Quantitative assessment of nano-plastic aerosol particles emitted during machining of carbon fiber reinforced plastic.

Focusing on the relatively unexplored presence of micro- and nano-plastic aerosol particles, this study quantitatively assessed the emission of nano-plastic particles during the machining of carbon fiber reinforced plastic (CFRP) in the working environment. Measurements of aerosol particles smaller than 1 µm in size were performed by aerosol mass spectrometry. The findings revealed that concentrations of carbonous aerosol particles (organic aerosol and refractory black carbon (rBC)) were higher during working hours than during non-working hours. Positive matrix factorization identified CFRP particles as a significant source, contributing an average of approximately 30% of concentration of carbonous aerosol particles during working hours. This source apportionment was corroborated by the presence of bisphenol A and F fragments, principal components of the epoxy resins used in CFRP, and was corroborated by similarities to the carbon cluster ion distribution observed in rBC during CFRP pipe-cutting operations. Further, the particle size distribution suggested the existence of plastic aerosol particles smaller than 100 nm. This study established the method to quantitatively distinguish nano-plastic aerosol particles from other aerosol particles in high temporal resolution and these techniques are useful for accurately assessing exposure to nano-plastic aerosol particles in working environments.

Characterisation of polycyclic aromatic hydrocarbons associated with indoor PM0.1 and PM2.5 in Hanoi and implications for health risks.

Polycyclic aromatic hydrocarbons (PAHs) associated with indoor PM pose a high risk to human health because of their toxicity. A total of 160 daily samples of indoor PM2.5 and PM0.1 were collected in Hanoi and analysed for 15 PAHs. In general, the concentrations of carcinogenic PAHs (car-PAHs) accounted for 21% ± 2%, 19.1% ± 2%, and 26% ± 3% of the concentrations of 15 PAHs in PM2.5, PM0.1-2.5, and PM0.1, respectively. Higher percentages of car-PAHs were found in smaller fractions (PM0.1), which can be easily deposited deep in the pulmonary regions of the human respiratory tract. The concentrations of 15 PAHs were higher in winter than in summer. The most abundant PAH species were naphthalene and phenanthrene, accounting for 11%-21% and 19%-23%, respectively. The PAH content in PM0.1 was almost twice as high as those in PM2.5 and PM0.1-2.5. Principal component analysis found that vehicle emissions and the combustion of biomass and coal were the main outdoor sources of PAHs, whereas indoor sources included cooking activities, the combustion of incense, scented candles, and domestic uses in houses. According to the results, 60%-90% of the PM0.1-bound BaP(eq) was deposited in the alveoli region, whereas 63%-75% of the PM2.5-bound BaP(eq) was deposited in head airways (HA), implying that most of the particles deposited in the HA region were PM0.1-2.5. The contributions of dibenz[a,h]anthracene and benzo[a]pyrene were dominant and contributed from 36% to 51% and 31%-50%, respectively, to the carcinogenic potential, whereas benzo[a]pyrene contributed from 30% to 49% to the mutagenic potential for both size fractions. The incremental lifetime cancer risk, simulated by Monte Carlo simulation, was within the limits set by the US EPA, indicating an acceptable risk for the occupants. These results provide an additional scientific basis for protecting human health from exposure to indoor PAHs.

Source apportionment of anthropogenic and biogenic organic aerosol over the Tokyo metropolitan area from forward and receptor models.

Organic aerosol (OA) is a dominant component of PM2.5, and accurate knowledge of its sources is critical for identification of cost-effective measures to reduce PM2.5. For accurate source apportionment of OA, we conducted field measurements of organic tracers at three sites (one urban, one suburban, and one forest) in the Tokyo Metropolitan Area and numerical simulations of forward and receptor models. We estimated the source contributions of OA by calculating three receptor models (positive matrix factorization, chemical mass balance, and secondary organic aerosol (SOA)-tracer method) using the ambient concentrations, source profiles, and production yields of OA tracers. Sensitivity simulations of the forward model (chemical transport model) for precursor emissions and SOA formation pathways were conducted. Cross-validation between the receptor and forward models demonstrated that biogenic and anthropogenic SOA were better reproduced by the forward model with updated modules for emissions of biogenic volatile organic compounds (VOC) and for SOA formation from biogenic VOC and intermediate-volatility organic compounds than by the default setup. The source contributions estimated by the forward model generally agreed with those of the receptor models for the major OA sources: mobile sources, biomass combustion, biogenic SOA, and anthropogenic SOA. The contributions of anthropogenic SOA, which are the main focus of this study, were estimated by the forward and receptor models to have been between 9 % and 15 % in summer 2019. The observed percent modern carbon data indicate that the amounts of anthropogenic SOA produced during daytime have substantially declined from 2007 to 2019. This trend is consistent with the decreasing trend of anthropogenic VOC, suggesting that reduction of anthropogenic VOC has been effective in reducing anthropogenic SOA in the atmosphere.

