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Children's environmental health : a comparison of risk assessment approaches taken by Canada, the United… Kinney, Elizabeth M. 2009

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 Children’s Environmental Health: A Comparison of Risk Assessment Approaches Taken by Canada, the United States, and the European Union by Elizabeth M. Kinney B.A., Pacific Lutheran University, 1999 LL. B., University of Victoria, 2002 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF LAWS in THE FACULTY OF GRADUATE STUDIES (Law) THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver) December 2009 © Elizabeth M. Kinney, 2009  ii  ABSTRACT Children come into contact with environmental pollutants on a daily basis.  Air pollution, pesticides, chemicals, and lead are a few of the toxic substances which are transferred to children through water, air, soil, food, and skin contact. Exposure to these substances has been linked to a variety of child chronic health conditions, including spontaneous abortions, congenital defects, neurodevelopmental disorders, reproductive dysfunctions, endocrine dysfunction, and cancers.  Because of this, governments have the responsibility to restrict exposures to these substances to ensure that intake is not unsafe. Governments have utilized a risk assessment process to determine what levels of exposure are considered safe.  The interpretation of the results of this process, however, has differed depending on which theory has been selected – the risk-based approach or the hazard-based approach.  The risk-based approach attempts to avoid unacceptable risks through the quantification of exposure and harm.  The hazard-based approach, aims to avoid exposures that result in significant harm and minimize all other exposures.  The difference between the two is that the risk-based approach is focused on controlling the risk while the hazard-based approach completely removes the most caustic substances. This thesis explores the impact the selected risk assessment approach may have on tolerances and standards set for children’s exposures to environmental pollutants.  The thesis will examine two case studies: (1) pesticide standards and (2) chemical standards.  The United States and Canada have chosen to use a risk-based approach to determine acceptable risks from exposure.  The European Union has utilized a hazard-based approach to set permissible exposure levels.  This thesis will argue that the hazard-based approach is preferable for children’s health and protection.  Since there are a great many unknowns regarding how toxic exposure impacts children’s health it is safer to avoid those chemicals which may negatively affect children’s health rather than attempt to control the risk at a “safe” level. The thesis will: (1) present information on what is known about health and toxic exposure, (2) illustrate that international efforts have failed to address environmental health, (3) discuss the differences between the two approaches to pesticide and chemical policies, and (4) provide policy recommendations.    iii  TABLE OF CONTENTS ABSTRACT................................................................................................................................................... ii TABLE OF CONTENTS ............................................................................................................................ iii ACRONYMS ............................................................................................................................................... vii ACKNOWLEDGEMENTS ........................................................................................................................ xi 1. INTRODUCTION ................................................................................................................................... 1 1.1 Introduction .............................................................................................................................................. 1 1.2 Children Are Not Little Adults ................................................................................................................ 2 1.3 A New Area Of Understanding: Children’s Environmental Health ........................................................ 3 1.4 Predicting Risks To Children’s Health Through An Uncertain Science ................................................. 5 1.5 The Failure To Consider Children In The Risk Assessment Process ...................................................... 8 1.6 Outline Of This Thesis ............................................................................................................................. 9 2. WHY ARE CHILDREN DIFFERENT? A REVIEW OF EPIDEMIOLOGY AND SCIENCE .... 10 2.1 Introduction ............................................................................................................................................ 10 2.2 The Vulnerability Of The Child ............................................................................................................. 11 2.2.1 The Developmental Stages ............................................................................................................. 13 Infancy ..................................................................................................................................... 14 Toddler And Childhood ........................................................................................................... 16 Adolescence ............................................................................................................................. 17 2.2.2 Exposure Pathways ......................................................................................................................... 19 Outdoor Air .............................................................................................................................. 20 Indoor Air ................................................................................................................................ 23 Food ......................................................................................................................................... 28 Water ........................................................................................................................................ 35 Soil ........................................................................................................................................... 38 2.2 Conclusion ............................................................................................................................................. 40  iv  3. CHILDREN’S ENVIRONMENTAL HEALTH: INTERNATIONAL EFFORTS ......................... 41 3.1 Introduction ............................................................................................................................................ 41 3.2 Focus On The Environment And Health: Tangential Agreements ........................................................ 41 3.2.1 Agenda 21 ....................................................................................................................................... 43 3.2.2 Regional Agreements ...................................................................................................................... 46 3.3 Children’s Environmental Health: International Agreements ............................................................... 49 3.3.1 The United Nations ......................................................................................................................... 50 3.3.2 The World Health Organization ..................................................................................................... 52 3.3.3 The Organisation For Economic Co-Operation And Development ................................................ 55 3.3.4 The Miami Declaration ................................................................................................................... 56 3.4 Regional Agreements: Europe ........................................................................................................... 59 3.5 Regional Agreements: North America .............................................................................................. 60 3.6 Children’s Environmental Health: International Agreements Addressing Chemicals and Pesticides ... 61 3.6.1 The Codex Alimentarius Commission ............................................................................................ 63 3.6.2 Cooperative Agenda For Children’s Health In North America ...................................................... 63 4. ADDRESSING CHILDREN’S ENVIRONMENTAL HEALTH AT A NATIONAL AND SUPRANATIONAL LEVEL ............................................................................................................... 65 4.1 Introduction ............................................................................................................................................ 65 4.2 The Differences In Risk Assessment: The Risk-Based Approach Versus The Hazard-Based Approach  ................................................................................................................................................................ 66 4.2.1 General Overview Of The Risk Assessment Process ..................................................................... 66 The Two Approaches To Risk Assessment: Risk- and Hazard-Based .................................... 67 4.3 Pesticide Legislation: An Example of How Amending The Risk-Based Approach Still Fails To Protect Children In The Same Way The Hazard-Based Approach Does ............................................................ 73 4.3.1 Pesticide Policy: A Unique Example Of The Risk- And Hazard-Based Approaches .................... 73 The Impetus For The Amendments To Pesticide Policy: Recognition That Children Were Not Accounted For ......................................................................................................................... 74 4.3.2 Risk Analysis Under Canada’s And The United States’ Pesticide Policies ................................... 77  v Defining “Acceptable” And “Safe” Risk ................................................................................. 77 Criticism of the Risk-Based Approach to Protect Children’s Health ...................................... 79 4.3.4 Risk Analysis Under The European Union’s Pesticide Policy ....................................................... 93 History:  Building On A Long Tradition Of A Non-Toxic Environment In Scandinavian Countries ................................................................................................................................. 94 Use Of A Three-Tiered Approach ........................................................................................... 97 4.3.5 Case Study: Pesticide Residues In Food Products – An Example Of The Failures Of The Risk- Based Approach ............................................................................................................................ 106 Food Residue Standards In Canada And The United States: Weaker Than That Of The EU 107 Food Residue Standards In The European Union: Greater Protection For Children’s Health  ............................................................................................................................................... 109 4.3.6 Conclusion .................................................................................................................................... 110 4.4 Chemicals ............................................................................................................................................ 111 4.4.1 Introduction ................................................................................................................................... 111 4.4.2 General Overview Of The Risk Assessment Process ............................................................... 114 4.4.3 Risk Analysis Under Canada’s And The United States’ Chemical Policies ............................. 114 The Standard Of Safety: Unreasonable And Unacceptable Risk ........................................... 116 4.4.4 Risk Analysis By The European Union: A Shift Towards A Hazard-Based Approach ........... 124 4.4.5 How The Hazard-Based Approach Resolves The Difficulties With The Risk-Based Approach In Favour Of Children’s Health ................................................................................................. 128 4.4.6 Conclusion ................................................................................................................................ 131 5. RECOMMENDATIONS AND CONCLUSIONS ............................................................................. 132 5.1 Introduction .......................................................................................................................................... 132 5.2 Obstacles That The US And Canada Face In Adopting A Hazard-Based Approach .......................... 132 5.3 Amendments That Should Be Made If The Use Of The Risk-Based Approach Continues ................ 135 5.3.1 Amendments To Be Made To The Pesticide Legislation ............................................................. 135 Minimizing The Errors Of Animal And Epidemiological Studies ........................................ 136 Reducing The Problems Associated With The Current Use Of Aggregate And Cumulative Data ....................................................................................................................................... 138  vi Instituting The Amendments Of The FQPA And PCPA: Use Of The Safety Factor ............ 141 5.3.2 Amendments To Be Made To The Chemical Legislation ........................................................ 143 5.3.3 Amendments To Be Made To The Legislation In General ....................................................... 151 5.4 Concluding Remarks ........................................................................................................................... 158 BIBLIOGRAPHY .................................................................................................................................... 161      vii  ACRONYMS 2, 4-D 2-4-Dichlorophenoxyacetic Acid ADI Acceptable Daily Intake ALARA  As Low As Reasonably Achievable ASHRAE American Society of Heating, Refrigerating, and Air- Conditioning Engineers BMD Benchmark Dose BPA Bisphenol A CDC Center for Disease Control (United States) CEHAPE Children’s Environment and Health Action Plan for Europe CHMS Canadian Health Measures Survey (Canada) COI Costs Of  Illness CRC Convention on the Rights of the Child (United Nations) CSD The Commission on Sustainable Development (United Nations) DCBP 1,2-Dibromo-3-Chloropropane DDE/DDT Dichloro-Diphenyl-Trichloroethane DEET N,N-Diethyl-Meta-Toluamide DEHP Di(2-ethylhexyl) Phthalate DINP Diisononyl Phthalate DRP Diesel Related Pollutant DSL Domestic Substances List EC European Community ECJ European Court of Justice EEA European Union European Environment Agency EEHC European Environment and Health Committee EPA Environmental Protection Agency’s (United States) ETS Environmental Tobacco Smoke EU European Union  viii  FAO Food and Agriculture Organization (United Nations) FDA Food and Drug Administration (United States) FEMA Federal Emergency Management Agency (United States) FFDCA Federal Food, Drugs, and Cosmetic Act (United States) FIFRA Federal Insecticide, Fungicide and Rodenticide Act (United States) FQPA Food Quality Protection Act (United States) G8 Group of Eight (Canada, France, Germany, Italy, Japan, Russia, United Kingdom, and the United States) GAO Government Accountability Office (United States) HCB Hexachlorobenzne HPV High Productive Volume IFM Integrated Farm Management KemI Kemikalieinspektionen (Swedish Chemical Agency) KSCA Kid Safe Chemical Act (United States) LOD Limit of Analytical Determination LOQ Level Of Quantification MCS Multiple Chemical Sensitivity MRL Maximum Residue Level NAAEC North American Agreement on Environmental Cooperation NAFTA North American Free Trade Agreement nDSL Non-Domestic Substances List NAS National Academy of Science (United States) NEHAPs National Environment Health Plans NHIS National Health Interview Survey (United States) NHANES  National Health And Nutrition Examination Survey (United States) NOAEL No Observed Adverse Effect Level   ix  OECD Organization for Economic Co-operation and Development OP Organophosphorous PAHs Polycyclic Aromatic Hydrocarbon PBDEs Polybrominated Diphenyl Ethers PBiT Persistence, Bioaccumulation, and Inherent Toxicity PCBs Polychlorinated Biphenyls PCDDs Polychlorinated Dibenzodiozins PCPA Pest Control Products Act (Canadian ) PCNB Pentachloronitrobenzene PFCs Perfluorocarbon PFOA Per-flu Octanoic Acid PM Particulate Matter PMRA Pest Management Regulatory Agency (Canada) POPs Persistent Organic Pollutants PRIMO  Pesticide RIsk Assessment Model PSL Priority Substances List PVCs Polyvinyl Chloride QALY Quality of Adjusted Life Years REACH Registration, Evaluation, Authorisation and Restriction of Chemicals (European Union) SCALE Science, Children, Awareness, Legislation and Evaluation (European Union) SIDS Sudden Infant Death Syndrome TSCA Toxic Substances Control Act (United States) UK United Kingdom UN United Nations US United States USDA US Department of Agriculture VEL Virtual Elimination List  x  VOCs Volatile Organic Compounds WHO World Health Organization WHO Europe World Health Organization Regional Office for Europe WTP Willingness To Pay      xi  ACKNOWLEDGEMENTS I would like to thank those who have made my time at UBC memorable, including peers, staff, and professors. Noteworthy amongst those is my supervisor, Dr. Shi-Ling Hsu.  I will always appreciate his willingness to take me on as a student and assist me though this often difficult process.  Thank-you for your help and support.  As well, I am grateful to Dean Bobinski for her feedback and assistance throughout my time at UBC Faculty of Law. I would also like to thank my family and friends who have supported me throughout my time at UBC.  I will always be grateful to my parents for all the years of encouragement; without it I could not have succeeded.  I am grateful to Dr. Michael Eisenhauer, my father, and my mother for their feedback and edits. Lastly but not least, I would like to thank my husband who been instrumental in my completion of this thesis.  I will forever be grateful for your willingness to proofread and make suggestions, as well as for your kindness, love, and patience. Thank-you.  1  1. INTRODUCTION 1.1 Introduction Children are often exposed to a myriad of environmental hazards, often simultaneously, in varying doses at different stages of their development.1 On a daily basis, children are exposed to a number of toxic substances, including lead, mercury, air pollution, chemicals, and pesticides.  These toxins are found in everyday life.  Children swallow polluted water and foods, breathe in ozone and chemicals from outdoor and indoor air pollution, and absorb through their skin pesticides found on playgrounds and chemicals used inside homes.  In order to control the level of exposure to these toxic substances responsible governments, especially in industrialized countries, have taken regulatory action restricting the use of and emissions from the offending agents. In many ways, the methods by which responsible governments have limited toxic exposure have been similar. Governments have relied on scientific evidence, mathematical models, and exposure data to analyze the risks associated with exposure to specific substances.  This data is used to determine what exposure rates or levels will be deemed legal or illegal, that is to say dangerous. Though science has evolved in the last half-century to provide governments with the ability to predict the impact chemical substances have on both humans and the environment, there remains a great deal of uncertainty.  Scientific understanding of the impact these toxic chemicals have on children’s health is in early development, as researchers have yet to fully grasp how chemicals affect a child’s endocrine system, reproductive development, neurodevelopmental growth, respiratory function, immune capacity, and behaviour.2 However, there exist two distinct methods for approaching this challenge of protecting children.  The risk-based approach aims at controlling the risk.  In contrast, the hazard-based approach aims to eliminate the most toxic substances, therefore removing the need to control the risk.  In order to understand how these interpretative assessment approaches make a measureable impact on children’s health, this introductory chapter will provide rationale as to why children’s environmental health is worth considering.  The five sections will include brief discussions of: (1) how children are different from adults, (2) the part environmental health plays on children’s health outcomes, (3) the role science plays in the assessment process, (4) how children often are not included in the policy process, and (5) an outline of the layout of the thesis.  1 P.J. Landrigan & J.E. Carlson, “Environmental Policy and Children’s Health” (1995) 5:2 Future Child 34 at 41. 2 E. Phipps, “Building a Dialogue Towards a National Strategy for Children’s Health and Environment in Canada” (National Policy Consultation Series on Children’s Health and Environment Interim Workshop Report, 14 September 2007) CPCHE at 35.  2  1.2 Children Are Not Little Adults Children have different physical, biological, and social environments than adults.3    The physical environment of a child includes parks, playgrounds and yards, along with school buildings, daycares, and homes.  Children spend eighty-five percent of their time indoors, in environments that may still contain lead paint, asbestos, or poor indoor air quality.4  Outside, children are exposed to a number of other chemicals that may not be part of an adult’s daily exposure.5  Playgrounds, sports fields, and yards tend to be treated with pesticides.  Since children spend more time playing and crawling in such areas than any adult, their contact with these pesticides is greater.6 Often these play areas are located near traffic zones, leading to an increased intake of particulate matter and ozone pollution.  Children inhale more air per kilogram of body weight than adults do, which adds to the impact outdoor air pollution has on their body.7  In addition, children have a greater intake of food and drink8 per kilogram of body weight, resulting in greater exposure to the toxins9 present in these dietary items.  “The average infant consumes six ounces of formula per kilogram of body weight.  For the average male adult, this is the equivalent to drinking thirty-five cans of soda pop a day.”10 The biological environment of a child consists of developmental changes that effects how toxins are absorbed by, distributed by, metabolized by, and interact with the biochemistry of the body.11  Children undergo a number of physical changes during each stage of growth, including fetus, infant, young child, child, and adolescent.12  During these periods of development, children are particularly vulnerable to harm from caustic substances.  Their gene regulation, nervous system, immune system, reproductive system, and endocrine system are still experiencing a number of changes which leave them physically vulnerable to harm.13  The negative outcomes of exposure to caustic substances include abnormalities at birth, low birth weight, childhood asthma, cancer, neurodevelopmental deficits, and behavioural disorders.14  3 E. M. Lewit & L.S. Baker, “Children’s Health and the Environment” (1995) 5:2 Future Child 8 at 8. 4 D.T. Wigle, Child Health and the Environment, (New York: Oxford University Press, 2003). 5 K. Cooper et al., Environmental Standard Setting and Children’s Health, (Toronto: C.E.L.A., 2000) at 40. 6 L.R. Goldman & S. Koduru, “Chemicals in the Environment and Developmental Toxicity to Children: A Public Health and Policy Perspective” (2000) Environ. Health Perspect. 443 at 443. 7 Cooper, supra note 5 at 41. 8In addition to food and water consumption , breast milk intake affects toxic intake. 9 Toxins include chemicals, lead, mercury, arsenic, cadmium, manganese, dioxins, and pesticides. Wigle, supra note 4. 10 Lewit supra note 3 at 15. 11 Ibid. at 12. 12 P.J. Landrigan et al., “Children’s Health and the Environment: Public Health Issues and Challenges for Risk Assessment” (2004) 112:2 Environ. Health Perspect., online: EHP <> (last modified: February 2004). 13 Wigle, supra note 4. 14 Ibid. at 1.  3  The social environment of a child consists of his/her interaction with other children and family members “as well as the laws and regulations that affect day-to-day living.”15  The places where children reside, the socio-economic class of their parents and care-takers, the school systems that they attend, and their access to health care influence exposure to and impact from toxins.  These cultural, political, and economic differences may influence nutrition, sanitation, and quality of medical care.16  Along with these differences in their social settings, children experience different exposures due to varying regulatory tools used in respective regions.17  Many governments have exercised their authority over water regulation, food control, school building requirements, consumer safety, and air pollution to prevent or reduce childhood exposures to chemicals.  However, these powers have been used in many ways and to varying degrees, resulting in differing levels of protection. 1.3 A New Area Of Understanding: Children’s Environmental Health The relationship humans have with their environment is ever-evolving.  Though the realization that humans have an impact on environment has long been understood18, the recognition of the impact environment can have on children’s health is relatively new.  In fact, the area of environmental health in general is fairly novel. Within the last century, a number of individual instances have occurred which have led to a better grasp of this relationship between environment and childhood health.  Research indicated that childhood exposure to lead paint often resulted in cognitive and neurobehavioural deficits as early as 1904.19  In the 1920s, there were reports that exposure to radiation during pregnancy led to childhood retardation.20  In the 1950s, the exposure to methyl mercury and its capacity to cause cerebral palsy in children was evident from the consumption of contaminated fish caught in Minamata Bay in Kyushu, Japan.21  The negative impact the chemical class of polychlorinated biphenyls (PCBs) had  15 C.F. Bearer, “Environmental Health Hazards: How Children Are Different from Adults” (1995) 5:2 Future Child11 at 11. 16 Wigle, supra note 4 at 1. 17 Bearer, supra note 15 at 22. 18 It has been argued that as early as biblical times there was a general understanding of the relationship environment had on health.  For instance, forbidden animal based foods were banned because they were “unclean”.  Research indicates that this religious principle aided in reducing human exposure to bacteria.   Scientific progress by the Romans led to an increase in knowledge on health consequences due to environmental exposures.  To address this, Romans instituted the first sewage system, hot and cold water, and regular bathing.  However, with the passage of time, there has been a shift from viewing the relationship between environment and health as one where environment affects humans, to one where humans affect the environment.  The 1962 publication, Silent Spring, by Rachel Carson highlighted this relationship, focusing on the harm pesticides were having on the environment, and therefore humans. H. Frumkin, “Beyond Toxicity Human Health and the Natural Environment” (2001) 20:3 Am. J. Prev. Med. 234 at 234; R. Carson, Silent Spring (New York: First Mariner Books, 1962); “History of Environmental Health” (Jersey, England: States of Jersey), online: States of Jersey <> (date accessed: 14 September 2009). 19 J.L. Gibson, “Painted Walls of Rooms as the Source of Lead Poisoning Amongst Queensland Children” (2005) 120 Public Health Rep. 301 at 301; J.J. Chisolm, “Removal of Lead Paint from Old Housing: The Need for a New Approach” (1986) 76:3 Am. J. Public Health 236 at 236. 20 R.W. Miller, “How Environmental Hazards in Childhood Have Been Discovered: Carcinogens, Teratogens, Neurotoxicants, and Others” (2004) 113:4 Peds. 945 at 945. 21 Ibid. at 946.  4  on children was discovered in 1968 when rice oil used in cooking had been contaminated by this substance.22  The exposure resulted in newborns and children having developmental delays, skin diseases, low birth weight, and cognitive deficits.23  Similarly, instances of childhood cancer from consumption of pesticides such as alachlor in the 1980s resulted in an awareness of the potential for harm from pesticides in general.24 In addition to these examples of cause-and effect between environment and childhood health, increases in chronic health conditions have led governments to begin to research additional relationships between exposure and harm, especially when government is the primary health insurer.  Globally there has been an increase in obesity, asthma, autism, and other developmental disorders among children.25  In the United States alone, almost five million children suffer from asthma.26  This figure has increased rapidly over the last few decades.27  Childhood cancer has increased, with melanoma, thyroid cancer, testicular cancer, and non-Hodgkin’s lymphoma being the most common and leukemia and brain tumours increasing the most rapidly.28  Birth defects have become the most common cause of infant mortality, with nearly one in every twenty-eight babies born with some form of birth abnormality.29 The specific instances of harm from exposure and the increasing incidents of childhood chronic health conditions have led to an understanding of the potential impact environmental pollution can have on children’s health.  Because of this, many enlightened governments have integrated the impact exposure to substances make on health as part of the assessment of environmental risk which is permitted under policy.30  Industrialized nations have initiated various efforts to include children’s physical, biological, and social environments in setting chemical exposure standards and controlling pollution.  22 Ibid; Y.L. Gao et al., “Blood Serum Levels of PCBs and PCDFs in Yucheng Women 14 Years after Exposure to Toxic Rice Oil” (1997) 33 Arch. Environ. Contam. Toxicol. 104 at 104; Y. J. Chen, “A 6-Year Follow-Up of Behavior and Activity Disorders in the Taiwan Yu-Cheng Children” (1994) 84:3 Am. J. Public Health 415 at 415. 23 Wigle, supra note 4 at 138. 24 G. Hoberg, Jr., “Risk, Science and Politics: Alachlor Regulation in Canada and the United States” (1990) 23 Can. J. Polt. Sci. 257 at 260. 25 J.E. Carlson, “Exposure and Toxicants and Child Health: Comments and Questions” (2005) 15:1 Children, Youth, and Environs. 224 at 225. 26 J. Wargo and L.E. Wargo, The State of Children’s Health and Environment, (Los Angeles: C.H.E.C. 2002) at 5. 27 Ibid. 28 Wigle, supra note 4 at 4; Wargo, supra note 26 at 5. 29 Wargo, supra note 26 at 5. 30 P. Bennett, “Governing Environmental Risk: Regulation, Insurance and Moral Economy” (1999) 23:2 Prgss. Hum. Geo. 189 at 191.  5  1.4 Predicting Risks To Children’s Health Through An Uncertain Science In attempts to control or prevent exposure to toxins found in a child’s daily environment, international and national policy has been drafted.  At an international level, a number of doctrines have provided awareness of the environmental health issues that children face, but few have included mandates which result in a reduction in exposure.  These doctrines will be discussed in chapter three.31 Although these international efforts have led to an increasing awareness of the vulnerabilities of children, they have failed to “actually act to specifically protect them”.32  As a result, federal governments are left to create regulatory policy on caustic substances.  