Person:

Wright, Rosalind Jo

Background: Although a number of studies have documented the relationship between lung function and traffic-related pollution among children, few have focused on adult lung function or examined community-based populations. Objective: We examined the relationship between black carbon (BC), a surrogate of traffic-related particles, and lung function among women in the Maternal–Infant Smoking Study of East Boston, an urban cohort in Boston, Massachusetts. Methods: We estimated local BC levels using a validated spatiotemporal land-use regression model, derived using ambient and indoor monitor data. We examined associations between percent predicted pulmonary function and predicted BC using linear regression, adjusting for sociodemographics (individual and neighborhood levels), smoking status, occupational exposure, type of cooking fuel, and a diagnosis of asthma or chronic bronchitis. Results: The sample of 272 women 18–42 years of age included 57% who self-identified as Hispanic versus 43% white, and 18% who were current smokers. Mean ± SD predicted annual BC exposure level was 0.62 ± 0.2 μg/m3. In adjusted analysis, BC (per interquartile range increase) was associated with a 1.1% decrease [95% confidence interval (CI), −2.5% to 0.3%] in forced expiratory volume in 1 sec, a 0.6% decrease (95% CI, −1.9% to 0.6%) in forced vital capacity, and a 3.0% decrease (95% CI, −5.8% to −0.2%) in forced mid-expiratory flow rate. We noted differential effects by smoking status in that former smokers were most affected by BC exposure, whereas current smokers were not affected. Conclusion: In this cohort, exposure to traffic-related BC, a component of particulate matter, independently predicted decreased lung function in urban women, when adjusting for tobacco smoke, asthma diagnosis, and socioeconomic status.

Background: There is a growing body of literature linking GIS-based measures of traffic density to asthma and other respiratory outcomes. However, no consensus exists on which traffic indicators best capture variability in different pollutants or within different settings. As part of a study on childhood asthma etiology, we examined variability in outdoor concentrations of multiple traffic-related air pollutants within urban communities, using a range of GIS-based predictors and land use regression techniques. Methods: We measured fine particulate matter (PM2.5), nitrogen dioxide (NO2), and elemental carbon (EC) outside 44 homes representing a range of traffic densities and neighborhoods across Boston, Massachusetts and nearby communities. Multiple three to four-day average samples were collected at each home during winters and summers from 2003 to 2005. Traffic indicators were derived using Massachusetts Highway Department data and direct traffic counts. Multivariate regression analyses were performed separately for each pollutant, using traffic indicators, land use, meteorology, site characteristics, and central site concentrations. Results: PM2.5 was strongly associated with the central site monitor (R2 = 0.68). Additional variability was explained by total roadway length within 100 m of the home, smoking or grilling near the monitor, and block-group population density (R2 = 0.76). EC showed greater spatial variability, especially during winter months, and was predicted by roadway length within 200 m of the home. The influence of traffic was greater under low wind speed conditions, and concentrations were lower during summer (R2 = 0.52). NO2 showed significant spatial variability, predicted by population density and roadway length within 50 m of the home, modified by site characteristics (obstruction), and with higher concentrations during summer (R2 = 0.56). Conclusion: Each pollutant examined displayed somewhat different spatial patterns within urban neighborhoods, and were differently related to local traffic and meteorology. Our results indicate a need for multi-pollutant exposure modeling to disentangle causal agents in epidemiological studies, and further investigation of site-specific and meteorological modification of the traffic-concentration relationship in urban neighborhoods.

