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27 records – page 1 of 3.

Arsenic concentrations in prediagnostic toenails and the risk of bladder cancer in a cohort study of male smokers.

https://arctichealth.org/en/permalink/ahliterature177829
Source
Am J Epidemiol. 2004 Nov 1;160(9):853-9
Publication Type
Article
Date
Nov-1-2004

Case study 1: asbestos--the TLV approach.

https://arctichealth.org/en/permalink/ahliterature251474
Source
Ann N Y Acad Sci. 1976;271:152-69
Publication Type
Article
Date
1976
Author
W J Nicholson
Source
Ann N Y Acad Sci. 1976;271:152-69
Date
1976
Language
English
Publication Type
Article
Keywords
Air Pollutants, Occupational
Asbestos - analysis - toxicity
Asbestosis - prevention & control
Canada
Carcinogens, Environmental
Cocarcinogenesis
Environmental health
Gastrointestinal Neoplasms - chemically induced
Humans
Lung Neoplasms - chemically induced
Male
Maximum Allowable Concentration
Mesothelioma - chemically induced
Occupational Diseases - chemically induced
Risk
Smoking - complications
Time Factors
United States
Abstract
A review of the control of carcinogenic exposures using the TLV approach presents a prospect of limited effectiveness. With asbestos, as with any carcinogen, no threshold is known below which no health effect may be manifest. At best, we have only limited dose-response information at levels much above those of practical concern. In the case of asbestos, current exposures can only be described crudely at any level of exposure, and health effects are only known for past high, but ill-defined, exposures. Limited information exists on the effects of synergistic interactions with other materials. The current U.S. TLV, based on data concerned with occurrence of asbestosis, has not been evaluated with regard to possible effectiveness in the prevention of asbestos cancer. Yet cancer is the heart of the asbestos-hazard problem. Finally, enforcement of the existing TLV, especially for asbestos has been limited, frequently absent, and often ineffective. Workers are exposed in many situations to levels much above the current standard. As discouraging as this picture may seem, a TLV can be useful for stimulating the development and application of engineering-control procedures. The application of these procedures, however, must be specified and mandated in future standards to lower worker exposures to the minimum commensurate with existing technology. As technology is developed that makes lower exposure levels possible in a large part of the industry, TLVs should be reduced to take advantage of that technology.
PubMed ID
1069498 View in PubMed
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Coffee, tea, tobacco, and cancer of the large bowel.

https://arctichealth.org/en/permalink/ahliterature23529
Source
Cancer Epidemiol Biomarkers Prev. 1994 Oct-Nov;3(7):565-70
Publication Type
Article
Author
J A Baron
M. Gerhardsson de Verdier
A. Ekbom
Author Affiliation
Cancer Epidemiology Unit, Uppsala University, Sweden.
Source
Cancer Epidemiol Biomarkers Prev. 1994 Oct-Nov;3(7):565-70
Language
English
Publication Type
Article
Keywords
Adenocarcinoma - epidemiology - etiology
Aged
Case-Control Studies
Cocarcinogenesis
Coffee - adverse effects
Colorectal Neoplasms - epidemiology - etiology
Confidence Intervals
Cross-Sectional Studies
Female
Humans
Incidence
Male
Middle Aged
Odds Ratio
Research Support, Non-U.S. Gov't
Risk factors
Smoking - adverse effects
Sweden - epidemiology
Tea - adverse effects
Abstract
The impact of tobacco use and coffee and tea intake on the risk of colorectal cancer is unclear. Previous research has suggested that coffee may be protective against these cancers, and investigation regarding tea or cigarette smoking has yielded inconsistent results. To clarify these issues, we evaluated coffee and tea intake and tobacco smoking as risk factors for cancer of the colon and rectum in a population-based case-control study from Stockholm, Sweden. Cases were ascertained from the regional cancer registry, and controls identified through population registers. Subjects completed a questionnaire requesting information regarding foods and beverages consumed, exercise, tobacco use, and personal characteristics. Logistic regression modelling was used to compute odds ratios. A total of 352 cases of colon cancer, 217 cases of rectal cancer, and 512 controls took part. High coffee intake was negatively associated with the risk of colon cancer: the odds ratio for those drinking 6 or more cups per day was 0.55 (95% confidence interval, 0.31-0.96) compared to those drinking one or fewer. There was no association with rectal cancer. For tea, the associations were the opposite: there was no association with colon cancer risk, but the odds ratio for rectal cancer was 0.56 (95% confidence interval, 0.34-0.90) for those drinking 2 or more cups per day compared with those drinking none. Smokers of 11 or more cigarettes per day had a 20 to 30% reduction in the risk of colon and rectal cancer, but these findings were consistent with chance. There was no association of long-term cigarette smoking with risk.
PubMed ID
7827586 View in PubMed
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Combined effect of smoking and human papillomavirus type 16 infection in cervical carcinogenesis.

