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Acute exacerbations of idiopathic pulmonary fibrosis are associated with high mortality and are of unknown cause. The effect of air pollution on exacerbations of interstitial lung disease is unknown. This study aims to define the association of air pollution exposure with acute exacerbation of idiopathic pulmonary fibrosis. Patients with idiopathic pulmonary fibrosis and corresponding air pollution data were identified from a longitudinal cohort. Air pollution exposures were assigned to each patient for ozone, nitrogen dioxide, particulate matter, sulfur dioxide and carbon monoxide based on geo-coded residential addresses. Cox proportional hazards models were used to estimate the association of air pollution exposures and acute exacerbations. Acute exacerbation was significantly associated with antecedent 6-week increases in mean level, maximum level and number of exceedances above accepted standards of ozone (hazard ratio (HR) 1.57, 95% CI 1.09-2.24; HR 1.42, 95% CI 1.11-1.82; and HR 1.51, 95% CI 1.17-1.94, respectively) and nitrogen dioxide (HR 1.41, 95% CI 1.04-1.91; HR 1.27, 95% CI 1.01-1.59; and HR 1.20, 95% CI 1.10-1.31, respectively). Increased ozone and nitrogen dioxide exposure over the preceding 6 weeks was associated with an increased risk of acute exacerbation of idiopathic pulmonary fibrosis, suggesting that air pollution may contribute to the development of this clinically meaningful event.

Background: More than two-fifths of the world’s population uses solid fuels, mostly biomass, for cooking. The resulting biomass smoke exposure is a major cause of chronic obstructive pulmonary disease (COPD) among women in developing countries.Objective: To assess whether lower woodsmoke exposure from use of a stove with a chimney, compared to open fires, is associated with lower markers of airway inflammation in young women.Design: We carried out a cross-sectional analysis on a sub-cohort of participants enrolled in a randomized controlled trial in rural Guatemala, RESPIRE.Participants: We recruited 45 indigenous women at the end of the 18-month trial; 19 women who had been using the chimney stove for 18–24 months and 26 women still using open fires.Measurements: We obtained spirometry and induced sputum for cell counts, gene expression of IL-8, TNF-α, MMP-9 and 12, and protein concentrations of IL-8, myeloperoxidase and fibronectin. Exhaled carbon monoxide (CO) and 48-hr personal CO tubes were measured to assess smoke exposure.Results: MMP-9 gene expression was significantly lower in women using chimney stoves. Higher exhaled CO concentrations were significantly associated with higher gene expression of IL-8, TNF-α, and MMP-9. Higher 48-hr personal CO concentrations were associated with higher gene expression of IL-8, TNF- α, MMP-9 and MMP-12; reaching statistical significance for MMP-9 and MMP-12.Conclusions: Compared to using an open wood fire for cooking, use of a chimney stove was associated with lower gene expression of MMP-9, a potential mediator of airway remodeling. Among all participants, indoor biomass smoke exposure was associated with higher gene expression of multiple mediators of airway inflammation and remodeling; these mechanisms may explain some of the observed association between prolonged biomass smoke exposure and COPD.

Background: More than two-fifths of the world's population uses solid fuels, mostly biomass, for cooking. The resulting biomass smoke exposure is a major cause of chronic obstructive pulmonary disease (COPD) among women in developing countries. Objective:

Recent changes in the global climate system have resulted in excess mortality and morbidity, particularly among susceptible individuals with preexisting cardiopulmonary disease. These weather patterns are projected to continue and intensify as a result of rising CO2 levels, according to the most recent projections by climate scientists. In this Pulmonary Perspective, motivated by the American Thoracic Society Committees on Environmental Health Policy and International Health, we review the global human health consequences of projected changes in climate for which there is a high level of confidence and scientific evidence of health effects, with a focus on cardiopulmonary health. We discuss how many of the climate-related health effects will disproportionally affect people from economically disadvantaged parts of the world, who contribute relatively little to CO2 emissions. Last, we discuss the financial implications of climate change solutions from a public health perspective and argue for a harmonized approach to clean air and climate change policies.

BackgroundWhile exposure to outdoor particulate matter (PM) has been associated with poor asthma outcomes, few studies have investigated the combined effects of outdoor and indoor PM (including secondhand tobacco smoke).ObjectiveTo examine the associations between PM and asthma outcomes.MethodsWe analyzed data from a cohort of adults with asthma and rhinitis (n=302; 82% both conditions; 13% asthma only; 5% rhinitis alone) including measures of home PM, tobacco smoke exposure (hair nicotine and self-report), ambient PM from regional monitoring, distance to roadway, and season (wet or dry). The outcomes of interest were frequent respiratory symptoms and forced expiratory volume in 1 second (FEV1) below the lower limit of normal (NHANES reference values). Multivariable regression analyses examined the associations (Odds Ratio [OR] and 95% Confidence Interval [95%CI]) between exposures and these outcomes, adjusted by sociodemographic characteristics.ResultsIn adjusted analyses of each exposure, the highest tertile of home PM and season of interview were associated with increased odds for more frequent respiratory symptoms (OR=1.64 95%CI: [1.00, 2.69] and OR=1.66 95%CI: [1.09, 2.51]). The highest tertile of hair nicotine was significantly associated with FEV1 below the lower limit of normal (OR=1.80 95%CI: [1.00, 3.25]). In a model including home PM, ambient PM, hair nicotine, and season, only two associations remained strong: hair nicotine with FEV1 below the lower limit of normal and season of measurement (dry, April-October) with increased respiratory symptoms (OR=1.85 95%CI: [1.00, 3.41] and OR=1.54 95%CI: [1.0, 2.37]). When that model was stratified by sex, the highest tertiles of ambient PM and hair nicotine were associated with FEV1 below the lower limit of normal among women (OR=2.23 95%CI: [1.08, 4.61] and OR=2.90 95%CI: [1.32, 6.38]), but not men. The highest tertile of hair nicotine was also associated with increased respiratory symptoms in women but not men (OR=2.38 95%CI: [1.26, 4.49]). When stratified by age, the middle quartile of ambient PM and the highest hair nicotine tertile were associated with increased respiratory symptoms (OR=2.07 95%CI: [1.01, 4.24] and OR=2.55 95%CI: [1.21, 5.36]) in those under 55 but not in the older stratum.ConclusionsExposure to PM from both home and ambient sources is associated with increased symptoms and lower lung function in adults with asthma, although these associations vary by type of PM, the respiratory outcome studied, sex and age.

Background: Estimating the burden of disease attributable to long-term exposure to fine particulate matter (PM2.5) in ambient air requires knowledge of both the shape and magnitude of the relative risk (RR) function. However, adequate direct evidence to id

OBJECTIVES: Shift work, such as alternating day and nights, causes chronobiologic disruptions which may cause an increase in hypertension risk. However, the relative contributions of the components of shift work ‒ such as shift type (eg, night work) and rotations (ie, switching of shift times; day to night) ‒ on this association are not clear. To address this question, we constructed novel definitions of night work and rotational work and assessed their associations with risk of incident hypertension. METHODS: A cohort of 2151 workers at eight aluminum manufacturing facilities previously studied for cardiovascular disease was followed from 2003 through 2013 for incident hypertension, as defined by ICD-9 insurance claims codes. Detailed time-registry data was used to classify each worker’s history of rotational and night work. The associations between recent rotational work and night work in the last 12 months and incident hypertension were estimated using adjusted Cox proportional hazards models. RESULTS: Elevated hazard ratios (HR) were observed for all levels of recent night work (>0–5, >5–50, >50–95, >95–100%) compared with non-night workers, and among all levels of rotational work (10–20, >20–30, and >30%) compared with those working

The ice cloud detection sensitivity of the millimeter cloud radar (MMCR) and the Ka-band Zenith radar (KAZR) is investigated using a collocated Raman lidar (RL) at the Atmospheric Radiation Measurement Program Southern Great Plains site. Only profiles that are transparent to the RL with ice clouds only are considered in this study. The MMCR underestimates the RL ice cloud optical depth (COD) by 20%. The MMCR detects no ice clouds in 37% of the profiles. These profiles where ice cloud goes undetected by the MMCR typically contain very optically thin clouds, with a mean RL ice COD of 0.03. Higher ice cloud detection sensitivity is found for the KAZR, which underestimates the RL ice COD by 15%. The decrease in the ice COD bias for the KAZR compared to the MMCR is largely due to a decrease in the ice COD bias for the situation where the transparent profiles with ice clouds are detected by both the RL and cloud radar. The climatic net ice cloud radiative effects (CREs) from the RL at the top of the atmosphere (TOA) and the surface are 3.2 W m−2 and −0.6 W m−2, respectively. The ice CREs at the TOA and surface are underestimated for the MMCR by 0.7 W m−2 and 0.16 W m−2 (21% and 29%) and underestimated for the KAZR by 0.6 W m−2 and 0.14 W m−2 (17% and 24%). The ice clouds undetected by the cloud radars led to underestimating the climatic net cloud heating rates below 150 hPa by about 0–0.04 K day−1.

