leslie london, university of cape town pesticides and health seminar for diploma in occupational...

Leslie London, University of Cape Town

Pesticides and HealthPesticides and Health

Seminar for Diploma in Occupational HealthSeminar for Diploma in Occupational Health

20052005

Leslie LondonLeslie London

With acknowledgement to E.E.Lekei, Tropical With acknowledgement to E.E.Lekei, Tropical Pesticides Research Institute, P.O.Box 3024 Pesticides Research Institute, P.O.Box 3024 Arusha – Tanzania; E Mail: [email protected] – Tanzania; E Mail: [email protected]



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OverviewOverview

Pesticides widely used developed AND Pesticides widely used developed AND developing countriesdeveloping countriesSeen as essential for food securitySeen as essential for food securityYet no evidence of Yet no evidence of world hunger, world hunger, despite growth in intern market last 3 despite growth in intern market last 3 decades +++decades +++1983 - 1998, 1983 - 1998, US$ 20 billion to US$34. US$ 20 billion to US$34.


World Pesticide Consumption World Pesticide Consumption (US$ billion)(US$ billion)

Compound annual increase

Region 1998 83-93 93-98 N Amer 9.0 6.3 4.0 Latin Am 3.0 6.3 5.4 W Eur 9.0 2.1 4.6 E Eur 3.2 -1.2 4.4 Africa/ME 1.6 2.9 5.1 Asia/Oc 8.4 3.0 4.4 TOTAL 34.2 3.0 4.4 (Yudelman et al, 1998)


Pesticides - Health issuesPesticides - Health issues

volumes in volumes in developeddeveloped countries; but ... countries; but ... hazard in hazard in developingdeveloping countries countries

Acute Poisoning: WHO EstimatesAcute Poisoning: WHO Estimates 2 million suicides2 million suicides700 000 occupational pois700 000 occupational pois300 000 non-occup300 000 non-occup220 000 fatalities220 000 fatalities

Long-term health and enviro impactsLong-term health and enviro impacts


Pesticides - Global concernsPesticides - Global concerns

Weak regulation in developing Weak regulation in developing countriescountries

Importation and dumping hazard Importation and dumping hazard pesticidespesticides

What role in food security? What role in food security? Chemical dependence?Chemical dependence?

Perceptions about risk and Perceptions about risk and safetysafety

How effective are preventive How effective are preventive measures?measures?

Global conventionsGlobal conventions (PIC, POPS)(PIC, POPS)Andrea Rother, UCT


CATEGORIES OF CATEGORIES OF PESTICIDES & USESPESTICIDES & USES

Leslie London, Leslie London, University of University of Cape TownCape Town

RodenticidesRodenticidesAcaricidesAcaricidesNematicides Nematicides (Fumigants)(Fumigants)Growth regulatorsGrowth regulatorsSeed treatmentsSeed treatmentsEtc.Etc.


Uses?Uses?

Agricultural production - pest and Agricultural production - pest and weed control, plant growth regulationweed control, plant growth regulation

Public health: vector controlPublic health: vector controlDomestic gardeningDomestic gardeningHousehold, Institutional pest controlHousehold, Institutional pest controlWood treatmentWood treatmentMedications for liceMedications for liceetcetc


Insecticides: Insecticides:

For insect pests For insect pests Ubiquitous, generally high hazardUbiquitous, generally high hazard Many formulations on Trade/ marketMany formulations on Trade/ market

OrganophosphatesOrganophosphates Carbamates Carbamates OrganochlorinesOrganochlorines PyrethroidsPyrethroids


Organochlorines Organochlorines (e.g. DDT, lindane, endosulfan)(e.g. DDT, lindane, endosulfan)

Synthetic organic insecticides with C, Cl, H and Synthetic organic insecticides with C, Cl, H and sometimes Oxygen.sometimes Oxygen.

Historical importanceHistorical importance chlorinated hydrocarbons, chlorinated organics.chlorinated hydrocarbons, chlorinated organics. Banned / Restricted in many countries – persistence Banned / Restricted in many countries – persistence Classic endocrine disruption (oestrogenic ring)Classic endocrine disruption (oestrogenic ring) Controversy DDT effects in humansControversy DDT effects in humans


OrganophosphatesOrganophosphates

Have replaced OrganochlorinesHave replaced OrganochlorinesBreak down faster than OCsBreak down faster than OCsHigh mammalian toxicityHigh mammalian toxicity - neurotoxic - neurotoxic

(Cholinesterase and others)(Cholinesterase and others)Short lived in the environment - hazards are Short lived in the environment - hazards are

therefore short termtherefore short termExamples: Chlorpyrifos, Fenthion, Examples: Chlorpyrifos, Fenthion,

Dichlorivos, Dimethoate, Malathion diazinon Dichlorivos, Dimethoate, Malathion diazinon etc.etc.


CarbamatesCarbamates

Developed after OCs, OPsDeveloped after OCs, OPsAre derivatives of carbamic AcidAre derivatives of carbamic AcidHave broad spectrum of activityHave broad spectrum of activityExamples: Examples: AldicarbAldicarb, Carbaryl, Propxur, , Carbaryl, Propxur,

Methiocarb Carbosulfan, Bendiocarb, Methiocarb Carbosulfan, Bendiocarb, carbofuran etc.carbofuran etc.


PyrethroidsPyrethroids

Pyrethrum developed from plant flowers Pyrethrum developed from plant flowers (chrysanthenum sp)(chrysanthenum sp)

Now heavily produced as synthetic pyrethroidsNow heavily produced as synthetic pyrethroids Break down faster in environmentBreak down faster in environment Have knock down effect (domestic products)Have knock down effect (domestic products) Low mammalian toxicity but highly toxic to fish Low mammalian toxicity but highly toxic to fish

/bees./bees. Parasthesiae, allergenicParasthesiae, allergenic


FUNGICIDESFUNGICIDESUsed to protect Fungal diseases - crops, Used to protect Fungal diseases - crops,

wood products, preserved foodstuffs, etc.wood products, preserved foodstuffs, etc.Often applied preventivelyOften applied preventivelyOften used for control of cosmetic Often used for control of cosmetic

disfigurementdisfigurementHeavy use in W Cape fruit (wet winters)Heavy use in W Cape fruit (wet winters) Examples: Mancozeb (dithiocarbamates), Examples: Mancozeb (dithiocarbamates),

Sulphur, Copper, CCA, Carboxim, Sulphur, Copper, CCA, Carboxim, Propiconazole, Dithianon, Propiconazole, Dithianon,


HERBICIDESHERBICIDES Used in Agricultural, Roadsides, Recreation areas.Used in Agricultural, Roadsides, Recreation areas. Types: Selective / non selective; Contact / Systemic; Types: Selective / non selective; Contact / Systemic;

Pre-emergence / Post emergence Pre-emergence / Post emergence e.g. Paraquat highly effective contact herbicide - e.g. Paraquat highly effective contact herbicide -

very dangerous for ingestionvery dangerous for ingestion Heavy use in grain farmingHeavy use in grain farming Examples: Glyphosate (Roundup), 2,4-D, atrazine, Examples: Glyphosate (Roundup), 2,4-D, atrazine,

etc.etc. 2,4 D related to 2,4,5-T, both = Agent Orange2,4 D related to 2,4,5-T, both = Agent Orange

Contamination with dioxin !!!Contamination with dioxin !!!


OTHERSOTHERS

Rodenticides (Rodents)Rodenticides (Rodents)Examples: Include difenacoum, brodifacoum, etc.Examples: Include difenacoum, brodifacoum, etc.

Nematicides (Nematodes) include OPs, Nematicides (Nematodes) include OPs, AldicarbAldicarb, methyl bromide, methyl bromideMethyl bromide = ozone depletorMethyl bromide = ozone depletor

Acaricides - attack spider mites.Acaricides - attack spider mites. Plant growth regulatorsPlant growth regulators Moluscicides (Slugs /Snails)Moluscicides (Slugs /Snails)


Type of Pes. FormulationsType of Pes. Formulations

Solids / Liquid formulations; Wettable Solids / Liquid formulations; Wettable Powder; granulesPowder; granules

Dust; AerosolsDust; AerosolsEmulsifiable Concentrates; Flowable Emulsifiable Concentrates; Flowable

ConcentratesConcentratesBaitsBaitsMicroencapsulated formulations.Microencapsulated formulations.


