Poluição atmosférica e função pulmonar em asmáticos: associação e interação gene-ambiente.

Abstract

Air pollutants induce the increase of inflammatory components in lung and the decrease of pulmonary function. The variability in the pulmonary response to exposition to air pollution has been associated to genetic polymorphisms, which modify the inflammatory and immunological response to the inhalation of those pollutants. The purpose of this study was to investigate the association between air pollution and pulmonary function in asthmatic children and teenagers as well as the potential modification of polymorphisms on inflammatory and antioxidant genes. This is a cross-sectional epidemiological study, with 112 asthmatic children and teenagers from 6 to 14 years old, within November to December 2016, all residents in the municipality of Rio de Janeiro. Cells from the buccal mucosa has been collected for researching polymorphisms of GSTM1, GSTT1 and GSTP1 genes and TNF-A The outcome variables were: forced expiratory flow in the first second (VEF1), forced vital capacity (CVF), forced expiratory flow between 25% and 75% of CVF (FEF25-75%), and peak expiratory flow (PFE). The polymorphisms have been genotyped using the polymerase chain reaction technique (PCR). Generalized Linear Models have been used, and the relation between PM10 and 03; VEF1, CVF, FEF25-75% and PFE has been estimated using Polynomial Distributed Lag Model (PDLM) methods. The effect modification of the genetic polymorphisms has been rated including the genotypes and pollutants in the work model. The increase of 10 μg /m3 at PM10 has been associated with a decline in VEF1 on current day, on the first lag day and at that accumulated in five days. At the other indicators, a negative association has been verified only at that accumulated in five days. With the increase of 10 μg/m3 of 03, a negative association was evidenced on the fourth lag day and fifth lag day, for VEF1 and CVF, and fifth lag day for FEF25-75 and PFE. In carriers of TNF-308 variant allele, a negative association has been observed between PM10 and VEF1 on the current day (-11,23; IC95%: -19,23, -2,45), on the first lag day (-5,6; IC95%: -10,16, -0,8), and at that accumulated of five days (-9,37; IC95%: -13,75, -4,76). The interaction has been observed for the GSTT1 null at VEF1 on the current day (-11,49; IC95%; -16,26, -6,45), in the first lag day (-6,23; IC95%: -8,81, -3,57) and at that accumulates of five days (-10,88; IC95%: -13,34, -8,35); at CVF, on the current day (-7,94; IC95%; -11,91, -3,8), on the first lag day (-4,38; IC95%: -6,48, -2,23) and at that accumulated of five days (-7,99; IC95%: -10,01, -5,93). The combination of the GSTM1/GSTT1 null genotypes has presented a significant negative association in the increase of 10 µg/m³ of PM10 and VEF1 as well as in CVF. Those results have evidenced the negative association between air pollutants and the pulmonary function, and also the modification of the effect of polymorphisms on the in the inflammatory and antioxidant genes in the association of the air pollutants with pulmonary function.