Allergens, Air Pollutants, and Childhood Allergic Diseases
I-Jen Wang a,b,c, Tao-Hsin Tung d,e, Chin-Sheng Tang d, and Zi-Hao Zhao da Department of Pediatrics, Taipei Hospital, Ministry of Health and Welfare, Taipei, Taiwan; b Institute of Environmental and Occupational Health Sciences, College of Medicine, National
Yang-Ming University, Taipei, Taiwan;
c Department of Health Risk Management, China Medical University, Taichung, Taiwan; d College of Public Health, Fu Jen Catholic University, Taipei, Taiwan;
e Department of Medical Research and Education, Cheng-Hsin General Hospital
Running title: Allergens, pollution & allergic disease
Corresponding author at: Dr. I-Jen Wang
Department of Pediatrics, Taipei Hospital, Ministry of Health and Welfare, No. 127, Su-Yuan Road, Hsin-Chuang Dist., New Taipei City 242, Taiwan. Phone: 886-2-2276-5566 ext. 2532
Fax: 886-2-2998-8028
E-mail addresses: [email protected] (I.J. Wang)
Abbreviations: SO2,sulfur dioxide; NO2, nitrogen dioxide;O3, ozone; CO, carbon monoxide; PM10, particulate matter ≤ 10 μm; PM2.5, particulate matter ≤ 2.5 μm;8hO3, 8-hour average ozone concentration; AD, atopic dermatitis; AR, allergic rhinitis.
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Abstract
Background: The synergistic effect of allergens and air pollutants on the risk of allergic diseases is unclear.
Objective: To evaluate the joint effect of outdoor pollutants and indoor allergens on the risk of allergic diseases.
Methods: We enrolled 2661 kindergarten children from the CEAS cohort. Data on allergic diseases and environmental exposure were collected. Skin prick tests were performed. Individual exposure to air pollution was estimated using a geographic information system with the mean concentration of air pollutants. Multiple logistic regression analysis was performed to estimate the association between air pollutants, allergen exposure and the risk of allergic diseases with adjustments for potential confounders.
Results: Overall, 12.6% of the children had asthma, 30.0% had allergic rhinitis (AR), and 14.4% had atopic dermatitis (AD). Mite sensitization significantly increased the risk of AD, AR, and asthma (OR (95%CI) 2.15 (1.53-3.03), 1.94 (1.46-2.58), and 2.31 (1.63-3.29), respectively). Exposure to PM10, PM2.5, CO, and O3 was associated with asthma (OR (95% CI) 1.39(1.03-1.87), 1.45(1.07-1.97), 1.36(1.01-1.83), and 0.68 (0.51-0.92), respectively). PM2.5 may have increased the risk of AR (OR (95% CI) 1.54 (1.03-2.32). Mite sensitization showed a synergistic effect with PM2.5 on the development of asthma (p<0.001). Moreover, mite allergens may modify the effect of air pollutants on allergic diseases.
Conclusion: Dust mites and PM2.5 play an important role on the risk of asthma and AR. Exposure to PM2.5 and mite allergens had a synergistic effect on the development of asthma. Avoiding co-exposure to allergens and air pollutants is important.
Key words: air pollutant, allergen, asthma 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
Introduction
Levels of traffic-related pollutants (TRAP) are increasing rapidly across many Asian countries in parallel with the level of urbanization and economic development (Leung et al., 2012). Air pollution increases asthma symptoms, the use of medication, bronchoconstriction, emergency room admissions and hospitalizations due to pollutants such as ozone (O3), nitrogen dioxide (NO2) and particulate matter (PM) (Sandström and Kelly, 2009).
Prenatal exposure to PM2.5 was reported to increase susceptibility to respiratory infections and may program respiratory morbidity in early childhood (Jedrychowski et al., 2013). Children appear to be most vulnerable to the harmful effects of ambient air pollutants. As their lungs have not completely developed, they may experience greater exposure to environmental pollutants than adults, and a higher amount of these pollutants may remain in their lungs for a greater duration (Tzivian, 2011). Particulate and gaseous pollutants can act on both the upper and lower airways to initiate and exacerbate cellular inflammation through interactions with the innate immune system (Bonay and Aubier, 2007).
