Concentrations Of Acrolein Research Articles

Development of nitrogen dioxide and volatile organic compounds land use regression models to estimate air pollution exposure near an Italian airport

The aim of this study was to evaluate the small scale spatial variability of nitrogen dioxide (NO2) and selected VOCs (benzene, toluene, acrolein and formaldehyde) concentrations using Land Use Regression models (LURs) in a complex multi sources domain (64 km2), containing a mid-size airport: the Ciampino Airport, located in Ciampino, Rome, Italy.46 diffusion tube samplers were deployed within a domain centred in the airport over two 2-weekly periods (June 2011–January 2012). GIS-derived predictor variables, with varying buffer size, were evaluated to model spatial variation of NO2, benzene, toluene, formaldehyde and acrolein annual average concentrations. The airport apportionment to air quality was investigated using a Lagrangian dispersion model (SPRAY). A stepwise selection procedure was used to develop the linear regression models. The models were validated using leave one out cross validation (LOOCV) method.In this study, the use of LURs was found to be effective to explain spatial variability of NO2 (adjusted-R2 = 0.72), benzene (adjusted-R2 = 0.53), toluene (adjusted-R2 = 0.50) and acrolein (adjusted-R2 = 0.51), while limited power was achieved with the formaldehyde modeling (adjusted-R2 = 0.24).For all pollutants LURs output showed that the small scale spatial variability was mainly explained by local traffic. The airport contribution to the observed spatial variability was adequately quantified only for acrolein (0.43 (±0.69) μg/m3 in an area of about 6 km2, SW located to the airport runway), while for NO2 and formaldehyde, only a little portion of the spatial variability in a limited portion of the study domain was attributable to airport related emissions.

Investigation of volatile organic compounds exposure inside vehicle cabins in China

This study assessed the concentrations of specific volatile organic compounds (VOCs) inside vehicle cabins under different practical vehicle driving conditions in China. The mean concentrations of the VOCs, including benzene, toluene, xylene, ethylbenzene, styrene, formaldehyde, acetaldehyde, acetone, and acrolein, were 16.73 μg/m3, 66.02 μg/m3, 14.20 μg/m3, 6.78 μg/m3, 28.09 μg/m3, 16.43 μg/m3, 12.47 μg/m3, and 20.65 μg/m3 (the sum of acetone and acrolein), respectively. All the specified VOCs inside vehicle cabins were not exceeded the limits of the national standard. The in-cabin VOCs concentrations were investigated for 16 private vehicles under three ventilation conditions: (i) fan off and recirculation (RC) off, (ii) fan on and RC off, and (iii) fan on and RC on. The VOCs concentrations increased 50.46% (mean of the measured VOCs) when the ventilation condition changed from (ii) to (i), and increased 51.38% (mean of the measured VOCs) when ventilation condition changed from (ii) to (iii). Two vehicle models (vehicle model A and vehicle model B) were tested in the study to investigate the influence on in-cabin VOCs concentrations of two typical interior trims (leather, fabric). The VOCs concentrations inside B vehicles (leather interiors) were averagely 1.42 times larger than the concentrations in A vehicles (fabric interiors). For new vehicles, the concentrations of benzene, toluene, xylene, ethylbenzene, formaldehyde, acetaldehyde, acetone and acrolein were larger than the concentrations inside old vehicles by 12.89%, 103.54%, 123.14%, 104.20%, 6.26%, 6.31%, and 10.67%, respectively. The VOCs concentrations significantly increased as the raise of ambient temperature. Toluene, styrene, ethylbenzene, and xylene were the most sensitive VOCs to temperature, which increased 513.6%, 544.8%, 767.0%, and 597.7% as the temperature increased from 11 °C to 25 °C.

A Potential Role for Acrolein in Neutrophil-Mediated Chronic Inflammation.

