Skip header and navigation

Refine By

24 records – page 1 of 3.

Accumulation of cadmium, zinc, and copper in maternal blood and developmental placental tissue: differences between Finland, Estonia, and St. Petersburg.

https://arctichealth.org/en/permalink/ahliterature198281
Source
Environ Res. 2000 May;83(1):54-66
Publication Type
Article
Date
May-2000
Author
M. Kantola
R. Purkunen
P. Kröger
A. Tooming
J. Juravskaja
M. Pasanen
S. Saarikoski
T. Vartiainen
Author Affiliation
Department of Chemistry, University of Kuopio, Finland. marjatta.kantola@uku.fi
Source
Environ Res. 2000 May;83(1):54-66
Date
May-2000
Language
English
Publication Type
Article
Keywords
7-Alkoxycoumarin O-Dealkylase - metabolism
Birth Weight - drug effects
Cadmium - analysis - blood
Copper - analysis - blood
Drug Interactions
Estonia
Female
Finland
Gestational Age
Humans
Infant, Newborn
Placenta - chemistry - enzymology
Pregnancy - blood
Pregnancy Trimester, First - blood
Regression Analysis
Russia
Smoking - blood - metabolism
Zinc - analysis - blood
Abstract
Cadmium, zinc, and copper from placental tissue and blood samples at the first trimester (n = 64) and at term (n = 152) were analyzed; the welfare of newborns and placental 7-ethoxycoumarin O-deethylase (ECOD) activities in vitro were determined. The study material was collected from Finland, Estonia, and Russia. The results demonstrate that Cd starts to accumulate in the placenta during the first trimester and that Zn and Cu contents were significantly higher at the first trimester than at term. Among nonsmokers a negative correlation was found between placental Cu content and birth weight of neonates. Among smokers a positive correlation between placental Zn content and birth weight and ECOD activity was found. The birth weights correlated inversely with the length of time the mothers smoked. The highest Cd concentrations were detected in the samples collected from St. Petersburg. The data demonstrate an inverse accumulation of Zn and Cd throughout the pregnancy in the placenta and maternal blood samples. Zn may act as a positive marker or even an enzymatic enhancement for the human placental vital functions. Smoking, parity, age, and especially the place of residence affect the Cd, Zn, and Cu contents and ratios in placenta and mother's blood.
PubMed ID
10845782 View in PubMed
Less detail

Association between chemical pattern in breast milk and congenital cryptorchidism: modelling of complex human exposures.

https://arctichealth.org/en/permalink/ahliterature125071
Source
Int J Androl. 2012 Jun;35(3):294-302
Publication Type
Article
Date
Jun-2012
Author
K. Krysiak-Baltyn
J. Toppari
N E Skakkebaek
T S Jensen
H E Virtanen
K-W Schramm
H. Shen
T. Vartiainen
H. Kiviranta
O. Taboureau
K. Audouze
S. Brunak
K M Main
Author Affiliation
Center for Biological Sequence Analysis, Technical University of Denmark, Lyngby, Denmark.
Source
Int J Androl. 2012 Jun;35(3):294-302
Date
Jun-2012
Language
English
Publication Type
Article
Keywords
Artificial Intelligence
Cryptorchidism - epidemiology
Denmark - epidemiology
Dioxins - analysis
Environmental Pollutants - analysis
Female
Finland - epidemiology
Halogenated Diphenyl Ethers - analysis
Humans
Logistic Models
Male
Milk, human - chemistry
Polychlorinated biphenyls - analysis
Systems Biology
Abstract
During the past four decades, there has been an increase in the incidence rate of male reproductive disorders in some, but not all, Western countries. The observed increase in the prevalence of male reproductive disorders is suspected to be ascribable to environmental factors as the increase has been too rapid to be explained by genetics alone. To study the association between complex chemical exposures of humans and congenital cryptorchidism, the most common malformation of the male genitalia, we measured 121 environmental chemicals with suspected or known endocrine disrupting properties in 130 breast milk samples from Danish and Finnish mothers. Half the newborns were healthy controls, whereas the other half was boys with congenital cryptorchidism. The measured chemicals included polychlorinated biphenyls (PCBs), polybrominated diphenyl-ethers, dioxins (OCDD/PCDFs), phthalates, polybrominated biphenyls and organochlorine pesticides. Computational analysis of the data was performed using logistic regression and three multivariate machine learning classifiers. Furthermore, we performed systems biology analysis to explore the chemical influence on a molecular level. After correction for multiple testing, exposure to nine chemicals was significantly different between the cases and controls in the Danish cohort, but not in the Finnish cohort. The multivariate analysis indicated that Danish samples exhibited a stronger correlation between chemical exposure patterns in breast milk and cryptorchidism than Finnish samples. Moreover, PCBs were indicated as having a protective effect within the Danish cohort, which was supported by molecular data recovered through systems biology. Our results lend further support to the hypothesis that the mixture of environmental chemicals may contribute to observed adverse trends in male reproductive health.
PubMed ID
22519522 View in PubMed
Less detail

