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Intervenciones en el lugar de trabajo para el abandono del hábito de fumar

Appendices

Appendix 1. Search Strategy for Register

Strategy for Tobacco Addiction Group Specialised Register
via Cochrane Register of Studies (CRS)
#1 workplace*:TI,AB,KY,XKY,MH,EMT
#2 worksite*:TI,AB,KY,XKY,MH,EMT
#3 work:KY,XKY,MH,EMT
#4 occupational health:KY,XKY,MH,EMT
#5 #1 OR #2 OR #3 OR #4

(KY, XKY, MH & EMT are keyword fields)

Appendix 2. Search strategies for electronic databases

Strategies used for update in 2013

Strategy for EMBASE

1. health behavior/
2. health promotion/
3. health education/
4. prevention/ or primary prevention/
5. mass screening/
6. 1 or 2 or 3 or 4 or 5
7. workplace/
8. (smok* or tobacco).mp.
9. 6 and 7 and 8
10. limit 9 to exclude medline journals
11. ("2008" or "2009" or "2010" or "2011" or "2012" or "2013").yr.
12. 10 and 11

Strategy for MEDLINE

1. exp Health Behavior/
2. exp Health Education/
3. Health Promotion/
4. Healthy People Programs/
5. exp Primary Prevention/
6. 1 or 2 or 3 or 4 or 5
7. Work/
8. Workplace/
9. Occupational Health/
10. 7 or 8 or 9
11. (smok* or tobacco).mp.
12. 6 and 10 and 11
13. ("2008" or "2009" or "2010" or "2011" or "2012" or "2013").yr.
14. 12 and 13

Strategy for PsycINFO

1. health behavior/
2. health promotion/
3. health education/
4. health care psychology/
5. prevention/ or preventive medicine/
6. health screening/
7. 1 or 2 or 3 or 4 or 5 or 6
8. occupational health/
9. workplace*.tw.
10. 8 or 9
11. (smok* or tobacco).mp.
12. ("2008" or "2009" or "2010" or "2011" or "2012" or "2013").yr.
13. 7 and 10 and 11 and 12

Appendix 3. Glossary of tobacco‐related terms

Term

Definition

Abstinence

A period of being quit, i.e. stopping the use of cigarettes or other tobacco products, May be defined in various ways; see also:
point prevalence abstinence; prolonged abstinence; continuous/sustained abstinence

Biochemical verification

Also called 'biochemical validation' or 'biochemical confirmation':
A procedure for checking a tobacco user's report that he or she has not smoked or used tobacco. It can be measured by testing levels of nicotine or cotinine or other chemicals in blood, urine, or saliva, or by measuring levels of carbon monoxide in exhaled breath or in blood.

Bupropion

A pharmaceutical drug originally developed as an antidepressant, but now also licensed for smoking cessation; trade names Zyban, Wellbutrin (when prescribed as an antidepressant)

Carbon monoxide (CO)

A colourless, odourless highly poisonous gas found in tobacco smoke and in the lungs of people who have recently smoked, or (in smaller amounts) in people who have been exposed to tobacco smoke. May be used for biochemical verification of abstinence.

Cessation

Also called 'quitting'
The goal of treatment to help people achieve abstinence from smoking or other tobacco use, also used to describe the process of changing the behaviour

Continuous abstinence

Also called 'sustained abstinence'
A measure of cessation often used in clinical trials involving avoidance of all tobacco use since the quit day until the time the assessment is made. The definition occasionally allows for lapses. This is the most rigorous measure of abstinence

'Cold Turkey'

Quitting abruptly, and/or quitting without behavioural or pharmaceutical support.

Craving

A very intense urge or desire [to smoke].
See: Shiffman et al 'Recommendations for the assessment of tobacco craving and withdrawal in smoking cessation trials'
Nicotine & Tobacco Research 2004: 6(4): 599‐614

Dopamine

A neurotransmitter in the brain which regulates mood, attention, pleasure, reward, motivation and movement

Efficacy

Also called 'treatment effect' or 'effect size':
The difference in outcome between the experimental and control groups

Harm reduction

Strategies to reduce harm caused by continued tobacco/nicotine use, such as reducing the number of cigarettes smoked, or switching to different brands or products, e.g. potentially reduced exposure products (PREPs), smokeless tobacco.

Lapse/slip

Terms sometimes used for a return to tobacco use after a period of abstinence. A lapse or slip might be defined as a puff or two on a cigarette. This may proceed to relapse, or abstinence may be regained. Some definitions of continuous, sustained or prolonged abstinence require complete abstinence, but some allow for a limited number or duration of slips. People who lapse are very likely to relapse, but some treatments may have their effect by helping people recover from a lapse.

nAChR

[neural nicotinic acetylcholine receptors]: Areas in the brain which are thought to respond to nicotine, forming the basis of nicotine addiction by stimulating the overflow of dopamine

Nicotine

An alkaloid derived from tobacco, responsible for the psychoactive and addictive effects of smoking.

Nicotine Replacement Therapy (NRT)

A smoking cessation treatment in which nicotine from tobacco is replaced for a limited period by pharmaceutical nicotine. This reduces the craving and withdrawal experienced during the initial period of abstinence while users are learning to be tobacco‐free The nicotine dose can be taken through the skin, using patches, by inhaling a spray, or by mouth using gum or lozenges.

