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PubMed1992

Studies on the prenatal toxicity of toluene in rabbits following inhalation exposure and proposal of a pregnancy guidance value.

Prenatal toxicity of toluene was determined in two separate studies by inhalation exposure of Himalayan rabbits. In the first study 15 artificially inseminated females per group were exposed to 30, 100, or 300 ppm and in the second study 20 artificially inseminated females per group inhaled 100 or 500 ppm. In each case the rabbits were exposed for 6 hours per day from day 6 post-insemination (p.i.) to day 18 p.i. The respective controls inhaled conditioned clean air under the same exposure conditions. No signs of maternal toxicity were observed. All data obtained on gestational parameters were found to be within the variation range reported for this rabbit strain. The fetal external, soft tissue and skeletal findings were seen in toluene exposed fetuses in a frequency similar to the corresponding and/or historical controls. Differences observed between the groups were not concentration dependent and were considered incidental rather than compound related. Therefore, toluene was not embryotoxic, fetotoxic, or teratogenic for rabbits exposed during the period of organogenesis. The highest concentration tested under these conditions (500 ppm) was found to be a no-observable-adverse-effect level (NOAEL) for both the adult and the fetal Himalayan rabbit. Based on these and previous results of animal studies of prenatal toxicity, a safety or uncertainty factor approach is considered for setting limits of exposure for women at workplaces. A pregnancy guidance value of 20 ppm is proposed.

Administration, Inhalation↗
PubMed1983

Concentration-dependent immunologic response to toluene diisocyanate (TDI) following inhalation exposure.

Little is known concerning industrial exposure conditions which lead to development of allergic sensitivity in exposed workers. This study investigated the relationship between exposure concentration and the induction of antibodies and sensitivity in a guinea pig animal model for inhalation exposure to isocyanates (Karol et al., Toxicol. Appl. Pharmacol. 53, 260-270, 1980). Groups of guinea pigs were exposed, via inhalation, to TDI concentrations ranging from 0.12 to 10 ppm. Exposure was for 3 hr/day on 5 consecutive days. Beginning on Day 22, animals were evaluated for TDI-specific antibodies, skin sensitivity, and pulmonary sensitivity to TDI. No antibodies were detected in animals exposed to 0.12 ppm TDI, whereas 55% of animals exposed to 0.36 ppm TDI or greater displayed TDI-specific antibodies in their sera. Exposure to higher TDI concentrations resulted in both a greater percentage of animals producing antibodies and higher antibody titers. Pulmonary sensitivity, assessed by bronchial provocation challenge with TDI-protein antigen, was not detected in animals exposed to 0.12 ppm TDI but was present in guinea pigs exposed to TDI concentrations of 0.36 ppm or greater. However, exposure concentrations higher than 2 ppm were pneumotoxic and resulted in few pulmonary hypersensitivity reactions. Exposure of animals to 0.02 ppm TDI for 15 weeks did not result in either dermal sensitivity, pulmonary sensitivity, or production of TDI-specific antibody. The exposure protocol, as well as the exposure concentration, was important for establishment of sensitivity. Recognition of the concentration-response relationship governing immune reaction to inhaled TDI should permit establishment of safe airborne exposure levels for industrial workers to prevent sensitization.

Animals↗
PubMed1996

Chronic inhalation exposure to ozone and nitric acid elevates stress-inducible heat shock protein 70 in the rat lung.

The ability of urban oxidant and acid air pollutants to induce heat shock proteins (HSPs) in the mammalian lung is not known. Such proteins are known to be correlated with environmental stress and pathophysiological conditions. In this study, stress-inducible HSP 70 was assessed by slot-blotting in rat lungs (N=10 per group) following inhalation exposures for 4 h per day, 3 days per week for 40 weeks to the following pollutants: (a) purified air;(b) 0.15 ppm ozone (O3);(c)50 micrograms/m3 nitric acid (HNO3); or(d) a combination of both 0.15 ppm O3 and 50 micrograms/m3 HNO3. At 24 h following the last exposure, samples from the right apical lobe of the lung were obtained for either slot-blotting or gel electrophoretic separation, subsequent protein immunoblotting, and chemiluminescence detection of HSP 70 levels. Experiments demonstrate that stress-inducible HSP 70 was present constitutively in the control lungs and was separable from the constitutive form of HSP 70. Slot-blotting analysis demonstrate that the O3 and HNO3 exposures alone produced significant elevations of HSP70. Specifically, either O3 or HNO3 alone significantly elevated lung stress-inducible HSP 70 levels by 277% and 221% respectively, above control levels. The group exposed to combined O3 and HNO3 showed a 177% elevation in lung stress-inducible HSP 70 that was significantly greater that the group inhaling purified air, but this effect was less than the effects of either pollutant component alone. Moreover, all exposure groups were significantly different from one another. These results indicate that stress-inducible HSP 70 in the rat lung is highly elevated after chronic inhalation exposures to both O3 and HNO3 when administered either alone or in combination within the range of urban ambient concentrations.

