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Quoted from Living Downstream:

Meanwhile, emerging environmental research indicated that trash incinerators routinely released troubling amounts of toxic and carcinogenic pollutants, including dioxin. In addition, several studies published in 1994 had demonstrated that dioxin is harmful at far lower exposures than anyone ever suspected. Even at a few parts per trillion, dioxin was capable, it seemed, of profoundly altering biological processes. Also in the fall of 1994, the EPA released a three-thousand-page draft reassessment of dioxin and was now soliciting public commentary and reaction. Three years in the making, the study reaffirmed dioxin’s classification as a probable human carcinogen.

The draft report also announced three other findings. First, dioxin’s effects on the immune system, reproduction, and infant development are much more significant than previously thought. Second, there is no safe dose below which dioxin causes no biological effect. Third, quantities of dioxin and dioxinlike chemicals present in most people’s bodies are already at or near levels shown to cause problems in animals. Finally, the report identified incineration—of both medical waste and common household garbage—as the leading source of dioxin emissions in the United States and food (meat, dairy, and fish) as the immediate source of 95 percent of the dioxin found in the bodies of the general population.

In the fifteen years since the release of this draft report, the case against dioxin has strengthened. A known endocrine disruptor, dioxin now appears on the Stockholm Convention’s list of chemicals slated for worldwide abolition. The International Agency for Research on Cancer upgraded dioxin from a probable to a known human carcinogen in 1997. The U.S. National Toxicology Program followed suit in 2001. The most potent carcinogen ever known, dioxin is the only substance in the Toxics Release Inventory whose annual emissions are tallied in grams rather than in pounds.


Incineration is not the only source of dioxins and furans. They can also form spontaneously during the manufacture of certain pesticides—especially phenoxy herbicides and chlorophenols—and during the bleaching of paper products, for example. What all three of these processes have in common is chlorine. Dioxin is synthesized when certain types of organic matter are placed together with chlorine in a reactive environment. Such conditions are created by combinations as banal as newspapers plus plastic wrap plus fire.


Ascertaining dioxin’s contribution to human cancers is one of the more frustrating challenges for public health researchers. Because dioxin is so potent at such vanishingly small levels, exposure is expensive to measure. Because it is so widely distributed, there remain no populations to serve as unexposed controls. Because dioxin so often rides the coattails of other carcinogens, confounding factors abound.

Animal studies provide a complex set of clues. In the laboratory, dioxin is an unequivocal carcinogen. As the dioxin researcher James Huff has noted, “In every species so far exposed to TCDD [the most toxic dioxin]. . . and by every route of exposure, clear carcinogenic responses have been found.” These include cancers of the lung, mouth, nose, thyroid gland, adrenal gland, lymphatic system, and skin. Dioxin also causes liver cancer in rats and mice, but it does so more often in females. Female rats whose ovaries have been removed, however, tend not to develop liver cancer when exposed to dioxin. On the other hand, they are far more likely to succumb to lung cancer. Clearly, an organism’s own internal hormones modulate dioxin’s carcinogenic powers, but through some unclear means.

We now know that dioxin perturbs many hormone systems and can do so through multiple mechanisms. It can alter the metabolism of hormones. It can alter their transport through the bloodstream. It can increase the number of hormone receptors, thereby leaving an organism more sensitive to its own hormones. Dioxin also alters a plethora of growth factors, including vitamin A, interferon, and interleukon. Dioxin can even affect the mobilization of calcium and impact serum triglyceride levels.

These particular effects do not just vary by species, they also vary by timing of exposure. Dioxin is now understood to be a developmental toxicant as well as an all-purpose carcinogen. Experiments with lab animals show that exposures in early life can permanently alter, for example, the structure of the mammary gland. Rats exposed to dioxin before birth develop breasts with more terminal end buds remaining in adulthood. (Recall from Chapter Seven that the pesticide atrazine has a similar effect.) Rather than promptly complete their pubertal metamorphosis into lobules, the terminal end buds within the breasts of dioxin-exposed rats remain suspended in an immature state. You could say that they do not know when to put away childish things. This dawdling pace of sexual maturation widens the window of sensitivity to carcinogenic damage. And so, through this mechanism, exposure to dioxin before birth predisposes rats to breast cancer.

Steingraber, Sandra (2010-03-23). Living Downstream: An Ecologist’s Personal Investigation of Cancer and the Environment (p. 215-16, 220, 224-25). Da Capo Press. Kindle Edition.