The Dawn of the domestic superbug

The huge popularity of antibacterial household cleaners is encouraging superbugs,
allergies, immune-system failure and dangerous environmental pollution. It’s time to
stop cleaning ourselves to death.

Superbugs don’t just appear out of nowhere. They aren’t invaders from Mars or the result of some mysterious process that science can’t fathom. They’re the consequence of human behaviour, and creating them is fairly easy. Expose bacteria to repeated doses of antibiotics, and they will genetically mutate into more robust and resistant strains. Keep repeating this process, and you will eventually produce a bacterium that no drug will kill. This is how ‘superbugs’ such as methicillin-resistant Staphylococcus aureus (MRSA) and other resistant strains of bacteria are created.

Indiscriminate use of antibiotics has received deserved criticism for provoking the rise of hospital superbugs. Less well publicised is the role that domestic antibacterial cleaners play in producing unique strains of resistant bacteria.

Today we use a variety of synthetic antibacterial chemicals, in particular quaternary ammonium compounds and the chlorophenol Triclosan, to keep the bugs at bay. Unlike soap and water, which work efficiently by physically loosening dirt and germs from surfaces and bodies and washing them down the drain, antibacterial chemicals are designed to kill. Worse, Dr Stuart Levy, director of the Center for Adaptation Genetics and Drug Resistance at Tufts University School of Medicine, Boston, and chairman of the Alliance for the Prudent Use of Antibiotics, says: ‘What is being touted as an antibacterial in household products is really, clinically, an antibiotic.’

Over the past decade our enthusiasm for fighting germs at home has become unstoppable. Today we can buy antibacterial hand soaps, laundry and dish detergents, surface cleaners, toothpastes, mouthwashes and hand wipes. Antibacterial agents, known as biocides, can be impregnated into clothing, furniture, blankets, insoles, the plastic lining of refrigerators, food-storage containers, shower curtains, rubbish bags, bins, chopping boards and even highchairs and toys.

Even so, five years ago the American Medical Association (AMA) issued a startling statement saying that antibacterial soaps were no more effective against germs than common soap. Manufacturers of toiletries and household cleaners, who had lobbied vociferously against the AMA taking any stand at all on this issue, greeted the statement with purple rage, defending their antibacterial products as both effective and desirable. They were, they claimed, simply giving consumers what they wanted – products to protect themselves and their families from the ‘germs’ that can cause disease.

Several recent studies suggest they do no such thing. Antibacterial hand soaps, for instance, may initially kill more bacteria and viruses on the skin than regular soaps. But within an hour or so after use, there is generally no difference in the number of microbes on the skin. Hardly surprising, given that the average adult touches approximately 300 different surfaces every 30 minutes. Similarly, while antibacterial surface cleaners may initially remove more organisms than soap and
water, within 90 minutes or so there is generally no difference in the numbers of bacteria and viruses that have repopulated cleaned areas.

While many antibacterial products do have a broad-spectrum action that encompasses the odd virus or fungus, most are only effective for bacteria, and even then only in a very limited way. Knowing this provides a context for the results of a widely publicised study originating from Columbia University in New York in March 2004, which showed that people who used antibacterial soaps and cleaners developed coughs, runny noses, sore throats, fever, vomiting, diarrhoea and other symptoms just as often as those who don’t use antibacterial products. The researchers also pointed out that many of these illnesses are typically caused by viruses, against which antibacterial soaps and cleaners provide no protection.

Tucked away in the AMA statement was another even more telling concern: that antibacterial chemicals used in the home could be contributing to the ongoing threat posed by drug-resistant bacterial strains. This concern is based on rapidly accumulating evidence, much of it originating from Levy and his team at Tufts. ‘There will always be people who say they don’t care what’s in the product,’ Levy says. ‘As long as it kills bacteria and other micro-organisms that’s better for them and their families and they’re going to buy it. But if you said on the label “this product contains an antibiotic”, people might not be so quick to buy them.’

