Associations of Personal Hourly Exposures to Air Temperature and Pollution with Resting Heart Rate in Chronic Obstructive Pulmonary Disease.

Previous studies linked higher daily ambient air temperature and pollution with increased cardiorespiratory morbidity, but immediate effects of personal, hourly exposures on resting heart rate remained unclear. We followed 30 older former smokers with chronic obstructive pulmonary disease (COPD) in Massachusetts for four nonconsecutive 30-day periods over 12 months, collecting 54,487 hourly observations of personal air temperature, fine particulate matter (PM2.5), nitrogen dioxide (NO2), ozone (O3), and resting heart rate. We explored the single lag effects (0-71 h) and cumulative effects (0-5 h, the significant lag windows) of air temperature and pollution on resting heart rate using generalized additive mixed models with distributed lag nonlinear models. Single lag effects of higher air temperature and pollutants on higher resting heart rate were most pronounced at lag 0 to 5 h. Cumulative effects of higher air temperature, PM2.5, O3, and NO2 (each interquartile range increment) on higher resting heart rate at lag 0-5 h, show differences of (beats per minute [bpm], 95% CI) 1.46 (1.31-1.62), 0.35 (0.32-0.39), 2.32 (2.19-2.45), and 1.79 (1.66-1.92), respectively. In conclusion, higher personal hourly air temperature, PM2.5, O3, and NO2 exposures at lag 0-5 h are associated with higher resting heart rate in COPD patients.

Weekly prenatal PM2.5 and NO2 exposures in preterm, early term, and full term infants: Decrements in birth weight and critical windows of susceptibility.

BACKGROUND: Previous studies have observed associations between birth weight and prenatal air pollution exposure, but there is not consensus on timing of critical windows of susceptibility. OBJECTIVE: We estimated the difference in birth weight among preterm, early term and full term births associated with weekly exposure to PM2.5 and NO2 throughout gestation. METHODS: We included all singleton live births in the Lower Peninsula of Michigan (United States) between 2007 and 2012 occurring at or after 32 weeks gestational age (n = 497,897). Weekly ambient PM2.5 and NO2 concentrations were estimated at maternal residences using 1-km gridded data from ensemble-based models. We utilized a distributed lag nonlinear model to estimate the difference in birth weight associated with weekly exposures from the last menstrual period (week 0) through 31 weeks gestation for preterm births; through 36 weeks gestation for early term births; and through 38 weeks gestation for full term births. RESULTS: In single-pollutant models, a 5 µg/m3 increase in PM2.5 exposure was associated with a reduction in birth weight among preterm births (-37.1 g [95% confidence interval [CI]: 60.8 g, -13.5 g]); early term births (-13.5 g [95% CI: 26.2 g, -0.67 g]); and full term births (-8.23 g [95% CI: 15.8 g, -0.68 g])]. In single-pollutant models, a 10 ppb increase in NO2 exposure was associated with a -11.7 g (95% CI: 14.46 g, -8.92 g) decrement in birth weight among full term births only. In models co-adjusted for PM2.5 and NO2, PM2.5 exposure was associated with reduced birth weight among preterm births (-36.9 g [95% CI: 61.9 g, -11.8 g]) and NO2 exposure was associated with reduced birth weight among full term births (-11.8 g [95% CI: 14.7 g, -8.94 g]). The largest decrements in birth weight were associated with PM2.5 exposure between approximately 10 and 26 weeks of pregnancy; for NO2 exposure, the largest decrements in birth weight in full term births were associated with exposure between weeks 6-18. CONCLUSION: We observed the largest and most persistent adverse associations between PM2.5 exposure and birth weight in preterm infants, and between NO2 exposure and birth weight in full term infants. Exposure during the first half of pregnancy had a greater impact on birthweight.

Associations between air pollution, residential greenness, and glycated hemoglobin (HbA1c) in three prospective cohorts of U.S. adults.

