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PubMed2002

Chlorination byproducts and nitrate in drinking water and risk for congenital cardiac defects.

Drinking water disinfection byproducts have been associated with an increased risk for congenital defects including cardiac defects. Using Swedish health registers linked to information on municipal drinking water composition, individual data on drinking water characteristics were obtained for 58,669 women. Among the infants born, 753 had a cardiac defect. The risk for a cardiac defect was determined for ground water versus surface water, for different chlorination procedures, and for trihalomethane and nitrate concentrations. Ground water was associated with an increased risk for cardiac defect when crude rates were analyzed but after suitable adjustments this excess rate was found to be determined by chlorination procedures including chlorine dioxide. Chlorine dioxide appears itself as an independent risk factor for cardiac defects (adjusted odds ratio 1.61 (95%CI 1.00-2.59)). The risk for cardiac defects increased with increasing trihalomethane concentrations (P=0.0005). There was an indicated but statistically nonsignificant excess risk associated with nitrate concentration. The individual risk for congenital cardiac defect caused by chlorine dioxide and trihalomethanes is small but as a large population is exposed to public drinking water, the attributable risk for cardiac defects may not be negligible.

Adult↗
PubMed2002

Risk assessment of ochratoxin: current views of the European Scientific Committee on Food, the JECFA and the Codex Committee on Food Additives and Contaminants.

The chlorinated isocoumarin compound, ochratoxin A (OTA), together with some related derivatives (ochratoxins B, C, alpha, beta) are produced by Penicillium verrucosum and by several spp. of Aspergillus, most notably A. ochraceus. P. verrucosum is the principal source of OTA contamination of stored foods in temperate climates while Aspergillus spp. predominate in warmer countries. The major dietary sources of OTA are cereals but significant levels of contamination may be found in grape juice and red wine, coffee, cocoa, nuts, spices and dried fruits. Because of the chemical stability of OTA and long half-life in mammalian tissues, contamination may also carry over into pork and pig blood products and into beer. OTA is potently nephrotoxic and carcinogenic, the potency varying markedly between species and sexes; it is also teratogenic and immunotoxic. There have been different approaches to the risk assessment of OTA in different jurisdictions, largely arising from whether or not the carcinogenicity of OTA is considered to arise through a thresholded or non-thresholded mechanism. Consequently the tolerable intakes have variously been estimated at 100 ng/kg bw/week (JECFA), 1.5 to 5.7 ng/kg bw/day (Canada) and not more than 5 ng/kg bw/day (European Commission). These differences are also reflected in risk management measures that have been implemented or proposed with different maximum contamination levels being applied to different commodities and to the same commodity in different countries. Prevention of contamination at source is considered to be the most effective public health measure. There is also a need to harmonise the risk assessment and management processes to a greater extent than currently exist if barriers to trade are to be avoided.

