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[Mustard--an important food allergen?]

https://arctichealth.org/en/permalink/ahliterature29823
Source
Tidsskr Nor Laegeforen. 2005 Mar 17;125(6):736-8
Publication Type
Article
Date
Mar-17-2005
Author
Martinus Løvik
Author Affiliation
Avdeling for miljøimmunologi, Divisjon for miljømedisin, Nasjonalt folkehelseinstitutt, Postboks 4404 Nydalen, 0403 Oslo. martinus.lovik@fhi.no
Source
Tidsskr Nor Laegeforen. 2005 Mar 17;125(6):736-8
Date
Mar-17-2005
Language
Norwegian
Publication Type
Article
Keywords
Cross Reactions
English Abstract
Food Hypersensitivity - diagnosis - etiology
Food Labeling
Humans
Mustard Plant - adverse effects
Abstract
BACKGROUND: The European Parliament and the Council of the European Union have issued a new directive on information on the label about the ingredients present in foodstuffs. Twelve foods causing hypersensitivity are now subject to particularly strict labelling rules. Among these foods is mustard, which until now has been little recognised as a food allergen in Norway. MATERIALS AND METHODS: Literature searches in Medline were performed and supplemented by manual searches of reference lists. RESULTS: Since the first published case of mustard allergy in 1980, a number of case reports and patient series have been published. Most reports come from certain regions of France, and a majority of the studies have been performed by a limited number of investigators. Symptoms triggered by mustard cover the whole range from full-blown systemic anaphylactic reactions to pollen-food allergy syndrome-like local reactions. Frequently, reactions appear to be serious. Mustard allergy has on many instances been found in small children. Cross-reactivity apart from that among different types of mustard does not appear to be a clinical problem. Mustard allergens are resistant to heat and food processing. INTERPRETATION: With more attention being given to mustard as a food allergen because of the new labelling rules, it will most likely soon become apparent whether mustard is a food allergen of importance in Norway. The Norwegian national reporting system and register of severe allergic reactions to food will be an important tool in this context.
PubMed ID
15776067 View in PubMed
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Pre-natal exposure to perfluoroalkyl substances may be associated with altered vaccine antibody levels and immune-related health outcomes in early childhood.

https://arctichealth.org/en/permalink/ahliterature116879
Source
J Immunotoxicol. 2013 Oct-Dec;10(4):373-9
Publication Type
Article
Author
Berit Granum
Line S Haug
Ellen Namork
Solvor B Stølevik
Cathrine Thomsen
Ingeborg S Aaberge
Henk van Loveren
Martinus Løvik
Unni C Nygaard
Author Affiliation
Division of Environmental Medicine, Norwegian Institute of Public Health , Oslo , Norway.
Source
J Immunotoxicol. 2013 Oct-Dec;10(4):373-9
Language
English
Publication Type
Article
Keywords
Alkanesulfonic Acids - blood
Alkenes - toxicity
Antibodies, Viral - blood
Asthma - epidemiology - immunology
Caprylates - blood
Child, Preschool
Cohort Studies
Common Cold - epidemiology - immunology
Female
Fluorocarbons - adverse effects - blood - toxicity
Follow-Up Studies
Gastroenteritis - epidemiology - immunology
Humans
Hypersensitivity - epidemiology - immunology
Immunosuppression
Incidence
Male
Norway
Pregnancy
Prenatal Exposure Delayed Effects - epidemiology - immunology
Prevalence
Prospective Studies
Treatment Outcome
Vaccines
Abstract
Perfluoroalkyl substances (PFAS) are suggested to have immunosuppressive effects; exposure in utero and in the first years of life is of special concern as fetuses and small children are highly vulnerable to toxicant exposure. The objective of this study was to investigate the effect of pre-natal exposure to PFAS on responses to pediatric vaccines and immune-related health outcomes in children up to 3 years of age. In the prospective birth-cohort BraMat, a sub-cohort of the Norwegian Mother and Child Cohort Study (MoBa), pregnant women from Oslo and Akershus, Norway, were recruited during 2007-2008. Three annual questionnaire-based follow-ups were performed. Blood samples were collected from the mothers at the time of delivery and from the children at the age of 3 years. As a measure of pre-natal exposure to PFAS, the concentrations of perfluorooctanoate (PFOA), perfluorononanoate (PFNA), perfluorohexane sulfonate (PFHxS), and perfluorooctane sulfonate (PFOS) were determined in maternal blood from 99 BraMat participants. Main outcome measures were anti-vaccine antibody levels, common infectious diseases and allergy- and asthma-related health outcomes in the children up to the age of 3 years. There was an inverse association between the level of anti-rubella antibodies in the children's serum at age 3 years and the concentrations of the four PFAS. Furthermore, there was a positive association between the maternal concentrations of PFOA and PFNA and the number of episodes of common cold for the children, and between PFOA and PFHxS and the number of episodes of gastroenteritis. No associations were found between maternal PFAS concentrations and the allergy- and asthma-related health outcomes investigated. The results indicate that pre-natal exposure to PFAS may be associated with immunosuppression in early childhood.
