2. Rev Environ Health. 2009 Oct-Dec;24(4):357-63.
Too much of a good thing? Nitrate from nitrogen fertilizers and cancer.
Ward MH.
Source: Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute,ExecutivePlazaSouth, Room 8006,6120 Executive Boulevard,Bethesda20892-7240,Maryland,USA.
Abstract: Nitrate levels in water supplies have been increasing in many areas of the world; therefore, additional studies of populations with well-characterized exposures are urgently needed to further our understanding of cancer risk associated with nitrate ingestion. Future studies should assess exposure for individuals (e.g., case-control, cohort studies) in a time frame relevant to disease development, and evaluate factors affecting nitrosation. Estimating N-nitroso compounds formation via nitrate ingestion requires information on dietary and drinking water sources of nitrate, inhibitors of nitrosation (e.g., vitamin C), nitrosation precursors (e.g., red meat, nitrosatable drugs), and medical conditions that may increase nitrosation (e.g., inflammatory bowel disease). Studies should account for the potentially different effects of dietary and water sources of nitrate and should include the population using private wells for whom exposure levels are often higher than public supplies. PMCID: PMC3068045 Free PMC Article
PMID: 20384045 [PubMed - indexed for MEDLINE]
3. Sci Total Environ. 2009 Jul 1;407(14):4189-206. Epub 2009 May 6.
Chowdhury S,ChampagneP, McLellan PJ.
Source: Department of Civil Engineering, Queen’s University, Kingston, Ontario, Canada. Shakhawat@ce.queensu.ca
Abstract: Disinfection for the supply of safe drinking water forms a variety of known and unknown byproducts through reactions between the disinfectants and natural organic matter. Chronic exposure to disinfection byproducts through the ingestion of drinking water, inhalation and dermal contact during regular indoor activities (e.g., showering, bathing, cooking) may pose cancer and non-cancer risks to human health. Since their discovery in drinking water in 1974, numerous studies have presented models to predict DBP formation in drinking water. To date, more than 48 scientific publications have reported 118 models to predict DBP formation in drinking waters. These models were developed through laboratory and field-scale experiments using raw, pretreated and synthetic waters. This paper aims to review DBP predictive models, analyze the model variables, assess the model advantages and limitations, and to determine their applicability to different water supply systems. The paper identifies the current challenges and future research needs to better control DBP formation. Finally, important directions for future research are recommended to protect human health and to follow the best management practices.
PMID: 19419751 [PubMed - indexed for MEDLINE]
4. Water Res. 2009 May;43(8):2057-92. Epub 2009 Feb 20.
Chlorination disinfection by-products, public health risk tradeoffs and me.
Hrudey SE.
Source: Steve E Hrudey & Associates Ltd, Canmore, Canada. steve.hrudey@ualberta.ca
Abstract: Since 1974 when trihalomethanes (THMs) were first reported as disinfection by-products (DBPs) in drinking water, there has been an enormous research effort directed at understanding how DBPs are formed in the chlorination or chloramination of drinking water, how these chlorination DBPs can be minimized and whether they pose a public health risk, mainly in the form of cancer or adverse reproductive outcomes. Driven by continuing analytical advances, the original DBPs, the THMs, have been expanded to include over 600 DBPs that have now been reported in drinking water. The historical risk assessment context which presumed cancer could be mainly attributed to exposure to environmental carcinogens played a major role in defining regulatory responses to chlorination DBPs which, in turn, strongly influenced the DBP research agenda. There are now more than 30 years of drinking water quality, treatment and health effects research, including more than 60 epidemiology studies on human populations, directed at the chlorination DBP issue. These provide considerable scope to reflect on what we know now, how our understanding has changed, what those changes mean for public health risk management overall and where we should look to better understand and manage this issue in the future.
PMID: 19304309 [PubMed - indexed for MEDLINE]
5. Mutat Res. 2007 Nov-Dec;636(1-3):178-242. Epub 2007 Sep 12.
RichardsonSD, Plewa MJ, Wagner ED, Schoeny R, Demarini DM.
