Non-volatile particle emissions from aircraft turbine engines at ground-idle induce oxidative stress in bronchial cells

Aircraft emissions contribute to local and global air pollution. Health effects of particulate matter (PM) from aircraft engines are largely unknown, since controlled cell exposures at relevant conditions are challenging. We examined the toxicity of non-volatile PM (nvPM) emissions from a CFM56-7B26 turbofan, the world's most used aircraft turbine using an unprecedented exposure setup. We combined direct turbine-exhaust sampling under realistic engine operating conditions and the Nano-Aerosol Chamber for In vitro Toxicity to deposit particles onto air-liquid-interface cultures of human bronchial epithelial cells (BEAS-2B) at physiological conditions. We evaluated acute cellular responses after 1-h exposures to diluted exhaust from conventional or alternative fuel combustion. We show that single, short-term exposures to nvPM impair bronchial epithelial cells, and PM from conventional fuel at ground-idle conditions is the most hazardous. Electron microscopy of soot reveals varying reactivity matching the observed cellular responses. Stronger responses at lower mass concentrations suggest that additional metrics are necessary to evaluate health risks of this increasingly important emission source

Road traffic noise and breast cancer:DNA methylation in four core circadian genes

Background: Transportation noise has been linked with breast cancer, but existing literature is conflicting. One proposed mechanism is that transportation noise disrupts sleep and the circadian rhythm. We investigated the relationships between road traffic noise, DNA methylation in circadian rhythm genes, and breast cancer. We selected 610 female participants (318 breast cancer cases and 292 controls) enrolled into the Malmö, Diet, and Cancer cohort. DNA methylation of CpGs (N = 29) in regulatory regions of circadian rhythm genes (CRY1, BMAL1, CLOCK, and PER1) was assessed by pyrosequencing of DNA from lymphocytes collected at enrollment. To assess associations between modeled 5-year mean residential road traffic noise and differentially methylated CpG positions, we used linear regression models adjusting for potential confounders, including sociodemographics, shiftwork, and air pollution. Linear mixed effects models were used to evaluate road traffic noise and differentially methylated regions. Unconditional logistic regression was used to investigate CpG methylation and breast cancer. Results: We found that higher mean road traffic noise was associated with lower DNA methylation of three CRY1 CpGs (CpG1, CpG2, and CpG12) and three BMAL1 CpGs (CpG2, CpG6, and CpG7). Road traffic noise was also associated with differential methylation of CRY1 and BMAL1 promoters. In CRY1 CpG2 and CpG5 and in CLOCK CpG1, increasing levels of methylation tended to be associated with lower odds of breast cancer, with odds ratios (OR) of 0.88 (95% confidence interval (CI) 0.76–1.02), 0.84 (95% CI 0.74–0.96), and 0.80 (95% CI 0.68–0.94), respectively. Conclusions: In summary, our data suggest that DNA hypomethylation in CRY1 and BMAL1 could be part of a causal chain from road traffic noise to breast cancer. This is consistent with the hypothesis that disruption of the circadian rhythm, e.g., from road traffic noise exposure, increases the risk of breast cancer. Since no prior studies have explored this association, it is essential to replicate our results. Graphical abstract: (Figure presented.

Short-lived reactive components substantially contribute to particulate matter oxidative potential.

Exposure to airborne particulate matter (PM) has been attributed to millions of deaths annually. However, the PM components responsible for observed health effects remain unclear. Oxidative potential (OP) has gained increasing attention as a key property that may explain PM toxicity. Using online measurement methods that impinge particles for OP quantification within seconds, we reveal that 60 to 99% of reactive oxygen species (ROS) and OP in secondary organic aerosol and combustion-generated PM have a lifetime of minutes to hours and that the ROS activity of ambient PM decays substantially before offline analysis. This implies that current offline measurement methods substantially underestimate the true OP of PM. We demonstrate that short-lived OP components activate different toxicity pathways upon direct deposition onto reconstituted human bronchial epithelia. Therefore, we suggest that future air pollution and health studies should include online OP quantification, allowing more accurate assessments of links between OP and health effects

