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While manyin vivoandin vitrotoxicology studies of multi-walled carbon nanotubes (MWCNTs) have already indicated that exposure to MWCNTs can potentially induce health effects in humans, the actual health effects of MWCNTs among exposed workers are not yet known. Moreover, the levels of exposure and internal doses of MWCNTs are becoming more and more important for estimating the health effects resulting from exposure to MWCNTs. However, information on biomonitoring and exposure to MWCNTs remains limited. Therefore, the authors conducted a health surveillance study in a workplace that manufactures MWCNTs, including assessment of the personal and area exposure levels to MWCNTs, a walk-through evaluation of the manufacturing process, and collection of blood and exhaled breath condensates (EBCs) from the MWCNT manufacturing and office workers. In addition, a pulmonary function test was also conducted on the MWCNT manufacturing workers (9) and office workers (4). The worker exposure to elemental carbon was found to be 6.2–9.3 μg/m3in the personal samplings and 5.5–7.3 μg/m3in the area samplings. Notwithstanding, the workers exhibited a normal range of hematology and blood biochemistry values and normal lung function parameters. When analyzing the EBCs, the malondialdehyde (MDA), 4-hydroxy-2-hexenal (4-HHE) and n-hexanal levels in the MWCNT manufacturing workers were significantly higher than those in the office workers. The MDA and n-hexanal levels were also significantly correlated with the blood molybdenum concentration, suggesting MDA, n-hexanal and molybdenum as useful biomarkers of MWCNT exposure. [ABSTRACT FROM PUBLISHER]

Single-walled carbon nanotubes (SWCNTs) have extensive potential industrial applications due to their unique physical and chemical properties; yet this also increases the chance of human and environment exposure to SWCNTs. Due to the current lack of hazardous effect information on SWNCTs, a standardized genotoxicity battery test was conducted to clarify the genetic toxicity potential of SWCNTs (diameter: 1–1.2 nm, length: ∼20 μm) according to Organization for Economic Cooperation and Development test guidelines 471 (bacterial reverse mutation test), 473 (in vitro chromosome aberration test), and 474 (in vivo micronuclei test) with a good laboratory practice system. The test results showed that the SWCNTs did not induce significant bacterial reverse mutations at 31.3–500 μg/plate in Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537 or in Escherichia coli strain WP2uvrA, with and without a metabolic activation system. Furthermore, the in vitro chromosome aberration test showed no significant increase in structural or numerical chromosome aberration frequencies at SWCNT dose levels of 12.5–50 μg/ml in the presence and absence of metabolic activation. However, dose-dependent cell growth inhibition was found at all the SWCNT dose levels and statistically significant cytotoxic effects observed at certain concentrations in the presence and absence of metabolic activation. Finally, the SWCNTs did not evoke significant in vivo micronuclei frequencies in the polychromatic erythrocytes of an imprinting control region mice at 25–100 mg/kg. Thus, according to the results of the present study, the SWCNTs were not found to have a genotoxic effect on the in vitro and in vivo test systems. [ABSTRACT FROM AUTHOR]

