can trigger asthmatic attacks. And the Donora catastrophe provided a striking example of local aggravation of asthmatics (with a number of deaths reported), caused by fumes emanating from steel and other manufacturing plants, under conditions favorable for their accumulation."

In New Orleans, epidemic outbreaks of "asthmatic attacks" have been associated with certain local wind conditions.", "5 At first, spontaneous underground combustion in abandoned city disposal dumps had seemed to be incriminated. However, a recent study suggests that there is more than one point source of air pollution causing an asthmatic-type disease in New Orleans, and there are probably multiple sources.

46

There have been other instances-one in Pasadena," another in Nashville 4. in which air pollutants have been shown, in epidemiological studies, to precipitate attacks of bronchial asthma in known cohorts of asthmatics. The mechanism by which airborne materials precipitate attacks of asthma is not yet known, but the significant fact is that asthma, or an asthmalike disease, can be induced by man-made community air pollutants.

For bronchial asthma due to natural airborne allergenic agents (pollen and spores), see below: Effects of aeroallergens.

"YOKOHAMA ASTHMA"

As long ago as 1946, many cases of a respiratory disorder commonly referred to as "Yokohama asthma" appeared among American troops stationed in the highly industrialized Yokohama area of Japan, and soon spread to dependents who were living in that area. Later the same condition was noted among our military personnel in the Tokyo area. 40, 50, 51, 52 Earlier studies indicated that the disease correlated best with air contaminants and smog. Severe attacks have been observed to be more frequent in the winter months, when smoke and fumes from the heavily industrialized Kanto Plain (Tokyo-Yokohama area) attain ground level concentrations so intense that they represent a hazard to low-flying small aircraft. Removal of affected personnel from the area, especially if early, usually results in recovery. However, permanent damage has resulted in patients who were not promptly removed from the area.

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53, 54

"Tokyo-Yokohama asthma" is still under detailed study, but several important conclusions have already been reached. Studies conducted in 1960 in a pulmonary function laboratory revealed that the patients were much more severely affected than was the original clinical impression. In these studies, the patients' incapacity due to shortness of breath became apparent, and their failure to respond to bronchodilators was documented. Starting in 1961, 182 men were studied on three occasions over an 18-month period, and 8 revealed a typical history of "T-Y asthma." Follow-up studies in 1962 on 244 cases who were returned to the United States revealed that 64 percent still had abnormal inflow patterns, and in some, significant emphysema was present. The evidence seems to be increasing that emphysema may occur in susceptible individuals if they stay too long in the Kanto Plain area. A total of 620 patients have been diagnosed as having “T-Y asthma" from 1960 to 1962. All have a negative history of clinical respiratory disease prior to coming to Japan. All but 18 were moderate-to-heavy cigarette smokers.

44 Lewis, R., et al: Air Pollution and New Orleans asthma; a preliminary report. Pub. Health Rep. 77 :947-954 (Nov.) 1962.

45 Weill, H., et al: Preliminary report: clinical and allergic study of New Orleans Asthma. Presented at Sixth Air Pollution Medical Research Conference, San Francisco, Calif. Jan. 28-29, 1963.

48 Weill, H., et al: Further observations on New Orleans asthma. Arch. Environ. Health 10:148-151 (Feb.) 1965.

47 Schoettlin, C. E.. and Landau, E.: Air Pollution and asthmatic attacks in the Los Angeles area. Pub. Health Rep. 76:545-548 (June) 1961.

48 Zeidberg. L. D., et al: The Nashville air pollution study: V. Mortality from diseases of the respiratory system in relation to air pollution. Presented at 91st Annual Meeting of the APHA meeting, Kansas City, Nov. 1963.

49 Huber, T. E., et al: New environmental respiratory disease (Yokohama asthma). A.M.A. Arch. Indust. Hyg. & Occupat. Med. 10: 399-408 (Nov.) 1956.

Phelps, H. W.. et al: Air pollution asthma among military personnel in Japan. J. A.M.A. 175:990-993 (March 18) 1961.

51 Phelps, H. W.: Air pollution asthmatic bronchitis among United States personnel in Japan. Japan Heart J. 27:180–186 (April) 1961.

52 Beard, R. R., et al: Observations on Tokyo-Yokohama asthma and air pollution in Japan. Pub. Health Rep. 79:5, 439-444 (May) 1964.

