Objective: In this study, we compared in vitro and in vivo bioactivity of nitrogen-doped multi-walled carbon nanotubes (NDMWCNT) to MWCNT to test the hypothesis that nitrogen doping would alter bioactivity.Materials and Methods: High-resolution transmission electron microscopy (TEM) confirmed the multilayer structure of MWCNT with an average layer distance of 0.36 nm, which was not altered by nitrogen doping: the nanomaterials had similar widths and lengths. In vitro studies with THP-1 cells and alveolar macrophages from C57BL/6 mice demonstrated that NDMWCNT were less cytotoxic and stimulated less IL-1β release compared to MWCNT. For in vivo studies, male C57BL/6J mice received a single dose of dispersion medium (DM), 2.5, 10 or 40 µg/mouse of NDMWCNT, or 40 µg/mouse of MWCNT by oropharyngeal aspiration. Animals were euthanized between 1 and 7 days post-exposure for whole lung lavage (WLL) studies.Results and Discussion: NDMWCNT caused time- and dose-dependent pulmonary inflammation. However, it was less than that caused by MWCNT. Activation of the NLRP3 inflammasome was assessed in particle-exposed mice by determining cytokine production in WLL fluid at 1 day post-exposure. Compared to DM-exposed mice, IL-1β and IL-18 were significantly increased in MWCNT- and NDMWCNT-exposed mice, but the increase caused by NDMWCNT was less than MWCNT. At 56 days post-exposure, histopathology determined lung fibrosis in MWCNT-exposed mice was greater than NDMWCNT-exposed mice.Conclusions: These data indicate nitrogen doping of MWCNT decreases their bioactivity, as reflected with lower in vitro and in vivo toxicity inflammation and lung disease. The lower activation of the NLRP3 inflammasome may be responsible. Abbreviations: NDMWCNT: nitrogen-doped multi-walled carbon nanotubes; MWCNT: multi-walled carbon nanotubes; TEM: transmission electron microscopy; HRTEM: high resolution transmission electron microscopy; IL-1ß: interleukin-1ß; DM: dispersion medium; WLL: whole lung lavage; IL-18: interleukin-18; GSD: geometric standard deviation; XPS: X-ray photoelectron spectroscopy; SEM: standard error of the mean; PMA: phorbol 12-myristate 13-acetate; LPS: lipopolysacharride; LDH: lactate dehydrogenase; AM: alveolar macrophage; PMN: polymorphonuclear leukocyte.

Boron nitride nanotubes (BNNTs) are an emerging engineered nanomaterial attracting significant attention due to superior electrical, chemical and thermal properties. Currently, the toxicity profile of this material is largely unknown. Commercial grade BNNTs are composed of a mixture (BNNT-M) of ∼50–60% BNNTs, and ∼40–50% impurities of boron and hexagonal boron nitride. We performed acute in vitro and in vivo studies with commercial grade BNNT-M, dispersed by sonication in vehicle, in comparison to the extensively studied multiwalled carbon nanotube-7 (MWCNT-7). THP-1 wild-type and NLRP3-deficient human monocytic cells were exposed to 0–100 µg/ml and C57BL/6 J male mice were treated with 40 µg of BNNT-M for in vitro and in vivo studies, respectively. In vitro, BNNT-M induced a dose-dependent increase in cytotoxicity and oxidative stress. This was confirmed in vivo following acute exposure increase in bronchoalveolar lavage levels of lactate dehydrogenase, pulmonary polymorphonuclear cell influx, loss in mitochondrial membrane potential and augmented levels of 4-hydroxynonenal. Uptake of this material caused lysosomal destabilization, pyroptosis and inflammasome activation, corroborated by an increase in cathepsin B, caspase 1, increased protein levels of IL-1β and IL-18 both in vitro and in vivo. Attenuation of these effects in NLRP3-deficient THP-1 cells confirmed NLRP3-dependent inflammasome activation by BNNT-M. BNNT-M induced a similar profile of inflammatory pulmonary protein production when compared to MWCNT-7. Functionally, pretreatment with BNNT-M caused suppression in bacterial uptake by THP-1 cells, an effect that was mirrored in challenged alveolar macrophages collected from exposed mice and attenuated with NLRP3 deficiency. Analysis of cytokines secreted by LPS-challenged alveolar macrophages collected after in vivo exposure to dispersions of BNNT-M showed a differential macrophage response. The observed results demonstrated acute inflammation and toxicity in vitro and in vivo following exposure to sonicated BNNT-M was in part due to NLRP3 inflammasome activation.

