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Molecular Research on Global Climate Change and Atmospheric Pollution

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Green Chemistry".

Deadline for manuscript submissions: closed (31 January 2017) | Viewed by 31368

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Prof. Dr. Marcello Iriti

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Department of Biomedical, Surgical and Dental Sciences, Università degli Studi di Milano, 20133 Milan, Italy
Interests: essential oils; bioactive phytochemicals; ethnopharmacology; antimicrobial resistance; one health; food security
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Dear Colleagues,

Global climate change refers to a pattern of change closely related to rising global temperatures. Therefore, global warming represents the most relevant trend which leads to more severe draughts, increase in extreme weather events, heavy precipitations, flooding, warmer oceans, shrinking sea ice, melting glaciers, rising sea level and so on. Anthropogenic factors are largely responsible for recent climate change. Over the past century, human activities have released large amounts of carbon dioxide and other greenhouse gases into the atmosphere. The majority of greenhouse gases come from burning fossil fuels to produce energy, although deforestation, industrial processes and some agricultural practices also emit gases into the atmosphere. Not least, human health, as well as the planet’s biodiversity, are at high risk from the changing climate. Extreme high air temperatures contribute to exacerbate cardiovascular and respiratory diseases, and strongly affect water- and insect-borne diseases. Climate variability also affects animals and plants in both their distribution and behaviour: many plants start to grow and bloom earlier in the spring and survive longer into the fall, some mammals wake from hibernation sooner, birds migrate at different times and lay eggs earlier, turtles lose their nesting beaches, and so on. In this scenario, we invite investigators to submit both original research and review articles that explore all the aspects of global climate change. Potential topics include, but are not limited to:

• Global change biology

• Atmospheric pollution

• Environmental toxicology

• Ecotoxicology

• Loss of biodiversity

• Chemical ecology

Prof. Dr. Marcello Iriti
Guest Editor

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Keywords

environmental change
tropospheric pollutants
biometeorology abiotic stresses

Published Papers (5 papers)

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Research

853 KiB

Open AccessArticle

Pulmonary Function and Incidence of Selected Respiratory Diseases Depending on the Exposure to Ambient PM₁₀

by Artur Badyda, Anna Gayer, Piotr Oskar Czechowski, Grzegorz Majewski and Piotr Dąbrowiecki

Int. J. Mol. Sci. 2016, 17(11), 1954; https://doi.org/10.3390/ijms17111954 - 22 Nov 2016

Cited by 33 | Viewed by 5013

Abstract

It is essential in pulmonary disease research to take into account traffic-related air pollutant exposure among urban inhabitants. In our study, 4985 people were examined for spirometric parameters in the presented research which was conducted in the years 2008–2012. The research group was divided into urban and rural residents. Traffic density, traffic structure and velocity, as well as concentrations of selected air pollutants (CO, NO₂ and PM₁₀) were measured at selected areas. Among people who live in the city, lower percentages of predicted values of spirometric parameters were noticed in comparison to residents of rural areas. Taking into account that the difference in the five-year mean concentration of PM₁₀ in the considered city and rural areas was over 17 μg/m³, each increase of PM₁₀ by 10 μg/m³ is associated with the decline in FEV₁ (forced expiratory volume during the first second of expiration) by 1.68%. These findings demonstrate that traffic-related air pollutants may have a significant influence on the decline of pulmonary function and the growing rate of respiratory diseases. Full article

(This article belongs to the Special Issue Molecular Research on Global Climate Change and Atmospheric Pollution)

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2076 KiB

Open AccessArticle

Comparative Analysis of Toxic Responses of Organic Extracts from Diesel and Selected Alternative Fuels Engine Emissions in Human Lung BEAS-2B Cells

by Helena Libalova, Pavel Rossner,, Jr., Kristyna Vrbova, Tana Brzicova, Jitka Sikorova, Michal Vojtisek-Lom, Vit Beranek, Jiri Klema, Miroslav Ciganek, Jiri Neca, Katerina Pencikova, Miroslav Machala and Jan Topinka

