Toxicologic Information About Insecticides
Used for Eradicating Mosquitoes
(West Nile Virus Control)
April 2005
Temephos (trade name Abate) is an organophosphate insecticide with such low toxicity to humans that it is occasionally used to treat potable water (HSDB 2003). Its primary use is as a larvicide for mosquitoes, midges, and blackflies on ponds, marshes, swamps, and neighboring ground. It also is used for cutworms, thrips, and lygus bugs on crops; for fleas on dogs and cats; and for lice on humans. Temephos has low toxicity for mammals but moderate toxicity for birds and high toxicity for certain aquatic organisms (HSDB 2003). Its low solubility in water (<1 ppm; INCHEM 2002) and low human toxicity make it a candidate for (potable) water treatment, but its toxicity for certain aquatic organisms and the scarcity of information about its environmental fate may limit its appropriateness.
Section 1. Environmental Factors
An atmospheric half-life of 2.8 hours has been calculated on the basis of an estimated rate constant of 1.4x10–10 cm³/molecule-second for the vapor-phase reaction of temephos with photochemically produced hydroxyl radicals, given an average hydroxyl radical concentration of 5x105 molecules/cm³. However, because of temephos’ very low vapor pressure (8.6x10–10 mm Hg at 25 ºC), it probably will exist largely as a particulate when airborne, greatly lowering its rate of hydroxylradical reaction. Dry deposition is probably the dominant atmospheric removal process.
The soil adsorption coefficient for temephos is calculated to be 9,000–42,000, indicating it probably is highly immobile in soil and highly likely to partition out of water into sediment/soil (HSDB 2003). Temephos is practically insoluble in water (0.27 mg/L at 20 ºC), a trait further supporting the likelihood of soil partitioning. Whether in water or soil, it is expected to volatilize extremely little. Its very low Henry’s Law Constant (2x10–9 atm-m³/mole at 25 ºC) indicates temephos would take thousands of days to volatilize from water (partitioning to soil instead), and its very low vapor pressure suggests it will not significantly volatilize from dry soil. It is expected to hydrolyze rapidly (within a few days) in highly basic or acidic conditions but to persist considerably longer at pH 5–7. When incubated in water from a sewage treatment lagoon, temephos slowly degraded after a lag period of 7 days. It did not biodegrade after 7 days in a natural pond water/sediment system. In the environment, a handful of studies found it to disappear rapidly from pond water and sediments (EPA 1999, also EXTOXNET 2002), but these data do not appear to be particularly thorough. When sprayed or dusted on vegetation, temephos has persisted for several days.
The estimated bioconcentration factor for Abate ranges from 1,300 to 20,000 according to its water solubility and octanol/water partition coefficient (log kow) of 5.96 (HSDB 2003). This suggests that bio-uptake is an important process. In the few marine samples (mainly shellfish) that have been taken, however, temephos did not persist long (EPA 1999; EXTOXNET 2002; HSDB 2003). One study found that temephos bioaccumulated in fish during a 28-day exposure period, but by the 14th day after exposure, 75% of temephos had been eliminated (EPA 1999).
In summary, information about the environmental fate of temephos is sparse. On the basis of theoretical and laboratory calculations, it probably hydrolyzes quickly in highly acidic or basic conditions or in situations suitable for biodegradation, but in neutral-pH conditions it might persist for longer periods, probably tightly bound to soil. The few environmental studies have found it does not persist in sediment or in aquatic organisms.
Section 2. Potential for Exposure
Because temephos is used primarily as a larvicide to treat bodies of water, the potential for incidental dermal or soil/dust exposure during this usage is minimal (HSDB 2003). Furthermore, its human toxicity is so low that it is used for dermal application (human lice or pet flea topical treatment) as well as for potable water treatment (in combination with its very low solubility, which limits water concentrations). Because of its low human toxicity, low solubility, and use as topical treatment, unintentional toxic exposure is difficult to envision, except perhaps in the event of an occupational accident. The public could conceivably be exposed to repeated very low (<1 ppm) doses in situations where potable bodies of water are continually treated, but its low toxicity (see next section) and low solubility, indicate that little cause exists for concern about harm to humans. The possibility of injury to aquatic organisms might exist in that type of situation, however.
