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19 APR 07 Dr. M. S. Prasad 1
EnvironmentEnvironment
&&
Child HealthChild Health
Dr. M. S. PrasadDr. M. S. Prasad
Consultant & Head
Dept. of Paediatrics
Safdarjung Hospital &
Vardhaman Mahavir Medical College
New Delhi
19 APR 07 Dr. M. S. Prasad 2
Environmental Hazards andEnvironmental Hazards and
their relationship to Healththeir relationship to Health
A neglected topic in the
Paediatric and General
Medical Textbooks.
19 APR 07 Dr. M. S. Prasad 3
HistoryHistory
• 1954:1954: Nuclear weapon test on Bikini IslandBikini Island
– Acute burns from beta-radiation in the neighboring islands.
– Hypothyroidism,
– Thyroid neoplasm, and
– Leukemia.
• 1957:1957: AAP CommitteeAAP Committee on Radiation Hazards and Congenital
Malformations.
• 1961:1961: CommitteeCommittee on Environmental Hazards.
• 1966:1966: First International ConferenceConference on Paediatric significance on
nuclear fall-outs.
• 1973:1973: ConferenceConference on the Susceptibility of the Fetus and Child to
Chemical Pollutants.
• 19811981:: ConferenceConference on Chemical and Radiation Hazards to Children.
• 1991:1991: CommitteeCommittee on Environmental Health.
19 APR 07 Dr. M. S. Prasad 4
HistoryHistory (Continued)
• 1996:1996: Food Quality Protection Act.
• April 21, 1997:April 21, 1997:
President Clinton issued Executive Order 13045: Protection of
Children from Environmental Health Risks and Safety Risks.
• October 1999:October 1999: First edition of the AAP
“Handbook of Pediatric Environmental Health”.
• 2000 & 2001:2000 & 2001: Workshops.
• 2002:2002: The Ambulatory Pediatric Association launched
3 years fellowship training programmefellowship training programme..
19 APR 07 Dr. M. S. Prasad 5
EnvironmentEnvironment
The term environment implies allThe term environment implies all
the external factors – living andthe external factors – living and
non-living, material and non-non-living, material and non-
material – which surround man.material – which surround man.
Everything except me is environment.
The term environment implies allThe term environment implies all
the external factors – living andthe external factors – living and
non-living, material and non-non-living, material and non-
material – which surround man.material – which surround man.
Everything except me is environment.
19 APR 07 Dr. M. S. Prasad 6
ClassificationClassification
• Physical:
– Macro-environment
– Microenvironment.
• Biologic:
Plant & animal life including bacteria, viruses, insects,
rodents and animals (including man).
• Social:
– Customs, culture, habits, income, occupation, religion etc.
• Chemical: Pesticides, Fluorine, Mercury, Lead, Solvent.
19 APR 07 Dr. M. S. Prasad 7
Areas of concernAreas of concern
• Physical:
– Radiation,
– Noise,
– Extreme heat/cold,
– Unsafe building,
– Traffic……..
• Chemical:
– Pesticides,
– Solvents,
– Lead,
– Mercury……….
• Biological:
– Disease Vector,
– Mould,
– Envenoming ……….
19 APR 07 Dr. M. S. Prasad 8
Why children?Why children?
19 APR 07 Dr. M. S. Prasad 9
Environment & DiseasesEnvironment & Diseases
• More than 1/4th
of global disease burden is
due to modified environmental factors.
• It is 1/3rd
of Paediatric Diseases burden.
[WHO, Preventing diseases through healthy environment 2000]
19 APR 07 Dr. M. S. Prasad 10
1. Different and unique exposures
2. Dynamic developmental physiology
3. Longer life expectancy
4. Politically powerless
Raphael, National Gallery of Art, Washington, DC
CHILDREN ARE NOT LITTLE ADULTSCHILDREN ARE NOT LITTLE ADULTS
19 APR 07 Dr. M. S. Prasad 11
1. DIFFERENT AND UNIQUE EXPOSURESDIFFERENT AND UNIQUE EXPOSURES
 Unique exposure pathways
– Transplacental
– Breastfeeding
 Exploratory behaviours leading to exposures
– Hand-to-mouth,
– Object-to-mouth
– Non-nutritive ingestion
 Stature and living zones, microenvironments
– Location – lower to the ground
– High surface area to volume ratio
 Children do not understand danger
– Pre-ambulatory
– Adolescence – “high risk” behaviors
19 APR 07 Dr. M. S. Prasad 12
Moore, Elsevier Inc, 1973
WINDOWS OF DEVELOPMENT
19 APR 07 Dr. M. S. Prasad 13
TRANSPLACENTAL EXPOSURETRANSPLACENTAL EXPOSURE
Maternal exposures do matter!
Lessons from pharmaceuticals: thalidomide, diethylstilbestrol (DES), alcohol
19 APR 07 Dr. M. S. Prasad 14
Breast-feedingBreast-feeding
Pollutants that may be
found in Human Milk
Chemical AgentsChemical Agents
DDT, DDE
PCB/PCDF
Dioxin
Chlordane
Heptachlor
Hexachlorobenzene
Volatile Organic Compounds
Nicotine
Metals
Lead
Methylmercury.
19 APR 07 Dr. M. S. Prasad 15
Breast-feedingBreast-feeding
• Halothane has been detected in the
milk of lactating anaesthesiologistanaesthesiologist..
• There is a single case of report of a child developed cholestatic
jaundice while being breastfed. His mother lunched daily with her
husband, who was a dry-cleaner, and perchloroethylene was found
in her milk.
Ref.:
– Br. J. Anaesth. 1976; 48-541 – 543.
– Can Med Assoc J 1977; 117: 1047 – 1048.
19 APR 07 Dr. M. S. Prasad 16
pembe yarapembe yara
• Weakness,
• Convulsions, and
• An annular papular rash.
• Case Fatality Rate: 95%.
• Cause: hexachlorobenzene in human milk.
• Turkey: 1957-59
19 APR 07 Dr. M. S. Prasad 17
Breathing ZonesBreathing Zones
• For an adult = 4 to 6 feet above the floor.
• For a child = closer to the floor.
• Chemicals heavier than air concentrate within lower
breathing zones near the floor.
19 APR 07 Dr. M. S. Prasad 18
Adult versus ChildrenAdult versus Children
• Microenvironment can differ enormously between
adults and children.
• Imagine a room which has air contaminated with mercury.
• Air near the floor may have a higher concentration
of mercury than air near the ceiling.
• The microenvironment of an infant lying on the floor therefore
would be different from that of a standing adult.
19 APR 07 Dr. M. S. Prasad 19
0
0.01
0.02
0.03
0.04
0.05
0.06
0.07
Surface Area/Body Mass
Newborn
Toddler
Child
Adult
SIZE AND SURFACE AREA
19 APR 07 Dr. M. S. Prasad 20
 Children lack the cognitive ability to recognize hazardous
situations.
 Pre-ambulatory children are unable to remove
themselves from danger
 Pre-reading children cannot read warning signs & labels
 Pre-adolescent / adolescent children may take unreasonable
risks due to cognitive immaturity and "risk-taking"
behaviours [Amir Khan in a film]
CHILDREN / ADOLESCENTS DO NOT RECOGNIZE DANGER
19 APR 07 Dr. M. S. Prasad 21
2. DYNAMIC DEVELOPMENTAL PHYSIOLOGY
Xenobiotics may be
handled differently by
an immature body
WHO
MORE VULNERABLEMORE VULNERABLE
19 APR 07 Dr. M. S. Prasad 22
3. LONGER LIFE EXPECTANCY
A safe and healthy environmentA safe and healthy environment
leads to a longer life expectancy.leads to a longer life expectancy.
WHO
Children inherit the world WE make!
19 APR 07 Dr. M. S. Prasad 23
4. POLITICALLY POWERLESS
 No political voice
 Advocacy by health sector
 Environmental laws and
regulations
– Local
– National
– International
WHO
19 APR 07 Dr. M. S. Prasad 24
SEARO, HRIDAY Educational Company
ENVIRONMENTAL RISK FACTORS AND CHILD LABOURENVIRONMENTAL RISK FACTORS AND CHILD LABOUR
 Over 171 million of the
352 million children
aged 5 – 17 years,
who work as Child
Labour, are exposed
to hazardous
conditions, including
chemical exposure
and poisoning.
 Child Abuse &
Neglect is another
environmental hazard
created by mankind.
19 APR 07 Dr. M. S. Prasad 25
WATER
19 APR 07 Dr. M. S. Prasad 26
Oh!Oh! The beautiful blue!
19 APR 07 Dr. M. S. Prasad 27
WATER IS ESSENTIAL FOR LIFE
 Access to safe water and sanitation
is a universal need and a basic
human right.
 70% of earth’s surface is water
 Only 2.5% to 3% is fresh water
 Less than 1% is accessible
 Pollution and other factors further
reduce access by 2/3
 1.1 billion people (1/6th
of the world’s
population) have no access to quality
drinking water Earth Observatory, NASA
19 APR 07 Dr. M. S. Prasad 28
wwwga.usgs.gov/edu/waterdistribution.html
19 APR 07 Dr. M. S. Prasad 29
Reykjavik
19 APR 07 Dr. M. S. Prasad 30
UNEP
19 APR 07 Dr. M. S. Prasad 31
UNEP
19 APR 07 Dr. M. S. Prasad 32
Waterborne diseasesWaterborne diseases
 Cholera
 Poliomyelitis
 Diarrhoeal diseases
 Roundworm
 Enteric fevers: typhoid
 Whipworm
 Hepatitis A
 Cryptosporidium
 Giardia
Water-washed diseasesWater-washed diseases
 Scabies
 Typhus
 Trachoma
 Louse infestation
Water-based diseasesWater-based diseases
 Schistosomiasis
 Dracunculiasis (guinea-worm)
Diseases transmitted by
water-related insect vectors
 Malaria
 Onchocerciasis
 Yellow fever
 Dengue
 Filariasis
 African trypanosomiasis
 Leishmaniasis
 Japanese Encephalitis
WATER - RELATED INFECTIONSWATER - RELATED INFECTIONS
19 APR 07 Dr. M. S. Prasad 33
 From natural erosion, discharge
from fertilizer and aluminium
factories, or added to drinking-water
 Bone disease, mottled teeth
 WHO guideline: 1.5 mg/L (ppm)
INORGANIC CHEMICAL: FLUORIDE (FL)INORGANIC CHEMICAL: FLUORIDE (FL)
A. K. Susheela. Fluorosis Research & Rural Development Foundation of India
19 APR 07 Dr. M. S. Prasad 34
Indoor HazardsIndoor Hazards..
19 APR 07 Dr. M. S. Prasad 35
SICK BUILDING SYNDROMESICK BUILDING SYNDROME
What is this syndrome?
 Discomfort not related to specific illness
 Effects appear to be linked to time spent inside the building
 Cause of symptoms is unknown
 Most complaints relieved soon after leaving the building
Building related illness:
Symptoms of identified illness attributed to airborne
contaminants in the building.
19 APR 07 Dr. M. S. Prasad 36
FIREFIRE
 Fire injuries can result from
Inhaled toxic chemicals and/or
Thermal burns.
 Make your home safer:
 Beware of matches and lighters
 Install smoke alarms
 Have a home fire escape plan
19 APR 07 Dr. M. S. Prasad 37
DUST MITESDUST MITES
CDC
19 APR 07 Dr. M. S. Prasad 38
MOULDMOULD
Occurs in dampOccurs in damp
indoor spacesindoor spaces
This home suffered only minor
exterior damage from
Hurricane Katrina, however
small leaks during the storm and
inadequate air flow, as the
house was vacant for weeks,
permitted this mold infestation
and resulted in homeowners
returning to this scene.
19 APR 07 Dr. M. S. Prasad 39
19 APR 07 Dr. M. S. Prasad 40
INDOOR AIR POLLUTIONINDOOR AIR POLLUTION
19 APR 07 Dr. M. S. Prasad 41
CHILDREN’S UNIQUE VULNERABILITYCHILDREN’S UNIQUE VULNERABILITY
 Inhale more pollutants per kilogram of body weight than do adults
 Because airways are narrower, irritation can result in
proportionately greater airway obstruction
WHO
19 APR 07 Dr. M. S. Prasad 42
Diagram showing effect of oedema onDiagram showing effect of oedema on
the cross-sectional airway diameterthe cross-sectional airway diameter
(R= radius)
Adult Airway
• D = 20 mm R = 10 mm
• Area = ∏ R2
= ∏ 102
= 100 ∏ mm2
(Normal)
• Oedema = 1 mm
• Area = ∏ 92
= 81 ∏ mm2
(81% of Normal)
Full Term Newborn
• D = 6 mm R = 3 mm
• Area ∏ R2
= ∏ 32
= 9 ∏ mm2
• Oedema = 1 mm
• Area = ∏ 22
= 4 ∏ mm2
(44% of Normal)
www.vh.org/pediatric/provider/pediatrics/ElectricAirway/Diagrams/AirwayDIaneterEdema.jpg
19 APR 07 Dr. M. S. Prasad 43
INDOOR AIR POLLUTION ALSO
AFFECTS OUTDOOR AIR QUALITY
Nigel Bruce/ITDG
19 APR 07 Dr. M. S. Prasad 44
SMOKY COOKING FUELS
WHO
19 APR 07 Dr. M. S. Prasad 45
CARBON MONOXIDE: THE "SILENT KILLER"
A COMMON CAUSE OF ACUTE AND LETHAL POISONING
www.cdc.gov/nceh/airpollution/carbonmonoxide/checklist.htm
19 APR 07 Dr. M. S. Prasad 46
CARBON MONOXIDE (CO): SOURCES
 Gas, kerosene, wood stoves and coal
 Room and water heaters
 Fireplaces, furnaces
 Leaking chimneys and vents
 Vehicle exhaust in closed garage
 Tobacco smoke
Any place where combustion is incomplete
EPA
19 APR 07 Dr. M. S. Prasad 47
Second-Hand Tobacco SmokeSecond-Hand Tobacco Smoke
(SHTS)
Children whose mothers smoke
 70% more respiratory problems
 Pneumonia and hospitalization in year 1 is 38% higher
 Infant mortality is 80% higher
 20% of all infant deaths could be avoided if all pregnant
smokers stopped by the 16th week of gestation
 5 times higher risk of sudden infant death syndrome (SIDS)
19 APR 07 Dr. M. S. Prasad 48
MOSQUITO COILSMOSQUITO COILS
 Major active ingredient –
PyrethrinsPyrethrins
 Long-term exposures linked
to asthma and wheezing
ehp.niehs.nih.gov/members/2003/6177/6177.html
19 APR 07 Dr. M. S. Prasad 49
RADONRADON
 Radon is a radioactive gas released from
soil and rocks
 It is the second leading cause of lung cancer
 Indoor Radon concentrations depend on
construction site and building materials
 Highest levels occur in basements and on the
ground floor
19 APR 07 Dr. M. S. Prasad 50
RADON MITIGATION SYSTEM
A – Gas-permeable layer
B - Plastic sheeting
C - Sealing and caulking
D - Vent pipe
E - Junction box
It is recommended thatIt is recommended that
homes be tested for radonhomes be tested for radon
on the lowest lived-in level –on the lowest lived-in level –
basement or ground floorbasement or ground floor
www.epa.gov/iaq/radon/construc.html
19 APR 07 Dr. M. S. Prasad 51
Radon in schoolsRadon in schools
Schools should also be tested for radon
Levels above 4 pCi/L call for action to reduce exposure
www.epa.gov/radon/pubs/schoolrn.html
19 APR 07 Dr. M. S. Prasad 52
ASBESTOSASBESTOS
Sources:
 Building construction materials used for insulation and as a fire-
retardant: asbestos cement, floor tiles, water pipes and others
 Levels increase if asbestos-containing materials are damaged
Health effects:
 NO acute toxicity
 Asbestosis results from occupational exposure
 Main risk for children: long-term exposure may cause cancer
 Lung cancer
 Malignant mesothelioma
19 APR 07 Dr. M. S. Prasad 53
LeadLead
19 APR 07 Dr. M. S. Prasad 54
LEAD POISONING IN THE ANCIENT WORLD
Did lead poisoning contribute to the fall of Rome?Did lead poisoning contribute to the fall of Rome?
