Exposure Guidelines for Residential Indoor Air Quality

4.0 Guidelines and Recommendations

Part A. Substances with Exposure Guidelines - Non-carcinogenic Effects

4.A.1 Aldehydes*

In cases where more than one aldehyde is detected in indoor air, the sum should not exceed 1, where c₁, c₂ and c₃ are the concentrations of formaldehyde, acrolein and acetaldehyde, respectively, as measured over a five-minute period, and C₁, C₂ and C₃ are as follows:

C₁ (formaldehyde) - 120 µg/m³ (0.10 ppm);
C₂ (acrolein) - 50 µg/m³ (0.02 ppm);
C₃ (acetaldehyde) - 9000 µg/m³ (5.0 ppm).

Aldehyde concentrations in indoor air generally exceed those outdoors. The primary sources include gas stoves, space heaters and tobacco smoke. Identities of all the aldehydes produced during incomplete combustion of organic fuels are not yet known, but measurements in indoor locations have shown that formaldehyde, acetaldehyde and acrolein are the major aldehydes present.

Concentrations of acrolein in indoor air range from 2 to 50 µg/m³ (0.001 to 0.02 ppm); limited data available indicate that levels of acetaldehyde average about 17 µg/m³ and range from 1 to 48 µg/m³.

The major effect on human health of airborne aldehydes is irritation of the eyes, nose and throat. In recently conducted clinical studies, significant increases in symptoms of irritation have been observed at levels of formaldehyde greater than 1200 mg/m³ (1 ppm) (exposure periods 1.5 to 30 minutes).

Data derived from observational studies of populations exposed to formaldehyde in the occupational environment or in public or residential buildings are less reliable owing to limitations of the investigations conducted to date. In the best-conducted studies, symptoms of irritation have not been associated with exposure to levels less than 600 µg/m³ (0.5 ppm).

There are few reliable data available concerning levels of the other aldehydes that induce symptoms. Acrolein is one of the most irritating of the aldehydes identified in indoor air, with most people reporting eye irritation at levels of less than 1 mg/m³. A significant increase in symptoms of eye irritation has been associated with exposure to levels as low as 210 µg/m³ (0.09 ppm); in the same study, however, eye irritation at a concentration of 800 µg/m³ was only slight. Severe irritation results from exposure to concentrations of 1900 µg/m³ (0.8 ppm). Chronic effects following exposure to acrolein have not been reported and there has been no evidence of carcinogenicity in long-term bioassays with laboratory animals.

Acetaldehyde is considerably less irritating than acrolein; symptoms of irritation have been associated only with exposure to levels greater than 46 mg/m³ (25 ppm). In a long-term bioassay in rats, significant increases in the incidence of nasal adenocarcinomas and squamous cell carcinomas were observed following inhalation of acetaldehyde; however, the administered dose levels (1400, 2700 and 5400 mg/m³ ; 750, 1500 and 3000 ppm) and mortality rates during the study were extremely high. Moreover, data given in the published report of the investigation were insufficient to permit meaningful quantitative risk estimation.

The recommended values for C l , C 2 and C 3 are five to ten times less than the concentrations reported to induce significant increases in symptoms of irritation. Concentrations satisfying the relationship given above should be low enough to minimize additive irritant effects of the specified aldehydes in the general population.

*Also see Section 4.B.1, "Formaldehyde".

4.A.2 Carbon Dioxide

Based on health considerations, the acceptable long-term exposure range (ALTER) for carbon dioxide in residential indoor air is ≤ 6300 mg/m³ (≤ 3500 ppm).

Carbon dioxide is a colourless, odourless and non-flammable gas, which is produced by metabolic processes and by the combustion of fossil fuels. The average concentration of carbon dioxide in the atmosphere is about 620 mg/m³ ( ≈ 340 ppm), but levels vary widely with time and location. Indoor levels tend to be higher than outdoor levels. Gas stoves and unvented kerosene heaters are major sources of carbon dioxide indoors, but, in poorly ventilated rooms, levels may exceed 5400 mg/m³ (3000 ppm) from human metabolism alone.

