Exposure to long-term air pollution and road traffic noise in relation to cholesterol: A cross-sectional study

BackgroundExposure to traffic noise and air pollution have both been associated with cardiovascular disease, though the mechanisms behind are not yet clear.ObjectivesWe aimed to investigate whether the two exposures were associated with levels of cholesterol in a cross-sectional design.MethodsIn 1993–1997, 39,863 participants aged 50–64 year and living in the Greater Copenhagen area were enrolled in a population-based cohort study. For each participant, non-fasting total cholesterol was determined in whole blood samples on the day of enrolment. Residential addresses 5-years preceding enrolment were identified in a national register and road traffic noise (L_den) were modeled for all addresses. For air pollution, nitrogen dioxide (NO₂) was modeled at all addresses using a dispersion model and PM_2.5 was modeled at all enrolment addresses using a land-use regression model. Analyses were done using linear regression with adjustment for potential confounders as well as mutual adjustment for the three exposures.ResultsBaseline residential exposure to the interquartile range of road traffic noise, NO₂ and PM_2.5 was associated with a 0.58 mg/dl (95% confidence interval: − 0.09; 1.25), a 0.68 mg/dl (0.22; 1.16) and a 0.78 mg/dl (0.22; 1.34) higher level of total cholesterol in single pollutant models, respectively. In two pollutant models with adjustment for noise in air pollution models and vice versa, the association between air pollution and cholesterol remained for both air pollution variables (NO₂: 0.72 (0.11; 1.34); PM_2.5: 0.70 (0.12; 1.28) mg/dl), whereas there was no association for noise (− 0.08 mg/dl). In three-pollutant models (NO₂, PM_2.5 and road traffic noise), estimates for NO₂ and PM_2.5 were slightly diminished (NO₂: 0.58 (− 0.05; 1.22); PM_2.5: 0.57 (− 0.02; 1.17) mg/dl).ConclusionsAir pollution and possibly also road traffic noise may be associated with slightly higher levels of cholesterol, though associations for the two exposures were difficult to separate.     

Associations between maternal exposure to air pollution and traffic noise and newborn's size at birth: A cohort study

BackgroundMaternal exposure to air pollution and traffic noise has been suggested to impair fetal growth, but studies have reported inconsistent findings.ObjectiveTo investigate associations between residential air pollution and traffic noise during pregnancy and newborn's size at birth.MethodsFrom a national birth cohort we identified 75,166 live-born singletons born at term with information on the children's size at birth. Residential address history from conception until birth was collected and air pollution (NO₂ and NO_x) and road traffic noise was modeled at all addresses. Associations between exposures and indicators of newborn's size at birth: birth weight, placental weight and head and abdominal circumference were analyzed by linear and logistic regression, and adjusted for potential confounders.ResultsIn mutually adjusted models we found a 10 μg/m³ higher time-weighted mean exposure to NO₂ during pregnancy to be associated with a 0.35 mm smaller head circumference (95% confidence interval (CI): 95% CI: − 0.57; − 0.12); a 0.50 mm smaller abdominal circumference (95% CI: − 0.80; − 0.20) and a 5.02 g higher placental weight (95% CI: 2.93; 7.11). No associations were found between air pollution and birth weight. Exposure to residential road traffic noise was weakly associated with reduced head circumference, whereas none of the other newborn's size indicators were associated with noise, neither before nor after adjustment for air pollution.ConclusionsThis study indicates that air pollution may result in a small reduction in offspring's birth head and abdominal circumference, but not birth weight, whereas traffic noise seems not to affect newborn's size at birth.     

Association between long-term exposure to air pollution and mortality in France: A 25-year follow-up study