Outcome

Often used to describe the result being measured in trials that is of relevance to the review. For example smoking cessation is the outcome used in reviews of ways to help smokers quit. The exact outcome in terms of the definition of abstinence and the length of time that has elapsed since the quit attempt was made may vary from trial to trial.

Pharmacotherapy

A treatment using pharmaceutical drugs, e.g. NRT, bupropion

Point prevalence abstinence (PPA)

A measure of cessation based on behaviour at a particular point in time, or during a relatively brief specified period, e.g. 24 hours, 7 days. It may include a mixture of recent and long‐term quitters. cf. prolonged abstinence, continuous abstinence

Prolonged abstinence

A measure of cessation which typically allows a 'grace period' following the quit date (usually of about two weeks), to allow for slips/lapses during the first few days when the effect of treatment may still be emerging.
See: Hughes et al 'Measures of abstinence in clinical trials: issues and recommendations'; Nicotine & Tobacco Research, 2003: 5 (1); 13‐25

Relapse

A return to regular smoking after a period of abstinence

Secondhand smoke

Also called passive smoking or environmental tobacco smoke [ETS]
A mixture of smoke exhaled by smokers and smoke released from smouldering cigarettes, cigars, pipes, bidis, etc. The smoke mixture contains gases and particulates, including nicotine, carcinogens and toxins.

Self‐efficacy

The belief that one will be able to change one's behaviour, e.g. to quit smoking

SPC [Summary of Product Characteristics]

Advice from the manufacturers of a drug, agreed with the relevant licensing authority, to enable health professionals to prescribe and use the treatment safely and effectively.

Tapering

A gradual decrease in dose at the end of treatment, as an alternative to abruptly stopping treatment

Titration

A technique of dosing at low levels at the beginning of treatment, and gradually increasing to full dose over a few days, to allow the body to get used to the drug. It is designed to limit side effects.

Withdrawal

A variety of behavioural, affective, cognitive and physiological symptoms, usually transient, which occur after use of an addictive drug is reduced or stopped.
See: Shiffman et al 'Recommendations for the assessment of tobacco craving and withdrawal in smoking cessation trials'
Nicotine & Tobacco Research 2004: 6(4): 599‐614

Risk of bias summary: review authors' judgements about each risk of bias item for each included study. Empty cells are for multiple studies within a single study report.
Figuras y tablas -
Figure 1

Risk of bias summary: review authors' judgements about each risk of bias item for each included study. Empty cells are for multiple studies within a single study report.

Comparison 1 Individual Treatments, Outcome 1 Group behavioural therapy (various endpoints).
Figuras y tablas -
Analysis 1.1

Comparison 1 Individual Treatments, Outcome 1 Group behavioural therapy (various endpoints).

Comparison 1 Individual Treatments, Outcome 2 Individual counselling (various endpoints).
Figuras y tablas -
Analysis 1.2

Comparison 1 Individual Treatments, Outcome 2 Individual counselling (various endpoints).

Comparison 1 Individual Treatments, Outcome 3 Any self‐help intervention (various endpoints).
Figuras y tablas -
Analysis 1.3

Comparison 1 Individual Treatments, Outcome 3 Any self‐help intervention (various endpoints).

Comparison 1 Individual Treatments, Outcome 4 Pharmacological treatments (various endpoints).
Figuras y tablas -
Analysis 1.4

Comparison 1 Individual Treatments, Outcome 4 Pharmacological treatments (various endpoints).

Comparison 1 Individual Treatments, Outcome 5 Social support (various endpoints).
Figuras y tablas -
Analysis 1.5

Comparison 1 Individual Treatments, Outcome 5 Social support (various endpoints).

Comparison 2 Worksite Treatments, Outcome 1 Environmental support (various endpoints).
Figuras y tablas -
Analysis 2.1

Comparison 2 Worksite Treatments, Outcome 1 Environmental support (various endpoints).

Comparison 2 Worksite Treatments, Outcome 2 Incentives (various endpoints).
Figuras y tablas -
Analysis 2.2

Comparison 2 Worksite Treatments, Outcome 2 Incentives (various endpoints).

Comparison 2 Worksite Treatments, Outcome 3 Comprehensive interventions.
Figuras y tablas -
Analysis 2.3

Comparison 2 Worksite Treatments, Outcome 3 Comprehensive interventions.

Study

Baseline/follow‐up

Smoking outcome

Validated ?

Bergstrom 2008

About 881 smokers across 4 companies risk‐assessed and given SC classes and NRT; about 98 controls assessed only

No MA data, but logistic regression results over 10 timepoints for 3½ years. Significant reductions in gradient relative to controls in Companies 1 (‐0.6), 2 (‐0.92) and 4 (‐0.45), not in Company 3 (‐0.09).

No indication of validation (all long‐term data collected by post or phone)

Cambien 1981

304 intervention smokers recalled at 2 yrs, and 306 control smokers. 195 participants lost to follow up, proportion of smokers not reported

21.4% of intervention smokers quit, vs 13.4% of control smokers. Point prevalence at 2 yrs, not a significant difference

Validation by blood CO levels

Campbell 2002

538 women in 9 worksites (4 exp, 5 control) completed all surveys (282 I, 256 C) to 18m.

No raw data given for smoking, but prevalence went down by around 3% in both groups. No significant differences, and no p values.

