Articles about Chloramine
http://www.epa.gov/athens/research/process/drinkingwater.html
August 9th, 2007
What is in Our Drinking Water?
Identification of New Chemical Disinfection By-products (DBPs)
What is a DBP? A drinking water disinfection by-product (DBP) is formed when the chemical used for disinfecting the drinking water reacts with natural organic matter and/or bromide/iodide in the source water. Popular disinfectants include chlorine, ozone, chlorine dioxide, and chloramine. Source waters include rivers, lakes, streams, groundwater, and sometimes seawater. We have only known about DBPs since 1974, when chloroform was identified by Rook as a DBP resulting from the chlorination of tap water. Since then, hundreds of DBPs have been identified in drinking water.
So what? Millions of people in the U.S. are exposed to these drinking water DBPs every day. While it is vitally important to disinfect drinking water, as thousands of people died from waterborne illnesses before we started disinfection practices in the early 1900s, it is also important to minimize the chemical DBPs formed. Several DBPs have been linked to cancer in laboratory animals, and as a result, the U.S. EPA has some of these DBPs regulated. However, there are many more DBPs that have still not been identified and tested for toxicity or cancer effects. Currently, we have only identified about 50% of the total organic halide (TOX) that is measured in chlorinated drinking water. There is much less known about DBPs from the newer alternative disinfectants, such as ozone, chlorine dioxide, and chloramine, which are gaining in popularity in the U.S. Are these alternative disinfectants safer than chlorine? What kinds of by-products are formed? And, what about the unidentified chlorine DBPs that people are exposed to through their drinking water--both from drinking and showering/bathing? The objective of our research is to find out what these DBPs are--to thoroughly characterize the chemicals formed in drinking water treatment--and to ultimately minimize any harmful ones that are formed.
Our research approach
• Gas chromatography/mass spectrometry (GC/MS), liquid chromatography/mass spectrometry (LC/MS), and gas chromatography/infrared spectroscopy (GC/IR) techniques are used to identify the unknown by-products
• NIST and Wiley mass spectral databases are used first to identify any DBPs that happen to be present in these databases
• Because many DBPs are not in these databases, most of our work involves unconventional MS and IR techniques, as well as a great deal of scientific interpretation of the spectra
• High resolution MS provides empirical formula information for the unknown chemical (e.g., how many carbons, hydrogens, oxygens, nitrogens, etc. are in the chemical’s structure)
• Chemical ionization MS provides molecular weight information when this is not provided in conventional electron ionization mass spectra
• IR spectroscopy provides functional group information (e.g., whether the oxygens are due to a carboxylic acid group, a ketone, an alcohol, or an aldehyde)
• LC/MS is used to identify compounds that cannot be extracted from water (the highly polar, hydrophilic ones), as well as the high molecular weight, nonvolatile DBPs. This is a major missing gap in our knowledge about DBPs--so far, most DBPs identified have been those that are easily extracted from water and are volatile enough to analyze by GC/MS
• Novel derivatization techniques are also applied to aid in the identification of highly polar DBPs
• Formation and fate & transport studies are conducted to better understand how certain priority DBPs are formed and transformed in treatment and distribution systems
Currently
We recently completed a major nationwide DBP occurrence study EPA/600/R-02/068 (also published in Dec. 1, 2006 issue of Environmental Science & Technology: ES&T, 2006, 40, 7175-7185), where we sampled drinking water across the U.S. (disinfected with the different disinfectants and with different water quality, including elevated levels of bromide in the source water). A group of >50 DBPs that resulted from a prioritization of >500 DBPs in the literature for predicted adverse health effects was quantified in these drinking waters. Fate and transport studies were also conducted in the drinking water distribution systems to determine whether these DBPs changed in concentration or were transformed in the distribution systems. In addition to obtaining important quantitative information on these new DBPs (to help in prioritizing health effects testing), important new discoveries were made regarding the use of alternative disinfectants. While the use of alternative disinfectants lowered the levels of the four regulated trihalomethanes and five haloacetic acids (as compared to chlorine), many of the other prioritized DBPs were formed at higher levels with these alternative disinfectants. For example, the highest levels of iodinated DBPs were found in chloraminated drinking water, the highest levels of halonitromethanes were found in pre-ozonated drinking water, and dihaloaldehydes were highest at a plant using chloramines and ozone.
Our new work includes obtaining quantitative occurrence information on the iodo-acids that were identified for the first time in the Nationwide DBP Occurrence Study. Chloraminated waters (where levels are expected to be highest) are targeted for this work. In addition, a toxicity-based identification approach (using mammalian cell and medaka fish assays) will be used to ensure toxicologically important DBPs are not being missed. The full study of the Four Lab Study is also expected to begin in 2005 (where drinking water is treated and concentrated, comprehensive DBP identifications are carried out, and drinking water concentrates are tested in a battery of in vivo and in vitro toxicity assays, with an emphasis on newer reproductive and developmental health effects). This Four Lab Study involves the collaboration of EPA's national laboratories and centers (NHEERL, NERL, NRMRL, and NCEA). Finally, work continues in determining how the toxicologically significant bromonitromethane DBPs are formed. These bromonitromethanes are more genotoxic and cytotoxic to mammalian cells than most of the DBPs currently regulated and are also currently the focus of in vivo testing at NHEERL (RTP, NC) and at the National Toxicology Program (NTP, NIEHS).
Recent results
• A recent Nationwide DBP Occurrence Study (ES&T, 2006, 40, 7175-7185) has provided important new quantitative information on unregulated DBPs that have the potential to cause adverse health effects based on a structure-activity analysis (Woo et al., 2002); several of these DBPs have concentrations similar to some that are already regulated
• The use of alternative disinfectants can produce higher levels of these DBPs, as compared to chlorine
• A recent study reveals that iodoacetic acid (one of five new iodo-acids recently identified in chloraminated drinking water) is a potent cytotoxin and genotoxin in mammalian cells (Plewa et al., 2004a) (work is in progress on the toxicity of other iodo-acids)
• The presence of natural bromide in the source water results in a tremendous shift from chlorine-containing DBPs to bromine-containing DBPs when chlorine or chloramine is used as a disinfectant (even in combination with ozone)
• New analytical methods have been developed (and are continuing to be developed) for the analysis of highly polar DBPs
• Collaborations have been forged with health effects researchers to study selected DBPs for potential adverse health effects
Gordon Research Conference on DBPs
A Gordon Research Conference on drinking water DBPs was held on August 13-18, 2006, at Mount Holyoke College in South Hadley, Massachusetts. Title of meeting: Drinking Water Disinfection By-products: Integrating Occurrence and Formation, Exposure, Toxicity, and Epidemiology. This meeting was highly successful, with a nice mix of chemists, epidemiologists, toxicologists, regulators, human exposure scientists, risk assessment scientists, clinicians, and engineers present. Scientists from 22 countries were represented. We were recently approved for on-going status, and will hold the next follow-up Gordon Conference on DBPs in the summer of 2009 (tentatively scheduled for early August). Ben Blount from the Centers for Disease Control and Prevention (CDC) will be the Chair of the 2009 conference. Contact Ben Blount (bkb3@cdc.gov) or Susan Richardson (richardson.susan@epa.gov) for more information.
Useful publications
1. Krasner, S. W., H. S. Weinberg, S. D. Richardson, S. Pastor, R. Chinn, M. J. Sclimenti, G. Onstad, and A. D. Thruston, Jr. 2006. The Occurrence of a New Generation of Disinfection Byproducts. Environmental Science & Technology, 40 (23): 7175-7185.
2. Weinberg, H. S., S. W. Krasner, S. D. Richardson, and A. D. Thruston, Jr. The Occurrence of Disinfection By-Products (DBPs) of Health Concern in Drinking Water: Results of a Nationwide DBP Occurrence Study. EPA/600/R02/068. U.S. Environmental Protection Agency, National Exposure Research Laboratory, Athens, GA. 2002.
3. Muellner, M. G., E. D. Wagner, K. McCalla, S. D. Richardson, Y.-T. Wood, and M. J. Plewa. 2007. Haloacetonitriles vs. Regulated Haloacetic Acids: Are Nitrogen Containing DBPs More Toxic? Environmental Science & Technology,41 (2): 645-651.
4. Zwiener, C., S. D. Richardson, D. M. DeMarini, T. Grummt, T. Glauner, and F. H. Frimmel. 2007. Drowining in Disinfection By-Products? Swimming Pool Water Quality Reconsidered. Environmental Science & Technology, 41 (2): 363-372.
5. Richardson. S. D. Environmental Mass Spectrometry: Emerging Contaminants and Current Issues. 2006. Analytical Chemistry, 78 (12): 4021-4046.
6. Richardson, S. D., and T. Ternes. 2005. Water Analysis: Emerging Contaminants and Current Issues. Analytical Chemistry, 77(12): 3807-3838.
7. Richardson, S. D., C. Rav-Acha, and G. D. Simpson. Chlorine Dioxide Chemistry, Reactions, and Disinfection By-Products. 2007. In Chlorine Dioxide in Drinking Water Treatment, American Water Works Association Research Foundation, in press.
8. Richardson, S. D., D. C. Wolf, M. J. Plewa, and R. Schoeny. Occurrence, Mutagenicity, and Carcinogenicity of Emerging Disinfection By-Products in Drinking Water. 2007. Mutation Research, in press.
9. Cemeli, E., E. D. Wagner, D. Anderson, S. D. Richardson, and M. J. Plewa. 2006. Modulation of the Cytotoxicity and Genotoxicity of the Drinking Water DBP Iodoacetic Acid by Suppressors of Oxidative Stress. Environmental Science & Technology, 40 (6): 1878-1883.
10. Vincenti, M., S. Biazzi, N. Ghiglione, M. C. Valsania, and S. D. Richardson. 2005. Comparison of Highly- Fluorinated Chloroformates as Direct Aqueous Sample Derivatizing Agents for Hydrophilic Analytes and Drinking Water Disinfection By-Products. Journal of the American Society for Mass Spectrometry, 16 (6): 803-813.
11. Plewa, M. J., E. D. Wagner, S. D. Richardson, A. D. Thruston, Jr., Y.-T. Woo, and A. B. McKague. 2004. Chemical and Biological Characterization of Newly Discovered Iodoacid Drinking Water Disinfection Byproducts. Environmental Science & Technology, 38(18): 4713-4722.
12. Zwiener, C., and S. D. Richardson. 2005. Drinking Water Disinfection By-Product Analysis by LC/MS and LC/MS/MS. Trends in Analytical Chemistry, 24(7): 613-621. (Invited review article for special thematic issue on Liquid Chromatography-Tandem Mass Spectrometry).
13. Plewa, M. J., E. D. Wagner, P. Jazwierska, S. D. Richardson, P. H. Chen, and A. B. McKague. 2004. Halonitromethane Drinking Water Disinfection Byproducts: Chemical Characterization and Mammalian Cell Cytotoxicity and Genotoxicity. Environmental Science & Technology, 38(1): 62-68.
14. Kundu, B., S. D. Richardson, P. D. Swartz, P. P. Matthews, A. M. Richard, and D. M. DeMarini. 2004. Mutagenicity in Salmonella of Halonitrometanes: A Recently Recognized Class of Disinfection By-Product in Drinking Water. Mutation Research, 562: 39-65.
15. Kundu, B., S. D. Richardson, C. A. Granville, D. T. Shaughnessy, N. M. Hanley, P. D. Swartz, A. M. Richard, and D. M. DeMarini. 2004. Comparative Mutagenicity of Halomethanes and Halonitromethanes in Salmonella TA100: Structure-Activity Analysis and Mutation Spectra. Mutation Research, 554: 335-350.
16. Richardson, S. D. 2004. Environmental Mass Spectrometry: Emerging Contaminants and Current Issues. Analytical Chemistry, 76(12): 3337-3364.
17. Simmons, J. E., L. K. Teuschler, C. Gennings, T. F. Speth, S. D. Richardson, R. J. Miltner, M. G. Narotsky, K. D. Schenck, E. S. Hunter, III, R. C. Hertzberg, III, and G. Rice. 2004. Component-Based and Whole-Mixture Techniques for Addressing the Toxicity of Drinking Water Disinfection Byproducts Mixtures. Journal of Toxicology & Environmental Health, 67: 741-754.
