Segment 1 Of 2 Next Hearing Segment(2)
SPEAKERS CONTENTS INSERTS
Page 1 TOP OF DOC Segment 1 Of 2 79379PS
HEALTH EFFECTS OF PARTICULATE AIR
POLLUTION: WHAT DOES THE SCIENCE SAY?
COMMITTEE ON SCIENCE
HOUSE OF REPRESENTATIVES
ONE HUNDRED SEVENTH CONGRESS
MAY 8, 2002
Serial No. 10760
Printed for the use of the Committee on Science
Available via the World Wide Web: http://www.house.gov/science
COMMITTEE ON SCIENCE
Page 2 PREV PAGE TOP OF DOC Segment 1 Of 2
HON. SHERWOOD L. BOEHLERT, New York, Chairman
LAMAR S. SMITH, Texas
CONSTANCE A. MORELLA, Maryland
CHRISTOPHER SHAYS, Connecticut
CURT WELDON, Pennsylvania
DANA ROHRABACHER, California
JOE BARTON, Texas
KEN CALVERT, California
NICK SMITH, Michigan
ROSCOE G. BARTLETT, Maryland
VERNON J. EHLERS, Michigan
DAVE WELDON, Florida
GIL GUTKNECHT, Minnesota
CHRIS CANNON, Utah
GEORGE R. NETHERCUTT, JR., Washington
FRANK D. LUCAS, Oklahoma
GARY G. MILLER, California
JUDY BIGGERT, Illinois
WAYNE T. GILCHREST, Maryland
W. TODD AKIN, Missouri
TIMOTHY V. JOHNSON, Illinois
MIKE PENCE, Indiana
FELIX J. GRUCCI, JR., New York
Page 3 PREV PAGE TOP OF DOC Segment 1 Of 2 MELISSA A. HART, Pennsylvania
J. RANDY FORBES, Virginia
RALPH M. HALL, Texas
BART GORDON, Tennessee
JERRY F. COSTELLO, Illinois
JAMES A. BARCIA, Michigan
EDDIE BERNICE JOHNSON, Texas
LYNN C. WOOLSEY, California
LYNN N. RIVERS, Michigan
ZOE LOFGREN, California
SHEILA JACKSON LEE, Texas
BOB ETHERIDGE, North Carolina
NICK LAMPSON, Texas
JOHN B. LARSON, Connecticut
MARK UDALL, Colorado
DAVID WU, Oregon
ANTHONY D. WEINER, New York
BRIAN BAIRD, Washington
JOSEPH M. HOEFFEL, Pennsylvania
JOE BACA, California
JIM MATHESON, Utah
STEVE ISRAEL, New York
DENNIS MOORE, Kansas
MICHAEL M. HONDA, California
Page 4 PREV PAGE TOP OF DOC Segment 1 Of 2
C O N T E N T S
May 8, 2002
Statement by Representative Sherwood L. Boehlert, Chairman, Committee on Science, U.S. House of Representatives
Statement by Representative Bob Etheridge, Member, Committee on Science, U.S. House of Representatives
Prepared Statement by Representative Nick Smith, Member, Committee on Science, U.S. House of Representatives
Prepared Statement by Representative Jerry F. Costello, Member, Committee on Science, U.S. House of Representatives
Page 5 PREV PAGE TOP OF DOC Segment 1 Of 2 Mr. Daniel S. Greenbaum, President, Health Effects Institute
Dr. Ronald E. Wyzga, Technical Executive, Electric Power Research Institute
ARIES: Aerosol Research Inhalation Epidemiology Study, EPRI Fact Sheet, March 11, 2002
Dr. Joel Schwartz, Associate Professor of Environmental Epidemiology, Harvard School of Public Health
Dr. Praveen K. Amar, Director, Science and Policy, Northeast States for Coordinated Air Use Management
Page 6 PREV PAGE TOP OF DOC Segment 1 Of 2 Financial Disclosure
Immediate Steps: Diesel Emissions
Immediate Steps: Carbonaceous Material
Retrofitting Diesel Vehicles: Cost Involved
Improving the Nation's Health: Cost-Benefit Analyses
Pollution Emissions From Industrial Plants
Determining Pollution as Cause of Death
Immunities to Pollutants
The Role of the Federal Government
Critique of the Studies: Determining ''Early'' and ''Premature'' Deaths
Appendix 1: Additional Material for the Record
''Understanding the Health Effects of Components of the Particulate Matter Mix: Progress and Next Steps,'' HEI Perspectives, April 2002
Solana Pyne, ''Small Particles Add Up to Big Disease Risk,'' Science, 15 March 2002
Andrew C. Revkin, ''Soot Particles Strongly Tied to Lung Cancer, Study Finds,'' The New York Times, 6 March 2002
Matthew L. Wald, ''Court Says Agency Can Tighten Smog Rules,'' The New York Times, 27 March 2002
Page 7 PREV PAGE TOP OF DOC Segment 1 Of 2 Submitted Statement of American Trucking Associations, Inc.
HEALTH EFFECTS OF PARTICULATE AIR POLLUTION: WHAT DOES THE SCIENCE SAY?
WEDNESDAY, MAY 8, 2002
House of Representatives,
Committee on Science,
The Committee met, pursuant to call, at 10:11 a.m., in Room 2318 of the Rayburn House Office Building, Hon. Sherwood L. Boehlert (Chairman of the Committee) presiding.
COMMITTEE ON SCIENCE
U.S. HOUSE OF REPRESENTATIVES
Health Effects of Particulate Air
Page 8 PREV PAGE TOP OF DOC Segment 1 Of 2 Pollution: What Does the Science Say?
WEDNESDAY, MAY 8, 2002
10:00 A.M.12:00 P.M.
2318 RAYBURN HOUSE OFFICE BUILDING
On Wednesday, May 8, 2002 at 10:00 a.m., the House Science Committee will hold a hearing to examine what is known about the impact of small particle air pollution on human health. The hearing will assess the state of our scientific knowledge about small particle air pollution and its effects on health and ask how we should go forward with a research agenda to address outstanding questions.
The Committee plans to explore several overarching questions:
1. What do we know about the relationship between particulate air pollution and adverse human health effects?
2. How has our knowledge improved since revised air quality standards were first proposed in 1997?
3. Are some components of particulate pollution more dangerous than others?
Page 9 PREV PAGE TOP OF DOC Segment 1 Of 2
4. What technologies are available to reduce emissions of this form of pollution?
2. Brief Background
In 1997, the Environmental Protection Agency (EPA) proposed revised regulatory standards for particulate matter (PM) air pollution, including an entirely new standard for particles 2.5 microns in diameterabout one-thirtieth the diameter of a human hairor smaller (PM2E). At the time, business groups and some Members of Congress criticized the Agency for not basing an important regulatory decision on sound science. In particular, the critics took issue with two key studies on which the PM2E standard was based: the Harvard Six-Cities study and the American Cancer Society study. In response, Harvard University and the American Cancer Society asked the Health Effects Institute (HEI), a research organization funded jointly by the auto industry and EPA, to oversee an independent re-analysis of the data from the two studies.
HEI's analysis, published in July of 2000, confirmed the results of the earlier studies establishing the link between particulate air pollution and human disease and death. Since that time, several new studies have strengthened our understanding of the relationship between particulate pollution and mortality. One study, published in March in the Journal of the American Medical Association, concluded that exposure to fine particle pollution significantly increases the risk of death from lung cancer, other pulmonary illness, and cardiovascular disease.
There has been much debate over the differential effects of constituents of PM (sulfates vs. carbon-based particles) on health, which has implications for how we control PM emissions (power plants vs. motor vehicles). While there are some studies that address this question, our knowledge about the relative toxicity and interactions between constituents is limited.
Page 10 PREV PAGE TOP OF DOC Segment 1 Of 2
The principal sources of particulate air pollution are coal-fired electricity generation plants and diesel engines used in trucks and buses. Cost-effective, well-understood technologies are commercially available for both mobile and stationary sources to control PM emissions. These include particulate traps combined with low sulfur fuel for diesel engines, and electrostatic precipitators and fabric filters for power plants.
Particulate matter (PM) is the term for solid or liquid particles found in the air. PM is classified by size; for example, PM2E designates particles that are less than 2.5 microns in diameter. Because particles originate from a variety of sources (dust, diesel vehicles, woodstoves, power plants, etc.), their chemical and physical compositions vary widely. Particulate matter can be directly emitted or can be formed in the atmosphere when gaseous pollutants such as SO and NOX react to form fine particles. In modern urban environments, particles from combustion generally represent more than half of all respirable particles.
Quantitative knowledge of the health effects of particulate air pollution dates back to 1952. During one week in December of that year, a high-pressure system set in over London, trapping coal emissions. Particle levels increased dramatically and then fell sharply over the week and counts of daily deaths showed a similar rise and fall.
Page 11 PREV PAGE TOP OF DOC Segment 1 Of 2 Because of its size, fine PM can bypass the body's defense system and become deposited deep into the lungs. There, it can be absorbed into the bloodstream or remain embedded for long periods of time. Researchers are still trying to discover how the particles cause disease. They may lodge in the lining of the lungs, inflaming them and contributing to infection. Fine particles can also generate highly reactive oxygen-containing chemicals that can trigger inflammation and allergies and might damage the heart. Studies have linked particulate matter to lung cancer, heart and lung disease, reduced lung function and asthma exacerbation.
There are two ways of studying the health effects of particulate matter: time-series studies and cohort studies. Time series studies track people over short pollution episodes, correlating morbidity (illness) and mortality with daily pollution levels. As of 1997, numerous time-series studies had reported associations between PM and daily mortality and morbidity. Landmark studies include Dockery and Pope (1994), Schwartz (1994), Katsouyanni, et al. (1997). These studies were criticized because they were largely conducted in single locations chosen for unspecified reasons and were analyzed with different statistical approaches.
In 2000, a Health Effects Institute study used explicit criteria to select cities from a well-defined sampling frame and analyzed them in a consistent fashion. The results from this 90-city study corroborated previous results, including the Katsouyanni 15-city study and a recent meta-analysis of 29 studies in 23 locations in Europe and North and South America (Levy, et al. 2000).
Cohort studies follow initially healthy people over longer periods to see how they develop disease or die. Landmark cohort studies include the Harvard Six Cities Study (Dockery, et al. 1993) and the American Cancer Society Study (Pope, et al. 1995). These studies followed large numbers of individuals over many years and observed their rates of mortality. They found that long-term average mortality rates were 17 percent to 26 percent higher in those living in communities with higher levels of PM2E even after accounting for the effects of other risk factors. The results have been used to demonstrate lifespan reduction attributable to exposure to PM2E pollution. Other researchers have independently confirmed the findings of both of these studies.
Page 12 PREV PAGE TOP OF DOC Segment 1 Of 2
A recent study reanalyzed the American Cancer Society (ACS) data (Pope, Thurston and Krewski 2002). This study tracked people over a longer time and controlled more extensively for individual risk factors. They compared data on particulate and gaseous air pollution with data on the cause of death among 500,000 people followed for 16 years by the ACS. After compensating for risk factors, as well as possible regional differences, the researchers found that every 10-microgram increase in fine particles per cubic meter of air produces a 6 percent increase in the risk of death by cardiopulmonary disease, and 8 percent for lung cancer. This is similar to the risk faced by those with long-term exposure to second-hand smoke.
Particulate matter is emitted from many sources both directly (primary particulate) and from interactions of gases such as NOX and SO in the atmosphere (secondary particulate). The major sources of particulate emissions vary regionally. For example, in Washington, DC, 47 percent of PM2E is sulfate derived from utilities and boilers and 35 percent is combustion products from vehicles, aircraft, and incineration. In Phoenix, Arizona only 14 percent of PM2E is sulfates and 57 percent is combustion related (other sources in both cities include nitrates from vehicles and dust from soil and roads). Control strategies for PM include both technologies that directly capture PM emissions and technologies that reduce the emissions of the precursor gases.
The primary mobile source of PM is diesel combustion in trucks, buses, construction and farm equipment. There are many technologies to reduce PM from diesel engines including particulate filters, oxidation catalysts, engine modifications and crankcase emissions controls. Diesel particulate traps are the technology of choice and, when combined with low sulfur diesel fuel, they can reduce PM emissions by more than 90 percent. The filters physically trap the particulate matter before it leaves the tailpipe and catalysts in the filter oxidize the trapped particles to form carbon dioxide and water. Particulate filters can be retrofitted to existing diesel engines, which is important because diesel engines have long operating lifetimes. Over 20,000 particulate filters have been retrofitted on diesel engines worldwide. The primary barrier to full deployment of particulate filters is the lack of availability of low sulfur fuel, which is necessary for the filter to perform. Low sulfur fuel should be widely available by 2006 because of EPA regulations.
Page 13 PREV PAGE TOP OF DOC Segment 1 Of 2
Major stationary sources of PM include power plants and industrial processes. Stationary sources, particularly power plants, emit NOX, SO and volatile organic compounds that lead to the formation of secondary particulate through atmospheric reactions. The major control strategies for direct PM (i.e., carbonaceous particles) from stationary sources are electrostatic precipitators and high-efficiency fabric filters. Electrostatic precipitators have been used for particulate control since 1923 and use electrical fields to remove particulates from boiler flue gas. The newest models can capture up to 99.5 percent of the PM emissions. Electrostatic precipitators are widely used, although many power plants have older, less efficient models. Fabric filters trap PM by passing flue gas through tightly woven fabric and are capable of 99.9 percent removal efficiency. While it is a proven technology, fabric filters are not yet widely deployed.
Other technologies to control PM emissions from stationary sources include wet scrubbers and mechanical collectors, and there are several emerging technologies as well. It is important to note that a large amount of PM emissions from stationary sources are formed from precursor gases emitted from the source. Thus, technologies that control NOX, SO and volatile organic compounds also control PM.
While a great amount is known about the correlation between particulate matter levels and health effects, many questions remain. These include:
What is the relative toxicity of the different components of PM? Are interactions between components significant?
Page 14 PREV PAGE TOP OF DOC Segment 1 Of 2
There has been much debate over the differential effects of constituents of PM (sulfates vs. carbon-based particles). This has implications for how we control PM emissions (power plants vs. motor vehicles). Not much is known about relative toxicity or the role of interactions between constituents.
Do ultrafine (less than 0.1 microns in diameter) particles have a different effect than fine (less than 2.5 microns in diameter) particles?
There is little evidence to indicate possible differences. Some have suggested that the ultrafines are the main culprit, while others argue that they are so small that they may accumulate or adsorb onto the side of the nose and throat where they would do little damage to the body.
Is there a threshold, under which levels of PM are safe?
It is unknown whether there is a threshold level. Daniels, et al. 2000 found that a threshold is possible, but would be well below current PM standards, and the cohort studies show no evidence of a threshold.
What is the physiological mechanism by which particulates cause damage?
While many hypotheses exist as to how particles cause health effects, there is no consensus as to the precise mechanism. The major potential biological responses that have been suggested include oxidative stress, pulmonary inflammation, airway hyperactivity, and alternations in the cardiovascular system such as heart rate variability.
Page 15 PREV PAGE TOP OF DOC Segment 1 Of 2
The following witnesses will address the Committee:
Mr. Daniel S. Greenbaum is the President of the Health Effects Institute (HEI), an independent, nonprofit corporation chartered in 1980 to provide high-quality, impartial, and relevant science on the health effects of pollutants from motor vehicles and from other sources in the environment. HEI is supported jointly by the U.S. Environmental Protection Agency (EPA) and industry. Dr. Greenbaum serves on the National Academy of Sciences Committee on Research Priorities for Airborne Particulate Matter. Prior to joining the Health Effects Institute, he served as Commissioner of the Massachusetts Department of Environmental Protection.
Dr. Ron Wyzga is the Technical Executive for Air Quality, Health, and Risk at the Electric Power Research Institute. He is a biostatician and has done extensive research on the health effects of particulate matter. His current research centers on how different components of particulate matter may have different health effects, and he will discuss his preliminary findings. He serves on, and has a chaired, several committees for the U.S. Environmental Protection Agency (EPA) Science Advisory Board Committees and National Academy of Sciences (NAS), including the NAS committee that will oversee the EPA's particulate matter research program through 2002. EPRI is a non-profit energy research consortium funded by the electric utility industry.
Dr. Joel Schwartz is Associate Professor of Environmental Epidemiology at the Harvard School of Public Health. His research looks at the health consequences of air pollution. He is one of the authors of the landmark Six Cities Study, a cohort study that documents a link between PM and mortality from respiratory and cardiovascular disease. Dr. Schwartz is the recipient of a MacArthur Genius Award for his work on the health effects of leaded gasoline. Dr. Schwartz will address the evidence of an adverse health effect from PM exposure, how our understanding has improved since 1997, and future research needs. The Harvard School of Public Health is one of the five EPA centers for the study of the health impacts of particulate matter.
Page 16 PREV PAGE TOP OF DOC Segment 1 Of 2
Dr. Praveen K. Amar is Director, Science and Policy at NESCAUM (Northeast States for Coordinated Air Use Management). NESCAUM's purpose is to exchange technical information, and to promote cooperation and coordination of technical and policy issues regarding air quality control among the member states. Before joining NESCAUM, Dr. Amar worked with the California Air Resources Board for fifteen years where he gained expertise in the technologies to control PM emissions. He has a Ph.D. in engineering and is a licensed Professional Mechanical Engineer.
Major Time-Series Studies
Dockery and Pope. 1994. Acute respiratory effects of particulate air pollution. Annual Review of Public Health 15:107132
Schwartz J. 1994. What are people dying of on high air pollution days? Environ Res 64:2635
Katsouyanni, et al. 1997. Short term effects of ambient sulfur dioxide and particulate matter on mortality in 12 European cities: results from time series data from the APHEA protect. British Medical Journal 314:16581663
Samet, et al. 2000. The National Morbidity, Mortality and Air Pollution Study, Part I: Methods and Methodologic Issues. Research Report 94, Part I. Health Effects Institute, Cambridge, MA
Page 17 PREV PAGE TOP OF DOC Segment 1 Of 2
Health Effects Institute. 1995. Particulate air pollution and daily mortality: replication and validation of selected studies. The Phase I report of the particle epidemiology evaluation project. Boston, MA
Levy, et al. 2000. Estimating the mortality impacts of particulate matter: What can be learned from between-study variability? Environ Health Perspect 108(2):109117
Daniels, et al. 2000. Estimating particulate matter-mortality dose-response curves and threshold levels: an analysis of daily time-series for the 20 largest US cities. American Journal of Epidemiology 152(5):407412
Major Cohort Studies
Dockery, et al. 1993. An Association Between Air Pollution and Mortality in Six US Cities. NEJM 329:17531759
Pope, et al. 1995. Particulate air pollution as a predictor of mortality in a prospective study of US adults. Am J Respir Crit Care Med 151:669674
Pope, Thurston and Krewski. 2002. Lung Cancer, Cardiopulmonary Mortality, and Long-term Exposure to Fine Particulate Air Pollution. Journal of the American Medical Association 287(9):11321141
Chairman BOEHLERT. Good morning. I want to welcome everyone here for this hearing on a vital environmental and public health issuethe impact of fine particle pollution on human health.
Page 18 PREV PAGE TOP OF DOC Segment 1 Of 2
When I became Chairman of this Committee, I said I hoped that the Committee would serve as a forum where members could undertake sober, calm, fair-minded reviews of the science underlying controversial policy decisions. We have done that a number of times in the past year-and-a-half, holding a hearing on the research into the impacts of arsenic in drinking water, for example, and today, again, we convene the Committee to get a timely overview of environmental science.
Our hearing is timely in two ways. First, the media have run numerous stories in recent months on new findings related to fine particles. Congress needs to understand the significance of those research results. And this hearing is timely because the Environmental Protection Agency is poised to begin its next review of the science concerning fine particles in advance of additional regulatory decisions. The President's Clear Skies Initiative has also focused renewed and needed attention on air pollution.
I was especially interested in holding a hearing on PM2E because I think the path that the scientific research in this area has taken is instructive. It is a good lesson in how to act in the face of scientific uncertainty.
In 1997, when EPA announced that it would regulate fine particles for the first time, the decision was extremely controversial. The science behind the decision was unsettled, the debate focused on a few key studies, and, as I put it in a speech last week, the critics of the regulation screamed uncertainty all the way to the Supreme Court.
Those of us who supported EPA back then, while acknowledging the uncertainty, argued that the evidence was strong enough to move ahead with regulation, especially given the long lead time necessary to implement any new rules. And time has borne us out, in this case.
Page 19 PREV PAGE TOP OF DOC Segment 1 Of 2
As today's hearing will indicate, our understanding of PM2E has grown much richer since 1997. And now there is a broad consensus, not only that fine particles are detrimental to human health, but that they are among the most potent of air pollutants.
The way that consensus has been reached is instructive, too. It owes a lot to the Health Effects Institute, which is jointly funded by the government and industry and has a reputation, in all quarters, as an honest broker in disputes over environmental science. HEI undertook major reviews of the studies that were at issue in 1997, as well as commissioning new work. That ability to take a step back and look at the data anew is an example of the scientific process at its best, and it has had important consequences in this case. I am pleased that we have Dan Greenbaum from HEI with us today.
