Skip header and navigation

Refine By

9 records – page 1 of 1.

Exposure of Inuit in Greenland to organochlorines through the marine diet.

https://arctichealth.org/en/permalink/ahliterature4827
Source
J Toxicol Environ Health A. 2001 Jan 26;62(2):69-81
Publication Type
Article
Date
Jan-26-2001
Author
P. Bjerregaard
E. Dewailly
P. Ayotte
T. Pars
L. Ferron
G. Mulvad
Author Affiliation
Section for Research in Greenland, National Institute of Public Health, Copenhagen, Denmark. p.bjerrgaard@dadlnet.dk
Source
J Toxicol Environ Health A. 2001 Jan 26;62(2):69-81
Date
Jan-26-2001
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Distribution
Aged
Aged, 80 and over
Canada
Case-Control Studies
Diet - adverse effects
Environmental Exposure - adverse effects - analysis
Environmental Monitoring - methods
Female
Food Habits - ethnology
Greenland
Health Surveys
Humans
Hydrocarbons, Chlorinated
Insecticides - adverse effects - analysis - blood
Inuits
Linear Models
Male
Middle Aged
Pesticide Residues - adverse effects - analysis - blood
Questionnaires
Research Support, Non-U.S. Gov't
Seafood - adverse effects - analysis
Sex Distribution
Abstract
High organochlorine concentrations have been found among the Inuit in eastern Canada and in Greenland. The present study was undertaken to assess the exposure to organochlorines in relation to age, sex, and diet in a general population sample of Inuit from Greenland. Survey data and plasma concentrations of 14 polychlorinated biphenyl (PCB) congeners and 16 pesticides, including 5 toxaphene congeners, were recorded in a random population survey of 408 adult indigenous Greenlanders. In a two-stage design, the survey response rate was 66%, and 90% of those randomly selected for blood testing participated. This was equivalent to an overall response rate of 59%. The median plasma concentration of the sum of PCB congeners was 13.3 microg/L; the lipid-adjusted value was 2109 microg/kg. The PCB concentration was twice as high as among the Inuit of Nunavik, Canada, 25 times higher than in a control group from southern Canada, and several times higher than the values found in European studies. Concentrations were similarly elevated for all PCB congeners and pesticides. The PCB congener pattern was similar to previous observations from the eastern Canadian Arctic and Greenland. Concentrations showed statistically significant positive associations with age, marine diet, and male sex in multiple linear regression analyses. The exceptionally high plasma concentrations of several organochlorines among the Inuit of Greenland are attributed to a lifelong high intake of seafood, in particular marine mammals. Concentrations of PCB adjusted for the consumption of marine food increased until approximately 40 yr of age, which is equivalent to the birth cohorts of the early 1950s. The age pattern indicates that bioaccumulation of PCB started in the 1950s, which is a likely date for the introduction of the compounds into the Arctic environment.
PubMed ID
11209822 View in PubMed
Less detail

Global methylmercury exposure from seafood consumption and risk of developmental neurotoxicity: a systematic review.

