Subclinical effects intoxication

A multiplicity of terms exists to describe lead poisoning. Strictly speaking frank means unmistakable, clinical is recognisable by a physician and classic as described in a textbook. Symptomatic is in the presence of well-defined symptoms and asymptomatic in the presence of an elevated blood lead without obvious symptoms. Other terms include subclinical and intoxication in which effects of lead are assumed but not yet proven. 

At lower exposures, the effects of lead are more difficult to examine. It appears that data from recent studies on developing rats with low blood levels (up to 100/(g Pb/lOOml) appear to show effects of lead on maturing and differentiated nerve cell populations. The relevance of these changes to human subclinical lead intoxication is not clear. However, the overall correspondence in lead-poisoned man and rat would make further investigation in this area appear necessary. 

Experimental animals exposed to sublethal doses of cyclodienes show a similar picture, with changes in EEG patterns, disorientation, loss of muscular coordination and vomiting, as well as convulsions, the latter becoming more severe with increasing doses (Hayes and Laws 1991). It is clear from these wide-ranging studies that a number of neurotoxic effects can be caused by cyclodienes at levels well below those that are lethal. In the human studies described here, subclinical symptoms were frequently reported when dieldrin blood levels were in the range 50-100 pg/L, an order of magnitude below those associated with lethal intoxication. 

Elovaara E, Tossavainen A, Savolainen H. 1978. Effects of subclinical hydrogen sulfide intoxication on mouse brain protein metabolism. Exp Neurol 62 93-98. 

Savolainen H, Tenhunen R, Elovaara E, et al. 1980. Cumulative biochemical effects of repeated subclinical hydrogen sulfide intoxication in mouse brain. Int Arch Occup Environ Health 46 87-92. 

Evidence indicates that OPs can induce chronic effects on both the peripheral and central nervous systems following acute intoxication (Jamal, 1997). The mechanisms for this condition are not related to the inhibition of AChE or NTE. Two types of such disorders have been documented type I, representing COPIND following an acute poisoning episode(s), and type II, representing COPIND following a chronic long-term exposure to subclinical doses. There is no distinction in the chemical nature of OPs for their apparent ability to cause COPIND. 

---