Exposure to other chemicals

Exposure of a thin-film composite membrane to a variety of organic compounds can result in swelling or dissolution of the polysulfone microporous support layer. Suspect chemicals include  

Note that only low-molecular solvents such as alcohols (isopropanol and smaller) are acceptable. 

Ridgeway, Harry R, Microbial Adhesion and Biofouling of Reverse Osmosis Membranes, in Reverse Osmosis Technology, Parekh Bipin S., Marcel Dekker, Inc., New York, New York, 1988. 

Standard Methods for the Examination of Water and Wastewater, 20 edition, published jointly by the American Public Health Association, the American Water Works Association, and the Water Pollution Control Federation. 

FilmTec Reverse Osmosis Membranes Technical Manual, Dow Liquid Separations, form number 609-00071-0705,2007. 

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The determinant is non-specific, since it is also observed after exposure to other chemicals. 

However, a sample taken in the doctor s office can be properly packed and shipped to a special laboratory, if necessary. Because endosulfan leaves the body fairly quickly, these methods are useful only for finding exposures that have occurred within the last few days. At this time, these methods can only be used to prove that a person has been exposed to endosulfan. The test results cannot be used to predict if you wiU have any adverse health effects. Exposure to other chemicals at the same time at hazardous waste sites could cause some confusion in understanding these results. More information about tests to find endosulfan in the body is presented in Chapters 2 and 6. 

Renal Effects. Triehloroethylene may have effeets in the kidney however, studies in humans are limited by having poor or no exposure data and by concomitant exposure to other chemicals. There was no evidence of kidney damage in 250 neurosurgery patients who underwent prolonged trichloroethylene anesthesia (Brittain 1948), nor in 405 women who had caesarean sections and were exposed to trichloroethylene anesthesia (Crawford and Davies 1975). 

Increases in miscarriages have been reported among nurses exposed to rmspecified concentrations of trichloroethylene and other chemicals in operating rooms (Corbett et al. 1974). The occurrence of miscarriages could not conclusively be attributed to trichloroethylene because there was concomitant exposure to other chemicals. 

Cancer. Workers who have been exposed to trichloroethylene show no higher incidence of cancer than controls in numerous epidemiologic studies (Axelson et al. 1978 Hardell et al. 1981 Malek et al. 1979 Novotna et al. 1979 Paddle 1983 Spirtas et al. 1991 Tola et al. 1980). Studies that did show an increased incidence of specific cancers in exposed workers were complicated by exposures to other chemicals, including known human carcinogens (Antilla et al. 1995 Blair et al. 1979 Hardell et al. 1994 Henschler et al. 1995). 

No studies were found on the health effects of diisopropyl methylphosphonate in humans following inhalation or oral exposure. The results of the one study that was located in which humans were exposed dermally to diisopropyl methylphosphonate was confounded by concurrent exposure to other chemicals. Limited animal data are available on the health effects of diisopropyl methylphosphonate following oral and dermal exposures. 

Hydrogen sulfide has not been shown to cause cancer in humans, and its possible ability to cause cancer in animals has not been studied thoroughly. Hydrogen sulfide has not been classified for its ability to cause or not cause cancer. There is some evidence that exposure to hydrogen sulfide may lead to an increase in spontaneous abortions in humans. However, the studies where this effect was reported are complicated by exposures to other chemicals and a lack of information on the amount of exposure to hydrogen sulfide. 

Intermediate-Duration Exposure. Intermediate-duration studies in humans are fairly limited and virtually all are complicated by exposures to other chemicals as well as rarely being accompanied with adequate exposure assessment. Additional epidemiologic studies, particularly prospective or case-control, of populations exposed environmentally to various levels of hydrogen sulfide (where other pollutants are monitored and ideally, do not vary) are needed. 

The information available regarding the association of occupational exposure to lead with increased cancer risk is generally limited in its usefulness because the actual compound(s) of lead, the route(s) of exposure, and level(s) of lead to which the workers were exposed were often not reported. Furthermore, potential for exposure to other chemicals including arsenic, cadmium, and antimony occurred, particularly in lead smelters, and smoking was a possible confounder (Cooper 1976 IARC 1987). These studies, therefore, are not sufficient to determine the carcinogenicity of lead in humans, and the following discussion is restricted to the most comprehensive of these studies. 

