OBJECTIVES:

Asthma is a highly prevalent childhood chronic disease, with particularly high rates among poor and minority youth. Psychosocial factors have been linked to asthma severity but remain poorly understood. This study examined (1) relationships between parent and child depression and posttraumatic stress disorder (PTSD) symptoms, family functioning, and child asthma control in a sample of urban minority youth with uncontrolled asthma and (2) family functioning as a pathway linking parent depression and asthma outcomes.

METHODS:

Data were drawn from the baseline cohort of a randomized trial testing community interventions for children aged 5 to 16 with uncontrolled asthma (N = 223; mean age = 9.37, SD = 3.02; 85.2% Hispanic). Asthma control was defined by using the Asthma Control Test and Childhood Asthma Control Test, activity limitation, and previous-12-month asthma severity. Psychosocial measures included parent and child depression and PTSD symptoms, family chaos, and parent social support.

RESULTS:

Parent and child depression symptoms, but not PTSD, were associated with worse asthma control (β = −.20 [SE = 0.06] and β = −.12 [SE = −.03]; P < .001). Family chaos corresponded to worse asthma control, even when controlling for parent and child depression (β = −.33; [SE = 0.15]; P < .05), and was a mediator of the parent depression-asthma path. Emotional triggers of asthma also mediated the parent depression-asthma relationship.

CONCLUSIONS:

Findings highlight family chaos as a mechanism underlying the relationship between parent depression and child asthma control. Addressing parent and child depression, family routines, and predictability may optimize asthma outcomes.

What’s Known on This Subject:

Child and parent psychosocial risk factors, including depression and anxiety, are consistent predictors of poorer child asthma outcomes. Yet the asthma literature has largely focused on univariate relationships, and few studies have explored mechanistic pathways underlying these relationships.

What This Study Adds:

Within our sample of urban minority youth, child and parent depression and family chaos were particularly relevant predictors of uncontrolled asthma. This is the first study to highlight family chaos as a mediator of asthma outcomes, with important clinical implications.

Current asthma rates among children remain high despite improvements in available therapies, with the highest morbidity and costs occurring in urban, low-income minority youth.1,2 Public health efforts have increasingly focused on the psychosocial factors that confer risk for uncontrolled asthma and contribute to asthma health disparities, suggesting that psychosocial effects are complex and multifactorial.3 Greater knowledge of the pathways linking mental health and asthma outcomes among high-risk populations holds promise for optimizing future intervention efforts.

Substantial evidence demonstrates links between pediatric asthma and psychosocial factors at the level of the child, parent, and family. Numerous studies suggest that child depression and anxiety symptoms predict negative asthma outcomes, including increased functional impairment,4,5 severity of asthma,6,8 rescue medication use,9,10 and frequency of emotional triggers.8 However, findings vary by study methodology, level of asthma severity, and focus on depression versus posttraumatic stress disorder (PTSD)4 or other anxiety disorders.5,6,11,13 

Considerable research has also found higher rates of depression and anxiety in mothers of children with asthma,14 and caregiver depression is associated with higher child asthma severity.10 Although few studies have explored mechanistic pathways, biopsychosocial models3 propose that family-level risk factors may explain these associations and warrant further study. For example, research has shown that increased family conflict15 and maternal criticism16 have been associated with greater asthma severity. Similarly, negative family emotional climate8 and lower family functioning11 have shown indirect effects on asthma severity and emotional triggering of asthma8 via child depressive symptoms.

A socioecological perspective is needed to understand the interplay between parent, child, family, and environmental variables in the transmission of asthma risk.3 Key questions remain about the relative roles of parent versus child psychopathology, differential pathways for depression versus anxiety, and disentangling how family-, parent-, and child-level factors influence asthma outcomes. This is complicated by previously inconsistent measurements of asthma control.17 To build on previous literature, we use well-validated clinical asthma-control instruments to explore (1) relationships among parent depression and PTSD symptoms, child depression and PTSD symptoms, and child asthma control in a sample at high risk for internalizing disorders and asthma morbidity and (2) potential family-level mechanisms connecting parent and child mental health and asthma outcomes. Guided by a socioecological framework,3 we focus on the child, parent, and family factors that have emerged in the extant literature as relevant for asthma morbidity (child and/or parent depression and PTSD4,10,14) and mechanistic pathways (family functioning3,8,11). This study used the baseline sample of the Asthma Action at Erie Trial (identifier NCT02481986), a randomized controlled trial testing community-based asthma interventions in high-risk urban children. On the basis of existing research and models, we hypothesized that (1) parent and child depression and PTSD would each demonstrate significant associations with asthma outcomes and (2) lower family functioning (operationalized as greater family chaos and lower social support) would be a significant pathway linking parent mental health and asthma outcomes. To further characterize asthma severity, exploratory analyses examined emotional triggers of asthma as an outcome as well as an indirect path linking psychosocial factors and asthma control.