IntroductionLong-term exposure to air pollution (AP) has been shown to have an impact on mortality in numerous countries, but since 2005 no data exists for France.ObjectivesWe analyzed the association between long-term exposure to air pollution and mortality at the individual level in a large French cohort followed from 1989 to 2013.MethodsThe study sample consisted of 20,327 adults working at the French national electricity and gas company EDF-GDF. Annual exposure to PM₁₀, PM_10–2.5, PM_2.5, NO₂, O₃, SO₂, and benzene was assessed for the place of residence of participants using a chemistry-transport model and taking residential history into account. Hazard ratios were estimated using a Cox proportional-hazards regression model, adjusted for selected individual and contextual risk factors. Hazard ratios were computed for an interquartile range (IQR) increase in air pollutant concentrations.ResultsThe cohort recorded 1967 non-accidental deaths. Long-term exposures to baseline PM_2.5, PM_10-25, NO₂ and benzene were associated with an increase in non-accidental mortality (Hazard Ratio, HR = 1.09; 95% CI: 0.99, 1.20 per 5.9 μg/m³, PM_10-25; HR = 1.09;95% CI: 1.04, 1.15 per 2.2 μg/m³, NO₂: HR = 1.14; 95% CI: 0.99, 1.31 per 19.3 μg/m³ and benzene: HR = 1.10; 95% CI: 1.00, 1.22 per 1.7 μg/m³).The strongest association was found for PM₁₀: HR = 1.14; 95% CI: 1.05, 1.25 per 7.8 μg/m³. PM₁₀, PM_10-25 and SO₂ were associated with non-accidental mortality when using time varying exposure. No significant associations were observed between air pollution and cardiovascular and respiratory mortality.ConclusionLong-term exposure to fine particles, nitrogen dioxide, sulfur dioxide and benzene is associated with an increased risk of non-accidental mortality in France. Our results strengthen existing evidence that outdoor air pollution is a significant environmental risk factor for mortality. Due to the limited sample size and the nature of our study (occupational), further investigations are needed in France with a larger representative population sample.     

Associations between short/medium-term variations in black smoke air pollution and mortality in the Glasgow conurbation,UK

ObjectivesTo examine associations between short/medium-term variations in black smoke air pollution and mortality in the population of Glasgow and the adjacent towns of Renfrew and Paisley over a 25-year period at different time lags (0–30 days).MethodsGeneralised linear (Poisson) models were used to investigate the relationship between lagged black smoke concentrations and daily mortality, with allowance for confounding by cold temperature, between 1974 and 1998.ResultsWhen a range of lag periods were investigated significant associations were noted between temperature-adjusted black smoke exposure and all-cause mortality at lag periods of 13–18 and 19–24 days, and respiratory mortality at lag periods of 1–6, 7–12, and 13–18 days. Significant associations between cardiovascular mortality and temperature-adjusted black smoke were not observed. After adjusting for the effects of temperature a 10 μg m^− 3 increase in black smoke concentration on a given day was associated with a 0.9% [95% Confidence Interval (CI): 0.3–1.5%] increase in all cause mortality and a 3.1% [95% CI: 1.4–4.9%] increase in respiratory mortality over the ensuing 30-day period. In contrast for a 10 μg m^− 3 increase in black smoke concentration over 0–3 day lag period, the temperature adjusted exposure mortality associations were substantially lower (0.2% [95% CI: − 0.0–0.4%] and 0.3% [95% CI: − 0.2–0.8%] increases for all-cause and respiratory mortality respectively).ConclusionsThis study has provided evidence of association between black smoke exposure and mortality at longer lag periods than have been investigated in the majority of time series analyses.     

Lower placental telomere length may be attributed to maternal residential traffic exposure; a twin study

BackgroundHigh variation in telomere length between individuals is already present before birth and is as wide among newborns as in adults. Environmental exposures likely have an impact on this observation, but remain largely unidentified. We hypothesize that placental telomere length in twins is associated with residential traffic exposure, an important environmental source of free radicals that might accelerate aging. Next, we intend to unravel the nature-nurture contribution to placental telomere length by estimating the heritability of placental telomere length.MethodsWe measured the telomere length in placental tissues of 211 twins in the East Flanders Prospective Twin Survey. Maternal traffic exposure was determined using a geographic information system. Additionally, we estimated the relative importance of genetic and environmental sources of variance.ResultsIn this twin study, a variation in telomere length in the placental tissue was mainly determined by the common environment. Maternal residential proximity to a major road was associated with placental telomere length: a doubling in the distance to the nearest major road was associated with a 5.32% (95% CI: 1.90 to 8.86%; p = 0.003) longer placental telomere length at birth. In addition, an interquartile increase (22%) in maternal residential surrounding greenness (5 km buffer) was associated with an increase of 3.62% (95% CI: 0.20 to 7.15%; p = 0.04) in placental telomere length.ConclusionsIn conclusion, we showed that maternal residential proximity to traffic and lower residential surrounding greenness is associated with shorter placental telomere length at birth. This may explain a significant proportion of air pollution-related adverse health outcomes starting from early life, since shortened telomeres accelerate the progression of many diseases.     

