Matiana Ramirez-Aguilar

International study of temperature, heat and urban mortality: the ‘ISOTHURM’ project

BACKGROUND This study describes heat- and cold-related mortality in 12 urban populations in low- and middle-income countries, thereby extending knowledge of how diverse populations, in non-OECD countries, respond to temperature extremes. METHODS The cities were: Delhi, Monterrey, Mexico City, Chiang Mai, Bangkok, Salvador, São Paulo, Santiago, Cape Town, Ljubljana, Bucharest and Sofia. For each city, daily mortality was examined in relation to ambient temperature using autoregressive Poisson models (2- to 5-year series) adjusted for season, relative humidity, air pollution, day of week and public holidays. RESULTS Most cities showed a U-shaped temperature-mortality relationship, with clear evidence of increasing death rates at colder temperatures in all cities except Ljubljana, Salvador and Delhi and with increasing heat in all cities except Chiang Mai and Cape Town. Estimates of the temperature threshold below which cold-related mortality began to increase ranged from 15 degrees C to 29 degrees C; the threshold for heat-related deaths ranged from 16 degrees C to 31 degrees C. Heat thresholds were generally higher in cities with warmer climates, while cold thresholds were unrelated to climate. CONCLUSIONS Urban populations, in diverse geographic settings, experience increases in mortality due to both high and low temperatures. The effects of heat and cold vary depending on climate and non-climate factors such as the population disease profile and age structure. Although such populations will undergo some adaptation to increasing temperatures, many are likely to have substantial vulnerability to climate change. Additional research is needed to elucidate vulnerability within populations.

Air pollution, airway inflammation, and lung function in a cohort study of Mexico City schoolchildren.

Background The biological mechanisms involved in inflammatory response to air pollution are not clearly understood. Objective In this study we assessed the association of short-term air pollutant exposure with inflammatory markers and lung function. Methods We studied a cohort of 158 asthmatic and 50 nonasthmatic school-age children, followed an average of 22 weeks. We conducted spirometric tests, measurements of fractional exhaled nitric oxide (FeNO), interleukin-8 (IL-8) in nasal lavage, and pH of exhaled breath condensate every 15 days during follow-up. Data were analyzed using linear mixed-effects models. Results An increase of 17.5 μg/m3 in the 8-hr moving average of PM2.5 levels (interquartile range) was associated with a 1.08-ppb increase in FeNO [95% confidence interval (CI), 1.01–1.16] and a 1.07-pg/mL increase in IL-8 (95% CI 0.98–1.19) in asthmatic children and a 1.16 pg/ml increase in IL-8 (95% CI, 1.00–1.36) in nonasthmatic children. The 5-day accumulated average of exposure to particulate matter < 2.5 μm in aerodynamic diamter (PM2.5) was significantly inversely associated with forced expiratory volume in 1 sec (FEV1) (p = 0.048) and forced vital capacity (FVC) (p = 0.012) in asthmatic children and with FVC (p = 0.021) in nonasthmatic children. FeNO and FEV1 were inversely associated (p = 0.005) in asthmatic children. Conclusions Exposure to PM2.5 resulted in acute airway inflammation and decrease in lung function in both asthmatic and nonasthmatic children.

GSTM1 and GSTP1 and respiratory health in asthmatic children exposed to ozone

Acute exposure to ozone has been related to a wide spectrum of health effects in susceptible individuals. Genetic factors may influence interindividual variation in ozone response. The current authors investigated the relationships between common polymorphisms in two genes involved in response to oxidative stress, i.e. glutathione S-transferases M1 (GSTM1) and P1 (GSTP1), and both respiratory symptoms and lung function in response to ozone among childhood asthmatics. A total of 151 asthmatic children, who were participants in a randomised controlled trial of antioxidant vitamin supplementation in Mexico City, were studied. Children were genotyped using PCR methods and followed from October 1998–April 2000. Increases in reported breathing difficulty were associated with ozone exposure in children with GSTM1 null (8%, 95% confidence interval (CI) 1–15%, per 20-ppb increase in 1-h maximum daily average over 7 days) or GSTP1 Valine/Valine (Val/Val) genotypes (14%, 95% CI 5–25%). In children with both GSTM1 null and GSTP1 Val/Val genotypes, the increase in breathing difficulty associated with a 20-ppb increase in ozone exposure was even greater (21%, 95% CI 5–39%). GSTP1 genotypes were not significantly associated with ozone-related lung function changes. In conclusion, asthmatic children with glutathione S-transferase M1 null and glutathione S-transferase P1 Valine/Valine genotypes appear more susceptible to developing respiratory symptoms related to ozone exposure.