In the Roman Empire, the upper classes were
exposed to high contents of lead in wine.
Lead water pipes
Glazed pottery
Signs and symptoms of lead poisoning recognized in
about half of the 38 Roman emperors
Nriagu, N Engl J Med. 1983 Mar 17;308(11):660
19 APR 07 Dr. M. S. Prasad 55
WHO ESTIMATESWHO ESTIMATES
 12 million children in developing countries suffer
from some form of permanent brain damage from
lead poisoning
 Hundreds of millions of children and pregnant
women are exposed to different sources of lead
 Worldwide, about 3.5% of minor mental retardation
is attributable to lead poisoning
19 APR 07 Dr. M. S. Prasad 56
X-RAY OF RECENT
LEAD INGESTION
A plain (flat) abdominal film
of a toddler with a recent
ingestion of lead-containing
paint chips
Lead particles are evident as
radio-opacities
Courtesy of John Graef, MD, Boston Children's Hospital
19 APR 07 Dr. M. S. Prasad 57
BASOPHILIC STIPPLING
 Classical 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
19 APR 07 Dr. M. S. Prasad 58
THE “LEAD LINE” SIGN
Abnormally heavy
mineralization of the
growth plate of long bones
in X-ray
The width and density of
“lead lines” reflect chronic
exposure
Courtesy of John Graef, MD, Boston Children's Hospital
19 APR 07 Dr. M. S. Prasad 59
LEADED PETROL – MAJOR SOURCELEADED PETROL – MAJOR SOURCE
Institute of Medicine, EPA, 1996
19 APR 07 Dr. M. S. Prasad 60
PESTICIDESPESTICIDES
Children's Health and the Environment
World Health Organization
www.who.int/ceh
August 2006 version
19 APR 07 Dr. M. S. Prasad 61
PESTICIDES – EXPOSURE
 Problems of spraying pesticides at home and in schools
 Higher concentrations near the floor
 Persistence in some surfaces: carpets, soft toys, …
 Overuse and misuse of pesticides
 Children’s behaviour and inhalation of pesticides
 Crawling
 Playing close to the floor
 Hand-to-mouth
 Object-to-mouth
19 APR 07 Dr. M. S. Prasad 62
CHILDREN'S EXPOSURECHILDREN'S EXPOSURE
WHO
19 APR 07 Dr. M. S. Prasad 63
Abusing DDT...
Norsk Barnemuseum
 DDT, DDE and their metabolites are weak
oestrogens and anti-androgens.
 Metabolites:
 o, p’ DDT
 p, p’ DDE
 Prenatal exposure to metabolites was
associated with a delay in mental and
psychomotor development at 13 months.
19 APR 07 Dr. M. S. Prasad 64
Persistent OrganicPersistent Organic
Pollutants (POPs) &Pollutants (POPs) &
Endocrine Disruptors.Endocrine Disruptors.
Children's Health and the Environment
World Health Organization
www.who.int/ceh
August 2006 version
19 APR 07 Dr. M. S. Prasad 65
WHAT ARE "POPs" ?
 Synthetic organic chemicals
 Persistent in environment
 Long-range transport leads
to global pollution
 Lipophilic
 Accumulate in food-chain
 High levels in fish and marine
mammals
Acute toxicity well-characterizedAcute toxicity well-characterized
NOAA
19 APR 07 Dr. M. S. Prasad 66
PESTICIDES
Aldrin
Dieldrin
Chlordane
DDT
Endrin
Heptachlor
Mirex
Toxaphene
INDUSTRIAL CHEMICALS
PCBs
HCB
UNINTENDED BY-PRODUCTS
Dibenzodioxins
Dibenzofurans
PERSISTENT ORGANIC POLLUTANTS (POPs)
Stockholm Convention: a global treaty
ratified by the international community lead by
UNEP – calls for the elimination and/or phasing
out of 12 POPs www.chem.unep.ch/pops/default.html
19 APR 07 Dr. M. S. Prasad 67
POPs – INDUSTRIAL CHEMICALS
PCBs:
Polychlorinated biphenyls
Trade Names for different mixtures (partial list):
Aroclor, Pyranol, Pyroclor, Phenochlor,
Pyralene, Clophen, Elaol, Kanechlor,
Santotherm, Fenchlor, Apirolio, Sovol
HCB:
Hexachlorobenzene
White monoclinic crystals or crystalline solid
UNEP
UNEP
19 APR 07 Dr. M. S. Prasad 68
PCB: HUMAN HEALTH INCIDENTS
"YUSHO" "YU-CHENG"
Adverse, persistent effects in newborns
• Low birth weight
• Reduced growth
• Hyperpigmentation
• Gingival hyperplasia
• Eye oedema
• Dentition at birth
• Skull calcifications
19 APR 07 Dr. M. S. Prasad 69
Dietary route of exposure to PCB
MARINE
MAMMALS
Whale
Seals
OTHER
Vegetables
Cereals
Fruits
ANIMAL
FAT
Meat
Poultry
COW'S
MILK
Butter
Dairy products
FISH
Salmon
Eel
Shellfish
Fish liver
Fish oils
WHO
19 APR 07 Dr. M. S. Prasad 70
BEYOND THE "DIRTY DOZEN"…
 In addition to POPs, other chemicals are characterized by their
persistence in the environment
 Persistent Toxic Substances (PTSs)
 Can be transported long distances
 Can accumulate in organisms and enter food-chain
 Not "POPs" – not listed in the Stockholm Convention
 Could include: mercury, cadmium, lead, polybrominated
diphenyl ethers (PBDE – flame retardants), others
19 APR 07 Dr. M. S. Prasad 71
Semi-persistent organic pollutants
Found in sewage, generated by waste incineration and traffic
PAHs, Phthalate esters, PBDEs, PCNs, BPA, Alkylphenols
Corra, Ceppi
19 APR 07 Dr. M. S. Prasad 72
In animals:
 Chloracne
 Lymphatic alteration
 Liver effects
 Gastric lesion
 Epidermal lesions
 Chicken: oedema, ascites
 Rats: fetal death and resorption,
endocrine alterations
 Mice: embryotoxicity,
malformations
IARC classification: carcinogen
AN EXAMPLE: DioxinDioxin – health effects
In humansIn humans::
 Chloracne
 Polyneuropathy
 Hepatomegaly
 Fatigue
 Depression
 Porphyria
IARC classification: 2,3,7,8-TCDD is a
possible human carcinogen (Group 2B)
19 APR 07 Dr. M. S. Prasad 73
Chemicals that mimic hormones could alter
the differentiation of some tissues.
Because organ systems in children, including
the reproductive system, continue to
differentiate, such chemical may have effect
on the development of those organs.
Such substances/chemicals are known as
“Endocrine Disrupting Chemicals (EDC)” or
Endocrine Disruptors.
ENDOCRINE DISRUPTING CHEMICALS (EDCs)
19 APR 07 Dr. M. S. Prasad 74
WHO
Children represent the future of nations.
19 APR 07 Dr. M. S. Prasad 75
Recognize, Prevent,
Assess and Manage
diseases linked to, or
triggered by,
environmental factors.
19 APR 07 Dr. M. S. Prasad 76
PaediatricPaediatric
EnvironmentalEnvironmental
HistoryHistory
19 APR 07 Dr. M. S. Prasad 77
• A set of basic and concise questions
• Part of the standard medical history
with additional questions to find out
child’s possible exposure to
hazardous environment.
• Tailored according to the local
situation, needs and capacities of:
– Industrialized countries
– Developing regions
WHAT IS THE PWHAT IS THE PAAEDIATRIC ENVIRONMENTAL HISTORYEDIATRIC ENVIRONMENTAL HISTORY
WHO
19 APR 07 Dr. M. S. Prasad 78
1. What are the potential
environmental hazards?
2. How, when and where are
children exposed?
3. What are the main effects?
KEY AREAS TO ADDRESS
WHO
19 APR 07 Dr. M. S. Prasad 79
OBJECTIVESOBJECTIVES
Help PaediatriciansHelp Paediatricians
• To understand the child’s
physical surroundings, and
• To offer appropriate suggestions
to promote a healthy environment.
19 APR 07 Dr. M. S. Prasad 80
Some Basic QuestionsSome Basic Questions
1. Where does the child live or spend time?
2. Does anyone in the home smoke?
3. What is source of drinking water?
4. Are there exposures from items in the diet?
5. Is the child protected from excessive sun
exposure?
6. What do parents/teenagers do for a living?
19 APR 07 Dr. M. S. Prasad 81
WHO
"Agreenpageintheclinicalrecord"
19 APR 07 Dr. M. S. Prasad 82
19 APR 07 Dr. M. S. Prasad 83
19 APR 07 Dr. M. S. Prasad 84
19 APR 07 Dr. M. S. Prasad 85
19 APR 07 Dr. M. S. Prasad 86
EXAMPLES OF QUESTIONS: WHERE DOES THE CHILD LIVE?
• What is the building made of (e.g. wood, brick, mud, cardboard,…)?
• Is there mould on the walls? Is it well-ventilated? Are there any odours?
• Has there been any recent painting or refurbishing?
• Do family members smoke at home? What do they smoke ? How much?
• Are pesticides used indoors? How? Are there cockroaches? Mites? Rats?
• Are there pets (dogs, cats, birds) or other animals?
• How often is the place cleaned? Which chemicals are used for cleaning?
• Where/how is the cooking done? How is the home heated? Stoves? Exhaust?
[Same applicable to playground and school]
19 APR 07 Dr. M. S. Prasad 87
EXAMPLES OF QUESTIONS: WHAT ARE THE CHILD'S ACTIVITIES?
Hobbies
Painting – paint and solvents?
Model-building – glue and solvents?
Pottery – pigments, paints?
Gardening – pesticides?
Woodwork – chemicals?
Activities
Eating habits (type of
diet, food quality)
Drinking habits (alcohol
use and abuse, soft
drinks)
Playing habits
Learning habits
Working habits
Scavenging (time spent
near garbage)
Exploring
Testing (trying drugs,
eating unknown
berries)
Sports
Type of sport
Sports area
Injuries
Toxic exposures
Use of energizing drugs
Application of poultices
WHOWHO
19 APR 07 Dr. M. S. Prasad 88
EXAMPLES OF QUESTIONS:EXAMPLES OF QUESTIONS: CHILD'S BEHAVIOURS?CHILD'S BEHAVIOURS?
Personal hygiene and
habits
How often does the child bathe?
Hand and face washed? How?
Where? With what?
Are clothes washed regularly?
What type of diapers are used?
Does the child have lice? How is
it treated?
Does the child play on the floor?
Carpet? Soil?
How and how often are the
child’s bedroom and play area
cleaned?
Which chemicals are used to
clean the home?
Does the child have pica?
Cultural history
Use of alternative
medicines or cosmetics
Cultural practices
Religious practices
Traditions involving the
use of chemicals
Transport
What transport does the
child use?
- individual or collective;
- bicycle;
- motorcycle;
- horse; or other?
Characteristics of bus?
Bus stop?
WHO
19 APR 07 Dr. M. S. Prasad 89
www.atsdr.cdc.gov/HEC/CSEM/pediatric/index.html
19 APR 07 Dr. M. S. Prasad 90
Some related websitesSome related websites
• http://www.atsdr.edc.gov
• http://www.aoec.org
• http://www.aoec.org/PedEnvHx_
files/frame.htm
• http://children.cape.ca
• http://children.cape.ca/history.html

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Child health & environment

  • 1. 19 APR 07 Dr. M. S. Prasad 1 EnvironmentEnvironment && Child HealthChild Health Dr. M. S. PrasadDr. M. S. Prasad Consultant & Head Dept. of Paediatrics Safdarjung Hospital & Vardhaman Mahavir Medical College New Delhi
  • 2. 19 APR 07 Dr. M. S. Prasad 2 Environmental Hazards andEnvironmental Hazards and their relationship to Healththeir relationship to Health A neglected topic in the Paediatric and General Medical Textbooks.
