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weight. Balmer et al. (2004) detected MTCS in fish in the range 4–370 ng g?1 and lower level of concentration were compared with previously measured in fish samples from different rivers. This difference is to be expected as concentrations of MTCS should typically be higher in river systems that receive inputs from WWTPs. A large monitoring study on TCS and MTCS was conducted by Boehmer et al. (2004) using fish tissues. Samples of tissues from breams (Abramis brama) from the period 1994–2003 were analyzed for TCS and MTCS. While TCS was only detected in a less number of samples, MTCS was present in all samples that were analyzed.
The increasing MTCS concentrations was observed in bream tissue from the mid 1990s until 2000, with levels of MTCS increasing from 10 to 26 ng g?1 of wet weight and ranged from below the limit of quantification up to 3.5 ng g?1. MTCS is a persistent pollutant with the potential to accumulate in the tissues of fish. Valters et al. (2005) detected TCS in the plasma samples of 13 fish species from the Detroit River, in the range of 750 to >10,000 pg g?1 of wet weight. Leiker et al. (2009) identified the MTCS in male carp (Cyprinus carpio) from the Las Vegas Bay and in the Las Vegas Wash, Nevada; MTCS was detected in all carp samples, with a mean concentration of 520–596 ?g kg?1 per wet weight basis. The concentrations of MTCS detected much higher, indicating that this might be due to the sediment foraging behavior of carp, which exposes them to higher levels of water-borne chemicals due to lipophilic nature. TCS and its metabolites have been detected in sediments, both freshwater and marine (Miller et al., 2008; Chalew and Halden, 2009). Lozano et al. (2010) in USA surveyed the presence of personal care products, in fish sampled from five effluent dominated rivers receiving discharge from WWTPs in large urban centers and rivers.
2.9.3 Marine mammals
Fair et al. (2009) characterized the presence of TCS in the plasma of bottlenose dolphins (Tursiops truncates), a top level predator, and then correlated biological levels with environmental concentrations and the bioaccumulation of TCS in a marine mammal with concentration of 5.5 to 20 ng l?1. TCS measured in estuarine water samples ranged from 4.9 to 13.7 ng l?1, averaging 7.5 ng l?1 and their plasma concentrations were 0.12–0.27 and 0.025–0.11 ng g?1 wet weight, at the two estuaries, respectively. Apparently, TCS has also been detected at a concentration of 9.0 ng g?1 of wet weight in the plasma of a captive killer whale (Orcinus orca) (Bennett et al., 2009) (Table 2.3). These studies further needed to monitor TCS and assess its effects in wild species.
Table.2.3. Concentration of Triclosan (TCS) in aquatic organisms
Organisms Type of Sample TCS (µg kg-1) References
Algae and invertebrates
Filamentous algae
(Cladophora spp.)
Whole organism
Coogan et al., 2007
Freshwater snails
(Helisoma trivolvis) Muscle 50–300 Coogan and La Point,
Vertebrates Rainbow trout
(Oncorhynchus mykiss) Bile 710- 17000 Adolfsson-Erici et al., 2002
Breams, male
(Abramis brama) Bile 14 000–80 000 Houtman et al., 2004
Pelagic fish Plasma 0.75–10 Valters et al., 2005
Atlantic bottlenose dolphins
(Tursiops truncates) Plasma 0.12–0.27 Fair et al., 2009
Killer whale
(Orcinus orca) Plasma 9.0 Bennett et al., 2009

Table.2.4. Acute toxicity of Triclosan on aquatic organisms
Compound Category Species Trophic group Duration LC 50 (mg L-1) References

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Antimicrobial Daphnia magna Invertebrate 48h 0.39 Balmer et al., 2004
Ceriodaphnia dubia Invertebrate 24, 48h 0.2, 125 Balmer et al., 2004
Pimephales promelas Fish 24,48, 72, 96h 0.36, 0.27, 0.27, 0.26 Balmer et al., 2004
Lepomis macrochirus Fish 24, 48, 96 h 0.44, 0.41, 0.37 Balmer et al., 2004
Oryzias latipes Fish 96 h 0.602 (larvae), 0.399
(embryos) Batscher, 2006a
Xenopus laevis Amphibian 96 h 0.259 Batscher, 2006b
Acris blanchardii Amphibian 96 h 0.367 Batscher, 2006b
Bufo woodhousii Amphibian 96 h 0.152 Batscher, 2006b
Rana sphenocephala Amphibian 96 h 0.562 Batscher, 2006b
Pseudokirch-neriella subcapitata Algae 72h growth 0.53
(l g L-1) Bazin et al., 2010

