How does social context influence appraisal and help-seeking for potential cancer symptoms in adults aged 50 and over? A qualitative interview study.

OBJECTIVE: To investigate how social context and social network activation influence appraisal and help-seeking for symptoms potentially indicative of cancer. METHODS: Semi-structured telephone interview study. Community dwelling adults who had experienced at least one symptom potentially indicative of cancer within the last month were sampled from a national symptom survey. RESULTS: Thirty-four interviews were conducted. Participants looked to peers and wider society to judge whether symptoms might be normal for their age. Involvement of others in symptom appraisal promoted an active management strategy, such as contacting a healthcare professional or trying a medication. There were practical, emotional, attitudinal, normative and moral barriers to involving others. Cancer narratives from significant others, public health campaigns and the media influenced symptom appraisal. Participants held mental representations of types of people who get cancer, for example, smokers and unfit people. This had two consequences. First, participants did not identify themselves as a candidate for cancer; impeding help-seeking. Second, social judgements about lifestyle introduced stigma. CONCLUSION: Involving friends/family in symptom appraisal facilitates help-seeking but barriers exist to involving others. Campaigns to promote earlier cancer diagnosis should incorporate age-appropriate narratives, address misconceptions about 'types' of people who get cancer and tackle stigma about lifestyle factors.

Patterns of symptoms possibly indicative of cancer and associated help-seeking behaviour in a large sample of United Kingdom residents-The USEFUL study.

BACKGROUND: Cancer awareness campaigns aim to increase awareness of the potential seriousness of signs and symptoms of cancer, and encourage their timely presentation to healthcare services. Enhanced understanding of the prevalence of symptoms possibly indicative of cancer in different population subgroups, and associated general practitioner (GP) help-seeking behaviour, will help to target cancer awareness campaigns more effectively. AIM: To determine: i) the prevalence of 21 symptoms possibly indicative of breast, colorectal, lung or upper gastrointestinal cancer in the United Kingdom (UK), including six 'red flag' symptoms; ii) whether the prevalence varies among population subgroups; iii) the proportion of symptoms self-reported as presented to GPs; iv) whether GP help-seeking behaviour varies within population subgroups. METHODS: Self-completed questionnaire about experience of, and response to, 25 symptoms (including 21 possibly indicative of the four cancers of interest) in the previous month and year; sent to 50,000 adults aged 50 years or more and registered with 21 general practices in Staffordshire, England or across Scotland. RESULTS: Completed questionnaires were received from 16,778 respondents (corrected response rate 34.2%). Almost half (45.8%) of respondents had experienced at least one symptom possibly indicative of cancer in the last month, and 58.5% in the last year. The prevalence of individual symptoms varied widely (e.g. in the last year between near zero% (vomiting up blood) and 15.0% (tired all the time). Red flag symptoms were uncommon. Female gender, inability to work because of illness, smoking, a history of a specified medical diagnosis, low social support and lower household income were consistently associated with experiencing at least one symptom possibly indicative of cancer in both the last month and year. The proportion of people who had contacted their GP about a symptom experienced in the last month varied between 8.1% (persistent cough) and 39.9% (unexplained weight loss); in the last year between 32.8% (hoarseness) and 85.4% (lump in breast). Nearly half of respondents experiencing at least one red flag symptom in the last year did not contact their GP about it. Females, those aged 80+ years, those unable to work because of illness, ex-smokers and those previously diagnosed with a specified condition were more likely to report a symptom possibly indicative of cancer to their GP; and those on high household income less likely. CONCLUSION: Symptoms possibly indicative of cancer are common among adults aged 50+ years in the UK, although they are not evenly distributed. Help-seeking responses to different symptoms also vary. Our results suggest important opportunities to provide more nuanced messaging and targeting of symptom-based cancer awareness campaigns.

Updating the evidence relating smoking bans to incidence of heart disease.

In our latest update of the evidence on smoking bans and heart disease we summarize 59 studies. We take account of the underlying trends in incidence rates as far as possible by using control data in eight studies, and by adjustment based on observed trends in cases pre- and post-ban in 40 studies, being unable to make an adjustment in the remaining 11 studies. Overall, based on 62 independent estimates from the 59 studies, we estimate that bans reduce incidence by 5.0% (95% CI 3.2-6.8%), though this estimate reduces to 2.9% (0.01-5.6%) when we exclude regional estimates where national estimates are available, and studies where trend adjustment is not possible. For 25 of the studies, quadratic rather than linear adjustment is possible, but this hardly affects the overall estimates. Ban effects are somewhat greater when the pre-ban period studied is relatively short, and in smaller studies. We compare our findings with those in other recent reviews, one of which totally ignored underlying trends and results from control populations. We discuss reasons why we believe there is likely to be a true small effect of smoking bans, and weaknesses in the data which preclude reaching any very confident conclusion.

