I am also the Director of the National Institute of Environmental Health Sciences' (NIEHS) Community Outreach and Education Program at NYU. A goal of this program is to provide an impartial scientific resource on environmental health issues to decision-makers, and that is my purpose in testifying to you here today.
I must take issue with much of the intent of Bill S 1084 and with the findings upon which it is based. First, the new ozone standard will not disrupt or delay ozone reductions, as implied by Finding 4: instead, it is S 1084 that would increase uncertainty in the marketplace and by regulators, thereby slowing air quality progress. Second, Findings 5 and 6 fail to acknowledge that, as stated in George Wolff's letters of closure to the Administrator, CASAC reached a consensus that a fine particulate matter (PM2.5) standard is needed, and that the ozone standard should be changed to an 8-hr basis, both of which the EPA promulgated on July 18, 1997. The revocation of these new ozone and PM2.5 standards that is called for in Bill S. 1084 would be unwise, and would be inconsistent with the intent of the Clean Air Act.
It is argued in the findings of Bill S. 1084 that significant progress has already been made, but this is not really the case for ozone over the last decade. As shown in the figure below, progress regarding ambient ozone levels in the U.S. had slowed in recent years under the old standards. In contrast, the new standards will engender a cleaning up of the air on a broader geographical basis than under the old standard. Thus, implementing the standards recently set by the EPA is the best way to ensure continued and even more rapid U.S. air quality improvements.
Moreover, Bill S 1084 wrongly seeks to fundamentally rewrite the Clean Air Act by restructuring who decides whether new standards are needed. The existing Clean Air Act requires that the EPA review the standards every five years, and then leaves that standard setting decision to the Administrator, with advice from CASAC. Bill S 1084, in contrast, seeks to shift that power to the Congress, by imposing a change back to the old O3 and PM standards. In addition, this bill says that the next science review of these standards may not occur any earlier than 4 years from now, but sets no requirement for the latest that this review may occur, which could possibly be interpreted as eliminating the Clean Air Act requirement for every five year reviews of these pollutants. These changes would represent a dramatic and unacceptable change in the Clean Air Act.
Source: U.S. EPA, National Air Quality and Emissions Trends Report, 1995.
EPA 454/R-96-005, October, 1996. RTP, NC.
The CAA has worked well for the last quarter of a century, right up to today. During the most recent O3 and PM standard reviews, CASAC reached consensus that the PM standard needed to be revised to directly control fine particles (PM2.5), and that the ozone standard needed to be changed to an eight hour average basis. The EPA followed that advice, and set standards that are in the best interest of the American public. The Congress should not try to "fix" something that isn't broken: the Clean Air Act is working just fine, and there is no need for the fundamental change in the Clean Air Act that is being proposed by S 1084.
The adverse health consequences of breathing ozone or particulate matter are serious and well documented, even at levels below the U.S. National Ambient Air Quality Standards (NAAQS) that were in effect before July 18, 1997. This documentation includes impacts demonstrated by controlled chamber exposures and by observational epidemiology showing consistent associations between each of these pollutants and adverse impacts across a wide range of human health outcomes. The implementation of the NAAQS promulgated by the U.S. EPA on July 18th will provide a substantial improvement in the public health protection provided to the American people by the Clean Air Act, but the passage of Bill S 1048 would block that much needed improvement in public health protection.
Ozone (O3) is a highly irritating gas that is formed in our atmosphere in the presence of sunlight from other "precursor" air pollutants, including nitrogen oxides and hydrocarbons. These precursor pollutants, which cause the formation of ozone, are emitted by pollution sources including automobiles, electric power plants, and industry.
Particulate Matter (PM) air pollution is composed of two major components: primary particles, or "soot", emitted directly into the atmosphere by pollution sources such as industry, electric power plants, diesel buses, and automobiles, and; "secondary particles" formed in the atmosphere from sulfur dioxide and nitrogen oxide gases, emitted by many combustion sources, including coal-burning electric power plants.
