Research conducted using small samples of persons exposed to extreme stressors has documented an association between parental and offspring posttraumatic stress disorder (PTSD), but it is unknown whether this association exists in the general population and whether trauma exposure mediates this association. We sought to determine whether mothers’ posttraumatic stress symptoms were associated with PTSD in their young adult children and whether this association was mediated by higher trauma exposure in children of women with PTSD.
Using data from a cohort of mothers (n=6924) and a cohort of their children (n=8453), we calculated risk ratios (RR) for child’s PTSD and examined mediation by trauma exposure.
Mother’s lifetime posttraumatic stress symptoms were associated with child’s PTSD in dose-response fashion (mother’s 1 to 3 symptoms, child’s RR=1.2; mother’s 4-5 symptoms, RR=1.3; mother’s 6-7 symptoms, RR=1.6, compared to children of mothers with no symptoms, p<0.001 for each). Mother’s lifetime symptoms were also associated with child’s trauma exposure in dose-response fashion. Elevated exposure to trauma substantially mediated elevated risk for PTSD in children of women with symptoms (mediation proportion, 74%, p<0.001).
Intergenerational association of PTSD is clearly present in a large population-based sample. Children of women who had PTSD were more likely than children of women without PTSD to experience traumatic events; this suggests, in part, why the disorder is associated across generations. Health care providers who treat mothers with PTSD should be aware of the higher risk for trauma exposure and PTSD in their children.
Posttraumatic stress disorder; trauma; childhood abuse; epidemiology; family studies; violence
Prenatal stress affects immunocompetence in offspring, although the underlying mechanisms are not well understood.
We sought to examine associations between maternal lifetime interpersonal trauma (IPT) and cord blood total IgE levels in a sample of urban newborns (n = 478).
Maternal IPT during childhood and adolescence (birth to 17 years), adulthood (18 years to index pregnancy), and the index pregnancy were ascertained by using the Revised Conflict Tactics Scale at 28.4 ± 7.9 weeks’ gestation. Cord blood IgE levels were derived by using a fluoroenzyme immunoassay. We examined effects of maternal IPT on increased cord blood IgE levels (upper quartile, 1.08 IU/mL) by using logistic regression, adjusting for confounders and mediating variables.
Maternal trauma was categorized as unexposed (n = 285 [60%]), early (childhood and/or teenage years only, n = 107 [22%]), late (adulthood and/or index pregnancy only, n = 29 [6%]), and chronic (early and late, n = 57 [12%]) exposure. Relative to no IPT, early (odds ratio [OR], 1.78; 95% CI, 1.05–3.00) and chronic maternal IPT (OR, 2.25; 95% CI, 1.19–4.24) were independently associated with increased IgE levels in unadjusted analyses. When adjusting for standard controls, including maternal age and race, season of birth, child’s sex, and childhood and current socioeconomic status, early effects became nonsignificant (OR, 1.48; 95% CI, 0.85–2.58). Chronic exposure remained significant in fully adjusted models, including standard controls, current negative life events, allergen exposure, and potential pathway variables (maternal atopy, prenatal smoking, and birth weight; OR, 2.18; 95% CI, 1.06–4.50).
These data link chronic trauma over the mother’s life course with increased IgE levels in infants at birth. Research examining associations between maternal trauma and indicators of offspring’s atopic risk might be particularly relevant in inner-city high-risk populations. (J Allergy Clin Immunol 2009;124:954–60.)
Interpersonal trauma; life course; pregnancy; cord blood IgE; urban asthma
This study investigated the relationship between growing up in a violent home and developmental trajectories of body mass index (BMI) in a cohort of adolescents followed longitudinally from 1996 to 2003-4.
6,043 girls and 4,934 boys aged 9–14 years in 1996 who reported height and weight at least two times and whose mothers completed intimate partner violence (IPV) questions at the 2001 Nurses’ Health Study. Main exposure was experiencing the first family violence during early (0–5 years) or later (6–11 years) childhood, based on mother’s year-specific exposure of IPV and the birth year of each participant. Mother’s report of IPV was ascertained by the abuse assessment screen. Four distinct BMI trajectory groups were estimated from age-specific BMI (age 12–20 years), using general growth mixture modeling.
