Monday, April 21, 2014

Gender, precaution, and DES

H-Environment recently re-posted a 2012 roundtable review of Nancy Langston's Toxic Bodies: Hormone Disruptors and the Legacy of DES (Yale UP, 2010), with comments by Jacob Darwin Hamblin, Mark Hamilton Lytle, Frederick Rowe Davis, Thomas R. Dunlap, and Stephen Bocking, along with an author response.

DES is familiar to law students as the harmful drug that gave rise to the novel tort theory of market-share liability in a 1980 California Supreme Court case, but Langston investigates its deeper history. The drug was banned by the FDA in 1940 based on precautionary thinking, but regulators later reversed themselves and allowed the substance to be used for many purposes, leading to all kinds of harm, including cancer in the daughters of women who took the drug. This is a rich history of toxic-substance regulation, including issues of gender, the history of science, and the precautionary principle.

Lytle, for instance, writes:
Langston is persuasive in connecting the FDA’s failure to follow the precautionary principle to a set of conditions, some specific to DES and others more a consequence of a generation’s commitment to “better living through chemistry.”  One factor involved the uncertainties over contemporary definitions of toxicology. Most scientists held to the belief “the dose makes the poison.”  As a Yale website states, “All chemical substances will exhibit toxic effect given a large enough dose.  If the dose is low enough, even a highly toxic substance will cease to have harmful effect.” The problem, as Langston explains, is that DES and other endocrine disrupters violate that principle.  They are not dose dependent. In fact, they have biological effects at dose levels far below those of other toxins.  Further, the effects do not correlate to an individual’s size but more to age. Exposed fetuses and infants face far higher risk than adults.  Finally, the effects often occur long after the initial exposure, so that affected fetuses may not face cancer or reproductive problems until puberty. 
Other uncertainties complicated matters further. Regulators do not treat evidence of harmful effects in animals as proof of risk to humans. Heavy drug company lobbying reinforced that disconnect.  Confusion existed about the difference in impact of synthetics and their natural counterparts.  Estrogens abound in nature. So why should synthetic versions have a harmful impact when natural ones did not?  Additionally, the benefits of using synthetic chemicals are realized collectively and obviously. Feeding DES to cattle increased the supply and lowered the cost of meat. Harm, in contrast, is often experienced privately, belatedly, and indirectly.  Affected individuals are often unaware that they are members of an aggrieved class rather than creatures of personal misfortune.  Only when researchers recognize a pattern do they connect the dots.

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