Self‐report on all outcomes, no biochemical validation

Dawley 1991

2 US oil refineries randomized to eenviornmental anti‐smoking campaign + SC programme, versus SC programme alone.

7/16 smokers in the comprehensive programme site had quit at 5m, versus 3/14 at the SC only site.

Self report only, no biochemical validation

DePaul 1987

425 smokers in 43 corporations, randomised to group support programmes or self‐help alone programmes
Attrition rate was 8% in both groups

6% vs 2% continuously abstinent (NS), 19% in both groups were abstinent at 12 months point prevalence.
Companies were the unit of analysis, similar results found using individual as unit of analysis.
(See also Cochrane Review 'Self‐help interventions for smoking cessation')

Partial validation by salivary cotinine, with family and colleague report

DePaul 1989

419 smokers in 38 worksites, randomised to experimental programme (206) and comparison programme (213). The attrition rate was 17% for Group worksites and 29% for Non Group worksite participants, so correcting the data for attrition would increase the apparent efficacy of the Group condition.

At the company level of analysis the 12 month point prevalence quit rates were Group 26% vs No Group 16% (p<0.06); continuous abstinence rates were 11% (Group) vs 3% (No Group) (p<0.05).
Reported rates were not based on Intention to Treat, but on participation in the programmes. Correcting for attrition would increase the efficacy of the Group programme.
At 24 months, 30% of the Group smokers were abstinent, comnpared with 19.5% of Non‐Group smokers (no p value).
(See also Cochrane Review 'Self‐help interventions for smoking cessation')

Partial validation by salivary cotinine, with family and colleague report

DePaul 1994

844 smokers in 61 worksites, randomised to Self‐help [SH] (289), Incentives [I] (281) or Group support [G] (283).
12 month attrition rates were 52.5% in SH, 47.2% in I, and 37.5% in G.

12 month quit rates for sustained abstinence were 5.1% (n=79) SH, 11% (n=91) I, 31.2% (n=109) G (p<0.01). An Intention to Treat analysis, taking account of attrition, would further favour the intervention groups.
(See also Cochrane Review 'Self‐help interventions for smoking cessation')

Validation by salivary cotinine at 6 months, and CO<9ppm at 12 months

Emmons 1999

2055 workers (28% smokers) completed all surveys from 22 worksites, and constituted the cohort.

At 3 yr final follow up, 8.0% of the intervention smokers had quit for 6m, and 8.1% of the control smokers. 25.6% and 21.8% respectively claimed 7‐day PP. Differences were non‐significant

Self‐report, with no biochemical validation

Erfurt 1991

Four sites were assessed at baseline; Site 1 had 1096 smokers (45%), Site 2 598 (44%), Site 3 844 (41%) and Site 4 834 (44%).
At 3 year follow‐up Site 4 had been significantly restructured.

Participation was affected by the intervention: 5% in Site 1, 9% in Site 2, 53% in Site 3 and 58% in Site 4.
Possible bias due to different baseline characteristics of people rescreened in site 3 & 4 limit interpretation of follow‐up smoking prevalences: 41.6%, 40.6%, 36.1%, 31.0%
All sites had significant relative reductions in smoking: 7.8% (p<0.01), 10.6% (p<0.01), 11.7% (p<0.001), 13.2% (p<0.001).
Of those smoking in 1985 who were re‐screened in 1988, 17.1% at Site 1 had quit, 17.6% at Site 2, 20.3% at Site 3 and 18.9% at Site 4 (NS).

Self‐report only, not biochemically validated

Frank 1986

48 smokers initially randomised to three groups, with varying levels of hypnosis, booster and self‐management training. A 4th group (15 smokers) was later recruited, with Group 2 interventions applied more intensively.
Attrition rate of 6% across the initial 3 groups at end of treatment, 17% at 3 months and 25% at 6 month follow‐up.

No difference between the groups for smoking cessation 6 months after treatment, regardless of the frequency, length between sessions, or addition of behavioural methods. Quit rate was 20% for all groups, based on Intention to Treat.
Intensive intervention produced initially higher quit rates (60% at end of treatment), but this reverted to 20% by 6 months
(See also Cochrane Review 'Hypnotherapy for smoking cessation')

Salivary cotinine measured at 3 months, but self‐report only at 6 months

Glasgow 1984

36 employees, randomised to abrupt reduction (13), gradual reduction (12) and gradual reduction + feedback (11).
Attrition at 6 months was respectively 4, 0 and 1.

At 6 months up to one third in the gradual condition were abstinent compared to no subjects in the abrupt condition (NS).
Intention to Treat analysis showed that the gradual reduction programme was more successful than the abrupt reduction (p<0.05)

CO<10 ppm at 6 months, weighing of cigarette butts

Glasgow 1986

29 employees randomised to Basic Programme (13) or Basic Programme + Social Support (16).
Attrition 7% at end of treatment, and a further 7% at 6 months

Consistent with previous findings, supportive social interactions were not related to treatment outcome.3/13 in the Basic Programme had quit at 6 months, and 3/16 in the Basic + Social Support Group (NS).
(See also Cochrane review 'Enhancing partner support to improve smoking cessation').

Self report, weighing of cigarette butts, CO monitoring and salivary thiocyanate

Glasgow 1993

19 worksites, random allocation to Incentive programme (474 smokers) or No Incentive programme (623 smokers).
Attrition rates at 1 year were 19% (I) and 24% (no I), and at 2 years were 27% and 32% respectively

At 2 year follow‐up 49/344 (14%) were abstinent in the Incentives group, and 49/426 (12%) in the No incentives group (NS). Intention to Treat analysis would give more conservative quit rates

CO monitoring and salivary cotinine

Glasgow 1995

26 worksites, randomised to early or delayed interventions. 1222 employees were followed up at all assessment points to 2 years. years.

