State of knowledge report
Environment Australia, 2001
ISBN 0 6425 4739 4
Part B: Indoor air quality (continued)
This section has drawn information from a number of key sources, particularly Brown (1997) and DHAC (2000).
Sources of indoor air pollutants include building operations and construction materials, household products, external factors and various human indoor activities. Table 7.1 identifies potential indoor pollutant sources and the range of pollutants that have been associated with these sources.
The following sections discuss some of the main indoor air pollutants under the following headings:
- criteria pollutants
- noncriteria pollutants
- biological contaminants.
These groupings have been made for convenience because of the wide range of pollutants covered. The order of the pollutants is not intended to convey their respective importance and impact on indoor air quality.
Table 7.2 summarises the main indoor air pollutants, their important sources and typical concentration ranges, as well as some possible responses.
In 1989, the NHMRC recommended that ambient (outdoor) air quality goals should also apply to the indoor environment. The national ambient air quality standards for the criteria pollutants, which have been defined by the NEPC, are detailed in Appendix D. The NHMRC recommendation was based on the simple premise that the adverse health effects of air pollutants will be the same whether the exposure occurs indoors or outdoors. The health effects of exposure to pollutants are shown in Section 6.3.
The State of the Environment report (DEST 1996) noted that the concentrations of the major indoor air pollutants can exceed the levels detected in the ambient environment. Levels of nitrogen dioxide, for example, can be up to an order of magnitude greater in the indoor environment than in outdoor air.
|Factors influencing indoor air quality Building operation and activity||Potentially emitted pollutant|
|Cigarette smoke (environmental tobacco smoke)||Respirable suspended particles, PAHs,benzene (See also Table 1.7)|
|Water cooling towers||Legionella|
|Human breath||Ethanol, methanol, carbon dioxide|
|Chlorinated water supplies used in washing activities||Chloroform|
|Petrol or car exhaust vapour entering building air from attached garages||Benzene, carbon monoxide, VOCs|
|Fuel-based heating and cooking appliances, especially if unflued||Butane, carbon monoxide, limonene, n-hexane, propane, respirable suspended particles, acrolein, NOx, formaldehyde|
|Construction products (wet)|
|Adhesives and sealants||Acetone, ethanol, formaldehyde, methanol, VOCs|
|Timber stains, paints, coatings||Ethanol, methanol, methyl chloroform, xylene, toluene, VOCs, lead|
|Polyurethane lacquer/floor varnish, including those used on concrete||Acetone, benzene, xylene, toluene, isobutyraldehyde|
|Construction products (dry)|
|Plastic and rubber flooring and carpet underlay||VOCs|
|Carpet||Dust mites, 4-vinylcyclohexene|
|Friable products||Asbestos, fibreglass|
|Furniture||Dust mites, VOCs, formaldehyde|
|Office equipment||Ozone, VOCs, respirable suspended particles|
|Drycleaned clothing||Methyl chloroform, tetrachloroethylene|
|Printed material||Formaldehyde, nonanal, toluene|
|Waxes and polishes||VOCs|
|Cleaners, disinfectants and detergents||Benzene, butane, ethanol, toluene formaldehyde, limonene, methanol,|
|Cosmetics||Ethanol, methanol, nonanal|
|Soil and rocks in the building site||Radon|
|Infiltration from outdoor environment||Sulfur dioxide, ozone|
PAH = polycyclic aromatic hydrocarbon;
VOC = volatile organic compound.
Source: Adapted from Brown (1996b), US EPA (Targeting Indoor Pollution, available at www.epa.gov/iaq/ ) and ANZEC (1990).
|Pollutanta||Typical concentration||Major source||Responsesb|
|Asbestos fibres||<0.002 fibres per mL||Friable asbestos products||Risk management, removal|
|Synthetic mineral fibres||Not characterised||Insulation products||Unknown|
|Radon||< 200 Bq/m³ per year (the NHMRC2 guidelinec) found 99.9% of time in conventional homes
< 200 Bq/m<³ per year found 91% of time in earth-constructed homes
|Soil under building earth walls||Siting of building, improved underfloor ventilation, material selection|
|Environmental tobacco smoke (ETS) and respirable suspended particles||High in recreational buildings, poorly characterised||Smoking (for ETS), cooking fuel combustion||Prohibition, well-ventilated designated smoking areas, education, improved ventilation|
|Legionella spp||30% of population potentially exposed||Water cooling towers||Maintenance, siting, regulation|
|House dust mites||10–40 µg of mite allergen marker protein per gram of dust in coastal areas||Bedding, carpet, furniture||Removal/control of habitat (humidity control)|
|Microbial||Range from hundreds of colony-forming units/m³ to 18 000 colony forming units/m³||Moist/damp surfaces||Control of moisture/ mould|
|Formaldehyde||< 100 ppb (the NHMRC2 guidelinec) in conventional homes
100–1000 ppb in mobile buildings
|Pressed-wood products||Source emission control, ventilation|
|Volatile organic compounds||Poorly characterised||Wet synthetic materials||Source emission control|
|Pesticides||Median value < 5 mg/m³ (limited data)||Pest control||Floor structure, inspection, clean-up, protocols for safe application|
|Nitrogen dioxide||Up to 1 ppm||Unflued gas heaters||Source emission control, flued systems, improved ventilation|
|Carbon monoxide||About 10% exceed 9 ppm (the NHMRC2 guidelinec)||Incomplete combustion||As for nitrogen dioxide above|
|Carbon dioxide||Poorly characterised||Exhaled air||Outdoor air ventilation|
|Lead||Poorly characterised||Lead paint, the fallout of accumulated roof space dust||Clean-up, education|
|Ozone||Poorly characterised||Some office equipment||Source emission control, ventilation|
a Note that no order of priority is implied in the listing of pollutants.
b In contrast to ambient (outdoor) environments, no regulations have been developed specifically for indoors except for workplaces.
c See Appendix D.
Source: DEST (1996).
NO2 is an oxidising gas. Exposure to high enough levels can lead to irritation of the eyes, nose, throat and lungs. The gas is primarily deposited in the large and small airways of the lung and can cause lung damage at high concentrations. There is no NHMRC indoor air goal for NO2, which occurs in building air due to indoor combustion sources. High concentrations have been found in buildings where unflued gas heaters have been widely used.
J. Ciuk, R.E. Volkmer and J.W. Edwards, (2000), 'Domestic nitrogen oxide exposure, urinary nitrate and asthma prevalence in preschool children' have examined the association between domestic exposure to nitrogen dioxide (NO2) and asthma prevalence. They discussed a South Australian preschool study carried out in 1993, which showed that respiratory symptom prevalence was significantly associated with the use of unflued natural gas appliances for cooking and heating. The results indicated that NO2 concentrations much higher in homes with natural gas appliances than other types of appliances (electric, solid fuel). Higher prevalence of asthma and respiratory symptoms was associated with higher levels of NO2 in the home. NO2 levels were lower in summer than in other seasons and higher in kitchens than bedrooms. The study concluded that there was a positive association between NO2 exposure from gas appliances and the prevalence of respiratory symptoms.
Most measurements of NO2 in Australia have been made in New South Wales, where unflued natural gas space heaters are widely used without restriction. In a 1992 winter NO2 survey of 195 dwellings that used unflued gas heaters in Sydney, Adelaide and Perth (Lyall 1993), 20% of the Sydney homes were found to exceed 300 ppb. This was similar to the findings of Ferrari et al (1998). However, only 4–5% of Adelaide and Perth dwellings exceeded this level, perhaps reflecting heater size limitations and the requirement for fixed wall vents for the latter). NO2 concentrations were 200 ppb (range 30–830 ppb) for Sydney, 100 ppb (range 0–340 ppb) for Adelaide and 100 ppb (range 30–600 ppb) for Perth. Evaluation of the 21 Sydney dwellings that exceeded 300 ppb found that servicing radiant heaters and modifying convection heaters could reduce concentrations, although not to levels much below 300 ppb.
