Combined adjuvant effects of ambient vapor-phase organic components and particulate matter potently promote allergic sensitization and Th2-skewing cytokine and chemokine milieux in mice: The importance of mechanistic multi-pollutant research.

Although exposure to ambient particulate matter (PM) is linked to asthma, the health effects of co-existing vapor-phase organic pollutants (vapor) and their combined effects with PM on this disease are poorly understood. We used a murine asthma model to test the hypothesis that exposure to vapor would enhance allergic sensitization and this effect would be further strengthened by co-existing PM. We found that vapor and PM each individually exerted adjuvant effects on OVA sensitization. Co-exposure to vapor and PM during sensitization further enhanced allergic lung inflammation and OVA-specific antibody production which was accompanied by pulmonary cytokine/chemokine milieu that favored T-helper 2 immunity (i.e. increased IL-4, downregulation of Il12a and Ifng, and upregulation of Ccl11 and Ccl8). TNFα, IL-6, Ccl12, Cxcl1 and detoxification/antioxidant enzyme responses in the lung were pollutant-dependent. Inhibition of lipopolysaccharide-induced IL-12 secretion from primary antigen-presenting dendritic cells correlated positively with vapor's oxidant potential. In conclusion, concurrent exposure to vapor and PM led to significantly exaggerated adjuvant effects on allergic lung inflammation which were more potent than that of each pollutant type alone. These findings suggest that the effects of multi-component air pollution on asthma may be significantly underestimated if research only focuses on a single air pollutant (e.g., PM).

Lung inflammation biomarkers and lung function in children chronically exposed to arsenic.

Evidence suggests that exposure to arsenic in drinking water during early childhood or in utero has been associated with an increase in respiratory symptoms or diseases in the adulthood, however only a few studies have been carried out during those sensitive windows of exposure. Recently our group demonstrated that the exposure to arsenic during early childhood or in utero in children was associated with impairment in the lung function and suggested that this adverse effect could be due to a chronic inflammation response to the metalloid. Therefore, we designed this cross-sectional study in a cohort of children associating lung inflammatory biomarkers and lung function with urinary As levels. A total of 275 healthy children were partitioned into four study groups according with their arsenic urinary levels. Inflammation biomarkers were measured in sputum by ELISA and the lung function was evaluated by spirometry. Fifty eight percent of the studied children were found to have a restrictive spirometric pattern. In the two highest exposed groups, the soluble receptor for advanced glycation end products' (sRAGE) sputum level was significantly lower and matrix metalloproteinase-9 (MMP-9) concentration was higher. When the biomarkers were correlated to the urinary arsenic species, negative associations were found between dimethylarsinic (DMA), monomethylarsonic percentage (%MMA) and dimethylarsinic percentage (%DMA) with sRAGE and positive associations between %DMA with MMP-9 and with the MMP-9/tissue inhibitor of metalloproteinase (TIMP-1) ratio. In conclusion, chronic arsenic exposure of children negatively correlates with sRAGE, and positively correlated with MMP-9 and MMP-9/TIMP-1 levels, and increases the frequency of an abnormal spirometric pattern. Arsenic-induced alterations in inflammatory biomarkers may contribute to the development of restrictive lung diseases.

Chemical reactivities of ambient air samples in three Southern California communities.