Now, I don't mean to suggest that we have nothing left to learn about fine particlesfar from it. Indeed, one thing we want to hear from our witnesses today is exactly which current research questions should be our top priority and what the implications of those questions are for policy. We also want to learn what kinds of technology are now, or could be, available to control fine particles.
So there is still much to discover. Today we want to thoughtfully review the current state of the science before any new policy proposals distort the debate. We are here to learn. I look forward to the testimony. The Chair is pleased to recognize the distinguished gentleman from North Carolina, Mr. Etheridge.
[The prepared statement of Mr. Boehlert follows:]
Page 20 PREV PAGE TOP OF DOC Segment 1 Of 2
PREPARED STATEMENT OF CHAIRMAN SHERWOOD L. BOEHLERT
I want to welcome everyone here for this hearing on a vital environmental and public health issuethe impact of fine particle pollution on human health.
When I became Chairman of this Committee, I said I hoped that the Committee would serve as a forum where Members could undertake sober, calm, fair-minded reviews of the science underlying controversial policy decisions. We've done that a number of times in the past year and a halfholding a hearing on the research into the impacts of arsenic in drinking water, for exampleand today, again, we convene the Committee to get a timely overview of environmental science.
Our hearing is timely in two ways. First, the media have run numerous stories in recent months on new findings related to fine particles. Congress needs to understand the significance of those research results. And this hearing is timely because the Environmental Protection Agency (EPA) is poised to begin its next review of the science concerning fine particles in advance of additional regulatory decisions. The President's ''Clear Skies'' initiative has also focused renewed, and needed, attention on air pollution.
I was especially interested in holding a hearing on PM2E because I think the path the scientific research in this area has taken is instructive. It's a good lesson in how to act in the face of scientific uncertainty.
In 1997, when EPA announced that it would regulate fine particles for the first time, the decision was extremely controversial. The science behind the decision was unsettled; the debate focused on a few key studies; and, as I put it in a speech last week, the critics of the regulation ''screamed 'uncertainty' all the way to the Supreme Court.''
Page 21 PREV PAGE TOP OF DOC Segment 1 Of 2
Those of us who supported EPA back then, while acknowledging the uncertainty, argued that the evidence was strong enough to move ahead with regulation, especially given the long lead time necessary to implement any new rules. And time has borne us out, in this case.
As today's hearing will indicate, our understanding of PM2E has grown much richer since 1997, and now there is a broad consensus not only that fine particles are detrimental to human health, but that they are among the most potent of air pollutants.
The way that consensus has been reached is instructive, too. It owes a lot to the Health Effects Institute (HEI), which is jointly funded by the government and industry, and has a reputation in all quarters as an honest broker in disputes over environmental science. HEI undertook major reviews of the studies that were at issue in 1997 as well as commissioning new work. That ability to take a step back and look at the data anew is an example of the scientific process at its best, and it has had important consequences in this case. I'm pleased that we have Dan Greenbaum from HEI with us today.
Now I don't mean to suggest that we have nothing left to learn about fine particlesfar from it. Indeed, one thing we want to hear from our witnesses today is exactly which current research questions should be our top priority and what the implications of those questions are for policy. We also want to learn what kinds of technology are now, or could be available to control fine particles.
So there's still much to discover. Today we want to thoughtfully review the current state of the sciencebefore any new policy proposals distort the debate. We are here to learn. I look forward to the testimony.
Page 22 PREV PAGE TOP OF DOC Segment 1 Of 2
Mr. ETHERIDGE. Thank you, Mr. Chairman, and, members of the Committee. I thank the Chairman for holding this hearing to enable us to hear about the current information we have on air pollution. Just last week, the Commerce Committee held a hearing to review the accomplishments of the 1990 Clean Air Act. We have accomplished a great deal since we passed the 1990 amendments, although that progress has not always come as easily as we would have liked.
The reality is, the activities that we rely upon to support our economy and our comfortable lifestyles also create some pollution. We haven't yet figured out a way around this problem, and I expect we never will totally, at least probably not completely.
Our lives will be very unpleasant and considerably more difficult without electricity, our transportation system, which moves goods and services to our markets and allows us to move freely across town and across the country. It is essential to our economy and to our way of life. We also know there is a connection between air pollution, asthma and other health-related problems, and we need to address these problems.
This Committee plays an essential role in highlighting the value of investing in science and technology to help us decide what emission reductions need to be made and to find the least costly and burdensome way to achieve these reductions. Investment in science is the key to developing improved technology and good policies so that we continue to enjoy the benefits of a healthy, robust economy, while also improving air quality to keep all of our citizens healthy and the horizons clear.
Page 23 PREV PAGE TOP OF DOC Segment 1 Of 2 I thank all the witnesses who are here this morning to appear before this Committee and look forward to hearing your testimony. Thank you, Mr. Chairman.
[The prepared statement of Mr. Smith follows:]
PREPARED STATEMENT OF REPRESENTATIVE NICK SMITH
I would like to thank Chairman Boehlert and Ranking Member Hall for holding this hearing today on the impacts of small particle air pollution on human health. I hope that today's hearing will provide answers to the many questions that we have concerning the role that particulate matter (PM) plays in the health of our nation.
As a farmer, I have been interested in the health effects for farmers that breathe grain dust, hay chaff, field dust, PM from animals and other farm-related air pollution. The study by the Health Effects Institute confirmed that there is a link between particulate air pollution and human disease and death.
Another recent study has shown that those exposed to fine particle pollution greatly increases the risk of death from lung cancer, other pulmonary illness, and cardiovascular disease. However, there are other studies that show that children that grow up on farms develop some immunity to such things as molds, pollens, etc.
More research is necessary to determine exactly how small and large inhaled particles can cause allergies and disease. Some scholars believe particles lodged in the lung's lining, causing inflammation and/or infection, lead to death, and others find that particles can generate highly reactive oxygen-containing chemicals can lead to inflammation and allergies that can damage the heart. Clearly, the key to understanding the direct relationship between PM and disease, lies in conducting more research based on sound science.
Page 24 PREV PAGE TOP OF DOC Segment 1 Of 2
I am inclined to support cohort studies over time-series studies. Cohort studies will produce more reliable answers because they are drawn out over longer periods of time and decrease the variability of certain defining factors, such as seasonality, production cycles, and genetic predisposition.
I look forward to today's hearing addressing the long-term solutions to air pollution and this cost/benefit evaluation.
[The prepared statement of Mr. Costello follows:]
PREPARED STATEMENT OF REPRESENTATIVE JERRY F. COSTELLO
Good morning. I want to thank the witnesses for appearing before our committee to discuss the impact of small particle air pollution on human health. Particulate matter is the term for solid or liquid particles found in air. Particulate matter's chemical and physical composition varies greatly because it originates from a variety of sources. Because of its size, these particles can bypass the body's defense system and become deposited deep into body tissue. While most agree that fine particulates can cause premature death, there is still uncertainty about the mechanisms that cause lung damage and premature deaths.
Particulate matter is important in my district because of the combustion of fossil fuels. As you may know, Southern Illinois is rich in high-sulfur coal and this coal is critically important to my district. I continue to support research and development of cleaner fossil fuel initiatives which includes a program to develop new technologies for cleaner, higher efficiency coal combustion with the hopes of achieving a healthier environment. Clean coal technology has improved the NOX and SOX emissions which have, in turn, reduced particulate matter in our area.
Page 25 PREV PAGE TOP OF DOC Segment 1 Of 2
While industry and the government continue to make great strides in reducing particulate matter, research still needs to be done on what portion of the fine particulate fraction is most harmful to human health. I believe further knowledge of how particulate matter effects lung function can suggest ways to target control strategies for state and local governments to gain the most public health benefit. I am interested to know what information on health effects of particulate matter would be most helpful to state and local governments in designing their implementation plans to achieve a goal of maximum health benefits for reduced emissions without hampering continued technology advances. In addition, I want to know what research results would be helpful to state and local regulators in designing strategies to reduce air pollution.
I welcome our panel of witnesses and look forward to their testimony.
Chairman BOEHLERT. Thank you very much, Mr. Etheridge. Now, we will have our witnesses. And I want to thank all of you for agreeing to serve as facilitators and sources of information for this Committee, we value highly your input and we hope to learn a great deal from it.
We have Mr. Daniel S. Greenbaum, President of the Health Effects Institute; Dr. Ron E. Wyzga, Technical Executive, Electric Power Research Institute; Dr. Joel Schwartz, Associate Professor of Environmental Epidemiology, Harvard School of Public Health; and Dr. Praveen Amar, Director of Science and Policy, Northeast States for Coordinated Air Use Management.
Page 26 PREV PAGE TOP OF DOC Segment 1 Of 2 The general procedure is that we ask you to try to summarize your statements in five minutes or thereabouts. We are not all that arbitrary. And then that gives us more time for questions. Mr. Greenbaum, we will start with you.
STATEMENT OF MR. DANIEL S. GREENBAUM, PRESIDENT, HEALTH EFFECTS INSTITUTE
Mr. GREENBAUM. I want to first thank you for holding this hearing. Thank you for the kind words about HEI, and for both you and Members of the Committee, tell you what a pleasure it is to appear before you to share the perspective of the Health Effects Institute on what we have learned and what we still need to learn about the health effects of particulate matter.
In 1997, the U.S. EPA promulgated a new set of national ambient air quality standards for OPM based on two types, primarily, of epidemiology studies. Nearly 40 short-term studies that found links between daily changes in air pollution and daily increases in health effects, and two long-term studies, the Harvard Six Cities Study and the American Cancer Society Study, that found that those who lived in the most polluted cities had between a 17 percent and 26 percent higher risk of premature death.
There were, at the time, a number of questions about these studies. The individual short-term studies were done by diverse investigators. Would a more systematic study find the same results? Could other pollutants, which occur along with PM, be responsible for the effects? Did the exposures measured in these studies at central air pollution monitors accurately represent the exposures of people who, in general, spend most of their time indoors? And could the Harvard Six Cities study and the American Cancer Society study stand up to intensive analysis from new independent investigators?
Page 27 PREV PAGE TOP OF DOC Segment 1 Of 2
But what have we learned? Well, substantial new research has been undertaken since 1997, much of it under the guidance of the National Academy of Sciences Committee on Research Priorities for Airborne Particulate Matter, on which Dr. Wyzga and I sit. HEI alone has invested in some 40 epidemiology, exposure and toxicology studies. Key among our work has been two effortsthe National Morbidity, Mortality and Air Pollution Study, or NMMAPS, and the Re-analysis of the Harvard Six Cities and American Cancer Society studies.
NMMAPS is a systematic study of air pollution, weather and mortality in the 90 largest cities in the United States, conducted under HEI oversight by investigators at Johns Hopkins University. NMMAPS also included similar analyses of air pollution in elderly hospitalization conducted in 14 U.S. cities by investigators at Harvard University.
NMMAPS found a consistent relationship between PM and mortality in the 90 largest cities and approximately .4 percent increase in mortality for every 10 micrograms increase in PM. This level of effect was about half the size of that found in earlier studies, but it was not substantially changed by any of the other gaseous pollutants. And I have provided a graph in your testimony that describes this result.
At the same time, this first nationwide analysis found differences in levels of effect across the U.S., suggesting that other factors, perhaps different mixes of pollution, could contribute along with particles.
In addition to NMMAPS, and in response to requests from Congress, U.S. EPA, industry, environmental organizations and others, HEI also convened a detailed re-analysis of the Harvard Six Cities and American Cancer Society studies. Given full access to the medical and air pollution data from those studies, HEI selected an entirely new team of investigators, conducted a detailed audit of the data, and then implemented a large number of analyses to test whether some other difference between the most and least polluted cities in those studies could explain the increased mortality.
Page 28 PREV PAGE TOP OF DOC Segment 1 Of 2
In brief, the re-analysis assured the quality of the data, replicated the original results, and tested those results against alternative explanations without substantively altering the original findings. At the same time, the re-analysis found that the effects on mortality appeared to increase for those with less education and therefore lower socioeconomic status. Using new analytic techniques, the effects of fine particles were somewhat smaller, but remained in the analysis. There was also an association found between sulfur dioxide and mortality, but not the other gaseous pollutants.
In a summary report, issued in June 2001 by the HEI Review Committee, our committee concluded epidemiologic evidence of PM's effects on mortality and morbidity persists even when alternative explanations have been largely addressed. At the same time they noted that many longer-term questions remain.
Key among those is the question, are all particles created equal? Particles, we know, are a complex mixture of pollutants, and over the longer term, it will be important to understand whether all particles have similar levels of toxicity or whether some particles and some sources contribute higher toxicity and should be more stringently controlled. This will be a critical area for new research.
Research studies are now underway at many institutions to begin to answer this question. Initial results are coming in. But identifying whether one or more of these components is especially toxic will require a systematic, multidisciplinary effort. The HEI Review Committee has just issued, ''Understanding the Health Effects of Components of the Particulate Matter Mix,''(see footnote 1) and I have provided this to your staff and it is available on our web site. And in that, our Committee calls for two key elements of such a systematic effortparallel epidemiology studies in selected cities throughout the United States with detailed daily characterization of what is in the particle mixture, and companion toxicology studies.
Page 29 PREV PAGE TOP OF DOC Segment 1 Of 2
Parts of such an effort are currently underway in EPA and other research programs, but a more systematic approach will require substantial resources dedicated over the next decade. The result of such an effort could be a better focused and more effective path to improve public health. Thank you for the opportunity to submit these comments.
[The prepared statement of Mr. Greenbaum follows:]
PREPARED STATEMENT OF DANIEL S. GREENBAUM
Mr. Chairman, Members of the Committee, it is a pleasure to have this chance to appear before you to share the perspective of the Health Effects Institute on what we have learned and what we still need to learn about the health effects of particulate matter. For the record, I am Dan Greenbaum, President of the Health Effects Institute, an independent research institute funded jointly and equally by the U.S. EPA and industry to provide impartial and high quality science on the health effects of air pollution.
The Data We Had in 1997Short- and Long-Term Epidemiology
In 1997, the U.S. EPA promulgated a new set of National Ambient Air Quality Standards (NAAQS) for fine particulate matter (PM2E). In large measure, that action was based on two types of epidemiology studies.
There were nearly 40 short-term studies that found a statistical relationship between daily changes in air pollution and daily small but relatively consistent increases in daily levels of death, hospitalization, and illness (e.g., one percent to two percent increases in mortality for every 10 microgram/cubic meter increase in PM);
Page 30 PREV PAGE TOP OF DOC Segment 1 Of 2
Two long-term ''cohort'' studiesthe Harvard Six Cities Study and the Pope/American Cancer Society Studythat tracked selected populations of people in a series of more- and less-polluted cities, and found that those who lived in the most polluted cities had between a 17 percent and 26 percent higher risk of premature death than those who lived in the least polluted cities.
These studies suggested that a measurable portion of mortality and respiratory and cardiac illness in the United States might be attributable to fine particle air pollution, and based on them, EPA set the new, more stringent NAAQS for PM2E. At the same time, there were a number of questions about these studies, key among them:
The individual short-term studies were done by diverse investigators using somewhat different methodswould a more systematic study find the same results?
Could other pollutants, which occur along with PM2E, be more likely to be responsible for the increased mortality?
Did the deaths measured in these short-term studies represent substantial losses of life years, or the advancing of death for critically ill people by a few days?
Did the exposures measured in these studiesat central air pollution monitorsaccurately represent the exposures of people who in general spend most of their time indoors?
Page 31 PREV PAGE TOP OF DOC Segment 1 Of 2 Could the Harvard Six Cities Study and the American Cancer Society Study, whose data had only been analyzed by the original investigators, stand up to intensive scrutiny and analysis from new, independent investigators? Could there be other differences between the cities (e.g., differences in socioeconomic status or health care) that would also explain the differences in mortality?
In addition to these questions about the epidemiology, there were also questions about the relative toxicity of the many different components of the complex PM mixture, and about the possible biological mechanisms that might explain the epidemiology results, questions that were laid out in a 1998 priority research agenda by the National Academy of Sciences Committee on Research Priorities for Airborne Particulate Matter of which Dr. Wyzga and I are members.
What Have We Learned Since 1997?
Since 1997, substantial new research has been undertaken to advance our understanding of the health effects of PM. As one part of the larger effort undertaken, HEI has invested in some 40 epidemiology, exposure, and toxicology studies to test the validity of the original studies, and to begin to answer the remaining questions.
Key among HEI's work have been two efforts to determine the validity of the short- and long-term epidemiology studiesthe National Morbidity, Mortality, and Air Pollution Study (or NMMAPS), and the Re-analysis of the Harvard Six Cities and American Cancer Society studies.
Page 32 PREV PAGE TOP OF DOC Segment 1 Of 2 NMMAPS is a systematic study of air pollution, weather and mortality in the 90 largest cities in the United States, conductedunder the oversight, quality assurance procedures, and review of HEIby investigators at Johns Hopkins University. NMMAPS also included similar analyses of air pollution and elderly hospitalization, conducted in 14 U.S. cities by investigators at Harvard University.
In brief, this systematic and rigorous study found a consistent relationship between PM and mortality in the 90 largest cities of an approximately 0.4 percent increase in mortality for every 10 micrograms increase in PM. This level of effect was about half the size of that found in the earlier study, but as the graph in my testimony illustrates, this effect was not substantially affected by any of the other gaseous air pollutants. (See Figure 1) The NMMAPS investigators also found that at least a portion of the mortality was not solely frail people dying a few days early, but deaths advanced 30 days or more, and conducted analyses that suggested that errors from using centrally monitored air pollution to estimate exposure were not likely to change the basic results.
At the same time, this first nationwide analysis found differences in levels of effect across the U.S., suggesting that other factors, perhaps different mixes of pollution, could contribute along with particles to the effect. (See Figure 2) Overall, the NMMAPS analyses provided greater confidence in the results of the short-term epidemiology.
Page 33 PREV PAGE TOP OF DOC Segment 1 Of 2 In addition to NMMAPS, and in response to requests from Congress, U.S. EPA, industry and others, HEI convened a detailed re-analysis of the Harvard Six Cities and American Cancer Society studies. Given full access to the entire medical and air pollution data base from the original investigators, HEI's Expert Panel selected an entirely new team of investigators, conducted a detailed quality assurance audit of the data and replication analyses, and then implemented a large number of sensitivity analyses to test whether some other difference between the most and least polluted cities (e.g., differences in the quality of medical care) could explain the increased mortality risk.
In brief, the re-analysis assured the quality of the data, replicated the original results, and tested those results against alternative risk models and analytical approaches without substantively altering the original findings of an association between indicators of particles and mortality. At the same time, the reanalyses extended and challenged our understanding of the original results:
the effects on mortality appeared to increase for those with less education (and likely therefore of lower socioeconomic status);
when the correlations among cities near one another were considered, the effects of fine particles remained but were diminished; and
an association between sulfur dioxide (SO) and mortality (but not other pollutants) was observed and persisted when other variables were included.
In conclusion, the re-analysis: identified relatively robust associations of mortality with fine particles, sulfate, and sulfur dioxide, and tested those associations in nearly every possible manner within the limitations of the data sets.
Page 34 PREV PAGE TOP OF DOC Segment 1 Of 2
In June 2001, the HEI Review Committee issued the first in its HEI Perspectives series: Airborne Particles and Health: HEI Epidemiologic Evidence, a summary of HEI's efforts to scrutinize, test, and understand the results of PM epidemiology that had been the basis of the 1997 standards. Based on that review, HEI concluded ''epidemiologic evidence of PM's effects on mortality and morbidity persists even when alternative explanations have been largely addressed.'' At the same time, the Review Committee noted that many questions remain; e.g., how does PM affect the cardiovascular and respiratory systems? What particle attributes are associated with toxicity?
Key Question for the Longer Term: Are All Particles Created Equal?
To date, most analyses of the effects of particulate matter have focused on the mass of PM. Particles are, however, a complex mixture of pollutants, and over the longer term, it will be important to understand whether all particles have similar levels of toxicity, or whether some particles, and therefore some sources, contribute higher toxicity, and should be more stringently controlled. While there are many actions underway already to reduce overall particle levelsfor example, to control diesel vehicle PM emissions and nitrogen oxide emissions (a precursor of nitrates) from power plantsin the years to come, it will be especially important to develop the most cost-effective control strategies aimed at the most toxic sources, or at the most toxic components of those sources' emissions. This will be a critical area for new research.
There are a number of components of PM that could cause toxicity. At a multidisciplinary workshop in July, 1998, which I co-chaired with Dr. Daniel Albritton of NOAA, we identified the following key PM characteristics and components:
Page 35 PREV PAGE TOP OF DOC Segment 1 Of 2
PM particle size, surface area
Ultra fine PM
Reactive transition metals
Organic compounds (e.g., diesel PM)
Sulfates and nitrates (e.g., from SO and NOX)
Co-pollutantsSO, CO, Ozone, etc.
Research studies are now underway at EPA, HEI, EPRI, NIEHS, and other research institutions to begin to identify the relative toxicity of some of these components. Initial indication of the potency of some of these elements (e.g., the metals attached to PM) are beginning to emerge. However, identifying whether one or more of these components is especially toxic will require a systematic, multidisciplinary effort.
