No abstract

Exposure to household air pollution (HAP) from solid fuel combustion affects almost half of the world population. Adverse respiratory outcomes such as respiratory infections, impaired lung growth and chronic obstructive pulmonary disease have been linked to HAP exposure. Solid fuel smoke is a heterogeneous mixture of various gases and particulates. Cell culture and animal studies with controlled exposure conditions and genetic homogeneity provide important insights into HAP mechanisms. Impaired bacterial phagocytosis in exposed human alveolar macrophages possibly mediates several HAP-related health effects. Lung pathological findings in HAP-exposed individuals demonstrate greater small airways fibrosis and less emphysema compared with cigarette smokers. Field studies using questionnaires, air pollution monitoring and/or biomarkers are needed to better establish human risks. Some, but not all, studies suggest that improving cookstove efficiency or venting emissions may be associated with reduced respiratory symptoms, lung function decline in women and severe pneumonia in children. Current studies focus on fuel switching, stove technology replacements or upgrades and air filter devices. Several governments have initiated major programmes to accelerate the upgrade from solid fuels to clean fuels, particularly liquid petroleum gas, which provides research opportunities for the respiratory health community.

Approximately 3 billion people around the world cook and heat their homes using solid fuels in open fires and rudimentary stoves, resulting in household air pollution. Household air pollution secondary to indoor combustion of solid fuel is associated with multiple chronic obstructive pulmonary disease (COPD) outcomes. The exposure is associated with both chronic bronchitis and emphysema phenotypes of COPD as well as a distinct form of obstructive airway disease called bronchial anthracofibrosis. COPD from household air pollution differs from COPD from tobacco smoke with respect to its disproportionately greater bronchial involvement, lesser emphysematous change, greater impact on quality of life, and possibly greater oxygen desaturation and pulmonary hypertensive changes. Interventions that decrease exposure to biomass smoke may decrease the risk for incident COPD and attenuate the longitudinal decline in lung function, but more data on exposure-response relationships from well-designed longitudinal studies are needed.

Rationale: It is hypothesized that the metabolic syndrome explains the association between body mass index (BMI) and asthma in adults. Objectives: Our objective was to longitudinally compare the relative strengths of the associations of the metabolic syndrome and BMI with incident asthma in adults. Methods: We included 4,619 eligible participants in the Coronary Artery Risk Development in Young Adults (CARDIA) cohort followed over 25 years. Incident asthma was defined by a new self-reported provider asthma diagnosis plus either the presence of asthma symptoms and/or use of asthma medications. Cox proportional hazard analyses were performed. Measurements and Main Results: Six hundred two subjects (417 women and 185 men) developed incident asthma over 25 years of follow-up. Metabolic syndrome predicted incident asthma among women but not men (unadjusted hazard ratios, 1.50 and 0.98; P ¼ 0.01 and 0.93, respectively). BMI had a similar predictive association among women but not men (unadjusted hazard ratios, 1.19 and 1.04 per 5 units of BMI; P , 0.001 and 0.60, respectively). The association of metabolic syndrome with incident asthma in women was no longer statistically significant after adjustment for BMI (P ¼ 0.44). In contrast, the association of BMI with incident asthma in women remained statistically significant after adjusting for the metabolic syndrome (P ¼ 0.01). In a stepwise model, BMI was a stronger predictor than the metabolic syndrome (P ¼ 0.001). Conclusions: BMI is a stronger predictor of incident asthma among women than the metabolic syndrome. Other obesity-associated factors that are not a part of the metabolic syndrome may play a role in the BMI-asthma association in women.Keywords: incident asthma; metabolic syndrome; body mass index Obesity and asthma are chronic diseases that have increased in prevalence across the world over the last 2 decades (1, 2). During the period 2009 to 2010, 1 in 12 American adults had asthma, and more than one-third of American adults were obese (3, 4). Obesity, as defined by elevated body mass index (BMI) of 30 kg/m 2 or more, is a risk factor for asthma, particularly among women. The basis for this association, however, remains unclear. The metabolic syndrome, as defined by the third Adult Treatment Panel (ATP-III) criteria (5), includes the presence of any three of the following five traits: abdominal adiposity (waist circumference . 102 cm in men and . 88 cm in women), hypertriglyceridemia (>150 mg/dl or drug treatment for high triglycerides), low high-density lipoprotein (HDL) cholesterol levels (,40 mg/dl in men and ,50 mg/dl in women or drug treatment for low HDL), elevated blood pressure (>130/85 mm Hg or drug treatment for elevated blood pressure), and impaired fasting blood glucose or diabetes mellitus (>100 mg/dl or antidiabetic drug treatment) (6). Some epidemiologic studies suggest that waist circumference-defined abdominal adiposity, one of the characteristics of the metabolic syndrome, is more strongly associated with prevalent asthma than is BMI-defined...

The current review focuses on the association between biomass smoke and common chronic respiratory diseases, discuss differences between biomass smoke-related COPD and tobacco smoke-related COPD, highlights chronic respiratory diseases that are specific for biomass smoke exposure such as hut lung and bronchial anthracofibrosis, and discusses the known impact of beneficial interventions.