Due to the number of different environmental pollutants, such as air pollution, water contamination, residues on foods, and indoor toxins, governments have relied on a number of different statutes respective to each.  Tools in statutes to regulate may include licensing requirements for substances prior to their use or production, pollution plans restricting the amount of a substance that may be present in the environment, and/or standards set in the statute for chemical exposure.33 In order to establish permissible tolerances of exposure, governing bodies rely on scientific evaluations.  These groups utilize data on toxicity and exposure to determine whether or not a standard for substance exposure needs to be legislated, and if so, at what level.  The use of scientific evidence in this way is a relatively new phenomenon, instigated both by the evolution of scientific capabilities and by a greater pressure by the public in developed nations to regulate industry.34 This process is now identified as the risk assessment process.  It has been defined as “principally a scientific activity” which “consists of an attempt to estimate the hazardous properties of a chemical in the environment and to determine the risks to human health that may result from exposure”.35  This process is the basis by which children’s health is considered and protected throughout environmental policy.  However, while the activity is science based there remains a great deal of unknowns or knowledge gaps.  Because the study of the impact substance exposure has on children is relatively new, there are a number of uncertainties as to what a negative outcomes therefore reducing the accuracy of this estimation.  “There are simply too many uncertainties inherent in the process in terms of 1) basic  31 Carlson, supra note 25 at 227. 32 Ibid. 33 Landrigan 1995, supra note 1 at 35. 34 Public pressure and awareness increased during the 1960s, due in part to Rachel Carson’s Silent Spring.   In response, a number of nation-states instituted a formal procedure mandating science as an evaluation tool. The United States was one of the first countries to document that a scientific evaluation shall be made.  The US National Research Council’s (NRC) report, Risk Assessment in the Federal Government: Managing the Process [hereinafter the “Red Book”], held that a risk analysis of substances shall be performed prior to political consideration of any standards. R.E. Lofstedt, “A European Perspective on the NRC Red Book, Risk Assessment in the Federal Government: Managing the Process” (2003) 9 Hum. Ecol. Risk Assess. 1327 at 1328; National Research Council, Risk Assessment in the Federal Government: Managing the Process (Washington, D.C.: National Academy Press, 1983); Carson, supra note 18; National Research Council, Risk Assessment in the Federal Government: Managing the Process (Washington, D.C.: National Academy Press, 1983). 35 Landrigan 1995, supra note 1 at 37.  6  insufficiency of data; 2) lack of methodologies for key steps in the process; and 3) the difficult of reproducing or ensuring consistency and equal levels of professionalism and expertise across highly complex analyses.”36 Because of these uncertainties, governments have relied on “a particular framing of knowledge”37 to aid in interpreting the outcomes of risk assessments.  The two primary frameworks that have been used by most developed nations are the risk-based approach and the hazard-based approach.  The objective of the risk-based approach is: “ avoid unacceptable risks.  These decisions are therefore based on unacceptable risk considerations using a quantitative and/or qualitative comparison between exposure and inherent properties.  The risk-based mechanisms are used to evaluate if the pressures imposed by exposure-based mechanisms are sufficient to reduce risks to an acceptable level or if additional measures are needed.”38 The hazard-based approach consists of three tiers.  At each level of evaluation, the substance is evaluated, and if it passes with the necessary requirements, it advances to the next tier.  The first tier is the hazard-based decision, where the objective is: “ avoid exposure to chemicals that pose a specific potential hazard.  These decisions are therefore based on risk avoidance considerations.  The risk avoidance considerations leading to hazard-based decisions are based on the conclusion that any exposure to a chemical with these specific inherent chemical properties is unacceptable regardless of whether or not the risks will actually occur.”39 If the substance does not possess the properties of harm which eliminate it in tier one, the review progresses to the second tier where exposure-based decisions are made.  The goal of this tier is: “...a clean(er) environment, based on pollution prevention.  These decisions are therefore based on exposure minimization considerations and are applied to all chemicals uniformly or to groups of chemicals used in certain processes.  The exposure-based decisions are made irrespective of the inherent chemical properties.  They provide continuous pressures to reduce pollution.”40 In those circumstances where the substance does not possess inherent chemical properties that cause it to be eliminated under tier one, and has not been selected for minimization under the second stage of the evaluation, then the substance will be evaluated for risk using the same criteria as the risk-based approach.41 As this thesis will argue, use of the hazard-based approach results in more protective standards and regulations than use of the risk-based approach.  One of the reasons for this is that the risk-based approach relies solely on scientific formulations to determine what levels of exposure are safe.  However, because of the great number of unknowns  36 T. McClenaghan et al., “Environmental Standard Setting and Children’s Health in Canada: Injecting Precaution into Risk Assessment” (2003) 12:2 J. Environ. Law Prct. 141 at 150. 37 Bennett, supra note 30 at 190. 38 B. Hansen & M. Blainey, “REACH: A Step Change in the Management of Chemicals” (2006) 15:3 Reciel. 270 at 273. 39 Ibid. at 274. 40 Ibid. 41 Ibid. at 275.  7  surrounding this field of science, particularly the impact toxic exposure has on children’s health, it is not very scientific.42  It has been said that “[w]hile [the risk-based approach] can provide a generally reliable means of predicting acute effects from high dose exposures, it falls far short in the most important areas of environmental concern: chronic effects from long-term, low dose exposure.”43  And, unfortunately, before this predictive tool can be validated, exposure for many years must occur to “obtain empirical feedback, which is necessary (for them as for all of us) to confirm or correct their theories.”44 The impact that these weak predictions, even when only slightly inaccurate, can make on children is substantial. Nearly seventy thousand chemicals are on the international market, and nearly five hundred of these substances are detectable in human tissue.45  Because a child is exposed to this many chemicals on a daily basis, any inaccuracy in the risk-based approach would make a negative impact on their health. This is particularly true as very little is understood about vulnerabilities due to exposure to a number of chemicals at once, known as Multiple Chemical Sensitivity (MCS).46  With an increase in childhood disease rates, as mentioned earlier, it may be that the imprecision in these estimates coupled with the scientific uncertainties is having a significant impact on children’s health. The hazard-based approach aims to eliminate some of the uncertainties which are inherent in the risk assessment process.  Based on the idea that precaution should be taken, this interpretation of the scientific process eliminates products that may cause substantial physical harm.  “If there is a potential for harm from an activity and if there is uncertainty about the magnitude of impacts or causality, then anticipatory action should be taken to avoid harm.”47 Using this overlay in the risk assessment process provides a safety net whereby caustic chemicals are immediately banned rather than an estimate of safe exposure made.  Since there are so many unknowns surrounding how chemicals affect children’s health, particularly their ability to cause cancer48, this approach rids the childhood exposure to the most likely offending toxins.  42 R. A. Pollak, “Government Risk Regulation” (1996) 545 Ann. Amrcn. Acad. Pltcl. Scnc. 25 at 25. 43 McClenaghan, supra note 36 at 9. 44 Pollak, supra note 42 at 28. 45 Wargo, supra note 26 at 4. 46 Ibid. at 8. 47 McClenaghan, supra note 36 at 19. 48 L. Goldman, “Chemicals and Children’s Environment: What We Don’t Know about Risks” (1998) 106:3 Environ. Health. Perspect. Supp. 875 at 875.  8  1.5 The Failure To Consider Children In The Risk Assessment Process It is more than the mere selection of an interpretative approach which aids or hinders in the protection of children’s health.  It is also the consideration, or lack thereof, of children in the first place.  “The fact that risk assessments do not usually consider children’s unique risks is a major flaw …”49  If children’s unique physical, biological, and social settings are not incorporated in the assessment process, then there is no way of knowing if harm occurs to a child at a specific dose. As already discussed, the differences between children and adults are vast, and therefore impact the type and quantity of exposures they have.  However, until the 1990s, assessments tended not to include children’s vulnerabilities in the estimate of harm.  While individual substances, such as lead, were evaluated for their impact on children, it was not a consistent process included in all environmental policy.  In fact, most of the efforts to do so were reactionary after a long period of harm was evident.  Due to a food scare in 1991 when it was found that the pesticide Aldicarb used on bananas left residues not “potentially high enough to make a child acutely ill”50, the US government commissioned a research report into the unknown effects pesticides were having on children.  Though this publication, Pesticides in the Diets of Infants and Children, was focused on pesticides, it did produce awareness that children are physically different in many ways than adults.51 What will be discussed throughout this thesis is that even in those circumstances where children are specifically mentioned in the environmental legislation, the interpretative approach to the assessment process makes a clear difference.  Those who utilize the risk-based approach continue to permit exposure to caustic substances, even though in limited amounts.  Meanwhile, those nations that have integrated children’s physiological differences into the assessment process and use the hazard-based approach tend to achieve more stringent standards and an overall elimination of potentially toxic substances, the outcome of which is a reduced childhood exposure to toxins.  49 Landrigan 1995, supra note 1 at 39. 50 Goldman, supra note 48 at 27. 51 While children are now integrated in the assessment process in most developed nations, there continues to be a fragmented approach whereby children may be protected under one environmental policy and not another, as will be highlighted in this thesis.  This needs to be remedied for children to be protected, no matter the approach taken. Landrigan 2004, supra note 12 at 257; J.L. Aber, J. Brooks-Gunn, & R.A. Maynard,  Effects of Welfare Reform on Teenage Parents and their Children” (1998) 106:3 Environ. Health. Perspect. Supp. 53 at 53.  9  1.6 Outline Of This Thesis This thesis will discuss in further detail the impact the interpretative approach taken to the risk assessment process can have on children’s health.  In doing so, three jurisdictions have been selected for review, Canada, the European Union (EU), and the United States (US).  The US and Canada both use the risk-based approach in regulating toxins, in contrast to the hazard-based approach employed by the EU.  In order to provide context about the different standards that result from these two approaches, two case studies have been selected.  The first case study is a review of pesticide regulation by each government.  The second case study is a review of chemical legislation in place in each jurisdiction. Chapter two of the thesis will provide an in-depth overview of the differences between children’s physical and biological settings which lead to an increase in the inhalation, absorption, and digestion of substances.  The purpose of this review is to put the prevalence of the problem into context.  It is not merely an issue of childhood consumption of pesticides or inhalation of chemicals, but rather an issue that affects every aspect of children’s daily life. Chapter three outlines the different international efforts which have been made pertaining to children’s environmental health.  What will be apparent from this chapter is though many developed nations have participated in international forums and doctrines that aim to reduce exposure, these doctrines do not mandate specific requirements of each signatory.  Without such requirements, little success has come from these doctrines.  In a limited number of instances, general environmental health issues have been addressed with specific requirements.  These policies have been capable of reducing or eliminating exposures to specific toxins.  However, the chemicals selected for these international efforts have only been the very most caustic. Chapter four provides a comparison of the level of risk to the children of the US and Canada with those of the EU. Because of the approaches taken by the North American jurisdictions, their policies have been weaker.  Their use of the risk-based approach aims to control the risk to children, yet because of the scientific uncertainties inherent in the process, this is an inaccurate process that results in children taking in more toxins than those residing in the EU.  The EU has applied a hazard-based approach which attempts to reduce the overall use of all toxins and endeavours to eliminate those substances with a significant impact on children’s health.  By banning these specific substances, the EU has effectively eliminated the concern that they may have, as the risk-based approach might not correctly estimating safe levels of exposure.  This chapter will utilize pesticide and chemical regulations as examples of each approach. The last chapter will provide recommendations for how the US and Canada can modify their current approach to risk assessment to provide better protection for children’s health.  This chapter will also include concluding remarks on the impact science makes on the approach and the advantages of utilizing a cautionary overlay in the assessment process.  10  2. WHY ARE CHILDREN DIFFERENT? A REVIEW OF EPIDEMIOLOGY AND SCIENCE 2.1 Introduction Before reviewing policy considerations relevant to children’s environmental health, it is important to understand the differences between children and adults. Children are a vulnerable subpopulation who have unique physiology, behaviour, and mental capacity. From conception to adulthood, a child has a limited capacity to ward off the negative consequences of environmental pollutants.52  Early stages of the developing immune system, nervous system, and endocrine system fail to offer the same levels of protection from environmental toxins that are active in adulthood. Additionally, behavioural and environmental differences, such as outdoor play, crawling, and school attendance, compound the susceptibilities of children. A child also has a reduced potential, compared to an adult, to combat toxins as they eat more food and drink more water relative to body weight and breathe more air per kilogram of body weight.53 Developing mental capacity leaves children unable to make reasonable decisions regarding exposure, particularly in early stages of life. The concept of exposure is foreign to children, and particular behaviours, such as hand-to-mouth actions, lead to added contact with pollutants. In this chapter, epidemiological studies obtained through databases, including Pubmed and Toxnet, are highlighted in the appropriate sections.   It is evident from these studies that further research needs to be conducted, particularly in the form of biomonitoring, which is the analysis of blood, tissue, and urine for a specific toxic substance. At this point, research performed tends to lack clear case-control groups or is unable to take into consideration confounding factors. These study concerns are not always attributable to poor research design but rather to the inability to isolate children from specific pollutants and control for genetic influences. What can be observed from these studies is that there is a clear basis for concern. Negative health outcomes due to environmental exposures indicate that there is a causational relationship, but what is yet to be defined is under what circumstances or what exposure levels the negative health outcomes occur.  It may be that these determinations need not be made before policy action is taken. This chapter is divided into two sections. The first provides an overview of the developmental stages of growth and the specific vulnerabilities during these times.  The developmental stages reviewed are that of infancy, toddler and young child, and adolescence. The second portion of the chapter provides an analysis of exposure pathways, i.e. what mediums expose children to pollutants. Pathways considered are outdoor air, indoor air, food, water, and soil. The objective of this chapter is to illustrate that the differences between a child’s and an adult’s daily life leave a children susceptible to unnecessary harm.  52 Wigle, supra note 4. 53 Ibid. at 1.  11  2.2 The Vulnerability Of The Child The medical community recognized physiological and behavioural differences of children during the late 1800s.54 First in Europe, then in North America, the specialization of children’s medicine took hold in medical practice and became a norm.55  Central to this medical specialization is that a child’s body is not that of a “little adult”56, but functionally and developmentally different during maturation. Awareness of childhood health has led to special consideration of pharmaceutical intake, surgical methods, and diagnostic tools. Within recent decades, the pediatric community has acknowledged that child health should be independently considered by more than solely by the medical community. There are a multitude of determinants of health, including social networks, education, employment conditions, culture, economic status, gender, health services, child development, biology, genetics, and physical environments.57  While no one determinant can be isolated when establishing the cause and prevention of disease, the consideration of environmental exposure has often been neglected. Because of this, the American Academy of Pediatrics has held out the determination of environmental exposures as essential in detecting, treating, and preventing diseases and offering an accurate diagnosis. Environment-related caused conditions result in over three million deaths of children under the age of five per year.58 This linkage between environmental pollutants and deaths and disease each year makes a lasting impact on the global society. Although the extent of exposure and the consequences of are naturally greater in developing nations, the exposure rates in countries such as Canada, the United States, and parts of Europe are alarming. While accidental injuries remain the leading cause of childhood death in Canada and the United States, there has been a disconcerting increase of environmentally induced diseases. From 1974 to 1984 the incidence rates of childhood cancer increased fifteen percent, and have remained relatively constant since.59  Incidence rates of childhood cancer vary from 144 to 159 per 1,000,000 children.60  Recent levelling trends may be an indication of a persistent rate of exposure to some  54 P.E. Luecke, Jr., “The History of Pediatrics at Baylor University Medical Center” (2004) 17(1) Bayl. Univ. Med. Cent. 56, online: PubMed Central  <> (last modified: January 2004). 55 E.A.C. Hubal et al., “Children’s Exposure Assessment: A Review of Factors Influencing Children’s Exposures, and the Data Available to Characterize and Assess that Exposure” (2000) 108:6 Environ. Health Perspect. 475, online: Environ. Health Perspect. < 0041.pdf> (last modified: June 2000). 56 P.S. Guzelian, C.J. Henry, & S.S. Olin, Similarities and Differences Between Children and Adults: Implications for Risk Assessment (Washington, D.C.: I.L.S.I. Press, 1992) at 1; M. Sharpe, “In Harm’s Way: Children’s Environmental Health” (2002) 4:6 J.E.M. 93, online: J.E.M. <> (last modified: December 2002). 57 I. Kickbusch, Health Promotion Glossary, WHO, WHO/HPR/HEP/98.1 (1998). 58 The Environment and Health for Children and their Mothers, WHO, (2005), online: WHO <> (date accessed: 13 July 2008). 59 Wigle, supra note 4, at 4. 60 National Cancer Institute of Canada, Canadian Cancer Statistics Special Topic: Childhood Cancer (Ages 0   to 14), (2008), online < wide/About%20cancer/Cancer%20statistics/Canadian%20Cancer%20Statistics/~/media/CCS/Canada%20wide/Files %20List/English%20files%20heading/pdf%20not%20in%20publications%20section/2008%20special%20topics%20 -CCS%20stats-English%20PDF_20526213.ashx> (date accessed: 2 January 2009).  12  cancer causing toxins, as well as reduced environmental tobacco smoke (ETS), chemical exposures (pesticides residues in foodstuff), and lead exposures.  Over the last twenty years, childhood asthma cases have escalated fourfold, with twelve percent of Canadian children treated for asthma and 29,000 children hospitalized for asthma related illnesses.61 While it is important to acknowledge that environmental contaminants and hazards affect or induce adult morbidity and mortality, children’s vulnerability is greater due to their disproportionately high exposure rate and biological susceptibility.62  This chapter examines how children are more vulnerable to the harmful effects of environmental hazards. Discussion will focus on the physiological and biological differences between children and adults, the exposure routes, and the conditions related to specific toxicants.  61 Canada, Environment Canada, “Children’s Environmental Health” (2005), online < http://www.environment->  (last modified: 21 May 2005). 62 P.J. Landrigan et al., “Children’s Health and the Environment: A New Agenda for Prevention Research” (1998) 106: Suppl 3 Environ. Health Perspect. 787, online: Environ. Health Perspect. <> (last modified: June 1998).  13  2.2.1 The Developmental Stages During a child’s transformation from fetus to young adult, he or she progresses through a number of developmental stages. These developmental stages of growth affect how, and with what impact, environmental exposures take place. While the terminology of children’s environmental health indicates that the focus is merely on exposure while a child, literature on the topic has established that the concern extends beyond childhood ages.63  Obviously exposure by a woman who is pregnant may affect the fetus. However, a mother’s exposure prior to conception may as well. For instance, epidemiological studies have determined that preconceptional exposure to carcinogens during sperm or oocyte maturation may result in transgenerational carcinogenesis (one of the steps in transmission of tumor susceptibility).64  Additionally a mother’s exposure before conception may affect her future children. For instance, the grandmother’s exposure may affect the mother’s ovum formation during her fetal stage of development, which, in turn, may harm her fetus when she is pregnant.65  Women exposed to PCBs prior to conception have been found to pass PCBs on to infants while breastfeeding due to the ability of PCBs to bioaccumulate in fatty tissue.66  Adult onset of cancer may be a result of fetal or childhood exposures.67  Japanese adults who are atomic bomb survivors have been found to have an increased risk of breast cancer, though exposed in childhood.68  Because toxin exposure can occur prior to conception and throughout childhood, and evidence of harm may not be evident until adulthood, it is necessary that developmental stages of the child considered must extend from preconception to adulthood. Literature on this topic tends to include preconception, fetus, infancy, toddler, young child, childhood, and adolescence.69  However, slight definitional differences exist. For some studies, consideration of pregnancy is segregated into trimesters. Studies have found that due to the developmental differences between the first trimester and the second through third trimesters, exposure concerns differ. For instance, during the first trimester, the fertilized embryo undergoes periods of cell proliferation and tissue differentiation, essential to DNA synthesis.70  The risk for cardiac defects has been associated with first trimester exposure to some herbicides and rodenticides, though  63Wigle, supra note 13, at 6; Canadian Partnership for Children’s Health and Environment, “Child Health and the Environment – A Primer” (2005), online: C.P.C.H.E. <>  (last modified: August 2005); Cooper, supra note 5 at 67. 64 L.S. Birnbaum & S.E. Fenton, “Cancer and Developmental Exposure to Endocrine Disruptors” (2003) 111:4 Environ. Health Perspect. 389 at 390. 65 C.F. Bearer, “Environmental Health Hazards: How Children Are Different from Adults” (1995) 5:11 Future Child. 11 at 14. 66 W.J. Rogan & B.C. Gladen, “PCBs, DDE, and Child Development at 18 and 24 months” (1991) Ann. Epidemiol. 407 at 407. 67 Cooper, supra note 5 at 13. 68A. Olshan et al., “Workshop to Identify Critical Windows of Exposure for Children’s Health: Cancer Work Group Summary” (2000) 108:S3 Environ. Health Perspect. Supp., online: Environ. Health Perspect. <> (date accessed: 19 November 2008); National Research Council, Committee on Biological Effects of Ionizing Radiation, Health Effects of Exposure to Low Levels of Ionizing Radiation (BEIR V) (Washington, D.C.: National Academy Press , 1990). 69 Wigle, supra note 4; Cooper, supra note 5. 70 Cooper, supra note 5 at 45.  14  not so in second or third trimesters.71 Throughout the pregnancy, exposure to environmental contaminants may occur since compounds are capable of crossing the placenta.72  It is thought that fat-soluble, lipophilic compounds (like that of polycyclic aromatic hydrocarbons and ethanol) are able to enter into the fetal circulation system.73  Little is known as to what ability, if any, the fetus has to protect itself from this exposure. The following subsections examine the developmental stages of infancy, toddler and young childhood, and adolescence, as these areas have been closely examined in epidemiological studies. Fetal exposure as well as adult onset of disease will be highlighted in the subsections dealing with the appropriate exposure pathways in the following section. Infancy Consideration of infancy by literature on children’s environmental health includes that of the newborn age to six months and six months to one year of age.74  Some prefer dividing the period of infancy between neonatal (up to one month) and postneonatal (one month to 1 year of age).75  With either method of analysis, what is noteworthy are the ongoing developmental changes prior to one year of age.  Infant growth is a period where the body undergoes rapid change, during which the organ systems are vulnerable and incapable of defence and repair of damage done.76 Exposure pathways, such as lungs, skin, and digestive tract, are still developing, leaving the body’s protective system less than optimal.77 Examples of harm done during this time period are prevalent in the literature; lead absorption is a case in point. As an infant’s body has a greater need for calcium during the developing months (this need continues into early childhood), absorption rates are greater.78  If lead is introduced into the system, the body absorbs it believing it to be calcium. Because of this, an adult’s body will take in ten percent of ingested lead, whereas a child who is two years of age will absorb fifty percent of lead introduced into the system.79 Inhalation during infancy is different than in childhood and adulthood.80  Infants and young children have a greater exchange of air than adults while having smaller lungs.81  The lung volume doubles within four months, and alveoli average half of that of an average adult.82  This higher surface to volume ratio provides a greater avenue for intake of  71 Wigle, supra note 4 at 1. 72 Bearer, supra note 15 at 19. 73 Ibid. 74 Canadian Partnership, supra note 63. 75 Wigle, supra note 4. 76 P.J. Landrigan, “Children as a Vulnerable Population” (2004) 17:1 Int. J. Occup. Med. Tox. 175 at 176. 77 Bearer, supra note 15 at 12. 78 Ibid. at 18. 79 Ibid. at 20. 80 E.E. Ziegler et al., “Absorption and Retention of Lead by Infants” (1978) 12:1 Pediatr. Res. 29 at 32. 81 W.S. Tyler et al., “Comparison of Daily and Seasonal Exposures of Young Monkeys to Ozone” (1988) 50:2 Toxicology 131 at 131. 82 A.A. Hislop, “Airway and Blood Vessel Interaction During Lung Development” (2002) 201:4 J. Anat. 325 at 330.  15  air pollutants.83  Behavioural differences, such as hand-to-mouth, eating, and playing on the floor, result in a greater level of exposure and intake of pollutants.84 Dermal exposure during infancy to pollutants and toxins is different than that of an adult or even a child. Young children and infants have a larger surface-to-volume ratio85 and therefore may take in three times the exposed pollutant than that of an adult. Infant production of the thick dead cell layer of the epidermis (keratin) is not produced until three to five days following birth.86  In pre-term infants, the susceptibility to absorption is even greater. A study of sodium salicylate (a non-steroidal anti-inflammatory drug (NSAID)) dermal exposure in preterm babies demonstrated that the absorption was greater in infants under thirty weeks of gestation87 and that there was little formation of keratinized stratum corneum (thick exterior skin cells).88 Other areas of dramatic development during infancy include that of the neurological system and the immune system. While neither acts as an exposure pathway like that of the digestive, respiratory, and dermal systems, the rapid development of these systems leaves them susceptible to permanent harm. Brain cells divide, migrate, differentiate, establish synaptic connections, and apoptosize during this developmental stage.89  The head circumference of an infant increases on average 2 cm per month until two months of age, and 1.5 cm from two months to four months of age.90  The posterior fontanel (a portion of the skull) does not close before the second month of infancy in order to allow for brain development. The blood-brain barrier, essential in the protection of the brain from pollutants, does not fully develop until about six months of age.91  Brain cells continue to increase in numbers for the first two years of life. A child’s immune system is not yet fully formed, with TH-2 (humoral immunity dominant) and TH-1 (cellular immunity dominant) phenotypes development not occurring until three to five days after birth.92  Interruption during any one of these stages can cause irreparable harm.93  Incidence of harm to brain function from exposure to alcohol94, eETS95, and lead96 has been well documented.  83 Wigle, supra note 4 at 13. 84 V.M. Weaver, T.J. Buckley, & J.D. Groopman, “Approaches to Environmental Exposure Assessment in Children” 106:S3 Environ. Health Perspect. 827 at 827. 85Wigle, supra note 4 at 165. 86 Ibid. 87 N. Barker, J. Hadgraft, & N. Rutter, “Skin Permeability in the Newborn” (1987) 88:4 J. Invet. Dermatol. 409 at 409. 88 K.T. Hoang, Dermal Exposure Assessment: Principles and Applications (Washington, D.C.: U.S. Environmental Protection Agency, 1992) (EPA/600/8-91/011B) at 30. 89 T. Schettler, “Toxic Threats to Neurologic Development of Children” (2001) 109:6 Environ. Health Perspect. 813 at 817. 90 “Developmental Milestones” (Washington, D.C.: NICHCY), online: NICHCY <> (date accessed: 16 October 2008); “Developmental Milestones” (Ann Arbor, MI: University of Michigan Health System), online: University of Michigan <> (date accessed: 16 October 2008). 