Hospitalization for community-acquired pneumonia (CAP) appears to be occurring more frequently (1, 2). Why is this? To answer this question we need to know why individuals develop this condition. Many predisposing factors to CAP have been described, such as the increased risk associated with extremes of age and comorbid diseases (3, 4).

Air pollution might also play a role as a predisposing factor to CAP. A previous study showed that elderly subjects hospitalized for chronic obstructive pulmonary disease (COPD) were at higher risk of dying on high–air pollution days (5). Similarly, such individuals with CAP could be more susceptible to the effects of air pollution, and prolonged exposure to air pollution might predispose them to pneumonia. Increased risk to CAP associated with direct inhalation of tobacco smoke is a finding common to virtually all studies (3, 4, 6), but despite much concern about possible effects of environmental pollution, this has been little studied. Those studies that have been performed have had a number of limitations including the study of only short-term pollution exposures, lack of robust pneumonia definitions, or lack of correction for other factors known to increase pneumonia frequency. These limitations have to a large extent been overcome in the study by Neupane and colleagues that appears in this edition of the Journal (pp. 47–53 ) (7).

Neupane and colleagues used a robust pneumonia definition that required emergency department presentation with the presence of at least two pneumonia signs or symptoms together with new radiographic findings compatible with pneumonia. Environmental pollutant levels were estimated from outdoor monitor readings over the course of 1 to 2 years before the year of the pneumonia presentation at residential addresses, with three different methods to take into account the spatial variability of the pollutants. Associations were corrected for the known association of CAP with age, sex, functional status, socioeconomic status, smoking, and history of regular exposure to air-polluting fumes. This robust approach identified an independent association between NO 2 and PM 2.5 levels in the previous 1 to 2 years and pneumonia hospitalization. It is worth mentioning that the effects were seen with pollutants derived mainly from traffic.

No study is perfect. Steps were not taken in Neupane's study to exclude pneumonia in patients who were immunocompromised or who had hospital-acquired pneumonia, but experience suggests that such cases were too few to have biased the findings. There were 136 potential cases that refused to take part—a proportion large enough to produce potential bias. The authors studied only those aged 65 years or older, so we do not know whether their findings apply to younger age groups. The lower frequency of pneumonia in younger age groups would make the association between CAP and air pollution harder to identify without a very large study population. The situation in children may indeed be different because lower cumulative exposure will have usually occurred.

Both the measurement of pollutant levels and the selection of cases and controls occurred during a 2-year period, which provides only a snapshot from a lifetime of exposure; it may be that earlier exposures could have been of greater importance. On the other hand, the 2-year average could represent the effect of prolonged or cumulative exposure over several years; other studies have used a 1-year average to represent longer-term exposures (8). Also, the importance of daily average as opposed to long-term pollutant levels has not been explored. The attempt to produce a figure for exposure at the residential address of the cases and controls necessarily omits exposures in transit or away from the place of residence; their exposure method is not the same as personal-level monitoring. Even though these were elderly subjects and outdoor activity might have been limited, it could have been of interest to explore the long-term effect of the average pollution concentrations among monitoring stations across the city. A comparison could have shown whether the effects estimated at the addresses yielded stronger associations (presumably due to less exposure measurement error) compared with the city-wide average exposure, which is commonly used in the literature.

Having said all of this, the authors have striven to ensure that the observed associations are likely to be valid. The associations identified are plausible and are convergent with other studies of short-term pollution. This then begs the question whether the association is causal. There are factors associated with pneumonia risk that were not controlled for (e.g., crowding, infant contact, nutritional status, and vaccination status), so it could be that the associations found are just surrogates for other CAP risks. If the association identified is causal it could be that the effect is to increase CAP incidence, but because only a subgroup of patients who were hospitalized with relatively more severe CAP were studied, it could also be that the effect is to increase the severity of illness without changing incidence. Separation of these effects could only be performed by studying CAP in the community. This is, however, difficult to do because of the logistics of radiographic confirmation in this setting.

There are certainly plausible biological mechanisms by which pollution could increase pneumonia risk. Epidemiologic studies indicate that hospitalizations for respiratory causes are strongly related to PM exposure. Several hypotheses have been advanced for possible underlying mechanisms (9). For example, some particles can cause epithelial cell damage, pulmonary edema, and eventually fibrosis (10). Respiratory tract deposition patterns depend on particle size and distribution within the inspired air. Biologic effects may also be a function of particle number, composition, and the total surface area of the particle. Various factors have been shown to influence particle deposition, such as age and ventilation patterns. Higher ventilation increases total deposition, and obstructive airway disease, such as chronic obstructive pulmonary disease or asthma, results in increased deposition in the lower respiratory tract (11). Chronic effects may also arise from recurring cycles of pulmonary injury and repair (12). Studies have shown that high doses of particles can trigger oxidative stress and the induction of inflammation, increased blood coagulation, impaired cellular defense, and modulation of the immune system (13, 14).

These findings of an association between CAP and long-term pollutant exposure have important implications for public health. They suggest that pneumonia is yet another disease outcome for which air pollution may contribute to enhanced susceptibility, and that reductions in air pollution should reduce disease burden.

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