Effect of prenatal exposure to diesel exhaust on dopaminergic system in mice

Yokota, Satoshi; Mizuo, Keisuke; Moriya, Nozomu; Oshio, Shigeru; Sugawara, Isamu; Takeda, Ken

doi:10.1016/j.neulet.2008.09.085

Cited by 98 publications

(76 citation statements)

References 24 publications

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“…In addition, serum testosterone concentration, a parameter of impulsive behavior such as aggression, was also increased by maternal exposure to DE (Yoshida et al, 2006). Furthermore, we showed that prenatal exposure to DE decreased locomotion as well as dopamine metabolites in the nucleus accumbens (Yokota et al, 2009), which was confirmed in a subsequent study (Suzuki et al, 2010).…”

supporting

confidence: 74%

Exposure to diesel exhaust during fetal period affects behavior and neurotransmitters in male offspring mice

et al. 2013

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supporting

confidence: 74%

Exposure to diesel exhaust during fetal period affects behavior and neurotransmitters in male offspring mice

et al. 2013

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“…Animal studies have confirmed these outcomes (25,38,40,44) and shown genetic and epigenetic changes in animals maternally exposed to air pollution (32). Consequences can be seen manifested as poor neurological outcomes (39,49), increased airway inflammation, and respiratory dysfunction (18). The combination of these factors leads to the hypothesis that air pollution causes an adverse intrauterine environment, altering regular development, which increases the likelihood of subsequent adult diseases.…”

mentioning

confidence: 91%

Early life exposure to air pollution induces adult cardiac dysfunction

Gorr

Velten²,

Nelin

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Exposure to ambient air pollution contributes to the progression of cardiovascular disease, particularly in susceptible populations. The objective of the present study was to determine whether early life exposure to air pollution causes persistent cardiovascular consequences measured at adulthood. Pregnant FVB mice were exposed to filtered (FA) or concentrated ambient particulate matter (PM2.5) during gestation and nursing. Mice were exposed to PM2.5 at an average concentration of 51.69 μg/m3 from the Columbus, OH region for 6 h/day, 7 days/wk in utero until weaning at 3 wk of age. Birth weight was reduced in PM2.5 pups compared with FA (1.36 ± 0.12 g FA, n = 42 mice; 1.30 ± 0.15 g PM2.5, n = 67 P = 0.012). At adulthood, mice exposed to perinatal PM2.5 had reduced left ventricular fractional shortening compared with FA-exposed mice (43.6 ± 2.1% FA, 33.2 ± 1.6% PM2.5, P = 0.001) with greater left ventricular end systolic diameter. Pressure-volume loops showed reduced ejection fraction (79.1 ± 3.5% FA, 35.5 ± 9.5% PM2.5, P = 0.005), increased end-systolic volume (10.4 ± 2.5 μl FA, 39.5 ± 3.8 μl PM2.5, P = 0.001), and reduced dP/d t maximum (11,605 ± 200 μl/s FA, 9,569 ± 800 μl/s PM2.5, P = 0.05) and minimum (−9,203 ± 235 μl/s FA, −7,045 ± 189 μl/s PM2.5, P = 0.0005) in PM2.5-exposed mice. Isolated cardiomyocytes from the hearts of PM2.5-exposed mice had reduced peak shortening (%PS, 8.53 ± 2.82% FA, 6.82 ± 2.04% PM2.5, P = 0.003), slower calcium reuptake (τ, 0.22 ± 0.09 s FA, 0.26 ± 0.07 s PM2.5, P = 0.048), and reduced response to β-adrenergic stimulation compared with cardiomyocytes isolated from mice that were exposed to FA. Histological analyses revealed greater picro-sirius red-positive-stained areas in the PM2.5 vs. FA group, indicative of increased collagen deposition. We concluded that these data demonstrate the detrimental role of early life exposure to ambient particulate air pollution in programming of adult cardiovascular diseases and the potential for PM2.5 to induce persistent cardiac dysfunction at adulthood.

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“…19,20 Laboratory studies in experimental animals have revealed neurodevelopmental and behavioral effects of PAH exposure during the prenatal and neonatal periods, including anxiety, depressionlike symptoms, and memory impairment. [20][21][22][23][24][25][26] Our previous research in a New York City birth cohort and in the present Krakow birth cohort revealed that prenatal exposure to PAH was associated with adverse cognitive outcomes at age 5 years 27,28 and with behavioral problems, including anxiety and depression, at ages 6 to 7 years in New York City. 29 Although there is some previous human evidence of interactions between socioeconomic factors and pollutants, [30][31][32][33][34] this is the first study assessing the interaction of PAHs and maternal psychological distress on neurobehavioral outcomes.…”

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confidence: 97%

Prenatal Exposure to Air Pollution, Maternal Psychological Distress, and Child Behavior

et al. 2013

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WHAT'S KNOWN ON THIS SUBJECT: Prenatal exposures to diverse pollutants and psychosocial stressors have been shown independently to adversely affect child development. Less is known about the potential interactions between these factors, although they commonly co-occur, especially in disadvantaged populations. WHAT THIS STUDY ADDS:The combination of high prenatal exposure to environmental polycyclic aromatic hydrocarbons and maternal demoralization adversely affects child behavior, and maternal demoralization has a greater effect among children with high prenatal polycyclic aromatic hydrocarbon exposure for a majority of behavioral symptoms. abstract BACKGROUND: Airborne polycyclic aromatic hydrocarbons (PAHs) are pollutants generated by combustion of fossil fuel and other organic material. Both prenatal PAH exposure and maternal psychological distress during pregnancy have each been associated with neurodevelopmental problems in children. The goal was to evaluate potential interactions between prenatal exposure to airborne PAHs and maternal psychological distress during pregnancy on subsequent behavioral problems in children. METHODS:In a longitudinal birth cohort study, 248 children of nonsmoking white women in the coal-burning region of Krakow, Poland, were followed from in utero until age 9. Prenatal PAH exposure was measured by personal air monitoring during pregnancy, maternal demoralization during pregnancy by the Psychiatric Epidemiology Research Instrument-Demoralization, and child behavior by the Child Behavior Checklist. RESULTS:Significant interactions between maternal demoralization and PAH exposure (high versus low) were identified for symptoms of anxious/ depressed, withdrawn/depressed, social problems, aggressive behavior, internalizing problems, and externalizing problems. The effects of demoralization on syndromes of anxious/depressed, withdrawn/depressed, rule-breaking, aggressive behavior, and the composite internalizing and externalizing scores were seen only in conjunction with high PAH exposure. Fewer significant effects with weaker effect sizes were observed in the low-PAH-exposure group.CONCLUSIONS: Maternal demoralization during pregnancy appears to have a greater effect on child neurobehavioral development among children who experienced high prenatal PAH exposure. The results provide the first evidence of an interaction between prenatal exposure to maternal demoralization and air pollution on child neurobehavioral development, indicating the need for a multifaceted approach to the prevention of developmental problems in children. Pediatrics 2013;132:e1284-e1294 AUTHORS:

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Effect of prenatal exposure to diesel exhaust on dopaminergic system in mice

Cited by 98 publications

References 24 publications

Exposure to diesel exhaust during fetal period affects behavior and neurotransmitters in male offspring mice

Exposure to diesel exhaust during fetal period affects behavior and neurotransmitters in male offspring mice

Early life exposure to air pollution induces adult cardiac dysfunction

Prenatal Exposure to Air Pollution, Maternal Psychological Distress, and Child Behavior

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