91 Cooper, supra note 5 at 46. 92 J. Schwartz, “Air Pollution and Children’s Health” (2004) 113:4 Pediatrics 1037 at 1037. 93 Landrigan 2004b, supra note 76 at 176; Schettler, supra note 89 at 816.  16 Toddler And Childhood There is a continuation of growth and maturation from toddler to that of child. As with the infant, lung capacity, neurological and immune system function, digestive faculty, and dermal protection is developing. External physical change takes place as the toddler is able to crawl and walk, and head weight and body length shift to become more proportionally similar to that of an adult.97 Many of the developmental concerns present later in infancy are also common in toddler and early childhood development. Although physiological differences play a part in exposure, behavioural differences have been found to result in greater susceptibility.98  As the infant grows, mobility, and therefore pathway exposure, increases. Hand-to- mouth behaviour, crawling, and increased touching of objects are just a few of the ways that toddlers are exposed to different contaminants than an infant is. Additionally, it is at this point in childhood that outdoor exposure may increase and the child is introduced to new indoor environments, such as in daycare and school. The US National Academy of Science, in the publication Pesticides in the Diets of Infants and Children [hereinafter NAS report], found that though children may be physically more susceptible to contaminants, it is the difference in exposure that more often leads to a greater intake of pesticides.99  The average child between the ages of one and five will take in three to four times more food per unit of body weight than an adult.100  Not only does the amount of consumption differ, but so does the diet. Children tend to eat more milk, dairy, vegetables, fruits, and soft drinks than adults.101  94 C.R. Goodlett, B.L. Marcussen, J.R. West, “A Single Day of Alcohol Exposure During the Brain Growth Spurt Induces Brain Weight Restriction and Cerebellar Paurkinje Cell Loss” (1990) 7:2 Alcohol 107 at 107. 95 J.R. DiFranza, C.A. Aligne, & M. Weitzman, “Prenatal and Postnatal Environmental Tobacco Smoke Exposure and Children’s Health” (2004) 113:4 Pediatrics 1007 at 1007. 96 P.M. Lavoie & B. Bailey, “Lead Poisoning from “Lead-Free” Paint” (2004) 170:6 Can. Med. Assoc. J. 956 at 956; D.R. Brown, “Neonatal Lead Exposure in the Rat: Decreased Learning as a Function of Age and Blood Lead Concentrations” (1975) 32:3 Toxicol. Appl. Pharmacol. 628 at 628; T.I. Lidsky & J.S. Schneider, “Lead Neurotoxicity in Children: Basic Mechanisms and Clinical Correlates” (2003) 126:1 Brain 5 at 5. 97 R. Tomanari, “Stages of Growth Child Development-Early Childhood (Birth to Eight Years), Middle Childhood (Eight to Twelve Years)” (State University), online: StateUniversity.Com <> (date accessed: 15 November 2008); U.S., Department of Education “Goals 2000:Reforming Education to Improve Student Achievement” (Washington, D.C.: Department of Education, 1998), online: US Department of Education <> (date accessed: 15 November 2008). 98 Sharpe, supra note 56 at 93. 99 National Research Council, Pesticides in the Diets of Infants and Children, (Washington, D.C.: National Academy Press, 1993) at 4. 100 Sharpe, supra note 56 at 94. 101 Children’s Environmental Health Network, A Child-Safe U.S. Chemical Policy, (Washington, D.C.: C.E.H.N., 2007), online: C.E.H.N. <>  (last updated: 10 May 2007); Wargo, supra note 26 at 6.  17  Evidence indicates that a toddler’s or young child’s exposure to some contaminants may be greater because of increased time spent on the floor or other indoor surfaces.102  An adult’s breathing space is on average four to six feet from the ground, whereas the child’s is much closer to the ground.103  Chemicals such as polyvinyl chloride (PVCs) found in vinyl flooring, insecticides used to control indoor pests, and pesticides in lawns are inhaled because of this close exposure.104  A well documented case of inhalation of mercury by a young child when exposed to interior latex paint occurred in Michigan. The four-year-old boy was diagnosed with acrodynia (which means “painful extremities”), a rare form of mercury poisoning, following the application of 17 gallons of paint that exceeded US Environmental Protection Agency’s (US EPA) standards for mercury (used as a paint preservative).  Other family members were asymptomatic. A number of factors influenced the young boy’s greater inhalation of mercury over that of other family members. As a toddler, his indoor environment was most often confined to the house. Secondly, at this age, a child is mobile and often spends a great deal of time on the ground surface where there was a larger concentration of mercury vapour because it is heavier than air.105  And lastly, the child’s intake of air per unit of body weight was greater than that an adult. Adolescence During adolescence, the body is more prepared for exposure to environmental hazards due to the increased lung function, developed dermal system, and matured neurological system. However, the body is undergoing many changes which cause it to be more susceptible to harm.  It is during this period that fertility (production of viable gametes) and a mature reproductive state through the development of secondary sex characteristics are achieved. Simultaneously, the body undergoes growth of skeleton, muscle, and viscera, and experiences changes in muscle and fat composition.106 It is during adolescence that certain effects of earlier exposure may be visible. Early onset of puberty and precocious puberty has both been linked with environmental hazards. Medical research has traditionally held that less than one percent of girls show signs of puberty (breast development or growth of pubic hair) before the age of eight years.107 Yet, recent studies have indicated that there may be a clear shift in these numbers. Herman-Giddens et al. found that  102 U.S., Environmental Protection Agency, A Decade of Children’s Environmental Health Research: Highlights from EPA’s Science to Achieve Results Program, (Washington, D.C.: U.S. Environmental Protection Agency, 2007) at 22. 103 Bearer, supra note 65 at 12. 104 Ibid; Sharpe, supra  56 at 94; Wigle, supra note 4 at 11-12. 105 P.S. Guzelian, C.J. Henry, & S.S. Olin Similarities and Differences Between Children and Adults: Implications for Risk Assessment (Washington, D.C.: ILSO Press International Life Sciences Institute, 1992). 106 S. Milligan, “Reproductive Life History” (London: King’s College London, 2003), online:  King’s College London < .pps+reproductive+life+history+powerpoint+puberty&hl=en&ct=clnk&cd=1> (date accessed: 14 November 2008); K. Parker Jones, The Beginning and End of Reproductive Life: Pubertal and Midlife Changes (Salt Lake: University of Utah College of Medicine, 1987), online: U of U College of Medicine <> (last accessed: 4 November 2008). 107 J.C. Rockett, C.D. Lynch, & G.M. Buck, “Biomarkers for Assessing Reproductive Development and Health: Park 1 – Pubertal Development” (2004) 112:1 Environ. Health Perspect. 105 at 105.  18  girls in the United States are developing pubertal characteristics as young as three-years-old (one to three percent), and 6.7 to 27.2 percent of girls are developing pubertal characteristics by age seven.108  Further research in the area has found that exposure to mycoestrogens (mycoestrogen zearalenone (ZEA)) and other estrogen disrupter pollution present in organochlorine pesticides, polychlorinated biphenyls, bisphenol-A, alkylphenolic chemicals, and some fungicides109, may produce central precocious puberty.110 Though research has begun to make progress on determining the cause-and-effect of precocious puberty, there remain a number of gaps in knowledge. One reason for this is that puberty is a multifaceted process and has a multitude of triggers.111  Furthermore, the exposures may have occurred earlier in life but take effect with the onset of puberty. Interestingly, rather than early onset of puberty, the Third National Health And Nutrition Examination Survey (NHANES III) found a link between lead levels and delayed first menstrual period and pubic hair for girls.112 Adolescence is more than the onset of puberty.  It is a time of change in behaviours, settings, and the introduction of the workplace environment. An increase in choice provides adolescents with greater exposure and accidental injury.113  This may include illegal drug and alcohol consumption, as well as increased use of prescription pharmaceuticals.114  One example of poor behavioural choices that resulted in pollutant exposure was shown when some children in Hamilton, Ontario, broke into a metal recycling plant and removed mercury and other materials from the site in September 1993.  Nearly 300 children displayed physical signs of mercury exposure.115  These changes in ingestion and inhalation may alter the affects of environmental exposures.116  This is often a time when adolescents begin to work, therefore incorporating another indoor or outdoor environment.117  Though occupational  108 M.E. Herman-Giddens et al., “Secondary Sexual Characteristics and Menses in Young Girls Seen in Office Practice: A Study from the Pediatric Research in Office Settings Network” (1997) 99:4 Pediatrics 505 at 507; Rockett, supra note 107 at 105; R.L. Rosenfield et al., “Current Age of Onset Puberty”, (2000) 106:3 Pediatrics 622 at 622; R.Y. Wang, L.L. Needham, & D.B. Barr, “Effects of Environmental Agents on the Attainment of Puberty: Considerations When Assessing Exposure to Environmental Chemicals in the National Children’s Study” (2005) 113:8 Environ. Health Perspect. 1100 at 1100. 109 C.R. Tyler, S. Jobling, & J.P Simpter, “Endocrine Disruption in Wildlife: A Critical Review of the Evidence” (1998) 28:4 Crit. Rev. Toxicol. 319 at 320. 110 F. Massart et al., “High Growth Rate of Girls with Precocious Puberty Exposed to Extrogenic Mycotoxins” (2008) 152:5 J. Pediatr. 690 at 690. 111 Rockett, supra note 107 at 105. 112 National Center for Health Statistics, Third National Health and Nutrition Examination Survey (NHANES III) Public-Use Data Files (Washington, D.C.: Center for Disease Control, 2008), online: CDC <> (last modified: 2 November 2008); Rockett, supra note 107 at 105; T. Wu, G.M. Buck, & P. Mendola, “Blood Lead Levels and Sexual Maturation in US Girls: The Third National   Health and Nutrition Examination Survey, 1988-1994” (2003) 111:5 Environ. Health Perspect. 737 at 739. 113 M.S. Golub, “Adolescent Health and the Environment” (2000) 108:4 Environ. Health Perspect. 355 at 356. 114 Cooper, supra note 5 at 47; S.G. Millstein et al., “Health-risk Behaviors and Health Concerns Among Young Adolescents” (1992) 89:3 Am. Acad. Pediatrics 422 at 422. 115 L. George et al., “The Mercury Emergency in Hamilton School Children: A Follow-Up Analysis” (1996) 87:4 Can. J. Public Health 224 at 224. 116 Golub, supra note 113 at 356. 117 Canadian Partnership, supra note 63.  19  environmental health is often addressed by governments, the thresholds for standards are set for adults, not developing children. 2.2.2 Exposure Pathways The prior section highlighted that exposure to contaminants at different developmental stages may affect the health outcomes from that exposure. As the child matures the body gains capacity to defend itself against pollutants. Nevertheless, the exposure pathways influence health outcomes even into adulthood. This section provides a general outline of how infants, children, and adults come into contact with environmental contaminants. The World Health Organization has stressed that environmental contaminants are only one factor affecting health outcomes.  Social, cultural, educational, and occupational settings play important roles. Some examples include: - Pesticide exposure has been found to be higher for those who live in rural areas.118 - Exposures to chemical by-products are greater for adults who have industrial occupations.119 - Where schools are located plays an essential role in how much pollution exposure a child has. Unfortunately, schools are often built on land sites which were considered unattractive for living or office space.120 - Economic status, and the often closely related topic of access to health services, commonly affects health outcomes. Low-income housing developments are often crowded and may be infested with pests. Use of pesticides and insecticides are often the first line of defense by landlords in these circumstances.121 - First signs of disease may be neglected due to healthcare costs, particularly where a government supported health care system is not in place. - Health outcomes are also affected by gender, biology, and genetics. Primary mediums of exposure identified by the US  EPA are outdoor air, indoor air, food, drinking water and soil.122 These exposure pathways are based on ingestion, inhalation, and dermal exposure.  Relevant examples of such will  118 T.E. Arbuckle, Z. Lin, & L.S. Mery, “An Exploratory Analysis of the Effect of Pesticide Exposure on the Risk of Spontaneous Abortion in an Ontario Farm Population” (2001) 109:8 Environ. Health Perspect. 851 at 851; L.S. Azaroff, “Biomarkers of Exposure to Organophosphorous Insecticides Among Farmers’ Families in Rural El Salvador: Factors Associated with Exposure” (1999) 80:2 Environ. Res. 138 at 138; J.S. LaKind et al., “Methodology for Characterizing Distributions of Incremental Body Burdens of 2,3,7,8-TCDD and DDE from Breast Milk in North American Nursing Infants” (2000) 59:8 J. Toxiocol. Env. Health Part A 605 at 605; Wigle, supra note 4 at 171. 119 Arbuckle, supra note 118 at 851; Wigle, supra note 4 at 304-306; T.E. Arbuckle & L.E. Sever, “Pesticide Exposures and Fetal Death: A Review of the Epidemiologic Literature” (1998) 28:3 Crit. Rev. Toxicol. 229 at 262. 120 S.K. Cummins & R.J. Jackson, “The Built Environment and Children’s Health” (2001) 48:5 Pediatr. Clin. N. Am., online: Pediatr. Clin. N. Am. <> (date accessed: 10 October 2008). 121 V.A. Rauh, G.L. Chew, & R.S. Garfinkel, “Deteriorated Housing Contributes to High Cockroach Allergen Levels in Inner-City Households” (2002) 110:2 Environ. Health Perspect. Supps. 323 at 327; S. Srinivasan, L.R. O’Fallon, & A. Dearry, “Creating Healthy Communities, Healthy Homes, Healthy People: Initiating a Research Agenda on the Built Environment and Public Health” (2003) 93:9 Am. J. Public Health 1446 at 1447. 122 E. Flynn et al., Indoor Air Pollutants Affecting Child Health, (Washington, D.C.: U.S. Agency for Toxic Substances and Disease Registry, 2000) at 11; Cooper, supra note 5.  20  be outlined below. However, it is important to note, as mentioned before, that during the stages of preconception and fetal development, exposure may take place through the ingestion, inhalation, or dermal exposure of the mother or father.  The mothers’ exposure through ingestion, inhalation, or absorption to pollutants may cross into the placenta and expose the fetus. Additionally, exposures to toxins prior to pregnancy that may be retained in fatty tissue may be released during pregnancy as the woman’s body uses up this tissue for nourishment. For instance, lead, retained in bone marrow, may be released during the third trimester of pregnancy when bone turnover increases.123 Health Canada has outlined specific exposure pathways for each medium of exposure. This includes inhalation, skin contact, and ingestion. Inhalation is defined by Health Canada as breathing in a substance such as gas, vapour, or airborne particles. Skin contact is considered as a pathway since water, soil, and air can be absorbed through the dermal layer. Ingestion is the swallowing of something containing a contaminant, during which the mouth, throat, stomach, and/or intestines can absorb the toxins.124 Outdoor Air Outdoor air pollution is taken into the body in two ways– inhalation and absorption. Exposure to air pollutants occurs during the fetal stage as well as from infancy through adulthood. Studies indicate that outdoor air pollution is positively associated with morbidity and mortality rates in both adults and children. Historical case studies have illustrated the harmful effects that may result from prolonged exposure. In Meuse Valley, Belgium (1930), Donora, Pennsylvania (1948), and London, United Kingdom (1952), change in weather pattern resulted in high levels of particulate matter trapped in one area.125  In each of these cases, deaths for the total population from respiratory conditions increased as did deaths from other causes with respiratory complications.126 Specific air pollutants of concern include ozone, carbon monoxide, nitrogen oxide, sulphur dioxide, total suspended particulate127, and particulate matter (PM). Toxic metals, such as lead, cadmium, and copper, are also often measureable in air. Inhalation of pesticides and chemicals may also occur. Major sources of air emissions are automobiles, industry, burning of coal and oil, combustion, and solvents.  123 Commission for Environmental Cooperation, Children’s Health and the Environment in North America; A First Report on Available Indicators and Measures, (Quebec: Secretariat – Commission for Environmental Cooperation, 2006), online: C.E.C. < > (last modified: 10 February 2008); E.K. Silbergeld, “Lead in Bone: Implications for Toxicology During Pregnancy and Lactation” (1991) 91 Environ. Health Perspect. 63 at 66. 124 Canada, Investigating Human Exposure to Contaminants in the Environment: A Handbook for Exposure Calculations (Ottawa: Minister of National Health and Welfare, Minister of Supply and Services Canada, 1995), online: Health Canada <> (date accessed: 12 November 2008). 125 J. Schwartz, “What Are People Dying of on High Air Pollution Days?” (1994) 64:1 Environ. Res. 26 at 26. 126 Schwartz, supra note 92 at 26-27. 127 Total suspended particulate (tsp) was replaced in 1987 by the US EPA with particulate matter (PM-10) which is a measurement of smaller particles.  Particulate matter is a measurement of molecules of solid or gas pollution.; U.S., Environmental Protection Agency, “Particulate Matter (PM-10)” (Washington, D.C.: Environmental Protection Agency, 2009), online: Environmental Protection Agency <> (lasted modified: 21 May 2009).  21  Literature on health conditions due to air pollution hold that exposure may increase infant mortality and incidence of upper and lower respiratory infections in children.128  Infant health, such as birth weight, appears to be associated with air pollutants, particularly exposure during prenatal or neonatal development to carbon monoxide.129  There is some indication that concentrations of elevated particulate matter PM-10130, though not PM-2.5, may be related to sudden infant death syndrome (SIDS).131  Observed ill-health effects in children have been linked to increased levels of PM-2.5, PM-10, nitrogen oxide, and sulphur dioxide.  Respiratory diseases often associated with air pollution are pneumonia, acute bronchitis, and asthma.132  There is an indication of increased asthma in Canada, where twelve percent of children, approximately one million, have been diagnosed. This is four times more children than were diagnosed with asthma in Canada twenty years ago.133  Research suggests that childhood asthma has increased due to air pollution, specifically exposure to PM, nitrogen oxide, and sulphur dioxide.134  Even neglect diagnosis twenty- five years ago would not explain this disparity. While infants have a more limited exposure to outdoor air, there is a diversification of inhalation areas for toddlers, children, and adolescents, as mobility and transportation increases with daycare, school, and work. Studies indicate that there is an association between traffic-related air pollution and coughing, though this appears to decrease with age.135  Traffic density, air composition, and the percentage of time downwind influence the components of air pollution that affect children during transport to school.136  Health complications of traffic related exposure include  128 J. Currie & M. Neidell, “Air Pollution and Infant Health: What Can We Learn from California’s Recent Experience?” (2005) 120:3 Q. J. Econ. 1003 at 1011; K.R. Smith et al., “Indoor Air Pollution in Developing Countries and Acute Lower Respiratory Infections in Children” 2000 55:6 Thorax 518 at 520; Schwartz, supra note 92 at 5; T.J. Woodruff, J.D. Parker, & K.C. Schoendorf, “Fine Particulate Matter (PM2.5) Air Pollution and Selected Causes of Postneonatal Infant Mortality in California” (2006) 114:5 Environ. Health Perspect. 786 at 788; T.J. Woodruff, J. Grillo, & K.C. Schoendorf, “The Relationship Between Selected Causes of Postneonatal Infant Mortality and Particulate Air Pollution in the United States” (1997) 105:6 Environ. Health Perspect. 608 at  608. 129 Woodruff 1997, supra note 128 at 608; B. Ritz & F. Yu, “The Effect of Ambient Carbon Monoxide on Low Birth Weight Among Children Born in Southern California Between 1989 and 1993” (1999) 107:17 Environ. Health Perspect. 17 at 22. 130 Particulate matter is defined as PM-10 or PM-2.5 determined by an aerodynamic diameter of 10 micrometers (PM-10) or a particle less than 2.5 micrometers (PM-2.5); U.S., Environmental Protection Agency, “Particulate Matter” (Washington, D.C.: Environmental Protection Agency, 2009), online: Environmental Protection Agency <> (last modified: 6 October 2009). 131 Woodruff 1997, supra note 128 at 610-611; Woodruff 2006, supra note at 786. 132 D.V. Bates, “The Effects of Air Pollution on Children” (1995) 103:S6 Environ. Health Perspect. Supps. 49 at 49; C. Braun-Fahrlander et al., “Air Pollution and Respiratory Symptoms in Pre-School Children” (1990) 45:5 Arch. Environ. Health; C.A. Pope, III, “Respiratory Hospital Admissions Associated with PM10 Pollution in Utah, Salt Lake, and Cache Valleys” (1991) 46:2 Arch. Environ. Health 90 at 90. 133 Canadian Partnership, supra note 63. 134A.G. Barnett et al., “Air Pollution and Child Respiratory Health: A Case-Crossover Study in Australia and New Zealand” (2005) 171:11 Am. J. Resp. Crit. Care 1271 at  1274; Pope 1991, supra note 132 at 90; Schwartz, supra note 92 at 6. 135 U. Gehring et al., “Traffic-Related Air Pollution and Respiratory Health During the First 2 Yrs of Life” (2002) 19:4 Eur. Respir. J. 690 at 690, 695-6. 136 Schwartz, supra note 92 at 1039.  22  allergic rhinitis, wheezing, and allergic reactions (to pollen, house dust mites, milk, and/or eggs).137  The method of transportation, i.e. automobile or bus, appears to influence ill-health effects. The University of California, Los Angeles (UCLA) Children’s School Bus Exposure Study found that diesel related pollutant (DRP) concentrations from self pollution were in fact higher when bus windows were closed or children were in older buses.138 Inhalation of hard metals, pesticides, and chemicals in outdoor air are also a concern. Children at play are often exposed to chemicals used to treat wood playground equipment139 or insecticides that have been used at school to prevent rodent infestation140.  Children tend to play outside in the afternoon which is the time that ozone levels are the highest.141  Although there has been a decrease in the number of American children living in locations where one or more measured air pollutants exceeded national air quality (down from 28 to 24 percent from 1990 to 1998)142, the increase in asthma rates indicates that the problem is far from solved.  137 U. Krämer et al., “Traffic-Related Air Pollution is Associated with Atopy in Children Living in Urban Areas” (2000) 11:1 Epidemiology 64 at 64. 138 L.D. Sabin, “Characterizing the Range of Children’s Air Pollutant Exposure During School Bus Commutes” (2005) 15 J. Expo. Anal. Environ. Epidemiol. 377 at 377 & 378; “Children’s Exposures Due to School Bus Commutes: Results from the Recent ARB-Sponsored Study” (Air Resources Board, California Environmental Protection Agency, 20 November 2003), online: CA Environmental Protection Agency <> (last modified: 20 November 2003). 139 Goldman, supra note 6 at 443; H.F. Hemond & H.M. Solo-Gabriele, “Children’s Exposure to Arsenic from CCA- Treated Wooden Decks and Playgrounds Structures” (2004) 24:1 Int. J. 51 at 51; R. Jagels, “Health Hazards of Natural and Introduced Chemical Components of Boatbuilding Woods” (1985) 8:3 Am. J. Ind. Med. 241 at 242. 140 Cooper, supra note 5 at 303-304. 141 Ibid. at 305. 142Sharpe, supra note 56 at 95.  23 Indoor Air Indoor air makes up a large part of our built environment. With people spending over ninety percent of their time indoors143, it is a necessary component of consideration when analyzing children’s environmental health. While both adults and children spend a great deal of time indoors, their exposure differs in many ways. As mentioned before, children have a lower inhalation space, therefore breathing in toxins from at ground level at a higher rate than adults.144  Infants and toddlers are often placed on the floor and ingest, inhale, and absorb chemicals associated with vinyl flooring and carpeting, such as volatile organic chemicals and formaldehyde. Pesticides used on indoor perimeter areas, such as flea bombs, emit chemicals inhaled by infants and small children at play on the ground.145 Furthermore, while adults tend to work in office space or manufacturing areas governed by occupational policy, children are often educated in school buildings that lack appropriate ventilation systems146, are built near landfills147, or are substandard structures.148  Whereas ventilation regulations pertaining to industrial buildings are under federal mandate, state and local building codes govern over school systems. Often responsibility for implication of building codes lies with local school boards and is poorly regulated. In 1999, a sample survey in New York City found that many public schools exposed children to a number of hazards, including lead.149  Similarly, a 1998 survey conducted by California Department of Health Services found seventy-eight percent of public schools contained lead paint, thirty-eight percent of the public schools had flaking or peeling lead paint, and eighteen percent had water-lead levels that exceeded US EPA drinking water standards.150  Poor air quality has been a result of prior recommendations by the American Society of Heating, Refrigerating, and Air-Conditioning Engineers (ASHRAE) that reduced classroom size during the 1930s and again in 1973 due to high heating costs. Revision of this recommendation to increase classroom size to a minimum of 15 cubic foot per minute per person (cfm/person) was made in direct response to poor indoor air quality. However, many schools remain at ventilation rates of 5 cfm/person or less.151 Lead is only one of the indoor pollutants to which infants and children may be exposed. Other contaminants include molds, carbon monoxide, pesticides, home products (shampoo, cosmetics, etc.), and chemical household cleaners.  143 P. Beamer, A. Castano, & J.O. Leckie, “Vertical Profile Particulate Matter Measurements in a California Daycare” (2002) Proceedings: Indoor Air 103 at 103. 144 Wigle, supra note 4 at 11-12. 145 Bearer, supra note 15 at 15. 146 G. Smedje, D. Norback, & C. Edling, “Asthma Among Secondary Schoolchildren in Relation to the School Environment” (1997) 27:11 Clin. Exp. Allergy 1270 at 1271. 147 M. Pastor, Jr., J.L. Sadd, & R. Morello-Frosch, “Who’s Minding the Kids? Pollution, Public Schools, and Environmental Justice in Los Angeles” (2002) 83:1 Soc. Sci. Quarterly 263 at 263-264. 148 Cummins¸ supra note 120. 149 Ibid. 150 Ibid; California Department of Health Services, “Lead Hazards in California’s Public Elementary Schools and Child Care Facilities: Report to the California State Legislature”, online: CA DHS <>  (date accessed: 20 November 2008). 151 U.S. Environmental Protection Agency, “IAQ Reference Guide Appendix C – Codes and Regulations”, online: US EPA <> (last modified: 23 December 2007).  24  Building materials, such as asbestos and formaldehyde, may be inhaled or absorbed by children. Dust mites, pet dander, and tobacco smoke may be part of the indoor air; but these aspects are typically outside the control of legislation and are within the realm of individual choice, and cannot be discussed within the context of this thesis.152 Literature indicates that lead exposure is still a concern for children’s health. Though lead content in gasoline and paint has been prohibited in many nations, inhalation, absorption, and ingestion of lead still occurs. Often this is a result of lead paint used in older homes in disrepair.153  It is one of the earliest contaminants recognized as harmful to children.  Exposure to lead as an infant or child has been shown to negatively affect behaviour and intelligence and cause learning disabilities, microcytic anemia, and reduced growth.154  Different families restoring pre-1930s homes are at risk. While the air pollutant carbon monoxide is often associated with outdoor air pollution, it is also a negative component of indoor air quality. Unlike ozone, which has a half-life and high reactivity and dissipates in seven to ten minutes155, PM, carbon monoxide, and nitrogen oxide are present indoors. Carbon monoxide tends to be one of the more concerning gases indoors due to the use of biomass fuels to heat and cook in many nations. While the jurisdictions considered in this thesis do not typically utilize biomass fuels, wood stoves are still a large component of heating within some of these locales.156  Carbon monoxide has long been associated with mortality, due to its interference with oxygen transport to the tissues.157  More recent studies have indicated that carbon monoxide is associated with infant mortality158, low birth weight159, and intrauterine growth retardation in rats160.  Housing developments located near heavy traffic areas are often are exposed to carbon monoxide. This is commonly affiliated with low-income housing since these developments are frequently constructed in areas near traffic – areas that are  152 With regards to environmental tobacco smoke, England has taken action to prevent foster children from exposure by prohibiting any new placements with carers who smoke. M. Horne, “Smoking Foster Carers to Lose Kids” The Sunday Times (9 April 2006), online: Sunday Times <> (last modified: 9 April 2006). 153 Srinivasan, supra  note 121 at 153. 154 J.M. Burns et al., “Lifetime Low-Level Exposure to Environmental Lead and Children’s Emotional and Behavioral Development at Ages 11-13 Years: The Port Pirie Cohort Study” (1999) 149:8 Am. J. Epidemiol. 740 at 747; Cummins, supra note 120; M. Smith et al., “The Effects of Lead Exposure on Urban Children: The Institute of Child Health/Southhampton Study” (1983) 47:1 Dev. Med. Child Neurol. Suppl. 1 at 1. 155 Schwartz, supra note 92 at 1038; C.J. Weschler, “Ozone in Indoor Environments: Concentration and Chemistry” (2000) 10:4 Indoor Air 269 at 271. 156 W.C. Maier et al., “Indoor Risk Factors for Asthma and Wheezing Among Seattle School Children” (1997) 105:2 Environ. Health Perspect. 208 at 211. 157 L.J. Folinsbee, “Human Health Effects of Air Pollution” (1993) 100:45 Environ. Health Perspect. 45 at 48. 158 Currie, supra note 128 at 1008. 159 Ritz, supra note 129 at 22. 160 D.J. Garvey & L.D. Longo, “Chronic Low Level Maternal Carbon Monoxide Exposure and Fetal Growth and Development” (1978) 19:1 Biol. Reprod. 8 at 12.  