Race, Genes and Preterm Delivery: Environmental Explanations
Population-level differences in outcomes can be attributable to differences in environmental exposures, differences in gene frequency or, more frequently, interaction between multiple genes and environment. Recurrent PTD contributes significantly to racial disparity in PTD, but risk of recurrence may simply represent continued exposure to environmental risk factors or biological predisposition as a result of an earlier environmental exposure. Environmental factors, particularly low socioeconomic status (SES), have been consistently linked to PTD, but existing measures of SES do not adequately capture differences by race in access to resources. In addition to household income, educational attainment and occupation, African Americans are disadvantaged relative to whites in terms of family wealth, debt levels, quality of schools, social networks, exposure to violence and environmental toxins, discrimination, differential exposure to infections, and social marginalization. Further¬more, cross-sectional measures of deprivation or stress do not adequately capture their cumulative impact on African-American health over an individual s life course. For example, childhood SES and the intrauterine environment can affect adult susceptibility to infection and metabolic function. Potentially, these early environmental factors could contribute to racial differences in prevalence and immunological response to urogential tract infections; greater prevalence of urogenital tract infections, particularly BV, represent a major contributor to racial disparity in PTD. Moreover, prepregnancy health status is an important risk factor for PTD and contributes to racial disparity in PTD.
Contextual factors may also contribute to racial disparity in PTD. For example, social networks—not individual level behavioral risk factors—primarily explain racial disparity in prevalence of urogenital tract infections. Risk of delivery of very-low (< 1,500 g)-birthweight (VLBW) infants has been linked to perceived discrimination during pregnancy; unsafe, stressful neighborhoods; and social support. Perceived discrimination along with maternal characteristics largely explained racial disparity in PTD in one study. Most studies of racial disparity in PTD have not adequately controlled for these factors.
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Comparisons of birth outcomes among African Americans, African immigrants and whites have been used to assess potential genetic effects. Mean birth-weights of African immigrant infants more closely resemble those of whites than African Americans. North African immigrants in the United States have lower rates of PTD than American or Flemish white women. However, these comparisons may be misleading. Immigrants have generally favorable birth outcomes in part because healthier women emigrate. Moreover, rates of VLBW or extreme PTD are 2-3 times higher among African or Caribbean immigrants in the United States and United Kingdom than white natives. Immigrants from sub-Saharan Africa may have higher rates of PTD than immigrants from North Africa, suggesting ethnic heterogeneity. Interestingly, racial disparity in PTD and hypertension are reportedly absent in Cuba. These findings suggest that these disparities are not immutable but are environmentally dependent.
Nongenetic mechanisms may conceivably contribute to racial disparity in intergenerational risk of PTD. According to the fetal origins of adult disease hypothesis, inadequate fetal nutrition increases the risk for subsequent cardiovascular disease and may contribute to intergenerational transmission of fetal growth restriction (FGR). Animal experiments and human observational studies suggest that intrauterine malnutrition results in endothelial dys function, reduction in nephron number and the development of hypertension. Both PTD and FGR are associated with impairment in flow-mediated, endothelial-dependent vasodilation and elevated lipoprotein(a) in adolescents and abnormal retinal vascularization in adults. Low maternal birthweight is also associated with hypertension during pregnancy and kidney failure. Thus, maternal environmental deprivation in previous generations may contribute to racial disparity in adult health and risk of PTD.
