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
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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
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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)
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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)
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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)
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6
Q

COGNITION “BENEFITS”

A
  • (smoking -> nicotine -> cognition)
  • Alzherimer’s
  • Parkinson’s
  • schizophrenia
  • depression
  • aging
  • anxiety
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7
Q

COGNITION LIMITATIONS

A
  • pregnant exposure
  • adolescent exposure
  • high-dose exposure
  • withdrawal effect
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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
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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
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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
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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
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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
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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
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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
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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
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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
  1. nicotine delivered to smoking
  2. nicotine travels to brain
  3. nicotine activates nicotinic receptors which stimulates release of dopamine
  4. dopamine released -> pleasant feelings of calmness/reward
  5. dopamine lvls reduce -> withdrawal symptoms of stress/anxiety
  6. 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