Associations between congenital cryptorchidism in newborn boys and levels of dioxins and PCBs in placenta.

https://arctichealth.org/en/permalink/ahliterature129015
Source
Int J Androl. 2012 Jun;35(3):283-93
Publication Type
Article
Date
Jun-2012
Author
H E Virtanen
J J Koskenniemi
E. Sundqvist
K M Main
H. Kiviranta
J T Tuomisto
J. Tuomisto
M. Viluksela
T. Vartiainen
N E Skakkebaek
J. Toppari
Author Affiliation
Departments of Physiology and Paediatrics, University of Turku, Turku, Finland. helena.virtanen@utu.fi
Source
Int J Androl. 2012 Jun;35(3):283-93
Date
Jun-2012
Language
English
Publication Type
Article
Keywords
Adult
Case-Control Studies
Cohort Studies
Cryptorchidism - etiology
Denmark
Dioxins - analysis
Female
Finland
Humans
Infant, Newborn
Luteinizing Hormone - blood
Male
Placenta - chemistry
Polychlorinated biphenyls - analysis
Pregnancy
Abstract
In animal studies, exposure to dioxins has been associated with disrupted development of the male reproductive system, including testicular maldescent. Some polychlorinated biphenyls (PCBs) have also dioxin-like effects. In addition, one previous case-control study has reported an association between congenital cryptorchidism and colostrum PCB levels. We performed a case-control study to evaluate whether congenital cryptorchidism in boys was associated with increased levels of dioxins or PCBs in placenta reflecting foetal exposure. In addition, associations between placenta levels of these chemicals and reproductive hormone levels in boys at 3 months were studied. Placentas were collected in a Danish-Finnish joint prospective cohort study on cryptorchidism (1997-2001). The boys were examined for cryptorchidism at birth and at 3 months. Altogether, 280 placentas [112 Finnish (56 cases, 56 controls) and 168 Danish (39 cases, 129 controls)] were analysed for 17 toxic polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and 37 PCBs (including 12 dioxin-like PCBs). Infant serum samples taken at 3 months were analysed for reproductive hormones. No significant differences between cases and controls were observed in either country in dioxin WHO-TEq levels (median 9.78 vs. 8.47 pg/g fat, respectively, in Finland, and 11.75 vs. 10.88 pg/g fat in Denmark) or PCB WHO-TEq levels (median 2.12 vs. 2.15 pg/g fat in Finland, 2.34 vs. 2.10 pg/g fat in Denmark) or total-TEq levels (median 11.66 vs. 10.58 pg/g fat in Finland, 13.94 vs. 13.00 pg/g fat in Denmark). Placenta WHO-TEq levels of dioxins were not associated with infant reproductive hormone levels at 3 months. In Finland, PCB WHO-TEq levels in placenta associated positively with infant LH levels. WHO-TEq levels of dioxins and PCBs and total-TEq levels were higher in Danish than Finnish samples. In conclusion, no association between placenta levels of dioxins or PCBs and congenital cryptorchidism was found. Significant country differences in chemical levels were observed.
Notes
Cites: Food Addit Contam. 2000 Apr;17(4):241-5910912239
