, and 9,059
respectively. The prevalence of arrhythmias was 11%. Among persons
without any arrhythmia, the means (SD) of PM10, SO2, NO2, CO, and O3
measured as one day prior their ECG and clinical examination were 29.5
(12.3) g/m3, 0.005 (0.004) ppm, 0.018 (0.008) ppm, 1.35 (0.60) ppm,
and 0.040 (0.017) ppm, respectively. For persons with arrhythmias, the
means (SD) were 30.0 (13.0) g/m3, 0.005 (0.003) ppm, 0.017 (0.008)
ppm, 1.33 (0.59) ppm, and 0.040 (0.017) ppm, respectively. Logistic
regression models were used to adjust for CVD risk factors, demographic
and socioeconomic variables, and relevant meteorological variables to
obtain the odds ratios (OR) and 95% confidence intervals (CI) of the
presence of arrhythmias associated with one standard deviation increase of
each ambient pollutant: the OR for PM10, SO2, NO2, CO, and O3 were
1.00 (0.99, 1.01), 0.94 (0.86, 1.04), 0.98 (0.90, 1.06), 0.94 (0.84, 1.05),
and 1.00 (0.91, 1.11), respectively. The frequency and complexity of
arrhythmias were not associated with any of the pollutants analyzed. In
conclusion, no statistically significant association between short-term
increase in ambient pollutants and the presence of arrhythmias was
observed in this in healthy, middle aged population.
ISEE-26
THE ASSOCIATION BETWEEN AMBIENT PM2.5 AND
BIOMARKERS OF AIRWAY INFLAMMATION IN PATIENTS
WITH ASTHMA
Samantha De Leon,* Kazuhiko Ito,* Hsien-Wen Hsu, Joan Reibman,
George Thurston*. *NYU School of Medicine, Nelson Institute of
Environmental Medicine; NYU School of Medicine, Division of
Pulmonary & Critical Care Medicine
Abstract: Many studies have shown that individuals with asthma are
adversely affected by short-term increases in ambient Particulate Matter
(PM) levels in terms of decreased lung function, increased occurrence of
respiratory symptoms (such as wheezing and coughing), and increased
hospital admissions and mortality. However, not as many studies have
considered why patients with asthma are sensitive to increases in ambient
pollution levels. Airway inflammation is one of the characteristic
symptoms of chronic asthma and asthma severity; therefore, levels of
chemokines associated with the recruitment of leukocytes, such as
eosinophils, into the lung airways were used to investigate the health
effects of ambient PM on those with asthma. Serum levels of several
chemokines (Regulated on Activation, Normal T-cells Expressed and
Secreted RANTES, Eotaxin, Thymus and Activation-Regulated
Chemokine TARC, and Interferon gamma Inducible Protein of 10 KDa
IP-10) were measured every 2 weeks, over a 3-month period in adult
subjects with asthma residing in New York City during the summer of
2001. PM2.5 (PM less than or equal to 2.5 um) data was collected over
the same 3-month period, and daily weather data were obtained from the
weather station located at New York Kennedy International Airport. All
analyses were conducted using linear mixed-effects models assuming
random intercepts and slopes for each subject. Biomarker levels were
included in the regression model as raw variables (pg/ml). Of the four
chemokines examined, only RANTES showed an association with PM2.5.
There was a general positive trend between the same day PM2.5 and
RANTES levels, with one outlier that weakened the overall positive slope.
The effect of PM2.5 on RANTES levels was estimated in the mixedeffects models adjusting for hot and humid days, day-of-week effects,
hours spent in air conditioning, number of puffs of albuterol, and serial
correlation between observations for each individual. After removal of one
outlier, RANTES levels (raw variable) were found to be increased by
11321 pg/ml (z-statistic 2.34) per Inter-Quartile Range (IQR) of PM2.5
(14.36 ug/m3), which corresponds to a 17% increase based on the study

