Chlorinated hydrocarbon exposure

Bopp, Richard Mount Sinai School of Medicine New York, New York Sources and pathways of persistent chlorinated hydrocarbon exposure in New York City NIEHS... 

Polystyrene. Polystyrene [9003-53-6] is a thermoplastic prepared by the polymerization of styrene, primarily the suspension or bulk processes. Polystyrene is a linear polymer that is atactic, amorphous, inert to acids and alkahes, but attacked by aromatic solvents and chlorinated hydrocarbons such as dry cleaning fluids. It is clear but yellows and crazes on outdoor exposure when attacked by uv light. It is britde and does not accept plasticizers, though mbber can be compounded with it to raise the impact strength, ie, high impact polystyrene (HIPS). Its principal use in building products is as a foamed plastic (see Eoamed plastics). The foams are used for interior trim, door and window frames, cabinetry, and, in the low density expanded form, for insulation (see Styrene plastics). 

Hexachloroethane is considered to be one of the more toxic chlorinated hydrocarbons. The 1991 ACGIH recommended time-weighted average (TWA) for hexachloroethane was 1 ppm or 10 mg /m of air. Skin adsorption is a route of possible exposure ha2ard. The primary effect of hexachloroethane is depression of the central nervous system (147). Pentachloroethane and tetrachloroethylene are primary metaboHtes of hexachloroethane in sheep (148). 

The resistance to heat and aging of optimized EPM/EPDM vulcanizates is better than that of SBR and NR. Peroxide-cured EPM can, for instance, be exposed for 1000 h at 150°C without significant hardening. Particularly noteworthy is the ozone resistance of EPM/EPDM vulcanizates. Even after exposure for many months to ozone-rich air of 100 pphm, the vulcanizates will not be seriously harmed. EPM/EPDM vulcanizates have an excellent resistance to chemicals, such as dilute acids, alkaUes, alcohol, etc. This is in contrast to the resistance to aUphatic, aromatic, or chlorinated hydrocarbons. EPM/EPDM vulcanizates swell considerably in these nonpolar media. 

This has a very high resistance to impact damage, even at subzero temperatures. It has good creep strength in dry conditions up to 115°C but degrades by continuous exposures to water hotter than 65°C. It is resistant to aqueous solutions of acids, aliphatic hydrocarbons, paraffins, alcohols (except methanol), animal and vegetable fats and oils, but is attacked by alkalis, ammonia, aromatic and chlorinated hydrocarbons. 

Liver cancer can also be a consequence of exposure to hepatotoxic chemicals. Natural hepatocarcinogens include fungal aflatoxins. Synthetic hepato-carcinogens include nitrosoamines, certain chlorinated hydrocarbons, polychlorinated biphenyls (PCBs), chloroform, carbon tetrachloride, dimethyl-benzanthracene, and vinyl chloride.Table 5.15 lists the chemical compounds that induce liver cancer or cirrhosis in experimental animals or... 

Dermal Effects. Some of the people in Woburn, Massachusetts, who had been chronically exposed to trace amounts of trichloroethylene and other substances in the drinking water reported skin lesions (Byers et al. 1988). These were maculopapular rashes that were said to occur approximately twice yearly and lasted 2-4 weeks. These skin conditions generally ceased 1-2 years after cessation of exposure to contaminated water. The limitations of this study are discussed in Section 2.2.2.8. A case study was published of a 63-year-old rural South Carolina woman exposed to trichloroethylene and other chlorinated hydrocarbons in her well water, who developed diffuse fascitis, although her husband did not (Waller et al. 1994). The level of trichloroethylene measured in the well water was 19 mg/L. Substitution of bottled water for drinking resulted in improved symptoms. 

The use of the methods for monitoring metabolites of trichloroethylene in blood and urine is, however, rather limited since the levels of TCA in urine have been found to vary widely, even among individuals with equal exposure (Vesterberg and Astrand 1976). Moreover, exposure to other chlorinated hydrocarbons such as tetrachloroethane, tetrachloroethylene, and 1,1,1-trichloroethane would also be reflected in an increase in urinary excretion of TCA. In addition, there may be sex differences regarding the excretion of trichloroethylene metabolites in urine since one experiment shows that men secrete more trichloroethanol than women (Inoue et al. 1989). The use of the level of trichloroethylene adduction to blood proteins as a quantitative measure of exposure is also possible, although obtaining accurate results may be complicated by the fact that several metabolites of trichloroethylene may also form adducts (Stevens et al. 1992). 