Printing devices are known to emit chemicals into the indoor atmosphere. Understanding factors that influence release of chemical contaminants from printers is necessary to develop effective exposure assessment and control strategies. In this study, a desktop fused deposition modeling (FDM) 3-dimensional (3-D) printer using acrylonitrile butadiene styrene (ABS) or polylactic acid (PLA) filaments and two monochrome laser printers were evaluated in a 0.5 m3 chamber. During printing, chamber air was monitored for vapors using a real-time photoionization detector (results expressed as isobutylene equivalents) to measure total volatile organic compound (TVOC) concentrations, evacuated canisters to identify specific VOCs by off-line gas chromatography-mass spectrometry (GC-MS) analysis, and liquid bubblers to identify carbonyl compounds by GC-MS. Airborne particles were collected on filters for off-line analysis using scanning electron microscopy with an energy dispersive x-ray detector to identify elemental constituents. For 3-D printing, TVOC emission rates were influenced by a printer malfunction, filament type, and to a lesser extent, by filament color; however, rates were not influenced by the number of printer nozzles used or the manufacturer's provided cover. TVOC emission rates were significantly lower for the 3-D printer (49-3552 µg h-1) compared to the laser printers (5782-7735 µg h-1). A total of 14 VOCs were identified during 3-D printing that were not present during laser printing. 3-D printed objects continued to off-gas styrene, indicating potential for continued exposure after the print job is completed. Carbonyl reaction products were likely formed from emissions of the 3-D printer, including 4-oxopentanal. Ultrafine particles generated by the 3-D printer using ABS and a laser printer contained chromium. Consideration of the factors that influenced the release of chemical contaminants (including known and suspected asthmagens such as styrene and 4-oxopentanal) from a FDM 3-D printer should be made when designing exposure assessment and control strategies.

Abstract The effects of acute pulmonary coexposures to silica and diesel particulate matter (DPM), which may occur in various mining operations, were investigated in vivo. Rats were exposed by intratracheal instillation (IT) to silica (50 or 233 µg), DPM (7.89 or 50 µg) or silica and DPM combined in phosphate-buffered saline (PBS) or to PBS alone (control). At one day, one week, one month, two months and three months postexposure bronchoalveolar lavage and histopathology were performed to assess lung injury, inflammation and immune response. While higher doses of silica caused inflammation and injury at all time points, DPM exposure alone did not. DPM (50 µg) combined with silica (233 µg) increased inflammation at one week and one-month postexposure and caused an increase in the incidence of fibrosis at one month compared with exposure to silica alone. To assess susceptibility to lung infection following coexposure, rats were exposed by IT to 233 µg silica, 50 µg DPM, a combination of the two or PBS control one week before intratracheal inoculation with 5 × 105 Listeria monocytogenes. At 1, 3, 5, 7 and 14 days following infection, pulmonary immune response and bacterial clearance from the lung were evaluated. Coexposure to DPM and silica did not alter bacterial clearance from the lung compared to control. Although DPM and silica coexposure did not alter pulmonary susceptibility to infection in this model, the study showed that noninflammatory doses of DPM had the capacity to increase silica-induced lung injury, inflammation and onset/incidence of fibrosis.

Exposure to crystalline silica results in serious adverse health effects, most notably, silicosis. An understanding of the mechanism(s) underlying silica-induced pulmonary toxicity is critical for the intervention and/or prevention of its adverse health effects. Rats were exposed by inhalation to crystalline silica at a concentration of 15 mg/m3, 6 hr/day, 5 days/week for 3, 6 or 12 weeks. Pulmonary toxicity and global gene expression profiles were determined in lungs at the end of each exposure period. Crystalline silica was visible in lungs of rats especially in the 12-week group. Pulmonary toxicity, as evidenced by an increase in lactate dehydrogenase (LDH) activity and albumin content and accumulation of macrophages and neutrophils in the bronchoalveolar lavage (BAL), was seen in animals depending upon silica exposure duration. The most severe histological changes, noted in the 12-week exposure group, consisted of chronic active inflammation, type II pneumocyte hyperplasia, and fibrosis. Microarray analysis of lung gene expression profiles detected significant differential expression of 38, 77, and 99 genes in rats exposed to silica for 3-, 6-, or 12-weeks, respectively, compared to time-matched controls. Among the significantly differentially expressed genes (SDEG), 32 genes were common in all exposure groups. Bioinformatics analysis of the SDEG identified enrichment of functions, networks and canonical pathways related to inflammation, cancer, oxidative stress, fibrosis, and tissue remodeling in response to silica exposure. Collectively, these results provided insights into the molecular mechanisms underlying pulmonary toxicity following sub-chronic inhalation exposure to crystalline silica in rats.

