Pesticide Exposure - HH-RA.org

Bibliography Tag: pesticide exposure

Benbrook et al., 2021a

Benbrook, Charles, Perry, Melissa J., Belpoggi, Fiorella, Landrigan, Philip J., Perro, Michelle, Mandrioli, Daniele, Antoniou, Michael N., Winchester, Paul, & Mesnage, Robin; “Commentary: Novel strategies and new tools to curtail the health effects of pesticides;” Environmental Health, 2021, 20(1); DOI: 10.1186/s12940-021-00773-4.

ABSTRACT:

BACKGROUND: Flaws in the science supporting pesticide risk assessment and regulation stand in the way of progress in mitigating the human health impacts of pesticides. Critical problems include the scope of regulatory testing protocols, the near-total focus on pure active ingredients rather than formulated products, lack of publicly accessible information on co-formulants, excessive reliance on industry-supported studies coupled with reticence to incorporate published results in the risk assessment process, and failure to take advantage of new scientific opportunities and advances, e.g. biomonitoring and “omics” technologies.
RECOMMENDED ACTIONS: Problems in pesticide risk assessment are identified and linked to study design, data, and methodological shortcomings. Steps and strategies are presented that have potential to deepen scientific knowledge of pesticide toxicity, exposures, and risks.
We propose four solutions:
(1) End near-sole reliance in regulatory decision-making on industry-supported studies by supporting and relying more heavily on independent science, especially for core toxicology studies. The cost of conducting core toxicology studies at labs not affiliated with or funded directly by pesticide registrants should be covered via fees paid by manufacturers to public agencies.
(2) Regulators should place more weight on mechanistic data and low-dose studies within the range of contemporary exposures.
(3) Regulators, public health agencies, and funders should increase the share of exposure-assessment resources that produce direct measures of concentrations in bodily fluids and tissues. Human biomonitoring is vital in order to quickly identify rising exposures among vulnerable populations including applicators, pregnant women, and children.
(4) Scientific tools across disciplines can accelerate progress in risk assessments if integrated more effectively. New genetic and metabolomic markers of adverse health impacts and heritable epigenetic impacts are emerging and should be included more routinely in risk assessment to effectively prevent disease.
CONCLUSIONS: Preventing adverse public health outcomes triggered or made worse by exposure to pesticides will require changes in policy and risk assessment procedures, more science free of industry influence, and innovative strategies that blend traditional methods with new tools and mechanistic insights.

FULL TEXT

Costello et al., 2009

Costello S, Cockburn M, Bronstein J, Zhang X, Ritz B; “Parkinson’s disease and residential exposure to maneb and paraquat from agricultural applications in the central valley of California.” American Journal of Epidemiology. 2009 Apr 15;169(8):919-26. DOI: 10.1093/aje/kwp006.

ABSTRACT:

Evidence from animal and cell models suggests that pesticides cause a neurodegenerative process leading to Parkinson’s disease (PD). Human data are insufficient to support this claim for any specific pesticide, largely because of challenges in exposure assessment. The authors developed and validated an exposure assessment tool based on geographic information systems that integrated information from California Pesticide Use Reports and land-use maps to estimate historical exposure to agricultural pesticides in the residential environment. In 1998-2007, the authors enrolled 368 incident PD cases and 341 population controls from the Central Valley of California in a case-control study. They generated estimates for maneb and paraquat exposures incurred between 1974 and 1999. Exposure to both pesticides within 500 m of the home increased PD risk by 75% (95% confidence interval (CI): 1.13, 2.73). Persons aged < or =60 years at the time of diagnosis were at much higher risk when exposed to either maneb or paraquat alone (odds ratio = 2.27, 95% CI: 0.91, 5.70) or to both pesticides in combination (odds ratio = 4.17, 95% CI: 1.15, 15.16) in 1974-1989. This study provides evidence that exposure to a combination of maneb and paraquat increases PD risk, particularly in younger subjects and/or when exposure occurs at younger ages. FULL TEXT

Abou et al., 2020

Abou Ghayda R, Sergeyev O, Burns JS, Williams PL, Lee MM, Korrick SA, Smigulina L, Dikov Y, Hauser R, Mínguez-Alarcón L; “Russian Children’s Study. Peripubertal serum concentrations of organochlorine pesticides and semen parameters in Russian young men.” Environment International. 2020 Nov;144:106085. DOI:10.1016/j.envint.2020.106085.

ABSTRACT:

Background: Epidemiologic literature on the relation of organochlorine pesticides (OCPs) with semen quality among adult men has been inconclusive, and no studies have prospectively explored the association between peripubertal serum OCPs and semen parameters in young men.

