3. What happens to triclosan in the environment?
- 3.1 How does triclosan reach the environment?
- 3.2 To what extent does triclosan break down or persist in the environment?
- 3.3 Are microbial populations in the environment affected by triclosan?
3.1 How does triclosan reach the environment?
The SCCS opinion states:
5.5. Triclosan in the environment
The widespread use of triclosan results in the discharge of this compound to wastewater. Incomplete removal of triclosan from wastewater treatment plants (WWTPs) as well as spreading the triclosan laden biosolids into soils, leads to triclosan being distributed in soils and surface waters.
Triclosan has been widely detected (see Table 4) in influents, effluents and biosolids of WWTPs, in lakes, rivers and sea water in various countries in Europe (Paxeus 1996, Lindström et al. 2002, Adolfsson-Erici et al. 2002, Kanda et al. 2003, Bester 2003, Sabaliunas et al. 2003, Samsø-Petersen et al. 2003, Xie et al. 2008, Singer et al. 2002, Tixier et al.2002, van Stee et al. 1999, Kantiani et al. 2008, Dye et al. 2007), in the USA (McAvoy et al. 2009, Coogan et al. 2007, Coogan et al. 2008, US EPA 2009, Cha and Cupples 2009, Fair et al. 2009, Halden and Paull 2005, Chalew and Halden 2009, Kumar et al. 2010), in Canada (Hua et al. 2005), in Australia (Ying and Kookana 2007, Fernandes et al. 2008), in Japan (Okumura and Nishikawa 1996) and in Hong Kong (Chau et al. 2008).
5.5.1. Fate of triclosan in the environment
Bacteria are able to survive triclosan exposure by activating specific or general genetic cascades (see 6.2.4). The environmental concentrations of triclosan may affect bacterial activities. Consequently it is important to evaluate the fate of triclosan in the environment such as in WWTPs, rivers, effluents, etc.
Triclosan is transported through the domestic waste stream to WWTPs. Municipal wastewater treatment helps to achieve average removal efficiencies in the range of 58- 99%, depending on the technical capabilities of sewage treatment systems (McAvoy et al. 2002, Kanda et al. 2003, Bester 2003, Singer et al. 2002, Federle et al. 2002, Lishman et al. 2006, Lindström et al. 2002, Lopez-Avila and Hites 1980, Thomson et al. 2005, Ternes et al. 2004). However, mass balance studies have demonstrated that triclosan also exhibits significant persistence, partitioning and sequestration in biosolids (by-product of wastewater treatment). Approximately 50 ± 19% of the incoming mass of triclosan was observed to persist and become sequestered in biosolids produced by a conventional WWTPs employing activated sludge treatment in conjunction with anaerobic biosolid digestion (Heidler and Halden 2007). Thus, important pathways of biocide release into the environment include WWTP effluent discharge into surface waters and the land application of biosolids. Effluent from WWTPs contains a complex mixture of anthropogenic and natural compounds. Soil samples from ten agricultural sites in Michigan previously amended with biosolids, collected over two years, revealed triclosan concentration 0.16-1.02 μg/kg (Cha and Cupples 2009). 90 to 7060 μg/kg triclosan was found in biosolids from 3 Michigan wastewater treatment plants.
Table 4: Environmental concentrations of triclosan
(data from worldwide sources)
