March 2015 Science Bulletin: Phthalates reduce sex drive in women; BPA and phthalates change sex ratio of offspring; IARC appraised; and more

March 9, 2015 at 2:05 pm | Posted in News and Science Bulletins | Leave a comment
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Don’t miss our recent feature article: “Science, Innovation, Politics and Controversy: How to Resolve Disagreement in Environmental Policy

Human research

Phthalates, reproduction | Environmental exposure to di-2-ethylhexyl phthalate is associated with low interest in sexual activity in premenopausal women. Women in the highest quartile of urinary concentrations of mono-2-ethyl-5-hydroxyhexyl phthalate, a DEHP metabolite, had 2.58 (95% CI 1.33, 5.00) times the adjusted odds of reporting that they almost always or often lacked interest in sexual activity, and results were similar for mono-2-ethyl-5-oxohexyl phthalate (aOR: 2.56, 95% CI 1.32, 4.95), another DEHP metabolite. Self-reported vaginal dryness was not associated with any phthalate metabolite concentration.

Pesticides, respiratory | Early-life Exposure to Organophosphate Pesticides and Pediatric Respiratory Symptoms in the CHAMACOS Cohort. In this study, higher prenatal markers of organophosphate exposure were non-significantly associated with respiratory symptoms in the previous 12 months at 5 or 7 years of age [adjusted odds ratio (aOR) per 10-fold increase = 1.44; 95% CI: 0.98, 2.12]. This association was strongest with total dialkyl phosphate and dimethyl (DM) metabolytes from the second half of pregnancy (aOR per 10-fold increase = 1.77; 95% CI: 1.06, 2.95; and 1.61; 95% CI: 1.08, 2.39, respectively). Childhood DAP, diethyl and DM concentrations were associated with respiratory symptoms and exercise-induced coughing in the previous 12 months at 5 or 7 years of age.

BPA, phthalates, sex ratio | Couples’ urinary bisphenol A and phthalate metabolite concentrations and the secondary sex ratio. “When maternal and paternal chemical concentrations were modeled jointly, paternal BPA (RR, 0.77; 95% confidence interval [CI], 0.62-0.95) and mono-isobutyl phthalate (RR, 0.82; 95% CI, 0.67-1.00) were significantly associated with a female excess. Contrarily, maternal BPA (RR, 1.16; 95% CI, 1.03-1.31), mono-isobutyl phthalate (RR, 1.28; 95% CI, 1.06-1.54), mono-benzyl phthalate (RR, 1.31; 95% CI, 1.08-1.58), and mono-n-butyl phthalate (RR, 1.24; 95% CI, 1.01-1.51) were significantly associated with a male excess.”

Non-human, policy and other research

Developmental origins of disease #1 | Developmental origins of health and disease: a paradigm for understanding disease cause and prevention. “The evidence in support of the developmental origins of the health and disease paradigm is sufficiently robust and repeatable across species, including humans, to suggest a need for greater emphasis in the clinical area. As a result of these data, obesity, diabetes, cardiovascular morbidity, and neuropsychiatric diseases can all be considered pediatric diseases. Disease prevention must start with improved nutrition and reduced exposure to environmental chemicals during development.”

Developmental origins of disease #2 |Evolution of DOHaD: the impact of environmental health sciences. “With mounting evidence connecting early-life exposures to later-life disease, we conclude that it is critical to expand the original DOHaD concept to include environmental chemical exposures, and to continue a research agenda that emphasizes defining sensitive windows of exposure and the mechanisms that cause disease.”

Adequacy of chemical safety test methods | Assessment of health risks resulting from early-life exposures: Are current chemical toxicity testing protocols and risk assessment methods adequate? “It is clear that sensitivity to chemical exposures during early-life can be similar, higher, or lower than that of adults, and can change quickly within a short developmental timeframe. Moreover, age-related exposure differences provide an important consideration for overall susceptibility. Differential sensitivity associated with a life stage can reflect the toxicokinetic handling of a xenobiotic exposure, the toxicodynamic response, or both. Each of these is illustrated with chemical-specific examples. The adequacy of current testing protocols, proposed new tools, and risk assessment methods for systemic noncancer endpoints are reviewed in light of the potential for differential risk to infants and young children.”

Evaluating IARC | IARC Monographs: 40 Years of Evaluating Carcinogenic Hazards to Humans. “The procedures employed by IARC to assemble Working Groups of scientists from the various discipline and the techniques followed to review the literature and perform hazard assessment of various agents provide a balanced evaluation and an appropriate indication of the weight of the evidence. Some disagreement by individual scientists to some evaluations is not evidence of process failure. The review process has been modified over time and will undoubtedly be altered in the future to improve the process. Any process can in theory be improved, and we would support continued review and improvement of the IARC processes. This does not mean, however, that the current procedures are flawed.”

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