The Asthma Action at Erie Trial, described in a previous publication,18 involves a partnership with Erie Family Health Centers, a Federally Qualified Health Center serving mainly low-income minority families across multiple sites in the Chicago area. Participants were enrolled as parent-child dyads. Inclusion criteria were as follows: (1) patient at a participating Erie clinic (6 sites; 10% total participants in 3 smaller sites, 35% in 2 middle-sized sites, and 55% from a larger site), (2) aged 5 to 16 years, (3) live with a caregiver at least 5 days per week, and (4) uncontrolled asthma (≥1.25 on the Asthma Control Questionnaire,19,21 <20 on the Asthma Control Test [ACT] or Childhood Asthma Control Test22,24 [cACT], or a report of at least 1 oral corticosteroid burst for asthma in the past year).25 Families were excluded if they could not speak English or Spanish, they did not have permanent housing, caregivers did not have permanent custody of the child, or the child had significant developmental delays or comorbidities limiting their participation. Recruitment occurred from March 2016 to August 2017. Of 1688 potentially eligible children, 223 families were enrolled and randomly assigned to 1 of 2 community interventions.18 

All study procedures were approved by institutional review boards and the Erie Research Committee. Caregivers and children older than 7 years provided signed consent and assent, respectively. Research assistants collected data in participants’ homes via computer. Research assistants asked questions verbally, showing prompt cards with responses. For privacy, caregivers completed depression and PTSD measures using computers. Asthma control was captured in multiple ways. Asthma control was measured by using the ACT (children aged 12 years and older) and cACT (children under 12 years of age).22,23 Families were also asked the number of days out of the past 14 with activity limitation to capture this powerful domain.26 The Asthma Functional Severity Scale (AFS)27 assessed symptoms over the past year. Families were asked about asthma medications. For children with an inhaled corticosteroid (ICS) controller, an electronic medication monitor was attached for 2 weeks to record daily actuations. Emotional triggers for asthma were asked of the child and/or caregiver via the item, “Do strong emotions trigger [child]’s asthma?” (yes, no, or do not know). Demographics, medications, triggers, and self-reported behaviors were assessed through questions and observations.

Parent Mental Health

Parent depression symptoms were measured via the 9-item Patient Health Questionnaire (PHQ-9).28,29 Parent PTSD symptoms were captured via the Short Form of the PTSD Checklist–Civilian Version,30 a 6-item measure widely used in trauma research.

Child Mental Health

Depression symptoms for children ages 7 years and older were assessed by using the Children’s Depression Inventory 2 (Short Form),31 a 12-item measure of the affective, behavioral, and cognitive symptoms of depression occurring over the past 2 weeks. The 28-item Child Report of Post-traumatic Symptoms32 assessed broad posttraumatic symptomatology experienced over the past 7 days for youth aged 7 years and older.

Family Functioning

Family chaos was examined by using the Confusion, Hubbub, and Order Scale (CHAOS),33 which assesses the level of commotion, disorganization, and routine within the household (eg, “We are usually able to stay on top of things”) on a yes-or-no scale. Total scores range from 0 to 15; higher scores reflect greater chaos and disorganization. The CHAOS has good validity, reliability, and stability over a 12-month period and thus is considered to capture chronic family conditions.33 Parent social support was assessed by using the 8-item Patient-Reported Outcomes Measurement Information System34 Emotional, Instrumental, and Informational Support scales, which were developed and validated to measure social function in adults.

Age-specific ACT measures were combined into a single measure to retain all subjects in the analyses by rescaling the ACT to the range of the cACT. Generalized linear regression models (GLMs) examined the key psychosocial predictors, identified a priori as guided by the literature, on asthma outcomes. All models controlled for demographic characteristics identified as significantly related to asthma outcomes by using backward elimination with P < .10 (child age, sex, ethnicity [Hispanic, yes or no], BMI, maternal education, and maternal language). Because of the multisite design, models also controlled for site effects. For brevity, only the effects for psychosocial predictors are discussed. Complete case analyses were implemented because the proportion of missing data was negligible. Residuals from all models were evaluated for normality and outliers; no departures from normality or outliers were identified.

To facilitate comparison with previous work and determine the relative weights of child-, parent-, and family-level factors, a series of GLMs examined the hypothesized relationships between psychosocial predictors and asthma outcomes through a 2-step process to identify the independent and relative associations with each independent variable. We were interested in child-parent associations and child-child associations separately as well as their joint associations on child outcomes. First, separate models examined the bivariate relationships between each parent- and family-level predictor and the ACT (controlling for significant demographics). Next, we examined the set of significant parent and/or family predictors identified in the bivariate models (P < .05), which allowed for the examination of adjusted effects of each predictor, controlling for all other parent and/or family and demographic variables in the model. Only significant factors were included to enhance parsimony and model fit. This approach was then followed for all child-level predictors. Last, a final GLM including all parent, child, and family factors that were identified as significant in the bivariate models was estimated to examine the relative contributions of each predictor, controlling for all other child-, parent-, and family-level predictors and demographic variables in the model. All models were repeated for the AFS and activity limitation. Additionally, separate logistic regression models examined each of the significant parent-, family- and child-level variables (identified in the GLMs described above) as predictors of emotional triggers of asthma symptoms (dichotomized as yes or no). Because of age restrictions of the child depression and PTSD measures, there were a total of 153 participants in select analyses.

