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Summary: Background: Air particulate matter is a ubiquitous environmental exposure associated with oxidation, inflammation, and age-related chronic disease. Whether particulate matter is associated with loss of bone mineral density and risk of bone fractures is undetermined. We did two independent studies with complementary designs, objectives, and measures to determine the relationship between ambient concentrations of particulate matter and bone health. Methods: In the first study, we examined the association of long-term concentrations of particulate matter less than 2·5 μm (PM2·5) and osteoporosis-related fracture hospital admissions among 9·2 million Medicare enrollees (aged ≥65 years) of the northeast-mid-Atlantic USA between January, 2003, and December, 2010. In the second study, we examined the association of long-term black carbon and PM2·5 concentrations with serum calcium homoeostasis biomarkers (parathyroid hormone, calcium, and 25-hydroxyvitamin [25(OH)D]) and annualised bone mineral density over 8 years (baseline, November, 2002–July, 2005; follow-up, June, 2010–October, 2012) of 692 middle-aged (46·7 years [SD12·3]), low-income men from the Boston Area Community Health/Bone Survey (BACH/Bone study) cohort. PM2·5 concentrations were estimated using spatiotemporal hybrid modelling including Aerosol Optical Depth data, spatial smoothing, and local predictors. Black carbon concentrations were estimated using spatiotemporal land-use regression models. Findings: In the Medicare analysis, risk of bone fracture admissions at osteoporosis-related sites was greater in areas with higher PM2·5 concentrations (risk ratio [RR] 1·041, 95% CI 1·030 to 1·051). This risk was particularly high among low-income communities (RR 1·076, 95% CI 1·052 to 1·100). In the longitudinal BACH/Bone study, baseline black carbon and PM2·5 concentrations were associated with lower serum parathyroid hormone (β=–1·16, 95% CI −1·93 to −0·38, p=0·004, for 1 IQR increase [0·106 μg/m3] in the 1-year average of black carbon concentrations; β=–7·39, 95% CI −14·17 to −0·61, p=0·03, for 1 IQR increase [2·18 μg/m3] in the 1-year average of PM2·5 concentrations). Black carbon concentration was associated with higher bone mineral density loss over time at multiple anatomical sites, including femoral neck (−0·08% per year for 1 IQR increase, 95% CI −0·14 to −0·02) and ultradistal radius (−0·06% per year for 1 IQR increase, −0·12 to −0·01). Black carbon and PM2·5 concentrations were not associated with serum calcium or serum 25(OH)D concentrations. Interpretation: Our results suggest that poor air quality is a modifiable risk factor for bone fractures and osteoporosis, especially in low-income communities. Funding: National Institutes of Health, Institute on Aging, National Institute of Environmental Health, the US Environmental Protection Agency, Consejo Nacional de Ciencia y Tecnología, and the Fundación México en Harvard.

Successful total shoulder arthroplasty is, in part, dependent on anatomic reconstruction of the glenohumeral joint. The purpose of this study was to evaluate the post-operative anatomy of total shoulder arthroplasty with an anatomic implant design in patients with primary glenohumeral osteoarthritis and compare it to published normative anatomic measurements. Fifty-one patients (56 shoulders) with primary glenohumeral osteoarthritis were treated with a press-fit humeral component as part of a total shoulder arthroplasty (Aequalis, Tornier, Edina, Minnesota). Analysis of postoperative true anterior posterior radiographs was performed with use of a custom software algorithm. The mean humeral inclination (head-shaft angle), mean humeral implant anatomical humeral axis, mean greater tuberosity height, and mean humeral head center offset (medial offset) were 135.4±5.1°, 1.73±1.7°, 6.9±2.4 mm, and 3.8±1.8 mm, respectively. All parameters were within the ranges reported in the literature for normal shoulders except the mean humeral head center offset, which was less than reported in the literature. Anatomic parameters of a total shoulder arthroplasty can be achieved with an anatomically designed, modular adaptable press-fit design. Reduced medial humeral head center offset was likely dependent upon implant specific design parameters.

