smoking-to chronic bronchitis, emphysema, lung cancer, pneumonia, and chronic heart disease. As an individual physician I have a particular concern with the effects of air pollution on brain function. Among my patients are some who become dizzy and confused, some stagger. They are apt to become irritable and then drowsy as a result of coming into the center of town. Such people, once their trouble is diagnosed, not only avoid coming into Washington, they even shun the business districts of Bethesda and Silver Spring. I can't help wondering how many fatigued and irritable people have this problem and don't know it.

Sick persons are not the only ones affected by air pollution. Just last March the Journal of the American Medical Association carried a report showing that the performance of runners in races was diminished in proportion to the concentration of certain smog irritants in the air. Effects were noted at levels we have in Washington. I have a copy of that for your record. Thus we have a clear and present need for cleaner air. Our metropolitan population is growing—1,989,000 in 1960, 2,468,000 in 1965. More people means more trash to burn, more heat for homes and other buildings, more automobiles all throwing more waste products into our already overburdoned atmosphere. We will have to make significant improvement just to keep even with the present highly unsatisfactory situation.

H.R. 6981 is a broad statement outlining specific problems of importance to this area. The bill also would

set conservative limits to certain of our worst sources of pollution. For instance we don't want to become a dumping ground for the cheap sulfur laden heating oil rejected by other jurisdictions. We don't want New York City rejects. This bill, by requiring permits for new heavy duty fuel burning equipment, by specifying standards for smoke emissions and by setting a limit on sulfur content of fuels used, would protect us from this eventuality.

It has been a year now since the Medical Society's statement that closing of the Kenilworth dump and better controls of auto exhausts were urgently needed. The fact that these conditions are still unchanged indicates that present instruments of government are insufficient to break through the inertia of the customary ways we use our air for waste disposal. For this reason the District of Columbia Medical Society endorses H.R. 6981 and begs that its effectiveness not be diminished by substitution of generalities for the specific recommendations made.

Mr. MULTER. Thank you. Your bibliography and the article you referred to, will be made a part of the record.

(The statement follows:)


[From Public Health Reports, Vol. 77, No. 10, Oct. 1962] Reprinted by the U.S. Department of Health, Education, and Welfare, Public



Richard A. Prindle, M.D., M.P.H., and Emanuel Landau Both authors are with the Division of Air Polludtion, Public Health Service. Dr. Prindle is deputy chief of the division, and Mr. Landau is chief of the Biometrics Section, Field Studies Branch. The paper was given before the Verein Deutscher Ingenieure (DI) Kommission (Commission for Clean Air) June 20, 1962, at Düsseldorf, Germany. It is scheduled to be published in Staub in October 1962.

One of the best documented facts in the whole complex field of air pollution is that it can, in certain circumstances, result in acute illness and sudden death. Everyone knows about the disasters in Belgium's Meuse Valley, in Donora, Pa., and in London. Continuing research is uncovering other such episodes, long after they have occurred. In the United States we plan to continue our search for further evidence from the past. We hope to develop eventually a warning system that will predict the weather and other conditions which made possible such abnormally high concentrations of air pollutants and thereby mitigate, or even eliminate, future air pollution disasters.

Nevertheless, although more Americans than ever before are doing research today in air pollution, an increasing proportion of this effort is devoted to the long-term effects of exposure to low pollutant levels.

Our approaches to the determination of chronic effects of pollution have been of two major kinds : (a) the repeated laboratory exposure of human and animal subjects to specific pollutants or mixtures; and (b) the epidemiologic approach, using the community as a field laboratory.


In pursuing the first kind of research, the Division of Air Pollution, Public Health Service, has encouraged attempts to develop techniques capable of measuring minute changes in physiology to supplement new knowledge of pollutant concentrations at levels which cause marked pathological variations or death. Accordingly, we have recently undertaken studies of physiological and metabolic activities. Unfortunately, because of lack of knowledge about the physiological effects of pollutants, the choice of metabolic activity to be studied must often be based on trial and error. In some cases, a chance observation by other investigators, discovered in a search of the literature or through personal communication, offers a clue which seems worth pursuing. In one such instance, because of the similarity of certain toxiocological effects of ozone to those produced by ionizing radiation, our researchers are following, in rats exposed to ozone, the urinary excretion pattern of creatine and creatinine, known to be affected by radiation. Possible alterations in protein and purine metabolism after exposure to various pollutants are being sought by analyses of the urinary excretion of uric acid and amino acid nitrogen. Measurements of oxygen consumption, also in progress, may yield useful information during long-term inhalation exposures. These approaches are then coupled with studies of pulmonary function for comparison with human disease states.