  • 3. 19 APR 07 Dr. M. S. Prasad 3 HistoryHistory • 1954:1954: Nuclear weapon test on Bikini IslandBikini Island – Acute burns from beta-radiation in the neighboring islands. – Hypothyroidism, – Thyroid neoplasm, and – Leukemia. • 1957:1957: AAP CommitteeAAP Committee on Radiation Hazards and Congenital Malformations. • 1961:1961: CommitteeCommittee on Environmental Hazards. • 1966:1966: First International ConferenceConference on Paediatric significance on nuclear fall-outs. • 1973:1973: ConferenceConference on the Susceptibility of the Fetus and Child to Chemical Pollutants. • 19811981:: ConferenceConference on Chemical and Radiation Hazards to Children. • 1991:1991: CommitteeCommittee on Environmental Health.
  • 4. 19 APR 07 Dr. M. S. Prasad 4 HistoryHistory (Continued) • 1996:1996: Food Quality Protection Act. • April 21, 1997:April 21, 1997: President Clinton issued Executive Order 13045: Protection of Children from Environmental Health Risks and Safety Risks. • October 1999:October 1999: First edition of the AAP “Handbook of Pediatric Environmental Health”. • 2000 & 2001:2000 & 2001: Workshops. • 2002:2002: The Ambulatory Pediatric Association launched 3 years fellowship training programmefellowship training programme..
  • 5. 19 APR 07 Dr. M. S. Prasad 5 EnvironmentEnvironment The term environment implies allThe term environment implies all the external factors – living andthe external factors – living and non-living, material and non-non-living, material and non- material – which surround man.material – which surround man. Everything except me is environment. The term environment implies allThe term environment implies all the external factors – living andthe external factors – living and non-living, material and non-non-living, material and non- material – which surround man.material – which surround man. Everything except me is environment.
  • 6. 19 APR 07 Dr. M. S. Prasad 6 ClassificationClassification • Physical: – Macro-environment – Microenvironment. • Biologic: Plant & animal life including bacteria, viruses, insects, rodents and animals (including man). • Social: – Customs, culture, habits, income, occupation, religion etc. • Chemical: Pesticides, Fluorine, Mercury, Lead, Solvent.
  • 7. 19 APR 07 Dr. M. S. Prasad 7 Areas of concernAreas of concern • Physical: – Radiation, – Noise, – Extreme heat/cold, – Unsafe building, – Traffic…….. • Chemical: – Pesticides, – Solvents, – Lead, – Mercury………. • Biological: – Disease Vector, – Mould, – Envenoming ……….
  • 8. 19 APR 07 Dr. M. S. Prasad 8 Why children?Why children?
  • 9. 19 APR 07 Dr. M. S. Prasad 9 Environment & DiseasesEnvironment & Diseases • More than 1/4th of global disease burden is due to modified environmental factors. • It is 1/3rd of Paediatric Diseases burden. [WHO, Preventing diseases through healthy environment 2000]
  • 10. 19 APR 07 Dr. M. S. Prasad 10 1. Different and unique exposures 2. Dynamic developmental physiology 3. Longer life expectancy 4. Politically powerless Raphael, National Gallery of Art, Washington, DC CHILDREN ARE NOT LITTLE ADULTSCHILDREN ARE NOT LITTLE ADULTS
  • 11. 19 APR 07 Dr. M. S. Prasad 11 1. DIFFERENT AND UNIQUE EXPOSURESDIFFERENT AND UNIQUE EXPOSURES  Unique exposure pathways – Transplacental – Breastfeeding  Exploratory behaviours leading to exposures – Hand-to-mouth, – Object-to-mouth – Non-nutritive ingestion  Stature and living zones, microenvironments – Location – lower to the ground – High surface area to volume ratio  Children do not understand danger – Pre-ambulatory – Adolescence – “high risk” behaviors
  • 12. 19 APR 07 Dr. M. S. Prasad 12 Moore, Elsevier Inc, 1973 WINDOWS OF DEVELOPMENT
  • 13. 19 APR 07 Dr. M. S. Prasad 13 TRANSPLACENTAL EXPOSURETRANSPLACENTAL EXPOSURE Maternal exposures do matter! Lessons from pharmaceuticals: thalidomide, diethylstilbestrol (DES), alcohol
  • 14. 19 APR 07 Dr. M. S. Prasad 14 Breast-feedingBreast-feeding Pollutants that may be found in Human Milk Chemical AgentsChemical Agents DDT, DDE PCB/PCDF Dioxin Chlordane Heptachlor Hexachlorobenzene Volatile Organic Compounds Nicotine Metals Lead Methylmercury.
  • 15. 19 APR 07 Dr. M. S. Prasad 15 Breast-feedingBreast-feeding • Halothane has been detected in the milk of lactating anaesthesiologistanaesthesiologist.. • There is a single case of report of a child developed cholestatic jaundice while being breastfed. His mother lunched daily with her husband, who was a dry-cleaner, and perchloroethylene was found in her milk. Ref.: – Br. J. Anaesth. 1976; 48-541 – 543. – Can Med Assoc J 1977; 117: 1047 – 1048.
  • 16. 19 APR 07 Dr. M. S. Prasad 16 pembe yarapembe yara • Weakness, • Convulsions, and • An annular papular rash. • Case Fatality Rate: 95%. • Cause: hexachlorobenzene in human milk. • Turkey: 1957-59
  • 17. 19 APR 07 Dr. M. S. Prasad 17 Breathing ZonesBreathing Zones • For an adult = 4 to 6 feet above the floor. • For a child = closer to the floor. • Chemicals heavier than air concentrate within lower breathing zones near the floor.
  • 18. 19 APR 07 Dr. M. S. Prasad 18 Adult versus ChildrenAdult versus Children • Microenvironment can differ enormously between adults and children. • Imagine a room which has air contaminated with mercury. • Air near the floor may have a higher concentration of mercury than air near the ceiling. • The microenvironment of an infant lying on the floor therefore would be different from that of a standing adult.
  • 19. 19 APR 07 Dr. M. S. Prasad 19 0 0.01 0.02 0.03 0.04 0.05 0.06 0.07 Surface Area/Body Mass Newborn Toddler Child Adult SIZE AND SURFACE AREA
  • 20. 19 APR 07 Dr. M. S. Prasad 20  Children lack the cognitive ability to recognize hazardous situations.  Pre-ambulatory children are unable to remove themselves from danger  Pre-reading children cannot read warning signs & labels  Pre-adolescent / adolescent children may take unreasonable risks due to cognitive immaturity and "risk-taking" behaviours [Amir Khan in a film] CHILDREN / ADOLESCENTS DO NOT RECOGNIZE DANGER
  • 21. 19 APR 07 Dr. M. S. Prasad 21 2. DYNAMIC DEVELOPMENTAL PHYSIOLOGY Xenobiotics may be handled differently by an immature body WHO MORE VULNERABLEMORE VULNERABLE
  • 22. 19 APR 07 Dr. M. S. Prasad 22 3. LONGER LIFE EXPECTANCY A safe and healthy environmentA safe and healthy environment leads to a longer life expectancy.leads to a longer life expectancy. WHO Children inherit the world WE make!
  • 23. 19 APR 07 Dr. M. S. Prasad 23 4. POLITICALLY POWERLESS  No political voice  Advocacy by health sector  Environmental laws and regulations – Local – National – International WHO
  • 24. 19 APR 07 Dr. M. S. Prasad 24 SEARO, HRIDAY Educational Company ENVIRONMENTAL RISK FACTORS AND CHILD LABOURENVIRONMENTAL RISK FACTORS AND CHILD LABOUR  Over 171 million of the 352 million children aged 5 – 17 years, who work as Child Labour, are exposed to hazardous conditions, including chemical exposure and poisoning.  Child Abuse & Neglect is another environmental hazard created by mankind.
  • 25. 19 APR 07 Dr. M. S. Prasad 25 WATER
  • 26. 19 APR 07 Dr. M. S. Prasad 26 Oh!Oh! The beautiful blue!
  • 27. 19 APR 07 Dr. M. S. Prasad 27 WATER IS ESSENTIAL FOR LIFE  Access to safe water and sanitation is a universal need and a basic human right.  70% of earth’s surface is water  Only 2.5% to 3% is fresh water  Less than 1% is accessible  Pollution and other factors further reduce access by 2/3  1.1 billion people (1/6th of the world’s population) have no access to quality drinking water Earth Observatory, NASA
  • 28. 19 APR 07 Dr. M. S. Prasad 28 wwwga.usgs.gov/edu/waterdistribution.html
  • 29. 19 APR 07 Dr. M. S. Prasad 29 Reykjavik
  • 30. 19 APR 07 Dr. M. S. Prasad 30 UNEP
  • 31. 19 APR 07 Dr. M. S. Prasad 31 UNEP
  • 32. 19 APR 07 Dr. M. S. Prasad 32 Waterborne diseasesWaterborne diseases  Cholera  Poliomyelitis  Diarrhoeal diseases  Roundworm  Enteric fevers: typhoid  Whipworm  Hepatitis A  Cryptosporidium  Giardia Water-washed diseasesWater-washed diseases  Scabies  Typhus  Trachoma  Louse infestation Water-based diseasesWater-based diseases  Schistosomiasis  Dracunculiasis (guinea-worm) Diseases transmitted by water-related insect vectors  Malaria  Onchocerciasis  Yellow fever  Dengue  Filariasis  African trypanosomiasis  Leishmaniasis  Japanese Encephalitis WATER - RELATED INFECTIONSWATER - RELATED INFECTIONS
  • 33. 19 APR 07 Dr. M. S. Prasad 33  From natural erosion, discharge from fertilizer and aluminium factories, or added to drinking-water  Bone disease, mottled teeth  WHO guideline: 1.5 mg/L (ppm) INORGANIC CHEMICAL: FLUORIDE (FL)INORGANIC CHEMICAL: FLUORIDE (FL) A. K. Susheela. Fluorosis Research & Rural Development Foundation of India
  • 34. 19 APR 07 Dr. M. S. Prasad 34 Indoor HazardsIndoor Hazards..
  • 35. 19 APR 07 Dr. M. S. Prasad 35 SICK BUILDING SYNDROMESICK BUILDING SYNDROME What is this syndrome?  Discomfort not related to specific illness  Effects appear to be linked to time spent inside the building  Cause of symptoms is unknown  Most complaints relieved soon after leaving the building Building related illness: Symptoms of identified illness attributed to airborne contaminants in the building.
  • 36. 19 APR 07 Dr. M. S. Prasad 36 FIREFIRE  Fire injuries can result from Inhaled toxic chemicals and/or Thermal burns.  Make your home safer:  Beware of matches and lighters  Install smoke alarms  Have a home fire escape plan
  • 37. 19 APR 07 Dr. M. S. Prasad 37 DUST MITESDUST MITES CDC
  • 38. 19 APR 07 Dr. M. S. Prasad 38 MOULDMOULD Occurs in dampOccurs in damp indoor spacesindoor spaces This home suffered only minor exterior damage from Hurricane Katrina, however small leaks during the storm and inadequate air flow, as the house was vacant for weeks, permitted this mold infestation and resulted in homeowners returning to this scene.
