CHAPTER 4
HEALTH EFFECTS OF SULFUR OXIDES

CHILDREN

A number of studies have focused on the effects of air pollutants in children. This is a useful group to study, in that their lesser mobility produces a more homogeneous pollution exposure and the effects of cigarette-smoking and occupational exposure are minimized. Furthermore, children appear to be at greater risk than healthy adults, owing presumably to their greater degree of mouth-breathing, relatively greater tidal volumes, and higher frequency of respiratory tract infections. The effects of air pollutants in children have been reviewed by a committee of the American Academy of Pediatrics (1970) and more recently by Wehrle and Hammer (1974).

An increase in the death rate of the very young has been noted in some, but not all, studies of air pollution episodes. Logan (1953) noted an increased neonatal and infant mortality in the December 1952 London fog episode, but Greenberg et al. (1967) did not observe any change in death rate in this age group during a less severe 2-week episode in New York in 1963. Lave and Seskin (1970), in their broad statistical analysis of the effects of air



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Air Quality and Stationary Source Emission Control CHAPTER 4 HEALTH EFFECTS OF SULFUR OXIDES CHILDREN A number of studies have focused on the effects of air pollutants in children. This is a useful group to study, in that their lesser mobility produces a more homogeneous pollution exposure and the effects of cigarette-smoking and occupational exposure are minimized. Furthermore, children appear to be at greater risk than healthy adults, owing presumably to their greater degree of mouth-breathing, relatively greater tidal volumes, and higher frequency of respiratory tract infections. The effects of air pollutants in children have been reviewed by a committee of the American Academy of Pediatrics (1970) and more recently by Wehrle and Hammer (1974). An increase in the death rate of the very young has been noted in some, but not all, studies of air pollution episodes. Logan (1953) noted an increased neonatal and infant mortality in the December 1952 London fog episode, but Greenberg et al. (1967) did not observe any change in death rate in this age group during a less severe 2-week episode in New York in 1963. Lave and Seskin (1970), in their broad statistical analysis of the effects of air

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Air Quality and Stationary Source Emission Control pollution in the United States, have suggested an association with neonatal mortality. A number of large-scale British studies have evaluated the effects of air pollution on the health of children. Colley and Reid (1970) surveyed respiratory disease prevalence in 1966 in over 10,000 children 6–10 years old in England and Wales with a questionnaire and measured peak expiratory flow rates. A social-class gradient was observed for chest disease, but a pronounced increase in prevalence was observed in each social class in association with greater pollution. This was particularly true in the children of unskilled and semiskilled workers. An unexplained excess in prevalence in Wales may represent an ethnic difference. Small differences in peak expiratory flow rate were found when the results were calculated independently for those with and without a history of respiratory disease or symptoms. The authors point out that differences may have been obscured by difficulties in standardizing the observers and the 70 peak flow meters used in the study. Another British study of over 10,000 children was performed at about the same time by Holland et al. (1969) in different areas of Kent. They observed independent and additive effects of social class, family size, history of significant respiratory disease, and area of residence on pulmonary function, as measured by peak expiratory flow rate. Residential area appeared to have the greatest influence on pulmonary function; this suggested an effect of air pollution. However, the authors note that all four factors together accounted for only about 10–15 percent of the total variation; other determinants, possibly including host factors, are probably also important. Only minimal pollutant monitoring data are presented that describe the monthly average smoke concentrations in three of the four areas studied for November 1966 to March 1967. In the most polluted area, which had the lowest peak expiratory flow rates, the highest recorded monthly average smoke shade was 96 ug/m3. A study by Douglas and Waller (1966) evaluated over 3,000 children 15 years old who

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Air Quality and Stationary Source Emission Control had been born in the first week of March 1946 and were followed regularly as part of a comprehensive health survey. Domestic coal consumption was used to divide areas into four pollution classes. The frequency and severity of lower respiratory tract infections were clearly related to air pollution. However, no consistent effect on upper respiratory infections, otitis, or tonsillitis was observed. The following factors demonstrated a gradient of air pollution effect, in that there was an increase at each succeeding stage of pollution severity: first lower respiratory tract infection before the age of 9 months and before age of 2 years; more than one attack in first 2 years for both boys and girls; hospital admission for bronchitis in first 5 years; pulmonary rales or rhonchi noted on two or more chest examinations or by the age of 15; excess episodes of school absences; and long periods of absence from primary school for bronchitis. Only small differences in social class among the air pollution categories were noted, and this factor was not evaluated further. Nor were other possible variables, such as crowding, assessed. Some data are given in the appendix concerning air pollution in 1962–1963. As indicated by the authors, this must be approached with caution, particularly as pollution was probably worse in earlier years. Taken as a whole, the data give an impression of linearity of response (lower respiratory infection) in children to air pollution beginning at somewhat higher than present U.S. standards for total suspended particles and sulfur dioxide. This cohort of children born in 1946 was reevaluated at the age of 20 (Colley and Reid 1970). The most noticeable finding was the dominant effect of cigarette-smoking on the respiratory symptoms of these young adults. A history of chest disease before the age of 2 also had a significant, but smaller, effect. After adjustment for these two variables, air pollution had only a small and not statistically significant effect. The same was true for socioeconomic class. There was a tendency for the air pollution effect to be greatest in the lower socioeconomic classes; this suggests an

