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.
ABSTRACT:
Not Avaialble
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.
ABSTRACT:
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.
ABSTRACT:
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
Donauer, Stephanie, Mekibib Altaye, Yingying Xu, Heidi Sucharew, Paul Succop, Antonia M. Calafat, Jane C. Khoury, Bruce Lanphear, Kimberly Yolton, “An Observational Study to Evaluate Associations Between Low-Level Gestational Exposure to Organophosphate Pesticides and Cognition During Early Childhood,” American Journal of Epidemiology, 2016, 184:5.
ABSTRACT:
Prenatal exposure to organophosphate pesticides, which is ubiquitous, may be detrimental to neurological development. We examined 327 mother/infant pairs in Cincinnati, Ohio, between 2003 and 2006 to determine associations between prenatal exposure to organophosphate pesticides and neurodevelopment. Twice during pregnancy urinary concentrations of 6 common dialkylphosphates, nonspecific metabolites of organophosphate pesticides, were measured. Aggregate concentrations of diethylphosphates, dimethylphosphates, and total dialkylphosphates were calculated. Bayley Scales of Infant Development, Second Edition-Mental and Psychomotor Developmental indices were administered at ages 1, 2, and 3 years, the Clinical Evaluation of Language Fundamentals-Preschool, Second Edition, at age 4, and the Wechsler Preschool and Primary Scale of Intelligence, Third Edition, at age 5. Mothers with higher urinary total dialkylphosphate concentrations reported higher levels of socioeconomic status and increased fresh fruit and vegetable intake. We found no associations between prenatal exposure to organophosphate pesticides and cognition at 1-5 years of age. In our cohort, exposure to organophosphate pesticides during pregnancy was not associated with cognition during early childhood. It is possible that a higher socioeconomic status and healthier diet may protect the fetus from potential adverse associations with gestational organophosphate pesticide exposure, or that dietary exposure to the metabolites is innocuous and not an ideal measure of exposure to the parent compound.
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.
ABSTRACT:
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
John Peterson Myers, Michael N. Antoniou, Bruce Blumberg, Lynn Carroll, Theo Colborn, Lorne G. Everett, Michael Hansen, Philip J. Landrigan, Bruce P. Lanphear, Robin Mesnage, Laura N. Vandenberg, Frederick S. vom Saal, Wade V. Welshons and Charles M. Benbrook. “Concerns over use of glyphosate-based herbicides and risks associated with exposures: a consensus statement,” Environmental Health, 2016, 15:19, DOI: 10.1186/s12940-016-0117-0.
ABSTRACT:
The broad-spectrum herbicide glyphosate (common trade name “Roundup”) was first sold to farmers in 1974. Since the late 1970s, the volume of glyphosate-based herbicides (GBHs) applied has increased approximately 100-fold. Further increases in the volume applied are likely due to more and higher rates of application in response to the widespread emergence of glyphosate-resistant weeds and new, pre-harvest, dessicant use patterns. GBHs were developed to replace or reduce reliance on herbicides causing well-documented problems associated with drift and crop damage, slipping efficacy, and human health risks. Initial industry toxicity testing suggested that GBHs posed relatively low risks to non-target species, including mammals, leading regulatory authorities worldwide to set high acceptable exposure limits. To accommodate changes in GBH use patterns associated with genetically engineered, herbicide-tolerant crops, regulators have dramatically increased tolerance levels in maize, oilseed (soybeans and canola), and alfalfa crops and related livestock feeds. Animal and epidemiology studies published in the last decade, however, point to the need for a fresh look at glyphosate toxicity. Furthermore, the World Health Organization’s International Agency for Research on Cancer recently concluded that glyphosate is “probably carcinogenic to humans.” In response to changing GBH use patterns and advances in scientific understanding of their potential hazards, we have produced a Statement of Concern drawing on emerging science relevant to the safety of GBHs. Our Statement of Concern considers current published literature describing GBH uses, mechanisms of action, toxicity in laboratory animals, and epidemiological studies. It also examines the derivation of current human safety standards. We conclude that: (1) GBHs are the most heavily applied herbicide