Assessing oxidative stress induction ability and oxidative potential of PM2.5 in cities in eastern and western Japan.

Oxidative stress is an important cause of respiratory diseases associated with exposure to PM2.5. Accordingly, acellular methods for assessing the oxidative potential (OP) of PM2.5 have been evaluated extensively for use as indicators of oxidative stress in living organisms. However, OP-based assessments only reflect the physicochemical properties of particles and do not consider particle-cell interactions. Therefore, to determine the potency of OP under various PM2.5 scenarios, oxidative stress induction ability (OSIA) assessments were performed using a cell-based method, the heme oxygenase-1 (HO-1) assay, and the findings were compared with OP measurements obtained using an acellular method, the dithiothreitol assay. For these assays, PM2.5 filter samples were collected in two cities in Japan. To quantitatively determine the relative contribution of the quantity of metals and subtypes of organic aerosols (OA) in PM2.5 to the OSIA and the OP, online measurements and offline chemical analysis were also performed. The findings showed a positive relationship between the OSIA and OP for water-extracted samples, confirming that the OP is generally well suited for use as an indicator of the OSIA. However, the correspondence between the two assays differed for samples with a high water-soluble (WS)-Pb content, which had a higher OSIA than would be expected from the OP of other samples. The results of reagent-solution experiments showed that the WS-Pb induced the OSIA, but not the OP, in 15-min reactions, suggesting a reason for the inconsistent relationship between the two assays across samples. Multiple linear regression analyses and reagent-solution experiments showed that WS transition metals and biomass burning OA accounted for approximately 30-40% and 50% of the total OSIA or the total OP of water-extracted PM2.5 samples, respectively. This is the first study to evaluate the association between cellular oxidative stress assessed by the HO-1 assay and the different subtypes of OA.

Factory site analysis of respirable fibers generated during the process of cutting and grinding of carbon fibers-reinforced plastics.

OBJECTIVES: Carbon fibers are used in a variety of industrial applications, based on their lightweight and high stiffness properties. There is little information on the characteristics and exposure levels of debris generated during the factory processing of carbon fibers or their composites. This study revisits the general assumption that carbon fibers or their debris released during composite processing are considered safe for human health. METHODS: The present interventional study was conducted at a factory located in Japan, and involved on-site collection of debris generated during the industrial processing of polyacrylonitrile (PAN)-based carbon-fiber-reinforced plastic (CFRP). The debris were collected before being exhausted locally from around different factory machines and examined morphologically and quantitatively by scanning electron microscopy. The levels of exposure to respirable carbon fibers at different areas of the factory were also quantified. RESULTS: The collected debris mainly contained the original carbon fibers broken transversely at the fiber's major axis. However, carbon fiber fragments morphologically compatible with the WHO definition of respirable fibers (length: > 5 µm, width: < 3 µm, length/width ratio: > 3:1) were also found. The concentrations of respirable fibers at the six examined factory areas under standard working conditions in the same factory were below the standard limit of 10 fibers/L, specified for asbestos dust-generating facilities under the Air Pollution Control Law in Japan. CONCLUSIONS: Our study identified potentially dangerous respirable fibers with high aspect ratio, which was generated during the processing of PAN-based CFRP. Regular risk assessment of carbon fiber debris is necessary to ensure work environment safety.

Early-Life Exposure to Traffic-Related Air Pollutants Induced Anxiety-like Behaviors in Rats via Neurotransmitters and Neurotrophic Factors.

