Assessment of the contribution of electron microscopy to nanoparticle characterization sampled with two cascade impactors.

This study assessed the contribution of electron microscopy to the characterization of nanoparticles and compared the degree of variability in sizes observed within each stage when sampled by two cascade impactors: an Electrical Low Pressure Impactor (ELPI) and a Micro-Orifice Uniform Deposit Impactor (MOUDI). A TiO(2) nanoparticle (5 nm) suspension was aerosolized in an inhalation chamber. Nanoparticles sampled by the impactors were collected on aluminum substrates or TEM carbon-coated copper grids using templates, specifically designed in our laboratories, for scanning and transmission electron microscopy (SEM, TEM) analysis, respectively. Nanoparticles were characterized using both SEM and TEM. Three different types of diameters (inner, outer, and circular) were measured by image analysis based on count and volume, for each impactor stage. Electron microscopy, especially TEM, is well suited for the characterization of nanoparticles. The MOUDI, probably because of the rotation of its collection stages, which can minimize the resuspension of particles, gave more stable results and smaller geometric standard deviations per stage. Our data suggest that the best approach to estimate particle size by electron microscopy would rely on geometric means of measured circular diameters. Overall, the most reliable data were provided by the MOUDI and the TEM sampling technique on carbon-coated copper grids for this specific experiment. This study indicates interesting findings related to the assessment of impactors combined with electron microscopy for nanoparticle characterization. For future research, since cascade impactors are extensively used to characterize nano-aerosol exposure scenarios, high-performance field emission scanning electron microscopy (FESEM) should also be considered.

Acute oral and inhalation toxicities in rats with cadmium telluride.

Cadmium telluride (CdTe) thin film photovoltaic has become one of the leading technologies in the solar renewable energy market. Little is known about CdTe's toxicological profile and regulatory agencies usually apply cadmium (Cd) criteria as a best approximation. However, CdTe may have different toxicological properties. The goal of this study is to determine the median lethal concentration/dose of CdTe and to compare these values with those of Cd. Using a rat model, the method followed conforms to that described in the Organisation for Economic Co-operation and Development (OECD) guidelines and in the US Environmental Protection Agency (EPA) Health Effects Test Guidelines. The median lethal concentration of CdTe was established at 2.71 mg/L, showing a very low variability between genders. The median lethal dose was determined to be greater than 2000 mg/kg. These results clearly show that CdTe is less toxic than Cd.

Dermal exposure to beryllium: a pilot case study.

The issue of dermal absorption of beryllium (Be) particles through intact healthy skin has not yet been demonstrated. The interest in Be dermal exposure as a potential pathway for toxic effects was emphasized in Quebec (Canada) when a recycling industry processing spent pot lining (SPL) related to the aluminum industry was recently requested by health authorities to conduct a Be particle size study and to provide a Tyvek coverall for full skin protection of workers. This study aimed to (1) calculate the dermal and inhalation exposures and (2) apply the results to the case study of a recycling SPL industry. Airborne dust was sampled in order to determine Be particles size. Exposure assessment via the skin and the respiratory routes was measured over a working day using standard calculations. The assessment of workers' clothing protection was obtained by swiping the skin on the forearm and upper front leg before and after exposure. Respirable Be (0.044 microg) was 23% of the total Be (0.19 microg). Be particles with a median mass aerodynamic diameter (MMAD) of 0.93 and below totaled 0.0103 microg (5% of BeT). The daily dose for the respiratory route was calculated to be 0.022 microg/kg/d, while the daily doses for the dermal route varied between 0.027 x 10(-7) microg/kg/d and 0.025 x 10(-3) microg/kg/d. After exposure, no Be was found on the skin of workers wearing a cotton coverall protection. When using a polyester coverall, minor amounts of Be were found. These results showed that dermal daily dose exposure is negligible. However, note that the case study did not involve handling of contaminated items by the workers, which lead to significant dermal exposure if care is not taken. Although daily dermal exposure may be small, because of uncertainties, a precautionary principle should be applied in an active sense.

Neuropathology, tremor and electromyogram in rats exposed to manganese phosphate/sulfate mixture.

