SPEAKER: Morton Lippmann, Ph. D., Professor of Environmental Medicine
AFFILIATION: New York University Medical Center
RELEVANT PERSONAL BACKGROUND
1. Academic Peer-Reviewed Research Incorporated into Ozone (O3) and PM Criteria Documents, on:
a) Respiratory tract deposition and clearance of airborne particles
b) Controlled human and animal inhalation studies of physiological responses to acidic particles
c) Field studies of population responses to air pollution exposures
d) Development and evaluation of air sampling and monitoring techniques
2. Federal Agency Service on Committees Focussing on Inhalation Hazards
a) Chair, Clean Air Scientific Advisory Committee (CASAC) (1983-'87)
b) Member, CASAC Subcommittees on O3 (1988-1997) and PM (1993-1997)
c) Chair, Physical Effects Review Subcommittee of Clean Air Act Advisory Council (1994-1997)
d) Chair, EPA Science Advisory Board (SAB) Review Committee for Risk Assessment for Environmental Tobacco Smoke (1991-1993)
e) Chair, SAB Review Committee for Risk Assessment for Dioxin and Related Compounds (1994-1997)
f) Co-Chair, 4th Task Force for Research Planning in Environmental Health Sciences, National Institute of Environmental Health Sciences (1992)
g) Chair, Board of Scientific Counselors, National Institute for Occupational Safety and Health (1990-1992)
3. Academic Air Pollution Research Study Advisement
a) Member and Chair of External Advisory Comm., Harvard 6-Cities Study (1978-1987)
b) Member of External Advisory Comm., Harvard - Health Canada - Mult-city Air Pollution Health Effects Study (1987-1991)
c) Chair of External Advisory Comm., USC - CA Air Resources Board Study of Effects of Air Pollution on Children (1992-present)
OUTLINE OF STATUTORY AND SCIENTIFIC BASIS FOR PROPOSED O3 AND PM STANDARDS
1. Statutory Requirement Mandates Periodic (Nominally 5 yr) Reviews of Adequacy of National Ambient Air Quality Standards (NAAQS)
2. There is growing Scientific Peer-Reviewed Evidence for Adverse Human Health Effects at Ambient Concentrations within Previous NAAQS for PM (revised in 1987) and O3 (last revised in 1979)
3. There have been extraordinarily Thorough Reviews of Evidence were Conducted by EPA, CASAC, and Public Sector. They provide an Open Record for EPA Administrator and Congress
4. There were Strong CASAC Consensus Conclusions with Respect to:
a) Need for more targeted indices of relevant exposure, e. g., 8-hr avg. O3, and 2.5 æm cut-size for PM (PM-2.5)
b) Need for more robust criteria for daily NAAQS exceedances, i. e., multiple times rather than single
c) Adverse health effects are occurring in U. S. communities currently in compliance with existing NAAQS
d) Adverse effects are evident for sensitive subpopulations and may not affect most people (very large numbers of affected people, but low % of total population)
e) There are no identifiable threshold exposures for associations between PM and O3 concentrations and adverse health effects
f) PM-2.5 and O3 are largely formed in the atmosphere from gaseous precursors, are relatively uniformly distributed over large regions (hydrocarbons and nitrogen oxides (NOx) react to form O3, and organic components of PM-2.5; NOx, SO2 and photochemical oxidants react to form inorganic components of PM-2.5 (sulfates and nitrates)
g) Control strategies for PM-2.5 and O3 need to be implemented together and on broad geographic scales
h) Existing statutes and evidence thus presents difficult policy dilemmas to EPA Administrator and Congress (reducing PM and O3 concentrations can reduce, but not eliminate, excess mortality and morbidity
5. Further Conclusions on PM by CASAC Panel Members with Relevant Experience in Environmental Epidemiology (excerpts from supplemental letter of 3/30/96 by Lippmann, Shy, Speizer, and Stolwijk-Appendix H of PM Staff Paper).
In our judgment, the studies reviewed in the criteria document, specifically those considered in Chapter 12 (Epidemiological Studies), are persuasive in demonstrating a causal relationship between particulate air pollution, as me asured by different methods in the various studies, and excess mortality and morbidity.
