Skip header and navigation

Refine By

467 records – page 1 of 47.

1,3-Butadiene and leukemia among synthetic rubber industry workers: exposure-response relationships.

https://arctichealth.org/en/permalink/ahliterature166384
Source
Chem Biol Interact. 2007 Mar 20;166(1-3):15-24
Publication Type
Article
Date
Mar-20-2007
Author
Hong Cheng
Nalini Sathiakumar
John Graff
Robert Matthews
Elizabeth Delzell
Author Affiliation
University of Alabama at Birmingham, Ryals School of Public Health, Department of Epidemiology, Birmingham, AL, USA. hcheng@ms.soph.uab.edu
Source
Chem Biol Interact. 2007 Mar 20;166(1-3):15-24
Date
Mar-20-2007
Language
English
Publication Type
Article
Keywords
Butadienes - adverse effects
Canada - epidemiology
Carcinogens - chemical synthesis - chemistry - toxicity
Chemical Industry - manpower - statistics & numerical data
Confidence Intervals
Dimethyldithiocarbamate - adverse effects
Humans
Leukemia, Lymphoid - chemically induced - epidemiology
Leukemia, Myeloid - chemically induced - epidemiology
Likelihood Functions
Male
Middle Aged
Occupational Exposure - statistics & numerical data
Proportional Hazards Models
Rubber - adverse effects - chemical synthesis - chemistry
United States - epidemiology
Abstract
Previous research updated the mortality experience of North American synthetic rubber industry workers during the period 1944-1998, determined if leukemia and other cancers were associated with several employment factors and carried out Poisson regression analysis to examine exposure-response associations between estimated exposure to 1,3-butadiene (BD) or other chemicals and cancer. The present study used Cox regression procedures to examine further the exposure-response relationship between several unlagged and lagged, continuous, time-dependent BD exposure indices (BD parts per million (ppm)-years, the total number of exposures to BD concentrations >100 ppm ("peaks") and average intensity of BD) and leukemia, lymphoid neoplasms and myeloid neoplasms. All three BD exposure indices were associated positively with leukemia. Using continuous, untransformed BD ppm-years the regression coefficient (beta) from an analysis that controlled only for age was 2.9 x 10(-4) (p
PubMed ID
17123495 View in PubMed
Less detail

1,3-Butadiene: exposure estimation, hazard characterization, and exposure-response analysis.

https://arctichealth.org/en/permalink/ahliterature186649
Source
J Toxicol Environ Health B Crit Rev. 2003 Jan-Feb;6(1):55-83
Publication Type
Article
Author
K. Hughes
M E Meek
M. Walker
R. Beauchamp
Author Affiliation
Existing Substances Division, Environmental Health Directorate, Health Canada, Environmental Health Centre, Tunney's Pasture PL0802B1, Ottawa, Ontario, Canada K1A 0L2.
Source
J Toxicol Environ Health B Crit Rev. 2003 Jan-Feb;6(1):55-83
Language
English
Publication Type
Article
Keywords
Animals
Butadienes - metabolism - toxicity
Canada - epidemiology
Carcinogens, Environmental - toxicity
Environmental Exposure
Hazardous Substances - toxicity
Humans
Mutagens - toxicity
Neoplasms - chemically induced - epidemiology
Occupational Diseases - chemically induced - epidemiology
Risk assessment
Abstract
1,3-Butadiene has been assessed as a Priority Substance under the Canadian Environmental Protection Act. The general population in Canada is exposed to 1,3-butadiene primarily through ambient air. Inhaled 1,3-butadiene is carcinogenic in both mice and rats, inducing tumors at multiple sites at all concentrations tested in all identified studies. In addition, 1,3-butadiene is genotoxic in both somatic and germ cells of rodents. It also induces adverse effects in the reproductive organs of female mice at relatively low concentrations. The greater sensitivity in mice than in rats to induction of these effects by 1,3-butadiene is likely related to species differences in metabolism to active epoxide metabolites. Exposure to 1,3-butadiene in the occupational environment has been associated with the induction of leukemia; there is also some limited evidence that 1,3-butadiene is genotoxic in exposed workers. Therefore, in view of the weight of evidence of available epidemiological and toxicological data, 1,3-butadiene is considered highly likely to be carcinogenic, and likely to be genotoxic, in humans. Estimates of the potency of butadiene to induce cancer have been derived on the basis of both epidemiological investigation and bioassays in mice and rats. Potencies to induce ovarian effects have been estimated on the basis of studies in mice. Uncertainties have been delineated, and, while there are clear species differences in metabolism, estimates of potency to induce effects are considered justifiably conservative in view of the likely variability in metabolism across the population related to genetic polymorphism for enzymes for the critical metabolic pathway.
PubMed ID
12587254 View in PubMed
Less detail

