ences encountered in occupational health and in the investigation of the effects of radiation on health. In occupational health, the development of values defining conditions of exposure which are safe and healthful for a wide variety of hazardous chemical and physical agents has been a slow and laborious process. Here, in many instances, we were dealing with a single substance, with an exposure relatively easily characterized qualitatively and quantitatively, with an exposed population which usually could be thoroughly evaluated-and frequently with instances of overt occupational disease clearly identifiied with higher exposure conditions. The extrapolation downward to safe levels for short-term exposure has been relatively easy. But, among the some 300 threshold limit values now accepted and applied in industry there are probably less than 10 with adequate documentation to justify their acceptance, if the true and rigid criterion were that of a safe and healthful environment over a full working lifetime. In spite of this deficiency, these threshold limit values serve a very useful purpose, and in the judgment of the majority of experienced observers, provide a good approximation to the longer term criterion. Among the various hazardous chemical and physical agents affecting health, ionizing radiation has certainly had the most extensive and best organized investigative program. In the search, as the target levels of radiation have been progressively reduced and as the end points of effect have been extended to include carcinogenesis, shortening of life span, and genetic changes, the technological complexities and the cost of meaningful studies have gone up in geometric proportion. We have progressed in our scientific jargon from such terms as "a million fruitflies" to "mega-mouse" and "mega-buck"-the latter meaning dollars rather than male deer. When, however, we attempt to study these smaller effects in man, a point is reached at which the identification of the component specific to radiation, in relation to all of the other variables to which our population is subject, becomes an almost impossible task. We have not reached this "diminishing return" effect in the study of air pollution but, as in the case of radiation, it is probable that we shall have to make important and far-reaching value judgments before we have acquired the human morbidity and mortality data which would in itself carry general conviction. THE COMPLEXITY OF THE RELATIONSHIP BETWEEN AIR POLLUTION AND RESPIRATORY HEALTH WILLIAM S. SPICER, JR. Associate Professor of Medicine and Head, Division for Pulmonary Diseases University of Maryland School of Medicine Baltimore, Md. That the relationship between air pollution and respiratory health is complex is obvious to the many who are attempting to evaluate it. A listing of the various known and probable factors involved, with the combinations and permutations possible, would adequately, but tediously, fill the allotted time. As the purpose of this conference is the presentation of the present status of our knowledge, we will sacrifice such completeness of listing in order to attempt to illustrate our level of understanding (or lack of understanding) of the complexities involved even in demonstrating this relationship. Respiratory health, in itself, is not a simple concept and has different meanings for different investigators. The recording of the symptoms of chronic bronchitis, e.g., cough, sputum, wheeze, breathlessness, etc., in a control population in relation to either daily or long-term levels of air pollutants differs from the recognition that individuals who have no clinical symptoms change in relation to environmental factors when tested by complex pulmonary function tests. The determination of the prevalence of acute respiratory infections or of carcinoma of the lung, the observation of disaster episodes or the tentative establishment of community air quality standards, which may be done in relation to air pollutant levels, differ from both of the former in interpretation. Certainly, all of these valuable approaches should and do complement each other. But, just as certainly, they can not be equated. Utter confusion and misinterpretation will result unless we are constantly clear as to which particular aspect of respiratory health is being evaluated in any particular investigation. Let us proceed step by step through a specific investigation. The primary purpose of this study is to determine whether there is a cause-and-effect relationship between environmental changes and the changes occurring in the respiratory status of a group of human beings living in a residential area in the center of an urban community. While the individuals undergo daily clinical and bacteriological evaluations, the primary tool utilized in assessing their respiratory status is a daily battery of objective pulmonary function tests. For orientation, we are discussing a 20- by 40block residential area, topographically low and flat, with a population of some 200,000 residing in row houses, 40 percent of which are heated by coal, kerosene, or wood burning stoves. The predominant winds over this area are either from the northwest or the southwest. To the southwest lies a major industrial complex; to the northwest, suburban residential and farming areas. The average yearly suspended particulate from urban stations is 130 micrograms per cubic