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The management of this web site believes that any opinions about the use of pesticides should be based on factual scientific evidence.  We are not scientists so we will strive to provide some basic information gathered from reliable sources and provide links to sources that have information of interest to average consumers. 

Pest Management Professionals and Pesticides:
Many problems with pesticides are caused by uninformed consumers who refuse to read labels and follow precautions. For this reason we suggest throughout this web site that  trained and licensed pest management professionals should be consulted.  Most of them will try to find Integrated Pest Management solutions that do not necessarily require the use of pesticides. If you use pesticides be sure to read and follow the label directions,  It's the law.
We welcome your feedback.


Pesticide information links

The Pros & Cons of Pesticides
Pesticide spills, disposal and shelf life
Pesticides and Cancer
Insect Repellant Safety Tips
Pesticide fears
Types of Pesticides 
Managing Pesticides in Canada
Alternatives to Chromated Copper- Arsenate (CCAP)  Wood Preservatives

Pest Control Supplies

Pesticide Labels.

Pesticides cause unfounded fears

Personal Insect repellants:
safety tips.

Pesticide Cross-reference table.

Pesticide regulation in Canada.

Pesticide information profiles


Some other pages of interest:

Ant nest photos 
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Getting rid of Carpenter ants 
Canadian Pest Management Association,
  Choosing a pro, Cockroaches, 
Controlling pests

Finding a Pro,

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,   Powder post beetles, Raccoons

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New Pest Control Products act
Canadian Pesticide labels
Pesticide Cross Reference Table
Pesticide terms dictionary
Pesticide info profiles
Pesticide toxicology handbook
Health Canada                       Français
National Contact(s):

Pest Management Information Service
Pest Management Regulatory Agency
Health Canada
2720 Riverside Drive
Ottawa, Ontario
K1A 0K9
Toll-free: 1-800-267-6315 (within Canada)
Telephone: (613) 736-3799
Fax: (613) 736-3798
Web site:
Green Cross Canada - Homeowner's Guide to Pesticides
Reading about pesticides on the internet can be very misleading for Canadians. Many of the pesticides on the market elsewhere in the world, are not available in Canada, and there are stringent regulations regarding importing them. This government web site has the details about importing pesticides:   

Types of Pesticides

A pesticide is any chemical which is used by man to control pests. The pests may be insects, plant diseases, fungi, weeds, nematodes, snails, slugs, etc. Therefore, insecticides, fungicides, herbicides, etc., are all types of pesticides. Some pesticides must only contact (touch) the pest to be deadly. Others must be swallowed to be effective. The way that each pesticide attacks a pest suggests the best way to apply it; to reach and expose all the pests. For example, a pesticide may be more effective and less costly as a bait, rather than as a surface spray.


Insecticides are chemicals used to control insects. Often the word "insecticide" is confused with the word "pesticide." It is, however, just one of many types of pesticides. An insecticide may kill the insect by touching it or it may have to be swallowed to be effective. Some insecticides kill both by touch and by swallowing. Insecticides called Systemics may be absorbed, injected, or fed into the plant or animal to be protected. When the insect feeds on this plant or animal, it ingests the systemic chemical and is killed.

Broad Spectrum. Insecticides vary in the numbers of different kinds of insects they kill. Some insecticides kill only a few kinds of insects. Sometimes you can choose these insecticides when you wish to kill only one insect pest and not other beneficial insects in the area. Many insecticides are general purpose or wide range killers. These "broad spectrum" pesticides are used when several different kinds of insects are a problem. One chemical can kill them all. No broad spectrum insecticide kills all insects; each varies as to the kinds of insects it controls.

Narrow Spectrum. While many insecticides are broad spectrum, killing a wide variety of animals by attacking a system common to all, such as the nervous system, a new group of insecticides are much more selective. The chitin inhibitors only affect animals with chitin in their exoskeleton (i.e. insects). Growth regulators are even more specific. They affect certain groups of species that have a particular hormone. Finally, pheromones are the most restrictive because they react with only one species or one sex of a single species.

Chitin synthesis inhibitors interfere with the development and molting of immature insects causing their death. Chitin is the primary structural chemical in an insects body wall. An immature insect treated with a chitin inhibitor dies the next time it attempts to molt.

Insect growth regulators or IGRs mimic the action of an insect's naturally occurring juvenile hormone. They interfere with certain normal processes and prevent immature insects from completing development into normal reproductive adults. The effects of IGRs on insects include abnormal molting, twisted wings, loss of mating behavior, and sometimes death to embryos in eggs. IGRs attack a growth process found only in insects, thus there is a great margin of safety for humans and other vertebrates. However, one disadvantage is that growth regulators act slowly, since they do not kill the insect until it molts into an adult.

Pheromones are naturally produced chemicals used by animals to communicate to each other. There are three basic types of pheromones. Aggregation pheromones attract many individuals together, for example, a site where food may be plentiful. Sex pheromones are used by one sex of a species to attract a mate. Trail pheromones are deposited by walking insects, such as ants, so that others can follow. Synthetic pheromones produced in laboratories mimic these natural chemicals. They are used to attract pest insects into traps, disrupt mating, and monitor populations of insects. Because they do not kill insects, they are often not considered to be pesticides.

Short Term vs. Residual. Insecticides also vary in how long they last as a killing agent. Some break down almost immediately into nontoxic by -products. These "short term" chemicals are very good in situations where the insects do not return or where long-term exposure could injure non-target plants or animals. For example, short-term insecticides are often used in homes and dwellings where people and domestic animals might be exposed. Other insecticides remain active killers for a fairly long period of time. These "residual" pesticides are very useful when the insects are a constant problem and where they will not be an environmental and/or health hazard. For example, residuals are often used for fly control in livestock buildings or for termite control in wooden structures.

Miticides and Acaricides

Miticides (or Acaricides) are chemicals used to control mites (tiny Insecticides spider-like animals) and ticks. The chemicals usually must contact the mites or ticks to be effective. These animals are so numerous and small, that great care must be used to completely cover the area on which the mites live. Miticides are very similar in action to insecticides and often the same pesticide kills both insects and mites. The terms "broad spectrum," "short term," and "residual" are also used.