2.9.4. On microbial community
Svenningsen et al. (2011) observed that effects of triclosan on microbial communities and observed that their degradation in simulated sewage-drain-field soil were decreased the microbial population about 22-fold in the presence of 4 mg kg-1 of triclosan. McLeod et al. (2001) reported that the broad range of TCS encompasses many types of Gram-positive and Gram-negative non-sporulating bacteria, some fungi, Plasmodium falciparum and Toxoplasma gondii. It is bacteriostatic (it stops the growth of microorganisms) at low concentrations, but at higher concentrations they are bactericidal (it kills microorganisms).
Doori et al. (2003) reported that the most sensitive organisms to triclosan are staphylococci, streptococci, mycobacteria, Escherichia coli and Proteus spp. In that sp, TCS is effective at concentrations that range from 0.01 mg L-1 to 0.1 mg L-1. Methicillin-resistant Staphylococcus aureus (MRSA) strains are also sensitive to triclosan in the range of 0.1–2 mg L-1. Russell (2003) reported that showering or bathing with 2% triclosan has been shown to be effective in decolonization of patients whose skin is carrying MRSA and also reported that Enterococci are much less susceptible than staphylococci and Pseudomonas aeruginosa is highly resistant.
Heath et al. (1999) had identified that triclosan blocks the active site of enoyl acyl carrier protein reductase enzyme which is essential for fatty acid synthesis in bacteria and it affects the cell membrane and reproduction by preventing bacteria from fatty acid synthesis. When leads to lower concentration, it acts as a bacteriostatic and works against to type II fatty acid synthase enoyl reductase (champlin et al., 2005). While at higher concentrations, it targets the cell membrane.
2.9.5. Triclosan toxicity in Animals
Miller et al. (1983) concerned TCS interfering with the body’s thyroid hormone metabolism led to hypothermic effect, lowering the body temperature, and overall causing a non-specific depressant effect on the central nervous system of mice. The exposure to low levels (0.03 mg L-1) of triclosan with disrupted thyroid hormone associated gene expression in tadpoles, which cause them to prematurely change into frogs (Veldhoen et al., 2006).
Kumar et al. (2009) reported that triclosan exposure leads to decreased sperm production in male rats and also it blocks the metabolism of thyroid hormone, because it chemically mimics thyroid hormone, and binds to the hormone receptor sites, blocking them, so that endogenous hormones cannot be used. James et al. (2010) showed that triclosan can hinder estrogen sulfotransferase in sheep placenta, an enzyme which helps metabolize the hormone and transport it to the developing fetus. The presence of TCS would be dangerous in pregnancy, if it gets through to the placenta to affect the enzyme.
The TCS enhances the production of chloroform in amounts up to 40% higher than levels in chlorine-treated tap water (Fiss et al., 2007). But Hao et al. (2007) reported that no formation of detectable chloroform levels over a range of expected tooth-brushing durations among subjects using toothpaste with triclosan and normal chlorinated tap water. U.S. EPA classifies chloroform as a probable human carcinogen. As a result, triclosan was the target of a UK cancer alert, even though the amount of chloroform generated was less than normally present in treated, chlorinated water and required brushing your teeth or washing your hands for times on the order of two hours or more.
2.10. Techniques to remove Triclosan
The phototransformation of the widely used biocide triclosan (5-chloro-2-(2, 4-dichlorophenoxy) phenol) was quantified (Tixier et al., 2002) for surface waters using artificial UV light and sunlight irradiation. Here, the pH of surface waters, commonly ranging from 7 to 9, determines the speciation of triclosan (pKa 8.1) and therefore its absorption of sunlight. Direct phototransformation of the anionic form with a quantum yield of 0.31 (laboratory conditions at 313 nm) was identified as the dominant photochemical degradation pathway of triclosan in swiss lake (Lake Greifensee). Hence, the direct phototransformation accounted for 80% of the observed total elimination of triclosan from the lake. Based on absorption spectra and quantum yield data, the phototransformation half-lives of triclosan were calculated under various environmental conditions typical for surface waters. Daily averaged half-lives were found to vary from about 2 to 2000 days, depending on latitude and time of year. The removal of TCS in municipal biosolid processing systems was determined (Ogunyoku and Young, 2014) from the measured concentration change after correcting for reductions in soild mass during sludge treatment. Removal of TCS in the digester systems ranged from 20 – 75% respectively. Increased solid retention times during sludge treatment operations were correlated with higher removals of TCS.
Singer et al. (2002) has identified an effective mechanism to remove triclosan from waste water by biodegradation and the biodegradability of triclosan is high under aerobic conditions rather than anaerobic conditions (McAvoy et al., 2002). Wu et al. (2012) found that the removal of triclosan is higher when treated with ozone during municipal sewage treatment and the adsorbing onto zeolites is the most vialble method to remove triclosan. Triclosan also removed through the process of phototransformation on surface water (Tixier et al., 2002).

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