2 - Health-based Guideline values

The health-based guideline values aim to protect people's health and well-being. They are generally designed to protect those who are most susceptible to experiencing health effects when a particular contaminant is inhaled. All the values are based on health effects, except the one for hydrogen sulphide, which is based on odour nuisance. They have been derived from epidemiological studies, international guidelines and, in some cases, laboratory research. The economic benefits and costs associated with achieving the values have not been taken into account. These must be considered when specific reduction strategies are developed (discussed further in section 3.3).

Potential health effects caused by inhaling contaminants range from relatively minor impacts, such as respiratory irritation, headaches and cough, to more serious health impacts, including asthma, cancer and advanced mortality in those already suffering serious illness. The following sections contain only brief descriptions of the human health effects of each contaminant (as opposed to the results of animal or laboratory research) and limited references. The reader is strongly advised to seek more detailed information and references in Chiodo and Rolfe (2000) and Denison et al. (2000).

The new contaminants (also referred to as 'hazardous air pollutants') were selected by prioritising those that are of greatest concern, are most likely to exist in New Zealand, and that should be monitored, assessed and, where necessary, reduced. The ranking method considered each contaminant's hazard to human health, toxicity, likelihood of being discharged, potential to cause public exposure, and ultimate fate in the environment (Chiodo and Rolfe, 2000).

In most cases the guideline value is based on the 'no observable adverse effect level' or 'lowest observable adverse effect level' of the contaminant, as determined through research studies. A safety factor may also be applied. Where research has been unable to determine such a threshold, a judgement has been made as to what constitutes an 'acceptable' health risk, taking into account the level of uncertainty in our understanding of the health effects caused by the contaminant. Given these different considerations, the result is inevitably a range of risk values, which are specified in Appendix 4.

Fluoride guideline values are now covered under Chapter 4 on ecosystem protection.

Table 1: Guideline values and the key health effects

Notes:

2.2.1 Guideline values

The guideline values are 30 mg/m³ (1-hour average) and 10 mg/m³ (8-hour average).

The guideline values aim to ensure that nobody will be exposed to levels of ambient carbon monoxide (CO) that would result in blood carboxyhaemoglobin (COHb) levels greater than 2.5%, at any level of physical activity. They are set to protect the more susceptible population sub-groups, including those with ischaemic heart disease, other forms of cardiac disease (including cyanotic heart disease), hypoxaemic lung disease, cerebrovascular disease, peripheral vascular disease, those with anaemia and haemoglobin abnormalities, children, and developing foetuses.

2.2.2 Health effects

When inhaled, CO combines with haemoglobin (Hb), the blood's oxygen-carrying protein, to form COHb. In this state the Hb is unable to carry oxygen (O₂). It takes about 4 to 12 hours for CO concentrations in the blood to reach equilibrium with the CO concentration in air, so any fluctuations in the ambient CO concentrations are only slowly reflected in the COHb levels in humans.

High exposures to CO can cause acute poisoning, with coma and collapse occurring at COHb levels of over 40%. Ambient exposures to CO are several orders of magnitude lower than those associated with acute poisoning. However, some exposures in urban settings have been shown to adversely affect the heart, brain and central nervous system.

Adverse cardiovascular effects of CO inhalation include decreased O₂ uptake and decreased work capacity. Those with angina may suffer decreased exercise capacity at onset of angina, and increased duration of angina. Adverse neurobehavioural effects of CO include a decrease in vigilance, visual perception, manual dexterity, ability to learn and perform complex sensorimotor tasks in healthy individuals, and reduced birth weight in non-smoking mothers.

Recent epidemiological studies have found effects in susceptible groups at levels lower than previously thought to be of concern. The Ministry therefore intends to review the CO guideline values within the next two years.

2.2.3 Description and sources

CO is a colourless, odourless and tasteless gas. It is a trace constituent of the atmosphere, with background levels normally ranging between 0.01 and 0.2 mg/m³. CO is formed from burning fuels, especially during incomplete combustion. It is produced both by natural processes (for example, from volcanoes) and by human activities (for example, the incomplete combustion of carbon-containing fuels, especially from motor vehicles). Industrial processes may also produce CO.

2.3.1 Guideline values

The PM₁₀ guideline values are 50 µg/m³ (24-hour average) and 20 µg/m³ (annual average).

Research has been unable to determine a threshold for PM₁₀ below which there are no adverse effects (WHO, 1999). Consequently, these guideline values are associated with a higher level of health risks than for many of the other contaminants. The values for PM₁₀ are designed to be the first step in reducing the health effects caused by particles in areas where concentrations breach the guideline values. Where PM₁₀ levels are within the guideline values, efforts should still be made to maintain and, where possible, further reduce levels (see also discussion in section 3.3).

The 1994 24-hour average guideline value of 120 µg/m³ is no longer appropriate given recent evidence of the acute (short-term) health effects of PM₁₀, and the annual average value has been amended to take account of recent evidence of the chronic (long-term) health effects of PM₁₀. The values are consistent with several current international guideline values and standards.

