Roberto A. Accinelli

Household air pollution is a major avoidable risk factor for cardiorespiratory disease.

Household air pollution (HAP) from biomass fuels, coal, and kerosene burned in open fires, primitive stoves, and lamps causes at least 2 million deaths per year. Many of these deaths occur in children <5 years of age with pneumonia and in women with COPD, lung cancer, and cardiovascular disease. HAP is inextricably linked to poverty, with activities to obtain fuel consuming a large proportion of the time and financial resources of poor households. Thus, fewer resources used in this way means less is available for basic needs like food, education, and health care. The burden of work and the exposure to smoke, particularly during cooking, are predominantly borne by women and children. Although historically HAP has not received sufficient attention from the scientific, medical, public health, development, and policy-making communities, the tide has clearly changed with the broad-based support and launch of the Global Alliance for Clean Cookstoves in 2010. There is now considerable reason for optimism that this substantial cause of cardiorespiratory morbidity and mortality will be addressed comprehensively and definitively. Drawing on our experience from four continents, we provide background information on the problem of HAP, health impacts of HAP, opportunities for research, and the current best solutions.

Genetic susceptibility to different clinical forms of tuberculosis in the Peruvian population

Racial variation, twin studies, segregation analyses, linkage and association studies all suggest that genetic factors play an important role in predisposition to tuberculosis. Many previous studies have been performed with pulmonary TB patients, as the most prevalent form of clinical TB (nearly 95%), and very few of them have considered extrapulmonary TB. The present study evaluates the effects of variation in eight candidate genes (LTA, TNF, IL1B, IL1RN, IL10, TGFB1, TIRAP and P2X7) with pulmonary, pleural, miliary and other extrapulmonary forms of TB in a Peruvian population from the North of Lima. 626 TB cases and 513 healthy controls were enrolled in this study. LTA(+368) and IL10(-592) were associated with different clinical forms of TB (P<0.05). LTA(+368) genotype A/A was protective for pleural TB, LTA(+368) G/A was correlated with susceptibility to miliary TB. Genotypes A/A and G/A were associated with protection and susceptibility respectively when considering all extrapulmonary TB forms versus either healthy controls or pulmonary TB patients. Carriers of IL10(-592)*C were under-represented among those with pulmonary TB and all TB forms (P<0.001). IL10(-1082)-IL10(-592) haplotypes showed different distributions among patients with pulmonary TB and all TB forms (P<0.01) when compared to healthy controls. In addition, IL10(-1082)-IL10(-592) haplotypes showed differences between pleural, miliary and all forms of extrapulmonary TB when compared with pulmonary TB (P<0.05). All findings are consistent with an under-representation of the IL10(-1082)*A-IL10(-592)*A haplotype in pulmonary TB patients. These results suggest that the polymorphisms LTA(+368) and IL10(-592), or variants in strong linkage disequilibrium, variably affect susceptibility to the differing clinical forms of TB in Peruvians.

Effect of reductions in biomass fuel exposure on symptoms of sleep apnea in children living in the Peruvian Andes: a preliminary field study.

Multiple studies have evaluated the prevalence of sleep apnea in pediatric populations. Although environmental exposures to cigarette smoke (ECS) increase the risk of habitual snoring, no studies have thus far examined the potential contribution of indoor pollution in children.

Algorithm for the diagnosis of smear-negative pulmonary tuberculosis in high-incidence resource-constrained settings

Diagnosis of smear‐negative pulmonary tuberculosis (SNPT) remains a challenge, particularly in resource‐constrained settings. We evaluated a diagnostic algorithm that combines affordable laboratory tools and a clinical prediction rule (CPR).

Ecological study on solid fuel use and pneumonia in young children: A worldwide association

Pneumonia constitutes one of the major causes of worldwide mortality in young children. Poverty has been traditionally assigned as the underlying factor accounting for these trends. However, the independent role of solid fuel use yielding biomass pollution on pneumonia rates among young children has not been extensively examined.

