Dataset Information

Ambient Air Pollution-related Mortality in Dairy Cattle: Does It Corroborate Human Findings?

ABSTRACT: Despite insights for humans, short-term associations of air pollution with mortality to our knowledge have never been studied in animals. We investigated the association between ambient air pollution and risk of mortality in dairy cows and assessed effect modification by season.We collected ozone (O3), particulate matter (PM10), and nitrogen dioxide (NO2) concentrations at the municipality level for 87,108 dairy cow deaths in Belgium from 2006 to 2009. We combined a case-crossover design with time-varying distributed lag models.We found acute and delayed associations between air pollution and dairy cattle mortality during the warm season. The increase in mortality for a 10 ?g/m increase in 2-day (lag 0-1) O3 was 1.2% (95% confidence interval [CI] = 0.3%, 2.1%), and the corresponding estimates for a 10 ?g/m increase in same-day (lag 0) PM10 and NO2 were 1.6% (95% CI = 0.0%, 3.1%) and 9.2% (95% CI = 6.3%, 12%), respectively. Compared with the acute increases, the cumulative 26-day (lag 0-25) estimates were considerably larger for O3 (3.0%; 95% CI = 0.2%, 6.0%) and PM10 (3.2%; 95% CI = -0.6%, 7.2%), but not for NO2 (1.4%; 95% CI = -4.9%, 8.2%). In the cold season, we only observed increased mortality risks associated with same-day (lag 0) exposure to NO2 (1.4%; 95% CI = -0.1%, 3.1%) and with 26-day (lag 0-25) exposure to O3 (4.6%; 95% CI = 2.2%, 7.0%).Our study adds to the epidemiologic findings in humans and reinforces the evidence on the plausibility of causal effects. Furthermore, our results indicate that air pollution associations go beyond short-term mortality displacement. (See video abstract at http://links.lww.com/EDE/B105.).

SUBMITTER: Cox B

PROVIDER: S-EPMC5400059 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature

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Ambient Air Pollution-related Mortality in Dairy Cattle: Does It Corroborate Human Findings?

Cox Bianca B Gasparrini Antonio A Catry Boudewijn B Fierens Frans F Vangronsveld Jaco J Nawrot Tim S TS

Epidemiology (Cambridge, Mass.) 20161101 6

<h4>Background</h4>Despite insights for humans, short-term associations of air pollution with mortality to our knowledge have never been studied in animals. We investigated the association between ambient air pollution and risk of mortality in dairy cows and assessed effect modification by season.<h4>Methods</h4>We collected ozone (O3), particulate matter (PM10), and nitrogen dioxide (NO2) concentrations at the municipality level for 87,108 dairy cow deaths in Belgium from 2006 to 2009. We combi ...[more]

PMID: 27468004

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Project description:BackgroundThe systematic evaluation of the results of time-series studies of air pollution is challenged by differences in model specification and publication bias.MethodsWe evaluated the associations of inhalable particulate matter (PM) with an aerodynamic diameter of 10 ?m or less (PM10) and fine PM with an aerodynamic diameter of 2.5 ?m or less (PM2.5) with daily all-cause, cardiovascular, and respiratory mortality across multiple countries or regions. Daily data on mortality and air pollution were collected from 652 cities in 24 countries or regions. We used overdispersed generalized additive models with random-effects meta-analysis to investigate the associations. Two-pollutant models were fitted to test the robustness of the associations. Concentration-response curves from each city were pooled to allow global estimates to be derived.ResultsOn average, an increase of 10 ?g per cubic meter in the 2-day moving average of PM10 concentration, which represents the average over the current and previous day, was associated with increases of 0.44% (95% confidence interval [CI], 0.39 to 0.50) in daily all-cause mortality, 0.36% (95% CI, 0.30 to 0.43) in daily cardiovascular mortality, and 0.47% (95% CI, 0.35 to 0.58) in daily respiratory mortality. The corresponding increases in daily mortality for the same change in PM2.5 concentration were 0.68% (95% CI, 0.59 to 0.77), 0.55% (95% CI, 0.45 to 0.66), and 0.74% (95% CI, 0.53 to 0.95). These associations remained significant after adjustment for gaseous pollutants. Associations were stronger in locations with lower annual mean PM concentrations and higher annual mean temperatures. The pooled concentration-response curves showed a consistent increase in daily mortality with increasing PM concentration, with steeper slopes at lower PM concentrations.ConclusionsOur data show independent associations between short-term exposure to PM10 and PM2.5 and daily all-cause, cardiovascular, and respiratory mortality in more than 600 cities across the globe. These data reinforce the evidence of a link between mortality and PM concentration established in regional and local studies. (Funded by the National Natural Science Foundation of China and others.).