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Air Quality and Stationary Source Emission Control interaction between these two variables in the production of respiratory symptoms. As pointed out by the authors, the nonresponders to the follow-up questionnaire were overrepresented in the high-pollution category, which might tend to bias the results. However, the results are consistent with those of other studies and indicate that the effects of air pollution on young adults are minimal at most, particularly in relation to cigarette-smoking. Lunn et al. (1970, 1967) evaluated children in Sheffield, England, in 1965 and were able to repeat the study on some members of the same group 4 years later, when air pollution had decreased. This type of study, in which a cohort is reevaluated after a change in the environment, has also been performed in Berlin, New Hampshire, and is of great value in ascertaining the effects of air pollution. At the time of the original study, there was a distinct gradient in air pollution in the four districts under evaluation. In 1964, the cleanest area had a mean daily sulfur dioxide concentration of 123 ug/m3 and mean daily smoke of 97 ug/m3. The mean daily sulfur dioxide and smoke values in the other areas were 183 and 230, 219 and 262, and 275 and 301 ug/m3. Questionnaires were sent to the parents of 5-year-olds living in the vicinity of the school. The children were then examined, and pulmonary function tests were performed. Socioeconomic class, number of children at home, and number of persons sharing the same bedroom all had some effect on the findings. However, when the data were evaluated within each social class, a distinct increase in respiratory morbidity for both upper and lower respiratory diseases was observed. For the lower socioeconomic classes, a history of persistent cough was obtained in 23.9 percent of the children in the cleanest area, and there were stepwise increments in from each area as the pollution increased—39.6 percent, 43.8 percent, and 60.9 percent. Lower-than-predicted forced expiratory volume (0.75 sec) and forced ventilatory capacity were observed only in the most polluted community. The 11-year-olds examined at the same time had similar, but less marked, differences between areas.

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Air Quality and Stationary Source Emission Control When the original 5-year-old group was reexamined 4 years later, in 1969, the differences between areas had narrowed and were not statistically significant. A major decrease in air pollution had occurred; in 1968, mean daily sulfur dioxide and smoke concentrations for the four areas were 94 and 48, 166 and 41, 186 and 118, and 253 and 169 ug/m3. There was also less respiratory disease in this 9-yearold group than in the 11-year-olds evaluated 4 years earlier. It should be emphasized that this lessening in a gradient of respiratory disease was associated with about a 45–80 percent decrease in particles, as measured by smoke, with only approximately a 10–25 percent decline in sulfur dioxide. Furthermore, during the latter part of the study, the smoke and sulfur dioxide concentrations were still appreciably above American air quality standards. Unfortunately, no data on ambient concentrations or gradients for sulfate are available. Biersteker and van Leeuwen (1970) evaluated peak flow rates in about 1,000 schoolchildren in two districts of Rotterdam: a wealthy suburban area in which winter mean smoke concentration was about 50 ug/m3 and winter mean sulfur dioxide concentration was 200 ug/m3, and a poorer urban area with about 50 percent higher pollutant concentrations. Air pollution monitoring techniques are not described. Although the children in the cleaner area generally had higher peak flow rates, this could be accounted for by differences in height and weight. In fact, following multiple regression analysis, there was a slight but statistically significant increase in peak flow rates in the polluted area. The authors also observed a statistically significant increase in the prevalence of childhood chronic bronchitis in the more polluted area (5.5 percent), compared with the cleaner area (1.0 percent). A smaller, nonsignificant increase in asthma rate was also found (2.2 percent vs. 1.7 percent). A number of Japanese investigators have also reported an association of sulfur dioxide and particles with prevalence of respiratory morbidity and a decrease in pulmonary function in children (Kagawa et al. 1974, Toyama 1964).

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Air Quality and Stationary Source Emission Control Responses appear to occur at relatively low pollutant concentrations. However, as discussed earlier, there is some question as to whether the results can be extrapolated to the U.S. population. As part of the Nashville air pollution study, Sprague and Hagstrom (1969) observed that sulfation rates correlated with middle-class deaths in the age range of 1–11 months and that dustfall was associated with neonatal deaths. However, the authors found it difficult to remove socioeconomic factors, which varied with air pollution, as well as with neonatal and infant mortality. Furthermore, their assignment of arbitrary linear numbers to different socioeconomic classes is questionable. Collins et al. (1971) studied environmental factors affecting child mortality in England and Wales during 1958–1964. Included in this analysis were indexes of domestic pollution, industrial pollution, proximity of a power station, social class, overcrowding, population density, and education. Each of these factors except power-station proximity was significantly correlated (p<0.001) with the mortality of infants less than a year old. Because all the social indexes were highly intercorrelated, it was difficult to disentangle their individual effects. However, partial correlation analysis showed that the bulk of the increased mortality could be attributed to domestic and industrial pollution. Unfortunately, the data are not presented in such a way as to permit assessment of a possible dose-response relationship. As part of the Berlin, New Hampshire, study (described in more detail later), Ferris (1970) investigated the relation of air pollution to school absences and pulmonary function. First-and second-graders from seven schools were studied in 1966–1967. No consistent effect of air pollution on total school absence rates or school absences due to respiratory illnesses were observed. A relationship may have been obscured by the fact that not all children lived close to their schools. There were some statistically significant differences in pulmonary function, particularly peak expiratory flow rate, that suggested an effect of air