18. Richardson, S.D., J. E. Simmons, and G. Rice. 2002. DBPs: The Next Generation. Environmental Science & Technology, 36(9): 198A-205A.
19. Woo, Y.-T., D. Lai, J. L. McLain, M. K. Manibusan, and V. Dellarco. 2002. Environmental Health Perspectives, 110 (Suppl. 1): 75-87.
20. Richardson, S. D., A. D. Thruston, Jr., C. Rav-Acha, L. Groisman, I. Popilevsky, V. Glezer, A. B. McKague, M. J. Plewa, and E. D. Wagner. 2003. Tribromopyrrole and Other DBPs Produced by the Disinfection of Drinking Water Rich in Bromide. Environmental Science & Technology, 37(17): 3782-3793.
21. Richardson, S. D. 2003. Water Analysis: Emerging Contaminants and Current Issues. Analytical Chemistry, 75(12): 2831-2857.
22. Richardson, S. D. 2003. Disinfection By-Products and Other Emerging Contaminants in Drinking Water. Trends in Analytical Chemistry, 22(10):666-684
23. Chen, P. H., S. D. Richardson, S. W. Krasner, G. Majetich, and G. L. Glish. 2002. Hydrogen Abstraction and Decomposition of Tribromonitromethane and Other Trihalo Compounds by GC/MS. Environmental Science & Technology, 36(15): 3362-3371.
24. Simmons, J. E., S. D. Richardson, T. F. Speth, R. J. Miltner, G. Rice, K. M. Schenck, E. S. Hunter, III, and L. K. Teuschler. 2002. Development of a Research Strategy for Integrated Technology-Based Toxicological and Chemical Evaluation of Complex Mixtures of Drinking Water Disinfection Byproducts. Environmental Health Perspectives, 110(Supp. 6): 1013-1024.
25. Arbuckle, T. E., S. E. Hrudey, S. W. Krasner, J. R. Nuckols, S. D. Richardson, P. Singer, P. Mendola, L. Dodds, C. Weisel, D. L. Ashley, K. L. Froese, R. A. Pegram, I. R. Schultz, J. Reif, A. M. Bachand, F. M. Benoit, M. Lynberg, C. Poole, and K. Waller. 2002. Assessing Exposure in Epidemiologic Studies to Disinfection By-products in Drinking Water: Report from an International Workshop. Environmental Health Perspectives, 110 (Supp. 1): 53-60.
26. Richardson, S. D., T. V. Caughran, T. Poiger, Y. Guo, and F. G. Crumley. 2000. Application of DNPH Derivatization with LC/MS to the Identification of Polar Carbonyl Disinfection By-products in Drinking Water. Ozone: Science & Engineering, 22: 653-675.
27. Richardson, S. D., A. D. Thruston, Jr., T. V. Caughran, P. H. Chen, T. W. Collette, T. L. Floyd, K. M. Schenck, B. W. Lykins, Jr., G.-R. Sun, and G. Majetich. 1999. Identification of New Ozone Disinfection By-products in Drinking Water. Environmental Science & Technology, 33: 3368-3377.
28. Richardson, S. D., A. D. Thruston, Jr., T. V. Caughran, P. H. Chen, T. W. Collette, T. L. Floyd, K. M. Schenck, B. W. Lykins, Jr., G.-R. Sun, and G. Majetich. 1999. Identification of New Drinking Water Disinfection By-products Formed in the Presence of Bromide. Environmental Science & Technology, 33: 3378-3383.
29. Richardson, S. D., A. D. Thruston, Jr., T. V. Caughran, P. H. Chen, T. W. Collette, K. M. Schenck, B. W. Lykins, Jr., C. Rav-Acha, and V. Glezer. 2000. Identification of New Drinking Water Disinfection By-products from Ozone, Chlorine Dioxide, Chloramine, and Chlorine. Water, Air, and Soil Pollution, 123: 95-102.
*For more information, contact Susan Richardson at richardson.susan@epa.gov
Last updated on Thursday, August 9th, 2007.
http://www.epa.gov/athens/research/process/drinkingwater.html
http://pubs.acs.org/cgi-bin/sample.cgi/ancham/2007/79/i12/html/ac070719q.html
Water Analysis: Emerging Contaminants and Current Issues
August, 2007
Susan D. Richardson
Drinking Water Disinfection Byproducts
In addition to new regulations and rules involving DBPs (e.g., the Stage 2 Disinfectants/DBP Rule and the UCMR-2, which requires monitoring of nitrosamines), there are also new, emerging issues with DBPs (91). New human exposure research is revealing that inhalation and dermal exposures (from showering, bathing, swimming, and other activities) can provide equivalent exposures or increased exposures to certain DBPs (91). Therefore, these exposure routes are now being recognized in new epidemiologic studies that are being conducted. And, epidemiology studies are beginning to focus more on reproductive and developmental effects-which recent studies have been shown to be important. A recent review article outlines these important routes of exposure, along with new, emerging DBPs (91).
Toxicologically Important DBPs. Toxicologically important DBPs include brominated, iodinated, and nitrogen-containing DBPs (so-called "N-DBPs"). Brominated DBPs are more carcinogenic than their chlorinated analogues (91), and new research is indicating that iodinated compounds may be more toxic than their brominated analogues (91). Brominated and iodinated DBPs form due to the reaction of the disinfectant (such as chlorine) with natural bromide or iodide present in source waters. Coastal cities, whose groundwaters and surface waters can be impacted by salt water intrusion, and some inland locations, whose surface waters can be impacted by natural salt deposits from ancient seas or oil-field brines, are examples of locations that can have high bromide and iodide levels. A significant proportion of the U.S. population and several other countries now live in coastal regions that are impacted by bromide and iodide; therefore, exposures to brominated and iodinated DBPs are important. Early evidence in epidemiologic studies also gives indication that brominated DBPs may be associated with the new reproductive and developmental effects, as well as cancer effects.
Specific DBPs that are of current interest include iodo acids, bromonitromethanes, iodo-THMs, brominated forms of MX (MX is 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone), haloaldehydes, haloamides, and NDMA, which is not brominated, but is classified as a probable carcinogen (91). Iodoacetic acid, one of five iodo acids identified for the first time in chloraminated drinking water, has recently been shown to be more genotoxic and cytotoxic to mammalian cells than all DBPs that have been studied, including the regulated HAAs and bromate (91). It is a factor of 2? more genotoxic than bromoacetic acid, which is the most genotoxic of the regulated HAAs. Other iodo acids identified-bromoiodoacetic acid, (Z)-3-bromo-3-iodopropenoic acid, (E)-3-bromo-3-iodopropenoic acid, and (E)-2-iodo-3-methylbutenedioic acid (91)-have been synthesized and are currently under investigation for genotoxic and cytotoxic effects. They were initially discovered in chloraminated drinking water extracts using methylation with GC/high-resolution-EI-MS. Analytical methods for the five iodo acids have been developed for a current occurrence study to determine their concentrations in chloraminated drinking water. These iodo acids are of concern not only for their potential health risks but also because early research indicates that they may be maximized (along with iodo-THMs) in waters treated with chloramines. Chloramination has become a popular alternative to chlorination for plants that have difficulty meeting the regulations with chlorine, and its use is expected to increase with the advent of the new Stage 2 D/DBP Rule. Chloramines are generated from the reaction of chlorine with ammonia, and it appears that the length of free chlorine contact time (before ammonia addition to form chloramines) is an important factor in the formation of iodo acids and iodo-THMs. Because of chlorine's competing reaction to form iodate as a sink for the natural iodide, it is likely that plants with significant free chlorine contact time before the addition of ammonia will not produce substantial levels of iodo acids or iodo-THMs.
The bromonitromethanes (including dibromonitromethane, tribromonitromethane, and bromonitromethane) are extremely cytotoxic and genotoxic to mammalian cells (91). Dibromonitromethane is at least 1 order of magnitude more genotoxic to mammalian cells than MX and is more genotoxic than all of the regulated DBPs, except for monobromoacetic acid. Bromonitromethanes have been found to be DBPs formed by chlorination or chloramination and have been shown to increase in formation when preozonation is used before chlorine or chloramine treatment. Bromonitromethanes, iodo-THMs, and brominated forms of MX (so-called BMXs), as well as other priority DBPs were the focus of a U.S. Nationwide DBP Occurrence Study, which was recently published in Environmental Science & Technology (92). This Nationwide Occurrence Study focused on approximately 50 priority DBPs that were selected from an extensive prioritization effort (according to predicted cancer effects). In this study, haloacetaldehydes represented the third major class formed on a weight basis (behind THMs and HAAs). An important finding was that while the alternative disinfectants significantly lowered the formation of regulated DBPs (THMs and HAAs), other high-priority DBPs were increased in formation with alternative disinfectants. For example, iodinated DBPs (iodo-THMs and iodo acids) were increased in formation with chloramination, dichloroacetaldehyde was highest at a plant using chloramines and ozone, and preozonation was found to increase the formation of halonitromethanes. This has important implications for drinking water treatment, as many plants in the United States have switched or are switching to alternative disinfectants to meet the Stage 1 and 2 D/DBP Rule requirements. This study also reports the highest levels of MX analogues to-date, with MX analogues and brominated MX analogues frequently being found at levels above 100 ng/L, and in two plants the sum of these analogues was at low-ppb levels. Finally, 28 new, previously unidentified DBPs were reported, including brominated and iodinated acids, a brominated ketone, and chlorinated and iodinated aldehydes. Despite the fact that more than 90 DBPs were measured in this study, only about 30 and 39% of the total organic halide (TOX) and total organic bromine (TOBr) were accounted for, respectively, by the sum of the measured DBPs. This is consistent with earlier studies that have shown that there is more TOX accounted for in chlorinated drinking water, as compared to drinking water treated with alternative disinfectants.
GC/MS continues to be an important tool for measuring DBPs and identifying new DBPs. However, LC/MS is being increasingly used for highly polar DBPs and high molecular weight DBPs. In fact, this was the focus of a recent review article by Zwiener and Richardson (93). Useful derivatization techniques, as well as related MS techniques, such as ESI-high field asymmetric waveform ion mobility spectrometry (FAIMS)-MS, IC-ESI-MS, and membrane introduction MS (MIMS), are also discussed. This review covered not only traditional DBPs that are formed by the reaction of the disinfectant (oxidant) with NOM but also newly identified DBPs that are formed by the reaction of the disinfectant with contaminants. Examples of those include reaction products with estrogens, alkylphenol ethoxylates, pesticides, and algal toxins.
Brominated and iodinated DBPs have been the focus of several new studies. In an innovative study, Becalski et al. investigated the potential formation of iodoacetic acids during cooking (94). In this study, municipal chlorinated tap water (containing NOM) was allowed to react with iodized table salt (containing potassium iodide) and with potassium iodide itself in boiling water. Samples were extracted with TAME and methylated prior to analysis with GC/MS. Iodoacetic acid and chloroiodoacetic acid were identified as byproducts, and iodoacetic acid was formed at 1.5 g/L levels when the water was boiled with 2 g/L iodized table salt. The concentration of chloroiodoacetic acid was estimated to be 3-5? lower. Hua et al. examined the effect of bromide and iodide on the formation of DBPs during chlorination (95). TOBr, total organic iodine (TOI), and total organic chlorine (TOCl) were measured in this study, as well as THMs, HAAs, and TOX. At higher levels of bromide, there was a decreasing level of unknown TOX and unknown TOCl, but an increasing level of unknown TOBr. The extent of iodine substitution was much lower than bromine substitution because a substantial amount of iodide was oxidized by chlorine to iodate. The tendency toward iodate formation resulted in the unusual situation where higher chlorine doses actually reduced levels of iodinated DBPs. However, this is not the case with chloramination, where iodo-DBPs preferentially form instead of iodate (92). The method for TOCl, TOBr, and TOI analysis is described in a separate paper by Hua and Reckhow (96). After investigating different pyrolysis-IC procedures, the optimum method included a pyrolytic analyzer that uses pure O2 and offline IC combined with a standard TOX carbon (coconut-based). This procedure allowed the most complete recovery of TOCl, TOBr, and TOI. Brominated and chlorinated acetaldehydes were the focus of another study by Koudjonou and Lebel (97). These DBPs were measured in Canadian drinking water with GC/electron capture detection (ECD), and their stability was investigated. Most of the haloacetaldehydes were found in the drinking waters, with chloral hydrate (trichloroacetaldehyde) comprising 7-51% of the total haloacetaldehydes measured, as well as a substantial portion of the total DBPs (as in the U.S. Nationwide Study). Mixed results were obtained for their stability in drinking water-the trihaloacetaldehydes degraded somewhat over time to the corresponding THMs at increasing pH and temperature.
