IISection
4.4 IndooR aIR pollutIon and health effeCts
where V is the volume of the room; C is the pollutant concentration in the room; CIN is the concentration entering the room; QIN is the airflow into the room; COUT is the concentration leaving the room; QOUT is the airflow leaving the room; S is the source term; and R is the removal term, which includes pollutant removal by using air cleaners and sinks.
From the well-mixed assumption, COUT equals C. The equation can be rewrit- ten as
IN IN OUT
dd .
V Ct =C Q −CQ + −S R (4.3)
This is the case with single compartment mass balance modeling (NRC, 1981).
It is applied to the spaces that are considered as well mixed at a given point of time and the pollutant concentration remains the same at all locations within the volume being modeled. Despite the widespread use of the well-mixed assumption, there is evidence that in many cases, indoor air concentrations are not spatially homoge- neous. Well-mixed models underestimate concentration near an emission source.
Recently developed models consider the “source proximate effect” (Furtaw et al., 1996), which is based on the premise that concentrations in proximity to the source are higher than those predicted by well-mixed models. Multicompartmental model- ing is the approach to modeling nonhomogeneous indoor air concentrations. This approach divides the space into two or more well-mixed zones that are connected by interzonal airflows (Furtaw et al., 1996). A compartment is defined as a region within which spatial variations in pollutant concentrations can be neglected over the timescale of interest. Depending on the ventilation conditions, a single room, a floor, or a whole building may be adequately approximated as a single compart- ment. However, if either sources or sinks are not uniformly distributed throughout the region of interest and the rate of mixing throughout the region of interest is low compared with characteristic residence time, then the single-compartment model may not provide an adequate description.
table 4.6 Indoor pollutants, their health effects, standards, and exposure limits pollutanthealth effects
limits epaoshaWho NO2Type: Immediate Causes: Irritation to the skin, eyes and throat, cough, etc.
0.09 mg/m3 (average over 1 year for 8 h exposure daily)9 mg/m3<0.19 mg/m3 COType: Immediate Causes: Headache, shortness of breath, higher concentration. May cause sudden death.
10 mg/m3 (average over 8 h period)55 mg/m3 (average over 8 h period)<2.0 mg/m3 CO2—9000 mg/m3— RSPMType: Cumulative Causes: Lung cancer0.15 mg/m3 (24 h average)5 mg/m3 (average over 8 h period)<0.01 mg/m3 SO2Type: Immediate Causes: lung disorders and shortness of breath0.13 mg/m3 (average over 1 year for 8 h exposure daily)13 mg/m3(average over 8 h period)<0.5 mg/m3 (short-term exposure) Radon Type: Cumulative Causes: Lung cancer4000 pCi/m3 of indoor air≈0.1 mg/m3— Formaldehyde Type: Immediate Causes: Irritation to the eyes, nose and throat, fatigue, headache, skin allergies, vomiting, etc.
0.12 mg/m3 (continuous exposure)3 mg/m3 (average over 8 h period)<0.06 mg/m3 (long-term and short-term exposure) Asbestos Type: Cumulative Causes: Lung cancer—200 fibers/m3 (8 h exposure period)≈0 fiber/m3 (long-term exposure) PesticidesType: Immediate Causes: Skin diseases——— O3Type: Immediate Causes: Eyes itch, burn, respiratory disorders, and lowers our resistance to colds and pneumonia.
—0.1 mg/m3 (continuous exposure)
<1800 mg/m3 Source:National Research Council. 1981. Indoor Pollutants. National Academy Press, USA.
whereas OSHA standards are for the occupants during their occupation. Quite recently, in 2003, the IAQ Management Group, Government of HKSAR, Hong Kong, gave the standards for “acceptable” IAQ for offices and public places, which are listed in Table 4.7.
The standards are prepared for 8-h exposure for both excellent class and good class IAQs. Exposure duration is of particular importance in assessing the IAQ exposures. In office buildings, exposure is generally 8–10 h a day, five days a week.
