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Canada Not Planning To Ban Popular Lawn Pesticide  2-4-D

Feb. 21 - Health Canada's Pest Management Regulatory Agency (PMRA) has determined, that 2,4-D can be used safely on lawns and turf when label directions are followed. Based on the available scientific information, PMRA, has conducted its re-evaluation of 2,4-D, a herbicide commonly used to control weeds on lawn and turf.  

The  decision on 2,4-D is consistent with those of other countries. The United States Environmental Protection Agency's re-evaluation, released in January 2005, is the most recent reassessment of 2,4-D. It also found 2,4-D to be acceptable for use on lawn and turf.   The PMRA also reviewed scientific assessments of 2,4-D from the European Union, New Zealand and the World Health Organization. 

Connie Moase of the PMRA told a news conference "We have determined that 2,4-D can continue to be used safely by homeowners who choose to use it on their lawns provided that label instructions are followed. The PMRA understands that the public may have concerns over domestic uses of pesticides and would like to convey that all registered pesticides undergo a thorough science-based risk assessment and must meet strict health and environmental standards before being approved for use in Canada. 

In order to make the determination that 2,4-D can be used safely on lawns and turf, the PMRA reviewed the available scientific data and other scientific related information on 2,4-D, and conducted stringent health and environmental risk assessments which included special consideration of children and pregnant women. In addition, the PMRA took into consideration the unique physiology, behaviors and play-habits of children, such as hand-to-mouth contact while playing on treated grass. 

The purpose of this re-evaluation is to determine if the pesticides currently on the market, that were registered before January 1, 1995 meet modern health and environmental standards. 

Before finalizing its decision, as part of its normal process, the Agency is seeking any additional information that may be relevant from the scientific community and all other interested parties before the approval of the product is final. The comment period ends on Monday, April 22, 2005.            

The PMRA is the federal regulatory body responsible for the regulation of pesticides in Canada. The regulation of pesticides in Canada is governed by the federal Pest Control Products Act.            


 About the Re-evaluation of 2,4-D            

The PMRA reviewed the extensive body of information available for 2,4-D which included the following:            

-  An extensive proprietary database. Manufacturers of the 2,4-D ingredient provided the PMRA with a database comprised of over 100 toxicity tests in animals. In addition to mammalian toxicity studies, numerous other studies on chemistry, exposure, environmental fate, environmental toxicity and on efficacy were also provided.            

-  Published scientific information. These include reports, epidemiological studies and all other relevant scientific information published in scientific journals and other publicly available documentation.            

-  Foreign reviews. The PMRA reviewed the scientific assessments of 2,4-D from the United States, the European Union, New Zealand and the World Health Organization.            

-  Use pattern information collected by the PMRA. The PMRA collected and examined all available information from a variety of sources in order to properly characterize the use pattern of 2,4-D in Canada.            

The re-evaluation included a science-based risk assessment to determine if the product can be used safely. This assessment consisted of the following:            

-  a health assessment that looked at the potential for 2,4-D to cause adverse health effects such as cancer, birth defects and Endocrine disruption;

-  an assessment of all sources and routes (oral, dermal, inhalation) of potential exposure to 2,4-D, including exposure from the diet, drinking water and from contact with treated areas like lawns and gardens;

-  homeowner as well as occupational exposure assessments (exposure encountered by the user/applicator of the product), both during and after application of 2,4-D;

-  a human health risk assessment that determined the toxicity in relation to the amount of exposure in all potentially exposed populations, including children;

-  an environmental risk assessment that considered risks to plants, birds, mammals, aquatic organisms as well as fate in the environment; and

-  an assessment of value as it relates to the efficacy of the product.            

Part of the human health assessment is to ensure that, when 2,4-D is used according to label directions, there is a large enough margin of safety between the level of exposure humans could be exposed to and any identified toxic effect during animal testing. The PMRA's assessment included the addition of extra safety factors to ensure that the most sensitive subpopulations, such as children and pregnant women, were also protected.

