Five studies [16–18,20,23] reported asthma as a risk factor for RRTIs in preschool children, and the heterogeneity test (I² = 93.80%, P < 0.001) was performed using a random-effects model. The results indicated that asthma was a significant risk factor for RRTIs in preschool children [OR = 3.84, 95% CI (1.97, 7.47), P < 0.001] (Figure 2B).

Three studies [16,20,23] identified allergy as a risk factor for RRTIs in preschool children, and the heterogeneity test (I² = 0, P = 0.606) was performed based on the fixed-effects model. It was found that allergy was a risk factor for RRTIs in preschool children, and there exists an obvious difference [OR = 2.27, 95% CI (2.06, 2.51), P < 0.001] (Figure 2C).

Five studies [17,19,22,24,25] mentioned dietary bias as a risk factor for RRTIs in preschool children, and the heterogeneity test (I² = 65.0%, P = 0.022) was performed based on the random-effects model. The results of the analysis reflected that dietary bias was a significant risk factor for RRTIs in preschool children [OR = 2.10, 95% CI (1.37, 3.24), P = 0.001] (Figure 2D).

Four studies [17,18,21,25] investigated co-residence with individuals having chronic respiratory disease as a risk factor for RRTIs in preschool children, and the heterogeneity test (I² = 68.3%, P = 0.024) was conducted based on the random-effects model. The results suggested that co-residence with individuals having chronic respiratory disease was not a significant risk factor for RRTIs in preschool children [OR = 1.57, 95% CI (0.87, 2.81), P = 0.132] (Figure 3A).

Figure 3.

Forest plots of meta-analyses for environmental and lifestyle factors. (A) Co-resident with chronic respiratory disease: Forest plot of 4 studies. The overall pooled OR is 1.57 (95% CI: 0.87–2.81), indicating moderate heterogeneity (I² = 68.3%, P = 0.024). (B) Smoking co-resident: Forest plot of 6 studies. The overall pooled OR is 1.83 (95% CI: 1.44–2.32), with low heterogeneity (I² = 42.7%, P = 0.121). (C) Preterm birth: Forest plot of 3 studies. The overall pooled OR is 1.14 (95% CI: 0.37–3.52), with significant heterogeneity (I² = 83.5%, P = 0.002). (D) Daily outdoor activity time ≤ 2 h: Forest plot of 2 studies. The overall pooled OR is 1.29 (95% CI: 0.53–3.17), with moderate heterogeneity (I² = 85.1%, P = 0.0009).

Six studies [17–19,21,24,25] mentioned smoking co-resident as a risk factor for RRTIs in preschool children, and the heterogeneity test (I² = 42.7%, P = 0.121) was conducted based on the fixed-effects model. It was found that smoking co-resident was a risk factor for RRTIs in preschool children, with obvious difference [OR = 1.83, 95% CI (1.44, 2.32), P < 0.001] (Figure 3B).

Preterm birth [20,22,24] was mentioned as a risk factor in three studies, and the heterogeneity test (I² = 83.5%, P = 0.002) was performed based on the random-effects model. The results indicated that preterm birth was not a statistically significant risk factor for RRTIs in preschool children [OR = 1.14, 95% CI (0.37, 3.52), P = 0.816] (Figure 3C).

Two studies [18,21] investigated daily outdoor activity time ≤ 2 h as a risk factor for RRTIs in preschool children, and the heterogeneity test (I² = 85.1%, P = 0.009) was conducted based on the random-effects model. It was found that daily outdoor activity time ≤ 2 h was not a significant risk factor for RRTIs in preschool children [OR = 1.29, 95% CI (0.53, 3.17), P = 0.574] (Figure 3D).

Two studies [19,25] mentioned low parental education level as a risk factor for RRTIs in preschool children, and the heterogeneity test (I² = 0, P = 0.629) was conducted based on the fixed-effects model. The results reflected that low parental education level was a significant risk factor for RRTIs in preschool children [OR = 3.17, 95% CI (1.76, 5.69), P < 0.001] (Figure 4A).

