In this large, geographically diverse community sample studied by standardized polysomnography we find novel evidence of pollution and temperature effects on sleep-disordered breathing. Increases in apnea or hypopnea, measured as the respiratory disturbance index, were associated with increases in short-term temperature over all seasons, and with increases in particle pollution levels in the summer months. In the summer months, pollution levels were associated with increased percentage of sleep time at less than 90% oxygen saturation. Previously we have demonstrated that SDB in this population is a risk factor for cardiovascular morbidity (7
). These data extend the growing literature demonstrating the contribution of air pollution to adverse pulmonary and cardiovascular health (13
Particles may influence sleep through effects on the central nervous system, as well as the upper airways. Particles have been shown to translocate from the nose up the olfactory nerve into the brain, including the striatum frontal cortex, and cerebellum (21
). This in turn is associated with increased brain inflammatory responses (23
) and changes in neurotransmitter levels (25
). In humans, diesel exhaust exposure has been shown to alter EEG responses, with patterns indicative of cortical stress (26
). Compared with less polluted cities, in polluted areas of Mexico City dogs had more prefrontal lesions, neuroinflammation, gliosis, and particle deposition. In these polluted areas, brain-imaging studies of children showed more prefrontal lesions; autopsy studies of accident victims showed up-regulation of cyclooxygenase-2 and CD14 (27
Prior research in rodents (30
) has shown that experimental exposure to increased ozone concentrations alters levels of serotonergic neurotransmitters in brainstem areas implicated in sleep–wake control (31
To our knowledge, the effects of pollutants on sleep architecture in humans have not been previously studied. However, environmental tobacco smoke exposure, which is a mix of particulate and gaseous pollution (33
), has been reported to be associated with symptoms of disrupted sleep and insomnia (30
). There is a growing literature that implicates low sleep efficiency, short sleep duration, and insomnia with adverse health outcomes (4
), with evidence that poor sleep may disproportionately afflict poor urban populations (35
). Our findings suggest that one mechanism for poor sleep and sleep health disparities may relate to environmental pollution levels.
In addition to effects on sleep architecture, during the summer elevation of ambient pollution levels is associated with an increased risk of SDB as measured by the RDI as well as sleep-related hypoxemia in this urban SHH study cohort. To our knowledge, this is the first study to demonstrate a link between air pollution exposure and SDB. We have done so in a cohort in which the prospective association of SDB with all-cause mortality and cardiovascular mortality has been demonstrated (37
). Pollution may increase SDB through influencing central ventilatory control centers. Pollutants may directly contribute to nasal or pharyngeal inflammatory responses that increase upper airway resistance and reduce airway patency. Fine and ultrafine particles may alter ventilation–perfusion relations, exacerbating the hypoxia of SDB (4
). In patients with asthma and SDB, elevated air pollution has been demonstrated to worsen lower airway inflammation and airflow obstruction through allergic and nonallergic mechanisms (19
); this may also contribute to the propensity for desaturation with sleep-associated reductions in ventilation. In patients with hay fever, upper airflow obstruction may worsen on an allergic basis when air pollution particles also contain allergen fragments (4
Sudden infant death syndrome (SIDS), which may occur because of brainstem ventilatory or autonomic control problems, abnormalities in cardiac function, or upper airway collapse, has been linked to ambient pollution levels in some (38
) but not all studies (39
). Familial aggregation studies suggest that there is an overlap of the etiologic factors for SIDS and for SDB (40
). Thus, the mechanisms that increase risk of SIDS in association with ambient pollutants may be similar to the mechanisms that may underlie risk of SDB. These factors may include pollutant-associated effects on central or peripheral neurotransmitters that influence sleep state stability (and thus also explain the sleep efficiency findings), upper airway patency, and/or ventilatory control.
Several studies have reported that temperature changes predict mortality. These findings, the mechanisms of which are poorly understood, are not restricted to extreme weather conditions, but are observed across the range of temperatures (41
). The association we found between short-term temperature and RDI could represent one possible mechanism. Alternatively, temperature could be confounded by ozone, as the two often covary.
Fifteen to 20 years ago, when the first of hundreds of studies demonstrating the adverse cardiac effects of air pollution were published, the plausibility of these associations was challenged because of the uncertain mechanistic links between the respiratory inhalation of air pollutants and subsequent cardiac morbidity or mortality (43
). Subsequently, demonstration of the autonomic (44
), inflammatory (46
), oxidative stress (48
), and procoagulant (49
) effects of particle pollution has lent biological plausibility to the epidemiologic observations. Nevertheless, up until this study, there has been relatively weak evidence of hypoxemia as a potential link between pulmonary exposure to air pollution and adverse cardiac outcomes. Small but significant reductions in oxygen saturation during waking hours were associated with elevation in particulate pollution in studies of elderly subjects from Utah (51
) and Boston, Massachusetts (8
); pollution effects on oxygen saturation during sleep were not evaluated in those studies.
The methodology for ascertainment of SDB outcomes in this cohort has been validated (10
). We present cross-sectional analyses; longitudinal analyses would be helpful to validate our findings. However, the major limitations of our study design relate, for the most part, to estimation of pollution exposure. Estimates of home-specific exposures could not be made, as geo-coded addresses were not available. The number of observations was limited by the location of EPA monitoring stations. Detailed information about air conditioning was not available, but summer pollution effects were lower in cities known to be hot, with a large amount of air conditioner use (e.g., Tucson, AZ). In the cities we studied, oxidant gases such as ozone and other secondary emissions are higher in the summer, and it is likely that mixtures of pollution contributed to the summer PM effects on SDB. More detailed study of effects of season-specific mixtures on SDB is warranted. Another limitation of the study is due to possible measurement error. Our exposure PM10
is based on an average concentration among several monitors, which serves as a surrogate for location-specific exposure. However, the error generated by this approximation is likely not a major issue, as the within-community correlation among monitors is high, and in our data varies between 0.62 and 0.82. Classical measurement error could bias the coefficient of PM10
in our analysis toward the null. On the other hand, Zeger and coworkers (52
) showed that exposure measurement error for short-term air pollution exposure is mainly Berkson. Therefore for our short-term exposure, the error is likely to be predominantly Berkson, which will result in a loss of power but not bias our estimate of the association between PM10
and sleep. Temperature levels vary geographically but their fluctuations are highly correlated, and hence measurement error is unlikely to be an issue. Other articles presented the magnitude of the potential bias due to measurement error (53
). Our study is also limited by the absence of data on ozone for Minneapolis, where we had the most outcome data. We were able to examine NO2
, and CO associations with sleep outcomes. The results were generally in the same direction as the PM10
results, but were weaker (results not shown).
The prevalence of SDB among adults is high in the United States (approximately 17%) (1
), and it may increase as the prevalence of obesity rises. Although therapies are available for this disorder, the majority of adults with SDB are not being treated, and many people are resistant to therapy. Along with reduction in obesity, these new data suggest that reduction in air pollution exposure might decrease the severity of SDB and nocturnal hypoxemia and may improve cardiac risk.