Latency periods

Depending on the concentration of agent vapor, the effects begin to appear from 30 seconds to 2 minutes after initial exposure. 

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Other courts addressing this problem have refused to adopt a rule of proportional recovery. Some have asserted that such a fundamental change of a basic tort principle is more appropriately a legislative function. Others have expressed concern that the long latency period renders any reconstmction of market shares highly speculative. The Restatement notes the opposing views but takes no position on this controversial issue. 

The replacement of asbestos fibers by other fibrous materials has raised similar health issues in relation to substitute materials. However, since lung cancer has a latency period of approximately 25 years, and since the fiber exposure levels in contemporary industries is far lower than those which prevailed half a century ago, the epidemiological data on most substitutes is insufficient. A possible exception is slag fibers for which several studies on worker populations are available over extended periods (44) some results show a substantial increase in lung cancer occurrence. Consequentiy, the toxicity of asbestos substitute fibers remains a subject of active investigation. 

Arguably, risk assessment from exposure to carcinogens merits special consideration because of the low levels of exposure capable of producing an adverse response in certain individuals coupled with the often long time-lag (latency period) between exposure and onset of disease. 

Environmentally induced cancers, for example, commonly involve latency periods of 15 to 30 years or more. 

A toxic reaction may take place during or soon after exposure, or it may only appear after a latency period. Chronic toxicity requires exposure of several years for a toxic effect to occur in humans. With respect to experimental animals, the animals are usually exposed for most or all of their life time to ascertain the occurrence of chronic toxicity. Acute toxic reactions that occur immediately are easy to associate with the exposure and the exposure-effect relationship can readily be demonstrated. The longer the time interval between exposure and effect, the more difficult it is to delineate the relationship between exposure and effect. 

Oral administration of 11.6 mg/kg/day of endosulfan to rats for up to 30 days also failed to induce chromosomal damage in bone marrow and spermatogonial cell systems, but it is not known how soon after treatment the animals were killed. As shown in mouse studies (Usha Rani and Reddy 1986), a latency period of 60 days was required to see chromosomal aberrations in spermatogonia. However, relatively significant changes were observed for mitotic indices (Dikshith et al. 1978). 

When potassium tert-butylate in the solid state comes into contact with a few drops of methanol, ethanol, or 1- or 2-propanol it causes the alcohols to combust after a latency period of two, seven, and one minute(s) respectively. If the alcohol is in the vapour state, ignition can also take place. However, if there is a large quantity of alcohol, there is no incident since alcohol in excess absorbs the heat produced. 

A homogeneous mixture of diethyl ether and nitric acid decomposes vigorously after a latency period during which the medium splits into two liquid phases. One of them was attributed to the formation of ethyl nitrate, which is unstable. 

Unfortunately, clinical trials in human volunteers usually have small sample sizes and adverse reactions are poorly documented. Also, adverse effects that have a long latency period such as carcinogenicity are difficult to account for. 

Arsine is extremely toxic and a potent hemolytic agent, ultimately causing death via renal failure. Numerous human case reports are available, but these reports lack definitive quantitative exposure data. The reports, however, affirm the extreme toxicity and latency period for the toxic effects of arsine in humans. 

Agent vapors of both series cause eye irritation. However, there is no significant difference in the concentration that will irritate the eyes and the one that will produce eye injury. Although impacts from exposure to vesicants occur almost at once, contact with vapors or the liquid agent neither irritates the skin nor produces visible dermal injuries until after a substantial latency period. In contrast, HL (C03-A010), sulfur mustard mixed with lewisite, produces immediate pain due to the arsenic mustard component. 

Urticants produce immediate irritation and pain of the eyes, respiratory tract, and skin. Blanching, reddening of the skin (erythema), and hives develop within minutes of exposure. Blisters, localized tissue death (necrosis), and formation of scabs may be delayed for 24 hours or more. Systemic effects, including pulmonary edema, from either inhalation or percutaneous absorption of the agent, do not occur until after a substantial latency period. 

Effects from vapor exposure begin to appear 1-2 minutes after exposure. Pulmonary edema, caused by inhalation of cyanogen halides, does not occur until after a substantial latency period. 

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