Airway and systemic biomarkers of health effects after short-term exposure to indoor ultrafine particles from cooking and candles - A randomized controlled double-blind crossover study among mild asthmatic subjects.

BACKGROUND: There is insufficient knowledge about the systemic health effects of exposure to fine (PM2.5) and ultrafine particles emitted from typical indoor sources, including cooking and candlelight burning. We examined whether short-term exposure to emissions from cooking and burning candles cause inflammatory changes in young individuals with mild asthma. Thirty-six non-smoking asthmatics participated in a randomized controlled double-blind crossover study attending three exposure sessions (mean PM2.5 µg/m3; polycyclic aromatic hydrocarbons ng/m3): (a) air mixed with emissions from cooking (96.1; 1.1), (b) air mixed with emissions from candles (89.8; 10), and (c) clean filtered air (5.8; 1.0). Emissions were generated in an adjacent chamber and let into a full-scale exposure chamber where participants were exposed for five hours. Several biomarkers were assessed in relation to airway and systemic inflammatory changes; the primary outcomes of interest were surfactant Protein-A (SP-A) and albumin in droplets in exhaled air - novel biomarkers for changes in the surfactant composition of small airways. Secondary outcomes included cytokines in nasal lavage, cytokines, C-reactive protein (CRP), epithelial progenitor cells (EPCs), genotoxicity, gene expression related to DNA-repair, oxidative stress, and inflammation, as well as metabolites in blood. Samples were collected before exposure start, right after exposure and the next morning. RESULTS: SP-A in droplets in exhaled air showed stable concentrations following candle exposure, while concentrations decreased following cooking and clean air exposure. Albumin in droplets in exhaled air increased following exposure to cooking and candles compared to clean air exposure, although not significant. Oxidatively damaged DNA and concentrations of some lipids and lipoproteins in the blood increased significantly following exposure to cooking. We found no or weak associations between cooking and candle exposure and systemic inflammation biomarkers including cytokines, CRP, and EPCs. CONCLUSIONS: Cooking and candle emissions induced effects on some of the examined health-related biomarkers, while no effect was observed in others; Oxidatively damaged DNA and concentrations of lipids and lipoproteins were increased in blood after exposure to cooking, while both cooking and candle emissions slightly affected the small airways including the primary outcomes SP-A and albumin. We found only weak associations between the exposures and systemic inflammatory biomarkers. Together, the results show the existence of mild inflammation following cooking and candle exposure.

Indoor PM2.5 from occupied residences in Sweden caused higher inflammation in mice compared to outdoor PM2.5.

We spend most of our time indoors; however, little is known about the effects of exposure to aerosol particles indoors. We aimed to determine differences in relative toxicity and physicochemical properties of PM2.5 collected simultaneously indoors (PM2.5 INDOOR ) and outdoors (PM2.5 OUTDOOR ) in 15 occupied homes in southern Sweden. Collected particles were extracted from filters, pooled (indoor and outdoor separately), and characterized for chemical composition and endotoxins before being tested for toxicity in mice via intratracheal instillation. Various endpoints including lung inflammation, genotoxicity, and acute-phase response in lung and liver were assessed 1, 3, and 28 days post-exposure. Chemical composition of particles used in toxicological assessment was compared to particles analyzed without extraction. Time-resolved particle mass and number concentrations were monitored. PM2.5 INDOOR showed higher relative concentrations (µg mg-1 ) of metals, PAHs, and endotoxins compared to PM2.5 OUTDOOR . These differences may be linked to PM2.5 INDOOR causing significantly higher lung inflammation and lung acute-phase response 1 day post-exposure compared to PM2.5 OUTDOOR and vehicle controls, respectively. None of the tested materials caused genotoxicity. PM2.5 INDOOR displayed higher relative toxicity than PM2.5 OUTDOOR under the studied conditions, that is, wintertime with reduced air exchange rates, high influence of indoor sources, and relatively low outdoor concentrations of PM. Reducing PM2.5 INDOOR exposure requires reduction of both infiltration from outdoors and indoor-generated particles.

Lung function and self-rated symptoms in healthy volunteers after exposure to hydrotreated vegetable oil (HVO) exhaust with and without particles.

