Issue link: https://hi.iaq.net/i/670243
Every breath we take: the lifelong impact of air pollution vulnerability. Generally, the effect sizes (risk estimates) are small, but important because they have an impact on a large number of people. To a statistician, factors that determine vulnerability modify the risk estimate; in other words, the size of the estimate varies according to the presence or absence of a vulnerability factor. Studies that set out to examine vulnerability need to be especially large and, in general, have used only crude measures of vulnerability such as age or sex. To complicate matters further, different factors that increase vulnerability often interact. For example, relatively socio-economically deprived communities will include a high proportion of individuals with diseases or poor diets that render them vulnerable to the effects of air pollution, and may be exposed to higher levels of pollution: a double injustice. These issues are discussed more fully below, but they beg several questions: • Are these differences inequalities or injustices? • Is it fair that those populations most exposed to air pollution are also more likely to have other stressors, such as poverty, poor housing, low educational attainment, obesity, long-term illnesses and higher levels of smoking? • How much do these factors affect individual and population health? • Which are the most important? • Are they inevitable? • Should we be reducing them and, if so, how do we do it? • What options, if any, are available to deprived communities to avoid or reduce exposure and its effects? • How much will intervention cost and who is responsible? 5.3 Biological (innate/acquired) susceptibility 5.3.1 Genetic and epigenetic influences Human defences against external hazards are determined in part by factors that are under genetic control. For example, the capacity to neutralise inhaled toxins is regulated by enzymes in the airway, whose nature and production are governed by inherited genes. Variation in these genes explains part of the difference in how individuals respond to air pollution. Several such genetically controlled factors have been identified (eg in asthma, polymorphism in the TNF (tumour necrosis factor) gene promoter and GSTM1 (glutathione S-transferase µ1) gene affects responsiveness to O 3 exposure), but even collectively they explain only a small part of individual variation in susceptibility. More recently, attention has moved to the 'epigenome', a term used to describe inheritable material other than the sequence of DNA (see Chapter 3). Epigenetic mechanisms include the switching on or off of genes, a process that may be fixed through life, but may also be prompted by environmental exposures including air pollutants such as PM. 2 These effects may vary by age. There is thus the intriguing possibility that past exposures to air pollution determine future responses, favourable or unfavourable, to the same pollutants (see Chapter 3). 5.3.2 Age There is consistent evidence that older people are particularly vulnerable to the adverse effects of air pollution. A systematic review of studies that examined deaths in association with exposure to PM, 3 70 © Royal College of Physicians 2016