Fungicides are chemicals used to control the fungi which cause molds, rots, and plant diseases. All fungicides work by coming in contact with the fungus, because fungi do not "swallow" in the normal sense. Therefore, most fungicides are applied over a large surface area to try to directly hit every fungus. Some fungicides may be systemic in that the plant to be protected may be fed or injected with the chemical. The chemical then moves throughout the plant, killing the fungi. to describe miticides.

Protectant vs. Eradicant. There are two basic approaches in the use of fungicides. One is designed to prevent the plant from getting the disease. These fungicides are used as "protectants" and are similar in purpose to polio and smallpox vaccinations for humans. They are applied before the disease gets a start. This type of fungicide is very useful when a particular disease or group of diseases are likely to attack a plant or crop, year after year. Protectants, for example, have often been used as a routine precaution on fruit and vegetable crops.

Most protectant fungicides are fungistatic. This means they prevent or inhibit fungal growth. Once the fungistatic action ceases, the controlled fungus may grow again or produce spores. Thus, a protectant fungicide may have to be applied at regular intervals to continue the protection from infection.

The other type of fungicide kills the disease after it appears on (or in) the plant. These fungicides, called "eradicants," are like penicillin or other antibiotics which cure diseases in humans after the sickness appears. Eradicants are less common than protectants because once the fungus is established in a plant, it is often difficult to destroy. Eradicants are often used when protectants aren't available, aren't applied in time, or are too expensive. Eradicants are also applied when the disease appears unexpectedly on a plant or in an area. For example, a common use is on fruit and vegetables when the protectant spray wasn't applied on time to prevent infection. Eradicants are also used by orchardists in combating diseases of fruit trees, such as apple scab.


Herbicides are chemicals used to control unwanted plants. These chemicals are a bit different from other pesticides because they are used to kill or slow the growth of some plants, rather than to protect them. Some herbicides kill every plant they contact, while others kill only certain plants.

Nonselective herbicides are toxic to all plants. These are often used when no plants are wanted in an area. For example, nonselective herbicides could be used for clearing under guardrails or for total control of weeds in industrial areas.

Selective herbicides kill some plants with little or no injury to other plants. Usually selective types will kill either broadleaved plants or grassy plants. These are useful for lawns, golf courses or in areas with desirable trees. Some very selective herbicides may kill only certain plants in a group; for example, crabgrass killers on lawns. 


Rodenticides are chemicals used to control rats, mice, bats and other rodents. Chemicals which control other mammals, birds, and fish are also grouped in this category by regulatory agencies. Most rodenticides are stomach poisons and are often applied as baits. Even rodenticides which act by contacting the pest are usually not applied over large surfaces because of the hazard to domestic animals or desirable wildlife. They are usually applied in limited areas such as runways, known feeding places, or as baits.

Nematicides Molluscicides Repellents

Nematicides are chemicals used to control nematodes. Nematodes are tiny hair-like worms, many of which live in the soil and feed on plant roots. Very few of these worms live above ground. Usually, soil fumigants are used to control nematodes in the soil. (See section on fumigants in Module XV.) However, a few contact insecticides and fungicides are also effective against these tiny worms.

Molluscicides are chemicals used to control snails and slugs. Usually the chemicals must be eaten by the pest to work. Baits are often used to attract and kill snails or slugs in an area.

A repellent is a pesticide that makes a site or food unattractive to a target pest. They are registered in the same way other pesticides are and must be used according to the label. Insect repellents are available as aerosols and lotions and can be applied to skin, clothing, or plants to repel biting and nuisance insects. Vertebrate repellents are available as concentrates to be mixed with water, powders, and granules. They can be sprayed or painted on nursery crops, ornamental plantings, orchards, vineyards, vegetables, and seeds. Repelling deer, dogs, birds, raccoons, and others can protect sites from damage.


Diatomaceous Earth

Diatomaceous Earth is all natural, safe for humans and pets, and easy and effective to use.

Diatomaceous earth is a remarkable, all-natural product made from tiny fossilized water plants (fossilized remains of diatoms, a type of hard-shelled algae). These plants have been part of the earth’s ecology since prehistoric times. It is used as a filtration aid, as a mild abrasive, as a mechanical insecticide, as an absorbent for liquids, as cat litter, as an activator in blood clotting studies, and as a component of dynamite. As it is also heat-resistant, it can be used as a thermal insulator.

To insects it is a lethal dust with microscopic razor sharp edges. These sharp edges cut through the insect’s protective covering drying it out and killing them when they are either dusted with it or if it is applied as a wettable powder spray. If they ingest the it, it will shred their insides. The fine powder absorbs lipids from the waxy outer layer of insects’ exoskeletons, causing them to dehydrate. Arthropods die as a result of the water deficiency. Medical-grade diatomite is sometimes used to de-worm both animals and humans. It can be used to help control and eventually eliminate a cockroach infestation. This material has wide application for insect control in grain storage.


About Health Canada’s re-evaluation of 2,4-D


Health Canada Online

The new Pest Control Products Act - pest management regulation in the 21st century

The Pest Control Products Act (PCPA) is the primary federal legislation to control the import, manufacture, sale and use of all pesticides, including insecticides, herbicides and fungicides, in Canada. The new pesticide legislation will strengthen Canada's rigorous safeguards against the risks to people and the environment from the use of pesticides.

Read more on this


Importance of Pesticides

 Plants are directly and indirectly mankind's main source of food. They are attacked by tens of thousands of diseases caused by viruses, bacteria, fungi, and other organisms. There are over thirty thousand kinds of weeds competing with crops worldwide; thousands of nematode species reduce crop vigour; and some ten thousand species of insects devour crops. It is estimated that one third of the world's food crop is destroyed by these pests annually.

Pesticides have also played an important role in improving world health. Canadians may not realize the role that pesticides (DDT in particular) have played in preventing disease, but developing nations have certainly benefited. Millions would not be alive today were it not for DDT used to control malaria-bearing mosquitoes, and tens of millions enjoy good health rather than suffer from malarial parasites. Even in Manitoba, pesticides are used to control the incidence of western equine encephalitis by reducing mosquito populations thus preventing the transmission of the disease.

Bed Bugs Remind Us of DDT's Benefits,

By: Harold S. Stein Jr.

The following is a letter published by the American Council for Health and Science from Crane Pest Control President and Pest Control Hall of Famer Harold S. Stein Jr.

A sidelight to the recent epidemic of bed bugs that appears to be blossoming all over the country is how it calls to mind a fundamental axiom of toxicology, namely, that it is important to weigh "risk vs. benefit."

