Respiratory Disease and Prevention Center

EPA Grant Number: R826708C003
Subproject: this is subproject number 003 , established and managed by the Center Director under grant R826708
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).

Center: Southern California Particle Center and Supersite
Center Director: Froines, John R.
Title: Respiratory Disease and Prevention Center
Investigators: Gong, Henry , Gilliland, Frank D.
Current Investigators: Gong, Henry , Gilliland, Frank D. , Jones, Craig , McConnell, Rob Scot
Institution: University of California - Los Angeles
Current Institution: Rancho Los Amigos Medical Center , University of California - Los Angeles
EPA Project Officer: Louie, Nica
Project Period: January 1, 1998 through January 1, 2002
Project Amount: Refer to main center abstract for funding details.
RFA: Centers for Children's Environmental Health and Disease Prevention Research (1998) RFA Text |  Recipients Lists
Research Category: Children's Health , Health Effects , Health


(1)  To design a carefully-controlled experiment for deposit accumulation and HC emission measurement.  (2)  To assess the effects of combustion chamber deposits on the hydrocarbon emissions from a modern production spark-ignition engine.  (3)  To measure the effect of CCD on HC emissions from single-component fuels.  (4)  To develop and validate a model for the mechanism(s) by which combustion chamber deposits lead to additional HC emissions.  (5)  To study the effects of combustion chamber deposits on NOx emissions.

Rationale:  Engine deposits (on intake valve and combustion chamber) increase HC emissions.  Some recent data suggest that combustion chamber deposits also increase NOx emissions.  To meet stringent future emissions standards, the emissions due to deposits will have to be reduced.  The first step towards that end is to better quantify these emissions and understand the mechanisms involved in their formation. 

Approach:  A four-cylinder, DOHC Saturn engine has been subjected to a standardized deposit build-up cycle.  An additized fuel (which keeps the intake valves and ports clean) was used to isolate the effects of the combustion chamber deposits on emissions.  HC and NOx emission measurements were taken continuously during the deposit accumulation process.  In parallel a model for the effect of deposits on HC emissions has been developed. 

Status:  The project has now been completed.  Four deposit build-up tests (100, 50, 25, and 35-hour tests) were carried out.  In these tests, the HC emissions stabilized after about 25 hours.  The HC emissions increased by an average of 14% due to deposit build-up.  The HC emissions returned to the clean engine baseline levels after the combustion chamber deposits were removed.  The NOx emissions, which were expected to increase slightly during these tests, showed substantial scatter and no clear trend was apparent. 

The deposit accumulation process developed has shown that deposits can be built up systematically and reproducibly in engine dynamometer tests.  The HC emissions trends were surprisingly repeatable.  The significant finding was that the HC emissions increased for the first 20 hours of operation and then stabilized, even though deposits continued to build up.  Thus engines will have to be very "clean" to largely eliminate this increase--an important practical issue.  The NOx emission variability noted above is believed due to variability in the engines EGR system.  Despite efforts to reduce this, no clear trends as deposits build up could be determined. 

A model has been developed to explain the observed increase in HC emissions as deposits build up, and the lack of sensitivity of this increase to fuel compound in the individual hydrocarbon fueled tests.  Critical to the development of this model were studies of the pore size distributions of the cylinder head and piston crown deposits (which had different characteristics). 

Three different mechanisms were examined to explain the effect of CCDs on the HC emissions.  The first is the displacement of fuel-air mixture into and out of the larger deposit pores as the cylinder pressure rises and falls.  The second consists of pressure driven bulk flow into the deposit pores, in the pore size range (1 - 0.1 micrometer ) where viscosity is important.  The deposits are treated as a porous medium with an estimated permeability.  Darcy?s Law for flow in a porous medium forms the basis of this model.  The third mechanism consists of ordinary diffusion of fuel molecules into the air (or exhaust gases) in the deposit pores.  The fuel molecules diffuse into the deposit pores during the intake, compression, and combustion processes and get released into the combustion gases during the expansion and exhaust processes.  During flow in, they are absorbed onto the pore surfaces.  By applying these models to the appropriate pore size range, and weighting the trapped HC by the relative importance of these size ranges, the individual mechanism contributions to the total deposits impact was quantified.  Only the crevice model of the larger (< 1 micrometer ) pores is significant, and the cylinder head deposits contribute many times what the piston deposits contribute.  The model indicates that the pore depth to which fuel penetrates becomes limiting ( ~ 100 micrometer  for the cylinder head) even though the deposit thickness steadily increases beyond that. 

The maximum amount of HC trapped in the deposits is reduced by oxidation and retention in the cylinder.  Allowing approximately for these effects produces estimates of the increase in engine HC emissions comparable to the measured increases. 