An increase in the ambient level of carbon dioxide brings about a rise in the acidity of the blood and an increase in the rate and depth of breathing. Over prolonged periods, of the order of days, regulation of blood carbon dioxide levels occurs by kidney action and the metabolism of bone calcium. The latter process leads to some demineralization of the bone. Exposure to levels of 27 000 mg/m³ (15 000 ppm) or more for several days has induced reversible changes in the lung membrane of guinea pigs. In humans, exposures to carbon dioxide levels of over 90 000 mg/m³ (50 000 ppm) have produced effects on the central nervous system, such as headache and dizziness and visual distortions; there is some evidence of cardiovascular effects at similar concentrations. Subjective symptoms such as fatigue, headaches and an increased perception of warmth and unpleasant odours have been associated with carbon dioxide levels of 900 to 5800 mg/m³ (500 to 3200 ppm). In some of these studies the symptoms may have been caused by other substances, with the carbon dioxide acting as a surrogate measure of air quality (see Section 2.3.1).

The lowest concentration at which adverse health effects have been observed in humans is 12 600 mg/m³ (7000 ppm), at which level increased blood acidity has been observed after several weeks of continuous exposure. A maximum exposure level of 6300 mg/m³ (3500 ppm) should provide a sufficient margin to protect against undesirable changes in the acid-base balance and subsequent adaptive changes such as the release of calcium from the bones. This level should also provide an adequate safety margin for sensitive groups. At such a level, the effect of carbon dioxide as a ventilatory stimulant is likely to be small and so would not greatly increase the dose received of other pollutants present in the air.

Changes in the acid-base balance and release of calcium from bones occur in response to chronic carbon dioxide exposure rather than to brief excursions in concentration. Thus, a short-term exposure range is not required for this substance.

4.A.3 Carbon Monoxide

The acceptable short-term exposure ranges (ASTER) for carbon monoxide in residential indoor air are:

• ≤ 11 ppm - eight-hour average concentration;
• ≤ 25 ppm - one-hour average concentration.

Carbon monoxide is a colourless, odourless gas that is produced by the combustion of carbonaceous materials and also in human metabolism. It combines with haemoglobin to form carboxyhaemoglobin (COHb), which reduces the oxygen supply to body tissues. Endogenous levels of carboxyhaemoglobin are approximately 0.5% of the total haemoglobin (written, 0.5 COHb%).

Sources of carbon monoxide in indoor air include gas and oil appliances, tobacco smoke and the infiltration of carbon monoxide in polluted outdoor air. Outdoor levels of 0.05 to 0.9 mg/m³ (0.04 to 0.8 ppm) have been measured in rural areas, and levels as high as 57 mg/m³ (50 ppm) have been found in urban areas, although levels of 1.1 to 11 mg/m³ (1 to 10 ppm) are more typical. Indoor levels generally follow outdoor levels except in houses with unvented or poorly vented combustion appliances or where there is tobacco smoking; carbon monoxide levels of approximately 115 mg/m³ (100 ppm) have been found in the kitchens of some houses immediately after gas stoves were used for cooking.

Exposure to carbon monoxide levels leading to carboxyhaemoglobin concentrations of approximately 2.5% to 10% has been shown to cause adverse effects on the cardio-vascular system, to decrease exercise capacity and to impair psychomotor performance. Elevated carboxyhaemoglobin levels in women who smoked during pregnancy have been associated with low birth weight and educational retardation of their children. Groups that may be at particular risk from the effects of carbon monoxide exposure include those with cardiovascular, cerebrovascular and peripheral vascular diseases, foetuses, the newborn, pregnant women and individuals living at high altitude.

Experimental results suggest that, in general, such sensitive individuals can tolerate increases in carboxyhaemoglobin levels of up to 1.5 COHb%: the guidelines are intended to ensure that increases due to ambient carbon monoxide remain below this limit. Since carboxyhaemoglobin levels depend on the concentrations of both carbon monoxide and oxygen, levels are expressed only as ratios (parts per million by volume) so that the guidelines will be independent of ambient pressure.