Table 1. Agrichemical Toxicity (WHO/FAQ) – LD50 Table 1. Agrichemical Toxicity (WHO/FAQ) – LD50 (mg/kg)(mg/kg)

ORALORAL DERMALDERMAL

SolidSolid LiquidLiquid SolidSolid LiquidLiquid

IA (Extremely Hazardous)IA (Extremely Hazardous) < 5< 5 < 20< 20 < 10< 10 < 40< 40

IB (Highly hazardous)IB (Highly hazardous) 5 – 505 – 50 20 – 20020 – 200 10 – 10010 – 100 40 – 40040 – 400

II (Moderately hazardous)II (Moderately hazardous) 50 – 50050 – 500 200 – 2000200 – 2000 100 – 1000 400 – 4000100 – 1000 400 – 4000

III (Slightly hazardous)III (Slightly hazardous) > 500> 500 > 2000> 2000 > 1000> 1000 > 4000> 40000 – Unlikely to cause hazard in normal use0 – Unlikely to cause hazard in normal use

BioaccumulationBioaccumulation Increased susceptibility: age (young children), pregnancy, under nutrition, liver disease.Increased susceptibility: age (young children), pregnancy, under nutrition, liver disease.

Exposure slidesExposure slides


Obsolete Pesticides in Obsolete Pesticides in Stellenbosch, 1995 and 2004Stellenbosch, 1995 and 2004

Occupational and Occupational and

Environmental Environmental

Health Research Health Research

Unit, UCTUnit, UCT

Leslie London, UCT


Obsolete PesticidesObsolete Pesticides

What are “Obsolete Pesticides?”What are “Obsolete Pesticides?”

No longer registered for use (banned or No longer registered for use (banned or withdrawn or lapsed registration)withdrawn or lapsed registration)

No longer wanted for use (ineffective, No longer wanted for use (ineffective, resistance, unsuited)resistance, unsuited)

Past expiry datePast expiry date

etcetc

Huge problem in developing world, esp AfricaHuge problem in developing world, esp Africa


Obsolete Pesticides in SAObsolete Pesticides in SA

Policy context (e.g. NEMA):Policy context (e.g. NEMA):

Polluter paysPolluter pays

Cradle-to-graveCradle-to-grave

Agri Industry audit, 1995 - postal Agri Industry audit, 1995 - postal questionare questionare

→ → poor responsepoor response


Stellenbosch Survey, 1995/6Stellenbosch Survey, 1995/6

Population = productive farms (+/- 800)Population = productive farms (+/- 800)

Audit information: Tradename, active Audit information: Tradename, active ingredient, amount, container information ingredient, amount, container information (type, size, condition), empty containers(type, size, condition), empty containers

233 farms surveyed233 farms surveyed

- 169 responded- 169 responded

- 41 (24%) had residual chemicals- 41 (24%) had residual chemicals

- Of these, 18 had DDT (11%)- Of these, 18 had DDT (11%)


Waste pesticides 1995 Waste pesticides 1995 (total 6196kg)(total 6196kg)

PesticidePesticide Amount (kg)Amount (kg)

DDTDDT 22512251

Other OCs Other OCs (dieldrin, chlordane, (dieldrin, chlordane, endosulfan, endosulfan, γγ-BHC)-BHC)

103103

ParathionParathion 6161

ParaquatParaquat 3333

Lead ArsenateLead Arsenate 99

Methyl bromideMethyl bromide 44

Herbicides (amitrole, 2,4D)Herbicides (amitrole, 2,4D) 2525

CyanamideCyanamide 325325

UnknownUnknown 10381038

Other knownOther known 23472347


Follow up 2003Follow up 2003

Repeated study in 2003Repeated study in 200373 farms included, 71 participated:73 farms included, 71 participated:

– 39 previous obsolete stocks39 previous obsolete stocks– 14 no previous stocks14 no previous stocks– 19 no previous participation because no stocks19 no previous participation because no stocks

Of the 39, 24 reported NEW obsolete stocksOf the 39, 24 reported NEW obsolete stocksOf the others, 16 accumulated NEW obsolete Of the others, 16 accumulated NEW obsolete stocksstocks

1.1. AN ONGOING PROBLEM !AN ONGOING PROBLEM !2.2. CRADLE-TO-GRAVE? CRADLE-TO-GRAVE?

PRODUCT STEWARDSHIP?PRODUCT STEWARDSHIP?


Waste pesticides Waste pesticides 1995 and 20031995 and 2003 (kg)(kg)

PesticidePesticide 1995/61995/6 20032003DDTDDT 22512251 132132

Other OCs Other OCs (dieldrin, chlordane, (dieldrin, chlordane, endosulfan, endosulfan, γγ-BHC)-BHC)

103103 23872387

ParathionParathion 6161 5151

ParaquatParaquat 3333 99

Lead ArsenateLead Arsenate 99 00

Methyl bromideMethyl bromide 44 00

Herbicides (amitrole, 2,4D)Herbicides (amitrole, 2,4D) 2525 10281028

CyanamideCyanamide 325325 240240

UnknownUnknown 10381038 28892889

Other knownOther known 23472347 50815081



Pattern of obsolete pesticidesPattern of obsolete pesticides

From old (e.g. DDT, Lead arsenate) to From old (e.g. DDT, Lead arsenate) to newer:newer:– Class I OrganophosphatesClass I Organophosphates– OrganochlorinesOrganochlorines– GlyphosateGlyphosate


Health Consequences of Health Consequences of Pesticide ExposurePesticide Exposure

AcuteAcute

Sub-AcuteSub-Acute

ChronicChronic

Acute Pesticide poisoningAcute Pesticide poisoning

Acknowledgements to Alison Acknowledgements to Alison JohnJohn


Exposure to unknown pesticidesExposure to unknown pesticidesmuscle fasciculationmuscle fasciculation organophosphates organophosphates

weakness, arrhythmiasweakness, arrhythmias and carbamatesand carbamates

respiratory failurerespiratory failure

bronchorrhoeabronchorrhoea

bleeding gumsbleeding gums warfarins andwarfarins and

gastrointestinal bleedinggastrointestinal bleeding superwarfarinssuperwarfarins

buccal ulcerationbuccal ulceration paraquat / diquatparaquat / diquat

pulmonary infiltratespulmonary infiltrates

renal failurerenal failure

transient burning of skin transient burning of skin permethrinspermethrins

and conjunctivaeand conjunctivae

nausea, vomiting, metHbnausea, vomiting, metHb chlorateschlorates


Acute OP (and carbamate) Acute OP (and carbamate) poisoning poisoning

The enzyme The enzyme acetylcholinesteraseacetylcholinesterase regulates the concentration of regulates the concentration of acetylcholine at the acetylcholine at the interneuronal and interneuronal and neuroeffector junctionsneuroeffector junctions

OPs and carbamates are OPs and carbamates are cholinesterase inhibitorscholinesterase inhibitors

Carbamates are reversible Carbamates are reversible inhibitorsinhibitors


Organophosphorus insecticidesOrganophosphorus insecticides

principal action is to attach on serine sites on principal action is to attach on serine sites on cholinesterases, particularly acetylcholinesterase, cholinesterases, particularly acetylcholinesterase, thus inhibiting themthus inhibiting them

the onset of symptoms and severity of poisoning is the onset of symptoms and severity of poisoning is dependent on the rate at which AChE is dependent on the rate at which AChE is inactivated, the rate of dissociation of inactivated inactivated, the rate of dissociation of inactivated AChE to release active enzyme, the rate at which AChE to release active enzyme, the rate at which ageing occurs, synthesis of new AChE by the liverageing occurs, synthesis of new AChE by the liver

those with pre-existing reduced AChE activities those with pre-existing reduced AChE activities are more susceptibleare more susceptible


