Toxicity Of Particulate Matter Research Articles

Annual variation of source contributions to PM10 and oxidative potential in a mountainous area with traffic, biomass burning, cement-plant and biogenic influences

Toxicity of particulate matter (PM) depends on its sources, size and composition. We identified PM10 sources and determined their contribution to oxidative potential (OP) as a health proxy for PM exposure in an Alpine valley influenced by cement industry. PM10 filter sample chemical analysis and equivalent black carbon (eBC) were measured at an urban background site from November 2020 to November 2021. Using an optimized Positive Matrix Factorization (PMF) model, the source chemical fingerprints and contributions to PM10 were determined. The OP assessed through two assays, ascorbic acid (AA) and dithiothreitol (DTT), was attributed to the PM sources from the PMF model with a multiple linear regression (MLR) model. Ten factors were found at the site, including biomass burning (34, 40 and 38% contribution to annual PM10, OPAA and OPDDT, respectively), traffic (14, 19 and 7%), nitrate- and sulphate-rich (together: 16, 5 and 8%), aged sea salt (2, 2 and 0%) and mineral dust (10, 12 and 17%). The introduction of innovative organic tracers allowed the quantification of the PM primary and secondary biogenic fractions (together: 13, 8 and 21%). In addition, two unusual factors due to local features, a chloride-rich factor and a second mineral dust-rich factor (named the cement dust factor) were found, contributing together 10, 14 and 8%. We associate these two factors to different processes in the cement plant. Despite their rather low contribution to PM10 mass, these sources have one of the highest OPs per µg of source. The results of the study provide vital information about the influence of particular sources on PM10 and OP in complex environments and are thus useful for PM control strategies and actions.

Oxidative potential associated with reactive oxygen species of size-resolved particles: The important role of the specific sources

Oxidative potential (OP) is a predictor of particulate matter (PM) toxicity. Size-resolved PM and its components that influence OP values can be generated from several sources. However, There is little research have attempted to determine the PM toxicity generated from specific sources. This paper studied the OP characterization and reactive oxygen species (ROS) formation of particles from specific sources and their effects on human health. OP associated with ROS of size-resolved particles was analyzed by using dithiothreitol (DTT) method and electron paramagnetic resonance (EPR) spectroscopy technology. And OP and ROS deposition of specific source PM were calculated for health through the Multi-path particle deposition (MPPD) model. The results evidenced that the highest water-soluble OP (OPws) from traffic sources (OPm: 104.50 nmol min−1·ug−1; OPv: 160.15 nmol min−1·m−3) and the lowest from ocean sources (OPm: 22.25 nmol⋅min−1⋅ug−1; OPv: 54.16 nmol min−1·m−3). The OPws allocation in PM from different sources all have a unimodal pattern range from 0.4 to 3.2 μm. ROS (·OH) displayed the uniform trend as PM OPws, indicating that PM< 3.2 is the major contributor to adverse health impacts for size-resolved PM because of its enhanced oxidative activity compared with PM> 3.2. Furthermore, this study predicted the DTT consumption of PM were assigned to different components. Most DTT losses are attributed to the transition metals. For specific sources, transition metals dominates DTT losses, accounting for 38%–80% of DTT losses from different sources, followed by Hulis-C, accounting for 1%–10%. MPPD model calculates that over 66% of pulmonary DTT loss comes by PM< 3.2, and over 71% of pulmonary ROS generation from PM< 3.2. Among these sources of pollution, traffic emissions are the primary contributors to reactive oxygen species (ROS) in environmental particulate matter (PM). Therefore, emphasis should be placed on controlling traffic emissions, especially in coastal areas.

