Skip header and navigation

Refine By

5 records – page 1 of 1.

Approach to risk assessment of PCDDs and PCDFs in Canada.

https://arctichealth.org/en/permalink/ahliterature219776
Source
Regul Toxicol Pharmacol. 1993 Dec;18(3):428-37
Publication Type
Article
Date
Dec-1993
Author
M M Feeley
D L Grant
Author Affiliation
Toxicological Evaluation Division, Bureau of Chemical Safety, Health and Welfare Canada, Ottawa, Ontario.
Source
Regul Toxicol Pharmacol. 1993 Dec;18(3):428-37
Date
Dec-1993
Language
English
Publication Type
Article
Keywords
Animals
Benzofurans - adverse effects - toxicity
Canada
Humans
Models, Statistical
Risk factors
Tetrachlorodibenzodioxin - adverse effects - analogs & derivatives - toxicity
Toxicology - methods
Abstract
The nongenotoxic classification for the ubiquitous environmental contaminants polychlorinated dibenzodioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) implies that a toxicity threshold may exist. Therefore, a minimal risk level or tolerable daily intake (TDI) value can be estimated by identifying no observable adverse effect levels (NOAELs) from animal toxicological investigations and extrapolating this dose to humans by the use of safety factors. When available, data from epidemiological investigations are utilized and carry a larger "weighting" than the animal studies (i.e., smaller safety factors required). A complete database review for the most toxic congener of this class of halogenated aromatic hydrocarbons, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), yields a NOAEL of 1.0 ng/kg body wt/day for rat carcinogenicity (Kociba et al., Toxicol. Appl. Pharmacol. 46, 279-303, 1978) and reproductive toxicity (Murray et al., Toxicol. Appl. Pharmacol. 50, 241-252, 1979) effects. By employing a 100-fold safety factor to compensate for inter- and intraspecies variability, a tentative TDI value can be estimated at 10 pg/kg body wt/day. For food intake purposes, a total of 17 2,3,7,8-substituted PCDD/PCDF congeners are included in this estimate by using an additive toxic equivalency (TEQ) approach based on international toxic equivalency factors (I-TEFs) developed by NATO (NATO Report No. 178, 1988). This implies that averaged over an individual's total lifespan (estimated at 70 years), 600 pg TCDD TEQs can be taken in daily (60 kg average body weight) without appreciable risk of deleterious effects. The current estimated Canadian daily intake for PCDDs and PCDFs from all sources is 2.0-4.2 pg TCDD TEQs/kg body wt/day (Gilman et al., Chemosphere 23, 1661-1667, 1990). Recent comprehensive epidemiological studies involving industrial/occupational scenarios suggest an increased cancer risk for workers exposed to TCDD-contaminated processes (products contaminated with TCDD) but only at relatively high exposure levels with long latency periods when compared to the background population. To date, the only sustained toxic effect in humans associated with PCDD/PCDF exposure has been chloracne and related dermatological lesions.
PubMed ID
8128004 View in PubMed
Less detail

Biomarkers for Great Lakes priority contaminants: halogenated aromatic hydrocarbons.