Int. J. Mol. Sci. 2016, 17(11), 1833; https://doi.org/10.3390/ijms17111833 - 03 Nov 2016

Cited by 29 | Viewed by 7037

Abstract

This study used toxicogenomics to identify the complex biological response of human lung BEAS-2B cells treated with organic components of particulate matter in the exhaust of a diesel engine. First, we characterized particles from standard diesel (B0), biodiesel (methylesters of rapeseed oil) in its neat form (B100) and 30% by volume blend with diesel fuel (B30), and neat hydrotreated vegetable oil (NEXBTL100). The concentration of polycyclic aromatic hydrocarbons (PAHs) and their derivatives in organic extracts was the lowest for NEXBTL100 and higher for biodiesel. We further analyzed global gene expression changes in BEAS-2B cells following 4 h and 24 h treatment with extracts. The concentrations of 50 µg extract/mL induced a similar molecular response. The common processes induced after 4 h treatment included antioxidant defense, metabolism of xenobiotics and lipids, suppression of pro-apoptotic stimuli, or induction of plasminogen activating cascade; 24 h treatment affected fewer processes, particularly those involved in detoxification of xenobiotics, including PAHs. The majority of distinctively deregulated genes detected after both 4 h and 24 h treatment were induced by NEXBTL100; the deregulated genes included, e.g., those involved in antioxidant defense and cell cycle regulation and proliferation. B100 extract, with the highest PAH concentrations, additionally affected several cell cycle regulatory genes and p38 signaling. Full article

(This article belongs to the Special Issue Molecular Research on Global Climate Change and Atmospheric Pollution)

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5728 KiB

Open AccessArticle

Testosterone-Mediated Endocrine Function and T_H1/T_H2 Cytokine Balance after Prenatal Exposure to Perfluorooctane Sulfonate: By Sex Status

by Shou-Qiang Zhong, Zan-Xiong Chen, Min-Li Kong, Yan-Qi Xie, Yang Zhou, Xiao-Di Qin, Gunther Paul, Xiao-Wen Zeng and Guang-Hui Dong

Int. J. Mol. Sci. 2016, 17(9), 1509; https://doi.org/10.3390/ijms17091509 - 12 Sep 2016

Cited by 18 | Viewed by 6547

Abstract

Little information exists about the evaluation of potential developmental immunotoxicity induced by perfluorooctane sulfonate (PFOS), a synthetic persistent and increasingly ubiquitous environmental contaminant. To assess potential sex-specific impacts of PFOS on immunological health in the offspring, using male and female C57BL/6 mice, pups were evaluated for developmental immunotoxic effects after maternal oral exposure to PFOS (0.1, 1.0 and 5.0 mg PFOS/kg/day) during Gestational Days 1–17. Spontaneous T_H1/T_H2-type cytokines, serum levels of testosterone and estradiol were evaluated in F1 pups at four and eight weeks of age. The study showed that male pups were more sensitive to the effects of PFOS than female pups. At eight weeks of age, an imbalance in T_H1/T_H2-type cytokines with excess T_H2 cytokines (IL-4) was found only in male pups. As for hormone levels, PFOS treatment in utero significantly decreased serum testosterone levels and increased estradiol levels only in male pups, and a significant interaction between sex and PFOS was observed for serum testosterone at both four weeks of age (p_interaction = 0.0049) and eight weeks of age (p_interaction = 0.0227) and for estradiol alternation at four weeks of age (p_interaction = 0.0351). In conclusion, testosterone-mediated endocrine function may be partially involved in the T_H1/T_H2 imbalance induced by PFOS, and these deficits are detectable among both young and adult mice and may affect males more than females. Full article

(This article belongs to the Special Issue Molecular Research on Global Climate Change and Atmospheric Pollution)

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1780 KiB

Open AccessArticle

Toxic Effects of the Major Components of Diesel Exhaust in Human Alveolar Basal Epithelial Cells (A549)

by Pavel Rossner, Simona Strapacova, Jitka Stolcpartova, Jana Schmuczerova, Alena Milcova, Jiri Neca, Veronika Vlkova, Tana Brzicova, Miroslav Machala and Jan Topinka

