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Landrigan, 2018

Philip J. Landrigan, “Pesticides and Human Reproduction,” JAMA Internal Medicine, 2018, 178:1, DOI:10.1001/jamainternmed.2017.5092

SUMMARY:

Invited commentary by Managing Weeds for Healthy Kids science team member Dr. Landrigan reports that herbicide use has increased sharply, with glyphosate use up 250-fold from 1974 to 2014. And, “measurable levels of multiple pesticides are found in the bodies of nearly all Americans…and pesticides are capable of causing a wide range of asymptomatic effects at levels of exposure too low to produce overt signs and symptoms.” New theories suggest that long term exposure to pesticides cause this kind of subclinical toxicity. Dr. Landrigan reviews the known linkages, including in utero chlorpyrifos exposure leading to neurodevelopmental deficits, and reproductive injury including adverse birth outcomes and birth defects. He recommends: “We need to overcome the strident objections of the pesticide manufacturing industry, recognize the hidden costs of deregulation, and strengthen requirements for both premarket testing of new pesticides, as well as postmarketing surveillance of exposed populations— exactly as we do for another class of potent, biologically active molecules—drugs.” FULL TEXT

Laugeray et al., 2014

Anthony Laugeray, Ameziane Herzine, Olivier Perche,1,2 Betty Hébert, Marine Aguillon-Naury, Olivier Richard, Arnaud Menuet, Séverine Mazaud-Guittot, Laurianne Lesné, Sylvain Briault, Bernard Jegou, Jacques Pichon, Céline Montécot-Dubourg, and Stéphane Mortaud, “Pre- and Postnatal Exposure to Low Dose Glufosinate Ammonium Induces Autism-Like Phenotypes in Mice,” Frontiers in Behavioral Neuroscience, 2014, 8:390, DOI: 10.3389/fnbeh.2014.00390

ABSTRACT:

Glufosinate ammonium (GLA) is one of the most widely used herbicides in agriculture. As is the case for most pesticides, potential adverse effects of GLA have not been studied from the perspective of developmental neurotoxicity. Early pesticides exposure may weaken the basic structure of the developing brain and cause permanent changes leading to a wide range of lifelong effects on health and/or behavior. Here, we addressed the developmental impact of GLA by exposing female mice to low dose GLA during both pre- and postnatal periods and analyzed potential developmental and behavioral changes of the offspring during infancy and adulthood. A neurobehavioral test battery revealed significant effects of GLA maternal exposure on early reflex development, pup communication, affiliative behaviors, and preference for social olfactory cues, but emotional reactivity and emotional memory remained unaltered. These behavioral alterations showed a striking resemblance to changes seen in animal models of Autistic Spectrum Disorders. At the brain level, GLA maternal exposure caused some increase in relative brain weight of the offspring. In addition, reduced expression of Pten and Peg3 – two genes implicated in autism-like deficits – was observed in the brain of GLA-exposed pups at postnatal day 15. Our work thus provides new data on the link between pre- and postnatal exposure to the herbicide GLA and the onset of autism-like symptoms later in life. It also raises fundamental concerns about the ability of current safety testing to assess risks of pesticide exposure during critical developmental periods. FULL TEXT

McDuffie et al., 2001

Helen H. McDuffie, Punam Pahwa, John R. McLaughlin, John J. Spinelli, Shirley Fincham, James A. Dosman, Diane Robson, Leo F. Skinnider and Norman W. Choi, “Non-Hodgkin’s Lymphoma and Specific Pesticide Exposures in Men: Cross-Canada Study of Pesticides and Health,” Cancer Epidemiology, Biomarkers, & Prevention, 2001, 10.

ABSTRACT:

