Green Solvent Selection for All Solution-Processed Inverted Quantum Dot Light Emitting Diode.

Quantum-dot light-emitting diodes (QD-LEDs) have gained attention as potential display technologies. However, the solvents used to dissolve a polymeric hole transport layer (HTL) are hazardous to both humans and the environment. Additionally, intermixing the HTL and QD layers presents a significant challenge when fabricating inverted QD-LEDs. Here, a green solvent selection procedure to achieve good device performance and environmental safety in QD-LEDs is established. This procedure utilizes Hansen solubility parameters and surface roughness to identify a set of solvents that do not lower the device performance by avoiding interlayer mixing or a rough interface. The CHEM21 solvent selection guide is used to screen for environmentally hazardous solvents. Finally, cyclopentanone (CPO) is selected as the optimal HTL solvent from among 16 candidates. Using CPO improves the maximum luminescence by ≈1.6 times and the maximum current efficiency by ≈12.6 times, compared to that of conventional devices using hazardous chlorobenzene. Solvent selection is critical for the fabrication of green and high-performance inverted QD-LEDs, particularly for large display panels that require n-type oxide thin-film transistors.

Insights from the COCOA birth cohort: The origins of childhood allergic diseases and future perspectives.

The ongoing COhort for Childhood Origin of Asthma and allergic diseases (COCOA) study is a prospective birth cohort investigating the origin and natural courses of childhood allergic diseases, including atopic dermatitis, food allergy, allergic rhinitis and asthma, with long-term prognosis. Initiated under the premise that allergic diseases result from a complex interplay of immune development alterations, environmental exposures, and host susceptibility, the COCOA study explores these dynamic interactions during prenatal and postnatal periods, framed within the hygiene and microbial hypotheses alongside the developmental origins of health and disease (DOHaD) hypothesis. The scope of the COCOA study extends to genetic predispositions, indoor and outdoor environmental variables affecting mothers and their offsprings such as outdoor and indoor air pollution, psychological factors, diets, and the microbiomes of skin, gut, and airway. We have embarked on in-depth investigations of diverse risk factors and the pathophysiological underpinnings of allergic diseases. By employing multi-omics approaches-proteomics, transcriptomics, and metabolomics-we gain deeper insights into the distinct pathophysiological processes across various endotypes of childhood allergic diseases, incorporating the exposome using extensive resources within the COCOA study. Integration with large-scale datasets, such as national health insurance records, enhances robustness and mitigates potential limitations inherent to birth cohort studies. As part of global networks focused on childhood allergic diseases, the COCOA study fosters collaborative research across multiple cohorts. The findings from the COCOA study are instrumental in informing precision medicine strategies for childhood allergic diseases, underpinning the establishment of disease trajectories.

Prenatal maternal anxiety promotes atopic dermatitis in offspring via placental DNA methylation changes.

BACKGROUND: Maternal anxiety during pregnancy has been previously reported to be associated with atopic dermatitis (AD) in offspring. The potential mechanism is not yet proven but epigenetic change may be suggested. OBJECTIVE: We examined whether maternal anxiety during pregnancy may alter placental DNA methylation, then develop AD in the offspring. METHODS: We evaluated maternal anxiety at 36 weeks of gestation by self-reported questionnaires, the State-Trait Anxiety Inventory-Trait subscale (STAI-T), in the Cohort for Childhood Origin of Asthma and Allergic Diseases (COCOA) study. AD was diagnosed at 6 months of age by pediatric allergists. We stratified the subjects into four groups according to the STAI score of mothers and diagnosis of AD in children. Placental genome-wide methylation microarray was analyzed using Infinium 450K BeadChip and selected genes were validated by pyrosequencing. RESULTS: From microarray, several differential methylation sites were identified in AD and healthy subjects and in total subjects, regarding to the STAI scores. Among differential methylation sites in microarray, six sites were selected for pyrosequencing. And site of matrix metalloproteinases 27 (MMP27) among 6 sites showed decreased methylation in AD infants with high STAI mothers compared to healthy infants with low STAI mothers. CONCLUSIONS: Epigenetic change in placenta can be a suggesting mechanism for the development of AD in offspring at 6 months of age associated with maternal anxiety during pregnancy and MMP27 may be a candidate gene.

