Institute and Clinic for Occupational, Social and Environmental Medicine, University Hospital, Ludwig Maximilian University of Munich; Comprehensive Pneumology Center (CPC) Munich, Member DZL, German Center for Lung Research, Munich, Germany; Institute of Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany; Department of Applied Social Sciences, Munich University of Applied Sciences, Munich, Germany
Depression and Anxiety With Exposure to Ozone and Particulate Matter: An Epidemiological Claims Data Analysis
Background: Depression and anxiety have complex etiologies and are associated with a significant burden of disease. Although air pollution has been hypothesized as a possible risk factor of these disorders, the associations are still under-investigated. We aimed to analyze associations between long-term exposure to ambient ozone and particulate matter with diameter <10 μm (PM10) and diagnoses of depression and anxiety in a general population.
Methods: We utilized data from a large statutory health insurance company from Saxony, Germany. Information on outpatient clinical diagnoses of depression and anxiety was available for the years 2005-2014. We assigned ambient ozone and PM10 estimates to residential districts of 1.13 million individuals aged 16 and older. Depression and anxiety were defined as diagnoses counts. Associations with depression and anxiety were assessed using adjusted generalized estimating equations models.
Results: In the ten-year study period, the observed prevalences of depression and anxiety were 7.40% and 3.82%, respectively. In the two-pollutant model, 10 more days with a maximum 8-h average ozone concentration exceeding 120 μg/m³ resulted in a relative risk (RR) of 1.010 with 95% confidence interval (CI) (1.005, 1.014) for depression and an RR of 1.007 (95% CI (1.000, 1.014)) for anxiety. The effect estimates of PM10 for depression and anxiety were 1.180 (95% CI (1.160, 1.201)) and 1.176 (95% CI (1.148, 1.205)) per 10 μg/m³ increase in PM10 concentration, respectively. Age, sex, and access to healthcare of the individual were also associated with the diagnosis of the disorders. The associations were consistent across one- and two-pollutant models.
Conclusions: Our findings indicate that increased levels of ambient ozone and PM10 may elevate the risk of a depression or anxiety diagnosis in the general population. However, given the lack of data on individual air pollutant exposure and socioeconomic status, our results should be interpreted with caution. Further well-designed epidemiological studies should replicate our findings.
October 10, 2018
Risk for Acute Myocardial InfarctionIncreased in Multiple Sclerosis
https://www.neurologyadvisor.com/confer ... sclerosis/
Individuals with multiple sclerosis are at increased risk for acute myocardial infarction, an association that has not been fully explained by normal vascular risk factors. This research was presented at the 34th Congress of the European Committee for Treatment and Research in Multiple Sclerosis held October 10-12, 2018, in Berlin, Germany. ,,
2005 Feb 8
Faculté de Médecine,, Toulouse Cedex, France
Ozone Air Pollution Is Associated With Acute Myocardial Infarction
..Conclusions: Observational data confirm that short-term O3 exposure within a period of 1 to 2 days is related to acute coronary events in middle-aged adults without heart disease, whereas NO2 and SO2 are not.
2020 Jun 20
Student Research Committee, Iran University of Medical Sciences, Tehran, Iran
Dysregulation of microRNAs regulating survivin in CD4+ T cells in multiple sclerosis
Background: Impaired elimination mechanisms of the autoreactive lymphocytes, like T lymphocytes, via apoptosis may be the cause of continues inflammatory state in multiple sclerosis (MS). BIRC5 gene codify for the survivin, which participates in the modulation of apoptosis and cell survival. The objective of this study was investigation of the role of important confirmed miRNAs, including miR-335, miR-485, miR-542, and miR-708, in the regulation of survivin mRNA in the CD4+ T cells of MS cases...
Conclusion: miRNAs play a role in the regulation of survivin, and therefore apoptosis of CD4+ T cells, and hence are probably participating in a persistent inflammatory condition in MS patients.
