Toxic exposures unknown

Grabo TN. 1997. Unknown toxic exposures. Arts and crafts materials. Aaohn Journal 45(3) 124-130. 

In this manner, a nearly universal and very nonselective detector is created that is a compromise between widespread response and high selectivity. For example, the photoionization detector (PID) can detect part-per-billion levels of benzene but cannot detect methane. Conversely, the flame ionization detector (FID) can detect part-per-billion levels of methane but does not detect chlorinated compounds like CCl very effectively. By combining the filament and electrochemical sensor, all of these chemicals can be detected but only at part-per-million levels and above. Because most chemical vapors have toxic exposure limits above 1 ppm (a few such as hydrazines have limits below 1 ppm), this sensitivity is adequate for the initial applications. Several cases of electrochemical sensors being used at the sub-part-per-million level have been reported (3, 16). The filament and electrochemical sensor form the basic gas sensor required for detecting a wide variety of chemicals in air, but with little or no selectivity. The next step is to use an array of such sensors in a variety of ways (modes) to obtain the information required to perform the qualitative analysis of an unknown airborne chemical. 

Although the mechanism of acrylamide toxicity is unknown, glycidamide may mediate the genotoxicity associated with acrylamide exposure. While both acrylamide and glycidamide bind to hemoglobin in vivo, only glycidamide forms adducts with DNA. 

If a toxic or unknown amount of a cephalosporin has been ingested, gastric decontamination and the administration of activated charcoal is usually all that is needed. In the symptomatic patient, evaluation of renal function and electrolytes may be necessary. Chronic exposure usually requires discontinuation of the drug and supportive care. Anaphylaxis should be treated with epinephrine and/or diphenhydramine. 

Cyclohexene is an irritant and defats skin on direct contact. It is also an anesthetic and central nervous system (CNS) depressant on inhalation exposure. The mechanism for this toxicity is unknown. 

No in vitro toxicity studies have been reported. The mechanism of phosgene oxime toxicity is unknown and long-term exposure effects have not been determined. 

Caution. The substance (CF jJig is a white crystalline and sublimable solid that should be handled in an efficient hood. Its toxicity is unknown, but upon prolonged exposure (CFi)JIg can cause eye irritation as well as irritation to the nasal membranes. 

Toxicity studies on trifluoroethanol show acute oral LD q, 240 mg/kg acute dermal LD q, 1680 mg/kg and acute inhalation L(ct) Q, 4600 ppmh. Long-term subchronic inhalation exposure to 50—150 ppm of the alcohol has caused testicular depression in male rats, but no effects were noted at the 10 ppm level (32). Although the significance of the latter observations for human safety is unknown, it is recommended that continuous exposure to greater than 5 ppm or skin contact with it be avoided. 

Health Hazards Information - Recommended Personal Protective Equipment Dust mask goggles or face shield protective gloves Symptoms Following Exposure Inhalation of dust irritates nose and throat. Contact with eyes causes irritation General Treatment for Exposure INHALATION move to fresh air. EYES flush immediately with physiological saline or water get medical care if irritation persists. SKIN flush with water Toxicity by Inhalation (Thresholdlimit Value) Data not available Short-Term Exposure Limits Data not available Toxicity by Ingestion Grade 1 oral LDjq 11.7 g/kg (rat) Late Toxicity Chronic effects in humans are unknown Vapor (Gas) Irritant Characteristics Not pertinent liqidd or Solid Irritant Characteristics Data not available Odor Threshold Data not available. 

The hazards of chemicals are commonly detected in the workplace first, because exposure levels there are higher than in the general environment. In addition, the exposed population is well known, which allows early detection of the association between deleterious health effects and the exposure. The toxic effects of some chemicals, such as mercury compounds and soot, have been known already for centuries. Already at the end of the eighteenth century, small boys who were employed to climb up the inside of chimneys to clean them suffered from a cancer of the scrotum due to exposure to soot. This was the first occupational cancer ever identified. In the viscose industry, exposure to carbon disulfide was already known to cause psychoses among exposed workers during the nineteenth century. As late as the 1970s, vinyl chloride was found to induce angiosarcoma of the liver, a tumor that was practically unknown in ocher instances. ... 

