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      Passive smoking at home is a risk factor for community-acquired pneumonia in older adults: a population-based case–control study

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          Abstract

          Objective

          To assess whether passive smoking exposure at home is a risk factor for community-acquired pneumonia (CAP) in adults.

          Setting

          A population-based case-control study was designed in a Mediterranean area with 860 000 inhabitants >14 years of age.

          Participants

          1003 participants who had never smoked were recruited.

          Primary and secondary outcome measures

          Risk factors for CAP, including home exposure to passive smoking, were registered. All new cases of CAP in a well-defined population were consecutively recruited during a 12-month period.

          Methods

          A population-based case-control study was designed to assess risk factors for CAP, including home exposure to passive smoking. All new cases of CAP in a well-defined population were consecutively recruited during a 12-month period. The subgroup of never smokers was selected for the present analysis.

          Results

          The study sample included 471 patients with CAP and 532 controls who had never smoked. The annual incidence of CAP was estimated to be 1.14 cases×10 –3 inhabitants in passive smokers and 0.90×10 −3 in non-passive smokers (risk ratio (RR) 1.26; 95% CI 1.02 to 1.55) in the whole sample. In participants ≥65 years of age, this incidence was 2.50×10 −3 in passive smokers and 1.69×10 −3 in non-passive smokers (RR 1.48, 95% CI 1.08 to 2.03). In this last age group, the percentage of passive smokers in cases and controls was 26% and 18.1%, respectively (p=0.039), with a crude OR of 1.59 (95% CI 1.02 to 2.38) and an adjusted (by age and sex) OR of 1.56 (95% CI 1.00 to 2.45).

          Conclusions

          Passive smoking at home is a risk factor for CAP in older adults (65 years or more).

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          Most cited references15

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          Smoking alters alveolar macrophage recognition and phagocytic ability: implications in chronic obstructive pulmonary disease.

          N Reynolds, Hubertus Jersmann, Jessica Ahern … (2007)
          Chronic obstructive pulmonary disease (COPD) is associated with defective efferocytosis (apoptosis and alveolar macrophage [AM] phagocytic function) that may lead to secondary necrosis and tissue damage. We investigated ex vivo AM phagocytic ability and recognition molecules (CD36, integrin alphaVbeta3, CD31, CD91, CD44) using flow cytometry. The transferrin receptor (CD71) was measured as an indicator of monocyte-macrophage differentiation in bronchoalveolar lavage (BAL). Proliferation was assessed with Ki-67. Based on evidence of systemic involvement in COPD, blood from 17 current smokers and 25 ex-smokers with COPD, 22 healthy smokers, and 20 never-smoking control subjects was also investigated. BAL was collected from 10 to 16 subjects in each group. Levels of recognition molecules and cAMP were assessed after exposure of AM to cigarette smoke in vitro. The phagocytic ability of AM was significantly decreased in both COPD groups and in healthy smokers compared with control subjects. However, phagocytic capacity was better in subjects with COPD who had ceased smoking, compared with those who were still smoking. AM from current smokers with COPD and healthy smokers exhibited reduced CD31, CD91, CD44, and CD71, and enhanced Ki-67 compared with healthy never-smoker control subjects. There were no differences in these markers in AM from ex-smokers with COPD compared with control subjects, or in blood monocytes from any group. Suppressive effects of cigarette smoke on AM recognition molecules associated with an increase in cAMP were confirmed in vitro. Our data indicates that a smoking-related reduction in AM phagocytic ability and expression of several important recognition molecules may be at least partially normalized in those subjects with COPD who have ceased smoking.
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            Parental and household smoking and the increased risk of bronchitis, bronchiolitis and other lower respiratory infections in infancy: systematic review and meta-analysis

            Laura L Jones, Ahmed Hashim, Tricia McKeever … (2011)
            Background Passive smoke exposure increases the risk of lower respiratory infection (LRI) in infants, but the extensive literature on this association has not been systematically reviewed for nearly ten years. The aim of this paper is to provide an updated systematic review and meta-analysis of studies of the association between passive smoking and LRI, and with diagnostic subcategories including bronchiolitis, in infants aged two years and under. Methods We searched MEDLINE and EMBASE (to November 2010), reference lists from publications and abstracts from major conference proceedings to identify all relevant publications. Random effect pooled odds ratios (OR) with 95% confidence intervals (CI) were estimated. Results We identified 60 studies suitable for inclusion in the meta-analysis. Smoking by either parent or other household members significantly increased the risk of LRI; odds ratios (OR) were 1.22 (95% CI 1.10 to 1.35) for paternal smoking, 1.62 (95% CI 1.38 to 1.89) if both parents smoked, and 1.54 (95% CI 1.40 to 1.69) for any household member smoking. Pre-natal maternal smoking (OR 1.24, 95% CI 1.11 to 1.38) had a weaker effect than post-natal smoking (OR 1.58, 95% CI 1.45 to 1.73). The strongest effect was on bronchiolitis, where the risk of any household smoking was increased by an OR of 2.51 (95% CI 1.96 to 3.21). Conclusions Passive smoking in the family home is a major influence on the risk of LRI in infants, and especially on bronchiolitis. Risk is particularly strong in relation to post-natal maternal smoking. Strategies to prevent passive smoke exposure in young children are an urgent public and child health priority.
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              Risk factors for community-acquired pneumonia in adults: a population-based case-control study.