Section 3. Health Effects/Toxicity
Health Effect in Humans Exposed to Temephos
Few health-effect studies in humans have been conducted on
temephos,, and no effects have been reported (HSDB 2003). Nevertheless, it acts
as an organophosphate cholinesterase inhibitor, for which much literature is
available. Health effects from a typical cholinesterase inhibitor are as
follows:
- Common early signs or mild symptoms of acute cholinergic poisoning include miosis (pinpoint pupils), headache, nausea/vomiting, dizziness, muscle weakness, drowsiness, lethargy, agitation, and anxiety.
- Moderate or severe poisoning can result in chest tightness, difficulty breathing, bradycardia, tachycardia, hypertension, pallor, abdominal pain, incontinence, diarrhea, anorexia, tremor/ataxia, fasciculation, lacrimation, heavy salivation, profuse sweating, blurred vision, poor concentration, confusion, and memory loss.
- Life-threatening or very severe signs and symptoms, such as coma, seizures, respiratory arrest, pulmonary edema, loss of reflexes, and flaccid paralysis, can occur at high doses, such as in the cases of attempted suicide.
Effects of temephos on humans have not been reported in the literature, presumably because of its low toxicity.
Experimental Studies in Humans
Only three studies of humans were found in the literature.
A 19-month study was conducted of temephos added to all cisterns and other potable water containers in a community of approximately 2,000 people (Laws et al., 1968). The treatment occurred once a month and consisted of 1% temephos adsorbed to sand, in sufficient quantity to achieve a calculated concentration of 1 ppm (19 g of sand per 50 gallon/188 liter drum). Only one water sample ever had a temephos concentration >0.5 ppm, attributable to the combined effects of adsorption, solubility, and dilution over time. No significant change was measured in either plasma or erythrocyte cholinesterase of the villagers at any time during the study. Urinary excretion of temephos reached steady state after 4 months. No illness attributable to the insecticides occurred, and all of eight babies born were normal.
Humans who ingested 256 mg/day for 5 days or 64 mg/day for 4 weeks had no symptoms or any detectable effects on plasma or erythrocyte cholinesterase activity (Laws et al. 1967). At 70 kg for an adult, the doses are equivalent to 3.7 mg/kg/day for 5 days or 0.9 mg/kg/day for 4 weeks. When the standard water ingestion rate of 2 liters/day and the solubility of temephos (<1 ppm) are considered together, adult humans would be expected to receive <2 mg/day from drinking water treated with temephos. This scenario is extreme because daily water treatments are unlikely, so concentrations of temephos would decrease between treatments. The concentrations may be considerably below saturation (~1 ppm) even at their peak (the time of treatment). Given the no-observed-adverse-effect level (NOAEL) of 64 mg/day for 4 weeks, temephos is not expected to present a health hazard when used for larvicide water treatment.
A 2% formulation of temephos in pyrax powder was applied to participants and their bedding from a shaker (57 g, equivalent to 1.1 g of temephos) or to clothed subjects from a powder duster (31 g, equivalent to 0.62 g) (Steinberg et al. 1972). The treatment was safe and effective.
Health Effects Possibly Related to Municipal Use of Temephos
for Mosquito Control
Temephos is not expected to pose a hazard to the public when used
for mosquito control because (1) it would most likely be used for
water (larvicide) treatment; (2) it has a low potential for toxicity
in humans; and (3) it has a very low water solubility. In regard to
people caught in aerial spray (or exposed to dust), temephos is used
to treat lice on humans (and fleas on pets) in quantities on the
orders of tens of grams. No instances were reported of human
toxicity from temephos (HSDB 2003).
For these reasons, temephos is not expected to be of concern in municipal scenarios, barring an extreme occupational accident.
Health Effects in Laboratory Animals
Studies in laboratory animals exposed to temephos orally and
dermally are summarized in Table 1, with NOAEL and
lowest-observed-adverse-effect levels (LOAELs) indicated. Very high
doses can cause death, but given the very low solubility of temephos,
such doses would not be expected in humans (barring an occupational
accident or intentional poisoning).
As expected, cholinesterase inhibition is a sensitive indicator. This effect was generally seen at approximately 10 mg/kg/day. Other effects also were noted at higher doses, including liver effects. However, a few chronic studies indicated organophosphate toxicity or other effects at 1 mg/kg/day.
Carcinogenicity
No studies or regulations regarding carcinogenicity were found.
The handful of existing chronictoxicity studies did not mention
cancer.