New DBPs continue to be identified. Often, low- and high-resolution EI-MS is used, and sometimes combinations of GC/MS or LC/MS with Fourier transform (FT)-infrared (IR) spectroscopy or NMR are used. In addition, derivatizing agents continue to be developed to aid in the identification of highly polar DBPs, which are largely unaccounted for. Gong et al. used FT-IR spectroscopy, EI-MS, 1H and 13C NMR spectroscopy, and single-crystal X-ray diffraction to identify a new DBP in chlorinated drinking water (98). This DBP was identified as 2,2,4-trichloro-5-methoxycyclopent-4-ene-1,3-dione. Ames test results showed it to be highly mutagenic. Vincenti et al. tested four newly developed fluorinated chloroformate derivatizing agents for identifying highly polar alcohol, carboxylic acid, and amine DBPs in drinking water with GC/negative chemical ionization (NCI)-MS (also referred to as electron capture negative ionization) (99). 2,2,3,3,4,4,5,5-Octafluoro-1-pentyl chloroformate performed the best, with good reaction efficiency, good chromatographic and spectroscopic properties, low detection limits (10-100 fmol), and a linear response over more than 2 orders of magnitude. The entire procedure from raw aqueous sample to ready-to-inject hexane solutions of the derivatives required less than 10 min. This method was used to identify three highly polar ozonation byproducts: malic acid, tricarballylic acid, and 1,2,3-benzenetricarboxylic acid.
Other Occurrence Studies. Huang et al. used GC/high-resolution-EI-MS to comprehensively identify DBPs formed by the ozonation of polluted source waters (100). Fifty-nine different organic compounds were identified, including low molecular weight carboxylic acids, benzoic compounds, aldehydes, bromoform, bromoacetic acid, dibromoacetic acid, 2,4-dibromophenol, and dibromoacetonitrile. When the NOM was fractionated from the source water into humic acid and hydrophilic neutral fractions, different distributions of DBPs were observed in the fractions. Malliarou et al. recently carried out a large survey of HAAs in UK drinking waters (101). Means ranged from 35 to 95 g/L, and a maximum of 244 g/L was observed. In two out of the three regions investigated, there was a high correlation between total THMs and total HAAs, and the ratio of total THMs to total HAAs was significantly correlated with temperature, pH, and free and total chlorine. This study is particularly important because HAAs are rarely measured in Europe, and most epidemiologic studies relate effects back to THMs only. Another large survey was carried out in Athens, Greece, over a 2-year period (102). DBPs measured (by GC/MS) included THMs, haloacetonitriles, haloketones, chloral hydrate, chloropicrin, and nine HAAs. All DBPs were identified in prechlorinated drinking water samples. The most commonly detected DBPs were chloroform, trichloroacetic acid, dichloroacetic acid, and chloroacetic acid. Annual mean concentrations ranged from 1.1 to 61.8 g/L.
Discovery Research for High Molecular Weight DBPs. More than 50% of the TOX formed in chlorinated drinking water remains unidentified, and much higher percentages of TOX are unaccounted for when alternative disinfectants are used (ozone, chloramine, chlorine dioxide). Earlier ultrafiltration studies indicate that >50% of the TOX in chlorinated drinking water is >500 in molecular weight, which would be missed with traditional GC/MS approaches. ESI-MS/MS is allowing researchers to investigate these high molecular weight DBPs. Most of this work is very preliminary, due to the complexity of the mass spectra obtained ("a peak at every mass" situation). Minear's group at the University of Illinois has carried out much of the pioneering work in this area. In a follow-up study to their earlier work, Zhang and Minear used radiolabeled chlorine (36Cl) to further probe high molecular weight DBPs formed upon chlorination of drinking water (103). Results of this study showed that oxidation was the dominant reaction compared to halogenation and that high molecular weight DBPs decreased when the chlorine contact time was increased. High molecular weight DBPs could not be separated into discrete LC peaks.
NDMA and Nitrosamines. NDMA is a probable human carcinogen, and NDMA and other nitrosamines were recently discovered to be DBPs in drinking water. NDMA can form in chloraminated or chlorinated water. 15N-Labeling studies have shown that the nitrogen present in monochloramine becomes incorporated into the structure of NDMA. And, as with iodo-DBP formation, the length of free chlorine contact time prior to ammonia addition to form chloramines can be an important factor in the formation of NDMA. Charrois and Hrudey published a recent study showing that a free chlorine contact time of 2 h (before ammonia addition) resulted in significant reductions (up to 93%) in NDMA formation (104). Chlorination can also form NDMA, when nitrogen precursors are present (e.g., natural ammonia in the source water or nitrogen-containing coagulants, such as diallyldimethylammonium chloride, used in water treatment). NDMA was initially discovered in chlorinated drinking waters from Ontario, Canada, and has since been found in other locations. The detection of NDMA in U.S. waters is largely due to improved analytical techniques that have allowed its determination at low-nanogram per liter concentrations. NDMA is generally present at low nanograms per liter in chloraminated/chlorinated drinking water, but it can be formed at much higher levels in wastewater treated with chlorine. Following its discovery in California well water, the State of California issued an action level of 0.002 g/L (2 parts per trillion) for NDMA, which was subsequently revised to 0.01 g/L, due to the analytical difficulty in measuring it at the original proposed level (www.dhs.ca.gov/ps/ddwem/chemicals/NDMA). NDMA is not currently regulated in the United States for drinking water, but is now included on the UCMR-2, where occurrence data are being collected on a national scale for NDMA and other nitrosamines. Ontario has issued an interim maximum acceptable concentration for NDMA at 9 ng/L (www.ene.gov.on.ca/envision/gp/4449e.pdf). Andrzejewski et al. published a nice review on NDMA in 2005, where its toxicological issues, mechanisms of formation in drinking water treatment, and physiochemical properties are discussed (105). This review also cites the possibility of NDMA being formed with chlorine dioxide disinfection.
To-date, all methods to measure NDMA have been GC/MS(/MS) or GC/ECD methods, including the EPA method created to measure nitrosamines (EPA Method 521). Zhao et al. created the first LC/MS/MS method to measure nitrosamines and, in doing so, identified two new nitrosamine DBPs in drinking water-nitrosopiperidine and nitrosodiphenylamine (106). LC/MS/MS was essential for detecting nitrosodiphenylamine, as it is thermally unstable and cannot be measured by GC/MS. An isotopically labeled NDMA standard was used as the surrogate standard for determining recovery, and isotopically labeled N-nitrosodi-n-propylamine was used as an internal standard for quantification. Detection limits ranged from 0.1 to 10.6 ng/L. Measurements in a drinking water distribution system revealed that nitrosamine concentrations increased with increasing distance from the water treatment plant, indicating that the amount of formation was greater than the amount of decomposition. Cheng et al. expanded and refined three previously existing GC/MS/MS methods for measuring nitrosamines in drinking water, wastewater, and recycled water (107). Detection limits for two SPE-GC/MS/MS methods ranged from 0.3 to 1.4 ng/L, and detection limits for a micro-liquid-liquid extraction-GC/MS/MS method ranged from 2 to 4 ng/L. These methods were used to measure NDMA and several other nitrosamines in drinking water, wastewater, and recycled water in California. In drinking water, NDMA was the only nitrosamine detected, but other nitrosamines were present in recycled water and wastewater. Cha et al. reported a new LC-fluorescence method for measuring NDMA in water (108). Samples were denitrosated and derivatized with dansyl chloride for fluorescence detection. Detection limits of 10 ng/L could be achieved. This method did not suffer interferences even in complex wastewater samples. Grebel et al. developed a new SPME method for extracting seven nitrosamines from water (109). SPME could be used with nitrogen chemiluminescence detection, nitrogen-phosphorus detection, or chemical ionization (CI)-MS. Detection limits for NDMA ranged from 30 to 890 ng/L.
Mechanistic Studies. Researchers continue to explore the mechanism of formation of nitrosamines. Schreiber and Mitch examined the importance of chloramine speciation and dissolved oxygen on the formation of nitrosamines (110). Dichloramine and dissolved oxygen were found to be critical in their formation, and a new nitrosamine formation pathway was proposed, in which dichloramine reacts with secondary amine precursors to form chlorinated dialkylhydrazine intermediates. Oxidation of these intermediates by dissolved oxygen to form nitrosamines competes with their oxidation by chloramines. This new model was able to explain the formation of nearly all nitrosamine species. Chen and Valentine developed a kinetic model to validate proposed reactions and predict NDMA formation in chloraminated drinking water (111). Inputs to this model include chloramine demand, a coefficient relating the amount of NDMA produced to the amount of NOM oxidized, and other kinetic parameters describing NOM oxidation. NOM oxidation was determined to be the rate-limiting step governing NDMA formation.
Mechanistic studies have also been carried out for other DBPs, including cyanogen chloride, N-chloroaldimines, and ozonation DBPs. Lee et al. examined 17 amino acids as potential precursors for CNCl in chlorinated drinking water (112). Among these amino acids, only glycine was found to produce detectable CNCl, and the glycine nitrogen was stoichiometrically converted to CNCl at pH <6. From examinations of river water, it was estimated that glycine may account for 42-45% of the CNCl formed (at pH 8.2). In another study by Freuze et al., amino acids were investigated as precursors to DBPs involved in an odor episode in Paris (113). The reaction of several amino acids with chlorine was investigated to solve the odor mystery. N-Chloroaldimines were identified in these amino acid-chlorine reactions by GC/MS, and they were suspected of being the DBPs responsible for the odor episode. Finally, These and Reemtsma used size exclusion chromatography with Q-TOF-MS to examine ozone DBP formation of different NOM fractions (114). A preferential reaction with fulvic acids at a low oxidation state (low O/C ratio) and a high degree of unsaturation (low H/C ratio) was observed, and the data suggested that molecules with a more extended carbon skeleton and fewer carboxylate substituents are more reactive with ozone.
Other New DBP Methods. Several new methods have been developed for the measurement of DBPs (beyond nitrosamines mentioned earlier). Khan et al. reported a new aqueous-phase aminolysis method to measure epoxides in water (115). This method also uses SPE, silylation, and GC/MS analysis. With this method, 1,2-epoxybutane, epichlorohydrin, and epifluorohydrin could be measured at 5-10 ng/L detection limits. Onstad and Weinberg created a refined method using liquid-liquid extraction, methylation, and GC with micro-ECD or ion trap-MS detection for measuring halogenated furanones (MX analogues) in drinking water (116). A preconcentration factor of 1000:1 allowed low-nanogram per liter detection limits. This method was used to measure the 12 halogenated furanone species in the U.S. Nationwide Study discussed earlier. Yang and Shang created a new MIMS method to quantify CNCl and cyanogen bromide in water (117). A linear response over 3 orders of magnitude was achieved, and CNCl and CNBr could be measured down to limits of 1.2 and 3.8 g/L, respectively. Recoveries were >93%. A new SPME-GC/ECD method to measure 2,4,6-trichloroanisole in chlorinated drinking water was also developed (118). Detection limits and quantification limits of 0.7 and 2.5 ng/L, respectively, were achieved. THMs could also be measured with this method. De Borba et al. created a new IC method to measure bromate in municipal and bottled drinking waters (119). This method utilized an electrolytically generated hydroxide eluent combined with a hydroxide-selective anion-exchange column and was able to provide significant noise reduction, along with 0.5 g/L detection limits.
Several new continuous, online methods have also been recently developed, and these have the promise of being used in water treatment plants to allow real-time determination of DBPs. Wang et al. developed a new continuous hollow-fiber, liquid-liquid membrane extraction-LC/UV method to measure HAAs in drinking water (120). Method detection limits were at sub-ppb levels. Simone et al. developed an online IC method for HAAs that uses a postcolumn reaction with nicotinamide and fluorescence detection (121). Detection limits of 0.5-5 g/L were achieved, and this on-line method was compared to EPA Method 552.3. Finally, Brown and Emmert developed a new on-line method for THMs, using capillary membrane sampling and GC/ECD detection (122). Method detection limits were in the 0.5 g/L range. This method was compared to EPA Method 502.2, and it offers advantages for monitoring a drinking water distribution system because it is a near real-time method and can be used at remote locations in the distribution system.
