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PubMed2000

Pollution of water sources and removal of pollutants by advanced drinking-water treatment in China.

The pollution of water resources and drinking water sources in China is described in this paper with basic data. About 90% of surface waters and over 60% of drinking water sources in urban areas have been polluted to different extents. The main pollutants present in drinking water sources are organic substances, ammonia nitrogen, phenols, pesticides and pathogenic micro-organisms, some of which cannot be removed effectively by the traditional water treatment processes like coagulation, sedimentation, filtration and chlorination, and the product water usually does not meet Chinese national drinking water standards, when polluted source water is treated. In some drinking-water plants in China, advanced treatment processes including activated carbon filtration and adsorption, ozonation, biological activated carbon and membrane separation have been employed for further treatment of the filtrate from a traditional treatment system producing unqualified drinking water, to make final product water meet the WHO guidelines and some developed countries' standards, as well as the Chinese national standards for drinking water. Some case studies of advanced water treatment plants are described in this paper as well.

China↗
PubMed1993

Effects of phencyclidine and dizocilpine on NMDA-, kainate-, and water deprivation-induced drinking in pigeons.

The excitatory amino acid (EAA) agonists, N-methyl-D-aspartate (NMDA) and kainate, elicit a copious drinking response in pigeons. NMDA-induced drinking, as compared with kainate- and water deprivation-induced drinking, is selectively antagonized by the competitive, NMDA receptor antagonist CGS 19755, and appears to be mediated by NMDA receptors located in brain. There have been several studies which have reported differences between competitive and non-competitive (PCP-like) NMDA antagonists in blocking various behavioral effects of NMDA, such as discriminative stimulus effects. The present studies examined the effects of the non-competitive antagonists, phencyclidine (PCP) and dizocilpine, on drinking elicited by NMDA, kainate, and water deprivation. PCP and dizocilpine were effective antagonists of NMDA-induced drinking, resulting in surmountable shifts to the right in agonist dose-response functions. These compounds had little effect on drinking evoked by either kainate or water deprivation. These results support the notion that the dipsogenic effects of NMDA are mediated by NMDA-type receptors, and also provide important information as to the characteristics of non-competitive NMDA antagonists. EAA-induced drinking provides a useful tool for the examination of the behavioral pharmacology of EAA agonists and antagonists.

Journal Article↗
PubMed1999

NTP Toxicity Studies of Methyl Ethyl Ketoxime Administered in Drinking Water to F344/N Rats and B6C3F1 Mice (CAS No. 96-29-7).

