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9 records – page 1 of 1.

Asbestos in drinking water: a Canadian view.

https://arctichealth.org/en/permalink/ahliterature241497
Source
Environ Health Perspect. 1983 Nov;53:177-80
Publication Type
Article
Date
Nov-1983
Author
P. Toft
M E Meek
Source
Environ Health Perspect. 1983 Nov;53:177-80
Date
Nov-1983
Language
English
Publication Type
Article
Keywords
Asbestos - adverse effects
Asbestos, Serpentine
Canada
Epidemiologic Methods
Humans
Neoplasms - epidemiology - etiology
Risk
Water supply
Abstract
For several years now, public health professionals have been faced with evaluating the potential hazards associated with the ingestion of asbestos in food and drinking water. In Canada, this is a subject of particular concern, because of the widespread occurrence of chrysotile asbestos in drinking water supplies. The results of available Canadian monitoring and epidemiologic studies of asbestos in drinking water are reviewed and discussed in light of other published work. It is concluded that the risk to health associated with the ingestion of asbestos, at the levels found in municipal drinking water supplies, is so small that it cannot be detected by currently available epidemiologic techniques.
Notes
Cites: Nature. 1971 Jul 30;232(5309):332-35094836
Cites: Arch Environ Health. 1977 Jul-Aug;32(4):185-190889357
Cites: Sci Total Environ. 1981 Apr;18:77-896262910
Cites: J Chronic Dis. 1981;34(5):211-247240361
PubMed ID
6319117 View in PubMed
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Approach to health risk determination for metals and their compounds under the Canadian Environmental Protection Act.

https://arctichealth.org/en/permalink/ahliterature213705
Source
Regul Toxicol Pharmacol. 1995 Dec;22(3):206-12
Publication Type
Article
Date
Dec-1995
Author
M E Meek
K. Hughes
Author Affiliation
Environmental Health Directorate, Health Canada, Ottawa, Ontario.
Source
Regul Toxicol Pharmacol. 1995 Dec;22(3):206-12
Date
Dec-1995
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Canada
Carcinogens - adverse effects
Child
Child, Preschool
Environmental Exposure - legislation & jurisprudence
Humans
Infant
Infant, Newborn
Metals - adverse effects
Neoplasms - etiology
Risk assessment
Abstract
The Canadian Environmental Protection Act (CEPA) authorizes the Ministers of the Environment and of Health in Canada to investigate a wide variety of substances that may contaminate the environment and cause adverse effects on the environment and/or on human health. Under the Act, assessments have been completed for 44 environmental contaminants on the first Priority Substances List, including four metals and their compounds. The principles developed for the assessment of risk to human health for priority substances under CEPA are outlined, with specific emphasis on the metals. These include general aspects such as estimation of total exposure from all media, the development of exposure potency indices for carcinogens in lieu of low-dose risk estimates, and incorporation of toxicokinetic and toxicodynamic data, where available, to modify traditionally adopted uncertainty factors for development of tolerable intakes, or concentrations, for nonneoplastic effects. Aspects of the approach to human health risk assessment more specific to the metals considered under CEPA (i.e., arsenic, cadmium, chromium, and nickel) and implications for the subsequent strategic options process are also addressed, including the extent to which various chemical forms could be assessed (i.e., speciation) and essentiality.
PubMed ID
8837844 View in PubMed
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Inhaled formaldehyde: exposure estimation, hazard characterization, and exposure-response analysis.

https://arctichealth.org/en/permalink/ahliterature186648
Source
J Toxicol Environ Health B Crit Rev. 2003 Jan-Feb;6(1):85-114
Publication Type
Article
Author
R G Liteplo
M E Meek
Author Affiliation
Existing Substances Division, Safe Environments Program, Health Canada, Ottawa, Canada.
Source
J Toxicol Environ Health B Crit Rev. 2003 Jan-Feb;6(1):85-114
Language
English
Publication Type
Article
Keywords
Air Pollutants - toxicity
Air Pollution, Indoor - adverse effects
Canada - epidemiology
Dose-Response Relationship, Drug
Formaldehyde - toxicity
Hazardous Substances - toxicity
Humans
Mutagens - toxicity
Neoplasms - chemically induced - epidemiology
Risk assessment
Abstract
Formaldehyde has been assessed as a Priority Substance under the Canadian Environmental Protection Act. Probabilistic estimates of exposure of the general population in Canada to formaldehyde in ambient and indoor air are presented. Critical health effects include sensory irritation and the potential to induce tumors in the upper respiratory tract (the nasal region in rodents and potentially the lungs of humans). The majority of the general population is exposed to airborne concentrations of formaldehyde less than those typically associated with sensory irritation (i.e., 0.1 mg/m3). Based primarily upon data derived from laboratory studies, the inhalation of formaldehyde under conditions that induce cytotoxicity and sustained regenerative proliferation within the respiratory tract is considered to present a carcinogenic hazard to humans. At airborne levels for which the prevalence of sensory irritation is minimal (i.e., 0.1 mg/m3), risks of respiratory-tract cancers for the general population estimated on the basis of a biologically motivated case-specific model are exceedingly low. This biologically motivated case-specific model incorporates two-stage clonal expansion and is supported by dosimetry calculations from computational fluid dynamics analyses of formaldehyde flux in various regions of the nose and single-path modeling for the lower respiratory tract. The degree of confidence in the underlying database and uncertainties in estimates of exposure and in characterization of hazard and dose response are delineated.
PubMed ID
12587255 View in PubMed
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Tools for the prioritization of substances on the Domestic Substances List in Canada on the basis of hazard.

