Evidence from episodes in the Orient which afflicted American servicemen and their dependents also shows that air pollution appears to be an etiologic agent for a condition that was originally called "Yokohama asthma" (17). This is now referred to as "air pollution asthma." Some of the servicemen and their dependents were relieved of asthmatic attacks when they were moved out of affected areas in Japan and Okinawa. Conversely, some persons who were not evacuated quickly from the areas continued to manifest asthmatic symptoms. Accordingly, it appears that for some susceptible individuals this kind of asthmatic response may be truly a chronic effect of air pollution.

A further bit of evidence is based on recent data on illnesses of employee groups. These data indicate a high degree of relationship between respiratory illnesses lasting 8 days or more and levels of sulfates in selected cities in the United States (18). If this relationship were to be more completely documented, it might explain some of the striking rise in the prevalence of chronic respiratory diseases which has been observed recently.

The best indication of all of the chronic effects of air pollution is undoubtedly provided by the statistics on chronic bronchitis in Great Britain (19). There, the disease is the third leading cause of death and the leading cause of disability. In the United States there has been increasing acceptance of the view that a group of chronic respiratory diseases in this country, comprising emphysema, chronic bronchitis, bronchiectasis, and "other chronic interstitial pneumonia," is similar to the chronic bronchitis syndrome observed in Great Britain and that the apparent differences reported in the two countries may merely reflect differences in medical diagnostic criteria and terminology in patients with cases of differing severity and degree of infection.

We are aware that in the United States no evidence has been produced to demonstrate that air pollution is an etiologic agent for the emphysema syndrome. Nonetheless, there is an ever-mounting accumulation of evidence linking the two. Well known is the phenomenal rise of deaths from emphysema in the American population as a whole since 1950 (20). One may, with considerable certainty, ascribe part of the increase to the increasing acceptance of this classification as a cause of death, which in turn is due to the increasing discussion of chronic respiratory disease in the medical literature. Nevertheless, we have no reservation in stating that part, perhaps most, of the sevenfold increase in the frequency of this diagnosis as a cause of death is due to the greater prevalence of the disease.

One reason for assuming an air pollution factor as a cause of emphysema is the urban-rural comparison of mortality in the United States. Certainly, when the age-adjusted urban rates are double the rural rates, there would appear to be some factor which is directly related to residence in cities. Attention has been drawn previously to the fact that smoking differences among males, by residence, are relatively small and presumably do not account for the urbanrural ratio found for emphysema (21). The well-documented greater pollution of urban atmospheres as compared with rural points to a possible causal relationship.

It is recognized, of course, that there may also be an occupational exposure factor. The records of the Social Security Administration show that emphysema is the second leading cause of disability among male workers 50 years of age and older (22). It is clear that the evaluation of the role of air pollution in the increase in mortality from emphysema will have to take account of the occupational history of the decedent as well as his smoking habits.

Because of the increased interest in chronic respiratory diseases there has been a growing awareness of the need to inform people of the importance of certain symptoms. Accordingly, the National Tuberculosis Association has announced its intention of conducting a campaign during the spring of 1963 to alert people to the significance of "shortness of breath" and "chronic cough” (23). It is quite possible that people become so accustomed to these symptoms that they pay little attention or attach no importance to them. An increasing amount of data on the prevalence of emphysema and chronic bronchitis should be forthcoming as this educational campaign progresses.

In order to learn more about the long-term effects of air pollution, it was found necessary to conduct extensive field studies on selected populations. In 1959 the Division of Air Pollution of the Public Health Service, in cooperation with the Pennsylvania Department of Health, the Pennsylvania Electric Co., and others, undertook a study of two small communities in Pennsylvania, Seward and New Florence (24). The study had the elements of a natural laboratory setting inasmuch as the towns were virtually identical demographically. These

towns, inhabited by about 1,000 persons each, are approximately 4 miles apart, with a soft-coal-burning electric power plant between them. The prevailing wind pattern was such that the town of Seward was subject to much higher levels of air pollution than New Florence. Thus, for the period of the study, the level of dustfall in Seward was three times that of New Florence, the level of sulfation was seven times as high, and the level of SO2 was at least nine times as high. Nevertheless, the SO2 level in Seward was below that generally found in London (25).