2014 Jun 15
Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, North Carolina; Curriculum in Toxicology, University of North Carolina, Chapel Hill, North Carolina; Center for Environmental Health and Susceptibility, Gillings School of Global Public Health, University of North Carolina, Chapel Hill
Air toxics and epigenetic effects: ozone altered microRNAs in the sputum of human subjects
Ozone (O3) is a criteria air pollutant that is associated with numerous adverse health effects, including altered respiratory immune responses. Despite its deleterious health effects, possible epigenetic mechanisms underlying O3-induced health effects remain understudied. MicroRNAs (miRNAs) are epigenetic regulators of genomic response to environmental insults and unstudied in relationship to O3 inhalation exposure. Our objective was to test whether O3 inhalation exposure significantly alters miRNA expression profiles within the human bronchial airways. Twenty healthy adult human volunteers were exposed to 0.4 ppm O3 for 2 h. Induced sputum samples were collected from each subject 48 h preexposure and 6 h postexposure for evaluation of miRNA expression and markers of inflammation in the airways. Genomewide miRNA expression profiles were evaluated by microarray analysis, and in silico predicted mRNA targets of the O3-responsive miRNAs were identified and validated against previously measured O3-induced changes in mRNA targets. Biological network analysis was performed on the O3-associated miRNAs and mRNA targets to reveal potential associated response signaling and functional enrichment. Expression analysis of the sputum samples revealed that O3 exposure significantly increased the expression levels of 10 miRNAs, namely miR-132, miR-143, miR-145, miR-199a*, miR-199b-5p, miR-222, miR-223, miR-25, miR-424, and miR-582-5p. The miRNAs and their predicted targets were associated with a diverse range of biological functions and disease signatures, noted among them inflammation and immune-related disease. The present study shows that O3 inhalation exposure disrupts select miRNA expression profiles that are associated with inflammatory and immune response signaling. These findings provide novel insight into epigenetic regulation of responses to O3 exposure.
2020 Jul 11
Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany
Interleukin-1 promotes autoimmune neuroinflammation by suppressing endothelial heme oxygenase-1 at the blood-brain barrier
The proinflammatory cytokine interleukin 1 (IL-1) is crucially involved in the pathogenesis of multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). Herein, we studied the role of IL-1 signaling in blood-brain barrier (BBB) endothelial cells (ECs), astrocytes and microglia for EAE development, using mice with the conditional deletion of its signaling receptor IL-1R1. We found that IL-1 signaling in microglia and astrocytes is redundant for the development of EAE, whereas the IL-1R1 deletion in BBB-ECs markedly ameliorated disease severity. IL-1 signaling in BBB-ECs upregulated the expression of the adhesion molecules Vcam-1, Icam-1 and the chemokine receptor Darc, all of which have been previously shown to promote CNS-specific inflammation. In contrast, IL-1R1 signaling suppressed the expression of the stress-responsive heme catabolizing enzyme heme oxygenase-1 (HO-1) in BBB-ECs, promoting disease progression via a mechanism associated with deregulated expression of the IL-1-responsive genes Vcam1, Icam1 and Ackr1 (Darc). Mechanistically, our data emphasize a functional crosstalk of BBB-EC IL-1 signaling and HO-1, controlling the transcription of downstream proinflammatory genes promoting the pathogenesis of autoimmune neuroinflammation.