Research is now showing that a whole range of antibacterial chemicals used as disinfectants in household cleaners and as preservatives and active ingredients in personal care products are producing resistant strains of bacteria. There is evidence, for example, showing that 7 per cent of Listeria monocytogenes strains (which cause severe gastrointestinal symptoms such as diarrhoea), isolated from the environment and from food, are now resistant to quaternary ammonium compounds, commonly used in household cleaners. Strains of Pseudomonas aeruginosa, which cause skin and wound infections, have also exhibited resistance to these chemicals. While the glare of the spotlight has focused on hospital-acquired MRSA, another type of the superbug –community-acquired MRSA (caMRSA) – is widely reported in the medical press in the US, Britain, Australia and Canada. This strain arises in people who have had no contact with the hospital environment and is principally resistant to penicillin-derived antibiotics, cephalosporins, carbapenems and monobactam (known collectively as beta-lactam antibiotics), but not, like the hospital-acquired variety, to multiple other types of antibiotics as well.

Studies from Japan suggest a strong link between caMRSA and the use of antibacterial cleaning solutions. When investigators there looked at the generational effects of exposure to the common antibacterial agent benzalkonium chloride (used in household cleaners and certain toiletries) in caMRSA strains, they found that as each new generation of bacteria evolved its resistance to the antibacterial grew stronger – as did its resistance to common antibiotics like methicillin and other betalactam antibiotics.

As resistance grows the minimum amount of antibacterial and antibiotic needed to kill bacteria also grows, in some cases dramatically. In another Japanese study, the concentration of the antibiotic oxacillin necessary to inhibit the growth of third-generation benzalkonium chloride-resistant caMRSA organisms was 32 times greater than first-generation resistant varieties.

Similar studies conducted with the bacteria Pseudomonas stutzeri, a common cause of wound infections, and the antibacterial chemical chlorhexidine found that as each generation grew resistant to the antibacterial, they also became more resistant to many antibiotics, including erythromycin and ampicillin, nalidixic acid, as well as other antibacterial agents such as Triclosan and quaternary ammonium compounds. When a bacterium exhibits simultaneous resistance to a number of antibiotics, all of which are chemically related and work in a similar way, this is known as cross-resistance. This phenomenon is well known in hospitals. But the possibility that bacteria can also develop a cross-resistance between common household antibacterial agents and antibiotics is particularly frightening because it means that the products we buy over the counter and use in our homes work in similar ways to antibiotics and have the same potential to create the kind of resistant bacteria that have up until now been confined to hospitals.

While a number of antibacterial chemicals used in the home can produce this cross-resistance to antibiotics, one in particular – Triclosan – towers above the rest. Although Triclosan (also known commercially as Microban) has been used in consumer products since 1967, it is only recently that scientists have discovered how it works. Most antibacterial agents have a non-specific action: that is, they kill bacteria in fairly general ways such as depriving them of oxygen or disrupting metabolic processes. This non-specific action was one of the things that differentiated them from antibiotics, which usually attack bacteria in very specific ways, often altering the genetic make-up of the organism to prevent it from reproducing. Until recently, Triclosan was classed as a non-specific antibacterial substance. But newer evidence reveals that, in common with many penicillin-derivative antibiotics, Triclosan produces a genetic change in bacteria such as Escherichia coli, Staphylococcus aureus (S. aureus) and Mycobacterium smegmatis, inhibiting an enzyme responsible for fatty acid synthesis and so preventing the organism from making a cell wall and replicating. This type of action means that Triclosan has more in common with antibiotics than antibacterials.

Resistance, both innate and acquired, to Triclosan is now well documented among several types of bacteria. Innate resistance among harmful bacteria, such as Pseudomonas aeruginosa, Enterococcus faecalis and Streptococcus pneumonia, would normally not cause much concern. However, in environments where Triclosan is overused and putting bacterial populations under pressure, this innate resistance can be passed on to other strains of bacteria to make them immune to the effects of Triclosan as well (see box ‘The bacterial community’ below).

Levy and his colleagues have discovered three types of E. coli that have already evolved to become Triclosan-resistant. Variants of S. aureus that are Triclosan-resistant have also been reported in the
medical literature.

In some cases Triclosan resistance also produces a cross-resistance to conventional antibiotics. For instance, Triclosan-resistant strains of E. coli are also resistant to the experimental antibiotic diazoborine. Triclosan-resistant strains of Mycobacterium smegmatis are also resistant to isoniazid – an antibiotic used against tuberculosis.