Page 36 PREV PAGE TOP OF DOC Segment 1 Of 2
To address these questions, the HEI Review Committee, in April 2002, issue the second in its HEI Perspectives series, entitled Understanding the Health Effects of Components of the Particulate Matter Mix: Progress and Next Steps. This review, which I have provided to your staff and is available on the HEI website at http://www.healtheffects.org/Pubs/Perspectives-2.pdf, summarizes recent HEI and other research on the effects of different components of the mix. It also lays out a systematic effort that will be necessary to achieve a better understanding, including:
Parallel epidemiology studies in carefully selected, representative cities throughout the U.S., with detailed daily characterization of the particle mixture;
Companion toxicology studies using concentrated ambient particles, source-specific particles, and model particles to test the full range of health endpoints and mechanisms for each particle type.
Many elements of such an effort are currently underway in the EPA research program and other efforts. A more systematic approach will require substantial resources dedicated over the next decade. However, the result of such an effort could be a better-focused and more effective path to improved public health.
Conclusion: Progress and Next Steps
In conclusion, we have made much progress in the last five years, especially in testing the validity of the short- and long-term epidemiology studies which served as the primary basis for the setting of the 1997 NAAQS for particulate matter. We have tested a number of possible confounding factors, explored whether errors in measuring exposure might explain the relationships between PM and health, and analyzed whether different statistical techniques could change the results. In reviewing the latest evidence, the HEI review Committee concluded ''epidemiologic evidence of PM's effects on mortality and morbidity persists even when alternative explanations have been largely addressed.'' Based on this evidence, a number of initial control measures are now moving forward.
Page 37 PREV PAGE TOP OF DOC Segment 1 Of 2
At the same, over the longer term, important questions remain, especially concerning the comparative toxicity of different components and sources of the PM mixture. Much research is underway to understand this important question and to inform and target future strategies for control at those emissions that may be most responsible. Only through a systematic effort to test and compare the toxicity of these diverse particles will be able to have the best chance of answering these key questions for the future.
Thank you again for the opportunity to present this testimony. I would be pleased to answer any questions you might have.
BIOGRAPHY FOR DANIEL S. GREENBAUM
Dan Greenbaum joined the Health Effects Institute as its President and Chief Executive Officer on March 1, 1994. In that role, Greenbaum leads HEI's efforts, supported jointly by U.S. EPA and industry, to provide public and private decision-makers with high quality, impartial, relevant and publicly credible research about the health effects of air pollution. To accomplish its mission, HEI selects, funds, oversees, and intensively peer reviews research by leading scientists in North America, Europe and Asia.
Greenbaum has focused HEI's efforts on providing timely and critical research and re-analysis on the air pollution mixture, including particulate matter (PM), air toxics, diesel exhaust and alternative technologies and fuels. In addition, HEI has recently published major scientific reviews on the health effects of Diesel Exhaust and of Oxygenates Added to Gasoline.
Page 38 PREV PAGE TOP OF DOC Segment 1 Of 2
Greenbaum recently chaired the EPA Blue Ribbon Panel on Oxygenates in Gasoline which issued its report Achieving Clean Air and Clean Water in July, 1999. Greenbaum also serves on the National Research Council Board of Environmental Studies and Toxicology, and its Committees for Research Priorities on Airborne Particulate Matter and Air Quality Management in the U.S., as well as on the U.S. EPA Clean Air Act Advisory Committee. He regularly presents the results of HEI's scientific work to U. S., international, and state audiences, the U.S. Congress, and the European Parliament.
From 1988 to 1994, Greenbaum served as Commissioner of the Massachusetts Department of Environmental Protection, where he was responsible for the Commonwealth's response to the Clean Air Act, as well as its efforts on water pollution and solid and hazardous waste. Under Greenbaum, DEP implemented a number of new approaches to achieving clean air, including regional initiatives on fuels and vehicle emissions. He also implemented two national award-winning programs: the Blackstone Project, a multi-media pollution prevention program; and a complete redesign of the state's Superfund program to accelerate the cleanup of hazardous waste sites in the state.
Greenbaum holds Bachelor's and Master's degrees from MIT in City Planning. Prior to becoming Commissioner, he worked for the Massachusetts Audubon Society, most recently as Vice President, and as Senior Planner for the Massachusetts Port Authority. Mr. Greenbaum lives in Gloucester, Massachusetts with his wife Deborah Cramer and their two daughters Abigail and Susannah.
Page 39 PREV PAGE TOP OF DOC Segment 1 Of 2 79379d.eps
Chairman BOEHLERT. Thank you very much, Mr. Greenbaum. Dr. Wyzga.
STATEMENT OF DR. RONALD E. WYZGA, TECHNICAL EXECUTIVE, ELECTRIC POWER RESEARCH INSTITUTE
Dr. WYZGA. Thank you for inviting me. Although I work for the Electric Power Research Institute, the comments that I make today are my personal comments and those basically reflect upon my scientific judgment.
The Committee has asked that I address three questions. Let me try to address each of these in my oral comments, although my backup written testimony provides much more detail.
The first question related to the health effects of small particles, the differential toxicity of its components, and the sources of toxic components and how our knowledge of particulates in health have changed since 1997. There are a large number of scientific studies that report a link between air pollution and health. From this literature I conclude there is a clear association between health and air pollution in the U.S. at current pollution levels.
Among the various pollutants examined, the strongest associations between pollution and health are for particulate matter, or PM. However, there is, as yet, no extensive biological explanation for the link between the pollution found in the U.S. today and observed health responses.
Page 40 PREV PAGE TOP OF DOC Segment 1 Of 2
There was limited data on the toxicity of the different components of particulate matter. Few toxicology experiments have been undertaken examining the different fractions of PM, but those that have been done have found significant differences in toxicity for the different samples.
The EPRI ARIES study was designed to examine the toxicity of various components of PM and air pollution. This study, conducted in metropolitan Atlanta, is unique in terms of the number of air quality parameters measured and the number of health effects examined.
In this study, we are examining both potential mortality and morbidity associations with air quality. For mortality of people over 65 years old, the results to date shows statistically significant associations for several pollutants. These include PM, fine particulates or PM2E, and the PM coarse fractionthat is the difference between PM and PM2E, as well as carbon monoxide, elemental carbon, and organic carbon.
The results today for morbidity show that in general different components of air pollution are associated with respiratory effects than those associated with cardiovascular effects. The respiratory effects appear to be related to the coarse fraction of PM and to the gaseous pollutantscarbon monoxide, ozone, NO, and SO. On the other hand, cardiovascular effects seem to be associated with fine particles, carbon monoxide, and NO. However, the only fraction of fine particles that show any statistically significant associations with these effects are carbon-containing particles, organic and elemental carbon.
There is little evidence to date of any health effects tied to acid aerosols, and no associations were found between any health effect and total soluble metals, ultrafine particles, or sulfates.
Page 41 PREV PAGE TOP OF DOC Segment 1 Of 2
The second question asked by the Committee related to what we know about the components of fine particulate matter regionally and how this correlates with sources. Particulate matter is a complex mixture and its composition varies over time and place. EPRI, EPA and others have undertaken studies in several different geographical regions of the U.S. to obtain a better understanding of particulate composition. When we analyze for the composition of particulate matter, we see there are broad regional differences.
In most urban areas of the eastern United States, carbon-containing components of PM are most prevalent, followed closely by sulfates. In the western United States, data are more limited, but carbon-containing compounds appear to be particularly significant; sulfates are less significant. In California, nitrates can be a major component of PM, while sulfates are relatively a small fraction of the PM mass.
Urban areas generally have greater concentrations of carbon-containing components than rural areas. This is because there are numerous local sources in urban areastraffic, fireplaces, factories, etcetera.
The last question related to the most important research needs with respect to health effects of air pollution. There is a great need for additional studies that focus upon the specific components of particulate matter and their relationship to public health. I would urge others to consider studies similar to ARIES in other geographic areas.
In addition, laboratory studies examining the toxic effects of specific components and sources of particulate matter should also be undertaken to help identify the pollution components that impact public health by developing a better biological understanding of the link between pollution found in the USA today and health effects.
Page 42 PREV PAGE TOP OF DOC Segment 1 Of 2
Let me recap my major points. Air pollution likely impacts the health of individuals in the U.S. today. Particulate matter is a likely candidate to explain these impacts. In our studies, the observed health impacts appeared to be most strong and associated with specific particle constituents. When health effects are associated with fine particles, our research points strongly to particles that contain carbon as the agent of concern.
In most U.S. cities, carbon-containing particles are the largest component by weight. Gaseous pollutants may still be of health concern. There is a strong need to identify with more certainty those specific components of air pollution that cause health effects. And decreasing the nontoxic part of particulate matter will not reduce health effects.
In summary, our latest results show that when health effects of fine particles are seen, these effects are most strongly associated with specific particle constituents. This may be an important fact in designing control strategies. Further research is needed to extend these human health studies to other geographic areas, and laboratory toxicology studies are also needed to supplement these.
I would like to thank the Committee for this opportunity to present my views and would be pleased to respond to any questions. Thank you.
[The prepared statement of Dr. Wyzga follows:]
PREPARED STATEMENT OF RONALD E. WYZGA
Page 43 PREV PAGE TOP OF DOC Segment 1 Of 2 Introduction
I am Dr. Ronald Wyzga. I am a Technical Executive and Program Manager for the Electric Power Research Institute (EPRI), in Palo Alto, California. EPRI is a non-profit corporation funded by voluntary contributions and has qualified as a tax-exempt scientific organization under Section 501(c)(3) of the Internal Revenue Code. EPRI, which performs scientific research for the benefit of the public, is over 25 years old and has an annual budget of approximately $350 million. EPRI's Environment Sector has an annual budget of approximately $50 million; this makes EPRI one of the largest privately-funded health and environmental research organizations in the world. Within the Environment Sector, I am responsible for air quality research, including research on the health effects of air pollution. The results of EPRI's health and environmental research is published and made publicly available, usually through the peer-reviewed scientific literature.
Personally I became interested in the topic of the relationship between air pollution and health (and specifically particulate matter) while a graduate student at the Harvard School of Public Health, and my doctoral dissertation in biostatistics in 1971 addressed this topic. Since then I have been actively engaged in environmental health issues. I have co-authored a book and published over 50 peer-reviewed papers on air pollution health issues. I have served on and chaired subcommittees of the National Research Council (NRC), National Academy of Sciences. I currently serve on the NRC Committee on Research Priorities for Airborne Particulate Matter. I have also served on or chaired several EPA Science Advisory Board Committees, and I have been appointed a Fellow of the American Statistical Association. The comments that I present today reflect my personal views and judgments as a scientist who has worked in this area for over thirty years. These comments should not be construed to be the views of my employer or of any associate.
Page 44 PREV PAGE TOP OF DOC Segment 1 Of 2
There are a large number of scientific studies that report a link between air pollution and human health. I have personally been involved in some, and EPRI has supported many more. In any consideration of the health and air pollution issue, it is important to keep in mind that air pollution is a complex mixture of many different types of gases and particles. Discerning specific causative agents is a challenge we in the scientific community are working to address. Given the large body of literature that has appeared in the past several years, I am led to the following conclusions:
1.) There is a clear association between air pollution and health in the U.S. at pollution levels we experienced in the 1990s and earlier. There are well over one hundred epidemiological studies that have found such an association to be statistically significant. Results from studies that relate the number of health effects on a given day to the air quality on that day and preceding days are particularly compelling.
2.) Among the various pollutants examined, the strongest associations between air pollution and health are for particulate matter. Several studies have included both particulate matter and other pollutants, such as ozone and carbon monoxide (CO), in their analyses. Particulate matter (PM) is most consistently associated with health responses although there are a number of studies where other pollutants, especially CO, are most highly associated with health responses. Interpretation of these study results is complicated because of technical issues such as differences in the actual personal exposures to the various pollutants, and statistical concerns about relative differences in measurement error of the various pollutants.
Page 45 PREV PAGE TOP OF DOC Segment 1 Of 2
3.) Laboratory studies have not provided an accepted biological explanation for the link between the pollution found in the U.S. today and observed health responses. Evidence from laboratory studies lags behind that obtained from epidemiologic studies; i.e., field studies. Some recent laboratory studies have found adverse biological responses of PM, but we still don't know enough to conclude that the biological mechanisms studied can explain the effects observed in human epidemiological studies.
4.) Particulate matter is a complex mixture and its composition varies over time and place. EPRI and others have undertaken studies in several different geographical regions. When we analyze the composition of PM, we see that there are broad regional differences. In most urban areas of the Eastern half of the U.S., carbon-containing components of PM are most prevalent, followed closely by sulfates. Sulfates are more prevalent in the summer season than in the winter season. In the Western U.S., data are more limited, but carbon-containing compounds appear to be particularly significant. In California, nitrates are a major component of PM, and sulfates are a relatively minor constituent. Urban areas generally have greater concentrations of carbon-containing components than rural areas.
5.) There are limited data on the toxicity of the different components of particulate matter. Few toxicology experiments have been undertaken examining the different fractions of PM, but those that have been done have found differences in toxicity for the different samples. Other results show that the total quantity of PM does not explain biological responses. Certain components in PM appear to explain the results more readily than total PM.
6.) The EPRI ARIES (Aerosol Research Inhalation Epidemiology Study) project was designed to examine the toxicity of the various components of PM and air pollution. This study is unique in terms of the number of air quality parameters measured and the number of health effects examined. This study, undertaken in Metropolitan Atlanta in conjunction with several universities, U.S. Department of Energy, and others, characterized the air quality on a daily or more frequent basis for over one hundred air quality variables. This characterization, accompanied by a suite of epidemiological studies, allowed us to examine the influence of the various components of air pollution on a variety of health outcomes. In general, the ARIES study is finding that different components of air pollution are associated with respiratory effects than are associated with cardiovascular effects (heart-related effects). More-detailed preliminary results are given in the detailed testimony, but in summary, the respiratory effects appeared to be related to the ''coarse'' fraction of PM (particles with size ranges between 2.5 and 10 microns or the difference between PM and PM2E) and the gaseous pollutants (CO, ozone, NO, and SO). Cardiovascular effects were associated with PM2E (particles 2.5 microns in size and smaller) and CO. However, the only fraction of PM2E that showed any association with these effects were carbon-containing particlesorganic and elemental carbon. It is the PM2E fraction that has been at the center of attention as the potential cause of negative health impacts.
Page 46 PREV PAGE TOP OF DOC Segment 1 Of 2
7.) There is a great need for additional studies that focus upon the specific components of particulate matter and their relationship to human health. Controlling the non-toxic fraction of air pollution or particulate matter will not result in any health benefits. I would urge others to consider studies similar to ARIES in other geographic areas. Atlanta is representative of the mix of pollutants found in many cities in the Eastern U.S. But as with all studies, we will have more confidence in the ARIES results when they are replicated in other places. Additional studies examining the toxic effects of the specific components and sources of particulate matter (PM) should also be undertaken to help identify the pollution components that impact public health.
There is a clear association between air pollution and health in the U.S. at pollution levels we have experienced in the 1990s and earlier. Several different types of epidemiological studies, undertaken at a wide variety of locations, have found associations between air pollution and human health effects in the U.S. The studies largely fall into two different types: ''chronic'' studies, which compare differences in the health and air quality in many different geographical areas, and ''acute'' studies which compare the health status of a group of individuals for many days with changes in air quality concentrations over the same time period. I personally have more confidence in the latter (''acute'' studies), primarily because there is a lower likelihood that unknown or unaddressed confounding factors influence the study results. For example, when comparing the health experience of several cities (as in chronic studies), it is important to characterize all the potential differences among those cities that may influence health and possibly be related to air quality; these could include many factors, such as economic status, quality of medical care, diet, exercise habits, weather, occupational exposure, smoking history, etc. Data for all of these are often not available, and it is difficult to include all of these factors in the analysis. For the ''acute'' studies, major sources of potential confounding are related to weather differences across days and to broad seasonal trends in health effects. Both of these can be treated reasonably well in the analysis of study results. Hence I find the results of these acute studies to be particularly compelling. Overwhelmingly they show a relationship between health effects and air pollution in the U.S. (indeed worldwide) for relatively recent time periods.
Page 47 PREV PAGE TOP OF DOC Segment 1 Of 2
Among the various pollutants examined, the strongest associations between air pollution and health are for particulate matter. Many of the earlier studies (pre-1990s) considered just one or a limited number of pollutants; in these studies, PM was frequently studied and found to be associated with health effects. Later studies more frequently examined multiple pollutants. Most of these studies also found associations between PM and health effects, although a subset of the studies found greater associations between health effects and other pollutants, especially carbon monoxide (CO). In interpreting the results of these studies, several factors must be taken into account. First, the pollution measurements used in these studies were made at outdoor monitoring sites; these are not necessarily representative of personal exposures to these pollutants. We now have some limited data on the differences between personal exposures and outdoor measurements. These differences are not the same for every pollutant measured, leading to possible statistical impacts on the results of the analyses of the relationships between air pollution and health.
Second, studies can only consider pollutants for which measurement data are available, and only a few pollutants/substances are generally measured. If the pollutant(s) that are truly responsible for health effects are not measured, then other pollutants that are measured and present at the same time as the responsible pollutants can be associated statistically with health effects. In such cases what we measure and use in our analyses could be a surrogate for something that is not measured. In all of our study results we need to keep this in mind. The only way to overcome this issue is to measure as many components of air pollution as possible, hopefully including the true culprit (or culprits), which only detailed analyses can reveal.
Page 48 PREV PAGE TOP OF DOC Segment 1 Of 2 There is as yet no accepted biological explanation for the link between the levels of pollution found in the U.S. today and observed health responses. Past research has focused on epidemiological studies. Laboratory research, which has been limited to date, can focus on establishing the underlying biological mechanisms that can cause negative health effects. Several biological explanations have been put forth to explain the results from epidemiological studies, and recent laboratory results support some of these hypotheses. For example, one study appeared to show that blood clotting can increase with exposure to higher levels of exposure to fine particulates. If this occurs, it could be an explanation for why some heart disease effects are related to fine particulate levels in epidemiological studies. At this time, I believe that the most likely scenario is that a combination of explanations is responsible for the effects observed, with different mechanisms acting for different air pollution/PM components. Different mechanisms may also be acting in susceptible individuals, such as asthmatics or those with hypertension. Clearly, much more work is needed to gain insight into the mechanism of PM action.
Particulate matter is a complex mixture and its composition varies over time and place. Appendix A summarizes particulate matter compositional data for many urban areas in the U.S. Some of these categories (e.g., organic matter) contain hundreds of chemical compounds. The charts show differences in the levels of fine particulates (PM2E) and in its composition for many U.S. cities. The results show that, except for Pittsburgh (Lawrenceville, PA), the carbon-containing compounds are the largest fraction in each city. Sulfates are a close second in most cities in the Eastern U.S. Nitrate can be an important fraction in California (and Salt Lake City). Data are not presented for rural areas. The composition of PM in rural areas is similar to that in nearby urban areas except that the concentrations of the carbon-containing species are lower. This is because of the more numerous local sources in urban areas (traffic, fireplaces, factories, etc.) There are also seasonal differences in the composition of PM. The concentration of sulfates is substantially higher in the warmer months than in the colder months; nitrate concentrations are higher in the winter months in the Eastern U.S.
Page 49 PREV PAGE TOP OF DOC Segment 1 Of 2
There are limited data on the toxicity of the different components of particulate matter. Several PM components have been hypothesized to play a role in toxic responses, including acid aerosols, metals, sulfates, nitrates, ultrafine particles (very tiny particles much smaller than the PM2E particles), bioaerosols (including pollen and mold spores), diesel exhaust particles, and organic compounds. Toxicological and human exposure evidence suggests that acid aerosols do not contribute much to the adverse respiratory outcomes observed in epidemiological studies; however, acid components have not been assessed thoroughly with respect to potential cardiovascular effects. Metals have been shown in multiple studies to cause cell injury and other effects. Particle size, specifically the ultrafine fraction, may also be important in the development of health effects. A number of studies have investigated the effects of ultrafines and found lung inflammation and other respiratory effects, although it appears that chemical composition may play a key role in the responses observed. Cardiovascular and systemic effects of ultrafine particles have been investigated to only a limited extent. Bioaerosols are not considered to account for the reported health effects of ambient PM as their concentrations are very low and effects can occur at times when bioaerosol concentrations are low. Toxicological evidence is accumulating to suggest that diesel PM can exacerbate the allergic response to inhaled allergenic material. Finally, the organic compounds associated with PM have been little-studied from a toxicological perspective, although they represent a substantial portion of the mass of ambient PM (1060% of total dry mass). Other fractions of PM including sulfates and nitrates appear to be of less concern. In a recent draft report, the Netherlands Aerosol Programme concluded: ''Based upon current toxicological and human clinical knowledge: water, sea salt, ammonium sulfate, ammonium nitrate and probably non-crystalline crustal material too, can be considered an inert part of PM at the ambient concentrations in the Netherlands.'' This report has not yet been finalized, and the conclusions are still under discussion.
