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Bisphenol A health risk
You may have never heard of bisphenol A before, even if it has caused quite a bit of commotion in the last few years. It belongs to the ever growing army of mainly anonymous xenobiotic chemicals inhabiting your body, and bodies of about every living human being, especially those living in developed countries.
Where does it come from, and what can it do to your health? More importantly, can it hurt the youngest and most vulnerable - babies?
Those familiar with available facts think it can. The evidence is convincing enough for California lawmakers to consider restriction of bisphenol A use in baby bottles and containers. If enacted, it would be the first law of this kind in the U.S. Similar bills are introduced in about a dozen other states.
Abroad, Canada intends to ban it as a component in baby bottles, but Europe seems to be - at least officially - at ease with it, noting that their limit to acceptable daily intake for this chemical is 1/5 of that established by the FDA.
What is it that makes bisphenol A concern?
Bisphenol A is industrial chemical used for production of plastics: epoxy resins, phenol resins, polycarbonates, polyacrylates and polyesters. These materials are used in great many industrial products, including those close to home: from water bottles and food packaging, to that whitish protective coating inside metal food containers. and to dental sealants. Billions pounds of it is produced every year.
Pharmacologically, bisphenol A is a hormonally active agent, specifically, environmental estrogen (xenoestrogen) - a compound which activates cell's estrogen receptors, disrupting endocrine function of the body (there is experimental evidence suggesting that at higher exposure levels it also affects thyroid function, and has broader effect on body's hormonal function).
Since 1997, well over 100 studies and scientific research papers provided plenty of evidence that it can adversely affect experimental animals in a number of ways. The effects of early exposure to bisphenol A include increased susceptibility to some cancers, alteration of brain development and sexuality, development of insulin resistance, obesity and/or hypertension later in life.
There is no direct evidence for its effect on humans, yet. In general, primates are less efficient than rodents at detoxifying and eliminating bisphenol A (Negishi et al, 2004), which does not ease the concerns. In humans, it also has shown the ability to selectively inhibit phase I detoxification in the liver (Niwa et al, 2001). A study on 45 woman with a history of 3 or more consecutive first-trimester miscarriages found that their bisphenol A level was four times higher than in the control group (2.6 vs. 0.77μg/L, Sugiura-Ogasawara et al, 2005).
However, whenever a substance is found to have significant detrimental effect on rodents at concentrations close to those of human exposure, it is warning not to be taken lightly. And the experimental evidence clearly indicates that bisphenol A can adversely affect rodents at exposure levels
- so called reference dose - of 50 µg/kg/day.
This is why 38 scientists, including long-time bisphenol A researchers Soto and Newbold, have joined together this past year to warn lawmakers of the potential harm to human health inflicted by this particular chemical (Chapel Hill bisphenol A expert panel consensus statement: Integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure, Reproductive Toxicology journal, corresponding author F.S. vom Saal).
The statement highlights following points:
1 } human exposure to bisphenol A is widespread, being present in blood and tissues within research-indicated biologically active range in over 95% of population sampled; bisphenol A concentration in humans is significantly above the level that can be expected from exposure to known sources, at the accepted rates of its degradation/elimination by the body
2 } average level of unmetabolized bisphenol A concentration in humans (central tendency is in the 0.3-4.4μg/L range) is above circulating bisphenol A levels in experimental animals after acute exposures (2μg/L or less) that resulted in adverse health effects
3 } likewise, bisphenol A level in the fetal mouse of 25μg/kg, that produced adverse health effects in multiple experiments, is well within the range of unmetabolized bisphenol A observed in human fetal blood (prenatal and/or neonatal low-level exposure of laboratory animals caused altered development of the prostate, breast, testis, mammary glands, body size, brain structure and chemistry, and behavior)
4 } substantial neurobehavioral and reproductive effects have been observed at low-level bisphenol A exposure in adult laboratory animals as well
5 } evidence of harm by low-level exposure to bisphenol A in wildlife is qualitatively consistent with that in experimental animals
6 } affinity of bisphenol A to recently discovered hormonal receptors on the outer cellular membrane equals that of estradiol (natural body's estrogen), making invalid its classification as "weak estrogen", based on its affinity to the receptors on the cellular nuclear membrane; this offers plausible explanation for bisphenol A bio-activity at very low-levels (in vitro studies indicate that bisphenol A can disrupt both animal and human cellular function at concentrations far bellow the levels typically found in humans - effects have been reported at levels as low as 0.00023μg/L)
7 } type of adverse effect caused by bisphenol A has been observed to vary in wide range of exposure levels, and does not follow monotonous dose-response curve; traditional acute high-level exposure animal studies do not reflect continuous low-level exposure of humans, nor they address long latency periods between actual exposure - particularly during development - and adverse health effect (at which time it is irrelevant whether or not bisphenol A is actually present in the system)
8 } recent trends in human diseases correlate with adverse health effects observed in experimental animals following low-level exposure to bisphenol A, including the increase in prostate and breast cancer, uro-genital abnormalities in male babies, a decline in semen quality in men, early onset of puberty in girls, metabolic disorders including diabetes 2 and obesity, and neurobehavioral problems such as attention deficit hyperactivity disorder (ADHD).
