Gerald M. Dill, R. Douglas Sammons, Paul C. C. Feng, Frank Kohn, Keith Kretzmer, Akbar Mehrsheikh, Marion Bleeke, Joy L. Honegger, Donna Farmer, Dan Wright, and Eric A. Haupfear, “Glyphosate: Discovery, Development, Applications, and Properties,” 2010, in Glyphosate Resistance in Crops and Weeds: History, Development, and Management, Edited by Vijay K. Nandula.
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Reigart, Routt, Roberts, James, “Recognition and Management of Pesticide Poisoning,” US EPA Office of Pesticide Programs, 2013, Sixth Edition.
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Wagner-Schuman M, Richardson JR, Auinger P, Braun JM, Lanphear BP, Epstein JN, Yolton K, Froehlich TE., “Association of pyrethroid pesticide exposure with attention-deficit/hyperactivity disorder in a nationally representative sample of U.S. children,” Environmental Health, 2015, 14:44.
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BACKGROUND: Pyrethroid pesticides cause abnormalities in the dopamine system and produce an ADHD phenotype in animal models, with effects accentuated in males versus females. However, data regarding behavioral effects of pyrethroid exposure in children is limited. We examined the association between pyrethroid pesticide exposure and ADHD in a nationally representative sample of US children, and tested whether this association differs by sex.
METHODS: Data are from 8-15 year old participants (N = 687) in the 2001-2002 National Health and Nutrition Examination Survey. Exposure was assessed using concurrent urinary levels of the pyrethroid metabolite 3-phenoxybenzoic acid (3-PBA). ADHD was defined by either meeting Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition criteria on the Diagnostic Interview Schedule for Children (DISC) or caregiver report of a prior diagnosis. ADHD symptom counts were determined via the DISC. Multivariable logistic regression examined the link between pyrethroid exposure and ADHD, and poisson regression investigated the link between exposure and ADHD symptom counts.
RESULTS: Children with urinary 3-PBA above the limit of detection (LOD) were twice as likely to have ADHD compared with those below the LOD (adjusted odds ratio [aOR] 2.42; 95 % confidence interval [CI] 1.06, 5.57). Hyperactive-impulsive symptoms increased by 50 % for every 10-fold increase in 3-PBA levels (adjusted count ratio 1.50; 95 % CI 1.03, 2.19); effects on inattention were not significant. We observed possible sex-specific effects: pyrethroid biomarkers were associated with increased odds of an ADHD diagnosis and number of ADHD symptoms for boys but not girls.
CONCLUSIONS: We found an association between increasing pyrethroid pesticide exposure and ADHD which may be stronger for hyperactive-impulsive symptoms compared to inattention and in boys compared to girls. Given the growing use of pyrethroid pesticides, these results may be of considerable public health import. FULL TEXT
Lanphear, Bruce, “The Impact of Toxins on the Developing Brain,” Annual Review of Public Health, 2015, 36:1, DOI: 10.1146/ANNUREV-PUBLHEALTH-031912-114413.
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The impact of toxins on the developing brain is usually subtle for an individual child, but the damage can be substantial at the population level. Numerous challenges must be addressed to definitively test the impact of toxins on brain development in children: We must quantify exposure using a biologic marker or pollutant; account for an ever-expanding set of potential confounders; identify critical windows of vulnerability; and repeatedly examine the association of biologic markers of toxins with intellectual abilities, behaviors, and brain function in distinct cohorts. Despite these challenges, numerous toxins have been implicated in the development of intellectual deficits and mental disorders in children. Yet, too little has been done to protect children from these ubiquitous but insidious toxins. The objective of this review is to provide an overview on the population impact of toxins on the developing brain and describe implications for public health. FULL TEXT
Laborde A, Tomasina F, Bianchi F, Bruné MN, Buka I, Comba P, Corra L, Cori L, Duffert CM, Harari R, Iavarone I, McDiarmid MA, Gray KA, Sly PD, Soares A, Suk WA, Landrigan PJ, “Children’s Health in Latin America: The Influence of Environmental Exposures,” Environmental Health Perspectives, 2015 Mar; 123(3), DOI: 10.1289/EHP.1408292.
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BACKGROUND: Chronic diseases are increasing among children in Latin America.