Recent epidemiological studies have reported significantly increasing hospital admission rates for mental disorders such as anxiety and depression, not only in adults but also in children and adolescents, indicating more research is needed for evaluation of the etiology and possible reduction and prevention of these disorders. The aim of the present study was to examine the associations between perinatal exposure to traffic-related air pollutants and anxiety-like behaviors and alterations in neurological and immunological markers in adulthood using a rat model. Sprague Dawley pregnant rats were exposed to clean air (control), diesel exhaust (DE) 101 ± 9 µg/m3 or diesel exhaust origin secondary organic aerosol (DE-SOA) 118 ± 23 µg/m3 from gestational day 14 to postnatal day 21. Anxiety-related behavioral tests including open field tests, elevated plus maze, light/dark transition tests and novelty-induced hypophagia were performed on 10-week-old rats. The hippocampal expression of neurotransmitters, neurotrophic factors, and inflammatory molecular markers was examined by real-time RT-PCR. Anxiety-like behaviors were observed in both male and female rat offspring exposed to DE or DE-SOA. Moreover, serotonin receptor (5HT1A), dopamine receptor (Drd2), brain-derived neurotrophic factor and vascular endothelial growth factor A mRNAs were significantly decreased, whereas interleukin-1ß, cyclooxygenase-2, heme oxygenase-1 mRNAs and microglial activation were significantly increased in both male and female rats. These findings indicate that brain developmental period exposure to traffic-related air pollutants may induce anxiety-like behaviors via modulation of neurotransmitters, neurotrophic factors, and immunological molecular markers, triggering neuroinflammation and microglia activation in rats.

Simulation of the transition metal-based cumulative oxidative potential in East Asia and its emission sources in Japan.

The aerosol oxidative potential (OP) is considered to better represent the acute health hazards of aerosols than the mass concentration of fine particulate matter (PM2.5). The proposed major contributors to OP are water soluble transition metals and organic compounds, but the relative magnitudes of these compounds to the total OP are not yet fully understood. In this study, as the first step toward the numerical prediction of OP, the cumulative OP (OPtm*) based on the top five key transition metals, namely, Cu, Mn, Fe, V, and Ni, was defined. The solubilities of metals were assumed constant over time and space based on measurements. Then, the feasibility of its prediction was verified by comparing OPtm* values based on simulated metals to that based on observed metals in East Asia. PM2.5 typically consists of primary and secondary species, while OPtm* only represents primary species. This disparity caused differences in the domestic contributions of PM2.5 and OPtm*, especially in large cities in western Japan. The annual mean domestic contributions of PM2.5 were 40%, while those of OPtm* ranged from 50 to 55%. Sector contributions to the OPtm* emissions in Japan were also assessed. The main important sectors were the road brake and iron-steel industry sectors, followed by power plants, road exhaust, and railways.

Source contributions to multiple toxic potentials of atmospheric organic aerosols.

Fine particulate matter (PM2.5) in the atmosphere is of high priority for air quality management efforts to address adverse health effects in human. We believe that emission control policies, which are traditionally guided by source contributions to PM mass, should also consider source contributions to PM health effects or toxicity. In this study, we estimated source contributions to the toxic potentials of organic aerosols (OA) as measured by a series of chemical and in-vitro biological assays and chemical mass balance model. We selected secondary organic aerosols (SOA), vehicles, biomass open burning, and cooking as possible important OA sources. Fine particulate matter samples from these sources and parallel atmospheric samples from diverse locations and seasons in East Asia were collected for the study. The source and atmospheric samples were analyzed for chemical compositions and toxic potentials, i.e. oxidative potential, inflammatory potential, aryl hydrocarbon receptor (AhR) agonist activity, and DNA-damage, were measured. The toxic potentials per organic carbon (OC) differed greatly among source and ambient particulate samples. The source contributions to oxidative and inflammatory potentials were dominated by naphthalene-derived SOA (NapSOA), followed by open burning and vehicle exhaust. The AhR activity was dominated by open burning, followed by vehicle exhaust and NapSOA. The DNA damage was dominated by vehicle exhaust, followed by open burning. Cooking and biogenic SOA had smaller contributions to all the toxic potentials. Regarding atmospheric OA, urban and roadside samples showed stronger toxic potentials per OC. The toxic potentials of remote samples in summer were consistently very weak, suggesting that atmospheric aging over a long time decreased the toxicity. The toxic potentials of the samples from the forest and the experimentally generated biogenic SOA were low, suggesting that toxicity of biogenic primary and secondary particles is relatively low.

