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PubMed1984

Study of chlorinated diphenyl ethers and chlorinated 2-phenoxyphenols as interferences in the determination of chlorinated dibenzo-p-dioxins and chlorinated dibenzo furans in biological samples.

Two classes of environmentally occurring chlorinated aromatic hydrocarbons which have mass spectral properties similar to the chlorinated dibenzo-p-dioxins (dioxins) and chlorinated dibenzofurans (furans) were studied. Standards of chlorinated diphenyl ethers (CDEs), and chlorinated 2-phenoxyphenols (CPPs) and their methyl ethers, along with the dioxins and furans were passed in steps through a simple method for the analysis of the latter compounds in biological samples. The CDEs, which interfere with the determination of furans by mass spectrometry, had similar extraction, high-performance liquid chromatographic and gas chromatographic properties as the furans but, in all cases studied, were well separated from them on an activated Florisil column using combinations of hexane and dichloromethane as eluting solvents. The higher CPPs on the other hand tended to generate dioxin residues by ring closure when exposed to strong hydrochloric acid solution during sample preparation. In addition, their methyl ethers containing four to six chlorines tracked completely through all stages of the method with the dioxins. Thus, if the methyl ethers of CPPs were present in a sample extract, additional mass spectral information would be needed to further differentiate them from dioxins in environmental samples.

Benzofurans↗
PubMed2002

Chlorination of bisphenol A in aqueous media: formation of chlorinated bisphenol A congeners and degradation to chlorinated phenolic compounds.

The chlorination of bisphenol A (BPA) in aqueous media was investigated in order to describe the degradation profile of this compound and the formation of chlorinated products. Aqueous solutions of BPA (approx. 1 mg/l) were chlorinated by sodium hypochlorite solution at room temperature and under weakly alkaline conditions. Chlorinated compounds were extracted with dichloromethane and determined by gas chromatography/mass spectrometry (GC/MS). BPA was consumed completely within 5 min of chlorination, when the initial chlorine concentration was 10.24 mg/l (molar ratio to BPA, 58.7). On the other hand, when the initial chlorine concentration was 1.03 mg/l (molar ratio, 6.56), 9.3% of BPA still remained after 60 min chlorination. Five chlorinated BPA congeners, 2-chlorobisphenol A (MCBPA), 2,6-dichlorobisphenol A (2,6-D2CBPA), 2,2'-dichlorobisphenol A (2,2'-D2CBPA), 2,2',6-trichlorobisphenol A (T3CBPA) and 2,2', 6,6'-tetrachlorobisphenol A (T4CBPA) were formed in the earlier stages of chlorination. Several chlorinated phenolic compounds, 2,4,6-trichlorophenol (T3CP), 2,6-dichloro-1,4-benzoquinone (D2CBQ), 2,6-dichloro-1,4-hydroquinone (D2CHQ), C9H10Cl2O2, C9H8Cl2O and C10H12Cl2O2, were also formed by further chlorination.

Benzhydryl Compounds↗
PubMed1993

Advances in research on carcinogenic and genotoxic by-products of chlorine disinfection: chlorinated hydroxyfuranones and chlorinated acetic acids.

The introduction of chlorination of public drinking water in the early 1900's was a major factor in the fight against waterborne disease. In the 1970's it was discovered that chlorine reacted with naturally occurring organic constituents, particularly in surface water, to yield small quantities of chlorinated by-products such as chloroform for which regulations were subsequently developed. Since then there has been shown to be a substantial number of other by-products some in concentrations of a few nanograms/l and others similar concentrations to the THM. Of particular note are the potent bacterial mutagen MX and the chlorinated acetic acids. Current research into the significance of these for man is described and the key issues for risk assessment are identified.

