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http://www.bund.net/themen_und_projekte/chemie/chemie_und_gesundheit/bundschwerpunkte/bisphenol_a/babyschnuller/

Hormonell wirksames Bisphenol A besonders für Säuglinge schädlich

Säuglinge und Kleinkinder reagieren besonders empfindlich auf hormonartige Schadstoffe wie BPA. Hormone spielen eine wichtige Rolle bei der Entwicklung von Organen. Ist der Körper künstlichen hormonähnlichen Stoffen ausgesetzt, können diese das empfindliche Gleichgewicht der natürlichen Hormone stören. Die höchsten Konzentrationen an BPA wurden in den Kunststoffschildchen gefunden, die den eigentlichen Schnullersauger halten. Die Kunststoffschildchen bestanden mit einer Ausnahme aus Polycarbonat, bei dessen Herstellung BPA eingesetzt wird.

BPA wird durch Speichel aus den Schnullern gelöst

Fünf von sechs in einem Folgetest untersuchten Schnullerfabrikaten, darunter vier mit Latex-Saugern und eines mit Silikon-Saugteil, hatten bereits nach einer Stunde BPA in Mengen zwischen ein und zehn Mikrogramm pro Liter in eine speichelähnliche Salzlösung abgegeben. Lediglich aus dem mit „BPA-free“ beworbenen Schnuller des Herstellers MAM sind keine nachweisbaren Mengen ausgetreten. Das von den Herstellern vor dem Einsatz empfohlene Auskochen der Schnuller hat in den Versuchen zu einer Erhöhung der BPA-Werte geführt.

Schadstoffe gehören nicht in Schnuller

Die Hersteller wurden vom BUND noch vor Vorliegen der Einzelergebnisse in schriftlicher Form befragt, ob und in welcher Weise Bisphenol A im Produktionsprozess eingesetzt wird und wie gewährleistet wird, dass keine hormonell wirksamen Chemikalien in ihren Schnullern vorhanden sind. Einige Hersteller räumten ein, dass die Kunststoffschildchen aus Polycarbonat bestehen und daher Bisphenol A enthalten.

Hersteller müssen Produktion umstellen

Der BUND fordert die Hersteller auf, bei der Produktion der Kunststoffschilde auf Polycarbonat zu verzichten. Es ist bekannt, dass Kinder gern alles in den Mund nehmen, das gilt auch für den ganzen Schnuller. Außerdem steht das Kunststoffschildchen beim Saugen in ständiger Berührung mit den Lippen des Kindes. In diesem sensiblen Anwendungsbereich haben hormonell wirksame Schadstoffe nichts verloren. Die Firmen müssen ihre Produktion umstellen und künftig auf BPA verzichten.

Handeln müssen auch die Behörden. Der BUND fordert ein Verbot von BPA und anderen hormonartig wirksamen Chemikalien nicht nur für Schnuller und Babyflaschen, sondern für alle Kleinkinderartikel und für Produkte, die mit Lebensmitteln in Berührung kommen.

Aktuell

Mehr Informationen

BUND-Schnullertests in der Diskussion

Der Ursprung

Bereits in der Antike wurden laut Überlieferungen Tonkrüge hergestellt, die eine gewisse Ähnlichkeit zu den heutigen Babyflaschen aufzeigten.

Im 16. Jahrhundert wurden dann die Tonkrüge durch Holz- und Ledergefäßen ersetzt. Die Sauger bestanden zu dieser Zeit entweder aus Leder oder aus Baumwollstoff, bis schließlich im 17 Jahrhundert Kuhhörner Einzug erhielten.

Erst ab dem 19. Jahrhundert kamen dann mit den gegenwärtigen Babyflaschen vergleichbare Modelle auf den Markt.

Der Siegeszug der Babyflaschen wird in Zukunft wohl nur durch völlig ausbleibende Geburten zu stoppen sein. Auch in den nächsten Jahren wird es keine ernsthafte Konkurrenz für die Babyflaschen geben.

http://www.krabbelstube.org/grundausstattung/babyflaschen

http://www.ourstolenfuture.org/NewScience/lowdose/lowdose.htm

SCHLIMMER: Low dose effects of endocrine disrupting chemicals

[link to examples of low-dose studies]

Sheldon Krimsky’s book, Hormonal Chaos, describes endocrine disruption as a paradigm shift in toxicology. At the core of this shift are scientific results demonstrating that endocrine disruption has impacts at contamination levels far beneath those of traditional concern to toxicologists. Some of these levels are so low that industry has asserted the results are not reliable.

The old paradigm focused on acute toxicity. How do high levels of contamination affect health? How do they cause cancer? How do they kill directly? How do they overcome the body’s defenses, like a massive invading army overwhelming the defenders simply by brute force and large numbers?

The new paradigm recognizes that there are other ways that contamination can work. Think of how terrorists overwhelm larger forces. Instead of using the brute force of large numbers, a small number of molecules can hijack the hormonal control of development and cause intense, life long damage, undermining the immune system, eroding intelligence, diminishing reproductive capacity.

