Infant Susceptibility of Mortality to Air Pollution in Seoul, South Korea
* Department of Preventive Medicine, College of Medicine, Ewha Medical Research Center, Ewha Womans University, Seoul, South Korea
Department of Epidemiology and Biostatistics and Institute of Health and Environmental Sciences, School of Public Health, Seoul National University, Seoul, South Korea
Department of Occupational and Environmental Medicine, College of Medicine, Inha University, Incheon, Korea
|| Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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Objective. Susceptibility of target populations to air pollution is an important issue, because air pollution policies and standards should be based on the susceptibilities of those at particular risk. To evaluate which age group is more susceptible to the adverse health effects of air pollution, we compared the effects of air pollution on mortality among postneonates, those aged 2 to 64 years, and those over 65 years of age.
Design. Daily counts of total and respiratory death along with daily levels of meteorological variables and air pollutants were analyzed using generalized additive Poisson regression. The relative risks (RR) of mortality for interquartile changes of the levels of particulate matter <10 µm (PM10) were calculated on the same day.
Results. For postneonates, the RR of total mortality for an interquartile change (42.9 µg/m3) in PM10 (RR: 1.142; 95% confidence interval [CI]: 1.096–1.190) was greatest among age groups. Next were the elderly over 65 years of age (RR: 1.023; 95% CI: 1.022–1.024). Regarding respiratory mortality, RR for an interquartile change of PM10 in postneonates (RR: 2.018; 95% CI: 1.784–2.283) was also greater than those in the other groups.
Conclusions. These results agree with the hypothesis that infants are most susceptible to PM10 in terms of mortality, particularly respiratory mortality.
Key Words: infant mortality • air pollution • PM10 • Seoul
Abbreviations: TSP, total suspended particle • CO, carbon monoxide • NO2, nitrogen dioxide • SO2, sulfur dioxide • O3, ozone • RR, relative risk • PM10, particles <10 µm in aerodynamic diameter • ppm, parts per million • ppb, parts per billion • CI, confidence interval
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INTRODUCTION |
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It has long been known that air pollution is associated with adverse health effects, morbidity, and mortality among humans.1–3 In particular, the elderly, infants, and persons with chronic cardiopulmonary disease, influenza, or asthma are considered susceptible to air pollution.4,5 Several studies of the effects of air pollution on mortality and morbidity have supported this susceptibility among the elderly.1,6–8 The increased mortality in London in 1952 was higher among the elderly, in terms of deaths from respiratory and cardiovascular diseases.1 Similar findings have been also reported in Philadelphia,1 Mexico,6 Edinburgh,7 and Quebec.8 In terms of effect size, the risk of mortality was about 3 times greater in persons older than 65 years of age than in persons younger than 65 for the increase of the total suspended particle (TSP) concentrations.1
Much of the evidence on susceptibility to air pollution involves its effects on the elderly population. However, there is less evidence about the susceptibility of infants to air pollution, although effects of air pollution on infants have more implications than those on any other age groups. Recently, a number of studies have dealt with mortality associated with air pollution, and have found that infants would be more susceptible to air pollution than the general population.5,9–11 In addition, Pope et al4 reported that earlier age of onset of the effects of fine particles result in greater overall loss of life, using the survival curve.
In response to air pollution exposure, different age groups may respond differently.12 Who is at risk or who is more susceptible to the adverse health effects of air pollution is an important question for air pollution management. However, the question of which age group is more susceptible to the adverse health effects of air pollution has not been fully considered. In this study, we compared the effect of air pollution on mortality among postneonates, those aged 2 to 64 years, and on those over 65 years of age.
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METHODS |
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Mortality Data
Daily records of mortality in Seoul were obtained from the Korean National Death Registry for the period January 1995 to December 1999. It provided the date of birth, place of residence, date of death, and the underlying cause. We used the code of the International Classification of Diseases, 10th Revision for the cause of death. Daily counts of total mortality were divided into 3 age groups: 1) aged 1 month to 1 year (postneonates), 2) aged 2 to 64 years, and 3) those over 65 years of age. We excluded neonates from this analysis, because neonates are influenced easily by perinatal conditions.13 We also excluded accidental deaths. In addition to total mortality, we calculated mortality from respiratory disease for each age group.
Exposure Assessment
Seoul is the largest metropolitan city in the country and is divided into 25 administrative areas. It has a distinct 4-season climate, and the major air pollution sources are the automobile exhaust and domestic heating. The Ministry of Environment provided data on air pollution.