In addition to air pollution, early and persistent allergic sensitization is known to be a risk factor for the development of asthma (Sly, 2011).Indoor allergens from dust mites, cockroaches and cats have been associated with asthma exacerbation in children (Sly, 2011). It has also been reported that allergen sensitization is associated with allergic diseases and also with air pollutants (Pénard-Morand et al., 2005). While many studies have focused on the association between TRAP and exacerbations of existing respiratory conditions, few studies have reported the impact of TRAP on the development of asthma and allergies over time. In addition, most of the studies on the relationship between exposure to air pollutants and the risk of asthma in children have been cross-sectional (Evans et al., 2014; Bowatte et al., 2015; Zhang et al., 2002). 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
Both air pollutants and allergens play important roles in the development of allergic diseases, however whether they synergistically increase the risk of developing allergic diseases is unclear. Therefore, the aim of this study was to evaluate the joint effect of long-term exposure to allergens and air pollutants on the risk of developing allergic diseases, and to investigate whether exposure to allergens modifies the effect of air pollutants on allergic diseases. 1 2 3 4 5 6
Methods
Study population
We conducted a school-based survey on allergic diseases in kindergarten children at 11 communities in Taipei in 2010 (Childhood Environment and Allergic Diseases Study cohort). A total of 3246 children were recruited with written informed consent. After excluding those who were multiple births, premature, had congenital and chronic diseases, were unable to answer questions in Chinese, had moved in or out of their current home, lived more than 10 km from air monitoring stations, 2661 children were entered into the analysis (Table 1).
Those who lived more than 10 km from air monitoring stations were excluded because of the relative lower correlation between monitoring station data and children’s real exposure for those living more than 10 km from air monitoring stations (Clark et al, 2010; Romieu et al, 1996; Rich et al, 2014). The average distance from monitoring stations to the children’s addresses was 2.14±0.72 km. The International Study of Asthma and Allergies in Childhood (ISAAC) questionnaires with extra questions on basic demographics, residential
environmental factors, and family history of allergic diseases were answered by parents. The study protocol was approved by the Institutional Review Board at our hospital, and this study complied with the principles outlined in the Helsinki Declaration.
Case definition
Cases of atopic dermatitis (AD) were identified through the questions, “ Has your child ever had AD diagnosed by a physician?” and “ Has your child ever had recurrent itchy rash for at least 6 consecutive half-month periods over elbows, knees, face, wrists, neck, peri-auricular and eyebrow areas?” Cases of allergic rhinitis (AR) were identified through the questions, 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23
“Has your child ever been diagnosed as having AR by a physician?” and “Has your child ever had a problem with sneezing, or a runny or blocked nose, when they did not have a cold or the flu?” Asthma was defined as positive responses to "physician-diagnosed asthma" and the presence of nocturnal cough or exercise wheeze in the past 12 months.
Exposure measurements
The long-term exposure to background air pollution was estimated by linking the home addresses to six air quality monitoring stations in six districts in Taipei FigureS1. The home addresses and the monitoring stations were geo-coded using a geographic information system. An expert identified the nearest and most representative background monitoring station for each child. The distance between the home and the nearest monitoring station was determined using Google's online maps Figure S1. The temperature and relative humidity in each
monitoring site were also recorded. The mean concentrations of sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), carbon monoxide (CO), and particulate matter ≤ 10 μm and ≤ 2.5 μm in aerodynamic diameter (PM10 and PM2.5) from when the children were born to the end of the study were measured at the relevant monitoring station, and averaged to represent long-term cumulative exposure to air pollutants for each child.
Laboratory methods
Skin prick tests to six common allergens (house dust mites including Der p, Der f, Der m, and Blot allergens, cockroaches, animal dander, milk, eggs, and crab allergens, all from ALK-Abell & Oacute, USA) were performed. The tests were read at 15 minutes. In the presence of a positive control (>3 mm), a mean wheal diameter of at least 3 mm greater than the negative control was taken to be positive.
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Statistical analysis
The daily average concentrations of each air pollutant (PM10, PM2.5, SO2, NO2, CO and O3) were calculated. More than 75% of the data (for at least 18 hours in a 24-hour period) had to be available to be included in the analysis. We then calculated the average concentration from birth until the end of the study to estimate long-term cumulative exposure. Adjustments were made for temperature and relative humidity at each monitoring site. The air pollutant data obtained from the geographic information system were taken as independent variables in the regression model.
