Within-city spatiotemporal variations in outdoor ultrafine particles and emergency room visits for cardiovascular outcomes.

Examining the social distributions in neighbourhood black carbon and ultrafine particles in Montreal and Toronto, Canada.

Predicting outdoor ultrafine particle number concentrations, particle size, and noise using street-level images and audio data

Do Diuretics Diminish the Predicted Benefits on Ischemic Heart Disease Events of Lowering Blood Pressure in Hypertension?

Airborne ultrafine particle concentrations and brain cancer incidence in Canada’s two largest cities

Particulate Air Pollution and Carotid Artery Stenosis

During winter 2006, indoor and outdoor ultrafine particle (UFP) size distribution measurements for particles with diameters from 5.6 to 165 nm were taken at five homes in a neighborhood directly adjacent to the Peace Bridge Complex (PBC), a major international border crossing connecting Buffalo, New York to Fort Erie, Ontario. Monitoring with 1-s time resolution was conducted for several hours at each home. Participants were instructed to keep all external windows and doors closed and to refrain from cooking, smoking, or other activity that may result in elevating the indoor UFP number concentration. Although the construction and age for the homes were similar, indoor-to-outdoor comparisons indicate that particle infiltration rates varied substantially. Overall, particle concentrations indoors were lower and less variable than particle concentrations outdoors, with average indoor-outdoor ratios ranging from 0.1 to 0.5 (mean 0.34) for particles between 5.6 and 165 nm in diameter. With no indoor sources, the average indoor-outdoor ratios were lowest (0.2) for 20-nm particles, higher (0.3) for particles <10 nm, and highest (0.5) for particles 70-165 nm. This study provides insight into the penetration of UFP into homes and the resulting change in particle size distributions as particles move indoors near a major diesel traffic source. Although people spend most of their time in their homes, exposure estimates for epidemiological studies are generally determined using ambient concentrations. The findings of this study will contribute to improved size-resolved UFP exposure estimates for near roadway exposure assessments and epidemiological studies.

Vulnerable blood in high risk vascular patients: Study design and methods

Penetration of freeway ultrafine particles into indoor environments

Airborne particles represent a very important pollutant with respect to healthy housing conditions. The snag is that in lack of indoor data epidemiological studies focusing on submicron and ultrafine (<100 nm in diameter) particles are usually forced to use outdoor particle concentrations only. On the other hand it is known that people spend most of their time indoors. The aim of this paper is therefore to give a short comprehensive overview of the indoor/outdoor problem with regard to submicron and ultrafine particles, investigating how indoor particle size distributions correlate with outdoor concentrations in the absence of significant indoor sources. In the absence of a major indoor source, total indoor particle number concentrations were always lower than outdoor concentrations. The highest ratios between indoor and outdoor concentrations tend to correlate with lower rather than higher total outdoor particle number concentrations. Concentration ratios depend on particle size. Time lags of the correlation coefficients between the concentrations of indoor and outdoor particles of different diameters have been determined to assess the time the particles need to enter the indoor site through closed modern-type windows. Typical lag times of 0.5-3 h between somewhat smaller indoor particles and somewhat larger outdoor particles have been observed. To assess the resulting particle burden for humans, a suitably weighted average emphasizing indoor aerosol particles must be used. To classify the health effects of particles of different diameters, different decreases of particle number concentrations depending on the particle sizes must be taken into account if indoor concentrations cannot be measured and outdoor concentrations are used in place of indoor measurements. In urban areas, ultrafine particles originate primarily from rapidly increasing traffic, which is the dominating source at many urban sites. The influence of traffic on outdoor and indoor concentrations is therefore of special interest.