The reasons for concluding that particulate air pollution is causally related to excess mortality and morbidity are summarized here:
A large number (20) of epidemiological time-series studies have consistently found a statistically significant association between daily variation in particulates and total mortality in cities of the U. S., Canada, Latin America, the U. K., and continental Europe. These findings argue against the associations being attributable to statistical sampling variation, i. e., the role of chance.
The results of these time-series studies cannot be attributed to the vagaries of statistical modeling, nor to confounding by season or weather.
The results of the time-series studies cannot be attributed to other criteria air pollutants. . . . Across the range of the 20 studies mentioned above, particulate air pollution is the only pollutant that is consistently associated with excess daily mortality, and the estimate of its effect is relatively stable when adjusted for the presence of co-pollutants. No monitored air pollutant, other than particulate matter, can account for the consistently observed excess mortality in these studies. Excess morbidity from cardiopulmonary diseases has also been observed in a considerable number of studies, and the morbidity relationship with ambient particulate concentrations is stronger overall and more consistent than for any other air pollutant.
There is considerable coherence between the observed mortality and morbidity effects of particulate air pollution. Not only is excess mortality from cardiovascular and respiratory diseases observed, but on days of higher particulates excess hospitalizations for cardiovascular and respiratory diseases are reported. On days of high particulates, there is an increased proportion of deaths from chronic obstructive pulmonary disease, pneumonia, heart disease and deaths among the elderly than on days of low particulates. These findings are supportive of a causal role for particulate air pollution, since they are health endpoints one would most anticipate from exposure by the inhalation route.
Given the striking consistency of the above studies, their robustness to variations in statistical modeling, the coherence among different but closely related health endpoints, and the empirical elimination of any alternative explanation for the findings, we conclude that a causal interpretation for particulate air pollution exposure is reasonable and defensible. This conclusion is further supported by longitudinal cohort studies of populations in which a geographical gradient in particulate air pollution was associated with a corresponding gradient in total mortality, in cardiopulmonary mortality and in lung cancer. These studies carefully controlled for other individual risk factors for these health endpoints.
Although population exposure to air pollution cannot be perfectly estimated based on central monitoring, these inherent errors in exposure estimation are more likely to cause an underestimation of the adverse health effects associated with pollution exposure, particularly in longitudinal cohort studies where individual risk factors and exposures are directly related to health effects. Thus the consistent positive findings cannot be attributed to exposure measurement error. Furthermore, there is growing evidence that fine particles are more uniformly distributed over large geographic areas than are coarse particles, that measurements at one site give a reasonable estimate of the fine particulate concentrations across a city, and that fine particles penetrate and have longer lifetimes indoors than coarse particles. This evidence supports using ambient measures of fine particulates at a central site as an acceptable estimate of the average exposure of people in the community. For these reasons, we judge that uncertainties arising from air monitoring and human exposure estimation do not negate the consistent excess mortality and morbidity associations discussed above.
We believe that the case has been made that fine particulates, as measured by PM-2.5, are the best surrogate currently available for the component of particulate air pollution that is associated with excess mortality and morbidity. We are not claiming that PM-2.5 is the causal agent, but rather that PM-2.5 is a better measure than any alternative metric, of the complex in the particulate mass that is causing excess mortality and morbidity. Excess mortality, hospital admissions for respiratory diseases and decreased lung function are more strongly and consistently associated with fine rather than with coarse mode particulates.