Background: Personal care product chemicals may be contributing to risk for asthma and other atopic illnesses. The existing literature is conflicting, and many studies do not control for multiple chemical exposures. Methods: We quantified concentrations of three phthalate metabolites, three parabens, and four other phenols in urine collected twice during pregnancy from 392 women. We measured T helper 1 (Th1) and T helper 2 (Th2) cells in their children's blood at ages two, five, and seven, and assessed probable asthma, aeroallergies, eczema, and lung function at age seven. We conducted linear and logistic regressions, controlling for additional biomarkers measured in this population as selected by Bayesian Model Averaging. Results: The majority of comparisons showed null associations. Mono-n-butyl phthalate (MnBP) was associated with higher Th2% (RR: 10.40, 95% CI: 3.37, 17.92), and methyl paraben was associated with lower Th1% (RR: −3.35, 95% CI: −6.58, −0.02) and Th2% at borderline significance (RR: −4.45, 95% CI: −8.77, 0.08). Monoethyl phthalate was associated with lower forced expiratory flow from 25 to 75% of forced vital capacity (FEF25–75%) (RR: −3.22 L/s, 95% CI: −6.02, −0.34). Propyl paraben (OR: 0.86, 95% CI: 0.74, 0.99) was associated with decreased odds of probable asthma. Conclusions: While some biomarkers, particularly those from low molecular weight phthalates, were associated with an atopic cytokine profile and poorer lung function, no biomarkers were associated with a corresponding increase in atopic disease. Keywords: Asthma, Allergy, Personal care products, Phthalates, Cytokines, Chemical mixtures

Background: Exposure to household air pollution from solid fuel combustion for cooking and heating is an important risk factor for premature death and disability worldwide. Current evidence supports an association of ambient air pollution with cardiovascular disease but is limited for household air pollution and for cardiac function. Controlled exposure studies can complement evidence provided by field studies. Objectives: To investigate effects of short-term, controlled exposures to emissions from five cookstoves on measures of cardiac function. Methods: Forty-eight healthy adults (46% female; 20–36 years) participated in six, 2-h exposures (‘treatments’), including emissions from five cookstoves and a filtered-air control. Target fine particulate matter (PM2.5) exposure-concentrations per treatment were: control, 0 µg/m3; liquefied petroleum gas, 10 µg/m3; gasifier, 35 µg/m3; fan rocket, 100 µg/m3; rocket elbow, 250 µg/m3; and three stone fire, 500 µg/m3. Participants were treated in a set (pre-randomized) sequence as groups of 4 to minimize order bias and time-varying confounders. Heart rate variability (HRV) and cardiac repolarization metrics were calculated as 5-min means immediately and at 3 h following treatment, for analysis in linear mixed-effects models comparing cookstove to control. Results: Short-term differences in SDNN (standard deviation of duration of all NN intervals) and VLF (very-low frequency power) existed for several cookstoves compared to control. While all cookstoves compared to control followed a similar trend for SDNN, the greatest effect was seen immediately following three stone fire (β = −0.13 ms {%}; 95% confidence interval = −0.22, −0.03%), which reversed in direction at 3 h (0.03%; −0.06, 0.13%). VLF results were similar in direction and timing to SDNN; however, other HRV or cardiac repolarization results were not similar to those for SDNN. Discussion: We observed some evidence of short-term, effects on HRV immediately following cookstove treatments compared to control. Our results suggest that cookstoves with lower PM2.5 emissions are potentially capable of affecting cardiac function, similar to stoves emitting higher PM2.5 emissions.

BackgroundThough SARS-CoV-2 outbreaks have been documented in occupational settings and in-person essential work has been suspected as a risk factor for COVID-19, occupational differences in excess mortality have, to date, not been examined. Such information could point to opportunities for intervention, such as vaccine prioritization or regulations to enforce safer work environments.Methods and findingsUsing autoregressive integrated moving average models and California Department of Public Health data representing 356,188 decedents 18-65 years of age who died between January 1, 2016 and November 30, 2020, we estimated pandemic-related excess mortality by occupational sector and occupation, with additional stratification of the sector analysis by race/ethnicity. During these first 9 months of the COVID-19 pandemic, working-age adults experienced 11,628 more deaths than expected, corresponding to 22% relative excess and 46 excess deaths per 100,000 living individuals. Sectors with the highest relative and per-capita excess mortality were food/agriculture (39% relative excess; 75 excess deaths per 100,000), transportation/logistics (31%; 91 per 100,000), manufacturing (24%; 61 per 100,000), and facilities (23%; 83 per 100,000). Across racial and ethnic groups, Latino working-age Californians experienced the highest relative excess mortality (37%) with the highest excess mortality among Latino workers in food and agriculture (59%; 97 per 100,000). Black working-age Californians had the highest per-capita excess mortality (110 per 100,000), with relative excess mortality highest among transportation/logistics workers (36%). Asian working-age Californians had lower excess mortality overall, but notable relative excess mortality among health/emergency workers (37%), while White Californians had high per-capita excess deaths among facilities workers (70 per 100,000).ConclusionsCertain occupational sectors are associated with high excess mortality during the pandemic, particularly among racial and ethnic groups also disproportionately affected by COVID-19. In-person essential work is a likely venue of transmission of coronavirus infection and must be addressed through vaccination and strict enforcement of health orders in workplace settings.

Millions of people are exposed to arsenic in drinking water, which at high concentrations is known to cause lung cancer in humans. At lower concentrations, the risks are unknown. We enrolled 196 lung cancer cases and 359 controls matched on age and gender from western Nevada and Kings County, California in 2002-2005. After adjusting for age, sex, education, smoking and occupational exposures, odds ratios for arsenic concentrations ≥85 µg/L (median = 110 µg/L, mean = 173 µg/L, maximum = 1,460 µg/L) more than 40 years before enrollment were 1.39 (95% CI = 0.55-3.53) in all subjects and 1.61 (95% CI = 0.59-4.38) in smokers. Although odds ratios were greater than 1.0, these increases may have been due to chance given the small number of subjects exposed more than 40 years before enrollment. This study, designed before research in Chile suggested arsenic-related cancer latencies of 40 years or more, illustrates the enormous sample sizes needed to identify arsenic-related health effects in low-exposure countries with mobile populations like the U.S. Nonetheless, our findings suggest that concentrations near 100 µg/L are not associated with markedly high relative risks.

