Association between adverse childhood experiences and asthma: a meta-analysis

Abstract

Objective

The study explored whether there is an association between adverse childhood experiences (ACEs) and asthma through meta-analysis.

Methods

PubMed, Embase, Cochrane Library, and Web of Science were systematically searched up to May 20, 2024. Observational studies reporting associations between adverse childhood experiences (ACEs) and asthma were included. Two reviewers independently screened studies, extracted data, and assessed study quality. Odds ratios (ORs) with 95% confidence intervals (CIs) were pooled using a random-effects model in Stata 15.0. Heterogeneity was evaluated using the I² statistic, publication bias was assessed with Egger’s test and funnel plots, and study quality was evaluated using established assessment tools.

Result

Sixteen articles (n = 1,291,133) were included. Experiencing ≥ 1 ACE was associated with an increased risk of asthma [adjusted OR = 1.18, 95% CI (1.12–1.24); I²=86.7%, P < 0.001]. Exposure to 2–3 ACEs was associated with asthma [adjusted OR = 1.55, 95% CI (1.45–1.66); I²=38.2%, P = 0.138], and ≥ 4 ACEs showed the highest risk [adjusted OR = 1.98, 95% CI (1.72–2.27); I²=63.3%, P = 0.012]. Sensitivity analyses using the leave-one-out method indicated that the pooled estimates were robust and stable.

Conclusion

The current study found a positive relationship between ACEs and asthma, and as the number of ACEs experienced increases, the likelihood of asthma also rises. These findings underscore the importance of early identification and psychosocial support for children exposed to adversity, which may help reduce the long-term risk of asthma and improve overall respiratory health.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12889-026-26363-y.

Introduction

Asthma is a common respiratory disease, and the Global Burden of Disease (GBD) study published by the World Health Organization (WHO) [1, 2] has shown it to be a globally prevalent chronic disease with a high burden of disease. Asthma is a chronic respiratory condition characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing. Symptoms often worsen at night or early morning, indicating a distinct temporal pattern [3–5]. A 2016 Global Burden of Disease study found that 334 million people worldwide suffer from asthma, asthma attacks, especially moderate-to-severe attacks [6], not only pose a serious risk of asthma deterioration and may even cause sudden asthmatic death, which seriously affects people’s quality of life and social functioning and creates a huge burden on society and families [7, 8]. Asthma occurs due to both genetic and environmental factors, including external environments such as family, school, and society [9].

Adverse environmental factors in early life, such as abuse, neglect, and household dysfunction, play a critical role in shaping long-term health outcomes [10]. Adverse childhood experiences (ACEs), a concept introduced in 1998, refers to traumatic experiences occurring before age 18, including abuse, neglect, and household dysfunction [11–13]. Studies have shown that greater exposure to ACEs, both in number and type, is associated with a higher likelihood of developing cardiovascular diseases and mental health issues, such as anxiety and depression, in adulthood, suggesting a dose-response relationship [14–16]. However, the association between ACEs and asthma remains controversial due to factors such as limited studies, inconsistent findings, and the lack of pooled data on this topic [17]. Therefore, the present study aims to explore the association between ACEs and asthma through meta-analysis, and to provide a new basis for the prevention and treatment of asthma.

Materials and methods

The study was constructed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines [18], this study was pre-registered with the International prospective register of systematic reviews (PROSPERO) under the registration number: CRD42024544950.

Literature retrieval

The PubMed, Embase, Cochrane library, and Web of Science databases were searched with a May 20, 2024, search deadline. Data analysis was conducted on June 20, 2024. The search was performed using subject and free words with the search terms adverse childhood experiences, asthma. The specific search strategy is described in Supplementary Material Table S1.

Study selection

The retrieved literature was screened for literature using endnote20 according to inclusion and exclusion criteria, where the main inclusion criteria were

• Population (P): Individuals diagnosed with asthma, without restrictions on age, gender, occupation and country.

