Letters▼ Triclosan research misreported? Your recent news story on research with the antimicrobial triclosan (1) sensationalized a relatively minor issue and was inappropriate in style and substance, particularly for a publication of the American Chemical Society, print or electronic. The background material was inaccurate and dated, the current issue overblown, and some of the quotes downright silly, with no perspective whatsoever. For example, the picture caption claims “triclosan . . . can react . . . to produce levels of chloroform that exceed EPA regulations.” Neither the ES&T research paper (2) nor the quotes from corresponding author Peter Vikesland support this statement. Another example is the statement “Vikesland’s research . . . including 2,4-dichlorophenol . . . could be producing dioxins.” A cited paper shows that 2,4-DCP is NOT related to dioxin production, according to the proposed pathway (3). The statement that “[if] someone who has triclosan-containing moisturizer [on jumps] into the pool . . . source for chloroform [and chlorinated dioxin] formation” is wild speculation and not supported by the research. These statements only serve to create confusion and fear in the public. Triclosan has an excellent overall safety and efficacy profile, demonstrated by over 30 years of safe use. It is one of the most extensively studied antimicrobial agents in the world. Triclosan has been extremely valuable in fighting antibiotic-resistant bacteria and nosocomial infections, as well as generally improving cleanliness and public health. The concerns regarding triclosan generally relate to speculation that triclosan acts as an antibiotic and thus causes resistant bacterial strains (4), despite peer-reviewed clinical studies showing otherwise (5–7). This speculation was the basis for the American Medical Associa© 2005 American Chemical Society
tion action in 2000, which dodged the real issue of medical overuse and misuse of antibiotics. It has since been demonstrated via NMR that triclosan intercalates into the bacterial cell membrane and thus does not behave as an antibiotic (8). Despite many laboratory studies purporting to show mechanisms of bacterial resistance, now at least seven clinical and field studies—including one coauthored by a prominent proponent of the resistance issue—show that triclosan does NOT cause resistant strains, (5–7, 9–12). I appreciate the need to examine and understand new and potential emerging pollutants; however, I am puzzled by the effort being invested in analyzing for triclosan in the environment relative to the potential risks. Several recent studies looking at the potential environmental impact of triclosan have generally found little to no risk to fish, aquatic invertebrates, or plants (13–16). In the introduction to Vikesland’s article, references cite concentrations of triclosan in the influent of waste treatment plants at only 0.062–22.0 ppb (2). Concentrations in streams and surface waters have been measured at a median of 0.14 ppb and a maximum of 2.3 ppb, with concentrations falling off rapidly away from waste treatment outlets. Research shows very low conversion rates to the lower dioxins (mono- and di-chloro) that represent lower, perhaps even little, risk to humans or the environment (3, 17). (Even under the worst conditions, there is no evidence that triclosan is converted to higher-level dioxins.) It is well known that the primary sources of dioxins in the environment are industry and burning, and I would expect any contribution from triclosan to be negligible by comparison. Similarly, the results from Vikesland’s paper, as well as his comments on subsequent work, show that the amount of chloroform to be expected from using triclosan is comparable to
what is normally present in treated water, which will vary depending on other organics in the water. On the basis of the above information, triclosan does not present a threat to human health or the environment. It should be noted that based on the huge media interest from articles overstating the significance of his research, Vikesland has been quoted as saying, “There isn’t a huge need to worry at the present” (18). WAYNE SWOFFORD Vice President Research & Development Microban Products Company