Prior to the U.S. ban on DDT, the incidence and significance of bed bug infestations was so inconsequential that my company charged the grand sum of $18 for a single treatment of a hotel room, with a 30-day guarantee. I do not recall a single incidence of having to schedule a second treatment. The key was the ability to treat not only the usual cracks and crevices but also the mattresses (especially the piping and little buttons) and bed frames without any fear of dermal irritation. We insisted then as now that the bed clothing, etc. be removed and cleaned, but since there would probably be some time delay before that was accomplished, the chemical treatment was having its effect.

DDT did not cause dermal or topical irritation. Remember its early use during World War II when it was liberally applied as a dusting powder to delouse infested civilians and military alike. In fact, DDT even was a recognized "drug" listed in the U.S. pharmacopeia with an accepted external and even internal oral dose!

Its beneficial uses, of course, were drowned out by the emotional crescendo that accompanied a long and politicized federal hearing prior to the ban. Recall, though, that the final verdict of the hearing was that DDT was relatively safe, a verdict that was administratively overturned — after the fact — by EPA's Administrator. The scientific community then and now recognizes that a strict adherence to the rule of judging the risk of an agent vs. the benefit of its careful use was totally abandoned here.

And during our current battle with what should in effect be a minor and easily removed incursion of bedbugs, there are few alternate substances registered for use with such efficacy and dermal safety; ergo, success is profoundly influenced by and dependent upon the thoroughness and speed of the housekeeping staff in tearing apart bed frames; perhaps disassembling furniture; bagging, removing, and sterilizing bed linens; and other inefficient and costly measures.

Granted, this all fades into inconsequence when compared to how this agent was removed from the arsenal for attacking diseases like malaria and fly-borne encephalitis, but the irony is the same: the public blames industry for problems caused by activists who, in their ignorance and fervor, were ostensibly acting in the public interest.

This is not a Canadian web site.
Some of the Pesticides listed here are not registered for use in Canada.


Search and Browse for EXTOXNET...
Pesticide Information Profiles (PIPs)

EXTOXNET is a cooperative effort of University of California-Davis, Oregon State University, Michigan State University, Cornell University, and the University of Idaho.
Primary files are maintained and archived at
Oregon State University.

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 Links to other selected web sites.
Using pesticides safely.  A University of Virginia site with some very sensible advice.     



The complete label information for all registered pest control products in Canada is now easily accessible on the Pest Management Regulatory Agency’s (PMRA) website. The labels on registered products contain important information on the legal uses of the product and vital safety information for users. To access this label information for any registered product, use the search engine.

Pesticide applicator Applicator Responsibility
Labels and the law.


Pesticide Label Label Information
Explanation of essential information provided on labels and tips to help understand label language.

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Pesticides Cause Unfounded Fears

Pesticides have one indisputable effect. They cause emotions to boil over. That's just what happened when a group of golfers noticed that a chemical sprayer was out on the course as they were completing their round. By the time they got into the clubhouse, several were complaining of headaches, rashes and general malaise. They were convinced that the use of pesticides is inherently unsafe. Are they right?

Asking if it is safe to use pesticides is like asking if it is safe to take medication. The answer is both "yes" and "no" because it depends on which medication, in what dose, how it is taken, by whom and for what reason. Salt, Vitamin B-6, Vitamin A and caffeine, on a weight-for-weight basis, are more toxic than many pesticides. Instead of classifying substances as "safe" or "dangerous," it is far more appropriate to think in terms of using substances in a safe or dangerous way.

In Canada, Health Canada’s Pest Management Regulatory Agency (PMRA) makes such judgments. Before a pesticide can be "registered" for use, the toxicologists, physicians, chemists and agronomists of the agency have to be convinced that the substance can effectively handle the problem it was designed for and that its risk profile is acceptable.

A "registration" is a long and involved process requiring acute, short-term and lifelong toxicology studies in animals as well as studies of carcinogenicity and possible damage to the nervous system. Proof of absence of birth defects is required. Effects on hormonal changes have to be studied in at least two species, along with the effects of the pesticide on non-target species. All routes of exposure are assessed, whether via ingestion, inhalation or skin contact. Cumulative effects are studied. PMRA also requires field-testing for environmental effects before a pesticide is approved.

Based on all the data, PMRA assesses the risk, taking into account exposure of children, pregnant women, seniors, pesticide applicators and agricultural workers. The potential level of exposure can be no more than 1/100th of the dose that showed no effect in animals.

Even once a pesticide is registered, there is a continuous re-evaluation system that includes the "inert" ingredients that are used in the formulations. Risk assessments are refined in accordance with new research findings. All ways of reducing pesticide risk are examined, with great emphasis on Integrated Pest Management, or IPM, which is aimed at reducing the reliance on pesticides as the sole approach to pest management. It is hard to imagine what more could be done to ensure that a pesticide has an acceptable risk-benefit ratio. But can even such a rigorous system ensure that we will have no consequences from the use of pesticides? > > Absolutely not.
Subtle effects in humans can show up only after years of exposure. This can be revealed only by long-term studies, not by anecdotal evidence. Pesticides cannot be linked to cancer on the basis of a heart-wrenching case that may appear in the media describing how a child who had repeatedly felt ill after exposure to lawn sprays was later diagnosed with cancer. Long-term epidemiological studies are required.

Several such investigations have been carried out. Workers in the agricultural chemical-production industries, who would be expected to have the highest exposures, do not show any unusual disease patterns, but the number of subjects in these studies is small. A widely reported study of farmers who sprayed their fields showed a weak link between acres sprayed and various cancers, but overall, the farmers had fewer cancer cases than the general population.

An often-cited U.S. study seemed to indicate a link between non-Hodgkin's lymphoma and acres sprayed with the herbicide 2,4-D, a chemical that is used in home lawn-care as well. But a long-term study of workers who manufactured 2,4-D, and had huge exposures over many years, showed no increased cancer incidence at all.

One of the developing concerns about the use of insecticides and herbicides is a possible effect on the immune system. Laboratory evidence indicates impaired activity of immune cells after exposure, and at least one study has shown increased respiratory infection in teenagers in villages where pesticide use is the heaviest. There is also the possibility of neurobehavioural effects. In a Mexican study, children in areas where pesticide use was extensive performed more poorly on co-ordination and memory tests. But these are very different conditions from those seen when a dilute solution of 2,4-D is occasionally used on a lawn by trained applicators. On the other hand, home gardeners who purchase such chemicals and use them improperly can put themselves and others at risk.