An understanding of the mechanisms underlying diseases is critical for their prevention. Excessive exposure to crystalline silica is a risk factor for silicosis, a potentially fatal pulmonary disease. Male Fischer 344 rats were exposed by inhalation to crystalline silica (15 mg/m3, six hours/day, five days) and pulmonary response was determined at 44 weeks following termination of silica exposure. Additionally, global gene expression profiling in lungs and BAL cells and bioinformatic analysis of the gene expression data were done to understand the molecular mechanisms underlying the progression of pulmonary response to silica. A significant increase in lactate dehydrogenase activity and albumin content in BAL fluid (BALF) suggested silica-induced pulmonary toxicity in the rats. A significant increase in the number of alveolar macrophages and infiltrating neutrophils in the lungs and elevation in monocyte chemoattractant protein-1 (MCP-1) in BALF suggested the induction of pulmonary inflammation in the silica exposed rats. Histological changes in the lungs included granuloma formation, type II pneumocyte hyperplasia, thickening of alveolar septa and positive response to Masson's trichrome stain. Microarray analysis of global gene expression detected 94 and 225 significantly differentially expressed genes in the lungs and BAL cells, respectively. Bioinformatic analysis of the gene expression data identified significant enrichment of several disease and biological function categories and canonical pathways related to pulmonary toxicity, especially inflammation. Taken together, these data suggested the involvement of chronic inflammation as a mechanism underlying the progression of pulmonary response to exposure of rats to crystalline silica at 44 weeks following termination of exposure.

Moisture-damaged indoor environments are thought to increase the toxicity of indoor air particulate matter (PM), indicating that a toxicological assay could be used as a method for recognizing buildings with indoor air problems. We aimed to test if our approach of analyzing the toxicity of actively collected indoor air PM in vitro differentiates moisture-damaged from non-damaged school buildings. We collected active air samples with NIOSH Bioaerosol Cyclone Samplers from moisture-damaged (index) and non-damaged (reference) school buildings (4+4). The teachers and pupils of the schools were administered a symptom questionnaire. Five samples of two size fractions [Stage 1 (>1.9 mu m) and Stage 2 (1-1.9 mu m)] were collected from each school. Mouse RAW264.7 macrophages were exposed to the collected PM for 24 h and subsequently analyzed for changes in cell metabolic activity, production of nitric oxide (NO), tumor necrosis factor (TNF)-alpha and interleukin (IL)-6. The teachers working in the moisture-damaged schools reported respiratory symptoms such as cough (p = 0.01) and shortness of breath (p = 0.01) more often than teachers from reference schools. Toxicity of the PM sample as such did not differentiate index from reference building, s but the toxicity adjusted for the amount of the particles tended to be higher in moisture-damaged schools. Further development of the method will require identification of other confounding factors in addition to the necessity to adjust for differences in particle counts between samples.