UNLABELLED: The potential adverse health effects of PM2.5 (particulate matter with an aerodynamic diameter<2.5 µm) and vapor samples from three communities that neighbor railyards, Commerce (CM), Long Beach (LB), and San Bernardino (SB), were assessed by determination of chemical reactivities attributed to the induction of oxidative stress by air pollutants. The assays used were dithiothreitol (DTT)- and dihydrobenzoic acid (DHBA)-based procedures for prooxidant content and a glyceraldehyde-3-phosphate dehydrogenase (GAPDH) assay for electrophiles. Prooxidants and electrophiles have been proposed as the reactive chemical species responsible for the induction of oxidative stress by air pollution mixtures. The PM2.5 samples from CM and LB sites showed seasonal differences in reactivities, with higher levels in the winter, whereas the SB sample differences were reversed. The reactivities in the vapor samples were all very similar, except for the summer SB samples, which contained higher levels of both prooxidants and electrophiles. The results suggest that the observed reactivities reflect general geographical differences rather than direct effects of the railyards. Distributional differences in reactivities were also observed, with PM2.5 fractions containing most of the prooxidants (74-81%) and the vapor phase most of the electrophiles (82-96%). The high levels of the vapor-phase electrophiles and their potential for adverse biological effects point out the importance of the vapor phase in assessing the potential health effects of ambient air. IMPLICATIONS: PM2.5 and its corresponding vapor phase, containing semivolatile organics, were collected in three communities in the Los Angeles Basin and examined with toxicologically relevant chemical assays. The PM2.5 phase contained most of the prooxidants and the vapor phase contained most of the electrophiles, whose content was highest in summer samples from a receptor site that reflected greater photochemical processing of the air parcel during its transport. As electrophiles initiate both adverse and adaptive responses to foreign substances by biological systems, their presence in the vapor phase emphasizes the importance of this phase in the overall health effects of ambient air.

Ambient vapor samples activate the Nrf2-ARE pathway in human bronchial epithelial BEAS-2B cells.

Ambient air pollutants have been reported to induce oxidative stress based inflammatory responses in humans and experimental animals. However, most of these reports describe the actions of the particulate phase of ambient and exhaust samples. We describe here results of studies investigating the actions of the vapor phase of ambient air samples collected in the midtown area of Los Angeles on human bronchial epithelial BEAS-2B cells using DNA microarray analysis. Among 26 genes whose expression increased fourfold or more, four genes were associated with detoxifying genes regulated by the transcription factor Nrf2. Consistent with these results, the vapor samples activate the Nrf2-ARE pathway, resulting in up-regulation of heme oxygenase-1 (HO-1), glutamate cysteine ligase modifier subunit, and cystine transporter (xCT) mRNA and proteins. No appreciable increases in pro-inflammatory genes were observed. These results suggest that ambient vapor samples activate the Nrf2-ARE pathway but not an inflammatory response. Also, treatment of the vapor samples with glutathione resulted in reduction in the Nrf2 activation and HO-1 induction, suggesting that electrophiles in vapor samples contribute to this Nrf2-dependent antioxidant or adaptive response.

Redox and electrophilic properties of vapor- and particle-phase components of ambient aerosols.

Particulate matter (PM) has been the primary focus of studies aiming to understand the relationship between the chemical properties of ambient aerosols and adverse health effects. Size and chemical composition of PM have been linked to their oxidative capacity which has been postulated to promote or exacerbate pulmonary and cardiovascular diseases. But in the last few years, new studies have suggested that volatile and semi-volatile components may also contribute to many adverse health effects. The objectives of this study were: (i) assess for the first time the redox and electrophilic potential of vapor-phase components of ambient aerosols and (ii) evaluate the relative contributions of particle- and vapor-fractions to the hazard of a given aerosol. To achieve these objectives vapor- and particle-phase samples collected in Riverside (CA) were subjected to three chemical assays to determine their redox and electrophilic capacities. The results indicate that redox active components are mainly associated with the particle-phase, while electrophilic compounds are found primarily in the vapor-phase. Vapor-phase organic extracts were also capable of inducing the stress responding protein, heme-oxygenase-1 (HO-1), in RAW264.7 murine macrophages. These results demonstrate the importance of volatile components in the overall oxidative and electrophilic capacity of aerosols, and point out the need for inclusion of vapors in future health and risk assessment studies.

Particulate matter (PM) research centers (1999-2005) and the role of interdisciplinary center-based research.