BACKGROUND:Blood pressure (BP) is a complex, multifactorial clinical outcome driven by genetic susceptibility, behavioral choices, and environmental factors. Many molecular mechanisms have been proposed for the pathophysiology of high BP even as its prevalence continues to grow worldwide, increasing morbidity and marking it as a major public health concern. To address this, we evaluated miRNA profiling in blood leukocytes as potential biomarkers of BP and BP-related risk factors. METHODS:The Beijing Truck Driver Air Pollution Study included 60 truck drivers and 60 office workers examined in 2008. On two days separated by 1-2 weeks, we examined three BP measures: systolic, diastolic, and mean arterial pressure measured at both pre- and post-work exams for blood NanoString nCounter miRNA profiles. We used covariate-adjusted linear mixed-effect models to examine associations between BP and increased miRNA expression in both pooled and risk factor-stratified analyses. RESULTS:Overall 43 miRNAs were associated with pre-work BP (FDR

OBJECTIVE To analyze the effect of air pollution and temperature on mortality due to cardiovascular and respiratory diseases. METHODS We evaluated the isolated and synergistic effects of temperature and particulate matter with aerodynamic diameter < 10 µm (PM10) on the mortality of individuals > 40 years old due to cardiovascular disease and that of individuals > 60 years old due to respiratory diseases in Sao Paulo, SP, Southeastern Brazil, between 1998 and 2008. Three methodologies were used to evaluate the isolated association: time-series analysis using Poisson regression model, bidirectional case-crossover analysis matched by period, and case-crossover analysis matched by the confounding factor, i.e., average temperature or pollutant concentration. The graphical representation of the response surface, generated by the interaction term between these factors added to the Poisson regression model, was interpreted to evaluate the synergistic effect of the risk factors. RESULTS No differences were observed between the results of the case-crossover and time-series analyses. The percentage change in the relative risk of cardiovascular and respiratory mortality was 0.85% (0.45;1.25) and 1.60% (0.74;2.46), respectively, due to an increase of 10 μg/m3 in the PM10 concentration. The pattern of correlation of the temperature with cardiovascular mortality was U-shaped and that with respiratory mortality was J-shaped, indicating an increased relative risk at high temperatures. The values for the interaction term indicated a higher relative risk for cardiovascular and respiratory mortalities at low temperatures and high temperatures, respectively, when the pollution levels reached approximately 60 μg/m3. CONCLUSIONS The positive association standardized in the Poisson regression model for pollutant concentration is not confounded by temperature, and the effect of temperature is not confounded by the pollutant levels in the time-series analysis. The simultaneous exposure to different levels of environmental factors can create synergistic effects that are as disturbing as those caused by extreme concentrations.

Background: Despite consistent evidence of a higher short-term risk of cardiovascular mortality associated with ambient temperature, there have been discrepant findings on the association between temperature and ischemic stroke. Moreover, few studies have considered potential confounding by ambient fine particulate matter air pollution 2.5) and none have examined the impact of temperature changes on stroke in the subsequent hours rather than days. The aim of this study was to evaluate whether changes in temperature trigger an ischemic stroke in the following hours and days and whether humid days are particularly harmful. Methods: We reviewed the medical records of 1,705 patients residing in the metropolitan region of Boston, Mass., USA, who were hospitalized with neurologist-confirmed ischemic stroke, and we abstracted data on the time of symptom onset and clinical characteristics. We obtained hourly meteorological data from the National Weather Service station and hourly PM2.5 data from the Harvard ambient monitoring station. We used the time-stratified case-crossover design to assess the association between ischemic stroke and apparent temperature averaged over 1-7 days prior to stroke onset adjusting for PM2.5. We assessed whether differences in apparent temperature trigger a stroke within shorter time periods by examining the association between stroke onset and apparent temperature levels averaged in 2-hour increments prior to stroke onset (0-2 h through 36-38 h). We tested whether the association varied by health characteristics or by PM2.5, ozone or relative humidity. Results: The incidence rate ratio of ischemic stroke was 1.09 (95% confidence interval 1.01-1.18) following a 5°C decrement in average apparent temperature over the 2 days preceding symptom onset. The higher risk associated with cooler temperatures peaked in the first 14-34 h. There was no statistically significant difference in the association between temperature and ischemic stroke across seasons. The risk of ischemic stroke was not meaningfully different across subgroups of patients defined by health characteristics. The association between ischemic stroke and ambient temperature was stronger on days with higher levels of relative humidity. Conclusions: Lower temperatures are associated with a higher risk of ischemic stroke onset in both warm and cool seasons, and the risk is higher on days with higher levels of relative humidity. Based on this study and the body of literature on ambient temperature and cardiovascular events, identifying methods for mitigating cardiovascular risk may be warranted.