Recent research has shown that particles less than 2.5 microns in diameter (PM_2.5) may responsible for specific health effects caused by fine particles. We therefore need to increase our understanding of PM_2.5 in New Zealand and to promote monitoring and source assessments. A monitoring value of 25 µg/m³ (24-hour average) can be used for assessing monitoring results and to judge whether further investigations are needed to quantify PM_2.5 sources. In suggesting this value, the Ministry aims to promote PM_2.5 monitoring and assessment. It is premature to use PM_2.5 as a target for air-shed management until further research can accurately determine its specific health effects and its sources. The Ministry will commence an investigation into PM_2.5 in 2002 with the aim of establishing an appropriate guideline value by 2004.

2.3.2 Health effects

The major health effects from airborne particles are:

• increased mortality
• aggravation of existing respiratory and cardiovascular disease
• hospital admissions and emergency department visits
• school absences
• lost work days
• restricted activity days.

People most susceptible to the effects of particles include the elderly; those with existing respiratory disease such as asthma, chronic obstructive pulmonary disease and bronchitis; those with cardiovascular disease; those with infections such as pneumonia; and children. As discussed above, the results of epidemiological studies have provided no evidence for the existence of a threshold value below which no adverse health effects are observed.

2.3.3 Description and sources

Particles are diverse in their chemical and physical characteristics and can span several orders of magnitude in size. Particles derive from many sources, including motor vehicles (especially diesels), solid-fuel burning for domestic heating, industry, photochemical processes, and natural sources such as dust, pollens and sea spray.

2.4.1 Guideline values

The nitrogen dioxide guideline values are 200 µg/m³ (1-hour average) and 100 µg/m³ (24-hour average).

The guideline values are based on a safety factor of 50% applied to the lowest observable adverse effect level in order to ensure adequate protection of the more vulnerable sub-groups in the population, including children, asthmatics of all ages (but especially children), and compromised adults with chronic respiratory and cardiac disorders. This value is consistent with the WHO guideline value of 200 µg/m³ (1-hour average) and the 1994 New Zealand 24-hour guideline value of 100 µg/m³.

2.4.2 Health effects

Exposure to nitrogen dioxide (NO₂) has been shown to cause reversible effects on lung function and airway responsiveness. It may also increase reactivity to natural allergens. Inhalation of NO₂ by children increases their risk of respiratory infection and may lead to poorer lung function in later life. Recent epidemiological studies have shown an association between ambient NO₂ exposure and increases in daily mortality and hospital admissions for respiratory disease. NO₂ has also been shown to potentiate the effects of exposure to other known irritants, such as ozone and respirable particles.

There is some evidence that acute exposure to NO₂ may cause an increase in airway responsiveness in asthmatic individuals. This response has been observed only at relatively low NO₂ concentrations, mostly in the range of 400-600 µg/m³. However, the findings of both clinical and epidemiological studies do not provide any clear quantitative conclusions about the health effects of short-term exposures to NO₂. The adverse health effects at low levels of NO₂ remain equivocal, with conflicting patterns of results obtained in both controlled exposure studies and in epidemiological studies. The contribution of NO₂ as one of a mixture of pollutants in the ambient environment has yet to be clearly defined.

2.4.3 Description and sources

NO₂ is a pungent, acidic gas. Corrosive and strongly oxidising, it is one of several oxides of nitrogen (NO_x) that can be produced as a result of combustion processes. Combustion of fossil fuels converts atmospheric nitrogen and any nitrogen in the fuel into its oxides, mainly nitric oxide (NO) but with small amounts (5-10%) of NO₂. NO slowly oxidises to NO₂ in the atmosphere. This reaction is catalysed in the presence of O₃. In the presence of sunlight, NOx, including NO₂, react with volatile organic compounds to form photochemical smog.

The main source of NO₂ resulting from human activities is the combustion of fossil fuels (coal, gas and oil). In cities, about 80% of ambient NO₂ comes from motor vehicles. Other sources include the refining of petrol and metals, commercial manufacturing, and food manufacturing. Electricity generation using fossil fuels can also produce significant amounts.

2.5.1 Guideline values

The guideline values for sulphur dioxide are 350 µg/m³ (1-hour average) and 120 µg/m³ (24-hour average).

These values are set to provide protection of lung function and prevent other respiratory symptoms of vulnerable sub-groups in the population, including asthmatics and those with chronic obstructive lung disease. They are in line with current international guideline values and standards. The annual guideline value for sulphur dioxide is now discussed in Chapter 4 on ecosystem-based guidelines. The short-term guideline value has been removed, as it is not appropriate for managing air quality in large air sheds, however, shorter-term criteria for sulphur dioxide may be appropriate for assessing industrial discharges.

