Pets Say NO to Smoking! PART 2

In Part 1 of this article, we took a look at exactly what cigarette smoke is and why it is so dangerous.

In this part, Part 2, we take a look at a random selection of a few of the thousands of studies published on the effects of smoking in humans, and especially children in SECTION B. There is less known about the negative effects of second-hand smoke on pets, but in SECTION C, we summarise the results of most of the studies that have been done in dogs and cats.

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Deaths estimated to be attributable to smoking. Statistics on Smoking, England – 2017. Image by NHS Digital. 2017


To set the stage for the devastating impact of smoking, and to give you an idea of what the human health professionals are up against, here is a chilling report on the influence of the tobacco industry itself on smoking.

Despite the overwhelming evidence that exposure of non-smokers to second hand smoke is dangerous and causes lung cancer, the tobacco industry persists in sophisticated and expensive campaigns to rubbish the science by manipulating the media and public opinion. For example, a huge European study by the International Agency for Research on Cancer confirmed the findings of previous studies that there was at least a 16% increase in risk of developing lung cancer in non-smokers (see also IARC, 2004). However, this study was reported by the tobacco industry, and from there in newspapers, as showing no increase in risk at all (Ong et al., 2000).

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Effects of passive smoking on humans health

1. A huge study conducted in 40 households in 31 different countries looked at the effects of exposure to second-hand tobacco smoke in women and children living with smokers (Wipfli et al., 2008). The nicotine levels in the air of smoking households was, on average, 17 times higher than that in non-smoking households. Furthermore, children assimilated higher levels of nicotine than the adults. The researchers concluded that women and children exposed to other people’s cigarette smoke suffered more illness and died sooner than those that were not exposed to smoking.

2. A German study looked at the role of smoking on sudden infant death syndrome by measuring the nicotine levels in the hair, which indicates long-term exposure to cigarette smoke, and in the tissues of the chest and in the brain, which indicates exposure in the last few hours before death. Babies of smoking parents had higher levels of nicotine in their hair, but nicotine was also found in babies of non-smoking parents, suggesting a link with passive smoking. There was also a link with how babies were fed. Nicotine levels where 5 times higher in babies of mothers who smoked and who did not breast feed, indicating that passive smoking was more dangerous than breast milk as the source of nicotine (Bajanowski et al., 2008).

3. Hair samples collected from toddlers and older children living together in the same household with smoking parents showed much higher nicotine levels in the toddlers than in the older children. The reason that toddlers are more at risk is probably because they spend more time close to their parents. Another important factor is that they spend more time putting their hands, and other contaminated objects like clothes and blankets, into their mouths and ingesting nicotine that way (Groner et al., 2011).

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4. In pregnant women that smoke, chronic exposure to nicotine also affects the unborn baby by altering the DNA of developing cells in the lungs. This contributes to the development of respiratory diseases such as bronchopulmonary dysplasia, cystic fibrosis, sudden infant death syndrome, and asthma (Schuller et al. 2000).

5. A study of 35 years of medical records of children showed strong evidence of the link between pre- and postnatal exposure to tobacco smoke and respiratory illness measured by coughing, phlegm production, wheezing and asthma attacks Jaakkola and Jaakkola, 2002).

6. Children with asthma living in a household with smokers suffered more asthma attacks and hospital admissions as a result than those that lived with non-smokers (Irani and Saliba, 2017; also see Gold, 2000).

There are many public health campaigns aimed at the effects of smoking on children
Image by HansMartinPaul [CC0 1.0]


Effects of passive smoking on canine health

Many thousands of non-human animals have been used in the past as surrogates to study the effects of smoking in humans. Here’s one from the 1970’s –

“Tracheal mucous velocity (TMV) was determined in eight purebred beagle dogs exposed to cigarette smoke (100 cigarettes per week) for 13.5 months, and four control dogs. By means of a mask, smoke was administered through both the mouth and nose for 1.5 hours twice daily.”

This horrendous account comes from the abstract of one of the many studies on the effects of cigarette smoke conducted using dogs (Wanner et al., 1973).