3.2 To what extent does triclosan break down or persist in the environment?
The SCCS opinion states:
Photodegradation of Triclosan
Despite its high chemical stability, being extremely resistant to high and low pH, triclosan is readily degraded in the environment via photodegradation. Eight photoproducts were tentatively identified, including chlorinated phenols, chlorohydroxydiphenyl ethers, 2,7- and 2,8-dichlorodibenzo-p-dioxin, and a possible dichlorodibenzodioxin isomer or dichlorohydroxydibenzofuran (Tixier et al. 2002; Sanchez-Prado et al. 2006a, 2006b, Canosa et al. 2005; Lores et al. 2005; Aranami and Readman 2007, Prada et al. 2004, Latch et al. 2005, Ingerslev et al. 2003). Some of these products show enhanced toxicity compared to triclosan but have been shown to be degraded in the environment by bacteria such as Pseudomonas, Burkholderia and Sphingomonas (Field et al. 2008a and 2008b). The end products are CO2 and chlorine with chlorocatechols as intermediates. Recently, Son et al. (2009) demonstrated that TiO2-photocatalytic degradation of triclosan is mainly achieved by radicals, and these radicals can further degrade dioxin-type intermediates once they are produced in photocatalysis. The presence of hydrogen peroxide enhanced the oxidation (Yu et al. 2006).
Triclosan is hydrolytically stable under abiotic and buffered conditions over the pH 4-9 range based on data from a preliminary test at 50°C. Photolytically, triclosan degrades rapidly under continuous irradiation from artificial light at 25°C in a pH 7 aqueous solution, with a calculated aqueous photolytic half-life of 41 minutes. One major transformation product was identified, 2,4-dichlorophenol, which was a maximum of 93.8-96.6% of the applied triclosan 240 minutes after treatment.
Hydrolysis is not expected to be an important environmental fate process due to the stability of triclosan in the presence of strong acids and bases. However, triclosan is susceptible to degradation via aqueous photolysis, with a half-life of <1 hour under abiotic conditions, and up to 10 days in lake water. An atmospheric half-life of 8 hours has also been estimated based on the reaction of triclosan with photochemically produced hydroxyl radicals. Additionally, triclosan may be susceptible to biodegradation based on the presence of methyl-triclosan following wastewater treatment.
Degradation in chlorinated water
Triclosan addition to chlorine spiked ultra-pure water or to chlorinated tap water led to the formation of two tetra- and one penta-chlorinated hydroxylated diphenyl ether, as well as 2,4-dichlorophenol. Chlorination of the phenolic ring and cleavage of the ether bond were identified as the main triclosan degradation pathways (Canosa et al. 2005). Free chlorine mediated oxidation of triclosan leads to the formation of chloroform and other chlorinated organics (Rule et al. 2005, Fiss et al. 2007).
Aerobic bacterial hydrolysis plays an important role in triclosan degradation. A consortium of bacteria able to partially degrade triclosan was isolated and one consortium member was shown to be a Sphingomonas-like micro-organism (Hay et al. 2001). In a different study, two strains of Pseudomonas putida TriRY and Alcaligenes xylosoxidans subsp. denitrificans TR1 were shown to utilise triclosan as sole carbon source (Meade et al. 2001). Zhao (2006) also isolated one strain of triclosan-degrading bacteria (Sphingomonas or Sphingopyxis) from activated sludge. Zhao also found that Nitrosomonas europaea, an important nitrification bacterium in wastewater treatment plants, has the ability to degrade triclosan through co-metabolism. Triclosan and its chlorinated degradation products can also be degraded by bacteria (Pseudomonas, Sphingomonas, Burkholderia) under aerobic conditions.
Very little is known of the biochemistry of the biodegradation of triclosan and nothing is documented in the Minnesota biodegradation database (http://umbbd.msi.umn.edu/
). There is a data gap on the degradation pathway of triclosan and its intermediary products.
Under anaerobic conditions and in the dark, triclosan is quite stable. Due to its low water solubility, triclosan is readily adsorbed to particles and tends to accumulate in sediments. Digested sludge concentrations of triclosan ranged from 0.5 to 15.6 μg/g (dry weight), where the lowest value was from an aerobic digestion process and the highest value was from an anaerobic digestion process. These results suggest that triclosan is readily biodegradable under aerobic conditions, but not under anaerobic conditions (McAvoy et al. 2009).
The limited data available indicate that effect levels of triclosan on activated sewage sludge micro-organisms vary depending on the level of acclimation. A concentration of 2 mg/L inhibited activated sludge micro-organisms that had not been acclimated to triclosan; however, the same concentration had no effect on acclimated organisms. Laboratory- derived IC50 values range from 20-239 mg triclosan/L based on carbon dioxide (CO2) evolution and glucose utilisation.
