Acrylamide (AA) is a chemical compound that occurs at room temperature in the form of colorless crystals or flakes. It is not found in the natural environment, but it can be produced in thermal food processes (frying, baking). It is also present in cigarette smoke. Acrylamide is categorized as a toxic substance that poses substantial health risk after long-term exposure via inhalation, ingestion or skin contact. It is a category 2 (1B) mutagen and category 2 (1B) carcinogen. AA is known to induce adverse effects on reproduction, eye irritation and allergic skin reactions. Acrylamide is produced in multitonnage quantities. It is mostly used to synthesize polyacrylamides applied in wastewater treatment, manufacturing paper, processing ore, manufacturing vinyl polymers; it is also used as a grouting agent in constructing dams and tunnels. Polyacrylamide gel is utilized in the process of electrophoresis (PAGE) commonly used in numerous laboratories.Occupational exposure to acrylamide may occur during the production, processing and distribution of this compound and also during its application in  construction and assembly works (e.g., construction of tunnels, sewer grouting work). In Poland occupational exposure to acrylamide is observed in chemical and pharmaceutical plants as well as in laboratories of research institutes and tertiary education schools. Over 2000 workers (mostly women) were exposed to this compound in the years 2005–2010 (2525 workers in 2010). According to the data produced by the Chief Sanitary Inspectorate in 2011 and 2012 there were no workers exposed to acrylamide at levels exceeding maximum allowable concentration (MAC) in the air, namely over 0.01 mg/m³. Acrylamide is found to exert neurotoxic effects. Clinical symptoms of acute and chronic poisoning are similar in humans, and symptoms of peripheral neuropathy, such as loss of sensation, paresthesia (numbness/tingling in hands and feet), reduced muscle tone and diminished tendon reflexes are most common. In addition, hand tremors and unsteady gait, diminished sensitivity to light and inability to distinguish colors can be observed. Peripheral neuropathy symptoms were significantly more frequent in workers exposed to AA concentrations exceeding 0.3 mg/m³. Based on the biological monitoring (acrylamide adducts with hemoglobin, AA-Hb) of AA-exposed workers no-observed adverse effect level (NOAEL) for numbness/tingling in hands/feet has been set at 0.51 nmol AA-Hb/g globin. This value corresponds to the air AA concentration of 0.1 mg/m³. In workers exposed to this compound dermatitis manifested by skin peeling, mostly in the palm, is also observed. The results of animal studies on acute AA toxicity have revealed symptoms of neurotoxicity, regardless of the exposure route. In the available literature there is no information about long-term inhalation studies on animals. Subchronic and chronic studies (after intraperitoneal and ingestion exposure) showed mainly neurotoxic effect of this compound. Clinical symptoms of animal AA exposure were manifested by incoordination, unsteady gait and diminished strength of hind limbs leading to paralysis. Histopathological examinations of animals most frequently showed degenerated axons and Schwann cells in the spinal cord and peripheral nerves. The NOAEL value for chronic neurotoxicity in rats has been set at 0.5 mg/kg b.w./day. Acrylamide induced male reproductive pathology (degeneration of the germinal epithelium in testes and seminiferous tubules, exfoliation of germ cells in the epididymis and atrophy of testes). Standard bacteria testing showed lack of AA ability to induce point mutations. The in vitro study of gene mutations on mammal cells yielded controversial results. Some researchers sup-pose that the AA activity may be associated with the clastogenic effect (a broken chromosome, which may lead to chromosome reorganization due to incorrect coupling of its fragments into a new configuration). Acrylamide induced chromosome aberrations, polyploidy and spindle disorders, which indicates its aneuploidal effect (the incorrect number of chromosomes in the cell). Acrylamide was responsible for DNA damage, unscheduled DNA synthesis, production of DNA adducts and induction of sister chromatid exchange. In vivo studies yielded positive results for chromosome aberration, production of micronuclei and aneuploidy in bone marrow, which suggests that acrylamide is a mutagen characterized by direct action, however, it is most likely that it exerts the clastogenic effect, but not gene mutations. Acrylamide showed the mutagenic effect in male reproductive cells. Positive results were obtained for such effects as chromosome aberrations, production of micronuclei, sister chromatid exchange, unscheduled DNA synthesis, dominant lethal mutations and hereditary translocations. It is likely that metabolite glycidamide, which exerts mutagenic and genotoxic effects in both in vivo and in vitro studies, is responsible for the mutagenic effect of acrylamide. Acrylamide was found to show a carcinogenic effect in rats and mice. Animal