Incidence of cardiovascular disease in a cohort of mine workers exposed to ultrafine aluminum powder in Ontario, Canada.

BACKGROUND: A retrospective cohort study was conducted to estimate associations between an ultrafine aluminum powder, McIntyre Powder (MP), and cardiovascular disease incidence in a cohort of mine workers from Ontario, Canada. Disease outcomes included ischemic heart disease (IHD), acute myocardial infarction (AMI), congestive heart failure (CHF), and strokes and transient ischemic attacks (STIA). METHODS: Using work history records from the Ontario Mining Master File (MMF) mine workers were followed for disease incidence in administrative health records. The analysis included 25,813 mine workers who were exposed to MP between 1943 and 1979 and followed for cardiovascular disease (CVD) diagnoses between 2006 and 2018. Cardiovascular disease cases were ascertained using physician, hospital, and ambulatory care records. Poisson regression models were used to estimate age and birth-year adjusted incidence rate ratios (RR) and 95% confidence intervals (CI) for associations between MP exposure and CVD outcomes. RESULTS: Ever-exposure to MP was positively associated with modest increases in the incidence rate of IHD, AMI, and CHF, but not STIA, using both assessment approaches. Duration of self-reported MP exposure was positively associated with monotonically increasing rates of IHD and AMI compared to never-exposed miners, with the greatest association observed among miners with >20 years of exposure (for IHD: RR 1.24, 95% CI: 0.91-1.68; and for AMI: RR 1.52, 95% CI 1.01-2.28). CONCLUSION: Mine workers ever-exposed to MP had modestly elevated rates of CVD. The rate of CVD diagnoses appeared to increase with longer duration of exposure when assessed by both self-reported exposure and through historical records.

Sub-23 nm Particles Dominate Non-Volatile Particle Number Emissions of Road Traffic.

Ultrafine particles (<100 nm) in urban air are a serious health hazard not yet fully understood. Therefore, particle number concentration monitoring was recently included in the WHO air quality guidelines. At present, e.g., the EU regulates particle number only regarding the emissions of solid particles larger than 23 nm emitted by vehicles. The aim of this study was to examine the non-volatile fraction of sub-23 nm particles in a traffic-influenced urban environment. We measured the number concentration of particles larger than 1.4, 3, 10, and 23 nm in May 2018. Volatile compounds were thermally removed in the sampling line and the line losses were carefully determined. According to our results, the sub-23 nm particles dominated the non-volatile number concentrations. Additionally, based on the determined particle number emission factors, the traffic emissions of non-volatile sub-10 nm particles can be even 3 times higher than those of particles larger than 10 nm. Yet, only a fraction of urban sub-10 nm particles consisted of non-volatiles. Thus, while the results highlight the role of ultrafine particles in the traffic-influenced urban air, a careful consideration is needed in terms of future particle number standards to cover the varying factors affecting measured concentrations.

Biological impact of sequential exposures to allergens and ultrafine particle-rich combustion aerosol on human bronchial epithelial BEAS-2B cells at the air liquid interface.

The prevalence of allergic diseases is constantly increasing since few decades. Anthropogenic ultrafine particles (UFPs) and allergenic aerosols is highly involved in this increase; however, the underlying cellular mechanisms are not yet understood. Studies observing these effects focused mainly on singular in vivo or in vitro exposures of single particle sources, while there is only limited evidence on their subsequent or combined effects. Our study aimed at evaluating the effect of subsequent exposures to allergy-related anthropogenic and biogenic aerosols on cellular mechanism exposed at air-liquid interface (ALI) conditions. Bronchial epithelial BEAS-2B cells were exposed to UFP-rich combustion aerosols for 2 h with or without allergen pre-exposure to birch pollen extract (BPE) or house dust mite extract (HDME). The physicochemical properties of the generated particles were characterized by state-of-the-art analytical instrumentation. We evaluated the cellular response in terms of cytotoxicity, oxidative stress, genotoxicity, and in-depth gene expression profiling. We observed that single exposures with UFP, BPE, and HDME cause genotoxicity. Exposure to UFP induced pro-inflammatory canonical pathways, shifting to a more xenobiotic-related response with longer preincubation time. With additional allergen exposure, the modulation of pro-inflammatory and xenobiotic signaling was more pronounced and appeared faster. Moreover, aryl hydrocarbon receptor (AhR) signaling activation showed to be an important feature of UFP toxicity, which was especially pronounced upon pre-exposure. In summary, we were able to demonstrate the importance of subsequent exposure studies to understand realistic exposure situations and to identify possible adjuvant allergic effects and the underlying molecular mechanisms.