Despite their useful physico-chemical properties, carbon nanotubes (CNTs) continue to cause concern over occupational and human health due to their structural similarity to asbestos. Thus, to evaluate the toxic and genotoxic effect of multi-wall carbon nanotubes (MWCNTs) on lung cells in vivo, eight-week-old rats were divided into four groups (each group = 25 animals), a fresh air control (0 mg/m3), low (0.17 mg/m3), middle (0.49 mg/m3), and high (0.96 mg/m3) dose group, and exposed to MWCNTs via nose-only inhalation 6 h per day, 5 days per week for 28 days. The count median length and geometric standard deviation for the MWCNTs determined by TEM were 330.18 and 1.72 nm, respectively, and the MWCNT diameters ranged from 10 to 15 nm. Lung cells were isolated from five male and five female rats in each group on day 0, day 28 (only from males) and day 90 following the 28-day exposure. The total number of animals used was 15 male and 10 female rats for each concentration group. To determine the genotoxicity of the MWCNTs, a single cell gel electrophoresis assay (Comet assay) was conducted on the rat lung cells. As a result of the exposure, the olive tail moments were found to be significantly higher ( p < 0.05) in the male and female rats from all the exposed groups when compared with the fresh air control. In addition, the high-dose exposed male and middle and high-dose exposed female rats retained DNA damage, even 90 days post-exposure ( p < 0.05). To investigate the mode of genotoxicity, the intracellular reactive oxygen species (ROS) levels and inflammatory cytokine levels (TNF-α, TGF- β, IL-1, IL-2, IL-4, IL-5, IL-10, IL-12 and IFN-γ) were also measured. For the male rats, the H2O2 levels were significantly higher in the middle (0 days post-exposure) and high- (0 days and 28 days post-exposure) dose groups ( p < 0.05). Conversely, the female rats showed no changes in the H2O2 levels. The inflammatory cytokine levels in the bronchoalveolar lavage (BAL) fluid did not show any statistically significant difference. Interestingly, the short-length MWCNTs deposited in the lung cells were persistent at 90 days post-exposure. Thus, exposing lung cells to MWCNTs with a short tube length may induce genotoxicity. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a nonessential toxic metal which is widely distributed in the environment. The general population is exposed to low levels of Cd and the kidney is the organ most sensitive to Cd toxicity. This study was performed to simultaneously evaluate Cd exposure, kidney function, and oxidative stress biomarkers in the general population. A total of 643 adults were interviewed to document demographic characteristics, lifestyles, past-medical history, and diet during the last 24 h. We estimated daily Cd intake based on the diet of study subjects who had not been exposed to Cd occupationally. Whole blood and urine samples were collected and analyzed to determine Cd concentrations and kidney function indices (β2-microglobulin [β2-MG], N-acetyl-β- D-glucosaminidase [NAG], metallothionein [MT]). The oxidative stress index (malondialdehyde [MDA]) was determined from the urine. The daily Cd intake from diet was established as 7.07 μg/day. The mean concentration of Cd measured in the blood was 1.22 μg/L and urine was 0.95 μg/g creatinine. The concentrations of Cd in blood and urine were higher in females than in males. The blood levels of Cd were affected by sex, age, and smoking, and urine Cd was influenced by sex, age, and blood Cd. The urine Cd was positively correlated with MT, NAG activity, and MDA in females, but with NAG only in males. The blood Cd was associated with MT in males. Increased NAG activity was observed when Cd in urine reached 1.0 μg Cd/g creatinine and was also affected by age, hypertension, and diabetes mellitus. Urinary MT only responded to Cd in urine or blood. In summary, exposure to Cd in the general population was influenced by various factors including sex, age, and smoking habits. Such exposure might eventually cause tubular damage in the kidneys through the oxidative stress mechanism, and females might be more susceptible than males to Cd exposure under the environment. © 2011 Wiley Periodicals, Inc. Environ Toxicol 28: 563-570, 2013. [ABSTRACT FROM AUTHOR]

To clarify the health risks related to silver nanoparticles (Ag-NPs), we evaluated the genotoxicity, acute oral and dermal toxicity, eye irritation, dermal irritation and corrosion and skin sensitisation of commercially manufactured Ag-NPs according to the OECD test guidelines and GLP. The Ag-NPs were not found to induce genotoxicity in a bacterial reverse mutation test and chromosomal aberration test, although some cytotoxicity was observed. In acute oral and dermal toxicity tests using rats, none of the rats showed any abnormal signs or mortality at a dose level of ∼ 2000 mg/kg. Similarly, acute eye and dermal irritation and corrosion tests using rabbits revealed no significant clinical signs or mortality and no acute irritation or corrosion reaction for the eyes and skin. In a skin sensitisation test using guinea pigs, one animal (1/20) showed discrete or patchy erythema, thus Ag-NPs can be classified as a weak skin sensitiser. [ABSTRACT FROM AUTHOR]