BackgroundArsenic exposure via drinking water increases the risk of chronic respiratory disease in adults. However, information on pulmonary health effects in children after early life exposure is limited.MethodsThis population-based cohort study set in rural Matlab, Bangladesh, assessed lung function and respiratory symptoms of 650 children aged 7-17 years. Children with in utero and early life arsenic exposure were compared with children exposed to less than 10 µg/l in utero and throughout childhood. Because most children drank the same water as their mother had drunk during pregnancy, we could not assess only in utero or only childhood exposure.ResultsChildren exposed in utero to more than 500 µg/l of arsenic were more than eight times more likely to report wheezing when not having a cold [odds ratio (OR) = 8.41, 95% confidence interval (CI): 1.66-42.6, P < 0.01] and more than three times more likely to report shortness of breath when walking on level ground (OR = 3.86, 95% CI: 1.09-13.7, P = 0.02) and when walking fast or climbing (OR = 3.19, 95% CI: 1.22-8.32, P < 0.01]. However, there was little evidence of reduced lung function in either exposure category.ConclusionsChildren with high in utero and early life arsenic exposure had marked increases in several chronic respiratory symptoms, which could be due to in utero exposure or to early life exposure, or to both. Our findings suggest that arsenic in water has early pulmonary effects and that respiratory symptoms are a better marker of early life arsenic toxicity than changes in lung function measured by spirometry.

RationaleAir pollution is a known asthma trigger and has been associated with short-term asthma symptoms, airway inflammation, decreased lung function, and reduced response to asthma rescue medications.ObjectivesTo assess a causal relationship between air pollution and childhood asthma using data that address temporality by estimating air pollution exposures before the development of asthma and to establish the generalizability of the association by studying diverse racial/ethnic populations in different geographic regions.MethodsThis study included Latino (n = 3,343) and African American (n = 977) participants with and without asthma from five urban regions in the mainland United States and Puerto Rico. Residential history and data from local ambient air monitoring stations were used to estimate average annual exposure to five air pollutants: ozone, nitrogen dioxide (NO₂), sulfur dioxide, particulate matter not greater than 10 μm in diameter, and particulate matter not greater than 2.5 μm in diameter. Within each region, we performed logistic regression to determine the relationship between early-life exposure to air pollutants and subsequent asthma diagnosis. A random-effects model was used to combine the region-specific effects and generate summary odds ratios for each pollutant.Measurements and main resultsAfter adjustment for confounders, a 5-ppb increase in average NO₂ during the first year of life was associated with an odds ratio of 1.17 for physician-diagnosed asthma (95% confidence interval, 1.04-1.31).ConclusionsEarly-life NO₂ exposure is associated with childhood asthma in Latinos and African Americans. These results add to a growing body of evidence that traffic-related pollutants may be causally related to childhood asthma.

BackgroundMillions of people worldwide are exposed to arsenic-contaminated water. In the largest city in northern Chile (Antofagasta), more than 250,000 people were exposed to high arsenic drinking water concentrations from 1958 until 1970 when a water treatment plant was installed. Because of its unique geology, limited water sources, and good historical records, lifetime exposure and long-term latency patterns can be assessed in this area with better accuracy than in other arsenic-exposed areas worldwide.MethodsWe conducted a population-based case-control study in northern Chile from October 2007 to December 2010 involving 232 bladder and 306 lung cancer cases and 640 age- and gender-matched controls, with detailed information on past exposure and potential confounders, including smoking and occupation.ResultsBladder cancer ORs for quartiles of average arsenic concentrations in water before 1971 (335 μg/L) were 1.00, 1.36 [95% confidence interval (CI), 0.78-2.37], 3.87 (2.25-6.64), and 6.50 (3.69-11.43), respectively. Corresponding lung cancer ORs were 1.00, 1.27 (0.81-1.98), 2.00 (1.24-3.24), and 4.32 (2.60-7.17). Bladder and lung cancer ORs in those highly exposed in Antofagasta during 1958 to 1970 but not thereafter were 6.88 (3.84-12.32) and 4.35 (2.57-7.36), respectively.ConclusionsThe lung and bladder cancer risks that we found up to 40 years after high exposures have ended are very high.ImpactOur findings suggest that prevention, treatment, and other mortality reduction efforts in arsenic-exposed countries will be needed for decades after exposure cessation.

BackgroundWhether long-term, low-level hydrogen sulfide (H2S) gas is a cause of health effects, including asthma, is uncertain. Rotorua city, New Zealand, has the largest population exposed, from geothermal sources, to relatively high ambient levels of H2S. In a cross-sectional study, the authors investigated associations with asthma in this population.MethodsA total of 1637 adults, aged 18-65 years, were enrolled during 2008-2010. Residences and workplaces were geocoded. H2S exposures at homes and workplaces were estimated using city-wide networks of passive H2S samplers and kriging to create exposure surfaces. Exposure metrics were based on (1) time-weighted exposures at home and work; and (2) the maximum exposure (home or work). Exposure estimates were entered as quartiles into regression models, with covariate data.ResultsNeither exposure metric showed evidence of increased asthma risk from H2S. However, some suggestion of exposure-related reduced risks for diagnosed asthma and asthma symptoms, particularly wheezing during the last 12 months, emerged. With the maximum exposure metric, the prevalence ratio for wheeze in the highest exposure quartile was 0.80 (0.65, 0.99) and, for current asthma treatment, 0.75 (0.52, 1.08). There was no evidence that this was caused by a "survivor effect".ConclusionsThe study provided no evidence that asthma risk increases with H2S exposure. Suggestions of a reduced risk in the higher exposure areas are consistent with recent evidence that H2S has signaling functions in the body, including induction of smooth muscle relaxation and reduction of inflammation. Study limitations, including possible confounding, preclude definitive conclusions.

Higher values of the environmental relative moldiness index (ERMI), a DNA-based method for quantifying indoor molds, have been associated with asthma in children. In this study, settled dust samples were collected from the homes of adults with asthma, rhinitis, or both conditions (n=139 homes) in Northern California. The ERMI values for these samples were compared to those from dust collected in homes from the same geographic region randomly selected as part of the 2006 American Healthy Home Survey (n=44). The median ERMI value in homes of adult with airway disease (6) was significantly greater than median ERMI value (2) in the randomly selected homes (p

The objective of this study was to assess the utility of urinary Clara cell protein (CC16) as a biomarker of increased lung epithelial permeability in non-smokers exposed to outdoor secondhand smoke. Twenty-eight healthy non-smoking adults visited outdoor patios of a restaurant and a bar where non-participants smoked and an open-air control with no smokers on three weekend days in a crossover study; subjects visited each site once for 3 h. Urine samples were collected at baseline, immediately post exposure and next morning, and analyzed for CC16. Changes in CC16 across location types or with cigarette count were analyzed using mixed-effect models, which included all subjects and stratified by gender. Urinary CC16 was higher in males (n=9) compared with females (n=18) at all measurement occasions (P

Abstract Background A travel mode shift to active transportation such as bicycling would help reduce traffic volume and related air pollution emissions as well as promote increased physical activity level. Cyclists, however, are at risk for exposure to vehicle-related air pollutants due to their proximity to vehicle traffic and elevated respiratory rates. To promote safe bicycle commuting, the City of Berkeley, California, has designated a network of residential streets as “Bicycle Boulevards.” We hypothesized that cyclist exposure to air pollution would be lower on these Bicycle Boulevards when compared to busier roads and this elevated exposure may result in reduced lung function. Methods We recruited 15 healthy adults to cycle on two routes – a low-traffic Bicycle Boulevard route and a high-traffic route. Each participant cycled on the low-traffic route once and the high-traffic route once. We mounted pollutant monitors and a global positioning system (GPS) on the bicycles. The monitors were all synced to GPS time so pollutant measurements could be spatially plotted. We measured lung function using spirometry before and after each bike ride. Results We found that fine and ultrafine particulate matter, carbon monoxide, and black carbon were all elevated on the high-traffic route compared to the low-traffic route. There were no corresponding changes in the lung function of healthy non-asthmatic study subjects. We also found that wind-speed affected pollution concentrations. Conclusions These results suggest that by selecting low-traffic Bicycle Boulevards instead of heavily trafficked roads, cyclists can reduce their exposure to vehicle-related air pollution. The lung function results indicate that elevated pollutant exposure may not have acute negative effects on healthy cyclists, but further research is necessary to determine long-term effects on a more diverse population. This study and broader field of research have the potential to encourage policy-makers and city planners to expand infrastructure to promote safe and healthy bicycle commuting.