OBJECTIVE: The U.S. Environmental Protection Agency funded five academic centers in 1999 to address the uncertainties in exposure, toxicity, and health effects of airborne particulate matter (PM) identified in the "Research Priorities for Airborne Particulate Matter" of the National Research Council (NRC). The centers were structured to promote interdisciplinary approaches to address research priorities of the NRC. In this report, we present selected accomplishments from the first 6 years of the PM Centers, with a focus on the advantages afforded by the interdisciplinary, center-based research approach. The review highlights advances in the area of ultrafine particles and traffic-related health effects as well as cardiovascular and respiratory effects, mechanisms, susceptibility, and PM exposure and characterization issues. DATA SOURCES AND SYNTHESIS: The collective publications of the centers served as the data source. To provide a concise synthesis of overall findings, authors representing each of the five centers identified a limited number of topic areas that serve to illustrate the key accomplishments of the PM Centers program, and a consensus statement was developed. CONCLUSIONS: The PM Centers program has effectively applied interdisciplinary research approaches to advance PM science.

Electrophilic and redox properties of diesel exhaust particles.

The adverse health effects of air pollutants have been associated with their redox and electrophilic properties. Although the specific chemical species involved in these effects are not known, the characterization of their general physical and chemical properties is important to our understanding of the mechanisms by which they cause health problems. This manuscript describes results of a study examining the partition properties of these activities in aqueous and organic media. The water and dichloromethane (DCM) solubility of redox active and electrophilic constituents of seven diesel exhaust particle (DEP) samples were determined with assays developed earlier in this laboratory. The constituents exhibiting redox activity, which included both metals and nonmetal species, were associated with the particles in the aqueous suspensions. Portions of the redox active compounds were also DCM-soluble. In contrast, the electrophilic constituents included both water-soluble and DCM-soluble species. The role of quinones or quinone-like compounds in redox and electrophilic activities of the DCM-soluble constituents was assessed by reductive acetylation, a procedure that inactivates quinones. The results from this experiment indicated that most of the activities in the organic extract were associated with quinone-like substances. The partition properties of the reactive species are important in exposure assessment since the toxicokinetics of particles and solutes are quite distinct.

Determination of metal-based hydroxyl radical generating capacity of ambient and diesel exhaust particles.

Numerous studies have suggested the association of reactive oxygen species (ROS) with adverse health effects derived from exposure to airborne particulate matter (PM) and diesel exhaust particles (DEP). This redox activity has been attributed to both inorganic and organic species present in these particles, but a clear distinction has not been established between the contribution of each. This article describes an application of an analytical procedure, based on the reaction of salicylic acid with hydroxyl radical to form dihydroxybenzoate (DHBA) isomers, to measure transition metal-based redox activity associated with ambient and diesel exhaust particles. In the procedure, ascorbic acid (AA) is used as electron source for reduction of metal ions and oxygen to generate superoxide, which is further reduced to hydroxyl radical in the presence of transition metal ions. Hydroxyl radical reacts with salicylate to generate DHBA isomers, which are measured by high-performance liquid chromatography (HPLC) with electrochemical detector. Both copper (Cu) and iron (Fe) ions generated DHBA isomers in a concentration-dependent manner but at different rates. The procedure was applied to DEP and ambient particles and the results showed Cu ion to be the major contributor to DHBA formation. The procedure provides a quantitative measure of transition metal-based redox activity associated with ambient samples with different physicochemical properties.

Redox cycling of 9,10-phenanthraquinone to cause oxidative stress is terminated through its monoglucuronide conjugation in human pulmonary epithelial A549 cells.