25  considered less than attractive to those with the economic capacity to be selective.161  Differentiation between indoor and outdoor exposure of carbon monoxide is difficult for studies and results in knowledge gaps. Indoor pesticide and chemical exposure has been linked with fetal deaths162, birth defects163, limb anomalies164, orofacial clefts165, cancers166, immunological disorders167, reproductive anomalies168, neurological disorders169, and behavioural disorders170. Within the United States, pesticides are used in over ninety percent of homes.171  If not applied in accordance with instructions, pesticides can remain in the indoor environment for weeks, months, or years.172  Due to the runoff of pesticides and insecticides on nearby farms, contaminated soil is brought indoors through footwear and clothing. Additionally, these pollutants are absorbed by soil and transported into the water system.173  Evidence indicates that those children who reside near agricultural areas have greater exposure than those in urban settings.174  Although increased exposure for children near agricultural areas occurs outdoors, it is also elevated indoors when one or more of the parents are employed in agriculture. Household dust and soil samples taken from families employed in farm work in Washington State tested for organophosphorous (OP) insecticides contained higher levels of toxins than comparative households nearby.175  This indoor contamination occurs through transport of outdoor soil to indoor floors and work clothes brought indoors.176  Although exposure is unavoidable in  161 S.A. Bashir, “Home Is Where the Harm Is: Inadequate Housing as a Public Health Crisis” (2002) 92:5 Am. J. Public Health 733 at  733. 162 T.E. Arbuckle et al., “Exposure to Phenoxy Herbicides and the Risk of Spontaneous Abortion” (1999) 10:6 Epidemiology 752 at 752. 163 Arbuckle 1998, supra note 119 at 230. 164Ibid. 165 Ibid. 166 Wigle, supra note 4 at 169-170. 167Flynn, supra   note 122 at 6 and 116. 168 Wigle, supra  note 13 at 168-169. 169 R.A. Fenske et al., “Lessons Learned for the Assessment of Children’s Pesticide Exposure: Critical Sampling and Analytical Issues for Future Studies” (2005) 113:10 Environ. Health Perspect. 1455 at  1456; Schettler, supra note 89 at 815. 170 Wigle, supra note 4 at 5. 171 B. Eskenazi et al., “Methodologic and Logistic Issues in Conducting Longitudinal Birth Cohort Studies: Lessons Learned from the Centers for Children’s Environmental Health and Disease Prevention Research” (2005) 113:10 Environ. Health Perspect. 1419 at 1423; P.J. Landrigan, “Risk Assessment for Children and Other Sensitive Populations” (1999) 895:1 Ann. N.Y. Acad. Sci. 1 at 3. 172 C. Baum & M. Shannon, “Environmental Toxins: Cutting the Risks” (1995) 12:7 Contemp. Pediatr. 20 at 20; Flynn, supra note 122 at 131. 173 In many jurisdictions, drinking water warnings are broadcast due to agricultural runoff.  R. Kellogg et al., “Environmental Indicators of Pesticide Leaching and Runoff from Farm Fields” (Agricultural Productivity: Data, Methods, and Measures, Washington, D.C., 9-10 March 2000), online: U.S. Department of Agriculture <> (last modified: March 2000). 174 N.J. Simcox et al., “Pesticides in Household Dust and Soil: Exposure Pathways for Children of Agricultural Families” (1995) 103:12 Environ. Health Perspect. 1126 at 1126. 175 Ibid. at 1133. 176 Ibid. at 1126.  26  agricultural regions, evidence indicates that it is unjustifiably high in some regions where farmers apply more than the recommended quantity.177  A study conducted in the United Kingdom (UK) found that only thirty-eight percent of produce manufacturers read the complete instructions before using a pesticide for the first time178, demonstrating how excessive use may occur. Other indoor exposure to pesticides occurs in a number of ways, including insect repellent, weed killer, rat poison, and some dog flea shampoos.179  The US EPA has found that levels of pesticides to be as high as 100 ug/g in carpet samples.180  Research indicates that pesticide use or storage indoors is immense, with one study determining ninety- seven percent of Minnesota homes store pesticide inside and eighty-eight percent using pesticides within the last year,181 and another study concluding that pesticides are used in ninety percent of all US households.182  Children who are of age to attend school often are exposed to additional pesticides used indoors to combat insect infestations and parameter sprays for pest prevention.183 Chemical exposure is of particular concern for those residing in sub-standard low-income housing. With over six million United States urban children living below the poverty level, the exposure rates are high and worth noting.184 One study conducted in Seattle, Washington, found concentrations of polycyclic aromatic hydrocarbon (PAHs) ranging from three to 290 micrograms/g, lead from 250 to 2250 micrograms/g, and PCBs from 210 to 1900 ng/g.185 Authors Roberts and Dickey concluded that with a reduction in exposure to these indoor pollutants, Seattle would be able to reduce immediate health costs and long-term health risks.186 Chemicals can be found throughout the home and school atmospheres. While the impact of both pesticides and chemicals will be expanded upon throughout this paper, it is noteworthy to explain their correlation with indoor air environments. Chemicals are present in clothing, food, packaging, toys, shampoos, computers, hospitals, and  177 M. Pollan, The Omnivore’s Dilemma: A Natural History of Four Meals, (New York: Penguin Group USA, 2006). 178 G. Avory & D. Coggon, “Determinants of Safe Behaviour in Farmers when Working with Pesticides” (1994) 44:5 Occup. Med. 236 at 237. 179 W. Baue, “Pesticides in Your Home” (2008), online: Healthy Child Healthy World <>  (last modified: 16 December 2008). 180 R.G. Lewis, R.C. Fortmann, & D.E. Camann, “Evaluation of Methods for Monitoring the Potential Exposure of Small Children to Pesticides in the Residential Environment” (1994) 26:1 Arch. Environ. Contam. Toxicol. 37 at 37. 181 J.L. Adgate et al., “Pesticide Storage and Use Patterns in Minnesota Households with Children” (2000) 10:2 J. Expo. Anal. Environ. Epidemiol. 159 at 159; G.S. Berkowitz et al., “Exposure to Indoor Pesticides during Pregnancy in a Multiethnic, Urban Cohort” (2003) 111:1 Environ. Health Perspect. 79 at 79. 182 Lewis, supra note 180 at 37; E.P. Savage et al., “Household Pesticide Usage in the United States” (1981) 36:6 Arch. Environ. Health 304 at 304. 183 T. Godish, “Indoor Environment Notebook: Everything You Wanted to Know about Indoor Air Pollution and More” (2008), online: Bell State University <>  (last modified: 01 September 2008). 184 Wigle, supra note 4 at 177. 185 J.W. Roberts & P. Dickey, “Exposure of Children to Pollutants in House Dust and Indoor Air” (1995) 143 Rev. Environ. Contam. Toxicol. 143 at 143. 186 Ibid. at 143.  27  workplaces along with other items and environments. While some are necessary for good health (hospital disinfectants, water chlorification, etc.) others have known negative effects (chlorinated pesticides, N,N-Diethyl- Meta_toluamide (DEET), persistent organic pollutants (POPs), etc.).187  Ingestion and inhalation of phthalates (diisononyl phthalate (DINP) and di(2-ethylhexyl) phthalate (DEHP)) in polyvinyl chloride (PVCs) found in some toys and plastic products have been associated with asthma188, birth defects and early onset of puberty189.  These chemicals have been identified as a human carcinogen.190 Indoor formaldehyde exposure, through inhalation, ingestion, and absorption, has been linked to increased allergic sensitization to common aeroallergens191 and airway irritation.192  Formaldehyde has been found in wood products, pressed wood furniture, environmental tobacco smoke, some drapes, and some glues.193 Evidence of high levels of exposure was found in house trailers provided by the Federal Emergency Management Agency (FEMA) for displaced Katrina and Rita hurricane and Iowa flood (2008) survivors.194 While some building substances, such as asbestos, have declined in use, a child’s exposure is still possible. Originally used for fireproofing and insulation between the 1940s and the 1970s195, inhalation of asbestos has been found to cause lung disease (asbestosis) and mesothelioma.196  Historically, much of a child’s exposure to asbestos was via a parent. If a parent worked in industrial areas where asbestos materials were common, work clothing brought home  187 Canadian Partnership, supra note 63. 188 K.M. Shea, “Pediatric Exposure and Potential Toxicity of Phthalate Plasticizers” (2003) 111:6 Am. Acad. Pediatrics 1467 at 1468; M.H. Garrett et al., “Indoor Airborne Fungal Spores, House Dampness and Associations with Environmental Factors and Respiratory Health in Children” (1998) 28:4 Clin. Exp. Allergy 459 at 461-462. 189 Wang, supra note 108 at 1100. 190 U.S. Department of Health and Human Services, National Toxicology Program, 11th Report on Carcinogens, (Washington, D.C.: NIH, 2008), online: NIH < FA60E922B18C2540>  (date accessed: 1 November 2008). 191 J.J. Quackenboss et al., “Formaldehyde Exposure and Acute Health Effects Study” (1989) 15 Environ. Int. 169 at 169. 192 Ibid; K.B. Rumchev et al., “Domestic Exposure to Formaldehyde Significantly Increases the Risk of Asthma in Young Children” (2002) 20:2 Eur. Respir. J. 403 at 403. 193 U.S., Environmental Protection Agency, An Introduction to Indoor Air Quality (Washington, D.C.: US Environmental Protection Agency, 2009), online: US EPA <> (last modified:27 October 2009). 194 C.Y. Rao et al., “Characterization of Airborne Molds, Endotoxins, and Glucans in Homes in New Orleans after Hurricanes Katrina and Rita” (2007) 73:5 Appl. Environ. Microbiol. 1630 at 1630. 195 American Academy of Pediatrics, How Can I Protect My Child from Environmental Hazards in Our Home?, (Illinois: Am. Acad. Pediatrics, 2005), online: AAP <>  (last modified: 5 March 2005). 196 CDC, Agency for Toxic Substances & Disease Registry, Toxicological Profile for Asbestos, (Washington, D.C.: CDC, 2008), online: CDC <> (last modified: September 2001).  28  provided another exposure route.197  Cases of women inhaling asbestos and then exposing her infant via breast milk have been documented.198 Food The consumption of food products are a source of exposure for infants, children, and adolescents. While regulatory agencies monitor what is sold, literature on children’s environmental health debates whether current food standards (permissible pesticides, chemicals, and metals) take into consideration the behaviour and lifestyle of a child.199 Exposure to pesticides, metals, and toxins via breast milk, infant formula, fruit, vegetable, and animal consumption may result in negative health impacts for the developing child. As mentioned earlier, a child’s behavioural and physiological differences greatly diverge from that of an adult. For the infant, breast milk tends to be the only source of nutrients. Use of infant formula and baby food may be introduced as the child gets older. Young children tend to consume larger quantities per body weight of fruit and vegetables.200  These various aspects of consumption lead to unique exposure pathways for infants and children. The consumption of breast milk during the first months of life is beneficial to growth and development. A number of international organizations, such as the World Health Organization (WHO) and the United Nations Children’s Fund (UNICEF), have recommended breastfeeding until two years of age or longer.201  National medical associations and government entities have stressed that “breast is best”.202  Breast milk provides the first defense from disease for the newborn. Antibodies (IgG, IgA, IgM, IgD, and IgE) are present in breast milk203, providing a barrier to pathogens introduced to a child. Evidence indicates that children are not capable of producing these antibodies on their own until six months of age, which is often an issue for infants who are only formula fed.204  For many decades the medical community has been aware that bottle-fed infants are more prone to neonatal infections.205  While there is little doubt that breast milk is the best option, exposure to environmental toxins may still take place.  Chemicals such  197 D. Ozonoff, Failed Warnings: Asbestos-Related Disease and Industrial Medicine (New York: Oxford University Press) 139 at 139. 198 J.J. Chisolm, “Fouling One’s Own Nest” (1978) 62:4 Pediatrics 614 at 615. 199 Children’s Environmental Health Network, Pesticides, (Washington, D.C.: C.E.H.N., 2007), online: C.E.H.N. <> (last updated: 13 October 2004); E. Groth et al. Do You Know what You’re Eating? An Analysis of US Government Data on Pesticide Residues in Foods (Washington, D.C.: Consumers Union of United States, 1999). 200 Cooper, supra note 5 at 41-42. 201 UNICEF, Division of Human Resources, Breastfeeding Guidelines, (New York: UN, 2000), online: UNICEF <> (last accessed: 12 November 2008). 202 UNICEF, Breast is Best. How UNICEF’s Baby Friendly Initiative is Supporting Breastfeeding in the UK, (London: UNICEF, 2008), online: UNICEF <> (last accessed: 21 November 2008). 203J. Newman, “How Breast Milk Protects Newborns” (1995) 273 Sci. Am. 58 at 58. 204 Ibid; L.K. Pickering, “Modulation of the Immune System by Human Milk and Infant Formula Containing Nucleotides” (1998) 110:2 Am. Acad. Pediatrics 242 at 242. 205 L.A. Hanson & J. Winberg, “Breast Milk and Defence Against Infection in the Newborn” (1972) 47:256 Arch. Dis. Child. 845 at 845-846.  29  as PCBs, dichloro-diphenyl-trichloroethane (DDT) , and polybrominated diphenyl ethers (PBDEs) present in a mother’s body may be transferred to the newborn via breast milk.206  These forms of POPs tend to bioaccumulate in fatty tissue and are transferable through breast milk. Furthermore, because they bioaccumulate in mammals, they tend to be transferred and biomagnify up the food chain.207  POPs tend to have a half-life of two to ten years, are persistent, fat-seeking (lipophilic), and are endocrine disruptors. The harmful effects of some POPs were identified as early as the 1970s.208  Responsible governments have restricted the use of DDT and PCBs, resulting in a reduction in exposure via breast milk.209  Within Canada, the US, and Europe, PCB levels in breast milk have decreased.210 211 Longitudinal monitoring of breast milk in Sweden212 demonstrated that PBDE levels in breast milk were increasing greatly, and therefore infant consumption was also on the rise. As a result, the government took regulatory action to phase out exposure. However, increased rates of PBDEs are still evident in North America where regulation on the chemical has not been passed.213 Even with government intervention, because of POPs’ long-term capacity to survive in the environment and animal life, exposure in future generations continues.  Subpopulations are often more susceptible to higher exposure levels due to their unique diets. Inuit women in Canada have been found to have ten times the PCB levels than that of women in southern Canada.214  Other arctic populations have shown similar increased levels of POPs, which  206 A. Larson, “Environmental Health: Chemicals in Breast Milk” (2008) SSRN, online: SSRN <> (last modified: 21 October 2008). 207 K. Hooper & T.A. McDonald, “The PBDEs: An Emerging Environmental Challenge and Another Reason for Breast-Milk Monitoring Programs” (2000) 108:5 Environ. Health Perspect. 387 at 387. 208 R.D. Kimbrough, “Toxicological Implication of Human Milk Residues as Indicated by Toxicological and Epidemiological Studies” Chemical Contaminants in Human Milk, (Boca Raton: CRC Press, 1991); D. McKeown, Environmental Threats to Children: Understanding the Risks, Enabling Prevention (Toronto: Toronto Public Health, 2005), online: Toronto Public Health <> (last modified: September 2005). 209 McKeown, ibid. 210 A.G. Crann & D.A. Haines, “Twenty-Five Years of Surveillance for Contaminants in Human Breast Milk” (1998) 35:4 Arch. Environ. Contam. Toxicol. 702 at 707-708. 211 The Stockholm Convention signed in 1995 calls for a global reduction of use of POPs; UN EP, Stockholm Convention on Persistent Organic Pollutants, UNEP/POPS/POPRC.4/INF/9 (2008), online: UNEP <> (last modified: 22 May 2001). 212 Sweden is one of the few countries that has established a government program that monitors breast milk for pollutants. The program began in 1967. G.M. Solomon & P.M. Weiss, “Chemical Contaminants in Breast Milk: Time Trends and Regional Variability” (2002) 110:6 Environ. Health Perspect. 339 at 339; The Collaborative on Health and the Environment, Breastmilk Biomonitoring (Bolinas, CA: Collaborative on Health and the Environment, 2003), online: CEH <>  (last modified: 20 March 2003). 213 Canada, Health Canada, PBDE Flame Retardants and Human Health (Ottawa: Minister of Health, 2006), online: Health Canada <> (last modified: August 2009). 214 Wigle, supra note 4 at 150; E. Dewailly et al., “Inuit Exposure to Organochlorines through the Aquatic Food Chain in Arctic Quebec” (1993) 101:7 Environ. Health Perspect. 618 at 618-619.  30  demonstrates the chemicals’ capability of travel and its longevity.215  Populations with high dietary intakes of aquatic wildlife, such as seals, whales, and sharks, tend to have elevated levels of POPs because of the chemicals’ ability to magnify (up to thousands of times greater than originating levels) in fatty tissues of these animals.216  Another source of contamination through ingestion by infants is baby formula. The water, the bottle, and the formula used influence the exposure levels.  Commercial infant formula has been approved by both medical communities and regulating government agencies as a safe and effective substitute to breast milk. Infant formula tends to fit into one of three categories: cow’s milk, soy-based, or protein hydrolysate (for those with milk allergies).217  Additionally, these types of infant formula come in either powdered, concentrated liquid, or ready-to-use form.218  While government entities, such as the US Food and Drug Administration (US FDA), approve infant formula prior to public sale, there are still uncertainties as to the effects of consumption of formula on infant health. Recent concern over detected trace amounts of industrial chemical melamine in the US has led consumer groups and the Illinois attorney general to pressure the EPA for a recall.219  The negative effects of melamine exposure include kidney and bladder stones, kidney failure, and death.220  In nations where manufacturing oversight is less stringent, infant formula has been found to contain diethylene glycol (thickening agent found in antifreeze)221 as well as purposefully including of melamine to raise protein levels.222 Even without the concerns pertaining to toxicity of infant formula, there are issues about the safety of the ingredients themselves.  Epidemiological studies and data on soy infant formula are lacking, though the product is being used by twenty-five percent of all US formula consumers.223  Similar to some of the recent studies on soy products and  215 B. Fängström et al., “A Retrospective Study of PBDEs and PCBs in Human Milk from the Faroe Islands” (2005) 4:12 Environ. Health Global Access Sci. Sourc 12 at 19. 216 Even with all this evidence against POPs, the benefits of breast milk greatly outweigh that of the risks from consumption.; United Nations Environment Programme Chemicals, A Guide to the Stockholm Convention on Persistent Organic Pollutants, (Geneva: UNEP, 2005), online: UNEP <> (date accessed: 11 December 2008). 217 Mayo Clinic, Infant Formula: Which Formula is Right for Your Baby?, (Rochester: Mayo Clinic, 2008), online: MayoClinic <> (date modified: 1 July 2008). 218 Ibid. 219 M. Mendoza, “Calls for National Infant Recall Spread” Associated Press (28 November 2008), online: AJC <> (last modified: 28 November 2008). 220 L. Layton, “FDA Draws Fire Over Chemicals In Baby Formula” The Washington Post (27 November 2008), online: Washington Post < dyn/content/article/2008/11/26/AR2008112600386.html>  (last modified: 27 November 2008). 221 E. Harris, “Nigerian Death Toll Rises in Tainted Formula Case” Seattle PI (12 November 2008), online: Seattle PI <>  (last modified: 12 November 2008). 222 M. Fan, “6 Chinese Infants Died in Milk Crisis” Washington Post (12 November 2008), online: Washington Post <>  (last modified: 12 November 2008). 223 A. Chen & W.J. Rogan, “Isoflavones in Soy Infant Formula: A Review of Evidence for Endocrine and Other Activity in Infants” (2004) 24:1 Annu. Rev. Nutr. 33 at 34; A. Karadag et al., “Soy Formulas and Hypothyroidism” (2004) 89:11 Arch. Dis. Child. 1077 at 1077.  31  thyroid complications for adults224, there is uncertainty whether soy-based formula affects the endocrine system.225 These formulas contain genistein and daidzein, which are phytoestrogens that affect hormonal activity.226 Historically, concerns surrounding infant formula focused on lead poisoning.  Lead was a component of solder used to seal cans, including those that contained infant formula.  In 1972, the US FDA worked with manufacturers to cease the use of lead solder in these foods.  Within fifteen years, lead levels in these products had been reduced eighty to ninety percent.227  While lead content in canning has basically been eliminated, recent literature indicates that the current use of plastics for bottles and packaging of infant formula is not safe.228  The use of bisphenol A (BPA) to strengthen plastics and make resins in cans has resulted in leaching of the toxin into the formula.  With ninety-three percent of people residing in the US possessing BPA in their bodies229, consumer groups have voiced concern over the continued use of this product.  BPA has been found to mimic anthropogenic estrogens.230  It has been linked to breast cancer, prostate cancer, hyperactivity, obesity, miscarriage, insulin resistance, and reproductive malformation.231 The current acceptable levels of BPA consumption as set by the US EPA is 50 ug/kg body weight/day.232  However, recent studies indicate that this level is not safe.233  Additionally, the ability to measure one’s intake is near  224 F. Balmir et al., “An Extract of Soy Flour Influences Serum Cholesterol and Thyroid Hormones in Rates and Hamsters” (1996) 126:12 J. Nutr. 3046 at 3046; W.A. Forsythe, III, “Soy Protein, Thyroid Regulation and Cholesterol Metabolism” (1995) 125:S3 J. Nutr. 619S at 620S. 225 Chen, supra note 223 at 34 & 48. 226 Ibid. at 34; K.D. Setchell et al., “Exposure of Infants to Phyto-Oestrogens from Soy-Based Infant Formula” (1997) 9070 Lancet 23, online: Lancet < b90f-266795192f03%40sessionmgr13&bdata=JnNpdGU9ZWhvc3QtbGl2ZQ%3d%3d#db=aph&AN=9707161061> (last modified: 5 July 1997). 227 U.S. Food and Drug Administration, FDA Efforts to Reduce Lead Levels in Food (Washington, D.C.: US FDA, 1988), online: US FDA <> (last modified: 5 August 1988). 228 “Preliminary Report finds Possible Link to Hormonal Problems” MSNBC News, (17 April 2008), online: MSNBC Online <> (last modified: 17 April 2008); C. Brede et al., “Increased Migration Levels of Bisphenol A from Polycarbonate Baby Bottles after Dishwashing, Boiling and Brushing” (2003) 20:7 Food Addit. Contam. 684 at 684. 229 D. Gutierrez, FDA Claims Cancer – Causing Chemical in Infant Formula is “Safe”, online: Natural News <> (last modified: 9 July 2008). 230 H.W. Kuo, “Trace Determination of Bisphenol A and Phytoestrogens in Infant Formula Powders by Gas Chromatography-Mass Spectrometry” (2004) 1027:1-2 J. Chromatogr. 67 at 67. 231 Healthy Legacy, Guide to Safer Children’s Products, online: Healthy Environment for Kids < hildren_Products.pdf> (last accessed: 6 December 2008); The Work Group for Safe Markets, Baby’s Toxic Bottle Bisphenol A Leaching from Popular Baby Bottles, online: CBS News <>  (last accessed: 12 November 2008). 232 Work Group for Safe Markets, Ibid. 233 R. Gibson, Toxic Baby Bottles Scientific Study Finds Leaching Chemicals in Clear Plastic Baby Bottles (Los Angeles: Environment California Research & Policy Center, 2007), online: Environment California <> (date accessed: 12 November 2008); G. Shaw, “Bisphenol A is Found Neurotoxic in Primates and is Associated with Health Risks in Humans: Questions Raised about Safe Exposure Levels” (2008) 8:19 Neurology Today 10 at 10.  32  impossible.234  Similar concern has been voiced over plasticizers used in baby food and infant formula.235  In a study on infant formula and baby food in glass jars, researchers found the presence of one or more of the eleven phthalates tested for in fifty percent of the sample.236  The most common phthalate found was DEHP, a chemical that may emulate estrogens.237 Aside from toxins directly from the formula or the bottle, the water mixed with the powdered formula may expose the child to additional toxins. A description of water contaminants is included in the following section. However, it is important to note that lead, POPs, and methylmercury may be present in the water used in powder infant formula. The average infant consumes six ounces of formula per kilogram of body weight, which is comparable to a male adult consuming thirty-five cans of soda a day.238  This results in a high intake of metals and toxins, including lead, which is not safe at any level.239  Furthermore, water standards are not set with the formula-fed infant in mind.240 As infants are weaned off breast milk and infant formula, consumption of vegetables and fruits increase. Throughout childhood a person’s dietary intake differs from that of an adult.  As mentioned earlier, there is a greater consumption by a child of fruit, vegetables, and fruit juice than an adult.  The use of pesticides and insecticides on commercial crops or personal gardens leaves residues that may be ingested.  It was estimated by one study that one out of every four times a child under the age of five eats a peach, the child is exposed to unsafe levels of organophosphate insecticides.241  The consumption of pesticides has been found to cause brain cancer, leukemia, non-Hodgkin’s lymphoma242, Wilms’ Tumor, and Ewing’s Sarcoma243 as well as affects the nervous system and endocrine system.244  Different developmental stages of children result in different organ susceptibility to chemical exposure. The toxiokenetic and tociodynamic functions of a young child have yet to fully develop, resulting in inability to expel toxins in the same fashion as an adult.245  234 Work Group for Safe Markets, supra note 231. 235 D. Feldman & A. Krishnan, “Estrogens in Unexpected Places: Possible Implications for Researchers and Consumers” (1995) 103 Environ. Health Perspect. Suppl. 129 at 132. 236 European Environment and Health Committee, Sweden, EEHC WHO, 2009, online: EEHC WHO <> (last modified: 17 February 2009). 237 P.K. Eagon et al., “Di (2-ethylhexyl) Phthalate-Induced Changes in Liver Estrogen Metabolism and Hyperplasia” (1994) 58:5 Int. J. Cancer 736 at 736; C.A. Harris et al., “The Estrogenic Activity of Phthalate Esters In Vitro” (1997) 105:8 Environ. Health Perspect. 802 at 802 & 808. 238 Bearer, supra note 15 at 15. 239 Lidsky, supra note 96 at 15. 240 Bearer, supra note 15 at 18. 241 S.H. Zahm & M.H. Ward, “Pesticides and Childhood Cancer” (1998) 106:S3 Environ. Health Perspect. Suppl. 893 at 893. 242 Wigle, supra note 4 at 169. 243 Zahm, supra note 241 at 898. 244 McKeown, supra note 208. 245 Sharpe, supra note 56 at 93.  33  Baby foods derived from pureed vegetables and fruits have been found to contain pesticides or pesticide metabolite residues.246  A study conducted by The Environmental Working Group and the National Campaign for Pesticide Policy Reform on eight brand-name baby foods found sixteen pesticides. Fifty-three percent of the baby food jars contained traces of one pesticide and eighteen percent contained two or more pesticides.247  Evidence of the effect of pesticides on the human population has been found in historical case-studies.  For instance, in 1959 over 4,000 people became ill due to contaminated seed.  Use of hexachlorobenzne (HCB) on seed grain between 1954 and 1959 caused negative health effects including skin lesions, colic, metabolic disorders, and adverse effects on infant reproductive systems.248  In the 1980s and early 1990s, there were incidents of illness due to aldicarb pesticides.  This pesticide is taken up through the root of the vegetable and is not able to be removed through washing the fruit or vegetable.249  Though aldicarb was used on banana crops within legal limits, because of the high consumption of the fruit by children, pesticide manufacturers prohibited sale of the pesticide for this produce within the US.250 Legislation has been passed to reduce pesticide exposure by children. For instance, the US 1996 Food Quality Protection Act (FQPA) amended prior law with the inclusion of a child specific safety factor. A ten-fold safety margin is applied in setting the maximum residue level (MRL).251 This new standard is to take into account specific food intake, average body weight, and the pesticide residue levels under good agricultural practices.252  While the ten-fold factor has reduced the ingestion of pesticides, there are still concerns around the current exposure levels. The standards do not take into consideration differences in consumption due to ethnicity, regional differences in diet, and exposure from home garden vegetables and fruits. The US FDA conducts daily tests of about forty food samples.253  Detectable traces of residues are found in fifty-six percent of fruit, forty-one percent of grain, thirty-two percent of fish or shellfish, and thirty-one percent of vegetable products.254  Residue levels that exceeded the maximum federal level were found on more than five percent of domestic strawberries, spinach, red beets, head lettuce, and leafy vegetables.255  In a study conducted by the Danish  246 Wigle, supra note 4 at 175. 247 “Forum: Pesticides in Baby Food” (1995) 103:12 Environ. Health Perspect., online: EHP <> (last modified: 27 November 1995). 248 Organic Ltd., “Pesticides”, online: Organic Ltd <> (last accessed: 23 November 2008). 249 Goldman, supra note 6 at 443. 250 Wigle, supra note 4 at 175-176. 251 Children’s Environmental Health Network, supra note 101. 252 B. Oh, “Pesticide Residues for Food Safety and Environment Protection” (2001) Food & Fertilizer Tech. Cntr., online: Food & Fertilizer Tech. Cntr. < > (last accessed: 6 November 2008). 253Goldman, supra note 6 at 444. 254 Wigle, supra note 4 at 176. 255 Ibid.  34  Veterinary and Food Administration in 1996 and 1997, high levels of mycotoxins, PCB, and nitrates were found in vegetables, grains, beef, and veal, despite regulatory action.256 Consumption of organic foods257 has increased as a result of this ongoing concern over pesticide consumption.  In Europe, there has been a five to seven percent increase in organic purchases per year.  Two of the largest Swedish groceries have reported an eighteen and thirty percent increase in organic purchases.258  Within the US, organic sales make up about two percent of the food market.259 Data is lacking to determine with certainty whether or not organic food products are always better than conventionally grown produce for children.  However, studies indicate that by increasing organic fruit, vegetable, and juice consumption a child’s exposure level will shift from that of uncertain risk to negligible risk.260  A study conducted at the University of Washington found a lower concentration of organophosphate insecticides in urine of children whose diet consists of organic foods than those who consume conventionally grown foods.261  Similarly, a study conducted at Emery University found that children who switched from conventional diets to organic diets for five days had a reduced level of pesticide by-products from organophosphates, including malathion and chlorphyrifos.262 Pesticides are not only a concern in produce. Due to the fact that conventionally grown feed is used in non-organic or non-free-fed animals, chemicals that bioaccumulate are transferred to humans during consumption.  Animal fat and hen eggs have been found to contain pesticides or pesticide metabolites.263  In the US, 11 x 10⁹lb of recycled animal fat per year is used in animal feed from animals which may have toxins that bioaccumulated during the animal’s lifetime.264  In addition to animal by-product and pesticide treated feed, antibiotics are used by some countries to increase growth in livestock.  It is estimated that more than seventy percent of antibiotics manufactured in the US are  256 European Environment and Health Committee, supra note 236. 257 The definition of organic foods has been established under US law, Organic Foods Protection Act of 1990. However, the definitions differ based on location and legislation (or lack thereof). Organic Foods Production Act of 1990 Title 21 of P.L. 101-624. 258 The Swedish Institute, Fact Sheet: Environment, (Stockholm: Swedish Institute, 2008), online: < nmental_%20policy/SI_FactSheetEnvironment-150DPI.pdf > (date accessed: 3 November 2008). 