BACKGROUND: Diesel engine exhaust causes adverse health effects. Meanwhile, the impact of renewable diesel exhaust, such as hydrotreated vegetable oil (HVO), on human health is less known. Nineteen healthy volunteers were exposed to HVO exhaust for 3 h in a chamber with a double-blind, randomized setup. Exposure scenarios comprised of HVO exhaust from two modern non-road vehicles with 1) no aftertreatment system ('HVOPM+NOx' PM1: 93 µg m-3, EC: 54 µg m-3, NO: 3.4 ppm, NO2: 0.6 ppm), 2) an aftertreatment system containing a diesel oxidation catalyst and a diesel particulate filter ('HVONOx' PM1: ~ 1 µg m-3, NO: 2.0 ppm, NO2: 0.7 ppm) and 3) filtered air (FA) as control. The exposure concentrations were in line with current EU occupational exposure limits (OELs) of NO, NO2, formaldehyde, polycyclic aromatic hydrocarbons (PAHs), and the future OEL (2023) of elemental carbon (EC). The effect on nasal patency, pulmonary function, and self-rated symptoms were assessed. Calculated predicted lung deposition of HVO exhaust particles was compared to data from an earlier diesel exhaust study. RESULTS: The average total respiratory tract deposition of PM1 during HVOPM+NOx was 27 µg h-1. The estimated deposition fraction of HVO PM1 was 40-50% higher compared to diesel exhaust PM1 from an older vehicle (earlier study), due to smaller particle sizes of the HVOPM+NOx exhaust. Compared to FA, exposure to HVOPM+NOx and HVONOx caused higher incidence of self-reported symptoms (78%, 63%, respectively, vs. 28% for FA, p < 0.03). Especially, exposure to HVOPM+NOx showed 40-50% higher eye and throat irritation symptoms. Compared to FA, a decrement in nasal patency was found for the HVONOx exposures (- 18.1, 95% CI: - 27.3 to - 8.8 L min-1, p < 0.001), and for the HVOPM+NOx (- 7.4 (- 15.6 to 0.8) L min-1, p = 0.08). Overall, no clinically significant change was indicated in the pulmonary function tests (spirometry, peak expiratory flow, forced oscillation technique). CONCLUSION: Short-term exposure to HVO exhaust concentrations corresponding to EU OELs for one workday did not cause adverse pulmonary function changes in healthy subjects. However, an increase in self-rated mild irritation symptoms, and mild decrease in nasal patency after both HVO exposures, may indicate irritative effects from exposure to HVO exhaust from modern non-road vehicles, with and without aftertreatment systems.

Underground emissions and miners' personal exposure to diesel and renewable diesel exhaust in a Swedish iron ore mine.

PURPOSE: Underground diesel exhaust exposure is an occupational health risk. It is not known how recent intensified emission legislation and use of renewable fuels have reduced or altered occupational exposures. We characterized these effects on multipollutant personal exposure to diesel exhaust and underground ambient air concentrations in an underground iron ore mine. METHODS: Full-shift personal sampling (12 workers) of elemental carbon (EC), nitrogen dioxide (NO2), polycyclic aromatic hydrocarbons (PAHs), and equivalent black carbon (eBC) was performed. The study used and validated eBC as an online proxy for occupational exposure to EC. Ambient air sampling of these pollutants and particle number size distribution and concentration were performed in the vicinity of the workers. Urine samples (27 workers) were collected after 8 h exposure and analyzed for PAH metabolites and effect biomarkers (8-oxodG for DNA oxidative damage, 4-HNE-MA for lipid peroxidation, 3-HPMA for acrolein). RESULTS: The personal exposures (geometric mean; GM) of the participating miners were 7 µg EC m-3 and 153 µg NO2 m-3, which are below the EU occupational exposure limits. However, exposures up to 94 µg EC m-3 and 1200 µg NO2 m-3 were observed. There was a tendency that the operators of vehicles complying with sharpened emission legislation had lower exposure of EC. eBC and NO2 correlated with EC, R = 0.94 and R = 0.66, respectively. No correlation was found between EC and the sum of 16 priority PAHs (GM 1790 ng m-3). Ratios between personal exposures and ambient concentrations were similar and close to 1 for EC and NO2, but significantly higher for PAHs. Semi-volatile PAHs may not be effectively reduced by the aftertreatment systems, and ambient area sampling did not predict the personal airborne PAHs exposure well, neither did the slightly elevated concentration of urinary PAH metabolites correlate with airborne PAH exposure. CONCLUSION: Miners' exposures to EC and NO2 were lower than those in older studies indicating the effect of sharpened emission legislation and new technologies. Using modern vehicles with diesel particulate filter (DPF) may have contributed to the lower ambient underground PM concentration and exposures. The semi-volatile behavior of the PAHs might have led to inefficient removal in the engines aftertreatment systems and delayed removal by the workplace ventilation system due to partitioning to indoor surfaces. The results indicate that secondary emissions can be an important source of gaseous PAH exposure in the mine.

