Current Smoking and Risk of Coronavirus Infection and Illness in a Highly Controlled Challenge Study: A Re-analysis of the British Cold Study.

INTRODUCTION: Meta-analyses have shown an association between smoking and the risk of Coronavirus Disease 2019 (COVID-19) disease severity, but the risk of smoking and coronavirus infection is less clear. AIMS AND METHODS: We re-analyzed data from the British Cold Study, a 1986-1989 challenge study that exposed 399 healthy adults to 1 of 5 "common cold" viruses (including n = 55 for coronavirus 229E). Participants with cotinine levels below 15 ng/mL (noncurrent smokers) were compared with participants with higher cotinine levels or self-reported smoking (current smokers). We calculated overall and coronavirus-specific unadjusted and adjusted relative risks (RRs) for current smoking and each outcome (infection and illness), and tested whether each association was modified by the type of respiratory virus. RESULTS: Current smokers had a higher adjusted risk than noncurrent smokers for infection (adjusted RR [aRR] = 1.12, 95% CI: 1.01, 1.25) and illness (aRR = 1.48, 95% CI: 1.11, 1.96). Neither association was modified by an interaction term for smoking and type of virus (infection: p = .44, illness: p = .70). The adjusted RR estimates specific to coronavirus 229E for infection (aRR = 1.22, 95% CI: .91, 1.63) and illness (RR = 1.14, 95% CI: .62, 2.08) were not statistically significant. CONCLUSIONS: These RRs provide estimates of the strength of associations between current smoking and infection and illness that can be used to guide tobacco control decisions. IMPLICATIONS: Systematic reviews and meta-analyses have found an association between smoking and COVID-19 disease severity, but fewer studies have examined infection and illness. The British Cold Study, a high-quality challenge study that exposed healthy volunteers to respiratory viruses including a coronavirus, provides an opportunity to estimate the RR for current smoking and infection and illness from coronaviruses and other viruses to guide tobacco control decisions. Compared with noncurrent smokers, current smokers had a 12% increased risk of having a laboratory-confirmed infection and a 48% increased risk of a diagnosed illness, which was not modified by the type of respiratory virus including a coronavirus.

Relationship between obesity and coronary heart disease among urban Bangladeshi men and women.

The aim of the study was to examine the association of different measures of obesity (body mass index or BMI, waist circumference or WC, waist to hip ratio or WHR and waist height ratio or WHtR) with coronary heart disease (CHD) in a Bangladeshi population. The study included 189 hospitalized CHD cases (133 men and 52 women) and 201 controls (137 men and 68 women). Logistic regression was done to assess the associations between obesity and CHD. The mean age was 53.1 ± 8.3 for men and 51.9 ± 8.4 for women. After adjustment for confounders the odds ratio (OR) of CHD for men was 1.69 (95% CI, 1.24-2.32), 1.94 (95% CI 1.40-2.70), and 1.32 (95% CI, 1.01-2.16) per 1 standard deviation (SD) increase in BMI, WC, and WHtR respectively. The OR for women was 2.64 (CI, 1.61-4.34), 1.82 (95% CI 1.12-2.95), 2.32 (95% CI, 1.36-3.96), and 1.94 (95% CI, 1.23-3.07) per 1 SD increase in BMI, WC, WHtR and WHR respectively. Since both total obesity and abdominal adiposity were associated with development of CHD and since measurement of WC and BMI are inexpensive, both should be included in the clinical setting for CHD risk assessment for this group of population.

The risk and burden of smoking related heart disease mortality among young people in the United States.

PURPOSE: Although cigarette smoking remains the most common risk factor for heart disease among the young, few studies have explored the relationship of smoking with heart disease mortality risk among young people. This prospective study assesses the risk and burden of all heart disease (HD) and coronary heart disease (CHD) mortality associated with smoking among younger adults from a nationally representative sample of the United States. METHOD: National Health Interview Survey respondents' data from 1997-2004 were linked to their death records through 2006. The analyses were restricted to individuals 18 to 44 years of age during follow up (n = 121,284). Cox proportional hazard ratios (HR) were estimated with adjustment for sample weights and design effects. Attributable fractions (AF) of smoking were calculated. RESULTS: After controlling for age, race, body mass index, history of hypertension and diabetes, and leisure time physical activity, current smoking related CHD mortality HR was 14.6 [95 % confidence interval or CI, 3.3-64.9] for females and 3.6 [95 % CI, 1.2-10.4] for males. The HR for all HD mortality was 3.1 [95 % CI, 1.3-7.6] for females and 2.4 [95 % CI, 1.2-4.7] for males. The AF of smoking for CHD deaths for female and male were 0.58 and 0.54 respectively. The AF of all HD mortality was 0.31 for male and 0.32 for female. The mean estimates of all HD deaths attributable to smoking during 1997-2006 among this age group were 52,214, of which 45,147 were CHD deaths. CONCLUSION: Even after adjustment for multiple risk factors and without addressing passive smoking, our result showed a strong relationship between smoking and HD and CHD mortality among young adults that is likely causal.

