Pyridine, a colorless liquid with a characteristic unpleasant odor, has been categorized as a highly flammable and harmful substance. It exerts harm-ful effects if inhaled, swallowed or absorbed through the skin.
Pyridine is used as a solvent in paints, rubber, pharmaceuticals, polycarbonate resins and textile fabric impregnating agents. Its large quantities are applied as a precursor in the production of pyridine derivatives, piperidine, pesticides, pharmaceuticals and other products.
Occupational exposure to pyridine may occur during its production, further processing and distribution, as well as during the process of pyridine release, yielding coal and tar breakdown products or pyridine-containing products.
In  the  second  half  of  the  20th  century  pyridine  air
concentration in the occupational environment ranged from 0.002 to about 20 mg/m³.
Based on the results of rather rare epidemiological studies no excess mortality among workers ex-posed to pyridine in three British plants was found in 1961–1983.
The studies of acute toxic effect of pyridine carried out on laboratory animals (rats, mice, guinea pigs, rabbits and dogs) have evidenced that pyridine is a harmful (Xn) compound. Pyridine induces mild irritation effects on the rabbit skin, but it does not generate dermal allergy in guinea pigs.
The studies of sub-chronic and chronic effects of pyridine, administered (per os or in drinking water) in different doses have revealed decreased body mass gain, liver and kidney damage  and reproductive disorders in laboratory animals.
Pyridine does not show mutagenic effects.  Based on the results of studies on rats and mice, per-formed under the NTP program, the absence of clear-cut evidence that pyridine exerts car-cinogenic effect on rats has been claimed, however, carcinogenic effect of pyridine on mice has been evidenced. The International Agency for Research on cancer has categorized pyridine with respect to its potential carcinogenic risk to group 3 as not classifiable as to its carcinogenicity to humans.
CNS  depression  observed  in  humans after repeated
exposure to pyridine, as well as the damage to liver and kidneys, the earliest symptoms of its toxic effect on rodents, are recognized as critical effects of this compound.
The LOAEL value of 7 mg/kg of body weight for pyridine corresponds with pyridine air concentration of 49 mg/m³ (15 ppm), providing that an adult person of 70 kg body weight inhales 10 m3 of the air during an 8-hour work shift.  After applying coefficients of uncertainty (total value, 8), the MAC value for pyridine was estimated at 6.13 mg/m³.
In the EU, the OEL value for pyridine has not been set, however, maintaining its air concentration below 5 ppm (16 mg/m³) is recommended.  The established pyridine MAC value  of 6.13 mg/m³ not only  meets this criterion but it is also close to the MAC value (5 mg/m³) for pyridine binding in Poland.
The authors of the documentation have suggested to keep the MAC value for pyridine at 5 mg/m³,  since according to the Chief Sanitary Inspectorate data for 2010–2011 in Poland there were no workers exposed to pyridine at concentrations exceed-ing 0.5 of the MAC value (2.5 mg/m³). The compound was labelled with “Sk” indicating dermal absorption of the substance.
There are no grounds for defining the maximum admissible short-term exposure level (STEL) for this compound. Therefore, it has been suggested to eliminate this value from the list of MAC values. The adherence to MAC value for pyridine of  5 mg/m³ should protect workers against harmful effects of pyridine on the CNS observed after exposure to its concentrations of 19 – 42 mg/m³.

