Populations in areas that contain hazardous waste sites may be exposed to Aldrin for brief periods. Exposure would most likely occur by the inhalation or oral routes, but dermal exposure is also possible. There are acuteduration oral exposure data in humans from cases of accidental or intentional poisonings that indicate that the central nervous system is a major target organ of Aldrin toxicity by the oral route. Convulsions have been observed following ingestion of very high concentrations of Aldrin.
Also, acute oral exposure in humans has been reported to cause renal toxicity. Renal toxicity has not been reported in studies in animals after acuteduration ingestion of high concentrations of Aldrin; however, the number of studies examining systemic effects associated with acuteduration exposures is quite limited. Studies in laboratory animals examining the effects of ingestion of Aldrin have supported the conclusion that the nervous system is a major target organ of Aldrin toxicity. In such studies, convulsions as well as impaired responding in operant behavioural paradigms were reported. In addition, immune suppression, and adaptive changes in the liver have been observed in acutely exposed animals. Results of these studies indicate that the immune system may be the most sensitive target organ for the effects of brief oral exposures to Aldrin.
An acuteduration oral MRL was derived for Aldrin based on a neurological effect (altered electroconvulsive shock threshold) and decreased body weight in offspring of treated mice.
No information is available regarding acuteduration inhalation exposure to Aldrin in humans, and extremely limited information is available from studies in animals. Although the volatility of Aldrin is quite low and levels in the atmosphere are expected to be quite low, absorption of this compound by the lungs occurs to a significant extent. Toxicokinetic data do not indicate that dissimilar target organs would be affected as a result of inhalation exposure to Aldrin.
Information regarding the acute effects of dermal exposure of Aldrin is limited to lethality studies in animals. Dermal exposure to Aldrin is possible in contaminated soil, and toxicokinetic studies indicate that dermally applied Aldrin is absorbed. Toxicokinetic data do not suggest that dissimilar target organs would be affected as a result of dermal exposure.

The World Health Organization has not listed Aldrin 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 aldrin formulations in Acute Toxicity Rankings in a Category 1 and 2, Moderately to Highly Toxic (Table below).

Study type Route Species Result Units
LD50 Dermal Rabbit 15 mg/m3
LD50 Dermal Rat 98 mg/m3
LD50 Oral Dog 65 mg/m3
LD50 Oral Duck 520 mg/m3
LD50 Oral Guinea pig 33 mg/kg
LD50 Oral Hamster 100 mg/kg
LD50 Oral Rabbit 50 mg/kg
LD50 Oral Rat 39 mg/kg

Few reports were located regarding effects in humans after intermediateduration exposure to aldrin by any route. These studies showed that the nervous system is a major target organ in humans after intermediateduration exposures and it confirmed by the studies in laboratory animals. Other targets identified in intermediateduration oral studies in animals include the immune system, the developing neonate, the reproductive system, the kidney, and the liver.  An intermediateduration oral MRL for aldrin was not derived due to lack of suitable effect levels. Intermediateduration studies of aldrin are essentially limited to studies that found frank neurotoxic effects (e.g., tremors, convulsions) at the lowest tested doses; LOAELs for serious end points are inappropriate for deriving MRLs.
No data were located regarding intermediateduration inhalation exposures in animals, and human exposure levels were not quantified. Therefore, no intermediateduration inhalation MRL was derived for aldrin. Also, only limited information was located regarding lethality, neurological effects, and dermal effects after intermediateduration dermal exposures. As noted above, absorption occurs by both the inhalation and dermal routes, and toxicokinetic data indicate that similar target organs would be affected following exposure to either route.

A number of epidemiological studies have been conducted on workers exposed chronically to aldrin. In these studies, doses are usually not well quantified and concomitant inhalation, dermal, and possibly oral exposures have occurred.
Data from the existing epidemiological studies indicate that the nervous system is a major target organ for chronic inhalation, dermal, and possibly oral exposures in humans. Chronic oral studies in animals also indicate that the nervous system is a major target organ, but additionally demonstrate adverse effects of aldrin on the kidney and liver. The liver was the most sensitive target of toxicity in chronicduration studies and hepatic effect levels in rats were used as the basis of chronic oral MRLs for aldrin. No chronic animal studies were located for the inhalation route. One animal study was located examining the effects of chronic dermal exposure. Studies examining the effects caused by lowlevel chronic exposures by both the inhalation and oral routes would be valuable for determining whether such exposures could cause toxicity in populations exposed to aldrin near hazardous waste sites for extended periods.

Structure formula of Aldrin

3D structure of Aldrin

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