Methyl ethyl ketoxime is used primarily as an antiskinning agent in alkyd coating resins. Methyl ethyl ketoxime was selected for study because of the potential for human exposure and because of interest in oximes as a chemical class. Toxicity studies of methyl ethyl ketoxime (greater than 99% pure) were carried out in male and female F344/N rats and B6C3F1 mice. The compound was administered in drinking water for 14 days or 13 weeks. In addition, the genetic toxicity of methyl ethyl ketoxime was evaluated by determining mutagenicity in Salmonella typhimurium and induction of sister chromatid exchanges and chromosomal aberrations in cultured Chinese hamster ovary cells in vitro, with and without S9 activation. The frequency of micronucleated normochromatic erythrocytes in the peripheral blood of mice from the 13-week study was also determined. In the 14-day studies, groups of five male and five female rats and mice were given drinking water containing 0, 106, 312, 625, 1,250, or 2,500 ppm methyl ethyl ketoxime. The mean body weight gain of male rats in the 2,500 ppm group was significantly less than that of the controls; the final mean body weight of male mice in the 2,500 ppm group was also less than that of the controls. Spleen weights were increased in male and female rats in the 1,250 and 2,500 ppm groups. No chemical-related gross lesions were observed. Microscopic tissue evaluations were not performed. In the 13-week studies, groups of 10 male and 10 female rats were given drinking water containing 0, 312, 625, 1,250, 2,500, or 5,000 ppm and groups of 10 male and 10 female mice were given drinking water containing 0, 625, 1,250, 2,500, 5,000, or 10,000 ppm. Mean body weights and body weight gains of 2,500 and 5,000 ppm male rats and 10,000 ppm male and female mice were less than those of the controls; mean body weight gains of male rats in the 1,250, 2,500 and 5,000 ppm groups and females in the 2,500 and 5,000 ppm groups were also less than those of the controls. Hematology results of this drinking water study indicate that methyl ethyl ketoxime induces a methemoglobinemia and a responsive Heinz body anemia. Liver and spleen weights were generally significantly greater than those of the controls in male and female rats exposed to 1,250 ppm or greater; spleen weights were also increased in male and female mice in the 10,000 ppm groups. Kidney weights were significantly greater in male rats in the 5,000 ppm group and in female rats exposed to 1,250 ppm or greater than those of the controls. Microscopically, there were exposure-related increases in the incidences and severities of hematopoietic cell proliferation in the spleen at exposure concentrations of 625 ppm or greater in male and female rats and at 5,000 and 10,000 ppm in male and female mice. A significant increase in the incidence of hematopoietic proliferation in the bone marrow was observed in rats exposed to 625 ppm or greater. Liver Kupffer cell erythrophagocytosis and hemosiderin pigmentation, as well as renal tubule hemosiderin pigmentation, occurred in exposed rats and mice. Other lesions observed include hyperplasia of the transitional epithelial lining of the urinary bladder in male and female mice exposed to 2,500 ppm or greater and degeneration of the nasal olfactory epithelium in male and female rats in the 2,500 and 5,000 ppm groups, male mice in the 5,000 and 10,000 ppm groups, and female mice exposed to 2,500 ppm or greater. Methyl ethyl ketoxime is extensively metabolized and does not accumulate in tissues. Single gavage doses of 2.7, 27, or 270 mg/kg administered to rats were primarily converted to carbon dioxide, mostly in the first 24 hours after dosing. After intravenous administration, less radioactivity on a percentage basis was excreted as carbon dioxide than in the gavage study, and more of the administered dose was excreted in urine and as volatiles. Following dermal administration, significantly greater amounts of volatiles were excreted than after gavage or intravenous administration. The 270 mg/kg gavage dose may result in saturation of a metabolic pathway(s). There is some evidence that the ketoxime is metabolized to the ketone and, presumably, hydroxylamine. Methyl ethyl ketoxime was mutagenic in Salmonella typhimurium strain TA1535 when tested in the presence of hamster liver S9 activation enzymes; results of mutagenicity testing were negative in strains TA97, TA98, and TA100, with and without exogenous metabolic activation. No induction of sister chromatid exhanges or chromosomal aberrations was observed in cultured Chinese hamster ovary cells treated with methyl ethyl ketoxime, with or without S9, and no increase in the frequency of micronucleated erythrocytes was noted in peripheral blood obtained from male and female mice administered methyl ethyl ketoxime in drinking water for 13 weeks. In summary, the major target of methyl ethyl ketoxime is the erythrocyte; the no-effect level for erythrotoxicity is 625 ppm in male rats and 312 ppm in female rats based on erythrocyte counts after 13 weeks of exposure. The no-effect level for hematopoietic toxicity is 312 ppm in rats based on erythroid cell hyperplasia in bone marrow and 2,500 ppm in mice based on hematopoietic cell proliferation in the spleen. Hematology results of this drinking water study indicate that methyl ethyl ketoxime induces a methemoglobinemia and a responsive Heinz body anemia. Methyl ethyl ketoxime was at most weakly genotoxic; it induced mutations in S. typhimurium under very specific conditions and increased the frequency of sister chromatid exchanges in cultured Chinese hamster ovary cells, but it did not induce sister chromatid exchanges or chromosomal aberrations in cultured Chinese hamster ovary cells in vitro or increase the frequency of micronucleated erythrocytes in mice treated in vivo.

Journal Article↗
PubMed2001

Toxicology and carcinogenesis studies of sodium nitrite (CAS NO. 7632-00-0) in F344/N rats and B6C3F1 mice (drinking water studies).