The PMRA also took into consideration the unique physiology, behaviors and play habits of children, such as their lower body weights and hand-to-mouth contact while playing on treated grass. 

In addition to the 2,4-D-specific animal toxicity data, the PMRA also considered the large body of epidemiological studies and reviews pertaining to 2,4-D and human health. The extensive body of scientific information examined by the PMRA included relevant data used by non-regulatory groups, such as the Ontario College of Family Physicians in their April 2004 Report.

While that report focussed on a subset of epidemiology studies from the public literature, the PMRA reviewed the extensive body of information available for 2,4-D to conduct a full human health risk assessment. The examination of animal toxicity data from internationally accepted guideline studies using doses well above those to which humans are typically exposed to, combined with exposure data obtained from well designed studies, is currently the best methodology available for assessing risks to human health. Based on the evaluation of the available information, as listed earlier, the PMRA determined that 2,4-D can be used safely when label directions are followed.            

Need More Information?            


1. PMRA | Information Note: 2,4-D and Use on Lawns and Turf
HTML Français. Contact Us. Help. Search. Canada Site. What's New. A-Z Index. Links. Site Map. Home. About PMRA. Responsible Pesticide Use. Applicants and Regist
Date: 24-Aug-2006, Size: 25K, Type: HTML


2. PMRA | 2,4-D Lawn and Turf Uses
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Date: 24-Aug-2006, Size: 17K, Type: HTML


3. meeting_report-e.pdf
PDF Page 1 of 12 Pest Management Advisory Council June 12 th - 13 th , 2006 Delta Hotel, Ottawa Draft Meeting Report The Pest Manageme nt Advisory Council (PMA
Date: 29-Sep-2006, Size: 25K, Type: Adobe PDF


4. PMRA | Information Notes
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Date: 27-Sep-2006, Size: 29K, Type: HTML


5. Questions and Answers Re-evaluation of Lawn and Turf Uses of the Herbicide 2,4-
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Date: 05-Oct-2006, Size: 53K, Type: HTML


6. PMRA | Information Note: The PMRA is implementing interim measures for products
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7. PMRA | Site Map
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8. PMRA | What's New
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Date: 27-Sep-2006, Size: 55K, Type: HTML


9. 2,4-Dqa-e.pdf
PDF Page 1 of 10 Questions and Answers Re-evaluation of Lawn and Turf Uses of the Herbicide 2,4-D Health Canada’s Pest Manageme nt Regulatory Agency has conduc
Date: 19-Sep-2006, Size: 26K, Type: Adobe PDF

Ontario College of Family Physicians Report




Information Note  Regarding Pesticide Safety in Canada

French version:


August 4, 2004
 Ontario College of Family Physicians Report

On April 23, 2004, the Ontario College of Family Physicians (OCFP) released a literature review on epidemiology studies on pesticides. The review linked pesticides to various illnesses, and stated that children are especially vulnerable to pesticides. In light of the public interest in this report, Health Canada’s Pest Management Regulatory Agency (PMRA) prepared this document to help Canadians better understand how human health and the environment are considered by the pesticide regulatory system in Canada. PMRA is the federal regulatory body responsible for the regulation of pesticides in Canada.

Pesticide Regulation in Canada

Pesticides are stringently regulated in Canada. Before a product is registered for use, it must undergo a comprehensive and rigorous scientific assessment to ensure the product does not pose unacceptable risks to human health or the environment and to assess its efficacy to ensure that the lowest rate possible is used. If the assessment does not indicate that a product can be used safely it is not registered for use in Canada. Currently, all pesticides registered prior to 1995 are being re-evaluated by using the most modern scientific risk assessment approaches to ensure they remain safe and effective for use.

The human health risk assessment looks for the short- and long-term potential of a pesticide to cause adverse health effects such as cancer, birth defects and endocrine disruption. All sources and routes (oral, dermal, inhalation) of potential exposure are assessed, including exposure from the diet, drinking water and from contact with treated areas like lawns and gardens. As well, occupational exposures, both during and after pesticide application, are specifically considered.