New Human Exposure Studies. Researchers have been investigating other routes of exposure, besides ingestion, in new human exposure studies of drinking water DBPs. And, in many cases, inhalation and dermal exposures that would result from bathing or showering offer greater exposures to particular DBPs than ingesting 2 L of water per day. Exhaled breath is often a convenient, noninvasive way to assess a person's exposure, either dermally or through inhalation. Once a DBP has been absorbed either through the lungs or through the skin, it is transported to the blood stream, where it can be released in exhaled breath from the lungs. Blood measurements are more invasive, but can be more precise measures of exposure. It is of particular interest to epidemiologic studies to know the entire dose of specific DBPs being investigated for effects. Xu and Weisel investigated the dermal absorption of 1,1-dichloropropanone, 1,1,1-trichloropropanone, and chloroform in human volunteers (in their exhaled breath) following a 30-min bath (123). The maximum haloketone breath concentration ranged from 0.1 to 0.9 ug/m3, which were approximately 2 orders of magnitude lower than the maximum chloroform breath concentrations. The permeability of chloroform was found to be much higher than the permeability of the haloketones. Gordon et al. carried out a human exposure study that investigated breath and blood THM levels from 12 common household water-use activities (124). Water, indoor air, blood, and exhaled breath samples were collected during each exposure activity. Although showering (10 min), bathing (14 min), machine washing of clothes, and opening dishwashers at the end of the cycle resulted in significant increases in indoor air chloroform levels, only showering and bathing caused significant increases in breath chloroform levels. For bromodichloromethane, only bathing produced significantly higher concentrations. For chloroform from showering, strong correlations were observed for indoor air and exhaled breath, blood and exhaled breath, indoor air and blood, and tap water and blood. Evidence of the importance of dermal and inhalation routes for DBPs, a new epidemiologic study by Villanueva et al. revealed a higher risk of bladder cancer from showering, bathing, and swimming in pools (125). Long-term THM exposure was associated with a 2-fold bladder cancer risk (odds ratio of 2.10) for average household THM levels of >49 g/L. The odds ratio for ingestion was 1.35 (compared to people who did not drink tap water), and the odds ratio from showering and bathing was 1.83.
New Swimming Pool Research. Related to other research involving alternate exposures to ingesting drinking water, swimming pool studies have shown a marked increase in the last 2 years. The Villanueva et al. epidemiologic study mentioned earlier showed an odds ratio of 1.57 for swimming in pools and developing bladder cancer (125). Zwiener et al. published a review article on swimming pool waters, detailing the adverse health effects (including asthma, bladder cancer, and endocrine effects), the formation of DBPs in swimming pool water, and precursor chemicals that give rise to them (126). Details on swimming pool operation and treatment are also given. Glauner et al. investigated the elimination of swimming pool DBPs using ozonation and advanced oxidation processes (ozone/UV and ozone/hydrogen peroxide) (127). Advanced oxidation processes (AOPs) substantially reduced the levels of TOC, adsorbable organic halogen, and THMs. A contact time of 3 min between the pool water and the oxidants was found to be sufficient for lowering DBP levels. Ozonation showed a small advantage to AOPs in removing THMs, and the combination of membrane filtration and AOPs resulted in the elimination of 10-90% of the DBPs and their precursors. The ozone/hydrogen peroxide process was recommended for pool water treatment because of higher elimination rates compared to ozonation alone and lower costs as compared to ozone/UV treatment.

http://www.spectroscopynow.com/coi/cda/detail.cda?id=18193&type=Feature&chId=7&page=1
March 1, 2008
Breathe easy when you're in the swim
Ernest Blatchley III and colleagues at Purdue University, Illinois, are learning how to reduce the production of irritating and unhealthy volatile compounds in swimming pools by turning to ultraviolet technology to complement the use of chlorinated disinfectants.
Most swimmers are familiar with the odour of their pool. That strong smell of "chlorine" is not, however, due to chlorine gas at all. Instead, it is the smell of volatile byproducts formed when chlorinated disinfectants react with sweat and urine in the water.
These volatile chloramines and other contaminants have in recent years been targeted as a possible risk factor for respiratory problems not only in pool users but among poolside staff, such as lifeguards and attendants. Understanding how these volatile contaminants are formed in various reactions could take us a stroke closer to making indoor swimming pools healthier.
"If the concentrations of those volatile byproducts gets high enough, then they can become an irritant to your respiratory system, to your skin and to your eyes," explains Blatchley. The issue received widespread media coverage in the US in 2007 when the U.S. National Swimming Championships in Indianapolis were interrupted after swimmers experienced difficulty breathing.
Unfortunately, the conventional chemical tests carried out on the poolside to evaluate pH and "chlorine" levels in the water, do not test for organic compounds, such as chloramines. However, Blatchley, working with post-doctoral research associate Jing Li in Purdue's School of Civil Engineering, published details last year in the journal Environmental Science & Technology explaining why these organic contaminants ought to be tested and outlining how this might be done. They now have new data, based on work by graduate students William Weaver and Yuli Wen and undergraduate student Jessica Johnston, which is scheduled to appear later this year in ES&T and will be presented to the World Aquatic Health Conference in Colorado Springs, Colorado during October.
Michael Beach, of the Centers for Disease Control and Prevention's National Center for Zoonotic, Vector-borne and Enteric Diseases, explains that the research is part of an effort to bring the scientific rigour of drinking-water chemistry to the wider aquatics industry. "If you don't understand what's in the soup, you can't know how to treat the water," he says, "The Purdue research is finding all sorts of compounds that could have potential health effects." He adds that as a major public health issue, such research is critical but more data are needed.
"It's amazing how little we know about swimming pool chemistry," Blatchley said. "And that's why we have pools being shut down for reasons that are probably avoidable. We want to solve this problem so that businesses and municipalities can operate their swimming pools in a manner that doesn't cause people to get sick." It is not just about byproducts of disinfectants reacting with sweat and urine, Blatchley and his team are also investigating the byproducts of personal care products, such as makeup, deodorants and perfume that for some reason many swimmers see fit to apply prior to taking a dip.
Using membrane introduction mass spectrometry, the researchers analysed swimming pool water for the presence of organic compounds formed from creatinine, urea and amino acids, which are found in human urine and sweat. Their results suggest possible mechanisms by which these compounds are formed. "We focused on a couple of the amino acids that we believe are representative of those that are present in sweat and urine and likely to be present at high concentrations in swimming pool water," Blatchley explains. They have tested numerous public pools and are building up a profile of volatile disinfection byproducts.
The next stage of the process is to figure out how these various byproducts might be broken down. After all, there is only so much policing of pool users that can be done to ensure they shower before swimming, not urinate in the pool and remove cosmetics and deodorants before diving in. The new research focuses on whether ultraviolet radiation might be used to degrade disinfection byproducts quickly and safely.
Blatchley explains that most are broken down to nitrates and nitrous oxide. "Currently, we know where about 75 percent of the nitrogen goes, and we think we know where most of the rest of it goes, but we need to do some experiments to confirm that," he concedes.
The same results may also have implications for drinking water quality in places where UV is used in conjunction with chlorinated disinfectants. "The chemistry is very similar in both settings," says Blatchley, "so our interest is broader than just swimming pools."
Related links:
• Environ Sci Technol, 2007, 41, 6732-6739
• World Aquatic Health Conference 2008
• Blatchley Page
Article by David Bradley
http://www.cdc.gov/healthyswimming/irritants.htm
April 25, 2007
Irritants (Chloramines) and Indoor Pool Air Quality
Pool operators may be getting complaints from swimmers and pool staff about stinging eyes, nasal irritation, or difficulty breathing after being in the water or breathing the air at swimming pools, particularly indoor pools. New research indicates that these symptoms may be an indication of poor water and indoor air quality at the pool caused by a build-up of irritants, known as chloramines, in the water and air.
Irritants in the air at swimming pools are usually the combined chlorine by-products of disinfection. These by-products are the result of chlorine binding with the sweat and urine from swimmers using the pool. As the concentration of by-products in the water increases, they move into the surrounding air as well. Breathing air loaded with irritants can cause a variety of symptoms depending on the concentration of irritants in the air and amount of time the air is breathed. The symptoms of irritant exposure in the air can range from mild symptoms such as wheezing, to severe symptoms such as lung disease and, potentially, asthma1-3. It is also known that routine breathing of irritants may increase sensitivity to other types of irritants such as fungi and bacteria.
The buildup of these irritants in the air is partially due to poor air turnover. The poor movement of fresh air over the pool surface, combined with the use of air recycling devices to control heating costs, leads to poor air exchange. Recyclers remove the moisture from the air, but they do not necessarily take in much fresh outside air. This may save money on heating, but the health risks to patrons and staff associated with the excessive use of these devices outweigh the financial benefits2. Without adequate fresh air, the recycled air flowing over the pool becomes saturated with chlorination by-products so that it can no longer absorb or pick up new by-products coming from the pool water. Because recyclers do not remove all of the by-products in the air, they allow the irritants to accumulate and reach unhealthy levels. In addition, if the air is saturated with irritants, new irritants produced in the water will stay in the pool water causing further irritation, such as stinging or red eyes, for swimmers. Fresh air is important; super chlorination can be an effective way to rid the pool water of these by-products but will not work if the air is saturated with irritants.
The problem of poor indoor air quality can be fixed through a combination of prevention measures. Improving air movement over the pool and increasing the air turnover rate will reduce irritant levels in the air. One option is to open all of the doors and windows in the pool area or use fans to boost airflow over the pool surface when many swimmers are using the pool. When super chlorinating, do the same. Also, ensure that the air recycling systems are bringing in enough fresh air. Adequate disinfectant levels and constant monitoring of water quality can also help reduce irritant levels by decreasing combined chlorine formation in the water. Combined chlorine levels in the water may be reduced by adding supplementary disinfection systems such as ultraviolet light or ozone. In addition, good hygiene is needed. Getting swimmers to shower before getting in the pool and promoting regular bathroom use to reduce the amount of urine in the pool will decrease the formation of irritants.
For the health of pool staff and patrons, remember that all indoor pools need adequate fresh air exchange and all pools need good water quality. This will help make all pools a healthier and more enjoyable place to play and work.
For more information on the topic:
1. Bowen A, Kile J, Austin C, Otto C, Blount B, Kazerouni N, Wong H-N, Mainzer H, Mott J, Beach MJ, Fry AM. Outbreaks of short-incubation illness following exposure to indoor swimming pools. Environ Health Perspect, 2007; 115: 267-271.
2. Emanuel BP. The Relationship Between Pool Water Quality and Ventilation. Environmental Health, 1998; 2: 17-20.
3. Ratner J, Griffiths T. Exercise-Induced Asthma and Indoor Swimming Pools. Parks and Recreation. 1995; 7: 46-51.
http://www.aquaticsintl.com/2006/oct/0610_air.html
October 2006
Air Sickness
New studies suggest indoor aquatic environments can trigger, or even cause, asthma and other respiratory ailments, opening the door for complaints and lawsuits. Here’s how to stay on top of this emerging issue and keep the air healthy. by Rin-rin Yu
The high school swim team was the first to notice. After practice, a handful of athletes would leave the pool coughing like smokers, their eyes red and noses swelling. Other swimmers suffered from dizzy spells, skin rashes, eye and nose irritations, and tight chests. The asthmatics in the group had it even worse, heaving and wheezing their way into the locker rooms. And their numbers seemed to be growing.
“Usually, we’d see one or two cases a year of kids with asthma,” says Dennis Majewski, director of district services at the Franklin Regional School District in Murrysville, Pa. “But we started seeing students who have no historical medical problems get irritations.”
Majewski carefully monitored the HVAC system and chlorine levels, but they remained within accepted parameters. Finally, he and his staff discovered the problem: The chlorine byproducts were making the swimmers sick. More precisely, they were making the air sick.
The main culprit, chloramines, are known asthma attack triggers. The higher the chloramine level, the more severe the attack. While Majewski and other aquatics professionals might be surprised that indoor aquatic environments can cause such health problems, scientists are not. Research has long suggested that prolonged exposure to chlorine byproducts can damage the lungs, which makes children and adults more susceptible to a host of respiratory illnesses. Chief among them is asthma, which shot up 160 percent between 1980 and 1994. Since then, rates have stabilized, but continue to climb.
