Bibliography Tag: other health risks

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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.

Landrigan and Goldman, 2011

Landrigan, Philip J, & Goldman, Lynn R; “Children’s vulnerability to toxic chemicals: a challenge and opportunity to strengthen health and environmental policy;” Health Affairs, 2011, 30(5), 842-850; DOI: 10.1377/hlthaff.2011.0151.


A key policy breakthrough occurred nearly twenty years ago with the discovery that children are far more sensitive than adults to toxic chemicals in the environment. This finding led to the recognition that chemical exposures early in life are significant and preventable causes of disease in children and adults. We review this knowledge and recommend a new policy to regulate industrial and consumer chemicals that will protect the health of children and all Americans, prevent disease, and reduce health care costs. The linchpins of a new US chemical policy will be: first, a legally mandated requirement to test the toxicity of chemicals already in commerce, prioritizing chemicals in the widest use, and incorporating new assessment technologies; second, a tiered approach to premarket evaluation of new chemicals; and third, epidemiologic monitoring and focused health studies of exposed populations.  FULL TEXT

Attina et al., 2016

Attina, T. M., Hauser, R., Sathyanarayana, S., Hunt, P. A., Bourguignon, J. P., Myers, J. P., DiGangi, J., Zoeller, R. T., & Trasande, L.; “Exposure to endocrine-disrupting chemicals in the USA: a population-based disease burden and cost analysis;” Lancet Diabetes and Endocrinol, 2016, 4(12), 996-1003; DOI: 10.1016/S2213-8587(16)30275-3.


BACKGROUND: Endocrine-disrupting chemicals (EDCs) contribute to disease and dysfunction and incur high associated costs (>1% of the gross domestic product [GDP] in the European Union). Exposure to EDCs varies widely between the USA and Europe because of differences in regulations and, therefore, we aimed to quantify disease burdens and related economic costs to allow comparison.

METHODS: We used existing models for assessing epidemiological and toxicological studies to reach consensus on probabilities of causation for 15 exposure-response relations between substances and disorders. We used Monte Carlo methods to produce realistic probability ranges for costs across the exposure-response relation, taking into account uncertainties. Estimates were made based on population and costs in the USA in 2010. Costs for the European Union were converted to US$ (euro1=$1.33).

FINDINGS: The disease costs of EDCs were much higher in the USA than in Europe ($340 billion [2.33% of GDP] vs $217 billion [1.28%]). The difference was driven mainly by intelligence quotient (IQ) points loss and intellectual disability due to polybrominated diphenyl ethers (11 million IQ points lost and 43 000 cases costing $266 billion in the USA vs 873 000 IQ points lost and 3290 cases costing $12.6 billion in the European Union). Accounting for probability of causation, in the European Union, organophosphate pesticides were the largest contributor to costs associated with EDC exposure ($121 billion), whereas in the USA costs due to pesticides were much lower ($42 billion).

INTERPRETATION: EDC exposure in the USA contributes to disease and dysfunction, with annual costs taking up more than 2% of the GDP. Differences from the European Union suggest the need for improved screening for chemical disruption to endocrine systems and proactive prevention.

FUNDING: Endocrine Society, Ralph S French Charitable Foundation, and Broad Reach Foundation. FULL TEXT