Yet Another Reason Not To Smoke

Tobacco pipes and car airbags don't mix, abstract:

Airbags have been shown to reduce injuries and save the lives of car occupants in a crash. Like any protection system, airbags potentially introduce some new risks if no appropriate countermeasures are taken. A case of a relatively moderate frontal impact is described where the driver of an airbag-equipped car suffered a severe penetrating eye injury after the airbag deployed. Since the airbag fabric itself was excluded as an injury-producing structure, other objects such as eyeglasses, a wrist-watch, a bracelet, and a large finger ring had to be assessed. The investigation of the car interior as well as the morphologic details of the injuries to the eye and the face revealed that the most likely candidate for the injury was a tobacco pipe, which was probably being held in one hand and was broken apart by the deploying airbag and projected into the face of the driver. This case illustrates the hazard of having any rigid object between the occupant and the deploying airbag. The desirability of warning car occupants of the potential hazards which can result from today's protection systems is also discussed.

Don't smoke.

Maternal Smoke Exposure And Cell Signaling

It is know that maternal smoke exposure can possibly cause problems to the fetus.  Here is a mouse study demonstrating that offspring of smoke-exposed pregnant female mice were underweight with deceased lung volume, and that there were alterations in important cell signaling pathways that may have caused the negative effects on the fetal mice  Abstract:

The present study tested the hypothesis that maternal smoke exposure results in fetal lung growth retardation due to dysregulation in various signaling pathways, including the Wnt (wingless-related integration site)/β-catenin pathway. Pregnant female C57BL/6J mice were exposed to cigarette smoke (100-150 mg/m3) or room air, and offspring were humanely killed on 12.5, 14.5, 16.5, and 18.5 d post coitum (dpc). We assessed lung stereology with Cavalieri estimation; apoptosis with proliferating cell nuclear antigen, TUNEL, and caspase assays; and gene expression with quantitative PCR (qPCR) and RNA sequencing on lung epithelium and mesenchyme retrieved by laser capture microdissection. Results demonstrated a significant decrease in body weight and lung volume of smoke-exposed embryos. At 16.5 dpc, the reduction in lung volume was due to loss of lung mesenchymal tissue correlating with a decrease in cell proliferation (n = 10; air: 61.65% vs. smoke: 44.21%, P < 0.05). RNA sequence analysis demonstrated an alteration in the Wnt pathway, and qPCR confirmed an increased expression of secreted frizzled-related protein 1 (sFRP-1) [n = 12; relative quantification (RQ) 1 vs. 2.33, P < 0.05] and down-regulation of Cyclin D1 (n = 7; RQ 1 vs. 0.61, P < 0.05) in mesenchymal tissue. Furthermore, genome expression studies revealed a smoke-induced up-regulation of Rho-GTPase-dependent actin cytoskeletal signaling that can lead to loss of tissue integrity.-Unachukwu, U., Trischler, J., Goldklang, M., Xiao, R., D'Armiento, J. Maternal smoke exposure decreases mesenchymal proliferation and modulates Rho-GTPase-dependent actin cytoskeletal signaling in fetal lungs.

The importance of pregnant women avoiding maternal smoke exposure is underlined with this study.

E-Cigarette And NRT Study

Does use of e-cigarettes and/or nicotine replacement therapy to replace regular cigarettes reduce intake of harmful materials? 

Here is a paper, conclusion from the abstract:

CONCLUSION:

Former smokers with long-term e-cigarette-only or NRT-only use may obtain roughly similar levels of nicotine compared with smokers of combustible cigarettes only, but results varied. Long-term NRT-only and e-cigarette-only use, but not dual use of NRTs or e-cigarettes with combustible cigarettes, is associated with substantially reduced levels of measured carcinogens and toxins relative to smoking only combustible cigarettes.

So, using e-cigarettes or NRT alone results in roughly the same nicotine intake but reduced carcinogens and toxins, which is good.  Using both e-cigarettes and NRT does not seem to lead to a reduction.  If you are a smoker, discuss with your physician; these results suggest to me to use either replacement but not both.  Of course, my father quit “cold turkey” which if you can do it, reduces intake of these substances to zero.  Best yet: do not start smoking to begin with, if you have not already done so.

Some Articles On Third Hand Smoke

We are all aware of the dangers of smoking, and most people have heard about "second hand smoke" - but what about "third hand smoke?"  

Smoking remnants can constitute a significant health hazard, and may be particularly problematical for infants.

If smokers needed yet another reason to quit, third hand smoke is something to consider.