While no one is solely blaming indoor pool environs, new studies are making the link to asthma and other respiratory illnesses difficult to deny. A controversial new Belgian study correlates high asthma rates with high numbers of indoor aquatics facilities. Meanwhile, new trends in aquatics design, everything from spraypads to energy-saving air systems, are only exacerbating the problem.
Indeed, indoor air quality issues have attracted the attention of the Centers for Disease Control in Atlanta. It is in the midst of a major study into the use of UV to control chloramines and improve air quality. Michael Beach, the CDC aquatics guru leading the fight against recreational water illnesses, calls air quality the next big issue for the aquatics industry.
It’s easy to see why. Connections between aquatic environments and respiratory illness could saddle indoor facilities with unhealthy reputations and set off a new round of lawsuits, warn experts. That, in turn, could hobble the growing aquatic exercise and therapy market, and the burgeoning waterpark resort industry. To avoid that fate, experts say, operators must recognize the problem and diffuse it or risk an industrywide air quality problem of epidemic proportions.
The diagnosis
In general, more children under age 5 are developing asthma every year. Out of 20 million Americans who suffer from this condition, 9 million are under age 18, according to the CDC’s National Center for Health Statistics. Scientists say lung damage can occur if children and adults are exposed regularly to disinfectant byproducts for long periods. And a number of studies show that young asthmatics who started swimming indoors are more likely to develop symptoms than those who swim outdoors or not at all.
In 1998, researchers at the National Jewish Medical and Research Center in Denver concluded that spray features, which created an aerosol of chlorinated water and byproducts, caused people to develop granulomatous lung disease, which they dubbed “lifeguard lung.” This disease also is caused by exposure to bacteria in inadequately ventilated air for long periods of time.
Mostly recently, a study at the Catholic University of Louvain in Brussels, Belgium, released in July found that for every extra pools per 100,000 inhabitants, European asthma rates increased by 2.7 percent in children 13-14; for 6- to 7-year-olds, rates increased 1.5 percent. “Trichloramine accumulating in the air of indoor swimming pools is one of the most concentrated lung toxicants to which children of developed countries are regularly exposed,” the study stated.
A similar study in Sweden examined the blood levels of a lung-specific protein called Clara cell protein, which protects the lungs. Those who went to indoor pools more often had significantly lower levels of Clara cells than those who did not.
Still, some doctors say this link is hardly conclusive. “I have not seen any harmful or negative effects [from swimming],” says Dr. Clifford Bassett, medical director at Allergy and Asthma Care of New York. “My opinion is based upon accumulated clinical data that swimming is generally a good thing and beneficial to most people with asthma.”
Others agree. “It’s highly unlikely that the rise [in asthma] we see across all industrialized countries is simply related to the presence of chlorinated swimming pools,” says Dr. Norman H. Edelman, chief medical officer of the American Lung Association in New York.
Jeff Sloan of the Chlorine Chemistry Council questions the measurement of the indoor air quality in the studies. “They don’t know what the kids were actually exposed to,” says the director of disinfection issues for the Arlington, Va.-based CCC. “Chlorine has been used for hundreds of years, safely and properly.”
But prominent aquatics experts admit the industry has a problem. “It’s very clear there’s a definite link between chronic chloramines and respiratory illnesses,” says Tom Griffiths, Ed.D., director of aquatics and safety officer for athletics at Penn State University in University Park, Pa. He calls air quality the “next new wave of litigation against facility operators.”
The cause
To understand why and how to head off that wave operators must first understand the relationship between air and water quality. As chlorine sanitizes, it creates an invisible vapor cloud of disinfection byproducts over the water. Concentrations depend on temperature, amount of chlorine, pH levels and air circulation.
When patrons complain of an overwhelming chlorine odor commonly referred to as the “pool smell,” what they’re really inhaling are chloramines, experts say. Chloramines result from chlorine killing off bacteria, and viruses and reacting with the ammonia found in sweat, urine and saliva. This process creates three types of chloramines: monochloramines, dichloramines and nitrogen trichloride, also known as trichloramines.
Another sanitization byproduct is trihalomethane, which in great amounts, can cause dizziness and respiratory issues. One common form of THM is chloroform, once used as an anesthetic by doctors. Studies with laboratory animals have shown that ingesting large amounts of THM can cause damage to the liver, kidneys and central nervous system. THM is a human carcinogen and may cause cancer if exposure happens regularly and for a prolonged period of time. According to the CDC, breathing 900 ppm can cause dizziness, fatigue and headaches. A typical natatorium contains up to .13 ppm; ambient air contains up to .00005 ppm.
Haloacetic acids form another sanitization byproduct that, when ingested in large quantities, can cause cancer in lab animals, though it has not been determined if it will affect humans. And it would be hard for someone to even know because these byproducts cause damage slowly over time, says June M. Weintraub, Sc.D., senior epidemiologist at the San Francisco Department of Public Health.
While damage may be prevalent in some, individual sensitivities vary. “Some might not notice there’s a chemical odor … but chemical odors can be problematic for others,” says Mike Tringale, director of communications at the Asthma and Allergy Foundation of America in Washington, D.C. “You can have a huge Olympic stadium vs. a hotel pool and get different outcomes.”
Further chlorination at higher levels can eliminate these odors, but other methods ventilation, filtration and UV systems exist to get rid of them. The problem, however, is that many facilities don’t apply these methods, experts say. As a result, patrons and staff constantly breathe in noxious fumes, sometimes with debilitating results.
At the same time, Griffiths says more cases of respiratory illnesses and asthma are occurring because more users are in the pool. He attributes the growth to the popularity of aquatic exercise, masters swimming and swim lessons for kids. Coaches are drilling swim teams to put in more mileage, extending their time in the pool and producing more sweat. The ammonia from the sweat binds with chlorine to produce chloramines. Griffiths personally receives more phone calls and written correspondence regarding chloramine problems from facilities around the country. In fact, he says he’s received “more this year than my entire career here.”
In addition, as traditional pools evolve into leisure pools, they offer more hours of sliding, splashing and spraying. This translates into more hours of chloramine exposure in the form of vapor hovering above the pool and in the fine aerosol that sprays from water cannons, jets and waterfalls. Meanwhile, the indoor waterpark has become a rising star, where children and families while away entire weekends for hours on end.
“We’re changing the types of pools we have to ones that spray and agitate from waterfalls to pop jets to hydrotherapy jets that just aerosolize [chloramines],” says Alison Osinski, Ph.D., president of Aquatic Consulting Services in San Diego. “We’re putting it in a form that’s easier to breathe.”
What’s also happening, she says, is that while more chloramines are filling the air, less fresh air is being exchanged. As facilities adopt more energy-efficient ventilation systems, the bad air is being recirculated to conserve heating costs. “In an attempt to be energy efficient, we’ve caused a problem in the natatorium,” she says. “We really didn’t have this problem 30 years ago. But we also had very energy-inefficient air handling systems.”
Griffiths blames energy-efficient systems for the heightened chloramine levels, too. “The pools with the best air quality will be the worst in terms of energy conservation,” he says.
In addition, many water supply companies now are using monochloramines to treat tap water. Because chlorine creates carcinogenic byproducts even though levels are strictly regulated by the Environmental Protection Agency, some areas have switched to disinfection that uses monochloramines. Unlike chlorine, monochloramines work slower, react with organic matter less often, and create fewer carcinogens in drinking water.
When fresh water is added to pools, the chloramine levels rise. In Majewski’s case, his chloramine levels were at 2.8 ppm, and he was fighting to lower them to 2.2 ppm. “We had 10 times the chloramines coming into the water than we were trying to maintain,” he says.
Some experts say breakpoint chlorination will reduce those levels, while others say it is impossible to shock a pool that often. In the pool, monochloramines will react to form dichloramines and nitrogen dichloride to produce the pool smell unless further chlorine is added, says Tom Lachocki, CEO of the National Swimming Pool Foundation in Colorado Springs, Colo. Because indoor pools can require up to a daily dose of fresh water, pools may need to be shocked daily as well, at 10 times the chloramine level.
The prescription
The problem is not easily solved, but there are some simple ways to bring down chloramine levels.
In its first International Recreational Water Guidelines, the World Health Organization of Geneva, Switzerland, recommends 10 liters of fresh air per second per square meter of water surface area in indoor swimming arenas. Many U.S. codes require only about 15 percent air turnover, whereas Osinski says a system should never exchange less than 40 percent fresh air. “One hundred percent fresh air is what we want,” she says. Higher rates of exchange are healthier, but more expensive.
A second method, also costly up front, is the installation of an ultraviolet system to zap chloramines. Systems cost approximately $30,000 to purchase and install, and $3,000 annual operating costs. But that price seems worth it to those who have tried it. Majewski has joined that camp. Since installing his UV system chloramine levels have never risen above 2 ppm. “It seemed too good to be true,” Majewski says. “But we monitor it every day.”
The swimmers at Lawrence Indoor Aquatic Center in Lawrence, Kan., also have been enjoying an odor-free pool for the past four years. “We were seeing a higher incidence of some respiratory distress,” says Jimmy Gibbs, aquatics manager. “We still have to have chlorine, but [the system] allowed us to put a significantly less amount.”
While all of the evidence so far is anecdotal, the CDC is working on a study to determine just how much UV systems can reduce chloramines. The results should be ready by the beginning of 2007, says Beach, who is team leader, water and environment activity, Division of Parasitic Diseases at the CDC.
Maintaining a proper pH level is another key way to minimize nitrogen trichloride formation. Nitrogen trichloride is formed when the water is more acidic, while monochloramines thrive in more alkaline water levels.
Installing and maintaining a thorough filtration system also will help improve air quality. Granular active carbon lowers chloramine levels and removes other compounds such as THM. Adding zeolite to filter mediums will retain ammonia in the tank, Griffiths says.
In addition, educating patrons about pool air quality and how they can take responsibility in its improvement can eliminate a large part of the problem. Explaining why showering beforehand is essential and enforcing it will send the message. Pool managers can form a working relationship with asthmatic swimmers who fear the air quality would be more detrimental to their health. “Managers have a responsibility to talk to members and have a plan if there are problems,” Tringale says.
Other experts say managers should encourage asthmatic patrons to talk to their doctors about what their potential triggers may be, and future studies should consider the same questions. “The critical components here are the timing,” says Mark Nieuwenhuijsen, Ph.D., reader in environmental epidemiology at the Imperial College in London. “Does swimming come before the onset of asthma or vice versa? And the exposure assessment what is the level of the contaminants?”
Tringale agrees. “[Asthma is] a custom-made disease. It really all depends on the person and the particular pool environment,” he says. “We encourage swimmers and parents of swimmers to talk to their doctors about better identifying what their triggers are.”
Operators should protect their staffs, too. Gibbs maintains close communication with his lifeguards and instructors to ensure they stay healthy on the job. “We take it very seriously,” he says. “If anybody feels something is wrong, we’ll do what we can to investigate it.” One suggestion: Rotate them regularly and encourage them to take a walk outside for fresh air. Sometimes staff members are the best measures for indoor air quality.
Finally, let the community know how safe and beneficial the pool can be, and the steps being taken to ensure excellent air quality. Lawrence Indoor Aquatic Center’s UV system made the local news, reinforced its positive image and, as word spread, other operators called Gibbs for information. Most importantly, the reassurance brought swimmers back.
“People want to feel safe,” Gibbs says. “They are more aware of their environments than they were in the past, and more people are sensitive about chemicals now.”
http://www.cdc.gov/mmwR/preview/mmwrhtml/mm5636a1.htm
September 14, 2007
Ocular and Respiratory Illness Associated with an Indoor Swimming Pool --- Nebraska, 2006
On December 26, 2006, the Nebraska Department of Health and Human Services (NDHHS) received a report of a child hospitalized in an intensive care unit for severe chemical epiglottitis and laryngotracheobronchitis after swimming in an indoor motel swimming pool. The pool was inspected the same day and immediately closed by NDHHS because of multiple state health code violations. NDHHS initiated an outbreak investigation to identify additional cases and the cause of the illness. This report describes the results of that investigation, which indicated that 24 persons became ill, and the outbreak likely was the result of exposure to toxic levels of chloramines* (1,2) that had accumulated in the air in the enclosed space above the swimming pool. This outbreak highlights the potential health risks from chemical exposure at improperly maintained pools and the need for properly trained pool operators to maintain water quality.