9,10-Phenanthraquinone (PQ), a component of airborne particulate matter, causes marked cellular protein oxidation and cytotoxicity through a two-electron reduction to 9,10-dihydroxyphenanthrene (PQH2), which is associated with the propagation of reactive oxygen species (K. Taguchi et al., Free Radic. Biol. Med. 43:789-799, 2007). In the present study, we explored a biotransformation pathway for the detoxification of PQ. Exposure of human pulmonary epithelial A549 cells to PQ resulted in a time-dependent appearance of an unknown metabolite in the medium that was identified as the monoglucuronide of PQH2 (PQHG). Whereas a variety of isozymes of uridine 5'-diphosphate glucuronosyltransferase (UGTs) are responsible for PQHG formation, UGT1A10 and UGT1A6 were particularly effective catalysts for glucuronide conjugation. In cell-free systems, PQ exhibited a rapid thiol oxidation and subsequent oxygen consumption in the presence of dithiothreitol, whereas PQHG did not. Unlike the parent compound, PQHG completely lost the ability to oxidize cellular proteins and cause cell death in A549 cells. In addition, deletion of the transcription factor Nrf2 decreased PQHG formation and increased PQ-mediated toxicity of mouse primary hepatocytes. Thus, we conclude that PQHG is a metabolite of PQ, generated through PQH2, that terminates its redox cycling and transports it to extracellular space.

Inhalation of concentrated ambient particulate matter near a heavily trafficked road stimulates antigen-induced airway responses in mice.

Motor vehicle exhaust emissions are known to exacerbate asthma and other respiratory diseases. Several studies have demonstrated significant associations between living near highly trafficked roadways and increased incidence of asthma and increased severity of asthma-related symptoms, medication usage, and physician visits. This study tested the hypotheses that (1) exposure to particulate matter (PM) near a heavily trafficked Los Angeles freeway would enhance inflammatory and allergic responses in ovalbumin (OVA)-sensitized BALB/c mice compared to sensitized, clean air controls, and (2) there would be differences in response at two distances downwind of heavily traveled freeways because of greater toxicity of PM closest to the freeway. An ambient particle concentrator was used to expose ovalbumin (OVA)-treated BALB/c mice to purified air, to concentrated fine ambient particles, and to concentrated ultrafine airborne particles (CAPs) at 2 distances, 50 m and 150 m, downwind of a roadway that is impacted by emissions from both heavy-duty diesel and light duty gasoline vehicles. Tissues and biological fluids from the mice were analyzed after exposures for 5 days/wk in 2 consecutive weeks. The biomarkers of allergic or inflammatory responses that were assessed included cytokines released by Type 2 T-helper cells (interleukin [IL]-5 and IL-13), OVA-specific immunoglobulin E (IgE), OVA-specific immunoglobulin G1 (IgG1), and pulmonary infiltration of polymorphonuclear leukocytes and eosinophils. IL-5 and IgG1 were significantly increased in mice exposed to CAPs 50 m downwind of the road, compared to responses in mice exposed to purified air, providing evidence of allergic response. No significant increases in allergy-related responses were observed in mice exposed to CAPs 150 m downwind of the road. The biological responses at the 50-m site were significantly associated with organic and elemental carbon components of fine and ultrafine particles (p < or = .05). The primary source of these contaminants at the roadway sites was motor vehicle emissions, suggesting that particulate matter from motor vehicle fuel combustion could exert adjuvant effects and promote the development of allergic airway diseases.

Chemical knockdown of protein-tyrosine phosphatase 1B by 1,2-naphthoquinone through covalent modification causes persistent transactivation of epidermal growth factor receptor.

