air pollution and health risks

Introduction

primary pollutants includes:
- sulfur oxides
- nitrogen oxides
  - may increase risk of breast cancer
- carbon monoxide
- Volatile organic compounds (VOC) - eg. produced from black gum, poplar, oak and willow trees
- particulate matter
- persistent free radicals
- toxic metals eg. lead, mercury
  - toxic iron rich metallic 15-40nm nanoparticles from roadside air pollution can find their way into the mitochondria of hearts with a negative impact on our health.²⁾
- chlorofluorocarbons (CFCs) which harm the ozone layer
- ammonia – emitted mainly by agricultural waste
- odors eg. methane
- radioactive pollutants
- persistent organic pollutants (POPs)
secondary pollutants form derived from the primary pollutants and include:
- admixtures creating smog
- ground level ozone formed from nitrogen oxides and VOCs
- peroxyacetyl nitrate

Airborne particulate matter

airborne particulate matter is generally regarded as particles less than 10micron in diameter (PM₁₀) and given they are able to pass through to the lungs are regarded as potentially a risk for ill health
- ambient particulate matter ranks as the sixth leading risk factor for premature death globally³⁾
- many can trigger attacks of asthma or exacerbate chronic obstructive pulmonary disease (COPD)
coarse particulate matter 2.5-10 microns includes:
- mold spores
- pollen
- settling dust
- cement dust
- fly ash
- aerosols
fine particulate matter <2.5 μm (PM_2.5) includes:
- biomass smoke
  - domestic solid fuel fireplaces are the main cause of high level particulate indoor air quality (IAQ) - whether closed or open fires ⁴⁾
- traffic emissions from spark ignition engines
- ultrafine magnetic iron-rich nanoparticles which can be taken up by cells and mitochondria
  - sources of iron-rich nanoparticles mainly from combustion or friction:
    - traffic:
      - brake and tyre wear and tear
      - emissions: iron impurities in fuel; in-cylinder melting of engine fragments; use of iron-rich lubricating oils and fuel additives (e.g. ferrocene)
    - industrial sources: power generation, incinerators, steelworks
    - indoors, they can be emitted from sources as diverse as open fires, and office printers
  - traffic-derived PM are ultrafine and mainly under 100nm
  - most comprise (semi-) volatile carbon-bearing aerosols (some with non-volatile cores)
  - the solid, inorganic fraction is dominated by transition metals, and especially by potentially bioreactive iron oxides, produced in abundance from brake-wear and from exhaust emissions
  - despite their toxicity and potential ability to gain access to any organ of the body via ingestion, inhalation and/or the circulation, ultrafine particles are neither monitored nor regulated at the current time.
  - ultrafine particle numbers show little correlation with current measurements of PM2.5
  - post mortem studies have demonstrated direct penetration of air pollution nanoparticles into the human brain and heart and, in particular, into mitochondria of these tissues even in young children, most of these were 15-40nm ⁵⁾
  - magnetic pollution particles translocated to the heart might feasibly induce heart electrical dysfunction, and cell damage, whether by magnetic rotation when under strong E-M fields or hyperthermia
- residual oil
- road dust
- allergens including house dust mite and cat
- aerosols
- soot (elemental carbon)
Exposure to fine particulate matter (PM2.5, <2.5 μm in aerodynamic diameter) in air pollution is reportedly the largest environmental risk factor contributing to cardiovascular mortality and morbidity, globally⁶⁾
WHO recommends no more than 3 days a year of exposures above 15mcg/cu.m
living near major roads has been associated with increased cardiopulmonary mortality
- RR 1.95 in a Dutch study
- RR 1.85 in a German study of those within 150m of a major road
PM_2.5 has been linked with:
- increased respiratory illness exacerbations
  - in Tasmania, a study published in May 2020 estimated 69 deaths, 86 hospital admissions, and 15 asthma emergency department visits in Tasmania were attributable to biomass smoke each year and more than 74% of these impacts were attributed to wood heater smoke, with average associated yearly costs of A$293 million ⁷⁾
- excess rates of cardiac arrhythmia hospitalizations, ischemic stroke hospitalizations⁸⁾
- acute myocardial infarction (AMI/STEMI/NSTEMI)
  - Short-term iron-rich PM2.5 exposure raises risk of acute myocardial infarction by up to 5% within a few days ⁹⁾
  - Longer-term (i.e. several years) iron-rich exposures incur higher risk (~20%) of cardiovascular events, ascribed partially to development of associated cardiometabolic conditions, e.g. hypertension, diabetes mellitus ¹⁰⁾
  - Exposure to higher ambient PM2.5 concentrations has also been linked specifically with the development of high-risk coronary plaques
- hypertension ¹¹⁾¹²⁾
- atherosclerosis and primary prevention ¹³⁾
- increase in preterm deliveries¹⁴⁾
- arrhythmias
  - a 10 μg/m³ increase in PM2.5 corresponded to a 26% rise in the hazard ratio (HR) for arrhythmias, esp, in women and older people, or the obese. ¹⁵⁾
- lung cancer
  - a 2013 study involving 312,944 people in nine European countries revealed that there was no safe level of particulates and that for every increase of 10 μg/m3 in PM₁₀, the lung cancer rate rose 22%; The smaller PM_2.5 were particularly harmful, with a 36% increase in lung cancer per 10 μg/m3 as it can penetrate deeper into the lungs¹⁶⁾
- breast cancer
  - a 2023 study¹⁷⁾ showed an increase of as little as 10 µg/m³ was found to be sufficient to increase oestrogen receptor–positive breast cancer risk by 2-13% in US women but no increase in oestrogen receptor–negative breast cancer risk
- increased prevalence of cleft lip/palate (CLP) births with maternal exposure to elevated PM and PM levels
- Parkinsons disease
  - a rather minimal 14% higher risk in the highest quintile of exposure compared to the lowest quintile ¹⁸⁾
- aberrant S-nitrosylation reactions which contribute to some forms of cancer, autism, Alzheimer's disease, Parkinson's disease and other conditions
  - S-nitrosylation of protein CRTC1, impairs its ability to regulate genes that are critical for forming and maintaining connections between brain cells, an essential process for learning and long-term memory¹⁹⁾
- impaired cognition long term ²⁰⁾

