Abstract
The objective of this study was to analyze the mechanisms by which exposure to ambient air pollutants influences respiratory health may include altered prenatal immune development. To analyze associations between elevated cord serum Immunoglobulin E (IgE) levels and maternal air pollution exposure during each month of gestation. Total cord serum IgE was determined by the CAP system and mothers' total IgE levels by nephelometry for 459 births in the Czech Republic from May 1994 to mid-January 1997. Concentrations of polycyclic aromatic hydrocarbons (PAHs) and particulate matter <2.5microns in diameter (PM2.5) were measured in ambient air, and arithmetic means were calculated for each gestational month. Log binomial regression models were used to estimate prevalence ratios (PR) for elevated cord serum IgE (≥0.9IU/ml) adjusting for district of residence, year of birth, and in further models, for maternal IgE (a surrogate for atopy) and gestational season. Heterogeneity by maternal atopy status was evaluated for associations of air pollution and of cigarette smoke. In adjusted models, PAH and PM2.5 exposures in the second month of gestation were each associated with a lower prevalence of elevated cord serum IgE. For an average increase of 100ng/m3 of PAHs, the PR was 0.69 (95% confidence interval (CI): 0.50, 0.95); for 25μg/m3 increase in PM2.5, the PR was 0.77 (95% CI: 0.55, 1.07). Conversely, exposures later in gestation were associated with a higher prevalence of elevated cord IgE: in the fifth month, the PR for PAH exposure was 1.64 (95% CI: 1.29, 2.08), while for PM2.5 in the sixth month, it was 1.66 (95% CI: 1.30, 2.13). In analyses stratified by maternal atopy, air pollutants were associated with altered cord serum IgE only among neonates with non-atopic mothers. Similarly, an association of cigarette smoke with elevated cord serum IgE was found only in non-atopic mothers. PAHs and PM2.5, constituents of both ambient air pollution and cigarette smoke, appear to influence fetal immune development, particularly among infants whose mothers are not atopic.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 75-84 |
| Number of pages | 10 |
| Journal | Pediatric Allergy and Immunology |
| Volume | 22 |
| Issue number | 1 PART 1 |
| DOIs | |
| State | Published - Feb 2011 |
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Keywords
- Air pollution
- Atopy
- Critical window
- Developmental immunology
- Immunoglobulin
- PM
- Polycyclic aromatic hydrocarbon
- Pregnancy
- Smoking and cord serum
ASJC Scopus subject areas
- Immunology and Allergy
- Pediatrics, Perinatology, and Child Health
- Immunology
Cite this
Exposure to air pollution in critical prenatal time windows and IgE levels in newborns. / Herr, Caroline E W; Ghosh, Rakesh; Dostal, Miroslav; Skokanova, Venuse; Ashwood, Paul; Lipsett, Michael; Joad, Jesse P.; Pinkerton, Kent E; Yap, Poh Sin; Frost, Joshua D.; Sram, Radim; Hertz-Picciotto, Irva.
In: Pediatric Allergy and Immunology, Vol. 22, No. 1 PART 1, 02.2011, p. 75-84.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Exposure to air pollution in critical prenatal time windows and IgE levels in newborns
AU - Herr, Caroline E W
AU - Ghosh, Rakesh
AU - Dostal, Miroslav
AU - Skokanova, Venuse
AU - Ashwood, Paul
AU - Lipsett, Michael
AU - Joad, Jesse P.
AU - Pinkerton, Kent E
AU - Yap, Poh Sin
AU - Frost, Joshua D.
