But-2-enal (crotonaldehyde) is a colourless liquid with a sharp odour. In commerce it is usually available as a mixture of Z (cis) and E (trans) isomers (with a predominance of an E isomer over 90%). Due to its easily recognizable and distinctive odour, but-2-enal was added to fuel gases as a marker to detect leakage and leakiness in transmission lines. Currently, but-2-enal is mainly used in the production of sorbic acid (trans, trans-2,4-hexadienoic acid), a food preservative.

According to the data of the Chief Sanitary Inspectorate, in Poland in the years 2013-2014, there were no workers exposed to but-2-enal in concentrations exceeding 0.1 TLV (Threshold Limit Value, TLV = 6 mg/m³), i.e. 0.6 mg/m³.

But-2-enal is well absorbed into the body by inhalation, through the skin and by ingestion. Because of the very sharp, irritating scent of but-2-enal, no cases of acute poisoning have been reported in humans. Volunteers and workers exposed to but-2-
-enal suffered from irritating effects on eyes and nasal mucosa. There are no available data on chronic exposure of but-2-enal in humans.

Acute toxicity of but-2-enal in experimental animals expressed in lethal dose mediators enable to classify this compound as toxic. It exhibits strong irritating effects on eyes, nasal mucous membranes and respiratory tract. There are no data on skin irritation and sensitization. In short-term and subchronic studies in mice and rats exposed intragastrically to but-2-enal for 13 weeks, predominant changes associated with the administration route were moted in the forestomach, including thickening of gastric mucosa with rickets (only in rats) and acute inflammation. Subchronic study (113 weeks) in rats, where but-2-enal was administered in drinking water (only at the lowest dose) resulted in tumours in liver and focal lesions in the liver cells. These effects have not been reported in rats exposed to two higher doses.

But-2-enal was not mutagenic in Ames tests, but was genotoxic, e.g., caused DNA adducts. Few data indicate that but-2-enal has harmful effects on germ cells. The compound is not classified by IARC in terms of carcinogenicity.

The major toxic effect of but-2-enal toxicity in humans and animals was a strong irritation to eyes and nasal mucosa. Irritation of respiratory tract in animals was also observed.

As a basis for calculating TLV for but-2-enal (mixture of isomers), and Z (cis) and E (trans) isomers, the low odour detection threshold (OT₅₀ » 0.20 mg/m³) was adopted. Moreover, results of study assessing respiratory rate in two mouse strains, where only slight differences in RD₅₀ was noted, was taken into account. One tenth of the value of 10.05 mg/m³ (3.5 ppm), i.e., 1 mg/m³, was used to determine the TLV. But-2-enal is strongly irritant, so the STEL (Short-Term Exposure Limit) value was proposed at 2 mg/m³. The reduction of valid values for but-2-enal (mixture of isomers) is also justified by the genotoxicity of the compound and possible carcinogenicity in experimental animals (which was due to the non-normative value of SCOEL and MAK). Norms are labelled with "skin" (absorption of the substance through the skin can be as important as exposure to the respiratory tract) and the letter "I" (irritant).

Hexafluoropropene (HFP) is a colorless gas. It is used mainly as a monomer for the production of thermoplastic fluoropolymers and as an extinguishing agent - heptafluoropropane. It has been classified for health hazards as a substance that is harmful if inhaled, may cause respiratory irritation and renal damage after a single exposure and through prolonged or repeated inhalation exposure.

Hexafluoropropene does not have Maximum Admissible Concentration (MAC) value in Poland. The reason for developing the documentation of proposal for MAC value was the production of hexafluoropropene in Poland. This substance was registered as an intermediate product in the European Chemicals Agency by the registrant (within the meaning of the REACH Regulation) sited in Tarnów.

There is lack of information on the toxic effects of occupational exposure to hexafluoropropene in humans. Degeneration and epithelial necrosis of the tubular lobules were observed in kidneys of laboratory animal after inhalation of hexafluoropropane. In the rodents exposed at higher concentrations of hexafluoropropene, pulmonary edema, coordination disorders and clonic contractions occurred. Exposure to hexafluoropropene induced changes in relative weight and activity of adrenal cortex, decrease in relative weight of spleen and changes in liver. Biochemical studies showed an increase of the level of fluoride ions and urinary lactate dehydrogenase activity and elevated serum creatinine and urea nitrogen in the exposed animals. Changes in blood parameters (count of lymphocytes, neutrophils and eosinophils) were also observed in rodents.