BackgroundShort‐term exposure to elevated air pollution has been associated with higher risk of acute cardiovascular diseases, with systemic oxidative stress induced by air pollution hypothesized as an important underlying mechanism. However, few community‐based studies have assessed this association. Methods and ResultsTwo thousand thirty‐five Framingham Offspring Cohort participants living within 50 km of the Harvard Boston Supersite who were not current smokers were included. We assessed circulating biomarkers of oxidative stress including blood myeloperoxidase at the seventh examination (1998–2001) and urinary creatinine‐indexed 8‐epi‐prostaglandin F2α (8‐epi‐PGF2α) at the seventh and eighth (2005–2008) examinations. We measured fine particulate matter (PM2.5), black carbon, sulfate, nitrogen oxides, and ozone at the Supersite and calculated 1‐, 2‐, 3‐, 5‐, and 7‐day moving averages of each pollutant. Measured myeloperoxidase and 8‐epi‐PGF2α were loge transformed. We used linear regression models and linear mixed‐effects models with random intercepts for myeloperoxidase and indexed 8‐epi‐PGF2α, respectively. Models were adjusted for demographic variables, individual‐ and area‐level measures of socioeconomic position, clinical and lifestyle factors, weather, and temporal trend. We found positive associations of PM2.5 and black carbon with myeloperoxidase across multiple moving averages. Additionally, 2‐ to 7‐day moving averages of PM2.5 and sulfate were consistently positively associated with 8‐epi‐PGF2α. Stronger positive associations of black carbon and sulfate with myeloperoxidase were observed among participants with diabetes than in those without. ConclusionsOur community‐based investigation supports an association of select markers of ambient air pollution with circulating biomarkers of oxidative stress.

BACKGROUND:Cumulative exposure to lead is associated with cardiovascular outcomes. Polymorphisms in the δ-aminolevulinic acid dehydratase (ALAD), hemochromatosis (HFE), heme oxygenase-1 (HMOX1), vitamin D receptor (VDR), glutathione S-transferase (GST) supergene family (GSTP1, GSTT1, GSTM1), apolipoprotein E (APOE),angiotensin II receptor-1 (AGTR1) and angiotensinogen (AGT) genes, are believed to alter toxicokinetics and/or toxicodynamics of lead. OBJECTIVES:We assessed possible effect modification by genetic polymorphisms in ALAD, HFE, HMOX1, VDR, GSTP1, GSTT1, GSTM1, APOE, AGTR1 and AGT individually and as the genetic risk score (GRS) on the association between cumulative lead exposure and incident coronary heart disease (CHD) events. METHODS:We used K-shell-X-ray fluorescence to measure bone lead levels. GRS was calculated on the basis of 22 lead-related loci. We constructed Cox proportional hazard models to compute adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for incident CHD. We applied inverse probability weighting to account for potential selection bias due to recruitment into the bone lead sub-study. RESULTS:Significant effect modification was found by VDR, HMOX1, GSTP1, APOE, and AGT genetic polymorphisms when evaluated individually. Further, the bone lead-CHD associations became larger as GRS increases. After adjusting for potential confounders, a HR of CHD was 2.27 (95%CI: 1.50-3.42) with 2-fold increase in patella lead levels, among participants in the top tertile of GRS. We also detected an increasing trend in HRs across tertiles of GRS (p-trend = 0.0063). CONCLUSIONS:Our findings suggest that lead-related loci as a whole may play an important role in susceptibility to lead-related CHD risk. These findings need to be validated in a separate cohort containing bone lead, lead-related genetic loci and incident CHD data.

