Grantee Research Project Results

2001 Progress Report: Exposure to Vehicular Pollutants and Respiratory Health

EPA Grant Number: R827352C007
Subproject: this is subproject number 007 , established and managed by the Center Director under grant R827352
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: UC Berkeley/Stanford Children’s Environment Health Center
Center Director: Tager, Ira
Title: Exposure to Vehicular Pollutants and Respiratory Health
Investigators: McConnell, Rob Scot , Lurmann, Fred
Current Investigators: McConnell, Rob Scot , Avol, Edward L. , Lurmann, Fred , Gauderman, William
Institution: University of Southern California , Sonoma Technology, Inc.
Current Institution: University of Southern California
EPA Project Officer: Chung, Serena
Project Period: June 1, 1999 through May 31, 2005 (Extended to May 31, 2006)
Project Period Covered by this Report: June 1, 2000 through May 31, 2001
RFA: Airborne Particulate Matter (PM) Centers (1999) RFA Text |  Recipients Lists
Research Category: Particulate Matter , Air Quality and Air Toxics , Air

Objective:

This project is one of four specific studies that focus on emission sources and related adverse health effects. The study hypotheses are:

• Hypothesis A: Mobile source emissions will exacerbate airway inflammation and allergic airway disease and produce cardiopulmonary effects.
• Hypothesis B: The magnitude of allergic airway disease and cardiovascular effects from mobile sources are a function of the size distribution of particulate matter (PM).
• Hypothesis C: Exposure in proximity to selected freeways with either heavy diesel or gasoline powered vehicles will cause exacerbation of inflammatory airway health effects, and exposure to ultrafine particles at very close proximity to a freeway will result in the most severe effects.

Two specific research studies are under way in the Children’s Health Study (CHS) to address the hypotheses, with a third study to follow next year.

A series of related studies take advantage of the long-standing, important CHS. The CHS has demonstrated chronic respiratory effects in children exposed to air pollutants, and continues to explore findings from a decade of investigation. Mobile source emissions appear to have direct relevance to the findings of the CHS. The SCPCS has determined its greatest potential contribution to the CHS is through participation in traffic density studies and support for enhanced exposure assessment at road sites and also with emphasis on organic products of atmospheric transformation. In particular, hypothesis A has direct relevance to the traffic density studies insofar as it seeks to better define etiologic agents with relevance to chronic health effects identified in the CHS. We are studying the role of quinones and polycyclic aromatic hydrocarbons (PAHs) at CHS sites. The freeway study (see R827352C014) will have direct relevance to traffic density research described here. The source/receptor study (see R827352C014) will provide insights to the findings of the CHS. The following hypotheses guide the SCPCS-CHS epidemiologic studies:

• Lung growth in children is permanently affected by air pollution in Southern California.
• Respiratory illnesses are more frequent and severe in children living in areas of high traffic density.
• Chronic health effects in children can be attributed to a specific pollutantor combination of pollutants derived from mobile sources.

Progress Summary:

We are examining the relationship between traffic assignment and primary respiratory health outcomes in the CHS. We are examining the relationship between traffic at schools and homes and:

• The resultant exposure to traffic-related pollutants such as PM₁₀, NO₂, and CO measured at schools and homes.
• The prevalence of asthma and wheeze at entry into the study and the incidence of asthma during followup.
• The level and growth in lung function during followup.
• In addition, we will examine how activity patterns such as time outside and mode of transportation to school, and polymorphisms of gene coding for enzymes involved in the metabolism of reactive species, modify the effect of traffic exposure.

We have geo-coded the home of each participant in the CHS and generated estimates of freeway related pollutants at these homes, using the CALINE4 model, and measured and estimated traffic counts available from the California Transportation Authority in each of the CHS communities. This line source air quality model was developed as a planning tool to predict roadways that would exceed short-term CO standards, and we are adapting it to examine chronic health effects in the CHS. We have used CO as a surrogate for pollutants in fresh vehicular exhaust. Prevalent wind direction and speed is modeled in estimating home concentrations. Predicted CO from measured short-term traffic counts has been validated in other studies against short CO measurements, and our preliminary results suggest that modeled CO reflects measured long-term concentrations.

Using these models, we have conducted extensive analyses of the effect on respiratory symptoms at entry into the CHS cohort of estimated CO at children’s homes. Our preliminary results suggest a large increased risk of parent-reported, physician-diagnosed asthma associated with exposure to local freeway derived CO. The effect of traffic was strongest for asthma diagnosed before age 6. In the CHS community with the highest estimated traffic exposures, there was almost a ten-fold increase in early onset asthma. We have also found that modeled traffic-related pollutants are associated with lower lung function (FEV-1). Another pollutant heavily influenced by local traffic, NO₂ at children’s homes, was measured (not modeled) in a smaller data set, and a similar large association with asthma prevalence was observed. These results provide important new evidence linking asthma with air pollution.

We do not believe that CO is responsible for the observed effects, rather that it may serve as a surrogate for the pollutants of interest. Therefore, in the next 3 years we will improve estimates of vehicular pollutants from surrounding freeways and from surface streets in each community. We will estimate exposure at CHS homes and schools to NO₂ as well as coarse and fine PM and elemental carbon, in addition to CO, using better models of emission factors recently available for California. Information on diurnal variability in traffic patterns, and in wind speed and direction and mixing levels, and the mix of diesel and light duty vehicles will improve these predicted pollutant concentrations at the times of day when children are exercising outside. We will validate these predictions against short-term and long-term historical measured exposures available for these pollutants in the CHS communities. We will re-examine the effect on asthma and lung function of these improved estimates of traffic related particulate matter. The CHS also provides a rich data set of information on more than 350 incident cases of asthma identified during the course of the study, and the relationship between traffic exposure and incident asthma in these older children will be examined. A large portion of the participating children have been genotyped for polymorphisms in genes involved in the metabolism of reactive oxygen species, and we will examine how this genetic variation modifies the effect of traffic related particulate and related pollutants.