The index patient was an otherwise healthy boy aged 6 years. The boy and his family attended a gathering with relatives at the motel on December 25, 2006, and he spent approximately 3 hours swimming in the pool. During this time, he had onset of coughing and dyspnea. He stopped playing in the pool but continued to cough, with one or two episodes of posttussive emesis. His parents had intended to spend the night at the motel but checked out early and returned to their home (approximately 15 miles away) the evening of December 25. During a period of 5 hours, the boy's condition worsened. He became agitated and more dyspneic and was taken to a local emergency department (ED) with erythematous eyes and nasopharynx, a barking cough, inspiratory stridor, expiratory wheezes, and respiratory distress. The parents told the physician that multiple persons in their group had developed burning eyes, nasal burning, congestion, and cough. Physical examination of the boy indicated croupy cough, stridor at rest, and moderate retractions. Oxygen saturation level was 98% on room air; lungs were clear on auscultation, and no chest radiograph was performed. In the ED, he received a dexamethasone injection, 3 doses of racemic epinephrine, and cool-mist respiratory therapy. He was transferred to the pediatric intensive care unit in stable condition for observation, with a guarded prognosis and a diagnosis of upper airway obstruction from chemical epiglottitis and laryngotracheobronchitis; drug therapy was discontinued, and no additional treatments were administered. The boy's condition gradually improved, and he was discharged the next morning. The attending physician recorded chlorine irritation as the cause of illness.
Investigators learned that the motel belonged to a national chain. The indoor, heated pool measured 40 ? 32 feet and had a maximum capacity of 70 persons. The immediate pool area was contained within a larger enclosed courtyard area with a single exhaust fan for ventilation in the ceiling directly above the pool. Adjacent guest rooms opened directly into the enclosed courtyard.
From the motel registry that recorded the name of a single guest per room, NDHHS identified 110 rooms with at least one guest registered during December 15--26, 2006, and attempted to contact these persons by telephone. Registered guests were asked whether they or other persons in their party experienced illness during their stay. Those who reported illness were asked to complete an online questionnaire; responses from persons without Internet access were collected by telephone. Information was collected regarding basic demographics; exposure to the pool, immediate pool area, or enclosed courtyard; time from exposure to illness onset; symptoms of illness; and whether medical treatment was required. A case was defined as ocular or respiratory illness in a motel guest during December 15--26, with illness onset after arrival and characterized by at least one of the following symptoms: burning eyes, sore throat, watery eyes, coughing, sneezing, burning inside the nose, wheezing, chest tightness, or shortness of breath.
NDHHS attempted to contact by telephone all 110 motel guests registered during December 15--26 and reached 67 (61%). Among those persons and other guests staying with them, 24 had illness consistent with the case definition; 16 were male, and eight were female, with a median age of 39 years (range: 4--71 years). In addition to the case definition symptoms, the 24 reported other symptoms (e.g., headache, blurry vision, or dry mouth) (Table 1).
Of 24 persons reporting illness, 20 (83%) had entered the immediate pool area, and four (17%) had entered the courtyard only. Among the 20 who entered the immediate pool area, 14 reported exposure for >1 hour, and six reported exposure for 30--60 minutes; 14 (70%) had onset of illness within 2 hours of entering the area (Table 2). Of five persons who sought medical care, three reported swimming in the pool, and two had entered the immediate pool area only. Four of the five persons were children aged <16 years; only the boy aged 6 years (the index patient) was hospitalized.
Nebraska health code regulations require clean and clear public swimming-pool water with a clearly visible main drain (3). Acceptable water-chemistry values for swimming pools are as follows: free chlorine, 2--10 ppm; pH, 7.2--7.8; and chloramine (measured as combined chlorine†), <0.5 ppm (3). Inspection of the motel pool on December 26 revealed multiple state health code violations, including cloudy water, a free chlorine level (0.8 ppm) less than half the minimum, a chloramine level (4.2 ppm) eight times the maximum, and a pH (3.95) approximately half the minimum. Less severe violations included low alkalinity, inadequate daily logs, and an inoperable flow meter. Review of operator logs indicated deterioration of the pool's water quality during the weeks preceding the outbreak.
Before pool closure, the operator recorded inadequate combined chlorine levels for 26 consecutive days. Each log entry for combined chlorine on these days was at least three times higher than the acceptable limit of 0.5 ppm, ranging from 1.8--7.0 ppm. During this same period, the operator also recorded pH levels below the lowest acceptable limit of 7.2 on 14 of 26 days and free chlorine levels below the lowest acceptable limit of 2.0 ppm on 5 of 26 days. In addition to improper management of the water chemistry, the ceiling exhaust fan was turned off at the time of the outbreak, and the outside windows of the enclosed courtyard were closed because of cold outdoor air temperatures.
The pool was closed on December 26 and subsequently drained. It reopened February 7, 2007, and no additional illnesses have been reported.
Reported by: T Safranek, MD, S Semerena, MBA, T Huffman, M Theis, Nebraska Dept of Health and Human Svcs. J Magri, MD, T Török, MD, Office of Workforce and Career Development; MJ Beach, PhD, Div of Parasitic Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases; B Buss, DVM, EIS Officer, CDC.
Editorial Note:
Swimming is the most popular recreational activity among children in the United States and the second most popular exercise activity for all ages, with approximately 360 million visits to recreational water venues each year (4). Throughout the country, swimming-pool operators are responsible for proper maintenance of public pools and receive minimal public health oversight (5). This outbreak in Nebraska highlights the public health risk of improperly managed public pools. Long-term deterioration of the pool water quality was documented by the operator, who failed to maintain acceptable levels set by state regulations. Although NDHHS is responsible for overseeing the training certification of municipal pool operators, Nebraska state regulations do not require training or certification for operators of state-licensed, nonmunicipal public pools; therefore, the operator of this swimming pool was not required to be certified and had no verifiable training.
Chloramines can remain in the water or evaporate into the air above the pool, causing a pungent smell. Trichloramine is more volatile than monochloramine and dichloramine and is released into the air more readily. In addition, trichloramine causes more severe irritation and forms more rapidly in water with a low pH, such as the water in this pool (2). Methods to test chloramine levels in the air exist but are neither routine nor rapid. Therefore, environmental air sampling was not performed as part of this outbreak investigation, and the outbreak could not be specifically linked to elevated levels of chloramines in the air. However, several factors strongly suggest that high chloramine levels in the air were the cause of illness. First, the water's combined chlorine level of 4.2 ppm (at least eight times the acceptable level), together with the water's extremely low pH (3.95), was favorable for formation of high levels of chloramines, particularly trichloramine. Second, all 24 ill persons reported that their symptoms began after they entered the pool courtyard environment, and 70% of ill persons who entered the immediate pool area reported illness onset within 2 hours of entering the area. Finally, ventilation was inadequate during the outbreak; the windows of the pool enclosure were closed, and the ceiling exhaust fan had been turned off, presumably to retain a warmer temperature in the enclosed courtyard.
Chloramines are not considered health hazards in outdoor swimming pools. However, in the enclosed space around indoor pools, they can reach dangerous concentrations and pose a substantial health risk. High concentrations cause acute eye and respiratory tract irritation in swimmers and other persons in the indoor pool environment (1,2) and might also contribute to asthma and respiratory disease (6,7).
In 2004, two similar outbreaks associated with exposure to indoor motel swimming pools were reported in Illinois (8). Within minutes of entering the indoor pool environments, 72 persons, predominantly children, reported illness with high attack rates and symptoms consistent with chloramine exposure. Water-chemistry abnormalities and inadequate pool maintenance were cited as contributing factors; the investigators suggested that standard education be mandatory for all public pool operators (8).
The findings of this investigation are subject to at least two limitations. First, NDHHS was unable to reach all 110 registered hotel guests, and those who were contacted were asked to complete an online survey. This passive method of data collection likely reduced the number of respondents, possibly resulting in an underestimation of the extent of the outbreak. Second, the association between exposure and illness could not be quantified because illness was not assessed in persons who were not exposed.
Clinicians and public health professionals should be vigilant for outbreaks of illness related to recreational water exposure, including those involving exposure to chloramines; such outbreaks should be reported to health departments. Chloramine-related outbreaks are thought to be common but seldom reported (8,9). Although NDHHS certification for nonmunicipal pool operators is not required, NDHHS training courses are open to both municipal and nonmunicipal pool operators. To ensure the safety of indoor swimming-pool environments, pool owners should ensure that pool operators are trained to maintain water chemistry within acceptable ranges and ensure adequate ventilation to prevent accumulation of unsafe levels of chloramines and minimize the associated health risks. In addition, swimmers should report an unusually strong chlorine odor and any instance of pool-associated respiratory or ocular irritation to pool operators and refrain from entering the implicated pool area and swimming in the pool.
References
1. Héry M, Hecht G, Gerber JM, Gendre JC, Hubert G, Rebuffaud J. Exposure to chloramines in the atmosphere of indoor swimming pools. Ann Occup Hyg 1995;39:427--39.
2. Massin N, Bohadana AB, Wild P, Héry M, Toamain JP, Hubert G. Respiratory symptoms and bronchial responsiveness in lifeguards exposed to nitrogen trichloride in indoor swimming pools. Occup Environ Med 1998;55:258--63.
3. Nebraska Health and Human Services. Nebraska Administrative Code, title 178, chapter 2. Operation and management of public swimming pools. Available at http://www.hhs.state.ne.us/reg/t178.htm.
4. US Bureau of the Census. Statistical abstract of the United States: 1995. 115th ed. Washington, DC: US Bureau of the Census; 1995.
5. CDC. Surveillance data from swimming pool inspections---selected states and counties, United States, May--September 2002. MMWR 2003;52:513--6.
6. Thickett KM, McCoach JS, Gerber JM, Sadhra S, Burge PS. Occupational asthma caused by chloramines in indoor swimming-pool air. Eur Respir J 2002;19:827--32.
7. Bernard A, Carbonnelle S, Dumont X, Nickmilder M. Infant swimming practice, pulmonary epithelium integrity, and the risk of allergic and respiratory disease later in childhood. Pediatrics 2007;119:1095--103.
8. Bowen AB, Kile JC, Otto C, et al. Outbreaks of short-incubation ocular and respiratory illness following exposure to indoor swimming pools. Environ Health Perspect 2007;115:267--71.
9. CDC. Surveillance for waterborne disease and outbreaks associated with recreational water---United States, 2003--2004. MMWR 2006;55(No. SS-12).
* Disinfection by-products formed when free chlorine, a common disinfectant used in swimming pools, combines with nitrogenous human wastes (e.g., sweat, urine, or feces) in pool water.
† Combined chlorine = total chlorine -- free chlorine.


http://www.americanfreepress.net/html/chloraminated_water.html
February 5, 2005
The Unhealthy Consequences of Chloraminated Water
By Christopher Bollyn
In order to meet standards set by the U.S. Environmental Protection Agency (EPA), municipal water districts across the United States are changing they way they disinfect public water supplies. In many cases this involves adding ammonia to chlorinated water to produce chloramines, or
chloraminated water.
While chloramination has been recommended by the EPA since the 1990s as a way to lower the level of carcinogenic disinfection byproducts (DBPs) created by chlorination, it has led to unintended consequences, in some cases making the water extremely toxic.
LEAD POISONING
In the nation’s capital, for example, the change to chloraminated water in 2000 caused a huge spike in lead levels in the water. The chloramines reacted with antiquated pipes causing toxic levels of lead in some Washingtonians’ drinking water.
When Washington’s Water and Sewer Authority (WASA) switched from using free chlorine to chloramines to disinfect the water, serious problems with lead leaching started to occur. Lead levels were found in Washington’s water 3,200 times the EPA’s “action level” and 4,800 times the UN’s acceptable level for the toxic heavy metal.
The Washington Post reported in October 2004 that the D.C. Water and Sewer Authority knew in 2001 that its water contained unsafe lead levels, but “withheld six high test results and said the water was fine.”
While the Post article did not mention chloramines, it did say that other cities have similar problems dealing with unacceptably high levels of lead in their water:
“Cities across the country are manipulating the results of tests used to detect lead in water, violating federal law and putting millions of Americans at risk,” the Post reported. “Some cities, including Philadelphia and Boston, have thrown out tests that show high readings or have avoided testing homes most likely to have lead.”
