Particulate matter (PM) is a growing public health concern due to growing economy rooted in the worldwide technological development. PM with a diameter of 2.5 μm (PM_2.5) enters the body due to its small size and can accrue in the lungs, enter circulation, and deposit itself along the endothelial walls. Understanding the different types of PM and the various biomarkers that accumulate in the body is imperative to understanding mechanisms of disease development to create potential treatment plans. Three main effects of PM_2.5are examined: pro-inflammatory cytokines release upon exposure, DNA conformation breakage, and cancer metabolite accumulation. The pro-inflammatory cytokines release after periodical exposure to PM_2.5revealed that despite the concentration of PM, the bodily release of tumor necrosis factor-α, interleukin (IL)-6, IL-8, and monocyte chemoattractant protein-1 was elevated. IL-8 was universally secreted in highest amounts by the body. The potential role that DNA conformation breakage could play in disease onset or progression in specifically hepatocyte cells showed that DNA conformation breakage was inevitable in disease progression. Cancer onset as a result of PM_2.5exposure was deemed attributable to reactive oxygen species properties in the PM as well as various metabolic dysfunctions. This mini-review examines some of the biomarkers that result from PM_2.5exposure and attempts to provide insight into how legislative and community efforts can curb the rising rates of PM in the air.

Background: Particulate matter under 2.5 μm (PM_2.5) is a major risk factor for nonalcoholic fatty liver disease (NAFLD). This study aimed to investigate whether PM_2.5could aggravate NAFLD, as well as its relative mechanisms. Materials and Methods: Male Sprague-Dawley rats were under PM_2.5exposure and filtered air with NAFLD for 4, 6, and 8 weeks. Blood lipids were measured by enzyme-linked immunosorbent assay (ELISA). The histopathology of liver was determined by hematoxylin and eosin staining. ELISA assay was conducted for detecting inflammatory markers including interleukin-17 (IL-17) or tumor necrosis factor alpha (TNF-α) and for assessing oxidative stress-associated proteins, including superoxide dismutase (SOD) and malondialdehyde (MDA). Apoptosis was assessed by detecting B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (BAX) by real-time polymerase chain reaction and Western blotting. Results: PM_2.5exposure for 8 weeks, but not 4 or 6 weeks, significantly aggravated NAFLD, which was associated with the enhanced expression of IL-17 and TNF-α and the enhanced oxidative stress (SOD and MDA). Meanwhile, exposure PM_2.5for 8 weeks, but not 4 or 6 weeks, regulated apoptosis (Bcl-2 and BAX). Conclusions: Exposure of PM_2.5for 8 weeks can aggravate NAFLD, which may be mediated by liver inflammation, oxidative stress, and apoptosis.

Purpose: This study measured the level of air pollution; carbon monoxide (CO) and air particulate matter caused by human activities in Aba metropolis. Ten sample locations were selected from the most busy and populated part of the city (Aba South), based on human activities such as burning of tires, wood, rubber materials, construction and factory activities, vehicular emission, and the use of combustion engines. Material and Methods: Level of pollution was measured in the ten sample locations using Gasman air monitor for CO and Haz-Dust monitor for perticulater matter; once a week, twice a month (the 1^st and 4^th week) for 4 months. Results: Data collected were analyzed using one-way analysis of variance; the highest mean average value of 66.81 ppm was recorded in Water Side Junction, 4.508 ppm in Asa/Azikiwe Junction, 42.506 and 42.166 ppm in Main Park and Ngwa Road Junction, 39.667 ppm in Opopo Junction, 36.009 ppm in Portharcut Road Junction, 35.833 in New Market Road Junction, 33.833 ppm in Milverton Junction, whereas 33.666 ppm in Bata Junction was recorded as the lowest mean value of CO. PPM gave an average mean value between 4.921 μg/m³ and 5.415 μg/m³. Conclusion: The result then indicates CO pollution in the sampled locations.

