Saturday, November 5, 2011

Delayed Mitigation Protects Our Children

The Long Road to EPA Considerations of Childhood Pesticide Exposure Begins with Congress, The National Academy of Sciences, and the National Research Council

In 1988, the U.S. Congress, concerned about the potential risk of pesticides in the diets of infants and children, requested the National Academy of Sciences (NAS) to appoint a committee that would study this issue through its National Research Council (NRC).  The ‘Committee on Pesticide Residues in the Diets of Infants and Children’ was appointed and became responsible for investigating scientific and policy issues faced by the EPA in regulating pesticide residues in foods consumed by infants and children.  In 1993 the NRC releases Pesticides In The Diets Of Infants And Children stating within “Current testing protocols do not, for the most part, adequately address the toxicity and metabolism of pesticides in neonates and adolescent animals or the effects of exposure during early developmental stages and their sequelae in later life.” [1] Finding that toxicology testing by pesticide manufacturers was designed primarily for sexually mature animals. (CLS p.4) 

This is highly concerning when considering the Natural Resource Defense Council released “Intolerable Risk: Pesticides In Our Children’s Food” which claimed “Preschoolers are being exposed to hazardous levels of pesticides in fruits and vegetables. Between 5,500 and 6,200 of the current population of American preschoolers may eventually get cancer solely as a result of their exposure before six years of age, to eight pesticides or metabolites commonly found in fruits and vegetables.”[2]

Seppo Leinonen,

In 2010 the EPA’s Office of Pesticide Programs released Protecting Children’s Health THE NATIONAL PESTICIDE PROGRAM

The EPA insists that pesticides are now so widely used, that children can be exposed in the home, school, play and work.  The document boasts of efforts to improve risk assessment and research requirements on pesticides as science and information improve.  They claim to recognize that over the past years, studies have documented the unique and particular vulnerability that infants and children have to toxins.  Therefore, the EPA now requires pesticide manufacturers to submit nuerotoxicity, immunotoxicity and reproductive studies in hopes of better assessing possible effects on fetal development and the maturing child.  They have only just begun to address effects of pesticides on the endocrine system by implemented pesticide screening on 67 chemical pesticides and inert ingredients into the endocrine disruptor screening program.[3]  A statement that they also hope to evaluate residential exposure, including exposure from home lawns and hand-to-mouth behavior is incorporated.  In what the EPA calls “Preliminary OP Cumulative Risk Assessment” it is explained that the occurrence of hand to mouth behavior and residential assessment of pesticide use; pesticide residue dissipation; and exposure contact and exposure factors have been estimated but chemical specific data and more research are required to get a better understanding of this exposure pathway.[4]   Finally, they believe, that they have made special efforts to reduce pesticide residue tolerance in food that are particularly consumed/in the diets of by infants and children.   They state: “Completed reassessment of all (over 9,700) tolerances (maximum residue levels in food), giving special consideration to consumption patterns and special susceptibility of infants and children;” but results only ended children’s food uses of methyl parathion and carbofuran.3

HOW Long do we want to wait for better protections for our children? 

This seems like a lot of studies, hopes and plans that could protect our children’s’ health and futures but are these matters being dealt with in a timely manner?  How long did it take to ban lead from use in wood playground equipment?  We should all be advised that this governmental protection agency fights with a lengthy process of science and law to determine and enforce better risk assessment through manufacturer funded and composed studies.  But while they battle multimillion dollar corporations, research presented by universities and medical facilities aim to enforce the precautionary principle, urging “Toxic exposures deserve special scrutiny because they are preventable causes of harm.”[5] (Greater Boston Physicians for Social Responsibility p.1) and “The inability of the current regulatory system to protect public health is not surprising, considering the disproportionate influence of special interests in the regulatory process.” (p.7)

Toxic Organochlorines are still on the Market

Research has shown that certain widely used synthetic pesticides, even now, years after being banned, are found in our environment and bloodstreams.  For example, Organochlorines (OC’s) were introduced in the 1940’s and 1950’s but widely banned in the 1970’ and 1980’s due to their ability to target the nervous system and potentially cause cancer.  However in a study by the Environmental Working Group in 2005, 21 of 28 organochlorines tested for, were found in the blood of newborns.[6]  Some of which are known to cause birth defects, developmental delays and cancer.  As well, many are considered probable for affecting our reproductive systems.  The EPA allows some OC’s to remain in use, including Endosulfan: Linked to autism, birth defects, and delayed puberty in humans, Lindane: An endocrine disruptor and likely carcinogen, still used in lice shampoo and Dicofol: a close relative of DDT, an endocrine disruptor and possible carcinogen.[7] 

