Scientists at Dana-Farber Cancer Institute and the Centers for Disease Control and Prevention have uncovered new evidence of the potential health risks of chemicals in tobacco and marijuana smoke.
In a study published online today by EClinicalMedicine, the researchers report that people who smoked only marijuana had several smoke-related toxic chemicals in their blood and urine, but at lower levels than those who smoked both tobacco and marijuana or tobacco only.
Two of those chemicals, acrylonitrile and acrylamide, are known to be toxic at high levels.
The investigators also found that exposure to acrolein, a chemical produced by the combustion of a variety of materials, increases with tobacco smoking but not marijuana smoking and contributes to cardiovascular disease in tobacco smokers.
The findings suggest that high acrolein levels may be a sign of increased risk of cardiovascular disease and that reducing exposure to the chemical could lower that risk.
This is particularly important for people infected with HIV, the virus that causes AIDS, given high rates of tobacco smoking and the increased risk of heart disease in this group.
“Marijuana use is on the rise in the United States with a growing number of states legalizing it for medical and nonmedical purposes—including five additional states in the 2020 election.
The increase has renewed concerns about the potential health effects of marijuana smoke, which is known to contain some of the same toxic combustion products found in tobacco smoke,” said the senior author of the study, Dana Gabuzda, MD, of Dana-Farber.
“This is the first study to compare exposure to acrolein and other harmful smoke-related chemicals over time in exclusive marijuana smokers and tobacco smokers, and to see if those exposures are related to cardiovascular disease.”
The study involved 245 HIV-positive and HIV-negative participants in three studies of HIV infection in the United States. (Studies involving people with HIV infection were used because of high tobacco and marijuana smoking rates in this group.)
The researchers collected data from participants’ medical records and survey results and analyzed their blood and urine samples for substances produced by the breakdown of nicotine or the combustion of tobacco or marijuana. Combining these datasets enabled them to trace the presence of specific toxic chemicals to tobacco or marijuana smoking and to see if any were associated with an increased risk of heart disease.
The investigators found that participants who exclusively smoked marijuana had higher blood and urine levels of several smoke-related toxic chemicals such as naphthalene, acrylamide, and acrylonitrile metabolites than non-smokers did. However, the concentrations of these substances were lower in marijuana-only smokers than in tobacco smokers.
Investigators also found that acrolein metabolites – substances generated by the breaking down of acrolein – were elevated in tobacco smokers but not marijuana smokers.
This increase was associated with cardiovascular disease regardless of whether individuals smoked tobacco or had other risk factors.
“Our findings suggest that high acrolein levels may be used to identify patients with increased cardiovascular risk,” Gabuzda said, “and that reducing acrolein exposure from tobacco smoking and other sources could be a strategy for reducing risk.”
moking is a primary risk factor associated with the prevalence and the incidence of neovascular macular degeneration and geographic atrophy.1,2
This link between smoking and age-associated macular degeneration (AMD) has recently been strengthened by three large epidemiologic studies, including the AREDS (Age-Related Eye Disease Study).3–5
Smoking is a cause of severe oxidative stress, due to the high concentrations of aldehydes and NOx in cigarette smoke, which markedly deplete ascorbic acid levels and protein sulfhydryl concentrations and cause oxidation of lipids and proteins.6–8
Six toxicants present in cigarette smoke are of particular concern as health risks: acrolein, acetaldehyde, acrylonitrile, benzene, 1,3-butadiene, and formaldehyde.9
Acrolein has a high hazard index and causes oxidative stress by reacting with sulfhydryl groups.10
It is more toxic (~10–1000 times) than formaldehyde, acetaldehyde, and 4-hydroxynonenal11 and can reach 80 µM in the respiratory tract fluid in smokers.12
Although the pathogenesis of AMD includes different clinical signs, the degeneration of RPE cells is often observed at early stages of the disease. Initial AMD pathogenesis includes abnormal RPE morphology and pigmentation, accumulation of lipofuscin in RPE cells, and accumulation of drusen between RPE and the underlying Bruch’s membrane. Electron microscopic and morphometric studies reveal qualitative and quantitative alterations of mitochondria in human RPE from AMD and from age- and sex-matched control subjects.13
The strong epidemiologic evidence linking smoking to AMD raises several questions that should be addressed: (1) What are the cellular and molecular mechanisms that underlie this link? (2)
Do cigarette smoke components such as acrolein cause injury, especially mitochondrial dysfunction, to RPE cells, as in other cellular and tissue models? (3)
Does lipoic acid, a potent inducer of phase-2 antioxidant and sulfhydryl protective enzymes, 14,15 protect RPE cells from smoke/acrolein-caused injury and mitochondrial dysfunction? (4)
Are there different responses to acrolein toxicity in a human RPE cell line and primary human fetal RPE cells?
In the present study, the ARPE19 cell line, was treated with acrolein, a major toxicant in tobacco smoke, and the effects on cellular toxicity and mitochondrial function were examined. A
crolein-induced toxicity was also studied using primary cultures of hfRPE, which are similar to native hfRPE.16 Both preparations were used to study the protective effects against acrolein-induced toxicity of α-lipoic acid (LA), which is a mitochondria-targeted antioxidant17 and mitochondrial nutrient.18
We hypothesize that smoking may cause oxidative mitochondrial damage in RPE cells and that the mitochondrial dysfunction may be a major cause in promoting the onset and progress of age-related macular degeneration.
reference link : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597695/
More information: EClinicalMedicine, DOI: 10.1016/j.eclinm.2020.100697