Triclosan is so much like a drug, in fact, that scientists are already working on ways to use it medicinally. Doctors are currently investigating the possibility of treating malaria with Triclosan. The parasite responsible for the transmission of malaria uses the same enzyme for fatty-acid synthesis as E. coli. Such innovations serve to reinforce the idea that Triclosan is simply an over-the-counter antibiotic that has slipped through the regulators’ net. Unmonitored and largely unregulated, the overuse of Triclosan in the home is likely to have the same devastating effect as overusing antibiotics in the hospital or clinic, producing increasingly resistant strains of bacteria that can’t be killed and have the potential to make people very sick.

Some argue that the number of resistant organisms produced by household antibacterials is small and unlikely to have much of an impact on human health. But this is a specious argument that harkens back to the early days of antibiotic resistance. When the first penicillin resistant strains of S. aureus were emerging in the 1950s, doctors dismissed them as mere blips on the medical radar. After four decades of complacency, during which time antibiotic resistance among S.aureus and other strains of bacteria multiplied, medical science finally had to admit that not only was the phenomenon of antibiotic resistance real, but that it was the result of doctors’ misuse and overuse of antibiotics – often for diseases, like colds and coughs, that were not even caused by bacteria in the first place. It also had to admit that, having come so far down the road without intervention, there was absolutely no way to reverse the trend. In the 20 years between 1980 and 2000 no truly new antibiotics were produced, and in the last 15 years only a trickle of new antibiotics has reached the market, and bacteria are already showing signs of resistance to these.

For people who are truly ill, and who desperately need the curative potential of an effective antibiotic, it is a bleak picture indeed. And while it can be difficult for the average person to make the mental leap from household cleaner to incurable disease the link inevitably exists. ‘Knowing antibiotics as well as we do, it just doesn’t make sense to say that exposure to these chemicals won’t result in resistant species,’ says Levy. ‘It’s just a matter of time.’

In the home, Triclosan can profoundly disrupt the micro-environment, killing off all but the most resistant strains of bacteria. Washed down the drain, it threatens the wider environment and human health. Triclosan is one of the most frequently detected compounds in rivers, streams and other bodies of water. It is highly toxic to aquatic life, especially algae. High levels of Triclosan have been found in fish, and, via our waterways, the compound has found its way back into the human body. A recent Swedish study found Triclosan in the breast milk of 60 per cent of women surveyed. This is a worrying finding given that no human data exists to show that it is safe to ingest. Similarly, no studies have examined what happens when Triclosan combines with other chemicals in the body, though evidence of what happens when Triclosan combines with chemicals in the wider environment provides some clue.

For years manufacturers have reassured consumers that Triclosan breaks down quickly in the environment. Depending on where it is and what other chemicals it comes into contact with in the environment, some Triclosan does break down. The rest, however, can be converted into even more toxic compounds.

Although vehemently denied by the manufacturers for years, evidence published in 2003 demonstrated that sunlight converts Triclosan into 2,8-dichlorodibenzo-p-dioxin, which has been described as a ‘mild’ form of dioxin. Given that 2,3,7,8- tetrachlorodibenzodioxin (TCDD), best known as a highly toxic impurity in the herbicide Agent Orange, has the same toxic profile as most other dioxins, the concept of a ‘mild’ dioxin would appear to be more of a figment of the industry’s collective imagination than a rigorous scientific classification.

Dioxins are hormone-disrupting chemicals that mimic the action of natural oestrogen. In the body, oestrogen levels are generally low and finely balanced. In excess, however, oestrogen is a recognised carcinogen. It accumulates in the environment and in the body and produces the kinds of excesses that, besides leading to cancer, are linked to reproductive and developmental problems and immune-system damage.

What is more, Triclosan in waterways can be altered further by repeated exposure to chlorine. If chlorine-exposed Triclosan is then exposed to sunlight it turns into a much more toxic form of dioxin.