Residential proximity to traffic and female pubertal development

BackgroundTraffic-related air pollution (TRAP) has been linked with several adverse health outcomes, including preterm birth and low birth weight, which are both related to onset of puberty. No studies to date have investigated the association between TRAP and altered pubertal timing.ObjectiveDetermine the association between residential proximity to traffic, as a marker of long-term TRAP exposure, and age at pubertal onset in a longitudinal study of girls.MethodsWe analyzed data for 437 girls at the CYGNET study site of the Breast Cancer and Environment Research Program. TRAP exposure was assessed using several measures of residential proximity to traffic based on address at study entry. Using accelerated failure time models, we calculated time ratios (TRs) and their corresponding 95% confidence intervals (CIs) for specified traffic metrics and pubertal onset, defined as stage 2 or higher for breast or pubic hair development (respectively, B2 + and PH2 +). Models were adjusted for race/ethnicity, household income, and cotinine levels.ResultsAt baseline, 71% of girls lived within 150 m of a major road. The median age of onset was 10.3 years for B2 + and 10.9 years for PH2 +. Living within 150 m downwind of a major road was associated with earlier onset of PH2 + (TR 0.96, 95% CI 0.93, 0.99). Girls in the highest quintile of either distance-weighted traffic density, annual average daily traffic, and/or traffic density also reached PH2 + earlier than girls in the lowest quintiles.ConclusionsIn this first study to assess the association between residential proximity to traffic and pubertal onset we found girls with higher exposure reached one pubertal milestone several months earlier than low exposed girls, even after consideration of likely confounders. Results should be expanded in larger epidemiological studies, and with measured levels of air pollutants.     

Respiratory medication sales and urban air pollution in Brussels (2005 to 2011)

BackgroundWe investigated the associations between daily sales of respiratory medication and air pollutants in the Brussels-Capital Region between 2005 and 2011.MethodsWe used over-dispersed Poisson Generalized Linear Models to regress daily individual reimbursement data of prescribed asthma and COPD medication from the social security database against each subject's residential exposure to outdoor particulate matter (PM₁₀) or NO₂ estimated, by interpolation from monitoring stations. We calculated cumulative risk ratios (RR) and their 95% confidence intervals (CI) for interquartile ranges (IQR) of exposure for different windows of past exposure for the entire population and for seven age groups.ResultsMedian daily concentrations of PM₁₀ and NO₂ were 25 μg/m³ (IQR = 17.1) and 38 μg/m³ (IQR = 20.5), respectively. PM₁₀ was associated with daily medication sales among individuals aged 13 to 64 y. For NO₂, significant associations were observed among all age groups except > 84 y. The highest RR were observed for NO₂, among adolescents, including three weeks lags (RR = 1.187 95%CI: 1.097–1.285).ConclusionThe associations found between temporal changes in exposure to air pollutants and daily sales of respiratory medication in Brussels indicate that urban air pollution contributes to asthma and COPD morbidity in the general population.     

Outdoor air pollution and term low birth weight in Japan

IntroductionEvidence has accumulated on the association between ambient air pollution and adverse birth outcomes. However, most of the previous studies were conducted in geographically distinct areas and suffer from lack of important potential covariates. We examined the effect of ambient air pollution on term low birth weight (LBW) using data from a nationwide population-based longitudinal survey in Japan that began in 2001.MethodsWe restricted participants to term singletons (n = 44,109). Air pollution concentrations during the 9 months before birth were obtained at the municipality level and were assigned to the participants who were born in the corresponding municipality. We conducted multilevel logistic regression analyses adjusting for individual and municipality-level variables.ResultsWe found that air pollution exposure during pregnancy was positively associated with the risk of term LBW. In the fully adjusted models, odds ratios following one interquartile range increase in each pollutant were 1.09 (95% confidence interval: 1.00, 1.19) for suspended particulate matter (SPM), 1.11 (0.99, 1.26) for nitrogen dioxide (NO₂), and 1.71 (1.18, 2.46) for sulfur dioxide (SO₂). Specifically, effect estimates for SPM and NO₂ exposure at the first trimester were higher than those at other trimesters, while SO₂ was associated with the risk at all trimesters. Nonsmoking mothers were more susceptible to SPM and NO₂ exposure compared with smoking mothers.ConclusionsAmbient air pollution increases the risk of term LBW in a nationally representative sample in Japan.     