OBJECTIVES: Water-based soluble and synthetic metalworking fluids (MWF) used in auto manufacturing may be contaminated by endotoxin from Gram-negative bacteria, a possible anticarcinogen via increased immuno­surveillance. The effectiveness of biocide, generally added to limit bacterial growth is unknown. We investigated whether an inverse relationship between lung cancer and synthetic MWF and biocide – as surrogates of endotoxin exposure – persisted in an extended follow-up of autoworkers. METHODS: A nested case–control analysis was performed within a retrospective cohort study of 46 399 auto manufacturing workers. Follow-up began in 1941 and was extended from 1985–1995. Mortality rate ratios (MRR) were estimated in Cox regression models for lung cancer as discrete and smoothed functions of cumulative exposure to synthetic MWF (mg/m^3 per year) and years exposed to biocide with both synthetic and soluble MWF. The analysis was also restricted to the subcohort hired on or after 1941 and stratified by follow-up period. RESULTS: The splines suggested a non-linear inverse exposure–response for lung cancer mortality with increasing endotoxin exposure. Overall, the greatest reduction in mortality was observed among those with the highest exposure [MRR 0.63, 95% confidence interval (95% CI) 0.39–0.98] at the 99^th percentile of exposure (15.8 mg/m^3 per year). Evidence for an inverse effect was limited to the earlier follow-up period. Effect modification by biocide was marginally significant (P=0.07); the protective effect of synthetic MWF was observed only for those who were co-exposed. CONCLUSIONS: The protective effect of synthetic MWF against lung cancer mortality persisted through the extended period of follow-up, although attenuated, and was observed only among workers with co-exposure to biocide and synthetic MWF.

High concentrations of particulate matter (PM) air pollution have been associated with death and hospital admissions due to cardiovascular morbidity. However, it is not clear a) whether high levels of non-anthropogenic PM from dust storms constitute a health risk; and b) whether these health risks are exacerbated in a particular demographic.This study comprised all patients above 18 years old admitted to Soroka University Medical Center (1000 bed tertiary hospital, Be'er-Sheva, Israel, 2001-2010) with a primary diagnosis of acute coronary syndrome (ACS). Data on meteorological parameters and PM10 (particulate matter

Feo-hifomicose causada por Veronaea bothryosa é muito rara. Os autores relatam dois casos, que acreditam ser o primeiro e o segundo no continente americano, mas quarto e quinto da literatura mundial, até o momento. Trata-se de dois pacientes, um transplantado renal e outro imunossuprimido não transplantado. Ambos apresentavam lesões no dorso do pé após trauma. O primeiro respondeu moderadamente ao tratamento com itraconazol, e o segundo respondeu muito bem à excisão cirúrgica.Phaeohyphomycosis caused by Veronaea bothryosa is very rare. We report two cases. To our knowledge, these are the first and second cases to be reported on the American continent, and fourth and fifth cases in the world literature. We report one case in a kidney transplant recipient, and another case in an immunosuppressed non-transplant patient. Both patients presented with a lesion on the dorsal aspect of the foot, following trauma. One patient responded moderately well to treatment with itraconazole. The other responded well to a surgical excision.

We describe a method for comparing the ability of different alert threshold algorithms to detect malaria epidemics and use it with a dataset consisting of weekly malaria cases collected from health facilities in 10 districts of Ethiopia from 1990 to 2000. Four types of alert threshold algorithms are compared: weekly percentile, weekly mean with standard deviation (simple, moving average, and log-transformed case numbers), slide positivity proportion, and slope of weekly cases on log scale. To compare dissimilar alert types on a single scale, a curve was plotted for each type of alert, which showed potentially prevented cases versus number of alerts triggered over 10 years. Simple weekly percentile cutoffs appear to be as good as more complex algorithms for detecting malaria epidemics in Ethiopia. The comparative method developed here may be useful for testing other proposed alert thresholds and for application in other populations.

