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Preventing exposure to ultrasonic noise in the work environment
Bożena Smagowska
This article discusses physical traits of ultrasonic noise, their influence on the human body during exposure in the work environment. However, the literature on this subject is limited. The article presents prevention activities for workersʼ protection against the effects of exposure to ultrasonic noise in the work environment.
It describes a method of assessing occupational risk resulting from exposure to ultrasonic noise at workstations as well as general technical, organizational and medical methods of reducing occupational exposure.
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Bromoethene. Documentation
Andrzej Sapota, Małgorzata Skrzypińska-Gawrysiak
Bromoethene (vinyl bromide,VB) is a colorless, flammable gas with a characteristic pungent odor. It is used as a transient compound in organic synthesis, and also in the production of polymers, copolymers, flame retardants, pharmaceutics and fumigants.
Occupational exposure to bromoethene may occur in production processes, processing and finishing. Because of its low boiling point (15.8 oC), bromoethene has the form of a gas in the occupational environment, and thus inhalation is the major route of exposure. In Poland, 100 workers involved in organic and polymer syntheses, as well as in the manufacturing of pharmaceutics and fumigants are exposed to this compound.
In the available literature, there are no data concerning toxic effects of bromoethene in humans.
In laboratory animals, high concentrations of bromoethene have an acute hepatoxic effect and a depressant effect on the central nervous system. It has been reported that chronic exposure of rats to a low concentration of 44 mg/m³ (10 ppm) induces hemangiosarcoma of the liver.
Bromoethene is an analog of vinyl chloride, a well documented human carcinogen. The carcinogenic effect of bromoethene is generated by its metabolism to 2-bromoethylene oxide that produces cyclic etheno adducts with DNA. Toxicokinetic data show that the carcinogenic potential of this compound within the range of low concentrations is about threefold higher than that of vinyl chloride.
As there are no data with evidence that bromo-ethene is carcinogenic to humans, in Poland this compound is categorized into group 2, and according to the International Agency for Research on Cancer (IARC) into group 2A – probably carcinogenic to humans.
A quantitative assessment of the carcinogenic effect of bromoethene, based on data on the incidence of hemangiosarcoma of the liver in rats exposed to this compound in concentrations of 44–1100 mg/m³, was adopted as the basis for calculating the MAC value. The concentration of bromoethene was calculated with the relationship between the concentration of bromoethene in the ambient air of the occupational environment and the probability of the development of hemangiosarcoma after 40-year occupational exposure.
A MAC value of 0.4 mg/m³ is suggested; it corresponds to the additional risk of hemangiosarcoma of 0.001. In population terms, this means that hemangiosarcoma of the liver may develop in one person per 1000 people exposed to bromoethene of 0.4 mg/m³ for 40 years.
There are no grounds for setting the value of short-term maximum admissible concentration or the value of maximum concentration in the biological material for bromoethene.
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Benzoyl chloride. Documentation
Andrzej Sapota, Małgorzata Skrzypińska-Gawrysiak
Benzoyl chloride is a colorless liquid with a characteristic pungent odor classified as a corrosive substance. Benzoyl chlorite is produced in high tonnages. In 1995 it was produced in 11 countries. There is no information on its production in Poland. Benzoyl chloride is used in the production of benzoyl peroxide and dyes, as well as in the acylation of alcohols, phenols and amines, and also as an analytical reagent.
Vapors of benzoyl chloride exert strong irritating effects on the eyes and mucous membranes. Exposure to benzoyl chloride at a concentration of 11.5 mg/m³ (2 ppm) for 1 min is not tolerable to humans. Epidemiological studies of workers employed in the production of chlorinated toluenes and benzoyl chloride have revealed excess mortality from lung cancer in this group of workers. These production processes involve
a combined exposure to a number of chemical compounds, mainly to benzotrichloride thought to be a carcinogenic compound.
Benzoyl chloride showed irritating effects on ocular and nasal mucous membranes and induced pulmonary emphysema in rats exposed to this compound via inhalation. Its irritating and corrosive effects on the skin and corrosive effect on the eye were also observed in rabbits. Most in vitro and in vivo studies have not reveal mutagenic effects of benzoyl chloride. The carcinogenic effect of benzoyl chloride has been investigated in animals after inhalation exposure and skin application, yet no significant increase in the incidence of lung and skin cancers, compared with the control group, has been observed. According to the International Agency for Research on Cancer (IARC) there is limited evidence that benzoyl chloride is carcinogenic in humans; there is insufficient evidence in laboratory animals. In the general assessment IARC has found that the combined exposure to α-chlorinated toluenes and benzoyl chloride is probably carcinogenic to humans (group 2A). Benzoyl chloride has been not classifiable as a human carcinogen by the American Conference of Governmental Industrial Hygienists (ACGIH) (group 4A). No data are available to assess the effect of benzoyl chloride on reproduction and developmental toxicity in humans or animals. Irritation of the eyes and mucous membranes in the upper respiratory tract has been recognized as a critical effect of benzoyl chloride.