2016 Mar 23
ArtImmune SAS13 Avenue Buffon, Orleans, France; CNRS, UMR7355, Experimental and Molecular Immunology and Neurogenetics Orleans, France
Inflammasome, IL-1 and inflammation in ozone-induced lung injury
Exposure to ambient ozone causes airway hyperreactivity and lung inflammation, which represent an important health concern in humans. Recent clinical and experimental studies contributed to the understanding of the mechanisms of epithelial injury, inflammation and airway hyperreactivity, which is reviewed here. The present data suggest that ozone induced oxidative stress causes inflammasome activation with the release of IL-1, other cytokines and proteases driving lung inflammation leading to the destruction of alveolar epithelia with emphysema and respiratory failure. Insights in the pathogenic pathway may allow to identify novel biomarkers of ozone-induced lung disease and therapeutic targets
Published - 1980
Mayoclinic, L. J. Melton, J. D. Bartleson
Spontaneous pneumothorax and multiple sclerosis
https://mayoclinic.pure.elsevier.com/en ... -sclerosis
Two patients with proved and one with clinically definite multiple sclerosis were found among 141 residents of Olmsted County, Minn., who were identified as incidence cases of spontaneous pneumothorax in an epidemiological study. Because the age- and sex-specific prevalence rates for multiple sclerosis had already been determined for this community, the expected prevalence of multiple sclerosis at the time spontaneous pneumothorax was diagnosed could be calculated. Even with both sexes combined, the presence of any patient with a history of multiple sclerosis in a group this small might be somewhat unusual. Three cases is an observation unlikely to have occurred by chance alone (p<0.01, based on exact confidence limits for the binomial distribution) and the authors could find no common explanation for this association.
2020 Jul 16
Emergency Department, CHU Besançon, 3 boulevard Alexandre Fleming, France
Short term association between air pollution (PM 10, NO 2 and O 3) and secondary spontaneous pneumothorax
Secondary spontaneous pneumothorax (SSP) occurs in the context of underlying pulmonary disease. Our objectives were to estimate the relationship between SSP and short term air pollution exposure with nitrogen dioxide (NO2), ozone (O3) and particulate matter with a diameter ≤ 10 μm (PM10). Patients with SSP were included between June 1, 2009 and May 31, 2013, in 14 Emergency Departments in France. In this case-crossover design study, PM10, NO2, and O3 data were collected hourly from monitoring stations. Quantitative values, fast increase in air pollutant concentration, and air quality threshold exceedance were retained. These assessments were calculated for each of the 4 days prior to the event (Lag 1-Lag 4) for all case and control period, and for the entire exposure period. A total of 135 patients with SSP were included, with a mean age of 55.56 (SD 18.54) years. For short term exposure of PM10, NO2 and O3, no differences were observed between case and control periods in terms of quantitative values of air pollutant exposure (P > 0.68), fast increase in concentration (P > 0.12) or air quality threshold exceedance (P > 0.68). An association between O3 exposures cannot be ruled out, especially when considering the Lag 2 prior to the event and in warm seasons.
wiki https://commons.wikimedia.org/wiki/Cate ... eumothorax
Department of Healthcare Administration, I-Shou University , Kaohsiung, Taiwan
Association between ozone air pollution levels and hospitalizations for depression in Taipei: a time-stratified case-crossover study
Epidemiologic studies reported an association between exposure to ambient air pollutants and increased mortality rate attributed to suicide and suicide attempts. The investigation sought to determine whether there is an association between short-term ambient ozone (O3) level exposure and daily hospital admissions for depression in Taipei from 2009 to 2013 using a time-stratified case-crossover design. In our single-pollutant model (with no adjustment for other pollutants), the % increase in daily hospital admissions for depression was 12% on warm days and 30% on cool days, per interquartile range (IQR) rise in O3 levels, respectively. Ozone levels were significantly correlated with daily number of depression admissions both on warm and cool days. In our two-pollutant models, O3 levels remained significant after adjusting for other air pollutants, including particulate matter (PM10, PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) both on warm and cool days. Although O3 levels tended to be higher on warm days, admissions for depression were higher on cool days, suggesting that the relationship between O3 concentrations and depression may be affected by temperature. Further study is needed to better understand these findings.
December 10, 2019
Disability worsening among persons with multiple sclerosis and depression
Objective Depression is common in multiple sclerosis (MS), but its impact on disability worsening has not yet been determined. We explored the risk of disability worsening associated with depression in a nationwide longitudinal cohort...