Fine and ultrafine particle- and gas-polycyclic aromatic hydrocarbons affecting southern Thailand air quality during transboundary haze and potential health effects.

Distribution of PM0.1, PM1 and PM2.5 particle- and gas-polycyclic aromatic hydrocarbons (PAHs) during the 2019 normal, partial and strong haze periods at a background location in southern Thailand were investigated to understand the behaviors and carcinogenic risks. PM1 was the predominant component, during partial and strong haze periods, accounting for 45.1% and 52.9% of total suspended particulate matter, respectively, while during normal period the contribution was only 34.0%. PM0.1 concentrations, during the strong haze period, were approximately 2 times higher than those during the normal period. Substantially increased levels of particle-PAHs for PM0.1, PM1 and PM2.5 were observed during strong haze period, about 3, 5 and 6 times higher than those during normal period. Gas-PAH concentrations were 10 to 36 times higher than those of particle-PAHs for PM2.5. Average total Benzo[a]Pyrene Toxic Equivalency Quotients (BaP-TEQ) in PM0.1, PM1 and PM2.5 during haze periods were about 2-6 times higher than in the normal period. The total accumulated Incremental Lifetime Cancer Risks (ILCRs) in PM0.1, PM1 and PM2.5 for all the age-specific groups during the haze effected scenario were approximately 1.5 times higher than those in non-haze scenario, indicating a higher potential carcinogenic risk. These observations suggest PM0.1, PM1 and PM2.5 were the significant sources of carcinogenic aerosols and were significantly affected by transboundary haze from peatland fires. This leads to an increase in the volume of smoke aerosol, exerting a significant impact on air quality in southern Thailand, as well as many other countries in lower southeast Asia.

Internal Exposure and Distribution of Airborne Fine Particles in the Human Body: Methodology, Current Understandings, and Research Needs.

Exposure to airborne fine particles (PM2.5, particulate matter with aerodynamic diameter <2.5 µm) severely threatens global human health. Understanding the distribution and processes of inhaled PM2.5 in the human body is crucial to clarify the causal links between PM2.5 pollution and diseases. In contrast to extensive research on the emission and formation of PM2.5 in the ambient environment, reports about the occurrence and fate of PM2.5 in humans are still limited, although many studies have focused on the exposure and adverse effects of PM2.5 with animal models. It has been shown that PM2.5, especially ultrafine particles (UFPs), have the potential to go across different biological barriers and translocate into different human organs (i.e., blood circulation, brain, heart, pleural cavity, and placenta). In this Perspective, we summarize the factors affecting the internal exposure of PM2.5 and the relevant analytical methodology and review current knowledge about the exposure pathways and distribution of PM2.5 in humans. We also discuss the research challenges and call for more studies on the identification and characterization of key toxic species of PM2.5, quantification of internal exposure doses in the general population, and further clarification of translocation, metabolism, and clearance pathways of PM2.5 in the human body. In this way, it is possible to develop toxicity-based air quality standards instead of the currently used mass-based standards.

Systematic ranking of filaments regarding their particulate emissions during fused filament fabrication 3D printing by means of a proposed standard test method.

The diversity of fused filament fabrication (FFF) filaments continues to grow rapidly as the popularity of FFF-3D desktop printers for the use as home fabrication devices has been greatly increased in the past decade. Potential harmful emissions and associated health risks when operating indoors have induced many emission studies. However, the lack of standardization of measurements impeded an objectifiable comparison of research findings. Therefore, we designed a chamber-based standard method, i.e., the strand printing method (SPM), which provides a standardized printing procedure and quantifies systematically the particle emission released from individual FFF-3D filaments under controlled conditions. Forty-four marketable filament products were tested. The total number of emitted particles (TP) varied by approximately four orders of magnitude (109  ≤ TP ≤ 1013 ), indicating that origin of polymers, manufacturer-specific additives, and undeclared impurities have a strong influence. Our results suggest that TP characterizes an individual filament product and particle emissions cannot be categorized by the polymer type (e.g., PLA or ABS) alone. The user's choice of a filament product is therefore decisive for the exposure to released particles during operation. Thus, choosing a filament product awarded for low emissions seems to be an easily achievable preemptive measure to prevent health hazards.

