...

Indoor_Air_Pollution-WHO.pdf

by user

on
Category: Documents
6

views

Report

Comments

Transcript

Indoor_Air_Pollution-WHO.pdf
TRAINING FOR THE HEALTH SECTOR
[Date …Place …Event…
Event…Sponsor…
Sponsor…Organizer]
INDOOR AIR POLLUTION
Children's Health and the Environment
WHO Training Package for the Health Sector
World Health Organization
www.who.int/ceh
July 2008 version
1
<<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.>>
<<NOTE TO USER: This is a large set of slides from which the presenter should
select the most relevant ones to use in a specific presentation. These slides cover
many facets of the problem. A number of slides refer to the specific issues related to
indoor air pollution in developing countries, as it represents a major determinant of
the burden of disease in children. Present only those slides that apply most directly
to the local situation in the region.>>
Indoor Air Pollution
LEARNING OBJECTIVES
TO UNDERSTAND, RECOGNIZE AND KNOW:
Hazards of indoor air pollution to children’s health
Different toxicants in indoor air, according to sources, settings
and activities
Characteristics and issues relating to indoor air pollution in
industrialized and developing countries
How to recognize, assess and address health effects
How to prevent exposure to indoor air contaminants
2
<<READ SLIDE>>
Indoor Air Pollution
OUTLINE
Scope of the problem of indoor air pollution
Particulate matter
Carbon monoxide
Secondhand tobacco smoke
Pesticides
Solvents
Volatile organic compounds
Biological pollutants
- Mites
- Allergens
- Moulds
Built environment
Radon
Asbestos
OccupationOccupation-related contaminants
<<READ SLIDE>>
<<NOTE TO USER: When selecting the slides to include in your presentation, please choose
only those of relevance to the region/country and/or the interests of your audience.>>
The indoor contaminants addressed in this module include:
•Particulate matter
•Carbon monoxide
•Secondhand tobacco smoke
•Pesticides
•Solvents
•Volatile organic compounds
•Biological pollutants
- Mites
- Allergens
- Moulds
•Built environment
•Radon
•Asbestos
•Occupation-related contaminants
3
Indoor Air Pollution
CHILDREN’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
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 J et al. Children’s behavior and physiology and how it affects exposure to
environmental contaminants. Pediatrics, 2004, 113:996.
•American Academy of Pediatrics Committee on Environmental Health. Pediatric
Environmental Health, 2nd ed. Etzel RA, Ed. Elk Grove Village, IL: American Academy of
Pediatrics, 2003.
•Children's Health and the Environment – A global perspective. A resource guide for the
health sector, WHO, 2005.
4
Indoor Air Pollution
SMALLER AIRWAYS MORE VULNERABLE
www.vh.org/pediatric/provider/pediatrics/ElectricAirway/Diagrams/AirwayDIaneterEdema.jpg
5
The effect of oedema on the adult airway is much less dramatic than it is on the newborn’s
airway. One millimetre of oedema reduces the diameter of the adult airway by about 19%
whereas it reduces the diameter of the infant airway by 56%.
Compared to that of adults, the peripheral airway (bronchioles) is both relatively and
absolutely smaller in infancy allowing intralumenal debris to cause proportionately greater
obstruction. In addition, infants have relatively larger mucous glands, with a concomitant
increase in secretions. They also have the potential for increased oedema because their
airway mucosa is less tightly adherent. Lastly, there are fewer interalveolar pores (Kohn’s
pores) in the infant, producing a negative effect on collateral ventilation and increasing the
likelihood of hyperinflation or atelectasis.
The resting minute ventilation normalized for body weight in a newborn infant (400
cc/min/kg) is more than double that of an adult (150 cc/min/kg).
Ref:
•Bar-on ME et al. Bronchiolitis. Prim Care, 1996, 23:805-19.
Picture:
www.vh.org/pediatric/provider/pediatrics/ElectricAirway/Diagrams/AirwayDIaneterEdema.jpg
- Copyright protected material used with permission of the authors: Drs. Michael and Donna
D'Alessandro - and the University of Iowa's Virtual Hospital, www.vh.org
Indoor Air Pollution
DEPOSITION OF POLLUTANTS IN RESPIRATORY TRACT
CDC
6
Respirable particles and gases affect different parts of the respiratory tree depending upon
their inherent characteristics. For gases, relative solubility is important. For particles, size is
important.
This slide shows the upper, middle and lower respiratory tract. Note that sulfur dioxide,
because it is highly water soluble, initially affects the upper airway, whereas ozone, which
has medium solubility, initially affects the middle airways, and nitrogen dioxide, which has
low solubility, initially affects the lower airways.
Indoor Air Pollution
SIZE MATTERS
Coarse particles (2.5–10
micrometres) deposited in
the upper respiratory tract
and large airways
Fine particles (< 2.5
micrometres) may reach
terminal bronchioles and
alveoli
7
Particle size is the most important factor in determining where particles are deposited in the
lung.
Compared with large particles, fine particles can remain suspended in the atmosphere for
longer periods and be transported over longer distances.
Some studies suggest that fine particles have stronger respiratory effects in children than
large particles.
This diagram shows that particles greater than 10 micrometres rarely make it past the upper
airways, whereas fine particles smaller than 2 micrometres can make it as far as the alveoli.
Ref:
•World Health Organization. Air Quality Guidelines. Geneva, World Health Organization:
Department of Protection of the Human Environment, 2005.
Indoor Air Pollution
RESPIRATORY DEVELOPMENT:
CONTINUES THROUGH LINEAR GROWTH
Growth/structure
• Second-hand
tobacco smoke
• Particulates
• Ozone
10 X 106 Alveoli
300 X 106 Alveoli Function
• Indoor air quality
(age 8)
• Ambient ozone
2 to 8
Dieter,t 2000
8
Like the nervous system, the respiratory system continues to grow and develop through
linear growth. The upper section of the diagram depicts the different developmental phases
of the lungs corresponding to the age of the embryo/fetus. It may be seen that at birth, a
baby has about 10 million alveoli, but at age 8 years, the lungs have grown and the number
of alveoli has reached 300 million. Exposures during this growth period are known to have
adverse consequences on both structure (growth of the lungs, as illustrated in the diagram)
and function (which is affected by indoor air quality and ozone exposure).
Figure: Dietert RR et al. Workshop to identify critical windows of exposure for children's
health: immune and respiratory systems – work group summary. Environmental Health
Perspectives, 2000, 108:483-90. Reproduced with permission from Environmental Health
Perspectives
Indoor Air Pollution
Attributable burden of disease 0–4 years
Illicit drugs
Alcohol
Ambient air pollution
Unsafe health care injections
Climate change
Lead exposure
Unsafe sex
Iron deficiency
Vitamin A deficiency
Zinc deficiency
Indoor smoke from solid fuels
Unsafe water, sanitation and hygiene
Underweight
0
20000
40000
60000
80000 100000 120000 140000 160000
1000 DALY
World Health Report 2002
9
In analyses by the World Health Organization (WHO) in 2002, the indoor smoke from solid
fuels accounted for the third highest disability-adjusted life years (DALYs) for children 0 to 4
years of age.
The DALY is a health measure that incorporates loss of quality of life as well as loss of years
of life. One DALY is the loss of one healthy life year.
Ref:
•World Health Report 2002 (www.who.int/whr/2002/en/).
Picture: World Health Report 2002
Indoor Air Pollution
CHILDREN’
CHILDREN’S INDOOR EXPOSURE
Level of economic development is a key factor
Developing and industrialized countries
Rural and urban areas
Local climate
Architecture/ventilation
In urban areas, children
may spend most of their time indoors.
WHO
Most exposure to air contaminants occurs
inside homes and schools.
10
<<READ SLIDE>>
The level of economic development is a key factor in determining children’s exposures and
the potential for responding to or improving their environment.
The level of social and economic development is linked closely to determinants of indoor air
pollution (IAP).
There are major differences between developing and industrialized countries: IAP results
from solid fuel use in the former, and from "chemicals" and "new substances" (e.g.
formaldehyde, insecticides and phthalates) in the latter. However, secondhand tobacco
smoke is a pollutant common to both settings.
IAP also differs between rural and urban areas due to the different economies and lifestyles.
For example, dust and organic particles are more common in agricultural areas and mites or
fungal contaminants in closed, unventilated urban dwellings.
The local climate conditions should also be taken into consideration, as they have an impact
on architecture (building materials used, structure, room distribution and characteristics) and
– particularly – on the ventilation of the dwelling.
Children in urban areas spend most of their time indoors, which means that their primary
exposure to air pollution may come from air inside homes and schools rather than outdoors.
There are numerous situations in homes and schools which may result in possible exposure
to contaminants, such as second-hand tobacco smoke, spraying of insecticides,
accumulation of pollutants in carpets, poor quality air and others. Children may also be
exposed where they play or at workplaces. The quality of children’s environments can cause
or prevent illness, disability and injury.
Picture: WHO.
Indoor Air Pollution
INDOOR AIR QUALITY
Indoor air quality is influenced by:
Outdoor air pollution: vehicles and industrial plants
Secondhand tobacco smoke
Fuels used for heating and cooking
Confined and poorly ventilated spaces
Overcrowded homes and insufficient living space
Customs, habits, traditions
Level of economic development:
Industrialized ≠ developing countries
11
Indoor air quality is influenced by concentrations of outdoor air pollutants, indoor sources of
pollution, characteristics of the building and the habits of the residents.