https://arctichealth.org/en/permalink/ahliterature148466
Source
Regul Toxicol Pharmacol. 2009 Dec;55(3):382-93
Publication Type
Article
Date
Dec-2009
Author
K. Hughes
J. Paterson
M E Meek
Author Affiliation
Safe Environments Directorate, Health Canada, AL 4904D, Ottawa, Ontario, Canada K1A 0K9. Kathy_hughes@hc-sc.gc.ca
Source
Regul Toxicol Pharmacol. 2009 Dec;55(3):382-93
Date
Dec-2009
Language
English
Publication Type
Article
Keywords
Animals
Canada
Environmental Exposure - adverse effects
Environmental Health - methods
Hazardous Substances - toxicity
Humans
Risk Assessment - methods
Abstract
A precedent setting legislative mandate under the Canadian Environmental Protection Act 1999 to establish priorities for assessment based on systematic consideration of all of the approximately 23,000 Existing Chemicals in Canada required the development and refinement of methodology in a number of important areas. This included development of simple and complex exposure and hazard tools for priority setting which draw maximally and efficiently on available data to systematically identify substances that are highest priorities in relation to their potential to cause adverse effects on the general population. The hierarchical approach in the simple and complex hazard tools described here efficiently and effectively sets substances aside as non-priorities, or prioritizes them for consideration additionally in assessment. The hazard tools efficiently incorporate previous work, contributing to consistency internationally, and involve hierarchical consideration of sources of information based on their relative weighting. They are health protective, based on their incorporated degree of conservatism, and provide direction for additional assessment for substances deemed to be priorities. Although designed for prioritization of Existing Substances in Canada, these tools have potential for broader application in other national and international programs to provide focus and increase efficiency in human health risk assessment.
PubMed ID
19766685 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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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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Releases from copper smelters and refineries and zinc plants in Canada: human health exposure and risk characterization.

https://arctichealth.org/en/permalink/ahliterature187312
Source
Sci Total Environ. 2003 Jan 1;301(1-3):23-41
Publication Type
Article
Date
Jan-1-2003
Author
R. Newhook
H. Hirtle
K. Byrne
M E Meek
Author Affiliation
Existing Substances Division, Health Canada, Environmental Health Centre, Tunney's Pasture 0802B1, Ottawa, Canada K1A 0L2. ron_newhook@hc-sc.gc.ca
Source
Sci Total Environ. 2003 Jan 1;301(1-3):23-41
Date
Jan-1-2003
Language
English
Publication Type
Article
Keywords
Air Pollutants - analysis
Canada
Carcinogens - adverse effects - analysis
Copper - adverse effects - analysis
Environmental Exposure
Epidemiologic Studies
Humans
Industry
Metallurgy
Metals, Heavy - adverse effects - analysis
Neoplasms - epidemiology - etiology
Public Health
Risk assessment
Zinc - adverse effects - analysis
Abstract
In these assessments of releases from copper smelters and refineries and from zinc plants as Priority Substances under the Canadian Environmental Protection Act (CEPA), available data were critically evaluated to determine if environmental exposure to selected components of these releases poses a risk to human health. The data on airborne levels of a variety of toxic substances near these facilities in Canada were obtained from the companies or provinces and systematically analyzed. Monitoring of ambient air near the Canadian copper smelters and refineries and zinc plants indicates that releases from these facilities result in increased potential for inhalation exposure of local human populations to several components of releases (As, Cd, Cr, Ni, Pb, SO(2) and PM(10)). Airborne levels in the vicinity of these metal-processing operations overlap those associated with cardiorespiratory effects for PM(10), and exceed health-based guidelines for SO(2) and, near some facilities, Pb. In addition, the margin between levels of As, Cd, Cr and Ni near these facilities in Canada and carcinogenic potency for each of these metals is relatively small near copper smelters, larger near copper refineries, and intermediate near zinc plants. On this basis, the risk to human health from environmental exposure to releases from these facilities is considered to be high compared with other Priority Substances assessed under CEPA, especially for facilities where copper is smelted.
PubMed ID
12493182 View in PubMed
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Speciation in health risk assessments of metals: evaluation of effects associated with forms present in the environment.

