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Reviews on Environmental Health

Editor-in-Chief: Carpenter, David O. / Sly, Peter

Editorial Board: Brugge, Doug / Edwards, John W. / Field, R.William / Garbisu, Carlos / Hales, Simon / Horowitz, Michal / Lawrence, Roderick / Maibach, H.I. / Shaw, Susan / Tao, Shu / Tchounwou, Paul B.

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Volume 32, Issue 4


Air pollution, aeroallergens and suicidality: a review of the effects of air pollution and aeroallergens on suicidal behavior and an exploration of possible mechanisms

Renee-Marie Ragguett / Danielle S. Cha / Mehala Subramaniapillai / Nicole E. Carmona / Yena Lee
  • Mood Disorders Psychopharmacology Unit, University Health Network, Toronto, ON, Canada
  • Institute of Medical Science, University of Toronto, Toronto, ON, Canada
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Duanduan Yuan / Carola Rong / Roger S. McIntyre
  • Corresponding author
  • Mood Disorders Psychopharmacology Unit, University Health Network, Toronto, ON, Canada
  • Institute of Medical Science, University of Toronto, Toronto, ON, Canada
  • Department of Psychiatry, University of Toronto, Toronto, ON, Canada
  • Department of Pharmacology, University of Toronto, Toronto, ON, Canada
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  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
Published Online: 2017-09-15 | DOI: https://doi.org/10.1515/reveh-2017-0011



Risk factors for suicide can be broadly categorized as sociodemographic, clinical and treatment. There is interest in environmental risk and protection factors for suicide. Emerging evidence suggests a link between environmental factors in the form of air pollution and aeroallergens in relation to suicidality.


Herein, we conducted a systematic review of 15 articles which have met inclusion criteria on the aforementioned effects.


The majority of the reviewed articles reported an increased suicide risk alongside increased air pollutants or aeroallergens (i.e. pollen) increase; however, not all environmental factors were explored equally. In specific, studies that were delimited to evaluating particulate matter (PM) reported a consistent association with suicidality. We also provide a brief description of putative mechanisms (e.g. inflammation and neurotransmitter dysregulation) that may mediate the association between air pollution, aeroallergens and suicidality.


Available evidence suggests that exposure to harmful air quality may be associated with suicidality. There are significant public health implications which are amplified in regions and countries with greater levels of air pollution and aeroallergens. In addition, those with atopic sensitivity may represent a specific subgroup that is at risk.

Keywords: aeroallergens; air pollution; inflammation; pollen; suicide


Suicide is a global phenomenon that represents one of the leading causes of death worldwide. Data collected in 2012 by the World Health Organization (WHO) (1) estimates that suicide accounts for 1.4% of deaths globally and is ranked as the second leading cause of death among individuals aged 15–29. Consequently, the WHO has made efforts to reduce these rates by identifying and implementing preventative strategies. The WHO (1) aims to continually implement and improve suicide prevention strategies (currently in place in 28 countries) through the use of several outlets (e.g. health care, media and education). Towards the foregoing aim, research has been conducted on the efficacy of various interventions for suicide prophylaxis. Effective suicide prevention strategies were found to be, physician education and restricting access to lethal means which could be used for suicide attempts (e.g. firearms, pesticides and gasses), while other preventative strategies (e.g. media reports and patient education) still require more rigorous assessments (2). The development of a successful and effective strategy towards suicide prevention relies heavily on the identification of suicide risk factors.

Risk factors for suicide are multivariate, consisting of both intrinsic and environmental factors (3), (4). The personal, cultural, societal and economic factors have been explored in detail previously and have been shown to vary greatly across these modalities and include, but are not limited to, age [high risk groups include youth (ages 15–19) and elderly (>75 years of age)] and gender [high risk groups differ by location wherein Western nations have a large male to female suicide ratio (three- to five-fold)] (5). Rates of suicide are also higher among individuals diagnosed with mental illnesses [e.g. major depressive disorder (MDD), schizophrenia and post-traumatic stress disorder] (6), (7).

Recently, a number of environmental risk factors have also been considered. For example, the effect of meteorological factors on suicide has been examined, exploring the consequences of climate change (e.g. droughts), seasonality and air temperature on suicidality with many of these aforementioned factors (i.e. air temperature increases and increased droughts) demonstrating a significant positive association with suicide completion (8), (9), (10). In addition, it has been demonstrated that environmental factors, such as air pollution and aeroallergens (i.e. any airborne substance which can cause an allergic reaction) may have deleterious effects on mental health. A review conducted on environmental pollutants and psychosis by Attademo et al. (11) (n=16 review articles; n=13 original research articles) found evidence of a tentative positive association between exposure to environmental pollution and psychosis. Similarly, a review conducted by Kolves et al. (12), exploring the link between allergies and suicidal behaviors (n=17 original research articles) found a positive association between the aforementioned factors. Suicide and decompensation of mental illness peak in spring and, to a lesser extent, in fall. This phenomena is represented in several recent studies wherein it has been reported that suicide and decompensation peaks coincided with spring and fall aeroallergen peaks (13). From low to high aeroallergen exposure, changes in anxiety symptom scores in patients with primary mood disorders are positively correlated with changes in allergy symptom scores (14).

The WHO defines air pollution as the modification of natural characteristics of the atmosphere through contamination of the environment by any chemical or agent. Furthermore, the WHO has developed standards reflecting the variability between pollutants, insofar as hazardous levels are dependent on respective pollutant concentration (15). Air pollutants do not act independently. For example, pollutants can also influence aeroallergens synergistically insofar as their atmospheric concentration may be increased, their allergenicity effects enhanced, and their transport in the air favored (16). While air pollution is a global phenomenon, higher levels are seen in low- and middle-income countries (17). The aforementioned trend is due to the primary use of unprocessed biomass fuels in developing countries; in contrast, developed countries tend to use cleaner fuels and methods of energy (e.g. petroleum and electricity) (18), (19). Dissimilarly, atopic diseases are more prominent in developed countries (20). There are various factors contributing to the increase of allergies, several theories established in the medical field include: the hygiene hypothesis wherein the immune system is affected due to decreased contact with microorganisms throughout childhood as hygiene standards are elevated, environmental contamination such as diesel exhaust particle pollutants and pesticides, and diverse diets in different countries (21). Notwithstanding global variation in levels of air pollution and atopic susceptibility, it is observed that these environmental urban factors at varying levels can have an impact on the population’s health in a number of ways, including impaired lung function (e.g. increased wheezing and asthma cases) (22), (23), (24). Additionally, air pollution concentrations have also been associated with reductions in life expectancy (25).

Components of air pollution

Air pollution is caused by any agent capable of altering the characteristics and natural composition of the atmosphere, including a combination of gasses, particulate matter (PM), metals, and organic and inorganic compounds (26). The following list is not inclusive of all current air pollution agents; however, they are those that are targeted for reduction by the WHO, which include PM, ozone (O3), nitrogen dioxide (NO2) and sulfur dioxide (SO2). Many air pollutants have been identified as health hazards, leading to negative health effects such as increased risk for cardiovascular diseases, and depressive symptomatology (27), (28). As such, the aforementioned agents are key targets according to the air quality guidelines, as lowering their levels could help lower the associated burden of disease (29). The air quality guidelines created by the WHO, are designed to offer guidance in the reduction of health impacts associated with air pollution. Given the detrimental health effects associated with air pollution, it is suggested these agents are not only able to penetrate into a variety of bodily systems; they are also exerting a negative effect on these systems (30).

PM is composed of a mixture of solid, liquid, inorganic/organic compounds and heavy metals suspended in the air. PM is often typified into two groups: PM equal to or less than 2.5 μm (PM2.5) and PM equal to or less than 10 μm (PM10). A third group, ultrafine particles (PM<0.1 μm), causes a greater inflammatory response when inhaled in comparison to larger PM (31). PM is produced by two sources 1) primary sources emit PM in particle form (e.g. forest fires), and 2) secondary sources expel gasses which form PM through a series of chemical reactions (e.g. power plants, car exhaust) (32).

Ozone is a gas which is present in both the stratosphere, earth’s upper atmosphere, and the troposphere, earth’s lower atmosphere (ground level). The role of O3 varies depending on the atmospheric layer, despite its identical molecular configuration in both layers. Ozone in the stratosphere, commonly known as the “ozone layer”, allows for a reduction of harmful UV penetration from incoming sunlight. Stratospheric O3 has had periods of localized and/or overall declines, and the reduction of this layer has been reported to have negative effects due to the important role of the ozone layer (e.g. UV protection) (33). In contrast, tropospheric O3 is considered an air pollutant which occurs by UV reactions to hydrocarbons released from a variety of sources (e.g. fossil fuels, refineries, plants and soil) and the dissension of stratospheric O3. Increased concentration of and exposure to the tropospheric O3 is harmful, as O3 is a highly oxidizing species associated with poor plant and human health (34). Specifically, O3 affects vegetation and humans by entering internal systems through the stomata and lungs, respectively. In vegetation, cellular damage can occur which results in reduced growth and/or yield and in humans increased O3 has shown a positive association with lung function in children (35), (36).