3 Motley, H. L., and Phelps, H. W.: Pulmonary function impairment produced by atmospheric pollution. Dis. Chest 45:154-162 (Feb.) 1964.

54 Phelps, H. W.: Follow-up studies in Tokyo-Yokohama respiratory disease. Environ. Health 10: 143–146 (Feb.) 1965.

Arch.

THE COMMON COLD AND OTHER RESPIRATORY DISEASES

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Common colds and other infections of the upper respiratory tract occur more frequently in areas with high pollution levels. This was indicated in a study in a small Maryland city as long ago as 1950, and has since been confirmed by studies in Great Britain, Japan," 1,50,59 and the Soviet Union. In connection with a study of air pollution in the Detroit-Windsor area by a U.S.-Canada International Joint Commission," responses to a Cornell Medical Index questionnaire indicated that people living in the two high-pollution areas in Detroit reported themselves afflicted with more symptoms of illness than people living in the two low-pollution areas. This was particularly true, and apparently statistically significant, in regard to prevalence of coughing and colds.

An interim analysis of the diaries of homogeneous groups of student nurses in a relatively polluted area, Los Angeles, and a relatively unpolluted one, Santa Barbara, California, showed that the mean frequencies of all respiratory and other symptoms in the former area were equal to or greater than the corresponding symptom frequencies in the latter. The probability of any one nurse reporting a cough on any one day of the period analyzed was 20 percent in Los Angeles and 6 percent in Santa Barbara. In the same study, a time-associated relationship between daily oxidant levels and the mean daily frequency of eye discomfort in the Los Angeles group was reported.

ALL RESPIRATORY DISEASES

That there is a definite link between air pollution and respiratory disease was further indicated when results were reported in November 1963 from a survey of deaths in and around Nashville, Tennessee, for a 12-year period ending in 1960. This would appear to provide evidence that normal city levels of air pollution correlate well with death rates from diseases of the respiratory system. Altogether, data on 38,207 deaths were studied and, even when full allowance was made for differences in age, color, and socio-economic status, the sections of the city subjected to heaviest air pollution were areas of maximum deaths from all respiratory diseases and from such specific respiratory diseases as tuberculosis, influenza, and pneumonia. Although smoking was not included in this study, it is not considered to be of significance for those specific diseases of the respiratory system. What is significant is that mortality ratios were correlated with air pollution levels in the ambient air.

Similar findings were made in a study conducted in the area of Buffalo, New York. A recent report on this study indicated that high levels of air pollution, as measured by suspended particulates, were correlated with elevated mortality from all causes and with mortality due to chronic respiratory diseases. Among white males 50 to 69 years old, the death rate for all causes was 50 percent higher in the area of heaviest particulate pollution than in the area of lowest particulate pollution. A similar mortality pattern was found among women, which supports the hypothesis that a non-occupational environmental factor was responsible. An even more striking relationship was found between particulate levels and mortality from chronic respiratory diseases. In this respect, the

Heimann, H. et al: Health and air pollution. A study on a limited budget. A. M. A. Arch. Indust. Hyg. & Occupat. Med. 3:399–407 (April) 1951.

Holland. W. W., et al: Influence of the weather on respiration and heart disease. Lancet 2:338-341 (Aug. 2) 1961.

Abe, S.: Air pollution in Sapporo. Science and Labor 13:98-108, 1958. (Quoted by Toyama, T. in Air Pollution and its Health Effects in Japan. Arch. Environ. Health

8:161-181 (Jan.) 1964.

Saruta. N.: Effects of air pollution on the health of people of northern Kyushue, Japan. (First Report) Kyushu J. Med. Sci. 12:167-176, 1961. (Quoted by Toyama, T. in Air Pollution and its Health Effects in Japan. Arch. Environ. Health 8:161-181 (Jan.) 1964.)

Suzuki, T.: Air Pollution and its health effects in Amagasaki City. Report of Air Pollution Control Committee of Amagasaki, 1962. (Quoted by Toyama, T. in Air Pollution and its Health Effects in Japan. Arch. Environ. Health 8:161-181 (Jan.) 1964.)

