Toxicity of Cancer-Causing Chemicals
 
by Kathryn Alexander (more info)
listed in environmental medicine
originally published in issue 112 - June 2005
 
Media coverage encourages us that we are winning the battle against cancer. Taking a closer look at the statistics, I find that in 2000, the estimated number of those suffering from cancer in the UK was 1.2 million �?or two percent of the population. However, as the rate of incidence (new cases per annum) is rising (currently averaging at 270,000 per annum) and the mortality rate is falling, the study admits that the figures are probably an underestimate.1 These figures simply mean that more people are getting cancer and living longer with cancer. As finding a cure for cancer seems to foil the scientific community, reducing mortality becomes the measure of their success, and the official response to this increase in cancer is two-fold �?early detection through better screening and a longer life-span account for the 'apparent' rise.

However, this doesn't tally with other statistical analysis that:

�?More young women are now being diagnosed with breast cancer;
�?The life-time risk for women of breast cancer in the 1940s was one in 16 but is currently one in eight;
�?Prostate and breast cancer have suddenly out-stripped both lung and colorectal cancer;
�?Non-Hodgkin's lymphoma, a rare form of cancer, has increased by 80% since the 1970s;2
�?Cancer is the highest cause of death in children under 15 years (one in 200 children are diagnosed with cancer per annum);
�?The government's own estimates now predict that our life-time risk of cancer is one in three for males and one in four for females.

Nor does the 'apparent rise' factor in the environmental impact of chemicals which have been unleashed onto the global community over the last 60 years. To the casual observer it would seem logical to draw a strong association between the increase in toxic chemicals and the parallel rise in the incidence of cancer, notwithstanding the bulk of animal studies and epidemiological evidence which support this correlation. So how is it that the environmental factor is ignored in the cancer equation? And how is it that we have reached a position where clinical observation is no longer a major consideration in any benefit/risk assessment? The answer is simple �?if we cannot scientifically prove cause and effect, then all other considerations pale into insignificance.

Scientific Proof

Let's examine the self-imposed rules of the scientific community. Scientific investigations seek to link the mode of action of an isolated, chemically defined active substance to a specific mechanical dysfunction and then measure the outcome. Evidence that falls outside this rationale may be dismissed on the basis that it can't be quantified within the set criteria. Hence the scientific fraternity often shields itself behind a code which focuses solely on the discovery of scientific truths, where any side-effects that have not been scientifically proven within the model can either be considered as unrelated to the action of the chemical (no evidence on available data), or simply put down to genetic variance. Although the clinical reality may be staring the observer in the face, the scientific fraternity, through its code, has given itself licence to ignore the reality and evade any responsibility. We only have to look as far as the tobacco industry, which was able to frustrate any attempt to link its product with lung cancer for over 40 years, and today can still successfully argue in court that no scientific proof exists to prove that smoking has caused the cancer. As industry now funds the majority of medical research, the public can no longer assume or trust the independence of scientific studies. This is due to the conflict of interest that the scientific fraternity is now experiencing as a direct consequence of having to serve the interests of their new paymasters. Corporate entities can only justify to their shareholders the funding of research which directly produces a commercially viable product, usually focused on high-yielding affluent Western markets.

The Role of Chemicals in Causing Cancer

The contention lies in proving which chemical causes what disease and at what dosage. When we examine the methods of evaluation based on epidemiological studies and animal toxicology research, we find that they are not only flawed but are also open to abuse by chemical manufacturers.

Let's start with animal studies. The purpose of these studies is to determine the carcinogenicity of a single substance and the dose at which it is likely to become toxic, and extrapolate from this data the risk to human populations. If the results are unfavourable (to the manufacturer) they may be disregarded on the basis that species sensitivity varies widely and the exact position of humans on the sensitivity spectrum is unknown.

The second loophole lies in the mandatory testing of single chemicals. The chemical that is usually tested is the 'active' ingredient �?or the one with killing power. However, commercial brands usually contain ingredients that are misleadingly called 'inert', which make the product more efficient.