Observational epidemiology studies have shown compelling and consistent evidence of adverse effects by ozone and PM below the old U.S. standards that Senate Bill 1084 seeks to regress back to, if passed. These scientific studies statistically evaluate changes in the incidence of adverse health effects in a single population as it undergoes varying real-life exposures to pollution over time, or across multiple populations experiencing different exposures from one place to another. They are of two types: 1) population-based studies, in which aggregated counts of effects (e.g., hospital admissions counts) from an entire city might be considered in the analysis; and, 2) cohort studies, in which selected individuals, such as a group of asthmatics, are considered. Both of these types of epidemiologic studies have shown confirmatory associations between ozone and PM air pollution exposures and increased adverse health impacts, including:
-- decreased lung function (a measure of our ability to breathe freely);
-- more frequent respiratory symptoms;
-- increased numbers of asthma attacks;
-- more frequent emergency department visits;
-- additional hospital admissions, and;
-- increased numbers of daily deaths.
The newly promulgated EPA air quality standards are appropriate, and are based on sound science.
In my own research, I have found that both ozone and particulate matter air pollution are associated with increased numbers of respiratory hospital admissions in New York City, Buffalo, NY, and Toronto, Ontario, even at levels below the current standards. My results have been confirmed by other researchers considering locales elsewhere in the world. The U.S. EPA used my New York City asthma results in their "Staff Paper" when estimating the health benefits of tightening the ozone standard.
In previous Congressional hearings, much discussion centered on the hospital admissions effects of ozone, but ozone's other impacts have been largely ignored. Indeed, hospital admissions in New York City are only a small fraction of the benefits to be accrued by lowering pollution levels. The effects of ozone on hospital admissions represent only the "tip of the iceberg" of all of the many adverse effects associated with this pollutant, and they are therefore best viewed as indicators of the much broader spectrum of adverse health effects being experienced unnecessarily by the public today as a result of air pollution exposures. Most of these adverse effects are not directly recorded, however, as no central records are kept of these related, but more numerous, adverse pollutant impacts, such as increased restricted activity days and doctors visits.
In order to give some insight into the much larger numbers of other effects lurking beneath the surface of the ozone hospital admissions effects noted by George Wolff in Table VI-2(revised) of the Ozone OAQPS Staff Paper (June, 1996) and during previous testimony to this Subcommittee, I have made working estimates of the other documented adverse impacts of ozone exposure that will also be reduced in New York City, if the EPA's new ozone standard were to be implemented as originally proposed.
The results of my analysis are presented in the figure below, entitled the "Pyramid of Annual New York City Adverse Impacts of Ozone Avoided by the Implementation of the Proposed New Standard (vs. "As Is"). This pyramid is intended to be illustrative of the enormous gaps in the table presented by Dr. Wolff, and is not presented as a peer-reviewed comprehensive documentation of all the benefits which would be accrued by achieving the EPA's proposed new standard. Please note that the figure could not be drawn "to scale". If it were drawn "to scale", the New York City (NYC) asthma admissions triangle would not even be visible, since it accounts for only approximately 0.01% of the total number of ozone related impacts noted for NYC. However, despite the fact that it visually overstates the relative size of the NYC hospital asthma admissions, and the fact that still other ozone effects cannot be considered in these calculations due to a lack of data, this figure still makes very clear that the New York City asthma admissions counts considered in the Wolff table represent only a small fraction (far less than 1 percent) of the adverse effects of air pollution which will be avoided through the implementation of the new standard being proposed by the EPA.
The starting point of the analysis I used to estimate the "pyramid" of effects noted in the attached figure is the 265 New York City asthma admissions estimated to be avoided as a result of the implementation of the new standard, as per the top line of the Wolff chart (i.e., 385-120 = 265 admissions). First, as I noted above, there are also non-asthma respiratory admissions effects. Based upon the average ozone impacts derived from my ozone-admissions regression results for New York City and Buffalo, this indicates that the non-asthma respiratory admissions avoided (for causes such as pneumonia and bronchitis) are about 90 percent of the size of the asthma admissions, or 240/yr. Now, based on the fact that New York City hospital records indicate that 12.6% of pediatric asthma emergency department (ED) visits result in an asthma hospital admission (Barton et al, 1993), it is estimated that the ED visits associated with the 505 ozone-related respiratory admissions would amount to approximately 3,500 ozone-induced ED visits (i.e., 505 x 1/.126). Furthermore, using the ozone adverse health effect coefficients derived from the published literature by the Empire State Electric Energy Research Corporation (ESEERCO) in the New York State Environmental Externalities Cost Study (Oceana Publications, Inc., December, 1995), and ratioing the ozone effect coefficients provided in that report with that for asthma hospital admissions in New York City (used to get the 265 admissions), effects for other outcomes were derived, based on the original 265 NYC hospital admissions/day estimate. In this way, estimated annual effects to be avoided in New York City each year were also derived for:
-- acute (i.e., daily) mortality,
-- asthma attacks,
-- restricted activity days (i.e., the total number of person-days during which some normal activities were curtailed), and
-- acute respiratory symptom days (i.e., the total number of person-days during which additional respiratory symptoms would be experienced).