https://arctichealth.org/en/permalink/ahliterature213704
Source
Regul Toxicol Pharmacol. 1995 Dec;22(3):213-20
Publication Type
Article
Date
Dec-1995
Author
K. Hughes
M E Meek
R. Newhook
P K Chan
Author Affiliation
Environmental Health Directorate, Health Canada, Ottawa, Ontario.
Source
Regul Toxicol Pharmacol. 1995 Dec;22(3):213-20
Date
Dec-1995
Language
English
Publication Type
Article
Keywords
Canada
Carcinogens - adverse effects - chemistry
Environmental Exposure - legislation & jurisprudence
Humans
Metals - adverse effects - chemistry
Neoplasms - etiology
Risk assessment
Abstract
Because metals occur in various forms in the environment, speciation is an issue which must be addressed in regulatory health risk assessment programs. The manner in which speciation was addressed in a federal program in Canada is discussed in this article. Under the Canadian Environmental Protection Act, four metals, including arsenic, cadmium, chromium, and nickel, and their compounds were assessed as priority substances to determine the risk to human health associated with exposure to levels present in the general environment in Canada. The extent to which the speciation of these metals could be considered in these assessments was largely determined by the nature of available data. Very few data were identified on speciation in environmental media to which humans are exposed. Based on available data on health effects, it was possible to conduct assessments on only one form each of arsenic and cadmium (i.e., inorganic arsenic and inorganic cadmium), two forms of chromium (trivalent and hexavalent), and four forms of inorganic nickel (oxidic, sulfidic, soluble, and metallic.
PubMed ID
8837845 View in PubMed
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Chloroform: exposure estimation, hazard characterization, and exposure-response analysis.

https://arctichealth.org/en/permalink/ahliterature189119
Source
J Toxicol Environ Health B Crit Rev. 2002 Jul-Sep;5(3):283-334
Publication Type
Article
Author
M E Meek
R. Beauchamp
G. Long
D. Moir
L. Turner
M. Walker
Author Affiliation
Existing Substances Division, Environmental Health Directorate, Health Canada, Ottawa, Ontario, Canada.
Source
J Toxicol Environ Health B Crit Rev. 2002 Jul-Sep;5(3):283-334
Language
English
Publication Type
Article
Keywords
Air Pollutants - adverse effects - analysis
Air Pollution, Indoor - adverse effects - analysis
Animals
Baths - adverse effects
Canada
Chloroform - adverse effects - analysis
Dose-Response Relationship, Drug
Environmental Exposure - adverse effects
Humans
Neoplasms - chemically induced
Risk assessment
Water Pollutants, Chemical - adverse effects - analysis
Abstract
Chloroform has been assessed as a Priority Substance under the Canadian Environmental Protection Act. The general population in Canada is exposed to chloroform principally through inhalation of indoor air, particularly during showering, and through ingestion of tap water. Data on concentrations of chloroform in various media were sufficient to serve as the basis for development of deterministic and probabilistic estimates of exposure for the general population in Canada. On the basis of data acquired principally in studies in experimental animals, chloroform causes hepatic and renal tumors in mice and renal tumors in rats. The weight of evidence indicates that chloroform is likely carcinogenic only at concentrations that induce the obligatory precursor lesions of cytotoxicity and proliferative regenerative response. Since this cytotoxicity is primarily related to rates of formation of reactive, oxidative metabolites, dose response has been characterized in the context of rates of formation of reactive metabolites in the target tissue. Results presented here are from a "hybrid" physiologically based pharmacokinetic (PBPK) animal model that was revised to permit its extension to humans. The relevant measure of exposure response, namely, the mean rate of metabolism in humans associated with a 5% increase in tumor risk (TC05), was estimated on the basis of this PBPK model and compared with tissue dose measures resulting from 24-h multimedia exposure scenarios for Canadians based on midpoint and 95th percentiles for concentrations in outdoor air, indoor air, air in the shower compartment, air in the bathroom after showering, tap water, and food. Nonneoplastic effects observed most consistently at lowest concentrations or doses following repeated exposures of rats and mice to chloroform are cytotoxicity and regenerative proliferation. As for cancer, target organs are the liver and kidney. In addition, chloroform has induced nasal lesions in rats and mice exposed by both inhalation and ingestion at lowest concentrations or doses. The mean rate of metabolism associated with a 5% increase in fatty cysts estimated on the basis of the PBPK model was compared with tissue dose measures resulting from the scenarios already described, and lowest concentrations reported to induce cellular proliferation in the nasal cavities of rats and mice were compared directly with midpoint and 95th percentile estimates of concentrations of chloroform in indoor air in Canada. The degree of confidence in the underlying database and uncertainties in estimates of exposure and in characterization of hazard and dose response are delineated.
PubMed ID
12162870 View in PubMed
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9 records – page 1 of 1.