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CHAPTER Approach to Common Poisoning in Punjab

115 Gursaran Kaur Sidhu

India is an agriculture based country with Punjab as ORGANOPHOSPHOROUS PIOSONING one of the leading food grain producing states, with poisoning results from exposure increasing burden to feed the growing population. This to (OPs),which cause the inhibition of has led to over-usage of pesticides which on one hand acetylcholinesterase (AChE), leading to the accumulation has contributed significantly to increase the crop yield of acetylcholine (ACh) in the body. It inhibits AChE, while on the other hand has led to sharp increase in the causing OP poisoning by phosphorylating the serine poisoning cases in the region. hydroxyl residue on AChE, which inactivates AChE. Common poisoning in Punjab are related to most easily AChE is critical for nerve function, so the irreversible available agricultural based products i.e. pesticides, blockage of this enzyme, which causes acetylcholine herbicides and preservatives. The nature of the poisoning accumulation, results in muscle overstimulation. This is more often due to accidental and sprays related causes disturbances across the cholinergic synapses. and suicidal. In parts of developing world pesticide Organophosphate compounds avidly bind to poisoning causes more deaths than infectious diseases. cholinesterase molecules as they share a similar Organophosphate account for more than 50% chemical structure. In human beings, the two principal of all acute poisoning in hospital practice; the majority cholinesterases are RBC, or true cholinesterase of patients are younger than 30 yrs.1 In teenagers and (acetylcholinesterase), and serum cholinesterase.3 adults the poisoning is generally due to suicidal intention Intoxication by inhalation and absorption through skin although accidental poisoning during spraying can also may occur during spraying. occur.2 Mortality ranges from 4% to 38% in Indian studies. Following absorption, OP compounds accumulate Poisoning as a mode of suicidal death is known from the rapidly in fat, liver, kidneys and salivary glands. The antiquity. Poisoning among all the age groups and both phosphorothioates (P=S), for example diazonin, , sexes is seen everywhere and the incidence of Poisoning and bromophos, are more lipophilic than phosphates with reference to insecticides, pesticides and (P=O), for example , and are therefore stored has become more common than others in the modern extensively in fat which may account for the prolonged times because of their easy availability, low cost, efficacy intoxication and clinical relapse after apparent recovery of action and rapid death. Also these days because of which has been observed in poisoning from these OP drug addiction, we see overdose of commonly abused insecticides. OP compounds generally are lipophilic and addictions of herione and Smack etc. therefore cross the blood / brain barrier in most cases.5 COMMONLY USED POISONS Metabolism 1. Pesticides: Organophosphorous compounds After absorption in skin, GI tract or inhalation, the i.e. Dichlorvos DDVD 76%, Chlorpyriphos, insecticides and their metabolites gets distributed Deltamiethin 1% + Trizophos 35%, quickly especially in liver kidneys, adipose tissue and 36%, 40% + 4% and tissues rich in lipids. The plasma half life after a single Pretilavhlor 50%. administration is from few minutes to several hours 2. Herbicides: Imidachlopride, Beldamycin and which depend on type of compound and rate and amount Propioconazone 25%. of administration. Metabolism is mainly due to oxidation, by cytocrome-p-450 system and hydrolysis of ester 3. bonds mediated by various esterases or paroxonases. 