To examine our hypothesis that family factors may mediate the link between parent mental health and child asthma outcomes, we estimated a full serial mediation model with family chaos and emotional triggers as potential mediators of parental depression and child ACT. The GLMs helped identify the key relationships to include in the mediation model (ie, parent depression and family chaos), and emotional triggers were included as an intermediary pathway between psychosocial factors and the ACT. Linear regression was used for family chaos, and logistic regression was used to model emotional triggers (dichotomized as yes or no), controlling for site, child age, and child ethnicity. Indirect effects were estimated as a product of regression coefficients with bootstrapped SEs. Analyses were conducted in SAS 9.4 (SAS Institute, Inc, Cary, NC) and Mplus 8.

Table 1 presents parent demographic characteristics. Caregivers were predominantly women (96.9%) and Hispanic (85.7%). Parents had low educational attainment (66.4% high school diploma or general education diploma or less) and income (62.3% made <$60 000). Child demographics and asthma characteristics are presented in Table 2.

TABLE 1

Parent Demographic Characteristics

Result (N = 223)
Female sex, n (%) 216 (96.9) 
Age, y, mean (SD) 36.3 (7.1) 
Relationship to child, n (%)  
 Parent 216 (96.9) 
 Grandparent 5 (2.2) 
 Other (legal guardian) 2 (0.9) 
Education, n (%)  
 Less than high school 64 (28.7) 
 High school graduate or GED 84 (37.7) 
 Some college 54 (24.2) 
 College graduate (baccalaureate) or more 21 (9.4) 
Hispanic, n (%) 191 (85.7) 
Place of birth, n (%)  
 Mainland United States 102 (45.7) 
 Mexico 99 (44.4) 
 Puerto Rico 6 (2.7) 
 Other outside mainland United States 16 (7.2) 
Race,an (%)  
 African American 34 (15.3) 
 White 68 (30.6) 
 Other 115 (51.8) 
 Unknown or refused to answer 5 (2.3) 
Household income in last y,b $, n (%)  
 <20 000 46 (20.9) 
 20 000–59 000 91 (41.4) 
 >60 000 13 (5.9) 
 Do not know 70 (31.8) 
Language of interview, n (%)  
 English 109 (48.9) 
 Spanish 70 (31.4) 
 Mixed English and Spanish 44 (19.7) 
Relationship status,cn (%)  
 Single 54 (24.4) 
 Living with partner or spouse 144 (65.2) 
 Separated, divorced, or widowed 23 (10.4) 
Result (N = 223)
Female sex, n (%) 216 (96.9) 
Age, y, mean (SD) 36.3 (7.1) 
Relationship to child, n (%)  
 Parent 216 (96.9) 
 Grandparent 5 (2.2) 
 Other (legal guardian) 2 (0.9) 
Education, n (%)  
 Less than high school 64 (28.7) 
 High school graduate or GED 84 (37.7) 
 Some college 54 (24.2) 
 College graduate (baccalaureate) or more 21 (9.4) 
Hispanic, n (%) 191 (85.7) 
Place of birth, n (%)  
 Mainland United States 102 (45.7) 
 Mexico 99 (44.4) 
 Puerto Rico 6 (2.7) 
 Other outside mainland United States 16 (7.2) 
Race,an (%)  
 African American 34 (15.3) 
 White 68 (30.6) 
 Other 115 (51.8) 
 Unknown or refused to answer 5 (2.3) 
Household income in last y,b $, n (%)  
 <20 000 46 (20.9) 
 20 000–59 000 91 (41.4) 
 >60 000 13 (5.9) 
 Do not know 70 (31.8) 
Language of interview, n (%)  
 English 109 (48.9) 
 Spanish 70 (31.4) 
 Mixed English and Spanish 44 (19.7) 
Relationship status,cn (%)  
 Single 54 (24.4) 
 Living with partner or spouse 144 (65.2) 
 Separated, divorced, or widowed 23 (10.4) 

GED, general education diploma.

a

N = 222.

b

N = 220.

c

N = 221.