In studies with the long-term effects of toxicity, hexafluoropropene was not mutagenic in bacterial systems or mammalian cells. In the in vitro tests, the compound induced chromosome aberrations in Chinese hamster ovary cells. In in vivo studies in mice, the formation of micronuclei in bone marrow was observed. The negative result was obtained in the assay for unplanned DNA synthesis test in rat hepatocytes and in the dominant rat mutation assay. No effect of hexafluoropropene on fertility was observed. There is no data on carcinogenicity.

The mechanism of hexafluoropropene toxicity is related to metabolism: path-way of S-conjugation with glutathione, in particular hydrolysis of the conjugate. During decomposition of the conjugate by the enzyme b-lyase, active thiols appeared. Nephrotoxic activity of hexafluoropropene is associated with high levels of enzymes (β-lyases and N-deacetylases), which contribute to the formation of active thiols in renal tubules.

The results of 3-month inhalation study on mice and rats were the basis for calculation of the MAC value of the hexafluoropropene. The critical organs of hexafluoropropene toxicity to rodents are kidneys. Based on the NOAEC value of 62 mg/m³, the MAC value for hexafluoropropene at 8 mg/m³ was proposed. Neither short-term value (STEL) nor biological tolerance limit was established.

N-hydroxyurea is an organic chemical compound – N‑hydroxydiamide of carbonic acid. At room temperature, it is a solid and white crystalline powder (needle), odorless, water-soluble.

N-hydroxyurea is an antineoplastic drug registered for the treatment of patients with chronic myelogenous leukemia and sickle cell anemia, and idiopathic thrombocytopenia and polycythemia.

Occupational exposure to N-hydroxyurea occurs during manufacturing, packing, using on a daily basis in hospitals and in veterinary practice. There is no data on the number of people exposed to N-hydroxyurea in Poland.

N-hydroxyurea is completely absorbed from the gastrointestinal tract. After oral administration, the maximum plasma concentration is within 1 ÷ 4 h after ingestion.

LD₅₀ value after intragastric administration to rats is 5760 mg/kg and mice 7330 mg/kg. N‑hydroxyurea does not meet the classification criteria established in the European Union for acute toxicity after oral administration established.

IARC classifies N-hydroxycarbamide into group 3, i.e., substances that cannot be classified for human carcinogenicity.

Main effects of N-hydroxyurea in humans include systemic toxicity manifested by suppression of bone marrow at therapeutic doses (the lowest therapeutic dose is 15 mg/kg). The side effect of hydroxycarbamide is bone marrow suppression resulting in neutropenia, granulocytopenia, thrombocytopenia, leukopenia and increased bone marrow mass.

In laboratory animals treated with N- hydroxyurea at doses higher than clinical doses established for humans, cardiovascular disorders (e.g., heart rate changes, blood pressure and ECG changes), haemolysis and methemoglobinemia were observed. In subchronic and chronic studies in rats, a dose-dependent, weak or moderate bone marrow hypoplasia and pulmonary congestion were observed. Dose of 50 mg/kg is the NOAEL value for the effect of N-hydroxyurea on blood parameters in rats treated with aqueous solution for 10 days.

The hydroxyurea-induced genotoxic effects in humans have been observed in bone marrow cells in the form of chromosome aberrations of various types. Hydroxyurea-induced toxicity was confirmed in in vitro and in vivo studies in animal models.

The lowest NOAEL and LOAEL values are 150 mg/kg/day and of 300 mg/kg/day, respectively.

Periodic medical examinations did not show any irritations and allergies, hair loss, epidermal keratosis, renal and hepatic changes and psychoneurological changes at employees in the manufacture of hydroxyurea, which perform homogenisation/granulation of tablets mass and encapsulation of a drug. The measured mean N-hydroxyurea concentration in the worker's breathing zone was 0.34 mg/m³.

Currently, the EU recommends the harmonized classification of N-hydroxyurea according to PE and Council Regulation 1272/2008: reproductive toxicity, reproductive function, fertility and the development of offspring in category 1B (Repr. 1B). The classification of substances in category 1B is largely based on the results of animal studies. Substances have been assigned a risk phrase H360FD "May cause harm to the fetus or to the unborn child."

In Poland, the MAC values of N- hydroxyurea have not been established. Occupational exposure limits have been determined by some manufacturers at a level from 0.01 to 0.1 mg/m³. According to NIOSH and the international pharmacists' association, N‑hydroxyurea is classified as a dangerous drug for which the pharmaceutical industry is required to use a workplace hygiene standard of less than 0.01 mg/m³ (10 μg/m³).

