The effect of industry-related air pollution on lung function and respiratory symptoms in school children

Background: Heavy industry emits many potentially hazardous pollutants into the air which can affect health. However, the effects of air pollution from heavy industry on lung function and respiratory symptoms have been investigated scarcely. Our aim was to investigate the associations of long-term air pollution from heavy industry with lung function and respiratory symptoms in school children. Methods: A cross-sectional lung function study was conducted among school children (7-13 years) in the vicinity of an area with heavy industry. Lung function measurements were conducted during school hours. Parents of the children were asked to complete a questionnaire about the health of their children. A dispersion model was used to characterize the additional individual-level exposures to air pollutants from the industry in the area. Associations between PM2.5 and NOX exposure with lung function and presence of respiratory symptoms were investigated by linear and/or logistic regression analysis. Results: Participation in the lung function measurements and questionnaires was 84% (665/787) and 77% (603/787), respectively. The range of the elevated PM2.5 and NOX five years average concentrations (2008-2012) due to heavy industry were 0.04-1.59 μg/m3 and 0.74-11.33 μg/m3 respectively. After adjustment for confounders higher exposure to PM2.5 and NOX (per interquartile range of 0.56 and 7.43 μg/m3 respectively) was associated with lower percent predicted peak expiratory flow (PEF) (B -2.80%, 95%CI -5.05% to - 0.55% and B -3.67%, 95%CI -6.93% to - 0.42% respectively). Higher exposure to NOX (per interquartile range of 7.43 μg/m3) was also associated with lower percent forced vital capacity (FVC) and percent predicted forced expiration volume in 1 s (FEV1) (B -2.30, 95% CI -4.55 to - 0.05 and B -2.73, 95%CI -5.21 to - 0.25 respectively). No significant associations were found between the additional exposure to PM2.5 or NOX and respiratory symptoms except for PM2.5 and dry cough (OR 1.40, 95%CI 1.00 to 1.94). Conclusion: Exposure to PM2.5 and NOX from industry was associated with decreased lung function. Exposure to PM2.5 was also associated with parents' reports of dry cough among their children

An immunoassay for the measurement of (1→3)-β-D-glucans in the indoor environment

An inhibition enzyme immunoassay was developed for quantitation of (1→3)-β-D-glucans in the indoor environment. Immunospecific rabbit antibodies were produced by immunization with bovine serum albuminconjugated laminarin.The laminarin calibration curve ranged from 40 to 3000 ng/ml.Another (1→3)-β-D-glucan (curdlan) showed a similar inhibition curve, but was less reactive on a weight basis. Pustulan, presumed to be (1→3)-β-D-glucan, also showed immunoreactivity in the assay. Control experiments indicated that this was due to (1→3)-β-D-glucan structures. Other non-(1→3)-β-D-glucan polysaccharides did not react. (1→3)-β-Dglucan was detectable in dust from a variety of occupational and environmental settings. We conclude that the new assay offers a useful method for indoor (1→3)-β-Dglucan exposure assessment

Use of passive diffusion sampling method for defining NO(2 )concentrations gradient in São Paulo, Brazil

BACKGROUND: Air pollution in São Paulo is constantly being measured by the State of Sao Paulo Environmental Agency, however there is no information on the variation between places with different traffic densities. This study was intended to identify a gradient of exposure to traffic-related air pollution within different areas in São Paulo to provide information for future epidemiological studies. METHODS: We measured NO(2 )using Palmes' diffusion tubes in 36 sites on streets chosen to be representative of different road types and traffic densities in São Paulo in two one-week periods (July and August 2000). In each study period, two tubes were installed in each site, and two additional tubes were installed in 10 control sites. RESULTS: Average NO(2 )concentrations were related to traffic density, observed on the spot, to number of vehicles counted, and to traffic density strata defined by the city Traffic Engineering Company (CET). Average NO(2)concentrations were 63μg/m(3 )and 49μg/m(3 )in the first and second periods, respectively. Dividing the sites by the observed traffic density, we found: heavy traffic (n = 17): 64μg/m(3 )(95% CI: 59μg/m(3 )– 68μg/m(3)); local traffic (n = 16): 48μg/m(3 )(95% CI: 44μg/m(3 )– 52μg/m(3)) (p < 0.001). CONCLUSION: The differences in NO(2 )levels between heavy and local traffic sites are large enough to suggest the use of a more refined classification of exposure in epidemiological studies in the city. Number of vehicles counted, traffic density observed on the spot and traffic density strata defined by the CET might be used as a proxy for traffic exposure in São Paulo when more accurate measurements are not available

How do you explain the risk of air pollution to your patients?

