Wednesday, March 25, 2015

Pesticide study shows Autism linked to pesticide use.

Pesticides first destroyed the neurological process of bees and other pollinators.
 Children now suffer the same neurological damage from the same pesticides.

Environ Health Perspect; DOI:10.1289/ehp.1307044

Neurodevelopmental Disorders and Prenatal Residential Proximity to Agricultural Pesticides: The CHARGE Study

Janie F. Shelton,1 Estella M. Geraghty,2 Daniel J. Tancredi,3,4 Lora D. Delwiche,1 Rebecca J. Schmidt,1 Beate Ritz,5,6,7 Robin L. Hansen,3,8 and Irva Hertz-Picciotto1,8
Author Affiliations open
PDF icon PDF Version (175 KB)
  • 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.


California is the top agriculture-producing state in the nation, grossing $38 billion in revenue from farm crops in 2010 (California Department of Food and Agriculture 2010). Each year approximately 200 million pounds of active pesticide ingredients are applied throughout the state [California Department of Pesticide Regulation (CDPR) 2014]. Although pesticides are critical for the modern agricultural industry, certain commonly used pesticides have been associated with abnormal and impaired neurodevelopment in children (Bouchard et al. 2010, 2011; Engel et al. 2007; Eskenazi et al. 2006; Grandjean et al. 2006; Guillette et al. 1998; Rauh et al. 2006; Ribas-Fito et al. 2006; Torres-Sánchez et al. 2007; Young et al. 2005). In addition, specific associations have been reported between agricultural pesticides and autism spectrum disorders (ASD) (Roberts et al. 2007) and the broader diagnostic category under which autism falls, the pervasive developmental disorder (PDD) (Eskenazi et al. 2007).
Developmental delay (DD) refers to significant delays young children experience reaching milestones in relation to cognitive or adaptive development. Adaptive skills include communication, self-care, social relationships, and/or motor skills. In the United States, DD affects approximately 3.9% of all children 3–10 years of age, and is approximately 1.7 times more common among boys than girls (Boyle et al. 2011).
Autism is a developmental disorder with symptoms appearing by 3 years of age. Specific deficits occur in domains of social interaction and language, and individuals show restricted and repetitive behaviors, activities, or movements (American Psychiatric Association 2000). The ASDs represent lower severity, usually with regard to language ability. ASDs affect boys 4–5 times more than girls, and the Centers for Disease Control and Prevention (2012) recently estimated a prevalence of 1.1% among children 8 years of age, a 78% increase since their 2007 estimate. Available evidence suggests that causes of both ASD and DD are heterogeneous and that environmental factors can contribute strongly to risk (Hallmayer et al. 2011; Mendola et al. 2002).
The majority of pesticides sold in the United States are neurotoxic and operate through one of three primary mechanisms: a) inhibition of acetylcholinesterase (AChE), b) voltage-gated sodium channel disruption, and/or c) inhibition of gamma-aminobutyric acid (GABA) (Casida 2009). AChE primarily functions as an inhibitory neurotransmitter, but also has critical roles in the development of learning, cognition, and memory. GABA is also an inhibitory neurotransmitter, and is necessary for development and maintenance of neuronal transmission.
Although limited research has assessed in utero exposures to pesticides, animal models (rats) of early exposure to organophosphates showed more severe neurodevelopmental effects for males than for females (Levin et al. 2001, 2010). On the basis of previously published epidemiology or mechanistic considerations, we selected the following pesticide families to investigate for this analysis: organophosphates, carbamates, organochlorines, and pyrethroids. Potential mechanisms linking these select pesticide groups to autism pathophysiology were recently reviewed (Shelton et al. 2012).
The aim of this paper was to explore the relationship between agricultural pesticide applications and neurodevelopmental outcomes by a) assessing the gestational exposure during pregnancy to CHARGE (Childhood Autism Risks from Genes and Environment) study mothers, b) testing the hypothesis that children with ASD or DD had higher risk of exposure in utero than typically developing children, and c) evaluating specific windows of vulnerability during gestation. Because of the well-defined case and control populations in the CHARGE study and the comprehensive availability of potential confounders, this analysis serves as exploratory research to identify environmental risk factors for ASD and DD, and contributes to a broader understanding of the potential risks to neurodevelopment from agricultural pesticides in a diverse population of California residents.