1 March 2018
Toxicology and Applied Pharmacology
Ozone modifies the metabolic and endocrine response to glucose: Reproduction of effects with the stress hormone corticosterone
https://www.sciencedirect.com/science/a ... 8X18300279
Air pollution is associated with increased incidence of metabolic disease (e.g. metabolic syndrome, obesity, diabetes); however, underlying mechanisms are poorly understood. Air pollutants increase the release of stress hormones (human cortisol, rodent corticosterone), which could contribute to metabolic dysregulation...
2020 Aug 3
Klinikum Bremen-Ost, Department of Neurology, Bremen, Germany; Institute of Psychology, University of Oldenburg, Oldenburg, Germany
Relation between cognitive fatigue and circadian or stress related cortisol levels in MS patients
Background Cortisol levels are increased in MS patients. However, the relation between cortisol, cognitive fatigue and load is still unknown and is investigated in this study.
Method: In 40 MS patients and 20 healthy controls, cortisol levels were assessed (in saliva) in the morning and afternoon, before and after 5 runs of a cognitively demanding divided attention task (lasting in total 25-minutes). MS patients were divided in those suffering from cognitive fatigue (MS-F) or not (MS-NF).
Results: MS-NF patients showed elevated cortisol levels in the morning and in the afternoon before the reaction time task compared to healthy controls. Differences in cortisol levels among the four measurements were also larger compared to healthy controls and MS-F patients. These differences could not be explained by medication, EDSS score, MS course, age or gender. MS-NF patients also produced more omissions on the attention task compared to healthy controls and MS-F patients. MS-F patients experienced more fatigue after the attention task, but they did not show a task related performance decline.
Conclusion: MS-NF patients, and not MS-F patients, deviate in cortisol release and task performance from healthy controls and from MS-F patients. We suggest that MS-NF patients suffer from a dysregulation of their circadian cortisol level.
American Journal of Respiratory and Critical Care Medicine 2020
[b]Ozone-Induced NF-kB Activation And IL-8 Gene Expression are Inhibited By Cyclopentenone A2-isoprostane In Human Bronchial Epithelial Cells [/b]
https://www.atsjournals.org/doi/abs/10. ... acts.A4955
Curcumin Exerted Neuroprotection against Ozone-Induced Oxidative Damage and Decreased NF-κB Activation in Rat Hippocampus and Serum Levels of Inflammatory Cytokines https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6332875/
2020 Aug 6
UQ Centre for Clinical Research, The University of Queensland Centre for Clinical Research, Brisbane, Australia
Reduced IκB-α Protein Levels in Peripheral Blood Cells of Patients with Multiple Sclerosis-A Possible Cause of Constitutive NF-κB Activation
NF-κB signaling pathways are dysregulated in both the central nervous system (CNS) and peripheral blood cells in multiple sclerosis (MS), but the cause of this is unknown. We have recently reported that peripheral blood mononuclear cells (PBMC) of patients with MS have increased constitutive activation and translocation of the transcription factor NF-κB to the nucleus compared to healthy subjects. NF-κB can be activated through either canonical or non-canonical pathways. In the canonical pathway, activation of NF-κB is normally negatively regulated by the inhibitor IκB. We therefore hypothesized that the increased activation of NF-κB could be caused by reduced IκB-α in the cells of patients with MS, possibly due to increased activity of the IκB kinase (IKK) complex, which regulates IκB-α. Alternatively, changes to the activity of key molecules in the non-canonical pathway, such as IKKα, could also lead to increased NF-κB activation. We therefore used Western blotting to detect IκB-α levels and ELISA to investigate NF-κB DNA binding activity and phosphorylation of IKKα and IKKβ in samples from PBMC of MS patients and controls. The level of full-length IκB-α protein in the cytosolic fraction of PBMC of MS patients was significantly reduced compared to healthy subjects, with significantly more evidence of multiple low molecular weight putative degradation products of IκB-α present in MS patients compared to healthy subjects. Conversely, the level of NF-κB DNA binding activity was increased in whole cell lysates from MS patients. Both IKKα and IKKβ showed increased overall activity in MS compared to healthy subjects, although not all of the MS patients showed increased activity compared to the healthy subjects, suggesting that there may be several different mechanisms underlying the constitutive activation of NF-κB in MS. Taken together, these findings suggest that there may be multiple points at which the NF-κB pathway is dysregulated in MS and that decreased levels of the full-length IκB-α protein are a major component in this.
