Air Pollution-Related Neurotoxicity Across the Life Span.

Air pollution is a complex mixture of gases and particulate matter, with adsorbed organic and inorganic contaminants, to which exposure is lifelong. Epidemiological studies increasingly associate air pollution with multiple neurodevelopmental disorders and neurodegenerative diseases, findings supported by experimental animal models. This breadth of neurotoxicity across these central nervous system diseases and disorders likely reflects shared vulnerability of their inflammatory and oxidative stress-based mechanisms and a corresponding ability to produce brain metal dyshomeo-stasis. Future research to define the responsible contaminants of air pollution underlying this neurotoxicity is critical to understanding mechanisms of these diseases and disorders and protecting public health.

Airborne Nanoparticle Concentrations Are Associated with Increased Mortality Risk in Canada's Two Largest Cities.

RATIONALE: Outdoor fine particulate air pollution (PM2.5) contributes to millions of deaths around the world each year, but much less is known about the long-term health impacts of other particulate air pollutants including ultrafine particles (a.k.a. nanoparticles) which are in the nanometer size range (<100 nm), widespread in urban environments, and not currently regulated. OBJECTIVES: Estimate the associations between long-term exposure to outdoor ultrafine particles and mortality. METHODS: Outdoor air pollution levels were linked to the residential addresses of a large, population-based cohort from 2001 - 2016. Associations between long-term exposure to outdoor ultrafine particles and nonaccidental and cause-specific mortality were estimated using Cox proportional hazards models. MEASUREMENTS: An increase in long-term exposure to outdoor ultrafine particles was associated with an increased risk of nonaccidental mortality (Hazard Ratio = 1. 073, 95% Confidence Interval = 1. 061, 1. 085) and cause-specific mortality, the strongest of which was respiratory mortality (Hazard Ratio = 1.174, 95% Confidence Interval = 1.130, 1.220). MAIN RESULTS: Long-term exposure to outdoor ultrafine particles was associated with increased risk of mortality. We estimated the mortality burden for outdoor ultrafine particles in Montreal and Toronto, Canada to be approximately 1100 additional nonaccidental deaths every year. Furthermore, we observed possible confounding by particle size which suggests that previous studies may have underestimated or missed important health risks associated with ultrafine particles. CONCLUSIONS: As outdoor ultrafine particles are not currently regulated, there is great potential for future regulatory interventions to improve population health by targeting these common outdoor air pollutants.

Chemically Resolved Respiratory Deposition of Ultrafine Particles Characterized by Number Concentration in the Urban Atmosphere.

Ultrafine particles (UFPs) dominate the atmospheric particles in number concentration, impacting human health and climate change. However, existing studies primarily rely on mass-based approaches, leading to a restricted understanding of the number-based and chemically resolved health effects of atmospheric UFPs. In this study, we utilized a high-mass-resolution single-particle aerosol mass spectrometer to investigate the online chemical composition and number size distribution of ultrafine, fine, and coarse particles during the summertime in urban Shenzhen, China. Human respiratory deposition dose assessments of particles with varying chemical compositions were further conducted by a respiratory deposition model. The results showed that during our observation, particles containing elemental carbon (EC) were the dominant components in UFPs (0.05-0.1 µm). Compared to fine and coarse particles, UFPs can deposit more deeply into the respiratory tract with a daily dose of ∼2.08 ± 0.67 billion particles. Among the deposited UFPs, EC-cluster particles constituted ∼85.7% in number fraction, accounting for a daily number dose of ∼1.78 billion particles, which poses a greater impact on human health. Simultaneously, we found discrepancies in the chemically resolved particle depositions among number-, surface area-, and mass-based approaches, emphasizing the importance of an appropriate metric for particle health-risk evaluation.

Physicochemical Characterization of the Particulate Matter in New Jersey/New York City Area, Resulting from the Canadian Quebec Wildfires in June 2023.