NO2 is an irritant gas produced by the combustion of carbon dioxide (CO2) and nitrogen monoxide (NO). NO2 itself is toxic and also reacts with other air pollutants and the environment, contributing to tropospheric O3, PM production, and lake acidification (37), (38). NO2 has been associated with adverse cardiovascular health effects such as strokes (39).

SO2 is a foul smelling gas produced by a variety of human sources (e.g. industrial activity and motor vehicles). SO2 has been shown to adversely affect both humans and the environment (40). In humans, exposure has been associated with cardiovascular and respiratory difficulties (41), (42). Moreover, a significant association exists between SO2 present in the atmosphere and the number of hospital admissions for ischemic heart diseases and cardiac diseases seen across seven European cities (i.e. Birmingham, London, Milan, Paris, Rome, Stockholm, and in the Netherlands) (41). Additionally, short-term exposure to SO2 can result in bronchoconstriction in asthmatic populations (43).


Aeroallergens are particulates in the air which induce an atopic response. Agents commonly associated with inducing an atopic response include, but are not limited to, pollen, fungal spores, mold and animal dander. Aeroallergens are of particular interest in relation to air pollutants as they have an interactive effect wherein air pollutants can increase the development of pollen allergies and pollen in heavily polluted areas contain more allergenic proteins (16), (44). In addition the term “polluen” has been coined to describe the pollen/pollutant interaction and describe the make-up of pollen materials as they are often carriers of allergenic proteins and non-allergenic pollutants (45). Given the association with pollution and the fact that pollen grains are the major source of outdoor aeroallergens we explore them in particular in this review (46).

Pollen grains are male gametophytes of seed plants ranging from 10 μm to 100 μm in size that carry proteins which compose the allergenic material. Allergy symptoms (e.g. sneezing, nasal congestion and itching) are collectively referred to as allergic rhinitis (AR) and has been reported in variable prevalence, such as 8%–24% self-report in China and in contrast 11%–30% self-report in the US (47), (48). AR is an immunoglobulin E (IgE) mediated response, and can result in both localized or systemic inflammation (49). Pollen counts have also been positively associated with asthma-related hospital admissions (50). Pollen types and concentrations vary both spatially and temporally (51). The major airborne pollen groups have been summarized in detail elsewhere; however, pollen can be classified in an overarching fashion into tree, grass and weed (52).

The recent emphasis on suicide prevention and preliminary evidence demonstrating an association between air pollution, allergens and mental health provides the impetus for exploring the effects of air pollution and aeroallergens in relation to the risk for suicide. The effects of air pollution and aeroallergens on suicidality have been scarcely investigated; however, there is initial evidence suggesting a positive correlation between air pollution, aeroallergens and suicidality (53), (54), (55), (56), (57), (58), (59), (60), (61), (62), (63), (64), (65), (66). Herein, the overarching aim is to provide a succinct review of the available literature on changes in air pollution, aeroallergens and their relationships to suicidal behavior, exploring potential mechanisms by which air pollution may influence suicide rates.


PubMed and Ovid MEDLINE, were searched from inception through May 15 2017 for published primary journal articles, reviews and meta-analyses exploring air pollution and aeroallergens in relation to attempted and completed suicide. The following keywords were used in various combinations for the search: air pollution, aeroallergens, pollen, suicide, suicide attempt, suicide completion, PM, NO2, SO2 and ozone. References from relevant reviews and the reference lists from included articles were screened manually. Articles selected for inclusion in this review were primary studies which discussed the overarching topic herein, examining changes in air pollution and/or aeroallergens in relation to suicidal behavior.


Results of our search criteria yielded 15 studies for review (Figure 1). Of the 15 studies, nine explored the relationship between air pollution and suicide, and six explored the relationship between aeroallergens and suicide, including both completed suicide and attempted suicide. The selected studies vary by length of study, location, and the components of air pollution and aeroallergens explored. Table 1 includes a summary of included studies investigating air pollutants and Table 2 includes a summary of studies investigating aeroallergens.

Flow diagram of article selection procedure.
Figure 1:

Flow diagram of article selection procedure.

Table 1:

Summary of available studies on air pollutants.

Table 2:

Summary of available studies on aeroallergens.

Air pollutants

All nine studies investigating the relationship between air pollution and suicide demonstrated a positive association between completed and attempted suicides with increased air pollution; however, the differences in design and methodology have produced variable results, insofar as not all components of air pollution explored [e.g. NO2, O3, PM10, PM2.5, SO2 and carbon monoxide (CO)] are equally expressed in study findings with regards to their effects on suicide.

Studies which included PM10 and PM2.5 as a measure (n=7), collectively demonstrated that PM has a positive significant association with completed and attempted suicide (28), (53), (55), (56), (57), (59), (60). The effect size per pollutant was not consistent and varied by study and was dependent on a variety of differences in study design, methodology and analysis including covariates (e.g. holidays and temperature) and group stratifications (e.g. age group and suicide method). Increased NO2 showed increase risk for suicide in four out of five studies (28), (56), (59), (60). Increased O3 was associated with increased risk for suicide in three out of four studies (55), (57), (61). SO2 increase demonstrated an increased risk for suicide in four out of five studies (28), (55), (56), (60). An increase in CO demonstrated a positive association with suicide risk in one out of three studies and a negative association in one of three studies (28), (55).


Four studies that examined the association between pollen and suicide found an increase in suicides with increases in pollen; however, the studies were very heterogeneous with many different variations of pollen studied (e.g. tree-cypress pollen and tree-elm pollen) as pollen type is dependent on geographical location (62), (63), (64), (66). In addition, one study by Woo et al. contrasted their own previous findings wherein they initially found a relationship between increasing pollen and increased rates of suicide; however, it was then speculated that this relationship may be explained by socioeconomic factors (e.g. median income, number of psychiatrists in location of study and rural or urban setting) which vary by geographical location (62), (65). Pollen types were often segregated into tree pollen (n=5), ragweed pollen (n=4), and grass pollen (n=2). Associations between suicide rates and pollen were mostly seen in tree pollen, where there was a significant positive association in three studies (62), (63), (64). Grass pollen had demonstrated a significant positive association with suicide risk in two studies; however, this relationship was not significant in Woo et al. after controlling for socioeconomic and demographic factors (62), (65).

Ragweed pollen had positive significant associations with suicide risk in one study, which was no longer significant after controlling for socioeconomic and demographic factors (65).


Air pollution studies vary in length from day of suicide to 191.1 months before suicide. The difference between effects of acute (i.e. less than or equal to 7 days before suicide) and prolonged exposure to air pollutants (i.e. greater than 7 days before suicide) on suicidality have not been explored in depth, such that the majority of the studies have explored acute effects, with few studies employing longitudinal designs examining prolonged exposure (59). There is evidence for both acute and prolonged exposure effects on suicide rate in air pollution. For example, one longitudinal study conducted by Yang et al. (55) found that exposure to gaseous pollutants SO2, O3 and CO continued to be a predictor of suicidality up to 15.9 years (r=0.365, p<0.001; r=0.338, p<0.001; r=−0.236, p=0.001, respectively). In contrast, there is evidence that acute exposure, even in very brief durations, has an influence on the risk of suicide. In particular, Bakian et al. (59) demonstrated that a single day of exposure to PM2.5 and NO2 on 2 days prior to suicide conferred an increased risk of suicidality [odd ratio (OR)=1.05, 95% confidence interval (CI): 1.01, 1.10; OR=1.13, 95% CI: 1.01, 1.27]. A trend exists in that increased air pollution lag days show decreased suicide risk (56), (60). However, the long-term impact of exposure to air pollution has yet to be fully elucidated and may have greater cumulative effects when combined with other risk factors for suicide.

Duration in aeroallergen studies was measured differently as pollen exposure is often typified into seasons. However, acute effects were initially demonstrated with grass-pollen wherein same-day or prior-day pollen counts predict the amount of daily emergency department events for self-directed violence (63). Interestingly, no aeroallergen studies looked specifically at long-term lag, perhaps given that atopic conditions are generally classified by seasons (e.g. tree pollen allergy season vs. grass pollen allergy season).


The effects of air pollution on suicide have a seasonal variation as demonstrated by trends seen typically divided by North American hot (i.e. April–September) versus cold months (i.e. October–March). When segregated by season, the effects of air pollutants on suicide risks were statistically significant in the cooler months, in contrast to no statistically significant trends seen in the hot months (56), (58). There also appears to be a critical transition period between spring and fall, where there is increased suicide risk with PM10 and PM2.5 (53), (59). This transition period may be reflective of the suicide trends seen in pollen as pollen levels demonstrate seasonal variation with increases in pollen counts occurring during their respective on-seasons which also vary spatially and temporally.