Perinatal Exposure to Diesel Exhaust-Origin Secondary Organic Aerosol Induces Autism-Like Behavior in Rats.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social communication, poor social interactions, and repetitive behaviors. We aimed to examine autism-like behaviors and related gene expressions in rats exposed to diesel exhaust (DE)-origin secondary organic aerosol (DE-SOA) perinatally. Sprague-Dawley pregnant rats were exposed to clean air (control), DE, and DE-SOA in the exposure chamber from gestational day 14 to postnatal day 21. Behavioral phenotypes of ASD were investigated in 10~13-week-old offspring using a three-chambered social behavior test, social dominance tube test, and marble burying test. Prefrontal cortex was collected to examine molecular analyses including neurological and immunological markers and glutamate concentration, using RT-PCR and ELISA methods. DE-SOA-exposed male and female rats showed poor sociability and social novelty preference, socially dominant behavior, and increased repetitive behavior. Serotonin receptor (5-HT(5B)) and brain-derived neurotrophic factor (BDNF) mRNAs were downregulated whereas interleukin 1 ß (IL-ß) and heme oxygenase 1 (HO-1) mRNAs were upregulated in the prefrontal cortex of male and female rats exposed to DE-SOA. Glutamate concentration was also increased significantly in DE-SOA-exposed male and female rats. Our results indicate that perinatal exposure to DE-SOA may induce autism-like behavior by modulating molecules such as neurological and immunological markers in rats.

Volatility Distribution of Organic Compounds in Sewage Incineration Emissions.

Intermediate volatility and semivolatile organic compounds (IVOC/SVOC) are important precursors of secondary organic aerosol (SOA) while SVOC is an important contributor to primary organic aerosol (POA). However, combustion emissions data for volatility classes are limited. This study reports the gas and particle emissions that were sampled with various dilution factors from a sewage sludge incinerator burning fuel oil. Volatility distributions were determined using measurements from online mass spectrometry and offline organic compound analyses. In the low volatility organic compound (LVOC) to IVOC range, volatility bins with organic saturation concentrations of 10-100 µg m-3 were most abundant, which was due to organic acids generated from sludge burning. Organic aerosol (OA) emission factors (EFOA) increased 1.4 times after cooling to ambient temperatures in comparison to those of the samples from the hot stack. Upon further isothermal dilution at 25 °C, the EFOA decreased while organic gas phase EFs increased with increasing dilution. Phase partitioning in volatility bins with saturation concentrations of 10-100 µg m-3 was sensitive to isothermal dilution that influenced the EFs. Therefore, gas- and particle-phase measurements alone cannot constrain EFs for these volatility classes. Low dilution factors may overestimate the particle phase and underestimate the gas phase EFs compared with real-world emission conditions.

Modeling Transition Metals in East Asia and Japan and Its Emission Sources.

Emission inventories of anthropogenic transition metals, which contribute to aerosol oxidative potential (OP), in Asia (Δx = 0.25°, monthly, 2000-2008) and Japan (Δx = 2 km, hourly, mainly 2012) were developed, based on bottom-up inventories of particulate matters and metal profiles in a speciation database for particulate matters. The new inventories are named Transition Metal Inventory (TMI)-Asia v1.0 and TMI-Japan v1.0, respectively. It includes 10 transition metals in PM2.5 and PM10, which contributed to OP based on reagent experiments, namely, Cu, Mn, Co, V, Ni, Pb, Fe, Zn, Cd, and Cr. The contributions of sectors in the transition metals emission in Japan were also investigated. Road brakes and iron-steel industry are primary sources, followed by other metal industry, navigation, incineration, power plants, and railway. In order to validate the emission inventory, eight elements such as Cu, Mn, V, Ni, Pb, Fe, Zn, and Cr in anthropogenic dust and those in mineral dust were simulated over East Asia and Japan with Δx = 30 km and Δx = 5 km domains, respectively, and compared against the nation-wide seasonal observations of PM2.5 elements in Japan and the long-term continuous observations of total suspended particles (TSPs) at Yonago, Japan in 2013. Most of the simulated elements generally agreed with the observations, while Cu and Pb were significantly overestimated. This is the first comprehensive study on the development and evaluation of emission inventory of OP active elements, but further improvement is needed.

The toxicological analysis of secondary organic aerosol in human lung epithelial cells and macrophages.