Image by kargo [CC0 1.0]
No studies like this are included here for 2 reasons. First, they are cruel and unethical. Second, which is more important, dogs don’t smoke and so these studies do not accurately reflect the long-term negative effects of passive smoking in dogs, which is what this article is about.

1. Reif et al. (1998) investigated 103 dogs diagnosed with nasal cancer and compared them with 378 dogs diagnosed with different cancers. They estimated the dogs exposure to tobacco smoke from the number of smokers in each of the dog’s households, the number of cigarettes smoked per day, the number of years the dogs had been exposed for and the amount of time the dogs spent indoors. Dolichocephalic (long-nosed) dogs were twice as likely to have nasal cancer compared with brachycephalic (short-nosed) dogs. In addition, the risk of nasal cancer rose with increased exposure to tobacco smoke. In short, passive smoking causes nasal cancer in dolichocephalic dogs.

2. The same researchers carried out a similar study, but this time looking for evidence of a link between lung cancer and exposure to tobacco smoke in dogs (Reif et al. 1992). What they found was not as conclusive as their nasal cancer study, but they did find a potential link of increased risk in breeds with short and medium length noses. This might be because in dogs with long noses, more of the carcinogenic (cancer-forming) compounds in the smoke become trapped on the nasal mucosa. This may also help to explain the higher incidence of nasal cancer in dolichocephalic dogs shown in the previous study. In short, there is a risk that passive smoking may cause cancer in brachycephalic dogs.

3. A more recent and larger study looking for a link between second-hand smoke exposure and lung cancer in dogs also found no association (Zierenberg‐Ripoll et al., 2017). This risk of lung cancer and smoking in humans is of course well-established, but dogs do seem to differ in this respect. It must be stated, however, that there is no information available for the risk of lung cancer in other species of household pets exposed to passive smoking.

4. An association between exposure to tobacco smoke and chronic cough in dogs has not been found (Hawkins et al., 2010).

5. However, Roza and Viegas (2007) looked at the long-term effects of passive smoking on Yorkshire Terriers in households where owners were smoking more than 20 cigarettes a day over a 2-year period. Compared to Yorkies living in non-smoking households, these dogs had many more inflammatory cells (macrophages and lymphocytes) in their respiratory systems and their macrophages were also anthracotic. Anthracosis is the accumulation of black carbon particles in cells and tissues and it is a classic abnormality in smokers (see image below). In short, passive smoking in dogs causes the same inflammatory pathologies in dogs as seen in humans that smoke.

Deposition of black carbon particles, mostly within the cytoplasm of macrophages.
Image by Yale Rosen from USA (Anthracosis) [CC BY-SA 2.0]
6. Nicotine build-up in hair is a very useful marker for exposure to cigarette smoke over the previous 2 to 3 months. Hair nicotine levels in children less than 5 years old have been found to be twice that found in older children (Wipfli et al., 2008). The same has been found in dogs; nicotine levels in hair samples has also been established as a reliable indicator of long-term exposure to cigarette smoke (Kim et al., 2009). Furthermore, higher relative levels of nicotine are also found in dogs, just like those found in children, when compared with adults (Knottenbelt et al., 2012). It should be noted that what is being measured here is not nicotine that has stuck to outside shafts of the hair, it is nicotine that has grown into their hair from the root, carried there in the blood stream. Hair samples are always washed before analysing them for nicotine content.

7. The above findings can be explained like this. Spend 5 minutes in a room with a smoker and the only way you can get rid of the smell of cigarettes is to launder your clothes and wash your hair. This is because cigarette smoke in the atmosphere, along with its nicotine load adheres to, and infuses deeply into, all nearby soft furnishings, clothes and hair. As dogs groom themselves, they ingest nicotine from the surface of their coats. They also ingest nicotine from the soft furnishings they are in regular contact with.

8. Nicotine levels in urine is a reliable indicator of recent exposure to cigarette smoke. In a study in dogs, urinary nicotine levels in those living with smokers was much higher than in dogs that lived in non-smoking households (Bertone-Johnson et al., 2008). In addition there was an association with the length of the dog’s nose. Nicotine levels were higher in short-nosed dogs compared to medium and long-nosed dogs.