“In New York City,” the Post wrote, “the nation’s largest water provider has for the past three years assured its 9.3 million customers that its water was safe because the lead content fell below federal limits. But the city has withheld from regulators hundreds of test results that would have raised lead levels above the safety standard in two of those years.”
The American Water Works Association (AWWA), an international nonprofit scientific society dedicated to the improvement of drinking water quality, reported that samples of Washington water collected after flushing were as high as 48,000 parts per billion (ppb). Some of the highest lead concentrations came from taps after one minute of flushing.
The EPA’s “action level” for lead in drinking water is 15 ppb, while the UN’s World Health Organization recommends that lead not exceed 10 ppb.
According to the EPA, “If the lead concentration of the drinking water at the tap is above the action level, the water supplier may be required to install corrosion-control equipment, monitor the water source, and replace lead service lines, as well as undertake a public education program.”
After switching to chloraminated water, children in Washington ingested more than 60 times the EPA’s maximum level of lead with one glass of water.
“[Lead] contaminated water is a greater risk to youth,” the EPA notes. A 2-year-old’s estimated daily intake of lead from all sources should not exceed 190 ppb per day, according to EPA guidelines.
In March 2004, after a number of 2-year-olds in Washington were found to have high levels of lead in their blood, D.C. City Administrator Robert Bobb said that 23,000 homes with lead service lines would receive filters
within 30 days.
Lead in the drinking water was a problem that plagued ancient Rome. Vitruvius, Roman architect and engineer, warned of lead in his 1st Century B.C. opus De Architectura: “Water from clay pipes is much more wholesome than that which is conducted through lead pipes, because lead is found to be harmful . . . hurtful to the human system. “Hence, water ought by no means to be conducted in lead pipes, if we want to have it wholesome,” Vitruvius wrote.
TOXIC BYPRODUCTS
The chlorination of water also creates a host of known and unknown organic byproducts, which experts say are “the chemicals of greatest concern” due to their toxicity and carcinogenic potential. To reduce the level of harmful DBPs (Disinfection By Products) and the odor in the water, the EPA began promoting chloramination of water in 1994.
While the chloramines reduce the level of known DBPs, they create a host of unknown DBPs, some of which are extremely toxic.
In Corpus Christi, Texas, for example, where the water is treated only with chloramines, the reaction with the bromide and iodide laden source water creates some of the “most toxic and genotoxic DBPs” ever found.
Although chlorine has been used to disinfect water for over 100 years, less than 50 percent of the DBPs in chlorinated drinking water are known. With chloramines, only 17 percent of the DBPs have been identified.
“The unintended generation of DBPs poses a chronic health risk,” Dr. Michael J. Plewa, a genetic toxicology expert at the University of Illinois, wrote. Plewa authored a 2004 EPA-funded study of the effects of chloramines in the water of Corpus Christi.
In the chloramine-treated water of Corpus Christi, Plewa’s study discovered a number of new and extremely toxic DBP’s: iodoacids.
“The iodoacetic acid is the most toxic and genotoxic DBP in mammalian cells reported in the literature,” Plewa wrote. Of the known DBPs, the iodoacetic acid found in the drinking water of Corpus Christi was “the most toxic and DNA-damaging.”
Plewa told AFP that Houston’s source water is probably very similar to the water of Corpus Christi. “Individuals who consume chlorinated drinking water have an elevated risk of cancer of the bladder, stomach, pancreas, kidney and rectum as well as Hodgkin’s and non-Hodgkin’s lymphoma,” Plewa wrote. “DBPs also have been linked to reproductive and developmental effects, including the induction of spontaneous abortions.”
‘A VASTLY BIG EXPERIMENT’
“I don’t want to sound glib,” Plewa said in an interview with American Free Press, “but we are participating in a vastly big experiment.”
The EPA is looking for an exit strategy from research on chloraminated water, Plewa said, while scientists are calling for more research about the toxicity of the halogenated organics, the unintended DBDs, in our drinking water.
Asked about a home water filtration system, Plewa said he and his wife, both veteran scientists, use a solid block carbon filter on the cold water intake for their kitchen in central Illinois.
The filter Plewa uses is about 10 inches long by 2 inches in diameter and requires a filter change every 4 months. The filter, which he buys from the local hardware store removes heavy metals, organics, and DBPs from his drinking water, he said.
CALIFORNIA’S ‘CHLORAMINE WARS’
In San Francisco, the addition of chloramines in February 2004 to the peninsula’s drinking water has provoked “chloramine wars,” pitting outraged citizens against the municipal water boards, The San Francisco Examiner noted last summer.
Chloraminated water kills fish and reptiles. When it was added to the San Francisco water supply it nearly had the same effect on some humans.
“I almost died,” Denise Kula Johnson of Menlo Park said the day after chloramines were added to her water supply. “I was in the shower and suddenly I could not breathe. I passed out on the floor. I was terrified.”
Leading the crusade against chloramines in drinking water is Winn Parker, a medical technologist from Milbrae, Calif.
“This is a national issue,” Parker told AFP. “The government is hiding the fact that the drinking water is not usable.”
Parker is calling for government funding of alternative disinfection methods, such as ultra-violet and reverse osmosis, which would make harmful chemical disinfection methods obsolete.
The most at-risk groups from chloraminated water are, according to Parker: the fetus in the first trimester, children to age three, people over age 60 and those with human immunodeficiency virus (HIV). Women in the 35-45 age group are at risk of recurring rashes on the inner thighs and chest, he added.
Twenty years ago the use of chloraminated water in Los Angeles was found to be potentially lethal to kidney patients during dialysis.
The increased nitrogen in the drinking water, which filters don’t remove, can severely affect people taking medications for hypertension, breast cancer and penile dysfunction, Parker said, “The side effects are close to death.”
“The government is being its own bio-terrorists,” Parker told AFP. Every day Parker considers the health risks faced by the 180 million Americans who consume chloraminated water.
“We need to amend the Constitution,” Parker said, “to give the people in each state the right to vote on what goes into their water.”
Christopher Bollyn is a correspondent with American Free Press newspaper and has developed a following among truth seekers around the globe. He was recently voted one of the “top 10 writers on the Internet” by an informal poll of patriots.
http://www.prism-magazine.org/nov04/feature_water.cfm
November 2004
THE WATER GUY
By Pierre Home-Douglas
FIRST, MARC EDWARDS DISCOVERED HIGH LEVELS OF LEAD IN WASHINGTON, D.C.'S, DRINKING WATER, THEN HE HAD TO PERSUADE THE BUREAUCRACY TO GET THE WORD OUT.
It was a problem that had baffled civil engineer Marc Edwards for a decade. By the time the Virginia Tech professor finally figured out the answer, he had stumbled across a health issue that ended up pitting him against the Environmental Protection Agency (EPA) and the utility that supplies Washington, D.C., with its drinking water. The resulting battle and stress affected his health, but Edwards persevered and was finally vindicated, assisted by three graduate students he credits with helping him through the ordeal.
Edwards is one of the world's leading experts in water corrosion in home plumbing. In the mid-90s he started getting calls from homeowners across America who had problems with pinhole leaks in their home plumbing systems. Edwards points out that plumbing may sound like a trivial asset in the grand scheme of things, but the value of pipes in all the buildings in America adds up to more than a trillion dollars.
One pinhole leak in a home isn't so bad, Edwards says, but once you have two, plumbers and insurers usually recommend replacing the plumbing, figuring that other leaks are bound to happen. That's typically a $2,000 to $6,000 investment. If those leaks cause mold problems inside the walls, the home's resale value could plummet. The problem was, Edwards discovered, that no one wanted to take responsibility for the problem. "Homeowners were basically left to fend for themselves," he says. "The historical mentality of the water industry is that its problem ends at the street. Anything that happens beyond that, it'll helpbut only to a certain extent, arguing that water may not be the cause. Some of the homeowners I dealt with literally lost their homes."
What baffled Edwards about the leaks was that they were occurring in copper pipes, which have been used for more than a century and typically last for 50 years. Some of the pipes he examined had developed leaks only 18 months after being installed. In one house the tube had a leak every inch. "It was like a sprinkler hose," Edwards recalls. The problems were often passed off as shoddy plumbing work, a rare batch of poor copper, or even lightning strikes and stray currents. Edwards thought otherwise. "I figured something must have changed in the water."
Flash forward to March 2003. A group of homeowners in Washington, D.C., had called Edwards in to find out what was eating up their copper pipe. He had heard that there were occasional problems with lead in the District's water, so he decided to sample for lead at the same time. The normally accepted limit of lead in drinking water is 15 parts per billion (ppb). Edwards's meter could register results as high as 140 ppb. The water he tested went right off the scale. Edwards diluted the sample to 10 percent of its original strength, and it was still off the scale, indicating that the levels were in the thousands of parts per billion. "Some of it would literally have to be classified as a hazardous waste," he says.
He was flabbergasted. "First off, I didn't believe my meter. But in the unlikely event that lead values were that high there was a serious problem that needed to be dealt with aggressively." Edwards immediately enlisted the help of graduate students and started taking samples at other District homes. Lacking conclusive proof and not wanting to raise an alarm unnecessarily, he didn't publicize his work. He continued experiments that, ultimately, unearthed another dimension to the problem.
In the past, the District of Columbia Water and Sewer Authority (WASA) had advised its customers to let water run from the tap for 30 seconds to 1 minute to flush all the lead out. Edwards's sampling, however, indicated that the lead levels were actually highest in water coming between 30 seconds and a few minutes. "The
water utility and the EPA were inadvertently causing some people to drink the very worst water possible," Edwards says.
EPA had subcontracted with Edwards to identify the problem with lead in the water, and WASA had solicited a proposal for urgent research. And yet when Edwards's sampling program proved there was a problem with the advice given to consumers, WASA did not issue any new instructions. "For me it was a basic moral question," Edwards declares. "If you were at all concerned about the health of the people you served, it was imperative to alert them the instant you discovered the problem and knew your well-intentioned advice was wrong."
Then the results from his sampling program stopped coming from the utility. On January 2 WASA called Edwards with an ultimatum: either stop working for the homeowners and work only for the utility, or be cut off from future monitoring data. "In other words, I was either with them or against them," Edwards says. The utility also said it would give the $110,000 of work Edwards had proposed to another researcher. Up to this point, Edwards had been paying for the full-time student research out of his own pocket. "There was no way I could compromise my integrity with the consumers for research funding, no matter how badly I needed the money." Edwards flatly refused WASA's demand.
EPA had another surprise. It suddenly discontinued its own subcontract with him. "That's when I suspected that WASA and EPA had both made mistakes and were in the same boat," Edwards recalls. "EPA's action stunned me. I mistakenly believed its job was to protect public welfare and enforce the law above all else, and instead EPA cut me out of my ongoing work on behalf of consumers." Edwards was so concerned about the lack of clear public warning to homeowners and the newly discovered dangers, he spent sleepless weeks worrying about the situation. A marathon runner, he lost 35 pounds in three weeks. He eventually checked into the emergency room of a hospital with heart problems.
Finding the Culprit
Then the Washington Post got hold of the story. In January 2004 the paper ran the first of a dozen front-page articles about the problem. "When that first article hit, people went berserk," Edwards recalls. The trouble was, the paper did not correct the flawed advice about flushing the lead out. In fact, the articles consistently repeated WASA's advice as a means to protect the consumer from lead exposure.
The publicity alerted politicians to the problem. Congresswoman Eleanor Holmes Norton (D-DC) pushed for a congressional hearing. Edwards testified in March, and Norton says he was "very, very credible on the excess amount of lead in D.C. water." "That credibility," she adds, "was enhanced by his reasonability. Some of the public health people took the position that the only safe amount of lead in the water was zero. He was not willing to say that, so he wasn't seen as someone who wanted to make it impossible for people to deliver water in the first place."
At the hearing, Edwards finally identified the culprit that had caused the lead leaching: chloramine. Made from chlorine and ammonia, the chemical had replaced chlorine as the disinfectant for drinking water in Washington, D.C., starting in March 2000. "I had read papers on the effect of chloramines on lead, and found that 50 years ago people noted some serious corrosion issues for brass, an alloy of copper, lead, and zinc," Edwards says. He adds that chloramine leachs lead not only out of lead pipes but even from so-called lead-free brass (which actually contains 8 percent lead) and lead-containing solder used to join copper tubes before it was banned in 1986.