Multiple logistic regression analyses were performed to estimate the association between air pollutants, allergen sensitization, and the development of allergic diseases. Odds ratios (ORs) and a 95% confidence intervals (CIs) were adjusted for important potential
confounders. Potential confounders which were selected based on the previous literatures, including age, gender, body mass index, environmental tobacco smoke, maternal history of atopy, maternal education and nationality, family income, duration of breast feeding, duration of sleep, number of siblings, dampness of the house, fungus on the house wall, residence, temperature, relative humidity, and distance from the home to the air monitoring station were all taken into consideration. Variables were included in the model if they changed the
univariate point estimate by at least 10% .
To further assess the joint effect and interactions between air pollutants and allergen sensitization, we stratified our subjects into four groups: low air pollutant exposure without allergen sensitization, high air pollutant exposure without allergen sensitization, low air pollutant exposure with allergen sensitization, and high air pollutant exposure with allergen sensitization. Bonferroni correction was used to address the problem of multiple comparisons. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
In addition, gene-environmental interaction was tested by adding a product term in the regression model. Within the allergen sensitization category, a one degree of freedom trend test was used to evaluate the possible exposure-response relationship across categories of the air pollutant variables. All tests assumed a two-sided alternative hypothesis and a 0.05 significance level. All analyses were conducted using SAS software version 9.1 (SAS Institute, Cary, NC, USA).
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Results
A total of 3264 children were recruited with written informed consent. After excluding those who were multiple births (n=27), premature (n=152), had congenital and chronic diseases (n=105), were unable to answer questions in Chinese (n=126), had moved in or out of their current home (n=114), and those living more than 10 km from air monitoring stations (n=79), 2661 children were entered into the analysis. Among 2661 children participated in the study, 384 (14.4%) had AD, 799 (30.0%) had AR, and 336 (12.6%) had asthma. Table 1 outlines the demographic characteristics of the study population. Mite (43.1%) was the most common sensitizing aeroallergen, and milk (15.9%) was the most common sensitizing food allergen (Table 2). Boys had a higher mite sensitization rate than girls (Table 2). The annual average PM10 was 48.14 ± 1.31 μg/m3, followed by PM2.5 (28.81 ± 0.84 μg/m3), NO2 (23.04 ± 0.73 ppb), and SO2 (6.30 ± 0.57 ppb). The hourly average levels of CO and O3 were 0.63 ± 0.03 ppm and 40.65 ± 1.01 ppb, respectively (Table 3).
Mite sensitization significantly increased the risk of AD, AR, and asthma with ORs (95%CI) of 1.70 (1.37-2.12), 1.94 (1.64-2.29), and 2.17 (1.71-2.74) (Table 4). Cockroach sensitization also increased the risk of asthma 1.43 (1.06-1.94) and AR 1.35 (1.07-1.71), whereas milk sensitization significantly increased the risk of AD 1.35 (1.02-1.78). There were no significant differences in the association of other allergen sensitizations with allergic diseases.
Since the correlation of each air pollutant was high, they were put into different
independent models to avoid collinearity in subsequent analysis (Supplement Table S2). After controlling for potential confounders, PM10, PM2.5, and CO were significantly associated with asthma with ORs (95%CI) of 1.39 (1.03-1.87), 1.45 (1.07-1.97), and 1.36 (1.01-1.83), respectively (Table 5). O3 showed a protective effect on asthma 0.68 (0.51-0.92), however 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
SO2 and NO2 were not significantly associated with allergic diseases. The air pollutants had a positive relationship with AD, but this did not reach statistical significance.
Since only mite sensitization was associated with asthma, the association between air pollutants and mite sensitization on allergic diseases was further examined. Mite sensitization showed a synergistic effect with PM2.5 on asthma with ORs (95%CI) of1.60 (1.06-2.42) for high PM2.5 exposure without mite sensitization, 1.75 (1.12-2.73) for low PM2.5 exposure with mite sensitization, and 3.06 (1.89-4.93) for high PM2.5 exposure with mite sensitization, compared to the children with low PM2.5 exposure and without mite sensitization (p for trend < 0.001) (Table 6).Therefore, the children who had mite sensitization and were exposed to PM2.5had an increased risk of asthma. After stratification by mite sensitization, we found that mite allergens may modify the effect of PM10 and CO on AR and AD. However, mite
sensitization did not show significant interactive effects with air pollutants on asthma, AR, or AD (Table 6). 1 2 3 4 5 6 7 8 9 10 11 12 13
Discussion
In this study, we investigated the potential association between air pollutants, allergen sensitization, and pediatric allergic diseases. We found that dust mite sensitization and PM2.5 played an important role on the risk of asthma and AR. Children with mite sensitization were most susceptible to the adverse effects of air pollutants. In addition, exposure to PM2.5 and mite allergens had a synergistic effect on the development of asthma.