1,2-Naphthoquinone (1,2-NQ), an atmospheric contaminant, causes the contraction of guinea pig trachea through the activation of epidermal growth factor receptor (EGFR) by inhibiting protein-tyrosine phosphatases (PTPs). Phosphorylation of EGFR is negatively regulated by PTPs, but details of the mechanism by which 1,2-NQ inhibits PTPs have not been elucidated. Results described in this report demonstrate that 1,2-NQ forms covalent bonds with PTP1B after exposure to human epithelial A431 cells. In this study, a concentration-dependent phosphorylation of EGFR was found to be coupled to the reduction of PTP activity in the cells. The reduction in PTP activity was due to the irreversible modification of PTP1B, and when PTP1B was overexpressed by the cells, the 1,2-NQ-mediated EGFR phosphorylation was suppressed. Studies with purified PTP1B and 1,2-NQ showed that the reduction in enzyme activity was due to a nucleophilic attack by the quinone on the enzyme, to form covalent bonds. Matrix-assisted laser desorption and ionization time-of-flight mass spectrometry analysis and mutation experiments revealed that PTP1B inactivation was primarily due to covalent attachment of the quinone to Cys-121 of the enzyme, with binding to His-25 and Cys-215 as well. Collectively, the results show that covalent attachment of 1,2-NQ to PTP1B is at least partially responsible for the reduction of PTP activity, which leads to prolonged transactivation of EGFR in the cells.

An approach to evaluate two-electron reduction of 9,10-phenanthraquinone and redox activity of the hydroquinone associated with oxidative stress.

Quinones are widely used as medicines or redox agents. The chemical properties are based on the reactions against an electron donor. 9,10-Phenanthraquinone (PQ), which is a quinone contaminated in airborne particulate matters, forms redox cycling, not Michael addition, with electron donors. Redox cycling of PQ contributes to its toxicity, following generation of reactive oxygen species (ROS). Detoxification of quinones is generally thought to be two-electron reduction forming hydroquinones. However, a hydroquinone of PQ, 9,10-dihydroxyphenanthrene (PQH(2)), has been never detected itself, because it is quite unstable. In this paper, we succeeded in detecting PQH(2) as its stable derivative, 9,10-diacetoxyphenanthrene (DAP). However, higher concentrations of PQ (>4 microM) form disproportionately with PQH(2), producing the 9,10-phenanthraquinone radical (PQ(-)) which is a one-electron reducing product of PQ. In cellular experiments using DAP as a precursor of PQH(2), it was shown that PQH(2) plays a critical role in the oxidative protein damage and cellular toxicity of PQ, showing that two-electron reduction of PQ can also initiate redox cycling to cause oxidative stress-dependent cytotoxicity.

Relationship between redox activity and chemical speciation of size-fractionated particulate matter.

BACKGROUND: Although the mechanisms of airborne particulate matter (PM) related health effects remain incompletely understood, one emerging hypothesis is that these adverse effects derive from oxidative stress, initiated by the formation of reactive oxygen species (ROS) within affected cells. Typically, ROS are formed in cells through the reduction of oxygen by biological reducing agents, with the catalytic assistance of electron transfer enzymes and redox active chemical species such as redox active organic chemicals and metals. The purpose of this study was to relate the electron transfer ability, or redox activity, of the PM samples to their content in polycyclic aromatic hydrocarbons and various inorganic species. The redox activity of the samples has been shown to correlate with the induction of the stress protein, hemeoxygenase-1. RESULTS: Size-fractionated (i.e. < 0.15; < 2.5 and 2.5 - 10 microm in diameter) ambient PM samples were collected from four different locations in the period from June 2003 to July 2005, and were chemically analyzed for elemental and organic carbon, ions, elements and trace metals and polycyclic aromatic hydrocarbons. The redox activity of the samples was evaluated by means of the dithiothreitol activity assay and was related to their chemical speciation by means of correlation analysis. Our analysis indicated a higher redox activity on a per PM mass basis for ultrafine (< 0.15 microm) particles compared to those of larger sizes. The PM redox activity was highly correlated with the organic carbon (OC) content of PM as well as the mass fractions of species such as polycyclic aromatic hydrocarbons (PAH), and selected metals. CONCLUSION: The results of this work demonstrate the utility of the dithiothreitol assay for quantitatively assessing the redox potential of airborne particulate matter from a wide range of sources. Studies to characterize the redox activity of PM from various sources throughout the Los Angeles basin are currently underway.

1,2-Naphthoquinone activates vanilloid receptor 1 through increased protein tyrosine phosphorylation, leading to contraction of guinea pig trachea.