Geigy s mothproofing agent was a stomach poison for moths and other keratin-eating insects. It had a strong affinity for woolens, was harmless to warm-blooded animals and people, and had no offensive odor. As a chlorinated hydrocarbon, it was extremely persistent despite exposure to light and moisture. 

Both hexachloroethane and its lipophilic metabolites can distribute to body fat. Only hexachloroethane can be used to confirm compound exposure by way of a fat biopsy, since some of its metabolites are also produced from other chlorinated hydrocarbons or are present as contaminants in the environment. Based on one worker occupationally exposed to hexachloroethane, Selden et al. (1993) estimated that the plasma half-life in humans was several days, but less than one week. A clearance half-life in rats of 2.5 days was reported for hexachloroethane absorbed from the diet (Gorzinski et al. 1985). Therefore, similar to measurement of hexachloroethane in blood, urine, and feces, hexachloroethane in body fat is representative of current exposures rather than exposures that occurred weeks or months before testing. 

Methods for Reducing Toxic Effects. There are no compound-specific methods for reducing the toxic effects of hexachloroethane. The mitigation procedures suggested (Bronstein and Currance 1988 Stutz and Ulin 1992) are applicable to exposure to volatile chlorinated hydrocarbons as a class and are not specific for hexachloroethane. 

TPUs are handicapped by a lower elasticity than conventional rubbers, the more so the higher the hardness certain risks of creep, relaxation and permanent set, the more so the higher the temperature higher cost than TPOs risks of hydrolysis especially for the polyester types UV exposure yellowing incompatibility between certain polyester and polyether grades aromatic and chlorinated hydrocarbon behaviour limited thermal behaviour density inherent flammability, but FR grades are marketed risks of fume toxicity in the event of fire. 

Rigid PVC natural UV sensitivity, but special grades benefit from long-time outdoor-exposure guarantees sensitivity to heat, creep, aromatic or chlorinated hydrocarbons, esters and ketones low-temperature brittleness high density toxicity and corrosivity of smoke in fires less easy injection. 

Although we can measure the amount of chloroform in the air that you breathe out, and in blood, urine, and body tissues, we have no reliable test to determine how much chloroform you have been exposed to or whether you will experience any harmful health effects. The measurement of chloroform in body fluids and tissues may help to determine if you have come into contact with large amounts of chloroform. However, these tests are useful only a short time after you are exposed to chloroform because it leaves the body quickly. Because it is a breakdown product of other chemicals (chlorinated hydrocarbons), chloroform in your body might also indicate that you have come into contact with those other chemicals. Therefore, small amounts of chloroform in the body may indicate exposure to these other chemicals and may not indicate low chloroform levels in the environment. From blood tests to determine the amount of liver enzymes, we can tell whether the liver has been damaged, but we cannot tell whether the liver damage was caused by chloroform. 

No correlation has been made between the exact environmental levels of chloroform and the amount of chloroform in the exhaled breath or in the blood. Furthermore, chloroform also can be detected in the breath after exposure to carbon tetrachloride and other chlorinated hydrocarbons (Butler 1961). Therefore, chloroform levels cannot be used as reliable biomarkers of exposure to this chemical. 

Exposure. Methods for detecting chloroform in exhaled breath, blood, urine, and tissues are available. Nevertheless, it is difficult to correlate chloroform levels in biological samples with exposure, because of the volatility and short half-life of chloroform in biological tissues. Several studies monitored chloroform levels in environmentally exposed populations (Antoine et al. 1986 Hajimiragha et al. 1986 Peoples et al. 1979) however, the measured levels probably reflect both inhalation and oral exposure. Moreover, increased tissue levels of chloroform or its metabolites may reflect exposure to other chlorinated hydrocarbons. Studies to better quantitate chloroform exposure would enhance the database. 

