Study hypotheses were partially supported by analysis results. The findings supported Hypothesis 1, that ACE scores have a positively graded relationship with asthma. Hypothesis 1 was supported by the results of the main effects model examining the independent relationship between ACEs, and race/ethnicity and asthma, as the risk of asthma increased significantly with each additional experience, accounting for control variables. Hypothesis 2 stated that the positive relationship between ACEs and asthma varies by race/ethnicity, with a stronger relationship experienced by racial/ethnic minority groups with higher rates of asthma and ACEs–Black/African American, Hispanic/Latino, AIAN, and multiracial individuals. Hypothesis 2 was partially supported by interactional models, with a significantly lower strength of relationship between ACEs and asthma for AIAN compared to the reference group, Asians, and no significant differences for other racial/ethnic groups. Hypothesis 3, stating that the positive relationship between ACEs and asthma varies by race/ethnicity and sex, with a disproportionate burden on Black/African American, Hispanic/Latino, AIAN, and multiracial women, was partially supported by sex-stratified interactional models, as the positive and significant relationship between ACEs and asthma was maintained for women but was no longer significant among men, and the strength of relationship between ACEs and asthma was, unexpectedly, significantly lower for Black/African American and AIAN women compared to Asian women.
Research has long established socially determined variations in health outcomes by ACEs, race/ethnicity and sex. Our paper contributes substantially to this work by considering the intersection of all three characteristics as related to one outcome, asthma. Our analysis reinforces prior work in this area: the number of ACEs and being female are independently and significantly related to the probability of a reported diagnosis of asthma. Contrary to our hypotheses, the results suggest that there were no significant differences in the relationship between ACEs and asthma for most racial/ethnic groups, with the exception of Black/African American and AIAN women, for whom the relationships between ACEs and asthma were actually weaker than for Asians. The findings allow a greater understanding of how various social identities and early life experiences interact with one another in relation to asthma likelihood, and provide insight for prioritizing potential strategies for asthma prevention.
Our findings show that negative social and environmental determinants of health expand health inequities across disadvantaged social groups and the general population. The odds of asthma increase significantly with each added ACE, independent of other factors related to race/ethnicity and other covariates. AIAN, Black/African American, White, and multiracial individuals experience a significantly greater risk of asthma than Asians related to their race/ethnicity, over and above ACEs and covariates. Additionally, AIAN and Black/African American women experience a significantly weaker relationship between ACEs and asthma compared to Asian women, while among men there was no significant relationship between ACEs and asthma, nor differences in the strength of relationship between ACEs and asthma across race/ethnicity. The findings suggest that women are particularly vulnerable to long-term asthma outcomes related to ACEs. This may contribute to higher rates of adult asthma for women compared to men. This merits the paying of increased attention to the prevention and early detection of ACEs for women in particular so as to mitigate long term health disparities.
While intersectionality theory would suggest the multiplicative effects of structural inequalities, an intersectional relationship was not fully supported for all racial/ethnic groups. The lack of significant interaction between most racial/ethnic groups and ACEs may lend some support to a multiple jeopardy hypothesis in which the effects of membership in such groups are instead additive. While social identities are interdependent on one another, results suggest that the relationship between ACEs and adult asthma differs in strength only between Asians, Blacks/African Americans, and AI/ANs. This also highlights the challenges and limitations inherent to using statistical methods, including interaction terms, to model intersectionality [43
Our findings point to childhood circumstances and sex as multiple intersecting identities that are important to wellbeing. However, they say little about causal mechanisms. We know little about what components at the intersection of experiences and social identity propel this vulnerability for some and not others. One potential explanation, in line with intersectionality, is that perceptions of adversity or the definitions of specific ACE survey items may differ across racial/ethnic groups, possibly intersecting with sex. Measures of childhood adversity may need to be expanded to include additional experiences, such as food insecurity, homelessness, or the prolonged absence of a parent [18
], or adversity occurring outside of the home, such as experiencing racism, bullying, or violence [44
]. For some AIAN groups, social support and community belonging may act as protective factors against the influence of ACEs on health outcomes [45
]. This could explain the observed significantly lower likelihood of asthma with respect to ACEs for AIAN women. It is also possible that other factors that influence asthma outcomes are more relevant than ACEs for some groups, such as neighborhood exposure to negative environmental impacts [47
], poor psychological wellbeing, and a family history of asthma [48
]. Another potential contributor could be that some groups spend more time in housing or work spaces that are constructed with toxic materials that heighten vulnerability to asthma [47
], which would be reflected in higher asthma rates but not the analyses presented in this study. Further research in this area could illuminate how specifically resources and supports may act as a buffer against negative health outcomes, or how influences other than ACEs more strongly affect asthma outcomes for some groups.
