Why are people who live in poverty disproportionately affected by mental illness? We review the interdisciplinary evidence of the bidirectional causal relationship between poverty and common mental illnesses-depression and anxiety-and the underlying mechanisms. Research shows that mental illness reduces employment and therefore income, and that psychological interventions generate economic gains. Similarly, negative economic shocks cause mental illness, and antipoverty programs such as cash transfers improve mental health. A crucial step toward the design of effective policies is to better understand the mechanisms underlying these causal effects.

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Poverty, depression, and anxiety: Causal evidence and mechanisms.

Air pollution exposure is estimated to contribute to approximately seven million early deaths every year worldwide and more than 3% of disability-adjusted life years lost. Air pollution has numerous harmful effects on health and contributes to the development and morbidity of cardiovascular disease, metabolic disorders, and a number of lung pathologies, including asthma and chronic obstructive pulmonary disease (COPD). Emerging data indicate that air pollution exposure modulates the epigenetic mark, DNA methylation (DNAm), and that these changes might in turn influence inflammation, disease development, and exacerbation risk. Several traffic-related air pollution (TRAP) components, including particulate matter (PM), black carbon (BC), ozone (O3), nitrogen oxides (NOx), and polyaromatic hydrocarbons (PAHs), have been associated with changes in DNAm; typically lowering DNAm after exposure. Effects of air pollution on DNAm have been observed across the human lifespan, but it is not yet clear whether early life developmental sensitivity or the accumulation of exposures have the most significant effects on health. Air pollution exposure-associated DNAm patterns are often correlated with long-term negative respiratory health outcomes, including the development of lung diseases, a focus in this review. Recently, interventions such as exercise and B vitamins have been proposed to reduce the impact of air pollution on DNAm and health. Ultimately, improved knowledge of how exposure-induced change in DNAm impacts health, both acutely and chronically, may enable preventative and remedial strategies to reduce morbidity in polluted environments.

/pdf/air-pollution-and-dna-methylation-effects-of-exposure-in-54stu75k28.pdf

Air pollution and DNA methylation: effects of exposure in humans

PM2.5 pollution has become a severe problem in China due to rapid industrialization and high energy consumption. It can cause increases in the incidence of various respiratory diseases and resident mortality rates, as well as increase in the energy consumption in heating, ventilation, and air conditioning (HVAC) systems due to the need for air purification. This paper reviews and studies the sources of indoor and outdoor PM2.5, the impact of PM2.5 pollution on atmospheric visibility, occupational health, and occupants’ behaviors. This paper also presents current pollution status in China, the relationship between indoor and outdoor PM2.5, and control of indoor PM2.5, and finally presents analysis and suggestions for future research.

/pdf/a-review-of-recent-advances-in-research-on-pm2-5-in-china-46fcybmmwe.pdf

A Review of Recent Advances in Research on PM2.5 in China

Mental disorders have been associated with various aspects of anthropogenic change to the environment, but the relative effects of different drivers are uncertain. Here we estimate associations between multiple environmental factors (air quality, residential greenness, mean temperature, and temperature variability) and self-assessed mental health scores for over 20,000 Chinese residents. Mental health scores were surveyed in 2010 and 2014, allowing us to link changes in mental health to the changes in environmental variables. Increases in air pollution and temperature variability are associated with higher probabilities of declined mental health. Mental health is statistically unrelated to mean temperature in this study, and the effect of greenness on mental health depends on model settings, suggesting a need for further study. Our findings suggest that the environmental policies to reduce emissions of air pollution or greenhouse gases can improve mental health of the public in China.

/pdf/declines-in-mental-health-associated-with-air-pollution-and-2bozcu91qa.pdf

Declines in mental health associated with air pollution and temperature variability in China.

Smoking is a major risk factor for a variety of diseases, including cancer and immune-mediated inflammatory diseases. Tobacco smoke contains a mixture of chemicals, including a host of reactive oxygen- and nitrogen species (ROS and RNS), among others, that can damage cellular and sub-cellular targets, such as lipids, proteins, and nucleic acids. A growing body of evidence supports a key role for smoking-induced ROS and the resulting oxidative stress in inflammation and carcinogenesis. This comprehensive and up-to-date review covers four interrelated topics, including 'smoking', 'oxidative stress', 'inflammation', and 'cancer'. The review discusses each of the four topics, while exploring the intersections among the topics by highlighting the macromolecular damage attributable to ROS. Specifically, oxidative damage to macromolecular targets, such as lipid peroxidation, post-translational modification of proteins, and DNA adduction, as well as enzymatic and non-enzymatic antioxidant defense mechanisms, and the multi-faceted repair pathways of oxidized lesions are described. Also discussed are the biological consequences of oxidative damage to macromolecules if they evade the defense mechanisms and/or are not repaired properly or in time. Emphasis is placed on the genetic- and epigenetic alterations that may lead to transcriptional deregulation of functionally-important genes and disruption of regulatory elements. Smoking-associated oxidative stress also activates the inflammatory response pathway, which triggers a cascade of events of which ROS production is an initial yet indispensable step. The release of ROS at the site of damage and inflammation helps combat foreign pathogens and restores the injured tissue, while simultaneously increasing the burden of oxidative stress. This creates a vicious cycle in which smoking-related oxidative stress causes inflammation, which in turn, results in further generation of ROS, and potentially increased oxidative damage to macromolecular targets that may lead to cancer initiation and/or progression.

