Other Health Risks - HH-RA.org

Bibliography Tag: other health risks

Mostafalou and Abdollahi, 2017

Sara Mostafalou and Mohammad Abdollahi, “Pesticides: an update of human exposure and toxicity,” Archives of Toxicology, February 2017, 91:2, DOI: 10.1007/s00204-016-1849-x.

ABSTRACT:

Pesticides are a family of compounds which have brought many benefits to mankind in the agricultural, industrial, and health areas, but their toxicities in both humans and animals have always been a concern. Regardless of acute poisonings which are common for some classes of pesticides like organophosphoruses, the association of chronic and sub-lethal exposure to pesticides with a prevalence of some persistent diseases is going to be a phenomenon to which global attention has been attracted. In this review, incidence of various malignant, neurodegenerative, respiratory, reproductive, developmental, and metabolic diseases in relation to different routes of human exposure to pesticides such as occupational, environmental, residential, parental, maternal, and paternal has been systematically criticized in different categories of pesticide toxicities like carcinogenicity, neurotoxicity, pulmonotoxicity, reproductive toxicity, developmental toxicity, and metabolic toxicity. A huge body of evidence exists on the possible role of pesticide exposures in the elevated incidence of human diseases such as cancers, Alzheimer, Parkinson, amyotrophic lateral sclerosis, asthma, bronchitis, infertility, birth defects, attention deficit hyperactivity disorder, autism, diabetes, and obesity. Most of the disorders are induced by insecticides and herbicides most notably organophosphorus, organochlorines, phenoxyacetic acids, and triazine compounds.

Islam et al., 2018

Faisal Islam, Jian Wang, Muhammad A. Farooq, Muhammad S.S. Khan, Ling Xu, Jinwen Zhu, Min Zhao, Stéphane Muños, Qing X. Li, Weijun Zhou, “Potential impact of the herbicide 2,4-dichlorophenoxyacetic acid on human and ecosystems,” Environment International, 2018, 111, DOI: 10.1016/j.envint.2017.10.020.

ABSRACT: The herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) is applied directly to aquatic and conventional farming systems to control weeds, and is among the most widely distributed pollutants in the environment. Non-target organisms are exposed to 2,4-D via several ways, which could produce toxic effects depending on the dose, frequency of exposure, and the host factors that influence susceptibility and sensitivity. An increasing number of experimental evidences have shown concerns about its presence/detection in the environment, because several investigations have pointed out its potential lethal effects on non-target organisms. In this review, we critically evaluated the environmental fate and behavior of 2,4-D along with its eco-toxicological effects on aquatic, plants and human life to provide concise assessment in the light of recently published reports. The findings demonstrate that 2,4-D is present in a low concentration in surface water of regions where its usage is high. The highest concentrations of 2,4-D were detected in soil, air and surface water surrounded by crop fields, which suggest that mitigation strategies must be implanted locally to prevent the entry of 2,4-D into the environment. A general public may have frequent exposure to 2,4-D due to its wide applications at home lawns and public parks, etc. Various in vivo and in vitro investigations suggest that several species (or their organs) at different trophic levels are extremely sensitive to the 2,4-D exposure, which may explain variation in outcomes of reported investigations. However, implications for the prenatal exposure to 2,4-D remain unknown because 2,4-D-induced toxicity thresholds in organism have only been derived from juveniles or adults. In near future, introduction of 2,4-D resistant crops will increase its use in agriculture, which may cause relatively high and potentially unsafe residue levels in the environment. The recent findings indicate the urgent need to further explore fate, accumulation and its continuous low level exposure impacts on the environment to generate reliable database which is key in drafting new regulation and policies to protect the population from further exposure.

Ranjbar et al., 2015

Mahsa Ranjbar, Michael A. Rotondi, Chris I. Ardern, and Jennifer L. Kuk, “The Influence of Urinary Concentrations of Organophosphate Metabolites on the Relationship between BMI and Cardiometabolic Health Risk,” Journal of Obesity, 2015, DOI: 10.1155/2015/687914

ABSTRACT:

The objective was to determine whether detectable levels of OP metabolites influence the relationship between BMI and cardiometabolic health. This cross-sectional study was conducted using 2227 adults from the 1999–2008 NHANES datasets. Urinary concentrations of six dialkyl phosphate metabolites were dichotomized to above and below the detection limit. Weighted multiple regression analysis was performed adjusting for confounding variables. Independent of BMI, individuals with detectable metabolites had higher diastolic blood pressure (for dimethylphosphate, diethylphosphate, and diethyldithiophosphate; ???? < 0.05), lower HDL (for diethyldithiophosphate; ???? = 0.02), and higher triglyceride (for dimethyldithiophosphate; ???? = 0.05) than those below detection. Contrarily, those with detectable dimethylthiophosphate had better LDL, HDL, and total cholesterol, independent of BMI. Individuals at a higher BMI range who had detectable diethylphosphate (interaction: ???? = 0.03) and diethylthiophosphate (interaction: ???? = 0.02) exhibited lower HDL, while little difference existed between OP metabolite detection statuses at lower BMIs. Similarly, individuals with high BMIs and detectable diethylphosphate had higher triglyceride than those without detectable levels, while minimal differences between diethylphosphate detection statuses were observed at lower BMIs (interaction: ???? = 0.02). Thus, cardiometabolic health outcome differs depending on the specific OP metabolite being examined, with higher BMIs amplifying health risk. FULL TEXT

Brändli et al., 2012

Dirk Brändli and Sandra Reinacher, “Herbicides found in Human Urine,” Ithaka Journal, 1/2012, 2012

SUMMARY:

Glyphosate is the main active substance used in most commercial herbicides. It poisons not only plants, but also animals and humans. When testing for glyphosate contamination in an urban population, a German university found significant contamination in all urine samples with levels 5 to 20 times above the legal limit for drinking water. Glyphosate background info, health risks, and reasons for contamination are discussed. FULL TEXT

Raines et al., 2014

Nathan Raines MPH, Marvin González MD MS, Christina Wyatt MD MS, Mark Kurzrok, Christopher Pool, Tiziana Lemma, Ilana Weiss MPH, Carlos Marín, Valerio Prado, Eugenia Marcas, Karina Mayorga, Jean Franco Morales, Aurora Aragón MD PhD, Perry Sheffield MD MPH, “Risk Factors for Reduced Glomerular Filtration Rate in a Nicaraguan Community Affected by Mesoamerican Nephropathy,” MEDICC Review, 2014, 16:2.

ABSTRACT:

INTRODUCTION: Mesoamerican nephropathy, also known as chronic kidney disease of unknown etiology, is widespread in Pacific coastal Central America. The cause of the epidemic is unknown, but the disease may be linked to multiple factors, including diet as well as environmental and occupational exposures. As many as 50% of men in some communities have Mesoamerican nephropathy.

OBJECTIVE: Describe prevalence of reduced glomerular filtration rate in a region of Nicaragua suspected to harbor high rates of Mesoamerican nephropathy; and investigate potential risk factors for such reduction associated with agricultural work (such as pesticide exposure and specific agricultural tasks associated with increased heat stress); sugar consumption; and traditional factors such as age, sex, diabetes, hypertension and nephrotoxic medication use.

METHODS: This study uses a cross-sectional design with nested case-control analysis. Cases were individuals with estimated glomerular filtration rates of <60 mL/min/1.73 m2 and controls were individuals with those >90mL/min/1.73 m2 , estimated using serum creatinine. Data on nutrition, past medical history, medication and substance use, and agricultural behaviors and exposures were collected using medical questionnaires from June through August, 2012. Venous blood and urine samples were collected to assess hemoglobin A1c, and dipstick proteinuria, respectively; anthropometry and blood pressure measurements were made using standard techniques. Analyses were conducted using chi square, and univariate and multiple logistic regression.

RESULTS: Of 424 individuals in the study, 151 had an occupational history in agriculture. Prevalence of glomerular filtration rate <60 mL/ min/1.73 m2 was 9.8% among women and 41.9% among men (male to female ratio = 4.3, p<0.0001). Proteinuria > or equal to 300 mg/dL was observed in <10% of participants with decreased glomerular filtration rate. Hemoglobin A1c and use of NSAIDs were not associated with decreased glomerular filtration rate. Although systolic and diastolic blood pressure was higher among participants with decreased glomerular filtration rate (p <0.001), hypertension was uncommon. Significant agricultural risk factors for reduced glomerular filtration rate included increased lifetime days cutting sugarcane during the dry season (OR 5.86, 95% CI 2.45–14.01), nondeliberate pesticide inhalation (OR 3.31, 95% CI 1.32–8.31), and sugarcane chewing (OR 3.24, 95% CI 1.39–7.58).