A 1989 investigation of over 700 New South Wales school-rooms with unflued gas heaters (most with a window or door open) found average concentrations of 145 ppb. Nearly one-quarter (23%) of cases exceeded 160 ppb and 7% exceeded 300 ppb (McPhail and Betts 1992). The major factors affecting the observed concentrations were gas leaks in the heaters (causing greater NO2 production) and room ventilation rates. In some trials, creating cross-ventilation by opening windows and doors reduced concentrations from 1000 ppb to 300 ppb, but such an approach may not be practicable in winter. Riley (ACT Government Analytical Laboratory, personal communication) reported that NO2 concentrations in ACT schools with unflued gas heaters ranged from 20 to 200 ppb.
In response to these findings, in 1990 the New South Wales Department of School Education began a major program to rectify gas leaks in all schools and to introduce heaters (still unflued) producing low levels of nitrogen oxides. McPhail and Betts (1992) reported that NO2 concentrations in 2645 rooms with conventional unflued heaters exceeded 100 ppb in 20% of cases and 300 ppb in 2.5% of cases; for 437 rooms with heaters producing low levels of oxides of nitrogen, the equivalent figures were 7.6% and 0%, respectively. This program in New South Wales’ schools is ongoing. All heaters found to cause NO2 concentrations above 300 ppb and heaters in colder areas of the State have been replaced with heaters producing low levels of oxides of nitrogen. The intention is to eventually replace all unflued gas convection heaters.
Between 1990 and 1994, the program measured NO2 concentrations in schoolrooms containing a total of 14 000 unflued gas convection heaters and found the median concentration to be 50 ppb, with 11% exceeding 160 ppb and 3% exceeding 300 ppb. (Note that these measurements were subsequent to the gas leak rectification and heater maintenance program for all New South Wales public schools and an Education Department directive requiring windows to be opened while heaters were operating. This may explain why the concentrations are significantly lower than those measured in 1989 by McPhail and Betts.) In the same period, schoolrooms with 519 heaters producing low levels of oxides of nitrogen (often two to a room) exhibited a median concentration of 40 ppb, with 4% of measurements exceeding 160 ppb and 0.5% exceeding 300 ppb. All low-NOx heaters were fuelled by LPG; preliminary investigation by New South Wales Public Works indicated that some supplies had a nonpropane content that caused high NO2 emissions.
CO disrupts the blood’s ability to carry oxygen; asphyxia can result if people are exposed to it at high enough levels for long enough durations. Other symptoms include headaches, confusion and collapse. The NHMRC2 indoor air goal concentration for carbon monoxide is 9 ppm (eight-hour average).
Carbon monoxide concentrations have been measured in Australian dwellings with unflued gas heaters, but the proportion exceeding the NHMRC indoor air goal is not known. Concentrations in other buildings have received little investigation; this inadequacy should be addressed for enclosed carparks and adjacent areas, which overseas research has shown may experience high concentrations.
Carbon monoxide is produced indoors primarily by fuel combustion (eg gas or wood-burning appliances, car exhausts) or infiltration of polluted outdoor air. Indoor carbon monoxide concentrations are expected to generally follow outdoor levels except where combustion occurs in buildings without full venting. Very high indoor residential concentrations have been measured in poisoning accidents; these generally resulted from malfunctioning or misused combustion appliances.
Outdoor levels in rural areas have been measured at < 1 ppm (Health and Welfare Canada 1989). Levels as high as 50 ppm, but typically 10–12 ppm, have been measured for vehicle occupants in heavy traffic (Coultas and Lambert 1991).
Levels higher than the NHMRC indoor air goal concentration have been experienced overseas in indoor parking areas and building locations attached to these (Coultas and Lambert 1991). Ferrari et al (1998) measured carbon monoxide concentrations in 52 Sydney dwellings, mostly with unflued gas heaters; three exceeded the NHMRC goal, possibly due to poor building ventilation or appliance servicing. Lyall (1993) measured carbon monoxide concentrations in 195 dwellings in Sydney, Adelaide and Perth, all of which had unflued gas heating. Median concentrations were 6 ppm (range 1-47 ppm) for Sydney, 0.6 ppm (range 0-37 ppm) for Adelaide and 5.3 ppm (range 0.3-22 ppm) for Perth. The proportion of dwellings exceeding the NHMRC goal was not reported. Pointon et al (1994) measured carbon monoxide concentrations in four central and one suburban office building in Perth with no known carbon monoxide sources other than underground parking. The concentrations varied with peak traffic flow outdoors; hourly averages ranged from 1 to 8 ppm, eight-hour averages from 1 to 5 ppm. Cummings et al (1990) measured carbon monoxide concentrations at 80 sites in recreational buildings with smoking permitted; levels ranged from 0 to 24 ppm and generally exceeded 9 ppm during peak activity periods, mainly because of increased outdoor levels.
The NHMRC2 indoor air goal for lead is 1.5 µg/m³, averaged over three months.
Atmospheric lead levels in suburban Australia are decreasing as more of the car fleet uses lead-free petrol; there have also been significant reductions in average levels of lead in children’s blood. However, old paint on buildings may contain large quantities of lead that could be released into the atmosphere with flaking and chalking of the paint, if painted wood is burnt or if old paint is burnt off prior to repainting during renovations. This could result in short-term but high exposure for some people. Lead exposure from old paint dust or flakes is cause for concern (AATSE 1997).
The Select Committee upon Lead Pollution (1994) identified lead abatement in public housing, childcare centres and lower socioeconomic housing as target areas. Penny (1994) discussed the issues from the paint industries’ perspective and recommended that products be managed in-place using purpose-designed encapsulants rather than being removed. The adoption of abatement strategies and the specification of these encapsulants and their effectiveness will be important factors in these activities.
Particles arise in indoor air from outdoor sources, environmental tobacco smoke and fuel-based heating appliances and cooking stoves. Wood-burning heaters and kerosene heaters can elevate short-term particles concentrations to levels similar to those described earlier for environmental tobacco smoke by either leakage or re-entrainment of polluted outdoor air. Airtight wood heaters will limit indoor leakage but still contribute substantially to outdoor air pollution. Ferrari et al (1998) found an average ‘respirable’ particle concentration of 86 µg/m³ in eight Sydney dwellings with wood fires compared to 28 µg/m³ in four dwellings without wood fires. Short-term concentrations during cooking (fuel unspecified) averaged 420 µg/m³ in seven Sydney dwellings. Movement of outdoor respirable particles into indoor air may also contribute to indoor particles but different particles may be involved (eg different amounts of soot and acid aerosols) (Dockery and Pope 1994).
Hitchins et al (2000) measured concentrations of particle emissions in buildings near a major road in Brisbane as part of a program to assess the risks associated with outdoor exposure to particulate matter. The study found that 15 m from a major road, exposure to submicrometre particles was seven times higher than average urban levels; 150 m from the road, the exposure was 3½ times higher than average urban levels. The study concluded that it was reasonable to assume that people living or working near an urban freeway are exposed to higher than average levels of submicrometre particles. It listed the following options for particle exposure control in indoor environments near major roads:
- avoid construction of buildings within 15–150 m of the road;
- install high-performance filtration systems for fine and ultrafine particles; and
- improve tailpipe emissions.
