Occupational Exposure and Environmental Release: The Case Study of Pouring TiO2 and Filler Materials for Paint Production.

Pulmonary exposure to micro- and nanoscaled particles has been widely linked to adverse health effects and high concentrations of respirable particles are expected to occur within and around many industrial settings. In this study, a field-measurement campaign was performed at an industrial manufacturer, during the production of paints. Spatial and personal measurements were conducted and results were used to estimate the mass flows in the facility and the airborne particle release to the outdoor environment. Airborne particle number concentration (1 × 103-1.0 × 104 cm-3), respirable mass (0.06-0.6 mg m-3), and PM10 (0.3-6.5 mg m-3) were measured during pouring activities. In overall; emissions from pouring activities were found to be dominated by coarser particles >300 nm. Even though the raw materials were not identified as nanomaterials by the manufacturers, handling of TiO2 and clays resulted in release of nanometric particles to both workplace air and outdoor environment, which was confirmed by TEM analysis of indoor and stack emission samples. During the measurement period, none of the existing exposure limits in force were exceeded. Particle release to the outdoor environment varied from 6 to 20 g ton-1 at concentrations between 0.6 and 9.7 mg m-3 of total suspended dust depending on the powder. The estimated release of TiO2 to outdoors was 0.9 kg per year. Particle release to the environment is not expected to cause any major impact due to atmospheric dilution.

Assessment of exposure determinants and exposure levels by using stationary concentration measurements and a probabilistic near-field/far-field exposure model.

Background: The Registration, Evaluation, Authorization and Restriction of Chemicals (REACH) regulation requires the establishment of Conditions of Use (CoU) for all exposure scenarios to ensure good communication of safe working practices. Setting CoU requires the risk assessment of all relevant Contributing Scenarios (CSs) in the exposure scenario. A new CS has to be created whenever an Operational Condition (OC) is changed, resulting in an excessive number of exposure assessments. An efficient solution is to quantify OC concentrations and to identify reasonable worst-case scenarios with probabilistic exposure modeling. Methods: Here, we appoint CoU for powder pouring during the industrial manufacturing of a paint batch by quantifying OC exposure levels and exposure determinants. The quantification was performed by using stationary measurements and a probabilistic Near-Field/Far-Field (NF/FF) exposure model. Work shift and OC concentration levels were quantified for pouring TiO 2 from big bags and small bags, pouring Micro Mica from small bags, and cleaning. The impact of exposure determinants on NF concentration level was quantified by (1) assessing exposure determinants correlation with the NF exposure level and (2) by performing simulations with different OCs. Results: Emission rate, air mixing between NF and FF and local ventilation were the most relevant exposure determinants affecting NF concentrations. Potentially risky OCs were identified by performing Reasonable Worst Case (RWC) simulations and by comparing the exposure 95 th percentile distribution with 10% of the occupational exposure limit value (OELV). The CS was shown safe except in RWC scenario (ventilation rate from 0.4 to 1.6 1/h, 100 m 3 room, no local ventilation, and NF ventilation of 1.6 m 3/min). Conclusions: The CoU assessment was considered to comply with European Chemicals Agency (ECHA) legislation and EN 689 exposure assessment strategy for testing compliance with OEL values. One RWC scenario would require measurements since the exposure level was 12.5% of the OELV.

Improving the foundation for particulate matter risk assessment by individual nanoparticle statistics from electron microscopy analysis.

Air pollution is one of the major contributors to the global burden of disease, with particulate matter (PM) as one of its central concerns. Thus, there is a great need for exposure and risk assessments associated with PM pollution. However, current standard measurement techniques bring no knowledge of particle composition or shape, which have been identified among the crucial parameters for toxicology of inhaled particles. We present a method for collecting aerosols via impaction directly onto Transmission Electron Microscopy (TEM) grids, and based on the measured impactor collection efficiency and observed impact patterns we establish a reproducible imaging routine for automated Scanning Electron Microscopy (SEM) analysis. The method is validated by comparison to scanning mobility particle sizer (SMPS) measurements, where a good agreement is found between the particle size distributions (PSD), ensuring a representative description of the sampled aerosol. We furthermore determine sampling conditions for achieving optimal particle coverage on the TEM grids, allowing for a statistical analysis. In summary, the presented method can provide not only a representative PSD, but also detailed statistics on individual particle geometries. If coupled with Energy-dispersive X-ray spectroscopy (EDS) analysis elemental compositions can be assessed as well. This makes it possible to categorize particles both according to size and shape e.g. round and fibres, or agglomerates, as well as classify them based on their elemental composition e.g. salt, soot, or metals. Combined this method brings crucial knowledge for improving the foundation for PM risk assessments on workplaces and in ambient conditions with complex aerosol pollution.