Deposition potential of 0.003-10 µm ambient particles in the humidified human respiratory tract: Contribution of new particle formation events in Beijing.

Ultrafine particles (UFPs) usually explosive growth during new particle formation (NPF) events. However, the risk of exposure to UFPs on NPF days has been ignored due to the prevalence of mass-based air quality standards. In this study, the daily deposited doses, i.e., the daily deposited particle number dose (DPNd), mass dose (DPMd), and surface area dose (DPSd), of ambient particles in the human respiratory tract in Beijing were evaluated based on the particle number size distribution (3 nm-10 µm) from June 2018 to May 2019 utilizing a Multiple-Path Particle Dosimetry Model (MPPD) after the hygroscopic growth of particles in the respiratory tract had been accounted for. Our observations showed a high frequency (72.6%) of NPF on excellent air quality days, with daily mean PM2.5 concentrations less than 35 µg m-3. The daily DPNd on excellent air quality days was comparable with that on polluted days, although the DPMd on excellent air quality days was as low as 15.6% of that on polluted days. The DPNd on NPF days was ~1.3 times that on non-NPF days. The DPNd in respiratory tract regions decreased in the order: tracheobronchial (TB) > pulmonary (PUL) > extrathoracic (ET) on NPF days, while it was PUL > TB > ET on non-NPF days. The number of deposited nucleation mode particles, which were deposited mainly in the TB region (45%), was 2 times higher on NPF days than that on non-NPF days. Our results demonstrated that the deposition potential due to UFPs in terms of particle number concentrations is high in Beijing regardless of the aerosol mass concentration. More toxicological studies related to UFPs on NPF days, especially those targeting tracheobronchial and pulmonary impairment, are required in the future.

Size-segregated particle number concentrations and outpatient-department visits for pediatric respiratory diseases in Shanghai, China.

BACKGROUND: Few studies have simultaneously explored which size of particles has the greatest impact on the risk for pediatric asthma, bronchitis and upper respiratory tract infections (URTIs). OBJECTIVES: To investigate the short-term association between size-segregated particle number concentrations (PNCs) and outpatient-department visits (ODVs) for major pediatric respiratory diseases. METHODS: Daily counts of pediatric ODVs for asthma, bronchitis and URTIs were obtained from 66 hospitals in Shanghai, China, from 2016 to 2018. Pollutant effects were estimated using Poisson generalized additive models combined with polynomial distributed lag models. We also fitted co-pollutant cumulative effects models included six criteria air pollutants and conducted stratifying analyses by gender, age, season and geographic distances. RESULTS: We identified a total of 430,103 patients with asthma, 1,547,013 patients with bronchitis, and 2,155,738 patients with URTIs from the hospitals. Effect estimates increased with decreasing particle size. Ultrafine particle (UFP) and PNCs of 0.10-0.40 µm particles (PNC0.10-0.40) were associated with increased ODVs for asthma, bronchitis and URTIs at cumulative lags up to 3d. Associations tended to appear stable after adjusting for criteria air pollutants. At the cumulative lag 0-2d, each interquartile range increase in UFP was associated with increased ODVs due to asthma (relative risk 1.21, 95% CI: 1.07, 1.38), bronchitis (1.20, 95% CI: 1.07, 1.34) and URTI (1.17, 95% CI: 1.06, 1.30), whereas the associations for PNC0.10-0.40 remained significant but attenuated in magnitude. CONCLUSIONS: UFP may be a leading contributor to the adverse respiratory effects of particulate air pollution and the effects increased with decreasing particle size.

The impact of solar activity on ambient ultrafine particle concentrations: An analysis based on 19-year measurements in Boston, USA.

