This information was prepared for the Zero Toxics Alliance.


Background: What are Xeno-Estrogens?

Xeno-Estrogen Effects:

Xeno-Estrogen Sources:

The Precautionary Principle


What are Xeno-Estrogens?

More than 50 years ago it was revealed that chemicals in the environment were having a profound affect on reproduction in many species. Despite this warning, humanity continued to embrace the quick fixes offered by the chemical industry.

Chlorine, widely used as a chemical weapon during World War I, was combined with other toxic chemicals to make PCBs, pesticides and plastic. We added chlorine to our drinking water and used it to bleach our paper and clothes. We bought disposable paper and plastic products, threw them out and then burned the waste, unaware that burning chlorine-contaminated waste created dioxins — one of the most toxic chemicals ever identified.

We’ve used heavy metals such as cadmium, mercury and lead, in a huge array of products. And, while some countries got the lead out of gasoline, cars and trucks still spew out a cocktail of toxics, including aromatic hydrocarbons.

Since the explosive, post-World War II expansion of the chemical industry, thousands of long-lasting toxic chemicals, which bioaccumulate in the tissues of animals, have been discharged into our environment.

A second warning was sounded in Rachel Carson’s award-winning 1960 book, “Silent Spring”, which detailed the dangers of pesticide use, including the impacts on the reproductive abilities of birds. This book played a pivotal role in the banning of DDT as an agricultural pesticide. (DDT is still extensively used to control malaria in developing countries — a short-term gain for a long-term loss.)

Some of these chemicals have now been identified as xenoestrogens — substances which cross the placenta and disrupt the hormone-regulating endocrine system by mimicking the female hormone estrogen.

Mixed Messages

Hormones are essential for the regulation of many biological processes in the body. Hormones act as messengers, relaying information to cells about how and when to grow, produce bodily substances, divide and die.

To exert their powerful effects, hormones must first bind with specifically tailored cell proteins called receptors. Hormones and receptors have an intricate and precise, lock-and-key fit. This hormone-receptor complex then binds to DNA in a cell’s nucleus to activate specific genes.

There are two ways xenoestrogens disrupt the function of the endocrine system. They can mimic natural hormones and “turn on” cell activity at the wrong time or they can “block” normal biological response by occupying the receptor site and preventing hormones from fitting.

The result is not genetic damage but inappropriate activation of genes, including incorrect timing or too much or too little cellular activity.

Interference with hormone function is particularly dangerous to the developing embryo and newborn. At this stage, alteration of sexual, physical or cognitive development is irreversible and potentially life threatening.

Damage from fetal exposure to xenoestrogens may be apparent at birth, but will probably not emerge until later in life when sexual maturity is reached. While exposed mothers may show not ill effects, their offspring may have trouble reproducing.

Even one small dose of a xenoestrogen at the point when a fetus is developing can cause permanent damage. For example, on day 56 of gestation, the human fetus begins the process of male/female differentiation and sexual organ development.

See below for information about the full range of threats to human and wildlife health.

Combined Effects

It is also important to note that low levels of various chemicals in the bodies of exposed wildlife and humans may be present and active at the same time. One experiment showed that, when 10 commonly encountered organochlorine chemicals were mixed at a tenth of their individually active dose, the potency (measured as cell proliferation) was 10 times higher than expected.

It has been estimated that each North American’s body contains hundreds, possibly thousands of synthetic chemicals.

Known Xeonestrogens

The following chemicals are considered to have serious reproductive and endocrinal disruptive effects:

  • PESTICIDES (Commercial and/or domestic)
  • 2,4,5-T, 2,4-D, alachlor, aldicarb, amitrole, atrazine, benomyl, lindane, carbaryl, chlordane, cypermethrin, DBCP, DDT, dicofol, dieldrin, endosulfan, esfenvalerate, ethyl parathion, fenvalerate, heptachlor, hexachlorobenzene, malathion, mancozeb, maneb, methomyl, methoxychlor, metiram, metribuzin, mirex, nitrofen, oxychlordane, permethrin and other synthetic pyrethroids, toxaphen, transnonachlor, tributyltin oxide, trifluralin, vinclozolin, zineb, ziram.
  • CADMIUM – Used in nickel/cadmium batteries, coatings, pigments, stabilizers in plastics and synthetic products and alloys, fossil fuels.
  • LEAD – Used in lead batteries, paints, pipes, leaded gasoline.
  • MERCURY – Used in nickel/cadmium batteries, fluorescent lighting ballasts, seed dressings, chlorine production, dental amalgams, fossil fuels.
  • DIOXIN – (2,3,7,8-TCDD) a byproduct of other organochlorine production, use and disposal (not intentionally produced). Examples include incinerator emissions, metal smelting, PVC (vinyl) plastic production, chlorine-bleached pulping.
  • PBBs & PCBs – Production now banned, but PCBs still used in electrical transformers. PCBs still reside in landfills, toxic waste dumps and sediments.
  • PENTACHLOROPHENOL Wood preservative, used in textile industry.
  • BISPHENOL A – Breakdown product of polycarbonate
  • PHTHALATES – POLYCARBONS – Used to make plastic soft
  • STYRENES – ALKYL/NONYL PHENOL ETHOXYLATES – Used in detergents, pulp & paper and textile industry, some plastic products, paints, pesticides.
  • PAHs – Present is crude oil and most fossil fuels, product of combustion of these fuels.

— Source: Eagle’s Eye, World Wildlife Fund, 1995


Why Women Should be Xeno-Estrogenophobic

Nobody knows exactly why hundreds of thousands of North American women develop breast cancer every year. The disease does have some established risk factors: early commencement of menstruation, never breastfeeding a child, late onset of menopause and inheritance of the long-researched “breast cancer gene”, BRCA1. These risks apply to approximately 30% of breast cancer cases, leaving the vast majority unexplained.

Or are they?

Some scientists are beginning to look at xenoestrogens (foreign estrogens) as a probable culprit. Xenoestrogens, contaminants introduced into the body from the environment, mimic the action of estrogen produced in cells or alter hormonal activity.

Some naturally occurring and easily degraded xenoestrogens, such as those found in soy products, broccoli and cauliflower, can reduce estrogen’s effects. Others, usually synthetic and difficult for the body to break down, can amplify the effects of estrogen. The latter xenoestrogens — found in certain pesticides, plastics, fuels and drugs — have proliferated since World War Two.

Evidence is steadily growing that xenoestrogens and other hormone mimicking substances are implicated in a wide range of human and wildlife health problems, including breast cancer.


Breast cancer develops when a cell escapes the usual restraints on replication and multiplies out of control. This escape is probably due to a build up of mutations in genes which regulate cell division and ensure accurate replication of DNA, although hormones and other substances around the cell may also prompt abnormal growth.

In attempting to explain the unexplained, scientists began to re-examine what was known. Linking most established risk factors is the fact that they promote breast cancer by elevating total lifetime exposure to the biologically active estrogen estradiol.

They began to hypothesize: If too much natural estrogen was dangerous, could prolonged exposure to xenoestrogens also be harmful? Not only might this theory explain breast cancer cases in women with no known risk factors, it made sense for another reason — breast cancer has been on the rise worldwide ever since the explosive growth of the chemical industry in the 1940s.

Natural estradiol can cause epithelial cells in breast tissue to multiply. It influences cell growth by binding to an estrogen receptor. Complexes of hormone and receptor can bind to DNA in the nucleus and activate genes which direct cell divisions, speeding the rate of DNA replication and so increasing the likelihood of a possibly carcinogenic mutation arising and going undetected.

At some point after it is formed, estradiol metabolizes into other forms of estrogen. Like “good” and “bad” cholesterol, the “good” estrogen (2-hydroxyestrone) activates the estrogen receptor only weakly. The “bad” estrogen (16-alpha-hydroxyestrone) strongly increases interaction of the receptor with growth-promoting genes, enhances breast cell proliferation and possibly damages DNA. Studies have already linked this “bad” estrogen to breast cancer.

