The relationship of air pollution to ED visits for asthma differ between children and adults
Original Contribution
The relationship of air pollution to ED visits for asthma differ between children and adults
Hai-Lun Sun MDa,b, Ming-Chieh Chou MD, PhDb, Ko-Huang Lue MDa,b,*
aDepartment of Pediatrics, Chung Shan Medical university hospital, Taichung 402, Taiwan
bInstitute of Medicine, Chung Shan Medical University Hospital, Taichung 402, Taiwan
Received 7 December 2005; revised 3 March 2006; accepted 4 March 2006
Abstract
The purpose of this study was to evaluate the relationship between air pollution and asthma exacerbation in children and adults. Pearson analysis was used to establish correlations between air pollutants—sulfur dioxide, Nitrogen dioxide, ozone, carbon monoxide, and particles with an aerodynamic diameter of 10 lm or less (PM10)-and ED visits for asthma in 2004. Among children, there were significant positive correlations between nitrogen dioxide (r = 0.72), carbon monoxide (r = 0.65), and PM10 (r = 0.63) and ED visits for asthma. Among adults, only weakly positive, non significant correlations between all air pollution measures and ED visits for asthma were found. This study suggests that air pollution plays a role in acute exacerbation of asthma in children but not in adults.
D 2006
Introduction
The prevalence of bronchial asthma has been increasing in many countries, the reasons as yet uncertain. Many factors, however, contribute to the exacerbation of asthma, including Respiratory tract infections, stress, exposure to allergens such as plant pollen and fungal spores, extreme Weather conditions, and air pollution [1-4]. ED visits for asthma are an indicator of asthma exacerbation. Several studies have assessed the relationship between levels of air pollution and asthma exacerbation, most of which have found positive associations between ED visits for asthma and levels of air pollutants in children [5-8]. Children spend more time outdoors and exercise more, thereby breathing in
* Corresponding author. Department of Pediatrics, Chung Shan Medical University Hospital, Taichung, Taiwan. Tel.: +886 4 24739595×34816; fax: +886 4 24710934.
E-mail address: [email protected] (K.-H. Lue MD).
a greater amount of pollution per pound of body weight than adults [9]. Furthermore, air pollutants may impair organo- genesis and other developmental processes in children. On the other hand, there are few studies investigating associ- ations between air pollution and asthma exacerbation in adults. Is there any difference in asthma attacks due to air pollution between children and adults? The purpose of this study was to evaluate the relationship between air pollution and ED visits for acute exacerbation of asthma in children and adults.
Methods
Data source
The National Health Insurance Research Database served as the data source for this study. The information in each computerized claim form included patients’ personal
0735-6757/$ - see front matter D 2006 doi:10.1016/j.ajem.2006.03.006
identification numbers (ID), age, sex, medical care institu- tions, and diagnosis. Both personal and medical care ins- titutions’ IDs in the database were scrambled in compliance with the Personal Electronic Data Protection Law in Taiwan.
Patients
Data were collected on all diagnoses for all patients younger than 55 years from January 1 to December 31, 2004, in 4 medical centers in central Taiwan. Patients older than 55 years were excluded because of a higher prevalence of chronic obstructive pulmonary disease. Individuals were included who had a diagnosis of asthma (International Classification of Diseases, Ninth Revision, Clinical Modi- fication code 493.xx) as a principal or secondary condition made at an ED visit. A maximum of 3 diagnoses could be listed. The study population was divided into a children (younger than 16 years) and an adult group (16-55 years).
Outdoor air pollution monitoring
Complete monitoring data for the air pollutants included sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone(O3), carbon monoxide (CO), and particles with an aerodynamic diameter of 10 lm or less (PM10). They were available from 11 Environmental Protection Agency monitoring stations in central Taiwan, located within 5 kilometers of the 4 medical centers in 2004. Concentrations of each pollutant were measured continuously and reported hourly-CO by non- dispersive infrared absorption, NO2 by chemiluminescence, O3 by ultraviolet absorption, SO2 by ultraviolet fluores- cence, and PM10 by b-gauge. The average monthly concentration of each air pollutant was calculated for 2004.
Statistical analysis
Data analysis was performed with the SPSS 12.0 for Windows software package (SPSS, Chicago, Ill). Pearson’s analysis was used to establish correlations (r) between each air pollutant and the number of ED visits for asthma. Multiple Correlation coefficients (R) (multiple regression analysis) were used to explain how much of the variance in the ED visits could be explained by a given set of air pollutants. P values (for F statistics) were calculated to
Fig. 1 Total numbers of asthmatic children and adult seen each month in the ED.
Fig. 2 Monthly mean of different airborne pollution counts. (A) CO; (B) SO2; (C) NO2, O3, and PM10.
determine the significance of regression relationships. P b.05 was considered significant.
