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Preterm birth is the leading cause of infant morbidity and mortality worldwide. Elevated levels of oxidative stress have been associated with an increased risk of delivering before term. However, most studies testing this hypothesis have been conducted in racially and demographically homogenous study populations, which do not reflect the diversity within the United States.We leveraged 4 cohorts participating in the Environmental Influences on Child Health Outcomes Program to conduct the largest study to date examining biomarkers of oxidative stress and preterm birth (N=1916). Furthermore, we hypothesized that elevated oxidative stress would be associated with higher odds of preterm birth, particularly preterm birth of spontaneous origin.This study was a pooled analysis and meta-analysis of 4 birth cohorts spanning multiple geographic regions in the mainland United States and Puerto Rico (208 preterm births and 1708 full-term births). Of note, 8-iso-prostaglandin-FApproximately 11% of our analytical sample was born before term. Relative to full-term births, an interquartile range increase in averaged concentrations of FHere, oxidative stress, as measured by 8-iso-prostaglandin-F

Background Atopic dermatitis is a common childhood disease, potentially influenced by prenatal nutritional exposures such as polyunsaturated fatty acids (PUFAs). Objective In a racially diverse cohort, we hypothesized that childhood atopic dermatitis would be associated with higher prenatal omega-6 (n-6) and lower omega-3 (n-3) PUFAs. Methods We included mother-child dyads, births 2006 to 2011, enrolled in the University of Tennessee Health Sciences Center Conditions Affecting Neurocognitive Development in Early Childhood cohort. Primary exposures included second trimester plasma n-3 and n-6 PUFA status and the ratio of the two (n-6:n-3). We assessed child current atopic dermatitis symptoms in the previous 12 months at age approximately 4 to 6 years. We investigated the association between PUFA exposures and atopic dermatitis using multivariable logistic regression, adjusting for potential confounders. We assessed for effect modification by maternal prenatal smoking, atopic disease history, and child sex. Results Among 1131 women, 67% were African American and 42% had an atopic disease history; 17% of children had atopic dermatitis. Higher prenatal n-6 PUFAs were associated with increased relative odds of child atopic dermatitis (adjusted odds ratio: 1.25; confidence interval: 1.01-1.54 per interquartile range difference), and interaction models demonstrated that this association was seen in dyads in which the women had a history of atopic disease. Neither prenatal n-3 PUFAs nor n-6:n-3 were associated with child atopic dermatitis. Conclusion In this racially diverse cohort, higher second trimester n-6 PUFAs were associated with atopic dermatitis in children of women with atopy. PUFAs may represent a modifiable risk factor for atopic dermatitis, particularly in individuals with a familial predisposition.

Background Individuals with spina bifida are at increased risk for urinary tract infection (UTI), however there are few population-based investigations of the burden of UTI hospitalizations. Objective We assessed rates and risk factors for UTI hospitalization in individuals with and without spina bifida. Methods We conducted a retrospective cohort study to estimate rates of UTI hospitalization by spina bifida status. We included individuals enrolled in Tennessee Medicaid who lived in one of the Emerging Infections Program’s Active Bacterial Surveillance counties between 2005 and 2013. Spina bifida was primarily defined and UTI hospitalizations were identified using International Classification of Diseases, Ninth Revision diagnoses. We also studied a subset without specific health conditions potentially associated with UTI. We used Poisson regression to calculate rate ratios (RR) of UTIs for individuals with versus without spina bifida, adjusting for race, sex and age group. Results Over the 9-years, 1,239,362 individuals were included and 2,493 met criteria for spina bifida. Individuals with spina bifida had over a four-fold increased rate of UTI hospitalization than those without spina bifida-in the overall study population and in the subset without specific, high-risk conditions (adjusted rate ratios: 4.41, 95% confidence intervals: 3.03, 6.43) and (4.87, 95% CI: 2.99, 7.92), respectively. We detected differences in rates of UTI hospitalization by race and sex in individuals without spina bifida that were not seen among individuals with spina bifida. Conclusions Individuals with spina bifida had increased rates of UTI hospitalizations, and associated demographic patterns differed from those without spina bifida.