Page 50 PREV PAGE TOP OF DOC Segment 1 Of 2
In order to more fully understand which components of PM are responsible for the health effects observed, additional toxicological studies must be conducted.
The EPRI ARIES study was designed to examine the toxicity of the various components of PM and air pollution. This study is unique in terms of the number of air quality constituents measured and the number of health effects examined. The best way to increase our understanding of the types and fractions of PM and air pollution that may be responsible for the health effects observed in other studies is to undertake a study in which all of the potentially relevant fractions of PM are measured. Traditionally we only measure what is required because of local, state or federal regulations. On occasion a research study may measure a larger array of air pollutants but it is rare to have a large number of constituents measured systematically over an extended period of time. ARIES addresses this need through detailed air quality characterization for a period of over two years and through undertaking several epidemiological studies to relate air quality characteristics to health effects. Appendix B provides further details about ARIES, as well as provisional results.
Extensive dailyand in some cases continuousmeasurements were made for all of the size fractions and constituents of PM about which concerns have been raised. At the same time several epidemiological studies were undertaken. Initial results from the analytical team focused upon the subset of air pollution measures tied to the major existing hypotheses about the pollution health relationship. Two years of data have been analyzed and manuscripts are now under preparation for peer review. The draft results are very informative, and I would like to share them with you.
Page 51 PREV PAGE TOP OF DOC Segment 1 Of 2
These results are complex and reflect a methodology that examined pollutants individually. Analyses which consider several pollutants simultaneously are planned and may help identify the pollution components that are greatest concern.
Several pollutants are statistically significantly associated with daily mortality of those over 65 years old; they include PM2E, PM, PM-''coarse,'' CO (carbon monoxide), and elemental and organic carbon. The latter are two classes of carbon-containing particles with the organic carbon fraction containing more volatile constituents than the elemental carbon fraction. (The technical definitions are tied to the methods used to measure them.) Results are available for several morbidity measures including emergency room admissions to Atlanta area hospitals, unscheduled physician visits to a health maintenance organization (HMO), and responses of defibrillator devices implanted in patients with erratic heart rhythms. Preliminary analyses of heart rate variability considered only PM2E and not its components nor gases; based on these limited data, PM2E was found to be associated with statistically significant changes in heart rates.
Lung and respiratory problems were related to PM and the ''coarse'' fraction of PM and to the pollutant gases including ozone, NO, CO, and SO.
Heart disease responses were much more likely to be related to PM2E, carbon monoxide, and NO. When the components of PM2E were considered, the only ones found to be significant were elemental and organic carbon. There was little evidence of any health effect tied to acid aerosols; no associations were found between any health effect and total soluble metals (additional analyses are planned to look at individual metals); no associations were found with ultrafine particles (however the concentrations of these particles change so rapidly over time and space, it is doubtful that the ARIES study could shed much light on the effects of these particles; nevertheless their concentrations are unrelated to the concentrations of other particle fractions; hence it is unlikely that ultrafine particles can explain the associations seen with other particles); organic compounds were associated with several cardiovascular effects; no cardiovascular or respiratory effects were associated with sulfates.
Page 52 PREV PAGE TOP OF DOC Segment 1 Of 2
ARIES did not look at sources of pollution directly. We did, however, undertake a source-attribution analysis of the organic compounds in Atlanta. Cardiovascular effects were found in the winter months only in this study. In the winter months organic compound concentrations were tied principally to wood smoke although diesel emissions were also a contributor. Diesel emissions were also a contributor in the summer months when no cardiovascular effects were related to organic pollution.
There is a great need for additional studies which focus upon the specific components of particulate matter and examine their relationship to human health. The ARIES study will provide an important piece of evidence in understanding which fractions of PM and of air pollution are the most important in affecting human health. ARIES results are from one metropolitan area, Atlanta. Atlanta is a logical place for a study; it has high pollution levels, many sources of pollution, and no unique sources of pollution that would yield a unique result. Nevertheless it is important to undertake similar studies in other metropolitan areas. We are now engaged in similar, although more limited, studies in St. Louis and Baltimore, where detailed monitoring is underway. Much of this monitoring is funded by EPA's supersites monitoring program. Undertaking such studies is expensive because the air quality monitoring itself is costly; hence governmental resources to undertake such studies are critical.
Secondly more laboratory studies are needed which examine specific fractions of particulate matter and its toxicity. Since it would be very costly and time-consuming to test all specific compounds rigorously in laboratories, special protocols should be considered which examine the mixture of pollutants associated with specific sources. For example, studies are now underway at the National Environmental Respiratory Center examining the toxicity of effluent streams from several sources. EPRI is planning some similar efforts, but clearly more research is needed. There are a large variety of emissions from different sources, and we need to learn how these emissions interact with other pollution elements once they enter the environment at large.
Page 53 PREV PAGE TOP OF DOC Segment 1 Of 2
An ongoing committee of the National Research Council, of which I am a member, will issue a report at the end of this year or early next year identifying the highest priority research needs to inform particulate matter-health policy issues.
1. Air pollution likely impacts the health of individuals in the U.S. today.
2. Particulate matter is a likely candidate to explain these impacts.
3. In our studies, the observed health impacts appear to be most strongly associated with specific particle constituents.
4. When health effects are associated with fine particles, our research points strongly to particles that contain carbon as the agent of concern.
5. In most U.S. cities, carbon-containing particles are the largest component by weight.
6. Gaseous pollutants may still be of health concern.
7. There is a strong need to identify with more certainty those specific components of air pollution which cause health effects.
8. Decreasing the non-toxic part of particulate matter will not reduce health risks.
Page 54 PREV PAGE TOP OF DOC Segment 1 Of 2
BIOGRAPHY FOR RONALD E. WYZGA
Area Manager, Air Quality, Health, and Risk Assessment, EPRI
1997presentTechnical Executive, EPRI, Palo Alto, CA
Responsible for all aspects of air quality research including particulate matter/ozone health, air toxics and visibility issues. Oversees annual research budget of over $15 million.
19751996Senior Manager, Program Manager, Project Manager, EPRI, Palo Alto, CA
Page 55 PREV PAGE TOP OF DOC Segment 1 Of 2
Sc.D.Biostatistics (1971), Harvard University School of Public Health, Boston, MA
M.S.Statistics (1966), Florida State University, Tallahassee, FL
A.B.Mathematics (1964), Harvard College, Cambridge, MA
Holds numerous advisory positions, including Consultant to EPA Science Advisory Board; Consultant to Environmental Health Committee; Consultant to Clean Air Scientific Advisory Committee; Member, National Academy of Sciences, National Research Council Committee on Research Priorities for Airborne particulate Matter; Chairman, Subcommittee on Biostatistics and Modeling; Member, Safe Drinking Water Oversight Committee; Chairman, Safe Drinking Water Committee on Mixtures; Member, Neurotoxicity and Risk Assessment; Member, Committee to Review the Effectiveness of the Health Effects Institute.
Elected Fellow of the American Statistical Association, 1990
Page 56 PREV PAGE TOP OF DOC Segment 1 Of 2 With L.J. Folinsbee, ''Health Effects of Acid Aerosol,'' Water, Air & Soil Pollution, 85(1):177188, 1995.
''Is the Current Fine Particulate Standard Protective of Public Health?'' Human and Ecological Risk Assessment, Volume 5, Number 3:493499, June 1999.
With F.W. Lipfert, Perry, Jr., M.H., Miller, J.P., Baty, J.D., Carmody, S., ''The Washington University-EPRI Veterans' Cohort Mortality Study: Preliminary Results,'' Inhalation Toxicology 12 (Supplement 4):4173, April 2000.
With F.W. Lipfert, J. Zhang, ''Infant Mortality and Air Pollution: A Comprehensive Analysis of U.S. Data for 1990,'' Journal of Air & Waste Management Association, Volume 50:13501366, August 2000.
With M. Van Loy, T. Bahadori, B. Harsell and E. Edgerton, ''The Aerosol Research and Inhalation Epidemiology Study (ARIES): PM2E Mass and Aerosol Component Concentrations and Sampler Intercomparisons,'' Journal of Air & Waste Management Association, Volume 50:14461458, August 2000.
Chairman BOEHLERT. Thank you, Dr. Wyzga. Dr. Schwartz.
STATEMENT OF DR. JOEL SCHWARTZ, ASSOCIATE PROFESSOR OF ENVIRONMENTAL EPIDEMIOLOGY, HARVARD SCHOOL OF PUBLIC HEALTH
Page 57 PREV PAGE TOP OF DOC Segment 1 Of 2
Dr. SCHWARTZ. Thank you very much, and thank you for inviting me here to speak to you. As you know, science is a process. It is not a body of knowledge. And so we will always have more to learn. I think the issue before us is whether we know enough to act.
And in 1997, when EPA set the standard, as you heard from Dan, there were considerable controversies. And among the criticisms were, as he said, that these daily studies were flawed because they failed to control well enough for other factors like weather and gaseous air pollutants. That even if those studies were correct, that the people who were dying were people who were going to die next week anyway. They were people on the brink of death, and so the public health significance was not great. That there were probably thresholds below which there were no effects. That there were, as you heard, flaws with the two prospective cohort studies. That there was no biological plausibility and that it couldn't possibly be true because exposure to particles was not well correlated with ambient levels. So I would like to try to go through those briefly and address them.
You have heard about the NMMAPS study, a systematic study of essentially all the urban areas in the United States. And the findings were, one, that there was no association between gaseous air pollutants, any of them, and daily death in that study. Okay. [Individual citiesyou saw things in other cities.] It was protective, on average it was zero. Two, that there was a PM association. Three, that it was not sensitive to how well you controlled for weather or for season. And last, that it wasn't sensitive to controlling the gaseous air pollutants. So I think that we have resolved that issue.
The second point, the harvesting phenomenon, the idea that the people who died today would have died next week. Well, if that is true, you could sort of average out today and next week and you would get nothing. And, in fact, I did two studies that took exactly that approach and tried to look at this phenomenon.
Page 58 PREV PAGE TOP OF DOC Segment 1 Of 2
In addition, we have another two studies that used an entirely different approachone of them, in ten European cities with a total population of 29 million people. And all four of those studies show the same thing. They show that when you look out to sort of longer term, instead of the net effect going down, it goes up. That, in fact, the effect is two-and-a-half times greater than the effect if you just looked at a single day's pollution correlated with daily deaths.
And there was another study from the investigators at Hopkins looking at Philadelphia data and they foundusing a third entirely different approach, and they found the same thing. At longer time scales, the effect size more than doubles. Now, the import of this is if you take these higher coefficients at the longer time scales, we are talking about 100,000 early deaths per year, which is more than AIDS, breast cancer, and prostate cancer put together.
But unlike those diseases, we know the cure. We know how to put scrubbers on power plants and we have commercially available busses that run on natural gas instead of diesel fuel to reduce the carbon particles you heard about.
In thresholds we have done some studies again indicating that there aren't thresholds and others have repeated those. Which types of particles, I agree, is an area where we need more research, but we do have some data that has been coming out.
We have a study, a multi-city study, and I think Dan is correct in saying that that is the direction of the future, where we looked at six cities in the United States, and we looked at particles from wind-blown dust, particles from traffic, particles from coal-burning power plants and particles from residual oil, simultaneously. And we saw significant associations with those sulfate particles, controlling for the others, significant associations with the traffic particles, controlling for the others, and an indication that the traffic particles may, indeed, be more toxic, although I think we need more work there.
Page 59 PREV PAGE TOP OF DOC Segment 1 Of 2
Biological plausibility is one area where there has been a tremendous amount of information. We had very little idea what might be going on in 1997. Today, we have animal studies, controlled human exposure studies, so there is no possibility of confounding by gaseous air pollutants there, and epidemiology studies, all of which show there are electrocardiogram changes associated with short-term exposure to combustion particles [that are in the direction] that puts you at risk of arrhythmia, which is one of the leading causes of sudden death, which is the death that we particularly see associated with particles.
We have animal studies, controlled human exposure studies and epidemiology studies that show airborne particles are associated with increases in inflammatory factors, clotting factors, and other blood markers that are known risk factors for having a heart attack. We have epidemiology studies and controlled chamber studies showing vascular changes, like increases in blood pressure and tighteningnarrowing of arteries, that are associated with particle exposure.
So we have a tremendous amount of new information that gives us too many potential mechanisms. The future will let us narrow down which of these are more important, but it can no longer be said that we don't see mechanistic pathways that get us from the exposure to the death.
And, lastly, on the exposure, we have multiple studies that show that if you look over time there is, in fact, quite good correlation between personal exposure to particles, particularly personal exposure to particles of outdoor origin, and the concentrations that the ambient monitors show. And we also have data that show that that is not true for any of the gaseous air pollutants, which makes them very unlikely to be confounders. Thank you.
Page 60 PREV PAGE TOP OF DOC Segment 1 Of 2
[The prepared statement of Dr. Schwartz follows:]
PREPARED STATEMENT OF JOEL SCHWARTZ
In 1997 When EPA set a standard for PM2E, there was considerable controversy about that decision. In particular, industry consultants attacked the scientific basis for the standards, arguing:
1. The dozens of studies showing day to day changes in airborne particle (PM) levels were associated with day to day changes in how many people died were flawed, due to inadequate control for weather, season, and other pollutants, or to only reporting results from cities where there was an association;
2. Even if those studies were true the deaths were only of persons who were going to die soon anyway, whose deaths were brought forward by a few days;
3. Even if those studies were true, there was a threshold below which no effects would be seen, and hence the health benefits of reducing pollution levels were low;
4. Even if those associations were true, we did not know which types of particles were associated with these deaths, and could not regulate until we resolved that question;
5. The two prospective studies, which followed groups of people over time, controlled for individual risk factors, and found higher death rates in more polluted cities were flawed, and would not stand up to more rigorous analysis. Because they contained confidential medical records of participants, they were not publicly available for re-analysis, and this was attacked as hiding the data.
Page 61 PREV PAGE TOP OF DOC Segment 1 Of 2
6. There were no biologically plausible mechanisms to support the epidemiological associations, or information on who is sensitive.
7. That the associations were implausible because personal exposures to particles were not related to ambient exposures.
Since then, great progress has been made resolving all of these issues. I will address these questions in turn.
1. Daily Time Series Studies
Since 1997, a number of studies have addressed the question of potential confounding by other factors such as season, weather, and other pollutants. For example, some studies have been conducted in locations where sulfur dioxide levels in the air are vanishingly small, making confounding by that pollutant impossible. I published studies from Tucson(see footnote 2) and Spokane,(see footnote 3) which are cities that have this characteristic, for example. Another set of studies from London and Santa Clara, were restricted to the winter, when ozone levels are trivial. These studies provide assurance that associations can be found in the absence of ozone exposure, and hence inadequate exposure to ozone is not the reason for the observed associations with particles. Recently, two large multi-city studies have addressed this issue further. Samet and co-workers, with funding from the Health Effects Institute, which is jointly funded by EPA and Industry, examined daily deaths and air pollution in the 90 most populous counties in the United States.(see footnote 4) This study addresses all of the questions above. First, there is no bias in reporting resultsessentially every city in the U.S. was studied and the names were announced publicly in advance of the analysis. Second, they performed extensive analyses of the sensitivity of the results to very substantial changes in the control for weather and season. They found little sensitivity. Third, they examined all criteria air pollutants, and not just PM. They found no evidence of a significant association between any other pollutant and daily deaths when examined one at a time (without control for PM or other pollutants), after control for PM, and after control for other criteria pollutants. They found consistent associations with PM that were little changed after control for any of the other criteria pollutants. I examined ten U.S. cities with daily PM monitoring (many cities only monitor one day in six), and found similar results.(see footnote 5) Since the Samet study examined all the major cities in the U.S., and was partially industry funded, there is no longer any basis for the arguments for confounding.
Page 62 PREV PAGE TOP OF DOC Segment 1 Of 2
Daily time series studies have also helped identify the types of illnesses that were being effected by PM. In 1994, Schwartz(see footnote 6) reported that the greatest relative increase in pollution-associated deaths in Philadelphia was for individuals who were ''dead on arrival'' to the hospital. Similarly, PM was primarily associated with deaths occurring out of the hospital in a ten-city study of air pollution and mortality. Since a substantial proportion of those deaths are due primarily to arrhythmias and myocardial infarctions, these results suggest that particulate air pollutants adversely impact the cardiovascular system. Further support for this theory is provided by recent time series studies that show particulate air pollution is associated with hospital admissions for nonfatal myocardial infarctions and other heart conditions.(see footnote 7),(see footnote 8),(see footnote 9)
The hypothesis that air pollution related deaths are only being brought forward by a few days is often called the harvesting hypothesis. If air pollution related deaths today are just in people who would have died in a few days or a week otherwise, then an air pollution episode today should result in fewer deaths in the following week. Netting out those two effects, we would find no significant reduction in lifespan. I addressed this idea, and constructed moving averages of daily deaths, which do net out these periods of subsequent lower than expected deaths. The size of the moving averages (7-day, 15-day, etc.) was varied, and the association of PM with these averages, which netted out harvesting over progressively larger timescales, was examined. Instead of going down, the estimated effect of particles on deaths more than doubled as the analysis went to longer averaging periods.(see footnote 10) This was subsequently extended to data from another city, and to hospital admissions.(see footnote 11) A second approach directly estimated the correlation between daily deaths and PM for up to 45 days after the air pollution exposure. This was applied to 10 cities with a population of 29 million, and a meta-analysis combined the results.(see footnote 12) The effect of PM was 2.5 times as great when taking these delayed effects into account. This analysis has been extended to examine cause-specific mortality (Zanobetti et al., in review).
Page 63 PREV PAGE TOP OF DOC Segment 1 Of 2
Zeger and co-workers took an entirely different approach.(see footnote 13) They used frequency domain regression to examine the issue, arguing that if the deaths were only brought forward by a few days to weeks, the pollution association would only be found in high frequencies. Their results (in Philadelphia) were the sameat longer frequencies, the effect size doubled. These results indicate the previous risk assessments have significantly underestimated the effects of PM on daily deaths.
A new methodology that allows the combination of smoothed dose-response curves from multiple locations was developed. Smoothing is a technique that makes no assumption about the shape of the dose-response curve, and lets the data determine it. Combining across multiple cities gives more stability and assures that results are not statistical flukes. The technique was tested using simulation studies, and applied to an analysis of PM data and daily deaths in 10 U.S. cities. There was no deviation from linearity down to the lowest exposure concentrations observed.(see footnote 14) A second study repeated this approach using data from 8 Spanish cities.(see footnote 15) Again no threshold was seen. This second study controlled for SO, which had no effect on the PM association. While these papers did not use PM2E as the exposure measure, in a subsequent study(see footnote 16) we applied the same method to the association between PM2E and daily deaths in six U.S. cities. These results are shown in Figure 1. The triangles are the combined (over 6 cities) estimated effects at each 2 mg/m increment, and the line is a straight line fit to the estimates. Once again, no evidence of a threshold was found.
Page 64 PREV PAGE TOP OF DOC Segment 1 Of 2
Daniels and co-workers took a related approach, applying regression splines to estimate the association between PM and daily deaths in 20 U.S. cities.(see footnote 17) Once again, they found no indication of a threshold, and evidence for a linear association. Schwartz and co-workers1B= (2002) have demonstrated that a linear association is what would be expected if there were a distribution of thresholds in individuals due to multiple risk factors.
4. Particle Specific Relations
While different PM components may have different toxicities, the most useful way to classify them is by their sources, since that is what ultimately will be regulated. Further, this approach directly addresses the question of relative benefits from regulating different PM sources. Laden and co-workers analyzed the elemental composition of PM from six U.S. cities each day for multiple years, in order to estimate the PM2E mass attributable to different sources.(see footnote 18) The estimated source specific mass concentrations were put into a model predicting daily deaths. There were significant mortality associations with PM from traffic and from coal-burning power plants, but not from earth crustal PM (wind blown dust). The traffic particles were more toxic. There was also a large effect of residual oil combustion PM, but it was not significant, possibly because the factor was only present in two cities, and concentrations were relatively small in those. The traffic PM was most strongly associated with cardiovascular deaths, and the coal powerplant PM with respiratory deaths.
Page 65 PREV PAGE TOP OF DOC Segment 1 Of 2 Janssen and co-workers(see footnote 19) (2001) approached this problem from a different direction. The examined the PM coefficient predicting hospital admissions for heart disease in 14 U.S. cities.(see footnote 20) As shown in Figure 2, they found that the larger the fraction of PM from traffic, the larger the coefficient for hospital admissions.
Figure 2. Association of Motor Vehicle PM and CVD Hospital Admissions
Sulfate particles from Coal combustion were also associated with hospital admissions, but had average toxicity for heart disease, as opposed to the Traffic particles, which were clearly more toxic than average.
