Active travel (cycling, walking) is beneficial for the health due to increased physical activity (PA). However, active travel may increase the intake of air pollution, leading to negative health consequences. We examined the risk-benefit balance between active travel related PA and exposure to air pollution across a range of air pollution and PA scenarios. The health effects of active travel and air pollution were estimated through changes in all-cause mortality for different levels of active travel and air pollution. Air pollution exposure was estimated through changes in background concentrations of fine particulate matter (PM2.5), ranging from 5 to 200μg/m3. For active travel exposure, we estimated cycling and walking from 0 up to 16h per day, respectively. These refer to long-term average levels of active travel and PM2.5 exposure. For the global average urban background PM2.5 concentration (22μg/m3) benefits of PA by far outweigh risks from air pollution even under the most extreme levels of active travel. In areas with PM2.5 concentrations of 100μg/m3, harms would exceed benefits after 1h 30min of cycling per day or more than 10h of walking per day. If the counterfactual was driving, rather than staying at home, the benefits of PA would exceed harms from air pollution up to 3h 30min of cycling per day. The results were sensitive to dose-response function (DRF) assumptions for PM2.5 and PA. PA benefits of active travel outweighed the harm caused by air pollution in all but the most extreme air pollution concentrations.
Indoor dust is a reservoir for commercial consumer product chemicals, including many compounds with known or suspected health effects. However, most dust exposure studies measure few chemicals in small samples. We systematically searched the U.S. indoor dust literature on phthalates, replacement flame retardants (RFRs), perfluoroalkyl substances (PFASs), synthetic fragrances, and environmental phenols and estimated pooled geometric means (GMs) and 95% confidence intervals for 45 chemicals measured in ≥3 data sets. In order to rank and contextualize these results, we used the pooled GMs to calculate residential intake from dust ingestion, inhalation, and dermal uptake from air, and then identified hazard traits from the Safer Consumer Products Candidate Chemical List. Our results indicate that U.S. indoor dust consistently contains chemicals from multiple classes. Phthalates occurred in the highest concentrations, followed by phenols, RFRs, fragrance, and PFASs. Several phthalates and RFRs had the highest residential intakes. We also found that many chemicals in dust share hazard traits such as reproductive and endocrine toxicity. We offer recommendations to maximize comparability of studies and advance indoor exposure science. This information is critical in shaping future exposure and health studies, especially related to cumulative exposures, and in providing evidence for intervention development and public policy.
Reduction of preterm births (<37 completed weeks of gestation) would substantially reduce neonatal and infant mortality, and deleterious health effects in survivors. Maternal fine particulate matter (PM2.5) exposure has been identified as a possible risk factor contributing to preterm birth. The aim of this study was to produce the first estimates of ambient PM2.5-associated preterm births for 183 individual countries and globally. To do this, national, population-weighted, annual average ambient PM2.5 concentration, preterm birth rate and number of livebirths were combined to calculate the number of PM2.5-associated preterm births in 2010 for 183 countries. Uncertainty was quantified using Monte-Carlo simulations, and analyses were undertaken to investigate the sensitivity of PM2.5-associated preterm birth estimates to assumptions about the shape of the concentration-response function at low and high PM2.5 exposures, inclusion of provider-initiated preterm births, and exposure to indoor air pollution. Globally, in 2010, the number of PM2.5-associated preterm births was estimated as 2.7 million (1.8-3.5 million, 18% (12-24%) of total preterm births globally) with a low concentration cut-off (LCC) set at 10μgm(-3), and 3.4 million (2.4-4.2 million, 23% (16-28%)) with a LCC of 4.3μgm(-3). South and East Asia, North Africa/Middle East and West sub-Saharan Africa had the largest contribution to the global total, and the largest percentage of preterm births associated with PM2.5. Sensitivity analyses showed that PM2.5-associated preterm birth estimates were 24% lower when provider-initiated preterm births were excluded, 38-51% lower when risk was confined to the PM2.5 exposure range in the studies used to derive the effect estimate, and 56% lower when mothers who live in households that cook with solid fuels (and whose personal PM2.5 exposure is likely dominated by indoor air pollution) were excluded. The concentration-response function applied here derives from a meta-analysis of studies, most of which were conducted in the US and Europe, and its application to the areas of the world where we estimate the greatest effects on preterm births remains uncertain. Nevertheless, the substantial percentage of preterm births estimated to be associated with anthropogenic PM2.5 (18% (13%-24%) of total preterm births globally) indicates that reduction of maternal PM2.5 exposure through emission reduction strategies should be considered alongside mitigation of other risk factors associated with preterm births.