Calcium hydroxide (Ca(OH)2), commonly known as slaked lime, is used to clean beet juice in the sugar industry, as a water softener, in fertilizer production and in flue gas desulphurisation in power. The term slaked lime (slaked lime) corresponds to an aqueous slurry of calcium hydroxide known as milk of lime. The aqueous slurry is used in chemical processes for painting and as a component of mortar. Hydrated lime, or dry powdered calcium hydroxide, is used to manufacture sodium carbonate by Solvay (Soda Ash), in deacidification of soils, disinfection, in bleach-ing households, farm buildings and tree trunks. Calcium hydroxide is an HPV substance. Calcium hydroxide is considered as a strong base, completely ionized in solution. Compared with the strong inorganic base, it has a similar effect, but 2.5-fold weaker. Mixtures of aqueous calcium hydroxide  are  strongly  alkaline  and   its  pH  is,  
depending  on the concentration, 12–13. Calcium hydroxide is corrosive after ingestion, especially in the esophagus and the stomach and causes redness, blisters and sores at the contact with the skin. Occupational exposure of workers to calcium hydroxide dusts takes place during the comminution of the substance, but also as a result of exposure to calcium oxide, which in humidity reacts with water to form calcium hydroxide. Particles of calcium hydroxide in humans are irritating to the eyes, upper respiratory tract and skin. In the available literature, there are no data about dose-response in humans and animals for calcium hydroxide. Given the similarities in the action of the oxide and calcium hydroxide, it was proposed to maintain the current value of TWA for inhalable fraction of calcium hydroxide 2 mg/m³ and adopt STEL of 6 mg/m³, and for respirable fraction of 1 mg/m³for TWA and STEL of 4 mg/m³.

The influence of a low frequency magnetic field causes biophysical effects in the human body, which may trigger the response of nervous cells, in both the central and peripheral nervous systems, such as magnetophospfenes or peripheral nervous excitation. This phenomenon determines the structure of requirements regarding the protection of workers against acute effects of the influence of a magnetic field of a frequency not exceeding a few hundreds of kilohertz.
Based on the results of numerical simulations of the relation between internal measures (measures of the electric field induced in the human body) and external measures (measures of the magnetic flux density of the field affecting workers) of the exposure to a low frequency magnetic field, the rules were worked out regarding assessment of hazards linked with electrodynamic interaction be-tween a worker’s body and a magnetic field of a frequency from the range 1–10000 Hz. Guide-lines on the assessment of hazards caused by the influence of sinusoidal time-varying and homogeneous in the work space magnetic field, which were published by International Commission on Non-Ionizing Radiation Protection (ICNIRP), have been used in developing the rules. The characteristics of exposure to the magnetic field in a real work-place, where fields are both spatially heterogeneous and non-sinusoidally timevarying, have been considered, as well technical conditions of performing such investigations. The proposal for rules on assessing exposure defines, among others, internal measures of exposure to a magnetic field, external measures applicable for exposure to a spatially homogeneous and/or heterogeneous magnetic field regarding the domain of workplace space, external measures regarding the time domain applicable for exposure to a harmonic or non-harmonic magnetic field, and exposure assessment criteria regarding individual sections of the human body (head, trunk and limbs). However, the rules for exposure as-sessment this article presents are not a legislative proposal in this field, but referring the outcome of research they are contributing to a discussion on the need and possible range of modifications of requirements of labour law in Poland, related to the coming  process  of  formal  implementation of the requirements of European Directive 2013/35/EU, which established the minimum requirements regarding the protection of workers against risks caused by the exposure to electro-magnetic fields in the workplace.

1,1-Dichloroethene (vinylidene chloride) is a low temperature boiling liquid with a sweet scent. 1,1-Dichloroethene is used as a chemical intermediate (usually with vinyl chloride) in the production of thermoplastic resins, lacquers, fibres for safety clothes, etc. In human, acute toxicity of 1,1-dichloroethene at concentration of ca. 16 000 mg/m³ was observed as a CNS depression (stunning and loss of consciousness). After acute inhalation or oral administration of 1,1-dichloroethene to laboratory animals some reversed adverse effects were observed in liver, kidneys and Clara cells. 1,1-Dichloroethene was mutagenic in Salmonella Typhimurium and  Escherichia coli only due to metabolic activation. IARC concluded that there was inadequate evidence in humans and limited evidence in laboratory animals of the carcinogenicity of 1,1-dichlo-roethene. This substance is not classifiable as to its carcinogenicity to humans (IARC Group 3). Results of a 17-month inhalation study in rats exposed to 1,1-dichloroethene concentration of 100 or 300 mg/m3 were considered in setting a maximum admissible concentration (MAC) value. Reversible fatty infiltration of the liver was reported in rats but no hematological alternations, no change in liver weight and no other indications of abnormal liver function were observed. Based on the LOAEC value for female rats (100 mg/m3) and the relevant uncertainty factors, a MAC value of 8 mg/m³ has been calculated. No STEL nor BEI value has been established.