Comprehensive programme; a 26% rate of cessation was noted across both longitudinal cohort groups (NS), and a 30% rate across both cross‐sectional groups (NS). No significant differences were seen between the 2 types of intervention

Self report, not biochemically validated

Gomel 1993a

28 ambulance stations randomized to 4 levels of risk reduction intervention. 128 baseline smokers followed for 1 yr

No significant differences between HRA and RFE groups at any follow‐up point, nor between BC and BCI groups. HRA and RFE groups (68 smokers) were pooled and compared with 60 smokers in pooled BC and BCI groups. Continuous abstinence rates at 6m were 1% for HRA+RFE and 10% for BC+BCI (Fisher's Exact Test P = 0.05); 12m rates were 0% and 7% (P = 0.05).

Serum cotinine validation used.

Groeneveld 2011

115 intervention smokers got MI + phone counselling, and 123 controls received 'usual care'.

PPA at 6 and 12m. Study used as denominators only those with complete follow‐up data, who had attended at least 5 sessions. On this basis, 6m quit rates were (I) 31.2%, (C) 13.4%, and 12m (I) 23.75, (C) 19.5. Our ITT analysis gives 6m: (I) 21.7%, (C) 8.9%: 12m: (I) 16.5%, (C) 13%.

No biochemical validation

Gunes 2007

200 smokers randomized to 7‐step behavioural programme or no intervention, followed for 6m

Main outcome was movement through stages of change. Smoking cessation at 6m was (I): 6/100, (C) 2/100.

Probably no validation (not mentioned)

Hennrikus 2002

24 worksites, randomised to 6 programmes, 4 worksites in each programme. 2402 smokers were surveyed at baseline and at 12 and 24 months. 85.5% response rate at 12 months, and 81.7% at 24.

407 (17%) smokers signed up to programmes. 15.4% at 12 months and 19.4% at 24 months reported themselves as non‐smokers.
Recruitment was significantly higher in the incentive sites (22% vs 12% p=0.0054), but did not translate into higher cessation rates.
Quit rates were consistently higher among programme registrants than among non‐registrants, but the differential was greater in the non‐incentive sites (15%) than in the incentive ones (6.7%), consistent with incentives attracting smokers less motivated to quit.

Self‐report, validated by family member or friend.
A sample of quitters were asked to supply saliva, and were paid $25 if they complied.
Winners of cessation prize draws had to supply a valid saliva sample.

Hishida 2010

257 smokers genotyped, given self‐help booklet; 276 controls assessment only.

At 12m, 15/257 intervention smokers had quit, versus 22/276 control smokers. Intervention smokers at genetically higher risk of smoking‐related cancers (5.6% and 7.1%) did not perform differently from the low‐risk smokers (4.9%, P = 0.723). Possible confounding by legislation preventing passive smoking.

Self report only, not verified.

Hymowitz 1991

Six worksites randomised to Full Programme or Group‐only interventions. Participation was 50% in the Full Programme sites, and 44% at Group‐only (NS).
193/252 smokers who began the quit programme completed it.
Randomisation was by worksite, but analysis was by individual.

At 12 months, 23/131 (18%) in the Full Programme arm had quit, while 27/121 (22%) in the Group‐only arm had quit (NS).

Self‐report and expired CO < 8 ppm.

Kadowaki 2000

263 male employees randomised to intervention (132) or control (131).
No attrition, as inclusion was compulsory.

Quit rates 17/132 (Intervention), 4/131 (Control) at 5‐month follow‐up (p=0.003). Male smoking decreased from 62.9% to 56.7% (p=0.04).
Delayed intervention in the control group lead to 13% quit rate (16/123)

Expired CO<9 ppm at baseline, 5 months and 12 months, and a urine test at 12 months

Klesges 1987

8 Oregon worksites (127 participating smokers), randomized to group behavioural intervention, + either a 2x2 competition component or a 2x2 relapse prevention component

At 6m, 15/127 had quit; Competition sites 12%, no‐competition 11%.

CO < 10 ppm and saliva thiocyanate

Kornitzer 1980

30 Belgian factories (16,230 men) randomized to intervention (risk assessment, physician and written advice) or control (assessment only). tested at 2 yrs.

High risk intervention group (n = 1268) reduced prevalence by 18.7% (84.5% to 68.7%), and high risk control group (n = 202) reduced by 12.2% (80.8% to 70.9%). P < 0.05.
Random sample comparison: 5% of intervention group (n = 327) reduced by 12.5%, compared with 10% control sample (n = 800) reduced by 12.6% (ns).

Self report only, no biochemical validation.

Kornitzer 1995

374 employees randomised to Group 1(149, active patch + active gum), Group 2(150, active patch + placebo gum) or Group 3 (75, placebo patch + placebo gum)

At 12 months, abstinence in Group 1 was 18.1% (NS), in Group 2 12.7% (NS) and in Group 3 13.3% (NS). Time to relapse was significantly longer in Group 1 compared with the other 2 groups (p=0.04).