ObjectivesWe estimated the extent to which socioeconomic status (SES) gradients in adult asthma and rhinitis outcomes can be explained by home and neighborhood environmental factors.MethodsUsing survey data for 515 adults with either asthma or rhinitis, or both, we examined environmental mediators of SES associations with disease severity, using the Severity of Asthma Scale, and health-related quality of life (HRQL), using the Rhinasthma Scale. We defined SES on the basis of education and household income. Potential environmental mediators included home type and ownership, exposures to allergens and irritants, and a summary measure of perceived neighborhood problems. We modeled each outcome as a function of SES, and controlled for age, gender, and potential mediators.ResultsGradients in SES were apparent in disease severity and HRQL. Living in a rented house partially mediated the SES gradient for both severity and HRQL (P < .01). Higher perceived levels of neighborhood problems were associated with poorer HRQL and partially mediated the income-HRQL relationship (P < .01).ConclusionsDifferences in home and neighborhood environments partially explained associations of SES with adult asthma and rhinitis outcomes.

BACKGROUND: Ambient air pollution (AAP) may be associated with increased risk for Pneumocystis pneumonia (PCP). The mechanisms underlying this association remain uncertain. OBJECTIVES: To determine if real-life exposures to AAP are associated with suppressed IgM antibody responses to P. jirovecii in HIV-infected (HIV+) patients with active PCP, and to determine if AAP, mediated by suppressed serologic responses to Pneumocystis, is associated with adverse clinical outcomes. METHODS: We conducted a prospective cohort study in HIV+ patients residing in San Francisco and admitted to San Francisco General Hospital with microscopically confirmed PCP. Our AAP predictors were ambient air concentrations of particulate matter of < 10 µm in diameter (PM10) and < 2.5 µm in diameter (PM2.5), nitrogen dioxide (NO2), ozone (O3), and sulfur dioxide (SO2) measured immediately prior to hospital admission and 2 weeks prior to admission. Our primary outcomes were the IgM serologic responses to four recombinant P. jirovecii major surface glycoprotein (Msg) constructs: MsgC1, MsgC3, MsgC8, and MsgC9. RESULTS: Elevated PM10 and NO2 exposures immediately prior to and two weeks prior to hospital admission were associated with decreased IgM antibody responses to P. jirovecii Msg. For exposures immediately prior to admission, every 10 µg/m(3) increase in PM10 was associated with a 25 to 35% decrease in IgM responses to Msg (statistically significant for all the Msg constructs), and every 10 ppb increase in NO2 was associated with a 19-45% decrease in IgM responses to Msg (statistically significant for MsgC8 and MsgC9). Similar findings were seen with exposures two weeks prior to admission, but for fewer of the Msg constructs. CONCLUSIONS: Real life exposures to PM10 and NO2 were associated with suppressed IgM responses to P. jirovecii Msg in HIV+ patients admitted with PCP, suggesting a mechanism of immunotoxicity by which AAP increases host susceptibility to pulmonary infection.

BackgroundQuantification of the disease burden caused by different risks informs prevention by providing an account of health loss different to that provided by a disease-by-disease analysis. No complete revision of global disease burden caused by risk factors has been done since a comparative risk assessment in 2000, and no previous analysis has assessed changes in burden attributable to risk factors over time.MethodsWe estimated deaths and disability-adjusted life years (DALYs; sum of years lived with disability [YLD] and years of life lost [YLL]) attributable to the independent effects of 67 risk factors and clusters of risk factors for 21 regions in 1990 and 2010. We estimated exposure distributions for each year, region, sex, and age group, and relative risks per unit of exposure by systematically reviewing and synthesising published and unpublished data. We used these estimates, together with estimates of cause-specific deaths and DALYs from the Global Burden of Disease Study 2010, to calculate the burden attributable to each risk factor exposure compared with the theoretical-minimum-risk exposure. We incorporated uncertainty in disease burden, relative risks, and exposures into our estimates of attributable burden.FindingsIn 2010, the three leading risk factors for global disease burden were high blood pressure (7·0% [95% uncertainty interval 6·2-7·7] of global DALYs), tobacco smoking including second-hand smoke (6·3% [5·5-7·0]), and alcohol use (5·5% [5·0-5·9]). In 1990, the leading risks were childhood underweight (7·9% [6·8-9·4]), household air pollution from solid fuels (HAP; 7·0% [5·6-8·3]), and tobacco smoking including second-hand smoke (6·1% [5·4-6·8]). Dietary risk factors and physical inactivity collectively accounted for 10·0% (95% UI 9·2-10·8) of global DALYs in 2010, with the most prominent dietary risks being diets low in fruits and those high in sodium. Several risks that primarily affect childhood communicable diseases, including unimproved water and sanitation and childhood micronutrient deficiencies, fell in rank between 1990 and 2010, with unimproved water and sanitation accounting for 0·9% (0·4-1·6) of global DALYs in 2010. However, in most of sub-Saharan Africa childhood underweight, HAP, and non-exclusive and discontinued breastfeeding were the leading risks in 2010, while HAP was the leading risk in south Asia. The leading risk factor in Eastern Europe, most of Latin America, and southern sub-Saharan Africa in 2010 was alcohol use; in most of Asia, North Africa and Middle East, and central Europe it was high blood pressure. Despite declines, tobacco smoking including second-hand smoke remained the leading risk in high-income north America and western Europe. High body-mass index has increased globally and it is the leading risk in Australasia and southern Latin America, and also ranks high in other high-income regions, North Africa and Middle East, and Oceania.InterpretationWorldwide, the contribution of different risk factors to disease burden has changed substantially, with a shift away from risks for communicable diseases in children towards those for non-communicable diseases in adults. These changes are related to the ageing population, decreased mortality among children younger than 5 years, changes in cause-of-death composition, and changes in risk factor exposures. New evidence has led to changes in the magnitude of key risks including unimproved water and sanitation, vitamin A and zinc deficiencies, and ambient particulate matter pollution. The extent to which the epidemiological shift has occurred and what the leading risks currently are varies greatly across regions. In much of sub-Saharan Africa, the leading risks are still those associated with poverty and those that affect children.FundingBill & Melinda Gates Foundation.

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

It is estimated that up to half of the world's population burns biomass fuel (wood, crop residues, animal dung and coal) for indoor uses such as cooking, lighting and heating. As a result, a large proportion of women and children are exposed to high levels of household air pollution (HAP). The short and long term effects of these exposures on the respiratory health of this population are not clearly understood. On May 9-11, 2011 NIH held an international workshop on the "Health Burden of Indoor Air Pollution on Women and Children," in Arlington, VA. To gather information on the knowledge base on this topic and identify research gaps, ahead of the meeting we conducted a literature search using PubMed to identify publications that related to HAP, asthma, and chronic obstructive pulmonary disease (COPD). Abstracts were all analyzed and we report on those considered by the respiratory sub study group at the meeting to be most relevant to the field. Many of the studies published are symptom-based studies (as opposed to objective measures of lung function or clinical examination etc.) and measurement of HAP was not done. Many found some association between indoor exposures to biomass smoke as assessed by stove type (e.g., open fire vs. liquid propane gas) and respiratory symptoms such as wheeze and cough. Among the studies that examined objective measures (e.g. spirometry) as a health outcome, the data supporting an association between biomass smoke exposure and COPD in adult women are fairly robust, but the findings for asthma are mixed. If an association was observed between the exposures and lung function, most data seemed to demonstrate mild to moderate reductions in lung function, the pathophysiological mechanisms of which need to be investigated. In the end, the group identified a series of scientific gaps and opportunities for research that need to be addressed to better understand the respiratory effects of exposure to indoor burning of the different forms of biomass fuels.