2nd Nordic Toxicology Congress, NordTox-92. Symposium proceedings. Aland Islands, Finland, May 1992.

https://arctichealth.org/en/permalink/ahliterature24280
Source
Pharmacogenetics. 1992 Dec;2(6):245-349
Publication Type
Conference/Meeting Material
Article
Date
Dec-1992
Source
Pharmacogenetics. 1992 Dec;2(6):245-349
Date
Dec-1992
Language
English
Publication Type
Conference/Meeting Material
Article
Keywords
Carcinogens, Environmental
Environmental Exposure
Humans
Neoplasms - chemically induced
PubMed ID
1363969 View in PubMed
Less detail

ABCG2/BCRP decreases the transfer of a food-born chemical carcinogen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in perfused term human placenta.

https://arctichealth.org/en/permalink/ahliterature92634
Source
Toxicol Appl Pharmacol. 2008 Oct 15;232(2):210-7
Publication Type
Article
Date
Oct-15-2008
Author
Myllynen Päivi
Kummu Maria
Kangas Tiina
Ilves Mika
Immonen Elina
Rysä Jaana
Pirilä Rauna
Lastumäki Anni
Vähäkangas Kirsi H
Author Affiliation
Department of Pharmacology and Toxicology, University of Oulu, PO Box 5000, 90014, Oulu, Finland. paivi.myllynen@oulu.fi
Source
Toxicol Appl Pharmacol. 2008 Oct 15;232(2):210-7
Date
Oct-15-2008
Language
English
Publication Type
Article
Keywords
ATP-Binding Cassette Transporters - physiology
Carcinogens - metabolism - toxicity
Cell Line, Tumor
Drug Resistance, Multiple - physiology
Female
Food - toxicity
Humans
Imidazoles - metabolism - toxicity
Maternal-Fetal Exchange - physiology
Neoplasm Proteins - physiology
Perfusion - methods
Placenta - drug effects - metabolism
Pregnancy
Abstract
We have studied the role of ATP binding cassette (ABC) transporters in fetal exposure to carcinogens using 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) a known substrate for ABC transporters as a model compound. In perfusion of human term placenta, transfer of (14)C-PhIP (2 microM) through the placenta resulted in fetal-to-maternal concentration ratio (FM ratio) of 0.72+/-0.09 at 6 h. The specific ABCG2 inhibitor KO143 increased the transfer of (14)C-PhIP from maternal to fetal circulation (FM ratio 0.90+/-0.08 at 6 h, p
PubMed ID
18680760 View in PubMed
Less detail

Acrylamide and cancer: tunnel leak in Sweden prompted studies.

https://arctichealth.org/en/permalink/ahliterature19084
Source
J Natl Cancer Inst. 2002 Jun 19;94(12):876-8
Publication Type
Article
Date
Jun-19-2002

Acrylamide-asparagine relationship in baked/toasted wheat and rye breads.