Pesticides are only registered if there is a wide enough margin of safety between what people are exposed to and the highest dose that causes no effects according to scientific research.

As the OCFP report notes, some population groups, such as children and pregnant women, may be more susceptible to potential effects of pesticides. This is why PMRA assessments include the application of extra safety factors to ensure that the most sensitive sub-populations are protected. For example, the PMRA pays special attention to the unique exposures and physiological characteristics of children, ensuring that factors such as their unique behaviours, different diets and lower body weights are considered.

Scientific Approaches to Understanding Pesticide Risk

The OCFP report is a review of epidemiology studies selected from the public scientific literature. There are many such studies published which suggest that there may or may not be associations between adverse health effects and pesticide exposure. As the report acknowledges, epidemiology studies are hard to interpret because of biases and confounding factors that make it very difficult to either establish or definitively rule out links between pesticide exposures and effects. For example, other chemical and physical environment effects are usually encountered at the same time as pesticide exposures and biases in the exposures remembered by study participants may affect the result. Without an actual exposure calculation, it is difficult to assess whether pesticides could have been responsible for an adverse health outcome.

When determining the acceptability of a pesticide, PMRA scientists critically examine the totality of the scientific database for pesticide active ingredients and end-use products, including the types of studies in the OCFP report. When new studies in the public literature are released, the PMRA examines them to determine if further regulatory action is required on the pesticides mentioned in the study.

Currently, much of the information submitted to the PMRA for pesticide risk assessments is protected under the Access to Information Act as confidential business information. Under the new Pest Control Products Act, the public will be able to view the data used in making pesticide registration decisions.

Responsible Pest Management

The PMRA agrees with the recommendation of the OCFP report that Canadians can and should seek opportunities to minimize their exposure to and reduce their reliance on pesticides. As such, the PMRA supports Integrated Pest Management (IPM) practices. IPM is an approach that combines biological, cultural, physical and chemical tools to manage pests so that benefits of pest control are maximized and health and environmental risks are minimized.

If Canadians choose to use pesticides, they should use products only for their intended and registered use while following all instructions on the label. The label instructions specify the conditions by which products can be used safely. The PMRA also agrees that, to prevent accidents, pesticides must always be stored out of the reach of children.

The PMRA is working with provincial and territorial governments on the Action Plan for Urban Use Pesticides that includes a Healthy Lawns Strategy ( This website provides information on IPM approaches to lawn and garden care. The PMRA also distributes a number of publications, including Pest Notes, that provide information on the safe use of pesticides and on controlling common household pests using the principles of IPM. These can be found on the Pest Notes page of, in the Responsible Pesticide Use section.

Need more information?

The following links on the PMRA website provide further information on the topics discussed in this document:

Risk assessment process:

Fact Sheet on The Regulation of Pesticides in Canada or in HTML format:

Children’s Health Priorities within the Pest Management Regulatory Agency (SPN2002-01)

A Decision Framework for Risk Assessment and Risk Management in the Pest Management Regulatory Agency (SPN2000-01)

Responsible Pest Management:

Healthy Lawns Strategy

Pest Notes

Action Plan on Urban Use Pesticides




Maximum Residue Limits for Pesticides on Foods in Canada

When pesticides are used on crops or when animals are fed crops treated with pesticides, residues may remain in or on the food when it is sold. Before registering a pest control product for use in Canada, the PMRA must determine that consumption of the residues that are likely to remain in or on the food when the pesticide is used according to label directions will not pose an unacceptable health risk. This amount is then legally established as a maximum residue limit (MRL) under the Food and Drugs Act New Window (FDA).

These MRLs apply to both domestic and imported food. In order to prevent residues in or on the imported food from posing an unacceptable health risk, MRLs are also established for pesticides not registered for use in Canada and for Canadian registered pesticides with respect to uses that are not authorized in Canada. If residues exceeding an MRL are found, the food is considered adulterated and is prohibited under the FDA from sale in Canada.
 More information...............




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.