Background: Disproportionate life stress and consequent physiologic alteration (i.e., immune dysregulation) has been proposed as a major pathway linking socioeconomic position, environmental exposures, and health disparities. Asthma, for example, disproportionately affects lower-income urban communities, where air pollution and social stressors may be elevated. Objectives: We aimed to examine the role of exposure to violence (ETV), as a chronic stressor, in altering susceptibility to traffic-related air pollution in asthma etiology. Methods: We developed geographic information systems (GIS)–based models to retrospectively estimate residential exposures to traffic-related pollution for 413 children in a community-based pregnancy cohort, recruited in East Boston, Massachusetts, between 1987 and 1993, using monthly nitrogen dioxide measurements for 13 sites over 18 years. We merged pollution estimates with questionnaire data on lifetime ETV and examined the effects of both on childhood asthma etiology. Results: Correcting for potential confounders, we found an elevated risk of asthma with a 1-SD (4.3 ppb) increase in NO2 exposure solely among children with above-median ETV [odds ratio (OR) = 1.63; 95% confidence interval (CI), 1.14–2.33)]. Among children always living in the same community, with lesser exposure measurement error, this association was magnified (OR = 2.40; 95% CI, 1.48–3.88). Of multiple exposure periods, year-of-diagnosis NO(_2) was most predictive of asthma outcomes. Conclusions: We found an association between traffic-related air pollution and asthma solely among urban children exposed to violence. Future studies should consider socially patterned susceptibility, common spatial distributions of social and physical environmental factors, and potential synergies among these. Prospective assessment of physical and social exposures may help determine causal pathways and critical exposure periods.

Background: DNA methylation is an epigenetic mark that regulates gene expression. Changes in DNA methylation within white blood cells may result from cumulative exposure to environmental metals such as lead. Bone lead, a marker of cumulative exposure, may therefore better predict DNA methylation than does blood lead. Objective: In this study we compared associations between lead biomarkers and DNA methylation. Methods: We measured global methylation in participants of the Normative Aging Study (all men) who had archived DNA samples. We measured patella and tibia lead levels by K-X-Ray fluorescence and blood lead by atomic absorption spectrophotometry. DNA samples from blood were used to determine global methylation averages within CpG islands of long interspersed nuclear elements-1 (LINE-1) and Alu retrotransposons. A mixed-effects model using repeated measures of Alu or LINE-1 as the dependent variable and blood/bone lead (tibia or patella in separate models) as the primary exposure marker was fit to the data. Results: Overall mean global methylation (± SD) was 26.3 ± 1.0 as measured by Alu and 76.8 ± 1.9 as measured by LINE-1. In the mixed-effects model, patella lead levels were inversely associated with LINE-1 (β = −0.25; p less than 0.01) but not Alu (β = −0.03; p = 0.4). Tibia lead and blood lead did not predict global methylation for either Alu or LINE-1. Conclusion: Patella lead levels predicted reduced global DNA methylation within LINE-1 elements. The association between lead exposure and LINE-1 DNA methylation may have implications for the mechanisms of action of lead on health outcomes, and also suggests that changes in DNA methylation may represent a biomarker of past lead exposure.

Rapidly expanding evidence increasingly strengthens the evidence linking psychological factors to asthma and allergy expression. Parallel studies in animals and humans demonstrating the influence of prenatal maternal stress and early caregiving experiences on the disrupted regulation of defensive biological systems [eg, sympathetic and adrenomedullary (SAM) system and the hypothalamicpituitary-adrenocortical (HPA) axis] provide strong proof of concept for this line of research. The consequent altered neuroimmune responses may influence the expression of immune-mediated disorders such as asthma as well as enhance an individual's susceptibility to other environmental factors that may also contribute to asthma risk.

