Environmental exposure to polychlorinated biphenyls and p,p\u27-DDE and sperm sex-chromosome disomy

Background: Chromosomal abnormalities contribute substantially to reproductive problems, but the role of environmental risk factors has received little attention. Objectives: We evaluated the association of polychlorinated biphenyl (PCB) and dichlorodiphenyldichloroethylene (p,p´-DDE) exposures with sperm sex-chromosome disomy. Methods: We conducted a cross-sectional study of 192 men from subfertile couples. We used multiprobe fluorescence in situ hybridization (FISH) for chromosomes X, Y, and 18 to determine XX, YY, XY, and total sex-chromosome disomy in sperm nuclei. Serum was analyzed for concentrations of 57 PCB congeners and p,p´-DDE. Poisson regression models were used to calculate incidence rate ratios (IRRs) for disomy by exposure quartiles, controlling for demographic characteristics and semen parameters. Results: The median percent disomy was 0.3 for XX and YY, 0.9 for XY, and 1.6 for total sex-chromosome disomy. We observed a significant trend of increasing IRRs for increasing quartiles of p,p´-DDE in XX, XY, and total sex-chromosome disomy, and a significant trend of increasing IRRs for increasing quartiles of PCBs for XY and total sex-chromosome disomy; however, there was a significant inverse association for XX disomy. Conclusions: Our findings suggest that exposure to p,p´-DDE may be associated with increased rates of XX, XY, and total sex-chromosome disomy, whereas exposure to PCBs may be associated with increased rates of YY, XY, and total sex-chromosome disomy. In addition, we observed an inverse association between increased exposure to PCBs and XX disomy. Further work is needed to confirm these findings

Environmental Exposure to Polychlorinated Biphenyls and p,p´-DDE and Sperm Sex-Chromosome Disomy

Background: Chromosomal abnormalities contribute substantially to reproductive problems, but the role of environmental risk factors has received little attention

Acoustic and perceptual analysis of speech adaptation to an artificial palate

The study investigated adaptation to a standard electropalatographic (EPG) practise palate in a group of eight adults (mean age=24 years). The participants read the phrase "a CVC" over four sampling conditions: prior to inserting the palate, immediately following insertion of the palate, 45 minutes after palate insertion, and 3 hours after insertion of the palate. Perceptual and acoustic analyses were conducted on the initial CV portion of the stimuli. Consonants examined included: /t/, /k/, /s/, and /f/ followed by the /i/, /a/, and /u/ vowels. Results revealed that individuals within the group were able to adapt their speech articulation to compensate for the presence of the artificial palate. Perceptually, mild consonant imprecision was observed upon insertion of the palate; however, this resolved following 45 minutes to 3 hours of adaptation. Acoustic findings indicated that the palate did not affect segment durations or vowel formant frequencies. However, a significant reduction in M 1 for /s/ persisted across the sampling periods. Overall, the results suggest that a period of between 45 minutes and 3 hours of adaptation is generally suitable for participation in EPG studies

Influence of a standard electropalatography artificial palate upon articulation

Objective: This study investigated the influence of a standard electropalatography (EPG) palate upon speech articulation in 3 normal speakers under standard EPG testing conditions. Patients and Methods: Three adult females aged 26, 31 and 34 years read the experimental phrase 'say CV again' 5 times under 3 experimental conditions: normal speech (without a palate in situ), 45 min after EPG palate insertion and 3 h after EPG palate insertion. Consonants and vowels commonly used in EPG research were studied and included /t/, /s/ and /int/ in the /i/, /a/ and /u/ vowel environments. Perceptual and acoustic analysis of the data was completed. Results: The results revealed varied patterns of adaptation across the 3 participants. Perceptual analysis suggested that 2 of the participants adapted to the presence of the palate; however, 1 did not. The presence of the palate resulted in significant changes to consonant duration for all 3 participants. Spectrally, production of /t/ was unaffected by the presence of the palate, while articulation of fricatives varied across the participants. Conclusion: Paired with a previous study examining the effects of an EPG palate upon speech articulation [McLeod S, Searl J: Am J Speech Lang Pathol 2006;15:192-206], the present data suggest that researchers and clinicians alike should be aware of the potential perturbing effects of the palate. Copyright © 2007 S. Karger AG, Base

The association between sperm sex chromosome disomy and semen concentration, motility and morphology

STUDY QUESTION: Is there an association between sex chromosome disomy and semen concentration, motility and morphology? SUMMARY ANSWER: Higher rates of XY disomy were associated with a significant increase in abnormal semen parameters, particularly low semen concentration. WHAT IS KNOWN ALREADY: Although some prior studies have shown associations between sperm chromosomal abnormalities and reduced semen quality, results of others are inconsistent. Definitive findings have been limited by small sample sizes and lack of adjustment for potential confounders. STUDY DESIGN, SIZE AND DURATION: Cross-sectional study of men from subfertile couples presenting at the Massachusetts General Hospital Fertility Clinic from January 2000 to May 2003. PARTICIPANTS/MATERIALS, SETTING, METHODS: With a sample of 192 men, multiprobe fluorescence in situ hybridization for chromosomes X, Y and 18 was used to determine XX, YY, XY and total sex chromosome disomy in sperm nuclei. Sperm concentration and motility were measured using computer-assisted sperm analysis; morphology was scored using strict criteria. Logistic regression models were used to evaluate the odds of abnormal semen parameters [as defined by World Health Organization (WHO)] as a function of sperm sex chromosome disomy. MAIN RESULTS AND THE ROLE OF CHANCE: The median percentage disomy was 0.3 for XX and YY, 0.9 for XY and 1.6 for total sex chromosome disomy. Men who had abnormalities in all three semen parameters had significantly higher median rates of XX, XY and total sex chromosome disomy than controls with normal semen parameters (0.43 versus 0.25%, 1.36 versus 0.87% and 2.37 versus 1.52%, respectively, all P< 0.05). In logistic regression models, each 0.1% increase in XY disomy was associated with a 7% increase (odds ratio: 1.07, 95% confidence interval: 1.02–1.13) in the odds of having below normal semen concentration (<20 million/ml) after adjustment for age, smoking status and abstinence time. Increases in XX, YY and total sex chromosome disomy were not associated with an increase in the odds of a man having abnormal semen parameters. In addition, autosomal chromosome disomy (1818) was not associated with abnormal semen parameters. LIMITATIONS, REASONS FOR CAUTION: A potential limitation of this study, as well as those currently in the published literature, is that it is cross-sectional. Cross-sectional analyses by nature do not lend themselves to inference about directionality for any observed associations; therefore, we cannot determine which variable is the cause and which one is the effect. Additionally, the use of WHO cutoff criteria for dichotomizing semen parameters may not fully define fertility status; however, in this study, fertility status was not an outcome we were attempting to assess. WIDER IMPLICATIONS OF THE FINDINGS: This is the largest study to date seeking to understand the association between sperm sex chromosome disomy and semen parameters, and the first to use multivariate modeling to understand this relationship. The findings are similar to those in the published literature and highlight the need for mechanistic studies to better characterize the interrelationships between sex chromosome disomy and standard indices of sperm health. STUDY FUNDING/COMPETING INTEREST(S): This work was supported by grants from NIOSH (T42 OH008416) and NIEHS (R01 ES009718, P30 ES000002 and R01 ES017457). The authors declare no competing interests. At the time this work was conducted and the initial manuscript written, MEM was affiliated with the Environmental Health Department at the Harvard School of Public Health. Currently, MEM is employed by Millennium: The Takeda Oncology Company. TRIAL REGISTRATION NUMBER: N/A