We also found that PM2.5, PM10, and CO were significantly associated with asthma. Gehring et al. also reported that PM constituents, reflecting poorly regulated non-tailpipe road traffic emissions, may increase the risk of asthma and allergy in schoolchildren (Gehring et al., 2015).Increased exposure to PM2.5 was associated with sensitization to both aero and food allergens and an increased risk of subsequent asthma in childhood. Moreover, the association between allergic rhinitis and PM2.5 absorbance was found to be significant in a study from Germany (Fuertes et al., 2013).Outdoor environmental exposure to O3, CO, NO, NO2, PM10, and SO2 has been well documented to exacerbate asthma. In addition to asthma exacerbation,
Clark et al. observed a statistically significantly increased risk of asthma development with increased early life exposure to CO, NO, NO2, PM10, SO2 and black carbon and the proximity to the point source (Clark et al., 2010).However, we failed to find significant associations between NO2, SO2, and O3and allergic diseases. Consistent with our study, Koo et al. also reported no association between O3 and respiratory symptoms among primary school children (Bernard et al., 2001). Different study populations, study design, different levels of exposure, and constituents of air pollutants (gas or particle) may explain differences between studies.
The biological mechanisms by which air pollutants exert toxic effects on asthma are not well understood. Aside from irritating the respiratory tract, Lin et al. reported that air
pollutants may cause elevated blood IgE (Donaldson et al., 2003).It is plausible that PM 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
stimulates dendritic cells and T cells to produce Th2 cytokines and activate pro-inflammatory genes in a process mediated by free radical and oxidative stress mechanisms. In contrast, some studies have reported that exposure to diesel exhaust particles (DEPs) did not significantly increase allergen-specific bronchial reactivity. However, adjuvant effects of DEPs on allergic inflammation have been reported (Riedl et al., 2012). After exposure to DEPs, elevated expressions of inflammatory mediators have been observed in the respiratory tract (Ghio et al., 2012). Therefore, DEPs are characterized by both adjuvant activity for sensitization against common allergens and enhancing the effects of allergic symptoms in sensitized patients. In addition, emerging evidence has shown that unique gene signatures and epigenetic control of immune- and inflammatory-based genes play important roles in the magnitude of the impact air pollutants have on respiratory health (Alexis and Carlsten, 2014).
After stratification by mite sensitization, the effects of PM10 and CO only remained in those with mite sensitization. Mite sensitization also showed a significant synergistic interaction with PM2.5 on asthma. Furthermore, the effect of air pollution from traffic on allergic diseases was modified by mite allergen sensitization. Exposure to TRAP during pregnancy may increase the risk of sensitization to allergens among asthmatic children (Mortimer et al., 2008).Curiously, children of dog owners were reported to be more likely to experience bronchitis symptoms following exposure to particulate matter than children living with a cat or no pets, suggesting that exposure to mammalian proteins could enhance the immune response to air pollution exposure (McConnell et al., 2006). Whether air pollutants-mediated up regulation of allergy is more likely to occur in association with mammalian proteins or those derived from arthropods requires further investigation. Previous studies suggest the ability of DEP to bind proteins (e.g. house dust mite allergens), which is why it may be considered to be a potential carrier of allergens. The majority of these particles are 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
small enough to penetrate deep into the respiratory tree and provoke allergic symptoms (Bernstein et al., 2012).DEPs have also been reported to enhance allergen sensitization, and to differentially affect the airway mucosa in healthy individuals and those with asthma (Stenfors et al., 2004).Moreover, early-life exposure to high DEP levels has been reported to be associated with significantly increased prevalence of asthma among allergic children but not among non-allergic children (Brandt et al., 2015). These findings suggest that exposure to DEPs results in accumulation of allergen-specific TH2/TH17 cells in the lungs, potentiating secondary allergen recall responses and promoting the development of allergic asthma (Brandt et al., 2015).