259 C.L. Curl, R.A. Fenske, & K. Elgethun, “Organophosphorus Pesticide Exposure of Urban and Suburban Preschool Children with Organic and Conventional Diets” (2003) 111:3 Environ. Health Perspect. 377 at 377. 260 Ibid. at 382. 261 Ibid. 262 C. Lu et al., “Organic Diets Significantly Lower Children’s Dietary Exposure to Organophosphorus Pesticides” (2006) 114:2 Environ. Health Perspect. 260 at 263. 263 Wigle, supra note 4 at 176. 264 P. Walker et al., “Public Health Implications of Meat Production and Consumption” (2007) 8:4 Public Health Nutr. 348 at 350.  35  used in livestock.265  Pesticides or pesticide metabolites are found in animal fat and eggs.  The most commonly detected chemicals are PCP (35%) and DDE (21%).266 Evidence indicates that wildlife is susceptible to high levels of accumulation of pesticides, depending on exposure. There may be an increase of toxicity in wildlife of up to one hundred times that of original exposure rates.267  This has a negative impact on children who consume wild game. Water Levels of exposure to environmental toxins found in water vary and are dependent upon the source of the water, the region, and the regulatory standards (or lack thereof).  Children may be exposed to water through inhalation, dermal absorption, or ingestion.  Toxins and chemicals of concern include lead, methyl mercury, pesticides, and POPs. Children have a greater intake of water relative to their body weight268 and have different physiological and behavioural traits which leave them more vulnerable than adults.  As referenced in the previous section, infants consuming water in place of milk or as an additive to infant formula are more susceptible to negative health effects from chemical exposure.  Young children often are exposed to water contaminants through play, such as swimming, or contaminated piping in schools. Water pollution is more apparent in developing nations where sewage, industrial waste, and agricultural run-off drain into the reservoir or river sources.  For instance, in India over 1500 million litres of sewage a day is generated, majority of which flows into rivers or other dumping sites.269  Illnesses directly associated with this high level of exposure include staph infections, diarrhoea, cholera, arsenicosis, E Coli, salmonella, and intestinal worms.270  While not as extreme, similar disease patterns have occurred in developed nations. Often these health effects are associated with low-income or impoverished locations. Low-rent areas often have become debilitated and neglected, resulting in lead piping or solder remaining tolerated or unknown to tenants.  Water provided to migrant farm workers in North Carolina tested positive for fecal coliform (26%) or coliform (44%).271  Much of this is a direct result of overcrowding, poor living accommodations, and the need for sanitation systems.272  For some, water from wells or  265 Ibid. at 353. 266 Wigle, supra note 4 at 176. 267 H.M. Thompson, “Interactions Between Pesticides; A Review of Reported Effects and their Implications for Wildlife Risk Assessment” (1996) 5:2 Ecotoxicology 59 at 70. 268 Cooper, supra note 5 at 41. 269 Centre for Science and Environment, “CSE Draft Dossier: Health and Environment” (2006), online: CSE < > (last accessed: 11 December 2008). 270 Ibid; UNICEF, supra note 202; World Health Organization, Food Safety and Foodborne Illness (Geneva: WHO, 2007), online: WHO <> (date accessed: 6 December 2008). 271 S. Ciesielski, “The Microbiologic Quality of Drinking Water in North Carolina Migrant Labor Camps” (1991) 81:6 Am. J. Public Health 762 at 762; G.W. Evans & E. Kantrowitz, “Socioeconomic Status and Health: The Potential Role of Environmental Risk Exposure” (2002) Annu. Rev. Publ. Health 303 at 307. 272 Ciesielski, Ibid. at 763.  36  rain basins serves as a drinking water source.  In some areas where ground or air pollution is at lower levels273 this may not be problematic.  However, in regions where industrial waste or air pollution contaminates the soil and air274, use of this water may expose children and adults to unnecessary toxins.  Evidence indicates that in the US, low- income populations bare the greatest burden of exposure with very little quality control.  For instance, Latino populations residing near the US and Mexico border in Texas consume polluted water which results in a large number of waterborne diseases.275  Only one percent of the over 842 Hispanic communities (colonias) in Texas, has public sewage systems.276  Over 200,000 people reside in these unincorporated subdivisions, a number of which are children.277  The Rio Grande has elevated levels of mercury content which exceed the state standards.278  A recent study conducted by the US Geological Survey found low levels of man-made chemicals in public water supplies after being treated for consumption.279  About 130 chemicals were found in the waters prior to being tested.  Around two- thirds remained after treatment.280 Lead is one of the pollutants detected in water.  Older piping and solder often contain lead which may leach into the water stream.281  In older school buildings and homes, replacement of these products may not have occurred. Furthermore, replacement may be the responsibility of the municipality if the lead piping lies within a public area. While lead piping use reduced in the 1950s, lead solder was used on copper pipes until the 1980s (1986 in the US).282 The US EPA has estimated that between ten and twenty percent of lead content in children is derived from tap water.283  Regional differences influence the levels of lead in water due to piping.  Those who live in an area with soft water tend to have greater amounts of leaching of lead into the water.284  Lead has been found to have a negative  273 Some examples of the least polluted cities include Flagstaff, Arizona, and Fairbanks, Alaska. For a complete list of the least polluted cities see: American Lung Association, State of the Air: 2008 (Washington, D.C.: American Lung Association, 2008), online: American Lung Association < cities/least-polluted-short-term-pm.html> (date accessed: 14 May 2009). 274 Some examples of the most polluted cities include Pittsburgh, Pennsylvania, and Los Angeles, California. For a complete list of the most polluted cities see: American Lung Association, ibid. 275 Evans, supra note 271 at 308. 276 R. Metzger, J.L. Delgado, & R. Herrell, “Environmental Health and Hispanic Children” (1995) 103:S6 Environ. Health Perspect. 25 at  30. 277 Ibid. 278 Ibid. 279 U.S. Department of the Interior, Man-Made Chemicals Found in Drinking Water at Low Levels (Washington, D.C.: U.S.G.S., 2008), online: USGS.Gov <> (last updated: 5 December 2008). 280 Ibid. 281 Cooper, supra note 5 at 44. 282 Ontario Ministry of Environment, Lead and Drinking Water – Questions and Answers, (Toronto: Ontario Ministry of Environment, 2007), online: ON Ministry of Environment <> (date accessed: 4 December 2008); J.L. Pirkle et al., “Exposure of the US Population to Lead, 1991-1994” (1998) 106:11 Environ. Health Perspect. 745 at 748. 283 L. Bower, Drinking Water: Lead-Pipe and Lead-Solder Concerns (Healthy House Institute , 2000), online: Healthy House Institute < Drinking_Water_Lead_Pipe_and_Lead_Solder_Concerns>  (date accessed: 2 December 2008). 284 U.S. Food and Drug Administration, supra note 227.  37  impact on intellectual and physical development, even with small amounts of consumption.285  Some schools have taken the precaution of running the faucets at the start of the day to ensure that children do not consume water which sat in piping overnight.286 The awareness of the harmful effects of lead has resulted in a reduction in exposure.  However, other chemicals and toxins remain in the water which may have negative health effects on infants and children.  In areas where ground water from well sources is used, consumption of pesticides may occur.  Agricultural run-off into surrounding areas is absorbed in the soil of these surrounding areas and is not capable of being monitored by government entities.287  Over 130 pesticides have been detected in groundwater, including aldicarb, atrazine, dichlorodiphenyldichloroethylene (DDE), dieldrin, and 1,2-dibromo-3-chloropropane (DCBP).288  Pesticides have been found in animals and wildlife as a result of consumption of pesticide-polluted water.289  Even if a child is not exposed to the polluted water directly, he or she may consume pesticides which have bioaccumulated in animal fat. The disinfection by-products (DBP) used to ensure water quality standards are met have been found to cause negative developmental outcomes, fetal deaths, birth defects, low birth weight, and cancer.290  The reaction of the chemical chlorine and the organic material in untreated water produces DBPs, which include trihalomethanes (THMs), haloacetic acids, haloacetonitriles, haloketones, halophenols, and halogenated furanones.291  There is still much debate over the negative effects of DBPs and data lacking as to linkage.  Nevertheless, some studies have found an association between THMs and stillbirth, spontaneous abortions, low birth weight, and birth defects.292  Due to the number of confounding factors, it is difficult to assess a clear linkage between DBPs and cancer.  However, some studies have established an association between exposure and brain cancer and adult bladder cancer.293 Exposure to water pollutants through dermal absorption occurs in many recreational settings.  For instance, by the mid-1980s the Great Lakes contained over 800 chemical substances as a result of industry, agricultural, and urban  285 U.S. Environmental Protection Agency, Actions You Can Take to Reduce Lead in Drinking Water, (Washington, D.C.: US EPA, 1993), online: US EPA < > (date accessed: 21 November 2008). 286 U.S. Environmental Protection Agency, Testing Schools and Child Care Centers for Lead in the Drinking Water, (Washington, D.C.: US EPA 2006), online: US EPA <> (date accessed: 3 December 2008). 287 Cooper, supra note 5 at 55. 288 Wigle, supra note 4 at 179. 289 P. Brown et al., “Identification of Pesticide Poisoning in Wildlife” (1996) 754:1-2 J. Chromatogr. A. 463 at 464; Thompson, supra 263 at 59. 290 Wigle, supra note 4 at 335-345. 291 Ibid. at 334-335. 292 Ibid; M.J. Nieuwenhuijsen, “Chlorination Disinfection Byproducts in Water and their Association with Adverse Reproductive Outcomes: A Review” (2000) 57:2 Occup. Environ. Med. 73 at 73 & 81. 293 Wigle, supra note 4 at 341-342; J.J. Cutler et al., “Childhood Leukemia in Woburn, Massachusetts” (1986) 101:2 Public Health Rep. 201 at 204; B.A. Mueller et al., “Residential Water Source and the Risk of Childhood Brain Tumors” (2008) 116:6 Differences 6 at 554.  38  surroundings.294  Though a concern for wildlife and the environment in general, it is especially worrisome for children and infants exposed to game and fish life that feeds off the lakes and for those who participate in recreational sports in those waters.295 Soil There are a variety of ways in which soil and ground pollution occurs.  Industrial sludge, agricultural run-off, automobile emissions, and construction by-products are just a few of the methods by which ground areas are polluted.  Children tend to spend more of their time near the ground, especially in play areas.296  They often have direct exposure to dirt and soil, which is not the case for most adults.  Because of a child’s hand-to-mouth behaviour, greater inhalation for body weight, and direct skin contact, contaminants that might be mitigated for adults are taken in by children.  It has been estimated that children between the age of two and six ingest 250 mg of dirt daily while at play outside.297  Some children, however, consume much more – up to twenty-five to sixty grams of soil a day.298 Because of the child’s ongoing developmental stages, the ability to expel these toxins is reduced and there is a greater susceptibility to disease.  The activity of eating dirt is not considered abnormal in young children who are undergoing an exploratory phase.299 Lead in play areas has reduced with the elimination of the metal from gasoline, exposure still is of concern for young children at play.  Within Ontario, residential areas tend to have lead levels less than 100 parts per million.300  Though there is minimal risk from this low level, some areas have greater amounts because of proximity to industry or in a historic region where lead-based products are still present.301  Garden areas may contain lead as a result of chipped  294 N.W. Tremblay & A.P. Gilman, “Human Health, the Great Lakes, and the Environmental Pollution: A 1994 Perspective” (1995) 103 Environ. Health Perspect. Suppl. 3 at 3. 295 Ibid. at 4; B.L. Johnson et al., “Public Health Implications of Persistent Toxic Substances in the Great Lakes and St. Lawrence Basins” (1998) 24:3 J. Great Lakes Res. 698 at 698. 296 Canadian Partnership, supra note 63. 297 J.K. Hawley, “Assessment of Health Risk from Exposure to Contaminated Soil” (1985) 5:4 Risk Anal. 289 at 292; M.L. Lepow et al., “Role of Airborne Lead in Increased Body Burden of Lead in Hartford Children” (1974) 7 Environ. Health Perspect. 99 at 100. 298 E. J. Calabrese et al., “Soil Ingestion: A Concern for Acute Toxicity in Children” (2008) 116:5 Gene 1354 at 1354 -1355. 299 “The Hazards and Benefits of Eating Dirt” About Kids Health News (2007), online: AboutKidsHealth < 38&categoryID=news-type” <date accessed: 3 January 2009). 300 Ontario, Lead and Drinking Water – Questions and Answers (Toronto: Ontario Ministry of the Environment, 2007), online: ON Ministry of Environment <> (date accessed: 4 December 2008); Ontario, What You Should Know about Lead in Soil (Toronto: Ontario Ministry of the Environment, 2007), online: ON Ministry of Environment <> (date accessed: 12 November 2008). 301 Ibid.  39  paint from the exterior of an older home.  Lead has been found to cause vomiting, diarrhea, convulsions, and intellectual development delay.302 Industrial waste and agricultural run-off influence the quality of soil and levels of pollution.  Children who reside near farmland or industry often have elevated exposure levels.  A number of studies have found that agricultural workers have increased health risks because of inhalation of pesticides.  In terms of children, direct contact with soil brought into the house from work areas may provide exposure.303  A study conducted in Central Valley, California, found that house dust may have contaminants transferred from outdoor rural soil.  Ingestion of diazinon and chlorphyrifos by children could exceed the US EPA levels because of this transfer from soil pollutants indoors.304 Literature indicates that these compounds, when inhaled, ingested, or absorbed by children, cause Hodgkin disease, brain cancer, and leukemia.305 Poor monitoring has led to incomplete conclusions as to the impact of sludge exposure.  This industrial by-product contains nutrients, organic matter, and chemical waste in varying quantities.  Though not scientifically linked, cases of infection presumed to be associated with sludge use have been reported.  In Menifee, California, reports of children and adults falling ill began after nearby farmland used sludge for fertilizer.306  As a result, the Californian county of Kern has banned Los Angeles from dumping nearly 250,000 tonnes of sewage sludge on county farms.307 There have been reports of illnesses associated with thirty-nine separate incidents of exposure to sewage sludge in fifteen states.308  Illnesses thought to be affiliated with exposure include respiratory, gastrointestinal, headaches, and skin disorders.309  Use of sludge on hayfields in Georgia310 resulted in the death of dairy cows who consumed the feed. 311  302 Canada, Effects of Lead on Human Health (Ottawa: Health Canada, 2008), online: Health Canada <>  (date accessed: 14 April 2009). 303 Simcox, supra note 174 at 1126. 304 M.A. Bradman et al., “Pesticide Exposures to Children from California’s Central Valley: Results of a Pilot Study” (1997) 7:2 J. Expo. Anal. Env. Epid. 217 at  217. 305 C.L. Curl et al., “Evaluation of Take-Home Organophosphorus Pesticide Exposure Among Agricultural Workers and their Children” (2002) 110:12 Environ. Health Perspect. A787 at A787; C. Leowenherz et al., “Biological Monitoring of Organophosphorus Pesticide Exposure among Children of Agricultural Works in Central Washington State” (1997) 105:12 Environ. Health Perspect. 1344 at 1350. 306 K. Brusch, “Residents Fear Renewed Use of Sludge on Farmland will Bring Health Problems” North Carolina Times (2004), online: NC Times <> (date accessed: 2 December 2008). 307 S. Chawkins, “LA Fights Kern County Sludge Ban” Los Angeles Times (2006). 308 E.Z. Harrison & S. R. Oakes, “Investigation of Alleged Health Incidents Associated with Land Application of Sewage Sludges” (2002) 12:4 New Sol. 387 at 390. 309 Ibid; C. Snyder & P.H. Snyder, “The Dirty Work of Promoting ‘Recycling’ of American’s Sewage Sludge” (2008) 11:4 Int. J. Occup. Environ. Health 415 at 419 -420. 310 $550,000 in damages was awarded to the Boyce family for death of cows due to sludge use. 311 J. Lee, “Sludge Spread on Fields is Fodder for Lawsuits” The New York Times (2008), online: NY Times <> (last modified: 26 June 2003).  40  The ASARCO Smelter in Ruston, Washington illustrates the impact industry can make on soil.  In operation from 1890 to 1986, this plant produced copper, emitting arsenic and lead into the air as a by-product.  As heavy metals, both fell to the ground and were absorbed by soil.312  With the company bankrupt, the necessary $164 million to clean up the site has yet to be produced by officials.313  Until the appropriate precautions have been taken the land the company occupied, as well as nearby land polluted by emissions, is not liveable.314 While pesticides have been covered under food consumption and air inhalation, it is important to note that direct contact with these chemicals may result in dermal absorption.  Pesticides and insecticides are used by schools, landlords, and home-owners to eliminate unwanted pests.  Caution has to be taken to prevent direct contact with these products, particularly since they have long staying power, particularly if applied incorrectly. 2.2 Conclusion This chapter has outlined how children differ from adults and how these differences facilitate exposure to environmental pollutants.   Chronic health conditions such as respiratory illnesses, asthma, allergies, and eczema are some of the less severe results of exposure. Linkages between pollutants and cancer, spontaneous abortion, birth defects and abnormalities, intellectual delay, and immunological and neurological disorders emphasize the seriousness of these exposures.  With nearly 120 million children in North America315 and over 100 million children residing in the Europe Union316, the costs to the health care system, of lost school days, of lost work days for parents, and to society as a whole due to these chronic health conditions are escalating.  Cancer remains one of the leading causes of disease-related deaths in children and asthma is increasing rapidly (one in five in children residing in Canada has asthma)317.  Within Canada alone, low birth weight and birth defects resulted in 30,000 hospitalizations and 1,500 deaths in one year.318  Because of the increasing incident rates of childhood onset of chronic health conditions, it is prudent that policy takes into account the uniqueness of a child.  312 T. Nguyen, “Be Alert in the Dirt: Keeping Children Safe in the Dirt” (Seattle: Public Health Seattle & King County, 2008), online: Public Health Seattle <> (date accessed: 2 December 2008). 313 D. Chircop, “Asarco Soil, Groundwater Cleanup in Everett at Risk” Snohomish County Herald (28 October 2008), online: HeraldNet <> (last modified: 28 October 2008). 314 Washington State, Asarco Ordered to Demolish Houses, Sample Soil and Conduct other Pre-Cleanup Activities in Northeast Everett (Olympia, WA: Department of Ecology, State of Washington, 1997), online: WA Department of Ecology <> (date accessed: 2 December 2008). 315 Growing Up in North America: Child Health and Safety in Canada, the United States and Mexico (The Annie E. Casey Foundation, 2007), online: Annie E. Casey Foundation <> (date accessed: 1 June 2009). 316 V. Holdsworth, Cool Facts and Figures about the EU (London: Europe in the UK, 2008), online: Europe in the UK <> (date accessed: 17 December 2008). 317 D. Coulombe, “$12 Million Invested in Improving the Health of Children Suffering from Asthma and Allergies” Medical News Today (10 June 2008), online: Medical News Today <> (last modified: 10 June 2008). 318Canadian Partnership, supra note 63.  41  3. CHILDREN’S ENVIRONMENTAL HEALTH: INTERNATIONAL EFFORTS 3.1 Introduction The last chapter’s outline of the numerous ill effects for children associated with environmental toxin. Children’s unique exposure to those toxins clearly mandates their respective government’s protection.  Due to the migrating impacts of pollutants, for instance chemical transport through waterways or the transfer of particle matter across boundaries, the issues associated with a child’s environmental exposure would be, in part, best addressed at the international level.  However, international agreements, have for the most part, failed to successfully reduce the exposures children face to outdoor pollution, water contamination, or built environmental toxins.  While efforts taken by worldwide organizations, such as the World Health Organization (WHO), the United Nations (UN), and the meetings of the Group of Eight (G8 – Canada, France, Germany, Italy, Japan, Russia, United Kingdom, and the United States) have assisted in bringing awareness to the issues, they have been unable to require nation-states to take specific actions with respect to exposure rates. International agreements which specifically link the harmful effects of environmental pollutants to negative health outcomes are few, and even less common when expressly considering the subpopulation of children. Those that do highlight children tend to be vague in language and do not stipulate well defined requirements, such as air quality standards, reduction of explicit water pollutants, reform of agricultural practices to diminish pesticide runoff, or the mandating of school building ventilation systems. This chapter provides a discussion of the international agreements and regional efforts which have relevance to children’s environmental health.  What is essential to take away from this chapter is that though children’s environmental health has been a topic of discussion at the international level, tangible objectives have not been required of nation-states.  Whereas policy on environmental health in general has gradually gained footing at both national and international levels, attention on children’s environmental health has been even more piecemeal.  The following section outlines some of the tangential agreements which have helped shape children’s environmental health at an international level.  Thereafter, attention is given to the international and regional agreements which are directly relevant to the field of children’s environmental health.  It should be noted that few of these agreements have demonstrated measurable changes in exposure rates or reduced pollution.  As this thesis utilizes the ill-effects of pesticide and chemical exposure on children’s health as a case study, the third section offers an assessment of international and regional agreements which directly address these toxins. 3.2 Focus On The Environment And Health: Tangential Agreements The topic of children’s environmental health is relatively new, with most relevant policy having taken effect in the later part of the twentieth century. Much of the early legislation was a reaction to specific pollutants, such as for lead, asbestos, and radon.  There are a number of reasons for policy progress in the area of children’s environmental health to have occurred recently.  Firstly, many common chemical pollutants were a product of industrialization and wartime efforts.319  “During the last 50 years hundreds of thousands of chemicals have been developed and the production of synthetic chemicals has increased from 1.3 billion lbs in 1940 to 320 billion lbs in 1980.”320  In part,  319 R. R. Orford, “Diagnosing and Treating Environmental Health Problems” (1991) 74:11 Minn. Med. 7 at 7. 320 Orford, Ibid. at 7; Children’s Environmental Health Network, supra note 101.  42  the recent legislative development has been due to the rapidly increasing measures taken in both environmental law and public health policy.  To provide an in-depth review of environmental law and public health policy would be impractical within the confines of this thesis, and that is not the purpose of this chapter.  However, it is noteworthy to highlight the relatively rapid growth in both environmental law and public health policy.  This has made a direct impact on the international environmental health forum.  Without awareness at a local or national level, the likelihood of the ability of international efforts to pressure industrialized nations to advance the protection of children’s health is improbable. The relationship between population health and the environment is one that grew over the course of the twentieth century, largely motivated by separate cases of epidemics directly linked to toxic exposure.  Instances of “killer smog” in Meuse Valley, Belgium (1930), Donora, Pennsylvania (1948), and London, United Kingdom (1952) resulted in death, respiratory disease, and hospitalizations.321  Recognition of the linkage between smog and negative health outcomes shaped US President Truman’s acknowledgement that government and industry must combat air pollution.  In his message to the United States Technical Conference on Air Pollution in 1950 Truman emphasized that “the health hazards arising from air pollution, as shown by the Donora disaster, are especially important.”322  In 1955, Los Angeles was one of the first regions in the US to set limits for nitrogen, ozone, sulphur dioxide, and carbon monoxide323, in response to dense smog which resulted in a halt of industry and schools in October 1954.324 Similar case studies can be found for mercury, lead, asbestos, and radium; a piecemeal approach taken by the judiciary and legislative bodies, acting after instances of harm were well documented. While lead paint was recognized as toxic when ingested as early as 1904325, it was not until 1970 that the US Surgeon General officially recognized the harmful effects lead had on children.  In 1978 household use of lead paint was banned, demonstrating the slow rate of linkage of a toxin and public health, and subsequent legal action.326  The relationship between public health and pollutant exposure rates is best illustrated by litigation surrounding the “Radium Girls”.  These “girls” were in fact women employed by the US Radium Corporation from 1917 to 1926 who suffered a number of illnesses,  321 A. Ciocco & D.J. Thompson, “A Follow-Up of Donora Ten Years After: Methodology and Findings” (1961) 51:2 Am. J. Public Health 155 at 155; B. Kovarik, “Environmental History Timeline”, online: Radford University <> (date accessed: 4 January 2009). 322 J.T. Woolley & G. Peters, “The American Presidency Project”(Santa Barbara, CA: The American Presidency Project), online: The American Presidency Project <> (date accessed: 4 January 2009). 323 L.C. McCabe, The Identification of the Air Pollution Problem (Geneva: World Health Organization, 1961) at 40. 324 B. Kovarik, supra note 321. 325 Identification of lead’s harmful effects on children was first presented by J.L. Gibson of Queensland, Australia, in 1904; Gibson, supra note 19 at 301. 326 S. Tong, Y.E. Schirnding, & T. Prapamontol, “Environmental Lead Exposure: A Public Health Problem of Global Dimensions” (2000) 78 Bull. World Health Organ. 1068, online: Bulletin of the WHO <> (date accessed: 14 October 2008).  43  often resulting in death, due to exposure to radium.  Evidence in the case indicated that the employer knew of the ramifications of exposure.  Victory for the “Radium Girls” lent itself to more stringent labour standards.327 While the advertised relationship between toxins and poor health assisted in closing the gap between health outcomes and the environmental issues, it is important to observe that the initial stages of environmental health regulation were due to the progression both of environmental law and public health policy.  Both medicine and the preservation of the environment have made progress technologically, scientifically, and legally within the last century. These are just a few of the reasons for the relatively new field of environmental health.  For instance public health has had a long history, routed in pandemics and outbreaks328, however epidemiological study of disease patterns is relatively new.329 The prevention of infectious diseases shifted medical attention towards chronic health conditions.  This move towards studying cause of chronic health conditions, rather than just infectious diseases, has allowed health professionals to recognize that environmental exposure leads to negative health outcomes. Health science has evolved; so has environmental law.  Early international environmental law was limited in scope and authority.  The 1968 Biosphere Conference recognized the lack of international governance on the matters of air and water pollution, deforestation, and overuse of land.330   “Until this point in history the nations of the world have lacked considered, comprehensive policies for managing the environment.  It has become clear, however, that earnest and bold departures from the past will have to be taken nationally and internationally if significant progress is to be made.”331  Following this, influential doctrines, such as the 1972 United Nations  Convention on the Human Environment (Stockholm Declaration), the 1987 Brundtland Report (Our Common Future), and the 1992 United Nations Conference on Environment and Development (UNCED)(Earth Summit), were formulated. 3.2.1 Agenda 21 One of the more noteworthy international agreements on environment health is Agenda 21. A product of the United Nations Conference on Environment and Development meeting held in Rio de Janeiro in June 1992, the agenda directly links health, environment, and sustainable development. The doctrine, adopted by 179 governments, emphasized the relationship between human health and the environment: “human beings are at the centre of concerns for sustainable development.  They are entitled to a healthy and productive life in harmony with nature.”332  The declaration set objectives to be met, with an emphasis on local authorities taking on much responsibility for  327La Porte V. United States Radium Corporation, 13 F. Supp. 263, 264 (D.N.J. 1935). 328 Notable outbreaks include the Black Death of 1348 and the Sixth cholera pandemic (1899-1923), both of which spread across Europe. 329 Physician John Snow is credited with the conception of epidemiology while studying the cholera outbreak in London, UK, in 1854; D. Cameron & I. Jones, “John Snow, the Broad Street Pump and Modern Epidemiology” (1983) 12:4 Int. J. Epidemiol. 393 at 393. 330 P. Sands, Principles of International Environmental Law, (Cambridge: Cambridge University Press, 2003) at 34. 331 Ibid. 332 Agenda 21, The Rio Declaration on Environment and Development, Distr. General (A/CONF.151/26) (1992); Y. Von Schirnding, “Health and Sustainable Development: Can We Rise to the Challenge?” (2002) 360:9333 The Lancet 632 at 632.  44  implementing these goals.  These targets were reaffirmed in the Millennium Summit of 2000, along with the goal of reducing the number of people living in poverty by half by 2015.333 Although Agenda 21 was not the first gathering where sustainable development was addressed at an international level334, it was innovative in linking health with environmental issues.335  Health, water, energy, biodiversity, and agriculture were identified as key areas of concern.  Chapter 25 of Agenda 21 addresses children and youth specifically, stressing the importance of including children in the dialogue on sustainable development.336  However, while there is great importance in bringing attention to these issues at an international level, the standards set by this declaration are nonbinding.  