meter. This would place the area as an "average dirty" community. The clinical pulmonary physiologist often thinks of the average human being as a lung which is intermittently flushed by the air of the surrounding environment through a connecting tube, or airway, as illustrated in figure 1. At the top of the diagram we have illustrated the lung and airway of a normal human being. At the top left this individual has filled his lung to its fullest extent with ambient air. The airway is thin, elongated, and distended. The cross section of the airway is shown at the top in each case. The maximum amount of gas that an individual's lung may contain is called the Total Lung Capacity. The clear area represents the amount of gas which he can expel from his lung, and is called the Vital Capacity. The gray area is the volume of gas remaining after he has exerted a maximal expiratory effort, and is named the Residual Volume. The dotted line is the volume of gas in his lung at the end of a normal respiration. This volume point is determined by the ease with which gas can pass through his airway, or the Airway Resistance, and the ease with which his lungs can collapse, and is known as the Functional Residual Capacity (FRC). In the middle illustration the normal individual has let air out of his lung to the normal resting respiratory position. His airway is shortened and its diameter narrowed. At this point the airway still does not present excessive resistance to the flow of gas. Expiring from full inspiration to full expiration is done easily until the FRC is passed, at which time it becomes increasingly difficult to collapse the lung and force the gas through an airway which is shortening and decreasing in size. Finally, the airway closes completely and expiration stops. During the late stages of expiration, airway resistance increases rapidly and considerably, secondary to the decrease in airway size. The bottom half of the diagram represents the disease state. It is applicable to an individual who has either permanent or transient pulmonary disease. Diagrammatically, we can summarize the effect of inhaled irritants upon the airway as leading to inflammation, with thickening of the wall and a resultant decrease in the diameter of the lumen. The airway widens and elongates with inspiration and shortens and narrows with expiration. Thickening of the wall will affect particularly the Expiratory Airway Resistance. This, in turn, will affect the lung volumes. Firstly, the airway will close earlier, increasing the Residual Volume. Secondly, the individual will breathe at a higher level in order to avoid the work of breathing out against the increased airway resistance at the lower volumes. Thirdly, the lung will be stretched more at full inspiration in order to build up more elastic recoil to aid in expelling gas through the narrowed airway. If, in addition, the individual has permanent lung damage, the lung tissues will have lost elasticity and the airways will tend to collapse. At the lower left the diseased lung is at full inspiration. The Total Lung Capacity is increased. As the individual expires fully the airways, which are already smaller than normal, close at an earlier point and also have a tendency to collapse. The result is that the residual volume, or the amount of gas remaining in the lung at the end of a full expiration, is considerably increased. In addition, the lung tissue itself is diseased and on expiration portions of it fail to collapse smoothly, as is illustrated in the diagram by the wavy appearance of the lung volume. Adjacent to each of the circular diagrams is a block diagram of the lung volumes, which may be used for graphic comparisons with air pollutant levels. In summary, one way in which either the normal or diseased lung responds to inhaled irritants is by an increase in expiratory airway resistance, often accompanied by an increase in the lung volumes noted. Now that we are prepared as pulmonary physiologists it would be well to immediately share in the difficulties encountered in measuring human beings. One of the first problems which we must face is the meaning of objective pulmonary function measurements. The physician is often inclined to feel, once he has made a measurement of a subject, that one measurement is valid for the individual over some period of time. In figure 2 we have illustrated the airway resistance and lung volumes obtained on one patient on three consecutive days. Note immediately the vast amount of the change in the pulmonary function tests in this relatively short period of time. For comparison his predicted normal values are seen on the right. On day 2 the patient has become obviously and grossly abnormal. However, in an additional 24 hours his pulmonary function tests have changed strikingly, with his total lung capacity having decreased by better than 2 liters. His studies now are borderline normal and, without objective pulmonary function tests, he might be judged normal. Consider our dilemma when faced with the problem of evaluating a large population group by a questionnaire and relatively simple pulmonary function tests, if, over the period of days or weeks which it will take to evaluate the group, their pulmonary function is changing to these extremes. In figure 3 the studies of a second patient for the same three-day period are shown. As with the previous patient there is a sharp rise in airway |