Oxidative potential of the inhalation bioaccessible fraction of PM10 and bioaccessible concentrations of polycyclic aromatic hydrocarbons and metal(oid)s in PM10

Atmospheric particulate matter (PM) has been related to numerous adverse health effects in humans. Nowadays, it is believed that one of the possible mechanisms of toxicity could be the oxidative stress, which involves the development of reactive oxygen species (ROS). Different assays have been proposed to characterize oxidative stress, such as dithiothreitol (DTT) and ascorbic acid (AA) acellular assays (OPDTT and OPAA), as a metric more relevant than PM mass measurement for PM toxicity. This study evaluates the OP of the bioaccessible fraction of 65 PM10 samples collected at an Atlantic Coastal European urban site using DTT and AA assays. A physiologically based extraction (PBET) using Gamble’s solution (GS) as a simulated lung fluid (SLF) was used for the assessment of the bioaccessible fraction of PM10. The use of the bioaccessible fraction, instead of the fraction assessed using conventional phosphate buffer and ultrasounds assisted extraction (UAE), was compared for OP assessment. Correlations between OPDTT and OPAA, as well as total and bioaccessible concentrations of polycyclic aromatic hydrocarbons (PAHs) and metal(oid)s, were investigated to explore the association between those compounds and OP. A correlation was found between both OP (OPDTT and OPAA) and total and bioaccessible concentrations of PAHs and several metal(oid)s such as As, Bi, Cd, Cu, Ni, and V. Additionally, OPDTT was found to be related to the level of K+.

Toxic Potencies of Particulate Matter from Typical Industrial Plants Mediated with Acidity via Metal Dissolution.

Acidity is an important property of particulate matter (PM) in the atmosphere, but its association with PM toxicity remains unclear. Here, this study quantitively reports the effect of the acidity level on PM toxicity via pH-control experiments and cellular analysis. Oxidative stress and cytotoxicity potencies of acidified PM samples at pH of 1-2 were up to 2.8-5.2 and 2.1-13.2 times higher than those at pH of 8-11, respectively. The toxic potencies of PM samples from real-world smoke plumes at the pH of 2.3 were 9.1-18.2 times greater than those at the pH of 5.6, demonstrating a trend similar to that of acidified PM samples. Furthermore, the impact of acidity on PM toxicity was manifested by promoting metal dissolution. The dramatic increase by 2-3 orders of magnitude in water-soluble metal content dominated the variation in PM toxicity. The significant correlation between sulfate, the pH value, water-soluble Fe, IC20, and EC1.5 (p < 0.05) suggested that acidic sulfate could enhance toxic potencies by dissolving insoluble metals. The findings uncover the superficial association between sulfate and adverse health outcomes in epidemiological research and highlight the control of wet smoke plume emissions to mitigate the toxicity effects of acidity.

Size Distributions and Health Risks of Particulate Polycyclic Aromatic Hydrocarbons in the Atmosphere at Coastal Areas in Ningbo, China.

Most current research focusing on the health risk assessments of particulate polycyclic aromatic hydrocarbons (PAHs) have not analyzed the size distributions and human respiratory deposition rates. In the present study, size-separated particulate matter (PM) was collected in the coastal area of Ningbo using an Anderson eight-stage air sampler over a 1-year period (2014-2015). The 16 US Environmental Protection Agency priority PAHs associated with PM were pretreated with rapid solvent extraction and analyzed by gas chromatography-mass spectrometry. The respiratory exposure assessment was determined using the multiple-path particle dosimetry (MPPD) model. The results show that all PAHs exhibited bimodal distribution with one mode peak in accumulation mode (0.43-0.65 µm) and another mode peak in coarse mode (4.7-5.8 µm). In addition, a low coefficient of divergence of PAHs between PM2.1 and PM2.1-10 indicated a high spatial heterogeneity in source factor contribution and formation mechanism. The deposition fluxes (tracheobronchial + pulmonary) of PM were highest for children in the size range of 3.3 µm < particle diameter (Dp) < 9 µm, while for males and females the highest fluxes occurred in the size range of 1.1 µm < Dp < 2.1 µm. The depositions of coarse PM in children were significantly higher than those in adults. The benzo[a]pyrene equivalent (BaPeq) depositions of dibenz[a,h]anthracene ranged from 1.4e-04 to 0.015 ng h-1, which were highest among the PAHs. The PAHs on particles with Dp >4.7 µm contributed approximately three times more to children than to males and females. Therefore, the toxicity of coarse PM to children needed attention. The incremental lifetime cancer risks (ILCR) for children, males, and females were estimated to be 2.92 × 10-7, 1.82 × 10-7, and 2.38 × 10-7, respectively, which were below the cancer risk guideline value (10-6). These ILCR values were much lower than the risks calculated without considering particle size distributions and respiratory depositions. The combination of the size-segregated sampling technique and the MPPD model can effectively avoid the overestimation of human respiratory exposure. Environ Toxicol Chem 2024;43:1364-1377. © 2024 SETAC.