PubMed ID
23350954 View in PubMed
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Prenatal exposure to polychlorinated biphenyls and dioxins from the maternal diet may be associated with immunosuppressive effects that persist into early childhood.

https://arctichealth.org/en/permalink/ahliterature120128
Source
Food Chem Toxicol. 2013 Jan;51:165-72
Publication Type
Article
Date
Jan-2013
Author
Solvor Berntsen Stølevik
Unni Cecilie Nygaard
Ellen Namork
Margaretha Haugen
Helle Margrete Meltzer
Jan Alexander
Helle Katrine Knutsen
Ingeborg Aaberge
Kirsti Vainio
Henk van Loveren
Martinus Løvik
Berit Granum
Author Affiliation
Norwegian Institute of Public Health, NO-0403 Oslo, Norway. solvor.berntsen@fhi.no
Source
Food Chem Toxicol. 2013 Jan;51:165-72
Date
Jan-2013
Language
English
Publication Type
Article
Keywords
Antibody formation
Child, Preschool
Dioxins - toxicity
Environmental Pollutants - toxicity
Female
Food Contamination
Humans
Infant
Maternal Exposure
Measles Vaccine - immunology
Norway
Polychlorinated Biphenyls - toxicity
Pregnancy
Prenatal Exposure Delayed Effects - chemically induced
Questionnaires
Regression Analysis
Respiratory Sounds - etiology
Respiratory Tract Infections - chemically induced - epidemiology
Abstract
We investigated whether prenatal exposure from the maternal diet to the toxicants polychlorinated biphenyls (PCBs) and dioxins is associated with the development of immune-related diseases in childhood. Children participating in BraMat, a sub-cohort of the Norwegian Mother and Child Cohort Study (MoBa), were followed in the three first years of life using annual questionnaires (0-3years; n=162, 2-3years; n=180), and blood parameters were examined at three years of age (n=114). The maternal intake of the toxicants was calculated using a validated food frequency questionnaire from MoBa. Maternal exposure to PCBs and dioxins was found to be associated with an increased risk of wheeze and more frequent upper respiratory tract infections. Furthermore, maternal exposure to PCBs and dioxins was found to be associated with reduced antibody response to a measles vaccine. No associations were found between prenatal exposure and immunophenotype data, allergic sensitization and vaccine-induced antibody responses other than measles. Our results suggest that prenatal dietary exposure to PCBs and dioxins may increase the risk of wheeze and the susceptibility to infectious diseases in early childhood.
PubMed ID
23036451 View in PubMed
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Prenatal exposure to polychlorinated biphenyls and dioxins is associated with increased risk of wheeze and infections in infants.