Acute OP poisoningAcute OP poisoning within 1-2 hours; nausea, vomiting, within 1-2 hours; nausea, vomiting, abdominal pain, diarrhoea, sweating, abdominal pain, diarrhoea, sweating, hypersalivation, chest tightnesshypersalivation, chest tightness

anxiety, agitation, confusion, tiredness, anxiety, agitation, confusion, tiredness, headache, amnesiaheadache, amnesia

miosis, bradycardia (tachycardia in 30%)miosis, bradycardia (tachycardia in 30%)

later; fasciculation and flaccid paralysis of later; fasciculation and flaccid paralysis of limbs, respiratory muscles and occasionally limbs, respiratory muscles and occasionally extraocular palsies may occurextraocular palsies may occur

coma and convulsions may also occurcoma and convulsions may also occur


Acute OP poisoningAcute OP poisoning

respiratory failure: respiratory muscle respiratory failure: respiratory muscle paralysis, bronchoconstriction and paralysis, bronchoconstriction and copious respiratory secretionscopious respiratory secretions

animal experiments suggest depression animal experiments suggest depression of respiratory drive is the single most of respiratory drive is the single most important factor in mortalityimportant factor in mortality


Severity and prognosis of acute Severity and prognosis of acute OP poisoningOP poisoning

clinical features are more helpful than clinical features are more helpful than cholinesterase measurements in determining cholinesterase measurements in determining severity of intoxication and prognosisseverity of intoxication and prognosis

AChE 50% in subclinical poisoning; 20-50% in AChE 50% in subclinical poisoning; 20-50% in mild poisoning; 10-20% in moderate poisoning mild poisoning; 10-20% in moderate poisoning and < 10% in severe poisoningand < 10% in severe poisoning[compare to biol monitoring 70%][compare to biol monitoring 70%]

Tolerance with ongoing exposureTolerance with ongoing exposure


Management of acute OP Management of acute OP poisoningpoisoning

decontamination; skin and clothingdecontamination; skin and clothing

gastric lavage + activated charcoal within gastric lavage + activated charcoal within 1 hour of ingestion1 hour of ingestion

confirm diagnosis by measuring AChE if confirm diagnosis by measuring AChE if possiblepossible

intensive supportive careintensive supportive care


Management of acute OP poisoningManagement of acute OP poisoning

10-20mg diazepam iv for an adult, to 10-20mg diazepam iv for an adult, to treat seizurestreat seizures

atropine (2mg iv for an adult) reduces atropine (2mg iv for an adult) reduces cholinergic features and should be cholinergic features and should be repeated every 10 minutes until signs of repeated every 10 minutes until signs of atropinisation occur (flushed dry skin, atropinisation occur (flushed dry skin, tachycardia, dilated pupils and dry tachycardia, dilated pupils and dry mouth). mouth).


Role of oximes in OP poisoningRole of oximes in OP poisoningpralidoxime mesylate (P2S), pralidoxime chloride (2-pralidoxime mesylate (P2S), pralidoxime chloride (2-PAM) and obidoxime (toxogonin) are helpful in severe PAM) and obidoxime (toxogonin) are helpful in severe poisoning as they reactivate AChE poisoning as they reactivate AChE

cessation of convulsions and fasciculation, improved cessation of convulsions and fasciculation, improved muscle power and recovery of consciousness usually muscle power and recovery of consciousness usually occurs within 20-30 minutes of oxime administrationoccurs within 20-30 minutes of oxime administration

the need for further therapy is guided by clinical the need for further therapy is guided by clinical improvement together with rbc AChE level, if availableimprovement together with rbc AChE level, if available

Typically, not helpful > 48 hours because of “ageing”Typically, not helpful > 48 hours because of “ageing”


Carbamate insecticidesCarbamate insecticides

same action as OPs on AChE except that same action as OPs on AChE except that enzyme-carbamate complex dissociates enzyme-carbamate complex dissociates spontaneously spontaneously

same features of acute poisoning as OPssame features of acute poisoning as OPs

same management as OPs including same management as OPs including atropine, except that oximes are not usedatropine, except that oximes are not used

Aldicarb!Aldicarb!


Organochlorine insecticidesOrganochlorine insecticidesinclude DDT, aldrin, dieldrin, chlordane, and include DDT, aldrin, dieldrin, chlordane, and lindane (lindane (-BHC), endosulfan-BHC), endosulfan

lipid soluble, sequestered in liver, kidneys, lipid soluble, sequestered in liver, kidneys, nervous system, adipose tissue, milknervous system, adipose tissue, milk

Oestrogenic, enzyme-inducing effect Oestrogenic, enzyme-inducing effect

NeurotoxicNeurotoxic

Acute poisoning: inhibits neuronal ATPases - Acute poisoning: inhibits neuronal ATPases - disrupts normal nerve conduction disrupts normal nerve conduction

Diff OC’s affect diff sites Diff OC’s affect diff sites diff effects diff effects


– NauseaNausea

– HHeadache eadache

– DizzinessDizziness

– ConfusionConfusion

– IncoordinationIncoordination

– TremorTremor

– ParesthesiasParesthesias

– ConvulsionsConvulsions

Organochlorine neuro effectsOrganochlorine neuro effects

Neuronal hyperactivity

Endosulfan the most toxic, easily absorbed dermally


Management of acute poisoning Management of acute poisoning with organochlorineswith organochlorines

Thorough skin decontamination if Thorough skin decontamination if appropriateappropriate

gastric lavage if ingestion within 1 hourgastric lavage if ingestion within 1 hour

activated charcoal or cholestyramine activated charcoal or cholestyramine should be given within 1 hourshould be given within 1 hour

control seizures with iv diazepamcontrol seizures with iv diazepam

ensure ventilationensure ventilation


ParaquatParaquatpoorly absorbed through skin or the resp tractpoorly absorbed through skin or the resp tract

however, irritant and corrosive effects on membranes, however, irritant and corrosive effects on membranes, cornea and skin cornea and skin

prolonged contact, particularly with concentrates, can prolonged contact, particularly with concentrates, can result in burns and systemic absorption (as little as 28% result in burns and systemic absorption (as little as 28% solutions on skin have caused death)solutions on skin have caused death)

in the lungs produces hydrogen peroxide and superanions in the lungs produces hydrogen peroxide and superanions alveolitis, haemorrhagic pulmonary oedema or adult alveolitis, haemorrhagic pulmonary oedema or adult respiratory distress syndrome, with subsequent fibrosisrespiratory distress syndrome, with subsequent fibrosis

death can also occur by hepatic death can also occur by hepatic renal failure renal failure


Deliberate ingestion of paraquatDeliberate ingestion of paraquat

serious and fatal paraquat poisoning is serious and fatal paraquat poisoning is most commonly due to deliberate most commonly due to deliberate ingestion of concentratesingestion of concentrates

lethal dose for an adult is 3-5g i.e. as little lethal dose for an adult is 3-5g i.e. as little as 10-15ml of a 20% solutionas 10-15ml of a 20% solution

death is usually due to pulmonary toxicity death is usually due to pulmonary toxicity and occurs about a week after ingestion, and occurs about a week after ingestion, though it may be delayed as long as 3 though it may be delayed as long as 3 weeksweeks


Ingestion of paraquatIngestion of paraquat

>6g>6g 3-6g3-6g 1.5-3g1.5-3g

fatal in 24-48h fatal in 24-48h more protracted but still fatalmore protracted but still fatal

nausea, vomitingnausea, vomiting nausea, vomiting nausea, vomiting nausea, vomitingnausea, vomiting

abdominal painabdominal pain dysphagia dysphagia diarrhoeadiarrhoea

diarrhoeadiarrhoea coughing, dyspnoea coughing, dyspnoea mild renal tubular mild renal tubular breathlessness, cyanosis creps and cyanosis breathlessness, cyanosis creps and cyanosis damage damage

metabolic acidosis metabolic acidosis start at 5-7d and start at 5-7d and resp damage starts 10-21dresp damage starts 10-21dimpaired consciousness progresses to death impaired consciousness progresses to death death may be as death may be as

late as 5 late as 5

convulsionsconvulsions renal failure renal failure weeks due to acute weeks due to acute

cardiovascular shock cardiovascular shock jaundice jaundice pneumonitispneumonitis


Diagnosis of paraquat poisoningDiagnosis of paraquat poisoning

usually made on the basis of history of usually made on the basis of history of ingestioningestion

screening test; blue-green colour when screening test; blue-green colour when sodium dithionite and sodium bicarbonate sodium dithionite and sodium bicarbonate is added to urineis added to urine

prognosis for individual cases can be prognosis for individual cases can be predicted from the Proudfoot (et al, 1979) predicted from the Proudfoot (et al, 1979) nomogram, which relates plasma paraquat nomogram, which relates plasma paraquat concentration and time since ingestion to concentration and time since ingestion to outcomeoutcome