Results
Fig. 1 shows the total number of ED visits for children and adults due to acute asthma in each month during 2004. In general, there were more ED visits due to asthma in the winter and spring and fewer during summer and early autumn in the children’s group. Except for fewer ED visits due to asthma in late spring and early summer, there was little variation in the adult group.
The distributions of the monthly mean air pollutant concentrations for the 11 monitoring stations are presented in Fig. 2. Most of the variation in air pollutant concen- trations was seen in PM10, whereas O3 and NO2 showed only slight lower concentrations in summer months. Sulfur
Table 1 Pearson correlation coefficient (r) between ED visits of asthmatic patients and the various environmental |
|||||
Factor |
Children r |
P |
Adult r |
P |
|
SO2 (ppb) |
0.128 |
.346 |
.423 |
.085 |
|
NO2 (ppb) |
0.72 |
.004 |
.428 |
.083 |
|
O3 (ppb) |
0.434 |
.079 |
.031 |
.462 |
|
CO (ppm) |
0.653 |
.011 |
.425 |
.084 |
|
PM10 (Ag/m3) |
0.626 |
.015 |
.384 |
.109 |
|
P b .05 means significant. |
dioxide and CO concentrations were nearly constant all throughout the year.
The cumulative total number of ED visits for asthma every month was compared with the corresponding cumu- lative mean of each of the air pollutants (Table 1). Significant ( P b .05) positive correlations were found between ED visits for asthma and the mean ambient concentrations of CO (r = 0.65), PM10 (r = 0.63), and NO2 (r = 0.72) in the
children’s group. There were no significant correlations in the adult group for any of the air pollutants.
Discussion
emergency visits for asthma increased with increased annual levels of 3 related pollutants (CO, NO2, and PM10) in children but not for any pollutants in adults in the present study.
Diesel- and gasoline-powered vehicular engines and coal- and oil-fired power plants are the main sources of ambient NO2 emissions, which typically result from the fixation of nitrogen in the air during high-temperature combustion [9]. Several studies have shown that NO2 is a risk factor for exacerbation of asthma in children. The risks of respiratory tract symptoms were associated with increased ambient NO2 in London and Japan [10,11]. In a cohort of infants living in New England, van Strien et al found that infants exposed to more than 17.4 ppb NO2 had significantly increased risk for respiratory diseases compared with those exposed to lower levels of NO2 [12]. Furthermore, in Santa Clara, Calif, NO2 levels were associated with childhood asthma exacerbations [13]. Chauhan et al [14] showed that increased indoor NO2 exposure was associated with increased severity of viral-induced exacerbation of asthma. There were about 23 million people living in Taiwan, an island of 12600 square miles, in 2004. The most popular modes of transportation were motorcycles and cars because of the lack of rapid mass transit systems, especially in central Taiwan. People frequently used gasoline-powered vehicles, which resulted in mean air concentrations of NO2 more than 20 ppb and as high as 26 ppb in 7 months in 2004 (Fig. 2). Our results are consistent with previous studies; NO2 was strongly correlated with acute asthma exacerbation in children.
In Helsinki, where air pollution levels are lower, Ponka
[15] found that NO2 and CO were strongly associated with ED visits and hospital admissions for asthma in 1991. In Rome, where air pollution comes mostly from motor vehicles, Fusco et al [16] also found that CO was associated with most of the respiratory conditions in all ages, and it remained an independent predictor in multipollutant analy- sis for total admissions. In our study, CO was also significantly associated with asthma exacerbation in chil- dren. Similar to NO2, CO is another marker of air pollution directly related to heavy traffic.PM10 was associated with increased ED visits from asthma in children. PM10 is a heterogeneous mixture of small solid or liquid particles of varying composition found in the atmosphere. In general, it is divided into 2 categories by Particle size: fine (diameter b2.5 lm) and coarse (diameter between 2.5 and 10 lm). Fine particles are emitted from combustion processes (such as power gener- ation, wood burning, and diesel-powered engines) and some from industrial activities. Coarse particles include wind- blown dust from dirt roads or soil and dust particles created by crushing and grinding operations [17]. Both fine and coarse particles have adverse effects on health. A positive association with PM10 has been reported by Pope [6] in the Utah valley where Hospital admission rates for asthma increased significantly during the periods when the local steel mill, the main source of particles, was operating. Schwartz et al [18], in Seattle, a city with low concentrations of PM10, found a positive and significant effect of this pollutant on emergency visits for asthma. But, there was similar regression coefficients for PM10 for age younger than 65 years in both children and adult groups. The destruction of the World Trade Center in New York City on September 11, 2001, released vast amounts of toxic material into the air. In general, air concentrations were highest on September 11 and in the first days and weeks thereafter, but PM from the World Trade Center fires remained in the air until all the fires were finally extinguished December 2001. New cases of asthma and exacerbations of existing cases have been reported in children despite pediatricians’ advise to parents and children in lower Manhattan to stay indoor and minimize outdoor exercise after September 11 [9]. This episode proves, once again, the unique vulnerability of children to outdoor air pollutants.
