2000 Progress Report: Acute Cardiopulmonary Responses to Fine Particulate Pollution and Copollutant Oxidant Gases in Los Angeles

EPA Grant Number: R827999
Title: Acute Cardiopulmonary Responses to Fine Particulate Pollution and Copollutant Oxidant Gases in Los Angeles
Investigators: Gong, Henry , Sioutas, Constantinos
Institution: University of Southern California , Rancho Los Amigos Medical Center
EPA Project Officer: Chung, Serena
Project Period: March 15, 2000 through March 14, 2003 (Extended to January 14, 2004)
Project Period Covered by this Report: March 15, 2000 through March 14, 2001
Project Amount: $613,894
RFA: Airborne Particulate Matter Health Effects (1999) RFA Text |  Recipients Lists
Research Category: Air , Health Effects , Particulate Matter

Objective:

This project addresses key goals of current research supported by the EPA and the Health Effects Institute to perform realistic controlled exposures of human volunteers to ambient particulate matter (PM), and to measure cardiac and respiratory health outcomes that can help to explain the increased mortality and morbidity associated with increases in ambient PM and gaseous copollutants. The specific goals of this study are to document short-term effects on symptoms, lung function, airway inflammation, hemostasis, and cardiac electrophysiology from controlled exposures to Los Angeles area ambient fine PM and nitrogen dioxide (NO2), separately and in combination. Experimental exposures are designed to represent extreme but still realistic ambient pollution conditions (200 µg/m3 PM, 0.4 ppm NO2, 2-hour duration with intermittent exercise). Volunteer subjects represent groups expected to be at high risk from ambient pollution, for example, elderly adults with chronic obstructive pulmonary disease (COPD), and healthy elderly adults.

Progress Summary:

As of June 10, 2001, four healthy elderly volunteers and four volunteers with COPD have completed all four experimental exposures?filtered air (FA), NO2 in FA, concentrated ambient particulate matter (CAP), and CAP plus NO2. Four additional volunteers with COPD have completed some, but not all, possible exposures. Thus, we are on or ahead of schedule at this point. (Progress might be similar or might be slower in the coming year, depending on the requirements of other projects that share the exposure facilities.)

Table 1 presents summary statistics for PM concentrations (from micro-orifice uniform-deposit impactor samples) and NO2 concentrations (from a continuous analyzer) measured during exposure studies so far. In FA and CAP exposures, NO2 concentrations were close to outdoor ambient levels, as NO2 is not removed by the concentrator or the filtration system. The somewhat higher NO2 concentrations with CAP than with FA reflect the fact that CAP exposures cannot be performed on very low pollution days. Similarly, pre-exposure ambient PM concentrations may differ systematically between exposures with FA and those with CAP. Statistical analyses will be performed to determine whether this influences subjects' pre-exposure physiological and symptom status. Chamber concentrations of generated NO2 were always close to the target level of 400 ppb. CAP concentrations averaged slightly below the target of 200 g/m3, and varied proportionately more than NO2 concentrations. This variation is expected, given the wide range of ambient conditions and inherent limitations of particle concentrator performance.

Table 1. Chamber concentrations in 43 exposure studies through 6/10/01

Exposure
Condition
PM Mean ? SD
( g/m3)
NO2 Mean ? SD
(ppb)
FA
29 ? 12
27 ? 12
FA NO2
26 ? 12
403 ? 13
CAP
194 ? 28
51 ? 21
CAP NO2
191 ? 50
396 ? 8

No subject has shown an untoward clinical response during an exposure or followup period. Interim statistical analyses of data from completed subjects show no significant changes in conventional lung function measures associated with either NO2 or CAP. Analyses of sputum and blood are pending. Holter electrocardiogram analyses are available for seven subjects (four healthy, three COPD) who completed all four exposures. Interim analyses of these data suggest an influence of exposures on cardiac autonomic function. Specifically, low-frequency power showed a significant (P < 0.05) tendency to increase immediately after exposure, relative to pre-exposure, when the atmosphere contained NO2 (regardless of whether CAP was present). Also, healthy elderly and COPD subgroups differed significantly (P < 0.05) in their responses to CAP: the COPD subjects' low-frequency power tended to change more negatively (or less positively) with CAP in the atmosphere (see graph below).

Figure 1

Future Activities:

Exposure studies are expected to continue in the present manner and to be completed partway through Year 3, by which time 24 volunteers will have completed all four exposures. The remainder of Year 3 will be devoted to data analysis and report preparation.

Journal Articles:

No journal articles submitted with this report: View all 6 publications for this project

Supplemental Keywords:

ambient air, mobile sources, risk assessment, health effects, human health, sensitive populations, dose-response, elderly, nitrogen oxides., RFA, Health, Scientific Discipline, Air, Geographic Area, Waste, particulate matter, air toxics, Environmental Chemistry, Health Risk Assessment, State, Risk Assessments, Susceptibility/Sensitive Population/Genetic Susceptibility, Biochemistry, genetic susceptability, tropospheric ozone, Atmospheric Sciences, Biology, Incineration/Combustion, copollutant exposures, elderly adults, health effects, sensitive populations, cardiopulmonary responses, fine particles, PM 2.5, stratospheric ozone, airway epithelial cells, inhaled pollutants, combustion-related pollutants, air pollution, chemical mixtures, susceptible subpopulations, cardiopulmonary response, chronic health effects, human exposure, lung inflammation, oxidant gas, particulate exposure, cardiopulmonary effects, Acute health effects, highrisk groups, inhaled, PM, PM2.5, chronic obstructive pulmonary disease, human susceptibility, California (CA), air quality, human health risk, toxics, concentrated particulate matter, environmental hazard exposures, air contaminant exposure

Relevant Websites:

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

Progress and Final Reports:

Original Abstract
  • 2001
  • 2002 Progress Report
  • Final Report