Cites: APMIS. 2001 Feb;109(2):96-10011399000
Cites: Lancet. 2000 Oct 7;356(9237):1240-111072947
Cites: Eur J Pediatr Surg. 2000 Oct;10(5):304-911194541
Cites: Eur J Endocrinol. 2002 Mar;146(3):357-6311888842
Cites: Int J Androl. 2003 Feb;26(1):2-1512534932
Cites: Chemosphere. 2004 Mar;54(10):1459-7314659948
Cites: Int Arch Occup Environ Health. 2004 Apr;77(3):153-814963712
Cites: Lancet. 2004 Apr 17;363(9417):1264-915094270
Cites: Environ Int. 2004 Sep;30(7):923-3215196840
Cites: Toxicol Appl Pharmacol. 1985 Jun 15;79(1):99-1114049410
Cites: Toxicol Appl Pharmacol. 1992 May;114(1):97-1071585378
Cites: Arch Dis Child. 1992 Jul;67(7):892-91355643
Cites: Lancet. 1993 May 29;341(8857):1392-58098802
Cites: Am J Epidemiol. 1994 Feb 1;139(3):272-818116602
Cites: Environ Health Perspect. 1996 Aug;104 Suppl 4:741-8038880001
Cites: Scand J Work Environ Health. 1996 Aug;22(4):267-738881015
Cites: J Clin Endocrinol Metab. 1998 Feb;83(2):675-819467591
Cites: Hum Exp Toxicol. 1998 Jul;17(7):365-729726532
Cites: Environ Health Perspect. 1998 Dec;106(12):775-929831538
Cites: J Urol. 1999 Sep;162(3 Pt 1):864-7110458397
Cites: Arch Dis Child. 1964 Dec;39:605-914230757
Cites: J Androl. 2005 Mar-Apr;26(2):205-1415713826
Cites: Placenta. 2005 Jul;26(6):512-415950066
Cites: J Clin Endocrinol Metab. 2005 Jul;90(7):4041-615870122
Cites: Chemosphere. 2006 Jan;62(3):390-516005046
Cites: Environ Health Perspect. 2006 Feb;114(2):270-616451866
Cites: J Clin Endocrinol Metab. 2006 Jul;91(7):2732-716595596
Cites: Environ Health Perspect. 2006 Jul;114(7):1133-816835070
Cites: Toxicol Sci. 2006 Oct;93(2):223-4116829543
Cites: Environ Health Perspect. 2006 Nov;114(11):1649-5417107848
Cites: Environ Health Perspect. 2006 Nov;114(11):1670-617107851
Cites: Food Chem Toxicol. 2007 Feb;45(2):259-6517029725
Cites: Chemosphere. 2007 Apr;67(9):S256-6217207515
Cites: Environ Health Perspect. 2007 Oct;115(10):1519-2617938745
Cites: Hum Reprod. 2008 Jan;23(1):201-1018025027
Cites: Hum Reprod Update. 2008 Jan-Feb;14(1):49-5818032558
Cites: Environ Pollut. 2008 Jul;154(2):172-8318055079
Cites: Hum Reprod. 2008 Aug;23(8):1708-1818503055
Cites: Eur Arch Paediatr Dent. 2008 Dec;9(4):224-719054476
Cites: Dokl Biol Sci. 2008 Nov-Dec;423:443-619213432
Cites: Environ Health Perspect. 2009 Sep;117(9):1472-619750116
Cites: Arch Dis Child. 2009 Nov;94(11):868-7219542061
Cites: Biol Reprod. 2010 Mar;82(3):636-4320007409
Cites: Environ Health Perspect. 2010 Apr;118(4):458-6420368131
Cites: Int J Androl. 2010 Apr;33(2):270-819780864
Cites: Int J Androl. 2010 Apr;33(2):413-2420059583
Cites: Front Neuroendocrinol. 2010 Oct;31(4):452-7820624415
Cites: Environ Health Perspect. 2011 May;119(5):713-821262597
Cites: Tissue Cell. 2001 Apr;33(2):169-7711392670
Cites: Food Addit Contam. 2000 Apr;17(4):275-8810912242
PubMed ID
22150420 View in PubMed
Less detail

Birth weight and sex of children and the correlation to the body burden of PCDDs/PCDFs and PCBs of the mother.