The Opiod Epidemic As A Model For The Tobacco Problem

Using the opioid epidemic as a model to deal with the broader tobacco problem may be a useful approach.  Read this:

On October 26, 2017, President Trump declared the opioid epidemic a public health emergency. Although some commentators have debated its merits, the declaration has already been successful in 1 regard: it has focused national attention on the problem of opioid misuse and abuse. Indeed, the opioid epidemic is a pressing problem. In 2015, opioids were implicated in 33 000 deaths, representing a 4-fold increase since the early 2000s.1 Mortality attributable to opioids is particularly concentrated among younger adults, with an estimated 1 million years of potential life lost annually.2

As devastating as the opioid epidemic is, however, its toll is modest compared to that of another substance: tobacco. Even though tobacco use has rarely made headlines in recent years, cigarette smoking is associated with an estimated 480 000 deaths in the United States annually, totaling approximately 5 million years of potential life lost each year.3,4 Of these deaths, approximately 41 000 are attributed to secondhand smoke exposure, a number that alone exceeds the number of US residents who die of an opioid overdose.3 Public outcry over the opioid crisis is by no means misplaced, but the contrast between the relative attention garnered by the opioid epidemic compared with tobacco use highlights the extent to which concern over tobacco has receded, despite the enormous adverse effects of tobacco on the health of society.

Why has the opioid crisis generated intense public concern and interest while tobacco has not? One reason might be that the trajectories of the 2 epidemics are quite different. The opioid epidemic is a relatively recent phenomenon that appears to be accelerating at a concerning pace. Tobacco use, by contrast, has been steadily decreasing in the United States, with smoking rates declining by more than half during the past 60 years.

The decline in smoking rates, while encouraging, can obscure the ways in which tobacco is still a real and pressing problem. First, the burden of disease attributable to tobacco remains substantial. For every person who dies from using tobacco, 30 live with serious tobacco-related illness.3 Second, and perhaps more insidiously, tobacco use has become more concentrated in vulnerable populations: among the poor, those with mental illness, and those with low educational attainment. Smoking prevalence has declined to less than 10% among those with a college education or more, whereas among those without a high school diploma, approximately 24% of the population smokes.5 Tobacco is becoming a key driver of health disparities in the United States.

The perceived importance of tobacco use has critical consequences for tobacco control and prevention efforts. Over the past decade, public funding for tobacco control has remained stagnant. State spending on tobacco control has been well below revenue generated by tobacco sales and represents a fraction of what tobacco companies spend on marketing. In some cases, states have elected to defund tobacco control programs entirely. For example, the state of New Jersey devoted zero state dollars to tobacco control and prevention between 2013 and 2017, suggesting that tobacco use was declining and that funding for tobacco control measures was not needed.

Despite declining or stagnant efforts on the state and local levels, tobacco control has received renewed attention from a key agency: the US Food and Drug Administration (FDA).6 In August 2017, the FDA announced a proposal to regulate and reduce the amount of nicotine in combustible cigarettes. High-quality (albeit short-term) data suggest that lowering nicotine levels in tobacco reduces nicotine dependence without promoting compensatory smoking.7 While the actual effects of such a policy remain to be seen, the policy represents a novel and aggressive approach to reducing cigarette consumption. The FDA has also proposed regulating noncombustible nicotine products, including electronic nicotine-delivery systems, and has suggested that these products may have a role in a broader harm-reduction strategy.

Implementing these policies will not be straightforward. The FDA’s authority to regulate nicotine in cigarettes was established by statute in 2009. Eight years have elapsed since this authority was granted, highlighting the difficulties of regulating nicotine. Vested interests, including tobacco companies, will surely oppose the policy. Policy makers concerned about local economic effects may also oppose and challenge the FDA’s authority. Even public health advocates and public health agencies wary of unintended consequences may challenge this approach.8

In many ways, the challenges faced by tobacco control are similar to those of the opioid epidemic: a profoundly addictive substance, use concentrated among marginalized and vulnerable populations, powerful interests that profit from consumption, and harm-reduction strategies that require a shift in approach. Perhaps a key difference is that the opioid epidemic has generated intense public concern as well as broad bipartisan political support. While the opioid epidemic has not yet abated, this public and political support has been critical at key policy junctures, including in shaping debate around the future of the Affordable Care Act and the structure of the Medicaid program, which are important in funding treatment for substance use disorders. Such support could likewise be critical in carrying the FDA proposal forward.

Perhaps public concern over the opioid epidemic can provide an opportunity to renew a sense of urgency around tobacco control. Indeed, the epidemics are not completely distinct. The communities most deeply affected by the opioid crisis also have some of the highest smoking rates, and individuals who use tobacco are also more likely to develop prescription opioid misuse. These overlapping epidemics suggest that common conditions may contribute to both and that common solutions may be useful. This moment, with attention focused intently on the opioid epidemic, may also provide the chance to address addiction to nicotine and thereby substantially reduce the harms caused by these 2 threats to health.

More On Cancer Prevention And Lifestyle

Here is recent news on yet another study linking lifestyle to cancer risk.  These are all things you, as a reader of this blog, should be well aware of by now.  The importance of curbing these behaviors to reduce cancer risk is underscored by these additional data.

Researchers with the American Cancer Society looked at data on cancer incidence and deaths, finding that 42 percent of all cancer cases in the United States -– and nearly half of all cancer deaths – are linked to preventable risk factors like cigarette smoking, exposure to secondhand smoke, excess body weight, alcohol intake and dietary choices.

