Standard Treatments Guidelines For Occupational Poisoning, DOH 1997

National Poison Control and Informa~r'" ".
,'
University of the Philippines· College of Medicine' !'til . j~\li8fll1 HosPital
Non·Communicable Disease Control SerVIt:8
Department of Health
Standard Treatment Guidelines for
..,..,
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EDITORS
o Nelia P. Cortes·Maramba, MD
>
-< lurenda Suplido, MD
~, laurence S. So. MO
-'
>
lynn Crisanta R. Panganiban, MD
0: Erie S. Castillo, MD
::>
iii
::>,
~'
~
CONTRIBUTORS
Allan R. Dionisio MD
"f Carissa Paz C. Dioquino, MD
,j Kenneth Hartlqan-Gn, MD
~I Irma R. Makalinao, MD
(CaJrrWaJl
llil~o@~~[ID §illJi
H44.45
S12
1997
]
r
,
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.
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ISBN 971·8650·03·2
ill December 1997 by the National Poison Control and Information Service
The publication of this book was funded by the Department of Health through the Regional
Occupational Toxicology and Non·Communicable Disease Information Center Project
This book isprotected by Philippine Copyright laws. All rights reserved. No part of this book may be reproduced
or transmitted in any form or by any manner, electronic or mechanical, including photocopy, recording, or any data
base or retrieVal system, without prior written permission from the copyright owners.
Printed in the Philippines .,

Standard Treatment Guidelines for
OCCUPATIONAl POISONING
Arsenic
Carbamates
Hydrogen Sulfide
Lead
Mercury
Organophosphates
r -------
Department of Heal~
I I I I !I I 'I I I~I I I
0462
H44.45 8121997 f Standardtreatment guidelinesfor occupational
-----J
The data in this book have been verified with reliable sources, and treatment
modalities discussed have been utilized in clinical practice. However. new re-
searches, changes in the medical sciences, and human error should be consid-
ered. Readers are advised to confirm data herein with other sources such as drug
information sheets for dosage, ccntraindications to administration, and other
data relevant to treatment. The editors, contributors and publisher are not re-
sponsible for errorsor omissions in patient management due to inaccuracies or
incompleteness of the information contained in this book.
MESSAGE
Worldwide, about 10 million chemical compounds have been synthesized in
laboratories since the beginning of the present century. There is virtually no
sector of human activity which does not make use of chemicals and many pred-
ucts have indeed brought beneficial effects toman. However, it isalso essential
tominimize adverse health effects ofchemicals on the environment and human
health.
In recent years, there has been growing concern worldwide about the harmful
effects of chemicals on human health and the environment. An important development in the past two decades
has been a shift offocus ofattention from acute tochronic effects which include neurological and genetic disor·
dars, mutagenic and teratogenic effects as well as other health concerns.
In this light, the Department, in partnership with the UP·National Poison Control and Information Service
under the Regional Occupational Toxicology and Non· Communicable Disease Information Center (ROTNIC) programme
has developed amanual on Standard liestment Guidelines for Occupational Poisoning for field health personnel. It
isfervently hoped that these guidelines will provide physicians in the countryside with basic information aswell as
emergency management procedures on occupational poisonings.
Iwould like toexpress my gratitude and appreciation tothe men and women who have provided their inputs
tothis manual which will serve asour legacy. Indeed, with the information contained in this manual, our physicians
can save and protect countless lives and conserve manpower resources for the greater good, productivity and
betterment ofsociety.
Mabuhay!
tt~t<·N:,.e~·~
CARMENCITA NORIEGA'REOOIcA. M.D.• M.P.H.
Secretary of Health
MESSAGE
The Department of Health has been continuously requested to reo

spend tohealth complaints brought about hy industrial and related activities in
the field. As health care providers, we are expected to respond to the health
needs of the community, including cases of industrial accidents or poisoning
incidents. In most cases, theDepartment isusually the first tobe called upon to
respond to these accidents. However, information is very limited at the field
level in terms of how to respond: the emergency management and treatment. to be administered, handling or
disposal ofhazardous waste materials, life support. decontamination and remediation.
With increasing advances in technology and industrialization in the countryside, the Department deems
itimperative toprovide the necessary information tohandle occupational poisonings. The Department, in partner-
ship with the UP·National Poison Control and Information Service. developed these Standard liestment Guidelines
as reference materials and information tools which can be used especiallv by medical personnel in the countryside.
It is hoped that the information contained herein will help save lives through the administration of appropriate
intervention measures.
A:iR.
M.D.• M.P.A.
nicable Disease Control Service
CONTENTS
Preface 4
User's Guide 5
Guidelines on Field Management 8
Guidelines on Hospital Management 10
Guidelines on Occupational Toxicologic Interventions 12
ARSENIC 14
CARBAMATES 22
HYOROGEN SULFIDE 35
LEAO 44
MERCURY 54
ORGANOPHOSPHATES 64
Annex A: Banned and Restricted Pesticides inthe Philippines 78
(as ofJune 30. 19971
Annex B: Use Categories of Pesticides According to Recommended 80
Restrictions on Availability
TOPIC OUTLINE
\Chemical Name Mechanisms ofToxicity

Chemical Formula Toxic Effects
Synonyms Toxidromes
Classification Acute Exposure
Sources Chronic Exposure
Physical States Specimen and Exams for Diagnosis
Physical and Chemical Properties Antidotes
Hazards Treatment
Carcinogenicity Potential Emergency Field Management
Teratogenicity Potential Emergency Hospital Management
Toxic Dose Occupational Toxicologic Interventions
Exposure Limits Hazards to the Environment andtheir
Toxicokinetics Prevention
Absorption References
Distribution
Metabolism
Excretion
PREFACE
This book is a product of the research and experience ofthe National Poison Control and Information
Service (NPCIS), with support from the Regional Occupational Toxicology and Non·Communicable
Disease Information Center (ROTNIC) Project of the Department ofHealth.
This manual was prepared for physicians and health workers in the field of occupational health and
toxicology. Data on environmental hazards have also been included.
This volume contains articles on some of the most frequently encountered occupational poisons: ar-
senic, carbamates, hydrogen sulfide, lead, mercury and organophosphates. Subsequent volumes will
contain information on benzene, cadmium, carbon monoxide, cyanide, organochlorines, paraquat,
pyrethroids, rodenticides, styrene, toluene and trinitrotoluene.
The reader is advised to review the guidelines on occupational toxicologic interventions, field manaqe-
ment, and hospital management at the beginning ofthis book since discussions for each toxic sub-
stance will contain only specific points regarding management.
.:»:
ACKNOWLEDGEMENTS
Our warmest thanks toOr. David lozada, Engr. Ana Francisco, Ms. Teresa Mendoza, Or. Cristina Oablo,
and to Secretary Carmencita Reodica ofthe Department ofHealth.
We appreciate the support given by the NPCIS staff: Or. Jojo Pascual, Jeanne Castaneda and Anton
Ozuna.
. The Editors and Contributors
4 Standard Treatment Guidelines

USER'S GUIDE
ACGIH - American Conference of Governmental Industrial Hygienists

Acute effect - with reference to chemicals. usually means a short exposure (5 24 hours) with an
immediate effect. I
ADI - Acceptable Daily Intake
Adverse Effect , change in morphology, physiology, growth. development or life span of an
organism resulting in:
- the impairment of functional capacity. or
. impairment in the capacity to compensate for additional stress, or
- an increase in susceptibility to the harmful effects of other environmental influences.'
BEl· Biological Exposure Indices
CAS - Chemical Abstract Service. A section of the American Chemical Society which assigns a
unique number to every chemical and publishes guides to chemical research. The CAS num-
ber is useful in overcoming confusion brought about by the many synonyms used for a single
substance. The number gives no information about the properties of the chemical.
Chemical Safety - The following steps can be taken to prevent and control workplace chemical
hazards:
identification of the hazard;
evaluation of the hazard and risk;
organization to prevent. control or eliminate the risk; and
controlling the hazard through specific actions.'
Hazard - the set of intrinsic properties of a chemical, mixture of chemicals or a process that.
under production. usage or disposal conditions. has the potential to adversely affect the cnvi-
ronmenl and the organisms therein. 1
Chronic effect - with reference to chemicals. usually refers to repeated exposure (>3 months)
with a long delay between the first exposure and note of adverse health effects.'
EPA - US Environmental Protection Agency
FAO ~ Food and Agriculture Organization of the United Nations
FDA ~ US Food and Drug Administration
IARC - International Agency for Reaseach on Cancer
IDLH - Immediately Dangerous to Life and Health
IPCS - International Program on Chemical Safety
Irreversible (permanent) effect - An effect that will have a lasting, damaging effect on the
body. even if exposure to the offending chemical ceases. An example is cancer caused by
chemical exposure. 1
JECFA - Joint Expert Committee on Food Additives
Latency period - The delay between the time of exposure and the onset of the adverse health
effect. I
LD~lI - Statistically derived single dose of a substance that can be expected to cause death in 50%
of animals tested."
Local effect - The harmful effect of a chemical at the point of contact or entry to the body. I
MCL - Maximum Contaminant Level
MCLG - Maximum Contaminant Level Goal
mg/m' - milligrams of the contaminant per cubic meter of air.
NIOSH - US National Institute for Occupational Safety and Health
Non-Adverse Effect - the absence of changes in morphology. growth. development. and life
span. Nonadverse effects do not result in impairment of the capacity to compensate for addi-
tional stress. They are reversible following cessation of exposure without detectable impair-
ment of the ability of the organism to maintain homeostasis. and do not enhance susceptibility
to the deleterious effects of other environmental influences.'
OCCUPATIONAL POISONING 5
Odor threshold - the concentration at which a substance can first be smelled by humans. It is
not a reliable way to ensure safety in the workplace since many chemicals are dangerous at
concentrations below the threshold. Furthermore. the capacity to smell varies greatly from
person to person. It can be affected by nose and throat infections or head injuries. Olfactory
fatigue or olfactory adaptation can occur when a person is exposed to a particular smell for
more than a few minutes and therefore a larger (and more dangerous) concentration may be
necessary for initial detection.'
OSHA - US Occupational Safety and Health Administration
PEL - Permissible Exposure Limit
Pesticides - any substance or mixture of substances used to control the presence of unwanted
organisms. The different chemical structures of pesticide compounds allow them to target a
certein species of pests. Their general names denote the type of organisms they control:
- acaricides spiders and ticks
- fungicides fungi
- herbicides weeds
- insecticides insects
- larvicides larvae of insects or other organisms
- miticidcs mites
- molluscicides snails
. rodenticidcs rodents such as rats and mice
Pesticides are not always selective. Those which tend to kill many types of organisms are
called broad-spectrum pesticides.
Pesticides are available as formulations. That is. they are composed of the active ingredient/s,
solvents. or other chemicals added to facilitate use. They may also contain impurities associ-
ated with the process of manufacturing. I
Ppb - parts of the chemical per billion parts of air or water; a ratio of volumes. 1 ppb::; I mcglL
Ppm - parts per million; I ppm is 1000 times more than I ppb; I ppm = I mcglml
Ppt - parts per trillion; I ppt is 1000 times smaller than I ppb.
PTWI I PTDI - Provisinnal Tnlerable Weekly I Daily Intake
REL . Recommended Exposure Limit
Reversible (temporary) effect - An effect that disappears if exposure to the offending chemical
ceases. Examples are contact dermatitis. headache and nausea from exposure to solvents.'
Risk - the expected frequency of adverse health effects arising from exposure to a chemical.
Estimates of risk may be expressed in absolute terms or in relative terms. The absolute risk is
the excess risk due to exposure. The relative risk is die ratio between risk in the exposed
population and risk in the unexposed. population.' Under certain circumstances. a "low risk"
may be acceptable to the people exposed. Safety standards attempt to define "acceptable
risk."!
Routes of Exposure - ways by which chemicals can enter the body:
inhalation (breathing in)
absorption (through the skin or eye)
ingestion (through the digestive system by swallowing chemicals or eating contaminated
food or drink); and
transplacental transfer (across the placenta of the pregnant woman to the fetus). I
Safety- the practical certainty that injury will not result from the substance when used in the
quantity and in the manner proposed for its use.' But because certainty cannot be achieved in
most circumstances. safely is defined as the extent to which a chemical may be used with a
minimum of risk or adverse health effects. Safety may thus be seen as a "socially acceptable"
level of risk.'
Systemic effect . The effect of a chemical on the organs and fluids of the body after absorption
and transport from the point of entry. I
Toxicity -thc capacity of a substance to cause harm or injury to a living organism. A highly toxic
6 Standard Treatment Guideline'
substance will damage an organism if administered in very small amounts; a substance of low
toxicity will not produce an effect unless the amount is very large. 2 Toxicity is defined in the
context of the following:
the quantity of a substance administered or absorbed (dose)
the route by which exposure to the chemical occurs (e.g .. inhalation. ingestion. absorp-
tion. transplacental transfer)
the duration of exposure to the chemical and the way the quantity administered is distrib-
uted in time (e.g., single dose. repeated doses)
the type and severity of injury. and
whether or not injury is temporary (reversible) or permanent (irreversible).'
TLVI T\VA • Threshold Limit Valueffime Weighted Average - the time-weighted average con-
centration for an 8-hour workday and a 40-hour workweek. at which nearly all workers are
exposed daily, without adverse effect."
UNEP - United Nations Environment Programme
WHO - World Health Organization
I IPCS, Users' manualfor the IPCS Health and Safety Guides. Geneva: World Health Organi-
zation. 1996.
2 International Programme on Chemical Safety (IPeS), Environmental Health Criteria # 6
Principles and Methods for Evaluating the Toxicity of Chemicals. Helsinki: World Health
Organization. 1978.
J International Programme on Chemical Safety (IPCS), Environmental Health Criteria # 170
Assessing Health Risks ofChemicals: Derivation ofGuidance Valuesfor Health-Based Ex-
posure Limits. Geneva: World Health Organization. 1994.
~ US Department of Health and Human Services. Case Studies in Environmental Medicine:
Lead Toxicity. Atlanta: Department of Health and Human Services. 1992.
5 Klaassen CD. Amdur MO. Doull J. cds .• Casareu and DOli" S Toxicology: The Basic Science
0/ Poisons, 5th ed. New York: Macflraw-Hill, 1996.
GUIDELINES ON FIELD MANAGEMENT
In the work· 1. RESCUE
Field rescuers must not contaminate themselves in the process of
place, assess- rescuing victims. They must wear proper protective equipment
ment of poten- such as gloves. full face mask and respirator or self contained
breathingapparatus. Employ a buddy system.
tial hazards Remove patient from area ofdanger or noxious stimuli. While trans-
should be done. porting the patient. take necessary precautions ifhead injury or
neck fractures arc suspected. Do not do resuscitation in the hot
zone.
Hazard zones
2. AIRWAY
should be All patients should be suspected of having a potentially compro-
classified: mised airway. Patients who are awake and talking arc likely to
have intact airways. but worsening intoxication can result in rapid
- "hot zone" loss of airway patency. In lethargic or obtunded patients, the gag
or cough reflex may give an indirect estimation of the patient's
. contamination ability to protect the airway.
reduction area If the airway is obstructed. place the patient in supine position and
apply the chin-lift and jaw-thrust maneuvers. Patients who are
. support area vomiting should be placed in the left lateral decubitus and
Trendelendberg position. If airway is still not patent. examine
the oropharynx and remove any obstruction or secretions. Air-
All poisoned way may be maintained with artificial oropharyngeal or nascpha-
patients should ryngeal devices.
Comatose patients should be intubated and mechanical ventilation
be treated as if initiated if equipment and trained personnel arc available.
they have a
J. BREATHING
potentially life- Poisoning patients may present with ventilatory failure. hypoxia or
bronchospasm. Ventilatory failure requires assisted ventilation
threatening which may be delivered manually with a bag-valve-mask or bag-
intoxication. valve-endotracheal tube device. Hypoxia requires oxygen supple-
mentation. Bronchospasm usually manifests as wheezing with
cyanosis and may also be treated with oxygen supplementation.
Remove patient from exposure to any noxious agent. If trained
personnel and medications arc available. patient may be given p-
ngcuists or epinephrine.
Note: Oxygen may be contraindicated in the initial management of
poisoning from paraquat and phosphides.
4. CIRCULATION
Check blood pressure. pulse rate and rhythm. If hypotension is
noted. elevate the legs about 15 em to increase venous return to
the heart. .
Perform cardiopulmonary resuscitation if there is no pulse or de-
tectable heartbeat. Secure venous access and' begin intravenous
infusion if equipment is available.
Hypotensive patients: Normal Saline
Crystalloid solutions

Adult maintenance: Normal Saline
D,NR
Pediatric maintenance: D,O.3NaCI
5. DECDNTAMINATION
Dermal Decontamination
Remove all items of clothing and thoroughly bathe patient with
alkaline soap and ' vatcr.
Evc Decontamination
Irrigate eyes with free flowing water for thirty minutes. Remove
contact lenses. Do 110t instill ophthalmic agents.
Gastric Decontamination
Generally. emesis may be done if antidotes arc unavailable and
the nearest medical facility is inaccessible.
Mechanical emesis is performed by instructing the patient to take
one to two glasses of warm water. Vomiting is then induced
by applying pressure on the posterior pharynx with a blunt
instrument.
Kinchay (Apium graveolcnss may be used as an emetic. Pound
the kinchay and instruct patient to take one tablespoon of the
juice from the herb. followed by one glass of warm water.
Comraindications to inducing emesis include:
depressed sensorium or impaired gag reflex Diazepam
late pregnancy Adult: 5 mg IV push
ingestion of caustics. hydrocarbons. convulsants, Pedia: D.3 mg/kg IV
arrhythmogenic agents May berepeated q' 2 . 5
presence of cardiac disease or aneurysm minutes up to 20 mg
total dose.
6. DRUGS Intubation may have to be
Severe acute encephalopathy can present with seizures. If trained done prior to giving
personnel and medications an: available. diazepam. phenytoin or additional doses.
lorazeparn may be given.
Phenytoin
7. TRANSPDRT Adult: 15·2D mg/kg IV
Bring patient to the nearest hospital. Take necessary precautions lD then 10D mg PD
for patients suspected of having head injuries or neck fracture. or IV q' 6·8h
Know the offending agent and inform receiving health person- ""dia: 15·2D mglkg IV
nel. lD then 5·7 mglkg in
3 divided doses q'
8h
May begiven for
uncontrolled seizures.
Administer at a rate of 1
mglkg/min or25 mgl
min.
lorazepam
Adult: 2 mg or D.04 mgl
'kg (whichever is I
lowerl
Pedia: 0.04 mglkg
Compatible with D~ W
OCCIIPATIONAl POISONING 9
GUIDELINES ON HOSPITAL MANAGEMENT
Clinical History 1. AIRWAY

1. Identification of Assess the patient's airway patency and determine the need for arti-
chemicals ficial airway devices or intubation. In patients that present with
2. Time of exposure coma. respiratory insufficiency, impaired gag reflex, or status
Mode of exposure epileptic us. intubation should be done and mechanical ventila-
4. Circumstances tion initiated.
surrounding
poisoning 2. BREATHING
5. Pre·existing medical Ifthere are signsof inadequate oxygenation, determinearterialblood
illnesses gases. Find out the nature of the oxygen deficiency:
6. Current medications Ventilatory failure- Start patient on mechanical ventilation.
7. Ba.ali•• heaith data Hypoxia - Start oxygen supplementation and determine depth of
8. Work environment or hypoxia with ABGs. Treat accordingly.
practices I use of Bronchospasm - Provide oxygen supplementation. J3-agonists or
personal protective epinephrine may be given.
equipment Note: Oxygen maybe contraindicated in the initial management of
9. Home remedies or paraquat and phosphide poisoning.
first aid administered
' - - - - - - - - - ' 3. CIRCULATION
Start intravenous fluid infusion with the following fluids:
Hypotensive patients: Normal Saline
Crystalloid solutions
Adult maintenance: Normal Saline
D,NR
Pediatric maintenance: D~0.3NaCI
lf there is persistent hypotension. give fluid chalJege with 200 ml of
normal saline for adults or 10 ml/kg of D50.3NaCI for children.
In cases of severe poisoning, a central venous line may be neces-
sary to monitor hydration status. Dopamine may be started if
hypotension cannot be corrected. Start at low doses to ensure
good urine output (1.0-2.5 mcglkg/min) then slowly increase to
maintain blood pressure.
4. OECONTAMINATION
Continue decontamination started in the field.
Dermal Decontamination
(See Field Management Guidelines)
Hospital Eye Decontamination
(See Field Management Guidelines)
personnel Gastric Decontamination
should wear Do not induce emesis unless there are no other decontamination
modalities available.
gloves and face Gastric lavage is generally safer than inducing emesis ifperfonned
mask when properly. Insert a nasogastric tube of appropriate size for the
patient's age. Infuse 50-60 ml (Podia: 10-20 mil tepid or luke-
handling warm water per NGT. After a few minutes. place patient in
poisoned Trendelenberg position and allow water to drain completely.
This procedure is contraindicated ill ingestion ofcaustics or kero-
patients. sene, and in the presence offrank seizures. Make sure the pa-
tient does not aspirate. Protect the airway accordingly. Charcoal Lavage
Charcoal lavage is useful in certain cases of poisoning by decreas-
Activated charcoal
ing absorption of some toxic substances. This is most effective if lAC)
10 parts activated charcoal (AC) is given for every I part poison Adult: 50·100 grams in
ingested. 200 ml water asa
Serial AC lavage may be administered with toxicants which undergo slurry
enterohepatic recirculation (e.g., organochlorines). See specific Pedia: 1 gm/kg in
treatment guidelines regarding its efficacy. proportionate
Alwaysfollow charcoal lavage with cathartics such as sodium sul- amount of liquid to
fate after the first dose ofAC and after the 4th dose in repeated make a 50%
charcoal lavage. suspension.
Give slurry per NGT
5. DRUGS while patient isin
For seizures Trendelenburg and left
Assess as to cause and treat accordingly. Diazepam, pheny- lateral decubitus
toin or lorazepam may be used (see Field Management Guidelines
position.
for dosages). Prevent recurrences.
Antidotal Therapy
Sodium Sulfala
Antidotes are often unnecessary especially if the appropriate Adult: 15gms in 10D
supportive treatments are given. Factors such as the patient's clini-
ml water
cal status. amount of toxic substance in the body, and the pharma- Pedia: 250 mg/kg
codynamics of the substance, dictate whether administration of an
given asa 10%
antidote is beneficial. solution
If there isno bowel
Antidotes movement within an
Arsenic DMSA. Dimercaprol. Penicillamina DMPS hour, another dose of
Benzene none sodium sulfate may
Cadmium EDTA. DMSA be given.
Carbamates Atropine Sodium containing
Carbon Monoxide none cathartics are
Cyanide Sodium sulfate and Sodium thiosulfate, Oxygen, contraindicated in
Hydroxocobalamine patiens with
Hydrogen Sulfide Sodium nitrite congestive heart
Lead DMSA. Penicillamina EDTA. NAPA failure.
Mercury DMSA. DMPS, NAPA, Penicillamine
Organochlorines none
Organophosphates Atropine, Pralidoxime
Paraquat Magnesium sulfate
Pyrethroids none
Rodenticides
zinc phosphida N·acetylcysteine
Styrena none
Toluene none
Trinitrotoluene none
OCCUPATIONAL POISONING /I
GUIDELINES ON
OCCUPATIONAL TOXICOLOGIC INTERVENTIONS
EMPLOYEE HEALTH MONITORING
Employees at risk of exposure should undergo annual medical evaluations. Monthly exami-
nations maybe requiredfor those at highestrisk, with particularattention given to signs and
symptomsof chronic poisoning. Confirmatory laboratory testing should be done as neces-
sary. Medica) records have to be meticulously kept for documentation of chronic effects.
HEALTH PERSONNEL ANO EMERGENCY FACILITIES