TABLE 2

Child Demographic and Asthma Characteristics

Result (N = 223)
Female sex, n (%) 98 (44.0) 
Age, y, n (%)  
 5–11 176 (78.9) 
 12–16 47 (21.1) 
Hispanic, n (%) 190 (85.2) 
Born in mainland United States, n (%) 215 (96.4) 
Race,an (%)  
 African American 39 (17.6) 
 White 63 (28.4) 
 Other 115 (51.7) 
 Unknown or refused to answer 5 (2.3) 
ACT,b mean (SD) 18.1 (4.82) 
AFS (past 12 mo),a mean (SD) 10.1 (4.7) 
 Low (0–4), n (%) 23 (10.4) 
 Mild (5–8), n (%) 62 (27.9) 
 Moderate (9–14), n (%) 96 (43.2) 
 Severe (15–24), n (%) 41 (18.5) 
No. d of activity limitation in past 2 wk, median (range) 2.0 (0–14) 
Oral corticosteroid for asthma in past 12 mo,a median (range) 2.0 (1–12) 
Observed quick-relief asthma medicine, n (%) 183 (82.1) 
Observed ICS medicine, n (%) 99 (44.4) 
Adherence to prescribed doses of ICS medicine in past 2 wk,cn (%) 53.4 (25.2) 
Emotions are a strong trigger, n (%) 82 (36.8) 
Result (N = 223)
Female sex, n (%) 98 (44.0) 
Age, y, n (%)  
 5–11 176 (78.9) 
 12–16 47 (21.1) 
Hispanic, n (%) 190 (85.2) 
Born in mainland United States, n (%) 215 (96.4) 
Race,an (%)  
 African American 39 (17.6) 
 White 63 (28.4) 
 Other 115 (51.7) 
 Unknown or refused to answer 5 (2.3) 
ACT,b mean (SD) 18.1 (4.82) 
AFS (past 12 mo),a mean (SD) 10.1 (4.7) 
 Low (0–4), n (%) 23 (10.4) 
 Mild (5–8), n (%) 62 (27.9) 
 Moderate (9–14), n (%) 96 (43.2) 
 Severe (15–24), n (%) 41 (18.5) 
No. d of activity limitation in past 2 wk, median (range) 2.0 (0–14) 
Oral corticosteroid for asthma in past 12 mo,a median (range) 2.0 (1–12) 
Observed quick-relief asthma medicine, n (%) 183 (82.1) 
Observed ICS medicine, n (%) 99 (44.4) 
Adherence to prescribed doses of ICS medicine in past 2 wk,cn (%) 53.4 (25.2) 
Emotions are a strong trigger, n (%) 82 (36.8) 
a

N = 222.

b

Combined scale.

c

N = 75.

The majority of the sample (55.7%) demonstrated uncontrolled asthma on the ACT. Asthma morbidity was significant, with high rates of oral corticosteroid bursts (60.4%), emergency department visits (38.3%), and hospitalizations (16.7%) for asthma in the past 12 months. Only 82.1% of children had a quick-relief medication, and 44% had an observed ICS controller medication. Children were taking approximately half (mean = 53.4) of prescribed ICS medications via monitor measurement. More than one-third (36.8%) reported strong emotions as an asthma trigger. Asthma outcomes (ACT, 12-month severity, and activity limitations) were moderately correlated (r = −0.448 to −0.511; P < .0001).

Table 3 presents mental health characteristics. Parents reported elevated depression and PTSD symptoms. Specifically, 14.8% endorsed moderate to severe depressive symptoms, 19.3% met criteria for PTSD, and 46.6% reported a traumatic event. Children reported similarly high levels of depression (18% elevated or very elevated), and 51.3% endorsed clinically significant PTSD symptoms. Families reported a wide range of chaos scores (0–13) but mean scores were low (3.2) comparable to other pediatric samples (2.8435 and 3.8936) and the original validation study (3.333). Family social support was within the normal range. Table 4 displays Pearson correlation coefficients for the psychosocial variables. Results suggest that psychosocial measures were related but largely distinct constructs.

TABLE 3

Parent, Child, and Family Psychosocial Characteristics

Result (N = 223)
Parent depression, mean (SD) 4.4 (5.0) 
 Moderate (score 10–15), n (%) 21 (9.4) 
 Moderate-severe to severe (score >15), n (%) 12 (5.4) 
Parent PTSD 1.0 (1.4) 
 No. stressful events, mean (SD) 13.0 (6.1) 
 PTSD score,a mean (SD) 43 (19.3) 
 PTSD in clinical range (score >13), n (%)  
Social support, mean (SD)  
 Emotionalb 54.0 (10.2) 
 Instrumentalc 52.8 (10.5) 
 Informationalc 55.1 (11.2) 
Family chaos, mean (SD) 3.2 (2.8) 
Child depression,d mean (SD) 54.3 (11.5) 
 Average, % 116 (74.4) 
 High average, % 12 (7.7) 
 Elevated, % 9 (5.8) 
 Very elevated, % 19 (12.2) 
Child posttraumatic stress symptoms,e mean (SD) 19.0 (8.4) 
 Clinical concern (≥19), % 79 (51.3) 
Result (N = 223)
Parent depression, mean (SD) 4.4 (5.0) 
 Moderate (score 10–15), n (%) 21 (9.4) 
 Moderate-severe to severe (score >15), n (%) 12 (5.4) 
Parent PTSD 1.0 (1.4) 
 No. stressful events, mean (SD) 13.0 (6.1) 
 PTSD score,a mean (SD) 43 (19.3) 
 PTSD in clinical range (score >13), n (%)  
Social support, mean (SD)  
 Emotionalb 54.0 (10.2) 
 Instrumentalc 52.8 (10.5) 
 Informationalc 55.1 (11.2) 
Family chaos, mean (SD) 3.2 (2.8) 
Child depression,d mean (SD) 54.3 (11.5) 
 Average, % 116 (74.4) 
 High average, % 12 (7.7) 
 Elevated, % 9 (5.8) 
 Very elevated, % 19 (12.2) 
Child posttraumatic stress symptoms,e mean (SD) 19.0 (8.4) 
 Clinical concern (≥19), % 79 (51.3) 
a

Parents reported a traumatic event (N = 104).

b

N = 221.

c

N = 222.

d

Youth (aged 7 years and older) completed measure (N = 156).

e

Youth (aged 7 years and older) completed measure (N = 154).