Emissions of soot, PAHs, ultrafine particles, NOx, and other health relevant compounds from stressed burning of candles in indoor air.

Burning candles release a variety of pollutants to indoor air, some of which are of concern for human health. We studied emissions of particles and gases from the stressed burning of five types of pillar candles with different wax and wick compositions. The stressed burning was introduced by controlled fluctuating air velocities in a 21.6 m3 laboratory chamber. The aerosol physicochemical properties were measured both in well-mixed chamber air and directly above the candle flame with online and offline techniques. All candles showed different emission profiles over time with high repeatability among replicates. The particle mass emissions from stressed burning for all candle types were dominated by soot (black carbon; BC). The wax and wick composition strongly influenced emissions of BC, PM2.5 , and particle-phase polycyclic aromatic hydrocarbons (PAHs), and to lower degree ultrafine particles, inorganic and organic carbon fraction of PM, but did not influence NOx , formaldehyde, and gas-phase PAHs. Measurements directly above the flame showed empirical evidence of short-lived strong emission peaks of soot particles. The results show the importance of including the entire burn time of candles in exposure assessments, as their emissions can vary strongly over time. Preventing stressed burning of candles can reduce exposure to pollutants in indoor air.

Exposure, respiratory symptoms, lung function and inflammation response of road-paving asphalt workers.

BACKGROUND: Controversy exists as to the health effects of exposure to asphalt and crumb rubber modified (CRM) asphalt, which contains recycled rubber tyres. OBJECTIVE: To assess exposures and effects on airway symptoms, lung function and inflammation biomarkers in conventional and CRM asphalt road pavers. METHODS: 116 conventional asphalt workers, 51 CRM asphalt workers and 100 controls were investigated. A repeated-measures analysis included 31 workers paving with both types of asphalt. Exposure to dust, nitrosamines, benzothiazole and polycyclic aromatic hydrocarbon (PAH) was measured in worksites. Self-reported symptoms, spirometry test and blood sampling were conducted prework and postwork. Symptoms were further collected during off-season for asphalt paving. RESULTS: Dust, PAHs and nitrosamine exposure was highly varied, without difference between conventional and CRM asphalt workers. Benzothiazole was higher in CRM asphalt workers (p<0.001). Higher proportions of asphalt workers than controls reported eye symptoms with onset in the current job. Decreased lung function from preworking to postworking was found in CRM asphalt workers and controls. Preworking interleukin-8 was higher in CRM asphalt workers than in the controls, followed by a decrement after 4 days of working. No differences in any studied effects were found between conventional and CRM asphalt paving. CONCLUSION: CRM asphalt workers are exposed to higher benzothiazole. Further studies are needed to identify the source of nitrosamines in conventional asphalt. Mild decrease in lung function in CRM asphalt workers and work-related eye symptoms in both asphalt workers were observed. However, our study did not find strong evidence for severe respiratory symptoms and inflammation response among asphalt workers.

Are urinary PAHs biomarkers of controlled exposure to diesel exhaust?

Urinary polycyclic aromatic hydrocarbons (PAHs) were evaluated as possible biomarkers of exposure to diesel exhaust (DE) in two controlled-chamber studies. We report levels of 14 PAHs from 28 subjects in urine that were collected before, immediately after and the morning after exposure. Using linear mixed-effects models, we tested for effects of DE exposure and several covariates (time, age, gender and urinary creatinine) on urinary PAH levels. DE exposures did not significantly alter urinary PAH levels. We conclude that urinary PAHs are not promising biomarkers of short-term exposures to DE in the range of 106-276 µg/m(3).

Indoor air levels of polycyclic aromatic compounds (PAC) in public buildings with creosote impregnated constructions - A pilot case study using passive samplers.