Yansheva, N. Ya.: The effect of air pollution from power and chemical plants on health. Gigiena i Sanitariya 8:15, 1957. (Transl. by Levine, B. S. in U.S.S.R. Literature on Air Pollution and Related Occupational Diseases, Vol. 1, 1960, U.S. Dept. of Commerce, Office of Technical Services, Wash. 25, D.C.)

1 Air Pollution in the Detroit-Windsor Area. Report of the Technical Advisory Board to the International Joint Commission United States and Canada. Washington. Ottawa. 1959.

Hammer. D. I., et al: Los Angeles air pollution and respiratory symptoms. Arch. Environ. Health 10: 475-480 (Mar.) 1965.

Zeidberg, L. D., et al: The Nashville air pollution study: I. Sulfur Dioxide and bronchial asthma-a preliminary report. Am. Rev. Resp. Dis. 84:489-503 (Oct.) 1961.

death rate in the area of highest pollution was nearly twice that in the lowest pollution area. This statistical relationship showed up even when allowance was made for age and socio-economic status of the deceased persons.

(1) Bronchial asthma

EFFECTS OF AEROALLERGENS

It is widely recognized that a number of airborne substances cause allergic responses in sensitized individuals. These substances, such a pollen, spores, rusts, and smuts, and known as aeroallergens, present a major public health problem."

Bronchial asthma and allergic rhinitis, and more commonly known as hay fever, are typical human responses to exposure to aeroallergens. Pathological symptoms may be severe, and the primary complications of bronchial asthma are numerous, in extreme cases sometimes even leading to death."

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Aeroallergens are primary causative agents in inducing bronchial asthma. Estimates of the national incidence of this disease vary widely, but a recent study of the epidemiology of asthma and hay fever in a total community. Tecumseh. Michigan, indicates that 5 percent of the inhabitants had a medical history of asthma." This and other studies indicate that many millions of persons in this country are or have been affected by this condition. For many of these it is a severe handicap.

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Allergenic pollens come from trees, grasses, and weeds. Ragweed presents the most serious problem in the pollen allergy in the United States. Although found primarily in the central portion of the continent, infestation is developing in other areas. Other aeroallergens, such as spores from the mold Alternaria, are found in every State.

(2) Allergic rhinitis

Allergic rhinitis, or hay fever, is even more prevalent than bronchial asthma. Studies of university student populations since 1950 show an incidence of ragweed pollinosis as follows: in Indiana, 18.7 percent; in the State of Washington. 16.7 percent; and in Michigan, 19.2 percent." The National Health Survey has estimated that about thirteen million persons throughout the country are being adversely affected by hay fever and/or asthma. Hay fever, unlike asthma, is rare in children under 10 years of age. The prevalence figure from the general population must therefore of necessity be smaller than the prevalence figure for selected young adult populations. The study of students mentioned above also shows that many foreign students develop ragweed pollinosis for the first time in their lives after a year or two of exposure to this potent aeroallergen. This fact has obvious public health significance when we consider that the ragweed plant appears to be migrating on this continent.

It might be thought that simple hay fever presents less of a hazard to health. Recent analyses indicate, however, that 5 to 10 percent of persons subject to allergic rhinitis will develop asthma if the disease runs unchecked." There is therefore ample reason to be seriously concerned about the effects on our national health and well-being of aeroallergens in general and of ragweed pollinosis in particular. There is little doubt that our agricultural, highway construction, and suburban land developments, which leave so much bare soil on which ragweed thrives, are leading to a wider distribution of ragweed pollen and of the asthma which it causes." There are a number of possibilities for controlling ragweed pollen and other aeroallergens. These control measures, however, are

4 Hewson, E. W.: Atmospheric pollution in relation to microclimatology and micrometeorology: Some problems. In: Proceedings of the Toronto Meteorological Conference 1953. Royal Meteorological Society, London, 1954, pp. 240-252. 65 Vaughn, W. T., and Black, J. H.: Practice of Allergy, C. V. Mosby Co., St. Louis, 1954. Sheldon, J. M., et al: A Manual of Clinical Allergy. W. B. Saunders Co., Philadelphia.

1953.

67 Rackemann, F. M.: Deaths from asthma. J. Allergy 15:249-258 (July) 1944. Broder, I. et al: The epidemiology of asthma and hay fever in a total community. Tecumseh, Michigan. I. Description of study and general findings. J. Allergy 33:513–523 (Nov.-Dec.) 1962.

