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About Trihalomethanes
Trihalomethanes are compounds consisting of a carbon atom bound to a hydrogen atom and three halogen atoms (i.e. like methane, but with three of the hydrogen atoms replaced with halogens such as fluorine, chlorine, and/or bromine). The halogen atoms can be of the same type or in different combinations. Chloroform is a well-known example of a trihalomethane that has many industrial and chemical applications; these compounds are not unique to drinking water and exposure to trihalomethanes can occur due to environmental contamination as well as through drinking water.
Trihalomethanes in Drinking Water
Chlorination and filtration of water supplies if often cited as one of the greatest public health achievements of the 20th century, greatly reducing the incidence of diseases such as cholera, dysentery, and typhoid (Calderon, 2000) where implemented. However, it was discovered in the 1970s that chlorine could react with naturally-occurring organic matter in the water to form trihalomethanes (THMs), especially chloroform.
THMs are sometimes also referred to as disinfection by-products, or DBPs. While THMs appear to be the first DBPs recognized, we are now aware of over 600 compounds that appear in drinking water as a result of a variety of disinfection processes (Richardson, 2012). However, only a few DBPs are regulated, and this discussion will be limited primarily to THMs formed as a result of chlorination.
There are four trihalomethanes that have historically been of concern in drinking water, which are sometimes grouped under the heading total trihalomethanes or TTHMs:
- Chloroform (CHCl3)
- Bromodichloromethane (CHCl2Br)
- Dibromochloromethane ( CHClBr2)
- Bromoform – (CHBr3)
Of these, it is chloroform that forms the basis for the minimum acceptable concentration of THMs in Canada (with respect to drinking water standards), because it the compound for which the most data on toxicological effects is available. The drinking water standard is based on the cumulative dose of all four THMs. Canada also has a separate standard for bromodichloromethane (even though it is also included within the trihalomethane guideline). The guidelines are primarily based on evidence from animal studies that identify chloroform as a potential carcinogen. Human studies have also suggested links to cancer, and at high levels reproductive effects. It has been suggested that trihalomethanes that contain bromine are more toxic than chloroform, and bromodichloromethane has been identified as a carcinogen in rodent studies (it is thought to be the most potent carcinogen of the four trihalomethanes being considered, at least in rodents)(Health Canada, 2006). Other guidelines are in effect elsewhere, as will be discussed in future reflections along with the rationale for these guidelines.
Other topics for reflection will included balancing the concern over trihalomethanes against the benefits of disinfecting water supplies, the importance of exposure routes, considering the risk of trihalomethanes relative to the risks of byproducts from alternate disinfection methods and relative to the hundereds of other disinfection by products.
References cited:
Calderon, R. L. (2000). The epidemiology of chemical contaminants of drinking water. Food and Chemical Toxicology, 38, Supplement 1(0), S13–S20.
Government of Canada, H. C. (2006, May 2). Guidelines for Canadian Drinking Water Quality: Guideline Technical Document: Trihalomethanes – Health Canada. publication. Retrieved September 10, 2013, from http://www.hc-sc.gc.ca/ewh-semt/pubs/water-eau/trihalomethanes/index-eng.php
Richardson, S. D., & Postigo, C. (2012). Drinking water disinfection by-products. In Emerging Organic Contaminants and Human Health (pp. 93–137). Springer. Retrieved from http://link.springer.com/chapter/10.1007/698_2011_125
toxcentre 
March 18, 2014 at 9:34 am
This topic is interesting because the public perception of risk is somewhat supported with regard to the risk associated with THMs. I enjoyed the article by Kerger et al. (2000) describing how one can decrease exposure concentrations of THM by bathing versus showering, decreasing time spent in the shower, choosing showerheads that produce less ‘vapour’, and having sufficient air ventilation in the bathroom.
Do you think inhalation is the primary pathway of exposure for THM for the average North American?
Kerger, B.D., C.E. Schmidt and D.J. Paustenbach. 2000. Assessment of airborne exposure to trihalomethanes from tap water in residential showers and baths. Risk Analysis. 20(5):637-651
March 18, 2014 at 9:34 am
Chloramination is another disinfection process that includes both chlorine and ammonia. The city of Saskatoon uses chloramination instead or chlorination to disinfect its drinking water because it has a longer half-life (www.saskatoon.ca). It would be interesting to compare which process produces more hazardous disinfectiontion bi-products: chlorination or chloramination.
http://www.saskatoon.ca/DEPARTMENTS/Utility%20Services/Water%20and%20Wastewater%20Treatment/Water%20Treatment%20Plant/Pages/Frequently%20Asked%20Questions.aspx#chemicals
March 18, 2014 at 9:34 am
As considered in class, when calculating the risk of a compound, the benefits should also be considered. In the case of Trihalomethanes, as you mention, the use improved human heath by decreasing the incidence of cholera and dysentery. Despite the risk of developing cancer as a result of Trihalomethanes exposure, are the benefits brought from this exposure greater than the risk of toxicity?
March 19, 2014 at 11:34 am
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Exposure Pathways and Uncertainty
Loosely following our flow chart of Health Canada’s approach to risk assessment, this week’s reflection is focused mainly on exposure pathways and the complexities related to exposure to trihalomethanes (THMs). Broadly, there will be two main areas of uncertainty when trying to calculated exposure to THMs: the concentrations in the water, and the relative importance and exposure amounts via different exposure pathways.
As mentioned previously, THMs are formed as a byproduct of the water treatment process. The concentration of each of the THMs formed depends on a wide variety of factors:
Organic precursor concentration (which is related to source water and can vary considerably over time for a given source; surface water is expected to have a higher concentration of organic matter than ground water sources)
Contact time with chlorine
Type of chlorination used (chlorine, chloramine, ozonation)
Presence of bromide ions in water (favors formation of brominated THMs)
Temperature (seasonal variation – increased rate of formation at higher temperatures)
pH (increased formation at higher pH)
location in distribution system (chlorine residuals in water protect water quality in the distribution system but result in increased contact times and therefore potential for elevated THM formation at extremities of distribution system)
Many of these factors relate to the sophistication of the water treatment system, which in turn tends to be associated with the size of the population served. Smaller centers generally have less sophisticated treatment systems and higher levels of THMs than larger centers (Health Canada, 2006). Health Canada did a survey from 1994-2000 of over 1200 water systems in eight provinces (collectively serving over 15 million Canadians) and found the mean concentration of THMs was 66 µg/L (below the Health Canada standard of 100ug/L). However, some systems had averages around 400 µg/L range, and some had peak values around 800 µg/L. 23% of the systems reported mean THM levels greater than 100 µg/L and 41% reported having at least one exceedance of the 100 µg/L standard. For systems providing data on bromodichloromethane (BDCM), mean concentrations were generally less than 10 µg/L, but some peak values were greater than 200ug/L. 8% of systems sampled reported mean BDCM concentrations over 10 µg/L. It is important to recognize that the systems where mean levels of both THM and BDCM were higher than the drinking water standards served a small proportion of the population – less than 4% of the population served by the sampled systems (Health Canada, 2006).
