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ALDRIN

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Aldrin is a chlorinated hydrocarbon insecticide.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C12-H8-Cl6

Available Forms Sources

    A) FORMS
    1) Chlorinated hydrocarbon insecticide compounds are very toxic because they are LIPHOPHILIC -- high solubility in fats makes the NERVOUS SYSTEM the major target organ (EOSH, 1983). Aldrin is rapidly metabolized to DIELDRIN , an experimental animal carcinogen (Proctor et al, 1988).
    B) USES
    1) Aldrin is a chlorinated hydrocarbon insecticide of the cyclodiene type; it is no longer manufactured in the USA, but some is imported solely for use in termite control by subsurface soil injection (Sittig, 1985; Budavari, 1989).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Aldrin is a chlorinated hydrocarbon insecticide in the cyclodiene family which is no longer manufactured in the US. This review is based on the properties of chlorinated hydrocarbon insecticides in general, with effects specific to aldrin identified. The primary target of action is the central nervous system. CNS excitation, myoclonic jerking, and recurrent convulsions may occur. Respiratory depression may occur concurrently with coma and is usually the immediate cause of death.
    0.2.3) VITAL SIGNS
    A) Respiratory depression can occur from exposure to aldrin. Fever and recurrent hypotension occurred in acute endrin poisoning.
    0.2.4) HEENT
    A) Hypersalivation and headache may occur.
    0.2.5) CARDIOVASCULAR
    A) Cardiac dysrhythmias can occur from cardiac sensitization.
    0.2.6) RESPIRATORY
    A) Irritation, reduced gas exchange, and chemical pneumonitis may occur.
    0.2.7) NEUROLOGIC
    A) Sensory disturbances, excitation with myoclonic jerking, convulsions, tremor, ataxia, agitation, nervousness, and amnesia may occur. Permanent damage may occur from acute exposure.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, and diarrhea may occur following ingestion.
    0.2.9) HEPATIC
    A) Aldrin is a liver enzyme inducer. Hepatic necrosis has been seen in animals.
    0.2.10) GENITOURINARY
    A) Renal tubular degeneration was seen in animals. Renal insufficiency occurred in a case of aldrin ingestion.
    0.2.11) ACID-BASE
    A) Severe metabolic acidosis may be a consequence of convulsions and an immediate cause of death.
    0.2.13) HEMATOLOGIC
    A) Aplastic and megaloblastic anemia, and rare blood dyscrasias have been associated with exposure to organochlorines.
    0.2.14) DERMATOLOGIC
    A) Extensive contact results in dermal irritation. Erythematobullous dermatitis has been reported from exposure to aldrin. Generally pure aldrin causes only minor erythema, but commercial formulations may contain more irritating components.
    0.2.15) MUSCULOSKELETAL
    A) Myoclonic jerks similar to those seen in grand mal seizures occur with acute exposure to aldrin.
    0.2.18) PSYCHIATRIC
    A) Alterations in mental function occur as a result of the neurotoxicity of chlorinated hydrocarbon insecticides.
    0.2.20) REPRODUCTIVE
    A) Aldrin has been fetotoxic and teratogenic in mice and hamsters. Mixed results have been obtained in rats, and it was not teratogenic in dogs. Higher doses have altered the estrus cycle and fertility in rats. Aldrin and dieldrin have been found in human breast milk.
    0.2.21) CARCINOGENICITY
    A) One occupational study which found no evidence that aldrin is a human carcinogen was judged inadequate by the IARC.
    0.2.22) OTHER
    A) Aldrin can cause systemic effects by the inhalation, oral, and dermal routes. It is efficiently absorbed through the skin. Aldrin is metabolized to dieldrin, both in animals and in the environment. Dieldrin is of approximately equal neurotoxicity. Persons with liver disease may be more sensitive.

Laboratory Monitoring

    A) Blood chlorinated hydrocarbon levels are not clinically useful following acute exposure. For most compounds, blood levels reflect cumulative exposure over a period of months or years rather than recent exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Emesis is not recommended due to potential CNS depression or seizures.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    D) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    E) Do not give oils by mouth.
    F) Do not administer adrenergic amines, which may further increase myocardial irritability and produce refractory ventricular arrhythmias.
    G) CHOLESTYRAMINE - Oral administration may enhance the excretion of kepone and chlordane which are trapped in the enterohepatic circulation.
    H) HEMODIALYSIS - Probably ineffective.
    I) EXCHANGE TRANSFUSION - Probably ineffective.
    J) HEMOPERFUSION - Probably ineffective.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) If clothing is contaminated remove, and wash skin and hair three times; do an initial soap washing followed by an alcohol washing followed by a soap washing. Leather absorbs pesticides. Hence, leather should not be worn in the presence of pesticides and all contaminated leather should be discarded.