Particulate matter exposure during pregnancy increases risk of childhood asthma: modified by gender and NRF2 genotype.

BACKGROUND: Exposure to particulate matter (PM) has been known to develop asthma in children and the oxidative stress-related mechanisms are suggested. For the development of asthma, not only the exposure dose but also the critical window and the risk modifying factors should be evaluated. OBJECTIVE: We investigated whether prenatal exposure to PM10 increases the risk of childhood asthma and evaluated the modifying factors, such as gender and reactive oxidative stress-related gene. METHODS: A general population-based birth cohort, the Panel Study of Korean Children (PSKC), including 1572 mother-baby dyads was analyzed. Children were defined to have asthma at age 7 when a parent reported physician-diagnosed asthma. Exposure to PM10 during pregnancy was estimated by land-use regression models based on national monitoring system. TaqMan method was used for genotyping nuclear factor, erythroid 2-related factor, NRF2 (rs6726395). A logistic Bayesian distributed lag interaction model (BDLIM) was used to evaluate the associations between prenatal PM10 exposure and childhood asthma by gender and NRF2. RESULTS: Exposure to PM10 during pregnancy was associated with the development of asthma (aOR 1.03, 95% CI 1.001.06). Stratifying by gender and NRF2 genotype, exposure to PM10 during 26-28 weeks gestation increased the risk of childhood asthma, especially in boys with NRF2 GG genotype. CONCLUSIONS: A critical window for PM10 exposure on the development of childhood asthma was during 26-28 weeks of gestation, and this was modified by gender and NRF2 genotype.

Analysis of national surveillance of respiratory pathogens for community-acquired pneumonia in children and adolescents.

BACKGROUND: Respiratory infections among children, particularly community-acquired pneumonia (CAP), is a major disease with a high frequency among outpatient and inpatient visits. The causes of CAP vary depending on individual susceptibility, the epidemiological characteristics of the community, and the season. We performed this study to establish a nationwide surveillance network system and identify the causative agents for CAP and antibiotic resistance in Korean children with CAP. METHODS: The monitoring network was composed of 28 secondary and tertiary medical institutions. Upper and lower respiratory samples were assayed using a culture or polymerase chain reaction (PCR) from August 2018 to May 2020. RESULTS: A total of 1023 cases were registered in patients with CAP, and PCR of atypical pneumonia pathogens revealed 422 cases of M. pneumoniae (41.3%). Respiratory viruses showed a positivity rate of 65.7% by multiplex PCR test, and human rhinovirus was the most common virus, with 312 cases (30.5%). Two hundred sixty four cases (25.8%) were isolated by culture, including 131 cases of S. aureus (12.8%), 92 cases of S. pneumoniae (9%), and 20 cases of H. influenzae (2%). The cultured, isolated bacteria may be colonized pathogen. The proportion of co-detection was 49.2%. The rate of antibiotic resistance showed similar results as previous reports. CONCLUSIONS: This study will identify the pathogens that cause respiratory infections and analyze the current status of antibiotic resistance to provide scientific evidence for management policies of domestic respiratory infections. Additionally, in preparation for new epidemics, including COVID-19, monitoring respiratory infections in children and adolescents has become more important, and research on this topic should be continuously conducted in the future.

Mid-pregnancy PM2.5 exposure affects sex-specific growth trajectories via ARRDC3 methylation.