Triclosan (≥2 mg/L) had a slight effect on chemical oxygen demand removal under laboratory conditions, but had a major inhibitory effect on the nitrification process. Anaerobic sludge digestion was significantly inhibited at a concentration of 10 mg/L. A NOEC for sewage microbes was not available (NICNAS 2009).
3.3 Are microbial populations in the environment affected by triclosan?
The SCCS opinion states:
5.5.2. Effect of triclosan on micro-flora and toxicity of metabolites
Inhibitory effects on micro-organisms were shown to begin at concentrations ranging from 25 to 80,000 μg⁄L for triclosan (Federle et al. 2002, Samsø-Petersen et al. 2003, Sivaraman et al. 2004, Neumegen et al. 2005, Stasinakis et al. 2007, Farre et al. 2008, Stickler and Jones 2008). It should be noted that the upper range minimum inhibitory concentrations (MICs) reported are well in excess of published solubility limit for triclosan. MIC threshold values for micro-organisms are exceeded by environmental levels of triclosan in several sediments, biosolids, and activated sludge. Lawrence et al. (2009) observed a change in the structure and composition of a river biofilm microcosm following exposure to triclosan (10 μg/L) over a 8-week period.
Waller and Kookana (2009) studied the effect of triclosan on selected microbiological activity and biochemical parameters in Australian soil. Substrate-induced respiration and nitrification, plus activities of four enzymes relevant for carbon turnover (acid and alkali phosphatase, 3-glucosidase, and chitinase) were measured. The effect of triclosan on enzymatic activity was minimal even at a high concentration (100 mg/kg). Likewise respiration was not affected. However, the study demonstrated that triclosan at concentrations below 10 mg/kg can disturb the nitrogen cycle in some soils.
McBain et al. (2003) showed that long-term exposure of domestic-drain biofilms to sublethal levels of triclosan (2-4 g/L, four times daily) did not affect bacterial viability or significantly alter antimicrobial susceptibility. This lack of effect may reflect the biofilm phenotype present in the microcosm, the presence of intrinsically tolerant bacteria and degradation of triclosan by the drain biofilm consortium. However, microbial diversity after exposure to triclosan was profoundly affected.
Studies reporting on the effect of repeated exposure of triclosan against complex oral microcosms failed generally to show an increase in resistance determined either by an increase in MIC or in Minimal Bactericidal Concentration (MBC) (Sullivan et al. 2003; McBain et al. 2004). In addition, McBain et al. (2004) did not observe any cross-resistance to other biocides or to some antibiotics (tetracycline and mitrodinazole) in a number of bacterial species such as Streptococcus sanguis, Sterptococcus oralis and Prevotella nigrescens with a decreased susceptibility to triclosan resulting from exposure to the bisphenol. However, these results contrasted with those obtained with E. coli, for which repeated exposure to increasing concentrations of triclosan led to a 400-fold increase in resistance (MBC from 0.2 to 39.1 mg/L) (McBain et al. 2004). Moreover, bacteria inside biofilms resist better to biocidal agents. For example, reduced susceptibility to triclosan was observed in Salmonella (Tabak et al. 2007) and Proteus/Providencia (Stickler and Jones 2008, Williams and Stickler 2008).
5.6. Triclosan in the human body
Triclosan enters the human body orally through toothpaste, mouthwashes and dental treatments. In humans, triclosan is rapidly and completely absorbed from the gastrointestinal tract, while a lower rate of absorption occurs dermally. It has been found in human blood, plasma and milk (Allmyr et al. 2006, 2008, Adolfsson-Erici et al. 2002) in Sweden and Australia. In the USA it was found in human urine (Calafat et al. 2008). A volunteer study in Sweden (Sandborgh-Englund et al. 2006) showed that the accumulated urinary excretion varied between the subjects, with 24 to 83% of the oral dose being excreted during the first 4 days after exposure.