Systems and effects

The respective ability of these components of air pollution to affect human health is dependent on their respective abilities to enter the body (Table 3), where they deposit in our bodies, and the methods by which they interact with their surroundings once they gain entrance. Primary routes of entry of air pollutants and aeroallergens for humans include ingestion and inhalation. In addition, air pollutants may affect a number of bodily systems (e.g. respiratory, cardiovascular, nervous, urinary and digestive), reviewed in detail elsewhere (69). Furthermore, aeroallergens are most often associated with detrimental effects to the immune system, cardiovascular system and respiratory system (70), (71), (72), (73). Of particular interest are the systems which have known effects on processes associated with suicidal ideation, specifically the respiratory system, immune system, and cardiovascular system.

Table 3:

Methods by which particles enter the lungs.

Air pollutants

Respiratory system

The respiratory tract is the main route of entry for air pollutants in humans. As such, there are many studies exploring the effects of air pollution on respiratory health. It has been proposed that air pollutants, particularly transitional metal particulates, disturb the airway by causing inflammation, as demonstrated by increased levels of C-reactive protein (CRP) in the circulatory system. CRP is an indiscriminate marker of inflammation produced by the liver (74). The inflammatory marker CRP has demonstrated a positive association with recent suicide attempts in the psychiatric population, wherein a higher concentration of CRP has been found in recent suicide attempters compared to those who have not recently attempted suicide (75). In addition, high CRP levels have also been associated with risk of depression and psychological distress in the general population (76). Therefore it is possible that increased levels of CRP caused by air pollutants may contribute to a suicidal state in certain populations.

Additionally, the pathogenesis of airway inflammatory disease may be mediated by the endoplasmic reticulum (ER) stress pathway, which has shown links to activation of major inflammatory pathways (e.g. NF-κB-IKK) (77). A study conducted by Bown et al. (78) demonstrated that subjects who died by suicide with MDD had higher levels of ER stress proteins (GRP78, GRP94, and calreticulin) present in their temporal cortex. Furthermore, the ER stress pathway has shown to have genetic variation, as such the susceptibility to deleterious effects of air pollution are not consistent across the whole population (79).

Prolonged exposure to air pollutants, specifically O3 and PM, has also been associated with reduced lung function and associated chronic illnesses which can result in reduced oxygen (e.g. asthma and emphysema) (69). It has been demonstrated that suicide rates are elevated in populations located at higher altitudes, where levels of hypoxia – oxygen deficiency – are high (80). This phenomenon has also been observed in other medical conditions associated with hypoxia, including smoking, asthma and chronic obstructive pulmonary disease (81). In contrast, it has been demonstrated that former episodes of hypoxia (e.g. former asthma) are not associated with suicidal ideation or attempts (82). Goodwin et al. (82) suggest that current asthma reflects an active disease whereas former asthma is an inactive disease, and the active state of the disease could be contributing to suicidal ideation. Hypoxia can alter a variety of systems including serotonin synthesis, wherein decreased oxygen is correlated with lower serotonin synthesis levels, possibly explaining the positive relationship suggesting that hypoxia may also be related to mood disturbances resulting from decreased serotonin (80), (83), (84). The affective disturbances present in MDD are mediated by disruptions in the neural serotonergic system; particularly a deficiency in serotonin (85).

Cardiovascular system

PM2.5 and O3 have been shown to affect systemic vasculature and cardiovascular processes (86). Affected cardiovascular processes include increased heart rate variability (i.e. interval between heartbeats), ectopic beats (i.e. disturbance of cardiac rhythm), blood inflammatory and coagulation markers, and mean red blood cell hemoglobin concentration (87). As such, a variety of cardiovascular ailments have been associated with exposure to air pollutants (e.g. anemia, myocardial infarctions and angina) (88), (89). Moreover, individuals with mood disorders, including a diagnosis of MDD, bipolar disorder, and those experiencing acute major depressive episodes, are more likely to experience suicide attempts and/or completion and are also more likely to experience cardiovascular diseases (90), (91), (92). In addition, several cardiovascular diseases have been found to have mood-altering side effects including adjustment disorder with depressed mood and, to a lesser extent, MDD (92).

Vascular depression, while absent from the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, is conceptualized as depressive symptoms with the accompaniment of vascular pathogenesis (93). One such factor postulated to be involved in the pathogenesis of vascular depression is brain lesion localization. Two theories have hypothesized different roles for brain lesion localization: 1) small lesions disrupting critical pathways related to depression (e.g. “lesion-depression pathway” – lesions involving left hemisphere prefrontal or basal ganglia structures, which have been shown to be associated with depressed moods), and 2) an accumulation of lesions exceeding a threshold [e.g. white matter hyperintensities (WMH) >10 cm2] (93), (94). Specifically, large quantities of WMH have been shown to be a factor in predicting future depression as WMH have been associated with the development of depressive symptoms (95), (96). Development of WMHs have further been associated with exposure to PM2.5 and O3 (97). Notwithstanding the aforementioned associations, there is a paucity of literature investigating the role of PM exposure in the development of vascular depression, either by changes in vasculature or by association with brain lesions.

Immune and neurological system

PM, particularly the heavy metals, interacts with the immune system in an antigen nonspecific fashion (69), (98). As such, these metals can lead to malfunction or disruption of regulatory systems (98). Specifically, lead exposure has been shown to result in changes to the dopaminergic and glutamatergic systems in the brain. For example, the density of N-methyl-D-aspartate receptors (NMDAR) has been reported in animal models to be elevated with exposure to lead (99). In addition, other neurological factors which are known to mediate the pathophysiology of mood disorders [e.g. serotonin (5HT) and brain-derived neurotropic factor (BDNF)] are also susceptible to dysregulation with air pollutants (100), (101).

The NMDAR is a glutamate receptor whose dysregulation is implicated in many mental disorders. Observed dysregulation of NMDAR systems across different disorders has included both an increase and a decrease in receptor densities. For example, Nudmamud and Reynolds (102) reported increases of NMDAR density bilaterally in the superior temporal cortex in schizophrenia patients. In contrast, Nudmamud-Thanoi and Reynolds (103) reported a decrease in NMDAR density in patients with MDD and bipolar disorder in the superior temporal cortex. Given the observed NMDAR dysregulation in various mental disorders, those exposed to particulate metals could be at risk for entering a state which promotes suicidal ideation.

Pro-suicidal ideation states are often associated with depressed mood and a deficiency in 5HT (104). In contrast to what would be expected by the monoamine hypothesis of depression [i.e. a deficit in certain neurotransmitters (e.g. 5HT) are responsible for depressive symptomatology], exposure to air pollutants, specifically O3 results in increased 5HT and its metabolites [i.e. 5-hydroxy-indole-acetic acid (5-HIAA)] in pre-clinical models (105), (106). While this increase would appear beneficial, it has been demonstrated that increased 5HT is associated with anxiety and decreased sleep quality (the latter through increased 5-HIAA) (106), (107). Sleep disturbances independent of mood symptomatology are demonstrated to be a risk factor for suicidal thoughts and behaviors as demonstrated in a meta-analysis conducted by Pigeon et al. (108) (adjusted effect size, risk ratio: 1.91, 95% CI: 1.64–2.23; p<0.001). Furthermore, anxiety disorders (e.g. panic disorder, post-traumatic stress disorder, social phobia, and agoraphobia) have been associated with increased odds of suicidal ideation in Canadian (unadjusted odds ratio 5.63, 95% CI: 4.59–6.90) and American (unadjusted odds ratio 8.36, 95% CI: 6.06–11.54) populations (107).

It has been suggested that decreases in BDNF reduces neural plasticity and the ability for coping with crisis situations (109). Various neuroprotective actions such as exercise and antidepressant pharmacological agents have been known to increase BDNF production (110), (111). The foregoing observations are further substantiated by reports indicating that BDNF is markedly downregulated among those who have completed suicide, independently of mood symptoms (112). Notable, it has been demonstrated that when exercising in air polluted conditions, specifically traffic-related air pollution, levels of BDNF are not increased compared to those exercising in a room with clean air (101). Despite exercise being known to increase BDNF this increase was only seen in those that exercised in a clean room. It has been further suggested that BDNF production is epigenetically mediated, wherein increased DNA methylation results in lower BDNF mRNA levels. Moreover, preliminary research has demonstrated that traffic-related air pollutants moderate DNA methylation (113), (114).