It would be great if we could get away from using pesticides. No exposure to pesticides means no exposure to their risks. At home, we can manage this. After all, a few dandelions on the lawn are not life threatening. In fact, quite the opposite. They can be made into a nutritious salad. But we cannot feed six billion people without the appropriate use of agricultural chemicals. So we do have to put up with risks, both real and imagined, because on a global scale they are outweighed by the benefits.

And just what was the dastardly chemical being sprayed on the golf course?

Good old H2O!


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Chemical Pesticide Cross-Reference Table

Chemical Product Names
2,4-D 2-4-D; 4-P Herbicide; Ace Weed & Feed; Amine 4(2,4-D); Banvel; Cenex Triplet; Class 40A; Class 40A Phenoxy Herbicide; Class 40-2,4-D; Country Club 12-4-8 w/ Trimec;Dissolve; Double 6; Double b; Ortho Weed B Gone; Riverdale Tri Power; Riverdale Triplet; Trimec 899; Trimec Classic; Trimec Encore; Barren Non-Selective Herbicide 
4-Aminopyridine Avitrol Whole Corn
Abamectin Whitmire PT 565; varieties of 'Avert' (320 Bait Gel, Bait, Bait Gel, Cockroach Bait Stations, Cockroach BTST)
Acephate Whitmire PT 280
Allethrin Ace Ant, Roach, & Spider Killer; Ace Wasp & Hornet Killer; Chemsearch Drop Dead; Raid Yard Guard; Wasp & Hornet Killer II; PT 240; PT515; PT 600 Optem; Wasp Freeze(PT515); Whitmire PT 310 Avert; Whitmire PT 565 Plus
Bendiocarb varieties of 'Ficam' (D, Dust, Granules, W, W 0.25%)
Borax Terro Ant Killer II
Boric Acid Borid; varieties of 'Drax' (Ant Bait, Ant Bait Gel, Ant Kill Gel, etc.) Ultracide
Brodifacoum Bolt; D Con; D Con Mouse Pruff II; Fib\nal Box; Talon G Rodenticide; Talon Weatherblock w/ Bitrex; Weather Block Rodenticide 
Bromacil Not Available
Bromadiolone Bell Lab Contrac Blox; varietes of 'Contrac' (Bait Blox, Bait Packs, Blocks, Mea Bait) Contrax Weather Blox
Chlorpyriphos Chem Tox; Dichloron LO; Dursban; Dursban Pro; Empire 20; Hydro Cide Residual; Ortho Home Pest Insect Control
Cyfluthrin varieties of 'Tempo' (Tempo 2 Insecticide, 2EC, 20 WP, WP) Whitmire PT 600 Optem
Cypermethrin Cynoff; Cynoff EC; Demand Pestabs; Demon EC
Deltamethrin Delta Dust
Diazinon Cit ATO Chem Knockout; Diazinon 2D Dust; Diazinon Granules; Drop Dead Insect Spray; Extermo; Extermo Liquid; Ortho Diazinon; Spectracide 
Dicamba 4-P Herbicide; Ace Weed & Feed; Cenex Triplet; Country Club 12-4-8 w/ Trimec; Riverdale Tri Power; Riverdale Triplet; Tri Mec Classic; Tri Power Selective Herbicide 
Dichlorvos(DDVP) Claire
Dimethoate Not Available
Diphacinone Diphacinone; Ditrac Blox; Ditrack 12455-29; 
Diquat Dibromide Aero Titanic
Esfenvalerate Conquer
Glyphosate Round Up by Monsato; Round Up; Round Up Pro; Round Up Ultra
Hydramethylnon Marc Wipe Out; Max Force Ant Killer Granular Bait; 
Hydroprene Gentrol IGR; Zoecon Control
Lambda-cyhalothrin Demand CS
Malathion Claire; Claire Golden Jet; Ortho Malathion
MCPA Ortho Weed B Gone
Mecaprop Not Available
Methidathion Turflon II
Orthoboric Acid Drax Ant Bait; Drax Ant Kill Gel; Drax Ant Bait Gel
Oxyfluorfen Triox
Permethrin Befco Insecticide; Chemsearch Drop Dead; Dead End; Raid Fumagator; Raid Ant & Roach; Raid Yard Guard; Ultracide; True Value Green Thumb Roach & Ant; True Value Green Thumb Weed & Feed etc.B112
Phenothrin PT 515; Wasp Freeze
Piperonyl Butoxide Befco Insecticide; Bidall Personal Insecticide; Bolt; Cessco 5E; Claire; Claire Golden Jet; Claire Lice Killer; Clean Drop Pramitol 25E; Davies Insect Killer No. 300; Defend; Defend Lice Killer; Dichloron L.O.; Drione; Drione Dust; Drop Dead Insect Spray; Drop Dead Liquid Insect Spray; Extermo Liquid; F/AM Drione; Raid Ant & Roach; Rid
Prodiamine Barricade 65 WO
Prometon  (Deoxi)Barrex Veg Killer; Triox Trophy Non Selective
Propetamphos Sandoz Catalyst; Safrotin
Propoxur Not Available
Resmethrin Bee Bopper Wasp & Hornet Spray; Claire Insect Spray; Hydro Cide Residual; varieties of 'Northwoods' (Dry Blast, Big Blast, Control, Direct Hit, Double Kill, Strike Insecticide)
Silica Gel Not Available
Sulfuramid Advance Dual Choice
Tetramethrin Befco Insecticide; Ortho Ant Stop; True Value Green Thumb Insect Killer; True Value Green Thumb Wasp+
Triclopyr Confront
Trifluralin Country Club Fertilizer
Warfarin D-Con
Zinc Phosphide Black Leaf Mole & Gopher Killer

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Chris F. Wilkinson
Department of Entomology
Cornell University
Ithaca, NY, 14853

Cancer is a special disease. Cancer of one type or another will eventually claim the life of one in every four or five Americans; indeed, few will escape the suffering of losing a friend or family member to the disease. Second only to heart disease as a leading cause of death in the United States, cancer is responsible for close to 500,000 deaths per year. Quite apart from its importance as a factor in human mortality, the very thought of cancer arouses a special dread in their minds of most individuals.