In Canada, Methylcyclopentadienyl manganese tricarbonyl (MMT) replaced tetraethyl lead in gasoline as an antiknock agent from 1976 until 2003. The combustion of MMT leads to increased manganese (Mn) concentrations in the atmosphere, and represents one of the main sources of human exposure to Mn. The nervous system is the major target of the toxicity of Mn and Mn compounds. The purpose of this study was to investigate exposure-response relationships for neuropathology and tremor, and the associated electromyogram (EMG), following subchronic inhalation exposure of rats to a mixture of Mn phosphate/sulfate particles. Rats were exposed 6 h per day, 5 days per week for 13 consecutive weeks at 30, 300 or 3000 microg m(-3) Mn phosphate/sulfate mixture and compared with controls. Half of the rats had EMG electrodes implanted in the gastrocnemius muscle of the hind limb to assess tremor at the end of Mn exposure. Two days after the end of Mn exposure, rats were killed by exsanguination and Mn concentrations in the brain (caudate putamen, globus pallidus and frontal cortex) were determined by neutron activation analysis while neuropathology was assessed by counting neuronal cells in 2.5 mm x 2.5 mm grid areas. Increased Mn concentrations were observed in all brain sections at the highest level of exposure. The neuronal cell loss was significantly different in the globus pallidus and the caudate putamen at the highest level of exposure (3000 microg m(-3)). No sign of tremor was observed among the rats. In conclusion, exposure to a high level of Mn phosphate/sulfate mixture brought on neuropathological changes in a specific area of the brain; however, no sign of tremor was observed.

Manganese distribution in the brain and neurobehavioral changes following inhalation exposure of rats to three chemical forms of manganese.

The central nervous system is an important target for manganese (Mn) intoxication in humans; it may cause neurological symptoms similar to Parkinson's disease. Manganese compounds emitted from the tailpipe of vehicles using methylcyclopentadienyl manganese tricarbonyl (MMT) are primarily Mn phosphate, Mn sulfate, and Mn phosphate/sulfate mixture. The purpose of this study is to compare the patterns of Mn distribution in various brain regions (olfactory bulb, frontal parietal cortex, globus pallidus, striatum and cerebellum) and other tissues (lung, liver, kidney, testis) and the neurobehavioral damage following inhalation exposure of rats to three Mn species. Rats (n=15 rats per Mn species) were exposed 6 h per day, 5 days per week for 13 consecutive weeks to metallic Mn, Mn phosphate or Mn phosphate/sulfate mixture at about 3000 microgm(-3) and compared to controls. At the end of the exposure period, spontaneous motor activity was measured for 36 h using a computerized autotrack system. Mn in tissues was determined by instrumental neutron activation analysis (INAA). The Mn concentrations in the brain were significantly higher in rats exposed to Mn phosphate and Mn phosphate/sulfate mixture than in control rats or rats exposed to metallic Mn. Exposure to Mn phosphate/sulfate mixture caused a decrease in the total ambulatory count related to locomotor activity. Our results confirm that Mn species and solubility have an influence on the brain distribution of Mn in rats.

Bioaccumulation and locomotor effects of manganese phosphate/sulfate mixture in Sprague-Dawley rats following subchronic (90 days) inhalation exposure.

Methylcyclopentadienyl manganese tricarbonyl (MMT) is an organic manganese (Mn) compound added to unleaded gasoline in Canada. The primary combustion products of MMT are Mn phosphate, Mn sulfate, and a Mn phosphate/Mn sulfate mixture. Concerns have been raised that the combustion products of MMT containing Mn could be neurotoxic, even at low levels of exposure. The objective of this study is to investigate exposure-response relationships for bioaccumulation and locomotor effects following subchronic inhalation exposure to a mixture of manganese phosphates/sulfate mixture. A control group and three groups of 30 male Sprague-Dawley rats were exposed in inhalation chambers for a period of 13 weeks, 5 days per week, 6 h a day. Exposure concentrations were 3000, 300, and 30 microg/m(3). At the end of the exposure period, locomotor activity and resting time tests were conducted for 36 h using a computerized autotrack system. Rats were then euthanized by exsanguination and Mn concentrations in different tissues (liver, lung, testis, and kidney) and blood and brain (caudate putamen, globus pallidus, olfactory bulb, frontal cortex, and cerebellum) were determined by neutron activation analysis. Increased manganese concentrations were observed in blood, kidney, lung, testis, and in all brain sections in the highest exposure group. Mn in the lung and in the olfactory bulb were dose dependent. Our data indicate that the olfactory bulb accumulated more Mn than other brain regions following inhalation exposure. Locomotor activity was increased at 3000 microg/m(3), but no difference was observed in resting time among the exposed groups. At the end of the experiment, rats exposed to 300 and 3000 microg/m(3) exhibited significantly decreased body weight in comparison with the control group. Biochemical profiles also revealed some significant differences in certain parameters, specifically alkaline phospatase, urea, and chlorate.

