Nanoparticle-rich Diesel Exhaust Research Articles

Effects of inhaled nanoparticle-rich diesel exhaust on regulation of testicular function in adult male rats

We investigated the effects of nanoparticle-rich diesel exhaust (NR-DE) on reproductive function. Eight-week-old male F344 rats were divided into 12 experimental groups and exposed to either whole NR-DE at low (15.37 μg/m3, 2.27 × 105 particles/cm3), middle (36.35 μg/m3, 5.11 × 105 particles/cm3), or high (168.84 μg/m3, 1.36 × 106 particles/cm3) concentrations or clean air for 4, 8, or 12 weeks (5 hours/day, 5 days/week). NR-DE exposure for 4 or 8 weeks did not affect body weight; however, body weight was significantly decreased in rats exposed to low- or high- concentration NR-DE for 12 weeks compared to the control group. Relative weights of testes, epididymides, seminal vesicles, and prostate had increased non-significantly in all NR-DE-exposed rats at 4, 8, and 12 weeks. Adrenal gland relative weights were significantly increased at 4 weeks in rats exposed to low-concentration NR-DE. Plasma luteinizing hormone and follicle stimulating hormone concentrations did not change significantly. Plasma testosterone concentrations were significantly increased after exposure to low- or middle-concentration NR-DE for 4 or 8 weeks compared to controls. Plasma immunoreactive (ir-) inhibin concentrations were significantly increased after exposure to high-concentration NR-DE for 4 weeks or middle- or high-concentration NR-DE for 12 weeks compared to controls. Testicular testosterone concentrations were significantly increased at 4, 8, and 12 weeks after exposure to low-concentration NR-DE compared to controls. In contrast, with exposure to low- or high-concentration NR-DE, testicular ir-inhibin concentrations were significantly greater than in controls, but only at 4 weeks. These results suggest that NR-DE inhalation disrupts the endocrine activity of the male reproductive system.

Extracellular glutamate level and NMDA receptor subunit expression in mouse olfactory bulb following nanoparticle-rich diesel exhaust exposure

In this present study, we aimed to investigate the extracellular glutamate level and memory function-related gene expression in the mouse olfactory bulb after exposure of the animals to nanoparticle-rich diesel exhaust (NRDE) with or without bacterial cell wall component. Lipoteichoic acid (LTA), a cell wall component derived from Staphylococcus aureus, was used to induce systemic inflammation. Male BALB/c mice were exposed to clean air (particle concentration, 4.58 μg/m3) or NRDE (148.86 μg/m3) 5 h per day on 5 consecutive days of the week for 4 wk with or without weekly intraperitoneal injection of LTA. We examined the extracellular glutamate levels in the olfactory bulb using in vivo microdialysis and high-performance liquid chromatography assay. Then, we collected the olfactory bulb to examine the expression of N-methyl-D-aspartate (NMDA) receptor subunits (NR1, NR2A, and NR2B) and calcium/calmodulin-dependent protein kinase (CaMK) IV and cyclic AMP response element binding protein (CREB)-1 using real-time reverse-transcription polymerase chain reaction (RT-PCR). NRDE and/or LTA caused significantly increased extracellular glutamate levels in the olfactory bulb of mice. Moreover, the exposure of mice to NRDE upregulates NR1, NR2A, NR2B, and CaMKIV mRNAs in the olfactory bulb, while LTA upregulates only NR2B and CREB1 mRNAs. These findings suggest that NRDE and LTA cause glutamate-induced neurotoxicity separately and accompanied by changes in the expression of NMDA receptor subunits and related kinase and transcription factor in the mouse olfactory bulb. This is the first study to show the correlation between glutamate toxicity and memory function-related gene expressions in the mouse olfactory bulb following exposure to NRDE.

Characterization of Dilution Conditions for Diesel Nanoparticle Inhalation Studies

Diesel exhaust nanoparticles easily coagulate during transportation from the engine to the inhalation chamber, depending on concentrations and residence times. Although dilution is effective in suppressing coagulation growth of nanoparticles, volatile organic carbon (OC) evaporates as a result of dilution. Thus, the design of an inhalation facility to investigate the health effects of nanoparticle-rich exhaust is important. In this study, we determined the optimum dilution conditions in consideration of coagulation growth and evaporation of OC for inhalation studies of nanoparticle-rich diesel exhaust. We found that a short residence time prevented coagulation growth in the primary dilution tunnel after the primary dilution or before the diluted exhaust reached the inhalation chamber after the secondary dilution. However, due to the longer residence time in the inhalation chamber, the coagulation growth occurred in the inhalation chamber depending on secondary dilution ratio which controlled exposure dose (particle concentration in the inhalation chamber). We determined that the secondary dilution ratio for the high-concentration chamber should be around 4.5 times to prevent coagulation growth and to obtain the desired exposure dose. We also found that the loss of OC was relatively independent of the secondary dilution ratio when the secondary dilution ratio was more than 10 times because it seemed to reach a gas–particle equilibrium in the inhalation chamber. We therefore set the secondary dilution ratios for the middle- and low-concentration chambers to 13.5 and 40.5 times, respectively.

