E-Cigarette Smoke Is Less Harmful For Human Heart Cells than Cigarette Smoke

This study has shown a significant difference in the way the human heart cells, especially the human coronary artery endothelial cells (HCAEC), respond to E-cigarette smoke and to the conventional cigarette smoke. 

E-cigarettes are designed in such a way that they dispense the main component of cigarette smoke, nicotine, in the form of an aerosol as compared to the conventional cigarette in which the smoke is directly inhaled. The level of harmful chemicals dispersed via the E-cigarette aerosol depends on different factors such as the solution used and the battery output voltage. 

The general consensus about E-cigarettes is that they are less harmful as compared to the conventional cigarettes since the smoke is not directly inhaled but there is a lack of enough data to back up this point of view. This called for a need to investigate the biological effects of E-cigarettes on various organ systems of the body and to compare them against the effects of conventional cigarettes at a very basic cellular level. 

E-Cigarettes Are Less Stressful For Heart 

The study was carried out by researchers at the Medical Research Council Integrative Epidemiology Unit (MRC IEU) at the University of Bristol. The basic aim of the study was to observe the stress response of the human coronary artery endothelial cells (HCAEC) when exposed to E-cigarette smoke and conventional cigarette smoke. The results of the study were later published in the journal Drug and Alcohol Dependence. 

During the course of the study, the researchers obtained aqueous filtered extracts of conventional cigarette smoke. The extract was prepared by passing the smoke from a cigarette through 10 ml of endothelial cell growth media MV2.

The researchers also prepared an aerosol extract from the E-cigarettes (eCAE) by employing the same tools. 5 cycles of 5 seconds of heat were used allowing at least 10 seconds in between the puffs which permitted the coils to cool down. Air was drawn through the device at a rate of 70 ml/minute during the process. The strength of the nicotine solution was 18 mg/ml. Cultures of heart cells were prepared and were exposed to both extracts. 

The research team then assessed the pattern of gene expression of the human coronary artery endothelial cells (HCAEC) to analyze whether the heart cells show a stress response to the E-cigarette aerosol extract or to the conventional cigarette smoke extract. The genes that were studied included the oxidative stress sensing transcription factor NFR2 (nuclear factor, erythroid 2-like 2, NFE2L2), and the cytochrome P450 family members. 

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According to Professor Marcus Munafò, one of the research team members, it was observed that heart cells exhibited a stress response when exposed to the conventional cigarette smoke extract through activation of NRF2 and up-regulation of cytochrome p450, but not to the E-cigarette aerosol extract. 

The study established that E-cigarette is a viable option for tapering off nicotine addiction in people trying to quit smoking. It also suggested that the tobacco users can use E-cigarettes to avoid the immediate harms associated with conventional cigarette smoking, particularly the cardiovascular risks. 

Cigarette Smoke Lowers Immunity by Increasing Resistance in Mouth Dwelling Bacteria

Cigarette smoke has been proven time and again to be injurious for health in a number of ways. In one of the latest researches, the chemicals present within the cigarette smoke have been shown to lower the immunity by prompting the growth and multiplication of the bacteria residing in the oral cavity. 

This study was carried out at the University Of Louisville School Of Dentistry and was led by David Scott. The primary result of the study was that the colonization and increase in the resilience of bacteria in the mouth increases upon exposure to cigarette smoke. The study was specifically aimed at studying the growth patterns of biofilms- a complex and intricately connected entity of different species of bacteria living and working together.

The researchers found that the growth of certain specific bacteria was affected more by the cigarette smoke as compared to others, including Staphylococcus aureus, Streptococcus mutans, Klebsiella pneumonia, and Pseudomonas aeruginosa. These bacteria give rise to conditions such as skin infections, oral diseases, vaginosis and pneumonia etc. 

Cigarette Smoke Promotes Bacterial Colonization and Resistance 

A lot of plausible explanations exist to support the exact mechanisms by which smoking weakens the immune system. However, very little data is available to shed light on the process by which the chemicals in cigarette smoke alter the bacterial growth pattern and build resilience in them. 

Very few previous researches explain the underlying association between smoking and enhanced bacterial resistance. Last year, the scientists discovered an unusual phenomenon that cigarette smoke leads to superbug development. In the start of the year 2016, another discovery was made which showed that cigarette smoke causes changes in the oral flora. This study is, however, the first of its kind to explore the effects of smoking on bacteria at a community level (biofilms). 

The study has established that killing of the bacteria in mouth is becoming steadily difficult as a result of buildup of resistance in bacterial biofilms. Overcoming a biofilm is particularly difficult because the biofilm works as a physical barrier against the immune responses and provides a sound niche for the spread of infections. 

During the course of the study, it was observed that bacteria increased their resistance to host immune system by altering specific genes and through protein expression. This led to increase in bacterial growth, causing the bacteria to colonize the oral cavity. These genetic changes were also found to be responsible for increased resilience of bacteria. 

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This study has paved way for further investigation into different kinds of mechanisms by which smoking can directly lead to various sorts of diseases. The recommendations put forward by the researchers include quitting smoking in order to prevent the mouth bacteria from becoming strong enough and resilient enough to cause diseases. 

This study might prove to be the stepping stone for building new treatment models for complex biofilms not only for the single species but also for multi-specie biofilms. With more complex bacterial biofilms being discovered every day, there is still a long way to go before precise treatments for the management of biofilm induced diseases can be formulated.