  • 39. 19 APR 07 Dr. M. S. Prasad 39
  • 40. 19 APR 07 Dr. M. S. Prasad 40 INDOOR AIR POLLUTIONINDOOR AIR POLLUTION
  • 41. 19 APR 07 Dr. M. S. Prasad 41 CHILDREN’S UNIQUE VULNERABILITYCHILDREN’S UNIQUE VULNERABILITY  Inhale more pollutants per kilogram of body weight than do adults  Because airways are narrower, irritation can result in proportionately greater airway obstruction WHO
  • 42. 19 APR 07 Dr. M. S. Prasad 42 Diagram showing effect of oedema onDiagram showing effect of oedema on the cross-sectional airway diameterthe cross-sectional airway diameter (R= radius) Adult Airway • D = 20 mm R = 10 mm • Area = ∏ R2 = ∏ 102 = 100 ∏ mm2 (Normal) • Oedema = 1 mm • Area = ∏ 92 = 81 ∏ mm2 (81% of Normal) Full Term Newborn • D = 6 mm R = 3 mm • Area ∏ R2 = ∏ 32 = 9 ∏ mm2 • Oedema = 1 mm • Area = ∏ 22 = 4 ∏ mm2 (44% of Normal) www.vh.org/pediatric/provider/pediatrics/ElectricAirway/Diagrams/AirwayDIaneterEdema.jpg
  • 43. 19 APR 07 Dr. M. S. Prasad 43 INDOOR AIR POLLUTION ALSO AFFECTS OUTDOOR AIR QUALITY Nigel Bruce/ITDG
  • 44. 19 APR 07 Dr. M. S. Prasad 44 SMOKY COOKING FUELS WHO
  • 45. 19 APR 07 Dr. M. S. Prasad 45 CARBON MONOXIDE: THE "SILENT KILLER" A COMMON CAUSE OF ACUTE AND LETHAL POISONING www.cdc.gov/nceh/airpollution/carbonmonoxide/checklist.htm
  • 46. 19 APR 07 Dr. M. S. Prasad 46 CARBON MONOXIDE (CO): SOURCES  Gas, kerosene, wood stoves and coal  Room and water heaters  Fireplaces, furnaces  Leaking chimneys and vents  Vehicle exhaust in closed garage  Tobacco smoke Any place where combustion is incomplete EPA
  • 47. 19 APR 07 Dr. M. S. Prasad 47 Second-Hand Tobacco SmokeSecond-Hand Tobacco Smoke (SHTS) Children whose mothers smoke  70% more respiratory problems  Pneumonia and hospitalization in year 1 is 38% higher  Infant mortality is 80% higher  20% of all infant deaths could be avoided if all pregnant smokers stopped by the 16th week of gestation  5 times higher risk of sudden infant death syndrome (SIDS)
  • 48. 19 APR 07 Dr. M. S. Prasad 48 MOSQUITO COILSMOSQUITO COILS  Major active ingredient – PyrethrinsPyrethrins  Long-term exposures linked to asthma and wheezing ehp.niehs.nih.gov/members/2003/6177/6177.html
  • 49. 19 APR 07 Dr. M. S. Prasad 49 RADONRADON  Radon is a radioactive gas released from soil and rocks  It is the second leading cause of lung cancer  Indoor Radon concentrations depend on construction site and building materials  Highest levels occur in basements and on the ground floor
  • 50. 19 APR 07 Dr. M. S. Prasad 50 RADON MITIGATION SYSTEM A – Gas-permeable layer B - Plastic sheeting C - Sealing and caulking D - Vent pipe E - Junction box It is recommended thatIt is recommended that homes be tested for radonhomes be tested for radon on the lowest lived-in level –on the lowest lived-in level – basement or ground floorbasement or ground floor www.epa.gov/iaq/radon/construc.html
  • 51. 19 APR 07 Dr. M. S. Prasad 51 Radon in schoolsRadon in schools Schools should also be tested for radon Levels above 4 pCi/L call for action to reduce exposure www.epa.gov/radon/pubs/schoolrn.html
  • 52. 19 APR 07 Dr. M. S. Prasad 52 ASBESTOSASBESTOS Sources:  Building construction materials used for insulation and as a fire- retardant: asbestos cement, floor tiles, water pipes and others  Levels increase if asbestos-containing materials are damaged Health effects:  NO acute toxicity  Asbestosis results from occupational exposure  Main risk for children: long-term exposure may cause cancer  Lung cancer  Malignant mesothelioma
  • 53. 19 APR 07 Dr. M. S. Prasad 53 LeadLead
  • 54. 19 APR 07 Dr. M. S. Prasad 54 LEAD POISONING IN THE ANCIENT WORLD Did lead poisoning contribute to the fall of Rome?Did lead poisoning contribute to the fall of Rome? In the Roman Empire, the upper classes were exposed to high contents of lead in wine. Lead water pipes Glazed pottery Signs and symptoms of lead poisoning recognized in about half of the 38 Roman emperors Nriagu, N Engl J Med. 1983 Mar 17;308(11):660
  • 55. 19 APR 07 Dr. M. S. Prasad 55 WHO ESTIMATESWHO ESTIMATES  12 million children in developing countries suffer from some form of permanent brain damage from lead poisoning  Hundreds of millions of children and pregnant women are exposed to different sources of lead  Worldwide, about 3.5% of minor mental retardation is attributable to lead poisoning
  • 56. 19 APR 07 Dr. M. S. Prasad 56 X-RAY OF RECENT LEAD INGESTION A plain (flat) abdominal film of a toddler with a recent ingestion of lead-containing paint chips Lead particles are evident as radio-opacities Courtesy of John Graef, MD, Boston Children's Hospital
  • 57. 19 APR 07 Dr. M. S. Prasad 57 BASOPHILIC STIPPLING  Classical 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
  • 58. 19 APR 07 Dr. M. S. Prasad 58 THE “LEAD LINE” SIGN Abnormally heavy mineralization of the growth plate of long bones in X-ray The width and density of “lead lines” reflect chronic exposure Courtesy of John Graef, MD, Boston Children's Hospital
  • 59. 19 APR 07 Dr. M. S. Prasad 59 LEADED PETROL – MAJOR SOURCELEADED PETROL – MAJOR SOURCE Institute of Medicine, EPA, 1996
  • 60. 19 APR 07 Dr. M. S. Prasad 60 PESTICIDESPESTICIDES Children's Health and the Environment World Health Organization www.who.int/ceh August 2006 version
  • 61. 19 APR 07 Dr. M. S. Prasad 61 PESTICIDES – EXPOSURE  Problems of spraying pesticides at home and in schools  Higher concentrations near the floor  Persistence in some surfaces: carpets, soft toys, …  Overuse and misuse of pesticides  Children’s behaviour and inhalation of pesticides  Crawling  Playing close to the floor  Hand-to-mouth  Object-to-mouth
  • 62. 19 APR 07 Dr. M. S. Prasad 62 CHILDREN'S EXPOSURECHILDREN'S EXPOSURE WHO
  • 63. 19 APR 07 Dr. M. S. Prasad 63 Abusing DDT... Norsk Barnemuseum  DDT, DDE and their metabolites are weak oestrogens and anti-androgens.  Metabolites:  o, p’ DDT  p, p’ DDE  Prenatal exposure to metabolites was associated with a delay in mental and psychomotor development at 13 months.
  • 64. 19 APR 07 Dr. M. S. Prasad 64 Persistent OrganicPersistent Organic Pollutants (POPs) &Pollutants (POPs) & Endocrine Disruptors.Endocrine Disruptors. Children's Health and the Environment World Health Organization www.who.int/ceh August 2006 version
  • 65. 19 APR 07 Dr. M. S. Prasad 65 WHAT ARE "POPs" ?  Synthetic organic chemicals  Persistent in environment  Long-range transport leads to global pollution  Lipophilic  Accumulate in food-chain  High levels in fish and marine mammals Acute toxicity well-characterizedAcute toxicity well-characterized NOAA
  • 66. 19 APR 07 Dr. M. S. Prasad 66 PESTICIDES Aldrin Dieldrin Chlordane DDT Endrin Heptachlor Mirex Toxaphene INDUSTRIAL CHEMICALS PCBs HCB UNINTENDED BY-PRODUCTS Dibenzodioxins Dibenzofurans PERSISTENT ORGANIC POLLUTANTS (POPs) Stockholm Convention: a global treaty ratified by the international community lead by UNEP – calls for the elimination and/or phasing out of 12 POPs www.chem.unep.ch/pops/default.html
  • 67. 19 APR 07 Dr. M. S. Prasad 67 POPs – INDUSTRIAL CHEMICALS PCBs: Polychlorinated biphenyls Trade Names for different mixtures (partial list): Aroclor, Pyranol, Pyroclor, Phenochlor, Pyralene, Clophen, Elaol, Kanechlor, Santotherm, Fenchlor, Apirolio, Sovol HCB: Hexachlorobenzene White monoclinic crystals or crystalline solid UNEP UNEP
  • 68. 19 APR 07 Dr. M. S. Prasad 68 PCB: HUMAN HEALTH INCIDENTS "YUSHO" "YU-CHENG" Adverse, persistent effects in newborns • Low birth weight • Reduced growth • Hyperpigmentation • Gingival hyperplasia • Eye oedema • Dentition at birth • Skull calcifications
  • 69. 19 APR 07 Dr. M. S. Prasad 69 Dietary route of exposure to PCB MARINE MAMMALS Whale Seals OTHER Vegetables Cereals Fruits ANIMAL FAT Meat Poultry COW'S MILK Butter Dairy products FISH Salmon Eel Shellfish Fish liver Fish oils WHO
  • 70. 19 APR 07 Dr. M. S. Prasad 70 BEYOND THE "DIRTY DOZEN"…  In addition to POPs, other chemicals are characterized by their persistence in the environment  Persistent Toxic Substances (PTSs)  Can be transported long distances  Can accumulate in organisms and enter food-chain  Not "POPs" – not listed in the Stockholm Convention  Could include: mercury, cadmium, lead, polybrominated diphenyl ethers (PBDE – flame retardants), others
  • 71. 19 APR 07 Dr. M. S. Prasad 71 Semi-persistent organic pollutants Found in sewage, generated by waste incineration and traffic PAHs, Phthalate esters, PBDEs, PCNs, BPA, Alkylphenols Corra, Ceppi
  • 72. 19 APR 07 Dr. M. S. Prasad 72 In animals:  Chloracne  Lymphatic alteration  Liver effects  Gastric lesion  Epidermal lesions  Chicken: oedema, ascites  Rats: fetal death and resorption, endocrine alterations  Mice: embryotoxicity, malformations IARC classification: carcinogen AN EXAMPLE: DioxinDioxin – health effects In humansIn humans::  Chloracne  Polyneuropathy  Hepatomegaly  Fatigue  Depression  Porphyria IARC classification: 2,3,7,8-TCDD is a possible human carcinogen (Group 2B)
  • 73. 19 APR 07 Dr. M. S. Prasad 73 Chemicals that mimic hormones could alter the differentiation of some tissues. Because organ systems in children, including the reproductive system, continue to differentiate, such chemical may have effect on the development of those organs. Such substances/chemicals are known as “Endocrine Disrupting Chemicals (EDC)” or Endocrine Disruptors. ENDOCRINE DISRUPTING CHEMICALS (EDCs)
  • 74. 19 APR 07 Dr. M. S. Prasad 74 WHO Children represent the future of nations.
  • 75. 19 APR 07 Dr. M. S. Prasad 75 Recognize, Prevent, Assess and Manage diseases linked to, or triggered by, environmental factors.
  • 76. 19 APR 07 Dr. M. S. Prasad 76 PaediatricPaediatric EnvironmentalEnvironmental HistoryHistory
  • 77. 19 APR 07 Dr. M. S. Prasad 77 • A set of basic and concise questions • Part of the standard medical history with additional questions to find out child’s possible exposure to hazardous environment. • Tailored according to the local situation, needs and capacities of: – Industrialized countries – Developing regions WHAT IS THE PWHAT IS THE PAAEDIATRIC ENVIRONMENTAL HISTORYEDIATRIC ENVIRONMENTAL HISTORY WHO
  • 78. 19 APR 07 Dr. M. S. Prasad 78 1. What are the potential environmental hazards? 2. How, when and where are children exposed? 3. What are the main effects? KEY AREAS TO ADDRESS WHO
  • 79. 19 APR 07 Dr. M. S. Prasad 79 OBJECTIVESOBJECTIVES Help PaediatriciansHelp Paediatricians • To understand the child’s physical surroundings, and • To offer appropriate suggestions to promote a healthy environment.
  • 80. 19 APR 07 Dr. M. S. Prasad 80 Some Basic QuestionsSome Basic Questions 1. Where does the child live or spend time? 2. Does anyone in the home smoke? 3. What is source of drinking water? 4. Are there exposures from items in the diet? 5. Is the child protected from excessive sun exposure? 6. What do parents/teenagers do for a living?
  • 81. 19 APR 07 Dr. M. S. Prasad 81 WHO "Agreenpageintheclinicalrecord"
  • 82. 19 APR 07 Dr. M. S. Prasad 82
  • 83. 19 APR 07 Dr. M. S. Prasad 83
  • 84. 19 APR 07 Dr. M. S. Prasad 84
  • 85. 19 APR 07 Dr. M. S. Prasad 85
  • 86. 19 APR 07 Dr. M. S. Prasad 86 EXAMPLES OF QUESTIONS: WHERE DOES THE CHILD LIVE? • What is the building made of (e.g. wood, brick, mud, cardboard,…)? • Is there mould on the walls? Is it well-ventilated? Are there any odours? • Has there been any recent painting or refurbishing? • Do family members smoke at home? What do they smoke ? How much? • Are pesticides used indoors? How? Are there cockroaches? Mites? Rats? • Are there pets (dogs, cats, birds) or other animals? • How often is the place cleaned? Which chemicals are used for cleaning? • Where/how is the cooking done? How is the home heated? Stoves? Exhaust? [Same applicable to playground and school]
  • 87. 19 APR 07 Dr. M. S. Prasad 87 EXAMPLES OF QUESTIONS: WHAT ARE THE CHILD'S ACTIVITIES? Hobbies Painting – paint and solvents? Model-building – glue and solvents? Pottery – pigments, paints? Gardening – pesticides? Woodwork – chemicals? Activities Eating habits (type of diet, food quality) Drinking habits (alcohol use and abuse, soft drinks) Playing habits Learning habits Working habits Scavenging (time spent near garbage) Exploring Testing (trying drugs, eating unknown berries) Sports Type of sport Sports area Injuries Toxic exposures Use of energizing drugs Application of poultices WHOWHO
  • 88. 19 APR 07 Dr. M. S. Prasad 88 EXAMPLES OF QUESTIONS:EXAMPLES OF QUESTIONS: CHILD'S BEHAVIOURS?CHILD'S BEHAVIOURS? Personal hygiene and habits How often does the child bathe? Hand and face washed? How? Where? With what? Are clothes washed regularly? What type of diapers are used? Does the child have lice? How is it treated? Does the child play on the floor? Carpet? Soil? How and how often are the child’s bedroom and play area cleaned? Which chemicals are used to clean the home? Does the child have pica? Cultural history Use of alternative medicines or cosmetics Cultural practices Religious practices Traditions involving the use of chemicals Transport What transport does the child use? - individual or collective; - bicycle; - motorcycle; - horse; or other? Characteristics of bus? Bus stop? WHO
  • 89. 19 APR 07 Dr. M. S. Prasad 89 www.atsdr.cdc.gov/HEC/CSEM/pediatric/index.html
  • 90. 19 APR 07 Dr. M. S. Prasad 90 Some related websitesSome related websites • http://www.atsdr.edc.gov • http://www.aoec.org • http://www.aoec.org/PedEnvHx_ files/frame.htm • http://children.cape.ca • http://children.cape.ca/history.html

Editor's Notes

  1. The artists of the Renaissance realized that children are not simply miniaturized adults: they have big heads, long trunks and short limbs, as seen in this "Madonna and Child" by Raphael. <<NOTE TO USER: Replace with culturally/regionally appropriate image to illustrate the physical differences between babies and adults.>> We now recognize that children, including the embryo, fetus, infant and all life stages until the completion of adolescence, are often at a different and increased risk from environmental hazards from that of adults, for reasons that can be divided into four major categories. 1. Children often have different, and sometimes unique, exposures to environmental hazards from those of adults. 2. Due to their dynamic developmental physiology children are often subjected to higher exposures to pollutants found in air, water and food. These exposures may be handled quite differently by an immature set of systems to the way they are dealt with in adults. Furthermore, the developmental component of a child’s physiology is changing: maturing, differentiating and growing in phases known as "developmental windows". These "critical windows of vulnerability" have no parallel in adult physiology and create unique risks for children exposed to hazards that can alter normal function and structure. 3. Children have a longer life expectancy. Therefore they have longer to manifest a disease with a long latency period, and longer to live with toxic damage. 4. Finally, children are politically powerless; they are defenceless. With no political standing of their own, they must rely on adults to protect them from toxic environmental agents. Each of these points is illustrated in more detail in the following slides. Image: National Gallery of Art, Smithsonian Institute, Washington, DC.