This terrorist attack on fetal development works because some chemicals act as imposters, insinuating themselves in the body’s natural hormone system that normally directs fetal development. These natural hormone signals work at very low concentrations. And the imposters do also, sometimes at levels tens of thousands of times lower than the brute force approach considered by traditional toxicology.

The implications of this new paradigm are profound. Every person living today carries measurable levels of several hundred synthetic chemicals, contaminants that did not exist prior to the 20th century. While we are fundamentally ignorant about the health impacts of most of these compounds–and profoundly so about their interactions–toxicologists had come to believe that background levels, the levels experienced by most people, the levels that are virtually unavoidable living in the world today, that those background levels were safe. This assumption of safety was allowed because scientists were considering them under the old paradigm, and with significant exceptions, they were not seeing dead bodies. The new paradigm indicates that an entire generation of science used to examine chemicals for safety was misguided, ignoring vital impacts at low levels of exposure, and likely to have given false assurances of safety.

Part of this new paradigm is also the acknowledgment that old assumptions about the nature of the relationship between dose and response may sometimes be violated. Traditional toxicology assumes that dose-response curves are always monotonic: that is, that higher doses have a greater effect than lower doses. This assumption underpins all regulatory testing: if no effect is found at high levels, then it is assumed that the contaminant is safe. It also usually assumes that there is a threshold level of exposure below which no effect occurs.

It turns out hormone systems aren’t always that simple. Sometimes high doses shut off effects that occur at lower levels. This can lead to dose response curves that are non-monotonic: low and intermediate doses produce effects that are larger than high levels. In mathematical terms, the slope of the dose response curve changes sign. The presence of non-monotonic dose response curves in endocrine disruption means that many toxicological tests have led to erroneous conclusions about safety.

Another important assumption of these regulatory approaches is that there is a threshold beneath which no effect occurs. Here, too, endocrine disrupting chemicals violate long-held, but not tested, assumptions.

What this means is that not only have we simply not tested the toxicological impacts of most chemicals, even those that have been tested have not been examined adequately. These tests were all done by beginning at high levels and working back down the dose response curve until the effect seen at high levels disappeared. Once that level of „no-effect“ is reached, testing stops, assuming a threshold and ignoring the possibility that non-monotonic effects occur at lower levels.

What are phthalates? How are they used?
Phthalates are a class of widely used industrial compounds known technically as dialkyl or alkyl aryl esters of 1,2-benzenedicarboxylic acid. There are many phthalates with many uses, and just as many toxicological properties.

Phthalates crept into widespread use over the last several decades because of their many beneficial chemical properties. Now they are ubiquitous, not just in the products in which they are intentionally used, but also as contaminants in just about anything. About a billion pounds per year are produced worldwide.

Intentional uses of phthalates include softeners of plastics, oily substances in perfumes, additives to hairsprays, lubricants and wood finishers. That new car smell, which becomes especially pungent after the car has been sitting in the sun for a few hours, is partly the pungent odor of phthalates volatilizing from a hot plastic dashboard. In the evening’s cool they then condense out of the inside air of the car to form an oily coating on the inside of the windshield.

What are the health concerns?
Much of the existing literature on phthalates‘ toxicological properties focuses on the old approach to toxicology: high level exposure for cancer endpoints, and occupational exposure leading to adult infertility. In the past several years, however, particularly led by Earl Gray’s laboratory at the US Environmental Protection Agency, attention has turned to low-dose toxicity of phthalates during crucial windows of fetal development. As these studies have advanced, they have fundamentally changed our perception of potential health risks of phthalates.
According to Hauser et al. (2006): „Phthalates are a class of multifunctional chemicals used in a variety of consumer and personal care products. Highmolecular- weight phthalates (eg, di-2-ethylhexyl phthalate –DEHP– and butylbenzyl phthalate –BBzP–) are primarily used as plasticizers in the manufacture of flexible vinyl, which is used in consumer products, flooring and wall coverings, food contact applications, and medical devices. Manufacturers use low-molecular-weight phthalates (eg, diethyl phthalate –DEP– and dibutyl phthalate –DBP-) in personal care products (eg, perfumes, lotions, cosmetics), as solvents and plasticizers for cellulose acetate, and in making lacquers, varnishes, and coatings, including those used to provide timed release in some pharmaceuticals.“

While high doses of phthalates do constitute risks in the sense of traditional toxicology, these low doses change the stakes dramatically. Gray’s work reveals that male reproductive development is acutely sensitive to some phthalates. For example, the phthalates dibutyl phthalate (DBP) and diethylhexyl phthalate (DEHP) produced dramatic changes in male sexual characteristics when exposure took place in utero, at levels far beneath those of previous toxicological concern. These changes included increases in the rates of hypospadias and other indications of demasculinization.

