Do you think a small dose of poison won’t hurt you? Think again.

In our previous post we told our readers about the strategies used by opponents of government regulation to prevent or delay regulation by undermining the science that informs us of environmental and health risks.  In this post, we will focus on the inadequacy of pesticide regulation in the US and the arguments used to justify inadequate regulation.

Paracelsus coined the adage "the dose makes the poison" in the 16th Century
Paracelsus coined the adage “the dose makes the poison” in the 16th Century

Pesticide regulation in the US—like all regulation of chemicals—is based on an assumption that there is a threshold of exposure below which the chemical is safe.  This assumption is often summarized as “the dose makes the poison.”  This old adage originates with a Renaissance medic who died in 1541 and it was employed at the dawn of the nuclear era to reassure the public that they were not being harmed by radiation.  Since radiation occurs naturally in the environment, some low level of exposure is assumed to be harmless.  (1)

But can we assume that the same is true of pesticides?  Does every pesticide have some threshold dose below which it is harmless?  There are many reasons why we cannot assume that there are safe levels of exposure to pesticides.

Bioaccumulation and Biomagnification

BiomagnificationMany chemicals accumulate in our bodies throughout our lives. Researchers at Brown University tested the blood of over 3,000 women between the ages of 16-49 for levels of mercury, lead, and PCBs. These three chemicals are known to harm brain development of fetuses and babies. The sample was designed to represent the national population of 134.4 million women of childbearing age. Here’s what they found:

  • “Nearly 23 percent of American women of childbearing age met or exceeded the median blood levels for all three chemical pollutants [combined].” (2)
  • “As women grew older, their risk of exceeding the median blood level in two or more of these pollutants grew exponentially to the point where women aged 30 to 39 had 12 times greater risk and women aged 40-49 [born before these chemicals were banned] had a risk 30 times greater than those women aged 16 to 19.(2)
  • The chemicals that accumulate in a woman’s body do not stop there. They are passed from one generation to the next in mother’s milk and across the placenta to her unborn child.  If we stopped all new discharges today and cleaned up all the PCBs already in the environment, “it would take six generations…until PCBs would no longer be detectable in the bodies of our offspring.” (3)
  • “Fish and alcohol consumption also raised the risk of having higher blood levels. Women who ate fish more than once a week during the prior 30 days had 4.5 times the risk of exceeding the median in two or more of these pollutants.” (2)

PCB  is an organochlorine (organic–carbon-based–chemicals that contain one or more chlorine atoms), as are all products derived from chlorine, such as polyvinyl chloride (PVC) and some pesticides, such as DDT.  Organochlorines accumulate in the fatty tissue of living things (bioaccumulation), magnifying in concentration as they are eaten by their predators (biomagnification).   Animals at the top of the food chain—such as humans—therefore receive larger doses of these chemicals than animals at the bottom of the food chain.

Some chemicals are not easily metabolized by our bodies and many persist in the environment for long periods of time, which contributes to the cumulative effect of each individual exposure:  “The increased stability of many organochlorines makes them more resistant to the body’s metabolic processes, so they are retained in the body for longer, may accumulate to higher and higher concentrations over time, and will cause more severe toxic effects for a longer period of time than if they were more easily metabolized.” (3)

In other words, a single dose of a chemical may not be harmful, but the accumulation of many doses from a variety of sources over a long period of time is much more likely to be harmful. 

Multiple exposure sources

Even if there were some safe dose of a particular chemical, we should assume that we are also exposed to multiple sources of that chemical, of which we may be unaware.  Taking organochlorines as an example of chemicals known to be toxic and to accumulate, if we are exposed to an organochlorine pesticide, we might also be exposed to organochlorine by-products of pulp paper manufacturers, and/or dry cleaning processes, and/or hazardous wastes generated by incinerators, and/or the PVC plumbing in our homes, and/or detergents and water disinfectants, etc.

Many of these chemicals are airborne and are found at high concentrations far from where they were applied:  “Airborne deposition of atrazine [herbicide] into the Great Lakes has become so significant that there is now about 36,000 kilograms of the pesticide in Lake Superior water…the bulk of organochlorine pesticides and other persistent pollutants that enter the waters of the Great Lakes come from as far away as the southeastern United States and Latin America.” (3)  These chemicals are volatized from where they were discharged, they travel on atmospheric currents and are deposited by rain and snow in colder regions where they stay.  Polar regions are the ultimate sink for persistent organochlorines, where they are far more persistent than in warmer climates, e.g., atrazine has a half life of 60 days at room temperature, but does not degrade at all below 43° F.

