2 ,4,5-Trichlorophenol contamination

In the course of making 24 5 trichlorophenol it al most always becomes contaminated with small... 

Tetrachlorodibenzo-p-dioxin (TCDD) (I), an occasional contaminant in 2,4,5-T and other trichlorophenol derivatives, is the most toxic of the commonly-encountered dioxins (8) and it received most of our attention. Its low solubility in common solvents and water (ca. 2 ppb) limited our experiments since the products were difficult to identify by the conventional techniques of organic chemistry. However, TCDD has an absorption maximum at 307 nm in methanol—well within the solar spectrum observed at the earth s surface and near the region of maximum intensity (310-330 nm) of the UV lamps used in previous experiments (H 29). 

Oevere toxicological responses have been associated with certain chloro- dibenzodioxins. One of these responses is chloracne, a folliculosis first associated with skin contamination by chlorohydrocarbons in 1899 (3). Serious outbreaks of chloracne-like lesions associated with runaway reactions in the production of 2,4,5-trichlorophenol occurred in Germany in the early 1950 s (5). 2,4,5-Trichlorophenol itself does not cause acne (S), but the contaminants which may be formed in the uncontrolled production of 2,4,5-trichlorophenol are extremely potent acnegens (5). 2,3,7,8-Tetrachlorodibenzo-p-dioxin and tri- and tetra-... 

Degradation of contaminants may occur with bacteria that have been isolated from pristine environments without established exposure to the contaminants, and exhibit no dependence on substrate concentration. For example, organisms from a previously unexposed forest soil were able to degrade 2,4,6-trichlorophenol at concentrations up to 5000 ppm, and terminal restriction fragment length polymorphism analysis revealed that at concentrations up to 500 ppm, the bacterial community was unaltered (Sanchez et al. 2004). 

TCP), and pentachlorophenol (PCP), in order of abundance. Minor amounts of other trichlorophenols and dichlorophenols may also be present, as well as recalcitrant polychlorinated phenoxyphenols (PCPPs) and PCDD/Fs as impurities [75, 76]. In Finland, approximately 30,000 tons of CP products were used between 1934 and 1988, when they were banned because of their potential toxicity to humans and the environment [77, 78]. The careless manufacturing and application of wood preservatives together with the lack of suitable waste disposal caused massive contamination of river sediments and sawmill sites. For example, the river Kymijoki in southern Finland was identified as the largest source of dioxins accumulating in fish in the entire Baltic area. Similar products were used in other European countries, especially Nordic countries with a large forestry industry, such as Sweden [79]. 

On July 10,1976, the trichlorophenol reactor went out of control, resulting in a higher than normal operating temperature and increased production of TCDD. An estimated 2 kg of TCDD was released through a relief system in a white cloud over Seveso. A subsequent heavy rain washed the TCDD into the soil. Approximately 10 square miles were contaminated. 

Fig. 20. A typical GC-MS trace of a phenol contaminated soil sample, Bitterfeld, Germany (after [254] with permission). Chlorophenols were extracted using ASE-SPME upper chromatogram, procedure B lower chromatogram, ASE conditions of water, 150°C, 15 min. Peak identifications (1) 2-chlorophenol, (2) 2,4-dichlorophenol, (3) 4-chlorophenol, (4) 4-chloro-3-methylphenol, (5) 2,3,5-trichlorophenol, (6) 2,4,6-trichlorophenol, (7) 2,3,4-trichlo-rophenol, (8) 2,3,4,6-tetrachlorophenol, (9) pentachlorophenol... 

The environmental burden of waterways with polychlorinated dibenzo-p-dioxins (PCDD) has been at the forefront of public and regulatory concern, because of the toxicity associated with particularly the 2,3,7,8-(laterally) substituted congeners, which have a tendency to bioaccumulate throughout the trophic food chain. Contamination of aquatic sediments by dioxins includes both non-point (e.g., atmospheric deposition) and point sources (e.g., industrial effluents, combined sewage overflows), and is generally characterized by a dominance of hepta- and octa-CDD, with minor contributions of hexa- to tetra-CDD [429]. Elevated concentrations of the 2,3,7,8-TCDD isomer tend to be associated with direct discharge from sources such as 2,4,5-trichlorophenol production [54,430]. 

Soil Under aerobic conditions, indigenous microbes in contaminated soil produced pentachlorocyclohexane. However, under methanogenic conditions, a-BHC was converted to chlorobenzene, 3,5-dichlorophenol, and the tentatively identified compound 2,4,5-trichlorophenol (Bachmann et al., 1988). Manonmani et al. (2000) isolated a microbial consortium from sewage and soil that could completely mineralize a-BHC in 14 d at 30 °C. The acclimated consortium could degrade up to 100 mg/L of a-BHC within 72 h at a degradation rate of 58 mg/L-day. 