https://arctichealth.org/en/permalink/ahliterature134515
Source
Food Chem Toxicol. 2011 Aug;49(8):1843-8
Publication Type
Article
Date
Aug-2011
Author
Solvor Berntsen Stølevik
Unni Cecilie Nygaard
Ellen Namork
Margaretha Haugen
Helen Engelstad Kvalem
Helle Margrete Meltzer
Jan Alexander
Joost H M van Delft
Henk van Loveren
Martinus Løvik
Berit Granum
Author Affiliation
Norwegian Institute of Public Health, NO-0403 Oslo, Norway. solvor.berntsen@fhi.no
Source
Food Chem Toxicol. 2011 Aug;49(8):1843-8
Date
Aug-2011
Language
English
Publication Type
Article
Keywords
Acrylamide - toxicity
Adult
Cohort Studies
Dioxins - toxicity
Eating
Environmental Pollutants - toxicity
Female
Humans
Infant
Maternal Exposure - adverse effects
Norway
Polychlorinated Biphenyls - toxicity
Pregnancy
Prenatal Exposure Delayed Effects
Questionnaires
Respiratory Sounds - physiopathology
Respiratory Tract Infections - chemically induced
Risk factors
Abstract
The birth cohort BraMat (n = 205; a sub-cohort of the Norwegian Mother and Child Cohort Study (MoBa) conducted by the Norwegian Institute of Public Health) was established to study whether prenatal exposure to toxicants from the maternal diet affects immunological health outcomes in children. We here report on the environmental pollutants polychlorinated biphenyls (PCBs) and dioxins, as well as acrylamide generated in food during heat treatment. The frequency of common infections, eczema or itchiness, and periods of more than 10 days of dry cough, chest tightness or wheeze (called wheeze) in the children during the first year of life was assessed by questionnaire data (n = 195). Prenatal dietary exposure to the toxicants was estimated using a validated food frequency questionnaire from MoBa. Prenatal exposure to PCBs and dioxins was found to be associated with increased risk of wheeze and exanthema subitum, and also with increased frequency of upper respiratory tract infections. We found no associations between prenatal exposure to acrylamide and the health outcomes investigated. Our results suggest that prenatal dietary exposure to dioxins and PCBs may increase the risk of wheeze and infectious diseases during the first year of life.
PubMed ID
21571030 View in PubMed
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Severe allergic reactions to food in Norway: a ten year survey of cases reported to the food allergy register.

https://arctichealth.org/en/permalink/ahliterature131413
Source
Int J Environ Res Public Health. 2011 Aug;8(8):3144-55
Publication Type
Article
Date
Aug-2011
Author
Ellen Namork
Christiane K Fæste
Berit A Stensby
Eliann Egaas
Martinus Løvik
Author Affiliation
Division of Environmental Medicine, Norwegian Institute of Public Health, P.O. Box 4404, Nydalen, Oslo NO-0403, Norway. ellen.namork@fhi.no
Source
Int J Environ Res Public Health. 2011 Aug;8(8):3144-55
Date
Aug-2011
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Distribution
Aged
Child
Child, Preschool
Female
Food Hypersensitivity - diagnosis - epidemiology - etiology
Humans
Immunoglobulin E - blood
Infant
Infant, Newborn
Lupinus - immunology
Male
Middle Aged
Norway - epidemiology
Registries
Sex Distribution
Trigonella - immunology
Abstract
The Norwegian Food Allergy Register was established at the Norwegian Institute of Public Health in 2000. The purpose of the register is to gain information about severe allergic reactions to food in Norway and to survey food products in relation to allergen labelling and contamination. Cases are reported on a voluntary basis by first line doctors, and submitted together with a serum sample for specific IgE analysis. The register has received a total of 877 reports from 1 July, 2000 to 31 December, 2010. Two age groups, small children and young adults are over-represented, and the overall gender distribution is 40:60 males-females. The legumes lupine and fenugreek have been identified as two "new" allergens in processed foods and cases of contamination and faults in production of processed foods have been revealed. The highest frequency of food specific IgE is to hazelnuts and peanuts, with a marked increase in reactions to hazelnuts during the last three years. The Food Allergy Register has improved our knowledge about causes and severity of food allergic reactions in Norway. The results show the usefulness of population based national food allergy registers in providing information for health authorities and to secure safe food for individuals with food allergies.