  2. Children have unique exposure pathways. They can be exposed in utero to toxic environmental agents which cross the placenta. Such exposures can be chemical (pollutants and pharmaceuticals), physical (radiation, heat) and biological (viral, parasitic). They can also be exposed to pollutants that pass into their mother’s milk. Neither of these routes of exposure occur in adults or older children. Children also have pathways of exposure that differ from those of adults due to their size and developmental stage. For example, young children engage in normal exploratory behaviours including hand-to-mouth and object-to-mouth behaviours, and non-nutritive ingestion which may dramatically increase exposure over that in adults. Children’s physical differences also cause them to reside in a different location in the world, i.e. closer to the ground. Heavy pollutants such as mercury are concentrated in their breathing zone and deliberate applications of pesticides and cleaning solutions make them more readily accessible to small children. Because they are small, they have a high surface area to volume ratio and can have dramatically higher absorption through dermal contact than adults. And, they may have much more limited ability to understand and move out of danger, both from toxic agents and dangerous situations which could result in injury. This characteristic is obvious in the pre-ambulatory phase, but persists through exploratory toddler behaviour and even into the high-risk behaviours seen in adolescence.
  3. Physiological differences manifest in more ways than immature metabolic pathways. Because important systems are still differentiating and growing, children have unique susceptibilities compared to adults — and critical time windows in those susceptibilities. Preconception Gestation – thalidomide, DES – ionizing radiation – methylmercury, Pb Postnatal – second-hand tobacco smoke – lead. There has been an explosion of knowledge about development in the past decade or so, and it is hard to remember that it was only about 50 years ago that the discovery was made that the fetus is vulnerable to exposures. The phocomelia epidemic resulting from use of thalidomide in pregnancy was an early and dramatic example of the ability of chemicals to cross the placenta and damage the fetus. Additionally, thalidomide administered during a small, 4-day window between gestational days 20 and 24, may increase the risk of autism (Stromland, 1994). More than one system can be susceptible and different pathology may occur depending upon the dose and timing of exposure. Now we know that other exposures during gestation can harm systems, and some are listed here. We also know that preconception exposure of either parent can cause harm to children, as well as postnatal exposures. <<NOTES TO USER: It is important to point out the different responses to insults shown on the bottom bar of the figure. Significant insult during the embryonic phase will result in pregnancy loss (first 2 weeks) or major organ malformation. During the fetal stage, damage is more subtle and related to system dysfunction.>> Ref: Stromland. Autism in thalidomide embryopathy: a population study. Developmental Medicine & Child Neurology, 1994, 36:351.Of a population of 100 Swedish thalidomide embryopathy cases, at least four met full criteria for DSM-III-R autistic disorder and ICD-10 childhood autism. Thalidomide embryopathy of the kind encountered in these cases affects fetal development early in pregnancy, probably on days 20 to 24 after conception. It is argued that the possible association of thalidomide embryopathy with autism may shed some light on the issue of which neural circuitries may be involved in autism pathogenesis. Figure: Reprinted from: Moore. The developing human. Elsevier Inc., 1973. Used with copyright permission (2004) from Elsevier.
  4. Until the disasters of phocomelia caused by thalidomide and clear cell carcinoma caused by diethylstilbesterol, it was widely believed that the placenta formed an impregnable, protective barrier between the mother and the child. Now we know that this is far from true. Many pharmaceuticals cross the placenta as do many pollutants. In addition, physical environmental hazards such as radiation and heat can harm a growing fetus. The issue of environmental health of children begins with the parents, and concerns about new exposures begin in utero. Refs: Brent. Environmental causes of human congenital malformations: The pediatrician’s role in dealing with these complex clinical problems caused by a multiplicity of environmental and genetic factors. Pediatrics, 2004, 113:957. Walkowiak. Environmental exposure to polychlorinated biphenyls and quality of the home environment: effects on psychodevelopment in early childhood. Lancet, 2001, 358:1602. There is uncertainty whether environmental levels of exposure to polychlorinated biphenyls (PCBs) adversely affect mental and motor development in early childhood. We aimed to establish whether such an effect is of only prenatal or additional postnatal origin, and if a favourable home environment can counteract this effect. Methods: Between 1993 and 1995 we recruited 171 healthy mother–infant pairs and prospectively measured psychodevelopment in newborn infants aged 7, 18, 30 and 42 months. We estimated prenatal and perinatal PCB exposure of newborn babies in cord blood and maternal milk. At 42 months we measured postnatal PCB concentrations in serum. At 18 months the quality of the home environment was assessed using the Home Observation for Measurement of the Environment scale. Mental and psychomotor development of the children were assessed using the Bayley Scales of Infant Development until 30 months and the Kaufman Assessment Battery for Children at 42 months. Findings: Negative associations between milk PCB and mental/motor development were reported at all ages, becoming significant from 30 months onwards. Over 30 months, for a PCB increase from 173 (5th percentile) to 679 ng/g lipids in milk (95th percentile) there was a decrease of 8.3 points (95% CI -16.5 to 0.0) in the Bayley Scales of Infant Development mental scores, and a 9.1 point decrease (95% CI -17.2 to -1.02) in the Bayley Scales of Infant Development motor scores. There was also a negative effect of postnatal PCB exposure via breastfeeding at 42 months. Home environment had a positive effect from 30 months onwards (Bayley Scales of Infant Development mental score increase of 9.4 points [95% CI 2.2–16.7]). Interpretation: Prenatal PCB exposure at current European background levels inhibits, and a favourable home environment supports, mental and motor development until 42 months of age. PCB exposure also has an effect postnatally. EHP Image from NIEHS Webpage
  5. DDE interferes with lactation performance. DDE has association with preterm birth.
  6. This difference in size and proportion means that dermal exposures may be greater. Except for premature infants and newborns, children’s skin presents the same barrier to dermal exposures as that of adults, but there is more of it on a surface area to volume basis. Babies have a surface area to volume ratio three times that of adults and in toddlers the ratio is twice that of adults. Also, children tend to have more skin exposed and more cuts, abrasions and rashes than adults; this could easily lead to increased dermal absorption as a proportion of body weight. Refs: Reed. Principles of drugs. In: Behrman RE et al. eds. Nelson Textbook of Pediatrics, 16th ed. Philadelphia, WB Saunders Co, 2000. Image derived from information in: Selevan, Identifying critical windows of exposure for children’s health. Environ Health Perspect, 2000, 108(Suppl 3):54.
  7. <<NOTE TO USER: Insert here a regionally appropriate picture of a child doing something dangerous despite an obvious warning label. >> Children are often exposed to dangerous chemicals or situations in which injury can occur and are unable or unwilling to respond with appropriate caution because of cognitive immaturity. Adolescents are known to exhibit risk-taking behaviour even if cognitively they are aware that the behaviour is dangerous (Dr Irena Buka, Director of Paediatric Environmental Health Specialty Unit, Misericordia Children's Health Centre, personal communication). <<READ SLIDE.>>
  8. Children have a dynamic physiology that is not only turned up to “high” because of growth demands, but also vulnerable to damage during differentiation and maturation of organs and systems. Their needs for energy, water and oxygen are higher, because they go through an intense anabolic process. Absorption is different and frequently increased because children are anabolic and active. They are geared to absorb nutrients very efficiently. This is exemplified most classically by lead. Lead follows calcium, which is essential for skeletal and cellular growth. A toddler will absorb between 40 and 70% of a given ingested dose of lead, whereas a non-pregnant adult will absorb from 5–20%. Nutritional deficiencies, particularly anaemia, which is common in rapidly growing children, will increase lead absorption. Some xenobiotics are dangerous as ingested and need to be detoxified by metabolism. Others are not dangerous when ingested but become dangerous when metabolized. Whatever the type of xenobiotic, these processes are likely to be different in children, but unfortunately not in predictable ways. Particularly during gestation and in the first 6–12 months of life, important metabolic pathways such as cytochrome P450 systems and glutathione conjugation are significantly less efficient than later in life. Most known toxicants are detoxified in the body, so immaturity of these systems increases the duration of residence and amount of any given internal dose. Distribution is different from that in adults and varies with age. For example, the blood–brain barrier is not fully developed for the first 36 months of life, so substances such as lead readily cross into the CNS. Elimination may be decreased in early postnatal life. For example the glomerular filtration rate (GFR) of newborns is less that 40% of that of adults. Premature infants may have only 5% of the adult GFR. All of these physiological processes are likely to be different in children from those in adults, but unfortunately not in predictable ways. Finally, children’s systems continue to grow, mature and change through adolescence. If disrupted during critical periods, damage may be severe and lifelong. Environmental hazards may operate to harm a developmentally dynamic child by mechanisms that do not operate in the adult.
  9. Children, ideally, are around longer in the world than adults. Not only do they live longer, allowing more time in which to develop diseases with long latency, but they also have longer to live with disabilities. In addition, they inherit the world we are creating, with all its problems and promises. So these three main characteristics of children: 1) unique and different types of exposures; 2) dynamic developmental physiology; and 3) longer life expectancy represent the scientific reasons that children are not little adults with respect to environmental hazards. An important difference is that the unique issues of the timing of exposure with respect to critical windows enlarges on the old concept of toxicology captured in the phrase “the dose makes the poison” to become “the dose and the timing make the poison”. <<NOTE TO USER: This image may be replaced with one showing a regionally appropriate baby.>>
  10. The fourth characteristic category takes us into the realm of laws, policy and advocacy. Children have no political voice. They are defenceless in a world that adults have created for them and vulnerable to environmental hazards. Children do not vote. There’s a long tradition of advocacy in paediatrics with respect to abuse, neglect, toy and product safety. In the 1990s paediatricians and other professionals (especially in the Northern countries) have begun to advocate changes in laws and regulations which will specifically protect children from environmental harm. There are a variety of mechanisms either proposed or in place designed to improve children’s environmental health. They range from very local initiatives, rules and laws to international treaties and resolutions. It is critical that practitioners of children’s environmental health become and stay politically active, in all countries.
  11. <<NOTE TO USER: Mention child labour only if relevant; include relevant local data, if available; state whether the country has ratified the ILO/IPEC conventions.>> IPEC: International Programme for the Eradication of Child Labour. Some of the worst forms of environmental exposure in children occur in the context of child labour. The drawing was done by a schoolchild from Delhi, India, in connection with a WHO educational event, after being told about environmental threats and the risks of exposure (March 2002, photo from HRIDAY, provided by WHO Regional Office for South-East Asia). Ref: ILO website (International Programme for the Eradication of Child labour – IPEC): www.ilo.org/public/english/standards/ipec
  12. Liquid water is responsible for life as we know it! Viewed from space the earth appears to be mostly water, but only 2.5% of that water is fresh, and most of that lies frozen and inaccessible. As a result, less than 1% of fresh water is accessible in lakes, river channels and under ground. Geography, environment and pollution from human activities reduce this amount by a further two thirds, and what remains is unequally distributed around the world. It should be noted that access to safe water, provision of sufficient supplies of water, and access to sanitation are three factors that together can contribute to the health and safety of the world’s population. A lack of adequate supplies of good-quality water, together with poor sanitation, exacts a high health toll, particularly in rural areas, hindering both social and economic development. This makes the promotion of hygienic behaviour a high priority. Ref: Water for health – taking charge. Geneva, World Health Organization, 2001.
  13. Where is Earth's water located and in what forms does it exist? The distribution of water is illustrated in the bar charts. The left-hand bar shows where the water on Earth exists; about 97% of all water is in the oceans. The middle bar represents the 3% of the "other" part of the left-hand bar (that portion of all of Earth's water that IS NOT in the oceans). Most (77%), is locked up in glaciers and icecaps, mainly in Antarctica and Greenland, and in saline inland seas. Twenty-two per cent of this portion of the Earth's water is groundwater. The right-hand bar shows the distribution of the "other" portion of the middle bar (the remaining 1%). Notice how rivers make up less than 4/10th of one per cent of this remaining water – yet this is where we get most of the water for our everyday use! This graph and the above text are in the Public Domain and can be found at wwwga.usgs.gov/edu/waterdistribution.html
  14. Pollutants move through the water cycle and can be transported long distances. Picture: www.unep.org/vitalwater/a1.htm
  15. Picture: www.unep.org/vitalwater/a3.htm
  16. The primary public health concern regarding water contamination is microbiological contamination of drinking-water. Water-related infections can be classified into four categories: waterborne diseases: directly acquired from drinking water (contaminated); water-washed: indirectly acquired diseases due to lack of hygiene; water-based diseases: caused by aquatic organisms that spend part of their life-cycle in the water and another part as parasites of animals; and diseases transmitted by water (or humidity!)-related insect vectors (includes African trypanosomiasis (tse-tse fly) and leishmaniasis (sandfly) that require only humid environments) (Dr D. Engels, WHO, personal communication). Microbial contamination usually results from the contamination of water with human or animal faeces. If drinking-water is contaminated with faeces, pathogens are likely to be widely and rapidly dispersed. If the contamination is recent, and if the faeces are from carriers of communicable enteric diseases, the microorganisms (bacteria, viruses or protozoa) that cause these diseases may be present in the water. The diseases range from mild gastroenteritis to severe and sometimes fatal diarrhoea, dysentery, hepatitis, cholera and typhoid. Helminths and amoebae may also be transmitted in water and are common in poor-quality water supplies. There are also some organisms in the environment that may cause disease in humans in certain circumstances, e.g. Legionella may be transmitted through aerosols. Adverse health effects arise primarily from the ingestion of pathogenic bacteria. People with low immunity, including infants, young children, the sick and the elderly are particularly vulnerable to microbial contamination even from ordinarily mild pathogens. Outbreaks of waterborne disease can lead to spread of infection across a wide community. Cryptosporidium and Giardia, for instance, cause regularly diarrhoea outbreaks. They cause problems due to the following factors: cyst formation (cysts are resistant in the water environment); cysts have a small size (problems in filtration processes); no specific hosts; cysts are resistant to chlorine. In addition, risks are posed by some toxins that occur naturally in water, particularly in nutrient-rich surface waters where there is profuse algal growth. Ref: Satterthwaite. The environment for children. New York, United Nations Children’s Fund & Earthscan, 1996.
