Skip to comments.Patterns: Smoking: Hazardous to Your Cat
Posted on 12/26/2002 8:50:00 AM PST by dennisw
Patterns: Smoking: Hazardous to Your CatBy JOHN O'NEIL
ats whose owners smoke are up to three times as likely to develop lymphoma, a form of cancer, as cats living with nonsmokers, a new study has found.
Dr. Antony S. Moore of the Tufts University Veterinary School, an author of the study, said cats in many ways were better subjects than people for studying secondhand smoke.
"Cats basically hang around inside the house, so they don't get exposed to as many possible environmental hazards," he said. "You can often smell the smoke on their fur, and when you consider that they're grooming all the time with their tongues, they're probably getting a fairly significant dose."
For the study, which was published in the August issue of The American Journal of Epidemiology, the researchers surveyed the owners of 80 cats with lymphoma and 114 cats with renal disease, which strikes cats at about the same age but is not linked to environmental factors.
They found not only that all cats exposed to tobacco smoke had a far higher risk of lymphoma, but also that the risk was directly related to how much smoke was in the house and how long the cat had been exposed.
Dr. Moore said that the study had been undertaken mainly to explore ways of preventing lymphoma in cats, but he added that he hoped it would raise awareness of the dangers of tobacco in a new way.
"People often think of their cats as members of their family, and they should realize that when we smoke we are increasing the risks faced by those around us," he said. "If we can prevent this disease in cats, I'd be happy. If in doing so we can decrease the risk of cancer in people, I'd be doubly happy."
Down here in Loozeana we prefer 'em cajun blackened w/ a nice crawfish etouffe...#8-)
Bull, Bull, Bull
This is just another BS study done by the antismoking Nazis. I guess if they can't make you quit by the harm you are causing yourself they are trying to make you feel guilty by trying to mke it look like you are killing your beloved pet.
I have the Abstract
Environmental tobacco smoke and risk of malignant lymphoma in pet cats.
Bertone ER, Snyder LA, Moore AS.
Department of Biostatistics and Epidemiology, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA 01003-9304, USA. firstname.lastname@example.org
Feline malignant lymphoma occurs commonly in domestic cats and may serve as a model for non-Hodgkin's lymphoma in humans. Several studies have suggested that smoking may increase the risk of non-Hodgkin's lymphoma. To evaluate whether exposure to household environmental tobacco smoke (ETS) may increase the risk of feline malignant lymphoma, the authors conducted a case-control study of this relation in 80 cats with malignant lymphoma and 114 controls with renal disease diagnosed at a large Massachusetts veterinary teaching hospital between 1993 and 2000. Owners of all subjects were sent a questionnaire inquiring about the level of smoking in the household 2 years prior to diagnosis. After adjustment for age and other factors, the relative risk of malignant lymphoma for cats with any household ETS exposure was 2.4 (95 percent confidence interval: 1.2, 4.5). Risk increased with both duration and quantity of exposure, with evidence of a linear trend. Cats with 5 or more years of ETS exposure had a relative risk of 3.2 (95 percent confidence interval: 1.5, 6.9; p for trend = 0.003) compared with those in nonsmoking households. These findings suggest that passive smoking may increase the risk of malignant lymphoma in cats and that further study of this relation in humans is warranted.
PMID: 12142262 [PubMed - indexed for MEDLINE]
First off right off the bat, this is a study done by questionaires and we all know how they word questionaires to get the results they want.
Secondly they did Adjustments for "Other Factors", Lord only knows what these other factors are.
Finally, The biggie. The control group is with cats with renal disease. Now a question to ask is why on Earth would you use for the control group cats with another type of disease instead of "Normal" healthly cats.
The reason and why the test is BS is that the nicotine in the cigarettes is probably good for Renal disease so cats whose owners are smokers are probably less likely to come down with renal disease and be less symptomatic if they suffer from it thus less likely to go to the vet and take part in this silly little survey. So yes since renal disease is a big killer of cats you can say second hand smoke is good for your kitty.
So the test is BS because there isn't more smokers with cats with lymphoma but instead there are less smokers with cats with renal disease which skews the results to make it look like smoking is causing lymphoma.
There are no (Public?) direct studies showing nicotine helps cats with renal disease but we can infer it to be a good possibility. I will try not to bore you with heavy science
Renal disease is Kidney failure where toxins that should be excreated in urine end up staying the blood. Nicotine has the effect of inhibiting the renal reflex and increasing urine flow which most likely helps prevent or delays the onset on renal disease. (Note: The renal reflex is what holds water & salts in the blood, If you are suffering from renal disease you want this shut off) 3 studys, 2 with cats and one with dog.
