TRAINING FOR HEALTH CARE PROVIDERS [Date …Place …Event…Sponsor…Organizer]
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TRAINING FOR HEALTH CARE PROVIDERSTRAINING FOR HEALTH CARE PROVIDERS [Date …Place …Event…Sponsor…Organizer] [Date …Place …Event…Sponsor…Organizer]
LEADLEAD
Children's Health and the EnvironmentWHO Training Package for the Health Sector
World Health Organization
www.who.int/ceh
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LEARNING OBJECTIVESLEARNING OBJECTIVES
To understand, recognize and know:To understand, recognize and know:
Characteristics of lead as a toxicant EEpidemiology of lead poisoningWho is vulnerable and why?Sources of contaminationToxicokinetics of leadDiagnosis and treatmentTrends in blood lead levels and action levelsPrevention: strategy and actionsCase studies
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LEAD PRODUCTION IN THE 20LEAD PRODUCTION IN THE 20THTH CENTURY CENTURY
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40Emissions
Production
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ctio
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Em
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on
s (t
ho
usa
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s m
etri
c to
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es)
Adapted from Nriagu, (1996) 272:223
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EVIDENCE OF INCREASED ACCUMULATION EVIDENCE OF INCREASED ACCUMULATION OF LEAD OVER THE YEARSOF LEAD OVER THE YEARS
Deposition of lead in Greenland ice (g/kg)
Sharp increase since 1940 attributed mainly to combustion of lead alkyl additives in petrol
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WHO ESTIMATESWHO ESTIMATES
Lead exposure accounts for about 1% of the global burden of disease and most exposure affects children in developing countries
In developing countries as much as 15-20% mental retardation could be caused by exposure to lead.
Hundreds of millions of children and pregnant women are exposed to different sources of lead.
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MORBIDITY, MORTALITY AND ESTIMATED COSTS MORBIDITY, MORTALITY AND ESTIMATED COSTS OF LEAD POISONING AMONG US CHILDRENOF LEAD POISONING AMONG US CHILDREN
Burden of disease for lead poisoning is 20 X higher than for asthma, and 120 X higher than for cancer
Estimated total annual costs:
- Lead exposure: 43.4 billion $US
- Childhood asthma: 2.0 billion $US
- Childhood cancer: 0.3 billion $US
- Neurobehavioural
disorders: 9.2 billion $US
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CHILDREN AT HIGHEST RISK CHILDREN AT HIGHEST RISK
High exposure: • Hand-to-mouth activity• Pica• Repeated ingestion of paint chips/dust• Inhalation of dust
High absorption• Fraction of absorption is 40% in children compared with 10%
in adults
High susceptibility• At the critical periods of brain development• Immature blood–brain barrier
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SOURCES OF EXPOSURE TO LEADSOURCES OF EXPOSURE TO LEAD
• Petrol additive • Old paint in houses• Improper de-leading or
renovation of old houses• Contaminated dust and soil• Industrial: smelters, battery recycling• Ceramic glazes, food can solder• Drinking water from old pipes • Cosmetics and folk remedies• Children of lead workers• Tattoos • Toys• Jewellery • Wax crayons • Candle wicks
WHO
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TRADITIONAL LEAD SMELTER, ARNOLDSTEIN, TRADITIONAL LEAD SMELTER, ARNOLDSTEIN, AUSTRIAAUSTRIA
A large lead smelter and a lead recycling plant that contributed to high lead exposure in the area - Drasch, 2000
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PAEDIATRIC ROUTES OF EXPOSURE (1)PAEDIATRIC ROUTES OF EXPOSURE (1)