TABLE 4

Pearson Coefficients Examining Pairwise Correlations Between Psychosocial Constructs (N = 223)

12345678
Parent depression — — — — — — — — 
Parent PTSD 0.589*** — — — — — — — 
Family chaos 0.504*** 0.426*** — — — — — — 
Support         
 Emotionala −0.498*** −0.314*** −0.406*** — — — — — 
 Instrumentalb −0.387*** −0.270*** −0.308*** 0.532*** — — — — 
 Informationalb −0.464*** −0.309*** −0.419*** 0.821*** 0.564*** — — — 
Child depressionc 0.195* 0.096 0.221** −0.163* −0.181* −0.074 — — 
Child PTSDd 0.150 0.081 0.071 −0.053 −0.127 −0.058 0.640*** — 
12345678
Parent depression — — — — — — — — 
Parent PTSD 0.589*** — — — — — — — 
Family chaos 0.504*** 0.426*** — — — — — — 
Support         
 Emotionala −0.498*** −0.314*** −0.406*** — — — — — 
 Instrumentalb −0.387*** −0.270*** −0.308*** 0.532*** — — — — 
 Informationalb −0.464*** −0.309*** −0.419*** 0.821*** 0.564*** — — — 
Child depressionc 0.195* 0.096 0.221** −0.163* −0.181* −0.074 — — 
Child PTSDd 0.150 0.081 0.071 −0.053 −0.127 −0.058 0.640*** — 

Numbers 1 to 8 (top row) correspond to variables as listed in the first column. —, not applicable.

a

N = 221.

b

N = 222.

c

N = 156.

d

N = 154.

*

P < .05; ** P < .01; *** P < .0001.

Parent and Family Models

Outcomes of the bivariate models examining each parent- and family-level predictor of the ACT are presented in Table 5 (top portion). This model summarizes variable associations in terms of estimated β coefficients, which represent the predicted change in outcome per 1-unit increase in covariate value. For example, a 1-point increase in parent PHQ-9 score corresponds to a decrease of 0.2 in predicted ACT scores (β = −.20; SE = 0.06). Parent depression, but not PTSD, symptoms were significantly related to ACT scores. Parent emotional support showed a modest but significant relationship with the children’s ACT scores. Instrumental and informational support were not significant. Family chaos demonstrated a robust effect on ACT scores. With all significant parent- and family-level predictors examined together in the multiple model (Table 5, bottom portion), only family chaos retained significance, suggesting that the associations between parent depression and parent emotional support with the ACT were accounted for by the effects of family chaos. This adjusted model accounted for 16.4% of the variance in ACT scores, with 31.5% of explained variance being attributed to family chaos.

TABLE 5

Parent Predictors of Child Asthma Control (ACT) Examined Separately (Bivariate Models) and in a Multiple Regression Model (N = 221)

PredictorEstimate95% CI
Separate bivariate modelsa   
 Depression −0.20** −0.32 to −0.08 
 PTSD −0.06 −0.17 to 0.04 
 Support   
  Emotional 0.06* 0.00 to 0.12 
  Instrumental 0.03 −0.04 to 0.08 
  Informational 0.05 −0.01 to 0.10 
 Family chaos −0.45*** −0.67 to −0.23 
Multiple modelb   
 Depression −0.11 −0.25 to 0.04 
 Support (emotional) 0.00 −0.07 to 0.07 
 Family chaos −0.36** −0.61 to −0.12 
PredictorEstimate95% CI
Separate bivariate modelsa   
 Depression −0.20** −0.32 to −0.08 
 PTSD −0.06 −0.17 to 0.04 
 Support   
  Emotional 0.06* 0.00 to 0.12 
  Instrumental 0.03 −0.04 to 0.08 
  Informational 0.05 −0.01 to 0.10 
 Family chaos −0.45*** −0.67 to −0.23 
Multiple modelb   
 Depression −0.11 −0.25 to 0.04 
 Support (emotional) 0.00 −0.07 to 0.07 
 Family chaos −0.36** −0.61 to −0.12 
a

Six separate bivariate models were conducted for each parent and family predictor listed on the ACT score; each bivariate test controlled for site, age, and ethnicity.

b

Significant predictors identified in bivariate models were retained in the multiple model, allowing for the capture of adjusted effects for each predictor while controlling for all other predictors in the model. Site, age, and ethnicity were included as controls.

*

P < .05; ** P < .01; *** P < .001.

Child Models

Table 6 presents the outcomes of the models examining child-level predictors. In the separate bivariate models (top portion), child depression and PTSD symptoms were each related to ACT scores, and family chaos was significant. To explore the relative influences of child depression versus PTSD symptoms, a second model examined child depression and PTSD symptoms together on the ACT; only depression remained significant at a trend level (P = .062). The multiple regression model (bottom portion) included child depression, PTSD, and family chaos; only family chaos remained significant. This model accounted for 26.2% of the variance in ACT scores, with family chaos contributing 23.8% of explained variance.