In practical terms, all of this means that there can be significant variation in the levels of trihalomethanes reaching a given household over time, dependent on characteristics of the source water, treatment practices, season and location in the distribution system, making exposure assessment difficult. For example, Rodriguez et al (2002) hypothesized that temperatures extremes might produce might produce variability in THMs between seasons, and found that in the Quebec City area, THM levels in summer were 2.5-5 times higher in summer than in winter. This difference could potentially be related to differences in source water quality in different seasons, as well as different rates of THM formation due to temperature.
THMs in Saskatoon’s water
How does Saskatoon measure up? The Ministry of Environment publishes water monitoring records from the municipal systems; following are the records for total THMS:
Saskatoon Water Works THM records (Source: SK Ministry of Environment)
Multiple samples are taken quarterly from various points in the distribution system. From the records it is apparent that the most recent measurements (July 2013) show concentrations approaching maximum acceptable levels, but these are unusually high (perhaps related to high river flows increasing the load of organic matter in the water?). Still, there is a lot of variation in the results and the question is: what concentration would you use in an exposure assessment for a Saskatoon resident?
Ways Water Treatment Plants can Reduce Exposure Levels – Alternative Treatments to reduce THMs?
Water treatment methods offer some options for minimizing the formation of THMS. The most efficient way to reduce the levels of THMs is to reduce the concentration of organic matter; coagulation, sedimentation, membrane filtration, carbon filtration, carbon adsorption and pre-oxidation can all be used to reduce the concentrations of precursors to THMs prior to chlorine contact. Chlorination practices can also reduce formation, such as optimal dosing and changing the point of contact (e.g. to after the water has been filtered). Alternatives to chlorination exist, as mentioned by Steven, but are not without issues. Chloramination is not as effective of a disinfectant as chlorine, and although it produces less THMs than chlorine, other, less well-characterized organic halogen compounds do form at higher levels than with chlorine (Krasner et al., 2006). Ozonation does produce some disinfection byproducts (though few THMS), while ultraviolet disinfection does not. However, ozonation and ultraviolet disinfection still require the addition of a residual disinfectant (typically chlorine or chloramine) to protect the water during its transit through the distribution system.
As an interesting aside, Health Canada recommends increased monitoring of lead levels when disinfection systems are changed. A switch to chloramination in Washington, D.C. resulted in increased levels of lead in drinking water as a result of destabilization of lead dioxide scales which had formed in the distribution system while chlorination had been used and had reached an equilibrium state under that system; the change resulted in lead leaching into the drinking water.
The relationship between THM formation and pH suggests that altering the pH could be used to control THM formation; however, at lower pH values the formation of haloacetic acids increase; haloacetic acids are the second most common group of disinfection by products, which are also regulated and are of concern due to potential health effects similar to those of THMs (Health Canada, 2006).
As Carla mentioned, the risks of exposure need to be balanced against the risks of non-exposure, which in this case is potential exposure to multiple pathogens. The final option for reducing exposure would be not treating our water. This brings with it tremendous risks; diarrheal disease from untreated water supplies is an enormous health burden in developing countries, and even where treatment is well-established, short- term failures of treatment have resulted in outbreaks of disease with had fatal consequences (Hrudey et al. 2003, Hoxie et al. 1997).
Exposure Pathways:
Although I titled my reflection THMs in Drinking Water, I have altered the title a bit to THMs in Tap Water. THMs are ingested via drinking water, but this is not the only important exposure pathway in water that reaches our homes via tap water. THMS readily volatilized from tap water into the air, and inhalation from indoor air via tap water is also a possible exposure route. Our hygiene habits also affect exposure to THMs by both inhalation from volatilization from shower or bath water, and dermal absorption from the same (Weisel and Jo, 1996). Therefore, any exposure assessment should include factors for exposure via bathing/showering in addition to tap water consumption rates. I did a quick exposure diagram:
THM pathways
Swimming was added to this diagram mainly as a consideration for possible contributions to background exposure because pools represent a significant source of THMs. Health Canada estimates that a one hour swim in a public indoor pool results in greater exposure than any tap water pathway (Health Canada, 2006). (I would be scared to estimate the THM exposure experienced by my kids over several summers in an above ground pool that took increasing amounts of chlorine to disinfect as the summers wore on due to vast amounts of organic matter accumulated over the season.) Hot tubs, due to their increased temperatures, are another potential source of significant background exposure.
Background exposure to THMs can also occur through pathways independent of disinfection byproduct formation, for example via food (e.g. chloroform has been detected in foods such as fish and dairy products as well a wide spectrum of other items) and relatively small amounts of emissions from consumer products (e.g. adhesives, fabrics, ink etc.).
Similar to the situation with the levels of THMs in municipal tap water, the various routes of exposure and their dependence on how water is handled makes exposure assessment difficult. For example, the volatilization of THMs from water depends on its temperature. If inhalation exposure is calculated based on the rates of volatilization from cold water, inhalation exposure will typically be underestimated for showers and bathing, and even simple things like the use of boiled water for drinking can affect exposures (Batterman et al, 2000). Individual differences can affect exposure assessment as well even when the tap water is the same – for example, as Lorelei pointed out, exposure can be modified by the length and temperature of showers, whether tap water or filtered or bottled water is consumed, and so on. Consumers can reduce their exposure by proper use in-home treatment devices to remove THMs from drinking water. Point-of-entry, point-of-use, and pour-through treatment devices certified to NSF/ANSI Standard 53 are certified to reduce the levels of THMs by 95%.
Furthermore, different assessments tend to make different assumptions and different defaults for calculating exposures, coming to different conclusions about the most important routes of exposure (e.g. Wang et al, 2007 ; Uyak 2006). And at least one study on routes of THM exposure suggested that the relative importance of different routes depends on the biologically active form of the compound being absorbed, the compound’s metabolism, and the target organ, so that although the amount absorbed by different routes is not necessarily as important as the actual load in the body resulting from a given route of exposure (Weisel and Jo, 1996).
Lorelei asked if inhalation exposure is the most significant pathway for North Americans. I believe this is hard to say given the complexities of considering different exposure pathways, and the relative importance of different THMs. I will write in more detail about exposure assessments in the future, but based on a study commissioned by Health Canada regarding total exposures (all pathways) cut comparing a daily 10 minute shower vs. a 30 minute bath and found that total exposure was greatest in the bath scenario, with the highest contribution from inhalation for Chloroform, but via ingestion for BDCM (Health Canada, 2006). Thus, if we assume chloroform to be the most commonly found THM, inhalation likely represents the most important exposure pathway (but not just from showering!). For other THMs, this may not be the case.
In conclusion, there are multiple pathways to consider for exposure, with a good deal of uncertainty associated with each in terms of what an average exposure might be, adding yet another layer of complexity to the question of how to calculate exposures. Next week I plan to examine in more detail how exposure assessments are calculated, considering the uncertainties around concentrations of THM in water and also in the relative importance of various exposure pathways.
