Introduction
Childhood asthma and allergic rhinitis (AR) are prevalent chronic respiratory diseases globally, significantly impacting children’s quality of life and health [1, 2]. In recent years, with the acceleration of industrialization and urbanization processes, environmental pollution has become increasingly severe, drawing considerable attention to the influence of various environmental factors (EFs) on childhood respiratory diseases [2, 3]. Existing studies indicated that EFs such as air pollution, exposure to second-hand smoke, household pet ownership, and indoor air quality may be closely associated with the incidence rates of childhood asthma and AR [4]. Asthma is characterized by chronic airway inflammation, presenting with recurrent episodes of wheezing, shortness of breath, chest tightness, and cough, often worsening at night and/or in the early morning [5]. AR, on the other hand, is inflammation of the nasal mucosa caused by allergens, with main symptoms including nasal itching, sneezing, rhinorrhoea, and nasal congestion. Both conditions frequently coexist and are common during childhood, with complex pathogenic mechanisms involving genetic, immunological, and EFs [6]. In recent years, research on the impact of EFs on the incidence rates of childhood asthma and AR has increased. Multiple studies indicated that air pollution is a notable environmental risk factor for both conditions. Specifically, exposure to high concentrations of particulate matter (PM2.5 and PM10), nitrogen oxides (NOx), ozone (O3), and other pollutants is notably associated with increased incidence rates of asthma and AR. Children exposed long-term in heavily trafficked areas show a notable increase in asthma incidence [7]. Indoor air quality is also considered a critical factor influencing children’s respiratory health. Household factors such as tobacco smoke, mould, pet dander, and dust mites can contribute to the onset or exacerbation of asthma and AR. Research indicated that children living in damp and poorly ventilated environments are at higher risk of developing asthma and AR [8]. Furthermore, studies indicated that maternal smoking during pregnancy or early childhood significantly increases the risk of children developing asthma and AR [9]. Climate change and seasonal factors such as temperature, humidity, and pollen concentrations also have a significant impact on the incidence of childhood asthma and AR. During pollen seasons, there is a notable increase in AR incidence, and higher temperatures may exacerbate air pollution, indirectly affecting asthma incidence [10]. Keeping pets at home, particularly cats and dogs, increases children’s exposure to pet dander and fur, which may trigger or worsen asthma and AR. However, some studies suggested that early exposure to pets may confer immune protection in certain children [11]. Diet and lifestyle are also focal points of research. Studies indicated that diets rich in antioxidants, vitamin D, and omega-3 fatty acids may offer protective effects against asthma and AR. Conversely, diets high in sugar and fats are associated with higher incidence rates of these diseases [11, 12]. Despite extensive research exploring the effects of various EFs on childhood asthma and AR, discrepancies in findings sometimes arise due to differences in the study design, sample size, regional variations, and other factors [13]. Therefore, further large-scale, long-term follow-up studies are needed to clarify the specific mechanisms through which EFs exert their effects, providing a basis for developing more effective prevention and control strategies. Genetic factors are also investigated in this era. Polymorphisms in the CD14 gene have been associated with asthma and atopy. CD14 is a receptor that plays a crucial role in the recognition of endotoxins, which are components of Gram-negative bacteria. Variants in the CD14 gene, such as the -260 polymorphism, have been shown to influence the expression of CD14 and the response to endotoxins. Studies have found that individuals with certain CD14 polymorphisms are more likely to develop asthma and atopy, particularly in response to exposure to endotoxins [14–16].
Aim
Therefore, this work investigated the impact of EFs on the incidence rates of childhood asthma and AR through a retrospective analysis. By systematically reviewing and comprehensively analysing existing data, it aimed to clarify the roles of various EFs in disease occurrence. This effort can provide scientific evidence to guide disease prevention and management strategies. Such findings are crucial for formulating effective public health policies aimed at improving children’s health outcomes, holding significant practical importance.
Material and methods
This work employed a retrospective cohort study design, selecting 120 paediatric patients diagnosed with asthma or AR at Xi’an Central Hospital from January 2022 to January 2024. All study participants met the inclusion criteria defined for this research. Guardians of the participants provided informed consent and agreed to participate in the study, including relevant investigations and assessments.