Objective: To evaluate prospective associations of peripubertal serum concentrations of hexachlorobenzene (HCB), β-hexachlorocylohexane (β-HCH), and p,p’-dichlorodiphenyldichloroethylene (p,p’-DDE) with semen parameters among young Russian men.

Methods: This prospective cohort study included 152 young men who enrolled in the Russian Children’s Study (2003-2005) at age 8-9 years and were followed annually until young adulthood. HCB, β-HCH, and p,p’-DDE concentrations were measured at the CDC by mass spectrometry in serum collected at enrollment. Between 18 and 23 years, semen samples (n = 298) were provided for analysis of volume, concentration, and progressive motility; we also calculated total sperm count and total progressive motile count. Linear mixed models were used to examine the longitudinal associations of quartiles of serum HCB, β-HCH and p,p’-DDE with semen parameters, adjusting for total serum lipids, body mass index, smoking, abstinence time and baseline dietary macronutrient intake.

Results: Lipid-adjusted medians (IQR) for serum HCB, βHCH and p,ṕ-DDE, respectively, were 150 ng/g lipid (102-243), 172 ng/g lipid (120-257) and 275 ng/g lipid (190-465). In adjusted models, we observed lower ejaculated volume with higher serum concentrations of HCB and βHCH, along with reduced progressive motility with higher concentrations of βHCH andp,ṕ-DDE. Men in the highest quartile of serum HCB had a mean (95% Confidence Interval, CI) ejaculated volume of 2.25 mL (1.89, 2.60), as compared to those in the lowest quartile with a mean (95% CI) of 2.97 mL (2.46, 3.49) (p = 0.03). Also, men in the highest quartile of serum p,ṕ-DDE had a mean (95% CI) progressive motility of 51.1% (48.6, 53.7), as compared to those in the lowest quartile with a mean (95% CI) of 55.1% (51.7, 58.5) (p = 0.07).

Conclusion: In this longitudinal Russian cohort study, peripubertal serum concentrations of selected OCPs were associated with lower ejaculated volume and progressive motility highlighting the importance of the peripubertal window when evaluating chemical exposures in relation to semen quality. FULL TEXT

Milesi et al., 2021

Milesi, M. M., Lorenz, V., Durando, M., Rossetti, M. F., & Varayoud, J. “Glyphosate Herbicide: Reproductive Outcomes and Multigenerational Effects.” Frontiers in Endocrinology, 12. 2021; DOI:10.3389/fendo.2021.672532.

ABSTRACT:

Glyphosate base herbicides (GBHs) are the most widely applied pesticides in the world and are mainly used in association with GBH-tolerant crop varieties. Indiscriminate and negligent use of GBHs has promoted the emergence of glyphosate resistant weeds, and consequently the rise in the use of these herbicides. Glyphosate, the active ingredient of all GBHs, is combined with other chemicals known as co-formulants that enhance the herbicide action. Nowadays, the safety of glyphosate and its formulations remain to be a controversial issue, as evidence is not conclusive whether the adverse effects are caused by GBH or glyphosate, and little is known about the contribution of co-formulants to the toxicity of herbicides. Currently, alarmingly increased levels of glyphosate have been detected in different environmental matrixes and in foodstuff, becoming an issue of social concern. Some in vitro and in vivo studies have shown that glyphosate and its formulations exhibit estrogen-like properties, and growing evidence has indicated they may disrupt normal endocrine function, with adverse consequences for reproductive health. Moreover, multigenerational effects have been reported and epigenetic mechanisms have been proved to be involved in the alterations induced by the herbicide. In this review, we provide an overview of: i) the routes and levels of human exposure to GBHs, ii) the potential estrogenic effects of glyphosate and GBHs in cell culture and animal models, iii) their long-term effects on female fertility and mechanisms of action, and iv) the consequences on health of successive generations. FULL TEXT

Crump et al., 2021

Crump, Casey, Groves, Alan, Sundquist, Jan, & Sundquist, Kristina; “Association of Preterm Birth With Long-term Risk of Heart Failure Into Adulthood;” JAMA Pediatrics, 2021, 175(7), 689-697; DOI: 10.1001/jamapediatrics.2021.0131.