When all this made the headlines in 2003 it was shocking to the public but hardly news to the scientific community. Triclosan is not a natural substance, and so must be synthesised in the lab. This process produces a number of harmful by-chlorinated products, including up to nine different dioxins and dibenzofurans. A similar range of toxins can be released from Triclosan-impregnated products at the end of their lifecycle, during incineration, for instance.

This year, research carried out at Virginia Tech University in the US found that chlorine in tap water and the Triclosan in some soaps and other products such as toothpastes and mouthwashes can react together to create harmful chloroform gas that can be absorbed through the skin or inhaled. If inhaled in large quantities, chloroform gas can cause depression, liver problems and, in some cases, cancer.

Five years ago the AMA called for regulators in the US to expedite their review of products containing Triclosan and other antibacterials and determine the extent to which they might actually be contributing to the health threat created by excessive use of antibiotics. No such reviews have taken place. In Britain we place our faith in a 2002 review paper by the European Commission’s Scientific Steering Committee, which concluded: ‘There is no convincing evidence that
Triclosan poses a risk to humans or the environment by inducing or transmitting antibacterial resistance under current conditions of use.’ This endorsement is still used by Ciba, Triclosan’s manufacturer, to defend the continued widespread use of the compound.

Nevertheless, other government agencies throughout Europe have taken the initiative and issued statements discouraging people from using antibacterial household and personal hygiene products. In 2000, six Finnish public authorities issued a joint statement urging consumers not to use antibacterial chemicals, stating that they were unnecessary and that their growing use increased the risk of spreading antibiotic resistance in microbial populations. The statement said: ‘Even Finnish hospitals don’t use such chemicals for routine cleaning operations… In households we see more disadvantages than advantages.’

That same year, Denmark’s Environmental Protection Agency (EPA), National Board of Health, National Central Laboratory and Consumer Information Centre issued a joint statement advising consumers against the routine use of antibacterial household and personal hygiene products, stating that it was unnecessary for domestic use and potentially harmful to the environment as such products were ‘extremely persistent and highly toxic in the marine environment’. In 2003, a report by the Danish EPA on Triclosan concluded that the chemical was ineffective in the home and devastating to the environment.

In 2001, German environment minister Jürgen Trittin called on consumers not to use cleaning agents containing antibacterial agents and on industry to stop marketing and advertising the antibacterial qualities of its products. Trittin called the use of anti-bacterial cleaners in households ‘superfluous and risky’, and he appealed to industry to stop suggesting to consumers that they were ‘surrounded by enemy germs which they had to fight aggressively’.

In the end, it’s not the spread of germs we need to fear; it’s the sheer volume of products that we use to fight them. We have no new antibiotics with which to fight serious infections, and every attempt we make to rectify this situation chemically, including using antibacterial cleaners in the home, leads us further down what has become a very dark path.

By placing our faith in antibacterial cleaners such as Triclosan we impose an utterly false sense of security on ourselves that leads to lax habits in hygiene. Why bother to wash your hands when you can simply spray and wipe or wash and go with any number of strong disinfectants? Yet our hands are the most important way in which bacteria and other micro-organisms are spread. Keeping them clean is the best way to keep ‘germs’ at bay. But the average hand wash takes a perfunctory three to five seconds (as opposed to the recommended 10 to 15), doesn’t always involve soap or warm water, and often ends with a quick wipe on your trousers. It’s a sign of the times when an organisation like the US Centers for Disease Control and Prevention feels compelled to post instructions on its website telling people how to wash their hands effectively.

More importantly, by allowing these products to remain on sale to the general public we are changing the basic ecology of our homes, turning them from places of safety into reservoirs of bacterial resistance. As the number of reservoirs of resistance throughout the world increases so does the likelihood that antibacterials of all kinds, including medicines and cleaning fluids, will be ineffective when and where we need them most – in hospitals and clinics.

It’s time regulators stopped kowtowing to the chemical/pharmaceutical industry. Antibacterial cleaners are nothing more than antibiotics. Selling them on demand over the counter and allowing them to be used widely and indiscriminately constitutes a clear, increasing and unacceptable threat to human health and the health of our environment. It is high time we faced this life-threatening growth in drug-resistant bacteria and pulled all products containing synthetic antibacterials off the shelves now.

