Hazard assessment study on organic compounds and heavy metals from using artificial turf.

Introduction: Artificial turf or synthetic grass releases hazardous substances such as heavy metals, polycyclic aromatic hydrocarbons (PAHs), and volatile organic compounds (VOCs). Objective: The current study aimed to evaluate the concentration levels of hazardous substances that are emitted from artificial turf as a result of sunlight effect; and to assess the expected exposure risks to such emitted substances during various activities.The current study aimed to evaluate the concentration levels of hazardous substances that are emitted from artificial turf as a result of the effect of sunlight. And to assess the expected risks of exposure to these substances emitted during the various activities. Study design: VOCs emitted from artificial turf samples were monitored and collected in the ambient air of three football fields, the ambient air around a piece of new artificial turf that has not yet been used on playing fields, but has been exposed to sunlight within one year and in the indoor air around a piece of new artificial turf. Which has not yet been used on the playgrounds and was placed at room temperature and away from sunlight. Results: The current study shows that average afternoon morning VOCs levels were 277, 333, 405 and 509 mg/m3 in winter, autumn, spring and summer, respectively. The most predominant PAHs compounds present in the samples were compounds with 3-rings and 4-rings.The average daily intake (ADI) for three exposure routes (ingestion, inhalation, and dermal contact) was calculated for different age categories (3-6, 7-15, 16-18, 19-22, 23-55, and 56-70 year). Non-Carcinogenic exposure risk as hazard quotient (HQ) and hazard index (HI) were detected. Conclusion: All HI values were <1, indicating that there is no potential adverse health effects occur as a result of a chemical exposure. Total carcinogenic risk (R) values for the different age categories were higher than 1E-04 for three football artificial grass fields, which indicated a high cancer risk development probability. HI and R probability increased in the age group of 7-15 year > 3-6 years.

Nephrotoxic effect of heavy metals and the role of DNA repair gene among secondary aluminum smelter workers.

This study aims to estimate the association between some heavy metals in suspended particulate matter (SPM) and kidney damage among workers at different departments in a secondary aluminum production plant. It also investigates the association between Xeroderma Pigmentosum complementation group D (XPD) gene polymorphisms and worker's susceptibility to kidney dysfunction. It was conducted on 30 workers from the administrative departments and 147 workers from different departments in the production line. Estimation of some heavy metals (Al, Co, Ni, Cu, Pb, and Cd) in suspended particulate matter (SPM) is done. Also, urinary levels of those metals were measured for all workers. Kidney injury molecule 1 (KIM-1), clusterin levels, and XPD protein level were estimated. Genotyping of XPD gene polymorphisms was performed. The measured annual average concentrations of the estimated heavy metals were lower than the permissible limits. Gravity area had the maximum concentration of metals with a higher Al average daily dose and hazardous index > 1. Kidney injury biomarkers (clusterin and KIM-1) were increased significantly (p < 0.05) while XPD protein showed the lowest levels among workers at the gravity and cold rolling areas. XPD Asn/Asp genotype was more dominant among those workers (85.7%). Conclusion: aluminum workers are at risk of kidney disorders due to heavy metal exposure. The individual's susceptibility to the diseases is related to the DNA repair efficiency mechanisms. The defect in XPD protein represents a good indicator of susceptibility to the disease. KIM-1 and clusterin estimation is a predictor biomarker for early-staged kidney diseases.

Lung cancer risk in workers occupationally exposed to polycyclic aromatic hydrocarbons with emphasis on the role of DNA repair gene.

OBJECTIVE: Workers in secondary aluminum production plants are occupationally exposed to polycyclic aromatic hydrocarbons (PAHs). We aimed to monitor the concentrations of PAHs in air and in serum of workers at two secondary aluminum production plants. We also investigated the potential risk of lung cancer development among PAHs exposed workers with emphasis on the role of A1AT mutation and APEX1 gene polymorphisms. METHODS: This study included 177 workers from administrative departments and production lines. Blood samples were obtained for estimation of benzo(a)pyrene diol epoxide albumin adduct (BPDE-Alb adduct), anti-Cyclin-B1 marker (CCNB1) and squamous cell carcinoma antigen (SCCAg). Genes' polymorphism for human apurinic/apyrimidinic endonuclease (APEX1) and alpha-1-anti-trypsin (A1AT) gene mutation were detected. RESULTS: There was a significant increase in the level of BPDE-Alb adduct among exposed workers in comparison to non-exposed group. Moreover, 41.67% of exposed workers in El Tebbin had BPDE-Alb adduct level ≥ 15 ng/ml versus 29.6% of workers in Helwan factory. There was a significant increase in tumor markers (SCCAg and CCNB1) among workers whose BPDE-Alb adduct ≥ 15 ng/ml. There was a significant increase in the level of BPDE-Alb adducts in exposed workers carrying homozygous APEX1 genotype Glu/Glu. Furthermore, exposed workers with the Glu/Glu genotype had high tumor markers levels. There was a significant increase in levels of BPDE-Alb adducts in workers carrying A1AT mutant allele. Moreover, workers with mutant A1AT genotype had significantly high tumor markers (SCCAg and CCNB1) levels. CONCLUSION: Therefore, we conclude that aluminum workers may be at a potential risk of lung cancer development due to PAHs exposure. Although PAHs concentrations in air were within the permissible limits, yet evidence of DNA damage was present as expressed by high BPDE-albumin adduct level in exposed workers. Also, elevation of tumor markers (SCCAg and CCNB1) in exposed workers points to the importance of periodic biological monitoring of such workers to protect them from cancer risk.

Seasonal Variation in the Biological Effects of PM2.5 from Greater Cairo.

Greater Cairo (Egypt) is a megalopolis where the studies of the air pollution events are of extremely high relevance, for the geographical-climatological aspects, the anthropogenic emissions and the health impact. While preliminary studies on the particulate matter (PM) chemical composition in Greater Cairo have been performed, no data are yet available on the PM's toxicity. In this work, the in vitro toxicity of the fine PM (PM2.5) sampled in an urban area of Greater Cairo during 2017-2018 was studied. The PM2.5 samples collected during spring, summer, autumn and winter were preliminary characterized to determine the concentrations of ionic species, elements and organic PM (Polycyclic Aromatic Hydrocarbons, PAHs). After particle extraction from filters, the cytotoxic and pro-inflammatory effects were evaluated in human lung A549 cells. The results showed that particles collected during the colder seasons mainly induced the xenobiotic metabolizing system and the consequent antioxidant and pro-inflammatory cytokine release responses. Biological events positively correlated to PAHs and metals representative of a combustion-derived pollution. PM2.5 from the warmer seasons displayed a direct effect on cell cycle progression, suggesting possible genotoxic effects. In conclusion, a correlation between the biological effects and PM2.5 physico-chemical properties in the area of study might be useful for planning future strategies aiming to improve air quality and lower health hazards.