4. Aluminum Poisoning Elimination mainly occurs via urine and faeces. Some compounds remain longer in body like and 5. Corrosives & Others Fenithrothion. The biological effects of OP compounds HOW TO APPROACH are a result of accumulation of endogenous acetyl choline at sites of cholinergic transmission. Ion binding by which Poisoning is a medical emergency. The patient should be enzyme AChE is inhibited, but eventually progressively immediately brought to hospital and shifted to ICU or any phosphorelated by covalent bonding, a process normally other high intensity unit of facility. History of inhaled or takes 24-48 hrs. This process is called “Ageing” and this suicidal intake of poisoning is of paramount importance period is known as the “critical interval” because during and maintaining the airway patency is the top priority. this time administration of antidote is still effective in CHAPTER 115 543 ENDOSULFAN POISONING ENDOSULFAN Acute EffectsAcute Endosulfan is highly and can be toxic fatal if inhaled, or absorbed through the skin. It directly swallowed affects the central nervous system and recurrent epileptic include poisoning of Symptoms are reported. seizures hyperactivity, excitement, dyspnea (breathing difficulty), anemia, diarrhea, of consciousness, loss apnea, salivation, tremor, dry vomiting, insomnia, blurred vision, cyanosis, mouth, lack of appetite, irritability, headache, decreased Caution succinycholine, aminophyline, Morphine, theophyline, reserpire and phenothiazine-type should transquilizers be avoided in patients with OP poisoning. Endosulfan is a pesticide belonging to the organochlorine in the 1950’s introduced It was group of pesticides. Health World pesticide. a leading broad spectrum as Organisation (WHO) classifies endosulfan asHazardous in category II. a Highly Endosulfan has now been banned in India, following the Supreme Court interim order on May 13, 2011, in a suicidal of no. the large of in the backdrop Writ Petition incidents reported in Kasargode, Kerala. In the cholinergic phase, the use of oximes as rejunevators as rejunevators of oximes the use phase, cholinergic In the The favour. has found cholinesterase enzyme of the beneficialeffects of the by cholinesterase of enzyme cleavage reactivation of oximes phosphorylated site and by is exerteda direct detoxifying effect on through the compound. organophosphorous the unbounded mg/kg Adults: 30 by administered (1-2 g), Dosage: Dosage 15–30 minutes. therapy over infusion intravenous at 6 60 minutes later and then 500 mg may be repeated a as be given also It can days. for next 3 hourly interval cases. IV infusion in severe 500 mg/hr continuous by a maintenance mg/kg Children: 20–50 followed infusions can lead infusion at 5–10 mg/kg/hr. Intravenous too quickly. arrest if given to respiratory or cardiac of in the dose administered was Atropine Atropine: fully atropinised till the patient is 0.6mg/min infusion, dryness, Tachycardia, i.e. toxicity appear of signs and Once atropinised, a dilated pupils, and urinary retention. target hourly. The given was mg 1-3 of dose maintenance clear chest on dry and end point of atropinisation was: heart rate >80/min, dilated wheeze, auscultation with no pressure >80 mmHg. pupil, dry axilla and systolic blood maintained for should be once achieved, Atropinisation, is Atropinisation atropine. of dose with low 3-4 days, evidenced by pupillary dilation, drying up of secretions shown and Roberts have and pulse rate >100. Tafuri beneficial effects of infusion of atropine 0.02-.08 obtained mg/kg was hourly. Sedation if required and analgesia administering midazolam and lorazepam. requiring ventilatory support: Patients Ventilatory and intubated and put on ventilator support were managed accordingly. 4 The term intermediate

