to a family which already had a daughter suffered sharply elevated mortality compared to other children. After sex-selective technology became widely available, the South Asian and South Korean data indicate that the use of this technology is strongly correlated with the sex composition of existing children<sup>11</sup> — just as in China.

It is striking that across East and South Asia all the indicators — sex ratios at birth, sex ratios of aborted fetuses, and sex ratios of child mortality — show the same pattern of manipulation of family composition by parents, consistent with strong son preference. Whether or not females “go missing” is determined by the existing sex composition of the family into which they are conceived. This suggests that cultural factors still provide the overwhelming explanation for the female deficit.

For Oster’s hypotheses to be consistent with the demographic data, women (or their husbands) would have to be especially prone to contracting hepatitis B if they had borne a daughter. Or the disease would have to somehow lead to women first bearing daughters followed by an excess of sons. Either of these scenarios would require a much more complex set of biological factors to be at work than is indicated by Oster or by the micro-studies she cites.

Is it possible that somehow hepatitis B works in these very complex ways? Lin and Luoh’s (2007) large medical dataset makes it possible to examine this issue. First, they show that the impact of maternal HBV status is fairly constant across birth orders (Figure 2). HBV+ and HBVwomen show a similar sharp rise in the sex ratio at birth by birth order. This is consistent with studies across Asia, which show that parents who have not yet borne a son have a higher probability of progressing to higher order births, and become increasingly desperate to assure that they have a son.<sup>12</sup> The fact that the HBV impact is fairly constant across birth orders suggests that this impact is unaffected by the sex composition of previous births.

But Lin and Luoh (2007: Table 6) go further to test the possibility that some complex biological factor makes women who are HBV+ more prone to bearing a son if they had previously borne girls. Their findings do not support this hypothesis. For women who have a third birth, the sex ratios at birth of HBV+ women remain marginally higher than that of HBV- women ⎯ but there is no significant _additional_ impact of HBV status on the sex ratio at birth of the third child if the previous children were all female. Table 3 summarizes the sex ratios at birth by sex composition of previous births and mother’s HBV status. It shows that women who have not yet borne a son have a much higher sex ratio of the third birth ⎯ but HBV status makes little difference to this.

# **_2.   The population-level evidence from Africa_**

Oster notes that Sub-Saharan Africa appears to offer evidence contrary to her hypothesis: “to the extent that it is possible to tell, it seems that Africa has relatively low sex ratios and relatively high HBV prevalence”. She notes that the absence of high-quality birth registration data from Africa make it difficult to use the data on sex ratios at birth. She therefore compiles data from the Demographic and Health Surveys (DHS) carried out in 18 Sub-Saharan African countries, cautioning that these survey data suffer from defects such as recall bias. She carries out some regressions on these data and concludes that “these results provide some comfort that Africa is not a particular challenge to the robustness of the HBV-sex ratio connection” (Oster 2005:1198).

But the limitations of African birth registration data apply also to many developing countries. ⎯ This is why the DHS data are widely used to obtain estimates of the sex ratio at birth including 5