Mortality in a cohort of men expressing the glucose-6-phosphate dehydrogenase deficiency.

The objective of this study was to test the hypothesis of a lower mortality from cancer and cardiovascular diseases among men expressing glucose-6-phosphate dehydrogenase (G6PD) deficiency. We designed a mortality study based on death certificates from January 1, 1982 through December 31, 1992 in a cohort of G6PD-deficient men. Cohort members were 1,756 men, identified as expressing the G6PD-deficient phenotype during a 1981 population screening of the G6PD polymorphism. The setting was the island of Sardinia, Italy. Outcome measures were cause-specific standardized mortality ratios (SMRs), which were computed as 100 times the observed/expected ratio, with the general Sardinian male population as the reference. Deaths from all causes were significantly less than expected due to decreased SMRs for ischemic heart disease (SMR, 28; 95% confidence interval [CI], 10 to 62), cerebrovascular disease (SMR, 22; 95% CI, 6 to 55), and liver cirrhosis (SMR, 12; 95% CI, 0 to 66), which explained 95.6% of the deficit in total mortality. All cancer mortality was close to the expectation, with a significant increase in the SMR for non-Hodgkin's lymphoma (SMR, 545; 95% CI, 147 to 1,395). A decrease in mortality from cardiovascular diseases was one of the study hypotheses, based on an earlier human report and experimental evidence. However, selection bias is also a likely explanation. Further analytic studies are warranted to confirm whether subjects expressing the G6PD-deficient phenotype are protected against ischemic heart disease and cerebrovascular disease. This cohort study is consistent with more recent case-control studies in rejecting the hypothesis of a decreased cancer risk among G6PD-deficient subjects. The observed increase in mortality from non-Hodgkin's lymphoma and decrease in mortality from liver cirrhosis were not previously reported.

Mortality of lead smelter workers with the glucose-6-phosphate dehydrogenase-deficient phenotype.

The mortality experience of 1345 male workers in a lead and zinc smelting plant was followed from 1973 to 1991. Information on the erythrocyte glucose-6-phosphate dehydrogenase (G6PD) phenotype was available for 1,222 (90.9%) cohort members, which provided the opportunity to compare the mortality experience of G6PD-deficient subjects to wild-type-G6PD coworkers with similar exposure to lead. A significant decrease in mortality was observed among the total cohort as well as among the subcohort of production and maintenance workers. Most deaths (27 of 31) and all cancer deaths occurred among production and maintenance workers. Lung cancer mortality was lower than expected. Two deaths from stomach cancer were observed versus 0.6 expected. Mortality from all causes and cancer mortality were lower among production and maintenance workers with the G6PD-deficient phenotype compared to coworkers with the wild-type phenotype. Although the low statistical power of this study prevents conclusive inference, lead smelter workers with the G6PD-deficient phenotype did not suffer adverse health outcomes in terms of mortality from all causes and cancer mortality compared to coworkers with the wild-type G6PD.