Administration, Inhalation↗
PubMed1999

Developmental toxicities of methacrylic acid, ethyl methacrylate, n-butyl methacrylate, and allyl methacrylate in rats following inhalation exposure.

The developmental toxicities of 4 methacrylates were studied in Sprague-Dawley rats after inhalation exposure for 6 h/day, during days 6 to 20 of gestation. The exposure concentrations were, for methacrylic acid, 0, 50, 100, 200, or 300 ppm; for ethyl methacrylate, 0, 600, 1200, 1800, or 2400 ppm; for n-butyl methacrylate, 0, 100, 300, 600, or 1200 ppm; and for allyl methacrylate, 0, 12, 25, 50, or 100 ppm. No significant increases in embryo/fetal lethality or fetal malformations were observed after exposure to any of these methacrylates. Fetal toxicity evidenced by statistically significant decreases in fetal body weights was observed at exposure levels > or = 1200 ppm ethyl methacrylate, > or = 600 ppm n-butyl methacrylate, and at 100 ppm allyl methacrylate. Statistically significant increases in the incidence of fetuses with skeletal variations and of fetuses with any variations were noted at 1200 ppm n-butyl methacrylate. These developmental effects were observed in the presence of overt signs of maternal toxicity. While maternal toxicity was observed, methacrylic acid caused no evidence of developmental toxicity up to 300 ppm.

Administration, Inhalation↗
PubMed2001

The effects of inhalation exposure to bromo-dichloromethane on specific rat CYP isoenzymes.

Several cytochrome P450 (CYP) isoenzymes may be involved in the metabolism of bromo-dichloromethane (BDCM), a drinking water disinfection byproduct. After 4-h inhalation exposures of male F344 rats to BDCM between 100 and 3200 p.p.m., hepatic microsomal methoxyresorufin demethylase (MROD), ethoxyresorufin de-ethylease (EROD) and pentoxyresorufin dealkylase (PROD) activities showed modest increases at low exposure levels and larger decreases at high exposure levels, compared with controls. Western blots for CYP1A2 and CYP2B1 showed similar trends. In addition, p-nitrophenol hydroxylase (PNP) activity was measured and Western blots for CYP2E1 were performed. CYP2E1 and CYP2B1 isoenzymes are known to metabolize BDCM (Thornton-Manning, J.R., Gao, P., Lilly, P.D., Pegram, R.A., 1993. Acute bromodichloromethane toxicity in rats pretreated with cytochrome P450 inducers and inhibitors. The Toxicologist 13: 361). When compared with a multiple gavage study of BDCM in female F344 rats (Thornton-Manning, J.R., et al., 1994. Toxicology 94, 3-18), the results of the two studies for EROD, PROD, and PNP activities were qualitatively the same; PNP activity did not change, while both PROD and EROD activities decreased at high exposures. In the current work, Western blots for CYP2E1, CYP2B1 and CYP1A2 supported the results from the PNP, PROD and MROD activities, respectively. The decreases in MROD and PROD activities and in Western blots for CYP1A2 and CYP2B1 at high exposures suggest that BDCM may be a suicide substrate for these CYP isoenzymes. Other important conclusions that can be drawn from the comparison between the current and prior work are that the liver response is similar for both sexes, and it is also similar for inhalation and gavage exposures under these conditions. Finally, the decrease in EROD activity at high doses, found in both studies, may be a further reflection of CYP1A2 activity, since little or no CYP1A1 activity is normally found in uninduced rat liver and CYP1A2 is known to metabolize ethoxyresorufin, although much more slowly than CYP1A1.

Administration, Inhalation↗
PubMed2006

Medical countermeasure against respiratory toxicity and acute lung injury following inhalation exposure to chemical warfare nerve agent VX.