4.A.4 Nitrogen Dioxide

The acceptable exposure ranges for nitrogen dioxide in residential indoor air are:

• ALTER: ≤ 100 µg/m ³ (≤ 0.05 ppm);
• ASTER: ≤ 480 µg/m ³ (≤ 0.25 ppm) - one-hour average concentration.

Nitrogen dioxide (NO₂) is the only oxide of nitrogen that has been shown to be detrimental to human health at concentrations that may be encountered in indoor air.

The primary outdoor sources of nitrogen dioxide are vehicular and industrial emissions. In general, nitrogen dioxide concentrations in urban atmospheres are higher than those in rural atmospheres, reflecting the large contribution of nitrogen dioxide from technological sources. In North America, the background level of nitrogen dioxide in rural areas is less than 19 µg/m³ (0.010 ppm). In urban centres, nitrogen dioxide levels are at least double this value. During the period 1977 to 1981, the average of nitrogen dioxide annual means for Canadian urban centres decreased from 60 to 44 µg/m³ (0.031 to 0.023 ppm). The highest annual mean reported in Canada for nitrogen dioxide (80 µg/m³ ; 0.042 ppm) occurred at a commercial site in 1981.

Gas stoves and unvented combustion appliances are major sources of nitrogen dioxide indoors. The indoor/outdoor ratio of nitrogen dioxide concentrations is generally less than unity in dwellings in which there are no major indoor sources, and greater than unity in dwellings with gas stoves or other combustion appliances. Families living in rural or low-pollution areas and who use gas for cooking are exposed to indoor nitrogen dioxide levels of roughly 30 µg/m³ (0.015 ppm), although average concentrations of 100 µg/m³ (0.050 ppm) have been recorded in some homes.

Interpretation of the results of available epidemiological studies on health effects associated with nitrogen dioxide exposure is rendered difficult by the lack of accurate exposure data and by confounding factors, such as exposure to other pollutants. Despite these limitations, the epidemiological studies have provided some useful data on exposure-effect relationships. In these studies an increased prevalence of respiratory illness was observed in adults and children chronically exposed to mean levels of near 200 µg/m³ (0.10 ppm) nitrogen dioxide.

The results of clinical studies indicate that both normal and asthmatic subjects can experience detrimental respiratory effects when exposed for brief periods to concentrations of approximately 960 µg/m³ (0.5 ppm). The short-term effects of nitrogen dioxide exposure below 960 µg/m³ (0.5 ppm) have been examined in only a few studies. A "no-adverse-effect level" cannot be clearly identified from the results of these studies; therefore a safety factor of two was applied to arrive at the recommended short-term exposure range.

4.A.5 Ozone (Oxidants)

The acceptable short-term exposure range (ASTER) for ozone in residential indoor air is ≤ 240 µg/m³(≤ 0.12 ppm) -one-hour average concentration.

Infiltration of outdoor air is the principal source of oxidants in indoor air. Ozone, nitrogen dioxide, hydrogen peroxide and peroxyacylnitrates are photochemical oxidants that may be present in indoor air. Nitrogen dioxide is examined in Section 4.A.4. Of the remaining oxidants, ozone is the most prevalent. Concentrations of ozone indoors are generally much lower than those outdoors, but may approach outdoor levels if windows are open. Indoor concentrations of ozone follow outdoor fluctuations with a time lag of one hour or less. The average annual outdoor concentration for urban centres in Canada was 30 µg/m³ (0.015 ppm) in 1979. Indoor ozone concentrations are typically less than 40 µg/m³ (0.02 ppm), although peak levels of 200 to 400 µg/m³ (0.1 to 0.2 ppm) have been reported. Ozone can be generated in the home by arcing of electric motors and by improperly installed or maintained electrostatic air cleaners.

Ozone is an irritant that can cause coughs, chest discomfort and irritation of the nose, throat and trachea. Ozone consistently causes detrimental effects on the lung function of healthy subjects at concentrations at or above 600 µg/m³ (0.30 ppm). Furthermore, ozone causes detrimental effects on the lung function of healthy subjects engaged in strenuous physical activity at concentrations lower than 600 µg/m³ (0.30 ppm), possibly as low as 240 µg/m³ (0.12 ppm). Results of epidemiological studies conducted to date support this finding. The available epidemiological data are, however, insufficient to serve as a basis for establishing an acceptable long-term exposure range.