In residential structures, exposure may be up to 24 h a day, seven days a week. As some substances build up in the body over time, 24-h exposure may result in an accu- mulation of pollutants and their subsequent impact on health effects. Thus the impact of a given concentration of air contaminant is less in office buildings than in resi- dences. Other areas that should be considered to have potential long-duration expo- sures include hospital patient rooms, hotels, mental wards, and prison cells. Individual sensitivity contributes a huge variable to the combination of factors affecting the health of building occupants. Infants, elderly people, and sick people are the most vulnerable to the health effects of air contaminants. Immune suppressed individuals, for example, AIDS patients and organ transplant recipients, and patients of genetic diseases, for example, Lupus erythematosus, are particularly sensitive to common molds. Individuals who drink alcohol in excess are more susceptible to air contami- nants that may affect the liver. People with dry skin are more susceptible to further drying and skin penetration by chemicals and those who smoke tobacco products
table 4.7
standards for acceptable Indoor air quality
parameters unit
8-h average
excellent Class good Class
CO2 mg/m3 <1500 <1800
CO mg/m3 <2 <10
Respiratory suspended particulate (RSP) mg/m3 <0.02 <0.18
NO2 mg/m3 <0.04 <0.15
Ozone (O3) mg/m3 <0.05 <0.12
Formaldehyde (HCHO) mg/m3 <0.03 <0.1
Total VOC mg/m3 <0.2 <0.6
Radon (Rn) Bq/m3 <150 <200
Airborne bacteria Cfu/m3 <500 <1000
Room temperature °C 20 to <25.5 <25.5
Relative humidity % 40 to <70 <70
Air movement m/s <0.2 <0.3
Note: “Excellent” class represents an excellent IAQ that a high-class and comfortable building should have.
“Good” class represents IAQ that provides protection to the public at large including the very young and the aged.
have a diminished body defense mechanism (Kousa, 2001). There is consistent evidence that exposure to indoor air pollution increases the risk of pneumonia among children under five years and chronic respiratory disease and lung cancer (in relation to coal use) among adults over 30 years old. The evidence for a link with lung cancer from exposure to biomass smoke and for a link with asthma, cataracts, and tubercu- losis was considered moderate. On the basis of the limited available studies, there is tentative evidence for an association between indoor air pollution and adverse preg- nancy outcomes, in particular, low birth weight, or ischemic heart disease and nasopharyngeal and laryngeal cancers (Smith, 1999).
The health effects from indoor air pollutants fall into two categories: short-term (immediate and/or acute) effects and long-term (cumulative and/or chronic) effects.
Short-term effects may show up after a single exposure or repeated exposures. These include irritation of the eyes, nose, throat, and skin, headache, dizziness, and fatigue.
These are treatable if identified. Most of the immediate effects are similar to those from cold or other viral diseases, so it is often difficult to determine if the symptoms are a result of exposure to indoor air pollution. Therefore, it is important to pay atten- tion to the time and place where the symptoms occur. Cumulative effects occur only after long or repeated periods of exposure to pollutants.
Indoor air pollution has been associated with a wide range of health outcomes, and the evidence for these associations has been classified as strong, moderate, or tentative in a recent systematic review. Most of the air pollutants directly affect the respiratory and cardiovascular systems. Increased mortality, morbidity, and impaired pulmonary function have been associated with elevated levels of SO2, and SPM or RSPM. While the precise mechanism of how exposure causes disease is still unclear, it is known that small particles and several of the other pollutants contained in indoor smoke cause inflammation of the airways and lungs and impair the immune response.
Acute and subacute health effects of the inhalation of biomass smoke include con- junctivitis, acute respiratory irritation/inflammation, and acute respiratory infection (ARI). Chronic effects of the inhalation of biomass smoke are chronic obstructive pulmonary disease (COPD), chronic bronchitis, cor pulmonale, adverse reproductive outcomes and pregnancy-related problems, such as stillbirths and low birth weight, and lung cancer. The health risks associated with some of the key pollutants present in smoke and their mechanism are listed in Table 4.8.
One study in Western India found a 50% increase in stillbirths in women exposed to indoor smoke during pregnancy. Likewise, a study in Africa found that cooking with wood greatly increased the risk of stillbirth. Considerable amounts of carbon monoxide have been detected in the bloodstream of women cooking with biomass in India and Guatemala. Studies in India, Nepal, and Papua New Guinea show that nonsmoking women who have cooked on biomass stoves for many years exhibit a higher prevalence of chronic lung disease (asthma and chronic bronchitis). In Mexico, women exposed to wood smoke for many years faced 75 times more risk of acquir- ing chronic lung disease, about the level of risk that heavy cigarette smokers face, than women not exposed to wood smoke. One recent Colombian study found that women exposed to smoke during cooking were three times more likely to suffer from chronic lung diseases. Studies in South America and India have shown that exposure to indoor air pollution severely reduces lung function in children.