Future Activities:

We plan more in-depth examination of the relationship of asthma with traffic related pollutants. These include a case control study of children in the CHS, which will measure traffic related pollutants at the homes and schools of children with and without asthma. In addition, we are planning to identify and follow a new cohort of children, among whom we will carefully characterize new onset asthma, and for whom we will further examine the relationship of asthma to measured home traffic related pollutants, and to interactions of traffic related pollutants with activity patterns of individual children and with measured indoor allergens. These efforts have been made possible in large part by the productive collaborations facilitated by the Center. Findings from the clinical toxicology studies on gene expression will be applied to studies of free-living human populations exposed to contrasting PM levels. The models of traffic related pollution will be used to study additional health outcomes in planned studies.

Journal Articles:

No journal articles submitted with this report: View all 7 publications for this subproject

Supplemental Keywords:

particulate matter, PM, quinones, polycyclic aromatic hydrocarbons, PAHs, aldehydes, ketones, metals, allergic airway disease, human exposure studies, asthma, cardiovascular effects, aerosol sampling, atmospheric aerosol, environmental monitoring, environmental statistics, California, CA, acute exposure, aerosols, air pollution, air quality, air toxics, airway disease, allergen, allergic response, ambient aerosol, assessment of exposure, asthma triggers, atmospheric chemistry, bioaerosols, biological response, childhood respiratory disease, children, dosimetry, environmental hazard exposures, environmental health hazard, environmental triggers, environmentally caused disease, epidemiology, exposure assessment, health effects, home, household, human exposure, human health effects, indoor air quality, inhaled particles, lead, outdoor air, particle concentrator, particle transport, particulate exposure, particulates, sensitive populations, toxicology, toxics, human health, air, geographic area, scientific discipline, health, RFA, physical aspects, health effects, risk assessments, health risk assessment, physical processes, biochemistry, particulate matter, environmental chemistry, mobile sources, state, automotive exhaust, engine exhaust, respiratory impact, airborne urban contaminants, urban air, respiratory disease, ultrafine particulate matter, diesel exhaust, air sampling, particulate emissions, human health risk, atmospheric particles, automobile exhaust, diesel exhaust particles, air pollution, airway disease, respiratory illness, automotive emissions, atmospheric particulate matter, exposure, motor vehicle emissions, PM characteristics, human exposure,, RFA, Scientific Discipline, Air, Geographic Area, HUMAN HEALTH, Health Risk Assessment, State, particulate matter, mobile sources, Environmental Chemistry, Health Effects, Air Pollutants, Environmental Monitoring, aerosols, indoor air quality, California (CA), particulate emissions, ambient aerosol, asthma, atmospheric chemistry, epidemiology, human exposure, motor vehicle emissions, automotive emissions, engine exhaust, quinones, dosimetry, children, allergens, PM characteristics, air pollution, human health effects, PAH, automobiles

Relevant Websites:

http://www.scpcs.ucla.edu Exit

Progress and Final Reports:

Original Abstract

1999

2000

2002 Progress Report

2003 Progress Report

2004 Progress Report

Final Report

Main Center Abstract and Reports:

R827352    UC Berkeley/Stanford Children’s Environment Health Center

Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R827352C001 The Chemical Toxicology of Particulate Matter
R827352C002 Pro-inflammatory and the Pro-oxidative Effects of Diesel Exhaust Particulate in Vivo and in Vitro
R827352C003 Measurement of the “Effective” Surface Area of Ultrafine and Accumulation Mode PM (Pilot Project)
R827352C004 Effect of Exposure to Freeways with Heavy Diesel Traffic and Gasoline Traffic on Asthma Mouse Model
R827352C005 Effects of Exposure to Fine and Ultrafine Concentrated Ambient Particles near a Heavily Trafficked Freeway in Geriatric Rats (Pilot Project)
R827352C006 Relationship Between Ultrafine Particle Size Distribution and Distance From Highways
R827352C007 Exposure to Vehicular Pollutants and Respiratory Health
R827352C008 Traffic Density and Human Reproductive Health
R827352C009 The Role of Quinones, Aldehydes, Polycyclic Aromatic Hydrocarbons, and other Atmospheric Transformation Products on Chronic Health Effects in Children
R827352C010 Novel Method for Measurement of Acrolein in Aerosols
R827352C011 Off-Line Sampling of Exhaled Nitric Oxide in Respiratory Health Surveys
R827352C012 Controlled Human Exposure Studies with Concentrated PM
R827352C013 Particle Size Distributions of Polycyclic Aromatic Hydrocarbons in the LAB
R827352C014 Physical and Chemical Characteristics of PM in the LAB (Source Receptor Study)
R827352C015 Exposure Assessment and Airshed Modeling Applications in Support of SCPC and CHS Projects
R827352C016 Particle Dosimetry
R827352C017 Conduct Research and Monitoring That Contributes to a Better Understanding of the Measurement, Sources, Size Distribution, Chemical Composition, Physical State, Spatial and Temporal Variability, and Health Effects of Suspended PM in the Los Angeles Basin (LAB)