Department of Occupational Health and Environment Health, School of Public Health, Anhui Medical University, China
The short-term effect of PM 2.5/O 3 on daily mortality from 2013 to 2018 in Hefei, China
This research intends to explore the short-term impacts of PM2.5/O3 on daily death in Hefei from 2013 to 2018. Data on daily death of Hefei residents, meteorological factors, and air pollutants were collected from Jan 1, 2013, to Dec 31, 2018. The correlation between PM2.5/O3 and daily death in Hefei during the research period was studied by time series analysis. From 2013 to 2018, there were 61,683 non-accidental deaths, including 27,431 cardiovascular deaths, 5587 respiratory deaths, 20,921 malignant tumor deaths, and 1674 diabetes deaths, in Hefei. Annual mean concentrations of PM2.5, PM10, NO2, SO2, CO, and O3 in Hefei were 66.18, 92.37, 39.75, 15.39, 930, and 79.08 μg m-3, respectively. An increase of 10 μg m-3 in PM2.5 was related with 0.53% (95% CI 0.31-0.75%), 0.93% (95% CI 0.60-1.26%), 0.90% and (95% CI 0.23-1.57%) increase in non-accidental, cardiovascular and respiratory diseases mortality, respectively. The association between ozone and mortality was not significant. In cold seasons, PM2.5 had a stronger effect on the deaths resulting from non-accidental, cardiovascular, and respiratory diseases. The effect of O3 on deaths was not significantly different between the cold season and the warm season. Women and the elders (over 65 years) were at high risk of being affected by PM2.5/O3. Short-term exposure to PM2.5 was positively correlated with increased deaths due to non-accidental, cardiovascular and respiratory diseases in Hefei. Females and elders were more vulnerable to PM2.5/O3 exposure. No significant associations were observed between ozone and deaths from non-accidental, cardiovascular, respiratory, malignant tumors, and diabetes diseases.
01 Feb 2001
journals.physiology.org, Steven R. Kleeberger, Yoshinori Ohtsuka, Liu-Yi Zhang and Malinda Longphre
Airway responses to chronic ozone exposure are partially mediated through mast cells
https://journals.physiology.org/doi/ful ... 188.8.131.523
Airways inflammation and epithelial injury induced by chronic ozone (O3) in genetically mast cell-deficient mice (KitW/KitW-v) were compared with those in mast cell-sufficient mice (+/+) and KitW/KitW-v mice repleted of mast cells (KitW/KitW-v-BMT). Mice were exposed to 0.26 ppm O3 8 h/day, 5 days/wk, for 1–90 days. Background was 0.06 ppm O3. Age-matched mice were exposed to filtered air for O3 controls. Reversibility of lesions was evaluated 35 days after exposure. Compared with KitW/KitW-v, O3 caused greater increases in lavageable macrophages, epithelial cells, and polymorphonuclear leukocytes in +/+ and KitW/KitW-v-BMT mice. O3 also caused lung hyperpermeability, but the genotypic groups were not different..
2020 Aug 17
Department of Basic Medical Sciences, Neurosciences and Sensory Organs, University of Bari Medical School, Bari, Italy
Mast cells and angiogenesis in multiple sclerosis
Multiple sclerosis (MS) is an autoimmune disease, characterized by multiple demyelination of axons in both white and gray matter in the Central Nervous System (CNS). There is increasing evidence to support the notion that angiogenesis and chronic inflammation are mutually related. Different immune cells, including monocytes-macrophages, lymphocytes, neutrophils, mast cells (MCs) and dendritic cells are able to secrete an array of angiogenic cytokines, which promote growth, migration, and activation of endothelial cells. MCs play various roles in MS pathogenesis, influencing the innate immune response in peripheral tissues and in CNS. The aim of this review article is to discuss the role of MCs in MS pathogenesis with particular reference to the involvement of these inflammatory cells in the angiogenic processes occurring during MS.
