TERMITE PROTECTION: AVAILABLE TREATMENTS AND HAZARD INFORMATION ABOUT TERMITICIDES Why are termites a problem in Australia?
Termites (often incorrectly called 'white ants') feed on wood and serve an important functionin nature by converting dead trees into organic matter. Unfortunately, the wood in buildingsand other structures such as wooden power poles is equally appetising to termites, so they cancause serious damage which may be very expensive to repair. There are many species oftermites in Australia, of which about 20 species can eat sound wood in buildings; thosecausing most damage to buildings are social insects that live in subterranean colonies that maycontain up to 200, 000 individuals.
In order to maintain humidity and to protect themselves from extreme weather conditions, acolony (or nest) of subterranean termites may be up to 6–7 metres below the soil surface andhave extensive tunnel networks that can extend up to 100 metres from the nest. In order toreach food sources above the soil surface, these subterranean termites construct mud tubes. These small mud tubes are often obscured by building structures and any infested wood isgenerally not obvious because termites take care to minimise damage to the outer surface inorder to maintain the humidity of their tunnel networks.
Termites occur throughout Australia; however, they are most common in warmer areas of thecountry (the tropics, temperate coastal regions and inland) and somewhat less common incooler regions (south eastern highlands and Tasmania). How can buildings be protected against termites?
Control techniques for termites can essentially be divided into two types, prevention and treatment. Preventative measures are easily applied during the construction of new buildings, but some (eg. stainless steel mesh, or a layer of granite chips) are not very suitable for existing buildings or structures. Prevention of infestation
Building design can reduce the chances of termite damage. Important strategies includereducing the amount of timber used in buildings, a properly designed concrete slab with edgesexposed for inspection for termite activity, or provision for easy under-floor inspections oftimber floors. Installation of a reticulated system under the concrete slab can also to allowchemical barriers to be applied and re-applied whenever necessary.
Many local building authorities require that preventative measures against termites be incorporated during the construction of new buildings. Published Standards outline the procedures that must be followed to protect new and existing buildings in Australia1. Since most termite-related damage to timber occurs from subterranean termites, preventative measures rely heavily on the establishment of barriers to stop the termites getting into the premises or timber from the underlying soil. Currently, two types of barriers are used, chemical or physical, often in combination. Physical barriers Metal shields, stainless steel mesh or granite chip barriers can all be used to stop termites getting into buildings.
Termite shields (caps and strip shields) are installed on all substructures (isolated piers orposts and along walls, etc) to provide a continuous barrier.
Continuous sheets of fine stainless steel mesh can be installed under buildings during concreteslab construction. In certain situations, it may be adapted for service openings or wall cavitiesin existing structures.
Graded stone barriers are made up of a thick layer of small granite chips graded to a size andshape that cannot be transported by the termites and spaces between the particles are too smallfor termites to get through. Such stone barriers can be installed underneath a concrete slab orbeneath a suspended floor. Such barriers are yet to be developed for tropical northern areas,which are inhabited by large termites (Mastotermes darwiniensis) that can make their waythrough the standard granite chip barrier. Chemical barriers
Chemicals that are used to kill termites are called termiticides. Termiticides have differing modes of action, and several methods are used to apply them.
For many new buildings, creation of a termiticide-treated layer of soil surrounding and underthe building form an integrated barrier together with the physical methods described above. The termiticide is applied to the soil under the slab and around the footings, pipes, conduitsand other structures of the house during construction to create a vertical barrier. Furtherloosened soil around the perimeter of the house, including around all pipes and servicefacilities, is treated during and after construction to from a horizontal barrier. Timberintended for use in the construction of houses, outbuildings, fences and other outdoorstructures is often treated with chemicals by dipping and pressure or vacuum impregnation.
1 The Australian Standards relating to termite management are: AS 3660.1— 2000 Termite Management – Part1: New Building Work; AS 3660.2 – 2000 Termite Management – Part 2: In and Around Existing Buildings andStructures – Guidelines; and AS 3660.3 – 2000 Termite Management – Part 3: Assessment Criteria for Termite
The termiticide used may repel termites, it may kill those that enter the treated area or attractthe insects and then kill them, or it may be taken back to the nest on the bodies of the termiteswhere it kills most of the colony by contact. With currently approved termiticides, an under-floor barrier may be effective for 4–10 years and an external barrier for 2–6 years, dependingon climate, soil conditions and soil disturbance (protection lasts longer in the cooler southernregions).