Neutrophils (PMNs) are key mediators of inflammatory processes throughout the body. In this study, we investigated the role of acrolein, a highly reactive aldehyde that is ubiquitously present in the environment and produced endogenously at sites of inflammation, in mediating PMN-mediated degradation of collagen facilitating proline-glycine-proline (PGP) production. We treated peripheral blood neutrophils with acrolein and analyzed cell supernatants and lysates for matrix metalloproteinase-9 (MMP-9) and prolyl endopeptidase (PE), assessed their ability to breakdown collagen and release PGP, and assayed for the presence of leukotriene A4 hydrolase (LTA4H) and its ability to degrade PGP. Acrolein treatment induced elevated production and functionality of collagen-degrading enzymes and generation of PGP fragments. Meanwhile, LTA4H levels and triaminopeptidase activity declined with increasing concentrations of acrolein thereby sparing PGP from enzymatic destruction. These findings suggest that acrolein exacerbates the acute inflammatory response mediated by neutrophils and sets the stage for chronic pulmonary and systemic inflammation.

Constituents of smoke from cigarettes made from diverted nicotine replacement therapy patches.

Anecdotes of nicotine replacement therapy patch misuse associated with the introduction of smoke-free prisons have been reported by media internationally, including Canada in 2006, New Zealand in 2011 and Australia in 2014. This study identifies chemical compounds released through diverted nicotine replacement therapy patches when they are smoked. Two samples were produced: (i) shredded 21 mg nicotine replacement therapy patches rolled with tea leaves into a cigarette; and (ii) patches boiled in water and tea leaves, and then dried tea leaves rolled into a cigarette. The smoke was tested for nicotine, caffeine and toxins. High-performance liquid chromatography, mass spectrometry and spectrophotometry were used to detect the presence and quantity of nicotine and caffeine. A specialised laboratory was contracted to test the presence of toxins. Nicotine was liberated when the two samples were burnt but not if the nicotine replacement therapy patches were boiled in water alone. High concentrations of formaldehyde, acetaldehyde, acrolein, toluene, xylene and heavy metals were also released. Nicotine is released when diverted nicotine replacement therapy patches are smoked, as are caffeine and harmful toxins. These toxins have the potential to cause short- and long-term health damage.

Cooking-related PM2.5 and acrolein measured in grocery stores and comparison with other retail types.

We measured particulate matter (PM), acrolein, and other indoor air contaminants in eight visits to grocery stores in California. Retail stores of other types (hardware, furniture, and apparel) were also sampled on additional visits. Based on tracer gas decay data, most stores had adequate ventilation according to minimum ventilation rate standards. Grocery stores had significantly higher concentrations of acrolein, fine and ultrafine PM, compared to other retail stores, likely attributable to cooking. Indoor concentrations of PM2.5 and acrolein exceeded health guidelines in all tested grocery stores. Acrolein emission rates to indoors in grocery stores had a mean estimate about 30 times higher than in other retail store types. About 80% of the indoor PM2.5 measured in grocery stores was emitted indoors, compared to only 20% for the other retail store types. Calculations suggest a substantial increase in outdoor air ventilation rate by a factor of three from current level is needed to reduce indoor acrolein concentrations. Alternatively, acrolein emission to indoors needs to be reduced 70% by better capturing of cooking exhaust. To maintain indoor PM2.5 below the California annual ambient standard of 12μg/m(3) , grocery stores need to use air filters with an efficiency rating higher than the MERV 8 air filters commonly used today.

Aldehydes in relation to air pollution sources: A case study around the Beijing Olympics