Four distinct BMI trajectories were identified separately for girls and boys: healthy growth; healthy to obese; steady overweight and consistently obese. Compared with boys not exposed to violence at home, boys raised in violent homes before 5 years were at increased risk of being in the consistently obese (OR =2.0; 95% CI 1.2 to 3.5) and steady overweight (OR 1.4; 95% CI 1.1 to 1.9) groups after adjusting for confounders. Girls raised in violent homes were more likely to be in the steady overweight group, but associations did not maintain statistical significance after adjusting for confounding.
These data link children’s exposure to domestic violence to a risk of unhealthy weight trajectories during adolescence in boys. Detrimental effects of exposure to a domestic violence environment may take root in the first few years of development for boys.
Exposure to environmental toxins during critical periods of prenatal and/or postnatal development may alter the normal course of lung morphogenesis and maturation, potentially resulting in changes that affect both structure and function of the respiratory system. Moreover, these early effects may persist into adult life magnifying the potential public health impact. Aberrant or excessive pro-inflammatory immune responses, occurring both locally and systemically, that result in inflammatory damage to the airway are a central determinant of lung structure-function changes throughout life. Disruption of neuroendocrine function in early development, specifically the hypothalamic-pituitary-adrenal (HPA) axis, may alter functional status of the immune system. Autonomic nervous system (ANS) function (sympathovagal imbalance) is another integral component of airway function and immunity in childhood. This overview discusses the evidence linking psychological factors to alterations in these interrelated physiological processes that may, in turn, influence childhood lung function and identifies gaps in our understanding.
maternal prenatal stress; postnatal stress; programming; hypothalamic-pituitary-adrenal axis; immunomodulation; autonomic nervous system; lung function; airway inflammation; airway hyperresponsiveness
Rationale: Critical periods for programming early wheeze risk may include pregnancy and infancy. Effects of timing remain poorly understood.
Objectives: Associations among prenatal and postnatal maternal stress and children’s wheeze were prospectively examined in 653 families. Effect modification by maternal sensitization was also examined.
Methods: Stress was indexed by a maternal negative life events (NLEs) score (range, 0–9) ascertained during pregnancy and between 1 and 2 years postpartum. Mothers reported child wheeze every 3 months up to age 2 years. Relationships of prenatal and postnatal maternal NLEs with repeated wheeze (≥2 episodes) were examined using logistic regression adjusting for covariates. Penalized splines were implemented to explore possible nonlinear associations. We also examined the interaction between prenatal stress and maternal sensitization indexed by allergen-specific IgE from maternal prenatal serum.
Measurements and Main Results: Adjusted models considering prenatal or postnatal NLEs alone both showed an exposure-response relationship between higher stress and child wheeze. When considering prenatal and postnatal stress concurrently, only children of mothers with high stress in both periods were significantly more likely to wheeze (adjusted odds ratio, 3.04; 95% confidence interval, 1.67–5.53) than children of mothers reporting low stress in both periods. Associations between high prenatal stress and wheeze were significant in children born to nonsensitized mothers (any IgE <0.35 kU/L) but not in the sensitized group (P for interaction = 0.03).
Conclusions: Although children have heightened sensitivity to maternal stress in utero and in early childhood, those with higher stress in both periods were particularly at risk for wheeze. The prenatal maternal immune milieu modified effects.
negative life events; stress; pregnancy; maternal sensitization; childhood wheeze
To date, there have been conflicting reports of the association of psychosocial stressors with prenatal corticotropin-releasing hormone (CRH) levels.
We examined whether racial discrimination, community violence, interpersonal violence (IPV), negative life events, considered independently, and as a composite measure of cumulative stress, were associated with prenatal CRH levels in the Asthma Coalition on Community, Environment, and Social Stress (ACCESS) project, a multiethnic pre-birth cohort in urban Boston. Blood was collected between 20 and 37 weeks gestation (Mean = 28.1, SD = 4.6 weeks gestation). During pregnancy, women were administered the Conflict Tactics Scale survey to assess IPV, the Crisis in Family Systems-Revised survey to assess negative life events, the My Exposure to Violence survey to assess community violence, and the Experiences of Discrimination survey. A cumulative stress measure was derived from these instruments to characterize exposure to high levels of multiple stressors.
None of the individual stressors or cumulative stress was associated with CRH in combined analyses including Whites (n=20), Blacks (n=46), and Hispanics (n=110). In separate analyses of Blacks and Hispanics, racial discrimination, community violence, and cumulative stress were associated with CRH in Blacks, but were not associated with CRH in Hispanics.