Prenatal
Lead crosses the placenta
Fetal/maternal ratio: 0.9
Graph with data of maternal-newborn (cord blood) blood lead level pairs
Adapted by Dr. Amitai from: Amitai, IMAJ (1999) 1: 250
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PAEDIATRIC ROUTES OF EXPOSURE (2)PAEDIATRIC ROUTES OF EXPOSURE (2)
IngestionNon-nutrient ingestionContaminated food/waterMinimal risk from breast milk
InhalationPolluted airDustGas sniffing
www.epa.gov/region02/health/leadpoisoning.htm
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ENVIRONMENTAL EXPOSURE PATHWAYSENVIRONMENTAL EXPOSURE PATHWAYS
Prenatal exposures
+
Postnatal multimedia exposures
paint
soil
dust
air
cans
pets
water
food
mouthing
Guzelian, ILSI, 1992
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TOXICOKINETICSTOXICOKINETICS
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TOXICOKINETICS: BIOTRANSFORMATIONTOXICOKINETICS: BIOTRANSFORMATION
Organic lead • Metabolized in the liver
Inorganic lead • No biotransformation
• Adults retain 1% of absorbed dose
• Children up to 2 years retain 1/3 absorbed dose
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TOXICOKINETICS: DISTRIBUTION & ELIMINATIONTOXICOKINETICS: DISTRIBUTION & ELIMINATION
Blood: distribution to other tissues
Soft tissues: liver > kidneys > lungs > brain
• Higher penetration into CNS in younger children
Mineralizing tissues: bones >> teeth
• Mobilization increased during pregnancy and lactation
• Exacerbated by calcium deficiency
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MECHANISMS OF TOXICITYMECHANISMS OF TOXICITY
No role for lead in the human body!
Several mechanisms of toxicity
• Interferes with Ca and Fe
• Forms complexes with sulfhydryl groups and others
Disrupts enzymes multisystem effects
• Other
Effect varies according to:
• Dose
• Timing and duration of exposure
• Age
• Health and nutritional status
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SYMPTOMS AND SIGNS: A WIDE SPECTRUMSYMPTOMS AND SIGNS: A WIDE SPECTRUM
Central and peripheral nervous system *
Gastrointestinal
Blood
Skeletal – reduced stature **
Cardiovascular – hypertension
Kidney – proteinuria (Fanconi)
Hearing – reduced
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SYMPTOMS AND SIGNS: A WIDE SPECTRUMSYMPTOMS AND SIGNS: A WIDE SPECTRUM
CNS: - Hyperactivity, restlessness- Behavioural disturbances- Learning disabilities (low score in
cognitive tests) ***- BLL > 70 (rare): headache, lethargy,
coma, seizures
PNS - Neuropathy (in adults!)
GI : - Anorexia, vomiting, constipation - Abdominal pain ****
Blood: - Anaemia, basophilic stippling
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POPULATION-LEVEL CONSEQUENCES OF POPULATION-LEVEL CONSEQUENCES OF BLOOD LEAD LEVELSBLOOD LEAD LEVELS
For each 1 μg/dL increase the IQ decrease is 0.25–0.5
For each 10 μg/dL increase: height decreases by 1 cm
BLL > 45 μg/dL: abdominal pain (colic, porphyria-like)
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TARGET TARGET ORGAN ORGAN
TOXICITYTOXICITY
• Toxicity at lower exposures
• Unique toxicities due to developmental immaturity
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RADIOGRAPH: RECENT RADIOGRAPH: RECENT LEAD INGESTIONLEAD INGESTION
A plain (flat) abdominal film of a toddler with a recent ingestion of lead-containing paint chips
Lead particles are evident as radiopacities
Courtesy of John Graef, MD, Boston Children's Hospital
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BASOPHILIC STIPPLING BASOPHILIC STIPPLING
Classical laboratory sign known since 1899Classical laboratory sign known since 1899
Inclusions of aggregated ribosomes found only in the red blood cells
Unspecific and inconstant
Courtesy of John Graef, MD, Boston Children's Hospital