Exposure to emissions from municipal solid waste incinerators and miscarriages: A multisite study of the MONITER Project

BackgroundMiscarriages are an important indicator of reproductive health but only few studies have analyzed their association with exposure to emissions from municipal solid waste incinerators.This study analyzed the occurrence of miscarriages in women aged 15–49 years residing near seven incinerators of the Emilia-Romagna Region (Northern Italy) in the period 2002–2006.MethodsWe considered all pregnancies occurring in women residing during the first trimester of pregnancy within a 4 km radius of each incinerator. Addresses were geocoded and exposures were characterized by a dispersion model (ADMS Urban model) producing pollution maps for incinerators based on PM₁₀ stack measurements and for other pollution sources based on NO_x ground measurements. Information on pregnancies and their outcomes was obtained from the Hospital Discharge Database. Simplified True Abortion Risks (STAR) × 100 estimated pregnancies were calculated. We ran logistic regressions adjusting for maternal characteristics, exposure to other sources of pollution, and sites, considering the whole population and stratifying by miscarriage history.ResultsThe study analyzed 11,875 pregnancies with 1375 miscarriages. After adjusting for confounders, an increase of PM₁₀ due to incinerator emissions was associated with an increased risk of miscarriage (test for trend, p = 0.042). The odds ratio for the highest quartile of exposed versus not exposed women was 1.29, 95% CI 0.97–1.72. The effect was present only for women without previous miscarriages (highest quartile of exposed versus not exposed women 1.44, 95% CI 1.06–1.96; test for trend, p = 0.009).ConclusionExposure to incinerator emissions is associated with an increased risk of miscarriage. This result should be interpreted with those of a previous study on reproductive health conducted in the same area that observed an association between incinerator exposure and preterm births.     

Air pollution exposure increases the risk of rheumatoid arthritis: A longitudinal and nationwide study

ObjectiveRheumatoid arthritis (RA) has been associated with inhaled pollutants in several studies, and it is a disease of chronic inflammation. The association between air pollution and the risk of RA remains unclear. Therefore, we conducted this nationwide, retrospective, sex-stratification study to evaluate this association.MethodsWe collected data from the Longitudinal Health Insurance Database (LHID), maintained by the Taiwan Bureau of National Health Insurance, and the Taiwan Air Quality-Monitoring Database (TAQMD), released by the Taiwan Environmental Protection Agency. The TAQMD provides the daily concentrations of particulate matter with the aerodynamic diameter < 2.5 μm (PM_2.5) and nitrogen dioxide (NO₂) from 74 ambient air quality-monitoring stations distributed all over Taiwan during 1998–2010. The LHID and TAQMD were linked according to the residential areas of insurants and the areas where the air quality-monitoring stations were located. A residential area was defined according to the location of the clinic and hospital that treated acute upper respiratory tract infections. The yearly average air pollutant concentrations were categorized into 4 levels based on quartiles. We evaluated the risk of RA in residents exposed to 4 levels of PM_2.5 and NO₂ concentrations.ResultsWe detected an increased risk of RA in participants exposed to PM_2.5 and NO₂. Among four quartiles of NO₂ concentration, namely Q1, Q2, Q3, and Q4, the adjusted hazard ratios (aHRs) in Q2, Q3, and Q4 compared with that in Q1 were 1.07 (95% confidence interval [CI] = 0.76–1.50), 1.63 (95% CI = 1.16–2.31),and 1.49 (95% CI = 1.05–2.12), respectively. Regarding the PM_2.5 concentrations, the aHRs after exposure to the Q2, Q3, and Q4 levels were 1.22 (95% CI = 0.85–1.74), 1.15 (95% CI = 0.82–1.62), and 0.79 (95% CI = 0.53–1.16), respectively.ConclusionThe results of this nationwide study suggest an increased risk of RA in residents exposed to NO₂.     