UNLABELLED: Sodium nitrite is used as a color fixative and preservative in meats and fish. It is also used in manufacturing diazo dyes, nitroso compounds, and other organic compounds; in dyeing and printing textile fabrics and bleaching fibers; in photography; as a laboratory reagent and a corrosion inhibitor; in metal coatings for phosphatizing and detinning; and in the manufacture of rubber chemicals. Sodium nitrite also has been used in human and veterinary medicine as a vasodilator, a bronchial dilator, an intestinal relaxant, and an antidote for cyanide poisoning. Sodium nitrite was nominated by the FDA for toxicity and carcinogenesis studies based on its widespread use in foods. Male and female F344/N rats and B6C3F1 mice were exposed to sodium nitrite (99% pure) in drinking water for 14 weeks or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, rat and mouse bone marrow, and mouse peripheral blood. 14-WEEK STUDY IN RATS: Groups of 10 male and 10 female rats were exposed to 0, 375, 750, 1500, 3,000, or 5000 ppm sodium nitrite (equivalent to average daily doses of approximately 30, 55, 115, 200, or 310 mg sodium nitrite/kg body weight to males and 40, 80, 130, 225, or 345 mg/kg to females) in drinking water for 14 weeks. Clinical pathology study groups of 15 male and 15 female rats were exposed to the same concentrations for 70 or 71 days. One female exposed to 3000 ppm died before the end of the study. Body weights of males exposed to 3000 or 5000 ppm and females exposed to 5000 ppm were significantly less than those of the controls. Water consumption by 5000 ppm males and 3000 and 5000 ppm females was less than that by the controls at weeks 2 and 14. Clinical findings related to sodium nitrite exposure included brown discoloration in the eyes and cyanosis of the mouth, tongue, ears, and feet of males exposed to 3000 or 5000 ppm and of females exposed to 1500 ppm or greater. Reticulocyte counts were increased in males and females exposed to 3000 or 5000 ppm. The erythron was decreased on day 19 but increased by week 14 in males and females exposed to 5000 ppm. Methemoglobin concentrations were elevated in almost all exposed groups throughout the 14 week study; a no-observed-adverse-effect level was not achieved. The relative kidney and spleen weights of males and females exposed to 3000 or 5000 ppm were significantly greater than those of the controls. Sperm motility in 1500 and 5000 ppm males was significantly decreased. Increased erythropoietic activity in the bone marrow of exposed males and females was observed. The incidences of squamous cell hyperplasia of the forestomach in 5000 ppm males and females were significantly increased. 14-WEEK STUDY IN MICE: Groups of 10 male and 10 female B6C3F1 mice were exposed to 0, 375, 750, 1500, 3000, or 5000 ppm sodium nitrite (equivalent to average daily doses of approximately 90, 190, 345, 750, or 990 mg/kg to males and 120, 240, 445, 840, or 1230 mg/kg to females) in drinking water for 14 weeks. Body weights of males exposed to 5000 ppm were significantly less than those of the controls. Water consumption by males exposed to 1500 ppm or greater was slightly less than that by the controls at week 13. Relative spleen weights of 3000 and 5000 ppm males and absolute and relative heart, kidney, liver, and spleen weights of females exposed to 3000 or 5000 ppm were greater than those of the control groups. Sperm motility was decreased in 5000 ppm males, and the estrous cycles of 1500 and 5000 ppm females were significantly longer than in the controls. There were increased incidences of squamous cell hyperplasia of the forestomach in 5000 ppm males and females, extramedullary hematopoiesis of the spleen in 3000 and 5000 ppm males and 1500 ppm or greater females, and degeneration of the testis in 3000 and 5000 ppm males. 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats were exposed to 0, 750, 1500, or 3000 ppm sodium nitrite (equivalent to average daily doses of approximately 35, 70, or 130 mg/kg to males and 40, 8d 40, 80, or 150 mg/kg to females) in drinking water for 2 years. For toxicokinetic studies of plasma nitrite and blood methemoglobin, 10 male and 10 female special study rats were exposed to the same concentrations for 12 months. Survival of exposed groups was similar to that of the controls. Mean body weights of males and females exposed to 3000 ppm were less than those of the controls throughout the study. Water consumption by males and females exposed to 3000 ppm was less than that by the controls throughout the study, and that by the other exposed groups was generally less after week 14. The incidences of hyperplasia of the forestomach epithelium in males and females exposed to 3000 ppm were significantly greater than those in the control groups. The incidence of fibroadenoma of the mam mary gland was significantly increased in females exposed to 1500 ppm, and the incidences of multiple fibroadenoma were increased in 750 ppm and 1500 ppm females; however, these neoplasms occur with a high background incidence, and no increase was seen in the 3000 ppm group. The incidences of mononuclear cell leukemia were significantly decreased in males and females exposed to 1500 or 3000 ppm. 2-YEAR STUDY IN MICE: Groups of 50 male and 50 female B6C3F1 mice were exposed to 0, 750, 1500, or 3000 ppm sodium nitrite (equivalent to average daily doses of approximately 60, 120, or 220 mg/kg to males and 45, 90, or 165 mg/kg to females) in drinking water for 2 years. Survival of exposed groups was similar to that of the controls; mean body weights of 3000 ppm females were less than those of the controls throughout the study. Exposed groups generally consumed less water than the control groups. The incidences of squamous cell papilloma or carcinoma (combined) in the forestomach of female mice occurred with a positive trend. The incidence of hyperplasia of the glandular stomach epithelium was significantly greater in 3000 ppm males than in the controls. GENETIC TOXICOLOGY: Sodium nitrite was mutagenic in Salmonella typhimurium strain TA100, with and without Aroclor 1254-induced hamster and rat liver S9 enzymes; no mutagenicity was observed in strain TA98. Results of acute bone marrow micronucleus tests with sodium nitrite in male rats and mice by intraperitoneal injection were negative. In addition, a peripheral blood micronucleus assay conducted with mice from the 14-week study gave negative results. CONCLUSIONS: Under the conditions of this 2-year drinking water study, there was no evidence of carcinogenic activity of sodium nitrite in male or female F344/N rats exposed to 750, 1500, or 3000 ppm. There was no evidence of carcinogenic activity of sodium nitrite in male B6C3F1 mice exposed to 750, 1500, or 3000 ppm. There was equivocal evidence of carcinogenic activity of sodium nitrite in female B6C3F1 mice based on the positive trend in the incidences of squamous cell papilloma or carcinoma (combined) of the forestomach. Exposure to sodium nitrite in drinking water resulted in increased incidences of epithelial hyperplasia in the forestomach of male and female rats and in the glandular stomach of male mice. Decreased incidences of mononuclear cell leukemia occurred in male and female rats.

