Pesticide Special Report

Organic NZ Magazine: February/March 2000
Author: Meriel Watts

This is the first in a series of articles on pesticide matters that require government action. Soil & Health will place these issues before government and request that action be taken on them.

The very first pesticide issue needing government action is that of banning spray drift. We expect the Labour government to keep its word and either to introduce the Agricultural Chemical Trespass Bill it has supported for three years, or to include its provisions in the Hazardous Substances and New Organisms regulations in a manner that results in spray drift of all pesticides being made illegal.

Since spray drift has been well covered in past issues and Environment Minister Marian Hobbs has already been acquainted with the legal options, the series starts with the second problem: endocrine disruptors.




The ground-breaking research by Lou Guillette on the Lake Apopca crocodiles with shrunken penises, and the book by Theo Colborn and colleagues, Our Stolen Future, rocketed endocrine disrupting pesticides into the world headlines several years ago. Even the New Zealand media responded. Then all went quiet. GE has grabbed the headlines, but the endocrine disruptors are still quietly doing their thing, undermining the fabric of life, human and non-human. Children and the young of other species are the most susceptible.

It has always been exceptionally difficult to establish a direct cause and effect relationship between pesticides and any one particular adverse effect on humans or the environment. Indeed, it is this inability of regular science to prove beyond doubt such connections that has allowed the indiscriminate poisoning of our environment and bodies to continue unabated. The old fall-back argument of the chemical supporters is that “harm hasn’t been proven”.

Slavish adherence to the scientific method of reductionism concentrates the mind on ever smaller details in order to establish proof of ill effect, and blinds us to the wider picture. When we look up from the microscopes and mathematical models, we see mass marine die-offs, mystery strandings, and collapsing fisheries stocks only in part due to overfishing. We see worldwide increases in testicular and breast cancer, and decreases in sperm quantity and quality. We see escalation of immune system disorders.

Many scientists are now linking these effects with disruption of the endocrine system by the all-pervasive synthetic chemicals with which humanity has doused the environment, its own food chain and its own bodies.


How endocrine disruptors work

The endocrine system is the body’s messenger system. Hormones are released by endocrine glands, such as the thyroid, thymus, pituitary, adrenals, testicles and ovaries, and carried by the blood stream to specific target sites where they latch on to receptors. In this way, they govern important functions such as growth and development, metabolism, reproduction, and the immune system.

Endocrine disruptors are chemicals that activate natural hormones or block their action, triggering a cascade of damaging biochemical changes that can affect development of the nervous, immune, reproductive and digestive systems. They can alter the pattern of hormone synthesis, metabolism, and excretion. Frequently thyroid, oestrogen and testosterone hormones are involved. Endocrine disruptors can mimic hormones by binding to receptor sites – oestrogen mimicry is the most well known endocrine disrupting mechanism. But there are other mechanisms and sites of action involved as well: endocrine disrupters also act on neurotransmitters, growth factors, corticosteroids, progestins, retinoids, and cytokines (Smolen 1999; Lyons 1999).

One chemical can work in several different ways. For example, DDT is mildly oestrogenic (mimics oestrogen), but its breakdown product pp-DDE is a very strong anti-androgen (blocks androgen). Another breakdown product, DDD, can affect neurotransmitters and cell membranes.

Often, the original pesticide is not the problem, but rather its breakdown products. Metabolites of the fungicide vinclozolin have been shown to be strong anti-androgens in laboratory mice. Like DDE, they bind to the androgen receptor blocking normal male development at a critical time. The result is undescended testes, vaginal pouches, reduced seminal vesicles and prostrate glands, and cleft penis (Smolen 1999).

Endocrine disruption can occur at any stage of life, but effects are most significant in the very early stages – in utero and during nursing – and the amounts of chemical required to cause those effects are much smaller. Correct development of the foetus and small child depends on a delicate balance of hormonal messengers involved in a complex feedback system that has evolved over many generations, without the relatively sudden bombardment of the endocrine disrupting chemicals that has faced humanity in the last 50 years.

