Maria Dolci1, Chiara Favero2, Valentina Bollati3, Laura Campo4, Andrea Cattaneo5, Matteo Bonzini3, Sonia Villani1, Rosalia Ticozzi1, Pasquale Ferrante1, Serena Delbue6. 1. Department of Biomedical, Surgical and Dental Sciences, University of Milan, Via Carlo Pascal, 36, Milano, Italy. 2. EPIGET - Epidemiology, Epigenetics and Toxicology Lab, Department of Clinical Sciences and Community Health, University of Milan, Via San Barnaba 8, Milano, Italy. 3. EPIGET - Epidemiology, Epigenetics and Toxicology Lab, Department of Clinical Sciences and Community Health, University of Milan, Via San Barnaba 8, Milano, Italy; Department of Preventive Medicine, Fondazione IRCSS Ca' Granda, Ospedale Maggiore Policlinico, Via San Barnaba 8, Milan, Italy. 4. Department of Preventive Medicine, Fondazione IRCSS Ca' Granda, Ospedale Maggiore Policlinico, Via San Barnaba 8, Milan, Italy. 5. Department of Science and High Technology, University of Insubria, Via Valleggio, 11, Como, Italy. 6. Department of Biomedical, Surgical and Dental Sciences, University of Milan, Via Carlo Pascal, 36, Milano, Italy. Electronic address: Serena.delbue@unimi.it.
Abstract
BACKGROUND: Human polyomaviruses (HPyVs) asymptomatically infect the human population during childhood and establish latency in the host. Viral reactivation and urinary excretion can occur when the immune system is impaired. Exposure to particulate air pollution, including the PM10/PM2.5 components, is a public health problem and has been linked to several disorders. Studies assessing the relationship between PM10/PM2.5 exposure and viral replication are lacking. OBJECTIVES: To investigate the relationship between HPyVs viruria and PM10/PM2.5 exposures. METHODS: Individual environmental exposure was assessed in 50 healthy adult volunteers using a chemical transport model (CTM) with a municipality resolution for daily PM10 and monitoring stations data for daily PM2.5 exposures. For each subject, a urine sample was collected, and HPyVs (JCPyV, BKPyV, MCPyV, HPyV6, HPyV7 and HPyV9) loads were determined. Zero-inflated negative binomial (ZINB) regression was used to model the count data, as it contained excessive zeros. Covariates were chosen by stepwise selection. RESULTS: HPyVs DNA was detected in 54% (median:87.6*105 copies/ml) of the urine samples. JCPyV was the prevalent (48%, (median viral load:126*105 copies/ml). Considering the load of the most frequently measured HPyVs, JCPyV, in the count-part of the ZINB model, every unitary in PM measured 2 days before urine collection (PM Day -2) was associated with an increase in JCPyV load (PM10: +4.0%, p-value = 0.002; PM2.5: +3.6%, p-value = 0.005). In the zero-part, the significant predictor was the PM10 measured 5 days before urine collection (+3%, p-value = 0.03). CONCLUSIONS: The environmental levels of PM10/PM2.5 increase the JCPyV viruria. Our findings emphasize the need for studies assessing the influence of air pollution exposure on the risk of viral reactivation.
BACKGROUND:Humanpolyomaviruses (HPyVs) asymptomatically infect the human population during childhood and establish latency in the host. Viral reactivation and urinary excretion can occur when the immune system is impaired. Exposure to particulate air pollution, including the PM10/PM2.5 components, is a public health problem and has been linked to several disorders. Studies assessing the relationship between PM10/PM2.5 exposure and viral replication are lacking. OBJECTIVES: To investigate the relationship between HPyVs viruria and PM10/PM2.5 exposures. METHODS: Individual environmental exposure was assessed in 50 healthy adult volunteers using a chemical transport model (CTM) with a municipality resolution for daily PM10 and monitoring stations data for daily PM2.5 exposures. For each subject, a urine sample was collected, and HPyVs (JCPyV, BKPyV, MCPyV, HPyV6, HPyV7 and HPyV9) loads were determined. Zero-inflated negative binomial (ZINB) regression was used to model the count data, as it contained excessive zeros. Covariates were chosen by stepwise selection. RESULTS: HPyVs DNA was detected in 54% (median:87.6*105 copies/ml) of the urine samples. JCPyV was the prevalent (48%, (median viral load:126*105 copies/ml). Considering the load of the most frequently measured HPyVs, JCPyV, in the count-part of the ZINB model, every unitary in PM measured 2 days before urine collection (PM Day -2) was associated with an increase in JCPyV load (PM10: +4.0%, p-value = 0.002; PM2.5: +3.6%, p-value = 0.005). In the zero-part, the significant predictor was the PM10 measured 5 days before urine collection (+3%, p-value = 0.03). CONCLUSIONS: The environmental levels of PM10/PM2.5 increase the JCPyV viruria. Our findings emphasize the need for studies assessing the influence of air pollution exposure on the risk of viral reactivation.
Authors: Jacopo Mariani; Chiara Favero; Michele Carugno; Laura Pergoli; Luca Ferrari; Matteo Bonzini; Andrea Cattaneo; Angela Cecilia Pesatori; Valentina Bollati Journal: Int J Environ Res Public Health Date: 2020-01-17 Impact factor: 3.390