Cancer. The information available on the carcinogenicity of lead in occupationally exposed humans is limited in its usefulness because the lead compound(s), the route(s) of exposure, and the levels of exposure were not always reported. Furthermore, concurrent exposure to other chemical (including arsenic, particularly in lead smelters) and confounding variables, such as smoking, were often not evaluated. Therefore, the data currently available do not support an assessment of the potential carcinogenic risk of lead in humans. 

Several studies of occupational exposures and one study with a human subject were located. In the occupational exposures (summarized in Table 5- 3), neurological symptoms consistent with cyanide intoxication were demonstrated, but the likelihood of concomitant exposure to other chemicals could not be ruled out. For example, cleaners and cutting oils, as well as sodium and copper cyanide, may be present in electroplating operations (ATSDR 1997). The experimental human study involved the exposure of a single subject and a dog to a high concentration for a short exposure period. 

Exposure to other chemicals can influence the metabolism of -hexane. The effect of oral pretreatment with methyl ethyl ketone (MEK) on the metabolism of inhaled -hexane was investigated in male Fischer 344 rats (Robertson et al. 1989). Groups of 2-4 rats were given MEK (1.87 mL/kg, approximately 1,500 mg/kg) by gavage for 4 days prior to a single 6-hour inhalation exposure to w-hexane (1,000 ppm). Animals were sacrificed at 0, 1, 2, 4, 6, 8, and 18 hours after exposure ended, and samples of blood, liver, testis, and sciatic nerve were obtained and analyzed for -hexane, MEK, and their metabolites. Significant increases in the levels of the neurotoxic metabolite 2,5-hexanedione and 2,5-dimethylfuran (derived from 2,5-hexanedione) were found in blood and sciatic nerve of rats pretreated with MEK. Levels of 2,5-hexanedione in blood were approximately 10-fold higher than control immediately after -hexane exposure in rats and fell rapidly to approximately 2-fold after 6 hours. In sciatic nerve, increases in 2,5-hexanedione were approximately 6-fold at 2 hours and 3-fold at 4 hours. Similar patterns were found with 2,5-dimethylfuran. 2,5-Hexanedione was not detected in the testis of non-pretreated rats levels were measurable but very low in pretreated rats (0.3-0.6 g/g compared to... 

Respiratory Effects. Respiratory effects were reported in workers involved in the manufacture of aldrin/dieldrin/endrin (Ditraglia et al. 1981). Increased deaths due to nonmalignant respiratory diseases such as pneumonia were observed in workers at one of two plants that manufactured endrin. However, simultaneous exposure to other chemicals occurred, and increased respiratory disease was not observed in the second endrin manufacturing facility. 

Hepatic Effects. Workers monitored for liver function had increased serum levels of liver enzymes (Hoogendam et al. 1965). Only limited conclusions should be drawn from these results as the levels returned to normal within 1 week to 3 months concurrent exposure to other chemicals and alcohol was not controlled. Diffuse degenerative hepatic lesions were observed in rabbits and mice exposed to lethal doses of endrin and in surviving animals (Treon et al. 1955). Rats, mice, guinea pigs, and hamsters administered a relatively high dose of endrin exhibited moderate hepatic histopathology (Hassan et al. 1991). 

No acute-, intermediate-, or chronic-duration inhalation MRLs were derived for cyanide because of the limitations associated with the available studies. Many of the animal and human studies used lethality, or serious effects, such as coma, as the end point. Two epidemiological studies are available however, one study lacked good exposure data, and the other study involved occupational exposure in the electroplating industry where exposure to other chemicals may have occurred. 

A number of effects from breathing phenol in air have been reported in humans. Short-term effects reported include respiratory irritation, headaches, and burning eyes. Chronic effects of high exposures included weakness, muscle pain, anorexia, weight loss, and fatigue effects of chronic low-level exposures included increases in respiratory cancer, heart disease, and effects on the immune system. Virtually all of the workplace exposures associated with these effects involved exposures to other chemicals, thus it is difficult to determine whether these are solely due to phenol, or are the result of mixed, multiple, or other chemical exposures. 

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