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Erschienen in: Environmental Health and Preventive Medicine 1/2019

Open Access 01.12.2019 | Research article

Association between gaseous pollutants and emergency ambulance dispatches for asthma in Chengdu, China: a time-stratified case-crossover study

verfasst von: Jianyu Chen, Xianyan Jiang, Chunli Shi, Ruicong Liu, Rong Lu, Li Zhang

Erschienen in: Environmental Health and Preventive Medicine | Ausgabe 1/2019

Abstract

Objectives

The association between concentrations of sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), ozone (O3), and emergency ambulance dispatches (EADs) for asthma was explored in the central Sichuan Basin of southwestern China for the first time.

Methods

EADs for asthma were collected from the Chengdu First-Aid Command Center. Pollutant concentrations were collected from 24 municipal environmental monitoring centers and including SO2, NO2, CO, daily 8-h mean concentrations of O3 (O3-8 h), and particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5). The climatic data were collected from the Chengdu Municipal Meteorological Bureau. All data were collected from years spanning 2013–2017. A time-stratified case-crossover design was used to analyze the data.

Results

After controlling for temperature, relative humidity, and atmospheric pressure, IQR increases in SO2 (13 μg/m3), NO2 (17 μg/m3), and CO (498 μg/m3) were associated with 18.8%, 11.5%, and 3.1% increases in EADs for asthma, respectively. The associations were strongest for EADs and SO2, NO2, and CO levels with 3-, 5-, and 1-day lags, respectively.

Conclusions

This study provides additional data to the limited body of literature for potential health risks arising from ambient gaseous pollutants. The results of the study suggest that increased concentrations of SO2, NO2, and CO were positively associated with emergency ambulance dispatches for asthma in Chengdu, China. Further studies are needed to investigate the effects of individual air pollutants on asthma.
Abkürzungen
AP
Atmospheric pressure
CI
Confidence interval
CO
Carbon monoxide
EADs
Emergency ambulance dispatches
IQR
Interquartile range
NO2
Nitrogen dioxide
O3
Ozone
O3-8 h
Daily 8-h mean concentration for O3
OR
Odds ratio
PM2.5
Particulate matter less than 2.5 μm in aerodynamic diameter
SD
Standard deviation
SO2
Sulfur dioxide
tpd
Times per day

Introduction

Asthma is one of the most common chronic diseases globally. As many as 300 million people currently have asthma, and it accounts for about 1 in 250 deaths worldwide. Moreover, the prevalence and patient burden from asthma have been sharply increasing [1]. Estimates for the costs of asthma in six developed countries range from $300 to $1300 per patient per year adjusted to 1990 US dollars [2]. Additional analyses indicate that asthma is estimated to cost 1–2% of the total health care budget of developed economies. In particular, asthma prevalence is sharply rising in developing countries and regions with increasing urbanization and westernization when compared to developed countries.
Previous studies have demonstrated the relationship between ambient air pollutants and asthma [36]. For example, associations have been detected between ambient air pollutant concentrations and the rate of pediatric asthma emergency department visits in Atlanta, USA [7]. Furthermore, Cai et al. (2014) reported that sulfur dioxide (SO2) and nitrogen dioxide (NO2) levels are more associated with asthma hospitalization events in Shanghai, China compared to levels of particulate matter with aerodynamic diameters less than 10 μm (PM10) [3]. The effects of air pollutants on asthma prevalence can also be associated with specific geographic terrains, weather conditions, and ethnic populations [811]. Following these previous analyses, the goal of the present study was to evaluate the association between short-term exposure to ambient gaseous pollutants (SO2, NO2, carbon monoxide (CO), and ozone (O3)) and emergency ambulance dispatches (EADs) for asthma in a typical basin of southwestern China.
The prevalence of gaseous pollutants including SO2, NO2, CO, and O3 were evaluated in comparison with asthma prevalence in the Sichuan Basin. The Sichuan Basin is a typical basin of southwestern China and exhibits severe air pollution [12]. To our knowledge, this report is the first to investigate the association between gaseous pollutants and asthma in this region, and thus, represents an important contribution to understanding the relationship between pollution and asthma for this region, and in general. The city of Chengdu was used as the study area, which comprises a population of over 15 million people [13]. Chengdu features its own unique geographical and meteorological conditions that are due to its location at the central region of the Sichuan Basin. EADs for asthma cases were investigated that encompassed cases across the whole city owing to data from the city’s Municipal First-Aid Command System. The association between air pollutants and EADs for asthma has rarely been explored in previous studies. However, some studies have explored the associations between air pollutants and EADs for cardiovascular diseases, respiratory diseases, and other systemic diseases [14, 15]. Consequently, we conducted a time-stratified case-crossover experimental design to explore the association between ambient gaseous pollutants and EADs for asthma in the central Sichuan Basin of China for the first time.

Materials and methods

Data collection

Data for EADs from asthma were collected from the Chengdu First-Aid Command Center from 1 January 2013 to 31 December 2017. The Chengdu First-Aid Command Center responds to all emergency calls for first aid in Chengdu, dispatches ambulances to transport patients to emergency hospitals, and serves residents of the entire city. EAD records include the patient identification number, gender, age, dispatch date, patient address, address code, chief complaint, and primary diagnosis. When a patient conducts an emergency call (number 120), their primary information including gender, age, and chief complaint is queried and recorded by operators at the Chengdu First-Aid Command Center. Patient identification numbers and dispatch dates are concomitantly generated automatically by the system. Primary diagnoses for patients are obtained by return calling the emergency hospital where the patient was dispatched immediately following the diagnosis. All case data from 1 January 2013 to 31 December 2017 were initially collected, and then only those with a primary diagnosis of asthma were used further.
Air pollutant concentrations were collected from all 24 Municipal Environmental Monitoring Centers in Chengdu from 1 January 2013 to 31 December 2017 (Fig. 1) and comprised data for SO2, NO2, CO, daily 8-h mean concentrations of O3 (O3-8 h), and particulate matter with aerodynamic diameters less than 2.5 μm (PM2.5). Daily mean concentrations for SO2, NO2, CO, O3-8 h, and PM2.5 were calculated using data for each pollutant from all 24 centers. Daily 8-h mean concentrations of O3 were defined as the highest 8-h mean concentration for O3 per day. If data from one or more centers were missing for a given day, data from the other centers would be used to calculate the mean concentrations that individuals were exposed to. Numerous previous analyses have considered weather conditions as confounding factors that should be adequately controlled for [16, 17]. Therefore, climatic parameters were collected from the Chengdu Municipal Meteorological Bureau from 1 January 2013 to 31 December 2017 that included daily mean temperature, relative humidity, and atmospheric pressure.