Our objective in the study was to investigate the putative associations of specific pesticides with non-Hodgkin’s Lymphoma [NHL; International Classification of Diseases, version 9 (ICD-9) 200, 202]. We conducted a Canadian multicenter population-based incident, case (n = 517)-control (n = 1506) study among men in a diversity of occupations using an initial postal questionnaire followed by a telephone interview for those reporting pesticide exposure of 10 h/year or more, and a 15% random sample of the remainder. Adjusted odds ratios (ORs) were computed using conditional logistic regression stratified by the matching variables of age and province of residence, and subsequently adjusted for statistically significant medical variables (history of measles, mumps, cancer, allergy desensitization treatment, and a positive history of cancer in first-degree relatives). We found that among major chemical classes of herbicides, the risk of NHL was statistically significantly increased by exposure to phenoxyherbicides [OR, 1.38; 95% confidence interval (CI), 1.06–1.81] and to dicamba (OR, 1.88; 95% CI, 1.32–2.68). Exposure to carbamate (OR, 1.92; 95% CI, 1.22–3.04) and to organophosphorus insecticides (OR, 1.73; 95% CI, 1.27–2.36), amide fungicides, and the fumigant carbon tetrachloride (OR, 2.42; 95% CI, 1.19–5.14) statistically significantly increased risk. Among individual compounds, in multivariate analyses, the risk of NHL was statistically significantly increased by exposure to the herbicides 2,4-dichlorophenoxyacetic acid (2,4-D; OR, 1.32; 95% CI, 1.01–1.73), mecoprop (OR, 2.33; 95% CI, 1.58–3.44), and dicamba (OR, 1.68; 95% CI, 1.00–2.81); to the insecticides malathion (OR, 1.83; 95% CI, 1.31–2.55), 1,1,1-trichloro-2,2-bis (4-chlorophenyl) ethane (DDT), carbaryl (OR, 2.11; 95% CI, 1.21–3.69), aldrin, and lindane; and to the fungicides captan and sulfur compounds. In additional multivariate models, which included exposure to other major chemical classes or individual pesticides, personal antecedent cancer, a history of cancer among first-degree relatives, and exposure to mixtures containing dicamba (OR, 1.96; 95% CI, 1.40–2.75) or to mecoprop (OR, 2.22; 95% CI, 1.49–3.29) and to aldrin (OR, 3.42; 95% CI, 1.18–9.95) were significant independent predictors of an increased risk for NHL, whereas a personal history of measles and of allergy desensitization treatments lowered the risk. We concluded that NHL was associated with specific pesticides after adjustment for other independent predictors. FULL TEXT

Steckel, 2012

Larry Steckel, “Glyphosate-Resistant Weeds: Lessons Learned in Tennessee,” Presentation to the Iowa Soybean Association, On-Farm Network Conference, Ames, IA, February 16, 2012

SUMMARY:

Describes aggressive spread of glyphosate reisistant weeds and the importance of proactive management, including prevention and early detection and recommends herbicide protocols to control weeds. FULL TEXT

Shaw, 2017

William Shaw, PhD, “Elevated Urinary Glyphosate and Clostridia Metabolites With Altered Dopamine Metabolism in Triplets With Autistic Spectrum Disorder or Suspected Seizure Disorder: A Case Study,” Integrative Medicine, 2017, 16:1.

CONTEXT: Autism is a neurodevelopmental disorder for which a number of genetic, environmental, and nutritional causes have been proposed. Glyphosate is used widely as a crop desiccant and as an herbicide in fields of genetically modified foods that are glyphosate resistant. Several researchers have proposed that it may be a cause of autism, based on epidemiological data that correlates increased usage of glyphosate with an increased autism rate.

OBJECTIVE: The current study was intended to determine if excessive glyphosate was present in the triplets and their parents and to evaluate biochemical findings for the family to determine the potential effects of its presence.

DESIGN: The author performed a case study with the cooperation of the parents and the attending physician.

SETTING: The study took place at The Great Plains Laboratory, Inc (Lenexa, KS, USA).

PARTICIPANTS: Participants were triplets, 2 male children and 1 female, and their parents. The 2 male children had autism, whereas the female had a possible seizure disorder. All 3 had elevated urinary glyphosate, and all of the triplets and their mother had elevated values of succinic acid or tiglylglycine, which are indicators of mitochondrial dysfunction.

INTERVENTION:
The participants received a diet of organic food only.

OUTCOME MEASURES:
The study performed organic acids, glyphosate, toxic chemicals and tiglylglycine, and creatinine testing of the participants’ urine.

RESULTS:
The 2 male triplets with autism had abnormalities on at least 1 organic acids test, including elevated phenolic compounds such as 4-cresol, 3-[3-hydroxyphenyl]-3-hydroxypropionic acid and 4-hydroxyphenylacetic acid, which have been previously associated with Clostridia bacteria and autism. The female, who was suspected of having a seizure disorder but not autism, did not have elevated phenolic compounds but did have a significantly elevated value of the metabolite tiglylglycine, a marker for mitochondrial dysfunction and/or mutations. One male triplet was retested postintervention and was found to have a markedly lower amount of glyphosate in his urine.

