The Endocrine Society calls for increased scrutiny and centralized regulation of suspected endocrine disruptors, including BPA. The American Medical Association does the same. The Obama Administration asks Congress to draft legislation allowing greater scrutiny and regulation of chemicals, including BPA. Such consumer activism is one response to concern over scientific evidence that BPA alters normal reproductive development in laboratory animals.
Our rodent brain research has also been challenged because of key anatomical differences between the rodent and human brains. Most significantly, in humans and other primates it appears that androgens, rather than estrogens, are primarily responsible for masculinizing the hypothalamus.
Therefore, disruption of AVPV organization in rats, the argument goes, may not predict a concomitant effect in humans. Disruption within the rat AVPV does, however, clearly show that BPA has the potential to interact with developmental estrogen pathways, an effect that may impact aspects of human brain development.
Another caveat is that humans have no AVPV. Humans do have kisspeptin neurons and discrete brain regions that coordinate GnRH release. These caveats again highlight the difficulties in translating results from rodents to humans but do not discount the importance of animal work by us or others.
It is important to keep in mind that the developmental period in which steroid-sensitive organization occurs in humans happens largely during gestation rather than in the first few days of neonatal life. Thus, when exposing rats neonatally it is imperative to select BPA doses that correspond to prenatal exposure levels in humans.
It is clear that BPA exposure can disrupt pubertal timing and compromise the capacity to maintain a regular ovulatory cycle in rodents. It is likely that these defects result from the abnormal organization of the hypothalamic- pituitary-gonadal axis, the crucial neuroendocrine pathway that regulates reproductive function. Our work has found evidence for effects in the brain, but growing evidence suggests that the entire axis is vulnerable. For example, National Institutes of Health researchers have identified numerous reproductive-tract abnormalities in aged female mice exposed to BPA in utero at doses as low as 0.
We have observed cyst-like structures in rats neonatally exposed to 50 milligrams BPA per kilogram. Increased numbers of blood-filled ovarian bursae indicative of advanced reproductive age , abnormal numbers of antral follicles, irregular chromosomes and decreased corpora lutea tissues vital to a fertilized ovum have also been observed by a number of research groups following exposure to BPA during development.
BPA has also been found to induce apoptosis and cell arrest in cultured ovarian granulosa cells, suggesting that BPA may also impact the adult ovary. These studies indicate that the ovary may be a particularly sensitive target of BPA. Other laboratories have observed that gestational exposure to BPA at doses below the reference dose can result in numerous uterine abnormalities including many that commonly precede carcinogenesis , alter mammary gland development, diminish the capacity to maintain pregnancy and induce abnormalities in the prostate.
It is also important to note that a handful of studies have found no effects from BPA at all. The most recent of these, published by EPA researchers in October of , found no changes in the timing of pubertal onset, sexual behavior or fecundity among female rats after exposure to BPA during gestation and lactation.
Inconsistent results continue to plague the field and make human risk assessment extraordinarily difficult. It is not readily clear why some effects are not easily replicated by other groups. Resolving how to interpret evidence from laboratory animals, and soon, is pivotal because BPA is not the only endocrine disruptor people are exposed to. Thousands of other compounds are also suspected of having similar properties, including some plasticizers, flame- retardants, pesticides and anti-microbials.
A research group at Washington State University recently reported that they could not replicate previously published BPA effects in the mouse ovary. The concept of mixture effects is an evolving area of endocrine-disruption research.
It could have profound implications for human health if these compounds are found to be more likely to produce significant health effects collectively rather than individually. Another sobering possibility is that endocrine disruptors could have transgenerational effects. For example, there is emerging concern that the children of DES daughters referred to as DES granddaughters might also develop reproductive problems. This concern arose from laboratory data indicating that the offspring of female mice exposed in utero were more likely than unexposed control animals to develop reproductive-tract lesions.
There are not enough human data to indicate a trend for deleterious effects in DES granddaughters. But this cohort is still quite young. Continued monitoring of these women as they age will be required. The precise mechanisms through which endocrine-disrupting effects transmit to subsequent generations are not well understood, but emerging evidence indicates that epigenetic mechanisms might be primary. Epigenetic inheritance involves changes in gene expression patterns without changes in gene sequence.