Source: National Exposure Research Laboratory, US Environmental Protection Agency, Athens, GA30605, USA. richardson.susan@epa.gov
Abstract: Disinfection by-products (DBPs) are formed when disinfectants (chlorine, ozone, chlorine dioxide, or chloramines) react with naturally occurring organic matter, anthropogenic contaminants, bromide, and iodide during the production of drinking water. Here we review 30 years of research on the occurrence, genotoxicity, and carcinogenicity of 85 DBPs, 11 of which are currently regulated by theU.S., and 74 of which are considered emerging DBPs due to their moderate occurrence levels and/or toxicological properties. These 74 include halonitromethanes, iodo-acids and other unregulated halo-acids, iodo-trihalomethanes (THMs), and other unregulated halomethanes, halofuranones (MX [3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone] and brominated MX DBPs), haloamides, haloacetonitriles, tribromopyrrole, aldehydes, and N-nitrosodimethylamine (NDMA) and other nitrosamines. Alternative disinfection practices result in drinking water from which extracted organic material is less mutagenic than extracts of chlorinated water. However, the levels of many emerging DBPs are increased by alternative disinfectants (primarily ozone or chloramines) compared to chlorination, and many emerging DBPs are more genotoxic than some of the regulated DBPs. Our analysis identified three categories of DBPs of particular interest. Category 1 contains eight DBPs with some or all of the toxicologic characteristics of human carcinogens: four regulated (bromodichloromethane, dichloroacetic acid, dibromoacetic acid, and bromate) and four unregulated DBPs (formaldehyde, acetaldehyde, MX, and NDMA). Categories 2 and 3 contain 43 emerging DBPs that are present at moderate levels (sub- to low-mug/L): category 2 contains 29 of these that are genotoxic (including chloral hydrate and chloroacetaldehyde, which are also a rodent carcinogens); category 3 contains the remaining 14 for which little or no toxicological data are available. In general, the brominated DBPs are both more genotoxic and carcinogenic than are chlorinated compounds, and iodinated DBPs were the most genotoxic of all but have not been tested for carcinogenicity. There were toxicological data gaps for even some of the 11 regulated DBPs, as well as for most of the 74 emerging DBPs. A systematic assessment of DBPs for genotoxicity has been performed for approximately 60 DBPs for DNA damage in mammalian cells and 16 for mutagenicity in Salmonella. A recent epidemiologic study found that much of the risk for bladder cancer associated with drinking water was associated with three factors: THM levels, showering/bathing/swimming (i.e., dermal/inhalation exposure), and genotype (having the GSTT1-1 gene). This finding, along with mechanistic studies, highlights the emerging importance of dermal/inhalation exposure to the THMs, or possibly other DBPs, and the role of genotype for risk for drinking-water-associated bladder cancer. More than 50% of the total organic halogen (TOX) formed by chlorination and more than 50% of the assimilable organic carbon (AOC) formed by ozonation has not been identified chemically. The potential interactions among the 600 identified DBPs in the complex mixture of drinking water to which we are exposed by various routes is not reflected in any of the toxicology studies of individual DBPs. The categories of DBPs described here, the identified data gaps, and the emerging role of dermal/inhalation exposure provide guidance for drinking water and public health research.
PMID: 17980649 [PubMed - indexed for MEDLINE]
6. Cancer. 2007 Jun 15;109(12 Suppl):2635-66.
Rudel RA, Attfield KR, Schifano JN, Brody JG.
Source: Silent Spring Institute, Newton, Massachusett 02458, USA. Rudel@SilentSpring.org
Abstract: Identifying chemical carcinogens in animal studies is currently the primary means of anticipating cancer effects in humans. Animal studies to evaluate potential chemical carcinogenicity are particularly important for breast cancer because environmental and occupational epidemiologic research is sparse. Chemicals that increased mammary gland tumors in animal studies were compiled from the International Agency for Research on Cancer (IARC), the U.S. National Toxicology Program (NTP), and other sources. Summary assessments of the carcinogenic potential for each chemical and potentially exposed populations were also compiled. In all, 216 chemicals were identified that have been associated with increases in mammary gland tumors in at least 1 study. These include industrial chemicals, chlorinated solvents, products of combustion, pesticides, dyes, radiation, drinking water disinfection byproducts, pharmaceuticals and hormones, natural products, and research chemicals. Twenty-nine are produced in the U.S.at >1 million pounds/year; 35 are air pollutants, 25 have involved occupational exposures to >5000 women, and 73 have been present in consumer products or as contaminants of food. Thus, exposure is widespread. Nearly all of the chemicals were mutagenic and most caused tumors in multiple organs and species; these characteristics are generally believed to indicate likely carcinogenicity in humans. To our knowledge, this is the most comprehensive list developed of animal mammary gland carcinogens and, along with associated data, is publicly available at URL: www.silentspring.org/sciencereview and at URL: www.komen.org/environment. Valuable information from cancer bioassays is not well utilized in risk assessment and regulatory processes, suggesting a need to strengthen chemicals testing and risk assessment as tools for breast cancer prevention. Free Article
PMID: 17503434 [PubMed - indexed for MEDLINE]
7. Environ Sci Technol. 2007 Jan 15;41(2):363-72.
Drowning in disinfection byproducts? Assessing swimming pool water.
