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Air Pollution Ozone

6. Are certain population groups particularly vulnerable?

    The source document for this Digest states:

    Are there specific population groups that should be brought into special attention?

    Explanation provided by the European Commission to this question:
    In the first report from WHO the effects on particular population groups is highlighted on several occasions. From the policy point of view it is important to have an understanding of the risks for the different groups (no single group would have to have unacceptable risks). WHO is invited to investigate the possibility to assess the sensitivity such groups and to assess the risks due to present air pollution levels for some important health endpoints, inter alia increased child mortality and asthma exacerbation due to exposure to PM and ozone.

    Answer:

    A number of groups within the population have potentially increased vulnerability to the effects of exposure to air pollutants. These groups comprise those who are innately more susceptible to the effects of exposure to air pollutants than others, those who become more susceptible for example as a result of environmental or social factors or personal behaviour and those who are simply exposed to unusually large amounts of air pollutants. Members of the last group are vulnerable by virtue of exposure rather than as a result of personal susceptibility.

    Groups with innate susceptibility include those with genetic predisposition that render them unusually sensitive, for example, to the broncho-constrictor effects of ozone or liable to produce an unusually marked inflammatory response on exposure to allergens. Very young children and unborn babies are also particularly sensitive to some pollutants.

    Groups which develop increased sensitivity include the aged, those with cardio-respiratory disease or diabetes, those who are exposed to other toxic materials that add to or interact with air pollutants and those who are socioeconomically deprived. When compared with healthy people, those with respiratory disorders (such as asthma or chronic bronchitis) may react more strongly to a given exposure both as a result of increased responsiveness to a specific dose and/or as a result of a larger internal dose of some pollutants than in normal individuals exposed to the same concentration of pollutants. Increased particle deposition and retention has been demonstrated in the airways of subjects suffering from obstructive lung diseases.

    Lastly, those exposed to unusually large amounts of air pollutants perhaps as a result of living near a main road or spending long hours outdoors, may be vulnerable as result of their high exposure.

    Introductory Remarks:

    The fact that some individuals are more affected than others by exposure to air pollutants has been known since the early years of air pollution research. Studies of the London fog of 1952 revealed that the elderly and the very young were most affected (Ministry of Health, 1954). The analysis of causes of death suggested that those suffering from cardiorespiratory disease might have been especially sensitive to the mixture of particles and sulphur dioxide that characterised the London smog of the period. More recent work has confirmed this perception and has identified a considerable number of groups of individuals who are likely to be at special risk when exposed to air pollutants.

    Concern about the impact of air pollution on children’s health has also increased recently. The European Commission has invited WHO to complement the current review (the work led by the Scientific Advisory Committee) by an in-depth review of this topic. The leading topic of the Fourth Ministerial Conference on Environment and Health, Budapest 2004 is the effects of environmental factors on children’s health: “The future for our children”. WHO is organizing a systematic review and assessment of the issue. This systematic review should be regarded as separate from the current work which has sought, specifically, to answer the follow-up questions posed by CAFE.

    In addition, the meta-analysis of time-series studies undertaken by experts at St George’s Hospital Medical School in London, on behalf of WHO, has looked specifically at the effect of age on coefficients linking air pollutants and health endpoints. The results of this analysis will be available on www.euro.who.int/air 

    The statement provided below is a summary of the thinking of the WHO working group and the Scientific Advisory Committee and does not purport to be a systematic review. To undertake such a review in all the areas mentioned below was not possible in the time available for this work.

    The terms sensitivity, susceptibility and vulnerability are used, sometimes interchangeably and incorrectly, to describe a greater than expected response of an individual or group of individuals to air pollutants. We use the terms susceptibility and vulnerability as defined below. We have not used the term sensitivity.

    Susceptibility: The likelihood of producing a significantly larger-than-average response to a specified exposure to air pollutants.

    Vulnerability: The likelihood of being unusually severely affected by air pollutants either as a result of susceptibility to the effects of these substances or as a result of a greater than average [exposure].

    Susceptibility
    Susceptibility can be subdivided into innate and acquired susceptibility. Innate susceptibility may be due to genetic predisposition or to incomplete development of normal (adult) physiological functions. A young child may be susceptible to a given pollutant because detoxification processes are not yet fully developed. Such susceptibility is transient and disappears with age and growth. Acquired susceptibility may be due to disease, socioeconomic status or age. A number of mechanisms are known to play a part and are discussed below. It should be noted, however, that “socioeconomic status” is not a precise identification of a causal factor.

    Vulnerability
    In addition to the susceptible groups outlined above some individuals are vulnerable to the effects of air pollutants as a result of their greater than average exposure to these substances. Such exposure may be due to living near busy roads or spending long hours outdoors each day. It is important to distinguish clearly between vulnerability due to increased exposure and vulnerability due to innate or acquired susceptibility.

    Innate susceptibility
    (a) Genetically predisposed It has been known since 1991 that the unusual sensitivity of some strains of mice to ozone is due to mutations of the Inf locus on chromosome 9. Further work has shown that more than one gene may be involved and one allele may be responsible for the extreme sensitivity to ozone seen in some animals. Kleeberger et al. (1996) described the MdSOD gene on chromosome 17 and the Trifa (pro-inflammatory cytokine TNF-ALPHA) gene, also on chromosome 17. Mice deficient in SOD (superoxide dismutase) show a greater than usual inflammatory response to ozone and higher levels of the cytokine IL-6 in bronchoalveolar lavage fluid. These studies show that genetic factors can, in animals, affect susceptibility to the effects of at least one classical air pollutant: ozone (Kleeberger et al., 1991; 1992; 1996; Carlsson et al., 1996).