Figure 4.

Forest plots of meta-analyses for early-life and parental factors. (A) low Parental education level: Forest plot of two studies. The overall pooled OR is 3.17 (95% CI: 1.76–5.69), with no significant heterogeneity (I² = 0, P = 0.629). (B) Initial use of antibiotic <6 months: Forest plot of two studies. The overall pooled OR is 1.70 (95% CI: 1.50–1.93), with no significant heterogeneity (I² = 0, P = 0.780). (C) Maternal BMI per 3 kg/m² increment: Forest plot of two studies. The overall pooled OR is 1.18 (95% CI: 1.08–1.28), with no significant heterogeneity (I² = 0, P = 0.661). (D) Breast feeding duration <6 months: Forest plot of two studies. The overall pooled OR is 1.26 (95% CI: 1.12–1.42), with no significant heterogeneity (I² = 0, P = 0.728).

Two studies [16,23] reported Initial use of antibiotic < 6 months as a risk factor for RRTIs in preschool children, and the heterogeneity test (I² = 0, P = 0.78) was performed based on the fixed-effects model. The results suggested that Initial use of antibiotic < 6 months was a statistically significant risk factor for RRTIs in preschool children [OR = 1.70, 95% CI (1.50, 1.93), P < 0.001] (Figure 4B).

Two studies [16,23] identified maternal BMI per 3 kg/m² increment as a risk factor for RRTIs in preschool children, and the heterogeneity test (I² = 0, P = 0.661) was conducted based on the fixed-effects model. It was found that maternal BMI per 3 kg/m² increment was a risk factor for RRTIs in preschool children, and there exists an obvious difference [OR = 1.18, 95% CI (1.08, 1.28), P < 0.001] (Figure 4C).

Two studies [16,23] mentioned breast feeding duration < 6 months as a risk factor for RRTIs in preschool children, and the heterogeneity test (I² = 0, P = 0.728) was performed based on the fixed-effects model. The results of the analysis indicated that breast feeding duration < 6 months was a risk factor for RRTIs in preschool children, with obvious difference [OR = 1.26, 95% CI (1.12, 1.42), P < 0.001] (Figure 4D).

The findings of this study indicate that asthma [OR = 3.84] and allergy [OR = 2.27] are risk factors for RRTIs in preschool children. The immune system in children is inherently predisposed to recurrent and persistent infections [27,28]. Allergic diseases, such as asthma, increase susceptibility to respiratory tract infections through multiple interrelated mechanisms. First, the airway epithelial barrier is typically impaired in individuals with allergic diseases [29]. Specifically, the airway epithelium constitutes a physical barrier that prevents the invasion of pathogens and allergens. In patients with asthma, chronic airway inflammation and structural remodeling are frequently observed. This chronic inflammation and structural remodeling —including goblet cell hyperplasia and ciliary damage — further compromise barrier function, manifesting as epithelial barrier dysfunction and impaired ciliary activity. These alterations facilitate pathogen penetration across the epithelial layer, thereby weakening the physical defense mechanisms of the respiratory tract against pathogens [30–32]. Second, the immune system in these patients tends to favor a Th2-dominant response, characterized by excessive production of IL-4, IL-5, and IgE, leading to enhanced eosinophilic infiltration. This Th2-skewed response diminishes the efficacy of Th1-mediated immune defense against viral and bacterial pathogens [33]. Furthermore, patients with asthma often require corticosteroids to manage symptoms. Although corticosteroids are effective in suppressing local airway inflammation, their long-term use can suppress both local and systemic immune function [34]. In addition, in children — particularly those under one year of age — acquired immunity is not yet fully developed, resulting in relatively low immune competence. Collectively, the combined effects of impaired barrier function and immune disbalance significantly increase susceptibility to respiratory tract infections in individuals with allergic diseases.