The Story of Endusulfan

The EPA website states that it is taking action on Endosulfan, “because it can pose unacceptable health risks to farmworkers and wildlife and can persist in the environment”[8]  yet has allowed a lengthy phase out lasting until July, 2016.  This is being allowed, even though residues of Endosulfan are considered highly mobile and shown to contaminate landscapes far outside of their used agricultural areas, including the Florida Everglades and the Alaskan Arctic.[9]  Furthermore, during this phase out of use, Endosulfan is used on a wide variety of vegetables and fruits in the U.S., including many vegetables in the cabbage family, as well as carrots, sweet potato, almonds and walnuts, plums, peaches, cherries, strawberries, and pineapples.  Find the full list here.

The EPA website explains, “Endosulfan is used on a very small percentage of the U.S. food supply and does not present a risk to human health from dietary exposure.”7  But what about the children who are eating these fruits and vegetables?

Autism Spectrum Disorders:  Our National Epidemic and Pesticide Links

A significant amount of medical literature has linked pesticides to both birth defects and genetic damage and these genetic factors are also considered a linking factor for autism.  In an abstract concerning the CHARGE Study, various environmental factors of autism will be studied through the University of California-Davis.  They seek to determine a suspected link between agricultural pesticides and autism through the mechanisms of birth defects and continual exposure.   Long term exposure also affects the neurological system, brain and other anatomical functions that pertain to behavioral disorders and autism spectrum disorders.

Over the past years rates of autism disorder have risen from 4–5 per 10,000 births[10] (Fombonne 1999) to a prevalence of 1-2 children per 1,000 births[11] (Fombonne 2005).  A recent publication in the journal Environmental Health Perspectives reported a possible connection between pesticide exposure, particularly endosulfan and dicofol, and autism in central California.  Cases and controls of this study were born between 1996 and 1998: Dicofol and endosulfan accounted for over 98% of the organochlorines applied during this time period.  Multiple databases were used to identify candidate exposures and analyze the relationship between the exposure and autism spectrum disorders (ASD). By linking these four databases, the researchers estimated which pregnant women were exposed to pesticides, when, and to how much (based on timing during pregnancy, amount applied, and residential proximity to application location). Using this information, researchers were able to stratify women into different exposure categories and compared rates of autism between those children whose mothers were exposed to the highest levels during a period of time surrounding conception, to those who were not exposed or exposed to lower levels.  Of particular interest, the researchers were also able to identify a critical time window just prior to and after embryogenesis during which the association is statistically highest.[12] (Hertz-Picciotto, Irva 2006)

Why should we be so concerned that mitigation is not fully covering all potential means of exposure to children? Widely-used pesticides that are potentially neurotoxic include: organophosphates, pyrethroids, carbamates, chlorophenoxy herbicides, and ethylenebisthiocarbamates.  While some of these pesticides are now banned, those in current use are thought to have the same toxic characteristics and mechanisms.  Since many pesticides by design are toxic to insect brains, the same could be true for people, specifically children.  Furthermore, because adverse side effects can be severe, long lasting and irreversible on brain development even at low exposure, preventing exposure should be a serious priority.  Philippe Grandjean of the Harvard School of Public Health advises, “While awaiting more definite evidence, existing uncertainties should be considered in light of the need for precautionary action to protect brain development.”[13]

Chipping Away at the Use of Organophosphates

The EPA attempts to complete tests that assess risk from cumulative organophosphate (OP) pesticide exposure, which they claim may warrant further risk mitigation.  The EPA says that the elimination of homeowner use of organophosphate (OP’s) pesticides was warranted because a particular risk to children had been identified.  However, according to EPA’s website the organophosphate insecticide, chlorpyrifos is used on an assortment of food crops.  Overall, 10 million pounds are sprayed annually in agriculture, with over half being used on corn.[14]   Statements on the EPA website dated February 2002, say that chlorpyrifos residues in food are considered safe and children are considered better protected with mitigation eliminating homeowner use yet studies find that exposure may be due instead to public areas and diet.

