1
Historical Overview of Drinking Water Contaminants and Public Water Utilities

Daniel A. Okun

A recent editorial in Science expressed a need for a more credible scientific basis for environmental regulations (Madia, 1998). The editorial goes on to point out that government regulators must rely on the research performed in their own laboratories as well as in private laboratories and universities in all of the agencies of government and not the U.S. Environmental Protection Agency (EPA) alone. It concludes that, "now is the time for science to close the gap."

My contention is that, under current circumstances, it may not be feasible to even begin to close the gap and that waiting for scientific evidence before adopting regulations is not adequate if protection of public health is the goal. History may help us understand what measures in the past, in the absence of scientific evidence, have been successful in helping reduce the risks to public health from assaults on the environment.

London, Nineteenth Century

In 1832 annual deaths from cholera in London ranged from 10 to 110 per 10,000 population. The introduction of tap water to the wealthier homes and the consequent introduction of the flush toilet led to the discharge of human wastewaters to the Thames River via the storm sewers that had been built to permit London's commercial center to remain active during rainy periods. By 1849 the death rates had increased to more than 200 per 10,000 for those taking water from the Thames in the center of the city.

At that time, decades before the germ theory of disease had been hypothesized and proven, the spread of cholera was attributed to poisons in the air emanating from the miasmas rising from the Thames during the occasional hot summers that frequented London. During such periods, the people of London avoided using London Bridge, the only crossing of the Thames in the city, obliging them to go far upstream to make the crossing.

John Snow, physician to Queen Victoria, hypothesized that the drinking water in London, which was drawn from the Thames by water companies and from private wells in the city, was responsible for the cholera outbreaks. The epidemic of 1854 helped demonstrate, if not prove, his theory. He mapped deaths in London's West End (see Figure 1-1) and identified a well on Broad Street as the focus for the



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--> 1 Historical Overview of Drinking Water Contaminants and Public Water Utilities Daniel A. Okun A recent editorial in Science expressed a need for a more credible scientific basis for environmental regulations (Madia, 1998). The editorial goes on to point out that government regulators must rely on the research performed in their own laboratories as well as in private laboratories and universities in all of the agencies of government and not the U.S. Environmental Protection Agency (EPA) alone. It concludes that, "now is the time for science to close the gap." My contention is that, under current circumstances, it may not be feasible to even begin to close the gap and that waiting for scientific evidence before adopting regulations is not adequate if protection of public health is the goal. History may help us understand what measures in the past, in the absence of scientific evidence, have been successful in helping reduce the risks to public health from assaults on the environment. London, Nineteenth Century In 1832 annual deaths from cholera in London ranged from 10 to 110 per 10,000 population. The introduction of tap water to the wealthier homes and the consequent introduction of the flush toilet led to the discharge of human wastewaters to the Thames River via the storm sewers that had been built to permit London's commercial center to remain active during rainy periods. By 1849 the death rates had increased to more than 200 per 10,000 for those taking water from the Thames in the center of the city. At that time, decades before the germ theory of disease had been hypothesized and proven, the spread of cholera was attributed to poisons in the air emanating from the miasmas rising from the Thames during the occasional hot summers that frequented London. During such periods, the people of London avoided using London Bridge, the only crossing of the Thames in the city, obliging them to go far upstream to make the crossing. John Snow, physician to Queen Victoria, hypothesized that the drinking water in London, which was drawn from the Thames by water companies and from private wells in the city, was responsible for the cholera outbreaks. The epidemic of 1854 helped demonstrate, if not prove, his theory. He mapped deaths in London's West End (see Figure 1-1) and identified a well on Broad Street as the focus for the

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--> Figure 1-1 Deaths from Cholera in Broad Street, Golden Square, London, and the  neighborhood, 19 August to 30 September 1854 (NCGIA, 1994).