High performance filtration was not considered fully effective for buildings such as schools, childcare centres or retirement villages, where occupants spend a significant amount of time outdoors. It was recommended that these buildings be situated further from the road. The study concluded that the most viable solution was to address the primary source of the particles through improved control of vehicle exhaust emissions of particles (Hitchins et al 2000).
This section deals with the main non-criteria chemical pollutants of significance to indoor air. Biological contaminants are discussed in a separate section.
Asbestos is a naturally occurring fibrous silicate mineral with high resistance to heat and acid. More information on asbestos and its impact on ambient air quality can be found in Section 1.3.7.
Asbestos is no longer allowed to be used in products for the home. Prior to the mid-1980s, products like cement sheet, roofing sheet, plastics, ceiling and vinyl floor tiles, pipe lagging and fire-resistant boards and blankets may have contained some asbestos. The health risk from asbestos in the home is generally very low, although this may not be the case during maintenance or renovation. The presence of products containing asbestos does not automatically lead to ill health. Much depends on whether the products are damaged and releasing fibres to the air, the type, size and concentration of fibres, the duration of the exposure and the susceptibility and health status of the individual.
Stringent precautions should be observed when removing asbestos as it can lead to prolonged periods of elevated indoor concentrations. Regulations may cover the removal and disposal of asbestos-containing products; before removing asbestos, individuals should seek professional advice, including from State and Territory occupational health and safety authorities.
Asbestos fibres were used widely in many building products in Australia up to the early 1980s; much of this material remains in place. The major manufactured building products were asbestos-cement sheet products for interior and exterior cladding, flooring products (high-density underlay sheets, vinyl-asbestos floor tiles, ‘cushion’ vinyl flooring) and fire, thermal or acoustic insulation products (asbestos millboard sheet and pipe preformed insulation panels, sprayed asbestos insulation) (Brown 1981). The types and amounts of asbestos and binders used in these products varied greatly; consequently there are large differences in their physical integrity (particularly friability, which is the ability of the material to be broken down to dust). Most insulation products are considered friable; many sprayed asbestos insulation products are so highly friable that minor disturbance can result in a large airborne release of asbestos fibres.
Sprayed asbestos insulation products were widely used in commercial and industrial buildings in Australia and can act as a major source of asbestos fibre exposure if they are damaged or deteriorate, particularly during building maintenance activities (Brown 1981). Local State regulations and guidance from the NOHSC (NOHSC 1988) help to manage risks from such products in workplaces. Rogers (1991) estimated that each year $300 million is spent in removing asbestos insulation products from Australian buildings.
Between 1968 and 1979 in the ACT, a specific contractor installed unbound asbestos ‘fluff’ as insulation in the ceiling spaces of approximately 1100 ACT houses and 100 houses in nearby New South Wales towns (Rist 1993). This material was largely amosite but also contained crocidolite in some (five to ten) cases. From 1989 to 1993, the asbestos fluff was removed from the ACT houses. It is believed that no removal program is planned for the nearby New South Wales houses also insulated with this material. Queanbeyan Shire has advertised for homeowners to supply insulation samples and this has led to seven positively identified cases of use of asbestos fluff. The shire has provided advice on procedures to isolate the insulation from living spaces by sealing gaps and openings and avoiding entry into the roof space.
Another aspect of Australian building practice that is different from other countries is the widespread use of asbestos cement sheet products. It has been estimated that, until production ceased in 1983, 1300 million square metres of asbestos cement building sheets were produced (Brown 1994a). Approximately one-half of this produce, if still installed in buildings, is over 30 years old. These products contained chrysotile, with lesser quantities of amosite or crocidolite (the latter until the late 1960s). The sheets were used for exterior cladding (roofing and walls) and interior lining of buildings of all types. Useable statistics on specific applications are available only for external walls of private dwellings – but these demonstrate the wide usage of these products (680 000 private dwellings had asbestos cement external walls). Environmental emission of asbestos from asbestos cement products is more likely to occur from outdoor products (particularly roofing) than indoor products, due to surface degradation of the former (Brown 1987). Asbestos concentrations around such buildings are generally extremely small and differ little from ambient levels in other urban areas, although they are persistent over time (Felbermayer and Ussar 1980; Western Australian Advisory Committee on Hazardous Substances 1990).
Radon (radon-222) is an inert gas that results from the decay of elements present in most soils and rocks, although at widely different levels. The gas leaves soil or rock and enters surrounding air or water; hence it is ubiquitous in indoor and outdoor air. Radon may enter building air via the soil under the building, but less significant sources include natural gas for cooking and heating and some building materials (Wadden and Scheff 1983). Radon concentrations in indoor air will be higher than outdoors because the dispersion of air is less restricted in buildings.
Although radon is an inert gas, its decay leads to emission of alpha particles that, if inhaled, can damage tissue, such as that of the lung. Radon has been classified as a class 1 (human) carcinogen following studies of lung cancer incidence in miners (IARC 1993).
There is widespread evidence (Brown 1999; Department of Environment Sport and Territories 1996) that the concentration of radon in most Australian buildings is well below the NHMRC’s2 indoor air goal and action limit of 200 Bq/m³ (see Table 6.3). Nevertheless, about 2000–3000 homes in Australia would be expected to exceed the action level of 200 Bq/m³, according to Selinger (1998). Radon levels in the United States and the United Kingdom often exceed guidelines, probably because of differences in building designs (eg the more common use of cellars and basements overseas) (DEST 1996) and the soil types and coastal proximity of much of Australian housing (Brown 1997).
In 1988, the Australian Radiation Laboratory carried out a survey of radon levels in 3413 Australian dwellings (Langroo et al 1990; Solomon 1990). The geometric mean radon activity concentration was 8 Bq/m³ nationally, approximately one-half of the world average, and significantly lower than the NHMRC indoor air quality goal and action limit (Table 6.3) of 200 Bq/m³. Three of the dwellings (0.09% of the survey population) exceeded the 200 Bq/m³ action limit.
Persily (1993) suggested that radon levels in high-rise buildings may become elevated due to stack effects. Hocking and Joyner (1994) found average levels of 15 Bq/m³ in three low to high-rise office buildings in Melbourne and Toussaint (1998) found average levels of 30 Bq/m³ in two high-rise buildings in Perth. Higher levels (but still below the action limit) were observed on upper floors and in basements.
Pesticides continue to deplete the quality of indoor air. The most common exposure to pesticides in dwellings is believed to occur through the use of consumer products, intrusion of termiticides from foundations and contamination of house dusts (Brown 1997). Residues from the past use of organochlorine termiticides such as chlordane may persist in the soil beneath buildings for many years. However, it is the mishandling of pesticides that is considered to provide the greatest potential for exposure (Lewis and Wallace 1988).
Some context to the potential magnitude of the problem can be found in a 1998 report from the Australian Bureau of Statistics (ABS 1998), which found from surveys that:
- around 79% of households reported using flysprays or baits inside their dwelling, with the highest use in Queensland (84%) and Western Australia (81%) and the lowest in Victoria (74%); and
- households with a dependent child (children) had a higher level of use than those with one person.
Health effects associated with pesticides include headaches, nausea, dizziness, and eye and skin irritation (EPA Victoria 1993). Many of the symptoms are associated with the group of chlorinated hydrocarbons which, as a group, tend to be biologically toxic; further attention is needed to identify their potential carcinogenicity.