The findings of this study indicate that initial use of antibiotics < 6 months [OR = 1.70], maternal BMI per 3 kg/m² increment [OR = 1.18], and breastfeeding duration < 6 months [OR = 1.26] are risk factors for RRTIs in preschool children. Although antibiotics confer significant health benefits in the treatment or prevention of bacterial infections, accumulating evidence suggests that they exert disruptive effects on host–microbiota homeostasis, posing a serious threat to global public health [35]. During infancy, due to the immaturity of the microbiota and the incomplete functional development of the immune system, the consequences of antibiotic treatment are more severe and persistent than those observed in adults [27]. This is primarily manifested in the following aspects: (1) Disruptive effects on the gut microbiota. The infant gut microbiota remains in a state of instability during the first 2–3 years of life [35]. Early-life antibiotic exposure disrupts the typical maturation trajectory of the gut microbiota, increases the abundance of antibiotic-resistant bacteria, enriches the resistance gene reservoir within the gut microbial community, and exerts adverse effects on child health [36]. A prospective controlled cohort study demonstrated that the timing of antibiotic exposure appears to be a critical determinant of gut microbiota alterations, with perinatal antibiotic exposure exerting a more pronounced impact on the gut microbiota of one-year-old infants than exposure occurring later in life [37]. (2) Long-term effects on immune system development. Antibiotic exposure during infancy may induce lasting consequences through microbiota–immune system crosstalk, potentially depleting key microbial taxa critical for normal immune maturation and leading to impaired local and systemic immune competence [38], Such disruption may affect both innate and adaptive immune responses to pathogens in infants [35], and has been associated with an increased risk of allergic diseases in childhood, including atopic dermatitis and asthma [39,40]. An additional cohort study confirmed that, compared with controls, children with early-life antibiotic exposure exhibited higher rates of subsequent infections and antibiotic usage later in childhood [41]. Although antibiotics are critical for infection treatment, their long-term effects on microbiome and immune development must be weighed. We therefore recommend a conservative antibiotic approach in infants and young children, and highlight the need to balance the risks and benefits of neonatal antibiotic exposure.

Due to the increasing prevalence of obesity and the trend of delayed childbearing, the number of children born to overweight or obese mothers is steadily rising [42,43]. Maternal obesity influences offspring susceptibility to long-term pediatric infectious morbidity [44]. Accumulating evidence suggests that children of obese mothers are at higher risk of hospitalization for respiratory diseases [45], including asthma [46] and respiratory symptoms such as wheezing [47]. The UK Bradford birth cohort study showed that higher maternal BMI was associated with an increased risk of respiratory tract infections (including lower respiratory tract infections, asthma, and otitis media) in offspring within the first year of life, with greater risk corresponding to higher obesity grades (class I obesity: RR = 1.18; class II obesity: RR = 1.31) [48]. A large Danish cohort study (n = 688,457) found that maternal BMI during early pregnancy was a risk factor for lower respiratory tract infections in offspring, particularly among children with an allergic predisposition [49]. Maternal pregnancy obesity has been associated with an increased risk of recurrent lower respiratory tract infections (e.g., bronchitis, pneumonia) in offspring during infancy, with a more pronounced effect observed among minority populations in low-income urban areas [50]. The potential underlying mechanisms may include the following. Studies have confirmed that offspring of obese mothers exhibit reduced pulmonary insulin sensitivity and elevated levels of allergen-specific IgE and IL-5 [51]. Furthermore, maternal BMI may influence fetal immune development through inflammatory states, metabolic abnormalities, or placental function, thereby increasing susceptibility to infections [52]. Maternal obesity during pregnancy leads to metabolic syndrome, chronic inflammation, and endocrine alterations, which can modify placental function and the maternal gut microbiome, as well as induce inflammation in the placenta and intrauterine environment. All of these factors collectively influence fetal growth and development, including brain and lung development [53]. From a population perspective, the finding suggests that maternal pre-pregnancy obesity may have a certain impact on children's respiratory health, warranting attention in public health research. However, its small effect size (OR = 1.18) limits its clinical utility, and it should not be a pediatric priority. Weight management in women of childbearing age should be pursued through preconception and population health efforts, rather than as a primary target in RRTI care.