Individuals exposed to concentrations of ozone between 200 and 800 µg/m³ (0.10 and 0.40 ppm) have exhibited an adaptive response, at least in terms of lung function. At present, it is not known if this adaptation is beneficial or detrimental in the long term. Available data are insufficient to serve as a basis for establishing an acceptable long-term exposure range for ozone.

4.A.6 Particulate Matter

The acceptable exposure ranges for fine particulate matter (≤ 2.5 µm mass median aerodynamic diameter -MMAD) in residential indoor air are:

• ALTER: ≤ 40 µg/m³;
• ASTER: ≤ 100 µg/m³ - one-hour average concentration.

Airborne particulate matter is a mixture of physically and chemically diverse substances, present in air as suspensions of solids or liquid droplets, varying in size from about 0.005 to 100 µm. The size range of concern when human health effects and indoor air quality are considered is from 0.1 to 10 µm in aerodynamic diameter, particles smaller than this generally being exhaled. Above 15 µm, most particles are too large to be inhaled. Virtually all particles between 10 and 15 µm are deposited in the nasopharyngeal region of the respiratory tract; health effects are associated primarily with the deposition of particles in the thoracic (tracheobronchial and pulmonary) regions. Particles have been further divided into a coarse fraction, normally around 2.5 µm and above, and a fine fraction under this size. It is this latter fraction that can reach the lung alveoli.

Indoor particles come from both indoor and outdoor sources, but the indoor matter differs in both size and chemical composition from that originating outdoors. Indoors, particles occur primarily in the fine fraction, because indoor sources such as combustion appliances and cigarettes tend to produce fine particles and the building envelope acts as a partial filter to screen out larger particles. Indoor particulate matter contains a much higher fraction of organic matter than that of outdoor air, largely because of household activities such as cooking, cleaning and use of consumer products.

Indoor concentrations of fine particulate matter tend to be higher than those outdoors. Average concentrations of particles under 3.5 µm (respirable suspended particulates or RSP) range between 20 and 30 µg/m³ Higher concentrations have been noted in "dirty" cities with high outdoor levels, and in homes with smokers or wood stoves. Cigarette smoke appears to be the most significant indoor source of particulate matter, and the presence of resident smokers has been shown to raise levels of fine particles in homes by between 12 and 40 µg/m³ per smoker.

Numerous epidemiological studies indicate that human health has improved as concentrations of airborne particulate matter have decreased. Despite the many uncertainties in these studies, they provide some useful information on levels at which adverse health effects might be expected. Increases in mortality have been observed especially among the elderly and those with pre-existing respiratory or cardiovascular disorders, when they were exposed to concentrations of particles (including coarse particles) above 500 µg/m³ accompanied by high sulphur dioxide levels for periods of one to four days. Increases in hospital admissions and in respiratory clinic visits were also noted at about the same levels, while increased prevalence of respiratory symptoms and discomfort in persons at increased risk because of pre-existing respiratory conditions were first observed at levels in the range 250 to 350 µg/m³. In children, marginal decrements in lung function lasting several weeks were also associated with short exposures at about these levels, which were correlated with outdoor and indoor RSP levels estimated to be about 80 µg/m³. Clinical studies, while not necessarily representing usual exposure conditions, also indicated that short exposures to concentrations of fine particulates (expressed as sulphuric acid) above 100 µg/m³ could result in irritation and alterations in respiratory function in asthmatic subjects and in slowing of bronchial clearance in normal individuals.

Chronic exposure for periods of several years to moderate levels of airborne particles estimated to be around 180 µg/m³ total suspended particulates or 80 µg/m³ fine particles (respirable suspended particulates or RSP) appear to be correlated with increased prevalence of respiratory symptoms and chronic respiratory disease, accompanied by reduced respiratory-function measurements, in adults and children.