1,2-Naphthoquinone (1,2-NQ) has recently been identified as an environmental quinone in diesel exhaust particles (DEP) and atmospheric PM2.5. We have found that this quinone is capable of causing a concentration-dependent contraction of tracheal smooth muscle in guinea pigs with EC50 value of 18.7 microM. The contraction required extracellular calcium and was suppressed by L-type calcium channel blockers nifedipine and diltiazem. It was found that 1,2-NQ activated phospholipase A2 (PLA2)/lipoxygenase (LO)/vanilloid receptor (VR1) signaling. Additionally, 1,2-NQ was capable of transactivating protein tyrosine kinases (PTKs) such as epidermal growth factor receptor (EGFR) in guinea pig trachea, suggesting that phosphorylation of PTKs contributes to 1,2-NQ-induced tracheal contraction. Consistent with this notion, this action was blocked by the PTKs inhibitor genistein and the EGFR antagonist PD153035, indicating that contraction was, at least in part, attributable to PTKs phosphorylation that activates VR1, resulting in increased intracellular calcium content in the smooth muscle cells.

Inhalation of concentrated ambient particulate matter near a heavily trafficked road stimulates antigen-induced airway responses in mice.

The goal of this study was to test the following hypotheses: (1) exposure to mobile emissions from mobile sources close to a heavily trafficked roadway will exacerbate airway inflammation and allergic airway responses in a sensitized mouse model, and (2) the magnitude of allergic airway disease responses will decrease with increasing distance from the roadway. A particle concentrator and a mobile exposure facility were used to expose ovalbumin (OVA)-sensitized BALB/c mice to purified air and concentrated fine and concentrated ultrafine ambient particles at 50 m and 150 m downwind from a roadway that was heavily impacted by emissions from heavy duty diesel-powered vehicles. After exposure, we assessed interleukin (IL)-5, IL-13, OVA-specific immunoglobulin E, OVA-specific immunoglobulin G1, and eosinophil influx as biomarkers of allergic responses and numbers of polymorphonuclear leukocytes as a marker of inflammation. The study was performed over a two-year period, and there were differences in the concentrations and compositions of ambient particulate matter across those years that could have influenced our results. However, averaged over the two-year period, exposure to concentrated ambient particles (CAPs) increased the biomarkers associated with airway allergies (IL-5, immunoglobulin E, immunoglobulin G1 and eosinophils). In addition, mice exposed to CAPs 50 m downwind of the roadway had, on the average, greater allergic responses and showed greater indications of inflammation than did mice exposed to CAPs 150 m downwind. This study is consistent with the hypothesis that exposure to CAPs close to a heavily trafficked roadway influenced allergic airway responses.

Redox activity of airborne particulate matter at different sites in the Los Angeles Basin.

Epidemiologic studies have shown associations between ambient particulate matter (PM) and adverse health outcomes including increased mortality, emergency room visits, and time lost from school and work. The mechanisms of PM-related health effects are still incompletely understood, but a hypothesis under investigation is that many of the adverse health effects may derive from oxidative stress, initiated by the formation of reactive oxygen species (ROS) within affected cells. While the adverse effects from PM have historically been associated with the airborne concentration of PM and more recently fine-particle PM, we considered it relevant to develop an assay to quantitatively measure the ability of PM to catalyze ROS generation as the initial step in the induction of oxidative stress. This ability of PM could then be related to different sources, chemical composition, and physical and spatial/temporal characteristics in the ambient environment. The measurement of ROS-forming ability in relation to sources and other factors will have potential relevance to control of redox-active PM. If oxidative stress represents a relevant mechanism of toxicity from PM, the measurement of redox activity represents a first step in the elucidation of the subsequent downstream processes. We have developed an assay for PM redox activity, utilizing the reduction of oxygen by dithiothreitol which serves as an electron source. We have found that PM will catalyze the reduction of oxygen and have examined the distribution and chemical characteristics of the redox activity of PM fractions collected in different sites in the Los Angeles Basin. Samples of concentrated coarse, fine, and ultrafine PM, obtained with aerosol concentrators, were studied with regard to their chemical properties and redox activity. Redox activity was highest in the ultrafine fraction, in agreement with results indicating ultrafines were the most potent toward inducing that heme oxygenase expression and depleting intracellular glutathione, which has relevance to induction of oxidative stress. Comparison of the redox activity with chemical composition showed a reasonable correlation of redox activity with elemental carbon (r(2)=0.79), organic carbon (r(2)=0.53), and with benzo[ghi]perylene (r(2)=0.82), consistent with species typically found in mobile emission sources.

