Table 2

Associations between ETS exposure and CIMT in children

StudyETS assessmentCIMT measurementExposure groupingMain results
Kallio et al
Circa Cardiovasc Qual Outcomes. 201028
  1. Exposure of prenatal maternal smoking: Delivery records used;

  2. Postnatal any exposure: biochemically measured- annual serum cotinine level assessment during 8–13 years

  1. Method: Acuson Sequoia 512 ultrasound mainframe (Acuson) with a 13.0-MHz linear-array transducer

  2. Location: maximal CIMT- the far (posterior) wall of the distal common carotid arteries 1–2 cm from the bulb on both sides

  3. Single blind analysis

(1) Prenatal maternal smoking- three groups:
5/160; 7/171; 10/163
(2)Postnatal any exposure-three groups
Low (n=160); Intermediate (n=171); High (n=163);
Average serum cotinine (ng/ml): 0.28 (0.27–0.29); 0.52 (0.51–0.53); 1.05 (1.00–1.11), respectively
(1) Between prenatal maternal smoking and CIMT, the association was not significant:
Single determinant regression coefficient: pregnancy maternal smoke: −0.004±0.013, p=0.77
(2) Postnatal ETS exposure: adolescents with higher ETS exposure level had thicker CIMT: CIMT mean values by groups: Low: 0.502±0.079 mm; Intermediate, 0.525±0.070 mm; High, 0.535±0.066 mm; p<0.001
P values: Low vs intermediate: 0.013; low vs high: <0.001; intermediate vs high: 0.57; No difference after adjustment
Geerts et al
Pediatrics. 201227
  1. Exposure of prenatal parental smoking: parental self-reported smoking condition by questionnaire;

  2. Postnatal maternal smoking: parental self-reported smoking conditions by questionnaire at children’s 5 years old

  3. Postnatal paternal smoking: parental self-reported smoking condition by questionnaire at children’s 5 years old

  1. Method: high-resolution echo-tracking technology (Art.laboratory) with a 128 radiofrequency line multiarray and a L10-5 40 mm linear array transducer

  2. Location: maximal CIMT-right common carotid artery

  3. Single blind anlaysis

(1) Prenatal maternal smoking-two groups
Yes (n=15); No (n=244)
(2) Prenatal both parents smoking-two groups
Yes (n=6); No (253)
(3)Postnatal any exposure–two groups
Yes (n=49); No (n=210)
(1) ETS exposure in utero could explain 0.57 SD of CIMT
Prenatal: pregnant women smoking led to a 0.0188 mm thicker CIMT in their offspring (p=0.04)
(2) The association between ETS and CIMT was strongest in children with both parents smoking during pregnancy (0.0277 mm thicker CIMT compared with their non-exposed peers)
Coefficient: crude: 0.0154 (−0.02, 0.0329), p=0.08; Mean CIMT (all children), mm: 0.384±0.03
Yang et al
J Renin-Angio-Aldo S. 201229
(1) Postnatal any exposure: biochemically assessment of serum cotinine level
  1. Method: High-resolution B-mode carotid ultrasonography (Vivid 7) with a 7.5-MHz linear transducer

  2. Location: maximal CIMT-both sides of common carotid artery proximal 1 cm to the bifurcation

  3. Single blind analysis

(1) Postnatal any exposure-three groups: low (n=209), intermediate (n=210), high (n=205); By averaged serum cotinine (ng/mL)- low: 0.26–0.57 (0.39±0.09); intermediate: 0.58–0.89 (0.74±0.11); high: 0.90–1.14 (1.00±0.08)(1) The mean CIMT (mm) had deteriorated in the high ETS exposure group than the low exposure group (p<0.001).
Low: 0.62±0.08; Intermediate: 0.66±0.09; High: 0.69±0.11;
P1 <0.001; P2 <0.001; P3=0.0024
P1: Comparison between low and intermediate groups; P2: Comparison between low and high groups; P3: Comparison between intermediate and high groups
Ayer et al
European Heart Journal. 201124
  1. Exposure of prenatal maternal smoking: parental self-reported smoking conditions by questionnaire

  2. Prenatal ETS exposure except for maternal smoking: questionnaire filled by mother

  3. Postnatal any exposure: home visit interview or phone call

  1. Method: high-resolution ultrasound;

  2. Location: maximal CIMT

(Details not applicable)
(1)Prenatal maternal smoking-two groups:
Yes (n=93); No (n=312)
  1. Prenatal other exposure-sample number not found

  2. Postnatal any exposure-sample number not found

(1) Prenatal maternal smoking:
Smoking in pregnancy: mean CIMT (mm): 0.59±0.06; No smoking in pregnancy, mean CIMT (mm): 0.60±0.06, p=0.31; CIMT mean difference (mm): 0.008 (0.007—0.02), p=0.31
(2) Postnatal maternal: 0.59,0.60, difference: 0.01 (-0.02 to 0.03); p=0.8 (data found in the article’s online supplemental material
Neither prenatal nor postnatal passive smoke exposure was linked to increase in CIMT
  • CIMT, carotid intima–media thickness; ETS, environmental tobacco smoke.