skip to Main Content

Project Bibliography

Bibliographies Grouped by Tag:
24 D | Adjuvants | Agricultural Health Study | Agrochemicals | AMPA | Analytical Methods | Atrazine | Autism | Biodiversity | Biomarkers | Biomonitoring | Birth Cohort Studies | Birth Defects | Birthweight | Cancer | Children | Chlorpyrifos | Climate Change | Communicating Science | Crop Science | Cumulative Toxicity | Cypermethrin | Cytotoxicity | DDT | Desiccation | Developmental Impacts | Diazinon | Dicamba | Dicamba Part I | Dicamba Part II | Dicamba Part III | Dicamba Watch | Diet | Dietary Risk | Diversified Weed Management/Integrated Pest Management (IPM) | DNA Damage | Economics | Endocrine Disruptors | Endosulfan | Environmental Health | Environmental Impacts | Environmental Racism | EPA Regulation | Epidemiological Studies | Epigenetic Impacts | Ethics and Environmental Justice | ethnicity | Exposure | Exposure at School and Public Spaces | Exposure in Pets | Female Reproductive Impacts | Fertility | Food Systems | Full Text Available | Fungicides | Gastrointestinal Impacts | GBH | Gender | Genetically Modified Crops | Genotoxicity | Gestational Length | Glufosinate | Glyphosate | Heartland Region | Herbicide Exposure | Herbicide Industry Labels and User Guides | Herbicide Use | Herbicides | HHRA Publication | Imidacloprid | Insecticides | Invertebrate Toxicity | Kidney Disease | Liver Damage | Lowdown on Roundup Part I | Lowdown on Roundup Part II | Lowdown on Roundup Part III | Lowdown on Roundup Part IV | Male Reproductive Impacts | Maternal Gut Microbiome | Meta-Analysis or Review Paper | Metolachlor | Microbiome | Miscarriage Rate | Multi-omics | National Cancer Institute | Neonicotinoids | Neurodevelopmental Toxicity | Nitric Oxide | Obesity | Occupational Exposure | Organic | Organic vs Conventional | Organochlorines | Organophosphates | Other Health Risks | Oxamyl | Oxidative Stress | Paraquat | Parkinson's Disease | Persistent Organic Pollutants | Pesticide Drift | Pesticide Effectiveness | Pesticide Exposure | Pesticide Legislation | Pesticide Registration | Pesticide Residues | Pesticide Resistance | Pesticide Toxicity | Pesticide Use | Policy and Politics | Pollinators | Pregestational Obesity | Pregnancy | prenatal | Public Health | Pyrethroids | Regenerative Agriculture | Remediation | Reproductive Impacts | Resistant Weeds | Risk Assessment | Roundup | Rural Health | Science Team Publication | Seasonal | Soil Health | Sperm Quality | Surfactants | Toxicity | Traizoles | Trends Analysis | Weed Management Systems
Combine bibliography tags from the above list:

Harris et al., 2015

Harris, DE, Aboueissa, N Baugh, & Sarton, C; “Impact of rurality on maternal and infant health indicators and outcomes in Maine;” Rural and Remote Health, 2015, 15(3278).

ABSTRACT:

INTRODUCTION: Rural residents may face health challenges related to geographic barriers to care, physician shortages, poverty, lower educational attainment, and other demographic factors. In maternal and child health, these disparities may be evidenced by the health risks and behaviors of new mothers, the health of infants born to these mothers, and the care received by both mothers and infants.

MEHTODS: To determine the impact of rurality on maternal and child health in Maine, USA, 11 years of data (2000–2010) for the state of Maine from the Pregnancy Risk Assessment Monitoring System (PRAMS) project were analyzed. PRAMS is a national public health surveillance system that uses questionnaires to survey women who had delivered live infants in the previous 2–4 months. Using a geographic information system, each questionnaire response was assigned a rurality tier (urban, suburban, large rural town, or isolated rural community) based on the rural–urban commuting area code of the town of residence of the mother. Results from the four rurality tiers were compared using the survey procedures in Statistical Analysis Software to adjust for the complex sampling strategy of the PRAMS dataset. Means (for continuous variables) and percentages (for categorical variables) were calculated for each rurality tier, along with 95% confidence intervals. Significant differences between rurality tiers were tested for using F-tests or χ2 tests. If significant differences between rurality tiers existed (p<0.05), specific tiers were judged to be different from each other if their 95% confidence intervals did not overlap.

RESULTS: A total of 12 600 mothers responded to the PRAMS questionnaire during the study period. Compared to mothers from more urban areas, rural mothers were younger (10.5% of mothers from isolated rural areas were teenagers compared to 6.2% of mothers from urban areas), less well educated, less likely to be married, and more likely to live in lower income households (39.6% of isolated rural mothers had household incomes ≤US$20 000/year vs 28.8% of urban mothers). Rural mothers had higher prepregnancy body mass indexes (BMIs; average BMI 26.1 for isolated rural women vs 25.3 for urban women) and were more likely to smoke but less likely to drink alcohol (both before and during pregnancy). Compared to mothers from more urban areas, rural mothers were not sure they were pregnant until a later gestational age but received prenatal care just as early and were just as likely to receive prenatal care as early as they wished. There were no differences among rurality tiers in Caesarean section rates, rates of premature births (<37 weeks gestation), or rates of underweight births (<2500 g). However infants born to rural mothers were less likely to be breastfed (52.9% of isolated rural vs 60.9% of urban infants breast fed for ≥8 weeks).