While experimental data raises concerns related to low-level exposure to bisphenol A in both, young and adults, the emphasis is on protection during the early development - from unborn babies in mother's womb to about 3 year olds - where the threat of harm is the highest. The research indicates that
during early development - particularly the fetal stage -
health conditions caused by hormonal, enzymatic and epigenetic alterations during this early development phase can surface much later in life, seemingly unrelated to their actual cause - or contributing factor - bisphenol A.
The bad news, as the researchers point out, is that we already have in our bodies significantly higher concentrations of this chemical than those capable of inflicting adverse health effects in animal experiments. Recent CDC (U.S. Centers for Disease Control, Calafat et al. 2004) publication puts the current average urine level of bisphenol A in humans at 2.7 nanograms/milliliter (parts per billion), or 2.7µg/liter, with
93% of over 2500 participants tested having measurable levels.
Bisphenol A half-life in the body is 5.4 hours. Since the human body has limited ability of detoxifying it (mainly via sulfotransferase enzymes), most of it - approximately 2/3 - is eliminated by urine excretion. The body is generally less efficient in getting rid of its metabolites, some of which can be much more toxic than bisphenol A itself.
The half-life figure indicates that about 95% of daily intake of bisphenol A is disposed of. With the average daily urine output of 2 liters (2,000 milliliters), it indicates the overall intake average of 5.4µg/person/day. However, average urine concentrations for children (over 6) and adolescents was higher, 4.5µg and 3µg/L, respectively, indicating less efficient elimination.
Children younger than 6 have not being tested, but the trend indicates that they may be having the highest bisphenol A concentration of all.
Note that your individual value for bisphenol A half-life may differ from the average, since it is mainly determined by the efficacy of your detox system - specifically, that of glucuronic acid pathway, whose main enzyme is zinc-dependant.
The industry was quick to point out that this is still much bellow the FDA/EPA maximum acceptable intake of 50 µg/kg/day. But how sound is this criterion? It is based on studies back in 1980s where the effect of bisphenol A on rodents - specifically weight loss - was observed at the intake level of 50mg/kg/day. No other dose was used, nor other possible effects were monitored. The FDA/EPA official "safe" level for humans, established in 1993, is arrived at after applying 1/1000 safety factor.
In the meantime, a number of studies - nearly 40 - have come up with the evidence that bisphenol A has adverse health effect on rodents in concentrations much lower than 50µg/kg/day.
Abnormal cell growth resulted
at doses 20 million times lower
(Murray et al. 2001), or 2.5 nanograms/kg/day. For comparison, infants can consume up to 13 µg/kg/day of bisphenol A leaching from baby food cans and polycarbonate bottles alone - over 500 times higher exposure (it is also higher than the official acceptable exposure limit for general population in Europe).
In vitro cellular experiments, when the cells were directly exposed to the chemical, have observed significant effects of bisphenol A
down to 0.23 ppt (parts per trillion),
more than 10,000 times lower than its average urine concentration in the general population.
And where does the FDA stand on this issue? As usual, it is sympathetic to the industry's cause (got to keep the economy going). It maintains that bisphenol A is safe, and doesn't intend to re-evaluate its approval which, by the way, was based on two industry funded studies. To them, the rest of research on bisphenol A is "inconclusive", with the final argument being that we don't know what the effect on humans is without a large controlled human study.
Since no such study is going to take place in the foreseeable future, don't expect from the government to take the action and ensure that your exposure to bisphenol A is reduced to reasonably safe. Since most of your bisphenol A (BPA) exposure comes from food consumption, you can have it significantly reduced by:
• avoiding food and drink containers made with bisphenol A (polycarbonate, marked with "PC" or "7" in or near the triangular recycling symbol, as well as type "3" plasics), particularly while pregnant, as well as in feeding your infant or small child (Born Free makes BPA-free plastic baby bottles)
• avoiding canned foods (some, like most Eden Foods canned products, are BPA-free)
• opt for dental sealant type not containing this chemical
Remember, it is babies in mother's womb, infants and small children that are most vulnerable.
Of course, as important is it can be, bisphenol A is only the tip of the iceberg. Many other chemicals present in foods and the environment are endocrine disruptors, or have some other adverse health effect. They include dioxins, PCBs, BHA (food additive), large number of pesticides, other plasticizers (phthalates, chemicals used in plastic production), arsenic, cadmium, lead, mercury, and so on. They have become our xenobiotic inheritance. R