in the world and usage continues to rise; (2) Worldwide, GBHs often contaminate drinking water sources, precipitation, and air, especially in agricultural regions; (3) The half-life of glyphosate in water and soil is longer than previously recognized; (4) Glyphosate and its metabolites are widely present in the global soybean supply; (5) Human exposures to GBHs are rising; (6) Glyphosate is now authoritatively classified as a probable human carcinogen; (7) Regulatory estimates of tolerable daily intakes for glyphosate in the United States and European Union are based on outdated science. We offer a series of recommendations related to the need for new investments in epidemiological studies, biomonitoring, and toxicology studies that draw on the principles of endocrinology to determine whether the effects of GBHs are due to endocrine disrupting activities. We suggest that common commercial formulations of GBHs should be prioritized for inclusion in government-led toxicology testing programs such as the U.S. National Toxicology Program, as well as for biomonitoring as conducted by the U.S. Centers for Disease Control and Prevention. FULL TEXT
Perry MJ, Venners SA, Barr DB, Xu X., “Environmental pyrethroid and organophosphorus insecticide exposures and sperm concentration,” Reproductive Toxicology, 2007, 23:1, DOI: 10.1016/J.REPROTOX.2006.08.005.
ABSTRACT:
BACKGROUND: There is growing concern that poisoning and other adverse health effects are increasing because organophosphorous (OP) insecticides are now being used in combination with pyrethroid (PYR) insecticides to enhance the toxic effects of PYR insecticides on target insects, especially those that have developed PYR resistance.
OBJECTIVES: We conducted a pilot biomonitoring study to determine whether men in our reproductive cohort study were being exposed to pesticides environmentally by virtue of frequenting an agricultural setting.
METHODS: We screened 18 randomly selected urine samples collected from male participants of reproductive age for 24 parent compounds and metabolites of pesticides and examined the results in relation to sperm concentration.
RESULTS: Results showed high prevalence of exposure to OP and PYR pesticides and our preliminary analyses provided some suggestion that the higher exposure group had lower sperm concentration.
CONCLUSIONS: The potential of OP/PYR mixtures to have enhanced human toxicity needs more research attention.
Melissa J. Perry, Anne Marbella, Peter M. Layde, “Nonpersistent Pesticide Exposure Self-report versus Biomonitoring in Farm Pesticide Applicators,” Annals of Epidemiology, 2006, 16:9, DOI: 10.1016/J.ANNEPIDEM.2005.12.004.
ABSTRACT:
PURPOSE: Few studies using biologic markers to examine nonpersistent pesticide exposure among pesticide applicators were conducted in field settings. This study compares self-reported dermal, inhalation, and ingestion exposures with urinalysis results after one-time application of the commonly used herbicide atrazine to field crops. It was hypothesized that: i) applicator reports of exposure would be associated positively with detection of urinary atrazine metabolites, and ii) applicator reports of personal-protective-equipment (PPE) use would be associated negatively with detection of urinary atrazine metabolites.
METHODS: Wisconsin dairy farmers were randomly selected to participate in 1997 to 1998 and were instructed to collect a urine sample 8 hours after the first pesticide application of the season. Farmers then were interviewed within 1 week of their first application to report on application practices. Eighty-six urine samples were analyzed for deethylatrazine, a major atrazine metabolite.
RESULTS: Comparing urinalysis results with self-reported dermal, inhalation, and ingestion exposure showed poor agreement between self-reported exposure and urinary deethylatrazine detections (all κ < 0.40). Multivariate linear regression modeling with deethylatrazine level as the outcome showed that self-reported practices did not significantly predict atrazine metabolite levels.
CONCLUSIONS: Possible explanations for the discrepancies between urinalysis results and self-reported data include: i) inaccuracies in self-reported data and ii) substantial interpersonal variation in atrazine metabolism, resulting in major differences in body burden for similar exposures. Either explanation poses challenges for epidemiologic studies of the health effects of pesticides, which rely solely on self-reported measures of exposure. Additional evaluation of determinants of accuracy in self-assessed occupational and environmental exposures is needed.
