Environmental Medicine - an overview

Rachel Nicoll from the British Society for Ecological Medicine

This talk was the introduction to a study day on Toxic Metals held by the Institute for Optimum Nutrition in June 2015.

(Image courtesy of Progessive Medical Education.)

What is environmental medicine?

Well, this is what Wikipedia has to say:

‘Environmental medicine is a multidisciplinary field?..studying the interactions between the environment and human health and the role of the environment in causing or mediating disease’. It overlaps with, but is distinct from, public, environmental or occupational health and it can certainly be argued that toxicology is a component of environmental medicine.?

So what does environmental medicine actually consider?

Environmental Medicine looks at the acute and chronic, short and long term effects of high and low dose exposures or environmental assaults on the body. These effects may be direct or indirect ? and they may result in long latency diseases. In other words, their effects in disease terms may not become evident for many years.

The human body is a dynamic environment, subject to multiple exposures which can affect multiple systems in which everything is interconnected. If you exclude congenital conditions there are only two causes of disease:

? too many toxins which the body cannot metabolise
? inadequate nutrients to protect against toxin damage.

The symptoms of toxic exposure symptoms are not uniform so the same toxin exposure could manifest as IBS in one person, as depression in another and produce no symptoms at all in a third person. Moreover, the problem is rarely just one toxin.? It is more usually a ‘total body burden’, with one final exposure tipping the body into a disease state.

The epidemic of chronic disease

In 2004, in a Journal of the American Medical Association (JAMA) editorial, Halsted Holman,?Professor Emeritus, Medicine - Immunology & Rheumatology at Stanford School of Medicine, ?stated that:
‘Chronic disease is now the principal cause of disability and of the ?use of health services, consuming 78% of health expenditures?. Chronic disease requires a practice of medicine quite different from that used for acute medicine’.

In 2002 Willett had already been claimed that 'despite the fact that potentially modifiable non-genetic factors (diet, weight, inactivity, smoking, environmental exposure) account for up to 70-90% of mortality in the US, clinical interventions are based primarily on drugs and surgery.' (Willett WC. Balancing life-style and genomics research for disease prevention. Science. 2002; 296: 695-97)

A 2001 report estimated that between US $568 billion and $793 billion is spent in the US and Canada on environmentally-caused disease while recent estimates suggest that between 5 and 10% of Disease Adjusted Life Years (DALYs) lost are due to environmental causes.

How has this come about?

? There is a large gap between scientific research and integration of new knowledge into clinical practice, particularly in the area of complex chronic disease.

? Many of the companies that make toxic chemicals also manufacture the pharmaceuticals that are prescribed to treat the damage.

? Newspapers report industrial poisoning or chemical spills causing cancer as if each were an isolated and unique incident. They do not consider our continual daily toxin exposure.

? The interaction between different individual toxicants in the body is unknown.

The result is that conventional/orthodox medicine denies the existence of environmental illness. This results in misdiagnosis, improper treatment and huge cost because successive ‘conventional’ medical treatments fail.

So what is the evidence that environmental illness exists and that environmental medicine can treat it?

For a start, there is a disconnect between science and orthodox/conventional medicine and nutritional medicine. This is partly because orthodox medicine will not adopt nutritional remedies despite clear evidence of benefit. But scientists are also unable to agree amongst themselves on environmental medicine. The evidence is unclear and this is not only as a result of political pressure and funding? by ‘big pharma’.

The problems with research studies

We cannot conduct randomised controlled trials of toxins on humans for ethical reasons. But in a world where the randomised controlled trial is everything, this puts recognition of environmental toxins in a poor position. Moreover, humans are surrounded by toxins every day, so there can be no true non-exposed control group against whom to ‘test’ your trial participants, although most researchers do not recognise this fact.

None the less, there is no shortage of research studies into all types of toxins, mostly animal or epidemiological but... There is no clear link between exposure and health conditions, not even between high dose exposure and acute conditions.? Nothing is simple, and here’s why.

High dose exposure and acute conditions

A precise measurement of exposure is almost impossible, particularly when it is being assessed retrospectively. Over time, researchers have improved research protocols and techniques but there are still many uncertainties. Moreover, toxins rarely occur in isolation and the combinations of toxins may have synergistic or antagonistic effects.
And then there is always the possibility of other causes of the condition in epidemiological or case control studies.
And finally, very few diseases are toxin specific ? can only be caused by one toxin ? asbestosis being a rare exception.