Furthermore, the issues of children’s environmental health differ greatly per region, and therefore the ability to set obligatory requirements that are regionally specific, becomes difficult.  The Commission on Sustainable Development (CSD) Indicators of Sustainable Development considers children only in the context of nutrition, mortality, infectious diseases, and educational status.337  Because of the economic, health, and environmental differences between nation-states, the objectives set by the UN have been ones already met by developed nations.  For instance, the disease rates of malaria and tuberculosis resulting from poor environmental standards is basically nonexistent in western nations, but it is a prominent problem in developing nations.  An international doctrine such as Agenda 21 is helpful in promoting awareness, but leaves the specific standards which may have been beneficial in diminishing childhood environmental exposures to be set by respective national governments. Local initiatives resulting from Agenda 21 have been influential in addressing negative effects on childhood health from to hazardous exposures.  Though unsuccessful in mandating specific efforts be taken by governments, Agenda 21 was significant in motivating a number of municipal-level projects.338  Because of the undefined methods by which local Agenda 21 (Local 21) projects are to be implemented, there is a great deal of variety in the projects. Therefore, some of these local efforts had a direct effect on childhood health, whereas others were responsible for improving of the general welfare of the population.  For instance, in Nottingham, UK, the local council has worked with the region’s largest employer to decrease traffic and car use through carpooling.339  In Sweden, local Agenda 21 projects have worked in conjunction with child daycare centres and schools in efforts to lessen behaviours which  333 United Nations Millennium Declaration, GA Res. A/55/L.2 (2000), online: UN <> (date accessed: 4 January 2009). 334 The term “sustainable development” was first used at the international level by the World Commission on Environment and Development (WCED), known as the Bundtland Commission, in 1983. Report of the World Commission on Environment and Development: Our Common Future, UNGA, 1983, UN A/42/427. 335 Von Schirnding, supra note 332. 336 Agenda 21, supra note 332. 337 Economic and Social Affairs United Nations, Indicators of Sustainable Development: Guidelines and Methodologies, UN ESC, 2007, No. E.08.II.A.2, online: UN ESC <> (date accessed: 3 June 2009). 338 B. Tuxworth, “From Environment to Sustainability: Surveys and Analysis of Local Agenda 21 Process Development in UK Local Authorities” (1996) 1:3 Local Environ. 277 at 277. 339 Friends of the Earth, Local Agenda 21 Must Have Hard Targets and Timetables, online: FOE <>  (last modified: 14 January 1998).  45  impact environment and health.340  In West Devon, UK341, the assessment of “quality of life” has been redefined to include personal safety, cheerfulness, and health.342 While Agenda 21 resulted in a number of local and municipal-level action plans, it has also been an awareness tool at a national level.  Many signatory nations created sustainable development plans following the summit.  Some national governments have been criticized for not incorporating economic development considerations, as well as failing to evaluate success or failures.343  Member states of the European Union, though, have published National Environment Health Plans (NEHAPs) as a result of the Agenda 21, and the 1994 World Health Organization Regional Office for Europe’s (WHO Europe) Second European Conference on Europe and Health, which have required greater accountability by governments.344 Agenda 21 may have made an impact in some locales, but it has not been safe from criticism.  The focus of the declaration was to force local authorities to take action to promote sustainable development.  Though Agenda 21 is recognized as an opportunity for municipal governments to take innovative actions, funding and the necessary authoritative control to do so may not be present.345  “The difficulty lies in establishing the relative balance between delegation and control which can create a strategy ... yet lay the groundwork for effective structures which will allow LA21 to develop its own momentum in the longer term.”346  Additionally, displeasure with the terminology used, which was influenced by industrialized language, has been voiced.347  Also, Agenda 21 did not take into consideration the differing political climates and unique roles non-governmental parties may play.348  Furthermore, implementation into the US political culture was not achieved.  The Bush administration of the time was hesitant to embrace the Rio Declaration as a monumental international doctrine because “the American life-style is not up for negotiation”.349  340 S.A. Jorby, “Local Agenda 21 in Four Swedish Municipalities: A Tool Towards Sustainability?” (2002) 45:2 J. Environ. Plann. Manage. 219 at 230. 341 Ibid. at 222. 342 Friends of the Earth, supra note 339. 343 C. F. Corvalán, T. Kjellström, & K.R. Smith, “Health, Environment and Sustainable Development. Identifying Links and Indicators to Promote Action” (1999) 10 Development 656 at 656. 344 Environmental Health Action Plan for Europe, (Copenhagen: World Health Organization Regional Office for Europe, 1994), online: WHO Europe <> (date accessed: 3 June 2009). 345 C. Freeman, S. Littlewood, & D. Whitney, “Local Government and Emerging Models of Participation in the Local Agenda 21 Process” (1996) 39:1 J. Environ. Plann. Manage. 65 at 65; T. Hart, G. Haughton, & J. Peck, “Accountability and the Non-Elected Local State: Calling Training and Enterprise Councils to Local Account” (1996) 30:4 Reg. Stud. 429 at 430; P. Selman, “Local Agenda 21: Substance or Spin?” (1998) 41:5 J. Environ. Plann. Manage. 533 at 550-551. 346 Freeman, supra note 345 at 68. 347 T. Doyle, “Sustainable Development and Agenda 21: the Secular Bible of Global Free Markets and Plurist Democracy” (1998) 19:4 Third World Q. 771. 348 Ibid. at 783. 349 P. Elmer-Dewitt, “Rich vs. Poor” (1992) 139:22 Time 22 at 22;  N. Low, Consuming Cities: The Urban Environment in the Global Economy After the Rio Declaration, (London: Routledge, 2000) at 56.  46  3.2.2 Regional Agreements Agenda 21 serves as an example of an international agreement which has made an impact on the field of children’s environmental health, though perhaps not intentionally.  Similarly, transnational agreements in both North America and Europe have been effective in linking health and the environment.  Just as with Agenda 21, the efforts have often been reactionary and do not necessarily assess the exposure rates with an awareness of the susceptibility of a child. However, regional agreements tend to include more specific requirements which may make an impact on a child’s exposure.  While many of these agreements are voluntary, because the agreement is often addressing an issue in urgent need of attention there is follow-through.  Within the EU, many of the standards or programs on environmental health are legal requirements. On a more practical level, the use of regional agreements have been beneficial in identifying transnational concerns and working towards remedying the environmental harms committed.  With over 120 regional environmental treaties, it is impossible and unnecessary to review them within the confines of this thesis.350  However, it is noteworthy to indicate that successful transnational agreements have been drafted, providing a context for future agreements with a focus on children’s environmental health. For the most part, these agreements have been retroactive, repairing damage done to the environment and the overall health of the population.  For instance, the US-Canada Great Lakes Binational Toxic Strategy351 aims at reducing persistent toxic substances currently present in the Great Lakes.  Signed in April 1997, this agreement specifies reduction targets for aldrin/dieldrin, benzo(a)pyrene, chlordane, DDT, hexachlorobenzene, alkyl-lead, mercury, mirex, octachlorostyrene, PCBs, dioxins and furans, and toxaphene.352  While one of the first agreements of this type signed between Canada and the United States, criticism has been made of the voluntary requirements and ability to revise timeframes introduced in the framework.353  Nevertheless, this agreement demonstrates that concern over specific pollutants and concentrated organizational efforts to combat those pollutants can be successful in reducing exposure rates.354  Similar agreements have been structured ?”between the United States and Mexico.  The Border Smog Reduction Act of 1998355 applies to the San Diego metropolitan area.  The objective of the act is to reduce  350 D. Vogel, “Trading Up and Governing Across: Transnational Governance and Environmental Protection” (1997) 4:4 J. Eur. Public Policy at  566. 351 U.S., Great Lakes Binational Toxics Strategy (Washington, D.C.: US EPA, 1997), online: US EPA <>  (last accessed: 15 January 2009). 352 Ibid. 353 T.C. Beierle & D.M. Konisky, “What Are We Gaining from Stakeholder Involvement? Observations from Environmental Planning in the Great Lakes” (2001) 19:4 Environ. Plann. C 515 at 516; Canada, Great Lakes Binational Toxics Strategy, (Ottawa: Environment Canada, 2001), online: Environment Canada <> (date accessed: 19 July 2008). 354 M. Valiante, P. Muldoon, & L. Botts, “Ecosystem Governance: Lessons from the Great Lakes” O. Young ed., Global Governance (Bonston: Massachusetts Institute of Technology, 1997) 197 at 223. 355 “Passed in 1998, the Border Smog Reduction Act was drafted by the US in response to the San Diego Air Pollution Control District’s finding that 7,000 vehicles registered in Mexico and driven daily to the US produce up to 14% of the region’s total air pollution.” R. Stern, Addressing Cross Boundary Air Pollution: A Comparative Case Study of the US-Mexico Border and the Hong Kong-Guangdong Board (Hong Kong:  Civic Exchange, 2001), online:  47  regional air pollution from non-commercial vehicles by preventing re-entry into the San Diego US border more than twice a month.356  Though the objective of the agreement is not children in particular, obviously reducing air pollutants in the region for the general public is beneficial to the vulnerable populations. The Canada-United States Border Air Quality Strategy is another example of a regional effort that has led to the positive reduction of air pollution exposure in children.  Signed in 1997, the agreement aims to reduce sulphur dioxide and nitrogen oxide emissions.  Projects and research borne out of this agreement have included consideration of children.  Health Canada has funded research on childhood respiratory disease using the BC Linked Health Database to review air quality in the British Columbia Georgia Basin and Washington State Puget Sound areas.357 Analysis of industrialized nations, such as Canada and the United States, indicates that the number of transboundary agreements have increased due to a growing awareness of environmental harm done, both in the science community and the general public.358  Within the United States, where strong lobbying groups exist, this external pressure on government for environmental protection has played an influential role in shaping regional agreements.359  The Great Lakes Binational Toxics Strategy illustrates how cooperation amongst a number of parties may influence regional action to reduce pollution.  Parties active in the efforts to reduce Great Lakes pollution included government at the federal, state/provincial, and local levels, as well as industry (American Automobile Manufacturers Association, Canadian Chemical Producers’ Association, etc.) and non-governmental organizations (Ecology Center of Ann Arbor, Great Lakes United, etc.).360  Although goals set, such as the reduction of mercury release into the Great Lakes Basin of ninety percent by Canada by 2000 and fifty percent by the US by 2006, have not been met, efforts by the two countries have been positive (78% and 40% respectively).361 Much of the regional attention given to transboundary pollution has been a result of economic and trade related agreements.  In Europe, the creation of the European Union has permitted a centralized power to govern over environmental issues which exceed the abilities and boundaries of a federal government.  Within North America, the pressures of environmentalists and public concerns influenced the formulation of the North American Free Trade  Civic-Exchange.Org <>  (last modified: October 2001) at 13. 356 U.S., Press Release: Border Smog Reduction Law to Take Effect Next Week (Washington, D.C.: U.S. Borders and Customs, 1999), online: U.S. Borders and Customs <> (last modified: 26 April 1999); “Selected Border-Related Environmental Laws and Regulations” (2002), online: University of San Diego <> (date accessed: 3 January 2009). 357 Canada, Canada-United States Border Air Quality Strategy: Georgia Basin Puget Sound International Airshed Strategy (Ottawa: Health Canada, 2006), online: Health Canada < ext/georgia_basin-eng.php> (last modified: 1 November 2006). 358 R.W. Hahn & K.R. Richards, “The Internationalization of Environmental Regulation” (1989) 30 Harv. Int. Law J. 421 at 423. 359 Ibid. at 426. 360 U.S., “Great Lakes Binational Toxics Strategy Five Year Perspective” (Washington, D.C.: U.S. Environmental Protection Agency, 2002), online: U.S. E.P.A. <> (online: 12 January 2009). 361 Ibid.  48  Agreement (NAFTA). As NAFTA, and the parallel agreement North American Agreement on Environmental Cooperation (NAAEC), has the capacity to positively influence children’s environmental health in both Canada and the United States, it will be covered in greater detail in the third section of this chapter. The European Union was originally formulated as a single economic market in efforts to create harmonization following the Second World War (WWII).362  It has been this unification and centralized governance which has led to the strengthening of environmental protection within member states.363  Although not one of the original objectives of the European Community (EC) (the predecessor to the European Union), “environmental policy is now one of the most important and highly regulated areas of EU competence.”364  This is a result of a number of factors, including increased distress by individuals over environmental deterioration, the global impact of heavily publicized environmental disasters, and “the politicization of the environmental movement in the 1970s and 1980s.”365  Much more than the strengthened concerns over environmental harms, it was the threat that member-state policy may disturb the single market that encouraged EU environmental policy-making.366  In 1997, the Amsterdam Treaty provided a basis for environmental consideration in Article 6, which states that “Environmental protection requirements must be integrated into the definition and implementation of the Community policies and activities referred to in Article 3, in particular with a view to promoting sustainable development.”367 While environmental law has clearly moved into an area of shared domain between the supranational government and federal control, public health policy still remains largely a national issue.368  Though the topic of a unified public health system is an area of great contention within the EU community, the need for some level of supranational governance in this field has been recognized.  Response to recent cases of “mad cow” disease and elevated levels of dioxin in Irish pork products illustrate the EU’s capacity to monitor and ban food products.369 Two EU programs tangentially relevant to children’s environmental health are the 2002 Sixth Environment Action Plan 2010: Our Future, Our Choice (6th EAP) and The European Environment and Health Action Plan 2004-2010 (Health Strategy). Both emphasize the link between the environment and health.  Two key pieces of legislation aiding in these objectives are: the Water Framework Directive (2000) and the 2006 Regulation on Registration and  362 J.J. Richardson, European Union: Power and Policy-Making (London: Routledge, 2005). 363 Vogel, supra note 350 at 566. 364 D. Dinan, Ever Closer Union: An Introduction to the European Union, (London: Macmillan, 1999) at 407. 365 Ibid. 366 Ibid. at 408-409. 367 E.C., Treaty of Amsterdam Amending the Treaty on European Union, the Treaties Establishing the European Communities and Certain Related Acts, [1997] O.J.L. C 325/5, online: Europa < http://eur-> (last modified: 24 December 2002). [hereinafter Treaty of Amsterdam]. 368 European Union, Public Health: Background Cross-Border Healthcare (Luxembourg: Publications Office of the European Union, 2009), online: EUROPA < border_healthcare_en.htm> (date accessed: 14 January 2009). 369 “EU Reaches Deal on Banning Toxic Pesticides” EurActiv (19 December 2008), online: EurActiv <> (last modified: 22 December 2008).  49  Evaluation and Authorisation of Chemicals (REACH).  In addition, there is a current proposal for a directive on ambient air quality for Europe and for a framework directive on pesticides.370  As a result of the 6th EAP, the Directorates-General of Environment, Health and Research and the Joint Research Centre published the Health Strategy. The strategy’s aim is to aid in information gathering and coordinate amongst all levels of the EU in reducing risk. Both Agenda 21 and the earlier transnational agreements demonstrate that though international recognition of health and environment has been made, these agreements tend to lack any binding or enforceable standards.  The relatively new paradigm of environmental health in relation with the varying abilities of developing and developed nations has produced little in effect of bettering westernized nations.  These same problems are evident in international doctrines which have focused on children directly. 3.3 Children’s Environmental Health: International Agreements It is well understood that children are not little adults, and, in fact, have a higher rate of susceptibility to harm from exposure to hazardous toxins.371  And though international bodies, non-governmental organizations, and even some national governments have begun to recognize the importance separate consideration and analysis of children is in policy, the number of effective international doctrines mandating clear requirements is few and far between.  In much of the literature on children’s environmental health, praise has been given to those agreements which have made any mention of children whatsoever.372  However, after decades of epidemiological studies indicating the physiological and behavioural differences of children there is sufficient scientific and public support in setting explicit exposure reduction rates.  Similar accomplishments have been made at an international level with regard to reducing lead, POPs, and hazardous materials as will be referenced in the following two sections. Therefore, it is reasonable that those agreements which have outlined children’s vulnerabilities could have taken it a step further and set forth standards, frameworks, and deadlines. This section will provide a general overview of some of those doctrines which have highlighted children’s environmental health, as well as some of the principles and conventions which are most often affiliated with the field. Transnational agreements which have made an impact on children’s environmental health will also be reviewed. It is worth noting that it would be difficult to mandate clear requirements and deadlines on a truly international scale.  The current status of children’s environmental health is divergent among nations.  A glaring contrast in policy protection for children’s health differs between that of industrialized and developed nations.  A child in Bangladesh is exposed to arsenic contamination in ground water and most likely does not live in an area where sanitation or solid waste  370 Communication from the Commission to the European Parliament, The Council, the European Economic and Social Committee and the Committee of the Regions on the Mid-Term Review of the Sixth Community Environment Action Programme, COM (2007) 225 Final, online: Commission of the European Communities <http://eur-> (last modified: 30 April 2007). 371 Landrigan 1999, supra note 171 at 1; Wargo, supra note 26. 372 Landrigan , ibid.; P.J. Landrigan & G. Tamburlini, “Editorial: Children’s Health and the Environment: A Transatlantic Dialogue” (2005) 113:10 Environ. Health Perspect. A646 at A646.  50  disposal is in place.373  The health effects of these problems for this child, though disproportionately higher than those of Bangladesh adults, are not a pressing issue where civil unrest routinely occurs and basic human rights have not been granted.374  This is in contrast to a child in Norway where the government is actively working towards including children in community planning375, infant mortality rates are extremely low376, and children are clearly identified in policy as a vulnerable subpopulation377.   Setting standards at an international level which would require both Bangladesh and Norway to better their environmental health protection is highly unlikely.  The standards would have to take into consideration the least progressive nation, therefore eliminating any binding requirements for industrialized nations such as Norway.  Nevertheless, this dichotomy between developing and developed nations does not excuse similar nation-states from taking action. 3.3.1 The United Nations International bodies have been fundamental in bringing children’s environmental health to the forefront of consideration.  As will be discussed in further detail in this section, this motivation has been in part due to national pressures (both from governmental bodies and non-governmental organizations) for an international discussion.  One such international organization that has been effective in bringing awareness to children’s environmental health at a global scale is the UN.  It is important to stress that this recognition, though useful, has been more effective in developing nations. Organizational bodies within the UN framework, as well as those at a national level, have taken on implementation of basic rights recognized by the UN and the signatory countries. Beginning with the UN Convention on the Rights of the Child (UN CRC), the UN has assisted in educating on the universal basic rights of health and care a child should have.  This has enveloped the right to safe drinking water, adequate sanitation, and healthy environmental conditions.378  Nevertheless, the functionality of these rights to require industrialized nations to improve their environmental conditions is not there.  The UN has, though, made an impact in increasing awareness  373 World Health Organization, Country Health System Profile Bangladesh – Health and Environment (Geneva: WHO, 2007), online: WHO <> (date accessed: 6 August 2008). 374 U.S., “Background Note: Bangladesh” (Washington, D.C.: U.S. Department of State, 2009), online: U.S. Department of State <> (date accessed: 3 January 2009). 375 European Union, “Norway – Steps Towards Implementation of Budapest Commitments” (Geneva: WHO/EUROPE European Environment and Health Committee, 2005), online: EEHC <> (last modified: 10 October 2005). 376 In 2004, 3.2 infants out of 1,000 live births in Norway die within the first year of life. Highlights on Health in Norway, (Copenhagen: World Health Organization Regional Office for Europe, 2005), online: WHO Europe <> (last modified: 2005); The Environment and Health for Children and their Mothers, (Copenhagen: World Health Organization Regional Office for Europe, 2005), online: WHO Europe <> (last modified: February 2005). 377 Norway, The Norwegian National Environment and Health Action Plan (Oslo: Norwegian Ministry of Environment and Ministry of Health and Social Affairs, 2001), online: < and-h.html?id=105635> (date accessed:15 January 2009). 378 Office of the United Nations High Commissioner for Human Rights & World Health Organization, The Right to Health UN Fact Sheet No. 31, 2008, online: UN <> (last modified: June 2008).  51  towards remedying the socioeconomic disparities that result in children in developing nations experiencing high levels of environmental exposures.379 The CRC was the result of ten years of efforts by the Working Group on the Question of a Convention on the Rights of the Child.380  While not directly focused on the relationship between children and exposure to environmental hazards, the doctrine has led to legal query by scholars and governments alike on how far these rights extend.  This convention built upon the Geneva Declaration of the Rights of the Child of 1924, the United Nations Declaration on the Rights of the Child adopted in 1959, the Universal Declaration of Human Rights, the International Covenant on Civil and Political Rights, and the International Covenant on Economic, Social and Cultural Rights.381  Children are highlighted as a subpopulation that “needs special safeguards and care, including appropriate legal protection, before as well as after birth.”382  Of particular relevance to children’s environmental health is Article 24, which holds that state parties “recognize the right of the child to the enjoyment of the highest attainable standard of health and to the facilities for the treatment of illness and rehabilitation of health”.383  It is within this article that the explicit right to clean water is mentioned.384  While the main objective of this convention was not to promote policy relevant to children’s environmental chemical and pollutant exposure, literature on the topic has looked to this doctrine as a relevant starting point.385  Discussion of the CRC stresses that this convention was a manifestation of a changing social environment where children were to be protected.386  For some nation-states, the CRC merely reaffirmed rights already assumed under domestic law.  The Finnish Child Custody and Rights of Access Act passed in 1983 and the Norwegian Children’s Act of 1981 are just two examples of domestic legislation which not only enforces the basic rights of the child (nutrition, freedom from poverty, health care), but also identifies the ability of children to actively participate in decision-making.387  However, other nations, such as the UK, have been criticized for failing to implement the convention to the fullest extent possible.388  Additionally, many of those authorities with direct  379 Critics hold that this awareness has not resulted in the reduction of infant mortality. A. Wagstaff et al., “Child Health: Reaching the Poor” (2004) 94:5 Am. J. Public Health 726 at 726-727. 380 S. Detrick, J. Doek, & N. Cantwell, The United Nations Convention on the Rights of the Child: A Guide to the “Travaux Préparatoires (Leiden, The Netherlands: Martinus Nijhoff Publishers, 1992) 1-3. 381 Convention on the Rights of the Child, GA Res. 44/25, UN GAOR, online: UN High Commissioner for Human Rights <> (date accessed: 15 July 2008). 382 Ibid. 383 Ibid. 384 Ibid. 385 S. Bartlett, The UN Convention on the Rights of the Child Reporting System and the Physical Environment, (Stockholm: Save the Children Sweden, 2002), online: Save the Children Sweden <> (date accessed: 12 December 2008); A. Davis & L.J. Jones, “Children in the Urban Environment: An Issue for the New Public Health Agenda” (1996) 2:2 Health Place 107 at 111; P.H. Gleick, “The Human Right to Water” (1998) 1:5 Water Policy 487 at 489-490. 386 M. Freeman, “The Future of Children’s Rights” (2000) 14:4 Child Society 277; M.A. Freeman & P.E. Veerman, The Ideologies of Children’s Rights (Leiden, The Netherlands: Martinus Nijhoff Publishers, 1992). 387 B. Franklin ed., The New Handbook of Children’s Rights: Comparative Policy and Practice (London: Routledge, 2002) at 23. 388 Ibid. at 97.  52  interaction with children, such as teachers and welfare practitioners, do not appear to be well informed about the CRC.389 3.3.2 The World Health Organization For developing nations, the recognition of the rights of the child may be a first step in moving towards a more progressive health and environmental policy which takes children into account.  Similar projects launched by the UN have aided in strengthening governance and reducing poverty, both of which are essential prior to tackling the hardships of environmental pollution.  While relevant to children’s environmental health in general, they are less influential in countries such as Canada, the US, and Sweden where these standards have been long ago instituted. International organizations, such as the World Health Organization (WHO) and the Organization for Economic Co- operation and Development (OECD), have had greater success in moving towards a better understanding of the field of children’s environmental health.  Both organizations have aided in data sharing and in the recognition of knowledge gaps in the field.  Interestingly, much of the efforts by both bodies have been in part due to collaboration with the European Union European Environment Agency (EEA). The WHO has played an important role in bringing awareness to a child’s susceptibility to environmental toxins.  For the most part, the focus of the WHO has been on morbidity and mortality of children in developing nations, in a great part because of toxic exposures.  It has been estimated that as much as thirty-six percent of deaths of children (0-14 years of age) is due to exposure to environmental toxins.390  Many of these deaths are due to respiratory infections, diarrhea, and vector borne disease391.392  A high percentage of these deaths occur within developing nations where use of biomass fuels, contaminated water, and poor sanitation are more common. Prioritization of what countries need to be the focus of the WHO necessarily results in concentration on developing nations with high levels of environmental burden of disease and communicable diseases.393 However, this is not to say that the efforts of the WHO have not been valuable to the increasing awareness and the development of policy within developed nations.  The WHO Europe has been able to assist western nations in addressing children’s environmental health issues.  Research supported by WHO Europe has produced data on the  389 Ibid.  at 112. 390 T.G. Gavidia, J. Pronczuk de Garbino, & P.D. Sly, “Children’s Environmental Health: An Under-Recognized Area in Paediatric Health Care” (2009) 9 BMC Pediatr. 10 at 11.  A. Prüss-Üstün & C. Corvalán, Preventing Disease through Healthy Environments (Geneva: WHO, 2006) at 6. 391 Vector borne diseases are those transmitted by mosquitoes. It is estimated that 1.3 million deaths for children under the age of five each year are a result of diarrhoea and 2 million die due to respiratory disease. World Health Organization, What Happens When Children Live in Unhealthy Environments? Healthy Environments for Children: Facts and Figures (Geneva: WHO, 2003), online: WHO <> (last modified: April 2003). 392 Ibid. 393 T. Boonyakarnkul, A.P. Kingston, & M.K. Shea, World Health Organization: Specific Environmental Threats: Sources of Exposure and Health Effects (Geneva: WHO, 2004), online: WHO <> (date accessed: 10 May 2009); D. Briggs, E. Rehfuess, & C. Corvalan, “Global Initiative on Children’s Environmental Health Indicators” (Workshop on Environmental Threats to the Health of Children in the Americas, Lima, 9-11 April 2003).  53  effects of air pollution in general, and more specifically on transport pollution and the effect of particulate matter on children.  Research conducted by WHO Europe indicates that though European children are exposed to fewer pollutants than developing nations, there is still need to address pollutant pathways.  “Between 1.8% and 6.4% of all deaths among European children up to 4 is caused by outdoor air pollution by fine particulates. Some 4.6% of deaths in the same group are attributed to indoor air pollution by smoke from solid fuel burning. A further 5.3% of deaths in children up to 14 are attributed to dirty water or sanitation.”394  In response to these numbers, the WHO Europe, in conjunction with European Union European Environment Agency, has commenced projects that target children`s vulnerability to environmental harms. In 1989, WHO Europe initiated a dialogue on environment and health, producing the European Charter on Environment and Health.  