Inclusion criteria: i) consistency with the Chinese Paediatric Respiratory Society’s 2008 revision of the Guidelines for the Diagnosis and Prevention of Childhood Bronchial Asthma; ii) children aged 0–16 years; iii) clinical diagnosis of asthma or AR; and iv) detailed medical history records, including onset time, symptom manifestations, and treatment history.
Exclusion criteria: i) patients with concurrent respiratory system diseases such as chronic obstructive pulmonary disease and pulmonary tuberculosis, which could potentially affect the study outcomes; ii) presence of congenital heart disease, immunodeficiency, or other conditions that could impact study results in children; iii) children who underwent surgery or severe infection within the 3 months prior to the study commencement; iv) children currently using medications that may interfere with study outcomes, such as long-term use of glucocorticoids and immunosuppressants; v) children outside the age range of 1 to 16 years; vi) children and families unable to complete the study follow-up due to reasons such as relocation and economic conditions; and vii) children unable to provide detailed or incomplete medical history records.
These inclusion and exclusion criteria were rigorously applied to ensure the selection of study participants with characteristics that are representative and consistent, thereby maintaining the reliability and scientific integrity of the study results.
Research methodologies
Medical history records of children, including diagnoses of asthma and AR, onset times, symptom presentations, and treatment details, were collected through the electronic health record system (EHR). Review and analysis of questionnaire survey results were conducted using the American Thoracic Society (ATS) Children’s Respiratory Diseases Survey Questionnaire (ATS-DLD-78-C) [17], modified slightly to fit the specific study context. Survey contents encompassed general conditions, family environment, lifestyle habits, family history, and respiratory health status, focusing on indicators such as asthma, current asthma status, AR, eczema, and asthma-related symptoms (e.g., wheezing, persistent cough, and persistent phlegm). Standard international definitions were applied for asthma, current asthma status, and asthma-related symptoms, while AR and eczema diagnoses were confirmed by medical professionals.
Environmental data for the study participants’ residential areas were obtained from environmental protection agencies, meteorological stations, etc. These data included concentrations of air pollutants, pollen, indoor air quality, and household environments (e.g., exposure to second-hand smoke, pet ownership).
Socioeconomic status of families was obtained through questionnaire surveys or public databases, including family income and parental education levels.
Genetic polymorphism evaluation
Blood samples were collected from participants of the study using a standardized protocol. A total of 5 ml of venous blood was drawn from each participant and collected in EDTA tubes. The samples were then labelled with a unique identifier and stored at –80°C until further processing. Genomic DNA was extracted from the blood samples using the QIAamp DNA Blood Mini Kit (Qiagen, Hilden, Germany) according to the manufacturer’s instructions. The extracted DNA was then quantified using a NanoDrop spectrophotometer (Thermo Fisher Scientific, Waltham, MA, USA) and stored at –20°C until further analysis. The extracted DNA was then amplified using polymerase chain reaction (PCR) to generate sufficient DNA for genotyping. The PCR reactions were performed using the TaqMan Universal Master Mix (Thermo Fisher Scientific, Waltham, MA, USA) and specific primers for each polymorphism. The PCR conditions were optimized for each polymorphism, and the reactions were run on a 7900HT Fast Real-Time PCR System (Thermo Fisher Scientific, Waltham, MA, USA).
The PCR products were then genotyped using the TaqMan allelic discrimination assay (Thermo Fisher Scientific, Waltham, MA, USA). The assay used fluorescent probes to detect the specific alleles of each polymorphism. The genotyping reactions were performed on a 7900HT Fast Real-Time PCR System (Thermo Fisher Scientific, Waltham, MA, USA), and the data were analysed using the TaqMan Genotyper software (Thermo Fisher Scientific, Waltham, MA, USA).
The following polymorphisms were examined: CD14: -159C/T (rs2569190), -550C/T (rs2915863), and 2758A/G (rs2569191).
The genotyping data were analysed using PLINK [18]. Hardy-Weinberg equilibrium was tested for each polymorphism to ensure that the genotypes were in equilibrium. The genotypes were then used to calculate allele frequencies, genotype frequencies, and minor allele frequencies for each polymorphism.