Hemolytic Properties of Fine Particulate Matter (PM2.5) in In Vitro Systems.

Epidemiological studies have suggested that inhalation exposure to particulate matter (PM) air pollution, especially fine particles (i.e., PM2.5 (PM with an aerodynamic diameter of 2.5 microns or less)), is causally associated with cardiovascular health risks. To explore the toxicological mechanisms behind the observed adverse health effects, the hemolytic activity of PM2.5 samples collected during different pollution levels in Beijing was evaluated. The results demonstrated that the hemolysis of PM2.5 ranged from 1.98% to 7.75% and demonstrated a clear dose-response relationship. The exposure toxicity index (TI) is proposed to represent the toxicity potential of PM2.5, which is calculated by the hemolysis percentage of erythrocytes (red blood cells, RBC) multiplied by the mass concentration of PM2.5. In a pollution episode, as the mass concentration increases, TI first increases and then decreases, that is, TI (low pollution levels) < TI (heavy pollution levels) < TI (medium pollution levels). In order to verify the feasibility of the hemolysis method for PM toxicity detection, the hemolytic properties of PM2.5 were compared with the plasmid scission assay (PSA). The hemolysis results had a significant positive correlation with the DNA damage percentages, indicating that the hemolysis assay is feasible for the detection of PM2.5 toxicity, thus providing more corroborating information regarding the risk to human cardiovascular health.

Oxidative potential apportionment of atmospheric PM1: a new approach combining high-sensitive online analysers for chemical composition and offline OP measurement technique

Abstract. Source apportionment models were widely used to successfully assign highly time-resolved aerosol data to specific emissions and/or atmospheric chemical processes. These techniques are necessary for targeting the sources affecting air quality and for designing effective mitigation strategies. Moreover, evaluation of the toxicity of airborne particulate matter is important since the classically measured particulate matter (PM) concentrations appear insufficient for characterizing the impact on human health. Oxidative potential (OP) measurement has recently been developed to quantify the capability of PM to induce an oxidative imbalance in the lungs. As a result, this measurement unit could be a better proxy than PM mass concentration to represent PM toxicity. In the present study, two source apportionment analyses were performed using positive matrix factorization (PMF) from organic aerosol (OA) mass spectra measured at a 15 min time resolution using a time-of-flight aerosol chemical speciation monitor (ToF-ACSM) and from 19 trace elements measured on an hourly basis using an online metal analyser (Xact 625i). The field measurements were carried out in summer 2018. While it is common to perform PMF studies individually on ACSMs and more recently on Xact datasets, here we used a two-step methodology leading to a complete PM1 source apportionment. The outputs from both OA PMF and Xact PMF, the inorganic species concentrations from the ACSM, and the black carbon (BC) fractions (fossil fuel and wood burning) measured using an Aethalometer (AE33) were gathered into a single dataset and subjected to a combined PMF analysis. Overall, eight factors were identified, each of them corresponding to a more precise source than performing single PMF analyses. The results show that besides the high contribution of secondary ammonium sulfate (28 %) and organic nitrate (19 %), about 50 % of PM1 originated from distinct combustion sources, including emissions from traffic, shipping, industrial activities, cooking, and biomass burning. Simultaneously, PM1 filters were collected during the experimental period on a 4 h sampling basis. On these filters, two acellular OP assays were performed (dithiothreitol; OPDTT and ascorbic acid; OPAA) and an inversion method was applied on factors issued from all PMFs to assess the contribution of the PM sources to the OP. This work highlights the sensitivity of OPAA to industrial and dust resuspension sources and those of OPDTT to secondary ammonium sulfate, shipping, and biomass burning.

Exhaled VOC Biomarkers from Rats Injected with PMs from Thirty-One Major Cities in China.