4.A.7 Sulphur Dioxide

The acceptable exposure ranges for sulphur dioxide in residential indoor air are:

• ALTER: ≤ 50 µg/m ³ (≤ 0.019 ppm);
• ASTER: ≤ 1000 µg/m ³ (≤ 0.38 ppm) - five-minute average concentration.

Sulphur dioxide is the main oxide of sulphur found in indoor air. Indoor concentrations are generally lower than those outdoors by a factor of about two, primarily because most sources are outdoors, and sulphur dioxide is readily absorbed by furnishings and fabrics.

Interpretation of the results of available epidemiological studies on health effects associated with exposure to sulphur dioxide is complicated by a paucity of representative exposure data and by confounding factors such as exposure to other air pollutants. However, such studies have provided some useful albeit uncertain data concerning exposure-effect relationships. Excess mortality, particularly among the elderly and those with pre-existing cardiopulmonary disease, has been observed in populations exposed to 24-hour pollution episodes in which sulphur dioxide concentrations exceeded 300 to 400 µg/m³ (0.12 to 0.15 ppm). Increases in hospital admissions and emergency room visits have also been associated with exposure to these levels. Increased prevalence of acute and chronic respiratory symptoms and impaired pulmonary function have been observed in adults and children exposed for extended periods (> 1 year) to mean levels of 100 µg/m³ (0.038 ppm) sulphur dioxide.

Relevant data have also been obtained from clinical studies; however, exposures in such investigations are short and do not necessarily represent usual exposure conditions. In normal subjects, increased airway and nasal flow resistance and a change in the mucociliary flow rate have been observed following exposure to 2600 µg/m³ (1.0 ppm) sulphur dioxide; reversible increases in specific airway resistance have been observed in asthmatics exposed by natural breathing for brief periods to concentrations exceeding 1000 µg/m³ (0.38 ppm).

4.A.8 Water Vapour

Based on health considerations, the acceptable short-term exposure ranges (ASTER) for water vapour in residential indoor air are:

• 30% to 80% relative humidity - summer;
• 30% to 55% relative humidity - winter*

*unless constrained by window condensation.

For purposes of indoor air quality, the most useful measure of water vapour levels is relative humidity, the ratio of the concentration of water vapour present to the concentration needed to saturate air at that temperature. Indoor humidity is determined by the humidity and temperature of outdoor air as well as by indoor sources and sinks of water vapour. The main indoor sources are human and animal metabolism, and such activities as bathing, cooking and the washing and drying of clothes. Small amounts of water vapour are also produced by combustion.

The moisture content of indoor air is reduced by dilution with drier outdoor air, by condensation on cold surfaces and by absorption or adsorption of water by materials in the home. Homes heated electrically are likely to have higher indoor relative humidities in winter than comparable homes heated by combustion furnaces, since the latter tend to increase the infiltration of dry outside air. Relative humidities in Canadian homes have been found to range from 21% to 68%.

In conjunction with temperature and air flow, relative humidity affects comfort; conditions of 20% to 60% relative humidity at temperatures between 20 and 25°C are usually judged comfortable. Long periods of low relative humidity are believed to cause dryness of the skin and mucous membranes, which may lead to chapping and irritation. High humidity at high temperatures leads to increased sweating and a loss of electrolytes from the blood; prolonged exposures may lead to heat exhaustion or heat stroke. Groups that may be at particular risk from high humidity are those suffering from cardiovascular disease, infants born two or three weeks before term and the elderly. Arthritis sufferers have been found to experience increased symptoms when a rise in humidity accompanies a drop in atmospheric pressure. People who suffer from asthma develop symptoms of bronchoconstriction after exercise more readily when breathing air at low humidity.

Several species of bacteria and viruses survive best at low or high, rather than intermediate, humidities. Humidity levels above 50% have been found to increase the population size of moulds, fungi and mites that may cause allergies. The evidence suggests that humidity levels should be maintained between 40% and 50% to reduce the incidence of upper respiratory infections and to minimize adverse effects on people suffering from asthma or allergies. Such a range would be hard to maintain, however, and exposure to higher or lower levels is unlikely to affect the health of most people.