Health effects of traffic-related air pollution (TRAP)

Peta Pippos, Senior Policy Analyst, Environmental Health Branch, Health Protection NSW
Richard Broome, Deputy Director, Environmental Health Branch, Health Protection NSW

Air quality in Australia is very good when compared to countries at similar levels of economic development. To control air quality, each state and territory is required to comply with a set of standards specified in the National Environment Protection (Ambient Air Quality) Measure.traffic-related air pollution in Sydney and other urban centres.

However, air pollution may still have health effects at levels below current standards,[1,2] and so reductions in exposure can be expected to provide benefit.

One of the roles of Health Protection NSW is to better understand the health impact of air pollution on the community; to work with the relevant agencies to identify the key sources of exposure, and to support reasonable and feasible actions to reduce exposure.

Traffic-related air pollution (TRAP) is a significant source of air pollution in Sydney and other urban centres.

Key air pollutants linked to traffic pollution

Important traffic-related air pollutants are particulate matter (PM), ozone, nitrogen dioxide (NO2), carbon monoxide (CO), polycyclic aromatic hydrocarbons (PAH) and volatile organic compounds (VOC).

Particulate matter

Particulate matter (PM) is a term used to describe airborne microscopic solid or liquid particles. PM is generally classified according to the size of the particles. Particles less than 10 micrometres in diameter are called PM10, particles less than 2.5 micrometres in diameter are PM2.5 and particles less than 0.1 micrometres in diameter are called ultrafine particles (UFPs). It is important to note that PM10 includes both PM2.5 and UFPs.

A key feature of PM is that no threshold has been identified below which exposure is not associated with adverse health effects. Therefore reductions in exposure to ambient concentrations may provide public health benefits. Recently, the International Agency for Research on Cancer (IARC) determined that PM was carcinogenic to humans.[3]

  • PM2.5: PM2.5 is generally produced by combustion. There is very good evidence that exposure to PM2.5 causes cardiovascular disease, respiratory disease and mortality. Associations have also been observed between PM2.5 exposure and reproductive and development effects such as low birth weight.[4]
  • PM10: Exposure to PM10 is also associated with cardiovascular disease, respiratory disease and mortality. However, because PM10 includes PM2.5, there is some uncertainty about how much of the observed effect is due to PM2.5 and how much is due to the larger particle fraction (PM10-2.5).
  • UFPs: Motor vehicle exhaust is an important source of ultrafine pollution in urban settings.[5] Ultrafine particles are thought to play a role in the adverse health impacts seen in association with exposure to particulate pollution, although the epidemiological evidence of their effects is limited.[5,6]

Ozone

Ozone is formed when precursor compounds (volatile organic compounds and oxides of nitrogen) photo-chemically react in the presence of sunlight. Ozone pollution can reach high levels on hot, still days and build up over a day, reaching its peak in the early evening.

Short term exposure to ozone can result in reduced lung function, exacerbation of asthma and chronic respiratory diseases, irritation and inflation of eyes, nose, throat and lower airways. There is a growing body of evidence to support that long term exposure to ozone may affect respiratory and cardiovascular mortality, and respiratory morbidity. There is currently inconsistent evidence to indicate there is a threshold below which exposure to ozone is not associated with adverse health effects.[6]

Nitrogen dioxide

Nitrogen dioxide (NO2) is produced by combustion and is a good marker of traffic-related pollution. Toxicological studies have found effects of NO2, but at levels far exceeding those normally found in ambient air. NO2 is highly correlated with other pollutants from combustion sources, which has made it very difficult to separate the effects of ambient NO2 from the effects of other traffic-related pollutants, especially PM. However, there is increasing evidence that indicates there are independent effects of NO2 separate from PM.[6]

Carbon monoxide (CO)

Carbon monoxide is produced during incomplete combustion of carbon containing fuels such as petrol.[7] Carbon monoxide can cause harmful health effects by reducing the amount of oxygen reaching the body’s organs (like the heart and brain) and tissues. At extremely high levels, carbon monoxide can cause death (carbon monoxide poisoning).