https://arctichealth.org/en/permalink/ahliterature265489
Source
Bull World Health Organ. 2014 Apr 1;92(4):254-269F
Publication Type
Article
Date
Apr-1-2014
Author
Mary C Sheehan
Thomas A Burke
Ana Navas-Acien
Patrick N Breysse
John McGready
Mary A Fox
Source
Bull World Health Organ. 2014 Apr 1;92(4):254-269F
Date
Apr-1-2014
Language
English
Publication Type
Article
Keywords
Adult
Biological Markers - blood
Environmental Exposure - adverse effects - analysis
Female
Global health
Hair - chemistry
Humans
Infant
Infant, Newborn
Male
Methylmercury Compounds - adverse effects - analysis
Neurotoxicity Syndromes - etiology
Pregnancy
Rivers
Seafood - adverse effects - analysis
Water Pollutants, Chemical - adverse effects - analysis
Young Adult
Abstract
To examine biomarkers of methylmercury (MeHg) intake in women and infants from seafood-consuming populations globally and characterize the comparative risk of fetal developmental neurotoxicity.
A search was conducted of the published literature reporting total mercury (Hg) in hair and blood in women and infants. These biomarkers are validated proxy measures of MeHg, a neurotoxin found primarily in seafood. Average and high-end biomarkers were extracted, stratified by seafood consumption context, and pooled by category. Medians for average and high-end pooled distributions were compared with the reference level established by a joint expert committee of the Food and Agriculture Organization (FAO) and the World Health Organization (WHO).
Selection criteria were met by 164 studies of women and infants from 43 countries. Pooled average biomarkers suggest an intake of MeHg several times over the FAO/WHO reference in fish-consuming riparians living near small-scale gold mining and well over the reference in consumers of marine mammals in Arctic regions. In coastal regions of south-eastern Asia, the western Pacific and the Mediterranean, average biomarkers approach the reference. Although the two former groups have a higher risk of neurotoxicity than the latter, coastal regions are home to the largest number at risk. High-end biomarkers across all categories indicate MeHg intake is in excess of the reference value.
There is a need for policies to reduce Hg exposure among women and infants and for surveillance in high-risk populations, the majority of which live in low-and middle-income countries.
Notes
Cites: Am J Public Health. 2005 Mar;95(3):393-715727965
Cites: Clin Toxicol (Phila). 2005;43(2):101-415822761
Cites: Sci Total Environ. 2005 Apr 1;341(1-3):45-5215833240
Cites: Environ Health Perspect. 2005 May;113(5):590-615866768
Cites: Occup Environ Med. 2005 Jun;62(6):368-7515901883
Cites: Environ Health Perspect. 2005 Oct;113(10):1376-8016203250
Cites: Environ Sci Pollut Res Int. 2001;8(4):280-411601365
Cites: Environ Health. 2005;4:2016202128
Cites: Sci Total Environ. 2005 Dec 1;351-352:165-24616297438
Cites: Environ Res. 2006 Mar;100(3):295-31816081062
Cites: Environ Geochem Health. 2006 Feb-Apr;28(1-2):67-7116528592
Cites: Environ Geochem Health. 2006 Feb-Apr;28(1-2):61-616528593
Cites: Arch Environ Health. 1992 May-Jun;47(3):185-951596101
Cites: Bull Environ Contam Toxicol. 1992 Apr;48(4):494-5011504492
Cites: Sci Total Environ. 1994 Jul 4;151(1):29-358079150
Cites: Chemosphere. 1995 Jan;30(1):127-337874463
Cites: J Trace Elem Electrolytes Health Dis. 1994 Jun;8(2):79-867881281
Cites: Neurotoxicology. 1995 Winter;16(4):653-648714870
Cites: Neurotoxicology. 1995 Winter;16(4):717-268714876
Cites: Neurotoxicol Teratol. 1997 Nov-Dec;19(6):417-289392777
Cites: Arch Environ Contam Toxicol. 1998 Jan;34(1):100-59419279
Cites: Environ Res. 1998 May;77(2):68-729600797
Cites: Environ Res. 1998 May;77(2):104-149600803
Cites: Arch Environ Health. 1998 Jul-Aug;53(4):299-3039709995
Cites: Environ Res. 1998 Oct;79(1):20-329756677
Cites: Risk Anal. 1998 Dec;18(6):701-139972579
Cites: Arch Environ Health. 1999 Jan-Feb;54(1):40-710025415
Cites: Int J Circumpolar Health. 1998;57 Suppl 1:582-510093346
Cites: Int J Circumpolar Health. 1999 Jan;58(1):4-1310208065
Cites: Environ Health Perspect. 1999 Jul;107(7):587-9110379006
Cites: Environ Res. 2005 Feb;97(2):220-715533338
Cites: Arch Environ Health. 2001 Jan-Feb;56(1):4-1011256856
Cites: Bull Environ Contam Toxicol. 2001 Apr;66(4):439-4211443304
Cites: Arch Environ Health. 2001 Jul-Aug;56(4):350-711572279
Cites: Am J Obstet Gynecol. 2006 Jun;194(6):1683-816635458