Though these results require replication, they suggest that the effects of stress on prenatal CRH levels may be mediated by factors that differ between racial/ethnic groups. Further studies in larger samples are warranted to clarify whether associations of chronic stressors and prenatal CRH levels differ by race/ethnicity and to better understand underlying mechanisms.
Background: Ambient air pollution may have neurotoxic effects in children. Data examining associations between traffic-related air pollution and attention domains remain sparse.
Objectives: We examined associations between black carbon (BC), a marker of traffic particles, and attention measures ascertained at 7–14 years of age among 174 children in a birth cohort based in the Boston, Massachusetts, area.
Methods: We estimated BC levels using a validated spatial–temporal land-use regression model based on residence during children’s lifetime. Children completed the Conner’s Continuous Performance Test (CPT) measuring omission errors, commission errors, and hit reaction time (HRT), with higher scores indicating increased errors or slower reaction time. Multivariable-adjusted linear regression analyses were used to examine associations between BC and each attention outcome.
Results: Children were primarily Hispanic (56%) and Caucasian (41%); 53% were boys. We found a positive association between higher BC levels with increased commission errors and slower HRT, adjusting for child IQ, age, sex, blood lead level, maternal education, pre- and postnatal tobacco smoke exposure, and community-level social stress. Notably, the association was weaker, though still positive, for the highest BC quartile relative to the middle two quartiles. Sex-stratified analysis demonstrated statistically significant associations between BC and both commission errors and HRT in boys, but BC was not significantly associated with any of the CPT outcomes in girls.
Conclusions: In this population of urban children, we found associations between BC exposure and higher commission errors and slower reaction time. These associations were overall more apparent in boys than girls.
attention; children; Conners’ Continuous Performance Test; hit reaction time; traffic-related air pollution; urban
Retrospective recall of smoking during pregnancy is assumed to be substantially biased, but this has rarely been tested empirically.
We examined the validity of an interview-based retrospective recall more than a decade after pregnancy, in a cohort with repeated, multimethod characterization of pregnancy smoking (N = 245). Retrospective smoking patterns were examined in relation to prospective reported and biological estimates of overall and trimester-specific smoking status and intensity. We also compared characteristics of women whose smoking status was misclassified by either prospective or retrospective measures with women whose status was congruent for nonsmoking across timepoints.
In general, sensitivity and specificity of recalled smoking were excellent relative to both prospective self-reported and cotinine-validated smoking status and trimester-specific intensity. However, measures were less congruent for amount smoked for women who recalled being heavy smokers. Further, retrospective measures captured some smokers not identified prospectively due to smoking that occurred prior to assessments. Women who would have been misclassified as nonsmokers based on either prospective or retrospective assessment differed significantly from congruently classified nonsmokers in a number of maternal, family, and neighborhood, but not child behavior, characteristics.
When epidemiological studies of the impact of smoking in pregnancy use retrospective methods, misclassification may not be a significant problem if prenatal smoking is assessed in terms of the pattern across pregnancy. This type of interview-based recall of pregnancy smoking may be relatively accurate, although optimal measurement should combine retrospective and prospective self-report and biological assays, as each provide unique information and sources of error.
The definition of the stressor criterion for posttraumatic stress disorder (“Criterion A1”) is hotly debated with major revisions being considered for DSM-V. We examine whether symptoms, course, and consequences of PTSD vary predictably with the type of stressful event that precipitates symptoms.
We used data from the 2009 PTSD diagnostic subsample (N=3,013) of the Nurses Health Study II. We asked respondents about exposure to stressful events qualifying under 1) DSM-III, 2) DSM-IV, or 3) not qualifying under DSM Criterion A1. Respondents selected the event they considered worst and reported subsequent PTSD symptoms. Among participants who met all other DSM-IV PTSD criteria, we compared distress, symptom severity, duration, impairment, receipt of professional help, and nine physical, behavioral, and psychiatric sequelae (e.g. physical functioning, unemployment, depression) by precipitating event group. Various assessment tools were used to determine fulfillment of PTSD Criteria B through F and to assess these 14 outcomes.
Participants with PTSD from DSM-III events reported on average 1 more symptom (DSM-III mean=11.8 symptoms, DSM-IV=10.7, non-DSM=10.9) and more often reported symptoms lasted one year or longer compared to participants with PTSD from other groups. However, sequelae of PTSD did not vary systematically with precipitating event type.
