Risk Factor For Asthma Research Articles

The Relationship Between Asthma Risk Factors and Disease Severity in Children with Asthma Aged 7 to 12 Years

The Relationship Between Asthma Risk Factors and Disease Severity in Children with Asthma Aged 7 to 12 Years

Association between visceral adipose tissue and asthma based on the NHANES and Mendelian randomization study.

Obesity is a crucial risk factor for asthma. Observational studies have examined the association between abdominal obesity and asthma symptoms. This study aimed to investigate the causal relationship between visceral adipose tissue (VAT) and asthma and its potential as an independent indicator. This study utilized data from the National Health and Nutrition Examination Survey spanning 2011-8. Multivariable logistic regression and stratified variable selection were employed to identify associations between asthma and VAT. Moreover, a two-sample Mendelian randomization analysis, using 221 genetic variants as instrumental variables, was conducted to assess this relationship further. Our findings indicated that individuals with higher VAT levels were more likely to develop asthma. Visceral obesity remained a significant risk factor for asthma after adjusting for demographic characteristics. Genetic predictions suggest a positive association between VAT and an elevated risk of asthma (odds ratio [OR] = 1.393, 95% confidence interval [CI]: 1.266-1.534, and P = 1.43E-11). No significant polymorphisms were detected using the Mendelian randomization-Egger intercept test. This study presents potential evidence supporting the causal role of VAT in asthma development. Furthermore, the findings from the Mendelian randomization analysis further reinforce the relationship between VAT and asthma risk.

Impact of obesity on airway remodeling in asthma: pathophysiological insights and clinical implications.

The prevalence of obesity among asthma patients has surged in recent years, posing a significant risk factor for uncontrolled asthma. Beyond its impact on asthma severity and patients' quality of life, obesity is associated with reduced lung function, increased asthma exacerbations, hospitalizations, heightened airway hyperresponsiveness, and elevated asthma-related mortality. Obesity may lead to metabolic dysfunction and immune dysregulation, fostering chronic inflammation characterized by increased pro-inflammatory mediators and adipocytokines, elevated reactive oxygen species, and reduced antioxidant activity. This chronic inflammation holds the potential to induce airway remodeling in individuals with asthma and obesity. Airway remodeling encompasses structural and pathological changes, involving alterations in the airway's epithelial and subepithelial layers, hyperplasia and hypertrophy of airway smooth muscle, and changes in airway vascularity. In individuals with asthma and obesity, airway remodeling may underlie heightened airway hyperresponsiveness and increased asthma severity, ultimately contributing to the development of persistent airflow limitation, declining lung function, and a potential increase in asthma-related mortality. Despite efforts to address the impact of obesity on asthma outcomes, the intricate mechanisms linking obesity to asthma pathophysiology, particularly concerning airway remodeling, remain incompletely understood. This comprehensive review discusses current research investigating the influence of obesity on airway remodeling, to enhance our understanding of obesity's role in the context of asthma airway remodeling.

German cockroach extract prevents IL-13-induced CCL26 expression in airway epithelial cells through IL-13 degradation.