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EFFECTS OF LEAD ON HEFFECTS OF LEAD ON HAEM AEM SYNTHESISSYNTHESISC
ourtesy of John Graef, M
D, B
oston Children's H
ospital
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THE “LEAD LINE” SIGNTHE “LEAD LINE” SIGN
Abnormally heavy mineralization of the growth plate of long bones in radiographs
The width and density of “lead lines” reflect chronic exposure
Courtesy of John Graef, MD, Boston Children's Hospital
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LABORATORY STUDIESLABORATORY STUDIES
BLL (blood lead levels)
(atomic absorption and/or electrochemical technique)
Action level: > 10 µg/dL
Chelation: > 45 µg/dL
Zinc protoporphyrin (ZPP) or erythroprotoporphyrin (EPP)*
BLL > 20 µg/dL
Aminolaevulinic acid dehydratase (ALAD)
BLL > 5–10 µg/dL
Pb in bone • "Lead lines" (> 45 µg/dL over 2 months)**
• X-ray fluorometry (XRF)
Pb in urine After chelation ***
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LEAD EXPOSURE AND TOXICITYLEAD EXPOSURE AND TOXICITY
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IMPORTANCE OF SCREENINGIMPORTANCE OF SCREENING
Lead poisoning is often SUBCLINICAL
Has NONSPECIFIC symptoms
Diagnosis relies on laboratory screening
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CORD BLL AND CORD BLL AND MENTAL MENTAL
DEVELOPMENT INDEXDEVELOPMENT INDEX
Bellinger, N Eng J Med. (1987)316:1037
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ASSOCIATION ASSOCIATION BETWEEN BETWEEN DENTINE DENTINE LEAD LEVELLEAD LEVEL AND AND CLASSROOM CLASSROOM BEHAVIOURBEHAVIOUR
Needleman, N. Engl J Med. (1979);300(13):689.
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SIGNIFICANCE OF 5 POINT IQ REDUCTIONSIGNIFICANCE OF 5 POINT IQ REDUCTION
www.prwventingharm.org/execsum.html
Schettler, GBPSR, 2000
5 Point Decrease in Mean IQ
160140120100806040
mean 95
70 130
2.4 million "gifted"
9.4 million
"mentally retarded"
57% INCREASE IN
"MentallyRetarded”Population
I.Q.
The Significance of Small Effects:EFFECTS OF A SMALL SHIFT IN IQ DISTRIBUTION IN A
POPULATION OF 260 MILLION
160140120100806040
70 130I.Q.
mean 100
6.0 million "gifted"
6.0 million "mentally retarded"
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TRENDS IN LEVEL OF CONCERN (ACTION TRENDS IN LEVEL OF CONCERN (ACTION LEVEL) FOR CHILDHOOD LEAD POISONING LEVEL) FOR CHILDHOOD LEAD POISONING
(1970–1990, CDC, USA)(1970–1990, CDC, USA)
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REDUCTION IN BLL (UG/ Dl) ACTION LEVELS
1970197519851990
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OUTCOME-EFFECTS: neurodevelopmental
impairment, learning disabilities, anaemia, GI upset
SUSCEPTIBILITIES
fetus, infant, toddler,
anaemia
ENVIRONMENTAL LEAD HAZARDS AND ENVIRONMENTAL LEAD HAZARDS AND POISONING IN CHILDRENPOISONING IN CHILDREN
HAZARDS:
old paint,
leaded petrol,
lead pipes,
water, soil
MEDIA: air, water, food, dust, cosmetics, traditional medicines
SETTINGS:
home,
playground, renovation of old houses
ACTIVITIES: hand–mouth activity, "pica", playing,
ingestion of paint, dust inhalation, chewing on windowsills
(photo credit US NIEHS CERHR logo)
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CATEGORIES OF BLL FOR ACTION CATEGORIES OF BLL FOR ACTION
LEVEL (μg/dL) ACTION
10–14 - repeat BLL within 3 months
- evaluate sources
- education: cleaning, hands and mouth
15–19 - repeat BLL within 2 months
- as above + referral to dept of health
20–44 - repeat BLL within 1 month
- as above
> 45 - as above + CHELATION therapy
> 70 - IMMEDIATE HOSPITALIZATION
- two-drug CHELATION
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MANAGEMENT (1)MANAGEMENT (1)
Complete assessmentRemove from source of exposureCorrect nutritional/iron deficienciesConsider chelation
