5
Building materials and furnishing
5.1 Introduction to building materials and furnishing as sources of indoor air pollution
The traditional design and construction of buildings is driven by functional, esthetic and economic values, but until recently little attention has been paid to the potential adverse health impact of indoor materials. This chapter describes how building materials and furniture partly determine indoor environmental conditions in homes and can be sources of emissions which may influence airways and respiratory health. Some of the available evidence comes from studies of other buildings such as office buildings, day-care centers and schools, but this evidence can be readily applied to homes.
The determinants of indoor air quality can be divided into (1) outdoor sources, (2) the building envelope, (3) occupants and their activities, (4) physical indoor sources and (5) heating, ventilating and air conditioning. Building materials and furnishing naturally represent potential physical indoor sources of gaseous and particulate air pollution, which may have direct health effects. However, all the other determinants, except outdoor sources, may play a role in human exposure from building materials and furnishing. The building envelope, including the structures, openings and the type of ventilation system, influences the elimination of air pollutants from building materials and furnishing. Occupant activities and heating, ventilating and air conditioning influence indoor temperature, relative humidity and air exchange, which modify the relations between emissions and human exposure. Indoor temperature, relative humidity and their variation influence the emission rates of pollutants and their elimination. Dampness in materials may lead to microbial growth and mold problems and some microbes produce volatile organic compounds (VOCs).
5.2 Emission of formaldehyde from building and interior surface materials
Formaldehyde (HCHO) is present in building materials (particleboard, fiber board and plywood), paintings and wall paints, glued wall papers, coatings, fabrics, fibers, draperies, carpets and insulation materials (Table 5.1). It is emitted more significantly from pressed wood products (particleboard, hardwood plywood panelling, medium density fiberboard) made using adhesives that contain urea-formaldehyde (UF) than those containing phenol-formaldehyde resins or conversion varnishes and latex paints. Experimental chamber studies have reported emission rates of different building materials including base coat floor finish (10, 800 μg/m2 h), pressed wood products (particleboard) (104-1580 μg/m2 h) and medium density fiber boards (210-264 μg/m2 h), most of which have been published by the WHO. Other sources of HCHO emissions include indoor ozone reactions with primary VOCs, or with fitted carpets or limonene, or with aliphatic hydrocarbons in photocopiers or laser printers. The first of these reactions is known experimentally to increase HCHO levels by a factor of 3.
Table 5.1 A summary of major chemical emissions from building materials and interior finishes and possible respiratory health effects Table 1 not mentioned?
| Building material and interior finishes source | Major chemical(s) emitted | Respiratory effects/symptoms |
| Textile wall materials | Naphthalene, methyl pyrrolidinone, styrene, aldehyde, phenol, formaldehyde, acrylonitrile, acetaldehyde, decane, tetradecane | Mucosal irritation, allergic reaction |
| Painted indoor surface (with water-based paints) | Propylene glycol, texanol, diethylene glycol monoethylene ether, diethyleneglycol monobutyl ether, dipropylene glycol monomethyl ether, ammonia, TXIBb, formaldehyde, butanol, aliphatic compounds (C8-C11) | Breathing difficulty, irritation of the eyes, nose and throat, nasal mucosal swelling, contact eczema, headache, wheezing, breathlessness,b asthma,b runny nose, hay fever |
| Painted indoor surfaces (with solvent-based paints) | Toluene, xylene, white spirit, isobutanole, trimethyl benzene, n-nonane, n-decane, n-undecane | Tiredness, eye irritation, nausea |