5. Prospective Cohort Studies
In 1997 two large studies had been published which followed subjects over years, controlled for individual risks such as smoking, and found that air pollution lowered life expectancy. These studies were criticized by industry scientists who argued that they failed to adequately examine other potential factors that might explain the association, and several industry groups asked for the data. Because of the confidentiality that had been promised to the participants, the investigators reached an understanding with the Health Effects Institute. HEI would fund a new research team to re-examine the data from both studies, while promising to maintain confidentiality, starting with re-extraction of data from paper records going back to the 1970's. They would then reanalyze the data, examining the stability of the association to control for these other potential explanatory factors. HEI, again using joint funding by Industry and EPA, convened a meeting to solicit ideas for the re-analysis to which all parties were invited, and formed a large advisory committee for the re-analysis, including industry scientists. After extensive analyses, the new investigators reported that they could replicate the results reported by the original investigators, and that the results were stable to control for a host of different factors. These new results add considerable support to the conclusions that PM is associated with important reductions in life expectancy.
Page 66 PREV PAGE TOP OF DOC Segment 1 Of 2
Recently, both sets of original investigators have followed up their cohort for additional years. The American Cancer Society cohort results, recently published, confirmed that the association with PM persisted, and reported that PM was associated with lung cancer deaths, as well as deaths from heart and lung disease.(see footnote 21)
We have followed up the Six City Study cohort, and found results of considerable public policy import. Pollution levels dropped substantially in one of our cities, and moderately in a second city, while remaining roughly stable in the remaining cities. When we analyzed deaths in the more recent follow-up period, we found that the death rates in those two cities had dropped relative to the rates in the other four cities. Again, this was after controlling for individual risk factors (smoking, hypertension, etc.). That is, reducing air pollution concentrations reduced mortality rates.
Another recent study has been reported from The Netherlands, where a large cohort of persons was followed. A key result is the preliminary report of the study of Hoek and co-workers.(see footnote 22) Using a prospective cohort study drawing on subjects from all over the Netherlands, they used geographical information systems methods to estimate exposures for each person. Significant associations were seen between mortality on follow-up and that exposure, with an effect size estimate similar to those in the U.S. cohort studies.
6. Biological Plausibility/Suceptibility
Page 67 PREV PAGE TOP OF DOC Segment 1 Of 2 Recent years have seen an explosion of papers examining potential pathways for the adverse effects of PM. The understanding the acute cardiovascular events, such as heart attacks and arrythmias, which produce sudden deaths, are the bulk of the problem has focused research on mechanisms for these cardiovascular deaths. These recent studies have included more focused epidemiology studies, controlled human exposure studies, and animal studies.
Results from both animal and human studies suggest several mechanisms by which particulate exposures can damage the heart. Consider deaths from arrhythmia, a leading cause of sudden death. These deaths result from the failure of the nervous system to coordinate the beating of the heart, so that the different parts of the heart do not beat in synch. Animal studies have shown that exposures to urban combustion particles can produce reductions in heart rate variability, a known risk factor for sudden death(see footnote 23) and, in compromised animals, death from arrhythmia.(see footnote 24) In another study, old rats (18 months) were used as a model of sensitivity of the elderly at NYU. Exposure to urban air particles, but not to SO, produced increased rates of spontaneous arrhythmia in those rats. Spontaneously hypertensive rats (12 months old) were found to have a persistent increase in heart rate following exposure to urban particles (two exposures at a concentration of 170 mg/m). Exposure of these same rats to NO (1 ppm) or CO (25 ppm) had no effect on heart rate. Exposure to SO at a concentration of 1 ppm, had no significant effect on heart rate even though exposures were repeated twice in young rats and 4 times in old rats (Nadziejko et al., in preparation).
Similarly, in recent panel studies of senior citizens, airborne particles were associated with decreases in heart rate variability(see footnote 25),(see footnote 26),(see footnote 27) and increased heart rate.(see footnote 28),(see footnote 29) Human volunteers were exposed to concentrated ambient PM2E in Los Angeles. Among the key findings were decreased heart rate variability in healthy young adults, and both decreased heart rate variability and increased arrhythmias in healthy elderly subjects (Report of EPA PM Research Centers).
Page 68 PREV PAGE TOP OF DOC Segment 1 Of 2
While prospective studies such as the Framingham Heart Study have demonstrated that reduced heart rate variability is a risk factor for sudden death from arrhythmia, they do not provide evidence that short term changes in heart rate variability convey short term risks of arrhythmia. A recent study in Boston provides key evidence in that regard. It examined patients who were at high risk of dying from arrhythmia, and had therefore had a defibrillator implanted in their chest, to save their lives if they went into ventricular fibrillation. Peters and co-workers found an association between PM2E and discharges of these implanted defibrillators.(see footnote 30), A recent follow-up study has confirmed the association with PM2E. Together, these results indicate that compromised nervous system control of the heart may play a role in the acute cardiovascular toxicity of particles. The controlled exposure studies provide further evidence that these associations are not due to failure to control for weather or other pollutants well enough, as does the failure to see the gaseous air pollutants associated with most of these mechanisms at all.
Progress has also been made on understanding how PM exposure can produce heart attacks. For example, a recent paper by Peters and co-workers(see footnote 31) used data from the Myocardial Infarction Onset Study(see footnote 32) to examine the association between non-fatal myocardial infarctions and airborne particles. Subjects were interviewed in the hospital about their activities immediately prior to their infarction and during control periods. Data were analyzed to identify numerous potential triggers of myocardial infarction, including physical, psychological and chemical stressors. Using hourly data on PM2E concentrations, the air pollution exposure of these subjects on the event and control days were also compared. PM2E was shown to have both an immediate effect (previous 2 hours exposure) and a delayed effect (24 hours before the infarct) on increasing the risk of myocardial infarctions, controlling for individual level covariates. For 24 hour exposure there was an OR of 1.69 (1.09, 2.02).
Page 69 PREV PAGE TOP OF DOC Segment 1 Of 2
Other studies have examined intermediary markers of pathways by which PM can affect cardiovascular disease, including factors associated with blood coagulation and plaque stability, which may explain the heart attack risk. Peters et al., for example, reported an association between plasma viscosity and airborne particles using data from the MONICA study.(see footnote 33) Consistent with this finding, Gardner and colleagues reported increased fibrinogen (a clotting factor) in animals exposed to urban particles.(see footnote 34) Ghio et al.(see footnote 35) showed similar increases for human volunteers exposed to concentrated air particles. We merged air pollution concentrations to subjects in the third National Health and Nutrition Examination Survey (NHANES III) in the U.S., and examined their association with fibrinogen levels, counts of platelets, and white blood cells. Regressions controlled for age, race, sex, body mass index, current smoking, and cigarettes per day. Consistent associations were found with PM but not the gaseous air pollutants. The odds ratio of being in the top 10 percent of fibrinogen for an interquartile range change in PM was 1.77 (95% CI 1.262.49). These results were stable with control for indoor exposures (wood stoves, ETS, gas stoves, fireplaces), dietary risk factors (saturated fat, alcohol, caffeine intake, n-3 fatty acids), and serum cholesterol.(see footnote 36) Also, an association of traffic pollutants and plasma fibrinogen was recently reported in London.(see footnote 37) The more specifically traffic related pollutants (black smoke, NO) showed stronger associations than PM. Other intermediate markers of cardiovascular disease, such as peripheral neutrophils,,(see footnote 38) c-reactive protein,(see footnote 39) endothelin (ET)1 and ET3,(see footnote 40) and blood pressure,(see footnote 41) have been shown to be elevated with particle exposures in an increasing number of studies. A recent controlled human exposure study to 300 mg/m of diesel particles for one hour, showed the exposure increased levels of peripheral neutrophils, a marker of systemic inflammation.(see footnote 42) The findings are consistent with a theory proposed by Seaton,(see footnote 43) in which particles cause damage by increasing pulmonary inflammation, penetrating into the bloodstream, interacting with platelets, and triggering systemic increases in blood coagulation and other risk factors for acute myocardial infarctions.
Page 70 PREV PAGE TOP OF DOC Segment 1 Of 2
One recent study(see footnote 44) has reported that exposure of particles was associated with increased athlerosclerotic plaque formation over time and decreased plaque stability in a rabbit model. The effects of controlled exposures to 60 mg/m of urban particles on ET1 and ET3 levels in humans may presage a chronic effect. The Los Angeles controlled exposure study also found increased levels of soluble intracellular adhesion molecule-1 (ICAM1), another marker of increased inflammation and blood coagulability that is predictive of future coronary events.
Ischemia was induced in dogs by Godleski and co-workers by occluding the coronary artery supplying blood to the heart. If that occlusion was accompanied by exposure to urban air particles, the increase in ST segment elevation on the dog's electrocardiogram was greater, and occurred earlier, than if the dog was exposed to filtered air. The finding that PM air pollution exacerbates acute myocardial ischemia suggests that vascular responses and pathophysiological events that lead to changes in vessels may be key mechanisms by which PM may trigger acute cardiac events.
In another study, healthy adults inhaled 150 mg/m of concentrated ambient fine particles and ozone (120 ppb) for two hours, and their vascular response was compared to when they inhaled clean air.(see footnote 45) Brachial artery vasoconstriction was significantly higher for the pollution inhalation than for the clean air inhalation.
Another recent study found that atherosclerosis development in rabbits was accelerated by exposure to PM, and that pollution exposure modified atherosclerotic lesions, making them more vulnerable to rupture. Compared to rabbits exposed to clean air, the PM exposed rabbits showed an increased systemic inflammatory response as well as progression of atherosclerotic lesions and increases in plaque cell turnover, extracellular lipid pools in coronary and aortic lesions, and the total lipids in aortic lesions.(see footnote 46) The plaques observed in the exposed rabbits were of the type more likely to trigger cardiac events (i.e., heart attacks).(see footnote 47)
Page 71 PREV PAGE TOP OF DOC Segment 1 Of 2
Heart disease is not the only area where we have found substantial evidence to support the association between PM and death risk. The NYU PM Center is using the combination of particle concentrator technology and animal infectivity models to investigate this question. A single 5 hr. inhalation exposure of bacterially-infected rats to concentrated ambient New York City (NYC) PM2E, at concentrations approximating or just greater than the 24 hr. NAAQS PM2E (65 mg/m), altered both pulmonary and systemic immunity, and exacerbated the infection process, in a time-dependent manner. Streptococcus pneumoniae-infected rats exposed to PM demonstrated increased burdens of pulmonary bacteria, numbers of circulating white blood cells, extent of pneumococcal-associated lung lesions, and incidence of bacteremia, compared to air-exposed, infected control rats (PM Research Centers Report). The hypothesis that patients with pre-existing respiratory, cardiovascular, or diabetic disease have an enhanced mortality response to PM exposures has been tested by several investigators. Respiratory illness modified the risk of cardiovascular hospital admissions associated with PM, and heart failure modified the risk of PM-associated COPD admissions.(see footnote 48) COPD has also been identified as a modifier of the effect of particles on deaths. Sunyer and co-workers reported that a cohort of COPD patients who required emergency room treatment during 19851989, when followed up for the next five years, showed a substantially larger risk of death associated with PM than the general population.(see footnote 49)
Diabetes affects a large number of people in America, and disproportionately impacts the elderly and minorities. An estimated 15.7 million people in the U.S. (almost 6 percent of the population) have diabetes, with about 800,000 new cases diagnosed per year.(2) Diabetes is most prevalent in people aged 65 and older (18%), and is more common among Latinos and blacks than among non-Hispanic whites. Common complications of diabetes include heart disease, high blood pressure, kidney disease, and increased risk of stroke. Diabetes is associated with reduced heart rate variability, increased plasma fibrinogen and C reactive proteins, and increased white cell counts. All of these have been associated with exposure to airborne particles as well. This suggested that a synergistic effect may occur. To test this, we examined hospital admissions for heart disease in persons aged 65 and over in Cook County, Illinois between 1988 and 1994. Daily counts of hospital admissions for heart disease were stratified into those with and without diabetes as a comorbidity.(see footnote 50) There were an average of 20 admissions per day for heart disease in patients with diabetes, and 82 per day in patients without diabetes. A 10 mg/m increase in PM was associated with a 2.0 percent increase in heart disease admissions in diabetics (95% CI 1.42.6%), vs. a 0.9 percent (0.61.3%) increase in patients without diabetes. This difference was statistically significant. This suggests that at least acutely, diabetes and airborne particles interact to increase the risk of cardiovascular disease, a result recently confirmed in three additional cities.(see footnote 51)
Page 72 PREV PAGE TOP OF DOC Segment 1 Of 2
Several developments clarified this issue. First, multiple studies demonstrated that there is high correlation between day to day changes in ambient PM and day to day changes in personal PM exposure. The previous low correlations came from only looking across subjects, and not time. Subjects differ substantially in how much PM from non-ambient sources (e.g., passive smoking, cooking fumes) they are exposed to.(see footnote 52) These differences are not correlated over time with ambient PM, and do not reduce the longitudinal correlations. Second, a recent paper by Sarnat et al.(see footnote 53) showed that day to day changes in ambient concentrations of gaseous air pollutants were more highly correlated with day to day changes in personal exposure to PM2E than with day to day changes in personal exposure to the gases. This indicates that real confounding by gaseous air pollutants is unlikely, and any association between daily deaths and those gases is probably because they are correlated with particles. Finally, a statistical paper by Zeger and colleagues(see footnote 54) showed that most of the exposure error was unimportant, as it was of a type that does not introduce bias.
Chairman BOEHLERT. Thank you very much, Dr. Schwartz. Dr. Amar.
Page 73 PREV PAGE TOP OF DOC Segment 1 Of 2
STATEMENT OF DR. PRAVEEN K. AMAR, DIRECTOR, SCIENCE AND POLICY, NORTHEAST STATES FOR COORDINATED AIR USE MANAGEMENT
Dr. AMAR. Thank you. I have some overheads here. Thank you for inviting me to give you a presentation on what technologies are there to control fine particles, what sources, and what various barriers are there to deployment.
First, a little background about NESCAUM. We are an association of the eight northeastern states' air quality agencies, including the six New England states, plus New York and New Jersey. And for the last 35 years, we have been providing scientific, technical, and policy support to our member statesstate governments.
I would first talk about the nature, the extent and the sources and then controlling technologies for PM. And then finally I will address the barriers to deployment. I think the thing to remember hereand if this thing worksI have this slide up there from Aristotle. I think the point to note there is that when we strive for solutions to complex issues such as PM, that involve science, technology, and, of course, policy, public policy, we should not strive for exactness when only an approximation of the truth is possible. And I think Dr. Schwartz mentioned that indirectly.
The extentthe problem here is thethe map of the three countries is part of the work we are doing with Canada and Mexico and the United States. The red dots is where the problem is. These are fine particle values over the standard, which is 15 micrograms per meter cubed. You could see essentially the east and then California where the values are over 15. That is the annual standard. The standard for the daily, which is 65, is not violated as often.
Page 74 PREV PAGE TOP OF DOC Segment 1 Of 2
Okay. The thing about fine particles is that it tells you what is in them. I mean, that is a good thing. When you are looking at those big pies, again, you can tell what is in those particles. And what you are finding there is a large fraction of sulfates and organics and, as Dr. Wyzga mentioned, in the east, and nitrates and organics in the west. Again, the point is, there is not a lot of coal-fired burning in California, so you don't see a lot of sulfates as we see here. And then obviously then there are other things in it, the crustal material. There are trace species, metals. There is ammonium from animal operationsthe ammonia gas, which makes really ammonium nitrate, and sulfate in the atmosphere.
The point is, these are complex mixtures. And the good thing about the mixtures is, they tell you what is in it once you start measuring them correctly. And then you can design your strategies to meet the standard.
And before I go into the technologies, the question to really ask is, you know, what technologies are available to reduce the emissions of gases that become particles in the airsecondary particles, that isand primary particles from stationary and mobile sources, both on road and off road. Here, it is important to note that PM is composed of traditional pollutants, many of which have beenwe have been controlling in this country for many, many years.
For example, for stationary sources, we have extensive experience in controlling primary PM emissions through the use of ESPs. This is a picture of electrostatic precipitators used in big power plants. And the next one is a baghouse. Again, these are also attached to power plants. The thing to remember here, I guess, is that ESPs don't do as good a job of fine particle controlling as baghouses do. But then again, about 80 percent of the power plants in this country have ESPs, and only one out of ten has a baghouse.
Page 75 PREV PAGE TOP OF DOC Segment 1 Of 2
And the thing to do would be to combine the two. In fact, EPRI has been working on what they call the baby baghouses, or polishing baghouse. You put a baghouse downstream of an ESP and you can collect fine particles, a lot more than you are able to collect with the ESPs.
The scrubbersand we have been controlling for quite some time sulfur dioxide in this country under Title IV, Acid Rain Program. And, again, only 27 percent of the capacity in the United States of power plants burning coal has scrubbers. So that is only about three out of 10 megawatts. And, again, there is this possibility of doing more.
This is a new technology which is coming up to control oxides of nitrogen. It has been applied since 1995 in this country and it is coming in a big way in the next three or four years. And the thing to remember about the scrubber and SCR, the combination of the two might work quite well for other issues, in this case, mercury.
The ChairChairman Boehlert mentioned about the Clear Skies Initiative. To the extent there is mercury in that initiative, one could be able to control mercury in a very big way without doing much additional costthe combination of the two.
The next one, of course, is the mobile sources. You asked me to address both of those. The diesel sources to fine particles, the contribution is obvious. Diesel sourcesthe trucks and busses and construction equipment, locomotives, marine vessels. And this is a picture of a truck where you see, at the bottom, the replacement of the muffler essentially with a brand new filter system. And same thing with the school bus. Here, under the bus, that is the way you replace the old muffler with the system, which is a filter.
Page 76 PREV PAGE TOP OF DOC Segment 1 Of 2
Here is a garbage truck and, again, you can see the stack, not any black smoke. And this is the best one. It is the Big Dig in Boston, where you can see two machines next to each other of the same type, and one has a filter, other doesn't, and obviously the slide is pretty clear.
And the final point I want to make, I think, this is the barriers to deployment. This is something we did about two years agoa report we did on relationship between environmental regulation and technology innovation. The key point there, which I am sure is valid for PM also, is that most of the technological progress in this country has come over the last 40, 50, 60 years whether it is power plant control for SOX and NOX or automobile controlsonce you have clear, well-established environmental drivers. You set clear deadlines. You set targets, not promote a certain technology or the other, and let industry figure out what is the best way to get there.
Thank you, and I thank you for your time.
[The prepared statement of Dr. Amar follows:]
PREPARED STATEMENT OF PRAVEEN K. AMAR
Good Morning. My name is Praveen Amar. I am the Director of Science and Policy, for the Northeast States for Coordinated Air Use Management (NESCAUM). I thank the Committee Chair; Mr. Boehlert, Ranking Member, Mr. Hall, and members of the Committee for the privilege and opportunity to share with you some ideas regarding the control technologies and strategies for fine particulate air pollution (popularly known as PM2E) in the U.S.
Page 77 PREV PAGE TOP OF DOC Segment 1 Of 2
First, a little background on NESCAUM. NESCAUM is a regional association of the eight northeastern states' air quality agencies. The eight states include the six New England states of Connecticut, Maine, Massachusetts, New Hampshire, Rhode Island, and Vermont, and New Jersey and New York. For the last 35 years, we have been providing scientific, technical and policy support to our member states on air pollution issues of regional interest. For example, in the recent past, we have evaluated the technical feasibility and cost effectiveness of various options to reduce emissions of major air pollutants (oxides of nitrogen [for ozone], sulfur dioxide [for acid rain], PM, mercury, hydrocarbons, and toxic air contaminants). We have also evaluated the role of long-range transport with wind of various air pollutants in affecting the ambient concentrations far from their sources of origin. This issue is of special importance for PM, since PM and its precursors tend to travel over hundreds to thousands of miles before eventually depositing on earth.
My testimony today will first provide a brief overview of the extent, nature and major sources of particulate air pollution, both stationary and mobile. Then, it will focus on the technologies for controlling PM emissions from these sources. Finally, I will address the barriers to deployment of many of the technologies and incentives and environmental drivers that are needed for their added deployment. It is also important to note that when we strive for solutions to complex issues such as PM, that involve science, technology, and public policy, we should not strive for exactness when only an approximation of the truth is possible (Slide 2).
The extent of the problem is summarized in the next slide (slide 3). Please note the annual standard for PM2E is 15 micrograms per cubic meter of air. Many locations in the eastern U.S. and California exceed this limit. Values above this standard have been measured in cities such as Atlanta, Boston, New York, Los Angeles, and Fresno, California. Additionally, the daily standard of 65 micrograms has been exceeded at some sites, but this is not as common as the exceedance of the annual standard.
Page 78 PREV PAGE TOP OF DOC Segment 1 Of 2
The next obvious question to ask is: What exactly is in this measured PM? The next slide (slide 4) shows that the major measured components of PM2E are: 1. sulfates (from sulfur dioxide emissions, primarily from coal fired electricity generating power plants), 2. organic carbon (from sources of hydrocarbons including gasoline and diesel combustion, biogenics, even meat cooking operations, industrial solvents use), 3. nitrates (from sources of oxides of nitrogen, including power plants, major industry, gasoline and diesel combustion), 4. black or elemental carbon or soot (primarily from diesel combustion including diesel trucks, construction and agricultural equipment, locomotives and marine vessels, also wood burning), 5. ammonium (from ammonia emissions from cattle operations, soils, and fertilizer applications), 6. crustal materials from soil and rock dust (oxides of silica, calcium, iron, etc.), and 7. other trace species (such as lead, mercury, copper, etc.).