Background: Extreme hot weather conditions have been associated with increased morbidity and mortality, but risks are not evenly distributed throughout the population. Previously, a heat vulnerability index (HVI) was created to geographically locate popula

ObjectivesThe aim of this study was to investigate whether exposure to a range of relatively low concentrations of aged secondhand smoke (SHS), similar to those encountered commonly in the community, would impair endothelial function in a concentration-dependent manner.BackgroundExposure to SHS impairs endothelial function in humans. The concentration-dependent relationship for aged SHS effects on endothelial function after an exposure of short duration is unknown.MethodsThirty-three healthy nonsmokers were exposed to 1 of 2 low levels of aged SHS or to conditioned filtered air for 30 min. The primary end point was change in maximal percent brachial artery flow-mediated dilation after exposure.ResultsIn a linear regression model for each increase in SHS exposure by 100 μg/m(3) respirable suspended particles, the absolute maximal percent brachial artery flow-mediated dilation was reduced by 0.67%. We did not find evidence of a threshold for the effect of SHS on flow-mediated dilation.ConclusionsShort-term exposure to real-world levels of aged SHS for 30 min resulted in a concentration-dependent decrease in endothelial function as measured by flow-mediated dilation.

PurposeEvidence suggests that arsenic in drinking water causes non-malignant lung disease, but nearly all data concern exposed adults. The desert city of Antofagasta (population 257,976) in northern Chile had high concentrations of arsenic in drinking water (>800 μg/l) from 1958 until 1970, when a new treatment plant was installed. This scenario, with its large population, distinct period of high exposure, and accurate data on past exposure, is virtually unprecedented in environmental epidemiology. We conducted a pilot study on early-life arsenic exposure and long-term lung function. We present these preliminary findings because of the magnitude of the effects observed.MethodsWe recruited a convenience sample consisting primarily of nursing school employees in Antofagasta and Arica, a city with low drinking water arsenic. Lung function and respiratory symptoms in 32 adults exposed to >800 μg/l arsenic before age 10 were compared to 65 adults without high early-life exposure.ResultsEarly-life arsenic exposure was associated with 11.5% lower forced expiratory volume in 1 s (FEV(1)) (P = 0.04), 12.2% lower forced vital capacity (FVC) (P = 0.04), and increased breathlessness (prevalence odds ratio = 5.94, 95% confidence interval 1.36-26.0). Exposure-response relationships between early-life arsenic concentration and adult FEV(1) and FVC were also identified (P trend = 0.03).ConclusionsEarly-life exposure to arsenic in drinking water may have irreversible respiratory effects of a magnitude similar to smoking throughout adulthood. Given the small study size and non-random recruitment methods, further research is needed to confirm these findings.

Rationale: Chronic air pollutant exposure has been associated with development of Acute Respiratory Distress Syndrome (ARDS) in patients at risk, particularly from severe trauma. We recently reported that shorter peripheral blood leukocyte (PBL) telomere length (TL) was associated with worse outcomes and higher severity of ARDS in critically ill patients. Since most major air pollutants are potent oxidants that can induce cellular oxidative stress, and oxidative stress can accelerate telomere shortening, we hypothesized that higher levels of chronic air pollutant exposure would be associated with shorter telomere length in critically ill patients including patients with ARDS. Methods: PBL-TL was measured in genomic DNA collected on the morning of ICU day 2 in 772 critically ill patients enrolled in a prospective observational study. Exposures to air pollutants including ozone (warm-season only), particulate matter

Rationale: Asthma is one of the most common chronic respiratory diseases in the United States. Several outdoor air pollutants have been associated with asthma morbidity. Previous studies of the effects of short-term air pollution exposure have been limited by potential exposure misclassification and limited spatial and temporal resolution of asthma outcome measures. Objectives: We aimed to assess the association of short-term air pollutant exposure with the use of short-acting beta-2 agonists (SABA) for asthma by monitoring the time and place of occurrence with electronic medication monitors. Methods: In a cohort of adults and children with asthma (n = 287; 60% female), we deployed electronic medication monitors fitted to metered-dose inhalers to monitor SABA use, capturing the date, time and location of use. We assigned pollutant exposures based on each actuation’s time and location (4-h mean measures for ozone and particulate matter of 2.5 µm or smaller (PM2.5)), assessed associations using generalized linear models and explored age-specific effects. Measurements and Main Results: Ambient ozone exposure was positively associated with SABA use (p = 0.01). Age-specific associations were identified (interaction p = 0.01), with a larger increase in SABA use for children (11.3%; 95% CI: 7.0%–18.2%) than adults (8.4%; 95% CI: 6.4%–11.0%) per IQR increase of ozone (16.8 ppb). Conclusions: These findings support existing evidence that short-term exposure to ozone can cause morbidity in individuals with asthma, and suggest that ozone exposures below the current U.S. EPA standard may be associated with increased SABA use. Keywords: Mhealth, Patient monitoring, Asthma, Air pollution, Ozone

Abstract The disease burden associated with air pollution continues to grow. The World Health Organization (WHO) estimates ≈7 million people worldwide die yearly from exposure to polluted air, half of which—3.3 million—are attributable to cardiovascular disease (CVD), greater than from major modifiable CVD risks including smoking, hypertension, hyperlipidemia, and diabetes mellitus. This serious and growing health threat is attributed to increasing urbanization of the world's populations with consequent exposure to polluted air. Especially vulnerable are the elderly, patients with pre‐existing CVD, and children. The cumulative lifetime burden in children is particularly of concern because their rapidly developing cardiopulmonary systems are more susceptible to damage and they spend more time outdoors and therefore inhale more pollutants. World Health Organization estimates that 93% of the world's children aged

Background: Exposure to household air pollution (HAP) from cooking with biomass fuel affects billions of people. We hypothesized that HAP from woodsmoke, compared to other household fuels, was associated with adverse cardiovascular outcomes, of which there have been few studies. Methods: A cross-sectional study was completed in 299 females aged 40–70 years in Kaski District, Nepal, during 2017–18. All participants underwent a standard 12-lead ECG, ankle and brachial systolic blood pressure measurement, and 2D color and Doppler echocardiography. Current stove type was confirmed by inspection. Blood pressure, height, and weight were measured using a standardized protocol. Hypertension was defined as ≥140/90 mmHg or prior diagnosis. Hemoglobin A1c (HbA1c) was obtained, with diabetes mellitus defined as a prior diagnosis or HbA1C ≥ 6.5%. We used adjusted linear and logistic multivariable regressions to examine the relationship of stove type with cardiac structure and function. Results: The majority of women primarily used liquified petroleum gas (LPG) stoves (65%), while 12% used biogas, and 23% used wood-burning cook-stoves. Prevalence of major cardiovascular risk factors was 35% with hypertension, 19% with diabetes mellitus, and 15% current smokers. After adjustment, compared to LPG, wood stove use was associated with increased indexed left atrial volume (β = 3.15, 95% CI 1.22 to 5.09) and increased indexed left ventricular end diastolic volume (β = 7.97, 95% CI 3.11 to 12.83). There was no association between stove type and systemic hypertension, left ventricular mass, systolic dysfunction, diastolic dysfunction, pulmonary hypertension, abnormal ankle-brachial index, or clinically significant ECG abnormalities. Conclusion: Biomass fuel use was associated with increased indexed left atrial volume and increased indexed left ventricular diastolic volume in Nepali women, suggesting subclinical adverse cardiac remodeling from HAP in this cross-sectional study. We did not find evidence of an association with hypertension or typical cardiac sequelae of hypertension. Future studies to confirm these results are needed.