Inhaled aeroallergens can directly activate airway epithelial cells (AECs). Exposure to cockroach allergens is a strong risk factor for asthma. Cockroach allergens mediate some of their effects through their serine protease activity; protease activity is also a major contributor to allergenicity. The Th2 cytokine interleukin-13 (IL-13) induces upregulation of the eosinophil chemotactic factor CCL26. CCL26 induces eosinophil migration in allergic inflammation. In this work, we studied the effect of cockroach proteases on IL-13-induced effects. Immersed cultures of the human bronchial epithelial cell line BEAS-2B and air-liquid interface (ALI) cultures of primary normal human bronchial epithelial (NHBE) cells were stimulated with IL-13, Blattella Germanica cockroach extract (CE), or both. IL-13-induced genes were analyzed with qRT-PCR. IL-13 induced upregulation of CCL26, periostin, and IL-13Rα2 in bronchial epithelial cells which were decreased by CE. CE was heat-inactivated (HICE) or pre-incubated with protease inhibitors. HICE and CE preincubated with serine protease inhibitors did not prevent IL-13-induced CCL26 upregulation. CE-degraded IL-13 and specific cleavage sites were identified. CE also decreased IL-4-induced CCL26 upregulation and degraded IL-4. Other serine proteases such as bovine trypsin and house dust mite (HDM) serine proteases did not have the same effects on IL-13-induced CCL26. We conclude that CE serine proteases antagonize IL-13-induced effects in AECs, and this CE effect is mediated primarily through proteolytic cleavage of IL-13. IL-13 cleavage by cockroach serine proteases may modulate CCL26-mediated effects in allergic airway inflammation by interfering directly with the pro-inflammatory effects of IL-13 invivo.

Airway Diseases Related to the Use of Cleaning Agents in Occupational Settings

Exposure to disinfectants and cleaning products (DCP) is now a well-established risk factor for work-related asthma (WRA). However, questions remain on the specific causal agents and pathophysiological mechanisms. Few studies have also reported an association between DCP and rhinitis or chronic obstructive pulmonary disease. This review discusses the recent evidence pertaining to airway diseases attributable to occupational exposure to DCP. In contrast to other agents, the incidence of WRA due to DCP has increased over time. The use of DCP in spray form has clearly been identified as an added risk factor. The mechanisms for WRA associated with DCP remain poorly studied, however, both allergic and nonallergic responses have been described, with irritant mechanisms thought to play a major role. An early diagnostic work-up based on clinical assessment accompanied by evaluation of lung function, immunological and airway inflammatory markers is important to guide optimal care and exposure avoidance to the implicated agent. Future research should focus on the effects of “green” products, pathophysiological mechanisms and quantitative exposure assessment including the use of barcode-based methods to identify specific agents. There is an urgent need to strengthen preventive measures and interventions to reduce the burden of airway diseases associated with DCP.

Prevalence of aeroallergen sensitization in children in Northern China

Objective This study aimed to analyze the sensitization rate of different aeroallergens in children of different age, sex, and disease groups, describe the changing trend of different aeroallergens in different ages, and analyze the sensitization risk factors for asthma. Methods Children (<18 years old) with suspected atopic diseases who visited the Department of Allergy of Children’s Hospital Affiliated to Capital Institute of Pediatrics and underwent a skin prick test (SPT) were retrospectively enrolled from January 2019 to November 2021. Results A total of 5465 patients (3514 boys, 1951 girls; mean age, 7 ± 3 years) were enrolled. Of them, 3703 patients (67.8%) were sensitized to at least one aeroallergen. Before 4 years of age, mold was the most prevalent aeroallergen (103/380 [27.1%]), whereas after 4 years of age, weed pollen was the most prevalent aeroallergen. After 6 years of age, tree pollen became the second most prevalent aeroallergen. After 12 years of age, the sensitization rate of indoor aeroallergens was lower than that of outdoor aeroallergens. Logistic regression showed that sensitization to mold (odds ratio [OR]:1.4, 95% confidence interval (CI): 1.2–1.7, p < 0.001), animal dander (OR: 1.6, 95% CI: 1.4–1.9, p < 0.001), and polysensitization (OR: 1.4, 95% CI: 1.0–1.8, p = 0.038) were potential sensitization risk factors for asthma. Conclusions Mold is an important allergen in early life. Different kinds of allergens affect different age groups. Patients who are sensitized to mold or animal dander or experience polysensitization should be carefully monitored for asthma risk.

Investigation analysis of the acute asthma risk factor and phenotype based on relational analysis with outdoor air pollutants in Xi'an, China.