Acetic acid is an organic compound from the group of carboxylic acids. It is a colorless, flam-mable, volatile liquid with a pungent odor. Acetic acid is used in organic synthesis in producing artificial silk, drugs (aspirin, antibacterials, antibiotics), film tape, synthetic fibers (carboxymethyl cellulose, cellulose acetate, PET bottles and as a descaler. In the form of a weak solution (acetic acid fermentation product), it is used as vinegar for preserving food and agricultural harvest. Acetic acid is registered as a non-selective contact herbicide. It is an HPV substance.
The main toxic effect of acetic acid vapor is irritating to the mucous membranes of the nose, eyes and skin. There have been reports of acute poisoning with acetic acid in humans following ingestion of acid by mistake or in suicides, and topical application of the acid to the skin for medicinal purposes, as a compress. Doses of 20-50 g or 60-70 ml of concentrated acetic acid are considered to be fatal to humans. After ingestion or upon contact with concentrated acetic acid, there are burns, necrosis, circulatory collapse, oliguria, hemolysis and hemoglobinuria, and anuria.
In animal studies, there is no NOAEL for irritant vapors of acetic acid. The concentration of acetic acid, resulting in a reduction of 50% (RD50) in respiratory rate in mice, is 408 mg/m³ (163 ppm)   560 mg/m³(227 ppm).
The  odor  threshold  of  acetic  acid  (OTH)  of 1.5 mg/m³ (0.6 ppm) and the lateralization limit ba-sed on the stimulation of the trigeminal nerve endings (LTH) of 100 mg/m³(40 ppm) have been set.
Studies in volunteers have shown that acetic acid in a concentration of 25 mg/m3 (10 ppm) does not cause any changes in the studied parameters. Only subjective feelings of acid odor perception have been reported. The effects of exposure in volunteers indicating sensory irritation of the trigeminal nerve, such as eye irritation, did not differ significantly at this concentration from the effects in a control group that was exposed to a vapor of acetic acid odor sensing threshold level, i.e. 1.5 mg/m³ (0.6 ppm). Acetic acid concentration of 25 mg/m³ (10 ppm) also had no effect on the frequency of blinking, the increase in airway resistance and concentration of the inflammatory mediators in the nasal lavage fluid.
It is proposed to establish the limit values of acetic acid taken as NOAEC value of 25 mg/m³ (10 ppm) determined in tests on volunteers. After applying appropriate uncertainty factors, it was suggested to adopt the concentration of 25 mg/m³ as the maximum admissible concentration (MAC-TWA) for this compound. It has been also recommended the short-term exposure limit (STEL) of 50 mg/m³. In addition, marking with the letter "C" (corrosive) is proposed.

At room temperature trinitrate(V)-propane-1,2,3-triyl (nitroglycerin, TNG) is an oily, colorless to pale yellow liquid with sweet, burning taste. It is classified as a highly toxic explosive substance. It shows very toxic effects by inhalation, in contact with skin and if swallowed.
Nitroglycerin  is a substance used in the manufacture of dynamite and other explosive materials as well as an active ingredient of rocket propellant. Nitroglycerin is also used medically as one of the most useful drug for treating angina pectoris, congestive heart failure (especially in acute myocardial infarction) and hypertension.
In industrial conditions inhalation of vapors via airways and contact with the skin are the potential routes of exposure to this compound.
Data on human exposure indicate that dilation of blood vessels is a critical effect of exposure to nitroglycerin. It is also the major pharmacological effect of TNG used as medication.