EPA Victoria concluded that a relatively small part of the total population is likely to be exposed through the application of pesticides to houses. A large proportion is likely to be exposed through the use of indoor pesticides (pesticides for flies, cockroaches, fleas and moths). Many of the pesticides are very toxic and some are carcinogens. Correct use and control of these should be a high priority (Dingle et al 1999).
Dingle et al (1999) reported that pesticides were detected in the indoor air of 19 of 22 dwellings treated with termiticides several years previously. Mean and range concentrations of the most frequently detected pesticides in homes where pesticides were detected are presented in Table 7.3.
|Pesticide||Mean concentration (µg/m³)||Range (µg/m³)||Standard deviation|
Source: Dingle et al (1999).
Of the pesticides detected, chlorpyrifos was found in the highest concentrations. This was attributed to its increasing use as an alternative to organochlorine pesticides for termite control in Western Australia (chlorpyrifos is an organophosphate).
The pesticide found at the highest level in the homes closely correlated with the organochlorine pesticide that the home occupant reported as previously being applied, except in the case of chlorpyrifos. Bedrooms had the highest levels of pesticides, followed by kitchens and general living areas.
Trends in the levels of pesticides over time were not uniform. Chlordane and heptachlor increased, possibly due to post-treatment care (eg ventilation, movement of soil or changes in climactic conditions). Levels of aldrin and dieldrin declined over time.
Misapplication (spills) of pesticides was reported in three of the 22 homes. Pesticide concentrations were higher in homes where spills were recorded, suggesting that misapplication of pesticides contributes significantly to contamination of indoor air.
Gunn et al (1994) summarised the findings of a two-year study into indoor air and blood dieldrin levels after 29 constructed dwellings were treated with aldrin to prevent termite infestation. The treatment was carried out using Australian Standard practice. The airborne aldrin concentrations 1–6 weeks after the treatment ranged from 0.08 to 51 µg/m³, with median concentrations of 0.7 to 2.6 µg/m³. Six dwellings exceeded a concentration of 10 µg/m³ after one week, two dwellings exceeded this level after six months, and one dwelling exceeded it after one year. Poor sub-floor ventilation and a ‘leaky’ floor were important contributors to indoor air pollution by aldrin (Pisaniello et al 1993). Blood dieldrin levels of occupants showed an increase of borderline statistical significance after the treatment. This was largely due to results from the two most heavily contaminated dwellings, where occupants showed clear and sustained increases in blood dieldrin levels.
Meaklim (1992) has suggested the following measures to reduce exposure to pesticides:
- in termite-prone areas, treat new buildings before construction;
- in existing buildings, perform all liquid termiticide treatment when the building is vacant for at least one day, preferably longer (buildings with poor subfloor ventilation should have the ventilation improved and a low-volatility chemical used);
- wherever possible, perform other pesticide applications when residents are absent for a few hours, especially if people especially sensitive to chemicals and solvents may be exposed;
- after each treatment, check the building for leaks and spillages, and clean up areas as required (normally carried out by the pest control company);
- if space spray is used, vacate the building and shut it until the treatment period is completed and the appropriate time allowed for ventilation;
- if a liquid pesticide is used, make sure the building is well ventilated (for at least half an hour with doors and windows open) prior to reoccupation;
- restrict the use of dichlorvos aerosols in buildings and rooms with plush fabrics (eg deep pile carpets, heavy curtains); and
- avoid dichlorvos ‘pest-strips’ in children’s bedrooms while children are sleeping (the level of ventilation required to safely use these reduces the effectiveness of the pest-strip anyway).
Section 1.3.2 of this report provides general information on agvet chemicals. Appendix A provides a more detailed description of the management framework for agvet chemicals.
At room temperature, formaldehyde is a colourless and flammable gas with a pungent odour. It is an irritant, causing a burning sensation to the eyes, nose, throat and lungs on exposure. Its major industrial application is in the production of resins that are widely used in indoor materials and in consumer products, particularly pressed-wood and building products such as particleboard and medium-density fibreboard. Formaldehyde is also emitted by gas stoves and in tobacco smoke.
Formaldehyde concentrations have been found to be low in conventional, established residences and offices, with mean concentrations of 30–85 µg/m³, well below the NHMRC2 goal of 130 µg/m³(0.1 ppm). However, concentrations up to 1500 µg/m³ with means of 120–920 µg/m³ have been reported in mobile buildings, probably due to the high content of pressed-wood products and low ventilation rates in these buildings. Concentrations exceeding the goal have also been observed in residences recently insulated with urea-formaldehyde foam insulation (UFFI), although, after several months, when the foam has dried, formaldehyde concentrations are generally below the NHMRC goal. There has been little investigation of concentrations in new or renovated buildings.
|Building type||Study||Number of buildings||Formaldehyde concentration (ppb)|
|Conventional dwelling||Dingle et al (1992)||100||0–97||26|
|Hooper et al (1994)||40||3–73||23|
|Caravan||Dingle et al (1992)||20||20–280||90|
|Caravan/mobile home||McPhail (1991)||24||80–1200||310|
|Conventional office||Dingle et al (1992)||3||15–70||21|
|Cliff (Simtars, Qld)||4||20–120||66|
|Ruksenas (Noel Arnold and Assoc)||8||10–80||40|
|Mobile office||Dingle et al (1992)||12||420–830||710|
UFFI has been used in 50 000–70 000 Australian dwellings; occupant health complaints arose in less than 1% of these. Soon after the installation of UFFI, formaldehyde indoor air concentrations could be in the 1000 ppb range, but after several months they were typically less than 100 ppb, the indoor air goal recommended by the NHMRC (Brown 1991). Concentrations found in Australian buildings are summarised in Table 7.4. Formaldehyde concentrations in conventional Australian buildings appear to be somewhat lower than those reported in North America; those in mobile buildings are similar.
General information on VOCs is presented in Section 1.3.4. The indoor ‘level of concern’ for VOCs established by the NHMRC2 is presented in Table 6.3. The NHMRC indoor goal for total VOCs concentration averaged over 1 hour is 500 µg/m³, with no single VOC contributing 50% or more of this concentration.
Generally, in any building, 50–150 different VOCs can be detected using sensitive analytical methods, which can detect concentrations around 1 µg/m³. It has been postulated that the individual compounds have an interactive effect on sensory irritation and should be considered together as a total VOC concentration (Molhave and Nielsen 1992). A recent European Commission report (European Commission 1997) recommended a definition of total VOCs and a method for sampling and analysis and specified the application of the total VOC concept in indoor air quality investigations.
Most reported total VOC concentrations in non-industrial indoor environments are below 1 mg/m³ and few exceed 25 mg/m³. Over this range the likelihood of sensory effects associated with VOC exposure increases. The sensory effects include sensory irritation, dryness, and weak inflammatory irritation in eyes, nose, airways and skin. At total VOC concentrations above 25mg/m³ other types of health effects become of greater concern (European Commission 1997).
Sources of indoor VOCs include cleaning agents, finishes applied to textiles, solvents, adhesives, floor varnishes, furniture and carpets (see Table 7.1). Outdoor sources of VOCs can be important causes of poor indoor air quality. Typically the problem is related to location, with motor vehicles being generally recognised as the major source of outdoor VOCs (Golding and Christensen 1999).
|Data source||Building type||Complaints(yes/no)||TVOC concentration (µg/m³)||Major compounds|
|CSIRO||Dwelling||No||143 (9 outdoor)||Limonene, alkanes, pinene|
New carpet 6 months later
|Styrene, 4-phenyl Cyclohexene, toluene, xylene|
|CSIRO||Office||No||69 (outdoor 27)||Limonene, ethanol, toluene|
|Healthy Buildings International||Offices (18)||Unknown||av <90
|Toluene, xylene, 1,1,1-trichloroethane Dichloromethane, toluene|
(D Cliff, pers comm)
|Toluene, xylene, trichloroethane Chloroform, acetone, dichloromethane, tetrachlorethylene|
|Noel Arnold and Assoc.