Zwiener C,RichardsonSD, DeMarini DM, Grummt T, Glauner T, Frimmel FH.
Source: Engler-Bunte-Institute, Universitaet Karlsruhe, Karlsruhe, Germany. christian.zwiener@ciw.uni-karlsruhe.de
Erratum in Environ Sci Technol. 2008 Mar 1;42(5):1812. De Marini, David M [corrected to DeMarini, David M].
Abstract: Disinfection is mandatory for swimming pools: public pools are usually disinfected by gaseous chlorine or sodium hypochlorite and cartridge filters; home pools typically use stabilized chlorine. These methods produce a variety of disinfection byproducts (DBPs), such as trihalomethanes (THMs), which are regulated carcinogenic DBPs in drinking water that have been detected in the blood and breath of swimmers and of nonswimmers at indoor pools. Also produced are halogenated acetic acids (HAAs) and haloketones, which irritate the eyes, skin, and mucous membranes; trichloramine, which is linked with swimming-pool-associated asthma; and halogenated derivatives of UV sun screens, some of which show endocrine effects. Precursors of DBPs include human body substances, chemicals used in cosmetics and sun screens, and natural organic matter. Analytical research has focused also on the identification of an additional portion of unknown DBPs using gas chromatography (GC)/mass spectrometry (MS) and liquid chromatography (LC)/MS/MS with derivatization. Children swimmers have an increased risk of developing asthma and infections of the respiratory tract and ear. A 1.6-2.0-fold increased risk for bladder cancer has been associated with swimming or showering/bathing with chlorinated water. Bladder cancer risk from THM exposure (all routes combined) was greatest among those with the GSTT1-1 gene. This suggests a mechanism involving distribution of THMs to the bladder by dermal/inhalation exposure and activation there by GSTT1-1 to mutagens. DBPs may be reduced by engineering and behavioral means, such as applying new oxidation and filtration methods, reducing bromide and iodide in the source water, increasing air circulation in indoor pools, and assuring the cleanliness of swimmers. The positive health effects gained by swimming can be increased by reducing the potential adverse health risks.
PMID: 17310693 [PubMed - indexed for MEDLINE]
8. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2005;23(2):163-214.
Carcinogenicity of the chlorination disinfection by-product MX.
McDonald TA, Komulainen H.
Source: Office of Environmental Health Hazard Assessment, CaliforniaEnvironmental Protection Agency, Oakland, USA. thomas.mcdonald@arystalifescience.com
Abstract: 3-Chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone, better known by its historical name ‘mutagen X’ or MX, is a chlorination disinfection byproduct that forms from the reaction of chlorine and humic acids in raw water. MX has been measured in drinking water samples in several countries at levels that ranged from non-detectable to 310 ng/L. Although the concentration of MX in drinking water is typically 100- to 1000-fold lower than other common chlorinated by-products of concern (e.g., trihalomethanes), some have hypothesized that MX might play a role in the increased cancer risks that have been associated with the consumption of chlorinated water. This hypothesis is based on observations that MX, in some test systems, is extremely potent relative to trihalomethanes in inducing DNA damage and altering pathways involved in cell growth, and that in some epidemiological studies increased cancer rates are associated with the bacterial mutagenicity of disinfected water of which MX contributes a significant portion. MX also appears to be more potent than other chlorination by-products in causing cancer in animals. This article reviews the available evidence on the carcinogenicity of MX. MX induced cancer at multiple sites in male and female rats, acted as a tumor initiator and promoter, enhanced tumor yields in genetically modified rodents, induced a myriad of genotoxic effects in numerous in vitro and in vivo test systems, and was a potent inhibitor of gap junction intercellular communication. Although the precise mechanism of MX-induced DNA damage is not known, MX is able to cause DNA damage through an unusual mechanism of ionizing DNA bases due to its extremely high reductive potential. MX may also cause mutations through DNA adduction. This article develops a mean cancer potency estimate for MX of 2.3 (mg/kg-d)(-1) and an upper 95% percentile estimate of 4.5 (mg/kg-d)(-1), and examines the potential health risks posed by this chlorination contaminant in drinking water. A discussion of additional data that would be desirable to better characterize the risks posed by MX and other halogenated hydroxyfuranones follows.
PMID: 16291527 [PubMed - indexed for MEDLINE]
9. Toxicology. 2004 May 20;198(1-3):255-62.
Risk analysis of drinking water microbial contamination versus disinfection by-products (DBPs).
Ashbolt NJ.