Analysis of Variance↗
PubMed1995

NTP Toxicology and Carcinogenesis Studies of t -Butyl Alcohol (CAS No. 75-65-0) in F344/N Rats and B6C3F1 Mice (Drinking Water Studies).

t -Butyl alcohol is widely used in the manufacture of perfumes and a variety of cosmetics. It is also used as a raw material in the production of isobutylene, which may be used to produce methyl tertiary butyl ether, a common gasoline additive, or to produce butyl elastomers used in the production of automobile tires. Male and female F344/N rats and B6C3F1 mice were given t -butyl alcohol (greater than 99% pure) in drinking water for 13 weeks or 2 years. The genetic toxicity of t -butyl alcohol was assessed by testing the ability of the chemical to induce mutations in various strains of Salmonella typhimurium and in L5178Y mouse lymphoma cells, sister chromatid exchanges and chromosomal aberrations in cultured Chinese hamster ovary cells, and by measuring the frequency of micronucleated erythrocytes in mouse peripheral blood. 13-WEEK STUDY IN RATS: Groups of 10 male and 10 female F344/N rats were given 0, 2.5, 5, 10, 20, or 40 mg/mL t -butyl alcohol in drinking water for 13 weeks. All males and six females given 40 mg/mL died during the study. Final mean body weights of 10 and 20 mg/mL males and of 40 mg/mL females were 12%, 17%, or 21% less than those of the corresponding controls, respectively. Serum sorbitol dehydrogenase activities in 10 and 20 mg/mL males were greater than that in the controls after 13 weeks. Serum alanine aminotransferase activity in 40 mg/mL females was greater than that in the controls after 2 weeks and greater in all exposed females after 13 weeks. Urine volumes of 10, 20, and 40 mg/mL males and females decreased, and urine specific gravity values increased. Transitional epithelial hyperplasia and inflammation of the urinary bladder were observed in 20 and 40 mg/mL males and 40 mg/mL females. Absolute and relative liver weights of all exposed groups of females and relative liver weights of 5, 10, and 20 mg/mL males were significantly greater than those of the controls. Absolute and relative kidney weights of all exposed groups of males and females were significantly greater than those of the controls. Incidences of mineralization of the kidney were significantly increased in 10, 20, and 40 mg/mL males. The severity of nephropathy in 2.5, 5, 10, and 20 mg/mL males was significantly greater than that of the controls as was the accumulation of hyaline droplets in the kidney of 5, 10, and 20 mg/mL males. The incidences of nephropathy in 10, 20, and 40 mg/mL females were significantly greater than that of the controls. 13-WEEK STUDY IN MICE: Groups of 10 male and 10 female B6C3F1 mice were given 0, 2.5, 5, 10, 20, or 40 mg/mL t -butyl alcohol in drinking water for 13 weeks. The deaths of two males and one female in the 40 mg/mL group were attributed to exposure to t -butyl alcohol. The final mean body weights of 20 and 40 mg/mL males and 40 mg/mL females were significantly lower than those of the controls. There were no biologically significant differences in hematology parameters of exposed and control groups of mice. Transitional epithelial hyperplasia and inflammation were observed in the urinary bladder of 20 and 40 mg/mL males and 40 mg/mL females. 2-YEAR STUDY IN RATS: Groups of 60 F344/N rats were given 0, 1.25, 2.5, or 5 mg/mL t -butyl alcohol (males) or 0, 2.5, 5, or 10 mg/mL t -butyl alcohol (females) in drinking water for 2 years. These correspond to average daily doses of approximately 90, 200, or 420 mg t -butyl alcohol/kg body weight for males and approximately 180, 330, or 650 mg t -butyl alcohol/kg body weight for females. Ten rats per group were evaluated after 15 months of chemical administration. Survival, Body Weights, and Water Consumption: Survival rates of 5 mg/mL males and 10 mg/mL females were significantly lower than those of the controls. The final mean body weights of exposed groups of males were 15% to 24% lower than that of the controls, and the final mean body weight of 10 mg/mL females was 21% lower than that of the controls. Water consumption by males increased with dose; water consumption by females decreased with dose. Hematology and Urinalysis: At the 15-month inte. Hematology and Urinalysis: At the 15-month interim evaluation, there were no significant differences in hematology parameters in males and females, and there were no significant differences in urinalysis parameters in males. Females given 5 or 10 mg/mL had increased urine specific gravities and decreased urine volumes. Pathology Findings: At the 15-month interim evaluation, relative kidney weights