Prenatal particulate matter <2.5 µm (PM2.5) is associated with adverse birth growth. However, the longitudinal growth impacts have been little studied, and no mechanistic relationships have been described. We investigated the association between prenatal PM2.5 exposure and growth trajectories, and the possible role of epigenetics. We enrolled 1313 neonates with PM2.5 data measured by ordinary kriging from the COhort for Childhood Origin of Asthma and allergic diseases, followed up at 1, 3, and 5 years to evaluate growth. Differential DNA methylation and pyrosequencing of cord blood leukocytes was evaluated according to the prenatal PM2.5 levels and birth weight (BW). PM2.5 exposure during the second trimester (T2) caused the lowest BW in both sexes, further adjusted for indoor PM2.5 levels [female, aOR 1.39 (95% CI 1.05-1.83); male, aOR 1.36 (95% CI 1.04-1.79)]. Bayesian distributed lag models with indoor PM2.5 adjustments revealed a sensitive window for BW effects at 10-26 weeks gestation, but only in females. Latent class mixture models indicated that a persistently low weight-for-height percentile trajectory was more prevalent in the highest PM2.5 exposure quartile at T2 in females, compared to a persistently high trajectory (36.5% vs. 20.3%, P = 0.022). Also, in the females only, the high PM2.5 and low BW neonates showed significantly greater ARRDC3 methylation changes. ARRDC3 methylation was also higher only in females with low weight at 5 years of age. Higher fetal PM2.5 exposure during T2 may cause a decreased growth trajectory, especially in females, mediated by ARRDC3 hyper-methylation-associated energy metabolism.

Prenatal PM2.5 exposure and vitamin D-associated early persistent atopic dermatitis via placental methylation.

BACKGROUND: The effects of prenatal particulate matter with an aerodynamic diameter ranging from 0.1 µm to 2.5 µm (PM2.5) and vitamin D on atopic dermatitis (AD) phenotypes have not been evaluated. DNA methylation and cord blood (CB) vitamin D could represent a plausible link between prenatal PM2.5 exposure and AD in an offspring. OBJECTIVE: To determine the critical windows of prenatal PM2.5 exposure on the AD phenotypes, if vitamin D modulated these effects, and if placental DNA methylation mediated these effects on AD in offspring. METHODS: Mother-child pairs were enrolled from the birth cohort of the Cohort for Childhood Origin of Asthma and allergic diseases (COCOA) study. PM2.5 was estimated by land-use regression models, and CB vitamin D was measured by chemiluminescence immunoassay. AD was identified by the parental report of a physician's diagnosis. We defined the following 4 AD phenotypes according to onset age (by the age of 2 years) and persistence (by the age of 3 years): early-onset transient and persistent, late onset, and never. Logistic regression analysis and Bayesian distributed lag interaction model were used. DNA methylation microarray was analyzed using an Infinium Human Methylation EPIC BeadChip (Illumina, San Diego, California) in placenta. RESULTS: PM2.5 exposure during the first trimester of pregnancy, especially during 6 to 7 weeks of gestation, was associated with early-onset persistent AD. This effect increased in children with low CB vitamin D, especially in those with PM2.5 exposure during 3 to 7 weeks of gestation. AHRR (cg16371648), DPP10 (cg19211931), and HLADRB1 (cg10632894) were hypomethylated in children with AD with high PM2.5 and low CB vitamin D. CONCLUSION: Higher PM2.5 during the first trimester of pregnancy and low CB vitamin D affected early-onset persistent AD, and the most sensitive window was 6 to 7 weeks of gestation. Placental DNA methylation mediated this effect.

Annual and seasonal patterns in etiologies of pediatric community-acquired pneumonia due to respiratory viruses and Mycoplasma pneumoniae requiring hospitalization in South Korea.