Asthma is a common chronic heterogeneous disease. Outdoor air pollutants are an important cause of acute asthma. Until now, the association between the risk of acute asthma and outdoor air pollutants is unclear. And the relationship between the different phenotypes of asthma and outdoor air pollutants has not been reported. Thus, an analysis of the association between outdoor air pollutants and daily acute asthma inpatient and outpatient visits in Xi'an, China, from January 1 to December 31, 2018, was conducted. A total of 3395 people were included in the study. The statistical analysis and relational analysis based on the logistic regression were used for illustrating the relatedness of the acute asthma risk factor and phenotype with outdoor air pollutants, while the age, gender, pollen peak and non-pollen peak periods, high type 2 (T2) asthma and non-high T2 asthma were also stratified. Results showed that particulate matter with particle size below 10μm and 2.5μm (PM10 and PM2.5), sulfur dioxide(SO2), nitrogen dioxide(NO2), and carbon monoxide(CO) increase the risk of acute asthma and that air pollutants have a lagged effect on asthma patients. PM10, NO2, CO, and Ozone (O3) are associated with an increased risk of acute attacks of high T2 asthma. PM10, PM2.5, SO2, NO2 and CO are associated with an increased risk of acute asthma in males of 0-16years old. PM10 and PM2.5 are more harmful to asthma patients with abnormal lung function.

Importance of GWAS Risk Loci and Clinical Data in Predicting Asthma Using Machine-learning Approaches.

To understand the risk factors of asthma, we combined genome-wide association study (GWAS) risk loci and clinical data in predicting asthma using machine-learning approaches. A case-control study with 123 asthmatics and 100 controls was conducted in the Zhuang population in Guangxi. GWAS risk loci were detected using polymerase chain reaction, and clinical data were collected. Machine-learning approaches were used to identify the major factors that contribute to asthma. A total of 14 GWAS risk loci with clinical data were analyzed on the basis of 10 times the 10-fold cross-validation for all machine-learning models. Using GWAS risk loci or clinical data, the best performances exhibited area under the curve (AUC) values of 64.3% and 71.4%, respectively. Combining GWAS risk loci and clinical data, the XGBoost established the best model with an AUC of 79.7%, indicating that the combination of genetics and clinical data can enable improved performance. We then sorted the importance of features and found the top six risk factors for predicting asthma to be rs3117098, rs7775228, family history, rs2305480, rs4833095, and body mass index. Asthma-prediction models based on GWAS risk loci and clinical data can accurately predict asthma, and thus provide insights into the disease pathogenesis.

Azithromycin therapy in infants hospitalized for respiratory syncytial virus bronchiolitis: Airway matrix metalloproteinase-9 levels and subsequent recurrent wheeze

BackgroundEarly life respiratory syncytial virus (RSV) bronchiolitis is a significant risk factor for childhood asthma. In vitro and in vivo studies suggested that decreasing levels of airway matrix metalloproteinase (MMP)-9 during RSV bronchiolitis may be associated with clinical benefits. ObjectiveTo investigate whether azithromycin therapy during severe RSV bronchiolitis reduces upper airway MMP-9 levels, whether upper airway MMP-9 levels correlate with upper airway interleukin IL-8 levels, and whether MMP-9 level reduction is associated with reduced post-RSV recurrent wheeze (RW). MethodsA total of 200 otherwise healthy 1- to 18-month-old infants hospitalized with RSV bronchiolitis were randomized into a double-blind, placebo-controlled trial of oral azithromycin (10 mg/kg daily for 7 days followed by 5 mg/kg daily for 7 days) or placebo. Infants were followed for 2 to 4 years for the outcome of RW (3 or more wheezing episodes). Nasal lavage samples for MMP-9 levels were obtained at baseline, day 14 (end of the study treatment), and after 6 months. ResultsUpper airway MMP-9 levels were highly correlated with IL-8 levels at all 3 time points: randomization, day 14, and 6 months (r = 0.80; P < .0001 for all time points). MMP-9 levels were similar between treatment groups at randomization, were lower on day 14 among children treated with azithromycin (P = .0085), but no longer different after 6 months. MMP-9 levels at baseline and change from baseline to day 14 were not associated with the development of RW (P = .49, .39, respectively). ConclusionAzithromycin therapy in children hospitalized with RSV bronchiolitis had a short-term anti-inflammatory effect in reducing upper airway MMP-9 levels. However, the reduction in MMP-9 levels did not relate to subsequent RW post-RSV. Trial RegistrationThis study is a secondary analysis of the Azithromycin to Prevent Wheezing following severe RSV bronchiolitis-II clinical trial registered at Clinicaltrials.gov (NCT02911935).