Solar radiation plays a major role in atmospheric photochemistry, contributing to the formation and growth of ultrafine particles (PN). PN affect global Earth's radiation balance, climate system, and human health. However, the impact of solar activity on ambient PN remains unclear. In this study, we investigated the associations between daily ambient PN concentrations [particle number (PN)/cm3] and solar radio flux [solar activity index (F10.7 in sfu)] as a solar activity parameter, shortwave solar radiation (SWR), daylight time (DL), cosmic ray-induced ionization (CRII), and air pollution [PM2.5, black carbon (BC) and SO2] over a 19-year period in Boston, MA. We used generalized additive models adjusted for local environmental conditions. We found that F10.7 was the strongest predictor for daily PN concentrations over all time lags (0-28 days of lags) and seasons. The effects were higher in winter and fall. In winter, an interquartile (IQR) of 60 sfu F10.7 corresponded to an increase of 5770 PN/cm3 in the day of PN collection. In fall, an IQR of 75.5 sfu F10.7 was associated with an increase of 5429 PN/cm3. The effects of F10.7 on PN concentrations were slightly greater when the models were adjusted for air pollution. In summer, ambient PN concentrations were statistically significantly associated with F10.7, SWR, and BC, with the strongest association found for PN and BC in the day of PN collection. Unlike the effects of F10.7, SWR and local pollutants on PN concentrations, DL and CRII were negatively associated with ambient PN in the analyses. These findings suggest that solar activity may have a significant impact on daily ambient PN concentrations that affect the Earth's climate system and human health.

Particulate matter air pollution and reduced heart rate variability: How the associations vary by particle size in Shanghai, China.

BACKGROUND: It remains unclear which size of particles has the strongest effects on heart rate variability (HRV). OBJECTIVE: To explore the association between HRV parameters and daily variations of size-fractionated particle number concentrations (PNCs). METHODS: We conducted a longitudinal repeated-measure study among 78 participants with a 24-h continuous ambulatory Holter electrocardiographic recorder in Shanghai, China, from January 2015 to June 2019. Linear mixed-effects models were employed to evaluate the changes of HRV parameters associated with PNCs of 7 size ranges from 0.01 to 10 µm after controlling for environmental and individual confounders. RESULTS: On the concurrent day, decreased HRV parameters were associated with increased PNCs of 0.01-0.3 µm, and smaller particles showed greater effects. For an interquartile range increase in ultrafine particles (UFP, those < 0.1 µm, 2453 particles/cm3), the declines in very-low-frequency power, low-frequency power, high-frequency power, standard deviation of normal R-R intervals, root mean square of the successive differences between R-R intervals and percentage of adjacent normal R-R intervals with a difference ≥ 50 ms were 5.06% [95% confidence interval (CI): 2.09%, 7.94%], 7.65% (95%CI: 2.73%, 12.32%), 9.49% (95%CI: 4.64%, 14.09%), 5.10% (95%CI: 2.21%, 7.91%), 8.09% (95%CI: 4.39%, 11.65%) and 24.98% (95%CI: 14.70%, 34.02%), respectively. These results were robust to the adjustment of criteria air pollutants, temperature at different lags, and the status of heart medication. CONCLUSIONS: Particles less than 0.3 µm (especially UFP) may dominate the acute effects of particulate air pollution on cardiac autonomic dysfunction.

Shenlian extract protects against ultrafine particulate matter-aggravated myocardial ischemic injury by inhibiting inflammation response via the activation of NLRP3 inflammasomes.