Public awareness and fear of cancer in the United States intensified during the late 1960s as a result of widely publicized associations between human cancer and a number of environmental factors associated with modern technology. In particular, attention was focused on the possible carcinogenic risks associated with the many products and byproducts of the chemical industry, and there was enormous public pressure for prompt legislative action to regulate human exposure to potential carcinogens.

As a result, legislation directed toward the protection of human health and the environment has increased dramatically during the past two decades. Approximately 30 such laws have been enacted, and although they differ in their objectives and regulatory authority, most are designed to control the carcinogenic and other health risks of chemicals introduced into commerce, released into the environment, or encountered in the workplace.

Despite substantial progress in the past few years, basic understanding of carcinogenic mechanisms and the major factors causing human cancer still leaves much to be desired. There remains considerable uncertainty in current procedures for identifying and regulating potential human carcinogens. Unfortunately, the development of an acceptable policy for the regulation of chemical carcinogens constitutes a particularly troublesome problem, because it seeks to match argument based on uncertain science against the deep-seated human fear of cancer. It is not surprising that the question of how to regulate cancer risks in the United States has become a highly divisive issue in which the limited amount of good science that is available either is not used to maximum advantage or rapidly becomes lost in a tangle of emotions and subjective value judgments.

Human exposure

It is frequently alleged, and widely and uncritically accepted by a large segment of the public, that the United States is currently in the midst of a veritable explosion of human cancer; futhermore, we are told, the situation continues to deteriorate. Although different statistical sources use different methods of analysis and data presentation , and although selective analyses can be used to support particular viewpoints, it is difficult to understand how the data can be interpreted as being indicative of a cancer epidemic.

No one will argue that more people are dying from cancer each year; some 433,795 Americans died of cancer in 1982, a 56% increase over the 278,562 deaths that occurred in 1962 (1). This is a sobering figure. However, when the trends are adjusted for the increased size of the population and for changes in age distribution the total cancer mortality rate from 1962 to 1982 has increased 8.7% (0.4%/year) and cancer incidence rate form 1973 to 1981 has increased 8.5% (1.1%/year) (1).

When site-specific analyses are conducted, the most obvious trends that become apparent during the past 35 years are the enormous increase in the incidence of lung cancer (greater than 200%) and the marked decrease in the incidence of stomach cancer; the incidence of cancers at most other sites has remained more or less constant. Lung cancer is of such dominance that if the mortality with which it is associated is excluded from the overall cancer mortality data over the last 30 years or so, the 8% increase in mortality becomes a 13% decrease (1). Indeed, when the effects of lung and skin cancer were excluded, a steady decline appeared in overall cancer mortality over the last 50 years in people under 65 years of age, according to a study by Doll and Peto (2). There is some evidence that, as a result of underreporting in the past, age-adjusted mortalities from many types of cancer (except lung cancer) have been declining significantly for decades (3).

Consequently, the only real evidence of a cancer epidemic in the American population (similar effects are also observed in other countries) is in relation to lung cancer, which is now generally considered to result primarily from smoking cigarettes (4). Sadly, this largely preventable disease is responsible for almost 30% of all human cancer deaths in the United States; it has been the major killer in males for some 20 years and now surpasses breast cancer as the major cause of cancer mortality in women.

Causes of human cancer

Not very many years ago it was generally believed that cancer was caused by a limited number of discrete chemical, physical, or biological (e.g., viruses) agents. Today, cancer is recognized as a highly complex, multifactorial disease caused, in part, by endogenous metabolic or other imbalances associated with age or genetic makeup and, in part, by a wide variety of exogenous factors including diet, lifestyle, and exposure to ionizing radiation and chemicals of natural or man-made origin.

As a result of early epidemiological studies suggesting the predominance of exogenous over hereditary factors in many human cancers, the search for causes of cancer was focused on the physical environment (4). At a time of intense public awareness of the potentially adverse impacts of technology on the environment it was perhaps inevitable that human cancer would be attributed to the many drugs, pesticides, plastics, food additives, and other materials generated by the chemical industry. Unfortunately, despite the absence of supporting data, a large segment of the public continues to believe that most human cancers are directly associated with exposure to synthetic chemicals.

There is now general consensus that the personal and cultural habits of individuals are the predominant determinants of human cancer (2,4,5). Thus cigarettes smoking alone accounts for about 30% of all male cancer in the United States, and other "bad" habits such as consumption of alcohol and sexual promiscuity may cause an additional 10%. Diet is a highly variable factor, and its importance can be expected to change markedly with geographic and ethnic background. It is estimated that factors associated with diet are responsible for about 35% of human cancer (2,5). Even in the most highly industrialized countries, it appears that very few cancers can be attributed to exposure to synthetic chemicals. Occupational exposure to a variety of chemicals or industrial processes probably accounts for no more than 5% of human cancer, and the total contribution of environmental pollution is estimated to be only 1-2% (2).

Naturally occurring carcinogens

The fact that human cancer incidence has not changed significantly during the last 50 years provides convincing evidence for the existence of a variety of long-established cancer risk factors not associated with modern technology. Consonant with the epidemiological association of cancer with diet, there is increasing evidence that the human diet contains substantial amounts of a wide variety of natural mutagens and carcinogens (6,7). Many of these -- such as the hydrazine derivatives in mushroom species, pierine, and safrole in black pepper and other plants, theobromine in cocoa and tea, chlorogenic acid in coffee, the pyrrolizidine alkaloids in many species, and the potent mycotoxins such as aflatoxin -- are established mutagens and animal carcinogens and often occur in plants at concentrations of 2-10% by weight (6,7). Clearly, a multitude of other naturally occurring materials of unknown toxicity remain to be isolated and characterized.

Other potent carcinogens are produced as a result of cooking various foods. These include the materials present in charred or browned protein and the mutagenic pyrolysis product methyglyoxal, which is present in coffee (6-8).

It is important to consider our current obsession with identifying, regulating, and generally worrying about what often appear to be trivial carcinogenic risks associated with many synthetic chemicals against the truly overwhelming background of natural carcinogens. The common belief that everything "natural" is good is simply not true, and we must consider naturally occurring chemicals as potentially important causative factors in human cancer. Indeed, in view of the fact that our total daily intake of natural carcinogens could exceed our intake of synthetic materials by as much as 10,000-fold (6,7), it is highly unlikely that, for the general population, the combined carcinogenic effects of all synthetic chemicals can ever be distinguished from the natural background.