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--> fatalities. The water had been clear and apparently very attractive as people sent carts to carry water from the well to homes even miles away. A "shoe leather" epidemiologist, Dr. Snow interviewed individuals in their homes and ascertained the presence of disease and deaths and concluded that the well was the common source of exposure for those affected (Snow, 1936). Two private water companies (all water distribution services were then private) were in competition to serve the south bank of the Thames with piped water drawn from the Thames in the center of the city. These supplies had been characterized as being among the worst of the water supplies of London. In 1852 the Lambeth Company, in an attempt to attract more customers by improving the aesthetic quality of its product, moved its intake upstream above the wastewater and storm water discharges from London. Dr. Snow seized the opportunity this offered to compare the impact on those taking water from the Lambeth Company with their neighbors who continued to subscribe to their larger competitor, the Southwark and Vauxhall Company. Table 1-1 shows the significance of the move of the intake in the Thames—an almost 90 percent decrease in the rate of fatalities. The relatively few deaths that occurred among customers of the Lambeth Company might be attributed to exposures of the residents elsewhere in London in connection with their employment. The affirmation of Dr. Snow's hypothesis provided a basis for water management for decades before there was scientific proof of causality—namely, the identification of the agent responsible for the disease, nor had he met many of the requirements of a modem epidemiological study. Nevertheless, a principle, which is valid today, emerged from that early work: that water should be taken from the highest-quality source available and be protected from contamination. United States, Twentieth Century Typhoid fever death rates in the United States during the early years of this century, before widespread acceptance of filtration and the introduction of chlorination, indicated that the death rates from typhoid were a function of the quality of the source, as shown in Table 1-2. Groundwater and upland watersheds showed the lowest rates of typhoid with a threefold higher rate in waters drawn from rivers (Kober, 1908). The introduction of filtration reduced the incidence of enteric disease generally and typhoid specifically, the latter dropping in rate by more than 55 percent (Ellms, 1928). Introduction of chlorine in the early years of this century, which combined with filtration virtually eliminated waterborne enteric disease in the United States, had one unfortunate consequence: filtration and chlorination appeared to make the quality of the source unimportant, and the principle of using the best source succumbed to the expedience of developing lower-cost polluted river sources and providing filtration and chlorination. Some large cities located on major rivers opted to take their water supply from these rivers despite the fact that upstream other cities, industries, and agricultural enterprises were discharging wastewaters into their water sources. Among these cities were Philadelphia, New Orleans, Cincinnati, and London, all of which had better-quality options that were more difficult to pursue and perhaps marginally more

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--> TABLE 1-1 Data of John Snow on Cholera in London, 1854 Water Service and Source Number of Houses Served Deaths from Cholera Deaths per 10,000 Households Southwark & Vauxhall Co.: from Thames River at London 40,046 1,263 315 Lambeth Co.: from Thames River above London 26,107 98 37 Rest of London: wells and surface sources 256,423 1,422 59   SOURCE: Adapted from Snow, 1936. TABLE 1-2 Mean Typhoid Death Rates in U.S., 1902-06 Source Number of Cities Death Rate per 100,000 Ground water 4 18.1 Impoundments and protected watersheds 18 18.5 Small lakes 8 19.3 Great lakes 7 33.1 Mixed surface and groundwater 5 45.7 Run-of-river supplies 19 61.6   SOURCE: Adapted from Kober, 1908. costly. The more costly options were rejected because filtration and chlorination gave assurance that the treated water would "meet the drinking water standards." (Unfortunately, today, most cities in Asia, Africa, and Latin America draw their water supplies from large rivers and do not provide filtration and chlorination effectively and have made few efforts at protecting their sources, with the result that infant mortality rates in these countries are more than 10-fold higher than in industrialized countries.) An interesting characterization of the status of drinking water in the United States in the first half of the twentieth century can be found in the book The Quest for Pure Water, published by the American Water Works Association