This study was carried out to characterize three aldehydes of health concern (formaldehyde, acetaldehyde, and acrolein) at a central Beijing site in the summer and early fall of 2008 (from June to October). Aldehydes in polluted atmospheres come from both primary and secondary sources, which limits the control strategies for these reactive compounds. Measurements were made before, during, and after the Beijing Olympics to examine whether the dramatic air pollution control measures implemented during the Olympics had an impact on concentrations of the three aldehydes and their underlying primary and secondary sources. Average concentrations of formaldehyde, acetaldehyde and acrolein were 29.3 ± 15.1 μg/m3, 27.1 ± 15.7 μg/m3 and 2.3 ± 1.0 μg/m3, respectively, for the entire period of measurements, all being at the high end of concentration ranges measured in cities around the world in photochemical smog seasons. Formaldehyde and acrolein increased during the pollution control period compared to the pre-Olympic Games, followed the changing pattern of temperature, and were significantly correlated with ozone and with a secondary formation factor identified by principal component analysis (PCA). In contrast, acetaldehyde had a reduction in mean concentration during the Olympic air pollution control period compared to the pre-Olympic period and was significantly correlated with several pollutants emitted from local emission sources (e.g., NO2, CO, and PM2.5). Acetaldehyde was also more strongly associated with primary emission sources including vegetative burning and oil combustion factors identified through the PCA. All three aldehydes were lower during the post-Olympic sampling period compared to the before and during Olympic periods, likely due to seasonal and regional effects. Our findings point to the complexity of source control strategies for secondary pollutants.

Ambient acrolein concentrations in coastal, remote, and urban regions in California.

Acrolein (2-propenal) is a reactive chemical that is very toxic and has many sources. Acrolein is commonly detected in the atmosphere, but understanding the ambient concentrations of this compound has been hampered by analytical difficulties. The objective of this research was to utilize an analytical method specifically designed for acrolein to determine acrolein concentrations in remote regions. The purpose was to determine the natural background concentrations of acrolein which were simply lacking in the literature. In addition, rural and urban areas were sampled to determine the degree of anthropogenic enrichment in polluted environments. The results from the coastal and remote inland areas suggest that the median natural summertime background of acrolein was near 40 ng/m(3), which was higher than the Environmental Protection Agency's Reference Concentration (RfC) of 20 ng/m(3). Acrolein concentrations in urban areas were approximately 3- to 8-fold higher than background concentrations, which was a lower degree of urban enrichment than expected. The results suggest that additional research is needed to understand the natural background concentrations of acrolein.

Analysis of mobile source air toxics (MSATs)—Near-road VOC and carbonyl concentrations

Exposures to mobile source air toxics (MSATs) have been associated with numerous adverse health effects. While thousands of air toxic compounds are emitted from mobile sources, members of a subset of compounds are considered high priority due to their significant contribution to cancer and noncancer health risks and the contribution of mobile sources to total exposure as evaluated by the U.S. Environmental Protection Agency (EPA) National-Scale Air Toxics Assessments (NATA). These pollutants include benzene, 1,3-butadiene, ethylbenzene, acrolein, acetaldehyde, formaldehyde, naphthalene, polycyclic organic matter, and diesel particulate matter/organic gases. This study provided year-long trends of benzene, 1,3-butadiene, acrolein, acetaldehyde, and formaldehyde in Las Vegas, NV. Results indicated that MSAT concentrations often did not exhibit trends typical of other primary emitted pollutants in this study. Instead, other mobile sources beyond the highway of interest contributed to the measured values, including a major arterial road, a large commercial airport, and a nearby parking lot. The data were compared with relevant census-tract NATA estimates, with estimated ambient 1,3-butadiene concentrations similar to the measured values. Measured benzene values were much lower relative to the NATA total ambient benzene concentrations. Measured acrolein values were much higher relative to the NATA total acrolein concentrations. Measured acetaldehyde and formaldehyde values were also higher relative to the NATA total acetaldehyde and formaldehyde concentrations for all wind conditions and downwind conditions. Some possible explanations for these differences include nearby sources influencing the measured values; meteorological influences that may not be well captured by the NATA modeling regime; chemical reactivity of measured compounds; and additional explanatory variables may be needed for certain urban areas in order to accurately disaggregate anthropogenic air toxics emissions. Implications: Comparison of air toxics concentrations measured at four long-term near-road sites in Las Vegas, NV, show generally good agreement with the EPA 2005 NATA total ambient concentrations. Measured concentrations did not compare as well with EPA 2005 NATA for the on-road mobile portion of the ambient concentrations. This highlights the complexity of air toxic emission sources and impacts in urban areas, especially around large highway facilities; NATA's inability to capture local-scale meteorology and fine-scale ambient gradients; and that additional explanatory variables may be needed for certain urban areas in order to accurately disaggregate anthropogenic air toxics emissions.