Pesticides are used to kill household insets, rats, cockroaches, and other pests. Pesticides can be classified based on their chemical nature or use as organophosphates, carbonates, chlorinated hydrocarbons, bipyridyls, coumarins and indandiones, rodenticides, fungicides, herbicides, fumigants, and miscellaneous insecticides. The common adverse effects are irritation of the skin, eyes, and upper respiratory tract. Prolonged exposure to some chemicals may cause damage to the central nervous system and kidneys [32,33]. 

Ideally, toxicology studies should mimic, as near as possible, human exposure. Thus, both the route of administration and the exposure should, where possible, be similar to that in man. The classic route of administration in man is oral and thus most toxicology studies are conducted by the oral route. Elowever, parenteral routes may be used either to mimic the clinical route or to ensure exposure. The administration of some medicines is directly on to highly differentiated surfaces such as the alveolar surface of the lungs or the skin. It is, therefore, important to assess the topical irritancy, absorption and subsequent systemic toxicity following such applications. It should be remembered that some compounds, for example, chlorinated hydrocarbons, may be more toxic when given by the inhalation route than when given orally or may directly affect... 

In a recent study of male operators employed in a chemical plant, it was concluded that long-term exposure to a mixture of chlorinated hydrocarbons, including hexachlorocyclopentadiene, below or near the current... 

Boogaard PJ, Rocchi, PSJ, van Sittert NJ Effects of exposure to low concentrations of chlorinated hydrocarbons on the kidney and liver of industrial workers. Br J Ind Med 50 331-339, 1993... 

Greenburg L, Mayers MR, Smith AR The systemic effects resulting from exposure to certain chlorinated hydrocarbons. J Ind Hyg Toxfro/21 29-38, 1939... 

Rats did not survive when exposed for longer than 12-18 minutes to 12,000ppm. When exposed repeatedly to 470 ppm, they showed liver and kidney injury. Cardiac arrhythmias owing to sensitization of the myocardium to epinephrine have been observed with certain other chlorinated hydrocarbons, but exposure of dogs to perchloroeth-... 

Exposure at waste sites is most likely to occur from the landfill disposal of waste by-products originating from chlorinated hydrocarbon manufacture. 

Occupational exposures can be significantly higher for individuals who work at plants that produce chlorinated hydrocarbons. Maximum air levels off plant property, at a plant boundary, and within a plant were reported to be 22 ppt, 938 ppt, and 43,000 ppt, respectively (Li et al. 1976). 

Production, Import/Export, Use, Release, and Disposal. Hexachlorobutadiene is not produced for commercial purposes in the United States, however small amounts are imported from Germany. Hexachlorobutadiene is mainly produced as a by-product of chlorinated hydrocarbon synthesis and is a primary component of "hex-wastes" (EPA 1982b). Its uses as a pesticide and fumigant have been discontinued. Hexachlorobutadiene is disposed chiefly by incineration, and to a lesser extent by deep well injection and landfill operations (EPA 1982b). More recent production and release data would be helpful in estimating human exposure to hexachlorobutadiene. 

Cardiovascular Effects. Most studies of humans exposed to carbon tetrachloride by inhalation have not detected significant evidence of cardiovascular injury, even at exposure levels sufficient to markedly injure the liver and/or kidney. Changes in blood pressure, heart rate, or right- sided cardiac dilation have sometimes, but not always, been observed (Ashe and Sailer 1942 Guild et al. 1958 Kittleson and Borden 1956 Stewart et al. 1961 Umiker and Pearce 1953), and are probably secondary either to fluid and electrolyte retention resulting from renal toxicity, or to central nervous system effects on the heart or blood vessels. Carbon tetrachloride also may have the potential to induce cardiac arrhythmias by sensitizing the heart to epinephrine, as has been reported for various chlorinated hydrocarbon propellants (Reinhardt et al. 1971). 

Plummer JL, de la Hall P, Isley AH, et al. 1990. Influence of enzyme induction and exposure profile on liver injury due to chlorinated hydrocarbon inhalation. Pharmacol Toxicol 67 329-335. 

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