Indoor air pollution may arise from the use of open fires, unsafe fuels or combustion of
biomass fuels, coal and kerosene. Gas stoves or badly installed wood-burning units with
poor ventilation and maintenance can increase the indoor levels of carbon monoxide,
nitrogen dioxide and particles.
Other pollutants not associated with fuel combustion include building materials such as
asbestos and cement, wood preservatives and others.
Volatile organic compounds may be released by various sources including paints, glues,
resins, polishing materials, perfumes, spray propellants and cleaning agents. Formaldehyde
is a component of some household products and can irritate the eyes, nose and airways.
Indoor Air Pollution
HOMES OF POOR CHILDREN MAY BE UNHEALTHY
2 000 000 deaths from ARI in
< 5 yr olds (½ due to solid fuel
use)
Rising trends of “wheezing”
WHO
Coal and biomass fuel: a major source of indoor air pollution
Suspended particulate matter increases the risk of acute respiratory infections
CO and other toxic gases may impair development and health
Secondhand tobacco smoke a major concern
12
The home is the first indoor environment a child will know. It should be a safe and healthy
place. But the homes of poor children may be unhealthy places.
ARI = acute respiratory illness
CO = carbon monoxide
<<READ SLIDE.>>
Picture: WHO, C. Gaggero. Child housework, Costa Rica.
Indoor Air Pollution
ADVERSE HEALTH EFFECTS OF AIR POLLUTANTS
Acute:
Irritation of the mucous membranes (eyes, nose, throat)
Cough, wheeze, chest tightness
Increased airway responsiveness to allergens
Increased incidence of acute respiratory illness:
"cold", pneumonia, otitis media
Tracheobronchitis
Exacerbation of asthma
13
<<READ SLIDE.>>
Indoor Air Pollution
ADVERSE HEALTH EFFECTS OF AIR POLLUTANTS
Chronic:
Long-term exposure decreases lung growth
Impairment of pulmonary function
Increased susceptibility to chronic obstructive lung
diseases, including asthma
Other
14
<<READ SLIDE.>>
Indoor Air Pollution
ENVIRONMENT AND POLLUTION
Indoor environments also reflect outdoor air quality
Industrial or agricultural activities
Treatment of industrial effluents and domestic residues
Traffic
Solid waste management
Cottage industries
Chemical incidents and spills
WHO
15
The indoor environment also reflects outdoor air quality and pollution. Outdoor pollution
primarily results from the combustion of fossil fuels by industrial plants and vehicles. This
releases carbon monoxide, sulfur dioxide, particulate matter, nitrogen oxides, hydrocarbons
and other pollutants. The characteristics of emissions and solid waste disposal may vary for
each specific industry (e.g. smelting, paper production, refining and others).
Picture: WHO, J. Vizcarra. Environmental Air Pollution
Indoor Air Pollution
INDOOR AIR POLLUTION ALSO AFFECTS OUTDOOR AIR
QUALITY
Nigel Bruce/ITDG
Indoor smoke polluting the ambient air in a small village in Nepal.
Picture: Nigel Bruce/ITDG. Used with permission.
16
Indoor Air Pollution
COMBUSTION PRODUCTS
Sources
Combustion products
Gas stoves and appliances
Wood and coal stoves
Gas and propane engines
Fireplaces
Tobacco smoke
Candles and incense
Mosquito coils
Carbon monoxide (CO)
Nitrogen dioxide (NO2)
Sulfur dioxide (SO2)
Nitrogenated compounds (NOx)
Particulate matter (PM)
17
A large number of combustion products originate from various different sources. The main
ones are listed here.
<<READ SLIDE.>>
Indoor Air Pollution
SMOKY COOKING FUELS
Open fire cooking stoves produce heavy smoke containing:
Fine particles
Carbon monoxide (CO)
Polycyclic aromatic hydrocarbons (PAHs)
Strongly linked to pneumonia
Suggested link to low birth weight
In adults: chronic obstructive
pulmonary disease, lung cancer
WHO
18
<<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.
•Smith KR et al. Chapter 18: Indoor smoke from household use of solid fuels. In: Ezzati Eds.
Comparative quantification of health risks: The global burden of disease due to selected risk
factors, Vol 2. Geneva: World Health Organization, 2004.
Indoor Air Pollution
HOUSEHOLD ENERGY, IAP AND HEALTH
3 billion people rely on solid fuels
Solid fuels comprise 10--15% of the
total fuels used worldwide
Dung
Wood
Agricultural
residues
Charcoal
Coal
Cooking and heating
levels indoor air pollution
Most concern: particulate matter and
carbon monoxide
Women and children heavily exposed
Nigel Bruce/ITDG
19
Some 3 billion people (half of the world’s population!) rely on solid fuels (e.g. dung, wood,
agricultural residues, charcoal, coal) for their basic energy needs.
Cooking and heating with solid fuels leads to high levels of indoor air pollution (IAP), a
complex mix of health-damaging pollutants (e.g. particulate matter and carbon monoxide).
Women and young children, who spend most time at home, experience the largest
exposures and health burdens.
IAP = indoor air pollution
Picture: Nigel Bruce/ITDG. Used with permission.
Indoor Air Pollution
INDOOR AIR POLLUTION LEVELS ARE VERY HIGH
Level of particulates in home
using biofuel: >1000 µg/m3
(24 hr mean)
Can reach 10 000 µg/m3 PM10 (if
using an open fire)
EPA: 50 µg/m3 PM10 annual mean
Women and young children have
greatest exposure
Nigel Bruce/ITDG
20
Standards and guidelines
US EPA standards are illustrated here. 150 µg/m3 PM10 is the 24-hour 99% percentile value, thus it
should be exceeded only on 1% of occasions. The recommended annual mean limit is 50 µg/m3 PM10
(PM10 are respirable particles ≤ 10 micrometre (µm) in diameter).
Levels of pollution in homes using biomass fuel
Numerous studies have shown that the levels of particulates are very high, with 24-hour means of around
1000 µg/m3 PM10, and even exceeding 10 000 µg/m3 PM10 when sampling is carried out during use of an
open fire. It is reasonable to compare the EPA recommended annual mean limit of 50 µg/m3 PM10 with
the typical 24-hour mean for a home in which biomass fuel is used, of 1000 µg/m3 PM10 quoted, as this
latter value is typical of the level every day (thus, annual mean levels can be expected to be around 1000
µg/m3 PM10). This comparison shows that average pollution levels are around 20 times the EPA
recommended limit.
Ambient pollution and personal exposure
Two important components are (a) the level in the home, and (b) the length of time for which each person
in the home is exposed to that level. We know that typically women and young children (until they can
walk), and girls (as they learn kitchen skills) are often exposed for at least 3–5 hours a day, often more. In
some communities, and where it is cold, exposure will be for a much longer period each day.
Ref:
•Addressing the links between indoor air pollution, household energy and human health. Based on the
WHO-USAID Consultation on the Health Impact of Household Energy in Developing Countries (Meeting
report).Geneva, World Health Organization, 2002.
Additional information can be found at: www.who.int/indoorair/publications/en/
Picture: Courtesy of Nigel Bruce/ITDG. Used with permission.
Indoor Air Pollution
Gordon, WHO, 2004
21
Cooking is central to our lives, yet the very act of cooking is a threat to children’s health and
well-being. Half of the world’s population relies on solid fuels, such as dung, wood, crop
waste or coal to meet their most basic energy needs. In most developing countries, these
fuels are burned in open fires or rudimentary stoves that give off black smoke. Children,
often carried on their mother’s back during cooking, are most exposed. The indoor smoke
inhaled leads to pneumonia and other respiratory infections – the biggest killer of children
under 5 years of age. Indoor air pollution is responsible for nearly half of the more than 2
million deaths each year that are caused by acute respiratory infections. Good ventilation
and improved cooking stoves can dramatically reduce children’s exposure to smoke.
Ultimately, making the transition to gas and electricity will save lives and reduce the physical
toll on women and children from gathering wood, freeing time for education and
development. This problem has been largely ignored by policy-makers.
Ref:
•Gordon B et al. Inheriting the world, the Atlas on Children's Health and the Environment.
Geneva, World Health Organization, 2004
Indoor Air Pollution
AGE DISTRIBUTION OF GLOBAL BURDEN OF DISEASE
ATTRIBUTABLE TO SOLID FUEL USE
Age
g ro u p
( y rs )
0–4
5–14
15–59
60+
A ttr ib u ta b le
m o r ta lity
A ttrib u ta b le
D ALYs
56
0
5
38
83
0
8
9
Young children at high risk due to:
Lung immaturity
High exposure to IAP: nearly 1 million
children under 5 yrs die every year due to
solid fuel use!
WHO
22
DALY = disability-adjusted life year. The DALY is a health measure that incorporates loss of
quality of life as well as loss of years of life. One DALY is the loss of one healthy life year.
IAP = indoor air pollution
Ref:
•The health effects of indoor air pollution exposure in developing countries. Concise
summary of the evidence for health effects of exposure to indoor air pollution from solid fuel
use in children and adults. Geneva, World Health Organization, 2002.
•Indoor air pollution: national burden of disease estimates. Geneva, World Health
Organization, 2007.