Resistance spot welding is a common process to join metals in the automotive industry. Adhesives are often used as sealers to seams of metals that are joined. Anti-spatter compounds sometimes are sprayed onto metals to be welded to improve the weldability. Spot welding produces complex aerosols composed of metal and volatile compounds (VOCs) which can cause lung disease in workers. Male Sprague-Dawley rats (n = 12/treatment group) were exposed by inhalation to 25 mg/m3 of aerosol for 4 h/day x 8 days during spot welding of galvanized zinc (Zn)-coated steel in the presence or absence of a glue or anti-spatter spray. Controls were exposed to filtered air. Particle size distribution and chemical composition of the generated aerosol were determined. At 1 and 7 days after exposure, bronchoalveolar lavage (BAL) was performed to assess lung toxicity. The generated particles mostly were in the submicron size range with a significant number of nanometer-sized particles formed. The primary metals present in the fumes were Fe (72.5%) and Zn (26.3%). The addition of the anti-spatter spray and glue did affect particle size distribution when spot welding galvanized steel, whereas they had no effect on metal composition. Multiple VOCs (e.g., methyl methacrylate, acetaldehyde, ethanol, acetone, benzene, xylene) were identified when spot welding using either the glue or the anti-spatter spray that were not present when welding alone. Markers of lung injury (BAL lactate dehydrogenase) and inflammation (total BAL cells/neutrophils and cytokines/chemokines) were significantly elevated compared to controls 1 day after exposure to the spot welding fumes. The elevated pulmonary response was transient as lung toxicity mostly returned to control values by 7 days. The VOCs or the concentrations that they were generated during the animal exposures had no measurable effect on the pulmonary responses. Inhalation of galvanized spot welding fumes caused acute lung toxicity most likely due to the short-term exposure of particles that contain Zn. Published by Elsevier Ireland Ltd.

Vapor grown carbon nanofibers (VGCF™-H) is an example of a two dimensional carbon based nanoparticle. In the present study, male C57Bl/6J mice were exposed to VGCF™-H (10–80 μg) by pharyngeal aspiration; dispersion medium (DM) was used as the vehicle. At 1, 7 and 28 days post-exposure, lung lavage and histopathology studies were conducted. VGCF™-H cytotoxicity was assessed by measuring acellular lavage fluid lactate dehydrogenase (LDH) activity, and determined that VGCF™-H exposure produced dose-dependent increases in LDH activity which decreased over time. Using polymorphonuclear leukocytes as a marker, VGCF™-H-exposure produced dose-dependent lung inflammation which decreased over time. Histologically, the incidence and severity of pulmonary inflammation was confirmed to be dose-dependent, and inflammatory infiltrates were characterized by increased numbers of alveolar macrophages with small numbers of neutrophils. VGCF™-H caused dose- and time-dependent increases in cathepsin activity and cytokines in the acellular lavage fluid, indicating activation of the NLRP3 inflammasome by VGCF™-H may contribute to lung inflammation. VGCF™-H exposure caused minimal to mild interstitial alveolar fibrosis, characterized by increased amounts of collagen fibers in the interstitium, and the incidence and severity of fibrosis tended to increase with the VGCF™-H dose. Accumulation of VGCF™-H fibers in the tracheobronchial lymph nodes was observed by 28 days after exposure at 40 and 80 μg doses.

Desktop three-dimensional (3D) printers are becoming commonplace in business offices, public libraries, university labs and classrooms, and even private homes; however, these settings are generally not designed for exposure control. Prior experience with a variety of office equipment devices such as laser printers that emit ultrafine particles (UFP) suggests the need to characterize 3D printer emissions to enable reliable risk assessment. The aim of this study was to examine factors that influence particulate emissions from 3D printers and characterize their physical properties to inform risk assessment. Emissions were evaluated in a 0.5-m(3) chamber and in a small room (32.7 m(3)) using real-time instrumentation to measure particle number, size distribution, mass, and surface area. Factors evaluated included filament composition and color, as well as the manufacturer-provided printer emissions control technologies while printing an object. Filament type significantly influenced emissions, with acrylonitrile butadiene styrene (ABS) emitting larger particles than polylactic acid (PLA), which may have been the result of agglomeration. Geometric mean particle sizes and total particle (TP) number and mass emissions differed significantly among colors of a given filament type. Use of a cover on the printer reduced TP emissions by a factor of 2. Lung deposition calculations indicated a threefold higher PLA particle deposition in alveoli compared to ABS. Desktop 3D printers emit high levels of UFP, which are released into indoor environments where adequate ventilation may not be present to control emissions. Emissions in nonindustrial settings need to be reduced through the use of a hierarchy of controls, beginning with device design, followed by engineering controls (ventilation) and administrative controls such as choice of filament composition and color.