Exposure measurements during the study period were taken from 27 monitoring sites, which represented all administrative areas. Measurements of particles <10 µm in aerodynamic diameter (PM10; ß-ray absorption method), carbon monoxide (CO; nondispersive infrared photometry), nitrogen dioxide (NO2; chemiluminescence), sulfur dioxide (SO2; ultraviolet photometry), and ozone (O3; ultraviolet photometry) were undertaken hourly. Twenty-four-hour pollutant concentration averages were constructed for the measurement sites. In the case of ozone, a daytime 8-hour average was used instead of a 24-hour average. Meteorological information from a station in the central part of Seoul was obtained from the National Meteorological Office. This included 24-hour average temperature and relative humidity.
Except for occasionally missing or excluded observations, data for air pollution and meteorological parameters were available for the period from January 1, 1995, to December 31, 1999.
Statistical Analysis
The mortality and exposure data were merged to create an analysis file with days as the units of observation. To compare the mortality among age groups, age-stratified analyses were performed for both total and respiratory mortality. To allow for nonlinear relations between mortality and predictor variables, we used a generalized additive model.14 To control long-term trends, seasonality, and meteorological influences (temperature and relative humidity), we used smoothing parameters with LOESS (locally-weighted smoother) function in S-PLUS.15 The Loess smoother that was used in this study has particular local behavior and therefore picked up awkward shapes in the data well.16 Dummy variables were used to allow for day-of-the-week and holiday effects. We added the individual pollutant concentrations of the same day, 1 to 7 lagged-days, or moving averages from 1 to 5 days. Because the best fit was obtained by Akaike’s information criteria, the concentrations of the same day for air pollutants were used. We analyzed with the same day levels of air pollutants in the results. In addition, we inserted autoregressive terms in the model to remove serial correlations of residuals when the remaining variation has systematic pattern.12
To compare the effect magnitude of pollutants on mortality, we calculated the relative risk (RR) of total or respiratory mortality for interquartile changes of levels of PM10 and other air pollutants for each age group.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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In total, 1045 postneonates, 67 597 persons aged 2 to 64 years, and 100 316 elderly over 65 years died during the study period. The average deaths per day were 0.6, 37.1, and 54.9, respectively (Table 1).
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Table 2 shows summary statistics of air pollution and weather in Seoul from 1995 to 1999. The 24-hour mean concentrations were 1.2 parts per million (ppm) for CO, 32.5 ppb for NO2, 11.1ppb for SO2, and 69.2 µg/m3 for PM10. The 8-hour average O3 level was 21.2 parts per billion (ppb).
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Table 3 shows the correlation matrix for the air pollutant concentrations during the study period. The concentrations of CO, NO2, SO2, and PM10 were positively correlated with each other (0.61 < r < 0.73). However, the concentration of O3 was negatively correlated with the other pollutants.
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Figure 1 shows plots of the relation between air pollutants and total death by age group. To allow direct comparison of the slope, the scale of Y axes are the same. For all age groups, total deaths increased with concentrations of PM10. In particular, the effect of PM10 on total mortality in postneonates was much greater than those in the other groups. The RR of total mortality for an interquartile change of PM10 was calculated on the same day (Table 4). For postneonates, RR of total mortality (RR: 1.142; 95% confidence interval [CI]: 1.096–1.190) for PM10 was highest among the age groups. This was followed by RR in the old age group over 65 (RR: 1.023; 95% CI: 1.022–1.024), and the least affected was the age 2 to 64 age group (RR: 1.008; 95% CI: 1.006–1.010). Figure 2 shows plots of the relation between air pollutants and respiratory deaths by age group. For respiratory disease, the relation between air pollutants and deaths are consistent with the result for total mortality. With respect to the effect size (Table 5), RR of respiratory mortality for an interquartile change of PM10 in postneonates (RR: 2.02; 95% CI: 1.78–2.28) was greater than that of total mortality. In addition, CO levels were significantly associated with respiratory-specific death, and the magnitude of risk was also largest in postneonates (RR: 1.39; 95% CI: 1.01–1.91).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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Researches in several countries have shown that infants are considered particularly susceptible to particulate air pollution (Table 6). Annual infant mortality rates in the Czech Republic were associated with annual average concentrations of TSP.10,17 In the United States, the odds ratio of overall postneonatal mortality in 86 cities was 1.04 for each 10 µg/m3 rise in PM10,11 and in Mexico City, excess infant mortality was associated with the level of environmental fine particles in the days before death.5
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In this study, we found that postneonatal infants are most susceptible to PM10 in terms of mortality, especially of respiratory mortality. Postneonatal mortality increased by 14.2% for each 42.9 µg/m3 rise in PM10. Although mortality of other groups was significantly associated with PM10, the effect size was smaller, 0.8% in persons aged 2 to 64 years and 2.3% in those over 65. Regarding the cause of death for postneonatal infants, PM10 had a greater effect on respiratory mortality than on total mortality, with an estimated risk ratio of 2.02 (95% CI: 1.78–2.28). This finding is consistent with the analyses of Bobak,10,16 who found that the effects of TSP on postneonatal mortality were greater and specific for respiratory causes.