•Fuel for life: household energy and health. Geneva, World Health Organization, 2006.
•Indoor air pollution from solid fuels and risk of low birthweight and stillbirth. Geneva, World
Health Organization, 2007.
•Indoor air pollution and respiratory tract infections in children. Geneva, World Health
Organization, 2007.
Additional information on these references can be found at:
www.who.int/indoorair/publications/en/
Picture: WHO. Americas.
Indoor Air Pollution
GLOBAL BURDEN OF DISEASE ATTRIBUTABLE TO
SELECTED MAJOR RISK FACTORS
Percentage
age of total
Percent
burden (within region)
Underweight
Unsafe sex
5% -
Tobacco
Overweight
Alcohol
Water, sanitation and hygiene (5.5%)
Solid fuel use (3.7 %)
Physical
inactivity
Zinc deficiency
Tobacco
1% -
Alcohol
Overweight
Occupational injuries
Ambient air Lead Climate
change
Occupational risks
Unsafe sex
Ambient air Water, sanitation and hygiene
Lead
Developing countries
Industrialized countries
(high mortality)
23
Household energy practices vary widely around the world, as does the resultant death toll
due to indoor smoke. In high-mortality developing countries, indoor smoke is responsible for
3.7% of the overall disease burden, making it the most important risk factor after malnutrition
(9%), unsafe sex (6%) and lack of safe water and adequate sanitation. In low-mortality
developing countries, indoor smoke occupies the 8th rank and accounts for 1.9% of the
disease burden. In contrast, in industrialized countries the impact of cooking and heating
with solid fuels becomes negligible in relation to risk factors such as tobacco, high blood
pressure and alcohol consumption. Notes taken from
www.who.int/indoorair/info/en/briefing2.pdf
Refs:
•Indoor air pollution in developing countries: a major environmental and public health
challenge. Bulletin of the World Health Organization, 2000.
•World Health Report 2002. Indoor Air Thematic Briefing 2
(www.who.int/indoorair/info/en/briefing2.pdf).
Additional information can be found at: www.who.int/indoorair/publications/en/
Indoor Air Pollution
WHAT INTERVENTIONS ARE AVAILABLE TO REDUCE
INDOOR AIR POLLUTION FROM SOLID FUELS?
Source of pollution
Home environment
- Improved stoves
- Cleaner fuels
(kerosene, gas,
electricity)
-Hoods and chimneys
-Windows, ventilation
holes, eaves spaces
-Separate kitchen
User behaviour
- Fuel drying
- Use of pot lids
- Good
maintenance
- Keeping children
away from smoke
24
<<READ SLIDE>>
Solid fuels comprise only 10–15% of fuel used.
•Nearly one half of the world’s population uses solid fuels for cooking and heating homes.
- 2 billion people are exposed to particulate matter (PM) and gases at levels up to 100 times
higher than in ambient (outdoor) air.
- Women and children are most exposed: levels may be 10 to 100 times above safety
standards for ambient air.
Combustion produces hundreds of toxic chemicals that concentrate inside homes.
Biomass (wood, agricultural produce, straw and dung) produces:
- a wide variety of liquids, suspended particles, gases and mixtures.
Coal produces:
- Polycyclic aromatic hydrocarbons (PAHs), benzene, formaldehyde, sulfur, heavy metals
and fluoride.
These pollutants affect the most vulnerable populations, women of childbearing age, infants
and children in the poorest circumstances.
Ref:
Air pollution: what a paediatrician needs to know. Leaflet published by the World Health
Organization in collaboration with the International Pediatric Association, 2003.
Additional information on these references can be found at:
www.who.int/indoorair/publications/en/
Indoor Air Pollution
CARBON MONOXIDE: THE "SILENT KILLER"
A COMMON CAUSE OF ACUTE AND LETHAL POISONING
Colourless, odourless gas formed by incomplete burning of
carbon-based fuels
CO’s affinity for Hb is 240–270 times greater than oxygen
Fetal Hb has higher affinity for CO
CO causes a leftward shift of the
oxyhaemoglobin (OHb) dissociation curve
Intoxication results in tissue hypoxia
Multiple organ systems are affected
www.cdc.gov/nceh/airpollution/carbonmonoxide/checklist.htm
25
• 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
Hb = haemoglobin
COHb = carboxyhaemoglobin
Refs:
• Carbon monoxide. In: Pediatric Environmental Health, 2nd ed. Etzel RA Ed. Elk Grove
Indoor Air Pollution
CARBON MONOXIDE (CO): SOURCES
Gas, kerosene, wood stoves and coal
Fires, fireplaces, furnaces
Leaking chimneys and vents
Room and water heaters
Vehicle exhaust in closed garage
Tobacco smoke
EPA
Any place where combustion is incomplete
26
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 secondhand tobacco smoke.
Picture: www.epa.nsw.gov.au/woodsmoke/heateruse.htm
Indoor Air Pollution
www.firstalert.com/index.asp?pageid=82
In a a single-family house in the industrialized world, CO can come from many sources.
Figure: www.firstalert.com/index.asp?pageid=82, Used with Copyright permission.
27
Indoor Air Pollution
PREVENTION OF EXPOSURE TO CO
Keep fuel-burning appliances in good
working condition
Check heating systems, chimneys and
vents regularly
Never burn charcoal indoors
Never leave a car running in a closed
garage
Consider CO detectors
28
Prevention is the key to avoiding carbon monoxide poisoning.
Primary prevention of carbon monoxide (CO) poisoning requires limiting exposure to known sources.
Proper installation, maintenance, and use of combustion appliances can help to reduce exposure to
CO.
The US Environmental Protection Agency (EPA) has set harm levels of:
•50 ppm (8-hour average)
•75 ppm (4-hour average)
•125 ppm (1-hour average).
Exposure to these levels can lead to COHb levels of 5 to 10% and cause significant symptoms in
sensitive individuals. The current US air quality standards for CO, intended to keep COHb below 2.1%,
recommend levels of not more than 9 parts per million (ppm) for 8 hours and 35 ppm for 1 hour for
outdoor air. No standards for CO have been agreed for indoor air.
Smoke and CO detectors may provide early warning and prevent unintentional CO-related deaths.
They should, however, be in good working condition and should not substitute for other prevention
measures (cleaning the chimney, etc.)
For more information on CO detectors, go to: www.epa.gov/iaq/pubs/coftsht.html
COHb = carboxyhaemoglobin
Ref:
•www.pinefire-85.org/Fire_safety_pages/CARBON_MONOXIDE/carbon_monoxide.html
Indoor Air Pollution
CARBON MONOXIDE POISONING CAN KILL
Symptoms:
Increasing COHb
Headache, dizziness, fatigue, dyspnoea
Nausea, vomiting
Irritability
Sleepiness, confusion, disorientation
Unconsciousness, coma
Death
Delayed neuropsychological sequelae (in
survivors)
29
The route of exposure is through inhalation. Unintentional exposure to carbon monoxide
(CO) can be attributed to smoke inhalation from inadequately vented combustion appliances,
and from vehicles and tobacco smoke.
The clinical features of CO poisoning are highly variable and symptoms vary from mild to
very severe. Acute effects are due to the formation of carboxyhaemoglobin in the blood,
which inhibits oxygen intake. At moderate concentrations, angina, impaired vision, and
reduced brain function may result. At higher concentrations, exposure to CO can be fatal.
Delayed neuropsychological sequelae have been reported in adults and children; these
usually occur 3 to 240 days following exposure and are estimated to occur in 10 to 30% of
victims.
Ref:
•California Poison Control System. Poisoning and drug overdose. Olson ed. Appleton and
Lange, 1999.
•Carbon monoxide. In: Pediatric Environmental Health, 2nd ed. Etzel RA Ed. Elk Grove
Village, IL: American Academy of Pediatrics. 2003.
•Hon KLet al. Neurologic and radiologic manifestations of three girls surviving acute carbon
monoxide poisoning. J Child Neurol. 2006 Sep;21(9):737-41.
We report the neurologic and radiologic manifestations of three adolescent girls with
acute carbon monoxide poisoning. The girls were found collapsed and unconscious
in a bathroom where liquid petroleum gas was being used as heating fuel. As
hyperbaric oxygen therapy was not available locally, they only received oxygen
supplementation via nasal cannula (4 L/minute) as treatment in the first 2 days. On
transfer to a tertiary center in Hong Kong, evolving neurologic manifestations of
visual acuity and field deficits, confusion, and focal motor weaknesses were
observed. Focal infarctions were evident in cerebral computed tomography in one
patient and cortical lesions on magnetic resonance imaging in all three patients.
[18F]Fluorodeoxyglucose (FDG) positron emission tomography (PET) revealed
additional decreased metabolism in the basal ganglia in two patients, which was
typical of carbon monoxide poisoning. The neurologic deficits resolved completely at
3 weeks after the exposure, but psychologic symptoms succeeded. This report
Indoor Air Pollution
MANAGEMENT
Diagnosis:
Measurement of COHb
nonsmokers 1–3 %
smokers 3–8%
Not useful:
Pulse oximeter
Arterial blood gases
Treatment:
Remove patient from
CO source
Life support
Oxygen 100%
Hyperbaric oxygen?