  17. Fluoride occurs naturally in soil and water, and is a by-product of industrial activities such as the aluminium and fertilizer industries. It is also added to drinking-water to help prevent dental caries. Concentrations in surface water are usually relatively low (< 0.5 mg/litre) while deeper groundwater wells in areas high in fluoride minerals may have concentrations as high as 10 mg/litre. An estimated 100 million people suffer health effects from overexposure to fluoride. A wide strip from North to South Africa, and including the Syrian Arab Republic, Jordan, Egypt, Sudan, Ethiopia, Kenya, the United Republic of Tanzania and South Africa, is known to have high concentrations of fluoride in groundwater. In one village of 2000 people, 95% of children are affected by dental fluorosis. Other effects, such as skeletal fluorosis and crippling fluorosis, are also seen in some inhabitants of this village, as in other parts of the so-called “African fluoride belt”. Fluoride is absorbed quickly following ingestion, but is not metabolized, and diffuses throughout the body. About 40% is excreted in urine within 9 hours, and 50% over 24 hours. Fluoride has an affinity for mineralizing tissues of the body – in young people the bones and teeth, and in older people the bones. As the excretion rate is greater in adults, mineralization is proportionally less than in children. The most readily identifiable health effects of consuming water with elevated levels of fluoride are a mottling of the teeth, known as fluorosis, and sclerosis of the bones. Children are particularly affected by fluorosis, because teeth take up fluoride during their formation. Fluoride has been shown to be effective in preventing dental caries, from the observed association of low incidence of dental caries with naturally occurring fluoride in drinking-water (at about 1 mg/litre). As a result, many health authorities around the world, including the World Health Organization, recommend fluoridation of public water supplies as an important public health measure. However, at concentrations above 1.5 mg/litre fluoride may affect tooth mineralization in children leading to a mottling of the teeth, which can in some cases be unsightly. The regular consumption of water with fluoride concentrations above 4 mg/litre, however, can cause progressively increasing skeletal fluorosis. Refs: Marcus. Agents affecting calcification and bone turnover. In: Hardman JG, Limbird LE. Goodman & Gillman’s The pharmacological basis of therapeutics, 9th ed. New York, McGraw-Hill, 1996. National Health and Medical Research Council. Australian drinking water guidelines and framework for management of drinking water quality (www.health.gov.au/nhmrc/publications/synopses/eh19syn.htm). Pictures: A. K. Susheela of Fluorosis Research & Rural Development Foundation of India (used with permission) Note the discoloured teeth of the children with fluorosis. Discoloration appears as brown or black streaks (lines) These have a horizontal orientation – not vertical. The discoloration is away from the gums. The discoloration is seen in the teeth in pairs and not in single teeth. The discoloration seen here is the classical depiction of dental fluorosis in children.
  18. When energy prices soared in the 1970s there was a movement to make buildings “tight” to preserve heat in winter and air conditioning in summer. The unexpected consequence, in some buildings, was an increase of indoor pollution due to inadequate ventilation. Pollutants from off-gassing from building materials together with other indoor pollutants were trapped in some structures and built up to levels that caused symptoms in sensitive individuals. "Sick building syndrome" is the name that was given to this phenomenon. Ref: Indoor Air Facts N° 4: Sick Building Syndrome. www.epa.gov/iaq/pubs/sbs.html
  19. Fire injuries can result from inhaled toxic chemicals and/or thermal burns. Smoke inhalation means breathing in the harmful gases, vapors, and particulate matter contained in smoke. Smoke inhalation impairs the body from acquiring oxygen from the environment and its ability to deliver and use oxygen at every step of respiration. Those caught in fires may suffer from smoke inhalation whether or not they present skin burns. However, the incidence of smoke inhalation increases with the percentage of total body surface area burned. The lungs and airways are affected in three ways: heat damage, tissue irritation, and oxygen starvation of tissues (asphyxiation). How to make your home safer: 1) Beware of matches and lighters around the house. Store them out of reach and sight. Teach toddlers to tell you when they find one and explain to them that these tools are only for adults. Never use them as an amusement. Children may imitate you. Practice and teach fire safe behaviours in your home: keep small children away from stoves when cooking, have your heating systems checked annually, use deep ashtrays and soak ashes in water if you are a smoker (or better: stop smoking!). Install smoke alarms Prepare a home fire escape plan. Draw a basic diagram of your house and mark all exits. Consider different fire scenarios and develop different escape plans. When escaping, crawl low under the smoke. Touch doors before opening: if they are hot, use an alternative route. Teach your children NEVER to go back inside the house Practice the fire escape plans and teach children how to cover their nose and mouth to reduce smoke inhalation. If there are babies and toddlers: keep a harness by the crib to be able to carry your baby and keep your hands free at the same time. Keep the child's bedroom closed. Ref: FEMA, A fact sheet on fire safety for babies and toddlers: usfa.fema.gov/downloads/usfaparents/508/USFA_FireFacts_508.pdf
  20. <<READ SLIDE>> The effectiveness of prevention measures against dust mite sensitization has been studied in a European multicentre randomized controlled trial. Intervention was a combination of education and mattress encasement. Of 566 preschool-aged children in the study’s first-year follow-up (mean age = 3.1 years), the incidence of sensitization to mite allergens was 10 (3%) of 330 in the intervention versus 20 (6.5%) of 306 in the control group. Likewise, in 213 school age children, 3 (2.56%) of 117 children in the intervention group and 9 (9.38%) of 96 in the control group developed sensitization to dust mite. Refs: Tsitoura. Randomized trial to prevent sensitization to mite allergens in toddlers and preschoolers by allergen reduction and education: one-year results. Arch Pediatr Adolesc Med, 2002, 156:1021. Arshad. Prevention of sensitization to house dust mite by allergen avoidance in school age children: a randomized controlled study. Clin Exp Allergy, 2002, 32:843.
  21. Infants and young children have a higher resting metabolic rate and rate of oxygen consumption per unit body weight than adults because they have a larger surface area per unit body weight and because they are growing rapidly. Therefore, their exposure to any air pollutant may be greater. In addition to an increased need for oxygen relative to their size, children have narrower airways than do adults. Thus, irritation caused by air pollution that would produce only a slight response in an adult can result in potentially significant obstruction in the airways of a young child. Ref: Moya. Children’s behavior and physiology and how it affects exposure to environmental contaminants. Pediatrics, 2004, 113:996.
  22. Indoor smoke polluting the ambient air in a small village in Nepal. Picture: Nigel Bruce/ITDG. Used with permission.
  23. <<READ SLIDE>> Girls are at most risk as they are often requested to help their mothers with household chores. Infants are exposed to pollutants when carried on the backs of their mothers as they tend fires. Irritation that would not affect adults may result in severe obstruction or damage to children’s lungs because they are more vulnerable. Ref: Environmental threats to children. In: Children in the New Millennium, Environmental Impact on Health. UNEP, UNICEF & WHO, 2002.
  24. CO is a colourless, odourless gas formed by incomplete burning of carbon-based fuels.  CO’s affinity for haemoglobin (Hb) is 240–270 times greater than that of oxygen: - it decreases the capacity of Hb for carrying oxygen. Fetal Hb has a higher affinity for CO. CO causes a leftward shift of the oxyhaemoglobin dissociation curve: - it decreases oxygen delivery to tissues. Intoxication results in tissue hypoxia. Multiple organ systems are affected: - Mainly systems with high metabolic rates; - CNS, cardiovascular system. Exposure to carbon monoxide reduces the blood's ability to carry oxygen. The chemical is odourless and some of the symptoms of exposure are similar to those of common illnesses. This is particularly dangerous because carbon monoxide's deadly effects may not be recognized until it is too late to take action. Exposure to carbon monoxide is particularly dangerous to unborn babies, infants and people with anaemia or a history of heart disease. Breathing low levels of the chemical can cause fatigue and increase chest pain in people with chronic heart disease. Breathing higher levels of carbon monoxide causes symptoms such as headaches, dizziness and weakness in healthy people. Carbon monoxide also causes sleepiness, nausea, vomiting, confusion and disorientation. At very high levels it causes loss of consciousness and death. Poisoning may have irreversible sequelae. These notes are taken from the US EPA website www.epa.gov/iaq/co.html Refs: Carbon monoxide. In: Pediatric environmental health, 2nd ed. American Academy of Pediatrics. 2003. Figure: www.cdc.gov/nceh/airpollution/carbonmonoxide/checklist.htm
  25. Incomplete oxidation during combustion in gas ranges and unvented gas or kerosene heaters may cause high concentrations of CO in indoor air. Worn or poorly adjusted and maintained combustion devices (e.g. boilers and furnaces) can be significant sources, especially if the fuel is of an unsuitable size, or if the system is blocked, or leaking. Car, truck, or bus exhaust from attached garages, nearby roads, or parking areas can also be a source. CO is one of the components of tobacco smoke. Picture: www.epa.nsw.gov.au/woodsmoke/heateruse.htm
  26. Children whose mothers smoke have an estimated 70% more respiratory problems than children whose mothers do not smoke. Pneumonia and hospitalization in the first year of life is 38% more frequent in children whose mothers smokes. Infant mortality was 80% higher in children born to women who smoked during pregnancy than in children of nonsmokers. An estimated 20% of all infant deaths could be avoided if all pregnant smokers stopped by the 16th week of gestation. Infants of mothers who smoke have an almost 5 times higher risk of sudden infant death syndrome (SIDS) than infants of mothers who do not smoke. Smoke released from cigarettes, cigars and pipes is composed of more than 3800 different substances. Airborne particulate matter is 2–3 times higher in homes of smokers. Exposure may occur at home, school, in child care settings, in relatives´ homes and other places. The importance of the need to reduce exposure to second-hand smoke justifies prohibiting smoking at home, in schools and in child care facilities. SHTS is covered extensively in a separate module. Refs: Etzel. Indoor air pollutants in homes and schools. Pediatric Clinics of North America, 2001, 48:1153. Wisborg. Exposure to tobacco smoke in utero and the risk of stillbirth and death in the first year of life. American Journal of Epidemiology, 2001, 154:322. The authors examined the association between exposure to tobacco smoke in utero and the risk of stillbirth and infant death in a cohort of 25,102 singleton children of pregnant women scheduled to deliver at Aarhus University Hospital, Aarhus, Denmark, from September 1989 to August 1996. Exposure to tobacco smoke in utero was associated with an increased risk of stillbirth (odds ratio = 2.0, 95% confidence interval: 1.4, 2.9), and infant mortality was almost doubled in children born to women who had smoked during pregnancy compared with children of nonsmokers (odds ratio = 1.8, 95% confidence interval: 1.3, 2.6). Among children of women who stopped smoking during the first trimester, stillbirth and infant mortality was comparable with that in children of women who had been nonsmokers from the beginning of pregnancy. Conclusions were not changed after adjustment in a logistic regression model for the sex of the child; parity; or maternal age, height, weight, marital status, years of education, occupational status, and alcohol and caffeine intake during pregnancy. Approximately 25% of all stillbirths and 20% of all infant deaths in a population with 30% pregnant smokers could be avoided if all pregnant smokers stopped smoking by the sixteenth week of gestation.
  27. Mosquito coils may represent a serious potential threat to children’s health. Prolonged use has been associated with increased incidences of asthma and persistent wheezing in children. Although the active ingredient is usually small amounts of pyrethrins (considered a low-toxicity insecticide), over 99% of the mass of the coil is so-called “inert” ingredients. When analysed, the smoke from coils was found to be entirely composed of respirable-sized particles, some quite small. The particles contain numerous PAH and carbonyl compounds including formaldehyde. One recent analysis found that the burning of one mosquito coil for 2 hours allowed a steady state of particulate matter to develop, and that the PM2.5 produced was the equivalent of that from burning 75–137 cigarettes (the formaldehyde produced was the equivalent of 51 cigarettes). Ref: Liu. Mosquito coil emissions and health implications. Environ Health Perspect, 2003, 111:1454. Burning mosquito coils indoors generates smoke that can control mosquitoes effectively. This practice is currently used in numerous households in Africa, Asia and South America. However, the smoke may contain pollutants of health concern. We conducted the present study to characterize the emissions from four common brands of mosquito coils from China and two common brands from Malaysia. We used mass balance equations to determine emission rates of fine particles (particulate matter < 2.5 µm in diameter; PM2.5), polycyclic aromatic hydrocarbons (PAHs), aldehydes and ketones. Having applied these measured emission rates to predict indoor concentrations under realistic room conditions, we found that pollutant concentrations resulting from burning mosquito coils could substantially exceed health-based air quality standards or guidelines. Under the same combustion conditions, the tested Malaysian mosquito coils generated more measured pollutants than did the tested Chinese mosquito coils. We also identified a large suite of volatile organic compounds, including carcinogens and suspected carcinogens, in the coil smoke. In a set of experiments conducted in a room, we examined the size distribution of particulate matter contained in the coil smoke and found that the particles were ultrafine and fine. The findings from the present study suggest that exposure to the smoke of mosquito coils similar to the tested ones can pose significant acute and chronic health risks. For example, burning one mosquito coil would release the same amount of PM2.5 mass as burning 75–137 cigarettes. The emission of formaldehyde from burning one coil can be as high as that released from burning 51 cigarettes. Picture: ehp.niehs.nih.gov/members/2003/6177/6177.html. NIEHS
  28. Radon is a radioactive gas that comes from the soil. Exposure to radon gas it the second-leading cause of lung cancer (after smoking) in the United States. About 14 000 people die each year from radon-related lung cancer. Radon is produced from the natural breakdown of thorium and uranium found in most rocks and soils. As it further breaks down, radon emits atomic particles. These particles are in the air we breathe and can be deposited in the lungs. The energy associated with these particles can alter DNA, leading to an increased risk of lung cancer. Radon does not usually present a health risk outdoors because it is diluted in the open air. Radon can, however, build up to dangerous levels inside a house. Radon can enter a new house through cracks or pores in concrete flooring and walls or through openings in the foundations, floor–wall joints or loose pipes. The differences in air pressure between the inside of a building and the soil around it also play an important role in radon entry. If the air pressure of a house is greater than that of the soil beneath it, radon will remain outside. However, if the air pressure of a house is lower than that of the surrounding soil (which is usually the case), the house will act as a vacuum, sucking radon gas inside. Because radon comes from the soil, a knowledge of the geology of an area can help to predict the potential for elevated indoor radon levels. These notes are taken from the US EPA website www.epa.gov/radon/index.html
  29. Gas-permeable layer. This layer is placed beneath the slab or flooring system to allow the soil gas to move freely underneath the house. In many cases, the material used is a 4-inch layer of clean gravel. Plastic sheeting. Plastic sheeting is placed on top of the gas-permeable layer and under the slab to help prevent the soil gas from entering the home. In crawlspaces, the sheeting is placed over the crawlspace floor. Sealing and caulking. All openings in the concrete foundation floor are sealed to reduce entry of soil gas into the home. Vent pipe. A 3- or 4-inch gas-tight or PVC pipe (commonly used for plumbing) runs from the gas permeable layer through the house to the roof to safely vent radon and other soil gases above the house. Junction box. An electrical junction box is installed in case an electric venting fan is needed later. Testing is not necessary above the second story. These notes are taken from the US EPA website www.epa.gov/iaq/radon/construc.html.