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MANAGEMENT (2) MANAGEMENT (2)
Education• Cleaning dust*
• Hand washing
Abatement of lead source• Residential de-leading
Long-term follow-up
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CHELATING AGENTSCHELATING AGENTS
GENERIC CHEMICAL ABBREVIATION
Edetate disodium calcium
Calcium disodium ethylenediamine-tetracetate
CaNa2EDTA
Succimer Meso-2,3-dimercaptosuccinic acid
DMSA
Dimercaprol 2,3-Dimercaptopropanol BAL
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IMPACT OF CHELATION ON IQIMPACT OF CHELATION ON IQ
NO SIGNIFICANT DIFFERENCE SUCCIMER vs PLACEBO Behaviour slightly worse in treated children Neurodevelopmental testing slightly better PRIMARY PREVENTION IS KEY
Rogan, NEJM (2001) 344:1421
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CASE STUDY ICASE STUDY I
5-year-old boy with hyperactivity and abdominal colic
History: mother worked in an automobile repair shop, where the child played
Exam: height and weight 10th percentile, short attention span, restlessness, delayed speech development, poor social skills
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CASE STUDY I LABORATORY CASE STUDY I LABORATORY
Laboratory: microcytic anaemia
BLL – 30 µg/dL
ZPP – 50 µg/dL (normal < 35)
Hgb – 10.7 gr/dL; MCV – 72 fL
Serum Ca – normal
Flat abdominal X-ray: no radio-opacities
BLL in mother – 40 µg/dL, referred for follow-up
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CASE STUDY I MANAGEMENT AND FOLLOW-UPCASE STUDY I MANAGEMENT AND FOLLOW-UP
Management: Abate source: cleaning, avoid further contact with dirty clothes, wash hands Treat anaemia with iron supplement No chelation
Repeat BLL: in 1 month – 26 µg/dL, in 2 months – 24 µg/dL in 3 months – 22 µg/dLFour months later – asymptomatic
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CASE STUDY IICASE STUDY II
7-year-old girl with anaemia
History: lives in Durban with parents, who say that she peels paint off the wall and digs putty out of the window frames and eats them
Exam: height and weight 20th percentile, otherwise appears normal
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CASE STUDY II LABORATORY CASE STUDY II LABORATORY
Laboratory: microcytic anaemia
Hgb – 19.4 g/dL; MCV – 70 fL
BLL – 47 µg/dL
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CASE STUDY II MANAGEMENT AND FOLLOW-UPCASE STUDY II MANAGEMENT AND FOLLOW-UP
Management: Remove from home while remediation occurs Treat anaemia with iron supplement No chelation
Repeat BLL: in 1 month – 38 µg/dL, in 2 months – 35 µg/dL in 3 months – 30 µg/dL
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CASE STUDY IIICASE STUDY IIIACUTE-ON-CHRONIC LEAD POISONINGACUTE-ON-CHRONIC LEAD POISONING
18-month-old African American child with mild-to-moderate lead poisoning: BLL 37 µg/dL
Admitted to the hospital with lethargy, vomiting and encephalopathy: BLL 130 µg/dL
Recent history: home de-leaded by sanding 3 days previously
Away from the house during day, inside at night.
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CASE STUDY III – FOLLOW-UP AND BLLCASE STUDY III – FOLLOW-UP AND BLLR
ey-Alvarez, P
ediatrics, 1987, 79(2):214.
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CASE SERIES CASE SERIES DELEADING-RELATED DELEADING-RELATED
EXPOSUREEXPOSURE
4 cases of acute-on-chronic lead poisoning
Subsequent to deleading without proper precautions
Amitai, Am J Dis Child, 1987,141(7):758.
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STUDY OF PRESTUDY OF PRE / MID / POST- DELEADING/ MID / POST- DELEADING
Study of 114 children in Boston whose houses were deleadedBlood lead levels (BLL)• before• during• after
Mean BLL were HIGHER during deleading due to improper precautions for safeguarding children
Amitai, Pediatrics (1991) 88(5):893.