Epidemiological evidence relating environmental smoke to COPD in lifelong non-smokers: a systematic review.

Background: Some evidence suggests environmental tobacco smoke (ETS) might cause chronic obstructive pulmonary disease (COPD). We reviewed available epidemiological data in never smokers. Methods: We identified epidemiological studies providing estimates of relative risk (RR) with 95% confidence interval (CI) for various ETS exposure indices. Confounder-adjusted RRs for COPD were extracted, or derived using standard methods. Meta-analyses were conducted for each exposure index, with tests for heterogeneity and publication bias. For the main index (spouse ever smoked or nearest equivalent), analyses investigated variation in RR by location, publication period, study type, sex, diagnosis, study size, confounder adjustment, never smoker definition, and exposure index definition. Results: Twenty-eight relevant studies were identified; nine European or Middle Eastern, nine Asian, eight American and two from multiple countries. Five were prospective, seven case-control and 16 cross-sectional. The COPD definition involved death or hospitalisation in seven studies, GOLD stage 1+ criteria in twelve, and other definitions in nine. For the main index, random-effects meta-analysis of 33 heterogeneous (p<0.001) estimates gave a RR of 1.20 (95%CI 1.08-1.34). Higher estimates for females (1.59,1.16-2.19, n=11) than males (1.29,0.94-1.76, n=7) or sexes combined (1.10,0.99-1.22, n=15 where sex-specific not available), and lower estimates for studies of 150+ cases (1.08,0.97-1.20, n=13) partly explained the heterogeneity. Estimates were higher for Asian studies (1.34,1.08-1.67, n=10), case-control studies (1.55,1.04-2.32, n=8), and COPD mortality or hospitalisation (1.40,1.12-1.74, n=11). Some increase was seen for severer COPD (1.29,1.10-1.52, n=7). Dose-response evidence was heterogeneous. Evidence for childhood (0.88,0.72-1.07, n=2) and workplace (1.12,0.77-1.64, n=4) exposure was limited, but an increase was seen for overall adulthood exposure (1.20,1.03-1.39, n=17). We discuss study weaknesses that may bias estimation of the association of COPD with ETS. Conclusions: Although the evidence suggests ETS increases COPD, study weaknesses and absence of well-designed large studies precludes reliable inference of causality. More definitive evidence is required.

The relationship of cigarette smoking in Japan to lung cancer, COPD, ischemic heart disease and stroke: A systematic review.

Background:  To present up-to-date meta-analyses of evidence from Japan relating smoking to major smoking-related diseases.  Methods:  We restricted attention to lung cancer, chronic obstructive pulmonary disease (COPD), ischemic heart disease (IHD) and stroke, considering relative risks (RRs) for current and ex-smokers relative to never smokers.  Evidence by amount smoked and time quit was also considered.  For IHD and stroke only, studies had to provide age-adjusted RRs, with age-specific results considered.  For each disease we extended earlier published databases to include more recent studies.  Meta-analyses were conducted, with random-effects RRs and tests of heterogeneity presented.  Results:  Of 40 studies, 26 reported results for lung cancer and 7 to 9 for each other disease.  For current smoking, RRs (95%CIs) were lung cancer 3.59 (3.25-3.96), COPD 3.57 (2.72-4.70), IHD 2.21 (1.96-2.50) and stroke 1.40 (1.25-1.57).  Ex-smoking RRs were lower.  Data for lung cancer and IHD showed a clear tendency for RRs to rise with increasing amount smoked and decrease with increasing time quit.  Dose-response data were unavailable for COPD and unclear for stroke, where the association was weaker.  Conclusions:  Compared to studies in other Asian and Western countries, current smoking RRs were quite similar for IHD and stroke.  The comparison is not clear for COPD, where the Japanese data, mainly from cross-sectional studies, is limited.  For lung cancer, the RRs are similar to those in other Asian countries, but substantially lower than in Western countries.  Explanations for this are unclear, but less accurate reporting of smoking by Japanese may contribute to the difference.

