Hypersensitization

The Red-Emitting Triphosphor. Eu + -activated Y2O2 phosphor is the universally used red-emitting triphosphor for lamps. The emission spectmm of this phosphor is almost ideal being dominated by one strong line at 611 nm. This SDg — transition is called hypersensitive because if, for... 

Toxicology. The acute oral and dermal toxicity of naphthalene is low with LD q values for rats from 1780—2500 mg/kg orally (41) and greater than 2000 mg/kg dermally. The inhalation of naphthalene vapors may cause headache, nausea, confusion, and profuse perspiration, and if exposure is severe, vomiting, optic neuritis, and hematuria may occur (28). Chronic exposure studies conducted by the NTP ia mice for two years showed that naphthalene caused irritation to the nasal passages, but no other overt toxicity was noted. Rabbits that received 1—2 g/d of naphthalene either orally or hypodermically developed changes ia the lens of the eye after a few days, foUowed by definite opacity of the lens after several days (41). Rare cases of such corneal epithelium damage ia humans have been reported (28). Naphthalene can be irritating to the skin, and hypersensitivity does occur. 

Skin and Eye Irritation. Fatty alkylamines are generally considered to be irritating to both the skin and eyes (83). The severity or degree of irritation is usually dependent on the type of alkylamine, concentration of the chemical, time of exposure to the chemical, and sensitivity to the chemical. A small percentage of the population who come into contact with fatty amines may develop a skin hypersensitivity to certain amines and diamines. 

Asthma is an extremely complex condition characterized by variable and reversible airways obstmction combiaed with nonspecific bronchial hypersensitivity (1 3). The cause of asthma, which is not always readily diagnosed (4), remains unknown. Days, if not weeks, ate needed to document the spontaneous reversal of the airways obstmction ia some patients. Asthmatics experience both an immediate hypersensitivity response and a delayed late-phase reaction, each mediated by a different pathway. Chronic asthma has come to be viewed as an inflammatory disease (5). The late-phase reaction plays a key role ia iaduciag and maintaining the inflammatory state which ia turn is thought to iaduce the bronchial hyperresponsiveness (6). The airways obstmction results from both contraction of airways smooth muscle and excessive bronchial edema. Edema, a characteristic of inflammatory states, is accompanied, ia this case, by the formation of a viscous mucus which can completely block the small airways. 

Blood dyscrasias are quite uncommon, but if they occur may be serious enough to cause discontinuance of the therapy. Both topical and systemic adrninistration of sulfas can cause hypersensitivity reactions, such as urticaria, exfoHative dermatitis, photosensiti2ation, erythema nodosum, and in its most severe form, erythema multiformexudativum. (Stevens-Johnson syndrome). In general, however, use of sulfonamide therapy is considered relatively safe. 

There should be sufficientiy large numbers of animals to allow a quantitative determination of the average response and the range of responses, including the demonstration of hypersensitive populations. When objective procedures are undertaken, these should be sufficient to allow vaUd statistical comparison to be made between treated and control groups. 

Experimental methods for determining the potential of materials to produce hypersensitivity reactions by inhalation use procedures to detect hyperreactivity of the airways as demonstrated by marked changes in resistance to air flow, and the detection of antibodies in blood semm (93). 

Chelated complexes such as sodium zirconium lactate [15529-67-6] or ammonium zirconium carbonate [22829-17-0] and acidic forms such as zirconium hydroxy oxide chloride [18428-88-1] have been used in preparations in deodorants or for treatment for poison oak and poison ivy dermatitis. In such occasions, when the skin had been cut or abraded, a few users developed granulomas which have been identified as a delayed hypersensitivity to zirconium (99). These may take several weeks to develop, and commonly persist for 6 months to over a year. 

The cephalosporins generally cause few side effects (80,132,219—221). Thrombophlebitis occurs as a result of intravenous administration of all cephalosporins. Hypersensitivity reactions related to the cephalosporins are the most common side effects observed, but these are less common than found with the penicillins. Clinically only about 5—10% of patients with allergic reactions to the penicillins manifest the same reactions to the cephalosporins, and data would contradict any tme cross-reactivity to cephalosporins in patients who have previously reacted to penicillin (80,132,219). 

The adverse effects iaclude digestive disturbances, neurological symptoms, and manifestations of allergic responses. As many as half of the patients taking it are iacapacitated by some of these adverse reactions for several hours. Whether these symptoms are caused by hypersensitivity to the dmg, the parasite, or by a manifestation of the disease is not known. Overall, effects are dose-related and transient. 