Mixture of glyphosate and aminopyralid sprayed on ivy in Glen Canyon Park, San Francisco
Mixture of glyphosate and aminopyralid sprayed on ivy in Glen Canyon Park, San Francisco

There are over 80,000 chemicals on the market of which only a small fraction have been tested and there are thousands more that are formed as accidental by-products, such as dioxins. These chemicals interact in unknown and unpredictable ways about which little is known: “Less than 0.25 percent of studies have evaluated the effects of mixtures of more than two chemicals.” (3)  Even if there were some safe level of exposure to a single chemical, that would tell us nothing about the synergistic (multiplicative or exponential effect by which the whole is greater than the sum of its parts) or additive effects of the multiple chemicals to which we are exposed.  A recent study by an international team of 174 scientists at leading research institutions reported that a “cocktail” of common chemicals found at exposure levels in the environment today can trigger the cellular mutations that result in cancer.

Limitations of testing

In the small minority of cases in which a chemical has been tested for toxicity, that test is only as accurate as the test protocol/test parameters/test procedures, etc.  There are many methodological limits of toxicological analysis:

  • Tests are conducted on laboratory animals in which the dose is limited to a single chemical. As we said before, in the real world, humans and other animals are subjected to many chemicals simultaneously in doses that are unknown and unknowable, because little testing is done of contamination in the environment.
  • Tests are done for relatively short periods of time, compared to the long lives of humans during which chemicals accumulate in our bodies.
  • The chemical threshold deemed “safe” is not the dose at which no adverse affect occurred. It is only the dose at which no adverse affect was observed:  “Subclinical affects—reduced fertility, compromised immune systems, and reduced intelligence, for example—are not observed not because they have not occurred but because they are seldom sought.” (3) In other words, the testing regimen does not test for many potential health problems.
  • The testing regimen also is limited to certain species and certain stages of development. For example, bees are the only species of insect on which pesticide tests are required and they are only tested at the adult stage.  Bee keepers will tell you that larvae stages of bee development are far more vulnerable to pesticides than adult bees, yet no tests are required on that stage of development.  Bees are probably less vulnerable to pesticides than caterpillars which eat vegetation, but caterpillars are not tested.  If caterpillars are killed, there are no moths and butterflies.
  • The test is only as accurate as the analytical tool. The test may not be sensitive enough to detect injury.  The history of lead regulation is an illustration of the evolving science of toxicology testing.  Lead poisoning was first detected in the 1920s among workers exposed to lead.  The first established threshold for lead exposure was 80 micrograms of lead per deciliter of blood.  In the 1960s Australian physicians reported a connection between lead levels in children and lead in household paint.  Industries with an economic interest in the issue organized a defense of their products, which prevented further regulation until the late 1970s when the threshold was lowered to 60 micrograms per deciliter.  A few years later, the threshold was reduced further to 40 micrograms, then 35 micrograms, then 30 micrograms, then 25 micrograms.  “In the 1990s the safe level for children was reduced to 10 micrograms…Today it is understood…that exposure to less than 10 micrograms per deciliter also impairs cognitive development, and there is most likely no threshold at all.” (3)

Manipulation and Obfuscation

The tests of toxicity required by law are conducted on a small minority of the tens of thousands of chemicals on the market.  When the tests required by law are conducted, they are inadequate to accurately determine toxicity.  So, in those rare cases when tests indicate that a chemical is harmful at the doses being used, you might think its use would be prohibited by law.  You would be wrong.  Regulation is prevented, even when tests clearly indicate that a chemical is harmful.

Atrazine is only one of many examples of how regulation is prevented by the disinformation campaigns of the manufacturers of chemicals and the industries which use them.  Professor Tyrone Hayes was hired by the manufacturer of atrazine to test the toxicity of that chemical on frogs, the animal that Professor Hayes studies.  Professor Hayes quickly reported that atrazine caused hermaphroditism and sterility in frogs.  Atrazine is a known endocrine (hormone) disrupter.  Very small quantities of hormones are capable of producing cascading effects throughout our bodies.  Despite this well known physiological fact, the primary means used by the manufacturer of atrazine to discredit Professor Hayes’ research was to argue about the doses that were used in his study:  “Atrazine is unlikely to have an adverse impact on frogs at existing levels of exposure” (4)  This criticism of Professor Hayes’ research is bogus because the dose he used was taken directly from the environment in which atrazine is used and contaminates surrounding water bodiesHe and his students continued the work, travelling to farming regions throughout the Midwest, collecting frogs in ponds and lakes, and sending three hundred pails of frozen water back to Berkeley. In papers in Nature and in Environmental Health Perspectives, Hayes reported that he had found frogs with sexual abnormalities in atrazine-contaminated sites in Illinois, Iowa, Nebraska, and Wisconsin.” (5)

African clawed frog was used in human pregnancy tests. Creative Commons
African clawed frog was used in human pregnancy tests. Creative Commons

