Relationship between in utero C-reactive protein levels and asthma in at-risk children.
BACKGROUND
Asthma research has focused on postnatal exposures, but there is recent evidence to indicate atopic immune responses might be initiated in utero. Systemic inflammation during pregnancy might indicate an environment that could increase propensity in the child to develop allergic disease.


OBJECTIVE
To investigate the association of systemic inflammation, as measured by C-reactive protein (CRP) levels, with asthma and wheezing in offspring within an at-risk, mostly Mexican, cohort.


METHODS
Using data from a randomized education intervention of families at risk for asthma from 1998 followed through 2009 in urban Chicago, asthma was defined as ever having a physician diagnosis of asthma by 3 years of age and wheezing before the third year. Logistic regression models controlling for confounders investigated the effect of prenatal CRP levels on these outcomes.


RESULTS
There were 244 mother-child pairs included in the study analysis with median prenatal CRP levels of 4.9 mg/L (interquartile range 3.2-7.7). Continuous prenatal CRP levels were predictive of asthma by year 3 (relative risk 2.4, 95% confidence interval 1.3, 3.6) and wheezing in year 3 (relative risk 1.7, 95% confidence interval 1.1, 2.4) after adjustment. Associations remained significant in mothers who were of Mexican ethnicity and were nonsmokers, suggesting that effects might be stronger in children at lower risk of disease.


CONCLUSIONS
Prenatal CRP levels are associated with asthma by year 3 and wheezing in year 3 within a high-risk, urban, mostly Mexican, cohort. Maternal systemic inflammation might reflect a prenatal environment that could increase offspring susceptibility to develop wheezing and asthma young in life.
Division of Epidemiology and Biostatistics, School of Public Health, University of Illinois at Chicago, Chicago, Illinois. Electronic address: brittany.lapin@gmail.com.
Brittany
B
Lapin
Section of Allergy and Immunology, Georgia Regents University, Augusta, Georgia.
Dennis
D
Ownby
Division of Epidemiology and Biostatistics, School of Public Health, University of Illinois at Chicago, Chicago, Illinois.
Mary
M
Turyk
Division of Epidemiology and Biostatistics, School of Public Health, University of Illinois at Chicago, Chicago, Illinois.
Julie
J
Piorkowski
Division of Epidemiology and Biostatistics, School of Public Health, University of Illinois at Chicago, Chicago, Illinois.
Sally
S
Freels
Community Health Sciences Division, School of Public Health, University of Illinois at Chicago, Chicago, Illinois.
Noel
N
Chavez
Division of Epidemiology and Biostatistics, School of Public Health, University of Illinois at Chicago, Chicago, Illinois.
Cynthia
C
Wagner-Cassanova
College of Nursing, University of Illinois at Chicago, Chicago, Illinois.
Eva
E
Hernandez
Mayo Clinic, Scottsdale, Arizona.
Darlene
D
Pelzel
Esperanza Health Centers, Chicago, Illinois.
Carmen
C
Vergara
Division of Epidemiology and Biostatistics, School of Public Health, University of Illinois at Chicago, Chicago, Illinois.
Victoria
V
Persky
D000328:Adult; D001249:Asthma / Q000097:blood / Q000175:diagnosis*; D002097:C-Reactive Protein / Q000032:analysis*; D002648:Child; D002675:Child, Preschool; D005260:Female; D006630:Hispanic or Latino; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000175:diagnosis; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000097:blood / Q000175:diagnosis*; D016032:Randomized Controlled Trials as Topic; D012135:Respiratory Sounds / Q000175:diagnosis; D012307:Risk Factors
D002097:C-Reactive Protein