Humans

Australia’s federal pesticide regulator has backed calls from researchers for further study into a potential link between the use of pesticides and increased risk of Parkinson’s disease. Australian Pesticides and Veterinary Medicines Authority (APVMA) spokeswoman Dr Raj Bhula told SBS the organisation believed further research was justified, but said there was not any: “clear-cut evidence that links the two together”. The call comes following the discovery of a Parkinson’s disease cluster in a barley, chickpea and lentil farming region of north-west Victoria.

One year ago, an agency of the World Health Organization’s International Agency for Cancer Research (IARC) declared that glyphosate (or Roundup), the world’s most widely used herbicide, probably causes cancer. Then, in the fall, the European Food Safety Agency’s (EFSA) responded with an assessment that disagreed with the WHO’s findings. In response, 94 scientists came out in support of the IARC’s original findings. This week, the group—which includes scientists from around the world—released their article in the peer-reviewed Journal of Epidemiology and Community Health saying: The most appropriate and scientifically based evaluation of the cancers reported in humans and laboratory animals as well as supportive mechanistic data is that glyphosate is a probable human carcinogen. On the basis of this conclusion and in the absence of evidence to the contrary, it is reasonable to conclude that glyphosate formulations should also be considered likely human carcinogens. And their endorsement is no small matter. In fact, as the U.S. Environmental Protection Agency (EPA) reassesses the safety of glyphosate, and the U.S. Food and Drug Administration (FDA) plans to begin testing food for its residue, this volley has important implications.

A latency period preceding neurotoxicity is a common characteristic in the dose-response relationship induced by organic mercury. Latency periods have typically been observed with genotoxicants in carcinogenesis, with cancer being manifested a long time after the initiating event. These observations indicate that even a very small dose may cause extensive adverse effects later in life, so the toxicity of the genotoxic compound is dose and time-dependent. In children, methylmercury exposure during pregnancy (in utero) has been associated with delays in reaching developmental milestones (e.g., age at first walking) and decreases in intelligence, increasing in severity with increasing exposure. Ethylmercury exposure from thimerosal in some vaccines has been associated, in some studies, with autism and other neurological disorders in children. In this paper, we have examined whether dose-response data from in vitro and in vivo organic mercury toxicity studies fit the Druckrey-Küpfmüller equation c·tn = constant (c = exposure concentration, t = latency period), first established for genotoxic carcinogens, and whether or not irreversible effects are enhanced by time of exposure (n≥ 1), or else toxic effects are dose-dependent while time has only minor influence on the adverse outcome (n < 1). The mode of action underlying time-dependent toxicity is irreversible binding to critical receptors causing adverse and cumulative effects. The results indicate that the Druckrey-Küpfmüller equation describes well the dose-response characteristics of organic mercury induced neurotoxic effects. This amounts to a paradigm shift in chemical risk assessment of mercurial compounds and highlights that it is vital to perform toxicity testing geared to investigate time-dependent effects.

Es wird in Bergbaubetrieben gefördert und beim Recycling von Autobatterien freigesetzt: Blei ist einer Studie zufolge das weltweit verheerendste Umweltgift. Etwa 26 Millionen Menschen in Ländern mit niedrigem und mittlerem Einkommensniveau sind demnach dem Schwermetall direkt ausgesetzt. Das geht aus dem Umweltgiftreport 2015 der Schweizer Stiftung Green Cross und der international tätigen Non-Profit-Organisation Pure Earth hervor. Zu den schädlichsten Umweltgiften zählen demnach auch Quecksilber, sechswertiges Chrom, Radionuklide, Pestizide und Kadmium. Etwa 95 Millionen Menschen seien unmittelbar von diesen Schadstoffen betroffen, heißt es in dem Bericht. Quecksilber wird oft von Kohlekraftwerken ausgestoßen und kommt in vielen Industrieprodukten wie Thermometern und Energiesparlampen vor. Sechswertiges Chrom findet sich unter anderem in gegerbtem Leder und Kochgeschirr aus Edelstahl. Radionuklide werden zum Beispiel beim Abbau von Uran und von radiologischen Produkten in der Medizintechnik freigesetzt. Pestizide kommen vor allem in der Landwirtschaft zum Einsatz. Kadmium entsteht etwa bei der Düngemittelherstellung.