Statistic analyses

Spearman’s correlational analyses were used to explore correlations between air pollutants and weather conditions. To estimate the association between gaseous pollutants and EADs for asthma, a time-stratified case-crossover methodology was used. The case-crossover method restricts the controls to the cases themselves. Consequently, the influence of confounding variables related to individual characteristics like gender, age, occupational hazards, smoking, and basic disease could be adequately controlled [18]. The R package “season” was used, allowing alternative values of controls to be set in the model. Time stratification was conducted to control for confounding variables due to long-term trends, seasonal patterns, and the day of the week [19]. Controls were restricted to the same weekday within the same month and year, relative to the corresponding cases. By controlling in this manner, the influences of trends due to time (long-term trends and seasonal patterns) and the day of the week are mitigated. The number of controls that were used was varied from three to four according to the number of days in a month. For example, if a case was dispatched to an emergency hospital on Friday, 23 September 2016, the case day was defined as the same day, and control days were assigned as all of the remaining Fridays in September 2016 (i.e., the 2nd, 9th, 16th, and 30th).
Delayed effects might exist between gaseous pollutant exposure and health outcomes [2022]. To assess the potential for delayed effects on EAD instances for asthma, a single-day lag model for each gaseous pollutant was conducted by ranging the lag days from one to seven.
The influence of confounding variables including daily mean temperature, relative humidity, and atmospheric pressure was controlled by using natural cubic splines (ns) in the R software environment with 3° of freedom for smoothing in all models [23].
Sensitivity analyses were conducted in several manners to assess the robustness of the results. First, the setting of controls was varied. Three controls were restricted to one case in the models, while ignoring if cases and controls originated from the same month [24, 25]. Second, a two-pollutant model was assessed for each pollutant. Third, a multi-day moving average was calculated for pollutant concentrations extending from the day of analysis and up to 3 days prior (lag 01, lag 02, and lag 03, respectively). The concentrations for each pollutant from the day of EAD to 1-, 2-, and 3-days prior were used to calculate moving average concentrations to approximate exposures, rather than calculating mean concentrations for each pollutant on each day.
Model results are presented as odds ratios (ORs) with 95% confidence intervals (95% CI) with increased concentrations of each pollutant given per interquartile range (IQR) [25, 26]. The season package for R (version 3.5.1) was used for fitting the time-stratified case-crossover model [27].

Results

A total of 2669 EADs for asthma were observed in Chengdu between 1 January 2013 and 31 December 2017. The mean concentrations of SO2, NO2, CO, O3-8 h, and PM2.5 were 21.6, 41.5, 1124.2, 92.4, and 70.5 μg/m3, respectively, while increases in their IQRs were 13, 17, 498, 74, and 53 μg/m3, respectively. The values for mean daily temperature, relative humidity, and atmospheric pressure were 17.0 °C, 77.7%, and 951.7 hpa, respectively (Table 1).
Table 1
Air pollutant, weather conditions, and emergency ambulance dispatches for asthma cases between 2013 and 2017 in Chengdu
 
Mean
SD
Min.
25%
50%
75%
Max.
IQR
SO2 (μg/m3)
21.6
10.5
6.0
14.0
20.0
27.0
71.0
13.0
NO2 (μg/m3)
41.5
13.2
13.0
32.0
39.0
49.0
89.0
17.0
CO (μg/m3)
1124.2
790.2
425.0
787.0
987.0
1285.0
16,608.0
498.0
O3-8 h (μg/m3)
92.4
49.6
11.0
54.0
82.0
128.0
285.0
74.0
PM2.5 (μg/m3)
70.5
48.9
9.0
36.0
56.0
89.0
372.0
53.0
Temperature (°C)
17.0
7.2
−1.9
10.3
17.9
23.2
30.0
12.9
Humidity (%)
77.7
9.7
41.0
72.0
78.0
85.0
98.0
13.0
AP (hpa)
951.7
7.4
933.1
945.6
951.2
957.4
977.3
11.8
EADs (tpd)
1.5
1.3
0.0
0.0
1.0
2.0
6.0
2.0
Abbreviations: SO2 sulfur dioxide, NO2 nitrogen dioxide, CO carbon monoxide, O3-8 h daily 8-h mean concentration of O3, PM2.5 particulate matter less than 2.5 μm in aerodynamic diameter, AP atmospheric pressure, EADs emergency ambulance dispatches, tpd times per day, SD standard deviation, IQR interquartile range
Spearman’s correlation analysis indicated the presence of correlations among several air pollutants, including SO2 and NO2 (r = 0.474, P < 0.05), SO2 and CO (r = 0.615, P < 0.05), SO2 and O3-8 h (r = − 0.047, P < 0.05), SO2 and PM2.5 (r = 0.622, P < 0.05), NO2 and CO (r = 0.678, P < 0.05), NO2 and O3-8 h (r = − 0.195, P < 0.05), NO2 and PM2.5 (r = 0.785, P < 0.05), CO and O3-8 h (r = − 0.383, P < 0.05), CO and PM2.5 (r = 0.817, P < 0.05), and O3-8 h and PM2.5 (r = − 0.205, P < 0.05). In addition, correlations were observed between air pollutants and weather conditions (Table 2). The concentrations of SO2, NO2, and CO were remarkably higher during winter than during summer, while O3 concentrations were highest in the summers of each year. The EADs were also relatively higher during winters (Fig. 2).
Table 2
Spearman’s correlation coefficients for relationships between air pollutants and weather conditions
 