5 This term is derived from the fact that it arises from the fact that This term is derived

6 syndrome was coined by Senanayake and Karalliedde L. by Senanayake coined was syndrome in 1987. between the period of early cholinergic syndrome and and syndrome cholinergic early of the period between is syndrome This peripheral neuropathy. onset the late , , commonly associated with OPs like monopcrotophos, methamidaphos, methylparathion, 12-96 hrs after It develops fenthion and ethylparathion. exposure and reflects a prolonged action of acetylcholine by characterized is and receptors the nicotinic on in the ocular, neck, bulbar, proximal weakness muscular limb and respiratory muscles. The sensory functions is characteristically remain normal and full recovery evident in 4-18 days. Polyneuropathy Delayed Organophosphate Induced following exposure to OPCs (OPIDN): OPIDN is common have anticholinesterase activity. OPCs weak which have been found to be neuropathic eg. , merphos, and trichloronat. , DEF, EPN, If the was in contact with skin or eyes, these these in contact with skin or eyes, If the insecticide was be Dirty clothes should be thoroughly washed. should in ICU gown. patient cleaned and redressed removed, maintaining respiratory airway to ICU, On admission clearance is a top priority. Oxygen, Endotracheal tube nasogastric A if required. ventilation intubation and of saline needs to be with 3-4L inserted & Stomach Wash done after securing clearance of respiratory passages. (1 ampoule -20ml contains 500mg): PAM-Pralidoxime Treatment Acute Cholinergic Crisis: OP’s lead to acute cholinergic lead OP’s Crisis: Cholinergic Acute crisis in the initial phase.The clinical findings are thereby a mixture of muscarinic effects, nicotinic effects resulting junctions at neuromuscular ACh of accumulation from and consequent depolarization and CNS effects causing CNS and subsequent inhibition of all initial excitation activity. lacrimation, diarrhea, are symptoms muscarinic The bradycardia, bronchospasm, bronchorrhoea, salivation, hypertension and may have Patient urination and miosis. tachycardia occurring due to nicotinic actions rather than receptors nicotinic The bradycardia. hypotension and to muscle during acute intoxication lead activated are a reliable sign paralysis. Fasciculations are seen and the and occur of paralysis may of poisoning. Progression intoxication Severe affected. get may respiration of muscles may cause emotional irritability, mental obtundation, because of and convulsions impairment, coma cognitive CNS effects. Intermediate Syndrome: Wadia et al first described this syndrome as type II paralysis. Three ClinicalThree Phases reversing the process. Once ageing is completed the completed is Once ageing process. the reversing recovers AChE Plasma reactivated. be cannot enzyme and takes longer AChE Red cell 4 weeks. within quickly may not be restored. Affected AChE recovers at the rate by activity occurs AChE of per day. Restoration 1% ~ of Ageing has an free enzyme. synthesis of slow denovo outcome. and treatment bearing on toxicity important 544 respiration, loss of memory, haematuria, albuminuria, ingestion is profound circulatory collapse, is confusion, dizziness, imbalance and lack of coordination.7 reportedly secondary to these toxins generated, which Autopsy examination of an intentional ingestion (suicide) lead due to direct effects on cardiomyocytes, fluid loss, case has revealed damage to liver, lung and brain. and adrenal gland damage. The signs and symptoms are non-specific, dose dependent and evolve with time. The Discussion & Treatment dominant clinical feature is severe hypotension refractory Convulsions are a common and severe manifestation. to dopamine therapy. Other features may include Endosulfan is also toxic to the liver, kidney and lung and dizziness, fatigue, tightness in the chest, headache, nausea, can cause rhabdomyolysis in higher doses. Liver function vomiting, diarrhoea, ataxia, numbness, paraesthesia, tests are abnormal in the form of deranged AST or ALT. tremor, muscle weakness, diplopia and jaundice. If Severe poisoning results in death due to status epilepticus severe inhalation occurs, the patient may develop acute that can lead to asphyxia, and rhabdomyolysis leading to respiratory distress syndrome (ARDS), heart renal failure. failure, arrhythmias, convulsion and coma. Treatment is symptomatic and supportive. Early Treatment & Management termination of convulsive status epilepticus by aggressive Detailed history need to be taken regarding number of POISONING treatment is the best way to prevent mortality. Refractory tablets, freshness of tablets, reason and mode of ingestion- seizures requires more aggressive treatment as it is whether dissolved in / liquid or ingested as such. associated with higher mortality and morbidity. All patients of suicidal AlP intake needs to be shifted to ALUMINUM POISONING IN PUNJAB ICU without any delay. Garlic odor in the breath is to phosphide poisoning (ALP) is a large be noticed and nasogastric tube put in and aspirate the problem, particularly in the Indian subcontinent. It is contents. It is recommended not to do gastric lavage readily available as a cheap solid fumigant for storing with water. Liquid paraffin/Coconut oil may be instilled cereal grains. It is sold under various brand names such through NG tube to give a protective coating over the as QuickPhos and Celphos and is highly toxic, especially mucosa and accelerate the excretion of aluminium when consumed from a freshly opened container. phophide and phosphate.Some authors recommend Unfortunately this has become the most common chemical gastric levage with potassium permagnate (1:10000) to agent used for the self poisoning. reduce the absorption of . Permagnate oxidizes

