Neonatal health of infants born to mothers with asthma

Mendola, Pauline; Männistö, Tuija; Leishear, Kira; Reddy, Uma M.; Chen, Zhen; Laughon, S. Katherine

doi:10.1016/j.jaci.2013.06.012

Cited by 59 publications

(68 citation statements)

References 31 publications

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“…Adjusted models include maternal age in years (<20, 20–24, 25–29, 30–34, ≥35, unknown); race/ethnicity (White, Black, Hispanic, Asian/Pacific Islander, Other Race, Unknown), pre-pregnancy body mass index (BMI, kg/m 2 ) (<18.5 underweight, 18.5–24.9 normal weight, 25–29.9 overweight, ≥30 obese, unknown), smoking and alcohol use (both yes/no), study site, parity (nulliparous, primiparous, multiparous), insurance status (private, public/government, self-pay/other, unknown), marital status (married, divorced/widowed, single, unknown), and maternal comorbidities (chronic hypertension, diabetes, thyroid disease and HIV). Covariates were selected a priori based on earlier analyses of preterm birth in association with maternal asthma (25;31). …”

Section: Methodsmentioning

confidence: 99%

Preterm birth and air pollution: Critical windows of exposure for women with asthma

Mendola

Wallace

Hwang

et al. 2016

Journal of Allergy and Clinical Immunology

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Background Ambient air pollutants may increase preterm birth (PTB) risk but critical exposure windows are uncertain. The interaction of asthma and pollutant exposure is rarely studied. Objective To assess the interaction of maternal asthma and air pollutant exposures in relation to PTB risk. Methods Electronic medical records for 223,502 U.S. deliveries were linked with modified Community Multiscale Air Quality model outputs. Logistic regression with generalized estimating equations estimated the odds ratio (OR) and 95% confidence intervals (CI) for PTB based on the interaction of maternal asthma and particulate matter <2.5 microns (PM2.5) and <10 microns (PM10), ozone (O3), nitrogen oxides (NOx), sulfur dioxide (SO2) and carbon monoxide (CO) per interquartile range. For each gestational week 23–36, exposures among women who delivered were compared to those remaining pregnant. Three-months preconception, whole pregnancy, weeks 1–28 and the last six weeks of gestation averages were also evaluated. Results Assessing PTB by gestational week, significant asthma interactions were sporadic before 30 weeks but more common during weeks 34–36 with higher risk among asthmatic mothers for NOx, CO and SO2 exposure and an inverse association with O3 in week 34. Odds of PTB were significantly higher among asthmatics for CO and NOx preconception and early in pregnancy. In the last six weeks of pregnancy, PM10 risk for PTB was higher among asthmatics. Conclusion Asthmatic mothers may experience higher risk for PTB after exposure to traffic-related pollutants such as CO and NOx particularly for exposures three-months preconception and in the early weeks of pregnancy.

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Section: Methodsmentioning

confidence: 99%

Preterm birth and air pollution: Critical windows of exposure for women with asthma

Mendola

Wallace

Hwang

et al. 2016

Journal of Allergy and Clinical Immunology

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Section: Methodsmentioning

confidence: 99%

“…Codes used to identify complications have been previously described [5, 14]. We evaluated neonatal and obstetric outcomes previously identified in our data as being associated with maternal asthma and retained outcomes with sufficient numbers to support analyses by race/ethnicity [5, 14]. Obstetric outcomes examined included gestational diabetes, gestational hypertension, preeclampsia, maternal hemorrhage, placental abruption, premature rupture of membranes (PROM) and preterm premature rupture of membranes (PPROM < 37 gestational weeks), and preterm delivery (<37 weeks).…”

Section: Methodsmentioning

confidence: 99%

“…To account for the varying prevalence of maternal asthma rates and obstetric and neonatal complications across groups, we chose to use women of the same racial/ethnic group without asthma as the reference group for comparisons. Except where noted, odds ratios were adjusted for covariates available in the electronic medical record selected a priori based on our previous studies of obstetric and neonatal complications among women with asthma [5,14]. These covariates included maternal age (continuous), marital status (not married/married/missing), insurance (private/public/other/missing), pre-pregnancy body mass index in kg/m 2 (under: <18.5, normal: 18.5 to <25, overweight: 25 to <30, obese: 30 to <35, severely obese: ≥35), smoking (yes/no) and alcohol use (yes/no) during pregnancy, history of chronic disease (pre-pregnancy diabetes, chronic hypertension, thyroid disease, or human immunodeficiency virus), parity (nulliparous/multiparous), cesarean delivery (yes/no), and clinical site.…”

Section: Methodsmentioning

confidence: 99%

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Does maternal asthma contribute to racial/ethnic disparities in obstetrical and neonatal complications?