To successfully complete termite barriers for existing buildings, strategic drilling throughconcrete slabs, porches, floors and wall footings may be needed, as well as under-floortreatment. This needs to be carefully worked out by a qualified pest control operator. Chemical baits
Strategically placed bait stations can be used to attract termites with an attractive food such asdry wood or paper refuse. About 30 bait stations are needed for a typical house and they needto be inspected regularly to assess termite activity. Once the termites are attracted to the baitstation, a particular termiticide is added. It is quickly spread through the colony by foragingtermites due to their communal grooming activity and ultimately reaches and kills the queen. This external 'bait and treat' approach is not always possible in built-up areas as some spacearound a building is needed for placement of the bait stations. Some simple preventative measures
Other simple prevention practices for existing buildings and other structures may also behelpful, such as:
§ ensuring good under-floor ventilation, which discourages termite activity;
§ not stacking timber against or near buildings;
§ not building wooden in-ground structures (eg. untreated timber retaining walls) close to
Treatment of infestation
Treatment of a termite infestation in an existing structure also requires an integrated approach,including destruction of termites within the timber structures, measures to locate and destroythe termite nest, re-establishment of a chemical and/or physical barrier, and regularinspections to detect any ongoing or new termite activity. For existing buildings, where signsof infestation have been detected, chemical treatment is usually the only option for destroyingtermites and re-establishing a barrier.
Treatment with a termiticide directly into tunnels of the nest where termites are known to beactive can reduce termite numbers but it rarely eliminates the colony altogether unless used inconjunction with another method. What chemicals are used as termiticides?
For many years, the prevention and treatment of termites relied heavily on the use of the so-called organochlorine insecticides, such as dieldrin, chlordane and heptachlor (knowncollectively as cyclodienes, because of their particular chemical structure). These chemicalshad some advantages in that they provided 20 to 30 years of protection against termitesbecause of their chemical stability, were extremely effective Australia-wide, and had noimmediate adverse health effects at the levels of exposure arising from the approved use. However, these chemicals were largely withdrawn from use in Australia from 1995 because ofconcerns about their environmental persistence, their tendency to accumulate in the fat ofanimals and humans, and the potential for them to exhibit toxic effects as their levels built upin the environment through continued use.
The elimination of these chemicals has presented a number of challenges because thereplacement chemicals do not provide such long-term protection. The need for more regularapplications of the newer, less-persistent chemicals means that there is an increased chancethat both householders and the pest control operators will be more frequently exposed to thechemicals.
In recent years there has therefore been much research into chemicals that have suitablepersistence, low mammalian toxicity and minimal environmental effects. However, integratedapproaches using physical and chemical methods have proved the most successful forprevention or treatment of termite damage.
A number of chemicals are currently approved in Australia as active constituents for use intermite control products. Separate inserts to this brochure outline some basic hazardinformation about each of the chemicals. For greater effectiveness, two different chemicalsmay be used in combination.
In the formulated products that are available for termite control, these active chemicals may bemixed with solvents, emulsifying agents or other components to aid application. Theseformulated products are sold under brand names but the chemical/generic name of the activeconstituent should always be shown on the label. Are termiticide chemicals safe?
Termiticides must be approved and registered by the Australian Pesticides and VeterinaryMedicines Authority (the APVMA). Before any agricultural or veterinary chemical can beused in Australia, it undergoes a rigorous approval process, including an assessment forpossible effects on human health (both of the public and of pest control operators who are toapply the chemical), and on the environment.
Issues related to toxicity and public health are assessed by the Commonwealth Department ofHealth and Ageing, issues related to health of pesticide applicators by the NationalOccupational Health and Safety Commission (NOHSC), and issues related to environmentalsafety, by Environment Australia (EA). Together with the APVMA, which assesses chemistryand efficacy issues, the combined work of these agencies forms what is known as the NationalRegistration Scheme (NRS).
Thus, chemical companies wishing to market a pesticide or other chemical must generate alarge number of studies to demonstrate that the chemical can be used safely, without causingunacceptable risks to users or the general public. As for other pesticides, the toxicologydatabase for a termiticide involves toxicity tests performed in animals, and is normally veryextensive.
In interpreting the toxicity data obtained in animals, it should be noted that toxicity testsgenerally use doses that are quite high relative to likely human exposures. The use of suchhigh doses increases the likelihood that potentially significant toxic effects will be identified. Toxicity tests also reveal doses at which toxic effects are not observed, known as ‘noobservable effect levels’ (NOELs). They are used, together with the application of generoussafety margins, to establish acceptable limits for exposure in humans at which no adversehealth effects would be expected. These limits are called the Acute Reference Dose (ARfD)and Acceptable Daily Intake (ADI), and are set for most pesticides to which humans maypotentially be exposed.
In addition to testing the 'pure' active ingredient, acute toxicity tests are also conducted on theformulated products containing the active termiticide chemical, solvents, emulsifiers,deodorants etc. Acute toxicity tests determine how poisonous the products are after a singledose by mouth, skin or inhalation, and whether they cause skin and eye irritation or skinsensitisation (allergies). What about smells that remain after treatment?
Many householders are concerned about the odour that remains after their house has beentreated. In the case of chlorpyrifos this may be due to the active constituent itself, which has adistinctive odour that may be noticeable after treatment, depending on the airflow andhumidity in the location where it was applied. Chlorpyrifos and pyrethroids (alpha-cypermethrin, bifenthrin and permethrin) are usually formulated with volatile organic orpetroleum solvents that may smell as they evaporate during and after application. Consequently, some manufacturers have marketed “low odour” termiticides. For example, tominimise the ‘petroleum odour’, a new bifenthrin product has been produced containing adifferent solvent to that previously used.