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Air Quality and Stationary Source Emission Control pollution. The worst school (school A) in terms of pulmonary function was subjected to much higher amounts of dustfall, but not of sulfur dioxide (as measured by lead peroxide candle), which suggests that the effect was due mainly to particles. However, school A’s pupils were of a lower socioeconomic class than those of most of the other schools. The only other school with pupils of a similarly low socioeconomic class (school J) was in an unpolluted area, and, although pupils in school A tended to have lower pulmonary function than those in school J, the difference was not reported to be statistically significant. Anderson and Larsen (1966), in a similar study of first-graders in British Columbia, were also unable to show an effect of air pollution on school absences. However, there was a statistically significant decrease in peak expiratory flow rate in the two towns affected by a Kraft pulp mill, compared with that in the clean town. This may have been related to ethnic differences, which were not studied. Air monitoring data are not presented. A recent study by Mostardi and Leonard (1974) reported a decrease in pulmonary function in high-school students in Barberton, Ohio, an industrialized area, compared with that in Revere, Ohio, a more rural community. These students had initially been evaluated in 1970 and were restudied in 1973. Socioeconomic factors were said to be similar. The Barberton students had a statistically significant and similar decrease in vital capacity in both periods: a decrease in 1-sec forced expiratory volume in 1970, but not 1973, and in maximal aerobic capacity on exercise (Vo2 max) when tested in 1973. No difference was observed in maximal midexpiratory flow rate, an index of small-airway disease. The finding of a difference in Vo2 max is of interest, in that this test is usually not performed in air pollution studies and has potential health significance. However, this result could conceivably be accounted for by a relative lack of routine exercise in the urban group, although participation in organized athletics was similar. The air monitoring data show that

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Air Quality and Stationary Source Emission Control Revere cannot be considered a low-pollution community, in that yearly mean concentration of total suspended particles, which decreased from 83 to 71 ug/m3 from 1969 to 1973, was generally greater than the U.S. air quality standard. Furthermore, the sulfur dioxide concentration (by lead peroxide candle, 0.96 mg of sulfur trioxide per 100 cm2 per day in 1971) was much higher than that recorded in Berlin, New Hampshire, although there is an unexplained decrease to 0.36 mg/100 cm2 per day in 1972. The air monitoring data for Barberton show a peak yearly mean 24-hr concentration of total suspended particles of 109 ug/m3 in 1969, which decreased to 77 ug/m3 in 1973, and peak yearly sulfur dioxide of 1.11 mg/100 cm2 per day. This study tends to support an association between a decrement in childhood pulmonary function with air pollution slightly above the current U.S. standards for total suspended particles and sulfur dioxide. The data, although suggestive, do not clearly indicate whether improvement in air quality had a positive effect. Potential criticism of the study includes the relatively small numbers of students tested and the lack of presented data on cigarette-smoking, although this question was apparently asked. In addition, a contemporary urban-rural difference in the use of nontobacco cigarettes is conceivable. The Community Health and Environmental Surveillance System (CHESS) program has conducted a number of extensive studies of the health of children (EPA 1974). In the Salt Lake area, four communities were selected for a retrospective study of lower respiratory infection on the basis of an expected gradient for sulfur dioxide and suspended sulfates (Nelson et al. 1974). Pollutant concentrations for the period before 1970 were estimated from monitoring and emission data, as well as meteorologic factors. Information about lower respiratory infection in children 5–12 years old was obtained by questionnaires mailed to parents and distributed through the schools. Almost 9,000 nonasthmatic students were studied; the results indicated an increased incidence of total lower respiratory infection, croup, and

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Air Quality and Stationary Source Emission Control bronchitis, but not of pneumonia or hospitalization, in the most polluted community. This high-pollution community had an estimated mean sulfur dioxide concentration in 1967–1970 of 91 ug/m3, compated with 33 ug/m3 in the next highest area, and an estimated mean suspended sulfate concentration of 15 ug/m3, compared with 9 ug/m3. The concentration of total suspended particles in the high-pollution community in 1967–1970 was 63 ug/m3, which was lower than the concentrations in two of the other communities. The concentrations of suspended nitrates were similarly low in all the communities. Other factors evaluated—including the educational status of the father, mean family size, and parental smoking habits—did not appear to account for the increased incidences of croup and bronchitis in the high-pollution community. Investigation of physicians’ records tended to validate the questionnaire findings and did not reveal any difference in diagnostic patterns between communities. An analysis of the duration of residence in each area showed that the increased attack rates for croup and bronchitis in the high-pollution community were observed solely in children who had lived there for 3 years or longer. In this subgroup, the data on croup, which had the largest gradient, showed a 3-year attack rate in the high-pollution area of 26.4 percent, compared with 14.5–16.9 percent in the other communities. The 3-year attack rate for bronchitis was 23.6 percent, compared with 16.5–17.1 percent in the cleaner communities. These attack rates were adjusted for age, sex, and socioeconomic status. It is noteworthy that people who had lived in the high pollution community for less than 3 years had much lower attack rates than short-term residents of the other communities. The explanations advanced for this finding are at best tentative. There were fewer short-term than long-term residents, so these anomalous findings decreased only slightly the overall gradient in lower respiratory infection attack rate for all residents. The questionnaire response rate was relatively low, 67 percent, and one-sixth of them had to be discarded because of inadequate information. Although a

