Association between Asthma Control and Exposure to Greenness and Other Outdoor and Indoor Environmental Factors: A Longitudinal Study on a Cohort of Asthmatic Children

Achieving and maintaining asthma control (AC) is the main goal of asthma management. Indoor and outdoor environmental factors may play an important role on AC. The aim of this longitudinal study was to evaluate the association between AC and exposure to greenness and other outdoor or indoor environmental factors in a cohort of asthmatic children. This study involved 179 asthmatic children (5–16 years). Parents were interviewed through a modified version of the SIDRIA questionnaire. AC was assessed at each visit. Exposure to greenness was measured using the normalized difference vegetation index (NDVI). A logistic regression model was applied for assessing risk factors for uncontrolled asthma (UA). Low NDVI exposure was a risk factor for UA (OR: 2.662, 95% CI (1.043–6.799)); children exposed to passive smoke during pregnancy had a higher risk of UA than those non-exposed to passive smoke during pregnancy (OR: 3.816, 95% CI (1.114–13.064)); and a unit increase in the crowding index was associated with an increased risk of UA (OR: 3.376, 95% CI (1.294–8.808)). In conclusion, the current study provided a comprehensive assessment of urban-related environmental exposures on asthma control in children, using multiple indicators of greenness and other outdoor or indoor environmental factors.

Association between early gestation passive smoke exposure and neonatal size among self-reported non-smoking women by race/ethnicity: A cohort study

Understanding implications of passive smoke exposure during pregnancy is an important public health issue under the Developmental Origins of Health and Disease paradigm. In a prospective cohort of low-risk non-smoking pregnant women (NICHD Fetal Growth Studies—Singletons, 2009–2013, N = 2055), the association between first trimester passive smoke exposure and neonatal size was assessed by race/ethnicity. Plasma biomarker concentrations (cotinine, nicotine) assessed passive smoke exposure. Neonatal anthropometric measures included weight, 8 non-skeletal, and 2 skeletal measures. Linear regression evaluated associations between continuous biomarker concentrations and neonatal anthropometric measures by race/ethnicity. Cotinine concentrations were low and the percent above limit of quantification varied by maternal race/ethnicity (10% Whites; 14% Asians; 15% Hispanics; 49% Blacks). The association between cotinine concentration and infant weight differed by race/ethnicity (Pinteraction = 0.034); compared to women of the same race/ethnicity, per 1 log-unit increase in cotinine, weight increased 48g (95%CI -44, 139) in White and 51g (95%CI -81, 183) in Hispanic women, but decreased -90g (95%CI -490, 309) in Asian and -93g (95%CI -151, -35) in Black women. Consistent racial/ethnic differences and patterns were found for associations between biomarker concentrations and multiple non-skeletal measures for White and Black women (Pinteraction<0.1). Among Black women, an inverse association between cotinine concentration and head circumference was observed (−0.20g; 95%CI −0.38, −0.02). Associations between plasma cotinine concentration and neonatal size differed by maternal race/ethnicity, with increasing concentrations associated with decreasing infant size among Black women, who had the greatest biomarker concentrations. Public health campaigns should advocate for reducing pregnancy exposure, particularly for vulnerable populations.

Association of passive smoking and lung cancer: Is there substantial evidence to prove the causation?

Cigarette smoking plays a crucial role in the development of lung cancer. Tobacco smoke positively influences lung cancer development in both smokers and never or non-smokers. The influence of passive smoke on lung cancer development is associated with toxic substances that cause chronic inflammation in the respiratory systems. Frequent or high exposure to second-hand or environmental tobacco smoke causes respiratory infections that impair lung function and triggers lung cancer development through cell damage, mitosis, and apoptosis. The toxic substances found in second-hand smoke, including carcinogens, ammonia, carbon monoxide, and nitrosamines, have a significant association with squamous cell carcinoma, small cell lung carcinoma, large cell carcinoma, and adenocarcinoma. Although some previously conducted studies showed no significant association between passive smoking and lung cancer, recent studies provide substantial evidence between their associations. Thus, exposure to passive smoke increases the risks of lung cancer.

