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2004 Progress Report: Research Project on Asthma: Prenatal and Postnatal Urban Pollutants and Childhood Asthma
EPA Grant Number: R832141C002Subproject: this is subproject number 002 , established and managed by the Center Director under grant R832141
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: Columbia Center for Children’s Environmental Health
Center Director: Perera, Frederica P.
Title: Research Project on Asthma: Prenatal and Postnatal Urban Pollutants and Childhood Asthma
Investigators: Rothman, Paul B. , Barr, R. Graham , Goldstein, Inge , Lederman, Sally Ann , Miller, Rachel L. , Sheares, Beverly
Current Investigators: Rothman, Paul B.
Institution: Columbia University
EPA Project Officer: Fields, Nigel
Project Period: November 1, 2003 through October 31, 2008
Project Period Covered by this Report: November 1, 2003 through October 31, 2004
RFA: Centers for Children's Environmental Health and Disease Prevention Research (2003)
Research Category: Children's Health , Health Effects
Description:
Objective:The specific objectives of this research project are to: (1) determine the relationship between environmental exposures experienced prenatally through early childhood and atopy and adverse respiratory outcomes and asthma at age 5-7 years; (2) determine the interaction between susceptibility factors and environmental exposures on respiratory outcomes and asthma through age 5-7 years; (3) determine whether antigen-induced cord blood mononuclear cell proliferation or cytokine production increases the risk for decreased lung function or atopy at age 5 years among children with physician diagnosis of probable asthma at age 2 years or allergen-specific IgE levels at ages 2 and 3 years are associated with decreased lung function or atopy at age 5 years; and (4) collaborate with the Community Outreach, Translation and Application Core to ensure that asthma risk factors of concern to the community are being addressed, translate research findings back to the community, and assist in developing interventions and policies to prevent exposures that contribute to asthma and adverse respiratory health in New York City and elsewhere.
Progress Summary:Recruitment of Study Participants
To date, 589 nonsmoking, African American and Dominican women have met the criteria for complete enrollment into the Mothers and Children Study cohort (i.e, underwent prenatal monitoring, provided a prenatal questionnaire, and had a blood sample collected at delivery from either the mother and/or her newborn).
Data Collected
Questionnaire completion rates are 589 prior to delivery, 466 at 3 months, 463 at 6 months, 422 at 12 months, 346 at 24 months, and 285 at 36 months. There were no significant differences in loss-to-followup by ethnic identity. This study involved analysis of 477 samples of cord blood and 405 samples of postpartum maternal blood by investigators in the Asthma Research Project Core.
Immunoassays Performed
A selected summary of the performed immunoassays is as follows: total IgE levels at birth by radioimmunoassay: 322; at age 2 years: 245; at age 3 years: 156; at age 5 years: 21; among the mothers during pregnancy: 326. Anti-cockroach, mouse, and dust mite-specific IgE (by fluorescence allergosorbent test or by Immunocap) at age 2 years: 139; anti-cockroach, mouse, and dust mite IgE levels at age 3 years: 74; anti-cockroach, mouse, and dust mite IgE levels at age 5 years: 12.
Findings
In utero Sensitization. There continues to be a high rate of sensitization to multiple inhalant indoor antigens, especially cockroach, in newborns. The rates have not been altered significantly from those previously reported.
Allergen-Specific IgE. There continues to be evidence of cockroach, mouse, and rarely dust mite allergy as early as age 2 years (Table 1). These allergic antibodies also are detected at age 3 years.
Table 1. Allergen-Specific IgE Age 2 Years
|
Cockroach IgE |
Mouse IgE |
Dust Mite IgE |
Frequency > 0.35 IU (%) |
9.6 |
11.3 |
3.6 |
Allergen-specific IgE levels (mouse and cockroach) at age 2 years have never been examined previously nor reported at such a level. The relationship between these IgE levels and the domestic exposures to allergens and environmental pollutants, as well as with antigen-induced cord blood mononuclear cell proliferation and respiratory symptoms, currently are being examined in our cohort.