Acetates↗
PubMed1986

NTP Toxicology and Carcinogenesis Studies of Chlorinated Paraffins (C23, 43% Chlorine) (CAS No. 108171-27-3) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

Toxicology and carcinogenesis studies of chlorinated paraffins (C23, 43% chlorine), an extreme-pressure lubricant and flame retardant, were conducted by administering the chemical in corn oil by gavage to groups of 50 F344/N rats and 50 B6C3F1 mice of each sex, 5 days per week for 103 weeks. Additional groups of 10 rats per sex and dose were examined at 6 and at 12 months. Male rats received doses of 0, 1,875, or 3,750 mg/kg body weight; female rats were given 0, 100, 300, or 900 mg/kg. Male and female mice received 0, 2,500, or 5,000 mg/kg. Doses selected for the 2-year studies were based on the results from 13-week studies in which rats of each sex received 0 to 3,750 mg/kg, and mice of each sex, 0 to 7,500 mg/kg. No toxicity of chlorinated paraffins (C23, 43% chlorine) was observed in male rats or in male or female mice in the 13-week studies. A dose-related inflammation of the liver was observed in female rats in the 13-week studies and in male and female rats in the 13-week studies and in male and female rats at 6 and 12 months in the 2-year studies. Chlorinated paraffins (C23, 43% chlorine) administration did not influence mean body weights of rats during the 2-year studies, but both male and female low dose mice gained less weight than did vehicle controls or the high dose groups. Survival of dosed and vehicle control groups was similar for each sex and species (male rats: vehicle control, 30/50; low dose, 32/50; high dose, 27/50; female rats: 34/50; 30/50; 33/50; 31/50; male mice: 29/50; 36/50; 28/50; female mice: 21/50; 22/50; 20/50). For female mice, 60%-70% of the early deaths in each group were attributed to utero-ovarian infection. The lower survival for female mice may have decreased the sensitivity of this study to detect a carcinogenic effect. Pheochromocytomas of the adrenal gland medulla occurred with an increased incidence in female rats exposed to chlorinated paraffins (C23, 43% chlorine) (vehicle control, 1/50; low dose, 4/50; mid dose, 6/50; high dose, 7/50). However, adrenal gland medullary hyperplasia was not increased (6/50; 3/50; 1/50; 6/50). Malignant lymphomas were increased in dosed male mice (6/50; 12/50; 16/50). High dose female mice showed a marginal increase in the incidence of hepatocellular carcinomas (1/50; 1/49; 6/50) and in the incidence of adenomas or carcinomas (combined) (4/50; 3/49; 10/50). The primary nonneoplastic lesion associated with chlorinated paraffins (C23, 43% chlorine) administration was a diffuse lymphohistiocytic inflammation in the liver and in the pancreatic and mesenteric lymph nodes of male and female rats. Splenic congestion was a secondary effect. These lesions occurred earlier and at lower doses in female rats than in male rats. No significant nonneoplastic lesions were considered compound related in mice. Chlorinated paraffins (C23, 43% chlorine) was not mutagenic in strains TA100, TA1535, TA97, or TA98 of Salmonella typhimurium in the presence or absence of Aroclor 1254-induced male Sprague-Dawley rat or male Syrian hamster liver S9 when assayed according to the preincubation protocol. An audit of the experimental data was conducted for these 2-year studies of chlorinated paraffins (C23, 43% chlorine). No data discrepancies were found that influenced the final interpretations. Under the conditions of these 2-year gavage studies, there was no evidence of carcinogenicity of chlorinated paraffins (C23, 43% chlorine) for male F344/N rats given 1,875 or 3,750 mg/kg per day. There was equivocal evidence of carcinogenicity of chlorinated paraffins (C23, 43% chlorine) for female F344/N rats as shown by an increased incidence of adrenal gland medullary pheochromocytomas. There was clear evidence of carcinogenicity of chlorinated paraffins (C23, 43% chlorine) for male B6C3F1 mice as shown by an increase in the incidence of malignant lymphomas. There was equivocal evidence of carcinogenicity of chlorinated paraffins (C23, 43% chlorine) for female B6C3F1 mice as shown by a marginal increase in the incidence of hepatocellular neoplasms. *The Chemical Abstract Service Seal increase in the incidence of hepatocellular neoplasms. *The Chemical Abstract Service Service (CAS) number that appeared on this technical report at the time of publication (63449-39-8) reflects the generic CAS number for chlorinated paraffins. This number has been replaced in the NTP Chemtrack chemical tracking system with the more appropriate number.