| PVC surface materials | Phthalate esters in dust (DEHP,b BBzPb), phthalate esters in air (DEHP, BBzP, DnBP), MEHP,a 2-butoxyethanol, 2-(2-butoxyethoxyl) ethanol, phenol, trimethyl benzene, TXIB, ammonia, acetic acid, hexanal, hexanoic acid, pentanoic acid, decane | Asthma,b allergic rhinitis,b eczema, wheezing, cough, phlegm, nasal congestion, bronchial hyper-reactivitya |
| Damp PVC flooring material | MEHP,a microbesb (Aspergillus veriscolor, Penicillium chrysogenum, Ulocladium botrytis, Fusarium culmorum, Cladosporium herbarum), MVOCsb (1-octen-3-ol, 2-ethyl-hexanol, dimethyl disulfide, 2-butanones, terpenes, 2-methyl furan, 3-methyl furan, 2-ethyl-1-hexanol, ammonia) | Eye,b noseb and throatb irritation, cough,b wheezing,b asthma,b tiredness, headache, airway infections,b bronchial hyperreactivitya |
| Damp interior finishes and building material like wall papers, woodchip etc. (excluding PVC materials) | Microbesb (A. veriscolor, P. chrysogenum, U. botrytis, F. culmorum, C. herbarum), MVOCsb (1-octen-3-ol, 2-ethyl- hexanol, dimethyl disulfide, 2-butanones, terpenes, 2-methyl furan, 3-methyl furan, 2-ethyl- 1-hexanol) | Eye,b noseb and throatb irritation, cough,b wheezing,b asthma,b tiredness, headache, airway infections |
| Particleboard panels, furniture, cabinetry, shelving, wooden house, newly built house | Formaldehyde,b limonene, acetaldehyde, hexanal, pentanal, butylacetate, cyclohexanone | Bronchial hyper-responsiveness, nose, throatb and eyeb irritation, asthmab |
| Carpets, new linoleum flooring, new synthetic carpeting, new carpets, wall-to-wall carpets | 4-Phenylcyclohexene, vinyl acetate, styrene, dodecanol, acetaldehyde, formaldehyde | Runny nose, allergic rhinitis, asthma, wheezing, bronchial hyper- responsivesness |
| Interior surface polished with oil-based varnishesc | Isobutanol, ethyl benzene, xylene, HCHOb | Eye,b noseb and throatb irritation, coughb |
Note: items in column 1 reported to possibly cause respiratory health effects in column 3.
aExpected respiratory health effects based on animal toxicity data.
bEmissions reported to possibly cause respiratory health effects.
cCould possibly cause respiratory health effects but nothing has been reported.
In a series of studies conducted in several European countries in the 1980s, HCHO concentrations between 72 and 3000 μg/m3 (0.06-2.50 ppm) were reported, with levels particularly high in houses containing particle board, UF insulation, glues for wall coverings or sealing-wax parquet flooring. Lower but significant concentrations have been reported more recently. For example, HCHO levels of <5-110 μg/m3 (0.004-0.090 ppm) were reported in selected Swedish homes, but in wooden houses, with wall-to-wall carpets and painted woods, the level of HCHO was above the Swedish limit value (100 μg/m3; 0.08 ppm). Lower concentrations (<3-72 μg/m3; 0.003-0.060 ppm) have also been noted in selected schools in Sweden and these were related to the fleece factor (area of fabrics in relation to room volume) and shelf factor (calculated as the length of open shelves in relation to room volume). Concentrations above 60 μg/m3 (>0.05 ppm) were also noted in newly painted living and bedrooms of children having new furniture and carpets as well as unflued gas heaters. In other studies the concentrations of HCHO were noted to decline with the age of the building [homes built in 2002, 123.5 ± 70 μg/m3 (0.10 ± 0.06 ppm), compared with those built in 1999 (83 ± 36 μg/m3 or 0.069 ± 0.03 ppm) and 1990-1998 (85 ± 21 μg/m3 or 0.07 ± 0.02 ppm)] and were higher in newly built houses containing computers and new furniture, and were significantly higher during summer than winter.
In some schools that continue to use particleboard panels in Eastern Europe, HCHO concentrations above the 1987 WHO threshold value (0.05 ppm; 60 μg/m3) have been reported. Formaldehyde concentrations of 34.4 ± 1.9 μg/m3 (0.03 ± 0.002 ppm) have also been measured in kitchens, living rooms and bedrooms in France, and these levels were associated with temperature and the age of the floor coverings.