• Exposure (E): Adverse childhood experiences (ACEs), including physical abuse, verbal abuse, sexual abuse, emotional abuse, discrimination, food insecurity, housing instability, community violence, and post-traumatic stress disorder (PTSD).

• Comparator (C): Individuals without exposure to ACEs.

• Outcome (O): The association between ACEs and asthma, assessed through multivariate regression models reporting adjusted effect estimates.

• Study (S): The types of study were cross-sectional studies, cohort studies and case control studies.

The following exclusion criteria were considered for this study: Types of literature included (conference abstracts, reviews, meta-analyses, protocols, case reports), articles for which full text was not available as well as articles for which no usable data was available.

Data extraction

The literature was screened independently by two authors (WLQ and CYG) in adherence to stringent inclusion and exclusion criteria. Any disparities were meticulously ironed out through negotiations or by soliciting input from third-party arbiters (WYQ), culminating in unanimous accord. Extracted from the incorporated studies are pivotal particulars, encompassing Author, publication year, study design, country, sample size, gender distribution, age demographics, ACEs types, regression model and outcome.

Risk of bias assessment

For cross-sectional study, the methodological quality of the studies included was assessed using an 11-item checklist which was recommended by Agency for Healthcare Research and Quality (AHRQ) [19]. An item would be scored ‘0’ if it was answered ‘no’ or ‘unclear’; if it was answered ‘yes’, then the item scored ‘1’. Article quality was assessed as follows: low quality = 0–3; moderate quality = 4–7; high quality = 8–11. risk of bias assessment by two authors (WLQ and CYG).

Statistical analysis

In this study, (WLQ and CYG) combined the multivariate analysis values (OR/RR/HR and 95% CI) and assessed heterogeneity using the Q-test and I² statistic. A fixed-effects model was used when I² ≤ 50%, indicating low heterogeneity, assuming the true effect is consistent across studies. A random-effects model was employed when I² > 50%, accounting for higher heterogeneity and providing more robust estimates. Sensitivity analyses were performed using the ‘leave-one-out’ method to assess the influence of individual studies, and publication bias was examined using the Egger test and funnel plot.

Result

Literature retrieval process

By searching PubMed, Embase, web of science, Cochrane library, China Knowledge, Wan fang and VIP databases, a total of 1,290 papers were retrieved after removing the literature by reading the title, abstract and full text. 16 literatures [20–35] were finally included. The literature search flowchart is shown in Fig. 1.

Fig. 1.

Literature search flow chart

Basic characteristics of literature

A total of 16 articles were included in this study involving a total of 1,291,133 individuals, the included studies were cross-sectional studies with sample sizes ranging from 54 to 466,556, the types of ACEs designed for the study included Physical abuse; verbal abuse; sexual abuse; PTSD; and emotional abuse. pairs of research AHRQ scores were performed, of which three studies [21, 28, 29] scored 7, five studies [20, 26, 30, 34, 35] scored 8, six studies [24, 25, 27, 31–33]scored 9, and two studies [22, 23] scored 10. The basic characteristics of inclusion are shown in Table 1.

Table 1.