Creosote has been used in Sweden as a wood preservative in buildings since the 19th century. These buildings can function as workplaces, homes, and cultural buildings to which the public has access. Creosote contains polycyclic aromatic hydrocarbons (PAH) which are well known carcinogens. To understand exposure and risks in an indoor environment, it is important to determine air levels of parent PAHs as well as the more toxic nitrated and oxygenated PAH derivatives (NPAH, OPAH). This study aims to investigate indoor air levels of polycyclic aromatic compounds (PACs) e.g., PAH, NPAH, OPAH and dibenzothiophenes in buildings containing creosote sources and whether these levels pose a health risk. Four cultural buildings were studied, all located within a radius of 130 m. Two were known to have creosote sources, and two had not. Polyurethane foam passive air samplers (PUF-PAS) were used to indicate possible point sources. PUF-PAS measurements were performed for one month in each building winter and summer. Simultaneously, PAC outdoor level measurements were performed. Buildings with creosote impregnated constructions had notably higher indoor air levels of PAC (31-1200 ng m-3) compared to the two buildings without creosote sources (14-45 ng m-3). The PAH cancer potency (sum of benzo[a]pyrene equivalents (BaPeq)) was more than one order of magnitude higher in the buildings containing creosote impregnated wood compared to reference buildings. The highest value was 5.1 BaPeq ng m-3 which was significantly higher than the outdoor winter measurement (1.3 BaPeq ng m-3). Fluoranthene and phenanthrene, with significant distribution in gas phase, but also several particulate NPAHs contributed significantly to the total cancer risk. Thus, creosote containing buildings can still contaminate the indoor air with PACs despite being over a hundred years old. The PUF-PAS was shown to be a good tool providing quantitative/semiquantitative measures of PACs exposure in indoor microenvironments.

An indoor air filtration study in homes of elderly: cardiovascular and respiratory effects of exposure to particulate matter.

BACKGROUND: Exposure to particulate air pollution increases respiratory and cardiovascular morbidity and mortality, especially in elderly, possibly through inflammation and vascular dysfunction. METHODS: We examined potential beneficial effects of indoor air filtration in the homes of elderly, including people taking vasoactive drugs.Forty-eight nonsmoking subjects (51 to 81 years) in 27 homes were included in this randomized, double-blind, crossover intervention study with consecutive two-week periods with or without the inclusion of a high-efficiency particle air filter in re-circulating custom built units in their living room and bedroom. We measured blood pressure, microvascular and lung function and collected blood samples for hematological, inflammation, monocyte surface and lung cell damage markers before and at day 2, 7 and 14 during each exposure scenario. RESULTS: The particle filters reduced the median concentration of PM2.5 from approximately 8 to 4 µg/m3 and the particle number concentration from 7669 to 5352 particles/cm3. No statistically significant effects of filtration as category were observed on microvascular and lung function or the biomarkers of systemic inflammation among all subjects, or in the subgroups taking (n = 11) or not taking vasoactive drugs (n = 37). However, the filtration efficacy was variable and microvascular function was within 2 days significantly increased with the actual PM2.5 decrease in the bedroom, especially among 25 subjects not taking any drugs. CONCLUSION: Substantial exposure contrasts in the bedroom and no confounding by drugs appear required for improved microvascular function by air filtration, whereas no other beneficial effect was found in this elderly population.

Simulated restaurant cook exposure to emissions of PAHs, mutagenic aldehydes, and particles from frying bacon.

This study investigated the exposure of cooks to polycyclic aromatic hydrocarbons (PAHs), higher mutagenic aldehydes, total particles, and ultrafine particles during cooking. Experiments were performed by pan frying fresh and smoked bacon on both electric and gas stoves, and with the gas alone. Detailed analyses of PAHs were performed, with analyses of the levels of 32 different PAHs. A TSI-3939 scanning mobility particle sizer system was used to measure the ultrafine particles. The results showed that total PAHs were in the range of 270-300 ng/m(3) air. However, the smoked bacon experiment showed a somewhat different PAH pattern, whereby retene constituted about 10% of the total PAHs, which is a level similar to that of the abundant gas phase constituent phenanthrene. The reason for the elevated retene emissions is unknown. The total cancer risk, expressed as toxic equivalency factors, showed a somewhat higher risk on the electric stove (p < 0.05) compared with the gas stove. Levels of trans, trans-2,4-decadienal were between 34 and 54 µg/m(3) air. The level of total particles was between 2.2 and 4.2 mg/m(3). Frying on a gas stove caused a statistically significant higher amount of ultrafine particles compared with frying on an electric stove. Large variations in the mobility diameter at peak particle concentration were found (74.4 nm-153.5 nm). The highest mobility diameter was found for frying on an electric stove. The gas flame itself showed a maximum production of 19.5-nm-sized particles and could not be the explanation for the difference between frying on the gas stove and frying on the electric stove. No single indicator for the exposure to cooking fume could be selected. Each compound should be measured independently to provide a comprehensive characterization of the cooking exposure.