The following examples illustrate some of the various approaches in the study of the long-term effects of air pollution on animals and man. In a study using classic laboratory techniques, repeated inhalation of ozone at a concentration of 1 ppm (2.6 mg./m.*), only slightly greater than that existing in some urban atmospheres, produced chronic bronchitis and bronchiolitis in small animals (1). The smaller bronchioles were partly occluded by hyperplastic or sloughed epithelium mixed with acute inflammatory exludate in guinea pigs which survived the experiments and were sacrified at the end of more than 400 days of exposure. The bronchiolar walls displayed fibrosis extending into the alveolar ducts and alveoli. A mild degree of emphysema was considered to be secondary to the bronchial occlusion. The changes were less marked in rats and hamsters and inconsistent in three mice examined. No evidence of intrapulmonary injury was detected in two dogs whose lungs were examined microscopically, but the trachea and major bronchi showed slight epithelial injury. Rats and guinea pigs which died during the course of exposure exibited massive pneumonia ; slight fibrosis was noted as early as the 25th day of exposure.

Groups of 9-month-old rats were exposed continuously up to 2 years to 1, 2, 4, 8, 16, and 32 ppm of sulfur dioxide to determine the long-term effects as manifested by survival, hematological response, and clinical symptoms (2).

Exposed rats exhibited changes in skin, fur, and conjunctiva and respiratory distress of increasing severity with increasing concentrations of the gas. A marked difference in the death rate of the group exposed to the 32 ppm concentration (84 mg./m.) was observed, as compared with controls, and groups exposed to lesser concentrations of sulfur dioxide also began to die before the control group. All control animals survived the first 9 months. By 18 months and until the end of the experiment, the survival rate of rats at all exposures to SO, except 32 ppm was similar but distinctly different from that of control animals. The earlier age at death of exposed animals was considered compatible with a process of accelerated aging, possibly resulting from the stress of such exposure.

It is becoming increasingly evident that oxides of sulfur, in concentrations attainable in community air, may affect the human respiratory tract. A research team at the Harvard School of Public Health has shown that the acute response in human beings resembles that in guinea pigs. Normal persons who inhaled either sulfuric acid mist or sulfur dioxide for brief periods exhibited markedly shallower, more rapid breathing (3,4). More recently another team of investigators at Harvard measured pulmonary function in healthy volunteers exposed to controlled levels of sulfur dioxide (5). During administration of the gas, all measurements of resistance showed an increase, greatest for pulmonary flow resistance (PFR) on quiet breathing, intermediate for PFR on panting and for airway resistance, and smallest for total respiratory resistance. Pulmonary flow resistance showed no change at 1 to 2 ppm of sulfur dioxide; it increased an average of 19 percent above control levels at 4 to 5 ppm and 49 percent at 8 to 19 ppm ; and when sulfur dioxide was combined with aerosol, the increase was 72 percent. However, investigators at St. Luke's Hospital in Cleveland observed no changes in resistance in normal subjects exposed briefly to sulfur dioxide in concentrations of 2.5 to 23 ppm, combined with particulates and aerosols, where emphysematous subjects exhibited a decrease in airway resistance (5).

Although the acute effects of exposure to high concentrations of carbon monoxide are well documented, the chronic effects from long-term subtosic doses are controversial. Recent findings suggest that, besides its known effects upon hemoglobin, carbon monoxide exposure may affect the eye and nervous system adversely. Since 1955, carbon monoxide levels in the Los Angeles atmosphere have been increasing by about 1 ppm (0.0012 mg./m.') per year. It is estimated that gasoline engine exhaust is the source of about 75 percent of the total carbon monoxide content of Los Angeles air, with significant contributions also from metallurgic and oil-refining operations.

Research workers (6, 7) have found an average blood carboxyhemoglobin of 3.8 percent, not markedly different from average levels in groups with lesser degrees of exposure, in subjects exposed to carbon monoxide in their working environment, from smoking, or while commuting to work in private automobiles. The carbon monoxide concentration in a garage and automobile inspection center where the exposed group worked ranged from 10 to 150 ppm, (0.06 mg./m.3); in the working environment of the control group, the ambient carbon monoxidelevel was less than 10 ppm (0.012 mg./m.”). Although 17 of 68 exposed subjects, compared with 3 of 25 controls, complained of headache, dizziness, or unusual fatigue at the end of the workday, no relationship could be found between carboxyhemoglobin levels and occurrence of those symptoms.