Antioxidant supplementation and nasal inflammatory responses among young asthmatics exposed to high levels of ozone

The inflammatory response to ozone in atopic asthma suggests that soluble mediators of inflammation are released in response to oxidant stress. Antioxidants may alleviate additional oxidative stress associated with photochemical oxidant pollution. This study investigates the impact of antioxidant supplementation on the nasal inflammatory response to ozone exposure in atopic asthmatic children. We conducted a randomized trial using a double‐blinded design. Children with asthma (n = 117), residents of Mexico City, were given randomly a daily supplement of vitamins (50 mg/day of vitamin E and 250 mg/day of vitamin C) or placebo. Nasal lavages were performed three times during the 4‐month follow‐up and analysed for content of interleukin‐6 (IL‐6), IL‐8, uric acid and glutathione (GSx). IL‐6 levels in the nasal lavage were increased significantly in the placebo group after ozone exposure while no increase was observed in the supplement group. The difference in response to ozone exposure between the two groups was significant (P = 0·02). Results were similar for IL‐8, but with no significant difference between the groups (P = 0·12). GSx decreased significantly in both groups. Uric acid decreased slightly in the placebo group. Our data suggest that vitamin C and E supplementation above the minimum dietary requirement in asthmatic children with a low intake of vitamin E might provide some protection against the nasal acute inflammatory response to ozone.

Traffic-related air pollution and respiratory symptoms among asthmatic children, resident in Mexico City: the EVA cohort study

BackgroundTaffic-related air pollution has been related to adverse respiratory outcomes; however, there is still uncertainty concerning the type of vehicle emission causing most deleterious effects.MethodsA panel study was conducted among 147 asthmatic and 50 healthy children, who were followed up for an average of 22 weeks. Incidence density of coughing, wheezing and breathing difficulty was assessed by referring to daily records of symptoms and childs medication. The association between exposure to pollutants and occurrence of symptoms was evaluated using mixed-effect models with binary response and poisson regression.ResultsWheezing was found to relate significantly to air pollutants: an increase of 17.4 μg/m3 (IQR) of PM2.5 (24-h average) was associated with an 8.8% increase (95% CI: 2.4% to 15.5%); an increase of 34 ppb (IQR) of NO2 (1-h maximum) was associated with an 9.1% increase (95% CI: 2.3% to16.4%) and an increase of 48 ppb (IQR) in O3 levels (1 hr maximum) to an increase of 10% (95% CI: 3.2% to 17.3%). Diesel-fueled motor vehicles were significantly associated with wheezing and bronchodilator use (IRR = 1.29; 95% CI: 1.03 to 1.62, and IRR = 1.32; 95% CI: 0.99 to 1.77, respectively, for an increase of 130 vehicles hourly, above the 24-hour average).ConclusionRespiratory symptoms in asthmatic children were significantly associated with exposure to traffic exhaust, especially from natural gas and diesel-fueled vehicles.

Ozone exposure, vitamin C intake, and genetic susceptibility of asthmatic children in Mexico City: a cohort study

BackgroundWe previously reported that asthmatic children with GSTM1 null genotype may be more susceptible to the acute effect of ozone on the small airways and might benefit from antioxidant supplementation. This study aims to assess the acute effect of ozone on lung function (FEF25-75) in asthmatic children according to dietary intake of vitamin C and the number of putative risk alleles in three antioxidant genes: GSTM1, GSTP1 (rs1695), and NQO1 (rs1800566).Methods257 asthmatic children from two cohort studies conducted in Mexico City were included. Stratified linear mixed models with random intercepts and random slopes on ozone were used. Potential confounding by ethnicity was assessed. Analyses were conducted under single gene and genotype score approaches.ResultsThe change in FEF25-75 per interquartile range (60 ppb) of ozone in persistent asthmatic children with low vitamin C intake and GSTM1 null was −91.2 ml/s (p = 0.06). Persistent asthmatic children with 4 to 6 risk alleles and low vitamin C intake showed an average decrement in FEF25-75 of 97.2 ml/s per 60 ppb of ozone (p = 0.03). In contrast in children with 1 to 3 risk alleles, acute effects of ozone on FEF25-75 did not differ by vitamin C intake.ConclusionsOur results provide further evidence that asthmatic children predicted to have compromised antioxidant defense by virtue of genetic susceptibility combined with deficient antioxidant intake may be at increased risk of adverse effects of ozone on pulmonary function.

Ozone exposure among Mexico city outdoor workers

Abstract In researching health effects of air pollution, pollutant levels from fixed-site monitors are commonly assigned to the subjects. However, these concentrations may not reflect the exposure these individuals actually experience. A previous study of ozone (O3 ) exposure and lung function among shoe-cleaners working in central Mexico City used fixed-site measurements from a monitoring station near the outdoor work sites as surrogates for personal exposure. The present study assesses the degree to which these estimates represented individual exposures. In 1996, personal O3 exposures of 39 shoe-cleaners working outdoors were measured using an active integrated personal sampler. Using mixed models, we assessed the relationship between measured personal O3 exposure and ambient O3 measurements from the fixed-site monitoring station. Ambient concentrations were approximately 50 parts per billion higher, on average, than personal exposures. The association between personal and ambient O3 was highly significant (mixed model slope p < 0.0001). The personal/ambient ratio was not constant, so use of the outdoor monitor would not be appropriate to rank O3 exposure and evaluate health effects between workers. However, the strong within-worker longitudinal association validates previous findings associating day-to-day changes in fixed-site O3 levels with adverse health effects among these shoe-cleaners and suggests fixed-site O3 monitors may adequately estimate exposure for other repeated-measure health studies of outdoor workers.