Respiratory and immune system

Similar to air pollutants, inhalation is the most common method of allergen entry into the human body; however, deposition of allergenic compounds along the respiratory tract is variable and is mediated by both particle diameter and breathing types (e.g. heavy through nose, light through mouth) (49). Ultimately, many pollen particles are too large to deposit in the lungs, although certain pollens, such as rye-grass pollen have demonstrated the ability to induce asthmatic effects similar to air pollutants. This is of relevance because asthma has shown positive associations with suicidal behaviors (115), (116). Interestingly it has been demonstrated that in contrast to air pollutants, non-allergic asthma has been associated with higher levels of CRP than allergic asthma (117). As such, there exists differences in the inflammatory pathways between air pollutants and aeroallergens.

Aeroallergens result in an IgE mediated immune response that is often localized and chronic (118), (119). Cytokines play a regulatory role in IgE-mediated atopic responses whereby increased interleukin-4 (IL-4) has a major role in IgE synthesis (120). Interestingly, the role of cytokines in suicidal behavior is contrary to what would be expected; previous evidence has suggested increases in interferon gamma (IFN)-γ, which down regulates the production of IgE. Moreover, an association between increased levels of IL-4 and suicide was only demonstrated in one study (121). Notwithstanding the foregoing results, IgE status has been associated with increased depression scores indicating worse mood symptoms (122).

Allergen-associated inflammation may also affect the brain. While the effects of this phenomenon in humans is poorly understood, there have been demonstrations of allergy-related neurological changes in murine models (49). For example, one study found that mice sensitive to allergies were found to have increased brain levels of IgE and immunoglobulin G. Furthermore, the presence of allergies was also found to increase phosphorylation of the tau protein which is a detrimental process towards the formation of Alzheimer’s disease (123). The aforementioned murine study made reference to Eriksson et al. (124), who demonstrated that atopy is associated with increased risk for Alzheimer’s disease and dementia in humans. Phosphorylated tau is associated with Alzheimer’s disease, it has been also associated with mild cognitive impairments (125). Interestingly, suicide has been positive associated with both Alzheimer’s disease and cognitive impairments (49). Collectively, these findings suggest that allergenic rhinitis may account for at least some of the increased risk of suicide seen in both Alzheimer’s disease and mild cognitive impairments, although this hypothesis warrants further investigation. In addition, the ability for allergens to influence brain function has been documented by Reeves et al. (126) where they proposed that alcohol disrupts the blood-brain barrier and, as such, allows the brain to be exposed to immune cells and cytokines which can influence mood symptomatology and result in behaviors such as suicide. Furthermore, in contrast to increases in 5HT seen with air pollutants, atopic rhinitis is associated with decreased 5HT (127). The aforementioned trend of 5HT under atopic rhinitis conditions is aligned with the monoamine hypothesis of depression, and may contribute to mood disturbances in this population.

Cardiovascular system

Atopic inflammatory processes have also been shown to influence vascular health insofar as factors associated with allergic diseases (e.g. increased IgE, cytokine secretion and low vitamin D concentration) can add to cardiovascular disorder pathogenesis (128). Further contributing to cardiovascular disease is the prolonged use of glucocorticoids, often used to control AR, as this treatment has been associated with metabolic dysregulation in the form of weight gain (128), (129). This is of significance as obese individuals are more likely to commit suicide than those with normal or low weight (130).

Discussion and conclusion

This review examined the relationship between air pollution, aeroallergens and suicide. We further explored the possible mechanisms by which exposure to air pollution and aeroallergens can lead to suicide attempts and/or completions. It is apparent that components of air pollution, particularly PM2.5, have the ability to negatively affect a variety of bodily systems (e.g. respiratory, cardiovascular and immune), ultimately resulting in alterations that are consistent with differences seen in those with mental disorders and/or in individuals who have attempted and/or completed suicide. In addition, it has been demonstrated that pollen alone can induce an immune response, which is potentially conducive to a suicidal state. However, the effects of pollen are exacerbated by the presence of air pollutants, as explained by the concept of “polluen” (45).

With the similarities and differences of the pathways affected by both air pollutants and aeroallergens, polluen may attack various systems simultaneously. It has been demonstrated that when pollen is exposed to specific air pollutants, it becomes more allergenic as more allergens are released from the pollen grain. In contrast SO2 resulted in decreased release of allergens from the pollen grain (46). Thus, it is possible that under certain pollution conditions the allergenic potential of aeroallergens is increased, potentially resulting in increased cases of allergenic rhinitis. In addition, there is also the concept of air pollutants carrying allergenic material, which could be activating both series of immune and system responses, contributing to a pro-suicidal internal environment.

There is a growing interest in ecological factors and their influence on suicidal behavior. While this review mainly focuses on pro-suicidal factors, there are also environmental factors that have been shown to reduce the rates of suicide. For example, lithium is a mood stabilizing agent and is known to have suicide protective effects. Trace amounts of lithium are found in drinking water; areas with higher lithium content in the drinking water have shown lower suicide rates in many existing studies (131), (132). For example, Kapusta et al. (133) explored the relationship between lithium in drinking water and suicide rates across 99 Austrian districts (average population 8,297,964, SD=65,050). The overall suicide rate was found to be inversely associated with the lithium levels in drinking water (B=−0.41, p>0.0001) (133). While the existing literature regarding air pollution, aeroallergens and suicide is very limited, the trends in the current literature would suggest that these ecological factors and their components demonstrate a pro-suicidal ecological effect.

The components of air pollution explored largely varied across studies. The recurring trend of the association between PM and suicide in the aforementioned studies and its systematic reappearance in suggests that it is an important component of air pollution with respect to suicidality. However, studies carried out prior to 2005 did not consider the effect of PM2.5, as this measurement was only implemented after this time. As PM is diverse in its composition, there could be a variety of components that affect suicidality. Exposure to heavy metals in the environment has been related to immunotoxic effects and has been targeted for direct reduction in consumption (e.g. consuming less foods with trace amounts of metals) (134). Heavy metals present in PM appear to be the main culprits impacting mental health via the respiratory system, cardiovascular system and immune system (69), (74), (86).

Available literature on the topic is limited insofar as the risk factors for suicide are multiplicative, involving a variety of different processes and systems, and direct inferences about the causal role of air pollution and aeroallergens in suicidality cannot be made at this point in time. Additionally, the possibility remains that there may have been pre-existing mental disorders among existing study samples. Interestingly when the aforementioned factor was controlled for by Postolache et al. (13), no differences were seen in suicide attempts in patients with MDD and bipolar disorder with or without allergy sensitivity in any pollen season. Moreover, only a limited number of locations were explored for air pollutants, excluding many of the cities with the highest amount of air pollution worldwide (e.g. Tokyo, Shanghai and Delhi) (135). Also, given the recent change in reporting standards (e.g. the introduction of PM2.5 in 2005), many historic data is incomplete, making it difficult to consider the effects of major pollution events such as the industrial revolution and the Bhopal gas leak on suicide rates. Large pollution events are important to analyze as they often have large effects on the population’s health, such as the Beijing fog in 2013 (136).

Limitations in the current studies include the lack of consistency in reporting air pollutants given the recent introduction of PM2.5, and the lack of many long-term exposure studies for both air pollutants and aeroallergens. Studies which reported on aeroallergens were also limited in diversity as there exists a large variety of aeroallergens. Additionally, only one study examined the effects of both pollen and air pollutants together. Future directions include exploring suicide statistics following major pollution events, exploring trends between studies comparing areas with high amounts of pollution to those with low pollution, and further exploring the specific composition of PM as a factor for suicide. Guo and Barnett (137) have completed a criticism on the methodology used for Bakian et al.’s study expressing the time-stratified case-crossover design with long strata durations (which has been widely repeated across other studies) is not as sensitive as desired and may not accurately control for pollutant seasonality. In addition gaps exist in the lack of controlling for the potential confounding variable of precipitation, and averaging air pollutant data across many stations (a practice which was repeated frequently) (137). It is possible that more accurate and representative studies of the interaction between air pollutants and suicide could be achieved if the aforementioned criticism was addressed.

Furthermore, studies are required that explore the effect of other aeroallergens on suicide and studies which explore combinatory effects of air pollutants and aeroallergens, also known as polluens. IgE mediated allergic reactions are not only seen with aeroallergens but also seen with some food allergies, which are recognized as the most common chronic non-communicable disease in children. With increasing global prevalence, there’s impetus for exploring the impact on suicide (138), (139).


  • 1.

    World Health Organization. Preventing suicide: a global imperative. Geneva: World Health Organization, 2014 [cited 2016 10 Nov]. Google Scholar

  • 2.

    Mann JJ, Apter A, Bertolote J, Beautrais A, Currier D, et al. Suicide prevention strategies: a systematic review. J Am Med Assoc 2005;294(16):2064–74. CrossrefGoogle Scholar

  • 3.

    Centers for Disease Control and Prevention. Suicide: risk and protective factors, 2016 [cited 2016 10 Nov]. Available from: https://www.cdc.gov/violenceprevention/suicide/riskprotectivefactors.html

  • 4.