Effects of a single intratracheal administration of phenanthraquinone on murine lung.

Although several studies have reported that diesel exhaust particles (DEP) affect cardiorespiratory health in animals and humans, the responsible components in DEP for the effects remain to be defined. Diesel exhaust particles contain quinones that can catalyse the generation of reactive oxygen species, resulting in the induction of oxidative stress. Oxidative stress can correlate with a variety of diseases and health effects. In the present study, we investigated the effects of phenanthraquinone--a relatively abundant quinone in DEP--on lung inflammation and the local expression of cytokine proteins in mice as a measure of oxidative damage. The animals were randomized into two experimental groups that received vehicle or phenanthraquinone by intratracheal instillation. The cellular profiles of bronchoalveolar lavage fluid (BALF) and local expression of cytokines were evaluated 24 and 48 h after the instillation. Phenanthraquinone challenge revealed an increase in the numbers of neutrophils and eosinophils in BALF as compared to vehicle challenge (P < 0.05 at 48 h post-instillation). Phenanthraquinone induced the lung expression of interleukin (IL)-5 and eotaxin 48 h and 24 h after the challenge, respectively. These results indicate that intratracheal exposure to phenanthraquinone induces recruitment of inflammatory cells, at least partly, through the local expression of IL-5 and eotaxin.

Size distribution and speciation of chromium in paint spray aerosol at an aerospace facility.

Spray painters are potentially exposed to aerosol containing Cr(VI) via inhalation of chromate-based paint spray. Two field studies were conducted at an aerospace facility to determine the size distribution and speciation of Cr(VI) in paint spray aerosol. Sampled paint products consisted of sparingly soluble strontium chromate in an epoxy resin matrix, a matrix generally known for its durability and toughness. Personal aerosol samples were collected using Sierra Marple personal cascade impactors and analyzed for Cr(VI) and total Cr. The size distribution of total Cr particles in the paint aerosol had a Mass Median Aerodynamic Diameter (MMAD) of 7.5 mum [Geometric Standard Deviation (GSD = 2.7 mum)] in both field studies. The MMAD of Cr(VI) particles was 8.5 mum (GSD = 2.2 mum). Particles >2 mum constituted 90% or more of the total Cr and the Cr(VI) mass, in all sampled paint aerosols and were lognormally distributed. The target site for respiratory deposition of Cr in the aerosol was estimated based on the mass distribution of Cr according to particle size. On an average, 62% of the Cr and Cr(VI) mass in the paint aerosol consisted of particles >10 mum. This study showed that 71.8% of Cr(VI) mass in paint spray aerosol potentially inhaled by a spray painter may deposit in the head airways region. Only 2.0 and 1.4% of Cr(VI) mass in the paint aerosol may potentially deposit in the alveolar and tracheobronchial region, respectively. The ratio of Cr(VI) mass to total Cr mass was determined in bulk paint and the data indicate that Cr was predominantly in the Cr(VI) valence state, before spraying. The ratio of Cr(VI) mass to total Cr mass was also determined in paint aerosol samples. The data indicated that there was a reduction of Cr(VI) regardless of Cr aerosol particle size. Cr(VI) reduction occurred most likely during the 8 h sample collection time period. These findings are in agreement with the findings that observed Cr(VI) reduction during collection of airborne Cr(VI) in samples of chromic acid mist. The use of Cr(VI) stabilizing sampling media and the storage of samples at lower temperatures (4 degrees C ) during and after sampling may avoid the underestimation of Cr(VI).

