Open a newspaper and on any given day you can usually find a story about the growing number of overweight and obese people throughout the UK, and indeed the world. Obesity is now officially an ‘epidemic’. GPs are ‘alarmed’. The Department of Health is ‘concerned’. And dozens of local authorities are gearing up to ‘do something about it’.
The figures are shocking. Globally the prevalence of overweight and obesity has increased steadily since 1970. In August of this year, it was reported that the number of overweight people in the world has topped one billion, considerably outnumbering the 800 million who are undernourished.
It’s not just an aesthetic problem. Obesity is a health risk associated with higher rates of diabetes, heart disease and cancer. In the UK, 43 per cent of men and 34 per cent of women are overweight and one in four adults, and one in 10 children under 15, are obese. The direct cost to the NHS is £480 million. The indirect costs are estimated to be in
the region of £2.5 billion per year, including costs to the NHS and costs to industry through sickness and absence. In the US, medical expenses for overweight and obesity accounted for 9.1 percent of total US medical expenditures in 1998, costing around $78.5 billion (equivalent to $92 billion today).
Most reports in the media trot out the same causes – the gluttony and sloth of modern society – and the same old solutions – eat less and exercise more. And yet if weight loss was simply a matter of cutting calories and being more active then our population should be in pretty good shape. At any given time as much as 50 per cent of the population in the UK is on a diet and/or exercise regime.
But one recent report contained a signpost to a truth about obesity that was nonetheless missed by almost everyone who read it. In September of this year a ‘fat map’ of Britain was published by Dr Foster Intelligence, an independent health research organisation that works closely with the NHS, and Experian, a market research company.
The analysis was a complex synthesis of data from two surveys – the Health Survey for England and the British Market Research Bureau’s quarterly survey of 25,000 Britons – that provided details of lifestyle, body mass index (BMI, an indication of how overweight a person is) and geographical location. Its conclusion was that people living in northern industrial towns were fatter than those living in London and more rural areas of the UK.
Across the board the reportage was unremarkable. The results, after all, echoed those of a survey produced by Experian two years ago. Having heard it all before, the newspapers avoided original analysis and focused instead on the marvels of modern technology that allow us to pinpoint, down to a street, the places where the fattest people live.
A rent-a-quote from Dr Foster Intelligence about the threat of obesity, and the benefits of surveys like this one, made all the papers: “We need to reduce levels of obesity, and detailed health maps like these show where the risks of obesity are highest,” commented the organisation’s marketing development manager, Dr Marc Farr. “This will enable health authorities to target weight-loss drives in areas where this is a problem. Until now they have not had access to this accurate database; this should make a difference.”
At first it may be difficult to see how knowing where people are fattest will make a dramatic difference to the problem of obesity. Surely the real question that needs answering is why are we so fat? On this point, Farr fell back on mainstream thinking to conclude: “The reasons for obesity [in these northern towns] are not uncommon and shared by many areas: availability of cheap, high sugar food products, unemployment, age-related failure to engage in physical activity, understanding the nature and dangers of obesity and changes to more sedentary forms of employment.”
This oft-repeated explanation, of course, has some merit but misses the vital point; that the where and the why of being overweight are intricately linked.
The reductionist explanation for the increase in overweight and obese individuals is a simple equation: calories in/calories out. A more global view, however, would acknowledge the multifaceted effect of urbanisation and industrialisation, which have had a devastating impact on what we eat, when we eat, how much we eat, how often we eat
and the quality of the food we eat, as well as on our levels of daily physical exertion.
In the West these simple ‘whys’ of obesity are rarely questioned anymore and have become largely obscured by the solution-oriented focus of quick weight-loss schemes. But in developing nations the startling parallel between the rise in obesity and the rapid acceptance of urban/industrial lifestyles and diets is all too apparent.