[email protected] (1) Betts, K. Chlorine and Antimicrobials Cause Concern. Environ. Sci. Technol. 2005, 39, 188A–189A. (2) Rule, K. L.; Ebbett, V. R.; Vikesland, P. J. Formation of Chloroform and Chlorinated Organics by Free-Chlorine-Mediated Oxidation of Triclosan. Environ. Sci. Technol. 2005, 39, 3176– 3185. (3) Latch, D. E.; et al. Aqueous Photochem istry of Triclosan: Formation of 2,4-Dichlorophenol, 2,8-Dichlorodibenzo-p-dioxin, and Oligomerization Products. Environ. Toxicol. Chem. 2005, 24, 517–525. (4) McMurry, L. M.; Oethinger, M.; Levy, S. B. Triclosan Targets Lipid Synthesis. Nature 1998, 394, 531–532. (5) Jones, C. L.; et al. The Effect of LongTerm Use of a Dentifrice Containing Zinc Citrate and a Non-ionic Agent on the Oral Flora. J. Dent. Res. 1988, 67 (1), 46–50. (6) Cox, A. R. Efficacy of the Antimicrobial Agent Triclosan in Topical Deodorant Products: Recent Developments in Vivo. J. Soc. Cosmet. Chem. 1987, 38, 223–231. (7) Zambon, J. J.; et al. Microbial Supragin gival Dental Plaque in Response to a Triclosan-Containing Dentifrice. Oral Microbiol. Immun. 1995, 10, 247– 255. (8) Guillen, J.; et al. Location and Orientation of Triclosan in Phospholipids Model Membranes. Eur. Biophys. J. 2004, 33, 448–453. (9) McBain, A. J.; et al. Exposure of Sink Drain Microcosms to Triclosan: Population Dynamics and Antimicrobial Susceptibility. Appl. Environ. Microbiol. 2003, 69 (9), 5433–5442. (10) Cole, E. C.; et al. Investigation of Antibiotic and Antibacterial Agent Cross-
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Resistance in Target Bacteria from Homes of Antibacterial Product Users and Nonusers. J. Appl. Microbiol. 2003, 95, 664–676. Lambert, R. J. W. Comparative Analysis of Antibiotic and Antimicrobial Biocide Susceptibility Data in Clinical Isolates of Methicillin-Sensitive Staphylococcus aureus, MethicillinResistant Staphylococcus aureus, and Pseudomonas aeruginosa between 1989 and 2000. J. Appl. Microbiol. 2004, 97, 699–711. Aiello, A. E.; et al. Relationship Between Triclosan and Susceptibilities of Bacteria Isolated from Hands in the Community. Antimicrob. Agents Chemother. 2004, 48 (8), 2973–2979. Reiss, R.; et al. An Ecological Risk Assessment for Triclosan in Lotic Systems Following Discharge from Wastewater Treatment Plants in the United States. Environ. Toxicol. Chem. 2002, 21, 2483– 2492. Orvos, D.; et al. Aquatic Toxicity of Triclosan. Environ. Toxicol. Chem. 2002, 21, 1338–1349. Federle, T.; Kaiser, S; Nuck, B. Fate and Effects of Triclosan in Activated Sludge. Environ. Toxicol. Chem. 2002, 21, 1330– 1337. McAvoy, D.; et al. Measurement of Triclosan in Wastewater Treatment Systems. Environ. Toxicol. Chem. 2002, 21, 1323–1329. Latch, D. E.; et al. Photochemical Conversion of Triclosan to 2,8-Dichlorodibenzo-p-dioxin in Aqueous Solution. J. Photochem. Photobiol. A 2003, 158, 63–66. Sturgeon, J. Professor Says Study Not Meant To Alarm. Roanoke Times, April 19, 2005, p A1.
Response Although the potential health and environmental ramifications of our research have yet to be firmly established, it is clear that triclosan readily degrades in the presence of free chlorine. The rates of these reactions are rapid enough that dermal and inhalation exposures to triclosan decomposition products could occur during household use of products that contain the antimicrobial. As a result, the significance of exposure to chloroform from the free chlorine/ triclosan-initiated reaction relative to other pathways needs to be addressed. Given the concentrations of triclosan (~0.3%) in many consumer products and the conditions under which they are used—water temperatures of ~40 °C and excess free chlorine—the rate of triclosan degradation and product formation is enhanced. This makes it imperative that these risk-assessment studies be initiated. Although published research suggests that triclosan itself is safe, the 272A ■ ENVIRONMENTAL SCIENCE & TECHNOLOGY / JULY 1, 2005
products and intermediates that the antimicrobial produces when it degrades in the outdoor environment or in the home have not been similarly scrutinized. The observation that photolysis of triclosan results in low yields of dichloro dioxins suggests that the chlorinated derivatives from the free chlorine/triclosan reaction could photolyze to higher chlorinated dioxins. This hypothesis, although unproven, is consistent with the photochemical literature. In addition, the statement in the news story speculating that “[if] someone who has triclosan-containing moisturizer [on jumps] into the pool . . . they’re a potential source for chloroform [and chlorinated dioxin] formation” is consistent with what we know about the reactivity of antimicrobial products that contain triclosan and should not be discounted. Although I have stated to the press, “There isn’t a huge need to worry at the present,” the quote was in response to tabloid and print-media stories that extrapolated our scientific results to scenarios we had not evaluated or considered. Not enough is known about the health and environmental ramifications of our results for us to recommend that consumers discontinue their use of triclosan-containing products. Nevertheless, it is in the public interest to inform the research community that these types of reactions can occur and that their implications should be considered. PETER VIKESLAND Department of Civil and Environmental Engineering Virginia Polytechnic Institute and State University
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