This declaration recognized the need for reliable scientific data and effective policy to promote environmental and health action.395  “Specific recommendations [have been] made in areas such as air quality, drinking-water and wastewater, solid waste and radiation. Target Ten in the policy states that, by the year 2015, people in the WHO European Region should live in a safer physical environment, with exposure to contaminants hazardous to health at levels not exceeding internationally agreed standards.”396  Further international promotion of environmental health was affirmed in June 1999, at the Third Ministerial Conference on Environment and Health hosted by WHO Europe.397  The Third Ministerial Conference recognized the “special vulnerability of children” and committed to “develop policies and actions to achieve a safe environment in which children can develop to their highest attainable levels of health”.398  Thus children’s health standards were elevated from that of “internationally agreed standards”399 to that of the “highest attainable level of health”400. Within WHO Europe sits the European Environment and Health Committee (EEHC) which is a coalition of health ministries, environment ministries, non-governmental organizations (NGOs), and intergovernmental organizations. This team of experts and government officials have been tasked with the responsibility of overseeing the implementation of Children’s Environment and Health Action Plan for Europe (CEHAPE) objectives.  CEHAPE, aimed at policy makers, was adopted by the European Ministers at the Fourth Ministerial Conference on Environment and Health (2004).  The purpose of the CEHAPE is to provide a framework for which member states  394 “WHO Talks Up Scale of Environment-Health Risks” ENDS Europe  (21 June 2004), online: ENDS Europe <> (last modified: 21 June 2004). 395 G.H Brundtland, “Environment and Health: Europe’s Partnership Can be a Model” (1999) 318:7199 Br. Med. J. 1635 at 1636. 396 WHO Working Group, Establishing the International Network on Children’s Health, Environment and Safety, WHO Europe, EUR/ICP/EHRO 02 06 02, online: WHO Europe <> (date accessed: 15 November 2008). 397 WHO, Fourth Ministerial Conference on Environment and Health, WHO Europe EUR/04/5046267/7, online: WHO Europe <> (last modified: 25 June 2004). 398 U.S., Environmental Protection Agency, 1997 Declaration of the Environment Leaders of the Eight on Children’s Environmental Health (Washington, D.C.: Environmental Protection Agency, 2009), online: Environmental Protection Agency <> (last modified: 27 November 2009). 399 Ibid. 400 Ibid.  54  can use in analyzing the current state of children’s environmental health within their jurisdiction.  CEHAPEs are advantageous to children for a few reasons.  One, the objectives are clearly defined.  Regional priority goals include: (1) ensure safe water and adequate sanitation, (2) ensure protection from injuries and adequate physical activity, (3) ensure clean outdoor and indoor air, and (4) aim chemical-free environments.  Also, the objectives are aimed at children.  Specifics have been outlined as to how each of these objectives can be met.  For instance, in order to reduce chemical exposure the EU aims to ensure that the obligations of the Stockholm Convention on Persistent Organic Pollutants, the Basel Convention on the Control of Transboundary Movements of Hazardous Wastes and their Disposal, and the Rotterdam Convention on the Prior Informed Consent Procedure for Certain Hazardous Chemicals and Pesticides in International Trade are fulfilled.401  Secondly, due to the relatively similar state of children’s environmental health within the region of WHO Europe and the EU, standards and recommendations are set for industrialized nations.  A third reason for the successfulness of the CEHAPE is that there is constant monitoring of progress and failure.  Evaluation by country is submitted to the CEHAPE Task Force on a regular basis.  Because the CEHAPE requires specific action to be taken by member-states, positive outcomes have resulted. For instance, within the UK government assessed in detail the current status of each priority goal within the nation for future policy development.402  Lastly, the project has a target audience of policy makers rather than the science community.  The EEHC and the WHO Europe have been fundamental in “facilitating, promoting and coordinating” international cooperation.403  The work conducted by the EEHC has incorporated the efforts of non-governmental entities, scientists, and representatives of national health and environment ministries.  It is this team of experts and governmental officials that has been tasked with the responsibility of overseeing the implementation of CEHAPE objectives.  401 WHO 2004, supra note 397. 402 U.K., Children’s Environment and Health Action Plan, (London: Health Protection Agency, 2007), online: HPA <> (date accessed: 3 June 2009). 403 L. Licari, L. Nemer, & G. Tamburlini, Children’s Health and Environment: Developing Action Plans, (Geneva: WHO European Office, 2005) at 43.  55  3.3.3 The Organisation For Economic Co-Operation And Development Similar to the WHO, the Organisation for Economic Co-Operation and Development has been fundamental in gathering data and fostering meetings with regard to standard setting relevant to children’s exposure rates.  The OECD actively works towards harmonizing testing and assessment protocols and preventing the repetition of research through data sharing.404  As children’s environmental health is one focus of the OECD’s environmental- social interface, the objective is to assist policymakers in making informed decisions pertaining to the health and safety of children.405  A portion of their efforts has been utilized to identify environmental health indicators which establish clear links between health impact and environmental hazards.406  For instance, the Valuation of Environment-Related Health Impacts program considers values used for monetisation of environment-related health impacts.407  Similar studies in the past have imposed adult values on children’s health outputs.  The OECD, in cooperation with the European Commission’s Directorate General for Research, has worked towards producing reports on willingness to pay (WTP) and quality of adjusted life years (QALY) frameworks with focus on children’s environmental health.408  The hope is that these studies and surveys will be of use in developing future policy within OECD member-states, and in particular the EU.  Funded by the European Commission’s Directorate General for Research, the OECD hopes to facilitate the gathering of information from the research teams on three objectives: (1) review of epidemiological studies, (2) review of economic studies on willingness to pay to reduce environmental risks to children’s health, and (3) evaluation of environment-related health impacts.409 While the majority of the efforts by the OECD have been on gathering data and formulating evaluative tools on children’s environmental health in general, specific areas of pollution have been targeted by the organization.  The OECD 1990 Decision-Recommendation on the Co-operative Investigation and Risk Reduction of Existing Chemicals (C(90) 163/Final) aims at reducing negative health outcomes due to chemicals released into the environment.410  404 H.B. Koëter & R. Visser, “Work in OECD on Chemical Safety: Approaches for Human Risk Assessment” (2000) 38:2 Ind. Health 109 at 110. 405 OECD Environment Directorate, Children’s Environmental Health (Paris: OECD, 2008), online: OECD <,3343,en_2649_32495306_35143376_1_1_1_1,00.html> (last modified: 14 November 2008). 406 Environment Directorate Environment Policy Committee, Children’s Environmental Health Indicators: A Survey, OECD, 2004, ENV/EPOC/WPNEP(2004)16/FINAL, online: OCED <$FILE/JT00189055.PDF> (date accessed: 12 December 2008). 407 Valuation of Environment-Related Health Impacts with a Particular Focus on Children, OECD, online: OECD <$FILE/JT00189055.PDF> (date accessed: 2 March 2009). 408 Ibid.; J. K. Hammitt, Methodological Review of WTP and QALY Frameworks for Valuing Environmental Health Risks to Children (OECD, 2005), online: OECD < tp+and+qaly+frameworks+&hl=en&as_sdt=2000> (date accessed: 14 July 2008). 409 Background Reading: Valuation of Environment-Related Health Impacts, (OECD), online: OECD <,3343,en_21571361_36146795_36283596_1_1_1_1,00.html> (date accessed: 14 July 2008). 410 Environment Directorate Environmental Health and Safety Division, Risk Reduction Monograph No. 1 Lead Background and National Experience with Reducing Risk, OECD, 1993, OCDE/GD(93)67, online: OCED  56  Additionally, the 1996 OECD Environment Ministers Declaration on Risk Reduction for Lead is an example of steps member states have taken under this declaration to diminish exposure in both adults and children.  This declaration has helped inform legislation in nations as well as industry behaviour.411  Elimination of exposure to lead from products intended for children are specifically outlined within the declaration.412  However, the declaration relies heavily on voluntary efforts to reduce exposure and production with no set deadlines or requirements to be met.413 For instance, though Canada is a signatory to the declaration which mandates reduction in exposure rates, Health Canada’s Consumer Product Safety group did not establish a procedure to prohibit consumer exposure to lead until 2004.414  Alternatively, the OECD’s efforts did result in the European Union’s Pan- European strategy to phase out leaded petrol by January 1, 2005.  Signed at the Fourth Ministerial Conference, motivation for this declaration included the health of the vulnerable populations, such as children.415  This was particularly effective for Eastern European nations that had not taken the necessary steps to mandate the use of unleaded gasoline.  Implementation remains a constant problem. 3.3.4 The Miami Declaration Although the UN, WHO, and OECD have made headway in bridging knowledge gaps and gathering intellectual and financial resources that aid in reducing children’s environmental hazard exposure, their main objectives have not been that of children’s environmental health.  The policy proposals they have produced do not mandate any specifics to be met, except in those cases where the EU has put in legislation with standard requirements.  These organizations have not produced international agreements which focus solely on children’s environmental health.  Due to the sparse number of international doctrines directly addressing children’s environmental health, those that do are often portrayed as successful.416  While these agreements may lend themselves to bringing awareness to the vulnerabilities that children face when exposed to toxins, they fail to hold signatories accountable or set specific standards.  The Miami Declaration is often cited as a landmark agreement in children’s environmental health, bringing the topic to  <> (date accessed: 3 June 2009); OECD, Council on the Co- operative Investigation and Risk Reduction of Existing Chemicals, Decision-Recommendation of the Council on the Co-operative Investigation and Risk Reduction of Existing Chemicals, OECD, 1991, C(90)163/Final, online: OECD <>  (last modified: 31 January 1991). 411 “International Lead Management Center Reducing the Risk of Lead Exposure” Lead Action News (18 February 2008), online: Lead Action News <> (last modified: 18 February 2008). 412 Declaration on Risk Reduction for Lead, OECD, 1996 C(96)42/Final, online: OECD <> (last modified: 19 February 1996). 413 “Reducing the Risk of Lead Exposure” Lead Action News (26 January 2009), online: Lead Action News <> (last modified: 26 January 2009). 414 W. Bell & K. O’Grady, “Lead Poisoning in Children” (2004) 171:5 C.M.A.J., online: CMAJ <> (last modified: 31 August 2004). 415 United Nations Economic Commission for Europe, Pan-European Strategy to Phase Out Leaded Petrol, UN ECE, 1998, online: UN Bibliographic Information System <!440 418~!6&ri=1&aspect=alpha&menu=search&source=~!horizon#focus> (date accessed: 15 December 2008); European Conference of Ministers of Transport, Resolution No. 99/6 on Phasing Out Lead in Petrol, CEMT/CM(99)25/FINAL. 416 Sharpe, supra note 56 at 96.  57  the forefront of policy dialogue in developed nations (G-8 nations).417  The efforts set forth in the declaration have been reaffirmed in the Banff Ministerial Statement on the World Summit on Sustainable Development in 2002. However, the Miami Declaration was a product of pressures by the US to bring attention to children’s environmental health, an effort which decreased in urgency with the following change of presidential administration.  Similarly, the efforts to bring attention to children’s environmental health in the North American context, under the pretext of NAFTA, failed to hold countries accountable to specific standards.  The following portion of this section will review these two agreements and their ineffectiveness in changing children’s environmental health. The 1997 Declaration of the Environment Leaders of the Eight on Children’s Environmental Health has provided an international forum on children’s environmental health.  A multitude of events led up to the Miami Declaration, including the 1990 EPA and International Life Sciences Institute symposia on Similarities and Differences Between Children and Adults: Implications for Risk Assessment418  and efforts to recognize children’s vulnerabilities in the US policy Food Quality Protection Act in 1996. 419  Prompted by the US EPA and President Clinton, this meeting of the G8 countries (Canada, France, Germany, Italy, Japan, the Russian Federation, the United Kingdom, the United States of America, and the European Union) outlined topics of focus, including lead reduction, providing microbiologically safe drinking water, undertaking research on air quality effects on children, eliminating environmental tobacco smoke exposure, gathering inventory on research concerning endocrine disrupting chemicals, and considering the impact of global climate change on children’s health.420  While this doctrine is legally non-binding, it has served as a motivational tool for nation-states for research and, to a lesser degree, relevant policy. Signatories of the declaration pledged “to establish national policies that take into account the specific exposure pathways and dose-response characteristics of children when conducting environmental risk assessments and setting protective standards.”421  Each nation-state has made efforts to address some if not all of the issues outlined in the doctrine.  The commitments made by the countries are helpful in highlighting the vulnerabilities of children, but fail to set standards or guidelines, or resolve issues surrounding knowledge gaps.  Each nation-state has made legislation citing the Miami Declaration, but the policy differs in consideration of children’s health.  Canada has focused on developing climate change human health impact assessment guidelines, while Germany committed to reducing carbon dioxide emissions by twenty-five percent of the 1990 levels by the year 2005.422  This illustrates that the science and the policy- making process may result in different outcomes though agreement has been made at an international level that action needs to be taken.  417 Ibid. 418 This was one of the first conferences on children’s environmental health. 419Sharpe, supra note 56 at 96. 420 1997 Declaration of the Environment Leaders, supra note 398. 421Ibid. 422 Canada, Status Report on Implementation of the 1997 Declaration of the Environment Leaders of the Eight on Children’s Environmental Health (Ottawa: Government of Canada, 2002), online: EPA <$File/G8report.pdf> (last modified: April 2002).  58  The Miami Declaration has instigated consultation at an international level on children’s environment health; however, it lacks clear requirements of compliance.  Some of the objectives of the declaration have merit, such as the request made that the International Organization on the Management of Chemicals and the US EPA to create an inventory on international research on endocrine disrupting chemicals.  However, the nations not only aren’t required to meet certain goals by predetermined deadlines, but follow-up on the issue is left to the devices of the nations with vested interests in the field.  The topic of environment and health first appeared on the G8 agenda in 1996.423  The 1997 Miami Declaration focused on environment and health in relation to children, with follow-up discussion at the 2002 Banff G8 meeting.  Additional consideration of the topic of children’s environmental health by the G8 ministers of environment has not been acted upon.  Though progress has been made in the area of children’s environmental health following the Miami Declaration, much of this would have taken place regardless of the agreement.  At the time the US administration was highly supportive of improving children’s health outcomes due to hazardous exposure and it is likely efforts taken by the US EPA in conjunction with Canada and Mexico to improve waterways would have occurred.424  Although the reduction of lead exposure is held out as a sign of progress in the 2002 review report, this was a recognized issue of concern long before the G8 meeting.425 The review of progress to date on the Miami Declaration conducted in 2002 illustrates that all G8 nations still had not yet explicitly considered children as a component of the risk assessment for water standards.426  The application of efforts to reduce exposure to endocrine disrupting chemicals has illustrated how the vague terminology of the Miami Declaration can result in differing outcomes. The G8 ministers of the environment pledged to develop “pollution prevention strategies, as major sources and environmental fates of endocrine disrupting chemicals are identified”.427 Relevant policy in Europe has banned the use of phthalates not only in toys but cosmetics, whereas Canada has done so for toys only, and the US EPA for none of the above.428  423 “G7 Environment Ministers’ Meeting” (G7 Meeting, Cabourg, France, 9-10 May 1996), online: U of T G8 Information Centre <> (date accessed: 3 June 2009). 424 C. Browner, “G-8 Environment Ministerial Follow up Report from Miami Meeting” (Leeds Castle, England, 4 April 1998), online: EPA < 3cc!OpenDocument> (last modified: 4 April 1998). 425 Environment Ministers’ Meeting, supra note 422. 426 Ibid. 4271997 Declaration of the Environment Leaders, supra note 398. 428 Sharpe, supra note 56 at 93; Canada, Chemical Substances Canada, Phthalates, (Ottawa: Chemical Substances Canada, 2007), online: Chemical Substances Canada < interet/phthalates_e.html> (last modified: 20 April 2007); J. Walsh, “EPA Should Pursue Cumulative Risk Assessment of Phthalates and Other Chemicals” Press Release from the National Academies (18 December 2008), online: National Academies <> (last modified: 18 December 2008).  59  3.4 Regional Agreements: Europe While the Miami Declaration may be heralded as a success in bringing awareness to the issue of children’s environmental health429, regional agreements have made a larger impact on actual exposure rates.  Regional agreements have been used specifically for the protection of children’s health.  Preventative measures with specific consideration of children’s environmental health have been employed to a great extent in Europe by the European Union and Nordic Committee of Senior Officials for Social and Health Affairs. The European Union’s Science, Children, Awareness, Legislation and Evaluation (SCALE)430 project focuses on children’s vulnerabilities with concentration on childhood respiratory diseases, neurodevelopmental disorders, cancer, and endocrine disrupting effects.431  Not only are children highlighted in this project, but it incorporates the monitoring of pollutant levels and childhood health indicators.432  Information gathered from this project led to the development of the European Environment and Health Action Plan 2004-2010.  Criticism has been made regarding the Action Plan’s slow progress in developing policy based on research outcomes from SCALE.  What makes this situation different from that of the Miami Declaration, though, is the willingness of EU officials to remedy the situation.  In 2005, EU Members of Parliament (MEPs) voted in favour of a report433  which provided on evaluation of the strategy and took necessary legislative action to reduce exposure to phthalates, chlorinated solvents, mercury, cadmium, and some pesticides.434 While the efforts by the EU are legislatively binding on member states, there are examples of voluntary transnational agreements which impact children’s environmental health.  The Nordic Council of Ministers, formed by Denmark, Finland, Norway, and Sweden, developed a working group to address children’s environmental health issues.  For instance, air pollution has been a topic of discussion where children’s health has been specifically outlined for consideration in areas such as the distance between schools and major traffic.435  Simple ideas, such as use of green space, have been addressed.  In August, 2005, the Council of Ministers adopted the Odense Declaration which recommended that daycare centers in Nordic countries be no further than five miles from green spaces which they could utilize.436  To follow-up on this declaration, the Council has commissioned a pilot study to review the policy  429 Sharpe, supra note 56 at 93. 430 E.C., Communication “A European Environment and Health Strategy” [2003] COM (2003) 338 final, online: EurActiv <> (last modified: 11 June 2003). [hereinafter Com(2003) 338 final]. 431 Ibid. 432 Ibid. 433  The EU ministers voted to ban the use of phthalates in children’s toys in 2004. Efforts have been taken by the EU to eliminate export of mercury and decrease use and emissions by 2011. Cadmium in consumer batteries has been partially banned, with exceptions for power tools. Additionally, 110 active substance found in pesticides have been removed from the market by the end of 2003. 434 “Industry Deplores MEP Vote on Environment and Health Plan” EurActiv News (24 November 2006), online: EurActiv News < plan/article-135911> (last  modified: 24 November 2006). 435 S. Herfelt, Nordic Synergy: The Day-Care Environment and Children’s Health (Copenhagen: Nordic Council, 2007), online: Nordic Council <> (date accessed:15 January 2009). 436 Ibid.  60  instruments needed to address the effect of local particle pollution and chemicals substances on children’s environmental health.437 3.5 Regional Agreements: North America Regional agreements addressing children’s environmental health are also present in North America.  Although the relationship between human health and the environment has been evolving in both Europe and North America, the method by which this topic has been approached differs.  Within the United States, a great deal of the success children’s environmental health has had at a national level has been linked to President Clinton.  The United States was fundamental in motivating international symposiums and declarations on the topic of children’s environmental health, mostly due to the EPA administration, President Clinton, and Vice President Gore.438  The Miami Declaration and the follow-up meeting, the World Summit on Sustainable Development (Johannesburg, 2002), elevated the awareness of the vulnerability of children to exposures.  However, what has been of value to regional responsiveness has been the NAAEC.  A parallel treaty to the North American Free Trade Agreement, this regional declaration was signed by Canada, Mexico, and the United States and came into effect on January 1, 1994.439  The NAEEC is overseen by the Commission for Environmental Cooperation (CEC) which consists of the Council, Joint Public Advisory Committee (JPAC) and the Secretariat.  The CEC’s Expert Advisory Board on Children’s Health was created to provide the CEC Council with advice and recommendations on “issues related to environmental threats to children’s health in North America”.440 Concern surrounding the NAFTA’s perceived ineffectual ability to address environmental issues, as well as environmental issues that had arisen under the General Agreement on Tariffs and Trade (GATT)441, led to the drafting of the NAAEC.  The agreement has been frowned upon for its reliance on litigation rather than cooperation442, as well as for its failure to address local polluters (the focus being on specific transboundary issues such as pollution in the Great Lakes).443  437 Ibid. 438 Goldman, supra note 6 at 445; Landrigan 1999, supra note 171 at 7. 439 Secretariat of the Commission for Environmental Cooperation, North American Agreement on Environmental Cooperation between the Government of Canada, the Government of the United Mexican States and the Government of the United States of America, 1993, online: Commission for Environmental Cooperation <>. 440 NAFTA, Expert Advisory Board, Children’s Heath and the Environment in North America, (Commission for Environmental Cooperation, 2008), online: CEC < eUSC_EN.pdf> (date accessed: 12 December 2008). 441 J.O. Saunders, “NAFTA and the North American Agreement on Environmental Cooperation: A New Model for International Collaboration on Trade and the Environment” (1994) 5:273 Colo. J. Int. Environ. Law Policy 273 at 274 & 282. 442 M. Spalding & J. Audley, “Promising Potential for the US-Mexico Border and for the Future: An Assessment of the BECC” (1997) NADBank Instit.; C. Deere & D.C. Esty, Greening the Americans: NAFTA’s Lessons for Hemispheric Trade, (Boston: MIT Press, 2002) at 187. 443 G.C. Hufbauer & J.J. Schott, North American Free Trade: Issues and Recommendations (New York: NYU Press, 1992) at 131.  61  Although the NAAEC has been criticized for being weak on requirements444, it has been recognized as a collective effort to discuss environmental issues in relation to international trade.445  The right to establish protection standards lies with each nation, independently.  However, the caveat is that these measures are to be based on “scientific principles” and risk assessment “as appropriate to the circumstances”.446  The relationship between health and environment is recognized in the agreement and throughout the CEC’s publications. The CEC has been constructive in providing a transboundary forum to discuss children’s environmental health. Published in 2006, Children’s Health and the Environment in North America: A First Report on Available Indicators and Measures, reviews three priority areas: (1)Asthma and Respiratory Disease, (2) Exposure to Lead and Other Toxic Substances, and (3)Waterborne Diseases.447  By producing this report, each nation gained an understanding of knowledge gaps and policy needed.  Similar reports on chemicals, metals, air pollution, and border traffic (US- Mexican Border) have been published. Though the CEC has been beneficial in information gathering and bringing awareness to the issues that children face in North America, it has not mandated standards or addressed local pollution.  As with other international agreements mentioned earlier, the differing pollution burdens amongst the parties may place an undue burden on Mexico or result in little change in Canada and the US to prevent this hardship.  The report recognizes that indicators and data gathering is only a first step and that further action is needed to truly improve the state of health for children in North America.  In 2002, Council Resolution 02-06: Cooperative Agenda for Children’s Health and Environment in North America was one such measure which strengthens trilateral efforts to reduce exposure rates.  Outlined in the agenda is an affirmation to reduce lead exposure in consumer products transferred by cross-border trade, continue to assess cross-border diesel exhaust’s impact on childhood health, and integrate children’s environmental health into the work of the CEC’s Sound Management of Chemicals program.448 3.6 Children’s Environmental Health: International Agreements Addressing Chemicals and Pesticides There are a number of international doctrines which address chemicals and pesticides in general.  The first section in this chapter outlined how international doctrines pertaining to pollutants, which are not specifically focused on children, can have a positive outcome on their health status.  The impact of international doctrines on chemical and pesticide management also do the same; however, they will only be referenced briefly in this section.  Rather, the objective is to provide context on international and transnational agreements which focus on children’s exposure to chemical toxins and pesticides.  444 C.A. Grant, “Transboundary Air Pollution: Can NAFTA and NAAEC Succeed Where International Law has Failed” (1994) 5 Colo. J. Int. Environ. Law Policy 439 at 447-450. 445 Saunders, supra note 441 at 279. 446 Ibid. at 281; Secretariat of the Commission for Environmental Cooperation, supra note 439. 447 Commission for Environmental Cooperation, supra note 123. 448 Cooperative Agenda for Children’s Health and the Environment in North America, CR 02-06, C/02- 00/RES/06/Final, online: CEC <> (last modified: 19 June 2002).  62  International agreements such as the Basel Convention on the Control of Transboundary Movements of Hazardous Wastes and their Disposal, the Rotterdam Convention, and the Stockholm Convention on Persistent Organic Pollutants are some of the more notable transnational agreements that made strides in reducing transboundary hazardous waste.  The Basel Convention was the first global environmental treaty to regulate hazardous waste, acting as a starting point for the following two conventions.449  Specifically aimed at preventing the transport of hazardous wastes from developed to developing nations, the Basel convention mandates that “Prior Informed Consent” be applied before shipments of waste are made and that wastes are managed in an environmentally sound manner (ESM).450  Building upon these principles, the Rotterdam Convention requires signatories to notify one another of pesticides or chemicals which have been banned due to harmful effects on the environment or health of the population.451  These doctrines provided a basis for the Stockholm Convention; an agreement which bans twelve persistent organic pollutants which are harmful to human health and the environment.452  Though the convention does not specify the consideration of vulnerable groups, one of the motivating factors for the agreement was the presence of POPs in breast milk thereby exposing infants to harmful pollutants.453  The Stockholm Convention does require signatories to include groups involved in the health of children in the implementation plan required under the agreement.454  449 Basel Convention on the Control of Transboundary Movements of Hazardous Wastes and Their Disposal, UNEP (1989), online: Secretariat of the Basel Convention <> (last modified: 22 March 1989); The Basel Convention at a Glance (Geneva: Secretariat of the Basel Convention), online: Secretariat of the Basel Convention <> (date accessed: 13 August 2008). 450 Ibid. 451 Rotterdam Convention Overview, UN EP, online: UNEP <> (date accessed: 15 January 2009). 452 Stockholm Convention on Persistent Organic Pollutants, supra note 211; Good Plant, Stockholm Convention, online: Good Plant < Stockholm-Convention> (date accessed: 14 January 2009); UN EP Chemicals, A Guide to the Stockholm Convention on Persistent Organic Pollutants, UNEP, online: UN <> (last modified: April 2005). 453 Landrigan 2004, supra note 12 at 259. 454 Good Plant, supra note 452; Stockholm Convention on Persistent Organic Pollutants, supra note 211.  63  3.6.1 The Codex Alimentarius Commission Efforts by the WHO and Food and Agriculture Organization of the UN (FAO) to standardize pesticide exposure by food sources has been fostered by the Codex Alimentarius Commission.  