J Physiol 1978 Oct;283:141-54
Electrophysiological characteristics of renorenal reflexes in the cat.
Calaresu FR, Kim P, Nakamura H, Sato A.
1. Experiments were done in anaesthetized, paralysed and artificially ventilated cats to determine the fibre composition of renal nerves and to study the functional characteristics of reflex responses recorded in efferent renal nerves during electrical stimulation of contralateral and ipsilateral afferent renal nerves. 2. Renal nerves were found to contain three afferent fibre groups (Abeta, Adelta and C); the majority of these fibres reach the sympathetic chain through the least splanchnic nerve. Efferent sympathetic nerves to the kidney were found to originate from the greater, lesser and least splanchnic nerves through a synapse in the coeliac ganglion. 3. Two contralateral renorenal reflex responses were demonstrated during selective stimulation of renal afferent A and C fibres. The first (A renorenal reflex) was elicited by stimulation with trains of pulses at low voltage and high frequency (200 Hz), had an onset latency of approximately 100 msec and was followed by post-excitatory depression. The second (C renorenal reflex) was demonstrated by trains of pulses at high voltage and low frequency (20--30 Hz), had an onset latency of approximately 350 msec and was also followed by post-excitatory depression. 4. Ipsilateral renorenal reflexes with characteristics similar to the contralateral reflexes were also demonstrated. 5. Renorenal reflexes were abolished by destruction of the spinal cord and administration of nicotine sulphate (5--20 mg/kg, i.v.), but were not affected by bicuculline (0.4 mg/kg, i.f.). 6. The significance and the physiological role of these renorenal reflexes as well as their pathways within the central nervous system remain to be determined.
The title says it all in the next one
Pflugers Arch 1987 Jun;409(1-2):145-51
Reflex inhibition of efferent renal sympathetic nerve activity by 5-hydroxytryptamine and nicotine is elicited by different epicardial receptors.
Mohr B, Bom AH, Kaumann AJ, Thamer V.
Intrapericardial administration of 5-hydroxytryptamine (5-HT) induced reflex effects consisting in an inhibition of renal sympathetic nerve activity (RSNA), bradycardia and a fall in blood pressure. Nicotine caused the same reflex effects as 5-HT. The reflex effects of both 5-HT and nicotine were abolished by vagotomy. MDL 72222, an antagonist at 5-HT M-receptors, abolished or attenuated the decreases in RSNA, heart rate and blood pressure induced by 5-HT, leaving the reflex effects of nicotine unchanged. In the absence of MDL 72222 the reflex bradycardia partially concealed a positive chronotropic response to 5-HT. After blockade of the bradycardia response by MDL 72222, 5-HT elicited a significant tachycardia, which was not altered by propranolol and phentolamine, but was prevented by phenoxybenzamine. 5-HT probably reaches the sinoatrial node and activates 5-HT receptors that mediate directly the increase in heart rate. The nicotine receptor antagonist hexamethonium selectively abolished or attenuated the reflex effects of nicotine without interfering with those of 5-HT. We conclude that 5-HT and nicotine elicit similar reflex effects in epicardial vagal nerve endings by stimulation of M-receptors or nicotine receptors, respectively.
PMID: 2886974 [PubMed - indexed for MEDLINE]
This one is done with Dogs no doubt the effects will be similar in cats
Actions of nicotine on renal function in dogs.
Pawlik WW, Jacobson ED, Banks RO.
