Specific Causes Of Infant Mortality Research Articles

Differential association of air pollution exposure with neonatal and postneonatal mortality in England and Wales: A cohort study.

BackgroundMany but not all studies suggest an association between air pollution exposure and infant mortality. We sought to investigate whether pollution exposure is differentially associated with all-cause neonatal or postneonatal mortality, or specific causes of infant mortality.Methods and findingsWe separately investigated the associations of exposure to particulate matter with aerodynamic diameter ≤ 10 μm (PM10), nitrogen dioxide (NO2), and sulphur dioxide (SO2) with all-cause infant, neonatal, and postneonatal mortality, and with specific causes of infant deaths in 7,984,366 live births between 2001 and 2012 in England and Wales. Overall, 51.3% of the live births were male, and there were 36,485 infant deaths (25,110 neonatal deaths and 11,375 postneonatal deaths). We adjusted for the following major confounders: deprivation, birthweight, maternal age, sex, and multiple birth. Adjusted odds ratios (95% CI; p-value) for infant deaths were significantly increased for NO2, PM10, and SO2 (1.066 [1.027, 1.107; p = 0.001], 1.044 [1.007, 1.082; p = 0.017], and 1.190 [1.146, 1.235; p < 0.001], respectively) when highest and lowest pollutant quintiles were compared; however, neonatal mortality was significantly associated with SO2 (1.207 [1.154, 1.262; p < 0.001]) but not significantly associated with NO2 and PM10 (1.044 [0.998, 1.092; p = 0.059] and 1.008 [0.966, 1.052; p = 0.702], respectively). Postneonatal mortality was significantly associated with all pollutants: NO2, 1.108 (1.038, 1.182; p < 0.001); PM10, 1.117 (1.050, 1.188; p < 0.001); and SO2, 1.147 (1.076, 1.224; p < 0.001). Whilst all were similarly associated with endocrine causes of infant deaths (NO2, 2.167 [1.539, 3.052; p < 0.001]; PM10, 1.433 [1.066, 1.926; p = 0.017]; and SO2, 1.558 [1.147, 2.116; p = 0.005]), they were differentially associated with other specific causes: NO2 and PM10 were associated with an increase in infant deaths from congenital malformations of the nervous (NO2, 1.525 [1.179, 1.974; p = 0.001]; PM10, 1.457 [1.150, 1.846; p = 0.002]) and gastrointestinal systems (NO2, 1.214 [1.006, 1.466; p = 0.043]; PM10, 1.312 [1.096, 1.571; p = 0.003]), and NO2 was also associated with deaths from malformations of the respiratory system (1.306 [1.019, 1.675; p = 0.035]). In contrast, SO2 was associated with an increase in infant deaths from perinatal causes (1.214 [1.156, 1.275; p < 0.001]) and from malformations of the circulatory system (1.172 [1.011, 1.358; p = 0.035]). A limitation of this study was that we were not able to study associations of air pollution exposure and infant mortality during the different trimesters of pregnancy. In addition, we were not able to control for all confounding factors such as maternal smoking.ConclusionsIn this study, we found that NO2, PM10, and SO2 were differentially associated with all-cause mortality and with specific causes of infant, neonatal, and postneonatal mortality.

Trends of Social Inequalities in the Specific Causes of Infant Mortality in a Nationwide Birth Cohort in Korea, 1995-2009.

The relationship between social disparity and specific causes of infant mortality has rarely been studied. The present study analyzed infant mortality trends according to the causes of death and the inequalities in specific causes of infant mortality between different parental social classes. We analyzed 8,209,836 births from the Statistics Korea between 1995 and 2009. The trends of disparity for cause-specific infant mortality according to parental education and employment were examined using the Cox proportional hazard model for the birth-year intervals of 1995–1999, 2000–2004, and 2005–2009. Adjusted hazard ratios were calculated after adjusting for infants' gender, parents' age, maternal obstetrical history, gestational age, and birth weight. An increasing trend in social inequalities in all-cause infant mortality according to paternal education was evident. Social inequalities in infant mortality were greater for “Not classified symptoms, signs and findings” (International Classification of Diseases 10th revision [ICD-10]: R00–R99) and “Injury, poisoning and of external causes” (S00–T98), particularly for “Ill-defined and unspecified causes” (R990) and “Sudden infant death syndrome (SIDS)” (R950); and increased overtime for “Not classified symptoms, signs and findings” (R00–R99), “Injury, poisoning and of external causes” (S00–T98) and “Conditions in perinatal period” (P00–P96), particularly for “SIDS” (R950) and “Respiratory distress syndrome of newborns (RDS)” (P220). The specific causes of infant mortality, in particular the “Not classified causes” (R00–R99 coded deaths) should be investigated more thoroughly to reduce inequality in health.

Socioeconomic position, health behaviors, and racial disparities in cause-specific infant mortality in Michigan, USA

ObjectivesStudies about racial disparities in infant mortality suggest that racial differences in socioeconomic position (SEP) and maternal risk behaviors explain some, but not all, excess infant mortality among Blacks relative to non-Hispanic Whites. We examined the contribution of these to disparities in specific causes of infant mortality. MethodsWe analyzed data about 2,087,191 mother–child dyads in Michigan between 1989 and 2005. First, we calculated crude Black–White infant mortality ratios independently and by specific cause of death. Second, we fit multivariable Poisson regression models of infant mortality, overall and by cause, adjusting for SEP and maternal risk behaviors. Third, Crude Black–White mortality ratios were compared to adjusted predicted probability ratios, overall and by specific cause. ResultsSEP and maternal risk behaviors explained nearly a third of the disparity in infant mortality overall, and over 25% of disparities in several specific causes including homicide, accident, sudden infant death syndrome, and respiratory distress syndrome. However, SEP and maternal risk behaviors had little influence on disparities in other specific causes, such as septicemia and congenital anomalies. ConclusionsThese findings help focus policy attention toward disparities in those specific causes of infant mortality most amenable to social and behavioral intervention, as well as research attention to disparities in specific causes unexplained by SEP and behavioral differences.

Infant mortality: The role of the macaque as a model for human disease

Factors which have been identified as the leading causes of infant mortality include birth defects, hemoglobinopathies, prematurity, and Sudden Infant Death Syndrome (SIDS). In order to further our understanding of the specific causes of infant mortality and the mechanisms by which they occur, suitable animal models will be required. Studies with nonhuman primates (specifically the macaque) have addressed malformation/functional deficit syndromes such as those associated with Fetal Alcohol Syndrome (FAS), nutritional deficiencies, and retinoid teratogenicity. These studies have provided critical information for further basic and preventive research. In addition, efforts to evaluate the safety of diagnostic ultrasound continue to aid in identifying safe methods for exposure. From a prenatal perspective, cellular transplantation has been shown to be a feasible method for treating individuals with inherited defects in utero, thereby avoiding postnatal transplantation and the associated risks. Longterm complications of prematurity have also been pursued with growth factors (i.e., epidermal growth factor) noted to play an important role in both pre- and postnatal development of the gastrointestinal tract and lung. As one of the most distressing causes of death in infancy, SIDS will require a concentrated effort to understand the basic mechanism(s) responsible for the characteristic respiratory complications. The nonhuman primate will continue to provide critical information as the model of choice for the human in determining the causes, mechanisms, and treatments for these significant causes of infant death. © 1994 Wiley-Liss, Inc.