Genotoxicity
The effect of temephos on several strains of bacteria has been
tested (EXTOXNET 2002). Although one strain showed weak mutagenicity,
the overall conclusion was that temephos is not mutagenic. Tests on
rabbits also have shown no signs of mutagenicity.
Table 1. Health Effect Levels of Temephos in Humans and
Laboratory Animals (PDF Version 66k)
The majority of an oral temephos dose in rats is excreted unchanged in the feces and urine (ExToxNet 2002; HSDB 2003; INCHEM 2002). 60% of the dose appeared in rat feces. Urinary excretion included sulfate ester and glucoside conjugates of phenolic hydrolysis. After oral administration of tritiated temephos in rats, radiation peaked in blood at 5–8 hours and then decreased, with a half-life of 10 hours. Radioactivity was found in the gastrointestinal tract and in fat. The mode of action of organophosphate cholinesterases is phosphorylation of the acetylcholinesterase enzyme at nerve endings. The toxicity of temephos could be altered by interactions with chemicals that interfere with its detoxication or with chemicals that have the same mechanism of action.
When temephos was applied dermally, <3% was absorbed across the skin in rats, rabbits, and dogs (HSDB 2003).
Section 5. Standards and Guidelines for Protecting Human Health
Regulatory standards and guidelines are shown in Table 2.
Perhaps because of temephos’ low toxicity and low expected concentrations, no agency has developed guidelines for chronic exposure. (Previous studies have indicated that its water concentration is not expected to be able to approach a level that would be toxic.) However, some occupational guidelines exist.
| Table 2. Regulatory Standards and Guidance Values | ||
| National Institute for Occupational Safety and Health/Centers for Disease Control and Prevention (NIOSH/CDC) Recommended Exposure Limit (REL): 10-hour time-weighted average (TWA, total dust) | 10 mg/m³ | NIOSH 2003 |
| NIOSH/CDC REL 10-hour TWA, respirable fraction | 5 mg/m³ | NIOSH 2003 |
| Occupational Safety and Health Administration (OSHA) Permissible Exposure Limit (PEL) 8-hour TWA, total dust | 15 mg/m³ | NIOSH 2003 |
| OSHA Permissible Exposure Limit (PEL): 8-hour TWA, respirable fraction | 5 mg/m³ | NIOSH 2003 |
EPA. 1999. Reregistration Eligibility Decision (RED) for Temephos: Revised environmental fate and effects assessment. Washington, DC: Environmental Protection Agency. Available at http://www.epa.gov/pesticides/op/temephos/rev_efed.pdf. Document is undated but hotlink from http://www.epa.gov/pesticides/op/temephos.htm says “Released 10/06/99.”
EXTOXNET. 2002.: Pesticide information profile for temephos. Available at http://pmep.cce.cornell.edu/profiles/extoxnet/pyrethrins-ziram/temephos-ext.html. Accessed December 2, 2002; PIP “published” September 1993 and “last modified” December 19, 2001.
Hayes WJ Jr. 1982. Pesticides studied in man. Baltimore/London: Williams and Wilkins: 377.
HSDB. 2003. Hazardous Substances Databank: Temephos. National Library of Medicine, National Toxicology Program. Available at http://www.toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?HSDB. Accessed February 19, 2003.
INCHEM. 2002. Data sheets on pesticides. No. 8 Rev. 1: Temephos. Geneva: Food and Agricultural Organization, World Health Organization. Available at http://www.inchem.org/documents/pds/pds/pest8_e.htm. Accessed November 26, 2002; Data sheet revision date August 1978.
Laws ER Jr, Morales FR, Hayes WJ Jr, Joseph CR. 1967. Toxicology of Abate in volunteers. Arch Environ Health 14:289–91.
Laws ER Jr, Sedlak VA, Miles JW, Romney-Joseph C, Lacomba JR, Diaz-Rivera A. 1968. Field study of the safety of Abate for treating potable water and observations on the effectiveness of a control programme involving both Abate and Malathion. Bull. World Health Org. 38:439–45.
NIOSH. 2003. NIOSH pocket guide to chemical hazards: Temephos. Atlanta: US Department of Health and Human Services, Centers for Disease Control and Prevention. Available at http://www.cdc.gov/niosh/npg/npgd0589.html. Accessed April 1, 2003.
Steinberg M, Cole MM, Miller TA, Godke RA. 1972. Toxicological and entomological field evaluation of Mobam and Abate powders used as body louse toxicants (Anoplura: pediculidae). J Med Entomol 9:73–7.
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