Salivary cotinine at baseline, and expired CO<10 ppm at subsequent checks

Lang 2000

30 worksite physicians (1095 smokers) were randomised to Group A (504, simple advice) or Group B (591, advice + support and 'contract').

2 physicians dropped out post randomisation.
3.4% of baseline non‐smokers in each group were smokers at 1 year follow‐up.
The sustained abstinence rate at 6 months or more (A: 4.6%; B: 6.1%) was non‐significant using the physician as the unit as analysis.
At 12 months, Group A had a quit rate of 13.5%, and Group B a rate of 18.4% (p=0.03)

Self‐report, with CO<7 ppm validation on a subset of 231 subjects whose physicians had access to a CO monitor.

Li 1984

871 employee smokers, randomised to Group 1 (simple warning) or Group 2(brief physician advice), stratified by normal/abnormal lung function.
After fine tuning, at 3 months 215 workers received counselling, while 361 received simple warning and 3 were excluded.
Attrition was 30%.

Counselled workers had an 8.4% abstinence rate at 11 months, compared with 3.6% in the control group (p<0.05).
Feedback on abnormal lung function was not significantly related to increased rates of quitting

Expired CO<10 ppm at 11 months follow‐up in all quitters, and in a random sample of 379 continuing smokers

Malott 1984

24 employees randomised to controlled smoking Group (1) or controlled smoking + partner support Group (2).
Attrition 4% at 6 months

Few differences were observed between controlled smoking and controlled smoking plus partner support conditions either during treatment or at the 6‐month follow‐up. 25% of Group 1, and 17% of Group 2 were abstinent at 6 months (NS).
(See Cochrane review 'Enhancing partner support to improve smoking cessation').

Self‐monitoring, butt counts, expired CO levels

Mayer 2010

275 abstainers randomized by company to proactive phone counselling (134) or to worksite‐based group counselling (141) for relapse prevention.

No significant differences at 9m: Phone counselling 57.5% and group counselling 61.7% remained abstinent (P = 0.552).

4‐wk CA assessed by CO < 10 ppm, and by urinary cotinine ≤ 317 ng/ml.

Milani 2009

Two sites chosen; 33 intervention smokers received comprehensive CV risk programme, including referral to SC programme, and 31 controls.

6/33 intervention smokers quit at 6m, versus 0/31 controls. Cost effectiveness analysis reported.

Not stated, but probably unvalidated.

Mishra 2010

Tobacco users in 4 call centres (63 control, 204 intervention) received increasing levels of support and bupropion; controls got self‐help leaflets. 99% received long‐term counselling.

6m PA at 12m rates were 4/63 (controls), 17/87 BPO2 (HE sessions + focus groups), 8/43 BPO3 (as BPO2 + individual counselling), and 15/74 BPO4 (as BPO3 + bupropion offered); high turnover (52.4%) but only 1% lost to follow‐up.

CO monitor < 6ppm.

Nilsson 2001

113 workers randomised to intervention (65) or control (63).
Attrition at 12 months was 32% for the intervention group, and 24% for the control group. At 18 months the respective attrition rates were 34% and 27%.

Baseline prevalence for both groups was 65%. At 12 months the intervention group point prevalence rate was 37%, and the control group 63%. At 18 months, the rates were 40% (of 43) and 59% (of 46) respectively. This difference influenced the decrease in mean risk score from 10.3 to 9.0 after 18 months in the intervention group (P = 0.042)

Self‐report, not biochemically validated

Noor 2011

77 male intervention smokers randomized to 24 wks of Viva QS tablets + brief counselling; 78 male control smokers randomized to placebo tablets. Attrtition was 1 intervention and 3 controls at start of study.

At wk 24 all pts had face‐to‐face meeting at workplace for smoking status. Intervention 20‐wk CA quit rate 19/75, controls 9/72. Similar AEs (sore throat: I 28.8%, C 36.6%; dry mouth: I 17.8%, C 16.9%).

All pts cotinine‐ (< 50 ng/ml) and CO‐ (< 8 ppm) tested at 24 wks, whether claiming abstinence or not. 54 24‐wk urine samples not analysed, so only CO reliable.

Okechukwu 2009

251 intervention smokers (4 sites) and 239 control smokers (6 sites) had 4m programme of counselling, self help, NRT and environmental cues. Attrition at 6m post‐programme was I 2%, C 1.7%.

At 6m, 22/245 intervention and 17/235 controls had PA quit. 2/10 sites had delayed assessment (8m and 9m).

Not verified (fear of 'drug‐testing, + possibility of industrial toxin contamination).

Omenn 1988

402 employee smokers randomised within their preference for group or self‐help programmes, to 3 programmes, MCP (1), RPP (2) or MTP (3).
7% attrition rate at 12 months.

Self‐reported quit rates similar across all three group preference conditions but more missing saliva samples in self‐help so validated rates lower.
All self‐help programmes similar.
Results: Group 1 8/51, Group 2 10/57, Group 3 4/51 (NS)
SH1 7/76, SH2 9/82, SH3 6/85 (NS)

Salivary cotinine at 12 months < 35 ng/ml

Prochaska 2008

48 smokers randomized to the HRI group, 40 to the MI group, and 48 to the TTM group. Attrition was 25.7% at 6m (distribution NK)

PPA at 6m ("at criteria") was estimated at 8/48 for HRI alone, 14/40 for HRI + MMI, 10/48 for HRI + TTM; 6m denominators not reported (no reply from authors), so we have applied 6m quit rates to baseline smoking rates.