SO2
NO2
CO
O3
PM2.5
Temperature
Humidity
AP
SO2
1
       
NO2
0.474a
1
      
CO
0.615a
0.678 a
1
     
O3-8 h
− 0.047a
− 0.195a
− 0.383a
1
    
PM2.5
0.622a
0.785a
0.817a
− 0.205a
1
   
Temperature
− 0.084a
− 0.431a
− 0.474a
0.680a
− 0.462a
1
  
Humidity
− 0.446a
− 0.137a
− 0.058a
− 0.428a
− 0.190a
− 0.078a
1
 
AP
0.079a
0.365a
0.363a
− 0.596a
0.335a
− 0.851a
− 0.002
1
Abbreviations: SO2 sulfur dioxide, NO2 nitrogen dioxide, CO carbon monoxide, O3-8 h daily 8-h mean concentration of O3, PM2.5 particulate matter less than 2.5 μm in aerodynamic diameter, AP atmospheric pressure
aP < 0.05
After controlling for temperature, relative humidity, and atmospheric pressure, an IQR increase (13 μg/m3) of SO2 was significantly and positively associated with EADs for asthma at lag 2 day (OR = 1.126, 95% CI 1.014–1.251) and lag 3 day (OR = 1.188, 95% CI 1.075–1.312). In addition, an IQR increase (17 μg/m3) for NO2 was significantly and positively associated with EADs for asthma at lag 0 day (OR = 1.086, 95% CI 1.009–1.168), lag 3 day (OR = 1.111, 95% CI 1.031–1.197), lag 4 day (OR = 1.093, 95% CI 1.015–1.176), lag 5 day (OR = 1.115, 95% CI 1.036–1.200), and lag 6 day (OR = 1.103, 95% CI 1.026–1.187). Finally, an IQR increase (498 μg/m3) of CO was significantly and positively associated with EADs for asthma at lag 1 day (OR = 1.031, 95% CI 1.003–1.059) (Fig. 3). The days corresponding to the greatest effects due to SO2, NO2, and CO were 3, 5, and 1 day lags, respectively.
In the two-pollutant models, there was an association between cases and SO2 at lag 3 day after adjusting for PM2.5 (OR = 1.204, 95% CI 1.058–1.371), NO2 (OR = 1.157, 95% CI 1.004–1.333), CO (OR = 1.193, 95% CI 1.077–1.321), and O3 (OR = 1.174, 95% CI 1.060–1.301). There was also an observed association between cases and NO2 at lag 5 day after adjusting for SO2 (OR = 1.158, 95% CI 1.042–1.288), CO (OR = 1.115, 95% CI 1.034–1.202), and O3 (OR = 1.111, 95% CI 1.031–1.197). Lastly, an association was observed for CO at lag 1 day after adjusting for SO2 (OR = 1.029, 95% CI 1.001–1.058) and O3 (OR = 1.032, 95% CI 1.004–1.060) (Table 3).
Table 3
Odds ratios (OR) for two-pollutant models including SO2, NO2, and COb
Air pollutants
 
OR
OR 95% CI
Lower bound
Upper bound
SO2
 
1.188a
1.075
1.312
+PM2.5
1.204a
1.058
1.371
+NO2
1.157a
1.004
1.333
+CO
1.193a
1.077
1.321
+O3
1.174a
1.060
1.301
NO2
 
1.115a
1.036
1.200
+PM2.5
1.068
0.960
1.189
+SO2
1.158a
1.042
1.288
+CO
1.115a
1.034
1.202
+O3
1.111a
1.031
1.197
CO
 
1.031a
1.003
1.059
+PM2.5
1.028
1.000
1.057
+SO2
1.029a
1.001
1.058
+NO2
1.027
0.999
1.056
+O3
1.032a
1.004
1.060
Abbreviations: SO2 sulfur dioxide, NO2 nitrogen dioxide, CO carbon monoxide, OR odds ratio, CI confidence interval
aP < 0.05
bORs for SO2, NO2, and CO are derived from 3-, 5-, and 1-day lags, respectively
Restricting three fixed controls to one case instead of restricting cases and controls to being from the same month resulted in similar values and trends of ORs for each pollutant (Fig. 4). In addition, ORs calculated via different lag-day structures (lag 01, lag 02, and lag 03, respectively) were similar to those from the single-day lag models (Table 4). Thus, these sensitivity analyses suggest that the results of the models were reliable.
Table 4
Odds ratios for different lag-day model structures of air pollutants
Air pollutants
Lag (days)
OR
OR 95% CI
Lower bound
Upper bound
SO2
0
1.043
0.934
1.166
1
1.065
0.955
1.187
2
1.126a
1.014
1.251
3
1.188a
1.075
1.312
01
1.072
0.945
1.216
02
1.131
0.986
1.298
03
1.219a
1.053
1.412
NO2
0
1.086a
1.009
1.168
1
1.065
0.988
1.148
2
1.073
0.996
1.157
3
1.111a
1.031
1.197
01
1.093a
1.007
1.187
02
1.111a
1.015
1.215
03
1.146a
1.040
1.263
CO
0
1.002
0.970
1.034
1
1.031a
1.003
1.059
2
1.007
0.972
1.044
3
1.005
0.974
1.037
01
1.030
0.992
1.071
02
1.036
0.988
1.088
03
1.038
0.983
1.096
O3
0
0.942
0.824
1.077
1
1.053
0.943
1.177
2
1.089
0.985
1.203
3
1.089
0.989
1.199
01
1.011
0.865
1.181
02
1.087
0.923
1.280
03
1.141
0.964
1.350
Abbreviations: SO2 sulfur dioxide, NO2 nitrogen dioxide, CO carbon monoxide, O3 ozone, OR odds ratio, CI confidence interval
aP < 0.05