Novel instrument to generate representative e-cigarette vapors for physicochemical particle characterization and in-vitro toxicity

The use of “electronic cigarettes” (e-cigs) has exponentially increased during the last decade. This drastic growth has been observed in smokers and never smokers, women and teenagers, with indicators for adverse effects related to nicotine, but also to e-liquid and vapor components. The aerosol characteristics depend on the e-cig features. Therefore, the introduction of many different e-cig types on the market leads to concerns regarding their potential Health effects. Our study aims to develop an instrument to generate representative vapors from e-cigarette devices, characterize the physicochemical properties of the aerosols and elucidate the adverse effects of inhaled vapors on normal human airway epithelia. E-cig vapors were produced using a specially developed aerosol generation instrument mimicking user puffing behavior. Aerosol particle size distribution and concentration were characterized with a Scanning Mobility Particle Sizer. Air-liquid interface cultures of differentiated human bronchial epithelial cells were exposed to 1 puff topography, i.e. to 21 puffs of 3 s with 22-second puff intervals using the Nano-Aerosol Chamber for In-Vitro Toxicity, which simulates particle deposition in the respiratory tract. Cell morphology was evaluated by light microcopy and induction of cell death by release of lactate Dehydrogenase at 4 and 24 h after aerosol exposure. Particle size in e-cig generated aerosols ranged from 20 to 430 nm and concentrations exceeded 1×10^6 particles/cm3. Deposited particle doses were 0.9–3 μg/cm2, depending on e-device type and number of puffs. A single exposure to e-cig vapors caused changes in epithelial cell shape but no massive cell death. We successfully developed an aerosol generation system to produce and deposit realistic vapors from e-cigs. The results obtained indicate that a single exposure to e-cig aerosols affects epithelial morphology and slightly increases cell death. Our interdisciplinary approach combining aerosol Technology and biology allows identifying adverse effects of e-cigs to the respiratory tract in vitro

Assessment of the oxidative potential of nanoparticles by the cytochrome c assay: assay improvement and development of a high-throughput method to predict the toxicity of nanoparticles

International audienceOxidative stress has increasingly been demonstrated as playing a key role in the biological response induced by nanoparticles (NPs). The acellular cytochrome c oxidation assay has been proposed to determine the intrinsic oxidant-generating capacity of NPs. Yet, there is a need to improve this method to allow a rapid screening to classify NPs in terms of toxicity. We adapted the cytochrome c assay to take into account NP interference, to improve its sensitivity and to develop a high-throughput method. The intrinsic oxidative ability of a panel of NPs (carbon black, Mn2O3, Cu, Ag, BaSO4, CeO2, TiO2 and ZnO) was measured with this enhanced test and compared to other acellular redox assays. To assess whether their oxidative potential correlates with cellular responses, we studied the effect of insoluble NPs on the human bronchial epithelial cell line NCI-H292 by measuring the cytotoxicity (WST-1 assay), pro-inflammatory response (IL-8 cytokine production and expression) and antioxidant defense induction (SOD2 and HO-1 expression). The adapted cytochrome c assay had a greatly increased sensitivity allowing the ranking of NPs in terms of their oxidative potential by using the developed high-throughput technique. Besides, a high oxidative potential revealed to be predictive for toxic effects as Mn2O3 NPs induced a strong oxidation of cytochrome c and a dose-dependent cytotoxicity, pro-inflammatory response and antioxidant enzyme expression. BaSO4, which presented no intrinsic oxidative potential, had no cellular effects. Nevertheless, CeO2 and TiO2 NPs demonstrated no acellular oxidant-generating capacity but induced moderate cellular responses. In conclusion, the novel cytochrome c oxidation assay could be used for high-throughput screening of the intrinsic oxidative potential of NPs. However, acellular redox assays may not be sufficient to discriminate among low-toxicity NPs, and additional tests are thus needed