Accumulation of antimony and lead in leaves and needles of trees: The role of traffic emissions.

Antimony (Sb) is a toxic metalloid, which has been increasingly used in the brake lining of vehicles, and increased concentrations have been found in soils near abundant traffic. However, since very few investigations of Sb accumulation in urban vegetation have been undertaken there exists a knowledge gap. We studied the concentrations of Sb in leaves and needles of trees in the Gothenburg City area, Sweden. In addition, lead (Pb), also associated with traffic, was investigated. Sb and Pb concentrations of Quercus palustris leaves at seven sites with contrasting traffic intensity varied substantially, correlated with the traffic-related PAH (polycyclic aromatic hydrocarbon) air pollution at the sites and increased during the growing season. Sb but not Pb concentrations were significantly higher in needles of Picea abies and Pinus sylvestris near major roads compared to sites at larger distances. In Pinus nigra needles at two urban streets both Sb and Pb were higher compared to an urban nature park environment, emphasising the role of traffic emissions for these elements. A continued accumulation of Sb and Pb in three years old needles of Pinus nigra, two years old needles of Pinus sylvestris and eleven years old needles of Picea abies was observed. Our data suggest a pronounced link between traffic pollution and Sb accumulation in leaves and needles, where the particles carrying Sb seem not to be transported very far from the source. We also conclude that there exists a strong potential for Sb and Pb bioaccumulation over time in leaves and needles. Implications of these findings are that increased concentrations of toxic Sb and Pb are likely to prevail in environments with high traffic intensity and that Sb can enter the ecological food chain by accumulation in leaves and needles, which is important for the biogeochemical cycling.

Effects on airways of short-term exposure to two kinds of wood smoke in a chamber study of healthy humans.

INTRODUCTION: Air pollution causes respiratory symptoms and pulmonary disease. Airway inflammation may be involved in the mechanism also for cardiovascular disease. Wood smoke is a significant contributor to air pollution, with complex and varying composition. We examined airway effects of two kinds of wood smoke in a chamber study. MATERIALS AND METHODS: Thirteen subjects were exposed to filtered air and to wood smoke from the start-up phase and the burn-out phase of the wood-burning cycle. Levels of PM(2.5) were 295 µg/m(3) and 146 µg/m(3), number concentrations 140 000/cm(3) and 100 000/cm(3). Biomarkers in blood, breath and urine were measured before and on several occasions after exposure. Effects of wood smoke exposure were assessed adjusting for results with filtered air. RESULTS: After exposure to wood smoke from the start-up, but not the burn-out session, Clara cell protein 16 (CC16) increased in serum after 4 hours, and in urine the next morning. CC16 showed a clear diurnal variation. Fraction of exhaled nitric oxide (FENO) increased after wood smoke exposure from the burn-out phase, but partly due to a decrease after exposure to filtered air. No other airway markers increased. CONCLUSIONS: The results indicate that relatively low levels of wood smoke exposure induce effects on airways. Effects on airway epithelial permeability was shown for the start-up phase of wood burning, while FENO increased after the burn-out session. CC16 seems to be a sensitive marker of effects of air pollution both in serum and urine, but its function and the significance need to be clarified.

Polycyclic aromatic hydrocarbon (PAH) accumulation in Quercus palustris and Pinus nigra in the urban landscape of Gothenburg, Sweden.

Trees have the potential to improve urban air quality as leaves and needles capture air pollutants from the air, but further empirical data has been requested to quantify these effects. We measured the concentration of 32 polycyclic aromatic hydrocarbons (PAHs) in leaves of pin oak (Quercus palustris) and needles of black pine (Pinus nigra) in the City of Gothenburg, Sweden, during the summer of 2018. Oak leaves were collected twice (June, September), while one-year-old (C + 1) and three-year-old (C + 3) pine needles were sampled in June to study the temporal development of leaf/needle PAH concentrations. Specific leaf area (SLA) was estimated, which permitted calculation of leaf/needle area-based PAH content that were compared with the mass-based concentration. In addition, the air concentration of PAHs and NO2 was measured using passive samplers. There was a strong correlation between air concentrations of PAH and NO2, indicating that the pollutants to a large degree originate from the same sources. In the oak leaves there was a significant decrease in low molecular mass PAHs (L-PAH, mainly gaseous) between June and September, but a significant increase in high molecular mass PAHs (H-PAH, mainly particle-bound). There was a strong correlation between L-PAH concentration in leaves and in air indicating an influence of equilibrium processes between ambient air and leaf. In the pine needles, there was a significant increase of both L-PAH and H-PAH in three-year-old needles compared to one-year-old needles. Pine was superior to oak in accumulating PAHs from the air, especially for L-PAHs when comparing area-based content. However, H-PAH concentrations were higher in oak leaves compared to pine needles on a leaf mass basis, emphasizing the importance of how concentrations are expressed. The results from this study can contribute to the development of urban planning strategies regarding the effect of vegetation on air quality.

