A limited number of studies have reported an association between long-term exposure to ambient air pollutants and lung function growth among children, with inconclusive results.
To assess the ...relationship between air pollutant exposure and lung function growth, and to examine potential sex differences in the susceptibility of lung function growth to air pollution.
We conducted a two-year prospective cohort study of Taiwanese children aged 12 at baseline who were followed from October 1, 2007 to November 31, 2009. The study population comprised 2941 non-smoking children who completed pulmonary function tests at both baseline and follow-up surveys. We applied spatial modeling for individual-level exposure assessment to capture relevant exposures and also attempted to eliminate potential community-level confounding. The exposure parameters were annual averages and values calculated from 24-hourly PM2.5 and 8-hourly ozone (O3) concentrations, corresponding to the residential addresses over the study period. The effect estimates were presented as lung function growth deficits per interquartile range (IQR) for PM2.5 and O3.
In a multiple linear mixed effect model, adjusted for confounding, growth deficits in the forced vital capacity (FVC), forced expiration volume in 1s (FEV1), and forced expiratory flow between the 25th and 75th percentiles of the FVC were associated with increased exposure to PM2.5 and O3. For example, greater exposure to PM2.5 (IQR, 17.92μg/m3) was associated with an annual deficit in FVC growth of 75mL in boys and 61mL in girls (p for interaction <0.05). Similar associations were found for O3.
The study provides evidence that long-term exposure to PM2.5 and O3 may have a detrimental effect on the development of lung function in children. The estimated deficits were generally larger in boys, compared to girls.
•We assessed the relationship between air pollutants and lung function growth.•Exposure to PM2.5 and O3 may increase the risk of deficits in FVC, FEV1, and MMEF.•The estimated deficits were generally larger for boys than girls.
Available prospective studies of obesity and asthma have used only body mass index (BMI) as an indicator for adiposity; studies using detailed obesity measures are lacking, and the role of physical ...fitness level and sedentary time remains unexplored in the link between obesity and asthma.
To compare various anthropometric measures of obesity in relation to childhood asthma, and to further characterize the interrelations among central obesity, physical fitness level, sedentary time, and asthma.
The nationwide Taiwan Children Health Study followed 2,758 schoolchildren from fourth to sixth grade, annually collecting data regarding physical fitness, sedentary time, obesity measures (comprising body weight and height, abdominal and hip circumference, skin fold thickness, and body composition), asthma, and pulmonary function tests. The generalized estimating equation was used for 3 years of repeated measurements to analyze the interrelation among obesity, sedentary time, physical fitness level, and asthma; a structural equation model was used to explore the pathogenesis among these factors. Asthma incidence was analyzed during a 2-year follow-up among centrally obese and nonobese groups in baseline children without asthma.
Central obesity most accurately predicts asthma. Low physical fitness levels and high screen time increase the risk of central obesity, which leads to asthma development. Obesity-related reduction in pulmonary function is a possible mechanism in the pathway from central obesity to asthma.
Central obesity measures should be incorporated in childhood asthma risk predictions. Children are encouraged to increase their physical fitness levels and reduce their sedentary time to prevent central obesity-related asthma.
Prenatal oxidative balance might influence cord blood IgE (cIgE) levels. We aimed to explore if certain prenatal dietary sources of antioxidants and pro-oxidants are associated with cIgE elevation ...and if they interact with IL4 and IL13 pathway genes. A structured questionnaire was completed during the third trimester of pregnancy for 1107 full-term newborns. Surveyed antioxidant-enriched food included fish, shellfish, and fruit, whereas surveyed pro-oxidant-contained food included fried fish sticks and canned fish. Cord blood was collected for measuring cIgE levels and genotyping IL13 rs1800925, rs20541, rs848, IL4 rs2243250, and STAT6 rs324011. Fairly lean fish consumption showed protection against cIgE elevation (odds ratio OR 0.66; 95% CI 0.49-0.90) in the whole sample, while daily fruit (OR 0.46; 95% CI 0.27-0.79) and ≥ monthly canned fish (OR 2.81; 95% CI 1.24-6.36) exhibited associations only in genetically susceptible babies. A prenatal food protective index, comprising any fairly lean fish, daily fruit, and the absence of any canned fish, exerted dose-response protection against cIgE elevation in babies carrying the IL13 rs20541 GA or AA genotype (P for trend < 0.0001; P for interaction = 0.004). We concluded that prenatal antioxidant-enriched and pro-oxidant-contained food consumption may influence cIgE, especially in genetically susceptible babies.