Effects of biological therapies on patients with Type-2 high asthma and comorbid obesity.

Over 20 million adults and 6 million children in the United States (US) have asthma, a chronic respiratory disease characterized by airway inflammation, bronchoconstriction, and mucus hypersecretion. Obesity, another highly prevalent disease in the US, is a major risk factor for asthma and a significant cause of diminished asthma control, increased submucosal eosinophilia, and reduced quality of life. A large subgroup of these patients experiences severe symptoms and recurrent exacerbations despite maximal dosage of standard asthma therapies. In the past two decades, the development of biological therapies has revolutionized the field and advanced our understanding of type 2 inflammatory biomarkers. However, patients with obesity and comorbid asthma are not principally considered in clinical trials of biologics. Large landmark cluster analyses of patients with asthma have consistently identified specific asthma phenotypes that associate with obesity but may be differentiated by age of asthma onset and inflammatory cell profiles in sputum. These patterns suggest that biologic processes driving asthma pathology are heterogenous among patients with obesity. The biological mechanisms driving pathology in patients with asthma and comorbid obesity are not well understood and likely multifactorial. Future research needs to be done to elicit the cellular and metabolic functions in the relationship of obesity and asthma to yield the best treatment options for this multiplex condition. In this review, we explore the key features of type 2 inflammation in asthma and discuss the effectiveness, safety profile, and research gaps regarding the currently approved biological therapies in asthma patients with obesity.

Presence of sputum IgG against eosinophilic inflammatory proteins in asthma.

Sputum immunoglobulin G (Sp-IgG) has been discovered to induce cytolytic extracellular trap cell death in eosinophils, suggesting a potential autoimmune mechanism contributing to asthma. This study aimed to explore the potential origin of Sp-IgG and identify clinically relevant subtypes of Sp-IgG that may indicate autoimmune events in asthma. This study included 165 asthmatic patients and 38 healthy volunteers. We measured Sp-IgG and its five subtypes against eosinophil inflammatory proteins (Sp-IgGEPs), including eosinophil peroxidase, eosinophil major basic protein, eosinophil-derived neurotoxin, eosinophil cationic protein, and Charcot-Leyden Crystal protein in varying asthma severity. Clinical and Mendelian randomization (MR) analyses were conducted. A positive Sp-IgGEPs signature (Sp-IgGEPs+) was defined when any of the five Sp-IgGEPs values exceeded the predefined cutoff thresholds, calculated as the mean values of healthy controls plus twice the standard deviation. The levels of Sp-IgG and Sp-IgGEPs were significantly elevated in moderate/severe asthma than those in mild asthma/healthy groups (all p < 0.05). Sp-IgG levels were positively correlated with airway eosinophil and Sp-IgGEPs. MR analysis showed causality between eosinophil and IgG (OR = 1.02, 95%CI = 1.00-1.04, p = 0.020), and elevated IgG was a risk factor for asthma (OR = 2.05, 95%CI = 1.00-4.17, p = 0.049). Subjects with Sp-IgGEPs+ exhibited worse disease severity and served as an independent risk factor contributing to severe asthma (adjusted-OR = 5.818, adjusted-95% CI = 2.193-15.431, adjusted-p < 0.001). Receiver operating characteristic curve analysis demonstrated that the combination of Sp-IgGEPs+ with non-allergic status, an ACT score < 15, and age ≥ 45 years, effectively predicted severe asthma (AUC = 0.84, sensitivity = 86.20%, specificity = 67.80%). This study identifies a significant association between airway eosinophilic inflammation, Sp-IgG, and asthma severity. The Sp-IgGEPs panel potentially serves as the specific biomarker reflecting airway autoimmune events in asthma.