Smoking and ischemic heart disease disparities between studies, genders, times, and socioeconomic strata.

Large, unexplained, but possibly related disparities exist between heart disease risks observed in differing genders, educational levels, times, and studies. Such heart disease disparities might be related to cumulative tobacco smoke damage (smoke load) disparities that are overlooked in standard assessments of point smoking status. So, I reviewed possible relationships between smoke load and heart disease levels across genders, educational strata, years, and leading studies. Smoker heart disease risk assessments in the Nurses Health Study (Nurses), Cancer Prevention Study-II (CPS-II), and British Doctors studies were compared and related to their likely selection and misclassification biases. Relationships between smoke loads and United States (US) education- and gender-related heart disease mortality disparities were qualitatively assessed using lung cancer rates as a smoke load proxy. The high heart disease mortality risks observed in smoking Nurses in 1980-2004 and in less educated US women in 2001 were qualitatively associated with their higher smoke loads and lower selection and exposure misclassification biases than in the CPS-II and Doctors studies. Smoking-attributable heart disease death tolls and disparities extrapolated from mortality ratios from the CPS-II and Doctors studies may be substantial underestimates. Such studies appear to have compared convenience samples of light smokers to lighter smokers instead of comparing representative smokers to the unexposed. Further efforts to minimize smoke exposures and better quantify cumulative smoking-attributable burdens are needed.

Male tobacco smoke load and non-lung cancer mortality associations in Massachusetts.

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.

Tobacco smoke overload and ethnic, state, gender, and temporal cancer mortality disparities in Asian-Americans and Pacific Islander-Americans.

BACKGROUND: Asians and Pacific Islanders (APIs) are important populations nationally and globally. So we assessed cumulative tobacco smoke overexposure (smoke overload)/cancer mortality associations across states, ethnicities, years, and genders among API-Americans. METHODS: Death rates were adjusted to the 2000 United States age standard, lung cancer death rates used as a smoke overload bio-index, and lung/non-lung cancer death rate linear regressions run. Cancer death rate smoking-attributable fractions (SAFs) are equal to 1--estimated unexposed rate/observed rate. RESULTS: The two lowest smoke overload and non-lung cancer death rates were in South Asian (Indo)-Californian females and males. The highest were in Korean-Californian males. Non-lung cancer death rates were tightly and steeply associated with smoke overload across ethnicity, state, year, or gender. Cancer death rate smoking-attributable fractions ranged from 0 in female and 6% in male Indo-Californians, to 39% in female and 57% in male API-Americans in 2002, to 71% in Korean-Californian and 69% in API Hawaiian males. DISCUSSION: Many API American cancer death rate disparities across genders, ethnicities, states, or years can be explained by smoke overload disparities. Tobacco control may greatly reduce cancer death rates and disparities among API-Americans and, likely, others.

Cancer death epidemics in United States Black males: evaluating courses, causation, and cures.

BACKGROUND: Estimates that smoking contributes 38-72% of the United States (US) Black male cancer death rate leave a wide range of uncertainty. This paper uses additional and regional data, and refined methods, to reassess that range. METHODS: This study uses lung cancer rates as an exposure index, linear regression, age adjusted US 1950-2001 and US regional 1969-2001 death rates (rates), and the formula: smoking-attributable fraction (SAF)=(1-((rate in the unexposed) / (rate in the exposed))). Estimated lung cancer rates in the unexposed range between rates predicted for a population with no smoking-attributable lung cancers to rates seen in "nonsmokers." RESULTS: Lung cancer death rates predicted 99.9% and 99.8% of the variances in non-lung non-stomach cancer death rates from 1950-1980 and 1950-1988, respectively (each P<0.0001). That suggests 2001 all-sites cancer death SAFs of 63% (sensitivity range 60-66%) nationally and from 43% in the Northeast to 67% in the South. CONCLUSIONS: Smoking may cause most premature cancer deaths and temporal and regional cancer death rate disparities in Black men.