Source: CRC for Water Quality and Treatment, School of Civil and Environmental Engineering, UNSW, Sydney, NSW 2052, Australia. N.Ashbolt@unsw.edu.au
Abstract: Managing the provision of safe drinking water has a renewed focus in light of the new World Health Organization (WHO) water safety plans. Risk analysis is a necessary component to assist in selecting priority hazards and identifying hazardous scenarios, be they qualitative to quantitative assessments. For any approach, acute diarrhoeal pathogens are often the higher risk issue for municipal water supplies, no matter how health burden is assessed. Furthermore, potential sequellae (myocarditis, diabetes, reactive arthritis and cancers) only further increase the potential health burden of pathogens; despite the enormous uncertainties in determining pathogen exposures and chemical dose-responses within respective microbial and chemical analyses. These interpretations are currently being improved by Bayesian and bootstrapping approaches to estimate parameters for stochastic assessments. A case example, covering the health benefits of ozonation for Cryptosporidium inactivation versus potential cancers from bromate exposures, illustrated the higher risks from a pathogen than one of the most likely disinfection by-products (DBPs). Such analyses help justify the industries long-held view of the benefits of multiple barriers to hazards and that microbial contamination of water supplies pose a clear public health risk when treatment is inadequate. Therefore, efforts to reduce potential health risks from DBP must not compromise pathogen control, despite socio-political issues.
PMID: 15138049 [PubMed - indexed for MEDLINE]
10. Toxicology. 2004 May 20;198(1-3):239-48.
Experimental cancer studies of chlorinated by-products.
Komulainen H.
Source: National Public Health Institute, Division of Environmental Health, Laboratory of Toxicology, P.O. Box95, FIN-70701 Kuopio, Finland. hannu.komulainen@ktl.fi
Abstract: Chlorinated drinking water contains a number of different by-products formed during the chlorination process from organic matter. The carcinogenicity of only a fraction of them have been evaluated in experimental animals. The focus has been on compounds and groups of compounds that are most abundant in chlorinated drinking water or the in vitro toxicity data have suggested genotoxic potential. From trihalomethanes, chloroform causes liver tumors in mice and female rats and renal tumors in male mice and rats. Tumor formation by chloroform is strongly associated with cytotoxicity and regenerative cell proliferation in tissues and that has been considered to be one determinant of its carcinogenicity. From halogenic acetic acids, dichloroacetic acid (DCA) and trichlotoacetic acid (TCA) are hepatocarcinogenic in mice and DCA in male rats. Their genotoxicity is equivocal and nongenotoxic mechanisms, such as peroxisome proliferation and hypomethylation of DNA in the liver, likely contribute to tumor development. From chlorinated furanones (CHFs), 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX) is a multisite carcinogen in rats (e.g. in thyroid glands and liver) and it has caused DNA damage in vivo. MX may be a complete carcinogen because it also has promoter properties in vitro. Chlorinated drinking water may also contain brominated by-products providing the raw water contains bromide. At least some of them (bromodichloromethane, bromoform) have been shown to be carcinogenic in laboratory animals. Altogether, although several by-products have been shown to have carcinogenic potential in laboratory animals, it not yet possible to state which compounds or groups of by-products cause the cancer risk in chlorinated drinking water. The cellular mechanisms of their effects and these effects at low concentrations are still poorly understood. The few studies with mixtures of these by-products suggest that the mixture effects may be complex and unpredictable (inhibitory, additive, synergistic).
PMID: 15138047 [PubMed - indexed for MEDLINE]
11. MedGenMed. 2002 Nov 6;4(4):16.
Cancer clusters: findings vs feelings.
Robinson D.
Source: American Council on Science and Health,New York,NY,USA.
Comment in MedGenMed. 2002 Nov 26;4(4):20; author reply 21.
Abstract: The issue of cancer clusters, which has been in the spotlight recently, is plagued by a wide disparity between public perceptions and scientific findings. Movies like Erin Brockovich have led the public to think that industrial pollution in the environment is causing local “cancer clusters” where cancer cases are more prevalent due to cancer-causing chemicals. There are many scientifically documented instances in which chemical exposure has caused cancer in humans, but the evidence for purely environmental exposures causing cancer is sparse. The clusters that scientists have been able to attribute successfully to a particular cause have been occupational (such as workers in a factory developing a particular type of cancer from daily exposure to a specific chemical), linked to a particular medicine, or linked to behaviors such as smoking or sunbathing. There is some indication that chemicals dissolved in drinking water may elevate the risk of gastrointestinal and bladder/urinary tract cancers and that living next to a smelter or other “point source” of air pollution may elevate risk of lung cancer. The many efforts that have been made to demonstrate links between other types of cancer and environmental contamination have not conclusively identified such links. Several challenges bedevil any cancer cluster investigation and can result in ambiguous or misleading conclusions. This report discusses the potential cancer clusters in Toms River, New Jersey andLong Island,New York, because they contain many elements typical of cancer cluster investigations and have received considerable media attention. Free Article
PMID: 12817212 [PubMed - indexed for MEDLINE]
12. Anim Reprod Sci. 2000 Jul 2;60-61:121-30.
Deteriorating trends in male reproduction: idiopathic or environmental?