The objective of the commission is to provide safe food practices and promote fair trade.455  With the signing of the GATT Agreement in 1994, the standards set by Codex have been used as “reference texts” by the World Trade Organization (WTO) and in international trade.456  Consideration is given of children’s vulnerabilities when suggesting standards for processed cereal-based foods for infants and young children.457  However, this voluntary agreement has been criticized by Consumers International, as well as the governments of Germany and France for its conclusion that additional safety factors for children, in addition to those currently used, are unjustified.458  Controversy amongst nations and NGOs as to the appropriate risk assessment procedures, including whether to expressly consider multiple pesticide exposure pathways, have slowed progress with regards to consideration of childhood exposure to food pesticides.459 3.6.2 Cooperative Agenda For Children’s Health In North America In an effort to address the rates of childhood exposure to chemicals and pollutants in North America, the CEC Council adopted the Cooperative Agenda for Children’s Health in North America in 2002.460  While not mandating standards or requirements, this effort to foster collaboration and gather data on environmentally caused childhood disease has resulted in specific recommendations for Canada, Mexico, and the United States.  Highlighting the fact that nearly half a million tons of chemicals “known or suspected to cause cancer” were used in Canada and the US in the year 2002, the report Toxic Chemicals and Children’s Health in North America calls for greater monitoring, improved scientific knowledge, increased awareness, and implementation of chemical-related disease tracking systems.461   For instance, the Action Plan to Enhance the Comparability of Pollutant Release and Transfer Registers in North America sets forth a framework that aims to harmonize the chemical use monitoring systems of all three countries, particularly requiring Mexico to move from a voluntary reporting system to a mandatory one.462  Though similar reports have been conducted at an international level by the WHO, what is unique about this one is that  455 FAO & WHO, Food Standards Codex Alimentarius, online: FAO/WHO <> (date accessed: 11 October 2008). 456 Consumers International, Codex Alimentarius for Consumers (Rome: FAO/Consumers International,  2000), online: FAO < 9B99-2475BEF47A7D_Doc378.pdf> (date accessed: 3 June 2009). 457 Committee on Nutrition and Foods for Special Dietary Uses, “Report of the 25th Session” (UN FAO/WHO, 3-7 November 2003) (ALINORM 03/27/26), online: FAO <>  (date accessed: 3 June 2009). 458 K. Racke, “IUPAC Representative Report” (32nd Session, Hague, 1-8 May 2000), online: IUPAC <> (date accessed:  3 June 2009). 459 Ibid. 460 Cooperative Agenda, supra note 448. 461 Commission for Environmental Cooperation, Toxic Chemicals and Children’s Health in North America, (Quebec: Secretariat – Commission for Environmental Cooperation, 2006), online: C.E.C. <> (date accessed: 3 June 2009). 462 Ibid.  64  recommendations are specific to each nation-state and based on data from government sources rather than aggregate data on a global scale. 3.7 Conclusion These previous sections provide an overview of international and regional agreements which may have indirectly impacted on children’s environmental health.  Though children’s vulnerabilities to pollutants may not be the sole focus of many international agreements, those agreements often influence exposure rates. What is unfortunate is that children are not specifically outlined as vulnerable and standards which are set tend to be based on the health of the general population.  Additionally, by failing to consider physiological differences of a child prior to implementation, it is difficult to measure whether these agreements have a monumental effect or a negligible consequence on childhood chronic health conditions, morality, and morbidity statistics.  Those agreements which have addressed children specifically have accomplished an escalated level of awareness, but fall short of producing standards and deadlines which must be accomplished by signatories.  Agreements which consider chemical and pesticide exposure, though they tend to be binding and mandate requirements, have not consistently considered children and infants. Furthermore, what is seen throughout all three sections is that much of the impetus for these global doctrines was present in the 1990s and early 2000s, but has steadily decreased, resulting in little monitoring and evaluation.  The result is that pesticide and chemical childhood exposure is left to the governance of nation-states.  65  4. ADDRESSING CHILDREN’S ENVIRONMENTAL HEALTH AT A NATIONAL AND SUPRANATIONAL LEVEL 4.1 Introduction Although the topic of children’s environmental health has achieved notoriety at an international level, little substantial change has come from this globally.  While international doctrines, such as the Stockholm Convention, have had the ability to reduce overall exposure to caustic substances, they have been narrowly focused and only address the most horrible offenders.   Because of this, the responsibility to determine how and what substances should be restricted or banned and how to do this remains with federal or regional jurisdictions.  This chapter will examine how the differing approaches to regulating toxic substances, specifically pesticides and chemicals, taken by Canada, the United States, and the European Union, have resulted in distinctive standards,  the consequence being that those children residing in North America are exposed to more toxins daily than those residing in Europe.  The objective of this chapter is to illustrate why the United States’ and Canada’s use of the risk-based approach in their risk assessment process fails to offer the same protection for children’s health as does the EU’s hazard-based approach.  The reasons for the different levels of protection will be discussed in detail, using the risk assessment of pesticides and chemicals as two case-studies. Indications of the prevalence and impact environmental pollution can have on children’s health were made in chapter two, thereby negating the need to review the epidemiological evidence supporting the assertion that toxic exposure can lead to chronic health conditions and even death.  In order to provide context, however, it is important to note that pesticides and chemicals are unavoidable by the general population, including children.  More than just agricultural or industrial products, pesticides are used in residential settings including schools, daycares, homes, gardens, and parks and are present on food products.  The United States alone used over 102 million pounds of pesticide active substances during the period between years 2000 and 2001.463  The exposures to chemicals are as great a concern as that of pesticides.  Of the 85,000 chemicals available worldwide, many are used in large quantities in schools, hospitals, and homes.464  Over 2,800 of these chemicals are produced in excess of 500,000 kilograms a year.465 In order to control the impact these chemicals and pesticides have on children, Canada, the US, and the EU have put in place legislation that mandates the assessment and management of the use of these substances.  This chapter will provide an overview of these pieces of legislation, focusing on the differences in standards that result because of the distinct risk assessment approaches taken.  Canada and the US have adopted a risk-based approach to risk assessment with the objective to determine what risks from exposures are considered acceptable.  Those substances that pose a  463 T. Kiely, D. Donaldson, & A. Grube, EPA, Pesticides Industry Sales and Usage 2000 and 2001 Market Estimates, (Washington, D.C., EPA, 2004), online: EPA <> (date accessed: 4 October 2009). 464 Wargo, supra note 26. 465 C.A. Mello-da-Silva & L. Fruchtengarten, “Environmental Chemical Hazards and Child Health” (2005) 81 J. Pediatr. 205, online: J. Pediatr. < 75572005000700011&script=sci_arttext&tlng=en> (last modified: November 2005).  66  risk that is unacceptable, often quantified in rates of chronic health conditions, are restricted to the point that exposure is acceptable.  Use of this method relies on science to ensure safety.  However, because of the number of unknowns related to toxic exposure and the governments’ inability to ensure that the necessary data is collected, the use of science alone fails to protect children’s health.  This is in contrast to the recently adopted EU hazard-based approach, which aims to avoid risk through the elimination of the substance when the risk is too great. The reason that this approach provides better protection for children’s health is that it eliminates substances completely rather than relying on a calculated standard to ensure that children’s exposure to a substance does not exceed a safe threshold. This chapter will be divided into three sections.  The first section will provide an overview of the risk assessment approaches taken by each jurisdiction.  The second section analyzes the pesticide legislation of each jurisdiction. This section explains why the risk-based approach used by Canada and the United States does not provide for the protection of children’s health, whereas the EU hazard-based approach reduces the pesticide exposure children experience.  This is particularly bothersome considering pesticide legislation is one of the few examples of environmental policy that has been amended in the US and Canada to account for children’s health.  Included in this section is a case study of how these policies have affected the standards set for pesticide residues on foodstuffs, resulting in higher intake of residue in Canada and the United States. The third section reviews the different legislative approaches to chemicals taken by each jurisdiction.  This section provides a glaring example as to how the risk-based approach fails to protect children from harmful exposure to substances.  This is in contrast to the EU’s legislation which aims at eliminating caustic chemicals to prevent any chance of exposure. 4.2 The Differences In Risk Assessment: The Risk-Based Approach Versus The Hazard-Based Approach Each of the jurisdictions utilizes a risk assessment process to review toxins, including pesticides and chemicals.466 Having evolved over the course of the last fifty years, this process is one that reviews the effects of exposure to toxins on health.  This information is then used to set standards to ensure that use of these pesticides and chemicals is “safe”.  Though the procedure of assessing substances is very similar among all three jurisdictions, the approach used to interpret the data differs. 4.2.1 General Overview Of The Risk Assessment Process Although Canada and the US and the EU have taken differing approaches to the risk assessment process, the mechanics of the procedure are still the same. The risk assessment process consists of four steps: (1) hazard identification, (2) dose-response assessment, (3) exposure assessment, and (4) risk characterization.467  First, the assessing agency aims to determine the harm associated with exposure to the substance, such as injury, disease, or  466 Also used for air pollution, water contamination, etc. 467 Canada, Pest Management Regulatory Agency, Science Policy Note: A Decision Framework for Risk Assessment and Risk Management in the Pest Management Regulatory Agency, (Ottawa: PMRA, 2000) at 6; U.S., Environmental Protection Agency, Standard Operating Procedures (SOPs) for Residential Exposure Assessment, (Washington, D.C.: EPA, 1997) at 8.  67  death.  Using this data, in the dose-response assessment step an analysis of exposure to specific doses of the substance is used to determine the possible severity of harm.  Third, consideration is given to the likelihood of frequent exposure, the possible duration of exposure, and the potential intensity of exposure.  Lastly, this data is used to establish the overall health risks associated with the estimated levels of exposure.468  Information submitted to the agency from the pesticide registrant applicant used in this four-step process includes toxicological data, animal bioassays, and/or epidemiological studies.469 Laboratory animals are exposed to the substance to determine what type of hazards occur at specified levels of exposure.  The purpose is to identify the level of exposure to the substance that results in no significant harm.  This numerical value, known as the “no observed adverse effect level” (NOAEL), is divided by two uncertainty factors to reduce the possibility of harm.  This process is to adjust the NOAEL for any differences between the animals and humans.  Each of these uncertainty factors range in value from one to ten.  One uncertainty factor is to account for any differences among humans, such as vulnerability to exposure, age differences, weight differences, and genetic variations.  The second uncertainty factor is to account for the differences between animals and humans since the studies used for calculation are based on animal laboratory research.  This calculation is used to establish a tolerance of exposure.  In situations where there is no NOAEL because significant harm is present at every dose of exposure, then a NOAEL is extrapolated from the data.  This process, known as the “weight of evidence” approach, is the selection of predictive model by the risk assessor based on all data on the exposure to the substance.  The model is used to set a standard that is thought to result in a specified rate of a particular disease, such as cancer.  Originally a product of the US EPA, the four-step process has been widely accepted as the global norm in scientific health and environmental assessment.  Documented in the 1983 US National Research Council’s report Risk Assessment in the Federal Government: Managing the Process470, is has become entrenched in the regulatory system of both pesticides and chemicals in the US and Canada.  By the mid-1990s the EU had adopted this process as well.471 The Two Approaches To Risk Assessment: Risk- and Hazard-Based The Risk-Based Approach The US and Canada have interpreted the outcomes of the four-step risk assessment process using the risk-based approach.  The primary objective of this approach is to control risk in a fashion that is “safe”.  However, “safe” does not guarantee that no harm will occur.  Instead this standard of safe is an “acceptable” level of risk of harm, determined by the government using the data from the risk assessment process.472  The belief is that the government  468 California, Environmental Protection Agency, A Guide to Health Risk Assessment, (Sacramento, CA: Office of Environmental Health Hazard Assessment, 2001), online: CA EPA <> (date accessed: 4 October 2009); U.S., Environmental Protection Agency, Risk Assessment Process (Washington, D.C.: Environmental Protection Agency, 2009), online: Environmental Protection Agency <> (last modified: 3 September 2009). 469 Description of these studies will be provided in the following pesticide section. 470 National Research Council 1983, supra note 34. 471 Lofstedt, supra note 34 at 1330. 472 McClenaghan, supra note 36 at 146.  68  is able to control the amount of exposure by setting tolerances, which results in a probability of a chronic health condition, such as cancer.  This method of using the risk assessment process to set standards to control the probability of risk was borne out of a series of legislative and judicial measures in the US. In the 1950s and 1960s, scientific advancements in toxicology assessment provided government agencies with the ability to evaluate substances for harm.  Because of the improved capacity, the US government instituted a “cancer policy”473 in the 1970s that outlined procedural methods for assessing the possibility of cancer from exposure to substances.474  At the same time that this “cancer policy” was developed, concerns surrounding the use of inference, when faced with uncertainty in the scientific process, came into question in a number of legal cases.  Originally the courts held that the government had the authority to make deductions when faced with scientific uncertainty.  Later on, however, the US judicial system narrowed this interpretation of authority to require the government to demonstrate scientific evidence supporting restrictions before any could be made. In the 1974 case, Industrial Union Department v. D. Hodgson475 [hereinafter Hodgson], the court indicated that the cause-effect relationship of exposure and substance may be surmised made when a government agency is faced with scientific uncertainty.  The court affirmed that government agencies have the capacity to make policy judgments when confronting insufficient data as to the effects of substance exposures.476  “Decision making must in that circumstance depend to a greater extent upon policy judgments and less upon purely factual analysis.”477 The Hodgson case provided the government with the authority to make regulations when lacking scientific evidence to support these standards, nevertheless , this agency capacity was short-lived.  In the 1980 case, Industrial Union Department v. American Petroleum Institute478 [hereinafter Benzene], the EPA Secretary’s powers were restrained to ensure that he does not have “unprecedented power over American industry”.479  The regulatory agency480 had reduced the standard of exposure to benzene in a workplace setting from ten parts per million (ppm) to one ppm due to uncertainty surrounding the health effects of this substance on those exposed.  The court found that this reduction in exposure was inappropriate given that there was “no finding that any of the provisions of the new standard were  473 National Research Council 1983, supra note 34. 474 McClenaghan, supra note 147; Even in establishing a cancer policy, the government recognized that there was a great deal of subjectivity in the risk assessment process.  The 1983 National Academy of Sciences report, Risk Assessment in the Federal Government: Managing the Process, identified at least fifty “inference choices” present in the scientific procedure. 475 Industrial Union Department, AFL-CIO, et al., Petitioners v. James D. Hodgson, Secretary, Department of Labor, Respondent, Environmental Defense Fund, Inc., Intervenor (1974)499 F.2d 467 (162 U.S.App.D.C. 331), online: OpenJurist <> (date accessed: 30 October 2009). 476 Ibid. at 20. 477 Ibid. at 26.;  J.S. Applegate, “The Perils of Unreasonable Risk: Information, Regulatory Policy, and Toxic Substances Control” (1991) 91 Colum. L. Rev. 261 at 268-269. 478 Industrial Union Department, AFL-CIO v. American Petroleum Institute, 448 U.S. 607 638 (S. Ct. 1980). [hereinafter Benzene Case ]. 479 Benzene Case, ibid. at 645. 480 The regulatory agency named in the case was the Secretary of Labor as part of the Occupational Safety and Health Administration (OSHA).  69  ‘reasonably necessary or appropriate to provide safe or healthful employment and places of employment’”. 481   The court held that there needed to be “substantial evidence” before such a standard could be valid.482 This decision was a shift away from the Hodgson finding that the EPA Secretary had authority to make deductions when faced with scientific uncertainty.  Not only did it rein in the authority originally given to government agencies, but also shaped future risk assessment procedures.  This case ensured that in future risk assessment the EPA must have the scientific evidence to support any regulatory standards on substance exposure.  Rather than interpret evidence when dealing with scientific uncertainty to construe a tolerance level, the government must have the evidence to prove that the standard is reasonable.  This is central to the difference between the risk- and hazard-based approaches.  The risk-based approach insists that the government have evidence to support the limitation on exposure.  As will be discussed later on, this is in contrast to the hazard-based approach that insists that industry have evidence to support removing limitations on exposure. Not only did the Benzene case require that scientific evidence justify the tolerance set, but it also shaped how the government interpreted the results of the four-step risk assessment process.  The court held that the chances of risk shall be interpreted as per individual, rather than to the society as a whole.483  The court’s statement that “ if the odds are one in a thousand that regular inhalation of gasoline vapors that are 2% benzene will be fatal, a reasonable person might well consider the risk significant and take appropriate steps to decrease or eliminate it” has been interpreted by the EPA as support for the calculation of risk per individual.484  Identified by the agency as the de minimis standard485, this probability of risk is often set as one-in-a-million and is used throughout the current risk-based approach.  This probability of harm eliminates the costs to society of lost days, quality of life, and defines “significant” risk not by disease but by individual chance of having that chronic health condition when exposed to that specific substance. This case law shaped future risk assessment, including that of pesticides and chemicals.  Because of these decisions, the EPA has established that “acceptable risk” is measured by individual risk, quantified, and must meet the de minimis standard.  These elements of calculating risk define the risk-based approach.  In the Benzene case it was stated that “legislative history also supports the conclusion that Congress was concerned, not with absolute safety, but with the elimination of significant harm.”486  As this indicates, the objective of the approach is controlling risk, not  481 Benzene Case, supra note 478 at 662. 482 Ibid. at 653; C.K. Findlay, Pollution Control, Administrative Discretion, and Science: A Journey Through the Maze of Environmental Law (LL.M., University of British Columbia, 1993) [unpublished] at 75. 483 Industrial Union, supra note 481 at 655. 484 Ibid.; M. Adler, “Risk, Death and Harm: The Normative Foundations of Risk Regulation” (2003) 87:1293 Minn. L. Rev. 1293 at 1432. 485 Confirmed in: Public Citizen, et al, Petitioners, v. Dr. Frank Young, Commissioner, Food and Drug Administration, et al, Respondent, 831 F.2d 1108 (D.C.Cir. 1987). [hereinafter Young]; Les, et al, Petitioners v. William K. Reilly, Administrator of the Environmental Protection Agency, et al., Respondent, 968 F.2d 985 (9th Cir. 1992). [hereinafter Les]. 486 Industrial Union, supra note 481 at 646.  70  eliminating it, in a way that risk is no longer “significant”.  Moving away from the Hodgson decision, the courts have indicated that this process is not to be qualitative, but rather quantitative.487 The Hazard-Based Approach The EU has utilized a hazard-based approach to interpret the outcomes of the four-step risk assessment process.  The purpose of this approach is to achieve a non-toxic environment.  It accomplishes this objective through the elimination of toxins when possible.  Because the eradication of use of all chemicals is impossible, however, the hazard-based approach aims at removing exposure to the most caustic substances.  It does this through a three-step procedure: (1) hazard, (2) exposure, and (3) risk.488  Each tier provides the government the ability to restrict or ban the substance based on the hazards associated with it. In the first tier the substance may be banned because it is associated with a significant hazard, such as cancer.  If the hazard associated with this substance is not too great then the product progresses to the second tier where it is compared with similar items already on the market.  In this step, the substitution principle is applied.  This principle holds that if the product is not more efficient than competitors and is more harmful it will be banned and replaced by a less caustic substance.489  If the substance has not yet been banned in tier one or tier two, in the third tier the product’s risk is assessed and controlled through regulation.490 The use of this three-tier approach by the EU is relatively new.  In the past, the EU’s authority over the assessment of health and environment was rather limited to issues related to trade and the reduction of trade barriers.  Because of this, risk assessment was only a priority insofar as it served to aid trade harmonization.491  Due to a number of public health and environmental concerns by member states, however, legislative and judicial changes led to a formal adoption of the four-step risk assessment process described earlier.492  Rather than interpreting this process in the same fashion as the US and Canada have, the EU has implemented a more cautionary policy. A series of events led the EU’s adoption of the hazard-based approach.  Historically, the EU had not developed a formal risk assessment procedure at a supranational level due to the fact that the government’s efforts were trade- focused.493  Instead, until the 1990s, the review authority sat with member states.  As member states that had embedded the protection of environmental health into their political culture joined the union during the 1990s,  487 Though these cases are American jurisprudence, the Canadian risk assessment process has been influenced by them as well.  Because of the close trade relationship between the two nations and the joint environment efforts on behalf of both countries, Canada has adopted the same procedural elements of risk assessment as the US. 488 Hansen, supra note 38 at 274. 489 Sweden’s use of the substitution principle does not include efficiency. Sweden, KEMI, The Substitution Principle (Stockholm: KEMI, 2007), online: KEMI <> (date accessed: 10 August 2009). 490 Ibid. 491 E. Vos, “EU Food Safety Regulation in the Aftermath of the BSE Crisis” (2000) 23 J. Consum. Policy 227 at 229. 492 Lofstedt, supra note 34 at 1330. 493 Vos, supra note 491 at  228.  71  however, they pressured the EU to do the same.494  At the same time, the EU faced an outbreak of disease from ingestion of cow meat contaminated by Bovine Spongiform Encephalopathy (BSE).495  Known as “mad cow disease”, this degenerative neurological disorder brought attention by member states and the general public to the lack of regulatory authority in the EU.496  Though the political focus was originally on food items when this outbreak occurred in 1997, the need for regulatory safety pertaining to other areas, including pesticides and chemicals, was soon recognized. In the 1999 Amsterdam Treaty, the EU outlined how this newly acquired authority over the regulation of substances should be carried out.  A “high level” of health was to be a priority in standard setting.497  In achieving this objective, the treaty declared that “scientific facts” should be the basis of assessment.498  Though these objectives are similar499 to that found in US environmental policy, the interpretation by the European Court of Justice (ECJ) differs from that of the US case law. Whereas the US judicial system imposed a requirement that the government have evidence supporting any restrictions, the ECJ chose to support the EU’s interpretative authority.  In similar circumstances to the US Hodgson case, the ECJ took the opposite position of the US judicial system and indicated that government shall have the ability to make policy judgments.500  Furthermore, the ECJ has held that it is not their role to determine whether or not the assessment is accurate: “[...] where a Community authority is called upon, in the perform of its duties, to make complex assessments, it enjoys a wide measure of discretion, the exercise of which is subject to a limited judicial review in the course of which the EC judicature may not substitute its assessment of the facts for the assessment made by the authority concerned.  Thus, in such cases, the EC judicature must restrict itself to examining the accuracy of the findings of fact and law made by the authority concerned and to verifying, in particular, that the action taken by that authority is not vitiated by a manifest error or a misuse of powers and that it did not clearly exceed the bounds of its discretion.”501 As a result of these judicial findings, the EU has been able to rely on a risk assessment procedure that includes a way of reasoning that is not solely based on scientific evidence.  The EU’s Risk Regulatory Framework held that “it is recognized that scientific risk assessment alone cannot, in some cases, provide all the information on which a risk  494 Austria, Finland and Sweden have been recognized for pressuring the EU to highten standards for environmental protection. E.C., Strengthened EU Environment Standards as a Result of the Enlargement with Austria, Finland and Sweden [1998] IP/98/1107, online: Europa <> (last modified: 14 December 1998). 495 Vos, supra note 491 at 227. 496 Ibid. 497 A. Alemanno, “The Role of Experts in Decision-Making and Judicial Review” (Young Researchers Workshop on Science and Law, ISUFI, 31 May – 1 June 2007) at 4. Treaty of Amsterdam, supra note 367. 498 Alemanno, Ibid. at 5; Vos, supra note 491 at 235. 499 Science is to take precedence, though if there is indication of doubt then caution should be taken.  This is in contrast to the US position that unless science indicates harm, then no action shall be taken. 500 Alemanno, supra 497 at 6. 501Alemanno, supra note 497 at 19.  E.C.J., Commission v. Ceva/Pfizer, Case C-196/03 P [2005], E.C.R. I-06357.  72  management decision should be based”.502  This is not the dismissal of scientific fact, rather support for the notion that “scientific knowledge is authoritative, but not exclusively so”.503  This cautious approach is a key difference between the risk-based approach and the hazard-based approach.  The US and Canada have interpreted scientific fact as authoritative, and when faced with uncertainty, have relied on mathematical adjustments in hopes to avoid subjectivity.  In contrast, the EU has recognized that uncertainty cannot be explained away by the calculation of risk alone. This cautionary approach is based on the EU’s precautionary principle504.  Originating in German environmental policy505, this principle has been interpreted by the EU to be the ability to take regulatory action to protect environment, human, animal, and plant health even when scientific evidence does not decisively conclude the action is necessary.506  Because the EU has recognized that “acceptable” risk for society is a political responsibility, “[d]ecision-makers faced with an unacceptable risk, scientific uncertainty and public concerns have a duty to find answers.  Therefore, all these factors have to be taken into consideration.”507  502 E.C., Council Regulation 1829/2003 on Genetically Modified Food and Feed [2003] O.J.L. 287 at 19. 503 Alemanno, Ibid. at 9; E.C., Commission Communication on the Precautionary Principle COM(2000)1 [2000], online: Europa <> (last modified: 2 February 2000). 504 Though all three jurisdictions have publicly embraced the precautionary principle at the Rio Declaration on Environment and Development, this concept of caution differs from the principle due to the specific requirements. Rather than merely acting as a theory for shaping future policy, the cautionary approach aims at having procedural requirements that are not negotiable, as will be discussed throughout the rest of this thesis. 505 The use of this principle in risk assessment is often controversial as critics argue that the approach is too open- ended and may allow bias to enter into the process.  Although these concerns are valid, within the context of pesticides and chemicals the EU has applied this principle in a fashion that reduces the possibility of subjectivity. First, it sits within the risk assessment process, rather than in the risk management portion of pesticide policy. Second, it has clear procedural tools by which caution can be implemented, such as the substitution principle and the objective to reduce overall exposures whether or not they are independently harmful.  Furthermore, one could argue that the mathematical adjustments utilized in a precautionary manner by the US and Canada in the risk-based approach provides an opportunity for bias as well.  The use of these p