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Journal Article Research Support, Non-U.S. Gov't Ppublish 15 citations

PubMed: 35234353 DOI: 10.1111/andr.13170

Exposure to polycyclic aromatic hydrocarbons and nicotine, and associations with sperm DNA fragmentation.

Andrology 10(4):740-748

Authors: Jonatan Axelsson, Christian H Lindh, Aleksander Giwercman

Affiliations

  • Reproductive Medicine Centre, SkÃ¥ne University Hospital, and Molecular Reproductive Medicine, Department of Translational Medicine, Lund University, Malmö, Sweden.
  • Division of Occupational and Environmental Medicine, Department of Laboratory Medicine, Lund University, Lund, Sweden.

Abstract

BACKGROUND

Tobacco smoking has been reported to cause DNA fragmentation and has been suggested to cause mutations in spermatozoa. These effects have been ascribed to the action of polycyclic aromatic hydrocarbons (PAH) present in the smoke. Simultaneously, DNA fragmentation has been associated with mutagenesis.

OBJECTIVE

The aim of this study was to investigate whether levels of urinary biomarkers of PAH and nicotine exposure were associated with sperm DNA fragmentation.

METHODS

In the urine of 381 men recruited from two cohorts of young men (17-21 years old) from the general Swedish population, the PAH metabolites 1-hydroxypyrene and 2-hydroxyphenanthrene, as well as the nicotine metabolite cotinine, were measured. The sperm DNA fragmentation index (DFI) was analysed using the sperm chromatin structure assay. Associations between the DFI, and PAH metabolite levels as continuous variables as well as in quartiles, were studied by general linear models adjusted for abstinence time. A similar analysis was carried out for cotinine levels, according to which the men were categorised as "non-smoking" (n = 216) and "smoking" (n = 165).

RESULTS

No association was found between levels of any of the three biomarkers and DFI, either as a continuous variable (p = 0.87-0.99), or when comparing the lowest and the highest quartiles (p = 0.11-0.61). The same was true for comparison of men categorised as non-smoking or smoking (DFI 11.1% vs. 11.8%, p = 0.31).

DISCUSSION

We found no evidence of PAH or nicotine exposure to be associated with DFI, which does not exclude that these exposures may have other effects on sperm DNA.

CONCLUSION

In these young men, levels of biomarkers of nicotine and PAH exposure were not associated with DFI.

MeSH

Andrology, Biomarkers, Dna Fragmentation, Cotinine, Polycyclic Aromatic Hydrocarbons, Nicotine, Hydrocarbons, Spermatozoa, Dna, Smoking, Hydrocarbons, Aromatic

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