Whether children with asthma are more susceptible to O3-induced respiratory tract injury is of great interest (Balmes 1993). Consistent with our study, previous study also found long term O3 exposure had protective effect on the lifetime prevalence of asthma (Guo, et al, 1999). However,some studies reported short term O3 exposure may increaseasthma
exacerbation frequency (Chen, et al., 2014). This may be because of the differences of long term and short term exposure (Sheffield, et al., 2015).Another reason is that high traffic density is inversely correlated with concentrations of O3, which is formed at some distance
from emission sources and scavenged in city centers by nitrogen monoxide from vehicle exhaust (Wjst, et al, 1993). Further investigations are necessary to search for the
pathophysiological mechanisms of O3 on asthma.
There are several limitations to this study that may influence the interpretation of the results. First, we failed to collect the distances of the subjects’ residential address to the nearest major traffic load. Assessing exposure from air monitoring stations is regarded to be a surrogate measurement of exposure to air pollutants, which may be subject to
misclassification bias. However, a more suitable quantitative biomarker for air pollutants was 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
not available. Further individual monitoring of air pollutants and sampling of indoor allergens are necessary to better assess exposure. Furthermore, the study subjects were likely to be exposed to other sources of pollutants in addition to allergens such as tobacco smoke at home. Therefore, we adjusted for these potential confounders in our model. Another possible
limitation is recall bias with regards the allergic diseases. We combined two specific questions in the ISAAC questionnaire to define each allergic disease, and this has been validated by many epidemiological studies. Recall of allergic diseases was assessed in a subset of the study population, and concordance between the parental reports and medical records was good.
One of the strengths of this study is its inclusion of a large and socio-demographically diverse population of children in the community, which minimizes the likelihood of selection bias and may enhance the generality. Because of the large sample size, we were able to control for numerous potential confounders in the statistical analysis. This allowed us to perform subgroup investigations. Moreover, our data represent exposure reasonably well as we had information on the children’s residential history to formally assess the lifetime exposure to air pollution. We also excluded children who lived more than 10 km from the air monitoring stations using a geographic information system which could reduce selection bias. In addition, although associations between air pollutants and many allergic diseases have been previously investigated, this is the first study to report the joint effects of air pollutants and allergen sensitization on allergic diseases.
Conclusion
In conclusion, exposure to both outdoor air pollutants and indoor allergens was associated with allergic diseases in children. Exposure to PM2.5 and mite allergens had a 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
synergistic effect on the development of asthma. Mite allergens may modify the effect of air pollutants on allergic diseases, and avoiding co-exposure of indoor allergens and outdoor air pollutants is important. These findings provide an insight into the etiology of allergic
diseases, and also suggest that control measures to avoid allergen and air pollutant
co-exposure such as increasing ventilation of the home and living away from busy roads may be beneficial.
Conflict of interest statement: None declared.
Acknowledgments
We thank the CEAS study group (Professor Mei-Lien Chen, Pau-Chung Chen, Chen-Chang Yang, Dr. Wen-Chiuo Wu, and the related colleagues for collecting the data).
This study was supported by grants from the National Science Council (NSC 102-2628-B-192 -001 -MY3) in Taiwan and Taipei Hospital, Ministry of Health and Welfare.
Appendix A. Supplementary data
Supplementary data associated with this article can be found, in the online version. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18
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Table 1
Comparison of basic demographics of the study population
Abbreviations: BMI, body mass index; ETS, environmental tobacco smoke; NT$, Taiwan dollar.