Results indicate the stressor criterion as defined by the DSM may not be informative in characterizing PTSD symptoms and sequelae. In the context of ongoing DSM-V revision, these results suggest that Criterion A1 could be expanded in DSM-V without much consequence for our understanding of PTSD phenomenology. Events not considered qualifying stressors under the DSM produced PTSD as consequential as PTSD following DSM-III events, suggesting PTSD may be an aberrantly severe but nonspecific stress response syndrome.
Criterion A; posttraumatic stress disorder; nosology; stress response syndromes; trauma exposure; diagnosis
Purpose of Review
While traditional disciplinary research theory and methods have focused separately on how social and physical environmental factors affect children’s health, evolving research underscores important integrated effects.
This review outlines the specific reasons why social determinants should be considered mainstream in children’s environmental health research with particular focus on interactive effects between social and physical hazards. These include (a) sensitivity of overlapping physiological systems, via epigenesis, programming, and plasticity to social and physical environmental moderation that may impact health across the life span; (b) ways in which social environmental vulnerabilities moderate the effects of physical environmental factors providing specific examples related to respiratory health and neurodevelopment; (c) overlapping exposure distribution profiles; and (d) relevance to pediatric health disparities.
Because of the covariance across exposures and evidence that social stress and other environmental toxins (e.g., pollutants, tobacco smoke) may influence common physiological pathways (e.g., oxidative stress, pro-inflammatory immune pathways, autonomic disruption), understanding the potential synergistic effects promises to more completely inform children’s environmental health risk. While this discussion focuses around the respiratory and neurological systems, these concepts extend more broadly to children’s psychological and physical development.
children; social toxins; physical hazards; health disparities
Prenatal exposure to both stress and aeroallergens (dust mite) may modulate the fetal immune system. These exposures may interact to affect the newborn immune response. We examined associations between prenatal maternal stress and cord blood total IgE in 403 predominately low-income minority infants enrolled in the Asthma Coalition on Community, Environment, and Social Stress (ACCESS) project. We also examined potential modifying effects of maternal atopy and maternal dust mite exposure.
The Crisis in Family Systems survey was administered to mothers prenatally and a negative life event domain score was derived to characterize stress. Dust mite allergen was quantified in dust from pregnant mothers’ bedrooms. Cord blood was analyzed for total IgE. Using linear regression, we modeled the relationship of stress with cord blood IgE and interactions of stress with dust mite and/or maternal atopy, adjusting for potential confounders.
Higher prenatal maternal stress (β=0.09; P=0.01) was associated with increased cord blood IgE. The interactive effects between stress and dust mite groups (high vs. low) were significantly different for children of atopic vs. nonatopic mothers (p for three-way interaction =0.005). Among children of atopic mothers, the positive association between stress and IgE was stronger in the high dust mite group. In children of mothers without a history of atopy, the positive association between stress and IgE was most evident in the low allergen group.
Prenatal stress was independently associated with elevated cord blood IgE. Mechanisms underlying stress effects on fetal immunomodulation may differ based on maternal atopic status.
Allergens; cord blood IgE; dust mite; prenatal stress; urban
Independent of current socioeconomic status (SES), past maternal SES might influence asthma outcomes in children.
We examined associations among the mother’s SES in the first 10 years of her life (maternal childhood SES), increased cord blood IgE levels (upper 20% [1.37 IU/mL]), and repeated wheeze (≥2 episodes by age 2 years) in an urban pregnancy cohort (n = 510).
Data on sociodemographics, discrimination, financial strain, community violence, interpersonal trauma, and other negative events were obtained prenatally. Prenatal household dust was assayed for cockroach and murine allergens, and traffic-related air pollution was estimated by using spatiotemporal land-use regression. Maternal childhood SES was defined by parental home ownership (birth to 10 years). Maternally reported child wheeze was ascertained at 3-month intervals from birth. Using structural equation models, we examined whether outcomes were dependent on maternal childhood SES directly versus indirect relationships operating through (1) cumulative SES-related adversities, (2) the mother’s socioeconomic trajectory (adult SES), and (3) current prenatal environmental exposures.
Mothers were largely Hispanic (60%) or black (28%), 37% had not completed high school, and 56% reported parental home ownership. When associations between low maternal childhood SES and repeated wheeze were examined, there were significant indirect effects operating through adult SES and prenatal cumulative stress (β = 0.28, P = .003) and pollution (β = 0.24, P = .004; P value for total indirect effects ≤ .04 for both pathways). Low maternal childhood SES was directly related to increased cord blood IgE levels (β = 0.21, P = .003). Maternal cumulative adversity (interpersonal trauma) was also associated with increased cord blood IgE levels (β = 0.19, P = .01), although this did not explain maternal childhood SES effects.