What is a carcinogen?

By analogy with previous experience with infectious diseases, the initial concept of a carcinogen was of some discrete physical, chemical, or biological entity. This view was strengthened by early studies showing that, under certain conditions, cancer could indeed be induced by exposing animals to single test chemicals. Today, although most of the public continues to subscribe to the concept of discrete causal agents of cancer, the scientist's view of what constitutes a carcinogen has become far more complex.

Cancer is now considered to be the end result of a multistage process in which a large number of endogenous and exogenous factors interact, simultaneously or in sequence, to disrupt normal cell growth and division (9,10). Cancer, therefore, is a complex disease that may involve a number of different mechanisms. Consequently chemical carcinogenicity should not be considered as an inherent property of a chemical but rather as an outcome of the interaction of a chemical with a complex biological system influenced by many factors.

Traditionally, the development of cancer has been divided into two major stages, initiation and promotion. Initiation describes the process whereby a chemical or other agent damages the DNA of the cell, and promotion refers to the subsequent progression and proliferation of the "transformed" cell through a variety of pathological states (e.g., hyperplasia, neoplasia) leading eventually to a malignant tumor (9,10). It is now recognized that initiation and promotion each consist of several stages and may involve distinct mechanisms; some of these stages are reversible and some are not, but probably all are susceptible to a variety of modulating factors through which they may be enhanced or inhibited.

Initiation can result directly from a mutagenic effect of the chemical (or its metabolite) on DNA, or indirectly from chronic cytotoxicity (resulting in cell turnover and natural errors in cell replication), the activation of cellular oncogenes, or other mechanisms. Initiation can be modulated by factors that change the efficiency of DNA repair or immune surveillance, and, in the case of chemicals that require metabolic activation, initiation will be affected by factors that modify metabolism.

Because these and a large number of other physiological (e.g., age, sex, hormone balance, nutritional status) and exogenous (e.g., stress, dietary fiber, and fat) factors are often key determinants in the development of cancer, should they be defined as carcinogens? Certainly an excess level of a natural hormone can be just as important a causal agent in human cancer as a pesticide residue. How to define carcinogen is not simply of academic importance; it has profound conceptual and practical implications in relation to the development of a reasonable national policy for the regulation of chemical carcinogens. It is also of importance to a confused public that constantly is being barraged by news of an ever-lengthening list of "carcinogens."

The International Agency for Research in Cancer (IARC) has defined chemical carcinogenesis as "the induction by chemicals of neoplasms that are not usually observed, the earlier induction by chemicals or neoplasms that are usually observed, and the induction by chemicals of more neoplasms than are usually found" (11). Although this is a useful operational definition, it does not attempt to address the fundamental distinction between direct-acting carcinogens and those acting indirectly through complex interactions with the test organism (12).

Clearly, a classification of carcinogens based on their mechanisms of action would be preferable, because, in some cases, this might provide an opportunity to adopt a more appropriate regulatory approach. A tilt in this direction is indicated by increasing use of terms like "genotoxic" and "nongenotoxic" (or "epigenetic") carcinogens to distinguish chemicals capable of damaging DNA from those apparently acting by other mechanisms (12,13). Unfortunately, current bioassay procedures do not allow us to classify all carcinogens according to their modes of action.

Although there is mounting evidence that some chemicals are acting through nongenotoxic mechanisms for which thresholds or no-effect dose levels might be anticipated, current regulatory policy requires that all are treated as though they are genotoxic "complete" carcinogens. In 1983, a somewhat simplistic and premature attempt by the EPA to place "epigenetic" carcinogens in a lower regulatory risk category than those considered to be "genotoxic" was greeted by such an uproar or dissent that it was quickly dropped from further consideration (14). A more fruitful approach, recommended by the Office of Science and Technology and others, evaluates each chemical on a case-by-case basis using all available data to understand its mechanism of action (9,15,16).

The search for chemical carcinogens

Efforts to identify chemicals likely to pose a potential cancer threat to humans have intensified in recent years and have relied mainly on the results of chronic bioassays with animals, short-term in vitro tests for genotoxicity, and epidemiological studies in human populations. Chronic bioassay with laboratory animals, mainly rats and mice, remains the major and most practical experimental procedure for identifying potential carcinogens. It is also a procedure beset by many practical and theoretical uncertainties relating to both the design and conduct of the test itself and the subsequent interpretation of the data.

Major limitations of chronic animal bioassays are that they are inherently insensitive and highly variable in nature. Furthermore, there is always a great deal of uncertainty associated with the fact that all such tests ultimately require the extrapolation of data obtained under one set of conditions (i.e., with rodents exposed to very high doses in the laboratory) to predict those likely to occur under an entirely different set of conditions (i.e., with humans exposed to very low doses in the real world). Such dose and species extrapolations are particularly troublesome in the generation of quantitative estimates of human cancer risk.

As a result of the increasing reliance of U.S. regulators on precise numerical estimates of theoretical, upper-bound, human cancer risk (e.g., 1 in a million or, worse, 1.3 or 1.33 in a million) and the matter-of-fact way in which these estimates are reported as real risks by the media, there are many who believe we have exquisitely sensitive testing capabilities. Nothing could be further from the truth. In a typical two-year rodent oncogenicity study utilizing a total of about 600 animals, a cancer occurring at a frequency of 5 in every 1000 would almost certainly go unnoticed. The practical implications of this are considerable because a cancer frequency of 5 in 1000 translates into more than 1 million cases of cancer in the current U.S. population.

In attempts to increase the sensitivity of the animal bioassay, high exposure levels at or approaching the maximum tolerated dose (MTD) are employed and, indeed, are required by most regulatory guidelines (17,18). The importance of the MTD in ensuring a successful outcome to the search for carcinogens is illustrated by the fact that of a group of 52 chemicals judged positive in NTP (National Toxicity Program) chronic bioassays, two-thirds would not have been so classified had the high dose selected been one-half of the MTD actually used (19). Does this increased "power of detection" really reflect true carcinogenic potential, or is it a false positive resulting from cytotoxicity or dose-dependent differences in metabolism and pharmacokinetics? Does it have any relevance to assessing low-dose effects in any species?