Cites: Int J Hyg Environ Health. 2006 Jul;209(4):337-4416735138
Cites: Sci Total Environ. 2006 Aug 31;367(2-3):586-9516549105
Cites: Biol Trace Elem Res. 2006 Jul;112(1):13-2916943613
Cites: Crit Rev Toxicol. 2006 Sep;36(8):609-6216973445
Cites: Yonsei Med J. 2006 Oct 31;47(5):626-3317066506
Cites: Sci Total Environ. 2006 Dec 15;372(1):76-8616963109
Cites: Environ Res. 2007 Jan;103(1):106-1116650842
Cites: Environ Int. 2007 Jan;33(1):84-9216962662
Cites: BJOG. 2007 Jan;114(1):81-517081179
Cites: Int J Hyg Environ Health. 2007 Jan;210(1):51-6017011234
Cites: Environ Res. 2007 Feb;103(2):205-1016831413
Cites: Environ Res. 2007 Feb;103(2):191-716890218
Cites: Sci Total Environ. 2007 Mar 1;374(1):60-7017258795
Cites: Int J Hyg Environ Health. 2009 Nov;212(6):588-9819481974
Cites: Environ Res. 2010 Jan;110(1):33-919811781
Cites: Environ Res. 2010 Jan;110(1):123-919878931
Cites: Arch Environ Contam Toxicol. 2009 Apr;56(3):615-2218836676
Cites: Public Health Nutr. 2010 Jan;13(1):54-6219490733
Cites: Environ Health Perspect. 2009 Nov;117(11):1760-620049129
Cites: Environ Health Perspect. 2010 Jan;118(1):137-4320056570
Cites: Sci Total Environ. 2010 Jan 15;408(4):806-1119914681
Cites: Sci Total Environ. 2010 Jan 15;408(4):713-2519945736
Cites: J Environ Health. 2010 Jan-Feb;72(6):37-4120104833
Cites: Food Chem Toxicol. 2013 Jul;57:161-923537601
Cites: Hum Exp Toxicol. 2013 Jun;32(6):591-923155199
Cites: Biol Trace Elem Res. 2013 Jun;153(1-3):145-5423661328
Cites: Int J Environ Res Public Health. 2013 Jun;10(6):2150-6323759951
Cites: Sci Total Environ. 2013 Oct 1;463-464:11-923787104
Cites: Sci Total Environ. 2013 Oct 1;463-464:319-2523827356
Cites: Int J Hyg Environ Health. 2013 Nov;216(6):682-923340120
Cites: Int Arch Occup Environ Health. 2014 Jul;87(5):501-1323824410
Cites: Environ Int. 2001 Oct;27(4):285-9011686639
Cites: Environ Health Perspect. 2001 Dec;109(12):1291-911748038
Cites: J Toxicol Environ Health A. 2002 Jan 25;65(2):165-8211820504
Cites: Environ Res. 2002 May;89(1):1-1112051779
Cites: Environ Health. 2003 Jun 4;2(1):812844364
Cites: Lipids. 2004 Jul;39(7):617-2615588018
Cites: Environ Res. 2005 May;98(1):14-2115721879
Cites: Environ Toxicol Pharmacol. 2013 Jul;36(1):103-723603462
Cites: Int J Hyg Environ Health. 2013 Jul;216(4):486-9323523155
Cites: Environ Res. 2007 Nov;105(3):390-917655840
Cites: Environ Health Perspect. 2007 Oct;115(10):1435-4117938732
Cites: Cad Saude Publica. 2007;23 Suppl 4:S622-918038043
Cites: J Expo Sci Environ Epidemiol. 2008 Jan;18(1):76-8717805232
Cites: Environ Res. 2008 Feb;106(2):270-618054904
Cites: Environ Int. 2008 Feb;34(2):162-717904222
Cites: Environ Health Perspect. 2008 Feb;116(2):263-718288328
Cites: J Expo Sci Environ Epidemiol. 2008 May;18(3):326-3117851449
Cites: Environ Health Perspect. 2008 May;116(5):674-918470301
Cites: Environ Int. 2008 May;34(4):476-8218155151
Cites: Environ Res. 2008 Jul;107(3):380-9218313043
Cites: Sci Total Environ. 2008 Aug 25;402(1):36-4218502474
Cites: Environ Health. 2008;7:2518518986
Cites: Environ Health Perspect. 2008 Aug;116(8):1085-9118709170
Cites: Ann Ig. 2008 May-Jun;20(3 Suppl 1):59-6418773607
Cites: Int J Hyg Environ Health. 2008 Oct;211(5-6):560-7918160343
Cites: Cad Saude Publica. 2008;24 Suppl 4:s503-2018797727
Cites: Asia Pac J Clin Nutr. 2008;17(3):461-7018818168
Cites: Environ Res. 2008 Nov;108(3):334-918675410
Cites: Environ Res. 2008 Nov;108(3):320-618814872
Cites: J Environ Health. 2008 Nov;71(4):44-5019004394
Cites: J Environ Sci (China). 2008;20(10):1258-6219143352
Cites: Environ Health Perspect. 2009 Jan;117(1):47-5319165386
Cites: Environ Sci Technol. 2009 Apr 15;43(8):2983-819475981
Cites: Regul Toxicol Pharmacol. 2009 Nov;55(2):219-2819589366
Cites: Sci Total Environ. 2011 Apr 15;409(10):1967-7521342703
Cites: Environ Res. 2011 Apr;111(3):442-5021257163
Cites: Environ Res. 2011 Apr;111(3):411-721277575
Cites: Int J Hyg Environ Health. 2011 Mar;214(2):79-10121093366
Cites: Sci Total Environ. 2011 May 1;409(11):2272-8020092877
Cites: Environ Health Perspect. 2011 May;119(5):607-1421220222
Cites: Xenobiotica. 2011 Jun;41(6):456-6321381896
Cites: Chemosphere. 2011 Jul;84(5):571-721524785
Cites: Environ Health Perspect. 2011 Aug;119(8):1156-6121543284
Cites: Environ Res. 2010 Apr;110(3):226-3620116785
Cites: J Environ Monit. 2009 Jul;11(7):1322-3020449220
Cites: J Intellect Disabil Res. 2010 May;54(5):448-5620537050
Cites: Int J Hyg Environ Health. 2010 Jul;213(4):243-5120417154