Air pollution is a growing public health burden associated with several negative health effects, especially cardiovascular disease. Shenlian extract (SL), a traditional Chinese medicine, has the effects of clearing heat-toxin and promoting blood circulation for removing blood stasis, and it has long been used to treat cardiovascular diseases and atherosclerosis. This study explored the underlying action mechanism of SL against ultrafine particle-induced myocardial ischemic injury (UFP-MI) through network pharmacology prediction and experimental verification. Male Sprague-Dawley rats with UFP-MI were pre-treated with SL intragastrically for 7 days. All the rats were then euthanized. Inflammatory cytokine detection and histopathological analysis were performed to assess the protective effects of SL. For the mechanism study, differentially expressed genes (DEGs) were identified in UFP-MI rats treated with SL through transcriptomic analysis. Subsequently, in combination with network pharmacology, potential pathways involved in the effects of SL treatment were identified using the Internet-based Computation Platform (www.tcmip.cn) and Cytoscape 3.6.0. Further validation experiments were performed to reveal the mechanism of the therapeutic effects of SL on UFP-MI. The results show that SL significantly suppressed inflammatory cell infiltration into myocardial tissue and exhibited significant anti-inflammatory activity. Transcriptomic analysis revealed that the DEGs after SL treatment had significant anti-inflammatory, immunomodulatory, and anti-viral activities. Network pharmacology analysis illustrated that the targets of SL were mainly involved in regulation of the inflammatory response, apoptotic process, innate immune response, platelet activation, and coagulation process. By combining transcriptomic and network pharmacology data, we found that SL may exert anti-inflammatory effects by acting on the NOD-like signaling pathway to regulate immune response activation and inhibit systemic inflammation. Verification experiments revealed that SL can suppress the secretion of the inflammatory cytokines Interleukin-1 (IL-1), Interleukin-18(IL-18) and Interleukin-33(IL-33) and suppress NLRP3 inflammasome activity. The results suggested that SL can directly inhibit the activation of NLRP3 inflammasomes and reduce the release of cytokines to protect against ultrafine particulate matter-aggravated myocardial ischemic injury.

Spatiotemporal Variations in Ambient Ultrafine Particles and the Incidence of Childhood Asthma.

Rationale: Little is known regarding the impact of ambient ultrafine particles (UFPs; <0.1 µm) on childhood asthma development. Objectives: To examine the association between prenatal and early postnatal life exposure to UFPs and development of childhood asthma. Methods: A total of 160,641 singleton live births occurring in the City of Toronto, Canada between April 1, 2006, and March 31, 2012, were identified from a birth registry. Associations between exposure to ambient air pollutants and childhood asthma incidence (up to age 6) were estimated using random effects Cox proportional hazards models, adjusting for personal- and neighborhood-level covariates. We investigated both single-pollutant and multipollutant models accounting for coexposures to particulate matter ≤2.5 µm in aerodynamic diameter (PM2.5) and NO2. Measurements and Main Results: We identified 27,062 children with incident asthma diagnosis during the follow-up. In adjusted models, second-trimester exposure to UFPs (hazard ratio per interquartile range increase, 1.09; 95% confidence interval, 1.06-1.12) was associated with asthma incidence. In models additionally adjusted for PM2.5 and nitrogen dioxide, UFPs exposure during the second trimester of pregnancy remained positively associated with childhood asthma incidence (hazard ratio per interquartile range increase, 1.05; 95% confidence interval, 1.01-1.09). Conclusions: This is the first study to evaluate the association between perinatal exposure to UFPs and the incidence of childhood asthma. Exposure to UFPs during a critical period of lung development was linked to the onset of asthma in children, independent of PM2.5 and NO2.

Ultrafine urban particle measurements in Budapest and their airway deposition distribution calculation.

OBJECTIVES: The aim of this study was to provide particle number and mass deposition rates of submicron particles in the human airways as inputs for toxicology and other areas of aerosol science. METHODS: Scanning Mobility Particle Spectrometer was used to measure the number concentrations and size distributions of the ultrafine urban particles during summer and winter in Budapest. The Stochastic Lung Model (SLM) was applied to calculate number and mass deposition rates of the inhaled particles in different anatomical regions of the airways. RESULTS: Our calculations revealed that for the selected days in summer and winter with PM10 values below the health limit 4.7 and 18.4 billion particles deposited in the bronchial region of the lungs. The deposition in the acinar region of the lung was even higher, 8.3 billion particles for the summer day, and 33.8 billion particles for winter day. CONCLUSIONS: Our results clearly demonstrate that large daily numbers of urban UFPs are deposited in the respiratory tract, which may play a key role in the health effects of particulate matter (PM) inhalation. Present results, connecting the ambient exposure parameters with the local burden of the airway epithelium, can be useful inputs of in vitro cell culture experiments. By the combination of urban UFP monitoring and numerical modeling of particle deposition with toxicological studies, the health risks of urban aerosols could be better assessed. The use of UFP data in addition to PM10 and PM2.5 in the epidemiological studies would also be indicated.