Not all symptoms after RCM exposure do resemble a hypersensitivity reaction. Toxic reactions related to the toxicity of RCM, imspecific reactions of unknown origin and or factors unrelated to RCM, such as chronic idiopathic urticaria, may occur (fig. 1) [3]. Hypersensitivity reactions to RCM may both present either under the clinical picture of anaphylaxis with the potential to result in fataUties or as delayed occurring... 

CX is an urticant, producing instant, almost intolerable pain and local tissue destruction immediately on contact with skin and mucous membranes. It is toxic through inhalation, skin and eye exposure, and ingestion. Its rate of detoxification in the body is unknown. 

Effects of Metabolism on Toxicity. Whether the toxic effects seen after exposure to diisopropyl methylphosphonate are caused by the parent compound or its metabolites is unknown. Studies of IMP A show that acute-duration exposure to IMPA results in reduced motor activity, prostration, and ataxia—effects also seen after exposure to diisopropyl methylphosphonate (EPA 1992). Other studies (Little et al. 1986, 1988) show that IMPA, the major metabolite of diisopropyl methylphosphonate, has an affinity for both lung and brain tissues and will bind to proteins in these tissues—effects that were not seen after exposure to diisopropyl methylphosphonate (EPA 1992 Little et al. 1988). These data and other data on the toxicity of IMPA neither support nor contradict the data found in the diisopropyl methylphosphonate studies, so it is not possible to attribute the effects after exposure to diisopropyl methylphosphonate to IMPA. Metabolites of IMPA other than MPA have not been identified. 

A pioneer study of the distribution of this substance in the tissues of rats to which it had been fed was made by Laug (3). He evaporated ether extracts in Erlenmeyer flasks, so that a deposit was left over the bottom. Female houseflies were confined in the flasks, and the mortalities after 20 hours were compared to those obtained with known amounts of 7-hexachlorocyclohexane. Because most of the inner surface of the flask was untreated, the flies were out of contact with the toxicant during an unknown fraction of the exposure period. The exposure period was so long that the insects had to be fed dur-... 

Mineral Oil Hydraulic Fluids and Polyalphaolefin Hydraulic Fluids. Limited information about environmentally important physical and chemical properties is available for the mineral oil and water-in-oil emulsion hydraulic fluid products and components is presented in Tables 3-4, 3-5, and 3-7. Much of the available trade literature emphasizes properties desirable for the commercial end uses of the products as hydraulic fluids rather than the physical constants most useful in fate and transport analysis. Since the products are typically mixtures, the chief value of the trade literature is to identify specific chemical components, generally various petroleum hydrocarbons. Additional information on the properties of the various mineral oil formulations would make it easier to distinguish the toxicity and environmental effects and to trace the site contaminant s fate based on levels of distinguishing components. Improved information is especially needed on additives, some of which may be of more environmental and public health concern than the hydrocarbons that comprise the bulk of the mineral oil hydraulic fluids by weight. For the polyalphaolefin hydraulic fluids, basic physical and chemical properties related to assessing environmental fate and exposure risks are essentially unknown. Additional information for these types of hydraulic fluids is clearly needed. 

Human toxicity data are limited to secondary citations. Because these citations provided no experimental details, they cannot be considered reliable. Deaths have occurred from aniline ingestion and skin absorption, but doses were unknown. Reviews of the older literature indicate that a concentration of 5 ppm was considered safe for daily exposures, concentrations of 7 to 53 ppm produced slight symptoms after several hours, a concentration of 40 to 53 ppm was tolerated for 6 h without distinct symptoms, a concentration of 130 ppm may be tolerated for 0.5 to 1 h without immediate or late sequalae, and 100 to 160 ppm was the maximum concentration that could be inhaled for 1 h without serious disturbance. In studies of accidents with unknown exposure concentrations, methemoglobin levels of up to 72% were measured. Recoveries occurred with a minimum of medical intervention following cessation of exposure. 

The exact mechanism by which chemical exposures cause MCS is unknown. It is believed that a two-step process occurs. First, an initial exposure or chronic exposures interacts with a susceptible individual, leading to loss of that person s prior, natural tolerance for everyday, low-level chemicals, as well as certain foods, drugs, alcohol, and caffeine. In the second stage, symptoms are thereafter triggered by extremely low doses of previously tolerated products and exposures.2 This theory is called toxicant-induced loss of tolerance or TILT. 3... 

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