(J Ruksenas, pers comm)
|DASCEM (Z Adamczyk, pers comm)||Office (1)||Unknown||20–1250
Note: TVOCs = total volatile organic compounds
There are limited data for VOC concentrations in Australian buildings. The CSIRO Division of Building, Construction and Engineering, Highett, is working on a project to characterise VOC concentrations in buildings; preliminary results are presented in Table 7.5 together with other measurements. Note that differences in analytical methods limit comparison of these data. Further investigation is needed to determine the level of exposure to VOCs for Australian populations.
Australians are exposed throughout their lives to VOCs in the workplace, schools, at home, in institutions and while travelling. Individuals with hypersensitivity may show symptoms at less than 1% of workplace exposure standards. Exposure to VOCs at the workplace is controlled by the NOHSC through the workplace exposure standards; the exposure levels are time dependant and are designed to prevent adverse effects in tolerant workers (Golding and Christensen 1999).
Smede et al (1997) have suggested that school indoor air quality was important and may affect asthma and perception even at low concentrations. Other studies have suggested that learning ability, sensory responses, eye physiology and performance may be affected.
Brown (1998a) reported problems with VOC exposure levels in a newly painted and carpeted classroom. Students and teachers experienced headaches, nausea, sore throats and increased asthma medication use over a three-year period. The total VOC level in the classroom was 550 µg/m³ after three years, which is higher than the NHMRC standard.
Environmental tobacco smoke is acknowledged to be one of the main contributors to poor indoor air quality. Some 4000 chemicals are contained in cigarette smoke, including carbon monoxide, nicotine, formaldehyde and ammonia, and including 43 chemicals known to be human carcinogens (US DHHS 1989). More information on toxic and carcinogenic agents can be found in Table 1.11. Information about the various management actions to address smoking can be found in Chapter 8.
Biological contaminants include viable and non-viable microbiological matter such as viruses, bacteria, fungi, protozoa, house dust mite and insect faeces and pollens. Their presence can result in infectious disease, toxics effects or allergic reaction. Much is known about the occurrence and health effects of Legionella spp and house dust mites but there has been little investigation on the impact of other microbial contaminants on indoor air quality in Australia.
Whilst all types of microorganisms can cause problems indoors, bacteria and fungi are most commonly associated with indoor air quality complaints. In any indoor environment a variety of species will be present at different times and in different micro-environments.
In order for airborne disease transmission to occur from microbes in buildings, there must be a source or reservoir for the microbes, some means for the microbes to multiply (amplifiers) and a mechanism for their release and dispersion into indoor air (Burge and Feeley 1991). The major indoor reservoir is stagnant water or moist interior surfaces. These can accumulate microbes that enter the building in outdoor air and act as amplifiers for bacteria. Fungi can grow in relatively dry environments (eg at relative humidities above 75% (Solomon and Burge 1984)). Airborne dispersion is relatively easy for microbes found in building ventilation systems (eg fungal and bacterial spores) or contaminated carpet.
Bioaerosols (which include bacteria, fungi, dust mites and other biological particles) are recognised as an important subgroup involved in building-related illness. Microbes, particularly fungi, which can contain mycotoxins, and VOCs, are now thought to be more involved as causative agents in mechanically ventilated indoor work environments (Phoon and Baker 1993). Several studies suggest that indoor air microbials may have a more common role in the sick building syndrome than previously thought (Rylander 1993a,b).
Several companies routinely screen buildings for airborne microbial levels; standardised test methods, which provide reproducible test results, are now readily available (Stuttard 1996). Some caution is required when evaluating any one-off microbial test results, because airborne microorganisms are ubiquitous in the environment, with ‘typical’ levels ranging from 50 to 1500 CFUs per cubic metre in outside city air. An external sample taken on the day of test can provide a useful baseline figure for the evaluation of results.
The Northern Territory Work Health Authority (1993) has stated that measurement of microorganisms in excess of about 1000 CFUs per cubic metre of air indicates that the indoor environment may need to be investigated for microbiological contamination. However, the report also stated that exceeding this level does not mean the air is unsafe or hazardous. Merely using a number to represent CFUs per cubic metre is an unreliable indicator of the actual hazard posed by airborne micro-organisms.
Because of the universal presence of microorganisms, it is critically important to obtain an indication of the ratios of organism groups present. This information will be of greatest value with periodic testing to provide data for a trend analysis of the microbial groups in a particular site. By differentiating these groups of organisms, the likely source, the risk potential and the need for any action can be established (Stuttard 1996).
Determining the groups of microorganisms present in a sample is significantly different from identifying all organisms present. The full identification of isolates from a sample would not generally provide any useful information and is certainly not cost-effective. A number of techniques have been recommended for sampling for microbial contamination in indoor environments (Phoon and Baker 1993).
Bacteria and viruses
Bacteria are ubiquitous in the air and general environment. They can cause adverse human health effects and deterioration of building materials when they proliferate in indoor environments (Stetzenbach 1998). The health effects of bacterial exposure in indoor air will depend on the species and the route of exposure.
The bacteria in building air can come from airborne sources from the wind’s action on soil and vegetation, compost, municipal landfills, sewage sludge, etc. They can also be a direct result of human activity, such as breathing, coughing and sneezing, or they may colonise the ductwork of the cooling systems, the water cooling towers (eg Legionella spp) or interior building materials and furnishings such as wallboard, wallpaper and flooring (Bates 2000).
In indoor environments, bacteria usually grow in areas with standing water such as water spray and condensation areas of air conditioning systems (Stetzenbach 1998). Dirty or poorly maintained air handling systems can become contaminated over time by bacterial populations that thrive on moisture-laden surfaces caused by water condensation. Legionella is probably the most common group of bacteria mentioned in association with airconditioning systems (see below).
Viruses are important airborne organisms and a significant contributor to occupational absenteeism. Examples of important viruses include the causative agent of the common cold (rhinoviruses) and the flu (influenza viruses types A, B, C, etc). The spread of these illnesses can be aided by inadequate ventilation levels within a building (Stuttard 1996). Viruses cannot multiply outside the human host, but can survive and remain infective for extended periods in the warm recirculating airspace of the modern air-conditioned building.
Routine testing for airborne viruses is expensive and not generally recommended. However a useful correlation between the levels of some airborne bacteria, particularly the Micrococcus group, and poor ventilation levels has been noted, and these can thus be used as an indicator of potential cross-infection problems (Stuttard 1996).
Prevention and control of legionnaire’s disease in Australia
Legionella bacteria are common microorganisms of concern. They occur naturally in small numbers within soil and water. However, the danger occurs when the bacteria are present in warm, moist environments such as cooling towers in air-conditioning plants, where they can multiply rapidly. Evaporative air conditioning units such as those used in homes and many business premises are not a likely source of legionella infection.
Most legionella infections are contracted outdoors, but predominantly in areas associated with cooling tower systems used to treat indoor air. Legionella infection control must therefore be included in discussions about indoor air quality. Legionella outbreaks have been recorded as a result of building air inlet pipes being positioned directly underneath air outlet pipes (Bates 2000).