https://arctichealth.org/en/permalink/ahliterature156290
Source
Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2008 Aug;25(8):921-9
Publication Type
Article
Date
Aug-2008
Author
Kit Granby
Nikoline Juul Nielsen
Rikke V Hedegaard
Tue Christensen
Mette Kann
Leif H Skibsted
Author Affiliation
Technical University of Denmark, National food Institute, Søborg, DK-2860, Denmark. kgr@food.dtu.dk
Source
Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2008 Aug;25(8):921-9
Date
Aug-2008
Language
English
Publication Type
Article
Keywords
Acrylamide - analysis
Asparagine - analysis
Bread - analysis
Carcinogens - analysis
Cooking - methods
Denmark
Diet
Flour
Food Technology - methods
Hot Temperature
Humans
Maillard Reaction
Risk Assessment - methods
Secale cereale
Triticum
Abstract
Acrylamide in baked and toasted wheat and rye bread was studied in relation to levels of asparagine in flour, dough, bread and toasts. Asparagine was consumed during bread preparation resulting in reduced acrylamide content in the products. In wheat bread, 12% of the asparagine initially present in the flour (0.14 g kg(-1)) remained after yeast fermentation and baking; for rye bread, 82% of asparagine remained after sourdough fermentation and baking. Asparagine present in untoasted wheat bread had totally reacted after hard toasting. Toasted wheat and rye bread slices contained 11-161 and 27-205 microg kg(-1) acrylamide, respectively, compared to untoasted wheat and rye bread with
PubMed ID
18608496 View in PubMed
Less detail

Active smoking and secondhand smoke increase breast cancer risk: the report of the Canadian Expert Panel on Tobacco Smoke and Breast Cancer Risk (2009).

https://arctichealth.org/en/permalink/ahliterature138696
Source
Tob Control. 2011 Jan;20(1):e2
Publication Type
Article
Date
Jan-2011
Author
Kenneth C Johnson
Anthony B Miller
Neil E Collishaw
Julie R Palmer
S Katharine Hammond
Andrew G Salmon
Kenneth P Cantor
Mark D Miller
Norman F Boyd
John Millar
Fernand Turcotte
Author Affiliation
Science Integration Division, Centre for Chronic Disease Prevention and Control, Public Health Agency of Canada, 785 Carling Avenue, Ottawa K1A0K9, Canada. ken_lcdc_johnson@phac-aspc.gc.ca
Source
Tob Control. 2011 Jan;20(1):e2
Date
Jan-2011
Language
English
Publication Type
Article
Keywords
Acetyltransferases - genetics
Breast Neoplasms - epidemiology - etiology - genetics
Canada - epidemiology
Carcinogens
Female
Humans
Organizations
Premenopause
Public Health
Risk factors
Smoking - adverse effects
Tobacco Smoke Pollution - adverse effects
Abstract
Four authoritative reviews of active smoking and breast cancer have been published since 2000, but only one considered data after 2002 and conclusions varied. Three reviews of secondhand smoke (SHS) and breast cancer (2004-2006) each came to different conclusions. With 30 new studies since 2002, further review was deemed desirable. An Expert Panel was convened by four Canadian agencies, the Ontario Tobacco Research Unit, the Public Health Agency of Canada, Physicians for a Smoke-Free Canada and the Canadian Partnership Against Cancer to comprehensively examine the weight of evidence from epidemiological and toxicological studies and understanding of biological mechanisms regarding the relationship between tobacco smoke and breast cancer. This article summarises the panel's full report (http://www.otru.org/pdf/special/expert_panel_tobacco_breast_cancer.pdf). There are 20 known or suspected mammary carcinogens in tobacco smoke, and recognised biological mechanisms that explain how exposure to these carcinogens could lead to breast cancer. Results from the nine cohort studies reporting exposure metrics more detailed than ever/never and ex/current smoker show that early age of smoking commencement, higher pack-years and longer duration of smoking increase breast cancer risk 15% to 40%. Three meta-analyses report 35% to 50% increases in breast cancer risk for long-term smokers with N-acetyltransferase 2 gene (NAT2) slow acetylation genotypes. The active smoking evidence bolsters support for three meta-analyses that each reported about a 65% increase in premenopausal breast cancer risk among never smokers exposed to SHS. The Panel concluded that: 1) the association between active smoking and breast cancer is consistent with causality and 2) the association between SHS and breast cancer among younger, primarily premenopausal women who have never smoked is consistent with causality.
PubMed ID
21148114 View in PubMed
Less detail

467 records – page 1 of 47.