Some xenoestrogens may promote cancer by enhancing production of “bad” estrogen. Others may act by binding to an estrogen receptor and inducing it to issue unneeded proliferation signals.

Chemicals with these properties may encourage the development of cancer in other ways. Some xenoestrogens seem to help cells generate the new blood needed for tumour growth and spread, others appear to damage DNA.


Xenoestrogens accumulate in fatty tissue, so food from animals at the top of the food chain are likely to deliver the largest doses — meat from animals which eat smaller animals or contaminated food or water would, for example, probably yield more exposure than a plate of vegetables carrying residues of estrogenic pesticides. Corn oil and related polyunsaturated fats seem to have estrogenic effects and can also be a source of exposure.

People who live in areas where air or water is highly polluted by industry or by the dumping or burning of wastes might take in xenoestrogens simply by breathing the air or drinking the water. Occupational exposures can also occur.

Evidence that synthetic chemicals could exert harmful estrogenic effects first emerged 50 years ago, when researchers reported that chemicals in the environment seemed to affect reproduction profoundly in many species.

Later research confirmed that DDT and other chlorinated organic pesticides could indeed disrupt the endocrine system. Injections of DDT have been found to accelerate the growth of existing mammary tumours in male mice. Growth of such tumours is a sign that a chemical is unusually carcinogenic, as male rodents are generally resistant to breast cancer. Injection into male rats of atrazine, a popular weed killer often found in groundwater, also increases the incidence of breast cancer.

In the past 15 years, studies have shown several compounds to be estrogenic and to cause mammary tumours in animals. These include certain aromatic hydrocarbons in fuels and some PCBs. PCBs are long-lived chlorinated organics, once used as electrical insulators. Although their manufacture has been banned in Canada and the US, they can still be found in old transformers and have been detected in soil, water, animals and human tissue.

Recent examinations of various pesticides support the idea that certain xenoestrogens promote breast cancer by shifting the balance of estradiol’s by products towards the “bad” estrogen. Natural plant xenoestrogens produce the opposite effect — broccoli, cabbage, brussel sprouts, cauliflower and soy products encourage the production of “good” estrogen. [1]


Evidence that plastics can also be estrogenic has emerged only in the past five years.

The first culprit to be exposed was the chemical bisphenol A, a breakdown product of polycarbonate, widely used in many plastics, including the lining in food cans and juice packages. Bisphenol A escapes when polycarbonate is subjected to high temperatures. The estrogenic effects of bisphenol A became clear when men working in the plastics industry developed breasts after chronically inhaling the chemical in dust.

Another link between plastics and breast cancer was uncovered by Drs Ana Soto and Carlos Sonnenschein in 1992. While working on research unconnected with xenoestrogens, they found cultures from breast cancer cells multiplying more rapidly than expected. Further research revealed that a chemical used to make plastic more flexible — nonylphenol [2] — was the culprit. This estrogen mimicking chemical had escaped from the laboratory’s plastic ware. Related substances can be found in polystyrene containers, intravenous tubing and some detergents and household cleaners.

Excerpted from “Can Environmental Estrogens Cause Breast Cancer?” by Drs Devra Lee Davis and Leon Bradlow, with permission. This article appeared in Scientific American, October 1995.


While breast cancer is unquestionably the most serious threat to women’s health linked with exposure to xenoestrogens, it is by no means the only problem.

Studies have also tied hormone mimicking chemicals with increases in vaginal and cervical cancers.

In addition, xenoestrogens have been implicated in the rising incidences of endometriosis, a painful condition which occurs when cells from the womb lining grow outside the uterus. Infertility can result.

Studies of rhesus monkeys show exposure to dioxin or PCBs increases risk of developing endometriosis, even at levels 7-8 times lower than the “safe” level proposed by the World Health Organization.

[1] US studies have revealed that white and African-American women with high levels of DDE (a breakdown product of DDT) and PCBs in their blood are two to three times more likely to develop breast cancer than those with lower levels. Asian women, who eat diets rich in soy products, cabbage, broccoli and other vegetables, seem to have no increased risk from higher blood levels of these contaminants.

[2] When Drs Soto and Sonnenschein identified plastic ware in their laboratory as the cause of cell multiplication, the manufacturer refused to provide them with a list of ingredients, as this was a “trade secret”. They broke the plastic down themselves to isolate the culprit, nonylphenol.

Why Men Should be Xeno-Estrogenophobic

In “The Children of Men”, novelist P D James described a futuristic society in which men were no longer capable of reproducing. As alarming as the premise was, it certainly wasn’t far fetched.

Studies have shown that in the past 50 years, the quality and quantity of male sperm has dropped by 42% and 50% respectively. In the past 20 years the decrease in sperm counts has occurred at a rate of 2% annually.

At the same time there has been a 3 to 4-fold increase in testicular cancer, making it the most common malignancy among younger men in the Western world.

UK research suggests the incidence of cryptorchidism (undescended testes) may have doubled since the 1950s. Studies in other countries also show an increase. Incidence of hypospadias (an urethral abnormality) has been reported on the increase in Scandinavian, Hungary and the UK.

These male reproductive disorders are closely linked. Testicular cancer risk is significantly increased in men with a history of cryptorchidism; many men with testicular cancer have impaired sperm production; sperm production is generally impaired by undescended testes. It is believed that all these testicular disorders can arise during fetal development and early childhood, so it is likely that some common factors could be responsible. A comprehensive Danish study of male reproductive disorders concluded that such remarkable increases in occurrences of these disorders over a relatively short period of time was probably the result of environmental, rather than genetic factors.


A prime suspect for this are environmental contaminants, man- made substances which can cross the placenta, mimic hormones and thereby alter fetal development. These substances, known as xenoestrogens (foreign estrogens), include some pharmaceuticals, chlorinated pesticides, PCBs, and certain chemicals used in plastics and solvents.

These chemicals, which have been introduced into the environment in the past 50 years are known to disrupt the endocrine system (which regulates hormones). Steroid hormones, which play a large role in regulating development and reproductive processes, seem to be particularly affected. Organs especially at risk from maternal exposure to hormone mimicking substances during development are male and female reproductive systems. Also affected are the skeleton, thyroid, liver, kidney and immune system. Effects, such as deformities, may be immediately apparent or may not be obvious until the child reaches maturity.

It has been established that development of male reproductive organs during fetal life can be affected by the female sex hormone estrogen. Higher than normal levels can result in reduced sperm counts and other problems.

The production of sperm is regulated by Sertoli cells in the testes. The number of sperm supported by each Sertoli cell is finite, so levels of sperm production are determined by the number of Sertoli cells which develop during fetal life. After birth, no more Sertoli cells can be formed. If Sertoli cell number is reduced by fetal exposure to estrogen, sperm production is also reduced in the male offspring for the rest of his life.

The discovery that synthetic estrogen could produce the same effects as excess natural estrogen was the highly unfortunate result of the widespread use of the drug DES (diethystilbestrol). Between 1945 and 1971 more than five million women were given DES to prevent miscarriages, before this synthetic estrogen was linked to a rare vaginal cancer. Further research revealed that prenatal exposure to DES resulted in a much greater incidence of cryptorchidism and hypospadias in male children. Many of the sons of women who took DES had reduced sperm counts as adults.

Scientists have since begun to question the role of estrogenic chemicals and have found them to be increasingly linked to the growing number of male reproductive disorders.


  1. 1929 PCBs introduced
  2. 1938 DDT first manufactured
  3. 1940s-WWII First widescale exposure to man-made chemicals
  4. 1940s-1950s First generation exposed postnatally
  5. 1950s-1970s First prenatally exposed generation born
  6. 1970s-1990s First prenatally exposed generation reaching reproductive age


Several studies have revealed that occupational exposure to some hormone mimicking chemicals has led to declines in male fertility.

A 1991 study of farmworkers in India exposed to organochlorine pesticides (such as DDT and endosulphan) showed a significant decrease in the number of fertile males. When the study was expanded to look at the children of workers, researchers discovered a notable increase in other reproductive disorders, including still births, neonatal deaths and congenital defects. These reproductive effects indicate chromosomal damage in the cells from which sperm is produced.