Low dose exposure

All the problems that arise with high dose exposure also apply to low dose exposure, plus?.

? The dose/response relationship in the low dose range may not be linear and there may be a threshold or an adaptive response.
In other words we may not apprently react to low dose exposures even though they may be having some effects on the body, or we may not react below a certain dose, or threshold. Alternatively, our bodies may adapt to cope with the low dose exposure even though we do not know what damage having to make that adaptation may cause.

? Very often, when the exposure is at a very low level or dose, the damage is initially very subtle. But most scientific research is constructed to measure gross and obvious changes in health from large and easily measurable exposures.

?? Also, researchers tend to look for effects in specific organs ? they do not look for effects on DNA, mitochondria or the immune system all of which are more likely to be affected by low dose exposures.

? Moreover, with low dose exposure the initial symptoms are generally non-specific (headache, IBS, fatigue, brain fog, sleep disturbance), all of which could also be caused by a number of conditions.

Animal studies: are they the answer?

The ethics governing animal studies are different so they can be controlled for uncertainties but there are always difficulties extrapolating results to humans. This is both because animals use different metabolic pathways to humans and because animals have a shorter lifespan than humans so may not live long enough for the long term effects of toxin exposure to become evident.?

Biomarkers: are they the answer?

Biomarkers from blood, urine, hair/nails are routinely used to assess exposure. but:

? Blood and urine biomarkers can indicate very recent exposure or, with metals, past exposure if mobilised by chelation ? a treatment which dislodges toxic metals from sites in the body where they may have settled back into the blood and the urine so that they can be excreted.

? Blood lymphocyte testing can indicate a sensitivity, which is indicative of a current toxin load but this is not conclusive because one remains sensitive for a time after the toxin has been removed. It can also only measure that specific toxin, not the total number of toxins (the total body burden) that person may be carrying.

? Hair and nail testing can indicate exposure in the recent past but the lab tests are not totally reliable.

? Moreover, no biomarker can give an accurate measure of past exposure and no biomarker can give an accurate measure of total body burden.

Safeguards: the precautionary principle

The 1994 Maastricht treaty established a European Environmental Health policy which comprised of:
? The Precautionary Principle.
This shifts the presumption that specific chemicals or activities are safe until proven dangerous, to a presumption in favour of protecting public health and the environment in the face of uncertain risks.
? The prevention of pollution at its source
? The ‘polluter pays’ principle.

So what is stopping the precautionary principle being practised?

? In the UK. The UK lags behind the rest of the developed world with no single department with overall responsibility for the impact of environmental toxins on human health. The Department of Health and others have an advisory role on public health but most of their advisors are industry-friendly ‘experts’. Basic pollution policy is set by the EU.

? Economics. No-one has yet found a mechanism to assign a monetary value to life, health or quality of life.

? There is little public pressure for more control as the general public believe that every substance in current use and on the market has been tested for toxicity, is safe and ‘approved’ for use ? but this is not the case.


Just because there are headlines saying a toxin is being or has been banned, you should not assume you can discount it as a source of toxic exposure because:

? It can take many years from the time that a toxin is ‘banned’ to actually implement the banning. (Although, for example, the 2013 Minamata Convention seriously restricted the mining and use of mercury worldwide, there are many countries that have either not yet ratified the convention or do not yet abide by it.)
? The ban may be disregarded by those using the toxin as it is cheaper to pay the fine than to stop using it.
? Many toxins have a long half life in the body.
? The toxin may have been acquired in a country with no ban.
? The toxin may have been? acquired from an import (e.g. lead in Traditional Chinese Medicines)
? Low dose exposure may take many years to manifest symptoms.

Why does not everyone with the same exposure not get sick? (Susceptibility)

Hippocrates (the father of modern medicine) allegedly stated:
‘Since some people who eat cheese do well on it, while others do not, the difference must lie in a constituent of the body which is hostile to cheese and is roused and stirred to action under its influence..?. if cheese were bad for the human constitution, without exception it would have hurt all’.

The concept of individual susceptibility

Current scientific thinking is that it is everything can be attributed to genes and to genetic factors affecting response to toxins. The new field of toxicogenomics investigates all the genes in the genome simultaneously to show the response to an environmental toxin. But although this research is growing, it is still in its infancy and so far the results are not encouraging.