Interventions targeting asthma or ACEs can be better informed by focusing on multiple vulnerable statuses to reduce health disparities. Effective evidence-based interventions for the primary prevention of asthma do not yet exist [51
], but interventions to reduce exposure to environmental triggers [52
], increase self-management skills, or incorporate psychological counseling or relaxation strategies are effective for asthma control and management [54
]. These interventions are most effective when they address the multiple physical and social factors that contribute to asthma, are tailored for participants’ needs and level of risk, and delivered in venues where the target audience can be effectively and widely reached [56
]. Such evidence highlights the need for asthma prevention and management interventions that address the social environment, in addition to resources focusing on reducing the exposure to allergens in homes, schools, and outdoors [57
Our findings support ongoing calls for standardized screening and referrals for ACEs and social needs more broadly in clinical settings [58
], as well as evidence-based prevention efforts and interventions in the wider community [61
]. One such approach is trauma-informed care, in which healthcare organizations systematically recognize the effects of childhood adversity and offer effective treatment options [62
]. Interventions that target those with multiple risk factors for adversity and chronic disease, and select home visitation programs and social work strategies that strengthen peer, family, and community social support, particularly in early childhood years, are effective in the prevention of child abuse and neglect [63
]. These approaches to preventing or buffering the effect of ACEs could contribute to reductions in asthma disparities across sex and racial/ethnic groups. More broadly, study findings reinforce the need for asthma prevention and treatment interventions that consider social determinants of asthma, such as stress, violence, socioeconomic conditions, and residential segregation, which drive disproportionate medical care access, exposure to pollutants and allergens, and levels of collective efficacy and other social resources [16
]. The Empower Action Model is one example of a systematic framework designed to prevent childhood adversity and associated negative health outcomes. This model consists of multilevel approaches that emphasize protective factors, such as developing resilience through interpersonal interventions that promote stress management skills in combination with corresponding policies to build healthy environments [65
]. The implementation of such interventions by organizations and communities would be consistent with calls from the CDC for investment in evidence-based strategies that support healthy relationships and supportive environments to prevent chronic disease in adulthood [66
]. Future research building on these findings could examine the potential differences in the severity of asthma according to ACEs and racial/ethnic groups so as to further untangle the nature of the relationship between ACEs and asthma across racial/ethnic groups. Additionally, this study sets the foundation for further research exploring the reasons behind unexpected findings for some racial and ethnic minority groups, and the effectiveness of multilevel, intersectional interventions to reduce the burden of ACEs on health.
Strengths and Limitations
This study has several strengths. Conventional analytic methods do not perfectly model intersectional health effects [26
]. However, our stratified interaction analysis does allow for conclusions about the effect of differential moderation of multiple racial/ethnic groupings on the relationship between ACEs and asthma. This represents some of the first evidence examining the relationship of ACEs with adult asthma by both sex and race/ethnicity—also unique in its examination of several racial/ethnic subpopulations.
This study also has a number of limitations. This is a cross-sectional study, and conclusions regarding causal relationships between exposures and outcome cannot be made. BRFSS is telephone-based and self-reported, and therefore it may miss U.S. residents without landline or cellular telephone access. Data for one key exposure variable, ACEs, were collected in only a subset of states, which may result in bias. Sample characteristics differed somewhat from U.S. population estimates. The overrepresentation of Whites in the BRFSS sample could conservatively skew estimates for asthma and ACEs, as well as the main effect of ACEs on asthma outcomes. Conversely, the overrepresentation of females may positively skew asthma estimates. The ACEs measurements used do not account for the timing of childhood adverse events, most notably whether experiences happened during particularly sensitive periods. Longitudinal data documenting the specific timing and frequency of adverse events would provide greater insight into cumulative disadvantage as a potential mechanism for the influence of ACEs on asthma. The retrospective measure of ACEs creates the potential for recall bias among participants. Asthma is measured using the self-report of a health professional’s asthma diagnosis, which excludes those who have not been formally diagnosed, potentially underestimating asthma prevalence. For the most part, potential biases would be expected to generate findings that underestimate ACEs and their contribution to asthma. The BRFSS data did not allow for incorporating specific built environmental exposures that may influence asthma, such as air pollution. Finally, the number of respondents in some analysis subgroups resulted in relatively wide confidence intervals, limiting the ability for comparisons.
In spite of these limitations, this study provides insight into the interplay of characteristics that may put individuals at risk of asthma. Our work strongly suggests that the increased attention paid to ACEs in recent years should include an accounting of sex and race/ethnicity to advance health equity. Building upon these findings, future studies might examine the relationships between ACEs, race/ethnicity, age, and other chronic diseases such as cardiovascular disease and type 2 diabetes that disproportionately affect minority populations, and the potential mediating influence of certain health behaviors.