Some may quarrel with the specific coefficients chosen here to model the other effects, but the overall point remains that these other effects collectively represent large multiples of the hospital admissions benefits noted for New York City in the chart presented at the hearing. Moreover, the categories of effects considered in the attached figure are not exhaustive by any means, but they still serve to show that the table presented by Dr. Wolff greatly underestimates the number of adverse health events that can be avoided by the meeting the standard.
Note that the numbers in this figure have been corrected to avoid double counting of adverse health "events". For example, the number of hospital admissions has been subtracted from the total number emergency department visits, assuming that the patients would have first passed through the ED before being admitted.
Note also that this figure can be used to consider other cases in Dr. Wolff's chart as well, since all estimates have been scaled to the asthma admissions number. For example, for the difference between the existing and the proposed new standard cases, the numbers in this figure would all be divided by three (= (210-120)/(385-120) = 90/265). However, this calculation underestimates the benefits of the new standard, since it fails to account for the more rapid progress which will no doubt be able to be achieved in New York City under the new standard, when upwind counties clean up. The comparison to the "as is" case contained in the above figure is the more apt comparison.
Finally, while there are about 7 million persons in New York City, there are a total of some 122 million persons throughout the U.S. who now live in areas exceeding the proposed O3 standard, and will therefore also be benefited by that new standard. Thus, the New York City hospital admissions effects are best viewed as an indicator of a much broader spectrum of potentially avoidable adverse health effects being experienced by the public today as a result of air pollution exposures.
Mr. Wolff's table also ignores the point that these pollution-related hospital admissions differ from other admissions, in that they are a violation of the law in the U.S., as embodied in the Clean Air Act. It is important to remember that these admissions are unlike most other admissions in this important way, and, thus, warrant the regulation and societal expense needed to eliminate them.
It is not illegal to be admitted to the hospital, but it is illegal for pollution to cause people to go to the hospital. In other words, it is right to go to the hospital if you are sick, but it is wrong to cause someone else to have to go. This is how air pollution induced hospital admissions differ from most others, and why it is inappropriate to treat them as equivalent to, or as a percentage of, other admissions in legislative deliberations and policy making decisions.
Thus, since polluters are today causing many people to get sick enough to go to the hospital, and even to die prematurely, who would otherwise not have this happen, and since the Clean Air Act has appropriately declared this to be unacceptable and illegal, then we must act as a society to stop it, even if it is only a small percentage of all admissions or deaths.
A relevant analogy is to homicides in the U.S.: approximately 2 million persons die in the U.S. each year, but only about 1 percent of these deaths are due to homicides. We as a society do not ignore these homicides because they are expensive to prevent and represent only a small fraction of all deaths. Homicide is wrong and illegal, so we as a society expend a great deal of money and effort trying to prevent homicides, and in bringing violators to justice, even though homicides represent only a small fraction of all deaths. If one were to apply the logic that we should do nothing about air pollution because it represents only one of many causes of hospital admissions to this case, we would therefore not try to prevent or prosecute killers because it is too expensive, relative to the small percentage of deaths that homicides represent. No one would make this argument for homicides, and neither should we make it for hospital admissions and deaths caused by pollution. The hospital admissions and deaths induced by polluters must also be stopped, even if it is expensive, as the Clean Air Act has declared them to be illegal.
I believe that this rationale is one reason why the legislative history of the Clean Air Act, as affirmed by the Courts, indicates that these NAAQS must be set without consideration of attainment costs.
Returning to the subject of air pollution health effects, among the important adverse effects noted above as also occurring in the New York region as a result of air pollution exposure are asthma attacks. The airway inflammation induced by present day ozone and PM is especially a problem for children and adults with asthma, as it makes them more susceptible to having asthma attacks. For example, recent controlled human studies (e.g., Molfino et al., 1991) have indicated that prior exposure to ozone enhances the reactivity of asthmatics to aeroallergens, such as pollens, which can trigger asthma attacks. In addition, the increased inflammation and diminished immune system ozone effects in the lung can make the elderly more susceptible to pneumonia, a major cause of illness and death in this age group.
