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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
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Availability of data on humans potentially exposed to suspected carcinogens in the Danish working environment.

https://arctichealth.org/en/permalink/ahliterature24170
Source
Pharmacol Toxicol. 1993;72 Suppl 1:77-85
Publication Type
Article
Date
1993
Author
J. Hansen
T. Schneider
J H Olsen
B. Laursen
Author Affiliation
National Institute of Occupational Health, København, Denmark.
Source
Pharmacol Toxicol. 1993;72 Suppl 1:77-85
Date
1993
Language
English
Publication Type
Article
Keywords
Carcinogens, Environmental - toxicity
Denmark - epidemiology
Humans
Occupational Exposure - adverse effects
Abstract
For the majority of suspected carcinogens only little or no human evidence exists, and in general on-going epidemiologic studies fail to address this fast growing group of chemicals. A survey based on a Danish occupational surveillance system concerning data on present and historical import, production and use of the 167 chemicals evaluated by the International Agency for Research on Cancer as possible or probable carcinogens, shows that about 110 of these chemicals are on the market in Denmark at present. Only 32 are used in industry in relatively large quantities. For some of these chemicals it is possible to identify clusters of companies, including historical cohorts of potentially exposed workers. Measurements of airborne pollutants are available for some few of the suspected carcinogens, indicating decreasing time trends and various levels in different industries. In spite of some limitations, this information on potential exposure has on ad hoc basis been linked to an existing cancer registry based occupational surveillance system, and various studies based on the total body of data are on-going, as a preliminary approach to give at least some human evidence to some widespread animal carcinogens.
PubMed ID
8474995 View in PubMed
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Carcinogenic chemicals in the occupational environment.

https://arctichealth.org/en/permalink/ahliterature221998
Source
Pharmacol Toxicol. 1993;72 Suppl 1:69-76
Publication Type
Article
Date
1993
Author
A. Anttila
M. Sallmén
K. Hemminki
Author Affiliation
Institute of Occupational Health, Helsinki, Finland.
Source
Pharmacol Toxicol. 1993;72 Suppl 1:69-76
Date
1993
Language
English
Publication Type
Article
Keywords
Carcinogens, Environmental - toxicity
Finland - epidemiology
Humans
Neoplasms - chemically induced - epidemiology
Occupational Exposure - adverse effects
Abstract
A survey of occupational carcinogens by the Institute of Occupational Health, Finland shows that more than 100,000 workers are exposed to carcinogenic substances. The most common exposures are silica, wood dust, tobacco smoke and lead compounds. Based on biological monitoring of workers over the years it appears that overall lead exposure has decreased but exposure to styrene, trichloroethylene and tetrachloroethylene has decreased only slightly or remained constant. The biological monitoring data are based on samples sent by the workplaces on their initiative presenting no scientifically selected sampling. Thus due caution is needed in the interpretation of the trends.
PubMed ID
8474994 View in PubMed
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Environmental health risk management in Canada.

https://arctichealth.org/en/permalink/ahliterature242151
Source
Regul Toxicol Pharmacol. 1983 Mar;3(1):75-81
Publication Type
Article
Date
Mar-1983
Author
E. Somers
Source
Regul Toxicol Pharmacol. 1983 Mar;3(1):75-81
Date
Mar-1983
Language
English
Publication Type
Article
Keywords
Animals
Canada
Carcinogens, Environmental - toxicity
Environmental Pollutants - toxicity
Humans
Legislation, Drug
Risk
Abstract
The legislative basis of the federal Canadian government's control of toxic chemicals is described and examples are given of the practical application, ranging from recommendations to a ban on the sale of the product. The ordered sequence of risk assessment and the application of risk estimation techniques are considered. It is clear that the ultimate political decision is not amenable to simplistic scientific analysis, although risk analysis is valuable in defining, rather than solving, the problem.
PubMed ID
6612005 View in PubMed
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[Evaluating occupational risk for firemen health due to exposure to chemicals].

https://arctichealth.org/en/permalink/ahliterature146412
Source
Med Tr Prom Ekol. 2010;(12):10-4
Publication Type
Article
Date
2010
Source
Med Tr Prom Ekol. 2010;(12):10-4
Date
2010
Language
Russian
Publication Type
Article
Keywords
Adult
Air Pollutants - adverse effects - chemistry
Carcinogens, Environmental - toxicity
Fires
Humans
Middle Aged
Occupational Diseases - epidemiology - etiology
Occupational Exposure - adverse effects
Risk
Risk assessment
Russia - epidemiology
Time Factors
Abstract
The authors present results of prognostic occupational risk evaluation in firemen of Chief Administration of Emergency Situations Ministry in Astrakhan region. Major risk is caused by exposure to chemicals produced in combustion. Findings are that health risk for the workers with long length of service is quite high and sufficient for occupational diseases and carcinogenic effects formation.
PubMed ID
21442934 View in PubMed
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[Exposure to carcinogens in work environment today. State of the art, problems and prospects raised by the Law 626/94].

