Severe Propanil [<i>N</i>-(3,4-Dichlorophenyl) Propanamide] Pesticide Self-Poisoning

Eddleston, Michael; Rajapakshe, Manjula; Roberts, Darren M.; Reginald, Kavita; Sheriff, M H Rezvi; Dissanayake, Wasantha P.; Buckley, Nicholas A.

doi:10.1081/clt-120016955

Cited by 21 publications

(36 citation statements)

References 14 publications

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“…However, such limitations are the norm throughout the developing world. For example, propanil's case fatality of 11% is unexpectedly high for an agent whose toxicity is largely due to methaemoglobinaemia and haemolysis, complications that should be relatively easily treated [24]. However, the difficulty in monitoring treatment response without cooximeters and problems with access to and dose adjustment of the antidote have all been suggested as major contributory causes to the high case fatality [24].…”

Section: Discussionmentioning

confidence: 99%

“…For example, propanil's case fatality of 11% is unexpectedly high for an agent whose toxicity is largely due to methaemoglobinaemia and haemolysis, complications that should be relatively easily treated [24]. However, the difficulty in monitoring treatment response without cooximeters and problems with access to and dose adjustment of the antidote have all been suggested as major contributory causes to the high case fatality [24]. Previous studies have also documented high complication rates from gastrointestinal decontamination in rural hospitals that may increase mortality [25].…”

Section: Discussionmentioning

confidence: 99%

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Acute Human Lethal Toxicity of Agricultural Pesticides: A Prospective Cohort Study

et al. 2010

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Acute Human Lethal Toxicity of Agricultural Pesticides: A Prospective Cohort Study

et al. 2010

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“…Researchers have shown some amounts of these agrochemicals to be present in water in small quantities (except phosphate in higher quantities in reservoir water) some of the affected areas [4,30,68,69], but no data exist indicating that any of these chemicals directly causing CKD-mfo [86][87][88]. In addition, these chemicals are used not only in the CKD-affected areas, but also throughout Sri Lanka and, in fact, globally.…”

Section: Agrochemical (Pesticides and Weedicides) Contaminationmentioning

confidence: 99%

“…Long-term exposure to high concentrations of propanil, chlorpyrifos, and glyphosate may cause various chronic diseases, predominantly neurological disorders, endocrine disruptions, liver disease, and CKD [68][69][70], but the pattern of the renal disease following exposure to these is quite different from that of CKD-mfo. On the other hand, some of the recently introduced pesticides, such as neonicotinoids, incorporate into plants and crops and thus directly contaminate the food chain.…”

Section: Agrochemical (Pesticides and Weedicides) Contaminationmentioning

confidence: 99%

Escalating chronic kidney diseases of multi-factorial origin in Sri Lanka: causes, solutions, and recommendations

Wimalawansa

2014

Environ Health Prev Med

125

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During the last two decades, Sri Lanka, located close to the equator, has experienced an escalating incidence of chronic kidney disease (CKD) of unknown aetiology (CKDue) in dry zonal areas. Similar incidences of unusual CKDs have been reported in the dry zonal, agricultural areas of several other equatorial countries. In Sri Lanka, the incidence of CKDue is highest in the North Central Province (NCP), where approximately 45 % of the country's paddy fields are located. However, in recent years, the disease has spread into areas adjacent to as well as distant from the NCP. The cause of CKD in Sri Lanka is unknown, and may likely due to interactions of different potential agents; thus, CKD is of multi-factorial origin (CKD-mfo). These factors include, the negative effects from overuse of agrochemicals. Nevertheless, the potential interactions and synergism between probable agents have not been studied. This systematic review discusses the proposed hypotheses and causes of CKD-mfo in Sri Lanka, and ways to decrease the incidence of this disease and to eradicate it, and provide some recommendations. During the past decade, a number of groups have investigated this disorder using different methodologies and reported various correlations, but failed to find a cause. Research has focussed on the contamination of water with heavy metals, agrochemicals, hard water, algae, ionicity, climate change, and so forth. Nevertheless, the levels of any of the pollutants or conditions reported in water in NPC are inconsistent not correlated with the prevalence of the disease, and are too low to be the sole cause of CKD-mfo. Meanwhile, several nephrotoxins prevalent in the region, including medications, leptospirosis, toxic herbs, illicit alcohol, locally grown tobacco, and petrochemicals, as well as the effects of changed habits occured over the past four decades have not been studied to date. Taken together, the geographical distribution and overall findings indicate that combinations of factors and/or their interactions are likely to precipitate CKD-mfo, which kills more than 5,000 people annually in Sri Lanka; most victims are middleaged male farmers. Much anecdotal evidence from this region suggests that consumption of contaminated water is the most likely source of this deadly disease. Although the aetiology is unknown, prevention of this ''environmentally acquired'' disease seems relatively straightforward. Solutions include (a) preventing environmental pollution, (b) stopping the irresponsible use and decreasing the usage of agrochemicals, and encouraging the use of environmentally friendly agricultural methods, (c) taking proper precautions when using agrochemicals and safe disposal of their containers, (d) changing the risky behaviour of farmers and educating them to preserve the environment, and (e) providing clean potable water to all affected regions. Implementing a well-coordinated, in-depth, region-wide, broad-based research study together with a long-term effective surveillance programme across the country i...