In general, the suggested composition of health personnel includes a first-aider, a part-time
occupational health nurse with previous training in handling poisoning, and an occupa-
tional health consultant. Adequate hospital facilities with trained personnel for handling
emergency poisoningshould be no morethan 5 krnaway, if situated in an urban area, or no
more than 25 minutes away by travel, if situated in a rural area. Arrangements must be
made between the company and the hospital for emergency cases.
HANOLING PRECAUTIONS
Properpersonal protective equipmentshould be madeavailableto employees. The equipment
should be cleaned immediately after use, tested regularly for effectivity and replaced as
necessary. Employees should be trained in the proper use of these equipment. The recom-
mended personal protective equipment varies with the type of toxic substance used. For
most purposes, the following equipmentare recommended:
overalls madeof double-weave cotton or cotton mixedwith polymerwith no pockets
or collars, long-sleeved, and fastened at the wrist and neck
safely helmetsor hard hats where injuryfrom fallingequipment is possible; washable
cotton cap if dusts and sprays are used
gauntlet gloves made from PVC, nitrile, or synthetic rubber (not natural rubber) to be
worn insidethe long sleeves
boots of similar material as the gloves to be worn insidethe overalls
face shields or goggles, as necessary, to prevent splashes
facemasksto prevent inhalation of dusts or vapors mayrange fromsimple dust masks
to full-face maskswithcanisterrespirators dependinguponthe conditionsin the work-
place
Usetoxic compoundsin a well-ventilated place. Makecertainthat sprayis not carriedby wind
toward the person sprayingor toward unprotected persons in the area. If exposureoccurs,
immediately clean the contaminated part of the body with soap and water.
Changingand washingfacilities equippedwith warm and cool watershould be provided. The
"dirty" room for washingshould be separated from the clean area in such a way that only
workerswho have showered after work can exit through the clean area.
Wash hands and face before smoking or eating. Work clothes should not be brought home.
Mixing implements should be separate from utensils used in preparingfood.
An emergency showershould be built within easyaccess(about S meters)from the hazardous
areas. Access to the shower should alwaysbe open. Showersshould drain into a contain-
ment area for contaminated sewage. Water should be availableduring working hours and
checkeddaily prior to start of operations.
Eye wash bottles or taps should be similarlyavailable and accessible in case of eye splashes.
STORAGE
Store compounds only in the original containers - never in containers for food, beverage.
animal feed, or seeds. Store compounds in rooms or storage areas that can be locked and
12 Standa,d T,.atmant Guidalin..
are not accessible to children. Keep substances away from food. animal feed. and seed
storage areas.
Self-scaling drums can be used for most toxic substances to prevent leakage.
SPillS
If a spill occurs during transport. alert the company and warn other traffic to keep away from
the area. Contain the spill by covering it with an absorptive material or earth while practis-
ing safety precautions. Do not allow materials to enter drainage systems or waterways.
Minimize absorption of material into the ground. Collect the absorbed spill. broken con-
tainers and all contaminated waste. Place them in properly labeled metal containers or
strong plastic bags. Ensure proper disposal of the contaminated material.
If a spill occurs at a warehouse or factory. do not hose down spills. Do not allow the toxic
materials to enter drainage systems or waterways. Liquid formulations should be collected
using absorbent material (sawdust. limc, sand, earth). The area ofthe spill should be scrubbed
with water and strong soap/detergent. Contaminated materials should be collected and
placed in marked metal or strong plastic containers and disposed of properly.
Solid formulation particles (dust. wet powders and granules) should be swept carefully to
avoid spreading them into the air. Sprinkling of damp sand or sawdust onto the spilled
particles can prevent this. The area of the spill should be scrubbed with water and strong
soap. Contaminated substances should be scaled in properly labeled metal containers or
strong plastic bags. Make sure the substances are disposed of properly.
LEAKS
Repack leaking material in a strong container made ofthe same materials as the original con-
tainer. Place small leaking containers in a large open-top drum.
REFERENCES
American Conference of Governmental Industrial Hygienists. Threshold Limit Values/or Chemical
Substances and Physical Agents and Biological Exposure Indices. Cincinnati: 1990.
Dreisback RH and Robertson WO, Handbook ofPoisoning. 12th edition. Prentice Hall lnterna-
tional, Inc.. 1987.
Ellenhorn MJ et al.. Ellenhorn s Medical Toxicology: Diagnosis and Treatment ofHuman Poi-
soning. 2nd edition. Baltimore: Williams and Wilkins. 1997.
Goldfrank RL ct al., Gold[rank s Toxicologic Emergencies 5th ed. Norwalk: Appleton and
Lange. 1994.
Gosselin et al., Clinical Toxicology ofCommerciol Products. Baltimore: Williams and Wilkins
Co.. 1976.
Haddad LM and Winchester JD, Clinical Management of Poisoning and Drug Overdose. WB
Saunders Company. 1990.
Olson KR. ed.. Poisoning and Drug Overdose. Norwalk:, Appleton and Lange. 1994.
Oudcjans JH. Agro-Pesticides: Propertiesand Functions in Integrated Crop Protection. Bangkok:
United Nations Economic Council and Social Commission for Asia and the Pacific. 1991.
So LS, Panganiban LCR. Makalinao. JR. cds.. Targeting the Poisoned Patient: II Manual of
Clinical Toxicology. Manila: National Poison Control and Information Service. 1997.
ARSENIC
CHEMICAL NAME SOURCES
ARSENIC wood preservative
Arsenite non-ferrous alloy
Arsenate manufacturing
pesticide
CHEMICAL FORMULA rodenticide
As herbicide
As(IlI) = Arsenite glassware manufacturing
As(V) = Arsenate veterinary antihelminthic
anti·fungal component iA
SYNONYMS paints and wallpaper
CAS number 7440-38-2 pigment production
semi-conductor
CLASSIFICATION manufacturing
Element folk remedies and tonics
trivalent (-3 or +3)
water runoff from volcanic
pentavalent (+5)
ash
PHYSICAL STATES
Solid, liquid and gas
PHYSICAL AND CHEMICAL PROPERTIES

Solid form of arsenic: gray, metallic crystals. Reacts with acids, oxidizing agents and halo-
gens, producing toxic fumes. Finely dispersed particlescan form explosive mixtures in air.
Arsine: colorless compressed liquefied gas with a characteristic odor. Most toxic form of
arsenic.
HAZARDS
Arsenic compounds are classified as very potent poisons. Toxicity ranking from the most
. toxic: arsenic gas, trivalent inorganic arsenites, inorganic pentavalent compounds, and
pentavalent organic compounds.
Evaporation at 200c is negligible. but it can react with acids, oxidizing agents and halogens,
producing toxic fumes.
Arsinegas is heavierthan air and maytravelalong the ground. Flowor agitation maygenerate
electrostatic charges resulting in ignition. Heating, light or moisture can decompose ar-
senic, producing toxic fumes.
Arsine may react with strong oxidants, fluorine, chlorine, nitric acid or nitrogen trichloride,
causing fires or explosions.
A harmful concentration in air may be reached very quickly if there is loss of containment.
Carcinogenicity Potential
Arsenic is a known human carcinogen because of its c1astogenic effects. Chronic inhalation
of compoundsof lowsolubility(e.g., galliumarsenide,calciumarsenate,elementalarsenic)
may increaserisk of lung cancer due to longertissue retention. Chronic ingestionmay also
increasethe risk of liver,kidney, bladderand even lung cancer. Skin cancer (intraepithelial
squamous cell carcinoma) mayalso develop with chronic exposure of up to 40 years. Leu-
kemias have been reported.
Teratogenicity Potential
Human data on the teratogenicity of inorganic arsenic are very limited. Studies in Sweden
i"nvolving children bornto womenwhoworkedduring pregnancy at a copper smeltershowed
a significantly higher frequency of congenital malformationsamong those whose mothers
were exposed to genotoxic substances including airborne arsenic and lead. Incidence of
congenital malformations was twice that of other children in the region. There was also a
five-fold higher frequency for multiple malformations. An earlier study around the same
site showed a significantly higher incidenceof abortions.
Animal studies have established the embryotoxicityand teratogenicity of arsenite in mice.
TOXIC DOSE
Trivalent arsenic is 2-10 times more toxic than pentavalent arsenic. The lethal dose oftriva-
lent arsenic in adults ranges from 100·200 mg. Ingestion of 1-2.5 mg/kg is lethal in the
pediatric age group. Chronic ingestion of 20-60 meg/kg/day in children (or 1-4 mg/day in
adults) may producesymptoms of chronic poisoning.
Arsinegas is the most toxic form of arsenic. Exposurefor 30 minutesat levelsof25 to 50 ppm
is lethal. Exposureat 100 ppm causes death in less than 30 minutes while exposure at 250
ppm may be instantly lethal.
EXPOSURE LIMITS
Air Arsenic Arsine

Arsenic inhaled per nV·TWA (my/m'l 0.01 0.05 (ACGIH 19901
day in unpolluted PEL (my/m'l 0.002 (OSHAI 0.002
areas is about 10LH 100 mg/m' 6 ppm
0.05mcg or less AOI PTWI 0.015 my/kg (JECFA 19881
(assuming that Calcium andlead A,sa.ata No AD! (1968)
about 20m3 of air is
inhaled per day).
Smokers inhale a larger amount of arsenic. The content of arsenic in tobacco grown on soils
not treated with arsenic compounds is usually below 3 mg/kg (or approximately 3 mcg per
cigarette), 10-15%of which have been recovered in main stream smoke, and the remainder
largelybeing distributed in the ash and butt. With the use of arsenic containing pesticides,
levels went up to as high as 52 mglkg in the 19505. At present, concentrations have de-
creased to below 8 mglkg due to the reduction in the use of these pesticides.
Drinking water
Drinking water MeL 0.05 mglL
Intake is estimated at 10 meg/day.
Surface water
The arsenic content of surface waters in unpollutedareas variesfrom 2.5-10 mcglL. Sea-water
contains from 1-8 mcgIL.
Food
Total daily intakefrom food is around45 megin adultsalthough it is higherwith a predomiantly
seafooddiet. Seafoods mayhaveas muchas 100mg/kg.Marine fish on the averagecontain
below 5 mg/kg wet weight. Edible seaweed has been reported to contain levels ranging
from 19-172 mg/kg. Marine organisms may contain large amounts of arsenobctaine, a
trimcthylated non-toxic compound which is excreted unchanged in the urine.
Plants grown on pesticide-free soils showed an arsenic content varying from 0.01-5.0 rnglkg
dry weight, while plants treated with arsenic show considerably higher levels, particularly
in the roots.
Soil
Uncontaminated soils contain arsenic levels between 0.2 and 40 rnglkg.
O~CUPATIONAL POISONING 15
TOXICOKINETICS
Absorption
Absorption from oral ingestion is almost complete. Absorption from the lungs depends on
particle size and chemical form of arsenic. Soluble forms of trivalent and pentavelent ar-
senic arc almostcompletely absorbed.
Distribution
Urine levels of total arsenic increase dramatically after chelation therapy. indicating that the
body stores arsenic if treatment is not instituted. It is possible that protein complex forma-
tion. which serves as the initial protectve mechanism, produces a depot or reservoir of
arsenic in the body since methylation and excretion of the complexes proceed slowly.
Arsenic can concentrate in nails and hair. and has a predilection for skin. It is also found in
human milk which contains around 3 mcg/L.
Excretion
Excretion is mainly via the urine.
Biological halflives:
inorganic arsenic (ingested) 10 hours
methylated arsenic 30 hours
Around 50-80% of inorganic arsenic is excreted in 3 days.
Arsenic can also be excreted from sweat and desquamation of skin.
MECHANISMS OF TOXICITY
When there is a surge of arsenite uptake, the initial protective mechanism of the cell is protein
binding. Arsine gas enters RBCs and forms a complex with oxygenated hemoglobin, re-
sulting in massive hemolysis. Animal studies show that the protein complex contains glu-
tathione, decreasing its detectable levels in the blood.
Arsenic disrupts enzymatic reactions vital to cellular metabolism. Trivalent arsenic (arsenite)
interacts with sulfhydryl groups of proteins while pentavalent arsenic (arsenate) substitutes
for phosphate.
It has been proposed that oxidative reactions cause RBe damage. Both arsenite and arsenate
decrease or uncouple mitochondrialoxidative phosphorylation. In arsenic poisoning. mito-
chondrial ATPase activity is stimulated, leading to the distortion of mitochondrial mem-
branes. Mitochondrial respiration is also inhibited through the suppression ofNAD-linked
substrates (pyruvate. glutamate, and a-ketoglutarate, in particular) by the reaction ofarsen-
ite with the dihydrolipoic acid cofactor needed for oxidation of the substrate. A depression
hi the activity of succinic acid dehydrogenase has also been demonstrated.
The most common cause of death is renal failure due to hemoglobinuria or the direct toxic
effects of the arsine-hemoglobin-haptoglobin complex deposited in the renal tubular cells.
Aside from protein complex formation. another detoxification pathway for arsenic is methyla-
tion to monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA). Animal studies
show that there are species differences in the ability to methylate arsenic. The lack ofMMA
methyltransfcrascs may have been an evolutionary advantage for animals exposed to
trypanosomal diseases since trivalent arsenic inhibits trypanothione reductase. causing a
lethal deficiency in trypanosomes. It is possible that similar genetic polymorph isms are
present among humans since different populations appear to have varying rates of MMA
formation.
More soluble arsenic compounds arc generally better absorbed after ingestion.or inhalation,
causing greatest risk for human intoxication. Inorganic arsenic dusts (such as arsenic triox-
ide) are direct irritants of the skin, mucous membranes, and respiratory and gastrointestinal
tracts. Systemic poisoning can also occur after percutaneous absorption.
The body is able to develop tolerance to large doses of inorganic arsenic if there is prior
exposure to small doses. This was seen among populations which used arsenious acid as a
/6 Standard Treatment Guidelines

health tonic. The mechanism of tolerance has not been elucidated. There is increasing
evidence that arsenic may be an essential element for humans.
TOXIC EFFECTS
Onset of Effects/Death
Symptoms of intoxication from arsenic appear within 10 minutes to several days after inges-
tion. There may be a delay in the appearance of symptoms if the arsenic is taken with food.
Exposure to 100 ppm of arsine gas causes death within 30 minutes. Odor threshold is
approximately 0.5 ppm.
TOXIDRDMES
ACUTE ARSENIC EXPOSURE
Ingestion
Cardiovascular: Initial vasodilation resulting in fluid transudation and acute circulatory col-
lapse. Decreasing cardiac preload then induces a reflex arteriolar constriction resulting in
peripheral cyanosis. Directly toxic to the heart; causes myocardial depression resulting in
decreased cardiac contractility. Voltage irregularities include QTc prolongation and T wave
inversion; rarely. atypical ventricular tachycardia (torsades des pointes) or ventricular fi-
brillation. Directly toxic to veins; gangrene may occur.
Gastrointestinal: Dilation of splanchnic vessels. causing submucosal vesicle formation and
hemorrhagic gastroenteritis. resulting in a protein-losing enteropathy. Fulminant gastroen-
teritis presents as abdominal pain. dysphagia. nausea and vomiting, bloody or rice-water
diarrhea. Garlic odor on breath and salivation may be present.
Hepatic: Jaundice secondary to fatty infiltration of the liver.
Neurologic: Cerebral edema may lead to headache. lethargy. delirium. coma. and convul-
sions. Peripheral neuropathy and hyperthermia may also be present.
Renal: Acute tubular necrosis. renal failure.
Inhalation
Neurologic: Headache. weakness. giddiness.
Pu lmonarv: Chest pain. cough.
Dermal Absorption
Integument: Palmar erythema. local edema. hyperkeratosis. hyperpigmentation. pyoderma.
Bowen's disease. alopecia and brittle fingernails. Mec's lines (transverse white striae in the
nails) may appear as later sequelae. May be absorbed through the skin. causing systemic
symptoms.
Transplacental Exposure
Placental transfer occurs: cord blood levels or arsenic are similar to maternal levels. A study
reported a case of ingestion of 400 mg of arsenic on the 3,d trimester of pregnancy. This Jed
to fetal death. assessed to be due to destruction of nprmal placental function.
ACUTE ARSINE GAS EXPOSURE

Latent period 01'2·24 hours with initial complaints of headache. lightheadcdncss. malaise. and
weakness: followed by onset of abdominal pain. hemolysis and renal failure.
Cardiac: Congestive heart failure
Gastrointestinal: Nausea. vomiting. diarrhea and abdominal pain predominate.
Hematologic: Arsine gas combines with hemoglobin in RBCs to produce severe hemolysis.
Hyperkalemia. anemia and hemoglobinuria as a result of hemolysis within a few hours.
Subsequent bronze-colored skin or jaundice may be severe.
Integulllent: Contact with liquid form causes frostbite.
Neurologic: CNS symptoms such as headache.
OCCUPATIONAL POISONING /7
Pulmonary: Pulmonary edema not apparent in the first few hours. Onset is associated with
and aggravated by physical effort.
Renal: Renal failure due to myoglobinuria or renal conversion of arsenate to a more toxic
arsenite form. An arsine-haptoglobin-hemoglobin complex is formed in the kidneys and is
difficult to remove. even with forced diuresis. Acute renal failure is frequent and often
fatal, occurring 1·3 days after exposure. Oliguria hematuria and proteinuria result from
acute tubular necrosis and renal cortical necrosis.
CHRONIC EXPOSURE
Dermal: Dermatitis manifesting as hyperkeratosis, warts and melanosis localized to the most
heavily exposed areas. Papular keratosis. ulcerative lesions, localized edema. pruritus, viti-
ligo. and alopecia have been described. Chronic exposure (up to 40 years) may cause squa-
mous cell carcinoma.
ENT: Mucous membrane lesions. nasal and oral tract irritation. stomatitis, lacrimation. sali-
vation, garlic odor on breath. and nasal-septal perforation.
Gastrointestinal: Nausea. vomiting. diarrhea and vague abdominal pains.
Hematologic: Bone marrow suppression manifesting as hypoplasia. anemia (occasionally
megaloblastic). leukopenia, thrombocytopenia, and leukemia.
Hepatic: Hepatomegaly. jaundice and angiosarcoma.
Neurologic: Resorption of myelin and destruction of axis cylinders leading to a distal sym-
metrical sensory neuropathy followed by muscle atrophy. Neuropathy occurs from any
route of exposure; generally involves long nerves of the legs. with paresthesia and loss of
vibratory or position sense. Delirium, coma and seizures can be present. Wernicke-like
encephalopathy may develop. Hearing loss and learning impairment have been observed in
chronically exposed children.
Pulmonary: Lung cancer
Renal: Proteinuria, casts. pyuria and hematuria.
SPECIMEN AND EXAMINATIONS FOR DIAGNOSIS

Arsenic
Urine for arsenic levels
Biologic limit: <50 mcg124 hr specimen
In the first 2-3 days after acute poisoning, may obtain values> /ODD meg and can remain
elevated for weeks.
Whole blood for arsenic levels
Biologic limit: <3 mcgldL
Elevated in acute poisoning but declines rapidly to normal.
Hair and nail clippings for arsenic levels
Biologic limit: <I mcglg
May be persistently elevatedfor months after urine levels normalize.
Rule 0111 external contamination.
Blood for esc
Blood for peripheral blood smear - may show basophilic stippling
Abdominal X-ray may detect radiopacities
Others: electrolytes, glucose. BUN. creatinine. liver enzymes, CPK, urinalysis. ECG,
chest X-ray
Arsine
Urine for arsenic levels
Biologic limit: <50 mcgl2-1 hr specimen
Whole blood for arsenic levels
Biologic limit: <3 mcgldL
Greater than OAmglL concentrations are associated with fatal cases.
/8 Standard Treatmant Guidelines

Blood for plasma free hemoglobin levels
Oimercaptosuccinic
Exceed 2g/dL in acute poisoning
acid (DMSAI
Blood for haptoglobin levels - decreased
10 mg/kg/dose PO q' 8
Blood for CBC - may show acute anemia
hours for5 days
Blood for peripheral blood smear - may show anisocytosis and
fragmented red cells then 10 mg/kg/dose
Urine for routine urinalysis- may show hemoglobinuriawith few PO q' 12hours for
intact RBCs another 5 days.
'Others: Blood type (cross match if needed), BUN, creatinine Not advisable if patient
presents with
ANTIDOTES gastroenteritis and
Penicillamine. Dimercaprol. Dimercaptosuccinic acid splanchnic edema
since gut absorption is
TREATMENT limited.
EMERGENCY FIELD MANAGEMENT (See Guidelinesl Itmay beused after an
1. Rescue acutely poisoned
2. Airway patient has been
3. Breathing stabilized, Dr in cases
4. Circulation ofchronic poisoning.
~. Decontamination
6. Drugs Dimercaprol
J. Transport Mild to moderate
poisoning
EMERGENCY HOSPITAL MANAGEMENT (See Guidelinesl 2 to 3 mg/kg/dose 1M
1. Airway q' 6 hours for 24
2. Breathing hours
3. Circulation then q'12 to 24
lf there is prolongationofQT intervals,avoid type la antiarrhyth- hours for 10days.
mic agents such as quinidine and procainamide. Severe poisoning
In arsine gas poisoning.hemolysis mayoccur, necessitatingblood 3 to 5 mg/kg/dose 1M
transfusion. If gas poisoning is severe, considerexchangetrans- q' 6 hours for 24
fusion if the patient's hemoglobin is above 150 g/dl. Because hours
renal tubular necrosis is common, maintain an adequate alka- then q'12 to 24
line urine flow by giving bicarbonate, fluids and mannitol. hours for 10 days.
4. Decontamination
Gastric Decontamination - Gastric lavage using an NGT and wa-
Penicillamine
ter may be done, especially in large ingestions. Charcoat tav-
25 mg/kg/dose q' 6
age is ineffective and cathartics are contraindicated.
hours for 5 days.
5. Drugs
Maximum single dose
Chelation can be instituted with any of the recommended anti-
should not exceed 1
dotes. After the initial regimen, allow for a 5 day respite then
evaluate need for repeat chelation. Therapeutic endpoints are '--- gram. --'
not defined. Generally. once urinary arsenic levels are <500
rncg/L, endogenous processes (biomcthylation and detoxifica-
tion) may be able to remove the remaining substance and no
further chelation is necessary.
Penicillamine.Dimercaprol and Dimcrcaptosuccinic acid are not
useful for arsine poisoning.
6. Dialysis
Consider hemodialysis curly in the management of the patient if
there is concomitant renal failure. Otherwise. dialysis contrib-
utes minimallyto arsenic clearance.
Maintenance
Maintain on NPO until patient is fully conscious.
Maintain adequate hydration and parenteral nutrition while patient is on NPO.
Correct any electrolyte or pH imbalance.
Monitor ECG and cardiac rhythm.
Monitor hematologic parameters.
Monitor fluid intake. urinary output and renal function.
Monitor hepatic function.
Specific Problems
Cerebral edema: mannitol therapy
Seizures: diazepam or lorazcpam, phenytoin, mannitol
Circulatory collapse: fluids and vasoconstrictors
Cardiac arrhythmia: lidocaine or magnesium sulfate
Hcmatochczia. diarrhea or protein. losing enteropathy: fluid maintenance, consider transfu-
sion and protein supplementation
Severe jaundice secondary to hemolysis: consider phototherapy, phenobarbital, hemodialysis
or exchangetransfusion
Acute tubular necrosis, hematuria or proteinuria: fluid maintenance, mannitol, diuretics and
consider dialysis
OCCUPATIONAL TOXICOLOGIC INTERVENTIONS (See Guidelinesl
HAZAROS TO THE ENVIRONMENT ANO THEIR PREVENTION

Arsenic levels are increased in areas around coal-fired power plants or smelters where coal
with a high arsenic content is used. Airborne arsenic levels of about I mcg/m', have been
detected in such areas. which would result in the inhalation of approximately 20 meg of
arsen ic per day.
Drinking-water can be severely contaminated through industrial operations particularly of
factories which produce arsenic compounds. Leaching can occur from coal preparation
wastes. Fly ash from coal-fired power plants may also contaminate uncovered sources of
water.
Arsenic formulating/utilizing plants should be situated away from populated areas and ground
water reservoirs. All arsenic containing compounds should be properly stored in self-
sealing drums 10 prevent leakage. These containers should be properly marked and stored.
Empty containers should be buried in a pit at least 50 cm deep in an isolated area away from
water supplies.
20 Standard T"atment Guideline.

REFERENCES
Aposhian HV • "Enzymatic methylation of arsenic species and other new approaches to ar-
senic toxicity," Annual Review of Pharmacology and Toxicology, Vol. 37. pp. 397-419.
1997.
American Conference of Governmental Industrial Hygienists. Threshold Limit Values for
Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati:
1990.
Dreisback RH and Robertson WOo Handbook a/Poisoning. 12th edition. Prentice Hall Inter-
·national.lnc., 1987.
Ellenhom MJ et at, £lIenhorn's Medical Toxicology: Diagnosis and Treatment of Human
Poisoning. 2nd edition. Baltimore: Williams and Wilkins, 1997.
Goldfrank RL et al., Goldfrank's Toxicologic Emergencies 5th ed. Norwalk: Appleton and
Lange. 1994.
Gosselin ct al., Clinical Toxicology a/Commercial Products. Baltimore: Williams and Wilkins
Co .• 1976.
Haddad LM and Winchester JD, Clinical Management ofPoisoning and Drug Overdose. WB
International Programme on Chemical Safety, Environmental Health Criteria Monograph #
18: Arsenic. Geneva: WHO. 1981.
International Programme on Chemical Safety & the Commission of the European Communi-
ties, International Chemical Safety Cards: Arsenic. IPCS, t 990.
Joint Expert Committee on tood Additives (JECFA) Monographs and Evaluations, Arsenic.
JECFA. 1988.
Klaassen CD, Amdur MO, Doull J. eds .• Casarett and Doul/'s Toxicology-The Basic Science
ofPotsons. 5th ed. New York: MacGraw-Hill, 1996.
Olson KR. ed., Poisoning and Drug Overdose. Norwalk: Appleton and Lange. 1994.
Department of Health
I I~I I I~I I il ~~ J',

0462
H~_.45 St2 1997
CARBAMATES
SOURCES
insecticides Discussion will concentrate on carbamate pesticides registered with the
fungicides PhilippineFertilizerand Pesticide Authority(FPA).
herbicides Thiocarbamates and dithiocarbamates have a different mode ofaction
nematocides and are not included in this discussion.
sprout inhibitors
CHEMICAL NAMES
Bendiocarb 1.3-benzodioxol- 4-yl, 2,2-dimethyl, methyl carbamate
Benamyl carbamicacid.]I-[(butylamino)-carbonyl]-IH- benzimidazole-2-yi]-,
methyl ester
Carbaryl I-naphthalcnylmethyl carbamate
Carbofufan 7-benzofuranol.2,3-dihydro-2,2-dimethyl-, methyl carbamate
Fenobucarb l-scc-butylphenylmethyl carbamate
Formetanate methanimidamide,N.N-dimethyl-N'- [3-[[(methylamino) carbonyl]oxy]-
phenyl]
Mathamyl ethanimidothioic acid,N -[[(methyl-amino)carhonyl]oxy]-, methylester
Oxamyl ethanimidothioic acid, 2-(dimethyl- amino)-N -[[(methyl-
amino)carbonyl]-oxy]-2-oxo-, methylester
Propoxur phenol, 2-( I -methyl ethcxy}. methyl carbamate
Thinphanate-methjl carbamic acid. methyl [1.2-phenylenebis-iminocarbonothioyl») bis-, dim-
ethyl ester
CHEMICAL FORMULAS
SYNONYMS
CAS Number
Bendiocarb
Bendiocarb
Oct
II
CH,NH-C-O
~ ,i 0\
0/ C(CH,I,
22781-23-3
Benamyl
r""'ir N
Benamyl 0NJLNH-C-OCH,
17804-35-2 I
Carbaryl O=C -NH-C.H,
63-25-2
Carbofuran
1563-66-2
Fenobucarb
Carbaryl
rt-g
CH,NH- C-O '1_"l.
BPMC ~ ,i
Formetanate
22259-30-9
Isoprocarb Carbofuran rt DD.
CH,NH-C-O
MIPC
Methamyl
16752-77-5 o (CH,),
o
Oxamyl
23135-22-0
Propoxur .
Formetanate 11-0
CH NH-C-O
, 'I "l. -N=CH-NICH)
"
114-26-1
o
Ihlopbenate-methvl
23564-05·8 Isoprocarb II
CH NH-C-O
, -0-
'I
"l. CHICH)
"
11 Standard Treatment GuidelinBs
o
II
Methomyl CH NH-C-O-N=C -SCH
, I'
CH,
o 0
II II
Oxamyl CH NH-C-O-N=C -C-NICH I
1 I n
SCH,
o
Propoxur 110-
CH J NH-C-O 'I_ ~ OCHICH J2I
S 0
II II
Thiophanate-methj!
(yNH-;-NH-t OCH,
~H-C-NH-C-OCH,
CLASSIFICATION
N-substituted esters of carbamicacid
PHYSICAL STATES
Solid and liquid
PHYSICAL ANO CHEMICAL PROPERTIES