table 4.8 mechanisms by Which some Key pollutants in smoke from domestic sources may Increase the Risk of Respiratory and other health problems s. no.pollutantsmechanismpotential health effects 1.Particles (<10 µm, and particularly <2.5 µm aerodynamic diameter)• Acute bronchial irritaion, inflammation, and increased reactivity • Reduced mucociliary clearance • Reduced macrophage response and reduced immunity
• Wheezing, exacerbation of asthma • Respiratory infection • Chronic bronchitis and COPD 2.CO• Binding with hemoglobin to produce carboxyhemoglobin, which reduces oxygen delivery to key organs and developing fetus• Low birth weight (carboxyhemoglobin is 2–10% higher) • Increased perinatal deaths 3. NO2• Acute exposure increases bronchial reactivity • Long-term exposure increases susceptibility to bacterial and viral lung infections
• Wheezing, exacerbation of asthma • Respiratory infection • Reduced lung function in children 4. SO2• Acute exposure increases bronchial reactivity • Long term: Difficult to dissociate from effects of particulates• Wheezing, exacerbation of asthma • Exacerbation of COPD, cardiovascular disease 5. Biomass smoke condensates including polyaromatics and metal ions
• Absorption of toxins into lungs leading to oxidative changes• Cataract 6.Polyaromatic HCs (benzopyrene)• Carcinogenic• Lung cancer • Cancer of mouth, nasopharynx, and larynx Source:From Bruce, N., Padilla, R.P., and Albalak, R. 2000. Bulletin of WHO, 78(9), 1078–1092. With permission.
There is growing concern about the fact that exposure to second-hand tobacco smoke is a serious and substantial public health risk. Tobacco smoke contains over 3800 compounds, including VOCs, inorganic gases, and metals, many of which are carcinogenic or can promote the carcinogenic properties of other pollutants. Small children and infants raised in the presence of passive smoke are more prone to lower respiratory tract and inner ear infections.
The health effects of airborne particulates depend on several factors that include particle dimensions, durability, and dose. In some instances, very small exposures can cause adverse health effects (hazardous exposures), while other seemingly large exposures do not cause any adverse effects (nuisance exposures). The health risk from exposure to particulate air pollution obtained by applying the mean risk per unit ambient concentration is based on the results of some urban epidemiological studies (Smith, 1996). The range of risk was found to be 1.2–4.4% increased mortal- ity per 10 mg/m3 incremental increase in the concentration of respirable suspended particles (PM10).
The CO emission poses a serious health problem when biomass fuels are used.
Incomplete combustion of fuels produces CO. Smith (1991) estimated that about 38, 17, 5, and 2 g/meal CO is released during household cooking by using dung, crop residues, wood, and kerosene, respectively. During the use of liquid petroleum gas (LPG), a negligible amount of CO is released. A study by the National Institute of Occupational Health (NIOH), Ahmedabad, reported indoor air CO levels of 144, 156, 94, 108, and 14 mg/m3 air during cooking by using dung, wood, coal, kerosene, and LPG, respectively. The short-term health effects of CO exposure are dizziness, headache, nausea, feeling of weakness, and so on. It also results in systemic effects by reducing the oxygen-carrying capacity of the blood. The association between a long-term exposure to CO from cigarette smoke, on the one hand, and heart disease and fetal development, on the other, has been described by Wynder (1979).
The formaldehyde is well recognized to be an acute irritant and long-term expo- sure can cause a reduction in vital capacity and chronic bronchitis. The formalde- hyde is well known to form cross-links with biological macromolecules. Inhaled formaldehyde forms DNA and DNA–protein cross-links. The formaldehyde mean levels are found to be 670, 652, 109, 112, and 68 µg/m3 of air for cattle dung, wood, coal, kerosene, and LPG, respectively (Patel and Raiyani, 1995).
The adverse health effects caused by VOCs in nonindustrial indoor environments fall under three categories: (1) irritant effects, including perception of unpleasant odors, mucous membrane irritation, and exacerbation of asthma; (2) systematic effects, such as fatigue and difficulty in concentrating; and (3) toxic, chronic effects, such as carcinogenicity.
