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One Minute of Marijuana Secondhand Smoke Exposure Substantially Impairs Vascular Endothelial Function

View Article: PubMed Central - PubMed

ABSTRACT

Background: Despite public awareness that tobacco secondhand smoke (SHS) is harmful, many people still assume that marijuana SHS is benign. Debates about whether smoke‐free laws should include marijuana are becoming increasingly widespread as marijuana is legalized and the cannabis industry grows. Lack of evidence for marijuana SHS causing acute cardiovascular harm is frequently mistaken for evidence that it is harmless, despite chemical and physical similarity between marijuana and tobacco smoke. We investigated whether brief exposure to marijuana SHS causes acute vascular endothelial dysfunction.

Methods and results: We measured endothelial function as femoral artery flow‐mediated dilation (FMD) in rats before and after exposure to marijuana SHS at levels similar to real‐world tobacco SHS conditions. One minute of exposure to marijuana SHS impaired FMD to a comparable extent as impairment from equal concentrations of tobacco SHS, but recovery was considerably slower for marijuana. Exposure to marijuana SHS directly caused cannabinoid‐independent vasodilation that subsided within 25 minutes, whereas FMD remained impaired for at least 90 minutes. Impairment occurred even when marijuana lacked cannabinoids and rolling paper was omitted. Endothelium‐independent vasodilation by nitroglycerin administration was not impaired. FMD was not impaired by exposure to chamber air.

Conclusions: One minute of exposure to marijuana SHS substantially impairs endothelial function in rats for at least 90 minutes, considerably longer than comparable impairment by tobacco SHS. Impairment of FMD does not require cannabinoids, nicotine, or rolling paper smoke. Our findings in rats suggest that SHS can exert similar adverse cardiovascular effects regardless of whether it is from tobacco or marijuana.

No MeSH data available.


Related in: MedlinePlus

Impairment of FMD by exposure to marijuana SHS at declining levels over a 30‐minute period. A, RSP levels over 30 minutes for each rat. Mean starting concentration, mean concentration over time, and total exposure derived from the area under the curve (AUC) are listed for each group ±SD. 670 and 210 μg/m3 correspond roughly to high and moderate levels of tobacco SHS in restaurants that allow smoking. B, Impaired FMD and (C) unchanged baseline artery diameter. Each line corresponds to an individual rat; colors track individual animals through panels A, B, and C. See Table for mean FMD values. There were no significant differences between the extents of FMD impairment by high‐dose, low‐dose, and THC‐marijuana smoke exposure, and no significant differences between the baseline diameter levels for the different exposure groups. FMD indicates flow‐mediated vasodilation; RSP, respirable suspended particles; SHS, secondhand smoke; THC, tetrahydrocannabinol.
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jah31602-fig-0002: Impairment of FMD by exposure to marijuana SHS at declining levels over a 30‐minute period. A, RSP levels over 30 minutes for each rat. Mean starting concentration, mean concentration over time, and total exposure derived from the area under the curve (AUC) are listed for each group ±SD. 670 and 210 μg/m3 correspond roughly to high and moderate levels of tobacco SHS in restaurants that allow smoking. B, Impaired FMD and (C) unchanged baseline artery diameter. Each line corresponds to an individual rat; colors track individual animals through panels A, B, and C. See Table for mean FMD values. There were no significant differences between the extents of FMD impairment by high‐dose, low‐dose, and THC‐marijuana smoke exposure, and no significant differences between the baseline diameter levels for the different exposure groups. FMD indicates flow‐mediated vasodilation; RSP, respirable suspended particles; SHS, secondhand smoke; THC, tetrahydrocannabinol.

Mentions: As in our tobacco cigarette SHS study,34 we exposed groups of rats to 30 minutes of marijuana SHS at 2 starting concentrations (≈670 and ≈210 μg/m3 RSP), typical of high and moderate tobacco SHS levels in smoky restaurants,36 and to smoke‐free air in the exposure chamber as a negative control (Figure 2A). Because THC can cause vasodilation directly, which might interfere with a functional assay based on vasodilation, we included an extra control group exposed to SHS from THC‐free marijuana (in which cannabinoids were removed) at ≈670 μg/m3 RSP.