Study design. The CHARGE study is an ongoing California population-based case–control study that aims to uncover a broad array of factors contributing to autism and developmental delay (Hertz-Picciotto et al. 2006). Since 2003, the CHARGE study has enrolled > 1,600 participants whose parents answer extensive questionnaires regarding environmental exposures including their place of residence during pregnancy. Here we report on ASD and DD in relation to gestational residential proximity to agricultural pesticide applications. The group of children with ASD includes approximately two-thirds with a diagnosis of full-syndrome autism or autistic disorder (68%) and one-third with a diagnosis of an autism spectrum disorder (32%).
Cases were recruited from children diagnosed with full-syndrome ASD or DD in one of the regional centers of the California Department of Developmental Services (DDS). Eligibility in the DDS system does not depend on citizenship or financial status, and is widely used across socioeconomic levels and racial/ethnic groups. It is estimated that 75–80% of the total population of children with an autism diagnosis are enrolled in the system (Croen et al. 2002). In addition to recruitment through the regional centers, some CHARGE participants are also recruited through referrals from other clinics, self-referral, or general outreach. The referents are recruited from the general population (GP) identified through California birth records, and are frequency matched to the autism case population on sex, age, and the catchment area for the regional they would have gone to, had they been a case. Children are eligible if they are 2–5 years of age, born in California, live with a biological parent who speaks either English or Spanish, and reside in the study catchment area. Currently, the catchment area for the CHARGE study participants consists of a 2-hr drive from the Sacramento area, but previously included participants from Southern California. Early in the study, recruitment in Southern California was terminated due to logistical difficulties that led to lower enrollment of general population controls.
Parents of children coming into the study with a previous diagnosis of ASD are administered the Autism Diagnostic Interview–Revised (ADI-R; Le Couteur et al. 2003; Lord et al. 1994, 1997), surveyed regarding a wide range of environmental exposures, and asked to report all addresses where they lived from 3 months before conception to the time of the interview.
Participating children are administered the Autism Diagnostic Observation Schedule (ADOS; Lord et al. 2000, 2003), which, combined with the ADI-R, is used to either confirm their diagnosis or reclassify them for purposes of our study. To rule out ASD, children who enter the study without an ASD diagnosis (from the DD or GP groups) are given the Social Communications Questionnaire (SCQ) (Rutter et al. 2003). Children with a previous diagnosis of DD are evaluated on both the Mullen Scales of Early Learning (MSEL) (Mullen 1995) and Vineland Adaptive Behavioral Scale (VABS) (Sparrow 2005). DD is confirmed if they scored ≥ 15 on the SCQ and ≤ 2 SDs lower than the mean (< 70) on the composite scores of MSEL and VABS. Those meeting criteria for one test, scoring < 77 on the other, and not qualifying for ASD, are classified as atypical and combined with the DD group (25 of the 168) for this analysis. For this sample, of those who entered the study as typically developing, 26 were reclassified with DD and 2 with ASD. Of those who entered as DD, 36 were reclassified with ASD. Only cases with completed diagnostic testing were included in the analysis presented here. Additional details on CHARGE study protocols have been published elsewhere (Hertz-Picciotto et al. 2006).
This study was approved by the institutional review boards for the State of California and the University of California. Written informed consent was obtained by the parent or guardian before collection of any data.
Estimation of pesticide exposures. Since 1990, California has required commercial application of agricultural pesticides to be reported to the CDPR, which makes data publically available in the form of the annual Pesticide Use Report (PUR). As described by CDPR (2014), the pesticide use report data includes
pesticide applications to parks, golf courses, cemeteries, rangeland, pastures, and along roadside and railroad rights-of-way. In addition, all postharvest pesticide treatments of agricultural commodities must be reported along with all pesticide treatments in poultry and fish production as well as some livestock applications. The primary exceptions to the reporting requirements are home-and-garden use and most industrial and institutional uses.
The PUR database includes all commercial applications at the county level, requiring spatially explicit (latitude and longitude) reporting for commercial agricultural applications. The PUR database then compiles agricultural pesticide applications throughout the state by square-mile areas (1.0 m2 or 2.6 km2) set by the U.S. Geological Survey, referred to as a meridian-township-range-section (MTRS). The amount of chemical applied is assigned to an MTRS by date, in pounds (each pound is 0.45 kg) of active ingredient only, excluding synergists and other compounds in the formulation. Mapping software (ArcGIS v10.0; ESRI, Redlands, CA) was used to create a geographic centroid (center-most point in the square mile) for each MTRS for use in this analysis.
From the CHARGE questionnaire administered to the parent, residential addresses were collected and assigned for each day of the pre-conception and pregnancy periods, beginning 3 months before conception and ending with delivery, thereby accounting for participants who changed residences during that time. Addresses were manually cleaned for spelling errors and standardized in ZIP+4 software ( Of the 1,043 diagnostically evaluated participants at the time of this study, 983 had given address data for the time period of interest. Overall, 99% of addresses (970 participants with 1,319 unique addresses) were successfully geocoded to obtain a longitude and latitude with a match rate of at least 80% in ArcMap (ArcGIS v10.0; ESRI) using the U.S. Rooftop search algorithm. Unmatched addresses (n = 5) or ties (n = 10) were manually matched to the most likely address.
Next, a spatial model was developed in ArcMap, which created three buffers of varying sizes around each residence with radii of 1.25 km, 1.5 km, and 1.75 km. Where the buffer intersected a centroid (or multiple centroids), the MTRS corresponding with that centroid was assigned to that residence; subsequently, pesticides applied in that MTRS (or multiple MTRSs) were considered exposures for that mother with the timing based on linking the date of application to the dates of her pregnancy. Each pregnancy therefore was assigned an exposure profile corresponding to applications made to the MTRS nearest the mother’s home and days of her pregnancy on which those applications occurred (for a visual representation of the exposure model, see Supplemental Material, Figure S1).
We classified chemicals in the PUR according to chemical structure as members of the organophosphate, carbamate, pyrethroid, or organochlorine classes of pesticides. Subclasses of pyrethroids were categorized as type 1 and type 2 because they induce distinct behavioral effects in animal studies (Agency for Toxic Substances and Disease Registry 2003; Breckenridge et al. 2009). In addition, chlorpyrifos, an organophosphate widely used in agriculture, was explored independently because previous research had associated higher levels of prenatal exposure with diminished psychomotor and mental development in children at 3 years of age (Rauh et al. 2006).
Statistical analysis. Most homes (~ 70%) received estimated agricultural pesticide exposure values of 0 because there was no pesticide applied within the buffer zone. For ease of interpretation, we created, for each time period, binary (1 = exposed vs. 0 = not exposed) indicators as independent variables. Multinomial (polytomous) multivariate logistic regression modeling with survey weights was used to estimate the association of prenatal residential proximity to applied pesticides with a binary exposure variable (1 = exposed vs. 0 = not exposed) and a 3-level case status outcome [ASD/DD/TD (typically developing)], using TD children as the reference group. Because it was the only chemical evaluated independently as opposed to an aggregated class of chemicals with varying toxicity levels, chlorpyrifos (an organophosphate) was evaluated both as a dichotomous (any exposure within the buffer area vs. none) and as a continuous variable (untransformed, per 100 lb). Separate models were run for each time period, for each pesticide class of interest, and for alternative residential buffer radii.
Potential confounders were first identified as a) variables that may influence one’s exposure to pesticides, and b) variables that are known to influence the risk of ASD or DD, with no requirement for statistical significance of the univariate association with either the exposure or outcome, but rather an initial evaluation of the relationship between those variables. Formal confounder identification and inclusion was assessed using the combined directed acyclic graph (DAG) and change-in-estimate (in this case, a 10% change in the β of the primary exposure variable in the regression model) criteria (Weng et al. 2009). The DAG was used to establish which variables could potentially confound the associations between ASD or DD and exposure to agricultural pesticides, and the change in estimate criteria was then used to exclude inclusion of those variables that induced minimal (< 10%) change in the β estimate. All other variables which were identified as confounders and met the criteria of a ≥ 10% change in the β were included in the final models.
During model selection, we tested the joint versus independent effects of two classes of pesticides (e.g., pyrethroids and organophosphates) in models that contained each independent variable (dichotomous) for the two pesticides and an interaction variable of those two dichotomous variables. We also explored the possibility that another pesticide was responsible for the observed association due to correlation between pesticides (i.e., if one class is applied, another is more likely to be applied in that same buffer zone) by treating other classes of pesticides as potential confounders.
Final models were adjusted for paternal education (categorical), home ownership (binary), maternal place of birth (United States, Mexico, or outside the United States and Mexico), child race/ethnicity (white, Hispanic, other), maternal prenatal vitamin intake (binary; taken during the 3 months before pregnancy through the first month), and year of birth (continuous). Prenatal vitamin consumption in this time window was found in previous work to have an inverse association with ASD, meaning that early prenatal vitamin intake may confer a lower risk of ASD (Schmidt et al. 2011). Other potential confounders explored but found not to satisfy criteria for confounding (based on inclusion in the DAG or the change in estimate criterion) were distance from a major freeway, maternal major metabolic disorders (diabetes, hypertension, and obesity), gestational age (days), latitude of residence, type of insurance used to pay for the delivery (public vs. private), maternal age, paternal age, and season of conception. Maternal age, though a known risk for ASD, does not differ significantly between cases and controls in the CHARGE study because the participating mothers of TD children are older than those of the GP (Table 1).
Table 1 - See HTML for full tableTable 1 – Characteristics [n (%) or mean ± SD] of the CHARGE study population (n = 970).
View Table (HTML Version)
View larger image (TIF File)
All statistical analyses were conducted using SAS software (version 9.3; SAS Institute Inc., Cary, NC). Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multinomial (polytomous) logistic regression models (PROC SURVEYLOGISTIC) with “survey” weights. Frequency-matching factors (regional center, age, and sex of child) were included to adjust for sampling strata using a STRATA statement.
The weights we used in exposure frequency and multinomial models adjusted for differential probabilities of enrollment in the study by case or control groups (ASD, DD, and GP controls) and by social and demographic factors (child race/ethnicity, maternal age, maternal education, insurance payment type at birth, regional center, parity, and maternal birth place) that influence voluntary participation in a case–control study. These weights represent the inverse of the probability of participation, within case and demographically defined groups. Thus, the weighted frequency distributions and regression models more accurately represent findings generalizable to the broader recruitment pools from which participants were drawn.