Basic features of literature

study	year	study design	country	samplesize	gender(M/F)	mean age	type of adverse childhood experiences	NOS scores
Bellis	2018	cross-sectional	UK	2452	1115/1337	18–69	Physical abuse; Verbal abuse; Sexual abuse	7
Chanlongbutra	2018	cross-sectional	USA	79,810	32,387/47,423	18–65	Physical abuse; Verbal abuse; Sexual abuse	9
Condon	2019	cross-sectional	USA	54	0/54	19–33	PTSD	9
Brew	2022	cross-sectional	Sweden	453,516	NR	NR	Physical abuse; Verbal abuse; Sexual abuse	8
Lam-Hine	2023	cross-sectional	USA	12,372	5778/6594	29	Physical abuse; Verbal abuse; Sexual abuse	8
Lê-Scherban	2018	cross-sectional	USA	350	280/70	42.7	Emotional abuse; Physical abuse; Sexual abuse	6
Lin	2021	cross-sectional	China	11,972	4390/7182	58.4	Physical abuse; Verbal abuse; Sexual abuse	7
Martinez	2024	cross-sectional	USA	147	91/56	7.66	discrimination; food insecurity; housing in stability; community violence	7
McCauley	2015	cross-sectional	USA	36,485	NR	50.5	Emotional abuse; Physical abuse; Sexual abuse	8
Merrick	2019	cross-sectional	USA	63,345	26,852/36,513	18–65	Physical abuse; Verbal abuse; Sexual abuse	6
Ospina	2021	cross-sectional	Canada	1207	595/612	17–94	Physical abuse; Verbal abuse; Sexual abuse	7
Pape	2021	cross-sectional	Denmark	466,556	227,156/239,400	25	Physical abuse; Verbal abuse; Sexual abuse	7
Wing	2015	cross-sectional	Greece	100	51/49	0–17	Physical abuse; Verbal abuse; Sexual abuse	8
Panisch	2022	cross-sectional	USA	49,000	NR	0–17	Physical abuse; Verbal abuse; Sexual abuse	8
Ross	2021	cross-sectional	USA	3691	NR	10.4	Physical abuse; Verbal abuse; Sexual abuse	9
Waehrer	2020	cross-sectional	USA	110,076	43,860/66,216	18–65	discrimination; food insecurity; housing in stability; community violence	9

M/F Male/female, PTSD Post-traumatic stress disorder, NR not reported

Meta-analysis results

Association between experiencing ≥ 1ACEs and asthma

Sixteen articles mentioned the relationship between experiencing ≥ 1 time ACEs and asthma, the test of heterogeneity (I² = 86.7%, P = 0.001), the data analysis using random effects model, the results (Fig. 2) of the analysis suggested that there was an association between those who have experienced ≥ 1 time ACEs and asthma [OR = 1.18, 95%CI (1.12, 1.24)]. Due to the large heterogeneity of this indicator, a sensitivity analysis was performed using the leave-one-out method, and the results of the analysis (Figure S1 in the Supplementary Material) suggested that the indicator was less sensitive, and the results were not influenced by a single study.

Fig. 2.

Forest plot of association between experiencing ACEs ≥ 1 and asthma

Association between experiencing 2-3ACEs and asthma

Seven articles mentioned the relationship between experiencing 2–3 times ACEs and asthma, the test of heterogeneity (I² = 38.2%, P = 0.138), the data analysis using fixed effects model, the results (Fig. 3) of the analysis suggested that there was an association between those who have experienced 2–3 times ACEs and asthma [OR = 1.55, 95%CI (1.45, 1.66)].

Fig. 3.

Forest plot of association between experiencing ACEs 2–3 and asthma

Association between experiencing ≥ 4ACEs and asthma

Seven articles mentioned the relationship between experiencing ≥ 4 times ACEs and asthma, the test of heterogeneity (I² = 63.3%, P = 0.012), the data analysis using random effects model, the results (Fig. 4) of the analysis suggested that there was an association between those who have experienced ≥ 4 times ACEs and asthma [OR = 1.98, 95%CI (1.72, 2.27)]. Due to the large heterogeneity of this indicator, a sensitivity analysis was performed using the leave-one-out method, and the results of the analysis (Figure S2 in the Supplementary Material) suggested that the indicator was less sensitive, and the results were not influenced by a single study.

Fig. 4.