Particulate air pollution is known to invoke alveolar inflammatory mediators and to increase blood viscosity, thereby leading to acute episodes of respiratory or cardiac death.18–23 Many studies on air pollution and mortality among adults or the elderly have dealt with respiratory mortality and cardiac mortality.6,8,24 An association between PM2.5 and respiratory mortality was found in Quebec among individuals older than 65 years at the time of death.8 Similar patterns were observed for respiratory deaths associated with fine particles 4 days previously in Mexico City.6 In Philadelphia, the risk of chronic obstructive pulmonary disease mortality associated with TSP was 3 times the risk of all-cause mortality.1 The mortality associated with increases in PM10 has been attributed to the exacerbation of preexisting lung disease in older individuals.25
Children or infants are reported to respond differently to particulate exposure from adults. Particulate air pollution was positively associated with respiratory hospital admission with bronchitis and asthma among children.12,13,26–28 We hypothesized that infants are more vulnerable to respiratory disease leading to death from particulate air pollution, because the infant lung and immune system is immature and unable to control adequately the inflammation resulting from exposure to ambient particle.12 Several studies indicated that the effects of air pollution on postneonatal respiratory mortality were greater than those on all-cause mortality. Expressed per 50 µg/m3 increase in TSP, the adjusted rate ratios for postneonatal respiratory mortality were 2.11 (95% CI: 1.35–3.29) and 1.95 (95% CI: 1.09–3.50) in 2 Czech studies10,16 and 1.58 (95% CI: 1.16–2.11) in the United States.11 These rate ratios are close to the increased risk of postneonatal respiratory mortality found in our analysis, which was 2.02 (95% CI: 1.78–2.28) for an increase of 42.9 µg/m3 in PM10.
In addition, our study showed that the increase in respiratory mortality was associated with CO exposure, and the risk estimates were also largest in postneonates. In agreement with this finding, Conceicao et al also reported that CO level was associated with mortality attributable to respiratory disease in children under 5 years.29 Saldiva et al30 found increased risk for respiratory mortality in children exposed to high levels of CO, although it did not reach statistical significance.
Our study has some limitations.31–34 First, environmental monitoring data do not necessarily represent individual exposures. However, this kind of measurement error is known to cause a bias toward the null and to underestimate pollution effects. Second, individual risk factors, such as underlying disease or exposure to smoking and infectious agents, were not considered in this analysis. However, there is no reason to believe that daily variations in the individual risk factors correlate with daily changes in air pollution; therefore, they are unlikely to be confounders in this time-series study. Third, the main cause of postneonatal death was congenital anomalies, which could confound the association between air pollution and mortality. We examined the association between death attributable to congenital anomalies and air pollution, however, we could not find any significant association between them (RR: 0.94; 95% CI: 0.84–1.05). Therefore, it would not confound the association between air pollution and mortality.
In addition, low temperature could be associated with excess deaths as well as air pollution episodes, confounding the association between air pollution and mortality. We controlled the short-term and prolonged effects of low temperature by adding the temperatures of the same day in addition to the seasonal factor in the analysis.
To our knowledge, this is the first study to determine that infants are the most susceptible age group after directly comparing with other age groups. This result has serious implications on the air pollution criteria, which should be based on the effects on infant health rather than adult health.
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ACKNOWLEDGMENTS |
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This study was supported by grant 2000-0-219-003-2 from the Basic Research Program of the Korea Science and Engineering Foundation.
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FOOTNOTES |
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Received for publication Dec 27, 2001; Accepted Jul 1, 2002.
Reprint requests to (E-H.H.) Department of Preventive Medicine, College of Medicine, Ewha Womans University, 911-1, Mok-6-Dong, Yangcheon-Gu, Seoul, South Korea 158-710. E-mail: eunheeha{at}ewha.ac.kr
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