Batterman, S., Huang, A.-T., Wang, S., & Zhang, L. (2000). Reduction of Ingestion Exposure to Trihalomethanes Due to Volatilization. Environmental Science & Technology, 34(20), 4418–4424. doi:10.1021/es991304s
Government of Canada, H. C. (2006). Guidelines for Canadian Drinking Water Quality: Guideline Technical Document: Trihalomethanes – Health Canada. publication. Retrieved September 10, 2013, from http://www.hc-sc.gc.ca/ewh-semt/pubs/water-eau/trihalomethanes/index-eng.php
Hoxie, N. J., Davis, J. P., Vergeront, J. M., Nashold, R. D., & Blair, K. A. (1997). Cryptosporidiosis-associated mortality following a massive waterborne outbreak in Milwaukee, Wisconsin. American Journal of Public Health, 87(12), 2032–2035. doi:10.2105/AJPH.87.12.2032
Hrudey, S. E., Payment, P., Huck, P. M., Gillham, R. W., & Hrudey, E. J. (2003). A fatal waterborne disease epidemic in Walkerton, Ontario: comparison with other waterborne outbreaks in the developed world. Water science & technology, 47(3), 7–14.
Krasner, S. W., Weinberg, H. S., Richardson, S. D., Pastor, S. J., Chinn, R., Sclimenti, M. J., … Thruston, A. D. (2006). Occurrence of a New Generation of Disinfection Byproducts†. Environmental Science & Technology, 40(23), 7175–7185. doi:10.1021/es060353j
Rodriguez, M. J., Vinette, Y., Sérodes, J.-B., & Bouchard, C. (2003). Trihalomethanes in Drinking Water of Greater Québec Region (Canada): Occurrence, Variations and Modelling. Environmental Monitoring and Assessment, 89(1), 69–93. doi:10.1023/A:1025811921502
Uyak, V. (2006). Multi-pathway risk assessment of trihalomethanes exposure in Istanbul drinking water supplies. Environment International, 32(1), 12–21. doi:10.1016/j.envint.2005.03.005
Wang, G.-S., Deng, Y.-C., & Lin, T.-F. (2007). Cancer risk assessment from trihalomethanes in drinking water. Science of The Total Environment, 387(1–3), 86–95. doi:10.1016/j.scitotenv.2007.07.029
Weisel, C. P., & Jo, W. K. (1996). Ingestion, inhalation, and dermal exposures to chloroform and trichloroethene from tap water. Environmental Health Perspectives, 104(1), 48–51.
March 19, 2014 at 11:35 am
This is a really interesting topic. I almost chose it myself, although I finally went for a more familiar variety, water fluoridation. I was wondering, given the halogen nature of fluoride, if there has been any incidence of fluoride-based THM’s and how, in your opinion the presence of this compounds could influence the already decided public opinion on water fluoridation.
March 19, 2014 at 11:36 am
Author –
That’s an interesting question and one I had myself. I have not been able so far to find any references to the formation of fluoride-based THMs. Chemistry was a long time ago for me, but perhaps there is something about the chemistry of fluoride such that it does not react this way, or perhaps nobody has looked in depth at such compounds if they do form. In any case, it seems like the issue of THMs ranks low on the scale of public perception of health risks so I am not sure how much concern over such compounds would add to the polarity of public opinion on fluoridation. It is interesting, as Lorelei pointed out, that THMs represent and area where risk perception is perhaps warranted, but it seems largely off the general public’s radar. Perhaps with high profile situations like Walkerton, people are more likely to accept risks inherent in disinfection, whereas they do not appreciate the public health benefits that fluoridation can afford to a risk as seemingly mundane as tooth decay (not that I see it as mundane – dental disease has far-reaching impacts – but maybe it is generally seen that way?).
March 19, 2014 at 11:36 am
This topic is very interesting to me as someone who enjoys hiking and travel and on occasion has the need to use water disinfecting agents. Point-of-use disinfectants like chlorine- and iodine-based tablets can often be necessary to adequately remove the cyst stage of parasitic pathogens that cannot be removed by other methods of water purification. After surveying various point-of-use devices, Smith et al 2010 found that the “Life Straw” water purifier contains an anion exchange resin and activated carbon as means to decrease exposure to THMs. Is this something that could be used on a larger scale or is already in use? I would also be curious to see what risk is involved with using the tradition tablets in water on a regular basis.
March 19, 2014 at 11:36 am
Author-
Interesting question! There are definitely means to reduce THM concentrations and point of use filtration can definitely reduce their concentrations. There are also numerous ways that water utilities can pre-treat drinking water to before disinfection to decrease the formation of disinfection by products.
There is speculation that iodinated disinfection by-products are more toxic (cytotoxic and genotoxic) than clorine or bromine based THMs (Richardson, 2007) but there is ongoing research into this area so I think it is difficult to assess at this point. I will try to look into this a bit more, perhaps for a future reflection.
March 21, 2014 at 1:28 pm
Author –
Exposure Assessment for Trihalomethanes
As noted in last week’s reflection, there are many complexities (and uncertainties) associated with exposure pathways and routes for trihalomethanes. These complexities are only compounded when we start to try to quantify exposure in the context of risk assessment.
Receptor Characteristics
As will be discussed in future reflections in more depth, one of the primary concerns associated with carcinogenesis. As such, exposure estimates would need to be, at least for this endpoint, on lifetime exposures. However, there are also chronic, non-cancer endpoints including possible reproductive effects, so critical receptors will need to be identified for the varied endpoints as well.
As noted in our lectures, Health Canada provides standard estimates water ingestion and inhalation rates for all age groups, as well as surface area which will be relevant for dermal exposure in the bath/shower. For inhalation, the rate of volatilization must also be estimated given that most of the chloroform in indoor air is thought to arise from volatilization from tap water (WHO, 2005). Air concentration estimates for chloroform are available (WHO, 2005) although some uncertainty is inherent because air concentrations will depend on household activities along with THM concentrations in the tap water. Showers, boiling water, and running a dishwasher have all been identified as activities that affect indoor air concentrations. Within the shower, water temperature, flow rates, droplet size, and shower stall volume (and likely other factors) could affect the rate of volatilization of chloroform and must be considered along with typical shower or bath length. The situation gets even more complex for dermal exposures. The relative importance of dermal exposures has been estimated by biomarker studies and breath concentrations (e.g. [Jo et al, 1990]), and more recently through modeling approaches [Wang et al, 2007]). It is important to note that most toxicological data is available for chloroform, the most common THM; this is the THM on which most published exposure assessments are based. The kinetics of the other THMs may be quite different, so with the exception of BDCM (for which some data is available), calculating exposure assessments based on chloroform could be misleading and could ultimately underestimate risks, especially considering that THMs occur in mixtures along with a multitude of other disinfection by-products. Looking at just chloroform is really just scratching the surface, but for now represent the best available information.