El asbesto, una epidemia todavía por controlar

El asbesto, formado por muy delgados hilos dispuestos en finas bras, es un compuesto de silicatos1 de cadena doble, resistente al alor, al fuego, a los ácidos y a la fricción, que por su alto punto de usión es un excelente aislante. Desde la revolución industrial, el sbesto tiene múltiples usos, como en la construcción de motores, alderos, barcos, automotores, trenes, material y ropa aislante al uego2.

Solid fuel use is associated with anemia in children

Abstract Over 3 billion people use solid fuels as a means of energy and heating source, and ˜ 50% of households burn them in inefficient, poorly ventilated stoves. In 2010, ˜ 43% of the 640 million preschool children in 220 countries suffered from a certain degree of anemia, with iron deficiency as the main cause in developed countries whereas its causes remained multifactorial in the undeveloped group. In this study, we explore the relations of country‐wide variables that might affect the peoples health status (from socioeconomic status to more specific variables such as water access). We found independent relationship between solid fuel use and anemia in children under five years old (p < 0.0001), taking into account the prevalence of anemia in pregnant woman and the access to improved water sources. Countries in which the population uses solid fuel the most have over three times higher anemia rates in children than countries with the lowest prevalence of solid fuels use. There is still a complex relationship between solid fuels use and anemia, as reflected in its worldwide significance (p < 0.05) controlled for measles immunization, tobacco consumption, anemia in pregnant mothers, girls primary education, life expectancy and improved water access but not (p > 0.05) when weighing for sanitation access or income per capita. Highlights3 billion people in the world use solid fuels.Globally 47.4% of children under five years old had anemia.There is an association between solid fuel uses and anemia in children.Liver hepcidin for macrophages IL‐6 production links to indoor particulates could explain anemia.

Enfermedades por exposición a la altura

En los últimos años la actividad turística, laboral y recreacional en la altura, es decir a niveles mayores a 2.000 msnm, se ha incrementado. En la altura disminuye la presión barométrica, y por tanto la de oxígeno, pues su proporción en el aire es siempre constante, por lo que conforme ascendemos respiramos este gas a una menor presión. Hay una serie de respuestas fisiológicas que ayudan a los individuos de menor altura a tolerar y adaptarse a las bajas condiciones de oxígeno. Sin embargo, no todos desarrollan estas respuestas adaptativas pudiendo presentar mal de montaña agudo (MMA), edema cerebral y/o edema pulmonar de gran altura1. Pero ¿por qué se producen? Durante la hipoxia, a nivel pulmonar se activan genes que a través de diferentes vías de señalización producen citocinas y quimiocinas proinflamatorias que promueven la migración de células transendoteliales y ejercen una potente acción proangiogénica. Hay inflamación alveolar local, liberándose otras moléculas a la circulación y desarrollándose una inflamación sistémica2. El tejido inflamado se vuelve severamente hipóxico, al incrementarse la distancia de difusión entre los vasos capilares y las células metabólicamente activas, lo que induce más inflamación3. Hay vasodilatación en estos tejidos, pero a nivel pulmonar se produce vasoconstricción, que en un inicio mejora la relación ventilación/perfusión, pero de persistir lleva a un incremento de la presión pulmonar que finalmente puede producir edema pulmonar y/o un incremento del flujo sanguíneo cerebral causando edema cerebral vasogénico4. Según la base genética estos procesos moleculares e inflamatorios, aún no completamente dilucidados, difieren en su expresión, lo que determina la variabilidad en la respuesta a la hipoxia hipobárica5. Entender la fisiopatología de la enfermedad por exposición aguda a la altura y el considerar los factores relacionados con su desarrollo, tales como la velocidad de ascenso, el nivel del mismo, las enfermedades subyacentes y el frío, permitirán realizar un diagnóstico y manejo oportuno. No existe una manera certera de realizar el diagnóstico del MMA o soroche porque sus síntomas y signos son atípicos6. El síntoma cardinal es la cefalea, que es expresiónRecent years have seen an increase in tourism, work, and recreational activities at high altitude, defined as heights greater than 2000 meters above sea level (MASL). Barometric pressure decreases with altitude, as does oxygen pressure, due to the constant proportion of oxygen in atmospheric air; therefore, the higher the altitude, the lower the pressure of inspired oxygen. A series of physiological responses help individuals from lower altitudes tolerate and adapt to low oxygen conditions. However not everyone develops these adaptive responses, and some individuals may present acute mountain sickness (AMS), cerebral edema and/or high-altitude pulmonary edema.1 But why do these phenomena occur? Hypoxia activates genes in the lungs that use various signaling pathways to produce proinflammatory cytokines and chemokines that promote the migration of transendothelial cells, exerting a potent proangiogenic effect. Local alveolar inflammation develops, releasing other molecules into the bloodstream and leading to systemic inflammation.2 The inflamed tissue becomes severely hypoxic, when the diffusion distance between the capillaries and the metabolically active cells increases, in turn causing more inflammation.3 Vasodilation is observed in these tissues, but vasoconstriction develops in the lung: initially this improves the ventilation/perfusion ratio, but as it persists, it causes an increase in pulmonary pressure that may eventually lead to pulmonary edema and/or an increase in blood flow to the brain, causing vasogenic cerebral edema.4 The expression of these molecular and inflammatory processes – not yet fully understood – varies according to genetic, which determine the variability in the response to hypobaric hypoxia.5 An understanding of the physiopathology of acute high-altitude illness and a study of the factors associated with its development, such as speed of ascent, height of ascent, underlying diseases, and cold conditions, are necessary for diagnosis and appropriate management. There is no accurate way of diagnosing AMS, also known as “soroche”, because the signs and symptoms are atypical.6 The cardinal symptom is headache, an indication of incipient cerebral