https://arctichealth.org/en/permalink/ahliterature21665
Source
Epidemiology. 1998 May;9(3):346-9
Publication Type
Article
Date
May-1998
Author
A O Olsen
J. Dillner
A. Skrondal
P. Magnus
Author Affiliation
Department of Population Health Sciences, National Institute of Public Health, Oslo, Norway.
Source
Epidemiology. 1998 May;9(3):346-9
Date
May-1998
Language
English
Publication Type
Article
Keywords
Adult
Case-Control Studies
Cell Transformation, Neoplastic
Cocarcinogenesis
DNA, Viral - analysis
Female
Humans
Norway - epidemiology
Papillomavirus - genetics - pathogenicity
Papovaviridae Infections - complications
Research Support, Non-U.S. Gov't
Smoking - adverse effects
Tumor Virus Infections - complications
Uterine Cervical Neoplasms - epidemiology - etiology - virology
Abstract
To study the combined effect of smoking and human papillomavirus (HPV) type 16 infection in high-grade cervical intraepithelial neoplasia, we analyzed data from a Norwegian population-based case-control study including 90 patients and 216 controls, 20-44 years of age. We assessed HPV-16 status both by polymerase chain reaction detecting virus DNA and by enzyme-linked immunosorbent assay detecting antibodies against virus capsid. Smoking was associated with cervical intraepithelial neoplasia grade II-III in HPV-16-positive individuals. Using the jointly unexposed (HPV-16 DNA-negative never-smokers) as the reference group, we determined the risk of cervical intraepithelial neoplasia grade II-III in HPV-16 DNA-positive never-smokers and HPV-16 DNA-positive ever-smokers (odds ratio = 15.7; 95% confidence limits = 3.2, 76.5, and odds ratio = 65.9; 95% confidence limits = 22.3, 194.3, respectively). The estimated proportion of cases among HPV-16-positive smokers that is attributable to the interaction between the two causes is 74%, based on HPV-16 DNA positivity.
PubMed ID
9583429 View in PubMed
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CYP2C9 genotype does not affect risk of tobacco-related cancer in the general population.

https://arctichealth.org/en/permalink/ahliterature145731
Source
Cancer Epidemiol. 2010 Apr;34(2):178-83
Publication Type
Article
Date
Apr-2010
Author
Diljit Kaur-Knudsen
Børge Grønne Nordestgaard
Stig Egil Bojesen
Author Affiliation
Department of Clinical Biochemistry and The Copenhagen General Population Study, Herlev Hospital, Copenhagen University Hospital, Herlev Ringvej 75, DK-2730 Herlev, Denmark.
Source
Cancer Epidemiol. 2010 Apr;34(2):178-83
Date
Apr-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aryl Hydrocarbon Hydroxylases - genetics - metabolism
Cocarcinogenesis
Cohort Studies
Denmark - epidemiology
Female
Genetic Predisposition to Disease
Genotype
Humans
Male
Middle Aged
Neoplasms - enzymology - epidemiology - genetics
Polymorphism, Genetic
Polymorphism, Single Nucleotide
Prospective Studies
Smoking - adverse effects - epidemiology - genetics - metabolism
Abstract
CYP2C9 enzymes are important in the metabolism of procarcinogenic chemicals such as polycyclic aromatic hydrocarbons (PAHs) found in tobacco smoke. Two functional variants in the CYP2C9 gene (CYP2C9*2 and CYP2C9*3) are known to be associated with decreased enzyme activity towards tolbutamide and warfarin, while this has not been investigated for PAHs. We hypothesised that these two variants in the CYP2C9 gene influence risk of tobacco-related cancer.
In a prospective study of the general population (n=10 392) with 60 years of follow-up, the Copenhagen City Heart Study, we associated two variants of CYP2C9 (CYP2C9*2 and CYP2C9*3) with risk of tobacco-related cancer and all cancer. All results were re-tested in a cross-sectional study of the general population (n=36 856), the Copenhagen General Population Study.
We found no association between any of the CYP2C9 genotypes and risk of tobacco-related cancer, individual tobacco-related cancers, or all cancer. For the combined carriers (any CYP2C9*2 or CYP2C9*3 heterozygotes or homozygotes) vs. non-carriers we had 90% statistical power to exclude measures of relative risks below/above 0.8/1.2 and 0.9/1.1 in the Copenhagen City Heart Study and below/above 0.8/1.3 and 0.9/1.1 in the Copenhagen General Population Study for tobacco-related cancer and all cancer, respectively.
Genetic variations in CYP2C9 do not affect risk of tobacco-related cancers.
PubMed ID
20117066 View in PubMed
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Exposure-response relationship between lung cancer and polycyclic aromatic hydrocarbons (PAHs).