Journal Article↗
PubMed1986

Reactions of aqueous chlorine and chlorine dioxide with model food compounds.

Chlorine and chlorine dioxide (ClO2), common disinfecting and bleaching chemicals used in the food industry, are potent oxidizing and chlorinating agents. Unfortunately, little is known about the nature of the reactions of chlorine with organic food constituents. This presentation reviews published information concerning the reactions of chlorine gas (Cl2[g]), aqueous chlorine, and ClO2 with model food compounds, the fate of chlorine during the chlorination of specific food products, and the potential toxicity of the reaction products. Fatty acids and their methyl esters react with chlorine with the degree of incorporation corresponding to their degree of unsaturation. Aqueous chlorine oxidizes and chlorinates lipids and amino acids much more readily than ClO2. Several amino acids are highly susceptible to oxidation and chlorination by chlorine compounds. Reactions of chlorine and ClO2 with several food products, including flour and shrimp, have also been characterized. In one model system, 99% of Cl2(g) either reacted with components of flour or was consumed by oxidation/chlorination reactions. The lipids extracted from the chlorinated flour contained significant amounts of chlorine. Exposure of shrimp to hypochlorous acid (HOCl) solution resulted in significant incorporation of chlorine into the edible portion. Although significant quantities of chlorine can be incorporated into specific model compounds and food products, the health risks associated with exposure to chlorinated organic products are unknown. Preliminary studies using the Ames Salmonella/microsome mutagenicity assay indicate that the reaction products from mixtures of aqueous chlorine and various lipids or tryptophan are nonmutagenic. Nevertheless, additional studies are warranted, so that the toxicological significance of these reaction products can be understood more fully.

Amino Acids↗
PubMed1986

NTP Toxicology and Carcinogenesis Studies of Chlorinated Paraffins (C12, 60% Chlorine) (CAS No. 108171-26-2*) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