Lower maternal childhood SES was associated with increased cord blood IgE levels and repeated wheeze through both direct and indirect effects, providing new insights into the role of social inequalities as determinants of childhood respiratory risk.
Childhood socioeconomic status; intergenerational; cord blood IgE; inner-city; childhood wheeze; structural equation models; life course
Respiratory sinus arrhythmia (RSA) is related to cardiac vagal outflow and the respiratory pattern. Prior infant studies have not systematically examined respiration rate and tidal volume influences on infant RSA or the extent to which infants' breathing is too fast to extract a valid RSA. We therefore monitored cardiac activity, respiration, and physical activity in 23 six-month old infants during a standardized laboratory stressor protocol. On average, 12.6% (range 0–58.2%) of analyzed breaths were too short for RSA extraction. Higher respiration rate was associated with lower RSA amplitude in most infants, and lower tidal volume was associated with lower RSA amplitude in some infants. RSA amplitude corrected for respiration rate and tidal volume influences showed theoretically expected strong reductions during stress, whereas performance of uncorrected RSA was less consistent. We conclude that stress-induced changes of peak-valley RSA and effects of variations in breathing patterns on RSA can be determined for a representative percentage of infant breaths. As expected, breathing substantially affects infant RSA and needs to be considered in studies of infant psychophysiology.
The current study examined associations between maternal posttraumatic stress disorder (PTSD) symptoms and infant emotional reactivity and emotion regulation during the first year of life in a primarily low-income, urban, ethnic/racial minority sample of 52 mother-infant dyads. Mothers completed questionnaires assessing their own trauma exposure history and current PTSD and depressive symptoms and their infants’ temperament when the infants were 6 months old. Dyads participated in the repeated Still-Face Paradigm (SFP-R) when the infants were 6 months old, and infant affective states were coded for each SFP-R episode. Mothers completed questionnaires assessing infant trauma exposure history and infant current emotional and behavioral symptoms when the infants were 13 months old. Maternal PTSD symptoms predicted infants’ emotion regulation at 6 months as assessed by (a) infant ability to recover from distress during the SFP-R and (b) maternal report of infant rate of recovery from distress/arousal in daily life. Maternal PTSD symptoms also predicted maternal report of infant externalizing, internalizing, and dysregulation symptoms at 13 months. Maternal PTSD was not associated with measures of infant emotional reactivity. Neither maternal depressive symptoms nor infant direct exposure to trauma accounted for the associations between maternal PTSD symptoms and infant outcomes. These findings suggest that maternal PTSD is associated with offspring emotion regulation difficulties as early as infancy. Such difficulties may contribute to increased risk of mental health problems among children of mothers with PTSD.
infant; emotion regulation; reactivity; maternal PTSD
While asthma has emerged as a major contributor to disease and disability in American children, the burden of this disease is unevenly distributed within the population. This paper provides a brief overview of social status variables that predict variation in asthma risks and social exposures such as stress and violence that are emerging as important risk factors. However, the central focus of the paper is on the distal social variables that have given rise to unhealthy residential environments in which the risk factors for asthma and other diseases are clustered. Effective initiatives for the prevention and treatment of childhood asthma need to address these non-medical determinants of the prevalence of asthma.
childhood asthma prevalence; low-income population; poverty; race; risk factors
Background To investigate lifetime history of interpersonal abuse and risk of pre-natal depression in socio-economically distinct populations in the same city.
Methods We examined associations of physical and sexual abuse with the risk of pre-natal depression in two cohorts in the Boston area, including 2128 participants recruited from a large urban- and suburban-managed care organization (Project Viva) and 1509 participants recruited primarily from urban community health centres (Project ACCESS). Protocols for the studies were designed in parallel to allow us to merge data to enhance ethnic and socio-economic diversity in the combined sample. In mid-pregnancy, the Personal Safety Questionnaire and Edinburgh Postnatal Depression Scale (EPDS) were administered in both cohorts. An EPDS score ≥13 indicated probable pre-natal depression. Logistic regression was used to estimate the odds ratio (OR) of pre-natal depression associated with lifetime abuse history.