Roundup's Toxic Effects

Take Roundup as an example. The active ingredient in Roundup is glyphosate and the 'inert' ingredient is a surfactant known as POEA. However, recommendations are based on tests using glyphosate alone. Although results indicate increased incidence of liver, thyroid, and testicular cancer in rats, the Environment Protection Agency in the US does not consider the 12% incidence of testicular cancer in treated animals of statistical significance to the 4.5% incidence in the non-treated group. Hence glyophosate is considered toxicologically benign.3 However, further tests show that Roundup is three times more lethal than glyphosate. This suggests that it is the synergistic "mix" of chemicals that may cause the problems �?not the single component. It should also be noted that epidemiological evidence supports a three-fold risk of non-Hodgkin's lymphoma in farm workers using Roundup. This is not an isolated case.

Other studies show that minute doses of multiple chemicals tend to be more lethal than a single chemical dose alone.4 Unfortunately, studies on single chemicals rather than the multi-chemicals in commercial products are accepted as sufficient evidence for assessing the toxicity of products �?as in the case of Roundup, which has never been tested in its product form for licensing.

The saga continues. Glyphosate is persistent and can remain in the soil and contaminate it and everything grown in it for up to three years. Its use has more than doubled from 17-20 million kilograms in 1995 to 45 million kilograms in 2001. We have no method of assessing the total residue of Roundup on crops. No government agency has even considered the issue of glyphosate on GE/GM crops �?thus nobody has included the effects of increasing the use of glyphosate in the risk/benefit analysis carried out on GE crops.2

So here is the rub: if GM crops are implicated in degenerative disease, will this be due to the genetic engineering of the crops, the vast toxic residue of herbicides that these crops carry, or Roundup's effect of inhibiting the protein synthesis of the plant, leading to a deficiency of two essential amino-acids and malnutrition? Will it be a deficiency disease, a toxic disease or a disease caused through genetic modification? We have no way of knowing, and nothing in place to determine the safety. In layperson's terms, this means there is no risk management.

High Exposure Groups

Next, we come to determining the toxic dose of a chemical. Epidemiological evidence concentrates on groups exposed to the highest levels of known contaminants such as hospital workers, farmers, carpenters (using treated wood), and chemical industry workers. The incidence of disease is noted and compared to the incidence in the general community. A positive correlation shows an increased incidence of disease in the exposed group above a certain threshold �?such as the six-fold risk of non-Hodgkin's lymphoma in agricultural workers using herbicides.

One of the best epidemiological examples which links organochlorine insecticides �?DDE (a metabolite of DDT), lindane and alpha benzene hexachloride (aBHC) �?to breast cancer, is the Israeli breast cancer anomaly noted during the 1970s to 1980s.

In the early 1970s, the incidence of breast cancer was twice the prediction. The Israeli government looked at levels of three organochlorine insecticides in milk and found between five and 100 times the amount found in US milk, and also higher levels in breast milk. By 1978, the government banned aBHC and, later, lindane from the milking shed. Breast cancer rates started to decline, but were steadily increasing in other countries.5

During the 1990s, scientists tried to forge a link between organochlorine insecticides and breast cancer. Studies from the USA, Canada and Finland compared malignant and non-malignant breast tissue samples and found a positive correlation between higher levels of organochlorine compounds in breast fat tissue and cancer. Levels of DDT and DDE were 50-300% higher in women with hormone-sensitive breast cancer than in those with benign breast disease. The estimated risk from higher exposure is two to four times greater than in those with lower exposure. But interestingly, other studies found no links at all. However, two isomers of DDE (p'p-DDE and o,p-DDE) have recently been identified which appear to have opposing actions, and depending upon which is more prevalent at the scene determines overall activity.6