CONCLUSIONS: Our findings demonstrate a high prevalence of chronic kidney disease not linked to traditional risk factors, and suggest it may be associated instead with occupational exposure to heat stress in conjunction with pesticide inhalation, sugarcane chewing and sugar intake during the workday. FULL TEXT

Mesnage et al., 2015b

Robin Mesnage, Matthew Arno, Manuela Costanzo, Manuela Malatesta, Gilles-Eric Séralini and Michael N. Antoniou, “Transcriptome profile analysis reflects rat liver and kidney damage following chronic ultra-low dose Roundup exposure,” Environmental Health, 2015, 14:70, DOI 10.1186/s12940-015-0056-1.

ABSTRACT:

BACKGROUND: Glyphosate-based herbicides (GBH) are the major pesticides used worldwide. Converging evidence suggests that GBH, such as Roundup, pose a particular health risk to liver and kidneys although low environmentally relevant doses have not been examined. To address this issue, a 2-year study in rats administering 0.1 ppb Roundup (50 ng/L glyphosate equivalent) via drinking water (giving a daily intake of 4 ng/kg bw/day of glyphosate) was conducted. A marked increased incidence of anatomorphological and blood/urine biochemical changes was indicative of liver and kidney structure and functional pathology. In order to confirm these findings we have conducted a transcriptome microarray analysis of the liver and kidneys from these same animals.

RESULTS: The expression of 4224 and 4447 transcript clusters (a group of probes corresponding to a known or putative gene) were found to be altered respectively in liver and kidney (p < 0.01, q < 0.08). Changes in gene expression varied from −3.5 to 3.7 fold in liver and from −4.3 to 5.3 in kidneys. Among the 1319 transcript clusters whose expression was altered in both tissues, ontological enrichment in 3 functional categories among 868 genes were found. First, genes involved in mRNA splicing and small nucleolar RNA were mostly upregulated, suggesting disruption of normal spliceosome activity. Electron microscopic analysis of hepatocytes confirmed nucleolar structural disruption. Second, genes controlling chromatin structure (especially histone-lysine N-methyltransferases) were mostly upregulated. Third, genes related to respiratory chain complex I and the tricarboxylic acid cycle were mostly downregulated. Pathway analysis suggests a modulation of the mTOR and phosphatidylinositol signalling pathways. Gene disturbances associated with the chronic administration of ultra-low dose Roundup reflect a liver and kidney lipotoxic condition and increased cellular growth that may be linked with regeneration in response to toxic effects causing damage to tissues. Observed alterations in gene expression were consistent with fibrosis, necrosis, phospholipidosis, mitochondrial membrane dysfunction and ischemia, which correlate with and thus confirm observations of pathology made at an anatomical, histological and biochemical level.

CONCLUSION: Our results suggest that chronic exposure to a GBH in an established laboratory animal toxicity model system at an ultra-low, environmental dose can result in liver and kidney damage with potential significant health implications for animal and human populations. FULL TEXT

Marc et al., 2004

Julie Marc, Robert Belle, Julia Morales, Patrick Cormier, and Odile Mulner-Lorillon, “Formulated Glyphosate Activates the DNA-Response Checkpoint of the Cell Cycle Leading to the Prevention of G2/M Transition,” Toxicological Sciences, 2004, 82, DOI:10.1093/TOXSCI/KFH281.

ABSTRACT:

A glyphosate containing pesticide impedes at 10 mM glyphosate the G2/M transition as judged from analysis of the first cell cycle of sea urchin development. We show that formulated glyphosate prevented dephosphorylation of Tyr 15 of the cell cycle regulator CDK1/cyclin B in vivo, the end point target of the G2/M cell cycle checkpoint. Formulated glyphosate had no direct effect on the dual specific cdc25 phosphatase activity responsible for Tyr 15 dephosphorylation. At a concentration that efficiently impeded the cell cycle, formulated glyphosate inhibited the synthesis of DNA occurring in S phase of the cell cycle. The extent of the inhibition of DNA synthesis by formulated glyphosate was correlated with the effect on the cell cycle. We conclude that formulated glyphosate’s effect on the cell cycle is exerted at the level of the DNA-response checkpoint of S phase. The resulting inhibition of CDK1/cyclin B Tyr 15 dephosphorylationleads to prevention of the G2/M transition and cell cycle progression. FULL TEXT

Jayasumana et al., 2015a

Channa Jayasumana, Sarath Gunatilake, and Sisira Siribaddana, “Simultaneous exposure to multiple heavy metals and glyphosate may contribute to Sri Lankan agricultural nephropathy,” BMC Nephrology, 2015, 16:103, DOI 10.1186/s12882-015-0109-2.