Although time spent at home vs. work is often important in characterizing receptors and exposure, I would propose that for THMs this may not be as important; most inhalation and dermal exposure would be expected to occur at home except for select occupational exposures (e.g. lifeguards, water treatment operators, dishwashers). Drinking water consumption could vary between home and work but I’m not sure how important this would be to consider since water consumption is typically considered on a per day basis (unless work and home water consumption was sourced from different water treatment plants in which case estimating the contribution of each would be important).
In class we touched on the issue of measuring vs. modeling. Modeling, of both disinfection by-product formation in water systems and personal exposures, has been proposed as a method to improve exposure assessments given the levels of uncertainties in the associated parameters (Arbuckle et al, 2002). Certainly, misclassification of exposure is a potential significant source of error in epidemiological studies of risks, especially where the magnitudes of associations are often low (Calderon, 2000). Modelling allows incorporation variability in formation of THMs in water and personal exposure and could potentially improve estimates of health effects, but models are prone to error as well. In particular, exposures models still require inputs of personal exposure factors (locations of residences and duration at each, estimates of water intake, shower lengths, etc.); these estimates can be prone to bias especially where information must be collected retrospectively i.e. estimated from memory. Given the variability and uncertainties associated with exposure, the development of good models may help provide better estimates of exposure, but also suggests a probabilistic approach might enhance risk assessments related to drinking water exposures (at least I hope so, given that this is the basis for my thesis project!).
Challenges in Calculating Dose
Theoretically, calculating the intake from drinking water is the simplest exposure calculation. However, even this relatively simple calculation has a potential for uncertainty. Consider this simple equation:
THM intake in drinking water (ug/day) = Concentration in drinking water (ug/L) * water consumed (L/day)
The uncertainties associated with concentrations in drinking water were discussed at length last week.
With respect to water consumption, we can note that this assumes that all water consumed is tap water directly from the tap (boiled, filtered, or bottled water is likely to have a lower THM concentration than the tap water). Standard values for water consumption rates vary: Health Canada estimates 1.5 L/day and the US EPA uses 2L/day. The US EPA Exposure Factors Handbook provides estimates based on NHANES data from 2003-2006 for various age groups, and provides an interesting look at water consumption patterns. For example, for those ≥21 years of age, the mean consumption was 1.0 L/day (13 ml/kg-day), and the upper 95th percentile was 3.0 L/day (40 ml/kg-day) (US Environmental Protection Agency, 2011). These data illustrate the point that water consumption is extremely variable within a population. These estimates also include water used in beverage preparation and cooking and therefore include water consumed after heating, in which the concentration of THMs is likely to be reduced due to losses to volatilization. Therefore, the simplest exposure estimate is prone to a great deal of uncertainty; uncertainty is only magnified when dealing with more complex exposure routes.
WHO Estimates
Based on a variety of studies, primarily from the US, Canada and Germany, WHO estimated mean rates of exposure to chloroform (the most common THM) through various pathways (WHO, 2005):
Indoor air: 0.3-1.1 µg/kg bw per day (primarily a result of volatilization from tap water)
Shower: 0.5 µg/kg bw per shower (70% inhalation, 30% dermal)
Ingestion via drinking water: < 0.7 µg/kg bw per day (based on an average concentration of <20 µg/L and ingestion rate of 2 L/day)
Ingestion via food: 1 µg/kg bw per day
Outdoor air is considered much lower than other exposure pathways (~ negligible)
Total Mean intake: 2-3 µg/kg bw per day (n.b. where chloroform concentrations were “high” (undefined) the total intake could be closer to 10 µg/kg bw per day)
An assessment for chloroform for the Canadian Environmental Protection Act, 1999 (CEPA) Priority Substances List calculated upper bounds of estimated exposures for Canadians at various ages; a summary table is available online. These estimates are based largely on Canadian values obtained through various surveys and monitoring data (Government of Canada, 2004). These rates are much higher than those from WHO, as they are based on the maximum exposures estimated from Canadian data (which for drinking water was a whopping 1224 µg/L, more than 10 times the maximum acceptable concentration).
Last week I mentioned that swimming in an indoor pool resulted in exposures much higher than these. (Lévesque et al, 1994) estimated that the dose of chloroform resulting from a 1-hour swim is 65 µg/kg bw in conditions found in public indoor swimming pools.
On their own these exposure rate estimates mean little, but do provide insight into the most important routes of exposure for most people in developed countries. Drinking water and showering/bathing are the primary routes of exposure that should be considered for most people, unless they swim a lot. I did note a discrepancy in the food exposures. Comparing the exposure routes from WHO, food may represent the largest daily contribution to chloroform exposure for most people. However, the CEPA data shows food as being relatively low in terms of relative contribution to potential exposure to THMs using the upper bounding estimates. I have not identified the source of this discrepancy, though it is most likely related to variability in data sources for food exposures (for example, the food data used by WHO is from the 1980s and I wonder if environmental contamination and thus food contamination have decreased due to tightening of regulations around the use of chloroform?).
Given the variability and assumptions required, the calculation of exposure looks rather daunting. What I took from our lectures in regards to dealing with uncertainty risk assessment, assumptions will have to be made and some arbitrary numbers chosen for calculations, but just make sure they are defensible. Ultimately, it is arguable that given the relatively low exposure rates reported above (WHO estimates), using any set of standardized rates of exposure is reasonable, since even relatively large variations in the estimates of water consumption, for example, will likely not affect the ultimate risk very much (for example, it might make a small change in the rate of cancer per 100,000, but this must be considered in the context of high background lifetime cancer risk). As I move into risk assessment in future reflections, I plan to try to quantify exposures for individuals in Saskatoon. However, there is more to consider, including even more uncertainty, before being able to reflect on the risks associated with THMs. Next week I will move from exposure to hazard, looking at the hazards associated with THMs.
Arbuckle TE, Hrudey SE, Krasner SW, Nuckols JR, Richardson SD, Singer P, Mendola P, Dodds L, Weisel C, Ashley DL (2002) Assessing exposure in epidemiologic studies to disinfection by-products in drinking water: report from an international workshop. Environ Health Perspect 110: 53.
Calderon RL (2000) The epidemiology of chemical contaminants of drinking water. Food Chem Toxicol 38, Supplement 1: S13–S20 doi:10.1016/S0278-6915(99)00133-7.
Government of Canada HC (2004) Canadian Environmental Protection Act, 1999: Priority Substances List Assessment Report: Chloroform. http://www.hc-sc.gc.ca/ewh-semt/pubs/contaminants/psl2-lsp2/chloroform/index-eng.php#t13
Government of Canada HC (2006) Guidelines for Canadian Drinking Water Quality: Guideline Technical Document: Trihalomethanes – Health Canada. http://www.hc-sc.gc.ca/ewh-semt/pubs/water-eau/trihalomethanes/index-eng.php
Jo WK, Weisel CP, Lioy PJ (1990) Routes of chloroform exposure and body burden from showering with chlorinated tap water. Risk Anal 10: 575–580.