Discussion

A significantly positive association was observed between EADs and gaseous pollutants when using a time-stratified case-crossover methodology. After controlling for temperature, relative humidity, and atmospheric pressure, IQR increases in SO2 (13 μg/m3), NO2 (17 μg/m3), and CO (498 μg/m3) were associated with 18.8%, 11.5%, and 3.1% increases in EADs for asthma, respectively. These effects were most notable for SO2, NO2, and CO at 3-, 5-, and 1-day lags, respectively. Furthermore, associations were observed between EADs for asthma and SO2 and NO2 when using lag models with other days of lag. Delay effects were only observed between asthma and exposure to SO2, CO, and EADs, but not between asthma incidences and NO2. Moreover, the health impacts of NO2 exposure as measured by EADS for asthma were similar among 3- to 6–day lag windows. IQR increases for NO2 at 3-, 4-, 5-, and 6-day lags were associated with 11.1%, 9.3%, 11.5%, and 10.3% increases in EADs for asthma, respectively, indicating that there may be a plateauing lag period for the association between NO2 and EADS for asthma. Several studies have suggested that further investigations are needed to evaluate the association between O3 and asthma in the Sichuan Basin [28, 29]. However, an association between exposure to O3 and EADs for asthma was not observed in our analyses. The major sources of SO2, NO2, CO, and O3 pollutants in Chengdu arise from industrial emissions and fuel combustion. In addition, traffic emissions also contribute to ambient NO2 and CO levels [30, 31]. The concentrations of gaseous pollutants exhibited typical seasonal trends. Specifically, the concentrations of SO2, NO2, and CO were remarkably higher during winters, which may be due to reduced dilution efficiency via air flow diffusion, and increases in biomass fuel combustion for heating. In addition, higher O3 concentrations in summer were likely caused by increased sunlight. Nevertheless, the aforementioned seasonal trends were accounted for in our analyses by using the case-crossover method.
The results reported here are consistent with those from previous studies. Ding et al. [32] explored the association between air pollution and hospital visits for asthma attack in children of Chongqing, China using a case-crossover analysis. The analysis indicated that increases of 10 μg/m3 concentrations in SO2, NO2, and CO were associated with 4.2%, 9.0%, and 0.4% increases in hospital visits for asthma attacks in children [32]. Furthermore, an analysis of several cities in the USA, including Atlanta, Dallas, and St. Louis [33], revealed associations between pollutant concentrations and asthma emergency department visits. In particular, the associations were strongest for patients in the 5–18-year age group, wherein the ratios per IQR (5 p.p.b. for SO2, 12 p.p.b. for NO2, 0.5 p.p.m. for CO, and 28 p.p.b. for O3) were 1.01%, 1.05%, 1.03, and 1.07%, respectively. Similarly, a cohort study in Denmark comprising 53,695 people [34] indicated that NO2 levels were associated with increased risk of hospitalization for asthma, with an adjusted hazard ratio per IQR (5.8 μg/m3) of 1.12. Likewise, a cohort study of 5349 children attending kindergarten and first grade in Southern California [35] revealed associations between new-onset asthma and NO2 levels.
The lag days exhibiting the greatest effect for each pollutant were used for two-pollutant models. Modeling revealed that ORs for NO2 decreased after adjusting for PM2.5, and a similar decrease was observed for CO after adjusting for PM2.5, and NO2. These results are consistent with those from previous studies [32], indicating the presence of synergistic effects among air pollutants towards disease incidence.
SO2 has long been considered an environmental cause of asthma. For example, Romanoff discussed the toxic effects of SO2 fume inhalation on bronchial asthma in 1939 [36]. One possible mechanism underlying aggravation of asthma by SO2 could be that SO2 derivatives increase the expression levels of EGF, EGFR, ICAM-1, and COX-2 proteins in BEP2D cells. The upregulation of these proteins then results in mucus over-production and inflammatory responses [37]. An experiment with newborn Sprague–Dawley rats sensitized to ovalbumin revealed that SO2 could be a universal factor in airway inflammatory processes that specifically exacerbates airway hyperresponsiveness (AHR) in asthmatics [38]. The underlying mechanism of this response could be due to increases in Penh (an indicator of AHR), that then increases antibody IL-4 production in serum and increases airway smooth muscle cell stiffness and contractility.
Exposure to ambient NO2 may enhance bronchial hypersensitivity to asthma, promote allergen sensitization to inhaled antigens, and increase the risk of exacerbating asthma following respiratory infections [3942]. Mechanisms underlying the exacerbation of asthma by NO2 that may be of particular significance include the following: (1) enhancing induction of apoptosis in normal human bronchial epithelial cells and inducing cell damage [43]. 2) Inducing an upregulation of IL-5, IL-10, IL-13, and ICAM-1 antibodies in the bronchial epithelium, thereby exerting a “pro-allergic” effect [44].
A relationship between ambient CO levels and asthma incidence has been demonstrated in many previous studies [7, 32, 33, 45, 46]. However, the biological mechanism underlying this association has not yet been determined. Norris et al. (1999) considered CO as a general indicator for the effects of air pollution [47]. In contrast to the above studies, recent studies have suggested that CO may potentially play a protective role in respiratory systems [48]. Ameredes et al. (2003) reported that exposure to CO could reduce airway hyperresponsiveness in mice [49]. Further, the study suggested that the response was associated with a guanosine-3,5-monophosphate (cGMP) mechanism both in the presence and absence of airway inflammation. Moreover, Song et al. (2002) suggested that CO could induce significant antiproliferative effects for human airway smooth muscle cells [50]. Thus, further studies are needed to more clearly discern the mechanism underlying the exacerbation of asthma by CO.
This study features three distinct strengths that increase the significance of the observations reported here. First, this is the first study to explore the association between gaseous pollutants and EADs for asthma in the central Sichuan Basin of southwestern China. Although the Bejing–Sichuan belt is located in one of two severe air pollution belts of China [12], investigations of pollution and pollution risks have lagged in the Sichuan Basin due to the relatively depressed economic conditions in the region [13]. The recent improvement and establishment of monitoring systems in the Sichuan Basin have provided opportunities to now conduct such investigations. In addition, several factors render the area a unique research resource that can help fill knowledge-gaps concerning pollution risks in the region. These include the uniquely dense population, different sources of air pollutants, different diffusional dilution conditions, and significantly different economic levels in the Sichuan Basin compared to eastern areas and cities. Second, emergency ambulance dispatch data for the whole city were used in our study due to the unique advantage of the Chengdu First-Aid Command System. City-wide data such as these have been rarely used in previous studies. Third, the city of Chengdu is large and densely populated, which is advantageous for assessing the effects of air pollutants on disease incidence.
However, some limitations were also evident in this study. First, concentrations of air pollutants were obtained from fixed municipal environmental monitoring centers, and thus, individual exposure data were not evaluated. Second, this study was conducted for the central Sichuan Basin. The specific geographical features and weather conditions of the region should be considered, and generalizations of these results should be treated cautiously. Third, not all asthma patients call for emergency ambulances when disease states occur. Consequently, we conducted a time-stratified case-crossover analysis based on individuals from which cumulative effects could not be obtained.

Conclusions

This study provides important data to advance our limited understanding of potential health risks due to ambient gaseous pollutants. Importantly, these data suggest that increased concentrations of SO2, NO2, and CO were significantly and positively associated with emergency ambulance dispatches for asthma in Chengdu, China. Further studies are needed to assess the effects of various individual air pollutants on asthma.

Acknowledgements

We thank the Chengdu First-Aid Command Center, the Chengdu Municipal Environmental Monitoring Center, and the Chengdu Municipal Meteorological Bureau for providing data.

Funding

This study was funded by the Special Foundation of Basic Science and Technology Resources Survey of the Ministry of Science and Technology (No. 2017FY101200), the China Short-Term Health Effects of Air Pollution Study (China SHEAP Study; No. 2016YFC0206500), the Sichuan Provincial Medical Research Youth Innovation Project (No. Q17070), and the Sichuan Provincial Cadre Health Care Research Project (No. ZH2018-1801).

Availability of data and materials

The datasets used in the current study are available from the corresponding author for reasonable requests.
Not applicable. This study does not involve experimental animals or individual information of human subjects. The Chengdu First–Aid Command Center provided the data used in this study.
Not applicable.

Competing interests

The authors declare that they have no competing interests.