Preterm birth (PTB) rates (11.4% in 2013) in the United States (US) remain high and are a substantial cause of morbidity. Studies of prenatal exposure have associated particulate matter <2.5microns in diameter (PM2.5) and other ambient air pollutants with adverse birth outcomes, yet, to our knowledge, burden and costs of PM 2.5-attributable PTB have not been estimated in the US.
Mammographic breast density is a well-established strong risk factor for breast cancer. The environmental contributors to geographic variation in breast density in urban and rural areas are poorly understood. We examined the association between breast density and exposure to ambient air pollutants (particulate matter <2.5 μm in diameter (PM2.5) and ozone (O3)) in a large population-based screening registry.
Fine particulate matter (PM2.5) has been linked to cardiovascular disease, possibly via accelerated atherosclerosis. We examined associations between the progression of the intima-medial thickness (IMT) of the common carotid artery, as an indicator of atherosclerosis, and long-term PM2.5 concentrations in participants from the Multi-Ethnic Study of Atherosclerosis (MESA).
Many residents in Beijing use disposable face masks in an attempt to protect their health from high particulate matter (PM) concentrations. Retail masks may be certified to local or international standards, but their real-life performance may not confer the exposure reduction potential that is marketed. This study aimed to evaluate the effectiveness of a range of face masks that are commercially available in China.
House dust exposure mediates gut microbiome Lactobacillus enrichment and airway immune defense against allergens and virus infection
- Proceedings of the National Academy of Sciences of the United States of America
- Published over 6 years ago
Exposure to dogs in early infancy has been shown to reduce the risk of childhood allergic disease development, and dog ownership is associated with a distinct house dust microbial exposure. Here, we demonstrate, using murine models, that exposure of mice to dog-associated house dust protects against ovalbumin or cockroach allergen-mediated airway pathology. Protected animals exhibited significant reduction in the total number of airway T cells, down-regulation of Th2-related airway responses, as well as mucin secretion. Following dog-associated dust exposure, the cecal microbiome of protected animals was extensively restructured with significant enrichment of, amongst others, Lactobacillus johnsonii. Supplementation of wild-type animals with L. johnsonii protected them against both airway allergen challenge or infection with respiratory syncytial virus. L. johnsonii-mediated protection was associated with significant reductions in the total number and proportion of activated CD11c(+)/CD11b(+) and CD11c(+)/CD8(+) cells, as well as significantly reduced airway Th2 cytokine expression. Our results reveal that exposure to dog-associated household dust results in protection against airway allergen challenge and a distinct gastrointestinal microbiome composition. Moreover, the study identifies L. johnsonii as a pivotal species within the gastrointestinal tract capable of influencing adaptive immunity at remote mucosal surfaces in a manner that is protective against a variety of respiratory insults.
Environmental exposure to chemicals has been considered a potential factor contributing to deteriorated semen quality. However, previous literature on exposure to air pollution and semen quality is inconsistent. We therefore investigated the health effects of short-term and long-term exposure to fine particulate matter (PM2.5) on semen quality in Taiwanese men from the general population.
Background Studies have shown that long-term exposure to air pollution increases mortality. However, evidence is limited for air-pollution levels below the most recent National Ambient Air Quality Standards. Previous studies involved predominantly urban populations and did not have the statistical power to estimate the health effects in underrepresented groups. Methods We constructed an open cohort of all Medicare beneficiaries (60,925,443 persons) in the continental United States from the years 2000 through 2012, with 460,310,521 person-years of follow-up. Annual averages of fine particulate matter (particles with a mass median aerodynamic diameter of less than 2.5 μm [PM2.5]) and ozone were estimated according to the ZIP Code of residence for each enrollee with the use of previously validated prediction models. We estimated the risk of death associated with exposure to increases of 10 μg per cubic meter for PM2.5 and 10 parts per billion (ppb) for ozone using a two-pollutant Cox proportional-hazards model that controlled for demographic characteristics, Medicaid eligibility, and area-level covariates. Results Increases of 10 μg per cubic meter in PM2.5 and of 10 ppb in ozone were associated with increases in all-cause mortality of 7.3% (95% confidence interval [CI], 7.1 to 7.5) and 1.1% (95% CI, 1.0 to 1.2), respectively. When the analysis was restricted to person-years with exposure to PM2.5 of less than 12 μg per cubic meter and ozone of less than 50 ppb, the same increases in PM2.5 and ozone were associated with increases in the risk of death of 13.6% (95% CI, 13.1 to 14.1) and 1.0% (95% CI, 0.9 to 1.1), respectively. For PM2.5, the risk of death among men, blacks, and people with Medicaid eligibility was higher than that in the rest of the population. Conclusions In the entire Medicare population, there was significant evidence of adverse effects related to exposure to PM2.5 and ozone at concentrations below current national standards. This effect was most pronounced among self-identified racial minorities and people with low income. (Supported by the Health Effects Institute and others.).