Such effects include DNA methylation and histone modifications. If epigenetic modifications occur within the germ cells, transmission to subsequent generations is possible. Randy Jirtle at Duke University found evidence in agouti mice that suggests that BPA has the potential to induce epigenetic effects. Other compounds, including polychlorinated biphenyls PCBs and the fungicide vinclozolin, have been shown to produce transgenerational effects, perhaps through epigenetic mechanisms.
This newly discovered and evolving area of research has once again challenged toxicologists and introduced a novel method by which endocrine disruptors and other toxicants may affect vertebrate physiology and behavior. Given this complex context, a clear, science-based strategy for identifying, screening and regulating suspected endocrine-disrupting compounds is badly needed. Nearly 40 years after DDT, the first recognized endocrine disruptor, was banned, new chemicals in the U.
Congress created the Endocrine Disruptor Screening and Testing Advisory Committee in to recommend how the EPA should test and screen these compounds, but progress has been frustratingly slow. A list of compounds to be screened was not compiled until April of , and it included only 67 chemicals, a tiny fraction of the thousands now suspected of having endocrine-disrupting properties.
It also has not yet been determined how the screening should be conducted and which biological endpoints should be used. Figure 9. While the science is not definitive regarding health risks from BPA, some consumers already try to limit their exposure.
Among the evidence is the growth in popularity of alternatives to hard-plastic containers, including stainless steel bottles and cups for adults and children. Top photograph courtesy of Klean Kanteen. Bottom photograph courtesy of Thermos L. It remains unclear how much evidence is needed to evaluate health risks from compounds such as BPA. The FDA, using far fewer, has so far insisted there is little to no risk.
Who is right? Most of the studies used by the NTP were conducted in university laboratories. In contrast, the FDA relied mostly on data provided by industry. This schism occurred because the NTP reviewed scores of studies by academic scientists. These guidelines specify how data must be organized and deal mostly with quality assurance, but they do not necessarily assure good study design, use of appropriate controls or robust statistical analysis.
GLP studies are expensive. Thus they are nearly all conducted by private industry or contract labs, not academic labs. Although research to date is not conclusive, there certainly is sufficient evidence to warrant concern about potential long-term effects from BPA exposure. Only a handful of studies have looked at associations between BPA exposure and disease outcomes in humans, some of which have found correlations. It is not ethically sound to expose people to a suspect compound and watch what happens.
Even if it were, it would take many years for our slow-to-mature species to display any effects from the encounters. Research in animals, however, is robust. It indicates that BPA may disrupt reproductive tract development, sex-specific neuroendocrine circuitry and fertility, even at doses considered relevant for humans.
Since laboratory animals are used in other aspects of human health research, including drug development, it is reasonable that evidence obtained from them should play a central role in any comprehensive human-risk assessment for BPA. When combined with human epidemiological studies, cell-culture assays and high-throughput genomic studies, evidence from experimental animals is likely the best tool we have to make predictions about human risk.
That is especially true for the long-term consequences of early exposures during critical developmental windows. That could open doors to long-term uncertainty and discord. Nearly 40 years later, the DDT debate is not over.
Most countries banned the agricultural use of DDT by the s, but it is still used in many parts of the world to control mosquitoes, especially where malaria, a disease that kills more people than cancer, heart disease or AIDS, is endemic. Whether DDT causes disease or impairs reproductive development remains the subject of investigation and a controversial topic.
Many scientists and policy makers are skeptical that it does; others are convinced. Of course, DDT undoubtedly saved lives, and likely still does. No such case can be made for BPA. It is time to develop a clear and comprehensive strategy for assessing the potential public health consequences of endocrine disruptors such as BPA that may contribute only economic value.
Failing to do so may put future generations at unnecessary risk. Skip to main content. Login Register. Page 30 DOI: Barbara Aulicino. Bibliography Aksglaede, L. Sorensen, J. Petersen, N. Skakkebaek and A. Recent decline in age at breast development: the Copenhagen Puberty Study. Pediatrics e— Calafat, A. Kuklenyik, J. Reidy, S. Caudill, J.