average of 66640 pg/ml. The results of this study suggest that chemokines
involved in airway inflammation in asthmatics, such as RANTES, can
increase in response to short-term elevations in ambient PM2.5 levels.
While controlled exposure experiments are needed to confirm these
results, they may provide insight into the mechanism(s) underlying asthma
exacerbations associated with acute episodes of increased ambient PM
levels.
ISEE-27
AIR POLLUTION AND ACUTE CARDIO-RESPIRATORY VISITS IN
AN AMBULATORY CARE SETTING: TWO YEAR AND
PRELIMINARY FOUR YEAR RESULTS
Amber H. Sinclair, Dennis Tolsma. Kaiser Permanente
Introduction: There is a lack of published research concerning the
possible associations between air pollution components and acute visits to
outpatient clinics. We investigated associations between various
components of air pollution and acute visits to clinics of a health plan in a
large urban area.
Methods: We used a time series analysis to determine the associations
between daily levels of suspended particulate matter and ambulatory care
acute visit rates during the 25-month period 8/1/98 to 8/31/00 and for the
four year period of 8/1/98 to 12/31/02. Acute visits of health plan
members to clinics with a respiratory diagnosis of asthma, COPD, upper
and lower respiratory infections (URI and LRI) and cardiovascular disease
were identified through electronic patient visit data. Pollutant data
included 24-hour measurements of PM2.5, coarse PM (2.510 um), PM10,
PM2.5 components (acidity, sulfates, OC, water-soluble transition metals
and elemental carbon), 10 100 nm PM area (ultra-fines), polar VOCs
(OHC); 8 hour maximum ozone; and 1 hour maximum NO2, CO and
SO2. Visit counts for each diagnosis group were modeled by air quality
metrics using general linear modeling, controlling for temporal trends and
meteorologic variables. Moving averages of the a priori 0 to 2 day lagged
air quality variables were investigated, as well as the 3 to 5 day average.
Results: For the 25-month data set, we found significant positive
associations for the 0 to 2 day lag for child asthma with OHC, URI with
ultrafine PM, and LRI with PM2.5 acidity and SO2. In comparison, we
found 14 significant positive associations for the 3 to 5 day lag: adult
asthma with ultrafine PM; child asthma with coarse PM, PM10, EC and
OC; URI with coarse PM; LRI with coarse PM, PM10, EC, OC and
PM2.5; and cardiovascular disease with NO2, CO and O3. There were
also a few significant negative associations. The magnitudes of the
significant risk ratios were less than 1.15. In addition to these findings,
preliminary results of the analysis of a four-year time-period of air quality
data will be presented.
Discussion: LRI and child asthma had the greatest number of significant
associations with air pollution, mainly for the 3 to 5 day lag structure, in
the 25-month data set. This study provides a unique evaluation of air
quality and health effects by investigating the relationships of air pollution
to uncommonly reported but readily measurable health effects.
This research was supported by a grant from the Electric Power Research
Institute (EPRI).
ISEE-28
ASSOCIATION BETWEEN FINE PARTICLES AND RESPIRATORY/
CARDIOVASCULAR ELDERLY HOSPITAL ADMISISONS IN NEW
YORK CITY
Kazuhiko Ito, Samantha De Leon, George Thurston. Nelson Institute of
Environmental Medicine, NYU School of Medicine
Abstracts
Abstract: Many studies reported associations between particlate mater

(PM)/gaseous pollutants and morbidity and mortality, but a question
remains as to what emission source types are responsible for the observed
associations. We examined associations between PM2.5/gaseous pollutants
(NO2, CO, SO2, and O3) and the cardiovascular and respiratory elderly
hospital admissions in NYC for period 1999 2001. The relationship
among PM2.5, gaseous pollutants, and weather variables were first
examined using cross-correlation functions (CCF) across seasons after
removing long-term and seasonal cycles. The associations between air
pollution and the elderly hospital admissions were examined in four
different ways: (1) single pollutant model; (2) two-pollutant model with or
without interaction terms; (3) single pollutant model stratified with the
level of a co-pollutant; and (4) model with factor-analysis derived
composite pollution indices. Poisson Generalized Linear Model was used
to estimate pollution effects, adjusting for temporal trends, day-of-week,
and temperature (quintile indicators with lags). The temporal relationships
between PM2.5 and NO2, SO2, or CO were relatively unchanged across
seasons with moderate to high (0.5 to 0.8) correlation. The short-term
correlation between O3 and PM2.5 was positive in warm season but
negative in cold season, apparently reflecting the association between cold
sunny clear day and O3 in winter. In single pollutant models, pneumonia
admissions were positively significantly associated with PM2.5 and CO
(percent excess 8% per 5th-to-95th percentile pollution increment for
both pollutants); COPD admissions were associated with CO (8%);
ischemic heart disease admissions were associated with NO2 and CO (6%
for both pollutants); and, heart failure admissions were associated with
PM2.5, NO2, and CO (9%, 9%, and 13%, respectively). Two pollutant
models generally resulted in attenuation of the risk estimates for one of
the pollutants while the other remaining significant without improving
model fit. In stratified analysis, PM2.5 risk estimates were larger for high
CO days than for low CO days for both pneumonia and heart failure
admissions. The factor-analysis derived components that represented the
common variation of PM2.5, NO2, and CO were not as good predictors of
these health outcomes as the individual pollutants. Overall, the pollution
mixture that includes PM2.5, NO2, and CO, likely traffic-related air
pollution, was associated with cardiovascular and respiratory elderly
hospital admissions in NYC.
This research was supported by U.S. EPA STAR grant (R827997010);
U.S. EPA Particulate Matter Health Research Center (R827351); and
NIEHS Environmental Health Center (ES00260).
ISEE-29
RELATIONSHIP BETWEEN GASEOUS AIR POLLUTANTS AND
CARDIOVASCULAR ADMISSIONS: A STUDY IN 14 SPANISH
CITIES
Ferran
Ballester,*
Paz
Rodrguez,*
Santiago
Pe rez-Hoyos,*
Juan Bellido, Federico Arribas, Carme Saurina, Inmaculada Aguilera,
Ana
Breznes,**
Margarita
Taracido,
Alvaro
Can ada,
Carmen In iguez* (EMECAS Group). *Valencian School of Studies for
Health-EVES; Miguel Herna ndez University; Departamento de Salud. C
Valenciana; Departamento de Salud. Arago n; Research Group on
Statistics, Applied Economics and Health (GRECS); Escuela Andaluza de
Salud Pu blica; **Departamento de Salud. C de Madrid; Universidad
de Santiago; Departamento de Salud. Asturias
Introduction: Since year 1997, the EMECAS project evaluates the effect
of current air pollution on the health of urban population in Spain. In this
paper we present the results for the association between gaseous air
pollution and hospital admissions for cardiovascular diseases.
Methods: Daily emergency admissions for all cardiovascular diseases
(CVS) (ICD-9: 390 459), heart diseases (HD) (ICD-9: 410 414, 427,
428); ischemic heart diseases (IHD) (ICD-9: 410 414), and
S25
Abstracts
cerebrovascular diseases (Stroke) (ICD-9: 430 438) were collected from