OBJECTIVE AND METHODS: To examine environmental risk factors for chronic disease in Latin American children and to develop a strategic initiative for control of these exposures, the World Health Organization (WHO) including the Pan American Health Organization (PAHO), the Collegium Ramazzini, and Latin American scientists reviewed regional and relevant global data.
RESULTS: Industrial development and urbanization are proceeding rapidly in Latin America, and environmental pollution has become widespread. Environmental threats to children’s health include traditional hazards such as indoor air pollution and drinking-water contamination; the newer hazards of urban air pollution; toxic chemicals such as lead, asbestos, mercury, arsenic, and pesticides; hazardous and electronic waste; and climate change. The mix of traditional and modern hazards varies greatly across and within countries reflecting industrialization, urbanization, and socioeconomic forces.
CONCLUSIONS: To control environmental threats to children’s health in Latin America, WHO, including PAHO, will focus on the most highly prevalent and serious hazards—indoor and outdoor air pollution, water pollution, and toxic chemicals. Strategies for controlling these hazards include developing tracking data on regional trends in children’s environmental health (CEH), building a network of Collaborating Centres, promoting biomedical research in CEH, building regional capacity, supporting development of evidence-based prevention policies, studying the economic costs of chronic diseases in children, and developing platforms for dialogue with relevant stakeholders. FULL TEXT
Jackson RJ, Minjares R, Naumoff KS, Patel BS, Martin LK, “Agriculture Policy is Health Policy,” Journal of Hunger and Environmental Nutrition, 2009; 4(3): 393-408, DOI: 10.1080/19320240903321367.
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The Farm Bill is meant to supplement and secure farm incomes, ensure a stable food supply, and support the American farm economy. Over time, however, it has evolved into a system that creates substantial health impacts, both directly and indirectly. By generating more profit for food producers and less for family farmers; by effectively subsidizing the production of lower-cost fats, sugars, and oils that intensify the health-destroying obesity epidemic; by amplifying environmentally destructive agricultural practices that impact air, water, and other resources, the Farm Bill influences the health of Americans more than is immediately apparent. In this article, we outline three major public health issues influenced by American farm policy. These are (1) rising obesity; (2) food safety; and (3) environmental health impacts, especially exposure to toxic substances and pesticides. FULL TEXT
Jackson RJ, Malloy TF, “Environmental public health law: three pillars,” The Journal of law, medicine & ethics : a journal of the American Society of Law, Medicine & Ethics, 2011; 39 Suppl 1: 34-6.
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Renata Sisto, Arturo Moleti, L’ubica Palkovičová Murínová, Soňa Wimmerová, Kinga Lancz, Juraj Tihányi, Kamil Čonka, Eva Šovčíková, Irva Hertz-Picciotto, Todd A. Jusko, and Tomáš Trnovec, “Environmental exposure to organochlorine pesticides and deficits in cochlear status in children,” Environmental Science and Pollution Research, 2015, 22:19, DOI: 10.107/S11356-015-489-5.
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The aim of this study was to examine the hypothesis that organochlorine pesticides (OCPs), hexachlorobenzene (HCB), β-hexachlorocyclohexane (β-HCH), 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane (p,p′-DDT) and its metabolite 1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene (p,p′-DDE) are ototoxic to humans. A Multivariate General Linear Model was designed, in which the statistical relation between blood serum concentrations of HCB, β-HCH, p,p′-DDT or p,p′-DDE at the different ages (at birth, 6, 16 and 45 months) and the DPOAEs were treated as multivariate outcome variables. PCB congeners and OCPs were strongly correlated in serum of children from our cohort. To ascertain that the association between DPOAEs at a given frequency and concentration of a pesticide is not influenced by PCBs or other OCP also present in serum, we calculated BMCs relating DPOAEs to a serum pesticides alone and in presence of confounding PCB-153 or other OCPs. We found that BMCs relating DPOAEs to serum pesticides are not affected by confounders. DPOAE amplitudes were associated with serum OCPs at all investigated time intervals, however in a positive way with prenatal exposure and in a negative way with all postnatal exposures. We observed tonotopicity in the association of pesticides with amplitude of DPOAEs as its strength was frequency dependent. We conclude that exposure to OCPs in infancy at environmental concentrations may be associated with hearing deficits. FULL TEXT
Vogt R, Cassady D, Frost J, Bennett DH, Hertz-Picciotto I, “An assessment of exposures to toxins through diet among California residents,” Environmental Health, 2012;11:83.