Regulatory policy continues to cling to the concept that there is no finite threshold below which carcinogens will not exert an effect. Consequently, although the true shape of the dose-response curve at doses lower than those actually used in the test is not known, low-dose effects can only be estimated by extrapolation to zero of effects observed at high doses (9,18,20). It should be noted that although chronic bioassays typically involve two or three doses spanning perhaps one order of magnitude, extrapolations are often four, five, or more orders of magnitude below the experimental range. Such extrapolations would not even be attempted in most areas of science.

The question of how to extrapolate has led to the development of a number of statistical models for the estimation of low-dose effects, and noisy debate over which is most appropriate has overemphasized this aspect to the problem. It has also led to the generation of precise mathematical risk estimates that are simply not justified by the quality of the toxicology data from which they are derived (21). The selection of the model to be used often dominates the results; although most models are in general agreement in the range of experimentally observed responses, they may provide estimates of low-dose responses that vary to several orders of magnitude (16,22). New and more biologically realistic models currently being developed will be described in future articles in this series (22,23).

It should be noted that risk estimates prepared by federal agencies are described as upper-bound estimates, not actual estimates, of risk. Real risks are judged to be below the upper-bound values and could be as low as zero. This is seldom made explicit in regulatory agency communications and is certainly not understood by either the media or the general public.

There is no question that the "no threshold" concept for carcinogens -- and the "zero tolerance," Delaney-type philosophy with which it is associated -- will continue to cause endless grief as long as it is a part of regulatory policy. Regardless of theoretical arguments for adopting a "no threshold" approach, it seems clear from a practical standpoint that thresholds must exist. If this were not the case the human race would have been long extinct as a result of exposure to natural carcinogens. Surely our regulatory policy must be based on realism rather than theory.

These are but some of the many sources of scientific uncertainty that severely limit current capabilities of interpreting the results of chronic animal bioassays for cancer. Others relate to properly identifying, quantifying, and assessing the relevance to humans of a variety of animal tumor types (pathology) and to evaluating the significance of tumors that occur spontaneously in several strains of test animals. Some of these uncertainties will undoubtedly be obviated as our understanding of the molecular biology of cancer and the mechanisms of carcinogenesis continue to improve. Some will not, however, and the need to extrapolate with respect to both dose and species will continue to present serious problems in evaluating the relevance of animal tests data to humans.

During the past two decades, a variety of short-term tests for genotoxicity have been developed to augment chronic animal bioassays for carcinogenesis (24). These include the well-known Ames Salmonella test for mutagenicity and several other in vitro and in vivo assays based on a number of genotoxic end points such as sister chromatid exchange, unscheduled DNA synethesis, and chromosome aberrations.

Many of these short-term tests have been widely used, but it has become increasingly apparent that there is often little correlation between the results of these tests and those of the chronic bioassays (25). Furthermore, there is considerable inconsistency among the results of different short-term tests themselves. The reasons for the former undoubtedly relate to the fact that carcinogenicity can occur through a variety of both genotoxic and nongenotoxic mechanisms and that many of the short-term tests simply fail to replicate the overall metabolic and pharmacokinetic conditions that exist in the intact test species. Differences between the results of the short-term tests probably reflect the different biological systems involved.

To avoid the problem of deciding which, if any, of the short-term tests is the most useful, it has become common practice to evaluate genotoxicity on the basis of the total weight of evidence from a battery of such tests.

Ashby has criticized this nonscientific approach (26) and has suggested a common-sense strategy that would reduce the number of short-term tests required to demonstrate genotoxic potential to just one or two in vitro tests (e.g., Ames) and one or two in vivo tests (e.g., mouse bone marrow micronucleus assay).

Doubt regarding the utility of many of the short-term tests for genotoxicity has also been raised by a recent NTP study that compared the results of chronic carcinogenesis bioassays and four short-term in vitro (not in vivo) tests for each of a group of 73 chemicals evaluated in the NTP/NCI program (27). Major conclusions from this rather limited study were

  • That a positive result in the Ames test carries a high probability (70%) that a chemical will be associated with carcinogenic activity,
  • That use of a battery of short-term tests does not improve predictability above that provided by Ames test,
  • That a tier system does not add to the utility of the tests, and
  • That the short-term tests correlated better with each other than with the chronic bioassay.

Human carcinogens

The IARC has developed a qualitative classification scheme that divides chemicals into groups with varying degrees of evidence for carcinogenicity in humans (28). These groupings are based on the strength of positive evidence available from animal studies, short-term tests, and human epidemiology, the evidence in each category being related as sufficient, limited, or inadequate. It is of interest that, of some 600 chemicals, chemical mixtures, or processes evaluated by IARC expert working groups, only 23 chemicals and 7 processes are considered causally associated with cancer in humans (Group 1). An additional 14 chemicals (Group 2A) are considered probably carcinogenic to humans. No new human carcinogens have been identified by IARC during the past 10 years; with improving tests procedures and decreasing levels of human exposure, it seems unlikely that many more will be identified.

The IARC has not been able to establish strong links with human cancer for more than a handful of chemicals, but it is equally true that very few chemicals tested are given an unequivocally clean bill of health. Of the first 192 bioassays conducted by the NCI, 98 were judged positive, 91 were judged suggestive or inconclusive, and only 3 were considered negative (29). The NCI guidelines require tests to be conducted on both sexes for each of two rodent species. A chemical is judged "positive" if it yields a positive response in one well-conducted test (i.e., in one sex of one species). A "negative" classification requires a uniformly negative response in each of the four tests. If the test results are equivocal or if the tests themselves are considered to have been inadequately designed or conducted, the conclusion with respect to carcinogenic potential is usually suggestive or inconclusive. Unfortunately, no matter how tenuous the data, these latter terms are frequently interpreted as positive by nonscientists who are unable to understand that a negative can never be demonstrated experimentally.

Regulatory goals and directions

The development of a sound regulatory policy that not only protects the public against the potentially adverse health effects of chemicals but also creates the incentive for industry to develop new materials of real benefit to society is, indeed, a difficult task. It is particularly difficult when, as is almost always the case today, the major focus of concern is cancer.

Despite the fact that there is no epidemic of human cancer in the United States and despite the fact that, of the cancer that does occur, only a very small percentage can be attributed to synthetic chemicals, we continue to pour billions of dollars worth of time, effort, and resources into attempts to identify carcinogens. Hindered by the scarcity and uncertainty of the science and complicated by the inevitable involvement of policy and value judgments, the results of such efforts are seldom clear-cut or cost-effective.