During pregnancy, residences of the CHARGE study participants were distributed broadly throughout California, with the greatest concentrations in Sacramento Valley, followed by the San Francisco Bay area and Los Angeles. One-third lived within 1.5 km of an agricultural pesticide application from one of the four pesticide classes evaluated. ASD and TD groups had similar sociodemographic profiles, with some variation by regional center, prenatal vitamin intake, and maternal place of birth, and more ASD cases were recruited earlier in the study than DD or TD children (Table 1). As described in “Methods,” early in the study, challenges were encountered recruiting non-ASD participants in Southern California, resulting in a greater proportion of ASD participants relative to TD participants from that regional center. The DD case group, which was not matched, differed from the reference group on many characteristics, including sex, race/ethnicity, maternal birth place, regional center, maternal education, and paternal education and appears to be of substantially lower socioeconomic status than either the ASD or TD groups (Table 1). Age of the child at enrollment was similar between the ASD and DD groups compared with the TD groups.
In the CHARGE study population, of the pesticides evaluated, organophosphates were the most commonly applied agricultural pesticide near the home during pregnancy. In the group exposed to organophosphates within 1.5 km of the home, 21 unique compounds were identified, the most abundant of which was chlorpyrifos (20.7%), followed by acephate (15.4%), and diazinon (14.5%) (see Supplemental Material, Table S1). The second most commonly applied class of pesticides was the pyrethroids, one-quarter of which was esfenvalerate (24%), followed by lamda-cyhalothrin (17.3%), permethrin (16.5%), cypermethrin (12.8%), and tau-fluvalinate (10.5%). Of the carbamates, approximately 80% were methomyl or carbaryl, and of the organochlorines, 60% of all applications were dienochlor. Among those exposed, only one-third were exposed to a single compound over the course of the pregnancy.
In the unweighted study population, little difference in exposure proportion was apparent, yet once the survey weights were applied, both case populations had higher exposure proportions than the TD controls, indicating that factors associated with exposure were also associated with study participation (Table 2). Because the study weights reflect the distributions of the three recruitment strata (ASD, DD, and TD controls) in the pool from which they were drawn, differences between case and control participation by regional center catchment area likely accounts for this effect. For example, DD cases proportionally under-enrolled in the CHARGE study from the Valley Mountain regional center compared with the recruitment pool. Because the Valley region had the highest proportion of exposed participants, weights that accounted for the discrepancy between the proportions of DD cases enrolled from the Valley region would more accurately represent the population distribution of cases and controls.
Table 2 - See HTML for full tableTable 2 – Exposure to pesticide applications (any vs. none) within 1.5 km of the home during the 3 months before conception through delivery according to outcome (ASD n = 486, DD n = 168, TD n = 316).
View Table (HTML Version)
View larger image (TIF File)
By pounds applied, the amount of pyrethroids and organophosphates (continuous, unweighted) applied within 1.5 km of the home were strongly correlated with each other (ρ = 0.74, p < 0.0001) and to a lesser extent organophosphates with carbamates (ρ = 0.45, p = 0.01) and carbamates with pyrethroids (ρ = 0.44, p < 0.0001). Because of the low prevalence of organochlorines and type 1 pyrethroids, these were excluded from the analyses, and carbamate exposure, though evaluated for pregnancy (any vs. none), was not evaluated by trimester due to small cell sizes of exposed participants. Overall, exposure to pesticides during gestation was slightly more common for male children than for female children (31% vs. 26%, p = 0.004).
For exposure (any vs. none) during pregnancy, children with ASD were 60% more likely to have organophosphates applied nearby the home [1.25 km distance; adjusted OR (aOR) = 1.60; 95% CI: 1.02–2.51] than mothers of TD children. Children with DD were nearly 150% more likely to have carbamate pesticides applied near the home during pregnancy (1.25 km distance; aOR = 2.48; 95% CI: 1.04–5.91). Both of these associations lessened as the buffer size grew larger (Tables 3 and 4), lending support to an exposure–response gradient.
Table 3 - See HTML for full tableTable 3 – Adjusted ORsa (95% CIs) for ASD and residential proximity to agricultural pesticide applications (any vs. none) within prespecified buffers, by time period.b
View Table (HTML Version)
View larger image (TIF File)
Table 4 - See HTML for full tableTable 4 – Adjusted ORsa (95% CIs) for DD and residential proximity to agricultural pesticide applications (any vs. none) within prespecified buffers, by time period.b
View Table (HTML Version)
View larger image (TIF File)
Examining specific gestational time windows, associations with pesticide applications of organophosphates and pyrethroids suggested an association between second- and third-trimester exposure to organophosphates and ASD, and preconception and third-trimester pyrethroid exposure (Table 3). Although those time periods describe the statistically significant associations, many of the effect estimates tended away from the null, which indicates a lack of precision in the specificity of any one time period and compound presented here.
For DD, the sample size permitted only temporal associations to be evaluated for organophosphates and pyrethroids, which were mostly > 1 (the null value), but only one statistically significant association was detected for third-trimester pyrethroid applications. In general, likely because a smaller sample of DD cases was exposed to agricultural pesticides, the estimates had a lower level of precision than the ASD case group. In addition, although carbamates were associated with DD for applications during pregnancy, the sample of exposed cases was too small to evaluate by trimester (Table 4).
For models evaluating the exposure to chlorpyrifos as a continuous variable with all other covariates remaining the same as above models, each 100-lb (45.4 kg) increase in the amount applied over the course of pregnancy (within 1.5 km of the home) was associated with a 14% higher prevalence of ASD (aOR = 1.14; 95% CI: 1.0, 1.32), but no association was detected with DD. Because aggregate classes of chemical do not have a uniform toxicity, we did not examine the pounds of classes (e.g., organophosphates) of chemicals as a continuous variable because compounds with a higher toxicity may be applied in lower volumes.
The role of simultaneous exposure to multiple classes of pesticides was evaluated in post hoc analyses. First, we evaluated combined categories of organophosphates and pyrethroids, organophosphates and carbamates, and pyrethroids or carbamates as a 3-level variable (0 = unexposed, 1 = exposed to one or the other, and 2 = exposed to both). However, effects from multiple exposures were not found to be higher than the observations of the individual classes of pesticides. Second, we adjusted models of one pesticide for the other. In models for organophosphates, adjusting for pyrethroids attenuated the third-trimester association with ASD slightly, but not substantially (< 10% change in β estimate) (data not shown). In additional analyses, we evaluated the sensitivity of the estimates to the choice of buffer size, using four additional sizes between 1 and 2 km: Results and interpretation remained stable (data not shown).