of 2.5 and 5 mg/mL males and absolute and relative kidney weights of 2.5, 5, and 10 mg/mL females were significantly greater than those of the controls. At 2 years, the incidence of mineralization in the kidney increased with dose and that of 5 mg/mL males was significantly greater than that of the controls. In the standard evaluation at the end of the study, the incidences of focal renal tubule hyperplasia and of adenoma were increased in exposed males and a carcinoma was observed in one 5 mg/mL male. Renal tubule hyperplasia occurred in one 10 mg/mL female. An extended evaluation of the kidney identified additional male rats with hyperplasia (control, 11/50; 1.25 mg/mL, 13/50; 2.5 mg/mL, 11/50; 5 mg/mL, 19/50) and renal tubule adenoma (7/50, 8/50, 15/50, 10/50); renal tubule carcinomas were identified in two 1.25 mg/mL males and in one 2.5 mg/mL male. Renal tubule adenoma was identified in one 5 mg/mL male from the 15-month extended evaluation. In the standard and extended evaluations combined, there were dose-related increased incidences of hyperplasia and adenoma. The severity of nephropathy and the incidence and severity of transitional cell hyperplasia of the kidney were increased in exposed male and female rats. Linear foci of mineralization were present in the renal papilla of exposed males. 2-YEAR STUDY IN MICE: Groups of 60 male and 60 female B6C3F1 mice were given 0, 5, 10, or 20 mg/mL t -butyl alcohol in drinking water for 2 years. Exposure levels of 5, 10, or 20 mg/mL delivered average daily doses of approximately 540, 1,040, or 2,070 mg t -butyl alcohol/kg body weight to males and approximately 510, 1,020, or 2,110 mg/kg to females. Survival, Body Weights, and Water Consumption: Survival of 20 mg/mL males was significantly lower than that of the controls. The final mean body weights of exposed groups of males were similar to those of the controls. The mean body weights of females given 20 mg/mL were 10% to 15% lower than those of the controls from week 13 to the end of the study. Water consumption by exposed groups of males and females was similar to that by the controls. Pathology Findings: Incidences of thyroid gland follicular cell hyperplasia were significantly increased in all exposed groups of males and in 10 and 20 mg/mL females. The incidence of follicular cell adenoma or carcinoma (combined) was marginally increased in 10 mg/mL males (0 mg/mL, 1/60; 5 mg/mL, 0/59; 10 mg/mL, 4/59; 20 mg/mL, 2/57). The incidence of follicular cell adenoma was significantly increased in 20 mg/mL females (2/58, 3/60, 2/59, 9/59). The incidences of chronic inflammation and transitional epithelial hyperplasia of the urinary bladder were increased in 20 mg/mL males and to a lesser extent in 20 mg/mL females. GENETIC TOXICOLOGY: t -Butyl alcohol was tested for induction of genetic damage in vitro and in vivo, and all results were negative. In vitro, t -butyl alcohol was negative in Salmonella typhimurium and mouse lymphoma cell mutation tests, and it did not induce sister chromatid exchanges or chromosomal aberrations in cultured Chinese hamster ovary cells. These in vitro studies were conducted with and without metabolic activation (S9). In vivo, no increase in micronucleated erythrocytes was observed in peripheral blood samples from mice administered t -butyl alcohol in drinking water for 13 weeks. CONCLUSIONS: Under the conditions of these 2-year drinking water studies, there was some evidence of carcinogenic activity of t -butyl alcohol in male F344/N rats based on increased incidences of renal tubule adenoma or carcinoma (combined). There was no evidence of carcinogenic activity in female F344/N rats receiving 2.5, 5, or 10 mg/mL t -butyl alcohol. There was equivocal evidence of carcinogenic activity of t -butyl alcohol in male B6C3F1 mice based on the marginally increased incidences of follicular cell adenoma or carcinoma (combined) of the thyroid gland. There was some evidence of carcinogenic activity of t -butyl alcohol in female B6C3F1 mice based on increased incidences of follicular cell adenoma of the thyroid gland. Exposure to t -butyl alcohol was associated with mineralization and renal tubule hyperplasia in male rats, transitional epithelial hyperplasia and increased severity of nephropathy of the kidney in male and female rats, follicular cell hyperplasia of the thyroid gland in male and female mice, and chronic inflammation and hyperplasia of the urinary bladder in male mice and to a lesser extent in female mice. Synonyms: 2-Methyl-2-propanol, 2-methylpropan-2-ol, TBA, t -butanol, tertiary butyl alcohol, t -butyl hydroxide, trimethyl carbinol, trimethyl methanol