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Literatur
1.
Zurück zum Zitat Masoli M, Fabian D, Holt S, Beasley R. The global burden of asthma: executive summary of the GINA dissemination committee report. Allergy. 2004;59(5):469–78.PubMed Masoli M, Fabian D, Holt S, Beasley R. The global burden of asthma: executive summary of the GINA dissemination committee report. Allergy. 2004;59(5):469–78.PubMed
2.
Zurück zum Zitat Sullivan S, Elixhauser A, Buist AS, Luce BR, Eisenberg J, Weiss KB. National Asthma Education and Prevention Program working group report on the cost effectiveness of asthma care. Am J Respir Crit Care Med. 1996;154(3_pt_2):S84–95.PubMed Sullivan S, Elixhauser A, Buist AS, Luce BR, Eisenberg J, Weiss KB. National Asthma Education and Prevention Program working group report on the cost effectiveness of asthma care. Am J Respir Crit Care Med. 1996;154(3_pt_2):S84–95.PubMed
3.
Zurück zum Zitat Cai J, Zhao A, Zhao J, Chen R, Wang W, Ha S, Xu X, Kan H. Acute effects of air pollution on asthma hospitalization in Shanghai, China. Environ Pollut. 2014;191:139–44.PubMed Cai J, Zhao A, Zhao J, Chen R, Wang W, Ha S, Xu X, Kan H. Acute effects of air pollution on asthma hospitalization in Shanghai, China. Environ Pollut. 2014;191:139–44.PubMed
4.
Zurück zum Zitat Chen K, Glonek G, Hansen A, Williams S, Tuke J, Salter A, Bi P. The effects of air pollution on asthma hospital admissions in Adelaide, South Australia, 2003–2013: time-series and case–crossover analyses. Clin Exp Allergy. 2016;46(11):1416–30.PubMed Chen K, Glonek G, Hansen A, Williams S, Tuke J, Salter A, Bi P. The effects of air pollution on asthma hospital admissions in Adelaide, South Australia, 2003–2013: time-series and case–crossover analyses. Clin Exp Allergy. 2016;46(11):1416–30.PubMed
5.
Zurück zum Zitat Nishimura KK, Galanter JM, Roth LA, Oh SS, Thakur N, Nguyen EA, Thyne S, Farber HJ, Serebrisky D, Kumar R, et al. Early-life air pollution and asthma risk in minority children. The GALA II and SAGE II studies. Am J Respir Crit Care Med. 2013;188(3):309–18.PubMedPubMedCentral Nishimura KK, Galanter JM, Roth LA, Oh SS, Thakur N, Nguyen EA, Thyne S, Farber HJ, Serebrisky D, Kumar R, et al. Early-life air pollution and asthma risk in minority children. The GALA II and SAGE II studies. Am J Respir Crit Care Med. 2013;188(3):309–18.PubMedPubMedCentral
6.
Zurück zum Zitat Pénard-Morand C, Raherison C, Charpin D, Kopferschmitt C, Lavaud F, Caillaud D, Annesi-Maesano I. Long-term exposure to proximity air pollution and asthma and allergies in urban children. Eur Respir J. 2010;36(1):33–40.PubMed Pénard-Morand C, Raherison C, Charpin D, Kopferschmitt C, Lavaud F, Caillaud D, Annesi-Maesano I. Long-term exposure to proximity air pollution and asthma and allergies in urban children. Eur Respir J. 2010;36(1):33–40.PubMed
7.
Zurück zum Zitat Strickland MJ, Darrow LA, Klein M, Flanders WD, Sarnat JA, Waller LA, Sarnat SE, Mulholland JA, Tolbert PE. Short-term associations between ambient air pollutants and pediatric asthma emergency department visits. Am J Respir Crit Care Med. 2010;182(3):307–16.PubMedPubMedCentral Strickland MJ, Darrow LA, Klein M, Flanders WD, Sarnat JA, Waller LA, Sarnat SE, Mulholland JA, Tolbert PE. Short-term associations between ambient air pollutants and pediatric asthma emergency department visits. Am J Respir Crit Care Med. 2010;182(3):307–16.PubMedPubMedCentral
8.
Zurück zum Zitat Bowatte G, Lodge C, Lowe AJ, Erbas B, Perret J, Abramson MJ, Matheson M, Dharmage SC. The influence of childhood traffic-related air pollution exposure on asthma, allergy and sensitization: a systematic review and a meta-analysis of birth cohort studies. Allergy. 2015;70(3):245–56.PubMed Bowatte G, Lodge C, Lowe AJ, Erbas B, Perret J, Abramson MJ, Matheson M, Dharmage SC. The influence of childhood traffic-related air pollution exposure on asthma, allergy and sensitization: a systematic review and a meta-analysis of birth cohort studies. Allergy. 2015;70(3):245–56.PubMed
9.
Zurück zum Zitat Grineski SE, Staniswalis JG, Peng Y, Atkinson-Palombo C. Children’s asthma hospitalizations and relative risk due to nitrogen dioxide (NO2): effect modification by race, ethnicity, and insurance status. Environ Res. 2010;110(2):178–88.PubMed Grineski SE, Staniswalis JG, Peng Y, Atkinson-Palombo C. Children’s asthma hospitalizations and relative risk due to nitrogen dioxide (NO2): effect modification by race, ethnicity, and insurance status. Environ Res. 2010;110(2):178–88.PubMed
10.
Zurück zum Zitat Guan W-J, Zheng X-Y, Chung KF, Zhong N-S. Impact of air pollution on the burden of chronic respiratory diseases in China: time for urgent action. Lancet. 2016;388(10054):1939–51.PubMed Guan W-J, Zheng X-Y, Chung KF, Zhong N-S. Impact of air pollution on the burden of chronic respiratory diseases in China: time for urgent action. Lancet. 2016;388(10054):1939–51.PubMed
11.
Zurück zum Zitat Samoli E, Nastos PT, Paliatsos AG, Katsouyanni K, Priftis KN. Acute effects of air pollution on pediatric asthma exacerbation: evidence of association and effect modification. Environ Res. 2011;111(3):418–24.PubMed Samoli E, Nastos PT, Paliatsos AG, Katsouyanni K, Priftis KN. Acute effects of air pollution on pediatric asthma exacerbation: evidence of association and effect modification. Environ Res. 2011;111(3):418–24.PubMed
12.
Zurück zum Zitat Han L, Zhou W, Li W, Li L. Impact of urbanization level on urban air quality: a case of fine particles (PM2.5) in Chinese cities. Environ Pollut. 2014;194:163–70.PubMed Han L, Zhou W, Li W, Li L. Impact of urbanization level on urban air quality: a case of fine particles (PM2.5) in Chinese cities. Environ Pollut. 2014;194:163–70.PubMed
