Background/Aims: The hydrocarbon solvent n-hexane is well known to cause polyneuropathy and its neurotoxicity is linked to the metabolite from the liver 2,5-hexanedione (2,5-HD). Increased urinary concentrations of 2,5-HD are shown in workers occupationally exposed to n-hexane. However, low urinary concentrations of 2,5-HD have also been detected in the general population possibly related to lipid peroxidation within the body or through microexposure to n-hexane in the environment. Less is known about the distribution of 2,5-HD within the general population and the relation to environmental exposures. Methods: Out of randomly selected referents in the general population from a previous survey 227 persons nonoccupationally exposed to n-hexane (age, 46–85 years) agreed to cast a morning urinary sample for analysis of 2,5-HD. The samples were analyzed after acid hydrolysis at the laboratory of Medicina del Lavoro in Perugia, Italy. Information on life style factors were collected through a questionnaire. A multiple linear regression analysis included as determinants liver toxic exposure, that is, organic solvents in occupation and leisure time, alcohol, drugs, and anesthesia during surgery at least once in the lifetime. Results: The mean 2,5-HD urinary concentration for women (n = 117) was 0.36 ± 0.23 mg/L and for men (n = 110) was 0.45 ± 0.27 mg/L. Men had significantly higher levels than women, hence the analysis was stratified for sex. The linear regression showed an inverse relation to age and a higher excretion in persons who never underwent general anesthesia. No other risk factor in the multiple linear regression was significant. None of these risk factors were significant for women in this regression. Conclusion: 2,5-HD is excreted in the urine in persons from the general population. Young men had consistently higher excretion than women in all the multivariate analyses. The background is still intriguing and the relevance as an etiology for development of polyneuropathy is unknown.

2,5-Hexanedione in the General Population: Environmental Exposure or Endogenous Production?

Nicola Murgia;
2011

Abstract

Background/Aims: The hydrocarbon solvent n-hexane is well known to cause polyneuropathy and its neurotoxicity is linked to the metabolite from the liver 2,5-hexanedione (2,5-HD). Increased urinary concentrations of 2,5-HD are shown in workers occupationally exposed to n-hexane. However, low urinary concentrations of 2,5-HD have also been detected in the general population possibly related to lipid peroxidation within the body or through microexposure to n-hexane in the environment. Less is known about the distribution of 2,5-HD within the general population and the relation to environmental exposures. Methods: Out of randomly selected referents in the general population from a previous survey 227 persons nonoccupationally exposed to n-hexane (age, 46–85 years) agreed to cast a morning urinary sample for analysis of 2,5-HD. The samples were analyzed after acid hydrolysis at the laboratory of Medicina del Lavoro in Perugia, Italy. Information on life style factors were collected through a questionnaire. A multiple linear regression analysis included as determinants liver toxic exposure, that is, organic solvents in occupation and leisure time, alcohol, drugs, and anesthesia during surgery at least once in the lifetime. Results: The mean 2,5-HD urinary concentration for women (n = 117) was 0.36 ± 0.23 mg/L and for men (n = 110) was 0.45 ± 0.27 mg/L. Men had significantly higher levels than women, hence the analysis was stratified for sex. The linear regression showed an inverse relation to age and a higher excretion in persons who never underwent general anesthesia. No other risk factor in the multiple linear regression was significant. None of these risk factors were significant for women in this regression. Conclusion: 2,5-HD is excreted in the urine in persons from the general population. Young men had consistently higher excretion than women in all the multivariate analyses. The background is still intriguing and the relevance as an etiology for development of polyneuropathy is unknown.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/2505080
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