Low vapor pressure: evaporate and sublimate slowly at usual room temperatures.
HAZAROS
Hazard classification for carbamates is based on the determined rat oral LD 50 •
Pesticides have been classified according to restrictions on use by the WHOIFAO/UNEP (See
Annex B)
Table 1. Fertilizer and Pesticide Authority IF PAl hazard classilicatio.
of carbamates based on rat orallDy"
Hazard Classification Rat Oral LO"lmg/kgl • solids

I poison 50 or less
II harmful 50·500
III caution 500·2.000
N . > 2.000
Table 2. The WHO recommended hazard classification of pesticides based on rat LOy.
RatLO"lmg/kgl
Hazard Classification Oral Oermal
Solids Liquids Solids Liquids
la Extremely hazardous :; or less 20orless 10or ~ss 40or less
Ib Highly hazardous 5·50 20 . 200 10 . 100 40 . 400
II Moderately hazardous 50 . 500 200 . 2000 100 . 1000 400 . 4000
III Slightly hazardous Over 500 Over 2000 OVOI 1000 Over 4000
0 Unlikelv to present acute hazard in normal use
----- -----
Table 3. Hazard cBtegory ofcarbamate pesticides usedin the Philippines

Carbamate Hazard Category
FPA WHO
Bendiocarb II II
Runomyl IV 0
Carbaryl II II
Aldicarb has been classied
Carbofuran I Ib as a restricted pesticide
Fenobucerb/BPMC III II by the FPA (see Annex AI.
formatanat_ I Ib
Isoprocarb/MIPC II II
Melhomyl I Ib
Dramyl I Ib
Propoxur II II
Thiophanat8·melhyl IV 0
Bendiocarb No effects on tumor profile ofmice.
Henomyl Dose-dependent increase in incidence of hepatocellular adenomas and car-
cinemas in mice.
Carbaryl Cannot be classified as to its carcinogenicity for humans. Animal studies
arc inadequate.
Carbofuran No evidence of carcinogenicity in rats. mice and dogs.
Methomyl No carcinogeniceffects in rats. mice nor hamsters.
Oxamyl No carcinogeniceffects in rats nor dogs.
Propoxur Note of hyperplasia, papilloma and carcinoma in the urinal')' bladder of fe-
male rats. No carcinogenic effects in mice.
Teratogenicity Pctentlal
Bendiocarb No teratogenic effects in rats nor rabbits.
Benomyl Teratogenic in mice: exencephaly. hydrocephaly. cleft palate. hydronephro-
sis. polydactyly. oligodactyly, umbilical hernia. fused ribs. fused verte-
brae and deformed tail.
Teratogenic in rats: microphthalmia, anophthalmia and hydrocephaly.
No teratogenicity in dogs. but with note of decreased testicular weight.
Carbaryl Teratogenic effects in dogs and guinea pigs at high doses.
Carbofuran No teratogenic effects in rats nor rabbits.
Methomyl No teratogenic effects in rats nor rabbits.
Oxamyl No teratogenic effects in rats.
Propoxur No teratogenic effects observed in rats and rabbits but there was note of
decreased fetal wdght and decreased food intake.
Table 4. Rat Oral LD§o of selected carbamates in their solid state

Carbamate RatorallO,. (mg/kg)
Bendiocarb 55
Benomyl + 10,000
Carbaryl 300
Carbofuran 8
Carbosulfan 250
FenobucarbfBPMC 620
Formetanate 21
IsoprocarblMIPC 403
Methomyl 17
Oxamyl 6
Propoxur 95
Ihicphanate-methvl +6.000
24 Standard Treatment Guideline.
TOXIC DOSE
Human LD50 may be estimated by dividing the rat LD511 values by a factor of 10 to 100 (Table
4).
EXPOSURE LIMITS
Carbamate nV·TWA PEL IOLH
Food (mg!m') (mglm') (mglm')
Bioaccumulation inthe foodchain Bendiocarb 0.2
occurs only to a limited extent.
Carbaryl 5 5 600
There is slightly greater accu-
mulation in fish. wheremetabc- Carbofuran 0.1 0.1
lism proceeds more slowly. Methomyl 2.5 2.5
Some carbamates are highly Propoxur 0.5
toxic to invertebrates and fish.
Generally. birds are not sensiti vc while bees are vcry sensitive to AOI(mg I kg BWl
toxic effects. Bendiocarb
Pesticide residues should be mon itored in agricultural products. 0-0.004 (1984)
Benomyl
Water 0-0.1 ( 1995)
May contaminate groundwater and subsequently, drinking water. Carbaryl
Early studies indicate that exp osure of the population is low, 0-0.003 (1996)
Carbofuran
S.il 0-0.002 (1996)
Canbe metabolized by soil microo rganisms. However, at high doses. Carbosulfan
microflora may be adversely affiected, thus limiting soil productiv- 0-0.01 ( 1986)
ity, Toxic to earthworms and other soil organisms but popula- M.thomyl
lions go back to normal levels quickly after cessation of pesticide 0-0.03 (1994)
use. Oxamyl
0-0.03 (1985)
TOXICOKINETICS Propoxur
Absorption 0-0.02 (1985)
Absorption is effective via the gas trointestinal and respiratory tracts, Ihlopbanate-methvl
but skin exposure is the main route of exposure for workers. Car- 0-0.02 (1995)
baryl applied to the forearm. for example. IS readily absorbed at
the rate of5% of the dose within 8 hours, and 74% after 5 days. The rate of skin penetration
by carbamates is influenced by other components of the pesticide formulation. Open
\v·ounds or abrasions facilitate absorption.
Distribution
Residues arc more readily detected in the liver. kidneys. brain. fat and muscle. Carbamatcs do
not bioaccumulate.
Metabolism
Biotransformation occurs via aryl- or alkyl oxidation. conjugation and hydrolysis. producing
more polar compounds with greater water solubility. Oxidation is carried out by mixed
function oxidase enzymes in the cytoplasmic reticulum of cells. The products of oxidative
metabolism (hydroxy-derivatives) arc conjugated and eliminated as 0- and N-glucuronides.
sulfides and mercapturates.
Excretion
Elimination is generally complete within 2-3 days for mammals. with the half life in the order
of3-8 hours. Around 80% is excreted through the urine. the rest in the feces. Animal studies
indicate that a variable fraction may be recovered from exhaled air.
MECHANISM OF TOXICITY
Effects on the central and peripheral nervoussystemsresult from increased cholinergicactiv-
ity.
Carbamates interfere with the action of acetylcholinesterase, the enzyme responsible for the
hydrolysis of the neurotransmitter acetylcholine to choline and acetic acid.
Acetylcholine is found in the autonomic nervoussystemand central nervous system. It is an
essential component of parasympathetic post- and pre-ganglionic synapses; sympathetic
pre-ganglionic synapses; and the neuromuscular junction.
Carhamatescause the carbamylation of the active serine-containing site of acetylcholinest-
erase. thus rendering it inactive. The consequent synaptic accumulation of acetylcholine
leads to continuous stimulation in the synapse and the onset of nicotinic, muscarinic or
central nervous system effects.
The mechanism of action of carbamates is similar to that of organophosphates. Generally,
however, carbamates are lesstoxicbecausethe regeneration rateof the carbamylated acetyl-
cholinesterase is relatively rapid compared with that of the phosphorylated enzyme result-
ingfromthe reactionwith organophosphates. Mostcarbamates also do not readilycrossthe
blood-brain barrier.
Carbamates cannot cause delayedtype neuropathy (OPIDN; see discussion on Organophos-
phales). Carbamatescan inhibit neurotoxic esterase (NTE), but since they are not able to
lose one alkyl residue(thus leavinga negativecharge on the molecule), they do not initiate
neuropathy.
Pesticides can cause disturbances in immune responses, decrease resistanceto antigens, and
increasethe likelihood of contractinginfectious diseasesor exacerbating pre-existing infec-
tions. Animal studieson aldicarband carbaryl, forexample, showdecreased T cell prolifera-
tive response; decreasedactivityof macrophages, neutrophilsand natural killer cells; and
variableeffects on humoral immunity and lymphocyte count. Carbamatesmay also affect
the immune system by binding or altering membrane-bound proteins on monocytes and
neutrophils. thereby suppressing their activity.
TOXIC EFFECTS
Onsel of Effects/Oeeth
Symptoms of intoxication from acuteexposure manifest within 2-10 hOUTS. Acetylcholinesterase
activityreturnsto normal within2 hOUTS post-exposure.
TOXIOROMES
ACUTE EXPOSURE
Sever-ity Syslem Involved l\1 anifestations
Mild Mainly Muscarinic Malaise, vomiting, nausea, diarrhea, sweating, abdomi-
nal pain, hypersalivation, miosis
Moderet. Muscarinic & Nicotinic Dyspnea, decreased muscular strength, bronchospasm,
bronchorrhea, speech impairment, muscle fasciculation.
tremor, motor incoordination, bradycardia, involuntary
urination/defecation, muscular cramps, hypotension,
hypertension
Severe Muscarinic, Nicotinic & eNS Coma, respiratory paralysis, extreme hypersecretion,
cyanosis, sustained hypotension, extreme muscle weak-
ness, muscular paralysis, convulsions, behavioral
changes
CHRONIC EXPOSURE
HearingMod eye problems, chroniccough,dizziness,headache, hypertension. aplastic anemia
and other relatedblooddyscrasia, photoallergenicity, and degeneration of liver, kidneysand
the testes.
26 Standard Treatment Guidalina.
l
Respiratory: Bronchospasm, wheezing, pulmonary edema. Dyspnea secondary to excessive
salivation and bronchial secretions. Chemical pneumonitis secondary to aspiration ofpetro-
lcum distillate carrier particularly in patients who present with vomiting or who have
decreased sensorium. In severe poisoning, muscle paralysis can contribute to respiratory
embarrassment. ARDS may occur in critical patients.
Neurologic: eNS manifestations occur in aldicarb, carbofuran or mixed organophosphate-
carbamatepoisoning.
Muscarinic:
dyspnea, cyanosis, pulmonary edema, anorexia, cramps, fecal incontinence, tenesmus,
hyperhydrosis. hypcrlacrimation, bradycardia, hypotension, miosis, urinaryincontinence,
bronchoconstriction, increased bronchial secretions
Nicotinic:
cramps, areflexia, muscle paralysis, hypertension, tachycardia, pallor, mydriasis
CNS:
restlessness. emotional lability, headache, tremor, drowsiness, confusion. slurred speech,
ataxia. generalized weakness, coma, convulsions, respiratory depression. cardiovascular
depression
Cardiovascular: Bradycardia in mild poisoning. Moderate to severe poisoning causes nicotinic
manifestations which result in tachycardia. Carbamates are arrhythmogenics.
Hepatic: Transient liver function and coagulation abnormalities.
Immunotoxicity: Increased incidence and severity of infectious disease; elicits hypersensitiv-
ity reactions.

5 ml heparinized blood kept at low temperature for red blood cell cholinesterase. Sampling
should be done immediately after the exposure. Samples should be stored refrigerated;
analysis and assay should be carried out as soon as feasible.
Normal values: n. 75-0.92 t:.pHIhour (Michel method)
Biofogicallimits:
RBC - 30% inhibition
Plasma - 50% inhibition
Whole blood - 30% inhibition
Classification of level of poisoning based on RBC cholinesterase determination
Mild poisoning: 20-40% depression
Moderate: 40-60% depression
Severe: >60% depression
200 ml urine (6 hour collection) for urine metabolitcls
Carbamate Urine metabolite
Carbaryl l-napthol
Propoxur Z-isopropoxyphenol
Carbofuran 2,3 dihydro-Zvl-dimethyl keso-I-hydroxy-benzofuran
Benomyl Carbendazim or its hydroxylated derivatives
blood for liver function tests, protimc
blood for high and low density lipoproteins, random blood sugar, electrolytes
blood for CBC with reticulocyte count
blood for AIlG
ECG
Chest x-ray
Atropine sulfate
The amount to be administered depends on the severity of the case.
Initial dosages are as follows:
Severity Dosage
mild Adult· 1 . 2 mg IV q'15 min
Padia . 0.01 mg/kg/doso IV q'15 min
moderate Adult· 2·3 mg IV q'15 min
Padia· 0.03 mg/kg/dosolV q'15min
sovero Adult· 3·5 mg IV q'15 min
Padia· 0.05 mg/kg/dosolV q'15min
Continue administering
atropine every 15 ANTIDOTE
minutes until the Atropine as physiologic antidote
following parameters
are reached: TREATMENT
heart rate ~ 140/min EMERGENCY FIELD MANAGEMENT ISoe Guidolinos)
pupils~ 4mm 1. Rescue
hypoactive bowel 2. Airway
sounds 3. Broathing
dry conjunctival and Patient should be removed from exposure to any noxious agent.
oral mucosa The patient may present with respiratory failure, hypoxia or
Parameters of 2/4 or bronchospasm. Respiratory failure requiresassisted ventilation
lower may indicate which maybedelivered manually witha bag-valve-mask or bag.
underatropinization. valve-endotracheal device. Hypoxia requires oxygen supple-
Dose and frequency of mentation. Bronchospasm, detected by wheezing with cyano-
atropine administration sis may be treated with oxygen supplementation and atropine
can be reduced by nebulization givenas I mg in 2 mlsalinesolution.
increments of 1 . 2 mg 4. Circulation
q' 2 . 4 hours if full 5. Decontamination
atropinization has been 6. Drugs
maintained for 3 to 4 . If trained personnel are presentand atropine sulfate is available,
doses. Upward or atropinization may be started.
downward titration is 7. Transport
done according to
patient's response. EMERGENCY HOSPITAL MANAGEMENT (Seo Guidelinos)
During maintenance 1. Airway
therapy, heart rate 2. Breathing
should not fall below If patient is cyanotic, detcnnine the nature of the oxygen defl-
6D/minute. In the ciency. If it is due to ventilatory failure, start mechanical venti-
lation. Ifit isdue to hypoxia, startoxygen supplementation and
elderly, beart rat~ of
determine depth of hypoxia withArterial BloodGas detennina-
SO·9D/min may be
tion. If bronchospasm is apparent, nebulize patient with atro-
sufficient.
pine I mg in 2 ml saline.
Cyanosis should be corrected prior to giving atropine IV since this
may cause ventricular fibrillation. Treat the cyanosis first and
give atropine1M until the patient's condition has stabilized.
3. Circulation
4. Decontamination
Gastric decontamination - Do not induce emesis unlessthereare no
otherdecontamination modalities available. Gastric lavage with
water may be done. Only a single dose of charcoal lavage is
28 Slnndnrd '"nlm..1 Guidnlinn!
necessary. A/waysfollow charcoal lavage with cathartics such as sodium sulfate.
5. Drugs
Seizures- Patients with moderate to severe aldicarb or carbofuran intoxication may present
with seizures and must be treated.accordingly.
Antidotal therapy with atropine.
Maintenance
Maintain on NPO until patient is fully conscious and atropine is given by oral route.
Maintain adequate hydration and parenteral nutrition while on NPO.
Correct any electrolyteor pH imbalances (metabolicacidosis).
Consider RBC transfusion in severe cases.
The followingdrugs should be avoided:
aminoglycosides
aminophylline
barbiturates
P-blockers
furosemide
local anesthetics- especially procaineand derivatives
morphine and other opiates
phenothiazincs
quinine
succinylcholine
sulfonamides
theophylline and other xanthines
Never give anticho/inesterases (e.g.. physostigmine. neostigmine).
Specific Problems
Pulmonaryedema: atropine I mg in 2 ml normalsaline solution as nebulization: furosemide I
mglkgldose for severecases .
Rhabdomyolysis: hydration, mannitol, sodium bicarbonate.
Seizures: diazepam or lorazepam. phenytoin. mannitol
Aspiration pneumonia: full antibiotic coverage until specific organism is identified; avoid
aminoglycosides .
Atropine toxicity: manifests as flushing, fever(temperature2: 39.SoC)and behavioral changes
in addition to the atropinizationparameters. If this occurs. temporarilydiscontinue or taper
atropinization and hydrate the patient. Consider administration of diazepam for possible
seizures.
Arrhythmia: Do not give Bbtockers or lidocaine. Instead, give calcium channel blockers or
phenytoin.
OCCUPATIONAL TOXICOLOGY INTERVENTIONS ISee Guideline.)

Employeesmust be educated on the possible health hazards posed by exposure to pesticides,
and the safety precautions which should be taken.
Regularmonthlymedicalevaluationsshould be done onthose at risk of exposure with particu-
lar emphasis on the neurologicexamination. Employeesshould be examined for signs and
symptoms of chronic poisoning with confirmatory laboratory testing done as necessary.
Regular monitoring of red cell cholinesterase should be done. depending on the duration.
frequency of exposure and type of job.
Medical records should be kept for at least 30 years due to the long latent period between
exposure and appearanceof ehronic effects.
Forcompaniesformulating categoryI and II pesticides, health personnelshould includea first-
aider. a pan-time occupational health nurse with previous training in handling pesticide
poisoning, and an occupational health consultant. This health personnel complement is
recommended for companies with 10 or less employees. For companies with II to 50
workers, the minimum required health personnel include a part time occupational health
physician, a full-time nurse and two first-alders.
Pesticidesare accompaniedby a hydrocarbon solvent that is often flammable. Fire extinguish-
ing agentsshould be readilyavailableand precautionsshould be taken to preventsparks that
may start fires.
Mix pesticides in a well-ventilated placeaway from homesand. Mixing implementsshould be
separate fromthe implementsused in preparingfood. When mixingand applying pesticides,
properpersonal protective equipment should be worn: face shieldsto protectagainstsplashes;
gauntlet gloves madeof nitrile, PVC, or synthetic rubber (not natural rubber); long sleeved
shirt with gloves worn inside the sleeves; boots made of the above materials worn inside the
long pants. The above equipment should be washed with soap and water after every use.
When applying the pesticide, make certain that the spray is not carried by wind toward the
person spraying, unprotected persons or homes. Do not allow family members to walk
through a newly sprayed field. Warning signs showing that spraying was done should be
installed, with the safe re-entry date specified. Ensure that well-water is not contaminated
by run-off from the fields being sprayed.
After applying pesticides, the worker should bathe with soap and water and change into clean
clothes. Washhands and face beforesmoking or eating,
Store pesticidesonly in the original containers- never in food, beverage,feed, or seed contain-
ers. Placethese in roomsor storageareasthat can be lockedand are not accessibleto children.
Store pesticides away from food, feed, and seed storage areas, preferably in self-sealing
drums to prevent leakage.
HAZARDS TO THE ENVIRONMENT AND THEIR PREVENTION

Soil microorganisms are able to hydrolyze carbamates but at high doses, soil rnicroflora arc
adverselyaffected, thus limiting soil productivity. Similarly, microorganisms in waterare able
to oxidize and hydrolyzecarbamatesto less toxic compounds but at high doses, carbamates
cause acute toxicity to aquatic life.
Agriculturallybeneficialorganismssuch as earthwormsand honey bees are particularlysensi-
tive to toxic effects.
Formulating plants should be sited away from populated areas and ground water reservoirs.
Dispersal of pesticides must be either by burying in a cemented pit with lime and sawdust to
prevent leakageinto ground water,or by incineratingat 1000oe. Emptypesticidecontainers
should be buried in a pit at least 50 cm deep in an isolated area away from water supplies.

c:.
l:l Tabl.5. Carbamate pesticides in the Philippines
~ Classification of
'"'=! Trade name Components Concentration Indication other components Manufacturer
~ 123 Household insecticide powder carbaryl household use lnt'l Pharmaceuticals Inc.
'"."
~
Baycarb 50 EC BPMC· 500g I liter agricultural Bayer Phils., Inc.
...5i!~ Baygon 20 EC
Baygon dust
propaxur
proporur
household use
household use
Bayer Phils.. Inc.
Bayer Phils.. Inc.
iii Baygon Aerosol evlluthrin household use Bayer Phils.. Inc.
'" OOVP··
propalur
organophosphate
pyrethroid
Baygon lIybait propaxur household use Bayer Phils., Inc.
Baygon hot fog ready us. prapuxur household use Bayer Phils., Inc.
BaygoR hot fog concentrate prupnxur household use Bayer PhiIs.. Inc.
BaygoR insect spray evlluthrin household use Bayer Phils., Inc.
OOVP·· organophosphate
propoxur pyrethroid
Baygon liquid waterbased killer propoxur household use Bayer Phils.. Inc.
tetramethrin pyrethroid
Baygon UlV propaxur household use Bayer Phils.. Inc.
Benlate 50 WP/OO Fungicide benomyl 500g/kg agricultural Ou Pont Far East, Inc.
Blattanex aerosol propoxuJ household use Bayer Phils., Inc.
Blattanex insect spray propaxur household use Bayer Phils.. Inc.
Brodan 31.5 EC chlorpyrifos 210 gIliter agricultural organophosphate Planters Products, Inc.
BPMC· 105 g I liter
Carbophen 6 G phenthoate 60 g I liter agricultural organophosphate Planters Products, Inc.
MTMC···
Carvil50 EC BPMC· 500 g Iliter agricultural Planters Products, Inc.
·BPMC: 1·sec·butylphenylmetbyl carbamate
"DDVP; 2.2·dicblorovinyldimethyl phosphate
...
- ·"MTMe: 4·tolylmethyl carbamate
~ Table 5. {continued} Carbamate pesticides in the Philippines
Classification of
Trade name Components Concentration Indication other components Manufacturer
Diacarb 50 EC BPMC· 500 9 I liter agricultural Transworld Trdg.
Oialuran 10 9 carbofuran lOOg/kg agricultural Transworld Trdg.
Iliafuran 3 9 carbofuran JOg/kg agricultural Transworld Trdg.
Oiaturan 5 9 carbofuran 50glkg agricultural Transworld Trdg.
Ilicarzul 20 SP tcrmetenete Hel 200g/kg agricultural Hoechst Phils.
Etrololan 50 WP isoprocarb 500 9 I kg agricultural Bayer Phils., Inc.
Ficam plus bendiocarb household use Thomas Cowan & Co., Inc.
pyrethrin pyrethroid
Ficam W bendiocarb housetIold use Thomas Cowan & Co.. Inc.
Furadan 10 G carbofuran lOOg/kg agricultural Bayer Phils., Inc./Marine Colloids Phils.
Furadan J G carbofuran JOg/kg agricultural Bayer Phils., Inc./Marine Colloids Phils.
Furadan 5 G carbofuran 50g/kg agricultural Bayer Phils., Inc./Marine Colloids Phils.
Garyox 20 WP bendiocarb 200g/kg agricultural Rhone·Poulenc Agro Chern. Phils., Inc.
Hoechst Phils.
Golden Marine Muscamone methomyl 1.00 9 I liter agricultural Sanofi Phil., Inc
Hopcin 50 EC BPMC· 500 9 I liter agricultural Hoechst Philippines
Hopkill50 EC BPMC· 500 9 I liter agricultural Zuellig Agrochem. Corp.
Hytox 50 WP MIPC·· 500g/kg agricultural Planters Products. Inc.
~ IMP Super Raid AE propoxur household use S.C. Johnson and Son, Inc.
"
l} permethrin pyrethroid
it neopynamin
:;t
IMP Super Raid L propoxur household use S.C. Johnson and Son, Inc.
=
..i permethrin pyrethroid
neopynamin
"
~
Lannate 40 SP methomyl 400g/kg agricultural Du Pont Far East, Inc.

