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Table 3 Additive joint interaction for included air pollutants exposure and genetic categories on the incident coronary artery disease

From: Association of air pollution exposure and increased coronary artery disease risk: the modifying effect of genetic susceptibility

Air pollutionb

CAD PRS (tertiles)c

 

Intermediatea

Higha

RERI (95% CI)

AP (95% CI)

RERI (95% CI)

AP (95% CI)

PM2.5

 High pollution

0.26 (0.20, 0.32)

0.28 (0.22, 0.33)

0.12 (0.05, 0.19)

0.09 (0.04, 0.14)

PM10

 High pollution

0.23 (0.17, 0.29)

0.25 (0.19, 0.31)

0.17 (0.10, 0.24)

0.12 (0.07, 0.18)

NO2

 High pollution

0.29 (0.24, 0.35)

0.31 (0.26, 0.36)

0.14 (0.07, 0.21)

0.11 (0.06, 0.16)

NOx

 High pollution

0.30 (0.25, 0.36)

0.32 (0.27, 0.37)

0.17 (0.10, 0.24)

0.13 (0.08, 0.18)

  1. Adjusted for age (continuous), sex (male/female), alcohol consumption (never, previous, current, missing), smoking status (never, previous, current, missing), body mass index (< 25 kg/m2, 25 to 29.9 kg/m2, ≥ 30 kg/m2, missing), education level (College or University degree, A/AS-level, O-level/GCSE, CSE, NVQ/HND/HNC, other qualifications, none), UK Biobank assessment center, physical activity (continuous, MET-min/week), diabetes at baseline (yes/no), cardiovascular disease at baseline (yes/no), genotyping batch, and the first 4 genetic principal components
  2. RERI relative excess risk due to interaction, AP attributable proportion due to interaction, CI confidence interval, PRS polygenic risk score, CAD coronary artery disease, PM2.5, fine particulate matter with diameter ≤ 2.5 μm, PM10 particulate matter with diameter ≤ 10 μm, NOx nitrogen oxides, NO2 nitrogen dioxide
  3. aDefined by polygenic risk score: low (lowest tertiles), intermediate (second tertiles) and high (highest tertiles)
  4. bDefined by median of air pollutants including PM2.5, PM10, NO2, and NOx concentration
  5. cTo estimate RERI and AP, the lower air pollution category and the lowest genetic risk (low PRS) groups were the reference categories