Most people detect HCHO odour at concentrations of 49.1-490 μg/m3 (0.04-0.4 ppm). In the literature, upper airway irritation of the nose and throat is reported to occurred at concentrations in excess of 1227 μg/m3 (1.02 ppm) and lower airway effects characterized by cough, chest tightness and wheezing occurred at HCHO levels ≥2454 μg/m3 (≥2.05 ppm) [1].
In mobile homes where UF glued particle board had been used for indoor panelling, high prevalences of nose and throat irritation and severe headache and tiredness were noted. Wall-to-wall carpets were also related to nocturnal breathlessness in Swedish adult populations. Eye irritation, headaches, nose and throat irritation and wheezing were also reported among children exposed to new synthetic carpet, wall covering, particleboard and furniture and recent painting. Among 88 children (cases) and 104 controls in Australia, a 10 μg/m3 (8.33ppb) increase in HCHO levels in living rooms and children’s bedrooms was associated with a 3% increase in risk of asthma, and HCHO levels >60 μg/m3 (0.05 ppm) were also related to a 39% increased risk of asthma in other case children. Several studies have also found strong associations between mucous membrane irritation and other respiratory problems among home occupants exposed to urea-formaldehyde foam insulation (UFFI). UFFI was used for housing insulation but was banned in many developed countries in the 1980s; variable but small levels of HCHO continue to be emitted depending on the age of building.
5.3 Emissions of volatile organic compounds
There is no clear and widely acceptable definition for VOCs, but in the loose sense the term describes organic compounds with a boiling point range of 50-250° C (excluding pesticides) which would have an effect on air quality. The introduction of new building materials is changing the profile of VOC to include oxygenated compounds (e.g. carboxylic acids, alcohols, aldehyde and ketones) and chlorinated aromatic compounds of higher boiling points.
Building materials, especially surface materials used on walls, floors and ceilings and interior finishes such as furniture, cabinets, carpet tiles and ceiling tiles, are major sources of primary VOC emissions (Table 5.1). Secondary emissions of VOCs formed through mechanisms such as reactions between ozone and aliphatic hydrocarbons (in photocopiers and laser printers), reactions between ozone and fitted carpets or limonene, microbiological emissions on damped surfaces (MVOCs), hydrolysis of wet PVC flooring materials or degradation of building and interior surface materials are also known. The most frequently reported VOCs include ethanol, limonene, carbonyls (aldehydes and ketones), aliphatic, cylic and aromatic hydrocarbons, methylene chloride, terpenes, glycols, acids and esters with their individual concentrations varying from 5 to 50 μg/m3 (0.004-0.041 ppm), but higher concentrations have been found in newly built houses. Hodgson and Levin [2] for example, observed 3 times higher concentrations of acetaldehyde, propionaldehyde, benzaldehyde, α-pinene and D-limonene in newly built houses compared with existing houses. High concentrations of pentanal, α-pinene and D-limonene, 1,4-dichlorobenzene and dichloro-methane are also known in residential accommodations compared with offices because of the relatively large wood products to air volume ratio in the former. The total VOC (TVOC) concentrations measured in various dwellings in Europe are ≥250 μg/m3 (≥0.250 ppm) but lower concentrations are also known.
Composite wood products and related products used for cabinet making and subfloors also emit aldehydes, terpenes and acetic acids and esters. Oil-based varnishes used as finishes on interior walls and ceilings also emit isobutanol, ethyl benzene, m,p,o-xylene and formaldehyde.