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“…Animal studies that have suggested that the kidney might be a target for propanil did not investigate the role of metabolites (Ambrose et al, 1972). Evidence for propanil-induced nephrotoxicity from human studies comes from case reports where renal function data are not always presented and little evidence of blood levels of propanil or its metabolites are available to calculate organ exposure (Wijekoon et al, 1974; De Silva and Bodinayake, 1997; Yamazaki et al, 2001; Eddleston et al, 2002). Thus, in humans, where propanil nephrotoxicity has been detected, the human studies have not examined the role of propanil metabolites in propanil nephrotoxicity.…”

Section: Discussionmentioning

confidence: 99%

In vitro nephrotoxicity induced by propanil

Rankin

Racine

Sweeney

et al. 2008

Environmental Toxicology

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Propanil is a postemergence herbicide used primarily in rice and wheat production in the United States. The reported toxicities for propanil exposure include methemoglobinemia, immunotoxicity, and nephrotoxicity. A major metabolite of propanil, 3,4-dichloroaniline (3,4-DCA), has been shown to be a nephrotoxicant in vivo and in vitro, but the nephrotoxic potential of propanil has not been examined in detail. The purpose of this study was to determine the nephrotoxic potential of propanil using an in vitro kidney model, determine whether in vitro propanil nephrotoxicity is due to metabolites arising from propanil hydrolysis, and examine mechanistic aspects of propanil nephrotoxicity in vitro. Propanil, 3,4-DCA, propionic acid (0.1–5.0 mM), or vehicle was incubated for 15–120 min with isolated renal cortical cells (IRCC; ~4 million cells/mL) obtained from untreated male Fischer 344 rats. Cytotoxicity was determined by measuring lactate dehydrogenase release from IRCC. In 120-min incubations, propanil induced cytotoxicity at concentrations >0.5 mM. At 1.0 mM, propanil induced cytotoxicity following 60- or 120-min exposure. Cytotoxicity was observed with 3,4-DCA (2.0 mM) at 60 and 120 min, while propionic acid (5.0 mM) induced cytotoxicity at 60 min. In IRCC pretreated with an antioxidant, cytochrome P450(CYP) inhibitor, flavin adenine dinucleotide monooxygenase activity modulator, or cyclooxygenase inhibitor before propanil exposure (1.0 mM; 120 min), only piperonyl butoxide (0.1 mM), a CYP inhibitor, pretreatment decreased propanil cytotoxicity. These results demonstrate that propanil is an in vitro nephrotoxicant in IRCC. Propanil nephrotoxicity is not primarily due to metabolites resulting from hydrolysis of propanil, but a metabolite resulting from propanil oxidation may contribute to propanil cytotoxicity.

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Severe Propanil [N-(3,4-Dichlorophenyl) Propanamide] Pesticide Self-Poisoning

Cited by 21 publications

References 14 publications

Acute Human Lethal Toxicity of Agricultural Pesticides: A Prospective Cohort Study

Acute Human Lethal Toxicity of Agricultural Pesticides: A Prospective Cohort Study

Escalating chronic kidney diseases of multi-factorial origin in Sri Lanka: causes, solutions, and recommendations

In vitro nephrotoxicity induced by propanil

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