June 15, 2009
Disrupting The “Endocrine Disruptor” Hypothesis
By Michael D. Shaw
In a lecture delivered on May 3, 1883, famed British scientist Baron William Thomson (Lord) Kelvin remarked that:
“I often say that when you can measure what you are speaking about, and express it in numbers, you know something about it; but when you cannot express it in numbers, your knowledge is of a meager and unsatisfactory kind; it may be the beginning of knowledge, but you have scarcely, in your thoughts, advanced to the stage of Science, whatever the matter may be.”
But, even the great Lord Kelvin could not foresee the type of intellectual, political, and social damage that might occur when fear entrepreneurs—armed with sophisticated instruments that can measure substances to extremely low levels—gain the bully pulpit. Promotion of danger based on the mere presence of a chemical, regardless of whether it is actually harmful or not, is the basis of untold government grants, questionable regulatory actions, and the banning of perfectly safe products.
At the heart of this is the so-called precautionary principle which states: “When an activity raises threats of harm to the environment or human health, precautionary measures should be taken even if some cause and effect relationships are not fully established scientifically.”
To the uninitiated, this principle may sound good, but in practice there have been virtually no demonstrated benefits to balance the well-documented failures and even catastrophes. All but the most strident Greens now agree that the banning of DDT was a tragic mistake, leading to the deaths of millions of Africans from malaria. Closer to the present, a mostly moronic Congress was quick to exploit the lead-poisoning death of young Jarnell Brown, with the patently absurd and destructive Consumer Product Safety Improvement Act—quite possibly the worst law passed in the last 50 years.
Not only were laws in place since 1978 that proscribed the lead charm that killed him, since CPSIA—incredibly—applies to ALL children’s products, ballpoint pens, books, bicycles, and countless other items, which present no conceivable hazard, are threatened. Among other catastrophes wrought by this precautionary principle based horror is the likelihood that specialized products vital to disabled youngsters could also be eliminated.
Arising from the nexus of regulatory zeal and chemophobia is the notion of “endocrine disruptors.” As you can see, the term is rather generic, and simply refers to exogenous substances that act like hormones in the endocrine system and disrupt the physiologic function of endogenous hormones. This is not necessarily a bad thing as many drugs work this way, and there are dozens of food items that can have similar effects. In fact, soy protein contains a potent disruptor called genistein, that is said to be protective against breast and prostate cancer.
The term “endocrine disruptor” first appeared with respect to how wildlife was being harmed by pesticides, but there is scant data to prove this concept.
What there is, though, is a body of literature examining the effects of various chemicals on rodents in the laboratory—usually at concentrations far greater than what would exist in the environment. However, rodents are not humans. What can we say about human exposure to these chemicals?
The rodent disruptor crew speaks of urogenital abnormalities associated with exposure to environmental endocrine disruptors such as phthalates: Decreased semen quality, increased rates of testis cancer, and hypospadias. A recently published article [Hypospadias rates in New York State are not increasing—J Urol. 2009 May;181(5):2291-4. Epub 2009 Mar 19] finds that this does not apply to humans. (Hypospadias is a developmental anomaly whereby the urinary opening on the penis is too low.)
Their conclusions? Hypospadias rates have not changed in New York State from 1992 to 2005. Combined with previous studies that demonstrate sperm counts are not declining, these data suggest that the testicular dysgenesis syndrome described in animal models may not be evident in humans.
Another recent study looked at how prenatal exposure to phthalates affects newborns, using the Brazelton Neonatal Behavioral Assessment Scale. [Prenatal phthalate exposure and performance on the neonatal behavioral assessment scale in a multiethnic birth cohort. Neurotoxicology doi:10.1016/j.neuro.2009.04.001.]
A strikingly odd finding was that higher exposure to phthalates improved the boys’ scores, while lowering the girls’ scores. However, the authors did list a number of limitations of the study, including the utility of making a single assessment of infant behavior shortly after delivery. They also noted that phthalate metabolites have short half-lives, and only a single measurement was made on the pregnant women during their third trimester. It had to be assumed that these levels would remain unchanged.
I would suggest that if one is looking at the effects of phthalates as endocrine disruptors, it would be of interest to focus on which hormone(s) are being disrupted. As it is, medical science proffers no gender-specific hormones affecting the measured parameters of attention, alertness, and movement.
In terms of methodology, the study relied on a questionnaire to garner information on demographics, medical history, and lifestyle factors on the subjects. Although the questionnaire was not reproduced in the study, many of the items were mentioned in the article, including whether they smoked, consumed alcohol, or engaged in illegal drug use during pregnancy.
As the authors admit, these—and several others—are confounding factors. Clearly, the ones I mention are important, and should have been verified by lab tests, rather than a simple yes/no answer from the patient. If lifestyle questions could explain the range of phthalate metabolite concentrations in the women, this was not discussed in the study.
In short, the study raises more questions than it answers, and surely does not advance the case for endocrine disruption in humans. Those of us who are not rodents can rest easy.