Management of acute paraquat ingestionManagement of acute paraquat ingestionsupportive if severe (keep comfortable supportive if severe (keep comfortable with local analgesics and morphine)with local analgesics and morphine)

active treatment active treatment – gastric lavage and activated charcoal or gastric lavage and activated charcoal or

Fuller’s earth within 1 hour of ingestion; anti-Fuller’s earth within 1 hour of ingestion; anti-emetics; NO INDUCTION OF VOMITINGemetics; NO INDUCTION OF VOMITING

– elimination techniques e.g. dialysiselimination techniques e.g. dialysis– corticosteroids, free-radical scavengers, corticosteroids, free-radical scavengers,

radiotherapyradiotherapy– no evidence above methods no evidence above methods mortality mortality


Management of paraquat Management of paraquat poisoning by other routespoisoning by other routes

eyes; wash for at least 15-20 minutes with eyes; wash for at least 15-20 minutes with waterwater

skin; remove clothes, wash with soap and skin; remove clothes, wash with soap and water for at least 20 minuteswater for at least 20 minutes

inhalation of diluted sprays; no measures inhalation of diluted sprays; no measures requiredrequired


Chlorophenoxyacetate herbicidesChlorophenoxyacetate herbicides““hormone” weedkillers (e.g. 2,4D, hormone” weedkillers (e.g. 2,4D, 2,4,5T)2,4,5T)

some toxicity results from additives some toxicity results from additives such as ioxynil and bromoxynil such as ioxynil and bromoxynil (uncouple oxidative phosphorylation) or (uncouple oxidative phosphorylation) or petroleum distillatespetroleum distillates

Difficult to confirm - HPLC assay aids Difficult to confirm - HPLC assay aids diagnosis but is not commonly availablediagnosis but is not commonly available


Chlorophenoxyacetate herbicidesChlorophenoxyacetate herbicidesToxicity: Pulmonary, GIT, renal, liver and CNSToxicity: Pulmonary, GIT, renal, liver and CNS

Non-specific: burning of the mouth and throat, with Non-specific: burning of the mouth and throat, with nausea, vomiting, diarrhoea and abdominal painnausea, vomiting, diarrhoea and abdominal pain

patient is often flushed, sweating and hypotensivepatient is often flushed, sweating and hypotensive

skin or eye exposure results in irritationskin or eye exposure results in irritation

Management: Gastric lavage, activated charcoal < Management: Gastric lavage, activated charcoal < 1hr; supportive care1hr; supportive care

haemodialysis will remove phenoxyacetates and haemodialysis will remove phenoxyacetates and ioxynilioxynil


Aluminium and zinc phosphideAluminium and zinc phosphide

used extensively against rodents and as a used extensively against rodents and as a preservative in grain stores and preservative in grain stores and transportationtransportation

reacts with moisture in air liberating reacts with moisture in air liberating phosphine gas which sinks through the phosphine gas which sinks through the graingrain

routes of exposure include inhalation and routes of exposure include inhalation and ingestioningestion


Mechanism of toxicity of Mechanism of toxicity of aluminium or zinc phosphidealuminium or zinc phosphide

direct gastrointestinal toxicitydirect gastrointestinal toxicity

phosphine generated on contact with fluid phosphine generated on contact with fluid and acid in the stomach is absorbed and and acid in the stomach is absorbed and inhibits cytochrome C oxidaseinhibits cytochrome C oxidase

Renal failure, jaundice (liver necrosis), Renal failure, jaundice (liver necrosis), ARDSARDS


Pyrethrum and pyrethroidsPyrethrum and pyrethroids

pyrethroids entered market in 1980s; pyrethroids entered market in 1980s; synthetic analogues of pyrethrum extractssynthetic analogues of pyrethrum extracts

Mechanism of toxicity of pyrethroids:Mechanism of toxicity of pyrethroids: blockade of sodium channels in neuronal blockade of sodium channels in neuronal membranes causes repetitive sensory and membranes causes repetitive sensory and motor dischargesmotor discharges

permethrin, cypermethrin and deltamethrin permethrin, cypermethrin and deltamethrin inhibit Ca/Mg ATPase leading to inhibit Ca/Mg ATPase leading to neurotransmitter releaseneurotransmitter release


Accidental and occupational Accidental and occupational exposure to pyrethroidsexposure to pyrethroids

use indoors has produced cutaneous paraesthesiae, use indoors has produced cutaneous paraesthesiae, or stinging or burning on the skin, especially or stinging or burning on the skin, especially deltamethrin, cypermethrin or fenvalerate and occur deltamethrin, cypermethrin or fenvalerate and occur several hours after exposure and last 12-18 hoursseveral hours after exposure and last 12-18 hours

upper respiratory tract irritation after flea-sprays with upper respiratory tract irritation after flea-sprays with 1.5% pyrethroids1.5% pyrethroids

allergic reactions to pyrethroids are well documented allergic reactions to pyrethroids are well documented and one death due to bronchospasm has been and one death due to bronchospasm has been reported after inhalation of a shampooreported after inhalation of a shampoo


Ingestion of pyrethroidsIngestion of pyrethroids

epigastric pain, nausea, vomiting, epigastric pain, nausea, vomiting, headaches, dizziness, fatigue, blurred headaches, dizziness, fatigue, blurred vision, paraesthesiae, coarse fasciculationvision, paraesthesiae, coarse fasciculation

coma, convulsions and pulmonary coma, convulsions and pulmonary oedema in severe cases, particularly oedema in severe cases, particularly where a large amount of a concentrated where a large amount of a concentrated product is swallowedproduct is swallowed


Management of poisoning by Management of poisoning by pyrethroidspyrethroids

features of occupational and accidental features of occupational and accidental exposure are reversibleexposure are reversible

skin and eye decontaminationskin and eye decontamination

gastric lavage within 1 hour of ingestion, gastric lavage within 1 hour of ingestion, together with symptomatic and together with symptomatic and supportive care is indicated for serious supportive care is indicated for serious poisoningpoisoning


Warfarin and other Warfarin and other anticoagulants as rodenticidesanticoagulants as rodenticidesNB haemorrhage 12-48 hours after NB haemorrhage 12-48 hours after ingestion, and lasts 3-4 daysingestion, and lasts 3-4 days

Management: as per anticoagulant Management: as per anticoagulant overdose -overdose - cholestyramine or activated cholestyramine or activated charcoal within 1 hour, tranfusion if neededcharcoal within 1 hour, tranfusion if needed


Diethyl toluamide or DEETDiethyl toluamide or DEET

insect repellent; lotions, sticks, sprays insect repellent; lotions, sticks, sprays

Typically children who swallow DEET - may Typically children who swallow DEET - may be mistaken for a viral infectionbe mistaken for a viral infection

Clinical features:Clinical features:– Nausea, vomiting, abdominal pain, diarrhoeaNausea, vomiting, abdominal pain, diarrhoea

– unconscious, fits, cerebellar signs, tremblingunconscious, fits, cerebellar signs, trembling

– liver damageliver damage

– systemic hypotension, tachycardiasystemic hypotension, tachycardia

– skin and eye irritation, including blisters, ulcersskin and eye irritation, including blisters, ulcers


Management of poisoning with Management of poisoning with DEETDEET

supportive and symptomaticsupportive and symptomatic

irrigate eyes, wash skinirrigate eyes, wash skin

gastric lavage with 1 hour of ingestiongastric lavage with 1 hour of ingestion

standard care for encephalopathystandard care for encephalopathy

treat convulsions with diazepam 10-20mg treat convulsions with diazepam 10-20mg iv for an adultiv for an adult


What symptoms would make you think of OP’s?What symptoms would make you think of OP’s?What steps would you take to:What steps would you take to:

Reach a diagnosis?Reach a diagnosis?Identify the source of the problem?Identify the source of the problem?Prevent recurrence or complicatoins?Prevent recurrence or complicatoins?Meeting your legal obligations?Meeting your legal obligations?

CaseCase: Three farm workers come to see you. They all have symptoms typical of organophosphate exposure. However, none of them report working with Ops. How would you being to address the problem?


