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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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          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/m 3 DEP (~1·10 6 particles/cm 3; mass median diameter ≅ 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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          In utero programming of chronic disease.

          D. J. Barker (1998)
          1. Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. 2. These 'programmed' changes may be the origins of a number of diseases in later life, including coronary heart disease and the related disorders stroke, diabetes and hypertension. 3. This review examines the evidence linking these diseases to fetal undernutrition and provides an overview of previous studies in this area.
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            Ambient Air Pollution and Pregnancy Outcomes: A Review of the Literature

            Radim J. Sram, Blanka Binkova, Jan Dejmek (posthumous) … (2005)
            Over the last decade or so, a large number of studies have investigated the possible adverse effects of ambient air pollution on birth outcomes. We reviewed these studies, which were identified by a systematic search of the main scientific databases. Virtually all reviewed studies were population based, with information on exposure to air pollution derived from routine monitoring sources. Overall, there is evidence implicating air pollution in adverse effects on different birth outcomes, but the strength of the evidence differs between outcomes. The evidence is sufficient to infer a causal relationship between particulate air pollution and respiratory deaths in the postneonatal period. For air pollution and birth weight the evidence suggests causality, but further studies are needed to confirm an effect and its size and to clarify the most vulnerable period of pregnancy and the role of different pollutants. For preterm births and intrauterine growth retardation (IUGR) the evidence as yet is insufficient to infer causality, but the available evidence justifies further studies. Molecular epidemiologic studies suggest possible biologic mechanisms for the effect on birth weight, premature birth, and IUGR and support the view that the relation between pollution and these birth outcomes is genuine. For birth defects, the evidence base so far is insufficient to draw conclusions. In terms of exposure to specific pollutants, particulates seem the most important for infant deaths, and the effect on IUGR seems linked to polycyclic aromatic hydrocarbons, but the existing evidence does not allow precise identification of the different pollutants or the timing of exposure that can result in adverse pregnancy outcomes.
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              Inhaled particles and lung cancer. Part A: Mechanisms.

              Theo J A Borm, Ad M Knaapen, Catrin Albrecht … (2004)
              Both occupational and environmental exposure to particles is associated with an increased risk of lung cancer. Particles are thought to impact on genotoxicity as well as on cell proliferation via their ability to generate oxidants such as reactive oxygen species (ROS) and reactive nitrogen species (RNS). For mechanistic purposes, one should discriminate between a) the oxidant-generating properties of particles themselves (i.e., acellular), which are mostly determined by the physicochemical characteristics of the particle surface, and b) the ability of particles to stimulate cellular oxidant generation. Cellular ROS/RNS can be generated by various mechanisms, including particle-related mitochondrial activation or NAD(P)H-oxidase enzymes. In addition, since particles can induce an inflammatory response, a further subdivision needs to be made between primary (i.e., particle-driven) and secondary (i.e., inflammation-driven) formation of oxidants. Particles may also affect genotoxicity by their ability to carry surface-adsorbed carcinogenic components into the lung. Each of these pathways can impact on genotoxicity and proliferation, as well as on feedback mechanisms involving DNA repair or apoptosis. Although abundant evidence suggests that ROS/RNS mediate particle-induced genotoxicity and mutagenesis, little information is available towards the subsequent steps leading to neoplastic changes. Additionally, since most of the proposed molecular mechanisms underlying particle-related carcinogenesis have been derived from in vitro studies, there is a need for future studies that evaluate the implication of these mechanisms for in vivo lung cancer development. In this respect, transgenic and gene knockout animal models may provide a useful tool. Such studies should also include further assessment of the relative contributions of primary (inflammation-independent) and secondary (inflammation-driven) pathways. Copyright 2004 Wiley-Liss, Inc.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Part Fibre Toxicol
                Title: Particle and Fibre Toxicology
                Publisher: BioMed Central
                ISSN (Electronic): 1743-8977
                Publication date Collection: 2008
                Publication date (Electronic): 11 March 2008
                Volume: 5
                Page: 3
                Affiliations
                [1 ]National Research Centre of the Working Environment, Lersø Parkallé 105, DK-2100 Copenhagen Ø, Denmark
                [2 ]Faculty of Pharmaceutical Sciences, University of Copenhagen, Universitetsparken 2, DK-2100 Copenhagen Ø, Denmark
                [3 ]National Food Institute, Technical University of Denmark, Mørkhøj Bygade 19, DK-2860 Mørkhøj, Denmark
                Article
                Publisher ID: 1743-8977-5-3
                DOI: 10.1186/1743-8977-5-3
                PMC ID: 2323399
                PubMed ID: 18331653
                SO-VID: 2643704f-9662-4391-a921-e517f3fe4311
                Copyright © Copyright © 2008 Hougaard et al; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 13 July 2007
                Date accepted : 11 March 2008
                Categories
                Subject: Research

                ScienceOpen disciplines: Toxicology
                Data availability:
                ScienceOpen disciplines: Toxicology

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