Some water-based products are available which do not leave any solvent odour after under-floor treatment (eg. the active ingredients, imidacloprid and fipronil are available in productsformulated in water). However, adequate ventilation is still recommended with all theseproducts.
Air monitoring studies have shown that if adequate ventilation is used, the concentrations oftermiticides in buildings after the initial spraying period are very low. What about pets and wildlife?
The potential for chemicals used in preventing or treating termite infestation to harm domesticanimals or wild animals (including birds, fish and beneficial insects) is assessed by theNational Registration Scheme for Agricultural and Veterinary Chemicals (the NRS). Becausetermiticides may have the potential to cause harm to domestic animals and wildlife in theenvironment, it is important not to unnecessarily expose the environment, includingcontaminating areas around treated premises, streams, rivers or waterways with excess unusedchemical or with waste washings from chemical containers. Licensed pest control operators(PCOs) should be trained in the correct disposal procedures. Hazard information on termiticides
Information on chemicals approved in Australia for use as a termiticide is given in theenclosed data sheets. The sheets outline the intrinsic characteristics of the chemicals (ie. whether they are hazardous or not). To reduce any potential health risks from chemicals, theaim is to reduce the likelihood of exposure. Since termiticides are commonly used aroundhomes, the correct volume and method of application are important considerations tominimise any exposure of applicators, householders, or bystanders. For this reason, registeredpest control operators who have completed an approved training course relating to the use andsafe application of termiticides normally perform termiticide application.
A number of the chemicals currently approved for the control of termites have relatively lowtoxicity (eg. imidacloprid and hexaflumuron), that is, they are not considered to be hazardouschemicals. In terms of the application method, hexaflumuron baits are likely to pose very lowrisk but the method requires a high level of vigilance over many years, with frequentmonitoring of the baits.
Pyrethroids are widely used in household insecticides and have a good safety record whenused as directed.
Organophosphorus compounds such as chlorpyrifos are widely used in agriculture as effectiveinsecticides, but need to be handled with caution because of their acute neurotoxicity inanimals and humans.
Arsenic trioxide is a well-known hazardous chemical but there is only a low probability thatthe public will become exposed to it. Small amounts are gently puffed into termite passageswith a hand blower to reduce an active infestation. It must be used at least two weeks beforeany other treatment as most other products repel termites, so that they would not be exposedto the arsenic.
Structural timber may be treated with a wide variety of insecticides. In addition to pyrethroids,timber may be impregnated with metal salts or organo-metals (based on arsenic, copper,chromium, tin or boron), fluorine, or creosote (a heavy petroleum hydrocarbon mixturesometimes referred to as coal tar). Fungicides may also be present in timber treatmentproducts to retard decomposition of wood. Under normal conditions, the chemicals remainwithin the treated timber and there is little potential for the public to become exposed to them. However, treated timber is unsuitable for use in situations where it could make contact withfood or drinking water, and requires care in handling to avoid human and environmentaltoxicity from the release of chemicals. People should work with treated wood outdoors, whilewearing a dust mask, goggles and gloves. Sawdust or scrap wood should never be disposed ofby mulching or composting and must not be burned, as toxic combustion products may bereleased. Arsenic and other heavy metals are especially hazardous when inhaled in smoke.
The enclosed hazard profiles give information about some of the active ingredients approved for termite control in Australia. Further details about the toxicity of the formulated products that contain these chemicals can be found on the relevant product containers. Poisons classification in Australia
In Australia, drugs and poisons are classified according to the 'Standard for the UniformScheduling of Drugs and Poisons', or SUSDP2. All termiticides are classified in PoisonsSchedule 5, 6 or 7 according to their availability and requirements for safe handling, asfollows:
Poisons of a hazardous nature that must be readily available to the public but
require caution in handling storage and use. Labels on containers of S5chemicals must bear the signal heading, 'Caution'. Schedule 6
Poisons that must be available to the public but are of a more hazardous or
poisonous nature than those classified in Schedule 5. Labels on containers ofS6 chemicals must bear the signal heading, 'Poison'. Schedule 7
Poisons that require special precautions in manufacturing, handling, storage or
use, or special individual regulations regarding labelling or availability. Labelson containers of S7 chemicals must bear the signal heading, 'DangerousPoison'.
To accommodate dilute products that are less toxic than the pure active ingredient, somechemicals have a ‘cut-off’ concentration. If a product contains less than the ‘cut-off’concentration of the active ingredient, then it is placed in a lower schedule, or even exemptedfrom scheduling.
2 This publication is a consolidation of recommendations made by the National Drugs and Poisons ScheduleCommittee, a national committee with State/Territory representation which meets on a regular basis.
List of some chemicals approved in Australia for use in products to be used for controlling termites.