Routes of ExposureRoutes of Exposure

Oral – SwallowingOral – Swallowing

Dermal – through the SkinDermal – through the Skin

Respiratory – breathe in fumes, Respiratory – breathe in fumes, vapousvapous

Ocular – splash in eyesOcular – splash in eyes


CHRONIC EFFECTS OF PESTICIDESCHRONIC EFFECTS OF PESTICIDES

Cancer:Cancer: Risk Exposures = FarmersRisk Exposures = Farmers Risk Chemicals = Arsenicals, dioxin, PCP ? OthersRisk Chemicals = Arsenicals, dioxin, PCP ? Others Risk cancers = lymphoma, sarcoma, brain, myeloma, ? OthersRisk cancers = lymphoma, sarcoma, brain, myeloma, ? Others

Immune System:Immune System: Reduced resistance to infectionReduced resistance to infection Reduced resistance to cancers (? lymphoma)Reduced resistance to cancers (? lymphoma)

Reproductive:Reproductive: Known reproductive toxins: e.g. DBCPKnown reproductive toxins: e.g. DBCP Endocrine disruptorsEndocrine disruptors

NeurotoxicityNeurotoxicityDifficulties of establishing causation are NBDifficulties of establishing causation are NB


NEUROTOXICITYNEUROTOXICITY

NB OrganophosphatesNB Organophosphates

Peripheral NeuropathyPeripheral NeuropathyIntermediate SyndromeIntermediate SyndromeSub-clinical CNS effects following Sub-clinical CNS effects following acute poisoningacute poisoningChronic effects following long term Chronic effects following long term exposure!exposure!


Peripheral Neuropathy = OPsPeripheral Neuropathy = OPs

OrganoPhosphate Induced Delayed Neuropathy OrganoPhosphate Induced Delayed Neuropathy ((O P I D N)O P I D N)Symmetrical distal sensori-motorSymmetrical distal sensori-motorUsually after massive exposure. (parasuicide)Usually after massive exposure. (parasuicide)Preceded by acute cholinergic phasePreceded by acute cholinergic phaseOnset 2 – 5 wks > intoxicationOnset 2 – 5 wks > intoxicationRecovery up to 1 yearRecovery up to 1 year± long-term residue: ± long-term residue: foot drop and spasticityfoot drop and spasticity

Mechanism: NeuroToxic Estrase = NTEMechanism: NeuroToxic Estrase = NTE Not cholinesterase!Not cholinesterase!

Leslie London, University of Cape TownPhoto from Leslie London, University of Cape Town


The intermediate syndromeThe intermediate syndrome

Minority of patients Minority of patients (Sri Lanka)(Sri Lanka)Proximal muscle weakness (24 – 96 hrs)Proximal muscle weakness (24 – 96 hrs)

Cranial nerve, brain-stem lesions; proximal neuropathy Cranial nerve, brain-stem lesions; proximal neuropathy starting 1-4 days > acute poisoning; lasts for approximately starting 1-4 days > acute poisoning; lasts for approximately 3 weeks3 weeks

respiratory depression criticalrespiratory depression critical

NO Cholinesterase depression NO Cholinesterase depression

Unresponsive to atropine and oximesUnresponsive to atropine and oximes


Sub-Clinical effects after Past PoisoningSub-Clinical effects after Past Poisoning

Laboratory Animals: EEG ChangesLaboratory Animals: EEG Changes

Case series human workers: EEG and Case series human workers: EEG and SPECT SPECT ChangesChanges

Case Control Studies Poisoning SurvivorsCase Control Studies Poisoning Survivors-- intellectual function intellectual function

-- motor skills motor skills

- - performance on WHO test batteries and other performance on WHO test batteries and other

Vibration sense loss in absence of nerve Vibration sense loss in absence of nerve conduction abnormalities or clinical conduction abnormalities or clinical symptomssymptoms


Long Term Exposure but NO poisoningLong Term Exposure but NO poisoning

Effects – vibration senseEffects – vibration sense - psychiatric - psychiatric changechangess

- Neurobehavioural - Neurobehavioural PerformancePerformance

- Neuroendocrine - Neuroendocrine changechangessEvidence equivocalEvidence equivocal


Neurotoxicity of Other PesticidesNeurotoxicity of Other Pesticides

PyrethroidsPyrethroids

OrganochlorinesOrganochlorines

Methyl BromideMethyl Bromide

OrganotinOrganotin

ParaquatParaquat

Manganese Manganese containing containing pesticides?pesticides?


NEUROTOXICITY OF CHEMICALSNEUROTOXICITY OF CHEMICALS

EXPOSURE – EFFECT RELATIONSHIPSEXPOSURE – EFFECT RELATIONSHIPS

What sort of ExposureWhat sort of Exposure?? What sort of EffectWhat sort of Effect??

ACUTE INTOXICATIONACUTE INTOXICATION ACUTEACUTE EFFECTSEFFECTS

EPISODICEPISODIC

ReversibleReversible

LONG-TERM LOW DOSELONG-TERM LOW DOSE CHRONIC EFFECTS CHRONIC EFFECTS

IrreversibleIrreversible

SP

EC

TR

UM

SP

EC

TR

UM

Progression

?

?

?


NEUROTOXICITY OF OP’s: SUMMARYNEUROTOXICITY OF OP’s: SUMMARY

EffectEffect Evidence Evidence Toxicolog Toxicolog MechMech

Acute Poisoning Acute Poisoning CLEAR CLEAR Cholinest inhib.Cholinest inhib.

Perip Neur Perip Neur CLEAR CLEAR ? NTE inhib? NTE inhib

> acute intox> acute intox

CNS effects CNS effects CLEAR CLEAR ? ?

> acute intox > acute intox

CNS + PN with CNS + PN with ? ? ? ?

long-term exposurelong-term exposure

Other conundrumsOther conundrums hypothetical hypothetical ?? ??

eg: GBSeg: GBS

EPIDEMIOLOGIC STUDIES EPIDEMIOLOGIC STUDIES OF PESTICIDE HAZARDS OF PESTICIDE HAZARDS

IN SAIN SA


Critical Issues in Occupational Critical Issues in Occupational EpidemiologyEpidemiology

Exposure AssessmentExposure Assessment

Outcome AssessmentOutcome Assessment

ConfoundersConfounders

NB - MisclassificationNB - Misclassification


STUDY DESIGNSTUDY DESIGN

Is there a comparison?

No

Descriptive Study

Yes

Is exposure controlled?

How are subjects selected?

Experimental R.C.T

Cohort Case Control

Before –

After

Between group comparison

Within goup compar.Within group comparison

By expos. By outcomeNeither: X sectional

YesNo

X sectional



South African Studies of Cholinesterase Depression amongst South African Studies of Cholinesterase Depression amongst farm workers exposed to Organophosphatesfarm workers exposed to Organophosphates

Authors and dateAuthors and date SettingSetting Main FindingsMain Findings ConstraintsConstraints

Fuller et al, 1990Fuller et al, 1990 40 farm workers and 11 40 farm workers and 11 nursery workers nursery workers handling pesticides – handling pesticides – large agribusiness fruit large agribusiness fruit farm in the W Cape farm in the W Cape Baseline and follow up Baseline and follow up over 6 weeksover 6 weeks

60% of fw and 72 % of 60% of fw and 72 % of nursery workers had nursery workers had PCE<referencePCE<reference

After withdrawl of 7 After withdrawl of 7 most affected workers, most affected workers, PCE increase 40 %PCE increase 40 %

Other exposed workers Other exposed workers decrease 5%decrease 5%

Reference group non-Reference group non-comparable – laboratory comparable – laboratory workersworkers

Rama and Jaga, 1992Rama and Jaga, 1992 69 coffee plantation 69 coffee plantation workers, N Provinceworkers, N Province

Cross-sectional studyCross-sectional study

77% low for RCE77% low for RCE

27% low for PCE27% low for PCE

About half of samples About half of samples discarded discarded

Unable to find rural Unable to find rural controlscontrols

No quantification of No quantification of exposureexposure

Not related to symptomsNot related to symptoms


Authors and Authors and datedate

SettingSetting Main FindingsMain Findings ConstraintsConstraints

Jaga et al, 1994Jaga et al, 1994 190 coffee plantation 190 coffee plantation workers in N Province workers in N Province with presumed high, with presumed high, medium and low medium and low exposureexposure

71 hospital patients and 71 hospital patients and

37 hospital staff as rural 37 hospital staff as rural controlscontrols

56 laboratory personnel 56 laboratory personnel as urban controlas urban control

Cross-sectional study.Cross-sectional study.