Cigarette smoking, in particular, was connected to far more cancer cases and deaths than any other single risk factor, accounting for 19 percent of all cancer cases and 28.8 percent of deaths. Overweight and obesity came in second, responsible for 7.8 percent of cases and 6.5 percent of deaths, while alcohol intake was the third most important factor, leading to 5.6 percent of cancer cases and 4 percent of deaths.

Although there are some sex-specific differences as to the relative importance of various risk factors, the bottom line is that these things – smoking/overweight/obese, bad diets, certain STDs, alcohol – are bad for everyone.  Be aware and adjust your life accordingly, to the extent you are able.

The Vices Of Men

By Vincent van Gogh - Scanned from Smoke: a global history of smoking (2004) ISBN 1-86189-200-4, Public Domain, https://commons.wikimedia.org/w/index.php?curid=3857076

The paper linked here is a fascinating review that looks at three major vices of men – drinking alcohol, being overweight/obese, and smoking tobacco – and how these activities can damage male fertility and also negatively affect the health of their offspring. Mechanisms by which these vices can affect fertility and the health of children include epigenetic changes to sperm DNA and non-coding RNA (changes to the modification to DNA and RNA, not including actual sequence mutation, that can affect gene expression), sperm DNA damage (which can cause actual sequence mutation affecting gene expression), changes in sperm chromatin structure (for example, changes in the chromosome structure that can affect which genes are expressed and which are silenced), and changes in seminal plasma (that can affect the function of the sperm cells themselves).  Abstract:

There is growing evidence from animal and human studies that demonstrate that acquired paternal traits can impair both a male's fertility and the health of his offspring, including advanced age, smoking, stress, trauma, under-nutrition, infection, toxin exposure, and obesity. Curiously, many of these factors manifest as impaired neurological, behavioural, and/or metabolic functioning in offspring. The underlying molecular mechanisms that respond to the paternal environment and act as vectors of intergenerational transmission are beginning to emerge. This review focuses on three vices of men (alcohol consumption, overweight/obesity, and tobacco smoking) that damage fertility and pose risks to offspring health. These vices are not only the three most prevalent but are also leading risk factors for death and disability adjusted life years (DALYs) worldwide. Clearly, any epigenetic/genetic alterations induced by the paternal exposures responsible for transmission need to escape/bypass the substantial post-fertilisation reprogramming that occurs during embryo development. For example paternal obesity alters the molecular composition of sperm, alters the developmental trajectory of resultant embryos, and increase the incidence of obesity and metabolic disorders in offspring. Mechanistic candidates of paternal programming include changes to the sperm epigenome (eg DNA methylation, histone/protamine modifications, and sperm borne small non-coding RNAs), increased sperm DNA damage, aberrant sperm DNA chromatin structure, and components of seminal plasma. Understanding the molecular mechanisms underpinning paternal programming may lead to the development of interventions designed to reduce the disease burden in future generations, who were born to fathers exposed to these initiating factors. Given that these vices are predominantly self-inflicted, interventions aimed at mitigating their consequences are readily identified.

Add this information to all the other reasons to avoid these vices.

Adenoma Detection Rates In Obese And Smoking Patients

At left, stained adenoma under the microscope.

By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=8273894

Here is a study showing higher detection rates for adenomas and serrated adenomas in obese and smoking patients undergoing colonoscopy. Adenomas are benign tumors that - if left in the colon - have a probability of turning into full-fledged cancer (e.g., for a given polyp, could be a 10% chance in 10 years). Therefore, when detected in endoscopic screening, adenomas are typically removed.  The more adenomas, the greater the chance for cancer, so it is not surprising that obese and smoking individuals tend to have higher rates of colorectal cancer, since they are developing more of the pre-cancerous adenomas.

This again underscores the fundamental importance of maintaining a healthy bodyweight and to refrain from smoking.  If you are already at a normal weight and do not smoke, great, keep it up; if not, lose weight and make every attempt to quit smoking.  In general people associate obesity with diabetes and smoking with lung cancer, and those associations are indeed correct; however, there are many, many diseases associated with both obesity and smoking - including colorectal cancer - so the health ramifications of weight control and no smoking are enormous.

Still smoking?

Paying people supports their will to undertake healthy changes, including this to quit smoking. Watch how smokers succeeded in quitting when paid. It seems that our health insurance providers should think about a monetary incentive for those who still smoke but are willing to change the habit. 

Another solution (or a complimentary solution) could be the application of cytisine, an over-the-counter remedy. Watch this New England Journal of Medicine video to find out about the spectacular effect of cytisine on smokers who want to quit.

GOLDEN RAIN TREE

Based upon this report, cytisine, an alkaloid from golden rain tree (Cytisus Laburnum), is very cheap to produce. In fact, it has been used for more than 50 years in Eastern Europe, where a 25-day (pill) treatment course costs approximately $10! 

I wonder why our health care givers and insurers are not offering this remedy. Probably because it is too cheap and too effective?