~
i: ·BPMC: 1·sec-butylphenylmetbyl carbamate
..
~ --MIPC: isoprocarb
Table 5. (continued) Carbamate pesticides in the Philippines
Classification of
lannate 90 Insecticide rnethornyl 900glkg agricultural Ou Pont Far East. Inc.
lannate l Insecticide methomyl 170 9 I liter agricultural Ou Pont Far East, Inc.
Marsbyl 50 WP carbaryl 500 9 I kg agricultural luellig Agrochem. Corp.
Marsbyl 85 Wp carbaryl 850 9 I kg agricultural luellig Agrochem. Corp.
Marshal 150 EC carbosulfan 150 9 I liter agricultural Bayer Phils., Inc./Marine Colloids Phils.
Mesurol 50 WP methioearb 500g/kg agricultural Bayer Phils., Inc.
Mipcin 50 WP MIPC" 500g/kg agricultural Transworld Trading
Reformulated Blitz AE OOVP'" + propoxur household use organophosphate Scientific Industries, Inc.
Reformulated Blitz l OOVP'" + propoxur household use organophosphate Scientific Industries, Inc.
Sevin 50 WP carbaryl 500glkg agricultural Rhone·Poulenc Agro Chern. Phils., Inc.
Sevin 85 WP carbaryl 850glkg agricultural Ahone·Poulenc Agro Chern. Phils., Inc.
Sevin XlR carbaryl 480 9 I liter agricultural Ahone·Poulene Agro Chern. Phils., Inc.
Shellcarb l BPMC' 500 9 I liter agriculturaJ Cyanamid Phils., Inc.
Supergran 3 G carbofuran 30g/kg agricultural Planters Products, Inc.
Sweep thiophanate methyl 700glkg agricultural Cyanamid Agricultural Prod. Phils.. Inc.
Tereyl B5 WP carbaryl 850 9 I kg agricultural Planters Products, Inc.
Top 70 WP thiophanate methyl 700g/kg agricultural Royal Biotech Corp.
Topsin M thiophanate methyl 700glkg agricultural Planters Products Inc.
Topsin . M 70 WP thiophanate methyl 700glkg agricultural Transworld Trading
Vindex Plus phenthoate 250 9 I liter agricultural organophosphate Bhcne-Poulenc Agro Chern. Phils., Inc.
BPMC' 100 9 I liter
Vydate l Insecticide ox amyl 240 9 I liter agricultural Ou Pont Far East, Inc.
lacarb 85 WP carbaryl 850g/kg agricultural luellig Agrichem. Corp.
lack 50 WP MIPC" 500glkg agricultural luellig Agrochem. Corp.
-BPMC: l·sec·butylphenylmethyl carbamate
--MIPC: isoprocarb ,
·--DDVP: 2,2·dichlorovinyldimethyl phosphate
REFERENCES
Amdur MO, Ooull J. and Klaassen, CD, eds.. Casarett and Doutt 's Toxicology: The Basic
Science ofPoisons, 4th ed. New York: Pergamon Press. Inc.. 1991.
Ellenhorn MJ and Barceloux DG.cds.. Medical Toxicology: Diagnosis and Treatment 01 Hu-
man Poisoning. New York: Elsevier Science Publishing Company, Inc.. 1988.
Fertilizer and Pesticide Authority. List a/Registered Agricultural Pesticide Products. FPA,30
June 1997.
Haddad LM and Winchester JF. eds .• Clinical Management ofPoisoning and Drug Overdose,
2nd ed. Philadelphia: w.B. Saunders Company, 1990.
International Programme on Chemical Safety, BasicAnalyticToxicology. Geneva: WHO/UNEP/
ILO.1995.
International Programmeon ChemicalSafety, Environmental Health Criteria Monograph #/48:
Benomy/: World Health Organization. 1993.
International Programmeon Chemical Safety. Environmental Health Criteria Monograph #64:
Carbamate Pesticides - A General Introduction. Geneva: World Health Organization, 1986.
InternationalProgrammeon ChemicalSafety. Environmental Health Criteria Monograph #/53:
Carbaryl. Geneva: World Health Organization. 1994.
International Programmeon ChemicalSafety. Environmental Health Criteria Monograph #/78:
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International Programmeon Chemical Safety, 711e WHO Recommended Classification ofPesti-
cides by Hazard and Guidelines to Classification, /996-/997. Geneva: World Health Orga-
nization. 1997.
Joint Meeting on Pesticide Residues, Propoxur: JMPR Evaluation. 1989.
Klaassen CD. Amdur MO. Doull 1. cds, Casarett and Dault s Toxicology: The Basic Science of
Poisons, 5th cd. New York: MacGraw-Hill. 1996.
Magallona ED, et al. Safety in Pesticide Handling. Manila: NCPC, 1986.
Manual on Occupational Health and Toxicology in the Management ofPesticide Poisoning.
Manila: National Poisons Control and Information Service and the Department of Health.
1994.
MarambaNPC. Panganiban LR and Hartigan-GoKY. Algorithms ofCommon Poisonings: Part
I. Manila: National Poisons Control and Information Service, 1991.
Maroni M. "Carbamate Pesticides," Biologicallndicatorsfor the Assessment afHuman Expo-
Sllre to Industrial Chemicals. Luxemburg: Commission of the European Communities,
1988.
National Poison Control and Information Service. Database on Commercial Products {unpub-
lished). NPCIS. 1996.
Olson KR. et al.. eds.. Poisoning and Drug Overdose. Norwalk: Appleton & Lange. 1990.
Oudejans J 1-1. Ag-o-pesticides: Properties and Functions in Integrated Crop Protection. United
Nations. 1991.
Repetto Rand Baliga SS. Pesticides and the Immune System: The Public Health Risks. Wash-
ington: World Resources Institute, 1996.
So LS. Panganiban LCR. Makalinao fR. Targeting the Poisoned Patient: A Manual on Clinical
Toxicology. Manila: National Poison Control and Information Service, 1997.
World Health Organization I Food and Agriculture Organization. Data Sheets on Pesticides #
52: Hendiocarb, 1982
World Health Organization / Food and Agriculture Organization. Data Sheets on Pesticides #
87: Bcnomyl. 1994.
World HealthOrganization I Food and AgricultureOrganization, Data Sheets on Pesticides # 3.-
Corbaryt. 1978.
World Health Organization / Food and Agriculture Organization, Data Sheets on Pesticides #
56: Carbofuran. Undated.
World Health Organization / Food and Agriculture Organization, Data Sheets on Pesticides #
.5~: Oxamyl. 1983.

HYDROGEN SULFIDE
SOURCES
by-product in:
geothermal plants
CHEMICAL NAME production of coke from
Hydrogen Sulfide sulfur-containing coal
refining sulfur-containing
CHEMICAL FORMULA crude oils
H,S production of carbon
disulfide
SYNONYMS manufacture of viscose
sulfuretted hydrogen rayon
hydrosulfuric acid theKraft process for
sulfur hydride producing wood pulp
hepatic gas sulfur extraction by the
Frasch process
CAS number 7783-06-4 petroleum refining
sewers and septic tanks
CLASSIFICATION volcanic gases
Sulfur compound production ofheavy water
for nuclear power
PHYSICAL STATES reactors
Gas and liquid tanning industry
paper pulp mills
PHYSICAL ANO CHEMICAL PROPERTIES
Colorlessgas: evaporatesfrom aqueoussolutions: highly flammable; heavier than air: gas/air
mixturesarc explosive.
Soluble in water, alcohol.ether.and solutions of amines,alkali carbonates.and bicarbonates.
Oxidation reaction yields sulfur dioxide. sulfuric acid. or elemental sulfur.
Lipid soluble; can penetrate biological membranes.
HAZAROS
Since it is slightly heavier than air. it can accumulate in toxic concentrations in low-lying or
enclosed areas. even when produced or leaking at very low rates.
Decomposes on burning and produces toxic gas including sulfur dioxide.
Use of alcoholic beverages enhances toxic effects.
The "rotten egg" odor is not an adequate warning. Prolonged exposure can lower the odor
threshold. At high concentrations (> I00 ppm), olfactory fatigue: prevents detection.
At present, there are no epidemiological data available on the potential effects of long-term,
low-level exposure.
Alterations in the growth patterns of neurons were noted in rat fetuses exposed to hydrogen
sulfide soon after conception. There was also note of decreased levels ofaspartate, glutamate
and GABA in the cerebrum; and aspartate and GABA in the cerebellum. The number of
cerebellar Purkinje cells increased. and normal perinatal reduction in number was not noted.
Levels of taurine were elevated early during gestation. but later returned to control levels.
Reports on human teratogenicity are scant. One study showed how breastfed children of
mothers working in rayon factories showed retarded development and listlessness.
TOXIC DOSE
Intoxication from hydrogen sulfide exposure is immediate.
Lethality is dependent on the concentration of H2S in the atmosphere and the duration of
exposure. Imminent death is expected in individuals exposed to hydrogen sulfide levels of
700-1000 ppm. At concentrationsof 1000-2000ppm (1500-3000 mg/m'). initial tachypnea
is followed by apnea. At higher concentrations, respiratory centers are paralyzed, causing
death due to asphyxia.
EXPOSURE LIMITS
Air nV·TWA 15 mgim'
Philippine ambient air quality 10 ppm (ACGIH)
standardfor short-term expo- STEL 15 ppm
sure (30 minutes): 0.3 mglm 3 PEL 10 mgim'
(0.2/ ppm) IOLH 300 mg/m'
Incomparison, countries suchas Note: The above exposure limits were established to pre-
Bulgaria, Czechoslovakia, vent eye injuries. Recent animal studies. however. show
Hungaryand Poland listedthe physiological changes in pulmonary function at lower
most stringent standards at air concentrations.
0.008 mgim' (0.006 ppm).
Concentrations in urban areas are usually in the range of 0.0015-0.050 mg/m'.
Near geothermal areas, l-hour mean concentrations may go as high as 2 mg/rn' (1.4 ppm).
There is less agreement regarding ambient air quality standards because the threshold for
detecting the nuisance odor has been variously placed at 0.0005-0.13 ppm.
Water
Marine environments near volcanic vents are rich in sulfide, prompting organisms in these
areas to develop means of detoxification. Sulfide is detoxified in the body, bound and
oxidized by blood components and cytosolic factors; oxidized by mitochondrial sulfide-
insensitive cytochrome c oxidase; and oxidized to produce ATP.
Drinking water
A concentration of 0.07 meg/litre (0.05 ppm) in drinking water can affect its taste.
Food
Emissions from geothermal plants may contaminate water and food.
Hydrogen sulfide is a problem in fish agriculture during harvests since anaerobic sediments of
fish ponds are disturbed during netting, increasing levels to the toxic range.
TOXICOKINETICS
Absorption
Rapid absorption takes place in the lungs. Absorption can also occur through the skin.
Distribution
Once absorbed. hydrogen sulfide is distributed to the following organs: brain. liver, kidney,
pancreas and small intestine. There is no evidence ofbioaccumulation because of fast rate
of metabolism.
Metabolism
There arc three pathways of metabolism:
I. Oxidation to sulfate - forms sulfate. thiosulfate or polysulfides
2. Methylation - by intestinal tract cells
3. Reaction with metallic ion or disulfide-containing proteins
Excretion
Elimination is primarily through the kidneys. Excretion also occurs via the lungs, even in
non-inhalational exposure.
Like hydrogen cyanide, hydrogen sulfide is a potent inhibitorof cytochrome c oxidase, but in
vitro experiments have shown that sulfide is a more potent enzyme inhibitorthan cyanide.
Hydrogen sulfideslowsdownoxidativemetabolism so tissuemetabolic demandscannot be
met. Tissues with high oxygen demandsare most sensitiveto its toxic effects.
The hydrogen sulfide ion (HS-) forms a dissociable complexwith ferric heme groups to pro-
duce sulfmethemoglobin which is relatively non-toxic and is reduced to hemoglobin by
polysulfides, thiosulfate or sulfate. .
In the brain, hydrogen sulfideelevatesendogenous brainsulfideconcentrations via increased
neuronal uptake. It also causesan increase in the concentrations of serotonin,dopamine,
epinephrine and norepinephrine, due to inhibition of monoamine'oxidase. Levelsof ala-
nine, aspartate, gamma aminobutyrate (GABA), glutamate, glycine and taurine are also
increased, possiblybecause hydrogen sulfide inhibitsdegradation of these aminoacids and
amines. Although acute exposure affects the entire brain, the brain stem appears to be the
site of most pathologicneural responses, impairing vital functions such'as respiration. Ef-
fectson other brain regionssuch as the hippocampus mayexplainmemory lossescommon
to survivorsof poisonings.
In chronic exposure, levelsof brainamino acid transmitters are decreased, secondaryto inhi-
bition of synthesis.
Electrophysiological effectsof hydrogen sulfidehave been elucidated in severalanimal stud-
ies:
I. Sodium sulfide administration depolarizes the sympathetic ganglion and increases the
hyperpolarizing effects of epinephrine and muscarine.
2. Sulfidesalts cause an initial block in action potential generation, followed by prolonged
enhancement of amplitude, then another briefinihibition. Highdoses cause irreversible
changes. There was no effecton the rate of conduction.
3. Sodiumcontainingreagents, eitheralone or incombination with taurineand cysteicacid,
completely and reversibly inhibittetrodotoxin-sensitive Nachanncls insympathetic gan-
glia. It is possiblethat taurine plays a significant role in hydrogen sulfide-induced eNS
depression.
4. Hippocampal CAI anddorsalrapheneuronsadministered sodiumsulfideexhibited rapid,
reversible, concentration-dependent hyperpolarization. This was followed by a further
hyperpolarization immediately afterwashout. Theseeffects wereattributedto changesin
the K' cbaancls and the inhibition of Na+/K+ ATPase.
Respiratory symptoms are due to increased bronchial reactivity or hypersensitivity following
exposure. Pulmonary function tests mayshowan obstructive patternamongasthmatics due
to increased airwayresistance and decreased specificairwayconductance. There is also an
inhibitory effecton alveolarmacrophages, increasing the likelihoodof pneumonia. Signifi-
cant hyperpnea mayalso be due to direct chemostimulation of the carotid body.
Animal studies on pulmonary system damage revealed the following:
I. In sub-chronic low-level inhalation, there was dose-related proliferation of ciliated cells
in tracheal and bronchiolarepithelium; and lymphocytic infiltration of the bronchialsub-
mucosa. Increased bronchial reactivity was attributed to the hyperpermeability of air-
way mucosa. Separation of tightjunctions maybe due to alterationsin the cytoskeleton
at the plasmamembrane, or it maybe affected by focal changes in intra-and intercellular
levelsof calcium.
2. Acute high-level inhalation also increased mucosal permeability. It is also possible that
smooth muscles in the airwayare directlyaffected.
3. Exposure to high air concentrations caused necrosis of the nasal epithelium, and exfolia-
tion of ciliated and olfactory mucosal cells. Cytotoxic effects, exudation of polymorpho-
nuclear cells. and pulmonary edema, were dose related. Pulmonary edema was charac-
terized by massive extravasation of eosinophilic fluid.
Hydrogen sulfide is a mucous membrane irritant. Exposure of mucous membranes of the eye
causes keratoconjunctivitis. Epithelial cells can subsequently swell. blister. and form vacu-
oles which could burst and ulcerate ("gas eye"). In severe cases. scar formation and penna-
nent loss of vision can occur.
Adverse effects on cardiac muscle may be due to the direct effect of hydrogen sulfide on
tissues with high oxygen demand. It could also be secondary to anoxia caused by pulmo-
nary edema and eNS dysfunction. Animal studies showed enzymatic changes in the rat
myocardium. leading to changes in ionic conductances. In humans, it is possible that 'car-
diac disease increases sensitivity to adverse effects.
A decrease in erythrocyte count was noted among workers exposed to hydrogen sulfide and
methylmercaptan. This was attributed to inhibition of enzymatic activities in the produc-
tion of heme.
Studies on rats showed no adverse effects in reproduction. However, at parturition. there was
an increased incidence of dystocia and subsequent fetal loss secondary to asphyxiation.
This could be due to inhibition or blockade of oxytocin receptors.
TOXIC EFFECTS
Concentration (ppm) Exposure time resulting in death
200·250 4 - 8 hours
300 I - 4 hours
500 30 min - I hour
TDXIDRDMES
Acute intoxication - Effects of a single exposure [seconds-minutes] to concentrations approxi-
. mating 1400 mg/m'. Rapidly produces signs of respiratory distress.
Sub-acute iatexicaticn- Effects of continuous exposure [up to several hours] to mid-level con-
centrations of 140 to 1400 mg/rn' (100 to 1000 ppm). Most commonly produces eye irrita-
tion (gas eye).
Chronic intoxication- Effects of'intcrmiuent exposures to lev..' to Intermediate concentrations of

70 to 140 mg! rn' (50 to 100 ppm). Characterized by largely subjective manifestations of
illness.
ACUTE EXPOSURE (S" Table 11

Inhalation
Neurologic: eNS depression which results in headache. lethargy, intense anxiety, dizziness,
vertigo, horizontal or vertical nystagmus, weakness of the extremities.. abnormal peripheral
reflexes. psychiatric symptoms (insomnia, depression, irritability, amnesia), seizures, coma
and respiratory failure. After resuscitation: poor coordination and psychiatric disturbances
such as hallucinations and retrograde amnesia.
Cardiovascular: Hypotension, bradycardia. dysrhythmia, myocardial depression, conduction
defects and abnormal ventricular repolarizaticn.
Pulmonary: At lower levels of exposure. causes irritation of the respiratory tract manifesting
8S rhinitis, pharyngitis or bronchitis. Exposure to higher concentrations causes dyspnea,
chest pain.. hemoptysis, pulmonary edema. cyanosis and respiratory distress syndromes.
38 Standard Treatment Guide/ines
~
§i.-----------------------------------------------------,
,.
::! Table 1. Effects of hydrogen sulfide exposure at different levels of air concentration.
~
~
." Concentration Physiological Responses
5! mg/m'
'"
~ Inhalation 0.0042 - 0.028 Odor threshold
.,;;; 4 - 14 Unpleasant odor
28 - 42 Smell of "rotten egg"
42 "Sickening sweet" odor
70 Marked dryness and irritation of nose and throat on prolonged exposure manifesting as
runny nose, cough, dyspnea
150 - 200 70 - 140 Olfactory paralysis
250 350 Prolonged exposure causes pulmonary edema
300· 500 420·700 Pulmonary edema
500 700 30 minute to I hour exposure causes excitement, headache, dizziness, staggering,
unconsciousness ("knockdown") and respiratory failure
500 - 1,000 700 - 1400 Acts as a systemic poison, causing loss of counsciousness, neural paralysis, cardiac
arrhythmias and death secondary to respiratory paralysis
1,000 1400 Rapid collapse, CNS and respiratory paralysis, imminent coma, death in several minutes
5.000 7000 Imminent death
Eye Contact 10 14 Eye irritation, tearing and burning sensation

> 50 70 Intense tearing. conjunctival irritation, blurring of vision, photophobia with possible
permanent eye damage
Dermal Absorption Direct contact may cause erythema and pain.

Contact with liquid form causes frostbite.
Ophthalmologic: Keratoconjunctivitis or "gas eye", visual "fogging", photophobia, tearing,
eye pain.
Gastrointestinal: Nausea, vomiting, anorexia, diarrhea, abdominal pain.
Dermal Absorption
Exposureto low concentrations «20 ppm) maycause skin irritation or allergies. High con-
centrationsmay producediscoloration, spots and rashes.
CHRONIC EXPOSURE
Headaches, weakness, nauseaand vomiting, weight loss, musclespasticity, cerebellarataxia,
pseudotumors. Exacerbation of exercise induced angina has been reported in personswho
presented with loss of consciousness and cyanosisafter a 30·minute exposure to hydrogen
sulfide.

Blood for serum sulfide determination
Normalsulfide level: <0.05 mglL
Blood concentrations in fatally poisoned victims: J. 70-3. 75 mglL
Air sulfide determination
Blood for sulfhemoglobin and methemoglobin levels
Other useful laboratory tests: electrolytes, glucose, arterial bloodgases, chest x-ray, ECG
Forensicdetection- findings in hydrogen sulfide poisoning:
greenish-blue discoloration ofthe viscera and brain
- sulfide levels elevated in blood (within 2 hours ofpoisoning) and in the brain
ANTIDOTES
Sodiumnitrite
Pyridoxine
TREATMENT
EMERGENCY FiElD MANAGEMENT ISoo Guidolinosl
1. Roseuo
Remove patient from toxic area to fresh air. Rescuers should be adequately equipped with
self-contained gas masks.
2. Airway
3.llroathing
In severecasesof poisoningwherethere is paralysisof respiratory centers, the heartcontin-
ues to beat for several minutes even after respiration has ceased. Artificial respiration
should thus be started imediately. There is no danger to the rescuer in giving mouth-to-
mouth resuscitation becauseof the low level of hydrogen sulfide exhaled. Appropriate
safetymeasures should be takensince hydrogen sulfidemaybe presenton the clothingof
the victim. Oxygen supplementation should be given at maximum flow until hydrogen
sulfide concentration in the blood decreases.
4. Circulation
5. Decontamination
Frostbitehas beenobserved on contactwith liquidform. Rinsepatientwith plentyof water.
Do not remove clothes.
6. Drugs
Antidotal therapy. Induction of 10%methemoglobinemia maybe started usinga nitrogly-
cerin patch. Nitritesare mosteffective when given within minutesafter exposure.
7. Transport
40 St,ndard Treatment Guid,lin"

Table 2. Patient hemoglobin levels with corresponding amount ofsodium nitrite needed forinduction
of 25% methemoglobinemia.
Patient Hemoglobin Level Sodium Nitrite (3% NaND, 30 mglml in 10mil
(gldll (mg/kg) (mllkg)
7 5.8 0.19
8 6.6 0.22
9 7.5 0.25
10 8.3 0.27
11 9.1 0.30
12 10.0 0.33
13 10.8 0.36
14 11.6 0.39
EMERGENCY HOSPITAL MANAGEMENT (S" Guidelines)

1. Airway
2. Breathing
Immediately start supplementation with maximum-flow humidi-
fiedoxygen and determine depthof hypoxia withArterial Blood
Gas determination.
Start mechanical ventilation, particularly in severe cases of poi-
soning where there is paralysis of the respiratory centers and
ventilatory failure. Give oxygen supplementation at maximum
flow until hydrogensulfideconcentrationinthe blood decreases.
3. Circulation
4. Decontamination
5. Drugs
Antidotal therapy - Induction of methemoglobinemia is done us- , - - - - - - - -
ing 3% sodium nitrite. Administration should be based on the Nitroglycerin patch
hemoglobin level and the weight of the patient (Table 2). The Adult: 1· 3 inches
goal is to convert at least 25% of the patient's hemoglobin to depending on severity,
methemoglobin. on non·hairy part of
Succeeding doses of sodium nitrite should be guided by meth- anterior chest wall.
emoglobin determinations. Methemoglobin levels should not Padi.: 1/2 to 1 inch on
exceed 40% of patient's total hemoglobin. anterior chest wall.
Pyridoxine should be given following methemoglobinization as a
sulfide acceptor. Sodium nitrite
Adult: determined amount
Maintenance of3% Sodium nitrite
Place patient on complete bed rest and in Trendelenburg position. given IV over 3 min at
Maintain on NPO until patient is fully conscious. a rate not to exceed 1
Maintain adequate hydration and parenteral nutrition while on NPO. ml/min.
Correct any electrolyte imbalance. Pedia: determined amount
Avoid giving patient food that may increase methemoglobinemia (c.g.. of 3% Sodium nitrite
tocino. chonios. given IV over 3 min at
Patient should avoid smoking while under treatment. a rate not to exceed
Do not administer adrenergic agents or eNS depressants. 0.5mllmin.
Specific Problem. Pyridoxine

Pulmonary edema: furosemide I rug/kg/dose: hyperbaric oxygen 25 mg/kg IV
OCCUPATIONAL POISONING 4/
Hypotension: leg elevation. ensure adequate hydration
Sodium Nitrite administration may cause the following problems:
Hypotension: lower dose of sodium nitrite or discontinue nitrite administration, elevate
legs and ensure adequate hydration
Cyanosis: may occur when methemoglobin levels reach >10% of total hemoglobin. Give
Ascorbic acid 500 mg to 1 gm IV every 6 hours.
OCCUPATIONAL TOXICOLOGY INTERVENTIONS ISee Guidelines)

Hydrogen sulfide producing geothermal plants should be sited away from populated areas and
ground water reservoirs. Regular evaluations should be done at these facilities to determine
the air levels of hydrogen sulfide.
Geothermal plants are required to conduct pre-placement. monthly, transfer. return to work
and exit health examinations for all workers. These examinations should consist.of com-
plete physical and laboratory examinations including determination of blood sulfides. sulf-
hemoglobin and methemoglobin levels among workers at high risk for hydrogen sulfide
exposure. Employees should be educated on the attendant heath risks.
The recommended number and type ofheallh personnel required in geothermal plants varies
according to the number of workers (Table 3). Health personnel must have undergone ap-
propriate training in occupational health specific for geothermal plant operations.
Proper personal protective equipment should be made available to the employees and they
should be trained on how to use them. Equipment should be cleaned immediately after use,
tested regularly for effectivity and replaced as necessary.
Recommended personal protective equipment are as follows:
mask fitted with activated charcoal filter or an 8-layer thick improvised mask (e.g. folded
handkerchief) with the outer surface kept wet
goggles or eyeglasses or face shield to protect eyes from dust particles; wearing of con-
tact lenses is not advised
long sleeved garments to cover exposed parts of the body
cold-insulating gloves for workers who handle hydrogen sulfide in liquid form
Individuals not wearing protective equipment and clothing should be kept away from areas of
Table 3. Recommended health personnel required for corresponding number ofhigh risk employees in
geothermal plants.
No. or Workers at High Risk 1\linimum Health Personnel Required
1·10 2 first eiders
1part-time nurse 14 hrslday, 5x/weekl
1 safety consultant
11 . 50 4 first elders
1 lull time nurse
1 part time physician
51·100 6 first aiders
1 full lime nurse
1 lull time physician
1 part lime dentist 12 hrs.day, 3:-:!weekl
101 ·300 3 first aiders
2 full time physicians
1 part time physician
1 full time dentist
301 & above 1 first aider per 30workers
1 full time nurse per 200 workers
1 full time physician per 300workers
1 full time dentist per 600workers
spills or leaks until clean up has been completed. Remove all ignition sources.
Once leaking containers are identified. attempt to stop the flow of gas. If the leak cannot be
stopped. remove the container to a safe place in open air' and repair the leak or allow the
container to empty. Ventilate the area. If the hydrogen sulfide is in liquid form. allow to
vaporize.
Use closed system ventilation. and explosion-proof electrical equipment and lighting. Pre-
vent build-up of electrostatic charges by grounding equipment. In case of fire. spray canis-
ters with water.

