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Greenwood M, Meechan JG. General medicine and surgery for dental practitioners: part 1. History taking and examination of the clothed patient. Br Dent J. 2014; 216:629-632 https://doi.org/10.1038/sj.bdj.2014.446
Gambhir R, Brar P, Anand S Oral health aspects of cannabis use. Ind J Multidis Dent. 2012; 2:507-511
Pertwee RG, Howlett AC, Abood ME International Union of Basic and Clinical Pharmacology. LXXIX. Cannabinoid receptors and their ligands: beyond CB1 and CB2. Pharmacol Rev. 2010; 62:588-631 https://doi.org/10.1124/pr.110.003004
Tossmann P, Boldt S, Tensil MD. The use of drugs within the techno party scene in European metropolitan cities. Eur Addict Res. 2001; 7:2-23 https://doi.org/10.1159/000050709
Office for National Statistics. Deaths related to drug poisoning by selected substances, England and Wales. 2022. https://tinyurl.com/32eftvsn (accessed July 2023)
Kaar SJ, Ferris J, Waldron J Up: The rise of nitrous oxide abuse. An international survey of contemporary nitrous oxide use. J Psychopharmacol. 2016; 30:395-401 https://doi.org/10.1177/0269881116632375
van Amsterdam J, Nabben T, van den Brink W. Recreational nitrous oxide use: prevalence and risks. Regul Toxicol Pharmacol. 2015; 73:790-796 https://doi.org/10.1016/j.yrtph.2015.10.017
Mental Health Foundation. Fundamental facts about mental health. https://tinyurl.com/enfcvhxk (accessed July 2023)
Kalant H. Adverse effects of cannabis on health: an update of the literature since 1996. Prog Neuropsychopharmacol Biol Psychiatry. 2004; 28:849-863 https://doi.org/10.1016/j.pnpbp.2004.05.027
Schulz-Katterbach M, Imfeld T, Imfeld C. Cannabis and caries – does regular cannabis use increase the risk of caries in cigarette smokers?. Schweiz Monatsschr Zahnmed. 2009; 119:576-583
Darling MR, Arendorf TM. Review of the effects of cannabis smoking on oral health. Int Dent J. 1992; 42:19-22
Hoffman D, Brunneman D, Gori G, Wynder E. On the carcinogenicity of marijuana smoke. Recent Adv Phytochem. 1975; 4:63-81
Donald PJ. Marijuana smoking – possible cause of head and neck carcinoma in young patients. Otolaryngol Head Neck Surg. 1986; 94:517-521 https://doi.org/10.1177/019459988609400420
Twardowski MA, Link MM, Twardowski NM. Effects of cannabis use on sedation requirements for endoscopic procedures. J Am Osteopath Assoc. 2019; https://doi.org/10.7556/jaoa.2019.052
Dickerson SJ. Cannabis and its effect on anesthesia. AANA J. 1980; 48:526-528
Quart AM, Small CB, Klein RS. The cocaine connection. Users imperil their gingiva. J Am Dent Assoc. 1991; 122:85-87
Kapila YL, Kashani H. Cocaine-associated rapid gingival recession and dental erosion. A case report. J Periodontol. 1997; 68:485-458 https://doi.org/10.1902/jop.1997.68.5.485
Bahdila D, Aldosari M, Abdullah A Cocaine, polysubstance abuse, and oral health outcomes, NHANES 2009 to 2014. J Periodontol. 2020; https://doi.org/10.1002/JPER.19-0509
Yagiela JA. Adverse drug interactions in dental practice: interactions associated with vasoconstrictors. Part V of a series. J Am Dent Assoc. 1999; 130:701-709 https://doi.org/10.14219/jada.archive.1999.0280
Goulet JP, Pérusse R, Turcotte JY. Contraindications to vasoconstrictors in dentistry: Part III. Pharmacologic interactions. Oral Surg Oral Med Oral Pathol. 1992; 74:(6)92-97 https://doi.org/10.1016/0030-4220(92)90367-y
Hill GE, Ogunnaike BO, Johnson ER. General anaesthesia for the cocaine abusing patient. Is it safe?. Br J Anaesth. 2006; 97:654-657 https://doi.org/10.1093/bja/ael221
Sacco R, Ball R, Barry E, Akintola O. The role of illicit drugs in developing medication-related osteonecrosis (MRONJ): a systematic review. Br J Oral Maxillofac Surg. 2021; 59:398-406 https://doi.org/10.1016/j.bjoms.2020.08.079
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Solowij N, Hall W, Lee N. Recreational MDMA use in Sydney: a profile of ‘Ecstacy’ users and their experiences with the drug. Br J Addict. 1992; 87:1161-1172 https://doi.org/10.1111/j.1360-0443.1992.tb02003.x
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Brazier WJ, Dhariwal DK, Patton DW, Bishop K. Ecstasy related periodontitis and mucosal ulceration – a case report. Br Dent J. 2003; 194:197-199 https://doi.org/10.1038/sj.bdj.4809908
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What's the deal? the importance of asking about recreational drug use in dental settings Onkar Mudhar Natalie Bradley Megan Samuel Dental Update 2024 50:7, 707-709.