Climate change,extreme events and increased risk of salmonellosis in Maryland,USA: Evidence for coastal vulnerability

BackgroundSalmonella is a leading cause of acute gastroenteritis worldwide. Patterns of salmonellosis have been linked to weather events. However, there is a dearth of data regarding the association between extreme events and risk of salmonellosis, and how this risk may disproportionately impact coastal communities.MethodsWe obtained Salmonella case data from the Maryland Foodborne Diseases Active Surveillance Network (2002–2012), and weather data from the National Climatic Data Center (1960–2012). We developed exposure metrics related to extreme temperature and precipitation events using a 30 year baseline (1960–1989) and linked them with county-level salmonellosis data. Data were analyzed using negative binomial Generalized Estimating Equations.ResultsWe observed a 4.1% increase in salmonellosis risk associated with a 1 unit increase in extreme temperature events (incidence rate ratio (IRR):1.041; 95% confidence interval (CI):1.013–1.069). This increase in risk was more pronounced in coastal versus non-coastal areas (5.1% vs 1.5%). Likewise, we observed a 5.6% increase in salmonellosis risk (IRR:1.056; CI:1.035–1.078) associated with a 1 unit increase in extreme precipitation events, with the impact disproportionately felt in coastal areas (7.1% vs 3.6%).ConclusionsTo our knowledge, this is the first empirical evidence showing that extreme temperature/precipitation events—that are expected to be more frequent and intense in coming decades—are disproportionately impacting coastal communities with regard to salmonellosis. Adaptation strategies need to account for this differential burden, particularly in light of ever increasing coastal populations.     

Associations of gestational and early life exposures to ambient air pollution with childhood respiratory diseases in Shanghai,China: A retrospective cohort study

BackgroundAssociations of ambient air pollutants with respiratory health are inconsistent.ObjectivesWe analyzed the associations of gestational and early life exposures to air pollutants with doctor-diagnosed asthma, allergic rhinitis, and pneumonia in children.MethodsWe selected 3358 preschool children who did not alter residences after birth from a cross-sectional study in 2011–2012 in Shanghai, China. Parents reported children's respiratory health history, home environment, and family lifestyle behaviors. We collected daily concentrations of sulphur dioxide (SO₂), nitrogen dioxide (NO₂), and particulate matter with an aerodynamic diameter ≤ 10 μm (PM₁₀) during the child's total lifetime (2006–2012) for each district where the children lived. We analyzed the associations using logistic regression models.ResultsAfter adjusting for covariates and the other studied pollutants, we found that exposure to NO₂ (increment of 20 μg/m³) during the first year of life was significantly associated with asthma [odds ratio (OR) = 1.77; 95% confidence interval (CI): 1.29–2.43] and allergic rhinitis (OR = 1.67; 95% CI: 1.07–2.61). Exposure to NO₂ during gestation, the first two and three years, and over total lifetimewas all consistently associated with increased odds of allergic rhinitis. Quartiles of NO₂ concentration during different exposure periods showed a slight dose–response relationship with the studied diseases. These diseases had significant associations with pollutant mixtures that included NO₂, but had no significant association with exposures to SO₂ and PM₁₀ individually or in mixtures.ConclusionsGestational and early life exposures to ambient NO₂ are risk factors for childhood respiratory diseases.     

Health effects for the population living near a cement plant: An epidemiological assessment

Epidemiological studies have shown the association between the exposure to air pollution and several adverse health effects. To evaluate the possible acute health effects of air pollution due to the emissions of a cement plant in two small municipalities in Italy (Mazzano and Rezzato), a case–control study design was used. The risks of hospital admission for cardiovascular or respiratory diseases for increasing levels of exposure to cement plant emissions were estimated, separately for adults (age > 34 years) and children (0–14 years). Odds ratios (OR) were estimated using unconditional regression models. Attributable risks were also calculated.Statistically significant risks were found mainly for respiratory diseases among children: OR 1.67 (95% CI 1.08–2.58) for the moderately exposed category (E1), OR 1.88 (95% CI 1.19–2.97) for the highly exposed category (E2), with an attributable risk of 38% of hospital admissions due to the exposure to cement plant exhausts. Adults had a weaker risk: OR 1.38 (95% CI 1.18–1.61) for group E1, OR 1.31 (95% CI 1.10–1.56) for group E2; the attributable risk was 23%. Risks were higher for females and for the age group 35–64. These results showed an association between the exposure to plant emissions and the risk of hospital admission for cardiovascular or respiratory causes; this association was particularly strong for children.     