              Ana Pinto, I Bolíbar, J Almirall … (1999)
              Although community-acquired pneumonia (CAP) remains a major cause of hospitalization and death, few studies on risk factors have been performed. A population-based case-control study of risk factors for CAP was carried out in a mixed residential-industrial urban area of 74,610 adult inhabitants in the Maresme (Barcelona, Spain) between 1993 and 1995. All patients living in the area and clinically suspected of having CAP at primary care facilities and hospitals were registered. In total, 205 patients with symptoms, signs and radiographic infiltrate compatible with acute CAP participated in the study. They were matched by municipality, sex and age with 475 controls randomly selected from the municipal census. Risk factors relating the subject's characteristics and habits, housing conditions, medical history and treatments were investigated by means of a questionnaire. In the univariate analysis, an increased risk of CAP was associated with low body mass index, smoking, respiratory infection, previous pneumonia, chronic lung disease, lung tuberculosis, asthma, treated diabetes, chronic liver disease, and treatments with aminophiline, aerosols and plastic pear-spacers. In multivariate models, the only statistically significant risk factors were current smoking of >20 cigarettes x day(-1) (odds ratio (OR)=2.77; 95% confidence interval (CI) 1.14-6.70 compared with never-smokers), previous respiratory infection (OR=2.73; 95% CI 1.75-4.26), and chronic bronchitis (OR=2.22; 95% CI 1.13-4.37). Benzodiazepines were found to be protective in univariate and multivariate analysis (OR=0.46; 95% CI 0.23-0.94). This population-based study provides new and better established evidence on the factors associated with the occurrence of pneumonia in the adult community.
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                Author and article information

                Journal
                Journal ID (nlm-ta): BMJ Open
                Journal ID (iso-abbrev): BMJ Open
                Journal ID (hwp): bmjopen
                Journal ID (publisher-id): bmjopen
                Title: BMJ Open
                Publisher: BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                ISSN (Electronic): 2044-6055
                Publication date Collection: 2014
                Publication date (Electronic): 13 June 2014
                Volume: 4
                Issue: 6
                Electronic Location Identifier: e005133
                Affiliations
                [1 ]Critical Care Unit, Hospital de Mataró, Universitat Autònoma de Barcelona, Ciber Enfermedades Respiratorias, CIBERES , Barcelona, Spain
                [2 ]Research Unit, Hospital de Mataró, CIBEREHD , Barcelona, Spain
                [3 ]Department of Clinical Epidemiology and Public Health, Institut de Recerca Biomedica (IIB Sant Pau) Barcelona, Universitat Autònoma de Barcelona, CIBERESP , Barcelona, Spain
                [4 ]Hospital Nostra Senyora de Meritxell , Escaldes-Engordany, Principat d'Andorra
                [5 ]Institut Català de la Salut (ICS) , Barcelona, Spain
                [6 ]IB-SALUT Balears , Palma de Mallorca, Spain
                [7 ]INSALUD , Valencia, Spain
                [8 ]Service of Pneumology, Institut Clínic del Torax, IDIBAPS, Hospital Clínic de Barcelona. Universitat de Barcelona, CIBERES , Barcelona, Spain
                Author notes
                [Correspondence to ] Dr Jordi Almirall; jalmirall@ 123456csdm.cat
                Article
                Publisher ID: bmjopen-2014-005133
                DOI: 10.1136/bmjopen-2014-005133
                PMC ID: 4067857
                PubMed ID: 24928592
                SO-VID: 012ea722-8411-42b1-8781-e2fc30af4e2b
                Copyright © Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions
                License:

                This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/3.0/

                History
                Date received : 25 February 2014
                Date revision received : 15 May 2014
                Date accepted : 22 May 2014
                Categories
                Subject: Respiratory Medicine
                Subject: Research
                Subject: 1506
                Subject: 1731
                Subject: 1692
                Subject: 1724

                ScienceOpen disciplines: Medicine
                Keywords: epidemiology
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: epidemiology

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