Results from genetics studies

The recent spate of research into the human genome has not brought about one single cure.

Research by Lichtenstein, Holm and Verkasalo in 2000 on cancer susceptibility concluded that:
‘Inherited genetic factors make a minor contribution to susceptibility to most types of neoplasm. This finding indicates that the environment has the principal role in causing sporadic cancer’. But even this does not explain susceptibility since environmental toxins affect different people differently. ?So the true answer to disease causation must be broader than just genetics.

To quote from the Institute of Functional Medicine's?textbook of Functional Medicine:
‘Genetics is not destiny. ?Merely because we have a susceptibility to a particular condition by virtue of our genes does not mean we will suffer from that condition ? diseases are not hard-wired into our genes. What determines whether or not we contract a disease is how our genes are expressed (epigenetics), which can be influenced by potentially modifiable factors (diet, weight, inactivity, smoking, environmental exposure). This also determines our biochemical individuality.’

So ? a comprehensive picture of the factors influencing disease aetiology ? the likelihood of you contracting a disease ? could look like this:

The ‘total load’ concept

The total of all exposures in a susceptible individual contribute to a breakdown of homeostatic mechanisms ? e.g. the body’s ability to cope.

? The multiplicative effect of certain toxins ? in combination they do not necessarily behave as you would expect them to. For example: animals given a dose of mercury combined with lead. You would expect 1% of animals poisoned with either mercury or lead to die. So if the animals are given the two toxins combined you would expect 2% to die. In fact all of the animals that received the combined dose died. But very little research has been carried out on this kind of multiple exposure.

? Individual susceptibility: Genetic predisposition such as polymorphisms [variations] in detoxification enzymes; gender; age; nutritional status; microbiome status and emotional and physical stress.

? Adaptive ability: the ability of an organism to adjust to gradually changing circumstances.

How does the body protect itself against toxins?

1. The immune system

The immune system includes three protective barriers although all can be breached: the skin, the gastrointestinal tract and the lung membranes. Toxins can enter and be absorbed into the circulation via intestinal permeability (leaky gut).
However 60% of the immune system is located in the mucosa (the internal lining of the gut) and this 'gut-associated lymphoid tissue' (GALT) produces IgA, IgE and IgG antibodies to fight toxins but requires a healthy gut microbiome to support GALT. Similarly in the body the 'mucosa-associated lymphoid tissue' (MALT) generates B + T cells which circulate in the blood search of toxins.

2. Detoxification

This occurs mainly in the liver followed by the intestinal mucosa. All cells have some capacity for metabolising toxins.
Phase 1:
Biotransformation enzymes (cytochrome p450, alcohol dehydrogenase etc) convert fat-soluble toxins to water-soluble (making them more polar) for eventual conjugation through oxidation, reduction or hydrolysis, followed by excretion.
Phase 2:
Conjugation enzymes attach polar groups (e.g. glutathione, glycine, glucuronic acid, taurine, methyl groups, sulphate) to the Phase 1 metabolites/molecules.

But?.. problems with detoxification

? Many toxins ?are lipophilic and can easily penetrate lipid (fat) cell membranes and accumulate in adipose tissue (body fat), particularly those such as PCBs/polychlorinated biphenyls that are resistant to biotransformation which would normally allow them to be excreted.

? Phase 1. The biotransformed metabolite/molecule may be more toxic than the original, binding to DNA, crosslinking with proteins or generating high levels of reactive oxygen species (chemically reactive molecules containing oxygen) or oxidative stress. Many of these metabolites are known carcinogens.

? Phase 1 and 2 enzymes may have polymorphisms (variations) which make them more or less efficient.

? Up-regulated Phase 1 and down-regulated Phase 2 is the worst combination! This is associated with many chronic diseases.

3. Endogenous (naturally occurring in the body) antioxidant enzymes such as glutathione peroxidase, superoxide dismutase, or catalase.

4. Natural DNA repair mechanisms such as methylation helped on by good nutrients, particularly folic acid and vitamin B12.

5. Apoptosis. When the DNA cannot be repaired, the cell may undergo programmed cell death before the altered DNA can be replicated and cause further damage.


For more information you can contact Rachel Nicoll via the BSEM.

July 2015