The bioaerosols—fungal spores, hyphae fragment, or metabolites—can cause a variety of respiratory diseases. These range from allergic diseases including allergic rhinitis and asthma to infectious diseases such as histoplasmosis, blastomycosis, and aspergillosis. Other than these major categories of illnesses, indoor air pollution is associated with blindness and changes in the immune system. Eighteen percent of blindness in India is attributed to the use of biomass fuels. Further, a 1995 study in Eastern India found the immune system of newborns to be depressed due to the presence of indoor air pollution.
4.4.1 diSproportionate impactSon cHildrenand women
Household energy practices vary widely around the world, as does the resultant death toll due to indoor air pollution. While more than two-thirds of indoor smoke- attributable deaths from acute lower respiratory infections in children occur in WHOE’s African and South East Asian Regions, over 50% of the COPD deaths due to indoor air pollution occur in the Western Pacific region. In most societies, women are in charge of cooking and—depending on the demands of the local cuisine—
they spend between 3 and 7 h per day near the stove preparing food. Thus 59% of all indoor air pollution-attributable deaths occur in females. Young children are often carried on their mother’s back or kept close to the warm hearth. Consequently, infants spend many hours breathing indoor smoke during their first year of life when their developing airways make them particularly vulnerable to hazardous pol- lutants. As a result, 56% of all indoor air pollution-attributable deaths occur in children under five years of age. In addition to the health burden, fuel collection can impose a serious time burden on women and children. Alleviating this work will free women’s time for productive endeavors and child care and can boost children’s school attendance and time for homework.
4.4.2 iaQ and HealtH effectS: indian eStimateS
In India, half a million deaths each year are attributed to indoor pollution from traditional biomass fuels. India and China together account for approximately 60%
of solid fuel using households in the developing world; this implies that, worldwide, about two million premature deaths each year could be attributed to household solid fuel use. Depending on the number of young children in total, indoor exposure would account for 4–6% of the global burden of disease. By comparison, urban air pollu- tion is estimated to be responsible for 1–2% of the global disease burden. These estimates would make the health impact of indoor exposure larger than the burden from all but two of the other major preventable risk factors that have been quantified:
malnutrition (15%) and lack of clean water and sanitation (7%). It surpasses the global burdens from sexually transmitted diseases, tobacco, illicit drugs, hyperten- sion, occupational hazards, alcohol, war, vehicle accidents, or homicide. It exceeds the global burden for many diseases except total ARIs, diarrhea, and the childhood cluster of vaccine-preventable diseases (measles, diphtheria, tetanus, polio, and per- tussis). If these estimates are accurate, the global burden of disease from indoor air pollution is larger than that for such well-known threats to human health as tuber- culosis, AIDS/HIV, malaria, heart disease, or cancer (Murray and Lopez, 1996).
ARI is the single largest disease category worldwide (about one-twelfth of the global disease burden); it accounts for about one-eighth of the disease burden in India. Odds ratio for young children: 2–3 (10 studies in developing countries).
Premature deaths: 290,000–410,000. COPDs such as chronic bronchitis account for about 1.5% of deaths among Indian women. Odds ratio for women cooking over biomass fires for 15 years: 2–4 (four studies in developing countries). Premature deaths: 19,000–34,000. Lung cancer in women is linked with cooking over open coal stoves; there is little evidence of a connection with biomass fuel. Odds ratio for
more than 20 Chinese studies: 3–5. Premature deaths: 400–800. Blindness is linked with the use of biomass fuels by women in India, which has the largest burden of blindness of any region of the world. Odds ratio for this group: 1.15–1.3. Blindness does not cause premature deaths, but puts a significant burden of disability.
Tuberculosis is responsible for 5% of the Indian burden of disease, a larger percent- age than in any other region. It causes premature deaths: 50,000–130,000. Perinatal effects (stillbirth; low birth weight; and death or illness during the first two weeks after birth) are responsible for 8.8% of the Indian burden of disease. But there is little evidence available to make estimates about premature deaths. Cardiovascular diseases (CVDs) and asthma are known to be related to outdoor air pollution and passive smoking in industrial countries but do not seem to have been studied in developing-country households (Smith, 1998).
The health bulletin of WHO has reported the results of studies conducted by Smith and Schwela on the number of deaths in developing and developed countries caused by indoor particle pollution for both the rural as well as urban population;
the results show that in rural households the particle pollution is responsible for 67–68% of the total deaths due to indoor particle pollution. This is due to the use of biomass fuel for cooking and heating purposes. A limited number of such studies has been done till now on the rural population of developing countries. Their results are shown in Table 4.9.