https://arctichealth.org/en/permalink/ahliterature206644
Source
Environ Health Perspect. 1998 Feb;106(2):61-6
Publication Type
Article
Date
Feb-1998
Author
T. Vartiainen
J J Jaakkola
S. Saarikoski
J. Tuomisto
Author Affiliation
Division of Environmental Health, National Public Health Institute, Kuopio, Finland.
Source
Environ Health Perspect. 1998 Feb;106(2):61-6
Date
Feb-1998
Language
English
Publication Type
Article
Keywords
Adult
Benzofurans - adverse effects - analysis
Birth Weight - drug effects
Body Burden
Diet
Education
Female
Finland - epidemiology
Follow-Up Studies
Humans
Infant, Newborn
Male
Milk, human - chemistry
Polychlorinated Biphenyls - adverse effects - analysis
Pregnancy
Rural Population
Seafood
Sex ratio
Socioeconomic Factors
Soil Pollutants - adverse effects - analysis
Tetrachlorodibenzodioxin - adverse effects - analogs & derivatives - analysis
Urban Population
Abstract
Polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) were analyzed in 167 random human milk samples from urban and rural areas in Finland. Dietary habits and background information on each mother and child were gathered by questionnaire. Body mass indexes (BMI) before pregnancy and delivery in the rural area were 5-10% higher than in the urban area, but fat content of mother's milk was about 10% higher in the urban area. The mean weights of children (+/- standard deviation) were similar in the rural and urban areas among primiparae, 3,500 +/- 597 g and 3,505 +/- 454 g, respectively, although dioxin international toxic equivalents (I-TEQs) were significantly higher in the urban area. The mother's level of education did not affect the weight of the child, but concentrations of PCDDs/PCDFs (I-TEQ, 2,3,4,7,8-Cl5 dibenzofuran,1,2, 3,7,8-Cl5 dibenzodioxin) and PCBs [sum of PCBs (sumPCB), PCB-TEQ, and most PCB congeners] increased with advanced education. This is considered to be due to differences in the mother's consumption of fish. The birth weight, especially of boys, slightly decreased with increasing concentrations of I-TEQ, 2,3,4,7,8-Cl5 dibenzofuran, 1,2,3, 7,8-Cl5 dibenzodioxin, and 2,3,7,8-Cl4 dibenzodioxin; however, when the analysis was restricted to primiparae, there was no statistically significant correlation between birth weight and the concentrations of PCDDs/PCDFs. No correlation was found between the weight of the child and PCBs, PCB-TEQs, or individual PCB congeners in the whole material or among primiparae, or among boys or girls. The concentrations of PCDDs/PCDFs and PCBs inhuman milk were modeled for primiparae by weighing fish consumption, age of mother, milk fat content, and BMI before pregnancy. The linear regression resulted in values of R = 0.67 and 0.30 for the modeled dioxin I-TEQs in the urban and rural areas, respectively, and the corresponding values for sumPCBs of R = 0.60 and 0.11. The increase of PCDD/PCDF body burden was calculated to be on average 0.58 pg I-TEQ/g milk fat/year in the urban area and 0.39 pg I-TEQ/g milk fat/year in the rural area.
Notes
Cites: J Pediatr. 1984 Aug;105(2):315-206431068
Cites: J Pediatr. 1986 Aug;109(2):335-413090217
Cites: Environ Health Perspect. 1994 Jan;102 Suppl 1:173-858187706
Cites: Crit Rev Toxicol. 1994;24(2):87-1498037844
Cites: Chemosphere. 1994 Nov-Dec;29(9-11):2261-57850373
Cites: Pharmacol Rev. 1994 Dec;46(4):483-5497899475
Cites: Chemosphere. 1995 Apr;30(8):1429-387743140
Cites: Regul Toxicol Pharmacol. 1995 Feb;21(1):136-507784626
Cites: Crit Rev Toxicol. 1995;25(2):133-637612174
Cites: Neurotoxicol Teratol. 1996 May-Jun;18(3):217-27; discussion 229-768725628
Cites: Crit Rev Toxicol. 1996 Nov;26(6):709-378958469
Cites: Chemosphere. 1997 Jun;34(12):2571-839204541
PubMed ID
9432971 View in PubMed
Less detail

Cancer incidence around an oil refinery as an example of a small area study based on map coordinates.