Particulate matter (PMs) of different origins can cause diverse health effects. Here, a homemade box was used to facilitate real-time measurements of breath-borne volatile organic compounds (VOCs) by gas chromatography-ion mobility spectrometry. We have tracked exhaled VOC changes in 228 Wistar rats that were injected with water-soluble PM suspension filtrates (after 0.45 μm) from 31 China cities for 1 h to up to 1-6 days during the experiments. Rats exposed to the filtrates exhibited significant changes in breath-borne VOCs within hours, featuring dynamic fluctuations in the levels of acetone, butan-2-one, heptan-2-one-M, acetic acid-M, and ethanol. Subsequently, on the fifth to sixth day after the injection, there was a notable increase in the proportion of aldehydes (including hexanal-M, hexanal-D, pentanal, heptanal-M, and (E)-2-hexenal). The 10 dynamic VOC fingerprint patterns mentioned earlier showcased the capability to indirectly differentiate urban PM toxicity and categorize the 31 cities into four distinct groups based on their health effects. This study provides valuable insights into the mechanisms of exhaled VOCs and underscores their critical role as biomarkers for differentiating the toxicity of different PMs and detecting the early signs of potential diseases. The results from this work also provide a scientific basis for city-specific air pollution control and policy development.

Particulate matter-mediated oxidative stress induces airway inflammation and pulmonary dysfunction through TXNIP/NF-κB and modulation of the SIRT1-mediated p53 and TGF-β/Smad3 pathways in mice

Exposure to particulate matter is currently recognized as a serious aggravating factor of respiratory diseases. In this study, we investigated the effects of particulate matter (PM) on the respiratory system in BALB/c mice and NCI-H292 cells. PM (0, 2.5, 5 and 20 mg/kg) was administered to mice by intra-tracheal instillation for 7 days. After a 7 day-repeated treatment of PM, we evaluated inflammatory cytokines/cell counts in bronchoalveolar lavage fluid (BALF) and conducted pulmonary histology and functional test. We also investigated the role of TXNIP/NF-κB and SIRT1-mediated p53 and TGF-β/Smad3 pathways in PM-induced airway inflammation and pulmonary dysfunction. PM caused a significant increase in pro-inflammatory cytokines, inflammatory cell counts in bronchoalveolar lavage fluid. PM-mediated oxidative stress down-regulated thioredoxin-1 and up-regulated thioredoxin-interacting protein and activation of nuclear factor-kappa B in the lung tissue and PM-treated NCI-H292 cells. PM suppressed sirtuin1 protein levels and increased p53 acetylation in PM-exposed mice and PM-treated NCI-H292 cells. In addition, PM caused inflammatory cell infiltration and the thickening of alveolar walls by exacerbating the inflammatory response in the lung tissue. PM increased levels of transforming growth factor-β, phosphorylation of Smad3 and activation of α-smooth muscle actin, and collagen type1A2 in PM-exposed mice and PM-treated NCI-H292 cells. In pulmonary function tests, PM exposure impaired pulmonary function resembling pulmonary fibrosis, characterized by increased resistance and elastance of the respiratory system, and resistance, elastance, and damping of lung tissues, whereas decreased compliance of the respiratory system, forced expired volume and forced vital capacity. Overall, PM-mediated oxidative stress caused airway inflammation and pulmonary dysfunction with pulmonary fibrosis via TXNIP pathway/NF-κB activation and modulation of the SIRT1-mediated TGF-β/Smad3 pathways. The results of this study can provide fundamental data on the potential adverse effects and underlying mechanism of pulmonary fibrosis caused by PM exposure as a public health concern. Due to the potential toxicity of PM, people with respiratory disease must be careful with PM exposure.

Oxidative potential, environmentally persistent free radicals and reactive oxygen species of size-resolved ambient particles near highways

Particulate matter (PM) is a group of atmospheric pollutants with an uncertain toxicity, particularly when collected near highways. This study examined the oxidative potential (OP) of, as well as the environmentally persistent free radicals (EPFRs) and reactive oxygen species (ROS) present in PM samples collected near highways in Xiamen, China. Our findings revealed that PM had a relatively high OP, ranging from 3.8 to 18.5 nmol/min/μg, surpassing values reported in previous research. The oxidative potential of the water-insoluble fraction (OPWIS), which accounted for 68% of the total oxidative potential (OPTotal), demonstrated rapid toxicity, whereas the oxidative potential of the water-soluble fraction (OPWS) displayed a steadier toxicity release pattern. The primary free radicals detected in PM were oxygen-centered. The measured concentration of EPFRs was 6.073 × 1014 spins/m3, which is lower than that reported in previous studies, possibly because of the high relative humidity of the road environment in Xiamen. We also investigated the interaction between PM and water near highways and observed the generation of R and OH radicals. Additionally, we analysed the sample composition and evaluated the contributions of the different components to OPTotal. Transition metals (Fe, Cu, and Zn) were identified as the major contributors, accounting for 33.2% of the OPTotal. The positive correlation observed between EPFRs and ROS suggests that EPFRs may be involved in ROS generation. The correlation analysis indicated that the oxidative potential measured using the DTT method (OPDTT) could serve as an indicator of ROS generation. Finally, based on the relationship between OPDTT, EPFRs, and ROS, we propose that reducing the emission of transition metals, particularly Fe, represents an effective control measure for mitigating PM toxicity near highways.