chronic studies revealed an increased incidence of cancers of thyroid, testes, mammary glands, pancreas, heart, oral cavity and skin and maybe also of the central nervous system (CNS) in rats as well as cancers of the Harderian gland, lungs, mammary glands, ovaries and foreestomach in mice. Glicydamide, AA metabolite, showed a similar effect. Epidemiological studies of people occupationally and environmentally (diet) exposed to acrylamide have not provided explicit evidence of the relationship between AA exposure and cancer risk. Acrylamide has been classified into group 2A (the agent probably carcinogenic to humans) by the International Agency for Research on Cancer and to group B (genotoxic carcinogen, for which the existence of a threshold cannot be sufficiently supported at present) by the Scientific Committee on Occupational Exposure Limit (SCOEL). Animal studies have evidenced an adverse effect of acrylamide on male reproduction/fertility, including a reduced number of sperm cells, morphological changes in sperm, altered sexual behavior, dominant lethal mutations. An increased fetal resorption and decreased litter size (resulting from lethal mutations) were observed in the progeny of males exposed to acrylamide. No effect on reproduction was found in females. In the studies of developmental toxicity the majority of symptoms were observed after administration of AA doses responsible for inducing maternal toxicity. Acrylamide is well absorbed via inhalation and ingestion (up to 98% in rats and up to 44% in mice), less absorbed through the skin; specifically bound to red blood cells and spermatids and permeats through the placental barrier. Acrylamide is rapidly metabolized through conjugation to glutathione or CYP2E1-mediated oxidation. The latter metabolic pathway leads to the production of glycidamide (GA), an epoxy derivative. Both acrylamide and GA can bind to hemoglobin and/or DNA. Acrylamide and its metabolites are excreted in the urine. In humans 50% of an orally administered dose was excreted in the urine in 24 h. Excretion half-time is estimated at approximately 3 h. Hemoglobin adducts of acrylamide, glycidamide and urinary metabolites can serve as biomarkers of acrylamide exposure. The neurotoxic AA effect on humans has been adopted as the basis for the proposed MAC value of this compound. In workers occupationally exposed to acrylamide at the concentration exceeding 0.3 mg/m³numbness in palms and feet was observed more frequently than in those exposed to lower concentrations (below 0.3 mg/m³). To establish a MAC value of acrylamide from the value of NOAEL 0.1 mg/m³, one uncertainty coefficient, related to individual differences in human sensitivity, has been adopted. The qualitative extrapolation of results obtained from carcinogenicity studies in laboratory animals to humans is practically impossible since the development of cancers observed in rats is significantly influenced by species-specific factors. The calculated MAC value for acrylamide is 0.05 mg/m³. It should be stressed that in the European Union the binding occupational exposure level value (BOELV) is most important. In 2012 the Advisory Committee for Safety and Health at Work (ACSH) accepted a proposal on BOELV for acrylamide concentration within the range of 0.07 – 0.1 mg/m³. Also in Germany MAC for acrylamide was proposed at 0.07 for acceptable risk 4 . 10-4. Bearing in mind the aforesaid stipulations MAC of 0.07 mg/m³ for acrylamide has finally been proposed. On account of acrylamide absorption through the skin the standard value for the compound is labeled “Sk”. Studies of workers occupationally exposed to acrylamide showed explicitly a relationship between the level of acrylamide     adducts    with     hemoglobin   (N-(2- -carbamoylethyl)-valine, AA-Hb) and the occurrence of symptoms in the peripheral nervous system. For numbness/tingling in feet or legs (the most commonly observed symptoms) the NOAEL value has been set at 0.51 nmol AA-Hb/g globin. This value corresponds to AA concentration in the air of 0.1 mg/m³. This is a binding MAC value for acrylamide in Poland.  Concentrations of acrylamide adducts with hemoglobin have been adopted to estimate admissible value in the biological material for acrylamide in blood. In Germany two values have been adopted, BLW (biologischer leitwert, biological limit value) of 550 pmol AA-Val/g globin and BAR (biologischer arbeitsstoff-referenzetwert, biological reference value) of 50 pmol AA-Val/g globin. SCOEL adopted an initial BGV (biological guidance value) for the non-smoking general population, which was set at 80 pmol AA-Val/g globin. None of these values was comparable with MAC values for acrylamide in workplace air; neither SCOEL nor Germany established such values. In view of great variations in the concentration of acrylamide adducts with hemoglobin in the population non-occupationally exposed to acrylamide as well as the fact measuring hemoglobin adducts involves an invasive procedure that requires highly specialized equipment, the establishment of BEI for acrylamide has been abandoned.