Timing is crucial. Developing organ systems go through brief windows of time during which they are particularly vulnerable to endocrine disruption. For example, days 56 to 80 of foetal development are crucial to the onset of the condition hypospadias in which the urethra does not open at the end of the penis. Changes that occur during this period cannot be undone; effects are irreversible and permanent. Subtle changes occurring at this early stage in life can lead, not only to birth defects and other developmental problems, but also to cancer later in life. Endocrine disrupting chemicals that accumulate in fat, and so pass from a nursing mother to her newly borne offspring, are a particular problem, for development of the nervous, reproductive and immune systems continues after birth. Such chemicals include many referred to frequently in Soil & Health over the years such as DDT, endosulfan and atrazine.

Thus while it is the mimicry of sex hormones, particularly oestrogen, that is the most well known aspect of endocrine disruption, it is not the only effect. Pesticides such as amitrole, ioxynil, maneb, mancozeb, zineb and alachlor (Lyons 1999) affect both the thyroid hormone and the brain. Recently, researchers have begun to pay attention to the interconnections between the endocrine, immune and nervous systems and how the impact of chemicals that affect one system can be felt throughout the others (Porter et al. 1993, 1998; Guillette et al. 1998). For example, organophosphate and carbamate insecticides – known primarily for their effect on the nervous system – may suppress the brain’s release of the gonadotrophic hormones (follicle stimulating hormone and leutinizing hormone) through their effect on acetylcholinesterase activity (Lyons 1999). Acetylcholinesterase is an enzyme involved in the transmission of nerve impulses. Some organophosphates have been linked to abnormal menses, amenorrhea and early menopause, again by disturbing the pituitary gland’s release of leutenizing hormone.

Perhaps of even greater concern are the sociological effect of pesticides, mediated via the interconnection between the endocrine and nervous systems in particular. Such effects include aggression, irritability, lowered IQ and other neuro-developmental problems indicative of brain dysfunction. (see boxes.) These recent findings imply grave consequences for the future of the individual, the family and society as a whole.


Endocrine disruptors in our air and in our food

Because endocrine disruptors exert their effects through interference in natural systems that operate on the level of minute amounts of natural chemicals, only minute amounts of pesticides are required to cause adverse effects. Therefore, exposure through spray drift and food residues is very important.

“Human dietary intake of synthetic hormonally active agents [endocrine disruptors] remains substantial,” said the USA’s National Research Council after a four-year study (Montague 1999). It cited a number of studies associating the consumption of food or water containing residues of endocrine disruptors with adverse effects:

  • atrazine in drinking water with cardiovascular, urogenital and limb-reduction birth defects
  • maternal consumption of fish containing PCB residues with lowered birth weight, shortened gestation, smaller head size and deficits in neurological development
  • eating fish containing residues of a variety of endocrine disruptors with reduced cognitive flexibility, word naming and auditory recall in people over 50 years
  • pre and post natal exposure of children to foods containing PCBs with deficit in cognitive development, such as short-term memory, visual discrimination, IQ.

Quite clearly, we have a problem in New Zealand with exposure to endocrine disruptors. The second most commonly used herbicide, and the most commonly drifted pesticide, is 2,4-D, an endocrine disruptor. There is anecdotal evidence that 2,4-D is involved in disturbances of the menstrual cycle of adult women and in precipitating early onset of menses in children in New Zealand. Ambient levels of vinclozolin were measured in the middle of Katikati township in 1997 – in other words the air contained background residual levels of this endocrine disruptor for all who entered Katikati to breathe. Permethrin and phenothrin are sprayed over passengers on aircraft arriving in New Zealand. MAF sprayed chlorpyrifos in suburban Auckland last year to control painted apple moth.

The latest survey of food residues, (Soil & Health Jan/Feb, Mar/April 1999) reveals the following endocrine disruptors in our food supply: chlorpyrifos, mancozeb, maneb, zineb, dicofol, pp-DDE, dimethoate, endosulfan, vinclozolin, fenitrothion (ESR 1997/98).

Thus, currently, very few if any New Zealanders can escape inhaling or ingesting endocrine disrupting pesticides if they eat non-organic food, live in the country or the city, or travel overseas.