TABLE 6

Child Predictors of Asthma Control (ACT) Examined Separately (Bivariate Model) and in Multiple Regression Models (N = 153)

PredictorEstimate95% CI
Separate bivariate modelsa   
 Child depression −0.12*** −0.18 to −0.05 
 Child PTSD −0.15*** −0.24 to −0.07 
 Family chaos −0.45*** −0.71 to −0.18 
Child depression and PTSD modelb   
 Child depression −0.08* −0.16 to 0.00 
 Child PTSD −0.09 −0.20 to 0.03 
Multiple modelc   
 Child depression −0.05 −0.13 to 0.03 
 Child PTSD −0.09 −0.21 to 0.02 
 Family chaos −0.35** −0.62 to −0.09 
PredictorEstimate95% CI
Separate bivariate modelsa   
 Child depression −0.12*** −0.18 to −0.05 
 Child PTSD −0.15*** −0.24 to −0.07 
 Family chaos −0.45*** −0.71 to −0.18 
Child depression and PTSD modelb   
 Child depression −0.08* −0.16 to 0.00 
 Child PTSD −0.09 −0.20 to 0.03 
Multiple modelc   
 Child depression −0.05 −0.13 to 0.03 
 Child PTSD −0.09 −0.21 to 0.02 
 Family chaos −0.35** −0.62 to −0.09 

Restricted to age ≥7 years for the depression measure.

a

Three separate bivariate models were conducted for each child and family predictor listed on the ACT; each model controlled for site, age, and ethnicity.

b

Model examined child depression and PTSD on the ACT, controlling for site, age, and ethnicity.

c

Multiple model examined the significant child and family predictors identified in the bivariate models, allowing for adjusted effects for each predictor and controlling for all others in the model. Site, age, and ethnicity were included as controls.

*

P < .10; ** P < .01; *** P < .001.

Combined Models

To evaluate the relative contributions of parent versus child influences on asthma, child and parent depression were examined together in a model (N = 153). Child depression retained significance (β = −.11; SE = 0.03; P = .002), but parent depression did not (β = −.11; SE = 0.07; P = .126). Last, when all significant child-, parent-, and family-level predictors were examined in a final multiple regression model (Table 7), only family chaos remained significant. To directly compare the magnitude of effects, semipartial standardized estimates were calculated for each predictor, providing an estimate of the adjusted correlation between the predictor and ACT and controlling for all other variables in the model. Family chaos showed the strongest relationship with the ACT, followed by child depression.

TABLE 7

Final Multiple Regression Model Examining Parent, Child, and Family Predictors of Asthma Control (ACT; N = 153)

PredictorEstimate95% CIStandardized Estimatea
Child depression −0.09 −0.20 to 0.02 −0.12 
Child PTSD −0.05 −0.13 to 0.03 −0.08 
Parent depression −0.02 −0.18 to 0.14 −0.02 
Family chaos −0.33* −0.64 to 0.03 −0.15 
PredictorEstimate95% CIStandardized Estimatea
Child depression −0.09 −0.20 to 0.02 −0.12 
Child PTSD −0.05 −0.13 to 0.03 −0.08 
Parent depression −0.02 −0.18 to 0.14 −0.02 
Family chaos −0.33* −0.64 to 0.03 −0.15 

Restricted to age ≥7 years for the depression measure. Model examined significant child, parent, and family variables on ACT score; model included covariates of site, age, and ethnicity not reported above.

a

Estimate of the adjusted correlation between each psychosocial predictor and the ACT, controlling for all other variables in the model, to compare magnitude of effects.

*

P < .05.

Analyses examining activity limitation revealed an identical pattern of results. Analyses examining the AFS produced the same pattern of results but weaker relationships. Logistic regression models indicated that the odds of emotional triggers were significantly increased with higher parent depression (odds ratio [OR] = 1.13; β = .12; SE = 0.03; P < .001), family chaos (OR = 1.13; β = .12; SE = 0.05; P = .02), and child depression (OR = 1.03; β = .03; SE = 0.02; P = .06).

We explored family chaos and emotional triggers as mediators of the parent depression-ACT association (Fig 1). Findings indicated significant indirect paths between parent depression and the ACT through family chaos and separately through emotional triggers. When controlling for family chaos and emotional triggers in the model, the parent depression-ACT direct path became nonsignificant, suggesting full mediation. The path via family chaos and emotional triggers was not significant. Findings suggest that the effect of parent depression on ACT scores is mediated separately through family chaos (β = −.09; SE = 0.04; bootstrapped bias corrected confidence interval [CI] = −0.17 to −0.02; 31% of total indirect effect) and emotional triggers (β = −0.17; SE = 0.11; CI = −0.48 to −0.03; 60% of total indirect effect).

FIGURE 1

Mediation model of the effect of parent depression on ACT scores via family chaos and emotional triggers. Solid lines are significant paths (P < .05); dashed lines are nonsignificant paths. Findings reveal full mediation, with the effect of parent depression on ACT scores being mediated separately through family chaos and emotional triggers.

