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Chemicals in Shampoos and Other Personal Care Damaging Our Hormones? We are what we put into and on our bodies. (Still a
truism) Scientists want to know if man-made chemicals that can interfere
with the hormonal system are responsible for plummeting sperm counts in
men in many parts of the world and for other problems such as the
dramatic increase in defects of the penis in the U.S. newborns? So far
the studies indicate that they are! Vom Saal says his research shows a chemical in
the lining of cans leaches into food in amount capable of disrupting
hormones in humans. 2002 Updated: A study published in September 2002 by a research group in the Netherlands documented associations between variations in background levels of in utero exposure to certain organochlorine chemicals and gender-specific play behavior in children (Vreugdenhil, et al. 2002). Boys with relatively higher levels of PCB exposure were less likely to engage in play behaviors typical for boys; girls more likely to engage in play behavior typical for boys. Boys with relatively higher levels of dioxin were more likely to engage in more feminine play behaviors, as were girls. These findings are especially noteworthy because the levels of exposure were not that high, but instead represented variations around background levels common in European women. Moreover, these outcomes are consistent with experiments carried out with laboratory animals examining exposure impacts on sex-specific behaviors. The same research group had recently published studies demonstrating impacts of in utero exposure on cognitive development and immune system function (Huisman, et al. 1996, Koopman-Esseboom, et al. 1996, Weisglas-Kuperus, et al. 2000). Their groundbreaking studies rest on detailed tracking of the development of a cohort of individuals beginning with measurements of the mothers' serum contamination during pregnancy, with careful attention paid to potential confounding variables. The same research group had recently published studies demonstrating impacts of in utero exposure on cognitive development and immune system function (Huisman, et al. 1996, Koopman-Esseboom, et al. 1996, Weisglas-Kuperus, et al. 2000). Their groundbreaking studies rest on detailed tracking of the development of a cohort of individuals beginning with measurements of the mothers' serum contamination during pregnancy, with careful attention paid to potential confounding variables. Traditional toxicology focuses on damage, such as cell death, mutations ,or genotoxicity, that occurs typically when cellular biochemical defense mechanisms are overwhelmed. At high exposure levels many chemicals implicated in message disruption are toxic in these traditional ways. At lower levels of exposure, however, their impacts instead involve, in essence, hijacking control of development, adding or subtracting to the body's own control signals at remarkably low levels of exposure. A vivid recent example is the discovery that a widely used herbicide, atrazine, causes tadpoles to develop into hermaphroditic adults at a level of exposure approximately 30,000 times lower than traditional toxicological work had identified as toxic to frogs (Hayes, et al. 2002). The mechanism appears to involve enhancement of aromatase conversion of testosterone to estrogen during development. Elegant theoretical and empirical work suggests that for activated signaling systems, there may be no threshold beneath which no effect occurs (Sheehan, et al. 1999). Re-examining Dosage Impacts of Many ChemicalsAnother key shift is the acknowledgment that the assumption that "the dose makes the poison" can be misleadingly simplistic, if it is used to imply that only high dose exposures induce effects. In fact, low exposure levels sometimes cause effects not seen at higher levels (e.g., vom Saal, et al. 1997, National Toxicology Program 2001, Cavieres, et al. 2002). Researchers are now intensely pursuing these "non-monotonic dose response curves" and the uncertainty about their underlying mechanisms, which likely vary from case to case. One plausible hypothesis is that at low, "physiological" levels, the contaminant interferes with developmental signaling but does not activate biochemical defenses against impacts that would be caused by higher exposures. At somewhat higher levels, these defenses are activated and the contaminant is successfully detoxified. At even higher levels, the defense mechanisms are overwhelmed by the toxicant and more traditional toxicological effects are induced. As scientific research has focused on mechanisms of message disruption, it has implicated a wide array of chemicals. This expansion has involved both ongoing identification of compounds capable of interfering with estrogen, which was the initial focus, and research broadening the range of message systems studied. Some of the most troubling discoveries about "new actors" is