Secondary organic aerosol (SOA) is a component of airborne particulate matter in urban areas. However, their toxicities remain incompletely understood. In this study, we investigated the oxidative and inflammatory potency of SOA derived from three different volatile organic compounds (α-pinene, m-xylene, and trimethylbenzene) using human bronchial epithelial cells (BEAS-2B) and macrophages (U937). In BEAS-2B cells, all types of SOA extracts increased the expression of the heme oxygenase 1 (HMOX1) and interleukin-8 (IL8) genes, a typical marker for oxidative stress and inflammatory responses, respectively. Among the three types of SOA, m-xylene-derived SOA showed the strongest induction of the HMOX1 and IL8 genes, and transcriptional activity via the antioxidant response element (ARE). A causal candidate for SOA induction of oxidative stress is 2,6-dimethyl-1,4-benzoquinone (DMBQ) because only this quinone compound increased the transcriptional activity via ARE among components tested in this study. Similar to the case of BEAS-2B cells, SOA extracts increased the expression of HMOX1 and IL8 genes in U937 cells, mainly through oxidative stress, but these responses in U937 cells were prolonged when compared with BEAS-2B cells. Together, these results show that SOA affects lung epithelial cells and macrophages mainly through oxidative stress and inflammation, suggesting their contribution to the development of respiratory diseases.

Contributions of Condensable Particulate Matter to Atmospheric Organic Aerosol over Japan.

Because emission rates of particulate matter (PM) from stationary combustion sources have been measured without dilution or cooling in Japan, condensable PM has not been included in Japanese emission inventories. In this study, we modified an emission inventory to include condensable PM from stationary combustion sources based on the recent emission surveys using a dilution method. As a result, emission rates of organic aerosol (OA) increased by a factor of 7 over Japan. Stationary combustion sources in the industrial and energy sectors became the largest contributors to OA emissions over Japan in the revised estimates (filterable-plus-condensable PM), while road transport and biomass burning were the dominant OA sources in the previous estimate (filterable PM). These results indicate that condensable PM from large combustion sources makes critical contributions to total PM2.5 emissions. Simulated contributions of condensable PM from combustion sources to atmospheric OA drastically increased around urban and industrial areas, including the Kanto region, where OA concentrations increased by factors of 2.5-6.1. Consideration of condensable PM from stationary combustion sources improved model estimates of OA in winter but caused overestimation of OA concentrations in summer. Contributions of primary and secondary OA should be further evaluated by comparing with organic tracer measurements.

Effects of diesel exhaust-derived secondary organic aerosol (SOA) on oocytes: Potential risks to meiotic maturation.

Particulate air pollution (PM 2.5) is a worldwide concern. Growing epidemiological evidence has shown pathophysiological effects of PM 2.5, not only on cardiovascular system but also on reproductive performance. The composition and physicochemical properties of PM 2.5 vary depending on the emission sources, climate conditions, and complex chemical reactions in the air. These factors make it difficult to understand the cause and mechanistic details of the adverse health effects of PM 2.5. Here, we show potential impacts of PM 2.5 on oocyte maturation in mice by utilizing diesel exhaust-derived secondary organic aerosol (SOA), a major component of urban PM 2.5. We found that the SOA destabilized microtubules of mouse oocytes and p-benzoquinone is one of the candidates for the microtubule-destabilizing compounds. We propose that some biologically reactive components of PM 2.5 should be prioritized for the regulation of atmospheric quality.

Role of TLR4 in olfactory-based spatial learning activity of neonatal mice after developmental exposure to diesel exhaust origin secondary organic aerosol.

Exposure to ambient air pollutants has been reported to have various adverse health impacts. Ambient particulate matter comprises primary particles released directly via engine exhaust and secondary organic aerosols (SOAs) formed from oxidative reactions of the ultrafine particle fraction of diesel exhaust (DE). Toll-like receptor 4 (TLR4) is well known to initiate the inflammatory cascade in the central nervous system. However, whether and how DE and DE-SOA exposure influences TLR4 signaling in the immature brain remains unclear. We attempted to evaluate the roles of TLR-4, inflammatory mediators and microglial markers in the impaired spatial learning ability of neonatal mice exposed to DE and DE-SOAs. Pregnant C3H/HeN (TLR4-intact) and C3H/HeJ (TLR4- mutated) mice were exposed to clean air, DE or DE-SOA from gestational day 14 to postnatal day (PND) 10 (5h/day for 5days) in exposure chambers. PND11 neonatal mice were examined for their performance in the olfactory-based spatial learning test. After the spatial learning test, the hippocampi of the mice were removed and real-time RT-PCR analysis was performed to examine the neurological and immunological markers. Both male and female C3H/HeN and C3H/HeJ neonatal mice exposed to DE and DE-SOAs showed poor performance in the test phase of spatial learning as compared to the mice exposed to clean air. However, this spatial learning deficit was prominent in C3H/HeJ neonatal mice. In the neonatal C3H/HeN male mice exposed to DE and DE-SOAs, the mRNA expression levels of the NMDA receptor subunits (NR1, NR2B), proinflammatory cytokines, tumor necrosis factor-α and cyclooxygenase-2, oxidative stress marker, heme oxygenase-1, and microglial marker, Iba1, in the hippocampus were significantly increased, but these changes were not observed in female mice. Our findings indicate that activation of the neuroimmune system and TLR4 signaling may possibly be involved in environmental pollutant-induced spatial learning impairment in neonatal mice.