The failure of the regulatory system

The pesticide regulatory system is based on the centuries-old belief that the dose makes the poison, i.e. the more you have of a substance the more poisonous it is. Therefore, when laboratory rats fail to show ill effects from high doses of pesticides, it is assumed that low doses will not cause harm to humans. But this theory falls apart with endocrine disruption, for four reasons:

The timing of the exposure of laboratory rats, and humans, is critical as already explained. If rats are not exposed at the equivalent time at which the human foetus is most sensitive to an endocrine disruptor, the effect may be missed altogether.

It has been demonstrated that where high doses of a chemical do not cause endocrine disruption, low doses will (Colborn et al. 1996). Natural chemicals occur in minute amounts – their normal working levels are measured in trillionths of a gram. They are highly susceptible to equally low doses of chemical mimics.

Some chemicals have effects at low doses that differ from those found at high doses.

The effects of mixtures of chemicals as shown in the studies by Dr Warren Porter and colleagues (refer box “Pesticides and aggression”) is not revealed.

The arena of endocrine disruption is immensely complicated and fraught with disagreement over how, why and what. To find all the answers will take decades and cost many millions of dollars, by which time it may well be too late to prevent large-scale dysfunction of the human population, and destruction of many other species. The list of chemicals recognised as a problem varies from publication to publication, depending in part on how broad a view of endocrine disruption is taken – some recognise only the effects on sex hormones. The chemical industry is reluctant to recognise even this limited view (Colborn et al. 1996). Endocrine disruption occurs in insects – that is the basis of the new class of pesticides known as Insect Growth Regulators such as tebufenozide (Mimic), cyromazine (Larvadex), methoprene (several flea killers), and diflubenzuron (Dimilin). These chemicals are specifically designed to disrupt the insects’ hormones. But while the chemical industry has been quick to capitalise on endocrine disruption in invertebrates, it has been very slow to acknowledge similar effects of chemicals on humans and other animals.

The United States Government has required the Environmental Protection Agency to screen chemicals for hormonal effects, and the Agency has produced a two volume report on the subject, known as the EDSTAC report. So far, apparently, there are still no conclusive tests that will determine whether or not a chemical is a hormone disruptor (Smolen 1999).

Meanwhile, the New Zealand government’s approach remains “if you can’t prove it occurs, we don’t need to worry about it”. When Alison White from PAN raised the issue with the Pesticides Board in 1997, the response was, “We see no reason why pesticides should be subject to more restrictions than they are at present.” Once again, the precautionary approach, more imperative in this arena than ever before, is overridden by the illogical, slavish adherence to undisputed scientific proof. But there are no ethical or scientific reasons for presuming pesticides to be safe until proven otherwise – that is simply a construct of the poison-pushers. Regulations under the HSNO Bill for the registration of pesticides, and other chemicals, do not even recognise endocrine disruption.

Now we have a new government that appears to be more environmentally and socially aware than the last one. It is imperative that it implements the precautionary approach with regard to endocrine disruptors. Where there is evidence from wildlife studies, animal laboratory trials or human epidemiological studies that a chemical may cause endocrine disruption, then that chemical should be de-registered and removed from the market. In other words, in the absence of scientific certainty the burden of proof must lie with the chemical manufacturers: if they cannot prove that the chemical concerned does not cause endocrine disruption it must be removed. Many endocrine disruptors have already been identified using the standard toxicological tests. Get rid of these. The precautionary approach does not mean adding an uncertainty factor of ten in the mathematical models that will tell you how much chemical you can put down a person’s throat before he or she gets sick. It means not using it at all unless we are certain it is safe.

The social costs of ill health, violence and lowered intelligence far outweigh any possible benefit of endocrine disrupting pesticides. After all, it must be remembered that not one single pesticide in the list provided here is necessary for New Zealand’s agricultural and horticultural industries. For all of these pesticides there is a less toxic alternative that does not threaten the fabric of life. Thus, to continue using unnecessary pesticides for which there is considerable evidence that they may be contributing to birth defects, chronic disease, lowered intelligence and increased aggression is unconscionable. Why should society bear the risk of these chemicals when we don’t need to, solely so that some people can make huge profits out of them?