Key Personnel 
Graduate Student:  Haissam Haidar Asthma is the most common chronic disease in childhood. Asthma is now associated with increasing frequency, hospitalization, and mortality, especially in nonwhite, poor, inner-city children. Research is needed to develop and evaluate comprehensive community-based programs designed to reduce asthma triggers in the home environment, such as house dust mites and cockroaches. In this study, inner-city, primarily minority, children with asthma are being identified through a school-based mobile asthma clinic, the Breathmobile, which delivers high quality asthma care to these children. Working with school nurses and community organizations and 3 Breathmobile units, we propose a community-based intervention aimed at reducing asthma triggers in the home. The major goal of this study is to determine whether a comprehensive environmental health education program, enhanced by least-toxic integrated pest management for cockroach control, will result in reduction of dust mites or cockroaches in children's homes and clinical improvement in asthma.Allergic rhinitis (hay fever) is a common illness involving the nose, throat, and eyes. Persons with this allergic condition of their upper airway often have allergic reactions in their lungs (asthma) as well. These reactions are caused by the presence of a particular antibody called immunoglobulin E (IgE) which reacts to foreign allergy material (e.g., pollen). The severity of allergic symptoms normally correlates with the levels of these antibodies. Several studies have compared antibody levels in children of smoking parents to those of non-smokers. Some have concluded that exposure to second-hand tobacco smoke (i.e., passive smoking) can increase the likelihood of producing IgE, while others have not been able to show such a link. These types of studies are complicated by other factors such as differences in lifestyle between the two groups being compared and the difficulties of accurately measuring smoke exposure.

The purpose of this new study is to investigate the ability of environmental tobacco smoke (ETS) to alter the amount and types of IgE and other mediators (cytokines). We will do this by taking a new direct approach. We will measure levels of these agents in the nasal secretions of adults and children before and after controlled experimental exposure to tobacco smoke in an environmentally controlled chamber. (All children will be from homes where parents smoke.) Some subjects will also be exposed to a common environmental allergen (ragweed pollen) with and without associated exposure to low levels of tobacco smoke (equivalent to one day's exposure for a child living with a smoking parent).

We will, therefore, determine if exposure to tobacco smoke plus pollen produces greater amounts of IgE and mediators in the nose than exposure to pollen alone. These experiments will also demonstrate whether children are more susceptible to tobacco smoke than adults. Similar studies will be performed in rats to address genetic and age-related questions that cannot be easily studied in humans. Overall, these studies will be important in determining the potential role of secondhand smoke in causing or exacerbating allergic disease.Lung disease is the most common chronic disease among children and the prevalence is rising worldwide. Chronic lung diseases may be preventable because they are, in part, caused by environmental exposures including air pollution and secondhand smoke. If children's exposures can be reduced and their lung defenses strengthened, we may be able to decrease the burden of lung disease.

Our research focuses on the effects of air pollution on children residing in Southern California. A large number of children breathe high levels of air pollutants and adverse respiratory effects at the levels found in some communities have been found. USC School of Medicine investigators are currently conducting a research project, the Children's Health Study, with funding from the California Air Resources Board, to find out how long-term exposure to air pollution in 12 southern California communities affects respiratory health among children and adolescents. Differences in the effect of air pollution on children's lungs suggest that some children may be more susceptible to air pollutants than others. Diet and genetic factors, as well as age, gender, and health status may affect susceptibility. As part of the new grant from EPA and NIEHS, we are investigating whether certain foods children eat - fruits, vegetables and antioxidant nutrients - along with genetic factors involved in lung defenses, might affect susceptibility to air pollution. Findings from this study have the potential to refine knowledge of the effects of air pollutants and improve strategies to protect children's health.

Publications and Presentations:

Publications have been submitted on this subproject: View all 10 publications for this subprojectView all 92 publications for this center

Journal Articles:

Journal Articles have been submitted on this subproject: View all 10 journal articles for this subprojectView all 61 journal articles for this center

Supplemental Keywords:

children, health, air, exposure, susceptibility., RFA, Health, Scientific Discipline, Geographic Area, Health Risk Assessment, State, Risk Assessments, Disease & Cumulative Effects, Biochemistry, Children's Health, health effects, air toxics, vulnerability, air pollutants, infants, lung disease, age-related differences, airway disease, gene-environment interaction, respiratory problems, second hand smoke, pulmonary disease, lead, air pollution, children, Human Health Risk Assessment, childhood respiratory disease, children's vulnerablity, genetic risk factors, lung dysfunction, disease resistance, human exposure, environmental health hazard, exposure pathways, harmful environmental agents, indoor air, California (CA), dietary exposure, tobacco smoke, dietary factors, environmental tobacco smoke, disease, genetic susceptibility, exposure assessment, cancer risk

Progress and Final Reports:

  • 1998
  • 1999
  • 2000 Progress Report
  • Final Report

  • Main Center Abstract and Reports:

    R826708    Southern California Particle Center and Supersite

    Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
    R826708C001 Asthma in Children: A Community-based Intervention Project
    R826708C002 Children's Exposure to Environmental Tobacco Smoke: Changes in Allergic Response
    R826708C003 Respiratory Disease and Prevention Center