Acute Air Pollution Exposure and Risk of Suicide Completion
Acute Air Pollution Exposure and Risk of Suicide Completion
To our knowledge, this is the first US-based study to have found an association between short-term air pollution exposure and heightened suicide risk. We found that increased suicide risk was associated with single-day and cumulative exposure to PM2.5 and nitrogen dioxide on and during the 2–3 days preceding a suicide in a sample of 1,546 completed suicides in Salt Lake County, Utah. Associations were strongest among males and persons aged 36–64 years. Suicide risk varied by season; it was heightened in both the spring and the spring/fall transition period following acute exposure to PM2.5 and in both the fall and the spring/fall transition period following acute exposure to nitrogen dioxide.
Previous research on suicide risk and air pollution is limited but includes investigations of the associations of criteria air pollutants with risk of suicide completion in the Republic of Korea (PM2.5 and PM10) and Taiwan (nitrogen oxide, carbon monoxide, sulfur dioxide, PM10) and with emergency room visits for suicide attempts in Vancouver, British Columbia, Canada (nitrogen dioxide, carbon monoxide, sulfur dioxide, PM10). Our findings advance support for an influential role of air pollution in suicide risk, but the study was conducted in Salt Lake County, Utah, a location possessing different climatic, geographical, and cultural characteristics than the locations considered in previous studies.
In this study, we found statistically significant associations of IQR increases in PM2.5 (but not in PM10) with maximum increased suicide risks of 5% in the entire study population on lag day 2. In comparison, Kim et al. found associations between IQR increases in both PM2.5 (10.1% maximum increase) and PM10 (9.0% maximum increase) and completed suicide, but the associations with PM10 were more consistent and were especially amplified during cumulative lags 1 and 2. Yang et al. identified a link between PM10 exposure in the spring and suicide in the early summer, while Szyszkowicz et al. measured an excess suicide-attempt risk of 16% in relation to an IQR increase in PM10 exposure during the cold period (October–March) on lag day 0 in males. Szyszkowicz et al. also explored the relationship between nitrogen dioxide exposure and suicide attempts and found a maximum increased risk of 23.9% among males exposed to nitrogen dioxide during the cold period on lag day 1. In our study, which explored the link between nitrogen dioxide and completed suicide, transient exposure to an IQR increase in nitrogen dioxide was associated with maximum increased suicide risks of 20% in the entire study population and 25% among males during cumulative lag 3.
A number of mechanisms have been proposed to explain the deleterious association between air pollutants, including fine particulate matter (PM2.5) and nitrogen dioxide, and suicide risk. Both PM2.5 and nitrogen dioxide may pose risks to physical and mental health, because they can efficiently permeate the thoracic airways due to their small size. They are potent oxidants, and their inhalation has been shown to reduce respiratory function, leading to decreased oxygen saturation, oxidative stress, and hypoxemia. Studies of hypobaric hypoxia have shown that exposure can cause an increase in brain dopamine and tyrosine hydroxylase levels and a decrease in serotonin and tryptophan hydroxylase levels. Decreased levels of serotonin have been implicated in the neurobiology of suicide.
Fine particulate matter and nitrogen dioxide also have strong inflammatory effects and may increase suicide risk by altering the functioning of the central nervous system through a proinflammatory response pathway. Inflammatory responses are linked to the pathophysiology of depression through the release of proinflammatory cytokines. Persons whose depression is exacerbated by air pollutants may be at increased risk for suicide. Similarly, exposure to PM2.5 has been shown to exacerbate physical health conditions such as cardiovascular and respiratory illness. Exacerbation of preexisting physical health conditions can trigger depression and depressive symptoms, which may ultimately increase a person's risk of suicide.
Although nitrogen dioxide and particulate matter share plausible biological mechanisms with regard to suicide, more research attention has historically been paid to the detrimental health effects of particulate matter than to those of nitrogen dioxide. However, both particulate matter exposure and nitrogen dioxide exposure have been linked to emergency room visits for depression and symptoms of depression. Further, outdoor PM2.5 and nitrogen dioxide concentrations have been found to be highly correlated, as they are both products of industrial and domestic combustion. This correlation can make it challenging to separate the contributions of individual pollutants, and investigators have reported that correlated air pollutants can have confounding or modifying effects. In contrast, other studies have found that controlling for multiple pollutants in an analysis did not have substantial impacts on an individual pollutant's risk estimate.
