Latency short

Key Latency Short = minutes to hours, Long = hours to days. Persistency Short = minutes to hours. Intermediate = hours to days, Long = days to weeks... 

Subchronic Studies. Although short-term repeated exposure studies provide valuable information about toxicity over this time span, they may not be relevant for assessment of ha2ard over a longer time period. For example, the minimum and no-effects levels determined by short-term exposure may be significantly lower if exposure to the test material is extended over several months. Also, certain toxic effects may have a latency which does not allow their expression or detection over a short-term repeated-exposure period for example, kidney dysfunction or disturbances of the blood-forming tissues may not become apparent until subchronic exposure studies are undertaken. 

Latency refers to the period of time that elapses between the first contact of a harmful agent and a host, and the development of identifiable symptoms or disease. Latency may be as short as a few hours, the time required for photochemical smog to induce watery eyes. Or it may stretch to 20 - 30 years for a chronic condition such as asbestosis or malignant neoplasm of the lung. The association between a gi en e.xposure and a disease is all that more difficult because of the passage of time. 

Acute clinical effects organ system specificity, short latency, high dose exposure ... 

Melatonin at doses of 0.5 to 5 mg taken at appropriate target bedtimes for east or west travel is becoming the drug of choice for jet lag. Melatonin significantly reduces jet lag and shortens sleep latency in travelers.50 Hypnotic agents with relatively short durations of action (3 to 5 hours) also may be used to sustain sleep during the initial adaptation to the new time zone. 

The occupational exposure of five workers to arsine was reported by Phoon et al. (1984). All cases involved hematuria and, except for one patient, abdominal pain and jaundice. One worker was exposed for approximately 1 3/4 h, while the others were exposed for approximately 2 1/4 h. The latency in appearance of toxic effects was unusually short U-3 h). The following day, the arsine level in the workers breathing zone was 0.055 mg/m3 (0.017 ppm), although no processing of arsenic-containing material was taking place at the time of measurement. It was hypothesized by the report authors that the arsine... 

The period of the test depends on whether long- or short-term effects are of interest. Acute toxicity is the effect of a single exposure or a series of exposures close together in a short period of time. Chronic toxicity is the effect of multiple exposures occurring over a long period of time. Chronic toxicity studies are difficult to perform because of the time involved most toxicological studies are based on acute exposures. The toxicological study can be complicated by latency, an exposure that results in a delayed response. 

Mouse Bioassay. When administered at 5 mg per mouse in 0.5 ml dose during the initial screening, the WSAP from G. toxicus caused death in all test mice within 120 minutes. The toxin had a latency period of approximately 30 minutes after which signs of toxicity were noticeable, and included in order of occurrance inactivity and piloerection followed by cyanosis of the tail and feet with concurrent hypothermia, vasodilation in the ears ( scarlet ears ), lacrimation, ptosis of the eye lid on the side of injection, ptosis of the abdomen (loss of muscular tone), asthenia, impairment of hind limb motor ability followed shortly by complete paralysis with the hind limbs extended posteriorly (complete prostration), and dyspnea (respiratory distress). Death occurred without convulsions and the eyes became cataracted just prior to or after death. 

The signs and symptoms of hypersensitivity include urticaria, contact dermatitis of the skin, and respiratory disorders ranging from sneezing, shortness of breath, and cyanosis to severe asthma. The latency period from the first contact with platinum to the occurrence of the first symptoms varies from a few weeks to several years. ... 

For short-term experiments, thorium-232 is considered radiologically inert since its half-life is so long. Therefore, the chemical toxicity of thorium was tested using this isotope. The low chemical toxicity of thorium was evidenced by the lack of initial systemic effects in patients injected with Thorotrast and in occupationally exposed workers. Animal studies also showed low toxicity (Guimaraes et al. 1955 Patrick and Cross 1948). Natural thorium (thorium-232) is toxic only after a latency period of 20-30 years, when the radiological effects are manifested. 

Following intravenous injection of Thorotrast in humans and animals, various malignancies were found, primarily liver cancers (latency period of 25-30 years), leukemia (latency period of 20 years), and bone cancers (latency period of about 26 years). Short-lived daughter products of thorium also resulted in the induction of bone sarcoma because of their short radioactive half-lives. Intravenous injection of thorium-228 resulted in dose-dependent induction of bone sarcoma in dogs (Lloyd et al. 1985 Mays et al. 1987 Stover 1981 Wrenn et al. 1986). At the highest administered level, the animals died from systemic radiological effects (e.g., radiation induced blood dyscrasia and nephritis) before the bone sarcoma could develop (Stover 1981 Taylor et al. 1966). A relationship was found between the amount of thorium-227 (half-life of 18.7 days) injected intraperitoneally and the incidence of bone sarcoma in mice (Luz et al. 1985 Muller et al. 1978). 

Elemental Be and its compounds are very poisonous by inhalation or intravenous route. Chronic inhalation of beryUium dusts or fumes can cause a serious lung disease, beryUiosis, after a latent period ranging from several months to many years. Inhalation of airborne dusts can also cause an acute disease manifested as dyspnea, pneumonitis and tracheobronchitis with a short latency period of a few days. Skin contact with soluble salts of the metal can cause dermatitis. Beryllium also is a carcinogen. There is sufficient evidence of its inducing cancer in animals and humans. 

In chnical trials, zolpidem shortened sleep latency, improved the quahty of sleep, and accelerated the restoration of normal sleep patterns (Lee, 2004). In insomniac patients it increased the amount of slow wave, restorative sleep as seen in normal sleepers. Zolpidem has high oral bioavailability (70%), a short duration of action (tj /2 = 2 h), and is relatively highly bound to plasma proteins (92%). The recommended dose is generally 10 mg/day as needed. Zolpidem is extensively metabolized, mainly by CYP3A4 but also by CYP1A2 and CYP2C9, and its major metabolites do not appear to have pharmacological activity. It has minimal daytime residual effects, and a low risk for tolerance and abuse. The safety profile showed a low incidence of adverse events, close to that observed with placebo. The medicine is available in over 80 countries. 

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