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Title
Tetrachloroethylene-contaminated drinking water in Massachusetts and the risk of
colon-rectum, lung, and other cancers.
Author
Paulu C; Aschengrau A; Ozonoff D
Address
Department of Environmental Health, Boston University School of Public Health, Boston,
MA 02118, USA.
Source
Environ Health Perspect, 1999 Apr, 107:4, 265-71
Abstract
We conducted a population-based case-control study to evaluate the relationship between
cancer of the colon-rectum (n = 326), lung (n = 252), brain (n = 37), and pancreas (n = 37),
and exposure to tetrachloroethylene (PCE) from public drinking water. Subjects were
exposed to PCE when it leached from the vinyl lining of drinking-water distribution pipes.
Relative delivered dose of PCE was estimated using a model that took into account
residential location, years of residence, water flow, and pipe characteristics. Adjusted odds
ratios (ORs) for lung cancer were moderately elevated among subjects whose exposure
level was above the 90th percentile whether or not a latent period was assumed [ORs and
95% confidence intervals (CIs), 3.7 (1.0-11.7), 3.3 (0.6-13.4), 6.2 (1.1-31.6), and 19.3
(2.5-141.7) for 0, 5, 7, and 9 years of latency, respectively]. The adjusted ORs for
colon-rectum cancer were modestly elevated among ever-exposed subjects as more years of
latency were assumed [OR and CI, 1.7 (0.8-3.8) and 2.0 (0.6-5.8) for 11 and 13 years of
latency, respectively]. These elevated ORs stemmed mainly from associations with rectal
cancer. Adjusted ORs for rectal cancer among ever-exposed subjects were more elevated
[OR and CI, 2.6 (0. 8-6.7) and 3.1 (0.7-10.9) for 11 and 13 years of latency, respectively]
than were corresponding estimates for colon cancer [OR and CI, 1.3 (0.5-3.5) and 1.5
(0.3-5.8) for 11 and 13 years of latency, respectively]. These results provide evidence for an
association between PCE-contaminated public drinking water and cancer of the lung and,
possibly, cancer of the colon-rectum.

Title
Chlorination, chlorination by-products, and cancer: a meta-analysis [published erratum
appears in Am J Public Health 1993 Sep;83(9):1257] [see comments]
Author
Morris RD; Audet AM; Angelillo IF; Chalmers TC; Mosteller F
Address
Division of Biostatistics, Medical College of Wisconsin, Milwaukee 53226.
Source
Am J Public Health, 1992 Jul, 82:7, 955-63
Abstract
OBJECTIVES. Individual epidemiological investigations into the association between
chlorination by-products in drinking water and cancer have been suggestive but
inconclusive. Enough studies exist to provide the basis for a meaningful meta-analysis.
METHODS. An extensive literature search was performed to identify pertinent case-control
studies and cohort studies. Consumption of chlorinated water, surface water, or water with
high levels of chloroform was used as a surrogate for exposure to chlorination by-products.
Relative risk estimates were abstracted from the individual studies and pooled. RESULTS.
A simple meta-analysis of all cancer sites yielded a relative risk estimate for exposure to
chlorination by-products of 1.15 (95% CI: 1.09, 1.20). Pooled relative risk estimates for
organ-specific neoplasms were 1.21 (95% CI: 1.09, 1.34) for bladder cancer and 1.38 (95%
CI: 1.01, 1.87) for rectal cancer. When studies that adjusted for potential confounders were
pooled separately, estimates of relative risks did not change substantially. CONCLUSIONS.
The results of this meta-analysis suggest a positive association between consumption of
chlorination by-products in drinking water and bladder and rectal cancer in humans.

Title
A case-control study of asbestos in drinking water and cancer risk.
Author
Polissar L; Severson RK; Boatman ES
Address
Source

