Toxaphene
| Units | Ref. | ||
|---|---|---|---|
| CAS | 008001-35-2 | - | - |
| Molecular formula | C10H10Cl8 | - | - |
| Molar weight | 413.82 | g mol-1 | - |
| Melting point | 65 | °C | [1] |
| Boiling point | 360 | °C | [2] |
| log KOW | 6.79 | - | [4] |
| Water solubility | 0.02911 | g m-3 | [4] |
| Vapor pressure | 27 | Pa | [3] |
| Henry's law constant | 4.35E-5 | atm m3 mol-1 | [4] |
| log KOA | 9.39 | - | [4] |
| log KOC | 4.888 | - | [4] |
Toxaphene (SC POPs) is a complex organochlorine mixture of at least 670 polychlorinated bicyclic terpenes consisting predominantly of polychlorinated camphenes (PCCs) with a wide range of molecular weights. Technical grade toxaphene is made from technical grade camphene reacted with chlorine gas using ultraviolet radiation and catalysts. Toxaphenelike mixtures of PCC congeners may also be released to the environment as unintentional byproducts from manufacturing processes involving chlorination, such as those used for paper and pulp. There are no known natural sources of the mixture. It was first produced commercially in 1947, by Hercules Powder Company, after 19 years of research and development. Found to be less toxic to bees than arsenical insecticides. It was largely used as a nonsystemic stomach and contact insecticide on cotton, corn, fruit, vegetables, and small grains and to control soybean pest. Toxaphene was also used to control livestock ectoparasites such as lice, flies, ticks, mange, and scab mites. Increased use occurred in the late 1960s to early 70s when it replaced DDT in formulations combined with methyl parathion. Toxaphene was at one time the most heavily manufactured pesticide in the United States with a maximum production volume of 23,000 tons in 1973. Through the early 1970s toxaphene or mixtures of toxaphene with rotenone were used widely in lakes and streams by fish and game agencies to eliminate biologic communities that were considered undesirable for sport fishing.
Toxaphene is an insecticide which is currently banned for all uses (SC POPs). Breathing, eating, or drinking high levels of toxaphene could damage the lungs, nervous system, and kidneys, and can even cause death. Toxaphene has been found in at least 58 of the 1,430 National Priorities List sites identified by the Environmental Protection Agency (EPA).
Toxaphene was formally used as a [nonsystemic] stomach and [contact insecticide] from the late 1940s until its peak in 1975 and then production and use dropped until 1982 when the EPA canceled all use of toxaphene as a pesticide or pesticide ingredient (ATSDR). It was used mainly on cotton, but also on flowers because it was persistent and relatively non-toxic to bees. The largest toxaphene production was in 1977, at around 40 million pounds, which dropped to 12 million pounds when it was canceled in 1982. Toxaphene was used to control insects on cotton, corn, fruit, vegetables, and small grains as well as to protect livestock from such pests as lice, fleas, ticks, mange, and scab mites. Up through the early 1970s, toxaphene, often mixed with rotenone, was used widely in lakes and rivers to eradicate certain organisms and species that were considered a detriment to sport fishing. This occurred most often in Canada and the Northern United States. It's use as a pesticide was canceled in 1982 and all uses were banned in 1990 and existing stocks were not to be sold in the United States after March 1, 1990. Toxaphen was included in the Stockholm Convention on persistent organic pollutants, which bans its production and use worldwide (SC POPs).
Toxaphene enters the environment after it is applied to a crop or poured into a lake. Toxaphene can enter the air (by evaporation), the soil (by sticking to soil particles), and the water (from runoff after rains). Toxaphene may also enter the environment from hazardous waste sites or when it accidentally spills or leaks during storage or transport. It does not dissolve well in water, so it is more likely to be found in air, soil, or the sediment at the bottom of lakes and streams. If toxaphene is found in surface water or groundwater, it is usually at very low levels. Once toxaphene is in the environment, it can last for years because it breaks down very slowly. This means there is still the chance of being exposed to toxaphene in the United States even though it has not been widely used for over 10 years. Because toxaphene breaks down slowly, exposure will probably be to the original material. Levels may be high in some predatory fish and mammals because toxaphene accumulates in fatty tissues. For example, when a raccoon eats a contaminated fish, some of the toxaphene in the fish is transferred to the raccoon. The more contaminated fish the raccoon eats, the more toxaphene it acquires. This means that even when toxaphene levels are low or confined to a certain area, they could be high in individual animals.