Effects of in utero exposure to nanoparticle-rich diesel exhaust on testicular function in immature male rats

We investigated the effects of in utero exposure to nanoparticle-rich diesel exhaust (NR-DE) on reproductive function in male rats. Pregnant F344 rats were exposed to NR-DE (148.86 μg/m 3, 1.83 × 10 6 particles/cm 3, 3.40 ppm CO, 1.46 ppm NOx), filtered diesel exhaust (F-DE; 3.10 μg/m 3, 2.66 particles/cm 3, 3.30 ppm CO, 1.41 ppm NOx), or clean air (as a control) from gestation days 1 to 19 (gestation day 0 = day of sperm-positivity). Male offspring were examined on postnatal day 28. The relative weights of the seminal vesicle and prostate to body weight were decreased after exposure to NR-DE or F-DE compared with controls. Serum concentrations of testosterone, progesterone, corticosterone, and follicle stimulating hormone and testicular concentrations of steroidogenic acute regulatory protein and 17β-hydroxysteroid dehydrogenase mRNA were decreased after exposure to NR-DE or F-DE compared with control levels. In contrast, serum concentrations of immunoreative inhibin were increased after exposure to NR-DE or F-DE compared with control levels, whereas transcription of follicle stimulating hormone receptor mRNA was increased in the NR-DE exposure group only. These results suggest that prenatal exposure to NR-DE or F-DE leads to endocrine disruption after birth and suppresses testicular function in male rats. Because both the NR-DE and F-DE-exposed groups reacted to the same extent, the nanoparticles in DE did not contribute to the observed reproductive toxicity.

Neurotoxic effect of nanoparticle-rich diesel exhaust in the mouse olfactory bulb

Neurotoxic effect of nanoparticle-rich diesel exhaust in the mouse olfactory bulb

In utero exposure to nanoparticle-rich diesel exhaust suppressed testicular function in immature male rats

In utero exposure to nanoparticle-rich diesel exhaust suppressed testicular function in immature male rats

Spatial learning and memory function-related gene expression in the hippocampus of mouse exposed to nanoparticle-rich diesel exhaust

Diesel exhaust particles are a major constituent of ambient particulate matter, and most particles emitted directly from diesel exhaust are smaller than 1 μm in diameter. Recently, the toxicity of diesel engine-derived nanoparticles has come to be recognized as an emerging social issue. In the present study, we investigated spatial learning ability and memory function-related gene expressions in mouse hippocampus after the exposure of animals to nanoparticle-rich diesel exhaust (NRDE) with or without a bacterial cell wall component. Lipoteichoic acid (LTA), a cell wall component derived from Staphylococcus aureus, was used to induce systemic inflammation. Male BALB/c mice were exposed to clean air (particle concentration, 4.58 μg/m 3) or NRDE (148.86 μg/m 3) for 5 h per day on 5 days of the week for 4 weeks in an exposure chamber, with or without the weekly intraperitoneal injection of LTA. On the day after the final day of exposure, we used a Morris water maze apparatus to examine the ability of the animals to perform a spatial learning task. After the completion of the test, the animals were sacrificed and the hippocampus was collected from each mouse; the expressions of NMDA receptor subunits (NR1, NR2A and NR2B), proinflammatory cytokines (IL-1β and TNF-α) and the oxidative stress marker heme oxygenase 1 were then investigated using real-time RT-PCR. In the Morris water maze task, NRDE/LTA (+) group took a longer time to reach the hidden platform than clear air/LTA (−) group. However, NRDE exposure alone did not affect it. The relative mRNA levels of the NMDA receptor subunits and proinflammatory cytokines were higher in hippocampus of NRDE/LTA (+) group compared to clear air/LTA (−) group. These results indicate that co-exposure of NRDE and LTA could affect spatial learning and memory function-related gene expressions in mouse hippocampus.

Prenatal Exposure to Nanoparticle-Rich Diesel Exhaust Suppressed Testicular Function in Immature Male Rats

Prenatal Exposure to Nanoparticle-Rich Diesel Exhaust Suppressed Testicular Function in Immature Male Rats