Ethyl   tertiary-butyl    ether   (ETBE,   2-ethoxy-2-methylpropane, CAS: 637-92-3) is a colorless, flammable liquid with a characteristic odor, which is obtained in a reaction of isobutene with ethanol. ETBE is used in an amount up to 15% as an additive, which improves the oxidizing properties and the octane number of gasoline. In Poland, PKN ORLEN SA and LOTOS Group produce ETBE (more than 170000 tonnes per year). Exposure of workers (usually by inhalation) occurs during manufacturing of ETBE, blending gasolines, and its transport and distribution. There are no data on the number of people exposed to ETBE in Poland and the concentrations, to which they are exposed. ETBE is readily absorbed into the body by inhalation. Its elimination from the blood is a four-phase process (the first two phases are very fast, t1/2 = 2 and 18 min). ETBE is rapidly metabolized by oxidation involving cytochrome P-450 to tert-buthyl alcohol (TBA), 2-methyl-1,2-propanediol (MPD) and 2-hydroxybutyric acid (HBA). In the second phase of metabolism, TBA is coupled, mainly with glucuronic acid. Unchanged ETBE is excreted in the expired air (about 45 – 50% of the dose) or as TBA (about 3% of the dose). The metabolites (representing approximately 40 to 70% of the dose) in the urine are excreted. There is little data on the effect of ETBE in humans. In volunteers exposed to ETBE by inhalation at the concentration of 106 or 212 mg/m³ (25 or 50 ppm), the mucous membrane of the nose and upper respiratory tract were irritated. After exposure to ETBE at the concentration of 212 mg/m³ irritation and slight changes in the parameters defining the functions of the lungs were recorded.
After intragastric administration of ETBE to rats, LD50 values 2000 mg/kg of body weight were exceeded. The compound was irritant to the skin and eyes of rabbits. No allergic effect was noted (maximization test on guinea pigs). In short-term experiments on animals, regardless of the route of exposure (inhalation or intragastric), dose-related (600 – 1800 mg/kg/day for 14 days) or concentration (2090 – 16720 mg/m3 for 4 weeks) increases in the relative weight of the liver and kidneys, but without histopathological changes in these organs were reported. After subchronic inhala-tion of rats to ETBE at the concentrations 2090 – 20900 mg/m³, reduced body weight gain and an increase in the mass of the liver and kidneys were observed. In the kidneys of males, histopathological changes and disorders in the functioning of the kidneys caused by the accumulation of α2-microglobulin in proximal tubular cells were reported. ETBE at the concentrations 7315 – 20900 mg/m3 caused an increase in urea nitrogen  (BUN)  in  the  blood  of  rats. After  13-week exposure of rats to ETBE at the concentrations 2090 – 20900 mg/m³, effects of neurotoxicity were noted. On the basis of a two-year study, in which ETBE was administered to animals in drinking water, the LOAEL value (kidney damage in rats) was 625 ppm (625 μg/l of water). No genotoxic nor carcinogenic effects were noted. ACGIH classifies ETBE as group 4A. ETBE did not affect the fertility and reproductive in laboratory animals, and did not cause embryotoxicity and teratogenicity. The value of the maximum admissible concentration (MAC) for ETBE was based on the results of tests carried out on vol-unteers. After exposure to ETBE at the concentration of 212 mg/m3 (LOAEL), the irritation of the mucous membranes of the eyes, nose and upper respiratory tract and a slight dysfunction of the lungs were observed. The Expert Group for Chemicals Agents suggest a MAC-TWA value of 100 mg/m³. Due to the irritant potential of ETBE, a MAC-STEL value of 200 mg/m3 (2 x MAC-TWA) has been proposed. It has been also proposed to label the substance with "I" (irritant).