BACKGROUND: While studies suggest impacts of individual environmental exposures on type 2 diabetes (T2D) risk, mechanisms remain poorly characterized. Glycated hemoglobin (HbA1c) is a biomarker of glycemia and diagnostic criterion for prediabetes and T2D. We explored associations between multiple environmental exposures and HbA1c in non-diabetic adults. METHODS: HbA1c was assessed once in 12,315 women and men in three U.S.-based prospective cohorts: the Nurses' Health Study (NHS), Nurses' Health Study II (NHSII), and Health Professionals Follow-up Study (HPFS). Residential greenness within 270 m and 1,230 m (normalized difference vegetation index, NDVI) was obtained from Landsat. Fine particulate matter (PM2.5) and nitrogen dioxide (NO2) were estimated from nationwide spatiotemporal models. Three-month and one-year averages prior to blood draw were assigned to participants' addresses. We assessed associations between single exposure, multi-exposure, and component scores from Principal Components Analysis (PCA) and HbA1c. Fully-adjusted models built on basic models of age and year at blood draw, BMI, alcohol use, and neighborhood socioeconomic status (nSES) to include diet quality, race, family history, smoking status, postmenopausal hormone use, population density, and season. We assessed interactions between environmental exposures, and effect modification by population density, nSES, and sex. RESULTS: Based on HbA1c, 19% of participants had prediabetes. In single exposure fully-adjusted models, an IQR (0.14) higher 1-year 1,230 m NDVI was associated with a 0.27% (95% CI: 0.05%, 0.49%) lower HbA1c. In basic component score models, a SD increase in Component 1 (high loadings for 1-year NDVI) was associated with a 0.19% (95% CI: 0.04%, 0.34%) lower HbA1c. CI's crossed the null in multi-exposure and fully-adjusted component score models. There was little evidence of associations between air pollution and HbA1c, and no evidence of effect modification. CONCLUSIONS: Among non-diabetic adults, environmental exposures were not consistently associated with HbA1c. More work is needed to elucidate biological pathways between the environment and prediabetes.

Impacts of long-term ambient particulate matter and gaseous pollutants on circulating biomarkers of inflammation in male and female health professionals.

BACKGROUND: Systemic inflammation may serve as a biological mechanism linking air pollution to poor health but supporting evidence from studies of long-term pollutant exposure and inflammatory cytokines is inconsistent. OBJECTIVE: We studied associations between multiple particulate matter (PM) and gaseous air pollutants and pro- and anti-inflammatory cytokines within two nationwide cohorts of men and women. METHODS: Data were obtained from 16,151 women in the Nurses' Health Study and 7,930 men in the Health Professionals' Follow-up Study with at least one measure of circulating adiponectin, C-Reactive Protein (CRP), Interleukin-6 (IL-6) or soluble tumor necrosis-factor receptor-2 (sTNFR-2). Exposure to PM with aerodynamic diameter ≤2.5, 2.5-10, and ≤10 µm (PM2.5, PM2.5-10, PM10) and nitrogen dioxide (NO2) was estimated using spatio-temporal models and were linked to participants' addresses at the time of blood draw. Averages of the 1-, 3-, and 12-months prior to blood draw were examined. Associations between each biomarker and pollutant were estimated from linear regression models adjusted for individual and contextual covariates. RESULTS: In adjusted models, we observed a 2.72% (95% CI: 0.43%, 5.95%), 3.11% (-0.12%, 6.45%), and 3.67% (0.19%, 7.26%) increase in CRP associated with a 10 µg/m3 increase in 1-, 3-, and 12- month averaged NO2 in women. Among men, there was a statistically significant 5.96% (95% CI: 0.07%, 12.20%), 6.99% (95% CI: 0.29%, 14.15%), and 8.33% (95% CI: 0.35%, 16.94%) increase in CRP associated with a 10 µg/m3 increase in 1-, 3-, and 12-month averaged PM2.5-10, respectively. Increasing PM2.5-10 was associated with increasing IL-6 and sTNFR-2 among men over shorter exposure durations. There were no associations with exposures to PM2.5 or PM10, or with adiponectin. Findings were robust to sensitivity analyses restricting to disease-free controls and non-movers. CONCLUSIONS: Across multiple long-term pollutant exposures and inflammatory markers, associations were generally weak. Focusing on specific pollutant-inflammatory mechanisms may clarify pathways.