https://arctichealth.org/en/permalink/ahliterature213763
Source
Environ Health Perspect. 1995 Dec;103 Suppl 9:7-16
Publication Type
Article
Date
Dec-1995
Author
M M Feeley
Author Affiliation
Bureau of Chemical Safety, Health Canada, Ottawa, Ontario. mfeeley@hpb.hwc.ca
Source
Environ Health Perspect. 1995 Dec;103 Suppl 9:7-16
Date
Dec-1995
Language
English
Publication Type
Article
Keywords
Adipose Tissue - chemistry
Adult
Benzofurans - adverse effects - analysis - blood
Biological Markers - analysis
Canada
Child
Environmental Exposure - adverse effects - analysis
Female
Food contamination - analysis
Great Lakes Region
Humans
Infant
Male
Milk, human - chemistry
Polychlorinated Biphenyls - adverse effects - analysis - blood
Tetrachlorodibenzodioxin - adverse effects - analogs & derivatives - analysis - blood
Water Pollutants, Chemical - adverse effects - analysis - blood
Abstract
One of the major goals of the Great Lakes Action Plan is to actively accumulate and assess toxicological information on persistent toxic substances found in the Great Lakes basin. As part of Health Canada's commitment to this plan, a review of biomarkers for the environmental contaminants polychlorinated biphenyls (PCBs) and polychlorinated dibenzodioxins/dibenzofurans (PCDDs/PCDFs) was conducted. In general, while food consumption was identified as the major source of human exposure to both contaminant groups, certain commodities, such as fish, milk and dairy products, and meat, were found to predominate. Due to the ubiquitous nature of these environmental contaminants and their propensity to bioaccumulate, all humans will have detectable body burdens, which in certain cases can be positively associated with the consumption of particular foods (i.e., PCBs and freshwater fish from the Great Lakes). When dealing with environmental exposure only, relating specific effect biomarkers to contaminant exposure or tissue levels was difficult, due in part to the complex nature of the exposure and the nonspecific nature of the effect. For PCBs, the most likely biomarkers of effect included some form of alteration in lipid metabolism (serum triglyceride/cholesterol levels) and elevation of hepatic-related enzymes, aspartate aminotransferase (AST) and gamma-glutamyltransferase (GGT). Cross-species extrapolation also indicates the potential for neurotoxicologic effects to occur in humans. For PCDDs/PCDFs, dermatologic lesions (chloracne) and indications of hepatic enzyme induction have been documented, but primarily due to occupational or high acute accidental exposures. Recent evidence suggests that neonates may represent a potential at-risk population due to relatively high exposure to PCDDs/PCDFs, as with PCBs, during breast feeding as compared to standard adult dietary intake. Future areas of potential benefit for biomarker development include immunologic and endocrine effects, primarily based on biologic plausibility from experimental animal research.
Notes
Cites: JAMA. 1992 Apr 22-29;267(16):2209-141348289
Cites: J Chromatogr. 1992 Mar 20;595(1-2):1-431577902
Cites: Toxicol Lett. 1992 Jul;61(2-3):141-71322574
Cites: Bull Environ Contam Toxicol. 1992 Nov;49(5):701-71392309
Cites: J Toxicol Environ Health. 1992 Oct;37(2):211-291404482
Cites: JAMA. 1992 Dec 9;268(22):3213-81433761
Cites: Sci Total Environ. 1992 Sep 11;126(1-2):89-1071439753
Cites: Environ Health Perspect. 1992 Nov;98:125-321336723
Cites: Environ Health Perspect. 1992 Nov;98:143-71486843