Inhalation exposure to multi-walled carbon nanotubes (MWCNT) in mice results in inflammation, fibrosis and the promotion of lung adenocarcinoma; however, the molecular basis behind these pathologies is unknown. This study determined global mRNA and miRNA profiles in whole blood from mice exposed by inhalation to MWCNT that correlated with the presence of lung hyperplasia, fibrosis, and bronchiolo-alveolar adenoma and adenocarcinoma. Six-week-old, male, B6C3F1 mice received a single intraperitoneal injection of either the DNA-damaging agent methylcholanthrene (MCA, 10 mu gg(-1) body weight) or vehicle (corn oil). One week after injections, mice were exposed by inhalation to MWCNT (5mgm(-3), 5hours per day, 5days per week) or filtered air (control) for a total of 15days. At 17months post-exposure, mice were euthanized and examined for the development of pathological changes in the lung, and whole blood was collected and analyzed using microarray analysis for global mRNA and miRNA expression. Numerous mRNAs and miRNAs in the blood were significantly up- or down-regulated in animals developing pathological changes in the lung after MCA/corn oil administration followed by MWCNT/air inhalation, including fcrl5 and miR-122-5p in the presence of hyperplasia, mthfd2 and miR-206-3p in the presence of fibrosis, fam178a and miR-130a-3p in the presence of bronchiolo-alveolar adenoma, and il7r and miR-210-3p in the presence of bronchiolo-alveolar adenocarcinoma, among others. The changes in miRNA and mRNA expression, and their respective regulatory networks, identified in this study may potentially serve as blood biomarkers for MWCNT-induced lung pathological changes. Copyright (c) 2015 John Wiley & Sons, Ltd.This study determined global mRNA and miRNA profiles in whole blood from mice exposed by inhalation to MWCNT that correlated with the presence of lung hyperplasia, fibrosis, and bronchiolo-alveolar adenoma and adenocarcinoma. At 17 months post-exposure, whole blood was collected and analyzed using microarray analysis for global mRNA and miRNA expression. The changes in miRNA and mRNA expression, and their respective regulatory networks, identified in this study may potentially serve as blood biomarkers for MWCNT-induced lung pathological changes.

Although classified as metal oxides, cobalt monoxide (CoO) and lanthanum oxide (La2O3) nanoparticles, as representative transition and rare earth oxides, exhibit distinct material properties that may result in different hazardous potential in the lung. The current study was undertaken to compare the pulmonary effects of aerosolized whole body inhalation of these nanoparticles in mice.

Gas metal arc welding fumes were generated from mild-steel plates and measured near the arc (30 cm), representing first-hand exposure of the welder, and farther away from the source (200 cm), representing second-hand exposure of adjacent workers. Measurements were taken during 1-min welding runs and at subsequent 5-min intervals after the welding process was stopped. Number size distributions were measured in real time. Particle mass distributions were measured using a micro-orifice uniform deposition impactor, and total mass concentrations were measured with polytetrafluorothylene filters. Membrane filters were used for collecting morphology samples for electron microscopy. Average mass concentrations measured near the arc were 45 mg/m3 and 9 mg/m3 at the farther distance. The discrepancy in concentrations at the two distances was attributed to the presence of spatter particles, which were observed only in the morphology samples near the source. As fumes aged over time, mass concentrations at the farther distance decreased by 31% (6.2 mg/m3) after 5 min and an additional 13% (5.4 mg/m3) after 10 min. Particle number and mass distributions during active welding were similar at both distances, indicating similar exposure patterns for welders and adjacent workers. Exceptions were recorded for particles smaller than 50 nm and larger than 3 μm, where concentrations were higher near the arc, indicating higher exposures of welders. These results were confirmed by microscopy analysis. As residence time increased, number concentrations decreased dramatically. In terms of particle number concentrations, second-hand exposures to welding fumes during active welding may be as high as first-hand exposures.