Death results from profound shock, myocarditis and multi- PH3 to form non-toxic phosphate. 8 organ failure. Aluminium phosphide has a fatal dose of On arrival in the ICU, the vital parameters are monitored- between 0.15 and 0.5 grams (0.0053 and 0.0176 oz).9 It has pulse, BP, SaO2 ,ABG, respiratory rate, and urine output. been reported to be the most common cause of suicidal Resuscitate the patient on the line of breathing and death in North India. Deaths have also been reported in circulation. Order Immediate investigations of arterial Iran, Thailand and Southeast Asia. blood gases, Na+ , K+ , and ionized Ca++. Establish I/V Mortality Rate access and given normal saline guided by CVP (apprx. The mortality rates 40 to 80 percent. The actual numbers 12cm of water). of cases may be much larger, as less than five percent of Low dose dopamine (4-6 ug/kg/min) to combat shock. those with AP eventually reach a tertiary care center. Since Oxygen is given for hypoxia. ARDS may require 1992, when aluminium phosphide became freely available mechanical ventilation. All types of arrthymias esp. atrial in the market, it had, reportedly, overtaken all other forms fibrillation are seen in these patients,and the management of deliberate poisoning, such as organophosphorus and has to be done accordingly. Magnesium sulphate used barbiturate poisoning, in North India. In a 25-year-long both high and low dose did not improve survival in study on 5,933 unnatural deaths in northwest India, controlled clinical trials. Hence Siwach et al do not aluminium phosphide poisoning was found to be the recommend its use. Metabolic acidosis are corrected by major cause of death among all cases of poisonings.10 intravenous sodium bicarbonate, requirement of which Mechanism of Toxicity are guided by base excess.

The toxicity of aluminium phosphide is attributed to the NaHCO3 required (meq) = 0.6 x body weight (kg) x Base liberation of phosphine gas, a cytotoxic compound that Excess causes free radical mediated injury, inhibits vital cellular Total requirement of sodium bicarbonate are given enzymes and is directly corrosive to tissues. The following immediately (full correction) and arterial blood gases are reaction releases phosphine when AlP reacts with water estimated after one hour and sodium bicarbonate was in the body: given accordingly. After that, arterial blood gas analysis  AlP + 3 H2O Al(OH)3 + PH3 are done again at one-hour intervals till two consecutive readings of arterial blood pH above 7.4 are obtained. AlP + 3 HCl  AlCl + PH (stomach) 3 3 Following which, ABG analysis is done at 2-, 4-, or 6- Signs, Symptoms & Diagnosis hourly intervals, according to requirement. Associated After ingestion, toxic features usually develop within a electrolyte imbalances are treated accordingly. few minutes. The major lethal consequence of aluminium CHAPTER 115 545

ts the The The ,

likely

including resection may be necessary if serious be necessary may resection including KEROSENE POISONING KEROSENE Laporatomy Laporatomy It i.e sequelae chronic The the stomach. haemorrhage from be managed can strictures pyloric the oesophageal and by repeated endoscopic dilatations and retrievable Accidental poisoning in children is oesophageal stents. is common. most frequent and deliberate self-poisoning as for lamps, as well Kerosene is an oil used as a fuel swallowing from effects harmful cooking.The and heating or breathing in kerosene. Symptoms Poisons ingredients like hydrocarbons lead to difficulty and ears, pain in eyes in breathing, throat swelling, abdominal pain with bloody stool, low BP - develops rapidly, unconsciousness, Drowsiness and skin burns. 1) Doraha (Figure Sidhu CollectedData Hospital, at In a retrospective study done in a rural setting at Sidhu analyzed the data of patients Hospital Doraha Punjab, we with poisoning. admitted were who years 6 the past from A total of 341 patients, 244 (72%) males and female 97 (28%) admittedwere to hospital from 2010 till November agent used was 2015. The most predominant poisonous Thimit, Organophosphorus (52%)(, Parathion, by (aluminium phosphide Celphos Baygon etc) followed rat poisons , like belladona, others and 24%) 2-4d, (), herbicides (Diquat, Paraquat, Glyphosate- Roundup), acid poisoning, kerosine oil, cases appx. 20 received has tablets. Hospital phenyl respiratory with severe overdose of heroine & smack depression. Management of Ingestion to hospital for assessment. should be referred case Every the to help neutralize given management is First aid cases the patient is unlikely to but severe in corrosive is it. Gastric emptying by any means be able to retain contraindicated. Analgesics and intravenous should acidosis metabolic required and are often blood fluids or treated appropriately. be sought and Oxygen and the larynx is if be required may intubation endotracheal involved. in limiting Corticosteroids- no convincing evidence the i.e oesophageal sequelae long term preventing or damage strictures. Endoscopy phase is hazardous Upper GI endoscopy in acute by an only be performed and should but is necessary a thinner instrument than using experienced endoscopist oesophageal of severity to establish the done It is usual. higher burns have and gastric burns. Circumferential causing mediastinitis. chances for perforation and even and oesophageal carcinoma may develop at sites such develop may carcinoma oesophageal and be can to acids due damage Gastric 20-30 years. after may (which gangrene with haemorrhage, severe equally and peritonitis. the whole stomach) involve