Background Previous studies of prenatal phthalate exposure and childhood asthma are inconsistent. These studies typically model phthalates as individual, rather than co-occurring, exposures. We investigated whether prenatal phthalates are associated with childhood wheeze and asthma using a mixtures approach. Methods We studied dyads from two prenatal cohorts in the ECHO-PATHWAYS consortium: CANDLE, recruited 2006–2011 and TIDES, recruited 2011–2013. Parents reported child respiratory outcomes at age 4–6 years: ever asthma, current wheeze (symptoms in past 12 months) and current asthma (two affirmative responses from ever asthma, recent asthma-specific medication use, and/or current wheeze). We quantified 11 phthalate metabolites in third trimester urine and estimated associations with child respiratory outcomes using weighted quantile sum (WQS) logistic regression, using separate models to estimate protective and adverse associations, adjusting for covariates. We examined effect modification by child sex and maternal asthma. Results Of 1481 women, most identified as White (46.6%) or Black (44.6%); 17% reported an asthma history. Prevalence of ever asthma, current wheeze and current asthma in children was 12.3%, 15.8% and 12.3%, respectively. Overall, there was no adverse association with respiratory outcomes. In sex-stratified analyses, boys’ phthalate index was adversely associated with all outcomes (e.g., boys’ ever asthma: adjusted odds ratio per one quintile increase in WQS phthalate index (AOR): 1.42; 95% confidence interval (CI): 1.08, 1.85, with mono-ethyl phthalate (MEP) weighted highest). Adverse associations were also observed in dyads without maternal asthma history, driven by MEP and mono-butyl phthalate (MBP), but not in those with maternal asthma history. We observed protective associations between the phthalate index and respiratory outcomes in analysis of all participants (e.g., ever asthma: AOR; 95% CI: 0.81; 0.68, 0.96), with di(2-ethylhexyl)phthalate (DEHP) metabolites weighted highest. Conclusions Results suggest effect modification by child sex and maternal asthma in associations between prenatal phthalate mixtures and child asthma and wheeze.

Background Prenatal and early life air pollution exposure may impair healthy neurodevelopment, increasing risk of childhood behavioral disorders, but epidemiological evidence is inconsistent. Little is known about factors that determine susceptibility. Methods Participants were mother-child dyads from the CANDLE study, an ECHO PATHWAYS Consortium birth cohort set in the mid-South United States, who completed a preschool visit. We estimated prenatal and childhood exposures to nitrogen dioxide (NO2) and particulate matter less than 10 μm (PM10) at participants' residences using a national annual average universal kriging model (land-use regression with spatial smoothing). Distance to nearest major roadway was used as a proxy for traffic-related pollution. Primary outcomes were children's internalizing and externalizing behavior problems. Regression models were adjusted for individual- and neighborhood-level socioeconomic measures, maternal IQ, and multiple other potential confounders. We tested for effect modification by select maternal and child characteristics. Results The analytic sample (N = 975 of 1503 enrolled) was 64% African American and 53% had a household annual income below $35,000; child mean age was 4.3 years (SD: 0.4). Mean prenatal NO2 and PM10 exposures were 12.0 ppb (SD: 2.4) and 20.8 μg/m3 (SD: 2.0); postnatal exposures were lower. In fully adjusted models, 2 ppb higher prenatal NO2 was positively associated with externalizing behavior (6%; 95% CI: 1, 11%). Associations with postnatal exposure were stronger (8% per 2 ppb NO2; 95%CI: 0, 16%). Prenatal NO2 exposure was also associated with an increased odds of clinically significant internalizing and externalizing behaviors. We found suggestive evidence that socioeconomic adversity and African American race increases susceptibility. PM10 and road proximity were not associated with outcomes. Conclusions Findings showed that air pollution exposure is positively associated with child behavior problems and that African American and low SES children may be more susceptible. Importantly, associations were observed at exposures below current air quality standards.

BackgroundFindings on prenatal polyunsaturated fatty acid (PUFA) intake and child wheeze and asthma have been inconsistent.ObjectiveWe sought to examine associations between prenatal PUFA status and child wheeze/asthma and modifying effects of maternal asthma/atopy, child sex, and maternal race.MethodsAnalyses included 1019 mother-child dyads with omega-3 (n-3) and omega-3 (n-6) PUFAs measured in second-trimester plasma; n-6/n-3 ratios were calculated. Child wheeze/asthma outcomes ascertained at age 4 to 6 years included ever physician-diagnosed asthma, current wheeze (symptoms past 12 months), current asthma (diagnosis and medication and/or symptoms past 12 months), and current diagnosed asthma. Each PUFA indicator and outcome was analyzed in separate models using modified Poisson regression with interaction terms.ResultsIn quartile (Q) analyses, higher n-6 PUFAs were associated with increased risk of ever (risk ratio [RR] high vs low [RR Q4 vs Q1], 1.70; 95% CI, 1.07-2.71) and current (RR Q4 vs Q1, 1.70; 95% CI, 1.07-2.71) diagnosed asthma, whereas n-3 PUFAs were associated with lower risk (RR Q4 vs Q1, 0.59; 95% CI, 0.33-1.03) of current diagnosed asthma (Ptrend< .05 for all). Higher n-6 PUFAs were associated with a higher risk of all respiratory outcomes among children born to women with asthma (Pinteraction< .05 for all outcomes). Asignificant 3-way interaction between child sex, maternal asthma, and n-6/n-3 PUFA indicated that male children born to women with asthma and a higher ratio had the highest risk across wheeze/asthma outcomes (Pinteraction< .05).ConclusionsAssociations between prenatal PUFA status and childhood wheeze/asthma were modified by maternal history of asthma and child sex.

