Wide disparities in obstetric outcomes exist between women of different race/ethnicities. The prevalence of preterm birth, fetal growth restriction, fetal demise, maternal mortality, and inadequate receipt of prenatal care all vary by maternal race/ethnicity. These disparities have their roots in maternal health behaviors, genetics, the physical and social environments, and access to and quality of health care. Elimination of the health inequities because of sociocultural differences or access to or quality of health care will require a multidisciplinary approach. We aim to describe these obstetric disparities, with an eye toward potential etiologies, thereby improving our ability to target appropriate solutions.
Profound racial and ethnic disparities have been documented in many areas of health and health care. Attempts to rectify these inequities in outcomes and processes of care must begin with an accurate account of their prevalence, with some attention to potential etiologies. Unfortunately, disparities in obstetric outcomes and care have persisted over time. Here we aim to summarize these obstetric disparities and their possible origins, with the hope of driving an agenda to resolve them.
The manner in which disparities in health and health care should be defined is not always straightforward. In an argument to standardize the definition, Le Cook et al described 3 definitions of disparities in health care. In the first, proposed by the Agency for Healthcare Research and Quality, disparities are defined by the mathematical difference in means or proportions between groups, without the use of statistical models. In the second, the residual direct effect method, disparities are defined by differences that persist after accounting for all measured potential confounding variables. The last definition, preferred by the authors, is that used by the Institute of Medicine, in which disparities are seen as differences above and beyond those that can be explained by differences in health status between groups.
Thus far, in investigations into obstetric disparities, the methodologies described in the first 2 definitions have been most common. It should be a goal in the field to design studies that also seek to use the third because this method is best able to highlight those disparities that might be amenable to interventions to reduce them.
The distinction between disparities in health outcomes and disparities in health care deserve mention. Both exist in obstetrics and both will be explored here. In general, disparities in health care are thought to contribute, although not exclusively, to disparities in health outcomes.
McGinnis and colleagues proposed that population health status, as measured by premature mortality, is contributed to by 5 domains, either individually or in conjunction with one another. The domains include behavioral patterns, which they estimate account for 40% of early deaths, genetic predispositions (30%), social circumstances (15%), environmental exposures (5%), and shortfalls in medical care (10%).
We propose that disparities in health status can also be considered using this framework. In this paper, we will outline major disparities in the outcomes most clearly associated with significant morbidity and mortality and will discuss the relative contributions of each of these domains, as indicated by our review of the relevant literature. We will also examine inequalities in obstetric care, whether in access to or quality of care. Table 1 presents a summary of our findings regarding racial/ethnic disparities in these outcomes, whereas Table 2 presents a summary of the strength of the evidence for contribution of each of the above-mentioned domains to these disparities.
| Outcome | American Indian/Alaska Native | Asian/Pacific Islander | Black | Hispanic |
|---|---|---|---|---|
| Pregnancy outcomes | ||||
| Congenital abnormalities | ↔ | ↔ | ↔ | ↑ (NTDs) |
| Fetal demise | ↔ | ↔ | ↑ | ↔ |
| Preterm birth | ↑ | ↔ | ↑ | ↑ (Puerto Ricans) |
| FGR | ↔ | ↔ | ↑ | ↔ |
| Maternal outcomes | ||||
| Mortality | ↔ | ↔ | ↑ | ↔ |
| Hypertensive disorders | ↔ | ↔ | ↑ | ↔ |
| Diabetes | ↑ | ↑ | ↑ | ↑ |
| Obesity | ↑ | ↑ | ↑ | ↑ |
| Obstetric care | ||||
| Prenatal care entry after first trimester | ↑ | ↔ | ↑ | ↑ |
| 1° cesarean delivery | ↓ | ↓ | ↑ | ↔ |
| Major perineal laceration | ↔ | ↑ | ↓ | ↔ |
| Outcome | Biology | Social circumstances | Environmental exposures | Behavioral patterns | Medical care |
|---|---|---|---|---|---|
| Pregnancy outcomes | |||||
| Congenital abnormalities | B | B | C | A | B |
| Fetal demise | C | B | C | B | C |
| Preterm birth | B | A | B | B | C |
| FGR | C | B | B | A | C |
| Maternal outcomes | |||||
| Mortality | B | A | C | B | A |
| Hypertensive disorders | B | C | C | C | C |
| Diabetes | B | B | C | B | B |
| Obesity | C | A | C | A | B |
| Obstetric care | |||||
| Early prenatal care | C | B | C | A | A |
| 1° cesarean delivery | C | B | C | C | A |
| Major perineal laceration | B | C | C | C | B |
For the purposes of this discussion, we will refer mostly to the maternal race/ethnicity categories of Asian/Pacific Islanders, black, Hispanic, American Indian/Alaska Native, and white. For most comparisons, white women serve as the referent group, merely to maintain consistency with the majority of the published literature on obstetric disparities.