Range Of Toxicity

    A) Acute oral exposures >10 mg/kg may cause illness. The lethal human oral dose has been estimated in the range of 3 to 7 grams.

Clinical Effects

Summary Of Exposure

    A) Aldrin is a chlorinated hydrocarbon insecticide in the cyclodiene family which is no longer manufactured in the US. This review is based on the properties of chlorinated hydrocarbon insecticides in general, with effects specific to aldrin identified. The primary target of action is the central nervous system. CNS excitation, myoclonic jerking, and recurrent convulsions may occur. Respiratory depression may occur concurrently with coma and is usually the immediate cause of death.

Vital Signs

    3.3.1) SUMMARY
    A) Respiratory depression can occur from exposure to aldrin. Fever and recurrent hypotension occurred in acute endrin poisoning.
    3.3.2) RESPIRATIONS
    A) RESPIRATORY DEPRESSION - Aldrin is a respiratory depressant.
    3.3.3) TEMPERATURE
    A) FEVER - Occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).
    3.3.4) BLOOD PRESSURE
    A) Recurrent hypotension occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).

Heent

    3.4.1) SUMMARY
    A) Hypersalivation and headache may occur.
    3.4.2) HEAD
    A) HEADACHE - Has been reported from aldrin exposure (EPA, 1985).
    3.4.6) THROAT
    A) HYPERSALIVATION - Foaming at the mouth has occurred with endosulfan and endrin ingestion (Shemesh et al, 1988; Runhaar et al, 1985).

Cardiovascular

    3.5.1) SUMMARY
    A) Cardiac dysrhythmias can occur from cardiac sensitization.
    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) High concentrations of organochlorine insecticides can cause cardiac dysrhythmias by increasing myocardial irritability (Morgan, 1993).

Respiratory

    3.6.1) SUMMARY
    A) Irritation, reduced gas exchange, and chemical pneumonitis may occur.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Irritation of respiratory membranes may result from inhalation of hexachlorobenzene (Dreisbach, 1983).
    B) HYPOXEMIA
    1) Severe convulsions can limit pulmonary gas exchange, and this may be an immediate cause of death (Morgan, 1993).
    C) PNEUMONITIS
    1) Aspiration of petroleum distillate solvent is likely to cause a hydrocarbon pneumonitis, which is potentially fatal.

Neurologic

    3.7.1) SUMMARY
    A) Sensory disturbances, excitation with myoclonic jerking, convulsions, tremor, ataxia, agitation, nervousness, and amnesia may occur. Permanent damage may occur from acute exposure.
    3.7.2) CLINICAL EFFECTS
    A) PARESTHESIA
    1) SENSORY DISTURBANCES - Early signs of organochlorine poisoning involve hyperesthesia and paresthesia of the face and extremities, headache, dizziness, and incoordination (Morgan, 1993).
    B) MYOCLONUS
    1) MYOCLONIC JERKING - As the severity of the poisoning increases, myoclonic jerking movements appear (Morgan, 1993).
    C) SEIZURE
    1) Generalized tonic-clonic seizures occur in severe poisonings. Coma and respiratory depression may ensue (Morgan, 1983). Aldrin is a CNS excitant and convulsant (Clinical Note, 1984).
    a) Seizures may appear as an early sign in the absence of other symptoms with the cyclodienes such as aldrin (EPA, 1985; Morgan, 1993).
    b) Seizures may recur over several days after an acute exposure (Morgan, 1993; Proctor et al, 1988).
    D) PSYCHOMOTOR AGITATION
    1) Kepone, mirex, endosulfan, and chlorbenzilate are more likely to produce tremors, ataxia, agitation, and nervousness than seizures.
    E) AMNESIA
    1) Amnesia following camphechlor ingestion has been reported (Dreisbach, 1983; Wells & Milhorn, 1983).
    F) CENTRAL NERVOUS SYSTEM FINDING
    1) PERMANENT DAMAGE - Severe mental impairment was evident one year after ingestion of endosulfan in one case. It is not clear if the brain damage was due to a direct effect of endosulfan, or to the hypoxemia accompanying convulsions and respiratory insufficiency (Shemesh et al, 1988).
    G) SECONDARY PERIPHERAL NEUROPATHY
    1) POLYNEUROPATHY - Occasional reports have associated peripheral neuropathy with exposure to organochlorines.