Lévesque B, Ayotte P, LeBlanc A, Dewailly E, Prud’Homme D, Lavoie R, Allaire S, Levallois P (1994) Evaluation of dermal and respiratory chloroform exposure in humans. Environ Health Perspect 102: 1082.
U.S. Environmental Protection Agency (EPA). (2011) Exposure Factors Handbook: 2011 Edition. National Center for Environmental Assessment, Washington, DC; EPA/600/R-09/052F. http://www.epa.gov/ncea/efh.
Wang G-S, Deng Y-C, Lin T-F (2007) Cancer risk assessment from trihalomethanes in drinking water. Sci Total Environ 387: 86–95 doi:10.1016/j.scitotenv.2007.07.029.
World Health Organization. (2005). Trihalomethanes in Drinking-Water: Background Document for Development of WHO Guidelines for Drinking-Water Quality. WHO: Geneva. http://www.who.int/water_sanitation_health/dwq/chemicals/en/trihalomethanes.pdf
March 21, 2014 at 1:29 pm
This topic ties in loosely with by reflection on triclosan. Studies have shown that modern water treatment techniques are not effective at removing a number of pharmaceuticals and personal card products, tricsloan being one example (Westerhoff et al. 2005). A number of studies have shown that triclosan in the presence of excess free chlorine under water treatment conditions can react to produce chloroform (Rule et al. 2005). This is one of the reasons that many groups are calling for the banning of triclosan. My questions is what proportion of the risk from THMs comes from the oxidation of triclosan in the presence of excess free chlorine? I’m guessing it is very small relative to the disinfection products we’re using already to treat water.
Westerhoff et al. 2005. Fate of endocrine-disruptor, pharmaceutical, and personal care product chemicals during simulated drinking water treatment processes. Environmental Science and Technology, 39:6649-6663.
Rule et al. 2005. Formation of chloroform and chlorinated organics by free-chlorine-mediated oxidation of triclosan. Environmental Science and Technology, 39:3176-3185.
March 21, 2014 at 1:29 pm
Author –
Good question, and one I’m not sure I can answer. I will look into this some more, but my first thoughts are that the amount of triclosan entering the water treatment process probably contribute relatively little to the overall THM production in the water leaving the treatment plant, although the proportion would depend on the relative amounts of organic matter in the water and the amount of triclosan. I am not sure, but I would imagine the amount of triclosan entering most plants is small compared to naturally occurring organic matter. I haven’t read the papers you cited, but under treatment conditions high amounts of free chlorine might be involved in these reactions, but I wonder whether any reaction could occur at point of use e.g. in the home between the residual chlorine in tap water and triclosan-containing products? Thanks for the interesting points to consider.
March 21, 2014 at 1:29 pm
Something I was completely unaware of until recently is the proposed link between chlorination byproducts and birth defects. Bove et al 2002 concluded that there is moderate evidence for a connection between THMs and birth defects while other byproducts are less well studied. I am curious to know what your thoughts are on this – is there actually a connection? I wonder because women are exposed to these byproducts all the time so I feel it would be hard to sort out any causation. Do you have any more information about fetal exposure?
March 21, 2014 at 1:30 pm
Author –
This is a good point; I haven’t had a chance to really look at the evidence for the reproductive effects, but Health Canada concluded that “neither a dose-response pattern of increasing risk with increasing concentration of THMs nor a clear evidence of a threshold has been found” with respect to reproductive effects of THM (Health Canada, 2006). The studies cited by Health Canada to arrive at this conclusion are detailed here, and reflect the conflicting nature of evidence that has been found. Comparison of studies is also difficult due to different ways of assessing exposure (range from being based on intake of chlorinated water in general to being based on measured THM levels in tap water, but even where THMs are measured, it is really difficult to make conclusions based on the epidemiologic studies because so many other factors, including other water contaminants, could be involved). Animal studies haven’t really found any teratogenic effects, and any adverse effects on the fetus appear to occur at levels that also produce toxic effects in the mother (in mouse and rat studies). A more recent review of the health effects of THM (Mohamadshafee and Taghavi, 2012) also concluded that the evidence is contradictory and not enough is available to make conclusions on the reproductive effects of THMs and other disinfection by products. In other words, I am not sure if there is a connection.
March 21, 2014 at 1:30 pm
Author –
Hazard Assessment, Part 1
As noted in last week’s reflection, there are many complexities (and uncertainties) associated with estimating exposure to THMs. This week, I wanted to start looking into the issues associated with hazard assessment for THMs.
As mentioned in the first reflection, the drinking water guidelines for total THMs are based primarily on information about chloroform, the most common THM formed in treated water and the one for which the most data is available for both exposure and hazard. In a future reflection I would like to examine the assumption that a guideline based on a single THM, i.e. chloroform, is sufficient to address all THMs.
As noted, the most data is available for chloroform, so I this week I will examine the evidence for the hazards posed by chloroform, particularly how an acceptable dose was derived. Next week I will move on to other THMs, before eventually coming back to the issue of treating THM as a group.
Chloroform is an interesting case, because some health effects in humans have indeed been directly observed as a result of its use as an early inhalant anesthetic agent in rather massive doses. Chlorofrom was administered at doses of 24-73 g/m3 for induction of anesthesia and at 12-48 g/m3 for prolonged maintenance of anesthesia (Watts et al, 2004). Its use was discontinued largely due to its toxic effects, which often included death due to cardiac arrhythmias and respiratory failure. Some patients who did survive were reported to suffer a range of side effects thought to be related to hepatic effects (nausea, vomiting, jaundice, coma) and hepatic necrosis has identified histologically (Goodman & Gilman 1970, cited in Watts et al, 2004). Ingestion is reported to have similar effects, and the lethal dose by ingestion was estimated at 45 g and serious effects can occur with 7.5 g (Winslow & Gerstner, 1978). These data are fascinating, but have little relevance in determining hazards from THM in drinking water, given that these doses were enormous: orders of magnitude greater than what we are exposed to incidentally.
In Vivo Studies
Chloroform’s toxic effects have been studied at length; finding have been well-summarized by the WHO (2004), Health Canada (2006) and very nicely in the US EPA IRIS Toxicological Review of Chloroform (2001). Chloroform has been assessed for the following effects with in vivo studies:
toxic effects in a variety of tissues (e.g. liver, kidney, thyroid, central nervous system, bone marrow, nasal lining)
reproductive and developmental effects (not well documented)
carcinogenicity and genotoxicity (discussed further below)
Chloroform Kinetics
A brief note about kinetics before I get to the key studies used to derive recommended doses. Chloroform is considered well absorbed by all routes (discussed in previous reflections). Its kinetics (and effects) are dependent on the route of exposure. The liver receives a greater dose from ingested chloroform, while other sites receive larger doses from inhalation and dermal absorption. Chloroform is distributed throughout the body, with highest concentrations in fat, blood, liver, kidney, lungs, and nervous system; placental transfer has also been documented in several species including humans (Health Canada, 2006).