In February, the results of a study I conducted on the effects of air pollution on children at a summer "asthma" camp in Connecticut were published. This study of a group of about 55 moderate to severely asthmatic children shows that these children experience diminished lung function, increased asthma symptoms, and increased use of unscheduled asthma medications as ozone pollution levels rise. As shown in the figure below, the risk of a child having an asthma attack was found to be approximately 40 percent higher on the highest ozone days than on an average study day, with these adverse effects extending to below the old 120 ppb O3 air quality standard.
The O3 - morbidity associations indicated by epidemiologic studies are supported by a large body of data from controlled exposure studies that give consistent and/or supportive results, and that have demonstrated pathways by which ozone can damage the human body when it is breathed. Clinical studies have demonstrated decreases in lung function, increased frequencies of respiratory symptoms, heightened airway hyper-responsiveness, and cellular and biochemical evidence of lung inflammation in healthy exercising adults exposed to ozone concentrations at the present standard, and at exposures as low as 80 parts per billion for 6.6 hours (e.g., Follinsbee et al., 1988, and Devlin et al, 1991).
Similarly, animal exposures to combustion-related fine particles (PM2.5) have also been shown by recent controlled exposure studies to have significant adverse effects on the lung, including diminished respiratory defense mechanisms, opening the lung to illness from other causes. In addition, repeated exposures to acidic fine particulate matter, a portion of the fine PM2.5 which the EPA now aims to focus on in the newly proposed reductions in the PM standard, has been shown to affect clearance in the lung in a manner similar to that of tobacco smoking, suggesting that these fine particles may have analogous long-term exposure effects on the development of Chronic Obstructive Pulmonary Disease.
The epidemiologic evidence indicating an association between PM and increased mortality and morbidity has been well documented by numerous investigators in the published literature (e.g., see Schwartz, 1997). The fact that these effects have both been shown so consistently across outcomes and from place to place is supportive of the interpretation of these associations as causal, and not due to some unknown confounder. Furthermore, controlled human and animal exposures of combustion aerosols have shown significant adverse effects by these fine particles, which are the class of particles which EPA now appropriately aims to regulate.
While the exact causal mechanism (i.e., the "smoking gun") of the PM-mortality association is not yet known at this time, there are biologically plausible mechanisms that are now known which could account for the associations. For example, PM stresses on the lung (e.g., by inducing edema), places extra burden on the heart, which could induce fatal complications for persons with cardiac problems. Recent animal experiments by Godleski and coworkers (1996, 1997) at Harvard University confirm that exposures to elevated concentrations of ambient PM can result in cardiac related death in animals. Thus, the situation with PM and mortality is similar to many public health risks in the past, such as cholera in London a hundred years ago, or smoking over the past few decades: the epidemiology shows biologically plausible effects, but the exact mechanism by which the documented adverse impacts are effected is not yet known. This uncertainty about the exact mechanism of effect did not stop us from taking societal action against epidemiologically documented health threats, such as smoking, in the past, and should not be a deterrent to controlling the adverse consequences of particulate matter air pollution now.
Epidemiological evidence has also accumulated over recent years indicating a role by O3 in daily human mortality, a factor not fully considered by the U.S. EPA in the latest O3 Staff Paper or in the EPA's recent Regulatory Impact Assessment (RIA) for ozone. For example, Verhoeff, et al. (1996) used Poisson regression analysis to analyze associations between daily mortality and air pollution concentrations in Amsterdam, The Netherlands during 1986-1992, finding a daily mortality RR=1.10 per 100 ppb 1-hr daily maximum O3, even after controlling for weather and co-pollutants. Anderson et al. (1996) investigated whether outdoor air pollution levels in London, England influenced daily mortality during 1987-1992, finding a daily mortality RR=1.10 per 100 ppb 8-hr O3 (RR=1.08 per 100 ppb 1-hr O3), even after controlling for weather and co-pollutants. Samet et al. (1997) considered total daily mortality and environmental data for Philadelphia during 1973-1980, finding that, when pairs of pollutants were considered simultaneously, only the ozone coefficient consistently remained unchanged and statistically significant, with a total mortality RR of 1.02 for a 20 ppb increase in 24-hr daily average ozone. Cause of death-specific regressions indicated the largest ozone RR for respiratory deaths, consistent with biological plausibility. More recently, I have found that daily mortality also rises after high ozone days in the U.S. cities of New York City, Atlanta, Detroit, Chicago, St. Louis, Minneapolis, San Francisco, Los Angeles, and Houston, even after accounting for other factors such as season and weather, and at ozone levels below the current NAAQS standard (Thurston, 1997). I find that the overall population's risk of death rises by about 6 percent on ozone days having a 1-hour maximum of ozone that is 100 ppb above the average. The many new studies released since the EPA Criteria Document was prepared that document associations between ozone air pollution and human mortality are listed in the attached Table 1.