Toxaphene has been detected in the atmosphere, soils, surface waters and sediments, rainwater, aquatic organisms, and foodstuffs. Historically, toxaphene has been released to the environment mainly as a result of its use as an agricultural insecticide. Current sources of toxaphene in the environment include atmospheric emissions from countries currently producing or using toxaphene and continued releases from previously contaminated soils, waters and waste lands. Toxaphene is highly insoluble in water and in surface waters, amounts that are not volatilized to the atmosphere, will be sorbed to sediments or suspended particulates, which are ultimately deposited in sediments. From a model river, one meter deep, with a flow rate of one meter/second and a wind velocity of 3 meters/second, a halflife of 6 hours has been estimated for the vaporization of toxaphene. Taking this model into consideration, the atmosphere is the most important environmental medium for transport of the toxaphene mixture. The chemical properties of toxaphene (low water solubility, high stability, and semivolatility) favour its long range transport, and toxaphene has been detected in arctic air. Atmospheric toxaphene may be transported back to soil and water surfaces by wet and dry deposition processes.Toxaphene released to soils will persist for long periods of time. The high soil sorption coefficient values for toxaphene (logKoc 2.475.00) suggest that the mixture should be strongly sorbed to soil particulates and, therefore, should be relatively immobile to leaching and inhibited from volatilizing from subsurface soils but toxaphene may be able to move into groundwater with the carrier hydrocarbon solvent (e.g., xylene). The halflife of toxaphene in soil ranges from 100 days up to 14 years, depending on the soil type and climate.
Acute oral exposure MRL of 0.005 mg/kg/day has been calculated for toxaphene on the 8 days 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. 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. No information is available for either humans or animals on the potential cancer risk following inhalation or dermal exposure to toxaphene. Although studies on the relationship between chronic exposure to toxaphene and cancer in humans are lacking, studies in rats and mice indicate that toxaphene causes cancer in rodents. Increased incidences of thyroid and hepatic carcinomas were observed in animals chronically exposed to high doses of toxaphene. Some populations may be exposed to higher amounts of toxaphene because a large portion of their diet is composed of game animals that bioaccumulate toxaphene. The Department of Health and Human Services (DHHS) determined that toxaphene may reasonable be anticipated to be a human carcinogen. The International Agency for Research on Cancer (IARC) determined that toxaphene may possibly cause cancer in humans. According to the U.S. EPA Carcinogen List there is a sufficient evidence of toxaphene carcinogenicity from animal studies with inadequate or no data from epidemiologic studies in humans, there for it is classified as a Category B2, Probable human carcinogen.
- AOAC Official Method 990.06 Organochlorine Pesticides in Water. Gas Chromatographic Method. 2005 AOAC International
- AOAC Official Method 990.06 Organochlorine Pesticide Contamination of Pesticide Formulations. ThinLayer Chromatographic Method. 2005 AOAC International
- EPA Method 8081A: Organochlorine Pesticides by Gas Chromatography (and ECD) EPA Method 8270C: Semivolatile Organic Compounds by Gas Chromatography/Mass Spectrometry (GC/MS)
- EPA Method 8270C: Semivolatile Organic Compounds by Gas Chromatography/Mass Spectrometry (GC/MS)
- ISO 6468 (1996) Water quality Determination of certain organochlorine insecticides, polychlorinated biphenyls and chlorobenzenes Gas chromatographic method after liquidliquid extraction
- ISO 10382 (2002): Soil quality Determination of organochlorine pesticides and polychlorinated biphenyls Gaschromatographic method with electron capture detection
[1] Howard, P.H., Editor (1991) Handbook of Environmental Fate and Exposure Data for Organic Chemicals. Pesticides. Vol. III. Lewis Publishers, Chelsea, Michigan.
[2] Tucker, W.A., Lyman, W.J., Preston, A.L. (1983) Estimation of the dry deposition velocity and scavenging ratio for organic chemicals. In: Precipitation Scavenging, Dry Deposition, and Resuspension. Pruppacher, et al., Editors, pp. 1242–1256, Elsevier Science Publishing Co., New York.
[3] Montgomery, J.H. (1993) Agrochemicals Desk Reference. Environmental Data. Lewis Publishers, Chelsea, Michigan.
[4] US EPA. [2009]. Estimation Programs Interface Suite™ for Microsoft® Windows, v 4.00]. United States Environmental Protection Agency, Washington, DC, USA
[5] IPCS: Intox Databank, http://www.intox.org/databank/index.htm
[6] ATSDR: Agency for toxic substances and disease registery, http://www.atsdr.cdc.gov/
[7] TOXNET: TOXikology Data NETwork TOXNET - http://toxnet.nlm.nih.gov/
[8] IRZ: Integrovaný registr znečišťování životního prostředí (IRZ) : http://www.irz.cz/