The following lists some chemicals (by their chemical, or generic name) which are used inAustralia to control termites. Alpha-cypermethrin
a member of the pyrethroid class of chemicals which are syntheticanalogues of the naturally occurring pyrethrums; it is used to form abarrier to repel or kill termites (see also deltamethrin, bifenthrin andpermethrin). Deltamethrin
a synthetic pyrethroid similar to alpha-cypermethrin (see above); it isused in some termiticide products. Bifenthrin
another member of the pyrethroid class of chemicals; it is used toform a barrier to repel or kill termites. Permethrin
another synthetic pyrethroid, pyrethrin is commonly used as a barrierto repel or kill termites, and is also used for treatment of timber. Chlorpyrifos
a member of the organophosphorus class of chemicals that is used asa barrier to repel/kill termites. Hexaflumuron
a member of the benzoylurea class of chemicals that inhibit chitinformation in insects. It is used in strategically placed bait stations toattract foraging termites, which transfer the chemical throughout thecolony. Triflumuron
another benzoylurea insecticide, triflumuron is applied directly totermite nests. Imidacloprid
a member of the relatively new class of chemicals calledchloronicotinyls. It is used to create a barrier or treated zone in thesoil where it attracts termites, which die within the treated zone(partly from the effect of the chemical and partly from infection withfungi and other soil microorganisms). Fipronil
an extremely active insecticide belonging to the phenylpyrazolefamily, which has also been developed relatively recently. It isapplied by spraying, trenching and soil rodding as a chemical soilbarrier around existing structures, and may also be used to protectpoles and fence posts. Arsenic trioxide
a compound used to directly kill termites in active passages (thismethod has variable effectiveness). ALPHA-CYPERMETHRIN Description and mode of action
Alpha-cypermethrin is a synthetic pyrethroid insecticide with a range of agricultural uses. It isalso used to form a barrier to repel or kill termites (see also bifenthrin).
The synthetic pyrethroids are man-made chemicals similar in structure to the naturallyoccurring pyrethrums. Like other pyrethroids, alpha-cypermethrin kills insects by affecting thesalt balance (sodium channels) in nerve cells. It has a broad spectrum of activity againstinsects with the main toxic effect on the nervous system. Toxicity
In mammals, alpha-cypermethrin is very toxic if swallowed. It is a type II pyrethrum, whichmeans that it affects the central nervous system (brain and spinal cord) causing writhing,salivation and clonic convulsions (muscle spasms). These effects are reversible andpyrethroids have a good safety record. Alpha-cypermethrin is less likely to cause poisoningafter contact with the skin, although facial skin contact may cause temporary facial numbness.
In laboratory animals, ingested alpha-cypermethrin is absorbed from the gastrointestinal tract. Most of the absorbed cypermethrin is broken down into other chemicals, and rapidly excretedin urine, with a small percentage (1%) stored in fat and excreted more slowly. It is poorlyabsorbed through the skin (only about 20% of the applied dose was absorbed when alpha-cypermethrin was applied to the skin of animals for four days).
Like other pyrethroids, alpha-cypermethrin can produce nerve damage. This can result intremors, abnormal gait, agitation and difficulty in standing or walking. It may also causevomiting and diarrhoea. If it is present in a water-based solution it is less toxic than when it ispresent in oils. It is less toxic by exposure on the skin, but signs of poisoning can includenumbness or an itching or burning sensation on the skin. Alpha-cypermethrin is a mild eyeirritant but minimally irritating to the skin. Some products containing alpha-cypermethrinmay cause allergic reactions when applied on the skin (skin sensitisation).
Long term exposure to cypermethrin at high doses has produced changes in the liver andkidneys of experimental animals. These effects were not seen in animals fed lower doses. Insome studies using very high doses in mice, alpha-cypermethrin produced benign (that is non-malignant, or unlikely to spread) tumours in the lungs. These effects were not seen in otherspecies.
Alpha-cypermethrin was negative in a range of genotoxicity tests (that is, tests to assess itspotential to damage the genetic material of cells and cause mutations or cancer).Alpha-cypermethrin did not cause birth defects or other reproductive problems in laboratory animals. Poisons scheduling in Australia
Alpha-cypermethrin products with a high concentration (more than 10% alpha-cypermethrin)are included in Schedule 7 of the Standard for the Uniform Scheduling of Drugs and Poisons(SUSDP). Products with 1.5 to 10% alpha-cypermethrin are included in Schedule 6, whileproducts at less than 1.5% are in Schedule 5. Schedule 5 chemicals are available for use inthe home garden. Alpha-cypermethrin products for termiticide treatment around the home canonly be applied by licensed pest-control operators who have been trained in their handlingand use. Ecological and environmental effects
Alpha-cypermethrin is not soluble in water, and tends to bind to the soil meaning that it isunlikely to contaminate ground water. It breaks down more rapidly in sandy soils than in claysoils, and is also broken down by bacteria and light.
Alpha-cypermethrin is of low toxicity to birds, but is very toxic to fish and invertebrateswhich live in the water. Fish are more sensitive to alpha-cypermethrin because they breakdown and excrete the chemical much more slowly than birds or mammals. Alpha-cypermethrin is also highly toxic to bees. Note: another type II pyrethrum chemical occasionally used in termiticide products is deltamethrin. Its physical and toxicological characteristics closely resemble those of alpha- cypermethrin. Deltamethrin is also in Schedule 7 with Schedule 6 and 5 classifications for some medium and low strength products. BIFENTHRIN Description and mode of action
Bifenthrin is a synthetic pyrethroid insecticide with a range of agricultural uses. It is also usedto form a barrier to repel or kill termites (see also alpha-cypermethrin).