A recent study among the Yaqui people of Mexico compared two groups of children sharing genetic, cultural and social backgrounds; one exposed to heavy pesticide use, and the other from an area where pesticide use is avoided. When chemical pesticides and fertilisers were embraced by many of the residents in the Yaqui valley in the late 1940s, a number of residents moved into the foothills in protest at the change, and stayed there. In the valley, up to 90 separate applications of pesticides are made per year, including “multiple organochlorine and organophosphate mixtures and pyrethroids”. In addition, household insecticides are used each day throughout the year. In contrast, the ranching lifestyle of the highlands requires no pesticide use, and the government DDT applications each spring for malaria control are their only contact with pesticides.

The survey revealed no differences in physical growth or other outward manifestations, but it did reveal significant differences in functional abilities. In the following areas valley children showed a marked decrease in function relative to highland children:

  • physical stamina
  • ability to catch a ball
  • fine hand-eye coordination
  • ability to draw a person: the valley children provided only random undifferentiated lines in comparison with the highland children’s easily recognisable human figures (refer drawings below)
  • recall after 30 minutes, although immediate recall was equivalent
  • group play: the valley children were less creative, roaming aimlessly or swimming in the irrigation canals with minimal group interaction.
  • Additionally, valley children were observed to be more aggressive, hitting siblings, and becoming more upset by minor corrective comment by a parent.

The researchers found no statistical difference between valley and highland women for problems such as spontaneous abortion, pre-maturity, neonatal death and birth defects. However, when the problems were viewed as a composite, the valley women had an elevated rate of pregnancy problems.

The researchers concluded that the differences they found in mental/neurological functioning were indicative of brain dysfunction and held implications for learning ability and social behaviour. This study provides possibly the only human data currently available on the neuro-developmental effects of exposure to a mixture of pesticides (Schmidt 1999). Whether the effects were the result of one chemical, or one class of chemicals, or a whole mixture of chemicals that may have been working additively, synergistically or independently, remains unknown. Endocrine disruption, however, is clearly implicated. (Source: Guillette et al. 1998.)



Recently published results of a five-year study by a group of biologists and medical researchers in the USA show a link between the ingestion of low levels of pesticides, endocrine disruption and aggression. Porter et al. (1999) voluntarily fed rats drinking water containing residues of the insecticide aldicarb, the herbicide atrazine and nitrate fertilizer. The chemicals used were those commonly found in US drinking water at legally allowed levels. They found changes in thyroid hormone levels and increases in aggression as a consistent response to the mixtures of chemicals, but not to individual chemicals. An earlier study had also found interactive effects between three pesticides (aldicarb, methomyl and metribuzin) on thyroxine levels in rats (Porter et al. 1993). The authors noted that “the same concentrations and mixtures of these three pesticides have now been shown to be implicated in learning impairment and other neurological functions, immune parameter changes, and endocrine changes”.

Disruption of the thyroid hormone is a significant effect of endocrine disruptors. As well as controlling the body’s rate of metabolism, the thyroid is essential to organ development and normal function. Interference with thyroid function can result in a variety of effects including reduced growth, minimal brain dysfunction syndrome and abnormal testicular development (Carpenter et al. 1998). It can also result in increased irritability and aggression. However, if the effect is seen at normal exposure levels, only with chemicals in combination as suggested by Porter et al. (1999), then traditional single chemical testing will not suffice for an accurate identification of pesticides that pose this hazard.


Other chemicals implicated in endocrine disruption:

  • Phthalate plasticisers – used in PVC, polyvinyl acetate, polyurethane and some polystyrene plastics. Also in paints, pesticides, inks, hairsprays, insect repellents.
  • Bisphenol A – in polycarbonate plastics used for making baby feeding bottles, water jugs, plastic dental sealants and in metal food can linings. Also in epoxy resins, coating thermosensitive paper, stabiliser for PVC softeners, tyre production.
  • Styrenes – drinking cups and food containers. Also used to produce polystyrene and released from some polystyrene applications.
  • Alkylphenolic chemicals, including 4-nonylphenol, 4-tert-octylphenol – breakdown products of industrial alkylphenol ethoxylate detergents and pesticide additives. Also used in paint, textiles, metal finishing, certain plastics and lubricating oils.
  • Polybrominated bisphenol-A – widely used as a flame retardant in plastics.
  • t-Butylhydroxyanisole (BHA) – used as an antioxidant especially in foods. Also used in cosmetics.
  • Lead – in batteries, production of chemicals, various metal products, ammunition, old paints.
  • Methylmercury – electrical equipment, batteries, production of chlorine gas, by-product of gold mining. Has been used in fungicides.
  • Cadmium – batteries and metal plating, pigments, plastics. Contaminant of superphosphate fertilizer.
  • Dimethyl formamide (DMFA) – common industrial and laboratory solvent, used in producing synthetic leather products.
  • Polyaromatic hydrocarbons – formed in burning of fossil fuels.
  • Ethylene glycol – common industrial and laboratory solvent; used in production of polymers for fabrics and in some food products.
  • 4-Cl-3-methylphenol – used in cosmetic products.
  • 4-Cl-2-methylphenol – additive in pesticides.
  • Perclorethylene (PERC) – solvent used in dry-cleaning.
  • Dioxins – by-products of processes in which chlorine and chlorine-derived chemicals are produced, used and disposed of, including waste incineration.