Solvent-based paints with high VOC emissions are rapidly being replaced in developed countries by water-based substitutes with lower VOC emissions. The latter contain complex chemical compositions of butanols, 2,2,4-trimethyl-1,3-pentanediol diisobutyrate (TXIB), 2,2,4-trimethyl-1,3-pentanediol monobutyrate (texanol) and low concentrations of aliphatic hydrcarbons (C8-C11). In European studies the TVOC concentrations in dwellings with water-based paints have been around 413 μg/m3 (0.337 ppm). In one such study, TXIB was detected in 57% of living rooms and 60% of bedrooms. The maximum level of TXIB was about 373 μg/m3 (0.304 ppm) and that of tetanol was 50 μg/m3 (0.041 ppm). The indoor concentrations of the n-alkanes and butanol were 25 μg/m3 (0.020 ppm) and 10 μg/m3 (0.008 ppm), respectively, their concentrations being particularly high in newly built houses. Other studies have suggested that TXIB may have a strong affinity for dust particles and thus may interfere with the mucous membrane.
Low geometric mean concentrations of acetaldehyde (10.7 ± 1.8 μg/m3; 8.9 ± 1.5 ppb), propionaldehyde (6.0 ± 2.2 μg/m3; 5.0 ± 1.8 ppb), pentaldehyde (8.9 ± 2.7 μg/m3; 7.4 ± 2.3 ppb) and hexanal (25.5 ± 2.6 μg/m3; 21.3 ± 2.2 ppb) were reported in recently refurnished rooms and kitchens with wall and floor coverings. Emissions of 2-ethyl-hexanol from wet PVC floor materials are also known. The growth of microbes of various genera in damp building and interior surface materials produces over 200 VOCs of microbial origin (MVOCs), but the most commonly reported of these include hydrocarbons (e.g. octane), alcohols (e.g. 2-methyl-1-propanol), sulfur compounds (e.g. dimethyl disulfide), ketones (e.g. 2-butanones), terpenes and terpene derivatives (e.g. geosmin), 2-methyl furan and 3-methyl furan. MVOC levels of 15-20 ng/m3 (0.012-0.016 ppb) have been reported, but concentrations of 423 ng/m3 (0.350 ppb) are also known.
VOCs may affect the airways and induce inflammation and airway obstruction. VOC from water-based paint was shown to increase the prevalence of asthma 2-fold in Swedish healthy adults. Work-related symptoms of eye irritation, cough with sputum and itchy hands are common among users of water-based paints. Wheezing, asthmatic and respiratory symptoms are also known effects among users of solventbased paints, but among indoor occupants newly painted surfaces were associated with asthma and allergic symptoms. Measured concentrations of texanol (0.89 μg/m3; 0.70 ppb), TXIB (1.64 μg/m3) and MVOC (423 ng/m3; 0.350 ppb) were also related to nocturnal breathlessness and doctor-diagnosed asthma in 1014 pupils. Although this evidence is from observational studies, intervention studies have also suggested that wet PVC flooring, moist building problem and microbe growth on interior finishes and building material could also cause asthma in both children and adult populations.
5.4 Emission of phthalates from PVC building and interior surface materials
Polyvinyl chloride (PVC) is a polymer and a major building material in which phthalates are used extensively as plasticizers to enhance its flexibility, viscosity, stability and other desirable physical properties. Plasticized PVC is used extensively indoors as wall and flooring coverings in kitchens, bathrooms and children’s playrooms and bedrooms because it is inexpensive and has easy-to-clean surfaces. Other indoor uses of plasticized PVC include roofing materials, shower curtains, electric cables, adhesives, synthetic leather, and so on. Because phthalate esters are not covalently bonded to the polymer with which they are mixed, they can migrate from PVC material and adhere to the surfaces of indoor particulate matter (PM) as well as house dust. Phthalate may also migrate to PM surfaces following wear and tear of PVC materials or during the use of other PVC products such as nail polishes.
Di-ethyl-hexyl phthalate (DEHP) is the main phthalate ester found in house dust in a concentration range of 0.24-0.94 mg/g dust, but concentrations of other phthalates such as di-n-butyl phthalate (DPB) (0.13-0.69 mg/g dust) and n-butyl benzyl phthalate (BBzP) (0.22-0.75 mg/g dust) have been reported. In a nested case-control study, the mean geometric concentrations of BBzP were 0.237-0.224 mg/g dust and that of DEHP was 0.966 mg/g dust. BBzP was mostly emitted from PVC flooring material, whereas DEHP concentration was a result of emissions from PVC flooring in older buildings. These findings confirmed the results of an earlier study in which the indoor concentration of BBzP (0.208 mg/g dust) and DEHP (0.638 mg/g dust) was related to PVC flooring in children’s room.