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Air Quality and Stationary Source Emission Control small-scale study appeared to show no difference between respondents and non-respondents, this may have been insufficient to rule out bias. The authors also state that there was a difference in attack rate between the community with mean suspended sulfates of 9 ug/m3 and the two communities with lower suspended sulfates but higher sulfur dioxide concentrations. This statement, does not appear to be completely warranted by the data. In general, the data do appear to substantiate an increase in lower respiratory disease in children exposed for a few years to sulfur dioxide at 90–100 ug/m3 and suspended sulfates at 15 ug/m3 in the presence of total suspended particles at concentrations below the air quality standard. No firm conclusions can be drawn, but the findings raise the suspicion of an effect of suspended sulfates. A similar retrospective study was performed in almost 6,000 children living in five Rocky Mountain communities (Finklea et al. 1974). The gradient in sulfur dioxide and total suspended particles was much greater than in the Salt Lake Basin, and there was also a difference in suspended sulfates. Unfortunately, the analysis of the data was complicated by distinct differences in socioeconomic status and parental smoking, which varied with air pollution. After adjustment for age, sex, and socioeconomic status, an increase in the attack rate for lower respiratory infections in nonasthmatics was observed in pooled data from the two high-pollution communities. (In 1968–1970, those two communities had sulfur dioxide concentrations of 177 and 375 ug/m3, total suspended particle concentrations of 63 and 102 ug/m3, and suspended sulfate concentrations of 7.2 and 11.3 ug/m3; of the three low-pollution communities, two had relatively negligible concentrations of each pollutant, and the third, “low III” had a mean sulfur dioxide concentration of 67 ug/m3, a total suspended particle concentration of 115 ug/m3, and a suspended sulfate concentration of 7.3 ug/m3.) However, the results in nonasthmatics tended to be significant only when calculated for people who had two or more episodes and only in the subgroup that had lived

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Air Quality and Stationary Source Emission Control in the same community for 3 years or longer. As in the Salt Lake study, croup rates correlated better with pollution than did bronchitis. There was also a tendency toward an increase in pneumonia and hospitalization rates in the high-pollution communities, but this was not statistically significant. Again, the finding of less disease in newcomers to the high-pollution areas than in newcomers to the low-pollution areas was puzzling. A more clearcut increase in the attack rate for lower respiratory illness was observed in asthmatics, but this was a smaller group and the findings were not adjusted for socioeconomic status, etc. Accordingly, the asthma data are inadequate to support firmly the investigators’ contention of a pollutant effect in the “low III” community. The findings are not as impressive as in the Salt Lake Basin, particularly in view of the larger gradient of sulfur dioxide and suspended particles (although not of suspended sulfates). Although comparison of these two similar studies is somewhat impeded by the larger difference in socioeconomic status between communities in the Rocky Mountain area, it should be noted that the relatively less polluted Salt Lake Basin area had higher adjusted attack rates—particularly multiple attack rates—of lower respiratory infection. Whether this represents physician diagnostic patterns, other local factors, or a difference in the administration of the two studies is unclear. Somewhat different studies were performed in Chicago and New York in which the attack rate of acute respiratory disease in family members was obtained by telephone interview of mothers. In Chicago, data were obtained in 1969–1970 on over 2,500 families that had at least one child in nursery school (Finklea et al. 1974). No information about those who did not volunteer for the study is given. Families were assigned to pollutant categories by place of residence with reference to nearby monitoring stations. The three exposure categories were defined as Intermediate, High, and Highest, and the 1969–1970 monitoring data on sulfur dioxide and total suspended particles were 57 and 111 ug/m3 for the Intermediate category, 51 and 126 ug/m3 for

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Air Quality and Stationary Source Emission Control respiratory disease symptoms in adults: 1970 survey of five Rocky Mountain communities, pp. 3–19 to 3–33. In U.S. Environmental Protection Agency, Office of Research and Development. Health Consequences of Sulfur Oxides: A Report from CHESS, 1970–1971. EPA-650/1–74–004. Washington, D.C.: U.S. Government Printing Office. Hewitt, D. (1956) Mortality in the London boroughs, 1950–52, with special reference to respiratory disease. Brit. J. Prev. Soc. Med. 10:45–57. Higgins, I.T.T., P.D.Oldham, A.L.Cochrane, and J.C.Gilson (1956). Respiratory symptoms and pulmonary disability in an industrial town. Survey of a random sample on the population. Brit. Med. J. 2:904–910. Higgins, I.T.T., and J.B.Cochran (1958). Respiratory symptoms, bronchitis and disability in a random sample of an agricultural community in Dumfriesshire. Tubercle 39:296–301. Higgins, I.T.T. (1974a). Background review: Epidemiology. Environ. Health Perspect. 8:110–118. Higgins, I.T.T. (1974b). Trends in respiratory cancer mortality in the United States and in England and Wales. Arch. Environ. Health 28:121–129. Higgins, I.T.T., and B.G.Ferris, Jr. (1974). Air pollution effects of the ventilatory function. Arch. Environ. Health 28:234. Hodgson, T.A., Jr. (1970). Short-term effects of air pollution on mortality in New York City. Environ. Sci. Technol. 4:589–597. Holland, W.W., and D.D.Reid (1965). The urban factor in chronic bronchitis. Lancet 1:446–448. Holland, W.W., D.D.Reid, R.Seltser, and R.W.Stone (1965). Respiratory disease in England and the United States. Studies of comparative prevalence. Arch. Environ. Health 10:338–343. Holland, W.W., T.Halil, A.E.Bennett, and A.Elliott (1969). Factors influencing the