Assessment of Modeled Indoor Air Concentrations of Particulate Matter, Gaseous Pollutants, and Volatile Organic Compounds Emitted from Candles

ABSTRACT Candle burning is regarded as an important source of airborne pollutants in indoor environments. Indoor concentrations of aldehydes, benzo(a)pyrene, sulphur dioxide (SO2), nitrogen oxides (NOx), and particulate matter (PM) produced from the burning of scented candles and raw materials with different melting point/oil content (50/1, 55/9, and 65/6) were predicted using a single compartment mass balance model and compared to regulatory or guideline limits. Scented candles may be responsible for indoor acrolein concentrations that could become relevant to health only in the case of chronic exposure. Indoor concentrations of fine PM and SO2 emitted from 65/6 wax burning under worst-case environmental and behavioral conditions were greater than their respective acute guideline limits. However, other waxes had levels of PM and SO2 well below the recommended values. Indoor concentrations of nitrogen dioxide emitted from raw wax burning should be further investigated. The degree of pureness of raw waxes significantly affected the predicted indoor concentrations of PM and SO2. In particular, 65/6 wax was criticized for its high content of impurities.

Source Apportionment of Personal Exposure to Carbonyl Compounds and BTEX at Homes in Beijing, China

Concentrations of carbonyl compounds (formaldehyde, acetaldehyde, acrolein and acetone) and BTEX (benzene, toluene and xylenes) were monitored at 128 residential homes (255) in Xicheng district, Beijing, during the period of November–December 2009. The indoor concentrations of formaldehyde, acetaldehyde, acrolein, acetone, benzene, toluene and xylenes were in the ranges of 1.3–85.6 µg/m 3 , 0.7–102.0 µg/m 3 , 0.3–102.1 µg/m 3 , 0.1–25.1 µg/m 3 , 1.0–47.5 µg/m 3 , 1.3–86.0 µg/m 3 and 0.2–78.7 µg/m 3 , respectively. The concentrations of all species during the investigation period were below the Chinese guideline values. Based on the measured concentrations, a receptor model (PMF; positive matrix factorization) coupled with the source information was applied to identify the major emission sources. The results showed that four major sources were identified by the PMF method, including (1) outdoor incursion factors, (2) emissions from building materials and paint solvent, (3) emissions from particle board and plywood flooring and (4) emissions from household cleaning chemicals. Our results also reveal that the health risks due to exposure to formaldehyde and benzene for Beijing residents were greater during this period than those for people living in Guangzhou and Hangzhou, China.

Using SPME‐GC/MS to Evaluate Acrolein Production in Cassava and Pork Sausage Fried in Different Vegetable Oils

AbstractThis work presents the quantification of acrolein in cassava and pork sausage fried (temperature of 170 °C) in five different vegetables oils: canola, palm, sunflower, soybean and corn using a method of solid‐phase microextraction (SPME) combined with gas chromatography and mass spectrometry. The results showed that the highest concentration of acrolein was found in samples fried in sunflower oil and canola oil. The concentration of acrolein in pork sausage (3.7 and 2.0 ng/g/g) was lower than in cassava (10.2 and 3.8 ng) when fried in sunflower and soybean oils, respectively. In contrast, when the denser oils (canola and palm) were used for frying, the concentration of acrolein in pork sausage (6.3 and 3.8 ng/g) was higher than in cassava (3.7 and 2.8 ng/g). Using corn oil, the concentrations of acrolein in both cassava and sausage were similar (approximately 5 ng/g). The viscosity of the oil, the fatty acid composition, especially the level of saturated and unsaturated fatty acids from the food, and oil uptake are factors that influence the acrolein concentration found in fried food.