Objective To examine healthcare resource utilization for acute respiratory illness in Latino infants compared with other racial/ethnic groups. Study design We studied 674 term-born, previously healthy infants brought in for an unscheduled healthcare visit for an acute respiratory illness. The predictor variable was infant race/ethnicity, and the primary outcome was healthcare resource utilization, adjusted for age and disease severity. Results The cohort was 14% Latino, 52% white, 22% African American, and 12% other race/ethnicity. More than one-third (37%) of the mothers of Latino infants were Spanish-speaking. The bronchiolitis severity score was higher (indicating more severe disease) in white infants (median, 6.0; IQR, 3.0-9.0 on a scale of 0-12) compared with Latino (median, 3.0; IQR, 1.0-6.0) and African American (median, 3.5; IQR, 1.0-6.0) infants ( P P = .96). Latino infants were the most likely to receive antibiotics (58%, compared with 47% of whites and 34% of African Americans; P = .005) and to have body fluid cultures drawn. Latino infants also were more likely than African American infants to undergo chest radiography and respiratory virus rapid antigen testing ( P ≤ .01). Latino infants from Spanish-speaking families had a higher rate of respiratory syncytial virus testing compared with those from English-speaking families (76% vs 51%; P = .016). Conclusion Providers caring for Latino infants with acute respiratory illness ordered more antibiotics and diagnostic testing for this group, particularly compared with African Americans, even though the 2 groups had similar disease severity and socioeconomic disparities. Language barrier may be a possible explanation for these differences.

Background Respiratory syncytial virus (RSV) and rhinovirus infections are the most common significant infant respiratory tract illnesses and are associated with increased but differential risks of childhood asthma. Objective We sought to determine whether maternal asthma is associated with higher odds of infant respiratory tract infection with rhinovirus versus RSV and increased infection severity. Methods Mother-infant dyads were enrolled from 2004-2008 during an infant respiratory tract infection (104 with rhinovirus and 279 with RSV). Mothers were classified into mutually exclusive groups (atopic asthma, nonatopic asthma, and no asthma). We determined viral cause using PCR and the severity of the infant's respiratory tract infection using the bronchiolitis severity score. Adjusted relative odds of maternal asthma with viral cause were calculated by using logistic regression. Proportional odds models assessed the association of maternal asthma and infant infection severity. Results Infants with a mother with atopic asthma compared with infants whose mothers did not have asthma were more likely to have rhinovirus versus RSV infection (adjusted odds ratio, 2.42; 95% CI, 1.19-4.90). Similarly, among infants with rhinovirus, having a mother with atopic asthma was associated with increased infection severity (adjusted odds ratio, 3.10; 95% CI, 1.21-7.98). This relationship was not seen among infants with RSV. Conclusions Clinically significant rhinovirus infection during infancy was more strongly associated with having a mother with atopic asthma than clinically significant RSV infection. Having a mother with atopic asthma was associated with increased severity of infant rhinovirus but not RSV infections. Infants with rhinovirus were more likely to have a familial atopic predisposition, which might partly explain the subsequent increased asthma risk.