Headache, pressure fall and nausea are the symptoms of TNG effects, resulting from the dilation of blood vessels. In occupational expo-sure these symptoms have been observed in workers exposed to nitroglycerin in concentrations of 0.3 ÷ 4.0 mg/m³. Similar symptoms have been noted in people after dermal exposure to TNG (patches releasing 5 mg of nitroglycerin). The dose absorbed corresponds to TNG air concentration of 0.5 mg/m³  (assuming that the lung ventilation is equal to 10 m³ during an 8-hour shift). Higher concentrations could induce depression, methemoglobinemia and cyanosis.
There are no reliable data on the increased human risk of coronary and cerebrovascular diseases induced by nitroglycerin. The results of the studies performed are conflicting and  the results of some cohort studies even suggest that  the incidence of these diseases is generated by ethylene glycol dinitrate (EGDN).
There is also lack of data on repeated exposure of experimental animals to nitroglycerin via inhalation.  In animals methemoglobinemia and toxic effects on the liver and testes were observed after intragastric administration of TNG in high doses. Studies on rats and dogs helped determine the value of no observed adverse effect level (NOAEL) for nitroglycerin in the range of doses 25 ÷ 40 mg/kg/day for the systemic effect of the compound, including reproductive toxicity, which corresponded to much higher TNG concentrations in the air than concentrations inducing toxic effects in humans.
The results of the in vitro study of the mutagenic effect of nitroglycerin have not evidenced   strong or even slight mutagenic effect of this substance.  All in vitro studies of the  TNG mutagenic effect produced negative results.
The International Agency for Research on Cancer (IARC) has not classified nitroglycerin as to its carcinogenicity to humans. In Germany TNG has been categorized into group 3B as to its carcinogenicity, whereas the Scientific Committee on Occupational Exposure Limits (SCOEL) has classified it as carcinogenic compound of group C – a genotoxic carcinogen for which it is possible to set the admissible practical value on the basis of existing data.
There are no data concerning the effect of nitro-glycerin on the human reproductive system. In  a three-generation reproductive toxicity study carried out on rats, the Fo generation showed no effect of TNG on the reproduction of these animals. Major disorders in reproduction were observed in the F1 group administered the highest dose of nitroglycerin, which was associated with the inhibition of spermatogenesis and significant decrease in the mass of testes. Other studies did not reveal any effect of TNG on reproduction. In Germany nitroglycerin has been categorized in group C – a substance not expected to damage embryos and fetuses if the MAC value is strictly observed.
Nitroglycerin enters the body through airways and skin. The capacity of absorption through the skin in humans accounts for 68 ÷ 76% . There are no data concerning nitroglycerin absorption in airways.
The results of the studies on workers showing no adverse effects after exposure to nitroglycerin in concentrations below 0.095 mg/m³ (0.01 ppm) have been suggested as the basis for setting MAC value for this compound  (Hanlon, Fredrick, 1966).
It has been suggested to adopt TNG concentra-tion of 0.095 mg/m³ (0.01 ppm) as the MAC value. In this case the determination of uncertainty coefficients was not necessary since this value was derived directly from the study out-come in workers occupationally exposed to nitroglycerin.
It has also been suggested to adopt the concentration of 0.19 mg/m³ (0.02 ppm) as the short-term exposure limit (STEL) value since irritation effect has been observed in workers exposed to nitroglycerin in concentrations equal to or higher than 0.3 mg/m³ of this compound (Hanlon, Fredrick, 1966).
In the concomitant presence of nitroglycerin and ethylene glycol dinitrate – a compound of the same mechanism of action, it is essential to consider the sum of  quotients of weighted average concentrations of both compounds relevant to the MAC value that must not exceed the value equal to 1.
It has been suggested to label the compound with “Sk” indicating dermal absorption of the substance since nitroglycerin shows very high capacity for absorption through the skin and induces systemic symptoms.  There are no data that allows to determine TNG maximum concentration in biological material.