Chronic health risks in retail buildings and their dependence on ventilation rates and filtration efficiencies

Background-Inhalation exposures to indoor pollutants in non-residential environments contribute largely to total daily exposures. Prioritizing pollutants to be controlled by energy-intensive methods (i.e.ventilation and filtration) is key to reducing the total chronic disease burden and achieve energy efficiency in retail buildings. Objective-Our objective was to model exposure to indoor pollutants measured in retail environments for customers and employees, and assess the role of ventilation and filtration in mitigating this exposure. Methods-Measured concentrations of pollutants in 140 stores in the U.S., available methods (IND and ID approaches) and toxicological data were employed in Monte Carlo simulations to calculate disability-adjusted-life-years (DALYs). Indoor emission factors for pollutants were calculated to assess the change in health risks under 9 scenarios of ventilation rates and filtration efficiencies. Results were compared with DALYs found in residences. Results-The estimated average DALYs due to PM2.5 and acrolein exposure contributed the largest to annual health impacts, with an estimated 122 DALYs per 100,000 persons, divided equally between PM2.5 and acrolein.Carbon tetrachloride, formaldehyde and ozone accounted for the vast majority of the cancer health effects, contributing for a total of 10 DALYs per 100,000 persons annually. Increasing the filtration efficiency, while reducing infiltration rate to a minimum, is found to be the most energy efficient method to decrease DALYs from PM2.5 exposure. As for acrolein, increasing the ventilation rates in the retail stores could not drive acrolein concentrations below the OEHHA chronic REL. Comparing the findings from this study to DALYs reported by Logue et al. (2012) for residences revealed that PM2.5 and acrolein are two common contaminants of concerns. Conclusions-This study found that polluatnt control startegies should focus on mitigating exposure to PM2.5 and acrolein. Cumulative health burden from all indoor pollutants contributed to 146 DALYs per 100,000 persons annually.

Identification of stable cytotoxic factors in the gas phase extract of cigarette smoke and pharmacological characterization of their cytotoxicity

Smoking is a major risk factor for atherosclerotic vascular diseases, but the mechanism for its genesis is unknown. We have recently shown that the gas phase of cigarette smoke (nicotine- and tar-free cigarette smoke extract; CSE) likely to reach the systemic circulation contains stable substances which cause cytotoxicity like plasma membrane damage and cell death in cultured cells, and also that the plasma membrane damage is caused through sequential activation of protein kinase C (PKC) and NADPH oxidase (NOX) and the resulting generation of reactive oxygen species (PKC/NOX-dependent mechanism), whereas cell death is caused through PKC/NOX-dependent and -independent mechanisms. To identify these stable substances, the CSE was prepared by passing the main-stream smoke of 10 cigarettes through a Cambridge glass fiber filter, trapping of the smoke in a vessel cooled at −80°C, and subsequent dissolution in 10ml of water. The CSE was fractionated into nine fractions using reversed-phase HPLC, and each fraction was screened for cytotoxicity in cultured cells, using propidium iodide uptake assay for cell membrane damage and MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium] reduction assay for cell viability. The cytotoxicity was positive in two of the nine fractions (Fr2 and Fr5). After extraction of the active fractions into dichloromethane, GC/MS analysis identified 2-cyclopenten-1-one (CPO) in Fr5 but none in Fr2. After derivatization of the active fractions with O-(2,3,4,5,6-pentafluorobenzyl) hydroxylamine hydrochloride, GC/MS analysis identified acrolein, acetone and propionaldehyde in Fr2, and methyl vinyl ketone (MVK) in Fr5. After 4-h incubation, authentic acrolein and MVK induced concentration-dependent cytotoxicity with EC50 values of 75.9±8.2 and 47.0±8.0μM (mean±SEM; n=3), respectively, whereas acetone, propionaldehyde and CPO were without effect. However, after 24-h incubation, CPO induced concentration-dependent cytotoxicity with an EC50 value of 264.0±16.9μM (n=3). The concentrations of acrolein, MVK and CPO in the CSE were 3368±334, 2429±123 and 392.9±31.8μM (n=4), respectively, which were higher than the cytotoxic concentrations. The cytotoxicity of acrolein and MVK consisted of plasma membrane damage and decreased cell viability: the plasma membrane damage was totally prevented by treatment with an inhibitor of PKC or NOX, whereas the decreased cell viability was only partially prevented by these inhibitors. The cytotoxicity of CPO consisted only of decreased cell viability, which was totally resistant to these inhibitors. These results show that acrolein and MVK are responsible for the acute cytotoxicity of the CSE through PKC/NOX-dependent and -independent mechanisms, whereas CPO is responsible for the delayed cytotoxicity of the CSE through a PKC/NOX-independent mechanism.