Polycyclic aromatic hydrocarbons (PAHs)

PAHs comprise over 100 different compounds. Some PAHs are carcinogens, for example benzo (a)pyrene. PAHs are often transported in the atmosphere attached to PM2.5, which means their effects cannot be separated from the effects of particles.[6]

Volatile organic compounds (VOCs)

Key VOCs from vehicle exhaust include benzene and formaldehyde.[8] These are typically present in low concentrations in the air but have toxic characteristics that may result in health effects from exposure even at low levels. Benzene and formaldehyde are classified as Group 1 carcinogens to humans.[9] Motor exhaust VOCs are also important precursors to the formation of ozone.[6]

Health effects from proximity to traffic

Adverse health effects have been observed in association with proximity to roads. These effects persist after adjusting for noise and socioeconomic status and are only partly explained by exposure to PM2.5. Therefore, it is likely that these effects result from exposure to other traffic-related pollutants, either individually or in combination.[6]

Evidence indicates that TRAP exposure causes exacerbation of asthma. There is also suggestive evidence linking TRAP to several other health outcomes (onset of childhood asthma, non-asthma respiratory symptoms, impaired lung function, total and cardiovascular mortality and cardiovascular morbidity).[8] An exposure zone extending up to 500m from a major road is the most affected by traffic emissions.[8]

Non-exhaust emissions (brake wear, engine abrasion, type wear) are a significant source of on-road particle emissions in Sydney.[10] As exhaust (tail pipe) emissions are further regulated and reduced, understanding non-exhaust emissions will increasingly become the focus to address health risks from future traffic pollution.[6,8]

Carcinogenicity of air pollution and its constituents

The IARC has classified outdoor air pollution and diesel engine exhaust as carcinogenic to humans.[3,11] Benzene and formaldehyde (VOCs linked to vehicle exhaust) have also been classified by IARC as Group 1 carcinogens.[9]

Conclusion

Although much remains unknown about TRAP, the evidence base is growing, and it is clear that exposure to TRAP does present a health risk, which is why it is prudent to minimise exposure.

Health Protection NSW continues to work with the NSW Environmental Protection Authority (which is responsible for the regulation of motor vehicle air emissions under the Protection of the Environment Operations (Clean Air) Regulation 2010) and other key agencies responsible for planning and road development to promote ways to reduce human exposure to TRAP.

References

  1. Barnett AG, et al (2006). The Effects of Air Pollution on Hospitalizations for Cardiovascular Disease in Elderly People in Australian and New Zealand Cities. Environmental Health Perspectives 140 (7) 1018-23
  2. Crouse DL, et al (2012) Risk of nonaccidental and cardiovascular mortality in relation to long-term exposure to low concentrations of fine particulate matter: a Canadian national-level cohort study. Environmental Health Perspectives 120 (5), 708
  3. Loomis D, et al. (2013). The carcinogenicity of outdoor air pollution. Lancet Oncology, 14 (13): 1262-1263.
  4. Pedersen M, et al (2013). Ambient Air Pollution and Low Birthweight: A European Cohort Study (ESCAPE). The Lancet Respiratory Medicine , 1(9): 695–704.
  5. HEI Panel on Ultrafine Particles. (2013). Understanding the health effects of Ambient Ultrafine Particles. Health Effects Institute, Boston. www.healtheffects.org accessed 7 January 2014.
  6. WHO Regional Office for Europe (2013). Review of evidence on health aspects of air pollution – REVIHAAP Project Technical Report. WHO Regional Office for Europe. www.euro.who.int/en/health-topics/environment-and-health/air-quality/publications/2013/review-of-evidence-on-health-aspects-of-air-pollution-revihaap-project-final-technical-report accessed 9 September 2013
  7. WHO Regional Office for Europe (2006). Air quality guideline global update 2005: particulate matter, ozone, nitrogen dioxide and sulphur dioxide. WHO Regional Office for Europe. http://www.euro.who.int/__data/assets/pdf_file/0005/78638/E90038.pdf accessed 6 February 2014
  8. HEI Panel on the Health Effects of Traffic-Related Air Pollution. (2010). Traffic-related air pollution: a critical review of the literature on emissions, exposure, and health effects – Special Report 17. Health Effects Institute, Boston www.healtheffects.org accessed 7 January 2014.
  9. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. (2009). A review of human carcinogens. Volume 100 Part F: Chemical agents and related occupations. International Agency for Research on Cancer, Lyon France. http://monographs.iarc.fr/ENG/Monographs/vol100F/mono100F.pdf accessed 17 January 2014
  10. NSW EPA (2012) 2008 calendar year air emissions inventory for the Greater Metropolitan Region of NSW https://www.epa.nsw.gov.au/your-environment/air/air-emissions-inventory/air-emissions-inventory-2008 accessed 27 February 2014
  11. Benbrahim-Tallaa L, et al. (2012). Carcinogenicity of diesel-engine and gasoline-engine exhausts and some nitroarenes. Lancet Oncolocy, 13 (7): 663-664.
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Page Updated: Monday 25 August 2014
Contact page owner: Health Protection NSW