The Health Effects Institute (HEI) reanalysis does not contradict any of the above conclusions. The HEI analysis conclusively demonstrated that the positive findings from the original studies selected for reanalysis were replicable, were not an artifact of statistical modeling, and were not confounded by idiosyncrasies in the method to control for season or weather. The HEI investigators appropriately concluded that, because of the high intercorrelations between pollutants in Philadelphia, mortality effects could not be attributed solely to particulates. More importantly, in their further report on this phase of their study, they concluded that "insights into the effects of individual criteria pollutants can be best gained by assessing effects across locations having different pollutant mixes and not from regression modeling of data from single locations. "
In our judgment, EPA has appropriately synthesized this evidence and drawn a responsible public health conclusion, namely, that particulate concentrations at current levels are causally associated with excess mortality and morbidity. Furthermore, we agree that fine particulates, as currently indexed by PM-2.5, are the most appropriate indicator for the component of the particulate air mass to which these adverse effects are attributed. We also agree that some adverse health effects may be related to the coarse particulate mode, and that therefore it is desirable to consider fine and coarse mode particulates as separate candidates for air quality standards.
MY RECOMMENDATIONS TO CONGRESS
1. Recognize that EPA Administrator has made a prudent public health judgment in her PM and O3 NAAQS selections.
The health benefits (cost avoidance) to be derived by implementation of the new PM-2.5 NAAQS will far exceed the costs of control implementations. The benefit/cost ratio for implementing compliance with the revised O3 NAAQS is not as great, but it should be recognized that reductions in O3 formation will also reduce PM-2.5 formation and ambient air concentrations and will also therefore contribute to the benefits associated with reductions in PM-2.5 exposures.
For O3, the current NAAQS of a 1-hr max of 120 ppb not be exceeded more than 4 times in 3 yrs is equivalent to an 8-hr max of 90 ppb based on the 3rd highest 8-hr value in a year. Thus, the proposed 8-hr max of 80 ppb is only a modest O3 NAAQS reduction. By contrast, the Air Quality Guideline for O3 of the World Health Organization-European Region (WHO-EURO), adopted late in 1996 is an 8-hr maximum of 60 ppb. In my view, the 8 hr-80 ppb proposal is a prudent step in the right direction at this time and recognizes that any lower limit is probably not achievable without draconian controls. The major advance is the shift to an 8-hr averaging time, providing a much sounder basis for evaluating the public health risk from community exposures.
For PM-10, the 50 æg/m3 annual average would be retained without change. and the 24-hr PM-10 would be relaxed by applying it only to the 98th% value (22nd highest) rather than to the 4th highest over 3 yrs. It is only by implementing the new PM-2.5 NAAQS that the degree of public health protection would be substantially advanced, and then only in the eastern U. S. and in some large cities in the west where fine particles are major %'s of PM-10.
2. Recognize that 1990 CAA-Title I implementation already underway (SO2 and NOx emission reductions) will reduce the numbers of communities in exceedance of the proposed PM-2.5 NAAQS relatively soon.
3. Recognize that the new PM-2.5 NAAQS cannot be implemented immediately, and prudent implementation schedules can be devised and implemented to minimize economic disruptions.
4. Recognize that the causal factors within PM-2.5 for the consistent and coherent associations between PM-2.5 in community air and excess daily and annual mortality, excess emergency room and hospital admissions for respiratory diseases, lost time from work and school, respiratory symptoms, and reduced lung functions are not yet established in terms of biological mechanisms. However, it has clearly been shown that they cannot be attributed to other hypothesized environmental factors such as other criteria air pollutants, aeroallegens, or meteorological variables. The situation is analogous to that for another commonly encountered respiratory irritant, i. e., environmental tobacco smoke, where the epidemiological evidence for adverse respiratory effects in children is overwhelming, and there is significant evidence for excess lung cancer in adults as well.
5. Recognize that more definitive laboratory and epidemiological research on causal factors is now becoming feasible as epidemiologic investigative techniques and animal models for susceptible segments of the population are being established and validated. With a reasonable and prudent level of additional research funding for EPA and NIEHS, identification of the biological mechanisms, the chemical and physical properties of the active components of PM, and the exposure-response relationships, can be more firmly established within the next five years. Such knowledge is essential for the design and implementation of cost-effective control strategies, and for the further revisions of the PM NAAQS that will be required early in the next century.
6. Recognize that while the costs of the research recommended above are substantial (on the order of $50x106 per year), they are quite small in relation to the control costs that can be more effectively targeted and reduced through the knowledge gained, and also small in comparison to the health benefits resulting from exposure reductions resulting from the controls.