Monitoring
30
The measurement of COHb confirms that exposure has occurred, but the severity of
poisoning is not correlated to COHb levels. Measurements of oxygen saturation by pulse
oxymetry and arterial blood gas are not helpful for diagnosis because they are normal,
although metabolic acidosis may be present. Normal levels of COHb range from 1 to 3% in
nonsmokers and 3 to 8% in smokers.
Blood tests have to be done as soon as possible after exposure. The gas company can also
complement the measurements.
Treatment of poisoning consists of supplemental oxygen, 100%, ventilatory support and
monitoring cardiac disrhythmias. Elimination half-life of COHb is approximately 4 hours in
room air, 1 hour with provision of oxygen, 100%, and 20–30 minutes with hyperbaric oxygen.
Hyperbaric oxygen is a treatment that is usually reserved for severe CO poisoning.
COHb = carboxyhaemoglobin
Indoor Air Pollution
CHRONIC EXPOSURE
Acute or chronic exposure to low levels of carbon monoxide
(research in animals and humans):
Linked to development of arteriosclerosis
?Aggravation of cardiovascular diseases
?Poor performance on certain psychomotor tasks
Limited exercise capacity
31
The main areas of concern that have arisen from acute or chronic exposure to low levels of carbon monoxide in
experimental and epidemiological research in animals and man are: (a) its role in the genesis of arteriosclerotic
vascular diseases; (b) its role in the aggravation of symptoms of cardiovascular diseases; (c) its contribution to
performance deficits in certain psychomotor tasks; and (d) its role in limiting the working capacity of exercising
man.
Cardiovascular system : Development of atherosclerotic cardiovascular disease
Extensive experimental work has been carried out over many years on animals, mainly rabbits, showing that
prolonged exposure to moderate levels of carbon monoxide can produce atherosclerotic changes, especially in the
presence of high cholesterol levels (1-2%) in the diet. The relevance of this work for man has not been
established. However, other animal work, and some epidemiologic studies of prolonged human exposures to
elevated carbon monoxide levels through smoking, occupation, or both, such as those carried out in Denmark,
Finland, and Japan, indicate the need for further investigation of the possible role of carbon monoxide in the
genesis of atherosclerotic vascular changes in animals and man. The degree of intermittency of exposure at
various levels should be taken into account as well as the possible contribution of other agents such as nicotine
and high-fat diets. There is some evidence of adaptation, but such changes may not be entirely beneficial.
Acute effects on existing heart illness
The few existing epidemiologic studies on the possible effects of carbon monoxide on the severity or fatality of
coronary occlusion are insufficient to allow any conclusions.
Acute effects on existing vascular disease
One study has been carried out on patients with intermittent claudication from peripheral vascular disease. Effects
on pain with exercise were observed in the same exposure range as with angina i.e., at carboxyhaemoglobin
concentrations of 2.5-3.1%, with a mean of 2.8%.
Nervous system
As for the role of carbon monoxide in affecting psychomotor functions, no definite conclusions can be drawn from
the existing data. The behavioural functions tested in such studies include vigilance and psychomotor
performance, visual acuity and sensitivity, the ability to estimate time intervals, complex motor coordination as
tested by driving simulators, and different perceptual and mental operations. Some workers observed detrimental
effects at carboxyhaemoglobin levels as low as 2%, whereas others were unable to detect significant impairment
even at levels from above 5% to about 20%. In evaluating these discrepancies, it should be mentioned, that these
behavioural functions are easily influenced by a number of other factors besides carbon monoxide-induced
hypoxia, e.g., degree of sensory deprivation, compensatory abilities, drugs, temperature, time of day, competition,
etc.
Work capacity
That elevated carboxyhaemoglobin levels affect work capacity has long been known. Levels of 40-50% will usually
prevent working entirely. Recent studies in the laboratory, on man, using maximum work capacity or maximum
aerobic capacity as indicators of performance, have been carried out in relation to carboxyhaemoglobin levels.
Here, dose-response data are available for maximum effort. The limitation appears at a carboxyhaemoglobin
concentration of about 4% and increases at higher levels. Lower exposure levels have been studied and do not
produce this effect. It should be noted that while levels of carboxyhaemoglobin of 2.5-4%, did not reduce
maximum work capacity, they did reduce the length of time for which such effort could be carried out. It is not
known what specific levels of carboxy- haemoglobin will reduce the capacity of individuals to perform at ordinary
work levels, such as 30-50% of their maximum capacity, for prolonged periods of time.
Notes from IPCS INCHEM: www.inchem.org/documents/ehc/ehc/ehc013.htm#SubSectionNumber:9.2.1
Indoor Air Pollution
CHRONIC EXPOSURE
Can lead mainly to :
Cardiovascular effects.
Central nervous system effects
Increased susceptibility to acute respiratory infections
32
Carbon monoxide can cause harmful health effects by reducing oxygen delivery to the body's organs (like the
heart and brain) and tissues.
Cardiovascular Effects. The health threat from lower levels of CO is most serious for those who suffer from heart
disease, like angina, clogged arteries, or congestive heart failure. For a person with heart disease, a single
exposure to CO at low levels may cause chest pain and reduce that person's ability to exercise; repeated
exposures may contribute to other cardiovascular effects.
Central Nervous System Effects. Even healthy people can be affected by high levels of CO. People who
breathe high levels of CO can develop vision problems, reduced ability to work or learn, reduced manual dexterity,
and difficulty performing complex tasks. At extremely high levels, CO is poisonous and can cause death.
Notes taken from EPA: www.epa.gov/air/urbanair/co/hlth1.html
Ref:
Estrella B et al. Acute respiratory diseases and carboxyhemoglobin status in school children of Quito, Ecuador.
Environmental Health Perspectives (2005) 113 (5): 607-11.
Outdoor carbon monoxide comes mainly from vehicular emissions, and high concentrations occur in areas with
heavy traffic congestion. CO binds to hemoglobin, forming carboxyhemoglobin (COHb), and reduces oxygen
delivery. We investigated the link between the adverse effects of CO on the respiratory system using COHb as a
marker for chronic CO exposure. We examined the relationship between acute respiratory infections (ARIs) and
COHb concentrations in school-age children living in urban and suburban areas of Quito, Ecuador. We selected
three schools located in areas with different traffic intensities and enrolled 960 children. To adjust for potential
confounders we conducted a detailed survey. In a random subsample of 295 children, we determined that average
COHb concentrations were significantly higher in children attending schools in areas with high and moderate
traffic, compared with the low-traffic area. The percentage of children with COHb concentrations above the safe
level of 2.5% were 1, 43, and 92% in low-, moderate-, and high-traffic areas, respectively. Children with COHb
above the safe level are 3.25 [95% confidence interval (CI), 1.65-6.38] times more likely to have ARI than children
with COHb < 2.5%. Furthermore, with each percent increase in COHb above the safety level, children are 1.15
(95% CI, 1.03-1.28) times more likely to have an additional case of ARI. Our findings provide strong evidence of
the relation between CO exposure and susceptibility to respiratory infections.
Indoor Air Pollution
FIRE INJURIES
From inhaled toxic chemicals and/or thermal burns.
The lungs and airways are affected in these ways:
tissue irritation
heat damage
Asphyxiation
potential cyanide poisoning
Make the home safer:
Beware of matches and lighters
Install smoke alarms
Have a home fire escape plan
33
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 the 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 the 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 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 the baby and keep 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
Indoor Air Pollution
SECONDHAND TOBACCO SMOKE
SCOPE OF THE PROBLEM
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)
34
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 RA. Indoor air pollutants in homes and schools. Pediatric Clinics of North America, 2001, 48:1153.
•Wisborg K et al. Exposure to tobacco smoke in utero and the risk of stillbirth and death in the first year of life.
American Journal of Epidemiology, 2001, 154:322-7.
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.
Indoor Air Pollution
SECONDHAND SMOKE INCREASES RISK OF:
Respiratory tract illness
Asthma
Middle ear effusions
Prenatal complications and low birth weight
Fire-related injuries
Sudden infant death syndrome (SIDS)
Cancers (childhood leukemia and others)
35
<<READ SLIDE>>
Sudden infant death syndrome (SIDS): death of an apparently healthy infant, usually before
the age of 1 year, that is of unknown cause and occurs especially during sleep.
Refs:
•Brondum J et al. Parental Cigarette Smoking and the Risk of Acute Leukemia in Children.
Cancer. 1999; 85:1380-1388.
•Ji BT et al. Paternal Cigarette Smoking and the Risk of Childhood Cancer Among Offspring
of Non-Smoking Mothers. J Natl Cancer Inst. 1997; 89:238-244.
•Shu XO et al. Parental Alcohol Consumption, Cigarette Smoking, and Risk of Infant
Leukemia: A Children’s Cancer Group Study. J Natl Cancer Inst. 1996; 88:24-31.
Indoor Air Pollution
THE LIFE CYCLE OF THE EFFECTS OF SMOKING ON
HEALTH
Asthma
Otitis Media
FireFire-related Injuries
SIDs
RSV/Bronchiolitis
Meningitis
Influences
to Start
Smoking
Childhood
Infancy
Adolescence
Nicotine Addiction
In utero
Adulthood
Low Birth Weight
Stillbirth
Cancer
Cardiovascular Disease
COPD
Aligne, 1997
36
This graphic depicts the life-cycle of the effects of tobacco smoking on health beginning in utero and
continuing throughout adulthood. Pregnant women will have babies with lower birth weight as well as
greater chances of stillbirth.