https://arctichealth.org/en/permalink/ahliterature213876
Source
Environ Res. 1995 Nov;71(2):128-34
Publication Type
Article
Date
Nov-1995
Author
J. Pekkanen
E. Pukkala
M. Vahteristo
T. Vartiainen
Author Affiliation
Unit of Environmental Epidemiology, National Public Health Institute, Kuopio, Finland.
Source
Environ Res. 1995 Nov;71(2):128-34
Date
Nov-1995
Language
English
Publication Type
Article
Keywords
Air Pollutants, Occupational
Cohort Studies
Environmental Exposure
Finland
Geography
Humans
Industrial Oils
Neoplasms - epidemiology
Poisson Distribution
Regression Analysis
Selection Bias
Abstract
The aim of the study was to create a rapid method for estimating cancer risk in areas defined by exact map coordinates and to test it using as an example incidence of leukemia near an oil refinery. The method can be used to investigate possible local excesses of cancer of suspected environmental origin in Finland. Map coordinates with an accuracy of 10 m for the place of residence of each Finn were obtained from national registers. Based on this data set, numbers of inhabitants and expected number of cancer cases by sex and age in squares of 500 x 500 m were calculated for all of Finland. Observed number of cancer cases in each square were obtained based on record linkage of the map coordinates with the Finnish Cancer Registry. The ratio of observed and expected number of cancer cases was modeled using Poisson regression. The example analysis included all 23 leukemia and 531 any cancer cases registered in an area around an oil refinery in 1983-1986. There was no significant association between distance from the oil refinery and risk of leukemia or any cancer. The method proved fast and efficient in comparing areal differences in cancer incidence in Finland. In cases of environmental concern, geographical analyses of existing registers is a rapid method to perform first analyses when evaluating the need for further studies.
PubMed ID
8977621 View in PubMed
Less detail

Changes in selenium, zinc, copper and cadmium contents in human milk during the time when selenium has been supplemented to fertilizers in Finland.

https://arctichealth.org/en/permalink/ahliterature192905
Source
J Trace Elem Med Biol. 2001;15(1):11-7
Publication Type
Article
Date
2001
Author
M. Kantol
T. Vartiainen
Author Affiliation
Department of Chemistry, University of Kuopio, Finland. Marjatta.Kantola@uku.fi
Source
J Trace Elem Med Biol. 2001;15(1):11-7
Date
2001
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Cadmium - metabolism
Copper - metabolism
Evaluation Studies as Topic
Fats - metabolism
Female
Fertilizers
Finland
Food Contamination
Humans
Milk, Human - drug effects - metabolism
Selenium - pharmacokinetics - pharmacology
Soil Pollutants - pharmacology
Zinc - metabolism
Abstract
Sodium selenate has been supplemented to all agricultural fertilizers used in Finland since 1984. We followed the changes in selenium, cadmium, zinc and copper content in Finnish human milk between the years 1987 and 1993-1995. A total of 257 milk samples was collected, four weeks after delivery, in two areas: In Helsinki, an urban area, and in Kuopio, a rural area, where elevated copper concentrations have been found in the bedrock. Direct atomic absorption spectrophotometric methods without digestion were used for the analyses. The dependence of trace element content on study time, living area, smoking habits, fish eating frequency, and parity of mothers was studied by analysis of covariance. Inter-element correlations and correlations with mothers' age and fat content in milk were studied by partial correlation. Significant increases were observed in mean selenium (16.4 microg/l and 18.9 microg/l, p
PubMed ID
11603821 View in PubMed
Less detail

Developmental dental defects in children who reside by a river polluted by dioxins and furans.

https://arctichealth.org/en/permalink/ahliterature190562
Source
Arch Environ Health. 2001 Nov-Dec;56(6):522-8
Publication Type
Article
Author
P. Hölttä
H. Kiviranta
A. Leppäniemi
T. Vartiainen
P L Lukinmaa
S. Alaluusua
Author Affiliation
Institute of Dentistry, University of Helsinki, Hospital for Children and Adolescents, Helsinki University Central Hospital, Finland.
Source
Arch Environ Health. 2001 Nov-Dec;56(6):522-8
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Animals
Breast Feeding
Child
Data Interpretation, Statistical
Dioxins - adverse effects
Female
Finland
Fishes
Food Contamination
Furans - adverse effects
Humans
Male
Milk, human - chemistry
Pregnancy
Risk factors
Tooth Demineralization - chemically induced
Tooth Diseases - chemically induced
Water Pollutants, Chemical - adverse effects
Abstract
The authors determined that demarcated hypomineralizations of developing teeth are a biological indicator of an early dioxin exposure in a healthy population of children. In the current study, the authors examined the prevalences of the demarcated hypomineralization lesions of teeth in 2 Finnish towns by the Kymijoki River--a river that is severely contaminated by dioxins and furans. The 4,120 permanent first molars of 1,030 children were studied. The prevailing levels of dioxins and furans in human milk were measured. The prevalences of the defects in children in Kotka and Anjalankoski were 14.2% and 5.6%, respectively, and the corresponding dioxins and furans in human milk were 13.4 pg/gm fat and 10.9 pg/gm fat (International Toxic Equivalents). In Anjalankoski, the duration of total breast-feeding was associated with the prevalence of the defects. Compared with the figures reported earlier in Finland, neither the prevalence of dental lesions nor the levels of dioxins and furans in human milk were increased in riverside residents.
PubMed ID
11958552 View in PubMed
Less detail