Renal excretory and circulatory responses to nicotine were investigated in anesthetized dogs under three sets of conditions: (a) infusion of nicotine into the left renal artery (ia) at a dose of 0.5 microgram X min-1 X kg body wt-1 X 15 min; (b) ia nicotine after 1.0 mg/kg ia propranolol; and (c) ia nicotine after bilateral adrenalectomy. Measured and calculated left and right renal excretory variables included sodium, potassium, and chloride excretion rates (UNaV, UKV, and UClV, respectively), total solute excretion (UOsV), glomerular filtration rate (GFR), fractional sodium excretion (FENa), and urine flow rate. Systemic arterial pressure and left renal artery blood flow (RBF) were also measured. In seven intact dogs administered nicotine alone, there were significant increases in UNaV, UClV, UOsV, GFR, and urine flow rates from both kidneys. However, nicotine did not significantly affect UKV, FENa, arterial pressure, or RBF. The lack of circulatory effects of nicotine was also observed after either propranolol or adrenalectomy. However, when nicotine was administered after propranolol, the drug evoked significant decreases in UOsV, UNaV, UClV, and GFR, compared with prenicotine values. When nicotine was administered after bilateral adrenalectomy, the drug evoked decreases in the excretory parameters similar to those observed after propranolol. These findings seem to support several inferences: (a) nicotine stimulates renal excretory functions-the alkaloid is saluretic and diuretic; (b) the action of nicotine on the kidney is mediated mainly by the release of catecholamines from the adrenal medulla; (c) catecholamines released by nicotine act mainly on beta-adrenergic receptors; and (d) the saluresis prompted by the release of catecholamines in response to nicotine is due to a subsequent increase in GFR.
PMID: 3983135 [PubMed - indexed for MEDLINE]
Study #1 - Nicotine Reduces aggressive behavior
Study #2 - Smoking makes you less likely to be allergic to your kitty
: Pharmacol Biochem Behav 1976 Sep;5(3):235-9 Related Articles, Links
Effects of nicotinic and muscarinic compounds on biting attack in the cat.
Berntson GG, Beattie MS, Walker JM.
Predatory-like biting attack on a rat, as well as hissing, growling, and other threat behaviors, could be induced in normally non-aggressive cats by systemic administration of the muscarinic agonist, arecoline (7-12 mg/kg). In contrast to arecoline, nicotine was found to suppress aggressive behaviors. Systemic administration of nicotine (0.5 mg/kg) prior to arecoline injection resulted in a significant reduction in elicited attack and threat behaviors. Furthermore, nicotine (0.075-0.500 mg/kg) was found to produce a dose-dependent suppression of natural predatory behavior as well. This nicotine-produced suppression of attack did not appear to be due to the induction of general malaise, since attack suppression could be seen in the absence of general behavioral inhibition, and doses of nicotine resulting in complete suppression of attack had little effect on food intake. Results indicate that muscarinic and nicotinic compounds can exert antagonistic control over some types of aggressive behaviors.
PMID: 1033569 [PubMed - indexed for MEDLINE]
The association of smoking with sensitization to common environmental allergens: results from the European Community Respiratory Health Survey.
Jarvis D, Chinn S, Luczynska C, Burney P.
Department of Public Health Sciences, Guy's King's and St Thomas' School of Medicine, Kings College, Guy's Hospital, London.
BACKGROUND: Smoking is a risk factor for sensitization to some occupational allergens, but its association with sensitization to common environmental allergens remains unclear. OBJECTIVE: We sought to determine the association of smoking with total IgE levels and with sensitization to 3 common environmental allergens in data from the European Community Respiratory Health Survey. METHODS: A detailed smoking history and blood sample for determination of serum total IgE and specific IgE levels to house dust mite, grass, and cat allergens was obtained from 13,002 randomly selected young adults living in the areas served by 34 centers in 14 countries. Associations with smoking status and amount smoked were determined. Because there was evidence of heterogeneity between centers in the association of age, sex, and smoking with sensitization, odds ratios (ORs) were determined for each center and combined by using random-effects meta-analysis. RESULTS: Compared with lifetime nonsmokers, current smokers were at an increased risk of sensitization to house dust mite allergen (OR, 1.13; 95% confidence interval [CI], 1.02-1.26) but a decreased risk of sensitization to grass (OR, 0.76; 95% CI, 0.67-0.88) and cat allergens (OR, 0.69; 95% CI, 0.59-0.80). Exclusion of those with symptoms suggestive of current asthma strengthened the association of smoking with sensitization to house dust mite allergen (OR, 1.29; 95% CI, 1.11-1. 50). The geometric mean total IgE level was higher in smokers and was higher among those who currently smoked the most compared with those who smoked less than 5 cigarettes per day. CONCLUSION: The association between smoking and sensitization to common environmental allergens is different for different allergens.
It looks like we're on our way to proving this study is bogus. When there were two heavy smokers in this house, the resident indoor-only cat lived 22 years.
Asinine comment. Truth is, we use our God-given common sense and past experience to guide us. Both prove there is no harm to healthy people or animals living with smokers.
Oh, yuck. You WOULD have to bring up Bill Clinton, Monica Lewinsky and that oral/anal thingy.
....and he lived 23 years.