Farm workers had Farm workers had lower RCE than urban lower RCE than urban controls but higher controls but higher than rural controls.than rural controls.

No relationship No relationship amongst farm amongst farm workers to degree of workers to degree of exposureexposure

Poor agreement RCE Poor agreement RCE and PCEand PCE

Different laboratories Different laboratories did analyses for 2 did analyses for 2 control groupscontrol groups

Gender discrepanciesGender discrepancies

Confounding for Confounding for medical illness, medical illness, anaemiaanaemia

Measurement bias?Measurement bias?

Environmental Environmental exposure?exposure?

Barnes et al, 1992 Barnes et al, 1992 (unpublished)(unpublished)

Spray operators Spray operators compared to Pack Store compared to Pack Store workers in apple farming workers in apple farming in W Cape Cohort: in W Cape Cohort: Changes in PCE across Changes in PCE across the spraying seasonthe spraying season

No difference No difference between controls and between controls and spray operatorsspray operators

Selection bias in Selection bias in controls – age, controls – age, education and jobeducation and job

Failed to do follow up Failed to do follow up bloods for controlsbloods for controls




London et al, 1998London et al, 1998 163 spraymen and 83 163 spraymen and 83 non-sprayers on fruit non-sprayers on fruit farms in the W Cape. farms in the W Cape. Cross-section. Cross-section. Sample selected on Sample selected on basis of long-term basis of long-term exposureexposure

No difference in RCE No difference in RCE or PCE between or PCE between sprayers and non-sprayers and non-sprayers, or between sprayers, or between recently exposed and recently exposed and non-exposed.non-exposed.

Fewer than 1 % Fewer than 1 % below normal rangebelow normal range

Design not suited for Design not suited for assessing acute assessing acute effectseffects


Long-term health impacts from pesticide exposureLong-term health impacts from pesticide exposure



Bouwman et al, 1990Bouwman et al, 1990 Women attending Women attending antenatal clinics: 132 antenatal clinics: 132 from malaria control from malaria control areas to 88 controlsareas to 88 controls

High level of DDT and High level of DDT and metabolites in breast milk metabolites in breast milk amongst exposed amongst exposed compared to controls.compared to controls.

Seasonal variation Seasonal variation consistent with malaria consistent with malaria sprayingspraying

No outcome No outcome measures linked to measures linked to exposuresexposures

Todd and London, Todd and London, 1995 (unpublished)1995 (unpublished)

197 fruit farm workers 197 fruit farm workers screened, 49 screened, 49 assessed for assessed for dermatosesdermatoses

Descriptive studyDescriptive study

23% any dermatosis23% any dermatosis

9% dermatitis of which 9% dermatitis of which 5/17 allergic5/17 allergic

11% acne bacterial 11% acne bacterial infection under-reportedinfection under-reported

1 patch + to pesticide of 1 patch + to pesticide of unknown significance.unknown significance.

May be under-May be under-estimated because estimated because 2 stage screen Path 2 stage screen Path series may not be series may not be specificspecific

Low atopyLow atopy



London et al, 1998London et al, 1998 163 spraymen and 83 163 spraymen and 83 non-sprayers on fruit non-sprayers on fruit farms in the W Cape. farms in the W Cape. Cross Section.Cross Section.

Exposure based on Exposure based on JEMJEM

Significant association Significant association past poisoning and past poisoning and neuro symptoms. neuro symptoms. Significant assoc. spray Significant assoc. spray man and neuro man and neuro symptoms. No symptoms. No evidence for assoc. evidence for assoc. long term exp and long term exp and psych/vibr sense loss.psych/vibr sense loss.

Impact of chronic Impact of chronic u/nutr-albumenu/nutr-albumen

Lack of specificity to Lack of specificity to particular OPparticular OP

High background High background alcohol and head injuryalcohol and head injury

HWE vs Sick Worker HWE vs Sick Worker EffectEffect

Dalvie et al, 1999Dalvie et al, 1999 62 spraymen exposed 62 spraymen exposed paraquat and 70 paraquat and 70 controls Cross-section controls Cross-section analytical studyanalytical study

Exposure based on Exposure based on JEMJEM

No association exp and No association exp and symptoms, LFTs and symptoms, LFTs and gas transfergas transfer

Significant association Significant association of long term exposure of long term exposure with O² desat.with O² desat.

Impact of chronic u/nutr Impact of chronic u/nutr – stunting– stunting

Exposure char subject Exposure char subject to misclassto misclass



London et al, 2005London et al, 2005

(in press)(in press)

Case series – 7 cases Case series – 7 cases GBS in agro-irrigation GBS in agro-irrigation farming N Capefarming N Cape

Significant cluster of Significant cluster of cases (4 x expected) cases (4 x expected) and sub-cluster (11 X) and sub-cluster (11 X) Ecological evidence for Ecological evidence for high OP usehigh OP use

No exposure No exposure characterisationcharacterisation

No ratesNo rates

No comparison groupNo comparison group

Maruping et al, 2005Maruping et al, 2005

(in preparation)(in preparation)

Mortuary review of Mortuary review of suicide in relation to suicide in relation to occupationoccupation

Farm workers had Farm workers had increased risk of suicide increased risk of suicide (appr RR = 2 to 3.5)(appr RR = 2 to 3.5)

RR for suicide WITH RR for suicide WITH pesticides about 5pesticides about 5

Not able to link job to Not able to link job to OP exposureOP exposure

Competing causes of Competing causes of death death

Major et al, 2005Major et al, 2005

(in preparation)(in preparation)

Cross sectional study of Cross sectional study of farm workers and farm workers and families in Worcester families in Worcester 20022002

High scores on suicide High scores on suicide and depression scalesand depression scales

Gender differencesGender differences

Past poisoning Past poisoning associated with associated with ↑risk↑risk

Still characterising long Still characterising long term OP exposureterm OP exposure

Surveillance for PesticidesSurveillance for Pesticides

Leslie LondonLeslie LondonOccupational and Environmental Occupational and Environmental Health Research Unit, University Health Research Unit, University of Cape Town, May 2005of Cape Town, May 2005


What kinds of Surveillance?What kinds of Surveillance?1.1. For ExposureFor Exposure

e.g How many workers handle Organophosphates?e.g How many workers handle Organophosphates?

2.2. For DiseaseFor Diseasee.g. How many workers have been poisoned by e.g. How many workers have been poisoned by Organophosphates?Organophosphates?

3.3. For Early markers before diseaseFor Early markers before diseasee.g How many workers have biochemical markers e.g How many workers have biochemical markers indicating early effects from Organophosphates?indicating early effects from Organophosphates?


increasing increasing exposureexposure

well-being

early changes

subclinical signs

illness

death

Used with permissions from Donna Mergler, CINBIOSE, University of Quebec at

Montreal


Exposure to Chemical

Uses OP

Early Biochemicalor Physiological

Cholinesterase

ReversibleDisease

Dizziness

IrreversibleDisease

Nervedamage

Surveillance for exposure

BiologicalSurveillance

Medical Surveillance

SubstitutionEngineering ControlsAdministrative ControlsPPETraining

Remove Worker from exposureCorrect exposureRetest Treatment

Remove from exposureReferral

CompensationRehabilitation

Leslie London, UCT

By Leslie London, University of Cape Town


Surveillance for ExposureSurveillance for Exposure

Pesticide PurchasesPesticide Purchases

Application recordsApplication records

Spray programmesSpray programmes

Pesticide store inspectionsPesticide store inspections

Reports of:Reports of:– Obsolete pesticidesObsolete pesticides– Empty containersEmpty containers– Environmental contamination: Soil, water, foliage, etcEnvironmental contamination: Soil, water, foliage, etc

Can only give crude idea of human hazard!Can only give crude idea of human hazard!


