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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 cCASHh-

project complex integrative approach, aims to improve our understanding

of future exposure, and adaptation possibilities and capacities to vector-

borne 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 vector-

borne 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 population’s 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

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 inventilation, 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), PAH’s (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.

Epidemiology • Volume 15, Number 4, July 2004 S15


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This research was sponsored by the Czech Ministry of Health, Project NJ/

5907-3.

ISEE-4

ESTIMATING HEALTH EFFECTS FROM EXPOSURES TOOUTDOOR 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

individual’s exposure. Source apportionment techniques can provide auseful 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

of fice 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

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 areference 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 1980 ’s.

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 on4039 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

Abstracts Epidemiology • Volume 15, Number 4, July 2004

© 2004 Lippincott Williams & WilkinsS16


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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;fi brinogen and CRP, which are known risk factors for cardiovascular

disease. The study was conducted in a mid sized Swedish city (Växjö)

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 fi brinogene and CRP results were first

inspected by plotting the ratio between each participant’s level at each

occasion and the mean level of all occasions against the measured

pollution levels (two day average). For fi brinogen 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 fi brinogen and CRP, respectively. The

estimated beta-coef ficients 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 fi brinogen 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 NationalInstitutes 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 period ’s risk divided by non-effect

period ’s 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: 0.91 – 1.38), 1.05 (95% CI: 0.89 – 1.23), 1.06

(95% CI: 0.93 – 1.19) and 1.07 (95% CI: 1.01 – 1.15) 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 TRAFFIC-

RELATED POLLUTANTS ON ISCHEMIC HEART DISEASES:

MAIN RESULTS OF THE HEAPSS PROJECT

Francesco Forastiere,* Pasi Aalto,† Tom Bellander,‡ Niklas Berglind,§

Daniela d ’Ippoliti,* 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; GSF-

National Research Center for Environment and Health; **IMIM-

Municipal Institute for Medical ResearchBackground: 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-of-

hospital 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 oneyear (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.




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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 all-

cause 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 0-

12) at lag 0-1.

Conclusions: Air pollution from traf fic 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).

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 Women’ s Hospital, Harvard

Medical School; ‡The Channing Laboratory, Brigham and Women’ s

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 wasassessed 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, IQR 38.5 ppb) were observed in the 14-

21 hours prior to the health assessment, as well as for the mean 48-hours

prior (OR 3.50, 95% CI: 1.62-7.55, IQR 21.7 ppb). For VE, long-term

exposures appeared the most important, with an OR of 1.72 (95% CI:

1.02-2.92, IQR 11.2 ug/m3) for 96-hour PM2.5 and an OR of 5.68 (95%

CI: 1.78-18.12, IQR 21.4 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

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

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 wereobtained 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.

Epidemiology • Volume 15, Number 4, July 2004 Abstracts

© 2004 Lippincott Williams & Wilkins S19


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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) fromthe 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

subject’s 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

subject’s age, sex, body mass index (BMI), disease status of coronaryheart 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.

Discussion: Our findings suggested that exposures to traf fic-related air

pollutants in urban environment, such as NO2 or CO, are associated with

decreased HRV in susceptible population.

ISEE-15CAN 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 thefish 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 HF-

HRV (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 Women’ s 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

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

Particulate




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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 PM2.5and 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-17CARDIOVASCULAR EFFECTS OF AIR POLLUTION IN ADULTS

IN CUBATÃO, SÃO PAULO, BRAZIL

Luiz Alberto Amador Pereira,* Gleice Margarete de Sousa Conceição,†

Alfesio L.F.Braga‡. *Catholic University of Santos; Brazil; † Department

of Internal Medicine, Federal University of Sã 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: Cubatão 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

80’s of the XX Century the “Valley of Death”. Since then, some air

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 Cubatão, from 1997 to 2000, and air pollution and weather

data provided by São 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 third-

degree 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 agegroups, 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 Cubatão 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, LIM05-

FMUSP, 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 case-

crossover 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 emergencyroom with a primary diagnosis of MI (ICD-9: 410), COPD (ICD-9: 490-

496, 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 case-

crossover 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 city-

specific 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%




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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 Women’ s 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: 0.1-

4.1) 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 Rückerl,† 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

Biological Signal Analysis, Deutsches Herzzentrum Mü 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 patientswas 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 Holter-

ECG 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 R-

827354) 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 defi brillators (ICDs). ICDs are electronic devices implanted in

patients at high risk for sudden cardiac death, ventricular tachycardia, and

ventricular fi brillation. 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




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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 traf fic-related particles. In order to examine the

associations between traf fic-related particles and systemic inflammation,

we conducted a study in which a panel of senior citizens was exposed to

elevated traf fic-related pollutant exposures through a series of bus trips.

Methods: Repeated blood samples were collected from forty-four non-smoking 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, c-

reactive protein, intracellular adhesion molecule – 1, fi brinogen, and von

willebrand ’s 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

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

Institute’s 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 evaluatethe 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

10-g/m3

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-dayEAP 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




10/15

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 5 – 10% 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 PM2.5surface (geostatistical kriging model; assigned exposures were mostly

within / 3 g/m3 of monitored values). We determined the cross-

sectional 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:

0.7 – 10.6%) 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 modi fiers

into account. Information on long-term, time-varying exposure to PM onvarious 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; 109:71 – 9.

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 PreventionAbstract: 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 (1987 – 1989) of the population-based Atherosclerosis Risk in

Communities study. We calculated the following pollutant exposures one-

day prior to each participant’s 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 EPA’s Aerometric Information Retrieval

System (AIRS). We assessed the presence, frequency, and complexity of

arrhythmias from standardized 2-minutes EKG rhythm strips recorded

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 theweather 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 mixed-

effects 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




11/15

(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 (2.5 – 10 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

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, pneumoniaadmissions 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 fi t. 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 traf fic-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 Rodr ı́guez,*† Santiago Pérez-Hoyos,*

Juan Bellido,‡ Federico Arribas,§ Carme Saurina, ¶ Inmaculada Aguilera,

Ana Breznes,** Margarita Taracido,†† Alvaro Cañada,‡‡Carmen Iñiguez* (EMECAS Group). *Valencian School of Studies for

Health-EVES; † Miguel Herná ndez University; ‡ Departamento de Salud. C

Valenciana; § Departamento de Salud. Aragó n; ¶ Research Group on

Statistics, Applied Economics and Health (GRECS); Escuela Andaluza de

Salud Pú 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




12/15

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

hospital records (1995 – 1999). 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: 0.2 – 2.5%) increase in the number of

hospital admissions for CVS, and 1.7% (95% CI: 0.7 – 2.9%) 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 coef ficients 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 Martı́nez, Luis Cirera,** Laura Ló pez,††Inez Aguinaga,‡ Ferran Ballester* (EMECAS Group). *Valencian School

of Studies for Health-EVES; † University Miguel Herná ndez; § Research

Group on Statistics, Applied Economics and Health (GRECS); ‡ Escuela

Andaluza de Salud Pú 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

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 7 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

6 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 5 0.91

(0.35; 1.47)

1.56

(0.82; 2.31)

1.58

(0.

Air Pollution and Acute Cardio Respiratory Visits.50

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