Dynamic behavior of indoor ultrafine particles (2.3-64 nm) due to burning candles in a residence.

A major source of human exposure to ultrafine particles is candle use. Candles produce ultrafine particles in the size range under 10 nm, with perhaps half of the particles less than 5 nm. For these small particles at typically high concentrations, coagulation and deposition are two dominant mechanisms in aerosol size dynamics. We present an updated coagulation model capable of characterizing the relative contributions of coagulation, deposition, and air exchange rates. Size-resolved coagulation and decay rates are estimated for three types of candles. Number, area, and mass distributions are provided for 93 particle sizes from 2.33 to 64 nm. Total particle production was in the range of 1013  min-1 . Peak number, area, and mass concentrations occurred at particle sizes of <3, 20, and 40 nm, respectively. Both the number and area concentrations greatly exceeded background concentrations in the residence studied. Contributions of coagulation, deposition, and air exchange rates to particle losses were 65%, 34%, and 0.3% at high concentrations (106  cm-3 ), while they are 17%, 81%, and 1.7% at lower concentrations (3 × 104  cm-3 ), respectively. The increased particle production for the very smallest particles (2.33-2.50 nm) suggests that even smaller particles may be important to study.

A new approach to estimate ultrafine particle respiratory deposition.

Ultrafine particles (UFPs) in workplaces have been and continue to be an important occupational health concern. The inhalation and the consequent deposition of UFPs in workers' lower airways can lead to many adverse health effects. Therefore, it is vital to study the deposition of UFPs in the human respiratory tract from the viewpoint of occupational health. In this study, a set of physiologically representative human tracheobronchial airway replicas were made using high-resolution 3D printers, and a new approach that was distinct from the traditional methods was developed to apply these airway replicas in estimating UFP respiratory deposition. The results showed that UFP respiratory deposition could be readily and systematically measured by the differential-based approach. The results of this study imply the feasibility of developing a mobile aerosol lung deposition apparatus in the future for on-site workplace UFP respiratory deposition to evaluate the UFP inhalation dosimetry for workers in the real workplaces.

Respiratory deposition of ultrafine welding fume particles.

The inhalation and the deposition of welding-generated ultrafine particles in welders' respiratory tracts have been linked to severe pulmonary impairments. In the present study, a mobile aerosol lung deposition apparatus (MALDA) was developed and applied to study the respiratory deposition of ultrafine welding fume particles. The MALDA was constructed with a set of physiologically representative human tracheobronchial airway replicas made with high-resolution 3D printers. Ultrafine welding fume particles were generated in a welding fume chamber and delivered to the MALDA. A series of respiratory deposition experiments were carried out using the MALDA to investigate the deposition of ultrafine welding fume particles in different airway generations of the tracheobronchial airways. The results showed that the fractional deposition of ultrafine welding fume particle in the human tracheobronchial airways down to the 9th airway generation could be readily and systematically measured by the MALDA. The estimated cumulative respiratory deposition ranged from approximately 9-31% for ultrafine welding fume particles between 10 and 100 nm in diameter. The results acquired demonstrated that the MALDA developed has the potential to become a useful apparatus in the future to estimate the respiratory deposition of ultrafine particles in real workplaces.

Ultrafine particle libraries for exploring mechanisms of PM2.5-induced toxicity in human cells.

Air pollution worldwide, especially in China and India, has caused serious health issues. Because PM2.5 particles consist of solid particles of diverse properties with payloads of inorganic, organic and biological pollutants, it is still not known what the major toxic components are and how these components induce toxicities. To explore this complex issue, we apply reductionism principle and an ultrafine particle library approach in this work. From investigation of 63 diversely functionalized ultrafine particles (FUPs) with adsorbed key pollutants, our findings indicate that 1) only certain pollutants in the payloads of PM2.5 are responsible for causing cellular oxidative stress, cell apoptosis, and cytotoxicity while the particle carriers are much less toxic; 2) pollutant-induced cellular oxidative stress and oxidative stress-triggered apoptosis are identified as one of the dominant mechanisms for PM2.5-induced cytotoxicity; 3) each specific toxic component on PM2.5 (such as As, Pb, Cr or BaP) mainly affects its specific target organ(s) and, adding together, these pollutants may cause synergistic or just additive effects. Our findings demonstrate that reductionism concept and model PM2.5 particle library approach are very effective in our endeavor to search for a better understanding of PM2.5-induced health effects.