To develop therapeutics against lung injury and respiratory toxicity following nerve agent VX exposure, we evaluated the protective efficacy of a number of potential pulmonary therapeutics. Guinea pigs were exposed to 27.03 mg/m(3) of VX or saline using a microinstillation inhalation exposure technique for 4 min and then the toxicity was assessed. Exposure to this dose of VX resulted in a 24-h survival rate of 52%. There was a significant increase in bronchoalveolar lavage (BAL) protein, total cell number, and cell death. Surprisingly, direct pulmonary treatment with surfactant, liquivent, N-acetylcysteine, dexamethasone, or anti-sense syk oligonucleotides 2 min post-exposure did not significantly increase the survival rate of VX-exposed guinea pigs. Further blocking the nostrils, airway, and bronchioles, VX-induced viscous mucous secretions were exacerbated by these aerosolized treatments. To overcome these events, we developed a strategy to protect the animals by treatment with atropine. Atropine inhibits muscarinic stimulation and markedly reduces the copious airway secretion following nerve agent exposure. Indeed, post-exposure treatment with atropine methyl bromide, which does not cross the blood-brain barrier, resulted in 100% survival of VX-exposed animals. Bronchoalveolar lavage from VX-exposed and atropine-treated animals exhibited lower protein levels, cell number, and cell death compared to VX-exposed controls, indicating less lung injury. When pulmonary therapeutics were combined with atropine, significant protection to VX-exposure was observed. These results indicate that combinations of pulmonary therapeutics with atropine or drugs that inhibit mucous secretion are important for the treatment of respiratory toxicity and lung injury following VX exposure.

Acetylcysteine↗
PubMed1992

Dose assessment to inhalation exposure of indoor 222Rn daughters in Korea.

Long-term, average indoor 222Rn concentrations were measured in 12 residential areas by passive CR-39 radon cups. Corresponding equilibrium-equivalent concentration of radon daughters were derived. The resulting effective dose equivalent for the Korean population due to inhalation exposure of this equilibrium-equivalent concentration of radon daughters was then evaluated.

Air Pollution, Indoor↗
PubMed2004

Effects of motorcycle exhaust inhalation exposure on cytochrome P-450 2B1, antioxidant enzymes, and lipid peroxidation in rat liver and lung.

The effects of motorcycle exhaust (ME) on metabolic and antioxidant enzymes and lipid peroxidation were determined using male rats exposed to 1:10 diluted ME by inhalation 2 h daily for 4 wk. For microsomal cytochrome P-450 enzymes, ME resulted in threefold increases of 7-ethoxyresorufin and pentoxyresorufin O-deethylase activities in liver and a sixfold increase of 7-ethoxyresorufin O-deethylase activity and an 80% decrease of pentoxyresorufin O-dealkylase activity in lung. The results of immunoblot analysis of microsomal proteins revealed that ME increased liver and lung cytochrome P-450 1A1 with minimal effects on cytochrome P-450 2E1. ME increased cytochrome P-450 2B1/2 proteins in liver but decreased cytochrome P-450 2B1 in lung. ME did not change microsomal cytochrome P-450 enzyme activity or protein level in kidney. For phase II enzymes, ME resulted in 53% and twofold increases of cytosolic NAD(P)H:quinone oxidoreductase activities in liver and lung, respectively, and no effect on microsomal UDP-glucuronosyltransferase activities. For antioxidant enzymes, ME produced 23% and 35% decreases of superoxide dismutase, 9% and 27% decreases of catalase, and no changes of glutathione peroxidase activities in liver and lung cytosols, respectively. For lipid peroxidation, the results of thiobarbituric acid assay showed that ME resulted in a twofold increase of formation of malondialdehyde by liver microsomes incubated with FeCl(3) -ADP. ME produced a threefold increase of malondialdehyde formation by lung microsomes. The present study demonstrates that ME inhalation exposure differentially modulates cytochrome P-450 2B1 and antioxidant enzymes and increases susceptibility to lipid peroxidation in rat liver and lung.

Animals↗
PubMed1983

Effects of the single or repeated inhalation exposure of Syrian hamsters to aerosols of 239PuO2.

Male Syrian hamsters were scheduled to be exposed by inhalation approximately every 60 days for 1 year (7 exposures) to aerosols of 239PuO2 beginning at 84 days of age. Other hamsters were exposed once when 84 or 320 days of age. Plutonium-239 deposited in the lungs by the repeated inhalation exposures was cleared from the lungs at a rate similar to that following a single inhalation exposure. The incidence of radiation pneumonitis, bronchiolar epithelial hyperplasia, and alveolar squamous metaplasia were the only lesions that were related to radiation dose. Only two primary lung tumours were found among the hamsters exposed to 239PuO2. No primary lung tumours were found in the control hamsters. It was concluded that the incidence of lung tumours was not increased by the protraction of the alpha radiation dose to the lungs from repeated inhalation exposure.