Children with parents who smoke will be more to likely develop respiratory problems, bronchiolitis,
meningitis, asthma and otitis media and are at a higher risk of fire-related injuries. Furthermore,
exposure to tobacco smoke damages the respiratory epithelium and decreases the ability to combat
the respiratory syncytial virus (RSV), the leading cause of hospital admissions of children under 1 year
of age.
Adolescence represents a high-risk period for taking up smoking behaviour.
As adults, children of smokers have a greater likelihood of developing cancer, chronic obstructive
pulmonary disease (COPD) and cardiovascular diseases (CVD) than children with non-smoking
parents. Also, children who have a parent who smokes are more likely to smoke as adults, so the
cycle continues from one generation to the next.
SIDS: sudden infant death syndrome
COPD: chronic obstructive pulmonary disease
Figure: Aligne A et al. Tobacco and children: An economic evaluation of the medical effects of parental
smoking. Arch Pediatr Adolesc Med, 1997, 151:652. Copyright (1997), American Medical Association.
Used with permission.
Ref:
• Aligne A et al. Tobacco and children: An economic evaluation of the medical effects of parental
smoking. Arch Pediatr Adolesc Med, 1997, 151:652.
•Tager IB et al. Longitudinal study of the effects of maternal smoking on pulmonary function in
children. N Engl J Med, 1983, 309:699-703.
•WHO Report on the Global Tobacco Epidemic 2008: The MPOWER Package, 2008.
Indoor Air Pollution
PESTICIDES
Spraying pesticides at home / school:
Higher concentrations near the floor
Persistence in some surfaces (carpets, soft toys)
Overuse and misuse
Children’s behaviour and inhalation of pesticides
Crawling
Playing close to the floor
Plush toys
Hand-to-mouth
Object-to-mouth
37
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 R et al. 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.
Indoor Air Pollution
PESTICIDES: INSECTICIDES
Classes commonly used for insect control indoors:
Pyrethroids: allergenic, CNS toxicity at high levels
Cholinesterase inhibitors: neurotoxicants,
neurodevelopmental toxicants
Insect repellents (DEET)
Mosquito coils
Health effects:
Acute poisoning
Allergic and general symptoms
38
<<READ SLIDE>>
Classes of insecticide commonly used for insect control indoors include the following:
•Pyrethroids: these are very allergenic and can lead to central nervous system (CNS) toxicity
at high levels of exposure.
•Cholinesterase inhibitors: these are neurotoxicants and neurodevelopmental toxicants
(organophosphosphates, carbamates).
•Insect repellents: diethyltoluamide (DEET).
•Mosquito coils.
The effects on health of exposure to these insecticides include:
•acute poisoning usually related to accidental ingestion in children;
•allergic and general symptoms
– headache, nausea, vomiting;
– cough, rhinitis, bronchitis, asthma and other allergic symptoms.
Indoor Air Pollution
MOSQUITO COILS
Household use in Africa, Asia, South America
Major active ingredient – pyrethrins
Long-term exposures linked to asthma
and wheezing
ehp.niehs.nih.gov/members/2003/6177/
6177.html
39
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 polycyclic aromatic hydrocarbons (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 W et al. Mosquito coil emissions and health implications. Environ Health Perspect, 2003,
111:1454-60.
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
Indoor Air Pollution
SOLVENTS AND VOLATILE ORGANIC COMPOUNDS
Alkanes, aromatic hydrocarbons, alcohols, aldehydes, ketones
Sources:
Solvents, fabric softeners, deodorizers and cleaning products
Paints, glues, resins, waxes and polishing materials
Spray propellants, dry cleaning fluids
Pens and markers
Binders and plasticizers
Cosmetics: hair sprays, perfumes
www.epa.gov/oppfead1/cb/10_tips/
40
Organic chemicals are widely used as ingredients in household products including paints,
varnishes, wax, cosmetics, degreasing agents, wood preservatives, aerosol sprays,
cleansers, disinfectants, moth repellents, air fresheners and hobby products. Fuels are also
made up of organic chemicals.
All of these products can release organic compounds while they are being used, and, to
some degree, when they are stored.
The average levels of several organic compounds in indoor air are 2–5 times higher than in
outdoor air. During certain activities, such as paint-stripping, and for several hours
immediately afterwards, levels may be 1000 times higher than outdoor levels.
These notes are taken from the US EPA Website www.epa.gov/iaq/voc.html
Picture: www.epa.gov/oppfead1/cb/10_tips/
Indoor Air Pollution
VOLATILE ORGANIC COMPOUNDS: HEALTH EFFECTS
Acute:
Irritation of eyes and respiratory tract
General: headache, dizziness, loss of coordination, nausea,
visual disorders
Allergic reactions, including asthma and rhinitis
Chronic:
Damage to liver, kidney, blood system and
central nervous system (CNS)
Some may cause cancer in humans (formaldehyde)
41
Volatile organic compounds (VOC) vary greatly in their health effects: some are highly toxic,
whereas some have no known effects on health.
As with other pollutants, the extent and nature of the effects on health will depend on many
factors including level of exposure and duration of exposure.
The immediate symptoms experienced after exposure to VOC may include eye, nose and
throat irritation; headaches; loss of coordination; nausea; dizziness; and visual disorders.
Memory impairment and damage to liver, kidneys and central nervous system (CNS) may
also occur. Little is yet known about what effects on health occur from exposure to the levels
of organics usually found in homes. Many organic compounds are known to cause cancer in
animals; some are suspected of causing, or are known to cause, cancer in humans.
Steps to reduce exposure
•Use household products according to manufacturer's directions.
•Make sure to provide plenty of fresh air when using these products.
•Throw away unused or little-used containers safely; buy in quantities that can soon be used.
•Keep out of reach of children and pets.
•Never mix household care products unless directed on the label.
These notes are taken from the US EPA website www.epa.gov/iaq/voc.html
Indoor Air Pollution
FORMALDEHYDE
Sources: differ according to country
Developing countries
Use of solid fuels indoors
Mosquito coils
Furniture (pressed wood)
Industrialized countries
Household cleaners and deodorizers
Glues and resins
Tobacco smoke
Carpeting
Furniture and dyed materials
Pressed wood products
Urea formaldehyde insulating foam (UFFI)
Others
Ref:
•www.epa.gov/iaq/formalde.html
42
Indoor Air Pollution
FORMALDEHYDE: HEALTH EFFECTS
Irritation of eyes, nose and throat
Breathing difficulties
Skin rash
Asthma and other allergic reactions
May be a sensitizer
May cause cancer
Prevention:
Reduce exposure
Provide adequate ventilation
Maintain moderate temperature and humidity levels
43
Formaldehyde, a colourless, pungent-smelling gas, can cause watery eyes, burning
sensations in the eyes and throat, nausea and difficulty in breathing (wheezing and
coughing) in some humans exposed to levels above 0.1 parts per million. High
concentrations may trigger attacks in people with asthma. There is evidence that some
people can develop a sensitivity to formaldehyde. It has also been shown to cause cancer in
animals and may cause cancer in humans.
Reducing exposure to formaldehyde in homes
•Ask about the formaldehyde content of pressed wood products, including building materials
and furniture before purchasing them.
•Maintain moderate temperature and humidity levels and provide adequate ventilation.
The rate at which formaldehyde is released is accelerated by heat and may also depend
somewhat on the humidity level. Therefore, the use of dehumidifiers and air conditioning to
control humidity and to maintain a moderate temperature can help reduce formaldehyde
emissions.
These notes are taken from the US EPA website www.epa.gov/iaq/formalde.htm
Indoor Air Pollution
BIOLOGICAL POLLUTANTS
Biological pollutants are/were living organisms:
Animal dander, dust mites, moulds, infectious agents, pollen
Sources of biological agents:
Water-damaged surfaces and materials
Humidifiers and stagnant water
Water vapour from cooking and showering
Air conditioning systems
Mattresses, upholstered furniture and carpets
Dirt
44
Dust mites, fungi and bacteria require moisture to proliferate. Permeation of rain or
groundwater into a building and condensation on cold interior surfaces can promote
proliferation of microbes. Water vapour is produced by people and pets, cooking and
showering and requires sufficient air exchange to prevent moisture problems. Mattresses,
upholstered furniture and carpets are reservoirs for dust mites.
Moulds have been associated with three types of effects: infections, allergic reactions and
toxic effects. Toxic effects may be caused by inhalation of mycotoxins.
These notes are taken from the US EPA website www.epa.gov/iaq/pubs/bio_1.html
Indoor Air Pollution
DUST MITES
Feed on human dander
Prefer warm, humid environments
Sources:
bedding, carpets, upholstery, soft toys
Prevention:
Encasing mattress and pillows
Washing bedding in hot water
Frequent vacuuming / damp mopping
Decreasing clutter
Removing carpets
CDC
45
Dust mites are acarians (Dermatophagoides spp.)
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 comparison (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 comparison (control) group developed sensitization to dust mite.
Refs:
•Tsitoura S et al. 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,
156:1021-7.
•Arshad SH et al. Prevention of sensitization to house dust mite by allergen avoidance in school age
children: a randomized controlled study. Clin Exp Allergy, 2002, 32:843.
•Arshad SH et al. Prevention of allergic disease during childhood by allergen avoidance: the Isle of
Wight prevention study. J Allergy Clin Immunol. 2007 Feb;119(2):307-13.