Disparities in obstetric outcomes
Pregnancy outcomes
Congenital abnormalities
the most consistent racial/ethnic difference in prevalence of congenital abnormalities appears to be a higher incidence of neural tube defects (NTDs), including spina bifida and anencephaly, among Hispanic women. Williams et al calculated a recent birth prevalence of spina bifida of 4.18 per 10,000 births among Hispanic women, as compared with 3.37 and 2.90 per 10,000 for non-Hispanic white and black women, respectively, similar to the findings of other studies.
In contrast, the Centers for Disease Control and Prevention (CDC) found a similar prevalence of spina bifida for Hispanic and white women. Although Hispanic women are at higher risk of NTDs in most studies, adequate intake of folic acid remains low in this group, despite the 1998 Food and Drug Administration mandate to fortify all cereal grains in the United States.
A difference in carrier frequencies of genetic polymorphisms associated with folate metabolism, among others, has been proposed as a mechanism for the increased risk of NTDs among Hispanic women, but findings have been inconsistent. Ascertainment of the true incidence of congenital abnormalities by race/ethnicity may be difficult because of known differences in rates of prenatal diagnosis among women of different backgrounds as well as differential rates of pregnancy termination for diagnosed anomalies.
Fetal demise
despite improvements in fetal death rates in the United States over time, significant racial disparities still persist. In 2004, the overall fetal death rate was 6.2 deaths per 1000 live births and fetal deaths; the rate for blacks (11.3 per 1000) was more than twice than for non-Hispanic whites (5.0 per 1000). Rates for Hispanic women, Asian/Pacific Islanders, and American Indian/Alaska Natives did not differ much from that of whites.
A review of fetal death rates for women enrolled in a large, prospective study of singleton pregnancies demonstrated an adjusted odds ratio (AOR) for fetal death less than 24 weeks’ gestation of 3.2 (95% confidence interval [CI], 2.2–4.8) for black women as compared with white women and 3.1 (95% CI, 1.5–6.2) for fetal death 24 weeks’ gestation or longer. Hispanic women and women of other races did not have fetal death rates significantly different from whites. The investigators adjusted their models for various maternal factors and pregnancy exposures, and the cohort was remarkable in that all women had to have had initiation of prenatal care in the first trimester to be eligible for inclusion.
These findings raise the possibility of contributions of unmeasured maternal social conditions and behaviors, quality of obstetric care content, and biological constructs to disparities in fetal demise.
Preterm birth
whereas congenital malformations and chromosomal disorders are the leading cause of infant mortality in the United States among most racial and ethnic groups, preterm birth/low birthweight is the most common cause of infant death for black and Puerto Rican (but not other Hispanic) women. It has been estimated that disparities in extremely preterm births are attributable for 80% of the black-white disparity in infant mortality. The overall rate of preterm birth in the United States in 2006 was 12.8%; black (18.4%) and American Indian/Alaska Native (14.1%) women have the highest risk of preterm delivery, as compared with white (11.7%), Asian/Pacific Islanders (10.9%), and Hispanic women (12.2%).
A recent investigation sought to explain racial and ethnic disparities in preterm birth using methodology akin to the residual direct effect method in a nationally representative birth sample. The author notes that in logistic regression models that account for biologic, sociodemographic, and behavioral factors in a stepwise fashion, the addition of behavioral factors (adequacy of prenatal care, pregnancy weight gain, use of prenatal vitamins, smoking and alcohol use) in the final model completely attenuates any residual increased risk of preterm birth for black women as compared with white women. This was not the case for American Indian/Alaska Native women, who had twice the odds of preterm birth as compared with white women after adjustment.