Industrial sources of hydrogen sulfide should be located away from residential areas. Hydro-
gen sulfide concentrations drop by a factor of 2 between the immediate neighborhood of a
source and a 2.5 km radius. Between a radius of2.5 km and 20 km, concentrations decrease
by 30% lip to a factor of 8.
Since sulfur may contaminate water and food. monitoring for residues must be conducted to
comply with allowable daily intake values. Contaminated food should be rinsed with sul-
fur- free water.
Thc lethal dose for animals such as dogs. cows, goats. monkeys. mice, guinea pigs, and rats is
around 100 ppm. Birds arc particularly sensitive. Hydrogen sulfide is also toxic to fish at
all stages of development. Fish reared in sublethal concentrations grow larger - probably
because offungicidal and bactericidal effects - but arc notably less active and show signs of
respiratory distress.
Environmental monitoring is strongly recommended. Air and water should be monitored for
concentrations of total sulfur. sultites. ammonium sulfate. zinc and vanadium.
At present, there are no epidemiological data available on the potential effects of long-term,
low-level exposure.
REFERENCES
Amdur MO. Doull J. and Klaassen CO eds .. Casoreu and Doull's Toxicology: The Basic
Science of Poisons. 4 1h ed. New York: Pergamon Press. 1991.
Department of Health and I-Iuman Services. Occupational Health Guidelines for Hydrogen
Sulfide. U.S. Department of Health and Human Services. 1978.
Dreisbach R and Robertson W. Handbook ofPoisoning, Norwalk: Appleton and Lange, 1987.
Gossel TA, Bricker JD. Principles ofToxicology, 3rd ed. New York: Raven Press, 1994.
Gosselin RE. Hodge HC. Smith RP and Gleason MN. Clinical Toxicology of Commercial
Products. 4th ed. Baltimore: Williams and Wilkins Company. 1976.
Haddad LM and Winchester JF eds .. Clinical Management ofPoisoning and Drug Overdose
2'" cd. Philadelphia: WIl Saunders. 1990.
lntcrnaticnnl Programme on Chemical Safety, Environmental Health Criteria # 19: Hydrogen
Sulfide. Helsinki: World Health Organization, 1981.
Klaasen CD. Amdur MO. Ooull J. eds, Toxicology: The Basic Science of Poisons, 5th ed.
New York: Macfiraw-Hill. 1996.
ReilTenstein RI. Hulbert we. Roth SH. "Toxicology of Hydrogen Sulfide," Annual Review oj
Pharmacology and Toxicology, Vol. 32, 1992, pp. 109-134.
LEAD
SOURCES
lead smelters
CHEMICAL NAME gasoline/automotive
LEAD exhaust
Inorganic lead paints/pigments
Organic lead lead·glazed ceramics
Tetraethyllead glass/painted glass
Tetramethyllead batterieslbetterv
reclamation process
CHEMICAL FORMULA radiator repair activities
Pb hair dyes
facial cosmetics
SYNONYMS cables
CAS number 7439-92-1 lead pipes
lead solders
CLASSIFICATION printing
Element colored newsprint
welding
PHYSICAL STATE ammunition
Solid building material
radiation shielding
PHYSICAL AND CHEMICAL PROPERTIES illicit distilled whisky
Bluish-white or silvery-gray soft metal; strong reducing agent. I"moonshine"'
HAZARDS
Although solid, lead decomposes on heating, producing toxic' fumes; can therefore be ab-
sorbed not only by ingestion, but also by inhalation, especially of its aerosol (e.g., sus-
pended paint particles).
Occupational exposure to lead is variable: highest among workers in smelters and storage
battery factories where lead concentration is often greater than 1 mg/rn', ten times higher
than what is considered safe; mining, refining and manufacture of lead-containing com-
pounds and products also expose workers to the substance, often in lower concentrations.
In homes. metal pipes and water storage tanks can be sources of lead. Water left standing in
plastic pipes could have higher lead levels due to the presence of lead stearate. a stablilizer
in the manufacture of poly vinyls. However, full assessment of hazard potentials of plastics
need more studies.
Lead may also be present in processed food from cans with lead-containing solders or from
improperly glazed earthenware containers. Among children, a notable hazard is the inges-
tion of non-food items. particularly lead-containing paint from surfaces in homes or from
lead-contaminated dust and soil.
The lead content of tobacco comes from lead arsenate used as an insecticide. The amount of
lead varies from 10.40-12.15 meg/cigarette. The amount of lead in mainstream smoke
show widely different values, ranging from 0.2-3.3 meg per cigarette.
Other less common sources of lead which have caused poisonings include illicit distilled
whisky. lead bullets which were not surgically removed. and the use of discarded automo-
bile battery casings as fuel.
Lead has been implicated as a potential renal carcinogen in humans but the association has not
been fully established. Lead and lead compounds belong to Category 2B (possible human
carcinogen with sufficent evidence in animal tests), as evaluated by fARe of the WHO.
Adverse reproductive outcomes from lead exposure include diminished or aberrant sperm
production, increased rate of miscarriage, decreased gestational age, low birth weight and
impaired neurologic development in humans since material readily crosses the placenta.
TOXI.C DOSE
Acute human ingestion of 15 g of lead oxide has resulted in death. The, LD511 for dermal
exposure in rabbits to tetraethyl lead is 532 rug/kg. Children appear to absorb lead more
rapidly than adults, and exhibit toxic effects at lower blood concentrations.
EXPOSURE LIMITS
Inorganic Lead Tetraethyl Lead Tetremethyl Leed

nV·TWA {mg/m'l 0.15 (ACGIH 1990·911 0.10 0.15
PEL (mg/m') 0.05 (OSHA) 0.075 0.075
10LH (mg/m'l 700 40 40
REL (mg/m'l 0.10 (NIOSHI
Air
US EPA regulation (3-month average):
U meglm' (0.0015 mglm')
The lead concentration in ambient air seldom exceeds 3 mcg/m'. Most particulate matter
containing lead are deposited near emission sources but small particulates can be trans-
ported over long distances. contaminating remote sites. Levels increase in direct propor-
tion to the density of automobile traffic: 2-25 rncg/m' in large cities: < 0.2 mcg/m' in
suburban and rural areas or in urban areas where leaded gasoline is not used: and only
0.0001-0.00 I mcg/m' in remote areas. Indoor levels are about 1/3 of outdoor air, except in
lead utilizing industries.
It has been estimated that blood lead levels.increase by 1-2 mcgldL for inhalation of every 1
mcg/rn' of lead in air. The respiratory uptake is influenced by total lead concentration,
particle size distribution, particle shape, chemical composition, physicochemical proper-
ties, and respiratory volume.
Blood lead levels of 50 mcgldL requires removal ofa worker from source of expo sure (OSHA).
Food
Adults absorb 10% of lead from food and beverages while children absorb about 50% of
dietary lead. The daily oral intake of adults ranges from 100 meg to >500 meg. Levels vary
according to eating habits and the lead content of water and food sources. Low dietary
intake of calcium and iron increases lead absorption while coingestion of food decreases
absorption. Blood lead levels are expected to increase by 6-18 mcgldL with each oral
intake of 100 meg of lead.
Lead can be detected in almost all foods. Vegetables normally contain 0-1.3 rug/kg, cereals 0-
1.39 rug/kg, condiments 0-1.5 mglkg, fish and seafood 0.2-2.5 rng/kg, meat and eggs 0-0.37
mg/kg. Wine and products stored in lead-soldered cans or lead-glazed pottery, markedly
increase the daily lead intake.
Children may be at higher risk because of their greater intake of cow's milk. which contains
lead at levels of5-12 megiL. A Provisional Tolerable Weekly Intake (PTWlj of25 meg/kg
BW of lead (from all sources) 'vas recommended (FAD/WHO 1993) based on a model
indicating that daily intake of lead between 3-4 meg/kg BW by infants and children is not
associated with an increase in blood lead concentration.
Drinking Water
WHO standards (1993): 0.01 mg/L (10 mcg/L), maximum allowable level
US EPA action level: 0.015 mgiL (15 rncg/L)
Drinking water generally contains less than 5 mcg/L of lead but levels are higher in areas
where water is soft (contains little calcium and magnesium) or with usage of lead pipes and
lead-lined water storage tanks.
Lead in water ingested independently of food may be more readily absorbed but the increase
in blood levels from lead in drinking water could best be estimated by a cube root relation-
ship rather than a linear relationship.
Ground and Surface Water

Lead concentrations in groundwater vary from 1·60 mcg/L. For natural surface waters, the
global mean for lakes and rivers is 1-10 mcg/L. Sea water contains only 0.08-0.4 mcg/L.
Concentrations at depths below 1000 m give a more uniform rangc of 0.03-0.04 mcg/L.
Although human activity increases lead levels. a self-cleaning process also occurs as water
flows though ecosystems.
Soil
Lead is found in the earth's crust at levels of around 13 rug/kg: lead ore deposits have higher
concentrations of lead. Surface soil shows different values; acidic soils generally contain
less lead than alkaline soils while organic matter which are rich in chelating components
bind lead or promote its movement out of the soil. In areas with little human activity.
concentrations range from 5-25 rug/kg.
TOXICOKINETICS
Absorption
Adults absorb 5-15% of ingested lead and retain less than 5%. Infants can absorb 41.5% and
retain 31.8% on regular diets. Lead absorption from the lungs depends on the particle size;
about 90% of lead particles deposited in the lungs from ambient air are retained.
Dermal absorption of organic (alkyl) lead compounds is rapid and extensive but absorption is
minimal for inorganic lead. Dermal absorption of inorganic lead compounds results in
elevated. levels of lead in human saliva and sweat. Lead acetate (in hair darkening cosmet-
ics) is absorbed at 0-0.3% of the applied dose even with intact skin. detectable in blood.
Distribution
Once in the blood. lead is distributed primarily among three compartments - blood. soft tissue
and mineralizing tissue (bones and teeth); the latter contains 95% of the total body burden
of lead in adults. A labile compartment in the bone readily exchanges lead with blood and
an inert pool which becomes a potential endogenous source of lead. More than 90% of lead
in the blood is in two major compartments within red blood cells: either in the membrane or
associated with hemoglobin. The total accumulation of lead may be as much as 200 mg to
over 500 mg for a worker with heavy occupational exposure.
Stores of lead in the body have been identified as having distinct half lives: blood lead, 28-36
days; soft tissue, 40 days: bone lead, 27 years.
In pregnancy. lead crosses the placenta. Fetal tissue accumulation of lead. including the brain.
is proportional to maternal blood lead levels.
Excretion
Renal excretion of lead is by glomerular filtration with some tubular resorption. At high lead
levels, excretion is increased through transtubular transport.
46 Standard Treatment Guidelinel

MECHANISMS OF TOXICITY
The multisystem toxicity of lead is mediated by at least two primary mechanisms: inhibition
of enzymatic processes as a result of sulfhydryl group binding, and interaction with essen-
tial cations (calcium. zinc and iron). Pathologic alterations in cellular and mitochondrial
membranes. heme and neurotransmitter synthesis. and nucleotide metabolism have been
observed. The primary organs affected are the eNS, kidneys. reproductive and hematopoi-
etic systems.
Lead-induced learning impairments have been attributed to changes in dopaminergic,
glutamincrgic and cholinergic systems.
1. Lead affects the regulation of autorcceptor-mcdiated dopamine synthesis. Lead alsco
decreases dopamine release either through changes in vesicular storage or decreased syn-
aptic transmission. The decreased availability of dopamine results in supersensitivity of
dopamine receptors- and an increase in dopamine (D2) binding sites. These changes in
dopamine systems impair behavior in various learning and cognitive tasks.
2. Lead decreases glutamine synthetase activity. It also decreases the activity of the NMDA
receptor complex which has been associated with learning and memory processes. Lead
also blocks the stimulus properties of MK-80 I by interacting with the zinc binding site,
causing impairment of learning accuracy.
3. Lead decreases acetylcholine release and function. These effects were noted in the cor-
tex. hippocampus. midbrain and striatum. Changes in the cholinergic system are associ-
ated with impairment in cognitive and attention-based tasks.
In fatal cases of lead poisoning. autopsies show cerebral edema, swelling of capillary endothe-
lial cells. and obliteration of the convolutions of the cerebral hemispheres with extravasa-
tion of RBCs and perivascular hemorrhage. The brain parenchyma may show patchy neu-
ronal loss, serous exudate. glial proliferation, and occasional areas of demyelinization.
Demyelination and axonal degeneration arc consistent findings in lead neuropathy.
Erythrocytes exposed to lead in vitro show increased osmotic resistance. increased mechani-
cal fragility, inhibition ofNa·K-ATPase. and increased loss ofintracelJular potassium. These
factors effectively shorten erythrocyte life span.
In vivo. anemia is due to the disruption of enzymatic steps in the production of heme and
globin. It inhibits aminolevulinic acid dehydratase (ALAD). ferrochelatase and
coproporphyrinogen oxidase. leading to the accumulation of aminolevulinic acid (ALA).
protoporphyrin IX (PP) and increased urinary excretion of coproporphyrin III. The mecha-
nism by which globin synthesis is impaired is thought to be secondary to decreased protein
synthesis in erythroid cells as a consequence oflead-induced inhibition of heme synthesis.
Iron deficiency and lead exposure have an additive effect: lead decreases the availability of
iron for coupling with protoporphyrin. Examination of developing RBCs in cases oflead
poisoning reveals accumulation of ferritin and iron micelles.
Children with poor nutritional status show toxic effects at lower blood lead concentrations. In
patients without iron-deficiency, however. serum iron may even be increased.
The earliest renal response to lead toxicity is the appearance of intranuclear inclusion bodies
followed by decreasing tubular reabsorption of glucose and alpha-amino acids leading to
amino aciduria and glycosuria. Impairment of cellular respiratory and phosphorylative
ability results in hyperphosphaturia. Hyperuricemia and gout may occur. Renal effects
have been associated with blood lead levels of 31.3 mcg/dL.
Diffuse interstitial and peri tubular fibrosis are seen in chronic lead nephropathy characterized
by arteriosclerotic changes. interstitial fibrosis. glomerular atrophy. and hyaline degcnera-
tion of the vessels. This pathology is progressive and can lead to renal failure years after
exposure has been terminated. Nephropathy is more common among those with high occu-
pational exposure of more than 10 years. Blood lead levels of more than 60 mcgldL may
give rise to chronic irreversible nephropathy.
Lead affects ~.he heart indirectly through the autonomic nervous system, causing R-R interval
Clinical Manifestations Blood Lead Levels Clinical Manifestations
in Children lmcg/dl) in Adults
Inverse relationship between blood 4 ·14
lead levels and 10 score can be
demonstrated
Transplacental transfer < 10
Level of concern for children 10 Hypertension I?l
Decreased hearing. growth
Increased erythrocyte protoporphyrin 15 Increased erythrocyte protoporphyrin Iwomenl
Decreased ViI. 0 metabolism I?l Associated with adverse pregnancy outcomes
Decreased nerve conduction velocity 20
25 Increased erythrocyte protoporphyrin Imenl
Headache. irritability. difficulty in concentra·
ting. slowed reaction time. neuropsychiatric
effects, anemia and subclinical slowing of
nerve conduction
· Decreased ViI. 0 metabolism > 30 Onset of renal effects
Increased systolic BP (menl
Decreased hearing acuity
· Decreased hemoglobin synthesis 40 Changes in autonomic nervous system function
Peripheral neuropathies
Infertility Imenl
50 Decreased hemoglobin synthesis Imenl
Lead colic > 50 Decreased longevity
Frank anemia Frank anemia
Nephropathy
> 60 Increased risk of irreversible nephropathy
Acute Of chronic encephalopathy 60 ·70
Medical emergency > 70
> BD Gastrointestinal symptoms and subclinical
renal effects
Abdominal pain lIead colicl and nephropathy
· Death > 100 Encephalopathy and neuropathy
variability on ECG tracings. There is no direct cytotoxic effect on the myocardium. There
appears to be a higher incidence of cerebrovascular deaths among populations exposed to
lead. A causal relationship cannot be established between high blood lead levels and hyper-
tension because of the presence of confounding factors.
Animal studies on the effects of lead on the lungs have shown that alveolar macrophages and
type I alveolarepithelial cells are damaged; 35% of inhaled lead particles are deposited in
the lungs. Lead fumes are particularly dangerous because most of its mass exists in the
respirable particle size range.
Reports of toxic hepatitis and impaired liver function occur among severe lead poisoning
cases. The mechanism of toxicity for hepatic, gastro-intestinal disorders, reproductive and
endocrinologic problems have not been elucidated.
TOXIC EFFECTS
Symptoms from acute toxicity of lead are rare. More common are manifestations ofsubacute
or chronic exposure. There is a relationship between blood lead levels and clinical find-
ings.
TOXIOROMES
At low levels of exposure, patients may present with constitutionalsymptoms such as fatigue,
malaise, irritability, anorexia, insomnia and weight loss, arthralgias and myalgias. fir/V
(lMw04>
ACUTE LEAD EXPOSURE ~ )
Ingestion'Inhalation
Gastrointestinal: Nausea, constipation or diarrhea, crampy abdominal pain (lead colic).
Hematologic: Increased frequency and severity of anemia at higher exposure levels.
Hepatic: Toxic hepatitis
Neurologic: Alkyl lead compounds are highly lethal. Convulsions and coma occur in the most
severe cases.
Dermal Absorption
Integument: Organic lead compounds are irritating to the skin.
Neurologic: Severe form of encephalopathy may present as seizures or coma.
CHRONIC LEAD EXPOSURE

Ingestion I Inhalation
Note: Some inhaled particulate mailer (> 7 micrometers) can be swallowed after mucocilliary
clearance from the respiratory tract.
Gastrointestinal: Nausea, constipation or diarrhea, and crampy abdominal pain (lead colic).
Patients may also complain of anorexia or metallic taste.
Renal: Lead toxicity produces lesions of the proximal tubule and loops of Henle. Laboratory
examinations would show aminoaciduria, phosphaturia, glycosuria, and renal tubular aci-
dosis (Fanconi syndrome). End-stage lead nephropathy is characterized by interstitial dis-
ease with sclerotic changes and interstitial fibrosis. Damage is progressive and renal failure
may result. Lead also decreases tubular secretion of uric acid, causing a higher incidence of
gout.
Hematologic: Anemia increases in frequency and severity at higher exposure levels. ( IA~/( ~)
Neurologic: Chronic lead exposure can cause lead encephalopathy, characterized as dullness,
restlessness, irritability, headaches, muscular tremors, hallucinations, loss of memory and
inability to concentrate. These signs and symptoms may progress to delirium, mania, con-
vulsions, paralysis, and coma.
Inorganic lead decreases peripheral nerve conduction velocity and impairs sensory motor func-
tion. It causes lead palsy, characterized as weakness of the extensor, muscles, hyperaesthe-
sia, analgesia, and anaesthesia.
For children. early signs of encephalopathy include irritability, lethargy, ataxia, bizarre behav-
ior, apathy and memory loss. The sequelae of lead encephalopathy may be severe and can
include cortical atrophy, hydrocephalus, and convulsive seizures.
More commonly, lead exposure in children manifests as decreased intelligence. Lead exerts a
direct effect in learning (as seen in animal studies) and also produces behavioral impair-
. ments. There is note of change in reaction time, postural disequilibrium, deficits in visual-
motor function, auditory acuity, perceptual integration, and verbal abstraction. Attention
deficits may be due to increased distractibility or perseverative behavior. Acquisition be-
haviors and difficult discriminations are also affected.
Epidemiologic studies do not set a threshold level at which effects on intelligence occur.
However, at levels as low as 4-14 mcgldL, 'an inverse relationship between intelligence
quotient (IQ) score and blood lead can already be demonstrated. A deficit of 0-5 IQ points
was noted for each 10 mgldL increment. Other studies showed decrements of71Q points
for blood levels greater than 20 mcg/dl., and a decrease by 4-6 points at levels of 30-40
mcgldL.
Alkyl lead intoxication presents differently from other lead exposures. Psychiatric problems
such as hallucinations, delirium, insomnia, delusions, and violent mood swings are com-
. monly reported. Symptomsmay be observed from 1-10 weeks.
Reproductive System
Women working in lead industries havea higher incidenceof ovulatory dysfunction. Adverse
pregnancyoutcomes have also been attributed to lead exposure. Decreased sperm count or
changes in sperm morphologyhave been noted in males. Increasedincidence of infertility
and loss of libido have been described for both sexes.
Endocrine System
Impairment of thyroid and adrenal function ~as been reported. Lead interferes with a hor-
monal form of Vitamin D which is involved in various processes including cell growth and
skeletal development.
Dermel Exposure
Use of hair darkening cosmetics can produce systemic manifestations.
Transplacental Exposure
Pre-termdelivery and decreased fetal growth have been associated with maternalblood levels
> 15 mcg/dl.,

Whole blood for lead levels - most important epidemiological index
10 mcgldL is the level a/concern/or children
> 50 mcg/dL in children is a medical emergency
Blood for aminolevulinic acid dehydrataseactivity - decreases with rising lead levels; useful
only with blood lead levels below 60 mcgldL
Blood for free erythrocyte protoporphyrin(FEP) or zinc protoporphyrin (ZPP)
Elevations> 35 mcg/dL reflect lead-induced inhibition ofheme synthesis in actively form-
ing red cells and not mature ones.
Elevations of lead level in the presence of a normal FfJl or ZPP therefore suggest very
recent exposure.
Blood for CBC, reticulocytecount
Blood for renalfunction tests
Blood for peripheral blood smear - punctate basophilia occurs in lead poisoning, but there is
no quantitative relationship between the number of stippled cells and blood lead levels.
Urine for coproporphyrin and aminolevulinic acid levels - increased when there is impaired
hematopoiesis; decreases quickly when exposure ceases; reflects average short-term level
of lead exposure; useful for early detection of elevated lead levels in the body.
X-ray fluorescence of lead in bone
Deciduous teeth and hair for lead levels - indicate integrated long-term exposure
NCV may document peripheral neuropathy
EMG may show fibrillation and diminished number of motor units on maximum contraction
ANTIDOTES
Dimercaptosuccinic acid
N-Acetyl-D,L-pen!cillamine
TREATMENT
EMERGENCY FIELD MANAGEMENT (S.e Guideline.)
1. Rescue
2. Airway
3. Breathing
50 Stand"d Traatmont Guidolina.
4. Circulation Dimercaptosuccinic
5. Decontamination acid 10MSA}
Gastric Decontamination - Emesis may be induced if a medical 10 mg/kg/dose PO q' 8
facility is inaccessible and if there are no contraindications. hours for 5 days
6.0rugs then 10 mg/kg/dose
J. Transport
PO q' 12hours for
another 5 days.
EMERGENCY HOSPITAL MANAGEMENT ISee Guidelines' Reassess patient after
1. Airway treatment and consider
2. Breathing repeat therapy if lead
3. Circulation levels are still
4. Decontamination elevated.
Gastric Decontamination - May do gastric lavage with single
dose of activated charcoal. Always follow charcoal lavage N·Acetyl-O,L·
with cathartics. If a post-catharsis radiograph of the abdo- penicillamine
men still shows the presence of lead, catharsis or enema should Podia: 5· 10 mg/kg/day
be repeated. PO in 3 divided
5. Drugs doses (maximum of 1
Current literature may cite higher therapeutic doses for N-acetyl- gm/day) given for 5
D.L-penicillamine; however. clinical experience at the Phil- days.
ippine General Hospital has shown response to chelation
Adults: 10· 20mg/kg/
therapy at the indicated doses. day PO in 3 divided
doses (maximum of 1
Maintenance gm/day) given for 5
Maintain on NPO until patient is fully conscious. days.
Maintain adequate hydration and parenteral nutrition while on NPO. Give at least 1 hour
before meals.
Reassess patient after
Specific Problems treatment and consider
Seizures: diazepam or lorazepam. phenytoin. mannitol repeat therapy after a
Status epilepticus: thiopental sodium, general anesthesia, or neu- 10 day rest if lead
romuscular blockade levels are still
Rhabdomyolysis: hydration. mannitol, sodium bicarbonate elevated.
Aspiration pneumonia: full antibiotic coverage until specific or- Toxic erythema and
ganism is identified erythema multiforme
Nephropathy: diuretics. adequate hydration
are signs ofallergic
Electrolyte imbalance/metabolic acidosis: correct accordingly reaction topenicil·
lamine. If noted,
OCCUPATIONAL TOXICOLOGIC INTERVENTIONS (See Guidelines) discontinue treatment
Regular monthly medical evaluations should be done on employ- immediately.
ees at risk of exposure, with particular emphasis given to blood Penicillamine has an
lead level monitoring. Workers with a single blood lead level antimetabolic effect.
exceeding 40 mcg/dL should be notified and given medical at- Discontinue treatment
tention. If a blood level reaches 60 mcg/dL or if three succes- if neutrophils drop
sive monthly tests average in excess of 50 mcg/dL. the worker below 1500/mm'.
should be removed from exposure until blood lead levels are
below 40 mcg/dL. and clinical manifestations oftoxicity are re-
solved.
Clothes of workers mining or using lead may contain lead-bearing
dusts which can be inhaled. or can settle on food and water.
Clothes used in work with exposure to lead should not be taken
home.
Workers should wash thoroughly prior to eating, drinking, close contact with other people,
and before leaving the place of work. Avoid eating, drinking, or staying unnecessarily in
areas where lead is handled, processed or stored.
Quality ventilation engineering can markedly decrease lead concentrations in air.

The most efficient clearing system for environmental lead pollution is rain. Water washes lead
into soil and bottom sediments where it is bound firmly by organic matter. Consequently,
natural waters and water supplies generally have low concentrations of lead even in pol-
luted areas.
Lead levels in air and soil are more difficult to control. Smelters of lead ores pose the greatest
problem to local communities. The zone of pollution can extend to 5·10 km in air, and 10
km in soil. Secondary smelters producing lead from scrap metal operate on a comparatively
smaller scale but are more numerous and are often situated closer to communities.
The production of electric storage batteries accounts for the largest lead consumption. 80% of
the lead content of batteries can be recovered and they serve as the main source of lead for
secondary smelters.
Industries that produce metal sheets, cable and printing metal also release lead to the environ-
ment but at comparatively lower levels. Alkyl lead content of fuel has decreased in the last
few years. prompted by legislation, increasing consumer awareness and the presence of
alternatives. However, these fuel additives remain the major source of inorganic lead in air.
Bioaccumulation of lead occurs. especially in shellfish. There is also secondary transfer from
soil to plants and from plants to animals. The highest levels have been found in the biota
around areas of intense air pollution. such as near smelters or roads with heavy traffic.
Studies on the amount of lead in mainstream cigarette smoke show widely different values,
ranging from 0.2-3.3 meg per cigarette. One report showed that smoking one packet of20
cigarettes would result in the direct inhalation of about 1-5 meg of lead.
Children of pre-school age are at greater risk for being affected by environmental sources of
lead because of their habit of licking, chewing or eating foreign objects such as household
items or walls painted with lead-based paints. In these patients. images of flaked paint were
seen in x-ray examinations of the abdomen. In other cases, the lead has been traced to
contaminated soil around homes where the outside walls are painted with lead-based paints.
Factors such as concentration of lead in soil, age and condition of housing, use of leaded
gasoline, urban density, play behavior and bioavailability of lead in the source material
influence the level of exposure of children.
Lead containing materials such as gasoline containers. facial cosmetics, food containers fin-
ished with lead-containing glazes. lead soldered cans or plumbing. contaminated work clothes,
colored ink on magazines, and even small pieces of metal should be out of reach of chil-
dren.