27%) patien 27%)

93( Male <5 Male >5 Female <5 Female >5 In the In rural area

2015

Celphos poison Celphos Belladonna Herbicides(Paraquat, 2-4D) OP poison 2014 Strong alkalies Lye Potassium hydroxide Sodium hydroxide

2013

Years 52% 2012

73%) patients was less than 5 days and and 5 days less than was patients 73%)

to females. Duration of Stay of Stay Duration Fig. 1: Percentile of Poisons used of Poisons 1: Percentile Fig. 15% 24%

2011

0% Percentile of Used Poisons Percentile

1%

0%

3%

0% 1% 2010

1% 2% Strong acids Hydrochloric acid Nitric acid Sulphuric acid 1% CORROSIVES Poisoning with strong alkalies and strong acids is strong acids with strong alkalies and Poisoning uncommon. Ingestion of strong acids and alkalies produces almost immediate burning pain in the lips, epigastrium. throat, substernal region and mouth, rapidly and may recur repeatedly. Vomiting occurs very may melena and Shock common. is Hypersalivation patient may look pale poisoning. The in severe develop and burns may be visible on the hands and face. of oesophageal or gastric necrosis depends Development commonly Alkalies ingested. alkali is or whether acid on gastric have oesophageal burns but only 20% produce to resistant lesions. Oesophageal mucosa is relatively particularly in the antrum gastric mucosa whereas acids may be present in vulneralble. Oesophageal necrosis is Oesophagus abnormalities. without buccal about 15% may perforate leading to mediastinitis but this is more The major likely to be a complication of oesophagoscopy. long term complication is oesophageal stricture formation Many poisons other than the strong acids and alkalis other than the strong acids Many poisons listed below effectscorrosive have on the gastrointestinal phenol, oxalic tract. They include iron salts, paraquat, acid and mercuric chloride. Continuous Veno-Venous Hemofiltration (CVVH) Hemofiltration Veno-Venous Continuous Continuous veno-venous hemofiltration (CVVH) in the early AP stages poisoning of may be beneficial before the AP causes because of multiple organ failure development resistant to medical and hypotension metabolic acidosis treatment. All the patients are given injection hydrocortisone 200 hydrocortisone injection given the patients are All hourly intervals. – at 8 mg then 150 and arrival IV on mg and dopamine with injections given is Inotropic support noradrenalin of the with the severity The outcome correlates hypotension the patient develops. The average time The average patient develops. hypotension the is 3 intake of poisoning and death between interval aggressive with most hrs with range o1-48hrs.Even rate is 10 to 40%. management the survival

0

10 20 30 40 No. of Patients Patients of No.

support.

ation of hospital stay in 248 ( hospital stay of ation

patients needed 127 (73%) only OP poisoning, of patients 173 (51%) total the Out of ventilator stayed more than 5 days. for stayed The duration of the of on hospital duration was average The 5 days less than an (73%),but stay patients than formore 5 days. support ventilatory stayed more and sick needed were who dur insecticides are lying freely in the fields, in the motor pump sheds making them very them freely making in motor pump fields, the sheds in the lying are insecticides has The available. shown study ofeasily increased prevalence inan incidence males as them twice making age group(52%), in lessthe 35 than especially years (72%), compared to consume poison as According tostudy, the According of suicidal90% where cases poisonings.

easily available. The study has shown an increased prevalence of incidence in males (72%), especially in the less than 35 years age group(52%), making them twice as likely to consume poison as compared to females. The easilyduration available. of the Thehospital study stay has on shown an average an increased was less prevalence than 5 days of incidence (73%), but in patientsmales who(72%), were especiallymore sick in and the neededless than ventilatory 35 years age support group(52%), stayed making for more them than twice 5 asdays. likely The durationto consume of hospital poison stay as comparedin 248 (73%) to females. patients was less than 5 days and 93(27%) patients stayedThe for duration more thanof the 5 hospitaldays. stay on an average was less than 5 days (73%), but patients who were more sick and needed ventilatory support stayed for more than 5 days. The duration of hospital stay in 248 (73%) patients was less than 5 days and 93(27%) patients stayed for more than 5 days. Duration of Stay Deaths from Poisoning 546