Int. J. Mol. Sci. 2016, 17(9), 1393; https://doi.org/10.3390/ijms17091393 - 26 Aug 2016

Cited by 33 | Viewed by 5177

Abstract

We investigated the toxicity of benzo[a]pyrene (B[a]P), 1-nitropyrene (1-NP) and 3-nitrobenzanthrone (3-NBA) in A549 cells. Cells were treated for 4 h and 24 h with: B[a]P (0.1 and 1 μM), 1-NP (1 and 10 μM) and 3-NBA (0.5 and 5 μM). Bulky DNA adducts, lipid peroxidation, DNA and protein oxidation and mRNA expression of CYP1A1, CYP1B1, NQO1, POR, AKR1C2 and COX2 were analyzed. Bulky DNA adducts were induced after both treatment periods; the effect of 1-NP was weak. 3-NBA induced high levels of bulky DNA adducts even after 4-h treatment, suggesting rapid metabolic activation. Oxidative DNA damage was not affected. 1-NP caused protein oxidation and weak induction of lipid peroxidation after 4-h incubation. 3-NBA induced lipid peroxidation after 24-h treatment. Unlike B[a]P, induction of the aryl hydrocarbon receptor, measured as mRNA expression levels of CYP1A1 and CYP1B1, was low after treatment with polycyclic aromatic hydrocarbon (PAH) nitro-derivatives. All test compounds induced mRNA expression of NQO1, POR, and AKR1C2 after 24-h treatment. AKR1C2 expression indicates involvement of processes associated with reactive oxygen species generation. This was supported further by COX2 expression induced by 24-h treatment with 1-NP. In summary, 3-NBA was the most potent genotoxicant, whereas 1-NP exhibited the strongest oxidative properties. Full article

(This article belongs to the Special Issue Molecular Research on Global Climate Change and Atmospheric Pollution)

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1032 KiB

Open AccessArticle

Do Variants in GSTs Modify the Association between Traffic Air Pollution and Asthma in Adolescence?

by Gayan Bowatte, Caroline J. Lodge, Adrian J. Lowe, Bircan Erbas, Martine Dennekamp, Guy B. Marks, Jennifer Perret, Jennie Hui, Matthias Wjst, Lyle C. Gurrin, Katrina J. Allen, Michael J. Abramson, Melanie C. Matheson and Shyamali C. Dharmage

Int. J. Mol. Sci. 2016, 17(4), 485; https://doi.org/10.3390/ijms17040485 - 01 Apr 2016

Cited by 21 | Viewed by 6582

Abstract

Polymorphisms in genes involved in the oxidative stress response may partially explain the documented heterogeneous associations between traffic-related air pollution (TRAP) exposure and asthma and allergies in children. We investigated whether the GSTT1, GSTM1 and GSTP1 gene polymorphisms modified the associations between TRAP exposure during the first year of life and asthma, wheeze and hay fever in adolescence. We used a birth cohort of 620 high risk infants from the Melbourne Atopy Cohort Study. TRAP exposure during the first year of life was defined as the cumulative length of major roads within 150 m of each participant’s residence during the first year of life. Wheeze, asthma and hay fever were measured at ages 12 (n = 370) and 18 (n = 434) years. The associations and interactions with glutathione S-transferases (GST s) were investigated using regression models. Overall, there was no relationship between TRAP exposure during the first year of life and current asthma, wheeze and hay fever at ages 12 or 18 years. However, in GSTT1 null carriers, every 100 m increase in cumulative lengths of major road exposure during the first year of life was associated with a 2.31-fold increased risk of wheeze and a 2.15-fold increased risk of asthma at 12 years. TRAP is associated with some respiratory outcomes in carriers of genetic polymorphisms in oxidative stress metabolism genes. Full article

(This article belongs to the Special Issue Molecular Research on Global Climate Change and Atmospheric Pollution)

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