Papular elastorrhexis is a rare acquired disease, first described in 1987 by Bordas, which has been very rarely reported in the literature. It is characterized by small asymptomatic non-follicular papules, mainly distributed in the trunk. Histology of the lesions shows homogenization of collagen and fragmentation of elastic fibers in the dermis. The rarity of this disease is probably due to the subtlety and benign nature of clinical and histopathological alterations, which can be easily confused with other pathologies. The authors report the case of a patient with exuberant clinical manifestations typical of elastorrhexis papular.Elastorrexe papulosa é uma doença adquirida rara, descrita em1987 por Bordas e poucas vezes relatada na literatura. Caracteriza-se por pequenas pápulas, não foliculares, assintomáticas, distribuídas essencialmente no tronco. A histologia das lesões demonstra homogeneização do colágeno e fragmentação de fibras elásticas dérmicas. A raridade dessa entidade provavelmente se deve à sutileza e benignidade das alterações clínicas e histopatológicas, que podem facilmente ser confundidas com inúmeras outras afecções. Os autores relatam o caso de uma paciente com quadro clínico exuberante e característico de elastorrexe papulosa.

Prior influenza infection is a risk factor for invasive meningococcal disease. Quantifying the fraction of meningococcal disease attributable to influenza could improve understanding of viral-bacterial interaction and indicate additional health benefits to influenza immunization.A time series analysis of the association of influenza and meningococcal disease using hospitalizations in 9 states from 1989-2009 included in the State Inpatient Databases from the Agency for Healthcare Research and Quality and the proportion of positive influenza tests by subtype reported to the Centers for Disease Control. The model accounts for the autocorrelation of meningococcal disease and influenza between weeks, temporal trends, co-circulating respiratory syncytial virus, and seasonality. The influenza-subtype-attributable fraction was estimated using the model coefficients. We analyzed the synchrony of seasonal peaks in hospitalizations for influenza, respiratory syncytial virus, and meningococcal disease.In 19 of 20 seasons, influenza peaked≤2 weeks before meningococcal disease, and peaks were highly correlated in time (ρ = 0.95; P

The underlying mechanisms of the association between ambient temperature and cardiovascular morbidity and mortality are not well understood, particularly for daily temperature variability. We evaluated if daily mean temperature and standard deviation of temperature was associated with heart rate-corrected QT interval (QTc) duration, a marker of ventricular repolarization in a prospective cohort of older men.This longitudinal analysis included 487 older men participating in the VA Normative Aging Study with up to three visits between 2000-2008 (n = 743). We analyzed associations between QTc and moving averages (1-7, 14, 21, and 28 days) of the 24-hour mean and standard deviation of temperature as measured from a local weather monitor, and the 24-hour mean temperature estimated from a spatiotemporal prediction model, in time-varying linear mixed-effect regression. Effect modification by season, diabetes, coronary heart disease, obesity, and age was also evaluated.Higher mean temperature as measured from the local monitor, and estimated from the prediction model, was associated with longer QTc at moving averages of 21 and 28 days. Increased 24-hr standard deviation of temperature was associated with longer QTc at moving averages from 4 and up to 28 days; a 1.9°C interquartile range increase in 4-day moving average standard deviation of temperature was associated with a 2.8 msec (95%CI: 0.4, 5.2) longer QTc. Associations between 24-hr standard deviation of temperature and QTc were stronger in colder months, and in participants with diabetes and coronary heart disease.In this sample of older men, elevated mean temperature was associated with longer QTc, and increased variability of temperature was associated with longer QTc, particularly during colder months and among individuals with diabetes and coronary heart disease. These findings may offer insight of an important underlying mechanism of temperature-related cardiovascular morbidity and mortality in an older population.