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, and diarrhea may occur following ingestion.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) When ingested, these agents cause nausea and vomiting (Clayton & Clayton, 1981; Hathaway et al, 1996), especially when contained in petroleum distillates.
    B) DIARRHEA
    1) Diarrhea may occur.

Hepatic

    3.9.1) SUMMARY
    A) Aldrin is a liver enzyme inducer. Hepatic necrosis has been seen in animals.
    3.9.2) CLINICAL EFFECTS
    A) HEPATIC NECROSIS
    1) Hepatic necrosis has been seen in animals acutely exposed to aldrin (Proctor et al, 1988).
    B) LIVER ENZYMES ABNORMAL
    1) ENZYME INDUCTION - Single doses of aldrin at 20 mg/kg induced liver enzymes in rats (HSDB , 1997).

Genitourinary

    3.10.1) SUMMARY
    A) Renal tubular degeneration was seen in animals. Renal insufficiency occurred in a case of aldrin ingestion.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) RENAL INSUFFICIENCY - occurred in a fatal case of endrin ingestion (Runhaar et al, 1985). Tubular generation was produced in animals acutely exposed to aldrin (Proctor et al, 1988).

Acid-Base

    3.11.1) SUMMARY
    A) Severe metabolic acidosis may be a consequence of convulsions and an immediate cause of death.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) METABOLIC ACIDOSIS - Severe metabolic acidosis may be a consequence of severe convulsions, and the acidosis may be an immediate cause of death (Morgan, 1993).

Hematologic

    3.13.1) SUMMARY
    A) Aplastic and megaloblastic anemia, and rare blood dyscrasias have been associated with exposure to organochlorines.
    3.13.2) CLINICAL EFFECTS
    A) APLASTIC ANEMIA
    1) Large exposures to lindane, chlordane, and dieldrin have been associated with rare individual cases of aplastic anemia (Morgan, 1993).
    B) MEGALOBLASTIC ANEMIA
    1) Megaloblastic anemia and other rare cases of blood dyscrasias have been associated with exposure to organochlorines (Infante et al, 1978; Sharp et al, 1986).
    C) THROMBOCYTOPENIC DISORDER
    1) Thrombocytopenia occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).

Dermatologic

    3.14.1) SUMMARY
    A) Extensive contact results in dermal irritation. Erythematobullous dermatitis has been reported from exposure to aldrin. Generally pure aldrin causes only minor erythema, but commercial formulations may contain more irritating components.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Some skin irritation results from extensive contact with these agents or with petroleum distillates in which they are contained.
    B) ERUPTION
    1) One case of erythematobullous dermatitis has been reported from exposure to aldrin, but dermatitis is unusual with this compound (Hathaway et al, 1996). Generally only minor erythema is caused by pure aldrin, but commercial formulations may contain more irritating components (Clayton & Clayton, 1981).

Musculoskeletal

    3.15.1) SUMMARY
    A) Myoclonic jerks similar to those seen in grand mal seizures occur with acute exposure to aldrin.
    3.15.2) CLINICAL EFFECTS
    A) MYOCLONUS
    1) MYOCLONIC JERKING has been reported with aldrin exposure (EPA, 1985).