Indoor and outdoor concentrations of fine particles, particle-bound PAHs and volatile organic compounds in Kaunas, Lithuania.

This complex study presents indoor and outdoor levels of air-borne fine particles, particle-bound PAHs and VOCs at two urban locations in the city of Kaunas, Lithuania, and considers possible sources of pollution. Two sampling campaigns were performed in January-February and March-April 2009. The mean outdoor PM(2.5) concentration at Location 1 in winter was 34.5 ± 15.2 µg m(-3) while in spring it was 24.7 ± 12.2 µg m(-3); at Location 2 the corresponding values were 36.7 ± 21.7 and 22.4 ± 19.4 µg m(-3), respectively. In general there was little difference between the PM concentrations at Locations 1 and 2. PM(2.5) concentrations were lower during the spring sampling campaign. These PM concentrations were similar to those in many other European cities; however, the levels of most PAHs analysed were notably higher. The mean sum PAH concentrations at Locations 1 and 2 in the winter campaign were 75.1 ± 32.7 and 32.7 ± 11.8 ng m(-3), respectively. These differences are greater than expected from the difference in traffic intensity at the two sites, suggesting that there is another significant source of PAH emissions at Location 1 in addition to the traffic. The low observed indoor/outdoor (I/O) ratios indicate that PAH emissions at the locations studied arise primarily from outdoor sources. The buildings at both locations have old windows with wooden frames that are fairly permissive in terms of air circulation. VOC concentrations were mostly low and comparable to those reported from Sweden. The mean outdoor concentrations of VOC's were: 0.7 ± 0.2, 3.0 ± 0.8, 0.5 ± 0.2, 3.5 ± 0.3, and 0.2 ± 0.1 µg m(-3), for benzene, toluene, ethylbenzene, sum of m-, p-, o-xylenes, and naphthalene, respectively. Higher concentrations of VOCs were observed during the winter campaign, possibly due to slower dispersion, slower chemical transformations and/or the lengthy "cold start" period required by vehicles in the wintertime. A trajectory analysis showed that air masses coming from Eastern Europe carried significantly higher levels of PM(2.5) compared to masses from other regions, but the PAHs within the PM(2.5) are of local origin. It has been suggested that street dust, widely used for winter sanding activities in Eastern and Central European countries, may act not only as a source of PM, but also as source of particle-bound PAHs. Other potential sources include vehicle exhaust, domestic heating and long-range transport.

Biomarkers after Controlled Inhalation Exposure to Exhaust from Hydrogenated Vegetable Oil (HVO).

Hydrogenated vegetable oil (HVO) is a renewable diesel fuel used to replace petroleum diesel. The organic compounds in HVO are poorly characterized; therefore, toxicological properties could be different from petroleum diesel exhaust. The aim of this study was to evaluate the exposure and effective biomarkers in 18 individuals after short-term (3 h) exposure to HVO exhaust and petroleum diesel exhaust fumes. Liquid chromatography tandem mass spectrometry was used to analyze urinary biomarkers. A proximity extension assay was used for the measurement of inflammatory proteins in plasma samples. Short-term (3 h) exposure to HVO exhaust (PM1 ~1 µg/m3 and ~90 µg/m3 for vehicles with and without exhaust aftertreatment systems, respectively) did not increase any exposure biomarker, whereas petroleum diesel exhaust (PM1 ~300 µg/m3) increased urinary 4-MHA, a biomarker for p-xylene. HVO exhaust from the vehicle without exhaust aftertreatment system increased urinary 4-HNE-MA, a biomarker for lipid peroxidation, from 64 ng/mL urine (before exposure) to 141 ng/mL (24 h after exposure, p < 0.001). There was no differential expression of plasma inflammatory proteins between the HVO exhaust and control exposure group. In conclusion, short-term exposure to low concentrations of HVO exhaust did not increase urinary exposure biomarkers, but caused a slight increase in lipid peroxidation associated with the particle fraction.

Field evaluation of a passive personal air sampler for screening of PAH exposure in workplaces.