Once the weight of this new evidence of biologically plausible associations between acute ozone exposures and increased daily human mortality is considered, it is clearer than ever that important reductions in public health risks can be achieved by going from the old standard (equivalent to about a 90 ppb 8-hour standard) down to an 80 ppb 8-hour O3 standard, as was promulgated by the EPA.
In conclusion, I would like to restate the key messages contained in the letter that I and 26 other air pollution researchers and physicians sent to President Clinton earlier this year:
-- Please listen to the medical and scientific community on this issue.
-- Exposures to O3 and PM air pollution have been linked to medically significant adverse health effects.
-- The pre-July 18, 1997 NAAQS for these pollutants were not sufficiently protective of public health.
Thus, the recently promulgated air quality standards for both ozone and particulate matter should be retained.
Thank you for the opportunity to testify on this important issue.
Anderson, H. R., Ponce de Leon, A, Bland, J.M., Bower, J.S., and Strachen, D.P. (1996) Air pollution and daily mortality in London: 1987-92. British Medical Journal, 312:665-669.
Barton, D.J.; Teets-Grimm, K.; and Kattan, M. (1993) Emergency room visit patterns of inner city children for asthma. Am. Rev. of Resp. Dis. 147: A577.
Devlin, R.B.; McDonnell, W.F.; Mann, R.; Becker, S.; House, D.E.; Schreinemachers, D., and; Koren, H.S.. (1991) Exposure of humans to ambient levels of ozone for 6.6 hours causes cellular and biochemical changes in the lung. Am. J. Respir. Cell Mol. Biol. 4: 72-81.
Follinsbee, L.J.; McDonnell, W.F., and; Horstman, D.H. (1988) Pulmonary function and symptom responses after 6.6 hour exposure to 0.12 ppm ozone with moderate exercise. JAPCA 38:28-35.
Godleski, J.J.; Sioutas, C.; Katler, M.; Catalano, P.; and Koutrakis, P. (1996) Death from inhalation of concentrated ambient air particles in animal models of pulmonary disease. Proceedings of the Second Colloquium on Particulate Air Pollution and Human Health, May 1-3, 1996, Park City, Utah.
Godleski, J.J., Sioutas, C., Verrier, R.L.; Killingsworth, C.R.; Lovett, E.; Murthy, G.G.; Hatch, V.; Wolfson, J.M.; Ferguson, T., and Koutrakis, P. (1997) Inhalation exposure of canines to concentrated ambient air particles. Am. J. Resp. and Crit. Care Med., 155:(4) A246.
Molfino, N.A.; Wright, S.C.; Katz, I.; Tarlo, S.; Silverman, F.; McClean, P.A.; Szalai, J.P.; Raizenne, M.; Slutsky, A.S., and; Zamel, N. (1991) Effect of low concentrations of ozone on inhaled allergen responses in asthmatic subjects. Lancet. 338(8761): 199-203.
Samet,, J.M.; Zeger, S.L.; Kelsall, J.E., Xu, J.; and Kalkstein, L.S. (1997) Air pollution, weather, and mortality in Philadelphia 1973-1988. Analyses of the Effects of Weather and Multiple Air Pollutants. The Phase I.B Report of the Particle Epidemiology Evaluation Project. Health Effects Institute, Cambridge, MA, March, 1997.
Schwartz, J. (1997) Health effects of air pollution from traffic: ozone and particulate matter. Health at the Crossroads: Transport Policy and Urban Health, T. Fletcher and A.J. McMichael Eds., John Wiley and Sons Ltd., New York, NY.
