Prenatal and postnatal mothering by diesel exhaust PM2.5-exposed dams differentially program mouse energy metabolism
Open accessAbstract
Obesity is one of the leading threats to global public health. It is consequent to abnormal energy metabolism. Currently, it has been well established that maternal exposure to environmental stressors that cause inappropriate fetal development may have long-term adverse effects on offspring energy metabolism in an exposure timing-dependent manner, known as developmental programming of health and diseases paradigm. Rapidly increasing evidence has indicated that maternal exposure to ambient fine particles (PM 2.5 ) correlates to abnormal fetal development. In the present study, we therefore assessed whether maternal exposure to diesel exhaust PM 2.5 (DEP), the major component of ambient PM 2.5 in urban areas, programs offspring energy metabolism, and further examined how the timing of exposure impacts this programming. The growth trajectory of offspring shows that although prenatal maternal exposure to DEP did not impact the birth weight of offspring, it significantly decreased offspring body weight from postnatal week 2 until the end of observation. This weight loss effect of prenatal maternal exposure to DEP coincided with decreased food intake but not alteration in brown adipose tissue (BAT) morphology. The hypophagic effect of prenatal maternal exposure to DEP was in concord with decreased hypothalamic expression of an orexigenic peptide NPY, suggesting that the prenatal maternal exposure to DEP impacts offspring energy balance primarily through programming of food intake. Paradoxically, the reduced body weight resulted from prenatal maternal exposure to DEP was accompanied by increased mass of epididymal adipose tissue, which was due to hyperplasia as morphological analysis did not observe any hypertrophy. In direct contrast, the postnatal mothering by DEP-exposed dams increased offspring body weight during lactation and adulthood, paralleled by markedly increased fat accumulation and decreased UCP1 expression in BAT but not alteration in food intake. The weight gain induced by postnatal mothering by DEP-exposed dams was also expressed as an increased adiposity. But it concurred with a marked hypertrophy of adipocytes. Prenatal and postnatal mothering by DEP-exposed dams differentially program offspring energy metabolism, underscoring consideration of the exposure timing when examining the adverse effects of maternal exposure to ambient PM 2.5 .
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Chen et al. did not observe an impact on birth weight in offspring of C57Bl/6 mice exposed to diesel exhaust PM2.5 during gestation; however, offspring body weight was found to be decreased from postnatal week two until the end of observation (20-22 weeks of age).
“Chen et al. [87] did not observe an impact on birth weight in offspring of C57Bl/6 mice exposed to diesel exhaust PM2.5 during gestation; however, offspring body weight was found to be decreased from postnatal week two until the end of observation (20-22 weeks of age).”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [87]
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Experimental — accuracy not yet measuredChen et al. applied 20 μg of a DEP suspension, representing an average daily dose of 8.6 μg/mouse, approximately equating to an inhalational exposure level of 160 μg/m3 PM2.5.
“For instance, Chen et al. [87] applied 20 μg of a DEP suspension, representing an average daily dose of 8.6 μg/mouse, approximately equating to an inhalational exposure level of 160 μg/m3 PM2.5.”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [87]
Reduced weight gain in the PM2.5-exposed mice correlated with decreased food intake.
“Reduced weight gain in the PM2.5-exposed mice correlated with decreased food intake.”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [87]
In a second exposure group, where control mice were fostered by PM2.5-exposed dams, offspring body weight increased during lactation and into adulthood (without marked food intake increases).
“In contrast, in a second exposure group, where control mice were fostered by PM2.5-exposed dams, offspring body weight increased during lactation and into adulthood (without marked food intake increases).”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [87]
Reduced weight gain corresponded with increased epididymal adipose tissue mass.