ABSTRACT Nine gas metal arc welding (GMAW) processes for stainless steel were assessed for fume generation rates, fume generation rates per g of electrode consumed, and emission rates for hexavalent chromium (Cr6+). Elemental manganese, nickel, chromium, iron emissions per unit length of weld, and labor plus consumables costs were similarly measured. Flux-cored arc welding and shielded metal arc (SMAW) processes were also studied. The objective was to identify the best welding processes for reducing workplace exposures, and estimate costs for all processes. Using a conical chamber, fumes were collected, weighed, recovered, and analyzed by inductively coupled atomic emission spectroscopy for metals, and by ion chromatography for Cr6+. GMAW processes used were Surface Tension Transfer, Regulated Metal Deposition, Cold Metal Transfer, short-circuit, axial spray, and pulsed spray modes. Flux-cored welding used gas shielding; SMAW used E308 rods. Costs were estimated as dollars per m length of a ¼ in (6.3 mm) thick horizontal butt weld; equipment costs were estimated as ratios of new equipment costs to a 250 ampere capacity SMAW welding machine. Results indicate a broad range of fume emission factors for the processes studied. Fume emission rates per g of electrode were lowest for GMAW processes such as pulsed-spray mode (0.2 mg/g), and highest for SMAW (8 mg fume/g electrode). Emission rates of Cr6+ ranged from 50–7800 µg/min, and Cr6+ generation rates per g electrode ranged from 1–270 µg/g. Elemental Cr generation rates spanned 13–330 µg/g. Manganese emission rates ranged from 50–300 µg/g. Nickel emission rates ranged from 4–140 µg/g. Labor and consumables costs ranged from $3.15 (GMAW pulsed spray) to $7.40 (SMAW) per meter of finished weld, and were measured or estimated for all 11 processes tested. Equipment costs for some processes may be as much as five times the cost of a typical SMAW welding machine. The results show that all of the GMAW processes in this study can substantially reduce fume, Cr6+, manganese and costs relative to SMAW, the most commonly used welding process, and several have exceptional capabilities for reducing emissions.

The early incorporation of exposure assessment can be invaluable to help design, prioritize, and interpret toxicological studies or outcomes. The sum total of the exposure assessment findings combined with preliminary toxicology results allows for exposure-informed toxicological study design and the findings can then be integrated, together with available epidemiologic data, to provide health effect relevance. With regard to engineered nanomaterial inhalation toxicology in particular, a single type of material (e.g. carbon nanotube, graphene) can have a vast array of physicochemical characteristics resulting in the potential for varying toxicities. To compound the matter, the methodologies necessary to establish a material adequate for in vivo exposure testing raises questions on the applicability of the outcomes. From insights gained from evaluating carbon nanotubes, we recommend the following integrated approach involving exposure-informed hazard assessment and hazard-informed exposure assessment especially for materials as diverse as engineered nanomaterials: 1) market-informed identification of potential hazards and potentially exposed populations, 2) initial toxicity screening to drive prioritized assessments of exposure, 3) development of exposure assessment-informed chronic and sub-chronic in vivo studies, and 4) conduct of exposure- and hazard-informed epidemiological studies.

Gas metal arc welding fumes were generated from mild-steel plates and measured near the arc (30 cm), representing first-hand exposure of the welder, and farther away from the source (200 cm), representing second-hand exposure of adjacent workers. Measurements were taken during 1 -min welding runs and at subsequent 5 -min intervals after the welding process was stopped. Number size distributions were measured in real time. Particle mass distributions were measured using a micro -orifice uniform deposition impactor, and total mass concentrations were measured with polytetrafluorothylene filters. Membrane filters were used for collecting morphology samples for electron microscopy. Average mass concentrations measured near the arc were 45 mg/m(3) and 9 mg/m(3) at the farther distance. The discrepancy in concentrations at the two distances was attributed to the presence of spatter particles, which were observed only in the morphology samples near the source. As fumes aged over time, mass concentrations at I the farther distance decreased by 31% (6.2 mg/m(3)) after 5 min and an additional 13% (5.4 mg/m(3)) after 10 min. Particle number and mass distributions during active welding were similar at both distances, indicating similar exposure patterns for welders and adjacent workers. Exceptions were recorded for particles smaller than 50 nm and larger than 3 where concentrations were higher near the arc, indicating higher exposures of welders. These results were confirmed by microscopy analysis. As residence time increased, number concentrations decreased dramatically. In terms of particle number concentrations, second-hand exposures to welding fumes during active welding may be as high as first-hand exposures.

