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Background: Several epidemiological studies have shown that blood pressure changes with temperature based on the daily temperature and linear relationship assumption. However, little is known about the true curve shape of the relationship between temperature and blood pressure. Objectives: The objective of this study was to investigate the non-linear relationship between hourly temperature and blood pressure. Methods: This is a prospective panel study comprising 100 participants in Suzhou, China. The blood pressure of each participant was measured >50 times between October 2013 and January 2016. Hourly temperature data were derived from the nearest monitoring station owned by the China Meteorological Administration. A Distributed Lag Nonlinear Model (DLNM) was used to investigate the relationship between hourly temperature and blood pressure. Results: We found that the relationship between hourly temperature and blood pressure was parabolic. Short-term exposure to hourly temperatures had significant cold and heat effects on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and mean arterial pressure (MAP). The hourly temperature had a significant lag effect on blood pressure, with a lag time of 0–5 h. Alcohol users were more sensitive to the cold effects of hourly temperature, and the diabetic population was more sensitive to the heat effects of hourly temperature on PP. Conclusion: Temperature imparts short-term effects on blood pressure. Therefore, timely protective measures during cold waves or cold weather are beneficial to maintain stable blood pressure levels to reduce the risk of blood pressure related diseases. Keywords: Hourly temperature, Blood pressure, Panel study, Repeated measurement

Background Air pollution is a leading contributor to premature mortality worldwide and is often represented by particulate matter (PM), a key contributor to its harmful health effects. Concentration-response relationships are useful for quantifying the effects of air pollution in relevant populations and in considering potential effect thresholds. Controlled human exposures can provide data on acute effects and concentration–response relationships that complement epidemiological studies. Objectives We examined PM concentration-responses after controlled human air pollution exposures to examine exposure–response markers, assess effect modifiers, and identify potential effect thresholds. Methods We reviewed primary research from published controlled human exposure studies where responses were reported at multiple target PM concentrations or summarized per unit change in PM to identify concentration-dependent effects. Results Of the 191 publications identified through PubMed and supplementary searches, 31 were eligible. Eligible studies collectively represented four pollutant models: concentrated ambient particles, engineered carbon nanoparticles, diesel exhaust, and woodsmoke. We identified concentration-dependent effects on oxidative stress markers, inflammation, and cardiovascular function that overlapped across different pollutants. Metabolic syndrome and glutathione s-transferase mu 1 genotype were identified as potential effect modifiers. Discussion Improved understanding of concentration–response relationships is integral to biomonitoring and mitigation of health effects through impact assessment and policy. Although we identified potential concentration–response markers, thresholds, and modifiers, our conclusions on these relationships were limited by a dearth of eligible publications, considerable variability in methodology, and inconsistent reporting standards between studies. More research is required to validate these observations. We recommend that future studies harmonize estimate reporting to facilitate the identification of robust response markers across research and applied settings.

Background: The link between PM2.5 exposure and adverse health outcomes is well documented from studies across the world. However, the reported effect estimates vary across studies, locations and constituents. We aimed to conduct a meta-analysis on associations between short-term exposure to PM2.5 constituents and mortality using city-specific estimates, and explore factors that may explain some of the observed heterogeneity. Methods: We systematically reviewed epidemiological studies on particle constituents and mortality using PubMed and Web of Science databases up to July 2015.We included studies that examined the association between short-term exposure to PM2.5 constituents and all-cause, cardiovascular, and respiratory mortality, in the general adult population. Each study was summarized based on pre-specified study key parameters (e.g., location, time period, population, diagnostic classification standard), and we evaluated the risk of bias using the Office of Health Assessment and Translation (OHAT) Method for each included study. We extracted city-specific mortality risk estimates for each constituent and cause of mortality. For multi-city studies, we requested the city-specific risk estimates from the authors unless reported in the article. We performed random effects meta-analyses using city-specific estimates, and examined whether the effects vary across regions and city characteristics (PM2.5 concentration levels, air temperature, elevation, vegetation, size of elderly population, population density, and baseline mortality). Results: We found a 0.89% (95% CI: 0.68, 1.10%) increase in all-cause, a 0.80% (95% CI: 0.41, 1.20%) increase in cardiovascular, and a 1.10% (95% CI: 0.59, 1.62%) increase in respiratory mortality per 10μg/m3 increase in PM2.5. Accounting for the downward bias induced by studies of single days, the all-cause mortality estimate increased to 1.01% (95% CI: 0.81, 1.20%). We found significant associations between mortality and several PM2.5 constituents. The most consistent and stronger associations were observed for elemental carbon (EC) and potassium (K). For most of the constituents, we observed high variability of effect estimates across cities. Conclusions: Our meta-analysis suggests that (a) combustion elements such as EC and K have a stronger association with mortality, (b) single lag studies underestimate effects, and (c) estimates of PM2.5 and constituents differ across regions. Accounting for PM mass in constituent's health models may lead to more stable and comparable effect estimates across different studies. Systematic review registration: PROSPERO: CRD42017055765. Keywords: Particulate matter constituents, Fine particulate matter (PM2.5), Mortality, Time series, Acute effects, Meta-analysis