Animals↗
PubMed1991

Long-term carcinogenesis studies on 2,3,7,8-tetrachlorodibenzo-p-dioxin and hexachlorodibenzo-p-dioxins.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and 1,2,3,6,7,8- and 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins (HCDDs) are among the most toxic and carcinogenic of "man-made" chemicals. These "dioxins," as well as many of the other polychlorinated dibenzodioxins (PCDDs) and dibenzofuran (PCDFs) derivatives, are chlorinated aromatic compounds which are chemically stable, insoluble in water, and highly soluble in fats and oils. TCDD acts as a complete carcinogen in several species, causing both common and uncommon tumors at multiple sites. It is a highly potent chemical carcinogen in chronic animal studies, producing carcinogenic effects in laboratory animals with doses as low as 0.001 micrograms/kg/day. In rats, TCDD induces neoplasms in the lung, oral/nasal cavities, thyroid and adrenal glands, and liver. In mice, TCDD induces neoplasms in the liver and subcutaneous tissue, thyroid gland, and thymic lymphomas. In hamsters, it induces squamous cell carcinomas of the facial skin. Tumors of the integumentary system are reported after oral (mice and rats), intraperitoneal (hamsters), and dermal (mice) administration. A mixture of HCDDS (defined as the mixture of the 1,2,3,6,7,8- and 1,2,3,7,8,9 isomers used in the NTP experiments) are potent liver carcinogens in mice and rats. Pharmacokinetic studies in laboratory animals indicate that 50-90% of dietary TCDD is absorbed. It concentrates in adipose tissue and the liver. In mammals, the TCDD present in the liver is slowly redistributed and stored in fatty tissue. Elimination of TCDD occurs via excretion of metabolites in the bile and urine and passively through the gut wall. Metabolism is slow: the biological half-life of TCDD varies from weeks (rodents) to years (humans), and is strongly dependent upon the rate of TCDD metabolism. Many of the toxic effects of TCDD, including teratogenicity, may arise by receptor-mediated mechanisms. The induction of cytochrome P-448 and related enzymes by TCDD occurs by such a mechanism, and is related to the binding of TCDD to the Ah receptor. The specific mechanism(s) by which TCDD exerts its carcinogenic effects is unclear: receptor-binding may be part of the story. The role of the Ah receptor has been indicated in a skin promotion assay. The evidence for mutagenicity is inconclusive. TCDD did not induce lethal mutations, chromosomal aberrations, micronuclei or sister chromatid exchanges in rodents treated in vivo, nor was it mutagenic to bacteria, but it did enhance transformation of mouse C3H 10T1/2 cells by N-methyl-N'-nitro-N-nitrosoguanidine and was mutagenic to mouse lymphoma cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Reductive dechlorination of 3-chlorobenzoate is coupled to ATP production and growth in an anaerobic bacterium, strain DCB-1.

Thermodynamic data that the reductive dechlorination of 3-chlorobenzoate is exergonic have led to the hypothesis that this reaction yields biologically useful energy. This hypothesis was tested with strain DCB-1, a dehalogenating bacterium. The organism was grown under strictly anaerobic conditions in vitamin-amended mineral medium with formate plus acetate as electron donor and 3-chlorobenzoate as electron acceptor. The cell yield increased stoichiometrically to the amount of 3-chlorobenzoate dechlorinated. No growth was observed in the absence of 3-chlorobenzoate, or when 3-chlorobenzoate was replaced by benzoate. To obtain further evidence on that energy is derived from dechlorination, 3-chlorobenzoate was added to starved cells. This amendment resulted in an increase in the ATP level of the cells at 10 nmol per mg protein versus 3 nmol per mg protein in non-amended controls. These data indicate that the reductive dehalogenation of chlorinated aromatic compounds can be coupled to a novel type of chemotrophy.

Adenosine Triphosphate↗
PubMed1990

Influence of environmental factors on 2,4-dichlorophenoxyacetic acid degradation by Pseudomonas cepacia isolated from peat.

A Pseudomonas cepacia, designated strain BRI6001, was isolated from peat by enrichment culture using 2,4-dichlorophenoxyacetic acid (2,4-D) as the sole carbon source. BRI6001 grew at up to 13 mM 2,4-D, and degraded 1 mM 2,4-D at an average starting population density as low as 1.5 cells/ml. Degradation was optimal at acidic pH, but could also be inhibited at low pH, associated with chloride release from the substrate, and the limited buffering capacity of the growth medium. The only metabolite detected during growth on 2,4-D was 2,4-dichlorophenol (2,4-DCP), and degradation of the aromatic nucleus was by intradiol cleavage. Growth lag times prior to the on-set of degradation, and the total time required for degradation, were linearly related to the starting population density and the initial 2,4-D concentration. BRI6001, grown on 2,4-D, oxidized a variety of structurally similar chlorinated aromatic compounds accompanied by stoichiometric chloride release.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1978

[On the toxicology of carbromal. IV. Binding of carbromal and its hypnotically active metabolites to human plasma proteins (author's transl)].