https://arctichealth.org/en/permalink/ahliterature205079
Source
Med Lav. 1998 Mar-Apr;89(2):102-9
Publication Type
Article
Author
F. Carnevale
A. Baldasseroni
Author Affiliation
UO PISSL G. Pieraccini Azienda Sanitaria di Firenze.
Source
Med Lav. 1998 Mar-Apr;89(2):102-9
Language
Italian
Publication Type
Article
Keywords
Carcinogens, Environmental - toxicity
Finland
Humans
Italy
Neoplasms - chemically induced - prevention & control
Occupational Diseases - chemically induced - prevention & control
Occupational Exposure - legislation & jurisprudence - prevention & control
Occupational health - legislation & jurisprudence
Risk factors
Abstract
The implementation in our country of recent legislation on carcinogenic risk assessment and management (VIIth title of Law 626/94) is considered. The authors describe potentialities and limits of the new legislation and of the derived Guidelines issued by the Regions. The health policy in this field and possible evolution in the near future are outlined, bearing in mind the experience of other countries. A short list of questions is suggested as a contribution to the discussion on the future scenario: whether exposure to carcinogens should be lower in the working environment than in the general environment; what is the relative importance of multifactoriality, individual biological variability, individual life-style in the genesis of cancers; whether medical health surveillance is worthwhile in terms of primary prevention; is it always true that there is no threshold limit value for carcinogens; what is the role of individual attitudes to prevention in exposure to carcinogens compared to "objective" protection; which balance between costs and benefits should be aimed at.
PubMed ID
9673099 View in PubMed
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Genetic determinant and environmental carcinogens.

https://arctichealth.org/en/permalink/ahliterature21551
Source
Mutat Res. 1998 Jun 18;402(1-2):85-91
Publication Type
Article
Date
Jun-18-1998
Author
M. Nagao
M. Ochiai
T. Ushijima
M. Watanabe
T. Sugimura
H. Nakagama
Author Affiliation
Carcinogenesis Division, National Cancer Center Research Institute, Tokyo, Japan. mnagao@gan2.ncc.go.jp
Source
Mutat Res. 1998 Jun 18;402(1-2):85-91
Date
Jun-18-1998
Language
English
Publication Type
Article
Keywords
Animals
Carcinogens, Environmental - toxicity
Colonic Neoplasms - chemically induced - genetics - pathology
Female
Genotype
Humans
Imidazoles - toxicity
Male
Mutagens - toxicity
Polymorphism, Genetic
Rats
Research Support, Non-U.S. Gov't
Species Specificity
Abstract
2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is the most abundant mutagenic heterocyclic amine (HCA) present in cooked foods. PhIP induces colon cancer in male Fischer 344 (F344) rats, and its role in human colon carcinogenesis has been suspected. To study the ecogenetics in PhIP colon carcinogenesis, rat system using aberrant crypt focus (ACF) formation as a phenotypic marker was applied. Among Buffalo (BUF), Brown Norway (BN), F344 and ACI/N (ACI) strains of rats, F344 rats produced a lower level of PhIP-DNA adducts than other three strains, and the number of ACFs/rat was highest in BUF, intermediate in BN and F344 and lowest in ACI. Thus there was no correlation between adduct levels and number of ACF induced by PhIP. F1 progenies of BUF and ACI developed ACF at a similar level to that of F344, and F1 progenies of F344 and ACI developed ACF at a similar level to that of F344. Thus it was indicated that susceptibility of F344 to the ACF induction was autosomally dominant over ACI rats. The results also suggest that BUF rats have at least two genes, one is autosomally recessive against ACI rats and one is autosomally dominant similar to that F344 has. A total of 170 progeny of ACI backcross of F344/ACI F1 were examined for number of ACFs and 65 progeny were phenotyped as F344 and 60 were ACI. Using these 125 rats, chromosomal mapping is being performed using markers of simple sequence length polymorphism (SSLP) and representational difference analysis (RDA). By mapping the gene, we will be able to identify humans who might belong to high risk group in general population, and cancer can be prevented more efficiently by attaining early diagnosis.
PubMed ID
9675250 View in PubMed
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Health risk assessment of 1,3-butadiene as a Priority Substance in Canada.

https://arctichealth.org/en/permalink/ahliterature194411
Source
Chem Biol Interact. 2001 Jun 1;135-136:109-35
Publication Type
Article
Date
Jun-1-2001
Author
K. Hughes
M E Meek
M. Walker
Author Affiliation
Environmental Health Directorate, Health Canada, Tunney's Pasture PL0802B1, Ottawa, Ontario, Canada K1A 0L2. kathy_hughes@hc-sc.gc.ca
Source
Chem Biol Interact. 2001 Jun 1;135-136:109-35
Date
Jun-1-2001
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 was included in the second list of Priority Substances to be assessed under the Canadian Environmental Protection Act. Potential hazards to human health were characterized on the basis of critical examination of available data on health effects in experimental animals and occupationally exposed human populations, as well as information on mode of action. Based on consideration of all relevant data identified as of April 1998, butadiene was considered highly likely to be carcinogenic to humans, and likely to be a somatic and germ cell genotoxicant in humans. In addition, butadiene may also be a reproductive toxicant in humans. Estimates of the potency of butadiene to induce these effects have been derived on the basis of quantitation of observed exposure-response relationships for the purposes of characterization of risk to the general population in Canada exposed to butadiene in the ambient environment.
PubMed ID
11397385 View in PubMed
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Lung cancer risk associated with occupational exposure to nickel, chromium VI, and cadmium in two population-based case-control studies in Montreal.