The relationship of snus use to diabetes and allied conditions.

A recent meta-analysis reported smoking to be associated with a 37% higher risk of type 2 diabetes in current smokers, rising to a 57% increase in heavy smokers, which declines on quitting. If the increase results from nicotine exposure, it is possible that using Swedish moist snuff ("snus"), which provides at least equivalent nicotine doses, might also increase diabetes risk. Following a recent publication reporting pooled results from five cohorts, we present a detailed meta-analysis of data from 18 studies. Based on covariate-adjusted estimates, no significant increased risk was seen in never smokers with RRs (95% CIs) of 1.08 (0.86-1.34), 0.93 (0.79-1.11) and 1.05 (0.94-1.18) for current, former and ever snus users. Significant increases were also not seen in the whole population, the corresponding RR estimates being 1.18 (0.94-1.48), 0.69 (0.49-0.96) and 0.95 (0.81-1.11). Nor was there an association of snus use with related endpoints, such as impaired glucose tolerance. However, dose-response analyses showed a relationship, with the highest levels of snus exposure associated with a diabetes RR of 1.65 (1.25-2.18) in never smokers. The evidence relating snus to type 2 diabetes is somewhat limited, requiring further studies to confirm any possible relationship.

Environmental Tobacco Smoke Exposure and Risk of Stroke in Never Smokers: An Updated Review with Meta-Analysis.

OBJECTIVES: The study aimed to review the epidemiological evidence relating environmental tobacco smoke exposure to stroke in never smokers. METHODS: The study is similar to our review in 2006, with searches extended to March 2016. RESULTS: Twelve further studies were identified. A total of 28 studies varied considerably in design, exposure indices used, and disease definition. Based on 39 sex-specific estimates and the exposure index current spousal exposure (or nearest equivalent), the meta-analysis gave an overall fixed-effect relative risk estimate of 1.23 (95% confidence interval: 1.16-1.31), with significant (P < .05) heterogeneity. There was no significant heterogeneity by sex, continent, fatality, disease end point, or degree of adjustment for potential confounding factors. Relative risks were less elevated in prospective studies (1.15, 1.06-1.24) than in case-control studies (1.44, 1.22-1.60) or cross-sectional studies (1.40, 1.21-1.61). They also varied by publication year, but with no trend. A significant increase was not seen in studies that excluded smokers of any tobacco (1.07, .97-1.17), but was seen for studies that included pipe- or cigar-only smokers, occasional smokers, or long-term former smokers. No elevation was seen for hemorrhagic stroke. Relative risk estimates were similar using ever rather than current exposure, or total rather than spousal exposure. Eleven studies provided dose-response estimates, the combined relative risk for the highest exposure level being 1.56 (1.37-1.79). Many studies have evident weaknesses, recall bias, and particularly publication bias being major concerns. CONCLUSIONS: Although other reviewers inferred a causal relationship, we consider the evidence does not conclusively demonstrate this. We repeat our call for publication of data from existing large prospective studies.

Epidemiological evidence on environmental tobacco smoke and cancers other than lung or breast.

We reviewed 87 epidemiological studies relating environmental tobacco smoke (ETS) exposure to risk of cancer other than lung or breast in never smoking adults. This updates a 2002 review which also considered breast cancer. Meta-analysis showed no significant relationship with ETS for nasopharynx cancer, head and neck cancer, various digestive cancers (stomach, rectum, colorectal, liver, pancreas), or cancers of endometrium, ovary, bladder and brain. For some cancers (including oesophagus, colon, gall bladder and lymphoma) more limited data did not suggest a relationship. An increased cervix cancer risk (RR 1.58, 95%CI 1.29-1.93, n = 17 independent estimates), reducing to 1.29 (95%CI 1.01-1.65) after restriction to five estimates adjusting for HPV infection or sexual activity suggests a causal relationship, as do associations with nasosinus cancer observed in 2002 (no new studies since), and less so kidney cancer (RR 1.33, 95%CI 1.04-1.70, n = 6). A weaker association with total cancer (RR 1.13, 95%CI 1.03-1.35, n = 19) based on heterogeneous data is inconclusive. Inadequate confounder control, recall bias, publication bias, and occasional reports of implausibly large RRs in individual studies contribute to our conclusion that the epidemiological evidence does not convincingly demonstrate that ETS exposure causes any of the cancers studied.

Long-Term Worries after Colposcopy: Which Women Are at Increased Risk?

