Manuel Oyarzún

Fine particulate matter and wheezing illnesses in the first year of life.

Background: Recent evidence implicates fine particulate matter (PM2.5), principally from vehicular exhaust, as a major cause of increased mortality and morbidity. However, there are limited data on the impact of PM2.5 on infant respiratory illnesses. Methods: We conducted a cohort study of 504 infants recruited at 4 months of age from primary health care units in southeastern Santiago, Chile. Project physicians followed infants through the first year of life via monthly check-ups and by appointments on demand. We obtained data for fine particulate matter, sulfur dioxide (SO2), and nitrogen dioxide (NO2) from the governmental monitoring network. Results: The most frequent diagnosis during follow-up was wheezing bronchitis, occurring 19.5 times per 100 infants per month. After adjusting for sex, socioeconomic level, family history of asthma, minimum temperature, and number of older siblings, we found that an increase of 10 μg/m3 of PM2.5 24-hour average was related to a 5% increase (95% confidence interval 0–9%) in the risk for wheezing bronchitis (1-day lag). This association was present for different lags, with a maximum observed for a 9-day lag (9%; 6–12%). No consistent association was detected with NO2 or SO2 ambient levels. Lower socioeconomic status and having older siblings were also associated with the risk of wheezing bronchitis. The association of PM2.5 and wheezing bronchitis was stronger among infants with a family history of asthma than among infants without. Conclusions: Air pollution in the form of fine particulates, mostly from vehicular exhaust, may adversely affect infants’ respiratory health with potential for chronic effects later in life.

Nutritional status, especially body mass index, from birth to adulthood and lung function in young adulthood.

Objective: The study assessed the impact of body mass index (BMI) at birth, infancy, and adulthood, and waist circumference on lung function. Methods: Using a longitudinal design 1221 Chilean young adults were studied. A standardized respiratory questionnaire was used. Forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), height, weight and waist circumference were measured. Data at birth and at 1 year were obtained from clinical notes. Results: Males with a BMI ≥ 30 and women with a BMI < 20 had a lower FEV1 (−230 mL, 95% CI −363 to −98; −106 mL, 95% CI −211 to −0.18, respectively). In both sexes those with a BMI 20–25 had the highest FEV1 and FVC. In males there was a negative association between waist circumference and FEV1 and FVC while in women the middle tertile had the highest FEV1 and FVC. There was an association between birthweight and BMI at birth, and FEV1 in men, when unadjusted for other measurements. Conclusions: BMI and waist circumference in adulthood make a greater impact on lung function in adulthood than anthropometric measurements at birth and infancy. Proxy measures of fatness in adulthood reduce lung function, but the pattern between fatness and lung function by sex may be different.

Rapid drop in infant blood lead levels during the transition to unleaded gasoline use in Santiago, Chile

This study was conducted to relate blood lead levels in infants to changes in lead emissions in Santiago, Chile, a heavily polluted setting where leaded gasoline began to be replaced with unleaded gasoline in 1993. Over an 18-mo period, 422 infants had blood lead levels, cotinine, and iron status determined at 12 mo. Blood lead levels fell at an average rate of 0.5 μ/dl every 2 mo, from 8.3 to 5.9 μ/dl, as the city experienced a net fall of 30% in the quantity of leaded gasoline sold. Time progression, car ownership, serum cotinine, and type of housing were significantly associated with a blood lead level ⩾ 10 μ/dl. In this study, the authors demonstrated that infant blood lead levels, even if relatively low, can drop very rapidly in conjunction with decreases in environmental lead exposure.

Mecanismos patogénicos en la enfermedad pulmonar obstructiva crónica causada por exposición a humo de biomasa

Chronic obstructive pulmonary disease (COPD) mortality and morbidity have increased significantly worldwide in recent decades. Although cigarette smoke is still considered the main risk factor for the development of the disease, estimates suggest that between 25% and 33% of COPD patients are non-smokers. Among the factors that may increase the risk of developing COPD, biomass smoke has been proposed as one of the most important, affecting especially women and children in developing countries. Despite the epidemiological evidence linking exposure to biomass smoke with adverse health effects, the specific cellular and molecular mechanisms by which this pollutant can be harmful for the respiratory and cardiovascular systems remain unclear. In this article we review the main pathogenic mechanisms proposed to date that make biomass smoke one of the major risk factors for COPD.

Role of Hypocapnia in the Alveolar Surfactant Increase Induced by Free Fatty Acid Intravenous Infusion in the Rabbit

Intravenous infusion of free fatty acid (FFA) produces an increase in the alveolar surfactant pool of the rabbit and pulmonary edema, hyperventilation, hypoxemia and hypocapnia. Previous studies suggested that alveolar PCO2 would be a regulator of intracellular storages of surfactant. In order to study the role of hypocapnia in the increase of lung surfactant in our experiments we administered 20 mg FFA X kg-1 X min-1 i.v. to rabbits breathing room air (n = 10) or 5% CO2, 21% O2, 74% N2 (n = 7). Disaturated phosphatidylcholine (DSPC) was determined in bronchial-alveolar lavage fluid as index of alveolar surfactant content, 5% CO2 in the inspired air prevented the hypocapnia and blocked the increase in DSPC induced by FFA (p less than 0.01). Pulmonary edema post-FFA was not changed by 5% CO2 administration. We conclude that hypocapnia produced by hyperventilation during FFA infusion would be an important factor in the increase of DSPC observed after FFA infusion.