Surveillance for DiseaseSurveillance for Disease

Function of reporting to Chief InspectorFunction of reporting to Chief InspectorCOIDA dataCOIDA dataData outside the DoLData outside the DoL

Acute Pesticide PoisoningAcute Pesticide PoisoningEasier to diagnose; Easier to diagnose; Easier to attribute to pesticide;Easier to attribute to pesticide;Seen at hospitals, clinics;Seen at hospitals, clinics;Needs to be reported, but … Needs to be reported, but … Many cases under-reportedMany cases under-reportedChronic Pesticide-related problemsChronic Pesticide-related problemsDifficult to diagnose;Difficult to diagnose;Very difficult to attribute to pesticidesVery difficult to attribute to pesticidesCould set up surveillance registry (e.g. cancer registry; Could set up surveillance registry (e.g. cancer registry; neurotoxicity register)neurotoxicity register)


2. Weak Surveillance for hazards & impact

0

5

10

15

20

25

30

35

40

45

Pre-Intervention

Post-intervention

Control Area Intervention Area

Intensified notification, South Africa, 1995/6Under-reporting of female and occupational poisoning


Surveillance for Biological Effects:Surveillance for Biological Effects:Biological MonitoringBiological Monitoring

Chemicals can cause early changes in the Chemicals can cause early changes in the body before the person actually develops body before the person actually develops a diseasea disease

Changes in an enzyme, hormone, Changes in an enzyme, hormone, metabolitemetaboliteIndicate EARLY effectsIndicate EARLY effectsReversible!Reversible!

Exposure to Chemical

Early Biochemicalor Physiological

ReversibleDisease Irreversible

Disease


Why Biological Monitoring?Why Biological Monitoring?

Primarily to detect changes Primarily to detect changes BEFORE BEFORE worker worker becomes illbecomes illSo that preventive intervention is put in placeSo that preventive intervention is put in placeCan signal problems in industrial hygieneCan signal problems in industrial hygieneCan draw attention to problem areasCan draw attention to problem areasCan help with subsequent compensationCan help with subsequent compensationCan help with proving causation of subsequent Can help with proving causation of subsequent chronic occupational illnesschronic occupational illness


What type of preventive actions?What type of preventive actions?Investigate workplace: condition of Investigate workplace: condition of equipment, appropriate maintenance, use, equipment, appropriate maintenance, use, PPEPPEInvestigate safety practicesInvestigate safety practicesRemoval from exposure (work placement)Removal from exposure (work placement)Search for other affected workersSearch for other affected workersHierarchy of controls: Engineering, Hierarchy of controls: Engineering, Administrative, Training, PPEAdministrative, Training, PPE


Examples of Early (Physiological) ChangeExamples of Early (Physiological) Change

Metabolites (breakdown products) in urineMetabolites (breakdown products) in urinee.g. organophosphates, paraquat, PCPe.g. organophosphates, paraquat, PCPEnzymes in bloodEnzymes in bloode.g. cholinesterasee.g. cholinesteraseGene damage in cellsGene damage in cellsDNA adducts, etcDNA adducts, etcHormone changesHormone changese.g. endocrine-disrupting chemicalse.g. endocrine-disrupting chemicalsImmune markersImmune markers

Marker depends on the Pesticide! (see EPA book; Marker depends on the Pesticide! (see EPA book; Haz Chem Regs)Haz Chem Regs)


What pesticides?What pesticides?

Organophosphates and Carbamates are Organophosphates and Carbamates are Cholinesterase-inhibiting pesticidesCholinesterase-inhibiting pesticides

Other pesticides less easyOther pesticides less easye.g. urine metabolites of many fungicides, e.g. urine metabolites of many fungicides, herbicidesherbicides

NOTE: Monitoring for Cholinesterase will NOTE: Monitoring for Cholinesterase will ONLY work for Organophosphates and ONLY work for Organophosphates and Carbamates – not for other pesticidesCarbamates – not for other pesticides


Acute OP (and carbamate) Acute OP (and carbamate) poisoning poisoning

The enzyme The enzyme acetylcholinesteraseacetylcholinesterase regulates the concentration of regulates the concentration of acetylcholine at the acetylcholine at the interneuronal and interneuronal and neuroeffector junctionsneuroeffector junctions

OPs and carbamates are OPs and carbamates are cholinesterase inhibitorscholinesterase inhibitors

Carbamates are reversible Carbamates are reversible inhibitorsinhibitors

Leslie London, University of Cape TownPhoto from Leslie London, University of Cape Town


What is cholinesterase?What is cholinesterase?

Enzyme in the blood and brainEnzyme in the blood and brainEssential for nerves to functionEssential for nerves to functionKeeps the level of acetyl choline constantKeeps the level of acetyl choline constantAcetyl choline = nerve transmitterAcetyl choline = nerve transmitterIf too much acetyl choline If too much acetyl choline nerve overactivity nerve overactivityIf you inhibit cholinesterase If you inhibit cholinesterase too much acetyl choline too much acetyl choline nerve nerve overactivity = poisoningoveractivity = poisoningTwo types of cholinesterase:Two types of cholinesterase:– Plasma cholinesterase = marker of recent exposurePlasma cholinesterase = marker of recent exposure– Red blood cell cholinesterase = marker of effects on brain, Red blood cell cholinesterase = marker of effects on brain,

nervous systemnervous system


How do you know How do you know cholinesterase is too low?cholinesterase is too low?

Variability between people for CHE is very Variability between people for CHE is very highhigh

Not good to compare between peopleNot good to compare between people

Better to compare person to their own Better to compare person to their own baselinebaseline


0

5

10

15

20

25

30

Jan Feb Mar April May June July Aug

Intervention

No intervention

Hypothetical Example of Cholinesterase Monitoring:a) With Intervention; b) Without Intervention

Start spraying

Remove fromexposure

Tox

icity

thre

shol

d


LessonsLessons

If you don’t have a baseline for EACH If you don’t have a baseline for EACH worker, cholinesterase testing is NOT very worker, cholinesterase testing is NOT very helpful!helpful!

Laboratories will often say what is “normal” Laboratories will often say what is “normal” and what is not – don’t believe them!and what is not – don’t believe them!

Laboratories often get results wrongLaboratories often get results wrong(Diraj Rama, 1997)(Diraj Rama, 1997)


How do you establish a baseline?How do you establish a baseline?

Test them BEFORE they start workTest them BEFORE they start work

If already at work, test them when they If already at work, test them when they return from leave (2 – 3 months away from return from leave (2 – 3 months away from pesticides!)pesticides!)

Recommend two tests within two days – Recommend two tests within two days – average of both testsaverage of both tests


How much of a decline is a How much of a decline is a problem?problem?

Red cell cholinesterase: Red cell cholinesterase: to 70% baseline to 70% baseline

Plasma cholinesterase: Plasma cholinesterase: to 60% baseline to 60% baseline(HCS regs don’t distinguish)(HCS regs don’t distinguish)


What action should be prompted?What action should be prompted?

Plasma Cholinesterase

75-85% Re-test worker

60-75% Re-test workerInvestigate hygiene

<60% Remove workerInvestigate hygien

Red blood cell cholineasterase

75-85% Re-test worker

70-75% Re-test workerInvestigate hygiene

<70% Remove workerInvestigate hygien


How frequently to test?How frequently to test?

Intended for PREVENTION, not for compliance Intended for PREVENTION, not for compliance with the regulations!with the regulations!

Therefore:Therefore:– At baselineAt baseline– As spraying begins to increaseAs spraying begins to increase– Regularly if a sprayerRegularly if a sprayer

e.g. In US: If > 6 days spraying in 30 day cyclee.g. In US: If > 6 days spraying in 30 day cyclee.g Continuous work in closed environmente.g Continuous work in closed environment

At discretion of OH practitionerAt discretion of OH practitioner


Testing technologyTesting technology

Blood samples can be Blood samples can be sent to laboratorysent to laboratory

Should be QC from Should be QC from laboratorylaboratory

Field kits give Field kits give immediate result immediate result (finger prick)(finger prick)

Leslie London, UCT


A Biological Monitoring Programme A Biological Monitoring Programme for Cholinesterase Inhibitorsfor Cholinesterase Inhibitors

What workers are included? [Risk What workers are included? [Risk Assessment]Assessment]

How often?How often?

What thresholds prompt preventive What thresholds prompt preventive actions? What actions?actions? What actions?

