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In developed countries, sudden infant death syndrome (SIDS) is the leading cause of death in infants in their first year of life. The risk of SIDS is increased if parents smoked during pregnancy and in presence of the child. Glutathione S-transferases ( GSTs ) catalyse the conjugation of glutathione with electrophilic compounds and toxins, making them less reactive and easier to excrete. As a gene dose effect was observed for  GSTM1  and  GSTT1 , the aim of this study was to investigate whether there is a connection between homozygous or heterozygous gene deletions of  GSTM1  or  GSTT1  and the occurrence of SIDS. We found that heterozygous deletion of  GSTM1  occurred significantly more frequently in the SIDS case group compared to the control group. A homozygous deletion of  GSMT1  was slightly more frequently in the control group. A homozygous gene deletion of  GSTT1  showed no significant difference between the SIDS group and the control group. We also found that in the SIDS group, the number of victims that were exposed to cigarette smoke was significantly higher than the number of victims without cigarette smoke exposure and that the mean lifetime of children whose mothers smoked was shorter in comparison with non-smoking mothers. In SIDS cases with homozygous gene deletions of  GSTM1 , the median life span of children with tobacco smoke exposure was 60 days shorter than without smoke exposure. In conclusion, the absence of these two genes is not the only trigger for SIDS but could be a critical aspect of SIDS aetiology, particularly in SIDS cases with smoking parents.

Sudden infant death syndrome: deletions of glutathione-S-transferase genes M1 and T1 and tobacco smoke exposure