Another organochlorine pesticide, DBCP (dibromochloropropane) has been scientifically proven to cause many cases of infertility in males who were occupationally exposed to this soil fumigant before it was banned in the US in 1979. Research on workers in the US, Israel and Central America all revealed fertility problems. In Costa Rica, where high doses of DBCP were used on banana plantations from 1971-78, an estimated 2500 workers became infertile as a result of exposure ~ 60-70% were diagnosed as azoospermic (no sperm count).

Occupational exposure to dioxins has also led to reproductive problems. Reduced testicular size of men involved in aerial spraying of dioxin-contaminated Agent Orange during the Vietnam war has been attributed to the amount of dioxin in their blood. A recent study of chemical workers uncovered alterations in three important reproductive hormones – decreased testosterone and increased follicle stimulating hormone (important in controlling Sertoli cell multiplication) and luteinizing hormone. The altered levels of all three were significantly related to dioxin levels in the workers’ blood, suggesting that dioxin can alter levels of reproductive hormones in adult men.

UK research has suggested that some male infertility problems in the London area may be linked to the drinking water supply which the drinking water supply, which contains sewage effluent and has been found to be contaminated with hormone- mimicking nonylphenols.

Sources: “Environmental Oestrogens: Consequences to Human Health and Wildlife”, Institute for Environment & Health, University of Leicester, 1995; “Body of Evidence”, Greenpeace, 1995; “An Environmental Assessment of Alkylphenol Ethoxylates & Alkylphenols”, Friends of the Earth, 1995; Eagle’s Eye, World Wildlife Fund, 1995.

Why Parents Should be Xeno-Estrogenophobic

There are glaring flaws in our current system of risk assessments, used to establish how much exposure to a chemical is deemed safe for human consumption. The most unforgivable flaws are that they do not consider combined effects of exposure to numerous chemicals and that the “safe” level is based on adult weight. This puts unborn and young children at considerably more risk.

The fetus is much more vulnerable to toxic damage for a number of reasons, including a lack of body fat to act as a reservoir for toxins, a susceptibility to chemically-induced cell injury, and a much slower rate for detoxifying toxic substances.

There is a large body of evidence linking xenoestrogens (synthetic chemicals which cross the placenta, mimic natural hormones and alter basic DNA) with dramatically increased cancer rates and with many reproductive problems in humans.

These chemicals have also been implicated in a wide array of other human health problems.


Numerous studies point to a connection.

For example, in Taiwan in the late 1970s, many people were poisoned consuming rice contaminated with PCBs and dioxins. A study carried out on the sexual development of the children of women who were pregnant at the time showed the penis size of 11 to 14-year-old boys to be significantly smaller than the penises of other children. This was attributed to prenatal exposure to estrogenic PCBs.

Although dioxins (unwanted by-products of industrial chlorine use) are not hormone mimicking chemicals, prenatal exposure in animals results in similar male reproductive disorders. Several recent experiments have shown that a single, very low dose of dioxin (which caused no maternal toxicity) given at a critical time of pregnancy resulted in a number of permanent alterations of male offspring, including reduced sperm count and reduced weight of testes.

No effect on other organ systems has ever been observed at such a low dose, leaving researchers to conclude that the male reproductive system is highly sensitive to prenatal and lactational exposure to dioxins. It was suggested that these effects resulted from altered hormone levels during development. Sexual behaviour of offspring was also affected (demasculinization and feminization) by low-level prenatal exposure.


Animal and human studies reveal that exposure to certain chemicals can result in fetal death and spontaneous abortion.

Human evidence comes mainly from women working in the dry cleaning and pharmaceutical industries, and in agriculture. (One Finnish study concluded that female dry cleaning workers exposed to the chemical perchloroethylene were three to four times more likely than the general population to spontaneously abort during pregnancy.) Recent studies of men also suggest that sperm abnormalities caused by workplace exposure to hormone mimicking chemicals may result in spontaneous abortions.

Delayed fetal growth — a condition known as intrauterine growth retardation and linked to sudden infant death syndrome — has also been associated with exposure to environmental pollution. Studies show infants with this condition have a greatly reduced number of nephrons (the basic filtration unit) in the kidneys.

The link between growth retardation and PCBs has been well documented. Studies of pregnant women in Japan and Taiwan who consumed PCB-contaminated rice and pregnant women in the Great Lakes region who consumed PCB-contaminated fish revealed reduced birth weight in their newborn children. Further studies showed the growth retardation still apparent at the age of four. Girls were particularly affected.

Following a report that cow’s milk had been highly contaminated with dioxins and PCBs from an incinerator in Rotterdam, the Dutch government initiated a study which revealed that babies of women who had dioxin and PCB-contaminated breast milk had a lower quality of muscle tone. More highly exposed babies also had less developed reflexes.


The brain has a strict timetable for development and if this is disturbed a permanent deficiency will result. Studies of children exposed in the womb to hormone mimicking chemicals show their behaviour and intelligence may be affected. The cause is not fully understood, but has been linked to the development of reproductive and thyroid hormones.

In birds, mammals and humans there are differences between male and female brain function and structure, which account for some of the distinctive differences in sexual behaviour. The development of sexually different areas of the brain is controlled by various reproductive hormones and other chemicals in the nervous system. If the balance of these hormones is altered during development, sexual behaviour can be altered.

Higher than normal levels of estrogen during development, for example, have dramatic and permanent influence on brain structure and function. Female rats exposed prenatally to synthetic estrogens have a masculine sexual behaviour pattern throughout their life, because increased levels of estrogen cause the sexually different region of the brain to develop the structural characteristics of a male brain. Increased testosterone exposure has the same effect, as it is broken down to estrogen in this region of the brain.

Thyroid hormones are essential for normal development of the human nervous system. They control growth rate, maturing of nerves, and organization of nerves in certain parts of the brain. Although disruption of adult thyroid function can be treated, disturbances during the critical period of nervous system development can produce irreversible nerve damage. For humans, this critical period begins in the womb and extends until the age of two.

Animal experiments have shown that dioxins and PCBs can block thyroid hormone action, as they are similar in structure and can bind to the same receptors. They also bind to a protein in the blood (which normally binds to thyroid hormones) and transport it around the body. The ability of dioxins and PCBs to mimic or decrease the biological action of thyroid hormones could have disastrous consequences during development. Even non-toxic, low level doses of dioxins and PCBs may alter neurological function.

Accidental exposure to dioxins and PCBs in pregnant women has resulted in behavioural and learning disabilities in their children. Evidence suggests this may be partly or entirely the result of the effects these chemicals have on thyroid hormones. Evidence also suggests PCBs may be toxic to the developing nervous system because they affect the level of dopamine, a chemical in the nervous system involved in sending nerve signals to the brain. PCBs are also considered to be toxic to the developing nervous system because they decrease the number of receptors for acetylcholine, another chemical involved in nerve impulse transmission.


Toxic effects on the nervous system and brain resulting from prenatal exposure to PCBs and dioxins can lead to various behavioural problems: reduced intelligence, learning difficulties, memory problems, hyperactivity and under-activity. These outcomes depend on the time of exposure, the specific chemicals involved, the dosage of exposure and other factors.

The study of offspring women who consumed PCB-contaminated rice during pregnancy showed that these children had consistently lower scores in annual intelligence tests given between the ages of 18 months and seven years. The results were very troubling as it appears the impairment of intellectual function in these children did not improve as they aged.

When the study was expanded to include children born by women up to 12 years after the contaminated rice episode, results showed these children were as or more affected than those born one year after the contamination, despite the fact that the level of toxins in women’s bodies had decreased. These children also suffered from mildly disordered behaviour and higher than normal activity levels.

Tests given to offspring of women who consumed PCB- contaminated Great Lakes fish during pregnancy also showed altered behaviour compared to a control group. At the age of four years, these children had deficits in short term memory and speed of thinking, sufficient to affect their ability to master basic reading and arithmetic skills.