Not stated, but probably no validation.

Rand 1989

47 employees randomised to contingent payment/frequent CO monitoring group (17), non‐contingent payment/frequent CO monitoring (16), non‐contingent payment/ infrequent monitoring (14).
4 participants failed to abstain for 5 days, and were excluded before randomisation.
At 6 months 11 more participants had dropped out. Analyses were Intention to Treat at randomisation.

Contingent payment combined with frequent CO monitoring delayed but did not ultimately prevent participant relapse to smoking by the end of the six month follow‐up. Contingent payment group had CO value at or less than 11 ppm significantly longer than the other two groups (p=0.03). CO monitoring alone had no effect on abstinence.
At six months, only 2 subjects ( 1contingent, 1 non‐contingent) had achieved sustained abstinence.

Expired CO monitoring <12 ppm

Razavi 1999

344 post‐cessation abstainers randomised to psychologist support (135), ex‐smoker support (88), or no formal support (121),

12 months abstinence rates were 59/135 (43.7%) in the PG group; 33/88 (37.5%) in the SG group; 43/121 (35.5%) in no support group (NS).

Expired CO and urinary cotinine. Unvalidated self‐report (higher) were also given.

Rodriguez 2003

218 smokers randomized to counselling + NRT (115) or minimal sporadic advice (103) in 3 Bilabao (Spain) worksites

12 months continuous abstinence rates were 23/114 (20.2%) for the intervention group, vs 9/103 (8.7%) in the control group (P = 0.025).
NNT was 9 people treated for 3mss to produce 1 quitter

Expired CO <+ 10 ppm

Schröter 2006

38 smokers assigned to standard behavioural (SB) programme, 41 to relapse prevention (RP) programme.
Assessed at 12m for continuous and PP abstinence

12m continuous abstinence rates were 8/38 (21.1%) for SB, and 5/41 (12.2%) for RP.

Self‐reported, no biochemical validation

Shi 1992

2887 workers (533 smokers) across 9 Californian sites, partially randomized to 4 intervention levels. No non‐intervention control group 

2 yr cross‐sectional survey of 1998 workers (250 smokers); Prevalence declined by 34% from 18% to 12% in Level 1 (p < 0.1); by 18% from 17% to 14% in Level 2 (p < 0.1); by 35% from 24% to 15% in level 3 (p < 0.01); by 44% from 14% to 8% in Level 4 (p < 0.01) 

Self‐reported PP at HRA, not biochemically validated 

Shimizu 1999

53 volunteer employee smokers, randomised to intervention and control groups.

After the 5 months of intervention, smoking cessation rate in the intervention group (19.2%) tended to be higher than that in the control group (7.4%), (NS).
Control group was given same programme after the 5 months for the intervention group. At six months after both groups were treated, overall cessation rate was 24.5%, and at one year was 13.2%.

Expired CO monitoring

Sorensen 1993

Eight worksites, randomised to intervention (1885 workers) or comparison (1479 workers).
At baseline, 9 months before intervention, 34% of respondents were current smokers (I:39%;C:31%)
Six‐month data were on only 7 of the 8 sites, because of ownership changes at the 8th. Six‐month survey was of all smokers then employed, = 66% of originally surveyed employees.
Analyses were by individual, while randomisation was by worksite.

Analysis of all smokers, not just participants.
At the 6‐month follow‐up, 12% of smokers in the intervention group reported quitting, compared with 8.8% in the control group (p<0.05), controlling for age, sex & occupation.

Self‐report only.
Baseline and follow‐up salivary cotinines obtained for 52% of baseline smokers. These data were not analysed.

Sorensen 1996

108 matched worksites (>28,000 workers), randomised to intervention or control conditions, though Florida center sites did not target smoking, leaving smoking outcomes available in only 84 worksites.

Worksite was the unit of allocation and analysis. Baseline smoking data were not reported in detail.
There was a difference of 1.53% (NS) in the 6‐month quit rates between intervention and control sites, and a reduction in prevalence from 24.5% to 21.2% (I), and from 25.8% to 21.8% (C), a difference between the 2 groups of 0.66% (NS).

Self‐reported, no biochemical validation

Sorensen 1998

Cohort analysis (2658 employees) of a randomised controlled study of 12 matched pairs of worksites.
Worksite was unit of allocation, but analysis was by individual.

PP abstinence for the 6 months prior to 2‐year follow‐up was 15% for intervention group and 9% for control group (p=0.123)
Blue‐collar cessation rates for the 2 groups were 18% (I) and 9% (C), while the white‐collar workers achieved higher rates in the control than in the intervention group; office worker rates were 2.5% (I) vs 5.1% (C), and professipnal/managerial rates were 14.2% (I) vs 18.6% (C).

Self‐reported, no biochemical validation

Sorensen 2002

Cross‐sectional analysis (9019 at baseline [80%] and 7327 [65%] ) at six months follow‐up, plus cohort analysis of 5156 employees who responded to both surveys (embedded cohort of 436 smokers).
Worksite was unit of allocation, but analysis was by individual.