https://arctichealth.org/en/permalink/ahliterature150148
Source
Occup Environ Med. 2009 Nov;66(11):740-6
Publication Type
Article
Date
Nov-2009
Author
B G Armstrong
G. Gibbs
Author Affiliation
London School of Hygiene and Tropical Medicine, Keppel St, London WC1E 7HT, UK. ben.armstrong@lshtm.ac.uk
Source
Occup Environ Med. 2009 Nov;66(11):740-6
Date
Nov-2009
Language
English
Publication Type
Article
Keywords
Cocarcinogenesis
Epidemiologic Methods
Female
Humans
Lung Neoplasms - chemically induced - mortality
Male
Metallurgy
Occupational Diseases - chemically induced - mortality
Occupational Exposure - adverse effects - analysis
Polycyclic Compounds - toxicity
Quebec - epidemiology
Smoking - adverse effects - epidemiology
Abstract
To estimate the exposure-response function associating polycyclic aromatic hydrocarbon (PAH) exposure and lung cancer, with consideration of smoking.
Mortality, occupational exposure and smoking histories were ascertained for a cohort of 16,431 persons (15,703 men and 728 women) who had worked in one of four aluminium smelters in Quebec from 1950 to 1999. A variety of exposure-response functions were fitted to the cohort data using generalised relative risk models.
In 677 lung cancer cases there was a clear trend of increasing risk with increasing cumulative exposure to PAH measured as benzo(a)pyrene (BaP). A linear model predicted a relative risk of 1.35 (95% CI 1.22 to 1.51) at 100 microg/m(-3) BaP years, but there was a significant departure from linearity in the direction of decreasing slope with increasing exposures. Among the models tried, the best fitting were a two-knot cubic spline and a power curve (RR = (1+bx)(p)), the latter predicting a relative risk of 2.68 at 100 microg/m(-3) BaP years. Additive models and multiplicative models for combining risks from occupational PAH and smoking fitted almost equally well, with a slight advantage to the additive.
Despite the large cohort with long follow-up, the shape of the exposure-response function and the mode of combination of risks due to occupational PAH and smoking remains uncertain. If a linear exposure-response function is assumed, the estimated slope is broadly in line with the estimate from a previous follow-up of the same cohort, and somewhat higher than the average found in a recent meta-analysis of lung cancer studies.
Notes
Comment In: Occup Environ Med. 2009 Nov;66(11):716-719837902
PubMed ID
19546103 View in PubMed
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Genetically lowered microsomal epoxide hydrolase activity and tobacco-related cancer in 47,000 individuals.