Thurston, G.D. (1997) Ozone Air Pollution and Human Mortality. Paper 97-MP9.04. For presentation at the Air & Waste Management Association's 90th Annual Meeting & Exhibition, June 8-13, 1997, Toronto, Ontario, Canada
Verhoeff, A.P., Hoek, G.; Schwartz, J.; and Wijnen, J.H. (1996) Air pollution and daily mortality in Amsterdam. Epidemiology. 7:225-230.
Not Considered by the U.S. EPA O3 Criteria Document or Staff Paper
Anderson et al. 1996. Air Pollution and Daily Mortality in London: 1987-1992. BMJ 312:665-669.
Bates, D. 1995. Ozone: A Review of Recent Experimental, Clinical and Epidemiological Evidence, with Notes on Causation, Part 2. Can. Respir. J. 2(3): 161-171.
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Hoek et al. 1997. Effects of Ambient Particulate Matter and Ozone on Daily Mortality in Rotterdam, The Netherlands. Accepted to: Arch. Environ. Health.
Ito, K. and Thurston, G.D. 1996. Daily PM10/Mortality Associations: An Investigation of At-Risk Subpopulations. J. Expo. Analysis Environ. Epidemiol. 6(1): 79-225.
Kinney et al. 1995. A Sensitivity Analysis of Mortality/PM10 Associations in Los Angeles. Inhal. Toxicol. 7:59-69.
Loomis et al. 1996. Ozone Exposure and Daily Mortality in Mexico City: A Time-Series Analysis. Health Effects Institute Research Report Number 75, October 1996.
Moolgavkar et al. 1995. Air Pollution and Daily Mortality in Philadelphia. Epidemiology 6(5): 476-484.
Ostro. 1995. Fine Particulate Air Pollution and Mortality in Two Southern California Counties. Environ. Res. 70: 98-104.
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Ozkaynak et al. 1995. Associations Between Daily Mortality, Ozone and Particulate Air Pollution in Toronto, Canada. Paper Presented at the Colloquium on Particulate Air Pollution, Irvine, CA, January 24-25.
Saldiva et al. 1994. Association Between Air Pollution and Mortality Due to Respiratory Diseases in Children in Sao Paulo, Brazil: A Preliminary Report. Environ. Res. 65: 218-225.
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Samet et al. 1996. Air Pollution and Mortality in Philadelphia, 1974-1988. Report to the Health Effects Institute on Phase IB: Particle Epidemiology Evaluation Project, March 25, 1996 (Accepted for publication).
Samet et al. 1997. Particulate Air Pollution and Daily Mortality: Analysis of the Effects of Weather and Multiple Air Pollutants. The Phase I.B Report of the Particle Epidemiology Evaluation Project. Health Effects Institute, March 1997.
Sartor, F. et al. 1995. Temperature, Ambient Ozone Levels, and Mortality during Summer 1994, in Belgium. Environ. Res. 70: 105-113.
Sunyer et al. 1996. Air Pollution and Mortality in Barcelona. J. Epidemiol. Community Health50(Suppl. 1): S76-S80.
Thurston, G.D. 1997. Ozone Air Pollution and Human Mortality. Paper 97-MP9.04. Presented at the Air and Waste Management Association's 90th Annual Meeting and Exhibition, June 8-13, 1997, Toronto, Canada.
Touloumi et al. 1997. Short Term Effects of Ambient Oxidants Exposure on Mortality: A Combined Analysis Within the APHEA Project. Am. J. Epidemiol. (In press).
Verhoeff, A.P. et al. 1996. Air Pollution and Daily Mortality in Amsterdam. Epidemiology 7(3): 225- 230.
Wyzga, R.E. and F.W. Lipfert. 1995. Temperature-Pollution Interactions with Daily Mortality in Philadelphia. In: Particulate Matter: Health and Regulatory Issues: Proceedings of an International Specialty Conference Sponsored by the Air and Waste Management Association, April, Pittsburgh, PA, pp. 3-42.
Wyzga, R.E. and F.W. Lipfert 1996. Ozone and Daily Mortality: The Ramifications of Uncertainties and Interactions and Some Initial Regression Results. In: Vostal, J.J., Ed., Tropospheric Ozone: Critical Issues in the Regulatory Process: Proceedings of a Specialty Conference Sponsored by the Air and Waste Management Association, May, 1994, Orlando, FL, pp. 453-487.
Zmirou et al. 1996. Short Term Effects of Air Pollution on Mortality in the City of Lyon, France, 1985-1990. J. Epidemiol. Community Health 50(Suppl. 1):S30-S35.