Personal exposure to ultrafine particles (UFP) can occur while people are cooking, driving, smoking, operating small appliances such as hair dryers, or eating out in restaurants. These exposures can often be higher than outdoor concentrations. For 3 years, portable monitors were employed in homes, cars, and restaurants. More than 300 measurement periods in several homes were documented, along with 25 h of driving two cars, and 22 visits to restaurants. Cooking on gas or electric stoves and electric toaster ovens was a major source of UFP, with peak personal exposures often exceeding 100,000 particles/cm³ and estimated emission rates in the neighborhood of 10¹² particles/min. Other common sources of high UFP exposures were cigarettes, a vented gas clothes dryer, an air popcorn popper, candles, an electric mixer, a toaster, a hair dryer, a curling iron, and a steam iron. Relatively low indoor UFP emissions were noted for a fireplace, several space heaters, and a laser printer. Driving resulted in moderate exposures averaging about 30,000 particles/cm³ in each of two cars driven on 17 trips on major highways on the East and West Coasts. Most of the restaurants visited maintained consistently high levels of 50,000-200,000 particles/cm³ for the entire length of the meal. The indoor/outdoor ratios of size-resolved UFP were much lower than for PM₂.₅ or PM₁₀, suggesting that outdoor UFP have difficulty in penetrating a home. This in turn implies that outdoor concentrations of UFP have only a moderate effect on personal exposures if indoor sources are present. A time-weighted scenario suggests that for typical suburban nonsmoker lifestyles, indoor sources provide about 47% and outdoor sources about 36% of total daily UFP exposure and in-vehicle exposures add the remainder (17%). However, the effect of one smoker in the home results in an overwhelming increase in the importance of indoor sources (77% of the total).

Rationale: Outdoor fine particulate air pollution (particulate matter with an aerodynamic diameter ⩽2.5 μm; PM2.5) contributes to millions of deaths around the world each year, but much less is known about the long-term health impacts of other particulate air pollutants, including ultrafine particles (a.k.a. nanoparticles), which are in the nanometer-size range (<100 nm), widespread in urban environments, and not currently regulated. Objectives: We sought to estimate the associations between long-term exposure to outdoor ultrafine particles and mortality. Methods: Outdoor air pollution levels were linked to the residential addresses of a large, population-based cohort from 2001 to 2016. Associations between long-term exposure to outdoor ultrafine particles and nonaccidental and cause-specific mortality were estimated using Cox proportional hazards models. Measurements and Main Results: An increase in long-term exposure to outdoor ultrafine particles was associated with an increased risk of nonaccidental mortality (hazard ratio = 1.073; 95% confidence interval = 1.061-1.085) and cause-specific mortality, the strongest of which was respiratory mortality (hazard ratio = 1.174; 95% confidence interval = 1.130-1.220). We estimated the mortality burden for outdoor ultrafine particles in Montreal and Toronto, Canada, to be approximately 1,100 additional nonaccidental deaths every year. Furthermore, we observed possible confounding by particle size, which suggests that previous studies may have underestimated or missed important health risks associated with ultrafine particles. Conclusions: As outdoor ultrafine particles are not currently regulated, there is great potential for future regulatory interventions to improve population health by targeting these common outdoor air pollutants.

The prognostic significance of acute pulmonary events in people with lower extremity peripheral artery disease (PAD) is unknown. We hypothesized that an acute pulmonary event (hospitalization for pneumonia and/or chronic lower respiratory disease (CLRD) exacerbation) would be associated with a higher rate of subsequent ischemic heart disease (IHD) events in PAD. A total of 569 PAD participants were systematically identified from among patients in Chicago medical practices and followed longitudinally. Hospitalizations after enrollment were evaluated and adjudicated for pulmonary events. The primary outcome was adjudicated myocardial infarctions, unstable angina, and IHD death. Of 569 PAD participants, 34 (6.0%) were hospitalized for a pulmonary event (11 CLRD exacerbation and 23 pneumonia) during a mean follow-up of 1.52 years±0.80. Participants hospitalized for a pulmonary event had a higher rate of subsequent IHD events than those not hospitalized for a pulmonary event (10/34 (29%) vs 38/535 (7.1%), p<0.001). After adjusting for age, sex, race, comorbidities, and other confounders, a pulmonary hospitalization was associated with an increased risk of a subsequent IHD event (hazard ratio (HR) = 12.42, 95% confidence interval (CI) = 5.35 to 28.86, p<0.001). Non-pulmonary hospitalizations were also associated with IHD events (HR = 3.39, 95% CI = 1.78 to 6.44, p<0.001), but this association was less strong compared to pulmonary hospitalizations and IHD events ( p = 0.011 for difference in the strength of association). In conclusion, hospitalization for an acute pulmonary event was associated with higher risk for subsequent IHD events in PAD. Future study should examine whether hospitalization for pulmonary events warrants increased surveillance or potential intervention to prevent IHD events in PAD.

