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Chloroacetyl chloride – determination method
Ewa Kozieł
The method is based on the chemisorption of chloroacetyl chloride on XAD-7 coated with 1-(2-pyri-dyl)piperazine, desorption of chloroacetyl chloride and 1-(2-pyridyl)piperazine derivative with acetonitryle and its determination in the obtained solution by high performance liquid chromatography.
The determination limit of the method is 0,02 mg/m³.
Methyl 2-cyanoacrylate – determination method
Joanna Kowalska
The determination method is based on the adsorption of methyl 2-cyanoacrylate vapours on phosphoric acid-treated XAD-7 sampling tubes (80/40 mg sections), desorption with 2 ml of 0.2%(v/v) phosphoric acid in acetonitryle and high performance liquid chromatographic (HPLC/UV) analysis of the resulting solution.
The determination limit of the method is 0.2 mg/m³.
Trimethyl phosphite – determination method
Anna Jeżewska
The method is based on the adsorption of trimethyl phosphite on glass fiber filter and resin XAD-7 and desorption with 1,5 mL of dichloromethane – methanol (95:5) mixture. The obtained solution is analyzed by gas chromatographic with a flame photometric detector (GC-FPD). The determination limit of the method is 0.5 mg/m³.
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Bis(2-ethylhexyl) adipate. Documentation
Lidia Zapór
Bis(2-ethylhexyl) adipate (DEHA) is used primarily as a plasticizer in the flexible vinyl industry and is widely used in flexible poly(vinyl chloride) food film. It is also used as a solvent and as a component of aircraft lubricants. It is important in the processing nitrocellulose and synthetic rubber and in the cosmetic industry (cellulose-based liquid lipsticks). Occupational exposure to DEHA may occur through inhalation or dermal contact during its manufacture and its use. Bis(2-ethylhexyl) adipate is rapidly and completely absorbed after oral administration, rapidly and extensively metabolized and excreted in humans and laboratory animals. In the available literature no data on the toxicity DEHA in humans have been found. The oral LD50 in rats is 9110 mg/kg body weight. DEHA exerts systemic action mainly on the liver in acute and chronic toxicity in laboratory animals. The critical effects of DEHA activity is induced hepatic peroxisome proliferation. DEHA did not show genotoxic and mutagenic effects in many experimental studies. In carcinogenicity testing this compound caused an increased hepatocellular tumor in mice but not in rats. There are no data on carcinogenicity in humans. DEHA exerts embryotoxic, fetotoxic and teratogenic effects in animals. There are no data on reproductive and developmental effects in humans. In setting the exposure limits, the results of chronic toxicity testing were considered. Based on the NOAEL value obtained in an experimental study (700 mg/kg bw per day) and appropriate uncertainty factors, a MAC (TWA) value has been calculated at 400 mg/m³. No STEL value has been established. With regard to fetotoxic effects of DEHA in laboratory animals an Ft notation is considered appropriate.
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Allyl chloride. Documentation
Katarzyna Miranowicz-Dzierżawska
Allyl chloride is a synonym of the compound 3-chloropropene, also referred to as 3-chloro, 1-propene. Allyl chloride is a volatile, highly reactive, liquid halogenated hydrocarbon with a characteristic purgent (garlic-like) odor. The high-temperature chlorination of propylene is believed to be the only production method of allyl chloride used commercially. Allyl chloride is used as an intermediate in chemical reactions. The major commercial derivative of allyl chloride is epichlorohydrin which is used in the manufacture of epoxy resins. Allyl chloride is also important in commercial glycerol production. The major routes for occupational exposure to allyl chloride are dermal and inhalation. Allyl chloride is irritating to eyes, the skin and the upper respiratory tract.
The effects of allyl chloride on human, after repeated or chronic exposure, are functional changes in the liver and kidneys. It also had an influence on CNS. Acute and chronic exposure to allyl chloride in animals has resulted in hepatic, renal and pulmonary damage. The LD50 value, following oral administration in rats, is 450 mg/kg body weight and 2026 mg/kg b.w. after dermal treatment. The International Agency for Research on Cancer has classified allyl chloride to Group 3 (not classifiable as to carcinogenicity to humans). The recommended maximum exposure limit (MAC) for allyl chloride is 2 mg/m³. No STEL and BEI have been proposed.
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Carbon monoxide. Documentation
Marek Jakubowski
Carbon monoxide (CO) is a colourless, odourless, flammable gas.
Anthropogenic emissions of carbon monoxide originate mainly from incomplete combustion. The largest proportion of these emissions are produced as exhaust of internal combustion engines. Other sources include power plants using coal and waste incinerators. Indoor concentrations are associated with combustion sources and are found in enclosed parking garages, service stations and restaurants. Passive smoking is associated with increasing a non-smoker’s exposure. Occupational groups include auto mechanics, garage and gas station attendants, police, firefighters. Industrial processes which can expose workers to carbon monoxide include steel production, coke ovens and petroleum refining.
Carbon monoxide is absorbed through lungs. Approximately 80-90% of the absorbed carbon monoxide binds with haemoglobin producing carboxyheamoglobin (CO-Hb). CO-Hb levels likely to result from external carbon monoxide exposure can be estimated reasonably well from the Coburn-Foster-Kane (CFK) equation.
Decrease of the oxygen carrying capacity of blood appears to be the principal mechanism of action of carbon monoxide. Its toxic effects on humans are due to hypoxia in organs and tissues with high oxygen consumption such as the brain , the hearth, exercising skeletal muscle and the developing fetus. In apparently healthy persons decreased oxygen uptake and the resultant work capacity under maximal exercise conditions have been shown starting at 5% CO-Hb. Hypoxia due to acute carbon monoxide poisoning may cause both reversible and long lasting neurological effects. Psychomotor effects, such as reduced coordination, tracking and driving ability have been revealed at CO-Hb levels as low as 5,1 – 8,2%. Therefore it seems that to protect the nonsmoking, healthy workers a Co-Hb level of 3,5% should not be exceeded. According to the Coburg-Foster-Kane equation 3,5% CO-Hb corresponds to the 8 h exposure to carbon monoxide concentration in the air of 30 mg/m³.At the proposed Occupational Exposure Limits (TWA and STEL)of 23 mg CO/m³(8 hours) and 117 mg CO/m³ (15 min) the CO-Hb levels of 3,5% and 5% respectively should not be exceeded. The Biological Exposure Index (BEI)of 3,5% CO-Hb was also proposed.
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Trimethyl phosphate. Documentation
Jerzy K. Piotrowski, Czesław Orłowski
Trimethyl phosphite (TMP) is a colorless liquid with a distinctive, pungent odor. It is mainly used as an intermediate in the manufacture of pesticides. Acute oral LD50 values for rats are between 2450 and 2890 mg/kg b.w. Superficial irritation of the cornea was observed in rats exposed at 50 and 100 ppm, and mild cataracts developed in female rats only. No effects were detected in animals exposed at 10 ppm (52 mg/m³). The substance was positive in a battery of Drosophila melanogaster mutagenicity assays and in a bacterial DNA amage/repair suspension assay using various strains of Escherichia coli and Salmonella typhimurium. The Expert Group for Chemical Agent established an 8-hour TWA value of 5 mg/m³, and a STEL value of 10 mg/m³.
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