2.5.2 Health effects

Sulphur dioxide (SO₂) is a potent respiratory irritant when inhaled. Asthmatics are particularly susceptible. SO₂ acts directly on the upper airways (nose, throat, trachea and major bronchi), producing rapid responses within minutes. It achieves maximum effect in 10 to 15 minutes, particularly in individuals with significant airway reactivity, such as asthmatics and those suffering similar bronchospastic conditions.

The symptoms of SO₂ inhalation may include wheezing, chest tightness, shortness of breath or coughing, which are related to reductions in ventilatory capacity (for example, reduction in forced expiratory volume in one second, or FEV₁), and increased specific airway resistance. If exposure occurs during exercise, the observed response may be accentuated because of an increased breathing rate associated with exercise. A wide range of sensitivity is evident in both healthy individuals and more susceptible people, such as asthmatics, the latter being the most sensitive to irritants.

Epidemiological studies have shown significant associations between daily average SO₂ levels and mortality from respiratory and cardiovascular causes. Increases in hospital admissions and emergency room visits for asthma, COPD and respiratory disease have also been associated with ambient SO₂ levels. These associations were observed with up to a two-day lag period. Long-term exposure to SO₂ and fine particle sulphates (SO₄^2-) has been associated with an increase in mortality from lung cancer and development of asthma and cardio-pulmonary obstructive disease. Increases in respiratory symptoms have also been associated with SO₂ levels.

2.5.3 Description and sources

SO₂ is a colourless, soluble gas with a characteristic pungent smell. It is mainly produced by the combustion of fossil fuels containing sulphur and some industrial processes.

2.6.1 Guideline values

The guideline values for ozone are 150 µg/m³ (1-hour average) and 100 µg/m³ (8-hour average).

Recent epidemiological studies demonstrate that there is no apparent threshold concentration for ozone (O₃) below which adverse health effects will not be observed. The proposed guideline values aim to provide reasonable protection for human health by protecting respiratory function in vulnerable sub-groups of the population, including those with asthma and chronic lung diseases, healthy young adults undertaking active outdoor exercise over extended periods, and the elderly, especially those with cardiovascular disease.

Guidelines to protect vegetation from the impacts of O₃ are provided in Chapter 4.

2.6.2 Health effects

Epidemiological evidence indicates that a wide variety of health outcomes are possible from exposure to O₃, including short-term effects on mortality, hospital admissions and emergency room attendances, respiratory symptoms and lung function. Experimental evidence has demonstrated short-term physiological and pathological changes in the respiratory system of humans. Although potentially more important, there is little evidence of long-term effects. Recently, ozone has been found to cause asthma, particularly in young children exercising in areas with higher ozone levels.

The health effects associated with exposure to ozone can be summarised as follows:

• increase in daily mortality, respiratory and cardiovascular disease
• increase in hospital admissions and emergency room visits
• increase in respiratory and cardiovascular disease
• decrease in lung function
• increase in symptoms of respiratory illness such as cough, phlegm and wheeze
• increase in bronchodilator usage.

These effects are observed in sensitive sub-populations, although effects on lung function have also been observed in the healthy normal population.

2.6.3 Description and sources

O₃ is a secondary air pollutant formed by reactions of primary pollutants - oxides of nitrogen (NO_x) and hydrocarbons - in the presence of sunlight. These primary pollutants arise mainly from motor-vehicle emissions, stationary combustion sources and industrial and domestic use of solvents and coatings.

O₃ is only one of a group of chemicals known as photochemical oxidants (commonly referred to as photochemical smog), but it is the predominant one. Also present in photochemical smog are formaldehyde, other aldehydes, and peroxyacetyl nitrate. Most epidemiological studies relate to O₃ plus the other oxidants, though it is usually only the former that is measured as an indicator of photochemical oxidants.

2.7.1 Guideline value

The guideline value for lead in PM10 is 0.2 µg/m³ (3-month moving average, calculated monthly).

This value aims to protect people from the health effects of inhaling lead - especially its effects on developing foetuses and on children's health, such as decreased intelligence and performance. With no apparent threshold for lead it is appropriate to have the ambient air quality guidelines for lead as low as possible.

The guideline value is reasonably consistent with the UK long-term objective of 0.25 µg/m³ (annual average) to be achieved by 2008, and the recommendation of their Expert Panel on Air Quality Standards (EPAQS), which concluded that the effects on the health of children at this level would be so small as to be negligible. The guideline value is more precautionary than that recommended by WHO (1999) of 0.5 µg/m³ (annual average).

This guideline value does not take account of other routes of exposure to lead, such as by eating contaminated food. Where other routes may be significant, they should also be considered when assessing the impacts of lead. Alternative sources of information and deposition criteria to use when considering exposure routes can be sourced from WHO (1999).

2.7.2 Health effects

The health effects of lead are related to the level of lead in human blood. Although there are some differences in the bio-availability of different lead compounds, the health effects caused by increased blood lead levels are the same, regardless of the lead compounds causing the exposure.