BACKGROUND: Early life allergen exposure may increase the risk of childhood allergy, but the
protective effect of reduction in allergen exposure remains uncertain. OBJECTIVE: To evaluate the
effect of reduction in food and house dust mite (HDM) allergen exposure in infancy in preventing
asthma and allergy. METHODS: Infants, at higher risk because of family predisposition, were recruited
prenatally and randomized to prophylactic (n = 58) and control (n = 62) groups. Prophylactic group
infants were either breast-fed with mother on a low allergen diet or given an extensively hydrolyzed
formula. Exposure to HDM was reduced by the use of an acaricide and mattress covers. The control
group followed standard advice. Development of allergic diseases and sensitization to common
allergens (atopy) was assessed blindly at ages 1, 2, 4, and 8 years in all 120 children. RESULTS:
Repeated measurement analysis, adjusted for all relevant confounding variables, confirmed a
preventive effect on asthma: adjusted odds ratio (OR), 0.24; 95% CI, 0.09-0.66; P = .005; atopic
dermatitis, OR, 0.23; CI, 0.08-0.64; P = .005; rhinitis, OR, 0.42; CI, 0.19-0.92; P = .03; and atopy, OR,
0.13; CI, 0.05-0.32; P < .001. The protective effect was primarily observed in the subgroup of children
with persistent disease (symptoms at all visits) and in those with evidence of allergic sensitization.
CONCLUSION: Allergic diseases can be reduced, for at least the first 8 years of life, by combined food
and HDM allergen avoidance in infancy. CLINICAL IMPLICATIONS: Strict food and HDM allergen
Indoor Air Pollution
ANIMAL ALLERGENS
Cat dander (most allergenic)
Dog dander
Birds
Cockroach parts and faeces
Prevention:
Remove animals from indoors
Allergens persist for many months after removal of source
Clean environment and pet(s) frequently
Ventilate adequately
Control dust and moisture
46
<<READ SLIDE>>
Cats are most allergenic.
Dogs are the most common household pet — allergy to dogs is uncommon.
Birds (harbour dust mites).
Cockroach parts (keratin) and faeces are an important cause of asthma morbidity.
Prevention
Avoid exposure: allergens persist for many months after removal of their source.
Clean the environment and pet(s) frequently.
Ensure adequate ventilation.
Control dust and moisture.
Use an air filtration system.
Refs:
•McConnell R et al. Cockroach counts and house dust allergen concentrations after
professional cockroach control and cleaning, Ann Allergy Asthma Immunol, 2003, 91:546-52.
•Becker AB. Primary prevention of allergy and asthma is possible. Clin Rev Allergy Immunol,
2005, 28:5-16.
Indoor Air Pollution
MOULDS
A frequently undetected environmental problem
Occur in damp indoor areas
Allergies and nonspecific symptoms are common, but
infections are rare
EPA
47
<<READ SLIDE>>
Ref:
•Etzel RA et al. Indoor mold and children's health. Environ Health Perspect, 1999, 107(Suppl)3:463.
Reactive airways disease in children is increasing in many countries around the world. The clinical
diagnosis of asthma or reactive airways disease includes a variable airflow and an increased
sensitivity in the airways. This condition can develop after an augmented reaction to a specific agent
(allergen) and may cause a life-threatening situation within a very short period of exposure. It can also
develop after a long-term exposure to irritating agents that cause an inflammation in the airways in the
absence of an allergen. (paragraph) Several environmental agents have been shown to be associated
with the increased incidence of childhood asthma. They include allergens, cat dander, outdoor as well
as indoor air pollution, cooking fumes, and infections. There is, however, increasing evidence that
mould growth indoors in damp buildings is an important risk factor. About 30 investigations from
various countries around the world have demonstrated a close relationship between living in damp
homes or homes with mould growth, and the extent of adverse respiratory symptoms in children.
Some studies show a relation between dampness/mould and objective measures of lung function.
Apart from airways symptoms, some studies demonstrate the presence of general symptoms that
include fatigue and headache and symptoms from the central nervous system. At excessive
exposures, an increased risk for haemorrhagic pneumonia and death among infants has been
reported. The described effects may have important consequences for children in the early years of
life. A child's immune system is developing from birth to adolescence and requires a natural,
physiological stimulation with antigens as well as inflammatory agents. Any disturbances of this normal
maturing process will increase the risk for abnormal reactions to inhaled antigens and inflammagenic
agents in the environment. The knowledge about health risks due to mould exposure is not
widespread and health authorities in some countries may not be aware of the serious reactions mould
exposure can provoke in some children. Individual physicians may have difficulty handling the patients
because of the lack of recognition of the relationship between the often complex symptoms and the
indoor environment.
Indoor Air Pollution
MOULDMOULD-RELATED DISEASES
Airway and conjunctival irritation
Headache
Difficulty in concentrating
Hypersensitivity reactions: asthma, rhinitis
Systemic infections (immunosuppressed child)
Acute exposure associated with pulmonary haemorrhage
in infants
48
Hypersensitivity to moulds is immediate (type 1) and includes: acute asthma, allergic rhinitis and
urticaria (hives) (which is uncommon).
Colonization associated with chronic asthma is rare and serious (allergic bronchopulmonary mycosis
and allergic mycotic sinusitis).
Deep fungal infections are uncommon: serious, life-threatening diseases are not usually caused by
common household moulds. The major exception is aspergillosis. Mould infection occurs only in an
immunocompromised children.
Ref:
•Etzel RA. Indoor mold and children's health. Environ Health Perspect, 1999, 107(Suppl 3):463.
•Etzel RA et al. Acute pulmonary hemorrhage in infants associated with exposure to Stachybotrys atra
and other fungi. Arch Pediatr Adolesc Med. 1998 Aug;152(8):757-62
BACKGROUND: A geographic cluster of 10 cases of pulmonary hemorrhage and hemosiderosis in
infants occurred in Cleveland, Ohio, between January 1993 and December 1994. STUDY DESIGN:
This community-based case-control study tested the hypothesis that the 10 infants with pulmonary
hemorrhage and hemosiderosis were more likely to live in homes where Stachybotrys atra was
present than were 30 age- and ZIP code-matched control infants. We investigated the infants' home
environments using bioaerosol sampling methods, with specific attention to S atra. Air and surface
samples were collected from the room where the infant was reported to have spent the most time.
RESULTS: Mean colony counts for all fungi averaged 29 227 colony-forming units (CFU)/m3 in homes
of patients and 707 CFU/m3 in homes of controls. The mean concentration of S atra in the air was 43
CFU/m3 in homes of patients and 4 CFU/m3 in homes of controls. Viable S atra was detected in filter
cassette samples of the air in the homes of 5 of 9 patients and 4 of 27 controls. The matched odds
ratio for a change of 10 units in the mean concentration of S atra in the air was 9.83 (95% confidence
interval, 1.08-3 X 10(6)). The mean concentration of S atra on surfaces was 20 X 10(6) CFU/g and
0.007 x 10(6) CFU/g in homes of patients and controls, respectively. CONCLUSION: Infants with
pulmonary hemorrhage and hemosiderosis were more likely than controls to live in homes with
toxigenic S atra and other fungi in the indoor air.
Indoor Air Pollution
CHEMICAL AGENTS PRODUCED BY MOULDS
Mycotoxins are associated with human disease and
cause acute and chronic effects
Mycotoxins
Aflatoxins
Tricothecenes
Ochratoxins and citrinin
Hundreds of others
Glucans (cell wall components)
Volatile organic compounds (irritating)
49
Mycotoxins are associated with human disease.
Tricothecenes inhibit protein synthesis and have many acute effects, including anemia and infant pulmonary
haemorrhage.
Ochratoxins and citrinin cause nephropathy and immunosuppression.
Aflatoxins are hepatotoxins and are carcinogenic.
(See module on Mycotoxins)
Refs:
•Etzel RA. What the primary care pediatrician should know about syndromes associated with exposures to
mycotoxins. Curr Probl Pediatr Adolesc Health Care. 2006;36(8):282-305.
Disease associated with exposure to mycotoxins is known as the "Great Masquerader" of the 21st century
because of its complex natural history involving different tissues and resembling different diseases at each stage
in its evolution. It can present with a variety of nonspecific clinical signs and symptoms such as rash, conjunctivitis,
epistaxis, apnea, cough, wheezing, nausea, and vomiting. Some cases of vomiting illness, bone marrow failure,
acute pulmonary hemorrhage, and recurrent apnea and/or "pneumonia" are associated with exposure to
mycotoxins. Familiarity with the symptoms of exposure to the major classes of mycotoxins enables the clinician to
ask pertinent questions about possible fungal exposures and to remove the infant or child from the source of
exposure, which could be contaminated food(s), clothing and furniture, or the indoor air of the home. Failure to
prevent recurrent exposure often results in recurrent illness. A variety of other conditions, including hepatocellular
and esophageal cancer and neural tube defects, are associated with consumption of foods contaminated with
mycotoxins. Awareness of the short- and long-term consequences of exposures to these natural toxins helps
pediatricians to serve as better advocates for children and families.
•Novak M et al. Beta-glucans, history, and the present: immunomodulatory aspects and mechanisms of action. J
Immunotoxicol. 2008 Jan;5(1):47-57.