2020 Jun 19
Department of Ophthalmology, Gil Medical Center, Gachon University College of Medicine, Incheon, South Korea
Different adverse effects of air pollutants on dry eye disease: Ozone, PM 2.5, and PM 10
To date, there have been no well-organized clinical studies evaluating which air pollutants affect dry eye disease (DED). In this study, we investigated changes in the clinical parameters of DED according to exposure to outdoor air pollutants, including PM2.5 (particulate matter with an aerodynamic diameter of less than 2.5 μm), PM10 (less than 10 μm), and ozone. A prospective observational study was conducted on 43 DED patients who had used the same topical eye drop treatment between 2016 and 2018 in South Korea. Ocular surface discomfort index (OSDI) score, tear film break-up time (TBUT), corneal fluorescein staining score (CFSS), and tear secretion were measured during each visit. Air pollution data of ambient PM10, PM2.5, and ozone, based on the patients' address, were obtained, and mean concentrations were computed for one day, one week, and one month before the examination. The relationships between air pollutants and DED were analyzed in single- and multi-pollutant models adjusted for demographic and clinical factors. In the multi-pollutant model, the OSDI score was positively correlated with ozone and PM2.5 exposure [ozone: β(exposure for 1 day/1 week) = 0.328 (95% CI: 0.161-0.494)/0.494 (0.286-0.702), p < 0.001/<0.001, per 1 ppb increase; PM2.5: β(1 day/1 week) = 0.378 (0.055-0.699)/0.397 (0.092-0.703), p = 0.022/ = 0.011, per 1 μg/m3 increase], and tear secretion decreased with increased ozone exposure [ozone: β(1 week/1 month) = -0.144 (-0.238 to -0.049)/-0.164 (-0.298 to -0.029), p = 0.003/ = 0.017, per 1 ppb increase]. Interestingly, increased PM10 exposure was only associated with decreased TBUT [β(1 day/1 week/1 month) = -0.028(-0.045 to -0.011)/-0.029(-0.046 to -0.012)/-0.023(-0.034 to -0.006), p = 0.001/ = 0.001/ = 0.018, per 1 μg/m3 increase]. Tear secretion and CFSS were not associated with PM10 exposure. Increased ozone and PM2.5 exposure led to aggravated ocular discomfort, and increased PM10 concentration aggravated tear film stability in patients with DED. Thus, each air pollutant may aggravate DED via different mechanisms of action.
2017 Jan 22
Department of Ophthalmology, Huashan Hospital Affiliated to Fudan University, Shanghai, China
Adverse Effect Profile of Topical Ocular Administration of Fingolimod for Treatment of Dry Eye Disease
..Our previous study indicated that fingolimod eyedrops was efficacious in inhibiting ocular inflammation in a dry eye disease (DED) model of non-obese diabetic (NOD) mice. In the current study, we evaluated potential adverse effects of fingolimod eyedrops. Inbred 10-week-old BALB/c mice were randomly divided into four groups, fingolimod-treated groups at three different concentrations (0.01%, 0.1% and 0.5%)
2019 Jun 30
The Case for a More Holistic Approach to Dry Eye Disease: Is It Time to Move beyond Antibiotics?
..Dry eye disease (DED) is an inflammatory disease that has many features in common with autoimmune disease
Department of Environmental Protection, Geophysics and Environmental Protection, Faculty of Geology, AGH University of Science and Technology, Krakow, Poland
The Condition of Air Pollution in Kraków, Poland, in 2005-2020, with Health Risk Assessment
..Results: Annual pollutant contents kept decreasing, with the exception of O3.