Background Urban children represent a group at high risk for asthma development and adverse asthma outcomes. Although rural children also encounter sociodemographic disparities that might be expected to worsen asthma, asthma in the rural United States is poorly studied. Objectives To determine rural-urban differences in childhood asthma diagnosis and morbidity. Methods We studied a statewide population of 117,080 children continuously enrolled in Tennessee Medicaid from birth through the sixth year of life, using linked Tennessee Medicaid, vital records, and pharmacy claims databases to determine asthma diagnosis and residence. Results The cohort was 45% urban, 23% suburban, and 33% rural. Compared with urban children, rural children were more likely to be white, have a history of bronchiolitis, and have mothers who smoked. Eleven percent of urban, 12% of suburban, and 13% of rural children met study criteria for asthma diagnosis (adjusted odds ratio for rural children, 1.16; 95% confidence interval, 1.09–1.24; adjusted odds ratio for suburban children, 1.22; 95% confidence interval, 1.14–1.30; with urban as the referent; P Conclusion In this pediatric Medicaid population, rural children had increased asthma prevalence and similar asthma morbidity compared with urban children but differences in patterns of asthma care and resource use, suggesting that optimal interventions for asthma may differ in rural compared with urban populations.

Background Risk factors for severe human rhinovirus (HRV)–associated infant illness are unknown. Objectives We sought to examine the role of HRV infection in infant respiratory tract illness and assess viral and host risk factors for HRV-associated disease severity. Methods We used a prospective cohort of term, previously healthy infants enrolled during an inpatient or outpatient visit for acute upper or lower respiratory tract illness during the fall-spring months of 2004-2008. Illness severity was determined by using an ordinal bronchiolitis severity score, with higher scores indicating more severe disease. HRV was identified by means of real-time RT-PCR. The VP4/VP2 region from HRV-positive specimens was sequenced to determine species. Results Of 630 infants with bronchiolitis or upper respiratory tract illnesses (URIs), 162 (26%) had HRV infection; HRV infection was associated with 18% of cases of bronchiolitis and 47% of cases of URI. Among infants with HRV infection, 104 (64%) had HRV infection alone. Host factors associated with more severe HRV-associated illness included a maternal and family history of atopy (median score of 3.5 [interquartile range [IQR], 1.0-7.8] vs 2.0 [IQR, 1.0-5.2] and 3.5 [IQR, 1.0-7.5] vs 2.0 [IQR, 0-4.0]). In adjusted analyses maternal history of atopy conferred an increase in the risk for more severe HRV-associated bronchiolitis (odds ratio, 2.39; 95% CI, 1.14-4.99; P = .02). In a similar model maternal asthma was also associated with greater HRV-associated bronchiolitis severity (odds ratio, 2.49, 95% CI, 1.10-5.67; P = .03). Among patients with HRV infection, 35% had HRVA, 6% had HRVB, and 30% had HRVC. Conclusion HRV infection was a frequent cause of bronchiolitis and URIs among previously healthy term infants requiring hospitalization or unscheduled outpatient visits. Substantial viral genetic diversity was seen among the patients with HRV infection, and predominant groups varied by season and year. Host factors, including maternal atopy, were associated with more severe infant HRV-associated illness.

The etiology and morbidity associated with asthma are thought to stem from both genetic factors and potentially modifiable environmental factors, such as viral infections.[1-7] Although it is unclear whether respiratory viral infections cause asthma, observational studies have demonstrated a high rate of asthma in children with a history of severe viral lower respiratory tract infections during infancy, and viruses are the associated with the majority of asthma exacerbations among both children and adults. This review will discuss the pathogens associated with virus-induced wheezing illnesses during infancy and early childhood, the association of bronchiolitis during infancy with an increased risk of childhood asthma, and the association of respiratory viruses with asthma exacerbations in older children and adults.

Background Asthma is a common condition during pregnancy. Objective We sought to determine the effect of asthma on the rates of adverse pregnancy and fetal outcomes. Methods We identified pregnancies among black and white women age 15 to 44 with singleton gestations enrolled in the Tennessee Medicaid program over a period of 9 consecutive years, from 1995to 2003, and used claims data to determine the relationship of maternal asthma and asthma exacerbations on pregnancy and infant outcomes. Results Among the 140,299 pregnancies, 6.5% were in women with asthma. Among women with asthma, 23% had a hospital or emergency department visit (exacerbated asthma); 40% of black and 23% of white women received hospital or emergency department care for asthma during pregnancy. After controlling for race and other covariates, birth weights among infants of women with asthma were, on average, 38 g lower, and among infants of women with exacerbated asthma they were, on average, 56 g lower. There were moderate, dose-dependent relationships between asthma alone and exacerbated asthma with hypertensive disorders of pregnancy, membrane-related disorders, preterm labor, antepartum hemorrhage, and cesarean delivery. Maternal asthma was not associated with preterm birth or birth defects. Conclusion Asthma is a risk factor for several common adverse outcomes of pregnancy, and poorly controlled asthma during pregnancy increases these risks. Clinical implications It is possible that both maternal and infant outcomes could be improved in this population with appropriate asthma care, especially among black women.