hospital records (19951999). Air pollutants data were obtained from local
networks. Variables for 24 hours daily levels of SO2, and NO2; 8 hours
maximum moving average of CO and ozone; and, lastly, 1 hour maximum
of SO2, NO2 and ozone were constructed. Magnitude of association in
each city was estimated using generalized additive models (GAM) of
Poisson controlling for confusion and overdispersion. Lagged effects, up
to three days, for each cause and pollutant were examined. Data were
analysed using S-Plus GAM function with more stringent convergence
criteria. Combined estimates were obtained under a fixed effects model,
and, if heterogeneity, under random effects one. For ozone the analyses
were restricted to the warm period (May to October).
Results: Concurrent and one day were the most consistent lags showing
associations, only ozone showed a more delayed relationship. In the
combined estimates an increase of 10 ug/m3 in SO2 daily levels was
associated with a 1.3% (95% CI: 0.22.5%) increase in the number of
hospital admissions for CVS, and 1.7% (95% CI: 0.72.9%) for HD. The
same increase in concentrations of NO2 was significantly associated with
a 0.4% increase in CVS, and 0.9% in HD admissions. For ozone the
corresponding estimates were 0.7 in both cases. An increase in 1 mg/m3
levels of CO was associated with an increase of 2.1% in CVS, and 4.2%
in HD admissions. Only ozone presented some suggestion of association
with stroke. In two pollutant models the coefficients of SO2 and NO2
were affected after control for other pollutants. On the contrary, CO and
ozone were unaffected by the inclusion of the second pollutant.
Conclusions: A short-term association between increases in daily levels
of air pollutants and the number of daily admissions for cardiovascular
diseases in the Spanish cities was found with greater estimates for heart
diseases. CO and ozone showed an independent effect of the other
pollutants.
EMECAS project has been supported by the Spanish Ministry of Health,
Fondo de Investigaciones Sanitarias (FIS 97/0051 and FIS 00/0010)
ISEE-30
URBAN
PARTICULATE
AIR
POLLUTION
AND
CARDIOVASCULAR ADMISSIONS IN SPAIN
Carmen Iniguez,* Paz Rodriguez,* Marc Saez, Antonio Daponte,
Elena Lopez, Teresa Martnez, Luis Cirera,** Laura Lo pez,
Inez Aguinaga, Ferran Ballester* (EMECAS Group). *Valencian School
of Studies for Health-EVES; University Miguel Herna ndez; Research
Group on Statistics, Applied Economics and Health (GRECS); Escuela
Andaluza de Salud Pu blica; Departamento de Salud. Canarias;
Departamento de Salud. Gobierno Vasco; Departamento de Salud.
Murcia; **Departamento de Salud. Madrid; Dep Salud. Ayuntamiento
de Pamplona
Introduction: The EMECAS project aims to evaluate the short-term
effects of air pollution on mortality and hospital admissions for
cardiovascular and respiratory diseases in Spain. We present the results of
the association between daily levels of particulate matter and the daily
number of cardiovascular admissions.
Methods: Data from fourteen cities accounting overall for 10 million
inhabitants were analysed. The number of daily emergency admissions for
all cardiovascular diseases (CVS) (ICD-9: 390 459), heart diseases (HD)
(ICD-9: 410 414, 427, 428); ischemic heart diseases (IHD) (ICD-9:
410 414), and cerebrovascular diseases (Stroke) (ICD-9: 430 438) was
obtained from hospital records. From local Air Pollution Networks we
collected data for the available particulate indicators, i.e., black smoke
(BS), total suspended particles (TSP), and PM10, and constructed variables
for 24 hours mean levels. The period of the study was 1995 to 1999.
Magnitude of association in each city was estimated using generalized
additive models (GAM) of Poisson controlling for confusion and
S26
overdispersion. For each cause lagged effects, up to three days, of each

pollutant were examined. Data were analysed using S-Plus GAM function
with stringent convergence criteria. Combined estimates were obtained
under a fixed effects model, and, if heterogeneity, under random
effects ones. Lastly, to explore potential confounding for the other
pollutants two-pollutant models were performed.
Results: Levels of PM10 ranked from 32 to 43 g/m3, BS from 18 to 80
g/m3; and TSP from 52 to 76 g/m3. Local estimates were, mostly,
positive and more consistent in lags 0 (concurrent day) and 1. Combined
estimates, expressed as the percent change in risk (and 95% confidence
interval) for an increase of 10 g/m3 particulate levels of lag 01 are
showed in the table below. In two pollutant models PM10 estimates were
not modified but BS and TSP were.
Particulate
indicator
Cities
(n)
CVS
HD
IHD
Stroke
TSP
0.07
(0.23; 0.36)
0.45
(0.04; 0.86)
0.29
(0.28; 0.86)
0.42
(1.03, 0.20)
Black
smoke
0.24
(0.18; 0.67)
0.71
(0.13; 1.29)
0.12
(0.69; 0.94)
0.49
(1.37; 0.39)
PM10
0.91
(0.35; 1.47)
1.56
(0.82; 2.31)
1.58
(0.09; 3.09)
0.76
(1.93; 0.41)
We found a short-term association between daily levels of

particulates and the number of daily admissions for cardiovascular
diseases in Spanish cities. The estimates were higher and more robust for
PM10 than for BS or TSP, with is a pattern of specificity in the effect:
greater estimates for hearth diseases than for all cardiovascular ones. No
effect with stroke has been found.
Conclusions:
The project was supported by the Spanish Ministry of Health, Fondo de

