Bibliography Tag: other health risks

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.


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


Haas et al., 2015

Haas, D. M., Parker, C. B., Wing, D. A., Parry, S., Grobman, W. A., Mercer, B. M., Simhan, H. N., Hoffman, M. K., Silver, R. M., Wadhwa, P., Iams, J. D., Koch, M. A., Caritis, S. N., Wapner, R. J., Esplin, M. S., Elovitz, M. A., Foroud, T., Peaceman, A. M., Saade, G. R., Willinger, M., Reddy, U. M., & NuMo, M. b study; “A description of the methods of the Nulliparous Pregnancy Outcomes Study: monitoring mothers-to-be (nuMoM2b);” American Journal of Obstetrics & Gynecology, 2015, 212(4), 539 e531-539 e524; DOI: 10.1016/j.ajog.2015.01.019.

ABSTRACT:

OBJECTIVE: The primary aim of the “Nulliparous Pregnancy Outcomes Study: monitoring mothers-to-be” is to determine maternal characteristics, which include genetic, physiologic response to pregnancy, and environmental factors that predict adverse pregnancy outcomes.

STUDY DESIGN: Nulliparous women in the first trimester of pregnancy were recruited into an observational cohort study. Participants were seen at 3 study visits during pregnancy and again at delivery. We collected data from in-clinic interviews, take-home surveys, clinical measurements, ultrasound studies, and chart abstractions. Maternal biospecimens (serum, plasma, urine, cervicovaginal fluid) at antepartum study visits and delivery specimens (placenta, umbilical cord, cord blood) were collected, processed, and stored. The primary outcome of the study was defined as pregnancy ending at <37+0 weeks’ gestation. Key study hypotheses involve adverse pregnancy outcomes of spontaneous preterm birth, preeclampsia, and fetal growth restriction.

RESULTS: We recruited 10,037 women to the study. Basic characteristics of the cohort at screening are reported.

CONCLUSION: The “Nulliparous Pregnancy Outcomes Study: monitoring mothers-to-be” cohort study methods and procedures can help investigators when they plan future projects.

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Saldana et al., 2007

Saldana, T. M., Basso, O., Hoppin, J. A., Baird, D. D., Knott, C., Blair, A., Alavanja, M. C., & Sandler, D. P.; “Pesticide exposure and self-reported gestational diabetes mellitus in the Agricultural Health Study;” Diabetes Care, 2007, 30(3), 529-534; DOI: 10.2337/dc06-1832.

ABSTRACT:

OBJECTIVE: To examine the association between pesticide use during pregnancy and gestational diabetes mellitus (GDM) among wives of licensed pesticide applicators.

RESEARCH DESIGN AND METHODS: Using data from the Agricultural Health Study (AHS), we estimated the association between self-reported pesticide-related activities during the first trimester of the most recent pregnancy and GDM among 11,273 women whose pregnancy occurred within 25 years of enrollment.

RESULTS: A total of 506 (4.5%) women reported having had GDM. Women who reported agricultural pesticide exposure (mixing or applying pesticides to crops or repairing pesticide application equipment) during pregnancy were more likely to report GDM (odds ratio [OR] 2.2 [95% CI 1.5-3.3]). We saw no association between residential pesticide exposure (applying pesticides in the home and garden during pregnancy) and GDM (1.0 [0.8-1.3]). Among women who reported agricultural exposure during pregnancy, risk of GDM was associated with ever-use of four herbicides (2,4,5-T; 2,4,5-TP; atrazine; or butylate) and three insecticides (diazinon, phorate, or carbofuran).

CONCLUSIONS: These findings suggest that activities involving exposure to agricultural pesticides during the first trimester of pregnancy may increase the risk of GDM.

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Hoppin et al., 2002

Hoppin, Jane A., Umbach, David M, London, Stephanie J., Alavanja, Michael, & Sandler, Dale P.; “Chemical Predictors of Wheeze among Farmer Pesticide Applicators in the Agricultural Health Study;” American Journal of Respiratory and Critical Care Medicine, 2002, 165, 683-689; DOI: 10.1164/rccm.2106074.