Authors
OnkarMudhar
Dental Core Trainee 2, Oral Surgery/OMFS, Mid and South Essex NHS Trust
This article looks at the dental implications of the most commonly abused recreational drugs in the UK. It emphasizes the need for clinicians to have honest discussions with their patients and obtain this often overlooked piece of information. We discuss not only the oral manifestations and health implications of various recreational drugs, but also the impacts their use may have on a range of dental treatment. Furthermore, tips are given on how to obtain this often sensitive information.
CPD/Clinical Relevance: The use of recreational drugs has oral health implications and may impact on a range of dental treatment.
Article
Recreational drug use in the UK is on the rise. In 2011, an estimated one in 11 adults aged between 16 and 59 years had taken a drug in the previous year (9.4% or approximately 3.2 million people), which was an increase from 8.6% in the year ending March 2010.1 Additionally, 2.1% of adults aged 16–59 years and 4.3% of adults aged 16–24 years were classed as ‘frequent’ recreational drug users (had taken a drug more than once a month in the previous year).1
This article explores the importance of including questions about recreational drug use as part of every patient assessment and the impact this can have on the provision of dental treatment.
Obtaining sensitive information: where to begin?
Within the dental profession, there can be a reluctance to enquire about recreational drug use, often due to its illegal nature. Like any other aspect of history taking, it is crucial that a non-judgemental, professional tone is used. The use of open-ended questions that encourage discussion may also be of benefit.2 Dental professionals must gauge the level of appropriateness when asking these questions because patients may need to establish trust and rapport before sharing this information.3 To obtain a detailed social history, clinicians may want to undertake training in basic and motivational interviewing, and challenge themselves to examine their own biases. Unexplored prejudices may influence the ability to obtain, or act on, important information.3
When approaching a social history, the impact of the delivery of dental treatment must be considered. As a minimum, it should include alcohol consumption and smoking status in a quantitative fashion (e.g. number of cigarettes smoked/or units of alcohol consumed). Patients may not often know the specific number of units of alcohol they consume, therefore a visual chart explaining the units system is often useful (e.g. a pint of 4% strength lager equates to 2 units, whereas a single measure of spirit is 1 unit). Asking about the patient's occupation, caring responsibilities and living status may also be relevant (especially in cases where overnight care may be required, such as for treatment under conscious sedation or general anaesthesia).4
Furthermore, asking a patient whether they are currently under the care of an addiction clinic or specialist drug and alcohol service may be of importance in order for liaison regarding medications (e.g. methadone, which often contains sugar), and coordination of care, for example, making sure dental appointments do not clash with allocated time slots for receiving medication.
Recreational drugs used in the UK
Cannabis
Cannabis is the most abused drug in the UK, with 18.7% of adults aged 16–59 years reported as using it within the previous year.1 In its most common form (dried leaves), it can either be smoked by itself or in combination with tobacco as hand rolled cigarettes. Additionally, it may also be smoked through a water pipe or an electric vaporizer, or the dried leaves can be mixed within food and consumed.5 Delta-9-tetrahydrocannabinol (THC), is one of sixty-six cannabinoids within cannabis, and is most associated with eliciting hallucinogenic/psychoactive effects.6 THC interacts with two main receptors: CB1, mainly found in the brain; and CB2, found within immune cells and the gastrointestinal tract.7
The most common route of administration is through smoking, in which 50% of the available THC is inhaled, while the remainder is lost as either heat or smoke. The ‘high’ is often felt within minutes and lasts 2–3 hours.8 Owing to its lipophilic nature, THC accumulates in adipose tissue and is slowly released back into the body. Total elimination can take up to 30 days.9
Cocaine
Cocaine (benzoylmethylecgonine, C17H21NO4) is derived from the leaves of Erythroxylum coca. It is the second most commonly abused drug in the UK, with approximately 873,000 of 16–59 year olds having used it within the previous year.1 The prevalence of powder cocaine use is now four times greater than in December 1995.1 It is most frequently used in its powder form and inhaled/snorted by the user.