The global increase in wildfires, primarily driven by climate change, significantly affects air quality and health. Wildfire-emitted particulate matter (WFPM) is linked to adverse health effects, yet the toxicological mechanisms are not fully understood given its physicochemical complexity and the lack of spatiotemporal exposure data. This study focuses on the physicochemical characterization of WFPM from a Canadian wildfire in June 2023, which affected over 100 million people in the US Northeast, particularly around New Jersey/New York. Aerosol systems were deployed to characterize WFPM during the 3 day event, revealing unprecedented mass concentrations mainly in the WFPM0.1 and WFPM0.1-2.5 size fractions. Peak WFPM2.5 concentrations reached 317 µg/m3, nearly 10 times the National Ambient Air Quality Standard (NAAQS) 24 h average limit. Chemical analysis showed a high organic-to-total carbon ratio (96%), consistent with brown carbon wildfires nanoparticles. Large concentrations of high-molecular-weight PAHs were found predominantly bound to WFPM0.1, with retene, a molecular marker of biomass burning and a known teratogen, being the most abundant (>70%). Computational modeling estimated a total lung deposition of 9.15 mg over 72 h, highlighting the health risks of WFPM, particularly due to its long-distance travel capability and impact on densely populated areas.

Indoor Emissions Contributed the Majority of Ultrafine Particles in Chinese Urban Residences.

Ultrafine particle (UFP) pollution should be controlled to reduce its effects on health. The design of control measures is limited owing to the uncertainty of source contributions in Chinese residences, where indoor UFP pollution is more severe than in Western residences. Herein, a source-specific, time-dependent UFP concentration model was developed by applying an infiltration factor model incorporating coagulation effects. A Monte Carlo framework with the UFP concentration model was employed to estimate the probabilistic distribution of source contributions in Chinese residences. The input parameter distributions were determined based on our survey and previous studies. The annually averaged indoor UFP concentration was estimated at (2.75 ± 1.71) × 104 #/cm3, ranging from 2.35 × 103 to 1.27 × 105 #/cm3 outside the kitchen, and at (5.48 ± 3.08) × 104 #/cm3, ranging from 2.90 × 103 to 1.94 × 105 #/cm3 in the kitchen. Indoor sources contributed more to indoor UFPs, accounting for 61% in the nonkitchen and 80% in the kitchen, surpassing their contribution to indoor PM2.5 in Chinese residences. Meanwhile, the indoor UFP emission contributions were higher than those in the United States, Canada, and Germany, owing to higher emissions from cooking and cigarette smoking. These results will aid in elucidating human exposure to UFPs and in designing more targeted control measures.

Diverse Metabolic Effects of Cooking Oil Fume from Four Edible Oils on Human BEAS-2B Cells: Implications for Health Guidelines.

The 2021 WHO guidelines stress the importance of measuring ultrafine particles using particle number concentration (PNC) for health assessments. However, commonly used particle metrics such as aerodynamic diameter and number concentrations do not fully capture the diverse chemical makeup of complex particles. To address this issue, our study used high-throughput mass spectrometry to analyze the properties of cooking oil fumes (COFs) in real time and evaluate their impact on BEAS-2B cell metabolism. Results showed insignificant differences in COF number size distributions between soybean oil and olive oil (peak concentrations of 5.20 × 105/cm3), as well as between corn oil and peanut oil (peak concentrations of 4.35 × 105/cm3). Despite the similar major chemical components among the four COFs, variations in metabolic damage were observed, indicating that the relatively small amount of chemical components of COFs can also influence particle behavior within the respiratory system, thereby impacting biological responses. Additionally, interactions between accompanying gaseous COFs and particles may alter their chemical composition through various mechanisms, introducing additional chemicals and modifying existing proportions. Hence, the chemical composition and gaseous components of COFs hold equal importance to the particle number concentration (PNC) when assessing their impact on human health. The absence of these considerations in the current guidelines underscores a research gap. It is imperative to acknowledge that for a more comprehensive approach to safeguarding public health, guidelines must be regularly updated to reflect new scientific findings and robust epidemiological evidence.