The finding reported by ACGIH that exposure to benzoyl chloride already in a concentration of 11.5 mg/m³ (2 pmm) for 1 min is not tolerable to humans has been adopted as the basis for calculating the MAC value for this substance. The concentration of 11.5 mg/m³ has been recognized as the LOAEL value. Using uncertainty coefficients at the total value of 4, the MAC value of 2.8 mg/m³ was obtained. Owing to the fact that benzoyl chloride exerts a strong irritating effect on the respiratory system, it has been suggested to adopt the value of the maximum admissible ceiling concentration (TLV-ceiling) equal to 2.8 mg/m³ instead of a MAC value. The proposed TLV-ceiling value should protect workers from potential irritating and systemic effects of benzoyl chloride. Standard was denoted “C”, substance with corrosive effect.
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1,2-Dibromoethane. Documentation
Anna Świdwińska-Gajewska, Sławomir Czerczak
1,2-Dibromoethane (DEB) is a colorless liquid with a sweet odor similar to chloroform. It is classified as a carcinogen category 2, which is toxic by inhalation, in contact with skin and if swallowed. It is irritating to the eyes, respiratory system and skin, and is dangerous to the environment.
1,2-Dibromoethane is obtained by bromination of ethylene, and in the reaction of acetylene with hydrobromic acid. The chemical was used to removing lead, as a pesticide and as a fumigant for fumigation of soil and grain. Now it is used as an intermediate product in chemical synthesis, and as a solvent for resin, rubber and wax.
Data collected by The Central Register of Data on Exposure to Substances, Preparations, Agents or Processes with Carcinogenic or Mutagenic Activity shows that in Poland exposure to 1,2-dibromoethane occurs mainly in laboratory workers at universities and chemical plants. In 2010, 336 people were recorded as exposed to this chemical in 10 plants. The Central Register has no information about the severity of the exposure (IMP 2011).
According to the Chief Sanitary Inspectorate, in 2010, no workers were exposed to 1,2-dibromoethane at a concentration above the maximum admissible concentration (MAC) of 0.5 mg/m³ (GIS 2010).
The first symptoms of poisoning in humans are gastrointestinal, followed by jaundice, liver and kidney damage, and inhibition of central nervous system. Inhalation exposure can result in inflammation and severe damage to the lungs.
In animals, exposure to 1,2-dibromoethane primarily produces changes in the respiratory tract (nasal cavity, trachea and lungs), and also in the liver, kidneys, adrenal gland and testes. The compound shows mutagenic and genotoxic activity, which numerous in vitro and in vivo tests on bacteria and animal cells have confirmed.
1,2-Dibromoethane can affect reproduction. A change in the quality of the semen was noted in workers exposed to 1,2-dibromoethane. In animals, this compound affects not only the spermatogenesis, but also the estrous cycle. Signs of embryotoxic and teratogenic activity of the compound were also observed in rats and mice.
Carcinogenicity of 1,2-dibromoethane in animals has been confirmed in numerous experiments, during which the animals were exposed to the substance in different ways. When given intragastrically, 1,2-dibromoethane caused cancer of the forestomach, lungs and circulatory system. Inhalation exposure to the compound resulted in tumors of the nasal cavity, lungs and circulatory system, while dermal exposure resulted in tumors of the skin and lungs.
1,2-Dibromoethane is metabolized in the body in the oxidative pathway by cytochrome P450 or by conjugation via glutathione S-transferase. The metabolites appear to be largely responsible for the toxic and carcinogenic effects of this compound, mainly by covalent binding to nucleic acids and proteins.
The carcinogenic effect of inhalation exposure of mice and rats has been accepted as the basis for establishing MAC values. The MAC value of 0.6 (mg/m³)-1 has been calculated on the basis of the individual risk estimated by the experts of the EPA. A decrease in the current MAC value of 1,2-dibromoethane from 0.5 to 0.01 mg/m³ has been suggested. It does not seem reasonable to establish a maximum short-term exposure limit (STEL), or the biological exposure index (BEI) for 1,2-dibromoethane. At the same time, maintaining current 1,2-dibromoethane notations Carc. Cat. 2, Ft, I and Sk is suggested.