Summary: Background: Asthma disproportionately affects communities of colour in the USA, but the underlying factors for this remain poorly understood. In this study, we assess the role of historical redlining as outlined in security maps created by the Home Owners' Loan Corporation (HOLC), the discriminatory practice of categorising neighbourhoods on the basis of perceived mortgage investment risk, on the burden of asthma in these neighbourhoods. Methods: We did an ecological study of HOLC risk grades and asthma exacerbations in California using the security maps available for the following eight cities: Fresno, Los Angeles, Oakland, Sacramento, San Diego, San Jose, San Francisco, and Stockton. Each census tract was categorised into one of four risk levels (A, B, C, or D) on the basis of the location of population-weighted centroids on security maps, with the worst risk level (D) indicating historical redlining. We obtained census tract-level rates of emergency department visits due to asthma from CalEnviroScreen 3.0. We assessed the relationship between risk grade and log-transformed asthma visit rates between 2011 and 2013 using ordinary least squares regression. We included potential confounding variables from the 2010 Census and CalEnviroScreen 3.0: diesel exhaust particle emissions, PM2·5, and percent of the population living below 2 times the federal poverty level. We also built random intercept and slope models to assess city-level variation in the relationship between redlining and asthma. Findings: In the 1431 census tracts assessed (64 [4·5%] grade A, 241 [16·8%] grade B, 719 [50·2%] grade C, and 407 [28·4%] grade D), the proportion of the population that was non-Hispanic black and Hispanic, the percentage of the population living in poverty, and diesel exhaust particle emissions all significantly increased as security map risk grade worsened (p

BackgroundDiverse environmental exposures, studied separately, have been linked to health outcomes in adult asthma, but integrated multi-factorial effects have not been modeled. We sought to evaluate the contribution of combined social and physical environmental exposures to adult asthma lung function and disease severity.MethodsData on 176 subjects with asthma and/or rhinitis were collected via telephone interviews for sociodemographic factors and asthma severity (scored on a 0-28 point range). Dust, indoor air quality, antigen-specific IgE antibodies, and lung function (percent predicted FEV1) were assessed through home visits. Neighborhood socioeconomic status, proximity to traffic, land use, and ambient air quality data were linked to the individual-level data via residential geocoding. Multiple linear regression separately tested the explanatory power of five groups of environmental factors for the outcomes, percent predicted FEV1 and asthma severity. Final models retained all variables statistically associated (p < 0.20) with each of the two outcomes.ResultsMean FEV1 was 85.0 +/- 18.6%; mean asthma severity score was 6.9 +/- 5.6. Of 29 variables screened, 13 were retained in the final model of FEV1 (R2 = 0.30; p < 0.001) and 15 for severity (R2 = 0.16; p < 0.001), including factors from each of the five groups. Adding FEV1 as an independent variable to the severity model further increased its explanatory power (R2 = 0.25).ConclusionsMultivariate models covering a range of individual and environmental factors explained nearly a third of FEV1 variability and, taking into account lung function, one quarter of variability in asthma severity. These data support an integrated approach to modeling adult asthma outcomes, including both the physical and the social environment.

Community-level approaches for pediatric asthma management rely on locally collected information derived primarily from two sources: claims records and school-based surveys. We combined claims and school-based surveillance data, and examined the asthma-related risk patterns among adolescent students.Symptom data collected from school-based asthma surveys conducted in Oakland, CA were used for case identification and determination of severity levels for students (high and low). Survey data were matched to Medicaid claims data for all asthma-related health care encounters for the year prior to the survey. We then employed recursive partitioning to develop classification trees that identified patterns of demographics and healthcare utilization associated with severity.A total of 561 students had complete matched data; 86.1% were classified as high-severity, and 13.9% as low-severity asthma. The classification tree consisted of eight subsets: three indicating high severity and five indicating low severity. The risk subsets highlighted varying combinations of non-specific demographic and socioeconomic predictors of asthma prevalence, morbidity and severity. For example, the subset with the highest class-prior probability (92.1%) predicted high-severity asthma and consisted of students without prescribed rescue medication, but with at least one in-clinic nebulizer treatment. The predictive accuracy of the tree-based model was approximately 66.7%, with an estimated 91.1% of high-severity cases and 42.3% of low-severity cases correctly predicted.Our analysis draws on the strengths of two complementary datasets to provide community-level information on children with asthma, and demonstrates the utility of recursive partitioning methods to explore a combination of features that convey asthma severity. Keywords: Asthma, Classification, Risk stratification, Statistical data analysis, Disease management

BACKGROUND: Although studies have demonstrated that air pollution is associated with exacerbation of asthma symptoms in children with asthma, little is known about the susceptibility of subgroups, particularly those with atopy. OBJECTIVE: This study was designed to evaluate our a priori hypothesis that identifiable subgroups of asthmatic children are more likely to wheeze with exposure to ambient air pollution. METHODS: A cohort of 315 children with asthma, 6-11 years of age, was recruited for longitudinal follow-up in Fresno, California (USA). During the baseline visit, children were administered a respiratory symptom questionnaire and allergen skin-prick test. Three times a year, participants completed 14-day panels during which they answered symptom questions twice daily. Ambient air quality data from a central monitoring station were used to assign exposures to the following pollutants: particulate matter

Abstract Background DNA methylation of CpG sites on genetic loci has been linked to increased risk of asthma in children exposed to elevated ambient air pollutants (AAPs). Further identification of specific CpG sites and the pollutants that are associated with methylation of these CpG sites in immune cells could impact our understanding of asthma pathophysiology. In this study, we sought to identify some CpG sites in specific genes that could be associated with asthma regulation (Foxp3 and IL10) and to identify the different AAPs for which exposure prior to the blood draw is linked to methylation levels at these sites. We recruited subjects from Fresno, California, an area known for high levels of AAPs. Blood samples and responses to questionnaires were obtained (n = 188), and in a subset of subjects (n = 33), repeat samples were collected 2 years later. Average measures of AAPs were obtained for 1, 15, 30, 90, 180, and 365 days prior to each blood draw to estimate the short-term vs. long-term effects of the AAP exposures. Results Asthma was significantly associated with higher differentially methylated regions (DMRs) of the Foxp3 promoter region (p = 0.030) and the IL10 intronic region (p = 0.026). Additionally, at the 90-day time period (90 days prior to the blood draw), Foxp3 methylation was positively associated with NO2, CO, and PM2.5 exposures (p = 0.001, p = 0.001, and p = 0.012, respectively). In the subset of subjects retested 2 years later (n = 33), a positive association between AAP exposure and methylation was sustained. There was also a negative correlation between the average Foxp3 methylation of the promoter region and activated Treg levels (p = 0.039) and a positive correlation between the average IL10 methylation of region 3 of intron 4 and IL10 cytokine expression (p = 0.030). Conclusions Short-term and long-term exposures to high levels of CO, NO2, and PM2.5 were associated with alterations in differentially methylated regions of Foxp3. IL10 methylation showed a similar trend. For any given individual, these changes tend to be sustained over time. In addition, asthma was associated with higher differentially methylated regions of Foxp3 and IL10.

BackgroundUnderstanding the progression from beryllium exposure (BeE) to chronic beryllium disease (CBD) is essential for optimizing screening and early intervention to prevent CBD.MethodsWe developed an analytic markov model of progression to cbd that assigns annual probabilities for progression through three states: from BeE to beryllium sensitization and then to CBD. We used calculations of the number in each state over time to assess which of several alternative progression models are most consistent with the limited available empirical data on prevalence and incidence. We estimated cost-effectiveness of screening considering both incremental (cost/case) and cumulative program costs.ResultsNo combination of parameters for a simple model in which risk of progression remains constant over time can meet the empirical constraints of relatively frequent early cases and continuing development of new cases with long latencies. Modeling shows that the risk of progression is initially high and then declines over time. Also, it is likely that there are at least two populations that differ significantly in risk. The cost-effectiveness of repetitive screening declines over time, although new cases will still be found with long latencies. However, screening will be particularly cost-effective when applied to persons with long latencies who have not been previously screened.ConclusionsTo optimize use of resources, the intensity of screening should decrease over time. Estimation of lifetime cumulative CBD risk should consider the declining risk of progression over time.