As noted in the State of the Environment report (DEST 1996), inhalation of droplet aerosols (very fine droplets of water) containing legionella bacteria can cause legionnaire’s disease. Sources of droplet aerosols include spray drifts vented from cooling towers into the atmosphere.
Poorly maintained spa pools can also be a source of legionella infection. Spas are normally heated to about 37°C and use air and water jets to produce turbulence. These conditions result in rapid growth of undesirable organisms, including legionella. These organisms may be transmitted readily to humans by inhalation of the aerosols created by the air and water jets.
In recent years there have been reports of legionnaire’s disease cases associated with the use of potting mix. Australian studies have found legionella species present in over 70% of commercial potting mix samples. The route of transmission of the bacterium from potting mix is not clearly established and is the subject of further studies.
Legionnaire’s disease is a rare form of pneumonia with a relatively high mortality rate of up to 20%. It represents 1% of pneumonia cases in Australia, with around 180 cases a year reported nationally. The most serious outbreak in Australia occurred in 1987 in Wollongong, when 44 cases were reported and 10 deaths resulted. Early symptoms resemble those of flu and include headache, fever, chills, muscle aches and pains and generally a dry cough followed by shortness of breath. Other body systems can sometimes be affected, resulting in diarrhoea, mental confusion and kidney failure. Legionnaire’s disease can be a very serious illness, particularly in the elderly, heavy smokers, people with respiratory diseases and people with an immune deficiency.
Currently, there is no vaccine for preventing legionnaire’s disease and total eradication is impossible because legionella is widespread in the environment. Instead, control measures aim to prevent exposure by preventing the growth of legionella in cooling towers, warm water systems and spas. Control mechanisms consist of regular maintenance, including chemical treatment.
The Australian Commonwealth, States and Territories do not have a common regulatory approach to the control of legionella. The National Environmental Health Forum (NEHF) has produced guidelines for the control of legionella (see below). The NEHF publication Water No. 1 Guidelines for the Control of Legionella includes an appendix on the regulatory approaches by Australian States and Territories.
AS/NZS 3666.3:2000 outlines a performance-based approach to the maintenance of cooling water systems and for the control of Legionella spp and other microorganisms in such systems. This approach combines automatically regulated water treatment with monitoring, assessment and control strategies to help create a low-risk environment in the cooling water system.
The Health (Infectious Diseases) Regulations 1990 require cooling towers, warm water systems and public spas in Victoria to be maintained and disinfected in accordance with set guidelines and standards (see below).
Relevant publications by the Victorian Department of Human Services include:
- Guidelines for the Control of Legionnaires’ Disease 1989;
- Water Purification Standards for Public Swimming Pools and Spa Pools 1990;
- Legionnaires’ Disease and Cooling Towers, Information for Owners and Managers 1996;
- Evaporative Coolers, An Operation and Maintenance Guide for Owners 1997; and
- Cooling Towers, Information for Dry Cleaners 1997.
To minimise the risk of infection, the Victorian Department of Human Services has also advised gardeners to take the following precautions when using potting mix:
- open bags with care to avoid breathing in airborne potting mix dust;
- moisten the contents in the bag to avoid creating dust;
- always wear gloves to avoid transferring the potting mix from hand to mouth; and
- always wash hands after handling potting mix even if gloves have been worn.
The same measures are advised when handling other gardening material such as compost.
In December 1999, the Victorian Minister for Health, the Hon Mr John Thwaites, established a Legionella Working Party to advise the Government on the enforcement of best practice for the maintenance of cooling towers to reduce the risk of legionnaire’s disease. The working party was also asked to review the roles and responsibilities of relevant agencies. The working party was subsequently asked to review the experience of the Melbourne Aquarium outbreak in making its final recommendations. The working party reported in June 2000 and recommended six broad strategies set out in Table 7.6 below.
|(i) That regulation of cooling towers and warm water systems be continued and upgraded to include improved levels of maintenance and enhanced standards of practice.|
|(ii) That improved and formalised partnership arrangements be introduced between agencies, including the Department of Human Services, local government, Victorian WorkCover Authority, Building Control Commission and Plumbing Industry Commission.|
|(iii) That ongoing legionella control education programs be provided jointly by these agencies.|
|(iv) That compulsory registration of cooling towers be required by the Department of Human Services in consultation with other agencies.|
|(v) That an ongoing program of inspections or audits be introduced and undertaken by authorised agencies.|
|(vi) That the revenue raised by registration fund the development and administration of the register and the inspection/audit process.|
The working party also proposed eight specific actions, within a strengthened regulatory framework. These actions are shown in Table 7.7, with the Government’s responses.
|Working party recommended actions||Government response|
|(i) Establish a comprehensive register of cooling towers, as part of a risk management strategy, under the Building Control Commission as a component of the existing buildings surveillance systems.||Agreed. Establish a comprehensive register of cooling towers, as part of a risk management strategy, by amendment of the Building Act 1993, to augment existing building systems, and legislative controls on plumbing work generally.|
|(ii) Require all registered premises to develop and implement risk management programs for the control of legionella. Actions required under the programs to be documented and detailed in the Annual Essential Services Report, currently required by the Building Control Commission, which should be available for review by accredited inspectors.||Agreed.|
|(iii) Require audits of risk management programs for the control of legionella of all registered premises on a regular basis, funded by industry, as a component of the existing Building Control Commission requirement for an audit of the Annual Essential Services Report.||Agreed. Audits to be conducted on an annual basis.|
|(iv) Provide for inspections to be undertaken by government on the basis of risk to the community as well as through information received through audit or to assist in outbreak investigation.||Agreed.|
|(v) Provide an enhanced technical advisory and outbreak investigation service for the control of legionella through the Department of Human Services.||Agreed.|
|(vi) Undertake cost recovery of recommendations (i), (iv) and (v) through registration fees payable by the registered premises to the Building Control Commission.||Agreed.|
|(vii) Extend the requirements of the Building Act 1993 and Building Regulations 1994, to enable the elements of the proposed approach to be actioned as quickly as possible for all buildings.||Agreed.|
|(viii) Upgrade existing systems which do not meet the Australian and New Zealand Standard (AS/NZS 3666) to require fitting of drift eliminators and automated biocide dosing and automated bleed off systems to all cooling towers.||Agreed. Undertake further consultation with industry to assess the impact of requiring the upgrading of existing systems which do not meet the Australian and New Zealand Standard (AS/NZS 3666) to require automated biocide dosing and bleed off systems and the fitting of drift eliminators.|
From 1 June 2000, the ACT will adopt a new Cooling Tower Code of Practice that aims to provide greater protection from diseases including legionnaire’s disease. The code will be enforceable under the ACT Public Health Act 1997.
The new code of practice strengthens existing maintenance and testing requirements of ACT cooling towers. It:
- adopts AS/NZS 3666, a nationally recognised standard, as the benchmark;
- requires owners/managers to conduct legionella testing and tower maintenance quarterly at a minimum and to provide the ACT Department of Health and Community Care with the quarterly test results and maintenance records;
- requires that owners/managers continuously monitor the bacterial load in their cooling towers;
- requires equipment that reduces the discharge of harmful vapour to be installed into every cooling tower; and
- requires owners/managers to notify the department within 24 hours of a high-risk event, such as a high legionella count.
ACT public health officers will inspect cooling towers and conduct record audits on a continual basis to ensure compliance with the code of practice and the Public Health Act 1997.
Currently, all cooling towers in the ACT are required to be licensed, with the exception of towers located in Commonwealth buildings, which are exempt from the requirements.