In this study, suicide risk fluctuated with season and peaked in the spring (PM2.5) and during the spring/fall transition period (nitrogen dioxide). The springtime peak observed in this study is consistent with the seasonality patterns associated with suicide rates—a well-documented phenomenon that is often attributed to the effects of meteorological factors. In this and previous studies, heightened suicide risk during the spring and the transition period persisted after controlling for the confounding effects of meteorological variables.
Salt Lake County, Utah, experiences wintertime temperature inversions that trap air pollutants, principally particulate matter, in a layer of cold air, a scenario which has been associated with poor physical health outcomes. Because particulate matter concentrations peak during the winter in Salt Lake County, we expected air pollution to be associated with the greatest risk of suicide during the winter. However, our findings did not support this hypothesis. In contrast, the suicide risk peaks observed during the spring and the transition period suggested that air pollution may interact with additional spring or spring/fall suicide risk factors to increase risk among susceptible individuals, such as those with certain psychiatric conditions (e.g., mood disorders) or pollen allergies.
This study supports previous findings that males and persons aged 35–64 years are subgroups for which the association between air pollution and suicide is especially strong. In the United States, men are at greater risk for suicide than women and, in general, suicide risk increases linearly with age. Persons in these subgroups may be more sensitive to air pollution because their exposure is greater. Alternatively, the individual-level susceptibility factors that increase a person's risk following exposure may be more common among men and persons aged 36–64 years. Conversely, limited sample sizes may have precluded the identification of heightened suicide risk in other subgroups, as insufficient power for detecting associations can be an issue in case-crossover analyses.
Although many of our findings are consistent with previous studies, there are a few possible explanations for between-study discrepancies. First, our daily PM10 data were 71.5% complete for our study period, and multiple imputation was conducted to estimate missing data. However, the approach we took of imputing a data set missing 30% of its data 5 times was expected to yield estimates with 94% precision, which suggests that incompleteness of PM10 data was not a study limitation. Second, air pollution compositions are likely to vary within and across urban study sites as a result of differences in meteorological, topographical, and environmental variables and differences in the type and location of emission sources. We and previous investigators used citywide or countywide daily average air pollutant concentrations to assign individual exposures, which may have biased estimates of association towards the null. To reduce bias, future studies should use air pollution exposure assessment tools with finer spatial and temporal resolution to characterize individual exposure, such as land-use regression models or interpolation methods. Third, population-level differences, including the incidence of comorbid conditions and personal risk factors, may be partly responsible for discrepancies between locations. In particular, Kim et al. showed that the association with PM10 exposure was especially acute in persons with cardiovascular disease. However, the incidence of conditions such as cardiovascular disease varies geographically among populations and may be considerably different between the Republic of Korea and Salt Lake County, Utah. Although our use of individual-level data was a study strength, we did not have access to data on other valuable individual-level characteristics, including the presence of physical and mental comorbidity, smoking behavior, and socioeconomic class. Another study limitation may have been the potential misclassification of some nonsuicide deaths as suicides. However, the Utah Department of Health's Office of the Medical Examiner considers interview data and evidence from the site of death in determining whether suicide was a cause of death, which may minimize misclassification. Air pollution data for this study were specific to Salt Lake County, Utah, and findings may not be generalizable to other parts of Utah or to the United States as a whole. Finally, exposure to air pollutants was assumed to occur among residents of Salt Lake County; alternative sources of air pollution exposure, including occupational and household exposures, were not considered in this study.
This study focused on suicide decedents and did not include persons who attempted suicide, because these 2 groups share some risk factors (e.g., the presence of a psychiatric diagnosis) but also have distinct risk factors (e.g., sex, the presence of stressful life events). We hypothesize that the relationship between air pollution and suicide differs between attempters and completers and that these differences are biologically meaningful. Variation in findings between our study and that of Szyszkowicz et al., which explored the relationship between ambient air pollution and suicide attempts, suggests that this might be the case.
In summary, we identified an increased risk of suicide associated with acute exposure to nitrogen dioxide and PM2.5 during the days preceding suicide in Salt Lake County, Utah. Previous studies of completed suicide focused largely on the relationship with particulate matter, and to our knowledge this was the first study to explicitly explore nitrogen dioxide's role. In the context of prior studies of air pollution and suicide, findings of overall positive associations between air pollution and suicide are consistent. Thus, the observed association appears to be present across environments with different meteorological conditions, geographical features, and population attributes.