Aldose reductase regulates acrolein-induced cytotoxicity in human small airway epithelial cells

Aldose reductase (AR), a glucose-metabolizing enzyme, reduces lipid aldehydes and their glutathione conjugates with more than 1000-fold efficiency (Km aldehydes 5–30µM) relative to glucose. Acrolein, a major endogenous lipid peroxidation product as well as a component of environmental pollutants and cigarette smoke, is known to be involved in various pathologies including atherosclerosis, airway inflammation, COPD, and age-related disorders, but the mechanism of acrolein-induced cytotoxicity is not clearly understood. We have investigated the role of AR in acrolein-induced cytotoxicity in primary human small airway epithelial cells (SAECs). Exposure of SAECs to varying concentrations of acrolein caused cell death in a concentration- and time-dependent manner. AR inhibition by fidarestat prevented the low-dose (5–10µM) but not the high-dose (>10µM) acrolein-induced SAEC death. AR inhibition protected SAECs from low-dose (5µM) acrolein-induced cellular reactive oxygen species (ROS). Inhibition of acrolein-induced apoptosis by fidarestat was confirmed by decreased condensation of nuclear chromatin, DNA fragmentation, comet tail moment, and annexin V fluorescence. Further, fidarestat inhibited acrolein-induced translocation of the proapoptotic proteins Bax and Bad from the cytosol to the mitochondria and that of Bcl2 and BclXL from the mitochondria to the cytosol. Acrolein-induced cytochrome c release from mitochondria was also prevented by AR inhibition. The mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinases 1 and 2, stress-activated protein kinase/c-Jun NH2-terminal kinase, and p38MAPK, and c-Jun were transiently activated in airway epithelial cells by acrolein in a concentration- and time-dependent fashion, which was significantly prevented by AR inhibition. These results suggest that AR inhibitors could prevent acrolein-induced cytotoxicity in the lung epithelial cells.

Acrolein detection based on alcohol dehydrogenase inhibition

This paper presents the effect of acrolein on three dehydrogenases and proposes a fast spectrometric method for acrolein analysis. We have found that alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (AlDH) are inhibited by low acrolein concentrations (0.2 mM) while inhibition of glutamate dehydrogenase (GDH) is not observed even at higher acrolein concentrations (1 mM). Acrolein is a suicide substrate for AlDH and ADH inhibition by acrolein is competitive. Cysteine (L-Cys) and glutathione (GSH) react with acrolein and thus reduce its expected inhibitory effect. ADH was chosen to develop a spectrophotometric method for acrolein analysis based on enzyme inhibition. The calibration curve is linear between 0.2 and 1.0 mM acrolein.

Personal exposure and source characteristics of carbonyl compounds and BTEXs within homes in Beijing, China