It can also be used as a solid for smoking through the addition of bicarbonate soda. This is often referred to as crack owing to the sound the product makes upon heating. The user may feel a euphoric sensation within minutes; however, this is often short lived (30–90 minutes).10 This short duration of action often leads to sizeable amounts being used in one sitting, often combined with alcohol.
Studies have shown that the combination of alcohol and cocaine tends to have greater additive effects on heart rate, owing to an increase in blood cocaine levels. Both prospective and retrospective data further reveal that co-use leads to the formation of cocaethylene, which may potentiate the cardiotoxic effects of cocaine or alcohol alone. More importantly, retrospective data suggest that the combination can potentiate the tendency towards violent thoughts and threats.11
Cocaine produces effects of euphoria through stimulation of the dopamine system. It diffuses across the lipid membranes of neurones, preventing the generation of an action potential and resulting in a reversible anaesthetic effect.10 Furthermore, it prevents the re-uptake of norepinephrine and dopamine, thus prolonging the effects of these neurotransmitters.12
MDMA
MDMA, (3,4-methylenedioxy methamphetamine), more commonly known as ecstasy was first synthesized in 1912 by Merck but was never marketed. During the 1960s, American chemist Alexander Shulgin reported that he synthesized MDMA while researching methylenedioxy compounds, but did not test its psychoactivity at that time. It gained traction as a ‘party drug’ in the USA during the late 1970s and 1980s, and it was estimated that in 2004, more than 8.3 million people worldwide had taken ecstasy.13 One can only assume that 18 years later this number would most certainly have risen.
Ecstasy is commonly taken in a tablet or powder form, and is frequently used in combination with other drugs, such as cannabis (71%) and alcohol (66%). Use with amphetamine (29%) or cocaine (25%) is also frequently reported.14 MDMA has major effects on serotonin pathways, but also dopamine and noradrenaline pathwats. MDMA binds to all three of the monoamine presynaptic transporters with the highest affinity for the 5-HT (serotonin) transporter. MDMA administration causes a surge in extracellular 5-HT through release from synaptic vesicles, blockade of 5-HT re-uptake into the presynaptic terminals and inhibition of monoamine oxidase.15 This leads to a surge in serotonin, leading to feelings of euphoria, alertness and feeling ‘close’ to others. Other symptoms include tachycardia, tremor, dilated pupils, an increased body temperature, nausea, suppressed appetite and insomnia. Body movements may be difficult to coordinate and users may clench and grind their jaw.16
Following oral ingestion of an ecstasy tablet, its onset can be seen within 20–60 minutes, peaking after 2 hours and lasting 4–6 hours.16 Owing to serotonin depletion, users may often feel anxious, irritable and paranoid for several days following usage.15 In addition, 1147 ecstasy-related deaths were registered in England and Wales between 1993 and 2020.17
Nitrous oxide
Nitrous oxide (N2O), referred to as laughing gas, was first synthesized in 1772 by Joseph Priestley. It is commonly used in the food industry as a mixing and foaming agent (E942) in the production of whipped cream and a fuel booster in the motoring industry. N2O combined with oxygen is used within dentistry as a conscious sedation technique owing to its anxiolytic properties.
