Smoking & Vaping Flashcards
1
Q
SMOKING PREVALENCE
A
- 2022; 12.9% people aged 18y+ in UK = current smokers (6.4 million)
- smoking prevalence = highest among 25-34y & is higher on average in men
2
Q
E-CIGARETTES & VAPING
A
- 5.2% people (16y) = currently daily users of e-cigarettes (aka. daily vapers)
- 3.5% = occasional vapers
- 2022; 16-24y = more likely to report daily/occasional vaping than all other ages
3
Q
HEALTH IMPACTS OF SMOKING
A
- 506,100 hospital admissions attributable to smoking; similar to 2018/19 BUT 10% higher than 2009/10 (461,700)
- 74,600 deaths attributable to smoking; decrease of 3% from 2018 (77,000)/9% from 2009 (82,000)
4
Q
SECONDHAND SMOKE EFFECTS
A
- NO safe lvl of exposure to secondhand smoke; adults who DON’T smoke BUT still experience secondhand smoke may have:
1. coronary heart disease
2. stroke
3. lung cancer
4. premature death
5. nasal irritation
6. adverse reproductive health effects (incl. low birth weight) - children may have:
1. sudden infant death syndrome
2. middle ear disease
3. respiratory issues (ie. impaired lung function; lower illness)
5
Q
SECOND/THIRDHAND SMOKE (AKA. AEROSOLS)
A
- secondhand vaping aerosols come from burning/heating tobacco via cigarette/cigar/pipe/hookah/e-cig
- also come from air smoker exhales
- thirdhand smoke stays in carpets/walls/furniture/clothing/hair/toys
- person/car/room continues to smell of smoke long after cig is put out
- both contain harmful/toxic cancer-causing chemicals; can be swallowed (ie. kids put hands/objects in mouths oft)
6
Q
COGNITION “BENEFITS”
A
- (smoking -> nicotine -> cognition)
- Alzherimer’s
- Parkinson’s
- schizophrenia
- depression
- aging
- anxiety
7
Q
COGNITION LIMITATIONS
A
- pregnant exposure
- adolescent exposure
- high-dose exposure
- withdrawal effect
8
Q
CONFOUNDS
A
- cigarette smoke contains many other compounds + nicotine than may have cognitive-enhancing effects
- amount of nicotine delivered via smoking = highly variable & dependent on type of cigarette/how individual smokes
- to avoid such limitations numerous studies on modulation of cognition by nicotine have used pure nicotine administered via nasal spray/transdermal patch/subcutaneous injection/oral inhaler/intravenous infusion
9
Q
NICOTINE
A
- addictive substance
- plays key role in initiating/maintaining tobacco use
- rapid delivery rate to brain (10-20s post puff) likely contributes to rewarding properties
- average terminal half-life of 2h; w/regular dosing blood nicotine lvls rise over 6-8h then plateau
10
Q
NICOTINIC ACETYLCHOLINE RECEPTORS (nAChRs)
A
- nicotine’s primary sites of drug action
- present in brain/throughout body:
1. blood vessels (endothelial cells)
2. epithelial cells
3. inflammatory cells (ie. T-cells; macrophages; astrocytes; microglia) - majority of neuronal nAChRs = excitatory/fast acting (millisecond range)
- activated -> modulate release of other neurotransmitters:
1. acetylcholine (ACh)
2. dopamine (DA)
3. serotonin
4. glutamate
5. GABA
6. norepinephrine
11
Q
SMOKING & CARDIOVASCULAR TOXICITY
A
- cigarette smoke contains > 9k chemicals & > 69 known carcinogens
- most concerning are:
1. oxidising chemicals
2. carbon monoxide
3. volatile organic compounds
4. particulates
5. heavy metals
6. nicotine
12
Q
NICOTINE & CARDIOVASCULAR TOXICITY
A
- nicotine ->
- sympathetic nervous system activation ->
- coronary vasoconstriction OR…
- increased HR/blood pressure/myocardial contractility ->
- increased myocardial demain for oxygen/nutrients ->
- myocardial ischemia/infarction ->
- sudden death
13
Q
CARBON MONOXIDE & CARDIOVASCULAR TOXICITY
A
- carbon monoxide ->
- reduced oxygen availability ->
- reduced myocardial blood/oxygen/nutrient supply & coronary occlusion ->
- myocardial ischemia/infarction ->
- sudden death
14
Q
OXIDANT CHEMICALS & CARDIOVASCULAR TOXICITY
A
- oxidant chemicals/particulares/other combustion products ->
- inflammation ->
- platelet activation/thrombosis & endothelial dysfunction ->
- coronary vasoconstriction & reduced myocardial blood/oxygen/nutrient supply & coronary occlusion ->
- myocardial ischemia/infraction ->
- sudden death
15
Q
NICOTINE & nAChRs
A
- nAChRs = widespread throughout brain (aka. thalamus; basal ganglia; PFC; hippocampus; cerebellum)
- acute effect of smoking = enhancement of neurotransmission through cortico-basal ganglia-thalamic circuits
16
Q
ACUTE EFFECTS
A
- acute nicotine administration & other nAChRs agonists result in improvements in:
1. attentional focus & flexibility