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PREVENTION IS ESSENTIALPREVENTION IS ESSENTIAL
Primary prevention: eliminate exposure• Regulations and laws
• Ban lead in petrol
• Ban lead-containing solder for packaging foods/beverages
• Remove lead from paint
• Regulate lead in toys/consumer products
• De-leading of houses
Secondary prevention: monitoring • SCREENING of asymptomatic children
• Optimize nutrition and health
• Remove from source of exposure
• Remediate environment
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LEADED PETROL – MAJOR SOURCELEADED PETROL – MAJOR SOURCE
Institute of Medicine, EPA, 1996
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TRENDS IN BLOOD LEAD LEVELS AMONGTRENDS IN BLOOD LEAD LEVELS AMONG CHILDREN AGES 1 – 5 YEARS (USA) CHILDREN AGES 1 – 5 YEARS (USA)
Years Mean BLL
µg/dL% BLL >10
µg/dLEstimated no. of
children >10 µg/dL
1976–1980 14.9 88.2 13 500 000
1988–1991 3.6 8.6 1 700 000
1991–1994 2.7 4.4 890 000
1999–2002 1.9 1.6 310 000
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GLOBAL SITUATIONGLOBAL SITUATION
16 countries still using leaded petrol (July 2008)
Afghanistan Algeria Bosnia-Herzegovina Iraq FYR Macedonia Laos Mongolia Montenegro Morocco Myanmar North Korea Palestine Serbia Tajikistan Tunisia Uzbekistan Yemen
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July 2008
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Gordon, WHO, Myriad Editions Ltd, 2004
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Diagnose and treat
Do research and publish• Detect sentinel cases• Inspire community-based
interventions
Educate• Patients and families• Colleagues and students
Advocate
Provide good role model
CRITICAL ROLES OFCRITICAL ROLES OFHEALTH & ENVIRONMENT PROFESSIONALSHEALTH & ENVIRONMENT PROFESSIONALS
WHO
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POINTS FOR DISCUSSIONPOINTS FOR DISCUSSION
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First draft prepared by Yona Amitai MD MPH (Israel)
With the advice of the Working Group on Training Package for the Health Sector: Cristina Alonzo MD (Uruguay); Yona Amitai MD MPH (Israel); Stephan Boese-O’Reilly MD MPH (Germany); Irena Buka MD (Canada); Lilian Corra MD (Argentina), Ruth A. Etzel MD PhD (USA); Amalia Laborde MD (Uruguay); Ligia Fruchtengarten MD (Brazil); Leda Nemer TO (WHO/EURO); R. Romizzi MD (ISDE, Italy); S. Borgo MD (ISDE, Italy)
Reviewers: D. Beltramino MD (Argentina); S. Boese O'Reilly MD MPH (Germany); I. Buka MD (Canada); Ruth A. Etzel, MD, PhD (USA)
Update July 2008WHO CEH Training Project Coordination: Jenny Pronczuk MDMedical Consultant: Katherine M. Shea MD MPH USATechnical Assistance: Marie-Noel Bruné MSc
ACKNOWLEDGEMENTSACKNOWLEDGEMENTS
WHO is grateful to the US EPA Office of Children’s Health Protection for the WHO is grateful to the US EPA Office of Children’s Health Protection for the financial support that made this project possible and for some of the data, financial support that made this project possible and for some of the data,
graphics and text used in preparing these materials.graphics and text used in preparing these materials.
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DISCLAIMERDISCLAIMER
• The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement.
• The mention of specific companies or of certain manufacturers’ products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.
• The opinions and conclusions expressed do not necessarily represent the official position of the World Health Organization.
• This publication is being distributed without warranty of any kind, either express or implied. In no event shall the World Health Organization be liable for damages, including any general, special, incidental, or consequential damages, arising out of the use of this publication
• The contents of this training module are based upon references available in the published literature as of the last update. Users are encouraged to search standard medical databases for updates in the science for issues of particular interest or sensitivity in their regions and areas of specific concern.
• If users of this training module should find it necessary to make any modifications (abridgement, addition or deletion) to the presentation, the adaptor shall be responsible for all modifications made. The World Health Organization disclaims all responsibility for adaptations made by others. All modifications shall be clearly distinguished from the original WHO material.