Love Canal killed how many people? Cancer risk from environmental pollution.

Love Canal Was Supposed to Cause Cancer. How Many People Died?


Health and medicine explained.
Aug. 28 2013 5:56 AM

How Many People Were Killed by Love Canal?

The surprising statistics of environmental cancers.

Love Canal Cleanup 1978
Love Canal cleanup in 1978

Photo courtesy of EPA

In the 1890s, William T. Love, foreseeing an economic boom along the banks of the Niagara River, began excavating a canal. It would skirt past Niagara Falls, allowing boats to travel between Lake Erie and Lake Ontario. More important, the diverted water would be used to generate hydroelectric power. Drawn by a seemingly inexhaustible supply of energy, new industries would spring up. Workers would commute to modern factories from a showcase urban development he would call Model City.

Love’s plan depended, in large part, on the need for power-hungry customers to come to the electricity, which in those days was generated in a form pioneered by Thomas Edison called direct current. Direct current could not be carried very far before it faded. But around the time Love’s canal broke ground, Nikola Tesla and his employer, George Westinghouse, introduced alternating current generators and transformers. Before long, electricity could be stepped up to high voltages and transported across the country. That and the great economic panic of 1893 put an end to the Love Canal project, leaving an unfinished ditch about 3,000 feet long and 100 feet wide.


In the years around World War II, the Hooker Electrochemical Company acquired it for use as a dump, eventually disposing of some 22,000 tons of toxic waste, including carcinogens like benzene and dioxin. In 1953, the land, closed and covered with dirt, was given for a token payment of $1 to the local school board with the understanding that it was filled with chemical waste. An elementary school was built there anyway, and the city envisioned turning part of the old dump site into a park.

Land bordering the canal was sold and developed, and in the late 1970s, after a couple of years of unusually high precipitation, residents began to complain of a sickening smell. When an official from the Environmental Protection Agency came to inspect, he saw rusting barrels of waste that had found their way to the surface. Potholes were oozing waste into several backyards, and it had seeped into the basement of one home. “The odors penetrate your clothing and adhere to your footwear,” he reported. Three days later his sweater still stank. The neighborhood was evacuated, a national emergency declared, and the investigations began.

The early results were confusing. At first the EPA estimated that people living along Love Canal stood a 1 in 10 chance of getting cancer during their lives just from breathing the polluted air. But several days later the agency admitted to a mathematical error: The increased risk was actually 1 in 100 and far less for people just a few blocks away. Another EPA report found that some of the 36 residents who volunteered for tests showed signs of chromosomal damage—more than considered normal. But it was dismissed by a panel of medical experts led by Lewis Thomas, chancellor of Memorial Sloan-Kettering Cancer Center, as “inadequate” and so poorly executed that it “damaged the credibility of science.” A later study found no excess of chromosomal aberrations.

Cancer can take decades to develop, and those who continued to follow the case awaited the results of a 30-year retrospective by the New York State Department of Health.


When the study was finally released, the epidemiologists reported that the birth defect rate for children born to parents who had lived near the canal was higher than for Niagara County and the rest of the state. But they found no convincing evidence that life by the canal had given people cancer. The overall rate was actually a little lower than for the general population.

Birth defects and cancer can both arise from mutations, so why would there be signs of one without the other? It seems plausible that the dividing cells of a developing embryo would be more sensitive to disruptive influences than cells in a fully formed person. And while a single mutation might be enough to derail a developmental pathway, several hits would usually be required for a cell to become cancerous. But even after three decades, the seeming head start provided by Love Canal hadn’t been enough to produce an obvious excess of malignancies.

For many of us who grew up during the exuberant beginnings of the environmental movement of the 1970s and 1980s, that outcome was almost beyond belief. We were influenced by scathing polemics like Samuel Epstein’s The Politics of Cancer. We worried about saccharine and Red Dye No. 2, and later about Alar on apples. We were told of a modern epidemic of cancer—“the plague of the 20th century”—that was being imposed on the public by irresponsible corporations and their effluents. Food additives, pesticides and herbicides, household cleaners—all of these were said to be corrupting our DNA. We were pawns in “a grim game of chemical roulette,” Russell Train, the administrator of the EPA, warned in a story that was picked up by newspapers across the country.