AU - Sram, Radim
AU - Hertz-Picciotto, Irva
PY - 2011/2
Y1 - 2011/2
N2 - The objective of this study was to analyze the mechanisms by which exposure to ambient air pollutants influences respiratory health may include altered prenatal immune development. To analyze associations between elevated cord serum Immunoglobulin E (IgE) levels and maternal air pollution exposure during each month of gestation. Total cord serum IgE was determined by the CAP system and mothers' total IgE levels by nephelometry for 459 births in the Czech Republic from May 1994 to mid-January 1997. Concentrations of polycyclic aromatic hydrocarbons (PAHs) and particulate matter <2.5microns in diameter (PM2.5) were measured in ambient air, and arithmetic means were calculated for each gestational month. Log binomial regression models were used to estimate prevalence ratios (PR) for elevated cord serum IgE (≥0.9IU/ml) adjusting for district of residence, year of birth, and in further models, for maternal IgE (a surrogate for atopy) and gestational season. Heterogeneity by maternal atopy status was evaluated for associations of air pollution and of cigarette smoke. In adjusted models, PAH and PM2.5 exposures in the second month of gestation were each associated with a lower prevalence of elevated cord serum IgE. For an average increase of 100ng/m3 of PAHs, the PR was 0.69 (95% confidence interval (CI): 0.50, 0.95); for 25μg/m3 increase in PM2.5, the PR was 0.77 (95% CI: 0.55, 1.07). Conversely, exposures later in gestation were associated with a higher prevalence of elevated cord IgE: in the fifth month, the PR for PAH exposure was 1.64 (95% CI: 1.29, 2.08), while for PM2.5 in the sixth month, it was 1.66 (95% CI: 1.30, 2.13). In analyses stratified by maternal atopy, air pollutants were associated with altered cord serum IgE only among neonates with non-atopic mothers. Similarly, an association of cigarette smoke with elevated cord serum IgE was found only in non-atopic mothers. PAHs and PM2.5, constituents of both ambient air pollution and cigarette smoke, appear to influence fetal immune development, particularly among infants whose mothers are not atopic.
AB - The objective of this study was to analyze the mechanisms by which exposure to ambient air pollutants influences respiratory health may include altered prenatal immune development. To analyze associations between elevated cord serum Immunoglobulin E (IgE) levels and maternal air pollution exposure during each month of gestation. Total cord serum IgE was determined by the CAP system and mothers' total IgE levels by nephelometry for 459 births in the Czech Republic from May 1994 to mid-January 1997. Concentrations of polycyclic aromatic hydrocarbons (PAHs) and particulate matter <2.5microns in diameter (PM2.5) were measured in ambient air, and arithmetic means were calculated for each gestational month. Log binomial regression models were used to estimate prevalence ratios (PR) for elevated cord serum IgE (≥0.9IU/ml) adjusting for district of residence, year of birth, and in further models, for maternal IgE (a surrogate for atopy) and gestational season. Heterogeneity by maternal atopy status was evaluated for associations of air pollution and of cigarette smoke. In adjusted models, PAH and PM2.5 exposures in the second month of gestation were each associated with a lower prevalence of elevated cord serum IgE. For an average increase of 100ng/m3 of PAHs, the PR was 0.69 (95% confidence interval (CI): 0.50, 0.95); for 25μg/m3 increase in PM2.5, the PR was 0.77 (95% CI: 0.55, 1.07). Conversely, exposures later in gestation were associated with a higher prevalence of elevated cord IgE: in the fifth month, the PR for PAH exposure was 1.64 (95% CI: 1.29, 2.08), while for PM2.5 in the sixth month, it was 1.66 (95% CI: 1.30, 2.13). In analyses stratified by maternal atopy, air pollutants were associated with altered cord serum IgE only among neonates with non-atopic mothers. Similarly, an association of cigarette smoke with elevated cord serum IgE was found only in non-atopic mothers. PAHs and PM2.5, constituents of both ambient air pollution and cigarette smoke, appear to influence fetal immune development, particularly among infants whose mothers are not atopic.
KW - Air pollution
KW - Atopy
KW - Critical window
KW - Developmental immunology
KW - Immunoglobulin
KW - PM
KW - Polycyclic aromatic hydrocarbon
KW - Pregnancy
KW - Smoking and cord serum
UR - http://www.scopus.com/inward/record.url?scp=78851470139&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=78851470139&partnerID=8YFLogxK
U2 - 10.1111/j.1399-3038.2010.01074.x
DO - 10.1111/j.1399-3038.2010.01074.x
M3 - Article
C2 - 20609135
AN - SCOPUS:78851470139
VL - 22
SP - 75
EP - 84
JO - Pediatric Allergy and Immunology
JF - Pediatric Allergy and Immunology
SN - 0905-6157
IS - 1 PART 1
ER -