CONCLUSIONS: These results show that, while rural women face significant demographic and behavior challenges, their access to prenatal care, the care they receive while pregnant, and the outcomes of their pregnancies are similar to those of urban women. These results highlight areas where focused pre-pregnancy and prenatal education may improve maternal and child health in rural Maine.


Villapiano et al., 2017

Villapiano, N., Iwashyna, T. J., & Davis, M. M.; “Worsening Rural-Urban Gap in Hospital Mortality;” Journal of the American Board of Family Medicine, 2017, 30(6), 816-823; DOI: 10.3122/jabfm.2017.06.170137.

ABSTRACT:

BACKGROUND: One out of every 5 Americans live in rural communities. Rural Americans have higher rates of early and preventable deaths outside of the hospital than their urban counterparts. How rurality relates to hospital mortality is unknown. We sought to determine the association between rural versus urban residence and hospital mortality.

METHODS: This is a retrospective observational study of 4,412,942 nonmaternal, nonneonatal hospitalizations in 2008, and 3899,464 nonmaternal, nonneonatal hospitalizations in 2013 using all-payer, all-age data from the National Inpatient Sample of the Health care Cost and Utilization Project. Using multivariable logistic regression, we report the association between rural versus urban location of residence and hospital mortality, adjusting for chronic disease burden, age, income, and insurance status.

RESULTS: The unadjusted probability of hospital mortality for urban patients decreased from 2.51% (95% CI, 2.40 to 2.62) in 2008 to 2.27% (95% CI, 2.22 to 2.32) in 2013 (P < .001). Hospital mortality did not change for rural patients over this same time period (2008: 2.66% [95% CI, 2.57 to 2.74], 2013: 2.66% [95% CI, 2.60 to 2.72]; P = .99). Adjusting for covariates accounted for the rural-urban hospital mortality difference in 2008 (rural: 2.13% [95% CI, 2.05 to 2.21], urban: 2.11% [95% CI, 2.02 to 2.20]; P = .67), but did not fully explain the difference in 2013 (rural: 1.92% [95% CI, 1.87 to 1.97]; urban: 1.76% [95% CI, 1.72 to 1.80], P < .001), resulting in 8416 excess deaths among hospitalized patients from rural areas.

CONCLUSION AND RELEVANCE: In 2013, patients living in rural areas of the United States had a greater probability of hospital mortality than their urban counterparts. Explaining excess rural hospital deaths will require further attention to the patient, community, and health system factors that distinguish rural from urban populations. FULL TEXT


Zahnd et al., 2009

Zahnd, W. E., Scaife, S. L., & Francis, M. L.; “Health literacy skills in rural and urban populations;” American Journal of Health Behavior, 2009, 33(5), 550-557; DOI: 10.5993/ajhb.33.5.8.

ABSTRACT:

OBJECTIVE: To determine whether health literacy is lower in rural populations.

METHOD: We analyzed health, prose, document, and quantitative literacy from the National Assessment of Adult Literacy study. Metropolitan Statistical Area designated participants as rural or urban.

RESULTS: Rural populations had lower literacy levels for all literacy types (P<0.001 for each). After adjusting for known confounders, there was no longer a difference in health or prose literacy (P>0.05). However, rural populations had higher document (P=0.04) and quantitative (P=0.01) literacy.

CONCLUSION: Health literacy is lower in the rural population although this difference is explained by known confounders.


Benbrook and Benbrook, 2021

Benbrook, Charles, & Benbrook, Rachel (2021). “A minimum data set for tracking changes in pesticide use.” In R. Mesnage & J. Zaller (Eds.), Herbicides: Elsevier and RTI Press.

ABSTRACT:

A frequently asked but deceptively simple question often arises about pesticide use on a given farm or crop: Is pesticide use going up, down, or staying about the same? Where substantial changes in pesticide use are occurring, it is also important to understand the factors driving change. These might include more or fewer hectares planted, a change in the crop mix, a higher or lower percentage of hectares treated, or higher or lower rates of application and/or number of applications. Or, it might arise from a shift to other pesticides applied at a higher or lower rate and/or lessened or greater reliance on nonpesticidal strategies and integrated pest management (IPM). Questions about whether pesticide use is changing and why arise for a variety of reasons. Rising use typically increases farmer costs and cuts into profit margins. It generally raises the risk of adverse environmental and/or public health outcomes. It can accelerate the emergence and spread of organisms resistant to applied pesticides. If the need to spray more continues year after year for long enough, farming systems become unsustainable. Lessened reliance on and use of pesticides, on the other hand, are typically brought about and can only be sustained by incrementally more effective prevention-based biointensive IPM systems (bioIPM).1–3 Fewer pesticide applications and fewer pounds/kilograms of active ingredient applied reduce the impacts on nontarget organisms and provide space for beneficial organisms and biodiversity to flourish. Such systems reduce the odds of significant crop loss in years when conditions undermine the efficacy of control measures, leading to spikes in pest populations and the risk of economically meaningful loss of crop yield and/or quality. FULL TEXT


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 &lt;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 &lt;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


Back To Top
Search