Discussion
To our knowledge, this is the first US-based study to have found an association between short-term air pollution exposure and heightened suicide risk. We found that increased suicide risk was associated with single-day and cumulative exposure to PM2.5 and nitrogen dioxide on and during the 2–3 days preceding a suicide in a sample of 1,546 completed suicides in Salt Lake County, Utah. Associations were strongest among males and persons aged 36–64 years. Suicide risk varied by season; it was heightened in both the spring and the spring/fall transition period following acute exposure to PM2.5 and in both the fall and the spring/fall transition period following acute exposure to nitrogen dioxide.
Previous research on suicide risk and air pollution is limited but includes investigations of the associations of criteria air pollutants with risk of suicide completion in the Republic of Korea (PM2.5 and PM10) and Taiwan (nitrogen oxide, carbon monoxide, sulfur dioxide, PM10) and with emergency room visits for suicide attempts in Vancouver, British Columbia, Canada (nitrogen dioxide, carbon monoxide, sulfur dioxide, PM10). Our findings advance support for an influential role of air pollution in suicide risk, but the study was conducted in Salt Lake County, Utah, a location possessing different climatic, geographical, and cultural characteristics than the locations considered in previous studies.
In this study, we found statistically significant associations of IQR increases in PM2.5 (but not in PM10) with maximum increased suicide risks of 5% in the entire study population on lag day 2. In comparison, Kim et al. found associations between IQR increases in both PM2.5 (10.1% maximum increase) and PM10 (9.0% maximum increase) and completed suicide, but the associations with PM10 were more consistent and were especially amplified during cumulative lags 1 and 2. Yang et al. identified a link between PM10 exposure in the spring and suicide in the early summer, while Szyszkowicz et al. measured an excess suicide-attempt risk of 16% in relation to an IQR increase in PM10 exposure during the cold period (October–March) on lag day 0 in males. Szyszkowicz et al. also explored the relationship between nitrogen dioxide exposure and suicide attempts and found a maximum increased risk of 23.9% among males exposed to nitrogen dioxide during the cold period on lag day 1. In our study, which explored the link between nitrogen dioxide and completed suicide, transient exposure to an IQR increase in nitrogen dioxide was associated with maximum increased suicide risks of 20% in the entire study population and 25% among males during cumulative lag 3.
A number of mechanisms have been proposed to explain the deleterious association between air pollutants, including fine particulate matter (PM2.5) and nitrogen dioxide, and suicide risk. Both PM2.5 and nitrogen dioxide may pose risks to physical and mental health, because they can efficiently permeate the thoracic airways due to their small size. They are potent oxidants, and their inhalation has been shown to reduce respiratory function, leading to decreased oxygen saturation, oxidative stress, and hypoxemia. Studies of hypobaric hypoxia have shown that exposure can cause an increase in brain dopamine and tyrosine hydroxylase levels and a decrease in serotonin and tryptophan hydroxylase levels. Decreased levels of serotonin have been implicated in the neurobiology of suicide.
Fine particulate matter and nitrogen dioxide also have strong inflammatory effects and may increase suicide risk by altering the functioning of the central nervous system through a proinflammatory response pathway. Inflammatory responses are linked to the pathophysiology of depression through the release of proinflammatory cytokines. Persons whose depression is exacerbated by air pollutants may be at increased risk for suicide. Similarly, exposure to PM2.5 has been shown to exacerbate physical health conditions such as cardiovascular and respiratory illness. Exacerbation of preexisting physical health conditions can trigger depression and depressive symptoms, which may ultimately increase a person's risk of suicide.
Although nitrogen dioxide and particulate matter share plausible biological mechanisms with regard to suicide, more research attention has historically been paid to the detrimental health effects of particulate matter than to those of nitrogen dioxide. However, both particulate matter exposure and nitrogen dioxide exposure have been linked to emergency room visits for depression and symptoms of depression. Further, outdoor PM2.5 and nitrogen dioxide concentrations have been found to be highly correlated, as they are both products of industrial and domestic combustion. This correlation can make it challenging to separate the contributions of individual pollutants, and investigators have reported that correlated air pollutants can have confounding or modifying effects. In contrast, other studies have found that controlling for multiple pollutants in an analysis did not have substantial impacts on an individual pollutant's risk estimate.