The immune system consists of a network of specialized cells which respond to foreign substances in the body in order to prevent infection or disease. The immune system can malfunction in two ways: It can be depressed and fail to provide protection against bacteria, parasites, viruses and some cancers, or it can become too active, leading to an increase in autoimmune diseases such as asthma and diabetes.

Evidence exists that prenatal exposure to some organochlorines and synthetic estrogens has a detrimental effect on the immune system.

In its four-year reassessment of the dangers of dioxin, the US Environmental Protection Agency concluded that sufficient evidence existed to assume that immune responses are suppressed following prenatal dioxin exposure.

Numerous studies were conducted on the children of women who were given the synthetic estrogen DES (diethylstilbestrol) to prevent miscarriages and it is clear that changes in their immune system may have occurred. Altered function of some immune system cells has been reported in a number of cases, as well as an increased lifetime prevalence of autoimmune diseases and a three- fold increase in rheumatic fever. Analysis of blood samples from exposed individuals revealed a significant difference in factors of the immune system associated with autoimmune diseases.

It remains to be seen whether these effects will worsen with time, but animal studies show the severity of immune systems defects associated with prenatal DES exposure increase with age.

Sources: “Dioxin Reassessment”, US Environmental Protection Agency, 1994; “Body of Evidence”, Greenpeace, 1995.

Listening to the Canaries

Just as miners once took canaries with them to provide a warning when the air became unsafe to breathe, wildlife everywhere are today providing us with warnings. They have been bombarded and contaminated with heavy metals, organochlorines and other man-made chemicals which can mimic hormones and cause many developmental and reproductive problems.

Fish, birds, reptiles and mammals around the world are showing signs that their hormonally-controlled functions have gone badly awry. Some species, such as the Florida panther, have been pushed to the brink of extinction.

Every day research reveals the dire consequences for wildlife of continued exposure to these substances. Every day it becomes more clear that just as the Florida panther goes, so, too, could humanity go.

Wildlife have been the innocent bystanders and victims of our addiction to chemicals. We must listen to and learn from their tragic lessons, only some of which follow.


Research has shown that all Great Lakes salmon over the age of two years have enlarged thyroids (essential for normal development of the nervous system). Some thyroids are over one million times their normal size and some are at the point of rupturing. (When these fish were fed to rats, the rats also developed thyroid enlargement.) Almost all the salmon examined have hermaphroditic reproductive systems.

Between 1980 and 1990 rates of survival to hatch for Lake Erie Pacific coho salmon decreased from as high as 48% in 1980 to less than 5% in 1990. There was also a high prevalence of embryo deformities and poor expression of secondary sexual characteristics in males, which is associated with environmental contaminants.

Canadian scientists have found that fish which swim through pulp mill pollution become sexually mature much later than normal, which could eventually effect their ability to breed and survive. Younger fish display both male and female features.

Male fish living near municipal sewage outlets are producing vitellogin, a female protein used to make egg yolks. Nonylphenol — a softener used by the plastics industry, which is also found in some industrial and commercial detergents and in some pulp processes — has been identified as the cause.

Experiments have shown that fertilized zebrafish eggs exposed to the pesticides lindane and atrazine exhibited increased deformities and decreased growth in the embryos and a reduction in the survival of hatched juveniles.

High embryo mortality rates in Great Lakes lake charr appear to be largely due to maternally transferred PCBs. This has continued despite the decrease in many Great Lakes fish contaminants in the past 20 years.

Female whelks around wharves and marinas in th Pacific northwest have grown penises as a result of the use of tributyltin paints.


In the 1950s, eggshell thinning, caused primarily by DDE, a breakdown product of the pesticide DDT, led to a dramatic decline in the British peregrine falcon population.

Many Great Lakes fish-eating birds decreased due to eggshell thinning, including a massive decrease in North American bald eagles in the 1950s and 1960s. Despite restrictions on DDT use since 1972, embryonic and chick survival along the shores of the Great Lakes is still not adequate to maintain stable populations. Female Great Lakes herring gulls have been found sharing nests with other females and together producing abnormally large clutches of predominantly infertile eggs. (Nest sharing is a sign that the male population has dwindled.) Biologists have also observed male young with feminized reproductive tracts, and behavioral changes in males characterized by a lack of interest in females.

Eagles and other Great Lakes birds have been born with deformities, including crossed beaks.


Abnormally small penises and altered hormone levels in alligators hatched in Lake Apopka, Florida, following a massive 1980 spill of Kelthane — a pesticide which at the time and until the late 1980s contained DDT as an “inert” ingredient. The population now is only one tenth of its size in the 1970s. Juvenile female have estrogen levels twice that of alligators in unpolluted lakes. Males had abnormally depressed levels of testosterone.

The sex of many reptilian species is determined by the temperature at which the egg is incubated. Previous research had shown that application of estrogen to eggshells during development can counteract the production of male offsprings at lower temperatures. A recent study of the red-eared slider turtle showed that spotting eggs with estrogenic PCBs had the same effect, causing an increase of female offspring. (The PCB levels which disrupted sex differentiation in the turtles were comparable to average levels of PCBs found in human breast milk in industrialized countries.)


European otters and mink populations have declined to the point that mink are now an endangered species. Studies on captive mink show they are highly sensitive to reproductive problems caused by organochlorines.

Estrogen mimicking organochlorines have been found in numerous Arctic marine mammals, including the fur seal, ringed seal, hooded seal, bearded seal, walrus, beluga, narwhal and polar bear.

St Lawrence beluga whales have 10-50 times higher levels of organochlorine contaminants than Arctic belugas. Only 21% of St Lawrence beluga females are breeding, compared to 65% in the Arctic. Lesions detected in mammary glands of 36% of St Lawrence females would seriously impact their ability to feed if calves were ever produced.

Reproductive failure of the common seal in the Wadden Sea has been attributed to PCBs.

A disease complex associated with high levels of PCBs and DDTs has caused reproductive failure and bone lesions in Baltic ringed seals and grey seals.

High levels of DDT residues in California sea lions has been cited as a cause of spontaneous abortions.

Most of the 35 remaining Florida panthers are exhibiting developmental and reproductive problems. Male sperm is of low quality and quantity. Undescended testes (cryptorchidism) has become common in male cubs. Females have high body burdens of various organochlorines and reproductive abnormalities have been blamed on contamination of the mothers by endocrine-disrupting chemicals.

Military dogs which served in Vietnam and were exposed extensively to the dioxin-laden defoliant Agent Orange, suffered twice the rate of testicular cancer and reproductive abnormalities compared to dogs serving elsewhere during the same period.


Hormone-mimicking substances have been linked to every one of the above wildlife tragedies, as well as numerous reproductive and developmental failures in humans. Urgent action is needed to protect ourselves and all the modern-day canaries we have harmed.

All chemicals — those in common use and those yet to be approved — must be screened for hormonal activity. Risk assessments based on acute toxicity and ability to cause cancer and gross birth defects are no longer sufficient, especially in assessing risks to embryos exposed to multiple chemicals.

Research must be devoted to looking at chemicals, their sources, exposed populations and the effects of multiple exposure to identify existing and emerging problems, and implement recovery action for both wildlife and human survival.

Precautionary action must be taken. Industrial, environmental and health policies must be based on pollution prevention. Cleaner, more efficient production will have numerous benefits.

We must consider how we use materials in industry, agriculture, commerce and our domestic lives: for the sake of wildlife and human health, and, ultimately, survival.

  • Demand action to phase out known hormone mimicking chemicals.
  • Demand and buy organic food and textiles.
  • Don’t use pesticides in your home.
  • Demand disclosure of information about hormone mimicking chemicals in consumer products, packaging, industrial emissions, pesticides and food.
  • Avoid chlorine-bleached paper products, PVC plastics and dry cleaners who use chlorinated solvents.

Sources: “Eagle’s Eye”, World Wildlife Fund, Summer 1995; “Body of Evidence: The effects of chlorine on human health”, Greenpeace, May 1995; “Sex Under Siege”, Canadian Broadcasting Corporation, 1995.