Veeramachaneni DN.
Source: Animal Reproduction and Biotechnology Laboratory, Department of Physiology, Collegeof Veterinary Medicineand Biomedical Sciences, ColoradoStateUniversity, Fort Collins80523-1683, USA. rao@cvmbs.colostate.edu
Abstract: Recent reports portend deterioration in male reproductive health in several human populations. Similar trends might exist in domestic animals, but data are not available because of the inherent nature of animal husbandry practices – culling of the reproductively inefficient food- and fiber-producing animals at an early age. Although the causes for this deterioration are unknown, a variety of endocrine-mimicking environmental pollutants have been implicated. Data for relevant laboratory animal models exposed to several classes of suspect chemicals indicate that a variety of chemicals ubiquitously present in the environment can disrupt normal reproductive phenomena in the male at exposure rates encountered in nature. Data are presented for occurrence of cryptorchidism, carcinoma in situ of the testis, acrosomal malformations, and impaired sexual function following in utero and/or postnatal exposures to pesticides (e.g., DDT and vinclozolin), high-volume industrial chemicals (e.g., alkylphenols and phthalates), and commonly occurring organic and inorganic chemical contaminants in drinking water (e.g., chemical mixtures and water disinfection byproducts). These observations are discussed in the context of similar, so-called idiopathic conditions encountered in stallions.
PMID: 10844189 [PubMed - indexed for MEDLINE]
13. Food Chem Toxicol. 2000;38(1 Suppl):S81-5.
Clues and uncertainties in the risk assessment of arsenic in drinking water.
Buchet J, Lison D.
Source: Catholic University of Louvain, MD/ESP/TOXI, Clos Chapelle-aux-Champs, 30.54, B-1200,Brussels,Belgium.
Abstract: On the basis of studies of the prevalence of skin cancer among users of As-rich well water inTaiwan, WHO experts recommended in 1984 a maximum As concentration of 50 microg/litre in drinking water. Since that time, a plethora of non-cancer as well as cancer effects has been observed in several other populations sustaining a chronic exposure to various As concentrations in drinking water. This prompted a revision of the standard and a provisional guideline of 10 microg/litre was recommended in 1993. While the uncertainty linked to the statistical inferences leading to the guideline are reduced by the fact that they are directly estimated from human data and result from extrapolations made relatively close to observed exposure levels, developed guideline depends strongly on the choice of the dose-response model (linear, quadratic, hockey-stick) and the accuracy of the exposure data. The potential exposure to As sources other than drinking water, dietary habits and genetic characteristics of the populations may also make more difficult the inference of a recommendation for As concentration in drinking water. Owing to the huge cost of strongly reducing the current As in water standard, many efforts are presently made to clarify the quantitative aspects of As-induced cancers, particularly at low dose levels. New data on the metabolism and carcinogenic mechanism of As in humans along with the results of epidemiological studies presently under way in several countries will help to reduce the uncertainty in the risk assessment of As.
PMID: 10717375 [PubMed - indexed for MEDLINE]
14. Occup Environ Med. 2000 Feb;57(2):73-85.
Nieuwenhuijsen MJ,ToledanoMB,EatonNE, Fawell J, Elliott P.
Source: Department of Epidemiology and Public Health,ImperialCollegeSchoolof Medicine at St Mary’s,London,UK.
Abstract:
OBJECTIVES AND METHODS: Chlorination has been the major disinfectant process for domestic drinking water for many years. Concern about the potential health effects of the byproducts of chlorination has prompted the investigation of the possible association between exposure to these byproducts and incidence of human cancer, and more recently, with adverse reproductive outcomes. This paper evaluates both the toxicological and epidemiological data involving chlorination disinfection byproducts (DBPs) and adverse reproductive outcomes, and makes recommendations for future research.