FIGURE 1

Mediation model of the effect of parent depression on ACT scores via family chaos and emotional triggers. Solid lines are significant paths (P < .05); dashed lines are nonsignificant paths. Findings reveal full mediation, with the effect of parent depression on ACT scores being mediated separately through family chaos and emotional triggers.

To explore what the family chaos construct may be capturing, post hoc analyses examined associations between family chaos and asthma management measures and income. Family chaos was significantly and inversely related to parental help with medication, as reported by the parent (r = −0.174) and child (r = −0.176; P = .009). The association with adherence was not significant (r = −0.070; P = .550; n = 75). Family chaos was not related to the presence of a controller (t[221] = −0.83; P = .408) or reliever medication (t[221] = −0.65; P = .517) and was unrelated to income (r = −0.069; P = .404). Additionally, we examined ACT scores at the top and bottom quartiles of family chaos scores. For youth with the greatest family chaos (top quartile), the average ACT was 15.58 (SD = 5.59), whereas for the lowest quartile of family chaos, the average ACT was 18.94 (SD = 6.75). This represents a clinically meaningful difference in levels of ACT scores across ranges of family chaos.37 Nonparametric methods confirmed that ACT scores worsened linearly with increasing levels of chaos.

In this study of urban minority youth with uncontrolled asthma, parents and children both demonstrated elevated rates of depression and PTSD symptomatology that exceed prevalence rates in the general population.14,38 We hypothesized that parent and child psychopathology would influence asthma outcomes and that family chaos and social support would serve as mechanisms underlying these relationships. Findings provided support for the hypotheses: parent and child depression symptoms were each predictors of worse asthma control, asthma severity, activity limitations, and emotional triggers of asthma when examined independently and showed stronger relationships with asthma than parent or child PTSD. Family chaos also emerged as a robust predictor of asthma outcomes even when controlling for parent and child depression and demographic covariates (eg, education level) as well as a mediator underlying the relationship between parent depression and asthma. Contrary to predictions, social support was less relevant to asthma control. To our knowledge, this study is the first to identify the key role of family chaos as a mechanism linking parent depression and child asthma outcomes.

Consistent with the asthma literature, parents in this study endorsed elevated rates of depression and anxiety.14,39,41 Although PTSD prevalence was high in this sample, parent PTSD was unrelated to asthma outcomes. Parent depression, however, showed significant associations with asthma control and severity. Numerous studies suggest that parent depression confers risk for child asthma severity.42,43 Complex transactional relationships underlying caregiver mental health and child asthma outcomes likely exist. The stress of caring for a child with chronic illness may influence the development of parent depression.3,44 Alternatively, maternal depression may play a role in the development and exacerbation of child asthma via influences on the infant stress response and immune function early in life.40,45,48 Parent depression may also give rise to a set of negative practices and beliefs that interfere with asthma management (eg, nonadherence and negative beliefs about asthma treatment).44,49 

As with previous literature, we also found that poorer asthma control was related to increased symptoms of child depression8,50 and PTSD.4,51 Yet only child depression, not PTSD, was associated with asthma when examined simultaneously. Given that our PTSD measure did not assess a specific trauma event, it may have tapped into more general distress that was highly correlated with depression. Correlation analyses support the strong relationship between these factors (ie, r = 0.640); hence, effects for PTSD may have been accounted for by the depression-asthma relationship. It is also possible that child depression is more influential than anxiety for asthma control, as past work has shown.5,8,11 Biological models8,52,54 support a specific depression-asthma mechanism whereby emotional dysregulation may lead to alterations in the autonomic nervous, hypothalamic-pituitary-adrenal, and immune and inflammatory systems that can impair child pulmonary function, particularly in the presence of stress. Notably, child depression remained significant when controlling for parent depression, suggesting a unique relationship with asthma outcomes.

Our findings also extend the literature on psychosocial mechanisms underlying asthma control. Specifically, mediation analyses suggest that increased parental depressive symptoms lead to greater family chaos, which in turn is associated with poorer child asthma control, although the cross-sectional design limits findings; thus, interpretations are made cautiously. Family chaos is a unique construct encompassing the high levels of stimuli, unpredictability, and lack of routine and rules in the home33,55 that is distinct from other measures of psychosocial adversity as well as family socioeconomic status.56 In the extant literature, family chaos was associated with worse glycemic control in youth with type 1 diabetes mellitus.57,58 Specific to asthma, other indicators of family organization, including children routinely sleeping away from home59 and single-parent households,60 were associated with asthma-related readmission, even when controlling for parent psychological distress, in a large sample of youth hospitalized for asthma. Consistent with our work, past research has demonstrated that family chaos is related to parent depression61,62 and is a mediator of the relationship between parent depression and negative child psychosocial outcomes.62 

Parents with depressive symptoms may experience executive functioning deficits and high levels of stressors that interfere with the establishment of consistent routines, stability, and organization in the home62 that are essential for asthma management.63,64 Indeed, we found that family chaos was related to lower parental medication management. Family chaos may also affect asthma via biological mechanisms. For example, family chaos and poor family routines predicted systemic inflammation and proinflammatory cytokine production in a study of healthy adolescents35 and youth with asthma, possibly via influences on medication use.65 Hence, our results are corroborated by research demonstrating the relevance of family chaos for multiple child health indicators. Interestingly, findings highlighted emotional triggers as a separate pathway linking parent depression and child asthma. Emotional triggers have been shown to mediate the child depression-asthma association,8 and our work extends this literature by demonstrating the importance of parental depressive symptoms for such triggers.