“Interestingly, reduced weight gain corresponded with increased epididymal adipose tissue mass.”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [87]
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Cites
Kinney, P. L., Aggarwal, M., Northridge, M. E., Janssen, N. A., & Shepard, P. (2000) · Environmental Health Perspectives · doi:10.1289/ehp.00108213 · Cited by 248 · see citing works
Rich, D. Q., Liu, K., Zhang, J., Thurston, S. W., Stevens, T. P., Pan, Y., Kane, C., Weinberger, B., Ohman-Strickland, P., Woodruff, T. J., et al. (2015) · Environmental Health Perspectives · doi:10.1289/ehp.1408795 · Cited by 174 · see citing works
Fleisch, A. F., Rifas-Shiman, S. L., Koutrakis, P., Schwartz, J. D., Kloog, I., Melly, S., Coull, B. A., Zanobetti, A., Gillman, M. W., Gold, D. R., et al. (2015) · Epidemiology · doi:10.1097/ede.0000000000000203 · Cited by 140 · see citing works
Hougaard, K. S., Jensen, K. A., Nordly, P., Taxvig, C., Vogel, U., Saber, A. T., & Wallin, H. (2008) · Particle and Fibre Toxicology · doi:10.1186/1743-8977-5-3 · Cited by 132 · see citing works
DIESEL EXHAUST AFFECTS THE ABNORMAL DELIVERY IN PREGNANT MICE AND THE GROWTH OF THEIR YOUNG
Tsukue, N., Tsubone, H., & Suzuki, A. K. (2002) · Inhalation Toxicology · doi:10.1080/08958370290084548 · Cited by 70 · see citing works
Flagged first, then by citations
Research works printed but not linked: 31
- [1]Ng M Global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013: a systematic analysis for the Global Burden of Disease Study 2013 Lancet 2014 384 9945 766 81 10.1016/S0140-6736(14)60460-8 24880830 PMC4624264 · DOI · Paper page
- [2]Grandjean P Life-long implications of developmental exposure to environmental stressors: new perspectives Endocrinology 2015 156 10 3408 15 10.1210/EN.2015-1350 26241067 PMC4588822 · DOI
- [3]Lim SS A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010 Lancet 2012 380 9859 2224 60 10.1016/S0140-6736(12)61766-8 23245609 PMC4156511 · DOI · Paper page
- [4]Bonzini M Impact of ambient air pollution on birth outcomes: systematic review of the current evidences Med Lav 2010 101 5 341 63 21105590
- [5]Valdiglesias V In vitro evaluation of selenium genotoxic, cytotoxic, and protective effects: a review Arch Toxicol 2010 84 5 337 51 10.1007/s00204-009-0505-0 20033805 · DOI
- [6]Schembari A Ambient air pollution and newborn size and adiposity at birth: differences by maternal ethnicity (the born in Bradford study cohort) Environ Health Perspect 2015 123 11 1208 15 10.1289/ehp.1408675 25978617 PMC4629735 · DOI
- [7]Sun X The association between fine particulate matter exposure during pregnancy and preterm birth: a meta-analysis BMC Pregnancy Childbirth 2015 15 300 10.1186/s12884-015-0738-2 26581753 PMC4650291 · DOI
- [10]Hyder A PM2.5 exposure and birth outcomes: use of satellite- and monitor-based data Epidemiology 2014 25 1 58 67 10.1097/EDE.0000000000000027 24240652 PMC4009503 · DOI
- [11]Savitz DA Ambient fine particulate matter, nitrogen dioxide, and term birth weight in New York, New York Am J Epidemiol 2014 179 4 457 66 10.1093/aje/kwt268 24218031 PMC3908629 · DOI
- [12]Dadvand P Maternal exposure to particulate air pollution and term birth weight: a multi-country evaluation of effect and heterogeneity Environ Health Perspect 2013 121 3 267 373 10.1289/ehp.1205575 23384584 PMC3621183 · DOI
- [13]Weldy CS In utero exposure to diesel exhaust air pollution promotes adverse intrauterine conditions, resulting in weight gain, altered blood pressure, and increased susceptibility to heart failure in adult mice PLoS One 2014 9 2 e88582 10.1371/journal.pone.0088582 24533117 PMC3922927 · DOI
- [14]Gorr MW Early life exposure to air pollution induces adult cardiac dysfunction Am J Physiol Heart Circ Physiol 2014 307 9 H1353 60 10.1152/ajpheart.00526.2014 25172901 PMC4217011 · DOI · Paper page
- [15]Valentino SA Maternal exposure to diluted diesel engine exhaust alters placental function and induces intergenerational effects in rabbits Part Fibre Toxicol 2016 13 1 39 10.1186/s12989-016-0151-7 27460165 PMC4962477 · DOI · Paper page
- [16]Veras MM Chronic exposure to fine particulate matter emitted by traffic affects reproductive and fetal outcomes in mice Environ Res 2009 109 5 536 43 10.1016/j.envres.2009.03.006 19394924 · DOI
- [17]Rocha ESIR Effects of ambient levels of air pollution generated by traffic on birth and placental weights in mice Fertil Steril 2008 90 5 1921 4 10.1016/j.fertnstert.2007.10.001 18222432 · DOI
- [19]Watanabe N Kurita M The masculinization of the fetus during pregnancy due to inhalation of diesel exhaust Environ Health Perspect 2001 109 2 111 9 10.1289/ehp.01109111 11266319 PMC1240629 · DOI
- [20]Bolton JL Auten RL Bilbo SD Prenatal air pollution exposure induces sexually dimorphic fetal programming of metabolic and neuroinflammatory outcomes in adult offspring Brain Behav Immun 2014 37 30 44 10.1016/j.bbi.2013.10.029 24184474 · DOI