Phenytoin s absorption is slow and variable yet almost complete absorption eventually occurs after po dosing. More than 90% of the dmg is bound to plasma protein. Peak plasma concentrations are achieved in 1.5—3 h. Therapeutic plasma concentrations are 10—20 lg/mL but using fixed po doses, steady-state levels are achieved in 7—10 days. Phenytoin is metabolized in the fiver to inactive metabolites. The plasma half-life is approximately 22 h. Phenytoin is excreted primarily in the urine as inactive metabolites and <5% as unchanged dmg. It is also eliminated in the feces and in breast milk (1,2). Prolonged po use of phenytoin may result in hirsutism, gingival hyperplasia, and hypersensitivity reactions evidenced by skin rashes, blood dyscrasias, etc... 

Prolonged contact with certain chromium compounds may produce allergic reactions and dermatitis in some individuals (114). The initial response is usually caused by exposure to Cr(VI) compounds, but once the allergy is estabUshed, it is extended to the trivalent compounds (111,115). There is also limited evidence of possible chromium associated occupational asthma, but there is insufficient data to estimate a dose for assumed chromium-induced asthma. Reference 116 provides a summary and discussion of chromium hypersensitivity. 

Dentifrices are also vehicles for agents that alleviate dentinal hypersensitivity. Among the materials that have given positive results in clinical tests are potassium nitrate [7757-79-1] (5%) and strontium chloride [10476-85-4] (10%). 

Chlorhexidine has found other medical appHcations, eg, in urology in preventing urinary tract infections (217), in obstetrics and gynecology (218), in controlling infection in bums and wounds (219), and in the prevention of oral disease (220). Hypersensitivity to chlorhexidine has been reported in Japan (221) but 0.05% concentration is considered to be safe. 

As is well known, the principal toxicity associated with penicillin therapy is the occurrence of hypersensitivity reactions. This and other aspects of pencillin toxicity have been recently reviewed 81MI51106). 

ATOPY Hypersensitivity where tendency to allergy is inherited. 

Population Adults (16-65) Fit for work possibly monitored All population including infants, aged, infirm hypersensitive subjects... 

Kimber, I. (1997) Toxicology of Chemical Respiratory Hypersensitivity, Taylor and Francis, London. 

In nonindustrial settings, MCS substances are the cause of indoor air pollution and are the contaminants in air and water. Many of the chemicals which trigger MCS symptoms are known to be irritants or toxic to the nervous system. As an example, volatile organic compounds readily evaporate into the air at room temperature. Permitted airborne levels of such contaminants can still make ordinary people sick. When the human body is assaulted with levels of toxic chemicals that it cannot safely process, it is likely that at some point an individual will become ill. For some, the outcome could be cancer or reproductive damage. Others may become hypersensitive to these chemicals or develop other chronic disorders, while some people may not experience any noticeable health effects. Even where high levels of exposure occur, generally only a small percentage of people become chemically sensitive. 

The threshold for toxic injury is not the same for everyone because sensitivity varies greatly among individuals. Most chemicals in consumer products remain untested for health effects, such as cancer, reproductive problems, and the impacts of long-term, low level exposure. How these substances affect women, children, and people with existing conditions is also little studied. Once a person s defenses have been broken down and he or she has become hypersensitive, a wide variety of common chemical exposures can trigger a reaction. Just what products and other chemicals which cause problems varies greatly among affected individuals. 

Hypersensitivity Pneumonitis a group of respiratory diseases that cause inflammation of the lung (specifically granulomatous cells). Most forms of... 

Sensitizer A sensitizer is defined by OSHA as "a chemical that causes a substantial proportion of exposed people or animals to develop an allergic reaction in normal tissue after repeated exposure to the chemical." The condition of being sensitized to a chemical is also called chemical hypersensitivity. Certain chemicals have no immediate health effect. But if you are exposed to them several times, they can make you allergic or sensitive to other chemicals. A classic example is formaldehyde (HCHO). Typical reactions to sensitizers can include skin disorders such as eczema. When working with sensitizers, always use proper protective equipment such as gloves, respirators, etc. Once you are sensitized to a particular chemical, even minute amounts will cause symptoms. Sensitization is usually a lifelong effect. 

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