Background: High blood pressure (BP) is associated independently with cocaine use and lead exposure. It is not known whether cocaine use and lead exposure act jointly to disrupt cardiovascular health. Objective: To determine whether cocaine use modifies the association between cumulative lead levels and elevated BP. Materials and Methods: We measured cumulative tibia lead levels in 35 adults: 20 with cocaine use disorder (CUD) and 15 non-CUD controls using in vivo K-shell X-ray fluorescence. Generalized estimating equation regression determined associations between log₂-transformed lead and BP (systolic, diastolic, and mean arterial pressure) and assessed the modifying association of cocaine use (as addiction severity) on the lead-BP relationship, adjusting for age, sex, smoking, and education. Sensitivity analyses included correction for potential selection bias. Results: Cases and controls differed by sex (%male: 90% vs. 67%), age (50.7 vs. 39.9 years), education (12.8 vs. 14.4 years), and tibia lead (3.50 vs. 2.35 μg/g). Lead was positively associated with systolic (P = 0.01) and diastolic BP (P = 0.01). We observed an interaction between lead and addiction severity on BP (P values for systolic BP: 0.01, diastolic BP: 0.003, and mean arterial BP: <0.0001); the association was stronger among individuals with more severe cocaine addiction: Systolic BP: Est.: 17.89, 95% confidence interval (CI): 9.52; 26.26, diastolic BP Est.: 17.89, 95% CI: 7.33; 13.79, mean arterial BP: Est.: 13.09, 95% CI: 10.34; 15.83. Conclusions: Lead was adversely associated with BP. This association was strongest among individuals with more severe cocaine addiction. The results from this small pilot study suggest that the interaction between lead and cocaine should be considered in studies of substance abuse-related health outcomes.

Study Background: Viral infection in children can elicit acute-phase response which can cause significant alterations in the level of acute-phase proteins such as fibrinogen. Aim and Objective: This work was designed to determine the possible viral immunochemical status of children aged 3–7 years with elevated blood fibrinogen of >6.0 g/L who received treatments as patients in herbal homes and hospitals in Nigeria. Materials and Methods: Children with elevated blood fibrinogen >6.0 g/L were recruited from 10 herbal homes (n = 27; 3–7 years) and three hospitals (n = 27; 3–7 years) and children with normal blood fibrinogen (3.1 ± 1.0 g/L; n = 30; 3–7 years) were also studied. Anti-hepatitis C virus (HCV), hepatitis B surface antigen, and human immunodeficiency virus type 1 (HIV1) p24 antigen were determined in each of the children immunochemically by ELISA, while blood fibrinogen was assayed using the Clauss method. Acid-fast bacilli were determined in the sputum by the Ziehl–Neelsen stain, and Plasmodium spp. identification was carried out using Giemsa staining -thick blood film technique. Results: The viral immunochemical status obtained in children with elevated blood fibrinogen who received treatments in herbal homes showed 3.7% (1) HIV mono-infection; 7.4% (2) HCV mono-infection; 18.5% (5) hepatitis B virus (HBV) mono-infection; 3.7% (1) HIV-HBV coinfection; and 7.4% (2) HCV-HBV coinfection with no coinfection of HIV-HCV and HIV-HCV-HBV, while those who received treatments in the hospitals showed only 11.1% (3) HBV mono-infection. The viral immunochemical status obtained in children with normal blood fibrinogen showed 3.3% (1) HBV mono-infection and 3.3% (1) HCV mono-infection with no HIV mono-infection and HIV-HBV, HIV-HCV, HCV-HBV, and HIV-HCV-HBV coinfections. Conclusion: Viral seromarkers of HCV, HBV, HIV, HIV-HBV, and HCV-HBV were more in children with elevated blood fibrinogen who received treatments in herbal homes than those who received treatments in the hospital and those with normal blood fibrinogen, which suggests blood fibrinogen as a possible diagnostic indicator in viral infection in herbal homes.