MAKING THE CASE
Little lungs, bigger problems
Development of the respiratory system begins early in pregnancy and continues throughout the fetal period and childhood. A healthy infant at full-term is born with approximately 10 x 106 alveoli, which proliferate to 300 x 106 by age 8 years.

A child’s minute ventilation per kg body weight per day is inversely related to age, reaching adult levels at around 16 years. This is due to the higher oxygen demand for growth and development. Throughout this process, therefore, it can be assumed that younger kids have the potential to inhale more pollutants per kg body weight. Also, because their airways are narrower, irritation from ambient pollutants may result in proportionately greater airway obstruction. Asthma prevalence from birth to 19 years in Canada has increased 4-fold in the last 2-3 decades. It continues to rise, particularly in kids ages 8-11 years. It’s estimated that 1 out of 6 children in Canada suffers from asthma.1

Diagnosis and management
Diagnosis and management of any respiratory disorder needs to include an environmental history see Table 1).

Asthma environmental control has up to now focused on the individual’s indoor climate — eliminating contaminants like tobacco smoke, animal allergens and dander, house dust mites, moulds, pollens, etc. Even here, new asthma triggers are being reported — chemical emissions from composite wood furniture that leaches formaldehyde, flexible plastics that emit plasticizers, and new paints in residences.2 The challenges we face from known asthma triggers are growing. In addition, traffic pollution is increasingly being recognized as a trigger for asthma in older kids, and that’s arguably more difficult to deal with.3

Home monitoring of symptoms, peak flow meter measurements, and medication treatment — all documented in an asthma diary — assist follow-up and identification of environmental triggers.

Counselling parents about outdoor air pollution and health links needs to be part of the consultation. Encourage them to:

• observe and act appropriately during smog health advisory warnings
• access provincially maintained air quality websites
• maintain awareness of potential outdoor air pollution — e.g. local industrial or traffic emissions
• restrict activities to the indoors at peak times — e.g. traffic congestion, high ozone levels on hot summer days
• postpone outdoor sports activities if higher air pollution is anticipated
• participate in community decisions — e.g. industrial development, planning of highways and residential communities
• promote use of public transit systems.

What are the sources of air pollution?
Interest on the adverse health effects of ambient air pollution is growing rapidly. Outdoors, the principal source of irritants is combustion of fossil fuels from domestic heating, power generation and motor vehicles. Depending on the area, this may be combined with industrial processes, oil and gas extraction and refining, manufacture of chemicals, production of pulp and paper, and metal mining and refining. Non-anthropogenic sources also exist from thunderstorms, forest fires, volcanoes and sand storms.

Sources of indoor air pollution include moulds, tobacco smoke, household products for cleaning and personal care, and volatile organic compounds (VOCs) from pressed woods, paints and glues. Emissions f! rom inadequately ventilated furnaces, gas appliances and wood stoves also contribute.

What's being tracked?
Some of the outdoor air pollutants tracked by the provincial or federal environment ministries are total particulate matter (TPM), particulate matter (PM) ≤ 10 µm (PM₁₀) or 2.5 µm (PM_2.5), as well as sulphur oxides, nitrogen oxides (NO_x), VOCs, carbon monoxide and ammonia. These all fall under the heading of criteria air contaminants. Ozone formation is dependent on primary chemical precursor VOCs, e.g. formaldehyde, combined with NO_x and ultraviolet radiation, and it becomes a major problem during warmer months, in the middle of the day. Prevailing wind direction and speed determine the transport of air pollutants away from major sources onto other areas.

In addition, toxic air pollutants comprise a broad category of substances — metals (e.g. lead and mercury), persistent organic pollutants (e.g. dioxins and furans), benzene, asbestos, polycyclic aromatic hydrocarbons and many others.4 

The majority of studies have focused on respiratory effects, including but not limited to asthma. They find an increased prevalence of asthma symptoms, emergency department visits and hospitalization.

Exposure to traffic-related air pollutants has been associated with dry cough at night, wheezing, runny/stuffy nose, otitis media and allergic rhinitis in kids. Evidence is in that air pollution may heighten the allergenicity of pollens as well as their exposure in humans by facilitating their penetration into the airways.5 During the Atlanta Olympic Games in 1996, successful attempts to reduce the numbers of vehicles on the road by ! substituting mass transportation resulted in a 42% decrease of hospital visits for asthma.

Of particular concern is a documented inverse relationship between exposure to criteria air pollutants and lung function growth, in both asthmatic and non-asthmatic children.6,7 There is optimism, though. Further studies in the U.S. showed that relocation to a healthier air environment stimulated lung function growth. Because the reverse is true as well, a call for more stringent regulatory action for emissions would be in order.

In 17 cities in Europe, cellular and humoral immunity in children has been studied and found to be adversely affected by ambient levels of criteria air pollutants. Animal toxicology studies point to the suppression of host immunity by air pollution.

Carbon monoxide and ozone have been linked to congenital heart defects. In babies, SIDS and post-neonatal mortality due to respiratory causes have been tied to air pollution, as have a host of effects related to pregnancy — premature birth, low birth weight, intrauterine growth retardation, abnormal birth length or head circumference and small size for gestational age.6,7 

Genomic studies are documenting gene-environment interactions involving epigenetic changes that have the potential of transmission of asthma to the next generation and beyond. This research, in time, could be used for identification of susceptible populations and prevention.8