The Group of Experts of Chemical Agents proposed the MAC value of N-hydroxyurea at the level of 0.1 mg/m³, i.e., at the level equivalent to 0.1% of the lowest recommended oral therapeutic dose. Following a discussion at the 86th meeting of the Interdepartmental Commission for MAC and MAI on July 5, 2017, the MAC value of 0.01 mg/m³ was accepted and submitted to the minister responsible for labor, since the low dose of compound was genotoxic, teratogenic, toxic for reproduction and developmental toxicity. There is no basis for determining the STEL value and the limit value in biological material (BEI).

Quantitative data on N-hydroxycarbamide absorption by skin were not found, but due to its low molecular weight (76.06) and unlimited water solubility, there is a potential for penetration of the substance through the skin. Skin contact is considered to be the most important risk factor for medical personnel exposed to cytostatics. Labeling the substance with the notation "skin" has been recommended - skin absorption can be as important as exposure to the respiratory tract. The substance was also marked with letters: "I" – irritant and "Ft" – substance harmful to a fetus.

Urea is a non-flammable, colorless or white crystalline solid. It has a faint aroma of ammonia and a cooling, saline taste. It is hygroscopic and highly soluble in water. During long-term storage and in aqueous solutions urea partly decomposes with the release of ammonia and carbon dioxide.

Urea is used as a component of fertilizer and animal feed; raw material for production of plastics, flame-proofing agents, adhesives, medicines, cosmetics and household products; reductant in selective catalytic reduction (SCR) systems used to reduce NOx emissions from stationary and mobile sources; deicing compound on roads, railroad tracks and airport runways; in the food industry as an additive in bakery products, alcoholic beverages and gelatine-based products and as a reagent in laboratories.

In 2012, world production of urea was estimated to be around 184 million tonnes and is predicted to increase further. In the European Chemicals Agency, urea was registered by 5 companies from Poland. The number of workers exposed to urea in 2 of these plants is 201.

Urea is an endogenous product, formed in a liver in the urea cycle from ammonia formed by the catabolism of amino acids and proteins, later is excreted by kidneys. An adult man excretes about 20 ÷ 35 g of urea in a urine during a day. Most of the information on the effects of urea in humans comes from patients with renal insufficiency who have elevated urea levels. Adverse effects of urea include headache, nausea, vomiting, syncope, confusion, electrolyte abnormalities in the blood. Urea has a slight irritating effect on the eyes and does not irritate skin. At concentrations above 10% urea has a keratolytic effect – it facilitates peeling and increases the permeability of the stratum corneum, thereby increasing the therapeutic activity of many topical medications.

Based on animal studies urea has low acute and chronic toxicity and no carcinogenic or reproductive toxicity. Urea does not meet the classification criteria as a CLP hazardous substance.

Due to very low vapor pressure, exposure is possible to urea dust only. Therefore, to protect workers from nuisance of particulate matter (dust) of urea, the MAC (TWA) value of 10 mg/m³ was recommended as for other dusts not classified for toxicity but posing a hazard for visibility reasons. There is no basis for determining the short-term exposurelimit value (STEL) and the biological exposure index value (BEI).

Ceramic fibers include a group of an amorphous or crystalline mineral fibers with flame retardant properties (i.e., high temperature stability). Ceramic fibers are produced from metal oxides (e.g., aluminum, silicon) or from non-oxide materials such as silicon carbide. Fibers produced for special purposes may contain such elements as zirconium, thorium, magnesium, beryllium, titanium, hafnium, yttrium and other additives such as potassium titanate. Ceramic fibers are characterized by high thermal resistance - the maximum application temperature is 1650 °C. Moreover, they have good electrical, acoustic and thermal insulating properties, and relatively high chemical resistance. Because of their properties, they are used as substitutes for asbestos in the production of insulating, sealing and filtering materials. Demand for ceramic fiber is very large and varied.

Ceramic mineral fibers enter the body almost exclusively through the respiratory tract. Based on the results of epidemiological studies of relatively large population exposed to ceramic fibers it have been demonstrated that they can be irritating to the skin and conjunctiva, and cause focal pleural fibrosis. Lung function impairment (reduction of FEV₁ and FVC) was also observed, but almost exclusively among smokers. Epidemiological studies have failed to provide convincing evidence of an increased risk of cancer associated with these fibers due to relatively short exposure period (since the production of this type of industrial fibers began in the early 1980s), and the fact that a significant proportion of workers in this industry were previously exposed to asbestos.