Telomere shortening and aortic plaque progression in Apoliprotein E knockout mice after pulmonary exposure to candle light combustion particles.

Particles from burning candles contribute to the overall indoor exposure to particulate matter (PM). However, little is known about the effects of indoor sources of particles on cardiovascular disease endpoints. This study investigated the effect of pulmonary exposure to particles from combustion of candles and progression of atherosclerosis. Telomere shortening was assessed in tissues due to its relationship to risk of cardiovascular diseases. The particles were collected from burning candles and used for toxicological studies in cultured endothelial cells and apolipoprotein E (ApoE) knockout mice. Three hours exposure to particles increased the production of reactive oxygen species in endothelial cells, whereas there was no effect on cytotoxicity. Intratracheal instillation of particles (0.5 or 5 mg/kg) once a week for 5 weeks in ApoE-/- mice was associated with an accelerated progression of atherosclerosis in aorta and telomere shortening in the lung and spleen, whereas there was no effect on inflammation in the lungs (i.e. cell numbers), cell damage (i.e. lactate dehydrogenase) and lung barrier damage (i.e. protein concentration) as measured in bronchoalveolar lavage fluid. The results indicate that particles from burning candles are hazardous and this indoor emission source is an important contribution to the health risk of exposure to PM.

Association between polycyclic aromatic hydrocarbon exposure and peripheral blood mononuclear cell DNA damage in human volunteers during fire extinction exercises.

This study investigated a number of biomarkers, associated with systemic inflammation as well as genotoxicity, in 53 young and healthy subjects participating in a course to become firefighters, while wearing personal protective equipment (PPE). The exposure period consisted of a 3-day training course where the subjects participated in various live-fire training exercises. The subjects were instructed to extinguish fires of either wood or wood with electrical cords and mattresses. The personal exposure was measured as dermal polycyclic aromatic hydrocarbon (PAH) concentrations and urinary excretion of 1-hydroxypyrene (1-OHP). The subjects were primarily exposed to particulate matter (PM) in by-stander positions, since the self-contained breathing apparatus effectively prevented pulmonary exposure. There was increased dermal exposure to pyrene (68.1%, 95% CI: 52.5%, 83.8%) and sum of 16 polycyclic aromatic hydrocarbons (Æ©PAH; 79.5%, 95% CI: 52.5%, 106.6%), and increased urinary excretion of 1-OHP (70.4%, 95% CI: 52.5%; 106.6%) after the firefighting exercise compared with the mean of two control measurements performed 2 weeks before and 2 weeks after the firefighting course, respectively. The level of Fpg-sensitive sites in peripheral blood mononuclear cells (PBMCs) was increased by 8.0% (95% CI: 0.02%, 15.9%) compared with control measurements. The level of DNA strand breaks was positively associated with dermal exposure to pyrene and Æ©PAHs, and urinary excretion of 1-OHP. Fpg-sensitive sites were only associated positively with PAHs. Biomarkers of inflammation and lung function showed no consistent response. In summary, the study demonstrated that PAH exposure during firefighting activity was associated with genotoxicity in PBMCs.

Cardiovascular health effects following exposure of human volunteers during fire extinction exercises.