Dietary intakes of polychlorinated dibenzo-p-dioxins, dibenzofurans and polychlorinated biphenyls in Finland.

https://arctichealth.org/en/permalink/ahliterature192790
Source
Food Addit Contam. 2001 Nov;18(11):945-53
Publication Type
Article
Date
Nov-2001
Author
H. Kiviranta
A. Hallikainen
M L Ovaskainen
J. Kumpulainen
T. Vartiainen
Author Affiliation
Division of Environmental Health, National Public Health Institute, Kuopio, Finland. hannu.kiviranta@ktl.fi
Source
Food Addit Contam. 2001 Nov;18(11):945-53
Date
Nov-2001
Language
English
Publication Type
Article
Keywords
Adult
Benzoates - analysis
Benzofurans - analysis
Biphenyl Compounds - analysis
Dairy Products - analysis
Diet Surveys
Dioxins - analysis
Female
Finland
Fish Products - analysis
Flour - analysis
Food analysis
Humans
Male
Meat Products - analysis
Middle Aged
Vegetables - chemistry
Abstract
Samples of cow milk, pork, beef eggs, rainbow trout, flours and vegetables were analysed for 17 polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/F) and 36 polychlorinated biphenyls (PCB). Daily dietary intake of PCDD/Fs as toxic equivalent (I-TEq) and PCBs (PCB-TEq) was assessed using food consumption data from a 24-h dietary recall study for 2862 Finnish adults. The calculated intake of PCDD/F was 46 pg I-TEq day(-1). The current level was about half of the earlier estimation of intake in Finland made in 1992. The assessed PCB intake was 53 pg PCB-TEq day(-1). Thus, the total intake of PCDD/Fs and PCBs was 100 pg TEqday(-1) (1.3pg TEqkg(-1) b.w. day(-1)), which is within the range of tolerable daily intake (TDI) proposed by the WHO (1-4pg TEqkg(-1) b.w. day(-1)).
PubMed ID
11665735 View in PubMed
Less detail

Drinking water chlorination and cancer-a historical cohort study in Finland.

https://arctichealth.org/en/permalink/ahliterature22167
Source
Cancer Causes Control. 1997 Mar;8(2):192-200
Publication Type
Article
Date
Mar-1997
Author
M. Koivusalo
E. Pukkala
T. Vartiainen
J J Jaakkola
T. Hakulinen
Author Affiliation
Finnish Cancer Registry, Helsinki, Finland.
Source
Cancer Causes Control. 1997 Mar;8(2):192-200
Date
Mar-1997
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Distribution
Aged
Child
Child, Preschool
Chlorine - adverse effects
Cohort Studies
Drinking
Environmental Exposure - adverse effects
Female
Humans
Incidence
Male
Middle Aged
Mutagens - adverse effects - analysis - chemistry
Neoplasms - epidemiology - etiology
Regression Analysis
Research Support, Non-U.S. Gov't
Risk assessment
Sex Distribution
Sweden - epidemiology
Time Factors
Water - chemistry
Water Purification - methods
Water Supply - analysis
Abstract
Chlorination of water rich in organic material is known to produce a complex mixture of organochlorine compounds, including mutagenic and carcinogenic substances. A historical cohort study of 621,431 persons living in 56 towns in Finland was conducted in order to assess the relation between historical exposure to drinking water mutagenicity and cancer. Exposure to quantity of mutagenicity was calculated on the basis of historical information of raw water quality and water treatment practices using an empirical equation relating mutagenicity and raw water pH, KMnO4 value and chlorine dose. Cancer cases were derived from the population-based Finnish Cancer Registry and follow-up time in the study started in 1970. Age, gender, time period, social class, and urban residence were taken into account in Poisson regression analysis of the observed numbers of cases using expected numbers of cases standardized for age and gender as a basis. Excess risks were calculated using a continuous variable for mutagenicity for 3,000 net rev/l exposure representing an average exposure in a town using chlorinated surface water. After adjustment for confounding, a statistically significant excess risk was observed for women in cancers of the bladder (relative risk [RR] = 1.48, 95 percent confidence interval [CI] = 1.01-2.18), rectum (RR = 1.38, CI = 1.03-1.85), esophagus (RR = 1.90, CI = 1.02-3.52), and breast (RR = 1.11, CI = 1.01-1.22). These results support the magnitude of excess risks for rectal and bladder cancers found in earlier epidemiologic studies on chlorination by-products and give additional information on exposure-response concerning the mutagenic compounds. Nevertheless, due to the public health importance of water chlorination, uncertainty related to the magnitude of observed risks, and the fact that excess risks were observed only for women, the results of the study should be interpreted with caution.
PubMed ID
9134243 View in PubMed
Less detail

