Page 9: Guidelines for Canadian Drinking Water Quality: Guideline Technical Document – Turbidity
Part II. Science and Technical Considerations (continued)
8.0 Health considerations
8.1 Microbial
The most important health-related function of turbidity is its use an indicator of the effectiveness of drinking water treatment processes, particularly filtration, in the removal of potential microbial pathogens. Several studies have evaluated the relationship between drinking water turbidity, pathogen occurrence and/or gastrointestinal illness in the population. The body of evidence indicates that there is not a universal mathematical relationship through which turbidity values can be used to predict an expected rate of gastrointestinal illness in a population. Significant increases in turbidity appear to have more relevance as a potential predictor of the potential for illness. Even so, it is the water industry's assessment that turbidity is an invaluable parameter for its functions in source assessment, drinking water system control and as an indicator of potential increases in concentrations of bacteria, Giardia cysts and Cryptosporidium oocysts (MWH, 2005).
Many drinking water-related outbreaks of gastrointestinal illness have coincided with reports of elevated turbidity levels (Kent et al., 1988; MacKenzie et al., 1994; Atherton et al., 1995; British Columbia Centre for Disease Control, 1996; PHAC, 2001; O'Connor, 2002). The 1993 outbreak of cryptosporidiosis in Milwaukee (Wisconsin) was preceded by a dramatic increase in turbidity at one of the city's drinking water treatment plants (MacKenzie et al., 1994). Heavy rains, flooding and a treatment plant overwhelmed by turbidity were identified as contributing factors to the Walkerton, Ontario, outbreak in 2000 (O'Connor, 2002). Increased finished water turbidity due to a malfunctioning solids contact unit was noted around the time of the 2001 outbreak of cryptosporidiosis in North Battleford, Saskatchewan (PHAC, 2001). Logsdon et al. (2004) have identified treatment issues, such as degraded filtered water quality (e.g., high turbidity) following filter ripening and turbidity breakthrough, as factors that can increase the risk of a waterborne outbreak.
Outbreaks have also been linked to municipal supplies where no treatment irregularities were reported and where water quality parameters (including turbidity) were below the acceptable limits recognized at the time (Hayes et al., 1989; Maguire et al., 1995; Goldstein et al., 1996). An outbreak of cryptosporidiosis in Clark County, Nevada (Goldstein et al., 1996), was associated with a drinking water facility that possessed state-of-the-art treatment capabilities and produced water of better quality than the current U.S. standards at the time of the occurrence. Post-outbreak troubleshooting performed at the Carrollton water treatment plant (Hayes et al., 1989; Logsdon et al., 1990) suggested non-optimized filtration and backwashing techniques may have led to increased passage of Cryptosporidium oocysts.
Investigations have been conducted to examine the potential association between the turbidity levels of public drinking water supplies and the rate of endemic (non-outbreak-related) gastrointestinal illness in the community. Schwartz et al. (1997, 2000) compared fluctuations in daily average turbidity levels with reported gastrointestinal illness-related hospital uses (emergency room visits and hospital admissions) for elderly and pediatric patients in the city of Philadelphia, Pennsylvania. Treated water turbidity levels were well below the regulated limits over the entire study period, having an average value of less than 0.20 NTU. Associations between turbidity and illness reporting were observed for turbidity values lagged by 4-6 and 10-13 days for children and 9-11 days for elderly patients. From the data, the authors further estimated that increases in turbidity of 0.04 NTU (roughly one quarter of the total range) correlated to a 9% increase in hospital admissions for elderly patients and up to a 31% increase for pediatric admissions.
A similar study was conducted by Aramini et al. (2000) in the city of Vancouver, British Columbia. Increases in raw water turbidity in the Greater Vancouver Regional District water supply (predisinfection, no filtration) were observed to correlate with increased illness rates when lagged at 3-6, 6-9, 12-16 and 21-29 days. The authors suggested that variations in turbidity exceeding 1.0 NTU (the previous Canadian guideline value) could explain as much as 2% of gastrointestinal illness-related physician visits and up to 1.3% of gastrointestinal illness-related hospitalizations.