Results Project ACCESS participants were twice as likely as Project Viva participants to report symptoms consistent with pre-natal depression: 22% of Project ACCESS participants had EPDS scores ≥13, compared with 11% of Project Viva participants. Fifty-seven percent of women in ACCESS and 46% in Viva reported lifetime physical and/or sexual abuse. In merged analysis, women reporting lifetime physical or sexual abuse had an OR for mid-pregnancy depression of 1.63 [95% confidence interval (95% CI): 1.29–2.07], adjusted for age and race/ethnicity. Lifetime histories of physical abuse [OR 1.48 (95% CI 1.15–1.90)] and sexual abuse [OR 1.68 (95% CI 1.24–2.28)] were independently associated with pre-natal depression. When child/teen, pre-pregnancy adult and pregnancy life periods were considered simultaneously, abuse in childhood was independently associated with an OR of 1.23 (95% CI 1.00–1.59), pre-pregnancy adult abuse with an OR of 1.70 (95% CI 1.31–2.21) and abuse during pregnancy with an OR of 1.77 (95% CI 1.14–2.74). Further adjustment for childhood socio-economic position made no material difference, and there were no clear interactions between abuse and adult socio-economic position.
Conclusions Physical and sexual abuse histories were positively associated with pre-natal depression in two economically and ethnically distinct populations. Stronger associations with recent abuse may indicate that the association of abuse with depression wanes with time or may result from less accurate recall of remote events.
Depression; pregnancy; violence; pre-natal care; adult survivors of child abuse; partner abuse; spouse abuse
A number of epidemiologic frameworks, exemplified through extant research examples, provide insight into the role of stress in the expression of asthma and other allergic disorders. Biological, psychological, and social processes interact throughout the life course to influence disease expression. Studies exploiting a child development framework focus on critical periods of exposure, including the in utero environment, to examine the influence of stress on disease onset. Early stress effects that alter the normal course of morphogenesis and maturation that affect both structure and function of key organ systems (e.g., immune, respiratory) may persist into adult life underscoring the importance of a life course perspective. Other evidence suggests that maternal stress influences programming of integrated physiological systems in their offspring (e.g., neuroendocrine, autonomic, immune function) starting in pregnancy, consequently stress effects may be transgenerational. A multi-level approach which includes an ecological perspective may help to explain heterogeneities in asthma expression across socioeconomic and geographic boundaries that to date remain largely unexplained. Evolving studies incorporating psychological, behavioral, and physiological correlates of stress more specifically inform underlying mechanisms operating in these critical periods of development. The role of genetics, gene by environment interactions, and epigenetic mechanisms of gene expression have been sparsely examined in epidemiologic studies on stress and asthma although overlapping evidence provides proof of concept for such studies in the future.
Although child abuse is associated with obesity, it is not known whether early abuse increases risk of type 2 diabetes.
To investigate associations of child and adolescent abuse with adult diabetes
Proportional hazards models were used to examine associations of lifetime abuse reported in 2001 with risk of diabetes from 1989 to 2005 among 67,853 women in the Nurses Health Study II. Data were analyzed in 2009.
Child or teen physical abuse was reported by 54% and sexual abuse by 34% of participants. Models were adjusted for age, race, body type at age 5 years, and parental education and history of diabetes. Compared to women who reported no physical abuse, the hazards ratio (HR) was 1.03 (95% CI: 0.91, 1.17) for mild physical abuse, 1.26 (1.14, 1.40) for moderate physical abuse, and 1.54 (1.34, 1.77) for severe physical abuse. Compared with women reporting no sexual abuse in childhood or adolescence, the HR was 1.16 (1.05, 1.29) for unwanted sexual touching, 1.34 (1.13, 1.59) for one episode of forced sexual activity, and 1.69 (1.45, 1.97) for repeated forced sex. Adult BMI accounted for 60% (32%, 87%) of the association of child and adolescent physical abuse and 64% (38%, 91%) of the association of sexual abuse with diabetes.
Moderate to severe physical and sexual abuse in childhood and adolescence have dose response associations with risk of type 2 diabetes among adult women. This excess risk is partially explained by the higher BMI of women with a history of early abuse.