The purpose of the study was to determine the long-term effects of low concentrations of air pollutants. An attempt was made to include the entire adult population of both sexes 30 years old and over. In addition to X-rays, the study used the long Medical Research Council questionnaire, with slight revisions, chiefly in terms of a much more detailed work-experience history. A battery of pulmonary function tests, including the body plethysmograph, was administered to the study group. The analysis, which was scheduled for completion in the summer of 1962, takes into account such variables as smoking and occupational and residence exposure of the townspeople.

In the preliminary report, one significant finding was that the average airway resistance (measured by the body plethysmograph) was higher in Seward than in New Florence even after differences in height and age were taken into account. A curious finding was that the male population of the polluted area was almost 1 inch shorter than that of New Florence. One would rightfully hesitate to attribute this difference in height to the difference in the environment. Yet this possibility should not be dismissed arbitrarily because of its apparent implausibility. One may only say that differences of this sort would have to be documented in many other communities before we could accept the hypothesis that the stature of the inhabitants was related to exposure to air pollutants rather than to ethnic or socioeconomic differences.

Since this study was completed, considerable effort has been made by the industry to reduce the pollution in the area. A restudy some time in the future might prove of considerable interest in evaluating the possible benefits of such reduction in pollutant levels as may have been achieved.

The long-term effects of the Donora disaster have also been studied in the United States (26). The resurvey of Donora 10 years after the disastrous smog of 1948 has shown that the persons who became ill during the outbreak have had a less favorable morbidity and mortality experience than the persons who were not affected in 1948. While it is true that those who became ill were probably less healthy to begin with than those who did not, it is quite likely that chronic effects due to unusually high levels of air pollution have been manifested in the affected group. Further, it is possible that repeated exposure to air pollution, even at very low levels, may have contributed to the long-term unfavorable experience.

The responsibility of air pollutants for the increasing frequency of lung cancer in the United States is at the moment a matter of some disagreement. Authoritative quantitative estimates of the role of air pollution as an etiologic agent do not exist, and only informed guesses can be made. Nevertheless, it is our thesis that, without decrying the importance of cigarette smoking as a factor, air pollution is also an important etiologic agent. This is not a novel idea. The World Health Organization report on lung cancer mentioned a number of possible etiologic agents and noted the prominence of air pollution in the list (27). Once again the sharp urban-rural differential in mortality rates for this disease is manifested. Also, lung cancer mortality rates appear to be related to the size of the urban area, the larger areas having the higher age-standardized mortality ratios.

The studies by Dean (28) and Eastcott (29) on migrants from Britain to South Africa and New Zealand suggest the role of air pollution as a causative factor in lung cancer. Unfortunately, there is no completed comparable study as yet in the United States. A study of British and Scandinavian migrants to the United States is underway, but we will have to wait several years for the results.

CONCLUSIONS

The great volume and variety of air pollutants in the United States offers unparalleled opportunities to study the chronic effects of low-level air pollution on health. In what other country is there amassed the concentration of automobiles found in Los Angeles with its resultant oxidant type of smog? The lethal concentration of pollutants in Donora in 1948 created a far different air pollution

problem than is found currently on the west coast. In the United States, air pollution arises from many and varied sources in every category, industrial, residential, residential, municipal, and automotive, and makes necessary a wider range of research activities than in many other countries.

In summary, we in the United States are devoting considerable time and effort to this important question: Does longtime exposure to low concentrations of air pollution result in adverse health effects? Our preliminary answer, based on both laboratory and epidemiologic studies, is yes. The evidence as yet is only qualitative; much more will have to be done before the necessary quantitative answers are found on which to base rational control standards. Hopefully, with the data the Public Health Service is able to collect and that amassed by researchers in Europe and throughout the world, this goal can be attained.