 Killer Car Pollution

A new car comes on to the world’s roads every second, nearly 100,000 every day. There were 53 million cars in the world 40 years ago, now there are 450 million. Add the number of trucks, and there are over 550 million vehicles, a figure likely to double again over the next 20 years.

Since Henry Ford’s time, inefficient internal combustion engines, relying on vast quantities of highly polluting oil, have been spewing carbon dioxide and a cocktail of other poisons into the air.

Cars have made many cities unliveable. Air pollution is common at levels which can kill children and elderly people. The public are regularly told to stay indoors and in Tokyo “pay for breath” oxygen dispensers have been installed on many street corners.

The car industry also fuels demand for the substance which symbolises 20th century growth and pollution – oil. Oil pollutes when we explore for it, when it is drilled, transported, spilt, refined or dumped. Oil also pollutes in normal everyday use, when it is burned in the engines of our cars. Transport now accounts for 50% of oil use worldwide.

The amount of carbon dioxide produced by cars is measured in billions of tonnes, amounting to 15-20% of all carbon dioxide produced through human activity. Carbon monoxide, nitrogen oxides, hydrocarbons and ozone-depleting CFCs are emitted in vast quanti- ties by the transport sector, an important and serious contributor to global warming.


One of the most lethal by-products of fossil fuel combustion are polycyclic aromatic hydrocarbons (PAHs). PAHs consist of carbon and hydrogen atoms with molecular structures based around two or more benzene rings linked together. Some examples are anthracene, pyrene, chrysene, phenanthrene and benzo[a]pyrene (the last being one of the most toxic, causing changes to DNA).

Many are present in crude oil and most fossil fuels, others are generated as products of combustion of these fuels. Acutely and chronically toxic, some PAHs are also carcinogenic. As a result of industrialisation and motorised transport, they are now ubiquitous in the environment and particularly abundant in urban areas.

PAHs from car exhaust, washed by rainfall into storm drains, are discharged into the marine environment. One of the most toxic components of urban runoff, PAHs are known to cause cancerous lesions, reproductive and developmental problems and immune system deficiencies in fish. An estimated 90% of Burrard Inlet English sole have cancerous lesions attributed to PAHs.

PAHs are included in the growing list of xenoestrogens ~ syn- thetic chemicals which wreak havoc with the hormone-regulating endocrine system ~ and have been linked with numerous human health problems.


Up to 50% of all car trips are short distances within cities. We need fewer cars, each producing little or no pollution. The answer to this problem lies in the design of our cities, and in the design and manufacture of our cars.

In order to protect human and environmental health from the ravages of the car, we must rethink the world’s urban centres. The sprawl which began with Los Angeles, the first city built for cars, not people, must be checked and reversed. Priority should be given to the most efficient and least polluting forms of transport.

Before cars, cities and towns were designed to be self con- tained. It’s time to take a step back and ensure future development plans are designed to make getting around without cars as easy as possible. Residential developments should include a shop selling everyday goods within easy walking or cycling distance of all homes.

The way people choose to travel depends enormously on the quality of options available. Dealing with traffic congestion by building more roads simply leads to more traffic. An extensive net- work of underground, bus and tram lines, on the other hand, encour- ages the use of public transport, just as a network of footpaths and bicycle lanes will promote walking and cycling.

While various levels of government argue about subsidies for public transport, few discuss the enormous subsidies granted to the private car.

Car and fuel taxes come nowhere near covering the cost of building and maintaining roads, let alone the environmental damage, air pollution-related health problems, deaths and injuries or impacts of climate change, the costs of which are borne by society as a whole. In the Lower Mainland, for example, each and every car is subsidised to the tune of $2700 a year ~ or $1.60 per litre of gas.

Real costs must be applied to each mode of transport. Increased car and fuel taxes, coupled with higher licensing and parking fees could be used to improve public transport systems, which would in turn increase employment (more buses, trams and trains need more drivers) and benefit the economy.


While improved urban planning and public transport will play a dramatic role in reducing automobile pollution, the demand for cars will continue. It is therefore essential that we deal with the threats posed by the fossil fuel-burning, carbon dioxide and PAH- spewing, internal combustion engine.

Car manufacturers could produce cars two or three times more efficient than the models currently on the market. These cars were designed as prototypes in the early 1980s, when the price of oil was high, but shelved when the price of oil came down.

It is within the power of the industry to produce low-emission cars, zero-emission cars, or better still, highly efficient public transport systems, but the industry has no desire to do so.

When we finally do demand change from manufacturers, we must choose wisely, lest the solution prove worse than the problem. When the car industry is forced to change, it will only do so once.


A switch to ethanol blended gasoline, for example, would reduce fossil fuel consumption and could provide a much needed market for forage crops, straw, wood chips and agricultural waste. However, these same wastes could be used to make paper and save the trees which help to absorb fossil fuel pollution. Also, a move to ethanol could, as it has in Brazil, result in valuable food crop land being devoted to feeding cars instead of people.

Lightweight-electric-vehicles (LEVs) being designed in Europe offer a promising solution. They perform as well as conventional cars – going distances of up to 400 kilometres before the batteries need recharging. Unfortunately, this is because their bodywork is made of moulded, unrecyclable plastic. Development of these vehicles should be promoted only after the plastic question (eliminating the toxicity of the ingredients with which it is made and ensuring it can either biodegrade or be truly recycled) has been resolved.

Another problem which must be dealt with is batteries. Today’s lead-acid batteries are heavy, inefficient and pose environmental risks in disposal. Some alternatives are of equal or greater concern, for example nickel-cadmium. Research into the potential of sodium-sulphur batteries should be encouraged.

One advantage of LEVs is that designs can be adapted for longer distance needs into “hybrids” which run on conventional fuels. These hybrids produce considerably less exhaust than internal combustion engines and, most importantly, could eventually be converted to the use of hydrogen, produced from renewable energy, virtually eliminating air pollution.

As communities in Europe begin to promote the use of electric cars by providing accessible public facilities for recharging batteries, another question must be addressed and that is the source of the electricity for recharging. In France, for example, the source is nuclear power.

Clearly, the world must develop carbon-free, renewable energy resources to power its transportation, if it is to be truly sustainable. Wind power, solar energy and bio-mass can be used to provide unlimited amounts of electricity or hydrogen.

Equally clearly, whatever route we take must involve less cars taking up less land. Life on earth depends on what we do.

  • Leave your car at home and walk, bicycle or take the bus whenever possible.
  • Buy only recycled motor oil. Use every drop. Return container to service station for recycling.
  • Write to the federal and provincial environment ministers, voicing your support for increased combustion-engine car and fuel taxes to fund improved public transport, and Canadian implementation of the California statute dictating a minimum percentage of all cars sold must be zero emission.
  • Write to car manufacturers demanding research and development of non-toxic, biodegradable or recyclable plastic and non-toxic batteries for use in lightweight electric vehicles.
  • Write to oil companies demanding research and development of carbon-free, renewable energy resources.

Sources: “Transport, Oil and Global Warming”, Greenpeace, 1993; “The New Automotive Revolution”, World Watch, Vol 6 No 4, July/August 1993; “Car Free Cities”, Greenpeace, 1993.

PCB’s — Polychlorinated Biphenyls

Polychlorinated biphenyls (PCBs) exist as a result of the automobile industry. As automobile use grew in the early 20th century, so did demand for gasoline. In extracting gasoline from crude oil, large amounts of other chemicals, including benzene, were left over. Chemists began trying to find a use for these unwanted by-products.

They discovered that heating benzene under the right conditions made it possible to glue two benzene rings together and create diphenyl. Exposing the diphenyl to chlorine gas created chlorinated diphenyls, or biphenyls as they are now known. Adding more or less chlorine gives compounds with differing properties.