Several studies have measured urinary concentrations of phthalates and other biomarkers to understand the pharmacokinetics of individual phthalates or the extent of exposure to phthalates in a given population. In a new study in a population at Erlangen, Germany, 10% of the population had DEHP concentration levels above the tolerable daily intake (TDI) acceptable in the EU (37 μg/kg body weight/day) and 31% had values higher than the reference dose (RfD) of the US Environmental Protection Agency (20 μg/kg body weight/day). In a Japanese study phthalate esters were measured in kitchens of newly built houses. The levels of DEHP and particularly DBP were surprisingly high (6.18 mg/g dust). These concentrations were attributed to vinyl cloth used as ceiling coverings and vinyl paints. The authors suggested that exposure to phthalate esters through inhalation (7.8-15 μg/day) indoors is as important as ingested phthalate exposure in Japan (14.3 μg/day).
Evidence of human hazards associated with phthalate exposure is very limited and most reports in the literature are based on animal studies. There is evidence of adverse effects such as increased weight, elevated enzyme levels and tumour development in rodents following administration of phthalates. Mono-2-ethylhexyl phthalate (MEPH) may modulate the immune response to allergen exposure in mice. At concentrations of 30 μg/m3 (0.024 ppm), calculated to be below the estimated level of human exposure to indoor MEHP, no effect was observed, as evident in a recent review of 14 animal laboratory studies. In a recent systematic review and meta-analysis based on 27 studies, the risk of asthma and respiratory symptoms in the adult population was related to fumes emitted from PVC films in occupational settings. In the same review, the relation between PVC surface materials indoors and the risk of asthma (OR = 1.55) and allergies was elevated (OR = 1.33) among children. Scandinavian, German and Bulgarian studies have noted BBzP in house dust (from indoor PVC material) and this was associated with rhinitis and eczema, whereas DEHP was related to asthma. In other studies the presence of both moisture and wet PVC flooring material was significantly related to asthma and this was attributed to mono (2-ethylhexyl) phthalate (MEHP), a product of the primary hydrolysis of DEHP.
5.5 Damp buildings and emissions of biological particles
Damp or moisture accumulates in building structures and/or interior finishes via leaks in roofs, windows or pipes; moisture from the ground penetrates into the building structure by capillary movement; moisture is created by humans and indoor activities such as cooking, bathing, respiration, humidifiers; and moisture may already be present in the building material from the time of construction. Damp may stimulate growth of microbes such as fungi, bacteria and in other situations protozoa, nematodes, mites and insects on material surfaces, thus defacing them and sometimes compromising the integrity of the material. Emissions of irritants and odorous substances from microbiological and chemical processes, e.g. HCHO and 2-ethyl-1-hexyl-hexanol, on building structures and interior finishes following dampness are known. The minimal water activity to support fungi growth is 0.67-0.75. Equilibrium relative humidity, temperature and pH are also in the ranges 0.70-0.90, 8-60 C and 2-11, respectively.
Several studies conducted in different parts of the world have shown that Aspergillus versicolor, Penicillum brevicompactum, P. chrysogenum and Cladosporum spp. are the most dominant species found on indoor surface materials and indoor ambient air. In wet rooms like bathrooms and kitchens (especially areas around the sink) Aureobasidium pullulans and Phoma exigua, Alternaria alternate, Cladosporium herbarum, C. sphaerospermum, Fusarium spp. and yeast have been identified on tiles, plasters and silicon caulking. Moist or damaged wallpapers such as woodchip, vinyl wallpapers, jute and cardboard containing cellulose may also support Acremonium strictum, Aspergillus niger, A. versicolor, Cladosporium herbarum, C. sphaerospermum, Epicoccum and yeast species. Stachybotrys chartarum, Aspergillus versicolo, Penicillum spinulosum and Streptomyces californicus have also been shown to grow on interior plasterboards at relative humidity 0.86-0.97. Some evidence exists that under limited nutrient conditions, some bacteria or fungi such as Streptomyces californicus can survive on the starch in plasterboards.