REFERENCES

(1) Stokinger, H. E., Wagner, W. D., and Dobrogorski, O. J.: Ozone toxicity studies. III. Chronic injury to lungs of animals following exposure at a low level. A.M.A. Arch. Indust. H. 16: 514-522, December 1957. (2) Ball, C. O. T., et al.: Survival of rats chronically exposed to sulfur dioxide. Physiologist 3: 15, August 1960.

(8) Amdur, M. O., Silverman, L., and Drinker, P.: Inhalation of sulfuric acid mist by human subjects. A.M.A. Arch. Indust. Hyg. & Occup. Med. 6: 305-313, October 1952.

(4) Amdur, M. O., Melvin, W. W., Jr., and Drinker, P.: Effects of inhalation of sulfur dioxide by man. Lancet 2: 758-759, October 10, 1953.

(5) Research in air pollution; conference report. Pub. Health Rep. 75: 11731189, December 1960.

(6) Hofreuter, D. H.: The automotive exhaust problem. A.M.A. Arch. Environ. H. 2: 559-563, May 1961.

(7) Hofreuter, D. H., Catcott, E. J., and Xintaras, C.: Carboxyhemoglobin in men exposed to carbon monoxide, A.M.A. Arch. Environ. H. 4: 81-85, January 1962. (8) Rose, A. H., Jr., Stahman, R. C., and Stevenson, H. J. R.: Exhaust contamination in passenger cars. Technical Report A61-2. Robert A. Taft Sanitary Engineering Center, Public Health Service, Cincinnati, Ohio, February 1961.

(9) U.S. Public Health Service: Six years of research in air pollution, July 1, 1955, to June 30, 1961. Washington, D.C., 1961 (a) p. 196, (b) pp. 204208, (c) p. 137. (10) Clayton, G. D., Cook, W. A., and Fredrick, W. G.: A study of the relationship of street level carbon monoxide concentrations to traffic accidents. Am. Indust. Hyg. A. J. 21: 46–54, February 1960.

(11) Wiseley, D. V., Kotin, P., Fowler, P. R., and Trivedi, J.: The combined effect of repeated viral infection on pulmonary tumor induction in C57 black mice. Proc. Am. A. Cancer Res. 3:278 (1961).

(12) Kotin, P.: Combination of stimuli in experimental lung cancer. Presented at the Fifth Air Pollution Medical Research Conference, Los Angeles, Calif., December 4-7, 1961.

(13) Greenburg, L., et al.: Report of an air pollution incident in New York City, November 1953. Pub. Health Rept. 77: 7-16. January 1962.

(14) Greenburg, L., Field, F. Reed, J. I., and Erhardt, C. L.: Air pollution and

morbidity in New York City. J.A.M.A. In press.

(15) Schoettlin, C. E., and Landau, E.: Air pollution and asthmatic attacks in

the Los Angeles area. Pub. Health Rep. 76: 545–548, June 1961.

(16) Zeidberg, L. D., Prindle, R. A., and Landau, E.: The Nashville air pollution study: I. Sulfur dioxide and bronchial asthma; a preliminary report. Am. Rev. Resp. Dis. 84: 489-503, October 1961.

(17) Phelps, H. W., Sobel, G. W., and Fisher, N. E.: Air pollution asthma among military personnel in Japan. J.A.M.A. 175: 990-993, March 18, 1961. (18) Dohan, F. C.: Air pollutants and incidence of respiratory disease. A.M.A. Arch. Environ. H. 3: 387-395, October 1961.

(19) Ogilvie, A. G., and Newell, D. J.: Chronic bronchitis in Newcastle-UponTyne. Livingstone, Ltd., Edinburgh and London, 1957, p. 2.