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Air Quality and Stationary Source Emission Control onset of chronic respiratory disease. Brit. Med. J. 1:205–208. Holland, W.W. (1972). Chapter 11, Clinical aspects, pathology and natural history of non-specific respiratory disease. In W.W. Holland, Ed., Air Pollution and Respiratory Disease. Westport, Connecticut: Technomic Publishing Co. Holma, B. (1967). Lung clearance of mono- and di-disperse aerosols determined by profile scanning and whole-body counting. A study on normal and sulfur dioxide exposed rabbits. Acta Med. Scand. Supplementum 473. pp. 1–102. House, D.E., J.F.Finklea, C.M.Shy, D.C.Calafiore, W.B.Riggan, J.W.Southwick, and L.J.Olsen (1974). Prevalence of chronic respiratory disease symptoms in adults: 1970 survey of Salt Lake Basin communities, pp. 2–14 to 2–54. In U.S. Environmental Protection Agency, Office of Research and Development. Health Consequences of Sulfur Oxides: A Report from CHESS, 1970–1971. EPA-650/1–74–004. Washington, D.C.: U.S. Government Printing Office. Howard P. (1974). The changing face of Chronic bronchitis with airways obstruction. British Medical Jorunal, April 13. pp. 89 ff. Hrubec, Z., R.Cederlof, L.Friberg, R.Horton, and G.Ozolins (1973). Respiratory symptoms in twins. Arch. Environ. Health 27:189–195. Ipsen, J., M.Deane, and F.E.Ingenito (1969). Relationships of acute respiratory disease to atmospheric pollution and meteorological conditions. Arch. Environ. Health 18:463–472. Ishikawa, S., D.H.Bowden, V.Fisher, and J.P.Wyatt (1969). The “emphysema profile” in two midwestern cities in North America. Arch. Environ. Health 18:660–666. Jaksch, J.A., and H.H.Stoevener (1974). Outpatient Medical Costs Related to Air Pollution in the Portland, Oregon Area. EPA-600/5–74–017. Prepared for Office of Research and Development, Washington

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Air Quality and Stationary Source Emission Control Environmental Research Center, U.S. Environmental Protection Agency. Kagawa, J., T.Toyama, and M.Nakaza (1974). Pulmonary Function Tests for Children Exposed to Air Pollution. Paper presented at the American Medical Association Air Pollution Medical Research Conference, December 5–6, San Francisco, California. Lambert, P.M., and D.D.Reid (1970). Smoking, air pollution, and bronchitis in Britain. Lancet 1:853–857. Laskin, S., M.Kuschner, and R.T.Drew (1970). Studies in pulmonary carcinogenesis, pp. 321–350. In M.G.Hanna, Jr., P.Nettesheim, and J.R.Gilbert, Eds. Inhalation Carcinogenesis. AEC Symposium Series 18. Oak Ridge, Tenn.: U.S. Atomic Energy Commission Division of Technical Information. Lave, L.B., and E.P.Seskin (1970). Air pollution and human health. The quantitative effect, with an estimate of the dollar benefit of pollution abatement is considered. Science 169:723–733. Lawther, P.J., T.R.Emerson, and F.W.O’Grady (1969). Haemophilus influenzae: Growth stimulation by atmospheric pollutants. Brit. J. Dis. Chest 63:45–47. Lawther, P.J., R.E.Waller, and M.Henderson (1970). Air pollution and exacerbations of bronchitis. Thorax 25:525–539. Lawther, P.J., A.G.F.Brooks, P.W.Lord, and R.E.Waller (1974). Day-to-day changes in ventilatory function in relation to the environment. Part I. Spirometric values. Environ. Res. 7:27–40. Lawther, P.J., A.G.F.Brooks, P.W.Lord, and R.E.Waller (1974). Day-to-day changes in ventilatory function in relation to the environment. Part II. Peak expiratory flow values. Environ. Res. 7:41–53. Lawther, P.J., A.G.F.Brooks, P.W.Lord, and R.E.Waller (1974). Day-to-day changes in ventilatory function in relation to the environment. Part III. Frequent measurements of peak flow. Environ. Res. 8:119–130.

