In Swan's study, higher concentrations of metabolites of two phthalates, di(2-ethylhexyl) phthalate (DEHP), and dibutyl phthalate (DBP), were associated with less male-typical behavior in boys on a standard play questionnaire. No other phthalate metabolites measured in-utero was linked to the less-masculine behavior. Girls' play behavior was not associated with phthalate levels in their mothers, the study concluded.
Swan hypothesized that phthalates may lower fetal testosterone production during a critical window of development -- somewhere within eight to 24 weeks gestation, when the testes begin to function -- thereby altering brain sexual differentiation.
To explore the question, researchers reconnected with mothers from the SFF sample and asked them to complete a standard research questionnaire, called the Preschool Activities Inventory (PSAI), for their children ages 3 1/2 to 6 1/2 years.
The PSAI is designed to discriminate play behavior within and between the sexes, and in the past has been shown to reflect the endocrine-disrupting properties of other toxins, such as PCBs and dioxins. The PSAI addressed three aspects of play: types of toys children choose (trucks versus dolls), activities (rough-and-tumble play, for example), and child characteristics.
The final survey scores are designed to reflect sex-typical play. Higher scores meant more male-typical play and lower scores meant more female-typical play.
Researchers then examined boys play-behavior scores in relation to the concentration of phthalate metabolites in their mothers' prenatal urine samples, finding that higher concentrations of DEHP and DBP metabolites were associated with less masculine play behavior scores.
Earlier studies by Swan and others have shown that phthalate exposure during pregnancy might affect the development of genitals of both male rodents and baby boys. Scientists refer to this cluster of genital alterations as the "phthalate syndrome," and research suggests that in rodent pups, the syndrome can have adverse consequences for later sexual development.
If endocrine disrupters such as phthalates can impair genital development and hormone levels in the body, the play-behavior study noted, then a deeper examination of how these chemicals impact the brain is warranted.
Previous studies about altered brain gender focused not on the reduction of hormones like testosterone, but of natural chemicals like androstendione that were produced by the mother and which blocked the receptors of the fetus from receiving testosterone. Androstendione is produced during periods of stress. It is theorized that this stress of the mother, during the first three months of pregnancy, could irreversably alter the brain gender of the fetus. Correlations have been found between maternal stress and homosexuality of their offspring.
This new study suggests that environmental toxins can also inhibit testosterone. But they do more than that. They strengthen the argument that homosexuality is not a chosen condition but a biological one.
Homosexuals continue to be discriminated against on every level in our society. The fundamental Christians condemn it as a "sin" and quote ancient Biblical passages which also called leprosy and epilepsy the work of the devil. This needs to change. More physicians and scientists must speak out and reveal the proof.
Or have we not come that far yet?
Common Plastics Chemicals Phthalates Linked to ADHD Symptoms
A new report by Korean scientists, published by Elsevier in the November 15th issue of Biological Psychiatry, adds to the potentially alarming findings about phthalates. They measured urine phthalate concentrations and evaluated symptoms of attention-deficit/hyperactivity disorder (ADHD) using teacher-reported symptoms and computerized tests that measured attention and impulsivity.
They found a significant positive association between phthalate exposure and ADHD, meaning that the higher the concentration of phthalate metabolites in the urine, the worse the ADHD symptoms and/or test scores.
Senior author Yun-Chul Hong, MD, PhD, explained that "these data represent the first documented association between phthalate exposure and ADHD symptoms in school-aged children." John Krystal, MD, the Editor of Biological Psychiatry, also commented: "This emerging link between phthalates and symptoms of ADHD raises the concern that accidental environmental exposure to phthalates may be contributing to behavioral and cognitive problems in children. This concern calls for more definitive research."
The U.S. Centers for Disease Control and Prevention, in the Summary of their 2005 Third National Report on Human Exposure to Environmental Chemicals, state that "very limited scientific information is available on potential human health effects of phthalates at levels" found in the U.S. population. Although this study was performed in a Korean population, their levels of exposure are likely comparable to a U.S. population.
The current findings do not prove that phthalate exposure caused ADHD symptoms. However, these initial findings provide a rationale for further research on this association.
Early-Life Exposure to BPA May Affect Testis Function in Adulthood
As reported in ScienceDaily on June 22, 2010m, exposure to environmental levels of the industrial chemical bisphenol A, or BPA, in the womb and early life may cause long-lasting harm to testicular function, according to a new study conducted in animals. The results were presented June 21 at The Endocrine Society's 92nd Annual Meeting in San Diego.
"We are seeing changes in the testis function of rats after exposure to BPA levels that are lower than what the Food and Drug Administration and Environmental Protection Agency consider safe exposure levels for humans," said Benson Akingbemi, PhD, the study's lead author and an associate professor at Auburn (Ala.) University. "This is concerning because large segments of the population, including pregnant and nursing mothers, are exposed to this chemical."
Many hard plastic bottles and canned food liners contain BPA, as do some dental sealants. BPA acts in a similar manner as the female sex hormone estrogen and has been linked to female infertility. This chemical is present in placenta and is able to pass from a mother into her breast milk. In their study of the male, Akingbemi and colleagues saw harmful effects of BPA at the cellular level, specifically in Leydig cells. These cells in the testis secrete testosterone, the main sex hormone that supports male fertility. After birth, Leydig cells gradually acquire the capacity for testosterone secretion, Akingbemi explained.
The process of testosterone secretion was decreased in male offspring of female rats that received BPA during pregnancy and while nursing. The mothers were fed BPA in olive oil at a dose of either 2.5 or 25 micrograms of BPA per kilogram of body weight. Akingbemi said this is below the daily upper limit of safe exposure for humans, which federal guidelines currently put at 50 micrograms per kilogram of body weight. A control group of pregnant rats received olive oil without BPA. Male offspring, after weaning at 21 days of age, received no further exposure to BPA.
Using a combination of analytical methods, the investigators studied the development of Leydig cells in male offspring. The capacity for testosterone secretion was assessed at 21, 35 and 90 days of age. The amount of testosterone secreted per Leydig cell was found to be much lower in male offspring after early-life exposure to BPA than in offspring from control unexposed animals.
"Although BPA exposure stopped at 21 days of age, BPA's effects on Leydig cells, which were seen immediately at the end of exposure and at 35 days, remained apparent until 90 days of age, when the rats reached adulthood," Akingbemi said. "Therefore, the early life period is a sensitive window of exposure to BPA and exposure at this time may affect testis function into adulthood."
Funding from this study came in part from the Graduate Research Scholars Program of Alabama EPSCoR (Experimental Program to Stimulate Competitive Research), Tuscaloosa, Ala., and the National Institute of Environmental Health Sciences.
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