The present paper represents a comprehensive up-to-date review of beta -glucans, their chemical and biological
properties, and their role in immunological reactions. beta -D-Glucans belong to a group of physiologically active
compounds called biological response modifiers and represent highly conserved structural components of cell
walls in yeast, fungi, or seaweed. Despite almost 150 years of research, the exact mechanisms of their action
remain unclear. The present review starts with the history of glucans. Next, attention is focused on sources and
structure, comparing the effects of physicochemical properties, and sources on biological effects. As glucans
belong to natural products useful in preventing various diseases, they have been highly sought after throughout
human history. Based on extensive recent research, this paper explains the various mechanisms of effects and the
ways glucans mediate their effects on defense reactions against infections. Despite the fact that predominately
pharmacological effects of glucans are positive, their unfavorable and potentially toxic side effects were not
overlooked. In addition, attention was focused on the future research, possible alternatives such as synthetic
oligosaccharides, and on clinical applications.
Indoor Air Pollution
INDOOR AIR QUALITY:
BUILDING COMPONENTS
The importance of:
Materials in houses and schools:
Asbestos, wood preservatives, paints and others
Ventilation
Heating
Use (overuse) and location of electric appliances
Air conditioning
50
Building components may be a source of indoor air pollution. The materials used in the
construction of a house or a school may release toxicants into the air. Indoor air pollutants
may have an effect on the health and performance of children in schools. Lack of ventilation
(and hygiene) increases the risk of exposure, which may be further enhanced by heating and
faulty air conditioning.
Knowledge of this issue has fueled interest in "green houses" and "green schools".
The “built environment” refers to the way a community is built, including how people get from
home to school, work, stores, places of worship. houses, offices and other manmade
structures in which people live, work and play.
Refs:
•Etzel RA. Indoor air pollutants in homes and schools. Pediatric Clinics of North America,
2001, 48:1153.
•Mendell MJ et al. Do indoor air pollutants and thermal conditions in schools influence
student performance? A critical review of the literature. Indoor Air 2005,15:27-52.
Indoor Air Pollution
SICK 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
An evolving area
Building related illness: symptoms of identified illness
attributed to airborne contaminants in the building
51
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
•Wang BL et al. Symptom definitions for SBS (sick building syndrome) in residential
dwellings. Int J Hyg Environ Health. 2008 Mar;211(1-2):114-20.
The potential risk factors for sick building syndrome (SBS) in newly built dwellings were
investigated. Two different definitions for SBS were used, a narrow definition (symptoms
related to home environment and continuously occurring in the last 3 months were regarded
as positive) and another relatively broad definition (symptoms related to home environment
and either continuously or sporadically occurring in the last 3 months were regarded as
positive). With both definitions indoor air chemicals, especially TVOC, and high stress during
work were found to be significantly associated with SBS symptoms. Allergic history was
more associated with narrow-sense symptoms and odor perception with broad-sense
symptoms. The results indicate that the broad definition be preferred to find more potential
risk factors.
Indoor Air Pollution
SICK BUILDING SYNDROME
Possible causes:
Inadequate building design
Occupant activities
Remodelled buildings operating in a manner
inconsistent with their original design
Inadequate ventilation
Inadequate maintenance
Chemical and biological contaminants
52
<<READ SLIDE.>>
Indoor Air Pollution
SICK BUILDING SYNDROME
Symptoms:
Headache
Irritation of eyes, nose or
throat
Dry cough
Dry or itchy skin
Difficulty in concentrating
Fatigue
Sensitivity to odours
Solutions:
Remove source of
pollutant
Increase ventilation
Air cleaning: filters
Education and
communication
53
<<READ SLIDE.>>
Indoor Air Pollution
RADON
Radioactive gas released from soil and rocks
Second leading cause of lung cancer (in adults)
Geology of the area can predict levels in soil and water
Concentrations indoors depend on construction site and building
materials
Highest levels occur in basements and on the ground floor
54
Radon is a radioactive gas that comes from the soil. Exposure to radon gas it the secondleading cause of lung cancer (after smoking) in the United States. About 14 000 adults die
each year in the USA 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
Indoor Air Pollution
RADON MITIGATION SYSTEM
A – GasGas-permeable layer
B - Plastic sheeting
C - Sealing and caulking
D - Vent pipe
E - Junction box
It is recommended that homes be
tested for radon on the lowest
livedlived-in level – basement or
ground floor
www.epa.gov/iaq/radon/construc.html
55
A.
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.
B.
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.
C.
Sealing and caulking. All openings in the concrete foundation floor are sealed to
reduce entry of soil gas into the home.
D.
Vent pipe. A 3- or 4-inch gas-tight or polyvinyl chloride (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.
E. 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.
Indoor Air Pollution
RADON IN SCHOOLS
www.epa.gov/radon/pubs/schoolrn.html
Schools should also be tested for radon:
Levels above 4 pCi/L call for action to reduce exposure
56
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
Indoor Air Pollution
ASBESTOS
Sources:
Used for insulation and as fire-retardant: asbestos cement, floor and roof tiles,
water pipes and others
Levels increase if asbestos-containing materials are damaged
Levels can be high in clothes of working parents
Health effects:
No acute toxicity
Asbestosis results from occupational exposure
Main risk for children: long-term exposure may cause cancer in adulthood
Malignant mesothelioma
Lung cancer
57
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:
•American Academy of Pediatrics Committee on Environmental Health. Pediatric
Environmental Health, 2nd ed. Etzel RA, Ed. Elk Grove Village, IL: American Academy of
Pediatrics, 2003.
Indoor Air Pollution
OCCUPATIONOCCUPATION-RELATED CONTAMINANTS
Parents “take home” exposures related to work:
Contaminated clothing, shoes and objects
Contaminated skin and exhaled breath
Empty containers (pesticide and others)
Children are directly exposed when:
Visiting parents’ workplaces
Participating in work
Prevention
Change work clothes and shower before hugging or playing
with children
58
Clothing contaminated with pesticides and other chemicals can be an important source of
exposure for children and a source of indoor air contamination. Exposures of family
members to pesticides have occurred from contact with contaminated skin, clothing or
shoes, contamination of the family car, and during visits to the workplace. Parents should
avoid hugging children or playing with them after coming home from work until they have
showered and changed their clothes.
Indoor Air Pollution
CHILDREN WORKING INDOORS
Child labour and adolescent work: exposure to
pesticides, solvents, cleaning agents and other
chemicals indoors
Young children employed illegally
Unregulated temporary work
School-based vocational training
Family businesses
Cottage industries
Indoor smoke from solid fuels (e.g. food stands)
Volunteer service projects
59
Children and adolescents are likely to work without proper training and protective equipment,
leading to their being exposed to dangerous products and pesticides, mainly when they are
being employed illegally or doing unregulated work.
Solvents and cleaning agents are important sources of exposure of employed adolescents.
Their workplaces include fast-food restaurants, automotive services, retail stores and others.
One of the most common types of exposure is to cleaning products containing ammonia or
other airway irritants. Other common sources of exposures include paints, glues and
solvents, caustic agents, hydrocarbons and bleach. Chemical burns have also been
reported.
Another group of adolescents or younger children who may suffer potentially hazardous
exposures to pesticides are the children of farm-workers working in the fields beside their
parents.
Indoor Air Pollution
SUMMARY SLIDE
HAZARDS:
Particulates,
CO, Solvents,
Pesticides,
Lead, moulds,
Mites, pollen
MEDIUM
Air
ACTIVITIES
Playing, Studying, Eating, Drinking, Working, Sleeping
SUSCEPTIBILITIES:
-Lungs still immature
-Higher breathing rate
-More time indoors
-Nutritional status
-Poverty
(photo credit US NIEHS CERHR logo)
SETTINGS:
-Home
-Child care
-School
-Workplace
Playground
Sports place
OUTCOME-EFFECTS:
- Acute poisonings
- Respiratory diseases
- Allergies
- Developmental
disturbances
- Cancer
60
Different hazards are presented by different settings and various children’s activities. The
effects of exposure are influenced by individual susceptibility which depends upon age,
developmental stage, and social support. Pollutants in the indoor environment are potentially
more hazardous to children than adults because their lungs are still growing and maturing;
younger children breathe more air than older children or adults; and they spend more time
indoors. All of these susceptibilities are modified by nutritional status and poverty.
Indoor Air Pollution
APPROACHES TO REDUCE INDOOR AIR POLLUTION
1. Eliminate or control the sources of pollution
Improved stoves
Clean fuels (kerosene, gas)
Venting stoves for cooking and heating
Regular maintenance of cooking, heating and cooling systems
Choose non-volatile, non-toxic building materials
Maintaining dry homes and schools
2. Ventilation – building design
Dilute and remove pollutants through ventilation with outdoor air
3. Air cleaning – NOT air fresheners!
Air filters and ionizers may remove some airborne particles
Gas adsorbing material is used to remove gaseous contaminants
61
It is always better to prevent rather than treat illness. To avoid problems due to indoor air
quality, the first approach is source reduction and elimination, and the second, proper
ventilation and maintenance of gas, oil and solid fuel cooking, heating and cooling systems.
Air cleaning is the least effective, and most expensive. Air fresheners, which contain
untested potentially harmful volatile organic compounds (VOCs), should not be used to cover
up stale air or unpleasant smells.