PCBs are not soluble in water, do not burn, conduct electricity or degrade during use, but they do conduct heat very well, which made them ideal candidates for use as insulators in electrical transformers and capacitors for the then new fields of electric power equipment and electronics. (PCBs have also been used as hydraulic fluids, and in metal finishing. They are found in some components of automobiles — one reason junked cars can be quite a health hazard. Carbon-less carbon paper was once made with PCBs.)

By 1914 enough PCBs were in the environment to leave measurable amounts in the feathers of birds exhibited in museums today.


In 1929 the US firm Monsanto began producing PCBs commercially. Within a few years PCBs had created sufficient health concerns to attract the attention of academics and the US Public Health Service, and the concern of several large industrial producers and users of PCBs.

A 1936 Public Health Service memo described the family of a chemical worker who developed chloracne (a combination of blackheads and pustules) merely from contact with his clothes. The writer added, “symptoms of systemic poisoning have occurred among workers inhaling these fumes.”

A 1947 internal Westinghouse memo admitted long-term exposure to PCB fumes “may produce internal bodily injury which may be disabling or could be fatal.”

A 1959 memo from Monsanto to its major customer, Westinghouse, said, “…sufficient exposure, whether by inhalation of vapours or skin contact, can result in chloracne which… we must assume could be an indication of a more systemic injury if the exposure were allowed to continue.”

In 1968, after residents of Kyushu, Japan, fell ill after eating PCB-contaminated rice, the global public health establishment began to thoroughly examine these now omnipresent chemicals.

Damning evidence against PCBs quickly mounted.

Scientists studying damage to wildlife from the pesticide DDT realized something else was causing the same problems, and soon identified PCBs as the culprit. They discovered that PCBs interfere with birds’ reproductive systems in the same way as DDT — by causing egg shells to become so thin, the eggs are crushed when the mother sits on them.

Occupational exposure to PCBs was linked to cancers of the liver, rectum, digestive system, lymphatic systems, blood-forming organs and skin.

Menstrual irregularities and hormonal changes were reported by Kyushu victims, and pregnant women who ate contaminated rice gave birth to children with numerous developmental and reproductive problems.

By the end of the 1970s PCB production had been banned in much of the western world.


Unfortunately, between 1929 and today, Monsanto had made, or licensed someone to make, a total of 1.2 million tons of PCBs.

Of this total, 31% (370,000 tons) has so far escaped into the global environment — 20% in the oceans and 11% in soil and sediments. An estimated 4% of original production has been fed into incinerators. This leaves 65% (780,000 tons) of PCBs still in use in transformers and capacitors, or sitting in landfills waiting to escape. Developed countries hold 85% of the world’s PCBs, developing countries 15%.

PCBs have a broad range of negative effects. They accumulate in fatty tissues of living things and readily pass through the walls of cells, causing widespread damage. PCBs cause cancer and promote cancer (ie, other chemicals when combined with PCBs develop the ability to cause cancer). PCBs also cause high blood pressure and strokes in humans.

In recent years PCBs have also been identified as xenoestrogens — manmade chemicals which can mimic and interfere with the hormones which control growth and development. PCBs cause birth defects in humans and animals. They damage the human immune system (and probably the immune systems of other creatures).

PCBs enter the ocean by two routes — rainfall and river drainage. Rainfall accounts for 98% of the PCBs arriving in the ocean as air pollution; only 2% arrives via river water.

Because PCBs can become airborne when they are released into the environment, they have polluted the entire planet. Recent studies in sparsely populated areas of northern Saskatchewan, Ontario and New Brunswick revealed that rainfall now carries 17 parts per trillion (ppt) of PCBs. By law, the Ontario government only allows 1 ppt of PCBs to be discharged into the environment, but it is difficult to get a court injunction against rainfall.


Between 1969 and 1984 levels of PCBs in Arctic polar bears quadrupled. At the current rate of increase, by the year 2005 the average polar bear will have 50 parts per million (ppm) PCBs in its fatty tissue, qualifying it to be treated as hazardous waste.

St Lawrence beluga whale corpses are already classified as hazardous waste. Other species of whales are faring equally badly. Orcas from the deep ocean have 410 ppm PCBs in their blubber, and blue-white dolphins off the coast of Europe have 833 ppm.

PCBs are soluble in fat and are retained in the bodies of fish and mammals. Each step in the food chain sees the concentration of PCBs increase. Animals at the top of an oceanic food chain, such as whales, will have a concentration of PCBs in their bodies 10 million times greater than the concentration in plankton at the bottom of the chain. (This is called biomagnification and is the reason dilution is no solution to pollution.)

Marine mammals, including porpoises, seals and whales, have a genetic tendency to reproductive failure caused by hormone mimicking PCBs, which interfere with their ability to reproduce.

According to Joseph Cummins, Associate Professor of Genetics at the University of Western Ontario, if even as little as 15% more of world PCB stocks gets into the oceans, “the extinction of marine mammals would be inevitable… The consequence of failing to control PCB releases to oceans will be the extinction of marine mammals and the chemical fouling of ocean fisheries, rendering them unsuitable for use by humans.”


Human exposure to PCBs is mostly through food, mainly meat and particularly fish. [Studies of the children of Japanese women who ate PCB-contaminated rice and US women who consumed PCB- contaminated Great Lakes fish are detailed in Why parents should be xeno-estrogenophobic.]

A North Carolina study followed 912 infants from birth. Their mothers had no unusual PCB exposures but, like all westerners, carry PCBs in their body tissues. Among 866 North Carolina infants tested, higher PCBs in mother’s milk was linked with loss of muscle tone and weak reflexes.

Subsequent studies of 802 of the North Carolina children at six and 12 months revealed those with higher levels of PCBs had poorer performance in tests requiring fine motor co-ordination.

Researchers reviewing the history of the Michigan and North Carolina children conclude, “There is consistent evidence that prenatal exposure to levels of PCBs commonly encountered in the US produce detectable effects on motor maturation and evidence of impaired infant learning.”

At age 4, children with higher PCB levels weighed 10% less than children with lower levels. The effect was most significant in girls. In addition, the children were ranked according to an “activity” index, and higher PCB levels were correlated with children who were unusually “inactive and quiet.” These effects on behaviour and growth were specifically linked with exposure to PCBs before, not after birth. This led researchers to conclude that PCBs attack the central nervous system more successfully during its earlier development.

The US Agency for Toxic Substances and Disease Registry has identified human populations with potentially high exposures as: individuals exposed in the workplace, breastfed infants of mothers who eat more than 6 pounds of fish per year, and people who live in the vicinity of incinerators and PCB disposal facilities.


The fact is no one has any idea what to do about PCBs. The problems posed by other xenoestrogens could be largely solved by banning their manufacture and use. In the case of PCBs, the stockpiles are too great. Some are in storage. Many are still in use and will have to be dealt with in the next decade as aging electrical equipment needs replacement.

Monsanto could accept responsibility for its product by devoting research funds to finding safe ways of dealing with PCBs and offering to buy back PCBs from developing nations with no facilities for safe storage. Instead, the company is fighting worker lawsuits and promoting their newest products — bovine growth hormone and Nutrasweet.

Sources: “Environmental Oestrogens: Consequences to Human Health and Wildlife”, Institute for Environment and Health, University of Leicester, UK, 1995; “Extinction: The PCB Threat to Marine Mammals”, Joseph Cummins, The Ecologist, Vol 18; “Rachel’s Hazardous Waste News”, Environmental Research Foundation.

Pesticides are Poison

Pesticides are highly toxic chemicals which are deliberately released into the environment. Accounting for only a small share of the 70,000 chemicals in common use, pesticides pose great potential hazards as they are designed to kill or repel living organisms. They threaten farm workers and the general population through contamination of drinking water and residues on food crops.

In 1985, for example, 1000 North Americans were poisoned by aldicarb-tainted watermelon. That same year, over 300 BC residents suffered aldicarb poisoning after eating tainted cucumbers.

