Inverse associations of cycling and gardening with respiratory mortality were closer to the null among subjects with high NO2 exposure (0.77; 95% CI: 0.54, 1.11 and 0.81; 95% CI: 0.55, 1.18, respectively) than among those with moderate/low NO2 (0.55; 95% CI: 0.42, 0.72 and 0.55; 95% CI: 0.41, 0.73, respectively). Only one similar study exists in a cohort of children, which, consistent with our findings, showed asthma development only in children living in areas with high ozone concentrations, and not in those living in areas with low ozone (). It is plausible that amplification of lung damage due to greater inhaled doses of air pollution through physical activity in urban areas with high air pollution may moderate the benefits of physical activity, which improves some of the same physiological mechanisms. Earlier studies have shown that hikers with a history of asthma had significantly greater air pollution–related acute reductions in pulmonary functions than did asthma-free hikers (), and that subjects with moderate asthma had greater acute lung function reductions after walking on a busy street in London than did those with mild asthma (; ). However, reduced physical activity was observed on days with poor air quality among respiratory disease patients (; ), but not among cardiovascular disease patients, as noted earlier. This implies an alternative explanation to our findings that reduced benefit from physical activity in subjects residing in areas with high air pollution may be attributable to abstaining from physical activity on days with high air pollution, and not from enhanced negative effects of greater exposure to air pollution during physical activity. Our findings were weakened by the fact that there was no dose–response relationship in reductions of respiratory mortality related to cycling by number of hours spent cycling and by increasing levels of air pollution (see Supplemental Material, Table S1). Although numbers are small in the interaction analyses, the lack of effect of duration of cycling may imply that the cyclists themselves differ from the noncyclists, and that in general, the effects of air pollution are minimal in healthy people. Finally, significant interactions of cycling and gardening with air pollution observed for respiratory mortality () could not be reproduced when considering levels of NO2 > 24.9 μg/m3 (the 90th percentile) as high exposure, or when considering the subset of subjects living in inner Copenhagen, where levels of air pollution and number of people cycling are at the highest in Denmark (see Supplemental Material, Tables S2 and S3). However, these analyses need to be interpreted with caution because in both sensitivity analyses, exposure levels were also increased in the “low” exposure category, possibly obscuring differences in associations between the lower and higher levels of exposure.
Our results—that long-term benefits of physical activity on all major types of mortality were not moderated by exposure to high levels of NO2—are novel. This may imply that acute stress and damage to the cardiovascular system induced by short-term exposure to air pollution during exercise, in terms of vascular impairment, arterial stiffness, and reduced blood flow, as shown in earlier studies (; ; ), seem to be transient and reversible and do not abate long-term benefits of physical activity on mortality. Our results may furthermore be explained by the short duration of the physical activities, with mean of 2–3 hr/week for most activities (); this implies that extra inhaled dose of air pollution during physical activity, which is a function of increased inhalation and duration, is only a small fraction of total inhaled dose of air pollution (), and is therefore not sufficient to increase the risk of premature mortality. Our results are furthermore in line with a study finding significantly lower levels of physical activity on days with poor air quality among respiratory disease patients, but not in cardiovascular patients, who do not seem immediately enough bothered by air pollution to change their outdoor physical activity habits (; ). Our study thus may imply that effects of long-term exposure to NO2 and physical activity on overall and cardiovascular mortality are independent of each other, with benefits of outdoor physical activity not being reduced by exposure to NO2.