https://arctichealth.org/en/permalink/ahliterature145190
Source
Am J Ind Med. 2010 May;53(5):476-85
Publication Type
Article
Date
May-2010
Author
Rachelle Beveridge
Javier Pintos
Marie-Elise Parent
Jérome Asselin
Jack Siemiatycki
Author Affiliation
Département de Médecine Sociale et Préventive, Université de Montréal, Montreal, QC, Canada.
Source
Am J Ind Med. 2010 May;53(5):476-85
Date
May-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Cadmium - toxicity
Carcinogens, Environmental - toxicity
Case-Control Studies
Chromium - toxicity
Confidence Intervals
Female
Humans
Logistic Models
Lung Neoplasms - chemically induced - epidemiology - etiology
Male
Middle Aged
Nickel - toxicity
Occupational Diseases - epidemiology - etiology
Occupational Exposure - adverse effects
Odds Ratio
Quebec - epidemiology
Questionnaires
Risk assessment
Risk factors
Abstract
Nickel, chromium VI, and cadmium have been identified as lung carcinogens in highly exposed cohorts. The purpose of this study was to examine the etiological link between lung cancer and these metals in occupations, that usually entail lower levels of exposure than those seen in historical cohorts.
Two population-based case-control studies were conducted in Montreal, from 1979 to 1986 and from 1996 to 2001, comprising 1,598 cases and 1,965 controls. A detailed job history was obtained to evaluate lifetime occupational exposure to many agents, including nickel, chromium VI, and cadmium compounds.
Lung cancer odds ratios were increased only among former or non-smokers: 2.5 (95% CI: 1.3-4.7) for nickel exposure, 2.4 (95% CI: 1.2-4.8) for chromium VI, and 4.7 (95% CI: 1.5-14.3) for cadmium. The metals did not increase risk among smokers.
While excess risks due to these metal compounds were barely discernable among smokers, carcinogenic effects were seen among non-smokers.
Notes
Comment In: Am J Ind Med. 2011 May;54(5):41920957675
PubMed ID
20187007 View in PubMed
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Multistage tumor development in the human esophagus - the first identification of cocarcinogens of the tumor promoter type as principal carcinogenic risk factors in a local life style cancer.

https://arctichealth.org/en/permalink/ahliterature242460
Source
Prog Clin Biol Res. 1983;132B:219-38
Publication Type
Article
Date
1983
Author
E. Hecker
D. Lutz
J. Weber
K. Goerttler
J F Morton
Source
Prog Clin Biol Res. 1983;132B:219-38
Date
1983
Language
English
Publication Type
Article
Keywords
Animals
Carcinogens - isolation & purification
Carcinogens, Environmental - toxicity
Diterpenes - toxicity
Esophageal Neoplasms - etiology
Female
Humans
Irritants - toxicity
Life Style
Male
Mice
Phorbol Esters - toxicity
Plant Extracts - toxicity
Plants, Toxic - analysis
Abstract
An experimental analysis is described which demonstrates that the epidemiologically established high rate of esophageal cancer among blacks and creoles in Curacao most likely is the result of a multistage process involving initiators and promoters. As part of local lifestyle, the group at risk utilizes for various purposes plant parts of an indigenous bush Croton flavens L. ("Welensali"). Moreover they consume, as an everyday beverage, a "bush tea" made from the leaves of the bush. The roots, leaves and tea are shown to contain a multitude of irritant croton factors which are characterized as diterpene esters of the tigliane type. In mouse skin these exhibit strong promoting activity comparable to that of TPA. As the latter, also the croton factors isolated, show no solitary carcinogenic activity. One cup of Welensali tea contains the equivalent of about 12-times the irritant dose of croton factor F1; in addition, the equivalent of about 1.4-times the irritant dose 50 of the corresponding "cryptic" promoter F1-20-decanoate is present. These amounts are considered sufficient to maintain chronic irritation of the esophagus as an important element of co-carcinogenesis, especially of tumor promotion. Also, persons at risk in Curacao have been exposed at times previously to certain initiators. Mice treated by an initiation/promotion protocol with DMBA (or other initiators) and TPA develop tumors of the forestomach. Therefore, esophageal cancer on Curacao may be considered the first case for cocarcinogens of the tumor promoter type being principal risk factors in a life style cancer.
PubMed ID
6634757 View in PubMed
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14 records – page 1 of 2.