One of the most widely recognised effects of lead exposure is a decrease in intelligence and general academic performance in children, especially when exposed to lead within the first two to three years of life. The sub-groups most vulnerable to lead are young children and developing foetuses. There is now clear epidemiological evidence of a close causal relationship between prenatal exposure to lead and early mental development indices, and it has not been possible to identify a clear threshold for its effects.

Where there is the likelihood of ingestion from deposited lead, this must be taken into account in conjunction with inhalation exposure when considering the total body burden. This is especially so when assessing potential health effects on children living in an area where lead may be inhaled and/or ingested.

2.7.3 Description and sources

Lead is a bluish or silvery-grey soft metal. With the significant reduction in the amount of lead allowed in petrol in New Zealand (current specifications allow a maximum of 13 mg/l) there is now very little lead in vehicle emissions. However, residual lead from historical vehicle emissions may still be present in the environment, although this is unlikely to be a concern for lead inhalation.

Airborne lead can also be found around some industrial discharges, such as at metal smelters, and houses or other structures where lead-based paint is being, or has been, removed without the proper safety precautions. Exposure for both adults and children can arise from inhaling fine lead particles in the air, or by ingesting soils or crops contaminated by lead deposition. In these cases, contaminated soils and dusts act as a continuous source of lead.

2.8.1 Guideline value

The guideline value for hydrogen sulphide is 7 µg/m³ (1-hour average).

Unlike other guideline values, the value for hydrogen sulphide (H₂S) is based on preventing odour annoyance and the resulting impacts on well-being rather than specific health effects. The guideline value may not be suitable for geothermal areas.

More recent work on odour has suggested that alternative management and assessment methods may be more appropriate. These will be considered in a forthcoming review of Odour Management under the Resource Management Act (Ministry for the Environment, 1995a).

Further monitoring and research is required to develop a guideline value for long-term exposure to hydrogen sulphide where natural background concentrations from geothermal activities occur above the odour-based guideline value. H₂S will be reviewed at the same time as PM_2.5 and CO.

2.8.2 Health effects

H₂S is a colourless gas with a distinctive odour at low concentrations. Humans detect it at levels of 0.2-2.0 µg/m³, depending on its purity. This is the odour threshold, which is defined as the concentration at which 50% of a group of people can detect an odour. At about three to four times this concentration range it smells like rotten eggs.

H₂S causes nuisance effects because of its unpleasant odour at concentrations well below those that cause health effects. Continuous exposure to H₂S reduces sensitivity to it.

In acute exposures H₂S acts on the nervous system to cause a range of symptoms characterised as H₂S intoxication. At levels above 15 mg/m³ it causes eye irritation, and above 70 mg/m³ it causes permanent eye damage. Above 225 mg/m³ it paralyses olfactory perception so that the odour is no longer a warning signal of the gas's presence. At concentrations above 400 ug/m³ there is a risk of pulmonary oedemea, and above 750 mg/m³ it over-stimulates the central nervous system, causing rapid breathing, cessation of breathing, convulsions, and unconsciousness. At 1400 mg/m³ it is lethal.

Adverse effects have been observed in occupationally exposed populations at an average concentration of 1.5-3.0 mg/m³. Symptoms include restlessness, lack of vigour, and frequent illness. In occupationally exposed groups, at levels of 30 mg/m³ or more 70% complained of fatigue, headache, irritability, poor memory, anxiety, dizziness and eye irritation.

2.8.3 Description and sources

H₂S occurs naturally in geothermal areas. It also forms under anaerobic conditions where organic material and sulphate are present. Human activities can release naturally occurring H₂S, such as when natural gas is extracted or when heat is extracted from geothermal waters. H₂S is also produced in industrial processes where sulphur and organic materials combine in oxygen-deprived environments. These include pulp and paper manufacturing, oil refining, tanning of animal hides, and wastewater treatment.

2.9.1 Guideline value

The guideline value for acetaldehyde is 30 µg/m³ (annual average).

This value aims to protect people from adverse health effects of acetaldehyde inhalation rather than its odour nuisance effects. It is based on the WHO upper risk level of 9 x 10^-7 per µg/m³, and an acceptable carcinogenic risk of between 1 in 10,000 and 1 in 100,000. The chosen value of 30 µg/m³ takes a reasonably precautionary approach as it comes from the lower end of the range of 12-120 µg/m³ derived from the WHO risk level and acceptable carcinogenic risk.

2.9.2 Health effects

The major route for exposure to acetaldehyde in humans is inhalation. The major toxic effects for acute exposure are eye, nose, skin and respiratory tract irritation; erythema; coughing; pulmonary oedema; and necrosis. Extremely high concentrations can cause respiratory paralysis and death. Depressed respiratory rates and elevated blood pressure have been observed in animals exposed to high concentrations of acetaldehyde. Chronic intoxication of acetaldehyde in humans can produce symptoms resembling alcoholism.

Human data regarding the carcinogenic potential of acetaldehyde are inadequate, but an increased incidence of nasal tumours in rats and laryngeal tumours in hamsters has been observed following acetaldehyde inhalation exposure (US EPA, 1998).