A study printed in the journal, Environmental Health Perspectives, released only one year before (2001) consistently finds common compounds of OP pesticides in the urine of preschool children living in different communities of the Seattle metropolitan area.  These breakdown products of OPs were consistently found through “season, community, sex, age, family income, or housing type” and did not differ due to reported use in residences or on household pets: signifying that pesticide exposure is due in part to diet and public areas such as schools or playgrounds.[15] (Lu C. 2001)  To determine if the source of chlorpyrifos and another commonly used OP pesticide, Malathion, found in the urine samples were from dietary intake, authors furthered their study in 2008 by placing children on a diet with organic fruits and vegetables for 5 days.  Urine samples tested after the five days showed  nearly undetectable levels of malathion and chlorpyrifos, supporting the possibility that most, if not all, of the exposure to organophosphorus pesticides in children is due to dietary intake.[16] (Lu C.  2008)  This research shows that the risk of childhood exposure to OP’s is evident in their food and therefore warrants further mitigation on organophosphates, especially since the EPA claims that risks to children has already been identified.

Seemingly concerned about the continued widespread use of chlorpyrifos in agricultural settings, experts continue research on chlorpyrifos found in maternal blood and cord blood samples to address the neurodevelopmental of participating children at age 7.  The Wechsler Intelligence Scales for Children (WISC-IV) is used to assess 7 year old development because of its improved ability to detect low-dose neurotoxic exposures, (as demonstrated by studies of lead toxicity in 6-7.5 year-old children). Results find concerning evidence that exposure to chlorpyrifos while in the womb produces early cognitive defects of working memory and IQ.[17] (Rauh V. 2011) 

Smoothed cubic splines, superimposed over scatterplots, examining the shape of the associations between CPF exposure and (A) Working Memory Index, (E) Full-Scale IQ (Rauh V. 2011) 

The Wechsler Intelligence Scale for Children-IV was also used to study 329 seven-year old children whose mothers had the OP pesticide metabolite, dialkyl phosphate (DAP), in urine collected during pregnancy.  Concentrations found were within the range of levels measured in the general U.S. population and were associated with poorer scores for Working Memory, Processing Speed, Verbal Comprehension, Perceptual Reasoning, and Full Scale IQ.[18] (Bouchard MF 2011)  Findings of these studies support the idea that although mothers do not show adverse health effects, exposure while pregnancy can cause lasting adverse effects on brain development in children.[19]   

Dr. Bouchard’s Powerful Study:  The Prevalence of Pesticides in Children w ADD/ADHD

Three doctors of Harvard University including Dr. Maryse Bouchard who is also associated with the University of Montreal, documented the prevalence of ADD/ADHD in children who had organophosphates in their urine.  The study showed a direct correlation between ADD/ADHD in children and the pesticides in their systems, and was a top health news story featured on Fox and CNN, and in the New York Times, Newsweek, the Utne Reader and elsewhere. 

In Dr. Bouchard’s study, children exhibited strong symptoms of ADD/ADHD such as, lack of focus, hyper-excitability, inability to sit still and complete school tasks.  Investigation revealed when placed on an organic diet for two weeks, most symptoms of ADD/ADHD disappeared.  Since the test group is representative of the entirety of children in the US, and not just those who congregate in areas with a high concentration of pesticides, these findings are startling, and according to the authors, presents a need for immediate action and extensive research regarding pesticides.[20] (Bouchard MF 2010)

Authors of this study also warn that pesticide exposure can change the function of immune and endocrine systems, making children even more vulnerable to permanent damage including altered intellectual function, ADD/ADHD and neurotoxicity. They state “While awaiting more definite evidence, existing uncertainties should be considered in light of the need for precautionary action to protect brain development.” (Bouchard MF 2010) 