New sampling methods are needed to simplify and enable frequent monitoring of workers' exposure to polycyclic aromatic hydrocarbons (PAHs). The sampler needs to fulfil some key operational requirements for occupational exposure assessments: (i) be usable as a personal sampler; (ii) work over 8 h exposure time; (iii) sequester PAHs both in gas and particle phase, (iv) yield reliable estimates of air concentrations. Here, a new smaller design of the traditional polyurethane foam (PUF) passive air sampler (PAS) (i.e. a 'mini-PUF') was introduced and assessed against these requirements in sites with elevated PAH concentrations. The exposure times were 2 weeks and 8 hours. The obtained sampling rates (R-values) were not significantly different between gas phase (0.4-3.3 m(3) day(-1), 0.3-2.3 L min(-1)) and particle associated PAHs (0.5-1.9 m(3) day(-1), 0.4-1.3 L min(-1)). The accuracy in estimating air concentrations was within +/-25% from the active sampler for half of the PAHs for the mini-PUF under 8 h exposures. Significant correlations (p < 0.003) were found between personally deployed mini-PUFs and a co-deployed personal active sampling method. This together with the low costs and ease-of-use of the mini-PUF encourage application in exposure assessments.

Emission factors and composition of PM2.5 from laboratory combustion of five Western Australian vegetation types.

This study investigated the emission of PM10 and PM2.5 (particulates with diameters of less than 10 µm and 2.5 µm, respectively) and the chemical composition of PM2.5 from laboratory combustion of five Australian vegetation types (three grasslands, a woodland and a forest). A mix of plants representative of Banksia (woodland) and Jarrah (forest) and three types of grasses (Spinifex - Triodia basedowii; Kimberley grass - Sehima nervosum and Heteropogon contortus; and an invasive grass (Veldt) - Ehrharta calycina) were burnt in 9 combustion conditions comprised of 3 fuel moisture levels (dry, moist, wet) and 3 air flow rates (no, low and high flow). PM (particulate matter) samples were collected onto filters and measured using gravimetric analysis. PM2.5 was then extracted and analyzed for water-soluble metals and polycyclic aromatic hydrocarbons (PAH) concentrations. The largest proportion of PM10 (98%) from vegetation fires was PM2.5. Banksia yielded the highest PM2.5 emission factor (EF), followed by Jarrah and Spinifex. Veldt grass combustion generated significantly higher emissions of PM2.5 compared with the other two grass types. High moisture contents and flow rates resulted in larger emissions of PM2.5. A strong correlation (R2 = 0.84) was observed between the EF for PM2.5 and combustion efficiency, suggesting higher PM emission with lower combustion efficiencies. Potassium and sodium were the most abundant PM2.5-bound water soluble metals, accounting for more than 97% of the total mass of metals analyzed. PAHs were found in significant concentrations, including the carcinogenic benzo(a)pyrene. Pyrene and fluoranthene were the most abundant PAHs detected, accounting for nearly 40% mass of the total PAHs. Indeno(1,2,3-cd)pyrene and benzo(g,h,i)perylene ratio (IND/IND + BghiP) appeared to be produced in a diagnostic ratio that indicated that the PAHs were derived from vegetation fires rather than other sources of emissions. The EF for PM2.5 and its chemical composition (water-soluble metals and PAHs) were strongly influenced by the type of vegetation burned. The results presented in this study could be useful in predicting the risks of human health effects on firefighters and the public who may be exposed to regular bushfires in Australia.

Urban PM2.5 Induces Cellular Toxicity, Hormone Dysregulation, Oxidative Damage, Inflammation, and Mitochondrial Interference in the HRT8 Trophoblast Cell Line.