The story is similar when we review prostate cancer. The development of androgen receptors in the prostate gland is governed by oestrogen. Overexposure to xeno-oestrogens (environmental oestrogens) results in an increase in the number of receptors, leading to a permanent sensitization to testosterone. This may result in either benign prostatic hypertrophy (enlargement of the prostate), which now affects 80% of males by the age of 70 years, or prostate cancer.7

Animal studies support these findings. Exposing adult animals to increased oestrogen leads to a 50% increase in androgen receptors and an increased incidence of prostate cancer. In an epidemiological study, an increased incidence of prostate cancer was reported in workers at a US manufacturing plant producing the (strongly oestrogenic) herbicide atrazine. Although this product is already banned in many European countries and will be banned totally by the EU in 2005, the US Environmental Protection Agency decided not to restrict its use. Currently, 60 million pounds of atrazine is applied annually to US soils.8

Invariably, the outcome of such studies does not lead to a ban of the product, but it may be required to carry additional warnings. This is the pattern of our Multi-National culture, where products are introduced with the full knowledge of their devastating effects as advised by the scientists they employ, in the confidence that it takes up to 30 years for a general consensus to occur as evidence builds on the overwhelming clinical effects on human beings and the environment (as we have experienced with lead, mercury, agent orange, smoking and asbestos).

Given this perspective, shouldn't we be factoring in the impact of environmental chemicals sooner rather than later? The reality is that research programmes are primarily focused on disease management rather than proving cause, where the fruits of public funding and charitable donations end up as patented intellectual property owned by the pharmaceuticals �?as in the case of AIDS research. The truth is that by proving cause the backlash on multi-nationals and governments, in terms of legal liabilities, could be monumental.

However, we have a choice: we may wait for scientific proof, wait for a cure (if you can have a cure without dealing with the cause) or take steps to limit our exposure. Most chemicals have been proved to be toxic, carcinogenic and incompatible with life. When we factor in the risk of bio-accumulation, it is doubtful that there is a safe dose for any chemical. Add to this the possible synergistic effects of multiple chemicals which have never been tested �?and you have a chemical mine-field. The to-do list is simple �?limit your personal exposure and support campaigns for a cleaner environment and groups that safeguard your access to natural medicine such as the Alliance for Natural Health (www.alliance-natural-health.org).

Further Information

If you are interested in options for chemical-free management and pesticide-free solutions you can visit www.pesticides.org/factsheets.html. There are also excellent scientific papers on numerous chemicals at www.pesticide.org/factsheets.html#pesticides

References

1. Cancer Research UK. Cancer Stats �?Incidence. UK. Feb 2004. www.cancerresearchuk.org/aboutcancer/statistics/statsmisc/pdfs/
cancerstats_incidence.pdf
2. New Study Links Monsanto's Roundup to Cancer. Organic Consumers Association Newsletter. Press Release. 22 June 1999. http://organicconsumers.org/ Monsanto/glyphocancer.cfm
3. Cox C. Herbicide Factsheet: Glyphosate. Journal of Pesticides Reform. Vol 24. No 4. Winter 2004. www.pesticide.org/gly.pdf
4. Colborn T, Dumanoski D and Myers P. Our Stolen Future. Abacus of Little, Brown and Company. London. p140. ISBN 0 349 10878 1. 1997.
5. Cox C. Pesticides and Breast Cancer: Prevention is Crucial. Journal of Pesticides Reform. Spring 1996. www.pesticide.org/BCancerReport.pdf
6. Breast Cancer Research Programme. California. Influence of localized DDT Exposure on Breast Cancer. 2003. www.cbcrp.org/research/PageGrant.asp?grant_id=1811).
7. Colborn T, Dumanoski D and Myers P. Our Stolen Future. Abacus of Little, Brown and Company. London. p178. ISBN 0 349 10878 1. 1997.
8. Natural Resources Defence Council. EPA won't Restrict Toxic Herbicide Atrazine despite Health Threat. Jan 2004. www.nrdc.org/health/pesticides/natrazine.asp