Background: Although blood pressure decreases in response to high ambient temperature, little is known about whether the ambient temperature can induce clinical hypotension events. Therefore, we conducted a time-series analysis to evaluate the association between hypotension hospital visits and ambient temperature in seven metropolitan cities of Korea. Methods: We used the National Health Insurance Database, which contains the complete hospital visit data of the entire Korean population. We collected hospital visit data of seven metropolitan cities and linked the number of daily hypotension hospital visits to city-level ambient temperature, relative humidity, and air pollution levels from 2011 to 2015. Time-series analysis using the Poisson generalized additive model was conducted for each metropolitan city and we meta-analyzed the time-series results using the random effect model. Results: There were 132,097 hospital visits for hypotension during our study period. A 1 degree Celsius (°C) increase in ambient temperature was associated with 1.1% increase in hospital visits for hypotension on lag day 0. Effects of ambient temperature lasted for 7 days, showing greater effects in shorter lag days. Subgroup analysis by sex and income groups showed similar results, but effects of ambient temperature on hypotension hospital visits was higher in the younger age group compared to older age group (aged over 65 years old). The results were unchanged when we applied cumulative lags, different case definitions, degrees of freedom per year, and multi-pollutant model adjusting for air pollutants. Conclusions: Hospital visits for hypotension were positively associated with ambient temperature. Increased hypotension events in response to increased ambient temperature might explain the high cardiovascular mortality on hot days. Keywords: Ambient temperature, Hypotension, Blood pressure, Time-series analysis

In Europe, the proportion of the population exposed to environmental noise above 65 dB(A) has increased during the past decade from 15% to 26%. While the acute effects of such noise exposure are well accepted, firm conclusions about long-term consequences for health are still hampered by inconsistent results. Apart from methodological shortcomings, lack of conceptual clarity in research designs has been blamed for the inconsistencies, but rarely has it been addressed. This paper illustrates the major conceptual models (general stress model, individual-situational difference model, transactional, and contextual model) applied in non-auditory health effects research. It discusses the inherent limitations of these models and evaluates their potential contribution to overcoming the conceptual deficiencies. The integration of physiological, psychological, and ecological approaches within a combined transactional-contextual research perspective provides the best available framework for future studies and reanalysis of earlier studies given the necessary information is provided.

In recent years, radon, formaldehyde, numerous solvents, asbestos, and nitrogen oxides have been repeatedly studied, both as they occur indoors and for their potential health effects. System studies encompassing pollutants in the context of their occurrence in an environment containing many other pollutants are, however, few and are primarily associated with the sick building syndrome (SBS). In general, indoor air pollutants can be categorized in two distinct groups. The first group consists of pollutants that are known to cause chronic effects such as cancer and chronic respiratory diseases. They can be assessed on the basis of their known or assumed dose response function. The second, and possibly more important group, consists of those pollutants that cause acute effects such as allergic reactions, irritation of the eyes and respiratory system discomfort, and similar effects. Their assessment requires the availability of a dose response function. Such a function will almost certainly have a threshold which is, however, not constant, and varies with the sensitivity and perception of individuals. This paper discusses these two groups, evaluates the assumed dose response functions, identifies those areas requiring a decision based on risk assessment, and provides a framework for regulations of indoor air pollutants.

Laboratory experiments and field measurements were carried out to determine relevant acute and long term effects of noise from low-flying military aircraft. Acute effects on the cardiovascular system were established under simulation conditions. Blood pressure, heart rate, and biochemical stress parameters (cortisol and catecholamines, renin and free fatty acids in blood) were measured as a function of time. Long-term effects of noise from low-flying aircraft were analyzed in 10 to 13-year-old children by comparative studies including a 75 m low-altitude flight area and a neighbouring area with flight altitudes of 150–450 m. Significantly higher blood pressure values were found in girls in the 75 m area. The hearing thresholds were significantly increased in boys and girls in the 75 m area. Altogether, acute effects of noise from low-flying aircraft on cardiovascular functions and hearing ability could be proved, and potential risks of long-term exposure to low-altitude flight noise are discussed.

Oxidants of significance to human health include ozone, nitrogen dioxide, and peroxyacetylnitrate. All of these compounds are involved in complex photochemical reactions which makes quantification and prediction of their individual health effects difficult. Ozone causes trauma to lung tissues and interferes with enzyme systems in the lungs and other tissues causing a broad range of symptoms. Measurable health impacts can occur at concentrations as low as 390 μg/m 3 . Acute effects of ozone exposure are reversible at normal urban concentrations (80–120 μg/m 3 ). A special problem of concern, however, is increased susceptibility to infectious diseases contracted through the lungs. Nitrogen dioxide also causes trauma to lung tissues and interferes with enzyme systems. Measurable impacts can occur at concentrations as low as 100 μg/m 3 , but recovery is rapid and it is not known whether repeated exposures at this level have cumulative effects or predispose the lungs to permanent damage. Chronic exposure of laboratory animals to higher nitrogen dioxide levels can cause emphysema-like conditions and reduction in resistance to respiratory infection. Epidemiological studies of children in houses with gas stoves confirm the finding of reduced resistance to respiratory infection. The U.S. EPA estimates that health effects may occur in young children exposed to concentrations in excess of 280 to 560 μg/m 3 one-hour average. These concentrations occur routinely in houses having gas stoves. Peroxyacetylnitrate is a powerful eye irritant in photochemical smog. Other health effects are similar to those of ozone, but less important because of the relatively low concentrations of this pollutant compared to other oxidants.

The effect of iron on algal samples obtained from Peoria, Farmington, and Princeton, IL, was studied. The Farmington and Princeton samples were found to be more sensitive to iron than the Peoria samples. Algae in all samples, however, showed no adverse effects from 1 mg/L total iron, which is the current Illinois water quality standard for general use.