CIGARETTE SMOKE INCREASES RISK FOR COLORECTAL NEOPLASIA IN INFLAMMATORY BOWEL DISEASE

Objective Patients with inflammatory bowel disease are at increased risk of colorectal neoplasia (CRN) due to mucosal inflammation. As current surveillance guidelines form a burden on patients and healthcare costs, stratification of high-risk patients is crucial. Cigarette smoke reduces inflammation in ulcerative colitis (UC) but not Crohn’s disease (CD) and forms a known risk factor for CRN in the general population. Due to this divergent association, the effect of smoking on CRN in IBD is unclear and subject of this study. Design In this retrospective cohort study, 1,386 IBD patients with previous biopsies analyzed and reported in the PALGA register, were screened for development of CRN. Clinical factors and cigarette smoke were evaluated. Patients were stratified for guideline-based risk of CRN. Cox-regression modeling was used to estimate the effect of cigarette smoke and its additive effect within the current risk stratification for prediction of CRN. Results 151 (11.0%) patients developed CRN. Previously described risk factors, i.e. first-degree family member with CRN in CD (p-value=0.001), presence of post-inflammatory polyps in UC (p-value=0.004), were replicated. Former smoking increased risk of CRN in UC (HR1.72;1.04–2.84), whereas passive smoke exposure yielded no effect. For CD, active smoking (2.52; 1.14–5.58) and passive smoke exposure (1.88;1.10–3.21) significantly increased CRN risk. Addition of cigarette smoking to the current risk-stratification model significantly improved model fit for CD. Conclusion This study is the first to describe the important role of cigarette smoke in CRN development in IBD patients. Adding this risk factor improves the current risk stratification for CRN surveillance strategies.

Abstract 15431: Childhood Passive Smoke Exposure is Associated With Subclinical Left Ventricular Dysfunction in Adulthood - Childhood Determinants of Adult Health Study

Introduction: Prolonged childhood passive smoke exposure may affect adult cardiovascular health but there are few studies of cardiac function. Subclinical left ventricular dysfunction detected by global longitudinal strain (GLS) is predictive of the subsequent development of heart failure. We investigated the association of passive smoke exposure during childhood with GLS in adults. Methods: Data were from the Childhood Determinants of Adult Health (CDAH) study 34-year follow-up (2014-19). Three measures of passive smoking (severity of exposure index [SEI], cumulative years of exposure [CYE], total household smokers [THS]) were derived retrospectively from a validated questionnaire. GLS was measured in clinics using a Siemens Acuson SC2000 ultrasound machine and 4V1c transducer with speckle tracking analysis. Linear regression adjusted for confounding factors (age, gender, childhood socioeconomic position, childhood smoking, adult smoking status, parental education level) examined the association between childhood passive smoke exposure and GLS in adulthood. Results: Among 781 participants (mean age 45.2 ± 2.5 SD years, 52.6% females, 54.2% exposed to passive smoking), GLS showed a decrease (β adjusted -0.17% 95% CI -0.32%, -0.02%) per SD of SEI (range: 0-318, mean 24.2 ± 35.8 SD). CYE (range: 0-106, mean 10.4 ± 13.9 SD) was associated with a decrease in GLS (β adjusted -0.18% 95% CI -0.33%, -0.05%) per SD of exposure. For each THS in childhood (range: 0-5, mean 0.9 ± 1.0 SD), there was a decrease in GLS (β adjusted -0.20% 95% CI -0.36%, -0.05%). Conclusion: Childhood passive smoke exposure, independent of own smoking, was associated with a reduction in GLS, a measure of subclinical cardiac dysfunction. Each 1% decrease in GLS has been associated with 12% higher risk of cardiovascular morbidity and mortality in low-risk general population. There are potential long-term consequences to cardiac function from childhood passive smoke exposure.

Longitudinal Asthma Patterns in Italian Adult General Population Samples: Host and Environmental Risk Factors

Background: Asthma patterns are not well established in epidemiological studies. Aim: To assess asthma patterns and risk factors in an adult general population sample. Methods: In total, 452 individuals reporting asthma symptoms/diagnosis in previous surveys participated in the AGAVE survey (2011–2014). Latent transition analysis (LTA) was performed to detect baseline and 12-month follow-up asthma phenotypes and longitudinal patterns. Risk factors associated with longitudinal patterns were assessed through multinomial logistic regression. Results: LTA detected four longitudinal patterns: persistent asthma diagnosis with symptoms, 27.2%; persistent asthma diagnosis without symptoms, 4.6%; persistent asthma symptoms without diagnosis, 44.0%; and ex -asthma, 24.1%. The longitudinal patterns were differently associated with asthma comorbidities. Persistent asthma diagnosis with symptoms showed associations with passive smoke (OR 2.64, 95% CI 1.10–6.33) and traffic exposure (OR 1.86, 95% CI 1.02–3.38), while persistent asthma symptoms (without diagnosis) with passive smoke (OR 3.28, 95% CI 1.41–7.66) and active smoke (OR 6.24, 95% CI 2.68–14.51). Conclusions: LTA identified three cross-sectional phenotypes and their four longitudinal patterns in a real-life setting. The results highlight the necessity of a careful monitoring of exposure to active/passive smoke and vehicular traffic, possible determinants of occurrence of asthma symptoms (with or without diagnosis). Such information could help affected patients and physicians in prevention and management strategies.