In our recent debate with a reader who does not believe that pesticides are harmful to humans, his response to this information about the affects of atrazine on frogs was that he does not care about frogs.  So, let’s take a moment to think about why this research should be a matter of concern to us, even if we don’t care about frogs.  One of the frogs that Professor Hayes used in his research on atrazine was the African clawed frog.  The reason why he used that particular species is that, although it is not a native frog, it is very commonly found in nature because it was used for decades in pregnancy tests on humans.  If the urine of a pregnant woman is injected into a female African clawed frog, the frog quickly lays eggs.   In other words, the reproductive and endocrine system of frogs is closely related to that of humans.  If the reproductive and developmental system of frogs is adversely affected by atrazine, we should assume that humans are probably also affected.

Agent Orange was used in Vietnam from 1965-1969 to defoliate the battlefield to make the guerilla enemy more visible.  It was discontinued when scientists reported that it caused birth defects in mice.  Subsequently, Vietnam veterans reported severe health problems that were suspected to be a result of exposure to Agent Orange.  The manufacturers of Agent Orange quickly circled the wagons.  With the active participation of the government, they were able to prevent compensation of Vietnam veterans for their health problems for over 20 years.  This was achieved by direct manipulation of the research data.  Specifically, exposed workers and soldiers were put into the unexposed control group so that no statistical difference in the groups was apparent. (3)

There are multitudes of ways to cook the books.  Atrazine and Agent Orange are two examples in which the manipulation was discovered.  We will never know how many more there are that we don’t know about.

Cost-benefit analysis

Current federal law regulating toxic chemicals requires a cost-benefit analysis be taken into consideration before a chemical can be taken off the market.  In the case of pesticides, the manufacturers and the primary users of pesticides have successfully defended against regulation by claiming that agricultural productivity would be drastically reduced and the price of food drastically increased without continued use of pesticides.  However, there is considerable evidence to the contrary:

  • Despite massive pesticide use, some 37 percent of all US crop production is lost to pests—significantly more than was lost before the advent of synthetic pesticides.” (3)
  • In 1989, the US National Academy of Science’s Board on Agriculture reported, “Reduced use of these [chemical] inputs lowers production costs and lessens agriculture’s potential adverse environmental and health effects without necessarily decreasing—and in some cases increasing—per acre crop yields and the productivity of livestock management systems.” (3)
  • “In Germany…a long-term study of 44 farms has found that yields of wheat, oats, and rye have steadily increased over a 17-year period following the farmers’ transition to strictly organic agriculture.” (3)
  • “While yields stay more or less the same, the impact on farmers’ profits can be very positive [because] pesticides account for as much as 20 percent of the variable costs of crop production.” (3)

As strong as the case is against economic benefits of pesticide use by agriculture, the case is much stronger against pesticide use for ecological “restorations.”  There is no empirical evidence that there is any benefit to ecological “restorations.”  They do not increase biodiversity.  They do not benefit wildlife.  If there is no benefit, there is no justification for using pesticides for this purpose.

We apologize for the length of this post.  After spending several months studying the issues, we felt compelled to take you on our journey to the inevitable conclusion.  There is no justification for using pesticides for the sole purpose of eradicating non-native plants because they are not doing any harm and therefore there is no benefit to killing them, particularly with harmful pesticides.

 (1) Naomi Oreskes & Erik Conway, Merchants of Doubt, Bloomsbury Press, 2010

(2) Marcella Remer Thompson, Kim Boekelheide, “Multiple environmental chemical exposures to lead, mercury, and polychlorinated biphenyls among child-bearing-aged women: Body burden and risk factors,” Elsevier, November 16, 2012

(3) Joe Thornton, Pandora’s Poison, MIT Press, 2000

(4) Jon Entine, “Scared to Death:  How chemophobia threatens public health,” A position paper of American Council on Science and Health, 2011

(5) Rachel Aviv, “A Valuable Reputation,” New Yorker, February 10, 2014

Regretting the use of pesticides

Spraying Milestone in Glen Canyon Park, June 2012

Recently visitors to Glen Canyon Park in San Francisco spotted a Pesticide Application Notice in their park, which states that Milestone herbicide was used on “sweet pea.”  Sweet pea is not classified as an invasive plant by the California Invasive Plant Council.  Milestone herbicide is classified as Tier I “Most Hazardous” pesticide by San Francisco’s IPM program because it persists in the ground for a long time.  The City’s IPM policy states that it is approved for use on “invasive species.”  Since sweet pea is not an invasive plant, we assume this pesticide application violated San Francisco’s IPM policy.