Exposure to indoor chemical air pollutants is expected to increase potentially the chance of developing cancer. Ambient levels of carbonyl (formaldehyde, acetaldehyde, acrolein and acetone) and BTEXs (benzene, toluene and xylenes) compounds were monitored at 210 residential homes in Xicheng district, Beijing, during the period of November–December 2009. The indoor concentrations of formaldehyde, acetaldehyde, acrolein, acetone, benzene, toluene and xylenes were in the range of 0.2–213.4 μg m−3, 0.7–140.9 μg m−3, 0.1–25.2 μg m−3, 0.3–102.1 μg m−3, 1.0–47.5 μg m−3, 1.3–552.6 μg m−3 and 0.2–150.6 μg m−3, respectively. Average concentrations of formaldehyde, acetaldehyde, acrolein, acetone, benzene, toluene and xylenes were 21.8 μg m−3, 16.3 μg m−3, 2.8 μg m−3, 10.7 μg m−3, 9.0 μg m−3, 32.1 μg m−3 and 12.3 μg m−3, respectively. The individual samples were mostly lower than the Chinese guideline values except formaldehyde and toluene, which showed higher values in 91 and 29 samples. Statistical analysis and I/O (indoor concentration/outdoor concentration) ratio results showed that the main sources of formaldehyde, acetaldehyde, benzene and toluene at homes with renovation age <5 years were organic solvents used in adhesives and decoration materials. Meanwhile, outdoor emission factors may have an impact on acetone, acrolein and xylenes concentrations of indoor air at different homes, and on formaldehyde, acetaldehyde, benzene and toluene concentrations of indoor air at homes with renovation age >5 years. Our results also showed that higher cancer risks for human exposure to formaldehyde, acetaldehyde and benzene than previous studies in Guangzhou and Hangzhou, China with one exception.

Acrolein cytotoxicity in hepatocytes involves endoplasmic reticulum stress, mitochondrial dysfunction and oxidative stress

Acrolein is a common environmental, food and water pollutant and a major component of cigarette smoke. Also, it is produced endogenously via lipid peroxidation and cellular metabolism of certain amino acids and drugs. Acrolein is cytotoxic to many cell types including hepatocytes; however the mechanisms are not fully understood. We examined the molecular mechanisms underlying acrolein hepatotoxicity in primary human hepatocytes and hepatoma cells. Acrolein, at pathophysiological concentrations, caused a dose-dependent loss of viability of hepatocytes. The death was apoptotic at moderate and necrotic at high concentrations of acrolein. Acrolein exposure rapidly and dramatically decreased intracellular glutathione and overall antioxidant capacity, and activated the stress-signaling MAP-kinases JNK, p42/44 and p38. Our data demonstrate for the first time in human hepatocytes, that acrolein triggered endoplasmic reticulum (ER) stress and activated eIF2α, ATF-3 and -4, and Gadd153/CHOP, resulting in cell death. Notably, the protective/adaptive component of ER stress was not activated, and acrolein failed to up-regulate the protective ER-chaperones, GRP78 and GRP94. Additionally, exposure to acrolein disrupted mitochondrial integrity/function, and led to the release of pro-apoptotic proteins and ATP depletion. Acrolein-induced cell death was attenuated by N-acetyl cysteine, phenyl-butyric acid, and caspase and JNK inhibitors. Our data demonstrate that exposure to acrolein induces a variety of stress responses in hepatocytes, including GSH depletion, oxidative stress, mitochondrial dysfunction and ER stress (without ER-protective responses) which together contribute to acrolein toxicity. Our study defines basic mechanisms underlying liver injury caused by reactive aldehyde pollutants such as acrolein.

Spatial variability of indoor air pollutants in schools. A multilevel approach

The measurement of indoor air pollutants and their health effects are less often studied due to the costs of collection of such data. We have analysed the variability in the measurement of five indoor school air pollutants: fine particulate matter of size ≤2.5 μm (PM2.5), nitrogen dioxide (NO2), and three Volatile Organic Compounds (VOC), namely formaldehyde, acetaldehyde and acrolein, objectively measured over five days of a week at representative points in more than 400 classrooms of 109 schools and courtyards in six French cities spread out over the year. Separate 3-stage multilevel models were fitted to partition the different nested variance components (i.e., classroom, school and city levels), and intra-class correlation (ICC) coefficients were computed to bring out the similarities of pollutants' concentrations among these spatial units. The indoor PM2.5 and NO2 concentrations showed a high degree of similarity (ICC coefficients equal to 76% and 81%, respectively) between the classrooms of a school (and city), whereas the formaldehyde, acetaldehyde and acrolein concentrations showed low to moderate degree of similarity (ICC coefficients equal to 25%, 36% and 57%, respectively) between the classrooms. We conclude that to investigate the impact of indoor air pollutants, a multilevel approach taking into account the full design of the study would be the most appropriate.