Physical activity. Physical activity was assessed by a self-administered, interviewer-checked questionnaire in which leisure time and transport-related (e.g., to and from work, shopping) physical activity was reported as hours per week spent on sports, cycling, gardening, walking, housework (cleaning, shopping), and “do-it-yourself” activities (e.g., house repair). Data were collected separately for winter and summer of the previous year, and the two values were averaged, so that being active implies at least half an hour spent on a specific activity per week. The physical activity questions have been validated in two studies that found high correlation between self-reported physical activity estimates with the accelerometer measurements of total metabolic equivalent in 182 subjects () and with combined heart rate and movement sensing measurements in 1,941 subjects (). We focused in this study on sports, cycling, and gardening, which were previously associated with lower mortality in the same cohort (), and additionally walking at least half an hour per week, which is relevant as an outdoor physical activity pertinent to exposure to air pollution. A previous analysis of data from the cohort indicated that accounting for the amount of physical activity did not substantially alter associations with mortality when activity was dichotomized as any participation versus none (). Therefore, our main analyses focused on the estimated effect of participation (yes/no) in sports, cycling, gardening, and walking on mortality, whereas associations with the amount of cycling (categorized as does not cycle, 0.5–4 hr/week, or > 4 hr/week) were estimated in sensitivity analyses.
The same researchers have also failed to adequately account for why the findings of this study and those of another of their own studies (Huesmann, Lagerspetz & Eron, 1984) absolutely contradict each other, with the former concluding that the media has a marginal effect on boys but no effect on girls, and the latter arguing the exact opposite (no effect on boys, but a small effect for girls).
(Lunenfeld, 206-7)." "My opinion is that the damaging effects the electronic media can have on children are not intrinsic to the media but grow out the ways the media are used much of the content of commercial TV shows may have a negative effect on children's social attitudes.
Adverse effects of chronic exposure to air pollution on total natural and cardiovascular mortality are well supported (), and positive associations were also evident in this Danish cohort, where air pollution levels are relatively low (, ; , ). Long-term exposure to air pollution was also associated with diabetes mortality in this cohort (), but not with respiratory mortality, in agreement with the recent meta-analyses of 16 European cohorts, including a subset of the cohort in the present analyses (). On the other hand, associations of air pollution with incidence of chronic respiratory disease—asthma and COPD (chronic obstructive pulmonary disease)—have been also found in this cohort (, ).
Relative to the entire study group results, odds of wheeze were 15–20% greater and statistically significant for EC, NO2, NO3, and PM10–2.5 when the analysis was restricted to children allergic to cat. Children allergic to Alternaria or Cladosporium were more likely than nonallergic children to wheeze when exposed to increased EC, NO2, or PM10–2.5. ORs were largest among the subgroup of boys with mild intermittent asthma for all pollutants except O3. A 3.7-μg/m3 increase in EC lag 6 was associated with an OR of 1.70 (95% CI, 1.35–2.13) among boys with mild intermittent asthma, a 52.6% increase in effect size relative to the full group [for effects in additional subgroups, see Supplemental Material, Figures 3–5 (doi:10.1289/ehp.0901292)].
After decades of stunted and rather irresponsible talk about media 'effects', the emphasis is hopefully changing towards a more sensitive but rational approach to media scholarship.
This is not a weakness of these studies, of course; the effects paradigm should be left to bury itself whilst prudent media researchers move on to explore these other areas.
However, whilst such studies may provide valuable reflections on the relationship between mass media and audiences, they cannot - for the same reason - directly challenge claims made from within the 'effects model' paradigm (as Miller & Philo (1996) have misguidedly supposed).
I have realised rather late that my own study (Gauntlett, 1997) in which children made videos about the environment, which were used as a way of understanding the discourses and perspectives on environmentalism which the children had acquired from the media, can be seen as falling broadly within this tradition.
The lack of firm theory has led to the effects model being based in the variety of assumptions outlined above - that the media (rather than people) is the unproblematic starting-point for research; that children will be unable to 'cope' with the media; that the categories of 'violence' or 'antisocial behaviour' are clear and self-evident; that the model's predictions can be verified by scientific research; that screen fictions are of concern, whilst news pictures are not; that researchers have the unique capacity to observe and classify social behaviour and its meanings, but that those researchers need not attend to the various possible meanings which media content may have for the audience.