Breathe easy at home: a web-based referral system linking clinical sites with housing code enforcement for patients with asthma.

Asthma, the most significant cause of pediatric morbidity and mortality, is exacerbated by adverse environmental conditions, especially substandard housing. The clinical care provider is often unable to address housing and environmental trigger issues. In Boston, Massachusetts, a web-based referral system called Breathe Easy At Home has been put in place, through which clinicians can refer patients to have their homes inspected for housing code violations that may be contributing to their asthma. Violations will then be brought to the attention of the landlord, who then has the option of redressing the issue or be taken to housing court. By bringing the local public health department, the city's inspectional services department, and the clinical care provider together with the help of a program coordinator, Breathe Easy At Home is able to provide comprehensive care to asthma patients. This program also serves as a replicable model for other cities and jurisdictions to follow.

Impact of gene patents and licensing practices on access to genetic testing for hearing loss.

Genetic testing for heritable hearing loss involves a mix of patented and unpatented genes, mutations and testing methods. More than half of all hearing loss is linked to inherited mutations, and five genes are most commonly tested for in the United States. There are no patents on three of these genes, but Athena Diagnostics holds exclusive licenses to test for a common mutation in the GJB2 gene associated with about 50% of all cases as well as mutations in the MTRNR1 gene. This fragmented intellectual property landscape made hearing loss a useful case study to assess whether patent rights in genetic testing can proliferate or overlap, and whether it is possible to gather the rights necessary to perform testing. Testing for hearing loss is widely available, primarily from academic medical centers. Based on literature reviews and interviews with researchers, research on the genetics of hearing loss has generally not been impeded by patents. There is no consistent evidence of a premium in testing prices attributable to patent status. Athena Diagnostics has, however, used its intellectual property to discourage other providers from offering some tests. There is no definitive answer about the suitability of current patenting and licensing of commonly tested genes because of continuing legal uncertainty about the extent of enforcement of patent rights. Clinicians have also expressed concerns that multiplex tests will be difficult to develop because of overlapping intellectual property and conflict with Athena's sole provider business model.

Long-term impact of PM2.5 mass and sulfur reductions on ultrafine particle trends in Boston, MA from 1999 to 2018.

Ultrafine particles (UFPs) pose a human health risk as they can penetrate deep into the respiratory system. The Harvard supersite in Boston, MA provides one of the longest time series of UFP concentrations. This study examined the hypothesis that long-term reductions in PM2.5 mass and sulfur have influenced UFP trends by limiting the ability of UFPs to coagulate onto the accumulation mode via polydisperse coagulation with larger particles. The study used Generalized Additive Models (GAMs) to assess whether changes in PM2.5 mass and sulfur concentrations resulted in smaller than expected (assuming no change in PM2.5 mass or sulfur) decreases in daily UFP trends over the 20-year period from 1999 to 2018. The impact of PM2.5 mass and sulfur changes were represented as UFP penalties. Bootstrapping was applied to calculate standard errors for the different trend and penalty estimates. Results showed that PM2.5 mass and sulfur concentrations declined significantly over the study period. The analysis found an estimated 7.3% (95% CI: 3.5, 11.1%) UFP penalty due to long-term PM2.5 mass trends, and a 9.9% (95% CI: 6.2, 13.7%) UFP penalty due to long-term sulfur trends. Findings from this study suggest that future UFP control efforts should account for the role of PM2.5 mass and sulfur changes. IMPLICATIONS: Using one of the longest available time series of UFP concentrations (1999 to 2018), this study examined the hypothesis that long-term trends of PM2.5 mass and sulfur concentrations have an impact on UFP trends. We found that PM2.5 mass and sulfur reductions had a small but significant impact, i.e., penalty, on UFP trends. Improved understanding of the impact of PM2.5 mass and sulfur concentrations on UFP trends can inform future air quality control efforts.