Investigaciones Sanitarias (FIS 97/0051 and FIS 00/0010).
ISEE-31
SOURCE LOCATION OF AIR POLLUTION AND CARDIAC
AUTONOMIC FUNCTION
Sung Kyun Park,* Marie Oneill,* Barbara Stunder, Pantel Vokonas,
David Sparrow, Petros Koutrakis,* Joel Schwartz*. *Department of
Environmental Health, Harvard School of Public Health; NOAA Air
Resources Laboratory; Normative Aging Study, Department of Veterans
Affairs Outpatient Clinic
Purpose: Several epidemiologic studies have shown associations between
air pollution and alterations in cardiac autonomic function. We
hypothesized that pollution originating in different locations would have
different associations with heart rate variability (HRV) among 512 male
participants from the Normative Aging Study.
Methods: Clinical data were collected during exams occurring November
14, 2000 through October 30, 2003 in Boston, MA, USA. HRV measures
included: the standard deviation of normal-to-normal (NN) intervals, the
square root of the mean of the squared differences between adjacent NN
intervals, power in high (HF, 0.15 to 0.40 Hz) and low frequency (LF,
0.04 to 0.15 Hz), and LF/HF ratio and were Log10 transformed. Potential
confounders were age, blood pressure, fasting blood glucose, smoking
status, use of beta-blocker and angiotensin-converting enzyme inhibitors,
room temperature, and outdoor apparent temperature matched on hour of
electrocardiogram measurement for each subject. We used the Hybrid
Single-Particle Lagrangian Integrated Trajectory (HYSPLIT4) model to
calculate 36-hour back-trajectories at heights of 500 and 1000 meters,
beginning at 9 a.m. of each exam date. Trajectory cluster analysis was
used to classify the trajectories into seven clusters, with each cluster
representing a different air transport regime.
Results: Trajectory clusters originating to the west and south of Boston,

and locally (short and slow-moving air masses) had significantly higher
concentrations of PM2.5, black carbon, NO2, and SO2 than clusters
originating from the north, northeast, and northwest, but ozone
concentrations differed little across clusters. Adjusting for potential
confounders, we found 61.4% (95% confidence interval (CI): 8.9%,
83.6%) and 61.0% (95% CI: 7.7%, 83.5%) lower HF on days with south
and west trajectories, respectively, compared to northeast trajectory days
at 1000 meters. LF/HF ratios on southwest, west, and northwest trajectory
days were higher than on northeast trajectory days: 89.2% (95% CI: 3.8%,
244.9%), 84.5% (95% CI: 0.8%, 237.8%), and 102.8% (95% CI: 10.8%,
271.2%) higher, respectively. Other HRV indices and 500 meter
trajectories showed no significant differences by source location.
Discussion: This study suggests that polluted air from the south and west
of Boston, where sources include vehicular traffic and coal burning power
plants, affects cardiac autonomic function more strongly than that from
the northeast. Though PM2.5 levels on northwest trajectory days were
relatively low, the strong associations with LF/HF ratios suggest that the
composition of air pollution from that area may be more toxic.
Supported by 5 T32 ES07069-22, 2 T32 ES07069-21, and EPAR827353.
ISEE-32
THE USE OF MONITOR DATA TO INVESTIGATE AIR
POLLUTION EFFECTS ON SUBCLINICAL ATHEROSCLEROSIS IN
AN EXISTING COHORT
Ana Diez Roux,* Amy Auchincloss,* Jeery Keeler,* Graham Barr,
Perry Samson*. *University of Michigan; Columbia University
Introduction: This presentation will discuss issues related to the use of
concurrent and historical monitor data to investigate associations of PM
exposures with inflammatory markers and subclinical atherosclerotic
disease in an existing multiethnic cohort study.
Methods: Data on recent and long-term exposure to PM and copollutants will be obtained for 6814 persons participating in the
Multiethnic Study of Atherosclerosis (MESA), an ongoing NHLBI-funded
longitudinal study of subclinical atherosclerosis. Retrospectively collected
residential history information will be used to link each participant to
measures of exposure.
Results:
The presentation will summarize: (1) the strengths and
limitations of the study design proposed; (2) success in obtaining and
geocoding residential history information; (3) problems encountered in the
construction of relevant exposure metrics using available monitor data;
and (4) the handling of analytical issues related to estimation of air
pollution effects.
Discussion:
Existing monitor data provides a valuable tool to
investigators interested in air pollution effects. The use of this data
however raises numerous practical and analytical issues which need to be
addressed if valid estimates of causal effects are to be obtained.
ISEE-33
EFFECTS OF PM1, PM2.5 AND PM10 ON HEART RATE
VARIABILITY IN SUSCEPTIBLE POPULATIONS
Chin-Sheng Tang,* Nan-Ting Chen, Chang-Chuan Chan*. *Department
of Public Health, College of Medicine, Fu-Jen Catholic University;
Institute of Industrial Hygiene and Occupational Medicine, College of
Public Health, National Taiwan University
Introduction: Researches have shown that both of the elderly people and
the cardio-vascular patients are susceptible populations for air pollution.
The decreases in heart rate variability (HRV) are important indices of
health effect caused by ambient air pollutants. The objective of this study
Abstracts
was to investigate the short-term effects of particulate matter (PM) on