BACKGROUND: Community-acquired pneumonia (CAP) is one of the leading worldwide causes of childhood morbidity and mortality. Its disease burden varies by age and etiology and is time dependent. We aimed to investigate the annual and seasonal patterns in etiologies of pediatric CAP requiring hospitalization. METHODS: We conducted a retrospective study in 30,994 children (aged 0-18 years) with CAP between 2010 and 2015 at 23 nationwide hospitals in South Korea. Mycoplasma pneumoniae (MP) pneumonia was clinically classified as macrolide-sensitive MP, macrolide-less effective MP (MLEP), and macrolide-refractory MP (MRMP) based on fever duration after initiation of macrolide treatment, regardless of the results of in vitro macrolide sensitivity tests. RESULTS: MP and respiratory syncytial virus (RSV) were the two most commonly identified pathogens of CAP. With the two epidemics of MP pneumonia (2011 and 2015), the rates of clinical MLEP and MRMP pneumonia showed increasing trends of 36.4% of the total MP pneumonia. In children < 2 years of age, RSV (34.0%) was the most common cause of CAP, followed by MP (9.4%); however, MP was the most common cause of CAP in children aged 2-18 years of age (45.3%). Systemic corticosteroid was most commonly administered for MP pneumonia. The rate of hospitalization in intensive care units was the highest for RSV pneumonia, and ventilator care was most commonly needed in cases of adenovirus pneumonia. CONCLUSIONS: The present study provides fundamental data to establish public health policies to decrease the disease burden due to CAP and improve pediatric health.

Is it necessary to evaluate urinary tract infection in children with lower respiratory tract infection?

AIM: Although the incidence of urinary tract infection (UTI) in children with lower respiratory tract infection (LRTI) has been reported as 3.1-10.0%, the exact concomitant prevalence is questionable. Here, we evaluated the prevalence and related risk factors of UTI associated with LRTI in children under 36 months of age. METHODS: We retrospectively reviewed the medical charts of 1574 patients under 36 months of age who were hospitalised with LRTI from January 2017 to December 2019 in a single centre, Seoul, South Korea. Among them, we analysed 278 patients who showed fever and performed urine evaluation. Urine was collected by catheterisation in children under 24 months of age and by voided urine between 24 and 36 months of age. RESULTS: The prevalence of concomitant UTI and LRTI was 13.6% in children under 24 months of age. Mean age was significantly younger in the UTI versus non-UTI group (6.93 ± 7.26 months vs. 12.61 ± 11.70 months; P < 0.001). When the participants were stratified by age, the prevalence of UTI was significantly higher in children younger than 24 months of age compared to older ones (P = 0.006). UTIs were more prevalent in boys than in girls (14.6% vs. 5.8%, P = 0.018). Peak body temperature, fever duration, premature birth and detected respiratory virus type did not differ between groups. CONCLUSIONS: It is not uncommon for children with LRTI with fever to be accompanied by UTI. When evaluating for UTI in children with febrile LRTI, age and sex must be considered.

Prenatal particulate matter affects new asthma via airway hyperresponsiveness in schoolchildren.

BACKGROUND: The most relevant time of PM10 exposure to affect airway hyperresponsiveness (AHR) and new development of asthma in school-aged children is unclear. The aims of this study were to investigate the most critical time of PM10 exposure to affect AHR and new diagnosis of asthma from AHR in school-aged children. METHODS: Elementary schoolchildren (n = 3570) have been enrolled in a nationwide prospective 4-year follow-up survey in Korea from 2005 to 2006. Individual annual PM10 exposure was estimated by using an ordinary kriging method from the prenatal period to 7 years of age. AHR at 7 years was defined by a methacholine PC20 ≤8 mg/mL. RESULTS: PM10 exposure during pregnancy and at 1 year of age showed significant effects on AHR (aOR: 1.694, 95% CI: 1.298-2.209; and aOR: 1.750, 95% CI: 1.343-2.282, respectively). PM10 exposure during pregnancy was associated with the risk of a new diagnosis of asthma (aOR: 2.056, 95% CI: 1.240-3.409), with the highest risk in children with AHR at age 7 (aOR: 6.080, 95% CI: 2.150-17.195). PM10 exposure in the second trimester was associated with the highest risk of a new diagnosis of asthma in children with AHR at age 7 (aOR: 4.136, 95% CI: 1.657-10.326). CONCLUSIONS: Prenatal PM10 exposure in the second trimester is associated with an increased risk of a new diagnosis of asthma in school-aged children with AHR at 7 years. This study suggests that PM10 exposure during a specific trimester in utero may affect the onset of childhood asthma via AHR.