9. Nicotine levels can also be measured in the blood of dogs and its concentration correlates with the number of cigarettes smoked in the household (Shek-Vugrovečki et al., 2016). Of course, the risk here is that the blood carries this nicotine to every organ and tissue in the body.

Chromosome showing telomeres capping off the ends of its DNA
Image by Samulili [CC GFDL 1.2]
10. Several strands of evidence show that second-hand cigarette smoke causes premature ageing in dogs (Hutchinson, 2017).

It shortens telomere length, which is an indicator of aging.

Telomeres protect the ends of strands of DNA in the nucleus of every cell in the body.

As animals naturally age the telomeres shorten, thus ultimately determining the lifespan of the cell because they can no longer protect the DNA from damage. In short, the dog prematurely ages.

Messenger RNA molecule.
Image by Corentin Le Reun [Public domain]
11. Messenger RNA (mRNA) is an important molecule that conveys the genetic information stored in the DNA molecules to the tissues where it can be expressed by activating enzymes that produce proteins and maintain all of the body’s functions.

Exposure to tobacco smoke reduces mRNA’s ability to do this, which in turn interferes with the normal process of tissue growth and repair (Hutchinson, 2017). In short, the dog prematurely ages.

Effects of passive smoking on feline health

Unlike other species, including dogs, cats have not been used for research into the effects of exposure to tobacco smoke. This is largely because, temperamentally, cats do not make ideal, easy-to-handle laboratory subjects.

Image by clickphoto [CC0 1.0]
A few studies have recently emerged specifically on the effects of passive smoking in cats and these are summarised here. There are many gaps in the information currently available for cats, but until we know otherwise, it would be perfectly reasonable to assume that the information summarised above for dogs is likely to be similar for cats.

1. A recent study found that cats living in households where humans smoked had much higher levels of nicotine in their hair (Smith et al., 2017). Interestingly, the duration of exposure to cigarette smoke did not make any difference. Neither did the cat’s lifestyle. Cats living exclusively indoors did not have higher nicotine levels in their hair compared with cats that had outdoor access. This latter finding can be explained by the cats indoor lifestyles. All the soft furnishings and carpets in the house, along with cats bedding, climbing frames, scratching posts etc., will become permanently infused and contaminated with chemicals from tobacco smoke. The cats frequent close contact with these materials, along with contact with owners, will be a significant contributing source of the nicotine found in the animals hair samples.

The cats bedding is a dangerous source of nicotine ingestion.
Image by 12019 [CC0 1.0]
2. Significant levels of carcinogens, only found in tobacco, have been confirmed in the urine of cats living in households with smokers (McNiel et al., 2007).

3. What this means in relation to the general health of cats and disease risk has not been well studied. However, there is some evidence of a possible link to cigarette smoke with cancer it cats, specifically oral squamous cell carcinoma (Snyder et al., 2004) and malignant lymphoma (Bertone et al., 2002).

Oral cancer. Histopathologic image illustrating well differentiated squamous cell carcinoma in the excisional biopsy specimen.
Image by KGH [CC GFDL 1.2]
Feline kidney malignant lymphoma.
Image by Richard Jakowski, DVM, PhD, DACVP, Tufts Open [CC BY-SA 3.0]

Final Take-Home Message

If you have read this article through and got to this point – THANK YOU.

Message to smokers: The article is not aimed at singling out and blaming smokers. There are many smokers who have tried to give up, but failed for all the reasons described above. Why not make 2018 the year when you finally achieve giving up once and for all.

Message to non-smokers: Please share this article everywhere and use the bite-sized chunks of information and images presented here to help those pet-owning smokers you know to take that vital step and finally quit smoking for good.

Let this be your slogan and symbol for action.

“Pets say NO to smoking.
Let’s work together to make the air we share better for pets everywhere.”

“Pets say NO to smoking. Let’s make the air we share better for pets everywhere.”
Let this be your slogan and symbol for action.
Image by GDJ2015 [CC0 1.0] and adapted by RFT
© copyright COAPE, 2018
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