Applications of two of the most common agricultural pesticides (organophosphates and pyrethroids) nearby the home may increase the prevalence of ASD. Specifically, we observed positive associations between ASD and prenatal residential proximity to organophosphate pesticides in the second (for chlorpyrifos) and third trimesters (organophosphates overall), and pyrethroids in the 3 months before conception and in the third trimester. Our findings relating agricultural pesticides to DD were less robust, but suggested an associated with applications of carbamates during pregnancy nearby the home. Because pesticide exposure is correlated in space and time, differences in time windows of vulnerability, if they exist, may be difficult to detect, and variation in associations according to time window of exposure may not represent causal variation.
These findings support the results of two previous studies linking ASD to gestational agricultural pesticide exposure. Using data from the California Department of Developmental Services and California Birth Records, Roberts et al. (2007) conducted a case–control study of 465 cases of autism and 6,975 controls. Although their main finding was an association between ASD and residential proximity to organochlorine compound applications (which we could not evaluate due to low exposure prevalence of this chemical class), they also reported associations with gestational exposures to organophosphates [β = 0.462, p-value 0.042 (confidence interval not reported) and bifenthrin (β = 1.57, p-value = 0.049 (confidence interval not reported)], a pyrethroid pesticide (Roberts et al. 2007). Eskenazi et al. (2007) found a relationship between symptoms of PDD and prenatal urinary metabolites of organophosphates in a cohort study (CHAMACOS; Center for the Health Assessment of Mothers and Children of Salinas) of mothers living in the Salinas valley. Each 10-fold increase in these metabolites doubled the odds (OR = 2.3, p = 0.05) of PDD at 2 years of age; postnatal concentrations showed some association as well (OR = 1.7, p = 0.04) (Eskenazi et al. 2007). Several studies have also reported evidence of an interaction between organophosphate exposure and polymorphisms for the PON1 gene, which codes for the enzyme paroxonase 1, in relation to neurodevelopment (Costa et al. 2005; D’Amelio et al. 2005; Furlong et al. 2005; Lee et al. 2013).
With regard to DD, several studies have reported associations of pesticide exposures with continuous scores on specific cognitive tests. For example, in a cross-sectional study of 72 children < 9 years of age in Ecuador, those prenatally exposed to pesticides as assessed by maternal occupation in the floriculture industry during pregnancy performed worse on the Stanford-Binet copying test than did children whose mothers did not work in floriculture during pregnancy (Grandjean et al. 2006). In another study of maternal occupation in the flower industry, exposed children performed worse on tests of communication, visual acuity, and fine motor skills, with delays of 1.5–2 years in reaching normal developmental milestones (Handal et al. 2008). In the CHAMACOS cohort, organophosphate urinary metabolites from the first and second halves of pregnancy were associated with an average deficit of 7.0 IQ points, comparing the highest quintile to the lowest (Bouchard et al. 2011). A study of inner city children at 3 years of age found that those with the highest (vs. lowest) umbilical cord concentrations of chlorpyrifos were 5 times more likely to have delayed psychomotor development and 2.4 times more likely to have delayed mental development as assessed by cut-off values of continuous scores on the Bayley Scales of Infant Development-II (Rauh et al. 2006).
Strengths of this study include well-defined case and control populations confirmed by standardized diagnostic instruments, extensive information on covariates, and a thorough confounder identification and control strategy. Because children can overcome developmental delay, or may move in or out of the ASD case definition over time, diagnostic confirmation at enrollment minimized outcome misclassification. Further, collection of information on all addresses during pregnancy likely reduced exposure misclassification, because 20% of the population had moved at least once during pregnancy.
Several limitations to this study were unavoidable in the exposure assessment, potentially producing misclassification. Primarily, our exposure estimation approach does not encompass all potential sources of exposure to each of these compounds: Among them were external nonagricultural sources (e.g., institutional use, such as around schools); residential indoor use; professional pesticide application in or around the home for gardening, landscaping or other pest control; and dietary sources (Morgan 2012). Other sources of potential error include errors in reporting to the PUR database, the assumption of homogeneity of exposure within each buffer, and potential geocoding errors. Seasonal variation and address changes mid-pregnancy were accounted for by assigning an address to each day instead of one address for the individual, but information on hours spent in the home or elsewhere was not available.
Use of the PUR data has been refined by some researchers who have enhanced the 1-mi2 resolution of the PUR data by incorporating land use data (Nuckols et al. 2007; Rull and Ritz 2003). This approach demonstrates higher correlation of PUR-based exposure estimates with in-home carpet dust pesticide concentrations than the PUR data alone (Gunier et al. 2011). In our case, land use reports were not available for about half the CHARGE study counties; given an already low prevalence of exposure, the loss of power by excluding those counties would have outweighed any benefit of increased specificity in exposure estimates from land use data.
Although organophosphate use drastically increased between the 1960s through the late 1990s (U.S. Department of Agriculture 2006), over the past decade, use has been declining (U.S. Environmental Protection Agency 2011). For indoor use, chlorpyrifos has largely been replaced with pyrethroids (Williams et al. 2008), but research indicates pyrethroids may not necessarily be safer. In an in vitro study comparing the toxicity of a common pyrethroid, cyfluthrin, with chlorpyrifos, at the same doses cyfluthrin induced either an equivalent or higher toxic effect on the growth, survival, and function of primary fetal human astrocytes, and induced inflammatory action of astrocytes that can mediate neurotoxicity (Mense et al. 2006). In another in vitro study comparing the neurotoxicity of fipronil to chlorpyrifos, fipronil induced more oxidative stress and resulted in lower cell counts for nondifferentiated PC12 cells than chlorpyrifos, and disrupted cell development at lower thresholds, leading the authors to conclude that fipronil was in fact more detrimental to neuronal cell development than chlorpyrifos (Lassiter et al. 2009). Although further studies are underway, because of the observed associations in humans and direct effects on neurodevelopmental toxicity in animal studies, caution is warranted for women to avoid direct contact with pesticides during pregnancy.


Children of mothers who live near agricultural areas, or who are otherwise exposed to organophosphate, pyrethroid, or carbamate pesticides during gestation may be at increased risk for neurodevelopmental disorders. Further research on gene–environment interactions may reveal vulnerable subpopulations.