Speaking in September at the International Congress on Obesity in Sydney Dr. Philip James, the British chairman of the International Obesity Task Force (IOTF), noted that in China the rate of obesity has risen from almost zero in the 1980s to about 10 percent of the population in 2006, and that the rise can be pinned down to the growing problems of urbanisation and the infiltration of a generally nutritionally poor Western diet, which favours high-fat, high-energy products over basic fruits and vegetables. Similar increases have been noted among more affluent urban dwellers in India.
And so we diet to fight the flab. Yet over and over again surveys show that the majority of people who lose weight on a given diet will subsequently regain that lost weight, and more besides. There is even evidence to suggest that dietary regimes that severely restrict calories as well as types of foods (fats, carbohydrates etc) in the short-term, actually encourage rebound weight gain over the long-term.
This rebound effect, which is well known to dieters and well documented in the medical literature, may have deep roots in human evolution. In our hunter-gatherer stage, when the next meal was not predictable, we became programmed to overeat when food was
available. In times of food deprivation (including when we diet), our hard-wiring changes. Our bodies develop mechanisms, largely driven by hormones, to store calories by over-riding signals of satiety and increasing hunger signals, even when food becomes plentiful again. In essence, the body is storing up calories in anticipation of the next period of food deprivation, even if it never comes.
According to the data, this effect is more dramatic when food and drink is freely available, when the foods available are calorie dense – such as crisps, sodas, Big Macs etc – and energy expenditure is low due to reduced physical activity.
Medical science has determined a biological basis for this storage effect. When we lose weight, our basal metabolic rate (BMR) – the minimum amount of energy the body requires at rest, to keep itself alive and to maintain weight at a constant ‘set point’ – decreases. BMR is related to the actual amount of body tissue so it naturally decreases when the amount of body tissue is reduced through dieting. Constant yo-yoing of weight through dieting and bingeing plays havoc with the body’s BMR and set point, in some cases wiping it out altogether, leaving the body with no blueprint for maintaining a healthy weight.
A more complex equation
In spite of the failure of conventional diets, the comforting equation of calories in/calories out still informs most weightloss initiatives, possibly because it makes the job of ‘doing something about it’ so effortless. Weight management programmes centred on this simple equation are easy to devise – anyone with a calculator, a calorie reference guide and an exercise manual can do it – and they shift the responsibility for the success or failure of the regime squarely onto the individual.
It’s an all too familiar scenario when faced with difficult cultural problems, where challenging the status quo could raise uncomfortable questions. Consider the way that individuals are encouraged to switch off standby electronics and change to energy efficient lightbulbs in order to ‘do something about’ climate change, or to recycle to end waste. Focusing on individual efforts – and failures – in this way deflects attention that away from bigger, and arguably more powerful influences, such as the government subsidies that keep polluting airlines and industries in business.
Nevertheless, the ongoing failure of ‘gold standard’ solutions like calorie counting has motivated some scientists to suggest that we must be missing something, and to look beyond the usual explanations. This year, a paper in the International Journal Of Obesity, for instance, attempted to explore the ‘roads less travelled’ in obesity research and suggested at least 10 additional causes of obesity that have nothing to do with gluttony and sloth.
The authors, made up of a panel of doctors from across the US, concluded that medical science had a tendency to “focus overwhelmingly on food-marketing practices and technology and on institution-driven reductions in physical activity (the ‘Big Two’), eschewing the importance of other influences.”
The panel went on to say that the influence of the Big Two on the global obesity epidemic is “largely circumstantial”, relying as it does on broad surveys – not unlike the recent Dr Foster report – rather than epidemiological data focused on individuals, or large randomised studies.
They further noted that the acceptance of the idea that too much food and too little exercise is the sole cause of obesity “…has created a hegemony whereby the importance of the Big Two is accepted as established and other putative factors are not seriously explored. The results may be well-intentioned, but ill-founded proposals for reducing obesity.”
In an effort to broaden the debate the authors recommended that other influential aspects of modern life (see box opposite) are influential. Among these and of particular relevance to the results of the Dr Foster survey, was exposure to hormone-disrupting pollutants – the kind you might find in excess in any industrial town in the North of the UK, where once there were mines, refineries, factories and tall chimneys belching out smoke and where now there are chemical factories, incinerators and waste transfer facilities regularly releasing toxins into the air, water and soil.