Ninety percent of cancer is environmental—we heard that again and again. Some of our fears were rooted in a misunderstanding. Epidemiologists define environment very broadly to include everything that is not the direct result of heredity—smoking, eating, exercise, the bearing of children, sexual habits, any kind of behavior or cultural practice. Viruses, exposure to sunlight, radon, cosmic rays—these are all defined as environmental. There was a chance of a person getting a head start on cancer by inheriting a damaged gene. But most of the mutations that triggered a malignancy were those acquired during life. That was encouraging news for public health and prevention. But it was often misconstrued to mean that almost all cancer was brought on by pollution, pesticides, and industrial waste.


There was more to the story than semantics. In 1973, the government Surveillance, Epidemiology and End Results Program began collecting data from state cancer registries on incidence and mortality—how frequently people got cancer and how often it killed them. For years, the mainstream view had been that except for lung cancer, overall rates were holding steady. But in 1976 when the new SEER data were compared with earlier surveys by the National Cancer Institute, the number of new cases seemed to be escalating abruptly, even when the aging of the population was allowed for. This appeared to be the vindication so many people sought.

Combining two sets of statistics, compiled from different sources according to different rules, is bound to cause trouble. Early on, epidemiologists warned that the comparisons were invalid and no conclusions should be drawn—that there was no evidence of a cancer epidemic. To get a clearer idea of what the public was facing, the U.S. Office of Technology Assessment commissioned a study by Richard Doll and Richard Peto, two Oxford University epidemiologists who had made names for themselves by establishing the link between cigarettes and cancer as well as the carcinogenic effects of asbestos.

Since it was published in 1981, Doll and Peto’s “The Causes of Cancer” has become one of the most influential documents in cancer epidemiology. It concluded that most cancer, by far, is “avoidable”—though not for the reasons so many people had come to believe. In 30 percent of cancer deaths, tobacco was a cause. For diet the proportion was 35 percent, and for alcohol it was 3 percent. Some 7 percent involved “reproductive and sexual behavior,” which included the hormonal effects of delaying or forgoing the bearing of children as well as promiscuous sex. (Having multiple partners was recognized as a risk for cervical cancer, although it was not yet known that the agent was human papillomavirus.) Another 10 percent of cancer was tentatively attributed to various infections and 3 percent to “geophysical” phenomena: exposure to sunlight and the naturally occurring background radiation from soil and cosmic rays. For deaths by artificially produced carcinogens, including radioisotopes, the percentages came out very low: 4 percent from occupational exposure, 2 percent from air, water, and food pollution, 1 percent from the side effects of medical treatment (including X-rays and radiotherapy), and less than 1 percent from either industrial products like paints, plastics, and solvents or food additives. Except for lung cancer, Doll and Peto concluded, “most of the types of cancer that are common today in the United States must be due mainly to factors that have been present for a long time.”

What a hard conclusion this was to swallow. Any specific case of cancer will have multiple causes—environmental (in the broadest sense) along with hereditary dispositions and the elusive influence of bad luck. But for the public at large, chemicals spewed from factories or the polysyllabic additives found in foods were apparently only minor parts of the equation. Most telling of all, Doll and Peto found that cancer had not been increasing rapidly, as one would expect if we were being subjected to an efflorescence of newly invented assaults. The lower mortality was not because we were getting much better at curing cancer, the authors concluded, but because the number of new cases was not escalating. Once SEER became better established and the quality of data improved, they confirmed that there was no alarming rise in either incidence or mortality.