Perfluorinated compounds (PFCs) are ubiquitous pollutants. Experimental data suggest that they may be associated with adverse health outcomes, including asthma. However, there is little supporting ...epidemiological evidence.
A total of 231 asthmatic children and 225 nonasthmatic controls, all from northern Taiwan, were recruited in the Genetic and Biomarkers study for Childhood Asthma. Structure questionnaires were administered by face-to-face interview. Serum concentrations of 11 PFCs and levels of immunological markers were also measured. Associations of PFC quartiles with concentrations of immunological markers and asthma outcomes were estimated using multivariable regression models.
Nine PFCs were detectable in most children (≥ 84.4%), of which perfluorooctane sulfonate (PFOS) was the most abundant (median serum concentrations of 33.9 ng/mL in asthmatics and 28.9 ng/mL in controls). Adjusted odds ratios for asthma among those with the highest versus lowest quartile of PFC exposure ranged from 1.81 (95% CI: 1.02, 3.23) for the perfluorododecanoic acid (PFDoA) to 4.05 (95% CI: 2.21, 7.42) for perfluorooctanic acid (PFOA). PFOS, PFOA, and subsets of the other PFCs were positively associated with serum IgE concentrations, absolute eosinophil counts (AEC), eosinophilic cationic protein (ECP) concentrations, and asthma severity scores among asthmatics.
This study suggests an association between PFC exposure and juvenile asthma. Because of widespread exposure to these chemicals, these findings may be of potential public health concern.
Background
Respiratory syncytial virus (RSV) infection is epidemiologically linked to asthma. During RSV infection, IL‐33 is elevated and promotes immune cell activation, leading to the development ...of asthma. However, which immune cells are responsible for triggering airway hyperreactivity (AHR), inflammation and eosinophilia remained to be clarified. We aimed to elucidate the individual roles of IL‐33‐activated innate immune cells, including ILC2s and ST2+ myeloid cells, in RSV infection‐triggered pathophysiology.
Methods
The role of IL‐33/ILC2 axis in RSV‐induced AHR inflammation and eosinophilia were evaluated in the IL‐33‐deficient and YetCre‐13 Rosa‐DTA mice. Myeloid‐specific, IL‐33‐deficient or ST2‐deficient mice were employed to examine the role of IL‐33 and ST2 signaling in myeloid cells.
Results
We found that IL‐33‐activated ILC2s were crucial for the development of AHR and airway inflammation, during RSV infection. ILC2‐derived IL‐13 was sufficient for RSV‐driven AHR, since reconstitution of wild‐type ILC2 rescued RSV‐driven AHR in IL‐13‐deficient mice. Meanwhile, myeloid cell‐derived IL‐33 was required for airway inflammation, ST2+ myeloid cells contributed to exacerbation of airway inflammation, suggesting the importance of IL‐33 signaling in these cells. Local and peripheral eosinophilia is linked to both ILC2 and myeloid IL‐33 signaling.
Conclusions
This study highlights the importance of IL‐33‐activated ILC2s in mediating RSV‐triggered AHR and eosinophilia. In addition, IL‐33 signaling in myeloid cells is crucial for airway inflammation.
Respiratory syncytial virus induces ILC2 to produce IL‐5 and IL‐13 through IL‐33, which is crucial for the development of airway hyperreactivity and airway inflammation. Myeloid cell‐derived IL‐33 and suppression of tumorigenicity 2‐positive myeloid cells contribute to cytokine production and cellular inflammation in airway. Both ILC2 and myeloid cell IL‐33 signaling contribute to local and peripheral eosinophilia.
The relationship between ambient air pollution exposure and mortality of cardiovascular and cerebrovascular diseases in human is controversial, and there is little information about how exposures to ...ambient air pollution contribution to the mortality of cardiovascular and cerebrovascular diseases among Chinese. The aim of the present study was to examine whether exposure to ambient-air pollution increases the risk for cardiovascular and cerebrovascular disease.