RESULTS AND CONCLUSIONS: Relatively few toxicological and epidemiological studies have been carried out examining the effects of DBPs on reproductive health outcomes. The main outcomes of interest so far have been low birth weight, preterm delivery, spontaneous abortions, stillbirth, and birth defects–in particular central nervous system, major cardiac defects, oral cleft, and respiratory, and neural tube defects. Various toxicological and epidemiological studies point towards an association between trihalomethanes (THMs), one of the main DBPs and marker for total DBP load, and (low) birth weight, although the evidence is not conclusive. Administered doses in toxicological studies have been high and even though epidemiological studies have mostly shown excess risks, these were often not significant and the assessment of exposure was often limited. Some studies have shown associations for DBPs and other outcomes such as spontaneous abortions, stillbirth and birth defects, and although the evidence for these associations is weaker it is gaining weight. There is no evidence for an association between THMs and preterm delivery. The main limitation of most studies so far has been the relatively crude methodology, in particular for assessment of exposure.
RECOMMENDATIONS: Large, well designed epidemiological studies focusing on well defined end points taking into account relevant confounders and with particular emphasis on exposure characterisation are ideally needed to confirm or refute these preliminary findings. In practice, these studies may be impracticable, partly due to the cost involved, but this is an issue that can be put right–for example, by use of subsets of the population in the design of exposure models. The studies should also reflect differences of culture and water treatment in different parts of the world. To identify the specific components that may be of aetiological concern and hence to fit the most appropriate exposure model with which to investigate human exposure to chlorinated DBPs, further detailed toxicological assessments of the mixture of byproducts commonly found in drinking water are also needed. PMCID: PMC1739910 Free PMC Article
PMID: 10711274 [PubMed - indexed for MEDLINE]
15. Chronic DisCan.1998;19(3):103-7.
Safe drinking water: a public health challenge.
Wigle DT.
Source: Bureau of Operations, Planning and Policy, Laboratory Centre for Disease Control, Health Canada, Tunney’s Pasture, AL: 0602E2, Ottawa, Ontario, K1A 0L2, Canada. Don_T_Wigle@hc-sc.gc.ca
Abstract: Disinfection of drinking water through processes including filtration and chlorination was one of the major achievements of public health, beginning in the late 1800s and the early 1900s. Chloroform and other chlorination disinfection by-products (CBPs) in drinking water were first reported in 1974. Chloroform and several other CBPs are known to cause cancer in experimental animals, and there is growing epidemiologic evidence of a causal role for CBPs in human cancer, particularly for bladder cancer. It has been estimated that 14 16% of bladder cancers in Ontario may be attributable to drinking water containing relatively high levels of CBPs; the US Environmental Protection Agency has estimated the attributable risk to be 2 17%. These estimates are based on the assumption that the associations observed between bladder cancer and CBP exposure reflect a cause-effect relation. An expert working group (see Workshop Report in this issue) concluded that it was possible (60% of the group) to probable (40% of the group) that CBPs pose a significant cancer risk, particularly of bladder cancer. The group concluded that the risk of bladder and possibly other types of cancer is a moderately important public health problem. There is an urgent need to resolve this and to consider actions based on the body of evidence which, at a minimum, suggests that lowering of CBP levels would prevent a significant fraction of bladder cancers. In fact, given the widespread and prolonged exposure to CBPs and the epidemiologic evidence of associations with several cancer sites, future research may establish CBPs as the most important environmental carcinogens in terms of the number of attributable cancers per year.
PMID: 9820833 [PubMed - indexed for MEDLINE]
16. Cancer Causes Control. 1997 May;8(3):292-308.
Cantor KP.
Source: Occupational Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute,Bethesda,Maryland20892,USA.
Abstract: Epidemiologic evidence on the relation between contaminants in drinking water and cancer is reviewed. The reviewed studies cover exposure to: disinfection byproducts; nitrate; arsenic and other metals; volatiles and contaminants from hazardous waste sites; asbestiform fibers; radionuclides; and fluoride. Most investigations are ecologic, with some confirmation of elevated risk from individual-based studies. In the case of waterborne arsenic, and possibly chlorination byproducts, there is a consistent but small body of epidemiologic evidence of an association with one or more types of cancer. Nitrate in groundwater has increased greatly over the years, and the demonstration of endogenous nitrosation among highly exposed subjects raises concern of elevated cancer risk. However, the epidemiologic data are not yet sufficient to draw a conclusion. There is a diversity of studies among populations exposed to water contaminated with pesticides, volatile organics, or mixtures from hazardous waste sites. Studies of asbestiform fibers and radionuclides in water are not conclusive, but there are suggested elevations of several cancer sites in highly exposed populations. There is no suggestion that fluoride in drinking water is linked with elevated risk of cancer. As topics for epidemiologic evaluation, drinking water contaminants pose methodologic problems common to studies designed to detect relatively small elevations in risk, with the added challenge of assessing exposures for many years in the past. Nevertheless, epidemiologic assessment is valuable and clearly warranted, given the potential public health impact of small risk elevations among very large exposed populations, and the limitations of toxicologic experiments in assessing carcinogenic risk of complex mixtures or of compounds for which appropriate animal models are not available.