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Pentabromodiphenyl ether. Documentation
Jadwiga A. Szymańska, Elżbieta Bruchajzer
Pentabromodiphenyl ether (pentaBDE) is an amber colour, transparent liquid, which occurs at room temperature in a semi-liquid form. This compound is obtained by bromination of diphenyl ether. The most common form in which pentabromodiphenyl ethers occurred, were the technical (commercial) mixtures. These consisted of compounds of varying degrees of brominated. The substance is listed as a priority to develop the limit values by SCOEL.
Pentabromodiphenyl ether is use as a flame retardant. Frequently used it in the production of flexible polyurethane foams: the production of furniture, automotive and aerospace industries. It also added to phenolic and epoxy resins, unsaturated polyesters, fabrics and materials used in electric cables.
Pentabromodiphenyl ether, due to their physicochemical properties (such as a weak water solubility, thermal and chemical stability) and the ability to accumulate and biomagnification in the food chain, belongs to POPs (persistent organic pollutants).
Pentabromodiphenyl ether has been found in the environment as a result of the use and recycling of the equipment containing this compound. The concentration of 0.0026 mg/m³ in the air was detected in the hall where computer equipment were dismantled.
So far, there have been no cases of poisoning people.
Pentabromodiphenyl ether in experiments on animals showed low acute toxicity. The mean lethal dose (LD50) for rats after oral administration ranged 2650-7400 mg/kg body weight. In rats were observed: decrease in motor activity, lethargy, muscle tremors, severe gastrointestinal motility and diarrhea. Similar toxic effects were observed in animals, both in the short-term experiments, and after repeated dosing. The most important changes were observed in the liver, and in functional of endocrine and nervous system. The first symptoms of this type (increase of the relative liver weight and induction of the microsomal enzymes in the liver) were found after a single administration of the compound in rats only after the dose of 300 mg/kg and in mice – at the dose of 100 mg/kg. The adverse effect of the compound on thyroid function was observed in mice after single dose administration of 4 mg/kg.
In short-term exposure (4-14 days of the intragastrical administration), in addition to the activities observed after a single exposure (effect on the liver, thyroid and nervous system), were also found immunotoxic effects, which were recorded after 14 days in rats and mice administered this compound at the doses of 18 mg/kg/day. The first symptoms of adverse effects on the thyroid (a decrease in serum T4 and T3) was observed after four days exposure at the dose of 3 mg/kg/day. At doses of 10-300 mg/kg/day, these effects are intensified. In addition, there were signs of the disturbance of liver function (dose dependent increase in relative liver weight, increase of the activity of O-dealkylase 7-etoxyresorufin (EROD) and O-dealkylase 7-pentoxyresorufin (PROD) in liver). The reduction of the T4 levels in serum were recorded after 14-day administration of pentabromodiphenyl ether to rats and mice. This effect was dependent on the administered dose of the compound (18-56 mg/kg/day in rats and 18-72 mg/kg/day in mice). Fourteen days of exposure to pentabromodiphenyl ether at the dose 18 mg/kg/day caused also in adverse effects in the liver: increase in relative liver weight and induction of microsomal enzymes in the liver (including EROD, PROD), intensified with dose (up to 72 mg/kg/day.)
After repeated (28- and 90-day) intragastrical exposure of rats to pentabromodiphenyl ether at the doses from 0.82 to 1.77 mg/kg/day did not show any toxic effects. After 28 days of the administration of pentaBDE at the dose 2.47 mg/kg/day were observed the decrease T4 levels in the serum and increase PROD activity in the liver. These symptoms enhanced with increasing doses (up to 200 mg/kg/day) of the compound.
After subchronic exposure (90 days) on pentabromodiphenyl ether at the dose 3.53 mg/kg/day, the microsomal enzyme induction was observed in the liver. This effect was growing with increasing doses (up to 14.12 mg/kg/day). After a three-month exposure of rats at a dose of 2 mg/kg/day were found the reduction of the T4 levels in the serum and increase of the cases of degeneration and necrosis of hepatocytes in females. After the doses of 10 or 100 mg/kg/day was also observed the porphyrogenic activity (dosedependent).
Pentabromodiphenyl ether was not genotoxic, embryotoxic and teratogenic. The EPA included pentabromodiphenyl ether to Class D, this compound not classified as a carcinogen for humans.
Polybrominated diphenyl ethers (PBDEs), including pentabromodiphenyl ether, act negatively on the: nervous, endocrine and immune systems. These compounds also cause the induction of hepatic microsomal enzymes, which may lead to changes in the metabolism of xenobiotics, and collected in large quantities cause changes in the liver. Pentabromodiphenyl ether can interact with the cytosolic Ah receptor, which is associated with induction of microsomal enzymes, especially CYP 1A1 and CYP 1A2. The EROD is an indicator of the binding of the aromatic hydrocarbon receptor (AhR). Both, PBDEs and their hydroxyleted derivatives are an estrogenic agonists and stimulate the in vitro luciferase activity through estrogenic receptor (ER). PBDEs can cause changes in the cholinergic system. These compounds can also affect the homeostasis of thyroid hormones, thus affecting on the development of the central nervous system.