Agency for Toxic Substances and Disease Registry. 2003. Toxicological Profile for Pyrethrins and Pyrethroids. Available:​55.pdf [accessed 22 February 2014].
American Psychiatric Association. 2000. Diagnostic and Statistical Manual of Mental Disorders-IV-TR. Washington, DC:American Psychiatric Association.
Bouchard MF, Bellinger DC, Wright RO, Weisskopf MG. 2010. Attention-deficit/hyperactivity disorder and urinary metabolites of organophosphate pesticides. Pediatrics 125(6):e1270–e1277.
Bouchard MF, Chevrier J, Harley KG, Kogut K, Vedar M, Calderon N, et al. 2011. Prenatal exposure to organophosphate pesticides and IQ in 7-year-old children. Environ Health Perspect 119:1189–1195; doi: 10.1289/ehp.1003185.
Boyle CA, Boulet S, Schieve LA, Cohen RA, Blumberg SJ, Yeargin-Allsopp M, et al. 2011. Trends in the prevalence of developmental disabilities in US children, 1997–2008. Pediatrics 127(6):1034–1042.
Breckenridge CB, Holden L, Sturgess N, Weiner M, Sheets L, Sargent D, et al. 2009. Evidence for a separate mechanism of toxicity for the Type I and the Type II pyrethroid insecticides. Neurotoxicology 30(suppl 1):S17–S31.
California Department of Food and Agriculture. 2010. California Agricultural Production Statistics. Available: [accessed 12 February 2012].
Casida JE. 2009. Pest toxicology: the primary mechanisms of pesticide action. Chem Res Toxicol 22(4):609–619.
CDPR (California Department of Pesticide Regulation). 2014. Pesticide Use Reporting (PUR). Available:​htm [accessed 22 May 2014].
Centers for Disease Control and Prevention. 2012. Prevalence of Autism Spectrum Disorders—Autism and Developmental Disabilities Monitoring Network, 14 Sites, United States, 2008. Available:​/ss6103a1.htm [accessed 27 May 2014].
Costa LG, Cole TB, Vitalone A, Furlong CE. 2005. Measurement of paraoxonase (PON1) status as a potential biomarker of susceptibility to organophosphate toxicity. Clin Chim Acta 352(1–2):37–47.
Croen LA, Grether JK, Hoogstrate J, Selvin S. 2002. The changing prevalence of autism in California. J Autism Dev Disord 32(3):207–215.
D’Amelio M, Ricci I, Sacco R, Liu X, D’Agruma L, Muscarella LA, et al. 2005. Paraoxonase gene variants are associated with autism in North America, but not in Italy: possible regional specificity in gene–environment interactions. Mol Psychiatry 10(11):1006–1016.
Engel SM, Berkowitz GS, Barr DB, Teitelbaum SL, Siskind J, Meisel SJ, et al. 2007. Prenatal organophosphate metabolite and organochlorine levels and performance on the Brazelton Neonatal Behavioral Assessment Scale in a multiethnic pregnancy cohort. Am J Epidemiol 165(12):1397–1404.
Eskenazi B, Marks AR, Bradman A, Fenster L, Johnson C, Barr DB, et al. 2006. In utero exposure to dichlorodiphenyltrichloroethane (DDT) and dichlorodiphenyldichloroethylene (DDE) and neurodevelopment among young Mexican American children. Pediatrics 118(1):233–241.
Eskenazi B, Marks AR, Bradman A, Harley K, Barr DB, Johnson C, et al. 2007. Organophosphate pesticide exposure and neurodevelopment in young Mexican-American children. Environ Health Perspect 115:792–798; doi: 10.1289/ehp.9828.
Furlong CE, Cole TB, Jarvik GP, Pettan-Brewer C, Geiss GK, Richter RJ, et al. 2005. Role of paraoxonase (PON1) status in pesticide sensitivity: genetic and temporal determinants. Neurotoxicology 26(4):651–659.
Grandjean P, Harari R, Barr DB, Debes F. 2006. Pesticide exposure and stunting as independent predictors of neurobehavioral deficits in Ecuadorian school children. Pediatrics 117(3):e546–e556.
Guillette EA, Meza MM, Aquilar MG, Soto AD, Garcia IE. 1998. An anthropological approach to the evaluation of preschool children exposed to pesticides in Mexico. Environ Health Perspect 106:347–353.
Gunier RB, Ward MH, Airola M, Bell EM, Colt J, Nishioka M, et al. 2011. Determinants of agricultural pesticide concentrations in carpet dust. Environ Health Perspect 119:970–976; doi: 10.1289/ehp.1002532.
Hallmayer J, Cleveland S, Torres A, Phillips J, Cohen B, Torigoe T, et al. 2011. Genetic heritability and shared environmental factors among twin pairs with autism. Arch Gen Psychiatry 68(11):1095–1102.
Handal AJ, Harlow SD, Breilh J, Lozoff B. 2008. Occupational exposure to pesticides during pregnancy and neurobehavioral development of infants and toddlers. Epidemiology 19(6):851–859.
Hertz-Picciotto I, Croen LA, Hansen R, Jones CR, van de Water J, Pessah IN. 2006. The CHARGE study: an epidemiologic investigation of genetic and environmental factors contributing to autism. Environ Health Perspect 114:1119–1125; doi: 10.1289/ehp.8483.
Lassiter TL, MacKillop EA, Ryde IT, Seidler FJ, Slotkin TA. 2009. Is fipronil safer than chlorpyrifos? Comparative developmental neurotoxicity modeled in PC12 cells. Brain Res Bull 78(6):313–322.
Le Couteur A, Lord C, Rutter M. 2003. Autism Diagnostic Interview–Revised (ADI-R). Los Angeles:Western Psychological Services.
Lee PC, Rhodes SL, Sinsheimer JS, Bronstein J, Ritz B. 2013. Functional paraoxonase 1 variants modify the risk of Parkinson’s disease due to organophosphate exposure. Environ Int 56:42–47.
Levin ED, Addy N, Nakajima A, Christopher NC, Seidler FJ, Slotkin TA. 2001. Persistent behavioral consequences of neonatal chlorpyrifos exposure in rats. Brain Res Dev Brain Res 130(1):83–89.
Levin ED, Timofeeva OA, Yang L, Petro A, Ryde IT, Wrench N, et al. 2010. Early postnatal parathion exposure in rats causes sex-selective cognitive impairment and neurotransmitter defects which emerge in aging. Behav Brain Res 208(2):319–327.
Lord C, Pickles A, McLennan J, Rutter M, Bregman J, Folstein S, et al. 1997. Diagnosing autism: analyses of data from the Autism Diagnostic Interview. J Autism Dev Disord 27(5):501–517.
Lord C, Rutter M, DiLavore PC, Risi S. 2000. The Autism Diagnostic Observation Schedule (ADOS). Los Angeles:Western Psychological Services.
Lord C, Rutter M, DiLavore PC, Risi S. 2003. Autism Diagnostic Observation Schedule Manual. Los Angeles:Western Psychological Services.
Lord C, Rutter M, Le Couteur A. 1994. Autism Diagnostic Interview–Revised: a revised version of a diagnostic interview for caregivers of individuals with possible pervasive developmental disorders. J Autism Dev Disord 24(5):659–685.
Mendola P, Selevan SG, Gutter S, Rice D. 2002. Environmental factors associated with a spectrum of neurodevelopmental deficits. Ment Retard Dev Disabil Res Rev 8(3):188–197.
Mense SM, Sengupta A, Lan C, Zhou M, Bentsman G, Volsky DJ, et al. 2006. The common insecticides cyfluthrin and chlorpyrifos alter the expression of a subset of genes with diverse functions in primary human astrocytes. Toxicol Sci 93(1):125–135.
Morgan MK. 2012. Children’s exposures to pyrethroid insecticides at home: a review of data collected in published exposure measurement studies conducted in the United States. Int J Environ Res Public Health 9(8):2964–2985.
Mullen EM. 1995. Mullen Scales of Early Learning. Circle Pines, MN:American Guidance Services Inc.
Nuckols JR, Gunier RB, Riggs P, Miller R, Reynolds P, Ward MH. 2007. Linkage of the California Pesticide Use Reporting Database with spatial land use data for exposure assessment. Environ Health Perspect 115:684–689; doi: 10.1289/ehp.9518.
Rauh VA, Garfinkel R, Perera FP, Andrews HF, Hoepner L, Barr DB, et al. 2006. Impact of prenatal chlorpyrifos exposure on neurodevelopment in the first 3 years of life among inner-city children. Pediatrics 118(6):e1845–e1859.
Ribas-Fito N, Torrent M, Carrizo D, Munoz-Ortiz L, Julvez J, Grimalt JO, et al. 2006. In utero exposure to background concentrations of DDT and cognitive functioning among preschoolers. Am J Epidemiol 164(10):955–962.
Roberts EM, English PB, Grether JK, Windham GC, Somberg L, Wolff C. 2007. Maternal residence near agricultural pesticide applications and autism spectrum disorders among children in the California Central Valley. Environ Health Perspect 115:1482–1489; doi: 10.1289/ehp.10168.
Rull RP, Ritz B. 2003. Historical pesticide exposure in California using pesticide use reports and land-use surveys: an assessment of misclassification error and bias. Environ Health Perspect 111:1582–1589; doi: 10.1289/ehp.6118.
Rutter M, Bailey A, Berument SK, Lord C, Pickles A. 2003. Social Communication Questionnaire (SCQ). Los Angeles:Western Psychological Services.
Schmidt RJ, Hansen RL, Hartiala J, Allayee H, Schmidt LC, Tancredi DJ, et al. 2011. Prenatal vitamins, one-carbon metabolism gene variants, and risk for autism. Epidemiology 22(4):476–485.
Shelton JF, Hertz-Picciotto I, Pessah IN. 2012. Tipping the balance of autism risk: potential mechanisms linking pesticides and autism. Environ Health Perspect 120:944–951; doi: 10.1289/ehp.1104553.
Sparrow S, Balla D, Cicchetti D. 2005. Vineland Adaptive Behavior Scales Interview Edition Expanded Form Manual. Circle Pines, MN:American Guidance Services Inc.
Torres-Sánchez L, Rothenberg SJ, Schnaas L, Cebrián ME, Osorio E, del Carmen Hernández M, et al. 2007. In utero p,p’-DDE exposure and infant neurodevelopment: a perinatal cohort in Mexico. Environ Health Perspect 115:435–439; doi: 10.1289/ehp.9566.
U.S. Department of Agriculture. 2006. Pest Management Practices. Available:​er.ashx?file=/media/873656/pestmgt.pdf [accessed 2 June 2014].
U.S. Environmental Protection Agency. 2011. Pesticide Industry Sales and Usage: 2006 and 2007 Market Estimates. Available:​pestsales/market_estimates2007.pdf [accessed 27 May 2014].
Weng HY, Hsueh YH, Messam LL, Hertz-Picciotto I. 2009. Methods of covariate selection: directed acyclic graphs and the change-in-estimate procedure. Am J Epidemiol 169(10):1182–1190.
Williams MK, Rundle A, Holmes D, Reyes M, Hoepner LA, Barr DB, et al. 2008. Changes in pest infestation levels, self-reported pesticide use, and permethrin exposure during pregnancy after the 2000–2001 U.S. Environmental Protection Agency restriction of organophosphates. Environ Health Perspect 116:1681–1688; doi: 10.1289/ehp.11367.
Young JG, Eskenazi B, Gladstone EA, Bradman A, Pedersen L, Johnson C, et al. 2005. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Neurotoxicology 26(2):199–209.