The good thing about PM2E measurements is that they provide us with extremely useful information about what exactly is in these particles. Different parts of the country, as well as urban and rural sites have different mix in their PM2E. This provides practical information about which control strategies and technologies should be pursued to effectively lower the concentrations to meet the ambient standards. The analysis of the data strongly suggests that sulfates and organic and elemental carbon are major components of PM2E in the east (they can be as much as 70 to 80 percent of the mass in the east). In California, carbon constituents and nitrates (nitrates replace sulfates in the west, since coal use is minimal in California) can make up most of the PM2E mass.
As I mentioned earlier, atmospheric transport plays a big role, such that upwind or regional sources can contribute a large fraction of the overall mass in cities such as Washington, DC, Atlanta, and many cities in the east including Boston and New York. On the other hand, cities like Los Angles are dominated by the urban or local sources.
Page 79 PREV PAGE TOP OF DOC Segment 1 Of 2
The next slide (slide 5) makes this point. Note, for example, how the local organic carbon (from diesel and gasoline powered mobile sources) is the key constituent (along with nitrate, not shown) in LA and that Atlanta has a strong regional influence. It is true for many cities in the east.
The next question to ask is: What control technologies are available to reduce the emissions of gases that become particles in the air (secondary particles) and primary particles from stationary and mobile sources (both on road and off road). Here it is important to note that PM is composed of traditional pollutants many of which we have been controlling for many years (since 1960s).
For example, for stationary sources, we have extensive experience in controlling primary PM emissions through the use of ESPs (electrostatic precipitators) and baghouses (slides 6 and 7). Baghouses do a much better job of controlling smaller particles than ESPs (80 to 95 percent for ESPs and 99 to 99.8 percent for baghouse). However, most of the coal boilers have ESPs (about 86 percent), but only about 1 in 10 has a baghouse. EPRI has been testing application of ''polishing or baby bag houses'' downstream of ESPs for additional collection of PM (which, by the way, has the added benefit of controlling mercury emissions. Mercury is included in the President's Clear Skies Initiative as well in many bills in the U.S. Senate and the House). Additionally, sulfates and nitrates in the PM can be reduced further by application of commercially available and cost effective, dry and wet SO scrubbers (slide 8) (currently only 27 percent of the utility boiler capacity has scrubbers), and by the application of widely available technologies for NOX control (such as Selective Catalytic Reduction (slide 9), which is currently being installed at many power plants in the east and in California). As a potentially substantial benefit, recent results indicate that the use of scrubbers and/or SCR can provide significant mercury reductions with minimal extra cost The main point I will like to make is that these are mature and extremely cost effective technologies, they are capable of delivering added benefits besides PM control, and we are fortunate to have substantial working experience with all of them.
Page 80 PREV PAGE TOP OF DOC Segment 1 Of 2
The contribution of diesel sources to fine particles is obvious. Diesel sources (trucks and buses, construction equipment) are present where people live. Here, technologies to control primary PM and organic and elemental carbon emissions from diesel source have been used in select applications over the last 15 years, and are rapidly emerging as retrofit control technology in diesel vehicles operating in an urban environment. Technologies such as diesel particulate filters (DPF) and diesel oxidation catalysts (DOCs) are examples of retrofit technology which can not only reduce PM mass but also toxic hydrocarbons by changing them into harmless exhaust products. Filters are efficient and are developing an impressive track record. They are capable of reducing PM mass and precursors by about 90 percent or more. Peugeot is already selling filter-equipped vehicles, with over one hundred thousand cars already sold. Over 50,000 systems have been retrofitted to heavy-duty diesel trucks and other equipment. Oxidation catalysts are efficient in reducing PM by 20 to 50 percent and toxic hydrocarbons by about 70 percent, and have gathered excellent operating experience. Thousands of U.S. buses and millions of light duty diesel vehicles in Europe are now equipped with oxidation catalysts.
Quite often, the difference between attainment (rural sites) and non-attainment sites (urban sites) is the incremental contribution of organic and elemental carbon to the PM mass at urban sites. There are additional issues related to toxicity of diesel exhaust. For example, California has declared diesel PM as a toxic air contaminant and is developing a control program. For these reasons, control of diesel sources has additional benefits.
The new diesel trucks will be required to meet increasingly stringent EPA's 2007 standards for PM and its precursors. Here, integrated approaches consisting of advanced engines, integrated emission control technologies and clean low-sulfur diesel fuels are the expected solution. High emitting older diesel vehicles will be in use for many years beyond 2007. We, therefore, can make great near-term progress by retrofitting existing, long-lived, on-road and off-road mobile source infrastructure with currently available and emerging integrated technologies. The next slides (slides 10, 11, 12, 13) show a diesel truck, a school bus, and a garbage truck, all retrofitted with particulate filters. The retrofit looks very much like the original equipment. The next slide (slide 14) shows NESCAUM's efforts in retrofitting diesel construction equipment used in the ''Big Dig.'' The slide speaks for itself.
Page 81 PREV PAGE TOP OF DOC Segment 1 Of 2
A final important point I wish to make is the historic relationship in the U.S. between environmental drivers and technology innovation (and implementation). We investigated the relationship between the two in a September 2000 NESCAUM report (slide 15) and looked at three case studies (automobile emissions controls, and SO and NOX emissions control technologies for power plants). What we always found was that these technologies became commercially available at attractive prices only after environmental drivers (in the form of federal and state requirements) were established in the form of performance standards with firm and fair time schedules, but without favoring any specific technology. The research and development efforts, before the environmental drivers were put in place, were helpful and necessary, but hardly sufficient in making major environmental progress. This should be no less valid for promoting wider application of existing, mature technologies for reducing unhealthful PM2E levels.
Thank for your time.
BIOGRAPHY FOR PRAVEEN K. AMAR
Dr. Praveen Amar is the Director of Science and Policy at NESCAUM (Northeast States for Coordinated Air Use Management). NESCAUM is an interagency association of eight northeastern states (New York, New Jersey, Connecticut, Maine, Massachusetts, Vermont, Rhode Island, and New Hampshire). NESCAUM provides high-level scientific and policy-relevant input to its member states on regional air pollution issues.
His key area of expertise is to ''translate'' the implications of findings of science and developments in technology into workable and cost-effective policy options for the states in the Northeast. These policy options have involved regional control of emissions of oxides of nitrogen and sulfur including market-based approaches, relative roles of local and regional sources, regional planning for achieving standards for fine particles and ozone, cost-effective technologies to reduce emissions of mercury from large utility boilers and municipal waste combustors, and promotion of environmentally friendly distributed generation technologies.
Page 82 PREV PAGE TOP OF DOC Segment 1 Of 2
He was NESCAUM's Project Manager for four NESCAUM reports in 1992, 1995, 1998, and 2000, on the status of NOX control technologies and their cost effectiveness for electricity-generating power plants and other large NOX sources including industrial boilers, gas turbines, large engines, and cement plants. These reports have been widely used in the technical and policy debates relating to NOX control in the United States.
More recently, he managed the publication of two NESCAUM reports on control of mercury emissions from large coal-fired boilers. The June 2000 report ''Assessment of Mercury Control Strategies for Electricity-Generating Boilers'' described the status and applicability of alternative technologies. The September 2000 report '' Environmental Regulation and Technology Innovation: Controlling Mercury Emissions from Coal-Fired Boilers'' investigated the historic relationship in the U.S. between environmental drivers and technology innovation. The report undertook three case studies (automobile emissions controls, and SO and NOX emission control technologies for power plants). A key finding of the report, that control technologies become commercially available only after environmental drivers (through federal and state requirements) are established in the form of performance standards with firm and fair time schedules, was found to be equally applicable to the need for establishing environmental drivers for mercury control from coal-fired boilers.
While at NESCAUM, he has served as a member of the EPA's New Source Review Advisory Subcommittee that has provided guidance to the EPA's effort to reform the NSR permitting program. He was a member of the Science Advisory Committee (19932001) for the Massachusetts Institute of Technology (MIT) and California Institute of Technology (CIT)'s joint Center on Airborne Organics. He is a member of the Synthesis Team for the NARSTO (North American Research Strategy for Tropospheric Ozone) that produced the July 2000 report '' An Assessment of Tropospheric Ozone Pollution'' and is currently working on a similar document on fine particles, to be published in March 2003. NARSTO has active participation of scientists from the U.S., Canada, and Mexico. He is a member of the modeling working group of the STAPPA/ALAPCO (State and Territorial Air Pollution Program Administrators/Association of Local Air Pollution Control Officials). Currently, Dr. Amar is serving as a member representing states interests in the EPA's Mercury MACT stakeholders workgroup. The joint state-industry-environmentalists workgroup is advising EPA on MACT development and is expected to finish its work by the end of 2002.
Page 83 PREV PAGE TOP OF DOC Segment 1 Of 2
Before joining NESCAUM, Dr. Amar was with the California Air Resources Board for fifteen years where he managed programs on air pollution research, strategic planning, and industrial source pollution control. For over 10 years, he has been a part-time faculty member at the University of California, Davis, and California State University at Sacramento, and Tufts University in Boston, teaching undergraduate and graduate courses in air pollution science, atmospheric chemistry and physics, mechanical engineering, and air pollution policy.
He received his Ph.D. in engineering from UCLA in 1977. He is a licensed Mechanical Engineer in the state of California.
Chairman BOEHLERT. Thank you very much, Dr. Amar. Just out of curiosity, that last slide you showed of the Big Dig and that one machine where all the gook is coming upwhat would be the PM concentration right there?
Dr. AMAR. I think it would .02 or .01 pounds per million BTU. I mean, that is the number. So it is hardly any. And you are talking 95 percent plus control over the unit on the right.
Page 84 PREV PAGE TOP OF DOC Segment 1 Of 2
Chairman BOEHLERT. Well, what would be the concentration of the unit on the right?
Dr. AMAR. Oh. The one
Chairman BOEHLERT. The bad guy.
Dr. AMAR [continuing]. With the black smoke.
Chairman BOEHLERT. That actor. Yeah.
Dr. AMAR. I would not know, but I think it isI am sure it is really, really large.
Chairman BOEHLERT. Yeah. Okay.
Dr. SCHWARTZ. I am sure it was thousands of micrograms per cubic meter right in the plume.
Chairman BOEHLERT. Yeah.
Dr. SCHWARTZ. And, obviously, it spreads out, but
Chairman BOEHLERT. And there is no regulation of that right now at all.
Page 85 PREV PAGE TOP OF DOC Segment 1 Of 2
Dr. AMAR. Most of these programs, sir, are voluntary, except for the mandatory bus program some time ago and the California, which is developing rules for various diesel equipment.
Chairman BOEHLERT. Yeah.
Dr. AMAR. These are voluntary where people raise money at a city level, state level, and try to do the things on a voluntary basis.
Chairman BOEHLERT. And not surprisingly all of you have indicated the need for more study, and we have got to constantly be expanding our body of knowledge so that we are dealing more with facts than with opinion. And there will be more study. But based upon your knowledge of the subject, if you could do just one thing that was doable and practical right now, to deal with this issue, what would you recommend that we do? Who wants to tackle that first and then we willDr. Amar.
Dr. AMAR. I will try to answer thatand I work in this practical field. I think if you are looking at the toxicity and other issues, diesel sources might be the first priority. People live where the diesel sources aretrucks and busses. And diesel has other environmental issues. I mean, California, for example, has recognized diesel as adiesel PM, that isas a toxic air contaminant. And so I would think that that might be, you know, the most beneficial and cost-effective way to reduce particles in urban areas.
Mr. GREENBAUM. If I could add to that?
Page 86 PREV PAGE TOP OF DOC Segment 1 Of 2
Chairman BOEHLERT. Mr. Greenbaum.
Mr. GREENBAUM. I would agree, perhaps, withand I think Praveen may have been saying this as well. There is actuallythere are actually in place already and, in fact, the court just upheld a series of rules that make new diesel engines increasingly clean and reduce sulfur in fuel and a number of other things. But, as his slide suggested, the diesel engines are pretty durable, and the quest, the biggest challenge, is really for the diesel engines that are on the road and continue to be on the road for many years.
Chairman BOEHLERT. To be retrofitted.
Mr. GREENBAUM. And thosethe older ones also tend to stay in the urban areas where you have higher populations for exposure. So it is not a simple process because you have diverse owners. This is no longer the responsibility of the manufacturers under the current law, but you have multiple owners who have rebuilt the engines and have different techniques for doing that. But coming up with strategies that actually get all of those either retired or retrofitted would probably be the single largest benefit that you could can see. And I think there is quite a lot of consensus, perhaps except from the owners of all those engines. But the engine manufacturers, I think, would like to see that.
Chairman BOEHLERT. But right now, if you are driving down and you see one of these big doubles traveling the highway and that plume of black gook coming out, there is no regulation of that under existing law. Is there?
Page 87 PREV PAGE TOP OF DOC Segment 1 Of 2 Mr. GREENBAUM. Well, there are some states that have smoke regulations. They are not often enforced. And I believe New Jersey has implementedPraveen knows this better than Isome form of emissions check for heavier duty vehicles. But there isn't a regular check for those things.
Chairman BOEHLERT. And it is a state by state
Mr. GREENBAUM. And it isat this point it is state by state. That is right.
Chairman BOEHLERT. Dr. Wyzga, any
Dr. WYZGA. I have no comments in terms of the regulation, but in terms of what needs to be done and I think, you know, in terms of the research, I think you canyou need to do more than just one thing. I think you need to come at it from several different angles. And I think you need to do more studies, as we have done with ARIES, and I think we also need to do some toxicology studies that are
Chairman BOEHLERT. But, no, I am acknowledging the need for more studies.
Dr. WYZGA. Okay.
Chairman BOEHLERT. We embrace that.
Page 88 PREV PAGE TOP OF DOC Segment 1 Of 2 Dr. WYZGA. Okay.
Immediate Steps: Diesel Emissions
Chairman BOEHLERT. You know, we accept that. But something more meaningful, something that we can do right now, initiate action right now other than just continue to study. Because I am reminded of a good friend of mine, Governor Tom Kean, the former Governor of New Jersey, when I used to argue about the need to do something for acid rain and my opponents would argue all the time, well, we need more study and don't have enough definitive information. And he would say, if all you do is continue to study the problem, you will end up with the best documented environmental disaster in history.
So I acknowledge we have to expand our body of knowledge. We have to have more study. But what action would you initiate right now if you were in charge and could initiate any single action that would help us address this problem in a meaningful way?
Dr. WYZGA. Okay. I am going to pass on that one because I want to stick with the science.
Chairman BOEHLERT. All right. He wants to stick with science. Science is a process. It is not a body of knowledge, as Dr. Schwartz reminded us in his testimony. Dr. Schwartz, what would you do?
Dr. SCHWARTZ. I guess I would go with most of the others, except Ron. I would say that, to my mind, diesel would be the thing that we need to do something about sooner rather than later. And I would focus on that. I think it is not yet clear the relative toxicity of different kinds of particles, but the studies we have done so far suggest that these traffic particles, which are predominantly from diesel engines, are more toxic than average. As you have heard, they tend to be emitted more in urban areas. So the probability of a diesel particle getting deposited in a lung is higher than for other particles.
Page 89 PREV PAGE TOP OF DOC Segment 1 Of 2
And there is also great disparity in the exposure. You know, we put monitors for PM2E 20 miles north of Boston, 20 miles south of Boston, and in Boston, and there is hardly any difference in the values that we get. Fine particles, because Brownian motion keeps them up in the air, they mix and the concentrations tend to be quite uniform over large geographic areas.
But these traffic particles are different. There are people who live right near the source. And we put up monitors outside 24 homes in Boston and we found a five-fold difference in the carbon concentrations between the highest and the lowest homes, but not much differenceyou know, not a huge difference in the total amount of PM2E. So that is the one where we sort of have the most inequity. Some people are getting a lot more than other people. So I think that also argues for focusing on it.
Mr. GREENBAUM. If I might just add to that, just to bring a fine point to this, think the general perception is that all of diesel engines are contributing to this. And, in fact, we have made progress in the diesel fleet. And we just published a study on a tunnel on the Pennsylvania Turnpike that has been studied over the last 25 years where you can actually characterize what is coming out of diesel and gasoline vehicles. And then you can document a 90 percent on-road improvement in particle emissions.
Now, these are engines on a turnpike running at hot temperatures so they are the most efficient, and also tend to be the newer engines because they are the ones that are out there used for long-distance hauling and transport. So, in fact, there are a lot of mechanisms in place that have been working, and I think we should understand that to improve the overall fleet. The focus needs to be more forcefully on the fleet of vehicles that is older and in the urban areas.
Page 90 PREV PAGE TOP OF DOC Segment 1 Of 2
I would also add that we need to be a little careful about jumping to one solution or another there. We need to move on it carefully. We have just seen results from studies in California, as well as elsewhere, that say that although diesels, older diesels are a problem, when you compare newer diesels to natural gas bus engines, there are pros and cons of both engines. Natural gas we think of as the clean solution, but there are issues with what comes out of any heavy-duty engine, whatever it is fueled by. So we need to move in this area. We need to have the technology research done, and absolutely get the older things off the road or retrofitted.
Chairman BOEHLERT. Dr. Wyzga.
Dr. WYZGA. I think one thing I would like to add to the diesel. I was on EPA's Science Advisory Board Committee. They were looking at the toxicity of diesel emissions. And I think people basically can trust the difference between the new engines and the old engines, but also we need to contrast the difference between the on-road and the off-road. There is far less controls in terms of off-road diesel enginesthose from the stationary type generators. And those maybe need to look at more detail.
Immediate Steps: Carbonaceous Material
The other thing that was interesting, maybe we need to look a little more carefully at, in some of our work in Atlanta we were looking at an inventory of some of the carbonaceous material, and found that in the winter something that was particularly important was wood combustion, through fireplaces, through agricultural burning, people burning trash, etcetera. And this was, perhaps, the largest contributor of carbonaceous materials in the winter in Atlanta. It also was the season where we tended to find much more in terms of cardiovascular impacts.
Page 91 PREV PAGE TOP OF DOC Segment 1 Of 2
Now, whether it is due to this type of pollution or due to differences in behavior, we don't know yet. We have a lot more work to do. But I think that we need to pay more attention to some of this wood burning. I saw a study in Illinois. I was there a couple of weeks agosome data was presented to me. And I was surprised, again, to see that the largest fraction of the carbonaceous material in Illinois was tied to wood burning in the winter as well. So that is something we also need to start thinking about.
Chairman BOEHLERT. Thank you very much. Mr. Hall.
Retrofitting Diesel Vehicles: Cost Involved
Mr. HALL. I want to be with the Chairman when he makes his first citizen's arrest out there on I95. But seriously, for diesel vehicles, for trucks, what do we have in retrofitting them and how often does that happen? And what do your studies cry out for? In other words, trucks and other diesel vehicles are expensive and they are not replaced very frequently. And I don't know how many checks through the year, quarterly, they go through. Like in my state, they have automobiles and our legislature has just passed an act that requires instead of a $13, $14 or $15 inspection, about a $40 inspection for automobiles. Well, a lettera word I have been trying to use ever since I got out of law school was A-for-sure-I. So I guess A-for-sure-I you would need a lot more studies for trucks, particularly diesel trucks. Would you not? And automobiles for fume and for pollutants.
Dr. SCHWARTZ. Well, I think Dr. Amar can probably tell you more about the technology. I did once see a study from Singapore which suggested that they looked at their municipal bus fleet. And they found that if they overhauled the engines every two years, that the emissions were much lower than if they did it every three or four years which is much more typical for an urban bus fleet.
Page 92 PREV PAGE TOP OF DOC Segment 1 Of 2
Mr. HALL. Are they lowered to a satisfactory amount or does that need more studying?
Dr. SCHWARTZ. Well, I think I indicated that we have a lot of studies that suggest there really are no thresholds. So satisfactory is a hard definition to come up with. Less is better than more. One could do cost benefit analyses, and I have done cost benefit analyses to ask you where to make that cut point, but I certainly haven't done it on diesel engine overhaul or retrofitting of filters. So I would
Chairman BOEHLERT. Would the gentleman yield for just a moment?
Mr. HALL. Sure. Yes, sir.
Chairman BOEHLERT. On that Singapore study, the study indicated the emissions were lower when they overhauled. Did they do anything on efficiency? Was the efficiency increased? In other words, I am trying to figure out a way to offset the cost of the overhaul. So if you get lower emissions and you have greater efficiency, and then there is an incentive to do the overhaul.
Mr. HALL. And that is the goal, Mr. Chairman, we are trying to get to, to try to find out if they have done any study on what the cost is and how cost-effective they were.
Dr. SCHWARTZ. I am afraid I don't know. I mean, it makes sense thatyeah. You may
Page 93 PREV PAGE TOP OF DOC Segment 1 Of 2
Dr. AMAR. Okay.
Dr. SCHWARTZ [continuing]. Address that, sir.