Hormones play a major role in determining and maintaining metabolism and the body’s set point. When levels of these hormones (produced by the thyroid, sympathetic nervous system and reproductive organs) deviate from the norm, problems with weight can ensue.
Thus in January 2004, at a conference titled Obesity: Developmental Origins and Environmental Influences, the US National Institutes of Health made an urgent call for more research on the link between hormone-disrupting chemicals and obesity, noting that exposure during adulthood and, crucially, in the womb, can permanently disrupt the body’s weight control mechanisms.
But, according to at least one scientist, if you look hard enough, the research is already out there. In 2002 Dr Paula Baillie-Hamilton, a visiting Fellow at the Occupational and Environmental Health Research Group, Stirling University, published a paper in which she proposed that chemical toxins were to blame for the global obesity epidemic.
Baillie-Hamilton’s hypothesis, the culmination of many years of forensic investigation into the way that pollution is changing us from the inside out, had its roots in an article she stumbled upon that explained how toxic chemicals in the environment were affecting the fertility of wildlife.
“I couldn’t understand how someone like myself, an academic with a load of scientific qualifications and papers behind me, had never heard of all these different chemicals that were out there. Yet if these chemicals were affecting the fertility of wildlife they must be affecting hormones significantly. And of course, hormones control a number of other functions in the body, including weight control.
“I spent a couple of years intensively identifying each major category of chemical and then working out how each individual substance affected the body’s weight control system. I looked at all the mechanisms involved, from the nerves and hormones to metabolism, and the levels of nutrients in the body, and found that the same chemicals that at high doses can cause weight loss, seemed to cause a fattening effect at very low levels – the same low levels that we are exposed to in everyday life.”
It was an arduous task made more difficult by the fact that weight gain is not always documented in trials of toxic chemicals. “For many years this data has been ignored or suppressed in the conclusions of scientific papers because there was no way to explain why it happened. And of course it wasn’t accepted at the time that weight gain in animals exposed to substances like DDT could be anything other than positive,” continues Baillie-Hamilton. “If weight gain was mentioned, it would be buried in the text of the paper, rather than the conclusion. Essentially what this meant was starting from scratch and reading through every single paper to find some mention of these effects.”
What else makes you fat?
Being overweight or obese is a modern problem and, as the results of a recent investigation in the International Journal Of Obesity show, many of the putative contributors to the problem have their roots in modern life. The authors suggest that even if some of these causes have only a small effect, they may interact with each other and with other factors in ways that greatly magnify their individual effects.
Sleep debt: Too many of us are getting too little sleep and the resulting ‘sleep debt’ can alter hormone levels and trigger an increase in body weight. Sleep debt is also associated with insulin resistance and diabetes, and with increased hunger and appetite.
Pollution: Hormones control body weight and many of today’s pollutants drastically alter levels of key hormones.
Air conditioning: We burn more calories when the environment is too hot or too cold for comfort. But more people than ever live and work in temperature-controlled homes and offices.
Decreased smoking: Smoking, because of its effects on circulation and the nervous system, reduces weight. In many developed countries people are smoking much less than they used to.
Prescription medications: Many different drugs – including contraceptives, steroid hormones, diabetes drugs, some antidepressants, and blood pressure drugs – can cause weight gain. Use of these drugs has risen exponentially in recent decades.
Population age and ethnicity: Middle-aged people and those of African and Hispanic origin have a tendency to be more obese than younger people of European descent. Throughout the world the population is getting older and more ethnically diverse.
Older mothers: There’s some evidence that the older a woman is when she gives birth, the higher her child’s risk of obesity. The average age at which a women has her first child is rising.
Ancestry and environment: Some health problems are passed down through the generations. A tendency towards gestational diabetes will produce a child prone to obesity (who are in turn more likely to produce obese children). Very high-fat diets during pregnancy have been shown, in animals, to skew the metabolism of offspring two generations down the line.