BackgroundDespite extensive evidence that air pollution affects childhood asthma, state-level and national-level tracking of asthma outcomes in relation to air pollution is limited.ObjectivesOur goals were to evaluate the feasibility of linking the 2001 California Health Interview Survey (CHIS), air monitoring, and traffic data; estimate associations between traffic density (TD) or outdoor air pollutant concentrations and childhood asthma morbidity; and evaluate the usefulness of such databases, linkages, and analyses to Environmental Public Health Tracking (EPHT).MethodsWe estimated TD within 500 feet of residential cross-streets of respondents and annual average pollutant concentrations based on monitoring station measurements. We used logistic regression to examine associations with reported asthma symptoms and emergency department (ED) visits/hospitalizations.ResultsAssignment of TD and air pollution exposures for cross-streets was successful for 82% of children with asthma in Los Angeles and San Diego, California, Counties. Children with asthma living in high ozone areas and areas with high concentrations of particulate matter < 10 microm in aerodynamic diameter experienced symptoms more frequently, and those living close to heavy traffic reported more ED visits/hospitalizations. The advantages of the CHIS for asthma EPHT include a large and representative sample, biennial data collection, and ascertainment of important socio-demographic and residential address information. Disadvantages are its cross-sectional design, reliance on parental reports of diagnoses and symptoms, and lack of information on some potential confounders.ConclusionsDespite limitations, the CHIS provides a useful framework for examining air pollution and childhood asthma morbidity in support of EPHT, especially because later surveys address some noted gaps. We plan to employ CHIS 2003 and 2005 data and novel exposure assessment methods to re-examine the questions raised here.

ObjectiveTo estimate the duration of work life among persons reporting a physician's diagnosis of COPD, asthma, or rhinitis compared to those with select non-respiratory conditions or none and to delineate the factors associated with continuance of employment.MethodsPersons ages 55 to 75 reporting a physician's diagnosis of COPD, asthma, or rhinitis as well as those without any of these conditions were identified by random-digit dialing (RDD) in the continental U.S and administered a structured survey. We used Kaplan-Meier life table analysis to estimate the duration of work life among persons with and without the three conditions and Cox proportional hazard regression to examine the role of demographic and work characteristics in the proportion leaving employment in each time interval.ResultsPersons with COPD, asthma, and rhinitis were no less likely than the remainder of the population to have ever worked, but those with COPD were less likely to be working when interviewed or as of age 65, whichever came first. As of age 55, only 62 percent of persons with COPD continued to work versus 72 and 78 percent of persons with asthma and rhinitis, respectively. Persons with COPD, asthma, and rhinitis all had an elevated risk of leaving work prior to age 65 relative to those without chronic conditions, with and without adjustment for demographic and work characteristics.ConclusionCOPD and to a lesser extent asthma and rhinitis were associated with a substantially shortened work life, an effect not due to demographic and work characteristics.

The Centers for Disease Control and Prevention in the U.S. Department of Health and Human Services is working with selected state and local health departments, academic centers, and others to develop an environmental public health tracking initiative to improve geographic and temporal surveillance of environmental hazards, exposures, and related health outcomes. The objective is to support policy strategies and interventions for disease prevention by communities and environmental health agencies at the federal, state, and local levels. The first 3 years of the initiative focused on supporting states and cities in developing capacity, information technology infrastructure, and pilot projects to demonstrate electronic linkage of environmental hazard or exposure data and disease data. The next phase requires implementation across states. This transition could provide opportunities to further integrate research, surveillance, and practice through attention to four areas. The first is to develop a shared and transparent knowledge base that draws on environmental health research and substantiates decisions about what to track and the interpretation of results. The second is to identify and address information needs of policy and stakeholder audiences in environmental health. The third is to adopt mechanisms for coordination, decision making, and governance that can incorporate and support the major entities involved. The fourth is to promote disease prevention by systematically identifying and addressing population-level environmental determinants of health and disease.

BackgroundAlthough personal cigarette smoking is the most important cause and modulator of chronic obstructive pulmonary disease (COPD), secondhand smoke (SHS) exposure could influence the course of the disease. Despite the importance of this question, the impact of SHS exposure on COPD health outcomes remains unknown.MethodsWe used data from two waves of a population-based multiwave U.S. cohort study of adults with COPD. 77 non-smoking respondents with a diagnosis of COPD completed direct SHS monitoring based on urine cotinine and a personal badge that measures nicotine. We evaluated the longitudinal impact of SHS exposure on validated measures of COPD severity, physical health status, quality of life (QOL), and dyspnea measured at one year follow-up.ResultsThe highest level of SHS exposure, as measured by urine cotinine, was cross-sectionally associated with poorer COPD severity (mean score increment 4.7 pts; 95% CI 0.6 to 8.9) and dyspnea (1.0 pts; 95% CI 0.4 to 1.7) after controlling for covariates. In longitudinal analysis, the highest level of baseline cotinine was associated with worse COPD severity (4.7 points; 95% CI -0.1 to 9.4; p = 0.054), disease-specific QOL (2.9 pts; -0.16 to 5.9; p = 0.063), and dyspnea (0.9 pts; 95% CI 0.2 to 1.6 pts; p < 0.05), although the confidence intervals did not always exclude the no effect level.ConclusionDirectly measured SHS exposure appears to adversely influence health outcomes in COPD, independent of personal smoking. Because SHS is a modifiable risk factor, clinicians should assess SHS exposure in their patients and counsel its avoidance. In public health terms, the effects of SHS exposure on this vulnerable subpopulation provide a further rationale for laws prohibiting public smoking.

ContextBiomass serves as a major fuel source for >50% of the world's population. The global burden of disease attributed to indoor air pollution from biomass combustion accounts for approximately 3% of worldwide disability-adjusted life-years lost. This is due to pneumonia in children and chronic obstructive pulmonary disease and lung cancer in women.Case presentationA 53-year-old man from Mexico was referred to the pulmonary clinic for evaluation of chronic productive cough and pulmonary nodules. In his youth, he worked at a charcoal plant in Mexico, where he burned wood and was exposed to massive amounts of smoke. His evaluation revealed thickened bronchovascular bundles with nodules on thoracic computed tomography, dark black plaques in large airways on bronchoscopy, and carbon-laden macrophages and fibrotic scars on lung biopsy.DiscussionThe patient was diagnosed with "hut lung," a term that refers to the noninfectious, nonmalignant respiratory manifestations of chronic, high-level exposures to biomass smoke. This is the first reported case of hut lung associated with charcoal production. This case highlights that histopathologic abnormalities of the lung parenchyma may be present in patients with only mild symptoms and that clinical progression is likely a function of both the duration and intensity of exposure.Relevance to clinical practiceAs residents of lesser developed countries continue to be exposed to high levels of biomass smoke at work or at home and continue to immigrate to developed countries, it is important that health care providers in developed countries be aware of biomass-smoke-related pulmonary disease.

Single short-term exposures to ozone are known to cause acute changes in pulmonary function and neutrophilic airway inflammation. The respiratory health effects of repeated exposures are not as well studied. Pulmonary function decrements are known to attenuate, but it is less clear how injury and inflammation are affected. Using sputum induction (SI) to sample respiratory tract lining fluid after single- and multiday exposures, we designed a study to test the hypothesis that neutrophils would increase after multiday exposure compared with single-day exposure. In a randomized, crossover design, 15 normal healthy subjects were exposed to O3 (0.2 ppm) under two conditions: for 4 hr for 1 day (1D) and for 4 hr for 4 consecutive days (4D). Pulmonary function testing was performed immediately before and after each 4-hr exposure. The SI was performed 18 hr after the end of the 1D and 4D conditions. The symptom and pulmonary function data followed a pattern seen in other multiday O3 exposure studies, with the greatest changes occurring on the second day. In contrast to previous studies using bronchoalveolar lavage, however, there was a significant increase in the percentage of neutrophils and a significant decrease in the percentage of macrophages after the 4D condition compared with the 1D condition. Given that SI likely samples proximal airways better than distal lung, these results add to the body of evidence that differential airway compartmental responses to O3 occur in humans and other species.