BACKGROUND: Firefighters have increased risk of cardiovascular disease and of sudden death from coronary heart disease on duty while suppressing fires. This study investigated the effect of firefighting activities, using appropriate personal protective equipment (PPE), on biomarkers of cardiovascular effects in young conscripts training to become firefighters. METHODS: Healthy conscripts (n = 43) who participated in a rescue educational course for firefighting were enrolled in the study. The exposure period consisted of a three-day training course where the conscripts participated in various firefighting exercises in a constructed firehouse and flashover container. The subjects were instructed to extinguish fires of either wood or wood with electrical cords and mattresses. The exposure to particulate matter (PM) was assessed at various locations and personal exposure was assessed by portable PM samplers and urinary excretion of 1-hydroxypyrene. Cardiovascular measurements included microvascular function and heart rate variability (HRV). RESULTS: The subjects were primarily exposed to PM in bystander positions, whereas self-contained breathing apparatus effectively abolished pulmonary exposure. Firefighting training was associated with elevated urinary excretion of 1-hydroxypyrene (105%, 95% CI: 52; 157%), increased body temperature, decreased microvascular function (-18%, 95% CI: -26; -9%) and altered HRV. There was no difference in cardiovascular measurements for the two types of fires. CONCLUSION: Observations from this fire extinction training show that PM exposure mainly occurs in situations where firefighters removed the self-contained breathing apparatus. Altered cardiovascular disease endpoints after the firefighting exercise period were most likely due to complex effects from PM exposure, physical exhaustion and increased core body temperature.

Lung inflammation and genotoxicity in mice lungs after pulmonary exposure to candle light combustion particles.

Candle burning produces a large amount of particles that contribute substantially to the exposure to indoor particulate matter. The exposures to various types of combustion particles, such as diesel exhaust particles, have been associated with increased risk of lung cancer by mechanisms that involve oxidative stress, inflammation and genotoxicity. The aim of this study was to compare pulmonary effects of candle light combustion particles (CP) with two benchmark diesel exhaust particles (A-DEP and SRM2975). Intratracheal (i.t.) instillation of CP (5mg/kg bodyweight) in C57BL/6n mice produced a significant influx of alveolar macrophages and polymorphonuclear leukocytes and increased concentrations of proteins and lactate dehydrogenase activity in bronchoalveolar fluid. Lower levels of these markers of inflammation and cytotoxicity were observed after i.t. instillation of the same dose of A-DEP or SRM2975. The i.t. instillation of CP did not generate oxidative damage to DNA in lung tissue, measured as DNA strand breaks and human 8-oxoguanine glycosylase-sensitive sites by the comet assay. The lack of genotoxic response was confirmed in lung epithelial (A549) cells, although the exposure to CP increased intracellular levels of reactive oxygen species. In conclusion, pulmonary exposure to particles from burning candles is associated with inflammation and cytotoxicity in the lungs.

In field conditions, commercial pigment grade TiO2 was not harmful to terrestrial isopods but reduced leaf litter fragmentation.

We investigated the effects of a commercial pigment grade rutile TiO2 on the terrestrial isopod Porcellio scaber in three locations that differed in terms of abiotic and biotic conditions: the laboratory, open air, and the closed barn. Mortality and isopod energy reserves (digestive gland total proteins, lipids and carbohydrates) were not affected following 14days exposure to up to 1000mg TiO2 per kg dry leaves (mg/kg) under any experimental scenario. However, in the field tests, isopods consumption of TiO2-coated leaves was reduced compared to that of uncoated leaves and the decrease was not dose-dependent. The highest reduction was in the closed barn (45-56%) rather than in the open-air (38-40%). In laboratory-based food choice tests, isopods neither preferred nor avoided leaves coated with TiO2, suggesting that rather than sensing the TiO2 on the leaves directly, the isopods under open-air and barn exposure responded to altered attractiveness and/or palatability of the TiO2 amended leaves. We propose that this could be due to altered microbial population on the leaves, a hypothesis that requires further investigation. Although short-term exposure to atmospheric deposition of up to 1000mg/kg commercial TiO2 is unlikely to pose an immediate threat to isopod mortality and energy balance, reduced leaf feeding may have implications for the decomposition of plant material.

Epoxy composite dusts with and without carbon nanotubes cause similar pulmonary responses, but differences in liver histology in mice following pulmonary deposition.

