From Silent Spring To Scientific Revolution
Two centuries ago, the industrial revolution began unleashing a vast array of new chemicals into the environment. For over a century, the benefits of that revolution were embraced and the side effects only rarely noted. Then in 1962, Rachel Carson published Silent Spring and sent a warning shot over the bow of unbridled progress. Now, four decades later, we are deep in the scientific revolution her work helped foment. We have begun to discover that these chemicals interfere with the systems that direct the development of plants and animals, including humans—the very stuff of life.
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It turns out that successfully bringing a healthy creature into the world—whether a human being, a mouse, a flower or a frog—depends not just on genes, but which genes are turned on and when, as the developing fetus or tadpole grows. Virtually all biological development is under the control of biochemical messaging systems that activate genes at precise moments. Normal healthy development depends on activating genetic instructions using the body's natural chemical messaging system: hormones and growth factors, among others. Interfering with these messages can cause effects ranging from disastrous birth defects to subtle functional disabilities that may not be evident until decades after exposure. Research now demonstrates that an array of chemicals can disrupt these messages without damaging the genes themselves. Scientists have begun to focus on disruption of hormonal signaling, known as endocrine disruption.
For example, a study by a research group in the Netherlands documented impacts of exposure in the womb on cognitive development and immune system function. Their groundbreaking studies rest on detailed tracking of the development of a group of individuals beginning with measurements of the mothers' contamination during pregnancy. They found that the kids with modestly higher exposures to PCBs showed delays in psychomotor development during infancy. During early childhood, they were more likely to have ear infections and chicken pox. None of the mothers had been exposed to abnormally high levels, for example through working in industry. Contamination was at levels regarded by experts as “background.”
Another example involves endometriosis, a painful and debilitating disease that affects millions of American women and forces, each year, over 100,000 hysterectomies. Evidence from experiments with monkeys and other animals now implicates dioxin as a contributing cause. Effects are seen in monkeys at dioxin levels 2- to 20-fold lower than the average levels of dioxin in American women today. Endometriosis is far more common today than 50 years ago, the typical age of onset is earlier in a woman's life now than before, and the disease has become more severe. These trends parallel increasing body burdens of dioxin.
New results like these are legion. They are forcing a series of conceptual shifts upon toxicology. Traditional toxicology focuses on drastic damage such as cell death or gene mutations that occur when organisms are exposed to massive amounts of toxins that overwhelm cellular biochemical defenses. At lower levels of exposure, however, contaminants can instead hijack control of development, adding or subtracting to the body's own control signals. 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. Elegant scientific work suggests that for these signaling systems, there may be no threshold beneath which no effect occurs.
Disrupting the messages
In fact, low exposure levels sometimes cause effects not seen at higher levels. One plausible hypothesis is that at low levels, the contaminant interferes with developmental signaling but does not activate biochemical defenses 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, obviously disastrous toxicological effects are induced.
As scientific research has focused on mechanisms of message disruption, it has implicated a wide array of chemicals. 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 compounds like bisphenol A, which leaches from polycarbonate plastic. This plastic is used in the jugs for filtered water dispensers, food containers and utensils, baby bottles, and the lining of metal food cans, such as those used for canned soups.
Another important issue is the powerful interactions that can occur within mixtures of chemicals, though toxicology, in order to establish laws and regulations, almost always studies only pure, single compounds. Two results published in 2002 emphasize the importance of chemical mixing. In the first, researchers demonstrated that a mixture of chemicals that mimic the hormone estrogen, each present at a level beneath that capable of producing a statistically detectable response, combined to more than double the response. The second study showed that a common off-the-shelf dandelion herbicide mixture strongly reduced fertility in mice at one-seventh the concentration considered safe for its main active ingredient, 2,4-D, by the EPA.
The issue of mixtures is complicated further by interactions now known to occur between contaminants and infectious diseases. Large increases in disease risk can be associated with simultaneous exposure to contaminants and germs. For example, one 1997 study reported a more than 20-fold increase in relative risk of non-Hodgkins 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 deaths caused by toxins are likely to be unrealistically low.
These findings point to conceptual shifts that challenge our current approach to regulating chemicals. The patterns underlying these conceptual shifts include:
- Lower dose does not always produce less effect;
- During development of an organism there are windows of vulnerability;
- In the real world, chemicals are not isolated and often mix together;
- Multiple chemicals can induce similar effects;
- The same chemical can cause different effects depending upon when exposure occurs;
There may be long lags between exposure and effects.
All this suggests that chemicals may have significant as-yet-undiscovered harmful effects.
We are confronting an enormous gap between what science now tells us about the links between contamination and health, and the antiquated approaches still used to safeguard public health. By completing Rachel Carson's scientific revolution, we can reinvigorate efforts to reduce our exposure to these chemicals that work so deeply into the fabric of life.
John Peterson Myers is senior advisor to the United Nations Foundation, a senior fellow at Commonweal, and co-author of Our Stolen Future. For more information see www.OurStolenFuture.org and www.protectingourhealth.org. This article was adapted from an article in San Francisco Medicine, November 2002.
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