Ref:
•www.epa.gov/iaq/pubs/ozonegen.html
For more information on indoor air pollution, you can obtain a guide (Indoor pollution: An
introduction for health professionals) recently published by the US EPA at:
www.epa.gov/iedweb00/pubs/hpguide.html
Ref:
Meklin T et al. Effects of moisture-damage repairs on microbial exposure and symptoms in
schoolchildren. Indoor Air. 2005;15 Suppl 10:40-7.
Effects of renovation on symptom prevalence and microbial status were studied in two
moisture-damaged schools and in two non-damaged schools with longitudinal crosssectional surveys before and after repairs. Over 1300 schoolchildren aged 6-17 returned
questionnaires before and after repairs. After full renovation in one of the damaged schools,
elevated concentrations and increased frequencies of indoor air fungi normalized and a
significant decrease in the prevalence of 10 symptoms of 12 studied was observed among
schoolchildren. No change in microbial conditions was seen after partial repairs in the other
damaged school, and only slight improvement was observed in symptom prevalence. The
change in the prevalence of symptoms in the reference schools was minor. The results
suggest that increased symptom prevalence among schoolchildren in moisture-damaged
schools can be managed with proper repair of the moisture damage. PRACTICAL
IMPLICATIONS: This longitudinal intervention study showed the positive effects of the
moisture and mold damage repairs of a school building on children's health. The success
necessitates however, a thorough renovation including appropriate ventilation. Monitoring of
airborne viable microbes revealed the damage status of the building and thus could be used
Indoor Air Pollution
OZONE GENERATORS – CAUTION
Ozone can be harmful to health
Chest pain, coughing, throat irritation
Ozone is ineffective in controlling indoor air pollution
below health standards levels
NIOSH / OSHA recommends an upper limit of 0.10 ppm ozone
High concentrations are used to decontaminate
unoccupied spaces from chemical and biological
contaminants or odours
62
Ozone generators have become popular in some industrialized countries. Ozone is a molecule
composed of three atoms of oxygen. The third oxygen atom can detach from the ozone molecule, and
re-attach to molecules of other substances, thereby altering their chemical composition. Scientific
evidence shows that, at concentrations that do not exceed public health standards, ozone has little
potential to remove indoor air contaminants: there is no approval for its use in occupied spaces.
When inhaled, ozone can damage the lungs. Relatively small amounts can cause chest pain,
coughing, shortness of breath and throat irritation. Ozone may also exacerbate chronic respiratory
diseases such as asthma and compromise the ability of the body to fight respiratory infections. People
vary widely in their susceptibility to ozone.
Ozone has been extensively used for water purification, but ozone chemistry in water is not the same
as ozone chemistry in air. High concentrations of ozone in air, when people are not present, are
sometimes used to help decontaminate an unoccupied space from certain chemical or biological
contaminants or odors (e.g., fire restoration). However, little is known about the chemical by-products
left behind by these processes (Dunston et al, 1997). While high concentrations of ozone in air may
sometimes be appropriate in these circumstances, conditions should be sufficiently controlled to insure
that no person or pet becomes exposed. Ozone can adversely affect indoor plants, and damage
materials such as rubber, electrical wire coatings, and fabrics and art work containing susceptible dyes
and pigments (U.S. EPA, 1996a).
These notes are taken from the US EPA website www.epa.gov/iaq/pubs/ozonegen.html
Refs:
US EPA, Air Quality Criteria for Ozone and Related Photochemical Oxidants. Research Triangle Park,
NC: National Center for Environmental Assessment-RTP Office; report nos. EPA/600/P-93/004aF-cF,
3v. NTIS, Springfield, VA; PB-185582, PB96-185590 and PB96-185608. 1996
Dunston et al. A Preliminary Investigation of the Effects of Ozone on Post-Fire Volatile Organic
Compounds. Journal of Applied Fire Science, 1997, 6(3): 231.
Indoor Air Pollution
EDUCATION AND ADVOCACY
Education of:
Children
Family and community
Health care providers
Environment policypolicy-making
Framework Convention on Tobacco Control
Clean indoor air regulations
Community actions
Research
63
A multi-level approach to prevention of indoor air-related illness is required. Education,
policy-making and research all have roles to play.
<<READ SLIDE>>
<<NOTE TO USER: Insert appropriate suggestions for tackling the specific indoor air
problems in your area.>>
Refs:
Eriksen MP et al. The diffusion and impact of clean indoor air laws. Annu Rev Public Health.
2008;29:171-85.
Over the past quarter century, primarily as a result of scientific discovery, citizen advocacy,
and legislative action, comprehensive clean indoor air laws have spread rapidly throughout
the world. Laws that establish completely smoke-free indoor environments have many
relative advantages including being low cost, safe, effective, and easy to implement. The
diffusion of these laws has been associated with a dramatic and rapid reduction in population
levels of serum cotinine among nonsmokers and has also contributed to a reduction in
overall cigarette consumption among smokers, with no adverse economic impact, except to
the tobacco industry. Currently, nearly half of the U.S. population lives in jurisdictions with
some combination of completely smoke-free workplaces, restaurants, or bars. The diffusion
of clean indoor air laws is spreading rapidly throughout the world, stimulated by the first
global health treaty, the Framework Convention on Tobacco Control.
Indoor Air Pollution
CRITICAL ROLES OF HEALTH & ENVIRONMENT
PROFESSIONALS
Diagnose and treat
Do research and publish
• Detect sentinel cases
• Inspire community-based
interventions
WHO
Educate
• Patients and families
• Colleagues and students
Advocate
Provide good role model
64
Health and environment professionals have a critical role to play in maintaining and
stimulating changes that will ensure children's health through a clean indoor environment.
•At the patient level it is important to include indoor air as an environmental etiology or
trigger of respiratory disease and in the preventive advice. Are the signs and symptoms
possibly linked to air pollutant exposure? Are there any potential indoor sources of
exposure?
•Health care providers should be alert and detect the "sentinel" cases of indoor air pollutant
exposure. Their detection and study will be essential for developing, proposing and
supporting family and community-based interventions. Publication of cases and research
studies allows the communication of knowledge and experience that will benefit other
communities and countries.
•It is important to inform and educate patients, families, colleagues and students didactically,
on the possibility of exposure to indoor air pollutants and its potential impact in children. Also
on how to avoid exposure and provide clean air.
•Finally, we can become vigorous advocates for the protection of children's environments
and prevention of exposure to indoor air pollutants. It is important to promote the measures
that are crucial for eliminating or mitigating sources of exposure in children (and pregnant
women!).
•Professionals with understanding of both health and the environment are powerful role
models. Their choices and opinions with respect to air pollutants and other environmental
factors will be noticed by patients and communities.
Indoor Air Pollution
POINTS FOR DISCUSSION
65
<<NOTE TO USER: Add points for discussion according to the needs of your
audience.>>
Indoor Air Pollution
ACKNOWLEDGEMENTS
WHO is grateful to the US EPA Office of Children’
Children’s Health Protection for the financial support
that made this project possible and for some of the data, graphics
graphics and text used in preparing
these materials.
First draft prepared by Ligia Fruchtengarten MD (Brazil)
With the advice of the Working Group on Training Package for the Health Sector:
Cristina Alonzo MD (Uruguay); Yona Amitai MD MPH (Israel); Stephan BoeseO’Reilly MD MPH (Germany); Irena Buka MD (Canada); Lilian Corra MD (Argentina),
PhD (USA); Ruth A. Etzel MD PhD (USA); Amalia Laborde MD (Uruguay); Ligia
Fruchtengarten MD (Brazil); Leda Nemer TO (WHO/EURO); R. Romizzi MD (ISDE,
Italy); S. Borgo MD (ISDE, Italy).
Reviewers: S. Bhave MD (India); S. Boese-O’Reilly MD MPH (Germany); Y. Amitai MD
MPH (Israel), E. Rehfuess (WHO), I. Buka MD (Canada)
Reviewer 2008: Ruth A. Etzel, MD, PhD (USA)
Update: July 2008
WHO CEH Training Project Coordination: Jenny Pronczuk MD
Medical Consultant: Katherine M. Shea MD MPH, USA
Technical Assistance: Marie-Noel Bruné MSc.
66
Indoor Air Pollution
DISCLAIMER
The designations employed and the presentation of the material in
in this publication do not imply the expression of any
opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city
or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent
approximate border lines for which there may not yet be full agreement.
agreement.
The mention of specific companies or of certain manufacturers’
manufacturers’ products does not imply that they are endorsed or
recommended by the World Health Organization in preference to others
others of a similar nature that are not mentioned.
Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.
The opinions and conclusions expressed do not necessarily represent
represent the official position of the World Health
Organization.
This publication is being distributed without warranty of any kind,
kind, either express or implied. In no event shall the World
Health Organization be liable for damages, including any general,
general, special, incidental, or consequential damages, arising
out of the use of this publication
The contents of this training module are based upon references available
available in the published literature as of the last
update. Users are encouraged to search standard medical databases
databases for updates in the science for issues of particular
interest or sensitivity in their regions and areas of specific concern.
concern.
If users of this training module should find it necessary to make
make any modifications (abridgement, addition or deletion) to
the presentation, the adaptor shall be responsible for all modifications
modifications made. The World Health Organization disclaims
all responsibility for adaptations made by others. All modifications
modifications shall be clearly distinguished from the original WHO
material.
67
Fly UP