Forest plot of association between experiencing ACEs ≥ 4 and asthma

Subgroup analysis

In the current study, subgroup analyses were performed according to the population, and the results of the subgroup analyses (Table 2) found that in children, ≥ 1 ACEs are associated with higher odds of asthma [OR = 1.16, 95%CI (1.10, 1.22)], and in adults, ≥ 1 ACEs are also associated with higher odds of asthma [OR = 1.27, 95%CI (1.09, 1.49)]. For 2–3 ACEs, in children, exposure is associated with higher odds of asthma [OR = 1.58, 95%CI (1.43, 1.74)], and in adults, the association remains significant [OR = 1.42, 95%CI (1.06, 1.90)]. For ≥ 4 ACEs, in children, the odds of asthma are significantly higher [OR = 2.12, 95%CI (1.92, 2.35)], and in adults, the odds are also elevated [OR = 1.52, 95%CI (1.26, 1.86)].

Table 2.

Results of subgroup meta-analysis

Outcomes	Subgroup	Number of Studies	Heterogeneity (%)	OR (95%CI)
≥ 1ACEs	Child	4	88.6	1.16(1.10, 1.22)
	Adult	12	43.0	1.27(1.09, 1.49)
2-3ACEs	Child	2	24.3	1.58(1.43, 1.74)
	Adult	5	71.4	1.42(1.06, 1.90)
≥ 4ACEs	Child	2	28.3	2.12(1.92, 2.35)
	Adult	5	0	1.52(1.26, 1.86)

Published bias

Egger’s test and funnel plot was used in the study to detect publication bias, and the results of the study suggested that Association between experiencing ACEs ≥ 1 and asthma (P = 0.02) may have publication bias, therefore, the association of ACE ≥ 1 May be slightly exaggerated. Association between experiencing ACEs 2–3 and asthma (P = 0.882), association between experiencing ACEs ≥ 4 and asthma (P = 0.467) were less likely to have publication bias, funnel plots are shown in Supplementary Material FigureS3-S5.

Discussion

To the best of our knowledge, this is the first time that a meta-analysis has been used to explore the link between ACEs and asthma, and the results of the current study found that there was a significant correlation between ACEs and asthma, and that the prevalence of asthma increased as the number of ACEs experienced increased. In this study, we found a significant positive correlation between experiencing at least one ACE and asthma (OR = 1.18, 95% CI [1.12, 1.24]). This means that individuals who have experienced one or more ACEs have an 18% higher risk of developing asthma compared to those who have not experienced ACEs, to better understand the relative importance of this result, we compared it to other known asthma risk factors. For example, smoking is a significant risk factor for asthma, and study [36] have shown that smokers have about a 35 per cent higher risk of developing asthma than non-smokers (RR = 1.35, 95%CI 1.04–1.75), this suggests that psychological and social factors should be included in a comprehensive consideration in asthma management strategies, this comparison is illustrative rather than exact, as the measures come from different study designs. In addition, future studies should further explore the underlying mechanisms linking ACEs to asthma and how this risk can be mitigated through interventions. Among the possible mechanisms linking ACEs to the development of asthma are the organic responses that occur in response to chronic psychosocial stress [37], due to the heterogeneity accounted for in this indicator, sensitivity analyses and subgroup analyses were conducted. Sensitivity analyses showed that no significant sources of heterogeneity were identified, but the main conclusions remained robust. Subgroup analyses further revealed differences in heterogeneity across the different feature groups. The high degree of heterogeneity, with an I² value of 86.7%, suggests that the pooled estimates may not apply uniformly across different settings, and effect sizes may differ meaningfully across populations, study designs, and regional characteristics. Thus, chronic exposure to stress leads to structural and functional abnormalities in the neural, endocrine, and immune systems, which work synergistically in response to stress [38, 39]. This negative exposure triggers specialized adaptive responses, including activation of different brain regions and the sympathetic nervous system, and leads to inflammatory processes that ultimately trigger neuroendocrine responses to stress and activation of the hypothalamic-pituitary-adrenal (HPA) axis [40]. While these integrated systems are effective in producing short-term adaptations to acute stress, their persistent stimulation may have deleterious effects on the organism [41]. Acute stress is associated with increased levels of cortisol, which leads to suppression of the inflammatory response [42]. Under the influence of stressors such as ACE, HPA axis function may be altered, leading to decreased cortisol levels and increased inflammatory markers, which would favor susceptibility to chronic disease. When we analyzed the association between ACEs ≥ 1 and asthma, the I² value was 86.7%, indicating that there was considerable heterogeneity among studies. This may be due to differences in study design, sample characteristics, regional differences, or measurement instruments. For example, some studies may focus on specific regions or specific populations, while others contain a broader group of subjects. High heterogeneity may affect the stability and accuracy of our results; therefore, we chose a random effects model to provide more reliable effect estimates when dealing with this heterogeneity. However, we are aware that this high heterogeneity may imply caution when synthesizing studies. There is a possibility of publication bias in our analysis, particularly when examining the association between ACE ≥ 1 and asthma exacerbations. As more positive findings are more likely to be published, this may lead to stronger associations being overestimated. Publication bias was found to be common in similar epidemiological studies, especially in small size and large effect studies. This bias may cause our observed association of ACE ≥ 1 to be stronger than the true effect; therefore, future studies should focus on more comprehensive bias assessment and adopt a more rigorous study design.

