Ntk Ntk

Influenza Probable Primary Spread Triggered By The Abiotic Vehicle Drinking Water

Background

a) Droplet infection, temperature and humidity: The triggering of human influenza epidemics by biotic droplet infection is unproven1. Lowen et al. have demonstrated that influenza virus transmission in a guinea pig model is most effective under cold and dry conditions2, 3. A fresh study from Oregon, USA has described a correlation between humidity and influenza virus survival and transmission. When absolute humidity is low - as in the peak influenza months of January and February - the virus appears to survive longer and transmission rates increase4, {5}.

b) Cluster: Influenza epidemics in Germany rarely occur together in recognizable clusters, e. g., in only 15% of the cases throughout the 2006/2007 season6.

c) Influenza subtypes: The herpes virus subtypes and strains involved in influenza epidemics are locally isolated. This is one indicator for why an easy homogeneous airborne -oevirus cloud-? for the initial spread of influenza is unlikely.

d) Geographical allocation: The emergence of influenza epidemics shows a certain and unexpected geographical pattern. They have maybe not been shown to arise mainly in large cities and densely populated areas. They appear predominantly in the colder parts of Germany, e. g., in the east in the winter using its cold continental climate, in the southeast, and at higher altitudes. They appear with maximum regularity in certain districts/cities.

e) Seasonal Influenza: An evident correlation may be observed between your parallel trends of influenza epidemics and the length of winter cooling. The influenza season starts and stops at a soil and water temperature of 7? C. Influenza incidence correlates to a much greater extent with soil and water than air temperature. Air temperature can be an random indicator for frost and thaw. Soil and water temperatures are long-term indicators for the course of cold weather cooling. Frost inhibits the input of secreted influenza viruses in water. Frost inhibited the start of the influenza season in Germany in 2006. The differences in the extent of influenza epidemics generally can be explained by the increased usage of analytical and rapid diagnostic tests, specifically since 2007, as a result of H5N1 avian influenza in Europe in the cold weather of 2006. In 2006 a 7-week frost inhibited the start of the influenza season until mid-February. Also, the seasonal virus secreted from infected animals may play a significant role in the differing extent of influenza epidemics. Within the next several years the epidemiological database will be more comprehensive because of further increases in the usage of rapid diagnostic tests. Each year in colder Saxony, with 74% of its normal water originating from surface water, the influenza season is significantly more severe than in Germany as a whole, where only 33% of the drinking water arises from surface water. Each year, as in week 11, 2007, the influenza peak in Saxony follows the thaw. Overall in Germany, there is no marked frost in 2007. The soil curves for Germany and Saxony are very similar, significantly more so compared to the air curves. For this reason we have included the soil curve for Saxony.

f) Influenza transmission: The transmission routes for the common cold and influenza remain debatable. The commonly held belief is that colds are spread by particles of infected mucous generated by coughs and sneezes. Immunohistological studies have shown that foci of virus-producing cells are clustered in the mucous layer of the respiratory system. Infected persons can shed countless virus particles within their mucus. However, there is increasing evidence that infection also occurs via contaminated surfaces as well as other abiotic vehicles. This may occur when surfaces such as handkerchiefs and tissues, water taps, door handles or telephones become contaminated by droplets shed from the nose of infected individuals. Herpes is offered to a different person if they touch a contaminated surface. Water can be an abiotic vehicle. It is not known which transmission routes would be the most important9. From a biological point of view, influenza infection is unlikely to be spread through saliva droplets, since saliva contains far fewer influenza virus particles than the substantially heavier droplets of mucus from the throat and nasal membranes10, 11. Coughs and sneezes tend to spray saliva from the pool at the front of the mouth instead of droplets of mucus from the throat and nose. Saliva contains little or no cold virus and so aerosolized saliva is unlikely to spread infection. Colds are not caught by kissing, as cold viruses do not infect the mouth and saliva contains very little virus. When volunteers infected with the common cold kissed cold-free volunteers for up to 1. {5 minutes}, only 1 case of cross-infection occurred in 16 trials12. Infected birds secrete the influenza virus through their saliva, nasal secretions and feces. Avian influenza viruses have been isolated from unconcentrated lake water, which indicates that waterfowl employ a efficient method of transmitting viruses, i. e. via fecal matter in the water supply13. Avian influenza viruses in wild aquatic birds are spread by fecal-oral transmission through the water supply14. Initial transmission of avian influenza viruses to mammals, including pigs and horses, probably also occurs by fecal contamination of water13. Shedding of the influenza virus into water results in transmission between waterfowl, and is a major threat for epidemics in poultry and pandemics in humans15. Just one human infectious dose of seasonal influenza virus might be between 100 and 1000 particles16-19. Needlessly to say, you can find no data on the human infectious dose of influenza virus concerning connection with drinking water or contact between water and oral mucous membranes, conjunctiva, eardrums or wounds. The human infectious dose of H5N1 avian influenza virus is also unknown.