Corelease of Genotoxic Polycyclic Aromatic Hydrocarbons and Nanoparticles from a Commercial Aircraft Jet Engine - Dependence on Fuel and Thrust.

Jet engines are important contributors to global CO2 emissions and release enormous numbers of ultrafine particles into different layers of the atmosphere. As a result, aviation emissions are affecting atmospheric chemistry and promote contrail and cloud formation with impacts on earth's radiative balance and climate. Furthermore, the corelease of nanoparticles together with carcinogenic polycyclic aromatic hydrocarbons (PAHs) affects air quality at airports. We studied exhausts of a widely used turbofan engine (CFM56-7B26) operated at five static thrust levels (idle, 7, 30, 65, and 85%) with conventional Jet A-1 fuel and a biofuel blend composed of hydro-processed esters and fatty acids (HEFA). The particles released, the chemical composition of condensable material, and the genotoxic potential of these exhausts were studied. At ground operation, particle number emissions of 3.5 and 0.5 × 1014 particles/kg fuel were observed with highest genotoxic potentials of 41300 and 8800 ng toxicity equivalents (TEQ)/kg fuel at idle and 7% thrust, respectively. Blending jet fuel with HEFA lowered PAH and particle emissions by 7-34% and 65-67% at idle and 7% thrust, respectively, indicating that the use of paraffin-rich biofuels is an effective measure to reduce the exposure of airport personnel to nanoparticles coated with genotoxic PAHs (Trojan horse effect).

Subchronic inhalation exposure to ultrafine particulate matter alters the intestinal microbiome in various mouse models.

Exposure to ultrafine particles (UFPs) has been associated with multiple adverse health effects. Inhaled UFPs could reach the gastrointestinal tract and influence the composition of the gut microbiome. We have previously shown that oral ingestion of UFPs alters the gut microbiome and promotes intestinal inflammation in hyperlipidemic Ldlr-/- mice. Particulate matter (PM)2.5 inhalation studies have also demonstrated microbiome shifts in normolipidemic C57BL/6 mice. However, it is not known whether changes in microbiome precede or follow inflammatory effects in the intestinal mucosa. We hypothesized that inhaled UFPs modulate the gut microbiome prior to the development of intestinal inflammation. We studied the effects of UFP inhalation on the gut microbiome and intestinal mucosa in two hyperlipidemic mouse models (ApoE-/- mice and Ldlr-/- mice) and normolipidemic C57BL/6 mice. Mice were exposed to PM in the ultrafine-size range by inhalation for 6 h a day, 3 times a week for 10 weeks at a concentration of 300-350 µg/m3.16S rRNA gene sequencing was performed to characterize sequential changes in the fecal microbiome during exposures, and changes in the intestinal microbiome at the end. PM exposure led to progressive differentiation of the microbiota over time, associated with increased fecal microbial richness and evenness, altered microbial composition, and differentially abundant microbes by week 10 depending on the mouse model. Cross-sectional analysis of the small intestinal microbiome at week 10 showed significant changes in α-diversity, ß-diversity, and abundances of individual microbial taxa in the two hyperlipidemic models. These alterations of the intestinal microbiome were not accompanied, and therefore could not be caused, by increased intestinal inflammation as determined by histological analysis of small and large intestine, cytokine gene expression, and levels of fecal lipocalin. In conclusion, 10-week inhalation exposures to UFPs induced taxonomic changes in the microbiome of various animal models in the absence of intestinal inflammation.

Indoor particulate matter concentrations and air cleaner intervention association with biomarkers in former smokers with COPD.