Reproductive

    3.20.1) SUMMARY
    A) Aldrin has been fetotoxic and teratogenic in mice and hamsters. Mixed results have been obtained in rats, and it was not teratogenic in dogs. Higher doses have altered the estrus cycle and fertility in rats. Aldrin and dieldrin have been found in human breast milk.
    3.20.2) TERATOGENICITY
    A) HUMAN DATA
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent or potential effects of exposure to this agent during pregnancy or lactation in humans.
    B) ANIMAL STUDIES
    1) Aldrin has been associated with eye, ear and musculoskeletal system developmental abnormalities in both the mouse and the hamster; post- implantation mortality and fetotoxicity in hamsters; and effects on the newborn live birth index in the mouse. In addition, effects on the uterus, cervix and the vagina have been observed in rats (RTECS , 1990).
    2) Fetotoxicity, structural malformations, and growth retardation were seen in hamsters exposed to 50 mg/kg (Hathaway et al, 1996).
    3) Cleft palate, eye and digit defects have been produced in mice and hamsters by aldrin (Ottolenghi et al, 1974; Schardein, 1985). Mixed results have been obtained in rats; aldrin has been either embryotoxic or teratogenic (Schardein, 1985).
    4) Neither aldrin nor its primary metabolite dieldrin were teratogenic in dogs (Kitselman, 1953).
    5) In rats, a low frequency of congenital malformations has been reported (Schardein, 1993).
    6) Dieldrin, a metabolite of aldrin, was not teratogenic in rabbits (Schardein, 1985).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) Disturbances in the estrus cycle of rats was produced at dietary doses of 10 and 20 ppm (Ball et al, 1953).
    2) Aldrin did not affect fertility or neonatal mortality in rats at 2.5 ppm, while dieldrin did (Treon & Cleveland, 1955).
    3) Aldrin affected fertility and gestation at 10 to 25 ppm (mixed with dieldrin or chlordane) in a two-generation feeding study in mice (Clayton & Clayton, 1981).
    4) Aldrin did not affect reproduction in the offspring of female rats fed it during gestation (HSDB , 1997).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Aldrin concentrations in breast milk samples from Quebec exceeded the Codex Alimentarius Commission maximum residue limits (0.041 +/- 0.068 mg/kg) for 3% of the samples. The mean content of aldrin in human breast milk was 0.002 ppm, and dieldrin was 0.20 ppm, in another study (HSDB , 1990). Aldrin and dieldrin were found in breast milk of women who were not occupationally exposed (Bakken & Seip, 1976).
    2) Aldrin affected lactation in a two-generation study on mice (Clayton & Clayton, 1981).
    3) Aldrin given in the diet increased the mortality of nursing dog pups (Kitselman, 1953).
    4) Highly lipophilic compounds which are stored in body fat such as dieldrin are likely to be transferred to breast milk (Morgan, 1993).
    5) The daily intake of total organochlorine pesticides residues calculated for the suckling infant was significantly higher when compared with the acceptable daily intake (ADI) as recommended by FAO/WHO (FAO/WHO, 1970).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS309-00-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Aldrin
    b) Carcinogen Rating: 3
    1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    3.21.2) SUMMARY/HUMAN
    A) One occupational study which found no evidence that aldrin is a human carcinogen was judged inadequate by the IARC.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) Increased deaths from hepatobiliary cancer were seen in workers manufacturing aldrin (SMR = 249), but exposures to other pesticides were also involved. The authors thought occupational exposures were not likely to have contributed (Amoatengadjepong et al, 1995).
    B) LACK OF EFFECT
    1) Aldrin was not implicated as a human carcinogen in an occupational study; however, IARC has determined that this study was inadequate for assessing the potential carcinogenicity of aldrin for humans (IARC, 1974; Hathaway et al, 1996)
    2) Epidemiological studies of groups of persons with heavy, prolonged occupational exposure to aldrin, dieldrin, and/or chlordane have found NO increase in mortality from cancer of from all causes of death combines (Hayes & Laws, 1991).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) In the mouse, aldrin was classified carcinogenic by RTECS criteria with liver tumors present. In the rat it was classified both as neoplastic and as an equivocal tumorigenic agent in two different studies (RTECS , 1997).
    2) Aldrin has been carcinogenic in three different strains of mice (C3H, CF1, B6C3F1), but seven studies in rats have been judged to be inadequate and inconclusive by the USEPA for assessing its carcinogenicity in that species (EPA, 1988).
    3) Dieldrin, the primary metabolite of aldrin, has induced liver tumors in mice (Proctor et al, 1988).
    4) In the NCI Carcinogenesis Bioassay (Feed), clear evidence was found for carcinogenicity in the mouse and equivocal evidence was found in the rat (RTECS , 1997).
    5) The International Agency for Research on Cancer (IARC) has listed some of these agents (eg, DDT) as "probably carcinogenic to humans", although it also categorizes them as being inadequately assessed for human carcinogenic potential (IARC, 1982).

