Person:

Kabir, Zubair

Background: To investigate whether primary prevention might be more favourable than secondary prevention (risk factor reduction in patients with coronary heart disease(CHD)).Methods The cell-based IMPACT CHD mortality model was used to integrate data for Ireland describing CHD patient numbers, uptake of specific treatments, trends in major cardiovascular risk factors, and the mortality benefits of these specific risk factor changes in CHD patients and in healthy people without recognised CHD. Results: Between 1985 and 2000, approximately 2,530 fewer deaths were attributable to reductions in the three major risk factors in Ireland. Overall smoking prevalence declined by 14% between 1985 and 2000, resulting in about 685 fewer deaths (minimum estimate 330, maximum estimate 1,285) attributable to smoking cessation: about 275 in healthy people and 410 in known CHD patients. Population total cholesterol concentrations fell by 4.6%, resultingin approximately 1,300 (minimum estimate 1,115, maximum estimate 1,660) fewer deaths attributable to dietary changes(1,185 in healthy people and 115 in CHD patients) plus 305 fewer deaths attributable to statin treatment (45 in people without CHD and 260 in CHD patients). Mean population diastolic blood pressure fell by 7.2%, resulting in approximately 170 (minimum estimate 105, maximum estimate 300) fewer deaths attributable to secular falls in blood pressure (140 in healthy people and 30 in CHD patients), plus approximately 70 fewer deaths attributable to antihypertensive treatments in people without CHD. Of all the deaths attributable to risk factor falls, some 1,715 (68%) occurred in people without recognized CHD and 815(32%) in CHD patients. Conclusion: Compared with secondary prevention, primary prevention achieved a two-fold larger reduction in CHD deaths. Future national CHD policies should therefore prioritize nationwide interventions to promote healthy diets and reduce smoking.

Background: Different methods exist to estimate smoking attributable cancer mortality rates (Peto and Ezzati methods, as examples). However, the smoking attributable estimates using these methods cannot be generalized to all population sub-groups. A simpler method has recently been developed that can be adapted and applied to different population sub-groups. This study assessed cumulative tobacco smoke damage (smoke load)/non-lung cancer mortality associations across time from 1979 to 2003 among all Massachusetts males and ages 30–74 years, using this novel methodology. Methods: Annual lung cancer death rates were used as smoke load bio-indices, and age-adjusted lung/all other (non-lung) cancer death rates were analyzed with linear regression approach. Non-lung cancer death rates include all cancer deaths excluding lung. Smoking-attributable-fractions (SAFs) for the latest period (year 2003) were estimated as: 1-(estimated unexposed cancer death rate/observed rate). Results: Male lung and non-lung cancer death rates have declined steadily since 1992. Lung and non-lung cancer death rates were tightly and steeply associated across years. The slopes of the associations analyzed were 1.69 (95% confidence interval (CI) 1.35–2.04, r = 0.90), and 1.36 (CI 1.14–1.58, r = 0.94) without detected autocorrelation (Durbin-Watson statistic = 1.8). The lung/non-lung cancer death rate associations suggest that all-sites cancer death rate SAFs in year 2003 were 73% (Sensitivity Range [SR] 61–82%) for all ages and 74% (SR 61–82%) for ages 30–74 years. Conclusion: The strong lung/non-lung cancer death rate associations suggest that tobacco smoke load may be responsible for most prematurely fatal cancers at both lung and non-lung sites. The present method estimates are greater than the earlier estimates. Therefore, tobacco control may reduce cancer death rates more than previously noted.

Background: Smoking causes 85% of all lung cancers in males and 70% in females. Therefore, birth cohort analysis and annual-percent-changes (APC) in age-specific lung cancer mortality rates, particularly in the youngest age cohorts, can explain the beneficial impacts of both past and recent anti-smoking interventions. Methods: A long-term time-trend analysis (1958-2002) in lung cancer mortality rates focusing on the youngest age-cohorts (30-49 years of age) in particular was investigated in Ireland. The rates were standardised to the World Standard Population. Lung cancer mortality data were downloaded from the WHO Cancer Mortality Database to estimate APCs in death rates, using the Joinpoint regression (version 3.0) program. A simple age-cohort modelling (log-linear Poisson model) was also done, using SAS software. Results: The youngest birth cohorts (born after 1965) have almost one-fourth lower lung cancer risk relative to those born around the First World War. A more than 50% relative decline in death rates among those between 35 and 39 years of age was observed in both sexes in recent years. The youngest age-cohorts (30-39 years of age) in males also showed a significant decrease in death rates in 1998-2002 by more than 3% every five years from 1958-1962 onwards. However, death rate declines in females are slower. Conclusions: The youngest birth cohorts had the lowest lung cancer risk and also showed a significant decreasing lung cancer death rate in the most recent years. Such temporal patterns indicate the beneficial impacts of both recent and past tobacco control efforts in Ireland. However, the decline in younger female cohorts is slower. A comprehensive national tobacco control program enforced on evidence-based policies elsewhere can further accelerate a decline in death rates, especially among the younger generations.

Objective: This study assesses the epidemiological pattern of lung cancer cell-types in Ireland, with identification of any underlying gender variations. Methods: Lung cancer incidence data, including the major cell-types: squamous-cell-carcinoma (SCC), adenocarcinoma (AC), small-cell-lung-carcinoma (SCLC) and large-cell-carcinoma (LCC) were obtained from the national cancer registry (1994–2000), together with individual characteristics, such as age, gender, smoking status, and the year of diagnosis. Age-standardised incidence rates (ASIR), male-to-female (M: F) rate ratios (RR) of ASIR for SCC and AC, as well as RR of AC: SCC according to smoking status for both sexes, were estimated. Estimated-annual-percent-changes for each of the cell-types were calculated. Results: AC incidence in females is rising annually (8.5%, p=0.008) from 1994 to 2000, while SCC is declining (−5.4%, p=0.01) in males. M: F ratios of ASIR are consistently greater than ‘one’, but converging recently. RR of AC: SCC is also approaching ‘unity’ across both sexes, irrespective of the smoking status. Conclusions: An apparent increase in lung AC incidence in females was observed in Ireland that might indicate some local environmental risk factors, in addition to changing smoking habits. The study findings do not support the hypothesis that females in general are at higher risk for lung cancer development, but tobacco and histologic-specific susceptibility cannot be ruled out.