(Sources: Smolen 1999; Nair 1999.)



Turmeric inhibits estrogenic effects of pesticides

A study published in 1998 indicated that curcumin, the major constituent of turmeric, is effective in inhibiting cancerous breast tumours caused by estrogenic pesticides and other chemicals. The effect is more marked with the addition of isoflavonoids, the synergistic combination achieving a 95% inhibition in growth of cancerous cells in laboratory trials, out-competing Tamoxofen, the drug favoured for breast cancer (70-80% inhibition) with none of its side effects.
(Source: Verma et al. 1998.)



Effects on human health

Endocrine disruptors have been cited as potential contributing factors to the following conditions in humans:

  • genital deformities such as hypospadias
  • cryptorchidism (undescended testes)
  • testicular cancer
  • decreased sperm counts
  • prostate cancer
  • breast cancer
  • endometriosis
  • infertility
  • precocious puberty
  • decreased lactation
  • goitre
  • attention deficit hypersensitivity disorder
  • learning disability
  • lower IQ
  • immune system dysfunction
  • increased susceptibility to disease
  • reduced growth
  • aggression, irritability.

(Sources: Smolen 1999; Quijano 1999; Lyons 1999.)


Pesticides registered in New Zealand known to cause endocrine disruption in animals

  • Herbicides
  • 2,4-D; alachlor; amitrole; atrazine; bromoxynil; ioxynil; metribuzin; picloram; simazine; trifluralin.


  • carbaryl; chlorpyrifos; cypermethrin; deltamethrin; dichlorvos; dicofol; dimethoate; endosulfan; esfenvalerate; fenitrothion; fenvalerate; fipronil; fluvalinate; Lambda-cyhalothrin; malathion; methomyl; methoxychlor; methyl parathion; permethrin; phenothrin; tributlytin.


  • benomyl; fenarimol; mancozeb; maneb; metiram; orthophenyl phenol; vinclozolin; zineb; ziram.

(Sources: Moses 1999; Smolen 1999; Lyons 1999.)




  • Carpenter, D.O., Arcaro, K.F., Bush, B., Niemi, W.D., Pang, S., Vakharia, D.D. 1998. Human health and chemical mixtures: an overview. Environmental Health Perspectives 106 (S.6):1263-1270.
  • Colborn, T., Dumanoski, D., Myers, J.P. 1996. Our Stolen Future. Little, Brown and Company, Boston, USA.
  • ESR 1997/98. 1997/98 New Zealand Total Diet Survey Raw Data Reports – Q1, Q2, Q3, Q4. Institute of Environmental Science & Research Ltd, Christchurch.
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  • Guillette, L.J.Jr, Gross, T.S., Masson, G.R., Matter, J.M., Percival, H.F., Woodward, A.R. 1994. Developmental abnormalities of the gonad and abnormal sex hormone concentrations in juvenile alligators from contaminated and control lakes in Florida. Environmental Health Perspectives 102:680-688.
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  • Porter, W.P., Green, S.M., Debbink, N.L., Carlson, I. 1993. Groundwater pesticides: interactive effects of low concentrations of carbamates aldicarb and methomyl and the triazine metribuzin on thyroxine and somatotropin levels in white rats. Journal of Toxicology and Environmental Health 40(1):15-34.
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