Safety data sheets (SDS5) and labelling are the basic hazard communication tools for hazardous chemicals as regards their manufacture, storage, transport and other handling activities. Thus, in the context of the growing use of nanomaterials and nanomaterial-containing materials, this study evaluated the information provided in 97 nanomaterial-related SDSs according to the criteria set by the GHS (Globally Harmonized System of Classification and Labelling of Chemicals) and found that most of the SDSs did not include sufficient information on the safety of nanomaterials, such as their toxicity and physicochemical properties. The reasons for this lack of information in the nanomaterial SDSs can mainly be attributed to (1) a lack of toxicity and physicochemical property information on nanomaterials, (2) unawareness of the effectiveness of conventional exposure controls, such as local exhaust ventilation and encapsulation, and personal protective equipment (PPE), in protecting against nanomaterial exposure, (3) a lack of information on emergency and firefighting measures and (4) a lack of knowledge on how existing regulations apply to nanomaterials. Therefore, to create a consistent standard for the information provided on safety, health and environmental matters for manufactured nanomaterial-containing products, guidance for the preparation of nanomaterial-specific SDSs, including both nanomaterials and mixtures of nanomaterials with conventional non-nanoscale materials, was recently initiated by the ISO TC 229. Their guidance, in the form of a technical report, recommends that nanomaterial-related SDSs should be prepared based on a precautionary approach in terms of the toxicity and other risks associated with the nanomaterial contents within the mixture in question. One of the key recommendations in the technical report is to include additional physicochemical properties, including the particle size (average and range), size distribution aggregation/agglomeration state, shape and aspect ratio, crystallinity, specific surface area, dispersibility and dustiness, which help to distinguish the characteristics of nanomaterials from those of non-nanoscale materials. The technical report also recommends the preparation of SDSs for all nanomaterials and mixtures that meet the GHS criteria for physical, health or environmental hazards, and for all mixtures containing nanomaterials that meet the criteria for carcinogenic, toxic to reproduction or specific target organ toxicity in concentrations exceeding the cut-off limits for an SDS specified by the criteria for mixtures. Finally, the technical report recommends that SDSs be prepared for all nanomaterials, unless there is evidence that they are not hazardous. [ABSTRACT FROM AUTHOR]

In a previous study, the lung function, as indicated by the tidal volume, minute volume, and peak inspiration flow, decreased during 90 days of exposure to silver nanoparticles and was accompanied by inflammatory lesions in the lung morphology. Therefore, this study investigated the recovery from such lung function changes in rats following the cessation of 12 weeks of nanoparticle exposure. Male and female rats were exposed to silver nanoparticles (14-15 nm diameter) at concentrations of 0.66 × 106 particles/cm3 (49 μg/m3, low dose), 1.41 × 106 particles/cm3 (117 μg/m3, middle dose), and 3.24 × 106 particles/cm3 (381 μg/m3, high dose) for 6 h/day in an inhalation chamber for 12 weeks. The rats were then allowed to recover. The lung function was measured every week during the exposure period and after the cessation of exposure, plus animals were sacrificed after the 12-week exposure period, and 4 weeks and 12 weeks after the exposure cessation. An exposure-related lung function decrease was measured in the male rats after the 12-week exposure period and 12 weeks after the exposure cessation. In contrast, the female rats did not show a consistent lung function decrease either during the exposure period or following the exposure cessation. The histopathology showed a gradual recovery from the lung inflammation in the female rats, whereas the male rats in the high-dose group exhibited persistent inflammation throughout the 12-week recovery period. Therefore, the present results suggest a potential persistence of lung function changes and inflammation induced by silver nanoparticle exposure above the no observed adverse effect level. [ABSTRACT FROM AUTHOR]