Aerosols↗
PubMed1992

Inhalation exposure of rats to metal aerosol. II. Study of mutagenic effect on alveolar macrophages.

The effects of inhalation exposure to metal aerosol derived from nickel refinery waste were studied on the frequency of chromosome aberrations in alveolar macrophages in Wistar rats. A 4-month exposure period resulted in significant (P less than 0.01) increases in chromosome aberrations. Relatively high variability without statistical significance was observed after a 4-week exposure period. Increase in damaged alveolar macrophages with the length of exposure seems to point to the role of pulmonary metal deposits. Comparison of the results with those found after 6 months of exposure in bone marrow cells confirmed that metal particles in nickel refinery waste are genotoxic. Thus, this study indicates that alveolar macrophages are suitable for monitoring the genotoxic potential of hazardous chemicals administered by inhalation.

Administration, Inhalation↗
PubMed2001

Potential dermal and inhalation exposure to chlorpyrifos in Australian pesticide workers.

Chlorpyrifos inhalation, dermal exposure and working practices of 28 pesticide applicators in Western Australia were assessed during a series of single property applications of a 0.5% (n=2) or 1% (n=26) concentration of active ingredient in water solution. Deposition on new cotton gloves worn beneath applicators' usual protective gloves was 2.4 (range 0.12-86.1) mg h(-1). Median deposition of chlorpyrifos onto a new cotton overall worn over other clothing (24 sections removed, corrected for body proportions) was 11.1 (range 0.2-41.9) mg h(-1). Deposition onto seven patches taped to the applicators' skin was 0.04 (range 0.01-4.7) mg h(-1). Inhalation concentration was 5.7 (range 0.7-219) microg m(-3) time weighted average. In one group of 17 applicators' applying to existing properties, breathing zone air concentration correlated (P<0.05) with ambient air temperature (15-38 degrees C). The questionnaire results (29 respondents) indicated applicators' practices led to increased exposure, in particular concerning poor usage and condition of protective equipment and a high frequency of splashes and spills onto the body. Prevention of deposition on clothing, in particular on the lower body is suggested, as well as improved working practices.

Chlorpyrifos↗
PubMed1999

Repeated 4-week inhalation exposure of rats: effect of low-, intermediate, and high-humidity chamber atmospheres.

A subacute nose-only inhalation study with low (approximately 3%), medium (approximately 40%), and high humidity (approximately 80%) has been performed on young adult Wistar rats. Exposure was 6-hr/day on 5 days/week for 4 consecutive weeks. Rats housed individually in the animal holding room, deprived of feed and water during exposure of the remaining groups, served as concurrent controls (sham controls). This study served the purpose to assess whether toxicologically significant effects occur when rats are repeatedly exposed to lower or higher humidity chamber atmospheres than proposed by current testing guidelines. For analysis, conventional end-points as required by common testing guidelines were considered, i.e., clinical observations before and after exposure, rectal temperatures, body weights, feed and water consumption. At the end of the 4-week exposure period, ophthalmological and gross pathological examinations were made and major organ weights determined. The histopathological examinations comprised the nasal cavities, larynx, trachea, and lungs. There was no apparent evidence of humidity-related effects on nose-only exposed rats. When compared with non-exposed sham controls, however, body weights, water and feed consumption were markedly reduced in all nose-only exposure groups. In summary, it can be concluded that rats tolerated either humidity atmosphere without any specific effects. As far as there were differences to sham controls they appear to be more controlled by the differences in the exposure patterns (nose-only versus normal housing) than differences in the humidity of chamber atmospheres. Thus, deviations of current testing guidelines for repeated exposure inhalation studies with regard to humidity, do not appear to have any appreciable impact on the study outcome.

Administration, Inhalation↗
PubMed1978

Continuous monitoring of temperature in laboratory animals during inhalation exposure.