Air pollution has been associated with increased systemic inflammation markers. We developed a new pathway analysis approach to investigate whether gene variants within relevant pathways (oxidative stress, endothelial function, and metal processing) modified the association between particulate air pollution and fibrinogen, C-reactive protein (CRP), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1). Our study population consisted of 822 elderly participants of the Normative Aging Study (1999-2011). To investigate the role of biological mechanisms and to reduce the number of comparisons in the analysis, we created pathway-specific scores using gene variants related to each pathway. To select the most appropriate gene variants, we used the least absolute shrinkage and selection operator (Lasso) to relate independent outcomes representative of each pathway (8-hydroxydeoxyguanosine for oxidative stress, augmentation index for endothelial function, and patella lead for metal processing) to gene variants. A high genetic score corresponds to a higher allelic risk profile. We fit mixed-effects models to examine modification by the genetic score of the weekly air pollution association with the outcome. Among participants with higher genetic scores within the oxidative stress pathway, we observed significant associations between particle number and fibrinogen, while we did not find any association among participants with lower scores (p(interaction) = 0.04). Compared to individuals with low genetic scores of metal processing gene variants, participants with higher scores had greater effects of particle number on fibrinogen (p(interaction) = 0.12), CRP (p(interaction) = 0.02), and ICAM-1 (pinteraction = 0.08). This two-stage penalization method is easy to implement and can be used for large-scale genetic applications.

Descreve-se caso de líquen aureus em paciente do sexo feminino, com 23 anos de idade que apresentava há dois anos lesão dolorosa, purpúrica, acastanhada tendendo por semelhante a cor de ferrugem e de aspecto liquenóide no antebraço. O exame anatomopatológico revelou denso infiltrado linfo-histiocitário na derme superior papilar, com extravasamento de hemácias. O líquen aureus é relativamente raro, sendo ainda mais raro o sintoma de dor.A case is described of lichen aureus in a 23 year old female with a 2-year history of painful, purpuric, rust-coloured to tan, lichenous lesion on forearm. A biopsy specimen demonstrated a dense lymphohistiocytic infiltrate in the upper dermis, with extravasation of red cells. The "algesiogenic" lichen aureus is a very rare dermatosis.

A micose fungóide hipopigmentar é uma forma rara de linfoma cutâneo de células T, em que lesões hipopigmentadas ocorrem na ausência de lesões clássicas dessa neoplasia. Na literatura latino-americana existem apenas três casos; relata-se aqui o caso de um homem negro, de 29 anos com lesões há 20 anos O tratamento é semelhante ao de outros tipos de linfomas T cutâneos, sendo o psoraleno mais ultravioleta A (Puva) e a mostarda nitrogenada tópica os mais relatados.Hypopigmented mycosis fungoides is a rare variant of the cutaneous T-cell lymphoma, in which hypopigmented lesions are seen without the classical lesions. Only three cases are found in the Latin-American literature. We report the case of a 29-year-old black male patient, who first presented with these lesions 20 years ago. The treatment is similar to the classical forms of the disease: psoralen plus ultraviolet A (PUVA) and topical nitrogen mustard are most often used.

Parkinson's disease (PD) is the second most common neurodegenerative disease. A key pathological feature of PD is Lewy bodies, of which the major protein component is α-synuclein (α-syn). Human genetic studies have shown that mutations (A53T, A30P, E46K) and multiplication of the α-syn gene are linked to familial PD. Mice overexpressing the human A53T mutant α-syn gene develop severe movement disorders. However, the molecular mechanisms of α-syn toxicity are not well understood. Recently, mitochondrial dysfunction has been linked with multiple neurodegenerative diseases including Parkinson's disease. Here we investigated whether mitochondrial motility, dynamics and respiratory function are affected in primary neurons from a mouse model expressing the human A53T mutation. We found that mitochondrial motility was selectively inhibited in A53T neurons while transport of other organelles was not affected. In addition, A53T expressing neurons showed impairment in mitochondrial membrane potential and mitochondrial respiratory function. Furthermore, we found that rapamycin, an autophagy inducer, rescued the decreased mitochondrial mobility. Taken together, these data demonstrate that A53T α-syn impairs mitochondrial function and dynamics and the deficit of mitochondrial transport is reversible, providing further understanding of the disease pathogenesis and a potential therapeutic strategy for PD.