Tuesday, February 24, 2015

Pesticides in Mississippi air and rain: a comparison between 1995 and 2007

Environ Toxicol Chem. 2014 Jun;33(6):1283-93. doi: 10.1002/etc.2550. Epub 2014 Apr 4.

Pesticides in Mississippi air and rain: a comparison between 1995 and 2007.

Author information

  • 1US Geological Survey, Sacramento, California.


A variety of current-use pesticides were determined in weekly composite air and rain samples collected during the 1995 and 2007 growing seasons in the Mississippi Delta (MS, USA) agricultural region. Similar sampling and analytical methods allowed for direct comparison of results. Decreased overall pesticide use in 2007 relative to 1995 generally resulted in decreased detection frequencies in air and rain; observed concentration ranges were similar between years, however, even though the 1995 sampling site was 500 m from active fields whereas the 2007 sampling site was within 3 m of a field. Mean concentrations of detections were sometimes greater in 2007 than in 1995, but the median values were often lower. Seven compounds in 1995 and 5 in 2007 were detected in ≥50% of both air and rain samples. Atrazine, metolachlor, and propanil were detected in ≥50% of the air and rain samples in both years. Glyphosate and its degradation product, aminomethyl-phosphonic acid (AMPA), were detected in ≥75% of air and rain samples in 2007 but were not measured in 1995. The 1995 seasonal wet depositional flux was dominated by methyl parathion (88%) and was >4.5 times the 2007 flux. Total herbicide flux in 2007 was slightly greater than in 1995 and was dominated by glyphosate. Malathion, methyl parathion, and degradation products made up most of the 2007 nonherbicide flux.
© 2014 SETAC.


Air; Deposition flux; Pesticides; Rain
[PubMed - indexed for MEDLINE]

Wednesday, December 24, 2014

Thurston County is the first county government in Washington state to ban the use of neonicotinoid insecticides on the property that it manages and owns.

Commissioners ban insecticide from Thurston County properties

Staff writer for The Olympian December 22, 2014 

 Last week, the Thurston County Commissioners approved a change in its policy; it will now ban the use of nenonictinoid insecticides on its managed lands, including parks and trails.
Thurston County is the first county government in Washington state to ban the use of neonicotinoid insecticides on the property that it manages and owns.
The chemical is highly toxic to honey bees and bumblebees, and is found in a variety of gardening products designed to keep insects away from plants.
The Board of County Commissioner’s decision came as good news for beekeepers who believe the chemical has contributed to the loss of bee populations and the collapse of bee colonies.
“I’m just elated,” said Rochester resident Mark Emrich, president of the Washington State Beekeepers Association. “I think it’s incredibly gutsy.”
The County Commissioners voted 3-0 last week to amend its pest and vegetation management policy and prohibit the use of neonicotinoids on its lands. That includes 77 acres of county facilities, 2,646 acres of parks, 47.1 miles of trails and one mile of right-of-way landscape.
“The goal of it is to send a big message to the public,” Thurston County commissioner Sandra Romero told The Olympian on Monday. “… We feel that it is a big enough issue and there could be a crisis if we have more bee colony collapses, more sick hummingbirds, more loss of our bats. All of the pollinators are in jeopardy.”
Neonicotinoid has been banned for municipal use in several cities, including Spokane and Seattle. Last month, the Olympia City Council passed a resolution stating the city would continue its policy to not purchase or use neonicotinoid pesticides for any purpose on its land, and that it would support “a national moratorium on the sale and use” of the products. In addition, the European Union instituted a two-year moratorium on products containing what many refer to as “neonics.”
Beekeeper Emrich said federal government agencies have been reluctant to take a stand, so the push for change is coming from local communities. He said some communities, including Long Island in New York, have banned the insecticide over concerns that it could pollute their water systems.
“I really think that municipalities are really starting to take on the role of it,” said Emrich, of Rochester . “If the EPA and the USDA aren’t going to take this on, we’re going to protect our own backyard.”
Romero said county officials don’t plan to ban the sale of neonicotinoids, which can be found in numerous lawn and gardening products. Some plants arrive from nurseries already containing it, Emrich said.
Romero said the ban for county properties is more about setting an example.
“We really think that the public, when they know and they have the information, will make the right choice,” she said. “We want to be known as a pollinator-friendly community.”
The county also is working with the cities of Lacey, Olympia and Tumwater, as well as LOTT, the Port of Olympia and the Nisqually Land Trust on a memorandum of understanding that would essentially extend the ban to their managed lands.
None of those groups use neonics, but the agreement would formalize that practice and urge participants to use “bee friendly” landscaping where feasible, Romero said.
Olympia naturalist Glen Buschmann of Bees, Birds & Butterflies said he supports the county’s ban of neonics on its properties.
He said he worries about the impact the chemicals may have on native bees, which can’t be tracked as well as honeybees.
Buschmann said insecticide companies have mounted a fight to keep their products on retail shelves.
“There’s some good reason for some push back (from counties and cities),” Buschmann said. “Way back in the ‘60s and ‘70s with DDT, manufacturers were saying, ‘There’s no problem. They’re safe.’ ”
Lisa Pemberton: 360-754-5433 @Lisa_Pemberton

Friday, December 19, 2014

Canadian beekeepers file lawsuit agianst Bayer, Syngenta over bee-killing neonicotinoids


 Canadian beekeepers have filed a class-action lawsuit against two pesticide manufacturers, seeking $400 million in damages for the devastating effects of the neonicotinoid pesticides that have been linked to the destruction of honeybee colonies.

"The goal is to stop the use of the neonicotinoids to stop the harm to the bees and the beekeepers," said Paula Lombardi, a lawyer with Siskinds LLP, the law firm that is handling the case.