Chloroform is ultimately metabolized to carbon dioxide and carbon monoxide, but intermediate metabolites are responsible for its toxic effects. Oxidative metabolism results in the production of both phosgene and hydrochloric acid, both of which have cytotoxic effects. Reductive metabolism can result formation of some mutagenic intermediates, but very high concentrations of chloroform are required for this pathway to be significant (IPCS 2000 cited in Health Canada, 2006). Chloroform is metabolized in multiple tissues, but the liver, nasal and kidney tissues appear to be the most active.
The Key Studies
As mentioned in class, it is important to look at the key studies involved in setting a guideline. Health Canada’s background document on setting the drinking water quality guidelines (2006) for THM identifies 2 key studies, both based on hepatotoxic effects of chloroform:
Authors
Model animal
Adminstration
Duration of Study
NOAEL
LOAEL
Endpoint
Heywood et al (1979)
dog
Via capsule, dosed in a toothpaste vehicle
7.5 years
n/a
13mg/kg/day
(corrected from 15 mg/kg/day given 6 days a week)
Fatty cysts in liver
Larson et al (1994)
mouse
Gavage in corn oil vehicle
3 weeks
7 mg/kg-day (corrected from 10 mg/kg/day given 5 days a week)
n/a
Cell death and regenerative hyperplasia
In drinking water ad libitum
3 weeks
No effects seen at dose as high as 329 mg/kg/day
n/a
n/a
Note that the LOAEL found in Heywood et al. was the lowest dose adminstered and consequently, no NOAEL was established. The study was designed to assess the safety of chloroform levels in toothpaste.
Of the above studies, Heywood’s was considered to be the more appropriate to use in derivation of a TDI, given its long duration and concern about the corn oil vehicle impact on toxicity (increased incidence of liver tumors have been seen in mice and rats when corn oil is used as a vehicle compared to water as a vehicle).
Health Canada therefore used the 13 mg/kg-day value, and applied an uncertainty factor of 2100, broken down as follows
100 – x10 for each of intra- and inter-species variation
7 – less than full lifetime exposure (reduced from 10 due to the fact that 7.5 years is a good portion of the dog’s natural lifetime)
3 – use of LOAEL instead of NOAEL (relatively low correction factor chosen given the use of a relatively subtle endpoint)
Therefore, 13 mg/kg-day / 2100 = a TDI of 6.2 ug/kg-day
As we discussed in class, development of TDIs is inherently uncertain; it is important to note that not all agencies use the same uncertainty factors and therefore derived different TDIs.
For example, the World Health Organization (WHO, 2004) also used the Heywood study, but then applied an uncertainty factor of 1000 (100 for intra- and interspecies variation and 10 for use of the LOAEL instead of a NOAEL and a subchronic study), resulting in a TDI of 13 ug/kg-day.
The US EPA (IRIS, 2001) used a similar approach to develop an oral RfD, citing Heywood for a NOAEL/LOAEL approach, applying a correction factor of 1000 (same as WHO) but based on 10 for interspecies variation, 10 to protect sensitive subpopulations, and 10 for used of the LOAEL. The EPA also used a benchmark modeling approach resulting in a BDML10 dose of 1.0 mg/kg-day to which an uncertainty factor of 100 was applied (10 for interspecies variation and 10 to protect sensitive populations) to obtain an RfD of 10ug/kg-day. EPA rates their confidence in the oral RfD as medium and no assessment of an inhaled RfC has been developed.
So while all the studies resulted in similar TDIs, they were derived using different uncertainty factors; one might speculated that the varied uncertainty factors used reflects the tremendous complexity of attempting to define a “safe” dose based on animal studies. In this case, the TDI derived by multiple agencies is based mainly on a 1979 study in dogs. I haven’t had a chance to review more recent toxicity studies to see how they might compare with Heywood’s findings — perhaps this would be a good project for a future reflection. However, in a comparison of studies of liver, kidney, and reproductive effects prior to the year 2000, the LOAEL found determined in the Heywood study was the lowest of the studies compared, and was also lower than any NOAEL identified in these studies (IRIS, 2001). A summary of studies examining the carcinogenic effects of chloroform over a similar time frame showed most LOAELs for a cancer endpoint were also higher than than the 13mg/kg/day LOAEL from Heywood’s study, suggesting that this is a reasonable and probably quite conservative value to use in setting guidelines.
I have further questions about using the Heywood study as the basis for the TDI. Concerns have been cited about route of administration regarding absorption and potentiation of effects whether water or oil is used, and yet a study using a toothpaste vehicle was chosen for derivation of an acceptable dose. I wonder about possible effects of other constituents of the toothpaste vehicle (a control group received the toothpaste vehicle for comparison, but I am thinking more about the potential for enhanced absorption and effect due to the vehicle). In any case, I believe this just adds more confusion to the issue of the uncertainties regarding the acceptable dose.
It is also worth noting that the key studies are based on an ingestion route of exposure. Fewer studies have looked at toxicity resulting from inhalation, but my previous exposure assessments the importance of the inhalation and dermal absorption pathways were stressed as being likely as important as the ingestion route from tap water. It stands to reason that from the kinetics discussed briefly above, a guideline based on the hepatic effects from ingestion alone could miss some important information about potential toxicity via other exposure routes.
A future reflection about risk assessment will cover how this TDI was used to derive a drinking water (i.e. tap water) guideline considering ingestion, inhalation and dermal exposures.
Why a TDI Based on a Threshold – Isn’t Chloroform a Carcinogen?
The EPA classifies chloroform as a Group B2 possible carcinogen, but its effect are still considered to be due to a threshold effect (IRIS, 2001; Health Canada, 2006). The carcinogenic effects of chloroform are hypothesized to be related only to its cytotoxic effects and resulting regenerative hyperplasia; the weight of evidence suggest there is no genotoxicity associated with chloroform. Carcinogenic effects are only thought to occur at doses that cause repeated and sustained cytotoxicity with resultant cell proliferation, producing a non-linear response curve with a threshold effect. The EPA considers the reference dose protective for these cytotoxic effect (IRIS, 2001).
Next week I will look at some of the evidence for toxicity of the other 3 common THMs, and in a future reflection I hope to return to the health effects of THMs by looking at role of evidence from epidemiological studies.
Government of Canada HC (2006) Guidelines for Canadian Drinking Water Quality: Guideline Technical Document: Trihalomethanes. http://www.hc-sc.gc.ca/ewh-semt/pubs/water-eau/trihalomethanes/index-eng.php
Heywood R, Sortwell RJ, Noel PRB, Street AE, Prentice DE, Roe FJC, Wadsworth PF, Worden AN, Van Abbe NJ (1979) Safety evaluation of toothpaste containing chloroform. III. Long-term study in beagle dogs. J Environ Pathol Toxicol 2: 835–851.
IRIS, US EPA (2001) Integrated Risk Information System Toxicological Review of Chloroform. http://www.epa.gov/iris/toxreviews/0025tr.pdf
Larson JF, Wolf DC, Butterworth BE (1994) Induced cytotoxicity and cell proliferation in the hepatocarcinogenicity of chloroform in female B6C3F1 mice: comparison of administration by gavage in corn oil vs ad libitum in drinking water. Toxicological Sciences 22: 90–102.