Obesity linked to fertility: Some evidence suggests that overweight and obese people are more fertile than lean ones. If obesity has a genetic component that makes it a dominant characteristic, the percentage of obese people in the population is likely to increase.
Unions of obese spouses: Obese women tend to marry obese men. If there are fewer thin people around – and if obesity is a dominant genetic characteristic – then these couples will produce obese children, who will then go on to produce more obese children.
A Chemical Cosh
Industrial chemicals – and specifically those that act like hormone disrupters – profoundly alter several aspects of human metabolism and appetite control. Research at the University of Laval in Quebec has added greatly to the understanding of just how wide-ranging the effects of an overpolluted body can be.
In the late 1990s Professor Angelo Tremblay and his team began to study, first in animals and then in people, the metabolic effects of organochlorines. Their interest was sparked by earlier Italian research which showed that overweight people who underwent gastric bypasses, to encourage weight loss, experienced dramatic increases in levels of the pesticide DDT and one of its breakdown products, DDE, in their blood as their bodyweight declined. The Laval studies of humans undergoing an average weight-loss programme also showed that concentrations of these chemicals rose as the pounds were shed.
Once in the body organochlorines and other industrial pollutants are generally stored in human fat cells. During weight loss the fat cells shrink and release these chemicals back into the bloodstream. The scientists at Laval found that as levels of these now freely circulating pollutants rose in dieters, levels of essential thyroid hormones – necessary for maintaining an efficient metabolism – fell dramatically.
A drop in basal metabolic rate (BMR) – the rate at which the body burns calories – is not uncommon in dieters. Studies into dieting show that as metabolism slows down during weight loss, levels of thyroid hormones also drop naturally. This slowdown is referred to as ‘adaptive thermogenesis’.
The worrying discovery of the Laval scientists was that higher levels of organochlorine compounds were associated with much lower levels of thyroid hormones than would be produced by weight loss alone. In dieters with these newly liberated toxins circulating throughout the body, BMR also slowed more dramatically, as did energy expenditure and levels of skeletal muscle oxidative enzymes (which determine how efficiently the muscles use energy – when levels are not optimum, energy gets stored as fat).
“If I were to put this in journalistic terms,” says Tremblay “I might say that the organochlorines essentially shut down the metabolic furnace that helps the body burn fat.”
Professor Tremblay’s research has focused on organochlorine compounds, for instance the pesticides DDT (and its breakdown product DDE), chlordane, aldrin, dieldrin and heptachlor, as well as PCBs, dioxins and chlorophenols. But the list of chemicals that can cause weight gain and promote obesity extends well beyond these to include a wide variety of everyday chemicals associated with manufacturing and a polluted environment (see Chemical calories, page 42).
A key effect, says Dr Baillie-Hamilton, is the way industrial pollutants interact with the sympathetic nervous system. This system releases hormones like adrenaline and noradrenaline that suppress our appetite, particularly for fat. These hormones also increase the ability and desire to exercise, as well as increasing body temperature, so that while you are exercising you are also burning calories more efficiently.
“Chemicals like organochlorines act directly on the sympathetic nervous system attacking each and every part of the way it works,” she explains. “It’s like a chemical cosh. They reduce levels of important hormones necessary for weight balance and also block and even destroy the hormone receptors in fat cells. This means the hormones can’t communicate with the fat cell and the cell becomes less sensitive to those metabolism-regulating hormones that are in circulation.”
Adapt and survive
Research at Laval continues to confirm that high circulating levels of organochlorines alter metabolism and may be one of the most important contributors to adaptive thermogenesis and the rebound weight gain so depressingly familiar to dieters.
But once liberated by weight loss these chemicals are also free to attack vital organs such as the brain, liver and kidneys, and this threat triggers an even more intriguing response. As chemicals build up beyond a level with which the body’s detoxification pathways can cope, the body begins to ‘dilute’ the amount of circulating toxins – the majority of which are fat soluble – by making new fat cells to store them in.
