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Toxicity

No information is available regarding the effects of acuteduration exposure to mirex in humans following inhalation, oral, or dermal exposure.
A large number of studies have been published for acuteduration oral exposure of rats and mice to mirex, many of them addressing interactions with other chemicals, such as the halogenated hydrocarbons, and adaptive liver effects. However, no information could be located for acuteduration inhalation or dermal exposure.
Mirex may lead to death after oral exposure, depending upon dose; some evidence exists that pregnant rats may be more sensitive to the lethal effects of mirex. The main targets of mirex toxicity following acute exposure by the oral route are the liver, nervous system, developing fetus, and eyes. Impaired hepatobiliary excretion and hepatic glycogen depletion have been described as the major hepatic effects. Tremors, hyperactivity or lethargy, and weakness were observed following acuteduration oral exposure to large doses of mirex. Prenatal acuteduration exposure to mirex resulted in cardiac and visceral anomalies, cataracts, increased resorptions, and lethality of offspring. Cataract formation in newborns occurs after early postnatal exposure. Diarrhoea, resulting from gastric irritation, has also been found with acuteduration oral mirex administration, especially in dying animals. The dose at which this effect occurs is not clear. Alterations in blood flow, in addition to changes in membranebound enzymes responsible for electrolyte flux in cardiac cells, occurs after acute oral exposure. The physiological significance of these changes to the experimental animal is not known. Thyroid toxicity has also been documented in rats, in addition to adrenal hypertrophy and hyperfunction. There was no indication that mirex was genotoxic in a dominant lethal assay. It is not possible to determine the target organ for mirex toxicity after inhalation or dermal exposure due to the complete lack of data in these areas for this duration of exposure. No acuteduration inhalation MRL could be derived for mirex because no inhalation data could be located. No acuteduration oral MRL was derived for mirex because serious effects, like heart block and arrhythmias in fetuses from dams exposed during gestation, were observed at the lowest dose tested.


The World Health Organization has not listed mirex 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 mirex formulations in Acute Toxicity Rankings in a Category 2, Moderately Toxic (Table below).

Study typeRouteSpeciesResultUnits
LC50InhalationBird (domestic or lab)1400ppm
LC50DermalRabbit800mg/kg
LC50OralDuck2400mg/kg
LC50OralHamster125mg/kg
LC50OralRat235mg/kg

No information is available regarding the toxicity of intermediateduration exposure of humans to mirex by any route of administration.
Information regarding exposure of animals to mirex for an intermediate duration is available for the oral route. Animals exposed orally to mirex for an intermediate period of time demonstrated increased lethality according to dose and species where mice and dogs may be more sensitive. Data from inhalation or dermal exposure to mirex could not be located; therefore, the concentration or dose that would be likely to cause death after these exposure routes cannot be established. The target organs of toxicity to orally administered mirex appear to be the liver, gastrointestinal system, and thyroid. Liver toxicity with intermediateduration oral exposure to mirex is similar to that occurring after acuteduration exposure, with the exception that lower doses cause hepatotoxicity. The most prominent hepatic effects are impaired biliary excretion and liver histopathology. Mild diarrhoea occurred in two studies in rats; in one study with mice, severe diarrhoea and haemorrhage of the intestines indicated a gastrointestinal origin for the disturbance. Histopathological changes in the thyroid have been reported after intermediateduration oral exposure of animals; however, no change in serum thyroid hormone levels was found.
Adrenal effects have been seen that are consistent with increased lipid utilization. Body weight decreases have been found in intermediateduration oral studies using mirex. No adverse cardiovascular effects were found in one study; however, the data reported from this study were limited. No renal toxicity was found after intermediateduration oral exposure to mirex, but these studies are flawed. No reports could be located describing the musculoskeletal effects of intermediateduration oral mirex administration.

No information is available regarding the toxicity of chronicduration exposure of humans to mirex by the inhalation or dermal route of administration.
Animal studies have not been located for chronic mirex administration by the inhalation or dermal routes.
Chronic exposure to mirex by the oral route results in mortality in animals, especially at higher doses and for longer durations. The major target organs for mirex after chronicduration exposures appear to be the kidney, nervous system, reproductive system, liver, cardiovascular system, and thyroid. Although acute and intermediateduration exposures to mirex are without renal effects, chronicduration exposure results in kidney toxicity.
Sufficient data exist to speculate that the kidney is a primary site of mirex toxicity.
Nephrotoxicity as characterized by histological changes like necrosis and nephritis was documented. Chronicduration exposures to mirex have been shown to increase excitability, hypoactivity, irritability, and tremors in treated rats, as was found in shorterterm oral exposures.
Reproductive effects of chronicduration mirex exposure included cataract formation and decreased survivol in offspring, and inhibition of reproduction. Histopathological examination of chronic exposure studies revealed hepatic necrosis. Thyroid effects occurred in chronicduration exposure to mirex. Several intermediateduration studies in rats also indicate that the thyroid is a target organ for mirex toxicity. These studies showed reduced colloid, thickening of the follicular epithelium, angular collapse of the follicles, and dilation of the rough endoplasmic reticulum of thyroid cells at 0.25 mg/kg/day for 28 days. A chronicduration oral MRL was derived using a NOAEL for hepatic, renal, and thyroid toxicity in a 2year feeding study in rats. Reproductive toxicity was tested at doses higher than the NOAEL from this study, and only less serious effects, nonsignificant decrease in litter size, were observed. No chronicduration inhalation MRL was derived for mirex because no data could be located for this duration and route. No reports could be located that addressed the effects of chronicduration exposure to mirex regarding gastrointestinal, hematological, musculoskeletal, dermal, or adrenal toxicity.


No human data regarding reproductive effects of mirex were located.
Studies in laboratory animals exposed orally to mirex derivative, chlordecone, have demonstrated reproductive effects similar to those produced by mirex in animals. Oral administration of these compounds decreased the fertility or fecundity and litter size, reduced the sperm count, and caused testicular atrophy in animals.
No studies in animals were found regarding reproductive effects of mirex via inhalation or dermal routes.

No human studies are available on developmental effects of mirex in humans for any exposure route.
No studies are available for animals via the inhalation or dermal routes.
Developmental effects of mirex via oral exposure have been well documented in animals.

 


Structure formula of Mirex


3D structure of Mirex