Experimental results in laboratory animals (rats and hamsters) exposed to ceramic fibers by inhalation or after their insertion into trachea indicate that certain ceramic mineral fibers can cause lung tumors (adenomas and cancers) and pleural tumors (mesothelioma). In some studies number of tumor cases was related to fiber concentration (or dose) or exposure time. Some types of fibers inserted directly into a body cavity (pleural cavity or tummy) caused mesothelial tumors – mesothelioma. Based on existing experimental data, it is not possible to quantify the carcinogenicity of ceramic fibers. The study on solubility of fibers in synthetic body fluids did not provide convincing evidence that poorly soluble fibers have a stronger carcinogenic effect, although theoretical considerations seem to indicate this.

In the opinion of the experts of the International Agency for Research on Cancer (IARC) there are sufficiently documented results of animal test indicating carcinogenic effect of ceramic fibers. Although, there are no data on the carcinogenic effect of ceramic fibers on humans, IARC classified them as a possible carcinogen in humans (group 2.B).

On the other hand, European Union experts classified refractory ceramic fibers for special purposes, called more specifically as synthetic silicates, without specific orientation with alkali and alkaline earth metal oxides (Na₂O + K₂O + CaO + MgO + BaO) of less than or equal to 18% wt. to carcinogens category 2, that is substances considered to be carcinogenic to humans, with assigned hazard statement H350i  "can cause cancer after respiratory exposure". The same classification applies in Poland under the provisions of Regulation (EC) No 1272/2008 of the European Parliament and Council.

The relationship between the level of exposure and the increased incidence of such symptoms as dyspnea, wheezing, chronic cough, decreased lung function, skin irritation, ocular and upper respiratory tract infections have been demonstrated by epidemiological studies conducted in Europe and the United States until 1980. Subsequent studies from years 1980–2004 indicate that occupational exposure of workers from the late 1980s had no harmful effects on lung function, no pleural plaques or cancer changes. The first lung function tests conducted in the US cohort showed statistically significant reductions in FVC and FEV₁ among the most exposed workers (> 60 fib./cm³ ž month) compared to the least exposed group (< 15 fib./cm³ ž month). However, in a following study, no significant decrease in lung function was observed in the study group in a 7-year period. Based on the estimated average cumulative concentrations in the most vulnerable workers and in the 60-year-old group, TWAs were estimated at 0.27 fib./cm³ and 0.34 fib./cm³. Given these values and no obvious side effects in these levels, the SCOEL proposed a limit value for refractory ceramic fibers at the level of 0.3 fib./cm³.

The authors of the documentation proposed the adoption of the highest concentration limit value (NDS) in Poland as it was proposed by SCOEL at 0.3 fib./cm³, but this value applies to fibers classified as carcinogenic category 1.B, in accordance with the CLP regulation, whose average geometric mean length-weighted fiber diameter reduced by two standard geometric errors is less than 6 μm. Compliance of this concentration should protect workers exposed to refractory ceramic fibers from its harmful effects.

Yttrium is a soft and a malleable metal. It is used in the metallurgical industry as a component of alloys, in electronics for manufacturing lamps and semiconductors, in the construction of reactors in nuclear technology and in the production of ceramic, laser and refractories. Radioactive yttrium is used in medicine.

Exposure limit values for yttrium and its compounds in the working environment, based on yttrium, are NDS – 1 mg/m^3.

The aim of the study was to amend the method for determining concentrations of yttrium and its compounds in workplace air in the range from 1/10 to 2 NDS values, in accordance with the requirements of Standard No. EN 482.

The developed method involves collection of yttrium and its compounds contained in the air on a membrane filter, filter mineralization with concentrated nitric acid (V) and chloric acid (VII), and the determination of yttrium in the solution prepared for analysis with atomic absorption spectrometry with flame atomization nitrous oxide-acetylene (F-AAS).

This method enables determination of yttrium in concentration range from 5.00 to 150.00 µg/ml. The obtained calibration curve yttrium has a correlation coefficient R² = 0.9999. The detection limit of yttrium (LOD) is 0.08 µg/ml, the limit of quantification (LOQ) is 0.25 µg/ml and a coefficient of recovery is 1.00.

The developed method enables determination of yttrium and its compounds in workplace air in the concentration range of 0.07 ÷ 2.08 mg/m³ (for a 720-L air sample), which represents 0.07 ÷ 2.1 of NDS. The method of determining yttrium and its inorganic compounds has been recorded as an analytical procedure (appendix).