amean ± SD
Characteristics Study population (n=2661) All participants (n=3246) Age (years)a 5.5 ± 1.1 7.7 ± 1.6 Gender (male) (%) 54.1 54.1 Weight (kg)a 18.8 ± 3.9 19.6 ± 6.4 Height (cm)a 107.6 ± 8.5 108.9 ± 11.5 BMI (kg/m2)a 16.2 ± 2.0 16.3 ± 2.3
Sleep duration (hours)a 9.0 ± 1.2 8.9 ± 1.2
ETS exposure (%) 64.1 57.8
Family history of atopy (%) 55.9 55.0
Breast feeding (%) 75.8 74.7
Family income per year (%)
< 1,000,000 NT$ 69.7 69.4
>1,010,000 NT$ 30.3 30.6
Maternal age (years)a 34.2 ± 4.3 29.3 ± 4.5 Maternal Education (%) <high school 27.6 27.4 high school 31.5 35.0 > college 40.8 37.7 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32
Table 2
The prevalence of allergic diseases and sensitization
Total Boys Girlsb
(N=2661) (N=1439) (N=1221)
Asthma(%)a 12.6 15.1 9.7
Allergic rhinitis(%)a 30.0 33.8 25.4
Atopic dermatitis(%) 14.4 14.9 13.8
Allergen sensitization rate(%)
Dust mitea 43.1 45.1 40.8 Cockroach 14.0 13.0 15.1 Animal dander 8.0 7.7 8.3 Milk 15.9 15.1 16.9 Egg 13.6 13.2 13.9 Crab 12.8 12.0 13.8
ap<0.05, represents a significant difference by gender using the chi-square test. bBoys vs. girls 1 2 3 4 5 6
Table 3
Meteorological factors and air pollutants in the study area in 2004-2011
Mean ± SD Median Min Max Quartile
Temperature(°C) 23.50 ± 0.29 23.47 21.58 29.10 23.33-23.64 Humidity (%) 72.11 ± 0.76 72.13 67.22 78.87 72.03-72.35 PM10 (μg/m3) 48.14 ± 1.31 48.32 27.75 52.77 47.08-49.24 PM2.5 (μg/m3) 28.81 ± 0.84 29.07 17.55 30.45 28.42-29.40 NO2 (ppb) 23.04 ± 0.73 23.03 16.48 26.03 22.86-23.28 SO2 (ppb) 6.30 ± 0.57 6.46 1.72 6.80 6.30-6.60 CO (ppm) 0.63 ± 0.03 0.63 0.39 0.82 0.62-0.64 O3 (ppb) 27.50 ± 0.61 27.62 23.58 31.37 27.43-27.84 8hO3 (ppb) 40.65 ± 1.01 40.84 28.49 42.40 40.58-41.19
Abbreviations: SO2,sulfur dioxide; NO2, nitrogen dioxide;O3, ozone; CO, carbon monoxide; PM10, particulate matter ≤ 10 μm; PM2.5, particulate matter ≤ 2.5 μm;8hO3, 8-hour average ozone concentration. 1 2 3 4 5 6 7
Table 4
The association of allergen sensitization with allergic diseases Allergen
sensitization
Allergic diseases
Asthma Allergic rhinitis Atopic dermatitis
OR (95% CI)a OR (95% CI) OR (95% CI)
Dust mite 2.17 (1.71-2.74)*** 1.94 (1.64-2.29)*** 1.70 (1.37-2.12)*** Cockroach 1.43 (1.06-1.94)* 1.35 (1.07-1.71)** 1.12 (0.83-1.52) Animal dander 1.38 (0.94-2.03) 1.23 (0.91-1.65) 1.19 (0.82-1.75) Milk 1.37 (1.02-1.84)* 1.03 (0.83-1.30) 1.35 (1.02-1.78)* Egg 1.32 (0.96-1.81) 1.10 (0.87-1.40) 1.23 (0.91-1.66) Crab 1.18 (0.85-1.64) 0.94 (0.73-1.21) 1.06 (0.77-1.46)
Abbreviations: OR, odds ratio; CI, confidence interval *p<0.05, **p<0.01, ***p<0.001
aModels are adjusted for age, gender, BMI, environmental tobacco smoke, maternal history of atopy, maternal education and nationality, duration of breast feeding, duration of sleep, number of siblings, temperature, relative humidity.