Aerosols

see also: aerosols
sea spray is by far the greatest contributor to aerosol generation and contains both inorganic and organic molecules and particles
cooling towers are a prime source in cities and may carry bacteria such as Legionella (Legionaire's disease)
oxidation of sulfur and nitrogen oxides may form secondary particles consisting of sulfuric acid or nitric acid which may combine with ammonia to form ammonium salts
organic material
oxidation of volatile organic compounds may form secondary organic matter particles
asphalt on hot days gives off semi-volatile organic compounds

Biomass smoke

the burning of organic material such as wood heaters, burning off crops and manure, bushfires, etc
smoke is toxic, and smoke from wood fired heaters is similar to that from bushfires
some types of smoke are more toxic than others (see below)
smoke can be a particular problem in Autumn when temperature inversions and light winds combine to trap the smoke in populated areas and create smog
A study in Sydney showed chronic exposure to even low levels of particulate matter was linked with an increased risk of death in those aged over 45yrs. Depending on the model used, it suggests between a 3-16% increased risk of dying occurred with each extra microgram of particulate matter per cubic metre of air.²¹⁾

Wood heaters

in 2020, Australia’s wood-fired heaters are estimated to cause health costs of around A$3,800 per wood heater each year.
a slow combustion heater will produce less pollution than a pot-belly stove or open fire because the fire is sealed in an airtight box
using wood with high water content increasing smoke production (freshly cut wood needs to be stored for 8-12 months to dry out)
modern wood heaters should be designed to ensure they produce no more than 1.5 grams of particle emissions per kilogram of fuel burnt²²⁾ but even so, 10 hours per day use in Autumn and Winter will produce 15g per day per heater which is equivalent output to a truck driving 500km. Older heaters may have 15x the emissions!
avoid allowing fires to smoulder overnight
- in winter, the highest concentrations of fine particles in the air occur after midnight. This suggests that most of fine particle pollution is caused by wood heaters left to smoulder over night.
- dampening down the fire overnight generates little heat but creates lots of smoke both indoors and outdoors.
some fuels are far more toxic than other fuels, these include:
- treated wood such as green pine used for outdoor uses which often contains an antifungal chemical called copper chrome arsenate
  - this has been associated with various cancers including liver, bladder, lung as well as affecting the bone marrow and cardiovascular system (reference needed)
- the bottom of old telegraph poles which are often saturated in creosote or other pesticides
- painted wood may have lead based paints
- trees that are very toxic if burnt
  - eg. oleander
- coal or coke as they give off sulphur dioxide
- household rubbish
https://www.mja.com.au/journal/2024/220/1/wood-heater-smoke-and-mortality-australian-capital-territory-rapid-health-impact
- data from the three ACT monitoring stations, we estimated that wood heater emissions contributed 1.16–1.73 μg/m3 to the annual mean PM2.5 concentration during the three colder years (2017, 2018, 2021), or 17–25% of annual mean exposure, and 0.72 μg/m3 (15%) or 0.89 μg/m3 (13%) during the two milder years (2016, 2022) and thus the estimated annual number of deaths attributable to wood heater PM2.5 pollution was 17 to 26 during the colder three years and 11 or 15 during the milder two years using the most conservative exposure–response function, or 43 to 63 (colder years) and 26 or 36 (milder years) using the least conservative exposure–response function