How do we "help the world breathe"?

infections that are accompanied by detection of bacterial pathogens such as S. pneumoniae are more likely to be symptomatic compared with RV infections without bacterial detection (5). Because symptomatic infections are more readily transmitted than asymptomatic infections (9, 10), cotransmission of RV and S. pneumonia (or perhaps other bacterial pathogens) could increase the probability of secondary symptomatic illnesses, and in turn could promote more efficient transmission of RV infection to other contacts. In addition increasing the probability of symptomatic respiratory illnesses, acquisition of both RV infection and pneumococcus could increase the risk for bacterial complications of viral respiratory infections, such as otitis media, sinusitis, and pneumonia. As a consequence, treatments that prevent or lessen the severity of RV infections could secondarily reduce the spread of pneumococcal colonization and these secondary infectious complications. As new therapies or vaccines targeting RV infections progress from preclinical investigations into clinical trials, it will be of great interest to determine whether inhibition of these picornavectors for pneumococcal transmission have benefits to respiratory health that extend beyond inhibition of RV infection. n

Biomass Pollution, Chimney Stove Interventions, and Discrepant Outcomes

Personal carbon monoxide (CO) exposures in the chimney woodstoves used in their study were only reduced by 30% following stove installation, while other chimney stoves, such as Patsari (Grupo Interdisciplinario de Tecnología Rural Apropiada), reduce personal exposures to CO by 78%. 2 Using the Patsari stove model, Romieu et al 3 reported a signifi cantly lower FEV 1 decline (31 mL) compared with open fi re use (62 mL) over 1 year of follow-up ( P 5 .012) for women 20 years of age and older. Zhou et al 4 found less deterioration in FEV 1 of 12, 13, and 16 mL/y in those who used biogas, improved ventilation, or both, respectively, compared with those who took up neither intervention, aft er adjustment for confounders. Th e longer the duration of improved fuel use and ventilation, the greater the benefi ts in slowing the decline of FEV 1 ( P , .05). 4