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BACKGROUND: In the absence of current cumulative dietary exposure assessments, this analysis was conducted to estimate exposure to multiple dietary contaminants for children, who are more vulnerable to toxic exposure than adults.
METHODS: We estimated exposure to multiple food contaminants based on dietary data from preschool-age children (2-4 years, n=207), schoolage children (5-7 years, n=157), parents of young children (n=446), and older adults (n=149). We compared exposure estimates for eleven toxic compounds (acrylamide, arsenic, lead, mercury, chlorpyrifos, permethrin, endosulfan, dieldrin, chlordane, DDE, and dioxin) based on selfreported food frequency data by age group. To determine if cancer and non-cancer benchmark levels were exceeded, chemical levels in food were derived from publicly available databases including the Total Diet Study.
RESULTS: Cancer benchmark levels were exceeded by all children (100%) for arsenic, dieldrin, DDE, and dioxins. Non-cancer benchmarks were exceeded by >95% of preschool-age children for acrylamide and by 10% of preschool-age children for mercury. Preschool-age children had significantly higher estimated intakes of 6 of 11 compounds compared to school-age children (p<0.0001 to p=0.02). Based on self-reported dietary data, the greatest exposure to pesticides from foods included in this analysis were tomatoes, peaches, apples, peppers, grapes, lettuce, broccoli, strawberries, spinach, dairy, pears, green beans, and celery.
CONCLUSIONS: Dietary strategies to reduce exposure to toxic compounds for which cancer and non-cancer benchmarks are exceeded by children vary by compound. These strategies include consuming organically produced dairy and selected fruits and vegetables to reduce pesticide intake, consuming less animal foods (meat, dairy, and fish) to reduce intake of persistent organic pollutants and metals, and consuming lower quantities of chips, cereal, crackers, and other processed carbohydrate foods to reduce acrylamide intake.
Janie F. Shelton, Estella M. Geraghty, Daniel J. Tancredi, Lora D. Delwiche, Rebecca J. Schmidt, Beate Ritz, Robin L. Hansen, and Irva Hertz-Picciotto, “Neurodevelopmental Disorders and Prenatal Residential Proximity to Agricultural Pesticides: The CHARGE Study,” Environmental Health Perspectives, 2014, 122:10, DOI: 10.1289/EHP.1307044.
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BACKGROUND: Gestational exposure to several common agricultural pesticides can induce developmental neurotoxicity in humans, and has been associated with developmental delay and autism.
OBJECTIVES: We evaluated whether residential proximity to agricultural pesticides during pregnancy is associated with autism spectrum disorders (ASD) or developmental delay (DD) in the Childhood Autism Risks from Genetics and Environment (CHARGE) study.
METHODS: The CHARGE study is a population-based case–control study of ASD, DD, and typical development. For 970 participants, commercial pesticide application data from the California Pesticide Use Report (1997–2008) were linked to the addresses during pregnancy. Pounds of active ingredient applied for organophophates, organochlorines, pyrethroids, and carbamates were aggregated within 1.25-km, 1.5-km, and 1.75-km buffer distances from the home. Multinomial logistic regression was used to estimate the odds ratio (OR) of exposure comparing confirmed cases of ASD (n = 486) or DD (n = 168) with typically developing referents (n = 316).
RESULTS: Approximately one-third of CHARGE study mothers lived, during pregnancy, within 1.5 km (just under 1 mile) of an agricultural pesticide application. Proximity to organophosphates at some point during gestation was associated with a 60% increased risk for ASD, higher for third-trimester exposures (OR = 2.0; 95% CI: 1.1, 3.6), and second-trimester chlorpyrifos applications (OR = 3.3; 95% CI: 1.5, 7.4). Children of mothers residing near pyrethroid insecticide applications just before conception or during third trimester were at greater risk for both ASD and DD, with ORs ranging from 1.7 to 2.3. Risk for DD was increased in those near carbamate applications, but no specific vulnerable period was identified.
CONCLUSIONS: This study of ASD strengthens the evidence linking neurodevelopmental disorders with gestational pesticide exposures, particularly organophosphates, and provides novel results of ASD and DD associations with, respectively, pyrethroids and carbamates. FULL TEXT