The lawsuit was filed in the Ontario Superior Court on September 2 by two of the largest honey producers in Ontario, Sun Parlor Honey Ltd. and Munro Honey. The next day, the Ontario Beekeepers Association publicly announced the lawsuit and invited other beekeepers to join in. By September 4, more than 30 beekeepers had already signed on.

Bee colonies devastated

The neonicotinoids, which include imidacloprid, clothianidin and thiamethoxam, are systemic pesticides applied to seeds prior to planting. The neurotoxic chemicals then coats the plant, making the entire thing poisonous. This means that birds or insects that visit the plant for nectar or pollen are also poisoned.

"The plants become poison not only for the insects that farmers are targeting, but also for beneficial insects like bees," said Jennifer Sass, a senior scientist with the Natural Resources Defense Council.

Numerous studies have shown that bees exposed to neonicotinoids experience trouble navigating, are more likely to fail to return to their hives, and have smaller colonies than non-exposed bees. In a 2013 study by Health Canada, 70 percent of all dead bees tested positive for exposure to neonicotinoids.

In response to these concerns, the European Commission has restricted the use of neonicotinoids for two years, and Ontario has announced plans to regulate them more tightly.

In the lawsuit, the beekeepers accuse Bayer CropScience Inc., Syngenta Canada Inc. and their parent companies of negligence in the design, manufacture, sale and distribution of the pesticides. The lawsuit claims that the negligent behavior of the companies has directly resulted in damage or death to bee colonies and breeding stock; contamination of beeswax, honeycomb and beehives; decreases in honey production; lost profit; and increased labor and supply costs. The plaintiffs are seeking $400 million in damages.

A global crisis

Over the past 20 years, neonicotinoids have become among the most popular of all pesticide varieties. In recent years, researchers have raised concerns that they may be a primary factor behind colony collapse disorder (CCD), a phenomenon marked by honeybees abandoning their hives and dying during the winter. Because honeybees pollinate a third of the entire global food supply -- 130 different crops, valued at $15 billion per year -- CCD has caused alarm at high levels of government and industry.

A pair of studies conducted by researchers from the Harvard School of Public Health and the Worcester County Beekeepers Association decisively linked neonicotinoids to CCD. The researchers found that exposing bees to neonicotinoids induced CCD in the majority of beehives over the winter, while non-exposed bees did not experience CCD. The researchers suggested that, in part, neonicotinoids may cause CCD by making bees more vulnerable to cold.

But it's not just honeybees that are affected by neonicotinoid poisoning; because the pesticides are systemic, any animal that even visits a treated crop may be affected. According to a comprehensive international review published in June 2014, neonicotinoids are severely damaging ecological integrity worldwide, on a scale comparable to the damage done by DDT prior to the 1970s.

Shockingly, there is no evidence that neonicotinoids are even particularly beneficial for farmers.

"We have been using these things for 20 years and there's not a single study that shows they increase yield," said researcher Dave Goulson of the University of Sussex, England. "If they don't benefit yield we should stop using them."

Sources for this article include: [PDF]

Monsanto’s New ‘Herbicide-Resistant’ GMO Crop Slammed by Food Experts ~ Natural Society

Christina Sarich
by Christina Sarich Originally  posted on
Posted on December 17, 2014
With all the talk of Monsanto’s herbicide glyphosate, it is likely that you haven’t heard of dicamba. This is another weapon in the Big Ag giant’s chemical arsenal that is being called yet another indiscriminate chemical that “will take agriculture back to the dark days of heavy, hazardous pesticide use that will seriously endanger human health and the environment.”
Monsanto is sowing GMO cotton and soybean that were created specifically to resist the dicamba herbicide. This herbicide is the subject of great scrutiny following the U.S. Department of Agriculture (USDA)’s final  Environmental Impact Statement (EIS) released last week.
Should both the EPA and USDA allow the as-yet-to-be-approved dicamba herbicide, the Center for Food Safety says it will pursue every legal option to make sure it is not used on US crops.
Dicamba is essentially Monsanto’s ‘solution’ to the glyphosate resistant crops that have already taken over US farmlands. Instead of yielding more food, glyphosate has caused an epidemic of super weeds that are so invasive that farmers in the Midwest cornbelt are dumbfounded. More than 60 million acres of US crops are now completely choked by glyphosate-driven super weeds.

( Glyphosate is Round-up, Razor Pro and other named products)
ButtsBees edit 

A Little About Dicamba

Dicamba was first introduced in 1967 to be used as a broadleaf herbicide. Even then it was linked to higher cancer rates in farmers who used it, as well as birth defects in their male offspring. The herbicide is especially notable for its ability to drift into neighboring farms, thereby damaging crops.
Additionally, dicamba poses a threat to flowering plants and their pollinators. If dicamba was added to the already devastated crops throughout the cornbelt, it could dramatically escalate both environmental damage while negatively impacting human health greatly.
Strangely, though up for review by the FDA, the USDA itself and many scientists suggest that the massively increased use of dicamba will rapidly generate the still more intractable weeds resistant to both dicamba and glyphosate – all this for some more GMO frankenfood.
Bill Freese, Center for Food Safety science policy analyst says:
“Monsanto’s dicamba-resistant crops are the latest fruits of a pesticide industry strategy to increase sales of their toxic herbicides. Genetic engineering is making American agriculture more chemical-dependent and less sustainable than ever before.”
The USDA also just approved GE 2,4-D-resistant corn and soybeans from Dow Chemical Company, and approvals of similar herbicide-resistant crops developed by other pesticide companies are to come.
They aren’t making food, dear friends, they are making a poisoned world.

Wednesday, December 3, 2014


As beekeepers we must see the whole insect world as our own. We can no longer blindly keep our precious honeybee as a separate part of this whole.



Two new studies published simultaneously in the highly respected American journal Science, March 29, 2012, highlight the role of two neonicotinoid insecticides most commonly used to explain the decline of bees.
Assessment procedures and authorization of pesticides are to be reviewed urgently.
The effect of some pesticides on pollinators is accurate.
Two studies published March 29, 2012 in the journal Science shows how two insecticides of the neonicotinoid family – introduced in the early 1990s and now has become the most commonly used pesticides on crops worldwide – affect the development and the behavior of honey bees and wild species of bumblebee pollinators. All – and this is a great first – in field conditions and not in the laboratory, as was the case until now.
The first study, led by Penelope Whitehorn and Dave Goulson of the University of Stirling in the UK could explain, at least in part, the decline of some of the 20,000 species of wild pollinators.
« Some bumblebee species have declined dramatically in number. In North America, for example, some species that were widespread have more or less disappeared from the continent. In the UK, three species are now extinct », says Dave Goulson. The researchers exposed colonies of Bombus terrestris bumblebees to low levels of a neonicotinoid called Imidacloprid, used to make the famous Gaucho. The doses used were comparable to those, which are exposed to insects foraging crops treated with these pesticides.
The researchers placed the colonies in an enclosed area where the bees were feeding for six weeks under natural conditions. At the beginning and the end of the experiment, the researchers weighed each bumblebee nests that included animals, wax, honey, larvae and pollen to determine how much the colony had increased. It turns out that the colonies exposed to imidacloprid took less weight compared to the control colonies, suggesting that they were fed less. At the end of the experiment, they were 8 to 12% smaller on average than the control colonies. They had also produced 85% less queens!
This is particularly important because the queen production is directly linked to the establishment of new nests after the winter dieback. Hence a significant reduction in their ability to regenerate, which could explain the observed decline found for a number of years.
« Bumblebees pollinate many crops and wildflowers. The use of neonicotinoids in crops is clearly a threat to their health and needs to be urgently reviewed », says Dave Goulson.
In the second article in Science, a French team found that the exposure to another neonicotinoid disrupted the ability of bees to find their hive, which caused the death of many of them. Mickaël Henry from the INRA of Avignon and his colleagues equipped 653 honeybees (Apis mellifera) with RFID microchips. This device allowed the researchers to track the bees in their back and forth between the hive and the environment. Then they gave half of them a small, non-lethal dose of Thiamethoxam, a substance of the neonicotinoid family with which the famous Cruiser is especially manufactured.
Compared to control bees that had not been exposed to the product, the treated bees were two to three times more likely to die outside the hive. The researchers argue that these deaths were likely to be produced because the pesticide interfered with the positioning system of the beehive.
In the second part of their study, the researchers used data from the tagging experiment with the bees to develop a mathematical model that simulates the dynamics of bee population. When mortality due to their lack of localization has been incorporated into these simulations, the model predicted that the bee populations exposed to pesticide were to decline to a level that did not allow their recovery.
Read more