The voicing of unsolicited observations by patients and families is a form of participation in the health care system. We investigated whether visits by patients of different race/ethnicities were equally represented in unsolicited complaints filed with a medical center's Office of Patient Affairs (OPA) regarding pediatric emergency visits.We conducted a population-based retrospective study, including pediatric emergency visits, at a large academic medical center between January 1999 and December 2002. We identified complaints to the OPA and conducted bivariate and multivariable analyses to determine whether patient race/ethnicity was associated with filing a complaint.Among 105 322 total visits, the overall complaint rate was 1.22/1000 visits. Visits by white children had a complaint rate of 1.78/1000 visits compared with 0.37/1000 visits by African American children (P.001). In multivariable analysis, visits by African American children remained less likely to be associated with a complaint to the OPA compared with visits by white children (adjusted odds ratio 0.30, 95% CI 0.17-0.55) after controlling for factors such as payer status.Emergency-department visits by African American children were less likely to be associated with a complaint than visits by white children. Programs that use complaints in service recovery, quality assurance, and risk management efforts may unintentionally exclude segments of the patient population served by the institution.

There is a population-based increased risk of early childhood asthma following infant bronchiolitis occurring during rhinovirus-predominant months compared to asthma following infant bronchiolitis during RSV-predominant months.

The in-vivo growth of respiratory viruses is dependent on replication in epithelial cell populations forming the mucosal lining of the respiratory tract. Primary epithelial cells have been established in tissue culture and are providing insight into the control of replication of viruses such as influenza, parainfluenza and respiratory syncytial virus. This review will focus on this system and more general exploration of the interactions of respiratory viruses with the epithelium.