Objective: Epidemiological studies have found air pollution to be a driver of adverse pregnancy outcomes, including gestational diabetes, low term birth weight and preeclampsia. It is unknown what biological mechanisms are involved in this process. A first trimester trophoblast cell line (HTR-8/SVneo) was exposed to various concentrations of PM2.5 (PM2.5) in order to elucidate the effect of urban particulate matter (PM) of size <2.5 µm on placental function. Methods: PM2.5 were collected at a site representative of urban traffic and dispersed in cell media by indirect and direct sonication. The HTR-8 cells were grown under standard conditions. Cellular uptake was studied after 24 and 48 h of exposure by transmission electron microscopy (TEM). The secretion of human chorionic gonadotropin (hCG), progesterone, and Interleukin-6 (IL-6) was measured by ELISA. Changes in membrane integrity and H2O2 production were analyzed using the CellToxTM Green Cytotoxicity and ROSGloTM assays. Protease activity was evaluated by MitoToxTM assay. Mitochondrial function was assessed through high resolution respirometry in an Oroboros O2k-FluoRespirometer, and mitochondrial content was quantified by citrate synthase activity. Results: TEM analysis depicted PM2.5 cellular uptake and localization of the PM2.5 to the mitochondria after 24 h. The cells showed aggregated cytoskeleton and generalized necrotic appearance, such as chromatin condensation, organelle swelling and signs of lost membrane integrity. The mitochondria displayed vacuolization and disruption of cristae morphology. At 48 h exposure, a significant drop in hCG secretion and a significant increase in progesterone secretion and IL-6 production occurred. At 48 h exposure, a five-fold increase in protease activity and a significant alteration of H2O2 production was observed. The HTR-8 cells exhibited evidence of increased cytotoxicity with increasing exposure time and dose of PM2.5. No significant difference in mitochondrial respiration or mitochondrial mass could be demonstrated. Conclusion: Following exposure to air pollution, intracellular accumulation of PM may contribute to the placental dysfunction associated with pregnancy outcomes, such as preeclampsia and intrauterine growth restriction, through their direct and indirect effects on trophoblast protein secretion, hormone regulation, inflammatory response, and mitochondrial interference.

Exposure to wood smoke particles leads to inflammation, disrupted proliferation and damage to cellular structures in a human first trimester trophoblast cell line.

The ongoing transition to renewable fuel sources has led to increased use of wood and other biomass fuels. The physiochemical characteristics of biomass combustion derived aerosols depends on appliances, fuel and operation procedures, and particles generated during incomplete combustion are linked to toxicity. Frequent indoor wood burning is related to severe health problems such as negative effects on airways and inflammation, as well as chronic hypoxia and pathological changes in placentas, adverse pregnancy outcome, preterm delivery and increased risk of preeclampsia. The presence of combustion-derived black carbon particles at both the maternal and fetal side of placentas suggests that particles can reach the fetus. Air pollution particles have also been shown to inhibit trophoblast migration and invasion, which are vital functions for the development of the placenta during the first trimester. In this study we exposed a placental first trimester trophoblast cell line to wood smoke particles emitted under Nominal Burn rate (NB) or High Burn rate (HB). The particles were visible inside exposed cells and localized to the mitochondria, causing ultrastructural changes in mitochondria and endoplasmic reticulum. Exposed cells showed decreased secretion of the pregnancy marker human chorionic gonadotropin, increased secretion of IL-6, disrupted membrane integrity, disrupted proliferation and contained specific polycyclic aromatic hydrocarbons (PAHs) from the particles. Taken together, these results suggest that wood smoke particles can enter trophoblasts and have detrimental effects early in pregnancy by disrupting critical trophoblast functions needed for normal placenta development and function. This could contribute to the underlying mechanisms leading to pregnancy complications such as miscarriage, premature birth, preeclampsia and/or fetal growth restriction. This study support the general recommendation that more efficient combustion technologies and burning practices should be adopted to reduce some of the toxicity generated during wood burning.

Roof cavity dust as an exposure proxy for extreme air pollution events.

Understanding exposure to air pollution during extreme events such as fire emergencies is critical for assessing their potential health impacts. However, air pollution emergencies often affect places without a network of air quality monitoring and characterising exposure retrospectively is methodologically challenging due to the complex behaviour of smoke and other air pollutants. Here we test the potential of roof cavity (attic) dust to act as a robust household-level exposure proxy, using a major air pollution event associated with a coal mine fire in the Latrobe Valley, Australia, as an illustrative study. To assess the relationship between roof cavity dust composition and mine fire exposure, we analysed the elemental and polycyclic aromatic hydrocarbon composition of roof cavity dust (<150µm) from 39 homes along a gradient of exposure to the mine fire plume. These homes were grouped into 12 zones along this exposure gradient: eight zones across Morwell, where mine fire impacts were greatest, and four in other Latrobe Valley towns at increasing distance from the fire. We identified two elements-barium and magnesium-as 'chemical markers' that show a clear and theoretically grounded relationship with the brown coal mine fire plume exposure. This relationship is robust to the influence of plausible confounders and contrasts with other, non-mine fire related elements, which showed distinct and varied distributional patterns. We conclude that targeted components of roof cavity dust can be a useful empirical marker of household exposure to severe air pollution events and their use could support epidemiological studies by providing spatially-resolved exposure estimates post-event.