g) Human influenza viruses in mammals: Human influenza viruses have been identified in the excretions of mammals, such as pigs (fecal and oronasal), wild boar (fecal and oronasal), cattle and goats. Hence in principle, from the virological point of view the transmission path from the environment to mammals and humans can be done via water, especially drinking water13, 20-30. Thus, it is highly probable that more animal species infected with influenza A is going to be discovered in future13. This way, human influenza viruses are secreted into the environment and water. Secreted influenza virus titers are usually very high. Avian influenza viruses have been isolated from unconcentrated lake water, which indicates that human influenza viruses can also be isolated from untreated water.

Effectiveness of elimination and inactivation of viruses during treatment of drinking water

To determine resistance of highly pathogenic H5N1 avian influenza virus to chlorination, Rice et al. 31 exposed allantoic fluid that contained two virus strains to chlorinated buffer at pH 7 and 8, at {5}? C. They figured free chlorine concentrations typically found in motor home water filters were sufficient to inactivate herpes by a lot more than three orders of magnitude. However, drinking water could be colder than {5}? C, e. g. 3? C. The pH value is frequently >8. 0, e. g. 9. {5}. In the cold and at high pH, virus inactivation by chlorine is rather poor. Rice et al. 31 used the utmost US chlorination amount of 2. 0 mg/L free chlorine. Only 0. 1-0. 3 mg/L free chlorine are allowed in Germany. The performance levels of water treatment units regarding virus inactivation32 are valid under the precondition that microorganisms in water come in suspension, maybe not embedded in particles32. In environmental waters, secreted influenza viruses are always embedded in particles. Hence the demonstrated amount of avian influenza virus inactivation in allantoic fluid diluted in buffer is not in line with real conditions. Moreover, the WHO32 requires virus inactivation/filtration rates from six (surface water) to four (groundwater) orders of magnitude. Rice et al. 31 only demonstrated three orders of magnitude. Hence the authors are not convinced that chlorinated water is safe. Real worst-case conditions are cold normal water at 3? C, pH 9. {5}, chlorination lower than 2 mg/L (or no chlorination but filtration), perhaps 0. 2 mg/L as in Germany, influenza viruses embedded in particles, and required virus inactivation/filtration performance from six to four orders of magnitude.

In Germany, normal water is frequently only roughly filtered or never. Thus, really small viruses are not filtered out reliably. In treating groundwater, the widespread filtration plants for the elimination of iron and manganese are ineffective in eliminating viruses32. The goals demanded by the WHO regarding elimination and inactivation of viruses can't be met32, even in Germany, having its efficient plants for flocculation and filtration, and the common disinfection procedures followed (chlorine, ozone treatment, and UV irradiation), whose efficiency declines with decreasing water temperature (chlorine and ozone treatment), because microorganisms clumped in water are only reduced to a limited extent.

"Cooling chain of the public water supply"

Coldness is the main parameter for the preservation of virulent influenza viruses in water33-38. The minimum temperature of water in German reservoirs is 3-5? C in the months of January and February. River water also reaches its minimum temperature in those months. Also, groundwater obtained from deeper wells can be colder when there is insufficient sealing involving the well pipes and the surrounding rocks. This enables the infiltration of surface water to influence the temperature of the groundwater, which might ensure it is colder compared to deeper groundwater. Moreover, surface water trickling from streams and coming to the wells within short distances might have the same effect. River bank filtrate pumped from wells which can be drilled near the bank assumes on the temperature of the cold river water, and the same pertains to wells that groundwater enriched with surface water is pumped. The 1-m deep soil temperatures match the temperatures of the underground, frost-protected, drinking water pipelines. In Germany, the minimum soil temperatures at a depth of 1 m are 3-5? C during February and March39. The temperature within the normal water pipelines and that of the drinking water transported in them adapts to the soil temperature. In cold weather, cold, untreated water arrives at the drinking-water treatment plants, and remains cold in the water tanks and pipelines after treatment, up to the houses of consumers. In particular, the minimum temperature of plain tap water corresponds to the cold winter temperature in the soil and water pipelines, and rises in February-March. Only at domestic taps could be the cold normal water mixed with tepid to warm water from the house. This technique is the -oecooling chain of the public water supply-?, from the water source to the consumers, with a normal water temperature of, as an example, 3-5? C in February-March. Cold, fresh normal water obtained from surface water, insufficiently protected groundwater near the surface, along with groundwater from rocks contaminated by influenza viruses, may be the abiotic vehicle that transports the virulent influenza viruses in winter at temperatures of 3-5? C. The viruses are conserved effectively in the cold and transported to humans via the cooling chain of the public hydrant.