Toxicology and carcinogenesis assessments of chlorinated paraffins (C12, 60% chlorine), a material widely used as a flame retardant and extreme-pressure lubricant, were conducted in male and female F344/N rats and male and female B6C3F1 mice in single-administration, 16-day, 13-week, and 2-year studies. Doses used in the 2-year studies were 0, 312, or 625 mg/kg body weight per day administered by gavage in corn oil five times per week to groups of 70 male and female rats and 0, 125, or 250 mg/kg administered to groups of 50 male and female mice. Ten male and 10 female rats were killed after 6 and 12 months of dosing and examined for toxicity. No chemically related toxicity was observed in single-administration studies in which male and female rats received doses of chlorinated paraffins (C12, 60% chlorine) up to 13,600 mg/kg body weight and male and female up to 27,200 mg/kg. In 16-day studies, deaths did occur in groups of male and female rats given 7,500 mg/kg and in groups of male and female mice given doses of 1,875 mg/kg or higher. In 13-week studies, no chemically related deaths occurred among male and female rats given up to 5,000 mg/kg or mice given up to 2,000 mg/kg. Increased liver weights were noted in dosed rats and mice of each sex in the short-term studies, and dosed male rats showed more severe nephropathy than did vehicle controls. Doses selected for the 2-year studies were those that caused a minimal increase in liver weight in the short-term studies. Liver and kidney weights were increased in dosed rats killed at 6 and 12 months. Morphometric measurements demonstrated hepatocyte hypertrophy in the livers of dosed rats. Lesions of the kidney tubules and interstitial inflammation increased with dose in male and female rats. During the 2-year studies, body weights of high dose male rats were 8%-12% lower than those of vehicle controls after week 20, and body weights of dosed female mice were about 10% lower than those of vehicle controls during the second year. Survival of dosed male rats was lower than that of vehicle controls after about week 85, perhaps due to toxicity to the kidney (final survival: vehicle control, 27/50; low dose, 6/50; high dose, 3/50). Survival of low dose female rats was lower than that of vehicle controls (34/50; 24/50; 29/50). Survival of dosed male mice was not significantly different from that of vehicle controls (34/50; 31/50; 31/50). Survival of high dose female mice was lower than that of vehicle controls after about week 75 (final survival: 36/50; 31/50; 25/50). Chemically related nonneoplastic lesions consisted of hypertrophy and minimal focal necrosis of the liver in rats; erosion, inflammation, and ulceration of the glandular stomach and forestomach a in male rats; and formation ofmultiple cysts in the kidney tubules of male rats. The incidence of nephropathy was also increased in dosed female rats and mice. The maximum tolerated dose may have been exceeded in male and female rats. Neoplastic lesions associated with chlorinated paraffins (C12, 60% chlorine) administration were found in the liver of rats and mice of each sex (see table p. 12 of Technical Report) Dosed male rats showed increased incidences of kidney tubular cell hyperplasia (1/50; 9/50; 12/49) and of tubular cell adenomas (0/50; 7/50; 3/49); two low dose males had tubular cell adenocarcinomas. The incidences of mononuclear cell leukemia were increased in dosed male rats (7/50; 12/50; 14/50) and in low dose female rats (11/50; 22/50; 16/50). Pancreatic acinar cell tumors occurred at increased incidences in low dose male rats (11/50; 22/50; 17/50). Follicular cell adenomas or carcinomas (combined) of the thyroid gland were found at increased incidences in both female rats (0/50; 6/50; 6/50) and female mice (8/50; 12/49; 15/49). Chlorinated paraffins (C12, 60% chlorine) was not mutagenic in Salmonella typhimurium strains TA97, TA98, TA100, or TA1535 in the presence or absence of Aroclor 1254-induced male Sprague-Dawley or male Syrian hamster liver S9 when tested according to the preincubational protocol. An ed according to the preincubational protocol. An audit of the experimental data was conducted for these 2-year studies on chlorinated paraffins (C12, 60% chlorine). No data discrepancies were found that influenced the final interpretations. Under the conditions of these 2-year gavage studies, there was clear evidence of carcinogenicity of chlorinated paraffins (C12, 60% chlorine) for F344/N rats based on increased incidences of hepatocellular neoplasms (primarily neoplastic nodules) in male and female rats, of adenomas or adenocarcinomas (combined) of the kidney tubular cells in male rats, and of follicular cell adenomas or carcinomas (combined) of the thyroid gland in female rats. Mononuclear cell leukemia in dosed male rats may have been related to administration of chlorinated paraffins (C12, 60% chlorine). There was clear evidence of carcinogenicity of chlorinated paraffins (C12, 60% chlorine) for B6C3F1 mice as shown by increased incidences of hepatocellular adenomas and of adenomas or carcinomas (combined) in dosed male and female mice and increased incidences of adenomas and of adenomas or carcinomas (combined) of thyroid gland follicular cells in dosed female mice.

Journal Article↗
PubMed2002

Sequential inactivation of Cryptosporidium parvum oocysts with chlorine dioxide followed by free chlorine or monochloramine.