A Nigerian study demonstrated that, compared with children breastfed for 1–6 months, those breastfed for 19–24 months exhibited significantly lower odds of recent acute respiratory illnesses after breastfeeding cessation (AOR = 0.37, 95% CI [0.15–0.79], P = 0.04). However, no significant difference was observed between feeding for 1–6 months and other shorter durations (e.g., 7–12 months) (P > 0.05) [54], suggesting that breastfeeding for <6 months may be insufficient to confer long-term immune protection. A prospective case–control study from China showed that among infants under 6 months of age, longer duration of exclusive breastfeeding was associated with lower recurrence rates of pneumonia, shorter hospital stays, and reduced hospitalization costs [55]. Early postnatal nutrition — particularly lactoferrin in breast milk — has profound implications for both development and long-term health, playing a crucial role in the growth of various biological systems and the prevention of numerous chronic diseases. Insufficient breastfeeding duration leads to lactoferrin deficiency, which may subsequently result in nutritional inadequacies and adversely affect the gut microbiota and immune pathways [56]. SIgA is the most abundant immunoglobulin subtype on mucosal surfaces and plays an important role in defending against pathogen invasion. Insufficient breastfeeding leads to reduced levels of SIgA in the infant respiratory and intestinal tracts, compromising the first-line mucosal defense and increasing the risk of respiratory mucosal immune disorders [57]. Breastfeeding is a key determinant in shaping the infant gut microbiota, and inadequate breastfeeding duration is associated with reduced microbial diversity and an increased abundance of potential pathogens (e.g., Enterobacteriaceae) [58]. In conclusion, breastfeeding reduces the risk of childhood respiratory diseases by modulating respiratory mucosal immunity and the gut microbiota while enhancing immune responses. Breastfeeding for less than six months may be insufficient to fully establish these protective mechanisms.

The findings of this study indicate that smoking co-resident [OR = 1.83], low parental education level [OR = 3.17], and dietary bias [OR = 2.10] are risk factors for RRTIs in preschool children. Preschool children, due to their immature immune systems, are a high-risk population for RRTIs. Passive smoking resulting from living with a smoking co-resident has been identified as one of the significant environmental risk factors [3]. A study from Spain reported that household secondhand smoke exposure was associated with significantly increased incidence and hospitalization rates for childhood asthma, otitis media, and lower respiratory tract infections [59]. Research from Poland also indicated that exposure to smoking environments in children under three years of age led to a significant increase in respiratory tract infections, as well as a higher incidence of otitis media. In households with smokers, children are more susceptible to passive secondhand smoke absorption, thereby significantly increasing the likelihood of frequent hospitalizations or antibiotic use due to respiratory infections [60]. When children co-reside with smokers, the passive smoking household environment may promote nasal biofilm formation, subsequently increasing the risk of persistent sinusitis and other respiratory tract infections [61]. Co-resident smokers may alter the microbial communities in the lower respiratory tract of children through secondhand smoke exposure, thereby increasing susceptibility to infections [62]. The impact of smoking on children's health is multifaceted. Exposing preschool children to smoking environments affects not only their physical health but also their development and behavior. For preschool children, such exposure is inequitable, and it is the responsibility of every parent to protect them from the harms of tobacco smoke.

A Finnish study investigating the relationship between parental education, income, employment status, and the risk of hospitalization for RSV bronchiolitis in infants demonstrated that lower parental education level significantly increased the risk of infant RSV hospitalization, with the risk increasing as education level decreased [63]. A study from Ethiopia showed that maternal occupation and education level were significantly associated with acute respiratory infections in children [64]. Parental knowledge regarding the management of respiratory tract infections may influence disease outcomes. Another study found that parents of children with frequent upper respiratory tract infections demonstrated a higher level of knowledge regarding wheezing management. During wheezing episodes, 91.8% of parents administered pharmacological treatment, while 80.1% used herbal remedies, suggesting that enhancing parental education may contribute to improved symptom recognition and management [65]. An association exists between parental education and childhood infectious diseases, with research indicating that parents with higher education levels are generally associated with higher coverage rates of voluntary vaccinations (e.g., varicella, mumps, and influenza) [66].