1 2 3 4 5 6 7 8 9
Table 5
The association between air pollutants and allergic diseases Air pollutants Allergic diseases Asthma OR (95% CI)b Allergic rhinitis OR (95% CI) Atopic dermatitis OR (95% CI) Outdoor PM10 1.39 (1.03-1.87)* 1.15 (0.79-1.66) 1.00 (0.70-1.44) PM2.5 1.45 (1.07-1.97)* 1.54 (1.03-2.32)* 1.25 (0.85-1.82) NO2 1.33 (0.99-1.78) 0.95 (0.74-1.20) 1.33 (0.98-1.79) SO2 1.10 (0.82-1.48) 1.00 (0.78-1.29) 1.24 (0.90-1.70) CO 1.36 (1.01-1.83)* 1.02 (0.80-1.29) 1.33 (0.98-1.80) O3 0.68 (0.51-0.92)* 1.01 (0.76-1.34) 1.03 (0.77-1.38) 8hO3 0.79 (0.59-1.07) 1.07 (0.85-1.36) 1.22 (0.93-1.60) Indoor ETS 1.28 (1.00-1.64)* 1.26 (1.05-1.49)* 0.90 (0.72-1.13) Dampness 1.10 (0.88-1.39) 0.90 (0.76-1.07) 1.03 (0.83-1.27) Heating 0.78 (0.62-0.98)* 0.83 (0.70-0.98)* 1.02 (0.82-1.27)
Abbreviations: SO2,sulfur dioxide; NO2, nitrogen dioxide;O3, ozone; CO, carbon monoxide; PM10, particulate matter ≤ 10 μm; PM2.5, particulate matter ≤ 2.5 μm;8hO3, 8-hour average ozone concentration; ETS, environmental tobacco smoke.
*p<0.05
aAir pollutant levels were dichotomized into high and low exposure groups with the cut off value of the median level; PM10 48.32μg/m3;PM2.5 29.07μg/m3;NO2 23.03ppb;SO2 6.46ppb;CO 0.63ppm;O3 27.62ppb;8hO3 40.84ppb;temperature 23.47°C;humidity 72.13%.The low
exposure group served as the controls.
bModels were adjusted for age, gender, body mass index, environmental tobacco smoke, maternal history of atopy, maternal education and nationality, duration of breast feeding, duration of sleep, number of siblings, temperature, relative humidity, and distance from the home to the air monitoring station
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
Table 6
Joint effect of exposure to air pollutants and mite allergens on allergic diseases
Asthma Allergic rhinitis Atopic dermatitis
Mite
sensitization ORb 95%CI OR 95%CI OR 95%CI
Air pollutanta PM2.5 Low - 1 1 1 High - 1.60 (1.06,2.42) 1.39 (1.01,1.90) 1.43 (0.95,2.15) Low + 1.75 (1.12,2.73) 1.78 (1.32,2.41) 2.33 (1.64,3.30) High + 3.06 (1.89,4.93) 2.50 (1.75,3.58) 2.27 (1.44,3.56) p for trend <0.001 <0.001 <0.001 p for interaction 0.756 0.966 0.137 PM10 Low - 1 1 1 High - 1.39 (0.90,2.15) 1.18 (0.86,1.61) 1.15 (0.77,1.73) Low + 1.44 (0.95,2.18) 1.77 (1.31,2.39) 2.34 (1.66,3.30) High + 2.64 (1.66,4.20) 2.14 (1.50,3.05) 1.80 (1.16,2.81) p for trend <0.001 <0.001 <0.001 p for interaction 0.318 0.910 0.119 O3 Low - 1 1 1 High - 0.64 (0.44,0.92) 0.89 (0.68,1.16) 0.93 (0.66,1.31) Low + 1.77 (1.23,2.55) 1.77 (1.32,2.37) 1.86 (1.29,2.69) High + 1.04 (0.68,1.59) 1.63 (1.20,2.24) 1.87 (1.28,2.72) p for trend <0.001 <0.001 <0.001 p for interaction 0.773 0.852 0.778 CO Low - 1 1 1 High - 1.25 (0.86,1.81) 0.99 (0.76,1.29) 1.25 (0.89,1.77) Low + 1.47 (0.98,2.21) 1.77 (1.32,2.38) 2.13 (1.50,3.03) High + 2.39 (1.58,3.61) 1.81 (1.32,2.49) 2.19 (1.47,3.25) p for trend <0.001 <0.001 <0.001 p for interaction 0.345 0.880 0.435
aAir pollutant levels were dichotomized into high and low exposure groups with the cut off value of the median level; PM10 48.32μg/m3; PM2.5 29.07μg/m3; CO 0.63ppm; O3 27.62ppb. The low exposure group served as the controls.
bModels were adjusted for age, gender, body mass index, environmental tobacco smoke, maternal history of atopy, maternal education and nationality, duration of breast feeding, duration of sleep, number of siblings, temperature, relative humidity, and distance from the home to the air monitoring station. p values were adjusted for multiple testing.
1 2 3 4 5 6 7 8 9 10
