Background Inequalities in infant mortality in England and Wales remain of concern. Patterns of risk for preterm babies (over 50% of infant deaths) are poorly understood, and may differ by cause of death and degree of prematurity. We aimed to describe ethnic and social variation in cause-specific infant mortality of preterm babies by level of prematurity, and examine the extent to which disadvantage might mediate ethnic variation, or ethnicity explain social variation.

Methods The Office for National Statistics linked birth and death registrations with other routine data for singleton live births at gestational age 24–36 weeks in England and Wales 2006–2012. Within three gestation categories (24–27, 28–31, 32–36 weeks), we fitted Poisson regression models with robust standard errors (adjusted for potential confounding by gestation week, birth year, and gender), relating ethnicity (9 groups) and/or area deprivation (IMD quintiles) to risk of infant death from congenital anomalies, immaturity-related conditions, or all other causes.

Results There were 2 56 142 births and 6480 deaths (26% from congenital anomalies, 52% immaturity-related).

Among 24–27 week births (5% of preterm babies, but 47% of those who died in infancy), infants of all minority ethnic groups had lower risk of immaturity-related death than White British, the lowest rate ratios being 0.65 (95% CI 0.51 to 0.83) for Black Caribbean, 0.76 (0.66–0.87) for Black African, and 0.76 (0.61–0.94) for Indian.

Among 32–36 week births, infants of all minority groups had higher risk of death from congenital anomalies than White British, the highest rate ratios being 4.86 (4.10–5.77) for Pakistani, 3.12 (2.28–4.28) for Bangladeshi, and 2.21 (1.71–2.87) for Black African. Risks of death from congenital anomalies and ‘other’ causes increased with disadvantage, rate ratios comparing the most with the least deprived quintile being respectively 2.01 (1.60–2.51) (attenuated to 1.54 (1.22–1.94) by adjustment for ethnicity) and 2.07 (1.57–2.73).

Except for social variation in death from congenital anomalies, adjusting disadvantage models for ethnicity, or vice versa, made little difference.

Conclusion Ethnic variation in infant mortality following preterm birth is driven by contrasting patterns of death from immaturity-related conditions in 24–27 week babies, and congenital anomalies in 32–36 week babies. Social variation is driven by deaths from congenital anomalies (perhaps in part explained by ethnicity) and ‘other’ causes. We found no evidence that ethnic variation was mediated by disadvantage. Further work is needed to establish reasons for ethnic variation in death from congenital anomalies. Future research should examine biological causes of very preterm birth.