HRV parameters in susceptible population.
Method: The study population consisted of 29 volunteers aged from 46
to 75 yrs, with 11 of them suffering from coronary heat disease. Personal
PM exposures were measured using direct-reading portable dust monitor
(GRIMM Model 1.108, Germany) in 1 minute interval, while each
subjects 24-hour electrocardiographics were recorded by PacerCorder
holter recorder (DELMAR Medical LLC, Model 461A, CA, USA). For
each subject, health status and environmental factors were assessed by
questionnaire and activity diary. The mass concentrations of PM1, PM2.5
and PM10 were measured and recorded as 5-minute average, and 1-hour,
2-hour, 3-hour, 4-hour, 5-hour, 6-hour, 7-hour, and 8-hour moving
averages. Linear mixed-effects model were applied to estimate the effects
of PM concentrations on time domain measures and frequency domain
measures of HRV. Time domain HRV parameters included the standard
deviation of normal RR intervals (SDNN), the square root of the mean of
the squared differences between adjacent normal RR intervals (r-MSSD),
and the probability of NN intervals more than 50 microsecond (pNN50).
Frequency domain HRV parameters included low frequency (LF), high
frequency (HF), LF/HF ratio, and Total Power.
Results: After adjusting for gender, age, body mass index, smoking,
sleeping hours, ?-block medicine, disease type, temperature, and relative
humidity, the 4-hour moving averages of PM concentrations were found
to have the strongest impact on HRV parameters. When the 4-hour PM10
levels increased 100?g/m3, the percentage changes of heart rate, SDNN, rMSSD, pNN50, LF, HF, LF/HF, and Total Power were 0.49%, 4.96%,
6.95%, 0.84%, 6.86%, 6.02%, 0.38%, and 4.73%, respectively
(all p0.05). Similarly, when the 4-hour PM2.5 average increased
100mg/m3, the percentage changes of above parameters were 0.44%,
5.44%, 7.76%, 0.96%, 7.54%, 6.43%, 0.41%, and 5.09%,
respectively (all p0.05). When the 4-hour moving PM1 average
increased 100mg/m3, the percentage changes of above parameters were
0.50%, 6.21%, 8.87%, 1.09%, 8.53%, 7.33%, 0.42%, and
5.71% (all p0.05).
Conclusions: Results of our study indicated that particulate matters may
have both of the short-term effects and the delay effects on heart rate
variability in susceptible populations. The fine particles showed more
prominent effects than coarse particles on heart rate variability.
The authors would like to thank all of the participants in this study. This
research was funded by National Science Council in Taiwan (project No.
91WFD0200236).
ISEE-34
IMPACT OF ACUTE AIR POLLUTION EXPOSURE ON MILITARY
FIREMEN CARDIORESPIRATORY PERFORMANCE
Alfe sio
L.F.
Braga,*
Raul
Santo
de
Oliveira,
Turbio Leite de Barros Neto, Sergio Ricardo Moreti,
Roberto Constantino Carneiro, Luiz Alberto Amador Pereira.
*Environmental Pediatrics Program, University of Santo Amaro Medical
School; School of Physical Education from Sa o Paulo State Police;
CEMAFE, School of Medicine, Federal University of Sa o Paulo;
Laboratory of Experimental Air Pollution, University of Sa o Paulo
Medical School
Abstract: This study was developed to assess the impact of acute air
pollution exposure on the physical cardio-respiratory fitness of military
fireman who lived and worked in the city of Guaruja, Sa o Paulo, Brazil.
A sample of 25 healthy and non-smoker firemen were selected from a
population of 40 volunteers. Their ages ranged from 24 to 45 years. The
tests were performed in two phases. Phase A, in Bertioga, a city with low
levels of air pollution, and phase B, in Cubata o, a polluted city. Both
cities are coastal cities of Sa o Paulo State. The cumulative loads exertion
S27
Abstracts
test on the treadmill was approximately 10 minutes 2 minutes long

with the first stage of 2 minutes and one load of 7 km/h, increasing the
intensity of the exertion on one km/h, per minute, until the maximum
individual limit. The results show that there are statistically significant
differences (p0.05) in the anaerobic threshold (AT) between Cubata o
(35.04 ml/kg/min 4.91) and Bertioga (36.98 ml/kg/min 5.62), in
the heart rate of anaerobic threshold (HRAT) (Cubata o 152.08 bpm
14.86; Bertioga 157.44 bpm 13.64) and in the anaerobic threshold
percentage in relation to the maximum oxygen consumption (%
ATVO2max) (Cubata o 64.56% 6.55; Bertioga 67.40% 5.35).
There were no differences regarding maximum consumption of oxygen
(VO2max), maximum heart rate (HR max) and anaerobic threshold
velocity (AT Velocity) between the cities. The acute exposition to
pollutants in the city of Cubata o, SP, caused a significant reduction in the
performance in terms of sub maximum levels of physical exertion, but did
not significantly affect the maximum aerobic potency.
ISEE-35
PARTICULATE AIR POLLUTION AND THE
CONGESTIVE HEART FAILURE IN 5 US CITIES
RISK
OF
Gregory Wellenius,* Antonella Zanobetti,* Murray Mittleman,