PMID: 9498894 [PubMed - indexed for MEDLINE]
17. Rev Environ Health. 1997 Apr-Jun;12(2):81-90.
Drinking water chlorination by-products and cancer.
Koivusalo M, Vartiainen T.
Source: Finnish Cancer Registry, Helsinki, Finland. meri.koivusalo@cancer.fi
Abstract: This review discusses the relation between by-products of drinking water chlorination and cancer in the light of present toxicological and epidemiologic evidence. During the chlorination of drinking water, a complex mixture of by-products forms from chlorine and the organic and inorganic compounds present in raw water. The quality and quantity of such compounds depend on the specific nature of the organic material in raw waters, the inorganic material in raw water, pH, temperature, other water treatment practices, and the chlorine timing and dose added. Chlorination by-products are important mainly when surface water is used for drinking water as more organic compounds are present in surface waters than in ground waters. The gastrointestinal and urinary tract are the cancer sites that are most often associated with the use of chlorinated surface water or with the quantity of chlorination by-products in the water-supply network. Yet the microbial quality of drinking water should not be compromised by excessive caution over the potential long-term effects of disinfection by-products because the risk of illness and death resulting from exposure to pathogens in untreated drinking water may be several orders of magnitude greater than the cancer risks from chlorination by-products.
PMID: 9273924 [PubMed - indexed for MEDLINE]
18.Environ Health Perspect. 1995 Nov;103 Suppl 8:225-31.
Morris RD.
Source: Department of Family and Community Medicine, Medical College of Wisconsin, Milwaukee, USA. morris@post.its.mcw.edu
Abstract: Any and all chemicals generated by human activity can and will find their way into water supplies. The types and quantities of carcinogens present in drinking water at the point of consumption will differ depending on whether they result from contamination of the source water, arise as a consequence of treatment processes, or enter as the water is conveyed to the user. Source-water contaminants of concern include arsenic, asbestos, radon, agricultural chemicals, and hazardous waste. Of these, the strongest evidence for a cancer risk involves arsenic, which is linked to cancers of the liver, lung, bladder, and kidney. The use of chlorine for water treatment to reduce the risk of infectious disease may account for a substantial portion of the cancer risk associated with drinking water. The by-products of chlorination are associated with increased risk of bladder and rectal cancer, possibly accounting for 5000 cases of bladder cancer and 8000 cases of rectal cancer per year in the United States. Fluoridation of water has received great scrutiny but appears to pose little or no cancer risk. Further research is needed to identify and quantify risks posed by contaminants from drinking-water distribution pipes, linings, joints, and fixtures and by biologically active micropollutants, such as microbial agents. We need more cost-effective methods for monitoring drinking-water quality and further research on interventions to minimize cancer risks from drinking water. PMCID: PMC1518976 Free PMC Article
PMID: 8741788 [PubMed - indexed for MEDLINE]
19. Pharmacol Toxicol. 1993;72 Suppl 1:108-15.
Carcinogenicity and drinking water.
Dayan AD.
Source: DH Dept of Toxicology, St Bartholomew’s Hospital Medical College, London.
Abstract: Water is a powerful solvent that readily dissolves many natural and synthetic substances from the environment (e.g. inorganic salts, humic acids and pesticide residues). The processes of purification, disinfection and preparation and storage necessary to provide and distribute drinking water may introduce further chemicals, including some used for these purposes and others derived by interaction between them and the compounds of natural origin. The composition of drinking water, therefore, is complex and varies between sites and with the seasons. Modern technology is employed to minimise the amounts of many of these substances, but some may persist, including derivatives generated by halogenation and ozonation for disinfection. Some of the substances are genotoxic in the laboratory and a few are proven experimental carcinogens–all at much higher concentrations than those normally found in a drinking water supply. Many ecological and epidemiological surveys have been done to compare the occurrence of various types of tumour in man with exposure to different types of drinking, but no consistent or reliable association has been found. There are serious and probably irremediable methodological weaknesses in these attempts, because of the difficulty of defining the nature of the waters consumed over a major part of life, and the variable composition of waters. The surveys do not permit even a realistic assessment of the upper confidence limit of the exclusion of the risk. Thus, although there is some experimental indication of the possible presence of carcinogenic substances in most or all drinking waters, and of how they are formed, the concentrations are very low and there is no realistic evidence that they have caused harm to man.(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 8474973 [PubMed - indexed for MEDLINE]
20. IARC Sci Publ. 1990;(104):298-306.
Drinking water and human cancer.