National Environmental Health Forum guidelines for the control of legionella
The NEHF has produced best practice guidelines of relevance to legionella, including Water No. 1 Guidance for the Control of Legionella (1996). This lists a total of 39 species of Legionella bacteria that have been identified since the outbreak of pneumonia amongst members of a convention in Philadelphia in 1976. The monograph describes how legionella are spread and cause infection, where they can be found, and under what conditions they proliferate. It describes the common sources of legionella, including cooling towers, condensers, hot water systems, potting mixes and composts, and gives advice on treatment of these systems and hazard minimisation.
Water No. 2 Guidance on Water Quality for Heated Spas (1996) was produced in recognition of the health risks associated with heated spa pools, which are now installed in many homes as well as within public hotels and resorts. It lists and discusses the properties of disinfectant chemicals and their applicability to spa pools. The monograph emphasises the importance of keeping the water ‘balanced’, (AS 2610 Part 1 – 1993 Appendix C) and provides guidance on how this may be achieved.
Fungi are ubiquitous microorganisms present in soil, dust and decaying organic matter. They produce spores that are capable of becoming airborne and being inhaled. Inhalation of fungal spores is known to cause clinical symptoms by various mechanisms, including active infection, allergenic activity and toxicity. A range of fungi can initiate infection, including Aspergillus fumigatus, which can cause acute respiratory disease (Stuttard 1996). However, fungi are more important for their role as initiators of hypersensitivity reactions, including sick building syndrome. The people most at risk are those exposed over long periods of their lives to visible mould growth, those who work where mould growth is inevitable and the aged or immunosuppressed, who have low resistance. Fungi are also associated with unpleasant odours, discolouring and degradation of building materials.
The fungi of interest in indoor air are usually described as moulds. Moulds can grow on virtually any substrate, including glass, paint, textiles and electrical equipment (Denizel 1974) and produce large quantities of spores in a short time.
The fungal population of indoor air generally reflects the extent to which outdoor air has been used to ventilate the building. The end result of the indoor air population of spores depends not only on the balance and levels of spores in the source (outdoor air) but also on the established source populations within the building. Activities such as cleaning, dusting and construction work can greatly increase the measured levels of airborne spores (Flannigan 1997).
Hargreaves and Parappukkaran (1999) noted that exposure to moulds and fungi is an everyday occurrence for most people, but that the collective literature points to three factors that may contribute to the promotion of elevated fungal populations:
- poor construction techniques;
- failure to rapidly identify/repair water incursion;
- failure to correctly operate and maintain airconditioning systems.
Specific guidelines have been supplied by the American Conference of Governmental Industrial Hygienists (ACGIH 1989). These relied primarily on site inspection for potential sources of microbes; air sampling was regarded as a secondary or last-resort action where occupant illness had occurred. Any indoor air sampling must be performed relative to outdoor air sampling and must determine both taxa and concentrations. The WHO (1990) guidelines for assessment of hazardous indoor airborne fungi used a similar approach, as summarised in Table 7.8.
|Result of air sampling||Acceptable level|
|A||Confirmed pathogens (eg Aspergillus fumigatus) or toxigenic fungi (eg Strachybotrys atra and toxigenic Penicillium, Fusarium species)||Not acceptable|
|B||Only one species other than Cladosporium or Alternaria||< 50 CFU/m³|
|C||A mixture of species reflective of outdoor flora||< 150 CFU/m³|
|D||Primarily Cladosporium or other common phylloplane fungi||< 500 CFU/m³|
Note: CFU = colony-forming units
Source: WHO (1990).
Published studies in Australian buildings have been limited. Godish et al (1993) investigated airborne mould and bacteria levels in 40 dwellings in the Latrobe Valley, Victoria. All dwellings had one or more occupants with persistent respiratory symptoms such as asthma or allergy. Seventy-five per cent of the houses had evidence of indoor mould growth, 25% of the houses had one or more rooms where viable mould concentrations exceeded 2000 CFU/m³ and 13% had concentrations exceeding 10 000 CFUs/m³. Outdoor mould levels contributed to indoor levels but indoor samples had much higher levels of Penicillium spp. Seneviratne et al (1994) reported measurements in three Sydney office buildings with histories of sick building syndrome symptoms. Two buildings exhibited low colony counts that were primarily Cladosporium, Aspergillus and Penicillium. The third, a building found to have damp walls but no visible mould growth, exhibited similar species but at high airborne levels (600–2500 CFU/m³).
The development of methods to estimate indoor allergen concentration has been important in both the assessment and risk of exposure and the evaluation of eradication procedures. Most work in this area has targeted the reduction of house dust mite allergen concentrations. This is accomplished by physically removing or denaturing the allergen. To be successful, a variety of measures needs to be used, depending on the particular climatic condition (Dr Connie Katelaris, Westmead Hospital, presentation on ‘Indoor allergens – risks and management’).
Allergens are substances that cause an allergic reaction. Many substances that are found indoors may act as allergens and have a significant impact on the health and quality of life of the 30–40% of individuals in our population who are atopic. Domestic allergen exposures may represent significant risks for the development of asthma and of acute asthma attack (Thomas et al 2000).
The prevalence of allergy and asthma has increased considerably in recent years, particularly in Western nations (Davies et al 1998; Peat et al 1994). The emergence of allergies in Western nations has been attributed to a number of factors, in particular, the changes in landscape from forest to pasture, and the trend for most people to lead an indoor, climate-controlled lifestyle (Platts-Mills et al (1996).
A wide range of trigger allergens have been identified, many of which are found in the indoor environment (Rutherford and Eigeland 1999). Findings in a study by Duffy et al (1998) suggest that house dust mite, cat and cockroach allergens may cause the onset of asthma while pollen and fungal allergens may exacerbate asthma or trigger episodes of asthma.
The National Academy of Sciences in the United States has found sufficient evidence to conclude that there is a causal relationship between exposure to cat, cockroach and house dust mite allergens and exacerbations of asthma in sensitised individuals. It also found that there was evidence of a causal relationship between environmental tobacco smoke exposure and exacerbations of asthma in preschool-aged children. An association (rather than causal relationship) was found for exposure to allergens of dogs, fungi and high-level exposures to nitrogen dioxide and oxides of nitrogen (at concentrations that may occur when gas appliances are used in poorly ventilated kitchens).
In Australia, house dust mite allergen appears to have the widest public health impact, with insect allergens (primarily cockroach) also important. Pets, particularly dogs and cats and to a lesser extent birds, impact on a smaller part of the community (Rutherford and Eigeland 1999).
Bedding, soft furnishings and carpets have been shown to act as reservoirs for allergens and it has been suggested that strategies to reduce asthma risk should be targeted at these sources (Thomas et al 2000).
House dust mites
House dust mites are microscopic organisms that live mainly in mattresses and carpets within the home, where they feed off human skin flakes and other products. These mites are a major source of allergens that can sensitise various organs, leading to inflammation at the next exposure. Black (1993) suggested that house dust mites were more likely to cause sensitisation than pollens or fungi since house dust mite exposure is perennial rather than seasonal and the level of allergen exposure can be 20 ng/hour for house dust mites compared to 1 mg/season for pollen and fungi. The sources of dust mites are well known and general health effects are understood, yet the risks of developing allergy to house dust mites is a more complicated issue relating to exposure and genetic predisposition.
House dust mite faeces, which contain the allergen, may become airborne if disturbed and build up in carpets, sofas, cushions, bedding etc. Allergic reaction in the lung leads to asthma; in the nose, to hay fever or allergic rhinitis; in the skin, to dermatitis or a form of eczema.
