Barr et al., 2005
Barr, D. B., Allen, R., Olsson, A. O., Bravo, R., Caltabiano, L. M., Montesano, A., Nguyen, J., Udunka, S., Walden, D., Walker, R. D., Weerasekera, G., Whitehead, R. D., Jr., Schober, S. E., & Needham, L. L.; “Concentrations of selective metabolites of organophosphorus pesticides in the United States population;” Environmental Research, 2005, 99(3), 314-326; DOI: 10.1016/j.envres.2005.03.012.
ABSTRACT:
We report population-based concentrations (stratified by age, sex, and composite race/ethnicity variables) of selective metabolites of chlorpyrifos (3,5,6-trichloro-2-pyridinol; TCPY), chlorpyrifos methyl (TCPY), malathion (malathion dicarboxylic acid; MDA), diazinon (2-isopropyl-4-methyl-6-hydroxypyrimidine; IMPY), methyl parathion (para-nitrophenol; PNP), and parathion (PNP). We measured the concentrations of TCPY, MDA, IMPY, and PNP in 1997 urine samples from participants, aged 6-59 years, of the National Health and Nutrition Examination Survey, 1999-2000. We detected TCPY in more than 96% of the samples tested. Other organophosphorus pesticide metabolites were detected less frequently: MDA, 52%; IMPY, 29%; and PNP, 22%. The geometric means for TCPY were 1.77 microg/L and 1.58 microg/g creatinine. The 95th percentiles for TCPY were 9.9 microg/L and 8.42 microg/g creatinine. The 95th percentiles for MDA were 1.6 microg/L and 1.8 microg/g creatinine. The 95th percentiles for IMPY and PNP were 3.7 microg/L (3.4 microg/g creatinine) and 5.0 microg/L (4.2 microg/g creatinine), respectively. Multivariate analyses showed that children aged 6-11 years had significantly higher concentrations of TCPY than adults and adolescents. Similarly, adolescents had significantly higher TCPY concentrations than adults. Although the concentrations between sexes and among composite racial/ethnic groups varied, no significant differences were observed. FULL TEXT
Castorina et al., 2010
Castorina, R., Bradman, A., Fenster, L., Barr, D. B., Bravo, R., Vedar, M. G., Harnly, M. E., McKone, T. E., Eisen, E. A., & Eskenazi, B.; “Comparison of current-use pesticide and other toxicant urinary metabolite levels among pregnant women in the CHAMACOS cohort and NHANES;” Environmental Health Perspectives, 2010, 118(6), 856-863; DOI: 10.1289/ehp.0901568.
ABSTRACT:
BACKGROUND:
We measured 34 metabolites of current-use pesticides and other precursor compounds in urine samples collected twice during pregnancy from 538 women living in the Salinas Valley of California, a highly agricultural area (1999-2001). Precursors of these metabolites included fungicides, carbamate, organochlorine, organophosphorus (OP), and pyrethroid insecticides, and triazine and chloroacetanilide herbicides. We also measured ethylenethiourea, a metabolite of the ethylene-bisdithiocarbamate fungicides. Repeat measurements of the compounds presented here have not been reported in pregnant women previously. To understand the impact of the women’s regional environment on these findings, we compared metabolite concentrations from the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) cohort with U.S. national reference data for 342 pregnant women sampled by the National Health and Nutrition Examination Survey (1999-2002).
RESULTS:
The eight metabolites detected in > 50% of samples [2,4-dichlorophenol (2,4-DCP); 2,5-dichlorophenol (2,5-DCP); 1- and 2-naphthol; ortho-phenylphenol (ORTH); para-nitrophenol (PNP); 2,4,6-trichlorophenol (2,4,6-TCP); and 3,4,6-trichloro-2-pyridinol (TCPy)] may be related to home or agricultural pesticide use in the Salinas Valley, household products, and other sources of chlorinated phenols. More than 78% of women in this study had detectable levels of at least one of the OP pesticide-specific metabolites that we measured, and > 30% had two or more. The 95th percentile values of six of the most commonly detected (> 50%) compounds were significantly higher among the CHAMACOS women after controlling for age, race, socioeconomic status, and smoking [(2,4-DCP; 2,5-DCP; ORTH; PNP; 2,4,6-TCP; and TCPy); quantile regression p < 0.05].