The binding of carbromal and its metabolites bromoethylbutyramide and ethylbutyrylurea to human plasma proteins was investigated in vitro by use of Sephadex-gelfiltration, equilibrium dialysis and ultrafiltration. No differences appeared in the binding characteristics of human plasma and of human albumine. In a concentration range between 3.10-8 and 1.5.10-6 moles/ml about 40% of the carbromal, and in a concentration range between 3.10-8 and 1.10-5 moles/ml about 30% of the bromoethylbutyramide are bound to plasma proteins. Proteinbinding of ethylbutyrylurea was found to be less than 5%. The binding constants, Ka, to human albumine and the binding energies deltaF 0 were found to be in the range of 0.5--1.2.10(3) L/Mol and 1.7--4.4 kcal/Mol, respectively. Protein binding of carbromal, bromoethylbutyramide, their chlorinated analgous compounds, chloroethylbutyrylurea and chloroethylbutyramide, and of ethylbutyrylurea is strongly correlated to the partition coefficients of these compounds between n-octanol and water, indicating that the intensity of proteinbinding depends on the hydrophobic character of the substances tested.

Blood Proteins↗
PubMed1989

Evidence of free radical (FR) involvement in ischemic colitis.

Early ischemic colitis was induced in rats to evaluate the roles of FRs and intraluminal content. After 30 minutes of ischemia, biopsies for histology, conjugated dienes (CD) and malonaldehyde (M), presumptive marker of lipid peroxidation, were obtained at 0, 30, and 60 minutes reperfusion. Histology was unchanged. CD and M were elevated in ischemic and saline controls, and rose progressively during reperfusion; CD and M were essentially the same as non-ischemic controls during reperfusion with intraluminal corticosteroid (c) and Alcide (A). These agents may be beneficial in early ischemic colitis.

Adrenal Cortex Hormones↗
PubMed1975

Inhibition of enzymatic reduction of delta 14-double bond of 5 alpha-cholesta-8,14-dien-3 beta-ol and 5 alpha-cholesta-7,14-dien-3 beta-ol by AY-9944.

AY-994 (trans-1,4-bis-(2-chlorobenzyl-aminomethyl) cyclohexane dihydrochloride), a potent inhibitor of the enzymatic reduction of the delta 7-double bond of delta 5,7-sterols, has been shown to inhibit, at higher concentrations (10-4 M), the enzymatic reduction of the delta 14-double bond of cholesta-8,14-dien-3 beta-ol and cholesta-7,14-dien-3 beta-ol.

Animals↗
PubMed1999

Sanitation of wallboard colonized with Stachybotrys chartarum.

Sections (8 cm2) of unused, nonsterile gypsum wallboard (dry wall) were inoculated with varying densities (10(4) to approximately 10(8)/ml) of conidia from 14- to 21-day cultures of Stachybotrys chartarum grown on cellulose agar. The sections were permitted to air dry and were placed into vessels with 86% or 92% RH and incubated at 22-25 degrees C for up to 12 weeks. The moisture content of the dryboard increased from near 10% to over 35%. Selected sections with confluent surface growth, mainly of S. chartarum, were obtained within 3 weeks. Sections were cleaned with a quaternary or quaternary and chlorine dioxide or a concentrated oxygen-saline solution and treated, in some cases, with a preservative system and returned to humidity vessels. Reemergence of S. chartarum from inoculated and treated surfaces occurred within 5 weeks only with sections treated with the quaternary alone. Other fungi, mostly species of Aspergillus, Chaetomium and Penicillium, slowly colonized (between 9-12 weeks) at least some areas of most treated surfaces and most uninoculated control surfaces. Stachybotrys chartarum was also found on several sections of uninoculated controls. Sections treated with a quaternary/acrylic and placed in a dynamic challenging chamber remained visually free of colonized fungi for over 90 days. These studies indicate that control samples of uninstalled wallboard, available from local distributors, can contain a baseline bioburden, including S. chartarum, that will colonize surfaces under high humidity conditions. Sanitation and preservation treatment of the wallboard can markedly delay regrowth of these fungi, particularly of S. chartarum.

Chlorine Compounds↗