The EPA and WASA were reluctant to accept this hypothesis until the water utility switched back to using chlorine for a regular cleanup of its pipes in April. The lead levels immediately dropped. When it switched back to using chloramine in May, the levels rose dramatically. Finally, in June 2004, the EPA ruled that WASA had violated federal law by not properly notifying the public about unsafe levels of lead in the water. "The wheels of justice turn slowly," Edwards says, "but they do turn."
That didn't mean a switch back to chlorine, however. As Edwards points out, when the EPA drew up its rules for water contamination in the '90s, it largely considered concerns about lead contamination an issue of the past, and inadvertently placed it much lower on the scale of health worries than substances called organochloridessuspected carcinogens caused as a byproduct of chlorination. The new EPA regulations pressured some utilities to switch to chloramine. Ironically, as Edwards points out, "The net result is that in D.C., we are exchanging a few parts per billion of a suspected carcinogen (organochlorides) for hundreds or even thousands parts per billion of leada known public-health threat, linked to birth defects and mental retardation." To counteract the corrosion problem, WASA has decided to include orthophosphate in its water treatment.
The whole experience has taught Edwards not only about the frustration of fighting bureaucracy but also something about the quality of today's engineering students. "You hear about the fact that North American students are so far behind their peers in some other countries, they don't have the same work ethic and they don't know this and they don't know that, but I will tell you that it almost brings tears to my eyes to think about the hours they invested and their commitment. It was really remarkable. You can't tell me that students of any era would have performed any better."
"At times," he adds, "I wanted to give up because I didn't have money and I was paying them piecemeal out of my own pocket, but they were so enthusiastic about working on something that would help consumerssomething that was also new scientificallyI didn't have the heart to tell them we had to stop."
Edwards grew up near Buffalo, where he completed an undergraduate degree in biophysics at SUNY Buffalo. He then went to graduate schoolin engineering. "I visited all kinds of programs and I had the best feel for the people in environmental engineering. I thought that this is an area where you can solve real problems that impact people's everyday lives." He completed a Ph.D. at the University of Washington in Seattle. Since then, he has worked as a consultant on corrosion problems with water authorities around the world, from Chile to Australia, from Korea to Germany. He joined Virginia Tech's department of civil and environmental engineering in 1997. Today, the 40-year-old teaches courses in water treatment. "The students are the best part of the job," he says. "It's great to work with young people who feel a deep sense of commitment, who are willing to sacrifice their time and effort to advance scientific understanding on behalf of the public." Edwards also serves as president of the Association of Environmental Engineering and Science Professors, which he says was very supportive during his battle with WASA and the EPA.
Edwards, his wife, and two pre-school children live in Blacksburg, Va., where he indulges his passion of growing exotic fruit and nut trees like pawpaws, kiwis, and persimmon. "Why I do it, I don't really know," he says with a chuckle. He finds the hobby fascinating even though he admits that it takes many years to see results. "Actually, it's a lot like research. You have to invest the years before you see the fruits of your labor. Some of the trees I planted take 10 years before there is even a hope of seeing results. He pauses for a couple of seconds. "Oddly, it took about the same time before we made any significant progress in understanding the problem of pinhole leaks in home plumbing."
Pierre Home-Douglas is a freelance writer based in Montreal.
Watch a video of Marc Edwards at Princeton: http://www.princeton.edu/WebMedia/lectures/
http://pubs.acs.org/subscribe/journals/esthag-w/2006/apr/science/rr_chloramines.html
Science News
April 12, 2006
Experiment confirms chloramine’s effect on lead in drinking water
The water chemistry that caused Washington, D.C.’s lead problem isn’t unique.
Chloramines, which have been linked to elevated levels of toxic lead in drinking water in Washington, D.C. [316KB PDF], and Greenville, N.C., have again been implicated in high lead concentrations, but this time the evidence comes from real-time experiments. In research published today on ES&T’s Research ASAP website (DOI: 10.1021/es052411r), chemist Jay Switzer at the University of MissouriRolla describes real-time corrosion studies that show that lead scales on pipes are more likely to dissolve into drinking water when chloramines are used as a disinfectant.
Lead water pipes Michael DeSantis Tetravalent lead scales (inset) have been found inside lead water pipes from several utilities. (a) In a free chlorine solution, tetravalent lead (triangular-faced crystals) are stable, but (b) in the presence of chloramine they dissolve into the water and only a different form of the toxic metal, lead carbonate (flakes), is left behind.
Concerns about lead in drinking water rocketed to prominence in 2004 following the discovery of concentrations of up to 48,000 parts per billion (ppb) in D.C. drinking water. The dangerously high levels came after the district’s water-treatment system switched from chlorine to chloramines for disinfection. Oddly, the switch to chloramine had been prompted by federal limits on another problemdisinfection byproducts (DBPs), potentially harmful compounds formed when chlorine reacts with organic matter in the water. Chloramine, a combination of chlorine and ammonia, is a weaker oxidizer than free chlorine, so it produces lower levels of the unwanted DBPs.
At the time of the D.C. lead crisis, EPA chemist Mike Schock hypothesized that the switch reduced the water’s oxidation potential and caused mineral scales made of relatively insoluble tetravalent lead inside pipes to dissolve. Before that, experts believed that a different form, divalent lead scales, dominated drinking-water systems.
Corrosion expert Marc Edwards at Virginia Polytechnic Institute and State University first identified the severity of the D.C. problem and says that the new research “provides yet another independent confirmation of Michael Schock’s hypothesis as to the importance of tetravalent lead in drinking water systems, and illustrates that the problems experienced in Washington, D.C., are likely to occur in many other systems that switch from free chlorine to chloramine disinfectant.”
Using a quartz-crystal microbalancea device capable of ultrasensitive mass measurementsSwitzer could track reactions between lead and chlorine or chloramine. Chlorine stabilized the lead film but “with the chloramines, the lead film almost completely dissolved,” he says. The experiment took 20 hours with concentrations about 10 to 12 times higher than those in drinking water; a real system would likely take longer, he notes.
“Confirmation by an independent third party using an entirely different experimental setup and analytical technique is gratifying,” says Schock, whose recent work shows that “tetravalent lead scales are not a freak occurrence.” He has found such scales in pipes from roughly a third of the systems he’s examined.
Schock is currently trying to identify a surrogate set of water-quality indicators to predict the occurrence of such scales. Tetravalent lead scales are associated with waters that have persistently high redox potentials. Such water chemistry can occur when engineers use high concentrations of free chlorine to combat bacteria, as was done in D.C.
But these conditions can also characterize pristine, hard, high-alkalinity groundwaters that are low in organic matter as well as various waters treated with other oxidative processes such as greensand filtration or ClO2, he says.
“A system with lead pipes, but lead concentrations that seem anomalously low, is a likely candidate for tetravalent lead scales,” says Schock. Managers must carefully evaluate the pipe-scale chemistry of such systems before they contemplate a switch to chloramines, he adds.
Switzer’s experiment and Schock’s studies focus on situations that involve lead water pipes. Elevated levels of lead were discovered in 2005 in drinking water and in the blood of two children in Greenville. Those levels were also associated with a switch to chloramine disinfection but occurred in a system with no lead service lines. Schock wonders if tetravalent lead scales may be present on solder or brass plumbing devices.
Given the conflict water utilities now face on how to reduce DBPs and keep lead levels low, perhaps the best solution is a new approach, says Schock. “Removing [DBPs] at the plant would be the ideal way to optimize the system,” he notes. This would take “a lot more research,” and he hopes that funding agencies and scientists are up to the challenge. REBECCA RENNER
http://www.medicalnewstoday.com/medicalnews.php?newsid=25017
24 May 2005
Fluoride Chemicals Leach Lead Into Water Supplies
Fluoride chemicals, combined with other water additives, pull health-damaging lead from plumbing systems into drinking water, according to University of North Carolina researchers reported a North Carolina newspaper on May 18, 2005 (a). Fluoride is added to water supplies to prevent cavities, not purify it as some believe.
A combination of chloramines and fluorosilicic acid, especially with extra amounts of ammonia, leaches lead from meters, solder and plumbing systems, according to Richard P. Maas, PhD and Steven C. Patch PhD, co-directors of the Environmental Quality Institute at the University of North Carolina, Asheville.
Chloramine, a combination of chlorine and ammonia, is a water supply disinfectant. Fluorosilicic acid, the chemical used by over 91% of U.S. fluoridating communities, attempts to improve dental health in those who drink it About 2/3 of U.S. public water supplies are fluoridated but tooth decay remains a national epidemic, according to the U.S. Surgeon General. (b)
Maas said, “Tests showed lead levels three and four times higher in water with that combination of chemicals …About 500 systems, across the country, have switched to chloramine treatment since 2001…and most also use fluorosilicic acid,” according to the North Carolina newspaper, the News & Observer.
Maas said this chemical interaction could be responsible for the elevated lead levels recently plaguing Greenville, North Carolina (c). Health authorities issued a lead advisory for water from the Greenville Utilities Commission when elevated lead levels showed up in 26 of 106 sampled homes.
Water leaving the plant and its distribution lines do not contain lead. But testing showed two children with harmful lead levels, leading health officials to speculate that corrosion of pipes within the home may be the cause. Greenville authorities warned pregnant and breastfeeding women and children under age six to avoid the tap water until it is tested for lead.
Maas, who heads a lead poisoning prevention program in Western North Carolina funded by the federal Centers for Disease Control and Prevention, said his lab has tested more than 150,000 homes across the country in the past 18 years and found that 10 to 15 percent have a significant lead contamination problem, according to the News & Observer article.
“No amount of lead is safe for a young child's developing brain,” says Paul Connett, PhD, Professor of environmental chemistry and toxicology at St. Lawrence University in Canton, NY and Executive Director of the Fluoride Action Network.
“If this new data is confirmed, it will further underscore the negligence of U.S. authorities using fluorosilicic acid as a fluoridating agent in the absence of any research establishing the safety of this particular fluoride chemical,” says Connett.
These new findings may help explain earlier published, peer-reviewed research by Roger Masters, PhD of Dartmouth College and Michael Coplan. Their studies show a link between water fluoridation status and elevated blood lead in children. (d)
Elevated blood lead levels are linked to developmental delays in children under age six and fetuses. Lead can adversely affect almost every organ and system in the body. The most sensitive is the central nervous system, particularly in children. Lead also damages kidneys and the reproductive system. The effects are the same whether it is breathed or swallowed.
According to the Centers for Disease Control and Prevention, "fluoride works primarily after teeth have erupted." (e)
"It really doesn't make any sense to ingest fluoride chemicals, anyway. Fluoridation is an outdated concept, wastes money, jeopardizes health and should be stopped everywhere," says Connett.
References:
(a) North Carolina News & Observer, “Water treatment process called potential risk Chemicals' mix with plumbing could put lead in tap water”
newsobserver.com/news/health_science/story/2417101p-8794959c.html
(b) “First-ever Surgeon General's Report on Oral Health Finds Profound Disparities in Nation's Population,” News Release, May 25, 2000 National Institutes of Dental and Craniofacial Research
nidcr.nih.gov/NewsAndReports/NewsReleases/NewsRelease05252000.htm
(c) “Pitt County Issues Advisory After Lead Discovered In Children.” May 3, 2005, WFMY News - Greensboro, NC
wfmynews2.com/news/local_state/local_article.aspx?storyid=40346
(d). Masters RD, Coplan MJ, et al., “Association of silicofluoride treated water with elevated blood lead,” Neurotoxicology. 2000 Dec;21(6):1091-100
(e) "Recommendations for Using Fluoride to Prevent and Control Dental Caries in the United States," August 2001
cdc.gov/mmwr/preview/mmwrhtml/rr5014a1.htm
Contacts:
Michael Connett, 802-355-0999, Project Director, Fluoride Action Network, info@fluoridealert.org
Dr. Paul Connett, Executive Director, Fluoride Action Network, paul@fluoridealert.org
Media Relations Director, Fluoride Action Network, carol@fluoridealert.org
SOURCE: FLUORIDE ACTION NETWORK
http://www.FluorideAlert.Org
PO Box 5111
Burlington VT 05402
E -mail: info@fluoridealert.org