The findings from the 2014 Global Drug Survey (GDS)18 confirm that N2O is a very common drug of abuse, in particular in the UK and US (38.6% and 29.4% lifetime prevalence), generally consumed via gas-filled balloons, at festivals and clubs in conjunction with other illicit substances.19 Additionally, 2.4% of adults aged 16–59 years and 8.7% of 16–24 year olds had used nitrous oxide, which is equivalent to around 796,000 and 549,000 individuals, respectively. This made it the second most prevalent drug among young adults (16–24 years) after cannabis.1
Users report a short euphoric sensation, feelings of disassociation and visual/sound hallucinations, which have a rapid onset, peaking around 1 minute after inhalation. The mechanism for N2O is also not fully known, but these effects are probably due to inhibition of the NMDA receptor, similar to that of ketamine.20
Heroin/opiates
Heroin is an opioid with diamorphine as its active component. It can be inhaled, smoked or injected. It causes users feelings of euphoria owing to the release of large amounts of dopamine.21 Heroin is extremely addictive, with users becoming dependent on the drug both physically and psychologically. Chronic use of heroin can result in a wide range of adverse effects on various body systems, including the cardiovascular, respiratory, central nervous, gastrointestinal and genitourinary systems.22 Furthermore, around 40% and 17% of heroin and intravenous heroin users, respectively, have been exposed to some form of hepatitis and/or HIV.23
In those trying to overcome heroin or other opiate addictions, methadone (a synthetic opiate) is often used. The aim of methadone therapy is to completely eliminate a user's dependence on opiates through a gradual dose reduction; however, patients may take methadone for extended periods of time.24
The impact of recreational drug use on dental care
Consent and capacity
Consent issues can arise if someone is under the influence of drugs at their dental appointments. Principles of the Mental Capacity Act, 2005 should be applied when assessing a person's capacity. Treatment may need to be deferred, if possible, to a time where the person is not under the influence of illicit substances, for example early mornings.
People who use recreational drugs also have higher incidences of mental health problems, which can affect capacity to consent.25
Should urgent dental treatment be needed while a person does not have capacity to consent, decisions should be made in their best interests and, if possible, a second opinion sought.
Multidisciplinary working
Managing the overall health and wellbeing of people using recreational drugs often involves multiple agencies. These agencies include additional services, general practitioners, mental health, housing and social care and learning disability teams. Dental professionals can use these agencies to provide holistic care for patients. Table 1 gives examples of multidisciplinary working.
Table 1. Examples of multidisciplinary working.
Referral pathways and signposting
Oral health promotion messages, e.g. increasing prescriptions of sugar-free medications
Escorting/chaperoning patients to their appointments to increase attendance and support during appointments
Liaison for further information, e.g. medical histories, recent blood tests, confirmation of dental exemption status
Cannabis
Cannabis has impacts on the respiratory, cardiovascular and central nervous system. The extent may vary between users owing to factors such as preparation, frequency of use and whether it has been used in combination with other substances.26 Studies have shown a direct correlation between cannabis use and reduced salivary flow. When coupled with the appetite enhancing nature of the drug (referred to as ‘munchies’) in which users often crave cariogenic food and drink, the xerostomic effect of the drug in conjunction with the reduced buffering capability of the user's saliva, increases the risk of caries.10,27,28 A survey found that 63% of those who felt hungry after cannabis use had consumed foods and drinks categorized as being sweet.29 Furthermore, regular cannabis users may present with poorer oral health than non-users, with higher decayed, missing and filled (DMF) teeth scores, higher plaque scores and poorer oral hygiene.30
Cannabis contains a number of carcinogens31 similar to those found in tobacco; however, the evidence to suggest it has a role to play in the development of oral cancer remains mixed. Some studies indicate that cannabis use increases the risk of oral cancer, including precancerous lesions and cancers, particularly at the anterior floor of the mouth and tongue.32,33 Additionally, a strong association between cannabis use and head and neck cancer has been reported among younger patients.34,35 Contrasting studies have also shown no association between cannabis use and the development of head and neck cancers or oral squamous cell carcinoma.33,36 A thorough oral cancer screening should be undertaken at each assessment.