One Minute of Marijuana Secondhand Smoke Exposure Substantially Impairs Vascular Endothelial Function
Impairment of FMD by exposure to marijuana SHS at declining levels over a 30‐minute period. A, RSP levels over 30 minutes for each rat. Mean starting concentration, mean concentration over time, and total exposure derived from the area under the curve (AUC) are listed for each group ±SD. 670 and 210 μg/m3 correspond roughly to high and moderate levels of tobacco SHS in restaurants that allow smoking. B, Impaired FMD and (C) unchanged baseline artery diameter. Each line corresponds to an individual rat; colors track individual animals through panels A, B, and C. See Table for mean FMD values. There were no significant differences between the extents of FMD impairment by high‐dose, low‐dose, and THC‐marijuana smoke exposure, and no significant differences between the baseline diameter levels for the different exposure groups. FMD indicates flow‐mediated vasodilation; RSP, respirable suspended particles; SHS, secondhand smoke; THC, tetrahydrocannabinol.
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jah31602-fig-0002: Impairment of FMD by exposure to marijuana SHS at declining levels over a 30‐minute period. A, RSP levels over 30 minutes for each rat. Mean starting concentration, mean concentration over time, and total exposure derived from the area under the curve (AUC) are listed for each group ±SD. 670 and 210 μg/m3 correspond roughly to high and moderate levels of tobacco SHS in restaurants that allow smoking. B, Impaired FMD and (C) unchanged baseline artery diameter. Each line corresponds to an individual rat; colors track individual animals through panels A, B, and C. See Table for mean FMD values. There were no significant differences between the extents of FMD impairment by high‐dose, low‐dose, and THC‐marijuana smoke exposure, and no significant differences between the baseline diameter levels for the different exposure groups. FMD indicates flow‐mediated vasodilation; RSP, respirable suspended particles; SHS, secondhand smoke; THC, tetrahydrocannabinol.
Mentions: As in our tobacco cigarette SHS study,34 we exposed groups of rats to 30 minutes of marijuana SHS at 2 starting concentrations (≈670 and ≈210 μg/m3 RSP), typical of high and moderate tobacco SHS levels in smoky restaurants,36 and to smoke‐free air in the exposure chamber as a negative control (Figure 2A). Because THC can cause vasodilation directly, which might interfere with a functional assay based on vasodilation, we included an extra control group exposed to SHS from THC‐free marijuana (in which cannabinoids were removed) at ≈670 μg/m3 RSP.

View Article: PubMed Central - PubMed

ABSTRACT

Background: Despite public awareness that tobacco secondhand smoke (SHS) is harmful, many people still assume that marijuana SHS is benign. Debates about whether smoke‐free laws should include marijuana are becoming increasingly widespread as marijuana is legalized and the cannabis industry grows. Lack of evidence for marijuana SHS causing acute cardiovascular harm is frequently mistaken for evidence that it is harmless, despite chemical and physical similarity between marijuana and tobacco smoke. We investigated whether brief exposure to marijuana SHS causes acute vascular endothelial dysfunction.

Methods and results: We measured endothelial function as femoral artery flow‐mediated dilation (FMD) in rats before and after exposure to marijuana SHS at levels similar to real‐world tobacco SHS conditions. One minute of exposure to marijuana SHS impaired FMD to a comparable extent as impairment from equal concentrations of tobacco SHS, but recovery was considerably slower for marijuana. Exposure to marijuana SHS directly caused cannabinoid‐independent vasodilation that subsided within 25 minutes, whereas FMD remained impaired for at least 90 minutes. Impairment occurred even when marijuana lacked cannabinoids and rolling paper was omitted. Endothelium‐independent vasodilation by nitroglycerin administration was not impaired. FMD was not impaired by exposure to chamber air.

Conclusions: One minute of exposure to marijuana SHS substantially impairs endothelial function in rats for at least 90 minutes, considerably longer than comparable impairment by tobacco SHS. Impairment of FMD does not require cannabinoids, nicotine, or rolling paper smoke. Our findings in rats suggest that SHS can exert similar adverse cardiovascular effects regardless of whether it is from tobacco or marijuana.

No MeSH data available.


Related in: MedlinePlus