14.
Zurück zum Zitat Liu R, Zeng J, Jiang X, Chen J, Gao X, Zhang L, Li T. The relationship between airborne fine particle matter and emergency ambulance dispatches in a southwestern city in Chengdu, China. Environ Pollut. 2017;229:661–7.PubMed Liu R, Zeng J, Jiang X, Chen J, Gao X, Zhang L, Li T. The relationship between airborne fine particle matter and emergency ambulance dispatches in a southwestern city in Chengdu, China. Environ Pollut. 2017;229:661–7.PubMed
15.
Zurück zum Zitat Michikawa T, Ueda K, Takeuchi A, Tamura K, Kinoshita M, Ichinose T, Nitta H. Coarse particulate matter and emergency ambulance dispatches in Fukuoka, Japan: a time-stratified case-crossover study. Environ Health Prev Med. 2015;20(2):130–6.PubMed Michikawa T, Ueda K, Takeuchi A, Tamura K, Kinoshita M, Ichinose T, Nitta H. Coarse particulate matter and emergency ambulance dispatches in Fukuoka, Japan: a time-stratified case-crossover study. Environ Health Prev Med. 2015;20(2):130–6.PubMed
16.
Zurück zum Zitat Chen R, Huang W, Wong CM, Wang Z, Thach TQ, Chen B, Kan H, Group CC. Short-term exposure to sulfur dioxide and daily mortality in 17 Chinese cities: the China air pollution and health effects study (CAPES). Environ Res. 2012;118:101–6.PubMed Chen R, Huang W, Wong CM, Wang Z, Thach TQ, Chen B, Kan H, Group CC. Short-term exposure to sulfur dioxide and daily mortality in 17 Chinese cities: the China air pollution and health effects study (CAPES). Environ Res. 2012;118:101–6.PubMed
17.
Zurück zum Zitat Tao Y, Mi S, Zhou S, Wang S, Xie X. Air pollution and hospital admissions for respiratory diseases in Lanzhou, China. Environ Pollut. 2014;185:196–201.PubMed Tao Y, Mi S, Zhou S, Wang S, Xie X. Air pollution and hospital admissions for respiratory diseases in Lanzhou, China. Environ Pollut. 2014;185:196–201.PubMed
18.
Zurück zum Zitat Yang C, Peng X, Huang W, Chen R, Xu Z, Chen B, Kan H. A time-stratified case-crossover study of fine particulate matter air pollution and mortality in Guangzhou, China. Int Arch Occup Environ Health. 2012;85(5):579–85.PubMed Yang C, Peng X, Huang W, Chen R, Xu Z, Chen B, Kan H. A time-stratified case-crossover study of fine particulate matter air pollution and mortality in Guangzhou, China. Int Arch Occup Environ Health. 2012;85(5):579–85.PubMed
19.
Zurück zum Zitat Guo Y, Tong S, Zhang Y, Barnett AG, Jia Y, Pan X. The relationship between particulate air pollution and emergency hospital visits for hypertension in Beijing, China. Sci Total Environ. 2010;408(20):4446–50.PubMed Guo Y, Tong S, Zhang Y, Barnett AG, Jia Y, Pan X. The relationship between particulate air pollution and emergency hospital visits for hypertension in Beijing, China. Sci Total Environ. 2010;408(20):4446–50.PubMed
20.
Zurück zum Zitat Belleudi V, Faustini A, Stafoggia M, Cattani G, Marconi A, Perucci CA, Forastiere F. Impact of fine and ultrafine particles on emergency hospital admissions for cardiac and respiratory diseases. Epidemiology. 2010;21(3):414–23.PubMed Belleudi V, Faustini A, Stafoggia M, Cattani G, Marconi A, Perucci CA, Forastiere F. Impact of fine and ultrafine particles on emergency hospital admissions for cardiac and respiratory diseases. Epidemiology. 2010;21(3):414–23.PubMed
21.
Zurück zum Zitat Kamouchi M, Ueda K, Ago T, Nitta H, Kitazono T. Fukuoka stroke registry I: relationship between asian dust and ischemic stroke: a time-stratified case-crossover study. Stroke. 2012;43(11):3085–7.PubMed Kamouchi M, Ueda K, Ago T, Nitta H, Kitazono T. Fukuoka stroke registry I: relationship between asian dust and ischemic stroke: a time-stratified case-crossover study. Stroke. 2012;43(11):3085–7.PubMed
22.
Zurück zum Zitat Yang Y, Cao Y, Li W, Li R, Wang M, Wu Z, Xu Q. Multi-site time series analysis of acute effects of multiple air pollutants on respiratory mortality: a population-based study in Beijing, China. Sci Total Environ. 2015;508:178–87.PubMed Yang Y, Cao Y, Li W, Li R, Wang M, Wu Z, Xu Q. Multi-site time series analysis of acute effects of multiple air pollutants on respiratory mortality: a population-based study in Beijing, China. Sci Total Environ. 2015;508:178–87.PubMed
23.
Zurück zum Zitat Hastie TJ. Generalized linear models. Statistical models in S; 1992. Hastie TJ. Generalized linear models. Statistical models in S; 1992.
24.
Zurück zum Zitat Janes H, Sheppard L, Lumley T. Case-crossover analyses of air pollution exposure data: referent selection strategies and their implications for bias. Epidemiology. 2005;16(6):717–26.PubMed Janes H, Sheppard L, Lumley T. Case-crossover analyses of air pollution exposure data: referent selection strategies and their implications for bias. Epidemiology. 2005;16(6):717–26.PubMed
25.
Zurück zum Zitat Jung CR, Young LH, Hsu HT, Lin MY, Chen YC, Hwang BF, Tsai PJ. PM2.5 components and outpatient visits for asthma: a time-stratified case-crossover study in a suburban area. Environ Pollut. 2017;231(Pt 1):1085–92.PubMed Jung CR, Young LH, Hsu HT, Lin MY, Chen YC, Hwang BF, Tsai PJ. PM2.5 components and outpatient visits for asthma: a time-stratified case-crossover study in a suburban area. Environ Pollut. 2017;231(Pt 1):1085–92.PubMed
26.
Zurück zum Zitat Lin H, An Q, Luo C, Pun VC, Chan CS, Tian L. Gaseous air pollution and acute myocardial infarction mortality in Hong Kong: a time-stratified case-crossover study. Atmos Environ. 2013;76:68–73. Lin H, An Q, Luo C, Pun VC, Chan CS, Tian L. Gaseous air pollution and acute myocardial infarction mortality in Hong Kong: a time-stratified case-crossover study. Atmos Environ. 2013;76:68–73.
27.