Indoor risk factors for cough and their relation to wheeze and sensitization in Chilean young adults

OBJECTIVES We assessed the effects of indoor risk factors, including smoking, on different types of cough and on cough and wheeze in combination. METHODS Our sample was composed of 1232 men and women residing in a semirural area of Chile. We used a standardized questionnaire, sensitization to 8 allergens, and bronchial hyperresponsiveness to methacholine to assess cough and wheeze characteristics. Information was gathered on dampness, mold, ventilation, heating, housing quality, smoking, and environmental tobacco smoke exposure. RESULTS Most exposures were associated with cough alone or cough in combination with wheeze. Smoking, past smoking, and environmental tobacco smoke exposure were strongly associated with dry cough and wheeze. The use of coal for heating was associated with dry cough. Leaks, mold, and lack of kitchen ventilation were associated with cough and wheeze. Nocturnal cough and productive cough were associated with specific types of sensitization, but dry cough was not. Productive cough was associated with hyperresponsiveness to methacholine. CONCLUSIONS Several different types of indoor exposures, including environmental tobacco smoke exposure, are important contributors to morbidity associated with cough and wheeze. A vigorous preventive strategy designed to lower exposures to indoor risk factors would lower rates of respiratory morbidity.

Effect of 0.25 ppm Ozone exposure on pulmonary damage induced by bleomycin

To study the effect of ozone in a chronically damaged lung, we used a bleomycin (BLM) induced pulmonary fibrosis model. Both endotracheal instillation of BLM and O3 exposure both produce lung inflammation and fibrosis. Oxidative stress would be a common mechanism of damage for both BLM and O3. Our aim was to assess lung injury induced by 5 and 60 days of intermittent exposure to 0.25 ppm O3 in rats with bleomycin-induced pulmonary fibrosis. Thirty-day-old Sprague Dawley rats were endotracheally instilled with BLM (1 U/100 g body weight) and, 30 days later, exposed to 0.25 ppm 03 (0.25 ppm 4 h per day, 5 days a week). Histopatology controls were instilled with saline and breathing room air. Histopathological evaluation of lungs was done 5 and 60 days after O3 exposure. BLM-induced lung damage did not change after 60 days of intermittent O3 exposure. Five days of O3 exposure increased the mean score of BLM-induced pulmonary inflammation and fibrosis (p=0.06). Frequency of bronchopneumonia increased from 1/7 to 6/6 (p <0.001), suggesting that a short-term exposure to O3 in a previously damaged lung might be a risk factor for developing further lung injury.

Thromboxane Mediates the Increase in Alveolar Surfactant Pool Induced by Free Fatty Acid Infusion in the Rabbit

Intravenous infusion of free fatty acid (FFA) produces pulmonary edema and an increase in the alveolar surfactant content of the rabbit. In order to identify a likely mediator of this lung response to FFA, we used inhibitors of cyclo-oxygenase (indomethacin, 15 mg X kg-1 i.v., or meclofenamate, 5 mg X kg-1 i.v.) and thromboxane synthetase inhibitors (imidazole, 50 mg X kg-1 i.v. or dazoxiben, 2 mg X kg-1 i.v.) which were administered before FFA, 20 mg X kg-1 X min-1 i.v., in four different experimental series (n = 54). Lung surfactant was measured in bronchial-alveolar lavage fluid by determining disaturated phosphatidylcholine (DSPC). Both kinds of inhibitors blocked the increase in FFA-induced DSPC. They increased the survival rate but they only slightly changed the post-FFA morphofunctional pulmonary alterations. We conclude that the increase in alveolar surfactant induced by FFA is likely mediated by thromboxane. This mediator would seem to play a minor role in the FFA-induced pulmonary edema observed.

Sodium Cholate Interactions with Rabbit’s Pulmonary Surfactant

In order to assay the possibility that sodium cholate interacts with pulmonary surfactant, we obtained bronchoalveolar lavage fluid from lungs of adult rabbits and measured the hysteresis area of surface tension-area loops of the bronchoalveolar lavage fluid in a Wilhelmy surface tension balance, before and after the addition of sodium cholate to reach different concentrations. We observed a biphasic behavior: at a low concentration of sodium cholate (1.5 x 10(5) mol/l; n = 6) the hysteresis area increased (p less than 0.05) as compared to its control (initial) area, meanwhile at a higher concentration (5 x 10(-5) mol/l; n = 6) the hysteresis area decreased (p less than 0.025), revealing a likely interaction of sodium cholate with pulmonary surfactant. We conclude that sodium cholate is able to interact in vitro with lung surfactant.