Under favorable conditions microbes may produce mycotoxins such as alternariols, chaetoglobosin, mycophenolic acid, satratoxin and sterigmatocystins – each with potential dermatoxic, immunosuppressive and carcinogenic effects. Biologically active nonallergenic compounds, spores and cellular debris may also be liberated, e.g. during microbiological activity on damp surfaces, which could stay longer in the air traveling through roofs, crevices and tiny cracks. The tiny fragments and spores could be carried by ultrasize particles and may enter the alveolar region when inhaled.
The first signs of dampness on interior surfaces includes visible molds, damp stains, condensation on window panes and/or walls and moldy and musty smells. Early symptoms in indoor occupants such as tiredness and complaints of cold and other allergic symptoms such as eye, nose and throat problems have also been reported. There has been a series of reviews by various multidisciplinary groups in the US and Europe on this subject. The earlier review by the Nordic group of researchers (NORDDAMP) provided strong evidence that damp in buildings increases the risk of cough, wheeze and asthma and the effect estimates were in the range (ORs) 1.4-2.2, but the strength of association for symptoms such as tiredness, headache and airway infections was weak. These authors suggested that there exists a causal association between damp in building and adverse airway health effects. In the second review by a European group (EURO-EXPO), which also included some members of the previous review, dampness in buildings and interior surfaces was related to health effects in non-atopics and atopics, but the causative agents, such as microbiological agents and organic chemicals from degraded building materials, were not conclusively identified. Moisture and microorganisms in buildings may affect health of indoor occupants through any one or more of the following ways: (i) allergic reactions (sensitization and immune response, i.e. asthma, allergic rhinitis or hypersensitivity reactions); (ii) infections (i.e. growth of the fungus in or on the body); and (iii) toxic responses. In a recent meta-analysis by Fisk and colleagues [3], a summary OR of 1.34-1.75 for several respiratory health problems was associated with building and indoor interior surface dampness and moldy conditions. About 30-50% of the increase in a variety of respiratory and asthma-related health problems were associated with building material damp or mold problems.
5.6 Specific diseases associated with exposures from building materials and furnishing
Chemical and biological emissions from building materials may contain specific compounds which can cause the onset of new asthma as well as asthma-related symptoms among subjects who already have asthma. There is also some evidence that the risk of allergic rhinitis is related to emissions from building materials. Asthma is characterized by airway inflammation and airway obstruction, which is reversible either spontaneously or with treatment, and increased airways responsiveness to a variety of stimuli. The main mechanisms in its etiology are specific sensitisation involving type I immune reactions and inflammatory processes. In principle, dust particles from textile surface and furnishing materials could serve as specific allergens and contribute to the etiology of asthma, but to our knowledge no such cases have been reported. Long-term low-level exposure to formaldehyde has been shown to increase the risk of asthma. Fortunately the use of formaldehyde in particle boards and furniture has decreased dramatically since the 1970s. There is accumulating evidence that semi-volatile phthalates from PVC surface materials may increase the risk of asthma. A recent systematic review and meta-analysis by Jaakkola and Knight reported that results from epidemiologic studies provide consistent support. In addition, damp PVC materials may lead to degradation and emission of materials such as 2-ethyl-hexanol, which may contribute towards the risk of asthma. Finally, damp materials may promote microbial growth.
5.7 Diagnosis and management issues
Diagnostic practice characteristic of occupational medicine can be applied to environmentally caused or environmental-related respiratory diseases. The following four areas of approach are applicable when suspecting indoor environmental causes: (1) a detailed history including both environmental and occupational exposures; (2) thorough physical examination; (3) pulmonary function testing; and (4) allergy testing.