As the years have passed, no epidemic has appeared. Adjusted for the aging of the population, the statistics amassed by SEER show that death rates from cancer did rise gradually by half a percentage point a year from 1975 to 1984—smoking no doubt was a factor—and at a slower pace until 1991, but then they began decreasing modestly and have been doing so ever since. Incidence rates tell a similar story, though the picture is a bit more complex. Like death rates they gradually rose from 1975 until the early 1990s with a burst of newly reported cases from 1989 to 1992, when the rate increased by 2.8 percent a year. The biggest driver for the spike appears to have been more assiduous screening for two of the most common cancers. The number of cases of prostate cancer that were detected shot up by 16.4 percent per year before sharply dropping and breast cancer by 4.0 percent. Then incidence rates, like death rates, began their slow decline.

A 25-year retrospective on “The Causes of Cancer” still attributed 30 percent of cancer to tobacco. Obesity and lack of exercise were believed to account for 20 percent, diet for 10 to 25 percent, alcohol for 4 percent, and viruses for 3 percent. Far down on the lists are occupational exposure and pollutants.

Throughout all of this, neighborhood cancer clusters, like the one fictionalized in Erin Brockovich, continue to be reported. But in almost every instance they turn out to be statistical illusions. Of those that do not, only a rare few have been associated with an environmental contaminant. Over the decades, unusual occurrences of cancer among workers have led to the identification of some carcinogens—the link between mesothelioma and asbestos, for example, and between bladder cancer and aromatic amines (substances also found in cigarette smoke). But even occupational clusters are uncommon.

One day, trying to absorb all of this, I holed up in my office and began unpacking the most recent SEER statistics. Concentrating on overall cancer rates can smear over some interesting details, and I wondered what might be lurking underneath. The prime mover in driving down the numbers has been a decline or leveling off in what are by far the most common cancers—cancer of the prostate in men, cancer of the breast in women, and lung and colorectal cancer in both women and men. At the same time, the cancers that appear to be rising—melanoma, for example, and cancer of the pancreas, liver, kidney, and thyroid—are among the rarest. The annual incidence of pancreatic cancer is 12.1 cases per 100,000, compared with 62.6 cases for lung and bronchial. Year by year the figures fluctuate ever so slightly. With numbers so low it can be difficult to tell if the increases are real or illusory—artifacts created by better reporting and early detection.


Every cancer tells a different story. For many years lung cancer declined among men because of the delayed effects of giving up cigarettes. Women started smoking later in the century and so their rates continued to climb. Only recently have they taken a downward turn. A spike in breast cancer in the last quarter of the 20th century—including the tiny, slow-growing “stage zero” tumors that some doctors don’t think should be classified as cancer—may be explained both by better diagnosis and earlier onset of puberty. (Each menstrual cycle adds incrementally to cancer risk.) The recent improvement in the numbers may be partly because of a drop in the use of hormone replacement therapy during menopause. Rising rates of melanoma, which began long before the discovery of the ozone hole, is often attributed to the popularity of sunbathing, tanning salons, and skimpier clothing that protects less flesh from ultraviolet rays. Another reason may be international travel. People from northern climes with lighter skin are now more likely to spend time in sunnier places. What may appear to be a climb in childhood malignancies, the National Cancer Institute suggests, is probably because of better imaging technologies and the reclassification of some benign tumors as malignant. Childhood obesity may conceivably be involved.

How much easier cancer would be if it were obviously driven by chemical contaminants. Instead there is a muddle of many little influences. High among them is entropy—the natural tendency of the world toward disorder. Of the multiple mutations it takes to start a cancer there is no way to know which was caused by what. Or, in the case of spontaneous mutations—DNA copying errors—if there was a cause at all.

I imagined an army of clones, genetically identical, going through life under the same conditions in the same geographic locales. They would eat the same foods, engage in the same behaviors, and some would die of cancer by the time they were 50 or 60 while others would succumb decades later to something else. As Doll and Peto put it, “Nature and nurture affect the probability that each individual will develop cancer.” But it is luck that determines which of us really do.

Excerpted from The Cancer Chronicles by George Johnson. Copyright (c) 2013 by George Johnson. Excerpted by permission of Knopf, a division of Random House LLC. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.