Genotoxicity

    A) Aldrin has been genotoxic at the level of primary DNA damage, mutagenicity, and chromosome aberrations.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Blood chlorinated hydrocarbon levels are not clinically useful following acute exposure. For most compounds, blood levels reflect cumulative exposure over a period of months or years rather than recent exposure.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Aldrin is rapidly metabolized to dieldrin. Both aldrin and dieldrin should be measured to account for the total toxic dose.
    2) Blood concentrations of dieldrin in unexposed persons averaged 0.0014 mg/L (Baselt & Cravey, 1989). Serum concentrations of aldrin in occupationally exposed persons averaged 0.0007 to 0.0023 mg/L, or 0.030 mg/L aldrin and 0.184 mg/L dieldrin in another study (Baselt & Cravey, 1989). Another study reported levels ranging from 0.25 mcg/100 g blood in laboratory staff to 7.08 mcg/100 g in manufacturing operators (Brown et al, 1964).
    3) The threshold concentration of dieldrin in blood for symptoms has been estimated as 0.16 to 0.25 mg/L (Baselt, 1988), 0.15 to 0.20 mg/L (Brown et al, 1964), or 0.105 mg/L (Anon, 1972). However, some persons have been symptomatic at 0.10 mg/L, and others were asymptomatic at 0.25 mg/L (Avar & Czegledi-Janko, 1970; Baselt & Cravey, 1989). The toxic concentration for blood is 0.0035 mg/L (0.0035 mcg/mL) (HSDB , 1997).
    a) These inconsistencies may be related to the relative amounts of dieldrin which may have been present by the time the blood samples were taken. The critical determinant is the total amount of dieldrin and aldrin, because they are of approximate equal potency.
    4) The probable concentration of dieldrin in the blood of five workers who developed convulsions or myoclonic limb movements was in the range of 16 to 62 mcg/100 g of blood (Proctor et al, 1988).
    5) Sixteen patients were examined to evaluate a possible correlation between serum aldrin and dieldrin levels and clinical complaints. It was concluded that: concentrations of <20 mcg/L were usually associated with mild poisoning (nausea, vomiting, epigastric pain); concentrations of 100-200 mcg/L represented moderate intoxication (nausea, vomiting, epigastric pain, headache, dizziness, convulsions); and severe or fatal cases were associated with levels above 700 mcg/L (Carvalho et al, 1991).
    4.1.3) URINE
    A) URINARY LEVELS
    1) Aldrin is not found in the urine. Urinary levels of dieldrin in occupationally exposed persons ranged up to 0.7 mg/L (Baselt, 1988).
    4.1.4) OTHER
    A) OTHER
    1) OTHER
    a) Dieldrin concentrations in fat of English persons averaged 0.21 mg/kg, while occupationally exposed persons averaged 6.12 mg/kg (Baselt, 1988). Levels in body fat of workers who had experienced convulsions were 60 and 140 ppm (Kazantzis et al, 1964).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Blood chlorinated hydrocarbon levels are not clinically useful following acute exposure. For most compounds, blood levels reflect cumulative exposure over a period of months or years rather than recent exposure.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Emesis is not recommended due to potential CNS depression or seizures.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    C) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    6.5.3) TREATMENT
    A) DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. Rescue personnel and bystanders should avoid direct contact with contaminated skin, clothing, or other objects (Burgess et al, 1999). Since contaminated leather items cannot be decontaminated, they should be discarded (Simpson & Schuman, 2002).
    B) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    C) CONTRAINDICATED TREATMENT
    1) Do NOT give oils by mouth. They tend to increase intestinal absorption of these lipophilic toxicants.
    2) Do NOT administer adrenergic amines, which further increase myocardial irritability and produce refractory ventricular arrhythmias (Dreisbach, 1983; Bryson, 1986).
    D) CHOLESTYRAMINE
    1) Cholestyramine (4 grams every eight hours) accelerated excretion of kepone and chlordane in excessively exposed workers, and probably would have a similar effect on other slowly excreted organochlorines which are trapped in the enterohepatic circulation (Cohn et al, 1978) Garrettson et al, 1984, 1985; Boylan et al, 1978).
    E) PULMONARY ASPIRATION
    1) Evaluate the patient for pulmonary complications, especially if the ingested product contained a petroleum solvent.
    F) EXPERIMENTAL THERAPY
    1) Peters et al (1982) report that symptoms of chronic exposure to hexachlorobenzene improved following treatment with intravenous and oral edetic acid therapy.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. Rescue personnel and bystanders should avoid direct contact with contaminated skin, clothing, or other objects (Burgess et al, 1999). Since contaminated leather items cannot be decontaminated, they should be discarded (Simpson & Schuman, 2002).
    2) Do an alcohol washing followed by a soap washing after the initial soap washing.