At six months, point prevalence in the HP/OHS sites fell from 20.4% to 16.3%, and in the HP sites from 18.6% to 17%.
In the embedded cohort (825 smokers) at 6m, the HP/OHS quit rate was 11.3%, compared with the HP rate of 7.5% (OR=1.57, p=0.17). Within the cohort, blue‐collar quit rates more than doubled in the HP/OHS sites (11.8%) compared with the HP sites (5.9%, p=0.04)

Self‐reported, no biochemical validation

Sorensen 2007

Baseline participants 674 workers, (354 Int/ 320 Cont).
188 smokers (101 Int, 87 Cont) completed baseline and 6m surveys

7‐day self‐reported PPA at 6m: Int: 19/101 (19%), Cont: 7/87 (8%) (P=0.03).
ITT analysis Int: 19/125 , Cont: 7/106, P = 0.04.

Self‐reported, no biochemical validation

Sutton 1987

270/334 interested smokers invited to nicotine gum cessation programme; the uninvited 64 represented a control group. 172 (64%) of invitees attended the 1st consultation, 163 the 2nd.
One‐year follow‐up rate was 99% (9% by phone).

12% (20/172) of those who attended the intervention course were abstinent at 12 months, compared with 1% (1/98) of those who did not accept the invitation, and 2% (1/64) of the control group; p values not given.

Expired CO<11 ppm

Sutton 1988a

Video programme (smoking, plus seat‐belt advice) was offered to all employees. 77 employees were randomised to DFF video (33) or seatbelt (44=control) videos.

Abstinence rates (DFF: 3%, SB [control] 0%) were not significantly different from each other at 12 months follow‐up, There was no significant difference in validated abstinence between the video groups and the non‐participant group.

Expired CO<11 ppm.

Sutton 1988b

150 employees (smokers only) participated. 46 watched the DFF video, 50 watched a confidence‐boosting version of the DFF video, and 54 (control group) watched LTK video.

Abstinence rates (DFF: 11%, DFF+C 8%, LTK [control] 9%) were higher than in the other 3 studies, but not significantly different from each other
at 12 months follow‐up. But there was a significant difference in abstinence rates between participant groups and the non‐participant group (4%, p<0.05).

Expired CO<11 ppm.

Sutton 1988c

197 employees (smokers only) participated. 56 watched the DFF video, 67 watched a less gory version of the DFF video, and 74 (control group) watched the TW video.
Non‐responder smokers at baseline had higher smoking prevalence (45%) than responders (29%), suggesting some response bias.

Abstinence rates (DFF: 4%, DFF‐G 3%, TW [control] 4%) were not significantly different from each other.
at 12 months follow‐up. There was no significant difference in abstinence rates between the video groups and the non‐participant group.

Expired CO<11 ppm.

Sutton 1988d

179 employees (smokers only) participated. 62 watched the DFF video, 59 watched SL video, and 58 (control group) watched TW video.
Non‐responder smokers at baseline had higher smoking prevalence (34%) than responders (22%), suggesting some response bias.

Abstinence rates (DFF: 3%, SL 2%, Tw [control] 5%) were not significantly different from each other at 12 months follow‐up. There was no significant difference in validated abstinence artes between the video groups and the non‐participant group.

Expired CO<11 ppm.

Sutton 1988e

Fourth study (D) of the video studies groups provided a nested RCT. 161 continuing smokers at 3‐month follow‐up were randomised to intervention (79) or control (82).
40.5% response rate, attending at least one consultation.

22% (7/32) of attenders in the intervention group were abstinent at 12 months, compared with 2% (1/47) of the non‐attending invitees, and compared with 2% (2/82)of the control group (p<0.001).
16% of intervention group achieved 'complete' sustained abstinence at 12 months, vs 2% control group (p<0.01).

Expired CO<11 ppm.

Tanaka 2006

Six intervention sites matched to 6 control sites; Of 1017 intervention smokers who completed baseline and 36m follow‐up, 125 participated in cessation campaign, and 79 accepted counselling + NRT.

6m sustained abstinence at 36m ITT analysis was 8.9% (123/1382) intervention vs 7.0% (121/1736) control (P = 0.0467). Quit rates in both groups rose steadily over 36m.

No biochemical confirmation

Terazawa 2001

228 smokers randomized to intervention (117) or control (111). 25 smokers in the intervention group made a supported quit attempt

PP 11.1% (13/117) in the intervention group at 12m, compared with 1.8% (2/111) controls. Continuous abstinence 6.8% (8/117) intervention, compared with 0.9% (1/111) controls. Fisher's Exact test 2‐tailed P = 0.04

Probably validated by expired CO

Volpp 2009

878 smokers randomized to intervention (436) or control (442); all got information about local SC programmes, and intervention also got stepped rewards for cessation efforts and goals. Attrition (losses + withdrawals) by 18m was 29% intervention and 24% controls.

At 15m or 18m 41/436 intervention and 16/442 control had quit (PA).

Confirmed by cotinine in saliva or urine.

Willemsen 1998

Four intervention worksites matched to 4 control sites (minimal self‐help), giving 498 smokers who completed baseline survey and enrolled in programmes.

Overall sustained abstinence quit rates at 6 months were 8% (9% for heavy smokers) in the comprehensive group, and 7% (4% for heavy smokers) in the minimal group (no p values given)

Self‐report, plus baseline Fagerstrom score.
At 4‐month follow‐up, 'bogus pipeline' procedure was used, and at 14 months salivary cotinines were collected from 41/79 quitters

Windsor 1988

387 smokers randomly assigned to four groups, in a 2x2 factorial pre‐/post‐test design.
37 were lost to follow‐up, and were counted as continuing smokers

As monetary incentives made no difference, groups 1&3 were compared with 2&4. Sustained abstinence at 1 year was 5.8% (11/190) in the self‐help only groups, and 14.4% (27/188) in the self‐help + counselling groups (p<0.001).