To examine the association between non-fasting serum glucose concentrations and major ischaemic heart disease (IHD) events (fatal and non-fatal myocardial infarction). A prospective study. A population based sample of 7735 middle aged British men. Known diabetics, men with a glucose concentration > or = 11.1 mmol/l at screening, and hypertensive patients taking regular medication were excluded from the analysis. With exclusions (n = 509) and missing glucose values (n = 49), there were 7177 men available for analysis. Major IHD events (fatal and non-fatal myocardial infarction) during 9.5 years follow up on all men. There were 505 major IHD events, 222 fatal and 283 non-fatal, in the 7177 men studied. There was a non-linear relation between the glucose concentration and the risk (per 1000 men per year) of all major IHD events and fatal IHD events, with the excess risk in the upper quintile of the glucose distribution (> or = 6.1 mmol/l). The unadjusted relative risks (RR) in the upper glucose concentration quintile compared with the first to the fourth quintiles combined were 1.4 (95% CI 1.1, 1.7) for all events and 1.3 (95% CI 1.0, 1.7) for fatal events. Adjustment for age, smoking, occupational status, body mass index, physical activity, systolic blood pressure, total and high density lipoprotein cholesterol, and triglyceride concentrations had a minimal effect on these relative risk estimates. This non-linear relationship between the serum glucose concentration and the risk of a major IHD event was observed in men with no evidence of IHD at screening (n = 5518) but not in men with IHD (n = 1659). In the former group, the RR (adjusted for major coronary risk factors) for all major IHD events in the upper quintile relative to the lower quintiles combined was 1.5 (95% CI 1.2, 2.0) and for fatal IHD events was 1.8 (95% CI 1.1, 2.6). These data suggest that asymptomatic hyperglycaemia is an independent risk factor for major IHD events.

Ultrafine particles (UFPs) significantly affect human health and climate. UFPs can be produced largely from the incomplete burning of solid fuels in stoves; however, indoor UFPs are less studied compared to outdoor UFPs, especially in coal-combustion homes. In this study, indoor and outdoor UFP concentrations were measured simultaneously by using a portable instrument, and internal and outdoor source contributions to indoor UFPs were estimated using a statistical approach based on highly temporally resolved data. The total concentrations of indoor UFPs in a rural household with the presence of coal burning were as high as 1.64 × 105 (1.32 × 105–2.09 × 105 as interquartile range) #/cm3, which was nearly one order of magnitude higher than that of outdoor UFPs. Indoor UFPs were unimodal, with the greatest abundance of particles in the size range of 31.6–100 nm. The indoor-to-outdoor ratio of UFPs in a rural household was about 6.4 (2.7–16.0), while it was 0.89 (0.88–0.91) in a home without strong internal sources. A dynamic process illustrated that the particle number concentration increased by ~5 times during the coal ignition period. Indoor coal combustion made up to over 80% of indoor UFPs, while in an urban home without coal combustion sources indoors, the outdoor sources may contribute to nearly 90% of indoor UFPs. A high number concentration and a greater number of finer particles in homes with the presence of coal combustion indicated serious health hazards associated with UFP exposure and the necessity for future controls on indoor UFPs.

Levels of ultrafine particles in different microenvironments — Implications to children exposure