CORRESPONDENCE
Short-Term Effects of Air Pollution on Mortality in New York City SIR: We have read with great interest the article by T. A. Hodgson (ENVIRON.SCI. & TECHNOL. 4, 589-597, 1970). Although not professing t o be statisticians and, therefore, admitting t o no competence to judge the validity of the statistical methods used, we are concerned about certain concepts expressed in the article and believe they need careful analysis and evaluation. These may be listed arld are discussed as follows: ONE. It seems to us that the opening sentence contains a contradiction. If “very little is known of the qualitative or quantitative nature of the relationship between air pollution and health,” then how can “considerable evidence” be present t o “support the belief. . .that air pollution affects health”? Evidence, we presume, means data, and data are either qualitative or quantitative knowledge. Is there another type of knowledge of which we are unaware ? Two. On page 590, Hodgson indicates that particulates were measured in coh units and sulfur dioxide in ppm. Later, on page 596 he indicates that he has used increments of 1 unit in the average coh units and 0.5 unit in the average concentration of sulfur dioxide. Presumably these are monthly averages. We have operated a n air monitoring station for over two years and have never observed a variation in monthly averages for smokeshade of 1 coh unit and of SO2 of 0.5 ppm. Hodgson stipulates day-to-day variations of as much as 5 coh units and 0.5 ppm of SO?. Monthly averages never have even approximated such wide swings. Such a change in monthly averages would represent a whopping change in air pollution levels. As a matter of fact, our monthly averages for smokeshade are about 0.5 t o 1.0 coh unit and for sulfur dioxide 0.04 to 0.08 ppm. If changes of monthly averages of the magnitude indicated by Hodgson did occur, then we would not be surprised at all if increased mortality occurred, since this would necessitate several days each month when coh units would exceed 9 or 10 and SO2 levels 2 or 3 ppm. Such levels of pollutants we would classify as “episodes.” THREE.On page 594, Hodgson states “the implication of a linear relation between mortality and the environmental factors is that a unit change in the level of air pollution in-
SIR: The criticism of Eckardt, Scala, and Brief is replete with misconception, misinterpretation, and factual error. Part of the difficulty they encountered can be attributed to their admitted lack of statistical knowledge. The bulk, however, is due to a careless reading of my paper and misstatement of certain facts. A thorough rebuttal requires a lengthy reply. However, I shall endeavor t o be as brief as possible and respond t o the five points made by Eckardt, et al., in the same order as in their letter: 548 Environmental Science & Technology
duces as great an increase in mortality a t low levels of pollution as at higher levels.” T o the toxicologist and pharmacologist, this is contrary t o any dose-response curve ever constructed unless the response is being measured in a very restricted area of the dose range. From what has been said above in paragraph 2 , this does not appear to be the case with Hodgson’s data on dose. Any toxicologist or pharmacologist knows that the dose-response curve is not linear but S-shaped. This means that for a unit increase at low doses the response is small, becoming large at intermediate doses and again tapering off t o be small at high doses. Only if one were comparing responses soley in the intermediate area of dose, or comparing responses in the low and high areas with each other, would that linearity exist. To propose linearity in the dose-response curve would be t o negate the thousands of toxicological and pharmacological experiments that have been conducted over the years which show that dose-respose curves are nonlinear. That Hodgson’s data imply linearity suggests some basic defect in the data which he was manipulating statistically. FOUR.The validity of using coh units as a measure of particulate concentration is open to serious question. They measure only the blackness of particles, not their concentration. Particulate concentrations are usually measured in units of micrograms per cubic meter. FIVE. That people 64 and under in age cannot be on the brink of death is an erroneous concept. Those ill at ages 64 or under are dying regularly regardless of air pollution levels, and since there are more people age 64 and under than over 65, one would expect more daily deaths among the 64 and under age group than among the 65 and over age group. R. E. Eckardt R. A. Scala R. S. Brief Esso Research and Engineering Co. Medical Research Dicision Linden, N . J. 07036
ONE. An exact quotation of my opening sentence is “Although there is considerable evidence t o support the belief, now widely held, that air pollution affects human health, very little is known of the qualitative or quantitative nature of the relationship between air pollution and health.” Referring t o the 1966 unabridged edition of the “Random House Dictionary” one will find that considerable means “worthy of respect, attention, etc.; important” (as well as “rather large or great, as in size, distance, extent, etc.”); support means