Am J Epidemiol, 1984 Mar, 119:3, 456-71
Abstract
The authors conducted a case-control, interview-based study of the risk of developing cancer
from asbestos in drinking water. The Everett, Washington area was selected for the study
because of the unusually high concentration of chrysotile asbestos in the drinking water it
draws from the Sultan River (200 X 10(6) fibers/liter). Through a population-based tumor
registry, the authors identified 382 individuals with cancer of the buccal cavity, pharynx,
respiratory system, digestive system, bladder, or kidney, diagnosed between 1977 and
1980, and then interviewed them or their next-of-kin. The authors conducted similar
interviews of a control group of 462 individuals. Finally, interviews were validated in
several ways, including comparing the collected data with that from secondary sources.
Estimates of exposure to asbestos in drinking water were based on residence and workplace
history, and on individual water consumption. Four different measures of exposure were
used. Cancer risk was estimated by logistic regression and other methods. The authors
found no convincing evidence for cancer risk from imbibed asbestos. Exposure was similar
between cases and controls. Confidence intervals for relative odds for almost all sites
included unity. Out of 84 dependent estimates of risk by sex, site, and exposure measure, 63
indicated a protective effect and 21 indicated an increased risk. In instances where relative
odds differed appreciably from unity for both males and females, the effect was protective.
The relative odds of cancer for 20 years of exposure to Sultan River drinking water varied
from 0.92 to 0.99 for females and 0.82 to 1.01 for males for all study sites grouped. For
cancer of the digestive system, the corresponding range was 1.03 and 1.08 for females and
0.85 to 1.00 for males. There were six statistically significant associations (p less than 0.05).
All involved male stomach (eight cases) and male pharynx (four cases), and indicate
elevated risk. This number of significant associations is close to that expected (for the
number of comparisons made). The female risks for these two sites indicate a protective
effect, and it is concluded that the male results are probably due to chance.

Title
Drinking water mutagenicity and gastrointestinal and urinary tract cancers: an ecological
study in Finland [see comments]
Author
Koivusalo M; Jaakkola JJ; Vartiainen T; Hakulinen T; Karjalainen S; Pukkala E; Tuomisto J
Address
Finnish Cancer Registry, Helsinki.
Source
Am J Public Health, 1994 Aug, 84:8, 1223-8
Abstract
OBJECTIVES. The purpose of this study was to investigate the relationship between
exposure to mutagenic drinking water and cancers of the gastrointestinal and urinary tract.
METHODS. Past exposure to drinking water mutagenicity was assessed in 56 Finnish
municipalities for the years 1955 and 1970. The cases of bladder, kidney, stomach, colon,
and rectum cancers were derived from two periods (1967 to 1976 and 1977 to 1986). Age,
sex, social class, urban living, and time period were taken into account in the Poisson
regression analysis. RESULTS. Statistically significant exposure-response association was
observed between exposure and incidence of bladder, kidney, and stomach cancers. In an
ordinary municipality using chlorinated surface water, this exposure would indicate a
relative risk of 1.2 for bladder cancer and of 1.2 to 1.4 for kidney cancer compared with
municipalities where nonmutagenic drinking water was consumed. CONCLUSIONS. The
acidic mutagenic compounds present in drinking water may play a role in the etiology of
kidney and bladder cancers, but, because the results are based on aggregate data, they should
be interpreted with caution.

Title
Case-control cancer mortality study and chlorination of drinking water in Louisiana.
Author
Gottlieb MS; Carr JK
Address
Source

Environ Health Perspect, 1982 Dec, 46:, 169-77
Abstract
Several Louisiana parishes (counties) using the Mississippi River for their source of public
drinking water have the highest mortality rates (1950-69) in the United States for several
cancers. Therefore, a case-control mortality study on cancer of the liver, brain, pancreas,
bladder, kidney, prostate, rectum, colon, esophagus, stomach, non-Hodgkin's lymphoma,
multiple myeloma, leukemia, Hodgkin's disease, lung; breast and malignant melanoma,
from 1960 to 1975 in South Louisiana parishes grouped for similarities in industrial
characteristics, having approximately equal exposure of the population to surface and
groundwater, was conducted. Noncancer deaths were randomly selected as controls and
matched to the case death on age, race, sex, and year and parish group of death. Water
source at death was assigned based on the residence at death and described as surface or
ground and chlorinated or nonchlorinated. A significantly increased risk for surface,
chlorinated water use was noted for rectal cancer. No risk could be demonstrated for colon
cancer. The risk noted for bladder cancer by other investigators is not substantiated. Brain
cancer risk appears to be associated with chlorinated groundwater, but this may be industrial
confounding. Breast cancer demonstrated a slight, but significant, risk associated with
surface chlorinated water. This risk, however, might be due to confounding of rural life
style, early childbearing and large families with nonchlorinated water found in these settings.
Chlorination risk for kidney cancer was not significant. No risk was observed in association
with surface water for other cancers of the gastrointestinal or urinary tract. Multiple
myeloma was significantly associated with a risk from ground water.