Strengths of this study include the focus on a high-risk population recruited and enrolled in a community setting. Additional strengths include the use of data from both children with asthma and their parents and the replication of findings with several measures of asthma control. Limitations must also be noted. The cross-sectional design precludes inference on the direction of effects and causality. Moreover, the magnitude of change in asthma outcomes vis-à-vis levels of family chaos are difficult to assess. Hence, prospective studies are necessary to confirm findings. Our measures of mental health, albeit well validated, did not provide clinical diagnoses, and findings may not generalize to clinical samples. Additionally, correlations between mental health variables may have influenced our analyses. Combining the cACT and ACT for analyses has not been examined in previous work. Because of age limits on the child measures, our sample was restricted. The sample was predominantly Hispanic, limiting generalizability to other populations. Although we focused on youth with uncontrolled asthma, the sample was not severely symptomatic and may better reflect a community sample. Last, family chaos captures only portions of the family environment, and a broader assessment of family functioning may aid in the interpretation of results.

Our results identify psychosocial pathways worthy of exploring in longitudinal and possible qualitative studies to understand the multifactorial etiology of pediatric asthma. Findings highlight the importance of assessing and addressing child and parent depression and family chaos to enhance asthma outcomes in high-risk samples. Effective, well-validated measures for screening youth and parent depression in primary care settings with minimal burden are readily available (eg, the Children’s Depression Inventory 2 [Short Form]31 and PHQ-928,29) and are increasingly being promoted by clinical guidelines.66 Additionally, the CHAOS33 may be an effective clinical discussion tool for illuminating areas of risk within the household. Integrated behavioral interventions that target a reduction in family chaos via development of family routines, structure, and predictability, particularly around medication,63 can help to optimize asthma care.

Dr Weinstein conceptualized and designed the psychosocial study analyses and drafted the initial manuscript; Dr Martin conceptualized and designed the study and the larger clinical trial from which this study is drawn; Dr Pugach designed the data collection process and conducted the main study analyses; Ms Rosales assisted with the design of the data collection process, collected data, and conducted preliminary analyses; Drs Mosnaim and Walton assisted with the conceptualization, design, and implementation of the study; and all authors reviewed and revised the manuscript, approved the final manuscript as submitted, and agree to be accountable for all aspects of the work.

This trial has been registered at www.clinicaltrials.gov (identifier NCT02481986).

FUNDING: Supported by the University of Illinois at Chicago and Erie Family Health Centers. Funded by the National Heart, Lung, and Blood Institute (grant 1R01HL123797; Dr Martin). Funded by the National Institutes of Health (NIH).

This study was funded by the National Institutes of Health and the National Heart, Lung, and Blood Institute (R01HL123797). We thank the staff who collected these data: Gizelle Alvarez, Daisy Cintron, Jazmin Morales, and Genesis Rosales. We also recognize the Asthma Action at Erie Trial Steering Committee who are not authors: Michael Berbaum, Ana Cesan, Hannah Chi, Andrea Fragoso, Denise Guerrero, Melissa Hernandez, Steven Rothschild, and Angkana Roy. The Chicago Asthma Consortium Community Advisory Board provided oversight for the study. We thank everyone at Erie Family Health Centers. This includes medical directors, providers, and staff at the Erie West Town Health Center, Erie Evanston–Skokie Health Center, Erie Helping Hands Health Center, Erie Humboldt Park Health Center, Erie Westside Health Center at Laura S. Ward Elementary School, and Erie Johnson School-Based Health Center. Finally, we thank all the families who made this research possible.

     
  • ACT

    Asthma Control Test

  •  
  • AFS

    Asthma Functional Severity Scale

  •  
  • cACT

    Childhood Asthma Control Test

  •  
  • CHAOS

    Confusion, Hubbub, and Order Scale

  •  
  • CI

    confidence interval

  •  
  • GLM

    generalized linear regression model

  •  
  • ICS

    inhaled corticosteroid

  •  
  • OR

    odds ratio

  •  
  • PHQ-9

    9-item Patient Health Questionnaire

  •  
  • PTSD

    posttraumatic stress disorder

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Competing Interests

POTENTIAL CONFLICT OF INTEREST: Dr Mosnaim receives research grant support from GlaxoSmithKline and Propeller Health, owns stock options in electroCore, and serves as a consultant and/or member of a scientific advisory board for electroCore, GlaxoSmithKline, Teva, Novartis, AstraZeneca, Boehringer Ingelheim, and Propeller Health; the other authors have indicated they have no potential conflicts of interest to disclose.

FINANCIAL DISCLOSURE: All authors have indicated they have no financial relationships relevant to this article to disclose other than those listed under the Potential Conflict of Interest section.