Racial disparities in infant mortality: what has birth weight got to do with it and how large is it?

Fu Fang,Erin K O'Neill,Timothy B Gage,A Gregory DiRienzo

doi:10.1186/1471-2393-10-86

Abstract

BackgroundIt has been hypothesized that birth weight is not on the causal pathway to infant mortality, at least among "normal" births (i.e. those located in the central part of the birth weight distribution), and that US racial disparities (African American versus European American) may be underestimated. Here these hypotheses are tested by examining the role of birth weight on racial disparities in infant mortality.MethodsA two-component Covariate Density Defined mixture of logistic regressions model is used to decompose racial disparities, 1) into disparities due to "normal" versus "compromised" components of the birth cohort, and 2) further decompose these components into indirect effects, which are associated with birth weight, versus direct effects, which are independent of birth weight.ResultsThe results indicate that a direct effect is responsible for the racial disparity in mortality among "normal" births. No indirect effect of birth weight is observed despite significant disparities in birth weight. Among "compromised" births, an indirect effect is responsible for the disparity, which is consistent with disparities in birth weight. However, there is also a direct effect among "compromised" births that reduces the racial disparity in mortality. This direct effect is responsible for the "pediatric paradox" and maybe due to differential fetal loss. Model-based adjustment for this effect indicates that racial disparities corrected for fetal loss could be as high as 3 or 4 fold. This estimate is higher than the observed racial disparities in infant mortality (2.1 for both sexes).ConclusionsThe results support the hypothesis that birth weight is not on the causal pathway to infant mortality among "normal" births, although birth weight could play a role among "compromised" births. The overall size of the US racial disparities in infant mortality maybe considerably underestimated in the observed data possibly due to racial disparities in fetal loss.

Highlights

It has been hypothesized that birth weight is not on the causal pathway to infant mortality, at least among “normal” births, and that US racial disparities (African American versus European American) may be underestimated
We investigate the effects of race on: (i) the logit of minimum mortality; (ii) the optimal standardized birth weight; and (iii) the particular shape of the reverse-J-shaped standardized birth weight specific mortality curve (i. e. a second possible indirect effect of race, not considered by Wilcox-Russell [2,4,5] but equivalent to the interaction of the stressor and birth weight proposed by Hernández-Diaz et al [6] as a possible alternative cause of the reverse-J shape of birth weight specific infant mortality)
The proportion of “normal” births is approximately 3% smaller and the means of both subpopulations are significantly smaller in African American births compared to European American births

Summary

Introduction

It has been hypothesized that birth weight is not on the causal pathway to infant mortality, at least among “normal” births (i.e. those located in the central part of the birth weight distribution), and that US racial disparities (African American versus European American) may be underestimated. The best developed argument, originating with the Wilcox-Russell hypothesis [2,4,5], is supported by qualitative analyses using directed acyclic graphs [6] Both of these approaches are based on simple graphical observations of the response of birth weight and birth weight specific infant mortality to exogenous stressors, such as smoking or altitude. The Wilcox-Russell hypothesis [2,4,5] suggests that in response to a stressor, the birth weight specific infant mortality curve and birth weight distribution. In this case, the reverse-J shape is entirely the result of unobserved covariates U. Wilcox and Russell [2,4,5] assume the shape of the birth weight specific mortality curve is constant

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