ABSTRACT:

Pesticides may contribute to respiratory symptoms among farmers. Using the Agricultural Health Study, a large cohort of certified pesticide applicators in Iowa and North Carolina, we explored the association between wheeze and pesticide use in the past year. Self-administered questionnaires contained items on 40 currently used pesticides and pesticide application practices. A total of 20,468 applicators, ranging in age from 16 to 88 years, provided complete information; 19% reported wheezing in the past year. Logistic regression models controlling for age, state, smoking, and history of asthma or atopy were used to evaluate associations between individual pesticides and wheeze. Among pesticides suspected to contribute to wheeze, paraquat, three organophosphates (parathion, malathion, and chlorpyrifos), and one thiocarbamate (S-ethyl-dipropylthiocarbamate [EPTC]) had elevated odds ratios (OR). Parathion had the highest OR (1.5, 95% confidence interval [CI] 1.0, 2.2).

Chlorpyrifos, EPTC, paraquat, and parathion demonstrated significant dose–response trends. The herbicides, atrazine and alachlor, but not 2,4-D, were associated with wheeze. Atrazine had a significant dose–response trend with participants applying atrazine more than 20 days/year having an OR of 1.5 (95% CI 1.2,1.9). Inclusion of crops and animals into these models did not significantly alter the observed OR. These associations, though small, suggest an independent role for specific pesticides in respiratory symptoms of farmers. FULL TEXT


Hernandez et al., 2006

Hernandez, A. F., Amparo Gomez, M., Perez, V., Garcia-Lario, J. V., Pena, G., Gil, F., Lopez, O., Rodrigo, L., Pino, G., & Pla, A.; “Influence of exposure to pesticides on serum components and enzyme activities of cytotoxicity among intensive agriculture farmers;” Environmental Research, 2006, 102(1), 70-76; DOI: 10.1016/j.envres.2006.03.002.

ABSTRACT:

Although the effects of acute pesticide poisoning are well known for the pesticides most currently used, hardly any data exist on health effects after long-term low-dose exposures. Major unresolved issues include the effect of moderate exposure in the absence of poisoning. The increased utilization of pesticides other than organophosphates makes it even more difficult to find associations. In this study a cohort of 106 intensive agriculture workers were assessed twice during the course of a spraying season for changes in serum biochemistry, namely enzymes reflecting cytotoxicity (AST, ALT, LDH, CK, and amino-oxidase) and other biochemical parameters, such as markers of nephrotoxicity (urea, creatinine) and lipid profile (cholesterol and triglycerides). Several criteria for estimating pesticide exposure were used, the most important one being serum cholinesterase depression greater than 25% from baseline to peak exposure. Our results revealed an association of pesticide exposure with changes in AST (increased activity), LDH, and amino-oxidase (decreased activity) as well as with changes in serum creatinine and phosphorus (lower and higher levels, respectively). These results provide support for a very slight impairment of the liver function, but overall these findings are consistent with no clinically significant hepatotoxicity. Intriguingly, paraoxonase-1 R allele was found to be an independent predictor of higher rates of AST and lower rates of amino-oxidase, so that it may play a supporting role as an individual marker of susceptibility on pesticide-induced health effects. In conclusion, different biomarkers might be used to detect early biochemical effects of pesticides before adverse clinical health effects occur. FULL TEXT


Caiati et al., 2019

Caiati, C., Pollice, P., Favale, S., & Lepera, M. E.; “The Herbicide Glyphosate and Its Apparently Controversial Effect on Human Health: An Updated Clinical Perspective;” Endocrine, Metabolic, and Immune Disorders: Drug Targets, 2019; DOI: 10.2174/1871530319666191015191614.

ABSTRACT:

BACKGROUND: Glyphosate (G) is the most common weed-killer in the world. Every year tons and tons of G are applied on crop fields. G was first introduced in the mid 1970s and since then its usage has gradually increased to reach a peak since 2005. Now G usage is approximately 100 -fold what it was in 1970. Its impact on human health was considered benign at the beginning. But over the years, evidence of a pervasive negative effect of this pesticide on humans has been mounting. Nonetheless, G usage is allowed by government health control agencies (both in the United States and Europe), that rely upon the evidence produced by the G producer. However, the IARC (International Agency for Research on Cancer) in 2015 has stated that G is probable carcinogenic (class 2A), the second highest class in terms of risk.

OBJECTIVE: In this review, we explore the effect of G on human health, focusing in particular on more recent knowledge.