This finding differs from TIBOSCH et al. [43], which examined psychological traits of parents linked to asthma attacks and acute exacerbations but did not conclusively identify a heightened risk of asthma attacks. This discrepancy may be due to the wider array of adverse childhood experiences (ACEs) considered in this review. Additionally, there is proof of interactions or “synergistic” effects between ACEs and physical environmental risk factors. When ACEs and environmental exposures are combined, there is a potential for increased sensitization and pro-inflammatory responses, which significantly heightens the risk of developing asthma [31]. Animal research has indicated that social stress can cause corticosteroid insensitivity and trigger mast cell degranulation, with these genes being implicated in many symptoms of atopic disorders like asthma [44, 45]. Multiple studies have demonstrated that stressful life events elevate the incidence of asthma [46, 47]. Maternal stress during prenatal and early postnatal periods is notably associated with early childhood wheezing [48]. One study revealed that mothers who encountered stressful life events during pregnancy, such as divorce, bereavement, or job loss, were 1.71 times more likely to have children who developed asthma than those who did not [49]. Furthermore, a large population-based study of adults found that high-intensity life stress doubled the risk of developing asthma [50]. Besides exacerbating asthma, stress exposure also predicts a higher incidence of asthma in children.

The study population included in this research consists of children with asthma, veterans with asthma, and elderly individuals with asthma. The pathological mechanisms and clinical characteristics of asthma in these groups may have significant differences. Therefore, we used a random effects model for analysis, hoping to reduce the impact of heterogeneity on our article to some extent. Although we integrated data from different populations, we remind readers to consider the potential impact of this heterogeneity when interpreting the results. Future studies should consider more detailed subgroup analyses or conduct independent studies in specific populations to supplement and validate our findings.

According to the results of our meta-analysis, there was a significant positive correlation between ACE exposure and the development of asthma, and the higher the number of exposures, the higher the risk of asthma. Therefore, early screening and interventions should be implemented for at-risk populations, especially individuals who have experienced multiple ACE exposures. Healthcare providers can develop personalized health management strategies based on the number of exposures, such as early screening and health education for individuals with ≥ 1 exposure, and regular health check-ups, psychological support, and lifestyle interventions for individuals with ≥ 4 exposures. At the same time, policy makers should focus on the socio-environmental factors of ACE exposure and implement effective preventive measures to reduce asthma risk in high-risk groups.