As chronic exposure to welding fumes causes pulmonary diseases, such as pneumoconiosis, public concern has increased regarding continued exposure to these hazardous gases in the workplace. In a previous study, the inflammatory response to welding fume exposure was analysed in rat lungs in the case of recurrent exposure and recovery periods. Thus using lung samples, well-annotated by histological observation and biochemical analysis, this study examines the gene expression profiles to identify phenotype-anchored genes corresponding to lung inflammation and the repair phenomenon after recurrent welding fume exposure. Seven genes (Mmp12, Cd5l, LOC50101, LOC69183, Spp1, and Slc26a4) were found to be significantly up-regulated according to the severity of the lung injury. In addition, the transcription and translation of Trem2, which was up-regulated in response to the repair process, were validated using a real-time polymerase chain reaction, Western blotting, and immunohistochemistry. The differentially expressed genes in the exposure and recovery groups were also classified using k-means and hierarchical clustering, plus their toxicological function and canonical pathways were further analysed using Ingenuity Pathways Analysis Software. As a result, this comprehensive and integrative analysis of the transcriptional changes that occur during repeated exposure provides important information on the inflammation and repair processes after welding-fume-induced lung injury. [ABSTRACT FROM AUTHOR]

With the increased production and widespread use of nanomaterials, human and environmental exposure to nanomaterials is inevitably increasing. Therefore, this study monitored the possible exposure to nanoparticles at workplaces that manufacture nano-TiO2 and nano-silver. To estimate the potential exposure of workers, personal sampling, area monitoring, and real-time monitoring using a scanning mobility particle sizer (SMPS) and dust monitor were conducted at workplaces where the workers handle nanomaterials. The gravimetric concentrations of TiO2 ranged from 0.10 to 4.99 mg/m3, which were lower than the occupational exposure limit 10 mg/m3 set by the Korean Ministry of Labor or American Conference of Governmental Industrial Hygienists (ACGIH). Meanwhile, the silver metal concentrations ranged from 0.00002 to 0.00118 mg/m3, which were also lower than the silver dust 0.1 mg/m3 and silver soluble compound 0.01 mg/m3 occupational exposure limits set by the ACGIH. The particle number concentrations at the nano-TiO2 manufacturing workplaces ranged from 11,418 to 45,889 particles/cm3 with a size range of 15--710.5 nm during the reaction, although the concentration decreased to 14,000 particles/cm3 when the reaction was stopped. The particle concentrations at the TiO2 manufacturing workplaces increased during the reactor and vacuum pump operations, and during the collection of the synthesized TiO2 particles. Similarly, the particle concentrations at the silver nanoparticle manufacturing workplaces increased when the sodium citrates were weighed or reacted with the silver nitrates, and during the cleaning of the workplace. The number of silver nanoparticles in the samples obtained from the workplace manufacturing silver nanoparticles using induced coupled plasma ranged from 57,789 to 2,373,309 particles/cm3 inside the reactor with an average size of 20--30 nm and 535--25,022 particles/cm3 with a wide range of particle sizes due to agglomeration or aggregation after the release of nanoparticles into the workplace air. In contrast, the silver nanoparticles manufactured by the wet method ranged from 393 to 3526 particle/cm3 with an average size of 50 nm. Thus, when taken together, the TiO2 and silver nanoparticle concentrations were relatively lower than existing occupational exposure limits. [ABSTRACT FROM AUTHOR]

Welder’s pneumoconiosis has generally been determined to be benign and unassociated with respiratory symptoms based on the absence of pulmonary-function abnormalities in welders with marked radiographic abnormalities. In previous studies, the current authors suggested a three-phase lung fibrosis process to study the pathological process of lung fibrosis and found that the critical point for recovery was after 30 days of welding-fume exposure at a high dose, at which point early and delicate fibrosis was observed in the perivascular and peribronchiolar regions. Accordingly, the current study investigated the inflammatory and genotoxic responses during a 30-day period of welding-fume exposure to elucidate the process of fibrosis. As such, rats were exposed to manual metal arc-stainless steel (MMA-SS) welding fumes at concentrations of 65.6 ± 2.9 (low dose) and 116.8 ± 3.9mg/m3 (high dose) total suspended particulate for 2h per day in an inhalation chamber for 30 days. Animals were sacrificed after the initial 2h exposure, and after 15 and 30 days of exposure. The rats exposed to the welding fumes exhibited a statistically significant (P < 0.05) decrease in body weight when compared to the control during the 30-day exposure period, yet an elevated cellular differential count and higher levels of albumin, LDH, and β-NAG, but not elevated TNF-α, and IL-1β in the acellular bronchoalveolar lavage fluid. In addition, the DNA damage resulting from 30 days of welding-fume exposure was confirmed by a comet assay and the inmmunohistochemistry for 8-hydroxydeoxyguanine (8-OH-dG). Consequently, the elevated inflammatory and genotoxic indicators confirmed the lung injury and inflammation caused by the MMA-SS welding-fume exposure. [Copyright &y& Elsevier]