Background: One in nine American women will meet criteria for the diagnosis of posttraumatic stress disorder (PTSD) in their lifetime. Although twin studies suggest genetic influences account for substantial variance in PTSD risk, little progress has been made in identifying variants in specific genes that influence liability to this common, debilitating disorder. Methods and design: We are using the unique resource of the Nurses Health Study II, a prospective epidemiologic cohort of 68,518 women, to conduct what promises to be the largest candidate gene association study of PTSD to date. The entire cohort will be screened for trauma exposure and PTSD; 3,000 women will be selected for PTSD diagnostic interviews based on the screening data. Our nested case-control study will genotype1000 women who developed PTSD following a history of trauma exposure; 1000 controls will be selected from women who experienced similar traumas but did not develop PTSD. The primary aim of this study is to detect genetic variants that predict the development of PTSD following trauma. We posit inherited vulnerability to PTSD is mediated by genetic variation in three specific neurobiological systems whose alterations are implicated in PTSD etiology: the hypothalamic-pituitary-adrenal axis, the locus coeruleus/noradrenergic system, and the limbic-frontal neuro-circuitry of fear. The secondary, exploratory aim of this study is to dissect genetic influences on PTSD in the broader genetic and environmental context for the candidate genes that show significant association with PTSD in detection analyses. This will involve: conducting conditional tests to identify the causal genetic variant among multiple correlated signals; testing whether the effect of PTSD genetic risk variants is moderated by age of first trauma, trauma type, and trauma severity; and exploring gene-gene interactions using a novel gene-based statistical approach. Discussion: Identification of liability genes for PTSD would represent a major advance in understanding the pathophysiology of the disorder. Such understanding could advance the development of new pharmacological agents for PTSD treatment and prevention. Moreover, the addition of PTSD assessment data will make the NHSII cohort an unparalleled resource for future genetic studies of PTSD as well as provide the unique opportunity for the prospective examination of PTSD-disease associations.

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.

Purpose

To assess the association between self-reported racial discrimination and prenatal depressive symptoms among black women.

Methods

Our study population consisted of two cohorts of pregnant women: the Asthma Coalition on Community, Environment, and Social Stress project (ACCESS) and Project Viva. We measured self-reported racial discrimination among black women using a modified Experiences of Discrimination scale (score 0–8). We assessed elevated depressive symptoms (EDS) with the Edinburgh Postnatal Depression Scale (≥13 on a 0–30 scale).

Results

Fifty-four percent of ACCESS and 78% of Viva participants reported experiencing racial discrimination. After adjusting for age, marital status, income, education, and nativity, a 1-U increment in Experiences of Discrimination score was associated with 48% increased odds of EDS (odds ratio, 1.48; 95% confidence interval, 1.24–1.76) for ACCESS participants but was not significantly associated among Viva participants (odds ratio, 1.12; 95% confidence interval, 0.92–1.37). In both cohorts, responding to unfair treatment by talking to others was associated with the lowest odds of EDS.

Conclusions

Our findings suggest that higher levels of perceived racial discrimination may increase depressive symptoms during pregnancy among U.S. black women. Interventions involving talking to others may aid in reducing the risk of depressive symptoms among black women experiencing higher levels of racial discrimination.

Population-based birth cohorts on asthma and allergies increasingly provide new insights into the development and natural history of the diseases. Over 130 birth cohorts focusing on asthma and allergy have been initiated in the last 30 years. A NIAID (National Institute of Allergy and Infectious Diseases), NHLBI (National Heart Lung and Blood Institute), MeDALL (Mechanisms of the Development of Allergy, Framework Programme 7 of the European Commission) joint workshop was held in Bethesda, MD, USA September 11–12, 2012 with 3 objectives (1) documenting the knowledge that asthma/allergy birth cohorts have provided, (2) identifying the knowledge gaps and inconsistencies and (3) developing strategies for moving forward, including potential new study designs and the harmonization of existing asthma birth cohort data. The meeting was organized around the presentations of 5 distinct workgroups: (1) clinical phenotypes, (2) risk factors, (3) immune development of asthma and allergy, (4) pulmonary development and (5) harmonization of existing birth cohorts. This manuscript presents the workgroup reports and provides web links (AsthmaBirthCohorts.niaid.nih.gov or www.medall-fp7.eu) where the reader will find tables describing the characteristics of the birth cohorts included in this report, type of data collected at differing ages, and a selected bibliography provided by the participating birth cohorts.

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.