|
|
| | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | |
|
|
 |
Beryllium. Documentation
Marek Jakubowski
Beryllium is a strategic and critical material for many industries. It is widely used because for certain critical applications it performs better than alternatives. The beryllium industry produces three primary forms of beryllium. Copper beryllium alloy is the largest, followed by pure beryllium metal and beryllium oxide ceramics.
As result of the increasing industrial use of beryllium, occupational exposure to the metal is an important issue. The estimated daily weighted average beryllium exposure levels in plant that extracted and pro-duced beryllium metal were > 50 μg/m³ during the mid-1960s, In mid-1970s, the exposure levels were > 30 μg/m³. At present, beryllium concentrations during different industrial processes tend to be below 2 μg/m³.
Exposures to beryllium are much more hazardous by the inhalation route than by the ingestion route. Beryllium and its compounds are poorly absorbed from the gastrointestinal tract. In general, inhalation exposure to beryllium results in long-term storage of beryllium in lung tissue and in the skeleton, which is the ultimate site of beryllium storage. Urinary beryllium concentrations are below the detection limits of 0,03 ÷ 0,06 μg/l.
Exposure to beryllium compounds has caused dermatitis, acute pulmonary inflammation, and chronic beryllium disease (CBD). Exposure to soluble beryllium salts may cause skin reactions such as edemat-ous, erythematous, and papulovesicular dermatitis. Those changes usually disappear after cessation of exposure. Granulomatous necrotic changes and ulcerations caused by skin penetration by insoluble beryllium salts were also observed. These changes are based on delayed allergic hypersensitivity. Acute toxicity of beryllium at concentrations usually > 25 μg/m³ is manifested by skin, eye, nose, and throat irritation, followed by upper and lower airway inflammation, pulmonary edema, and (> 100 μg/m³ ) chemical pneumonitis.
Chronic beryllium disease is the most common health problem caused by exposure to beryllium. CBD is a T-cell-mediated disorder. Beryllium, acting as a hapten, interacts with the antygen-presenting cells in the lungs. The beryllium blood lymphocyte proliferation test (BLPT) is used as a medical surveillance tool for assess persons at risk for developing clinical and subclinical CBS. The LOAEL for beryllium sensitization and CBD progression was suggested as 0.55 μgBe/m³. However, recent reports suggest that sensitization and CBD were associated with beryllium time weighted average air levels exceeding 0.2 μg/m³. These results suggest that to avoid sensitization and CBD, occupational exposure limits should be < 0.2 μg/m³.
An excess in lung cancer was found in persons occupationally exposed to beryllium and was higher for individuals after recovery from acute beryllium pneumonitis than those with CBD. IARC classified beryl-lium in 1993 as a group 1 carcinogen. The US EPA unit risk is 2.4 · 10-3 per μg/m³. In general it seems that the lung cancer observations related to occupational exposure to beryllium are linked to higher exposure levels that were associated with acute beryllium pneumonitis and predominated before the 1950s.
|
4-Chlorophenol. Documentation
Tadeusz Dutkiewicz
4-Chlorophenol is a white to straw-colored crystal (yellow or pink when impure) with a characteristic phenolic odor. Occupational exposure takes place during manufacturing 4 chlorophenol, chlorinating of phenols, pharmaceutics and dyes production. It is corrosive in the case of skin or eye contact; the extent of tissue damage depends on the duration of contact. Eye contact can result in corneal damage or blindness. Skin contact can produce inflammation and blistering. Inhalation of dust will produce irritation to gastro-intestinal or respiratory tracts, characterized by burning, sneezing and coughing. Severe overexposure can produce lung damage, choking, unconsciousness or death. Inflammation of the eye is characterized by redness, watering, and itching. Skin inflammation is characterized by itching, scaling, reddening or, occasionally, blistering. IARC classifies 4-chlorophenol 2B (a possible carcinogen for human) by. Repeated or prolonged exposure to the substance can produce damage of target organs. The substance may be toxic to the liver, brain, gastrointestinal tract, upper respiratory tract and the central nervous system. MAC values have been based on hepatotoxic effects of 4-chlo-rophenol in rats. LOAEL of 0.64 mg/kg/day has been established in a subchronic experiment. The Expert Group for Chemical Agent established an 8-hour TWA value of 0.5 mg/m3 and a STEL value of 1.5 mg/m³ .
|
1,2-Dichloropropane. Documentation
Jolanta Gromadzińska, Wojciech Wąsowicz
1,2-Dichloropropane (1,2-DCP) is a colorless liquid, with a chloroform-like odour, used as an industrial solvent (resins, lubricants, bitumens, asphalts, paints) for specific technological processes or as a cleaning and soil fumigant.
In experiments on animals, exposure to high levels of 1,2-DCP caused injury of the liver, kidneys and the respiratory tract. Respiratory effects were reported in humans following oral and dermal exposure. A case of dermatitis resulting from dermal exposure to mixtures of solvents containing 1,2-DCP was reported.
