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The endocrine system in humans and other animals has an important job. It produces the hormones that regulate the body's various processes, such as metabolism and reproduction, which are vital to the chemistry of life. One example of a hormone is insulin, which breaks down sugar. Another is adrenalin, which pumps us up so we can deal with stress or danger. Estrogens are hormones that impart female characteristics and androgens impart male characteristics.
Endocrine-active chemicals (sometimes called "endocrine disruptors") received wide publicity in 1996 with the publication of "Our Stolen Future", which dramatized the impact of accidental chemical spills and other isolated incidents on wildlife - and hypothesized that humans could also be harmed. What gave the book an added fear factor was its emphasis on potential effects on sexual development and reproduction. The book speculated that even extraordinarily low levels of some chemicals, delivered at just the wrong time, may currently be having calamitous consequences on human sexual structure, function, behavior and even identity. Some have coined a catchy phrase for such chemicals - "gender benders."
A few chemicals and some natural substances (for example, soybeans are weakly estrogenic), can impact the endocrine system to some degree. However, there is no scientific agreement on how to define or test for an endocrine-active effect. Nor is there a consensus whether human reproductive capacity in the general population has changed in recent years, let alone what may be responsible. Nevertheless, lists of alleged human endocrine disruptors continue to circulate. Given the lack of consensus on the definition and consequence of an endocrine-active effect, the relevance of these lists of alleged endocrine disruptors is in serious doubt.
The World Health Organization International Programme on Chemical Safety (WHO IPCS) conducted a global assessment of the state of the science relative to endocrine disruption. In its August 2002 report, the WHO IPCS states that "Analysis of the human data by itself, while generating concerns, has so far failed to provide firm evidence of direct causal associations between low-level (i.e., levels measured in the general population) exposure to chemicals with [endocrine disrupting effects] and adverse health outcomes." The report concludes: "studies examining [endocrine disrupting chemical]-induced effects in humans have yielded inconsistent and inconclusive results, which is responsible for the overall data being classified as weak." The report does point out, however, this classification "is not meant to downplay the potential effects of [endocrine disrupting chemicals]" and instead "highlights the need for more rigorous studies."
Phthalates are frequently referred to as endocrine disruptors, or endocrine mimics, by some anti-chemical lobbies and pressure groups, but those characterizations are highly misleading. The major phthalates in commerce today do not interfere with or mimic either the estrogen or androgen receptors when tested in laboratory animals. That is, they neither activate the male or female hormone receptors nor prevent activation by natural hormones.
High doses of some phthalates can however interfere with normal sexual development in male rodents. Sexual development in rodents happens rapidly and shortly before birth. High doses of some phthalates administered to pregnant rats shortly before they gave birth suppressed levels of testosterone, a male hormone key to sexual development in the male fetuses, and interfered with the development of male reproductive organs. However, there were also lower doses at which there were no effects, and even these "no effect doses" were far above those that any human being would be exposed to under any realistic scenario.
In a significant new study first presented at the Society of Toxicology and published in 2006, researchers found that very high doses of DEHP administered to juvenile marmoset monkeys (which are much closer to humans in both physiology and development than are rodents) from weaning to sexual maturity had no negative effects on the development of the male reproductive tract. As marmosets are primates, the research indicates that the reproductive effects observed in rodents may not be relevant to humans.
A study published in 2004 may help explain the different reactions from species to species. In the study by Kessler, et al2, female rats and marmosets were fed equivalent doses of DEHP, then tested for levels of MEHP, which is a major metabolite of DEHP. Blood levels of MEHP were as much as 7.5 times lower in the marmosets, and the total internal dose of MEHP was as much as16 times lower. In other words, one reason why primates appear to be less vulnerable to DEHP is that primates experience lower internal doses at equivalent external exposures. They simply do not adsorb the DEHP as efficiently as the rodent, nor do they convert it as efficiently to MEHP.
The Phthalate Esters Panel and the chemical industry continue to devote significant financial and human resources to further research.
1. Tomonari Y., Kurata Y., Kawasuso T., David R., Gans G., Tsuchitani M., Katoh M. Effect of di(2-ethylhexyl) phthalate (DEHP) from juvenile common marmosets. Journal of Toxicology and Environmental Health, Part A, 69:1651-1672, 2006.
2. Kessler, W., Numtip, W., Grote, K., Csanady, G., Chahoud, I., and Filser, J. (2004). Blood burden of di(2-ethylhexyl) phthalate and its primary metabolite mono(2-ethylhexyl) phthalate in pregnant and nonpregnant rats and marmosets. Toxicology and Applied Pharmacology 195:142-153.
Last Updated: June 18, 2007
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