Characterization particulate matter from several Chinese cooking dishes and implications in health effects.

Cooking fume produced by oil and food at a high temperature releases large amount of fine particulate matter (PM) which have a potential hazard to human health. This chamber study investigated particle emission characteristics originated from using four types of oil (soybean oil, olive oil, peanut oil and lard) and different kinds of food materials (meat and vegetable). The corresponding emission factors (EFs) of number, mass, surface area and volume for particles were discussed. Temporal variation of size-fractionated particle concentration showed that olive oil produced the highest number PM concentration for the entire cooking process. Multiple path particle dosimetry (MPPD) model was performed to predict deposition in the human respiratory tract. Results showed that the pulmonary airway deposition fraction was the largest. It was also found that particles produced from olive oil led to the highest deposition. We strongly recommend minimizing the moisture content of ingredients before cooking and giving priority to the use of peanut oil instead of olive oil to reduce human exposure to PM.

Inhalation exposure to three-dimensional printer emissions stimulates acute hypertension and microvascular dysfunction.

Fused deposition modeling (FDM™), or three-dimensional (3D) printing has become routine in industrial, occupational and domestic environments. We have recently reported that 3D printing emissions (3DPE) are complex mixtures, with a large ultrafine particulate matter component. Additionally, we and others have reported that inhalation of xenobiotic particles in this size range is associated with an array of cardiovascular dysfunctions. Sprague-Dawley rats were exposed to 3DPE aerosols via nose-only exposure for ~3h. Twenty-four hours later, intravital microscopy was performed to assess microvascular function in the spinotrapezius muscle. Endothelium-dependent and -independent arteriolar dilation were stimulated by local microiontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP). At the time of experiments, animals exposed to 3DPE inhalation presented with a mean arterial pressure of 125±4mmHg, and this was significantly higher than that for the sham-control group (94±3mmHg). Consistent with this pressor response in the 3DPE group, was an elevation of ~12% in resting arteriolar tone. Endothelium-dependent arteriolar dilation was significantly impaired after 3DPE inhalation across all iontophoretic ejection currents (0-27±15%, compared to sham-control: 15-120±21%). Endothelium-independent dilation was not affected by 3DPE inhalation. These alterations in peripheral microvascular resistance and reactivity are consistent with elevations in arterial pressure that follow 3DPE inhalation. Future studies must identify the specific toxicants generated by FDM™ that drive this acute pressor response.

Preparation of an Ultrafine Rebamipide Ophthalmic Suspension with High Transparency.

A 2% commercially available, milky-white, rebamipide micro-particle suspension is used to treat dry eyes, and it causes short-term blurring of the patient's vision. In the current study, to improve the transparency of a rebamipide suspension, we attempted to obtain a clear rebamipide suspension by transforming the rebamipide particles to an ultrafine state. In the initial few efforts, various rebamipide suspensions were prepared using a neutralizing crystallization method with additives, but the suspensions retained their opaque quality. However, as a consequence of several critical improvements in the neutralizing crystallization methods such as selection of additives for crystallization, process parameters during crystallization, the dispersion method, and dialysis, we obtained an ultrafine rebamipide suspension (2%) that was highly transparent (transmittance at 640 nm: 59%). The particle size and transparency demonstrated the fewest level of changes at 25°C after 3 years, compared to initial levels. During that period, no obvious particle sedimentation was observed. The administration of this ultrafine rebamipide suspension (2%) increased the conjunctival mucin, which was comparable to the commercially available micro-particle suspension (2%). The corneal and conjunctival concentration of rebamipide following ocular administration of the ultrafine suspension was slightly higher than that of the micro-particle suspension. The ultrafine rebamipide suspension (eye-drop formulation) with a highly transparent ophthalmic clearness should improve a patient's QOL by preventing even a shortened period of blurred vision.