While adult hypothalamic-pituitary-adrenocortical (HPA) axis functioning is thought to be altered by traumatic experiences, little data exist on the effects of cumulative stress on HPA functioning among pregnant women or among specific racial and ethnic groups. Individuals may be increasingly vulnerable to physiological alterations when experiencing cumulative effects of multiple stressors. These effects may be particularly relevant in urban poor communities where exposure to multiple stressors is more prevalent. The goal of this study was to explore the effects of multiple social stressors on HPA axis functioning in a sample of urban Black (n = 68) and Hispanic (n = 132) pregnant women enrolled in the Asthma Coalition on Community, Environment, and Social Stress (ACCESS). Pregnant women were administered the Revised Conflict Tactics Scale (R-CTS) survey to assess interpersonal violence, the Experiences of Discrimination (EOD) survey, the Crisis in Family Systems-Revised (CRISYS-R) negative life events survey, and the My Exposure to Violence (ETV) survey, which ascertains exposure to community violence. A cumulative stress measure was derived from these instruments. Salivary cortisol samples were collected five times per day over three days to assess area under the curve (AUC), morning change, and basal awakening response in order to characterize diurnal salivary cortisol patterns. Repeated measures mixed models, stratified by race/ethnicity, were performed adjusting for education level, age, smoking status, body mass index and weeks pregnant at time of cortisol sampling. The majority of Hispanic participants (57%) had low cumulative stress exposure, while the majority of Black participants had intermediate (35%) or high (41%) cumulative stress exposure. Results showed that among Black but not Hispanic women, cumulative stress was associated with lower morning cortisol levels, including a flatter waking to bedtime rhythm. These analyses suggest that the combined effects of cumulative stressful experiences are associated with disrupted HPA functioning among pregnant women. While the etiology of racial/ethnic differences in stress-induced HPA alterations is not clear, this warrants further research.
In large epidemiological studies, many researchers use surrogates of air pollution exposure such as geographic information system (GIS)-based characterizations of traffic or simple housing characteristics. It is important to evaluate quantitatively these surrogates against measured pollutant concentrations to determine how their use affects the interpretation of epidemiological study results. In this study, we quantified the implications of using exposure models derived from validation studies, and other alternative surrogate models with varying amounts of measurement error, on epidemiological study findings.
We compared previously developed multiple regression models characterizing residential indoor nitrogen dioxide (NO2), fine particulate matter (PM2.5), and elemental carbon (EC) concentrations to models with less explanatory power that may be applied in the absence of validation studies. We constructed a hypothetical epidemiological study, under a range of odds ratios, and determined the bias and uncertainty caused by the use of various exposure models predicting residential indoor exposure levels. Our simulations illustrated that exposure models with fairly modest R2 (0.3 to 0.4 for the previously developed multiple regression models for PM2.5 and NO2) yielded substantial improvements in epidemiological study performance, relative to the application of regression models created in the absence of validation studies or poorer-performing validation study models (e.g. EC).
In many studies, models based on validation data may not be possible, so it may be necessary to use a surrogate model with more measurement error. This analysis provides a technique to quantify the implications of applying various exposure models with different degrees of measurement error in epidemiological research.
Exposure misclassification; exposure measurement error; fine particulate matter; nitrogen dioxide; elemental carbon
Rationale: Stress-elicited disruption of immunity begins in utero.
Objectives: Associations among prenatal maternal stress and cord blood mononuclear cell (CBMC) cytokine responses were prospectively examined in the Urban Environment and Childhood Asthma Study (n = 557 families).
Methods: Prenatal maternal stress included financial hardship, difficult life circumstances, community violence, and neighborhood/block and housing conditions. Factor analysis produced latent variables representing three contexts: individual stressors and ecological-level strains (housing problems and neighborhood problems), which were combined to create a composite cumulative stress indicator. CBMCs were incubated with innate (lipopolysaccharide, polyinosinic-polycytidylic acid, cytosine-phosphate-guanine dinucleotides, peptidoglycan) and adaptive (tetanus, dust mite, cockroach) stimuli, respiratory syncytial virus, phytohemagglutinin, or medium alone. Cytokines were measured using multiplex ELISAs. Using linear regression, associations among increasing cumulative stress and cytokine responses were examined, adjusting for sociodemographic factors, parity, season of birth, maternal asthma and steroid use, and potential pathway variables (prenatal smoking, birth weight for gestational age).
Measurements and Main Results: Mothers were primarily minorities (Black [71%], Latino [19%]) with an income less than $15,000 (69%). Mothers with the highest cumulative stress were older and more likely to have asthma and deliver lower birth weight infants. Higher prenatal stress was related to increased IL-8 production after microbial (CpG, PIC, peptidoglycan) stimuli and increased tumor necrosis factor-α to microbial stimuli (CpG, PIC). In the adaptive panel, higher stress was associated with increased IL-13 after dust mite stimulation and reduced phytohemagglutinin-induced IFN-γ.