- [21]Zeltser LM Developmental influences on circuits programming susceptibility to obesity Front Neuroendocrinol 2015 39 17 27 10.1016/j.yfrne.2015.07.002 26206662 PMC4681591 · DOI
- [22]Kyjovska ZO DNA strand breaks, acute phase response and inflammation following pulmonary exposure by instillation to the diesel exhaust particle NIST1650b in mice Mutagenesis 2015 30 4 499 507 10.1093/mutage/gev009 25771385 · DOI
- [24]Ying Z Ambient particulates alter vascular function through induction of reactive oxygen and nitrogen species Toxicol Sci 2009 111 1 80 8 10.1093/toxsci/kfp004 19182107 PMC2726294 · DOI
- [25]Ying Z Long-term exposure to concentrated ambient PM2.5 increases mouse blood pressure through abnormal activation of the sympathetic nervous system: a role for hypothalamic inflammation Environ Health Perspect 2014 122 1 79 86 24240275 PMC3888575
- [26]Fangstrom B A retrospective study of PBDEs and PCBs in human milk from the Faroe Islands Environ Health 2005 4 12 10.1186/1476-069X-4-12 16014177 PMC1226148 · DOI
- [29]Thaler JP Hypothalamic inflammation: marker or mechanism of obesity pathogenesis? Diabetes 2013 62 8 2629 34 10.2337/db12-1605 23881189 PMC3717869 · DOI
- [30]Tang W White fat progenitor cells reside in the adipose vasculature Science 2008 322 5901 583 6 10.1126/science.1156232 18801968 PMC2597101 · DOI · Paper page
- [31]Sanchez-Gurmaches J Guertin DA Adipocyte lineages: tracing back the origins of fat Biochim Biophys Acta 2014 1842 3 340 51 10.1016/j.bbadis.2013.05.027 23747579 PMC3805734 · DOI
- [32]Hirsch J Han PW Cellularity of rat adipose tissue: effects of growth, starvation, and obesity J Lipid Res 1969 10 1 77 82 5764119
- [33]Cristancho AG Lazar MA Forming functional fat: a growing understanding of adipocyte differentiation Nat Rev Mol Cell Biol 2011 12 11 722 34 10.1038/nrm3198 21952300 PMC7171550 · DOI · Paper page
- [34]Veldhuis JD Somatotropic and gonadotropic axes linkages in infancy, childhood, and the puberty-adult transition Endocr Rev 2006 27 2 101 40 10.1210/er.2005-0006 16434512 · DOI
- [35]Gillman MW The first months of life: a critical period for development of obesity Am J Clin Nutr 2008 87 6 1587 9 18541543 PMC4407661
- [36]Richard D Cognitive and autonomic determinants of energy homeostasis in obesity Nat Rev Endocrinol 2015 11 8 489 501 10.1038/nrendo.2015.103 26122319 · DOI
- [37]Harada K Resistance to high-fat diet-induced obesity and altered expression of adipose-specific genes in HSL-deficient mice Am J Physiol Endocrinol Metab 2003 285 6 E1182 95 10.1152/ajpendo.00259.2003 12954598 · DOI
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Johnson, N. M., Hoffmann, A. R., Behlen, J. C., Lau, C., Pendleton, D., Harvey, N., Shore, R., Li, Y., Chen, J., Tian, Y., et al. (2021) · Environmental Health and Preventive Medicine · doi:10.1186/s12199-021-00995-5 · Cited by 339 · see citing works
“[87] C57BL/ 6J mice Concentrated ambient particles, PM2.”
BackgroundMethodInfluentialXie, P., Zhao, C., Huang, W., Yong, T., Chung, A. C. K., He, K., Chen, X., & Cai, Z. (2019) · Science of The Total Environment · doi:10.1016/j.scitotenv.2018.12.007 · Cited by 28 · see citing works
- Authors
- Chen, M., Liang, S., Zhou, H., Xu, Y., Qin, X., Hu, Z., Wang, X., Qiu, L., Wang, W., Zhang, Y., & Ying, Z.
- Affiliations
- University of Maryland, Baltimore (US)
- Fudan University (CN)
- Corresponding author
- Ying, Zhekang
- ORCID
- Venue
- Particle and Fibre Toxicology
- Published
- 2017-01-18
- Volume
- 14
- Issue
- 1
- Pages
- 3-3
- ISSN
- 1743-8977 (ISSN-L)
- PMC
- PMC5423412
- OpenAlex
- W2574706107
- Cited by
- 48
- References
- 5
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 2 · 2023: 6 · 2022: 4 · 2021: 17 · 2020: 2 · 2019: 5 · 2018: 3 · 2017: 4
- FWCI
- 4.18
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Particle and Fibre Toxicology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institute of Environmental Health Sciences (R01ES024516)
- American Heart Association (13SDG17070131)
- National Natural Science Foundation of China (81270342, 21407082, 81302452)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- 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
- Keywords
- diesel exhaust particles, PM2.5, maternal exposure, developmental programming, energy metabolism, obesity, offspring body weight, dietary intake, brown adipose tissue, UCP1, adipocyte hypertrophy, epididymal adipose tissue, exposure timing
- MeSH terms
- Animals, Vehicle Emissions, Behavior, Animal, Energy Metabolism, Female, Male, Mice, Inbred C57BL, Pregnancy, Prenatal Exposure Delayed Effects, Maternal Exposure, Mice, Particulate Matter
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