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Air Quality and Stationary Source Emission Control Lebowitz, M.D. (1973). A comparative analysis of the stimulus-response relationship between mortality and air pollution, Weather Env. Research 6, 106–118. Lebowitz, M.D., E.J.Cassell, and J.D.McCarroll (1972). Health and the urban environment. XV. Acute respiratory episodes as reactions by sensitive individuals to air pollution and weather. Environ. Res. 5:135–141. Lebowitz, M.D., and F.A.Fairchild (1973). The effects of sulfur dioxide and A2 influenza virus in pneumonia and weight reduction in mice. An analysis of stimulus-response relationships. Chem. Biol. Interact. 7:317–326. Lebowitz, M.D., P.Bendheim, G.Cristea, D.Van Wyck (1974). The effect of air pollution and weather on lung function in exercising children and adolescents. Amer. Rev. Resp. Dis. 109:262–273. Lee, A.M., and J.F.Fraumeni, Jr. (1969). Arsenic and respiratory cancer in man: An occupational study. J. Nat. Cancer Inst. 42:1045–1052. Logan, W.P.D. (1953). Mortality in London fog incident. Lancet 1:336–338. Loudon, R.G., L.C.Brown, and S.K.Hurst (1965). Cough frequency in a group of males. Arch. Environ. Health 11:372–374. Loudon, R.G., and J.F.Kilpatrick (1969). Air pollution, weather, and cough. Arch. Environ. Health 18:641–645. Love, G.J., A.A.Cohen, J.F.Finklea, J.G.French, G.R.Lowrimore, W.C.Nelson, and P.B.Ramsey (1974). Prospective surveys of acute respiratory disease in volunteer families: 1970–1971 New York studies, pp. 5–49 to 5–69. In U.S. Environmental Protection Agency, Office of Research and Development. Health Consequences of Sulfur Oxides: A Report from CHESS, 1970–1971. EPA-650/1–74–004. Washington, D.C.: U.S. Government Printing Office. Lunn, J.E., J.Knowelden, and A.J.Handyside (1967). Patterns of respiratory illness in Sheffield infant schoolchildren. Brit. J. Prev. Med. 21:7–16.

OCR for page 58
Air Quality and Stationary Source Emission Control Lunn, J.E., J.Knowelden, and J.W.Roe (1970). Patterns of respiratory illness in Sheffield junior schoolchildren. A follow-up study. Brit. J. Prev. Soc. Med. 24:223–228. Ma, T., D.Isbandi, S.Khan, and Y.Tseng (1973) Low level of SO2 enhanced chromatid aberrations in trandescantia pollen tubes and seasonal variation of the aberration rates. Mutation research, 21:93–100. Martin, A.E. (1964) Mortality and morbidity statistics and air pollution. Proc. Roy. Soc. Med. 57:969–975. McCarroll, J. and W.Bradley (1966) Excess mortality as an indicator of health effects of air pollution. Amer. J. Pub. Health 56: 1933–1942. McCarroll, J., E.J.Cassell, D.W.Wolter, J.D.Mountain, J.R.Diamond, and I.M.Mountain (1967) Health and the urban environment. Arch. Environ. Health 14:178–184. McDonald, J.C., J.S.Wilson, W.B.Thorburn, W.W.Holland, and B.E.Andrews (1958) Acute respiratory disease in the RAF, 1955–1957. Brit. Med. J. 1:721–724. Mills, C.A. (1943) Urban air pollution and respiratory diseases. Amer. J. Hyg. 37:131–141. Mills, C.A. (1952) Air pollution and community health. Amer. J. Med. Sci. 224:403–407. Mills, C.A. and M.Mills-Porter (1948) Health costs of urban air pollution. Occup. Med. 5: 614–633. Mostardi, R.A. and D.Leonard (1974) Air pollution and cardiopulmonary functions. Arch. Environ. Health 29:325–328. Mukai, F., I.Hawryluk, and R.Shapiro (1970) The mutagenic specificity of sodium bisulfite. Biochem. Biophys. Res. Communications 39:983–988. National Academy of Sciences (1974) Air quality and automobile emission control, vol. 2: health effects of air pollutants. September. U.S. Government Printing Office, Washington, D.C. Nelson, W.C., J.F.Finklea, D.E.House, D.C.Calafiore, M.B.Hertz, and D.H.Swanson (1974) Frequency of acute lower respiratory disease in children: Retrospective survey of

OCR for page 58
Air Quality and Stationary Source Emission Control Salt Lake Basin communities, 1967–1970, pp. 2–55 to 2–73. In U.S. Environmental Protection Agency, Office of Research and Development. Health Consequences of Sulfur Oxides: A Report from CHESS, 1970–1971. EPA-650/1–74–004. Washington, D.C.: U.S. Government Printing Office. Peacock, P.R. and J.B.Spence (1967) Incidence of lung tumours in LX mice exposed to (1) free radicals; (2) SO2. Brit. J. Cancer 21:606–618. Pemberton, J. and C.Goldberg (1954) Air pollution and bronchitis. Brit. Med. J. 2:557–570. Petrilli, F.L., G.Agnese, and S.Kanitz (1966) Epidemiologic studies of air pollution effects in Genoa, Italy. Arch. Environ. Health 12:733–740. Phelps, H.W. (1965) Follow-up studies in Tokyo-Yokohama respiratory disease. Arch. Environ. Health 10:143–147. Pirila, V. (1954) Skin allergy to simple gaseous sulfur compounds. Acta Allergol. 7:397–402. Pirila, V., H.Kajanne, and O.P.Salo (1963) Inhalation of sulfur dioxide as a cause of skin reaction resembling drug eruption. J. Occup. Med. 5:443–445. Ramazzini, B. (1964) Diseases of Workers (1964) translated from the Latin text by W.C. Wright. New York: Hafner Publishing Company, page 51, 1713. Rao, M., P.Steiner, Q.Qazi, R.Padre, J.E.Allen, and M.Steiner (1973) Relationship of air pollution to attack rate of asthma in children. J. Asthma Res. 11:23–26. Reid, D. (1962) Diagnostic standardization in geographic comparisons of morbidity. Amer. Rev. Resp. Dis. 86:850–854. Reid, D. (1969) The beginnings of bronchitis. Proc. Roy. Soc. Med. 62:311–316. Reid, D.D. (1956) General epidemiology of chronic bronchitis. Proc. Roy. Soc. Med. 49:767–771. Reid, D.D. and A.S.Fairbairn (1958) The natural history of chronic bronchitis. Lancet 1: 1147–1152. Ridker, R.G. (1967) Economic Costs of Air Pollution. New York: Praeger, 241 pp.