(20) U.S. National Office of Vital Statistics: Vital Statistics of the United States: 1950, 1959. U.S. Government Printing Office, Washington, D.C., 1952, 1961.

82-615-67- -5

(21) Prindle, R. A.: Some considerations in the interpretation of air pollution health effects data. J. Air Pollut. Control A. 9: 12-19 (1959).

(22) U.S. Social Security Administration: Disability applicants under the OldAge Survivors and Disability Insurance Program, 1960. Social Security Administration, Washington, D.C., January 1962, tables 10 and 11. (23) Williams, G.: Program possibilities in respiratory diseases. Presented at the 58th annual meeting of the National Tuberculosis Association, Miami Beach, Fla., May 20-23, 1962.

(24) Prindle, R. A., et al.: Comparison of pulmonary function and other parameters in two communities with widely different air pollution levels. Am. J. Pub. Health. In press.

(25) World Health Organization: Air pollution WHO Monograph Series No. 46, Geneva, 1961.

(26) Ciocco, A., and Thompson, D. J.: A follow-up of Donora ten years after: methodology and findings. Am. J. Pub. Health 51: 155-164, February 1961. (27) World Health Organization: Epidemiology of cancer of the lung; report of a study group. WHO Technical Report Series No. 192, Geneva, 1960, p. 5-6.

(28) Dean, G.: Lung cancer among white South Africans. Report on a further study. Brit. M.J. 16: 1599-1605, December 16, 1961.

(29) Eastcott, D. F.: The epidemiology of lung cancer in New Zealand. Lancet 1: 37-39, January 7, 1956.

BIBLIOGRAPHY

1. Heggestad, H. E., Air Pollution Control Ass'n. J., Dec. 1966, 16:691. See also Heggestad Testimony before Air Pollution Hearings, Senator Tydings, March 8, 1967.

2. Prindle, R. A. and Landau, E., Public Health Reports, Oct. 1962, 77:901. See also the 29 references in this bibliography-copy attached.

3. Personal communication, Dr. Leonard Girsh, Chairman, Committee on Air Pollution, American Academy of Allergy.

4. Girsh, L. S., Shubin, E., Dick, C., Schulener, F. A., J. Allergy, June, 1967, 39:347.

5. Hourly tabulations obtained from Air Quality Section Laboratory, Div., Air Pollution, Robert A. Taft Sanitary Engineering Center. Original data obtained at Washington, D.C. CAMP Station.

6. Air Quality Criteria for Sulfur Oxides, HEW, PHS, Bureau of Disease Prevention and Environmental Control, At Washington, D.C., March, 1967. See page 1 vi.

7. Miranda, J. M., Konopinski. V. J., Larsen, R. I., Arch. Environmental Health, July, 1967 15:16. (Calculates effects of carbon monoxide on persons with anemia and cardiac conditions.)

8. Six Years of Research in Air Pollution, July 1, 1955 to June 30, 1961. HEW, PHS, Washington, D.C. Note: contains 623 bibliographic citations.

9. Surgeon-General Luther Terry: Report to U.S. Congress in Compliance with Public Law 86-493, The Schenck Act, June 1962. Especially pages 44-45.

10. Experimental evidence of damage from air pollution appears in almost every issue of Archives of Environmental Health recently. For instance August, 1967, Vol. 15, Page 160, contains an article by R. E. Easton and S. D. Murphy describing how ozone exposure makes guinea pigs suspectible to histamine in amounts which do not bother non-exposed guinea pigs. This may be part of the reason allergic persons here have so much difficulty from our ozone containing summer smog.

11. Walborg, S. W., Wehrle, P. F., and Carroll, R. E., JAMA, March 20, 1967, 199:151.

Oxidant Air Pollution

and Athletic Performance

Walborg S. Wayne, MS, Pad F. Wehrle, MD,

and Robert E. Carroll, MD, MPH