/pdf/relationships-among-smoking-oxidative-stress-inflammation-3s2jakrhj3.pdf

Relationships among smoking, oxidative stress, inflammation, macromolecular damage, and cancer.

Epidemiology studies indicated that air pollution has been associated with adverse neurological effects in human. Moreover, the secretion of glucocorticoid (GC) affects the mood regulation, and the negative feedback of hippocampal glucocorticoid receptors (GR) inhibits the GC secretion. Meanwhile, the over secretion of GC can interfere the immune system and induce neurotoxicity. In the present study, the human test showed that the secretion of the cortisol in plasma was elevated after exposure in heavy air pollution. In the mouse model, we found that breathing the highly polluted air resulted in the negative responses of the mood-related behavioral tests and morphology of hippocampus, as well as the over secretion of GC in plasma, down regulation of GR, and up-regulation of cytokine and chemokine in the hippocampus. When considering the interrelated trends between the hippocampal GR, inflammatory factors, and plasmatic GC, we speculated that PM2.5 exposure could lead to the increased secretion of GC in plasma by decreasing the expression of GR in hippocampus, which activated the inflammation response, and finally induced neurotoxicity, suggesting that PM2.5 exposure negatively affects mood regulation. When combined with the results of the human test, it indicated that exposure to ambient air particles increased the risk of mental disorder.

https://www.mdpi.com/1660-4601/15/1/160/pdf

Exposure to Ambient Air Particles Increases the Risk of Mental Disorder: Findings from a Natural Experiment in Beijing.

The symptoms of asthma, breathlessness, insomnia, etc. all have relevance to pulmonary rhythmic disturbances. Epidemiology and toxicology studies have demonstrated that exposure to ambient air particles can result in pulmonary dysfunction. However, there are no data directly supporting a link between air pollution and circadian rhythm disorder. In the present study, we found that breathing highly polluted air resulted in changes of the molecular clock genes expression in lung by transcriptome profiling analyses in a rodent model. Compared to those exposed to filtered air, in both pregnant and offspring rats in the unfiltered group, key clock genes (Per1, Per2, Per3, Rev-erbα and Dbp) expression level decreased and Bmal1 expression level increased. In both rat dams and their offspring, after continuous exposure to unfiltered air, we observed significant histologic evidence for both perivascular and peribronchial inflammation, increased tissue and systemic oxidative stress in the lungs. Our results suggest that chronic exposure to particulate matter can induce alterations of clock genes expression, which could be another important pathway for explaining the feedbacks of ambient particle exposure in addition to oxidative stress and inflammation.

/pdf/transcriptome-profiling-of-the-lungs-reveals-molecular-clock-147pv6s6ho.pdf

Transcriptome Profiling of the Lungs Reveals Molecular Clock Genes Expression Changes after Chronic Exposure to Ambient Air Particles

The global DNA and RNA methylation and their reversal in lung under different concentration exposure of ambient air particulate matter in mice.

Genomic DNA methylation signatures in different tissues after ambient air particulate matter exposure

Tissue phenotypic plasticity facilitates rapid adaptation of organisms to biotic and/or abiotic pressure. The reproductive capacity of honey bee workers (Apis mellifera) is plastic and responsive to pheromones produced by broods and the queen. Egg laying workers (ELWs), which could reactivate their ovaries and lay haploid eggs upon queen lost, have been commonly discussed from many aspects. However, it remains unclear whether midgut homeostasis in ELWs is affected during plastic changes. Here, we found that the expression of nutrition- and autophagy-related genes was up-regulated in the midguts of ELWs, compared with that in nurse workers (NWs) by RNA-sequencing. Furthermore, the area and number of autophagosomes were increased, along with significantly increased cell death in the midguts of ELWs. Moreover, cell cycle progression in the midguts of ELWs was increased compared with that in NWs. Consistent with the up-regulation of nutrition-related genes, the body and midgut sizes, and the number of intestinal proliferation cells of larvae reared with royal jelly (RJ) obviously increased more than those reared without RJ in vitro. Finally, cell proliferation was dramatically suppressed in the midguts of ELWs when autophagy was inhibited. Altogether, our data suggested that autophagy was induced and required to sustain cell proliferation in ELWs’ midguts, thereby revealing the critical role of autophagy played in the intestines during phenotypic plasticity changes.

/pdf/autophagy-is-required-to-sustain-increased-intestinal-cell-1o82v4iy.pdf

Nannan Li

Papers

Exposure to Ambient Air Particles Increases the Risk of Mental Disorder: Findings from a Natural Experiment in Beijing.

Transcriptome Profiling of the Lungs Reveals Molecular Clock Genes Expression Changes after Chronic Exposure to Ambient Air Particles

The global DNA and RNA methylation and their reversal in lung under different concentration exposure of ambient air particulate matter in mice.

Genomic DNA methylation signatures in different tissues after ambient air particulate matter exposure

Autophagy Is Required to Sustain Increased Intestinal Cell Proliferation during Phenotypic Plasticity Changes in Honey Bee (Apis mellifera)