Women cooking with biomass fuels have increased respiratory symptoms and a slight average reduction in lung function compared with those cooking with gas.

Women exposed domestically to biomass develop chronic obstructive pulmonary disease with clinical characteristics, quality of life, and increased mortality similar in degree to that of tobacco smokers.

A case-control study was performed in women older than 40 yr of age to evaluate the risk of cooking with traditional wood stoves for chronic bronchitis and chronic airway obstruction (CAO). The subjects were recruited from patients attending a referral chest hospital in Mexico City. We selected 127 patients with chronic bronchitis or CAO, of which 63 had chronic bronchitis alone, 23 had CAO alone (FEV1 less than 75% of predicted), and 41 had both chronic bronchitis and CAO (cases). Four control groups were selected: 83 patients with pulmonary tuberculosis, 100 patients with interstitial lung diseases, 97 patients with ear, nose and throat ailments, and 95 healthy visitors to the hospital (controls). Exposure to wood smoke, assessed as any or none, and as hour-years (years of exposure multiplied by average hours of exposure per day) was significantly higher in cases than in controls. Crude odds ratios for wood smoke exposure were 3.9 (95% CI, 2.0 to 7.6) for chronic bronchitis only, 9.7 (95% CI, 3.7 to 27) for CAO plus chronic bronchitis, and 1.8 (95% CI, 0.7 to 4.7) for CAO only. Differences in exposure to wood smoke persisted after adjusting by stratification and logistic regression for age, income, education, smoking, place of residence, and place of birth. Risk of chronic bronchitis alone and chronic bronchitis with CAO increased linearly with hour-years of cooking with a wood stove; odds ratios for exposure to more than 200 hour-years compared with nonexposed were 15.0 (95% CI, 5.6 to 40) for chronic bronchitis only and 75 (95% CI, 18 to 306) for chronic bronchitis with CAO. The findings support a causal role of domestic wood smoke exposure in chronic bronchitis and chronic airflow obstruction.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), is a global health threat with the potential to cause severe disease manifestations in the lungs. Although COVID-19 has been extensively characterized clinically, the factors distinguishing SARS-CoV-2 from other respiratory viruses are unknown. Here, we compared the clinical, histopathological, and immunological characteristics of patients with COVID-19 and pandemic influenza A(H1N1). We observed a higher frequency of respiratory symptoms, increased tissue injury markers, and a histological pattern of alveolar pneumonia in pandemic influenza A(H1N1) patients. Conversely, dry cough, gastrointestinal symptoms and interstitial lung pathology were observed in COVID-19 cases. Pandemic influenza A(H1N1) was characterized by higher levels of IL-1RA, TNF-α, CCL3, G-CSF, APRIL, sTNF-R1, sTNF-R2, sCD30, and sCD163. Meanwhile, COVID-19 displayed an immune profile distinguished by increased Th1 (IL-12, IFN-γ) and Th2 (IL-4, IL-5, IL-10, IL-13) cytokine levels, along with IL-1β, IL-6, CCL11, VEGF, TWEAK, TSLP, MMP-1, and MMP-3. Our data suggest that SARS-CoV-2 induces a dysbalanced polyfunctional inflammatory response that is different from the immune response against pandemic influenza A(H1N1). Furthermore, we demonstrated the diagnostic potential of some clinical and immune factors to differentiate both diseases. These findings might be relevant for the ongoing and future influenza seasons in the Northern Hemisphere, which are historically unique due to their convergence with the COVID-19 pandemic.

The main objective of this study is to describe the presence of infections in patients with pulmonary haemorrhage and systemic lupus erythematosus. Patients with systemic lupus erythematosus and pulmonary haemorrhage were thoroughly evaluated in the first 48 hours with imaging plus bronchoscopy and bronchoalveolar fluid analysis. If needed, videoassisted thoracoscopy and lung biopsy were performed too. In all, search for bacterial, mycobacterial and fungal infections proceeded. Appropriate blood, bronchoalveolar fluid and tissue cultures were taken. Patients were treated with antibiotics and corticosteroids in case of infection. Otherwise, they received initial intravenous methylprednsiolone pulses for 3 days as standard therapy for pulmonary haemorrhage in systemic lupus erythematosus. Additional treatment with immunosuppressives was further decided by the treating physicians. Fourteen events in 13 patients were evaluated. In eight events (57%), an infection was demonstrated. Aetiological agents included Pseudomonas sp. and Aspergillus fumigatus. Four patients died, three of them because of the pulmonary infection and one because of cerebral haemorrhage secondary to severe systemic hypertension, 48 hours after methylprednisolone treatment. Patients with systemic lupus erythematosus and pulmonary haemorrhage have a high prevalence of infections. The influence of pulmonary haemorrhage in the setting of systemic lupus erythematosus needs further study to establish adequate treatment and to reduce the high mortality of this complication.