The Ability of Airborne Microalgae and Cyanobacteria to Survive and Transfer the Carcinogenic Benzo(a)pyrene in Coastal Regions.

Air pollution has been a significant problem threatening human health for years. One commonly reported air pollutant is benzo(a)pyrene, a dangerous compound with carcinogenic properties. Values which exceed normative values for benzo(a)pyrene concentration in the air are often noted in many regions of the world. Studies on the worldwide spread of COVID-19 since 2020, as well as avian flu, measles, and SARS, have proven that viruses and bacteria are more dangerous to human health when they occur in polluted air. Regarding cyanobacteria and microalgae, little is known about their relationship with benzo(a)pyrene. The question is whether these microorganisms can pose a threat when present in poor quality air. We initially assessed whether cyanobacteria and microalgae isolated from the atmosphere are sensitive to changes in PAH concentrations and whether they can accumulate or degrade PAHs. The presence of B(a)P has significantly affected both the quantity of cyanobacteria and microalgae cells as well as their chlorophyll a (chl a) content and their ability to fluorescence. For many cyanobacteria and microalgae, an increase in cell numbers was observed after the addition of B(a)P. Therefore, even slight air pollution with benzo(a)pyrene is likely to facilitate the growth of airborne cyanobacteria and microalgae. The results provided an assessment of the organisms that are most susceptible to cellular stress following exposure to benzo(a)pyrene, as well as the potential consequences for the environment. Additionally, the results indicated that green algae have the greatest potential for degrading PAHs, making their use a promising bioremediation approach. Kirchneriella sp. demonstrated the highest average degradation of B(a)P, with the above-mentioned research indicating it can even degrade up to 80% of B(a)P. The other studied green algae exhibited a lower, yet still significant, B(a)P degradation rate exceeding 50% when compared to cyanobacteria and diatoms.

Benzo[a]pyrene-Environmental Occurrence, Human Exposure, and Mechanisms of Toxicity.

Benzo[a]pyrene (B[a]P) is the main representative of polycyclic aromatic hydrocarbons (PAHs), and has been repeatedly found in the air, surface water, soil, and sediments. It is present in cigarette smoke as well as in food products, especially when smoked and grilled. Human exposure to B[a]P is therefore common. Research shows growing evidence concerning toxic effects induced by this substance. This xenobiotic is metabolized by cytochrome P450 (CYP P450) to carcinogenic metabolite: 7ß,8α-dihydroxy-9α,10α-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE), which creates DNA adducts, causing mutations and malignant transformations. Moreover, B[a]P is epigenotoxic, neurotoxic, and teratogenic, and exhibits pro-oxidative potential and causes impairment of animals' fertility. CYP P450 is strongly involved in B[a]P metabolism, and it is simultaneously expressed as a result of the association of B[a]P with aromatic hydrocarbon receptor (AhR), playing an essential role in the cancerogenic potential of various xenobiotics. In turn, polymorphism of CYP P450 genes determines the sensitivity of the organism to B[a]P. It was also observed that B[a]P facilitates the multiplication of viruses, which may be an additional problem with the widespread COVID-19 pandemic. Based on publications mainly from 2017 to 2022, this paper presents the occurrence of B[a]P in various environmental compartments and human surroundings, shows the exposure of humans to this substance, and describes the mechanisms of its toxicity.

The association of airborne particulate matter and benzo[a]pyrene with the clinical course of COVID-19 in patients hospitalized in Poland.

Air pollution can adversely affect the immune response and increase the severity of the viral disease. The present study aimed to explore the relationship between symptomatology, clinical course, and inflammation markers of adult patients with coronavirus disease 2019 (COVID-19) hospitalized in Poland (n = 4432) and air pollution levels, i.e., mean 24 h and max 24 h level of benzo(a)pyrene (B(a)P) and particulate matter <10 µm (PM10) and <2.5 µm (PM2.5) during a week before their hospitalization. Exposures to PM2.5 and B(a)P exceeding the limits were associated with higher odds of early respiratory symptoms of COVID-19 and hyperinflammatory state: interleukin-6 > 100 pg/mL, procalcitonin >0.25 ng/mL, and white blood cells count >11 × 103/mL. Except for the mean 24 h PM10 level, the exceedance of other air pollution parameters was associated with increased odds for oxygen saturation <90%. Exposure to elevated PM2.5 and B(a)P levels increased the odds of oxygen therapy and death. This study evidences that worse air quality is related to increased severity of COVID-19 and worse outcome in hospitalized patients. Mitigating air pollution shall be an integral part of measures undertaken to decrease the disease burden during a pandemic of viral respiratory illness.

Air pollution might affect the clinical course of COVID-19 in pediatric patients.

Air pollution, to which children are more susceptible than adults, can promote airway inflammation, potentially exaggerating the effects of respiratory viral infection. This study examined the association between the clinical manifestation of COVID-19 in unvaccinated pediatric patients hospitalized in Poland (n = 766) and levels of particulate matter 2.5 (PM2.5) and benzo(a)pyrene (B(a)P) within a week before hospitalization. Children aged ≤ 12 years exposed to mean and max 24 h B(a)P levels > 1 ng/m3 revealed higher odds of cough, dyspnea, fever, and increased concentrations of inflammatory markers (C-reactive protein, interleukin-6, procalcitonin, white blood cell count). In older patients (13-17 years), elevated mean 24 h B(a)P levels increased odds of dyspnea, fever, and diarrhea, and higher concentrations of C-reactive protein and procalcitonin. Exposure to max 24 h PM2.5 levels > 20 µg/m3 was associated with higher odds of cough, increased concentrations of C-reactive protein (group ≤12 years), and increased procalcitonin concentration (groups ≤12 years and 13-17 years). In both age groups, length of stay was extended in patients exposed to elevated levels of max 24 h PM2.5, mean and max 24 h B(a)P. This study suggests that worse air quality, particularly reflected in increased B(a)P levels, might affect the clinical course of COVID-19 in pediatric patients and adds to the disease burden during a pandemic.

Degradation of SARS-CoV-2 receptor ACE2 by the E3 ubiquitin ligase Skp2 in lung epithelial cells.

An unexpected observation among the COVID-19 pandemic is that smokers constituted only 1.4%-18.5% of hospitalized adults, calling for an urgent investigation to determine the role of smoking in SARS-CoV-2 infection. Here, we show that cigarette smoke extract (CSE) and carcinogen benzo(a)pyrene (BaP) increase ACE2 mRNA but trigger ACE2 protein catabolism. BaP induces an aryl hydrocarbon receptor (AhR)-dependent upregulation of the ubiquitin E3 ligase Skp2 for ACE2 ubiquitination. ACE2 in lung tissues of non-smokers is higher than in smokers, consistent with the findings that tobacco carcinogens downregulate ACE2 in mice. Tobacco carcinogens inhibit SARS-CoV-2 spike protein pseudovirions infection of the cells. Given that tobacco smoke accounts for 8 million deaths including 2.1 million cancer deaths annually and Skp2 is an oncoprotein, tobacco use should not be recommended and cessation plan should be prepared for smokers in COVID-19 pandemic.