Few studies have looked at the interaction between cannabis and sedative agents, with one study showing that patients who were regular users of cannabis required a higher dose of sedative prior to their procedure.37 Cannabis may compound the effects of anaesthetic agents, thus increasing arterial pressure and heart rate to possibly life threatening levels. Patients should be advised not to use cannabis (for at least 72 hours) before treatment under conscious sedation in order to reduce the likelihood of drug interactions and unpredictable sedation quality.38
Cocaine
The oral impacts of cocaine include gingival lesions at the site of application owing to the rubbing of cocaine powder topically onto the gingivae (usually the maxillary anterior teeth). These often resolve upon abstaining from use of the drug (within 2 weeks to 18 months).39,40,41
Bahdila et al showed that cocaine users may present with a higher burden of periodontal disease and untreated dental caries compared with never-users. Established cocaine users had a higher prevalence of any periodontitis, severe periodontitis, and untreated dental caries compared with that of never-users.42
Users can suffer from bruxism, commonly leading to pain around the temporomandibular joint and muscles of mastication, in addition to tooth attrition and abrasion. Repeated intranasal snorting can lead to chronic congestion and a runny nose. Long-term irritation of the nasal mucosa can lead to the development of ulcers, nosebleeds and, at worst, nasal septal or palatal perforations.43
Cocaine blocks nerve conduction similarly to lidocaine and articaine, therefore enhancing the body's response to adrenaline, which is used as a vasoconstrictor in local anaesthetics.44 Administration of a local anaesthetic after recent cocaine use may lead to an acute increase in blood pressure. Furthermore, the use of lidocaine in a cocaine-using patient may increase the chance of convulsions. In these cases, dental treatment should be delayed for at least 6 hours following cocaine use, with only adrenaline-free local anaesthetics and retraction cords being used.45
Cocaine users are at an increased risk of undergoing treatment under general anaesthesia,46 particularly if ketamine (a reuptake inhibitor of endogenously released noradrenaline) is included in the anaesthetic regimen.47 Furthermore, there links between chronic cocaine usage and the developmental of cluster headaches, often characterized by mostly unilateral, moderately severe, headaches starting around the eye or lateral side of the nose, radiating to the maxillary teeth, zygomatic or mastoidal area have been seen.48 Be wary should any such patient present with these symptoms alongside atypical nasal symptoms, such as frequent nosebleeds or maxillary sinusitis because this may hint toward regular/frequent cocaine usage.48
Studies have shown that users presenting with palatal erosion as a result of chronic cocaine use may be more at risk of developing osteonecrosis of the jaw (ONJ) in the maxilla; however, more research is required.49 Palatal erosions or perforations may create challenges for constructing dentures. When taking impressions, care should be taken to ensure that material does not become locked into undercuts, for example, by using gauze to pack any defects.
MDMA
MDMA elicits mental and physical effects on the entire body. MDMA can cause bruxism, with studies showing users reported that jaw clenching persisted for up to 24 hours following use of the drug.50 Furthermore, evidence suggests that larger doses of ecstasy are related to more severe jaw clenching.51 Users combat these symptoms through the use of chewing gum or lollipops. Bouts of xerostomia may also be experienced during use. These symptoms may persist following initial use, with 93–99% of users experiencing a dry mouth.52 To alleviate this, users may consume excess acidic fluid (either alcohol, sugary or carbonated drinks), which, in conjunction with reduced salivary flow and bruxism, may lead to an increased risk of damage to tooth structure.53
Studies have also shown links between the use of MDMA and the development of oral ulcers. Biancardi et al reported a case of two young patients who presented with painful multifocal oral erosions and ulcerations. Histopathology revealed superficial ulceration surrounded by acanthotic squamous epithelium with marked spongiosis, interstitial oedema and perivascular lymphoid infiltrate, suggestive of drug-induced oral mucositis.54 Similarly, Brazier et al outlined a case of a 15-year-old patient who presented with swelling around the maxillary labial vestibule alongside mobility of both maxillary central incisors following storage of an ecstasy tablet in his upper anterior vestibule 24 hours prior to the onset of his symptoms. This was treated with sub- and supra-gingival debridement, topical fluoride application and fixation of the mobile maxillary central incisors. The mucosal ulcer had healed at 1 week review and 4 months after presentation, the teeth were firm and vital; however, a 2–3-mm localized defect of the alveolar gingivae remained.55
If a patient who has recently taken ecstasy needs to undergo dental treatment, caution should be taken when administering local anaesthetic containing adrenaline. Ecstasy induces a systemic increase in blood pressure, which may be enhanced by this vasoconstrictor and the anticipated stress of treatment.56 Lastly, soft tissue injuries of the oral mucosa requiring surgical closure may sometimes be seen.57