BACKGROUND: The toxicity of dusts from mechanical abrasion of multi-walled carbon nanotube (CNT) epoxy nanocomposites is unknown. We compared the toxic effects of dusts generated by sanding of epoxy composites with and without CNT. The used CNT type was included for comparison. METHODS: Mice received a single intratracheal instillation of 18, 54 and 162 µg of CNT or 54, 162 and 486 µg of the sanding dust from epoxy composite with and without CNT. DNA damage in lung and liver, lung inflammation and liver histology were evaluated 1, 3 and 28 days after intratracheal instillation. Furthermore, the mRNA expression of interleukin 6 and heme oxygenase 1 was measured in the lungs and serum amyloid A1 in the liver. Printex 90 carbon black was included as a reference particle. RESULTS: Pulmonary exposure to CNT and all dusts obtained by sanding epoxy composite boards resulted in recruitment of inflammatory cells into lung lumen: On day 1 after instillation these cells were primarily neutrophils but on day 3, eosinophils contributed significantly to the cell population. There were still increased numbers of neutrophils 28 days after intratracheal instillation of the highest dose of the epoxy dusts. Both CNT and epoxy dusts induced DNA damage in lung tissue up to 3 days after intratracheal instillation but not in liver tissue. There was no additive effect of adding CNT to epoxy resins for any of the pulmonary endpoints. In livers of mice instilled with CNT and epoxy dust with CNTs inflammatory and necrotic histological changes were observed, however, not in mice instilled with epoxy dust without CNT. CONCLUSIONS: Pulmonary deposition of epoxy dusts with and without CNT induced inflammation and DNA damage in lung tissue. There was no additive effect of adding CNT to epoxies for any of the pulmonary endpoints. However, hepatic inflammatory and necrotic histopathological changes were seen in mice instilled with sanding dust from CNT-containing epoxy but not in mice instilled with reference epoxy.

Worker Exposure and High Time-Resolution Analyses of Process-Related Submicrometre Particle Concentrations at Mixing Stations in Two Paint Factories.

The paint and coatings industry is known to have significant particulate matter (PM) emissions to the atmosphere. However, exposure levels are not studied in detail especially when considering submicrometre (PM1) and ultrafine particles (particle diameter below 100nm). The evidence is increasing that pulmonary exposures to these size fractions are potentially very harmful. This study investigates particle emissions during powder handling and paint mixing in two paint factories at two mixing stations in each factory. In each case measurements were made simultaneously at the mixing station (near-field; NF), as well as at 5-15 m distance into the workroom far-field (FF), and in the workers breathing zone. Particle concentrations (5nm to 30 µm) were measured using high time-resolution particle instruments and gravimetrically using PM1 cyclone filter samplers. The PM1 filters were also characterized by scanning electron microscopy (SEM). The NF particle and dust concentration levels were linked to pouring powder and were used to characterize the emissions and efficiencies of localized controls. NF particle number concentrations were 1000-40000cm(-3) above FF concentrations. NF particles were mainly between 100 and 500nm and emissions appeared to occur in short bursts. Personal PM1 exposure levels varied between 0.156 and 0.839mg m(-3) and were 1.6-15 times higher than stationary NF PM1 concentrations. SEM results verified that the personal exposure and NF particles were strongly dominated by the pigments and fillers used. Better understanding of the entire temporal personal exposure could be improved by using real-time particle monitors for personal exposure measurements. This study provides better insight into PM exposure characteristics and concentration levels in the paint industry.

Exposure and preventive measure to reduce high and daily exposure to Bacillus thuringiensis in potted plant production.

