Silent Spring: Chapter 14 Summary & Analysis

This chapter takes up the question of pesticides’ carcinogenic (cancer-causing) effects. The first awareness of environmental cancer-causing agents was in 1775 when Sir Percivall Pott made the link between scrotal cancer in chimney sweeps and the arsenic laden soot that they interacted with so much as part of their jobs. Arsenic was also found to cause cancer among copper smelters and mine workers during the early days of the industrial revolution. As the industrial era progressed, more occupational exposures to industrial chemicals were identified as cancer-causing.

In the modern era, exposure is no longer merely an occupational hazard, but rather an environmental one—we are all vulnerable wherever we go, exposed to rapidly increasing number of carcinogens. Cancer rates are rising, argues Carson – 45,000,000 Americans now living will develop cancer at some point. Children, for whom cancer was a rarity as recently as a quarter century ago, are also increasingly vulnerable, with more children dying of cancer in America than any other disease. The question is: could the pesticides we are using to try and control nature be one cause of this increase?

The circumstantial evidence is compelling. A monograph by Dr. Hueper tells the story of Reichenstein, a mining city in Silesia, Germany, where arsenic waste had accumulated near mine shafts and contaminated streams. This exposure caused disease and cancer, as has also been seen in Córdoba, Argentina, where arsenic leaches from the rocks. We may be creating the same circumstance for ourselves by using arsenic based pesticides and polluting streams. In Saxony, in Germany, arsenic fumes from smelters caused environmental degradation reminiscent of those accounts of pesticides recounted in previous chapters.

Arsenic is not the only carcinogenic pesticide, however. One chemical widely used against mites and ticks is an example of ways in which slow-moving legal processes can allow cancer-causing agents to remain in use even though danger is suspected. Although the FDA’s scientists had interpreted initial testing of the pesticide as possibly cancer-producing, the chemical’s manufacturer filed an appeal of their initial ruling of ‘zero-tolerance’ for crop residues, and the committee’s decision was changed to a tolerance of one part per million, an unenforceable level that essentially made the public into unwitting guinea pigs.

Even after the chemical’s cancer-causing effects were further confirmed by testing with lab animals two years later, it took another year of legal work before the tolerance level could be reduced back to zero in 1958 – and the agency’s ability to enforce this level is open to questions.

Dr. Hueper also rates DDT as a carcinogen, and two herbicides (IPC and CIPC) have been shown to produce skin tumors in mice. The FDA found aminotriazole, an herbicidal chemical widely used by cranberry growers, to cause thyroid cancer at any level of exposure, and subsequently seized contaminated berries. Some questioned this choice, but further testing confirmed that more than half of lab rats exposed to the chemical at a rate of 100 parts per million in their drinking water developed tumors.

15-30 years of latency may pass between exposure to a carcinogen and development of disease, so the full maturing of the threat has yet to arrive. Leukemia has a shorter latency period, and anecdotes show chemicals have a causal relation to all types of blood and lymph diseases, which are on the rise at a rate of 4-5% each year. Dr. Hargraves sees an unmistakable link between these blood diseases and environmental exposure to toxic substances.

Carson recounts a series of cases in which exposure to DDT seems to have led to the development of cancer. One housewife who sprayed repeatedly against spiders with DDT died of acute leukemia. A business man embarrassed of the roaches in his building used a 25 percent DDT concentrate to spray the basement, quickly developing internal bleeding and received 59 transfusions over the next six months. He recovered, but died nine years later after the development of leukemia. More cases from around the world support the causal link between pesticides and leukemia.

Researchers must again examine the body on a cellular level to understand cancer’s origins. Professor Otto Warburg believes that when respiration is disrupted in individual cells, which can happen as a result of pesticide exposure, the race to compensate might cause cancerous growths. Another theory suggests that disruption of chromosome replication, another effect of pesticide exposure, causes unregulated cell division, a hallmark of cancerous growth. Exposure that disrupts the liver’s normal workings can also cause estrogen to accumulate in a way that might stimulate the growth of cancer cells.

Again, Carson emphasizes that interactions between chemicals that are now omnipresent in the environment may also amplify their carcinogenic effects, and radioactive contamination could also change the nature of individual chemicals. We cannot know the full extent of these dangers with certainty, but the development of cancer in fish is an early warning sign for human health, as Dr. Hueper notes.

Dr. Hueper believes that, just as the previous generation of medical researchers found success eliminating disease-carrying pathogens and focusing on prevention, we must work to clear our environment of the carcinogens with which we are populating it on an increasing basis. This will be more effective than a magic bullet ‘cure’ for cancer. There is hope. Since we have created these carcinogens, we can also eliminate them from our lifestyles if we act collectively.