Joel Schwartz*. *Harvard School of Public Health; Beth Israel
Deaconess Medical Center
Abstract: Patients with congestive heart failure (CHF) may remain
asymptomatic for extended periods if compensatory mechanisms are
sufficient to balance the cardiac dysfunction. The identification of factors
that lead to cardiac decompensation and subsequent hospitalization for an
acute exacerbation of CHF is of considerable public health interest. Prior
studies using administrative data suggest that fine particulate matter
(aerodynamic diameter 10 m, PM10) may be a precipitating factor,
but this hypothesis has not been evaluated across multiple cities in a
systematic manner. Therefore, we evaluated the association between daily
PM10 and the risk of hospitalization from the emergency room for CHF
(ICD-9: 428.0 and 428.1) among Medicare recipients (age 65) in 5
US cities. We analyzed the data using a two-stage hierarchic model. In
the first stage, we used the case-crossover design to separately estimate
the effect of a 10 g/m3 increase in PM10 in Chicago, IL, Cleveland,
OH, Detroit, MI, Minneapolis/St. Paul, MN, and Seattle, WA. Within
each city, referent exposure days were chosen using the time-stratified
approach such that exposures on the case day were compared to exposures
occurring on all other days of the same month as the case day. In the
second stage, a combined random-effects estimate was obtained from the
city-specific effect estimates. In total, there were 242,462 emergency room
admissions with a primary diagnosis of CHF during the observation
period. Overall, a 10 g/m3 increase in PM10 was associated with a 1.0%
(95% CI: 0.6, 1.4) increase in risk of admissions for CHF on the same
day. PM10 levels at lag 0 were positively associated with the risk of
admissions for CHF in all cities, with estimates ranging from 0.7% in
Detroit to 2.8% in Seattle. There was no significant change in risk
associated with PM10 at lags 1 to 3 days. These results support the
hypothesis that elevated levels of particulate air pollution are a risk factor
for acute cardiac decompensation and subsequent hospitalization in heart
failure patients. Further studies are needed to elucidate the mechanisms of
this effect.
This study was supported by grants R827353 from the U.S.
Environmental Protection Agency and HL07118 from the National
Institutes of Health.
S28
ISEE-36
A CASE-CONTROL STUDY ON LONG-TERM EXPOSURE TO AIR
POLLUTION AND MYOCARDIAL INFARCTION
Mats Rosenlund,* Niklas Berglind,* Tom Bellander,* Johan Hallqvist,
Go ran Pershagen. *Dept. of Occupational and Environmental Health,
Stockholm County Council, and Institute of Environmental Medicine,
Karolinska Institute, Sweden; Dept. of Social Medicine, Stockholm
County Council, and Dept. of Public Health Sciences, Karolinska
Institute, Sweden; Institute of Environmental Medicine, Karolinska
Institute, Sweden
Introduction: Cross-sectional and mainly large-scale differences in
exposure to air pollution have been associated with a long-term increase
in risk for cardiopulmonary mortality in cohort studies. Our objective is to
study the association between myocardial infarction (MI) and the
historical residential exposure to combustion-related air pollution during
30 years in a population-based case-control study.
Methods: The study population includes all first events of MI in people
aged 4570 during 19921994, and population controls matched on age,
gender, and hospital catchment area. The subjects or next-of-kin have
answered an extensive questionnaire covering a large set of potential risk
factors for MI. A supplementary telephone interview was conducted and a
health examination was carried out on hospitalized cases and their
controls to collect data on biological parameters. Information of historical
home-addresses was collected for 4,069 subjects since 1960 using a
questionnaire. The 10,662 addresses have been transformed into
geographical coordinates using GIS in combination with a regional
geographical address database. Based on a detailed regional emission
database from 1993 and statistics of changes in traffic and other historical
land-use variations from 1960, emission databases for air pollution have
been reconstructed for the years 1960, 1970, and 1980. These databases
describe emissions of nitrogen oxides (NOX, NO2) and sulfur dioxide
(SO2) from traffic-related line sources, different point sources, area
sources, and grid sources. The emission databases provide information
used in dispersion calculations to obtain annual mean levels of NOX,
NO2, and SO2 throughout the study area, with a resolution of 500*500 m
in rural areas and 25*25 m in the inner-city area. In addition, historical
dispersion models of carbon monoxide (CO) and current particulate matter
(PM10 and PM2.5) under development will be used. The study design and
the long-term exposure assessment makes it feasible to investigate the
importance of different aspects of the exposure, such as cumulative dose,
intensity and duration of exposure, and different time windows for
individual exposure.
Results: In a preliminary analysis, using exposure assessment with lower
geographical resolution, an association between the 30-year average
residential level of combustion-related air pollution and myocardial
infarction was suggested. We will present results from epidemiological
analyses of the association between MI and air pollution using more
detailed exposure assessment during several decades.
ISEE-37
AIR POLLUTION AND CARDIOVASCULAR DISEASE EVENTS IN
THE WOMENS HEALTH INITIATIVE OBSERVATIONAL (WHIOS) STUDY
Kristin A. Miller,* David A. Siscovick,* Lianne Sheppard,*
Kristen Shepherd,* Garnet L. Anderson, Joel D. Kaufman*. *University
of Washington; Fred Huchinson Cancer Research Center, Womens
Health Initiative Clinical Coordinating Center
Introduction: Particulate Matter (PM) air pollution has been associated
with cardiovascular disease (CVD) in studies of long-term exposure;
however, prior studies have had limited geographical variability and
individual level information on prior medical history, and did not assess
nonfatal events. We examined the association of long-term exposure to
PM with CVD in the WHI-OS prospective cohort study.
Methods: We assigned air pollution exposures to 66,801 postmenopausal
US women with no history of CVD, using year 2000 averaged exposure
data from the nearest representative PM2.5 monitor (within 30 miles) of
subject residential zipcode centroid. Monitor characteristics and annual
average pollutant concentrations were obtained from EPA AirData
database. Median follow-up was 6.0 years including events through
August, 2003. Events were ascertained by review of hospital and medical
records or death certificates with local adjudication according to
standardized criteria. There were 421 fatal CVD events and 3061 incident
nonfatal CVD events. Specific events included CHD death 162,