Achieving health-oriented air pollution control requires integrating unequal toxicities of industrial particles

Protecting human health from fine particulate matter (PM) pollution is the ambitious goal of clean air actions, but current control strategies largely ignore the role of source-specific PM toxicity. Here, we proposed health-oriented control strategies by integrating the unequal toxic potencies of the most polluting industrial PMs. Iron and steel industry (ISI)-emitted PM2.5 exhibit about one order of magnitude higher toxic potency than those of cement and power industries. Compared with the current mass-based control strategy (prioritizing implementation of ultralow emission standards in the power sector), the proposed health-oriented control strategy (priority control of the ISI sector) could generate 5.4 times higher reduction in population-weighted toxic potency-adjusted PM2.5 exposure among polluting industries in China. Furthermore, the marginal abatement cost per unit of toxic potency-adjusted mass of ISI-emitted PM2.5 is only a quarter of that of the other two sectors under ultralow emission scenarios. We highlight that a health-oriented air pollution control strategy is urgently required to achieve cost-effective reductions in particulate exposure risks.

A review on potential approach for in silico toxicity analysis of respirable fraction of ambient particulate matter.

Epidemiological and toxicological studies have shown the adverse effect of ambient particulate matter (PM) on respiratory and cardiovascular systems inside the human body. Various cellular and acellular assays in literature use indicators like ROS generation, cell inflammation, mutagenicity, etc., to assess PM toxicity and associated health effects. The presence of toxic compounds in respirable PM needs detailed studies for proper understanding of absorption, distribution, metabolism, and excretion mechanisms inside the body as it is difficult to accurately imitate or simulate these mechanisms in lab or animal models. The leaching kinetics of the lung fluid, PM composition, retention time, body temperature, etc., are hard to mimic in an artificial experimental setup. Moreover, the PM size fraction also plays an important role. For example, the ultrafine particles may directly enter systemic circulations while coarser PM10 may be trapped and deposited in the tracheo-bronchial region. Hence, interpretation of these results in toxicity models should be done judiciously. Computational models predicting PM toxicity are rare in the literature. The variable composition of PM and lack of proper understanding for their synergistic role inside the body are prime reasons behind it. This review explores different possibilities of in silico modeling and suggests possible approaches for the risk assessment of PM particles. The toxicity testing approach for engineered nanomaterials, drugs, food industries, etc., have also been investigated for application in computing PM toxicity.

P04-06: Toxicity of particulate matter from experimental burning of domestic waste

P04-06: Toxicity of particulate matter from experimental burning of domestic waste

Can l-ascorbic acid and trans-resveratrol protect HaCaT cells from fine particulate matter toxicity?

Continuous exposure of human skin to air pollution can result in a range of undesirable skin conditions. In our recent study, UV and visible light were found to increase cytotoxicity of fine particulate matter (PM2.5 ) against human keratinocytes. Since it is impossible to avoid exposure of human skin to PM2.5 , effective strategies are needed to reduce their damaging effects. l-ascorbic acid and resveratrol were tested as potential topical agents against pollution-related skin impairment. Although these agents were previously found to ameliorate PM-dependent damage, the effect of light and seasonal variation of particles were not previously studied. EPR spin-trapping, DPPH assay, and singlet oxygen phosphorescence were used to determine the scavenging activities of the antioxidants. MTT, JC-10 and iodometric assays were used to analyze the effect on PM2.5 -induced cytotoxicity, mitochondrial damage and oxidation of lipids. Live-cell imaging was employed to examine wound-healing properties of cells. Light-induced, PM2.5 -mediated oxidative damage was examined by immunofluorescent staining. Both antioxidants effectively scavenged free radicals and singlet oxygen produced by PM2.5 , reduced cell death and prevented oxidative damage to HaCaT cells. l-ascorbic acid and resveratrol, especially when applied in combination, can protect HaCaT cells against the dark and light induced toxicity of PM2.5 .