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--> (Baker, 1948). The 27-page index to this 527-page book does not include the words "typhoid," "cholera," "bacteria," "health," "standards," or "regulations." A brief epilogue states: In the last 60 years (from about 1880), with advances in the arts and sciences, including the acceptance of the germ theory of disease and of water as one of the chief means of spreading cholera and typhoid, standards for the quality of water have been raised. The standards then were directed almost exclusively at the prevention of transmission of enteric pathogens, with E. coli serving as a useful surrogate for the waterborne diseases prevalent during that period. As we are now aware, this surrogate is no longer useful and the search is on for some other approach to ensuring microbial safety without having to test for every likely pathogen. The Chemical Revolution The chemical revolution that accompanied the increasingly technical sophistication of the major combatants of World War II led to the creation of thousands of synthetic organic chemicals (SOCs). They were designed for the most part to be toxic to biota and to be long lasting to achieve economy in their application. That these compounds would reach the environment and drinking water sources was slow to be recognized. Among the first to draw attention to the potential was W.C. Hueper of the National Cancer Institute who wrote: It is obvious that with the rapidly increasing urbanization and industrialization of the country and the greatly increased demand placed on the present resource of water from lakes, rivers, and underground water reservoirs, the danger of cancer hazards from the consumption of contaminated drinking water will grow considerably within the foreseeable future. (Hueper, 1960) Only two years later, Rachel Carson's Silent Spring (1962) raised the issue throughout the nation and the industrialized world. The U.S. Public Health Service recognized the issue with its 1962 Drinking Water Standards, the first to include mention of organic compounds with a limit for chloroform extractables. This test measured the total of all organic compounds, both natural and synthetic, toxic and nontoxic, that would be adsorbed by passing the water through a granular activated carbon (GAC) column and desorbed with chloroform. (It should have been no surprise that GAC filters would show up well in studies for the treatment of water for the removal of these organics.) It was not until the early 1970s that the EPA recognized there were hundreds of SOCs in drinking water sources, particularly in the Mississippi River at New Orleans near its mouth. A large number of these compounds were believed to be carcinogenic, teratogenic, and/or mutagenic in animals and possibly in humans. These findings, together with epidemiological studies comparing populations in New Orleans who drank treated Mississippi River

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--> water with nearby populations using untreated groundwater, revealed somewhat higher rates of some forms of cancer in those using the Mississippi River water, led to passage of the Safe Drinking Water Act (SDWA) in 1974. EPA's Interim Primary Drinking Water Regulations included, for the first time in federal regulations, six widely used pesticides (EPA, 1976). The EPA also contracted with the National Research Council (NRC) to prepare a series of volumes, ultimately nine over a 13-year period, entitled Drinking Water and Health to provide guidance on methodologies for selecting contaminants and establishing maximum contaminant levels (MCLs) for contaminants known to be in drinking water (NRC, 1977-1989). One quote from Volume 2 is of interest: Over 700 volatile organic compounds have been identified in drinking water ... These compounds make up only a small fraction of the total organic matter ... Approximately 90% of the volatile organic compounds that can be analyzed by gas chromatography have been analyzed, but this represents no more than 10% by weight of the total organic material. Only 5-10% of the non-volatile organic compounds that comprise the remaining 90% of the total organic matter have been identified. (NRC, 1980) Two problems were largely ignored in assessing the problems with organics in drinking water and regulations for their control: MCLs were established for each contaminant individually, with no account taken of the impact of several compounds being present in a sample and no consideration of the possible synergistic effects of one of the contaminants with another. This problem still faces us. No attention was given to the impact of using chlorine for disinfection. Being a strong oxidant, chlorine reacts with other organic compounds in the water being treated to create what are now termed disinfection byproducts (DBPs). This problem was addressed by the addition of trihalomethanes to the regulations in 1979. Amendments to the SDWA in 1986 obliged EPA to establish MCLs and MCL goals for many more contaminants, including primarily SOCs. A requirement was that every three years 25 new contaminants would be added to the drinking water regulations. Figure 1-2 shows the rate at which contaminants have been added to the regulations since early in this century. The unreasonableness of this approach was addressed with the SDWA amendments of 1996, which established new protocols for incorporating contaminants in the regulations. The World Health Organization and the European Community, as well as other industrialized countries, have been incorporating contaminants either as guidelines or regulations in about the same numbers over the past several decades. EPA's focus on the problems of SOCs and DBPs arose from their potential for causing cancer. The selection of compounds of concern and setting their acceptable MCLs were difficult because the onset of cancer requires decades-long exposure and the epidemiology to date had not been sufficiently