The Korean Version of the Test for Respiratory and Asthma Control in Kids (TRACK): Reliability and Validity.

BACKGROUND: Test for Respiratory and Asthma Control in Kids (TRACK) questionnaires were developed and validated in various languages to monitor respiratory control in preschool-aged children. We aimed to assess the reliability and validity of the Korean version of the TRACK questionnaire. METHODS: We administered the linguistically validated TRACK questionnaires to caregivers of asthmatic preschool children on two separate visits 4-6 weeks apart. Each physician graded the level of the guideline-based asthma control, assessed the timing of symptoms, and adjusted the therapeutic level at each visit. RESULTS: A total of 137 children were enrolled in the study. Cronbach's alpha was 0.65 for a questionnaire as a whole. The test-retest reliability was 0.72. The median TRACK scores were significantly different between asthma control status categories, with the lowest scores in children classified as poorly controlled and the highest in the well-controlled group (P < 0.001). They were different among groups classified according to the physician adjusted therapeutic levels, with the lowest values in children prescribed step-up therapy (P < 0.001), and according to the recency of respiratory symptoms (P < 0.001). Finally, the changes in TRACK scores between visits were highest in subjects showing improved control, followed by unchanged, and worsened control. When we applied the traditional cut-off of 80 for a well-controlled condition, a sensitivity of 75.6% and a specificity of 70.9% were calculated. CONCLUSION: The Korean translated version of the TRACK questionnaire is valid and reliable to assess respiratory and asthma control in Korean preschool children with asthma symptoms.

Clinical phenotypes of bronchial hyperresponsiveness in school-aged children.

BACKGROUND: Bronchial hyperresponsiveness (BHR), one of the key features of asthma, has a diverse natural course in school-aged children, but studies on BHR phenotypes are lacking. OBJECTIVE: To classify BHR phenotypes according to onset age and persistence in children and investigate the characteristics and factors associated with each phenotype in a longitudinal study. METHODS: This study analyzed 1,305 elementary school children from the Children's Health and Environmental Research (CHEER) study, a 4-year, prospective, follow-up study with 2-year intervals starting at a mean age of 7years. Total serum IgE levels and blood eosinophil counts were measured, and allergy workup, including methacholine challenge tests with the International Study of Asthma and Allergies in Childhood questionnaire, was performed at each survey. RESULTS: The 4 BHR phenotypes were classified as non-BHR (n = 942 [72.2%]), early-onset transient BHR (n = 201 [15.4%]), late-onset BHR (n = 87 [6.7%]), and early-onset persistent BHR (n = 75 [5.7%]). Early-onset persistent BHR is characterized by an increased eosinophil count, total serum IgE level, sensitization rate, decreased lung function, and increased risk of newly diagnosed asthma during follow-up (adjusted odds ratio, 3.89; 95% confidence interval, 1.70-8.88). The 2 early-onset phenotypes were associated with peripheral airway dysfunction. The late-onset BHR phenotype was related to increased risks of allergic rhinitis symptoms at baseline and later sensitization against inhalant allergens. CONCLUSION: The early-onset persistent BHR phenotype in school-aged children is associated with high atopic burden and increased risk of newly diagnosed asthma, whereas the late-onset BHR phenotype related with later sensitization and allergic rhinitis symptoms. Diverse BHR phenotypes in children have specific characteristics that require targeted follow-ups.

Association of atopy phenotypes with new development of asthma and bronchial hyperresponsiveness in school-aged children.