Outdoor Health Risk of Atmospheric Particulate Matter at Night in Xi'an, Northwestern China.

The deterioration of air quality via anthropogenic activities during the night period has been deemed a serious concern among the scientific community. Thereby, we explored the outdoor particulate matter (PM) concentration and the contributions from various sources during the day and night in winter and spring 2021 in a megacity, northwestern China. The results revealed that the changes in chemical compositions of PM and sources (motor vehicles, industrial emissions, coal combustion) at night lead to substantial PM toxicity, oxidative potential (OP), and OP/PM per unit mass, indicating high oxidative toxicity and exposure risk at nighttime. Furthermore, higher environmentally persistent free radical (EPFR) concentration and its significant correlation with OP were observed, suggesting that EPFRs cause reactive oxygen species (ROS) formation. Moreover, the noncarcinogenic and carcinogenic risks were systematically explained and spatialized to children and adults, highlighting intensified hotspots to epidemiological researchers. This better understanding of day-night-based PM formation pathways and their hazardous impact will assist to guide measures to diminish the toxicity of PM and reduce the disease led by air pollution.

The evolution of atmospheric particulate matter in an urban landscape since the Industrial Revolution

Atmospheric particulate matter (PM) causes 3.7 million annual deaths worldwide and potentially damages every organ in the body. The cancer-causing potential of fine particulates (PM2.5) highlights the inextricable link between air quality and human health. With over half of the world’s population living in cities, PM2.5 emissions are a major concern, however, our understanding of exposure to urban PM is restricted to relatively recent (post-1990) air quality monitoring programmes. To investigate how the composition and toxicity of PM has varied within an urban region, over timescales encompassing changing patterns of industrialisation and urbanisation, we reconstructed air pollution records spanning 200 years from the sediments of urban ponds in Merseyside (NW England), a heartland of urbanisation since the Industrial Revolution. These archives of urban environmental change across the region demonstrate a key shift in PM emissions from coarse carbonaceous ‘soot’ that peaked during the mid-twentieth century, to finer combustion-derived PM2.5 post-1980, mirroring changes in urban infrastructure. The evolution of urban pollution to a recent enhanced PM2.5 signal has important implications for understanding lifetime pollution exposures for urban populations over generational timescales.

Microfluidic paper-based analytical devices for simultaneous detection of oxidative potential and copper in aerosol samples.

The potential reach of point-of-care (POC) diagnostics into daily routines for exposure to reactive oxygen species (ROS) and Cu in aerosolized particulate matter (PM) demands that microfluidic paper-based analytical devices (μPADs) take into consideration the simple detection of these toxic PM components. Here, we propose μPADs with a dual-detection system for simultaneous ROS and Cu(II) detection. For colorimetric ROS detection, the glutathione (GSH) assay with a folding design to delay the reaction yielded complete ROS and GSH oxidation, and improved homogeneity of color development relative to using the lateral flow pattern. For electrochemical Cu(II) determination, 1,10-phenanthroline/Nafion modified graphene screen-printed electrodes showed ability to detect Cu(II) down to pg level being low enough to be applied to PM analysis. No intra- and inter-interference affecting both systems were found. The proposed μPADs obtained LODs for 1,4-naphthoquinone (1,4-NQ), used as the ROS representative, and Cu(II) of 8.3 ng and 3.6 pg, respectively and linear working ranges of 20 to 500 ng for ROS and 1 × 10-2 to 2 × 102 ng for Cu(II). Recovery of the method was between 81.4 and 108.3% for ROS and 80.5-105.3% for Cu(II). Finally, the sensors were utilized for simultaneous ROS and Cu(II) determination in PM samples and the results statistically agreed with those using the conventional methods at 95% confidence.