House dust mites thrive in warm, humid environments, conditions found at least in parts of most Australian households. The State of the Environment report (DEST 1996) notes that the level of mite allergens in very dry or cold regions is generally low (less than 2 mg/g), because mites require humidity above 40–50% for survival at normal indoor temperature. In contrast, regions with one season suitable for growth have mean mite allergen levels of 2–15 mg/g. Allergen levels are higher in coastal areas of Australia, where the climate is suitable for mites for most of the year; mean levels of 10–40 mg/g have been recorded (Tovey 1992).
For any region, mite allergen levels fluctuate widely between dwellings. The reason for this is not known, although indoor humidity is a possible controlling factor (Tovey 1993; Brown et al 1994). Limited studies of public buildings in Sydney (Green et al 1992) and Melbourne (Brown et al 1994) have shown virtually zero house dust mite levels compared to nearby dwellings. This may be due to greater ventilation rates and lower indoor humidities in public buildings, but these factors have yet to be investigated. However, localised artificial environments created in many heated buildings in cooler climates can also sustain substantial house dust mite populations. In these circumstances, it is the design of the building that inadvertently results in suitable conditions in which house dust mites can live (Rutherford and Eigeland 1999).
It has been suggested that at allergen levels above 2 µg of Der p 1 per gram1 of fine dust (equivalent to 100 house dust mites per gram of fine dust) there is an increased risk of sensitisation, bronchial reactivity and symptomatic asthma. At levels above 10 µg of Der p 1 per gram of fine dust (500 house dust mites per gram) the risk of acute or severe asthma attacks is increased (Platts-Mills and de Weck 1988).
Thomas et al (2000) measured the concentrations of the major allergens of the mite Dermatophagoides pteronyssinus (Der p 1) in homes of preschool children in Adelaide, South Australia. Geometric mean Der p 1 concentrations were significantly higher in beds of asthmatic children (8.30 µg/g dust) than nonasthmatic (3.16 µg/g dust). In asthmatics, bed levels exceeded those of bedroom floor (3.16 µg/g) and living room floor (1.62 µg/g). For nonasthmatics, concentrations in bed and bedroom samples were the same (4.80 µg/g) but exceeded those of living room floors (1.21 µg/g). The study showed that while mite allergen levels found in homes in Metropolitan Adelaide were slightly lower than those reported in the eastern states of Australia, they exceeded proposed levels of risk for allergy and asthma. The study also confirmed that levels of mite allergen in beds were higher than in bedroom floors, and that these were higher than levels found in living room.
Most Australian households have pets, but there is little information on pet allergens. Allergen sources include animal dander, saliva, faeces and urine. A review by Ahlbom et al (1998) found that the levels of pet allergens were high in homes with pets (especially if the standard of cleaning was poor and ventilation inefficient) and that they were greatest during seasons when heating was likely to be used.
The potential for exposure to pet allergens can be seen from the estimates of households with pets (45% dogs, 30% cats, 20% birds) (Rutherford and Eigeland 1999). Anecdotal evidence suggests that dogs with woolly coats and short-haired cats have less effect on sensitised individuals. Dog and cat allergens are readily transported by air currents and attachment to objects like clothes which then are moved.
Allergens from pets, particularly dogs and cats, appear to be ubiquitous, even in houses that do not have pets. A study of houses of allergy clinic patients in Baltimore (United States) showed that there were significant differences in the levels of pet allergens between houses with and without pets, but that many of the houses without resident pets still had high concentrations of pet allergens (Wood et al 1988).
Allergic reactivity to cats appears to be stronger than that seen with other animals; exposure to cat allergen in the first year of life is an important factor in the development of sensitisation and asthma (Dr Connie Katelaris, Westmead Hospital, presentation on ‘Indoor allergens – risks and management’). Allergen in cat saliva is transferred to the fur in grooming. The salvia then dries, detaches from the fur and commonly becomes airborne with the particle it is attached to. As with dust mites, allergens build up in carpets, furnishings and beddings.
The major allergen of domestic cats is Fel d 1. Thomas et al (2000) found very high levels of Fel d 1 in homes of preschool children in Adelaide, South Australia. The levels found in the beds of asthmatic children were significantly higher than in non-asthmatic (2.60 mg/g versus 0.89 mg/g). For asthmatics, bed levels exceeded bedroom and living room levels, but for non-asthmatics no differences were seen in samples from the three locations.
This study concluded that the very high level of cat allergen exceeded proposed levels of risk for allergy and asthma and represented a significant risk of asthma in Adelaide. The results suggested that it is likely that pet cats are permitted to sleep on beds and that this practice should be discouraged.
The primary allergens in dogs are from tongue tissues and tongue glands. Dog fur rarely causes an allergic response.
Cockroach allergen (present in cockroach saliva, gut and faeces) is found throughout the home, but kitchens usually have the highest levels. The allergen has also been found in schools (Sarpong et al 1997). It has been found to be associated with particles greater in size than 10 µm and is found in the air only after vigorous disturbance.
Although the health risks are less than those associated with house dust mites, the allergen has a significant consequences for some individuals.
Pollen is the popular term for the microspores (male spores) of seed-producing plants. The symptoms associated with pollen allergy, hayfever and allergic rhinitis can be either acute or chronic. It is not unusual for 10–20% of a population to be pollen sensitised.
As part of the ambient aerosol, pollens are readily transported into the indoor environment through windows, doors, air intakes and even humans. There has been little or no systematic investigation of indoor/outdoor pollen concentrations across Australia. (Rutherford 1999).
In Australia, work by Bass and Morgan (1997) illustrates the seasonal nature of airborne pollen concentrations, as well as the contribution various species – trees, grasses, herbs – make to overall concentrations.
The major source of pollen exposure is the outdoor environment, so exposure would be expected to be low in mechanically ventilated buildings with well maintained systems. Indoor plants may produce allergenic pollen. Carpets are a reservoir for particles but regular cleaning will reduce pollen load provided the equipment used captures the particles.
Humans release a variety of odorous gaseous bioeffluents (eg body odours) that influence the perceived acceptability of indoor air. Carbon dioxide, which is odourless, is one of the gaseous human bioeffluents in exhaled air. Humans are normally the main indoor source of carbon dioxide. The outdoor carbon dioxide concentration is approximately 350 ppm, whereas indoor concentrations are usually in the range of 500 ppm to a few thousand parts per million. At these concentrations, carbon dioxide is not thought to be a direct cause of adverse health effects; however, carbon dioxide is an easily measured surrogate for other occupant-generated pollutants, such as body odours.
Human breath emissions may be a significant source of VOCs. Fenske and Paulson (1999) used data from previous studies to calculate the proportion of VOCs attributable to human emissions in places where people congregate indoors, such as schools and offices. They calculated that human emissions are likely to be the source of at least 10–20%, and sometimes more than 50%, of VOCs in these places.
1 Der p 1 is the allergen specific to Dermatophagoides pteronyssinus.
2 On 19 March 2002, the National Health and Medical Research Council rescinded its publication "Ambient Air Quality Goals and Interim National Indoor Air Quality Goals". The Council has made this publication available on its Internet Archives site as a service to the public for historical and research purposes only.
The publication is available at: http://www.nhmrc.gov.au/publications/synopses/eh23.htm
The Internet Archives site also contains the following statement made by the National Health and Medical Research Council:
Rescinded publications are publications that no longer represent the Council's position on the matters contained therein. This means that the Council no longer endorses, supports or approves these rescinded publications.
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