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--> Figure 1-2 Number of drinking water contaminants regulated by the U.S.  government. The large increase in regulated contaminants that begins after 1976  is due to regulations issued under the Safe Drinking Water Act and its subsequent  amendments. SOURCE: Reprinted, with permission, from Okun (1996).  Copyright © 1996, the American Society of Civil Engineers.

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--> robust to distinguish the significance of any single contaminant if ingested for 70 years, the exposure period adopted in establishing risk. Several epidemiological studies by the National Cancer Institute were contradictory (Cantor et al., 1978, 1998). A controversial metanalysis on the significance of chlorine consumption on cancer rates, which combined 10 previously published epidemiology studies, reported increased relative risk for bladder and rectal cancers in proportion to the exposure to chlorinated water (Morris et al., 1992). EPA's concern for the formation of DBPs and its belief that they might be responsible for cancers after long-term exposures led to one unfortunate side effect, illuminated by the cholera epidemic that surfaced in Peru in 1991 and rapidly spread throughout much of Latin America. Some of the blame for the spread was attributed by Peruvian officials to the EPA because its considerable concern for the deleterious effects of chlorine had been responsible for Peru reducing and even ceasing chlorination of its water supplies. With the high infant mortality rates in developing countries, most of which are attributable to waterborne infectious diarrheal diseases such as typhoid and cholera that have largely been eliminated in the industrialized world, disinfection of water is absolutely essential. Chlorine is the disinfectant of choice in the developing countries because it is by far the lowest in cost and easiest to apply. Yet the ubiquity of radio and television throughout the world and the spread of news that EPA is urging reduced chlorination because chlorine is said to contribute to cancer have induced many authorities in developing countries to reduce or even abandon the use of chlorine. The Microbial Revival EPA's focus on DBPs and SOCs led the Milwaukee Journal to adopt the title "Fatal Neglect" for a special reprint following the devastating April 1993 cryptosporidiosis outbreak (Rowen and Behm, 1993). The newspaper asserted that EPA had sufficient knowledge about Cryptosporidium and its effects because of six earlier outbreaks in the United States and several in England but that this knowledge had not been translated into any type of meaningful response. The Surface Water Treatment Rule, promulgated in 1989, did focus on giardiasis, which is a far less serious disease than cryptosporidiosis and one for which there is adequate therapy. More importantly, Cryptosporidium oocysts, as was the case with the cysts of amoebic dysentery, a serious waterborne pathogen that flourished a half a century earlier, are not inactivated by conventional chlorination and, being smaller in size than Giardia cysts, would more easily pass through conventional filters. A particularly serious problem is that fecal coliform is not an appropriate surrogate for the oocysts of Cryptosporidium. Moreover, while the oocysts are relatively large, determination of their presence has been very difficult. A problem that arises with diarrheal diseases is that their endemicity is not easily recognized as the symptoms do not generally require medical attention and, even if a physician becomes involved, seldom is the stool sent off for examination. The International Life Sciences Institute held a conference in August 1992 entitled "Balancing the Risk" (Craun, 1993). One day was devoted to microbial risk and another to chemical risk. An informal poll among the conferees indicated that, at the time, microbial risks were more important and