BACKGROUND: Indoor pollutants have been associated with worse clinical outcomes in chronic obstructive pulmonary disease (COPD). Elevated biomarkers are associated with ambient pollution exposure, however the association with indoor pollution remains unclear. METHODS: Former smokers with spirometry-confirmed COPD were randomized to portable air cleaner or placebo. Indoor particulate matter (PM2.5, PM10, and ultrafine particles [UFP; PM<0.1]) and biomarkers were measured longitudinally at pre-specified intervals and course PM fraction (PM10-2.5) was calculated. Biomarkers were categorized based on associations with biologic mechanisms: inflammation (white blood cell count, interleukin [IL]-6, IL-8, IL-1ß, tumor necrosis factor-α, interferon-γ, serum amyloid A), platelet activation (P-selectin, CD40 ligand [CD40L], 11-dehdydro-thromboxane-B2 [11dTxB2]), endothelial dysfunction (Vascular Cell Adhesion Molecule [VCAM]-1, Intercellular Adhesion Molecule [ICAM]-1), and oxidative stress (thiobarbituric acid reactive substances [TBARS], 8-hydroxydeoxyguanosine, 8-isoprostane). Associations between PM concentrations and each biomarker were analyzed using multivariable linear mixed models. An intention-to-treat analysis was performed to evaluate the air cleaner intervention on the biomarker levels longitudinally. RESULTS: Fifty-eight participants were randomized to each group. Finer PM was more strongly associated with higher IL-8 (mean difference per doubling: UFP 13.9% [p = 0.02], PM2.5 6.8% [p = 0.002], PM10-2.5 5.0% [p = 0.02]) while interferon-γ was associated with UFP and IL-1ß with PM10-2.5. UFP and PM2.5 were associated with elevated levels of the oxidative stress biomarkers TBARS and 8-isoprostane respectively. For platelet activation markers, UFP was associated with higher 11dTxB2 while PM2.5 was associated with higher P-selectin and CD40L. Pollutants were not associated with biomarkers of endothelial dysfunction. In intention-to-treat analysis there was no association of the air cleaner intervention with any of the biomarkers. DISCUSSION: Among former smokers with COPD, elevated levels of indoor air pollutants, particularly ultrafine particles (PM<0.1), were associated with elevated biomarkers of inflammation, platelet activation, and oxidative stress. However, an air cleaner intervention that reduced PM did not significantly reduce biomarker levels.

Air pollution exposure in active versus passive travel modes across five continents: A Bayesian random-effects meta-analysis.

Epidemiological studies on health effects of air pollution usually estimate exposure at the residential address. However, ignoring daily mobility patterns may lead to biased exposure estimates, as documented in previous exposure studies. To improve the reliable integration of exposure related to mobility patterns into epidemiological studies, we conducted a systematic review of studies across all continents that measured air pollution concentrations in various modes of transport using portable sensors. To compare personal exposure across different transport modes, specifically active versus motorized modes, we estimated pairwise exposure ratios using a Bayesian random-effects meta-analysis. Overall, we included measurements of six air pollutants (black carbon (BC), carbon monoxide (CO), nitrogen dioxide (NO2), particulate matter (PM10, PM2.5) and ultrafine particles (UFP)) for seven modes of transport (i.e., walking, cycling, bus, car, motorcycle, overground, underground) from 52 published studies. Compared to active modes, users of motorized modes were consistently the most exposed to gaseous pollutants (CO and NO2). Cycling and walking were the most exposed to UFP compared to other modes. Active vs passive mode contrasts were mostly inconsistent for other particle metrics. Compared to active modes, bus users were consistently more exposed to PM10 and PM2.5, while car users, on average, were less exposed than pedestrians. Rail modes experienced both some lower exposures (compared to cyclists for PM10 and pedestrians for UFP) and higher exposures (compared to cyclist for PM2.5 and BC). Ratios calculated for motorcycles should be considered carefully due to the small number of studies, mostly conducted in Asia. Computing exposure ratios overcomes the heterogeneity in pollutant levels that may exist between continents and countries. However, formulating ratios on a global scale remains challenging owing to the disparities in available data between countries.

Los Angeles Basin's air quality transformation: a long-term investigation on the impacts of PM regulations on the trends of ultrafine particles and co-pollutants.