The synthetic pyrethroids are synthetic chemicals similar in structure to the naturally-occurring pyrethrums. Like other pyrethroids, bifenthrin kills insects by affecting the saltbalance (sodium channels) in nerve cells. It has a broad spectrum of activity against insectswith the main toxic effect on the nervous system. Toxicity
In mammals, bifenthrin is very toxic if swallowed. It is a type I pyrethrum (as compared withtype II pyrethrums such as alpha-cypermethrin), which means that it mainly affects theperipheral nervous system causing tremors; it may also cause difficulties in walking. Theseeffects are reversible and pyrethroids have a good safety record.
In laboratory animals, ingested bifenthrin is poorly absorbed from the gastrointestinal tractand is excreted unchanged in the faeces. It does not accumulate in the body after repeateddoses. When applied to the skin, bifenthrin is of low toxicity, is not irritating and does notcause allergic reactions (skin sensitisation). However, bifenthrin is a slight eye irritant. Bifenthrin products are typically of low toxicity by inhalation.
After long-term exposure to high levels in the diet, mice developed benign (that is non-malignant, or unlikely to spread) tumours of the urinary bladder. These tumours are thought toresult from chronic inflammation of the bladder wall, and were not seen in other species, or atlower doses. Bifenthrin was negative in most genotoxicity tests (that is, tests to assess itspotential to damage the genetic material of cells and cause mutations or cancer). Bifenthrindid not cause birth defects or other reproductive problems in laboratory animals. Poisons scheduling in Australia
Bifenthrin is included in Schedule 7 of the Standard for the Uniform Scheduling of Drugs andPoisons, with products containing less than 10% included in Schedule 6. Products containingless than 0.5% bifenthrin are exempt from scheduling. Bifenthrin products for termiticidetreatment around the home can only be used by licensed pest control operators who have beentrained in their handling and use. Ecological and environmental effects
Bifenthrin is poorly soluble in water and exhibits strong soil binding properties and lowmobility in soils. Neither plants nor animals metabolise bifenthrin extensively. Thesecharacteristics tend to make bifenthrin very stable in the environment. The chemical is highlytoxic to fish, aquatic invertebrates and bees, but only slightly toxic to birds. PERMETHRIN
Permethrin is a synthetic pyrethroid insecticide, which has the same mode of action as otherpyrethroids including alpha-cypermethrin and bifenthrin. Technical grade permethrin is amixture of four isomers, known as trans-(R), trans-(S), cis-(R) and cis-(S) permethrin. Theproportions of the isomers vary with the method of synthesis. The chemical has foundwidespread use in agricultural and veterinary settings, and forms the active constituent ofnumerous products that are applied as a barrier treatment to kill or repel termites. Oftencombined with anti-bacterial agents and fungicides, permethrin is also used in preservativesfor timber, which may be treated by dipping or vacuum impregnation. Toxicity
Permethrin is classified as a type I pyrethrum that affects the central and peripheral nervoussystems, causing tremors, hyper-excitability, salivation and paralysis. In rodents, a single highdose exposure to permethrin has been shown to cause degeneration in the peripheral nerves. However, these effects are reversible and pyrethroids have a good safety record. In mammals,permethrin is of moderate to low acute oral toxicity, influenced by the ratio of the trans andcis isomers in the chemical. The cis isomer is more toxic than the trans isomer. Permethrinhas low dermal toxicity, is of very low toxicity by inhalation, is slightly irritating to the skinand eyes of rabbits and causes skin sensitisation in guinea pigs. Permethrin-based productstend to be of low toxicity but their irritation potential varies, ranging from nil to moderatedepending on their strength and on the properties of other chemicals in the product. Similarly,some permethrin products cause allergic skin reactions whereas others do not. Information onhuman toxicity of permethrin is limited, but paraesthesia (numbness, itching, tingling andburning sensations) has been reported.
Following oral administration, permethrin is rapidly absorbed, distributed and excreted. Thetrans isomer is metabolised and excreted in the urine more readily than the cis isomer, whichis more stable and tends to be eliminated in the faeces. A variety of metabolic products areformed. The trans isomer may deposit in adipose tissue and milk fat, although the extent ofaccumulation is very low. Permethrin is absorbed across the skin of experimental animals.