Household air pollution (HAP) due to solid fuel use is a major public health threat in low-income countries. Most health effects are thought to be related to exposure to the fine particulate matter (PM) component of HAP, but it is currently impractical to measure personal exposure to PM in large studies. Carbon monoxide (CO) has been shown in cross-sectional analyses to be a reliable surrogate for particles

In September–October 2015, El Niño and positive Indian Ocean Dipole conditions set the stage for massive fires in Sumatra and Kalimantan (Indonesian Borneo), leading to persistently hazardous levels of smoke pollution across much of Equatorial Asia. Here we quantify the emission sources and health impacts of this haze episode and compare the sources and impacts to an event of similar magnitude occurring under similar meteorological conditions in September–October 2006. Using the adjoint of the GEOS-Chem chemical transport model, we first calculate the influence of potential fire emissions across the domain on smoke concentrations in three receptor areas downwind—Indonesia, Malaysia, and Singapore—during the 2006 event. This step maps the sensitivity of each receptor to fire emissions in each grid cell upwind. We then combine these sensitivities with 2006 and 2015 fire emission inventories from the Global Fire Assimilation System (GFAS) to estimate the resulting population-weighted smoke exposure. This method, which assumes similar smoke transport pathways in 2006 and 2015, allows near real-time assessment of smoke pollution exposure, and therefore the consequent morbidity and premature mortality, due to severe haze. Our approach also provides rapid assessment of the relative contribution of fire emissions generated in a specific province to smoke-related health impacts in the receptor areas. We estimate that haze in 2015 resulted in 100 300 excess deaths across Indonesia, Malaysia and Singapore, more than double those of the 2006 event, with much of the increase due to fires in Indonesia’s South Sumatra Province. The model framework we introduce in this study can rapidly identify those areas where land use management to reduce and/or avoid fires would yield the greatest benefit to human health, both nationally and regionally.

OBJECTIVE: Whether underlying chronic respiratory diseases are susceptible factors for symptomatic episodes, which lead to primary-level care, in association with air pollutant exposures is unknown. We evaluated and compared association lag structures between daily ambient levels of nitrogen dioxide (NO2) and total suspended particulates (TSP) and respiratory symptom-related doctor visits in adults with different patterns of underlying chronic respiratory disease. METHODS: In a time-stratified case-crossover analysis nested within a diary panel study, 459 Swiss adult participants with asthma, chronic bronchitis, chronic obstructive pulmonary disease (COPD) and healthy participants recorded occurrence of respiratory-symptom related doctor visits (n = 1,048) in one to six four-week intervals over two years. For each disease subgroup, odds ratios (ORs) for doctor visit were estimated as a function of NO2 or TSP concentrations (per 10 micrograms per cubic meter [µg/m3]) lagged between 0–13 days in a polynomial distributed lag model. RESULTS: Higher ORs for NO2 in participants with COPD (OR: 1.17, 95%CI: 1.02–1.35) and asthma (OR: 1.15, 95%CI: 1.02–1.30) occurred at exposure lags of two and five days, respectively. Doctor visits increased by 9.1% (95%CI: 3.2–15.4%) and 4.2% (95%CI: 1.2–7.2%) over the first week following a 10 µg/m3 increase in NO2 concentration in the COPD and chronic bronchitis subgroups, respectively. The percent increase in the COPD subgroup was significantly greater (p

