Epidemiology of Stress and Asthma: From Constricting Communities and Fragile Families to Epigenetics

Neighborhood violence increases children’s risk for a variety of health problems. Yet, little is known about biological pathways involved or neural mechanisms that might render children more or less vulnerable. Here, we address these questions by considering whether neighborhood violence is associated with the expression of a proinflammatory phenotype and whether this relationship is moderated by resting-state functional connectivity (rsFC) of the central executive network (CEN).

The study involved 217 children (13.9 years old; 66.4% female; 36.9% Black; 30.9% Latinx), enrolled in eighth grade and reassessed 2 years later. At time 1, geocoding was used to estimate murder frequency in children’s neighborhoods, and functional magnetic resonance imaging was used to characterize CEN rsFC. At both visits, children gave antecubital blood for ex vivo studies, where leukocytes were incubated with stimulators and inhibitors of inflammation, and cytokine production was measured.

Consistent with our hypotheses, the relationship between neighborhood murder and inflammatory activity was moderated by CEN rsFC. Among children with lower rsFC, neighborhood violence covaried with a proinflammatory phenotype, reflected in larger cytokine responses to triggering stimuli and lower sensitivity to inhibitory agents. These associations were generally not apparent for children with higher rsFC, although occasionally they ran in the opposite direction. The same patterns were apparent 2 years later.

These results advance the understanding of neighborhood violence and its relationship with processes involved in the initiation and resolution of inflammation. They also deepen understanding of variability in children’s immunologic responses to stress and suggest that the CEN may be a neurobiological contributor to resilience.

This population-based study of 21,902 Finnish adults examined whether adulthood risk factors for asthma mediate the association between the exposure to multiple adverse childhood experiences (ACEs) assessed retrospectively and the risk of new-onset asthma in adulthood.

Baseline characteristics, occurrence of ACEs, and risk factors of asthma in adulthood were collected with a postal survey at baseline in 1998. The participants were linked to records on incident asthma from national health registers from 1999 to 2012. Counterfactual mediation analysis was used to examine the effects of multiple ACEs (≥2) on asthma through adulthood risk factors of asthma (mediators).

Of the 21,902 participants without asthma at baseline, 7552 (34%) were exposed to multiple ACEs during childhood. During the follow-up period, 2046 participants were diagnosed with incident asthma. Exposure to multiple ACEs increased the risk of asthma onset by 31% compared with ≤1 ACE. The association between ACEs and asthma onset was partly mediated by the following adulthood risk factors: severe life events (29%), smoking (15%), allergic rhinitis (8%), low education level (6%), and obesity (3%). Specific stressful life events mediating the ACE–asthma association were ‘severe financial difficulties’ (24%), ‘emotional, physical or sexual violence’ (15%), ‘major increase in marital problems’ (8%), ‘severe conflicts with supervisor’ (7%), and ‘divorce or separation’ (5%).

Exposure to multiple ACEs increased the risk of asthma in adulthood. Adulthood risk factors of asthma mediated a significant proportion of the effect of ACEs on the risk of asthma onset.

Early-life stress is becoming an important determinant of immune system programming. Maternal prenatal distress is found to be associated with atopic disease in offspring but the separate effects of postnatal distress are not well-studied.

Does the likelihood of asthma and atopic dermatitis in children increase when they are exposed to maternal distress pre- and postnatally in a sex-specific manner?

Using data from a provincial newborn screen and health-care database for 12,587 children born in 2004, maternal distress (depression or anxiety) was defined as prenatal, self-limiting, recurrent, or late-onset postpartum. Atopic dermatitis (AD) and asthma at ages 5 years and 7 years of age were diagnosed by using hospitalization, physician visit, or prescription records. Associations between maternal distress and childhood asthma and AD were determined by using multiple logistic regression.

After adjusting for risk factors, a significant association between maternal prenatal (OR, 1.27; 95% CI, 1.11-1.46), recurrent postpartum (OR, 1.28; 95% CI, 1.11-1.48), and late-onset postpartum (OR, 1.19, 95% CI, 1.06-1.34) distress was found with AD at age 5 years. Asthma at age 7 years was also associated with maternal prenatal distress (OR, 1.57; 95% CI, 1.29-1.91) and late-onset postnatal distress (OR, 1.22; 95% CI, 1.01-1.46). Self-limiting postnatal distress was not found to be a risk factor for either atopic condition. Associations with AD or asthma were of a similar magnitude in boys and girls; the exception was recurrent postnatal distress, which increased risk for asthma in boys only.

This population-based study provides evidence for sex-specific associations between maternal prenatal and postnatal distress, as well as the development of AD and asthma. The findings support recommendations for greater psychosocial support of mothers during pregnancy and early childhood to prevent childhood atopic disease.

Evidence on the association between residential surrounding greenness (RSG) in urban areas with asthma and asthma symptoms is inconsistent.

To examine the association of RSG with respiratory outcomes in a sample of Mexican American children living in inner-city Chicago, Illinois.

This study is based on parent-reported data on 1915 Mexican American children. We calculated RSG using the normalized difference vegetation index based on satellite imagery within buffers of 100, 250, and 500 m of each child's residence. Multivariable multilevel mixed-effect logistic regression was used to estimate adjusted odds ratios (aORs) for the effect of a 1-interquartile range increase in greenness.

In adjusted analyses, a protective effect of greenness within 100 m was observed for lifetime wheezing (aOR, 0.82; 95% CI, 0.69-0.96). Environmental tobacco smoke (ETS) exposure modified the association of RSG with lifetime asthma and current dry cough at night. For all buffer distances, increased greenness was associated with lower odds of lifetime asthma among children with current ETS exposure (100 m: aOR, 0.43; 95% CI, 0.22-0.87; 250 m: aOR, 0.39; 95% CI, 0.18-0.84; 500 m: aOR, 0.48; 95% CI, 0.26-0.90) and lower odds of current dry cough at night among children with perinatal ETS exposure (100 m: aOR, 0.53; 95% CI, 0.31-0.92; 250 m: aOR, 0.55; 95% CI, 0.31-0.98; 500 m: aOR, 0.55; 95% CI, 0.35-0.87).

Our results suggest inverse associations of urban greenness with respiratory outcomes, especially in children exposed to ETS. Further research is needed to examine the mechanisms through which RSG may be associated with the risk of asthma and contribute to health.