    Moscicki EK. Identification of suicide risk factors using epidemiologic studies. Psychiatr Clin North Am 1997;20(3): 499–517. CrossrefPubMedGoogle Scholar

  • 5.

    Goldsmith SK, Pellmar TC, Kleinman AM, Bunney WE. Reducing suicide: a national imperative. In: Goldsmith SK, Pellmar TC, Kleinman AM, Bunney WE, editors. Reducing suicide: a national imperative. Washington, DC: The National Academies Press, 2002. Google Scholar

  • 6.

    Harris EC, Barraclough B. Suicide as an outcome for mental disorders. A meta-analysis. Br J Psychiatry 1997;170:205–28. PubMedCrossrefGoogle Scholar

  • 7.

    Sokero TP, Melartin TK, Rytsala HJ, Leskela US, Lestela-Mielonen PS, et al. Prospective study of risk factors for attempted suicide among patients with DSM-IV major depressive disorder. Br J Psychiatr 2005;186:314–8. CrossrefGoogle Scholar

  • 8.

    Hanigan IC, Butler CD, Kokic PN, Hutchinson MF. Suicide and drought in New South Wales, Australia, 1970–2007. Proc Natl Acad Sci USA 2012;109(35):13950–5. CrossrefGoogle Scholar

  • 9.

    White RA, Azrael D, Papadopoulos FC, Lambert GW, Miller M. Does suicide have a stronger association with seasonality than sunlight? BMJ Open 2015;5(6):e007403. CrossrefPubMedGoogle Scholar

  • 10.

    Kurokouchi M, Miyatake N, Kinoshita H, Tanaka N, Fukunaga T. Correlation between suicide and meteorological parameters. Medicina 2015;51(6):363–7. CrossrefGoogle Scholar

  • 11.

    Attademo L, Bernardini F, Garinella R, Compton MT. Environmental pollution and risk of psychotic disorders: a review of the science to date. Schizophr Res 2016;181:55–9. PubMedGoogle Scholar

  • 12.

    Kolves K, Barker E, De Leo D. Allergies and suicidal behaviors: a systematic literature review. Allergy Asthma Proc 2015;36(6):433–8. PubMedCrossrefGoogle Scholar

  • 13.

    Postolache TT, Roberts DW, Langenberg P, Muravitskaja O, Stiller JW, et al. Allergen specific IgE, number and timing of past suicide attempts, and instability in patients with recurrent mood disorders. Int J Child Health Hum Dev 2008;1(3):297–304. PubMedGoogle Scholar

  • 14.

    Postolache TT, Langenberg P, Zimmerman SA, Lapidus M, Komarow H, et al. Changes in severity of allergy and anxiety symptoms are positively correlated in patients with recurrent mood disorders who are exposed to seasonal peaks of aeroallergens. Int J Child Health Hum Dev 2008;1(3):313–22. PubMedGoogle Scholar

  • 15.

    World Health Organization. WHO air quality guidelines for particulate matter, ozone, nitrogen dioxide and sulfur dioxide, 2005 [cited 2016 10 Nov]. Available from: http://apps.who.int/iris/bitstream/10665/69477/1/WHO_SDE_PHE_OEH_06.02_eng.pdf

  • 16.

    Bartra J, Mullol J, del Cuvillo A, Davila I, Ferrer M, et al. Air pollution and allergens. J Investig Allergol Clin Immunol 2007;17(Suppl 2):3–8. PubMedGoogle Scholar

  • 17.

    World Health Organization. Ambient (outdoor) air quality and health, 2016 [cited 2016 10 Nov]. Available from: http://www.who.int/mediacentre/factsheets/fs313/en/

  • 18.

    World Reseources Institute, United Nations Environment Programme, United Nations Development Programme, Bank W. The urban environment. A guide to the global environment. A special reprint from World Resources, 1996–97. New York, NY: Oxford University Press, 1996. Google Scholar

  • 19.

    Bruce N, Perez-Padilla R, Albalak R. Indoor air pollution in developing countries: a major environmental and public health challenge. Bull World Health Organ 2000;78(9):1078–92. Google Scholar

  • 20.

    Sublett JL. The environment and risk factors for atopy. Curr Allergy Asthma Rep 2005;5(6):445–50. PubMedCrossrefGoogle Scholar

  • 21.

    Kulis M, Wright BL, Jones SM, Burks AW. Diagnosis, management, and investigational therapies for food allergies. Gastroenterology 2015;148(6):1132–42. PubMedCrossrefGoogle Scholar

  • 22.

    Chan-Yeung M. Air pollution and health. Hong Kong Med J 2000;6(4):390–8. PubMedGoogle Scholar

  • 23.

    D‘Amato G. Environmental urban factors (air pollution and allergens) and the rising trends in allergic respiratory diseases. Allergy 2002;57(Suppl 72):30–3. PubMedCrossrefGoogle Scholar

  • 24.

    Atis S, Tutluoglu B, Sahin K, Yaman M, Kucukusta AR, et al. Sensitization to sunflower pollen and lung functions in sunflower processing workers. Allergy 2002;57(1):35–9. PubMedGoogle Scholar

  • 25.

    de Keijzer C, Agis D, Ambros A, Arevalo G, Baldasano JM, et al. The association of air pollution and greenness with mortality and life expectancy in Spain: a small-area study. Environ Int 2017;99:170–6. CrossrefGoogle Scholar

  • 26.

    Akimoto H. Global air quality and pollution. Science 2003;302(5651):1716–9. CrossrefPubMedGoogle Scholar

  • 27.

    Bonyadi Z, Ehrampoush MH, Ghaneian MT, Mokhtari M, Sadeghi A. Cardiovascular, respiratory, and total mortality attributed to PM2.5 in Mashhad, Iran. Environ Monit Assess 2016;188(10):570. CrossrefPubMedGoogle Scholar

  • 28.

    Szyszkowicz M, Kousha T, Kingsbury M, Colman I. Air pollution and emergency department visits for depression: a multicity case-crossover study. Environ Health Insights 2016;10:155–61. PubMedGoogle Scholar

  • 29.

    Krzyzanowski M, Cohen A. Update of WHO air quality guidelines. Air Qual Atmos Health 2008;1(1):7–13. CrossrefGoogle Scholar

  • 30.

    Block ML, Calderon-Garciduenas L. Air pollution: mechanisms of neuroinflammation and CNS disease. Trends Neurosci 2009;32(9):506–16. CrossrefPubMedGoogle Scholar

  • 31.

    Oberdorster G. Pulmonary effects of inhaled ultrafine particles. Int Arch Occup Environ Health 2001;74(1):1–8. PubMedGoogle Scholar

  • 32.

    Centers for Disease Control and Prevention. Particle pollution, 2014 [cited 2016 10 Nov]. Available from: https://www.cdc.gov/air/particulate_matter.html

  • 33.

    Peter T. The stratospheric ozone layer-an overview. Environ Pollut 1994;83(1–2):69–79. CrossrefPubMedGoogle Scholar

  • 34.

    McKee D. Tropospheric ozone: human health and agricultural impacts. Boca Raton, Florida: CRC Press, 1993. Google Scholar

  • 35.

    Hwang BF, Chen YH, Lin YT, Wu XT, Leo Lee Y. Relationship between exposure to fine particulates and ozone and reduced lung function in children. Environ Res 2015;137:382–90. CrossrefPubMedGoogle Scholar

  • 36.

    Wilkinson S, Mills G, Illidge R, Davies WJ. How is ozone pollution reducing our food supply? J Exp Bot 2012;63(2):527–36. PubMedCrossrefGoogle Scholar

  • 37.

    World Health Organization. WHO guidelines for indoor air quality: selected pollutants. WHO, 2010. Available from: http://www.euro.who.int/__data/assets/pdf_file/0009/128169/e94535.pdf

  • 38.

    Vitousek PM, Aber JD, Howarth RW, Likens GE, Matson PA, et al. Human alteration of the global nitrogen cycle: sources and consequences. Ecol Appl 1997;7(3):737–50. Google Scholar

  • 39.

    Tsai SS, Goggins WB, Chiu HF, Yang CY. Evidence for an association between air pollution and daily stroke admissions in Kaohsiung, Taiwan. Stroke 2003;34(11):2612–6. PubMedCrossrefGoogle Scholar

  • 40.

    Rall DP. Review of the health effects of sulfur oxides. Environ Health Perspect 1974;8:97–121. PubMedCrossrefGoogle Scholar

  • 41.

    Sunyer J, Ballester F, Tertre AL, Atkinson R, Ayres JG, et al. The association of daily sulfur dioxide air pollution levels with hospital admissions for cardiovascular diseases in Europe (The Aphea-II study). Eur Heart J 2003;24(8):752–60. CrossrefPubMedGoogle Scholar

  • 42.