Ambient air pollution and visit of asthma patients: case study in DKI Jakarta 2017

Asthma is a worldwide disease that affects all races, ages, and genders. In 2017, asthma attacked 300 million people in the world. One risk factor for asthma is air pollution. The design of this study is a time-stratified case crossover, with secondary data types consisting of asthma visit data (ICD-10: J45) and pollutant data (PM10, O3, and NOx) in DKI Jakarta in 2017. The results from this study: Ozone exposure lag day 3 p = 0.04, OR = 1.0016 (95% CI 1,0001-1.003) and lag day 1 of NOx exposure p = 0.04, OR = 1.0050 (95% CI 1, 0003-1,010) which influences the visit of asthma patients in DKI Jakarta. It can be concluded that ozone and NOx are associated with asthma patient visits in DKI Jakarta, and this study on PM10 pollutants did not show any relationship with patient visits due to Asthma in DKI Jakarta.

How early life respiratory viral infections impact airway epithelial development and may lead to asthma.

Childhood asthma is a common chronic disease of the airways that results from host and environment interactions. Most risk factor studies of asthma point to the first year of life as a susceptibility window of mucosal exposure that directly impacts the airway epithelium and airway epithelial cell development. The development of the airway epithelium, which forms a competent barrier resulting from coordinated interactions of different specialized cell subsets, occurs during a critical time frame in normal postnatal development in the first year of life. Understanding the normal and aberrant developmental trajectory of airway epithelial cells is important in identifying pathways that may contribute to barrier dysfunction and asthma pathogenesis. Respiratory viruses make first contact with and infect the airway mucosa. Human rhinovirus (HRV) and respiratory syncytial virus (RSV) are mucosal pathogens that are consistently identified as asthma risk factors. Respiratory viruses represent a unique early life exposure, different from passive irritant exposures which injure the developing airway epithelium. To replicate, respiratory viruses take over the host cell transcriptional and translational processes and exploit host cell energy metabolism. This takeover impacts the development and differentiation processes of airway epithelial cells. Therefore, delineating the mechanisms through which early life respiratory viral infections alter airway epithelial cell development will allow us to understand the maturation and heterogeneity of asthma and develop tools tailored to prevent disease in specific children. This review will summarize what is understood about the impact of early life respiratory viruses on the developing airway epithelium and define critical gaps in our knowledge.

Prevalence and Risk Factors of Childhood Asthma in Jazan Region, Saudi Arabia.

The prevalence of asthma among children has been on the rise worldwide, leading to significant morbidity and mortality. Our study was conducted to determine the prevalence of asthma and its related risk factors among school-age children in the Jazan Region, Saudi Arabia. The study was a cross-sectional prospective study that used Phase I ISAAC protocol and was conducted from March to June 2023. The sample size was calculated to be 1600 among school-age children in the Jazan Region Saudi Arabia. This study complies with the Declaration of Helsinki. Data was analyzed using SPSS version 23.0, Descriptive statistics were calculated for study variables, and appropriate tests of significance were performed to determine statistical significance. The total study population was 1368 the majority of them, 96.6% (n=1321), were Saudi nationals, and most of them lived in rural areas (70.6%, n=966). The prevalence of life-long wheezing, wheezing in the last 12 months, and exercise-induced wheezing was 28.0%, 29.2%, and 30.9%, respectively. Risk factors such as having indoor plants, having a pet, and a smoker in the household were reported by 48.0%, 24.6%, and 36.4% of participants, respectively. Living near an industrial area was determined as a risk factor in 98 (7.2%) of the children. Asthma-related symptoms were strongly correlated with all risk factors based on the chi-square test, and some risk factors based on multivariate linear regression. The prevalence of asthma among children in the Jazan Region is higher than previously reported, and the reported risk factors are significantly correlated with symptoms of asthma.