REFERENCES
Cory-Slechta DA,"Relationships between lead-induced learningimpairments and changes in
dopaminergic, cholinergic, and glutarninergic neurotransmittersystem fucntions," Annual
Review ofPharmacology and Toxicology. Vol 35, pp. 391-415, 1995.
Ellenhorn MJ et aI., Ellenhorn s Medical Toxicology: Diagnosis and Treatment of Human
Poisoning, 2nd edition. Baltimore: Williams and Wilkins, 1997.
Haddad LM and WinchesterJO, Clinical Management afPoisoning and Drug Overdose. WB
Saunders Company, 1990.
International Programmeon Chemical Safety, Environmental Health Criteria Monograph #
165: Inorganic Lead. Geneva: WHO, 1995.
International Programmeon Chemical Safety, Environmental Health Criteria Monograph #
3: Lead. Geneva: WHO, 1977.
ties, International Chemical Safety Cards: Lead. International Programme on Chemical
Safely, 1990.
Klaascn CD, Amdur MO, Doull J, cds, Toxicology: The Basic Science ofPoisons, 5th ed. New
York: MacGraw-Hill, 1996.
Olson KR. ed., Poisoning and Drug Overdose. Norwalk: Appleton and Lange, 1994.
US Department of Health and Human Services. Case Studies in Environmental Medicine:
Lead Toxicity. Atlanta: Department of Health and Human Services. 1992.
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MERCURY
SOURCES CHEMICAL NAME
Elemental/lnor.ganic MERCURY
extraction and
processing of ore,
including gold
CHEMICAL FORMULA
Hg
..
working fluid in Mercurous mercury (+ I)
instruments Mercuric mercury (+2)
!thermometers.
barometers. SYNONYMS
sphygmomanom- Quicksilver, metallic mercury, liquid silver, mercurio
eters) CAS number 7439-97-6
amalgams in dental
fillings CLASSIFICATION
manufacture of Inorganic mercury: elemental mercury
electrical appliances mercury 5'al15
fluorescent or mercury (mercurous and mercuric salts)
lamps Organic mercury:ethylmercury
felt making methylmercury
disinfectants phenylmcrcury
production of chlorine PHYSICAL STATES
gas and caustic Solid. liquid and gas
soda
button I disk batteries PHYSICAL AND CHEMICAL PROPERTIES
pigments (mercuric Odorless, shiny, silvery liquid; non-flammable; produces poisonous
sullideJ gas in fire: evaporation ofmetatlic mercury occurs to some extent
at room temperature.
Organic Combines readily with sulfur, chlorine or oxygen to form inorganic
agricultural fungicide mercury. Binds with carbon to form organic mercury. Forms
medical bactericidal amalgams with most metals except iron, nickel, cadmium, alumi-
and fungicidal num and platinum.
agents Reactsexothermically withalkalinemetals;reactsviolentlywith acety-
bioaccumulated in lene.chlorine and ammonia.
food chain Corrosive, particularly to copper and copper alloy materials.
Attacked by nitric acid but not by hydrochloric acid.
HAZARDS
Vapor pressure is high; may produce hazardous concentrations of
mercury vapor at usual room temperatures. At 24"C. a saturated
atmosphere of mercury vapor would have a concentration of 18
mg/nr'. 360 times more than permissible levels.
Studies are few and causality has not been adequately established.
The IARC has included mercury in Group D (not classifiable as to
human carcinogenicity).
The fetus has been observed to be more sensitive to methylmercury
than adults since a relatively greater amount passes into the brain
54 Standa,d Treatment Guid.lin••

and because methylmercury interferes with brain development. Exposed pregnant women
may give birth to children with mental retardation. cerebral palsy. tremors. seizures. motor
disability and low birth weight.
Elemental mercury vapor and methylmercury compounds rapidly cross the placenta. Plasma
methylmercury concentrations are similar in the mother and newborn but concentration in
fetal RBCs is 30% higher. compared to the mother. Placental infiltration with lytic lympho-
cytes has been noted.
Breastmilk may contain around 5% of mother's blood mercury levels. Suckling infants may
accumulate high blood levels if rnothers are continuously exposed.
TOXIC DOSE
Lethal dose for mercuric chloride: 10-42mglkg
Most of the reported toxicities of mercury stem from chronic exposure. Long term daily intake
of methylmercury at levels between 3-7 meg/kg/day causes initial toxic symptoms like
paresthesia.
The fetus is more sensitive to the effects of mercury and may show untoward effects at lower
levels.
EXPOSURE LIMITS
nV·TWA Im9/m') REllmg/m'j 10lH Img/m')

Inorganic Mercury
(metal! 0.05IACGIH 19901 O.lINIOSH 19921
!inorganic cpdsl O.lIACGIH 19921 0.1 (NIOSH 1992)
lvaporl 0.05 nglm 3 281NIOSH 19901
(NIOSH 19921·
Organic Mercury
(alkyl compoundsl D.D1IACGIH 19921 D.mINIOSH 19921 10 INIOSH 1990)
(aryl compoundsl D.l IACGIH 1992) D.l(NIOSH 19921
Exposure toair mercury levels of0.1 mglm 3leads 10 anincrease inthe incidence 01 intentional tremors. lower air cencenne-
tions. however, have been observed tocause non·specific signs and symptoms such as anorexia, weighlloss. and psychological
disturbances like shyness and nervousness. II is therefore difficult to eslab~sh alower limit at which no effects occur.
AOI
PTWI 5 mcglkg (JECFA 1978; WHO 1976)
Air
The concentration of atmospheric mercury is very low (10-20 ng/rn') and does not contribute
much to total daily Intake. A concentration of 50 ng/m? would mean a daily intake of
approximately I mcg. In areas of high mercury production such as mines. smelters and
refineries, daily intake can go as high as 30 meg.
Occupational exposure to the acceptable level of0.05 rng/m' represents an intake ofaround 480
mcg andmanlfests as blood concentrations of3.5 mcg/dL. The corresponding ambient air
concentration for the general population is 0.0 IS mgzm'.
Surface Water
EPA limits (inorganic) 144 ppt
Levels are generally <Sng/l., though various studies have measured levels in oceans as <300 ngl
L. and <200 nglL for uncontaminated bodies of'frcshwater. Soon after the contamination of
Minamata bay. water mercury levels increased to 600 nglL. Rivers in heavily industrialized
areas have values as high as 700 ng/L.
Drinking Water
MCL 0.002mglL(EPA 1991)
MCLG (inorganic) 0.002 mglL (EPA 1991)
EPA and FDA limits 2 ppb
WHO (1971) advised upper limit I mcglL
Since most sources have mercury levels of not more than 50 nglL, intake from drinking water
amounts to only about <0.1-0.4 mcg daily. However. natural waters from areas with
mineralized mercury deposits may have levels as high as 300 nglL.
Soil
Levels range from 20·625 nglg ofsoil.
Food
Limit for seafood products I ppm (FDA 1984)
Limit for treated seed grain 1 ppm (FDA 1980)
Thc total intake ofmcrcury varies according to diet. Average daily intake from food is 50 ngl
kg BW.or 3.5 meg for an adult. Highest intake (levels of around 200-300 mcg) was reported
among those from coastal areas where fish is the main source of protein. In areas of high local
pollution. levels may be much higher than 300 mcg.
Intake oftish and fish products is the greatest source of non-occupational exposure to mercury.
Methylation of inorganic mercury in water allows it to be transported in aquatic food chains,
accumulating according to trophic level, until it reaches its highest concentration in large
carnivorous fish such as tuna and swordfish. "
Freshwater fish from uncontaminated waters contain mercury at levels between 100-200 meg!
kg wet weight. In contaminated areas, levels can be as high as 500- 700 mcg/kg. For oceanic
fish. the usual level is about 150 meg/kg. Large fish, however, may contain 200·1500 mcglkg.
Large carnivorous species caught in highly polluted waters may have as much a..s 5000 meg/
kg.
In food other than fish. mercury is present at concentrations of below 60 meg/kg. Levels may
increase in areas where methylmercury fungicides arc used.
TOXICOKINETICS
AbsDrption
Absorption is high for inhaled metallic mercury vapor (80%), low for oral ingestion of liquid
metallic mercury (40%), and also low for oral intake of inorganic mercury (2-38%). Oral
absorption oforganic mercury is almost complete. When ingested, inorganic mercury (such
as those found in thcrmometers) call be converted to organic mercury in the presence of acid
pH in the stomach.
DistributiDn
Inhaled metallic mercury readily passes through the blood-brain barrier and oxidation to inor-
ganic divalent cation can result in retention in the brain. Inorganic mercury can reach most
organs but their low lipcphilicity reduces their transport to the brain and fetus. The
distribution of methyl mercury is similar to metallic mercury, with high levels in the brain
and fetus. Both inorganic and organic mercury compounds are excreted in breast milk.
Inorganic mercury ccumulates primarily in the kidneys and brain as metallic mercury or
mercuric chloride. It is also found in the liver. spleen. bones. RBC. intestine: skin and
respiratory mucosa.
Animal data show that the kidneys accumulate the most mercury. regardless of the type of
mercury absorbed,
Hair may show trace amounts and has been used as an indicator of exposure since concentration
of mercury in hair is directly proportional 10 blood levels at the time of hair formation.
Excretion
Urinary and fecal routes are the main excretory pathways of metallic and inorganic mercury in
humans. with a body burden half-life of about 1-2 months (40 days) for inorganic mercury,
and 35-90 days for elemental mercury. The fecal pathway is the main excretory route for
organic mercury. with a biological half-time 01'70 days.
The rate of absorption of mercury is determined by its affinity for proteins containing SUlfhy-
dryl or thiol groups. Toxicity is related to its subsequent accumulation in specific tissues.
Mercury is transported to the kidneys as a glutathione complex and is bound by a
metallothioneine-like protein. Mercury is also able to cross the blood-brain-barrier as a
cysteine complex.
In the kidneys, mercury complexes cause epithelial cell damage, probably secondary to radical
formation and lipid pcroxidation. Defense mechanisms against glutathione. superoxide
dismutase. catalase and glutathione peroxidase are impaired. Acute renal failure may be due
to decreased reabsorption of sodium and chloride in the proximal tubules. increasing their
levels in the macula densa and prompting renin production. Subsequent vasoconstriction of
the afferent arteriole leads to filtration failure.
Early studies have already established that mercury causes neuronal degeneration, glial prolif-
eration in the cortex and cerebellum; adverse effects on Purkinje. basket. stellate and granule
cells: and peripheral nerve degeneration. It is possible that increased formation of reactive
oxygen species are particularly toxic to neurons which have either low endogenous glu-
tathione or inefficient glutathione redox activit)'. Increased intracellular calcium may also be
a factor since this causes proteolysis. endonuclease activation. and phospholipid hydroly-
sis.
In the developing brain. an immature transport system and an immature blood brain barrier
allow greater entry of mercury. Mercury affects microtubulcs by binding with tubulin, a
sulfhydryl rich protein. Damage to the mitotic spindle inhibits cell proliferation. Further-
more. cytoskcletal defects cause derangements in neuronal migration causing abnormal cell
organization and alignment distortion in the cerebral cortex. Neuronal migration starts at the
7th week of'gcstation and continues on to the third trimester and so exposure during this time
predisposes the infant to eNS disturbances.
An autoimmune response to mercury is also being entertained since it causes modifications in
the following: major histocompatibility complex class II, selfpeptides, T-cell receptors and
cell-surface adhesion molecules. Mercury also inhibits B cells by suprcssing proliferation.
expression of surface antigens. and synthesis of IgG and IgM. It is possible that increased
intracellular calcium initiates adverse changes in 9 cells.
TOXIC EFFECTS
Effects of toxic exposure to mercury are cumulative in nature, although some symptoms may
manifest acutely. Inhalation of toxic levels of elemental mercury may cause non-specific
symptoms within several hours. Ingestion ofa toxic dose of mercuric chloride can soon after
cause severe nausea. vomiting. diarrhea. and abdominal pain, culminating in cardiovascular
collapse. Azotemia and anuria develop within a few hours to three days. Death may occur
within 6-23 days post- ingestion.
Effects of chronic exposure depend on the type and amount of mercury consumed. Long-term
daily intake of 4 meg/kg ofmethylmercury. for example. increases the frequency of'paresthe-
sia by about 5%. There is a latent period of weeks to months between cessation of exposure
and onset of symptoms.
TOXIOROMES
ACUTE EXPOSURE TO ELEMENTAL MERCURY
Inhalation
Exposure is primarily through inhalation. eNS and renal problems are most prominent allow
levels ofexposure, while respiratory, cardiovascular and gastrointestinal effects occur 01
high levels.
Initial symptoms may include fatigue. fever, chills and elevated leukocyte count ('"metal fume
fever"),
Pulmonary: Cough, dyspnea. acute pneumonitis with respiratory failure, chest tightness.
pneumomediastinum and pulmonary fibrosis. Bronchiolar obstruction causes emphysema.
alveolar dilatation and bilateral pneumothorax. Subcutaneous emphysema has been ob-
served. Severeintoxication cancausenon-cardiogenic pulmonary edemawith cyanosisand
chest radiograph findings of bilateral infiltrates. Aspiration may occur. resulting in necrotiz-
ing bronchiolitis. granuloma formation and progressive pulmonary fibrosis. Death is sec-
ondary to respiratory fnilure.
Ren ..l: Accumulation of mercury in the kidney: proteinuria. changes in urinary acid excretion.
hematuria. nligura, acute renal failure with proximal convoluted tubule necrosis or degenera-
tion.
Neurologic: Symptoms do not vary according to duration of exposure. Some symptoms may
intensify or become permanent as exposure duration and concentration increase.
Neuromuscular changes (tremors. fasciculations, weakness. myoclonus. muscle atrophy.
muscle pains. unsteady gait. slurred speech. seizures)
Polyneuropathy (paresthesia. stocking-glove sensory loss. hyperactive tendon reflexes.
slowed sensory-motor nerve conduction velocities)
Sensory disturbances (hearing loss. visualfield cuts. numbness. tingling. decreased pinprick
and vibration sensations. photophobia) .
Personality changes/psychiatric problems (emotional lability. nervousness, excessive shy-
ness. confidence loss. lack of ambition, loss of libido. auditory hallucinations).
Neurobehavioral changes characterized by anxiety, depression. irritability, emotional in-
stabilityand regressive behavior. are labeled as erethism.
Cognitive disturbances (memory loss. poor concentration)
Cardiovascular: Increased blood pressure and heart rate; palpitations
Gastrointestinal: Nausea. vomiting. diarrhea. anorexia and abdominal cramps: stomatitis. ex-
cessive salivation. difficulty swallowing, gingivitis.
Hematologic: Elevated leukocyte count with neutrophilia: thrombocytopenia and nosebleeds.
Hepatic: Hepatocellular dysfunction ~ elevated SGPT. ornithine carbamyl transferase and
serum bilirubin: decreased synthesis of hepatic coagulation factors. Hepatomegaly and
central lobular vacuolation on autopsy.
Ophthalmologic: Redness. burning sensation. conjunctivitis
Reproductive: No apparent effect in fertility but with note of increased rate of spontaneous
abortions. stillbirths. congenital malformations and materna! complications on parturition.
Dysmenorrhea and meno/metrorrhagia noted in exposed women.
Others: May simulate mucocutaneous lymph node syndrome (Kawasaki Disease)
Subcutaneous I Intramuscular Injection

Note: Cases have been admitted at the Philippine General Hospital wherein toxic manifesta-
tions ofpoisoning were seen after subcutaneous or intramuscular injection ofmercury: the
patients believed that mercury is a IOnicand injection increases muscular strength.
Pulmonao': Embolization can result in restrictive lung disease
Dermal: Local inflammation. abscess formation and localized ischemia or gangrene.

Dermal Exposura
Erythema, purpura, heavy perspiration. skin peeling on palms and sales.
CHRONIC EXPOSURE TO ELEMENTAL MERCURY

Inhalation
The classic triad of chronic elemental mercury poisoning includes:
oral manifestations of gingivitis. salivation and stomatitis
intentional tremors
erethism
NeurologicIPsychological: (See discussion on acute exposure.) Motor system disturbances
may be reversible upon cessation of exposure. Cognitivedeficits may be permanent.
Renal: Proximal tubulardamage; glomerulosclerosis; changesin foot processes of glomerular
basement membrane-associated cells with deposition of IgG and C3; nephrotic syndrome
(proteinuria,albuminuria, hyalinecasts in urine, edema). Other possiblelab findings:
increased urinespecificgravity
increased urinaryN-acetyl-Jl-glucosaminidase
increased urinaryexcretion ofTamm-Horsfall glycoprotein
increased urinaryexcretion of tubularantigens
decreased urinary pH
excretionof glycoaminoglycans, prostaglandin E2 and F2a, and thromboxane 82
Cardiovascular: Palpitations, hypertension, decreased cardiovascular reflex responses; pos-
sible increased likelihood of death secondaryto ischemic heart disease or cardiovascular
disease.
Gastrointestinal: Stomatitis, increased salivation, soregums,oral ulcers,diarrhea.
Hematologic: Decreased hemoglobin and hematocrit, increased mean corpuscularhemoglobin
concentration, decreased delta-aminolevulinlc acid dehydratase activity in erythrocytes.
Ophthalmologic: Greyish-brown or yellow haze on the anterior surface of the lens.
Immunologic: Idiosyncratic hypersensitive response: Acrodynia (Pink Disease or Swift's
Disease), characterized by erythematous rash, painful pink fingers, fever, splenomegaly,
.cardiovascular and neurologic symptoms. Various studies show both increases and de-
creases in immune activity.
Endocrinologic: Anecdotal reportof thyroidenlargement, elevatedtriiodothyronine and thy-
roxine, decreased thyroidstimulating hormone levels.
Note: Silver-colored dental amalgams typically contain about 50% metallic mercury. Dental
fillings may slowly release small amounts ofmercury which can be absorbed by inhalation,
absorption through the oral mucosa and ingestion. Preparation ofamalgams is an occupa-
;ional hazard/or dentists.
ACUTE EXPOSURE TO MERCURY SALTS

Ingestion
Intoxication is mainly due to ingestion. Patient may presentinitiallywith fatigue, weakness,
lowgrade intermittent fever.
Gastrointestinal: Irritation of thegastrointestinal tract manifests as stomatitis, severegingivi-
tis, sore throat, laryngeal erosion, nausea, vomiting, diarrhea and abdominal pain. Gas-
trointestinallesions range from mildgastritisto severe necrotizing ulcers and hemorrhage.
Mercuric chloride produces more severe symptoms compared 10 mercurous chloride.
Cardiovascular: Tachycardia, hypertension. Hematemesis and hematochezia maylead to car-
diovascular collapse.
Renal: Progressive renal dysfunction; initially manifests as proteinuria and hematuria; can lead
to acutetubularnecrosis, albuminuria, anuriaand uremia. Cardiovascular collapsecan result
in acute renal failure; rhabdomyolysis maybe a contributingfactor.
Neurologic: In children: drooling. dysphagia. irregular arm movements, disturbed gait.
Respiratory: Pulmonary edema. dyspnea
Hematologic: Pallor and anemia secondary to gastrointestinal bleeding; thrombocytopenia.
Musculoskeletal: Skeletal muscle degeneration. twitching, cramps.
Hepatic: Jaundice. elevated LFTs.enlarged and softened liver.
Dermatologic: Flushing. itching, swelling, desquamation of palms and soles; morbiliform
rashes. excessive perspiration. allergic reaction.
Dermal Exposure
Urticaria and vesicle formation. acrodynia, tachycardia and hypertension. irritability, restless-
ness, sleeplessness, weakness, photophobia. muscle twitching. hyperlhypoactive tendon
reflexes,confusion
CHRONIC EXPOSURE TO MERCURY SALTS

Ingestion
Dermatitis, gingivitis. stomatitis, tremors. erethism. renal dysfunction and acrodynia.
Chronic abuse of mercurous chloride can lead to chronic renal failure, severe colitis, irritability
and dementia. On autopsy: low brain weight and decreased neurons in the cerebellum.
O.,mal Exposu,.
Traditional medicines containing mercury may cause renal failure when applied to wounds.
Skin ointments may cause impaired renal function, edema, nephrotic syndrome, tremors,
anxiety. depression. delusions.
ACUTE EXPOSURE TO ORGANIC MERCURY

Ingestion
Exposure is primarily through the oral route.
Gastrointestinal: Diarrhea or constipation, vomiting. tenesmus, mucosal irritation, ulcers in
the upper gastrointestinal tract.
Neurologic:Ataxia, paresthesia, malaise.blurred vision, fasciculations, absence of deep reflexes
in arms. Babinski reflex,muscle wastingand weakness,musclepain. cerebellar ataxia, speech
dlfflcultics. paraplegia, spasticity, impaired sensation (taste, sight. hearing and smell), loss
of consciousness. Irritability. memory loss. depression. insomnia, hallucinations. excite-
ment.
Renal: Renal failure. tubular necrosis
Dermal: Rash. flushing. exfoliative dermatitis on hands and feet.
Cardiovascular: Changes in blood pressure and heart rate: myocarditis; ECG changes (ST
segment depression. T wave inversion, prolonged QT interval).
Respiratory: Bronchopneumonia, edematous alvcolitis.
Reproductive: Adverse effects on sperm and male reproductive organs; abortions and still-
births.
Inhalation
Respiratory: Dyspnea. respiratory depression. increased mucus production. bronchopneu-
monia.
Ncurologic: Death secondary to profound neurotoxicity.
Gastrointestinal: Inflammation of the mouth, excessive salivation. sore gums. carious teeth,
thin blue line at thc gums. infected and swollen posterior pharyngeal wall. nausea.
Dermal Exposure
Application of methylmercury or phenylmercury can cause rashes. blisters. hypersensitivity
reactions.
CHRONIC EXPOSURE TO ORGANIC MERCURY
Ingestion
Chronic methylmercury exposure leads to a triad of:
dysarthria
ataxia
visual field constriction
Neurologic: Damage to the cerebellum manifests as progressive Dimercaptosuccinic
incoordination, dysarthria, ataxia, loss of voluntary movement. acid 10MSA)
Also causes paresthesia. loss of sensation in the digits, decreased 10mg/kg/dosa PO q' 8
auditory acuityand erethism. Increased incidenceof noninflam- hours for 5 days
matory eNS disease. then 10mg/kg/dosa
Gastrointestinal: Necrosis and ulceration of intestinal tract. PO q' 12 hours for
Ophthalmologic: Degeneration of the calcarine cortical cells can another5 days.
produce"tunnel vision"and multiplescotomata. Insevereexpo- Reassess patient after
sure, visual field constriction may lead to complete blindness. treatment and
Cardiovascular: Increased incidence ofnon- ischemic heart disease. consider repeat
Renal: Polyuria,polydipsia.albuminuria,nephritis,tubular degen- therapy if mercury
eration. levels are still
elevated.
Inhalation
A report on chronic exposure to diethylmercury vapors showed N.Aeelyl.O,L.
pronounced gastrointestinal pathologies on autopsy. Another penicillamine
case of chronic exposureto phenylmercuric acetate showed liver Padia: 5· 10mg/kg/day
necrosis. PO in 3 divided
doses(maximum of
SPECIMEN ANO EXAMINATIONS FOR OIAGNOSIS 1 gm/day) given for
whole blood for mercury levels 5 days.
Biological limits: Adu)ts: 10· 20 mg/kgl
< J mcg/dL (inorganic mercury) day PO in 3 divided
< I mcg/dL (methyl mercury) doses(maximum of
Tentative maximum permissible concentration: 1 gm/day) given for
2 mcg/dL (inorganic mercury) 5 days.
10 mcgldL (methyl mercury) Give at least 1 hour
24-hour urine for mercury levels before meals.
Biological limits: <5 mcglg creatinine (inorganic mercury) Reassess patient after
Tentative maximum permissible concentration: treatment and
50 mcg/dL (inorganic mercury) consider repeat
Hair for mercury-levels therapy after a 10
Segmental hair analysis (I cmeach)is useful in determining expo- day rest if lead levels
sure or uptake of mercury through diet. Not a good biomarker are still elevated.
for inorganic mercuryexposure. Toxic erythema and
erythema mu)tiforme
ANTIOOTES are signs of allergic
Dimercaptosuccinic acid (DMSA) forms an inactivecomplex with reaction to penicil·
mercury. The chelate is less toxic than mercury and is more lamine. If noted,
rapidly excreted. discontinue treatment
N-Acetyl-DL-Penicillamine increasesthe excretion of mercuryaf- immediately.
ter acute exposure to mercury vapor. and can relieve symptoms Penicillamine has an
of chronic poisoning by both mercury vapor and alkylmercury. antimetabolic effect.
It has also been observed to be effective in preventing brain Discontinue treatment
damage in offspringof exposedanimals. if neutrophils drop
2,3-dimercaptopropanolol (BritishAntilewisite-BAL) has beenrec- below 15001mm'.
OCCUPATIONAL POISONING 6/
om mended for poisoning with mercury salts but u is contraindicated in alkylmercury poi-
soning and in neurological disorders caused by mercury vapor exposure.
TREATMENT
EMERGENCY FiElD MANAGEMENT (See Guidelines)
1. Rescue
2. Airway
3. Breathing
4. CirculatiDn
5. Decontamination
Gastric Decontamination - Elemental merCUD'
Inorganic mercury can be absorbed since it is converted into organic mercury in the stomach
Catharsis should be initiated 10 ensure immediate elimination. Give sodium sulfate only
if trained personnel arc present (see Guidelines), A second dose may be given if there is
no bowel movement within an hour.
Gastric Decontnmination· Mercury salt ingestion
Mercury salt ingestion may be treated with egg whites within 6 hours post-ingestion as
follows:
Adult: 10- 12 eggwhiles
Pedia: 6·8 egg whites
If trained personnel arc present and sodium sulfate is available. catharsis may be initiated
with sodium sulfate. A second dose may be given ifthere is no bowel movement within an
hour.
6. Drugs
7. Transport
EMERGENCY HOSPITAL MANAGEMENT (See Guidelinesl

1. Airway
2. Breathing
3. Circulation
4. Decontamination
Continue decontamination as described above. Procedures will depend on the type of
mercury and route of poisoning.
An X-ray may be done after catharsis to ensure evacuation of the mercury.
5. Drugs
Seizures
Patients with severe intoxication may present with seizures and must be treated accordingly.
Antidotal Therapy
Current literature may cite higher therapeutic doses for N·acetyl.D,L·penicillamine; how-
ever. clinical experience at the Philippine General Hospital has shown response to chela-
tion therapy at the indicated doses.
Maintenance
Maintain on NPO until patient is fully conscious.
Maintain adequate hydration and parenteral nutrition while on NPO.
Determine the presence ofdental amalgams and suggest removal.
Specific Problems
Status cpilepticus: thiopental sodium. general anesthesia. or neuromuscular blockade