Environmental pollution and COVID-19 outbreak: insights from Germany
The impact of environmental pollutants and climate indicators on the outbreak of COVID-19 has gained considerable attention in the recent literature. However, specific investigation of industrial economies like Germany is not available. This provides us motivation to examine the association between environmental pollutants, climate indicators and the COVID-19 cases, recoveries, and deaths in Germany using daily data from February 24, 2020, to July 02, 2020. The correlation analysis and wavelet transform coherence (WTC) approach are the analytical tools, which are used to explore the association between variables included in the study. Our findings indicate that PM2.5, O3, and NO2 have a significant relationship with the outbreak of COVID-19. In addition, temperature is the only significant climate indicator which has significant correlation with the spread of COVID-19. Finally, PM10, humidity, and environmental quality index have a significant relationship only with the active cases from COVID-19 pandemic. Our findings conclude that Germany's successful response to COVID-19 is attributed to environmental legislation and the medical care system, which oversaw significant overhaul after the SARS and MERS outbreaks. The current study implicates that other industrial economies, especially European economies, that are still facing COVID-19 outbreak can follow the German model for pandemic response.
Key Laboratory of Environmental Remediation and Ecological Health, Ministry of Education; Research Center for Air Pollution and Health, College of Environmental and Resource Science, China
Unexpected rise of ozone in urban and rural areas, and sulfur dioxide in rural areas during the coronavirus city lockdown in Hangzhou, China: implications for air quality
The outbreak of coronavirus named COVID-19, initially identified in Wuhan, China in December 2019, has spread rapidly at the global scale. Most countries have rapidly stopped almost all activities including industry, services and transportation of goods and people, thus decreasing air pollution in an unprecedented way, and providing a unique opportunity to study air pollutants. While satellite data have provided visual evidence for the global reduction in air pollution such as nitrogen dioxide (NO2) worldwide, precise and quantitative information is missing at the local scale. Here we studied changes in particulate matter (PM2.5, PM10), carbon monoxide (CO), NO2, sulfur dioxide (SO2) and ozone (O3) at 10 urban sites in Hangzhou, a city of 7.03 million inhabitants, and at 1 rural site, before city lockdown, January 1-23, during city lockdown, January 24-February 15, and during resumption, February 16-28, in 2020. Results show that city lockdown induced a sharp decrease in PM2.5, PM10, CO, and NO2 concentrations at both urban and rural sites. The NO2 decrease is explained by reduction in traffic emissions in the urban areas, and by lower regional transport in rural areas during lockdown, as expected. SO2 concentrations decreased from 6.3 to 5.3 μg m-3 in the city, but increased surprisingly from 4.7 to 5.8 μg m-3 at the rural site: this increase is attributed both to higher coal consumption for heating and emissions from traditional fireworks of the Spring Eve and Lantern Festivals during lockdown. Unexpectedly, O3 concentrations increased by 145% from 24.6 to 60.6 μg m-3 in the urban area, and from 42.0 to 62.9 μg m-3 in the rural area during the lockdown. This finding is explained by the weakening of chemical titration of O3 by NO due to reductions of NOx fresh emissions during the non-photochemical reaction period from 20:00 PM to 9:00 AM (local time). During the lockdown, compared to the same period in 2019, the daily average concentrations in the city decreased by 42.7% for PM2.5, 47.9% for PM10, 28.6% for SO2, 22.3% for CO and 58.4% for NO2, which is obviously explained by the absence of city activities. Overall, we observed not only the expected reduction in some atmospheric pollutants (PM, SO2, CO, NO2), but also unexpected increases in SO2 in the rural areas and of ozone (O3) in both urban and rural areas, the latter being paradoxically due to the reduction in nitrogen oxide levels. In other words, the city lockdown has improved air quality by reducing PM2.5, PM10, CO, and NO2, but has also decreased air quality by augmenting O3 and SO2.