CONCLUSIONS:
Findings suggest that the CHAMACOS cohort has an additional burden of precursor pesticide exposure compared with the national sample, possibly from living and/or working in an agricultural area. FULL TEXT
Alexander et al., 2006
Alexander, B. H., Burns, C. J., Bartels, M. J., Acquavella, J. F., Mandel, J. S., Gustin, C., & Baker, B. A.; “Chlorpyrifos exposure in farm families: results from the farm family exposure study;” Journal of Exposure Science and Environmental Epidemiology, 2006, 16(5), 447-456; DOI: 10.1038/sj.jes.7500475.
ABSTRACT:
We used urinary biological monitoring to characterize chlorpyrifos (O,O-diethyl-O-(3,5,6-trichloro-2-pyridinyl) phosphororthioate) exposure to farm family members from Minnesota and South Carolina who participated in the Farm Family Exposure Study. Five consecutive 24-h urine samples were obtained from 34 families of licensed pesticide applicators 1 day before through 3 days after a chlorpyrifos application. Daily 3,5,6-trichloro-2-pyridinol (TCP) urinary concentrations characterized exposure profiles of the applicator, the spouse, and children aged 4-17 years. Self-reported and observed determinants of exposure were compared to the maximum postapplication TCP concentration. All participants had detectable (> or = 1 microg/l) urinary TCP concentrations at baseline. Applicators’ peak TCP levels occurred the day after the application (geometric mean (GM) = 19.0 microg/l). Postapplication TCP change from baseline in the spouses and children was negligible, and the only reliable predictor of exposure was assisting with the application for children aged 12 years and older. The applicators’ exposure was primarily influenced by the chemical formulation (GM = 11.3 microg/l for granular and 30.9 microg/l for liquid), and the number of loads applied. Repairing equipment, observed skin contact, and eating during the application were moderately associated TCP levels for those who applied liquid formulations. Estimated absorbed doses (microg chlorpyrifos/kg bodyweight) were calculated based on TCP excretion summed over the 4 postapplication days and corrected for pharmacokinetic recovery. The GM doses were 2.1, 0.7, and 1.0 microg/kg bodyweight for applicators, spouses, and children, respectively. Chlorpyrifos exposure to farm family members from the observed application was largely determined by the extent of contact with the mixing, loading, and application process. FULL TEXT
Arnold et al., 2015
Arnold, S. M., Morriss, A., Velovitch, J., Juberg, D., Burns, C. J., Bartels, M., Aggarwal, M., Poet, T., Hays, S., & Price, P.; “Derivation of human Biomonitoring Guidance Values for chlorpyrifos using a physiologically based pharmacokinetic and pharmacodynamic model of cholinesterase inhibition;” Regulatory Toxicology and Pharmacology, 2015, 71(2), 235-243; DOI: 10.1016/j.yrtph.2014.12.013.
ABSTRACT:
A number of biomonitoring surveys have been performed for chlorpyrifos (CPF) and its metabolite (3,5,6-trichloro-2-pyridinol, TCPy); however, there is no available guidance on how to interpret these data in a health risk assessment context. To address this gap, Biomonitoring Guidance Values (BGVs) are developed using a physiologically based pharmacokinetic and pharmacodynamic (PBPK/PD) model. The PBPK/PD model is used to predict the impact of age and human variability on the relationship between an early marker of cholinesterase (ChE) inhibition in the peripheral and central nervous systems [10% red blood cell (RBC) ChE inhibition] and levels of systemic biomarkers. Since the PBPK/PD model characterizes variation of sensitivity to CPF in humans, interspecies and intraspecies uncertainty factors are not needed. Derived BGVs represent the concentration of blood CPF and urinary TCPy associated with 95% of the population having less than or equal to 10% RBC ChE inhibition. Blood BGV values for CPF in adults and infants are 6100 ng/L and 4200 ng/L, respectively. Urinary TCPy BGVs for adults and infants are 2100 mug/L and 520 mug/L, respectively. The reported biomonitoring data are more than 150-fold lower than the BGVs suggesting that current US population exposures to CPF are well below levels associated with any adverse health effect. FULL TEXT
Cai et al., 2020
Cai, Wenyan, Zhang, Feng, Zhong, Lixin, Chen, Dongya, Guo, Haoran, Zhang, Hengdong, Zhu, Baoli, & Liu, Xin; “Correlation between CYP1A1 polymorphisms and susceptibility to glyphosate-induced reduction of serum cholinesterase: A case-control study of a Chinese population;” Pesticide Biochemistry and Physiology, 2020, 162, 23-28; DOI: 10.1016/j.pestbp.2019.07.006.