Pesticides are generally classified according to their purposes, such as insecticides (including flea sprays for pets), herbicides, fungicides, and rodenticides. These are used mostly in agriculture but also for lawns and landscapes, roadsides, schools, playgrounds, parks, libraries, and offices. Pesticide residues have been found everywhere, including human tissue, wildlife, groundwater, sediments of rivers, dust, and even rain and fog. They can travel thousands of miles from the original point of application and have even been found in the fat of Antarctic penguins.


More than one billion pounds of pesticides are applied in Canada and the US each year at a cost of over $4.5 billion. North American agricultural pesticide use nearly tripled between 1965 and 1985.

Chemical pesticides were generally not used as widely or intensively in developing countries, but usage has grown dramatically as more and more land is devoted to producing cash crops for export. In India, pesticide use increased from about 2000 tons annually in the 1950s to more than 80,000 tons in the mid- 1980s.



2,4,5-T, 2,4-D, alachlor, aldicarb, amitrole, atrazine, benomyl, lindane, carbaryl, chlordane, cypermethrin, DBCP, DDT, dicofol, dieldrin, endosulfan, esfenvalerate, ethyl parathion, fenvalerate, heptachlor, hexachlorobenzene, malathion, mancozeb, maneb, methomyl, methoxychlor, metiram, metribuzin, mirex, nitrofen, oxychlordane, permethrin and other synthetic pyrethroids, toxaphen, transnonachlor, tributyltin oxide, trifluralin, vinclozolin, zineb, ziram.


Pesticides cause a variety of health problems in humans, from acute impacts such as damage to eyes and respiratory system, nausea, skin burns and even death, to chronic effects such as cancer, various reproductive problems, nerve damage and immune system and hormonal disruption.

Environmental damage includes degradation of ground and surface water quality, soil fertility, beneficial insects, plants and animals, and aquatic and terrestrial ecosystems. Toxic agricultural runoff is, for example, a major source of pollution in the Fraser River and threatens the entire Georgia Basin ecosystem.

In addition to the known effects of pesticides on human and environmental health, there are many impacts which are poorly understood.

In Canada, laws governing pesticide registration and use have recently been transferred from Agriculture Canada to Health Canada. All data on testing and registration of pesticides are considered proprietary information, and by law cannot be released to the public. Nor does the public have any right to know about non-agricultural applications of pesticides, such as in schools or restaurants.

US decisions on regulation of pesticides are not based on whether or not they are safe, but on cost-benefit analyses which weigh the financial benefits to industry over the cost in terms of human and environmental health. These costs are paid for by consumers and taxpayers. The annual environmental and social costs of pesticide use in Canada and the US has been estimated at over $8 billion, including nearly $1 billion in public health impacts, $2.1 billion in bird losses, and $1.8 billion in groundwater contamination.

According to the US National Academy of Sciences (NAS) there is adequate testing to assess hazards for only 10% of pesticides. For 38% nothing useful is known, and the remaining 52% fall somewhere in between. The US Environmental Protection Agency (EPA) says 70 of the pesticides used on food are considered to cause cancer and many more are suspected to be carcinogens.


Testing is done on “active” ingredients (the part designed to kill the target pest), but not on “inert” ingredients. Inerts — such as the known carcinogens toluene, asbestos, formaldehyde, benzene and xylene — can constitute up to 99% of the pesticide formulation and can be more toxic than the active ingredient. Inert ingredients are considered “trade secrets” and are not revealed to the public.

EPA does not take into account any combined effects, or effects on children or other sensitive populations when determining exposure levels. A report by NAS found that children are more susceptible to pesticides, particularly those which affect the nerves, and that exposure during critical times at levels believed to be safe for adults could result in permanent loss of brain function.

Up to two million pesticide poisonings occur worldwide each year, most among farmers in developing countries. In North America, farmworkers have the highest rate of exposure to toxic poisons of any occupational group and 4.7 times the average of acute poisoning. More than 300,000 Canadian and US farmworkers are injured or made sick by pesticides every year.


As well as harming human and environmental health, pesticides are becoming less effective as pests mutate quickly and become resistant. Between the 1940s and 1970s, insecticide use increased ten-fold, while crop losses to insects doubled.

Many chemicals banned in industrial countries because of known health and environmental effects are still being used in developing countries.

DDT and benzene hexachloride (BHC), banned in the US and most of Europe and unregistered in Canada, are still used widely in the rest of the world and account for about 75% of total pesticide use in India. Present use of DDT in developing countries (mainly for control of malaria) probably exceeds the level of its historical use. The US exports one billion kilograms of pesticides each year to other countries.



In Brazil, IPM used on soybean crops reduced pesticide use 80- 90% over seven years.

In China, IPM used on cotton crops led to 90% reduction in pesticide use and 84% decrease in pest control costs, while improving yields.

In the US, the use of IPM on cotton crops led to an 88% decrease in insecticide use, with an average net return to farmers of $77/hectare.

In Costa Rica, biological control on banana crops through the reintroduction of natural enemies allowed for total discontinuation of pesticide use.


Alternatives to chemical pesticides exist. The problem lies in getting information about alternatives into the hands of users.

Integrated Pest Management (IPM) is used increasingly around the world to effectively control problem pests, including weeds, in agriculture, homes and gardens, schools, and office buildings. IPM is an ecosystem-based approach to pest control which emphasizes prevention, physical or biological control where possible, and the use of least-toxic chemicals only when necessary.

The efforts of some farmers to reject toxic pesticide use are being rewarded. Sales of organically-grown produce in the US total over $1.5 billion dollars a year and are increasing about 25% annually. To be classified organic, the food must be grown according to strict guidelines which control what compounds can be used.

NAS reported in 1989 that farmers could adopt organic farming methods, reduce or eliminate the use of synthetic pesticides and enhance their profits and crop yields. In 1990, scientists at the University of California analyzed more than 600 crop pest situations and found alternatives to synthetic pesticides exist for 75% of them.

  • Eat only organically grown produce.
  • Seek out least toxic pest control options for your home and garden.
  • Demand full disclosure of ingredients of pesticide labels.
  • Demand funds for research to help farmers get off the pesticide treadmill.
  • Work to keep carcinogenic pesticides out of your food supply.
  • Insist on knowing when and where pesticides are applied.
  • Urge your school to eliminate pesticide use and employ alternatives.
  • Join your local or regional environmental group working to reduce toxics.

Sources: “Beyond Pesticides: Biological Approaches to Pest Management in California”, Division of Agriculture and Natural Resources, University of California, 1992; “Basic Guide to Pesticides”, Shirley Briggs, Hemisphere Publishing, Washington DC, 1992; “Pesticides in the Diets of Infants and Children”, National Research Council, Washington DC, National Academy Press, 1993; “The Pesticide Question: Environment, Economics and Ethics”, David Pimentel, New York: Chapman & Hall, 1993.

Plastic Plague

Giant corporations such as Dow and Dupont have spent a great deal of time and money trying to persuade the public that plastic is environmentally safe. This simply isn’t true. From manufacture to generally short-term use to disposal — plastics pose numerous hazards.

Plastic production requires an array of toxic chemicals which have been associated with long term, adverse health effects, including reproductive problems, developmental disorders, hormone disruption, birth defects and cancer.

In 1993 alone, the US plastics industry admitted releasing 283 million kilograms of toxic chemicals into the nation’s air, water and land.


Polyvinyl chloride (PVC), commonly known as vinyl, may be the most toxic plastic on the market today. PVC is identified by the #3 recycling code.

Most fire-related injuries and fatalities are caused by smoke inhalation. This is largely the result of the preponderance of PVC plastic in pipes, cable and wire insulation, flooring, wallpaper, shower curtains, siding, moulded furniture and Venetian blinds, to name but a few common uses. PVC is also used for toys, food wrappings and containers.

PVC is the product of an extremely hazardous industrial process, which combines chlorine with ethylene dichloride (EDC), a known carcinogen, to produce vinyl chloride monomer (VCM) — the basic building block of PVC. Approximately one third of global chlorine production is devoted to making PVC. Over 24 million kilos of PVC were produced in 1994.

