Quantile regression to examine the association of air pollution with subclinical atherosclerosis in an adolescent population

BACKGROUND: Air pollution has been associated with carotid intima-media thickness test (CIMT), a marker of subclinical atherosclerosis. To our knowledge, this is the first study to report an association between ambient air pollution and CIMT in a younger adolescent population. OBJECTIVE: To investigate the associations beyond standard mean regression by using quantile regression to explore if associations occur at different percentiles of the CIMT distribution. METHODS: We measured CIMT cross-sectionally at the age of 16 years in 363 adolescents participating in the Dutch PIAMA birth cohort. We fit separate quantile regressions to examine whether the associations of annual averages of nitrogen dioxide (NO(2)), fine particulate matter (PM(2.5)), PM(2.5) absorbance (a marker for black carbon), PM(coarse) and ultrafine particles up to age 14 assigned at residential addresses with CIMT varied across deciles of CIMT. False discovery rate corrections (FDR, p < 0.05 for statistical significance) were applied for multiple comparisons. We report quantile regression coefficients that correspond to an average change in CIMT (μm) associated with an interquartile range increase in the exposure. RESULTS: PM(2.5) absorbance exposure at birth was statistically significantly (FDR < 0.05) associated with a 6.23 μm (95% CI: 0.15, 12.3) higher CIMT per IQR increment in PM(2.5) absorbance in the 10th quantile of CIMT but was not significantly related to other deciles within the CIMT distribution. For NO(2) exposure we found similar effect sizes to PM(2.5) absorbance, but with much wider confidence intervals. PM(2.5) exposure was weakly positively associated with CIMT while PM(coarse) and ultrafine did not display any consistent patterns. CONCLUSIONS: Early childhood exposure to ambient air pollution was suggestively associated with the CIMT distribution during adolescence. Since CIMT increases with age, mitigation strategies to reduce traffic-related air pollution early in life could possibly delay atherosclerosis and subsequently CVD development later in life.