Measurements of personal exposure to nitrogen dioxide in four Mexican cities in 1996.

Abstract Nitrogen dioxide is a ubiquitous pollutant in urban areas. Indoor NO2 concentrations are influenced by penetration of outdoor concentrations and by indoor sources. The objectives of this study were to evaluate personal exposure to NO2, taking into account human time-activity patterns in four Mexican cities. Passive filter badges were used for indoor, outdoor, and personal NO2 measurements over 48 hr and indoor workplace measurements over 16 hr. Volunteers completed a questionnaire on exposure factors and a time-activity diary during the sample period. An unpaired t test, an analysis of variance (ANOVA), and a linear regression were performed to compare differences among cities and mean personal NO2 concentrations involving housing characteristics, as well as to determine which variables predicted the personal NO2 concentration. Sampling periods were in April, May, and June 1996 in Mexico City, Guadalajara, Cuernavaca, and Monterrey. All 122 volunteers in the study were working adults, with a mean age of 34 (SD ± 7.38); 64% were female, and the majority worked in public offices and universities. The highest NO2 concentrations were found in Mexico City (36 ppb for outdoor, 57 ppb for indoor, and 39 ppb for personal concentration) and the lowest in Monterrey (19 ppb for outdoor, 24 ppb for indoor, and 24 ppb for personal concentration). Significant differences in NO2 concentrations were found among the cities in different microenvironments. During the sampling period, volunteers spent 85% of their time indoors. The highest personal NO2 concentration was found when volunteers kept their windows closed (p = 0.03). In the regression model adjusted by city and gender, the best predictors of personal NO2 concentration were outdoor levels and time spent outdoors (R2 = 0.68). These findings suggest that outdoor NO2 concentrations were an important influence on the personal exposure to NO2, due to the specific characteristics and personal behavior of the people in these Mexican cities.

Morbilidad infantil por causas respiratorias y su relación con la contaminación atmosférica en Ciudad Juárez, Chihuahua, México

Objective: To assess the impact of atmospheric pollutants on the respiratory health of children of different age groups in Juarez City, Chihuahua, Mexico. Material and Methods: Data on emergency room visits between 1997 and 2001 for respiratory diseases in children less than 17 years old were obtained from hospitals in the Juarez City belonging to the Mexican Social Security Institute (IMSS). Diseases were classified into three groups according to ICD 9th and 10th codes: a) upper respiratory diseases, b) lower respiratory diseases, and c) asthma attacks. This information was stratified by age group ( 5 years). Daily air pollution data (ozone and PM 10 ) and weather conditions were obtained from the Monitoring Network System in Juarez City. Statistical analysis was carried out using a Generalized Additive Model assuming a Poisson distribution. Results: Ozone concentrations, but not PM 10 , were statistically associated with emergency room visits for respiratory diseases, mainly among children 5 years old or younger. In this group, an increase of 20 ppb 1-hr maximum for ozone was associated with an increase of 8.3% in the number of emergency room visits for upper respiratory diseases, with a 3day exposure lag; and an increase of 12.7% in the number of emergency room visits for lower respiratory diseases when considering a 4-day exposure lag in a maximum 8-hr mobile average. The largest effect for the complete sample and for

Effect of Personal Exposure to PM2.5 on Respiratory Health in a Mexican Panel of Patients with COPD.

Background: Air pollution is a problem, especially in developing countries. We examined the association between personal exposure to particulate matter with an aerodynamic diameter less than 2.5 µm (PM2.5) on respiratory health in a group of adults with chronic obstructive pulmonary disease (COPD). Methods: All participants resided in Mexico City and during follow-up, personal exposure to PM2.5, respiratory symptoms, medications, and daily activity were registered daily. Peak expiratory flow (PEF) was measured twice daily, from February through December, 2000, in 29 adults with moderate, severe, and very severe COPD. PEF changes were estimated for each 10 µg/m3 increment of PM2.5, adjustment for severity of COPD, minimum temperature, and day of the sampling. Results: For a 10-µg/m3 increase in the daily average of a two-day personal exposure to PM2.5, there was a significant 33% increase in cough (95% CI, range, 5‒69%), and 23% in phlegm (95% CI, range, 2‒54%), a reduction of the PEF average in the morning of −1.4 L/min. (95% CI , range, −2.8 to −0.04), and at night of −3.0 L/min (95% CI, range, −5.7 to −0.3), respectively. Conclusions: Exposure to PM2.5 was associated with reductions in PEF and increased respiratory symptoms in adults with COPD. The PEF reduction was observed both at morning and at night.