Exposure to fine particle matter,nitrogen dioxide and benzene during pregnancy and cognitive and psychomotor developments in children at 15 months of age

BackgroundPrenatal exposure to air pollutants has recently been identified as a potential risk factor for neuropsychological impairment.ObjectivesTo assess whether prenatal exposure to fine particulate matter (PM_2.5), nitrogen dioxide (NO₂) and benzene were associated with impaired development in infants during their second year of life.MethodsRegression analyses, based on 438 mother–child pairs, were performed to estimate the association between mother exposure to air pollutants during pregnancy and neurodevelopment of the child. The average exposure to PM_2.5, NO₂ and benzene over the whole pregnancy was calculated for each woman. During the second year of life, infant neuropsychological development was assessed using the Bayley Scales of Infant Development. Regression analyses were performed to estimate the association between exposure and outcomes, accounting for potential confounders.ResultsWe estimated that a 1 μg/m³ increase during pregnancy in the average levels of PM_2.5 was associated with a − 1.14 point decrease in motor score (90% CI: − 1.75; − 0.53) and that a 1 μg/m³ increase of NO₂ exposure was associated with a − 0.29 point decrease in mental score (90% CI: − 0.47; − 0.11). Benzene did not show any significant association with development. Considering women living closer (≤ 100 m) to metal processing activities, we found that motor scores decreased by − 3.20 (90% CI: − 5.18; − 1.21) for PM_2.5 and − 0.51 (− 0.89; − 0.13) for NO₂, while mental score decreased by − 2.71 (90% CI: − 4.69; − 0.74) for PM_2.5, and − 0.41 (9% CI: − 0.76; − 0.06) for NO₂.ConclusionsOur findings suggest that prenatal residential exposure to PM_2.5 and NO₂ adversely affects infant motor and cognitive developments. This negative effect could be higher in the proximity of metal processing plants.     

Exposure to traffic-related air pollution and the risk of developing breast cancer among women in eight Canadian provinces: A case–control study

A few recent studies have reported positive associations between long-term exposure to traffic-related air pollution and the incidence of breast cancer. We capitalized on an existing Canadian multi-site population-based case–control study to further investigate this association.We used the National Enhanced Cancer Surveillance System, a population-based case–control study conducted in eight of 10 Canadian provinces from 1994 to 1997. A total of 1569 breast cancer cases and 1872 population controls who reported at least 90% complete self-reported addresses over the 1975–1994 exposure period were examined. Mean exposure levels to nitrogen dioxide (NO₂) (an indicator of traffic-related air pollution) were estimated for this period using three different measures: (1) satellite-derived observations; (2) satellite-derived observations scaled with historical fixed-site measurements of NO₂; and (3) a national land-use regression (LUR) model. Proximity to major roads was also examined. Using unconditional logistic regression, stratified by menopausal status, we estimated odds ratios (ORs) adjusted for many individual-level and contextual breast cancer risk factors.We observed positive associations between incident breast cancer and all three measures of NO₂ exposure from 1975 to 1994. In fully adjusted models for premenopausal breast cancer, a 10 ppb increase in NO₂ exposure estimated from the satellite-derived observations, the scaled satellite-derived observations, and the national LUR model produced ORs of 1.26 (95% confidence intervals (CIs): 0.92–1.74), 1.32 (95% CI: 1.05–1.67) and 1.28 (95% CI: 0.92–1.79). For postmenopausal breast cancer, we found corresponding ORs of 1.10 (95% CI: 0.88–1.36), 1.10 (95% CI: 0.94–1.28) and 1.07 (95% CI: 0.86–1.32). Substantial heterogeneity in the ORs was observed across the eight Canadian provinces and reduced ORs were observed when models were restricted to women who had received routine mammography examinations. No associations were found for road proximity measures.This study provides some support for the hypothesis that traffic-related air pollution may be associated with the development of breast cancer, especially in premenopausal women. With the few studies available, further research is clearly needed.     

Long-term air pollution exposure and diabetes in a population-based Swiss cohort

Air pollution is an important risk factor for global burden of disease. There has been recent interest in its possible role in the etiology of diabetes mellitus. Experimental evidence is suggestive, but epidemiological evidence is limited and mixed. We therefore explored the association between air pollution and prevalent diabetes, in a population-based Swiss cohort.We did cross-sectional analyses of 6392 participants of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults [SAPALDIA], aged between 29 and 73 years. We used estimates of average individual home outdoor PM₁₀ [particulate matter <10 μm in diameter] and NO₂ [nitrogen dioxide] exposure over the 10 years preceding the survey. Their association with diabetes was modeled using mixed logistic regression models, including participants' study area as random effect, with incremental adjustment for confounders.There were 315 cases of diabetes (prevalence: 5.5% [95% confidence interval (CI): 2.8, 7.2%]). Both PM₁₀ and NO₂ were associated with prevalent diabetes with respective odds ratios of 1.40 [95% CI: 1.17, 1.67] and 1.19 [95% CI: 1.03, 1.38] per 10 μg/m³ increase in the average home outdoor level. Associations with PM₁₀ were generally stronger than with NO₂, even in the two-pollutant model. There was some indication that beta blockers mitigated the effect of PM₁₀. The associations remained stable across different sensitivity analyses.Our study adds to the evidence that long term air pollution exposure is associated with diabetes mellitus. PM₁₀ appears to be a useful marker of aspects of air pollution relevant for diabetes. This association can be observed at concentrations below air quality guidelines.     