During the 2009 H1N1 pandemic (pH1N1), morbidity and mortality sparing was observed among the elderly population; it was hypothesized that this age group benefited from immunity to pH1N1 due to cross-reactive antibodies generated from prior infection with antigenically similar influenza viruses. Evidence from serologic studies and genetic similarities between pH1N1 and historical influenza viruses suggest that the incidence of pH1N1 cases should drop markedly in age cohorts born prior to the disappearance of H1N1 in 1957, namely those at least 52-53 years old in 2009, but the precise range of ages affected has not been delineated.To test for any age-associated discontinuities in pH1N1 incidence, we aggregated laboratory-confirmed pH1N1 case data from 8 jurisdictions in 7 countries, stratified by single year of age, sex (when available), and hospitalization status. Using single year of age population denominators, we generated smoothed curves of the weighted risk ratio of pH1N1 incidence, and looked for sharp drops at varying age bandwidths, defined as a significantly negative second derivative. Analyses stratified by hospitalization status and sex were used to test alternative explanations for observed discontinuities. We found that the risk of laboratory-confirmed infection with pH1N1 declines with age, but that there was a statistically significant leveling off or increase in risk from about 45 to 50 years of age, after which a sharp drop in risk occurs until the late fifties. This trend was more pronounced in hospitalized cases and in women and was independent of the choice in smoothing parameters. The age range at which the decline in risk accelerates corresponds to the cohort born between 1951-1959 (hospitalized) and 1953-1960 (not hospitalized).The reduced incidence of pH1N1 disease in older individuals shows a detailed age-specific pattern consistent with protection conferred by exposure to influenza A/H1N1 viruses circulating before 1957.

Extreme heat events are associated with spikes in mortality, yet death rates are on average highest during the coldest months of the year. Under the assumption that most winter excess mortality is due to cold temperature, many previous studies have concluded that winter mortality will substantially decline in a warming climate. We analyzed whether and to what extent cold temperatures are associated with excess winter mortality across multiple cities and over multiple years within individual cities, using daily temperature and mortality data from 36 US cities (1985–2006) and 3 French cities (1971–2007). Comparing across cities, we found that excess winter mortality did not depend on seasonal temperature range, and was no lower in warmer vs. colder cities, suggesting that temperature is not a key driver of winter excess mortality. Using regression models within monthly strata, we found that variability in daily mortality within cities was not strongly influenced by winter temperature. Finally we found that inadequate control for seasonality in analyses of the effects of cold temperatures led to spuriously large assumed cold effects, and erroneous attribution of winter mortality to cold temperatures. Our findings suggest that reductions in cold-related mortality under warming climate may be much smaller than some have assumed. This should be of interest to researchers and policy makers concerned with projecting future health effects of climate change and developing relevant adaptation strategies.

Air quality is heavily influenced by weather conditions. In this study, we assessed the impact of long-term weather changes on air quality and health in the US during 1994–2012. We quantified past weather-related increases, or ‘weather penalty’, in ozone (O _3 ) and fine particulate matter (PM _2.5 ), and thereafter estimated the associated excess deaths. Using statistical regression methods, we derived the weather penalty as the additional increases in air pollution relative to trends assuming constant weather conditions (i.e., weather-adjusted trends). During our study period, temperature increased and wind speed decreased in most US regions. Nationally, weather-related 8 h max O _3 increases were 0.18 ppb per year (95% CI: 0.06, 0.31) in the warm season (May–October) and 0.07 ppb per year (95% CI: 0.02, 0.13) in the cold season (November–April). The weather penalties on O _3 were relatively larger than PM _2.5 weather penalties, which were 0.056 μ g m ^−3 per year (95% CI: 0.016, 0.096) in warm months and 0.027 μ g m ^−3 per year (95% CI: 0.010, 0.043) in cold months. Weather penalties on O _3 and PM _2.5 were associated with 290 (95% CI: 80, 510) and 770 (95% CI: 190, 1350) excess annual deaths, respectively. Over a 19-year period, this amounts to 20 300 excess deaths (5600 from O _3 , 14 700 from PM _2.5 ) attributable to the weather penalty on air quality.