cerebrovascular death 145, CVD death 114; nonfatal MI 597, angina 854,
revascularization 165, coronary artery disease 148, CHF 382, stroke 570,
and TIA 345. For the first incident event since enrollment, we calculated
hazard ratios per 10 g/m3 increment of annual average PM2.5 exposure
using Cox proportional hazards regression, adjusting for age, smoking
status, years smoked, cigarettes/day, diabetes, hypertension, systolic and
diastolic blood pressure, BMI, and elevated cholesterol.
Results: After adjustment for confounding factors, each 10 g/m3 of
PM2.5 was associated with a 17% increased risk of incident nonfatal and
fatal CVD events, relative hazard (RH) 1.17 (95% CI: 1.06, 1.28). Risk
was increased by 14% for incident nonfatal CVD events (RH 1.14; 95%
CI 1.03, 1.26) and by 32% for fatal CVD events (RH 1.32; 95% CI: 1.01,
1.73). Further adjustment for second-hand smoke, occupation, SES, diet,
exercise and medications did not appreciably change estimates.
Discussion: Our results suggest that long-term exposure to PM2.5 is
associated with both CVD mortality and with nonfatal CVD events.
Chronic air pollution exposure may influence CVD incidence in
postmenopausal women.
ISEE-38
AMBIENT AIR POLLUTION AND HEART RATE VARIABILITY
(HRV) IN TWO SENSITIVE POPULATIONS
Helen Suh,* Amanda Wheeler, Diane Gold, Joel Schwartz*. *Harvard
School of Public Health; Health Canada; Channing Laboratory
Introduction. Significant associations between ambient fine particle
(PM2.5) concentrations and decreased heart rate variability (HRV) have
been shown in epidemiological studies. To examine further the effects of
ambient pollution concentrations on HRV, a cardiovascular health study
was conducted in Atlanta, GA during Fall 1999 and Spring 2000.
Methods. Holter monitoring was conducted for 31 individuals living in
metropolitan Atlanta, 19 of which had chronic obstructive pulmonary
disease (COPD) and 12 had recent MIs. Each participant was monitored
on seven days in either or both the fall and spring seasons. Holter data
were analyzed for measures of HRV. Hourly ambient pollution
concentrations were obtained from stationary ambient monitoring (SAM)
sites in Atlanta. The association between ambient pollution and logtransformed HRV was examined using linear mixed effects models
(LME). Models controlled for subject as a random effect, body mass
index, gender, age, medication use, season, temperature, relative humidity,
hour and day of week. Models were also run including baseline FEV1 as
interaction terms. Results were scaled by an inter-quartile range (IQR)
increase in ambient PM2.5 (10.6 ug/m3) and EC (1.2 ug/m3).
Results. Disease status or lung function level modified the associations of
4-hour mean ambient pollution with HRV. Increased pollution levels were
associated with increased HRV for those with COPD or marked airway
obstruction, and with no change or decreases in HRV for those with MI
diagnosis or normal lung function levels. For individuals with COPD, the
standard deviation of normal RR intervals (SDNN) rose by 7.5% (95%
Abstracts
CI: 1.513.9%) per IQR increase in ambient PM2.5. Similarly for those
with marked airway obstruction (a subset of those with COPD; baseline
FEV135% of predicted), an IQR increase in 4-h ambient PM2.5 was
associated with a 10.2% (95% CI: 3.8 17.0%) increase in SDNN. In
contrast, those with MI and/or with normal FEV1 percent predicted had a
small, not statistically significant decrease in SDNN in response to PM2.5.
For 24-h ambient EC, SDNN decreased significantly by 4.9% (95% CI:
8.7 to 1.0%) per IQR increase in persons with a normal baseline
FEV1, while subjects with an FEV1 of only 35% of predicted showed an
insignificant 2.9% increase (95% CI: 1.2 to 7.1%) in SDNN per the
same IQR increase in ambient EC.
Discussion. Results suggest that the association between ambient air
pollution and HRV varies with either disease status or baseline pulmonary
function. Further research should be conducted to determine whether this
association is generalizable to other study populations.
ISEE-39
SHORT-TERM EFFECT OF DIFFERENT SIZE PARTICULATE
MATTERS ON PEAK EXPIRATORY FLOW RATE OF ASTHMATIC
CHILDREN IN ELEMENTARY SCHOOL
Li-Te Chang,* Chin-Sheng Tang, Chang-Chuan Chan. *Department of
Environmental Engineering, Feng Chia University; Department of Public
Health, Fu Jen Catholic University; Institute of Occupational Medicine
and Industrial Hygiene, National Taiwan University
Abstract: Many respiratory disease studies have examined pulmonary
function and respiratory symptoms in relation to particulate matters (PM).
Pulmonary function studies were suggestive of short-term effects resulting
from ambient PM exposures, where peak expiratory flow rates showed
decrease in the range of 2 to 5 L/min due to an increase of 50 ug/m3 in
24-hr PM10 concentrations. Although there are many studies available for
the respiratory effects of PM10, the effects of different size PM on
asthmatic subjects are still limited. The objective of this study was to
assess the contribution of different size PM to peak expiratory flow rate
(PEFR). An ongoing panel study is conducted to examine the pulmonary
effect of particulate air pollution on asthmatic children in primary school.
The panel will consist of 26 children of age 712 in a primary school of
Taipei County, Taiwan. The peak flow rate is measured both in the
morning on childrens arrival at school and in the evening after departing
from school for 12 days during three periods in the years of 2003 and
2004. During the study, continuous PM (sizes from 0.3 to 20 um)
exposures are measured (using GRIMM 1.108, Germany) for 5 days for
each subject. Integrated particle samples are also collected for elemental
analysis using energy dispersive XRF. In addition, ambient air pollutant
concentrations will be obtained from the Taiwan EPA fixed-site
particulate super-station located on the campus. All participants shall live
in private residences (i.e., either single-family houses or apartments),
where they are also asked to complete activity diaries to report
information on the nature and location of their activities, as well as other
factors (e.g., incense burning) that may affect personal exposures.
Preliminary results showed that the mean 24-hr PM1, PM2.5, and PM10
concentrations were 33.0 (29.6), 40.8 (35.7), and 80.5 (104.4)
ug/m3. Mean wake-hour (7am to 11pm) PM1 exposures were found to be
approximately two times higher than the mean exposure levels during
sleep hours (11pm to 7 am). Results for characterizing the influence of
activity patterns on childrens exposures will also be presented. Our
research findings will inform policy makers, local officers and the general
public of the significant health impact of particulate air pollution, and also
offer important insights to improve childrens health in Taiwan.
S29