The lifecycle of PVC — its production, use and disposal — has been identified as the single biggest source of dioxin in the environment. Samples taken from PVC production facilities in Louisiana and Texas had some of the highest concentrations of dioxin and PCBs ever reported in chemical processing wastes.

At the Vulcan Chemical plant in Louisiana, dioxin concentrations were 200,750 parts per billion. This contamination level is comparable to the amounts of dioxin previously found only in waste from Agent Orange, the chemical defoliant extensively used by US forces during the Vietnam War.

Dioxins are only one of the many groups of by-products formed in the manufacture of VCM. Others include hexachlorobenzene, hexachlorobutadiene, hexachloroethane and carbon tetrachloride.

  • In January 1996 the Danish Environmental Protection Agency released a report linking PVC production, manufacture, use and disposal with endocrine disruption, reproductive disorders, immune system suppression and a variety of cancers.
  • In November 1995, the Swedish Parliament initiated steps towards a PVC ban by endorsing the following statement: “It is possible to make an overall assessment of today’s PVC in all its parts from chlorine manufacture to waste. Such an assessment shows that PVC can not be a part of an eco-cycle society. Today’s plasticized PVC, as well as rigid PVC with environmentally harmful additives, should therefore be phased out. The phase-out should begin speedily.”
  • More than 200 communities in Germany and Austria have banned the use of PVC construction materials in public buildings.
  • Large retail chains and supermarkets in Germany have virtually eliminated PVC packaging. Switzerland, the Netherlands and Australia are also phasing out PVC packaging.


A great deal of PVC packaging ends up in waste incinerators, as it is the least recyclable of all plastics. PVC is a major source of chlorine in municipal waste and contributes to dioxin formation in incinerators.

One German study revealed that PVC packaging, while it makes up only 0.5% of the waste stream, is responsible for about 50% of the total chlorine in our garbage.

In its recent dioxin reassessment, the US Environmental Protection Agency (EPA) identified solid and medical waste incinerators as the two largest sources of dioxin in the environment. The study revealed that much of the food chain (particularly meat, fish and dairy produce) has been contaminated by dioxins, which are now found in the bodies of all North Americans at dangerously high levels.

The study also revealed that dioxins cause cancer, hormonal changes, birth defects, infertility and learning disorders.


In addition to chlorine, PVC requires a number of highly toxic additives, many of which are known to cause serious injury to human and environmental health. PVC stabilizers are based on heavy metals: lead, cadmium, tin, barium and zinc, primarily.

These and other additives — including foaming agents, brominated flame retardants, biocides and phthalates — make the recycling of PVC products impossible. According to the Danish EPA, phthalates are “the most abundant environmental pollutant.” Many phthalates disrupt the endocrine system, causing an array of effects including decreased sperm counts, testicular cancer, reduced penis size and undescended testicles in males.

Approximately 75% of world production of carcinogenic DEHP (diethylhexylpthalate) is used as a plasticizer for PVC. In some European countries it has been banned for use in packaging which comes into contact with food and in the manufacture of toys for children under the age of three. It is on the priority pollutant list in both the Netherlands and the US.


Evidence that plastics ingredients work as xenoestrogens (synthetic chemicals which can mimic hormones) has emerged only in the past five years.

The first substance to be exposed was the chemical bisphenol A, a breakdown product of polycarbonate, widely used in many plastics, including the lining in food cans and juice packages. Bisphenol A escapes when polycarbonate is subjected to high temperatures. The estrogenic effects of bisphenol A became clear when men working in the plastics industry developed breasts after chronically inhaling the chemical in dust.

A link between plastics and breast cancer was uncovered by Drs Ana Soto and Carlos Sonnenschein in 1992. While working on research unconnected with xenoestrogens, they found cultures from breast cancer cells multiplying more rapidly than expected. Further research revealed that nonylphenol — a chemical used to make plastic more flexible — was the culprit. This estrogen-mimicking chemical had leached from the laboratory’s plastic ware. Related substances can be found in polystyrene containers, intravenous tubing and some detergents and household cleaners.


Where exactly does the plastic we put in our blue boxes and depots end up? In 1992, Greenpeace set out to follow the trail of recycled plastics. The journey led through Indonesia, Hong Kong, China and the Philippines, where thousands of people eke out a meagre income and endanger their health “recycling” North America’s waste.

In a slum outside Jakarta, for example, women work without protective clothing in a crowded, unventilated room, separating poor quality and highly contaminated plastic from reusable plastics. Huge piles of plastic bags, liquid soap bottles, food wrappers and jugs bear familiar logos: Dow, DuPont, Monsanto, Mobil.

Discards are sent to a local dump. One Indonesian recycler estimated that up to 40% of imported waste is landfilled. Workers shovel “good” plastic into large grinding machines which turn out plastic pellets or flakes. The pellets, often mixed with new plastic or other additives, are melted and formed into plastic cords. Once cooled, cords are again chipped and sent to plants in Asia to be made into containers, shoe soles or toys.

US and Canadian companies began shipping plastic waste overseas in the 1980s. In 1989, US corporations used over 12 billion pounds of disposable plastic packaging. This figure is expected to double. Rather than reduce plastic wrap, industry tried to revamp the image of plastics with a $150 million PR campaign.

First they tried adding corn starch and claiming plastic was “biodegradable”. When the public figured out the corn starch would degrade, but the plastic wouldn’t, industry jumped on the recycling bandwagon. Now most plastic packages on supermarket shelves are stamped “recyclable.” The plastic hasn’t changed, only its label.

Industry’s recycling claims are badly misleading. Recycling plastic cannot remove most toxic chemicals which are passed on to new products and those who handle them. Paper, glass and metal waste can be turned back into essentially the same product, but plastic cannot. Each time plastic is heated its chemical composition changes and its quality decreases. Turning plastic into low-grade products, makes no dent in the amount of toxic chemicals used to make the original product. And all this plastic still ends up being landfilled or burned.

  • Never microwave food in plastic containers, as dangerous chemicals can leach into food.
  • SNUB (Say No to Useless Bags)
  • Avoid purchasing over packaged products. If you have no other choice, leave packaging in stores. (They will soon demand less packaging from manufacturers.)
  • Demand and buy beverages in reusable glass bottles.
  • Write to the prime minister and premier demanding full disclosure of plastic formula ingredients — currently considered trade secrets.

Sources: “Can Environmental Estrogens Cause Breast Cancer?” Scientific American, October 1995; “Where do all our ‘recycled’ plastics go?” Greenpeace, 1992; “Plagued by Plastic Packaging”, Washington Citizens for Recycling, 1995, “PVC: Primary Contributor to the Global Dioxin Crisis”, Greenpeace, 1995.

The Precautionary Principle

It seems more than coincidental that dramatic increases in these developmental problems should parallel so exactly the increased discharge of hormone-mimicking chemicals into our environment.

Immediate action is needed to:

  • Establish the hormone-mimicking potential of commonly used materials such as fuels, plastics and drugs — and any proposed alternative.
  • Discover the consequences of long-term exposure to xenoestrogens, both individually and in combination with other chemicals.
  • Ban the use of inessential xenoestrogens.
What are persistent and bio-accumulative toxics?

The US-Canadian International Joint Commission defines persistent toxic substances as all toxic substances with a half life in any medium (water, air, sediment, soil or biota) of greater than eight weeks, as well as those which bioaccumulate in the tissue of living organisms.

There are many known persistent, bioaccumulative toxics such as PCBs, TCDD, lead, mercury and dieldrin. But an all-inclusive list of these substances does not exist. Identifying substances which lead to persistent and bioaccumulative toxic pollutants will be an important part of phasing out their production, use and release. Some substances which are not persistent or bioaccumulative should also be eliminated.

It should be noted that groups working together for phase-outs of the production, use and discharge of chlorinated pollutants have expressly stated they are not targeting the tiny percentage of chlorine used in pharmaceuticals. They are especially not interested in calling for the elimination of chlorine-based medicines, when good alternatives need to be developed.

This information package was compiled by members of the Zero Toxics Alliance. Special thanks to Delores Broten and Miranda Holmes.