Dr. AMAR. These days, if you are trying to retrofit these diesel trucks with what is known as filter traps or particulate filters or oxidation catalysts, these things would go about $5,000 to $6,000 per big truck, 400 horsepower or so. But the people who do these things when they estimate in the future if there are requirements for many, many of these engines, the prices could come down tooas low as about $250 to about $600 per retrofit.
Mr. HALL. Per vehicle?
Dr. AMAR. Per big diesel truck. Yes. Per vehicle.
Mr. HALL. How much?
Dr. AMAR. About $500$250 to about $600 to about maybe $1,000, in that range, in the future. But presently, because there aren't many being retrofitted, because there aren't many requirements, these are voluntary programs at state levels and local levels where people raise money to do these things through private and public sector, the costs are high, as high as about $5,000 to $6,000 per truckin that range. But, again, in terms of
Page 94 PREV PAGE TOP OF DOC Segment 1 Of 2 Mr. HALL. And how often would that need to be done at $5,000 or $6,000 per truck?
Dr. AMAR. Pardon me?
Mr. HALL. How often would that need to be done at $5,000 or $6,000 per truck?
Dr. AMAR. Well, I think that they have very low maintenance costs. These things have a long life just like diesel trucks have.
Mr. HALL. Yes.
Dr. AMAR. So I think that the real cost comes up frontthe capital cost itself.
Mr. HALL. Initial.
Dr. AMAR. Yes, sir.
Mr. HALL. At the factory.
Dr. AMAR. At the factory or the retrofit of an existing engine, which is in the field.
Page 95 PREV PAGE TOP OF DOC Segment 1 Of 2 Chairman BOEHLERT. But that would be a one-time cost, though. Wouldn't it.
Dr. AMAR. Yes, sir.
Chairman BOEHLERT. Okay. Thank you.
Mr. HALL. Well, now I am talking about these trucks that are not replaced frequently, say, 20 years from now. If you have that in effect today and they spend that $5,000 or $6,000 bucks at the factory and pass that on to whoever buys the vehicle, or the truck, I presume they would.
Dr. AMAR. Well, the brand new trucks in the year 2007 will have these requirements of EPA which will be met by, you know, the engine modifications, number one, ultra-low sulfur diesel as low as about 15 parts per million, and the integrated control equipment. So I think the cost of a brand new diesel engine in 2007 is going to be much less than what we would estimate today.
Mr. HALL. Yeah. I think that is fine if it is done at the factory, but for those trucks out there that have been out there for years and years that have not been retrofitted, is there any technology or cost-effective technology available for retrofitting these existing diesel vehicles or trucks?
Dr. AMAR. Yeah. I would say thesethe oxidation catalyst and the filters, I would think, are cost-effective. The way we calculate cost effectiveness in our businessyou look at dollars you spend per ton of emissions removed. For example, for oxides and nitrogen, you know, if you are spending about $1,000 per ton of air pollution removed, we think it is very cost-effective. Same thing for PM or other pollutants.
Page 96 PREV PAGE TOP OF DOC Segment 1 Of 2
So cost effectiveness is done by comparing not only, you know, mobile sources like trucks and diesels, but also what we do for cars and power plants and refineries and cement plants. So you kind of look at the overall industry and what people are paying for every ton of pollution removed.
Mr. HALL. My last questionand because my time is upisand is it your testimony that if you retrofit the existing diesel vehicles that have been out on the road for all this time that the cost is about what it would be at the factory or $5,000 or $6,000 per vehicle?
Dr. AMAR. The cost in the future of the retrofit of diesel will be, I think, the same as almost at the factory. At this time it isn't.
Mr. HALL. I yield back my time. Thank you, Mr. Chairman.
Chairman BOEHLERT. Thank you very much, Mr. Hall.
Mr. HALL. And I will go with you when you make that first arrest out there.
Chairman BOEHLERT. Thank you. That will be an interesting exercise. Dr. Bartlett.
Improving the Nation's Health: Cost-Benefit Analyses
Page 97 PREV PAGE TOP OF DOC Segment 1 Of 2
Mr. BARTLETT. Thank you very much. I think before we make a public policy decision as to what we do about this, we need to know who is dying and why. If, for instance, it is a smoker, where this is essentially the straw that broke the camel's back and they would have died next week anyhow, this is a pretty different thing than taking out a baby who would look forward to maybe 90 years of productive life, except for this. So I think that we need to determine who dies and why before we make any decisions of what to do about it.
And then I would like to reflect for just a moment and get your response on cost benefit. Today, 3,000 of our kids will start smoking cigarettes and 1,000 of them will die prematurely. This year 40-couple thousand people will die from automobile accidents and hundreds of thousands of our people will sustain life-altering injuries as a result of automobile accidents. Now, it is obvious that in both of these cases we could drastically reduce deaths and health assaults.
For instance, if we would just quit smoking, there wouldn't be any deaths from smoking. Would there? And if we equipped each of our cars like we equip racing cars, where they can run into the wall at 150 miles an hour, they go end over end, the wheels fly off, they burst into flamesthen you put the fire out, and if the seat belt was fastened, they generally crawl out without any meaningful injury.
Now, obviously if each of our cars was equipped with a steel crash cage and you put on a flame suit and a crash helmet and strapped yourself in the car, there is almost no accident we have on the road which comes anywhere close to these accidents with racing cars and, therefore, we could reduce deaths to very, very few. You would have to be run over by a tractor-trailer or something to die in a car equipped like that. And there would be very few life-altering injuries.
Page 98 PREV PAGE TOP OF DOC Segment 1 Of 2
Now, why don't we do that? We don't do that because our society has determined that 40-couple thousand lives lost a year and hundreds of thousands of life-altering injuries is a reasonable price to pay for the convenience of using the car the way we do. And why don't we just say you can't smoke? Because if you quit smoking, the last year of which I saw data, 419,000 people died from smoking. That is four times the estimate of maybe the 100,000 whose deaths might have been precipitated a bit early by breathing these pollutants. Don't you think that at the end of the day, no matter what the science tells us, that what we do about it has to be determined in the broad context of where we can best spend our monies to improve health in this country?
Dr. SCHWARTZ. Can I respond?
Mr. BARTLETT. Yes, sir. I hope so.
Dr. SCHWARTZ. Okay. Many thingsso let me try to address them. Who is dying? I did a study in Philadelphia looking at who was dying on high air pollution days. And the answer is, these deaths were out of hospital and they were mostly dead on arrival. These are sudden deaths. So they are primarily dying from heart attacks and arrhythmias, although we do get some pneumonia deaths.
Mr. BARTLETT. But what was their health status before that? Was this just the straw that broke the camel's back or did this take out of
Dr. SCHWARTZ. Well, andokay. So let me go on with that. So that is exactly what I did these harvesting related studies for. I have done four of these studies and there is another study that the folks at Hopkins did, and I think they have another one underway that will be out soon.
Page 99 PREV PAGE TOP OF DOC Segment 1 Of 2
And what those studies look at is, is it, in fact, true that these people would have died in the next week or the next month anyway? Were they desperately ill? And the answer was, no, that, in fact, the effect estimates didn't go down; they went up. And it is important to pin that with what people are dying of. I mean, if you have a heart attack and you don't die within the first 30 days, your life expectancy isn't bad for your age. Most of the deaths associated with a heart attack occur within, in fact, the first week of having the event.
So if we don't see this harvesting showing up pretty quickly, then these people's risks, you know, are going back to normal and they probably have years of life expectancy available. The latest data from the prospective cohort studies do suggest that on average many years of life are lost per event.
In the ACS study, on average, a high polluted city has a life expectancy, an average life expectancy, that is a year less than a clean city. But since most of those deaths aren't the ones associated with air pollution, that translates to about an average of 10 years lost for the average air pollution associated death. Now, some of them may only be three weeks, but on average, it is on the order of 10 years. So we are not looking at a trivial reduction in life expectancy as far as we can tell.
Now, that said, I do think that we should do cost benefit analyses. You mentioned some others. I would, by the way, love to drive one of those cars, but I don't think I could afford it. But not only couldn't I afford it, it would be very inconvenient for me to put on all that equipment and stuff like that.
Page 100 PREV PAGE TOP OF DOC Segment 1 Of 2 If somebody can change the pollution control equipment that my car comes equipped with, and, you know, I don't notice it and all it does is cost me a little more money, or if the price per kilowatt hour of my electricity goes up by three percent, that is a lot different now. It still doesn't mean that the benefits are worth the cost, but at least there is not these great inconveniences or great costs imposed on certain people that are there.
And the cost benefit analyses that have been done on particulate standards have shown that the benefits do exceed the cost because, you know, the benefits of reducing mortality risks by that much are fairly substantial. That doesn't mean that that is true for every possible control strategy. And that is what Dr. Amar was getting at. You have got to look at, you know, what is the cost per ton for this versus controlling over there. It might be that we don't want to put any controls on certain emission sources because it is just not worth it, and there are other ones where, hey, you know, it is pretty cheap to control this, and we want to buy more. And we certainly should do those kinds of things, and I have done those kinds of analyses, and I think they are important for public policy.
The last thing, in terms of who is dying, is we have recent data from three studies that have come out and a fourth that is in process that suggest that diabetics are considerably more susceptible to particulate air pollution than non-diabetics. And that is interesting because the mechanisms I spoke about before, the changes in electrocardiogram patterns, the increases in systematic inflammationthese mechanisms that are associated with cardiovascular death are also associated with diabetes. These are what are thought to be the mechanisms behind the increased cardiovascular risks of diabetics. So it could be that particles are sort of hitting the same pathways that diabetes are hitting and you are getting a double whammy, and that is why those people are more at risk. But we need to look at that some more.
Page 101 PREV PAGE TOP OF DOC Segment 1 Of 2
Chairman BOEHLERT. Well, thank you very much. Mr. Etheridge.
Pollution Emissions From Industrial Plants
Mr. ETHERIDGE. Thank you, Mr. Chairman. And, again, let me thank you for holding this important hearing. And let me turnwe talked earlier in the testimony, I believe, by the distinguished panelists about sulfur dioxides and some other things. Let me change it just a bit and refocus it, if I may, because there was just a recent report in our local paper on an issue, released in a report on May 4 of this year actually, about bad air in one of the counties that is adjacent to my district. That report found that an industrial center in that county, which is really a rural county, but it just has a concentration of plants in one corner of the county. The report studied the release of chemicals ranging from sulfur dioxide to formaldehyde emitted from eight of the manufacturing and chemical plants in the rural area.
The study found that the county is in the top 10 percent of sulfur dioxide emissions in the United States. Although the report paints a very unflattering view of what is happening infrom those plants, they do not violate any of the permitted emission levels that are permitted according to the North Carolina Department of Air Quality, and have not since, once, I think, in the early '90's.
Although individual plants may not be violating the state standards or Federal standards, I am concerned about the cumulative effect of this many plants in a cluster, if it would happen not only here, but anywhere in the country, and what kind of harmful effects they may produce for individuals. So my question to you is this, do I have any reason to be concerned about this problem? And, number two, how detrimental is the emission of pollution from plants, as well as diesels and otherwise to the health of individuals living in communities such as this one where plants may be?
Page 102 PREV PAGE TOP OF DOC Segment 1 Of 2
Mr. GREENBAUM. I might take a first stab at that briefly. Most of the concern around sulfur dioxide and the setting of standards for sulfur dioxide in this country has been based mostly on the sort of acute resultsthe acute effects of very high exposures. And as a result, we have such standards. They have been largely met in many parts of the country. In some cases, historically, they were met by tall stacks, which created problems downwind, as we know. And that has been where the attention has been. So that it is not surprising that today these plants are meeting those standards.
Having said that, our re-analysis of the American Cancer Society study and the recent further analysis in that database that was published in the Journal of the American Medical Association found relationships between not only particles and mortality, but also sulfur dioxide. Now, our review committee, in looking at that, was not convinced that it was sulfur dioxide itself that was doing that, because the health data and the toxicology data might not support that.
But a suggestion that other pollutants that we don't even measure that are traveling may be coming from the same sources, may be the cause of that. So I think it is fair to say that we are learning more about this and that the data is suggesting that we need to look at these things, whether that means revisiting specifically the standards for sulfur dioxide, or whether that means looking at the whole suite of those pollutants and seeing what kinds of control actions could cost effectively reduce all of them at the same time and thereby get you the benefit even if you are not sure exactly which one is there.
Mr. ETHERIDGE. Anyone else?
Page 103 PREV PAGE TOP OF DOC Segment 1 Of 2
Dr. AMAR. Yeah. Yeah. I would like to maybe add to that. I think when we look at a state level of what needs to be doneand you mentioned, you know, chemical plants and sulfur dioxideand we are obviously discussing here PM2E. But all these things are connected. You have PM2E. You have ozone. There are issues of acid deposition, regional haze, visibility, even mercury. So when you are looking at many of these measures, you have to look them in a combined way.
For example, you know, we mentioned diesel a number of times here. But just looking at sulfur dioxide and sulfates, and the power plants in this countryyou know, we still, I think, have about 15 million tons of SO from power plants burning coal, and sulfate is still the second largest part of what you see in PM2E. Even though organics in urban areas dominate, sulfates are not that far behind.
But, again, under the Clean Air Act of 1990, you know, we reduced sulfur dioxide by 50 percent. Whereas technology is able to do that up to 90, 95 percent. Soand, again, you know, 12 years after the Clean Air Act, we still have only 27 percent of capacity in the United States with the scrubbers, which means three out of four megawatts don't have a scrubber. And that is because we required 12 years ago only 50 percent reduction.
Under Clear Skies Initiative, I think that is about 70 percent. There are other bills before your House and also Senate which are requiring larger reductions, which are very doable, but also they have benefits besides just the health effects of PM2E. They improve visibility in national parks. They reduce acid deposition in a big way. So I think one has to look at all these things in one place, rather than looking at, you know, PM and ozone.
Page 104 PREV PAGE TOP OF DOC Segment 1 Of 2
I will give you one other example. I mean, one of the things we have doneoxides and nitrogen control in this country. You know, we said it was, well, only to reduce ozone levels. So we have controls now in power plants with these huge devices I showed you, selective catalytic reduction, which turn on May 1 and turn off on September 30, because we said, NOX was bad for you only because it made ozone, but ozone is made only during 153 days of the year, May 1 through September 30. So you can have this billions of dollars of investment which are not used after October 1.
It is like your cars with catalytical converters where you turn them off saying, you know, NOX only makes ozone, and we don't need to control this after October 1. So I think sometimes we have ended up making bad decisions. But looking back on this initiative, I think the President's initiative and other bills are requiring NOX control, not for just five months a year, but all 12 months.
Dr. WYZGA. I would like to go back to your problem in North Carolina. You have to realize that air pollution is a complex mixture. And I think we have been handicapped in terms of looking at exposures and concentrations by looking at a lamppost. We only measure a small number of things, namely those that we regulate directly.
And it is very conceivable that there are things in that mixture that we are not measuring that could be pretty noxious. I think one of the things that would be particularly important would be to get some good measures of what concentrations or exposures are to people in those communities and to try and really look at the specific components to see are there any in there that might be of particular concern to that population.
Page 105 PREV PAGE TOP OF DOC Segment 1 Of 2
Chairman BOEHLERT. Thank you very much. The gentleman's time has expired. Mr. Smith.
Determining Pollution as Cause of Death
Mr. SMITH OF MICHIGAN. Thank you, Mr. Chairman. I am a farmer and I need to get some things sort of out of the hay mall and down on the ground floor where we can chew on it a little better. How do you know when somebody died because of pollutants or PMs?
Dr. SCHWARTZ. That is easy. We also don't know whether they died of smoking or anything else. You know, all we know is that, on average, there is more of a risk of having a heart attack if you smoke cigarettes, but we can't tell you which heart attacks were due to the fact that you smoked. And we know there is more of a risk for air pollution, but we can't tell you which people it was.
Mr. SMITH OF MICHIGAN. Are there studies of autopsies where you look at the inside of the lungs to determine the collection of pollutants, whether it might be from a coal mine or whether it might be a farmer breathing grain dust or animal dust or whatever?
Mr. GREENBAUM. There are limited autopsy studies. The one challenge is that the percentage of the population who tend to have autopsies after death is not representative of the general population and tends to have a much higher number of people who engaged in drugs, drinking, and a variety of other things. So that the ability to tell whether or not air pollution was a factor is clouded at the best. You know, we are talking here about usually people who have been involved in crime, for the most part.
Page 106 PREV PAGE TOP OF DOC Segment 1 Of 2
But there other ways of doing this. We funded a study in Montreal which took advantage of the fact that with their government health system they actually track every single individual's health care. And we could tie in these daily studies, every death on a given day, to the person's health care and diagnoses for the previous five years, the medications they were having and others. This was the first study that Dr. Schwartz referred to that found that there was a relationship between people, for example, who have had diabetes and people dying early on these days.
But these are averages. They are not individual cases of doing it. What you can do is be pretty sure that you have controlled for other things that likely would have contributed to their early death.
In the American Cancer Society's study you have information, detailed information, on each person's smoking behavior, which we know is a risk. You have information on their body mass index, how obese they are, which we also know is a significant risk. There is other information, as well, that can lend insight to that. So you can eliminate the other possible explanations to a large extent, not totally, but to a large extent. And then when you still see differences between the most polluted city and the least polluted city
Immunities to Pollutants
Mr. SMITH OF MICHIGAN. How about the capacity of this wonderful body that we live in to develop some natural protections? Are there studies that show where a youngster growing up might develop the kind of whateverthe resistance, the immunities, or to put those inhaled pollutants aside? We briefly talked to Dr. Schwartz earlier about the study on allergies, but how about other PMs? The more you get, the worse off you are, or is there a situation
Page 107 PREV PAGE TOP OF DOC Segment 1 Of 2
Dr. WYZGA. There is a set of literature suggesting that Vitamin C may be protective of some of the impacts of air pollution, but, you know, whether or not that could be replicated in other studies, I don't know.
Mr. GREENBAUM. There is not evidence currently on PM protective mechanisms. There is some suggestion that people exposed over long periods of time to ozone develop a thickening of the lung lining, which may be a protective mechanism to some extent. There is also some evidence, limited evidence, and this will be ironic for most people, that those who smoke may also develop that thickening of the lung lining and may be less sensitive to things like ozone.
Mr. SMITH OF MICHIGAN. Yeah. Dr. Schwartz, I was happy to read thatof the study that those of us that grew up on a farm might be more resistant to allergies.
Dr. SCHWARTZ. To asthma. That is correct. But that has to doI mean, the theory behind that, as opposed to the observation, is that early in life the direction of emphasis of your immune system is set and it can go in more than allergenic direction or more of a direction that tends to attack, say, bacteria. And there is a lot of bacterial products, not even necessary live bacteriabroken down cell walls of bacteria. There is a lot of exposure to that in a farm, and that may push your immune system that way and keep it from becomingdeveloping an allergic phenotype is the theory. Whether that happens with particulate air pollution exposure, I don't think we have any evidence.
Page 108 PREV PAGE TOP OF DOC Segment 1 Of 2 Mr. SMITH OF MICHIGAN. But I guess you all agree, a little more scientific study and research wouldn't hurt.
Chairman BOEHLERT. Oh, yeah. And we all do.
Dr. SCHWARTZ. None of us are retiring immediately.
Chairman BOEHLERT. Thank you. The Chair recognizes Ms. Woolsey.
The Role of the Federal Government
Ms. WOOLSEY. Thank you, Mr. Chairman. And, again, a wonderful Panel. Thank you very much. Survival of the fittest, I think, is what Congressman Smith is talking about. And maybe I have seen too many sci-fi movies or something, but I am trying to think what we all are going to look like in order to adapt to particulates if we don't do something about it.
There is good science and science we need more of, I am sure. There is also good common sense. I mean, you would probably do exactly what I would do if you are in your car and you pull upor you see one of those dirty busses or dirty trucks in front of youI make distance. I get really polite and I let all kinds of people go in front of me. I mean, there is just somethingI mean, it is just a survival reaction. And so, I have a question that is kind of not too serious and then I do have a serious question.
I mean, are we only trying to convince Members of Congress that this is important and we need a lot more science, or does the public not haveis there not an outcry from the public that they don't want any more of these busses and trucks on the streets and they know that they are dangerous, and why aren't we doing something about it? Because that is what I hear. So with that, I am going to ask a two-part question. What role do you think the Federal Government should play in responding to that outcry? So let us start with you, Mr. Greenbaum, and just go down the line. And we have to go vote. I think you heard
Page 109 PREV PAGE TOP OF DOC Segment 1 Of 2
Mr. GREENBAUM. Yeah. So I will be very brief. There are campaigns in a number of cities around the United States being run by environmental organizations in those cities dealing with busses, trying to get busses either retrofitted or converted to other sources or replaced. And there are programs, probably most progressively in California, where they actually have a bond issue where they have been funding those retrofits for school districts and others who are strapped for dollars. Also, New York City has made an agreement to do similar things.
So there are efforts underway. As we said earlier, there is no Federal effort underway, no Federal mechanism. And we have to remember that many of these busses are owned by public agencies, either public transit authorities or by school districts, none of whom have a lot of money to make these changes. So there is a public responsibility that isn't fully addressed.