ABSTRACT:

Preterm birth has been associated with increased risk of heart failure (HF) early in life, but its association with new-onset HF in adulthood appears to be unknown. To determine whether preterm birth is associated with increased risk of HF from childhood into mid-adulthood in a large population-based cohort. This national cohort study was conducted in Sweden with data from 1973 through 2015. All singleton live births in Sweden during 1973 through 2014 were included. Gestational age at birth, identified from nationwide birth records. Heart failure, as identified from inpatient and outpatient diagnoses through 2015. Cox regression was used to determine hazard ratios (HRs) for HF associated with gestational age at birth while adjusting for other perinatal and maternal factors. Cosibling analyses assessed for potential confounding by unmeasured shared familial (genetic and/or environmental) factors. A total of 4 193 069 individuals were included (maximum age, 43 years; median age, 22.5 years). In 85.0 million person-years of follow-up, 4158 persons (0.1%) were identified as having HF (median [interquartile range] age, 15.4 [28.0] years at diagnosis). Preterm birth (gestational age <37 weeks) was associated with increased risk of HF at ages younger than 1 year (adjusted HR [aHR], 4.49 [95% CI, 3.86-5.22]), 1 to 17 years (aHR, 3.42 [95% CI, 2.75-4.27]), and 18 to 43 years (aHR, 1.42 [95% CI, 1.19-1.71]) compared with full-term birth (gestational age, 39-41 weeks). At ages 18 through 43 years, the HRs further stratified by gestational age were 4.72 (95% CI, 2.11-10.52) for extremely preterm births (22-27 weeks), 1.93 (95% CI, 1.37-2.71) for moderately preterm births (28-33 weeks), 1.24 (95% CI, 1.00-1.54) for late preterm births (34-36 weeks), and 1.09 (95% CI, 0.97-1.24) for early term births (37-38 weeks). The corresponding HF incidence rates (per 100 000 person-years) at ages 18 through 43 years were 31.7, 13.8, 8.7, and 7.3, respectively, compared with 6.6 for full-term births. These associations persisted when excluding persons with structural congenital cardiac anomalies. The associations at ages 18 through 43 years (but not <18 years) appeared to be largely explained by shared determinants of preterm birth and HF within families. Preterm birth accounted for a similar number of HF cases among male and female individuals. In this large national cohort, preterm birth was associated with increased risk of new-onset HF into adulthood. Survivors of preterm birth may need long-term clinical follow-up into adulthood for risk reduction and monitoring for HF.

Messina and Goodis, 2020

Messina, Edward & Goodis, Mike; “Overview of EPA’s Pesticide Program”; Presented at the Farm, Ranch, and Rural Communities Committee Meeting; November 13, 2020. Environmental Protection Agency, 2020.

PRESENTATION OUTLINE

Background
Office of Pesticide Programs Structure and Responsibilities
Pesticide Legislation
Pesticide Registration and Registration Review Process
Risk Assessment, Risk Characterization, and Risk Management
Public Involvement
Collaboration with Domestic & International Partners
Updates on EPA Issues

FULL PRESENTATION

Benbrook et al., 2021

Benbrook, Charles, Kegley, Susan, & Baker, Brian; “Organic Farming Lessens Reliance on Pesticides and Promotes Public Health by Lowering Dietary Risks;” Agronomy, 2021, 11(7); DOI: 10.3390/agronomy11071266.

ABSTRACT:

Organic agriculture is a production system that relies on prevention, ecological processes, biodiversity, mechanical processes, and natural cycles to control pests and maintain productivity. Pesticide use is generally limited or absent in organic agroecosystems, in contrast with non-organic (conventional) production systems that primarily rely on pesticides for crop protection. Significant differences in pesticide use between the two production systems markedly alter the relative dietary exposure and risk levels and the environmental impacts of pesticides. Data are presented on pesticide use on organic and non-organic farms for all crops and selected horticultural crops. The relative dietary risks that are posed by organic and non-organic food, with a focus on fresh produce, are also presented and compared. The results support the notion that organic farms apply pesticides far less intensively than conventional farms, in part because, over time on well-managed organic farms, pest pressure falls when compared to the levels on nearby conventional farms growing the same crops. Biopesticides are the predominant pesticides used in organic production, which work by a non-toxic mode of action, and pose minimal risks to human health and the environment. Consequently, eating organic food, especially fruits and vegetables, can largely eliminate the risks posed by pesticide dietary exposure. We recommend ways to lower the pesticide risks by increased adoption of organic farming practices and highlight options along organic food supply chains to further reduce pesticide use, exposures, and adverse worker and environmental impacts. FULL TEXT

Ledda et al., 2021

Ledda C, Cannizzaro E, Cinà D, Filetti V, Vitale E, Paravizzini G, Di Naso C, Iavicoli I, Rapisarda V. “Oxidative stress and DNA damage in agricultural workers after exposure to pesticides.” Journal of Occupational Medicine and Toxicology. 2021 Jan 7;16(1):1. DOI: 10.1186/s12995-020-00290-z.

ABSTRACT:

BACKGROUND: Recent epidemiological studies on workers describe that exposure to pesticides can induce oxidative stress by increased production of free radicals that can accumulate in the cell and damage biological macromolecules, for example, RNA, DNA, DNA repair proteins and other proteins and/or modify antioxidant defense mechanisms, as well as detoxification and scavenger enzymes. This study aimed to assess oxidative stress and DNA damage among workers exposed to pesticides.