that they involve compounds in widespread use in consumer products, including plastic additives like phthalates and plastic monomers like bisphenol A, which leaches from polycarbonate products (e.g., Gray, et al. 2000, Masuno, et al. 2002). That is not to say that we have complete understanding of even the best known contaminants. This reality was highlighted by a study published in 2001 about DDT, in which Longnecker, et al. (2001) report a highly significant association between DDT in maternal serum and the likelihood of preterm birth. Their study used birth records and stored serum from the mid-1950s to the 1960s. They concluded that the U.S. had experienced a hitherto undetected epidemic of preterm birth during this period because of DDT use. Longnecker went further to estimate that because of the close association between preterm birth and infant mortality, up to 15 percent of infant mortality during that period may have been attributable to DDT use. Disrupting chemicals have been identified that interfere with estrogen, androgen, progesterone, thyroid, insulin and glucocorticoid signaling, among others. The mechanism does not always involve mimicking (or inhibiting) ligand-receptor binding. For example, as noted above, atrazine appears to enhance aromatase conversion of testosterone to estrogen. Interactions of Toxicants Appear CrucialSignal disruption may also intercede in steps leading to gene activation after ligand-receptor binding. This was established by in vitro experiments showing that arsenic selectively inhibits gene activation by the glucocorticoid- receptor complex after normal ligand-receptor binding and subsequent entry into the cell nucleus, at arsenic concentrations far beneath cytotoxic levels (Kaltreider, et al. 2001). While human health impacts have yet to be demonstrated via this mechanism, dysfunctions in glucocorticoid action have been linked to weight gain/loss, protein wasting, immunosuppression, insulin resistance, osteoporosis, growth retardation, and hypertension. Another important issue raised by emerging science is the powerful interactions that can occur within mixtures of chemicals, even though regulatory toxicology is conducted virtually exclusively on pure single compounds. Two results published in 2002 emphasize the importance of considering mixtures: In the first, Rajapakse, et al. (2002) demonstrated that a mixture of estrogenic compounds, each present at a level beneath that capable of producing a statistically detectable estrogenic response in an in vitro system, combined to more than double the response of the system to 17ß-estradiol. In the second, Cavieres, et al. (2002) found that a common off-the-shelf dandelion herbicide mixture strongly reduced fetal implantation rates in mice at one-seventh the concentration considered safe for its principal herbicidal component, 2,4-D, by the U.S. Environmental Protection Agency. The issue of mixtures is complicated further by interactions now known to occur between contaminants and infectious agents. Large increases in disease risk can be associated with simultaneous exposure to contaminants and infectious agents. For example, Rothman, et al. (1997) reported a >20-fold increase in relative risk to non-Hodgkin's lymphoma with combined exposure to elevated (but still background) PCBs and Epstein-Barr virus. The mechanism underlying this result is unknown, but is possibly due to well-established immune system impairment by PCBs. If this mechanism is widespread, then current estimates of morbidity and mortality due to contamination are likely to be unrealistically low. Immune system interference by a variety of contaminants is widely reported (e.g., Baccarelli, et al. 2002). Together these conceptual shifts are also challenging the adequacy of current epidemiology to guide regulatory standards. The patterns underlying these conceptual shifts-including (1) non-monotonic dose response curves; (2) windows of vulnerability during development; (3) the ubiquity of mixtures; (4) the likelihood that multiple chemicals can induce similar impacts via disruption of developmental processes; (5) the same chemical can cause different impacts depending upon when exposure occurs; (6) long latencies between exposure and manifestation of impact in a mobile population, etc.-all increase the likelihood of false negatives in epidemiology as it is currently practiced. Thus, the revolution in science that Rachel Carson stimulated raises today a series of troubling questions about whether current health standards truly protect public health. Effects of low level, background exposures are likely to be far more widespread than acknowledged, and involve many more health endpoints than traditionally considered, yet these new mechanisms of toxicity thwart the epidemiological tools now available to establish human harm. Americans Shrinking!! BEER CANS FOR THE COMPOST
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