# **_3. Lin and Luoh’s (2007) study from Taiwan (China)_**

Fortunately, there is a very large national longitudinal dataset from Taiwan (China), which permits a robust estimation of the impact of mother’s HBV status on sex ratios at birth. These data were collected for a national Hepatitis B immunization program, covering up to 90 percent of births. It was especially important to test pregnant women’s HBV status, because an additional dose of Hepatitis B immune globulin had to be given within 24 hours of birth to babies born to women who had tested positive.

Using the data collected between 1988 and 1999, Lin and Luoh (2007) were able to track the sex ratio of births to women whose HBV status was known. They found that women who were infected had only a 0.25 percent higher probability of having a son than other women. With a prevalence of hepatitis B infection as high as 15 percent in the population, this translates into an increase of only 0.16 percent in the overall sex ratio at birth, raising it from a baseline of 105 to 105.165. The sex ratio at birth for all the births in the dataset was 109, so the exercise of son preference accounts for all but a tiny part of the elevation in the overall sex ratio at birth.

Oster estimates that the prevalence of HBV among pregnant women in China is 11.24%, and that this should result in a sex ratio at birth of 1.10 (2005:Table 10). This is the basis for her estimate that HBV accounts for the bulk of excess male births in China (Oster 2005: 1201-2). However, the findings from the detailed medical dataset from Taiwan (China), indicate that she has massively overestimated the impact of maternal hepatitis B infection on the sex ratio at birth.

# **_4.   Oster’s (2007) new hypothesis_**

In response to Lin and Luoh’s (2007) study, Oster has revised the premise of her argument. She now concludes that the effect of HBV on the sex ratio at birth is driven largely by the _father’s_ HBV status, and that mother’s HBV status plays at most a much weaker role (Blumberg and Oster 2007). As in her previous paper, she uses multiple approaches to arrive at her conclusions<sup>8</sup> : “We present three pieces of evidence that this may be the case. First, using two of the original datasets on this topic we find that father’s infection is more strongly correlated with sex ratio than mother’s infection. Second, in population-level data from Taiwan we find that paternal cohort infection rates are more important that maternal cohort infection rates. Finally, we show using the IPUMS dataset that children born in the United States to men born in China are more likely to be boys, but this finding does not hold for children born to women from China.” Each of these analytical approaches raises some questions. First, she revisits the three individuallevel datasets on the basis of which Chahnazarian, Blumberg and London (1988) concluded that sex ratios at birth were elevated if either parent was an HBV carrier, and that the data did not permit them to conclude that one parent’s status was more important that the other’s. Oster selects two of these three datasets (Greece 1 and the Philippines), and runs regressions on them to show that only the father’s HBV status is significantly associated with a more masculine sex ratio at birth, not the mother’s. This conclusion is at odds with the previous analyses.

This conclusion is also at odds with the evidence from the larger study in Greece, which includes information only on _mother’s_ HBV status (Livadas et al 1979, reproduced here in Table 1). This study records a similar increase in sex ratio at birth associated with _mother’s_ HBV status as the two datasets Oster re-analyzes to conclude that elevated sex ratios at birth are related solely to _father’s_ HBV status. Unless there was a near-perfect correlation between mother’s and father’s 3