Title
Impact of nitrates in drinking water on cancer mortality in Valencia, Spain.
Author
Morales Suárez Varela MM; Llopis Gonzalez A; Tejerizo Perez ML
Address
Unit of Public Health and Environmental Care, Faculty of Pharmacy, University of
Valencia, Burjassot, Spain.
Source
Eur J Epidemiol, 1995 Feb, 11:1, 15-21
Abstract
The concentrations of nitrates in public drinking water in the Mediterranean coastal province
of Valencia are not only the highest in Spain but also in the whole of Europe. Intensive
agricultural practices involve a traditional and growing use of nitrogen fertilizers. This and
the terrain--poorly consolidated and porous in areas--favors the accumulation of nitrates in
underground aquifers, thereby perhaps accounting for this contamination. The possible
conversion of nitrates to nitrites under certain conditions of gastric achlorhydria, followed by
their transformation to nitrosamines--substances known to be carcinogenic in experimental
models--has led to a number of epidemiological studies of the possible relationship between
high nitrate levels in public drinking water and mortality due to different cancers. The aim of
the present study was to analyze the relationship between different levels of exposure to
nitrates in the drinking water of the 258 municipalities in the province of Valencia and
mortality due to cancer of the stomach, bladder, prostate and colon in this population. The
cancer mortality rate was found to rise with increasing exposure to nitrates in the case of
gastric cancer in both sexes, and in prostate cancer. These same results were obtained on
calculating relative risk for the different age groups associated with the consumption of
drinking water containing different levels of nitrates.(ABSTRACT TRUNCATED AT 250
WORDS)

Title
Drinking water and the prevalence of colorectal adenomas: an epidemiologic study in
Telemark, Norway.
Author
Hoff G; Moen IE; Mowinckel P; Rosef O; Nordbö E; Sauar J; Vatn MH; Torgrimsen T
Address
Medical Department, Telemark Sentralsykehus, Skien, Norway.
Source
Eur J Cancer Prev, 1992 Oct, 1:6, 423-8
Abstract
This study was based on an endoscopic screening study for detection of polyps in the
rectum and sigmoid colon in a randomized, normal population sample of 400 individuals
aged 50-59 years. Family disposition for cancer and indicators of lifestyle (including dietary
registration) were recorded. The 310 individuals received domestic drinking water from one
out of four public water supplies. The participants were categorized according to the water
supply connected to their house of residence. Drinking water was analysed monthly during
2 years for chloroform, total organic carbon, colour index, calcium, magnesium and
chlorine. The overall prevalence of colorectal polyps was significantly higher in residents
receiving chlorinated water with a high organic content when compared with recipients of
water with a low organic content. There was no association between polyp prevalence and
chloroform concentration in the drinking water. Multivariate analysis revealed that age, male
sex, high BMI, smoking, few stools per week, high protein intake and low intake of fibre,
iron and cruciferous vegetables were far more important for the presence of polyps than the
total organic content in chlorinated drinking water.

Title
Cancer mortality in U.S. counties with hazardous waste sites and ground water pollution.
Author
Griffith J; Duncan RC; Riggan WB; Pellom AC
Address
U.S. Environmental Protection Agency, Health Effects Research Laboratory, Research
Triangle Park, North Carolina.
Source
Arch Environ Health, 1989 Mar, 44:2, 69-74
Abstract
Since the late 1950s, more than 750 million tons of toxic chemical wastes have been
discarded in an estimated 30,000 to 50,000 hazardous waste sites (HWSs). Uncontrolled
discarding of chemical wastes creates the potential for risks to human health. Utilizing the
National Priorities Listing (NPL) of hazardous waste sites developed by the United States
Environmental Protection Agency (EPA), this study identified 593 waste sites in 339 U.S.
counties in 49 states with analytical evidence of contaminated ground drinking water
providing a sole source water supply. For each identified county, age-adjusted, site-specific
cancer mortality rates for 13 major sites for the decade 1970-1979, for white males and
females, were extracted from U.S. Cancer Mortality and Trends 1950-1979. Also, HWS
and non-HWS counties that showed excess numbers of deaths were enumerated for each
cancer selected. Significant associations (p less than .002) between excess deaths and all
HWS counties were shown for cancers of the lung, bladder, esophagus, stomach, large
intestine, and rectum for white males; and for cancers of the lung, breast, bladder, stomach,
large intestine, and rectum for white females when compared to all non-HWS counties.
There were no consistent geographical patterns that suggested a broad distribution of
gastrointestinal cancers associated with HWSs throughout the United States, although we
did identify a cluster of excess gastrointestinal cancers in counties within states located in
EPA Region 3 (Delaware, Maryland, Pennsylvania, Virginia, West Virginia).(ABSTRACT
TRUNCATED AT 250 WORDS)