The bacterium Bacillus thuringiensis (Bt) is the active organism in a variety of commercially available products used worldwide as biopesticides. Bt products are applied in large outdoor areas as well as in indoor environments. Even though it has been sold for decades, not much is known about the occupational exposure to Bt. The aim of this study was to obtain knowledge about the exposure to Bt subspecies israelensis (Bti) in a propagation section in a greenhouse, where Bti is applied hourly by a spray boom, and to test a preventive measure to reduce the exposure to airborne Bti. Furthermore, we wanted to study the exposure during work with potted plants treated earlier with Bti. Exposure to aerosols with Bti was measured repeatedly by personal and stationary samplers before and after the intervention. Bti was identified by polymerase chain reaction in air and soil samples. Personal exposure to inhalable Bti in the propagation section was 3×10(5) cfu m(-3) (median level, n = 22); the personal exposure of people working with plants treated earlier with Bti was 3200 cfu m(-3) (median level, n = 17). The highest single measure was found for the person working with the spray boom (7×10(5) cfu m(-3)) but airborne Bti was present at all sampling stations in the propagation section. Bti constituted a high share of the airborne cultivable bacteria and a smaller share of the soilborne bacteria in the propagation section. In a human cell assay, spiking an aerosol sample with a product with Bti increased the inflammatory potential of an aerosol sample from the greenhouse significantly. Based on the inflammatory potential and the high personal exposure, a cover around the spray boom was built as an attempt to reduce the daily exposure to Bti. The cover reduced the personal exposure to Bti from 3.0×10(5) cfu m(-3) to 1.8×10(4) cfu m(-3). The exposure was thus reduced by a factor 17, which is a considerable reduction. Bti was present in different particle size fractions with the majority, both before and after the intervention, in the fraction of airborne particles with an aerodynamic diameter between 1.2 and 3.0 µm. The measured occupational exposure to Bti is discussed in relation to risk evaluation.

Inflammatory and genotoxic effects of sanding dust generated from nanoparticle-containing paints and lacquers.

Nanoparticles are increasingly used in paints and lacquers. Little is known of the toxicity of nanoparticles incorporated in complex matrices and released during different phases of the life cycle. DNA damaging activity and inflammogenicity of sanding dust sampled during standardised sanding of boards painted with paints with and without nanoparticles were determined 24 h after intratracheal instillation of a single dose of 54 µg in mice. Dusts from nanoparticle-containing paints and lacquers did not generate pulmonary inflammation or oxidative stress. Sanding dust from both the nanoparticle-containing and the conventional lacquer and the outdoor acrylic-based reference paint increased the level of DNA strand breaks in bronchoalveolar fluid cells. In conclusion, addition of nanoparticles to paint or lacquers did not increase the potential of sanding dust for causing inflammation, oxidative stress or DNA damage, suggesting that the paint/lacquer matrix is more important as determinant of DNA damage than the nanomaterial.

Conceptual model for assessment of inhalation exposure to manufactured nanoparticles.

As workplace air measurements of manufactured nanoparticles are relatively expensive to conduct, models can be helpful for a first tier assessment of exposure. A conceptual model was developed to give a framework for such models. The basis for the model is an analysis of the fate and underlying mechanisms of nanoparticles emitted by a source during transport to a receptor. Four source domains are distinguished; that is, production, handling of bulk product, dispersion of ready-to-use nanoproducts, fracturing and abrasion of end products. These domains represent different generation mechanisms that determine particle emission characteristics; for example, emission rate, particle size distribution, and source location. During transport, homogeneous coagulation, scavenging, and surface deposition will determine the fate of the particles and cause changes in both particle size distributions and number concentrations. The degree of impact of these processes will be determined by a variety of factors including the concentration and size mode of the emitted nanoparticles and background aerosols, source to receptor distance, and ventilation characteristics. The second part of the paper focuses on to what extent the conceptual model could be fit into an existing mechanistic predictive model for ''conventional'' exposures. The model should be seen as a framework for characterization of exposure to (manufactured) nanoparticles and future exposure modeling.

Comparison of dust released from sanding conventional and nanoparticle-doped wall and wood coatings.

Introduction of engineered nanoparticles (ENPs) into traditional surface coatings (e.g., paints, lacquers, fillers) may result in new exposures to both workers and consumers and possibly also a new risk to their health. During finishing and renovation, such products may also be a substantial source of exposure to ENPs or aggregates thereof. This study investigates the particle size distributions (5.6 nm-19.8 µm) and the total number of dust particles generated during sanding of ENP-doped paints, lacquers, and fillers as compared to their conventional counterparts. In all products, the dust emissions from sanding were found to consist of five size modes: three modes under 1 µm and two modes around 1 and 2 µm. Corrected for the emission from the sanding machine, the sanding dust, was dominated by 100-300 nm size particles, whereas the mass and surface area spectra were dominated by the micrometer modes. Adding ENPs to the studied products only vaguely affected the geometric mean diameters of the particle modes in the sanding dust when compared to their reference products. However, we observed considerable differences in the number concentrations in the different size modes, but still without revealing a clear effect of ENPs on dust emissions from sanding.