Dr. Warren Porter spoke at the 25th National Pesticide Forum, discussing scientific data collected on children with regard to pesticide poisoning. He explains how pesticides are built to be fat and water soluble via inert ingredients that help penetrate the surface of plants, which are very similar to our own skin and lungs.  Porter finds startling evidence through school records that our children are being affected negatively.  In his local Madison school district,  he determined  that disabilities,  including emotional and learning, as well as birth defects had all jumped at least 70% in a five year period. Porter extended his research to find Wisconsin, California, Pennsylvania and even Australia, were noticing huge increases of learning disabilities and behavioral disorders between 1990 and 1995.  These astounding increases lead to added costs for school, families and local governments.[21] 

Continued Exposure and Lasting Effects in Our Children and the Environment  

The study, “Association Of Prenatal Exposure To Environmental Contaminant With Intellectual Function In Childhood” suggests the ability of pesticides to endure in anaerobic settings.  Children born to women who had eaten large quantities of contaminated Lake Michigan fish were found to have adversely affected intellectual function.  “Poorer recognition memory in infancy, lower scores on a preschool IQ test, and poorer verbal IQ and reading comprehension at 11 years of age” was determined because of this exposure.[22] (Jacobson JL, 2002)  It seems further education and mitigation rather than re-registration of pesticides should be more prompt and promised to protect the livelihood of children.

The EPA now requires neurotoxicity testing but as new research arises, prompt action is not taken to protect us against potential risks.  Pyrethrins and pyrethroids are replacing organophosphate insecticides and include 3,500 registered products which are currently under registration review from 2010 to 2012.    These products are used in homes, on pets, in mosquito control and agriculture. The EPA states that issues may arise, for example: urban runoff, potentially exposing aquatic life to harmful levels in water and sediment.[23]  As well, these products are formulated with synergists, piperonyl butoxide and MGK-264, to enhance the pesticidal properties of the chemical pesticide.  Much like studies on Roundup have shown the additive ingredients that assist Glyphosate in permeating cell membranes present a higher potential risk than the active ingredient alone[24],[25] pyrethrin synergists are showing their own risks.  A study presented in the Journal of Pediatrics tests whether there is an association between 36-month neurodevelopment and prenatal exposure to permethrin (a common pyrethroid) and piperonyl butoxide (a pyrethroid synergist).  Results found prenatal exposure to piperonyl butoxide to be directly and negatively associated with lower scores on the Bayley Mental Developmental Index from the Bayley Scales of Infant Development.[26]

HEAD Start and Early Childhood Education and Pesticides

Of future activities scheduled by the EPA a year ago, includes “Take full advantage of opportunities to improve children’s health through education and training initiatives.”[27]  These initiatives include informing health care providers, educating parents, enhancing web pages and utilizing social media.  They claim, “OPP, partnering with the National Head Start Association and the Department of Health and Human Services’ Child Care Bureau, launched a national awareness campaign on the safe use of pesticides directed at child care center staff and parents.“[28]  But I wonder if this reached the hearts and brains of our local day cares, schools and parents.

A pamphlet designed for Head Start staff encourages them to educate families about the possible health effects that pesticides may have on children.  Specific educational points include children’s particular susceptibility, limited detoxification ability and critical stages of development.  It states “The effects are not always immediate, and may show up years later as unknown illnesses.  Because their bodies are still growing, children have less natural defenses and can develop serious health effects if overexposed to pesticides.” (EPA 2010)  The pamphlet warns that children may have a higher risk for pesticide exposure that may cause serious damage to their health from contact to applied or stored pesticides throughout interior and exterior areas that they inhabit throughout normal daily activities.  This includes playing on floors and grass of the home, daycares, parks or around pets and further exposing themselves by putting their hands in their mouths.  The pamphlet goes on to urge Head Start staff to inform families of long term exposure and its health effects, such as:

• Birth defects;
• Learning disabilities;
• Behavioral changes;
• Organ damage;
• Forms of cancer, including leukemia, breast cancer, and brain tumors; or
• Asthma symptoms.

It has become essential that the precautionary principle on synthetic pesticides involves avoiding exposure to even low levels during pregnancy and developing ages until new tests have been completed, including cumulative and chemical combination risk analysis.  As for products currently on the market that are currently under reexamination, our chances of being exposed are high. 