Rhabdomyolysis: hydration. mannitol. sodium bicarbonate
Aspiration pneumonia: full antibiotic coverage until specific organism is identified
Nephropathy: diuretics. adequate hydration
Pneumothorax/pneumomediastinum: thoracostomy tube and air evacuation
Respiratory Distress Syndrome: place patient on mechanical ventilation with PEEP
OCCUPATIONAL TOXICOLOGY INTERVENTIONS (See Guidelinesl

Workers in manufacturing or processing industries which use mercury should be educated on
the possible health hazards and the proper safety precautions to take when handling this
substance. Dentists preparing amalgams may be exposed through dermal absorption or
inhalation. .
Regular monthly medical evaluations should be done on employees at risk of exposure with
particular emphasis on blood mercury level monitoring and neurological examination.
The health personnel complement of manufacturing or processing plants should include a first-
aider. a part-time occupational health nurse with previous training in handling mercury
poisoning. and an occupational health consultant.
In case of fire. all extinguishing agents may be used.
HAZARDS TO THE ENVIRONMENT ANO THEIR PREVENTION

Natural sources of mercury arc greater than anthropogenic sources. However. the latter cause
more harmful local contamination. Examples of epidemics of mercury poisoning include: a
fire in a mercury mine in 19lh century India. spillage of metallic mercury from a British
warship in the 1800s. the major methylmercury poisonings of Minamata Bay and Agano
River in the 1960s. and poisoning from bread prepared from cereals treated with mercury
fungicides in Iraq in the 1970s.
Mining plants and refineries should be sited away from populated areas and ground water
reservoirs. Environmental monitoring should be done to check for water pollution and its
danger to aquatic life. Bioaccumulation is observed in game fish, shellfish, and fish-eating
birds and mammals. thus posing a threat to the food chain important to humans.
Alkylmercury fungicides arc still being used. Accumulation of mercury occurs in seed eating
rodents and birds. and subsequently carnivorous birds. There is a potential hazard to
humans in thc consumption of game birds from areas where methylmercury fungicides are
used. and from consumption of bread or porridge prepared from contaminated cereals.
REFERENCES
Casarett LJ and Doull J, Toxicology:The Basic Science of Poisons. New York: Macmillan
PublishingCompany. 1991.
Ellenhorn MJ et al., Ellenhom oS Medical Toxicology: Diagnosis and Treatment of Human
Poisoning, 2ndcdition. Baltimore: Williams and Wilkins, 1997.
Haddad LM and Winchester JD, Clinical ManagementofPoisoning and Drug Overdose, WB
ties, InternationalChemicalSafety Cards: Mercury. International Programme on Chemical
Safety. 1988
Klaassen CD. Amdur MO, Doull J. eds .. Casarettand Doutt s Toxicology: The BasicScience of
Poisons, 5th ed. New York: Macflraw-Hill. 1996.
Olson KR. cd.• Poisoning and Drug Overdose. Norwalk: Appleton qnd Lange. 1994.
U.S. Department of Health and 1·luman Services. ToxicologicalProfilefor Mercury(Updote).
Atlanta: US Department of Health and Human Services. May 1994.
World Health Organization. Environmental HealthCriteriaMonograph # I: Mercury. Geneva:
WIIO. 1976.
ORGANOPHOSPHATES
SOURCES
CHEMICAL NAME insecticides
Selected organophosphates currently registered with the Philippine fungicides
Fertilizerand PesticideAuthority:
Chlorpy,ifos· O,O-diethyl 0-(3.5.6-trichloro-2-pyridyl) phosphoro-thioate
Oia,inon . O,O-diethyl 0-[6-methyl-2-(l-methylethyl)-4-yrimidinyl] phosphorothioate
Diehlo,vos I OOVP . 2.2-dichlorovinyldimethyl phosphate
Oimethoato . Phosphorodithioic acid. O.O-dimethyl S-[2-(methylamino)-2-oxoethyl] ester
Fenitrothion . O,O-Dimethyl 0-(3-methyl-4-nitrophenyl) phospho-rothioate
Fenthion . O,O-Dimethyl-O-(4-methylthio-m-tolyl) phosphorothioate
Malathion· Diethyi-2-(dimethoxyphosphoinothioylthio) succinate
Omethoato . O,O-dimethyl-S-methylcabamoylmethyl-phospho-rothiate
Mothamidophos O.S-Dimethyl phosphoramidothioate
Mevinphos . 2-methoxycarbonyl-l-methylvinyldimethyl phosphate
Phonamiphos . Ethyl-3-methyl-4-(methylthio)phenyl( I-methyl-ethyl)phosphoram idate
Phosphamidon . 0, 0-Dimethyi-0-(2-chloro-2-diethylcarbamoyl-l-methylvinyI) phosphate
Temephos ·0,0'-tthiodi-a.I-phenylene) bis(0,O-dimethylphospho-rothioate)
Banned organophosphates (See Annex A):

Parathion othyl . O,O-diethyl-0-4-nitrophenylphosphorothioate
Loptophos . 0-(4-bromo-2.5-dichlorophenyl) O-methyl phenyl-phosphonothioate
EPN . 0-ethyl-0-4-nitophenyl phenyl-phosphorothioate
A,inphos othyl· O,O-diethyl S-[(4-oxo-I.2,3-benzotriazin-3(4H )-yl)methyl] phosphorodithioate
Methyl parathian- O,O-dimethyl 0-(4-nitro-phenyl) phosphorothioate
Monoerotophos . (E)-dimethyl-l-methyi-3-(methylamino)-3-oxo-l-propenyl phosphate (9CI);
dimethyl phosphate ester with (E)-3-hydroxy-N-methylcrotonamide (8 CI)
SYNONYMS CHEMICAL FORMULA

CAS Number
Diazinon RI and R2: alkyl or aryl groups
RI
,,--II0 RI fI
"--P-X
333-41-5 X: wide variety of structures; aliphatic, /P-X
R2
/
Diehlo,vos I OOVP aromatic or heterocyclic R2
62-73-7
Dimethoate PHYSICAL STATES
60-51-5 Solid and liquid
Fenitrothion
122-14-5 PHYSICAL AND CHEMICAL PROPERTIES
Fenthion Esters, arnides, or thiol derivatives of phosphoric. phosphonic,
55-38-9 phosphorothioic, or phosphonothioic acids.
Malathion Slightly soluble in water; high oil-to-water partition coefficient; low
121-75-5 vapour pressure.
Methamidophos
CLASSIFICATION
10265-92-6
Phosp hate chlorlenvinphos, crotoxyphos, dichlorvos, dicrotophos, heplenphos, mevinphos,
Phenamiphos ,
monocrotophos, naled, phosphamidon, TEPP, lelrachlorvinphos, lriazophos
Fenamiphos
O-alkyl phosphorothioate _
22224-92-6
amiton, demeton-S-methyl, cmethcate, crydemetcn-mathyl, phanm,
Phosphamidon
vamidothion, azcthcata, bremcphcs. bromophos-ethyl, chlorpyriphos,
13171-21-6 chlorpyriphos-methyl, coumaphos, diazinon, dichlcfenthicn, fenchlorphos,
Temephos lenitrothion. fenthion, iodofenphos, parathion, parathion-melhyl. pyrazophos,
3383-96-8 pyrimiphos·ethyl, pyrirniphos-methyl. sulfolep, temephos, thionazin
t'hosphorodithioatl 1lIIi~_. azinophoHthyl, azinopIm<nethyi. dinathoa te, lIo'athion, lisullot", at/'Oon.
formothion. malathion. mecarbam. menazon. methidathion, morphothion. phenthoate.
phOl'ate, phasllone. phosmet, prothoate. thiometon
s- alkyl phosphorothioatl. profenofos. trifenofos
S· Ilkyl phosphorodithioate prottiofos, sulprofos
Phosphoremidltt erutermate, fenamiphos. fosthietan
Phosphorotriamidlte rrihiphos
Phasphorothioamidate m8thanidophos. isofenphos
Phosphonate butonate. trichlorfon
Phosphonothioate EPN. trichlornat,leptophos. cyanotenphos
HAZARDS
Hazard classification lor organophosphates is basedon the determined rat oral LDj W
Pesticideshave beenclassified according to restrictions on use by the WHO/FAO/UNEP (See
AnnexB).
Table 1. Hazard category of selected organophosphate pesticides as determined byoral LOy in rats
Organophosphate FPA Physical state Rat oral lD~
Hazard Category (mg/kg)
Azinphos-ethyl I solid 12
Azinphos-methyl 1 solid 16
Chlorpyrifos II solid )35
Dilzinon II liquid 300
Milithion II liquid 100
Methyl parathion I 14
Mevinphos I liquid 4
Monocrotophos I solid 14
Phospamidon I liquid 7
Organophosphates are generally not strongmammalian mutagens or carcinogens.
Diazinon Has been linkedto chromosomal damage in humans, possiblyincreasing the
riskof cancer.
Dichlorvos Someevidenceof carcinogenicity incertainspeciesof rats. Datastill incon-
clusive.
Dimethoate Havebeenlinked tochromosomal damage in humans, possibly increasing the
risk of cancer. Several studies showed presence of spleen and livercarcino-
mas in exposed rats but studies are not adequate (0 ascertain presence or
absence of carcinogenic response.
Fenitrothion No evidenceof carcinogenicity in rats and mice.
For the majority of organophosphorus pesticides, no adverseeffectswere notedin experimen-
tal animals. However, at very high doses, these compounds are embryotoxic and can
significantly retard the growth of the fetus. Some offspringexposed to high dose organo-
phosphates during gestation were noted !t> have cholinergic symptoms.
Studieswith trichlorfon showed offspringwith hypoplasia ofthe cerebellum. accompanied by
severeataxiaand tremors.
TOXIC DOSE
Mean fatal dose for malathion: 60g
Lethal dose for diazinon: approximately 25g
Acuteoral LDj U of organophosphates in rats ranges from 4_0-2018 mglkg. HumanLDj O may
be estimatedby dividingthe rat LD,,, valuesby • factorof 10 to 100.
ADllmg I kg BWI Solvents such as toluene. xylene, kerosene or isopropanol present in
Chlorpyrilos organophosphateformu/ations can themselves produce toxic effects.
0-0.0 \ (1982)
Diazinon EXPOSURE LIMITS
0-0.002 (1993)
Dichlorvos Organophosphatt TLV-TWA PEL IDLH
0-0.004 (1993) (mg!m') (mg/m') (mg/m')
Dimethoate Chlorpyrifol 0.20.2
0-0.002 (1996) Dilzinan 0.10.1
Edilenphos DicblorvoslDDVP 0.1 I 200
0-0.003 (1981) Malathion 10 5000
Ethoprophos total dust 10
0-0.0003 (\987) respirable fraction 5
Fenitrothion Methyl parathion 0.20.2
0-0.005 (1988) M,vinpbol 0.092 0.\ 4 ppm
Fenthion Monocrotophol 0.25 0.25
0-0.007 (1995)
Malathion Food
0-0.02 (1996) Generally, organophosphales havemoderate to hightoxicity forfresh-
Methamidophos water and estuarine fish; moderate to high toxicity for birds; very
0-0.004 (\990) high toxicity for honey bees.
Methidathion There is no evidence of bioaccumulation but direct poisoning can
0-0.001 (1992) occur from consumption of sprayed food or contaminated meat
Omethoate products.
ADI (1996)
withdrawn Air
With the exception of dichlorvos, organophosphates have low vola-
Phenthoata
tility. Aerosols may be spread by wind but there is no evidence of
0-0.003 (1984) contamination beyond 1·2 km from a spraying source.
Phorate
0-0.0005 (1996) Water
Phosalone Organophosphates may contaminate water through industrial waste
0-0.00\ (1993) or effluents, seepage of buried toxic wastes, or from agricultural
Phosphamidon run-off Bacteria can degrade some organophosphates into less
0-0.0005 (\986) toxic compounds, depending on the temperature and pH of the
Pirimiphos methyl waterand half-lifeof the pesticide,though these mechanismsmay
0-0.03 (1992) be overwhelmed by large-scalecontamination.
Pyrazophos
0-0.004 (1992) TOXICOKINETICS
Terbufos
Absorption
Absorption occurs by all routes of exposure: inhalation, dermal ab-
0-0.0002 (1989) sorption and ingestion. Most organophosphates are lipophilic
Triazophos and are not ionized, thus facilitatingcellular uptake.
0-0.001 (1993)
Distribution
Tracking the distribution of unchanged compounds is difficult because of rapid metabolism.
The half life is comparatively short, though in acute poisonings, significant amounts may
remain in the body, particularly in adipose tissue.
Metabolism
Biotransformation reactions involve mixed-function oxidases, hydrolases and transferases.
Organophosphate oxons may also bind to tissues. Cytochrome P450, flavin-containing
monooxygenases and glutathione Svtransfcrases contributeto detoxification.
Excretion
Most organophosphates are degraded quickly. Accumulation does not occur, though removal
from fatty tissues proceeds more slowly. Elimination is mostly via the urine, with the rest
removed via the feces and expired air.
Effects on the central and peripheral nervous systems result from increased cholinergic activ-
ity. Organophosphates and their potent sulfoxidation (voxon") metabolites interfere with
the action of acetylcholinesterase, the enzyme responsible for the hydrolysis ofacetylcho-
line to choline and acetic acid.
Acetylcholine is an important neurotransmitter in the CNS. It is an essential component of
parasympathetic post- and pre-ganglionic synapses; sympathetic pre-ganglionic synapses:
and the neuromuscular junction. I
Phosphate radicals from organophosphates bind the active serine-containing site of acetylcho-
linesterase, thus rendering it inactive. The consequent synaptic accumulation ofacetylcho-
line leads to continuous stimulation in the synapse and the onset of nicotinic, muscarinic or
central nervous system effects.
In Organophosphate Induced Delayed Neuropathy (OPIDN), there is inhibition ofNTE (neu-
ropathy target esterase or neurotoxic esterase). It is also possible that neurotoxic organo-
phosphates phosphorylate calmodulin kinase II (CaM kinase II) in nerve cells. increasing
intracellular calcium and enhancing proteolysis of cytoskcletal proteins. Increased CaM
kinase II activity also affects u- and p-tubulin, MAP·2 and neurofilaments, causing disas-
sembly of cytoskeletal proteins. Axonal transport is therefore impaired; further internodal
swelling and proteolysis lead to axonal degeneration.
The following organophosphates have been associated with OPIDN: cyanofenphos, diisopropyl
phosphorofluoridate, EPN. leptophos, mcrphos, methamidophos, methylparathion, mipafox,
ornethoate. parathion. trichlornat, trichlorphon.
Recent studies on the effects of organophosphates on the immune system show that these bind
to or alter membrane-bound proteins on monocytes and ncutrophils. thereby suppressing
their activity. There is also evidence that these elicit autoimmune reactions. Disturbances in
immune responses decrease resistance to antigens, thereby increasing the likelihood ofcon-
tracting infectious diseases or exacerbating pre-existing infections. Chromosomal damage to
lymphocytes. or decreased host resistance to cancer-initiating viruses, may be possible.
mechanisms for increased incidence of cancer.
TOXIC EFFECTS
Onset of EffectslOeath
Death may occur within 5 minutes to 24 hours of exposure. depending on the type and
concentration of pesticide.
TOXIOROMES
Severity System Involved 1\1 a nifesla lions
Mild Mainly Muscarinic Malaise, vomiting. nausea, diarrhea, sweating, abdomi-
nal pain, hypersalivation, miosis
Moderate Muscarinic & Nicotinic Dyspnea, decreased muscular strength, bronchospasm,
bronchorrhea, speech impairment, muscle fasciculation.
tremor, motor incoordination, bradycardia, involuntary
urination/defecation, muscular cramps, hypotension,
hypertension
Severe Muscarinic. Nicotinic & eNS Coma, respiratory paralysis, extreme hypersecretion.
cyanosis, sustained hypotension. extreme muscle weak-
ness. muscular paralysis, convulsions, behavioral
changes
ACUTE EXPOSURE
Ingestion
Pulmonary: Respiratorydistress may be observed due to the following:
• excessive salivation and production of bronchial secretions, bronchospasmand wheezing
- pulmonary edema
- chemical pneumonitisafter aspiration of petroleumdistillate carrier
- aspiration pneumonia in patients with vomiting and depressed sensorium
- muscle paralysis contributing to respiratory embarrassment
-ARDS
Neurologic:
Muscarinic:
dyspnea. cyanosis, pulmonary edema, anorexia, cramps, fecal incontinence, tenesmus,
hyperhydrosis, hyperlacrimation, bradycardia, hypotension, miosis.urinaryincontinence,
bronchoconstriction, increased bronchial secretions
Nicotinic:
cramps. fasciculations, tremors, areflexia, muscle paralysis, decreased muscle strength,
speech impairment, hypertension, tachycardia, pallor, mydriasis, motor incoordination
eNS:
restlessness, emotional lability, headache,tremor,drowsiness,confusion,slurred speech,
ataxia generalized weakness, coma, convulsions,respiratorydepression, cardiovascular
depression
The intermediate syndrome may be noted 1-4days after acute poisoning. It is characterizedby
proximallimb paralysisnot responsiveto atropine, and may progressto involvesensorimo-
tor muscles.
Organophosphate Induced Delayed Neuropathy (OPION) is a sensory-motor axonopathy
occuring 6 days to I month (usually 2 weeks) after exposure.
Progressive Phase (lasts 3-6 months after initial onset):
Lower extremity cramps, burning sensation, tightness, pain; followed by numbness and
tingling. weaknessand atrophy of peroneal muscles(foot drop), hypoesthesia, steppage
gait. positive Rhomberg, absent knee and ankle jerk; may progress to bilateral flaccid
paralysis 2-4 weeks after; may also involve the hands (weaknessand hypoesthesia).
Stationary Phase (lasts 3-12 months after initial onset):
Paralysis is stationary (bilateral paraplegia or quadriplegia); sensory symptoms may
disappear.
Improvement Phase (lasts 6-18 months after initial onset):
Definitive improvement in upper extremitiesand extensor movementsof lower extremi-
ties. Recovery depends on severity of exposure, with complete return of function for
mild exposure and persistence of lower extremityparalysis in severe cases.
CHRONIC EXPOSURE
Inhalation
Neurologic: Central nervous system effects may include memory impairment, depression,
confusion and thought disorders. Symptoms of OPION may be observed since weak
OPION action of organophosphates can manifest in chronic exposures. It is also possible
that neuropathiesare due to prolonged inhibitionof acetylcholinesterase rather than inhibi-
tion of neurotoxicesterase.
Hematologic: Aplastic anemiaand other related blood dyscrasia
Renal: Renaltubular abnormalities
Genetic: Chromosomal damage
Immunotoxicity: Increasedincidenceand severityof infectiousdisease;elicits hypersensltjv-
ity reactions
Others: Organ-specific toxicity to the heart and liver.
68 Standard Treatment Guideline.

Dermal Absorption
Atropine sulfate
Dermal:Necrotizingexfoliativedermatitisand
erythema multiforme (Stevens-Johnson The amount to be administered depends on the
Syndrome), chloracne, allergic sensitization, severity of the case.
and contact dermatitis. Initial dosages are as follows:
Severity Dosage
SPECIMEN AND EXAMINATIONS FOR DIAGNOSIS mild Adult· 1 ·2 mg IV q'15 min
5 ml heparinizedblood kept at low Pedia· 0.01 mg/kg/dose IV q'15
temperaturefor red blood cell cholinesterase min
Normal values: 0.75-0.92 spll/nour moderate Adult· 2 . 3 mg IV q'15 min
[Michel method) Pedia . 0.03mg/kg/dose IV q'15
Biologicallimits: min
RBC - 3()% inhibition severe Adult' 3 . 5 mg IV q'15 min
Plasma - 50% inhibition
Pedia . 0.05mg/kg/dose IV q'15
Whole blood - 30% inhibition
min
Classification of level of poisoning based on
Continue administering atropine every 15 minutes
RBC cholinesterase determination
until the following parameters are reached:
Mild poisoning: 20-40% depression
heart rate.?. 140lminute
Moderate: 40-60% depression
pupils~ 4 mm
Severe: >60% depression
200 ml urine (6 hour collection) for urine
hypoactive bowel sounds
metabolite dry conjunctival and oral mucosa
blood for liver function tests, prothrombin Parameters of 2/4 or lower may indicate
time underatropinization.
blood for high and low density lipoproteins, Dose a~d frequency of atropine administration can
random blood sugar. electrolytes bereduced by increments of 1 . 2 mg q' 2 . 4
blood for CRC with reticulocyte count, plate- hours if full atropinization has been maintained
let count for 3 to 4 doses. Upward or downward
blood for ABG titration is done according to patient's
ECG and Chest x-ray response.
During maintenance therapy, heart rate should not
ANTIDOTE fall below SO/minute. In the elderly. heart rate
Atropine as physiologic antidote of SO·SO/min may be sufficient.
Pralidoxime as pharmacologic antidote(an
oximeenxymeactivator).
TREATMENT
EMERGENCY FiElD MANAGEMENT (See Guidelines)
1. Rescue
2. Airway
3. Breathing
Poisoning patients may present with ventilatory failure. hypoxia or bronchospasm. Respi-
ratory failure requires assisted ventilation which may be delivered manually with a bag-
valve-mask or bag-valve-endotracheal device. Hypoxia requiresoxygensupplementation.
Bronchospasm. detected by wheezingwith cyanosis may be treated with oxygen supple-
mentationand atropine I mg in 2 ml saline given as nebulization.
4. Circulation
5. Decontamination
Gastric decontamination - Emesismay be done if antidotes arc unavailable and the nearest
medicalfacilityis inaccessible.
6. Drugs
If trained personnel are present and atropine sulfate is available. atropinization may be
started.
7. Transport
r-------, EMERGENCY HOSPITAL MANAGEMENT
Pralidoxime
(See Guidelines)
Adult: 1 gm in 250 ml
DsW to run for 1
1. Airway
2. Breathing
hour
Ifpatient is cyanotic determine the nature of the oxygen deficiency. If
Pedia: 50 . 100 mglkg
it is due to ventilatory failure. start mechanical ventilation. Ifit is due to
in 125 ml O,W to
hypoxia. start oxygen supplementation and determine depth of hypoxia
run for 1 hour
with Arterial Blood Gas determination. If bronchospasm is apparent.
Ifthere is a response,
nebulize patient with atropine I mg in 2 ml saline.
continue for 3 more Cyanosis should he correctedprior to giving atropine IV since this may
doses given every 6 cause ventricularfibrillation. Treat the cyanosis first and give atropine
hours. 1M until the patient has stabilized.
For severe cases, the 3. Circulation
second dose may be 4. Decontamination
given 1 hour after Gastric decontamination - Do not induce emesis unless there are no
initial dose and the other decontamination modalities available. Gastric lavage with water
subsequent doses at 6 may be done. Only a single dose of charcoal lavage is necessary. Always
hour intervals. follow charcoal lavage with cathartics such as sodium sulfate.
Caution should be 5. Drugs
observed in the use of Seizures - Patients with moderate to severe intoxication may present
pralidoxime in patients with seizures and must be treated accordingly.
who are severely Antidotal therapv • Start pralidoxime and atropine.
poisoned with Start diazepam and phenytoin for patients with nicotinic manifesta-
dichlorvos. malathion tions.
and methylparathion For intermediate syndrome. atropine maynot alter progressionof muscle
formulations. paralysis. Respiratory support should be provided until recovery oc-
Pralidoxime is eontrain- curs.
dicated in carbamate Treatment for OPIDN is symptomatic since the organophosphorus com-
poisoning and pounds arc already cleared by the time symptoms of OPIDN apear.
ineffective in the Diazepam may be useful in treating spasticity.
following:.
crotoxyphos (ciodrinJ Maintenance
dimefox Maintain on NPO until patient is fully conscious and atropine is given
dimethoate by oral route.
methyl diazinon Maintain adequate hydration and parenteral nutrition while on NPO.
methyl phencapton Correct any electrolyte or pH imbalance.
ph orate Consider RBC transfusion in severe cases.
schradan
triamiphos (wepsin) Specific Problems
'- Pulmonary edema: atropine I mg in 2 ml normal saline solution as
-1
nebulization: furosemide 1mglkg/dose
Rhabdomyolysis: hydration. mannitol. sodium bicarbonate.
Seizures: diazepam. phenytoin. lcrazeparn, mannitol
Aspiration pneumonia: full antibiotic coverage until specific organism is identified; avoid
aminoglycosides
Atropine toxicity: manifests as flushing and irritability in addition to the atropinization param-
eters. If this occurs. temporarily discontinue or taper atropinization and hydrate the pa-
tient. Consider administration of diazepam for possible seizures.
Arrhythmia: Do not give p-blockers or lidocaine. Instead, give calcium channel blockers or
phenytoin.
Never give ontocholincstcrascs (physostigmine/neostigmine).
The following drugsshouldbeavoided:

aminoglycosides morphine and other opiates
aminophylline phenothiazines
barbiturates quinine
B-blockers succinylcholine
sulfonamides furosemide
local anesthetics especially procaine and derivatives
theophylline and other xanthincs
OCCUPATIONAL TOXICOLOGY INTERVENTIONS ISee Guidelines)

Employees must be educated on the possible health hazards posed by exposure to pesticides.
and the safety precautions which should be taken.
Regular monthly medical evaluations should be done on those at risk of exposure with particu-
lar emphasis on the neurologic examination. Employees should be examined for signs and
symptoms of chronic poisoning with confirmatory laboratory testing done as necessary.
Red cell cholinesterase should be done regularly depending on duration and frequency of
exposure. and type ofjob.
Medical records should be kept for at least 30 years due to the long latent period between
exposure and appearance of chronic effects.
For companies formulating category I and 11 pesticides, health personnel should include a first-
aider. a part-time occupational health nurse with previous training in handling pesticide
poisoning. and an occupational health consultant. This health personnel complement is
recommended for companies with 10 or less employees. For companies with 11 to 50
workers. the minimum required health personnel include a part time occupational health
physician. a full-time nurse and two first-eiders.
Pesticides arc accompanied by a hydrocarbon solvent that is often flammable. Fire extinguish-
ing agents should be readily available and precautions should be taken to prevent sparks that
may start Fires.
Mix pesticides in a well-ventilated place away from homes and. Mixing implements should be
separate from the implements used in preparing food. When mixing and applying pesticides.
proper personal protective equipment should be worn: face shields to protect against splashes:
gauntlet gloves made of nitrile, PVC. or synthetic rubber (not natural rubber); long sleeved
shirt with gloves worn inside the sleeves: boots made of the above materials worn inside the
long pants. The above equipment should be washed with soap and water after every use.
When applying the pesticide. make certain that the spray is not carried by wind toward the
person spraying, unprotected persons or homes. Do not allow family members to walk
through a newly sprayed field. Warning signs showing that spraying was done should be
installed, with the safe re-entry date specified. Ensure that well-water is not contaminated
by run-off from the fields being sprayed.
After applying pesticides. the worker should bathe with soap and water and change into clean
clothes. Wash hands and face before smoking or eating.
Store pesticides only in the original containers - never in food. beverage, feed. or seed contain-
ers. Place these in rooms or storage areas that can be locked and are not accessible to children.
Store pesticides away from food. feed. and seed storage areas. preferably in self-scaling
drums to prevent leakage.
In case of spills, the following agents can be used to hydrolyze organophosphorous com-
pounds: sodium hypochlorite (bleach), 10% sodium carbonate solution (washing soda). 5%
sodium hydroxide (caustic soda).
HAZAROS TO THE ENVIRONMENT ANO THEIR PREVENTION