In a preliminary study performed by Public Health Service scientists at Cincinnati, Ohio (8), the levels of carbon monoride in the passenger compartment of stationery vehicles in heavy traffic were greatly increased, reaching a maximum of 370 ppm (0.44 mg./m.»). Investigators at the University of Michigan (9a, 10) sought to determine whether atmospheric carbon monoxide levels in urban areas might interfere with the driver's ability to operate his vehicle. Data collected from appropriate sites in Detroit for 1 year showed that median daily values of atmospheric carbon monoxide ranged between 0 and 20 ppm. During periods of high atmospheric stability and heavy traffic, concentrations reached 100 ppm at some sampling sites and persisted at this level for several hours. A later study on Los Angeles freeways showed significant build-up of carbon monoxide in drivers in rush-hour traffic to dangerous levels with respect to driving judgment. In homes several hundred feet from street sampling sites, concentrations approximated those in the street. Analysis of reports of more than 4,000 consecutive accidents involving almost 5,000 persons failed to reveal a higher accident rate associated with occupations in which high carbon monoxide exposure would be expected. In an attempt to relate the carbon monoxide content of the blood to air levels, a cigar smoker and a nonsmoker traveled in a police scout car for 8 hours for a distance of 130 miles. The carbon monoxide in the vehicular air, monitored continuously-reflecting outside traffic conditions and not influenced by any tobacco smoke in the car-averaged 17 ppm with a peak of 120 ppm when the engine was idling. The smoker's loaded carboxyhemoglobin rose from 3.4 to 3.9 percent, the nonsmoker's from 0.8 to 1.2 percent.

In a study of 237 persons involved in traffic accidents (including both drivers and pedestrians) and brought to the hospital for treatment, 50 percent of the drivers had less than 3 percent carboxyhemoglobin, 50 percent of the pedestrians bad less than 2 percent, and only 3 persons had levels of 10 percent or more; in

1 of these the carboxyhemoglobin was 31.5 percent. It was concluded by the investigators that carbon monoxide concentrations in the general atmosphere of Detroit do not impair driving ability (10), but further work is now underway to substantiate or amend these findings.

Studies undertaken on animals have demonstrated that guinea pigs exposed to automobile exhaust, at a concentration several times normal, for 1, 2, and 4 weeks, were especially susceptible to severe pulmonary disease (96). This came to light accidentally following an epidemic which produced pneumonia in the test animals. Significantly higher mortality occurred in the animals exposed to irradiated exhaust, comparable to heavy photochemical smog, than in animals exposed to nonirradiated exhaust or in control animals, which also experienced the epidemic but were exposed only to pure air. This finding parallels the results of another study in which animals exposed for only 2 hours to pure nitrogen dioxide at levels similar to those occasionally found in community atmospheres were much fore susceptible to infection by certain pneumonia organisms (personal communication, Richard Ehrlich, Armour Research Institute, Chicago). More serious illnesses and more deaths occurred in this group than in the control animals, which were exposed to the same organisms but otherwise breathed only pure air.

Irradiated exhaust, that is, automobile exhaust which has been diluted with air and then exposed either to sunlight or to artificial light with ultraviolet components, is chemically different from exhaust which has not been irradiated. It has been shown that this irradiated gas is chemically similar to the so-called "photochemical smog” so notorious on our west coast. It also causes the same types of damage to vegetation as the "smog” found in California. Constituents include ozone, "oxidants" (oxygen-containing compounds of high reactivity), other hydrocarbons, and oxides of nitrogen.

These ingredients appear to result from complex interactions due to photochemical action on the unburned hydrocarbons and oxides of nitrogen found in exhaust gases. Merely mixing ozone with hydrocarbons, such as gasoline vapors, can simulate this process to some degree. Because these ingredients appear to be more biologically potent, causing damage to plants and eye irritation in people, our recent studies have been focused on them to a large extent.

Physiological experimentation in which measures were made of respiratory function of guinea pigs, including pulmonary resistance, respiratory rate, and minute volume, has shown that the greatest changes occurred in those animals exposed to irradiated exhaust. In general, these changes have occurred when the animals have been exposed to concentrations two or more times the usual ambient levels. However, some physiological changes have occurred in animals at “community" levels, and certain specific pollutants have been observed to produce effects at or near these concentrations. This would appear to indicate that the observed maximum levels present in communities at this time are borderline with respect to causing immediate effects such as changes in pulmonary function and may be highly significant in their long-term effects.