Air pollution,ethnicity and telomere length in east London schoolchildren: An observational study

BackgroundShort telomeres are associated with chronic disease and early mortality. Recent studies in adults suggest an association between telomere length and exposure to particulate matter, and that ethnicity may modify the relationship. However associations in children are unknown.ObjectivesWe examined associations between air pollution and telomere length in an ethnically diverse group of children exposed to high levels of traffic derived pollutants, particularly diesel exhaust, and to environmental tobacco smoke.MethodsOral DNA from 333 children (8–9 years) participating in a study on air quality and respiratory health in 23 inner city London schools was analysed for relative telomere length using monochrome multiplex qPCR. Annual, weekly and daily exposures to nitrogen oxides and particulate matter were obtained from urban dispersion models (2008–10) and tobacco smoke by urinary cotinine. Ethnicity was assessed by self-report and continental ancestry by analysis of 28 random genomic markers. We used linear mixed effects models to examine associations with telomere length.ResultsTelomere length increased with increasing annual exposure to NO_x (model coefficient 0.003, [0.001, 0.005], p < 0.001), NO₂ (0.009 [0.004, 0.015], p < 0.001), PM_2.5 (0.041, [0.020, 0.063], p < 0.001) and PM₁₀ (0.096, [0.044, 0.149], p < 0.001). There was no association with environmental tobacco smoke. Telomere length was increased in children reporting black ethnicity (22% [95% CI 10%, 36%], p < 0.001)ConclusionsPollution exposure is associated with longer telomeres in children and genetic ancestry is an important determinant of telomere length. Further studies should investigate both short and long-term associations between pollutant exposure and telomeres in childhood and assess underlying mechanisms.     

Occupational exposure to asthmagens and adult onset wheeze and lung function in people who did not have childhood wheeze: A 50-year cohort study

BackgroundThere are few prospective studies that relate the development of adult respiratory disease with exposure to occupational asthmagens.ObjectiveTo evaluate the risk of adult onset wheeze (AOW) and obstructive lung function associated with occupational exposures over 50 years.MethodsA population-based randomly selected cohort of children who had not had asthma or wheezing illness, recruited in 1964 at age 10–15 years, was followed-up in 1989, 1995, 2001 and 2014 by spirometry and respiratory questionnaire. Occupational histories were obtained in 2014 and occupational exposures determined with an asthma-specific job exposure matrix. The risk of AOW and lung function impairment was analysed in subjects without childhood wheeze using logistic regression and linear mixed effects models.ResultsAll 237 subjects (mean age: 61 years, 47% male, 52% ever smoked) who took part in the 2014 follow-up had completed spirometry. Among those who did not have childhood wheeze, spirometry was measured in 93 subjects in 1989, in 312 in 1995 and in 270 subjects in 2001 follow-up. For longitudinal analysis of changes in FEV₁ between 1989 and 2014 spirometry records were available on 191 subjects at three time points and on 45 subjects at two time points, with a total number of 663 records. AOW and FEV₁ < LLN were associated with occupational exposure to food-related asthmagens (adjusted odds ratios (adjORs) 95% CI: 2.7 [1.4, 5.1] and 2.9 [1.1, 7.7]) and biocides/fungicides (adjOR 95% CI: 1.8 [1.1, 3.1] and 3.4 [1.1, 10.8]), with evident dose-response effect (p-trends < 0.05). Exposure to food-related asthmagens was also associated with reduced FEV₁, FVC and FEF_25–75% (adjusted regression coefficients 95% CI: − 7.2 [− 12.0, − 2.4], − 6.2 [− 10.9, − 1.4], and − 13.3[− 23.4, − 3.3]). Exposure to wood dust was independently associated with AOW, obstructive lung function and reduced FEF_25–75%. Excess FEV₁ decline of 6-8ml/year was observed with occupational exposure to any asthmagen, biocides/fungicides and food-related asthmagens (p < 0.05).ConclusionsThis longitudinal study confirmed previous findings of increased risks of adult onset wheezing illness with occupational exposure to specific asthmagens. A novel finding was the identification of food-related asthmagens and biocides/fungicides as potential new occupational risk factors for lung function impairment in adults without childhood wheeze.     