Acetaldehyde has been classified as a Group B2 carcinogen of low potency by the US EPA, and a Group 2B carcinogen by IARC (IARC, 1998).

2.9.3 Description and sources

Acetaldehyde, like formaldehyde, is very reactive and is important in photochemical smog reactions. Major sources of acetaldehyde are motor vehicle exhaust and domestic solid-fuel combustion. It is also released from some industrial processes.

2.10.1 Guideline values

The guideline value for benzene is 10 µg/m³ (annual average), with a guideline value of 3.6 µg/m³ (annual average) to be achieved by 2010.

These values are based on a combination of the European Council and UK approaches and the need to set reducing, precautionary guideline values for a carcinogen such as this.

2.10.2 Health effects

The most significant chronic adverse effects from prolonged exposure to benzene are haemotoxicity, genotoxicity and carcinogenicity (WHO, 1996). Haemotological effects of varying severity have occurred in workers occupationally exposed to high levels of benzene. Decreased red and white blood cell counts in humans have been reported above median levels of approximately 120 mg/m³. There is only weak evidence for effects below 32 mg/m³, and no reported effects at 0.03-4.5 mg/m³.

Data from animal and human exposures indicate that benzene is both mutagenic and carcinogenic. Increased mortality from leukaemia has been demonstrated in occupationally exposed workers. Benzene has been classified as a Group A carcinogen of medium potency by the US EPA, and a Group 1 carcinogen by IARC (see Appendix 3).

2.10.3 Description and sources

Benzene (C₆H₆) is a colourless, clear liquid with a density of 0.87 g/cm³ (at 20°C) and a boiling point of 80.1°C. Chemically it is fairly stable but it undergoes substitution and addition reactions.

Motor vehicles and household fires are significant sources of benzene in New Zealand's air. There are also some industrial activities that use and discharge benzene. Motor vehicle exhaust emissions of benzene are thought to derive partly from unburnt benzene in the fuel, and partly from the dealkylation of other aromatic hydrocarbons. Other sources of benzene that may impact locally include oil refining, petrochemical production, and synthetic rubber manufacture.

2.11.1 Guideline value

The guideline value for 1,3-butadiene is 2.4 µg/m³ (annual average).

This guideline value is designed to reduce ambient concentrations to as low a level as reasonably practicable such that 1,3 butadiene inhalation represents an exceedingly small risk to human health. The value is consistent with the UK's Air Quality Objective to be achieved by 2003. The evidence that 1,3-butadiene is a genotoxic carcinogen is ambivalent, but has been accepted by expert panels in the UK and in the US, and by IARC. A precautionary approach in setting the ambient guideline value for New Zealand has therefore been taken.

2.11.2 Health effects

The main route for 1,3-butadiene exposure in humans is inhalation. Adverse health effects from acute exposure include irritation of the eyes, throat, lungs and nasal passages, and neurological effects such as blurred vision, fatigue, headache and vertigo. Chronic non-cancer effects in exposed humans include cardiovascular and blood diseases.

The US EPA classifies 1,3-butadiene as a Group B2 carcinogen of medium potency. The IARC classification is Group 2A (IARC, 1998). The UK Expert Panel accepts that 1,3-butadiene is a genotoxic carcinogen (UK Expert Panel on Air Quality Standards, 1998).

WHO considers that the uncertainties in current estimates of carcinogenic risks to humans do not allow a specific guideline value to be recommended. Given that there is some equivocal evidence of carcinogenicity, they recommend prudence in developing ambient air quality guidelines/standards.

The UK EPAQS (1998) recommended a 1,3-butadiene standard of an annual running average of 2.4 µg/m³. The panel concluded that on the basis of current data, the increased risks of lymphomas and leukaemias would be unlikely to be detectable by any practicable means in workers from a lifetime exposure to 2,400 µg/m³ of 1,3-butadiene. The recommended standard was arrived at by applying a safety factor of 100 to account for differences in chronological and working life, and in susceptibility). The panel believed that standards for genotoxic carcinogens should be set as low as practicable. Since ambient levels in the UK on current data have not exceeded 2.4 µg/m³, the panel has recommended this level as the standard, implying an additional safety factor of 10.

2.11.3 Description and sources

1,3-butadiene (C₄H₆) is a colourless, highly reactive gas, with a mild aromatic odour. Emission sources include motor vehicle exhausts, and production of synthetic rubber, latex and resin. The atmospheric half-life of 1,3-butadiene is quite short (several hours) compared to benzene (several days).

2.12.1 Guideline value

The ambient guideline value for formaldehyde is 100 µg/m³ (30-minute average).

This guideline value is based on the WHO value and is designed to protect most individuals. However, some people may be (or have become) hypersensitive to formaldehyde, so it is important to consider whether there are such people in the population, particularly in areas where formaldehyde levels may be elevated. If so, full health risk assessments should be carried out.