Comparative Computational Modeling of Airflows and Vapor Dosimetry in the Respiratory Tracts of Rat, Monkey, and Human

Computational fluid dynamics (CFD) models are useful for predicting site-specific dosimetry of airborne materials in the respiratory tract and elucidating the importance of species differences in anatomy, physiology, and breathing patterns. We improved the imaging and model development methods to the point where CFD models for the rat, monkey, and human now encompass airways from the nose or mouth to the lung. A total of 1272, 2172, and 135 pulmonary airways representing 17±7, 19±9, or 9±2 airway generations were included in the rat, monkey and human models, respectively. A CFD/physiologically based pharmacokinetic model previously developed for acrolein was adapted for these anatomically correct extended airway models. Model parameters were obtained from the literature or measured directly. Airflow and acrolein uptake patterns were determined under steady-state inhalation conditions to provide direct comparisons with prior data and nasal-only simulations. Results confirmed that regional uptake was sensitive to airway geometry, airflow rates, acrolein concentrations, air:tissue partition coefficients, tissue thickness, and the maximum rate of metabolism. Nasal extraction efficiencies were predicted to be greatest in the rat, followed by the monkey, and then the human. For both nasal and oral breathing modes in humans, higher uptake rates were predicted for lower tracheobronchial tissues than either the rat or monkey. These extended airway models provide a unique foundation for comparing material transport and site-specific tissue uptake across a significantly greater range of conducting airways in the rat, monkey, and human than prior CFD models.

Reactive Secondary Sequence Oxidative Pathology Polymer Model and Antioxidant Tests.

AimsTo provide common Organic Chemistry/Polymer Science thermoset free-radical crosslinking Sciences for Medical understanding and also present research findings for several common vitamins/antioxidants with a new class of drugs known as free-radical inhibitors.Study DesignPeroxide/Fenton transition-metal redox couples that generate free radicals were combined with unsaturated lipid oils to demonstrate thermoset-polymer chain growth by crosslinking with the α-β-unsaturated aldehyde acrolein into rubbery/adhesive solids. Further, Vitamin A and beta carotene were similarly studied for crosslink pathological potential. Also, free-radical inhibitor hydroquinone was compared for antioxidant capability with Vitamin E.Place and Duration of StudyDepartment of Materials Science and Engineering and Department of Biomaterials, University of Alabama at Birmingham, between June 2005 and August 2012.MethodologyObservations were recorded for Fenton free-radical crosslinking of unsaturated lipids and vitamin A/beta carotene by photography further with weight measurements and percent-shrinkage testing directly related to covalent crosslinking of unsaturated lipids recorded over time with different concentrations of acrolein. Also, hydroquinone and vitamin E were compared at concentrations from 0.0–7.3wt% as antioxidants for reductions in percent-shrinkage measurements, n = 5.ResultsUnsaturated lipid oils responded to Fenton thermoset-polymer reactive secondary sequence reactions only by acrolein with crosslinking into rubbery-type solids and different non-solid gluey products. Further, molecular oxygen crosslinking was demonstrated with lipid peroxidation and acrolein at specially identified margins. By peroxide/Fenton free-radical testing, both vitamin A and beta-carotene demonstrated possible pathology chemistry for chain-growth crosslinking. During lipid/acrolein testing over a 50 hour time period at 7.3wt% antioxidants, hydroquinone significantly reduced percent shrinkage greatly compared to the standard antioxidant vitamin E, %shrinkage at 11.6 ±1.3 for hydroquinone and 27.8 ±2.2 for vitamin E, P = .001.ConclusionFree radicals crosslinked unsaturated lipid fatty acids into thermoset polymers through Fenton reactions when combined with acrolein. Further, hydroquinone was a superior antioxidant to vitamin E.