Biomonitoring Human Exposure to Household Air Pollution and Association with Self-reported Health Symptoms – A Stove Intervention Study in Peru

BackgroundHousehold air pollution (HAP) from indoor biomass stoves contains harmful pollutants, such as polycyclic aromatic hydrocarbons (PAHs), and is a leading risk factor for global disease burden. We used biomonitoring to assess HAP exposure and association with self-reported symptoms in 334 non-smoking Peruvian women to evaluate the efficacy of a stove intervention program.MethodsWe conducted a cross-sectional study within the framework of a community randomized control trial. Using urinary PAH metabolites (OH-PAHs) as the exposure biomarkers, we investigated whether the intervention group (n = 155, with new chimney-equipped stoves) were less exposed to HAP compared to the control group (n = 179, with mostly open-fire stoves). We also estimated associations between the exposure biomarkers, risk factors, and self-reported health symptoms, such as recent eye conditions, respiratory conditions, and headache.ResultsWe observed reduced headache and ocular symptoms in the intervention group than the control group. Urinary 2-naphthol, a suggested biomarker for inhalation PAH exposure, was significantly lower in the intervention group (GM with 95% CI: 13.4 [12.3, 14.6] μg/g creatinine) compared to control group (16.5 [15.0, 18.0] μg/g creatinine). Stove type and/or 2-naphthol was associated with a number of self-reported symptoms, such as red eye (adjusted OR with 95% CI: 3.80 [1.32, 10.9]) in the past 48 h.ConclusionsEven with the improved stoves, the biomarker concentrations in this study far exceeded those of the general populations and were higher than a no-observed-genotoxic-effect-level, indicating high exposure and a potential for increased cancer risk in the population.     

Respiratory hospital admissions in young children living near metal smelters,pulp mills and oil refineries in two Canadian provinces

BackgroundIndustrial plants emit air pollutants like fine particles (PM2.5), sulfur dioxide (SO2) and nitrogen dioxide (NO2) that may affect the health of individuals living nearby.ObjectiveTo assess the effects of community exposure to air emissions of PM2.5, SO2, and NO2 from pulp mills, oil refineries, metal smelters, on respiratory hospital admissions in young children in Quebec (QC) and British Columbia (BC), Canada.MethodsWe assessed QC, BC and pooled associations between the following estimates of exposure and hospital admissions for asthma and bronchiolitis in children aged 2–4 years for the years 2002–2010: i) Crude emission exposures at the residential postal codes of children, calculated by multiplying estimated daily emissions of PM2.5, SO2, or NO2 from all nearby (< 7.5 km) pulp mills, oil refineries, metal smelters emitting yearly ≥ 50 t and their total emissions, by the percent of the day each postal code was downwind; ii) Daily levels of these pollutants at central ambient monitoring stations nearby the industries and the children's residences.ResultsSeventy-one major industries were selected between QC and BC, with a total of 2868 cases included in our analyses. More cases were exposed to emissions from major industries in QC than in BC (e.g. 2505 admissions near SO2 industrial emitters in QC vs 334 in BC), although air pollutant levels were similar. Odds ratios (ORs) for crude refinery and smelter emissions were positive in QC but more variable in BC. For example with PM2.5 in QC, ORs were 1.13 per 0.15 t/day (95% CI: 1.00–1.27) and 1.03 (95% CI: 0.99–1.07) for refinery and smelter emissions, respectively. Pooled results of QC and BC for crude total SO2 emissions from all sources indicated a 1% increase (0–3%) in odds of hospital admissions per 1.50 t/day increase in exposure. Associations with measured pollutant levels were only seen in BC, with SO2 and NO2.ConclusionHospital admissions for wheezing diseases in young children were associated with community exposure to industrial air pollutant emissions. Future work is needed to better assess the risk of exposure to complex mixture of air pollutants from multiple industrial sources.