Last year workers at the University of Southern California were able to produce true squamous cancers in the lungs of mice, similar in type to those found in human beings, by exposing the animals first to infection, then to air containing ozonized gasoline. In this experiment, one group of animals was exposed to a virus type of influenza and another was unexposed. Each of these groups was divided after recovery into two further groups, one exposed to purified air and the other to ozonized gasoline. In the animals receiving the infection alone, approximately 8 percent showed squamous changes in the bronchi consistent with healing processes after infection and occasionally demonstrated metaplastic changes. In the animals exposed to ozonized gasoline alone, there were no sig. nificant findings. In the uninfected animals exposed to pure air, the findings were negative. A striking 30 percent of the animals which had been infected and subsequently exposed to ozonized gasoline demonstrated the presence of squamous carcinoma. Interestingly enough, the male-female ratio was approximately :3 to 1, similar, in fact, to that found in humans and obviously not associated with smoking habits or occupation (11, 12).


Considerable epidemiologic research has also been undertaken with the community used as a laboratory. While increasing effort has been devoted to the chronic effects of normal low levels of community pollutants, the Public Health Service has continued to support research into the extent of previously unre ported air pollution disasters.

The literature of air pollution disasters was enriched recently by the publica-tion of a paper reporting excess mortality, presumably due to elevated levels of pollutants resulting from an extended temperature inversion in New York City as long ago as November 1953. This excess mortality in the largest metropolis in the United States was determined retrospectively by an examination of death records (13). It parallels in that respect the experience of the 1952 disaster in London, the largest metropolitan area in Great Britain. However, while the London episode was studied almost concurrently, the study in the United States was made more than 5 years after the event.

In the 1953 incident, 220 excess deaths were attributed to cardiac and respiratory diseases, again paralleling the London episodes. These deaths must have been accompanied by increased morbidity. Unfortunately, the precise magnitude of this morbidity is uncertain, since it is extremely difficult to obtain reliable morbidity data for past years.

There are some possible source of illness data, such as hospital admissions, physician visits, group medical practice usage, health surveys, and the like. It is obvious that it is no easy matter to collect such data after the lapse of nearly a decade. The less current the records, the greater is the danger that they may no longer exist. Therefore, it was gratifying to find that an examination of the records on emergency room visits to the largest New York City hospitals for November 15–24, 1953, undertaken recently by the same group which reported on mortality in New York City, revealed about twice the expected number of visits by patients with respiratory and cardiac conditions (14).

The line of demarcation between an acute air pollution episode and the chronic long-term effects of low levels of air pollution can become quite blurred. This difficulty is exemplified when we look for causes of the large number of asthmatic responses to sublethal levels of pollutants which have been observed in New Orleans, Pasadena, and Nashville.

In New Orleans, it was demonstrated that there had been sharp periodic increases in emergency clinic visits to Charity Hospital by nonwhite asthmatics. This has occurred often enough so that adequate documentation is now possible (90). The usual number of visits to Charity Hospital by asthmatics was 25 per day for the period 1953 to 1961.

Frequently, however, outbreaks of asthmatic attacks have seriously strained the facilities of the hospital. In August 1958, for example, an outbreak of asthma involved 100 people, with 3 deaths. There have been instances of daily admissions of 150 and even 200 Negro adult patients. Asthma outbreaks have been accurately predicted in advance on at least two occasions; the predictions were made on the basis of meteorological data which had shown that the outbreaks were associated with particular wind movements.

We are now able to report that these asthma outbreaks are thought to be related to particles of a silicon-containing compound emitted into the atmosphere as a result of poor combustion of garbage and refuse in the New Orleans city dumps. This could very possibly be an instance of an air pollutant acting as an allergen and creating an allergic response in certain susceptible individuals. Obviously, testing of skin and pulmonary sensitivity and further research are indicated to verify or disprove this hypothesis.

How are we to consider the response of asthmatics to insults to the respiratory tract in such diverse air pollution areas as Los Angeles and Nashville? Are these responses the product of acute or chronic insults? In the Los Angeles area a study was conducted from September 3 to December 9, 1946, of 137 bronchial asthma patients of 5 practicing physicians (15). The study revealed that the average number of patients afflicted on days when oxidant values were above a level that caused eye irritation was significantly greater than the average number on days when oxidant values were below this level. Similarly, the number of persons who had att cks on days when plants showed damage from air pollutants, a biological indicator, was significantly greater than the number on other days.

In Nashville, also, it was found that attack rates were significantly different when comparison was made of days with the highest and the lowest sulfur dioxide levels (16). The statistical significance was even greater when the daily data on asthma attacks were lagged 1 day to take account of possible delayed rections to sulfur dioxide. A possibly corroborative finding was that the pattern of attacks for adult asthmatics reflected differences in air pollution levels. in different sections of the city. Thus, the attack rate was three times as high in an area of high pollution as it was in a low-pollution area. It is particularly noteworthy that the sulfur dioxide levels in Nashville are not very high even at their worst.

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