Statistical analysis
A database was established using Excel to record demographic characteristics, environmental exposure levels, and the incidence of asthma and AR among study subjects. Data were processed using SPSS 19.0 statistical software. Categorical data were denoted as percentages (%), and normally distributed continuous data were presented as mean ± standard deviation. Single-factor analyses of factors influencing asthma and AR, including symptoms, were performed using the χ2 test. Multiple logistic regression models were employed to analyse the independent effects of various EFs on the incidence of childhood asthma and AR, with confounding variables controlled. Differences were statistically significant at p < 0.05.
Results
A χ2 test was conducted on a sample of 120 patients with asthma and allergic rhinitis to examine the association between various factors and the disease. The results showed significant associations between the disease and age (χ2 = 34.48, p < 0.001), with the 3–5 years age group being overrepresented. Weight status was also significantly associated with the disease (χ2 = 63.1, p < 0.001), with normal weight and underweight individuals being more likely to have the disease. A personal history of allergies was also significantly associated with the disease (χ2 = 54.1, p < 0.001), with food allergies and eczema being the most common allergies. Furthermore, three CD14 polymorphisms (-159C/T, -550C/T, and 2758A/G) were significantly associated with the disease (χ2 = 23.5, p < 0.001; χ2 = 20.63, p < 0.001; χ2 = 24.5, p < 0.001, respectively). In contrast, birth situation (p = 0.377) and mode of delivery (p = 0.273) were not significantly associated with the disease (Table 1).
Table 1
Asthma and allergic rhinitis patient characteristics
Table 2 reveals a χ2 test conducted to examine the associations between various factors and the presence of asthma and allergic rhinitis in a cohort of patients. The results showed that the prevalence of the conditions was significantly different between categories of father’s educational level (p = 0.03), mother’s educational level (p = 0.002), history of asthma in parents (p = 0.001), parent’s allergy history (p = 0.001), caesarean section (p = 0.003), house decoration history (p = 0.003), contact with pets (p = 0.001), exposure to house dust (p = 0.002), contact with pollen (p = 0.001), contact with plush toys (p = 0.002), contact with cold air (p = 0.004), long-term smoking by family members (p = 0.001), number of cars near the residence (p = 0.003), and outdoor activities (p = 0.002). Additionally, sex (p = 0.051) and winter gas heating and natural gas (p = 0.001) approached significance in terms of differences in prevalence. Premature delivery (p = 0.76) did not show a significant difference in prevalence between categories.
Table 2
Univariate analysis results of risk factors for asthma and AR diseases
Discussion
This study identified significant associations between asthma and allergic rhinitis in paediatric patients and various factors, including age, weight status, personal history of allergies, and CD14 polymorphisms, as well as environmental and lifestyle factors such as parental education level, exposure to pets and dust, and long-term family smoking. Our study found that CD14 -550C/T and CD14 2758A/G polymorphisms were significantly higher in childhood asthma and allergic diseases patients, whereas the CD14 -159C/T polymorphism was not. This finding contrasts with a previous meta-analysis by Zhao and Bracken, which reported a protective dose-response relationship between the CD14 -260T allele (also known as -159) and atopic asthma susceptibility [19]. The discrepancy between the two studies may be attributed to differences in the study design, population characteristics, and outcome measures. However, a study by Şahin et al. found that the CD14 -159C/T polymorphism was associated with total IgE levels and asthma severity in adult Turkish asthma patients. Specifically, they found that the C allele was correlated with low total IgE levels and the T allele with high total IgE levels in atopic patients, and that the CC+CT genotype was more frequent in moderate and severe asthma groups. These findings are in contrast to our study, which did not find an association between the CD14 -159C/T polymorphism and childhood asthma and allergic diseases [20]. The differing results may be due to differences in study populations, age groups, and asthma phenotypes, highlighting the complexity of the relationship between CD14 polymorphisms and asthma susceptibility.