  30. A USA survey of radon levels in schools estimated that nearly one in five schools has at least one schoolroom with a short-term radon level above 4 pCi/L (picoCuries per litre) – the level at which EPA recommends that schools take action to reduce the level. EPA estimates that more than 70 000 schoolrooms in use today have high short-term radon levels. Ref: www.epa.gov/radon/pubs/schoolrn.html
  31. Asbestos is a fibrous mineral product and is classified into six types: amosite, chrysotile, crocidolite, tremolite, actinolite and anthophyllite. It is very resistant and almost indestructible and has been used widely in manufactured products and building materials. Inhalation of microscopic fibres is the major route of exposure. Fibres are liberated from deterioration, destruction or renovation of asbestos-containing materials. Asbestos produces no acute toxicity. Workers exposed to asbestos in industry may develop asbestosis. The main risk for children is the long-term exposure that may lead to cancers, such as lung cancer and malignant mesothelioma. These notes are taken from the US EPA websites www.epa.gov/iaq/asbestos.html and www.epa.gov/asbestos/ashome.html Ref: Etzel. Asbestos. In: Pediatric environmental health, 2nd ed. American Academy of Pediatrics, 2003.
  32. Lead poisoning has been a problem throughout history and possibly contributed to the fall of the Roman Empire. Lead was used as the glaze for wine jars, because it gave the wine a special sweet taste. Due to the acidity of the wine, lead leached from the jars and reached a high concentration in the wine, which was popular among aristocrats and emperors in Rome. Nriagu analysed historical testimonies on the health and behaviour of 38 Roman emperors, and concluded that about half of them had neuropsychiatric symptoms, as well as other symptoms of lead poisoning (e.g. gout). Neron Caesar and Caius Caligula are just two well-known examples. Ref: Nriagu. Saturnine gout among Roman aristocrats. Did lead poisoning contribute to the fall of the Empire? N Engl J Med, 1983, 308:660.
  33. Children are the major victims of lead poisoning. Current estimates from WHO are that about 15 to 18 million children in developing countries may suffer permanent brain damage due to lead poisoning. Ref: Prüss-Üstün. Lead exposure. In: Ezzati eds. Comparative quantification of health risks. Geneva, World Health Organization, 2004. <<READ SLIDE.>>
  34. The diagnosis of lead poisoning requires a high index of suspicion and it is confirmed by measurement of blood lead level. Plain X-Ray of the abdomen can confirm the source of recent lead paint chip ingestion. High-dose poisoning occurs in children when they ingest lead from sources such as leaded paint chips, toys or mini-blinds painted with lead paint or when they eat food from ceramic pots and jars with lead-containing glazes. <<READ SLIDE.>>
  35. <<READ SLIDE>> Basophilic stippling of red blood cells (BSC) has been noted in lead intoxication since 1899 and has been considered a classic laboratory sign of lead poisoning since that time. BSC are inclusions of aggregated ribosomes found only in the red blood cells and may be confused with siderotic (iron) granules, Heinz bodies or even reticulocytes. BSC are an inconstant finding in lead intoxication. In a review of peripheral blood smears from 1000 consecutive internal medicine patients, we found BSC in 27%. These occurred in a variety of malignant, rheumatological, haematological, cardiovascular, and other diseases, frequently with associated anaemia. BSC may even be found in a small percentage of normal people; thus, it must be emphasized that BSC is a nonspecific finding. Furthermore, BSC has been replaced by measurement of blood lead (since the 1940s) and zinc protoporphyrin (since the 1970s) levels for biological monitoring of lead-exposed workers.Ref: Cheson. Basophilic stippling of red blood cells: a non-specific finding of multiple etiology. Am J Ind Med, 1984, 5:327.
  36. <<READ SLIDE>> Lead lines are a sign of significant chronic exposure to lead. The threshold for the occurrence of “lead lines” is a BLL of about 45 μg/dL. Bone is the long-term "sink" for lead and builds up at areas of high bone metabolism during growth. This X-ray shows heavy “lead lines” at the distal part of the femur, and the proximal side of the tibia and fibula in a child.
  37. This graph demonstrates very clearly the effect of primary prevention – removal of lead from petrol in the USA closely paralleled the reduction of average blood lead levels in the American population. Ref: books.nap.edu/books/NI000651/html/103.html#p2000321cmmm00010 Institute of Medicine. Lead in the Americas: A call for action. EPA, 1996.
  38. <<NOTE TO USER: Please add details of the date, time, place and sponsorship of the meeting for which you are using this presentation in the space indicated.>>
  39. Spraying pesticides in the home results in increased risks to children because of higher concentrations near the floor and persistence of insecticides in carpets and soft toys. The typical activities of young children also contribute to their higher exposure. Pesticides are covered extensively in a separate module. Ref: Reigart. Pesticides in children. Pediatric Clinics of North America, 2001, 48:1185. Children are exposed to a wide range of pesticides, including insecticides, herbicides, fungicides and rodenticides. They differ from adults in their exposures and responses to exposures. Acute and chronic toxicity are discussed, and important chronic effects, such as carcinogenesis, endocrine disruption, and neurodevelopmental effects are reviewed. Laws and regulations are also discussed. Recommendations are made to pediatricians regarding treatment and advising families regarding avoidance of pesticide exposures and their effects.
  40. Pesticides are considered one of the main environmental threats to children’s health because: A large variety of chemicals and mixtures are used as pesticides. Many pesticides are used at the same time in the same place (agricultural regions). They are ubiquitous in the environment – and in individual environments (micro-environments) of children – there may be several sources of exposure to the same or a different chemical. Multiple exposures may occur from the preconception period throughout the child's growth into adolescence and adulthood.
  41. Fig: Norsk Barnemuseum. www.norskbarne.museum.no/html/barn100.htm Used with copyright permission.
  42. <<NOTE TO USER: Please add details of the date, time, place and sponsorship of the meeting for which you are using this presentation in the space indicated.>>
  43. The POPs are: Synthetic (man-made) organic chemicals – they are all synthetic chemicals, either intentionally or non-intentionally produced/released. Some are pesticides, others are industrial products or unintended by-products resulting from industrial processes or combustions (see next slide). Persistent in the environment – their persistence in the environment is remarkable – it may take them decennia or centuries to be degraded. Long-range transport leads to global pollution – Some POPs will almost always be found if tested for in tissues or environmental samples from different parts of the world. As is the case with many environmental pollutants, it is most difficult to establish that illness or disease are directly attributable to exposure to a specific persistent organic pollutant or to a group of POPs. This difficulty is further underscored by (a) the fact that POPs rarely occur as a single compound, and (b) that individual field studies are insufficient to provide compelling evidence of cause and effect in their own right. Lipophilic – they have a tendency to remain in fat-rich tissues. This affinity for the adipose tissues means that POPs are likely to accumulate, persist and bioconcentrate and could, eventually, achieve toxicologically relevant concentrations – even though exposure episodes may appear limited. Accumulate in food-chain – POPs enter into a cycle in nature, accumulating in the bigger animals as they eat the smaller ones. Highest levels found in marine mammals – immune dysfunction is considered as a plausible cause for increased mortality among marine mammals. It is postulated that the consumption by seals of fish contaminated with POPs may lead to vitamin and thyroid deficiencies and cause increased susceptibility to microbial infections and reproductive disorders. Acute, high-level toxicity is well characterized – acute effects after high-level exposure have been described for some of the organochlorine pesticides (e.g. aldrin, dieldrin and toxaphene). PCBs have caused well-documented episodes of mass poisoning called "Yusho" and "Yu Cheng“, that occurred in China, Province of Taiwan, and in Japan. Pregnant women exposed had no or minor symptomatology, but their children presented adverse effects and developmental disorders. Some are potential endocrine disrupters – this will be addressed later in the presentation. Ref: www.pops.int/documents/background/assessreport/en/ritteren.pdf Picture above: NOAA, NURP, Wicklund. Humpback whales cruising beneath a diver. www.photolib.noaa.gov/nurp/nur02001.htm Picture below: NOAA, Captain Budd Christman. Humpback whale. www.photolib.noaa.gov/animals/anim0800.htm
  44. These are the persistent organic pollutants – grouped according to their use and origin: 8 pesticides 2 industrial chemicals 2 unintended industrial by-products. <<READ SLIDE.>> PCBs: polychlorinated biphenyls HCB: hexachlorocyclohexane DDT: dichlorodiphenyl trichloroethane. The Stockholm Convention is a global treaty ratified by the international community and led by the United Nations Environment Programme (UNEP) that calls for the elimination and/or phasing out of 12 POPs, called the "dirty dozen". More information is available at: www.chem.unep.ch/pops/default.html
  45. Polychlorinated biphenyls (PCBs) are mixtures of chlorinated hydrocarbons that have been used extensively since 1930 in a variety of industrial uses, including as dielectrics in transformers and large capacitors, as heat exchange fluids, as paint additives, in carbonless copy paper and in plastics. There are 209 possible PCBs. PCBs in the environment may be expected to associate with the organic components of soils, sediments and biological tissues, or with dissolved organic carbon in aquatic systems, rather than being in solution in water. Association between elevated exposure to PCB mixtures and alterations in liver enzymes, hepatomegaly, and dermatological effects such as rashes and acne has been reported. Adverse effects are predominantly associated with higher blood concentrations. Contamination of rice oil by PCBs in Japan (1968) and China, Province of Taiwan (1979) has resulted in the exposure of a large number of people to PCBs and their contaminants PCDFs. Signs and symptoms of exposure from these incidents include enlargement and hyper secretion of the Meibomian glands of the eyes, swelling of the eyelids, and pigmentation of the nails and mucous membranes, occasionally associated with fatigue, nausea and vomiting. This was followed by hyperkeratosis and darkening of the skin with follicular enlargement and acneform eruptions, often with a secondary staphylococcal infection. Children born up to 7 years after maternal exposure in the Taiwan incident had hyperpigmentation, deformed nails and natal teeth, intrauterine growth delay, poorer cognitive development up to 7 years of age, behavioural problems and higher activity levels. The affected children appeared to "catch up" with controls at 12 years of age. Children born 7–12 years after maternal exposure experienced mildly delayed development, but no differences in behaviour. Effects observed in these children are probably a result of the persistence of PCBs in the human body, resulting in prenatal exposure long after the exposure took place. These effects are consistent with the observations of poorer short-term memory functioning in early childhood, in children exposed prenatally by mothers who had high consumption of Lake Michigan sports fish containing PCBs, amongst other POPs. People exposed in the Yucheng incident had low resistance, and suffered from a variety of infections. Examination during the first year revealed decreased concentrations of IgM and IgA, decreased percentages of total T-cells, active T-cells and helper T-cells, but normal percentages of B-cells and suppressor T-cells; suppression of delayed type response to recalling antigens; enhancement of spontaneous proliferation of lymphocytes and an enhancement in lymphoproliferation to certain mitogens. After 3 years, some, although not all, of the effects had disappeared. Cancer deaths in both male and female workers involved in the manufacture of electrical capacitors were significantly increased. A significant increase in haematological neoplasms and gastrointestinal cancers was observed in male workers. The persistence of PCBs, combined with the high partition coefficients of various isomers (log KOW ranging from 4.3 to 8.26) provide the necessary conditions for PCBs to bioaccumulate in organisms. Concentration factors in fish exposed to PCBs in their diet were lower than those for fish exposed to PCBs in water, suggesting that PCBs are bioconcentrated (taken up directly from the water) as opposed to being bioaccumulated (taken up by water and in food). The main source of PCB exposure to the general population is through food, especially fish. Hexachlorobenzene (HCB) is a fungicide that was first introduced in 1945 for seed treatment, especially for control of bunt of wheat. HCB is also a byproduct of the manufacture of industrial chemicals including carbon tetrachloride, perchlorethylene, trichloroethylene and pentachlorbenzene. It is quite volatile and can be expected to partition into the atmosphere as a result. It is known to bioconcentrate in the fat of living organisms as a result. The most notable episode involving the effects of HCB on humans involved the ingestion of HCB-treated seed grain in eastern Turkey between 1954 and 1959. The patients who ingested the treated seed experienced a range of symptoms including photosensitive skin lesions, hyperpigmentation, hirsutism, colic, severe weakness, porphyrinuria, and debilitation. Approximately 3000–4000 people developed porphyria turcica, a disorder of haem biosynthesis. Mortality was up to 14%. Mothers who ingested the seeds passed the HCB to their children by placental transfer and through maternal milk. Children born to these women developed "pembe yara" or pink sore, with a reported mortality rate of approximately 95%. A study of 32 individuals 20 years after the outbreak showed that porphyria can persist years after the ingestion of HCB. HCB is very persistent. This persistence, combined with a high partition coefficient (log KOW = 3.03–6.42), provides the necessary conditions for HCB to bioconcentrate in organisms. The chemical properties of HCB favour its long-range transport, and HCB has been detected in arctic air, water and organisms. HCB is ubiquitous in the environment, and has been measured in foods of all types. HCB was one of two organochlorines detected in all samples of Spanish meat and meat products. These chemicals are banned and restricted in many countries, please see UNEP website for more information. Notes and pictures taken from UNEP website: www.chem.unep.ch/pops/alts02.html <<NOTE TO USER: PCBs will be addressed more in detail further on in the module.>>
  46. Two important mass-poisoning episodes have occurred: one in Japan ("Yusho") and one in China, Province of Taiwan ("Yu-Cheng"). The main symptoms in Yusho and Yu-Cheng patients have frequently been attributed to contaminants in PCB mixtures, specifically, to PCDFs. Expert groups concluded that the symptoms may have been caused by the combined exposure to PCBs and PCDFs. However, some of the symptoms, principally, the chronic respiratory effects, may have been caused specifically by the methylsulfone metabolites of certain PCB congeners. The signs of intoxication in Yusho and Yu-Cheng patients included: eye irritation and lacrimation, swelling of the eyelids, hyperpigmentation of the nails and mucous membranes, occasionally associated with fatigue, nausea and vomiting. This was usually followed by hyperkeratosis and darkening of the skin with follicular enlargement and acneiform eruptions. Furthermore, oedema of the arms and legs, liver enlargement and liver disorders, central nervous system disturbances, respiratory problems (e.g. bronchitis-like) and changes in the immune status of the patients were also reported. Children of Yusho and Yu-Cheng patients presented: reduced growth, dark pigmentation of the skin and mucous membranes, gingival hyperplasia, xerophthalmia, oedematous eyes, dentition at birth, abnormal calcification of the skull, rocker bottom heel. A high incidence of low birth weight was reported. Infants born to women who had been exposed to PCBs exhibited numerous effects, including  neurobehavioural deficits and lower overall age-adjusted developmental scores among the exposed children.  The link between exposure and the occurrence of malignant neoplasms in these patients could not be definitely established, because the number of deaths was too small. However, a statistically significant increase in liver and lung cancer was observed in male patients, in the context of mortality due to all types of neoplasms (Kuratsune, 1986). Refs: www.atsdr.cdc.gov/DT/pcb007.html Kuratsune. Analysis of deaths seen among patients with Yusho, (Abstract FL17), In: Dioxin 86, Proceedings of the VI International Symposium on Chlorinated Dioxins and Related Compounds, Fukuoka, Japan. 1986, p.179.