Cites: Environ Health Perspect. 1992 Nov;98:179-821336724
Cites: Environ Res. 1993 Jan;60(1):124-358432263
Cites: Vet Hum Toxicol. 1993 Feb;35(1):68-778434461
Cites: Z Lebensm Unters Forsch. 1993 Feb;196(2):126-308456563
Cites: Arch Environ Health. 1993 Mar-Apr;48(2):98-1048476311
Cites: Arch Environ Contam Toxicol. 1993 May;24(4):504-128507107
Cites: Environ Health Perspect. 1993 Apr 22;101(1):36-448390353
Cites: Bull Environ Contam Toxicol. 1993 Jul;51(1):146-528318765
Cites: Environ Health Perspect. 1993 Apr;100:189-2008394802
Cites: Food Addit Contam. 1993 Jul-Aug;10(4):419-288405581
Cites: Life Sci. 1993;53(26):1995-20068255162
Cites: Am J Epidemiol. 1994 Feb 1;139(3):272-818116602
Cites: Regul Toxicol Pharmacol. 1995 Feb;21(1):136-507784626
Cites: Crit Rev Toxicol. 1995;25(2):133-637612174
Cites: Environ Health Perspect. 1985 Feb;59:99-1063921372
Cites: Environ Health Perspect. 1985 May;60:151-74029098
Cites: Environ Health Perspect. 1985 May;60:193-93928345
Cites: Scand J Work Environ Health. 1985 Jun;11(3 Spec No):165-712930898
Cites: Sci Total Environ. 1985 Nov;46:9-183936176
Cites: JAMA. 1986 Apr 18;255(15):2031-83959286
Cites: J Pediatr. 1986 Aug;109(2):335-413090217
Cites: JAMA. 1986 Nov 21;256(19):2687-952877102
Cites: Eur J Epidemiol. 1985 Jun;1(2):139-442946601
Cites: J Toxicol Environ Health. 1987;22(4):381-4033694702
Cites: Arch Environ Health. 1988 Jan-Feb;43(1):54-83128188
Cites: Environ Health Perspect. 1987 Dec;76:79-872834196
Cites: Clin Pharmacol Ther. 1977 Aug;22(2):140-6407043
Cites: Bull Environ Contam Toxicol. 1979 Jan;21(1-2):273-8109143
Cites: J Occup Med. 1982 Feb;24(2):109-146799628
Cites: Arch Environ Health. 1982 May-Jun;37(3):141-76284069
Cites: Environ Res. 1982 Jun;28(1):106-126179776
Cites: Br J Ind Med. 1982 Nov;39(4):361-96128023
Cites: Environ Res. 1983 Feb;30(1):169-746403348
Cites: Am J Ind Med. 1984;5(1-2):31-446422748
Cites: Am J Ind Med. 1984;5(3):161-826142642
Cites: JAMA. 1984 May 11;251(18):2372-806231388
Cites: Environ Health Perspect. 1985 Feb;59:85-903921370
Cites: Can J Public Health. 1988 May-Jun;79(3):150-83135931
Cites: Am J Ind Med. 1988;14(1):47-623136647
Cites: Arch Environ Health. 1988 Jul-Aug;43(4):273-83415353
Cites: Br J Ind Med. 1988 Oct;45(10):689-933143397
Cites: Sci Total Environ. 1989 Jan;78:99-1162717930
Cites: Food Addit Contam. 1989 Jul-Sep;6(3):365-752498139
Cites: Bull Environ Contam Toxicol. 1989 Nov;43(5):641-62508801
Cites: J Toxicol Environ Health. 1989;28(3):285-952585536
Cites: Arch Environ Health. 1989 Nov-Dec;44(6):351-42514628
Cites: Cancer Res. 1990 Mar 1;50(5):1585-902302718
Cites: Food Addit Contam. 1990 Mar-Apr;7(2):143-742113010
Cites: Neurotoxicol Teratol. 1990 Jul-Aug;12(4):319-262118230
Cites: Environ Res. 1990 Dec;53(2):175-921701383
Cites: N Engl J Med. 1991 Jan 3;324(1):8-121898530
Cites: Bull Environ Contam Toxicol. 1990 Nov;45(5):681-82124937
Cites: Br J Addict. 1990 Dec;85(12):1661-32289067
Cites: Fundam Appl Toxicol. 1990 Nov;15(4):722-312128284
Cites: J Toxicol Environ Health. 1991 Apr;32(4):357-661826746
Cites: Environ Health Perspect. 1991 Feb;91:157-641674906
Cites: J Pediatr. 1991 Jul;119(1 Pt 1):58-631906100
Cites: Sci Total Environ. 1991 May 1;104(1-2):97-1271871593
Cites: Sci Total Environ. 1991 Jul 1;106(1-2):33-411948013
Cites: Hum Exp Toxicol. 1991 Sep;10(5):311-221683543
Cites: Int Arch Occup Environ Health. 1991;63(5):325-71837285
Cites: Teratog Carcinog Mutagen. 1991;11(2):77-821686676
PubMed ID
8635442 View in PubMed
Less detail