Watts P, Long G, Meeks ME (2004) Chloroform: International Program on Chemical Safety (IPCS) Concise international chemical assessment document 58. World Health Organization: Geneva. http://www.who.int/ipcs/publications/cicad/en/cicad58.pdf
Winslow SG, Gerstner HB (1978) Health aspects of chloroform-a review. Drug Chem Toxicol 1: 259–275.
WHO (2005). Trihalomethanes in Drinking-Water: Background Document for Development of WHO Guidelines for Drinking-Water Quality. WHO: Geneva. http://www.who.int/water_sanitation_health/dwq/chemicals/en/trihalomethanes.pdf
March 21, 2014 at 1:31 pm
Author –
In this final reflection I want to briefly touch on the issue of risk assessments. First, I will very briefly review the toxicity data on the other THMs
Bromodichloromethane (BDCM)
Studies have primarily been done on mice and rats. Summaries of the studies and the various NOAELs derived can be found in the WHO (2004) and Health Canada (2006) summary documents. NOAELs varied from 25-150 mg/kg-day in the short term studies based on a variety of effects including liver, kidney and thyroid lesions, changes in serum liver enzymes, body weight depression and fetotoxic effects. BDCM has also been identified as carcinogenic in animal studies (liver, kidney, large intestinal tumors in rats, liver and kidney tumors in mice), and also a probably mutagen (recall chloroform was not found to be genotoxic)(WHO, 2004). It is considered to be the most potent carcinogen among the THMs (Health Canada, 2006).
Dibromochoromethan (DBCM)
WHO (2004) also identified several short and long term studies on mice and rats. A variety of liver, kidney, thyroid lesions, serum liver enzyme elevations, loss of body weight, NOAELs were found ranging from 10-125 mg/kg-day. DBCM was found to be a probable mutagen, but there was only equivocal evidence for carcinogenicity in mice (WHO, 2004).
Bromoform
Bromoform has been found to have primarily liver effects in short and long term liver studies along with diminished growth rates and body weight. Based primarily on its liver effects, NOAELS ranged from 18-100 mg/kg-day, and one study identified a LOAEL of 100 mg/kg-day. No reproductive or teratogenic effects were found, but bromoform was identified as a probable mutagen and potential carcinogen (WHO, 2004).
Drinking Water Guideline Values
Chloroform
As discussed last week Health Canada derived a TDI of 6.2 ug/kg-day for chloroform, and this TDI was used to form a guideline that encompasses the total THM concentration in drinking water.
Daily drinking water intake for Canada is set at 1.5 L day (for an adult) for risk assessment, but as discussed in a previous reflection, individuals are also exposed to THM in tap water via inhalation and dermal absorption. Health Canada used modelling to convert these other exposure routes to the equivalent of ingestion in L, and estimated an adult is exposure as equivalent to 4.11 L/day based on taking a 30 minute bath per day. This bath scenario resulted in the highest exposure levels, so using this estimate should result in a conservative guideline given that most adults would not exposed to levels this high. Equivalent doses were also calculated for children, which would likely be a more sensitive receptor, but I could not track these down and the Health Canada guideline is based on the adult value.
An adult body weight of 70 kg/day, and an allocation factor of 0.8 for chloroform exposure via tap water that was specified by CEPA were used to make the calculation of the guideline as follows:
(6.2 ug/kg-day * 70 kg * 0.8) / 4.11 L equivalent/day ≈ 80 ug/L
However, 80 ug/L was deemed economically difficult for many water treatment plants and the guideline was increased to 100 ug/L (an increase deemed unlikely to significantly increase health risks) to be a more reasonable target. This is an example where a cost-benefit analysis was used to in setting the final guideline, an area we touched on in class.
The WHO takes a slightly different approach, and does not calculate a total trihalomethand guideline, as such. However a guideline was developed for chloroform which could be compared to the Health Canada Guideline considering the Health Canada guideline is based on the TDI for chloroform. The WHO assumed a body weight of 60 kg, an allocation factor of 0.5, and intake of 2 L/day (therefore based solely on drinking water ingestion as exposure), and used a TDI if 13 Ug/kg-day.
13 ug/kg-day * 60 kg * 0.5 / 2 L/day ≈200 ug/L
The WHO, however, does not consider the chloroform guideline a suitable “umbrella” guideline for all TMS, so set guidelines for each of the THMs as well as how to consider them jointly (more on this shortly).
Interestingly, EPA has set their guideline at 80 ug/L.
Bromodichloromethane
In my first reflection, I erroneously stated that Canada has a separate guideline for BDCM; a guideline was set in the 2006 assessment of THMs, but was rescinded in 2009 in light of more recent research which rated BDCM as less of a health concern (studies not cited; I ran out of time to request a copy of supporting document from Health Canada). Initially Health Canada used a modeling approach [based on kidney tumors in mice (NTP 1987)] and applied a conversion to human cancer risks shown in the table below. Based on the lowest concentration for a cancer risk of 10-5, a guideline of 16 ug/L was initially set before the guideline was rescinded.
Excess lifetime cancer risks
BDCM concentration
10-5
15.8-48.5
10-6
1.6-4.9
10-7
0.2-0.5
WHO considered the same study as Health Canada and also used a linearized multistage model but with different outcome; I wasn’t able to ascertain the differences in the calculations but perhaps it is due to the process to convert to lifetime human risks by Health Canada. Note that the WHO guidelines lifetime cancer risks differ by an order of magnitude so their table is not directly comparable to the Health Canada table; the Health Canada guidelines are just a bit more conservative.
Excess lifetime cancer risks
BDCM concentration
10-4
600 µg/litre
10-5
60 µg/litre
10-6
6 µg/litre
Dibromochloromethane and Bromoform
Health Canada considers the evidence for the toxicity of these two THMs insufficient to develop a guideline. The WHO did develop guidelines for these THM, as shown in the table below. What is interesting is that the proportion of the TDI attributed to drinking water is much lower than for chloroform, (i.e. the usual 20% set out in a single exposure risk assessment).
Guideline
NOAEL
TDI
Uncertainty factor
Proportion of TDI attributed to water
Dibromochloromethane
100 ug/L
30 mg/kg-day
21.4 µg/kg (NTP 1985)
1000
20%
Bromoform
100 ug/L
25 mg/kg
17.9 µg/kg (NTP 1989)
1000
20%
Total ThM
Finally the WHO does approach the issue of total THMs by recommended that the proportions of each THM should add to less than 1.0 according to the following formula:
C(chloroform)/GV(chloroform) + C(BDCM)/GV(BDCM) + C(DBCM)/GV(DBCM) + C(bromoform)/GV(bromoform) <= 1
where C is the concentration and GV is the guideline value for each THM.