Recent evidence even suggests that the presence of some industrial pollutants such as bisphenol-A and organotins can signal dormant ‘baby’ fat cells, known as preadipocytes, to grow into fully mature fat cells, or adipocytes. As the number of fat cells increases it can become harder to keep weight down. In addition, with increasing weight the body detoxification system, which would normally facilitate the excretion of toxins, appears to shut down in preference to simply storing any toxins in available fat.
Professor Tremblay admits there is still much that is unknown about the way these chemicals interfere with metabolism. But, apart from triggering hormonal changes, the presence of organochlorines and other toxins can also act as inflammatory triggers.
Some physicians such as Dr. Leo Galland, author and internationally recognised expert in nutrition, believe industrial pollutants can also trigger allergies and allergic responses that can cause, or worsen, the problem of chronic systemic inflammation.
For Dr. Galland, it is the problem of chronic inflammation that is most relevant to rising levels of obesity. Inflammation, he argues, causes the body to release a range of chemicals that make the system resistant to the relatively recently discovered hormone, leptin. Professor Tremblay agrees that this is “entirely possible”.
The discovery of leptin 12 years ago in New York at the Rockefeller Institute changed the whole map of our understanding of obesity.
“Prior to that,” says Galland, “the way that everyone thought about fat was that it was just a bag of unused calories that was totally inert. The key thing about leptin is not just that it is a hormone that affects appetite, metabolism and fat stores. It’s that leptin is produced
by fat cells exclusively. So all of a sudden fat became an active player in the body. Really, fat is an organ and its function is just as intricate as any other organ in the body in that it interacts with the immune system, with the nervous system and with other systems
and can produce changes that can be very complex.”
Galland admits that the science is difficult, and yet some understanding of it is crucial if we are to get to grips with the problems of hard to shift overweight and obesity.
“Whenever there is inflammation, the cells respond by producing anti-inflammatory chemicals known as SOCS – suppressors of cytokine signalling. Two of these, SOCS1 and SOCS3, interfere with leptin by blocking the signal in the cells. The mechanism is very similar to the development of insulin resistance, which is also due to inflammation. In fact, inflammation also causes production of the fight or flight hormone cortisol from the adrenal glands. Cortisol blocks leptin and it also raises blood sugar, which in turn decreases the response to any given amount of insulin.”
The bigger picture of what these scientists are saying is staggering. Inflammation is fundamentally a protective process necessary, for instance, for wound healing as well as for curing infection. If inflammation arises in a polluted body it’s highly likely that it is a protective response to the presence of toxins.
Body fat also has a protective effect. For example, studies show that animals that are exposed to environmental toxins while at the same time encouraged to gain weight through a high calorie diet will survive better than exposed animals that are not allowed to gain weight. In other words, body fat, because it is a repository of these toxins, also becomes a survival mechanism. Thus it is possible that the obesity epidemic, as Tremblay postulated as far back as 2000, is in reality an adaptive response by the body to a chemically toxic environment.
The bigger picture
Viewed in this way, obesity could be seen as the response of an intelligent body trying to cope and maintain balance in an overwhelmingly polluted world. Sadly, in an environment where we are overwhelmed with pollutants, this intelligent adaptation is proving lethal and continued advice to simply decrease calorie intake dramatically in order to speed weight loss may even be making the problem worse.
Clinical practice has been frustratingly slow to catch up with the conceptual changes prompted by the link between environmental pollutants and obesity.
Says Dr Baillie-Hamilton, “There is still no academic textbook that brings it all together and it takes time to get through to people’s consciousness. If you are talking to an obesity specialist, whose professional life has been spent telling people that if they eat too much
and don’t exercise they are going to gain weight, he may not have a clue about the link between industrial pollutants and weight gain. And until the professionals do get a clue their conclusions, and the solutions they propose, will continue to be very limited.”
Dr Galland agrees. “There is a worldwide epidemic and it is definitely associated with industrialisation and pollution. And yes, of course, there may be confounding factors because industrialisation and pollution are also associated with dietary changes and changes in activity patterns. But the reality is that the results of most weight loss treatments are lousy and creative new approaches are urgently needed.”
