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Toxics
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Environmental Drivers of Chronic Disease: From Population Landscapes to Molecular...
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Environmental Drivers of Chronic Disease: From Population Landscapes to Molecular Mechanisms

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Human Toxicology and Epidemiology".

Deadline for manuscript submissions: 22 May 2026 | Viewed by 2130

Special Issue Editors

Dr. Jian Hou

E-Mail Website
Guest Editor
Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, Zhengzhou 450001, China
Interests: air pollution; persistent organic pollutants; human health risk assessment; environmental epidemiology; aging-related diseases
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Weidong Wu

E-Mail Website
Guest Editor
School of Public Health, Xinxiang Medical University, Xinxiang 453003, China
Interests: health effects of air pollution and underlying mechanisms
Dr. Yanjun Guo

E-Mail Website
Guest Editor
Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Interests: environmental epidemiology; genetic epidemiology

Special Issue Information

Dear Colleagues,

This Special Issue is dedicated to exploring the epidemiology of chronic diseases including diabetes, cardiovascular diseases, respiratory disorders and metabolic dysfunction-associated steatotic liver disease (MASLD) and their connections with a range of environmental factors. Among these, indoor and outdoor air pollution, meteorological conditions and light pollution are of particular interest. We also examine how these relationships are modified by socioeconomic status and unhealthy lifestyle behaviors, such as active and passive smoking, as well as the role of gene–environment interactions in disease development. In addition to epidemiological investigations, this issue welcomes studies that delve into potential biological mechanisms underlying environment-related health impairments. Research focusing on oxidative stress, gut microbiota dysbiosis, and other pathways through which air pollutants exert adverse effects will be highly valued. By integrating both population-based and mechanistic evidence, we aim to build a multidimensional understanding of how environmental exposures contribute to chronic disease burden.

Ultimately, this collection seeks to provide a robust scientific foundation for the creation of healthier living environments and to support medical practitioners in addressing the clinical challenges posed by ambient pollution. We hope the findings presented will inform public health strategies, inspire targeted interventions and promote both environmental and individual health resilience.

Dr. Jian Hou
Prof. Dr. Weidong Wu
Dr. Yanjun Guo
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxics is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • environmental epidemiology
  • chronic non-communicable diseases
  • gene–environment interaction
  • gut microbiota
  • oxidative stress
  • human health

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

12 pages, 1467 KB  
Article
Ground-Level Ozone as Community-Acquired Pneumonia Risk Factor in Different Population Groups in Summer: The Case of Moscow
by Nina Dudorova, Boris Belan and Sergey Kotel’nikov
Toxics 2026, 14(1), 83; https://doi.org/10.3390/toxics14010083 - 16 Jan 2026
Viewed by 560
Abstract
A correlation between the near-surface ozone concentration in the urban atmosphere and hospitalizations of community-acquired pneumonia patients has been analyzed based on a long-term (five years) series of observations in the warm season in Moscow, Russia. The study included hospitalization records for patients [...] Read more.
A correlation between the near-surface ozone concentration in the urban atmosphere and hospitalizations of community-acquired pneumonia patients has been analyzed based on a long-term (five years) series of observations in the warm season in Moscow, Russia. The study included hospitalization records for patients over 15 years old. One of the main goals was to reveal vulnerable groups of the urban population that react most strongly to increased ozone concentrations. It has been shown that increased near-surface ozone concentrations lead to increased hospitalizations. Older people (over 60 years old) are most sensitive to the negative impact of air pollution. Women in this age group are more sensitive to the effects of ozone air pollution than men. In the middle-aged group (31–60 years), the highest correlation between the number of community-acquired pneumonia cases and the ozone level in the atmospheric surface layer, conversely, was in men, but it was still lower than the rate in older people. The young people (15–30 years old) group turned out to be insensitive to the near-surface air pollution. Full article
(This article belongs to the Special Issue Environmental Drivers of Chronic Disease: From Population Landscapes to Molecular Mechanisms)
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14 pages, 864 KB  
Article
Gene–Environment Interactions of Apoptosis-Related Polymorphisms and Urinary Polycyclic Aromatic Hydrocarbon (PAH) Metabolites in Relation to Sperm Cell Apoptosis Among Men Attending Infertility Clinics
by Shiting Yi, Sitong Lin, Jiabin Xie, Zhihong Yang, Junxia You, Ximei Zhong, Hui Yang, Haiqing Lin, Qian Wang, Yajie Gong, Pan Yang, Yan Bai and Yingjun Chen
Toxics 2026, 14(1), 50; https://doi.org/10.3390/toxics14010050 - 31 Dec 2025
Viewed by 1220
Abstract
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental endocrine disruptors (EDCs) that enter the human body through respiratory, digestive, and dermal exposure. Prolonged exposure has been associated with adverse health outcomes, including carcinogenicity, mutagenicity, and reproductive toxicity. However, whether genetic variation in apoptosis-related pathways [...] Read more.
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental endocrine disruptors (EDCs) that enter the human body through respiratory, digestive, and dermal exposure. Prolonged exposure has been associated with adverse health outcomes, including carcinogenicity, mutagenicity, and reproductive toxicity. However, whether genetic variation in apoptosis-related pathways modifies the reproductive effects of PAH exposure remains unclear. To investigate gene-environment interactions between urinary PAH metabolites and polymorphisms in apoptosis-related genes in relation to sperm apoptosis, we conducted a cross-sectional study involving 176 male participants from an infertility clinic in Wuhan, China, who completed structured questionnaires and provided biological samples. Ten OH-PAH metabolites in repeated urine samples were measured, along with genotyping of single-nucleotide polymorphisms (SNPs) at apoptosis-related genes (Fas, FasL, and caspase-3) in whole blood DNA, and sperm apoptosis. Multivariable linear regression evaluated the interaction between urinary OH-PAH levels and apoptotic gene SNPs on apoptotic sperm, with genotype-stratified analyses. PAH exposure appeared to interact with SNPs in FasL rs763110, Fas rs2234767, and caspase-3 rs12108497 to jointly influence sperm cell apoptosis. Specifically, for the FasL rs763110, higher 9-OHFlu was associated with fewer viable sperm and more apoptotic sperm, and this association was more pronounced among CC genotype homozygotes. For the caspase-3 rs12108497, higher 2-OHFlu was associated with more dead sperm, and this association was significant among TC and TC/CC genotypes. These findings suggest that genetic variation in apoptosis-related genes may modify susceptibility to PAH-induced sperm apoptosis, highlighting the importance of gene–environment interactions in male reproductive toxicity. Full article
(This article belongs to the Special Issue Environmental Drivers of Chronic Disease: From Population Landscapes to Molecular Mechanisms)
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