The main objective of this study was to assess the effect of temperature (4-30 degrees C) on the inactivation kinetics of Cryptosporidium parvum oocysts with sequential disinfection schemes involving the use of chlorine dioxide as the primary disinfectant and free or combined chlorine as the secondary disinfectant in synthetic water. The synergy previously reported for sequential inactivation of C. parvum oocysts with ozone/free chlorine or ozone/combined chlorine did not occur when chlorine dioxide was used. instead of ozone, as the primary disinfectant within the temperature range (4-30 degrees C) and the pre-treatment levels investigated. Sequential ozone/chlorine dioxide and chlorine dioxide ozone experiments revealed that the lower level or absence of synergy for chlorine dioxide/free chlorine and chlorine dioxide, monochloramine was likely the result of chlorine dioxide reacting with oocyst chemical groups that are mostly different from those reacting with ozone, free chlorine, or monochloramine. The CT concept was found to be valid for the primary inactivation kinetics of C. parvum oocysts with chlorine dioxide, thus allowing the use of the simpler CT approach for the development of C. partum inactivation requirements with chlorine dioxide. General consistency was found between the secondary inactivation kinetics of C. parvum oocysts with free chlorine and monochloramine after chlorine dioxide pretreatment obtained in this study with oocyst viability determined by a modified in vitro excystation method and those reported in the literature for the same sequential disinfection schemes based on an animal infectivity assay.

Animals↗
PubMed1993

Assessment of the carcinogenic potential of chlorinated water: experimental studies of chlorine, chloramine, and trihalomethanes.

BACKGROUND: Water chlorination has been one of the major disease prevention treatments of this century. While epidemiologic studies suggest an association between cancer in humans and consumption of chlorination byproducts in drinking water, these studies have not been adequate to draw definite conclusions about the carcinogenic potential of the individual byproducts. PURPOSE: The purpose of this study was to investigate the carcinogenic potential of chlorinated or chloraminated drinking water and of four organic trihalomethane byproducts of chlorination (chloroform, bromodichloromethane, chlorodibromomethane, and bromoform) in rats and mice. METHODS: Bromodichloromethane, chlorodibromomethane, bromoform, chlorine, or chloramine was administered to both sexes of F344/N rats and (C57BL/6 x C3H)F1 mice (hereafter called B6C3F1 mice). Chloroform was given to both sexes of Osborne-Mendel rats and B6C3F1 mice. Chlorine or chloramine was administered daily in the drinking water for 2 years at doses ranging from 0.05 to 0.3 mmol/kg per day. The trihalomethanes were administered by gavage in corn oil at doses ranging from 0.15 to 4.0 mmol/kg per day for 2 years, with the exception of chloroform, which was given for 78 weeks. RESULTS: The trihalomethanes were carcinogenic in the liver, kidney, and/or intestine of rodents. There was equivocal evidence for carcinogenicity in female rats that received chlorinated or chloraminated drinking water; this evidence was based on a marginal increase in the incidence of mononuclear cell leukemia. Rodents were generally exposed to lower doses of chlorine and chloramine than to the trihalomethanes, but the doses in these studies were the maximum that the animals would consume in the drinking water. The highest doses used in the chlorine and chloramine studies were equivalent to a daily gavage dose of bromodichloromethane that induced neoplasms of the large intestine in rats. In contrast to the results with the trihalomethanes, administration of chlorine or chloramine did not cause a clear carcinogenic response in rats or mice after long-term exposure. CONCLUSION: These results suggest that organic byproducts of chlorination are the chemicals of greatest concern in assessment of the carcinogenic potential of chlorinated drinking water.

Animals↗
PubMed2002

Effects of isocyanuric acid on the monochlorodimedone chlorinating rates with free chlorine and ammonia chloramine in water.