CONCLUSIONS:
The pattern of metabolites in the urine samples of the males with autism are consistent with a recent theory of autism that connects widespread glyphosate use with alteration of animal and human gastrointestinal flora. That theory is that the normally beneficial bacteria species that are sensitive to glyphosate are diminished and harmful bacteria species, such as Clostridia, that are insensitive to glyphosate, are increased following exposure to glyphosate. Excessive dopamine, caused by inhibition of dopamine-beta-hydroxylase by Clostridia metabolites, in turn, produces oxidative species that damage neuronal Krebs cycle enzymes, neuronal mitochondria, and neuronal structural elements such as the neurofibrils. FULL TEXT

Kriebel et al., 2016

David Kriebel, ScD, Polly J. Hoppin, ScD, Molly M. Jacobs, MPH, Richard W. Clapp, DSc, “Environmental and Economic Strategies for Primary Prevention of Cancer in Early Life,” Pediatrics, 2016, 138:s1, DOI: 10.1542/peds.2015-4268

ABSTRACT:

This article summarizes the evidence for environmental toxic exposures contributing to cancers in early life, focusing on the most common cancer sites in this age group. It provides examples of widespread avoidable exposures to human carcinogens through air, water, and food and then describes recent examples of successful initiatives to reduce exposure to chemicals linked to these cancer sites, through government policy, industry initiatives, and consumer activism. State government initiatives to reduce toxic chemical exposures have made important gains; the Toxics Use Reduction Act of Massachusetts is now 25 years old and has been a major success story. There are a growing number of corporate initiatives to eliminate toxics, especially carcinogens, from the products they manufacture and sell. Another important opportunity for cancer prevention is provided by online databases that list chemicals, their toxicity, and lower-toxicity alternatives; these can be used by businesses, health care institutions, consumers, and workers to reduce exposures to chemicals of concern. The article concludes by inviting pediatricians and public health professionals to include elimination of carcinogen exposures in their work to promote primary prevention of cancer in early life. FULL TEXT

Lerro et al., 2017

Catherine C. Lerro, Laura E. Beane Freeman, Lützen Portengen, Daehee Kang, Kyoungho Lee, Aaron Blair, Charles F. Lynch, Berit Bakke, Anneclaire J. De Roos, and Roel C.H. Vermeulen, “A longitudinal study of atrazine and 2,4-D exposure and oxidative stress markers among Iowa corn farmers,” Environmental and Molecular Mutagenesis, 2017, 58, DOI: 10.1002/em.22069

ABSTRACT:

Reactive oxygen species, potentially formed through environmental exposures, can overwhelm an organism’s antioxidant capabilities resulting in oxidative stress. Long-term oxidative stress is linked with chronic diseases. Pesticide exposures have been shown to cause oxidative stress in vivo. We utilized a longitudinal study of corn farmers and non-farming controls in Iowa to examine the impact of exposure to the widely used herbicides atrazine and 2,4-dichlorophenoxyacetic acid (2,4-D) on markers of oxidative stress. 225 urine samples were collected during five agricultural time periods (pre-planting, planting, growing, harvest, off-season) for 30 farmers who applied pesticides occupationally and 10 controls who did not; all were non-smoking men ages 40–60. Atrazine mercapturate (atrazine metabolite), 2,4-D, and oxidative stress markers (malondialdehyde [MDA], 8-hydroxy-2′-deoxyguanosine [8-OHdG], and 8-isoprostaglandin-F_2α [8-isoPGF]) were measured in urine. We calculated β estimates and 95% confidence intervals (95%CI) for each pesticide-oxidative stress marker combination using multivariate linear mixed-effect models for repeated measures. Farmers had higher urinary atrazine mercapturate and 2,4-D levels compared to controls. In regression models, after natural log transformation, 2,4-D was associated with elevated levels of 8-OHdG (β=0.066, 95%CI=0.008–0.124) and 8-isoPGF (β=0.088, 95%CI=0.004–0.172). 2,4-D may be associated with oxidative stress because of modest increases in 8-OHdG, a marker of oxidative DNA damage, and 8-isoPGF, a product of lipoprotein peroxidation, with recent 2,4-D exposure. Future studies should investigate the role of 2,4-D-induced oxidative stress in the pathogenesis of human diseases. FULL TEXT

Winston et al., 2016

Jennifer J. Winston, Michael Emch, Robert E. Meyer, Peter Langlois, Peter Weyer, Bridget Mosley, Andrew F. Olshan, Lawrence E. Band, Thomas J. Luben and the National Birth Defects Prevention Study, “Hypospadias and maternal exposure to atrazine via drinking water in the National Birth Defects Prevention study,” Environmental Health, 15:76, DOI: 10.1186/s12940-016-0161-9

ABSTRACT:

BACKGROUND: Hypospadias is a relatively common birth defect affecting the male urinary tract. It has been suggested that exposure to endocrine disrupting chemicals might increase the risk of hypospadias by interrupting normal urethral development.