BACKGROUND: Although previous studies have investigated the association between atopy phenotypes and allergic diseases, atopy characterizations in association with the development of allergic diseases remain poorly understood. OBJECTIVE: To identify atopy phenotypes in school-age children and to evaluate the association between atopy phenotypes and allergic diseases. METHODS: We enrolled 616 children with atopy defined as 1 or more positive allergen responses on skin prick tests and 665 children without atopy from the Children's Health and Environmental Research (CHEER) study. All children were followed up for 4 years at 2-year intervals. Atopy phenotypes were classified using latent class analysis. RESULTS: Four atopy phenotypes were characterized: later sensitization to indoor allergens (cluster 1); multiple early sensitization (cluster 2); early sensitization to outdoor allergens, especially Alternaria, and later sensitization to indoor allergens, including Aspergillus (cluster 3); and early sensitization to indoor allergens and later sensitization to outdoor allergens (cluster 4). New cases of asthma during follow-up were increased in clusters 2 and 3 (adjusted odds ratio [aOR], 2.76 and 4.25, respectively). The risk of new-onset bronchial hyperresponsiveness was highest in cluster 3 (aOR, 5.03). Clusters 2 and 4 had an increased risk of allergic rhinitis (aOR, 7.21 and 2.37, respectively). CONCLUSION: Identification of atopy phenotypes facilitates prediction of the development of asthma and bronchial hyperresponsiveness in school-age children. Our study suggests prevention of additional sensitization is required to modify the progression of allergic diseases.

Persistent asthma phenotype related with late-onset, high atopy, and low socioeconomic status in school-aged Korean children.

BACKGROUND: Treatment guidelines for asthma have been established based on asthma severity; there are limitations in the identification of underlying pathophysiology and prediction of prognosis in heterogeneous phenotypes of asthma. Although the complex interactions between environmental and genetic factors affect the development and progression of asthma, studies on asthma phenotypes considering environmental factors are limited. This study aimed to identify asthma phenotypes using latent class analysis including environmental factors in school-age children. METHODS: We included 235 children (6-8 years) with parent-reported, physician-diagnosed asthma from the Children's HEalth and Environmental Research (CHEER) study, which is a 4-year prospective follow-up study with 2-year intervals. At every survey, pulmonary function tests, methacholine challenge tests and blood tests with questionnaire were conducted. RESULTS: Four asthma phenotypes were identified. Cluster 1 (22% of children) was characterized by high prevalence of atopy and mild symptoms; subjects in cluster 2 (17%) consisted of less atopy and normal lung function, but intermittent troublesome; cluster 3 (29%) experienced late-onset atopic troublesome asthma with decreased lung function in combination with low socioeconomic status; and cluster 4 was associated with early-onset and less-atopic infrequent asthma. CONCLUSIONS: Late-onset, high atopy, and low socioeconomic status are associated with troublesome persistent asthma phenotype in school-age children. Environmental factors might be implicated in the clinical heterogeneity of asthma. Asthma phenotypes considering diverse factors might be more helpful in the identification of asthma pathogenesis and its prevention.

A rhinitis phenotype associated with increased development of bronchial hyperresponsiveness and asthma in children.

BACKGROUND: Allergic rhinitis (AR) has a wide range of clinical features and may be accompanied by comorbid allergic diseases. OBJECTIVE: To identify rhinitis phenotypes in school aged children and to predict the prognosis for developing bronchial hyperresponsiveness (BHR) and asthma. METHODS: This prospective follow-up study involved schoolchildren from the Children's Health and Environment Research cohort with current rhinitis, which was defined based on parental-reported, physician-diagnosed rhinitis and symptoms of rhinitis in the previous 12 months. All participants were followed up at 2 and 4 years later. Rhinitis clusters were identified by latent class analysis that used demographic, clinical, and environmental variables. RESULTS: In 512 eligible children (age range, 6-8 years), 4 rhinitis phenotypes were identified: cluster 1 (25% of children) was associated with nonatopy and a low socioeconomic status; cluster 2 (36%) was associated with a high-atopic burden but normal lung function; cluster 3 (22%) was associated with a high-atopic burden and impaired lung function; and cluster 4 (17%) was associated with low atopy and a high socioeconomic status. Cluster 3 was associated with the highest total serum IgE levels and blood eosinophil percentages at enrollment and the highest incidence of new cases of BHR (P = .04) and asthma symptoms (P = .005) during follow-up. CONCLUSION: The rhinitis cluster of schoolchildren with atopy and impaired lung function is associated with allergic march. This identification of distinct rhinitis phenotypes in affected children may help to prevent allergic march in children with rhinitis.