To an intelligent health service the ‘fat map’ of Britain would be seen as a wakeup call, an opportunity to get to grips with a difficult and challenging problem. Instead, NHS and government advice remains stubbornly allied to the calories in/calories out equation. For example, the latest Department of Health (DoH) patient leaflet ‘Your Weight, Your Health’ makes clear that excess weight is due to ‘energy imbalance’, explains the number of calories needed per day, suggests ways to reduce the calories you take in each day and lists the benefits of being active.
Another booklet from the DoH, The Obesity Care Pathway, for health professionals advises much the same thing and suggests that a sensitive, empathetic, non-judgemental approach should underpin all obesity-related interventions – advice that is intended to complement the National Institute of Clinical Excellence (NICE) guidelines on the prevention, identification, assessment, treatment and weight management of overweight and obesity in adults and children due to be published this month (November).
Certainly, not blaming the victims when conventional diets fail would be a good first step. Given the available data on the environmental complexity of obesity this is rather like blaming the poverty striken of the world for being lazy and feckless, the victims of starvation for not having had the foresight to stock up on food, and the people murdered in the twin towers for going to work that day.
There also needs to be a much more comprehensive and honest focus on the double bind in which some of the nation’s poorest people find themselves in relation to good health. People in lower income brackets may already be subsisting on poor quality food that is high in sugar and fat and low in nutrition. Their general level of health will already be
compromised. Add the chemical cosh of industrial pollution to the mix and the metabolic and detoxification pathways that should be protecting the body may break down entirely.
There is also a need to address the obvious question of why the people in polluted cities like London and New York remain slimmer than those in industrial towns and cities. Given what is already known about polluted bodies, it is a fair bet that such research might show that being thin is not the only, or even the best indicator, of a healthy population. That the particulate pollution from traffic and lighter forms of industry in and around major capitals like these behaves in a distinct way in the body and causes its own kind of chemical chaos. New Yorkers and Londoners may be thinner, but are they also, for example, more infertile or more prone to allergies and asthma and generally more immune compromised?
What stands in the way of recognising the need for such solutions, says Professor Tremblay, is simply that the concept of industrial pollutants altering body chemistry invites far too many uncomfortable questions about the world in which we live. Most of these pertain to the economic consequences of acknowledging this issue.
“There is a global context here,” says Tremblay. “You see it with George W Bush’s position regarding the Kyoto agreement. He says it is out of the question to move towards any solution that might lead to what he sees as economic vulnerability. It’s the same with
obesity. The response is always framed by the politics and economics of addressing the reality, not by the potential health problems of exposure to substances like organochlorines.”
But just as the US President should be worried about global warming, he should also be worried about the fact that the ‘fat map’ of Britain was not unique to the UK. A just-published survey by the Trust for America’s Health found that the 10 fattest states in the US – Mississippi, Alabama, West Virginia, Louisiana, Kentucky, Tennessee, Arkansas, Indiana, South Carolina and Texas – were in located in the industrial South of the nation. The report failed to mention any aspect of environment, yet the Mississippi River, which runs through several of these states, is officially the most polluted river in the US. Likewise, West Virginia, Texas, Indiana, Alabama, Louisiana and Georgia are home to some of the top 20 mercury polluting power plants in the US. Fish and wildlife in some southern states like Alabama, Arkansas and Tennessee are regularly found contaminated by organochlorines like DDT and PCBs – due to the former production of these chemicals in these areas.
Instead of falling over ourselves to promote a lot of PC nonsense about not being judgemental about overweight and obesity, perhaps it would be more productive to acknowledge that the most pressing human problems, the biggest human disasters, don’t just apparate out of thin air. They evolve in the industrial, environmental and politcial milieu of modern life – and modern life can be a much dirtier business in certain parts of the country.