    Recent work in man has shown that abnormalities of the members of the glutathionine-S- transferase super family (GSTM1, GSTT1 and GSTP1) can affect responses of children to oxidant air pollutants. Gilliland et al. (2004) have shown that individuals with the GSTM1-null or GSTP1 Ile105 wildtype genotypes produced an enhanced allergic response to diesel-exhaust particles. Individuals with GSTM1-null genotype produced a larger than usual increase in conversion of IgE and histamine in nasal lavage fluid after challenge with allergen or diesel exhaust particles than individuals with the functional genotype. Hong et al. (2003) have shown that these polymorphisms are important in controlling neonatal vulnerability to maternal smoking. A further example is provided by the –308 promotor polymorphism of TNFa which has been shown to enhance the lung function response to sulphur dioxide in chamber studies (Winterton et al., 2001). Interestingly, polymorphisms of the TNFa gene have been shown to be associated with asthma. In communities with the lowest ozone concentrations, variant TNF genotypes were associated with a higher risk of wheezing outcomes (Witte et al., 2002; Gilliland et al., 2003).

    A number of studies has focused on the possible effects of maternal exposure to air pollutants on fetal growth (birth weight), prematurity (gestational age at delivery) and the incidence of stillbirths. The studies reported between 1996 and 2001 have been reviewed by Glinianaia et al. (2004). The authors concluded that the evidence was compatible either with a small adverse effect of particulate air pollution on fetal growth and duration of pregnancy or with no effect. Recent work from the United States argued that over 70% of the overall reduction in infant mortality during the first year of life could be attributed to the, on average, 15 µg/m3 decline in TSP that occurred during the economic recession of 1981–1982 (Chay & Greenstone, 2003). A number of studies, for example, Bobak (2000) has reported associations between sulphur dioxide and low birth weight. Other studies have not found such effects. The general impression is that maternal exposure to air pollutants is related to decreased fetal growth and prematurity. An interesting implication of such a conclusion relates to the increased prevalence of asthma in children with low birth weight. Mortimer showed that asthmatic children who were born either before the thirty-seventh week of gestation or with a low birth weight (<2500 g) had a significantly increased risk of symptoms and a reduction in lung function in response to summertime air pollution in the eastern half of the United States (Mortimer et al., 2000).

    Acquired susceptibility
    There is convincing evidence that the elderly and those suffering from cardio-respiratory disorders are susceptible to the effects of air pollutants (Gordon & Reibman, 2000; Pope, 2000; Takafuji & Nakagawa, 2000; Donaldson et al., 2001). In addition, it has long been known that patients with asthma are more affected by exposure to irritant air pollutants such as sulphur dioxide than other individuals (Linn et al., 1983; Sheppard et al., 1981). A recent study has shown a differential sensitivity of patients with and without asthma exposed to diesel exhaust (Stenfors et al., 2004). The cytokine profile of lavage fluid was counter-intuitively found to contain more classical inflammatory cytokines in the non-asthmatic group. Earlier work had shown a more marked neutrophil response in asthmatic subjects (Scannell et al., 1996). It has also been shown that the inflammatory response induced by exposure to ozone is longer lasting in asthmatic subjects than in controls (Balmes et al., 1997; Frampton et al., 1997a; 1997b). Work by Zanobetti et al. (2000) has focused on subgroups of patients with cardio-respiratory disorders and showed that those with acute respiratory infections and with defects in the electrical control of heart rate and rhythm appeared to be at particular risk of adverse effects on exposure to particles measured as PM10.

    These effects may be in part explained by the greater instability or susceptibility to insult likely in disease states, for example, an already inflamed airway and also by the increased deposition of both fine and ultrafine particles known to occur in diseased lungs. Such enhanced deposition leads to what could be regarded as an increased internal dose of particles on exposure to a given concentration of particles (Kim & Kang, 1997; Brown et al., 2002).

    Zanobetti & Schwartz (2001) have recently shown that patients with diabetes are of increased risk of admission to hospital for treatment of heart disease on exposure to raised concentrations of particles. The risk amongst diabetics was twice that in the non-diabetic population. The authors hypothesized that the possible links between exposure to particles and clotting factors might explain this effect, as diabetes itself is characterized by abnormalities in such factors. It is interesting that the authors pointed out that they had not found age to be a modifying factor of the effects of PM10 on hospital admissions for disorders of the heart and lungs (Zanobetti & Schwartz, 2001). Systematic analysis will be needed to clarify the possible effects of age on susceptibility to particulate air pollution.

    Increased vulnerability due to increased exposure
    A number of studies have shown increased effects associated with living near busy roads (Roemer & Wijnen, 2001; Janssen et al., 2003; Hoek et al., 2002). Children may also be exposed to a greater extent than adults because of their greater physical activity and likelihood that they spend a larger part of the day outdoors. The higher metabolic rate of children, revealed in a higher minute volume per unit mass also increased the internal dose of pollutants for a given ambient concentration. This point applies also to athletes and others exercising outdoors.

    Source & ©: WHO Regional Office for Europe  Health Aspects of Air Pollution - answers to follow-up questions from CAFE (2004), Section 6


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