Direct-reading instruments have been widely used for characterizing airborne nanoparticles in inhalation toxicology and industrial hygiene studies for exposure/risk assessments. Instruments using electrical mobility sizing followed by optical counting, e.g., scanning or sequential mobility particle spectrometers (SMPS), have been considered as the “gold standard” for characterizing nanoparticles. An SMPS has the advantage of rapid response and has been widely used, but there is little information on its performance in assessing the full spectrum of nanoparticles encountered in the workplace. In this study, an SMPS was evaluated for its effectiveness in producing “monodisperse” aerosol and its adequacy in characterizing overall particle size distribution using three test aerosols, each mimicking a unique class of real-life nanoparticles: singlets of nearly spherical titanium dioxide (TiO2), agglomerates of fiber-like multi-walled carbon nanotube (MWCNT), and aggregates that constitutes welding fume (WF). These aerosols were analyzed by SMPS, cascade impactor, and by counting and sizing of discrete particles by scanning and transmission electron microscopy. The effectiveness of the SMPS to produce classified particles (fixed voltage mode) was assessed by examination of the resulting geometric standard deviation (GSD) from the impactor measurement. Results indicated that SMPS performed reasonably well for TiO2 (GSD = 1.3), but not for MWCNT and WF as evidenced by the large GSD values of 1.8 and 1.5, respectively. For overall characterization, results from SMPS (scanning voltage mode) exhibited particle-dependent discrepancies in the size distribution and total number concentration compared to those from microscopic analysis. Further investigation showed that use of a single-stage impactor at the SMPS inlet could distort the size distribution and underestimate the concentration as shown by the SMPS, whereas the presence of vapor molecules or atom clusters in some test aerosols might cause artifacts by counting “phantom particles.” Overall, the information obtained from this study will help understand the limitations of the SMPS in measuring nanoparticles so that one can adequately interpret the results for risk assessments and exposure prevention in an occupational or ambient environment.

There is a need for toxicity tests capable of recognizing indoor environments with compromised air quality, especially in the context of moisture damage. One of the key issues is sampling, which should both provide meaningful material for analyses and fulfill requirements imposed by practitioners using toxicity tests for health risk assessment. We aimed to evaluate different existing methods of sampling indoor particulate matter (PM) to develop a suitable sampling strategy for a toxicological assay. During three sampling campaigns in moisture-damaged and non-damaged school buildings, we evaluated one passive and three active sampling methods: the Settled Dust Box (SDB), the Button Aerosol Sampler, the Harvard Impactor and the National Institute for Occupational Safety and Health (NIOSH) Bioaerosol Cyclone Sampler. Mouse RAW264.7 macrophages were exposed to particle suspensions and cell metabolic activity (CMA), production of nitric oxide (NO) and tumor necrosis factor (TNFα) were determined after 24 h of exposure. The repeatability of the toxicological analyses was very good for all tested sampler types. Variability within the schools was found to be high especially between different classrooms in the moisture-damaged school. Passively collected settled dust and PM collected actively with the NIOSH Sampler (Stage 1) caused a clear response in exposed cells. The results suggested the higher relative immunotoxicological activity of dust from the moisture-damaged school. The NIOSH Sampler is a promising candidate for the collection of size-fractionated PM to be used in toxicity testing. The applicability of such sampling strategy in grading moisture damage severity in buildings needs to be developed further in a larger cohort of buildings.

A field study was conducted to estimate the amount of Cr, Mn, and Ni deposited in the respiratory system of 44 welders in two facilities. Each worker wore a nanoparticle respiratory deposition (NRD) sampler during gas metal arc welding (GMAW) of mild and stainless steel and flux-cored arc welding (FCAW) of mild steel. Several welders also wore side-by-side NRD samplers and closed-face filter cassettes for total particulate samples. The NRD sampler estimates the aerosol's nano-fraction deposited in the respiratory system. Mn concentrations for both welding processes ranged 2.8–199 μg/m3; Ni concentrations ranged 10–51 μg/m3; and Cr concentrations ranged 40–105 μg/m3. Cr(VI) concentrations ranged between 0.5–1.3 μg/m3. For the FCAW process the largest concentrations were reported for welders working in pairs. As a consequence this often resulted in workers being exposed to their own welding fumes and to those generated from the welding partner. Overall no correlation was found between air velocity and exposure (R2 = 0.002). The estimated percentage of the nano-fraction of Mn deposited in a mild-steel-welder's respiratory system ranged between 10 and 56%. For stainless steel welding, the NRD samplers collected 59% of the total Mn, 90% of the total Cr, and 64% of the total Ni. These results indicate that most of the Cr and more than half of the Ni and Mn in the fumes were in the fraction smaller than 300 nm.