Short-, medium and long-term studies in laboratory species have revealed the liver is themain target organ of permethrin at moderate oral doses. Enlargement of the liver was seen,sometimes with activation of metabolic enzymes. Some studies showed that the effects werereversible if treatment was withdrawn. Neurological abnormalities occurred in dogs fed
permethrin at high doses for at least a year. However, low doses of permethrin did not causeany toxic effects. Permethrin does not damage genetic material and does not cause cancer,have adverse effects on reproduction, or cause deformities in the developing foetus. Poisons scheduling in Australia
Permethrin is in Schedule 6 for preparations containing more than 25% of permethrin,Schedule 5 for preparations containing between 2 and 25% permethrin, and exempt fromScheduling when present at concentrations of 2% or less. Ecological and environmental effects
Permethrin is moderately stable in soil, to which it binds strongly and degrades with a half-life of 28 days or less. The decline of permethrin residues from crops is moderately fast, andit disappears rapidly from foliage and the soil surface when exposed to sunlight. Permethrinis of low mobility and shows little tendency to accumulate in the environment. Permethrin isof low oral toxicity to birds but highly toxic to insects, fish and aquatic arthropods such ascrabs. However, permethrin’s toxicity in the field is limited by its tendency to bind tosediment and degrade in sunlight. CHLORPYRIFOS Description and mode of action
Chlorpyrifos is an organophosphate insecticide that has widespread agricultural uses. It is alsofound in a number of insecticide products that are used in or around homes and gardens,including use as a termiticide. It has a mild mercaptan (sulphurous) odour, sometimesnoticeable after treatment of buildings.
Like other organophosphate insecticides, chlorpyrifos kills insects by interfering with theactivity of an enzyme (acetylcholinesterase) in the nervous system. This interference causes anincrease in levels of the nerve transmitter chemical, acetylcholine, leading to over-stimulationof the nervous system and rapid twitching and paralysis of muscles. Toxicity
In mammals, the main signs of organophosphate poisoning are increased swallowing,excessive saliva, rapid breathing, pinpoint pupils, loss of coordination, excitement, twitchingand rapid contractions of the neck and jowl muscles, coarse generalised body tremors,secretion of tears, urination, defecation, depression, prostration, convulsions, respiratoryfailure and death. The severity of signs increases with the amount of exposure, but there is aneffective antidotal treatment for chlorpyrifos poisoning. Regardless of the route of exposure(oral, dermal or inhalation), the toxic effects of chlorpyrifos are similar.
In laboratory animals, ingested chlorpyrifos is rapidly absorbed from the gastrointestinal tract,but does not remain for long periods in the tissues or organs. It is broken down into otherchemicals and excreted relatively quickly from the body, mostly in urine. Inhaled chlorpyrifosis also absorbed but relatively little is absorbed through skin. Chlorpyrifos is a very slight eyeand skin irritant but does not cause allergic reactions when applied on the skin (skinsensitisation).
Long-term exposure to low concentrations of chlorpyrifos in the diet was without seriousconsequences in animal studies, although high concentrations caused similar symptoms tothose listed above after single high doses. Both chlopyrifos and its main metabolite gavenegative results in a range of genotoxicity tests (that is, tests to assess its potential to damagethe genetic material of cells and cause mutations or cancer). Similarly, exposure tochlorpyrifos did not cause cancer, reproductive problems or birth defects in experimentalanimals.
The possibility of chronic neurological effects after repeated exposures to low levels oforganophosphate insecticides has been investigated. Health studies in workers producing and
packaging chlorpyrifos products have not shown any differences in the levels of illness ordiseases compared with a matched control group not exposed to chlorpyrifos. Air monitoring studies
Air monitoring studies have shown that if adequate ventilation is used, the concentration oftermiticides in buildings after the initial spraying period is very low. For example, in 1992 theWorkCover Authority of New South Wales monitored chlorpyrifos concentrations in the air ofseven Sydney houses that had been sprayed in the under-floor area (the treatment proceduremost likely to cause the highest concentrations of the termiticide). Average chlorpyrifosconcentrations in the houses did not exceed 1 microgram per cubic metre (µg/m³). Breathingair at this concentration is calculated to give an exposure that is approximately 200-fold lessthan the lowest dose of chlorpyrifos that causes significant reduction in plasma cholinesteraseactivity in humans (the most sensitive marker of exposure). Poisons scheduling in Australia
Chlorpyrifos products with high concentrations of the active ingredient are listed in schedule 6of the Standard for the Uniform Scheduling of Drugs and Poisons (SUSDP). Termiticidetreatments around the home are restricted to licensed pest-control operators who have beentrained in the handling and use of these products. A schedule 5 classification exists forpreparations containing 5% or less of chlorpyrifos, controlled release granular preparationscontaining 10% or less, and for microencapsulated chlorpyrifos when present at 20% or less inaqueous preparations. Potting or soil mixtures containing 100 g/m3 or less are exempt fromscheduling. Ecological and environmental effects
Chlorpyrifos does not dissolve easily in water. It is strongly adsorbed by most soils and isrelatively immobile in the soil. The half-life of chlorpyrifos in the soil has been shown torange from 11 to 141 days depending on the soil type; it is thus considered to be moderatelypersistent. Chlorpyrifos was least persistent in soils with high pH values. Soil micro-organisms break down chlorpyrifos. Chlorpyrifos is hydrolysed at a moderate rate. Based ondata from available studies, chlorpyrifos is unlikely to leach into ground water in measurablequantities under most typical use scenarios.