In this study, suicide risk fluctuated with season and peaked in the spring (PM2.5) and during the spring/fall transition period (nitrogen dioxide). The springtime peak observed in this study is consistent with the seasonality patterns associated with suicide rates—a well-documented phenomenon that is often attributed to the effects of meteorological factors. In this and previous studies, heightened suicide risk during the spring and the transition period persisted after controlling for the confounding effects of meteorological variables.
Salt Lake County, Utah, experiences wintertime temperature inversions that trap air pollutants, principally particulate matter, in a layer of cold air, a scenario which has been associated with poor physical health outcomes. Because particulate matter concentrations peak during the winter in Salt Lake County, we expected air pollution to be associated with the greatest risk of suicide during the winter. However, our findings did not support this hypothesis. In contrast, the suicide risk peaks observed during the spring and the transition period suggested that air pollution may interact with additional spring or spring/fall suicide risk factors to increase risk among susceptible individuals, such as those with certain psychiatric conditions (e.g., mood disorders) or pollen allergies.
This study supports previous findings that males and persons aged 35–64 years are subgroups for which the association between air pollution and suicide is especially strong. In the United States, men are at greater risk for suicide than women and, in general, suicide risk increases linearly with age. Persons in these subgroups may be more sensitive to air pollution because their exposure is greater. Alternatively, the individual-level susceptibility factors that increase a person's risk following exposure may be more common among men and persons aged 36–64 years. Conversely, limited sample sizes may have precluded the identification of heightened suicide risk in other subgroups, as insufficient power for detecting associations can be an issue in case-crossover analyses.
Although many of our findings are consistent with previous studies, there are a few possible explanations for between-study discrepancies. First, our daily PM10 data were 71.5% complete for our study period, and multiple imputation was conducted to estimate missing data. However, the approach we took of imputing a data set missing 30% of its data 5 times was expected to yield estimates with 94% precision, which suggests that incompleteness of PM10 data was not a study limitation. Second, air pollution compositions are likely to vary within and across urban study sites as a result of differences in meteorological, topographical, and environmental variables and differences in the type and location of emission sources. We and previous investigators used citywide or countywide daily average air pollutant concentrations to assign individual exposures, which may have biased estimates of association towards the null. To reduce bias, future studies should use air pollution exposure assessment tools with finer spatial and temporal resolution to characterize individual exposure, such as land-use regression models or interpolation methods. Third, population-level differences, including the incidence of comorbid conditions and personal risk factors, may be partly responsible for discrepancies between locations. In particular, Kim et al. showed that the association with PM10 exposure was especially acute in persons with cardiovascular disease. However, the incidence of conditions such as cardiovascular disease varies geographically among populations and may be considerably different between the Republic of Korea and Salt Lake County, Utah. Although our use of individual-level data was a study strength, we did not have access to data on other valuable individual-level characteristics, including the presence of physical and mental comorbidity, smoking behavior, and socioeconomic class. Another study limitation may have been the potential misclassification of some nonsuicide deaths as suicides. However, the Utah Department of Health's Office of the Medical Examiner considers interview data and evidence from the site of death in determining whether suicide was a cause of death, which may minimize misclassification. Air pollution data for this study were specific to Salt Lake County, Utah, and findings may not be generalizable to other parts of Utah or to the United States as a whole. Finally, exposure to air pollutants was assumed to occur among residents of Salt Lake County; alternative sources of air pollution exposure, including occupational and household exposures, were not considered in this study.
This study focused on suicide decedents and did not include persons who attempted suicide, because these 2 groups share some risk factors (e.g., the presence of a psychiatric diagnosis) but also have distinct risk factors (e.g., sex, the presence of stressful life events). We hypothesize that the relationship between air pollution and suicide differs between attempters and completers and that these differences are biologically meaningful. Variation in findings between our study and that of Szyszkowicz et al., which explored the relationship between ambient air pollution and suicide attempts, suggests that this might be the case.
In summary, we identified an increased risk of suicide associated with acute exposure to nitrogen dioxide and PM2.5 during the days preceding suicide in Salt Lake County, Utah. Previous studies of completed suicide focused largely on the relationship with particulate matter, and to our knowledge this was the first study to explicitly explore nitrogen dioxide's role. In the context of prior studies of air pollution and suicide, findings of overall positive associations between air pollution and suicide are consistent. Thus, the observed association appears to be present across environments with different meteorological conditions, geographical features, and population attributes.
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