BACKGROUND: A colposcopy examination is the main management option for women with an abnormal cervical screening test result. Although some women experience adverse psychological effects after colposcopy, those at greatest risk are unknown. We investigated predictors of worries about cervical cancer, sex, future fertility and general health during 12 to 30 months after colposcopy. METHODS: We invited 1,515 women, aged 20 to 59 years with low-grade cervical cytology who attended colposcopy to complete questionnaires at recruitment (∼8 weeks after cytology result) and after 12, 18, 24, and 30 months of follow up. Outcomes were worries about having cervical cancer, having sex, future fertility, and general health at any time during follow-up. Factors significantly associated with each outcome were identified using multiple logistic regression. RESULTS: At one or more time points during follow-up, 40% of women reported worries about having cervical cancer, 26% about having sex, 24% about future fertility, and 60% about general health. For all outcomes except sex, worries reported at recruitment were associated with significantly increased risk of worries during follow-up. Significant anxiety at recruitment was associated with all worries during follow-up. Women diagnosed with CIN2+ had significantly higher risks of worries about cervical cancer and future fertility. Management received was associated significantly with worries about cervical cancer and having sex. Younger women significantly more often reported worries about future fertility, whereas women who had children had reduced risk of future fertility worries but increased risk of cervical cancer worries. CONCLUSION: Clinical, sociodemographic, lifestyle, and psychological factors predicted risk of reporting worries after colposcopy.

Estimating the decline in excess risk of cerebrovascular disease following quitting smoking--a systematic review based on the negative exponential model.

We attempted to quantify the decline in stroke risk following quitting using the negative exponential model, with methodology previously employed for IHD. We identified 22 blocks of RRs (from 13 studies) comparing current smokers, former smokers (by time quit) and never smokers. Corresponding pseudo-numbers of cases and controls/at risk formed the data for model-fitting. We tried to estimate the half-life (H, time since quit when the excess risk becomes half that for a continuing smoker) for each block. The method failed to converge or produced very variable estimates of H in nine blocks with a current smoker RR <1.40. Rejecting these, and combining blocks by amount smoked in one study where problems arose in model-fitting, the final analyses used 11 blocks. Goodness-of-fit was adequate for each block, the combined estimate of H being 4.78(95%CI 2.17-10.50) years. However, considerable heterogeneity existed, unexplained by any factor studied, with the random-effects estimate 3.08(1.32-7.16). Sensitivity analyses allowing for reverse causation or differing assumed times for the final quitting period gave similar results. The estimates of H are similar for stroke and IHD, and the individual estimates similarly heterogeneous. Fitting the model is harder for stroke, due to its weaker association with smoking.

Psychological, surgical, and sociodemographic predictors of pain outcomes after breast cancer surgery: a population-based cohort study.

Chronic postsurgical pain (CPSP) is a common postoperative adverse event affecting up to half of women undergoing breast cancer surgery, yet few epidemiological studies have prospectively investigated the role of preoperative, intraoperative, and postoperative risk factors for pain onset and chronicity. We prospectively investigated preoperative sociodemographic and psychological factors, intraoperative clinical factors, and acute postoperative pain in a prospective cohort of 362 women undergoing surgery for primary breast cancer. Intraoperative nerve handling (division or preservation) of the intercostobrachial nerve was recorded. At 4 and 9months after surgery, incidence of chronic painful symptoms not present preoperatively was 68% and 63%, respectively. Univariate analysis revealed that multiple psychological factors and nerve division was associated with chronic pain at 4 and 9months. In a multivariate model, independent predictors of CPSP at 4months included younger age and acute postoperative pain (odds ratio [OR] 1.34, 95% confidence interval [CI] 1.12 to 1.60), whereas preoperative psychological robustness (OR 0.70, 95% CI 0.49 to 0.99), a composite variable comprising high dispositional optimism, high positive affect, and low emotional distress, was protective. At 9months, younger age, axillary node clearance (OR 2.97, 95% CI 1.09 to 8.06), and severity of acute postoperative pain (OR 1.17, 95% CI 1.00 to 1.37) were predictive of pain persistence. Of those with CPSP, 25% experienced moderate to severe pain and 40% were positive on Douleur Neuropathique 4 and Self-Complete Leeds Assessment of Neuropathic Symptoms and Signs pain scales. Overall, a high proportion of women report painful symptoms, altered sensations, and numbness in the upper body within the first 9months after resectional breast surgery and cancer treatment.