Concentrations of bisphenol A in the composite food samples from the 2008 Canadian total diet study in Quebec City and dietary intake estimates.

https://arctichealth.org/en/permalink/ahliterature134088
Source
Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2011 Jun;28(6):791-8
Publication Type
Article
Date
Jun-2011
Author
X-L Cao
C. Perez-Locas
G. Dufresne
G. Clement
S. Popovic
F. Beraldin
R W Dabeka
M. Feeley
Author Affiliation
Food Research Division, Bureau of Chemical Safety, Food Directorate, Health Canada, 251 Sir Frederick Banting Driveway, Ottawa, Ontario, Canada. Xu-Liang.Cao@hc-sc.gc.ca
Source
Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2011 Jun;28(6):791-8
Date
Jun-2011
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Animals
Benzhydryl Compounds
Canada
Child
Cooking
Databases, Factual
Diet
Diet Surveys
Endocrine Disruptors - administration & dosage - analysis - isolation & purification
Fast Foods - analysis - standards
Female
Food Contamination - statistics & numerical data
Food, Preserved - analysis - standards
Humans
Infant
Infant Food - analysis - standards
Legislation, Food
Male
Phenols - administration & dosage - analysis - isolation & purification
Quebec
Abstract
A total of 154 food composite samples from the 2008 total diet study in Quebec City were analysed for bisphenol A (BPA), and BPA was detected in less than half (36%, or 55 samples) of the samples tested. High concentrations of BPA were found mostly in the composite samples containing canned foods, with the highest BPA level being observed in canned fish (106 ng g(-1)), followed by canned corn (83.7 ng g(-1)), canned soups (22.2-44.4 ng g(-1)), canned baked beans (23.5 ng g(-1)), canned peas (16.8 ng g(-1)), canned evaporated milk (15.3 ng g(-1)), and canned luncheon meats (10.5 ng g(-1)). BPA levels in baby food composite samples were low, with 2.75 ng g(-1) in canned liquid infant formula, and 0.84-2.46 ng g(-1) in jarred baby foods. BPA was also detected in some foods that are not canned or in jars, such as yeast (8.52 ng g(-1)), baking powder (0.64 ng g(-1)), some cheeses (0.68-2.24 ng g(-1)), breads and some cereals (0.40-1.73 ng g(-1)), and fast foods (1.1-10.9 ng g(-1)). Dietary intakes of BPA were low for all age-sex groups, with 0.17-0.33 µg kg(-1) body weight day(-1) for infants, 0.082-0.23 µg kg(-1) body weight day(-1) for children aged from 1 to 19 years, and 0.052-0.081 µg kg(-1) body weight day(-1) for adults, well below the established regulatory limits. BPA intakes from 19 of the 55 samples account for more than 95% of the total dietary intakes, and most of the 19 samples were either canned or in jars. Intakes of BPA from non-canned foods are low.
Notes
Cites: Food Addit Contam. 2001 Jan;18(1):69-7511212549
Cites: J Nutr. 2001 Feb;131(2):409S-20S11160571
Cites: Food Addit Contam. 2002 Aug;19(8):796-80212227943
Cites: Food Addit Contam. 2003 Jun;20(6):596-60612881134
Cites: J AOAC Int. 1993 Jan-Feb;76(1):14-258448438
Cites: Food Addit Contam. 2005 Jan;22(1):65-7215895613
Cites: J Toxicol Environ Health A. 2009;72(21-22):1327-3520077204
Cites: J Agric Food Chem. 2008 Mar 26;56(6):2041-718284199
Cites: J Agric Food Chem. 2008 Sep 10;56(17):7919-2418702469
Cites: Food Chem Toxicol. 2009 Feb;47(2):506-1019121362
Cites: J Agric Food Chem. 2009 Feb 25;57(4):1307-1119170636
Cites: J Agric Food Chem. 2009 Jun 24;57(12):5345-5119459630
Cites: Food Addit Contam. 2007 Jan;24(1):103-1217164221
PubMed ID
21623504 View in PubMed
Less detail

Environmental contaminants and human health in the Canadian Arctic.

https://arctichealth.org/en/permalink/ahliterature99174
Source
Sci Total Environ. 2010 Aug 20;
Publication Type
Article
Date
Aug-20-2010
Author
S G Donaldson
J. Van Oostdam
C. Tikhonov
M. Feeley
B. Armstrong
P. Ayotte
O. Boucher
W. Bowers
L. Chan
F. Dallaire
R. Dallaire
E. Dewailly
J. Edwards
G M Egeland
J. Fontaine
C. Furgal
T. Leech
E. Loring
G. Muckle
T. Nancarrow
D. Pereg
P. Plusquellec
M. Potyrala
O. Receveur
R G Shearer
Author Affiliation
Chemicals Surveillance Bureau, HECSB, Health Canada, 269 Laurier Ave West, Ottawa, ON, Canada K1A 0K9; Carleton University, 1125 Colonel By Drive, Ottawa, ON, Canada K1S 5B6.
Source
Sci Total Environ. 2010 Aug 20;
Date
Aug-20-2010
Language
English
Publication Type
Article
Abstract
The third Canadian Arctic Human Health Assessment conducted under the Canadian Northern Contaminants Program (NCP), in association with the circumpolar Arctic Monitoring and Assessment Programme (AMAP), addresses concerns about possible adverse health effects in individuals exposed to environmental contaminants through a diet containing country foods. The objectives here are to: 1) provide data on changes in human contaminant concentrations and exposure among Canadian Arctic peoples; 2) identify new contaminants of concern; 3) discuss possible health effects; 4) outline risk communication about contaminants in country food; and 5) identify knowledge gaps for future contaminant research and monitoring. The nutritional and cultural benefits of country foods are substantial; however, some dietary studies suggest declines in the amount of country foods being consumed. Significant declines were found for most contaminants in maternal blood over the last 10years within all three Arctic regions studied. Inuit continue to have the highest levels of almost all persistent organic pollutants (POPs) and metals among the ethnic groups studied. A greater proportion of people in the East exceed Health Canada's guidelines for PCBs and mercury, although the proportion of mothers exceeding these guidelines has decreased since the previous assessment. Further monitoring and research are required to assess trends and health effects of emerging contaminants. Infant development studies have shown possible subtle effects of prenatal exposure to heavy metals and some POPs on immune system function and neurodevelopment. New data suggest important beneficial effects on brain development for Inuit infants from some country food nutrients. The most successful risk communication processes balance the risks and benefits of a diet of country food through input from a variety of regional experts and the community, to incorporate the many socio-cultural and economic factors to arrive at a risk management decision that will be the most beneficial in Arctic communities.
PubMed ID
20728918 View in PubMed
Less detail