Cites: Environ Sci Pollut Res Int. 2010 Sep;17(8):1422-3220411344
Cites: Sci Total Environ. 2010 Sep 15;408(20):4841-720619878
Cites: Sci Total Environ. 2010 Sep 15;408(20):4848-5420655095
Cites: J Health Econ. 2010 Sep;29(5):674-8520609487
Cites: Br J Nutr. 2010 Oct;104(8):1096-10020487582
Cites: J Prev Med Public Health. 2010 Sep;43(5):377-8620959708
Cites: Regul Toxicol Pharmacol. 2010 Dec;58(3):482-920804806
Cites: Environ Health Perspect. 2011 Feb;119(2):245-5120980220
Cites: Environ Int. 2011 Apr;37(3):597-60421239061
Cites: Environ Res. 2004 Nov;96(3):257-6315364592
Cites: Sci Total Environ. 1991 Mar;100 Spec No:235-822063184
Cites: J Environ Monit. 2011 Aug;13(8):2143-5221738945
Cites: Nutr Rev. 2011 Sep;69(9):493-50821884130
Cites: Biol Trace Elem Res. 2011 Nov;143(2):815-2421225477
Cites: Environ Res. 2011 Nov;111(8):1180-421807364
Cites: Environ Res. 2011 Nov;111(8):1201-721835399
Cites: Sci Total Environ. 2011 Dec 1;410-411:26-3322000783
Cites: Biol Trace Elem Res. 2011 Dec;144(1-3):118-3221476008
Cites: Bull Environ Contam Toxicol. 2012 Feb;88(2):135-922147084
Cites: Arch Environ Contam Toxicol. 2012 Feb;62(2):323-3221713402
Cites: Int J Hyg Environ Health. 2012 Feb;215(2):109-1922014893
Cites: Am J Epidemiol. 2012 Apr 1;175(7):645-5222302120
Cites: J Biomed Biotechnol. 2012;2012:13287622619491
Cites: Environ Health Perspect. 2012 Jun;120(6):799-80622275730
Cites: Biol Trace Elem Res. 2012 Sep;148(3):292-30122419376
Cites: Environ Health. 2012;11:4422747793
Cites: Neurotoxicology. 2012 Aug;33(4):676-8222525937
Cites: Environ Res. 2012 Oct;118:124-922749111
Cites: Neurotoxicol Teratol. 2000 Jan-Feb;22(1):21-910642111
Cites: Sci Total Environ. 2000 Jan 17;245(1-3):195-20210682367
Cites: Neurotoxicology. 2010 Jan;31(1):10-619833149
Cites: Environ Health. 2010;9:120064246
Cites: Sci Total Environ. 2010 Mar 1;408(7):1538-4320100624
Cites: Int J Environ Health Res. 2009 Aug;19(4):267-7720183195
Cites: Environ Health Perspect. 2010 Mar;118(3):437-4320194072
Cites: Biol Trace Elem Res. 2012 Nov;149(2):155-6222592844
Cites: Public Health Nutr. 2011 Dec;14(12):2236-4421896241
Cites: PLoS One. 2012;7(10):e4738823077607
Cites: Sci Total Environ. 2012 Nov 15;439:220-923069934
Cites: Environ Res. 2013 Jan;120:7-1722999706
Cites: Environ Health. 2013;12:223289850
Cites: J Environ Health. 2013 Jan-Feb;75(6):8-1523397644
Cites: J Environ Health. 2013 Jan-Feb;75(6):38-4323397648
Cites: Environ Health. 2013;12:323289875
Cites: Int J Occup Med Environ Health. 2013 Mar;26(1):58-7223526195
Cites: Int Arch Occup Environ Health. 2000 Apr;73(3):195-20310787135
Cites: JAMA. 2000 Apr 19;283(15):2008-1210789670
Cites: Sci Total Environ. 2000 Oct 2;259(1-3):55-6011032135
Cites: Environ Res. 2000 Oct;84(2):108-2611068924
Cites: Environ Res. 2000 Oct;84(2):186-9411068932
Cites: Environ Res. 2000 Nov;84(3):204-1011097793
Cites: An Acad Bras Cienc. 2000 Dec;72(4):497-50711151017
Cites: Environ Health Perspect. 2007 Jan;115(1):42-717366817
Cites: Ambio. 2007 Feb;36(1):3-1117408186
Cites: Public Health Nutr. 2007 May;10(5):508-1717411472
Cites: Environ Health Perspect. 2007 Apr;115(4):609-1517450232
Cites: Environ Health Perspect. 2007 Jun;115(6):841-717589589
Cites: Int J Occup Med Environ Health. 2007;20(1):31-717708016
Cites: Environ Sci. 2007;14(4):167-7517762840
Cites: Invest Clin. 2007 Sep;48(3):305-1517853790
Cites: Rev Environ Health. 2007 Apr-Jun;22(2):91-11317894202
Cites: Food Addit Contam. 2007 Nov;24(11):1236-4617852400
Cites: J Environ Monit. 2011 Mar;13(3):563-7121184002
Cites: BJOG. 2002 Oct;109(10):1121-512387464
Cites: Environ Res. 2002 Oct;90(2):69-7512483796
Cites: Environ Res. 2002 Oct;90(2):98-10312483799
Cites: Environ Health Perspect. 2003 Apr;111(4):637-4112676628
Cites: Cad Saude Publica. 2003 Jan-Feb;19(1):199-20612700799
Cites: Tohoku J Exp Med. 2003 Mar;199(3):161-912703660
Cites: Environ Health Perspect. 2003 Sep;111(12):1465-7012948885
Cites: Tohoku J Exp Med. 2003 Jun;200(2):67-7312962403
Cites: Ambio. 2003 Nov;32(7):440-614703901
Cites: Environ Health Perspect. 2004 Apr;112(5):562-7015064162
Cites: Environ Res. 2004 Jul;95(3):305-1415220065
Cites: Environ Res. 2004 Jul;95(3):363-7415220070
Cites: Environ Res. 2004 Jul;95(3):414-2815220075
Cites: J Epidemiol Community Health. 2004 Sep;58(9):756-715310801
Comment In: Bull World Health Organ. 2015 Feb 1;93(2):13225883408
PubMed ID
24700993 View in PubMed
Less detail