Transmission paths of normal water - basic principle

Infections through normal water are not only transmitted through drinking the water, but in addition through the inhalation of aerosols during showers and experience of drinking water. The entry sites in humans are the conjunctiva, nasal and oral mucous membranes, eardrums, wounds, and contaminated catheters infecting other mucous membranes.

Influenza transmission in temperate climates and tropical regions

In temperate regions, influenza epidemics recur with marked seasonality around the end of winter, in the northern as well as the southern hemisphere. Although seasonality is among the most familiar top features of influenza, it's also one of the least understood. Indoor crowding during winter, seasonal fluctuations in host immune responses, and environmental factors, including relative humidity, temperature and UV radiation, have all been assumed to take into account this phenomenon, but none of those has been tested directly. Influenza also causes significant morbidity in tropical regions; however, contrary to the problem in temperate zones, influenza in the tropics just isn't strongly of a certain season.

In the tropics, clear links are observed involving the cold rainy seasons, floods and the spread of influenza. There exists a widespread link between avian influenza and water, e. g. in Egypt, with respect to the Nile delta, or in Indonesia, with regards to the less prosperous residential districts with backyard flocks of birds, and with no central hydrant, as in Vietnam40. However, the direct biotic transmission from birds, poultry or humans to humans can't be determined by the cold rainy seasons or floods. Water is a very efficient abiotic vehicle for the spread of viruses - particularly, the fecal viruses, as well as those excreted through the mouth, nose and eyes. Infected humans, mammals, birds and poultry can contaminate normal water everywhere, and all humans require water frequently and also have very intensive contact with water in general, and not only through drinking.

The virulence of influenza viruses depends on the temperature and time. Especially in cases of local water supplies freshly contaminated with influenza virus from wells nearby the surface, cisterns, tanks, rain barrels, ponds, rivers, or rice paddies, this pathway can explain the little clusters in households. For instance, at 24? C in the tropics, the virulence of influenza viruses in water persists limited to 2 days. However, in temperate climates with central water supplies, the temperature of the -oeolder-?, less fresh contaminated water is decisive for virus virulence. At 7? C, the influenza virus virulence in water reaches {14 days}.

Ducks and rice paddies may be critical factors in spreading avian influenza41. Ducks, rice paddies and people, but not chickens, have emerged as the most significant factors in the spread of avian influenza in Thailand and Vietnam42. Also, these factors are presumed to be behind the persistent outbreaks in other countries, such as Cambodia and Laos. In Thailand, for example, the proportion of young ducks in flocks was found to peak in September-October; these rapidly growing young ducks can thus benefit from the peak of the rice harvest in November-December, at the beginning of the winter. Thailand, Vietnam, Cambodia and Laos, instead of Indonesia, are located in the northern hemisphere. This peak in the congregation of ducks in November-December indicates the period by which there is a rise in the probability of virus release and exposure, where rice paddies often become a temporary habitat for wild-bird species. The influenza season in humans begins close to this peak.

Conclusions

In temperate climates, the strict dependence of influenza infection on environmental temperature helps it be improbable that the primary human-to-human transmission of influenza is through warm biotic droplet infection. Influenza must be triggered by an abiotic vehicle that is increasingly efficient in spreading infection with increasing cold environmental temperatures. Therefore, the question arises regarding which abiotic vehicles are determined by cold environmental temperatures for the transmission of influenza viruses. Normal water is this abiotic vehicle.

This informative article shows that cold normal water may be the abiotic vehicle by which virulent human influenza viruses from the infection reservoirs reach humans, and which is responsible predominantly for triggering the seasonal influenza epidemics. And also this applies specifically to the new H1N1 influenza virus with vomiting or/and diarrhoea (38% of cases) and the lethal H5N1 avian influenza virus, whose potential transmission via water is more successful.