This study investigates the long-term trends of ambient ultrafine particles (UFPs) and associated airborne pollutants in the Los Angeles Basin from 2007 to 2022, focusing on the indirect effects of regulations on UFP levels. The particle number concentration (PNC) of UFPs was compiled from previous studies in the area, and associated co-pollutant data, including nitrogen oxides (NOx), carbon monoxide (CO), elemental carbon (EC), organic carbon (OC), and ozone (O3), were obtained from the chemical speciation network (CSN) database. Over the study period, a general decrease was noted in the PNC of UFPs, NOx, EC, and OC, except for CO, the concentration trends of which did not exhibit a consistent pattern. UFPs, NOx, EC, and OC were positively correlated, while O3 had a negative correlation, especially with NOx. Our analysis discerned two distinct subperiods in pollutant trends: 2007-2015 and 2016-2022. For example, there was an overall decrease in the PNC of UFPs at an annual rate of -850.09 particles/cm3/year. This rate was more pronounced during the first sub-period (2007-2015) at -1814.9 particles/cm3/year and then slowed to -227.21 particles/cm3/year in the second sub-period (2016-2023). The first sub-period (2007-2015) significantly influenced pollutant level changes, exhibiting more pronounced and statistically significant changes than the second sub-period (2016-2022). Since 2016, almost all primary pollutants have stabilized, indicating a reduced impact of current regulations, and emphasizing the need for stricter standards. In addition, the study included an analysis of Vehicle Miles Traveled (VMT) trends from 2007 to 2022 within the Los Angeles Basin. Despite the general increase in VMT, current regulations and cleaner technologies seem to have successfully mitigated the potential increase in increase in PNC. Overall, while a decline in UFPs and co-pollutant levels was observed, the apparent stabilization of these levels underscores the need for more stringent regulatory measures and advanced emission standards.

Impact of Ambient Ultrafine Particles on Cause-Specific Mortality in Three German Cities.

Rationale: Exposure to ambient air pollution has been associated with adverse effects on morbidity and mortality. However, the evidence for ultrafine particles (UFPs; 10-100 nm) based on epidemiological studies remains scarce and inconsistent. Objectives: We examined associations between short-term exposures to UFPs and total particle number concentrations (PNCs; 10-800 nm) and cause-specific mortality in three German cities: Dresden, Leipzig, and Augsburg. Methods: We obtained daily counts of natural, cardiovascular, and respiratory mortality between 2010 and 2017. UFPs and PNCs were measured at six sites, and measurements of fine particulate matter (PM2.5; ⩽2.5 µm in aerodynamic diameter) and nitrogen dioxide were collected from routine monitoring. We applied station-specific confounder-adjusted Poisson regression models. We investigated air pollutant effects at aggregated lags (0-1, 2-4, 5-7, and 0-7 d after UFP exposure) and used a novel multilevel meta-analytical method to pool the results. Additionally, we assessed interdependencies between pollutants using two-pollutant models. Measurements and Main Results: For respiratory mortality, we found a delayed increase in relative risk of 4.46% (95% confidence interval, 1.52 to 7.48%) per 3,223-particles/cm3 increment 5-7 days after UFP exposure. Effects for PNCs showed smaller but comparable estimates consistent with the observation that the smallest UFP fractions showed the largest effects. No clear associations were found for cardiovascular or natural mortality. UFP effects were independent of PM2.5 in two-pollutant models. Conclusions: We found delayed effects for respiratory mortality within 1 week after exposure to UFPs and PNCs but no associations for natural or cardiovascular mortality. This finding adds to the evidence on the independent health effects of UFPs.

Communities catalyzing change with data to mitigate an invisible menace, traffic-related air pollution.

OBJECTIVES: To identify strategies and tactics communities use to translate research into environmental health action. METHODS: We employed a qualitative case study design to explore public health action conducted by residents, organizers, and public health planners in two Massachusetts communities as part of a community based participatory (CBPR) research study. Data sources included key informant interviews (n = 24), reports and direct observation of research and community meetings (n = 10) and project meeting minutes from 2016-2021. Data were coded deductively drawing on the community organizing and implementation frameworks. RESULTS: In Boston Chinatown, partners drew broad participation from community-based organizations, residents, and municipal leaders, which resulted in air pollution mitigation efforts being embedded in the master planning process. In Somerville, partners focused on change at multiple levels, developer behavior, and separate from the funded research, local legislative efforts, and litigation. CONCLUSIONS: CBPR affords communities the ability to environmental health efforts in a way that is locally meaningful, leveraging their respective strengths. External facilitation can support the continuity and sustainment of community led CBPR efforts.