Human biomonitoring to optimize fish consumption advice

https://arctichealth.org/en/permalink/ahliterature4439
Source
American Journal of Public Health. 2005 Aug;95(8):1304; author reply 1304-1305
Publication Type
Article
Date
Aug-2005
  1 website  
Author
Knobeloch, L
Anderson, HA
Author Affiliation
Wisconsin Department of Health and Family Services, Madison
Source
American Journal of Public Health. 2005 Aug;95(8):1304; author reply 1304-1305
Date
Aug-2005
Language
English
Publication Type
Article
Keywords
Alaska - epidemiology
Animals
Environmental monitoring
Female
Fishes
Humans
Mercury Poisoning - etiology
Nutrition Policy
Pregnancy
Pregnancy Complications - chemically induced
Public Health
Risk assessment
Seafood - adverse effects - analysis - poisoning
United States
United States Environmental Protection Agency
United States Food and Drug Administration
Abstract
The public is confused and concerned about the quality of the fish it eats. People worry about chemicals that can accumulate in their bodies. Telling worried people not to worry is seldom an effective risk communication strategy. Unless clear fish consumption guidelines are issued by credible federal and local agencies, the public is likely to respond by avoiding all fish.
Notes
Comment On: American Journal of Public Health. 2005 Mar;95(3):393-397
PubMed ID
16006410 View in PubMed
Online Resources
Less detail