Changes in monochlorodimedone (MCD) chlorinating rates with free chlorine (mixture of HOCl and OCl-) and ammonia monochloramine (NH2Cl) in water at pH 7 by the addition of isocyanuric acid (H3Cy) were determined at room temperature. Decreases in MCD absorbance at 290nm in equimolar (0.04mM) reactions of MCD and free available chlorine solutions containing H3Cy (0.01-1.60 mM) were recorded in a stopped-flow spectrophotometer. The rates indicate second-order reactions. Since the rate with free chlorine was high (> 7.6 x 10(6) M(-1) s(-1)), the amounts of free chlorine in the solutions could be distinguished from that of chlorinated cyanurates. The chlorinating rates with chlorinated cyanurates decreased with an increase in H3Cy concentrations. Plotting the rates against the molar ratio of chlorine to H3Cy showed a linear correlation and the rates with chlorinated cyanurates (H2ClCy) was estimated at 0.5 x 10(5) M(-1) s(-1). In contrast, the rates with the NH2Cl solution containing H3Cy increased with an increase in H3Cy concentrations, increasing from 1.2 x 10 to 2.7 x 10 M(-1) s(-1) by the addition of 1.55 mM H3Cy. The DPD color development rates (OD512/t1/2/M) with free available chlorine (0.015mM) declined from 1.3 x 10(5) to 0.9 x 10(5)M(-1) by the addition of 0.61 mM H3Cy.

Chloramines↗
PubMed1964

KILLING OF CHLORINE-RESISTANT BACTERIA BY CHLORINE-BROMINE SOLUTIONS.

The disinfective power of chlorine, bromine, and mixtures of chlorine and bromine at different ratios was compared. The influence of pH was also studied. The experiments were carried out in "purified" water and in natural waters of swimming pools, river, and sea. In the presence of high amounts of nitrogenous growth-promoting material (at neutral pH), bromine was more effective than chlorine; in waters containing low amounts of nitrogenous growth-promoting material, chlorine was found superior. Mixtures of chlorine and bromine at various ratios were found to increase in effectiveness inversely to the percentage of hypobromite generated, down to 10 or 5%. Such effectiveness was found at pH levels of 5.4 to 8.6 in both purified and natural water containing high and low amounts of nitrogenous growth-promoting material. Therefore, the above mixtures seem of practical value for the disinfection of various natural waters. Escherichia coli isolated in the presence of chlorine, either from swimming pools or after deliberate exposure to the halogen, were shown to be chlorine-resistant mutants. Their resistance was maintained for at least nine passages in the absence of the disinfectant, which accounts for the number of passages tested. Chlorine-resistant mutants were not affected by bromine alone but did show a marked sensitivity to low concentrations of bromine active in the presence of chlorine. This was achieved by admixing small amounts of bromide to hypochlorite. A hypothetical model is presented to explain the synergistic sequential block by the two disinfectants. Some chlorine-resistant mutants were found to have changed into relatively slow-growing organisms with a changed phase-sensitivity pattern.

Bromides↗
PubMed1989

Formation of chlorinated PAH--a possible health hazard from water chlorination.

Four PAH compounds, fluorene, anthracene, fluoranthene and benzo(a)pyrene were dissolved in humus poor (lake) and humus rich water. The samples were chlorinated, stored for three days, and extracted with cyclohexane. Chlorinated derivatives of the four compounds were synthesised and used as calibration standards for quantitative analysis of the corresponding chlorinated PAH formed during the experiment. The synthesized chlorinated PAH were tested for mutagenic activity by the Ames test, and their octanol/water partition coefficient (Pow) were determined by thin layer chromatography. Chlorinated fluorene, fluoranthene and benzo(a)pyrene were formed during chlorination of PAH polluted lake water, but not during chlorination of the humus rich water samples. All chlorinated PAH except 9,10-dichloroanthracene, acted as strong mutagens both in the presence and in the absence of metabolic activation, while benzo(a)pyrene was the only mutagen active parent PAH. The determined Pow showed high lipophilicity for all chlorinated PAH. Theoretically determined bioconcentration factors (BCF) were found to be extremely high, and increased with increasing ring number and increasing number of chlorine atoms attached to the ring.

Anthracenes↗
PubMed2002

Chlorination of natural organic matter: kinetics of chlorination and of THM formation.