Vorgestern Nacht erklärte EU-Gesundheitskommissar Vytenis Andriukaitis gegenüber Mitgliedern des Europäischen Parlaments, die EU-Kommission werde die seit Dezember 2013 überfälligen wissenschaftlichen Kriterien für die Charakterisierung hormonell schädigender Chemikalien noch vor Sommer vorlegen. Bisher hatte sich die Kommission trotz Verurteilung durch den EuGH geweigert, eine diesbezügliche Frist zu nennen. Sie argumentierte, sie wolle zuerst das Ergebnis des “Impact Assessments“ über die sozio-ökonomischen Auswirkungen des 2009 beschlossenen gesetzlichen Verbots hormonell wirksamer Pestizide abwarten. Da die EU-Kommission die mit Dezember 2013 gesetzte Frist für die Vorlage dieser Kriterien tatenlos verstreichen ließ, konnten die in den EU-Pestizid- und Biozid-Verordnungen festgelegten gesetzlichen Verbote hormonschädigender Stoffe nicht rechtswirksam werden. Im Sommer 2014 klagte Schweden die Kommission wegen Untätigkeit. EU-Parlament und EU-Rat schlossen sich der Klage an. Am 16. Dezember 2015 urteilte das Gericht der Europäischen Union: Die EU-Kommission verstoße gegen Unionsrecht, indem sie keine Rechtsakte zur Festlegung wissenschaftlicher Kriterien zur Bestimmung endokrin schädigender Eigenschaften erlassen habe. „Alles hängt nun davon ab, ob die Kriterien, welche die Kommission im Juni vorlegen wird, auch tatsächlich auf den wissenschaftlichen Grundlagen des von der Kommission selbst beauftragten Kortenkamp-Reports basieren oder aber die Vorstellungen und Wünsche der chemischen Industrie widerspiegeln.“ meint dazu DI Dr. Helmut Burtscher, Umwelt-Chemiker von GLOBAL 2000.

Neonicotinoids—the world’s most widely used and fastest growing type of insecticide—have been at the center of the conversation about bee die-offs for several years. Even the U.S. Environmental Protection Agency (EPA) recently acknowledged that very small quantities can impact pollinators. But what about human health? “There is an amazing lack of information for such widely used pesticides,” Mount Sinai professor of pediatrics and preventative medicine and dean for global health Philip Landrigan told Civil Eats. Now, a number of scientists, including those at the U.S. National Toxicology Program, say a closer look is needed.

A commonly used pesticide may alter the development of the brain's dopamine system -- responsible for emotional expression and cognitive function -- and increase the risk of attention deficit hyperactivity disorder in children, according to a new Rutgers study. The research published Wednesday in the Journal of the Federation of American Societies for Experimental Biology (FASEB), by Rutgers scientists and colleagues from Emory University, the University of Rochester Medical Center, and Wake Forest University discovered that mice exposed to the pyrethroid pesticide deltamethrin in utero and through lactation exhibited several features of ADHD, including dysfunctional dopamine signaling in the brain, hyperactivity, working memory, attention deficits and impulsive-like behavior. These findings provide strong evidence, using data from animal models and humans, that exposure to pyrethroid pesticides, including deltamethrin, may be a risk factor for ADHD, says lead author Jason Richardson, associate professor in the Department and Environmental and Occupational Medicine at Rutgers Robert Wood Johnson Medical School and a member of the Environmental and Occupational Health Sciences Institute (EOHSI). "Although we can't change genetic susceptibility to ADHD, there may be modifiable environmental factors, including exposures to pesticides that we should be examining in more detail," says Richardson.

We previously determined a metabolite of acetamiprid, N-desmethyl-acetamiprid in the urine of a patient, who exhibited some typical symptoms including neurological findings. We sought to investigate the association between urinary N-desmethyl-acetamiprid and the symptoms by a prevalence case-control study. Spot urine samples were collected from 35 symptomatic patients of unknown origin and 50 non-symptomatic volunteers (non-symptomatic group, NSG, 4–87 year-old). Patients with recent memory loss, finger tremor, and more than five of six symptoms (headache, general fatigue, palpitation/chest pain, abdominal pain, muscle pain/weakness/spasm, and cough) were in the typical symptomatic group (TSG, n = 19, 5–69 year-old); the rest were in the atypical symptomatic group (ASG, n = 16, 5–78 year-old). N-desmethyl-acetamiprid and six neonicotinoids in the urine were quantified by liquid chromatography-tandem mass spectrometry. The detection of N-desmethyl-acetamiprid was the most frequent and highest in TSG (47.4%, 6.0 ppb (frequency, maximum)), followed by in ASG (12.5%, 4.4 ppb) and in NSG (6.0%, 2.2 ppb), however acetamiprid was not detected. Thiamethoxam was detected in TSG (31.6%, 1.4 ppb), in ASG (6.3%, 1.9 ppb), but not in NSG. Nitenpyram was detected in TSG (10.5%, 1.2 ppb), in ASG (6.3%, not quantified) and in NSG (2.0%, not quantified). Clothianidin was only detected in ASG (6.3%, not quantified), and in NSG (2.0%, 1.6 ppb). Thiacloprid was detected in ASG (6.3%, 0.1 ppb). The cases in TSG with detection of N-desmethyl-acetamiprid and thiamethoxam were aged 5 to 62 years and 13 to 62 years, respectively. Detection of N-desmethyl-acetamiprid was associated with increased prevalence of the symptoms (odds ratio: 14, 95% confidence interval: 3.5–57). Urinary N-desmethyl-acetamiprid can be used as a biomarker for environmental exposure to acetamiprid. Further multi-centered clinical research in larger patients groups with more metabolites analysis is needed