ABSTRACT:
Glyphosate (GLP) is one of the most common herbicides worldwide. The serum cholinesterase (ChE) may be affected when exposed to glyphosate. Reduction of serum ChE by herbicides is probably related to cytochrome P450 (CYP450) family polymorphisms. We suspect that the abnormal ChE caused by GLP could be correlated with the CYP family members. To determine whether CYP1B1 (rs1056827 and rs1056836) and CYP1A1 (rs1048943) gene polymorphisms and individual susceptibility to GLP-induced ChE abnormalities were interrelated in the Chinese Han population, we performed this genetic association study on a total of 230 workers previously exposed to GLP, including 115 cases with reduced serum ChE and 115 controls with normal serum ChE. Two even groups of cases and controls were enrolled. The CYP1A1 and CYP1B1 polymorphisms in both groups were genotyped using TaqMan. Subjects with the CYP1A1 rs619586 genotypes showed an increased risk of GLP-induced reduction of serum ChE, which was more evident in the following subgroups: female,>35 years old, history of GLP exposure time<10 years and>10 years, nonsmoker and nondrinker. The results show that CYP1A1 rs619586 was significantly associated with the GLP-induced reduction in serum ChE and could be a biomarker of susceptibility for Chinese GLP exposed workers. Because of a large number of people exposed to glyphosate, this study has a significance in protecting their health. FULL TEXT
Perro, 2019
Perro, Michelle, “Childhood Leukemia, the Microbiome, and Glyphosate: A Doctor’s Perspective,” GMOScience.org, January 15, 2019.
SUMMARY:
- Childhood leukemia is on the rise
- Exposure to pesticides is known to increase the risk of childhood leukemia, as well as other types of cancer
- New research links an impoverished gut microbiome (bacterial community) and chronic inflammation with increased risk of childhood leukemia
- Diet-related ways are being sought to improve the microbiome and prevent the inflammation that triggers childhood leukemia
- Glyphosate herbicides are used on around 90% of GM crops; glyphosate has been classified as a probable carcinogen by the World Health Organization’s cancer agency IARC
- Exposure to glyphosate-based and other pesticides has been shown to disrupt the gut microbiome in laboratory animals
- People who eat organic food have been found to have a 25% reduced risk of cancer
- Clinical experience shows that switching to an organic and non-GMO diet improves people’s health
- Controlled studies are needed to verify how switching to an organic and non-GMO diet affects the microbiome and certain disease conditions.
Perro and Adams, 2017
Perro, Michelle and Adams, Vincanne, “What’s Making Our Children Sick? How Industrial Food Is Causing an Epidemic of Chronic Illness, and What Parents (and Doctors) Can Do About It,” Chelsea Green Publishing, 2017.
SUMMARY:
With chronic disorders among American children reaching epidemic levels, hundreds of thousands of parents are desperately seeking solutions to their children’s declining health, often with little medical guidance from the experts. What’s Making Our Children Sick? convincingly explains how agrochemical industrial production and genetic modification of foods is a culprit in this epidemic. Is it the only culprit? No. Most chronic health disorders have multiple causes and require careful disentanglement and complex treatments. But what if toxicants in our foods are a major culprit, one that, if corrected, could lead to tangible results and increased health? Using patient accounts of their clinical experiences and new medical insights about pathogenesis of chronic pediatric disorders—taking us into gut dysfunction and the microbiome, as well as the politics of food science—this book connects the dots to explain our kids’ ailing health.