Association Between Prenatal Airborne Pyrene Exposure and Antigen-Induced Sensitization and IgE
We have begun to analyze the relationship between prenatal pyrene exposure, increased antigen-induced cord blood, mononuclear cell proliferation, and elevated serum IgE at birth and age 2 years. Results on 265 newborns (those with history consistent with elevated cotinine levels excluded) yielded the following preliminary findings: regression analysis demonstrated that antigen-induced cord blood proliferation and prenatal pyrene exposure were weakly associated with increased IgE level at birth (OR 1.52 [CI 1.22, 13.04] p = 0.14, n = 185) and increased total IgE at age 24 months (p = 0.12, n = 99). Mouse antigen-induced cord blood proliferation in the presence of high prenatal pyrene exposure was associated with increased mouse IgE level at age 2 months (p = 0.04). In addition, increased prenatal pyrene exposure was significantly correlated with increased mouse (r = 0.47, p < 0.0001, n = 65) and dust mite (r = 0.35, p = 0.02, n = 43) IgE levels at age 24 months. These results suggest that prenatal pyrene exposure may be an important coexposure in the development of indoor antigen-specific B and T cell immune responses.
Association Between Prenatal PAH, Postnatal ETS, and Respiratory Symptoms Age 12-24 Months
We collected 48-hour personal polycyclic aromatic hydrocarbon (PAH) exposure measurements and histories of environmental tobacco smoke (ETS) exposure on 303 women during pregnancy and followed their children prospectively for adverse respiratory effects. We found that by 12 months of age, more cough and wheeze were reported among children exposed to PAH in concert with ETS postnatally (PAH x ETS OR 3.26 p < 0.01, 3.38 p < 0.05, respectively). By 24 months, difficulty breathing and probable asthma were reported more frequently among children exposed to PAH and ETS postnatally (PAH x ETS OR 5.37 p < 0.05, 7.52 p < 0.01, respectively) (Miller, et al., 2004). Our results suggest that early exposure to PAH and ETS can lead to frequent respiratory symptoms and probable asthma by age 12-24 months.
Significance
Their full significance with respect to asthma causation is not known, but these results suggest that sensitization to indoor allergens occurs as early as in utero. Our cohort appears to be demonstrating elevated total and allergen-specific IgE levels, and possibly early signs of asthma, in relation to environmental exposures. Prenatal PAHs, and possibly pyrene exposure specifically, may be important cofactors in the development of allergic immune responses.
Future Activities:We plan to continue expanding data collection and analysis. Evaluation of the relationship between birth biomarkers and findings at age 2 through 5 years is ongoing. Evaluation of the contribution of maternal stress and nutritional status to onset of asthma is underway. Lung functions studies and allergy testing at age 5 years have begun.
Journal Articles on this Report: 1 Displayed | Download in RIS Format
| Other subproject views: | All 2 publications | 2 publications in selected types | All 2 journal articles |
| Other center views: | All 100 publications | 89 publications in selected types | All 86 journal articles |
| Type | Citation | ||
|---|---|---|---|
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Miller RL, Garfinkel R, Horton M, Camann D, Pereral FP, Whyatt RM, Kinney PL. Polycyclic aromatic hydrocarbons, environmental tobacco smoke, and respiratory symptoms in an inner-city birth cohort. Chest 2004;126(4):1071-1078. |
R832141 (2006) R832141C002 (2004) R827027 (2002) |
not available |
children’s health, health effects, health risk assessment, asthma, genetics, assessment of exposure, PAH, ETS, environmental risks, environmental exposure, exposure assessment, genetic risk factors, genetic susceptibility, maternal exposure, nutritional risk factors,
,
HUMAN HEALTH, ENVIRONMENTAL MANAGEMENT, Scientific Discipline, Health, RFA, Health Effects, Risk Assessment, Health Risk Assessment, Epidemiology, Children's Health, Biochemistry, Genetics, exposure assessment, genetic risk factors, children's environmental health, diesel exhaust, assessment of exposure, prenatal exposure, genetic susceptibility, maternal exposure, nutritional risk factors, genetic mechanisms, environmental risks, asthma
Relevant Websites:
Progress and Final Reports:
Original Abstract
2005 Progress Report
2006 Progress Report
Main Center Abstract and Reports:
R832141 Columbia Center for Children’s Environmental Health
Subprojects under this Center:
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R832141C001 Growth and Development Research Project: Prenatal and Postnatal Urban Pollutants and Neurobehavioral Developmental Outcomes
R832141C002 Research Project on Asthma: Prenatal and Postnatal Urban Pollutants and Childhood Asthma
R832141C003 Mechanistic Research Project
R832141C004 Community-Based Intervention Project: Reduction of Exposure and Risk from Pesticides and Allergens
R832141C005 Community Translation and Application Core (COTAC)
R832141C006 Exposure Assessment Facility Core
R832141C007 Data Management, Statistics and Community Impact Modeling Core
R832141C008 Administrative Core