The federally mandated Material Safety Data Sheet (MSDS) for Milestone advises users to, “Prevent [Milestone] from entering into soil, ditches, sewers, waterways and/or groundwater.”  The MSDS also says that Milestone “is not readily biodegradable according to OECD/EEC guidelines.”

For these reasons, the manufacturer of Milestone herbicide withdrew its application to sell Milestone in the State of New York, after the State of New York determined, “The [New York State] Department [of Environmental Conservation] could not ensure that the labeled use of aminopyralid [the active ingredient in Milestone] would not negatively impact groundwater resources in sensitive areas of New York State.”  In other words, the sale of Milestone herbicide is banned in the State of New York.

Kid playing in Glen Canyon Park. Courtesy San Francisco Forest Alliance

Since Glen Canyon is a watershed to Islais Creek, we believe it is irresponsible to use Milestone in that park.  And clearly there is no justification for using this persistent herbicide on a plant as benign as sweet peas.  Since Glen Canyon park is the home of a year-round day care center as well as a summer camp which leads children throughout the park, it is outrageous that these pointless risks were taken there.

We have learned nothing….

As we celebrate the 50th anniversary of Rachel Carson’s ground-breaking book, Silent Spring, there is renewed media interest in this issue.  We welcome this reminder that Rachel Carson informed the public in 1962 that DDT was having a devastating impact on wildlife.  DDT had been used for about 20 years, but it took that long for us to notice that some species of birds had been poisoned nearly to extinction.  And it took another 10 years for DDT to finally be banned in 1972.

Rachel Carson was vilified for her revelations, just as critics of the so-called Natural Areas Program are being vilified by supporters of that program.  We have been called “chemophobes” and “anti-chemical crazies.” 

Frank Graham, editor of Audubon Magazine, recently wrote an article for Yale University’s “environment 360” blog about the abuse that Rachel Carson endured after the publication of Silent Spring.  He recounts several anecdotes about the attacks on her character.  For example, “An official with the federal Pest Control Review Board drew laughter from his audience when he remarked, ‘I thought she was a spinster.  What’s she so worried about genetics for?’”

Forty years after DDT was banned in the United States we have a local example of the persistence of this dangerous chemical in our environment.  From 1947 to 1966, several companies on the harbor in Richmond, California formulated, packaged, and shipped pesticides, including DDT.  The site was designated a State Superfund site in 1982, and in 1990 the EPA placed the site on a national priorities list for clean up.  “Remedial actions took place on the site from 1990 to 1999.”  Twelve years later, the EPA tells us, “Although actions were taken to reduce the risk from the pesticides found on site…sediments and the water [in that location] are still contaminated with pesticides, primarily DDT and dieldrin.”

In other words, we fouled our water with dangerous pesticides; we then spent many years and probably a lot of money trying to clean up after ourselves, and 40 years later we are still living with the consequences of our foolishness.

What have we learned from that experience?  Now we are using a very persistent chemical (Milestone) on a benign plant (sweet pea) in our public parks.  We have learned nothing.  And those who have some economic gain from poisoning our parks—or are clueless about the risks they are taking—are defending the use of pesticides and trying to shut us up, just as they tried to shut Rachel Carson up 50 years ago.  We are proud to be in her company and we are inspired by her leadership.

Some people have learned

Peaches at “Organic U-Pick” Courtesy Arnita Bowman

We prefer to end our stories on a positive note when we can, so we turn to a book we read recently about a fruit farmer in California’s Central Valley.  David Mas Masumoto wrote Epitaph for a Peach to tell us about his transition from the traditional farming methods used by his father to organic methods.  He has abandoned rigorous weed and pest control and he is learning to live in harmony with his orchards rather than fighting against nature.  He tells us about the difficult decision to quit using pesticides:

“I am reminded that in some valley wells they have found traces of a chemical called DBCP in ground water aquifers.  DBCP was linked to sterility in males and is now banned in the United States.  My dad used some DBCP years ago…No one knew it would contaminate drinking water.  Neighboring city folks are angry with farmers for damaging their water supply.  ‘How could you farmers poison the water?’ they ask.  My dad didn’t choose to pollute the water table.  He did nothing illegal.  He simply trusted the chemical company and the governmental regulatory agencies.

Mr. Masumoto has learned from bitter experience.  What we know about pesticides today is not necessarily what we will learn about them tomorrow.  We often look back on our use of pesticides with regret.  So, shouldn’t we at least avoid using them when we don’t need to—such as on flowers just because they aren’t native—or in places where the risks are great—such as public parks occupied by children?

Let’s turn that rhetorical question into the affirmative statement that it deserves to be:  We should not be using pesticides in our public parks or on plants that aren’t doing any harm.  We will live to regret it when we do.  And let’s express our gratitude to Rachel Carson for inspiring us to keep informing the public of the needless risks that are being taken in their parks.