We conducted a retrospective cohort study among humans to examine the association between compound-air pollutants particulate matter <10 µm in aerodynamic diameter (PM(10)), sulfur dioxide (SO(2)) and nitrogen dioxide (NO(2)) and mortality in Shenyang, China, using 12 years of data (1998-2009). Also, stratified analysis by sex, age, education, and income was conducted for cardiovascular and cerebrovascular mortality. The results showed that an increase of 10 µg/m(3) in a year average concentration of PM(10) corresponds to 55% increase in the risk of a death cardiovascular disease (hazard ratio HR, 1.55; 95% confidence interval CI, 1.51 to 1.60) and 49% increase in cerebrovascular disease (HR, 1.49; 95% CI, 1.45 to 1.53), respectively. The corresponding figures of adjusted HR (95%CI) for a 10 µg/m(3) increase in NO(2) was 2.46 (2.31 to 2.63) for cardiovascular mortality and 2.44 (2.27 to 2.62) for cerebrovascular mortality, respectively. The effects of air pollution were more evident in female that in male, and nonsmokers and residents with BMI<18.5 were more vulnerable to outdoor air pollution.
Long-term exposure to ambient air pollution is associated with the death of cardiovascular and cerebrovascular diseases among Chinese populations.
Memory T helper (Th) and regulatory T (Treg) cells play key roles in asthma. Certain sialyl carbohydrate determinants for selectins profoundly affect the migratory properties of memory Th cells, and ...the suppressive function of Treg cells. Previous studies have shown that the proportion of CCR4
memory Th cells expressing sialyl 6-sulfo Lewis X (Le
) is elevated in asthma patients. We aim to investigate the roles of different sialyl glycans on T cell subsets in asthma. Using flow cytometry, we assessed the expression of three sialyl glycans, sialyl 6-sulfo Le
, cyclic sialyl 6-sulfo Le
, and sialyl Le
on memory Th and Treg cells, in the peripheral blood of asthmatic children. We also assessed the relationships between glycan-expressing cell percentages and asthma clinical parameters. Compared with controls, asthmatic children showed higher proportions of memory Th cells expressing sialyl Le
and sialyl 6-sulfo Le
. The proportions of memory Th cells with sialyl 6-sulfo Le
and cyclic sialyl 6-sulfo Le
expression in asthmatic children correlated with absolute eosinophil count and IgE level, respectively. Children with moderate-to-severe asthma had lower numbers of sialyl Le
positive Treg cells. Our study suggests that sialyl glycans on T cells may play important roles in the pathogenesis of asthma.
There were limited studies concerning ambient air pollution exposure on development of bronchitic symptoms among children. These studies provided suggestive but inconclusive results. Therefore, the ...objective of this study is to assess the association between air pollutants and the prevalence of bronchitic symptoms in the Taiwan Children Health Study.
We conducted a nationwide cross-sectional study of 5,049 Taiwanese children in 2007. Routine air pollution monitoring data were used for sulfur dioxide (SO(2)), nitrogen dioxides (NO(2)), ozone (O(3)), carbon monoxide (CO), and particles with an aerodynamic diameter ≤ 2.5 μm (PM(2.5)). The exposure parameters were calculated using the between-community 3-year average concentration. The effect estimates were presented as odds ratios (ORs) per interquartile changes for SO(2), NO(2), O(3), CO, and PM(2.5).
In the two-stage hierarchical model adjusting for confounding, the prevalence of bronchitic symptoms with asthma was positively associated with the between-community 3-year average concentrations of NO(2) (adjusted OR, 1.81 per 8.79 ppb; 95% CI, 1.14-2.86), and CO (OR, 1.31 per 105 ppb; 95% CI, 1.04-1.64). The prevalence of phlegm with no asthma was related to O(3) (OR, 1.32 per 8.77 ppb; 95% CI, 1.06-1.63).
The results suggest that long-term exposure to outdoor air pollutants, such as NO(2), CO, and O(3), may increase the prevalence of bronchitic symptoms among children.
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