Human biomonitoring to optimize fish consumption advice: Reducing uncertainty when evaluating benefits and risks

https://arctichealth.org/en/permalink/ahliterature3086
Source
American Journal of Public Health. 2005 Mar;95(3):393-397
Publication Type
Article
Date
Mar-2005
  1 website  
Author
Arnold, SM
Lynn, TV
Verbrugge, LA
Middaugh, JP
Author Affiliation
Alaska Division of Public Health, Section of Epidemiology, 3601 C St, Ste 540, PO Box 240249 Anchorage, AK 99524-0249, USA. scott_arnold@health.state.ak.us
Source
American Journal of Public Health. 2005 Mar;95(3):393-397
Date
Mar-2005
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Alaska - epidemiology
Animals
Chemistry, Analytical - trends
Counseling - standards
Environmental Monitoring - methods - standards
Environmental Pollutants - adverse effects - poisoning
Female
Fishes
Hair - chemistry
Humans
Mass Screening
Mercury Poisoning - diagnosis - epidemiology - prevention & control
Methylmercury Compounds - adverse effects - analysis - poisoning
Middle Aged
No-Observed-Adverse-Effect Level
Nutrition - education
Nutrition Policy - trends
Pregnancy
Pregnancy Complications - diagnosis - epidemiology - prevention & control
Public Health - standards - trends
Risk assessment
Risk factors
Seafood - adverse effects - analysis - poisoning
Uncertainty
United States
United States Environmental Protection Agency
United States Food and Drug Administration
Abstract
National fish consumption advisories that are based solely on assessment of risk of exposure to contaminants without consideration of consumption benefits result in overly restrictive advice that discourages eating fish even in areas where such advice is unwarranted. In fact, generic fish advisories may have adverse public health consequences because of decreased fish consumption and substitution of foods that are less healthy. Public health is on the threshold of a new era for determining actual exposures to environmental contaminants, owing to technological advances in analytical chemistry. It is now possible to target fish consumption advice to specific at-risk populations by evaluating individual contaminant exposures and health risk factors. Because of the current epidemic of nutritionally linked disease, such as obesity, diabetes, and cardiovascular disease, general recommendations for limiting fish consumption are ill conceived and potentially dangerous.
Notes
Comment In: American Journal of Public Health. 2005 Aug;95(8):1304; author reply 1304-1305
PubMed ID
15727965 View in PubMed
Online Resources
Less detail

Human isolates of Listeria monocytogenes in Sweden during half a century (1958-2010).

https://arctichealth.org/en/permalink/ahliterature259026
Source
Epidemiol Infect. 2014 Nov;142(11):2251-60
Publication Type
Article
Date
Nov-2014
Author
G. Lopez-Valladares
W. Tham
V Singh Parihar
S. Helmersson
B. Andersson
S. Ivarsson
C. Johansson
H. Ringberg
I. Tjernberg
B. Henriques-Normark
M-L Danielsson-Tham
Source
Epidemiol Infect. 2014 Nov;142(11):2251-60
Date
Nov-2014
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Distribution
Aged
Aged, 80 and over
Animals
Child
Child, Preschool
Databases, Factual
Electrophoresis, Gel, Pulsed-Field - methods
Female
Food Contamination - prevention & control - statistics & numerical data
Humans
Infant
Listeria monocytogenes - classification - pathogenicity
Listeriosis - diagnosis - epidemiology
Male
Middle Aged
Pregnancy
Prevalence
Retrospective Studies
Risk assessment
Salmon
Seafood - adverse effects - analysis
Serotyping - methods
Sex Distribution
Sweden - epidemiology
Time Factors
Young Adult
Abstract
Isolates of Listeria monocytogenes (n = 932) isolated in Sweden during 1958-2010 from human patients with invasive listeriosis were characterized by serotyping and pulsed-field gel electrophoresis (PFGE) (AscI). Of the 932 isolates, 183 different PFGE types were identified, of which 83 were each represented by only one isolate. In all, 483 serovar 1/2a isolates were distributed over 114 PFGE types; 90 serovar 1/2b isolates gave 32 PFGE types; 21 serovar 1/2c isolates gave nine PFGE types; three serovar 3b isolates gave one PFGE type; and, 335 serovar 4b isolates gave 31 PFGE types. During the 1980s in Sweden, several serovar 4b cases were associated with the consumption of European raw soft cheese. However, as cheese-production hygiene has improved, the number of 4b cases has decreased. Since 1996, serovar 1/2a has been the dominant L. monocytogenes serovar in human listeriosis in Sweden. Therefore, based on current serovars and PFGE types, an association between human cases of listeriosis and the consumption of vacuum-packed gravad and cold-smoked salmon is suggested.
PubMed ID
24480252 View in PubMed
Less detail

Modelling the intake of polychlorinated dibenzo-p-dioxins and dibenzofurans: impact of energy under-reporting and number of reporting days in dietary surveys.