Aerosol Health Effects from Molecular to Global Scales.

Poor air quality is globally the largest environmental health risk. Epidemiological studies have uncovered clear relationships of gaseous pollutants and particulate matter (PM) with adverse health outcomes, including mortality by cardiovascular and respiratory diseases. Studies of health impacts by aerosols are highly multidisciplinary with a broad range of scales in space and time. We assess recent advances and future challenges regarding aerosol effects on health from molecular to global scales through epidemiological studies, field measurements, health-related properties of PM, and multiphase interactions of oxidants and PM upon respiratory deposition. Global modeling combined with epidemiological exposure-response functions indicates that ambient air pollution causes more than four million premature deaths per year. Epidemiological studies usually refer to PM mass concentrations, but some health effects may relate to specific constituents such as bioaerosols, polycyclic aromatic compounds, and transition metals. Various analytical techniques and cellular and molecular assays are applied to assess the redox activity of PM and the formation of reactive oxygen species. Multiphase chemical interactions of lung antioxidants with atmospheric pollutants are crucial to the mechanistic and molecular understanding of oxidative stress upon respiratory deposition. The role of distinct PM components in health impacts and mortality needs to be clarified by integrated research on various spatiotemporal scales for better evaluation and mitigation of aerosol effects on public health in the Anthropocene.

Exposure of BALB/c Mice to Diesel Engine Exhaust Origin Secondary Organic Aerosol (DE-SOA) during the Developmental Stages Impairs the Social Behavior in Adult Life of the Males.

Secondary organic aerosol (SOA) is a component of particulate matter (PM) 2.5 and formed in the atmosphere by oxidation of volatile organic compounds. Recently, we have reported that inhalation exposure to diesel engine exhaust (DE) originated SOA (DE-SOA) affect novel object recognition ability and impair maternal behavior in adult mice. However, it is not clear whether early life exposure to SOA during the developmental stages affect social behavior in adult life or not. In the present study, to investigate the effects of early life exposure to DE-SOA during the gestational and lactation stages on the social behavior in the adult life, BALB/c mice were exposed to clean air (control), DE, DE-SOA and gas without any PM in the inhalation chambers from gestational day 14 to postnatal day 21 for 5 h a day and 5 days per week. Then adult mice were examined for changes in their social behavior at the age of 13 week by a sociability and social novelty preference, social interaction with a juvenile mouse and light-dark transition test, hypothalamic mRNA expression levels of social behavior-related genes, estrogen receptor-alpha and oxytocin receptor as well as of the oxidative stress marker gene, heme oxygenase (HO)-1 by real-time RT-PCR method. In addition, hypothalamic level of neuronal excitatory marker, glutamate was determined by ELISA method. We observed that sociability and social novelty preference as well as social interaction were remarkably impaired, expression levels of estrogen receptor-alpha, oxytocin receptor mRNAs were significantly decreased, expression levels of HO-1 mRNAs and glutamate levels were significantly increased in adult male mice exposed to DE-SOA compared to the control ones. Findings of this study indicate early life exposure of BALB/c mice to DE-SOA may affect their late-onset hypothalamic expression of social behavior related genes, trigger neurotoxicity and impair social behavior in the males.

Nano-Sized Secondary Organic Aerosol of Diesel Engine Exhaust Origin Impairs Olfactory-Based Spatial Learning Performance in Preweaning Mice.