René Glynnis English, Melissa Perry, Mary M. Lee, Elaine Hoffman, Steven Delport, Mohamed Aqiel Dalvie, “Farm residence and reproductive health among boys in rural South Africa,” Environment International, 2012, 47, DOI: 10.1016/J.Envint.2012.06.006.
ABSTRACT:
Few studies have investigated reproductive health effects of contemporary agricultural pesticides in boys. To determine the association between pesticide exposure and reproductive health of boys. We conducted a cross-sectional study in rural South Africa of boys living on and off farms. The study included a questionnaire (demographics, general and reproductive health, phyto-estrogen intake, residential history, pesticide exposures, exposures during pregnancy); and a physical examination that included sexual maturity development ratings; testicular volume; height, weight, body mass index; and sex hormone concentrations. Among the 269 boys recruited into the study, 177 (65.8%) were categorized as farm (high pesticide exposures) and 98 (34.2%) as non-farm residents (lower pesticide exposures). Median ages of the two groups were 11.3 vs 12.0 years, respectively (p<0.05). After controlling for confounders that included socioeconomic status, farm boys were shorter (regression coefficient (RC)=-3.42 cm; 95% confidence interval (CI): -6.38 to -0.45 cm) and weighed less (RC=-2.26 kg; CI: -4.44 to -0.75 kg). The farm boys also had lower serum lutenizing hormone (RC=-0.28 IU/L; CI: -0.48 to -0.08 IU/L), but higher serum oestradiol (RC=8.07 pmol/L; CI: 2.34-13.81 pmol/L) and follicle stimulating hormone (RC=0.63 IU/L; CI: 0.19-1.08 U/L). Our study provides evidence that farm residence is associated with adverse growth and reproductive health of pubertal boys which may be due to environmental exposures to hormonally active contemporary agricultural pesticides.
Heather A Young, John D Meeker, Sheena E Martenies, Zaida I Figueroa, Dana Boyd Barr and Melissa J Perry, “Environmental exposure to pyrethroids and sperm sex chromosome disomy: a cross-sectional study,” Environmental Health, 2013, 12:111, DOI: 10.1186/1476-069X-12-111.
ABSTRACT:
BACKGROUND: The role of environmental pesticide exposures, such as pyrethroids, and their relationship to sperm abnormalities are not well understood. This study investigated whether environmental exposure to pyrethroids was associated with altered frequency of sperm sex chromosome disomy in adult men.
METHODS: A sample of 75 subjects recruited through a Massachusetts infertility clinic provided urine and semen samples. Individual exposures were measured as urinary concentrations of three pyrethroid metabolites ((3-phenoxybenzoic acid (3PBA), cis- and trans- 3-(2,2-Dichlorovinyl)-1-methylcyclopropane-1,2-dicarboxylic acid (CDCCA and TDCCA)). Multiprobe fluorescence in situ hybridization for chromosomes X, Y, and 18 was used to determine XX, YY, XY, 1818, and total sex chromosome disomy in sperm nuclei. Poisson regression analysis was used to examine the association between aneuploidy rates and pyrethroid metabolites while adjusting for covariates.
RESULTS: Between 25-56% of the sample were above the limit of detection (LOD) for the pyrethroid metabolites. All sex chromosome disomies were increased by 7-30% when comparing men with CDCCA and TDCCA levels above the LOD to those below the LOD. For 3PBA, compared to those below the LOD, those above the LOD had YY18 disomy rates 1.28 times higher (95% CI: 1.15, 1.42) whereas a reduced rate was seen for XY18 and total disomy (IRR = 0.82; 95% CI: 0.77, 0.87; IRR = 0.93; 95% CI: 0.87-0.97), and no association was seen for XX18 and 1818.
CONCLUSIONS: Our findings suggest that urinary concentrations of CDCCA and TDCCA above the LOD were associated with increased rates of aneuploidy. However the findings for 3BPA were not consistent. This is the first study to examine these relationships, and replication of our findings is needed before the association between pyrethroid metabolites and aneuploidy can be fully defined. FULL TEXT