Estimation of annual Mn emissions from MMT source in the Canadian environment and the Mn pollution index in each province.

Methylcyclopentadienyl manganese tricarbonyl (MMT), is an organic derivative of Mn used as an anti-knock agent in Canadian unleaded gasoline since 1976. This study aims to estimate Mn emissions from MMT source in the Canadian environment as well as the Mn pollution index per capita in each of the Canadian provinces. In concomitance, lead emissions will also be addressed. The quantities of Mn and Pb used in gasoline were calculated from data on annual gasoline sales in Canada supplied by Statistics Canada. Obviously, the Pb emission profile shows a substantial decrease with an annual average of -28% until 1991, when MMT totally replaced Pb in Canadian gasoline. The case of Mn is quite different. Since emission rates of Mn at the tailpipe vary between 6 and 45%, the quantities released into the atmosphere were calculated for each of these rates, as well as for 100 and 25% emission rate scenarios. For 1981 and 1999, the quantities of Mn used in gasoline were estimated at 101122 and 344880 kg, respectively. Based on the realistic 25% emission rate scenario and a concentration of 0.009 g/l of Mn in gasoline, Mn emissions from car exhausts were estimated to 25280 and 86220 kg, respectively. The mean annual increase in emission rate between 1981 and 1999 is 7.34%. The atmospheric Mn pollution index seems to be stable over time, and it varies from 0.0024 kg/capita to 0.0041 kg/capita in 1999. In the context of a notable decrease in Mn emissions from industrial sources, these results suggest that the combustion of MMT used in gasoline may be an important factor contributing to maintaining stable atmospheric Mn concentrations instead of a significant decrease due to reduced industrial emissions.

Assessment of bioaccumulation, neuropathology, and neurobehavior following subchronic (90 days) inhalation in Sprague-Dawley rats exposed to manganese phosphate.

Methylcyclopentadienyl manganese tricarbonyl (MMT) is an organic manganese (Mn) compound added to unleaded gasoline. It has been suggested that the combustion products of MMT containing Mn, such as manganese phosphate, could cause neurological symptoms similar to Parkinson's disease in humans. The aim of this work was to investigate the exposure-response relationship of bioaccumulation, neuropathology, and neurobehavior following a subchronic inhalation exposure to manganese phosphate in Sprague-Dawley male rats. Rats were exposed 6 h/day, 5 days/week for 13 consecutive weeks at 30, 300, or 3000 microg/m(3) Mn phosphate and compared to controls. Some rats were implanted with chronic EMG electrodes in the gastrocnemius muscle of the hind limb to assess tremor at the end of Mn exposure. Spontaneous motor activity was measured for 36 h using a computerized autotrack system. Rats were then sacrificed by exsanguination and Mn level in different brain tissues and other organs was determined by instrumental neutron activation analysis. Neuronal cell counts were obtained by assessing the sum of five grid areas for the caudate/putamen and the sum of two adjacent areas for the globus pallidus. Increased manganese concentrations were observed in all tissues of the brain and was dose-dependent in olfactory bulb and caudate/putamen. In fact, beginning with the highest level of exposure (3000 microg/m(3)) and ending with the control group, Mn concentrations in the olfactory bulb were 2.47 vs 1.28 vs 0.77 vs 0.64 ppm (P < 0.05) while for the caudate/putamen, Mn concentrations were 1.06 vs 0.73 vs 0.62 vs 0.47 ppm (P < 0.05). The Mn concentrations in lung were also dose-dependent (10.30 vs 1.40 vs 0.42 vs 0.17 ppm; P < 0.05). No statistical difference was observed for loss of neurons in caudate/putamen and globus pallidus. Locomotor activity assessment and tremor assessment did not reveal in neurobehavioral changes between the groups. Our results reinforce the hypothesis that the olfactory bulb and caudate/putamen are the main brain tissues for Mn accumulation after subchronic inhalation exposure.