Baseline salivary cotinine, and follow‐up salivas at 6 weeks, 6 months and 1 year.

Figuras y tablas -
Analysis 3.1

Comparison 3 Results of included studies, Outcome 1 Results of included studies.

Summary of findings for the main comparison. Smoking cessation interventions for the workplace

Smoking cessation interventions for the workplace

Patient or population: Employees who smoke
Settings: Workplaces
Intervention: Smoking cessation interventions

Outcomes

Illustrative comparative risks* (95% CI)

Relative effect
(95% CI)

No of Participants
(studies)

Quality of the evidence
(GRADE)

Comments

Assumed risk

Corresponding risk

Control

Smoking cessation interventions

Group therapy
Follow‐up: 6‐24 months

51 per 1000

84 per 1000
(54 to 131)

OR 1.71
(1.05 to 2.80)

1309
(8 studies)

⊕⊕⊕⊝
moderate1,2,3

Individual counselling
Follow‐up: 6‐24 months

61 per 1000

113 per 1000
(89 to 141)

OR 1.96
(1.51 to 2.54)

3516
(8 studies)

⊕⊕⊕⊝
moderate3,4,5

Self‐help interventions
Follow‐up: 6‐24 months

45 per 1000

52 per 1000
(34 to 79)

OR 1.16
(0.74 to 1.82)

1906
(6 studies)

⊕⊕⊕⊕
high2,3

Pharmacological interventions
Follow‐up: 6‐24 months

77 per 1000

142 per 1000
(95 to 206)

OR 1.98
(1.26 to 3.11)

1092
(5 studies)

⊕⊕⊕⊕
high3,4

Limiting to NRT only (4 studies) reduced OR to 1.81 (1.07 to 3.08).

Incentives
Follow‐up: 6‐18 months

73 per 1000

113 per 1000
(82 to 154)

OR 1.60
(1.12 to 2.3)

1928
(5 studies)

⊕⊕⊕⊝
moderate3,6

Multiple interventions
Follow‐up: 6‐36 months

63 per 1000

95 per 1000
(71 to 126)

OR 1.55
(1.13 to 2.13)

5018
(6 studies)

⊕⊕⊕⊝
moderate3,4,7

*The basis for the assumed risk (e.g. the median control group risk across studies) is provided in footnotes. The corresponding risk (and its 95% confidence interval) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI).
CI: Confidence interval; OR: Odds ratio;

GRADE Working Group grades of evidence
High quality: Further research is very unlikely to change our confidence in the estimate of effect.
Moderate quality: Further research is likely to have an important impact on our confidence in the estimate of effect and may change the estimate.
Low quality: Further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate.
Very low quality: We are very uncertain about the estimate.

11 +outlier (Glasgow 1994); removing this study reduced the OR to 1.62 (0.98 to 2.66).
2Removing self‐reported (non‐validated) abstinence studies made no significant difference to the results.
3No funnel plot ‐ too few studies.
4Removing trials at high risk of bias made no difference
5Possibility of publication bias
6One trial (Volpp 2009) has 37% of the weight and is the only trial with positive findings. Removing it eliminates the statistical significance (OR 1.16 [0.73 to 1.83]).
7Two non‐validated, two partial validation, one 'bogus pipeline' and one CO.

Figuras y tablas -
Summary of findings for the main comparison. Smoking cessation interventions for the workplace
Comparison 1. Individual Treatments

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Group behavioural therapy (various endpoints) Show forest plot

10

Odds Ratio (Fixed, 95% CI)

Subtotals only

1.1 Cessation

8

1309

Odds Ratio (Fixed, 95% CI)

1.71 [1.05, 2.80]

1.2 Relapse prevention

2

484

Odds Ratio (Fixed, 95% CI)

1.15 [0.80, 1.65]

2 Individual counselling (various endpoints) Show forest plot

8

3516

Odds Ratio (Fixed, 95% CI)

1.96 [1.51, 2.54]

3 Any self‐help intervention (various endpoints) Show forest plot

6

1906

Odds Ratio (Fixed, 95% CI)

1.16 [0.74, 1.82]

4 Pharmacological treatments (various endpoints) Show forest plot

5

1092

Odds Ratio (Fixed, 95% CI)

1.98 [1.26, 3.11]

5 Social support (various endpoints) Show forest plot

2

53

Odds Ratio (Fixed, 95% CI)

0.69 [0.18, 2.62]

Figuras y tablas -
Comparison 1. Individual Treatments
Comparison 2. Worksite Treatments

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Environmental support (various endpoints) Show forest plot

4

3851

Odds Ratio (Fixed, 95% CI)

1.00 [0.60, 1.65]

2 Incentives (various endpoints) Show forest plot

5

1928

Odds Ratio (Fixed, 95% CI)

1.60 [1.12, 2.30]

3 Comprehensive interventions Show forest plot

6

5018

Odds Ratio (Fixed, 95% CI)

1.55 [1.13, 2.13]

Figuras y tablas -
Comparison 2. Worksite Treatments
Comparison 3. Results of included studies

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Results of included studies Show forest plot

Other data

No numeric data

Figuras y tablas -
Comparison 3. Results of included studies