Toxicity/toxic effects subclinical

Stratification of lead s toxicity in humans into diagnosable disease or probabilistic risks of disease is not simply defined by where exposures and toxic effects align across the full spectrum of lead s dose—response relationships. That is, one cannot infer that only historic clinical effects at high Pb exposures comprise diagnosable disease and that subclinical effects always require population or epidemiological approaches. See the historical scientific perspective on these topics by Mushak (1992). 

Low-level SM exposure with or without symptoms but with delayed or long-term health effects has been described in detail (Mandel and Gibson, 1917 Hurst and Smith, 2001 Balali-Mood et al., 2005a,b Balali-Mood and Hefazi, 2006). Subclinical exposure to SM in some Iranian combatants induced delayed toxic effects (Ghanei et al., 2004a-c). Chronic SM exposure is usually occupational. Some factory workers in Japan and in the United Kingdom were reported to have had SM... 

Effect. Potential biomarkers of the subclinical effects of hydrogen sulfide are decreases in the activities of the heme synthesis enzymes, ALA-S and Haem-S (Jappinen and Tenhunen 1990). These effects have nothing to do with the mechanism of toxicity, however. Neurological indices are also used as biomarkers of effect for hydrogen sulfide (Gaitonde et al. 1987 Kilbum 1993 Stine et al. 1976 Tvedt et al. 1991b). 

Youssef, S.A.H., Effect of subclinical lead toxicity on the immune response of chickens to Newcastle s disease virus vaccine, Res. Vet. Sci. 60, 13, 1996. 

Hathaway J A Subclinical effects of trinitrotoluene A review of epidemiology studies. In Richert DE (ed) Toxicity of Nitroaromatic Compounds, pp 255-274. New York, Hemisphere Publishing, 1985... 

Subclinical effects are often observed when molybdenum levels in soil exceed 3 pg/g an excess of molybdenum in forage is toxic to livestock. Deficiency diseases have been observed in livestock when soil molybdenum levels are below 0.5 pg/g. 

Toxicities included an infusion reaction consisting of fever, chills, pain, asthenia, nausea, and vomiting. This syndrome was typically observed after the initial infusion, was self-limited, and frequently did not recur with subsequent infusions. The most serious toxicity was cardiac dysfunction, defined as clinical findings of congestive heart failure and/or subclinical declines in cardiac ejection fraction, which was seen in 5% of patients. Cardiotoxicity was unanticipated, as it had not been detected in previous studies. The mechanism for this effect is unclear, but is likely related to trastuzumab s antiproferative effect on HER2-mediated homeostasis and response to injury. 

Other populations are unusually susceptible to the aromatic EC5-EC9 fraction. People with P-thalassemia may be at risk for benzene exposure because some forms of P-thalassemia may exacerbate the adverse effects of benzene on the hematopoietic system. Children and fetuses may be at increased risk to benzene toxicity because their hematopoietic cell populations are expanding and dividing cells are at a greater risk than quiescent cells. Developmental effects in animals are the basis for intermediate inhalation MRLs for ethylbenzene and mixed xylene, indicating that the embryo/fetus may be particularly sensitive to these two BTEXs. People with subclinical and clinical epilepsy are considered at increased risk of seizures from xylene because of its central nervous system effects. 

Fernandez JM, Croom WJ, Johnson AD, et al. 1988. Subclinical ammonia toxicity in steers effects on blood metabolite and regulatory hormone concentrations. J Anim Sci 66(12) 3259-3266. 

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