On the basis of LOAEL for the irritation effect of the upper respiratory tract obtained from an animal study, the TLV value was calculated at 50 mg/m³ .
|
1,2-Epoxypropane. Documentation
Andrzej Sapota, Elżbieta Bruchajzer
1,2-Epoxypropane (EP), propylene oxide, is a colorless liquid, most frequently obtained from propylene and chlorine by means of the chlorohydrin method. It is used as an indirect product in the synthesis of propylene glycols and propylene glycol ethers to produce polyurethanes and polyester resins. This com-pound also finds its application in the pharmaceutical, food (fruit conservation fumigant) and cosmetic industries. In 1997, its world production accounted for 4.1 million tones, whereas in Poland, it was over 25 000 tones and about 200 persons were exposed to its effects.
Irritation of the skin, eyes, nose or airways is the most common manifestation of the acute toxic effect of 1,2-epoxypropane in humans. In exposures to high EP concentrations, symptoms, such as cyanosis, loss of consciousness, pulmonary edema and signs of neurotoxic effects have been observed. Severe irritation or even burn has been found after a direct EP contact with the skin. It may also induce allergy in humans. In the available literature, there are no epidemiological data on occupational exposure to EP alone.
1,2-Epoxypropane is a compound that exerts moderate acute toxic effects in animals. The value of DL50 obtained in various experiments amounts to 380 ÷ 1140 mg/kg, which indicates that the compound has been categorized (according to EU classification) in the group of harmful substances. Irritation and depressive influence on the central nervous system are the major manifestations observed in acute animal EP toxicity.
Following a 28-month exposure of rats to 1,2-epoxypropane at a concentration of 72 mg/m³ , degenerative and proliferative changes in the nose mucous membrane have been observed. Exposure of rats to EP at a concentration of 240 mg/m³ for two years caused inflammation of mucous membrane in upper airways. EP exposure increased to 482 mg/m³ induced rhinitis. The aforesaid symptoms intensified after a 24 ÷ 28-month exposure of rats to EP at a concentration of 723 mg/m³ . The highest EP concentrations, the mice were exposed to for two years, accounted to 964 mg/m³ . In the experimental animals, a significant body weight loss, an increased rate of animals with rhinitis and a significant increase in the number of cases with metaplasia to squamous epithelium and purulent inflammation of nose mucous, have been observed.
The mutagenic and genotoxic (increased rates of chromosome aberration and sister chromatid exchange) effects of EP have already been evidenced.
Inhalation exposure to 1,2-epoxypropane increases cancer risk in laboratory animals (mostly cancer of nasal cavity but also of adrenal gland and mammary gland in females).
No significant effect of EP on the animal reproduction (both genders) has been found. EP toxic effect on the fetus (deformity of ribs) was visible after exposure of pregnant rats to very high (1200 mg/m³ ) con-centrations of the compound.
Absorption of 1,2-epoxypropane by lungs as well as its distribution and metabolism are very fast processes. EP is covalently bound to DNA (mostly with guanine). There are two routes of EP biotrans-formation, mediated by the liver S-glutathione transferase to mercapturic acid and/or by 1,2-propandiol to lactic and pyruvic acids. EP metabolites are mainly excreted (96% of an absorbed dose) with urine.
The mechanism by which EP exerts its toxic effect is associated with the promotion of covalent binding to DNA (mostly nasal cavity), which may induce degenerative changes and mucous membrane proliferation, leading finally to the mutation and cancer development. Data on EP combined action with other compounds are not accurate and they mostly apply to human exposures in the chemical industry, where exposure to a large number of compounds, including those of carcinogenic properties, has been recorded. In such cases, an enhanced risk of deaths from cancers at different sites has been found. Even a fifty fold difference in the values of maximum admissible concentrations (MAC) for 1,2-epoxypropane can be found between different countries. The majority of European countries adopted for EP the concentration of 12 mg/m3 (5 ppm) or 50 mg/m³ (20 ppm) as its MAC (TWA) value. Observations made during long-term (28 months) experiments have provided the basis for the MAC value calculation. After using relevant uncertainty coefficients, the MAC value of 9 mg/m³ has been calculated and proposed to be approved in Poland.
|
Hydroquinone. Documentation
Krystyna Sitarek
Hydroquinone is a white crystalline substance. It has been used in photography as a developer, and a raw material in the rubber industry, a stabilizer in oils, paints and as a chemical intermediate in dyes. LD50 for laboratory animals ranges from 70 to 550 mg/kg. Hydroquinone is negative in mutagenicity tests but it is a clastogenic agent. This chemical is absorbed from the gastrointestinal tract and is eliminated as a sulfate and glucuronide conjugates in the urine.
Acute human exposure causes irritation, photophobia, lacrimation and corneal ulceration. The symptoms of acute severe poisoning include tinnitus, nausea, dizziness, increased respiration, pallor, headache and dyspnoea.
The Expert Group recommended a MAC of 1.0 mg/m³ and MAC-STEL 2.0 mg/m³ and the “A” – allergic substance – notation.
|
Iodomethane. Documentation
Sławomir Czerczak, Hanna Grunt
Iodomethane is a clear liquid with a characteristic odor. Iodomethane is readily absorbed by all routs of exposure. After inhalation exposure there were neurological disorders and irritation effects to the eyes, nose and throat. The concentration of iodomethane of 56 mg/m³ was accepted as an NOAEL value.
The Expert Group for Chemical Agents has recommended MAC of 7 mg/m³ and because of its irritative effect MAC-STEL of 20 mg/m³. Because percutaneous absorption of iodomethane has caused systemic toxicity in laboratory animals, “Sk” notation is considered appropriate; “I” – irritation notation is also recommended.
|
|