https://arctichealth.org/en/permalink/ahliterature133868
Source
Cancer Epidemiol Biomarkers Prev. 2011 Aug;20(8):1673-82
Publication Type
Article
Date
Aug-2011
Author
Julie Lee
Morten Dahl
Børge G Nordestgaard
Author Affiliation
Department of Clinical Biochemistry, Herlev Hospital, Herlev, Denmark.
Source
Cancer Epidemiol Biomarkers Prev. 2011 Aug;20(8):1673-82
Date
Aug-2011
Language
English
Publication Type
Article
Keywords
Aged
Cocarcinogenesis
Denmark - epidemiology
Epoxide Hydrolases - genetics - metabolism
Female
Genetic Predisposition to Disease
Genotype
Humans
Male
Middle Aged
Neoplasms - enzymology - epidemiology - etiology - genetics
Questionnaires
Smoking - adverse effects - epidemiology - genetics - metabolism
Abstract
Two functional polymorphisms of the microsomal epoxide hydrolase (mEH) gene (EPHX1), Tyr113His (rs1051740) and His139Arg (rs2234922), have variably been found to influence susceptibility to various cancer forms. We tested whether genetically lowered mEH activity affects risk of developing cancer in the general population.
We genotyped 47,089 individuals from the Danish general population for the Tyr113His and His139Arg polymorphisms in the EPHX1 gene and divided them into groups with predicted fast, intermediate, and slow mEH activity. Using Cox proportional hazards models, we calculated HRs for 26 individual cancer diagnoses and for groups of any cancer, tobacco-related cancers, estrogen-related female cancers, and other cancers.
Of the 47,089 individuals, 7,590 experienced a cancer event, and of these, 1,466 were tobacco-related. After multifactorial adjustment, the HRs (95% CI) for tobacco-related cancer were 1.1 (0.8-1.5) and 1.5 (1.1-2.0) in individuals with intermediate and slow mEH activity versus individuals with the fast phenotype (P(trend) = 0.003). The corresponding HRs among ever-smokers were 1.1 (0.8-1.5) and 1.5 (1.1-2.0; P(trend) = 0.003), whereas HRs among never-smokers did not differ from 1.0.
Our results indicate that genetically lowered mEH activity is associated with increased risk of developing tobacco-related cancer among smokers in the general population; however, additional studies are needed to confirm our findings.
To our knowledge, this is the largest study to investigate the association of mEH phenotype and genotype with tobacco-related cancers combined in the general population.
PubMed ID
21653646 View in PubMed
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Genetic bases of estrogen-induced tumorigenesis in the rat: mapping of loci controlling susceptibility to mammary cancer in a Brown Norway x ACI intercross.

https://arctichealth.org/en/permalink/ahliterature81225
Source
Cancer Res. 2006 Aug 1;66(15):7793-800
Publication Type
Article
Date
Aug-1-2006
Author
Schaffer Beverly S
Lachel Cynthia M
Pennington Karen L
Murrin Clare R
Strecker Tracy E
Tochacek Martin
Gould Karen A
Meza Jane L
McComb Rodney D
Shull James D
Author Affiliation
Department of Genetics, Eppley Institute for Research in Cancer, University of Nebraska Medical Center, 985805 Nebraska Medical Center, Omaha, NE 68198, USA.
Source
Cancer Res. 2006 Aug 1;66(15):7793-800
Date
Aug-1-2006
Language
English
Publication Type
Article
Keywords
Animals
Chromosome Mapping
Cocarcinogenesis
Estradiol - pharmacology
Female
Genetic Predisposition to Disease
Mammary Neoplasms, Experimental - chemically induced - genetics
Pituitary Neoplasms - genetics
Rats
Rats, Inbred ACI
Rats, Inbred BN
Abstract
Exposure to estrogens is associated with an increased risk of breast cancer. Our laboratory has shown that the ACI rat is uniquely susceptible to 17beta-estradiol (E2)-induced mammary cancer. We previously mapped two loci, Emca1 and Emca2 (estrogen-induced mammary cancer), that act independently to determine susceptibility to E2-induced mammary cancer in crosses between the susceptible ACI rat strain and the genetically related, but resistant, Copenhagen (COP) rat strain. In this study, we evaluate susceptibility to E2-induced mammary cancer in a cross between the ACI strain and the unrelated Brown Norway (BN) rat strain. Whereas nearly 100% of the ACI rats developed mammary cancer when treated continuously with E2, BN rats did not develop palpable mammary cancer during the 196-day course of E2 treatment. Susceptibility to E2-induced mammary cancer segregated as a dominant or incompletely dominant trait in a cross between BN females and ACI males. In a population of 251 female (BN x ACI)F(2) rats, we observed evidence for a total of five genetic determinants of susceptibility. Two loci, Emca4 and Emca5, were identified when mammary cancer status at sacrifice was evaluated as the phenotype, and three additional loci, Emca6, Emca7, and Emca8, were identified when mammary cancer number was evaluated as the phenotype. A total of three genetic interactions were identified. These data indicate that susceptibility to E2-induced mammary cancer in the BN x ACI cross behaves as a complex trait controlled by at least five loci and multiple gene-gene interactions.
PubMed ID
16885383 View in PubMed
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27 records – page 1 of 3.