Maternal interpersonal trauma and cord blood IgE levels in an inner-city cohort: a life-course perspective.

BACKGROUND: Prenatal stress affects immunocompetence in offspring, although the underlying mechanisms are not well understood. OBJECTIVE: 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). METHODS: 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. RESULTS: 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). CONCLUSION: 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.

Synergistic effects of traffic-related air pollution and exposure to violence on urban asthma etiology.

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 NO(2) 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.

Ambient pollution and blood pressure in cardiac rehabilitation patients.

BACKGROUND: Multiple studies have demonstrated a consistent association between ambient particulate air pollution and increased risk of hospital admissions and deaths for cardiovascular causes. We investigated the associations between fine particulate pollution (PM2.5) and blood pressure during 631 repeated visits for cardiac rehabilitation in 62 Boston residents with cardiovascular disease. METHODS AND RESULTS: Blood pressure, cardiac risk factor, and exercise data were abstracted from records of rehabilitation visits between 1999 and 2001. We applied mixed-effect models, controlling for body mass index, age, gender, number of visits, hour of day, and weather variables. For an increase from the 10th to the 90th percentile in mean PM2.5 level during the 5 days before the visit (10.5 microg/m3), there was a 2.8-mm Hg (95% CI, 0.1 to 5.5) increase in resting systolic, a 2.7-mm Hg (95% CI, 1.2 to 4.3) increase in resting diastolic, and a 2.7-mm Hg (95% CI, 1.0 to 4.5) increase in resting mean arterial blood pressure. The mean PM2.5 level during the 2 preceding days (13.9 microg/m3) was associated with a 7.0-mm Hg (95% CI, 2.3 to 12.1) increase in diastolic and a 4.7-mm Hg (95% CI, 0.5 to 9.1) increase in mean arterial blood pressure during exercise in persons with resting heart rate > or =70 bpm, but it was not associated with an increase in blood pressure during exercise in persons with heart rate <70 bpm. CONCLUSIONS: In patients with preexisting cardiac disease, particle pollution may contribute to increased risk of cardiac morbidity and mortality through short-term increases in systemic arterial vascular narrowing, as manifested by increased peripheral blood pressure.