Measurement artifacts in the dithiothreitol (DTT) oxidative potential assay caused by interactions between aqueous metals and phosphate buffer

Metals in particulate matter (PM) are hypothesized to have enhanced toxicity based on their ability to catalyze reactive oxygen species (ROS) formation. Acellular assays are used to measure the oxidative potential (OP) of PM and its individual components. Many OP assays, including the dithiothreitol (DTT) assay, use a phosphate buffer matrix to simulate biological conditions (pH 7.4 and 37 °C). Prior work from our group observed transition metal precipitation in the DTT assay, consistent with thermodynamic equilibria. In this study, we characterized the effects of metal precipitation on OP measured by the DTT assay. Metal precipitation was affected by aqueous metal concentrations, ionic strength, and phosphate concentrations in ambient PM sampled in Baltimore, MD and a standard PM sample (NIST SRM-1648a, Urban Particulate Matter). Critically, differences in metal precipitation induced differing OP responses of the DTT assay as a function of phosphate concentration in all PM samples analyzed. These results indicate that comparison of DTT assay results obtained at differing phosphate buffer concentrations is highly problematic. Further, these results have implications for other chemical and biological assays that use phosphate buffer for pH control and their use to infer PM toxicity.

57 Particles in Outdoor Air: are they all Equal?

Abstract Statement from the Committee on the Medical Effects of Air Pollutants (COMEAP) on the differential toxicity of particulate matter according to source or constituents Particulate matter in outdoor air comes from a wide range of different sources and contains many different chemical components. Understanding which of these sources and components are particularly harmful would help to focus policies and interventions to reduce impacts on health. COMEAP recently (July 2022) published an updated statement on this topic, drawing on recent reviews of the available evidence. It noted that particulate matter, and constituents of particulate matter, associated with combustion and road traffic have received the most research attention. However, there was insufficient coherence in the epidemiological evidence to conclude that these sources of particulate matter play a significantly greater role in the health effects of particulate air pollution than other sources or constituents. A comprehensive review of the evidence reveals that toxicity has been attributed to a wide variety of constituents and sources, possibly acting by a number of different mechanisms. However, the complexity of sources, sizes and chemical composition of particulate matter makes it extremely difficult to identify which characteristics of particles might make them less harmful or more toxic than others. Future research assessing the influence of chemical composition of particulate matter should offer greater insights into toxicity. But, at present, PM2.5 (the mass concentration of fine particulate matter in air) remains the most suitable metric for evaluating health impacts and regulating particulate air pollution.

A novel laboratory method for simulating pollinator exposure to agrochemical-laden particulate matter.

Environmental transport and deposition of particulate matter (PM) associated with toxic chemicals has begun to receive attention as a source of risk to pollinators. For example, dust arising from manipulations of insecticide-treated seed has potential to exert toxic effects among non-target insects. Similarly, synthetic steroid growth promoters, antibiotics and multiple insecticides and parasiticides detected in fugitive beef cattle feedyard PM may also negatively impact pollinators since many of these chemicals have been detected on wildflowers and pollinators collected near beef cattle feedyards. Therefore, there is a need to assess risk to pollinators posed by deposition of agrochemical-laden PM, both in the field and the laboratory. Unfortunately, established laboratory methods for simulating PM exposure or toxicity associated with contaminated PM are few and highly situation-specific. Herein we describe development and use of a PM circulation system that can be employed to evaluate toxicity of agrochemical-contaminated PM in the laboratory under controlled conditions. Two model organisms (honeybees (Apis mellifera) and mason bees (Osmia lignaria)) were exposed to agrochemical-free PM in the circulator system, and post-exposure mortality was compared with controls. No significant differences in mortality between exposed and control bees were observed. Next, honeybees and mason bees were exposed to PM spiked with an insecticide known to exert toxic effects to pollinators (thiamethoxam). Bees experienced significantly higher mortality when exposed to thiamethoxam-laden PM at environmentally relevant concentrations as compared to bees exposed to agrochemical-free PM. These results confirm the validity of these methods for use in controlled laboratory PM toxicity tests and offer a source of positive and negative control groups for laboratory and field experiments examining exposure of pollinators to potentially toxic agrochemical-laden PM. This method facilitates generation of more realistic toxicity data than standard contact toxicity tests when pollinator exposure scenarios involve particulate-based agrochemicals or other toxic chemicals.