40 40 OP cases 30 30 Male <5 Death of OP 20 20 Male >5 Out of the total 173 (51%) patients of OP poisoning, only 127 (73%) patients needed Celphos Cases 10 10 No. of Patients Female <5 No. of patients ventilator support. Death of Celphos 0 Female >5 0 2010 2011 2012 2013 2014 2015 2010 2011 2012 2013 2014 2015 Other Cases Years Years Death of Other

RequirementFig. 2: Duration of Ventilation of Stay Fig. 4: Deaths from Poisoning

40 Out of the total 173 (51%) patients of OP poisoning, only 127 (73%) patients REFERENCESneeded 30 1. Karalliedde, Senanayake N. Organophosphorous Male: Yes ventilator support.20 insecticide poisoning. Br J Anesthesia 1989; 63:739-750. Male: No 10 2. Franklin CA. Modi’s medical jurisprudence and toxicology. No. of patient Female: Yes 22nd edn. Mumbai. N M Tripathi Private Limited 1991:p.85- 0 Female: No

POISONING 87. 2009Requirement2010 2011 2012of Ventilation2013 2014 Years 3. L Haddad, J Winchester. Clinical management of poisoning 40

Fig. 3: Requirement of Ventilation and overdose. Philedelphia, WB Saunders, 1983, 575-586. 30 4. International Journal of Health Sciences & Research (www. According to the study, 90% of cases where suicidalMale: Yes ijhsr.org) 255 Vol.4; Issue: 8; August 2014. OP poisoning20poisonings. had the leastIn thenumber rural of deathsarea, as the compared insecticides to Celphos are poisoning lying having a Male: No 5. Wadia RS, SAdagopan C, Amin RB et al. Neurological 98% survival10 rate. No. of patient freely in the fields, in the motor pump sheds making them Female: Yes manifestations of organophosphorous insecticide very easily available. The study has shown an increased 0 Female: No poisoning. J Neurology, Neurosurgery and Psychiatry 1974; prevalence2009 of2010 incidence2011 in2012 males 2013(72%), 2014especially in the 137:841-47. less than 35 years age group(52%),Years making them twice as 6. Senanayake N, Karalliedde L. Neurotoxic effects of likely to consume poison as compared to females. organophosphorous insecticides - An Intermediate The duration of the hospital stay on an average was less syndrome. NEJM 1987; 316:761-63. than 5 days (73%), but patients who were more sick and 7. Mirkin DB. Benzene and related aromatic hydrocarbons. needed ventilatory support stayed for more than 5 days In: Shannon MW, Borron SW, Burns MJ, eds. Haddad and (Figure 2). The duration of hospital stay in 248 (73%) Winchester’s Clinical Management of Poisoning and Drug patients was less than 5 days and 93(27%) patients stayed Overdose. 4th ed. Philadelphia, Pa: Saunders Elsevier; for more than 5 days. 2007:chap 94. 8. Mathai, Ashu; Bhanu, Madhuritasingh. “Acute aluminium Out of the total 173 (51%) patients of OP poisoning, only phosphide poisoning: Can we predict mortality?”. Indian 127 (73%) patients needed ventilator support (Figure 3). Journal of Anaesthesia 2010; 54:302–7.doi:10.4103/0019- 5049.68372. PMC 2943698. PMID 20882171. OP poisoning had the least number of deaths as compared to Celphos poisoning having a 98% survival rate (Figure 9. A Wahab; MS Zaheer; S Wahab; RA Khan. “Acute 4). aluminium phosphide poisoning: an update” (PDF). Hong Kong Journal of Emergency Medicine: 152. RECOMMENDATIONS 10. Singh, D; Dewan, I; Pandey, AN; Tyagi, S. “Spectrum Prevention is better than cure. It is recommended that of unnatural fatalities in the Chandigarh zone of north- these insecticides should be rationed and not freely west India—a 25 year autopsy study from a tertiary care available and farmers using them should be made aware hospital”. Journal of Clinical Forensic Medicine 2003; 10:145– to dispose them completely after spraying in the fields, so 52. doi:10.1016/S1353-1131(03)00073-7. PMID 15275009. that poisonings can be prevented.