2.12.2 Health effects

The major route for exposure to formaldehyde in humans is inhalation. The main toxic effects for acute exposure are eye, nose and throat irritation and effects on the nasal cavity. Other effects include coughing, wheezing, chest pains and bronchitis. Chronic exposure has also been associated with respiratory symptoms and eye, throat and nose irritation.

WHO notes that there is substantial inter-individual variability in human formaldehyde responses. Significant increases in signs of irritation occur at levels above 0.1 mg/m³ in healthy subjects, and a progression of symptoms occur above 1.2 mg/m³. No lung function alterations were noted in healthy non-smokers and asthmatics exposed to formaldehyde levels up to 3.7 mg/m³, leading to the conclusion that the observed effects were related more to peak than to mean concentrations (WHO, 1996).

Formaldehyde is classified as a Group B1 carcinogen of medium potency by the US EPA, and as a Group 2A carcinogen by IARC (1998).

The WHO ambient air quality guideline value is 100 µg/m³, 30-minute average, for protection of the general population. This is based on a no observable adverse effects level of 100 µg/m³ and an uncertainty factor of 1. WHO also recommend that for groups within the general population that show hypersensitivity reactions without immunological signs, the formaldehyde concentration should be kept to a minimum and not exceed 10 µg/m³ (30-minute average).

2.12.3 Description and sources

Formaldehyde (HCHO) is the simplest and most common aldehyde found in the environment. At normal temperatures it is a colourless gas with a pungent odour, and is soluble in water.

Motor vehicles and domestic solid-fuel combustion are major sources of formaldehyde in the urban environment. Industrial sources can be locally important, and include the manufacture of particleboard, plywood, fabrics and furnishings. Formaldehyde emissions from furnishings and fittings can be important for indoor air quality.

The atmospheric half-life is quite short (a few hours), so the main impacts are relatively close to the source. However, formaldehyde is highly reactive and is an important contaminant in widespread photochemical smog formation.

2.13.1 Guideline value

The guideline value for benzo(a)pyrene (as an indicator of polyaromatic hydrocarbons) is 0.0003 µg/m³ (annual average).

This is based on an acceptable risk to the community of between 1 in 10,000 and 1 in 100,000 which has been applied to the WHO unit risk values to provide an annual average guideline value for benzo(a)pyrenein the range 0.00012-0.0012 µg/m³.

The Ministry intends to review this guideline in five years to work towards a toxic equivalency scheme for polyaromatic hydrocarbons (PAHs) similar to that for organochlorines.

2.13.2 Health effects

There are no human data on the effects of acute exposure to benzo(a)pyrene (BaP) and other PAHs. Chronic exposure to BaP in humans has resulted in dermatitis, photosensitisation, eye irritation, and cataracts. Epidemiological studies have reported increases in lung cancer in humans from exposure to coke-oven and roof-tar emissions and cigarette smoke, all of which contain a number of PAHs.

WHO notes that the carcinogenicity of PAH mixtures may be influenced by other compounds emitted with PAHs during incomplete combustion, and also points out the poor quality of available data sets from which to derive a risk assessment for BaP (WHO, 1996).

WHO has determined an inhalation unit risk of 8.7 x 10^-2 per µg/m³ BaP, based on interpolation from risk estimates for PAHs in coke-oven emissions. WHO has also determined an inhalation unit risk from studies of animals exposed to complex mixtures of PAHs of 2 x 10^-5 per µg/m³ BaP 10^-5 per ng/m³ (WHO, 1996). They recommend that unit risks be used to set ambient air quality guidelines.

The US EPA has classified BaP as a Group B2 carcinogen of medium potency. The IARC classification is Group 2A (IARC, 1998). The US EPA has not determined an inhalation unit risk for BaP.

The UK has proposed a new objective for BaP of 0.00025 µg/m³ (annual average at 20°C) to be achieved by the end of 2010.

2.13.3 Description and sources

PAHs are a large group of organic compounds with two or more benzene rings. They are semi-volatile compounds that occur in both the gaseous phase or attached to particles. PAHs with low vapour pressures are almost totally adsorbed onto particles. BaP is an indicator species for PAHs. Although a relatively minor component of PAHs, BaP is extremely important because of its highly toxic and carcinogenic properties and, as discussed above, most guideline values are based on BaP.

PAHs arise from incomplete combustion of solid and liquid fuels. Main sources of PAHs in New Zealand include vehicles, home-heating fires and some industrial processes.

2.14.1 Guideline values

The guideline values for mercury are 0.33 µg/m³ (annual average) for inorganic mercury and 0.13 µg/m³ for organic mercury (annual average).

The guideline values aim to protect people from adverse health effects caused by inhaling mercury fumes or particles.

The value for inorganic mercury is derived from the occupational health standards for inorganic mercury and the US EPA reference concentration (RfC) and the Californian Air Resources Board's reference exposure level (REL) values (Chiodo and Rolfe, 2000). The value for organic mercury is derived from the value for inorganic mercury by scaling according to the occupational health standards.