Using particle dimensionality-based modeling to estimate lung carcinogenicity of 3D printer emissions.

The use of 3D printing technologies by industry and consumers is expanding. However, the approaches to assess the risk of lung carcinogenesis from the emissions of 3D printers have not yet been developed. The objective of the study was to demonstrate a methodology for modeling lung cancer risk related to specific exposure levels as derived from an experimental study of 3D printer emissions for various types of filaments (ABS, PLA, and PETG). The emissions of 15 filaments were assessed at varying extrusion temperatures for a total of 23 conditions in a Class 1,000 cleanroom following procedures described by ANSI/CAN/UL 2904. Three approaches were utilized for cancer risk estimation: (a) calculation based on PM2.5 and PM10 concentrations, (b) a proximity assessment based on the pulmonary deposition fraction, and (c) modeling based on the mass-weighted aerodynamic diameter of particles. The combined distribution of emitted particles had the mass median aerodynamic diameter (MMAD) of 0.35 µm, GSD 2.25. The average concentration of PM2.5 was 25.21 µg/m3 . The spline-based function of aerodynamic diameter allowed us to reconstruct the carcinogenic potential of seven types of fine and ultrafine particles (crystalline silica, fine TiO2 , ultrafine TiO2 , ambient PM2.5 and PM10, diesel particulates, and carbon nanotubes) with a correlation of 0.999, P < 0.00001. The central tendency estimation of lung cancer risk for 3D printer emissions was found at the level of 14.74 cases per 10,000 workers in a typical exposure scenario (average cumulative exposure of 0.3 mg/m3 - years), with the lowest risks for PLA filaments, and the highest for PETG type.

Ambient Particulate Matter Induces In Vitro Toxicity to Intestinal Epithelial Cells without Exacerbating Acute Colitis Induced by Dextran Sodium Sulfate or 2,4,6-Trinitrobenzenesulfonic Acid.

Inflammatory bowel disease (IBD) is an immunologically complex disorder involving genetic, microbial, and environmental risk factors. Its global burden has continued to rise since industrialization, with epidemiological studies suggesting that ambient particulate matter (PM) in air pollution could be a contributing factor. Prior animal studies have shown that oral PM10 exposure promotes intestinal inflammation in a genetic IBD model and that PM2.5 inhalation exposure can increase intestinal levels of pro-inflammatory cytokines. PM10 and PM2.5 include ultrafine particles (UFP), which have an aerodynamic diameter of <0.10 µm and biophysical and biochemical properties that promote toxicity. UFP inhalation, however, has not been previously studied in the context of murine models of IBD. Here, we demonstrated that ambient PM is toxic to cultured Caco-2 intestinal epithelial cells and examined whether UFP inhalation affected acute colitis induced by dextran sodium sulfate and 2,4,6-trinitrobenzenesulfonic acid. C57BL/6J mice were exposed to filtered air (FA) or various types of ambient PM reaerosolized in the ultrafine size range at ~300 µg/m3, 6 h/day, 3-5 days/week, starting 7-10 days before disease induction. No differences in weight change, clinical disease activity, or histology were observed between the PM and FA-exposed groups. In conclusion, UFP inhalation exposure did not exacerbate intestinal inflammation in acute, chemically-induced colitis models.

A review on vulnerable atmospheric aerosol nanoparticles: Sources, impact on the health, ecosystem and management strategies.