“to add strength to,” and not necessarily sustain completely and adequately; and beliefrefers to “acceptance of, or confidence in, an alleged fact or body of facts as true or right without positive knowledge or proof.” That there are many who believe air pollution affects human health is obvious from even a cursory search of the literature in the fields of medicine, the physical and social sciences, and law. Repeated observation of excess mortality and morbidity during air pollution episodes, at least since 1930 to the present, in many widely scattered areas of the world such as the Meuse River Valley in Belgium, Donora (Pa.), London, and New York is important and worthy of attention. This observation adds strength to the belief and has spurred further research. Nevertheless, much remains unknown. What is the effect of continuous exposure over a prolonged time (Le., decades) t o the commonly occurring levels of urban air pollution? Is air pollution a factor in initiating disease, or does pollution only aggravate already existing conditions ? Which diseases, which pollutants? What is the role of time, the extent to which health effects are delayed and (or) cumulative with respect t o past exposure? What is the relative importance of massive short-term exposure, exposure to periods of high, but not extraordinary, levels of pollution, exposure at lower levels over longer periods of time? Are harmful effects of several pollutants taken together additive or synergistic? What are the threshold levels of noxious pollutants at which deleterious effects begin to occur? What are the effects of different levels of the many air pollutants and combinations of pollutants, over varying exposure times, on various health indexes? These unanswered questions demonstrate there are many qualitative and quantitative aspects of the relationship between air pollution and human health which are still to be ascertained. Two. Eckardt, Scala, and Brief are confused concerning the monthly and daily models in my paper, the difference between units of measurement and differences is observed values, and they apparently do not understand the role of regression coefficients as estimates of the change in the expected value of the dependent variable resulting from a unit change in the corresponding explanatory variable. The air pollution data employed in my study, as described on page 590, consist of 12 coh observations, one every two hours, and 24 hourly sulfur dioxide readings for each day in the study period. The averages of the 12 coh and 24 sulfur dioxide readings, respectively, give an index of coh and sulfur dioxide pollution for each day. The averages of the daily values occurring each month give a series of monthly coh values and a series of monthly sulfur dioxide values. These two series are the observations used in the monthly models, while two-day moving averages of the daily indexes (including the present and previous day) form the observations on coh and sulfur dioxide in the daily regression models. Eckardt et al., are mistaken in presuming the discussion they refer to on page 596 concerns monthly averages, as the opening sentence clearly indicates the daily models are to be discussed. They also fail to comprehend that the 1 unit increase in coh concentration and 0.5 unit increase in sulfur dioxide concentration are simply assumed (and reasonably SO for New York City during the study period) in order to discuss the magnitude of the response in mortality induced by changes in coh and sulfur dioxide as estimated by the regression equations, and have nothing to do with the variance of the observed values for coh or sulfur dioxide during the study period. It is not clear to me whether uuriution to Eckardt et al.,
means variance, as defined statistically, or simply the range. It is true the variances of the 31 monthly values for coh and sulfur dioxide between November 1962 and May 1965 employed in my paper are less than 1 coh unit and 0.5 pprn of sulfur dioxide. And the range of the monthly values for sulfur dioxide is also less than 0.5 ppm. However, the range of the monthly coh index is 2.4. The observations made at the station operated by Eckardt et al., whose location is a mystery, are irrelevant for discussion of my paper if they were not collected in New York City during the period of my study. The monthly values 1 employ indicate levels of air pollution greatly in excess of those observed by Eckardt et al. For coh (to the nearest tenth) the monthly mean is 1.8, the maximum is 3.4, and the minimum is 1.0, giving a range of 2.4. For sulfur dioxide, the mean of themonthly values is 0.15, the maximum is 0.26, and the minimum is 0.04, giving a range of 0.22. These monthly values are calculated from daily values of coh and sulfur dioxide having, of course, means equal to the monthly means but larger ranges and variances. The validity of the magnitudes of coh and sulfur dioxide levels in my paper is substantiated by Green (1966) who points out that between November 1962 and March 1964 daily averages for sulfur dioxide of 0.7 ppm and smokeshade of 6 and 7 coh were recorded on more than one occasion in New York City. Although it may surprise Eckardt et al., increased mortality occurred in New York City as air pollution increased within the range of levels discussed above, levels which are greater than observed at their monitoring station, but less than they presume necessary. THREE. Not all authorities, if, indeed, any, agree with the assertion Eckardt et al., appear to be making that ‘ . , .any dose-response curve ever constructed’ is “S-shaped.” Good. man and Gilman (1965) state “A dose-effect curve may be linear, concave upward, concave downward, or sigmoid. Moreover, if the observed effect is the composite of several effects of the drug,. . .the doseeffect curve need not be monotonic.” Be this as it may, it is not a major point of contention. Contrary to what Eckardt et al., think, I do not propose linearity over the total conceivable range of air pollution exposure; only over the range observed in New York City during the study period, and only when mortality and air pollution are both plotted on arithmetic scales. TO obtain the sigmoid-shaped curve desired by Eckardt et al., when mortality is the response would require a range of air pollution levels such that 100% of the population at risk succumbed when the maximum levels occurred. Actual levels of air pollution do not even come close to approaching the median lethal dose, let alone the dose required for 100% response. This is true whether the population at risk is the total population of New York City or only those individuals with the preexisting and predisposing heart and respiratory diseases discussed in my paper. In this sense, response is being measured in only part of the dose range required to produce a sigmoid curve, but over the total dose range that, in fact, occurred in New York City. The high and low levels I discuss on page 594 are high and low in terms of the observed range in New York City. A linear relation between two variables on arithmetic scales will be nonlinear on semilog paper and a linear relation on semilog paper will be nonlinear on arithmetic scales. The purpose of the discussion on page 594 was to demonstrate that the best explanation of mortality in terms of the explanatory variables themselves is linear, which transforms into a nonVolume 5, Number 6, June 1971 549