Organophosphates can pollute the environment through discharge from formulating plants.
seepage of buried toxic wastes. agricultural run-off or accidental leaks and spills.
Dispersal of pesticides must be either by burying in it cemented pit with lime and sawdust to
preventleakage into ground water. or by incinerating at IOOO"C. Empty pesticide containers
should be buried in a pit at least 50 cm deep in an isolated area away from water supplies.
OCCUPAnONALPWSONING 71
~
Table 2. Organophosphate pesticides in the Philippines
Classification of
Abate 50 EC temephos 500 g I lite, agricultural Cyanamid Agricultural Prod. Phils.. Inc.
Abate 56 temepbos lOglkg agricultural Cyanamid Agricultural Prod. Phils.. Inc.
Acardust esbiol household use Zuellig Pharrna Corp.
piperonyl butoxide pyrethroid
Actellic 25 EC pirimiphos methyl 250 g I liter agricultural Jardine Davies. Inc.
Actellic PH pirimiphos methyl household use Jardine Davies. Inc.
Afugan 30 EC pyrazophos 300 9 I lite, agricultural Hcechst Philippines
Ambithion 100 E malathion 410 9 I lite, agricultural Cyanamid Agricultural Prod. Phils.. Inc.
fenitrothion 410 9 I liter
Apache 10 6 cadusafos 100glkg agricultural Bayer Phils., Inc.
Azocord 137 monocrotophos 126 9 I lite, agricultural Cyanamid Agricultural Prod. Phils., Inc.
cypermethrin 12.5 9 I liter pyrethroid
Azod,in 202 R monocrotophos 285 9 I liter agricultural Cyanamid Agricultural Prod. Phils., Inc.
Basudin 40 WP diazinon 400glkg agricultural Novartis Agro Phils.• Inc.
Basudin 400 EC diazinon 400 9 I liter agricultural Novartis Agro Phils., Inc.
Basudin 5 G diazinon 50 I kg agricultural Novartis Agro Phils.• Inc.
Basudin 600 EC diazinon 600 9 I liter agricultural Novartis Agro Phils.• Inc.
Baygon 24 hour roach killer chlorpyrifos household use Bayer Phils., Inc.
Baygon Aerosol DOVP' household use Baver Phils., Inc.
'"i;; cyfluthrin pyrethroid
"ll- propoxur carbamate
't Baygon insect spray DDVP' household use Bayer Phils .• Inc.
~ cyfluthrin pyrethroid
..s" Bavte, 40 WP
propoxur
fenthion household use
carbamate
Baver Phils., Inc.
"
~
Bavte, 50 EC
Bavtex HN 60
fenthicn
fenthion
household use
household use
Baver Phils., Inc.
Baver Phils., Inc.
~
..
§:
~
*DDVP: 2.2·dichlorovinyldimethyl phosphate
'"~ Table 2. (continued) Organophosphate pesticides in the Philippines
§i Classification of
'"
:::! Trade name Components Concentration Indication other components Manufacturer
'"~
~
Blink 275 EC chlorpvrifos
cypermethrin
250 9 I liter
25 9 I liter
agricultural
pyrethroid
Novartis Agro Phils.. Inc.
." Brodan 31.5 EC chlorpyrifos 210 9 I liter agricultural Planters Products. Inc.
...Si! BPMC· 105 9 I liter carbamate
1il Carbophen 6 G phenthoate 60 9 I liter agricultural Planters Products, Inc.
~ MTMC·· carbamate
'" Counter 10 G terbulos lOg/kg agricultural Cyanamid Agricultural Prod. Phils.. Inc.
Cythion 57 EC malathion 570 9 I liter agricultural Cyanamid Agricultural Prod. Phils., Inc.
Diagran 5 G diazinon 50g/kg agricultural Aldiz Inc.
Cyanamid Agricultural Prod. Phils., Inc.
Diazinon 40 EC diazinon 400 9 I liter agricultural Cyanamid Agricultural Prod. Phils., Inc.
Oiazinon 60 EC diazinon 600 9 I liter agricultural Asiatic Agrochem
2uellig Agrochem. Corp.
Oiazol40 EC diazinon 400 9 I liter agricultural Zuellig Agrochem. Corp.
Diazol 60 EC diazinon 600 9 I liter agricultural Zuellig Agrochem. Corp.
Dimecron 500 SCW phosphamidon 500 9 I liter agricultural Novartis Agro Phils., Inc.
Dursban TC chlorpyrifos 4BO 9 I liter agricultural Dow Chemical Pacific ltd.
Fenom 0 225 diazinon 200 9 I liter agricultural Novartis Agro Phils., Inc.
cypermethrin 25 9 I liter
Folithion 1% Oust fenitrothion household use Bayer Phils., Inc.
Folithion 50 EC fenitrothion 500 9 I liter agricultural Bayer Phils., Inc.
Folithion 50 EC fenitrothion household use Bayer Phils., Inc.
Guardsman insecticide OOVP· •• household use Keuer . Beckitt & Colman, Inc.
laerosoll neopynamin
permethrin pyrethroid
• BPMC: 1·sec-butylphenylmethyl carbamate
•• MTMe: 4-tolylmethyl carbamate
••• OOVP: 2.2·dichlorovinyldimethyl phosphate
..,"
Table 2. (continued) Organophosphate pesticides in the Philippines
Classification of
Guardsman insecticide DDVp· household use Keller· Reckitt & Colman, Inc.
(liquid spray) neopynamin
permethrin pyrethroid
Hawk 50 EC malathion 200 9 I liter agricultural Cyanamid Agricultural Prod. Phils.. Inc.
fenitrothion 200 9 I liter
Hinosan 50 EC edifenphos 500 9 I liter agricultural Bayer Phils.. Inc.
Hnaehst malathion 57 EC malathion 570 9 I liter agricultural Hoechst Philippines
Hostathion 20 EC triazophos 200 9 I liter agricultural Hoechst Philippines
Hostathion 40 EC triazophos 400 9 I liter agricultural Hoechst Philippines
Iva pyratiline 20 PE MIB chlorpyrifos 200 glkg agricultural Intervet Agricultural Prod. Inc.
Lebaycid 50 EC tenthlon 500 9 I liter agricultural Bayer Phils., Inc.
Lentrek TC ehlorpyrifos 480 9 I liter agricultural Cyanamid Agricultrural Prod. Phils., Inc.
Lorsban 3E chlorpyrifos 300 9 I liter agricultural Dowelanco B.V., Phils.
Lorsban 40 EC chlorpyrifos 400 9 I liter agricultural Dowelanco B.V., Phils.
Lorsban IPE chlorpyrifos 10 gl kg agricultural Arc-men industries. Inc.
Dowelanco B. V.. Phils.
Malu 25 EC DDVp· household use Bayer Phils., Inc.
Mafu hot fog concemtrate ODVp· household use Bayer Phils., Inc.
Maladrin 2 EC dichlorvos 195 9 I liter agricultural Cyanamid Agricultural Prod. Phils.. Inc.
Malathion 50 WP malathion 500glkg agricultural Cyanamid Agricultural Prod. Phils., Inc.
Malathion 57 E Premium malathion 570 9 I liter agricultural Cyanamid Agricultural Prod. Phils.. Inc.
Malathion 57 EC malathion 570 9 I liter agricultural Cyanamid Agricultural Prod. Phils., Inc.
Zuellig Agrochem, Corp
Malathion UlV malathion 960 9 I liter agricultural Cyanamid Agricultural Prod. Pbils., Inc.
Matador 60 SC methamidophos 600 9 I liter agricultural Cyanamid Agricultural Prod. Phils.. Inc.
Miral 10 G isazofos 100 9 I kg agricultural Novartis Agro Phils.. Inc.
Miral 3 G isazofos 30g/kg agricultural Novartis Agro Phils.• Inc.
-DDVP: 2.2·dichlorovinyldimethyl phosphate
'"~ Table 2. {continuedl Organophosphate pesticides in the Philippines
'"
.i1!
::! Trade name Components Concentration Indication
Classification of
other components Manufacturer
'"~
~
Mist" C dichlorvos 10 9 I liter agricultural Cyanamid Agricultural Prod. Phils., Inc.
."
Mocap 10 9 ethoprophos 100glkg agricultural Rhone-Paulenc Agro Chern. Phils., Inc.
51 Nemacur 10 G phenamiphos 100 9 I kg agricultural Bayer Phils.. Inc.
'"
lil Nemacur 250 EW
Nemacur 400 EC
phenamiphcs
phenamiphos
250 9 I liter
400 9 / liter
agricultural
agricultural
Bayer Phils., Inc.
Bayer Phils., Inc.
~
'" Neocidol 40 WP
New Nuvan aerosol
diazinon
OOVP·
household use
household use
Ciba :Geigy Phils, Inc.
Keller· Reckitt & Colman, Inc.
esbial pyrethroid
New Nuvan liquid OOVP· household use Keler . Reckitt & Colman, Inc.
esbial
Nurelle 0 chlorpyrifos 250 9 I liter agricultural Oowelanco B.V.. Phils.
cypermethrin 25 9 / liter pyrethroid
Nuvan 50 EC OOVP· household use Keller· Reckitt & Colman, Inc.
Ort~ene 75 SP acephate 750 9 I kg agricultural Cyanamid Agricultural Prod. Phils.. Inc.
Asiatic Agrochem
Parapest 0 400 EC diazinon 400 9 I liter agricultural Planters Products, Inc.
Pennant 50 EC phenthoate 500 9 I liter agricultural Rhone-Poulenc Agro Chern. Phils., Inc.
Perfekthion 40 EC dimethoate 400 9 I liter agricultural Hoechst Philippines
Planters Oiazinon 60 EC diazinon 600 9 I liter agricultural Planters Products, Inc.
Planters Malation 57 EC malathion 570 9 I liter agricultural Planters Products, Inc.
Polytrin C 440 EC profenofos 400 9 I liter agricultural Novartis Agra Phils. Inc.
cypermethrin 40 9 I liter pyrethroid
Predator EC chlorpyrifos 300 9 I liter agricultural Bayer Phils., Inc.
Predator Plus chlorpyrifos 250 9 I liter agricultural Bayer Phils.. Inc.
cypermethrin 25 9 I liter
Pyfos 20 EC chlorpyrifos 200 9 I liter agricultural luellig Agrochem. Corp.
pyritiline 1 Blue chlorpyrifos 12 9 I kg agricultural luellig Agrochem. Corp.
• DDVP: 2,2·dichlorovinyldimethyl phosphate
~
Manufacturer
Scientific Industries, Inc.
Scientific Industries, Inc.
Novartis Agro Phits., Inc.

The Shell Chemicals (Phils.l. Inc
The Shell Chemicals (Phils.l. Inc
Cyanamid AliriCtlltural Prod. PhiIs.. Inc.

Novartis Agro Phils., Inc.
Bayer Phils.. Inc.
Aldi' Inc.
Novartis Agro Phils., Inc.
Rhone·Poulenc Agro Chern. Phils., Inc.
Hunter Mktg. & Dev. Corp

Zuellig Agrochem. Corp.
Zuellig Agrochem. Corp.
Hhone-Poulenc Agro Chern. Phils., Inc.
REFERENCES
Abou-Donia MB and Lapadula DM. "Mechanism of Organophosphorus ester-induced
delayed neurotoxicity: Type I and Type II," Annual Review of Pharmacology and
Toxicology. Vol 30. pp. 405-440. 1990.
Amdur. M.D.• Dou11. J.. and Klaassen, CD., cds. Casarett and Doull s Toxicology: The
Basic Science a/Poisons, 4th ed. New York: Pergamon Press, 1991.
Ballantyne 13, MarrsT. TurnerP. General and Applied Toxicology. London: The Macmillan
Press. Ltd" 1993.
Ellenhorn, MJ. and Barceloux, D.G.,cds. Medical Toxicology: Diagnosis and Treatment of
Human Poisoning. New York: Elsevier Science Publishing Company, Inc.. 1988.
Fertilizerand Pesticide Authority, List afRegistered Agricultural Pesticide Products. FPA,30
June 1997.
Haddad, L.M. and Winchester. J.E Clinical Management ofPoisoning and Drug Overdose.
3rd ed, Philadelphia: WB. SaundersCompany. 1990.
International Programme on Chemical Safety, Basic Analytic Toxicology. Geneva: WHO/ONEP/
ILa.1995.
International Programme on Chemical Safety. Environmental Health Criteria # 79: Dichlorvos.
Geneva: World Health Organization. 1989.
International Programme on Chemical Safety. Environmental Health Criteria # 90: Dimethoate.
Geneva: World HealthOrganization. 198'l.
International Programme on Chemical Safety. Environmental Health Criteria # 133: Fenitrothion.
Geneva: World HealthOrganization. 1992.
International Programme on Chemical Safety. Environmental Health Criteria # 63:
Organophosphorous Insecticides - A Genera/Introduction. Helsinki: World HealthOrgani-
zation. 1987.
International Programme on Chemical Safety. The WHO Recommended Classification 0/Pesti-
cides by Hazard and Guidelines to Classification, 1996-1997. Geneva: World Health Orga-
nization. 1997.
Klaassen CD. AmdurMO. OoullJ. cds, Toxicology: The Basic Science ofI'oisons. 5th ed. New
York: Macflraw-Hill, 1996.
Magallona, E.D" et al. Safety in Pesticide Handling. NCPC. 1986.
Manual on the Occupational Health and Toxicology in the Management ofPesticide Poisoning.
Manila: National Poisons Control and Information Service and the Department of Health,
1994.
Maramba NPC. Panganiban LRand Hartigan-Go KY. Algorithms ofCommon Poisonings: Part
I. Manila: National PoisonsControl and Information Service. 1991.
National PoisonControl and Information Service. Database on Commercial Products (unpub-
lished). NPCIS. 1996.
Olson. K.R.. et aI., eds. Poisoning and Drug Overdose. Norwalk: Appleton & Lange, 1990.
Oudejans, J.H. Agro-pesticides Properties and Functions in Integrated Crop Protection.
United Nations. 1991.
Repetto Rand BaligaSS. Pesticides and the Immune System: The Public Health Risks.
Washington: World Resources Institute. 1996.
ANNEX A
Banned and Restricted Pesticides in the Philippines
- Fertilizer and Pesticide Authority (April 30. 1997)
I. Banned Pesticides
I. Parathion ethyl 25. Brestan
2. Copper Aceto-arsenite (Paris Green) 26. Aquatin EC
3. DDT containing mosquito coils 27. Telustan 60 WP
4. DBCP 28. Torque 50% WP
5. Nitrogen 29. Gusathion 400 EC
6. Leptophos 30. Marsathion 10 EC
7. EPN 31. Bionex 10 EC
8. Endrin 32. Telothion 10 EC
9, Mercuric fungicides 33. Folidol M 50 EC
to. Toxaphene 34. Methyl Fosfemo 50 EC
11. Elemental phosphorus 35. Methion 50 EC
12.Thalium sulfate 36. Meptox 50 EC
13. I-Napthylthiourea (ANTU) 37. Parapest M 50 EC
14. Gophaeide 38. Penneap M (EN CAP)
15. Sodium Fluoroacetate 39. Wofatox 50 EC / 80 EC
16. Sodium Fluoroacetamide 40. Wofatox Konzentra "I" 50 EC / 80 EC
17. Stryobhine 41. Thioearb 17 EC
18.2,4,5-T 42. Thiodan 35 WP
19. Aldrin 43. Thiodan 35 EC
20. Dieldrin 44. Endosulfax 35 EC
21. Heptachlor 45. Endox 35 EC
22. Chlordimeform 46. Thiodan 2.5 G
23. EDB 47. Endosulfan 36 EC
24. HCH / BHC
II. Restricted Pesticides

A. Importation Not Allowed Except in Cases of Emergency as Determined by the Author-
ity
I. Aldiearb
2. Chlorobenzilate
B. ForTermite Control Only

I. Chlordane - its use is limited for pre-construction treatment.
C. ForUsc Under Specified Limitations

I. DDT· All uses canceled exceptformalaria control purposes by the Department of
Health.
2. Not for use near Aquatic Ecosystems
a. Chlordane
b. Endosulfan
3. Too Hazardous forGeneral Use (For Institutional Use Only)'
3. Paraquat - Restricted forInstitutional Use Only. Approval of use will be based
on strict compliance by theimporter/cnd-user of the requirement set foritsusc.
b. Phenamiphos - for use in banana and pineapple plantations.
c. Etroprop , for use in banana plantations only.
7,8 Standard Treatment Guidelines
d. Methidathion • for use in banana plantations only.
e. Inorganic Arsenicals (Arsenic Trioxide) - for usc by FPA accredited wood treat
ment and preserving plants only.
f. Lindane (Gamma BHC) - The only allowed use to date is on pineapple planta
tions by soil pre-plant application.
g. Pentachlorophenol - for use in wood treatment only by FPA accredited wood
treating plants and institutions.
D. Fumigants and Other Chemicals for Use Only by Certified Fumigators

Adequate time for aeration is required after treatment before commodities arc processed
into food or feed.
I. Methyl bromide
2. Carbon disulfide
3. Phosphine generating compounds
4. HCN-generating materials
5. Carbon tetrachloride
6. Chloroform
7. Ethylformate
E. Endosulfan- the concentration will be reduced to 5% or lower for other uses.
F. Monocrotophos - the allowed use is for bcanfly control on legumes only.

1. Nuvaeron 30 sew
2. Azodrin 168
3. Azodrin 202 R
4. Azodrin 150
5. Azodrin 202
6. Azodrin 137
1 Strict compliance to guideline lor pesticides lor Institutional Use as stipulated in the FPA Pesticide Regu-
latory Policies. 1987 edition. and such other requirements as may be imposed by the Authority.
ANNEX B
Use Categories of Pesticides According to
Recommended Restrictions on Availability
- WHO IFAO I UNEP
Category 1
Pesticides in this category should be available only to professional operators, individually
licensed, who have demonstrated good knowledge of the chemical. its US~S, hazards and the
precautions to be taken in use. This category includes only a few very highly toxic pesticides.
(E.g .. Leptophos. sodium fluoroacetate)
Category 2
Pesticidesin this categoryshould be available only to contractors, pest control operators, ctc.,
who will apply the pesticidesunder strictly-controlled and supervised conditions.using trained
operators. The application of pesticides will normally be the major part of their commercial
operation. This categoryincludesmostofthe veryhighly toxic pesticidesand other pesticides
for which it is felt that special training or supervision in use is necessary. (E.g., Aldicarb (all
formulations). carbofuran (liquid formulation, 4%and above:solid. 16%and above),methomyl
(liquid, 85% arid above; solid, 35% and above), zinc phosphide (all formulations))
Category 3
Pesticidesin this categoryshould be availableto commercial applicators (farmers, fruit grow-
ers, foresters, and those responsible for bulk food storage) for whom the application of pesti-
cide is not necessarilya major part of their operations,subject to a permit being received from
competent authority specifying the pesticide. conditions of usc, and the precautions to be
taken. This category includes pesticides that are highly toxic and those that have adverse
effectson the environmentto the extent that their uncontrolled use without permit is undesir-
able. (E.g., Bendiocarb (solid, >10%), chlorpyrifos (liquid, >50%), cypermethrin (liquid,
>15%), dimethoate (liquid, 10% and above; solid, >25%), diazinon (liquid, >20%; solid,
>50%)) .
Category 4
. Pesticides in this categoryshould be available in the same manneras those in Category 3, but
without the requirement of a permit. This category includes toxic pesticides that may be
distributed for commercial use, but should not be available to the general public. (E.g., 2,4·0
(all formulations, >10%), deltamethrin (all liquid formulations, >20%»
Category 5
Pesticides in this category may be available to the general public for specified uses.

EDITORS
Nelia P. Cortes·Maramba, M.D., F.P.P.S. F.P.S.E.C.P.
Professor, Department of Pharmacology
U.P. College of Medicine .
Clinical Professor. Department ofPediatrics
U.P. College ofMedicine·Philippine General Hospital
Haad, National Poison Control and Information Service
Erie S. Castillo, M.D.
Clinical Assistant Professor, Department of Family and Community Medicine
U.P. College of Medicine·Philippine General Hospital
Consultant, Department of Emergency Medicine Services
Philippine General Hospital
Consultant, National Poison Control and Information Service
Lynn Crisanta R. Panganiban, M.D., D.P.A.F.P.

Associate Professor, Department of Pharmacology
U.P. College ofMedicine
Consultant, Department of Family and Community Medicine
Laurence S. So, M.D.

Toxicology Research Associate
National Poison Control and Information Service
Lurenda Suplido. M.D.
Toxicology Research Associate
CONTRIBUTORS
Allan R. Dionisio, M.D., F.P.A.F.P.
Clinical Assistant Professor, Department of Family and Community Medicine
Carissa Paz C. Dioquino. M.D., F.P.N.A.

Clinical Assistant Professor, Section ofNeurology, Department of Internal Medicine
Kenneth Y. Hartigan-Bn, M.D., F.P.C.P.. F.P.S.E.C.P.
Associate Professor, Department of Pharmacology
U.P. College ofMedicine .
Clinical Associate Professor, Department of Internal Medicine
Irma R. Makalinao. M.D.• D.P.P.S..

Assistant Professor, Department of Pharmacology
U.P. College ofMedicine
Clinical Associate Professor, Department of Pediatrics
r
ISBN 971·8650·03·2

University of the Philippines College of Medicine . il1
Philippine General Hospital ;
Ward 14·A Room 100, Taft Avenue, Manila 1000

,
'~.
,.;
.,
PHILIPPINES '
·1
Tel: (63·2) 524-1078 "
(63-2) 521·8450 Loe. 2311 '-". -

Fax: (63·2) 526·0062

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National Poison Control and Informa~r'" ".

Standard Treatment Guidelines for

Printed in the Philippines .,

The Department of Health has been continuously requested to reo

\Chemical Name Mechanisms ofToxicity

. The Editors and Contributors

4 Standard Treatment Guidelines

ACGIH - American Conference of Governmental Industrial Hygienists

8 Standard Treatment Guidelines

Clinical History 1. AIRWAY

HEALTH PERSONNEL ANO EMERGENCY FACILITIES

PHYSICAL AND CHEMICAL PROPERTIES

Air Arsenic Arsine

/6 Standard Treatment Guidelines

ACUTE ARSINE GAS EXPOSURE

SPECIMEN AND EXAMINATIONS FOR DIAGNOSIS

/8 Standard Treatmant Guidelines

OCCUPATIONAL TOXICOLOGIC INTERVENTIONS (See Guidelinesl

HAZAROS TO THE ENVIRONMENT ANO THEIR PREVENTION

20 Standard T"atment Guideline.

I I~I I I~I I il ~~ J',

PHYSICAL ANO CHEMICAL PROPERTIES

Hazard Classification Rat Oral LO"lmg/kgl • solids

Table 3. Hazard cBtegory ofcarbamate pesticides usedin the Philippines

Table 4. Rat Oral LD§o of selected carbamates in their solid state

SPECIMEN AND EXAMINATIONS FOR DIAGNOSIS

OCCUPATIONAL TOXICOLOGY INTERVENTIONS ISee Guideline.)

HAZARDS TO THE ENVIRONMENT AND THEIR PREVENTION

30 Standard Treatment Guidelines

Lannate 40 SP methomyl 400g/kg agricultural Du Pont Far East, Inc.

34 Standard Treatment Guidelines

Chronic intoxication- Effects of'intcrmiuent exposures to lev..' to Intermediate concentrations of

ACUTE EXPOSURE (S" Table 11

Eye Contact 10 14 Eye irritation, tearing and burning sensation

Dermal Absorption Direct contact may cause erythema and pain.

SPECIMEN AND EXAMINATIONS FOR DIAGNOSIS

40 St,ndard Treatment Guid,lin"

EMERGENCY HOSPITAL MANAGEMENT (S" Guidelines)

Specific Problem. Pyridoxine

OCCUPATIONAL TOXICOLOGY INTERVENTIONS ISee Guidelines)

HAZARDS TO THE ENVIRONMENT AND THEIR PREVENTION

Inorganic Lead Tetraethyl Lead Tetremethyl Leed

Ground and Surface Water

46 Standard Treatment Guidelinel

CHRONIC LEAD EXPOSURE

SPECIMEN AND EXAMINATIONS FOR DIAGNOSIS

HAZARDS TO THE ENVIRONMENT AND THEIR PREVENTION

52 Standard Treatment Guidelines

54 Standa,d Treatment Guid.lin••

nV·TWA Im9/m') REllmg/m'j 10lH Img/m')

Subcutaneous I Intramuscular Injection

58 Standard Treatment Guidelines

CHRONIC EXPOSURE TO ELEMENTAL MERCURY

ACUTE EXPOSURE TO MERCURY SALTS

CHRONIC EXPOSURE TO MERCURY SALTS

ACUTE EXPOSURE TO ORGANIC MERCURY

EMERGENCY HOSPITAL MANAGEMENT (See Guidelinesl

62 Standard Treatment Guidelines

OCCUPATIONAL TOXICOLOGY INTERVENTIONS (See Guidelinesl

HAZARDS TO THE ENVIRONMENT ANO THEIR PREVENTION

Banned organophosphates (See Annex A):

SYNONYMS CHEMICAL FORMULA

68 Standard Treatment Guideline.