References

Brankston G, Gitterman L, Hirji Z, Lemieux C, Gardam M. Transmission of influenza A in people. Lancet Infect Dis. 2007 Apr; 7(4): 257-65. Available from http: //www. ncbi. nlm. nih. gov/sites/entrez? Db=pubmedCmd=ShowDetailViewTermToSearch=17376383ordinalpos=1itool=EntrezSystem2. PEntrez. Pubmed. Pubmed_ResultsPanel. Pubmed_RVDocSum visited: 9 June 2008.

Lowen AC, Mubareka S, Steel J, Palese P. Influenza virus transmission depends on relative humidity and temperature. PLoS Pathog 3(10): e151. doi: 10. 1371/journal. ppat. 0030151. Available from http: //www. plospathogens. org/article/info: doi/10. 1371/journal. ppat. 0030151 visited: 9 June 2008.

Lowen AC, Steel J, Mubareka S, Palese P. Temperature (30? C) blocks aerosol however, not contact transmission of influenza virus. Journal of Virology, June 2008, p. 5650-5652, Vol. 82, No. 11. Available from http: //jvi. asm. org/cgi/content/abstract/82/11/5650 visited: 9 June 2008.

Shaman J, Kohn M. Absolute humidity modulates influenza survival, transmission, and seasonality. PNAS 2009 106: 3243-48.

Lipsitch M, Viboud C. Influenza seasonality: Lifting the fog. PNAS 2009 106: 3645-46.

Robert Koch-Institut (RKI). Infektionsepidemiologisches Jahrbuch meldepflichtiger Krankheiten f? 1/4 r 2007, Datenstand: 1. M?? rz 2008.

Arbeitsgemeinschaft Influenza. Available from http: //influenza. rki. de/agi visited: 9 June 2008.

Robert Koch-Institut (RKI). Datenbank der nach Infektionsschutzgesetz meldepflichtigen Infektionskrankheiten in Deutschland. Available from http: //www3. rki. de/SurvStat/ visited: 9 June 2008.

Goldmann DA. Transmission of viral respiratory infections in the house. Paediatr Infect Dis J 2000; 19: 97-102. Available from http: //www. ncbi. nlm. nih. gov/pubmed/11052396 visited: 9 June 2008.

International Scientific Forum on Home Hygiene IFH. Colds, flu along with other respiratory infections. May 2003. Available from http: //www. ifh-homehygiene. org/2003/2downloadabledoc/SARS. pdf visited: 9 June 2008.

Goldmann DA. Epidemiology and prevention of pediatric viral respiratory infections in health-care institutions, Children's Hospital and Harvard Medical School, Boston, Massachusetts, USA, Emerging Infectious Diseases, Special Issue. Available from http: //www. cdc. gov/ncidod/eid/vol7no2/goldmann. htm visited: 9 June 2008.

D'Alessio DJ, Meschievitz CK, Peterson JA, Dick CR, Dick EC. Short-duration exposure and the transmission of rhinoviral colds. J Infect Dis 1984; 150: 189-194.

Webster RG. Influenza: An emerging disease. Emerging Infectious Diseases 4(3) July-September 1998, Special Issue. Available from http: //www. cdc. gov/ncidod/eid/vol4no3/webster. htm visited: 9 June 2008.

Hinshaw VS, Webster RG. The natural history of influenza A viruses. In: Beare AS, editor. Basic and applied influenza research. Boca Raton (FL): CRC Press; 1982. p. 79-104.

Khalenkov A, Laver WG, Webster RG. Detection and isolation of H5N1 influenza virus from large volumes of natural water. J Virol Methods, Volume 149, Issue 1, April 2008, Pages 180-183. Available from http: //www. ncbi. nlm. nih. gov/pubmed/18325605 visited: 9 June 2008.

G? 1/4 rtler L. Virology of Human Influenza. Influenza Report 2006, Edited by Kamps BS, Hoffmann C, Preiser W. Flying Publisher. Available from www. InfluenzaReport. com visited: 9 June 2008.

Nicholson KG, Webster RG, Hay AJ. Textbook of Influenza. Blackwell Science, Oxford, 1998.

Lamb RA, Krug RM. Orthomyxoviridae: The viruses and their replication. In: Fields Virology fourth edition, Knipe DM, Howley PM eds, Lippincott, Philadelphia 2001, pp 1487-1531.