What’s Making Our Children Sick? explores the frightening links between our efforts to create higher-yield, cost-efficient foods and an explosion of childhood morbidity, but it also offers hope and a path to effecting change. The predicament we now face is simple. Agroindustrial “innovation” in a previous era hoped to prevent the ecosystem disaster of DDT predicted in Rachel Carson’s seminal book in 1962, Silent Spring. However, this industrial agriculture movement has created a worse disaster: a toxic environment and, consequently, a toxic food supply. Pesticide use is at an all-time high, despite the fact that biotechnologies aimed to reduce the need for them in the first place. Today these chemicals find their way into our livestock and food crop industries and ultimately onto our plates. Many of these pesticides are the modern day equivalent of DDT. However, scant research exists on the chemical soup of poisons that our children consume on a daily basis. As our food supply environment reels under the pressures of industrialization via agrochemicals, our kids have become the walking evidence of this failed experiment. What’s Making Our Children Sick? exposes our current predicament and offers insight on the medical responses that are available, both to heal our kids and to reverse the compromised health of our food supply.
Zanardi et al., 2020
Zanardi, M. V., Schimpf, M. G., Gastiazoro, M. P., Milesi, M. M., Munoz-de-Toro, M., Varayoud, J., & Durando, M.; “Glyphosate-based herbicide induces hyperplastic ducts in the mammary gland of aging Wistar rats;” Molecular and Cellular Endocrinology, 2019, 501, 110658; DOI: 10.1016/j.mce.2019.110658.
ABSTRACT:
Glyphosate-based herbicide (GBH) exposure is known to have adverse effects on endocrine-related tissues. Here, we aimed to determine whether early postnatal exposure to a GBH induces long-term effects on the rat mammary gland. Thus, female Wistar pups were injected with saline solution (Control) or GBH (2 mg glyphosate/kg/day) on postnatal days (PND) 1, 3, 5 and 7. At 20 months of age, mammary gland samples were collected to determine histomorphological features, proliferation index and the expression of steroid hormone receptors expression, by immunohistochemistry, and serum samples were collected to assess 17beta-estradiol (E2) and progesterone (P4) levels. GBH exposure induced morphological changes evidenced by a higher percentage of hyperplastic ducts and a fibroblastic-like stroma in the mammary gland. GBH-treated rats also showed a high expression of steroid hormone receptors in hyperplastic ducts. The results indicate that early postnatal exposure to GBH induces long-term alterations in the mammary gland morphology of aging female rats. FULL TEXT
McDermott et al., 2019
McDermott, S., Hailer, M. K., & Lead, J. R.; “Meconium identifies high levels of metals in newborns from a mining community in the U.S;” Science of the Total Environment, 2019, 135528; DOI: 10.1016/j.scitotenv.2019.135528.
ABSTRACT:
BACKGROUND: This pilot study was conducted to determine if we could identify intrauterine exposure to metals in meconium, as a measure of exposure for mother-child pairs living in proximity to a mining operation.
OBJECTIVES: We used meconium as a means to measure metal exposure in utero. We set out to quantify the exposure to selected metals that are currently being mined and also are found in the Superfund site in Butte, Montana, and to compare it to that of Columbia, South Carolina, US, where mining is not occurring.
METHODS: This cross-sectional study was conducted between May and November 2018. We received Institutional Review Board approval and we consented women following the birth of their newborns, and collected meconium within 24 h of birth, without any identifiers. Each laboratory used the same protocol for collection, transport, and storage; and the same laboratory protocol was used for the analysis of all samples. Samples were digested using standard acid/peroxide digestion methods and measured by inductively coupled plasma mass spectroscopy.
RESULTS: We collected meconium specimens from 17 infants in Columbia, South Carolina and 15 infants in Butte, Montana. The concentrations found in Columbia were in the low mug kg(-1) range (or less) and were similar to the low levels that have been identified in other studies of meconium. The magnitude of the differences in concentrations found in Butte compared to Columbia was 1792 times higher for Cu, 1650 times higher for Mn, and 1883 times higher for Zn.
CONCLUSION: Using meconium to measure exposure of newborns has implications for risk assessment in a mining-exposed population. This approach was inexpensive and thorough. The magnitude of the differences in the metal levels identified from the two study sites suggests there is an urgent need for further research to learn if there are health consequences to these highly exposed infants. FULL TEXT
Ostrea et al., 2006
Ostrea, E. M., Bielawski, D. M., & Posecion Jr., N C; “Meconium analysis to detect fetal exposure to neurotoxicants;” Archives of Disease in Childhood, 2006, 91(8), 628-629; DOI: 10.1136/adc.2006.097956.
ABSTRACT:
Not Available.