Ekong and L. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Environmental Health Perspectives — Durando, M. Kass, J. Piva, C. Sonnenschein, A. Soto, E. Luque and M. Prenatal bisphenol A exposure induces preneoplastic lesions in the mammary gland in Wistar rats.
Jirtle, R. Environmental epigenomics and disease susceptibility. Nature Reviews Genetics — Joensen, U. Several studies show that BPA can negatively affect many aspects of both male and female fertility. Most studies — but not all — have observed that children born to mothers exposed to BPA at work weigh up to 0. In addition, children born to mothers with higher BPA levels were more hyperactive , anxious, and depressed. They also showed 1. Finally, BPA exposure during early life is also thought to influence prostate and breast tissue development in ways that increase cancer risk.
However, while there are ample animal studies to support this, human studies are less conclusive 29 , 30 , 31 , 32 , 33 , BPA exposure during early life may influence birth weight, hormonal development, behavior, and cancer risk in later life. However, some studies found no links between BPA and these diseases 40 , 41 , Higher BPA levels are associated with an increased risk of type 2 diabetes, high blood pressure, and heart disease. Interestingly, similar patterns have been observed in children and adolescents 48 , Although prenatal exposure to BPA is linked to increased weight gain in animals, this has not been strongly confirmed in humans 50 , BPA exposure is linked to an increased risk of obesity and waist circumference.
However, more research is needed. BPA exposure has also been linked to several other health problems, such as issues with brain, liver, thyroid, and immune function. More research is needed to confirm these findings. Although eradicating it completely may be impossible, there are some effective ways to reduce your exposure:. In particular, pregnant women may benefit from avoiding BPA — especially during the early stages of pregnancy. That said, swapping plastic containers for BPA-free ones requires very little effort for a potentially big health impact.
Three new studies link the common chemical BPA to numerous conditions, including obesity, prostate cancer, and undescended testicles. Researchers have discovered that some alternative materials designed to be an alternative to bisphenol A BPA could be leaching from plastic into…. Some foods contain ingredients and chemicals that are harmful in large amounts. Here are 7 food "toxins" that are actually concerning. New test may help experts find out if people are being exposed to dangerous levels of chemicals.
This could have effects on social behavior and anxiety after birth, says one study. Scientists believe BPA, with its estrogen-like behavior, could increase the risk of breast , prostate , and other cancers in people who experienced exposure to the chemical in the womb.
In , a group of researchers concluded that exposure to BPA before birth could have long-term effects on carcinogenesis in certain organs. This in turn could lead to the development of hormone-related cancers. In , scientists reported that BPA could interfere with the effectiveness of chemotherapy in breast cancer treatment. Research suggests there may be a link between exposure to BPA before or after birth and a higher risk of wheezing or asthma.
The CDC note that people commonly experience exposure to low levels of BPA when they consume food or water stored in containers made with the chemical. Children may also experience exposure by touching items made with BPA and then putting their hands in their mouths or by putting their mouths on the item.
Other means of exposure include having dental sealants that contain BPA and working in places that manufacture products with BPA in them. Thermal paper and carbonless paper may also contain varying levels of BPA, which gets onto the hands and fingers. Thermal paper is commonly used in boarding passes, luggage tags, and receipts. BPA may enter the system through the skin or when a person places their fingers in their mouth.
A study of 77 Harvard College students found 1 week of drinking water from polycarbonate bottles increased the levels of BPA by two-thirds. BPA features in some baby feeding bottles, so breastfeeding an infant is likely to reduce levels of BPA exposure. In , the CDC noted that there was evidence BPA affects reproduction in laboratory animals, but added that more research is necessary.
While experts recognize that BPA may be hazardous, a report about the dangers of BPA for the World Health Organization WHO points out that, in investigations, exposure tends to be higher than what it usually is in most environments. The EPA is continuing to monitor the findings but is not currently planning to recommend new guidance.
It is difficult to avoid BPA, because it is so prevalent. However, a person can try to minimize their exposure by doing the following :. They found that levels of BPA fell significantly during this time. BPA is a chemical that is present in hard plastics, including drinking water bottles and many household items.
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