Egorov et al. (2003) examined daily variations in drinking water turbidity and gastrointestinal illness among a study cohort in Cherepovets, Russia. Drinking water was shown to be in compliance with existing microbiological standards over the entire study period. However, the authors reported that local public health officials consider the water to be microbiologically unsafe and advise the public to boil their drinking water. Turbidity recorded during the study exceeded 1 NTU more than 80% of the time. The authors determined that individuals who reported drinking non-boiled tap water had statistically significant elevated risks of gastrointestinal illness at lags of 1, 2 and 7 days. The subset of participants who reported consuming only boiled drinking water did not demonstrate such significant association.
A group of related studies also retrospectively examined the possibility for a gastrointestinal illness-turbidity relationship to have been present at and around the time of the Milwaukee outbreak. Morris et al. (1996) reported that during the outbreak, cases of gastroenteritis were closely associated with drinking water turbidity at a lag of 7 days among children and 8 days among adults. In a follow-up analysis (Morris et al., 1998) determined that in the 434 days leading up to the outbreak, gastrointestinal events among children and adults living in the service area of one of the treatment plants (the North Plant, where a higher average effluent turbidity was observed over that period) were strongly associated with turbidity lagged by 8 days and 9 days respectively. Lastly, Naumova et al. (2003) reported a strong association between gastrointestinal illness-related hospital admissions among the elderly and drinking water turbidity lagged by 5 to 6 days. In each of the studies (Morris et al., 1996, 1998; Naumova et al., 2003), the authors concluded that the lag times observed were consistent with the incubation period for Cryptosporidium.
Some other investigations have failed to find evidence of a link between turbidity and endemic illness. A study equivalent to the Vancouver study was conducted in the city of Edmonton, Alberta (Lim et al., 2002). The researchers found no significant relationship between lagged finished water turbidity values and reported rates of gastroenteritis among city residents. Most recently, Tinker et al. (2010) reported finding no association between filtered water turbidity values and rates of gastrointestinal illness during a time-series comparison of drinking water turbidity and gastrointestinal illness-related emergency department visits in the city of Atlanta, Georgia. A modest turbidity-illness association was noted by the authors when raw water turbidity values were examined.
Turbidity and community gastrointestinal illness linkages have also been examined using other surveillance mechanisms. Gilbert et al. (2006) reported an association between treated water turbidity and gastrointestinal illness-related calls to a health information telephone line. Beaudeau et al. (1999) found a positive correlation between raw water turbidity increases and increases in sales of over-the-counter anti-diarrheal medicine in the city of Le Havre, France.
Mann et al. (2007) conducted a systematic review of the literature on the subject of drinking water turbidity and endemic gastrointestinal illness. In summing up their findings, the authors noted that to date, study results have been varied: relationships between drinking water turbidity and community gastrointestinal illness have been observed in some studies, whereas other studies did not support these findings. The authors further noted that methodological differences between the studies may help explain some of the contradicting results. Presently there is no standard approach for the analysis of associations between turbidity level and health outcomes, making it difficult to directly compare studies.
8.2 Chemical
Particulate matter in water is generally not considered to pose a chemical health risk. The types of particles that are most frequently encountered are not regarded as significant chemical hazards.
There are some indirect links between the chemical quality of turbidity particles and health that can be noted as a result of particles interacting with other chemical contaminants. Clay and natural organic matter particles can adsorb heavy metals as well as some pesticides, such as dichlorodiphenyltrichloroethane (DDT), chlordane and dieldrin (Health Canada, 1995; Ritter et al., 2002). It is known that adsorbed chemicals can dissociate from particles upon experiencing a change in conditions, such as pH changes. Therefore, the possibility exists that when particles enter a different environment, such as the stomach, release of the adsorbed contaminants could occur.
Nevertheless, at the finished water turbidity levels specified in this document, it is not expected that particulate chemical contaminants will be in sufficient concentrations to present a chemical health hazard. In addition, the minerals and metals most commonly encountered (e.g., calcium, manganese, iron, aluminum) are either considered essential nutrients or have not demonstrated evidence of adverse health effects attributed to drinking water ingestion that would result from any concentration that may occur at turbidity levels recommended herein (Health and Welfare Canada, 1987a,b,c; Health Canada, 1998). In general, food and occupational routes are considered more significant contributors to metal and pesticide exposures (Ritter et al., 2002).
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