Research on the impact of EFs on the incidence of childhood asthma and AR is of significant importance. Rosário Filho et al. [21] indicated that air pollution is a major risk factor and contributor to the incidence and mortality rates of chronic diseases. Due to physiological immaturity and prenatal/postnatal lung development, children are greatly impacted by environmental influences. Poor air quality is associated with increased prevalence of allergic asthma and rhinitis clinical manifestations [21]. Our study also found that environmental factors, including exposure to pollutants, are prevalent in childhood asthma and allergic rhinitis. Geller-Bernstein and Portnoy [22] highlighted the impact of varying pollen levels on health, indicating a notable correlation between pollen and allergic health conditions. Pollen can trigger or exacerbate asthma, especially allergic asthma. Inhalation of pollen leads to inflammation and constriction of airways in allergic asthma patients, exacerbating asthma symptoms. Our study also found that exposure to pollen is a significant environmental risk factor for childhood asthma and allergic rhinitis. Allergic diseases have a significant genetic predisposition. Children with one or both parents affected by asthma or AR have a drastically increased risk of developing these conditions.
Nolte et al. [23] indicated that pollen can exacerbate symptoms of AR. When pollen enters the respiratory tract of sensitive individuals, the immune system identifies these pollen particles as harmful substances and produces IgE antibodies. IgE antibodies bind to mast cells and basophils, triggering the release of histamine and other inflammatory mediators, leading to allergic symptoms. Allergic diseases have a significant genetic predisposition. Children with one or both parents affected by asthma or AR have a drastically increased risk of developing these conditions. Our study found that genetic factors, including CD14 polymorphisms, are prevalent in childhood asthma and allergic rhinitis.
Our study found that caesarean section delivery, home renovations, pet exposure, household dust, and other EFs are seen in most childhood asthma and AR patients. These EFs can trigger allergic reactions and exacerbate respiratory inflammation by increasing exposure to indoor allergens and air pollutants. Additionally, factors such as cold air exposure, family smoking, and proximity to vehicle emissions can further contribute to respiratory inflammation and allergic responses. In contrast, a similar study conducted in the southern edge of the plateau grassland region of northern China found that sensitization to Artemisia and Humulus pollen was a significant risk factor for AR and AR combined with asthma, with approximately 70% of subjects with AR and < 30% of asthma patients sensitized to these pollen types [24].
Furthermore, outdoor activities can have both positive and negative effects, with moderate activities enhancing immunity and lung function, but excessive or activities in polluted environments increasing the risk of asthma exacerbations. These EFs can interact with each other, amplifying their effects and highlighting the need for comprehensive assessment and management of environmental factors to prevent and treat childhood asthma and AR. A systematic review of 25 years of literature on allergic rhinitis (AR) and asthma in paediatric patients identified several risk factors that contribute to the development of these conditions, including exposure to ambient polycyclic aromatic hydrocarbons, living in an industrialized city with elevated traffic, dampness and mould exposure, electric cooking, male gender, genetic predispositions, and certain dietary habits. Additionally, the review found that children with AR are at increased risk of developing asthma, and that the onset of asthma can worsen AR symptoms [25]. The study also highlighted the complex interplay between genetic and environmental risk factors, leading to epigenetic, microbiota, and immunological changes that contribute to the development of AR and asthma in children. These findings are consistent with our study, which identified environmental factors such as caesarean section delivery, home renovations, pet exposure, and household dust as common triggers for childhood asthma and AR.
Limitations of this work include its cross-sectional design that does not have a control cohort and single-centre data, which may lead to selection bias and information bias. Future research should consider larger-scale, multicentre prospective cohort studies to validate the findings of this study. In summary, it is suggested by this work that reducing exposure to adverse EFs, particularly improving household and surrounding environments, may be crucial measures to lower the incidence of childhood asthma and AR. This provides a scientific basis for public health interventions and practical guidance for families in preventing childhood allergic diseases.
Conclusions
This work found distinct variations in multiple EFs’ prevalence. Specifically, factors such as parental education levels, history of asthma and allergies, caesarean section delivery, home renovation history, exposure to pets, dust mites, pollen, plush toys, cold air, long-term family smoking, number of cars near the residence, frequency of outdoor activities, and winter heating methods (coal gas, natural gas) were all correlated with the incidence of childhood asthma and AR. These findings suggest that reducing exposure to adverse EFs, particularly improving household and surrounding environments, can help lower the incidence of childhood asthma and AR. This provides a scientific basis for public health interventions and serves as a reference for parents and families in preventing childhood asthma and allergic diseases.