More information about Triclosan and other anti-microbial chemicals and how they contribute to bacterial resistance can be found on the Alliance for Prudent Use of Antibiotics website at

The campaign Beyond Pesticides also produces several informative and in-depth documents
on Triclosan.

Bacteria police themselves
In each bacterial community – whether it exists on your skin, in your gut, on a hospital floor or in your kitchen sink – there are billions of benign bacteria that pose no threat to humans. By their sheer numbers these benign bacteria keep populations of the minority of more virulent bacteria in check. When we use antibiotics and antibacterial cleaners we kill off large number of these benign bacteria, thus giving more virulent strains room to reproduce and thrive.

Bacteria support each other
Many bacteria, both benign and virulent, possess an innate resistance to a range of common drugs and chemicals. When exposed to an antibiotic, which specifically attacks some part of the organism’s DNA, bacteria can also adapt their genetic make-up to become resistant to the toxin. In any bacterial community the organisms can also share their genetic material with each other, passing on innate or acquired resistant genes to their neighbours and relatives.

Bacteria are masters in the art of self-defence
Many bacteria also have what is known as an ‘efflux pump’ mechanism. This mechanism forcefully expels substances that the organism recognises as toxic, much like a baby spitting out its medicine. As the bacteria are exposed to more and more toxic substances, the efflux mechanism learns to respond to each of these in turn.

Trying to kill members of the bacterial community in the home has important implications for the human community at large. ‘We really need to be thinking ecologically about this issue,’ says Dr Stuart Levy of the Center for Adaptation Genetics and Drug Resistance. ‘One man’s misuse is another man’s problem down the line. There are millions and millions of microbes around us and they interact, and they have a very intimate involvement with us. We’ve evolved, our skin flora has evolved and our environment has evolved to deal with the normal bacteria around us. We think of these micro-organisms as intrinsically harmful, even though the vast majority of “germs” are harmless to all but the most immune-compromised humans. If we continue to be super-clean and remove relatively benign bacteria that we’ve learned to live with, we are essentially removing the very thing that
protects us from harm.’

Manufacturers of antibacterial products prey heavily on parents’ fears about the health of their children. Yet by using antibacterial products in otherwise healthy homes, we may be condemning our children to a future of chronic ill health.

Evidence exists to show a link between early childhood infections and a lower risk of developing atopic diseases such as allergies, asthma and eczema. This idea forms one part of what is known as the ‘hygiene hypothesis’: a theory that developed out of scientists’ inability to explain why children in developed countries were experiencing escalating rates of atopic diseases.

The theory goes that in ‘protecting’ children from exposure to dirt and germs, and by preventing disease from taking its full course in childhood, we are inadvertently destroying the body’s ability to respond appropriately to infection and other stimuli which involve the immune system. In formulating this theory, researchers have found a link between too much hygiene and increased incidence of allergies.

The hypothesis came into being in 1989, when David Strachan, an epidemiologist at the London School of Hygiene and Tropical Medicine, noticed that children from big families, among whom infections are likely to circulate freely, were less likely to develop atopy.

Studies that have been published since 1989 suggest Strachan was on the right track. A report in the British Medical Journal in 2001 found that repeated viral infections (other than lower respiratory tract infections) in the fi rst three years of life had a striking protective effect against asthma in later life.

Another study, conducted by the Institute of Social and Preventive Medicine in Basel, Switzerland, and published in the prestigious New England Journal of Medicine in 2002, looked at more than 800 children aged six to 13. Researchers found that kids who lived in the dustiest environments were less likely to suffer from asthma and hay fever.
According to the researchers, farms offer one of the best places for the immune system to be exposed to infection.

That same year, the results of a 10-year study carried out at the Henry Ford Hospital in Detroit were published in the Journal of the American Medical Association. They showed that children who were exposed to furry pets during their first year of life were half as likely to develop common allergies by the age of six than those living in petless homes.

And last year a study, published in the Journal of Allergy and Clinical Immunology revealed that not only were children who had fevers early in life less allergy-prone, but the more fevers they had the more allergy-resistant they became. There is also a growing body of evidence showing that children who receive antibiotics early in life are also more prone to allergies later on.

This article first appeared in the Ecologist July 2005

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