Abstract

It is known that sperm aneuploidy contributes to early pregnancy losses, and to congenital abnormalities. Although the causes are unknown, environmental contaminants are suspected. Previously published data on 90 Faroese men showed that organochlorine exposure is associated with sperm disomy. Associations based on cord blood samples from a Faroese birth cohort (n=40) was apparent, but not statistically significant. This study aims to evaluate whether a significant association can be detected with a larger sample size.Serum and semen samples were obtained from 22-year-old men (n=100) who belonged in the birth cohort and participated in Faroe Islands health studies from 2009 to 2010. Serum samples were analyzed for p,p-DDE and major PCB congeners (118, 138, 153, and 180) and adjusted for total lipids. Cord blood and age-14 serum were available and were also analyzed for p,p-DDE and PCBs. Sperm fluorescence in situ hybridization (FISH) for chromosomes X, Y, and 18 was used to determine rates of XX18, XY18, YY18, and total disomy. Multivariable adjusted Poisson models (SAS GENMOD procedure) were used to estimate the relationship between organochlorine exposure and sperm disomy outcomes. The Poisson model was fitted using disomy measures (XX18, YY18, XY18, or total sex chromosome disomy) as the outcome variable, the natural logarithm of the number of sperm counted as the offset variable, the organochlorine exposure of interest as the independent variable. Age, abstinence time, smoking status, log of sperm concentration, motility, and morphology were all potential confounders controlled for in the adjusted analysis. Incidence rate ratios (IRRs) and 95% confidence intervals were calculated for each model.Because associations between cord blood concentrations of p,p-DDE and PCBs and sperm disomy in adulthood were not consistently significant in the original 40 men, we hypothesize that the addition of 50 men to this original cohort will yield more consistent results.

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