ABSTRACT:

BACKGROUND: Sri Lankan Agricultural Nephropathy (SAN), a new form of chronic kidney disease among paddy farmers was first reported in 1994. It has now become the most debilitating public health issue in the dry zone of Sri Lanka. Previous studies showed SAN is a tubulo-interstitial type nephropathy and exposure to arsenic and cadmium may play a role in pathogenesis of the disease.

METHODS: Urine samples of patients with SAN (N = 10) from Padavi-Sripura, a disease endemic area, and from two sets of controls, one from healthy participants (N = 10) from the same endemic area and the other from a non-endemic area (N = 10; Colombo district) were analyzed for 19 heavy metals and for the presence of the pesticide- glyphosate.

RESULTS: In both cases and the controls who live in the endemic region, median concentrations of urinary Sb, As, Cd, Co, Pb, Mn, Ni, Ti and V exceed the reference range. With the exception of Mo in patients and Al, Cu, Mo, Se, Ti and Zn in endemic controls, creatinine adjusted values of urinary heavy metals and glyphosate were significantly higher when compared to non-endemic controls. Creatinine unadjusted values were significant higher for 14 of the 20 chemicals studied in endemic controls and 7 in patients, compared to non-endemic controls. The highest urinary glyphosate concentration was recorded in SAN patients (range 61.0-195.1 μg/g creatinine).

CONCLUSTIONS: People in disease endemic area exposed to multiple heavy metals and glyphosate. Results are supportive of toxicological origin of SAN that is confined to specific geographical areas. Although we could not localize a single nephrotoxin as the culprit for SAN, multiple heavy metals and glyphosates may play a role in the pathogenesis. Heavy metals excessively present in the urine samples of patients with SAN are capable of causing damage to kidneys. Synergistic effects of multiple heavy metals and agrochemicals may be nephrotoxic. FULL TEXT

Jayasumana et al., 2014

Channa Jayasumana, Sarath Gunatilake, and Priyantha Senanayake, “Glyphosate, Hard Water and Nephrotoxic Metals: Are They the Culprits Behind the Epidemic of Chronic Kidney Disease of Unknown Etiology in Sri Lanka?,” International Journal of Environmental Research and Public Health, 2014, 11, DOI:10.3390/IJERPH 110202125.

ABSTRACT:

The current chronic kidney disease epidemic, the major health issue in the rice paddy farming areas in Sri Lanka has been the subject of many scientific and political debates over the last decade. Although there is no agreement among scientists about the etiology of the disease, a majority of them has concluded that this is a toxic nephropathy. None of the hypotheses put forward so far could explain coherently the totality of clinical, biochemical, histopathological findings, and the unique geographical distribution of the disease and its appearance in the mid-1990s. A strong association between the consumption of hard water and the occurrence of this special kidney disease has been observed, but the relationship has not been explained consistently. Here, we have hypothesized the association of using glyphosate, the most widely used herbicide in the disease endemic area and its unique metal chelating properties. The possible role played by glyphosate-metal complexes in this epidemic has not been given any serious consideration by investigators for the last two decades. Furthermore, it may explain similar kidney disease epidemics observed in Andra Pradesh (India) and Central America. Although glyphosate alone does not cause an epidemic of chronic kidney disease, it seems to have acquired the ability to destroy the renal tissues of thousands of farmers when it forms complexes with a localized geo environmental factor (hardness) and nephrotoxic metals. FULL TEXT

Skinner, 2007

Skinner MK1, “Endocrine disruptors and epigenetic transgenerational disease etiology,” Pediatric Research, 2007, 61:5 Pt 2.

ABSTRACT: Exposure to an environmental factor (e.g. endocrine disruptor) during embryonic gonadal sex determination appears to be epigenetically reprogram the male germ-line and subsequently promote transgenerational adult-onset disease. Disease phenotypes resulting from this epigenetic phenomenon include testis abnormalities, prostate disease, kidney disease, tumor development, and immune abnormalities. The epigenetic mechanism is hypothesized to involve the induction of new imprinted-like DNA sequences in the germ-line to transgenerationally transmit disease phenotypes. This epigenetic transgenerational disease mechanism provides a unique perspective from which to view adult onset disease and ultimately offers new insights into novel diagnostic and therapeutic strategies. FULL TEXT

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