Source Although not produced commercially, TCDD is formed as a by-product in the synthesis of 2,4,5-trichlorophenol. TCDD was found in 85% of soil samples obtained from a trichlorophenol manufacturing site. Concentrations ranged from approximately 20 ng/kg to 600 g/kg (Van Ness et al, 1980). TCDD may be present in the herbicide 2,4-D which contains a mixture of dichloro-, trichloro-, and tetrachlorodioxins. TCDD is commonly found as a contaminant associated with pulp and paper mills (Boddington, 1990). In addition, during the manufacture of 2,4,5-T and silvex from trichlorophenol, TCDD was found at concentrations averaging 20 parts per billion (Newton and Snyder, 1978). 

The most heavy exposure is most likely during purification as the residues are by far more contaminated than the purified produts (2j. However, only limited information is available on the levels of PCDD contamination of products prepared prior to the 1970 s and no information at all is available on the levels of TCDD in the residues. Consequently it is quite difficult to estimate the levels of exposure. Moreover, the TCDD content seems to be dependent on the experimental conditions during the preparation of 2,U,5-trichlorophenol, but these conditions are very seldom given in the literature. 

In the course of making 2,4,5-trichlorophenol, it al- amounts of 2,3,7,8-tetrachlorodibenzo-p-dioxin, bet-most always becomes contaminated with small ter known as dioxin. 

Chlorinated phenols are among the most important contaminants in the environment (aqueous systems and soils) due to their widespread use in industry and agriculture and for domestic purposes for over 50 years. It is well-known that chlorophenols are toxic at low levels. The more highly chlorinated phenols such as trichlorophenols and pentachlorophenol are also persistent. Five of the chlorophenols (2-chlorophenol, 2,4-dichlorophenol, 4-chloro-3-methylphenol, 2,4,6-trichlorophenol and pentachlorophenol) have been classified as priority pollutants by the US Environmental Protection Agency (EPA). 

Perhaps the most catastrophic industrial accident involving dioxin occurred in S6veso, Italy in July, 1976. Here an entire community surrounding a trichlorophenol feedstock plant was contaminated 736 individuals were in the maximum exposure zone 4699 were in a less exposed zone, and 31.800 individuals were in the zone of least exposure. There were four spontaneous abortions and thirty voluntary interrupted pregnancies. The dose-related increase in chloracne occurred, but the spate of voluntary abortions obscured the teratogenicity data. 

The chlorinated phenols, particularly pentachlorophenol (Figure 16.7) and the trichlorophenol isomers, have been widely used as wood preservatives. Applied to wood, these compounds prevent wood rot through their fungicidal action and prevent termite infestation because of their insecticidal properties. Both cause liver malfunction and dermatitis. Contaminant polychlorinated dibenzodiox-ins may be responsible for some of the observed effects. 

Gastrointestinal Effects. Earlier studies of individuals with exposure to substances contaminated with 2,3,7,8-TCDD found significant elevations in self-reported ulcers (Bond et al. 1983 Suskind and Hertzberg 1984), but a study of Vietnam veterans (USAF 1991) failed to find such effects. A more recent study evaluated the gastrointestinal effects of exposure to substances contaminated with 2,3,7,8-TCDD in an occupational cohort (Calvert et al. 1992). More than 15 years earlier, the workers were employed in the manufacture of trichlorophenol and its derivatives at 2 chemical plants. A total of 281 workers participated in the medical study the control group consisted of 260 unexposed subjects who lived in the same communities as the workers. The participants underwent a comprehensive physical examination of the abdomen and rectum. The mean serum 2,3,7,8-TCDD level (on a lipid basis) for the workers was 220 ppt and was found to be highly correlated with years of exposure to 2,3,7,8-TCDD-contaminated substances controls had a mean serum 2,3,7,8-TCDD concentration of 7 ppt. At the time of examination, the workers were not found to be at increased risk for any gastrointestinal diseases. Moreover, neither... 

Accidental exposure to 2,3,7,8-TCDD in a 1949 explosion in a trichlorophenol plant in Nitro, West Virginia, resulted in an outbreak of severe chloracne. Moses et al. (1984) conducted a cross-sectional survey of workers in this plant in 1979. In reviewing the impact of the accident, the authors indicated that 117 workers had severe chloracne as a result of the explosion however, 111 additional workers were found to have had chloracne prior to the explosion. A cross-sectional study of 226 workers in 1979 indicated that 52% had chloracne which persisted for 26 years, and in 29 subjects it was still present after 30 years. Blood levels were not measured, but the air dust in the plant was suspected to have contained 2,4,5-T contaminated with 6 ppm 2,3,7,8-TCDD compared to 0.1 ppm in later years. Similarly, high incidences of chloracne were also found in other facilities (Jirasek et al. 1976 May 1973 Poland et al. 1971 Vos et al. 1978). Appearance of chloracne after accidental occupational exposure may be immediate or delayed since workers may not always be removed from the work environment, the duration of exposure and total exposure is difficult to assess. 

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