To the Editor: The etiology of asthma remains unclear but is thought to include non-modifiable risk factors such as family history and genetic predisposition, as well as potentially modifiable risk factors including viral bronchiolitis in infancy(1;2). During the winter months, the predominant virus detected in infants with viral bronchiolitis is respiratory syncytial virus (RSV)(3). By 1 year of age approximately 70% of children have been infected with RSV, and this increases to almost 100% by 2 years of age(4). Infant RSV bronchiolitis is associated with recurrent wheeze or asthma throughout childhood and even into early adulthood(5;6), with a dose-response relationship identified between the severity of the bronchiolitis and the risk of developing asthma(7), and evidence for a causal relationship(8). The aim of our study was to determine what proportion of childhood asthma is associated with infant bronchiolitis during RSV season. We analyzed cohort data of children born from 1996–2003 cared for at Northern California Kaiser Permanente (KPNC), an integrated healthcare delivery system, and children born from 1995–2003 enrolled in Tennessee Medicaid (TennCare). KPNC and TennCare provide health insurance for approximately one-third of Northern California residents and approximately one-half of infants born in Tennessee, respectively. Eligible infants had a minimum gestation age of 32 weeks, no chronic lung disease, and were continuously enrolled in either TennCare or KPNC during the first year of life. The main predictor variable was infant bronchiolitis during RSV season defined by ICD-9 codes for bronchiolitis and limited to the RSV season, October through March, during the first year of life. The main outcome variable was early childhood asthma determined using an algorithm of ICD-9 codes for asthma and asthma-specific medication utilization between ages 4.5–6 years. The Vanderbilt University Institutional Review Board and the KPNC Institutional Board for the Protection of Human Subjects approved the study. The Bureau of TennCare approved use of Tennessee Medicaid data. To ascertain the proportion of childhood asthma in the TennCare or KPNC population that is associated with bronchiolitis exposure during RSV season, we calculated both the attributable risk of infants with a bronchiolitis event during infancy, and the population attributable risk. We estimated the attributable fraction of bronchiolitis from adjusted risk ratios that were calculated from multivariable Poisson regression models with a robust error variance for the early childhood asthma outcome. Adjustment covariates included gender, race, gestational age, birthweight, siblings, maternal age, and maternal smoking. Statistical analyses were performed with R version 2.12.1 software. A total of 264,010 infant births (KPNC 81,550, TennCare 182,460) were included in this study and followed until 6 years of age. Table I highlights key characteristics of the two cohorts. Compared to the TennCare population, the KPNC population had more Hispanic and Asian participants, less African American participants, higher rates of maternal education beyond high school, and lower rates of maternal smoking. Overall, 15% of infants had bronchiolitis during RSV season. The proportion of children diagnosed with asthma among the KPNC and TennCare cohorts was 8% and 12%, respectively, for those without a history of infant bronchiolitis during RSV season, and 16% and 23%, respectively, for those with a history of infant bronchiolitis during RSV season. The population attributable risk for asthma contributed by infant bronchiolitis during RSV season was 10% for the KPNC cohort, and among the subset of children with infant bronchiolitis during RSV season, the attributable risk was 49% (95% CI:47%,52%); in TennCare, it was 13% and 47% (95% CI:45%,48%), respectively (See Fig 1). The unadjusted risk ratio of childhood asthma following infant bronchiolitis during RSV seaso100 n for KPNC was 1.97 (95% CI:1.87,2.09) and the multivariate adjusted risk ratio of childhood asthma following infant bronchiolitis during RSV season was 1.94 (95% CI:1.84,2.05); for TennCare it was 1.87 (95% CI:1.82,1.92) and 1.81 (95% CI:1.77,1.86), respectively. In our analysis restricting to term infants (gestational age ≥37 weeks), results remain unchanged (data not shown). FIG 1 Attributable risk of asthma due to infant bronchiolitis during RSV season. *Multivariable Poisson regression analyses were used to calculate risk ratios within the KPNC and TennCare populations. In both the KPNC and TennCare cohorts, the proportion of children who developed asthma was almost two times higher in children with a history of infant bronchiolitis during RSV season as compared to the children who did not have a history of infant bronchiolitis during RSV season. The almost identical attributable risk and population attributable risk findings are notable given the significant differences between the two populations. Adjustment of risk ratios for potential confounders did not change the results. Despite the strengths of our large population-based study, several limitations deserve mention. This study relied on existing electronic data; however, the use of electronic data has been previously validated as both sensitive and specific(9). Secondly, the study was unable to detect infants with asymptomatic or mild bronchiolitis during RSV season as well as those who did not seek treatment. In addition, we were unable to confirm the diagnosis of RSV as the etiology of bronchiolitis events although prior studies support that the majority of infant bronchiolitis events during RSV season are attributable to RSV(3). In a retrospective study by Stemple et al. in which bronchiolitis was defined by ICD-9 codes for bronchiolitis, RSV was detected in the nasal wash samples of 77% of children under 2 years of age collected between October and April(10). By limiting our study to bronchiolitis episodes during the winter months, RSV is likely to be the associated viral pathogen. Lastly, while human rhinovirus (RV) infection has also been implicated in asthma inception, infant RV bronchiolitis is far less common than infant RSV bronchiolitis, and occurs in older infants, those born to parents with asthma, or those who have already been allergically sensitized, suggesting that rather than being causal, that RV bronchiolitis is a clinical biomarker of future asthma risk(11–13). In summary, in two representative US populations with significantly varying baseline characteristics, there were consistent findings that nearly 50% of asthma cases in children with a history of infant bronchiolitis during RSV season were associated with bronchiolitis. On a population level, 13% of asthma was associated with infant bronchiolitis during RSV season. The mechanism to explain how infant RSV infection results in the subsequent development of asthma remains unclear, but if truly causal in nature as supported by observational(8) and mechanistic(14) studies, our findings indicate up to 13% of asthma cases could be prevented by eliminating infant bronchiolitis during RSV season. Thus, next steps are to determine if preventing or altering host response to infant RSV infections decreases both the incidence and severity of childhood asthma as a primary asthma prevention strategy.

Objective The objective of the study was to investigate the association of maternal vitamin D and maternal asthma and infant respiratory infection severity. Study Design The study included cross-sectional analyses of 340 mother-infant dyads enrolled from September to May 2004-2008 during an infant viral respiratory infection. Maternal vitamin D levels were determined from enrollment blood specimens. At enrollment, we determined self-reported maternal asthma and infant respiratory infection severity using a bronchiolitis score. We assessed the association of maternal vitamin D levels and maternal asthma and infant bronchiolitis score in race-stratified multivariable regression models. Results The cohort was 70% white, 19% African American, and 21% had asthma. Overall, the median maternal vitamin D level was 20 ng/mL (interquartile range, 14–28). Among white women, a 14 ng/mL increase in vitamin D was associated with a decreased odds of asthma (adjusted odds ratio, 0.54; 95% confidence interval, 0.33–0.86). Maternal vitamin D was not associated with infant bronchiolitis score. Conclusion Higher maternal vitamin D levels were associated with decreased odds of asthma.