The basis for the proposed value of the maximum allowable concentration (MAC) are data in the literature regarding the adverse effects of the compound on the functioning of the liver and thyroid. To calculate the value NDS has been proposed the adoption of the NOAEL value as the dose 0.82 mg/kg/day with a 28-day experiment performed on rats given intragastrically pentabromodiphenyl ether. After determining the coefficients of uncertainty has been proposed the adoption of the concentration of 0.7 mg/m³ for the value of the maximum allowable concentration (MAC, TWA). No MAC-STEL values have been established.
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Cadmium is a silver-white metal. Documentation
Marek Jakubowski
Cadmium is a silver-white metal, oxidation state +2. Of the many inorganic cadmium compounds, several are quite soluble in water (e.g. cadmium acetate, chloride, and sulfate); cadmium oxide and cadmium sulfide are almost insoluble. The use of cadmium compounds falls into five categories: active electrode materials in nickel-cadmium batteries (79%); pigments used mainly in plastics, ceramics, and glasses (11%); coatings on steel and some nonferrous metals (7%); stabilizers for polymers (2%), and component of various specialized alloys (1%). Most exposure to cadmium compounds in the working environment occurs through inhalation among people manufacturing nickel-cadmium batteries or pigments. High acute inhalation exposure may occur among workers welding cadmium-plated materials or using silver-cadmium solder.
In 2007, according to the State Sanitary Inspection, 52 persons were employed in Poland at cadmium concentrations in the air exceeding the occupational exposure limit of 0.01 mg/m³ .
Cadmium is absorbed from the lungs and the gastrointestinal tract. In humans, on average, 4-6% of the total oral intake is absorbed. Between 5 and 20% of inhaled cadmium is deposited in the lungs. Cadmium is mainly stored in the liver and kidneys (about 40 – 80 % of the body burden) bound to metallothionein. Elimination is normally slow. Biological half-times after cessation of occupational exposure were 75-130 days during the first phase and to about 16 years during the second phase of elimination.
Long-term occupational exposure to cadmium causes severe chronic effects, predominantly in the lungs and kidneys. The kidney is the critical organ. The accumulation of cadmium in the renal cortex leads to renal tubular dysfunction with impaired reabsorption of proteins, glucose, and amino acids. An increase of low molecular weight proteins in urine is a characteristic sign of tubular dysfunction. There is evidence that long-term occupational exposure to cadmium may contribute to the development of cancer of the lung.
Impaired tubular reabsorption of low-molecular weight proteins or increased glomerular permeability occurred mainly when cadmium levels in urine exceeded 10 –15 μg/g creatinine corresponding to the renal cortex concentration of about 200 mg/kg. For a long time tubular proteinuria was considered irreversible. Experimental and fields data suggested, however, that the persistence of this kind of proteinuria depended on the intensity of cadmium exposure as well as the severity of cadmium-induced renal tubular changes. In a study on workers chronically exposed to cadmium when the microproteinuria was mild and historical Cd-U values never exceeded 20 μg/g creatinine, there was an indication of a reversible tubulotoxic effect of cadmium.
According to IARC there was sufficient evidence to classify cadmium and cadmium compounds as human carcinogens ( group I). This assessment to a great extent depended on the significant relation between the risk of lung cancer and estimated cumulative exposure to cadmium in an analysis of mortality among a cohort of workers from a single cadmium recovery plant in the USA. These findings were criticized mainly because there was no control for exposure to arsenic. The results of a later reevaluation suggest that the evidence for cadmium as a human carcinogen is rather weak, and thus classifying cadmium as probably carcinogenic to humans would be more appropriate. This conclusion complies with the EC ( carcinogenic category 2), US EPA ( category B1) and ACGIH ( category A2) classifications. According to US EPA the unit risk is 0.0016.
On the basis of the results of epidemiological examinations the MAC values for cadmium and its inorganic compounds were established at 0.01 mg/m³ and 0.002 mg/m³ for inhalable and respirable fractions, respectively.
The proposed admissible levels of in urine ( Cd-U) and in blood (Cd-B) are 5 μg/g creatinine and 5 μg/l, respectively. The level of Cd-B can be considered an indicator of current exposure, whereas Cd-U, in absence of renal damage , reflects the cadmium body burden.
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