There has been increasing interest in explorations of genetic contributions to racial/ethnic disparities in preterm birth. Most have focused on identifying candidate genes involved in inflammatory pathways. A recent review of this topic summarizes the literature to date, including evidence that polymorphisms in maternal and fetal genes for tumor necrosis factor, interleukin (IL)-1, and IL-6 may be associated with an excess risk of preterm premature rupture of the membranes and spontaneous preterm birth among black women. Such genetic differences may modify the risk of preterm birth associated with genital tract infections among black women in an example of possible gene-environment interaction.
Results of studies that examine differences in adverse outcomes between foreign-born and United States-born women of the same race/ethnicity demonstrate the need to look beyond a genetic explanation for disparities in obstetrics. In 2002, the CDC reported that foreign-born women had better birth outcomes than their United States-born racial/ethnic counterparts despite later initiation of prenatal care and less education, similar to findings from other national- and state-level data: compared with their United States-born equivalents, foreign-born blacks, Asians, Hispanics, and Filipinos have lower infant mortality, low birthweight, and preterm births.
The role of social circumstances such as poverty and maternal stress has been explored as contributors to disparities in preterm birth. Poor socioeconomic conditions at the individual and neighborhood levels are associated with prematurity and may modify the effect of race on preterm birth risk. Hispanic women, who often have socioeconomic statuses similar to that of black women, on average, have notably better birth outcomes, a phenomenon often referred to as the Hispanic paradox. However, evidence exists that with acculturation comes worse birth outcomes for Hispanic women, a fact that may explain higher rates of preterm birth among Puerto Ricans, who may have had longer exposure to mainland US culture, as compared with recent immigrants from Mexico and Central America.
Maternal stress also contributes to preterm birth risk, and black and American Indian/Alaska Native women are most likely to report exposure to chronic stressors during pregnancy. The search for a biological explanation for the pathways through which stress might affect preterm birth risk has led to an extensive literature on the role of corticotropin-releasing hormone (CRH) as a potential mediator of this relationship. Whereas some studies have shown higher levels of CRH in women destined to have a preterm birth, these findings have not been consistent. It remains likely, however, that neuroendocrine pathways underlie the relationship between acute and chronic stressors on preterm birth and low birthweight risk.
An interesting line of investigation explores the role of maternal perceived racism on preterm delivery risk; most studies find that life experiences with racism, as well as living in especially segregated residential areas, increase the risk of adverse birth outcomes, a fact that may help to explain racial and ethnic disparities in these outcomes.
Fetal growth restriction (FGR)
black women are more likely to experience FGR, a significant contributor to neonatal morbidity and mortality, than are women of other races and ethnicities. Factors such as maternal prepregnancy weight and nutrition, substance abuse and exposure to cigarette smoke, and maternal health status prior to pregnancy have been shown to contribute to fetal growth. Black and American Indian/Alaska Native women are more likely to have inadequate weight gain during pregnancy; some evidence suggests that black women are more likely than others to decrease their risk of FGR by achieving adequate weight gain during pregnancy.
Black women are more likely than other groups to experience food insecurity during pregnancy; participation in such public programs as the Special Supplemental Food Program for Women, Infants, and Children may have a beneficial effect on FGR risk among women. Historical factors such as maternal low birthweight has also been shown to be a risk factor for FGR among black women but does not fully explain the disparity between groups.
Use of substances such as tobacco and alcohol during pregnancy is known to increase the risk of FGR. White women are more likely to use tobacco, and white women and American Indian/Alaska Native women more likely to use alcohol during pregnancy than are other groups. However, it appears that minority (American Indian/Alaska Native, Asian/Pacific Islander, black, and Hispanic) women may be less likely to discontinue use during pregnancy than are white women, and for smoking, third-trimester exposure may be more predictive of poor fetal growth.
Several investigators have found an association between other environmental pollutants such as polycyclic aromatic hydrocarbons and pesticides and small-for-gestational-age neonates. Racial and ethnic minorities are more likely to live and work in areas with greater exposure to such agents. The impact of several of these substances seems to be modified by race/ethnicity, having been found to contribute to growth restriction among black Americans but not Dominican Americans in studies conducted in New York City.
Authors who have found this association suggest that protective factors among Hispanic immigrants may outweigh adverse effects of environmental pollutants, as has been argued in other instances of the Hispanic paradox. As with preterm birth, social isolation and deprivation appear also to play a role in the risk of FGR.