Zurück zum Zitat Guo Y, Tong S, Li S, Barnett AG, Yu W, Zhang Y, Pan X. Gaseous air pollution and emergency hospital visits for hypertension in Beijing, China: a time-stratified case-crossover study. Environ Health. 2010;9(1):57.PubMedPubMedCentral Guo Y, Tong S, Li S, Barnett AG, Yu W, Zhang Y, Pan X. Gaseous air pollution and emergency hospital visits for hypertension in Beijing, China: a time-stratified case-crossover study. Environ Health. 2010;9(1):57.PubMedPubMedCentral
28.
Zurück zum Zitat Lin S, Liu X, Le LH, Hwang S-A. Chronic exposure to ambient ozone and asthma hospital admissions among children. Environ Health Perspect. 2008;116(12):1725–30.PubMedPubMedCentral Lin S, Liu X, Le LH, Hwang S-A. Chronic exposure to ambient ozone and asthma hospital admissions among children. Environ Health Perspect. 2008;116(12):1725–30.PubMedPubMedCentral
29.
Zurück zum Zitat McDonnell WF, Abbey DE, Nishino N, Lebowitz MD. Long-term ambient ozone concentration and the incidence of asthma in nonsmoking adults: the Ahsmog study. Environ Res. 1999;80(2):110–21.PubMed McDonnell WF, Abbey DE, Nishino N, Lebowitz MD. Long-term ambient ozone concentration and the incidence of asthma in nonsmoking adults: the Ahsmog study. Environ Res. 1999;80(2):110–21.PubMed
30.
Zurück zum Zitat Chen T-M, Kuschner WG, Gokhale J, Shofer S. Outdoor air pollution: nitrogen dioxide, sulfur dioxide, and carbon monoxide health effects. Am J Med Sci. 2007;333(4):249–56.PubMed Chen T-M, Kuschner WG, Gokhale J, Shofer S. Outdoor air pollution: nitrogen dioxide, sulfur dioxide, and carbon monoxide health effects. Am J Med Sci. 2007;333(4):249–56.PubMed
31.
Zurück zum Zitat Li J, Wang Z, Akimoto H, Yamaji K, Takigawa M, Pochanart P, Liu Y, Tanimoto H, Kanaya Y. Near-ground ozone source attributions and outflow in central eastern China during MTX2006. Atmos Chem Phys. 2008;8(24):7335–51. Li J, Wang Z, Akimoto H, Yamaji K, Takigawa M, Pochanart P, Liu Y, Tanimoto H, Kanaya Y. Near-ground ozone source attributions and outflow in central eastern China during MTX2006. Atmos Chem Phys. 2008;8(24):7335–51.
32.
Zurück zum Zitat Ding L, Zhu D, Peng D, Zhao Y. Air pollution and asthma attacks in children: a case–crossover analysis in the city of Chongqing, China. Environ Pollut. 2017;220:348–53.PubMed Ding L, Zhu D, Peng D, Zhao Y. Air pollution and asthma attacks in children: a case–crossover analysis in the city of Chongqing, China. Environ Pollut. 2017;220:348–53.PubMed
33.
Zurück zum Zitat Alhanti BA, Chang HH, Winquist A, Mulholland JA, Darrow LA, Sarnat SE. Ambient air pollution and emergency department visits for asthma: a multi-city assessment of effect modification by age. J Exposure Sci Environ Epidemiol. 2015;26:180. Alhanti BA, Chang HH, Winquist A, Mulholland JA, Darrow LA, Sarnat SE. Ambient air pollution and emergency department visits for asthma: a multi-city assessment of effect modification by age. J Exposure Sci Environ Epidemiol. 2015;26:180.
34.
Zurück zum Zitat Andersen ZJ, Bønnelykke K, Hvidberg M, Jensen SS, Ketzel M, Loft S, Sørensen M, Tjønneland A, Overvad K, Raaschou-Nielsen O. Long-term exposure to air pollution and asthma hospitalisations in older adults: a cohort study. Thorax. 2011;67(1):6–11.PubMed Andersen ZJ, Bønnelykke K, Hvidberg M, Jensen SS, Ketzel M, Loft S, Sørensen M, Tjønneland A, Overvad K, Raaschou-Nielsen O. Long-term exposure to air pollution and asthma hospitalisations in older adults: a cohort study. Thorax. 2011;67(1):6–11.PubMed
35.
Zurück zum Zitat McConnell R, Islam T, Shankardass K, Jerrett M, Lurmann F, Gilliland F, Gauderman J, Avol E, Künzli N, Yao L, et al. Childhood incident asthma and traffic-related air pollution at home and school. Environ Health Perspect. 2010;118(7):1021–6.PubMedPubMedCentral McConnell R, Islam T, Shankardass K, Jerrett M, Lurmann F, Gilliland F, Gauderman J, Avol E, Künzli N, Yao L, et al. Childhood incident asthma and traffic-related air pollution at home and school. Environ Health Perspect. 2010;118(7):1021–6.PubMedPubMedCentral
36.
Zurück zum Zitat Romanoff A. Sulfur dioxide poisoning as a cause of asthma. J Allergy. 1939;10:166–9. Romanoff A. Sulfur dioxide poisoning as a cause of asthma. J Allergy. 1939;10:166–9.
37.
Zurück zum Zitat Li R, Meng Z, Xie J. Effects of sulfur dioxide derivatives on four asthma-related gene expressions in human bronchial epithelial cells. Toxicol Lett. 2007;175(1):71–81.PubMed Li R, Meng Z, Xie J. Effects of sulfur dioxide derivatives on four asthma-related gene expressions in human bronchial epithelial cells. Toxicol Lett. 2007;175(1):71–81.PubMed
38.
Zurück zum Zitat Song A, Liao Q, Li J, Lin F, Liu E, Jiang X, Deng L. Chronic exposure to sulfur dioxide enhances airway hyperresponsiveness only in ovalbumin-sensitized rats. Toxicol Lett. 2012;214(3):320–7.PubMed Song A, Liao Q, Li J, Lin F, Liu E, Jiang X, Deng L. Chronic exposure to sulfur dioxide enhances airway hyperresponsiveness only in ovalbumin-sensitized rats. Toxicol Lett. 2012;214(3):320–7.PubMed
39.
Zurück zum Zitat Bevelander M, Mayette J, Whittaker LA, Paveglio SA, Jones CC, Robbins J, Hemenway D, Akira S, Uematsu S, Poynter ME. Nitrogen dioxide promotes allergic sensitization to inhaled antigen. J Immunol. 2007;179(6):3680–8.PubMedPubMedCentral Bevelander M, Mayette J, Whittaker LA, Paveglio SA, Jones CC, Robbins J, Hemenway D, Akira S, Uematsu S, Poynter ME. Nitrogen dioxide promotes allergic sensitization to inhaled antigen. J Immunol. 2007;179(6):3680–8.PubMedPubMedCentral
40.