Journal Article↗
PubMed2003

Phosphorus limitation on bacterial regrowth in drinking water.

Assimilable organic carbon (AOC) test and bacterial regrowth potential (BRP) analysis were used to investigate the effect of phosphorus on bacterial regrowth in the drinking water that was made from some raw water taken from a reservoir located in northern China. It was shown that AOC of the drinking water samples increased by 43.9%-59.6% and BRP increased by 100%-235% when 50 microg/L PO4(3-)-P(as NaH2 PO4) was added alone to the drinking water samples. This result was clear evidence of phosphorus limitation on bacteria regrowth in the drinking water. This investigation indicated the importance of phosphorus in ensuring biological stability of drinking water and offered a novel possible option to restrict microbial regrowth in drinking water distribution system by applying appropriate technologies to remove phosphorus efficiently from drinking water in China.

Bacteria↗
PubMed2004

[Study on the application of benchmark dose and biological monitoring indexes of fluorides in drinking water].

OBJECTIVE: By using Benchmark Dose (BMD) approach to explore the relations among drinking water fluoride, urine fluoride, serum fluoride and dental fluorosis; and to evaluate the significance of urine fluoride and serum fluoride in control and prevention of endemic fluorosis. METHODS: 512 children (290 in Xinhuai Village, 222 in Wamiao Village) aged 8-13 years were recruited in the study. Epidemiological methods were used to investigate the prevalence of dental fluorosis, and the levels of urine fluoride, serum fluoride, and drinking water fluoride in superficial well. The children were divided into six subgroups by the concentration of fluoride in drinking water: < 0.5 mg/L, 0.5-mg/L, 1.0-mg/L, 2.0-mg/L, 3.0-mg/L and > or = 4.0 mg/L. RESULTS: There was significant dose-response relationship between the drinking water fluoride and the prevalence of dental fluorosis or the prevalence of defect dental fluorosis. The BMDLs (Benchmark Dose Lower Bound) were 1.01 and 1.30 mg/L, respectively. Urine fluoride and serum fluoride also had significant dose-response relationship to the prevalence of dental fluorosis or defect dental fluorosis. The correlation coefficient between drinking water fluoride and urine fluoride was 0.717, and it was 0.855 between drinking water fluoride and serum fluoride, and 0.617 between urine fluoride and serum fluoride. CONCLUSIONS: The currently national standard of fluoride in drinking water in China is safe and reasonable. As a biological monitoring index, the levels of fluoride in serum may be more useful than that in urine in the control and prevention of endemic fluorosis.

Adolescent↗
PubMed2005

An assessment of drinking-water supplies on the Hanford site: an evaluation conducted at a federal nuclear facility in southeastern Washington state.

Drinking water is supplied to most U.S. Department of Energy (DOE) facilities on the Hanford Site by DOE-owned, contractor-operated pumping and distribution systems. Water is primarily obtained from the Columbia River, but some facilities use water from on-site groundwater wells. Because of the large amount of radioactive and chemical waste produced, stored, and disposed of at Hanford, some people are concerned that waste materials are contaminating on-site drinking-water supplies. This paper describes the drinking-water facilities and treatment requirements on the Hanford Site and summarizes radiological and non-radiological water quality data obtained from water samples collected from each drinking-water system in use during 2001 and 2002. Monitoring data show that Hanford-produced radionuclides are measurable in some drinking-water samples. The only non-radiological contaminants detected either were by-products of the chlorination process or came from off-site agricultural activities. Contaminant level values were, in all cases, below state and federal drinking-water limits. This information will provide assurance to current employees and future site developers that drinking water on the Hanford Site is safe for public consumption.

Agriculture↗
PubMed2005

Supplementary effect of carbohydrate-electrolyte drink on sports performance, lactate removal & cardiovascular response of athletes.

BACKGROUND AND OBJECTIVE: Carbohydrate-electrolyte drink has a significant role on energy balance during exercise. The present study was designed to investigate the effect of oral carbohydrate-electrolyte supplementation on sports performance and cardiovascular status of the national level male athletes during exercise and recovery. METHODS: A total of 10 male athletes (age range: 20-25 yr) were selected. The experiment was performed in laboratory (25 degrees C and 60% relative humidity) in two phases; phase 1 - no supplementation, and phase 2 - a 5 g per cent carbohydrate-electrolyte drink was given orally during exercise and a 12.5 g per cent carbohydrate-electrolyte drink during recovery. Subjects performed an exercise test at 70 per cent of VO(2)max. Performance time, heart rate during exercise and recovery were noted, blood samples were collected during exercise and recovery for the analysis of glucose and lactate levels in both the phases. RESULTS: Significant improvements were noted in total endurance time, heart rate responses and blood lactate during exercise at 70 per cent VO(2)max after the supplementation of 5 g per cent carbohydrate-electrolyte drink. However, no significant changes were noted in blood glucose and peak lactate level irrespective of supplementation of carbohydrate-electrolyte drink. Significant improvement in cardiovascular responses, blood glucose and lactate removal were noted during recovery following a 12.5 g per cent carbohydrate-electrolyte drink. INTERPRETATION AND CONCLUSION: Carbohydrate-electrolyte drink can increase endurance performance as well as enhance lactate removal and thereby delaying the onset of fatigue.

Analysis of Variance↗
PubMed2006

Drinking water and health research: a look to the future in the United States and globally.

Drinking water supplies continue to be a major source of human disease and death globally because many of them remain unsafe and vulnerable. Greater efforts are needed to address the key issues and questions which influence the provision of safe drinking water. Efforts are needed to re-evaluate and set new and better priorities for drinking water research and practice. More stakeholders need to be included in the processes of identifying key issues and setting priorities for safe drinking water. The overall approach to drinking water research and the provision of safe drinking water needs to become more rational and scientific, and become more visionary and anticipatory of the ever-present and emerging risks to drinking water safety. Collectively, we need to do a better job of making safe water available, accessible and affordable for all. One such approach to safe water for all is household water treatment and safe storage, which is being promoted globally by the World Health Organization and many other stakeholders and partners to reduce the global burden of waterborne disease.

Global Health↗
PubMed2005

[Viability of a native isolate of Lactobacillus brevis in a fermented milky drink].