The effect of quitting smoking on HDL-cholesterol - a review based on within-subject changes.

A higher concentration of high density lipoprotein cholesterol (HDL-C) in ex-smokers than smokers has consistently been observed. Better evidence of quitting effects comes from within-subject changes. We extend an earlier meta-analysis to quantify the reduction, and investigate variation by time quit and other factors. We conducted Medline and Cochrane searches for studies measuring HDL-C in subjects while still smoking and later having quit. Using unweighted and inverse-variance weighted regression analysis, we related changes (in mmol/l) to intra-measurement period, and estimated time quit, and to study type, location and start year, age, sex, product smoked, validation of quitting, baseline HDL-C, baseline and change in weight/BMI, and any study constraints on diet or exercise. Forty-five studies were identified (17 Europe, 16 North America, 11 Asia, 1 Australia). Thirteen were observational, giving changes over at least 12 months, with most involving >1000 subjects. Others were smoking cessation trials, 12 randomized and 20 non-randomized. These were often small (18 of <100 subjects) and short (14 of <10 weeks, the longest a year). Thirty studies provided results for only one time interval. From 94 estimates of HDL-C change, the unweighted mean was 0.107 (95% CI 0.085-0.128). The weighted mean 0.060 (0.044 to 0.075) was lower, due to smaller estimates in longer term studies. Weighted means varied by time quit (0.083, 0.112, 0.111, 0.072, 0.058 and 0.040 for <3, 3 to <6, 6 to <13, 13 to <27, 27 to <52 and 52+ weeks, p=0.006). After adjustment for time quit, estimates varied by study constraint on diet/exercise (p=0.003), being higher in studies requiring subjects to maintain their pre-quitting habits, but no other clear differences were seen, with significant (p<0.05) increases following quitting being evident in all subgroups studied, except where data were very limited. For both continuing and never smokers, the data are (except for two large studies atypically showing significant HDL-C declines in both groups, and a smaller decline in quitters) consistent with no change, and contrast markedly with the data for quitters. We conclude that quitting smoking increases HDL-C, and that this increase occurs rapidly after quitting, with no clear pattern of change thereafter.

Systematic review with meta-analysis of the epidemiological evidence relating smoking to COPD, chronic bronchitis and emphysema.

BACKGROUND: Smoking is a known cause of the outcomes COPD, chronic bronchitis (CB) and emphysema, but no previous systematic review exists. We summarize evidence for various smoking indices. METHODS: Based on MEDLINE searches and other sources we obtained papers published to 2006 describing epidemiological studies relating incidence or prevalence of these outcomes to smoking. Studies in children or adolescents, or in populations at high respiratory disease risk or with co-existing diseases were excluded. Study-specific data were extracted on design, exposures and outcomes considered, and confounder adjustment. For each outcome RRs/ORs and 95% CIs were extracted for ever, current and ex smoking and various dose response indices, and meta-analyses and meta-regressions conducted to determine how relationships were modified by various study and RR characteristics. RESULTS: Of 218 studies identified, 133 provide data for COPD, 101 for CB and 28 for emphysema. RR estimates are markedly heterogeneous. Based on random-effects meta-analyses of most-adjusted RR/ORs, estimates are elevated for ever smoking (COPD 2.89, CI 2.63-3.17, n = 129 RRs; CB 2.69, 2.50-2.90, n = 114; emphysema 4.51, 3.38-6.02, n = 28), current smoking (COPD 3.51, 3.08-3.99; CB 3.41, 3.13-3.72; emphysema 4.87, 2.83-8.41) and ex smoking (COPD 2.35, 2.11-2.63; CB 1.63, 1.50-1.78; emphysema 3.52, 2.51-4.94). For COPD, RRs are higher for males, for studies conducted in North America, for cigarette smoking rather than any product smoking, and where the unexposed base is never smoking any product, and are markedly lower when asthma is included in the COPD definition. Variations by sex, continent, smoking product and unexposed group are in the same direction for CB, but less clearly demonstrated. For all outcomes RRs are higher when based on mortality, and for COPD are markedly lower when based on lung function. For all outcomes, risk increases with amount smoked and pack-years. Limited data show risk decreases with increasing starting age for COPD and CB and with increasing quitting duration for COPD. No clear relationship is seen with duration of smoking. CONCLUSIONS: The results confirm and quantify the causal relationships with smoking.