Project description:Exposure to ozone and fine particulate matter (PM2.5) can cause adverse health effects, including premature mortality due to cardiopulmonary diseases and lung cancer. Recent studies quantify global air pollution mortality but not the contribution of different emissions sectors, or they focus on a specific sector.We estimated the global mortality burden of anthropogenic ozone and PM2.5, and the impact of five emissions sectors, using a global chemical transport model at a finer horizontal resolution (0.67° × 0.5°) than previous studies.We performed simulations for 2005 using the Model for Ozone and Related Chemical Tracers, version 4 (MOZART-4), zeroing out all anthropogenic emissions and emissions from specific sectors (All Transportation, Land Transportation, Energy, Industry, and Residential and Commercial). We estimated premature mortality using a log-linear concentration-response function for ozone and an integrated exposure-response model for PM2.5.We estimated 2.23 (95% CI: 1.04, 3.33) million deaths/year related to anthropogenic PM2.5, with the highest mortality in East Asia (48%). The Residential and Commercial sector had the greatest impact globally-675 (95% CI: 428, 899) thousand deaths/year-and in most regions. Land Transportation dominated in North America (32% of total anthropogenic PM2.5 mortality), and it had nearly the same impact (24%) as Residential and Commercial (27%) in Europe. Anthropogenic ozone was associated with 493 (95% CI: 122, 989) thousand deaths/year, with the Land Transportation sector having the greatest impact globally (16%).The contributions of emissions sectors to ambient air pollution-related mortality differ among regions, suggesting region-specific air pollution control strategies. Global sector-specific actions targeting Land Transportation (ozone) and Residential and Commercial (PM2.5) sectors would particularly benefit human health. Citation: Silva RA, Adelman Z, Fry MM, West JJ. 2016. The impact of individual anthropogenic emissions sectors on the global burden of human mortality due to ambient air pollution. Environ Health Perspect 124:1776-1784;?http://dx.doi.org/10.1289/EHP177.

Project description:ImportanceThyroid hormones are critical for fetal growth and development. Prenatal particulate matter (PM) air pollution exposure has been associated with altered newborn thyroid function, but other air pollutants have not been evaluated, and critical windows of exposure are unknown.ObjectivesTo investigate the association of prenatal exposure to ambient and traffic-related air pollutants with newborn thyroid function and identify critical windows of exposure.Design, setting, and participantsThis cohort study used data from 2050 participants in the Children's Health Study. Statistical analyses were conducted from 2017 to 2018 using pregnancy and birth data from 1994 to 1997 for a subset of participants recruited from schools in 13 southern California communities in 2002 to 2003 when participants were 5 to 7 years of age. Participants were included in statistical analyses if they could be linked to their newborn blood spot and had complete monthly exposure measures for at least 1 air pollutant across pregnancy.ExposuresPrenatal monthly averages of ambient (PM diameter <2.5 ?m [PM2.5] or <10 ?m [PM10], nitrogen dioxide, and ozone) and traffic-related (freeway, nonfreeway, and total nitrogen oxides) air pollutant exposures were determined using inverse distance-squared weighting of central monitoring data and the California Line Source Dispersion model, respectively.Main outcomes and measuresNewborn heel-stick blood spot total thyroxine (TT4) measures were acquired retrospectively from the California Department of Public Health.ResultsParticipants included 2050 newborns (50.5% male), with a median (interquartile range) age of 20 (15-29) hours. The majority of newborns were Hispanic white (1202 [58.6%]) or non-Hispanic white (638 [31.1%]). Sixty-six (3.2%) were black and 144 (7.0%) were from other racial/ethnic groups. The mean (SD) newborn TT4 measure was 16.2 (4.3) ?g/dL. A 2-SD increase in prenatal PM2.5 (16.3 ?g/m3) and PM10 (22.2 ?g/m3) was associated with a 1.2-?g/dL (95% CI, 0.5-1.8 ?g/dL) and 1.5-?g/dL (95% CI, 0.9-2.1 ?g/dL) higher TT4 measure, respectively, in covariate-adjusted linear regression models. Other pollutants were not consistently associated with newborn TT4. Distributed lag models revealed that PM2.5 exposure during months 3 to 7 of pregnancy and PM10 exposure during months 1 to 8 of pregnancy were associated with significantly higher newborn TT4 concentrations (P?<?.05).Conclusions and relevancePrenatal PM exposure, particularly in early pregnancy and midpregnancy, is associated with higher newborn TT4 concentrations. Future studies should assess the health implications of PM-associated differences in newborn TT4 concentrations.

Project description:Background The association between fine particulate matter and cardiovascular disease has been convincingly demonstrated. The role of traffic-related air pollutants is less clear. To better understand the role of traffic-related air pollutants in cardiovascular disease development, we examined associations between NO2, carotid atherosclerotic plaque, and cardiometabolic disorders associated with cardiovascular disease. Methods and Results Cross-sectional analyses were conducted among 2227 patients (62.9±13.8 years; 49.5% women) from the Stroke Prevention and Atherosclerosis Research Centre (SPARC) in London, Ontario, Canada. Total carotid plaque area measured by ultrasound, cardiometabolic disorders, and residential locations were provided by SPARC medical records. Long-term outdoor residential NO2 concentrations were generated by a land use regression model. Associations between NO2, total carotid plaque area, and cardiometabolic disorders were examined using multiple regression models adjusted for age, sex, smoking, and socioeconomic status. Mean NO2 was 5.4±1.6 ppb in London, Ontario. NO2 was associated with a significant increase in plaque (3.4 mm2 total carotid plaque area per 1 ppb NO2), exhibiting a linear dose-response. NO2 was also positively associated with triglycerides, total cholesterol, and the ratio of low- to high-density lipoprotein cholesterol (P<0.05). Diabetes mellitus mediated the relationship between NO2 and total carotid plaque area (P<0.05). Conclusions Our results demonstrate that even low levels of traffic-related air pollutants are linked to atherosclerotic plaque burden, an association that may be partially attributable to pollution-induced diabetes mellitus. Our findings suggest that reducing ambient concentrations in cities with NO2 below current standards would result in additional health benefits. Given the billions of people exposed to traffic emissions, our study supports the global public health significance of reducing air pollution.

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Ambient Air Pollution-related Mortality in Dairy Cattle: Does It Corroborate Human Findings?

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Ambient Air Pollution-related Mortality in Dairy Cattle: Does It Corroborate Human Findings?

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