The objective of this research was to test the viability of a native isolate of Lactobacillus brevis in two fermented milky drinks: a drink without prebiotic ingredient and another drink with oat flour (0.5%, p/v) as prebiotic ingredient. The viability of L. brevis was tested at 7, 14, and 21 after inoculation. Drink pH and lactic acid concentration was measured as a function of time (2, 7, 14, and 21 days after inoculation). The isolate was viable in both drinks because its counting plates was higher than 10(6) CFU/mL until day 21st. Between the 7th and 14th day, the rate of growth was higher in the drink that included oat flour, however, at the day 21st the colony density was similar in both drinks.

Animals↗
PubMed1991

Drinks and dental health.

The average daily requirement for water in man is 2-3 litres, of which more than half comes from drinks. Although the total consumption of various drinks is quite stable, the choices of beverages are slowly changing. In many Western countries e.g. the use of milk is declining while consumers drink greater amounts of soft drinks, including fruit juices and carbonated beverages. These changes may also affect dental health because of the potential risk of sugar and acid-containing drinks to cause dental caries and erosion. The effects of drinks in the human mouth are, however, strongly related to many individual factors and prediction of dental effects is therefore difficult. Anyway, there are risk patients who should be recognized, and risk products which should be noticed in product formulation. If attention is paid to such factors in the future harmful effects of drinks on teeth may be minimized.

Beverages↗
PubMed1990

[Criticism and recommendations for improvements of the drinking water regulation and of the European Community guideline 80/778/EWG].

The prevention of possible outbreaks as they occurred hundred years ago is still the object of the control of drinking water by the EC-guideline and the Drinking Water Regulations, respectively. At that time, the principle of faecal indicator bacteria was developed and it proved very useful. Now, however, drinking water is no longer supplied by wells but by plants. In comparison with the situation during the last century the relative risks of infectious diseases by faecal organisms are now drastically lower. An intelligent strategy of prevention of drinking water epidemics has to take into consideration that enteropathogens have become too rare so that it is hardly possible to detect them by the frequently occurring faecal markers E. coli and total coliforms. The alternative is the control of the "good manufacturing practices" (GMP) during the processing of drinking water. The colony counts seem to be better markers than the coliforms. Today, more than 90 per cent of infections by drinking water are due to legionellas and ubiquitous mycobacteria occurring in warm water. Therefore, warm water has to be included in the normal control. Furthermore, legionellae and ubiquitous mycobacteria should be tested regularly. Against that, the investigation of total coliforms and/or faecal streptococci seems superfluous. Finally, the future safety of drinking water demands the investigation of at least two additional chemical contaminants, i.e. asbestos and radon, whereas the cyanide test does not appear necessary.

Colony Count, Microbial↗
PubMed1990

The effects of actinidia sinensis planch (kiwi) drink supplementation on athletes training in hot environments.

On the basis of studying the problems and experimental data of athletes training in hot environments, we designed an athletic drink choosing actinidia sinensis planch (ASP), also known as kiwi fruit, as the basic component, and assessed its effects in athletes both at site of training and in the laboratory. The main results were as follows: (1) In athletes riding on a Monark ergometer (maintaining HR at 150 beat/min), the work time to exhaustion was longer (149 +/- 3 min vs 120 +/- 1 min), and the work load was larger (947 +/- 36 KJ vs 833 +/- 28 KJ) when supplementing the ASP drik than when they drank the placebo, P less than 0.01) (2) Supplements with the ASP drink expanded the blood volume of athletes. Hematocrit increased significantly after exercise in athletes consuming placebo, but no significant changes were found in those consuming the ASP drink. (3) The ASP drink which contained 5% carbohydrate maintained the blood glucose concentration of athletes at a normal level even when training lasted more than 2.5 hours and without noticeable effect on plasma insulin levels. (4) Supplement of small amount of multi-minerals in the ASP drink helped to decrease the mineral level changes in serum and sweat after intensive training, but it did not cause kaliemia or affect urinary output. (5) Data on urinary vitamin C content indicated that the vitamin C status of athletes supplementing the ASP drink improved. The ASP drink is not only effective but also fragrant, tasty, refreshing and thirst quenching, and it appears to have no side effects.

Adolescent↗
PubMed1995

Drink composition and the electrolyte balance of children exercising in the heat.

Twelve 9- to 12-year-old children (6 boys, 6 girls) performed four exercise-in-heat (35 degrees C, 45% RH) trials which differed in the composition of the fluids they drank. In each trial, subjects cycled for one 20-min and two 15-min bouts at 50% peak VO2 with 10-min rest periods in between. In a fourth bout, they cycled at 90% peak VO2 until exhaustion. Drinks had the same grape flavor and were assigned in a double-blind design and in a Latin-square order. Subjects drank 7 ml.kg-1.h-1 to keep them euhydrated. Three of the drinks had 6% carbohydrates (CHO), with different [Na+]: 0, 8.8, 18.5 mmol.l-1 and one drink had neither CHO nor Na+ (WATER). Among drink trials, there were no differences in the increase in rectal temperature, HR, or performance time to exhaustion. Despite the larger Na+ deficit induced by the Na(+)-free drinks compared with the Na+ drinks (11.8 +/- 1.4 vs 5.7 +/- 0.9 mmol.h-1), neither plasma [Na+] nor osmolality were affected. These results suggest that electrolyte, as in the above conditions, did not affect electrolyte balance, thermoregulatory responses, or aerobic performance of children exercising in the heat. The greater Na+ deficit induced by ion-free drinks was of minor biological importance.