Drinking water mutagenicity and gastrointestinal and urinary tract cancers: an ecological study in Finland.

https://arctichealth.org/en/permalink/ahliterature217573
Source
Am J Public Health. 1994 Aug;84(8):1223-8
Publication Type
Article
Date
Aug-1994
Author
M. Koivusalo
J J Jaakkola
T. Vartiainen
T. Hakulinen
S. Karjalainen
E. Pukkala
J. Tuomisto
Author Affiliation
Finnish Cancer Registry, Helsinki.
Source
Am J Public Health. 1994 Aug;84(8):1223-8
Date
Aug-1994
Language
English
Publication Type
Article
Keywords
Case-Control Studies
Chlorine - adverse effects
Environmental Exposure
Environmental monitoring
Epidemiological Monitoring
Finland - epidemiology
Gastrointestinal Neoplasms - chemically induced - epidemiology
Humans
Incidence
Linear Models
Mutagens - adverse effects
Population Surveillance
Risk factors
Urban Population
Urologic Neoplasms - chemically induced - epidemiology
Water Supply - analysis
Abstract
The purpose of this study was to investigate the relationship between exposure to mutagenic drinking water and cancers of the gastrointestinal and urinary tract.
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.
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.
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.
Notes
Cites: Res Commun Chem Pathol Pharmacol. 1974 Aug;8(4):703-64153624
Cites: Science. 1980 Jan 4;207(4426):90-26985746
Cites: Environ Res. 1994 Jan;64(1):90-1018287844
Cites: Mutat Res. 1983 May;113(3-4):173-2156341825
Cites: Int J Epidemiol. 1983 Sep;12(3):290-66629617
Cites: Mutat Res. 1986 Jan-Feb;169(1-2):29-343511365
Cites: Scand J Soc Med. 1986;14(1):39-473704580
Cites: Prev Med. 1986 Mar;15(2):127-383714667
Cites: Soc Sci Med. 1987;24(7):601-63589754
Cites: Mutat Res. 1987 Dec;189(4):363-732960893
Cites: J Natl Cancer Inst. 1987 Dec;79(6):1269-793480378
Cites: Mutat Res. 1988 Oct;206(2):177-823050498
Cites: Sci Total Environ. 1988 Aug 1;74:75-963065939
Cites: Health Phys. 1989 Sep;57(3):417-272777548
Cites: Toxicol Lett. 1991 Dec;59(1-3):187-951755025
Cites: Int J Epidemiol. 1992 Feb;21(1):6-151544760
Cites: Am J Public Health. 1992 Jul;82(7):955-631535181
Cites: Pharmacol Toxicol. 1992 Jun;70(6 Pt 1):424-81438020
Cites: Mutat Res. 1993 Mar;299(1):25-87679189
Comment In: Am J Public Health. 1994 Aug;84(8):1211-38059872
Comment In: Am J Public Health. 1995 Sep;85(9):1298-3007661248
PubMed ID
8059876 View in PubMed
Less detail

24 records – page 1 of 3.