https://arctichealth.org/en/permalink/ahliterature143880
Source
Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2010 Aug;27(8):1170-6
Publication Type
Article
Date
Aug-2010
Author
Tero Hirvonen
Harri Sinkko
Anja Hallikainen
Hannu Kiviranta
Pirjo Pietinen
Liisa Valsta
Jouni T Tuomisto
Author Affiliation
Finnish Food Safety Authority, Risk Assessment Unit, FI-00790 Helsinki, Finland. terohirvonen69@gmail.com
Source
Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2010 Aug;27(8):1170-6
Date
Aug-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Animals
Benzofurans - administration & dosage
Diet - adverse effects
Diet Records
Diet Surveys
Dioxins - administration & dosage
Energy intake
Environmental Pollutants - administration & dosage
Female
Finland
Fishes
Food Contamination
Humans
Male
Middle Aged
Models, Statistical
Risk Assessment - methods
Seafood - adverse effects - analysis
Statistics as Topic
Abstract
A probabilistic long-term intake estimation of dioxins was carried out using food consumption data obtained from the National FINDIET 2007 Survey (Paturi et al. 2008). The study population consisted of 606 participants who were first interviewed with a 48-h recall and then filled in a 3-day food record twice. The concentrations of dioxins were obtained from previously published studies. The intake was estimated using a semi-parametric Monte Carlo simulation. The analyses were done separately for the whole study population and for the population excluding energy under-reporters. To diminish the impact of intra-individual variation and nuisance effects, adjustment with software (C-SIDE) was also done after Monte Carlo simulation. It was found that when C-SIDE was used, the 95th percentile of intake and its confidence limit was higher with 2 reporting days than with a higher number of days. However, with a crude intake estimation (no adjustment), the confidence intervals of the 95th percentile were also smaller with a higher number of days, but the 95th percentiles were higher with a higher number of reporting days. When under-reporters were excluded the intakes increased, but the impact of energy under-reporting was smaller with 8 reporting days than with 2 days and smaller using C-SIDE than with a crude estimation. To conclude, adjustment for intra-individual variation and taking energy under-reporting into account are essential for intake estimation of dioxins with food consumption data of a limited number of reporting days.
PubMed ID
20432100 View in PubMed
Less detail

Prenatal mercury exposure and infant birth weight in the Norwegian Mother and Child Cohort Study.

https://arctichealth.org/en/permalink/ahliterature263497
Source
Public Health Nutr. 2014 Sep;17(9):2071-80
Publication Type
Article
Date
Sep-2014
Author
Kristine Vejrup
Anne Lise Brantsæter
Helle K Knutsen
Per Magnus
Jan Alexander
Helen E Kvalem
Helle M Meltzer
Margaretha Haugen
Source
Public Health Nutr. 2014 Sep;17(9):2071-80
Date
Sep-2014
Language
English
Publication Type
Article
Keywords
Birth Weight - drug effects
Cohort Studies
Databases, Factual
Female
Fetal Growth Retardation - chemically induced - epidemiology - ethnology
Food Contamination
Food Habits - ethnology
Humans
Infant, Newborn
Infant, Small for Gestational Age
Male
Maternal Nutritional Physiological Phenomena - ethnology
Mercury - analysis - toxicity
Norway - epidemiology
Pregnancy
Prenatal Exposure Delayed Effects - ethnology
Prospective Studies
Risk
Seafood - adverse effects - analysis
Water Pollutants, Chemical - analysis - toxicity
Abstract
To examine the association between calculated maternal dietary exposure to Hg in pregnancy and infant birth weight in the Norwegian Mother and Child Cohort Study (MoBa).
Exposure was calculated with use of a constructed database of Hg in food items and reported dietary intake during pregnancy. Multivariable regression models were used to explore the association between maternal Hg exposure and infant birth weight, and to model associations with small-for-gestational-age offspring.
The study is based on data from MoBa.
The study sample consisted of 62 941 women who answered a validated FFQ which covered the habitual diet during the first five months of pregnancy.
Median exposure to Hg was 0·15 µg/kg body weight per week and the contribution from seafood intake was 88 % of total Hg exposure. Women in the highest quintile compared with the lowest quintile of Hg exposure delivered offspring with 34 g lower birth weight (95 % CI -46 g, -22 g) and had an increased risk of giving birth to small-for-gestational-age offspring, adjusted OR = 1·19 (95 % CI 1·08, 1·30). Although seafood intake was positively associated with increased birth weight, stratified analyses showed negative associations between Hg exposure and birth weight within strata of seafood intake.
Although seafood intake in pregnancy is positively associated with birth weight, Hg exposure is negatively associated with birth weight. Seafood consumption during pregnancy should not be avoided, but clarification is needed to identify at what level of Hg exposure this risk might exceed the benefits of seafood.
PubMed ID
24103413 View in PubMed
Less detail

