Electronic cigarettes (E-cigs) have been promoted as harm-free or less-risky than smoking, even for women during pregnancy. These claims are made largely on E-cig aerosol having fewer number of toxic chemicals compared to cigarette smoke. Given that even low levels of smoking are found to produce adverse birth outcomes, we sought to test the hypothesis that vaping during pregnancy (with or without nicotine) would not be harm-free, and would result in vascular dysfunction that would be evident in offspring during adolescent and/or adult life. Pregnant female Sprague Dawley rats were exposed to E-cig aerosol (1-hour/day, 5 days/week, starting on gestational day 2 until pups were weaned) using e-liquid with 0 mg/ml (E-cig0) or 18 mg/ml nicotine (E-cig18) and compared to ambient air exposed controls. Body mass at birth and at weaning were not different between groups. Assessment of middle cerebral artery (MCA) reactivity revealed a 51-56% reduction in endothelial-dependent dilation response to acetylcholine (ACh) for both E-cig0 and E-cig18 in 1-month, 3-month (adolescent), and 7-month old (adult) offspring (p<0.05 compared to air, all time points). MCA response to sodium nitroprusside (SNP) and myogenic tone were not different across groups suggesting that endothelial-independent responses were not altered. The MCA vasoconstrictor response (5-hydroxytryptamine, 5-HT) was also not different across treatment and age groups. These data demonstrate that maternal vaping during pregnancy is not harm-free and confers significant cerebrovascular health risk/dysfunction to offspring that persists into adult life.

Temporal influences of electronic cigarettes (Ecigs) on blood vessels are poorly understood. In this study, we evaluated a single episode of cigarette versus Ecig exposure on middle cerebral artery (MCA) reactivity and determined how long after the exposure MCA responses took to return to normal. We hypothesized that cigarette and Ecig exposure would induce rapid (<4 h) reduction in MCA endothelial function and would resolve within 24 h. Sprague-Dawley rats (4 months old) were exposed to either air (n = 5), traditional cigarettes (20 puffs, n = 16) or Ecigs (20-puff group, n = 16; or 60-puff group, n = 12). Thereafter, the cigarette and Ecig groups were randomly assigned for postexposure vessel myography testing on day 0 (D0, 1-4 h postexposure), day 1 (D1, 24-28 h postexposure), day 2 (D2, 48-52 h postexposure) and day 3 (72-76 h postexposure). The greatest effect on endothelium-dependent dilatation was observed within 24 h of exposure (∼50% decline between D0 and D1) for both cigarette and Ecig groups, and impairment persisted with all groups for up to 3 days. Changes in endothelium-independent dilatation responses were less severe (∼27%) and shorter lived (recovering by D2) compared with endothelium-dependent dilatation responses. Vasoconstriction in response to serotonin (5-HT) was similar to endothelium-independent dilatation, with greatest impairment (∼45% for all exposure groups) at D0-D1, returning to normal by D2. These data show that exposure to cigarettes and Ecigs triggers a similar level/duration of cerebrovascular dysfunction

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The effects of vaping with electronic cigarettes (e‐cigs) on cardiovascular health are still under investigation. An important question that still remains unknown is the role of individual constituents within the e‐liquid used for vaping. In this study, we examine the sole effect of either vegetable glycerin (VG) or propylene glycol (PG), without the presence of any flavors or nicotine, on aortic reactivity. Healthy C57BL/6J mice were exposed to e‐cig vapor for 4 weeks (5d/wk, 1‐hour/day, 60 puffs/day) to e‐cig aerosol from either 100% VG or 100% PG e‐liquid using a whole‐body chamber exposure system (SCIREQ InExpose). Control mice were exposed to ambient air. E‐cig aerosol was produced by a Joyetech eGRIP OLED device at 17.5 watts, with 5‐second puff duration. Mice were sacrificed >24 hours after their final exposure, and thoracic aortas were excised, cleaned of perivascular adipose tissue, and were cut into 2mm ring segments. Aortic rings were mounted on wire myograph system (DMT, AD Instruments) containing warm aerated Krebs‐Henseleit buffer solution. The vessels were pre‐constricted with 50 µL of U46619 [7.5e‐9 M], and then exposed to a serial dilution of methacholine [MCh 10‐9 to 10‐5 M] to assess endothelial‐dependent (EDD) vasodilation, and separately to serial dilutions of sodium nitroprusside [SNP 10‐9 to 10‐5 M] to assess endothelium‐independent (EID) vasodilation. In PG‐exposed mice, max aortic EDD was reduced by 18±2% (P<0.05) compared to controls, and reduced by 14±2% (P<0.05) compared to VG‐exposed mice. VG‐exposed mice were not significantly different compared to controls. Maximal aortic EID was slightly impaired in PG‐ mice compared to control (8±2% P<0.05) and VG (5±1% P<0.05) groups. In summary, chronic exposure to e‐cig aerosol from PG in the base solution resulted in aortic EDD and EID dysfunction, however VG‐exposed mice were not affected. These data suggest that both endothelial‐dependent and ‐independent mechanisms are adversely affected by PG, and therefore vaping with PG in the base solution alone poses a significant risk for adverse cardiovascular health effects.