Maternal outcomes
Maternal mortality
pregnancy-related mortality, although rare, is on the rise in the United States. In 2005, the death rates for white women was 11.7 per 100,000 live births, 9.6 for Hispanic women, and 39.2 for non-Hispanic black women. To compare, the Healthy People 2010 goal for maternal deaths is 3.3 per 100,000 live births. Tucker et al attempted to understand whether higher rates of pregnancy-related mortality among black women is due to a higher prevalence of certain high-risk conditions vs a higher risk of death from these conditions (or both). They found that black women in a national sample did not have a higher prevalence of preeclampsia/eclampsia, postpartum hemorrhage, placenta previa, or placental abruption, but for all 5 conditions, black women had a case-fatality rate 2.4-3.3 times higher than that of white women.
This case-fatality ratio accounted for the majority of the disparity in mortality. The authors were not able to comment upon differences in severity of conditions, presence of comorbidities, or timing or quality of care received but postulate that any of these might contribute to this black-white disparity. Harper and colleagues examined some of these variables in their investigation of black and white women with pregnancy-related morbidity in North Carolina.
Black women had higher degrees of hypertension and lower hemoglobin levels on admission and had presented for prenatal care later, on average, than white women. Black women were no more likely to have a chronic medical condition, were more likely to be obese and to use cocaine, and were less likely to smoke. In the cohort with obstetric hemorrhage, black women were less likely to undergo a surgical intervention, although there were no differences in medical management or the likelihood of transfusion, suggesting a similar severity of disease.
Maternal morbidity
black women are more likely to experience morbidity during pregnancy. In California, black women had an AOR for 1 or more maternal morbidities of 1.25 (95% CI, 1.23–1.27) as compared with white women. Asian and Hispanic women had lower risks of maternal morbidities as compared with white women. Asian women are at particular risk of third- and fourth-degree lacerations (AOR, 1.36; 95% CI, 1.32–1.40), considered a metric of obstetric care quality.
Black women are more likely to experience hypertensive disorders of pregnancy, some of which may be attributable to excess cases of prepregnancy hypertension. Whereas black women have the highest risks of pregnancy-related hypertension, among Asian women, Filipina, and Samoan women have risks higher than women from other subgroups, arguing for the careful and thorough collection of race/ethnicity data for the purposes of assessing maternal risk. Thus far, few data exist regarding racial differences in biological mediators of preeclampsia, such as endothelial dysfunction or responsiveness to angiotensin, to explain disparities in hypertensive disorders, but more investigation in this area is warranted. There is also evidence that paternal race/ethnicity may be associated with preeclampsia with Asian paternity associated with a reduction in the risk and racial/ethnic discordance between parents associated with a small increased risk.
Wide variations in risk of diabetes in pregnancy exist by race/ethnicity. As compared with white women, racial/ethnic minorities are at higher risk of entering pregnancy with preexisting diabetes, and Hispanic and Asian/Pacific Islander women are at particularly high risk for the development of gestational diabetes. Among Asians, women of Filipina and Native Hawaiian descent appear to be at highest risk, and data suggest that these women are more likely than white women or women of other Asian groups to have macrosomic infants in the setting of gestational diabetes. There is also evidence that pregnancies of white women fathered by Asian men are at increased risk of gestational diabetes as well, suggesting potential biologic or nutritional explanations.
Disparities similarly exist in the prevalence and severity of other maternal morbidities in pregnancy, such as asthma, connective tissue diseases, human immunodeficiency virus, genitourinary infections, and periodontal disease, with evidence that minorities, in particular black women, with these conditions fare worse in pregnancy than do their white counterparts.
Disparities in maternal obesity in pregnancy deserve special mention. Racial/ethnic minorities are at increased risk of prepregnancy overweight and obesity, and these conditions are associated with an ever-growing list of pregnancy complications, including preterm birth, fetal death, macrosomia, gestational diabetes, and cesarean delivery. Furthermore, the effects of obesity on the pregnancy and the severity of outcomes at higher body mass indices may differ by racial/ethnic group. Contributors to maternal overweight and obesity are many, including poor nutrition and physical and built environments, which are not conducive to exercise, and are often more prevalent among minority populations. The contribution of genetics and in utero exposures to later childhood and adult obesity are also an area of active investigation.
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