2. reduces distractability
3. improve hippocampus & PFC-dependent working memory
4. increased activity in thalamus/lateral PFC/ACC
5. reduced activity in ventromedial prefrontal cortex/posterior cingulate cortex/parahippocampus & regions involved w/task-irrelevant mental operations (ie. mind wandering)
17
Q
GRUNDEY ET AL. (2015)
A
- clinical results show WM performance improved in smokers post taking nicotine in n-back letter task
- accuracy in nonsmokers decreased (aka. number of errors increased)
- adolescents = more sensitive to beneficial effects of nicotine; may be why many start smoking during adolescence
18
Q
STRESS REDUCTION
A
- nicotine delivered to smoking
- nicotine travels to brain
- nicotine activates nicotinic receptors which stimulates release of dopamine
- dopamine released -> pleasant feelings of calmness/reward
- dopamine lvls reduce -> withdrawal symptoms of stress/anxiety
- withdrawal triggers desire for another cigarette
19
Q
CLINICAL POPULATIONS
A
- nicotine & smoking can help w/cognitive impairment in Alzheimer’s/Parkinson’s disease
- cognitive impairment = associated w/defects in cholinergic neurotransmission system in brain
- nAChR = reduced in elderly individuals w/age-related neurodegenerative diseases
- postmortem & lab studies = smokers have widespread up-regulation of nAChRs; likely related to desensitisation of receptors from nicotine exposure
20
Q
MOST EVIDENCE SUPPORTS NEGATIVE EFFECTS OF SMOKING
A
- early onset smoking = related to LONG-LASTING decreases in attention/inhibitory control
- teen e-cigarette use -> lower academic achievement
21
Q
DAI ET AL. (2022)
A
- longitudinal assessments of neurocognitive performance & brain structure associated w/initiation of tobacco use in children
- 2016-2021
22
Q
SMOKING & PFC
A
- cognitive effects = thought to be related to nicotine-induced damage to PFC
- nicotine acting on nAChr hampers PFC function & interferes w/PFC maturation
- decreased inhibitory presynaptic mGluR2 protein expression -> decreased adolescence
- increase in dopamine (D1) receptors
- beh disturbances & mental health issues = strongly correlated w/adolescent nicotine use
23
Q
NICOTINE-INDUCED EPIGENETIC ALTERATIONS PERSIST ACROSS GENERATIONS: PRENATAL
A
F1
- altered DNA methylation & CpG sites
F2
- early childhood asthma w/parallel downregulation of PPAy & altered DNA methylation patterns in lungs; increased likelihood of autism
24
Q
NICOTINE-INDUCED EPIGENETIC ALTERATIONS PERSIST ACROSS GENERATIONS: POSTNATAL/PERINATAL
A
F1
- remodeled DNA methylation in spermatozoa
-deficits in proBDNF proteolysis
- anomalies in glucocorticoid receptor activation
- enhanced nicotine preference & hyperactivity
F2
- deficits in proBDNF proteolysis
- anomalies in glucocorticoid receptor activation
- enhanced nicotine pref & hyperactivity
25
Q
NICOTINE-INDUCED EPIGENETIC ALTERATIONS PERSIST ACROSS GENERATIONS: ADOLESCENT
A
F1
- learning & cognitive deficits
- nicotine sensitisation
F2
- cognitive & beh impairment
- nicotine sensitisation
26
Q
COGNITION
A
- individuals w/lower executive functions & higher impulsivity = more likely to report smoking
- lower inhibitory control predicts cigarette dependence
- degree to which rewards are discounted by smokers = positively related to number of cigarettes smoked/nicotine lvls & their experience of withdrawal
27
Q
SMOKING RELAPSE
A
- 60% smokers make at least 1 attempt to quit each year BUT 5% of them attempt abstinence 12 months later
- even w/intensive combination treatment at least 70% smokers relapse within 1y
- baseline measures of delay discounting = strong predictors of abstinence post treatment
- decreased discounting = also associated w/increased likelihood of LTM abstinence from smoking in pregnant women/adolescents/heavy drinkers
- steeper delay discounting & greater cognitive impulsiveness independently predict lesser likelihood of abstinence in low SES group
28
Q
NEUROMODULATION & SMOKING
A
- rTMS/tDCS over dIPFC reduced cravings for cigarettes even in non-motivated smokers & helps w/quitting
29
Q
GRAPHIC WARNING LABELS
A
- elicit emotional response associated w/increased activity in:
1. amygdala
2. hippocampus
3. inferior frontal gyri
4. insula - higher ER warning lebel = graphic (ie. “cigarettes cause cancer” w/body trauma picture)
- low ER warning label = non-graphic but relevant pic (ie. “quitting smoking now greatly reduces serious risks to health” w/pic of woman blowing bubbles)
- aka. neural reactivity = predictor of campaign success
