Is triclosan harming your microbiome?

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Science  22 Jul 2016:
Vol. 353, Issue 6297, pp. 348-349
DOI: 10.1126/science.aag2698

Antibacterial soaps were originally used only in hospitals, but since the 1990s, their use has expanded into households. Antimicrobial chemicals are now found in many soaps, wipes, hand gels, cutting boards, detergents, cosmetics, and toothpastes, as well as toys and plastics. One of the most common antibacterials, triclosan [5-chloro-2-(2,4-dichlorophenoxy)phenol], is found in ∼75% of antibacterial soaps (1). In 2008, it was detected in ∼75% of urine samples in the United States (2). There are concerns that triclosan use contributes to the development of antibiotic resistance and may adversely affect human health. Partial bans exist in the European Union and the U.S. state of Minnesota (3, 4). However, recent studies exploring triclosan's effect on the microbiome have given conflicting results.

Triclosan works by inhibiting the final step of the bacterial fatty acid synthesis pathway. At low concentrations it stops microbial growth, but at high concentrations it is bactericidal. Bacterial resistance to triclosan is readily obtained in the laboratory, but it is not clear that resistance is widespread in the environment. A 10-year study of triclosan exposure found no change in the antibiotic tolerance of methicillin-resistant Staphylococcus aureus or Pseudomonas aeruginosa (5). However, in a recent report, prolonged treatment with triclosan produced clinical resistance to ampicillin and/or ciprofloxacin in S. aureus and Escherichia coli (6).

To explore the effectiveness of triclosan, Kim et al. (7) recently compared the bactericidal effects of plain and triclosan-containing soaps under conditions that mimic handwashing. They found no differences in the soaps' ability to reduce bacterial abundance during a brief (20 s) exposure. The exposure time may have been too short to see an effect, or soap surfactants may have reduced triclosan's activity. Triclosan is bactericidal in water-based solution with 24 hours of exposure.

Exposure to antimicrobial compounds can disrupt the community of microorganisms that colonize the human body. Perturbations in the microbiota have been linked to a wide array of diseases and metabolic disorders, including obesity, inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), and behavioral and metabolic disorders. However, it remains unclear whether triclosan can disrupt the microbiome to such an extent that it influences health and well-being (8).

To elucidate the effect of triclosan on the microbiome, Gaulke et al. exposed adult zebrafish to high oral doses of triclosan over the course of 7 days (9). This acute exposure resulted in changes in community structure, interaction networks, and an increase in triclosan resistance. However, the microbiome of fish exposed for only 4 days with 3 days of no exposure was no different from that of the control fish. This observation suggests either resilience to temporary disturbance or that changes are reversible.

Narrowe et al. studied the effects of triclosan exposure on the microbiome of fathead minnows (10). They used environmentally relevant doses of triclosan in the fishes' habitat, which led to substantial shifts in the microbiome, which again recovered after triclosan was removed. However, in a study of riverine biofilms, Lawrence et al. found that even after the removal of triclosan, the microbiome remained disrupted (11).

To explore the effects of triclosan on human microbiota, Poole et al. gave seven volunteers personal products (toothpaste, hard and liquid soap, and dish soap) containing triclosan to use at will for 4 months; the same volunteers then switched to 4 months of products without triclosan. A second group started with non-triclosan products and then switched to the triclosan products (12). Urinary concentrations of triclosan were higher in all volunteers during the triclosan period, but the composition of the stool, molar, or incisor microbiomes did not change, nor were there changes in serum endocrine markers.

There are a few possible explanations for the disparities among these studies. In both the zebrafish and minnow studies, the fish were exposed to triclosan for much longer durations than those generally experienced by humans. The fish consumed triclosan in food or were immersed in triclosan, whereas humans typically encounter the compound in products such as soap and toothpaste that are rinsed off immediately. It is also possible that triclosan exposure is so ubiquitous, starting as early as prenatal exposure, that the human microbiota has already adapted. Even in the human trial with periods of no triclosan, the compound was still detectable in urine, although at lower concentrations (12).

Uncertain effects.

The antimicrobial compound triclosan, found in many soaps and other household products, can change the gut microbiota of fish and rats. It remains unclear whether such effects occur in humans and, if so, what the health effects are.


Future research should explore the role of dose, timing, and route of triclosan exposure. Humans are exposed to triclosan transiently and in small doses, but the presence of triclosan in surface, ground, and drinking water indicates its potential to persist and accumulate in the environment (5). Triclosan is readily absorbed through the skin and gastrointestinal tract, but in humans, it tends to be applied topically and is thus not subject to metabolic alteration in the gastrointestinal tract, whereas this may have been the case in the fish studies. Therefore, it is important to determine whether the metabolic by-products of triclosan also affect the structure of the microbiota.

It is also possible that prenatal, perinatal, and postnatal triclosan exposure is more detrimental than adult exposure. Cox et al. have suggested that there are key developmental windows during which microbiome perturbations can leave lasting impacts on neurological and immune development (13). Hu et al. recently showed that the adolescent rat microbiota are more vulnerable to chemical perturbation than that of adult rats (14). They administered oral doses of triclosan sufficient to recapitulate observed human urinary levels and found substantial differences between the microbiota of triclosan-exposed and control adolescent rats. These changes were attenuated in adult rats, implying that low-dose postnatal exposure to triclosan may modulate microbiota composition but that the microbiota may recover.

Triclosan and disinfectants containing other antimicrobials are used even more frequently and in higher concentrations in hospitals than in the home. Given that more than 98% of infants are delivered in hospitals and that infants are particularly naïve to microbes, their microbiota is vulnerable at this developmental stage. Thus, triclosan should be investigated for its potential to perturb microbial community assembly and succession.


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