Lead (Pb, atomic weight 207.19) in inorganic compounds usually has the oxidation state II, but state IV also occurs.
Lead is a soft, silvery grey metal. In the Earth’s crust it is present in various minerals  such as sulfide, carbonate and sulfate. The metallurgy of lead consists of three separate operations: concentrating ,smelting and refining. Occupational lead exposure occurs in the wide variety of settings during primary and secondary lead smelting, working in non-ferrous foundries, production of electric storage batteries, as well as scraping and sanding lead paint. Exposure to lead, both in the occupational and environmental settings decreased significantly during last 20 years. In 2004-2005, in Poland, 3297 persons were exposed to lead in occupational settings in concentrations higher than the Polish OEL amounting to 0.050 μg/m³. In the occupational setting, inhalation is then most significant route of exposure to lead.  However, improvements in industry resulted in a reduction of lead concentrations in the air, making the gastrointestinal absorption increasingly important. Deposition and absorption of inhaled lead-containing particles are influenced by their size and solubility in water. About 30 – 50% of lead containing particles is deposited in the lungs. That which is not deposited in alveoli is cleared by the mucociliary  escalator and ingested. Only small fraction of ingested lead (about 10 %) in absorbed in adults. Under steady-state conditions, lead in blood is found primarily in the red blood cells  (99%). In human adults,  approximately 90%  of the total  body burden  is found in the bones. This compartment contains two different pools of lead with  different turnover rates, trabecular bone (23%) and cortical bone (69%). At the steady state conditions T1/2 of elimination of lead from blood amounts to about one month and from bones to 5 – 10 years. Most of the information on human exposure to lead , and the health effects resulting from it, is based on the lead in blood (B-Pb) levels. At  steady state B-Pb reflects a combination of recent lead exposure to that which occurred several years ago. The relationship of B-Pb to air lead (A-Pb) exposure concentrations is as the bridge between A-Pb and possible damage to health of workers.  The  relationship  varied  from  0.3  to 1.9 μg/L blood per μg Pb/m³air. In adults, the health effects of exposure to lead may include inhibition of  several enzymes involved in heme synthesis, influence on the functions of the kidney, peripheral and central nervous system, and an increase of blood pressure, which is a significant risk factor for cardiovascular diseases. The threshold for these effects in adults amounts to about 300 μg/L B-Pb.  The central nervous system is the main target organ for lead toxicity in children. There is no evidence of a threshold below which lead does not cause neurodevelopmental toxicity in children. Lead is carcinogenic in animal experiments, but there is only limited evidence for carcinogenicity in humans (IARC category 2A). Identifying of a blood lead level in workers that would be protective during a working lifetime was necessary for recommending a TLV, because B-Pb values, rather than A-Pb concentrations, were most strongly related to health effects. The recommended BEI of 300 μgL is designed to minimize the possible effects on the mentioned  above organs and systems in adults. Certain studies have reported effects at B-Pb below the proposed BEI value. However, the observed effects were transient, did not constitute a decrement in the worker’s functional  capacity, or was contradicted by other adequately conducted studied. If the steepest slope representing the relationship between B-Pb and A-Pb concentration in the workplace (1.9 μg/L of lead in blood per μg/m³ air) is used for judging the contribution of airborne concentrations to B-Pb  the proposed TLV-TWA of 0.050 mg/m³ would contribute an airborne, work-related fraction of B-Pb concentration of 95 μg/L.  Therefore contributions from community sources  and nonairborne workplace contamination  should be controllable such that the total B-Pb  concentrations could be kept below the BEI of 300 μg/L. For example in  Germany  geometric mean concentration of B-Pb in the general population amounted to 31 μg/L and 95% percentyles to 70 μg/L in women and 90 μg/L in men Thus, the persons responsible for occupational hygiene  must keep in mind that  B-Pb,  rather than A-Pb is the principal means for moniotoring lead exposure control.

A new procedure has been developed for determining 1,1-dichloroethene with gas chromatography with a flame ionisation detector. This method is based on the adsorption of 1,1-dichloroethene on active charcoal, desorption with carbon disulfide and chromatographic analysis of the obtained solution. The working range is 0.8 to 16.0 mg/m³ for a 12-L air sample. Limit of quantification: 11.1 µg/m³. The developed method of determining 1,1-dichloroethene has been recorded as an analytical procedure, which is available in the Appendix.