The aims of our present study were to establish a novel olfactory-based spatial learning test and to examine the effects of exposure to nano-sized diesel exhaust-origin secondary organic aerosol (SOA), a model environmental pollutant, on the learning performance in preweaning mice. Pregnant BALB/c mice were exposed to clean air, diesel exhaust (DE), or DE-origin SOA (DE-SOA) from gestational day 14 to postnatal day (PND) 10 in exposure chambers. On PND 11, the preweaning mice were examined by the olfactory-based spatial learning test. After completion of the spatial learning test, the hippocampus from each mouse was removed and examined for the expressions of neurological and immunological markers using real-time RT-PCR. In the test phase of the study, the mice exposed to DE or DE-SOA took a longer time to reach the target as compared to the control mice. The expression levels of neurological markers such as the N-methyl-d-aspartate (NMDA) receptor subunits NR1 and NR2B, and of immunological markers such as TNF-α, COX2, and Iba1 were significantly increased in the hippocampi of the DE-SOA-exposed preweaning mice as compared to the control mice. Our results indicate that DE-SOA exposure in utero and in the neonatal period may affect the olfactory-based spatial learning behavior in preweaning mice by modulating the expressions of memory function-related pathway genes and inflammatory markers in the hippocampus.

Effects of diesel engine exhaust origin secondary organic aerosols on novel object recognition ability and maternal behavior in BALB/c mice.

Epidemiological studies have reported an increased risk of cardiopulmonary and lung cancer mortality associated with increasing exposure to air pollution. Ambient particulate matter consists of primary particles emitted directly from diesel engine vehicles and secondary organic aerosols (SOAs) are formed by oxidative reaction of the ultrafine particle components of diesel exhaust (DE) in the atmosphere. However, little is known about the relationship between exposure to SOA and central nervous system functions. Recently, we have reported that an acute single intranasal instillation of SOA may induce inflammatory response in lung, but not in brain of adult mice. To clarify the whole body exposure effects of SOA on central nervous system functions, we first created inhalation chambers for diesel exhaust origin secondary organic aerosols (DE-SOAs) produced by oxidation of diesel exhaust particles caused by adding ozone. Male BALB/c mice were exposed to clean air (control), DE and DE-SOA in inhalation chambers for one or three months (5 h/day, 5 days/week) and were examined for memory function using a novel object recognition test and for memory function-related gene expressions in the hippocampus by real-time RT-PCR. Moreover, female mice exposed to DE-SOA for one month were mated and maternal behaviors and the related gene expressions in the hypothalamus examined. Novel object recognition ability and N-methyl-D-aspartate (NMDA) receptor expression in the hippocampus were affected in male mice exposed to DE-SOA. Furthermore, a tendency to decrease maternal performance and significantly decreased expression levels of estrogen receptor (ER)-α, and oxytocin receptor were found in DE-SOA exposed dams compared with the control. This is the first study of this type and our results suggest that the constituents of DE-SOA may be associated with memory function and maternal performance based on the impaired gene expressions in the hippocampus and hypothalamus, respectively.

Effects of exposure to nanoparticle-rich diesel exhaust on 8-OHdG synthesis in the mouse asthmatic lung.

It has been demonstrated that exposure to diesel exhaust (DE) is associated with the induction and exacerbation of respiratory disorders; however, the impacts of DE containing mainly nanoparticles have been less studied. We have previously demonstrated that inhalation exposure to nanoparticle-rich DE (NR-DE) exacerbated allergic pulmonary inflammation, in the context of enhanced local expression of proinflammatory molecules. However, the underlying mechanisms have not been fully elucidated. 8-Hydroxydeoxyguanosine (8-OHdG) is a marker of oxidative damage, particularly in DNA. This study examined the effects of NR-DE on 8-OHdG synthesis in the lung in the presence or absence of an allergen. Institute for Cancer Research (ICR) mice were exposed by inhalation to four different gas compositions (control air, low-concentration DE, high-concentration DE and high-concentration DE without particulate matter) for 8 weeks, in the presence or absence of repetitive intratracheal administration of ovalbumin (OVA). Thereafter, we assessed the levels of 8-OHdG synthesis and expression in the lungs by means of enzyme immunoassay (EIA) and immunohistochemistry. The EIA revealed that the level of 8-OHdG was significantly higher in the high-concentration NR-DE-exposed and allergen-sensitized/stimulated group compared with that in the control air-exposed and allergen-treated group. The immunohistochemistry results demonstrated that the level of immunoreactive 8-OHdG was higher in the NR-DE-exposed and allergen-treated lungs compared with that in the corresponding control air-exposed lungs. The results suggested that NR-DE exposure enhanced 8-OHdG formation in asthmatic lungs. This, at least in part, is involved in the NR-DE-mediated exacerbation of the allergic pathophysiology that was identified in our previous study.