Lifetime prevalence of childhood eczema and the effect of indoor environmental factors: Analysis in Hispanic and non-Hispanic white children.

BACKGROUND: The prevalence of eczema varies markedly across the globe. It is unclear whether the geographic variation is due to race and/or ethnic differences, environmental exposures, or genetic factors. OBJECTIVE: We investigated the effects of ethnicity and environmental exposures on eczema in Hispanic white and non-Hispanic white children who participated in the Southern California Children's Health Study. METHODS: We performed a cross-sectional study with sociodemographic predictors and environmental exposures among Hispanic white and non-Hispanic white children ages 4-8 years enrolled in the Children's Health Study, 2002-2003. RESULTS: Eczema prevalence differed by ethnicity: Hispanic whites showed lower prevalence (13.8%) compared with non-Hispanic whites (20.2%), and adjustment for sociodemographic factors did not account for the ethnic difference (odds ratio [OR] 0.79 [95% confidence interval {CI}, 0.65-0.95]). Parental history of allergic disease had a larger effect in Hispanic whites than in non-Hispanic whites (p for interaction = 0.005). High maternal education level (OR 1.46 [95% CI, 1.14-1.87]), parental history of allergic disease (OR 2.21 [95% CI, 1.78-2.76]), and maternal smoking during pregnancy (OR 1.44 [95% CI, 1.06-1.95]) increased the risk of eczema. Indoor environmental factors (e.g., mold, water damage, humidifier use) increased the risk of eczema in non-Hispanic whites independent of a parental history of allergic disease, but, in Hispanic whites, increased risks were observed, primarily in children without a parental history of allergic disease. CONCLUSION: Hispanic white children in southern California had a lower prevalence of eczema than non-Hispanic whites, and this ethnic difference was not accounted for by sociodemographic differences. The effects of a parental history of allergic disease and indoor environmental exposures on eczema varied by ethnicity, which indicated that the etiology of eczema may differ in Hispanic whites and in non-Hispanic whites.

Exhaled nitric oxide as a better diagnostic indicator for evaluating wheeze and airway hyperresponsiveness in preschool children.

OBJECTIVE: Fractional concentration of exhaled nitric oxide (FeNO) is a known marker of airway inflammation. The aims of this study were to evaluate FeNO, impulse oscillometry (IOS), and spirometry in preschool children and to investigate their relationship with wheeze and airway hyperresponsiveness (AHR). METHODS: We performed a population-based, cross-sectional study with 561 children aged 5-6 years. A total of 544 children completed a modified International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire and eligible for the study. We measured FeNO, spirometry, methacholine bronchial provocation, and IOS. AHR was defined as the induction of a 20% decrease in FEV(1)(PC(20)) by a methacholine concentration ≤8.0 mg/dL. RESULTS: Children who had wheeze or AHR had higher FeNO levels than children without these symptoms. However, neither IOS nor spirometry parameters showed significant differences between children with wheeze or AHR and those without. FeNO was associated with AHR, whereas IOS or spirometry parameters showed no association. Mean FeNO levels were positively correlated with a dose-response slope for methacholine, but neither IOS nor spirometry parameters showed significant correlations. CONCLUSIONS: FeNO is a more sensitive measurement of AHR and wheeze than spirometry or IOS in preschool children.

Modification of additive effect between vitamins and ETS on childhood asthma risk according to GSTP1 polymorphism: a cross -sectional study.