The health problems associated with polluted bodies are usually unseen. Some, like cancer or Alzheimer’s disease, can take decades to develop. The problems of overweight and of obesity offer us a rare and very visible cue that tells us that pollution is killing us, inch by everexpanding inch.
The recognition that chemical pollutants could have such a direct effect on our bodies is possibly one of the most important new ideas in public health; one which demands a difficult but necessary shift in our conceptual understanding of the dynamics of weight control. Allied to this there is an urgent need to acknowledge the way that our actions shape our environment and our environment, in turn, shapes our lives.
In July of this year members of the Women’s Institute in the UK took the initiative and dumped carloads of unnecessary food packaging back on the doorstep of supermarkets countrywide, with the message ‘you created this problem, now you clean it up’. The time has come to dump the problem of overweight and obesity back on the doorstep of industry and government with the same unflinching message.
In addition to organochlorines, a range of other industrial and everyday chemicals are known to encourage weight gain. These include:
Organophosphate pesticides, such as malathion, dursban, diazanon and carbonates, constitute 40 per cent of all pesticides used. These chemicals are mainly used inside buildings as opposed to in agriculture. They are neurotoxins and hormone disrupters.
Including aldicarb, bendiocarb, carbaryl, propoxur and thiophanate methyl, are used extensively in agriculture, forestry and gardening, and are suspected hormone disrupters.
These chemicals, which include tributyltin (TBT) and the mono and dibutyltins (MBT, DBT), have many applications, including stabilisers in PVC and catalysts in chemical reactions. They are also found in glass coatings, agricultural pesticides, biocides in marine antifoulant paints and wood treatments and preservatives. They are damaging
to the thyroid and immune system and potential hormone disrupters.
A Estrogen mimic used to make clear, hard, reusable plastic products; also used in the manufacture of polymers, fungicides, antioxidants, dyes, polyester resins, flame retardants and rubber chemicals and some dental resins.
Hormone disrupting chemicals, produced in large volumes, and commonly detected in groundwater, rivers and drinking water as well as in meat and dairy products. Around 95 per cent of phthalate production over the last few decades is tied to the PVC industry. Can be found in many plastics and consumer products – everything from hair spray and nail varnish to plastic water bottles and tshirts.
Added to many products, including computers, TVs and household textiles to reduce fire risk. Also found in baby mattresses, foam mattresses, car seats and PVC products. Office workers who use computers, hospital cleaners and workers in electronics-dismantling plants are at particular risk from these chemicals. Polybrominated flame-retardants are oestrogen mimics and can also affect the thyroid.
A common food pollutant that belongs to a family of chemicals known as polycyclic aromatic hydrocarbons (PAHs). It is derived from coal tar and enters the atmosphere as a result of incomplete combustion of fossil fuels. In animals it has been shown to cause weight gain in the absence of any detectable change in food intake. It is possible that other PAHs may have a similar effect.
Neurotoxic chemicals that include xylene, dichlorobenzene, ethylphenol, styrene, toluene, acetone and trichloroethane are commonly found in human blood samples. Necessary for a wide range of industrial processes and found widely in adhesives, glues, cleaning fluids, paint and felt-tip pens, perfumes, paints, varnishes, pesticides, petrol, and household cleaners and waxes.
Principally used as a protective plating for steel, in electrode material in nickel-cadmium batteries and as a component of various alloys. It is also present in phosphate fertilisers, fungicides and pesticides. Cadmium in the soil is taken up through the roots of plants and distributed to edible leaves, fruits and seeds, and eventually passed on to humans and other animals, where it can build up in milk and fatty tissues. Neurotoxic and a potential hormone disrupter.
Professions that put their employees at risk of exposure to this neurotoxin include lead-smelting, -refining and -manufacturing industries, brass/bronze foundries, the rubber and plastics industries, steel-welding and -cutting operations, and battery manufacturing plants. Construction workers and people who work in municipal waste incinerators, in the pottery and ceramics industries, radiator-repair shops and other industries that use lead solder may also be among the high-exposure groups.
This article first appeared in the Ecologist November 2006