Toxic metals and essential trace elements in placenta and their relation to placental function

Introduction: Placental function is essential for fetal development, but it may be susceptible to malnutrition and environmental stressors. Objective: To assess the impact of toxic and essential trace elements in placenta on placental function. Methods: Toxic metals (cadmium, lead, mercury, cobalt) and essential elements (copper, manganese, zinc, selenium) were measured in placenta of 406 pregnant women in northern Sweden using ICP-MS. Placental weight and birth weight were obtained from hospital records and fetoplacental weight ratio was used to estimate placental efficiency. Placental relative telomere length (TL) and mitochondrial DNA copy number (mtDNAcn) were determined by quantitative PCR (n = 285). Single exposure-outcome associations were evaluated using linear or spline regression, and joint associations and interactions with Bayesian kernel machine regression (BKMR), all adjusted for sex, maternal smoking, and age or BMI. Results: Median cadmium, mercury, lead, cobalt, copper, manganese, zinc, and selenium concentrations in placenta were 3.2, 1.8, 4.3, 2.3, 1058, 66, 10626, and 166 μg/kg, respectively. In the adjusted regression, selenium (>147 μg/kg) was inversely associated with placental weight (B: −158; 95 % CI: −246, −71, per doubling), as was lead at low selenium (B: −23.6; 95 % CI: −43.2, −4.0, per doubling). Manganese was positively associated with placental weight (B: 41; 95 % CI: 5.9, 77, per doubling) and inversely associated with placental efficiency (B: −0.01; 95 % CI: −0.019, −0.004, per doubling). Cobalt was inversely associated with mtDNAcn (B: −11; 95 % CI: −20, −0.018, per doubling), whereas all essential elements were positively associated with mtDNAcn, individually and joint. Conclusion: Among the toxic metals, lead appeared to negatively impact placental weight and cobalt decreased placental mtDNAcn. Joint essential element concentrations increased placental mtDNAcn. Manganese also appeared to increase placental weight, but not birth weight. The inverse association of selenium with placental weight may reflect increased transport of selenium to the fetus in late gestation

Toxicity of particles derived from combustion of Ethiopian traditional biomass fuels in human bronchial and macrophage-like cells

The combustion of traditional fuels in low-income countries, including those in sub-Saharan Africa, leads to extensive indoor particle exposure. Yet, the related health consequences in this context are understudied. This study aimed to evaluate the in vitro toxicity of combustion-derived particles relevant for Sub-Saharan household environments. Particles (< 2.5 µm) were collected using a high-volume sampler during combustion of traditional Ethiopian biomass fuels: cow dung, eucalyptus wood and eucalyptus charcoal. Diesel exhaust particles (DEP, NIST 2975) served as reference particles. The highest levels of particle-bound polycyclic aromatic hydrocarbons (PAHs) were found in wood (3219 ng/mg), followed by dung (618 ng/mg), charcoal (136 ng/mg) and DEP (118 ng/mg) (GC–MS). BEAS-2B bronchial epithelial cells and THP-1 derived macrophages were exposed to particle suspensions (1–150 µg/mL) for 24 h. All particles induced concentration-dependent genotoxicity (comet assay) but no pro-inflammatory cytokine release in epithelial cells, whereas dung and wood particles also induced concentration-dependent cytotoxicity (Alamar Blue). Only wood particles induced concentration-dependent cytotoxicity and genotoxicity in macrophage-like cells, while dung particles were unique at increasing secretion of pro-inflammatory cytokines (IL-6, IL-8, TNF-α). In summary, particles derived from combustion of less energy dense fuels like dung and wood had a higher PAH content and were more cytotoxic in epithelial cells. In addition, the least energy dense and cheapest fuel, dung, also induced pro-inflammatory effects in macrophage-like cells. These findings highlight the influence of fuel type on the toxic profile of the emitted particles and warrant further research to understand and mitigate health effects of indoor air pollution