Association of Environmental tobacco smoke exposure with depression among non-smoking adults

Environmental tobacco smoke exposure (ETSE) is the exposure to smoke arising from the burning of any form of tobacco product(s) or exhalation by a person who smokes any form of tobacco product [1, 2]. Several pieces of evidence suggest that ETSE may be a major modifiable risk factor for morbidity and mortality globally [3, 4]. Also, ETSE has been suggested to be associated with productivity losses [5] and responsible for 600,000 deaths per year in the United States (US) [3, 6]. A recent report revealed a decline in the prevalence of tobacco smoking among males and females [7] without itemizing ETSE rates and implications on mental health. Depression is a widespread mood disorder [8, 9] associated with morbidity and mortality worldwide [5]. It affects one out of every five people in a lifetime and is one of the leading causes of disability worldwide [10]. It is characterized by symptoms associated with imbalance(s) in emotional, motivational, cognitive, and physiological wellbeing [10, 11].

Several studies have reported the relationship between smoking and depressive symptoms [8, 12‐17], which prompted legislative interventions [18, 19] to minimize smoking rates. However, ETSE is an evolving phenomenon worldwide with the potential of making vulnerable populations at odds of adverse health outcomes [20‐24]. Some animal studies [25‐29] have reported the potential inhibitory effect of ETSE on dopamine transport and metabolism. Dopamine is a neurotransmitter with multiple functions in neurological processes and mental health [30]. For example, dopamine-receptor localization attributable to ETSE [27] has been linked with psychologically-related deformities in rat models [28]. Whether similar exposures can affect mental health in human populations is yet to be clearly understood.

It is not yet clear whether ETSE is associated with alteration(s) that could promote depressive symptoms and/or disorders in the neural network among humans. Understanding the importance of ETSE in depression outcomes could offer useful new information to guide the design of well-articulated public health policies, guidelines or advisory for the effective management of ETSE to avoid depressive symptoms and adverse health conditions.

The current analysis examined the association of ETSE with depression among non-smokers in the National Health and Nutrition Examination Survey (NHANES). We hypothesized ETSE had a null association with depression and assessed whether the association differed by sex and age in the same population.

The current study provides evidence for the association of ETSE with depression in the 2015-2016 NHANES data from the US. First, the rates of ETSE was relatively high. Second, depression was relatively prevalent. Third, females and young adults exposed to ETSE were at higher odds of being depressed. However, males exposed to ETSE were not at higher odds of being depressed.

Several reports [7, 12, 16, 36, 37] have attempted to present evidence on the burden of smoking in different populations with limited information on ETSE rates. In our study, we found about two in every ten non-smokers reported ETSE. Our findings on the burden of ETSE among non-smokers were comparable to a nationally representative tobacco survey among never-smoking youths from 168 countries between 1999 and 2008 [38]. In that study, about 23% of never-smoking youth were secondarily exposed to tobacco. In contrast, findings from a similar population in other climes revealed ETSE was as high as over 70% in China [39] and Spain [40]. Despite the recent decline in tobacco use, ETSE remains a potential threat to public health [41], and continuous efforts to reduce the burden of ETSE is vital. Globally, daily smoking rates appear lower, but the number of people using tobacco has increased [7]. In principle, passive exposure to tobacco smoke among non-smokers remains a public health threat in most regions of the world [42‐45] and has been reported as a leading cause of death in the US [46]. However (in the light of our findings), evidence-based intervention efforts are necessary not only to meet reduction targets to manage the escalating burden of morbidity and mortality attributable to tobacco use but also ETSE. Also, more studies evaluating the potential contributions of ETSE to specific causes of morbidity/mortality are necessary.

In our study, the proportion of respondents with ETSE was significantly higher among young adults than old adults. Similarly, we found respondents exposed to ETSE at higher odds of being depressed in the overall population with aggravated odds among young adults and females. Our findings are in tandem with similar reports [47‐54], where ETSE was observed to be associated with odds of psychological/mental distress. In contrast, other reports [47, 55, 56] found no significant association between ETSE and depression. These results can be explained in several ways.

First, ETSE is a proxy for discerning stressful living conditions [57, 58]. It may imply respondents exposed to ETSE might have been subjected to living and working conditions that predispose them to depression. In tandem with this assertion, lesser odds of depression and higher tendencies of a healthier lifestyle have been reported among persons from homes where smoking is prohibited [59]. Also, a diathesis-stress model has posited the association of ETSE with depression might be a function of stress [60]. Susceptibilities to the stressful environment (which may be evident by ETSE) may promote stress-induced depressive symptoms.

Second, the ETSE-depression relationship may be plausible. Using animal models, a neuro-biological route (via the dopamine complex assembly) has been reported for the causal association between ETSE and depression [25‐29]. For example, caudate-putamen localization of dopamine D1 and D2 receptors was observed in rats with ETSE [27]. Similarly, alterations in the magnitude of dopamine D1 and γ-aminobutyric acid β2 receptors in the caudate-putamen may up-regulate dopamine transporter mRNA expression to promote neuropsychological disorders related to the midbrain abnormalities in rats [28]. Also, ETSE was observed to inhibit dopamine reuptake in the in-vivo [26], and low dopamine activity was associated with increased odds of major depressive disorders [61].

Contrary to the expectation, we found ETSE was inversely associated with depression among males. Our findings were in tandem with a report in Germany [55] highlighting a similar observation among males. On the one hand, suggesting high exposure to ETSE is likely to be associated with lower odds of being depressed (independent of sex, race and marital status) would be implausible. On the other hand, it is tedious to hypothesize that the latent noxious effect of ETSE on depression might be counteracted by an unknown factor(s) primarily related to social livelihood and systems patronizing males more than females. First, some reports [20, 55, 62] have suggested that females are likely to be vulnerable to ETSE from family members and colleagues who smoke at home and the workplace. Second, sex-related hormonal difference(s) that accompany mechanistic change(s) in the pathophysiology of diseases [63] is a plausible explanation for the difference in odds of depression between males and females in this study. In tandem with this postulation, gender-related differences have been reported in the onset of depression events in the entire life course [64]. Similarly, a correlation between the prevalence of depression and hormonal changes (during puberty, pregnancy, and perimenopause) has been hypothesized among females [65]. However, this observation does not connote the simplification of the potential effects of ETSE on the odds of being depressed among males. Future studies might consider discerning underlying genetic differences that confer different response(s) to depression in the light of ETSE.

Some limitations in this study are worth mentioning. The cross-sectional method excludes causal interpretations for the ETSE-depression relationship. ETSE was self-reported. It would be necessary to clarify the significance of the magnitude and duration of ETSE in future studies. The possibility of ETSE as an indicator for poor living conditions cannot be ruled out. Depression is likely to have been subjectively estimated given that it was self-reported and not a physician-administered assessment. Also, data on proximal drivers of depression (such as; living conditions, emotional stressors, coping and/or adapting mechanisms, etc.) were unaccounted for in our study. Howbeit, our data source and methodologies greatly enhanced the quality and reliability of our data. Hence, the main conclusions of this study remain valid and largely unaffected in the light of the large sample size, sampling strategy, statistical adjustment for potential confounding factors and weighting, which improved the statistical power of the study to be representative of the US population. Future longitudinal studies are essential to determine the causal association between ETSE and depression.

Females exposed to ETSE (compared to those unexposed) were at higher odds of being depressed, but males exposed to ETSE were not at higher odds of being depressed. Intervention efforts targeted at policy formulation and behavioural change should be directed at tobacco control and the prevention of ETSE.