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--> should not, in effect, be neglected under the assumption that they were well under control. In fact, considerably more attention has begun to be given to microbial risks of all types. New pathogens are continually appearing on the scene, and the search for a suitable surrogate for determining microbial safety enjoys a high priority. Return of Trace Chemical Contaminants This was pretty much the situation when I prepared a paper entitled "From Cholera to Cancer to Cryptosporidiosis" (Okun, 1996). In the few years since, new problems with SOCs have begun to take center stage. Uncertainties remain about the roles of SOCs and DBPs in connection with reproductive anomalies which, if shown to be a problem, will change our assessment of DBPs (Bove et al., 1995; Savitz et al., 1995; Swan et al., 1998). Currently, our concern is with long-term exposures, so that averaging concentrations of DBPs is adequate for monitoring water quality. With reproductive effects, a three-month period of exposure would become significant, which would require more frequent monitoring and a concern for seasonal variations in DBP concentrations. Another manifestation of the role of anthropogenic impacts on our water supply emerged from Europe, where it was found that all the drinking waters withdrawn from sources that had received human wastewaters were showing trace concentrations of the pharmaceutical compounds commonly used by people with a wide range of ailments—heart disease to mental stress to control of conception (Stan and Heberer, 1997; Buser and Muller, 1998). More recently, evidence from England indicates that waters impacted by human wastes were responsible for "feminizing fish" (Jobling et al., 1998). This last observation may have special significance in that fish may be a better source of information about trace contaminants in water than samples of water themselves. In studies related to the safety of San Francisco delta water for drinking, analyses failed to show the presence of trace concentrations of SOCs in the water. However, the fish did reveal their presence, which had been inferred from the sanitary survey conducted on the watershed. This revealed that hundreds of thousands of tons of pesticides were being applied annually to lands draining into the rivers feeding the delta but had not shown up in analyses of water samples (Okun et al., 1985). The more important concern exhibited by the fish is that the impact on them might well be a signal for us to be concerned about impacts on humans drinking these waters for long periods of time. The fish may be our canaries. The Challenge Is science now able to identify all of the trace chemical contaminants and microbials in water, let alone determine their concentration? Can science establish methods for their reduction or removal and characterize their health significance?

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--> A currently appropriate metaphor, football talent, might give us a clue as to the difficulties that face science today if it is to provide the basis for regulations. In football, if a team were to spend 100-fold more on its offensive players than its opponents did on their defensive players, the likelihood of the defense containing the offense would be small indeed. Football teams, if they are to contend, recognize that they must invest as much in defense as in offense. But this imbalance between offense and defense is precisely the situation facing environmental sciences today in the protection of the public health. Billions of dollars are invested annually by industry in inventing new chemical compounds—all potential contaminants and parents of daughter contaminants born of reactions of these compounds with other compounds in the aquatic environment. How much money is available to support the scientists who have the responsibility to identify these chemical compounds that are developed in secrecy? The offensive is carried out in secret to protect patents and licenses. Regulatory agencies only learn about them when they are cleared for marketing and the water utilities much later. Only then can their scientists begin to determine their presence and concentrations and establish the significance and fate of these chemical compounds in the aquatic environment. The regulators are handicapped because there is little literature describing the birth and development of these compounds. (While the literature may be replete with papers that address methods for identifying, characterizing, and determining the health effects of these chemicals.) This is not to imply that these developments of industry are not valuable. They have been seized on and perceived as improving the quality of life. In fact, it is the great value placed on these very important developments, such as pesticides for agriculture, chemicals for plastics and pharmaceuticals, radiation, and myriad new breakthroughs that result in the very heavy assault on water quality. The offense will continue to be strong. Our role is to create a defense that has the potential to contain the offense. This may oblige some to communicate not only with our science colleagues but also with those who have the power to support the defense. In the meantime, as scientists provide the data for regulators and public officials who are responsible for the initiatives of the defense, they might consider introducing the "precautionary principle" (Hileman, 1998) onto the playing field. Application of the principle would reduce the power of the offense by placing the burden of demonstrating the harmlessness of a new product or technology on its proponents rather than on the general public. References Baker, M. N. 1948. The Quest for Pure Water. Denver, Colo.: American Water Works Association. Bove, F. J., M. C. Falcomer, J. B. Klotz, J. Esmart, E. M. Dufficy, and J. E. Savrin. 1995. Public drinking water contamination and birth outcomes. American Journal of Epidemiology 141(9):850-862. Buser, H. R., and M.D. Muller. 1998. Occurrence of the pharmaceutical drug clofibric acid and the herbicide mecropop in various Swiss lakes and the North Sea. Environmental Science and Technology 32(1):188-192.