The above levels should be viewed as applicable where exposure to mercury is mainly through inhalation. They will need to be adjusted downwards where dietary intake is significant.

2.14.2 Health effects

The effects of chronic exposure to elemental mercury include central nervous system (CNS) effects (such as erethism, irritability, insomnia), severe salivation, gingivitis and tremor, kidney effects (including proteinuria), and acrodynia in children. The primary effect of chronic exposure to methyl mercury is CNS damage, while chronic exposure to inorganic mercury induces kidney damage (US EPA, 1998). Acute inhalation exposure to high levels of elemental mercury in humans results in CNS effects such as hallucinations, delirium and suicidal tendencies; gastrointestinal effects; and respiratory effects such as chest pains, dyspnoea, cough, pulmonary function impairment, and interstitial pneumonitis. Acute exposure to high levels of methyl mercury also results in CNS effects, including blindness, deafness, impaired level of consciousness and death.

Studies of the effects on human reproduction and development from exposure to inorganic mercury are ambivalent. There is no information on reproductive and developmental effects on humans, but animal studies have reported effects including testicular changes and developmental abnormalities. Studies on the carcinogenic effects of elemental mercury on humans are inconclusive. No studies are available on the carcinogenic effects of methyl mercury on humans.

The US EPA has classified inorganic and methyl mercury as Group C carcinogens, and elemental mercury as Group D (unclassifiable). IARC has classified methyl mercury compounds as a Group 2B carcinogen, and mercury and inorganic compounds as Group 3 (unclassifiable) (IARC, 1998).

No unit risk factors are available for mercury and mercury compounds. Their status as carcinogens is ambivalent. WHO recommends a guideline for inorganic mercury of 1 µg/m³ as an annual average. This is based on a lowest observable adverse effects level for renal tubular effects on humans of 20 µg/m³ and an uncertainty factor of 20.

The US EPA RfC for elemental mercury is 0.3 µg/m³, and the reference dose (RfD) for methyl mercury is 0.3 µg/kg/day (US EPA, 1993). The California Air Resources Board (CARB) RELs are as follows:

• elemental mercury 0.3 µg/m³ (chronic REL)
• inorganic mercury and mercury compounds 30 µg/m³ (acute REL)
• methyl mercury 1 µg/m³ (chronic REL).

The acute REL for inorganic mercury is under review, and a draft value of 1.8 µg/m³ is to be reviewed by the Scientific Review Panel on Toxic Air Contaminants.

2.14.3 Description and sources

Elemental mercury exists almost totally in the gas phase in the atmosphere, as does methyl mercury, while inorganic mercury compounds are usually particle-bound (CARB, 1998).

Volcanic and geothermal activities are the most important sources of mercury in New Zealand. Specific sources include fossil fuel combustion such as vehicles, trucks and power stations. Other sources are crematoria, waste incinerators, gold-recovery plants and chlor-alkali plants.

2.15.1 Guideline values

The guideline value for chromium VI is 0.0011 µg/m³ (annual average) and for other chromium (chromium III and chromium metal) it is 0.11 µg/m³ (annual average).

The guideline value for chromium VI recognises that it is a human carcinogen of high potency, and that a risk level of 1 in 100,000 (which is at the lower end of the range considered acceptable by the US EPA) is appropriate for New Zealand. This guideline value for chromium VI is at the top end of WHO values but lower than the US value.

For chromium metal and III compounds, concentrations 100 times larger than those for chromium VI is appropriate on the basis of their much lower toxicity and non-carcinogenicity.

As is the case for mercury, these values may need to be adjusted downwards if dietary intake is significant.

2.15.2 Health effects

Chromium VI compounds are more toxic than chromium III. The respiratory tract is the major target organ for acute inhalation exposure to chromium VI. Dyspnoea, coughing, and wheezing in humans have been reported following exposure to very high levels. Gastrointestinal and neurological effects have also been reported. Chronic inhalation exposure has been associated with effects on the respiratory tract. Perforations and ulcerations of the septum, bronchitis, decreased pulmonary function, pneumonia, asthma, and nasal itching and soreness have also been reported in humans following exposure. Other effects of chronic inhalation exposure have been reported on the liver, kidney, gastrointestinal and immune systems, and possibly the blood.

Complications during pregnancy and childbirth in humans have been reported following inhalation exposure. Reproductive effects have not been reported in animal studies, but oral exposure has been reported to cause severe developmental effects in mice. Epidemiological studies of workers have established that inhaled chromium is a human carcinogen, resulting in increased risk of lung cancer, although the studies were unable to differentiate between chromium VI and chromium III compounds.

The US EPA has classified chromium VI as a Group A carcinogen of high potency, and chromium III as not classifiable (Group D). IARC has classified chromium VI as a Group 1 carcinogen, and chromium III as Group 3 (unclassifiable) (IARC, 1998).