Wright PF, Webster RG. Orthomyxoviruses. In: Fields Virology fourth edition, Knipe DM, Howley PM eds, Lippincott, Philadelphia 2001, pp 1533-1579.

Brown IH. Part 1: Swine, avian human influenza viruses, OIE/FAO/EU International Reference Laboratory for Avian Influenza, Veterinary Laboratories Agency, Weybridge, New Haw, Addlestone, Surrey KT15, 3NB, UK. Available from http: //www. pighealth. com/influenza. htm visited: 9 June 2008.

Brown IH. Part 2: Transmission between pigs along with other species, OIE/FAO/EU International Reference Laboratory for Avian Influenza, Veterinary Laboratories Agency, Weybridge, New Haw, Addlestone, Surrey KT15, 3NB, UK. Available from http: //www. pighealth. com/influenzaB. htm visited: 9 June 2008.

Graves IL, Oppenheimer JR. Human viruses in animals in West Bengal: An ecological analysis, Human Ecology, Volume 3, {Number 2} / April, 1975, 105-130. Available from http: //www. springerlink. com/content/u5408wx5t622ll82/ visited: 9 June 2008.

Kaden V, M? 1/4 ller T. Gef?? hrliche Verwandtschaft Schwarzwild - ein nat? 1/4 rliches Reservoir f? 1/4 r Infektionserreger und Ansteckungsquelle f? 1/4 r Hausschweine? Bundesforschungsanstalt f? 1/4 r Viruskrankheiten der Tiere Forschungsreport 1/2001: 24-28. Available from http: //ticker-grosstiere. animal-health-online. de/20010902-00002/ visited: 9 June 2008.

Kawaoka Y, Bordwell E, Webster RG. Intestinal replication of influenza A viruses in two mammalian species, Archives of Virology, Volume 93, Numbers 3-4/December, 1987, 303-308. Available from http: //www. springerlink. com/content/g352726672xj5703/ visited: 9 June 2008.

Markowska-Daniel I, Pejsak Z. Seroprevalence of influenza virus among wild boars in Poland. National Veterinary Research Institute, Swine Diseases Departement, Pulawy, Poland. Available from http: //www. medwet. lublin. pl/Year%201999/vol99-05/art222-98. htm visited: 9 June 2008.

Robert Koch-Institut (RKI). Merkblatt f? 1/4 r?,, rzte, Influenza - Verh? 1/4 tung und Bek?? mpfung (Stand 1999).

Vicente J, Le?? n-Vizca? -no L, Gort?? zar C, Jos? (C) Cubero M, Gonz?? lez M, Mart? -n-Atance P. Antibodies to selected viral and bacterial pathogens in European wild boars from southcentral Spain. J Wildl Dis. 38(3): 649-52. Available from http: //www. ncbi. nlm. nih. gov/entrez/query. fcgi? cmd=Retrievedb=PubMedlist_uids=12238391dopt=Abstract visited: 9 June 2008.

Zhou N, He S, Zhang T, Zou W, Shu L, Sharp GB, Webster RG. Influenza infection in humans and pigs in southeastern China. Archives of Virology, Volume 141, Numbers 3-4/March, 1996, 649-661. Available from http: //www. springerlink. com/content/p220471r1r337521/ visited: 9 June 2008.

Landolt GA, Karasin AI, Phillips L, Olsen CW. Comparison of the pathogenesis of two genetically different H3N2 influenza A viruses in pigs. J Clin Microbiol. 2003 May; 41({5}): 1936-1941. Available from http: //www. pubmedcentral. nih. gov/articlerender. fcgi? tool=pmcentrezrendertype=abstractartid=154671 visited: 9 June 2008.

Zimmermann W. Krankheiten des Schweines. Universit?? t Bern, Departement klinische Veterin?? rmedizin, Schweineklinik, Vorlesungsskript WS 2001-2002, 49-51.

Rice EW, Adcock NJ, Sivaganesan M, Brown JD, Stallknecht DE, Swayne DE. Chlorine inactivation of highly pathogenic avian influenza (H5N1) virus. Emerg Infect Dis (serial on the Internet). 2007 Oct (date cited). Available from http: //www. cdc. gov/EID/content/13/10/1568. htm visited: 9 June 2008.