Welders working in a confined space, as in the shipbuilding industry, are at risk of being exposed to high concentrations of welding fumes and developing pneumoconiosis or other welding-fume exposure related diseases. Among such diseases, manganism resulting from welding-fume exposure remains a controversial issue, as the movement of manganese into specific brain regions has not yet been clearly established. Accordingly, to investigate the distribution of manganese in the brain after welding-fume exposure, male Sprague–Dawley rats were exposed to welding fumes generated from manual metal arc-stainless steel (MMA-SS) at concentrations of 63.6 ± 4.1 mg/m3 (low dose, containing 1.6 mg/m3 Mn) and 107.1 ± 6.3 mg/m3 (high dose, containing 3.5 mg/m3 Mn) total suspended particulate (TSP) for 2 h per day in an inhalation chamber over a 60-day period. Blood, brain, lung, and liver samples were collected after 2 h, 15, 30, and 60 days of exposure and the tissues analyzed for their manganese concentrations using an atomic absorption spectrophotometer. Although dose- and time-dependent increases in the manganese concentrations were found in the lungs and livers of the rats exposed for 60 days, only slight manganese increases were observed in the blood during this period. Major statistically significant increases in the brain manganese concentrations were detected in the cerebellum after 15 days of exposure and up until 60 days. Slight increases in the manganese concentrations were also found in the substantia nigra, basal ganglia (caudate nucleus, putamen, and globus pallidus), temporal cortex, and frontal cortex, thereby indicating that the pharmacokinetics and distribution of the manganese inhaled from the welding fumes were different from those resulting from manganese-only exposure. [Copyright &y& Elsevier]

Welders with radiographic pneumoconiosis abnormalities have exhibited a gradual clearing of the X-ray identified effects following removal from exposure. In some cases, the pulmonary fibrosis associated with welding fumes appears in a more severe form in welders. Accordingly, to investigate the disease and recovery process of pneumoconiosis induced by welding-fume exposure, rats were exposed to welding fumes with concentrations of 63.6±4.1 mg/m3 (low dose) and 107.1±6.3 mg/m3 (high dose) of total suspended particulate for 2 h per day in an inhalation chamber for a total of 2 h or 15, 30, 60 or 90 days. Thereafter, the rats were no longer exposed and allowed to recover from the welding fume-induced lung fibrosis for 90 days. When compared to the unexposed control group, the lung weights significantly increased in both the low- and high-dose rats from day 15 to 90. A histopathological examination combined with fibrosis-specific staining revealed that the lungs from the low-dose rats did not exhibit any significant progressive fibrotic changes. Whereas, the lungs from the high-dose rats exhibited early delicate fibrosis from day 15, which progressed into the perivascular and peribronchiolar regions by day 30. Interstitial fibrosis appeared at day 60 and became prominent by day 90, along with the additional appearance of pleural fibrosis. Recovery, evaluated based on the body and lung weights and a histopathological examination, was observed in both the high and low-dose rats that were exposed up to 30 days. The rats exposed for 60–90 days at the low dose also recovered from the fibrosis, yet the rats exposed for 60–90 days at the high dose did not fully recover. Consequently, recovery from pneumoconiosis induced by welding-fume exposure was observed when the degree of exposure was short-term and moderate. [Copyright &y& Elsevier]