Blood Glucose↗
PubMed1995

Mutagenicity of stable dust and drinking water on swine and cattle farms.

Single pilot examinations of mutagenicity of stable dust and drinking water were made on three swine farms (D., M., T.) and one cattle farm (N.) in the district of Hodonín in summer 1994. The mutagenicity was examined by the Ames test using the indicator strains Salmonella typhimurium TA 98 and TA 100 with (+S9) or without (-S9) metabolic activation. At the same time the contents of selected pesticides (PES) and polychlorinated biphenyls (PCB) in stable dust and drinking water and that of polycyclic aromatic hydrocarbons in stable dust were determined. Increased mutagenicity was demonstrated in drinking water (strain TA 98 with metabolic activation; index Rt/Rk 3.6-7.7) and stable dust (strain TA 100 with metabolic activation; index Rt/Rk 2.2) collected on the swine farm M. High contents of PAH (8.246 mg/kg) and PCB (0.263 mg/kg) were also found in the dust samples collected on this farm. Only drinking water showed mutagenic activity (strain TA 98 without metabolic activation; index Rt/Rk 2.6) on the swine farm D. On both the farms, the number of revertants was dose-dependent. Increased content of PAH (2.553 mg/kg) was also demonstrated on the dust samples collected on the farm D. No significant increase (twofold or higher when compared with negative controls) of mutagenic activity of stable dust or drinking water was demonstrable on the swine farm T. and the cattle farm N. Substances responsible for the mutagenicity of drinking water on the farms D. and M. have not yet been identified. Anyway, the increase of mutagenicity of stable dust and drinking water should be taken as a warning that mutagens that can jeopardise animal and human health have penetrated into the stable environment.

Animals↗
PubMed1996

Perceived workplace harassment experiences and problem drinking among physicians: broadening the stress/alienation paradigm.

Sociologists who embrace the stress or alienation paradigms generally focus on explaining problem drinking in low status occupations. By contrast, this paper argues that a broadened conceptualization of stress and alienation which incorporates abusive work relationships has utility for explaining male and female drinking outcomes in both high and low status occupations. We provide empirical data on the relationship between perceived abusive experiences and drinking outcomes in a cohort of male and female physicians in their internship year of training. The data show that perceived sexual harassment, discriminatory treatment and psychological humiliation relate to various drinking outcomes in men and women, controlling for drinking prior to the internship year. While females were more likely to report experiencing abuse, these perceived experiences had deleterious effects on drinking outcomes for both genders. Personal vulnerability (narcissism) brought into the training environment somewhat influenced the later reporting of abusive experiences by males but not by females. Regression analyses showed that, for both males and females, work-place abusive experiences in interaction with personality vulnerability best explained drinking outcomes. The implications of these results for the design of future alcohol-related work-place studies are discussed.

Adult↗
PubMed2000

Kappa-opioid receptors and relapse-like drinking in long-term ethanol-experienced rats.

RATIONALE: The role of the dynorphin/kappa-opioid receptor system in ethanol reinforcement is unclear. OBJECTIVE: Examination of the effects of the highly selective kappa-opioid receptor agonist CI-977 (enadoline) and of the long-acting selective kappa-opioid receptor antagonist nor-binaltorphimine (nor-BNI) on relapse-like drinking measured by the alcohol deprivation effect (ADE) in long-term ethanol-experienced rats. METHODS: Rats were either implanted with mini-osmotic pumps delivering 0 or 0.01 mg/kg per h CI-977 or received two injections (12 h apart) of nor-BNI (0 or 5 mg/kg i.p.) before representation of alcohol after 2 weeks of alcohol deprivation in a four-bottle home cage drinking paradigm. In a second experiment, long-term ethanol-experienced rats trained in an operant ethanol self-administration paradigm received either acute CI-977 treatment (0, 0.003-0.1 mg/kg i.p.) or two injections (12 h apart) of nor-BNI (0 or 5 mg/kg i.p.) before a 23-h session. RESULTS: Chronic CI-977 potentiated ethanol intake and preference during the ADE. Acute CI-977 dose-dependently reduced total lever pressing activity demonstrating an unspecific sedative effect, except for the lowest dose (0.003 mg/kg), which selectively increased lever pressing for ethanol during basal drinking. Nor-BNI did not affect relapse-like drinking at all. CONCLUSIONS: Stimulation of kappa-opioid receptors can increase ethanol intake, at least in long-term ethanol-experienced rats. Since kappa-opioid receptor agonists have aversive motivational consequences, increased ethanol drinking might be an attempt to counteract the aversive effects of this treatment. On the other hand, the nor-BNI experiments indicate that endogenous kappa-opioid receptor stimulation does not seem to be involved in relapse-like drinking after protracted abstinence.

Alcohol Drinking↗