Nitrous oxide
When released from a pressurized canister N2O is extremely cold. This can cause hypothermic skin trauma (frost burns) in the mouth, vocal cords and lungs. Users may try to extend the effects by exhaling into, and re-inhaling from, balloons filled with N2O, which may cause hypoxia or even asphyxia.58 The lack of oxygen can cause users to become disorientated with a risk of tripping, falling and collapse which is increased with alcohol;59 however, at present there is no evidence to suggest a concrete link between N2O use and increased risks of dental trauma. Traffic accidents may also occur when N2O has been used, as studies show driving is impaired for up to 30 minutes after initial use.60
Chronic abuse of N2O can cause permanent neurological damage, while rebreathing in an enclosed space can cause hypoxia and death via asphyxia. Fatalities can occur through contaminated supplies, through trauma or aspiration, particularly when taken with other drugs or alcohol. Dentists should be aware of the various presentations and dangers of this drug.61
Heroin/methadone/opiates
The impacts of heroin and methadone are well documented and include personal neglect, suboptimal oral hygiene, xerostomia, rampant caries and periodontal disease.62 Chronic opioid use is known to cause altered taste preferences by modulating the kappa and mu receptors. This may explain why users prefer highly cariogenic foods and beverages.63,64 Studies have shown that users are susceptible to smooth surface, buccal and cervical caries, often present prior to beginning methadone therapy. Because heroin acts as a powerful analgesic, users may only present with dental problems once they are stabilized on methadone and their dental pain becomes a main complaint.65
Methadone can be prepared in both sugar-containing and sugar-free formulations. The sugar-containing formula is more palatable.
Chronic use of sugar-based methadone formulations has been associated with widespread, rapidly progressing caries, although it is unlikely that sugar-based methadone is the primary cause for rapid disease progression. Other factors, such as poor oral health and neglect, are more likely to be the main cause with methadone exacerbating these problems.66 Methadone users are known to retain the syrup in the mouth for some time, resulting in a prolonged attack on the teeth.67 This may be done to increase the absorption time or with a view of regurgitating it for later sale or intravenous use.68
In patients with a history of IV drug abuse (such as opiates), venous access can be challenging, and can affect the success of intravenous sedation. Additionally, this cohort of patients may present with an increased tolerance to opiates and require more than standard therapeutic doses to achieve adequate sedation. Potentially serious drug interactions, resulting in hypotension, cardiac arrest and respiratory depression can occur between IV sedative drugs and opiate agonists and other central nervous system depressant drugs, therefore referral to secondary care or a specialist sedation service should be considered if intravenous sedation is required.23
Heroin use can cause thrombocytopenia putting patients at risk of post-operative bleeding, particularly if liver function is impaired due to concomitant alcohol use or viral hepatitis.69 Patients may require blood tests for a platelet count, prothrombin time (PT), partial thromboplastin time (PTT) and international normalized ratio (INR) prior to treatment in order to ascertain this risk.
Intravenous drug use is one of the leading causes of infective endocarditis (IE) in developed countries.70 Although antibiotic prophylaxis prior to dental treatment is not routinely recommended,71 if a patient has had a previous episode of IE, they will fall into the special consideration group at higher risk of IE. This means that they might require antibiotic prophylaxis for invasive dental procedures in consultation with their cardiologist. The patient should also be educated about their risk, and the importance of maintaining good oral health by treating any dental infections promptly and maintaining good oral hygiene.72
Conclusion
There is a clear role for clinicians, in both primary and secondary care, to ask a patient about recreational drug use (past and present) within their social history, similarly to how one would enquire about alcohol or nicotine use. In these cases a set, formulated approach may not be successful, therefore flexibility and open discussion is recommended. Furthermore, it is evident that illicit drug use can affect a patient's general and oral health, increasing the risks for caries, periodontal disease, temporomandibular disorder and of developing oral cancer. The importance of regular dental assessments, detailed oral hygiene advice, including the prescription of high fluoride toothpaste (5000ppm) in this patient category is recommended. The risks of treating these patients under both local anaesthetic and IV sedation are well documented, and caution should be taken, with referrals to secondary care being considered where appropriate.
Discussion of these often sensitive issues with patients should be encouraged, even if it is difficult owing to the taboo surrounding them. It will ensure patient safety, and where desired, the opportunity for referral to cessation/rehabilitation services.