linear semilog relation. If one takes the linear equation for R t on page 594, substituting 0.0 for St (which is not significant in this equation), 17.0 for D t (its mean value) and plots R t for C t = 1, . , 6 on semilog paper, he will obtain a concave upward function, which may be the beginning of the sigmoid dose-response curve Eckardt et al., desire. What is especially bothersome in the comments by Eckardt et al., is their apparent belief that any relation between air pollution and health (morbidity as well as mortality) which is not “S-shaped” cannot be valid. Mortality is ostensibly a composite effect of air pollution; coh and sulfur dioxide are only indexes of air pollution and harmful pollutants probably act in a synergistic or additive manner; exposure does not take place in a controlled laboratory experiment and the poplation is being subjected to other stimuli that affect health status. Thus, it is inadequate to use the shape of the curve as the sole criterion for judging data or method and rejecting a statistically significant, positive relation between air pollution and mortality from respiratory and heart diseases. FOUR. I agree micrograms per cubic meter is a more desirable measure of particulate matter. It permits, for example, combination of particulate concentration with sulfur dioxide measurements to form an index which reflects adsorption of sulfur dioxide by airborne particulates. This type of index would aid in the study of synergistic health effects. However, if micrograms per cubic meter are more highly correlated with some causal factor in the relation between mortality and air pollution than are coh units, the substitution of micrograms per cubic meter for coh units will improve the estimated regression equations. Any single air pollutant can provide only an index of a complex atmospheric situation and a less than optimal index is far better than none at all. Micrograms per cubic meter were not available to us at the time of the study and cob units were valid measurements to employ. The fact that the study obtained such significant results helps to confirm that air pollution influences the level of mortality. FIVE. I neither state nor infer that persons age 64 and under cannot be on “the brink of death.” Of course the deaths of many persons under age 65, and 65 and over for that matter, are unrelated to air pollution. But the fact is, there is a strong correlation between the level of air pollution and mortality in both age groups. The higher the level of air pollution, the
more deaths there are from heart and resipratory diseases in both age groups. This correlation and other aspects of the study support the hypothesis that increases in air pollution are an environmental stress which results in death for substantial numbers of persons who would not otherwise have died at that time. Eckardt et al., are quite mistaken in their statement concerning relative mortality in the two age groups. It is true that there are more people age 64 and under. According to the 1960 United States Census, only 1 0 . 5 x of the population of New York City was age 65 or older. However, Eckardt et al., should realize that the number of deaths in an age group depends on the age specific mortality rates as well as the number of persons at that age. The age specific mortality rates for those 65 and over are so much higher than the rates for those 64 and under that, contrary to what Eckardt et al., say, there are many more deaths among those 65 and over than among those 64 and under. Had they not overlooked the figures in Table VI, they would have seen that for every category of mortality listed there are more dying who are 65 and over than 64 and under, and for respiratory and heart diseases as a group the number dying who are 65 and over is more than twice the number 64 and under. For all causes of death the ratio is 1.35 for New York City. And this is not a local phenomenon, since the Center for Disease Control reports (“Morbidity and Mortality,” 1970) that in 1969 in 122 United States cities 1.34 times as many deaths occurred among persons age 65 and over as among those age 64 and under. Literature Cited
Goodman, L. S., Gilman, A,, “The Pharmacological Basis of Therapeutics,” third ed., Macmillan, New York, N.Y., 1965, p 20. Green, M. H., Air Pollut. Contr. Ass. J . 16,703 (1966). U.S. Dept. H.E.W., Public Health Service, Center for Disease Control, “Morbidity and Mortality,” 18 (54), 28 (1970).
Thomas A. Hodgson, Jr. Cornell Unicersity Medical College Department of Public Health Dicision of’ Epidemiologic Research New York, N . Y . IO021
CORRECTION
SPECTROPHOTOMETRIC DETERMINATION OF ATMOSPHERIC FLUORIDES In this article by P. W. West, G. R . Lyles, and J. L. Miller [ENVIRON. Scr. TECHNOL.4,487 (1970)], paragraph 4, page 489, should read as follows: Lanthanum nitrate buffer (2 x lO-3M). Dissolve 0.886 g. La(N0J3.6H20 and 102 g. NaOAc (anhy) in 250 ml. H?O. Add 222 ml. glacial HOAc and 76 ml. HCL (conc.). Dilute to 1 liter with HzO. The pH of this solution, when diluted 1 : 10, and containing acetone to the extent of 25 (v.,h.) (see Sampling Technique), should be 4.1 to 4.2.
x
550 Environmental Science & Technology