Cues to action

Considering the observed association between adverse childhood experiences (ACEs) and asthma, several evidence-informed actions may help mitigate exposure to adversity and its long-term respiratory consequences. First, integrating systematic screening for psychosocial stressors into routine pediatric and primary care encounters may facilitate early identification of children at elevated risk. Second, strengthening family-focused interventions—such as evidence-based parenting programs, mental health services, and support for households affected by violence or instability—could reduce the occurrence of ACEs at the domestic level. Third, community and policy initiatives aimed at improving neighborhood safety, ensuring food and housing security, and expanding access to social and behavioral health resources may further limit exposure to chronic stressors. Additionally, training clinicians to recognize psychosocial determinants of health and to initiate timely referrals can enhance multidisciplinary responses. Collectively, these actions may contribute to lowering ACE exposure and, ultimately, reducing the burden of asthma attributable to early-life adversity.

Strengths and limitations

This study has several strengths. It is the first to explore the association between ACEs and asthma using a meta-analysis approach, utilizing a large dataset and robust statistical methods to assess the relationship between ACEs and asthma. Additionally, our study incorporates dose-response analysis, which allows us to examine how the risk of asthma changes with increasing exposure to ACEs. Sensitivity testing was also conducted to assess the robustness of our findings and ensure the reliability of our results. These methodological approaches strengthen the validity and generalizability of our conclusions.

This study also has several important limitations. First, all included studies were cross-sectional in design, which inherently limits causal inference. Although associations between adverse childhood experiences and asthma were identified, the temporal sequence between exposure and outcome cannot be firmly established, and reverse causality cannot be completely excluded. Therefore, the observed associations should be interpreted with caution, and future longitudinal or prospective cohort studies are needed to better clarify causal relationships. Second, the included studies were predominantly conducted in the United States and Europe, which may limit the generalizability of our findings to populations in other regions with different socioeconomic and environmental backgrounds. Third, some of the included studies were based on adult populations, while others focused on pediatric participants. Due to limited data availability, subgroup analyses by age were not feasible in this meta-analysis. Such analyses could provide more comprehensive insights and may help reduce heterogeneity across studies. Fourth, differences in the types of adverse childhood experiences reported across studies represent a key limitation of this analysis. Different studies included various forms of adverse childhood experiences—such as abuse, neglect, family dysfunction, or emotional abuse—but the definitions and measurement methods for these exposures varied. This inconsistency may have contributed to the observed heterogeneity and limited the ability to identify which specific types of adverse childhood experiences are most strongly associated with asthma. Finally, there was variability in the time interval between exposure to adverse childhood experiences and the onset of asthma. Some studies assessed exposures during early life, whereas others focused on more recent experiences, potentially leading to differences in the observed associations.

Conclusion

The current study found a positive relationship between ACEs and asthma, and as the number of ACEs experienced increases, the chance of asthma increases. Interventions may help mitigate this risk, though causality is not yet established, however, since there are more limitations in the study, future studies need to be multicenter, large sample studies to support our findings.

Authors’ contributions

Liqiong Wang has expertise in systematic reviews and meta-analyses, with a particular focus on epidemiological research design and quantitative data synthesis. Yungai Cheng specializes in statistical analysis and methodological quality assessment, with experience in evidence-based medicine. Yuqi Wang has a background in clinical research and scientific writing, with strengths in data interpretation and manuscript development. Liqiong Wang, Yungai Cheng, and Yuqi Wang contributed to the study conception and design. Liqiong Wang and Yuqi Wang performed the literature search and data extraction. Liqiong Wang and Yungai Cheng conducted the statistical analyses. Liqiong Wang, Yungai Cheng, and Yuqi Wang contributed to manuscript drafting. Yungai Cheng and Yuqi Wang critically revised the manuscript for important intellectual content. Liqiong Wang supervised the study and provided final approval of the version to be published. All authors read and approved the final manuscript and agree to be accountable for all aspects of the work.

Funding

None.

Data availability

The authors confirm that the data supporting the findings of this study are available within the article and its supplementary materials.

Declarations

Ethics approval and consent to participate

This meta-analysis does not involve human subjects. IRB review is not required.

Competing interests

The authors declare no competing interests.