Unit risk factors for chromium VI compounds for inhalation exposure adopted by various groups are as follows: 1.2 x 10^-3 per µg/m³ (US EPA, 1998), 1.5 x 10^-1 per µg/m³ (CARB, 1998) and 1.1-13 x 10^-2 per µg/m³ (WHO, 1996).

Because chromium VI is considered a human carcinogen, WHO has not specified a guideline for ambient air quality, but recommends that unit risk factors be applied.

The US EPA specifies an RfD for chromium VI of 5 µg/kg/day, and 1000 µg/kg/day for chromium III (US EPA, 1993). RfCs for both groups of compounds are under review.

CARB specifies a non-cancer chronic REL of 2 x 10^-3 µg/m³ for chromium VI, considering effects on the respiratory tract, kidney, and gastrointestinal system as the toxicological targets. An REL has not been established for chromium III.

2.15.3 Description and sources

Chromium (Cr) is a grey, hard metal most commonly found in the trivalent state in nature, but hexavalent compounds are found in small quantities.

Emissions of chromium in New Zealand are mostly associated with particles emitted when burning fossil fuels, which includes power stations, cars and trucks. The emissions largely depend on the chromium content of the fuel, which varies with both the fuel type and source. Specific sources of chromium include metal smelting and foundries, cement production, pulp and paper mills, chrome plating, timber treatment using copper/chrome/arsenic preservatives, cooling towers and leather tanning.

2.16.1 Guideline values

The guideline value for inorganic arsenic is 0.0055 µg/m³ (annual average). For arsine the guideline value is 0.055 µg/m³ the (annual average).

The ambient guideline value for inorganic arsenic is based on an acceptable risk value of 1 in 100,000 for a high-potency carcinogen.

As is the case for mercury and chromium, these values may need to be adjusted downwards if dietary intake is significant. Contaminated soils may be a significant source of exposure for children.

2.16.2 Health effects

Acute inhalation exposure to inorganic arsenic may result in gastrointestinal effects, haemolysis, and central and peripheral nervous system disorders in humans. Effects of acute exposure to arsine (a gaseous compound of arsenic) include haemolytic anaemia, haemoglobinuria and jaundice, and can lead to kidney failure. Acute inhalation exposure to arsine can lead to death: it has been reported that exposure to 87-170 mg/m³ arsine for half an hour can be lethal.

Chronic inhalation exposure to, and contact with, inorganic arsenic is associated with irritation of the skin and mucous membranes, including dermatitis, conjunctivitis, pharyngitis and rhinitis. Several studies of women working or living near metal smelters, and in the electronics industry, have associated exposure to arsenic and arsine gas with an increased incidence of spontaneous abortions and lower birth weights. However, the studies have limitations due to simultaneous exposure to other pollutants, and small numbers in some studies. Human inhalation studies have reported that inorganic arsenic exposure is strongly associated with lung cancer. Human exposure by ingestion has also been associated with an increased risk of skin, bladder, liver and lung cancer (US EPA, 1998).

The US EPA has classified inorganic arsenic as a Group A carcinogen of high potency, but it has not classified arsine. IARC has not classified either inorganic arsenic or arsine.

Unit risk factors for inorganic arsenic for inhalation exposure adopted by various groups are as follows: 4.3 x 10^-3 per µg/m³ (US EPA, 1998), 3.3 x 10^-3 per µg/m³ (CARB, 1998) and 1.5 x 10³ per µg/m³ (WHO, 1996).

Since inorganic arsenic is considered a human carcinogen, WHO has not specified a guideline for ambient air quality, but recommends that unit risk factors be applied.

The US EPA specifies an RfD of 0.3 µg/kg/day for inorganic arsenic, but it has not established an RfC. For arsine, the US EPA has not established an RfD, but it does specify a non-cancer RfC of 0.055 µg/m³ (US EPA, 1993).

CARB specifies a non-cancer chronic REL of 0.55 µg/m³ for inorganic arsenic, considering blood disorders as the toxicological endpoint, and a non-cancer chronic REL of 140 µg/m³ for arsine, for which the toxicological endpoints are considered to be the respiratory system, the central and peripheral nervous systems, and the skin (CARB, 1998).

2.16.3 Description and sources

Arsenic and its compounds are ubiquitous in the environment and exhibit both metallic and non-metallic properties. The trivalent and pentavalent forms are the most common oxidation states. At least six groups are present in the environment, with inorganic forms (such as arsenic trioxide and arsenic pentoxide) and gaseous inorganic and organic arsenic compounds (for example, arsine) being the most important for air quality.

Specific sources of arsenic include timber treatment using copper/chrome/arsenic preservatives, and previous pesticide application. Emissions are largely to land or water. Arsine can be released into the air from old chemical landfill sites. The burning of treated timber releases volatile arsenic oxides, either in the gaseous form or associated with particle emissions. Health and environmental guidelines for selected timber treatment chemicals are available (Ministry for the Environment, 1997b).