Human toxicity delayed toxic effects

A limited study in animals also presents evidence for increased susceptibility to Streptococcus zooepidomicus (Aran d et al. 1986). Immune system effects observed in mice exposed orally to trichloroethylene included inhibition of cell-mediated immunity, delayed type hypersensitivity, and inhibition of antibody-mediated immunity (Sanders et al. 1982). Female mice appeared to be more sensitive than male mice. A study in which a susceptible strain of mice was treated with intraperitoneal injections of trichloroethylene suggests that trichloroethylene can accelerate the autoimmune response (Khan et al. 1995). The immune system may be a sensitive end point for toxic effects from low-level exposure to trichloroethylene however, no firm conclusions can be drawn from the available information. Additional human and animal studies are needed to better characterize this end point and determine the potential for immunological effects for people exposed to trichloroethylene at hazardous waste sites. 

No NOAELs or LOAELs were identified for toxic effects in humans after inhalation exposure to organophosphate ester hydraulic fluids. Reliable NOAELs and LOAELs for acute inhalation exposure are restricted to 4-hour NOAELs for systemic effects in rats exposed to Fyrquel 220 or Durad MP280 and 4-hour LOAELs for mild lethargy in rats exposed to Durad MP280 and Fyrquel 220 (Gaworski et al. 1986). The study identifying these NOAEL and LOAEL values did not measure cholinesterase inhibition, did not allow sufficient follow-up time for the development of delayed neurotoxic effects, and used a... 

No clinical or experimental evidence is available to indicate that VX causes delayed neuropathy in humans (Munro et al., 1994). Chickens injected subcutaneously with supralethal doses of VX (10, 100, or 150 /rg/kg, following treatment with antidotes to protect against acute toxicity) exhibited no signs of a delayed neurotoxic response (Goldman et al., 1988). However, QL, a chemical intermediate of VX, has been reported to cause delayed neurotoxic effects in hens dosed at 635 mg/kg (Olajos et al., 1986). The available data indicate that delayed neuropathy in humans exposed to VX is unlikely. 

Data regarding the toxic effects of hydrazines in humans are limited to a few case studies of accidental exposure and chemotherapy trials in cancer patients. Studies consistently indicate that the central nervous system is the primary target for hydrazine and 1,1 -dimethylhydrazine following inhalation, oral, and dermal exposures. In some cases, neurological effects were delayed, but most effects were observed either during exposure or soon after. Quantitative data on human exposures are available only for oral exposures of intermediate durations. 

Information on toxic effects of acute-duration exposure to PCBs by routes other than oral are limited to LD50 values for dermal exposure (Fishbein 1974 Puhvel et al. 1982), but these data may not be reliable due to possible delayed lethality. PCBs are well absorbed after exposure by all routes, and distribution to and retention by adipose tissue has been observed in humans after inhalation, oral, and/or dermal exposure (Brown and Lawton 1984 Fait et al. 1989 Jensen 1987). Mobilization of PCBs from adipose tissue to target organs is likely to be similar regardless of the route of exposure. Additional acute dermal studies are relevant because the skin is a route of concern for exposure at or near hazardous waste sites, particularly due to possibilities for brief contact. Acute inhalation toxicity studies may be relevant due to the potential for inhalation exposure from electrical appliances in buildings and downwind from PCB disposal facilities and incinerators. 

There are many different cholinesterase inhibitors which find use, particularly as insecticides but also as nerve gases for use in chemical warfare. Organophosphorus insecticides are the most widely used and the most frequently involved in fatal human poisonings. They may be absorbed through the skin and there have been accidental poisoning cases arising from such exposure. Accidental contamination of food with insecticides such as parathion has led to a significant number of deaths. There are two types of toxic effects inhibition of cholinesterases and delayed neuropathy. 

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