The kinetics of the formation of trihalomethanes (THMs) and of chlorine consumption for the chlorination of natural organic matter with an excess of chlorine (50 microM > [Cl2]o >210 microM) was investigated. THM precursors could be divided into a fast and a slowly reacting fraction. Long term chlorine demand and the formation of THM could be described by second order kinetics. Rate constants were between 0.01 and 0.03 M(-1) s(-1) in the pH range 7-9 for surface waters and humic materials extracted from surface waters. A groundwater gave a higher rate constant of 0.124 M(-1) s(-1). Resorcinol-type structures were tested with respect to kinetics and yield of THM formation. They could possibly be responsible for the fast reacting THM precursors. which represent 15-30% of the THM precursors of natural waters. Additional classes of compounds that might contribute to the initial THM formation include readily enolizable compounds such as beta-diketones and beta-ketoacids. Experiments with phenol showed that slowly reacting THM precursors may consist of phenolic compounds. The influence of pretreatments (UV/visible irradiation, ozone and chlorine dioxide) on chlorine demand and THM formation from NOM was also studied: UV/visible irradiation does not alter THM formation but leads to a higher chlorine demand. Preoxidation with ozone leads to a lower THM formation with an unaltered chlorine demand and preoxidation with chlorine dioxide reduces THM formation and the chlorine demand.

Chlorine Compounds↗
PubMed2002

Chlorine and chlorine dioxide treatment to reduce or remove EBDCs and ETU residues in a solution.

Calcium hypochlorite (Ca(OCl)(2)) and chlorine dioxide (ClO(2)), common disinfecting and bleaching chemicals used in the food industry, are potent oxidizing agents. In this paper, the degradation effects of chlorine dioxide on mancozeb and ethylenethiourea (ETU) residues were investigated in a model system and compared with those of liquid chlorine, under various conditions such as differing concentration, pH, reaction time, and temperature. All samples were analyzed for residues by GLC and HPLC. Rate of mancozeb degradation was dependent on pH, with pH 4.6 being the most effective. Mancozeb residues decreased 40-100% with chlorine and chlorine dioxide treatments. ETU residue concentrations in mancozeb solutions were monitored over 60 min. Under controlled conditions, the ETU residue concentrations increased up to 15 min reaction time and then decreased in all three pH ranges. Treatment with both chlorine and chlorine dioxide at pH 4.6, yielded no ETU residues at both 10 and 21 degrees C. The results show that chlorine dioxide gives excellent degradation effects at lower concentrations than liquid chlorine.

Calcium Compounds↗
PubMed1984

Inactivation of simian rotavirus SA11 by chlorine, chlorine dioxide, and monochloramine.

The kinetics of inactivation of simian rotavirus SA11 by chlorine, chlorine dioxide, and monochloramine were studied at 5 degrees C with a purified preparation of single virions and a preparation of cell-associated virions. Inactivation of the virus preparations with chlorine and chlorine dioxide was studied at pH 6 and 10. The monochloramine studies were done at pH 8. With 0.5 mg of chlorine per liter at pH 6, more than 4 logs (99.99%) of the single virions were inactivated in less than 15 s. Both virus preparations were inactivated more rapidly at pH 6 than at pH 10. With chlorine dioxide, however, the opposite was true. Both virus preparations were inactivated more rapidly at pH 10 than at pH 6. With 0.5 mg of chlorine dioxide per liter at pH 10, more than 4 logs of the single-virus preparation were inactivated in less than 15 s. The cell-associated virus was more resistant to inactivation by the three disinfectants than was the preparation of single virions. Chlorine and chlorine dioxide, each at a concentration of 0.5 mg/liter and at pH 6 and 10, respectively, inactivated 99% of both virus preparations within 4 min. Monochloramine at a concentration of 10 mg/liter and at pH 8 required more than 6 h for the same amount of inactivation.