When examining a patient with new-onset asthma, special emphasis should be paid not only to existing exposures but also to recent changes in the home or work environment. A move to a new home or recent refurbishment during the past 1-2 years may have produced new, intensive exposures. New houses or apartments with synthetic materials, large painted surfaces and new furnishing and textiles may contain substantial sources of volatile organic compounds and phthalates whose emission rates are highest when the first occupants arrive. Refurbishment may include installation of new surface material, painting of large surfaces, use of various glues and putties and the opening of roofs, floors or ventilation ducts, which may contribute many types of potential respiratory sensitizers and irritants. Furthermore, changes in heating, ventilating and air conditioning systems may be directly or more often indirectly related to increase in exposures and their respiratory effects. In particular, a decrease in air changes will increase the concentration of all indoor airborne air pollutants. The start of use of heating systems after the summer or hot season may also introduce changes which may trigger asthmatic symptoms.
The diagnosis of environmental asthma is based on both the report of intermittent respiratory symptoms and evidence of variable airway obstruction. Typical symptoms include wheezing, cough, phlegm, shortness of breath and chest tightness, and repeated bronchitis episodes. Symptoms in the eyes and upper respiratory tract may occur concomitantly with asthma-like symptoms when related to environmental factors. The relation of asthma to the home environment may follow several patterns: symptoms occur only at home, symptoms improve when away from home and symptoms improve after changing the home environment. Naturally the work environment may also contain exposures responsible for symptoms and/or the initiation of asthma and should receive systematic attention. With persistent exposure the symptoms may become chronic and any obvious time-relation to the home environment may be lost.
Intermittent and home-related respiratory symptoms among other family members may also offer a clue to the role of building materials and furnishing as a cause of asthma or allergic rhinitis. Detection of wheezing on chest auscultation will be a helpful indicator of asthma, expiratory wheezing being typical. However, auscultation is frequently normal in mild asthma, being present only during respiratory infections or special exposure periods, e.g. the pollen season. Examination of the heart, upper airways and skin should also be included. Blocked nose and redness of eyes indicate allergic rhinitis and conjunctivitis. Dry, itchy eczema will indicate an atopic propensity.
Spirometry for forced expiratory volume in one second (FEV1) and forced ventilatory capacity (FVC) are the best methods for assessing bronchial obstruction. Serial recording of peak expiratory flow (PEF) over periods of days or weeks is the best way to document whether home or work environment plays a role in the etiology of asthma or symptoms. Pocket-size spirometers can similarly be used in serial measurements. A 20% or greater diurnal variation in PEF or FEV1 indicates asthma and repeated declines in lung function when at home provide strong evidence of the role of the home environment. Serial PEF measurements have become routine in diagnosis and treatment of occupational asthma, but they can be as beneficial in identifying causes of bronchial obstruction in the home or other microenvironments. The measurements should be conducted preferably four but at least twice a day. Allergy tests are useful in the early phase of asthma, because they may reveal important triggers of asthma and allergic rhinitis. Skin prick tests and allergen-specific IgE antibodies in serum are informative in assessing the role of specific inhalation allergen occurring in indoor and outdoor environments.
Expert assessment of home environment for potential causes and triggers of asthma would be useful in both diagnosis and treatment of environmental asthma, but these types of services are not yet part of routine clinical practice.
Removal of hypothesized causal agents is the best treatment. This can be achieved by removing suspicious building materials or furnishing from the home of the asthmatic or individual with home-related asthma-like symptoms. Sometimes moving to another home is the best solution. Drug treatment follows the usual pattern of asthma treatment.