Title
Evaluation of mutagenic and carcinogenic properties of brominated and chlorinated
acetonitriles: by-products of chlorination.
Author
Bull RJ; Meier JR; Robinson M; Ringhand HP; Laurie RD; Stober JA
Address
Source

Fundam Appl Toxicol, 1985 Dec, 5:6 Pt 1, 1065-74
Abstract
The present study was undertaken to determine if chlorinated and brominated acetonitriles
formed during the chlorination of drinking water possess mutagenic and/or carcinogenic
properties. Chloroacetonitrile (CAN), dichloroacetonitrile (DCAN), trichloroacetonitrile
(TCAN), bromochloroacetonitrile (BCAN), and dibromoacetonitrile (DBAN) were tested
for their ability (1) to produce point mutations in the Salmonella/microsome assay, (2) to
induce sister chromatid exchanges (SCE) in Chinese hamster ovary (CHO) cells in vitro,
(3) to produce micronuclei in polychromatic erythrocytes in CD-1 mice, and (4) to act as
tumor initiators in the skin of Sencar mice. DCAN and BCAN were found to be
direct-acting mutagens in Salmonella. All five haloacetonitriles induced SCE in CHO cells
in vitro. This activity paralleled the extent of chlorine substitution and was further enhanced
in the dihaloacetonitrile series when bromine was substituted for chlorine. None of the
haloacetonitriles showed evidence of activity in the mouse micronucleus assay. DBAN,
BCAN, and CAN initiated tumors in the mouse skin with topical applications followed by a
20-week promotion schedule of 12-O tetradecanoylphorbol-13-acetate applications (p less
than 0.02). These data indicate that the haloacetonitriles do display mutagenic and
carcinogenic properties in some test systems and the hazard associated with their occurrence
in drinking water and production within the gastrointestinal tract require further evaluation.

Title
Carcinogenic activity associated with halogenated acetones and acroleins in the mouse skin
assay.
Author
Robinson M; Bull RJ; Olson GR; Stober J
Address
Environmental Toxicology Division, U.S. Environmental Protection Agency, Cincinnati,
OH 45268.
Source
Cancer Lett, 1989 Dec, 48:3, 197-203
Abstract
Several chlorinated acetones have been identified in drinking water and these, as well as a
number of chlorinated acroleins, are produced by chlorination of humic acid solutions.
Many of these chlorinated compounds and the brominated acrolein analog were positive in
the Ames Assay in the laboratory. To determine if carcinogenic activity was associated with
these chemicals the following acetone derivatives: monochloro (MCA); 1,1-dichloro
(1,1-DCA), 1,3-dichloro (1,3-DCA), 1,1,1-trichloro (1,1,1-TCA), 1,1,3-trichloro
(1,1,3-TCA), and substituted acroleins: 2-chloro (CAC), 3,3-dichloro (DCAC),
2,3,3-trichloro (TCAC) and 2-bromo (BAC), were applied topically to SENCAR mice (25,
30, or 40/group) at the following dose levels: 50 mg/kg (MCA and 1,1,3-TCA); 50, 75 and
100 mg/kg (1,3-DCA); 100, 200 and 400 mg/kg (CAC, DCAC, and TCAC); 200 and 300
mg/kg (BAC); and 400, 600, and 800 mg/kg (1,1-DCA, and 1,1,1-TCA). Doses were
applied six times over a 2-week period in 0.2 ml ethanol per application. 1,3-DCA was also
tested with single doses of 37.5, 75, 150 and 300 mg/kg in 0.2 ml ethanol. Control animals
received 0.2 ml ethanol per application as a single dose or multiple doses to match
corresponding studies. Two weeks after the final dose, 1.0 microgram TPA in 0.2 ml
acetone was applied three times weekly for 20 weeks. After 24 weeks the percentage of
animals with tumors for dose groups above were: MCA (8); 1,1,3-TCA (10); 1,3-DCA,
multiple doses (48, 45, 32); CAC (30, 28, 38); DCAC (3, 0, 0); TCAC (10, 5, 0); BAC (54,
43); 1,1-DCA (0, 5, 0); 1,1,1-TCA (10, 5, 0); 1,3-DCA, single doses (47, 47, 63, 20);
controls (12--Table 3, 9--Table 4 average). These data show that 1,3-DCA, CAC and BAC,
when applied topically, initiate tumors in the mouse skin. These chemicals administered
orally in a 2% emulphor solution, at doses described in Table 3, did not initiate tumors in the
mouse skin.

 

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