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.




Safety Tips on Using Personal Insect Repellents

General Use Information for Personal Insect Repellents

Always read the entire label carefully before using.

Apply the repellent sparingly, and only on exposed skin surfaces or on top of clothing. Do not use under clothing. Heavy application and saturation are unnecessary for effectiveness.  Repeat applications only as necessary.  Do not get in eyes. If you do get repellent in your eyes, rinse immediately with water.  Do not use the repellent on open wounds, or if your skin is irritated or sunburned.  Avoid breathing spray mists and never apply sprays inside a tent. Use only in well-ventilated areas. Do not use near food.

Wash treated skin with soap and water when you return indoors or when protection is no longer needed.

Keep all insect repellent containers out of the reach of children.

Always supervise the application on children.  Avoid applying repellent to children’s hands to reduce the chance of getting the repellent in their eyes and mouths.

If you suspect that you or your child are reacting to an insect repellent, stop using the product immediately, wash treated skin and seek medical attention. When you go to the doctor, take the product container with you.  If you are concerned that you are sensitive to a product, apply the product to a small area of skin on your arm and wait 24 hours to see if a reaction occurs.

Choosing A Product

Choose a product that meets your needs.  For example, if you plan to be outdoors for a short period of time, choose a product with a lower concentration of repellent (shorter protection time) and repeat only if you need a longer protection time.

Use only personal insect repellents that are registered in Canada. They have a registration number granted under the Pest Control Products Act and are labelled as insect repellents for use on humans. Never use a product labelled as an insecticide on your body.

PMRA’s re-evaluation of Personal Insect Repellents containing citronella and lavender oil has not yet been completed. As a precaution, it is recommended that these not be used on children under 2 years of age. Re-evaluations involve a comprehensive review of the scientific data that supports the registration of a pesticide.  The citronella oil repellents registered in Canada protect people against mosquito bites for less than one hour. The registered lavender oil repellent protects for half an hour or less. Based on animal studies, citronella-based products appear to be potential dermal sensitizers.  Therefore, allergic reactions may occur in some individuals.

Updated Information on Using Insect

Repellents that Contain DEET

The following safety tips are based on the PMRA’s re-evaluation of DEET which involved a comprehensive review of the scientific data that supported its registration. For a complete explanation of the DEET re-evaluation process and its conclusions, please refer to Reevaluation Decision Document RRD2002-01, Personal insect repellents containing DEET (N,N-diethyl-m-toluamide and related compounds).

Children under 6 months of age

DO NOT use personal insect repellents containing DEET on infants. (Advice unchanged)

Children aged 6 months to 2 years

In situations where a high risk of complications from insect bites exist, the use of one application per day of DEET may be considered for this age group.  The least concentrated product (10% DEET or less) should be used. (New advice.)

The product should be applied sparingly and not be applied to the face and hands.  Prolonged use should be avoided.

Children between 2-12 years of age

The least concentrated

product (10% DEET or less) should be used.

Do not apply more than three times per day.
(New advice) Do not apply to the face and hands.

Prolonged use should be avoided.

Adults and Individuals 12 Years of Age or Older:

Products containing DEET at concentrations above 30% will no longer be acceptable for registration, based on a human health risk assessment that considered daily application of DEET over a prolonged period of time. Studies show that products with lower concentrations of DEET are as effective as the high concentration products, but they remain so for shorter periods of time. Products containing no more than a 30% concentration of DEET will provide adults with sufficient protection. (New advice)

30% DEET will provide approximately 6.5 hours of protection; 15% DEET will provide approximately 5 hours of protection; l0% DEET will provide approximately 3 hours of protection and 5% DEET will provide approximately 2 hours of protection.

Re-apply after these protection time have elapsed if necessary.

Note: There is no indication that there is a hazard to the unborn or nursing child associated with the use of DEET by pregnant or lactating women. However, there are non-chemical methods to reduce mosquito bites (e.g., protective clothing, avoiding mosquito habitat and times of peak mosquito activity) which could be considered.



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