Zurück zum Zitat Linaker CH, Coggon D, Holgate ST, Clough J, Josephs L, Chauhan AJ, Inskip HM. Personal exposure to nitrogen dioxide and risk of airflow obstruction in asthmatic children with upper respiratory infection. Thorax. 2000;55(11):930–3.PubMedPubMedCentral Linaker CH, Coggon D, Holgate ST, Clough J, Josephs L, Chauhan AJ, Inskip HM. Personal exposure to nitrogen dioxide and risk of airflow obstruction in asthmatic children with upper respiratory infection. Thorax. 2000;55(11):930–3.PubMedPubMedCentral
41.
Zurück zum Zitat Orehek J, Massari JP, Gayrard P, Grimaud C, Charpin J. Effect of short-term, low-level nitrogen dioxide exposure on bronchial sensitivity of asthmatic patients. J Clin Invest. 1976;57(2):301–7.PubMedPubMedCentral Orehek J, Massari JP, Gayrard P, Grimaud C, Charpin J. Effect of short-term, low-level nitrogen dioxide exposure on bronchial sensitivity of asthmatic patients. J Clin Invest. 1976;57(2):301–7.PubMedPubMedCentral
42.
Zurück zum Zitat Strand V, Rak S, Svartengren M, Bylin G. Nitrogen dioxide exposure enhances asthmatic reaction to inhaled allergen in subjects with asthma. Am J Respir Crit Care Med. 1997;155(3):881–7.PubMed Strand V, Rak S, Svartengren M, Bylin G. Nitrogen dioxide exposure enhances asthmatic reaction to inhaled allergen in subjects with asthma. Am J Respir Crit Care Med. 1997;155(3):881–7.PubMed
43.
Zurück zum Zitat Ayyagari VN, Januszkiewicz A, Nath J. Effects of nitrogen dioxide on the expression of intercellular adhesion molecule-1, neutrophil adhesion, and cytotoxicity: studies in human bronchial epithelial cells. Inhal Toxicol. 2007;19(2):181–94.PubMed Ayyagari VN, Januszkiewicz A, Nath J. Effects of nitrogen dioxide on the expression of intercellular adhesion molecule-1, neutrophil adhesion, and cytotoxicity: studies in human bronchial epithelial cells. Inhal Toxicol. 2007;19(2):181–94.PubMed
44.
Zurück zum Zitat Pathmanathan S, Krishna MT, Blomberg A, Helleday R, Kelly FJ, Sandström T, Holgate ST, Wilson SJ, Frew AJ. Repeated daily exposure to 2 ppm nitrogen dioxide upregulates the expression of IL-5, IL-10, IL-13, and ICAM-1 in the bronchial epithelium of healthy human airways. Occup Environ Med. 2003;60(11):892–6.PubMedPubMedCentral Pathmanathan S, Krishna MT, Blomberg A, Helleday R, Kelly FJ, Sandström T, Holgate ST, Wilson SJ, Frew AJ. Repeated daily exposure to 2 ppm nitrogen dioxide upregulates the expression of IL-5, IL-10, IL-13, and ICAM-1 in the bronchial epithelium of healthy human airways. Occup Environ Med. 2003;60(11):892–6.PubMedPubMedCentral
45.
Zurück zum Zitat Clark NA, Demers PA, Karr CJ, Koehoorn M, Lencar C, Tamburic L, Brauer M. Effect of early life exposure to air pollution on development of childhood asthma. Environ Health Perspect. 2010;118(2):284–90.PubMed Clark NA, Demers PA, Karr CJ, Koehoorn M, Lencar C, Tamburic L, Brauer M. Effect of early life exposure to air pollution on development of childhood asthma. Environ Health Perspect. 2010;118(2):284–90.PubMed
46.
Zurück zum Zitat Lin M, Chen Y, Burnett RT, Villeneuve PJ, Krewski D. Effect of short-term exposure to gaseous pollution on asthma hospitalisation in children: a bi-directional case-crossover analysis. J Epidemiol Community Health. 2003;57(1):50–5.PubMedPubMedCentral Lin M, Chen Y, Burnett RT, Villeneuve PJ, Krewski D. Effect of short-term exposure to gaseous pollution on asthma hospitalisation in children: a bi-directional case-crossover analysis. J Epidemiol Community Health. 2003;57(1):50–5.PubMedPubMedCentral
47.
Zurück zum Zitat Norris G, YoungPong SN, Koenig JQ, Larson TV, Sheppard L, Stout JW. An association between fine particles and asthma emergency department visits for children in Seattle. Environ Health Perspect. 1999;107(6):489–93.PubMedPubMedCentral Norris G, YoungPong SN, Koenig JQ, Larson TV, Sheppard L, Stout JW. An association between fine particles and asthma emergency department visits for children in Seattle. Environ Health Perspect. 1999;107(6):489–93.PubMedPubMedCentral
48.
Zurück zum Zitat Ryter SW, Kim HP, Nakahira K, Zuckerbraun BS, Morse D, Choi AMK. Protective functions of heme oxygenase-1 and carbon monoxide in the respiratory system. Antioxid Redox Signal. 2007;9(12):2157–73.PubMed Ryter SW, Kim HP, Nakahira K, Zuckerbraun BS, Morse D, Choi AMK. Protective functions of heme oxygenase-1 and carbon monoxide in the respiratory system. Antioxid Redox Signal. 2007;9(12):2157–73.PubMed
49.
Zurück zum Zitat Ameredes BT, Otterbein LE, Kohut LK, Gligonic AL, Calhoun WJ, Choi AMK. Low-dose carbon monoxide reduces airway hyperresponsiveness in mice. Am J Phys Lung Cell Mol Phys. 2003;285(6):L1270–6. Ameredes BT, Otterbein LE, Kohut LK, Gligonic AL, Calhoun WJ, Choi AMK. Low-dose carbon monoxide reduces airway hyperresponsiveness in mice. Am J Phys Lung Cell Mol Phys. 2003;285(6):L1270–6.
50.
Zurück zum Zitat Song R, Mahidhara RS, Liu F, Ning W, Otterbein LE, Choi AMK. Carbon monoxide inhibits human airway smooth muscle cell proliferation via mitogen-activated protein kinase pathway. Am J Respir Cell Mol Biol. 2002;27(5):603–10.PubMed Song R, Mahidhara RS, Liu F, Ning W, Otterbein LE, Choi AMK. Carbon monoxide inhibits human airway smooth muscle cell proliferation via mitogen-activated protein kinase pathway. Am J Respir Cell Mol Biol. 2002;27(5):603–10.PubMed
Metadaten
Titel
Association between gaseous pollutants and emergency ambulance dispatches for asthma in Chengdu, China: a time-stratified case-crossover study
verfasst von
Jianyu Chen
Xianyan Jiang
Chunli Shi
Ruicong Liu
Rong Lu
Li Zhang
Publikationsdatum
01.12.2019
Verlag
BioMed Central
Erschienen in
Environmental Health and Preventive Medicine / Ausgabe 1/2019
Print ISSN: 1342-078X
Elektronische ISSN: 1347-4715
DOI
https://doi.org/10.1186/s12199-019-0773-0

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