Chlorpyrifos is moderately to very highly toxic to birds and bees when exposed to directtreatment. Terrestrial non-food application of chlorpyrifos to sites such as turf represents anacute hazard to birds. Run-off from such applications could be hazardous to fish and aquaticinvertebrates, as chlorpyrifos is highly toxic to aquatic organisms. Various uses ofchlorpyrifos may pose a risk to small birds and small mammals. HEXAFLUMURON Description and mode of action
Hexaflumuron is a chemical of the benzoylurea class, which regulates insect growth byinhibiting chitin (outer skeleton) formation. Toxicity
In laboratory animals, hexaflumuron has very low acute toxicity if ingested, inhaled orexposed on the skin. It is not irritating to the skin or eyes and does not cause allergic reactionswhen applied on the skin (skin sensitisation). Hexaflumuron is absorbed only to a limitedextent when swallowed, is metabolised extensively, and excreted rapidly via the urine andfaeces.
Short- and long-term exposure to low concentrations of hexaflumuron in the diet was withoutserious consequences in animal studies. High doses produced some damage to the liver,oxidation of haemoglobin, and elevated red blood cell production in the spleen. It did notcause birth defects.
As hexaflumuron is mainly used in bait stations, significant public exposure is unlikely tooccur. Poisons scheduling in Australia
As a reflection of its low toxicity, hexaflumuron is currently exempt from poisonsscheduling. Ecological and environmental effects
Hexaflumuron is strongly adsorbed by a wide range of soils. It is highly toxic to aquaticinsects under field conditions, but is of low toxicity to bees and birds. Note:Triflumuron, another benzoylurea chemical, has closely similar toxicological characteristics to hexaflumuron, and is applied directly to termite nests when in a powder formulation. Triflumuron is in Poisons Schedule 5. IMIDACLOPRID Description and mode of action
Imidacloprid belongs to a relatively new class of nitromethylene chemicals calledchloronicotinyls, which kill insects by blocking nerve impulses. Toxicity
In mammals, imidacloprid is broken down to a compound that has toxic effects on the nervoussystem. This compound is either broken down and excreted, or converted to a protein that isused in the body. The toxic effects on the nervous system may include apathy, reduced muscletone, tremors and, in extreme cases, muscle cramps and difficulties in breathing due to effectson the muscles associated with respiration.
In laboratory animals, ingested imidacloprid is rapidly absorbed from the gastrointestinal tract. Around 96% of an ingested dose is excreted within two days (predominantly in the form ofmetabolites) in urine, with some excretion in the faeces. Ingested imidacloprid is moderatelytoxic but even large doses are of low toxicity when applied to skin. Dust formulations ofimidacloprid are of low toxicity when inhaled. Imidacloprid is not irritating to the eyes or skinand does not cause allergic reactions when applied to the skin (skin sensitisation). Someimidacloprid products may contain clay as a binding agent, which can irritate the eyes.
Long-term exposure to low concentrations of imidacloprid in the diet was without seriousconsequences in animal studies. At high doses, bodyweight loss, tremors and evidence of livertoxicity were seen. There was also premature ageing in the thyroid of rats.
Imidacloprid did not cause cancer in mice or rats. Similarly, it did not affect reproduction orcause birth defects. It was negative in most genotoxicity tests (that is, tests to assess itspotential to damage the genetic material of cells and cause mutations or cancer), although itcaused chromosome damage in cultured cells. However, tests for chromosome damage inanimals were negative. Poisons scheduling in Australia
Imidacloprid is in Schedule 6 of the Standard for the Uniform Scheduling of Drugs andPoisons. Products containing 20% or less of imidacloprid are included in Schedule 5, andthose containing 5% or less are exempt from scheduling. Ecological and environmental effects
Imidacloprid has quite a long half-life in soil (from about 6 weeks up to about 6 months). It isbroken down more quickly in soils with plant cover than in bare earth. Imidacloprid ismoderately soluble in water with a half-life of greater than 31 days, and can bind to organicmatter in soils. In some soils that are very porous or gravelly, there may be potential forimidacloprid to move into ground water.
Imidacloprid is toxic to birds and highly toxic to bees by direct application. In studies wherebirds were allowed to eat seed treated with imidacloprid, they had short-term toxic effectsincluding retching and loss of coordination. They recovered rapidly, and learnt to avoidtreated seed. Imidacloprid is of moderately low toxicity to fish, but may be highly toxic toaquatic invertebrates. It is unlikely that there will be significant effects on birds and non-targetinsects from soil treatment if care is taken during application. FIPRONIL Description and mode of action
Fipronil belongs to a relatively new class of chemicals called phenylpyrazoles, which killinsects by blocking nerve impulses. The chemical has a stronger binding affinity within thenervous system of insects than in animal nerves, and therefore has enhanced toxicity toinsects. Toxicity
In laboratory animals, there is moderately extensive absorption of ingested fipronil from thegastrointestinal tract. Once absorbed, fipronil is metabolised rapidly but is excreted slowly, asthe metabolism products tend to become deposited in the body fat. The major route ofexcretion is the faeces. Fipronil is moderately toxic by ingestion and inhalation, and inlaboratory animals causes abnormal gait and posture, ruffled fur, lethargy, tremors andconvulsions. However, fipronil is poorly absorbed across the skin and is therefore of lowtoxicity when applied dermally. Fipronil does not cause skin or eye irritation, but somefipronil-based products are skin and eye irritants due to the presence of other chemicals in theformulations. Fipronil may cause skin sensitisation in sensitive individuals.