Health Canada’s approach was to develop a guideline based on chloroform, under the assumption that a guideline protective for chloroform will be protective against other THMs too (which is a big assumption), and the THM concentrations are added to make sure they fit within this guideline in total (based primarily on the toxicity data showing similar modes of action for each of the THM).
Going back to the Saskatoon data, the average total THMs over 2005-2013 (data I linked to in my exposure reflection) was 42 ug/L. For an adult, using Health Canada’s equivalency factor to account for inhalation and dermal exposures as well as ingestion, the EDI from our tap water for an average adult could be estimated at 2.5 ug/kg-day. This is higher than the 0.2 hazard quotient discussed in class based on Health Canada’s TDI of 6.2 ug/kg-day, but based on the WHO TDI of 13 ug/kg-day this would be just under 0.2. Then again, CEPA determined that exposure through drinking water comprises 80% of total intake of chloroform so perhaps the cut of hazard quotient of 0.2 is considered conservative? I have to admit I still find the issue of hazard quotients and what is considered acceptable a bit confusing. In any case, I think this all underscores the uncertainties associated with the guidelines on which safe exposures are based.
Mixtures
Although we didn’t get a chance to delve into mixtures in class, it is likely that developing an approach to assess mixtures will be important to the future of assessing THMs. A wider issue that THMs do not occur in isolation as a disinfection by product, and it is possible that the range of other by-products with which they occur could have effects on their toxicity. Despite this, considering them in isolation is the best we can do at this point, although this leads to the prospect of an ever-increasing list of guidelines to be followed as more research is done on the potential health impacts of newly identified disinfection by products.
The Great Trade-Off
After all of this, let’s return to a cost benefit analysis. I briefly mentioned the economic cost-benefit analysis used by Health Canada in setting the guideline for THMs. And although I have mentioned it before, I want to finish off my reflections by emphasizing the most important cost-benefit consideration of all: the benefits of water disinfection.
I’ve made a point of contrasting the Health Canada and WHO approaches to developing guidelines, however there is one point on which both entities emphatically agree: efforts should be made to reduce the formation of THMs, but never at the cost of compromising the effective disinfection of drinking water. To quote the WHO:
“It is cautioned that where local circumstances require that a choice be made between
meeting microbiological guidelines or guidelines for disinfection by-products such as
chloroform, the microbiological quality must always take precedence. Efficient
disinfection must never be compromised.” (WHO, 2004)
While the issue of THMs should not be taken lightly as there do appear to be risks associated with exposure, it must be emphasized that these risks are quite small, especially compared with the risks of not disinfecting a water supply. Clean drinking water is something many people in developed countries might take for granted, although the United Nations estimates that 1.8 million people die every year from diarrheal disesase attributed to unsafe water and poor sanitation, most of them children living in poverty (UN Water, 2011). There have been 7 global pandemics of cholera including one that is ongoing — the number of cholera cases globally increased by 130% in the decade from 2000 to 2010 (UN Water); proper water disinfection readily prevents cholera. Closer to home, a failure in disinfection practices combined with contamination of a well due to extreme weather resulted in an outbreak of E. coli in Walkerton, ON that claimed 7 lives and made over 2000 people ill. The formation of THMs in our water supplies should be minimized to the lowest possible levels without compromising disinfection; the risks posed by THMs seem like a very reasonable trade-off in light of how important disinfection of the water supply is to our health.
Government of Canada HC (2006) Guidelines for Canadian Drinking Water Quality: Guideline Technical Document: Trihalomethanes – Health Canada. http://www.hc-sc.gc.ca/ewh-semt/pubs/water-eau/trihalomethanes/index-eng.php#a11
NTP (1985) Toxicology and carcinogenesis studies of chlorodibromomethane in F344/N rats and B6C3F1 mice (gavage studies). Research Triangle Park, NC, US Department of Health and Human Services, National Toxicology Program (TR 282). http://ntp.niehs.nih.gov/ntp/htdocs/LT_rpts/tr282.pdf
NTP (1987) Toxicology and carcinogenesis studies of bromodichloromethane in F344/N rats and B6C3F1 mice (gavage studies). Research Triangle Park, NC, US Department of Health and Human Services, National Toxicology Program (TR 321). http://ntp.niehs.nih.gov/ntp/htdocs/LT_rpts/tr321.pdf
NTP (1989) Toxicology and carcinogenesis studies of tribromomethane (bromoform) in F344/N rats and B6C3F1 mice (gavage studies). Research Triangle Park, NC, US Department of Health and Human Services, National Toxicology Program (TR 350).
Click to access tr350.pdf
UN Water (2011) Water Quality: Policy Brief. http://www.unwater.org/downloads/waterquality_policybrief.pdf
UN Water Web Site http://www.unwater.org/statistics_san.html
World Health Organization (2004) Trihalomethanes in Drinking Water. WHO: Geneva. http://www.who.int/water_sanitation_health/dwq/chemicals/en/trihalomethanes.pdf
March 21, 2014 at 1:31 pm
This is a very thorough closure to your topic. The concluding paragraph really hit home for me. I think in Canada we often forget that complaining about things like disinfection byproducts and flouride in our water is a luxury. So many people in this world live without clean water and would love to be able to drink our tap water.
Great job, I did not know anything about THMs and other disinfection byproducts until I read your posts so thanks for enlightening me!
March 21, 2014 at 1:32 pm
I really like the topic you chose. I’ve been following all your comments, and I think you did a great job approaching different aspects of the risk assessment of Trihalomethanes.
As we learnt during classes, the exposure to some compounds can be higher in children due to their hand-to-mouth behavior. This week I attended to a flame retardant seminar, and the results in infants exposure presented follow the same trend, higher in infants than adults.
Your previous comment, regarding the duration of bathing and common children activities, e.g. go to swimming pool, could increase the exposure to Trihalomethanes. Additionally, you also commented that children are likely to be more sensitive. I read a paper that presents suggestive results of association of childhood acute lymphoblastic leukemia with trihalomethanes in drinking water (1).
I wonder if the TDI and the rates of exposure should be different and specific for this age group. And I would like to know if you read any paper evaluating the exposure in infants and children.
1- 1- Infante-Rivard et al. GSTT1 and CYP2E1 Polymorphisms and Trihalomethanes in Drinking Water: Effect on Childhood Leukemia. Environtal Health Perspective, 110(6): 591–593, 2001.
March 21, 2014 at 1:32 pm
Great job indeed, i really enjoyed the topic. Just wanted to throw a final comen on the lines of what i said before about some similarities about our topics. I liked that you mentioned the cost benefit analisys and the WHO coment about putting effort on reducing THM’s as long as water disinfection is ensured. Even though water fluoridation might seem like a trivial thing, not that long ago, death by systemic infection from tooth decay was a comon thing. In current times, with fluoride exposure from multiple other products, developed countries are starting to consider wether the investment is worth it. As the WHO said about THM’s, not everybody is a lucky as us, and while we could afford the costs of other technologies and being “picky” about the way our water is being treated, there are still a lot of people around the world for wich basic water treatment is still a luxory.