Saturday, October 25, 2014

Pathogen-associated self-medication behavior in the honeybee Apis mellifera

, Volume 68, Issue 11, pp 1777-1784
Date: 09 Aug 2014

Pathogen-associated self-medication behavior in the honeybee Apis mellifera

Honeybees, Apis mellifera, have several prophylactic disease defense strategies, including the foraging of antibiotic, antifungal, and antiviral compounds of plant products. Hence, honey and pollen contain many compounds that prevent fungal and bacterial growth and inhibit viral replication. Since these compounds are also fed to the larvae by nurse bees, they play a central role for colony health inside the hive. Here, we show that honeybee nurse bees, infected with the microsporidian gut parasite Nosema ceranae, show different preferences for various types of honeys in a simultaneous choice test. Infected workers preferred honeys with a higher antibiotic activity that reduced the microsporidian infection after the consumption of the honey. Since nurse bees feed not only the larvae but also other colony members, this behavior might be a highly adaptive form of therapeutic medication at both the individual and the colony level.

Monday, September 1, 2014

After 90 Percent Decline, Federal Protection Sought for Monarch Butterfly ; Genetically Engineered Crops Are Major Driver in Population Crash

Center for Biological Diversity

For Immediate Release, August 26, 2014
Contact:  Tierra Curry, Center for Biological Diversity, (928) 522-3681
Abigail Seiler, Center for Food Safety, (443) 854-4368
Lincoln Brower, Sweet Briar College, (434) 277-5065
Sarina Jepsen, Xerces Society, (971) 244-3727
After 90 Percent Decline, Federal Protection Sought for Monarch Butterfly
Genetically Engineered Crops Are Major Driver in Population Crash
WASHINGTON The Center for Biological Diversity and Center for Food Safety as co-lead petitioners joined by the Xerces Society and renowned monarch scientist Dr. Lincoln Brower filed a legal petition today to the U.S. Fish and Wildlife Service seeking Endangered Species Act protection for monarch butterflies, which have declined by more than 90 percent in under 20 years. During the same period it is estimated that these once-common iconic orange and black butterflies may have lost more than 165 million acres of habitat — an area about the size of Texas — including nearly a third of their summer breeding grounds.
Monarch butterfly
Photo courtesy Wikimedia Commons/Tiago J. G. Fernandes. Photos are available for media use.
“Monarchs are in a deadly free fall and the threats they face are now so large in scale that Endangered Species Act protection is needed sooner rather than later, while there is still time to reverse the severe decline in the heart of their range,” said Lincoln Brower, preeminent monarch researcher and conservationist, who has been studying the species since 1954.
“We’re at risk of losing a symbolic backyard beauty that has been part of the childhood of every generation of Americans,” said Tierra Curry, a senior scientist at the Center for Biological Diversity. “The 90 percent drop in the monarch’s population is a loss so staggering that in human-population terms it would be like losing every living person in the United States except those in Florida and Ohio.”
The butterfly’s dramatic decline is being driven by the widespread planting of genetically engineered crops in the Midwest, where most monarchs are born. The vast majority of genetically engineered crops are made to be resistant to Monsanto’s Roundup herbicide, a uniquely potent killer of milkweed, the monarch caterpillar’s only food. The dramatic surge in Roundup use with Roundup Ready crops has virtually wiped out milkweed plants in midwestern corn and soybean fields.

“The widespread decline of monarchs is driven by the massive spraying of herbicides on genetically engineered crops, which has virtually eliminated monarch habitat in cropland that dominates the Midwest landscape,” said Bill Freese, a Center for Food Safety science policy analyst. “Doing what is needed to protect monarchs will also benefit pollinators and other valuable insects, and thus safeguard our food supply.”
Monarch butterflies are known for their spectacular multigenerational migration each year from Mexico to Canada and back. Found throughout the United States during summer months, in winter most monarchs from east of the Rockies converge in the mountains of central Mexico, where they form tight clusters on just a few acres of trees. Most monarchs west of the Rockies migrate to trees along the California coast to overwinter.
The population has declined from a recorded high of approximately 1 billion butterflies in the mid-1990s to only 35 million butterflies last winter, the lowest number ever recorded. The overall population shows a steep and statistically significant decline of 90 percent over 20 years. In addition to herbicide use with genetically engineered crops, monarchs are also threatened by global climate change, drought and heat waves, other pesticides, urban sprawl, and logging on their Mexican wintering grounds. Scientists have predicted that the monarch’s entire winter range in Mexico and large parts of its summer range in the states could become unsuitable due to changing temperatures and increased risk of drought, heat waves and severe storms.
Monarchs need a very large population size to be resilient to threats from severe weather events and predation. Nearly half of the overwintering population in Mexico can be eaten by bird and mammal predators in any single winter; a single winter storm in 2002 killed an estimated 500 million monarchs — 14 times the size of the entire current population.
“We need to take immediate action to protect the monarch so that it doesn’t become another tragic example of a widespread species being erased because we falsely assumed it was too common to become extinct,” said Sarina Jepsen, endangered species director at the Xerces Society. “2014 marks the 100th anniversary of the extinction of the passenger pigeon, which was once so numerous no one would ever have believed it was at risk of extinction. History demonstrates that we cannot afford to be complacent about saving the monarch.”
“The purpose of the Endangered Species Act is to protect species like the monarch, and protect them, now, before it’s too late,” said George Kimbrell, senior attorney at the Center for Food Safety. “We’ve provided FWS a legal and scientific blueprint of the urgently needed action here.”
“The monarch is the canary in the cornfield, a harbinger of environmental change that we’ve brought about on such a broad scale that many species of pollinators are now at risk if we don’t take action to protect them,” said Brower, who has published hundreds of scientific studies on monarchs.
The Fish and Wildlife Service must now issue a “90-day finding” on whether the petition warrants further review.
The Center for Biological Diversity is a national, nonprofit conservation organization with more than 775,000 members and online activists dedicated to the protection of endangered species and wild places.
Center for Food Safety is a nonprofit, public interest organization with half a million members nationwide. CFS and its members are dedicated to protecting public health and the environment by curbing the use of harmful food production technologies and instead promoting sustainable alternatives.
The Xerces Society is a nonprofit organization that protects wildlife through the conservation of invertebrates and their habitat. Established in 1971, the Society is at the forefront of invertebrate protection worldwide, harnessing the knowledge of scientists and the enthusiasm of citizens to implement conservation programs.
Related Posts Plugin for WordPress, Blogger...