Clinical profiles, severity, and risk factors of pediatric asthma in Baghdad: A comparative study of early-onset and late-onset cases

Clinical profiles, severity, and risk factors of pediatric asthma in Baghdad: A comparative study of early-onset and late-onset cases

A Study on the Correlation between Allergic Asthma and Cardiovascular Metabolic Risk Factors

A Study on the Correlation between Allergic Asthma and Cardiovascular Metabolic Risk Factors

Allergy/Atopic March and United Airway Disease: What We Know and What We Need to Know?

Abstract “Allergy/atopic march” refers to a typical sequence in which the allergic or atopic features appear at a certain age, and may or may not persist thereafter. In general, atopic dermatitis or atopic eczema occurs first, which progresses to immunoglobulin-E-mediated food allergy, asthma, and then allergic rhinitis (AR). However, this sequence may not be conspicuous in many cases. AR is an independent risk factor for asthma; in fact, AR often precedes that of asthma. United airway disease (allergic rhino-bronchitis) means the coexistence of AR and asthma. This has been shown in clinical and experimental studies, which suggest a similar immune pathology between the upper and lower airways in allergic subjects. In children with asthma, coexistent AR leads to an increased risk of asthma exacerbation leading to hospitalization and/or emergency visits as well as increased health-care cost. Treatment of AR in asthmatic children results in a lowered risk of asthma-related hospitalizations and emergency visits, and improved quality of life. In this article, we have discussed the current evidence for the clinically relevant effects that allergic conditions (from food allergies to atopic march, united airways disease, and AR) can have on children with asthma along with the future of allergic diagnosis (precision allergy molecular diagnosis) and allergen immunotherapy.

Genetic analyses of the bidirectional associations between common mental disorders and asthma.

Although extensive research has explored the link between mental disorders and asthma, the characteristics and patterns of this association are still unclear. Our study aims to examine the genetic causal links between common mental disorders (specifically, anxiety and depression) and asthma. We conducted genetic analyses including linkage disequilibrium score regression (LDSC) and bidirectional two-sample Mendelian randomization (MR) analyses, and utilized summary statistics from recent large-scale Genome-Wide Association Studies (GWASs) in European populations, covering sensation of anxiety or depression, anxiety sensation, depression sensation, anxiety disorders, major depression disorder (MDD), and asthma. LDSC revealed significant genetic correlations among sensation of anxiety or depression, MDD and asthma (P < 0.017), highlighting potential genetic correlation between anxiety disorders and asthma (P < 0.05 yet > 0.017). In bidirectional two-sample MR, inverse-variance weighted (IVW) analyses suggested that genetic liability to asthma was significantly associated with an increased risk of sensation of anxiety or depression (OR = 4.760, 95%CI: 1.645-13.777), and MDD (OR = 1.658, 95%CI: 1.477-1.860). Conversely, IVW analyses indicated that genetic liability to anxiety disorders was not associated with an increased risk of asthma (P > 0.01), nor was genetic liability to asthma associated with an increased risk of anxiety disorders (P > 0.01). Furthermore, no significant genetic causal relationships were observed for other studied traits. Multivariate MR, after adjusting for body mass index and alcohol consumption, further corroborated the independent causal effect of genetic predisposition to MDD on the risk of asthma (OR = 1.460, 95% CI: 1.285-1.660). Our study establishes MDD as a predisposing factor for asthma. Meanwhile, anxiety disorders are not causal risk factors for asthma, nor is the reverse true. It is recommended to closely monitor asthma symptoms in patients with MDD.