In long-term feeding studies with fipronil, the main effects in laboratory animals weredecreased weight gain and degenerative lesions in the liver. Convulsions and other signs ofnervous system toxicity occurred at high doses. In rats, fipronil caused a disturbance ofthyroid hormone regulation, leading to an increased incidence of benign tumours of thethyroid gland. However, rats are highly sensitive to this condition and fipronil is very unlikelyto pose a carcinogenic hazard to humans when used as a termiticide. Fipronil did not causemutations, damage genetic material or have adverse effects on foetal development, but didimpede the growth and survival of rat pups at high doses. Poisons scheduling in Australia
Fipronil is included in Schedule 6 of the SUSDP, with cut-offs to Schedule 5 when present inpreparations at 10% or less, and is unscheduled in products containing 0.05% or less. Ecological and environmental effects
Fipronil is an extremely active insecticide and is highly toxic to birds, fish and aquaticinvertebrates. It is stable in water in the dark but rapidly breaks down in the presence of light. Laboratory and field studies have demonstrated that fipronil is also broken down by lightwhen on plant and soil surfaces. The main degradation products retain high insect and non-target organism toxicity. Fipronil and its degradation products are relatively immobile in soil,and therefore the risk of residues leaching into groundwater is considered to be low. ARSENIC TRIOXIDE Description and mode of action
Arsenic is highly toxic following both short-term exposure to high doses and long-termexposure to lower doses. However, for termite control, arsenic is generally used in baitstations, or in direct application to termite nests. In both of these situations, the potential forexposure of the public is limited. Toxicity
Arsenic is very poisonous if ingested in large doses, with signs including vomiting, diarrhoeaand stomach cramping.
In laboratory animals arsenic is quite well absorbed from the gastrointestinal tract followingingestion and is mostly excreted in the urine (up to 80%), with less than 20% in the faeces. The arsenic is combined with other compounds by the body to aid in urinary excretion. Onlong-term administration, arsenic can build up in the liver, kidneys and lungs.
There is some evidence that a certain level of arsenic is required for normal body functioning. However exposure to increased levels can cause a range of problems. Long-term exposure toincreased arsenic levels has occurred due to naturally high arsenic levels in the water supplyor contamination following mining activities. Long-term ingestion of relatively high levels ofarsenic causes thickening of the skin and changes in the pigmentation. Arsenic has also beenassociated with increased cancer of the liver, lung, skin, bladder and kidneys. It is believedthat exposure to arsenic after exposure to an agent which is known to cause cancer (such asultraviolet light or cigarette smoke) can increase the chance of developing cancer.
Arsenical chemicals are genotoxic in cultured bacterial and mammalian cells and in insects. Mutagenic effects have been identified, together with damage to chromosomes, inhibition ofDNA repair and interference with cell division. These chemicals can also increase the effectof other DNA-damaging agents. Workers exposed to arsenic trioxide in a smelter showedincreased mortality from tuberculosis, respiratory cancer, heart disease and emphysema.
Arsenic is teratogenic (causes birth defects) in experimental animals. In a number of humanstudies where there was enough arsenic exposure to cause changes in the skin, there was someevidence of increased numbers of spontaneous abortions and babies being stillborn. Theseeffects were only seen at these relatively high levels, with lower levels of arsenic producing noproblems with mammalian development. Poisons scheduling in Australia
Like all arsenic-containing chemicals, arsenic trioxide is a very hazardous chemical. Onlyvery small amounts (several grams) are used by licensed pest control operators. It is classifiedas a Schedule 7 poison. Ecological and environmental effects
Inorganic arsenic compounds are moderately toxic to fish and aquatic invertebrates. However,they are highly toxic to algae, and low concentrations may have considerable impact onaquatic ecosystems. Inorganic arsenic trapped in sediments may be released into ground waterover long periods of time. Biological transformations result in the production of less toxicorganic arsenic compounds, but soil pollution resulting in ground water contamination hasproved to be a serious human health problem in some parts of the world. Although persistentand taken up by plants and other organisms, inorganic arsenic is not subject to significantbiomagnification in food chains.
Information prepared for the Department of Health and Ageing by the Chemicals Review and InternationalHarmonisation Section, Office of Chemical Safety, Therapeutic Goods Administration, and by Dr Janet Salisburyof Biotext, Canberra.
The KPC Student Health Clinic is recommending all students and staff evaluate their risk for pertussis infection and get immunized if possible. Adults can become ill and/or carry the pertussis bacterium to high risk groups such as non or under immunized infants, children and the frail elderly. Pertussis has been increasing in Alaska due to the outbreak in Washington State and the frequent tra
CURRICULUM VITAE B323 Clinical Center Bldg., Dept. of Medicine, Michigan State University, East Lansing, MI 48824 Endocrinology and Metabolism, College of Human Medicine, Michigan State University, East Lansing, MI M.D. (Internal Medicine) Post Doctoral Degree in Medicine All India Institute of Medical Sciences, New Delhi, India - May 1967 American Board of Internal Medicine - Internal Med