The current obsession for regulating carcinogenic risk in the United States seems to be based more on the public's perception of risk and fear of cancer than on risks that actually can be demonstrated. We are caught up in a vicious circle in which, in attempting to respond to public pressure, regulators are focusing on and identifying increasingly smaller risks that in turn further alarm the public and create yet more pressure to regulate. We seem unable, in a regulatory sense, to distinguish toxicological trivia from more clear-cut problems, and as a society we spend our time worrying about cancer risks that are orders of magnitude smaller than those risks most of us face driving to work each day.

Surely the time has come to pause and take serious stock of our regulatory goals and directions. We have limited resources, and we must concentrate these on resolving real problems that require immediate attention. Despite the inherent difficulties it entails, we must address the issue of what constitutes a significant health risk; in developing policy, we must balance this against what we as a nation can afford in terms of remedial action to reduce risks. We cannot afford to go blindly along, throwing large amounts of money into attempts to resolve imaginary problems. Instead, we must carefully identify and rank the areas of real health concern and develop appropriate strategies by which the associated risks can be avoided or minimized.


(1) Bailar, K.C. III; Smith, E.M. N. Engl. J. Med. 1986, 314, 1226-32.

(2) Doll, R.; Peto, R. The Causes of Cancer; Oxford University Press: New York, 1981.

(3) Gori, G.B.; Lynch , C.J. Reg. Toxicol. Pharmacol. 1986, 6(3), 261-73.

(4) Higginson, J.; Muir, C.S. J. Natl. Cancer Inst. 1979, 63 1291-98.

(5) Higginson, J. Environ. Mutagen. 1983, 5, 929-40.

(6) Ames, B.N. Science 1983, 221, 1256-64.

(7) Ames, B.N.; Magaw, R.; Gold, L.S. Science 1987, 236, 271-80.

(8) Sugimura, T.; Sato, S. Cancer Res. 1983, 43, 2415s.

(9) Office of Science and Technology Policy. "Chemical Carcinogens: A Review of the Science and its Associated Principles"; Fed. Regist. 1985, 50, 10371-442.

(10) Farber, E. Cancer Res. 1984, 44, 5463-74.

(11) International Agency for Research on Cancer (IARC). "IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans"; IARC: Lyons, France, 1982; Vol. 29, p. 16.

(12) Weisburger, J; Williams, G. In Toxicology: The Basic Science of Poisons, 2nd ed.; Doull, J.; Klaassen, C.D.; Amdur, M. O., Eds.; MacMillan: New York, 1980; pp. 84-138.

(13) Weisburger, J. Jpn. J. Cancer Res. 1985, 76, 1244-46.

(14) Marshall, E. Science 1983, 220, 36-37.

(15) Squire, R.A.. Science 1981, 214-877-80.

(16) Panel report; Science 1984, 225, 682-87.

(17) International Life Science Institute (ILSI). In Current Issues in Toxicology; Grice, H.C., Ed.; Springer-Verlag: New York, 1984; pp. 9-49.

(18) Environmental Protection Agency (EPA). "Guidelines for Carcinogen Risk Assessment"; Fed. Regist. 1986, 51, 33993-34014.

(19) Haseman, J. K. Fund. Appl. Toxicol. 1985, 5, 66-78.

(20) National Toxicology Program (NTP). "Report of the NTP Ad Hoc Panel on Chemical Carcinogenesis Testing and Evaluation"; U.S. Dept. of Health and Human Services: Washington, D.C. 1984.

(21) Krewski, D.; Van Ryzin, J. In Statistics and Related Topics; Csorgo, M. et al., Eds.; Elsevier/North Holland: Amsterdam, 1981; pp. 201-31.

(22) Menzel, D. ES&T, in press.

(23) Sielken, R. ES&T, in press.

(24) Weisburger, J.H.; Williams, G. In Chemical Carcinogens; 2nd ed.; Searle, C.E., Ed.; American Chemical Society: Washington, D.C., 1984; Vol. 2, pp. 1323-73.

(25) Shelby, M.D.; Stasiewicz, S. Environ. Mutgen. 1984, 6, 871-76.

(26) Ashby, J. Mutagenesis 1986, 1, 3-16.

(27) Tennant, R..W. et al. Science 1987, 236, 933-41.

(28) International Agency for Research on Cancer (IARC). "IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans"; IARC: Lyons, France, 1982; Supplement 4, pp. 7-23.

(29) Hottendorf, G.H.; Pachter, J. Toxicol. Pathol. 1982, 10, 22-26.


Alternatives to Chromated Copper Arsenate (CCAP)

  Wood Preservatives

As of December 31, 2003, the pressure treated wood industry discontinued the use of chromated copper arsenate (CCA) as the primary wood preservative used for most residential and general consumer construction. Existing CCA-treated stockpiles may be used until exhausted; however, the transition to CCA alternatives is already in progress. There are several arsenic-free wood pressure treatment alternatives to CCA already on the market including ACQ, Copper Azole, and Bardac 22C50. There are also several alternative building materials to pressure treated wood that are available today.

Environmental and health concerns have been raised over the use of CCA-treated wood. It is likely that CCA alternatives will circumvent some of these concerns simply because they do not contain arsenic. Because they have been developed relatively recently and/or have been used infrequently, only limited research has been conducted on their potential leaching and environmental impact.

Though slightly more expensive than CCA, the appearance, strength, and handling characteristics of CCA alternatives are very similar to those of CCA. However, the treated wood costs from 10% to 30% more than CCA-treated wood. (Lebow, USDA 2004)

The increased use of the CCA alternative pressure treatments has triggered concerns of hardware corrosion. Please refer the hardware portion of the Safety and Precautions page for hardware recommendations when working with the new wood treatments. Here you can also find handling and disposal recommendations.

Some helpful links to related resources

Lebow, Stan T. 2004. Alternatives to chromated copper arsenate for residential
construction. Res. Pap. FPL-RP-618. Madison, WI: U.S. Department of
Agriculture, Forest Service, Forest Products Laboratory. 9 p.  

American Wood-Preservers' Association  

Osmose, Inc.  

Wolmanized Wood by Arch Wood Protection, Inc. presented by Chemical Specialties Inc.  

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