69 Maternowski, C. J., and Mathews, K. P.: The prevalence of ragweed pollinosis in foreign and native students at a midwestern university and its implications concerning methods for determining the inheritance of atopy. J. Allergy 33: 130-140 (MarchApril) 1962.

70 Broder, I., et al: The epidemiology of asthma and hay fever in a total community. Tecumseh, Mich. II. The relationship between asthma and hay fever. J. Allergy 33: 524-531 (Nov.-Dec.) 1962.

Wagner, W. R., Jr., and Beals. R. F.: Perennial ragweeds (Ambrosia) in Michigan with the description of a new intermediate taxon. Rhodora 60: 177-204, 1958.

administratively very complex; for example, they involve a change in agricultural practice wherein the farmers would spray the fields after the crop has been harvested. Such control methods should be evaluated and the effectiveones adopted for use until such time as adequate immunochemical means of desensitization become available.

EFFECTS ON LABORATORY ANIMALS (EXCLUDING CANCER)

Laboratory research has provided important information concerning the effects of specific pollutants on animals. Mice, rabbits, guinea pigs, rats, and monkeys have been utilized to demonstrate the toxic properties of such air pollutants as sulfur dioxide, sulfuric acid, hydrogen sulfide, ozone, nitrogen dioxide, and some dusts.

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In one recent experiment, the respiratory response of guinea pigs inhaling low concentrations of acrolein was characterized by an increase in total respiratory flow resistance, accompanied by decreased respiratory rates and increased tidal volumes. The changes in respiratory function were reversible when the animals were returned to clean air. In another study of considerable relevance, conducted by Dr. Mary Amdur, guinea pigs which had relatively higher initial flow resistance values, corresponding roughly to humans with respiratory disease, were exposed to an irritant aerosol or to an irritant gas. These animals showed a greater resistance than did control animals, particularly at the lower concentrations. at which the latter group had shown only a slight change. Animals which were exposed to both an inert aerosol and an irritant gas showed an enhancement of the effect over that shown by the irritant gas alone.

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Other experiments with animals have shown that certain irritants common in polluted air can slow down, and even stop, ciliary activity in the air passages.” This impairment results in less effective cleansing of the mucus carpet of those air passages, and hence greater susceptibility to respiratory infection. A twohour exposure of mice to as little as 3.5 parts per million of nitrogen dioxide significantly increased their susceptibility to respiratory infection initiated by challenge with an aerosol of Klebsiella pneumoniae. Infected animals exposed to 25 ppm of nitrogen dioxide for two hours showed an increased mortality rate and decreased survival time."5

Thus, information which has been obtained by artificial exposure of animals is providing some indexes of both human and animal effects to be expected from natural exposure.”

On the other hand, knowledge of the toxic potentialities of some air pollutants, such as peroxyacyl nitrates, ketenes, free radicals or radical formers, and air ions, is grossly incomplete and unsatisfactory. Similarly, only a beginning has been made in the more important area of toxicological interactions in which the presence of one air pollutant may, at one extreme, completely abolish the effects of another or, at the other extreme, enhance the effects out of all proportion to the toxicity of either alone.

RADIOACTIVE MATERIALS

In this brief survey of the part played by radioactive materials in the overall contamination of the atmosphere, no attempt will be made to cover the possible wartime use of nuclear devices and resultant civil defense requirements. Our concern here is rather with the increasing peacetime uses of all forms of ionizing radiation, and specifically with radioactive materials which are airborne. (1) Sources

The sources of radioactive materials which may be present in our environment include: natural sources (radium and thorium in earth and cosmic rays): nuclear weapons testing (fallout); nuclear power production (waste disposal); nuclear fuel processing (waste disposal); and radioisotope use and disposal (industry and research)."

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Murphy, S. D.. et al: Respiratory response of guinea pigs during acrolein inhalation and its modification by drugs. J. Pharmacol. and Exp. Therap. 141: 79-83 (July) 1963. Amdur. M. O.: The effect of high flow-resistance on the response of guinea pigs to irritants. 25:564-568 (Nov.-Dec.) 1964.

Falk, H. L., and Kotin. P.: Chemical and biological considerations of atmospheric carcinogenic agents. J. APCA 7:12-14 (May) 1957.