17q21 Variants Disturb Mucosal Host Defense in Childhood Asthma.

Rationale: The strongest genetic risk factor for childhood-onset asthma, the 17q21 locus, is associated with increased viral susceptibility and disease-promoting processes.Objectives: To identify biological targets underlying the escalated viral susceptibility associated with the clinical phenotype mediated by the 17q21 locus.Methods: Genome-wide transcriptome analysis of nasal brush samples from 261 children (78 healthy, 79 with wheezing at preschool age, 104 asthmatic) within the ALLIANCE (All-Age-Asthma) cohort, with a median age of 10.0 (range, 1.0-20.0) years, was conducted to explore the impact of their 17q21 genotype (SNP rs72163891). Concurrently, nasal secretions from the same patients and visits were collected, and high-sensitivity mesoscale technology was employed to measure IFN protein levels.Measurements and Main Results: This study revealed that the 17q21 risk allele induces a genotype- and asthma/wheeze phenotype-dependent enhancement of mucosal GSDMB expression as the only relevant 17q21-encoded gene in children with preschool wheeze. Increased GSDMB expression correlated with the activation of a type-1 proinflammatory, cell-lytic immune, and natural killer signature, encompassing key genes linked to an IFN type-2-signature (IFNG, CXCL9, CXCL10, KLRC1, CD8A, GZMA). Conversely, there was a reduction in IFN type 1 and type 3 expression signatures at the mRNA and protein levels.Conclusions: This study demonstrates a novel disease-driving mechanism induced by the 17q21 risk allele. Increased mucosal GSDMB expression is associated with a cell-lytic immune response coupled with compromised airway immunocompetence. These findings suggest that GSDMB-related airway cell death and perturbations in the mucosal IFN signature account for the increased vulnerability of 17q21 risk allele carriers to respiratory viral infections during early life, opening new options for future biological interventions.The All-Age-Asthma (ALLIANCE) cohort is registered at www.clinicaltrials.gov (pediatric arm, NCT02496468).

Predicting asthma using imbalanced data modeling techniques: Evidence from 2019 Michigan BRFSS data

Studies in the past have examined asthma prevalence and the associated risk factors in the United States using data from national surveys. However, the findings of these studies may not be relevant to specific states because of the different environmental and socioeconomic factors that vary across regions. The 2019 Behavioral Risk Factor Surveillance System (BRFSS) showed that Michigan had higher asthma prevalence rates than the national average. In this regard, we employ various modern machine learning techniques to predict asthma and identify risk factors associated with asthma among Michigan adults using the 2019 BRFSS data. After data cleaning, a sample of 10,337 individuals was selected for analysis, out of which 1,118 individuals (10.8%) reported having asthma during the survey period. Typical machine learning techniques often perform poorly due to imbalanced data issues. To address this challenge, we employed two synthetic data generation techniques, namely the Random Over-Sampling Examples (ROSE) and Synthetic Minority Over-Sampling Technique (SMOTE) and compared their performances. The overall performance of machine learning algorithms was improved using both methods, with ROSE performing better than SMOTE. Among the ROSE-adjusted models, we found that logistic regression, partial least squares, gradient boosting, LASSO, and elastic net had comparable performance, with sensitivity at around 50% and area under the curve (AUC) at around 63%. Due to ease of interpretability, logistic regression is chosen for further exploration of risk factors. Presence of chronic obstructive pulmonary disease, lower income, female sex, financial barrier to see a doctor due to cost, taken flu shot/spray in the past 12 months, 18–24 age group, Black, non-Hispanic group, and presence of diabetes are identified as asthma risk factors. This study demonstrates the potentiality of machine learning coupled with imbalanced data modeling approaches for predicting asthma from a large survey dataset. We conclude that the findings could guide early screening of at-risk asthma patients and designing appropriate interventions to improve care practices.