    French JG, Lowrimore G, Nelson WC, Finklea JF, English T, et al. The effect of sulfur dioxide and suspended sulfates on acute respiratory disease. Arch Environ Health 1973;27(3):129–33. CrossrefPubMedGoogle Scholar

  • 43.

    Horstman DH, Folinsbee LJ. Sulfur dioxide-induced bronchoconstriction in asthmatics exposed for short durations under controlled conditions: a selected review. Susceptibility to inhaled pollutants. West Conshohocken, PA, USA: ASTM International, 1989:195–206 Google Scholar

  • 44.

    Obtulowicz K. Air pollution and pollen allergy. Folia Med Cracov 1993;34(1–4):121–8. PubMedGoogle Scholar

  • 45.

    Senechal H, Visez N, Charpin D, Shahali Y, Peltre G, et al. A review of the effects of major atmospheric pollutants on pollen grains, pollen content, and allergenicity. ScientificWorldJ 2015;2015:940243. Google Scholar

  • 46.

    Behrendt H, Becker WM, Fritzsche C, Sliwa-Tomczok W, Tomczok J, et al. Air pollution and allergy: experimental studies on modulation of allergen release from pollen by air pollutants. Int Arch Allergy Immunol 1997;113(1–3):69–74. PubMedCrossrefGoogle Scholar

  • 47.

    Zhang L, Han D, Huang D, Wu Y, Dong Z, et al. Prevalence of self-reported allergic rhinitis in eleven major cities in china. Int Arch Allergy Immunol 2009;149(1):47–57. PubMedCrossrefGoogle Scholar

  • 48.

    Nathan RA, Meltzer EO, Derebery J, Campbell UB, Stang PE, et al. The prevalence of nasal symptoms attributed to allergies in the United States: findings from the burden of rhinitis in an America survey. Allergy Asthma Proc 2008;29(6):600–8. CrossrefGoogle Scholar

  • 49.

    Janeway CA Jr, Travers P, Walport M, Shlomchik MJ. Effector mechanisms in allergic reactions. In: Immunobiology, 5th edition. The Immune System in Health and Disease. New York: Garland Science, 2001. Google Scholar

  • 50.

    Ghosh D, Chakraborty P, Gupta J, Biswas A, Roy I, et al. Associations between pollen counts, pollutants, and asthma-related hospital admissions in a high-density Indian metropolis. J Asthma 2012;49(8):792–9. CrossrefGoogle Scholar

  • 51.

    Emberlin J, Jaeger S, Dominguez-Vilches E, Soldevilla CG, Hodal L, et al. Temporal and geographical variations in grass pollen seasons in areas of western Europe: an analysis of season dates at sites of the European pollen information system. Aerobiologia 2000;16(3):373–9. CrossrefGoogle Scholar

  • 52.

    Weber RW. Pollen identification. Ann Allergy Asthma Immunol 1998;80(2):141–8. CrossrefPubMedGoogle Scholar

  • 53.

    Kim C, Jung SH, Kang DR, Kim HC, Moon KT, et al. Ambient particulate matter as a risk factor for suicide. Am J Psychiatry 2010;167(9):1100–7. CrossrefPubMedGoogle Scholar

  • 54.

    Yackerson NS, Zilberman A, Todder D, Kaplan Z. The influence of air-suspended particulate concentration on the incidence of suicide attempts and exacerbation of schizophrenia. Int J Biometeorol 2014;58(1):61–7. CrossrefPubMedGoogle Scholar

  • 55.

    Yang AC, Tsai SJ, Huang NE. Decomposing the association of completed suicide with air pollution, weather, and unemployment data at different time scales. J Affect Disord 2011; 129(1–3):275–81. PubMedCrossrefGoogle Scholar

  • 56.

    Lin GZ, Li L, Song YF, Zhou YX, Shen SQ, et al. The impact of ambient air pollution on suicide mortality: a case-crossover study in Guangzhou, China. Environ Health 2016;15(1):90. CrossrefPubMedGoogle Scholar

  • 57.

    Kim Y, Myung W, Won HH, Shim S, Jeon HJ, et al. Association between air pollution and suicide in South Korea: a nationwide study. PLoS One 2015;10(2):e0117929. PubMedCrossrefGoogle Scholar

  • 58.

    Szyszkowicz M, Willey JB, Grafstein E, Rowe BH, Colman I. Air pollution and emergency department visits for suicide attempts in vancouver, Canada. Environ Health Insights 2010;4:79–86. PubMedGoogle Scholar

  • 59.

    Bakian AV, Huber RS, Coon H, Gray D, Wilson P, et al. Acute air pollution exposure and risk of suicide completion. Am J Epidemiol 2015;181(5):295–303. CrossrefPubMedGoogle Scholar

  • 60.

    Ng CF, Stickley A, Konishi S, Watanabe C. Ambient air pollution and suicide in Tokyo, 2001–2011. J Affect Disord 2016;201: 194–202. CrossrefPubMedGoogle Scholar

  • 61.

    Biermann T, Stilianakis N, Bleich S, Thurauf N, Kornhuber J, et al. The hypothesis of an impact of ozone on the occurrence of completed and attempted suicides. Med Hypotheses 2009;72(3):338–41. PubMedCrossrefGoogle Scholar

  • 62.

    Postolache TT, Stiller JW, Herrell R, Goldstein MA, Shreeram SS, et al. Tree pollen peaks are associated with increased nonviolent suicide in women. Mol Psychiatry 2005;10(3):232–5. PubMedCrossrefGoogle Scholar

  • 63.

    Jeon-Slaughter H, Claassen CA, Khan DA, Mihalakos P, Lee KB, et al. Temporal association between nonfatal self-directed violence and tree and grass pollen counts. J Clin Psychiatry 2016;77(9):1160–7. PubMedGoogle Scholar

  • 64.

    Stickley A, Sheng Ng CF, Konishi S, Koyanagi A, Watanabe C. Airborne pollen and suicide mortality in Tokyo, 2001–2011. Environ Res 2017;155:134–40. CrossrefPubMedGoogle Scholar

  • 65.

    Woo JM, Gibbons RD, Rogers CA, Qin P, Kim JB, et al. Pollen counts and suicide rates. Association not replicated. Acta Psychiat Scand 2012;125(2):168–75. CrossrefGoogle Scholar

  • 66.

    Qin P, Waltoft BL, Mortensen PB, Postolache TT. Suicide risk in relation to air pollen counts: a study based on data from Danish registers. BMJ Open 2013;3(5): 1–9. Google Scholar

  • 67.

    Carvalho TC, Peters JI, Williams RO, 3rd. Influence of particle size on regional lung deposition – what evidence is there? Int J Pharm 2011;406(1–2):1–10. CrossrefPubMedGoogle Scholar

  • 68.

    Lippmann M, Yeates DB, Albert RE. Deposition, retention, and clearance of inhaled particles. Br J Ind Med 1980;37(4):337–62. PubMedGoogle Scholar

  • 69.

    Kampa M, Castanas E. Human health effects of air pollution. Environ Pollut 2008;151(2):362–7. CrossrefPubMedGoogle Scholar

  • 70.

    Wilson AF, Novey HS, Berke RA, Surprenant EL. Deposition of inhaled pollen and pollen extract in human airways. N Engl J Med 1973;288(20):1056–8. CrossrefPubMedGoogle Scholar

  • 71.

    Thomas WR, Hales BJ. Immune responses to inhalant allergens. World Allergy Organ J 2008;1(6):89–95. CrossrefPubMedGoogle Scholar

  • 72.

    Stieb DM, Beveridge RC, Brook JR, Smith-Doiron M, Burnett RT, et al. Air pollution, aeroallergens and cardiorespiratory emergency department visits in Saint John, Canada. J Expo Anal Environ Epidemiol 2000;10(5):461–77. CrossrefGoogle Scholar

  • 73.

    Yeates DB, Mauderly JL. Inhaled environmental/occupational irritants and allergens: mechanisms of cardiovascular and systemic responses. Introduction. Environ Health Perspect 2001;109(Suppl 4):479–81. PubMedCrossrefGoogle Scholar

  • 74.

    Hampel R, Peters A, Beelen R, Brunekreef B, Cyrys J, et al. Long-term effects of elemental composition of particulate matter on inflammatory blood markers in European cohorts. Environ Int 2015;82:76–84. PubMedCrossrefGoogle Scholar

  • 75.

    Loas G, Dalleau E, Lecointe H, Yon V. Relationships between anhedonia, alexithymia, impulsivity, suicidal ideation, recent suicide attempt, C-reactive protein and serum lipid levels among 122 inpatients with mood or anxious disorders. Psychiatry Res 2016;246:296–302. PubMedCrossrefGoogle Scholar

  • 76.