Dietary bias refers to an unreasonable and unhealthy dietary tendency in children, characterized by imbalanced dietary structure, uneven nutrient intake, or poor eating behaviors. Dietary bias can lead to deficiencies in immune-related nutrients such as vitamin A, vitamin D, calcium, and zinc, which may subsequently increase the risk of RRTIs through various immune mechanisms. A study from China demonstrated that low serum vitamin A concentration in children is associated with a high incidence of RRTIs; both low serum vitamin A concentration and current RTI symptoms are associated with the occurrence of RRTIs; and low intake of vitamin A-rich foods is also linked to the development of RRTIs [67]. It has been reported that vitamin A influences respiratory health by maintaining epithelial integrity and exerting anti-infective effects [68]. Additionally, studies have shown that low vitamin D levels constitute a risk factor for RRTIs, with serum 25(OH)D levels being significantly lower in children with recurrent infections compared to healthy controls [69]. Furthermore, hypocalcemia has also been identified as a risk factor associated with RRTIs [70]. Collectively, these studies indicate that dietary bias in preschool children may lead to nutritional deficiencies and inadequate intake of specific nutrients, ultimately increasing the risk of RRTIs. However, the underlying mechanisms require further investigation for validation.

The findings of this study suggest that daily outdoor activity time ≤ 2 h, co-residence with individuals having chronic respiratory disease, and preterm birth are not risk factors for recurrent respiratory tract infections in preschool children, which differs from the perspectives of some previous studies. Studies have found that higher physical activity levels in preschool children are significantly associated with fewer days of upper respiratory tract infection symptoms, while low physical activity levels may increase susceptibility to respiratory tract infections [71]. Considering the high heterogeneity associated with this factor, it can be inferred that the impact of outdoor activity on immunity may be characterized by "quality outweighing duration." A short duration of regular outdoor activity (e.g., one hour of outdoor play daily) may suffice to meet immune regulation requirements. Due to the high heterogeneity among the included studies, it was not possible to distinguish between the effects of "duration" and "quality," and the pooled results ultimately showed no significant association. Meanwhile, indoor activities with adequate ventilation may also reduce infection risk; therefore, insufficient duration per se may not constitute an independent risk factor. Studies have indicated that recurrent respiratory tract infections may be associated with chronic inflammation or abnormal immune responses [72]. If co-residing household members have chronic respiratory diseases, this may indirectly increase the risk of infection in children through genetic or environmental pathways. However, the present study showed that co-residence with individuals having chronic respiratory disease was not an independent risk factor. Possible explanations include the following: most chronic respiratory diseases are non-communicable, with extremely low pathogen shedding during stable phases; additionally, the compensatory effect of household protective behaviors may mitigate exposure risk. Therefore, future research still needs to further investigate the specific impact of the co-residence environment on recurrent respiratory tract infections in preschool children. Multiple studies have demonstrated that the incidence of lower respiratory tract infections in preterm infants at 1–2 years of age is significantly higher than that in term infants [73], and the proportion of moderate-to-late preterm infants hospitalized for lower respiratory tract infections is significantly higher than that of term infants [74]. Conversely, the results of this study indicated that preterm birth was not a risk factor for recurrent respiratory tract infections in preschool children. This may be attributed to substantial variability in follow-up durations among the included studies — for instance, some studies only followed up to infancy, while others extended into the preschool period — resulting in inconsistent temporal associations between exposure and outcome and consequently unstable pooled effect estimates. Meanwhile, given the high heterogeneity, it can be inferred that the impact of preterm birth on respiratory tract infections is age-dependent. Specifically, the risk may be higher during infancy, but as children enter the preschool period, with improved lung function and immune maturation, their infection risk gradually approaches that of term-born children. However, due to the substantial heterogeneity among the included studies, this dynamic change could not be precisely captured, and the pooled results ultimately showed no significant association.