Smoking as a determinant of high organochlorine levels in Greenland.

https://arctichealth.org/en/permalink/ahliterature3452
Source
Arch Environ Health. 2003 Jan;58(1):30-6
Publication Type
Article
Date
Jan-2003
Author
Bente Deutch
Henning Sloth Pedersen
Eva C Bonefeld Jørgensen
Jens C Hansen
Author Affiliation
Centre of Arctic Environmental Medicine, Aarhus University, Aarhus, Denmark. bd@mil.au.dk
Source
Arch Environ Health. 2003 Jan;58(1):30-6
Date
Jan-2003
Language
English
Publication Type
Article
Keywords
Adult
Body mass index
Diet - adverse effects
Environmental Exposure - adverse effects - analysis
Greenland - epidemiology
Health Surveys
Humans
Hydrocarbons, Chlorinated
Insecticides - adverse effects - blood
Inuits
Life Style
Linear Models
Male
Pesticide Residues - adverse effects - blood
Research Support, Non-U.S. Gov't
Seafood - adverse effects - analysis
Smoking - epidemiology
Abstract
The authors investigated the accumulation of organochlorines among smoking and nonsmoking Inuit hunters (n = 48) in Uummanaq, Greenland, a population with high dietary exposure to persistent organic pollutants (POPs). Human plasma organochlorine levels were positively correlated with age, marine diet, and smoking or plasma cotinine in multiple linear-regression models (p
PubMed ID
12747516 View in PubMed
Less detail

Substitution of meat and fish with vegetables or potatoes and risk of myocardial infarction.

https://arctichealth.org/en/permalink/ahliterature282791
Source
Br J Nutr. 2016 Nov;116(9):1602-1610
Publication Type
Article
Date
Nov-2016
Author
Anne M L Würtz
Mette D Hansen
Anne Tjønneland
Eric B Rimm
Erik B Schmidt
Kim Overvad
Marianne U Jakobsen
Source
Br J Nutr. 2016 Nov;116(9):1602-1610
Date
Nov-2016
Language
English
Publication Type
Article
Keywords
Animals
Cohort Studies
Denmark - epidemiology
Diet, Fat-Restricted - adverse effects - ethnology
Diet, High-Fat - adverse effects - ethnology
Female
Fishes
Follow-Up Studies
Healthy Diet - ethnology
Humans
Incidence
Male
Meat - adverse effects
Middle Aged
Myocardial Infarction - epidemiology - ethnology - etiology - prevention & control
Plant Roots - adverse effects
Proportional Hazards Models
Risk factors
Seafood - adverse effects - analysis
Self Report
Sex Factors
Solanum tuberosum - adverse effects
Vegetables - adverse effects
Abstract
Red meat has been suggested to be adversely associated with risk of myocardial infarction (MI), whereas vegetable consumption has been found to be protective. The aim of this study was to investigate substitutions of red meat, poultry and fish with vegetables or potatoes for MI prevention. We followed up 29 142 women and 26 029 men in the Danish Diet, Cancer and Health study aged 50-64 years with no known history of MI at baseline. Diet was assessed by a validated 192-item FFQ at baseline. Adjusted Cox proportional hazard models were used to calculate hazard ratios (HR) and 95 % CI for MI associated with specified food substitutions of 150 g/week. During a median follow-up of 13·6 years, we identified 656 female and 1694 male cases. Among women, the HR for MI when replacing red meat with vegetables was 0·94 (95 % CI 0·90, 0·98). Replacing fatty fish with vegetables was associated with a higher risk of MI (HR 1·23; 95 % CI 1·05, 1·45), whereas an inverse, statistically non-significant association was found for lean fish (HR 0·93; 95 % CI 0·83, 1·05). Substituting poultry with vegetables was not associated with risk of MI (HR 1·00; 95 % CI 0·90, 1·11). Findings for substitution with potatoes were similar to findings for vegetables. Among men, a similar pattern was observed, but the associations were weak and mostly statistically non-significant. This study suggests that replacing red meat with vegetables or potatoes is associated with a lower risk of MI, whereas replacing fatty fish with vegetables or potatoes is associated with a higher risk of MI.
PubMed ID
27774916 View in PubMed
Less detail

9 records – page 1 of 1.