[1] Pesticides In The Diets Of Infants And Children  Commission on Life Sciences, National Research Council, National Academy Press. p.4 (1993)
[2] “Intolerable Risk: Pesticides In Our Children’s Food” Natural Resources Defense Council. (1989)
[3] Endocrine Disruptor Screening Program (EDSP)
[4] “Preliminary OP Cumulative Risk Assessment” accessed Oct. 2011
[5] In Harms Way: Toxic Threats to Child De¬velopment  Shettler, T., et al., (2000)
[6] Body Burden, The Pollution In Newborns. Houlihan, J., et al, Environmental Working Group, (2005)
[7] Organochlorines.
[8] Endosulfan Phase-out
[10] “The Epidemiology Of Autism: A Review” Fombonne, Eric Psychological Medicine, 29: 769-786 Cambridge University Press  (1999)
[11] “The Changing Epidemiology of Autism” Fombonne, E. Journal of Applied Research in Intellectual Disabilities, 18: 281–294 (2005)
[12] “The CHARGE Study: An Epidemiologic Investigation of Genetic and Environmental Factors Contributing to Autism.” Hertz-Picciotto, Irva et al. Environmental Health Perspectives, 114(7): 1119–1125 (2006)
[13] “Potential Developmental Neurotoxicity Of Pesticides Used In Europe” Bjorling MA, Andersen HR and Grandjean P., Environmental Health, 7:50 (2008)
[14] “Chlorpyrifos Facts”  EPA 738-F-01-006 (2002)
[15] “Biological Monitoring Survey Of Organophosphorous Pesticide Exposure Among Pre-School Children In The Seattle Metropolitan Area”  Lu C. et al., Environmental Health Perspectives 109(3):299-303 (2001)
[16] “Dietary Intake And Its Contribution To Longitudinal Organophosphorus Pesticide Exposure In Urban/Suburban Children” Lu C. et al., Environmental Health Perspectives, 116(4):537-542. (2008)
[17] “Seven-Year Neurodevelopmental Scores and Prenatal Exposure to Chlorpyrifos, a Common Agricultural Pesticide” Rauh V. et al., Environmental Health Perspectives 119(8) (2011)
[18] “Prenatal Exposure to Organophosphate Pesticides and IQ in 7-Year-Old Children.” Bouchard MF, Chevrier J, Harley KG, Kogut K, Vedar M, et al. Environmental Health Perspectives 119(8) (2011)
[19] “Neurobehavioral Deficits and Increased Blood Pressure in School-Age Children Prenatally Exposed to Pesticides.” Harari R et. al, Environmental Health Perspectives 118(6) (2010)
[20] “Attention-Defecit/Hyperactivity Disorder And Urinary Metabolites Of Organophosphate Pesticides.” Bouchard MF et al., Pediatrics 125(6):1270-1277 (2010)
[21] “Facing Scientific Realities, Debunking The “Dose Makes The Poison” Myth The Big Picture: Linking Pesticide Science And Health Effects” Porter W. Pesticides and You 27(4):16-23 (2008)
[22] “Association Of Prenatal Exposure To Environmental Contaminant With Intellectual Function In Childhood.” Jacobson JL, Jacobson SW, Journal of Toxicology. Clinical Toxicology, 40: 467-475 (2002)
[23] Pyrethroids and Pyrethrins August 2011
[24] “Glyphosate Formulations Induce Apoptosis And Necrosis In Human Umbilical, Embryonic And Placental Cells.”  Benachour, N, et al.  Chemical Research in Toxicology 22(1):97-105 (2009)
[25] “Effects Of Roundup And Glyphosate Formulations On Intracellular Transport, Microtubules And Actin Filaments In Xenopus Laevis Melanophores”  Hedberg D., Wallin M. Toxicology in Vitro. 24(3):795-802 (2010)
[26] “Impact Of Prenatal Exposure To Piperonyl Butoxide And Permethrin On 36-Month Neurodevelopment” Megan K. Horton M.K. et al., Pediatrics 127(3):699-706 (2010)
[27] “Protecting Children’s Health: THE NATIONAL PESTICIDE PROGRAM” US EPA Office of Pesticide Programs, Washington, DC EPA-735-K-10-001 (Oct. 2010)
[28] “Head Start Staff: What You Need to Know About Pesticide Poisoning”  EPA 735-F-07-011

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