The Earth's atmosphere contains ultrafine particles known as aerosols, which can be either liquid or solid particles suspended in gas. These aerosols originate from both natural sources and human activities, termed primary and secondary sources respectively. They have significant impacts on the environment, particularly when they transform into ultrafine particles or aerosol nanoparticles, due to their extremely fine atomic structure. With this context in mind, this review aims to elucidate the fundamentals of atmospheric-derived aerosol nanoparticles, covering their various sources, impacts, and methods for control and management. Natural sources such as marine, volcanic, dust, and bioaerosols are discussed, along with anthropogenic sources like the combustion of fossil fuels, biomass, and industrial waste. Aerosol nanoparticles can have several detrimental effects on ecosystems, prompting the exploration and analysis of eco-friendly, sustainable technologies for their removal or mitigation.Despite the adverse effects highlighted in the review, attention is also given to the generation of aerosol-derived atmospheric nanoparticles from biomass sources. This finding provides valuable scientific evidence and background for researchers in fields such as epidemiology, aerobiology, and toxicology, particularly concerning atmospheric nanoparticles.

The role of nanoparticles in bleed air in the etiology of Aerotoxic Syndrome: A review of cabin air-quality studies of 2003-2023.

Aerotoxic Syndrome may develop as a result of chronic, low-level exposure to organophosphates (OPs) and volatile organic compounds in the airplane cabin air, caused by engine oil leaking past wet seals. Additionally, acute high-level exposures, so-called "fume events," may occur. However, air quality monitoring studies concluded that levels of inhaled chemicals might be too low to cause adverse effects. The presence of aerosols of nanoparticles (NPs) in bleed air has often been described. The specific hypothesis is a relation between NPs acting as a vector for toxic compounds in the etiology of the Aerotoxic Syndrome. These NPs function as carriers for toxic engine oil compounds leaking into the cabin air. Inhaled by aircrew NPs carrying soluble and insoluble components deposit in the alveolar region, where they are absorbed into the bloodstream. Subsequently, they may cross the blood-brain barrier and release their toxic compounds in the central nervous system. Olfactory absorption is another route for NPs with access to the brain. To study the hypothesis, all published in-flight measurement studies (2003-2023) of airborne volatile (and low-volatile) organic pollutants in cabin air were reviewed, including NPs (10-100 nm). Twelve studies providing data for a total of 387 flights in 16 different large-passenger jet aircraft types were selected. Maximum particle number concentrations (PNC) varied from 104 to 2.8 × 106 #/cm3 and maximum mass concentrations from 9 to 29 µg/m3. NP-peaks occurred after full-power take-off, in tailwind condition, after auxiliary power unit (APU) bleed air introduction, and after air conditioning pack failure. Chemical characterization of the NPs showed aliphatic hydrocarbons, black carbon, and metallic core particles. An aerosol mass-spectrometry pattern was consistent with aircraft engine oil. It is concluded that chronic exposure of aircrew to NP-aerosols, carrying oil derivatives, maybe a significant feature in the etiology of Aerotoxic Syndrome. Mobile NP measuring equipment should be made available in the cockpit for long-term monitoring of bleed air. Consequently, risk assessment of bleed air should include monitoring and analysis of NPs, studied in a prospective cohort design.

Personal exposure to gaseous and particulate phase polycyclic aromatic hydrocarbons (PAHs) and nanoparticles and lung deposited surface area (LDSA) for soot among Norwegian chimney sweepers.