Conclusions: Prenatal stress was associated with altered innate and adaptive immune responses in CBMCs. Stress-induced perinatal immunomodulation may impact the expression of allergic disease in these children.
psychological stress; cord blood; cytokines; innate; adaptive
Both physical environmental factors and chronic stress may independently increase susceptibility to asthma; however, little is known on how these different risks may interact. We examined the relationship between maternal intimate partner violence (IPV), housing quality and asthma among children in the Fragile Families and Child Wellbeing Study (N=2013).
Maternal reports of IPV were obtained after the child’s birth and at 12 and 36 months. At the 36 month assessment, interviewers rated indoor housing conditions, regarding housing deterioration (i.e., peeling paint, holes in floor, broken windows) and housing disarray (i.e., dark, cluttered, crowded or noisy house). At the same time, mothers reported on housing hardships (i.e., moving repeatedly, and hardships in keeping house warm). Maternal-report of physician-diagnosed asthma by age 36 months which was active in the past year was the outcome.
Asthma was diagnosed in 10% of the children. In adjusted analysis, an increased odds of asthma was observed in children of mothers experiencing IPV chronically (OR 1.8, 95% CI 1.0, 3.5) and in children experiencing housing disarray (OR 1.5, 95% CI 1.1, 2.0) compared to those not exposed to these risks. In stratified analyses, a greater effect of IPV on asthma was noted among children living in disarrayed or deteriorated housing or among children whose mothers were experiencing housing hardship.
IPV and housing disarray are associated with increased early childhood asthma. Exposure to cumulative or multiple stressors (i.e. IPV and poor housing quality) may increase children’s risk of developing asthma more than a single stressor.
intimate partner violence; asthma; housing quality; built environment
To examine the relationship between maternal intimate partner violence (IPV) and asthma onset in children and the role of supportive caregiving factors in modifying this relationship.
Prospective birth cohort.
In-person interview at enrollment as well as in-home interviews during study follow-up.
Children (N=3116) enrolled in the Fragile Families and Child Wellbeing Study.
Maternal-report of IPV assessed after the child’s birth and at 12 and 36 months. In addition mothers indicated how many days a week they participated in activities with the child and the amount and type of educational/recreational toys available for the child.
Maternal-report of physician-diagnosed asthma by age 36 months.
Asthma was diagnosed in 19% of children. In adjusted analysis, children of mothers experiencing IPV chronically, compared to those not exposed, had a 2-fold increased risk of developing asthma. In stratified analysis, children of mothers experiencing IPV and low levels of mother-child activities (RR 2.7, 95% CI 1.6, 4.7) had a significant increased risk for asthma. Those exposed to IPV and high levels of mother-child activities had a lower risk for asthma (RR 1.6, 95% CI 0.9, 3.2). A similar buffering effect was noted among children with high numbers of educational/recreational toys.
IPV is associated with increased early childhood asthma risk. Maternal ability to maintain positive caregiving processes in this context may buffer the effects of violence on child asthma risk. The best way to promote positive health in toddlers may be to help their mothers.
domestic violence; asthma; parent-child interactions; self-regulation
While community violence has been linked to psychological morbidity in urban youth, data on the physiological correlates of violence and associated posttraumatic stress symptoms are sparse. We examined the influence of child posttraumatic stress symptoms reported in relationship to community violence exposure on diurnal salivary cortisol response in a population based sample of 28 girls and 15 boys ages 7–13, 54% self-identified as white and 46% as Hispanic.
Mothers’ reported on the child’s exposure to community violence using the Survey of Children’s Exposure to Community Violence and completed the Checklist of Children’s Distress Symptoms (CCDS) which captures factors related to posttraumatic stress; children who were eight years of age or greater reported on their own community violence exposure. Saliva samples were obtained from the children four times a day (after awakening, lunch, dinner and bedtime) over three days. Mixed models were used to assess the influence of posttraumatic stress symptoms on cortisol expression, examined as diurnal slope and Area Under the Curve (AUC), calculated across the day, adjusting for socio-demographics.
In adjusted analyses, higher scores on total traumatic stress symptoms (CCDS) were associated with both greater cortisol AUC and with a flatter cortisol waking to bedtime rhythm. The associations were primarily attributable to differences on the intrusion, arousal and avoidance CCDS subscales.
Posttraumatic stress symptomatology reported in response to community violence exposure was associated with diurnal cortisol disruption in these community-dwelling urban children.
community violence; cortisol rhythm; posttraumatic stress symptoms