Purvis, M. R., and Ehrlich. R.: Effect of atmospheric pollutants on susceptibility to respiratory infection. II. Effect of nitrogen dioxide. J. Infect. Dis. 11: 72-76. 1963.

Catcott. E. J. Effects of air pollution on animals. In Air Pollution, SHO Monograph Series no. 46. Geneva. 1961 pn. 221-231.

Terrill. J. G. Jr.: Radiological Health Activities Related to Weapons and Missile Testing. A statement prepared for the Senate Committee on Public Works, Subcommittee on Air and Water, June 30, 1964.

The greatest source is from natural deposits of radioactive materials. The predominant component of radioactivity in air is the noble gas, radon-222, which is formed in the earth from decay of radium-226. A portion escapes to the atmosphere, where further decay results in a series of radioactive atoms which become a part of the normal atmospheric aerosol by attachment to other existing particles.

Great quantities of radioactive debris have been injected into the atmosphere by nuclear testing. Debris injected into the upper atmosphere remains for several months to years during which most of the radionuclides decay to insignificant concentrations, so that only the longer-lived nuclides, such as strontium-90 and sesium-137, enter the lower atmosphere. The debris injected into the lower atmosphere remains airborne long enough for the freshly formed fission products to be transported around the earth, contributing enroute to ground-level contamination. Fortunately, great dilution, washout in precipitation, and decay occur prior to population exposures, so that the probability of inhaling significant amounts has been slight. With the limited test ban treaty, this source has declined significantly. Radiation exposures from such radioactive fallout occur primarily from whole-body exposure from gamma-emitting nuclides deposited on the surface, and from radionuclides deposited in tissues through ingestion.

The processing, manufacturing, and use of nuclear fuels and radioisotopes, and the disposal of associated wastes, have incorporated engineering and procedural controls which have maintained these minimal sources. Several incidents at nuclear installations which have aroused concern appear to have been of the nature of industrial "accidents," and precautions have been taken to minimize the likelihood of their recurrence.

Inhalation has been recognized as a major, if not the most important, route of entry to the body of potentially hazardous materials for occupational exposures. Nonoccupational exposures may occur from external gamma radiation and ingestion, as mentioned above, as well as through inhalation.

(2) Effects

A great deal is known about the effects on human beings of large doses of radiation-such as would be encountered in a nuclear war-but comparatively little about the effects of small doses of radiation, for example, natural background radiation and fallout from nuclear tests.78 79

The biological effects of radiation are either somatic, that is, ocurring during the lifetime of the exposed organism, or genetic, the effects on germ cells. These effects depend on the type and quality of radiation and the quantity absorbed in tissues. Because of the difficulty of detecting effects of very low exposures, it is not known whether or not there is a "threshold" for any of the radiation effects: i.e., a dose below which there is no effect. There is some evidence from studies of experimental animals that suggests there is no "threshold" for genetic effect. If this is true for all effects, any amount of radiation causes damage, and the damage increases with increase in total cumulated exposure.

Somatic Effects.-The time of appearance of somatic effects is dependent on the magnitude of exposure. Following very large acute exposures, effects may appear within a few hours or less. Such early effects include central nervous system disorders, nausea, decrease in formed blood elements, intestinal disorders, and radiation burns. Longterm effects which may appear after many years from acute and chronic exposures, both large and small, include leukemia, bone and other cancers, cataracts, and overall shortening of life span.

Genetic Effects.-Genetic effects result from radiation damage to germ cell chromosomes, i.e.. cell constituents responsible for transmitting characteristics from generation to generation. These effects can appear in subsequent generations. The effect may produce undetectable defects in the offspring; some may appear unspecifically as health impairments which may be minor or which may result in premature death or permanent serious illness. Studies with experimental mammals indicate that genetic damage increases with increase in exposure rate as well as total exposure.

Exposure in the U.S. population to fallout is slight compared to natural and other manmade health hazards. However, since the application of radiationproducing machines and materials, such as nuclear reactors, radioactive nuclides, and X-rays, will continue to increase in the future, radiation exposure will also

United Nations, 1962. Report of the United Nations Scientific Committee on the Effects of Atomic Radiation. New York.

National Academy of Sciences--National Research Council. The biological Effects of Atomic Radiation. Washington. 1956 and 1960 Reports.