Notes
Cites: J Allergy Clin Immunol. 2001 May;107(5):891-611344358
Cites: Allergy. 2010 Jun 1;65(6):671-8020148805
Cites: Allerg Immunol (Paris). 2002 Jun;34(6):194-812134641
Cites: Allergy. 2003 Nov;58(11):1204-514616143
Cites: J Investig Allergol Clin Immunol. 2004;14(1):70-915160445
Cites: Int Arch Allergy Immunol. 2004 Sep;135(1):36-915286444
Cites: Allergy. 1999 Mar;54(3):261-510321562
Cites: Allergy. 1999 Apr;54(4):380-510371098
Cites: Eur Ann Allergy Clin Immunol. 2005 Feb;37(2):54-715859362
Cites: Proc Nutr Soc. 2005 Nov;64(4):413-716313682
Cites: J Allergy Clin Immunol. 2006 Dec;118(6):1375-8117157669
Cites: Thorax. 2007 Jan;62(1):91-616950836
Cites: J Allergy Clin Immunol. 2007 Nov;120(5):1172-717935766
Cites: J Allergy Clin Immunol. 2007 Dec;120(6):1413-718073126
Cites: Allergy. 2008 Mar;63(3):370-318028245
Cites: Pediatr Allergy Immunol. 2008 Jun;19(4):368-7318482082
Cites: Int J Biometeorol. 2008 Sep;52(7):667-7418481116
Cites: Allergy. 2008 Nov;63(11):1418-2718925878
Cites: Allergy. 2008 Nov;63(11):1562-318925896
Cites: Curr Allergy Asthma Rep. 2009 Jan;9(1):57-6319063826
Cites: J Allergy Clin Immunol. 2009 Jan;123(1):187-9418930518
Cites: Eur Ann Allergy Clin Immunol. 2009 Feb;41(1):17-2219496348
Cites: Clin Pediatr (Phila). 2010 Jun;49(6):579-8520075031
Cites: J Allergy Clin Immunol. 2010 Jun;125(6):1327-3520451985
Cites: J Allergy Clin Immunol. 2010 Jun;125(6):1322-620462634
Cites: J Allergy Clin Immunol. 2001 Nov;108(5):861-611692116
PubMed ID
21909296 View in PubMed
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Urinary biomarkers for phthalates associated with asthma in Norwegian children.

https://arctichealth.org/en/permalink/ahliterature118838
Source
Environ Health Perspect. 2013 Feb;121(2):251-6
Publication Type
Article
Date
Feb-2013
Author
Randi J Bertelsen
Karin C Lødrup Carlsen
Antonia M Calafat
Jane A Hoppin
Geir Håland
Petter Mowinckel
Kai-Håkon Carlsen
Martinus Løvik
Author Affiliation
Department of Food, Water and Cosmetics, Norwegian Institute of Public Health, Oslo, Norway. randi.jacobsen.bertelsen@fhi.no
Source
Environ Health Perspect. 2013 Feb;121(2):251-6
Date
Feb-2013
Language
English
Publication Type
Article
Keywords
Asthma - chemically induced
Biological Markers - urine
Body Burden
Child
Cross-Sectional Studies
Humans
Norway
Phthalic Acids - pharmacokinetics - toxicity - urine
Abstract
High-molecular-weight phthalates in indoor dust have been associated with asthma in children, but few studies have evaluated phthalate biomarkers in association with respiratory outcomes.
We explored the association between urinary concentrations of phthalate metabolites and current asthma.
In a cross-sectional analysis, 11 metabolites of 8 phthalates [including four metabolites of di(2-ethylhexyl) phthalate] were measured in one first morning void collected from 2001 through 2004 from 623 10-year-old Norwegian children. Logistic regression models controlling for urine specific gravity, sex, parental asthma, and income were used to estimate associations between current asthma and phthalate metabolite concentrations by quartiles or as log10-transformed variables.