    Wium-Andersen MK, Orsted DD, Nordestgaard BG. Elevated C-reactive protein, depression, somatic diseases, and all-cause mortality: a mendelian randomization study. Biol Psychiatry 2014;76(3):249–57. CrossrefPubMedGoogle Scholar

  • 77.

    Hotamisligil GS. Endoplasmic reticulum stress and the inflammatory basis of metabolic disease. Cell 2010;140(6): 900–17. CrossrefPubMedGoogle Scholar

  • 78.

    Bown C, Wang JF, MacQueen G, Young LT. Increased temporal cortex ER stress proteins in depressed subjects who died by suicide. Neuropsychopharmacology 2000;22(3):327–32. CrossrefPubMedGoogle Scholar

  • 79.

    Huls A, Kramer U, Herder C, Fehsel K, Luckhaus C, et al. Genetic susceptibility for air pollution-induced airway inflammation in the SALIA study. Environ Res 2017;152:43–50. CrossrefPubMedGoogle Scholar

  • 80.

    Brenner B, Cheng D, Clark S, Camargo CA Jr. Positive association between altitude and suicide in 2584 U.S. counties. High Alt Med Biol 2011;12(1):31–5. PubMedCrossrefGoogle Scholar

  • 81.

    Young SN. Elevated incidence of suicide in people living at altitude, smokers and patients with chronic obstructive pulmonary disease and asthma: possible role of hypoxia causing decreased serotonin synthesis. J Psychiatry Neurosci 2013;38(6):423–6. PubMedCrossrefGoogle Scholar

  • 82.

    Goodwin RD, Demmer RT, Galea S, Lemeshow AR, Ortega AN, et al. Asthma and suicide behaviors: results from the Third National Health and Nutrition Examination Survey (NHANES III). J Psychiatr Res 2012;46(8):1002–7. PubMedCrossrefGoogle Scholar

  • 83.

    Nishikawa M, Kumakura Y, Young SN, Fiset P, Vogelzangs N, et al. Increasing blood oxygen increases an index of 5-HT synthesis in human brain as measured using alpha-[(11)C]methyl-L-tryptophan and positron emission tomography. Neurochem Int 2005;47(8):556–64. CrossrefPubMedGoogle Scholar

  • 84.

    Shukitt BL, Banderet LE. Mood states at 1600 and 4300 meters terrestrial altitude. Aviat Space Environ Med 1988;59(6):530–2. PubMedGoogle Scholar

  • 85.

    Coppen A. The biochemistry of affective disorders. Br J Psychiatry 1967;113(504):1237–64. CrossrefPubMedGoogle Scholar

  • 86.

    Brook RD, Brook JR, Urch B, Vincent R, Rajagopalan S, et al. Inhalation of fine particulate air pollution and ozone causes acute arterial vasoconstriction in healthy adults. Circulation 2002;105(13):1534–6. PubMedCrossrefGoogle Scholar

  • 87.

    Riediker M, Cascio WE, Griggs TR, Herbst MC, Bromberg PA, et al. Particulate matter exposure in cars is associated with cardiovascular effects in healthy young men. Am J Respir Crit Care Med 2004;169(8):934–40. CrossrefPubMedGoogle Scholar

  • 88.

    Huang YC, Ghio AJ. Vascular effects of ambient pollutant particles and metals. Curr Vasc Pharmacol 2006;4(3): 199–203. PubMedCrossrefGoogle Scholar

  • 89.

    Vermylen J, Nemmar A, Nemery B, Hoylaerts MF. Ambient air pollution and acute myocardial infarction. J Thromb Haemostasis 2005;3(9):1955–61. CrossrefGoogle Scholar

  • 90.

    Coryell W, Young EA. Clinical predictors of suicide in primary major depressive disorder. J Clin Psychiatry 2005;66(4):412–7. PubMedCrossrefGoogle Scholar

  • 91.

    Chen YW, Dilsaver SC. Lifetime rates of suicide attempts among subjects with bipolar and unipolar disorders relative to subjects with other Axis I disorders. Biol Psychiatry 1996;39(10):896–9. PubMedCrossrefGoogle Scholar

  • 92.

    Hare DL, Toukhsati SR, Johansson P, Jaarsma T. Depression and cardiovascular disease: a clinical review. Eur Heart J 2014;35(21):1365–72. PubMedCrossrefGoogle Scholar

  • 93.

    Alexopoulos GS, Bruce ML, Silbersweig D, Kalayam B, Stern E. Vascular depression: a new view of late-onset depression. Dialogues Clin Neuroscience 1999;1(2):68–80. Google Scholar

  • 94.

    Morris PL, Robinson RG, Raphael B, Hopwood MJ. Lesion location and poststroke depression. J Neuropsychiatry Clin Neurosci 1996;8(4):399–403. CrossrefPubMedGoogle Scholar

  • 95.

    Teodorczuk A, O’Brien JT, Firbank MJ, Pantoni L, Poggesi A, et al. White matter changes and late-life depressive symptoms: longitudinal study. Br J Psychiatry 2007;191:212–7. CrossrefPubMedGoogle Scholar

  • 96.

    Park JH, Lee SB, Lee JJ, Yoon JC, Han JW, et al. Epidemiology of MRI-defined vascular depression: a longitudinal, community-based study in Korean elders. J Affect Disord 2015;180:200–6. CrossrefPubMedGoogle Scholar

  • 97.

    Calderon-Garciduenas L, Reynoso-Robles R, Vargas-Martinez J, Gomez-Maqueo-Chew A, Perez-Guille B, et al. Prefrontal white matter pathology in air pollution exposed Mexico City young urbanites and their potential impact on neurovascular unit dysfunction and the development of Alzheimer’s disease. Environ Res 2016;146:404–17. PubMedCrossrefGoogle Scholar

  • 98.

    Mishra KP. Lead exposure and its impact on immune system: a review. Toxicol In Vitro 2009;23(6):969–72. CrossrefPubMedGoogle Scholar

  • 99.

    Lasley SM, Green MC, Gilbert ME. Rat hippocampal NMDA receptor binding as a function of chronic lead exposure level. Neurotoxicol Teratol 2001;23(2):185–9. CrossrefPubMedGoogle Scholar

  • 100.

    Gonzalez-Pina R, Paz C. Brain monoamine changes in rats after short periods of ozone exposure. Neurochem Res 1997;22(1):63–6. CrossrefPubMedGoogle Scholar

  • 101.

    Bos I, Jacobs L, Nawrot TS, de Geus B, Torfs R, et al. No exercise-induced increase in serum BDNF after cycling near a major traffic road. Neurosci Lett 2011;500(2):129–32. CrossrefGoogle Scholar

  • 102.

    Nudmamud S, Reynolds GP. Increased density of glutamate/ N-methyl-D-aspartate receptors in superior temporal cortex in schizophrenia. Neurosci Lett 2001;304(1–2):9–12. CrossrefPubMedGoogle Scholar

  • 103.

    Nudmamud-Thanoi S, Reynolds GP. The NR1 subunit of the glutamate/NMDA receptor in the superior temporal cortex in schizophrenia and affective disorders. Neurosci Lett 2004;372(1–2):173–7. CrossrefPubMedGoogle Scholar

  • 104.

    Jacobsen JP, Medvedev IO, Caron MG. The 5-HT deficiency theory of depression: perspectives from a naturalistic 5-HT deficiency model, the tryptophan hydroxylase 2Arg439His knockin mouse. Phil Trans R Soc B 2012;367(1601):2444–59. CrossrefGoogle Scholar

  • 105.

    Murphy SR, Schelegle ES, Miller LA, Hyde DM, Van Winkle LS. Ozone exposure alters serotonin and serotonin receptor expression in the developing lung. Toxicol Sci 2013;134(1): 168–79. PubMedCrossrefGoogle Scholar

  • 106.

    Gonzalez-Pina R, Alfaro-Rodriguez A. Ozone exposure alters 5-hydroxy-indole-acetic acid contents in dialysates from dorsal raphe and medial preoptic area in freely moving rats. Relationships with simultaneous sleep disturbances. Chem Biol Interact 2003;146(2):147–56. CrossrefPubMedGoogle Scholar

  • 107.

    Raposo S, El-Gabalawy R, Erickson J, Mackenzie CS, Sareen J. Associations between anxiety disorders, suicide ideation, and age in nationally representative samples of Canadian and American adults. J Anxiety Disord 2014;28(8):823–9. PubMedCrossrefGoogle Scholar

  • 108.

    Pigeon WR, Pinquart M, Conner K. Meta-analysis of sleep disturbance and suicidal thoughts and behaviors. J Clin Psychiatry 2012;73(9):e1160–7. CrossrefPubMedGoogle Scholar

  • 109.

    Dwivedi Y. Brain-derived neurotrophic factor: role in depression and suicide. Neuropsychiatr Disease Treat 2009;5:433–49. Google Scholar

  • 110.