The most efficient means of primary prevention is through architecture and building engineering and the use of building materials with low chemical emissions is an important part of environmental management. Several macro-scale activities are likely to reduce population exposure from material emissions. Producers of building materials should develop and produce materials with lower emissions. Testing of new materials entering the market is a critical point, but can be difficult, because the amount of surface material used can vary in different microenvironments and emission rates depend on air change, temperature humidity and building structures. Special emphasis should be paid to materials covering large surfaces, such as walls and floors. Consumers should be informed about the emission rates of different materials and educated to demand ‘healthy’ materials, probably the most efficient way to influence the market. Classification of materials, paints and chemical would help consumers to choose their products and guide both builders and manufacturers. Finally the maintenance of buildings and heating, ventilation and air conditioning practices are important in the primary prevention of the harmful effects of emissions from building materials and furnishing.
References
1. Paustenbach, D., Alarie, Y., Kulle, T. et al. (1997) A recommended occupational exposure limit for formaldehyde based on irritation. J. Toxicol. Environ. Health 50(3): 217-263.
2. Hodgson AT, Bea J, McIlvaine JE. (2002) Sources of formaldehyde, other aldehydes and terpenes in a new manufactured house. Indoor Air 12: 235-242.
3. Fisk, W.J., Lei-Gomez, Q., Mendell, M.J. (2007) Meta-analyses of the associations of respiratory health effects with dampness and mold in homes. Indoor Air 17(4): 284-296.
Further reading
Afshari, A., Gunnarsen, L., Clausen, P.A. et al. (2004) Emission of phthalates from PVC and other materials. Indoor Air 14(2): 120-128.
Bornehag, C.G., Blomquist, G., Gyntelberg, F., Jarvholm, B., Malmberg, P., Nordvall, L., Nielsen, A., Pershagen, G., Sundell, J. (2001) Dampness in buildings and health. Nordic interdisciplinary review of the scientific evidence on associations between exposure to “dampness” in buildings and health effects (NORDDAMP). Indoor Air 11(2): 72-86.
Bornehag, C.G., Sundell, J., Bonini, S., Custovic, A., Malmberg, P., Skerfving, S., Sigsgaard, T., Verhoeff, A. (2004) EUROEXPO. Dampness in buildings as a risk factor for health effects, EUROEXPO: a multidisciplinary review of the literature (1998-2000) on dampness and mite exposure in buildings and health effects. Indoor Air 14(4): 243-257.
Bornehag, C.G., Sundell, J., Weschler, C.J. et al. (2004) The association between asthma and allergic symptoms in children and phthalates in house dust: a nested case-control study. Environ. Health Perspect. 112(14): 1393-1397.
Bornehag, C.G., Lundgren, B., Weschler, C.J. et al. (2005) Phthalates in indoor dust and their association with building characteristics. Environ. Health Perspect. 113(10): 1399-1404.
Brown, V.M., Crump, D.R., Mann, H.S. (1995) Concentrations of volatile organic compounds and formaldehyde in five UK homes over a three year period. In J.J. Knight and R. Perry (eds), Volatile Organic Compounds in the Environment (pp. 289-301). Indoor Air International: London.
COST Project 613. (1989) Formaldehyde emissions from wood based materials: guideline for the establishment of steady state concentrations in test chambers. Report No. 2. Prepared by Working Group 3 on behalf of the Community-COST Concertation Committee. Commission of the European Communities, Directorate-General for Science, Research and Development, Joint Research Centre, Ispra Establishment. EUR 121 96 EN.
Hansen, M.K., Larsen, M., Cohr, K.H. (1987) Waterborne paints. A review of their chemistry and toxicology and the results of determinations made during their use. Scand. J. Work. Environ. Hlth 13(6): 473-485.
Institute of Occupational Medicine (2004) Damp Indoor Spaces and Health. National Academy Press: Washington, DC.
Jaakkola, M.S., Jaakkola, J.J.K. (2004) Indoor molds and asthma in adults. Adv. Appl. Microbiol. 55: 309-338.
Jaakkola, J.J.K., Knight, T. (2008) The role of exposure to di(2-ethylhexyl) phthalate in the development of asthma and allergies. Environ. Hlth Perspect. 116: 845-853.
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