OCR for page 58
Air Quality and Stationary Source Emission Control Rosenbaum, S. (1961) Home localities of national servicemen with respiratory disease. Brit. J. Prev. Soc. Med. 15:61–67. Rumford, J. (1961) Mortality studies in relation to air pollution. Amer. J. Pub. Health 51:165–173. Rylander, R. (1969) Alterations of lung defense mechanisms against airborne bacteria. Arch. Environ. Health 18:551–555. Rylander, R. (1970) Studies of lung defense to infections in inhalation toxicology. Arch. Int. Med. 126:496–499. Rylander, R., M.Ohrstrom, P.A.Hellstrom, and R.Bergstrom (1971) SO2 and particles—synergistic effects on guinea-pig lungs, pp. 535–541. In W.H.Walton, Ed. Inhaled Particles III. Proceedings of an International Symposium organized by the British Occupational Hygiene Society in London, 14–23 September, 1970. Surrey, England: Unwin Brothers, Limited. Schimmel, H. and L.Greenburg (1972) A study of the relation of pollution to mortality. New York City, 1963–1968. J. Amer. Pollut. Control Assoc. 22:607–616. Schimmel, H., T.J.Murawski, and N.Gutfeld (1974) Relation of pollution to mortality. New York City, 1963–1972. Presented at the 67th Annual Meeting, Air Pollution Control Association, Denver Colorado, June 9–13. Schneider, L.K. and C.A.Calkins (1970) Sulfur dioxide-induced lymphocyte defects in human peripheral blood cultures. Environ. Res. 3:473–483. Schrenk, H.H., H.Heimann, G.D.Clayton, W.Gafafer, and H.Wexler (1949) Air Pollution in Donora, Pennsylvania. Epidemiology of the Unusual Smog Episode of October 1948. Public Health Bulletin 306. Washington, D.C.: U.S. Government Printing Office, 173 pp. Shapiro, R. R.E.Servis, and M.Welcher (1970) Reactions of uracil and cytosine derivatives with sodium bisulfite. A specific deamination method. J. Amer. Chem. Soc. 92: 422–424. Shy, C.M., V.Hasselblad, R.M.Burton, C.J.Nelson, and A.A.Cohen (1973) Air pollution

OCR for page 58
Air Quality and Stationary Source Emission Control effects on ventilatory function of U.S. schoolchildren. Results of studies in Cincinnati, Chattanooga, and New York. Arch. Environ. Health 27:124–128. Shy, C.M., C.J.Nelson, F.B.Benson, W.B. Riggan, V.A.Newill, and R.S.Chapman (1974) Ventilatory function in schoolchildren: 1967–1968 testing in Cincinnati neighborhoods, pp. 6–3 to 6–14. In U.S. Environmental Protection Agency, Office of Research and Development. Health Consequences of Sulfur Oxides: A Report from CHESS, 1970–1971. EPA-650/1–74–004. Washington, D.C.: U.S. Government Printing Office. Shy, C.M., V.Hasselblad, J.F.Finklea, R.M. Burton, M.Pravda, R.S.Chapman, and A.A.Cohen (1974) Ventilatory function in schoolchildren: 1970–1971 New York studies, pp. 4–109 to 5–119. In U.S. Environmental Protection Agency, Office of Research and Development. Health Consequences of Sulfur Oxides: A Report from CHESS, 1970–1971. EPA-650/1–74–004. Washington, D.C.: U.S. Government Printing Office. Spicer, W.S. and D.H.Kerr (1966) Variation in respiratory function. Arch. Environ. Health 12:217–226. Spicer, W.S. and D.H.Kerr (1970) Effects of environment on respiratory function. Arch Environ. Health vol. 21:635–642. Sprague, H.A. and R.Hagstrom (1969) The Nashville air pollution study: Mortality multiple regression. Arch. Environ. Health 18:503–507. Stebbings, J.H., Jr. (1971) Chronic respiratory disease among nonsmokers in Hagerstown, Maryland. IV. Effects of urban residence on pulmonary function values. Environ. Res. 4:283–304. Sterling, T.D., S.V.Pollack, and J.Weinkam (1969) Measuring the effect of air pollution on urban morbidity. Arch. Environ. Health 18:485–495. Stocks, P. (1959) Cancer and bronchitis mortality in relation to atmospheric deposit and smoke. Brit. Med. J. 1:74–79.