    Hunsberger J, Austin DR, Henter ID, Chen G. The neurotrophic and neuroprotective effects of psychotropic agents. Dialogues Clin Neurosci 2009;11(3):333–48. PubMedGoogle Scholar

  • 111.

    Ahlskog JE. Does vigorous exercise have a neuroprotective effect in Parkinson disease? Neurology 2011;77(3):288–94. CrossrefPubMedGoogle Scholar

  • 112.

    Dwivedi Y. Brain-derived neurotrophic factor and suicide pathogenesis. Ann Med 2010;42(2):87–96. PubMedCrossrefGoogle Scholar

  • 113.

    Ding R, Jin Y, Liu X, Zhu Z, Zhang Y, et al. Characteristics of DNA methylation changes induced by traffic-related air pollution. Mutat Res Gen Toxicol Environ Mutagen 2016;796:46–53. CrossrefGoogle Scholar

  • 114.

    Dwivedi Y. Brain-derived neurotrophic factor in suicide pathophysiology. The Neurobiological Basis of Suicide: Boca Raton, FL, 2012. Google Scholar

  • 115.

    Suphioglu C, Singh MB, Taylor P, Bellomo R, Holmes P, et al. Mechanism of grass-pollen-induced asthma. Lancet 1992;339(8793):569–72. PubMedCrossrefGoogle Scholar

  • 116.

    Barker E, Kolves K, De Leo D. The relationship between asthma and suicidal behaviours: a systematic literature review. Eur Respir J 2015;46(1):96–106. CrossrefPubMedGoogle Scholar

  • 117.

    Olafsdottir IS, Gislason T, Thjodleifsson B, Olafsson I, Gislason D, et al. C reactive protein levels are increased in non-allergic but not allergic asthma: a multicentre epidemiological study. Thorax 2005;60(6):451–4. PubMedCrossrefGoogle Scholar

  • 118.

    Holgate ST. The epidemic of allergy and asthma. Nature 1999;402(Suppl 6760):B2–4. PubMedCrossrefGoogle Scholar

  • 119.

    Galli SJ, Tsai M, Piliponsky AM. The development of allergic inflammation. Nature 2008;454(7203):445–54. CrossrefPubMedGoogle Scholar

  • 120.

    Tan HP, Lebeck LK, Nehlsen-Cannarella SL. Regulatory role of cytokines in IgE-mediated allergy. J Leukoc Biol 1992;52(1):115–8. PubMedGoogle Scholar

  • 121.

    Gananca L, Oquendo MA, Tyrka AR, Cisneros-Trujillo S, Mann JJ, et al. The role of cytokines in the pathophysiology of suicidal behavior. Psychoneuroendocrinology 2016;63:296–310. CrossrefPubMedGoogle Scholar

  • 122.

    Manalai P, Hamilton RG, Langenberg P, Kosisky SE, Lapidus M, et al. Pollen-specific immunoglobulin E positivity is associated with worsening of depression scores in bipolar disorder patients during high pollen season. Bipolar Disord 2012;14(1):90–8. PubMedCrossrefGoogle Scholar

  • 123.

    Sarlus H, Hoglund CO, Karshikoff B, Wang X, Lekander M, et al. Allergy influences the inflammatory status of the brain and enhances tau-phosphorylation. J Cell Mol Med 2012;16(10):2401–12. PubMedCrossrefGoogle Scholar

  • 124.

    Eriksson UK, Gatz M, Dickman PW, Fratiglioni L, Pedersen NL. Asthma, eczema, rhinitis and the risk for dementia. Dement Geriatr Cogn Dis 2008;25(2):148–56. CrossrefGoogle Scholar

  • 125.

    Arai H, Ishiguro K, Ohno H, Moriyama M, Itoh N, et al. CSF phosphorylated tau protein and mild cognitive impairment: a prospective study. Exp Neurol 2000;166(1):201–3. CrossrefPubMedGoogle Scholar

  • 126.

    Reeves GM, Tonelli LH, Anthony BJ, Postolache TT. Precipitants of adolescent suicide: possible interaction between allergic inflammation and alcohol intake. Int J Adolesc Med Health 2007;19(1):37–43. PubMedGoogle Scholar

  • 127.

    Ciprandi G, De Amici M, Tosca M, Alesina R, Marseglia G, et al. Serotonin in allergic rhinitis: a possible role for behavioural symptoms. Iranian J Allergy Asthma Immunol 2011;10(3):183–8. Google Scholar

  • 128.

    Bergmann K, Sypniewska G. Is there an association of allergy and cardiovascular disease? Biochem Med 2011;21(3):210–8. Google Scholar

  • 129.

    Trangsrud AJ, Whitaker AL, Small RE. Intranasal corticosteroids for allergic rhinitis. Pharmacotherapy 2002;22(11):1458–67. CrossrefPubMedGoogle Scholar

  • 130.

    Klinitzke G, Steinig J, Bluher M, Kersting A, Wagner B. Obesity and suicide risk in adults – a systematic review. J Affect Disord 2013;145(3):277–84. CrossrefPubMedGoogle Scholar

  • 131.

    Vita A, De Peri L, Sacchetti E. Lithium in drinking water and suicide prevention: a review of the evidence. Int Clin Psychopharm 2015;30(1):1–5. CrossrefGoogle Scholar

  • 132.

    Lewitzka U, Severus E, Bauer R, Ritter P, Muller-Oerlinghausen B, et al. The suicide prevention effect of lithium: more than 20 years of evidence-a narrative review. Int J Bipolar Disord 2015;3(1):32. PubMedGoogle Scholar

  • 133.

    Kapusta ND, Mossaheb N, Etzersdorfer E, Hlavin G, Thau K, et al. Lithium in drinking water and suicide mortality. Br J Psychiatry 2011;198(5):346–50. CrossrefPubMedGoogle Scholar

  • 134.

    Bernier J, Brousseau P, Krzystyniak K, Tryphonas H, Fournier M. Immunotoxicity of heavy metals in relation to Great Lakes. Environ Health Perspect 1995;103(Suppl 9):23–34. CrossrefPubMedGoogle Scholar

  • 135.

    Nations U. World Urbanization Prospects: The 2014 Revision, Highlights (ST/ESA/SER. A/352). New York: United, 2014. Google Scholar

  • 136.

    Peplow M. Beijing smog contains witches’ brew of microbes. Nature 2014;10. doi:10.1038/nature.2014.14640. Google Scholar

  • 137.

    Guo Y, Barnett AG. Invited commentary: assessment of air pollution and suicide risk. Am J Epidemiol 2015;181(5):304–8. PubMedCrossrefGoogle Scholar

  • 138.

    Sampson HA. Utility of food-specific IgE concentrations in predicting symptomatic food allergy. J Allergy Clin Immunol 2001;107(5):891–6. CrossrefPubMedGoogle Scholar

  • 139.

    Prescott SL, Pawankar R, Allen KJ, Campbell DE, Sinn J, et al. A global survey of changing patterns of food allergy burden in children. World Allergy Organ J 2013;6(1):21. PubMedGoogle Scholar

About the article

Corresponding author: Dr. Roger S. McIntyre, MD, FRCPC, Professor of Psychiatry and Pharmacology, University of Toronto, Head, Mood Disorders Psychopharmacology Unit, University Health Network, 399 Bathurst Street, Toronto, ON, Canada

Received: 2017-03-23

Accepted: 2017-08-01

Published Online: 2017-09-15

Published in Print: 2017-12-20

Author Statement

Research funding: Authors state no funding involved. Conflict of interest: Roger McIntyre has the following disclosures: AstraZeneca, advisory board/researcher, consulting fees and speaker fees, no equity; Bristol-Myers Squibb, advisory board/researcher, consulting fees and speaker fees, no equity; Eli Lilly, advisory board/researcher, consulting fees and speaker fees, no equity; Lundbeck, advisory board/researcher, consulting fees and speaker fees, no equity; Pfizer, advisory board/researcher, consulting fees and speaker fees, no equity; Merck, advisory board/researcher, consulting fees and speaker fees, no equity; Sunovion, advisory board/researcher, consulting fees and speaker fees, no equity; Otsuka, advisory board/researcher, consulting fees and speaker fees, no equity; Takeda, advisory board/researcher, consulting fees and speaker fees, no equity; Allergan, advisory board/researcher, consulting fees and speaker fees, no equity; Janssen-Ortho, researcher, speaker fees, no equity; Shire, Research, funding for research, no equity. Duanduan Jaung is a health journalist whom has interviewed many families in China who have chronic atopic symptoms and have reported suicidal behavior. Informed consent: Informed consent is not applicable. Ethical approval: The conducted research is not related to either human or animal use.

Citation Information: Reviews on Environmental Health, Volume 32, Issue 4, Pages 343–359, ISSN (Online) 2191-0308, ISSN (Print) 0048-7554, DOI: https://doi.org/10.1515/reveh-2017-0011.

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