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ABSTRACTS

Epidemiology Volume 15, Number 4, July 2004

40 g/m3, respectively. Linear regression suggested that the quantity of

Epidemiology Volume 15, Number 4, July 2004

environmental tobacco smoke exposure and air change rate, were

2004 Lippincott Williams & Wilkins

Epidemiology Volume 15, Number 4, July 2004

2004 Lippincott Williams & Wilkins

Epidemiology Volume 15, Number 4, July 2004

periods risk) was calculated. A Poisson regression model was used to

2004 Lippincott Williams & Wilkins

Epidemiology Volume 15, Number 4, July 2004

There was variation between cities with respect to effect modification by

analyses will examine pollution associations with the counts of

2004 Lippincott Williams & Wilkins

Introduction: The Harvard Six Cities study was seminal in establishing

Epidemiology Volume 15, Number 4, July 2004

Discussion: Our findings suggested that exposures to traffic-related air

FIGURE 1. Odds Ratios from Logistic Regression Model v. Fine

2004 Lippincott Williams & Wilkins

Epidemiology Volume 15, Number 4, July 2004

the PM-mediated acute cardiac effects. Although these epidemiologic

2004 Lippincott Williams & Wilkins

pollution control policies were adopted in order to decrease air pollution

Epidemiology Volume 15, Number 4, July 2004

Biological Signal Analysis, Deutsches Herzzentrum Mu nchen, Department

2004 Lippincott Williams & Wilkins

Epidemiology Volume 15, Number 4, July 2004

2004 Lippincott Williams & Wilkins

inflammatory markers will be presented using the results of longitudinal

Abstract: Long-term exposure to fine ambient particulate matter (PM2.5)

Epidemiology Volume 15, Number 4, July 2004

during the baseline clinical examination. After excluding missing data on

2004 Lippincott Williams & Wilkins

Epidemiology Volume 15, Number 4, July 2004

(14.36 ug/m3), which corresponds to a 17% increase based on the study

2004 Lippincott Williams & Wilkins

Abstract: Many studies reported associations between particlate mater

Epidemiology Volume 15, Number 4, July 2004

cerebrovascular diseases (Stroke) (ICD-9: 430 438) were collected from

overdispersion. For each cause lagged effects, up to three days, of each

We found a short-term association between daily levels of

The project was supported by the Spanish Ministry of Health, Fondo de

2004 Lippincott Williams & Wilkins

Epidemiology Volume 15, Number 4, July 2004

Results: Trajectory clusters originating to the west and south of Boston,

2004 Lippincott Williams & Wilkins

was to investigate the short-term effects of particulate matter (PM) on

Epidemiology Volume 15, Number 4, July 2004

test on the treadmill was approximately 10 minutes 2 minutes long

Gregory Wellenius,* Antonella Zanobetti,* Murray Mittleman,

2004 Lippincott Williams & Wilkins

Epidemiology Volume 15, Number 4, July 2004

2004 Lippincott Williams & Wilkins

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