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Hällsten, Anna-Lena
Publications (3 of 3) Show all publications
Persson, B., Vrethem, M., Murgia, N., Lindh, J., Hällsten, A.-L., Fredrikson, M. & Tondel, M. (2013). Urinary 2,5-hexanedione excretion in cryptogenic polyneuropathy compared to the general Swedish population. Journal of Occupational Medicine and Toxicology, 8
Open this publication in new window or tab >>Urinary 2,5-hexanedione excretion in cryptogenic polyneuropathy compared to the general Swedish population
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2013 (English)In: Journal of Occupational Medicine and Toxicology, ISSN 1745-6673, E-ISSN 1745-6673, Vol. 8Article in journal (Refereed) Published
Abstract [en]

Background

2,5-hexanedione (2,5-HD) is the main neurotoxic metabolite of methyl-n-butyl ketone (MBK) and n-hexane, and known to cause polyneuropathy. The aim of our study was to compare the urinary levels of 2,5-HD between cases with cryptogenic polyneuropathy and the general Swedish population, and to elucidate the role of certain external factors.

Methods

Morning urine samples were collected from 114 cases with cryptogenic polyneuropathy (77 men and 37 women) and 227 referents (110 men and 117 women) randomly selected from the population registry. None had any current occupational exposure to n-hexane or MBK. The urine samples were analysed by a gas chromatographic method based on acidic hydrolysis.

Results

Cases had statistically higher urinary levels of 2,5-HD (0.48 mg/L) than the general population (0.41 mg/L) and men higher excretion than women (0.48 mg/L and 0.38 mg/L, respectively). There was no difference in 2,5-HD levels between current smokers and non-smokers. Occupational exposure to xylene, alcohol consumption and ever exposed to general anaesthesia were associated with lower excretion in men while for occupational exposure to nitrous oxide in women higher excretion was seen. Higher excretion of 2,5 HD was inversely related to increasing age.

Conclusions

Significantly higher levels of urinary 2,5-HD were seen in men and cryptogenic polyneuropathy cases seemingly unexposed to n-hexane. Hypothetically, this might be due to either differences in metabolic patterns or some concealed exposure. The difference in means between cases and the general population is small and can therefore not allow any firm conclusions of the causality, however.

Place, publisher, year, edition, pages
BioMed Central, 2013
Keywords
Polyneuropathy, Cryptogenic, Urine, 2, 5-hexanedione, General population, Sweden, Occupational exposure
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-96984 (URN)10.1186/1745-6673-8-21 (DOI)000322598500001 ()
Note

Funding Agencies|Swedish Council for Work Life and Social Research||Medical Research Council of Southeast Sweden (FORSS)||

Available from: 2013-09-02 Created: 2013-09-02 Last updated: 2017-12-06
Dick, F., De Palma, G., Ahmadi, A., Osborne, A., Scott, N., Prescott, G., . . . Tondel, M. (2007). Gene-environment interactions in parkinsonism and Parkinson's disease: The Geoparkinson study. Occupational and Environmental Medicine, 64(10), 673-680
Open this publication in new window or tab >>Gene-environment interactions in parkinsonism and Parkinson's disease: The Geoparkinson study
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2007 (English)In: Occupational and Environmental Medicine, ISSN 1351-0711, E-ISSN 1470-7926, Vol. 64, no 10, p. 673-680Article in journal (Refereed) Published
Abstract [en]

Objectives: To investigate associations of Parkinson's disease (PD) and parkinsonian syndromes with polymorphic genes that influence metabolism of either foreign chemical substances or dopamine and to seek evidence of gene-environment interaction effects that modify risk. Methods: A case-control study of 959 prevalent cases of parkinsonism (767 with PD) and 1989 controls across five European centres. Occupational hygienists estimated the average annual intensity of exposure to solvents, pesticides and metals, (iron, copper, manganese), blind to disease status. CYP2D6, PON1, GSTM1, GSTT1, GSTM3, GSTP1, NQO1, CYP1B1, MAO-A, MAO-B, SOD 2, EPHX, DATl, DRD2 and NAT2 were genotyped. Results were analysed using multiple logistic regression adjusting for key confounders. Results: There was a modest but significant association between MAO-A polymorphism in males and disease risk (G vs T, OR 1.30, 95% C1 1.02 to 1.66, adjusted). The majority of gene-environment analyses did not show significant interaction effects. There were possible interaction effects between GSTM1 null genotype and solvent exposure (which were stronger when limited to PD cases only). Conclusions: Many small studies have reported associations between genetic polymorphisms and PD. Fewer have examined gene-environment interactions. This large study was sufficiently powered to examine these aspects. GSTM1 null subjects heavily exposed to solvents appear to be at increased risk of PD. There was insufficient evidence that the other gene-environment combinations investigated modified disease risk, suggesting they contribute little to the burden of PD.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-39589 (URN)10.1136/oem.2006.032078 (DOI)49969 (Local ID)49969 (Archive number)49969 (OAI)
Available from: 2009-10-10 Created: 2009-10-10 Last updated: 2017-12-13
Semple, S., Dick, F., Cherrie, J., Study Group, G., Axelson, O., Hällsten, A.-L. & Tondel, M. (2004). Exposure assessment for a population-based case-control study combining a job-exposure matrix with interview data.. Scandinavian Journal of Work, Environment and Health, 30(3), 241-248
Open this publication in new window or tab >>Exposure assessment for a population-based case-control study combining a job-exposure matrix with interview data.
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2004 (English)In: Scandinavian Journal of Work, Environment and Health, ISSN 0355-3140, E-ISSN 1795-990X, Vol. 30, no 3, p. 241-248Article in journal (Refereed) Published
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-22016 (URN)1044 (Local ID)1044 (Archive number)1044 (OAI)
Available from: 2009-10-07 Created: 2009-10-07 Last updated: 2017-12-13
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