BACKGROUND: Asthma is characterized by airway inflammation, and bronchial airways are particularly susceptible to oxidant-induced tissue damage. OBJECTIVE: To investigate the effect of dietary antioxidant intake and environmental tobacco smoke (ETS) on the risk of childhood asthma according to genotypes susceptible to airway diseases. METHODS: This cross-sectional study included 1124 elementary school children aged 7-12 years old. Asthma symptoms and smoking history were measured using the International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire. Intake of vitamin A (including retinol and ß-carotene), C, and E was measured by a semi-quantitative food frequency questionnaire (FFQ). GSTP1 polymorphisms were genotyped from peripheral blood samples. RESULTS: ETS was significantly associated with presence of asthma symptoms (adjusted odds ratio [aOR], 2.48; 95 % confidence interval [CI], 1.29-4.76) and diagnosis (aOR, 1.91; 95 % CI, 1.19-3.06). Dietary antioxidant intake was not associated with asthma symptoms, although ETS plus low vitamin A intake showed a significant positive association with asthma diagnosis (aOR, 2.23; 95 % CI, 1.10-4.54). Children with AA at nucleotide 1695 in GSTP1 who had been exposed to ETS and a low vitamin A intake have an increased risk of asthma diagnosis (aOR, 4.44; 95 % CI,1.58-12.52) compared with children who had not been exposed to the two risk factors. However, ETS exposure and low vitamin A intake did not significantly increase odds of asthma diagnosis in children with AG or GG genotypes. CONCLUSION: Low vitamin A intake and ETS exposure may increase oxidative stress and thereby risk for childhood asthma. These relationships may be modified by gene susceptibility alleles of GSTP1.

Pulmonary lymphomatoid granulomatosis in a 4-year-old girl.

Lymphomatoid granulomatosis is a rare lymphoproliferative disease associated with the Epstein-Barr virus that commonly affects the lung. There is limited literature on cases of pediatric lymphomatoid granulomatosis. Half of all cases of lymphomatoid granulomatosis develop during the treatment of leukemia. Herein, we describe a case of lymphomatoid granulomatosis in a previously healthy child without leukemia.

Effect of antibiotic use and mold exposure in infancy on allergic rhinitis in susceptible adolescents.

BACKGROUND: Antibiotic use in infancy induces alteration in intestinal microbiota and is associated with the development of allergic diseases. Mold exposure is also associated with allergic diseases. Genetic susceptibility may interact with specific environmental factors in allergic disease development. OBJECTIVE: To investigate independent and combined effects of antibiotic use and mold exposure in infancy on the risk of allergic rhinitis (AR) in adolescents. METHODS: Data on AR and environmental factors were collected using the International Study of Asthma and Allergies in Childhood questionnaire from 7,389 adolescents from Seoul, Korea. TaqMan genotyping was performed for interleukin 13 (IL-13) (rs20541) and Toll-like receptor 4 (rs1927911) polymorphisms in 1,395 adolescents. RESULTS: Age, parental history of AR, antibiotic use in infancy, and pet ownership during pregnancy or infancy were associated with an increased risk of current AR (diagnosis of AR and symptoms of AR within the preceding 12 months). Having older siblings was a protective effect. The adjusted odds ratio (aOR) for current AR for combined antibiotic use and mold exposure in infancy was 1.45 (95% confidence interval [CI], 1.01-2.09). For each factor separately, aORs were 1.25 (95% CI, 1.04-1.50) and 0.99 (95% CI, 0.75-1.31), respectively. Antibiotic and mold exposure in infancy, GA or AA genotypes of IL-13 (rs20541) (aOR 4.53; 95% CI, 1.66-12.38; P for interaction = .05), and CT+TT genotype of Toll-like receptor 4 (rs1927911) (aOR, 3.20; 95% CI, 1.24-8.26; P for interaction = .18) increased the risk of current AR. CONCLUSION: Antibiotic use and mold exposure in infancy have additive effects on the risk of current AR in genetically susceptible adolescents. Gene-environment interactions between IL-13 (rs20541) and antibiotics or mold may play a role in AR.