Enough questions about phthalates have been raised during the last few years for the National Toxicology Program, under the auspices of its recently established „Center for the Evaluation of Risks to Human Reproduction“ (CERHR), to convene a panel of independent experts in 1999 to review scientific evidence addressing developmental threats of phthalates. The panel issued a draft report in August 2000. Its conclusions are severely restricted by the fact that few of studies necessary to address fetal impacts of phthalates have been done. For a least one of the phthalates they addressed, DEHP, the panel had serious concern about health impacts. Not surprisingly, given the state of research the report’s conclusions are tentative, establishing plausible but uncertain risk. One of the key points is DEHP’s impact on developing Sertoli cells, cells in the male reproductive tract that are central to sperm formation. Damaged Sertoli cells during development lead to sperm maladies in adulthood, including low sperm count. DEHP does not cause Sertoli damage directly; damage instead is caused by a metabolite of DEHP, monoethylhexyl phthalate (MEHP).

In summer 2006, two papers upped the ante considerably on possible low-level effects of phthalates. The ranges at which Gray et al. have conducted their experiments are close to the range of common human exposure, but still somewhat above. These new papers reveal biological impacts in animals well within the range of common human exposure, and show show non-monotonic action of DEHP at environmentally-relevant levels. One examined impacts on the activity of the enzyme aromatase, which is essential for masculinizing male brains. The second experimented with DEHP’s ability to exacerbate allergic reactions to an allergen, providing a possible clue as to why allergy rates have gone up so much in the developed world. Non-monotonic dose response curves are important because they invalidate current approaches to developing health standards.

In May 2005: For the first time, researchers have identified an association between pregnant women’s exposure to phthalates and adverse effects on genital development in their male children. The pattern of genital changes seen in these baby boys is consistent with the „phthalate syndrome“ previously observed in rodents prenatally exposed to phthalates. It is also suggestive of „testicular dysgenesis syndrome,“ a human health condition proposed to be linked to exposure to endocrine-disrupting compounds. The adverse effects are seen at phthalate levels below those found in one-quarter of women in the United States, based on a nation-wide survey by the Centers for Disease Control. More…

In August 2000, Puerto Rican scientists reported on an association between exposure to DEHP and premature breast development in young girls, possibly linking phthalates to trends in puberty.

In September 2000, the US Centers for Disease Control released the first substantial assessment of phthalate exposure in the American public. Their study analyzed urine metabolite residues of seven phthalates. Levels were high for several of the compounds studied, particularly the metabolite of DBP. Of greatest concern was the discovery that in their sample, an disproportionate number of women of child-bearing age bore high levels of this metabolite. Given Gray’s data on fetal vulnerability, this is precisely the population that should minimize exposure to this anti-androgen.

In winter/spring 2002-2003, three studies linked phthalate exposure to reductions in semen quality. All were of men exposed to background, environmental levels of phthalates, not higher occupational levels. One showed DNA damage in sperm. Two others (one from the US, the other from India) found reductions in sperm quality in men with slightly elevated phthalate levels. Phthalate levels associated with the damage were well within the range experienced by many Americans.

The debate about regulation and public health protection
Over the past several years, debate has grown in the regulatory world about what to do about phthalates. Industry argues that years of phthalate use without visible harm prove product safety. Critics counter that animal studies establish plausible risk but that the relevant human epidemiological studies focused specifically on the impacts of fetal exposure simply haven’t been done. They point, moreover, to the fact that human health endpoints consistent with phthalate damage are found in animal experiments. They also point out that certain exposures, particularly those associated with children chewing on soft polyvinyl chloride toys and patients receiving intravenous medication through polyvinyl chloride equipment may lead to very high exposures. [The CDC report, above, adds to that list of high exposure concern: the fetuses of pregnant women using cosmetics containing phthalates.]

European regulators kicked off this debate when they began to explore the possibility of bans on toys intended for infants that contained DEHP. This set in motion fierce industry lobbying from the United States to head off the ban, an effort that not only proved unsuccessful ultimately in Europe, but one that was matched in the US by a call by the Consumer Products Safety Commission for a voluntary phase-out by US manufacturers, not only from pacifiers and toys but also from certain medical devices. Several large US toy manufacturers, including Disney and Mattel, made public commitments supporting the phase-out.

The debate heated up further in the US when an industry PR firm that masquerades as a public health organization, the American Council on Science and Health, put together a panel to review the safety of phthalates. Headed by retired Surgeon General C. Everett Koop, the panel ultimately issued a flawed report that concluded phthalates were safe. Their report failed to consider several key recent publications and misrepresented another, citing the latter as stating that no kidney damage was caused when in fact the research did not assess kidney damage. They committed an even more basic error, moreover, by accepting the absence of data as proof of safety. Absence of data proves only ignorance. A devastating critique of this report was published by Health Care Without Harm (a PDF file; long download on slow modems).

The American Academy of Pediatrics entered the debate in June 2003, issuing a report in Pediatrics that recommends research on phthalates effects on the fetus and infants. Their review of the literature found that no studies had directly addressed this issue, yet animal research clearly documents harm and data from the US Centers for Disease Control shows widespread exposure.

More…

http://www.ourstolenfuture.org/newscience/oncompounds/phthalates/phthalates.htm

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