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Cited by 132Air Quality and Health ImpactsToxic Organic Pollutants ImpactCarcinogens and Genotoxicity Assessment

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Effects of prenatal exposure to diesel exhaust particles on postnatal development, behavior, genotoxicity and inflammation in mice

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Hougaard, Karin S, Jensen, Keld A, Nordly, Pernille, Taxvig, Camilla, Vogel, Ulla, Saber, Anne T, Wallin, Håkan·2008·Particle and Fibre Toxicology
DOI 10.1186/1743-8977-5-3PMC PMC2323399
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Abstract

BACKGROUND: Results from epidemiological studies indicate that particulate air pollution constitutes a hazard for human health. Recent studies suggest that diesel exhaust possesses endocrine activity and therefore may affect reproductive outcome. This study in mice aimed to investigate whether exposure to diesel exhaust particles (DEP; NIST 2975) would affect gestation, postnatal development, activity, learning and memory, and biomarkers of transplacental toxicity. Pregnant mice (C57BL/6; BomTac) were exposed to 19 mg/m3 DEP (~1.106 particles/cm3; mass median diameter congruent with 240 nm) on gestational days 9-19, for 1 h/day. RESULTS: Gestational parameters were similar in control and diesel groups. Shortly after birth, body weights of DEP offspring were slightly lower than in controls. This difference increased during lactation, so by weaning the DEP exposed offspring weighed significantly less than the control progeny. Only slight effects of exposure were observed on cognitive function in female DEP offspring and on biomarkers of exposure to particles or genotoxic substances. CONCLUSION: In utero exposure to DEP decreased weight gain during lactation. Cognitive function and levels of biomarkers of exposure to particles or to genotoxic substances were generally similar in exposed and control offspring. The particle size and chemical composition of the DEP and differences in exposure methods (fresh, whole exhaust versus aged, resuspended DEP) may play a significant role on the biological effects observed in this compared to other studies.

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Crossref · 10.1186/1743-8977-5-3

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Figures

Figure 1 Average particle number distribution during DEP-exposure compared to the average particle size distribution in exposure to controls.n = 26. Error bars denote the SD of the average concentrations calculated based on the average for each N exposure.
Figure 1 Average particle number distribution during DEP-exposure compared to the average particle size distribution in exposure to controls.n = 26. Error bars denote the SD of the average concentrations calculated based on the average for each N exposure.CC BY · PubMed Central
Figure 2 Average mass number distribution during DEP-exposure compared to the average mass distribution in exposure to controls.n = 26. Error bars denote the SD of the average concentrations calculated based on the average for each N exposure.
Figure 2 Average mass number distribution during DEP-exposure compared to the average mass distribution in exposure to controls.n = 26. Error bars denote the SD of the average concentrations calculated based on the average for each N exposure.CC BY · PubMed Central
Figure 3 Average litter weight during lactation. Litters were either controls or exposed to DEP during gestation. Data represent mean+SEM. Mean Offspring exposed to DEP during fetal life gained statistically significantly less weight during the latter half of lactation compared to control offspring. n = 12. *p < 0.05.
Figure 3 Average litter weight during lactation. Litters were either controls or exposed to DEP during gestation. Data represent mean+SEM. Mean Offspring exposed to DEP during fetal life gained statistically significantly less weight during the latter half of lactation compared to control offspring. n = 12. *p < 0.05.CC BY · PubMed Central
Figure 4 mRNA expression of inflammatory cytokines in liver from pups at PND 2. Expression of mRNA is normalized to 18S rRNA. Empty squares: Controls; filled squares: DEP. Horisontal line: mean value. Levels of mRNA of IL-6, MCP-1, and MIP-2 were normalized to the 18S levels. n = 6–7.
Figure 4 mRNA expression of inflammatory cytokines in liver from pups at PND 2. Expression of mRNA is normalized to 18S rRNA. Empty squares: Controls; filled squares: DEP. Horisontal line: mean value. Levels of mRNA of IL-6, MCP-1, and MIP-2 were normalized to the 18S levels. n = 6–7.CC BY · PubMed Central
Figure 5 T4 plasma hormone levels in mothers and offspring. Blood for T4 plasma hormone levels were collected at the time of weaning and measured by immunoassay. Data represent mean+SEM, n = 11–12 for the dams. Data for male and female pups were similar and were therefore collapsed within each prenatal exposure group, n = 9.
Figure 5 T4 plasma hormone levels in mothers and offspring. Blood for T4 plasma hormone levels were collected at the time of weaning and measured by immunoassay. Data represent mean+SEM, n = 11–12 for the dams. Data for male and female pups were similar and were therefore collapsed within each prenatal exposure group, n = 9.CC BY · PubMed Central
Figure 6 Memory in the Morris water maze for female offspring. Data represent mean+SEM. Latency to locate the hidden platform is presented for memory (three days, i.e. trial 1–12; reversal, trial 13–16, and new, trial 17–20). DEP exposed offspring located the platform faster than controls on the first trial of reversal learning. n = 10. *p < 0.05.
Figure 6 Memory in the Morris water maze for female offspring. Data represent mean+SEM. Latency to locate the hidden platform is presented for memory (three days, i.e. trial 1–12; reversal, trial 13–16, and new, trial 17–20). DEP exposed offspring located the platform faster than controls on the first trial of reversal learning. n = 10. *p < 0.05.CC BY · PubMed Central

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Metadata

Authors
Hougaard, K. S., Jensen, K. A., Nordly, P., Taxvig, C., Vogel, U., Saber, A. T., & Wallin, H.
Affiliations
  • National Research Centre for the Working Environment (DK)
  • University of Copenhagen (DK)
  • Technical University of Denmark (DK)
ORCID
Venue
Particle and Fibre Toxicology
Publisher
Springer Science and Business Media LLC
Published
2008
Volume
5
Issue
1
Pages
3
ISSN
1743-8977 (ISSN-L)
DOI
10.1186/1743-8977-5-3
PMC
PMC2323399
OpenAlex
W2102523805
Cited by
132
References
54
Citations by year
2026: 1 · 2025: 4 · 2024: 5 · 2023: 4 · 2022: 8 · 2021: 5 · 2020: 7 · 2019: 13 · 2018: 10 · 2017: 11 · 2016: 5 · 2015: 11 · 2014: 6 · 2013: 10 · 2012: 7
FWCI
5.76
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Particle and Fibre Toxicology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
  • Technical University of Denmark, DTU Orbit (Technical University of Denmark, DTU) (submittedVersion, other-oa)
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
Keywords
diesel exhaust particles, prenatal exposure, postnatal development, weight gain, lactation, cognitive function, learning and memory, genotoxicity, inflammation, particulate matter pollution, endocrine activity, gestation, mice

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