Ms. WOOLSEY. Dr. Wyzga.
Dr. WYZGA. Yes. Let me comment first on, I guess, your avoidance experience. I am not sure that sort of letting those carskeeping a distance is really going to protect you. We have been
Ms. WOOLSEY. You just feel like it will.
Dr. WYZGA. We have been involved in a study and I saw some data that actually blew my mind where we were looking at personal exposures to people to PM2E. And these are people who were basically riding in a van that was designed to protect them from, I guess, emissions of the van. And when they were riding on roads in St. Louis, the personal exposures went up by a factor of about 5 or 6 and they were not trying to go near trucks that were emitting lots of pollutants.
Page 110 PREV PAGE TOP OF DOC Segment 1 Of 2
But just simply that, you know, there are areas, and roads include them, where we have incredibly high exposures. And I am not sure basically what we could do. I guess we can try andyou know, try and find the offenders and limit them. But, on the other hand, wemaybe we have to find, you know, alternative transportation systems or, you know, find ways to limit people being stuck in congested traffic. Because that certainly is going to lead to some very high exposures.
Dr. SCHWARTZ. Well, I would just like to mention that in response to one thing, I think people came up with doing something to reduce diesel emissions, but hopefully there is room for more than one thing, and there are other sources of particle exposures. And so wesome of which may be less expensive to control and that might be a worthwhile thing to think about, is, well
Ms. WOOLSEY. Like wood?
Dr. SCHWARTZ. Like wood. In fact, where Ron lives there was a study done by David Fairly showing that more than 50 percent of the PM in the air in the winter is wood smoke. And if you figure PM2E, it has got to more like 70 percent of the PM2E in the air is wood smoke. All around the bay area there is a lot of wood smoke exposure to populations in the winter.
Chairman BOEHLERT. Thank you very much. We will get on now. We have to complete because we have 8 minutes before we vote, and Mr. Nethercutt and Mr. Rohrabacher both agreed to take two minutes of questions. Mr. Nethercutt.
Page 111 PREV PAGE TOP OF DOC Segment 1 Of 2
Mr. NETHERCUTT. Thank you, Mr. Chairman. Thank you
Chairman BOEHLERT. And then excuse you.
Critique of the Studies: Determining ''Early'' and ''Premature'' Deaths
Mr. NETHERCUTT. Thank you, gentlemen. I noticed in some of your testimony, written testimony, that there is reference to early death and premature death, which seems to me to be a challenging conclusion since we don't know what early is and we don't know what premature is. It may be days. It may beI think it said up to 30 days, as I understand it. Yet, is it my understanding that you didn't follow individual patients for any period of time to determine their lifestyle or their habits or, you know, whether they smoked or didn't smoke or drank or didn't drink or involved in sort of risky behavior? Is that correct?
Dr. SCHWARTZ. Well, there were two kinds of studies. First of all, we used the word early death because we are all going to die. And we
Mr. NETHERCUTT. Exactly.
Dr. SCHWARTZ [continuing]. Don't want to say avoided death, so you got to say something.
Mr. NETHERCUTT. Right.
Page 112 PREV PAGE TOP OF DOC Segment 1 Of 2 Dr. SCHWARTZ. There are two kinds of studies. The time series studies are based on the assumption that, you know, your smoking history today and your smoking history on Thursday are
Mr. NETHERCUTT. Well, let me
Dr. SCHWARTZ [continuing]. Pretty similar.
Mr. NETHERCUTT. I understand. Let me justbecause I
Dr. SCHWARTZ. These cohort studies did look at whether you smoked.
Mr. NETHERCUTT. Well, I understand. But didyou didn't follow individual patients for a period of years. Like we are going to study these 50 people and
Dr. SCHWARTZ. In the cohort studies, we did.
Mr. NETHERCUTT. Yeah. But for how long a time?
Dr. SCHWARTZ. The latest follow-up of the Six Cities study, we look atwe are following people from 1976 to 2000.
Page 113 PREV PAGE TOP OF DOC Segment 1 Of 2 Mr. NETHERCUTT. I see. Okay. And diabetesdid your reference to diabetes involve Type I or Type II? What is the higher risk based on
Dr. SCHWARTZ. Type II. Type II.
Mr. NETHERCUTT. Okay. And, finally, have you done any analysis of the cost of any solutions to prevent premature or early death, assuming that your conclusions are correct?
Dr. SCHWARTZ. I mean, I have
Mr. NETHERCUTT. What would cause society to not have early deathlike that is related to the causes that you see
Dr. SCHWARTZ. To the pollution?
Mr. NETHERCUTT. Yes, sir.
Dr. SCHWARTZ. Well, that gets down to these costs per ton removed. I mean, for sulfur dioxide control to reduce sulfatesyou know, that is traded on the Chicago Board of Trade. You can look at what SO emission reduction credits go for. And it is, I don't know
Mr. NETHERCUTT. So now
Page 114 PREV PAGE TOP OF DOC Segment 1 Of 2 Dr. SCHWARTZ [continuing]. About 120
Mr. NETHERCUTT. So now if the forecast initially was in excess of 1,000, it is below 100 bucks.
Dr. SCHWARTZ. Right. Hundred bucks.
Mr. NETHERCUTT. Right.
Dr. SCHWARTZ. So that is what that costs. For diesel emissions it is going to be more, but it is probably going to be under $1,000 a time.
Mr. NETHERCUTT. Thank you. My time is up. Thanks.
Chairman BOEHLERT. Mr. Rohrabacher.
Mr. ROHRABACHER. Thank you very much. First of all, let me say to the Chairman, now that he can hear me, thank you very much for this hearing. I think that when we study omissions and emissions, I think it is important for us to focus on health and the health of human beings rather than focusing on other issues like global warming, which I consider to be nonsense. So, thank you very much to the Panel. Thank you very much to the Chairman for taking a health issue very, very seriously.
Page 115 PREV PAGE TOP OF DOC Segment 1 Of 2 Let me note that I think that it is very much of a health challenge, but is it not getting better? In Southern California, when I was a kid, we used to have all kinds of things. You couldn't go out and do gym, you know, twice a week, and now it happens maybe once a semester for kids. Aren't the health emissionsare we getting
Mr. GREENBAUM. The emissions have gone down. There is no question about that.
Mr. ROHRABACHER. Right.
Mr. GREENBAUM. And Southern California is probably the best example of that. I am actually the Vice Chairman of the National Academy Committee that was established by Congress to look at the air quality management system in the United States. And there is
Mr. ROHRABACHER. Right. So that
Mr. GREENBAUM [continuing]. No question there has been progress.
Mr. ROHRABACHER. And that is aMr. Chairman, that is really an important issue right here, that we are on a good trend when it comes to these emissions, as compared to 100 years ago or 50 years ago. So, number one, the health effect of emissions is vitally important, but it is getting better. Let me note that most kids today think it is just the opposite. I always ask kids who come into my office, is the air pollution worse today or better today than what it used to be when I was going to high school? And they all say, oh, you are so lucky to have gone to high school 35 years ago in Southern California. The air was so much better then. And if we need to get any information out, it is that we have made progress. Health does count. Progress is being made.
Page 116 PREV PAGE TOP OF DOC Segment 1 Of 2
One last very quick question is, when we are talking about making further progress, is it engine configuration, or should we go to thingsthink about things like fuel additives that might actually make us burn fuel more efficiently? Which would be the best way to go?
Dr. SCHWARTZ. Well, I think we need toand you want to buy the cheapest tons first. So we are not going to do any one thing. You know, SO emission reductions are pretty cheap. Some early diesel reductions are going to be pretty cheap. And then if you want more, you are going to have to go to a more expensive technologyand depending on what you are trying to control, baghouses, things like that. So you need to look at all the industries that produce this stuff and look at what the cost per ton is for controls in different places and buy the cheapest tons first.
Mr. ROHRABACHER. All right. Thank you very much. Thank you, Mr. Chairman.
Chairman BOEHLERT. Thank you. And I want to thank all of you for being facilitators. And I really want to thank youyou might get Mr. Rohrabacher to cosponsor my bill, H.R. 25, which requires further reductions in NOX, SOX, and addresses mercury for the first time. Thank you very much. We would have more questions, however, we are rudely interrupted by votes in the House. And it is a series of votes. So to be fair to you, I don't want to keep you here. This meeting is now adjourned. Thank you.
Dr. SCHWARTZ. Thank you, Mr. Chairman.
Page 117 PREV PAGE TOP OF DOC Segment 1 Of 2
[Whereupon, at 11:33 a.m., the Committee was adjourned.]
Additional Material for the Record
Next Hearing Segment(2)
(Footnote 1 return)
Full text of article included in Appendix 1, pp. 7291.
(Footnote 2 return)
Schwartz J. Air pollution and hospital admissions for cardiovascular disease in Tucson. Epidemiol 1997; 8:371377.
(Footnote 3 return)
Schwartz J. Short term fluctuations in air pollution and hospital admissions of the elderly for respiratory disease. Thorax 1995; 50:531538.
(Footnote 4 return)
Samet JM, Zegar SL, Dominici F, Curriero F, Coursac I, Dockery DW, Schwartz J, Zanobetti A. The National Morbidity, Mortality, and Air Pollution Study Part II: Morbidity, Mortality, and Air Pollution in the United States. Health Effects Institute 2000; 94:184.
(Footnote 5 return)
Schwartz J. Assessing Confounding, Effect Modification, and Thresholds in the Association between Ambient Particles and Daily Deaths. Environ Health Perspect 2000; 108:563568.
(Footnote 6 return)
Schwartz J. What are people dying of on high air pollution days? Environ Res 1994; 64:2635.
(Footnote 7 return)
Schwartz J, Morris R. Air pollution and hospital admissions for cardiovascular disease in Detroit, Michigan. Am J Epidemiol 1995; 142:2235.
(Footnote 8 return)
Schwartz J. Air Pollution and Hospital Admissions for Heart Disease in Eight U.S. Counties. Epid 1999:10:1722.
(Footnote 9 return)
Burnett RT, Dales R, Krewski D, Vincent R, Dann T, Brook JF. Associations between ambient particulate sulfate and admissions to Ontario hospitals for cardiac and respiratory diseases. Am J Epidemiol 1995; 142:1522.
(Footnote 10 return)
Schwartz J. Harvesting and long-term exposure effects in the relationship between air pollution and mortality. Am J Epidemiology 2000; 151:440448.
(Footnote 11 return)
Schwartz J. Is There Harvesting in the Association of Airborne Particles with Daily Deaths and Hospital Admissions? Epidemiol 2001; 12:5561.
(Footnote 12 return)
Zanobetti A, Schwartz J, Samoli E, Gryparis A, Touloumi G, Atkinson R, Le Tertre A, Bobros J, Celko M, Goren A, Forsberg B, Michelozzi P, Rabczenko D, Ruiz EA, Katsouyanni K. The Temporal Pattern of Mortality Responses to Air Pollution. Epidemiol 2002; 13:8793.
(Footnote 13 return)
Zeger SL, Dominici F, Samet J. Harvesting-resistant estimates of air pollution effects on mortality. Epidemiology 1999 March; 10(2):171175.
(Footnote 14 return)
Schwartz J and Zanobetti A. Using meta-smoothing to estimate dose-response trends across multiple studies, with application to air pollution and daily death. Epidemiology 2000; 11(6):666672.
(Footnote 15 return)
Schwartz J, Ballester F, Saez M, Pérez-Hoyos S, Bellido J, Cambra K, Arribas F, Cañada A, Pérez-Boillos MJ, and Jordi Sunyer J. The Concentration Response Relation between Air Pollution and Daily Deaths. Environmental Health Perspectives 2001; 109:10011006.
(Footnote 16 return)
Schwartz J, Laden F, Zanobetti A. The Concentration-Response relation between air pollution and daily deaths. Environ Health Perspect, in press.
(Footnote 17 return)
Daniels MJ, Dominici F, Samet JM, Zeger SL. Estimating particulate matter-mortality dose-response curves and threshold levels: an analysis of daily time-series for the 20 largest U.S. cities. Am J Epidemiol 2000 Sep 1; 152(5):397406.
(Footnote 18 return)
Laden F, Neas LM, Dockery DW, Schwartz J. Association of fine particulate matter from different sources with daily mortality in six US cities. Environ Health Perspect 2000; 108:941947.
(Footnote 19 return)
Janssen NAH, Schwartz J, Zanobetti A, Suh HH. Air conditioning and combustion related particles as modifiers of the effect of PM10 on hospital admissions for heart and lung diseases. Environ Health Perspect 2002; 110:4349.
(Footnote 20 return)
Samet JM, Zeger SL, Dominici F, Curriero F, Coursac I, Dockery DW, Schwartz J, Zanobetti A. The National Morbidity, Mortality, and Air Pollution Study Part II: Morbidity, Mortality, and Air Pollution in the United States. Health Effects Institute 2000; 94:184.
(Footnote 21 return)
Pope CA 3rd, Burnett RT, Thun MJ, Calle EE, Krewski D, Ito K, Thurston GD. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA 2002 Mar 6; 287(9):113241.
(Footnote 22 return)
Hoek G, Brunekreef B, Goldbohm S, Fischer P, and van den Brandt P. Long-term exposure to traffic related air pollution is associated with mortality in a Dutch Cohort Study. Proceeding of Health Effects Institute Annual Meeting, 2001, p. 36. Health Effects Institute, Cambridge MA.
(Footnote 23 return)
Godleski JJ, Lovett EG, Sioutas C, Killingsworth CR, Krishnamurthi GG, Hatch V, Wolfsom M, Ferguson ST, Koutrakis P, Verrier RL. Impact of inhaled concentrated ambient air particles on canine electrocardiographic patterns. Health Effects Institute Annual Meeting, 1997: 15.
(Footnote 24 return)
Watkinson WP, Campen MJ, Costa DL. Cardiac arrhythmia induction after exposure to residual oil fly ash particles in a rodent model of pulmonary hypertension. Toxicol Sci Feb 1998; 41(2):20916.
(Footnote 25 return)
Pope CA III, Verrier RL, Lovett EG, Larson AC, Raizenne ME, Kanner RE, Schwartz J, Villegas GM, Dockery DW. Heart Rate Variability Associated with Particulate Air Pollution. Am Heart J. 1999; 138:890899.
(Footnote 26 return)
Liao D, Creason J, Shy C, Williams R, Watts R, and Zweidinger R.Daily Variation of Particulate Air Pollution and Poor Cardiac Autonomic Control in the Elderly. Environ Health Perspect 1999; 107:521525.
(Footnote 27 return)
Gold DR, Litonjua A, Schwartz J, Verrier M, Milstein R, Larson A, Lovett E, Verrier R. Ambient Pollution and Heart Rate Variability. Circulation 2000; 101:12671273.
(Footnote 28 return)
Pope CA, Dockery DW, Kanner RE, Villegas GM, Schwartz J. Oxygen saturation, pulse rate, and particulate air pollution: a daily time series panel study. Am J Resp Crit Care Med 1999; 159:365372.
(Footnote 29 return)
Peters A, Perz S, Doring A, Stieber J, Koenig W, Wichmann HE. Increases in heart rate during an air pollution episode. Am J Epidemiol Nov 15 1999; 150(10):10948.
(Footnote 30 return)
Peters A, Liu E, Verrier RL, Schwartz J, Gold DR, Mittleman M, Baliff J, Oh A, Allen G, Monahan K, Dockery D. Air pollution and incidence of cardiac arrhythmia. Epidemiology 2000; 11:1117.
(Footnote 31 return)
Peters A, Dockery DW, Muller JE, Mittleman MA. Increased particulate air pollution and the triggering of myocardial infarction. Circulation, 2001, in press.
(Footnote 32 return)
Mittleman MA, Maclure M, Tofler GH, Sherwood JB, Goldberg RJ, Muller JE. Triggering of acute myocardial infarction by heavy physical exertion. Protection against triggering by regular exertion. Determinants of Myocardial Infarction Onset Study Investigators. N Engl J Med 1993 Dec 2; 329(23):167783.
(Footnote 33 return)
Peters A, Doering A, Wichmann HE, Koenig W. Increased plasma viscosity during an air pollution episode: a link to mortality? Lancet 1997; 349: 9054, 15827.
(Footnote 34 return)
Gardner SY and Costa DL. Particle-Induced Elevations In White Blood Cell Count And Plasma Fibrinogen Levels In Rats. Am J Resp Crit Care Med 1998; 157:A152.
(Footnote 35 return)
Ghio AJ, Kim C, Devlin RB. Concentrated ambient air particles induce mild pulmonary inflammation in healthy human volunteers. Am J Resp Crit Care Med 2000; 162:98188.
(Footnote 36 return)
Schwartz J. Air Pollution and Blood Markers of Cardiovascular Risk. Environ Health Perspect, in press.
(Footnote 37 return)
Pekkanen J, Brunner EJ, Anderson HR, Tiittanen P, Atkinson RW. Daily concentrations of air pollution and plasma fibrinogen in london. Occup Environ Med 2000 Dec; 57(12):81822.
(Footnote 38 return)
Salvi S, Blomberg A, Rudell B, Kelly F, Sandstrom T, Holgate ST, Frew A. Acute inflammatory responses in the airways and peripheral blood after short-term exposure to diesel exhaust in healthy human volunteers. Am J Respir Crit Care Med 1999 Mar; 159(3):7029.
(Footnote 39 return)
Peters A, Frohlich M, Doring A, Immervoll T, Wichmann H-E, Hutchinson Wl, Pepys MB, Koenig W. Particulate air pollution is associated with an acute phase response in men:Results from the MONICA-Augsburg Study. Eur Heart J., in press.
(Footnote 40 return)
Vincet R, Jumarathasan P, Mukherjee B, Gravel C, Bjarnason S, Urch B, Speck M, Brook J, Tarlo S, Zimmerman B, Siverman F. Exposure to urban particles (PM2E) causes elevations of the plasma vasopeptides Endothelin (ET)1 and ET3 in humans. Am J Resp Crit Care Med 2001; 163:A313.
(Footnote 41 return)
Ibald-Mulli A, Stieber J, Wichmann HE, Koenig W, Peters A. Effects of air pollution on blood pressure: a population-based approach. Am J Public Health 2001 Apr; 91:5717.
(Footnote 42 return)
Salvi S, Blomberg A, Rudell B, Kelly F, Sandstrom T, Holgate ST, Frew A. Acute inflammatory responses in the airways and peripheral blood after short-term exposure to diesel exhaust in healthy human volunteers. Am J Respir Crit Care Med 1999 Mar; 159(3):7029.
(Footnote 43 return)
Seaton A, MacNee W, Donaldson K, Godden D. Particulate air pollution and acute health effects. Lancet 1995; 345:17678.
(Footnote 44 return)
Suwa T, van Eeden SF, Quinlan K, Ohgami A, Hards J, Vincent R, and JC Hogg. The effect of PM10 on conronary ateroslerosis. Am J Resp Crit Care Med 2001; 163(5):A311.
(Footnote 45 return)
Brook RD, Brook JR, Urch B, Vincent R, Rajagopalan S, Silverman F. Inhalation of fine particulate air pollution and ozone causes acute arterial vasconstriction in healthy adults. Circulation 2002; 105:15341536.
(Footnote 46 return)
Suwa T, Hogg JC, Quinlan KB, Ohgami A, Vincent R, van Eeden SF. Particulate air pollution induces progression of atherosclerosis. Journal of the American College of Cardiology 2002; 39:93542.
(Footnote 47 return)
Glantz SA. Air pollution as a cause of heart disease. Time for action*. Journal of the American College of Cardiology 2002; 39:9435.
(Footnote 48 return)
Zanobetti A, Schwartz J, Gold DR. Are there sensitive subgroups for the health effects of airborne particles? Environ Health Perspect 2000; 108:841845.
(Footnote 49 return)
Sunyer J, Schwartz J, Tobias A, MacFarlane D, Garcia J, Anto JM. Patients with chronic obstructive pulmonary disease area susceptible population of dying due to urban particles. Am J Epidemiol 2000; 151(1):506.
(Footnote 50 return)
Zanobetti A, Schwartz J. Are diabetics more susceptible to the health effects of airborne particles? Am J Resp Crit Care Med, in press.
(Footnote 51 return)
Zanobetti A, Schwartz J. Cardiovascular damage by airborne particles: Are Diabetics more susceptible? Epidemiology, 2002, in press.
(Footnote 52 return)
Sarnat JA, Koutrakis P, Suh H. Assessing the relationship between personal particulate and gaseous exposures of senior citizens living in Baltimore, Md. J Air Waste Mange Assoc 2000; 50:118498.
(Footnote 53 return)
Sarnat JA, Schwartz J, Catalano PJ and Suh HH. Confounder or Surrogate: The Role of Gaseous Pollutants in Particulate Matter Epidemiology. Environ Health Perspect 2001; 109:10531061.
(Footnote 54 return)
Zeger SL, Thomas D, Dominici F, Samet J, Schwartz J, Dockery D, Cohen A. Exposure measurement error in time-series studies of air pollution: concepts and consequences. Environ Health Perspect 2000; 108:419426.