World Health Organization (WHO). Guidelines for drinking-water quality, third edition, incorporating first addendum. Available from http: //www. who. int/water_sanitation_health/dwq/gdwq3/en/print. html visited: 9 June 2008.

Halvorson DA, Kelleher CJ, Senne DA. Epizootiology of Avian Influenza: Effect of Season on Incidence in Sentinel Ducks and Domestic Turkeys in Minnesota. Appl Environ Microbiol. 1985 April; 49(4): 914-919. Available from http: //aem. asm. org/cgi/content/abstract/49/4/914 visited: 9 June 2008.

Stallknecht DE, Shane SM, Kearney MT, Zwank PJ. Persistence of avian influenza viruses in water. Avian Dis. 1990 Apr-Jun; 34(2): 406-11. Available from http: //www. ncbi. nlm. nih. gov/pubmed/2142420? ordinalpos=1itool=EntrezSystem2. PEntrez. Pubmed. Pubmed_ResultsPanel. Pubmed_DiscoveryPanel. Pubmed_Discovery_RAlinkpos=3log$=relatedarticleslogdbfrom=pubmed visited: 9 June 2008.

Stallknecht DE, Kearney MT, Shane SM, Zwank PJ. Effects of pH, temperature, and salinity on persistence of avian influenza viruses in water. Avian Dis. 1990 Apr-Jun; 34(2): 412-8. Available from http: //www. ncbi. nlm. nih. gov/pubmed/2142421? ordinalpos=1itool=EntrezSystem2. PEntrez. Pubmed. Pubmed_ResultsPanel. Pubmed_DiscoveryPanel. Pubmed_Discovery_RAlinkpos=5log$=relatedarticleslogdbfrom=pubmed visited: 9 June 2008.

World Health Organization. Avian influenza H5N1 infection in humans: urgent have to eliminate the animal reservoir - update {5}, 22 January 2004. Available from http: //www. who. int/csr/don/2004_01_22/en/ visited: 9 June 2008.

World Health Organization. Avian influenza A(H5N1)- update 31: Situation (poultry) in Asia: importance of a long-term response, comparison with previous outbreaks, 2 March 2004. Available from http: //www. who. int/csr/don/2004_03_02/en/ visited: 9 June 2008.

Brown JD, Swayne DE, Cooper RJ, Bums RE, Stallknecht DE. Persistence of H5 and H7 avian influenza viruses in water. Avian Dis. 2007; 51(Suppl): 285-9. Available from http: //www. ncbi. nlm. nih. gov/pubmed/17494568 visited: 9 June 2008.

Deutscher Wetterdienst (DWD). Wetterstation Erfurt-Bindersleben, Erdbodentemperaturen aus 100 cm Tiefe, mittlere Lufttemperatur; Wetterstation Fichtelberg, mittlere Lufttemperatur.

Dinh PN, Long HT, Tien NTK, Hien NT, Mai LTQ, Phong LH, et al. Risk factors for human infection with avian influenza A H5N1, Vietnam, 2004. Emerg Infect Dis (serial on the Internet). 2006 Dec. Available from http: //www. cdc. gov/ncidod/EID/vol12no12/06-0829. htm visited: 9 June 2008.

United nations agency. Ducks and rice major factors in bird flu outbreaks, says UN agency, 26 March 2008. Available from http: //www. un. org/apps/news/story. asp? NewsID=26096Cr=Cr1 visited: 9 June 2008.

Gilbert M, Xiao X, Pfeiffer DU, Epprecht M, Boles S, Czarnecki C, Chaitaweesub P, Kalpravidh W, Minh PQ, Otte MJ, Martin V, Slingenbergh J. Mapping H5N1 highly pathogenic avian influenza risk in Southeast Asia. Proc Natl Acad Sci U S A. 2008 Mar 25; 105(12): 4769-74. Epub 2008 Mar 24. Available from http: //www. ncbi. nlm. nih. gov/pubmed/18362346 visited: 9 June 2008.

Dipl. -Ing. Wilfried Soddemann

M? 1/4 hlenstra?? e 5b

D - 48351 Everswinkel

soddemann-aachen@t-online. de

http: //sites. google. com/site/trinkwasservirenalarm/Trinkwasser-Viren? pageUrlChanged=Trinkwasser-Viren

NTK (Need to Know) (Omaha World-Herald)

News you need as you start your day.

Omaha World-Herald

NTK Premium Bluetooth Keyboard Leather Case for HP Touchpad 16GB 32GB