Exposure to polycyclic aromatic hydrocarbons (PAHs) of high molecular weight from chimney soot can cause cancer among chimney sweepers. These sweepers may also be exposed to high concentrations of nanosized particles, which can cause significant inflammatory responses due to their relatively greater surface area per mass. In this study, the authors aimed to assess the exposure profiles of airborne personal exposure to gaseous and particulate PAHs, and real-time samples of the particle number concentrations (PNCs), particle sizes, and lung-deposited surface areas (LDSAs), for chimney sweepers in Norway. Additionally, the authors aimed to assess the task-based exposure concentrations of PNCs, sizes, and LDSAs while working on different tasks. The results are based on personal samples of particulate PAHs (n = 68), gaseous PAHs (n = 28), and real-time nanoparticles (n = 8) collected from 17 chimney sweepers. Samples were collected during a "typical work week" of chimney sweeping and fire safety inspections, then during a "massive soot" week, where larger sweeping missions took place. Significantly higher PAH concentrations were measured during the "massive soot" week compared to the "typical work week," however, the time-weighted average (TWA) (8-hr) of all gaseous and particulate PAHs ranged from 0.52 to 4.47 µg/m3 and 0.49 to 2.50 µg/m3, respectively, well below the Norwegian occupational exposure limit (OEL) of 40 µg/m3. The PNCs were high during certain activities, such as emptying the vacuum cleaner. Additionally, during 2 days of sweeping in a waste sorting facility, the TWAs of the PNCs were 3.6 × 104 and 7.1 × 104 particles/cm3 on the first and second days, respectively, which were near and above the proposed nano reference limit TWA value of 4.0 × 104 particles/cm3 proposed by the International Workshop on Nano Reference Values. The corresponding TWAs of the LDSAs were 49.5 and 54.5 µm2/cm3, respectively. The chimney sweepers seemed aware of the potential health risks associated with exposure, and suitable personal protective equipment was used. However, the PNCs reported for the activities show that when the activities change or increase, the PNCs' TWAs can become unacceptably high.

Characterization of carbonaceous components and PAHs on ultrafine particles in Phnom Penh, Cambodia.

This study investigated seasonal fluctuations in particulate matter (PM) concentrations, including carbon and polycyclic aromatic hydrocarbon (PAH) components, in Phnom Penh, Cambodia, focusing on ultrafine particles (UFPs or ≤ 100 nm). UFP levels were notably higher during the dry season, averaging 23.73 ± 3.7 µg/m3 compared to 19.64 ± 3.4 µg/m3 in the wet season, attributed to increased emissions from vehicles and agricultural burning. In contrast, lower concentrations during the wet season were due to scavenging effect of rain. When compared to other Southeast Asian cities, UFP levels in Phnom Penh were significantly higher during the dry season, surpassing those in cities like Bangkok and Kuala Lumpur. Seasonal variations in carbonaceous components showed higher elemental carbon (EC) and total carbon (TC) during the dry season, with EC/TC ratios suggesting substantial influence from vehicular emissions and biomass burning. PAH analysis revealed seasonal disparities, with higher concentrations of benzo[b]fluoranthene (BbF) and benzo[k]fluoranthene (BkF) during the wet season, whereas fluoranthene (Flu) and pyrene (Pyr) were consistently present, indicating diverse PAH sources. The Flu/(Flu + Pyr) ratios, indicative of biomass burning, were higher in the dry season. Correlations between PAHs and carbon components confirmed combustion as a significant source of PAHs, aligning with global trends. This emphasizes the need to address distinct PM sources during various season in Phnom Penh.

Impact of Mobile Monitoring Network Design on Air Pollution Exposure Assessment Models.

Short-term mobile monitoring campaigns are increasingly used to assess long-term air pollution exposure in epidemiology. Little is known about how monitoring network design features, including the number of stops and sampling temporality, impacts exposure assessment models. We address this gap by leveraging an extensive mobile monitoring campaign conducted in the greater Seattle area over the course of a year during all days of the week and most hours. The campaign measured total particle number concentration (PNC; sheds light on ultrafine particulate (UFP) number concentration), black carbon (BC), nitrogen dioxide (NO2), fine particulate matter (PM2.5), and carbon dioxide (CO2). In Monte Carlo sampling of 7327 total stops (278 sites × 26 visits each), we restricted the number of sites and visits used to estimate annual averages. Predictions from the all-data campaign performed well, with cross-validated R2s of 0.51-0.77. We found similar model performances (85% of the all-data campaign R2) with ∼1000 to 3000 randomly selected stops for NO2, PNC, and BC, and ∼4000 to 5000 stops for PM2.5 and CO2. Campaigns with additional temporal restrictions (e.g., business hours, rush hours, weekdays, or fewer seasons) had reduced model performances and different spatial surfaces. Mobile monitoring campaigns wanting to assess long-term exposure should carefully consider their monitoring designs.