An automatic system was developed to monitor continuously the colonic temperature of laboratory animals during inhalation exposure to toxic chemicals. It includes: an automatic switchbox, a control circuit, a recorder and a digital voltmeter. The system was calibrated for different temperature ranges and used for a year to assess the effects of household solvents on temperature of Sprague-Dawley rats. Reliable monitoring of temperature in 16 rats was carried out in a sequential manner in the manual mode or in the automatic mode for several consecutive days. Very slight changes (.01 - .02 degrees C) in temperature can be measured with this system.

Animals↗
PubMed1990

Effect of repeated benzene inhalation exposures on benzene metabolism, binding to hemoglobin, and induction of micronuclei.

Metabolism of benzene is thought to be necessary to produce the toxic effects, including carcinogenicity, associated with benzene exposure. To extrapolate from the results of rodent studies to potential health risks in man, one must know how benzene metabolism is affected by species, dose, dose rate, and repeated versus single exposures. The purpose of our studies was to determine the effect of repeated inhalation exposures on the metabolism of [14C]benzene by rodents. Benzene metabolism was assessed by characterizing and quantitating urinary metabolites, and by quantitating 14C bound to hemoglobin and micronuclei induction. F344/N rats and B6C3F1 mice were exposed, nose-only, to 600 ppm benzene or to air (control) for 6 hr/day, 5 days/week for 3 weeks. On the last day, both benzene-pretreated and control animals were exposed to 600 ppm, 14C-labeled benzene for 6 hr. Individual benzene metabolites in urine collected for 24 hr after the exposure were analyzed. There was a significant decrease in the respiratory rate of mice (but not rats) pretreated with benzene which resulted in lower levels of urinary [14C]benzene metabolites. The analyses indicated that the only effects of benzene pretreatment on the metabolite profile in rat or mouse urine were a slight shift from glucuronidation to sulfation in mice and a shift from sulfation to glucuronidation in rats. Benzene pretreatment also had no effect, in either species, on formation of [14C]benzene-derived hemoglobin adducts. Mice and rats had similar levels of hemoglobin adduct binding, despite the higher metabolism of benzene by mice. This indicates that hemoglobin adduct formation occurs with higher efficiency in rats. After 1 week of exposure to 600 ppm benzene, the frequency of micronucleated, polychromatic erythrocytes (PCEs) in mice was significantly increased. Exposure to the same level of benzene for an additional 2 weeks did not further increase the frequency of micronuclei in PCEs. These results indicate that repeated exposures to benzene, such as might be encountered by humans as a result of occupational or environmental exposures, are not likely to change or increase benzene metabolism.

Administration, Inhalation↗
PubMedDate not supplied

Blood pharmacokinetics of tertiary amyl methyl ether in male and female F344 rats and CD-1 mice after nose-only inhalation exposure.

Interest in understanding the biological behavior of aliphatic ethers has increased owing to their use as gasoline additives. The purpose of this study was to investigate the blood pharmacokinetics of the oxygenate tertiary amyl methyl ether (TAME), its major metabolite tertiary amyl alcohol (TAA) and acetone in rats and mice following inhalation exposure to TAME. Species differences in the area under the curve (AUC) for TAME were significant at each exposure concentration. For rats, the blood TAME AUC increased in proportion with an increase in exposure concentration. For mice, an increase in exposure concentration (100-500 ppm) resulted in a disproportional increase in the TAME AUC. Mice had greater (two- to threefold) blood concentrations of TAA compared with rats following exposure to 2500 or 500 ppm TAME. Mice had a disproportional increase in the TAA AUC with an increase in exposure concentration (100-500 ppm). This difference could result from saturation of a process (e.g. oxidation, glucuronide conjugation) that is involved in the further metabolism of TAA. For each species, gender and exposure concentration, acetone increased during exposure and returned to control values by 16 h following exposure. The source of acetone could be both as a metabolite of TAA or an effect on endogenous metabolism produced by exposure to TAME.

Acetone↗
PubMed2005

Characterization of complex mixtures in urban atmospheres for inhalation exposure studies.