.@ERStalk Environ & Health committee workshop concludes: HCPs vital to raising awareness of air pollution to patients http://ow.ly/pfOe301FoIg

Long-Term Traffic-Related Exposures and Asthma Onset in Schoolchildren in Oslo, Norway

BACKGROUND: Whether there is a causal relation between long-term exposure to traffic and asthma development is so far not clear. This may be explained by inaccurate exposure assessment. OBJECTIVE: We investigated the associations of long-term traffic-related exposures with asthma onset assessed retrospectively and respiratory symptoms in 9- to 10-year-old children. METHODS: We collected information on respiratory outcomes and potential confounding variables by parental questionnaire in 2,871 children in Oslo. Nitrogen dioxide exposure was assessed by the EPISODE dispersion model and assigned at updated individual addresses during lifetime. Distance to major road was assigned at birth address and address by date of questionnaire. Cox proportional hazard regression and logistic regression were used. RESULTS: We did not find positive associations between any long-term traffic-related exposure and onset of doctor-diagnosed asthma. An interquartile range (IQR) increase of NO(2) exposure before asthma onset was associated with an adjusted risk ratio of 0.82 [95% confidence interval (CI), 0.67-1.02]. Handling early asthma cases (children /= 4 years of age) were positive but not statistically significant. For current symptoms, an IQR increase of previous year's NO(2) exposure was associated with adjusted odds ratios of 1.01 (95% CI, 0.83-1.23) for wheeze, 1.10 (95% CI, 0.79-1.51) for severe wheeze, and 1.01 (95% CI, 0.84-1.21) for dry cough. CONCLUSIONS: We were not able to find positive associations of long-term traffic-related exposures with asthma onset or with current respiratory symptoms in 9- to 10-year-old children in Oslo

Air pollution and the development of asthma from birth until young adulthood

We used data of 3687 participants of the prospective Dutch PIAMA (Prevention and Incidence of Asthma and Mite Allergy) birth cohort and linked asthma incidence until age 20 years to estimated concentrations of nitrogen dioxide (NO2), particulate matter with a diameter <2.5 μm (PM2.5), <10 μm (PM10), and 2.5-10 μm, and PM2.5 absorbance ("soot") at the residential address. We assessed overall and age-specific associations with air pollution exposure with discrete time-hazard models, adjusting for potential confounders

Reducing the health effect of particles from agriculture

This autumn, the European Union (EU) Parliament will have a crucial vote on the future of air pollution policy in Europe. For discussion is a commission proposal for new national emission ceilings, as amended by the European Parliament Environment Committee in July, 2015. The proposed emission ceilings cover not only emissions of primary, directly emitted particulate matter but also emissions from precursor gases. These gases include ammonia, sulphur dioxide, and nitrogen oxides, which react in the atmosphere to form solid (particulate) ammonium sulphates and nitrates

House dust endotoxin, asthma and allergic sensitization through childhood into adolescence

We used data of 854 participants of the prospective Dutch PIAMA birth cohort study with house dust endotoxin measurements at 3 months and/or 5-6 years and data on asthma and/or allergic sensitization from at least one of 11 follow-ups until age 17. We assessed overall and age-specific associations of the prevalence of asthma and sensitization with mattress and living room floor dust concentrations (per gram of dust) and loads (per m2 of sampling surface)

The influence of industry-related air pollution on birth outcomes in an industrialized area

Recent studies suggests that air pollution, from among others road traffic, can influence growth and development of the human foetus during pregnancy. The effects of air pollution from heavy industry on birth outcomes have been investigated scarcely. Our aim was to investigate the associations of air pollution from heavy industry on birth outcomes. A cross-sectional study was conducted among 4488 singleton live births (2012–2017) in the vicinity of a large industrial area in the Netherlands. Information from the birth registration was linked with a dispersion model to characterize annual individual-level exposure of pregnant mothers to air pollutants from industry in the area. Associations between particulate matter (PM10), nitrogen oxides (NOX), sulphur dioxide (SO2), and volatile organic compounds (VOC) with low birth weight (LBW), preterm birth (PTB), and small for gestational age (SGA) were investigated by logistic regression analysis and with gestational age, birth weight, birth length, and head circumference by linear regression analysis. Exposures to NOX, SO2, and VOC (per interquartile range of 1.16, 0.42, and 0.97 μg/m3 respectively) during pregnancy were associated with LBW (OR 1.20, 95%CI 1.06–1.35, OR 1.20, 95%CI 1.00–1.43, and OR 1.21, 95%CI 1.08–1.35 respectively). NOX and VOC were also associated with PTB (OR 1.14, 95%CI 1.01–1.29 and OR 1.17, 95%CI 1.04–1.31 respectively). Associations between exposure to air pollution and birth weight, birth length, and head circumference were statistically significant. Higher exposure to PM10, NOX, SO2 and VOC (per interquartile range of 0.41, 1.16, 0.42, and 0.97 μg/m3 respectively) was associated with reduced birth weight of 21 g to 30 g. The 90th percentile industry-related PM10 exposure corresponded with an average birth weight decrease of 74 g