METHODS: For this purpose, 52 pesticide exposed workers and 52 organic farmers were enrolled. They were assessed: the pesticide exposure, thiobarbituric acid reactive substances (TBARS), total glutathione (TG), oxidized glutathione levels (GSSG), and 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG), levels.

RESULTS: Correlation between pesticide exposure was positively associated with high TBARS and 8-oxodG levels (p < 0.001). A negative association was founded with TG and GSSG and pesticide exposure.

CONCLUSIONS: The present investigation results seem to indicate a mild augment in oxidative stress associated with pesticide exposure, followed by an adaptive response to increase the antioxidant defenses to prevent sustained oxidative adverse effects stress. FULL TEXT

Mesnage et al., 2021C

Mesnage R, Mazzacuva F, Caldwell A, Halket J, Antoniou MN. “Urinary excretion of herbicide co-formulants after oral exposure to roundup MON 52276 in rats.” Environmental Research. 2021 Jun;197:111103. DOI: 10.1016/j.envres.2021.111103.

ABSTRACT:

The toxicity of surfactants, which are an integral component of glyphosate-formulated products is an underexplored and highly debated subject. Since biomonitoring human exposure to glyphosate co-formulants is considered as a public health priority, we developed and validated a high-resolution mass spectrometry method to measure the urinary excretion of surfactants present in Roundup MON 52276, the European Union (EU) representative formulation of glyphosate-based herbicides. Quantification was performed measuring the 5 most abundant compounds in the mixture. We validated the method and showed that it is highly accurate, precise and reproducible with a limit of detection of 0.0004 μg/mL. We used this method to estimate the oral absorption of MON 52276 surfactants in Sprague-Dawley rats exposed to three concentrations of MON 52276 via drinking water for 90 days. MON 52276 surfactants were readily detected in urine of rats administered with this commercial Roundup formulation starting from a low concentration corresponding to the EU glyphosate acceptable daily intake. Our results provide a first step towards the implementation of surfactant co-formulant biomonitoring in human populations. FULL TEXT

Lee et al., 2017

Lee KM, Park SY, Lee K, Oh SS, Ko SB. “Pesticide metabolite and oxidative stress in male farmers exposed to pesticide.” Annals of Occupational and Environmental Medicine. 2017 Feb 28;29:5, DOI: 10.1186/s40557-017-0162-3.

ABSTRACT:

BACKGROUND: The objective of this study was to measure malondialdehyde (MDA) and isoprostane which has been used as an index of lipid injury, 8-hydroxy-2′-deoxyguanosine (8-OHdG), which has been used as an index of DNA damage, and dialkyl-phosphate (DAP), which has been used to quantify pesticide exposure, and to investigate the relationship between pesticide exposure and oxidative stress.

METHODS: This study was a cross-sectional study that evaluated 84 male farmers exposure to pesticide. In this study, 8-OHdG, isoprostane, and MDA were measured as oxidative stress indices, and dialkyl-phosphate (dimethylphosphate(DMP), diethylphosphate(DEP), dimethylthiophosphate(DMTP), and diethylthiophosphate (DETP)) excreted in the urine was also measured to evaluate pesticide exposure. A linear regression analysis was performed to investigate the relationship between pesticide metabolites, and oxidative stress biomarkers.

RESULTS: A Correlation analysis was performed for pesticide exposure month (PEI), cumulative exposure index (CEI), and DAP as well as the concentration of the oxidative stress biomarkers. The PEM significantly and positively correlated to the levels of 8-OHdG, isoprostane, CEI, and DMP. CEI showed a correlation to 8-OHdG and PEM. DMP, DEP, and DETP showed a positive correlation to 8-OHdG, isoprostane, and MDA. A correlation analysis was adjusted some demographic characteristics, such as age, smoking, drinking, and exercise to determine the relationship between pesticide exposure and oxidative stress. The 8-OHdG, isoprostane, and MDA levels were significantly related to the DMP (ß = 0.320), DEP (ß = 0.390), and DETP (ß = 0.082); DMP (ß = 0.396), DEP (ß = 0.508), and DETP (ß = 0.504); and DMP (ß = 0.432), DEP (ß = 0.508), and DETP (ß = 0.329) levels, respectively.

CONCLUSIONS: The concentration between oxidative stress biomarkers and the pesticide metabolite were a positive correlation. Indicators of oxidative stress was associated with a pesticide metabolite DMP, DEP, and DETP. Therefore, Pesticide exposure and oxidative stress were relevant. FULL TEXT

Bibliography Index