Size distribution of chromate paint aerosol generated in a bench-scale spray booth.

Spray painters are potentially exposed to aerosols containing hexavalent chromium [Cr(VI)] via inhalation of chromate-based paint sprays. Evaluating the particle size distribution of a paint spray aerosol, and the variables that may affect this distribution, is necessary to determine the site and degree of respiratory deposition and the damage that may result from inhaled Cr(VI)-containing paint particles. This study examined the effect of spray gun atomization pressure, aerosol generation source and aerosol aging on the size distribution of chromate-based paint overspray aerosols generated in a bench-scale paint spray booth. The study also determined the effect of particle bounce inside a Marple personal cascade impactor on measured size distributions of paint spray aerosols. Marple personal cascade impactors with a modified inlet were used for sample collection. The data indicated that paint particle bounce did not occur inside the cascade impactors sufficiently to affect size distribution when using uncoated stainless steel or PVC substrate sampling media. A decrease in paint aerosol mass median aerodynamic diameter (MMAD) from 8.2 to 7.0 mum was observed as gun atomization pressure increased from 6 to 10 psi. Overspray aerosols were sampled at two locations in the spray booth. A downstream sampling position simulated the exposure of a worker standing between the painted surface and exhaust, a situation encountered in booths with multiple workers. The measured mean MMAD was 7.2 mum. The distance between the painted surface and sampler was varied to sample oversprays of varying ages between 2.8 and 7.7 s. Age was not a significant factor for determining MMAD. Overspray was sampled at a 90 degrees position to simulate a worker standing in front of the surface being painted with air flowing to the worker's side, a common situation in field applications. The resulting overspray MMAD averaged 5.9 mum. Direct-spray aerosols were sampled at ages from 5.3 to 11.7 s. Overspray and direct-spray results indicated that most of the change in aerosol size distribution occurred between the time the paint aerosol impacted the painted surface and the time the overspray became 2.8 s old. The overall mean MMAD of overspray in the study was 6.4 mum and may have been underestimated due to sampling efficiency biases. If inhaled by a worker, the overspray aerosols evaluated in this study would mostly deposit in the head airways region of the respiratory tract. Paint overspray aerosols contained Cr primarily in the Cr(VI) state.

The efficiency of alkaline extraction for the recovery of hexavalent chromium (CrVI) from paint samples and the effect of sample storage on CrVI recovery.

Workplace exposures to CrVI, a human carcinogen, are significant in spraying operations of chromate-containing paints. Accurate determination of CrVI in paint aerosol air samples is important in assessing a worker's exposure to CrVI. National Institute for Occupational Safety and Health method 7604 is widely used for determining CrVI in air samples. It utilizes an alkaline extraction procedure. It was historically validated for paint aerosol samples containing 24.5 to 61.5 microg of CrVI. The literature documented potential airborne CrVI exposures greater than 61.5 microg in recent paint spraying operations. The efficiency of the alkaline method at extracting CrVI from paint samples containing 250 to 3000 microg of CrVI was determined. Paint was prepared, sampled, extracted twice and then digested. Extracts were analyzed for CrVI and digestates of the residual Cr were analyzed for total Cr. Alkaline extraction of paint samples using NIOSH method 7604 resulted in quantitative recoveries for paint samples with CrVI filter loadings from 250 to 3000 microg. A decrease in CrVI extraction efficiency was observed in samples containing > 1000 microg of CrVI. A second extraction improved the recovery of CrVI in these samples. Refrigerating paint aerosol samples for up to 2 weeks did not affect their CrVI content.