OCR for page 58
Air Quality and Stationary Source Emission Control Stocks, P. (1960) On the relations between atmospheric pollution in urban and rural localities and mortality from cancer, bronchitis and pneumonia, with particular reference to 3:4 benzopyrene, beryllium, molybdenum, vanadium and arsenic. Brit. J. Cancer 14:397–418. Sultz, H.A., J.G.Feldman, E.R.Schlesinger, and W.E.Mosher (1970) An effect of continued exposure to air pollution on the incidence of chronic childhood allergic disease. Amer. J. Pub. Health 60:891–900. Summers, G.A. and J.W.Drake (1971) Bisulfite mutagenesis in bacteriophage T4. Genetics 68:603–607. Thomas, O.C. and J.P.McGovern (1971) Air pollution and respiratory allergic disease. Southern Medical Journal vol. 65, no. 12:1453–1458. Thompson, J.R. and D.M.Pace (1962) The effects of sulfur dioxide upon established cell lines cultivated in vitro. Canad. J. Biochem. Physiol. 40:207–217. Toyama, T. (1964) Air pollution and its health effects in Japan. Arch. Environ. Health 8:153–173. U.S. Department of Health, Education, and Welfare (1974) Mortality Trends for Leading Causes of Death, United States. 1950–1969, (p. 39) Vital and Health Statistics, Series 20, No. 16 (HRA) 74–1853. Washington, D.C.: U.S. Government Printing Office. U.S. Environmental Protection Agency (1974) Office of Research and Development. Health Consequences of Sulfur Oxides: A Report from CHESS, 1970–1971. EPA-650/1–74–004. Washington, D.C.: U.S. Government Printing Office, 420 pp. Verma, M.P., F.J.Schilling, and W.H.Becker (1969) Epidemiological study of illness absences in relation to air pollution. Arch. Environ. Health 18:536–543. Waddell, T.E. (1973) The Economic Damages of Air Pollution. EPA-R5–73. National Environmental Research Center, Office of Research and Monitoring, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina.

OCR for page 58
Air Quality and Stationary Source Emission Control Wehrle, P.F. and D.I.Hammer (1974) Summary Report: Illnesses of Children. Presented at American Medical Association Air Pollution Medical Research Confernece, December 5–6, San Francisco, California. Weill, H., M.M.Ziskind, V.Derbes, R.Lewis, R.J.M.Horton, and R.O.McCaldin (1964) Further observations on New Orleans asthma. Arch. Environ. Health 8:184–187. Williams, J.R. and C.G.Justus (1974) Evaluation of nationwide health costs of air pollution and cigarette smoking. J. Air Pollut. Control Assoc. 24:1063–1066. Winkelstein, W., Jr. (1970) Utility or futility of ordinary mortality statistics in the study of air pollution effects, pp. 539–554. In Proceedings of the Sixth Berkeley Symposium on Mathematical Statistics and Probability, University of California, University of California Press, June and July. Winkelstein, W., Jr. and S.Kantor (1969) Respiratory symptoms and air pollution in an urban population of northeastern United States. Arch. Environ. Health 18:760–767. Winkelstein, W., Jr. and S.Kantor (1969) Stomach cancer. Positive association with suspended particulate air pollution. Arch. Environ. Health 18:544–547. Winkelstein, W., Jr., S.Kantor, E.W.Davis, C.S.Maneri, and W.E.Mosher (1967) The relationship of air pollution and economic status to total mortality and selected respiratory system mortality in men. I. Suspended particulates. Arch. Environ. Health 14:162–171. Winkelstein, W., Jr., S.Kantor, E.W.Davis, C.S.Maneri, and W.E.Mosher (1968) The relationship of air pollution and economic status to total mortality and selected respiratory system mortality in men. II. Oxides of sulfur. Arch. Environ. Health 16:401–405. Wolozin, H. (ed.) (1966) The Economics of Air Pollution. A Symposium. New York: W.W. Norton and Company, Inc. Zarkower, A. (1972) Alterations in antibody response induced by chronic inhalation of

OCR for page 58
Air Quality and Stationary Source Emission Control sulfur dioxide and carbon. Arch. Environ. Health 25:45–50. Zavrotskii, V.K. (1959) Effect of chronic low concentration sulfur dioxide poisoning on the immuno-biological reactivity of rabbits. Gig. Sanit. 24:21–25. Zeidberg, L.D., R.A.Prindle, and E.Landau (1961) The Nashville air pollution study. I. Sulfur dioxde and bronchial asthma. A preliminary report. Amer. Rev. Respiratory Dis. 84:489–503. Zeidberg, L.D., R.A.Prindle, and E.Landau (1964) The Nashville air pollution study. III. Morbidity in relation to air pollution. Amer. J. Public Health 54:85–97. Zeidberg, L.D., R.J.M.Horton, and E.Landau (1967) The Nashville air pollution study. V. Mortality from diseases of the respiratory system in relation to air pollution. Arch. Environ. Health 15:214–224. Zeidberg, L.D., R.J.M.Horton, and E.Landau (1967) The Nashville air pollution study. VI. Cardiovascular disease mortality in relation to air pollution. Arch. Environ. Health 14:225–236. Zweiman, B., R.G.Slavin, R.J.Feinberg, C.J.Falliers, and T.H.Aaron (1972) Effects of air pollution on asthma: A review. J. Allergy Clin. Immunol. 50:305–314.