Neither SO2 nor O3 were significantly associated with
ED visits for asthma in our study. Our findings for SO2 and O3 are consistent with the results of Castellsague et al [19] in Barcelona where no association was observed. Another study in Taiwan, based on a nationwide survey of asthma prevalence in middle-school children, showed no consistent relationship with O3 and sulfur [20]. Similarly, the Seattle study showed SO2 was not related to ED visits for asthma, although in this city, the station monitoring SO2 levels was not representative of the population exposure [18]. In contrast, negative correlations were found between O3 concentrations and asthma visits in some studies [11,21].
Acute asthma attacks may have been relatively rare during the summer months when O3 levels were highest because of other factors such as low community rates of respiratory tract infections and relatively low pollen counts. White et al [22], who found that peak O3 concentrations greater than
0.11 ppm correlated with asthma visits to ED, also found there was no such correlations at peak O3 concentrations below 0.11 ppm. Annual temperatures in Taiwan were around 23.28C F 0.18C, especially in central Taiwan. Because of minimal variation in temperatures, O3 concen- trations may not have been as affected as in other countries. Unlike the children in our study, there were no significantly positive correlations between ED visits for asthma and air pollution in the adults. This may be because of the vulnerability of children to the adverse affects of air pollution compared with adults. Organogenesis of the lungs begins in fetal life and is especially rapid in early childhood. Eighty percent of alveoli are formed postnatally, and changes in the lungs continue through adolescence [23]. Posing further problems is the incomplete development of lung epithelium causing increased permeability of the epithelial layer in young children. Exposure to air pollution alters the normal developmental process, leading to greater lung damage, which may have a lasting effect on respiratory health. In addition, air pollution may affect the child’s developing immune system. Molecular studies suggest that environmental exposures influence the development of humoral immunity-dominant (TH2) vs cellular immunity-
dominant (TH1) phenotypes [24].
Children have increased exposure to many air pollutants compared with adults because of higher minute ventilation and higher levels of physical activity. In California, children were found to spend an average of 124 min/d participating in active sports, walking-hiking, or outdoor recreation, more than 5 times the 21 min/d spent by adults engaging in the same activities [9]. Children spend more time outdoors than adults, so they have increased exposure to outdoor air pollution. The peripheral airways of infants are more susceptible to inflammatory narrowing than those of adults [25]. In infancy the chest wall is nearly 3 times as compliant as the lung, and by the second year of life, chest wall stiffness increases to the point that the chest wall and lung compliance are nearly equal as in adults [26]. Thus, irritation caused by inhaled air pollution can result in proportionally greater airway obstruction and fatigue of breathing muscles than in adults. occupational exposures, smoking habits, stress, emotional factors, and systemic diseases are other major confounders in adult asthmatic patients and may explain why outdoor air pollution was not associated with ED visits in the adults in our study.
There were some limitations in our study. First, this is a retrospective study. Inclusion was completely dependant on the final coding of the claim data. If mistakes were made in the final diagnosis coding, patients could have been inappropriately included or excluded from the study. We did not review the charts to evaluate the accuracy of the
diagnosis of asthma, but according to the previous studies, the mistakes were usually minimal and could be ignored [27,28]. Second, some adults with asthma may not go to the ED for an asthma attack, rather, they may self-treat with an inhaled bronchodilator or oral steroid at home. Only if symptoms persist or severe exacerbate would they ever visit the ED for treatment. In contrast, parents may worry more about asthma exacerbation of their children; they may perhaps rush to the ED with just mild wheezing or shortness of breath, especially in the first couple years of asthma diagnosis. For this reason, we may have underestimated the real frequency of asthma exacerbations in adults. Thirdly, only outdoor exposures were assessed, although personal exposure to some pollutants such as NO2 also occurs indoors at levels sometimes higher than those found outdoors. The lack of personal exposure data for both indoor and outdoor pollutants prohibited analysis comparing individual exposure and asthma exacerbation. Data from German and Mexican cities provide consistent evidence that the outdoor NO2 level is a better predictor of exposure than the personal NO2 level [29,30]. Therefore, further studies using the adjusted mean level of air pollutants in every month to determine relationships with the asthma attacks might be necessary. Finally, in this study, no informa- tion was collected on fungal spore, pollen spore, viral epidemics, and barometric pressure, although they have also been associated with the triggering of asthma attacks [1-4]. Thus, the relationship between concentrations of air pollution and asthma exacerbation rate is mainly driven by the pollination period, yet there could also be subtle relationship for susceptible persons with asthma that should be deeply examined using the data at individual levels in another research.
In summary, the present study provides additional evidence that exposure to outdoor air pollutants increases the risk of childhood asthma ED visits. Our study also showed a significant association between NO2, CO, and PM10 and asthma exacerbation for children. These results suggest that emissions from motor vehicles may play an important role. Similar associations were not found in the adults, possibly because many other factors such as smoking habits and occupational exposures might contrib- ute to adult asthma.
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