McMichael AJ.
Source: Department of Community Medicine, University of Adelaide, S.A., Australia.
Abstract: The relatively low concentrations of the various natural and man-made contaminants of drinking water, together with the methodological problems of obtaining valid and complete exposure histories for individuals and of controlling for confounding factors, have made it difficult for epidemiological studies to detect and estimate risks of cancer. Nearly all studies to date, with some exceptions for the halogenated hydrocarbons, have been at the ecological level. For these and other reasons, quantitative risk assessment of the cancer risks due to this complex environmental exposure remains rudimentary. If, eventually, risks are assessed to be non-trivial, primary prevention could be sought by alternative choices of either methods of water treatment or of water sources. However, since we cannot eliminate all trace carcinogens from our environment, we need simultaneously to minimize both the exposures and the biological impact of such exposures. The latter will require studies of cancer chemoprevention, using biochemical and molecular epidemiological approaches.
PMID: 2228127 [PubMed - indexed for MEDLINE]
21. Crit Rev Oral Biol Med. 1990;1(4):261-81.
Fluoride: benefits and risks of exposure.
Kaminsky LS, Mahoney MC, Leach J, Melius J, Miller MJ.
Source: Wadsworth Center for Labs and Research, New York State Department of Health, Albany 12201-0509.
Abstract: This summarizes current knowledge of the benefits and risks of fluoride ingestion. The preponderance of evidence indicates that fluoride can reduce the incidence of dental caries and that fluoridation of drinking water can provide such protection. Due to the ubiquitous nature of exposures to fluoride sources other than drinking water, it is currently impossible to draw firm conclusions regarding the independent effect of fluoride in drinking water on caries prevalence using an ecologic study design. Moderate dental fluorosis occurs in 1 to 2% of the population exposed to fluoride at 1 mg/l in drinking water and in about 10% of the population at 2 mg/l; moderate/severe fluorosis occurs in variable percentages ranging up to 33% of the population exposed to fluoride at 2.4 to 4.1 mg/l in drinking water. The issue of whether moderate or severe dental fluorosis represents an adverse health effect is still controversial. There is no evidence of skeletal fluorosis among the general U.S. population exposed to drinking water fluoride concentrations lower than 4 mg/l. Radiographically detected osteosclerosis after chronic exposure to fluoride in drinking water at 8 mg/l was not associated with clinical symptoms. Reports of crippling skeletal fluorosis associated with low concentrations of fluoride in drinking water in tropical countries have been attributed to other dietary factors. The available data suggest that some individuals may experience hypersensitivity to fluoride-containing agents. Further studies on hypersensitivity are required. There is no evidence of increased incidence of renal disease or renal dysfunction in humans exposed to up to 8 mg fluoride per liter in drinking water. Structural changes in kidneys of experimental animals have been detected at doses exceeding 1 to 5 mg fluoride per kilogram per day. Based on four case reports, individuals with renal insufficiency who consume large volumes of naturally fluoridated water at 2 to 8 mg/l are possibly at increased risk of developing skeletal fluorosis. Studies on the effects of fluoride in individuals with renal insufficiency are needed. There is no evidence that chronic exposure to concentrations of fluoride reported to be greater than 2 mg/l in drinking water increases human cancer mortality or incidence. A study of lifetime exposure to fluoride on cancer incidence in rats and mice has been completed, but assessment for cancer has not been completed. There is no evidence that fluoride is genotoxic except in some in vitro assays at cytotoxic concentrations. There is no in vivo evidence that fluoride affects human cellular enzyme activities.(ABSTRACT TRUNCATED AT 400 WORDS) Free Article
PMID: 2129630 [PubMed - indexed for MEDLINE]
22. Sci Total Environ. 1985 Dec;47:461-72.
Epidemiologic studies of organic micropollutants in drinking water.
Craun GF.
Abstract: Epidemiologic studies have been conducted in order to make a quantitative statement about associations between drinking water contaminants and disease. The basic measures of the association are a rate ratio or relative risk and rate difference or attributable risk. The appropriateness of this measure is dependent on components of study design, data collection, and the analysis of epidemiologic data, and these must be evaluated for each study to determine precision (lack of random error) and validity (lack of systematic error). Internal validity includes considerations for preventing selection bias, minimizing observation bias, and assessing, preventing, and controlling confounding bias within a particular study. No single epidemiologic study is likely to provide a definitive answer, and the results of epidemiologic studies must be interpreted in the context of other scientific information. Epidemiologic studies of organic micropollutants in drinking water have been reviewed and are summarized based on these considerations.
PMID: 3911420 [PubMed - indexed for MEDLINE]
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