BackgroundExposure to environmental tobacco smoke (ETS), which contains potent respiratory irritants, may lead to chronic airway inflammation and obstruction. Although ETS exposure appears to cause asthma in children and adults, its role in causing COPD has received limited attention in epidemiologic studies.MethodsUsing data from a population-based sample of 2,113 U.S. adults aged 55 to 75 years, we examined the association between lifetime ETS exposure and the risk of developing COPD. Participants were recruited from all 48 contiguous U.S. states by random digit dialing. Lifetime ETS exposure was ascertained by structured telephone interview. We used a standard epidemiologic approach to define COPD based on a self-reported physician diagnosis of chronic bronchitis, emphysema, or COPD.ResultsHigher cumulative lifetime home and work exposure were associated with a greater risk of COPD. The highest quartile of lifetime home ETS exposure was associated with a greater risk of COPD, controlling for age, sex, race, personal smoking history, educational attainment, marital status, and occupational exposure to vapors, gas, dusts, or fumes during the longest held job (OR 1.55; 95% CI 1.09 to 2.21). The highest quartile of lifetime workplace ETS exposure was also related to a greater risk of COPD (OR 1.36; 95% CI 1.002 to 1.84). The population attributable fraction was 11% for the highest quartile of home ETS exposure and 7% for work exposure.ConclusionETS exposure may be an important cause of COPD. Consequently, public policies aimed at preventing public smoking may reduce the burden of COPD-related death and disability, both by reducing direct smoking and ETS exposure.

Disease surveillance has a century-long tradition in public health, and environmental data have been collected at a national level by the U.S. Environmental Protection Agency for several decades. Recently, the Centers for Disease Control and Prevention announced an initiative to develop a national environmental public health tracking (EPHT) network with "linkage" of existing environmental and chronic disease data as a central goal. On the basis of experience with long-established disease surveillance systems, in this article we suggest how a system capable of linking routinely collected disease and exposure data should be developed, but caution that formal linkage of data is not the only approach required for an effective EPHT program. The primary operational goal of EPHT has to be the "treatment" of the environment to prevent and/or reduce exposures and minimize population risk for developing chronic diseases. Chronic, multifactorial diseases do not lend themselves to data-driven evaluations of intervention strategies, time trends, exposure patterns, or identification of at-risk populations based only on routinely collected surveillance data. Thus, EPHT should be synonymous with a dynamic process requiring regular system updates to a) incorporate new technologies to improve population-level exposure and disease assessment, b) allow public dissemination of new data that become available, c) allow the policy community to address new and emerging exposures and disease "threads," and d) evaluate the effectiveness of EPHT over some appropriate time interval. It will be necessary to weigh the benefits of surveillance against its costs, but the major challenge will be to maintain support for this important new system. Key words: environmental health, evaluation, intervention, registries, surveillance.

BackgroundThe Beta-Carotene and Retinol Efficacy Trial (CARET) tested the effect of daily beta-carotene (30 mg) and retinyl palmitate (25,000 IU) on the incidence of lung cancer, other cancers, and death in 18,314 participants who were at high risk for lung cancer because of a history of smoking or asbestos exposure. CARET was stopped ahead of schedule in January 1996 because participants who were randomly assigned to receive the active intervention were found to have a 28% increase in incidence of lung cancer, a 17% increase in incidence of death and a higher rate of cardiovascular disease mortality compared with participants in the placebo group.MethodsAfter the intervention ended, CARET participants returned the study vitamins to their study center and provided a final blood sample. They continue to be followed annually by telephone and mail self-report. Self-reported cancer endpoints were confirmed by review of pathology reports, and death endpoints were confirmed by review of death certificates. All statistical tests were two-sided.ResultsWith follow-up through December 31, 2001, the post-intervention relative risks of lung cancer and all-cause mortality for the active intervention group compared with the placebo group were 1.12 (95% confidence interval [CI] = 0.97 to 1.31) and 1.08 (95% CI = 0.99 to 1.17), respectively. Smoothed relative risk curves for lung cancer incidence and all-cause mortality indicated that relative risks remained above 1.0 throughout the post-intervention follow-up. By contrast, the relative risk of cardiovascular disease mortality decreased rapidly to 1.0 after the intervention was stopped. During the post-intervention phase, females had larger relative risks of lung cancer mortality (1.33 versus 1.14; P = .36), cardiovascular disease mortality (1.44 versus 0.93; P = .03), and all-cause mortality (1.37 versus 0.98; P = .001) than males.ConclusionsThe previously reported adverse effects of beta-carotene and retinyl palmitate on lung cancer incidence and all-cause mortality in cigarette smokers and individuals with occupational exposure to asbestos persisted after drug administration was stopped although they are no longer statistically significant. Planned subgroup analyses suggest that the excess risks of lung cancer were restricted primarily to females, and cardiovascular disease mortality primarily to females and to former smokers.

BackgroundThe Beta-Carotene and Retinol Efficacy Trial (CARET) tested the effect of daily beta-carotene (30 mg) and retinyl palmitate (25,000 IU) on the incidence of lung cancer, other cancers, and death in 18,314 participants who were at high risk for lung cancer because of a history of smoking or asbestos exposure. CARET was stopped ahead of schedule in January 1996 because participants who were randomly assigned to receive the active intervention were found to have a 28% increase in incidence of lung cancer, a 17% increase in incidence of death and a higher rate of cardiovascular disease mortality compared with participants in the placebo group.MethodsAfter the intervention ended, CARET participants returned the study vitamins to their study center and provided a final blood sample. They continue to be followed annually by telephone and mail self-report. Self-reported cancer endpoints were confirmed by review of pathology reports, and death endpoints were confirmed by review of death certificates. All statistical tests were two-sided.ResultsWith follow-up through December 31, 2001, the post-intervention relative risks of lung cancer and all-cause mortality for the active intervention group compared with the placebo group were 1.12 (95% confidence interval [CI] = 0.97 to 1.31) and 1.08 (95% CI = 0.99 to 1.17), respectively. Smoothed relative risk curves for lung cancer incidence and all-cause mortality indicated that relative risks remained above 1.0 throughout the post-intervention follow-up. By contrast, the relative risk of cardiovascular disease mortality decreased rapidly to 1.0 after the intervention was stopped. During the post-intervention phase, females had larger relative risks of lung cancer mortality (1.33 versus 1.14; P = .36), cardiovascular disease mortality (1.44 versus 0.93; P = .03), and all-cause mortality (1.37 versus 0.98; P = .001) than males.ConclusionsThe previously reported adverse effects of beta-carotene and retinyl palmitate on lung cancer incidence and all-cause mortality in cigarette smokers and individuals with occupational exposure to asbestos persisted after drug administration was stopped although they are no longer statistically significant. Planned subgroup analyses suggest that the excess risks of lung cancer were restricted primarily to females, and cardiovascular disease mortality primarily to females and to former smokers.

Several components of air pollution have been linked to asthma. In addition to the well-studied critera air pollutants, such as nitrogen dioxide, sulfur dioxide, and ozone, diesel exhaust and diesel exhaust particles (DEPs) also appear to play a role in respiratory and allergic diseases. Diesel exhaust is composed of vapors, gases, and fine particles emitted by diesel-fueled compression-ignition engines. DEPs can act as nonspecific airway irritants at relatively high levels. At lower levels, DEPs promote release of specific cytokines, chemokines, immunoglobulins, and oxidants in the upper and lower airway. Release of these mediators of the allergic and inflammatory response initiates a cascade that can culminate in airway inflammation, mucus secretion, serum leakage into the airways, and bronchial smooth muscle contraction. DEPs also may promote expression of the T(subscript)H(/subscript)2 immunologic response phenotype that has been associated with asthma and allergic disease. DEPs appear to have greater immunologic effects in the presence of environmental allergens than they do alone. This immunologic evidence may help explain the epidemiologic studies indicating that children living along major trucking thoroughfares are at increased risk for asthmatic and allergic symptoms and are more likely to have objective evidence of respiratory dysfunction.