  47. As with many POPs, the main source of human exposure is dietary. Over the years, thousands of different food samples have been analysed, in several countries, for contaminants, including PCBs. Most samples have been from fish, meat and milk. Food becomes contaminated with PCBs through three main routes: a) uptake from the environment by fish, birds, livestock (via food-chain), and also into crops; b) migration from packaging materials into food (around 1 mg/kg, but in some cases up to 10 mg/kg); c) direct contamination of foodstuff or animal feed as the result of an industrial accident or incident. The levels of PCBs found in different foodstuff are: animal fat: 20 to 240 µg/kg; cow's milk: 5 to 200 µg/kg; butter: 30 to 80 µg/kg; fish: 10 to 500 µg/kg, on a fat basis. Certain fish species (eel) and fish products (fish liver and fish oils) may contain much higher levels, up to 10 mg PCBs/kg; vegetables, cereals, fruits, and a number of other products: <10 µg/kg. Main causes of concern regarding PCBs are: large fish, shellfish, marine mammals, meat, milk, and other dairy products. The median levels reported in fish, in various countries, are of the order of 100 µg/kg (on a fat basis). However, it seems that the levels of PCBs in fish are slowly decreasing. Refs: INCHEM. Environmental Health Criteria 140, Polychlorinated Biphenyls and Terphenyls (Second Edition). Geneva, World Health Organization, 1993 www.inchem.org/documents/ehc/ehc/ehc140.htm Pictures: WHO.
  48. <<NOTE TO USER: These are not POPs but it is foreseen that they will be included in further conventions or expanded international agreements.>> In addition to POPs, other chemicals are characterized by their persistence in the environment. They are called persistent toxic substances (PTSs) and may pose a serious threat to humans and the environment. They can remain in the environment for a long time and be transported long distances, far away from their site of origin. They can accumulate in organisms and enter the food-chain. Their levels in food may be of concern to human health. They are not "POPs" as they are not listed in the Stockholm Convention. However, there is growing concern that these chemicals, which are somehow similar to the 12 listed in the UNEP convention, may harm the environment, and through the environment, endanger human health. The list of PTS has not been defined, but could include, for example: mercury, cadmium, lead, the polybrominated diphenyl ethers (PBDE-flame retardants).
  49. A growing number of chemicals are now recognized as persistent or semi-persistent in the environment – they are found in sewage and may originate from waste or traffic, among other sources. There is no general agreement on the terminology to be used for these substances, but in the future they may be included under the PTS. The list includes, for example: PAHs – polycyclic aromatic hydrocarbons. The high-molecular-weight molecules originate mainly from vehicle exhaust, and the lower-molecular-weight PAHs from low-temperature combustion, from fossil fuels (e.g. diesel), and spillage from ships and boats (Mai, 2003). Phthalate esters – used as plasticizers in polyvinyl chloride (PVC) products to make them soft. In 1999, the EU placed bans on these phthalates in toys and child care articles. The main phthalates are: DEHP, DBP, BBP, DINP, DIDP and DNOP (Hileman, 2004). PBDEs – polybrominated diphenyl ethers. PCNs – polychlorinated naphthalenes. BPA (bisphenol A) – high-volume production chemical used in the synthesis of polycarbonates and epoxy resins found in plastic bottles and in the lining of food cans. Small amounts may migrate into food. Reports suggest it may be estrogenic in animals and may have effects on the thyroid. (Kamrin, 2004, Zoeller, 2004). Alkyl phenols – widely used in industrial and domestic detergents as a surfactant, also used as an antioxidant for polymer resin, wall and floor coverings. They are found in sewage wastewater and also in the indoor air of newly built houses. Refs: Hileman. Toys in phtalates. Chemical and Engineering News, 2004, 82 (40). Kamrin. Bisphenol a: a scientific evaluation. Med Gen Med, 2004, 6:7. Mai. Distribution of polycyclic aromatic hydrocarbons in the coastal region off Macao, China: assessment of input sources and transport pathways using compositional analysis. Environ Sci Technol, 2003, 37:4855. Zoeller. Bisphenol-A, an environmental contaminant that acts as a thyroid hormone receptor antagonist in vitro, increases serum thyroxine and alters RC3/neurogranin expression in the developing rat brain. Endocrinology, 2005, 146:607. Picture: L. Corra and R. Ceppi. Argentina.
  50. At present, the only persistent effect associated with dioxin exposure in humans is chloracne. Other health effects that have been reported include peripheral neuropathies, fatigue, depression, personality changes, hepatitis, enlarged liver, abnormal enzyme levels and porphyria cutanea tarda though causal relationships were not established in every case. Results of a study on 1520 workers known to have been exposed to 2,3,7,8-TCDD for a period of at least 1 year, and with a latency of at least 20 years between exposure and diagnosis of disease, revealed a slightly, but significantly elevated mortality from soft tissue sarcoma and cancers of the respiratory system. As with other studies, interpretation of results was limited by the small number of deaths and by possible confounders including smoking and other occupational exposures. Two recent studies followed a young population from the area of Seveso, Italy following an industrial accident. The first, a cancer study, examined a cohort of people aged 0–19 years living in the area at the time of the accident, for the period 1977–1986. Wheras a consistent tendency toward increased risk was apparent, none of the relative risks were significantly elevated. Non-significant increases in thyroid cancer and myeloid leukaemia were also observed. The study is limited, however, by the relatively short latency periods, the definition of exposure based on place of residence and the limited number of events. The second study examined the mortality of the same cohort of people for the same time period. Among those exposed, mortality owing to all causes did not deviate from expectations, however, as noted above, this study provides only limited evidence. In animals, effects of dioxin exposure that are common to most, and sometimes all, species include wasting, lymphoid involution, hepatotoxicity, chloracne and epidermal changes, and gastric lesions. Other characteristic responses include oedema and ascites in chickens; fetal death and resorption in rats and fetal wastage, embryotoxicity and malformations in mice. Dioxins are associated with a variety of adverse effects on the reproductive systems of both male and female rats. Male reproductive toxicity has included altered regulation of luteinizing hormone secretion, reduced testicular steroidogenesis, reduced plasma androgen concentrations, reduced testis and accessory sex organ weights, abnormal testis morphology, decreased spermatogenesis, and reduced fertility. Signs of female reproductive toxicity included hormonal irregularities in the estrous cycle, reduced litter size and reduced fertility. IARC has concluded that while there is inadequate evidence for the carcinogenicity of 2,3,7,8-TCDD in humans, there is sufficient evidence in experimental animals. IARC has classified 2,3,7,8-TCDD as a possible human carcinogen (Group 2B). As with most other organochlorines, food is a major source of dioxins and furans in the general population, with food of animal origin contributing the most to human body burdens. Notes taken from UNEP website: www.chem.unep.ch/pops/alts02.html <<NOTE TO USER: A reminder of IARC (International Agency for Research on Cancer) standard group classification: 1: "Carcinogenic to humans": there is enough evidence to conclude that it can cause cancer in humans. 2A: "Probably carcinogenic to humans": there is strong evidence that it can cause cancer in humans, but at present it is not conclusive. 2B: "Possibly carcinogenic to humans": there is some evidence that it can cause cancer in humans but at present it is far from conclusive. 3: "Unclassifiable as to carcinogenicity in humans": there is no evidence at present that it causes cancer in humans. 4: "Probably not carcinogenic to humans": there is strong evidence that it does not cause cancer in humans.>>
  51. <<READ SLIDE>> Endocrine disrupting chemicals (EDCs) were defined by the EDC-IPCS Working Group as: “exogenous substance or mixture that alters the function(s) of the hormonal system and consequently causes adverse effects in an intact organism, or its progeny or its subpopulation”. The substances may be of natural or synthetic origin. An example of EDCs of natural origin is the "phytoestrogens“ present in plants. The synthetic ones include some pesticides, industrial by-products, chemicals used in plastics, pharmaceuticals that enter the natural environment, and persistent organic pollutants (POPs) (addressed in the next slides). The potential effects are FUNCTIONAL and not a toxic end-point. These functional changes may or may not lead to an adverse event. It is difficult to distinguish between the direct and indirect effects and to distinguish the primary from the secondary effects. The effects are complex as they result from multiple mechanisms of action on a hormonal system with close interconnections and "cross-talk".
  52. Prevention of exposure through cleaner, safer and healthier environments – free of persistent organic and other pollutants – is the single most effective means of protecting children against environmental threats. Education about the environment and human health will enable our children to become informed individuals, contributing members in their own societies and promoters of sustainable development.
  53. The PEH is a set of basic and concise questions, part of the standard medical history, a tool and a mechanism for interaction that covers: – general issues that are similar throughout the world (e.g. access to safe drinking-water and sanitation; waste disposal and quality of the air); – specific issues, that depend on the local situation (e.g. pesticide use in agricultural areas and local traditional medicines and practices); and – age- and gender-related issues (different questions are used when addressing the behaviour, diet or activities of toddlers or adolescents, or of boys or girls). The questions should be adapted to suit the local situation, needs and capacities of: – industrialized countries where there is concern about heavy traffic, injuries, noise, food additives and diet; where physicians and nurses see the children and may ask the questions; and there are good mechanisms for recording case data (using electronic clinical records). – developing regions where there are concerns about other risk factors such as unsafe water, lack of sanitation, misuse of pesticides and unsafe buildings. Physicians and nurses may not be available and primary health care workers should take the PEH – which may have to be recorded very succinctly on paper or in a notebook. Picture: WHO
  54. << READ SLIDE.>> The photo illustrates a typical situation in rural and suburban areas, where children play in creeks, and are exposed to chemical contaminants, to vectors of disease and to the risk of drowning. Picture: WHO
  55. The GREEN PAGE is presented as an example of a concise PEH – where just a core set of basic details is recorded. This format is being tested by WHO/PAHO with health care providers in a small health care centre in Argentina (2003). The data collection form is GREEN, to make it clearly visible within the clinical records (which are still kept in paper form in most primary health care centres). The GREEN PAGE has about 50 fields for recording information about the child, his or her built and ambient environments, the characteristics of the community and other data. It also allows a basic assessment to be made of the state of the child's environment (the "ABC" of environmental risks).
  56. Example of the detailed questions on HOUSING that may be asked while taking the PEH. Many more questions may need to be asked and the answers recorded. These represent a few examples. << READ SLIDE.>> << NOTE TO USER: give examples of questions that are applicable to the country or local community.>>
  57. Example of the detailed questions on ACTIVITIES that may be asked by those in charge of collecting environmental information at the health care centre, while taking the PEH. << READ SLIDE.>> << NOTE TO USER: give examples of questions that are applicable to the country or local community.>> Pictures: WHO
  58. Example of the detailed questions on BEHAVIOURS AND HABITS that may be asked while taking the PEH. << READ SLIDE.>> << NOTE TO USER: state examples of questions that are applicable to the country or local community.>> Pictures: WHO
  59. Another example: the Case Studies in Environmental Medicine series of the Agency for Toxic Substances and Disease Registry devoted to PEDIATRIC ENVIRONMENTAL HEALTH, which presents interesting case-studies (on mercury and lead) and provides a summary of questions for an environmental history. This ATDSR document focuses not so much on the history to be taken at the clinician's office, but rather on the details of an exposure history.