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) HEMODIALYSIS: Has not proven effective.
    2) HEMOPERFUSION: Effectiveness not known due to limited experience.
    3) Exchange transfusion, extracorporeal, and peritoneal dialysis have not proven effective in management of these poisonings. There has been little or no experience with charcoal hemoperfusion in organochlorine poisonings.

Range Of Toxicity

Summary

    A) Acute oral exposures >10 mg/kg may cause illness. The lethal human oral dose has been estimated in the range of 3 to 7 grams.

Minimum Lethal Exposure

    A) ADULT
    1) The fatal dose for man has been estimated at 3 to 7 grams (Baselt, 1988), or between 7 drops or one ounce for a 150 pound adult human (EPA, 1985).
    B) ANIMAL DATA
    1) FELINE - Exposure over a few days to 76 parts per million aldrin in soil (5.2 parts per million dieldrin) was sufficient to kill 6-week-old kittens (Klemmer et al, 1977).
    2) OTHER - For one- to two-week old calves, the minimum toxic oral dose was 5.0 mg/kg and for cattle and sheep it was 25 mg/kg (HSDB , 1997).

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) ORAL -
    a) Acute oral exposures exceeding 10 milligrams/kilogram cause illness (Clayton & Clayton, 1981).
    b) Severe symptoms may result from ingestion or percutaneous absorption of 1 to 3 grams, especially in the presence of liver disease (Budavari, 1996).
    2) DERMAL -
    a) Solutions containing 10% or more aldrin are rapidly absorbed by the skin. Formulations containing less than 10% may be fatal by skin contact, inhalation or swallowing (NFPA, 1986).
    3) OCCUPATIONAL -
    a) Occupational exposure to aldrin at 1 to 2.6 milligrams/cubic meter caused no ill effects (Clayton & Clayton, 1981).
    B) ANIMAL DATA
    1) Rats tolerated dietary levels as high as 20 parts per million for 6 weeks with no apparent effects (HSDB , 1997).
    2) Based on a rat chronic feeding study, a lowest effect level (LEL) of 0.025 mg/kg/day has been calculated (EPA, 1988).
    C) CASE REPORTS
    1) Toxic doses of organochlorines vary enormously with route and rate of absorption. Based on reports of poisonings and laboratory studies, aldrin would be considered in the group of highest toxicity of the organochlorines.

Workplace Standards

    A) ACGIH TLV Values for CAS309-00-2 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Aldrin
    a) TLV:
    1) TLV-TWA: 0.05 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: IFV, Skin
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    b) IFV: Inhalable fraction and vapor.
    c) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): CNS impair; liver and kidney dam
    d) Molecular Weight: 364.93
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS309-00-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Aldrin
    2) REL:
    a) TWA: 0.25 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    e) Skin Designation: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s): See Appendix A
    3) IDLH:
    a) IDLH: 25 mg/m3
    b) Note(s): Ca
    1) Ca: NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

    C) Carcinogenicity Ratings for CAS309-00-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Aldrin
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    2) EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: Aldrin
    a) B2 : Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals.
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 3 ; Listed as: Aldrin
    a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Aldrin
    a) Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS309-00-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Aldrin
    2) Table Z-1 for Aldrin:
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.25
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: Yes
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1997 HSDB, 1997
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 50 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 44 mg/kg
    3) LD50- (INTRAPERITONEAL)RAT:
    a) 150 mg/kg
    4) LD50- (ORAL)RAT:
    a) 39 mg/kg
    5) LD50- (SKIN)RAT:
    a) 98 mg/kg
    6) LD50- (SUBCUTANEOUS)RAT:
    a) 62 mg/kg

Physicochemical

Physical Characteristics

    A) Aldrin is a brown to white crystalline solid (Lewis, 1993; AAR, 1996).
    B) Aldrin is an odorless, white solid (pure) or tan to dark brown solid with a mild chemical odor (technical) (EPA, 1985).
    C) Solid sinks in water; solution floats on water (CHRIS , 1997).
    D) Physical state at 15 degrees C and 1 atm: solid (CHRIS , 1997).

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 364.93 (CHRIS , 1997; ACGIH, 1991)
    B) 364.91 (Budavari, 1996)
    C) 364.90 (RTECS , 1997; Lewis, 1996)

References

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