RESULTS: We have attempted to untangle the controversy about the dangers of the product for human beings in view of a very recent development, when the so -called Monsanto Papers, consisting of Emails and memos from Monsanto came to light, revealing a coordinated strategy to manipulate the debate about the safety of glyphosate to the company’s advantage.

CONCLUSIONS: The story of G is a recurrent one (see the tobacco story), that seriously jeopardizes the credibility of the scientific study in the modern era.


Alarcon et al., 2005

Alarcon, W. A., Calvert, G. M., Blondell, J. M., Mehler, L. N., Sievert, J., Propeck, M., Tibbetts, D. S., Becker, A., Lackovic, M., Soileau, S. B., Das, R., Beckman, J., Male, D. P., Thomsen, C. L., & Stanbury, M.; “Acute illnesses associated with pesticide exposure at schools;” JAMA, 2005, 294(4), 455-465; DOI: 10.1001/jama.294.4.455.

ABSTRACT:

CONTEXT: Pesticides continue to be used on school property, and some schools are at risk of pesticide drift exposure from neighboring farms, which leads to pesticide exposure among students and school employees. However, information on the magnitude of illnesses and risk factors associated with these pesticide exposures is not available.

OBJECTIVE: To estimate the magnitude of and associated risk factors for pesticide related illnesses at schools.

DESIGN, SETTING AND PARTICIPANTS: Analysis of surveillance data from 1998 to 2002 of 2593 persons with acute pesticide-related illnesses associated with exposure at schools. Nationwide information on pesticide-related illnesses is routinely collected by 3 national pesticide surveillance systems: the National Institute for Occupational Safety and Health’s Sentinel Event Notification System for Occupational Risks pesticides program, the California Department of Pesticide Regulation, and the Toxic Exposure Surveillance System.

MAIN OUTCOME MEASURES: Incidence rates and severity of acute pesticide-related illnesses.

RESULTS: Incidence rates for 1998-2002 were 7.4 cases per million children and 27.3 cases per million school employee full-time equivalents. The incidence rates among children increased significantly from 1998 to 2002. Illness of high severity was found in 3 cases (0.1%), moderate severity in 275 cases (11%), and low severity in 2315 cases (89%). Most illnesses were associated with insecticides (n=895, 35%), disinfectants (n=830, 32%), repellents (n=335, 13%), or herbicides (n=279, 11%). Among 406 cases with detailed information on the source of pesticide exposure, 281 (69%) were associated with pesticides used at schools and 125 (31%) were associated with pesticide drift exposure from farmland.

CONCLUSIONS: Pesticide exposure at schools produces acute illnesses among school employees and students. To prevent pesticide-related illnesses at schools, implementation of integrated pest management programs in schools, practices to reduce pesticide drift, and adoption of pesticide spray buffer zones around schools are recommended.

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Chung and Herceg, 2020

Chung, F. F., & Herceg, Z.; “The Promises and Challenges of Toxico-Epigenomics: Environmental Chemicals and Their Impacts on the Epigenome;” Environmental Health Perspectives, 2020, 128(1), 15001; DOI: 10.1289/EHP6104.

ABSTRACT:

BACKGROUND: It has been estimated that a substantial portion of chronic and noncommunicable diseases can be caused or exacerbated by exposure to environmental chemicals. Multiple lines of evidence indicate that early life exposure to environmental chemicals at relatively low concentrations could have lasting effects on individual and population health. Although the potential adverse effects of environmental chemicals are known to the scientific community, regulatory agencies, and the public, little is known about the mechanistic basis by which these chemicals can induce long-term or transgenerational effects. To address this question, epigenetic mechanisms have emerged as the potential link between genetic and environmental factors of health and disease.

OBJECTIVES: We present an overview of epigenetic regulation and a summary of reported evidence of environmental toxicants as epigenetic disruptors. We also discuss the advantages and challenges of using epigenetic biomarkers as an indicator of toxicant exposure, using measures that can be taken to improve risk assessment, and our perspectives on the future role of epigenetics in toxicology.

DISCUSSION: Until recently, efforts to apply epigenomic data in toxicology and risk assessment were restricted by an incomplete understanding of epigenomic variability across tissue types and populations. This is poised to change with the development of new tools and concerted efforts by researchers across disciplines that have led to a better understanding of epigenetic mechanisms and comprehensive maps of epigenomic variation. With the foundations now in place, we foresee that unprecedented advancements will take place in the field in the coming years.

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