METHODS: Using data from the National Birth Defects Prevention Study, a population-based case-control study, we considered the role of maternal exposure to atrazine, a widely used herbicide and potential endocrine disruptor, via drinking water in the etiology of 2nd and 3rd degree hypospadias. We used data on 343 hypospadias cases and 1,422 male controls in North Carolina, Arkansas, Iowa, and Texas from 1998–2005. Using catchment level stream and groundwater contaminant models from the US Geological Survey, we estimated atrazine concentrations in public water supplies and in private wells. We assigned case and control mothers to public water supplies based on geocoded maternal address during the critical window of exposure for hypospadias (i.e., gestational weeks 6–16). Using maternal questionnaire data about water consumption and drinking water, we estimated a surrogate for total maternal consumption of atrazine via drinking water. We then included additional maternal covariates, including age, race/ethnicity, parity, and plurality, in logistic regression analyses to consider an association between atrazine and hypospadias.

RESULTS: When controlling for maternal characteristics, any association between hypospadias and daily maternal atrazine exposure during the critical window of genitourinary development was found to be weak or null (odds ratio for atrazine in drinking water = 1. 00, 95 % CI = 0.97 to 1.03 per 0.04 μg/day increase; odds ratio for maternal consumption = 1.02, 95 % CI = 0.99 to 1.05; per 0.05 μg/day increase).

CONCLUSIONS: While the association that we observed was weak, our results suggest that additional research into a possible association between atrazine and hypospadias occurrence, using a more sensitive exposure metric, would be useful. FULL TEXT

Lebov et al., 2016

Jill F. Lebov, MSPH, PhD, Lawrence S. Engel, PhD, David Richardson, PhD, Susan L. Hogan, PhD, Jane A. Hoppin, ScD, and Dale P. Sandler, PhD, “Pesticide use and risk of end-stage renal disease among licensed pesticide applicators in the Agricultural Health Study,” Occupational and Environmental Medicine, 2016, 7, DOI: 10.1136/oemed-2014-102615

ABSTRACT:

OBJECTIVES: Experimental studies suggest a relationship between pesticide exposure and renal impairment, but epidemiological evidence is limited. We evaluated the association between exposure to 41 specific pesticides and end-stage renal disease (ESRD) incidence in the Agricultural Health Study (AHS), a prospective cohort study of licensed pesticide applicators in Iowa and North Carolina.

METHODS: Via linkage to the United States Renal Data System, we identified 320 ESRD cases diagnosed between enrollment (1993-1997) and December 2011 among 55,580 male licensed pesticide applicators. Participants provided pesticide use information via self-administered questionnaires. Lifetime pesticide use was defined as the product of duration and frequency of use and then modified by an intensity factor to account for differences in pesticide application practices. Cox proportional hazards models, adjusted for age and state, were used to estimate associations between ESRD and: 1) ordinal categories of intensity-weighted lifetime use of 41 pesticides, 2) poisoning and high-level pesticide exposures, and 3) pesticide exposure resulting in a medical visit or hospitalization.

RESULTS: Positive exposure-response trends were observed for the herbicides alachlor, atrazine, metolachlor, paraquat, and pendimethalin, and the insecticide chlordane. More than one medical visit due to pesticide use (HR = 2.13; 95% CI: 1.17, 3.89) and hospitalization due to pesticide use (HR = 3.05; 95% CI: 1.67, 5.58) were significantly associated with ESRD.

CONCLUSIONS: Our findings support an association between ESRD and chronic exposure to specific pesticides and suggest pesticide exposures resulting in medical visits may increase the risk of ESRD. FULL TEXT

Agopian et al., 2013a

A.J. Agopian, PhD, Yi Cai, MS, Peter H. Langlois, PhD, Mark A. Canfield, PhD, and Philip J. Lupo, PhD, “Maternal Residential Atrazine Exposure and Risk for Choanal Atresia and Stenosis in Offspring,” Journal of Pediatrics 2013, 162:3, DOI: 10.1016/j.jpeds.2012.08.012

ABSTRACT:

OBJECTIVE: To assess the relationship between estimated residential maternal exposure to atrazine during pregnancy and the risk for choanal atresia or stenosis in offspring.

STUDY DESIGN: Data for 280 nonsyndromic cases and randomly selected, population-based controls delivered between 1999 and 2008 were obtained from the Texas Birth Defects Registry. County-level estimates of atrazine levels obtained from the US Geological Survey were assigned to cases and controls based on maternal county of residence at delivery. Unconditional logistic regression was used to assess the relationship between maternal residential atrazine exposure and the risk for choanal atresia or stenosis in offspring.

RESULTS: Compared with offspring of mothers with low levels of estimated residential atrazine exposure, those with high levels had nearly a 2-fold increase in risk for choanal atresia or stenosis (aOR, 1.79; 95% CI, 1.17-2.74). A significant linear trend was also observed with increasing levels of atrazine exposure (adjusted P = .002).

CONCLUSION: A link between maternal exposure to endocrine disruptors, such as atrazine, and the risk of choanal atresia is plausible based on previous findings. Our results lend further support to this hypothesis. FULL TEXT

Bibliography Index