What follow up needed?What follow up needed?

How long to keep records? [30 years]How long to keep records? [30 years]

Informed consentInformed consent


Common problemsCommon problems

Don’t use BM as substitute for proper Don’t use BM as substitute for proper safety programmesafety programme

Should be evaluated – not just for Should be evaluated – not just for compliance with regulationscompliance with regulations

Are the results used and interpreted Are the results used and interpreted meaningfully? Not good enough to rely on meaningfully? Not good enough to rely on “normal” result from lab.“normal” result from lab.


THE HAZARDOUS CHEMICAL THE HAZARDOUS CHEMICAL SUBSTANCE REGULATIONSSUBSTANCE REGULATIONS

Provides for Risk AssessmentProvides for Risk Assessment

Right-to-knowRight-to-know

Biological and environmental monitoringBiological and environmental monitoring

Obligations on employers and employeesObligations on employers and employees

Threshold levels of chemicals Threshold levels of chemicals (carcinogens and non-carcinogens)(carcinogens and non-carcinogens)

Hierarchy of controlsHierarchy of controls


What type of preventive actions?What type of preventive actions?Investigate workplace: condition of Investigate workplace: condition of equipment, appropriate maintenance, use, equipment, appropriate maintenance, use, PPEPPEInvestigate safety practicesInvestigate safety practicesRemoval from exposure (work placement)Removal from exposure (work placement)Search for other affected workersSearch for other affected workersHierarchy of controls: Engineering, Hierarchy of controls: Engineering, Administrative, Training, PPEAdministrative, Training, PPE


Future trends of PesticidesFuture trends of Pesticides

Use of modern / new FormulationsUse of modern / new Formulations Use less acutely toxicUse less acutely toxic Use products that need less ApplicationUse products that need less Application Safe package designsSafe package designs Alternative pest control methodsAlternative pest control methods Eliminating POP’sEliminating POP’s Avoiding unnecessary and hazardous imports Avoiding unnecessary and hazardous imports

(Rotterdam Convention = International Code of (Rotterdam Convention = International Code of Conduct)Conduct)


Control of Pesticide HazardsControl of Pesticide Hazards

• Surveillance: for Surveillance: for exposure, biological exposure, biological effect, and pesticide-effect, and pesticide-related illnessrelated illness

Leslie London, UCT



• Training: farm Training: farm workers, farmers, workers, farmers, public health public health personnelpersonnel

Leslie London, UCT



LegislationLegislation

•RationalizedRationalized•PracticalPractical•EnforceableEnforceable•facilitate surveillance and monitoringfacilitate surveillance and monitoring•public access; worker’s right-to-knowpublic access; worker’s right-to-know

Leslie London, UCT


Points about the law to rememberPoints about the law to rememberWorkers have the Workers have the right to knowright to know about the hazards about the hazards of chemicals they useof chemicals they useWorkers must receive Workers must receive trainingtrainingWorkers who are exposed to pesticides must be Workers who are exposed to pesticides must be monitoredmonitored to prevent their health being affected to prevent their health being affectedEmployers must provide proper Employers must provide proper protectiveprotective clothing clothing only after they have tried all other methods to only after they have tried all other methods to prevent workers exposureprevent workers exposureWashing and changing facilitiesWashing and changing facilities must be provided must be providedWorkers must also do everything reasonable to Workers must also do everything reasonable to prevent their exposureprevent their exposure



• Safe chemical waste Safe chemical waste disposaldisposal

• IPMIPM

Leslie London, UCTLeslie London, UCT



• Workplace Workplace interventionsinterventions

• Contextual : Contextual : Education, housing, Education, housing, alcohol, etc alcohol, etc [ A PHC approach !!!!][ A PHC approach !!!!]

Andrea Rother, UCT

HAZARD COMMUNICATIONHAZARD COMMUNICATION


PURPOSE OF HAZARD PURPOSE OF HAZARD COMMUNICATIONCOMMUNICATION

Provide sufficient information to recipients on workplace Provide sufficient information to recipients on workplace hazards so that they may be able to protect themselves and/or hazards so that they may be able to protect themselves and/or their family from exposures, and adverse consequences.their family from exposures, and adverse consequences.

Forms of Hazard CommunicationForms of Hazard Communication

Labels (including pictograms)Labels (including pictograms)Information insets to chemical containersInformation insets to chemical containersMSDS’sMSDS’sEducation and Training programmesEducation and Training programmesWarnings in advertisementsWarnings in advertisementsAdvisory services (Agrichemical sales representatives, Advisory services (Agrichemical sales representatives, Government Agricultural Extension Officers)Government Agricultural Extension Officers)


Labels and Information Insets to ContainersLabels and Information Insets to Containers

a)a) Present? Torn off, wrinkled or damaged? Decanting to an unlabelled Present? Torn off, wrinkled or damaged? Decanting to an unlabelled container.container.

b)b) User understanding; Information inset not openedUser understanding; Information inset not opened

c)c) Inappropriate language; Functional illiteracy highInappropriate language; Functional illiteracy high

d)d) Technical language, aimed at scientifically literateTechnical language, aimed at scientifically literateTranslation difficultiesTranslation difficultiesConceptual non-currency; e.g. understanding “witholding” periodsConceptual non-currency; e.g. understanding “witholding” periods

Labels as insurance for industry?Labels as insurance for industry?

Hazard Communication for Hazard Communication for Pesticides: Pesticides:

Key ProblemsKey Problems


PictogramsPictograms

AssumptionsAssumptionsPictograms are universally understoodPictograms are universally understoodBy simplifying, increase comprehensibilityBy simplifying, increase comprehensibilityPictograms are realisticPictograms are realistic

BUT:BUT: Empirical evidence not presentEmpirical evidence not present Even if understood, what action?Even if understood, what action? Culturally specific – graphic conventions not universalCulturally specific – graphic conventions not universal Like any language, must be taughtLike any language, must be taught Preliminary SA research – workers prefer “realistic” Preliminary SA research – workers prefer “realistic”

pictures (photographs as hazard communication pictures (photographs as hazard communication tools.tools.


Colour CodesColour Codes

Users unaware of implications (toxicity, Users unaware of implications (toxicity, precautions)precautions)

Even if aware, no control over the Even if aware, no control over the availabilityavailability

Colour Codes need to be taughtColour Codes need to be taught


Applicability in Developing Applicability in Developing CountryCountry

Triple rinsing needs water – availability in Triple rinsing needs water – availability in communities?communities?

Symbol Symbol glove use – but what if unable glove use – but what if unable to afford, or unavailable?to afford, or unavailable?


South African Hazard Communication South African Hazard Communication LegislationLegislation

HCS RegulationsHCS Regulations::

Employer obliged to provide information to employee on:Employer obliged to provide information to employee on:

Content, scope regsContent, scope regs ** Sources exposureSources exposure

Health risksHealth risks ** Reproductive impactsReproductive impacts

Protective measuresProtective measures ** Precautions to preventPrecautions to prevent

Use of Safety equipmentUse of Safety equipment ** Sampling, surveillanceSampling, surveillance

Industrial hygieneIndustrial hygiene ** Safe working proceduresSafe working procedures

Accident proceduresAccident procedures


South African Hazard Communication South African Hazard Communication LegislationLegislation

General Administrative RegulationsGeneral Administrative RegulationsAny hazardous substance must be supplied with a MSDS, which should include:Any hazardous substance must be supplied with a MSDS, which should include:

Product, company IDProduct, company ID * Info on ingredients* Info on ingredientsHazards IDHazards ID * First aid measures* First aid measuresFire-fighting measuresFire-fighting measures * Accidental release measures* Accidental release measuresHandling, storageHandling, storage * Control of exposure* Control of exposurePhys + chem. PropertiesPhys + chem. Properties * Stability, reactivity* Stability, reactivityToxicologyToxicology * Ecological info* Ecological infoDisposal considerationsDisposal considerations * Transport info* Transport infoRegulatory infoRegulatory info * Other info as needed* Other info as needed

Available to employees, interested or affected persons Available to employees, interested or affected persons Annexure = standardsAnnexure = standards

How complete are MSDS’s in practice?How complete are MSDS’s in practice?Not very complete – Dalvie and Ehrlich, 1999Not very complete – Dalvie and Ehrlich, 1999

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