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--> Cantor, K. P., R. Hoover, T. J. Mason and L. I. McCabe. 1978. Associations of cancer mortality with halomethanes in drinking water. Journal of the National Cancer Institute 61(4):979-985. Cantor, K. P., C. F. Lynch, M. E. Hildesheim, M. Posemeci, J. Lubin, M. Alvanja, and G. Craun. 1998. Drinking water source and chlorination byproducts in Iowa: I. Risk of bladder cancer. Epidemiology 9(1):21-28. Carson, R. 1962. Silent Spring. New York: Houghton Mifflin. Craun, G.F., ed. 1993. Safety in Water Disinfection: Balancing Chemical and Microbial Risks. Washington, D.C.: ILSI Press. Ellms, J. W. 1928. Water Purification. New York: McGraw-Hill. EPA (U.S. Environmental Protection Agency). 1976. National Interim Primary Drinking Water Regulations. Federal Register 40:59565. Hileman, B. 1998. Precautionary principle. Chemical and Engineering News (Feb.):16-18. Hueper, W. C. 1960. Cancer Hazards from natural and artificial water pollutants. Proceedings from Conference on Physiological Aspects of Water Quality. Washington, D.C.: U.S. Public Health Service. Jobling, S., M. Nolan, C. R. Tyler, G. Brighty, and J. P. Sumpter. 1998. Widespread sexual disruption in wild fish. Environmental Science and Technology 32(17):2498-2506. Kober, G. M. 1908. Conservation of life and health by improved water supply. Engineering Record. 57(June). Madia, W. J. 1998. A call for more science in EPA regulations. Science 282(Oct. 2):45. Morris, R. D., A. M. Audet, I. F. Angelilo, T. C. Chalmers, and F. Mosteller. 1992. Chlorination, chlorination byproducts and cancer. A meta-analysis. American Journal of Public Health 82(7):955-963. NCGIA (National Center for Geographic Information and Analysis). 1994. Snow's Cholera Map. Online. NCGIA, Geography Department. Available: http://www.ncgia.ucsb.edu/pubs/snow/map.gif [10 January 1994]. NRC (National Research Council). 1980. Drinking Water and Health, Vol. 2. Washington D.C.: National Academy Press. Okun, D. A., R. H. Harris, and R. Tardiff. 1985. Water Quality Considerations in Source Selection. Prepared for East Bay Municipal Utilities District. Okun, D. A. 1996. From Cholera to Cryptosporidiosis. Journal of Environmental Engineering 122(6):453-458 Rowen, J., and D. Behm. 1993. Fatal neglect. The Milwaukee Journal, Sept. 19-26. Savitz, D. A., K. W. Andrews, and L. M. Pastore. 1995. Drinking water and pregnancy outcome in central North Carolina: Source, amount, and trihalomethane levels. Environmental Health Perspectives 103(6):592-596. Snow, J. 1936. Snow on Cholera London: Oxford University Press. Stan, H. J., and T. Heberer. 1997. Pharmaceuticals in the aquatic environment. Analusis 25(7):M20-M23. Swan, S. H., K. Waller, B. Hopkins, G. Windham, L. Fenster, C. Schaefer, and R. R. Neutra. 1998. A prospective study of spontaneous abortion: Relation to amount and source of drinking water consumed in early pregnancy. Epidemiology 9:126-133.