Animals↗
PubMedDate not supplied

Reactions of aqueous chlorine in vitro in stomach fluid from the rat: chlorination of tyrosine.

Aqueous chlorine reacts with tyrosine to form ring-chlorinated products. Ring substitution occurs at Cl:tyrosine mole ratios greater than 1. Because the nitrogen function of amides is much less reactive than that of amines, the aromatic ring of N-acetyltyrosine is chlorinated at chlorine:substrate mole ratios less than 1. When an aqueous solution of the gastric protein pepsin was chlorinated (37 degrees C, 45 min), tyrosine residues were chlorinated at pH 2 but not at pH 8. The carbohydrate, protein, and chloride concentrations in stomach fluid from fasted rats were determined. When varying concentrations of aqueous chlorine (20-180 mg/L Cl2) were added to the stomach fluid at pH 2, tyrosine residues were mono- and dichlorinated on the aromatic ring. The amount of mono- to dichlorination products varied with the concentration of aqueous chlorine. A mechanism is proposed. The implications for toxicological studies involving chlorinated drinking water are discussed.

Animals↗
PubMed2000

Ascorbic acid reduction of active chlorine prior to determining Ames mutagenicity of chlorinated natural organic matter (NOM).

Many potable water disinfection byproducts (DBPs) that result from the reaction of natural organic matter (NOM) with oxidizing chlorine are known or suspected to be carcinogenic and mutagenic. The Ames assay is routinely used to assess an overall level of mutagenicity for all compounds in samples from potable water supplies or laboratory studies of DBP formation. Reduction of oxidizing disinfectants is required since these compounds can kill the bacteria or react with the agar, producing chlorinated byproducts. When mutagens are collected by passing potable water through adsorbing resins, active chlorine compounds react with the resin, producing undesirable mutagenic artifacts. The bioanalytical and chemoanalytical needs of drinking water DBP studies required a suitable reductant. Many of the candidate compounds failed to meet those needs, including 2,4-hexadienoic (sorbic) acid, 2,4-pentanedione (acetylacetone), 2-butenoic (crotonic) acid, 2-butenedioic (maleic and fumaric) acids and buten-2-ol (crotyl alcohol). Candidates were rejected if they (1) reacted too slowly with active chlorine, (2) formed mutagenic byproducts, or (3) interfered in the quantitation of known chlorination DBPs. L-Ascorbic acid reacts rapidly and stoichiometrically with active chlorine and has limited interactions with halogenated DBPs. In this work, we found no interference from L-ascorbic acid or its oxidation product (dehydroascorbic acid) in mutagenicity assays of chlorinated NOM using Salmonella typhimurium TA100, with or without metabolic activation (S9). This was demonstrated for both aqueous solutions of chlorinated NOM and concentrates derived from the involatile, ether-extractable chlorinated byproducts of those solutions.

Ascorbic Acid↗
PubMed2003

Effects of chlorine content and position of chlorinated phenols on their oxidation kinetics by potassium permanganate.

Chlorine content and position of chlorinated phenols have many significant effects on the reactivity of oxido-reduction. The effects of chlorine content and position of chlorinated phenols on their oxidation kinetics by potassium permanganate were evaluated through different kinetics studies. Since chlorine was an electron withdrawing atom, the substitution of chlorine on the aromatic ring decreased the oxidation rate constant by sigma-electron withdrawing conductive effect. The substitution of chlorine at ortho or para position on the aromatic ring increased the oxidation rate constant by pi-electron donating conjugative effect, and the conjugative effect could counteract the negative impact of the conductive effect to some extent. On the other hand, the substitution of chlorine at ortho position on the aromatic ring decreased the oxidation rate constant by steric hindrance effect. The oxidation rate constants of phenol and chlorinated phenol studied decreased as follow order: 4-chlorophenol > 2,4-dichlorophenol > phenol > 2,6-dichlorophenol.

Chlorine Compounds↗