A real-world assessment of the source-to-receptor pathways for ambient particulate matter (PM), as opposed to in a laboratory environment, was crucial for gaining a better understanding of the types of particles to which people are actually exposed in their daily lives, and of the human-health risks for source-specific PM. However, obtaining scientific evidence linking specific source emissions to health responses was not an easy task; ambient PM possesses diverse chemical, physical and thermodynamic properties, and is subjected to numerous complex atmospheric processes in which source type, source strength, sinks, and meteorology interact continuously. Our collaborative PM health research studies utilized an integrated approach that employs detailed characterization of ambient PM concurrent with inhalation toxicology studies using animal models and concentrated fine air particulates (CAPs). Ambient PM2.5 (PM less than 2.5 microm in mean aerodynamic diameter) was concentrated with a Harvard fine particle concentrator housed in AirCARE1, a unique mobile air research laboratory which enables inhalation exposure studies in real-world settings. This paper discusses the importance of comprehensive characterization of ambient PM2.5, CAPs and their sources, and the associated challenges. In a southwest Detroit community where the pediatric asthma rate is about three times the national average, a detailed assessment was performed including: characterization of ambient PM2.5 and CAPs; identification of major emission sources of PM2.5; and quantification of trace elements in lung tissues of laboratory rats that were exposed to CAPs, all in an effort to define source-receptor pathways for ambient PM2.5. Our findings to date constitute evidence of the retention of ambient urban particulates from local combustion sources within animal tissues from short-term exposures, and possible associations between the observed health effects and source-specific PM2.5. However, a complete understanding of the effects of complex mixtures of air pollutants and their toxicological impacts still faces many challenges.

Air Pollutants↗
PubMedDate not supplied

Inhalation exposure to JP-8 jet fuel alters pulmonary function and substance P levels in Fischer 344 rats.

In a simulated military flightline exposure protocol, Fischer 344 rats (F344) were used to investigate the pulmonary effects of JP-8 jet fuel inhalation. Exposures were nose only and for 1 h daily. Groups were exposed for 7 days (7D) or 28 days (28D). Each exposure group had a matched longitudinal control group (LC7 and LC28). Exposure concentrations of 520 mg m-3 caused an increase in dynamic compliance after 7 days of exposure, but compliance changes were not seen with continued exposure (28D, 495 mg m-3). Pulmonary resistance was increased in both 7- and 28-day JP-8-exposed groups. Changes in pulmonary function were accompanied by a decrease in substance P concentrations from the bronchoalveolar lavage fluid (BALF). No significant change was observed in BALF levels of 6-keto-PGF1 alpha, the stable metabolite of prostacyclin, which is a marker of endothelial cell function. The JP-8-exposed rats gained significantly less weight during the study period than the LC7 and LC28 groups, and the lungs of the 7D group were heavier by wet lung/body weight ratio (WtL/WtB). Alveolar clearance of technetium-labelled diethylenetriamine pentaacetate ([99mTc]DTPA) was increased in jet fuel-exposed groups. Light microscopy showed no pathological evidence of lung injury. Recovery from the early pulmonary effects of JP-8 inhalation occurred with continued exposure, as seen by recovery of pulmonary compliance and WtL/WtB.

6-Ketoprostaglandin F1 alpha↗
PubMed2006

Design, construction, and characterization of a novel robotic welding fume generator and inhalation exposure system for laboratory animals.

Respiratory effects observed in welders have included lung function changes, metal fume fever, bronchitis, and a possible increase in the incidence of lung cancer. Many questions remain unanswered regarding the causality and possible underlying mechanisms associated with the potential toxic effects of welding fume inhalation. The objective of the present study was to construct a completely automated, computer-controlled welding fume generation and inhalation exposure system to simulate real workplace exposures. The system comprised a programmable six-axis robotic welding arm, a water-cooled arc welding torch, and a wire feeder that supplied the wire to the torch at a programmed rate. For the initial studies, gas metal arc welding was performed using a stainless steel electrode. A flexible trunk was attached to the robotic arm of the welder and was used to collect and transport fume from the vicinity of the arc to the animal exposure chamber. Undiluted fume concentrations consistently ranged from 90-150 mg/m(3) in the animal chamber during welding. Temperature and humidity remained constant in the chamber during the welding operation. The welding particles were composed of (from highest to lowest concentration) iron, chromium, manganese, and nickel as measured by inductively coupled plasma atomic emission spectroscopy. Size distribution analysis indicated the mass median aerodynamic diameter of the generated particles to be approximately 0.24 microm with a geometric standard deviation (sigma(g)) of 1.39. As determined by transmission and scanning electron microscopy, the generated aerosols were mostly arranged as chain-like agglomerates of primary particles. Characterization of the laboratory-generated welding aerosol has indicated that particle morphology, size, and chemical composition are comparable to stainless steel welding fume generated in other studies. With the development of this novel system, it will be possible to establish an animal model using controlled welding exposures from automated gas metal arc and flux-cored arc welding processes to investigate how welding fumes affect health.

Aerosols↗