We examined the relationship between infant and maternal outcomes and asthma complicating pregnancy, using historical cohort analysis of singleton live deliveries in New Jersey hospitals between 1989 and 1992 (n = 447,963). Subject mother-infant dyads were identified from linked birth certificate and maternal and newborn hospital claims data. Women with an International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) diagnosis code (493) for asthma (n = 2,289) were compared with a fourfold larger randomly selected control sample (n = 9,156) from the remaining pool of women. After controlling for the effects of important confounding variables, maternal asthma was associated with the following adverse infant outcomes: preterm infant (odds ratio [OR] = 1.36; 95% confidence interval [CI], 1.18 to 1.55), low birth weight (OR = 1. 32; 95% CI, 1.10 to 1.58), small-for-gestational age (OR = 1.26; 95% CI, 1.10 to 1.45), congenital anomalies (OR = 1.37; 95% CI, 1.12 to 1.68), and increased infant hospital length of stay (OR = 1.44; 95% CI, 1.25 to 1.65). The adverse maternal outcomes associated with maternal asthma were: pre-eclampsia (OR = 2.18; 95% CI, 1.68 to 2. 83), placenta previa (OR = 1.71; 95% CI, 1.05 to 2.79), cesarean delivery (OR = 1.62; 95% CI, 1.46 to 1.80), and increased maternal hospital length of stay (OR = 1.86; 95% CI, 1.60 to 2.15). The results emphasize the need for maternal asthma to be added to the list of conditions that increase the risk of adverse pregnancy outcomes.

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The results of this study provide evidence that maternal asthma is a risk factor for transient tachypnea of the newborn and differences in gestational age and sex were apparent in this association. The mechanism for this association remains to be determined.

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To determine the relation between placenta previa and male sex at birth, the authors conducted two types of analysis: 1) a historical cohort analysis of singleton live births in New Jersey hospitals during 1989-1992 (N = 447,963); and 2) a meta-analysis of previously published studies on the subject. For the cohort analysis, subject mother-infant dyads were identified from linked birth certificate and maternal and infant hospital claims data. The infant's sex for mothers with an International Classification of Diseases, Ninth Revision, Clinical Modification, code of 641.0-641.1 for placenta previa (n = 2,685) was compared with infant's sex for mothers without placenta previa (n = 445,270). For the meta-analysis, seven published articles were located and summary effects were calculated using both fixed-effect and random-effects models. In the present cohort study, the male:female ratio at birth was significantly higher in women with placenta previa (1.19) than in those without placenta previa (1.05) (p<0.001). The association of placenta previa with male sex persisted when the analysis was either stratified or adjusted for the effects of maternal age, maternal parity, maternal smoking during the index pregnancy, race/ethnicity, the infant's gestational age, and the infant's birth weight. The meta-analytic results from the fixed-effect and random-effects models showed a 14% excess of placenta previa when women were carrying a viable male fetus as compared with a viable female fetus during pregnancy. The results were the same regardless of whether the present cohort study was included in the meta-analysis. In conclusion, the evidence obtained from these analyses strongly argues for an association between placenta previa and male sex at birth. The mechanism for this association remains to be determined.

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