Human health implications of environmental contaminants in Arctic Canada: A review.

https://arctichealth.org/en/permalink/ahliterature3072
Source
Sci Total Environ. 2005 Dec 1;351-352:165-246
Publication Type
Article
Date
Dec-1-2005
Author
J. Van Oostdam
S G Donaldson
M. Feeley
D. Arnold
P. Ayotte
G. Bondy
L. Chan
E. Dewaily
C M Furgal
H. Kuhnlein
E. Loring
G. Muckle
E. Myles
O. Receveur
B. Tracy
U. Gill
S. Kalhok
Author Affiliation
Environmental Contaminants Bureau, Safe Environments Program, Health Canada, Rm 4-046, BMO Building, 269 Laurier Avenue W., AL4904B, Ottawa, ON, Canada K1A 0K9. jay_van_oostdam@hc-sc.gc.ca
Source
Sci Total Environ. 2005 Dec 1;351-352:165-246
Date
Dec-1-2005
Language
English
Publication Type
Article
Abstract
The objectives of this paper are to: assess the impact of exposure to current levels of environmental contaminants in the Canadian Arctic on human health; identify the data and knowledge gaps that need to be filled by future human health research and monitoring; examine how these issues have changed since our first assessment [Van Oostdam, J., Gilman, A., Dewailly, E., Usher, P., Wheatley, B., Kuhnlein, H. et al., 1999. Human health implications of environmental contaminants in Arctic Canada: a review. Sci Total Environ 230, 1-82]. The primary exposure pathway for contaminants for various organochlorines (OCs) and toxic metals is through the traditional northern diet. Exposures tend to be higher in the eastern than the western Canadian Arctic. In recent dietary surveys among five Inuit regions, mean intakes by 20- to 40-year-old adults in Baffin, Kivalliq and Inuvialuit communities exceeded the provisional tolerable daily intakes (pTDIs) for the OCs, chlordane and toxaphene. The most recent findings in NWT and Nunavut indicate that almost half of the blood samples from Inuit mothers exceeded the level of concern value of 5 microg/L for PCBs, but none exceeded the action level of 100 microg/L. For Dene/M?tis and Caucasians of the Northwest Territories exposure to OCs are mostly below this level of concern. Based on the exceedances of the pTDI and of various blood guidelines, mercury and to a lesser extent lead (from the use of lead shot in hunting game) are also concerns among Arctic peoples. The developing foetus is likely to be more sensitive to the effects of OCs and metals than adults, and is the age groups of greatest risk in the Arctic. Studies of infant development in Nunavik have linked deficits in immune function, an increase in childhood respiratory infections and birth weight to prenatal exposure to OCs. Balancing the risks and benefits of a diet of country foods is very difficult. The nutritional benefits of country food and its contribution to the total diet are substantial. Country food contributes significantly more protein, iron and zinc to the diets of consumers than southern/market foods. The increase in obesity, diabetes and cardiovascular disease has been linked to a shift away from a country food diet and a less active lifestyle. These foods are an integral component of good health among Aboriginal peoples. The social, cultural, spiritual, nutritional and economic benefits of these foods must be considered in concert with the risks of exposure to environmental contaminants through their exposure. Consequently, the contamination of country food raises problems which go far beyond the usual confines of public health and cannot be resolved simply by risk-based health advisories or food substitutions alone. All decisions should involve the community and consider many aspects of socio-cultural stability to arrive at a decision that will be the most protective and least detrimental to the communities.
PubMed ID
16297438 View in PubMed
Less detail