| Pesticides with reproductive and
endocrine disrupt- ing effects(2) |
| Herbicides |
| 2,4-D |
| 2,4,5-T |
| alachlor |
| amitrole |
| atrazine |
| metribuzin |
| nitrofen |
| trifluralin |
| Fungicides |
| benomyl |
| hexachlorobenzene |
| mancozeb |
| maneb |
| metiram-complex |
| PCP |
| tributyltin |
| zineb |
| ziram |
| Insecticides |
| carbaryl |
| chlordane |
| dicofol |
| dieldrin |
| DDT and metabolites |
| endosulfan |
| heptachlor H-epoxide |
| lindane (y-HCH) |
| methomyl |
| methoxyclor |
| mirex |
| oxychlordane |
| parathion |
| synthetic pyrethroids |
| toxaphene |
| transnonachlor |
| Nematicides |
| aldicarb |
| DBCP |
Many synthetic organic chemicals are
capable of disrupting endocrine (hormonal) processes in animals and humans,
often because their molecules mimic natural hormones and act instead of them in
the cell. This may add to a natural hormone process or compete with it.
In 1991 an unusual meeting of scientists took place in
Wisconsin in the US. Endocrinologists studying the effects of the synthetic
hormone diethylstilbestrol (DES)—given to prevent miscarriage—met scientists
studying reproductive dysfunction in the wildlife around the Great Lakes. DES
has been found to cause reproductive system malformations and cancers in
children whose mothers took it during pregnancy. Similar malfunctions have been
found in shellfish, birds, fish, mammals and turtles in the Great Lakes, and
have been connected with pollutants that interfere with hormonal processes.
After the conference the scientists agreed a consensus
statement recognising the existence of environmental endocrine disrupters(1).
Since then, Dr. Theo Colborn, of the World Wildlife Fund US, who brought the
scientists together, has stated that action should be taken to reduce the
exposure of endocrine disrupters, both from old discharges and from new
chemicals likely to be released.
Pesticides such as DDT are prominent in a diverse list (see
box) of chemicals found to disrupt hormone action or reproduction in laboratory
experiments, in wildlife and in humans. Endocrine activity is difficult to
predict from simple examination of the molecule. Organochlorines may be
especially risky because of their persistence: they can remain in the body for
many years.
Human effects
Data on the health effects on humans of environmental
oestrogens is fragmentary, but suggestive and worrisome. Sperm counts have
halved in all industrial nations since 1940. Over the same period, there have
been worrying trends in testicular cancer, male reproductive system defects,
female breast cancer and endometriosis (the growth outside the uterus of cells
that normally line the uterus)(3).
Wildlife disruption
There is now strong evidence that environmental
oestrogens cause abnormal sexual development and impaired reproduction.
Alligators in Florida are failing to hatch, and the males that do hatch have
abnormally small penises(4). Two- to four-year-old salmon in the Great Lakes
have been found to have enlarged thyroid glands. Precocious sexual maturity,
poor egg survival and low thyroid content in eggs are also common(5). Many
reproductive anomalies have been found in birds.
Screening for endocrine toxicity
At present, screening for the endocrine disruption
potential of pesticides, prior to release in the market, is not specifically
required, although some aspects are de facto assessed. Dr Colborn suggests that
screening for activity using hormone-responsive cells should be required.
Regulators’ views on endocrine studies
Regulators say that aspects of endocrine toxicology
are required prior to pesticide approval. The Pesticides Trust [now PAN UK]
contacted several
leading regulatory agencies to seek clarification.
The US position was outlined by Richard Mountfort of the
Environmental Protection Agency (EPA): “Endocrine organs/tissues are examined
in long-term and [medium-term] animal studies using the active ingredient as the
test substance. In developing and describing test results to US authorities,
companies may attempt to determine if a specific effect is hormonally mediated,
and if quantification by methods other than linear extrapolation may be
appropriate. Normal levels of hormones are variable and it is not clear, at this
time, that endocrine disruption tests would be useful data”(6).
In Canada the regulatory view is that “if the available
toxicity data suggest a potential for treatment-related endocrine disruption by
the chemical, additional data on endocrine functions/hormone levels pertinent to
the specific area of concern would be requested”, according to Dr C. Warfield
of the Health and Welfare Department(7). In cases in which concerns have been
raised about possible adverse health effects of particular chemicals, Australian
regulatory authorities can request sponsor companies to provide further studies.
For example, Dr BG Priestly of the Australian Department of Health says: “we
currently are awaiting the submission of endocrine effect data on triazine
herbicides from the relevant company”(8).
Groups call for endocrine screening
The Pesticides Trust (PAN UK) and Women’s Environmental
Network (WEN) agree with Dr Colborn of the World Wildlife Fund that the
regulatory authorities should require pre-approval testing to assess endocrine
disruption by pesticides and to develop relevant protocols. As with predicting
carcinogenicity, it is unlikely that there will be an easy-to-adopt ideal test.
The real possibility of endocrine disruption being already part of the burden on
women pesticide sprayers must make improvement of their conditions an even
greater priority, according to WEN. The problems raised here also add to the
argument raised by environmentalists suggesting a general reduction in pesticide
use, whilst maintaining adequate pest control.