Acute oral exposure MRL of 0.005 mg/kg/day has been calculated for toxaphene on the 8days exposure study. This study represented the lowest LOAEL for hepatic toxicity. Since the liver has been identified as a target of toxaphene toxicity, the LOAEL from this study was used to calculate the acute oral exposure MRL.
Data from animal studies indicate that dermal exposure to toxaphene can be lethal, but at doses that are an order of magnitude higher than those for oral administration of the pesticide because absorption through the skin is much less efficient.
The World Health Organization has not listed toxaphene in WHO Acute Hazard Rankings because as an active ingredient is believed to be obsolete or discontinued for use as a pesticide.Studies performed by the U.S. EPA placed toxaphene formulations in Acute Toxicity Rankings in a Category 1 and 2, Moderately to Highly Toxic (Table below).
Limited information is available on subchronic toxicity in both humans (inhalation and oral) and experimental animals (oral only). The exact duration and level of exposure in the human studies generally cannot be quantified because the information is derived from case reports rather than controlled studies. Most of the information on human exposure is from combinations of pesticides; only one study was located in which oral exposure to toxaphene alone was clearly linked with adverse effects in humans. The animal studies described predominantly neurological, hepatic, renal, developmental, and immunological end points. Sufficient data were available to calculate an Oral intermediateduration MRL of 0.001 mg/kg/day was derived based on NOAEL hepatic effects in rats exposed to toxaphene intermittently for 13 weeks, and the liver has been identified as a target organ of toxaphene toxicity.
Little or no reliable information on respiratory, cardiovascular, gastrointestinal, hematological, musculoskeletal, dermal, or ocular effects in animals is available. The health effects data available on inhalation and dermal exposure to toxaphene in animals come primarily from secondary unpublished sources and, therefore, do not have sufficient details for evaluation. Since wastesite toxaphene may leak into surrounding areas or evaporate, both the inhalation and dermal routes are possible means of exposure for individuals living near hazardous waste sites.
Chronic inhalation exposure to toxaphene in humans has been reported to cause reversible respiratory toxicity.Chronic toxicity studies conducted in animals have found predominantly hepatic, renal, and neurological effects. The health effects data available on chronic inhalation exposure to toxaphene in animals come primarily from secondary unpublished sources, and therefore, do not have sufficient details for evaluation. No information is available on the health effects of chronic dermal exposure to toxaphene. Since wastesite toxaphene may leak into surrounding areas or evaporate, both the inhalation and dermal routes are possible means of exposure for individuals living near hazardous waste sites.
ATSDR has calculated an oral intermediate minimal risk level (MRL) of 0.001 mg/kg/day based on no adverse liver effects in rats. The MRL is an estimate of the daily human exposure to a hazardous substance that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration of exposure. Exposure to a level above the MRL does not mean that adverse health effects will occur.
No information on the reproductive effects of toxaphene in humans is available. The available information from multigeneration studies in rats indicates that toxaphene does not adversely affect reproductive end points. Since it is likely that the distribution of dermally and orally administered toxaphene is similar, dermally absorbed toxaphene should not be expected to cause reproductive toxicity.
Information on the developmental effects of toxaphene in humans resulting from ingestion was not found. Data in experimental animals indicate that toxaphene can cause offspring behavioural toxicity and immunosuppression at doses that are not maternally toxic. However, only one dose was used in these studies that demonstrated behavioural effects, no NOAEL was identified, and the effect was no longer apparent after 16 weeks.