Flores¹,

Robledo²,

Hwang³

et al. 2015

Annals of Epidemiology

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Purpose Examine whether maternal asthma contributes to racial/ethnic differences in obstetric and neonatal complications. Methods Data on White (n=110,603), Black (n=50,284) and Hispanic (n=38,831) singleton deliveries came from the Consortium on Safe Labor. Multi-level logistic regression models, with an interaction term for asthma and race/ethnicity, estimated within-group adjusted odds ratios (aOR) for gestational diabetes, gestational hypertension, preeclampsia, placental abruption, premature rupture of membranes, preterm delivery, maternal hemorrhage, NICU admissions, small for gestational age (SGA), apnea, respiratory distress syndrome, transient tachypnea of the newborn, anemia and hyperbilirubinemia after adjustment for clinical and demographic confounders. Non-asthmatics of the same racial/ethnic group were the reference group. Results Compared to non-asthmatics, White asthmatics had increased odds of preeclampsia (aOR 1.28; 95% CI: 1.15–1.43) and maternal hemorrhage (1.14; 1.04–1.23). White and Hispanic infants were more likely to have NICU admissions (1.19; 1.11–1.28; 1.16; 1.02–1.32, respectively) and be SGA (1.11; 1.02–1.20; 1.26; 1.10–1.44, respectively) and Hispanic infants were more likely to have apnea (1.32; 1.02–1.69). Conclusions Maternal asthma did not impact most obstetric and neonatal complication risks within racial/ethnic groups. Despite their increased risk for both asthma and many complications, our findings for Black women were null. Asthma did not contribute to racial/ethnic disparities in complications.

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“…Asthma during pregnancy substantially increases risks of adverse pregnancy outcomes, including preeclampsia (↑54%), preterm birth (↑41%), SGA (↑22%), and LBW (↑46%) (Murphy et al 2011). Risks of adverse neonatal outcomes including admission to neonatal intensive care (↑12%), respiratory distress syndrome (↑9%) and transient tachypnoea of the newborn (↑10%) are also increased when the mother has asthma, even after correction for prematurity as a comorbidity (Mendola et al 2014). …”

Section: Evidence For Maternal Asthma and Allergy During Pregnancy Asmentioning

confidence: 99%

Pre-birth origins of allergy and asthma

Gatford¹,

Wooldridge

Kind

et al. 2017

Journal of Reproductive Immunology

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Highlights Key points (3-5 dot points, max 85 characters including spaces)  Prenatal exposures alter later disease risk, including for allergy  Epidemiological and experimental evidence suggests IUGR protects against allergy  Elevated methyl donor abundance in late pregnancy may predispose progeny to allergy  Maternal asthma and allergy during pregnancy predispose progeny to allergy Abstract: Allergy is a chronic disease that can develop as early as infancy, suggesting that early life factors are important in its aetiology. Variable associations between size at birth, a crude marker of the fetal environment, and allergy have been reported in humans and require comprehensive review. Associations between birth weight and allergy are however confounded in humans, and we and others have therefore begun exploring the effects of early life events on allergy in experimental models. In particular, we are using ovine models to investigate whether and how a restricted environment before birth protects against allergy, whether methyl donor availability contributes to allergic protection in IUGR, and why maternal asthma during pregnancy is associated with increased risks of allergic disease in children. We found that experimental intrauterine growth restriction (IUGR) in sheep reduced cutaneous responses to antigens in progeny, despite normal or elevated IgE responses. Furthermore, maternal methyl donor supplementation in late pregnancy partially reversed effects of experimental IUGR, consistent with the proposal that epigenetic pathways underlie some but not all effects of IUGR on allergic susceptibility. Ovine experimental allergic asthma with exacerbations reduces relative fetal size in late gestation, with some changes in immune populations in fetal thymus suggestive of increased activation. Maternal allergic asthma in mice also predisposes progeny to allergy development. In conclusion, these findings in experimental models provide direct evidence that a perturbed environment before birth alters immune system development and postnatal function, and provide opportunities to investigate underlying mechanisms and develop and evaluate interventions.

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Neonatal health of infants born to mothers with asthma

Cited by 59 publications

References 31 publications

Preterm birth and air pollution: Critical windows of exposure for women with asthma

Preterm birth and air pollution: Critical windows of exposure for women with asthma

Does maternal asthma contribute to racial/ethnic disparities in obstetrical and neonatal complications?

Pre-birth origins of allergy and asthma

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