Current asthma was associated with both mono(carboxyoctyl) phthalate (MCOP) and mono(carboxynonyl) phthalate (MCNP), although the association was limited to those in the highest quartile of these chemicals. The adjusted odds ratio (aOR) for current asthma was 1.9 (95% CI: 1.0, 3.3) for the highest MCOP quartile compared with the lowest quartile, and 1.3 (95% CI: 0.98, 1.7) for an interquartile-range increase. The aOR for current asthma was 2.2 (95% CI: 1.2, 4.0) for the highest MCNP quartile and 1.3 (95% CI: 1.0, 1.7) for an interquartile-range increase. The other phthalate metabolites were not associated with current asthma.
Current asthma was associated with the highest quartiles of MCOP and MCNP, metabolites of two high molecular weight phthalates, diisononyl phthalate and diisodecyl phthalate, respectively. Given the short biological half-life of the phthalates and the cross-sectional design, our findings should be interpreted cautiously.
Notes
Cites: Environ Health Perspect. 2010 Dec;118(12):1748-5420797930
Cites: Environ Health Perspect. 2011 Jan;119(1):50-520870567
Cites: Mol Nutr Food Res. 2011 Jan;55(1):7-3120564479
Cites: Int J Hyg Environ Health. 2011 Jun;214(3):188-9521371937
Cites: Environ Res. 2011 Jul;111(5):656-6321429484
Cites: Toxicology. 2010 May 27;271(3):73-8220371260
Cites: Am J Ind Med. 2001 Jan;39(1):100-1111148020
Cites: Environ Health Perspect. 2002 May;110(5):515-812003755
Cites: Environ Health Perspect. 2003 Feb;111(2):139-4512573895
Cites: Pediatr Allergy Immunol. 2002;13 Suppl 15:29-3112688621
Cites: Environ Health Perspect. 2003 Nov;111(14):1719-2214594621
Cites: Environ Health Perspect. 2004 Mar;112(3):331-814998749
Cites: Environ Health Perspect. 2004 Apr;112(5):571-415064163
Cites: Environ Health Perspect. 2004 Oct;112(14):1393-715471731
Cites: Eur Respir J. 1994 Sep;7(9):1660-87995397
Cites: Environ Health Perspect. 1997 Sep;105(9):972-89374082
Cites: J Expo Sci Environ Epidemiol. 2010 Nov;20(7):625-3320354564
Cites: Indoor Air. 2010 Dec;20(6):494-50121070375
Cites: Am J Public Health. 1999 Feb;89(2):188-929949747
Cites: Environ Health Perspect. 2004 Dec;112(17):1734-4015579421
Cites: Hum Reprod. 2005 Mar;20(3):604-1015591081
Cites: Int J Androl. 2006 Feb;29(1):134-9; discussion 181-516466533
Cites: Allergy. 2006 Apr;61(4):454-6016512808
Cites: Am J Epidemiol. 2006 Oct 15;164(8):742-916877535
Cites: Int J Hyg Environ Health. 2007 Jan;210(1):35-4217185035
Cites: Int J Hyg Environ Health. 2007 May;210(3-4):319-3317400024
Cites: J Expo Sci Environ Epidemiol. 2007 Jul;17(4):378-8717006438
Cites: J Environ Monit. 2007 Dec;9(12):1419-2518049782
Cites: J Chromatogr B Analyt Technol Biomed Life Sci. 2007 Dec 1;860(1):106-1217997365
Cites: Environ Health Perspect. 2008 Jan;116(1):98-10318197306
Cites: Toxicol Lett. 2008 May 5;178(2):110-618407439
Cites: Environ Health Perspect. 2008 Jul;116(7):845-5318629304
Cites: Allergy. 2008 Aug;63(8):1054-6018691307
Cites: Int J Hyg Environ Health. 2009 Sep;212(5):481-9119394271
Cites: Int J Hyg Environ Health. 2009 Nov;212(6):685-9219729343
Cites: Inhal Toxicol. 2010 Feb;22(2):140-5019938896
Cites: J Expo Sci Environ Epidemiol. 2010 Mar;20(2):169-7519277068
Comment In: Environ Health Perspect. 2013 Feb;121(2):a5923380156
PubMed ID
23164678 View in PubMed
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6 records – page 1 of 1.