Water and Air Quality Bureau

Ottawa, Canada

Water and Air Quality Bureau

Ottawa, Canada
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PubMed | Water and Air Quality Bureau, Air Quality Research Division and Environment Canada
Type: | Journal: Environmental research | Year: 2015

A large landfill fire occurred in Iqaluit, Canada in spring/summer 2014. Air quality data were collected to characterize emissions as well as potential threats to public health. Criteria pollutants were monitored (PM2.5, O3, NO2) along with dioxins/furans, polycyclic aromatic hydrocarbons, and volatile organic compounds. Median daily dioxin/furan concentrations were 66-times higher during active burning (0.2 pg/m(3) Toxic Equivalency Quotient (TEQ)) compared to after the fire was extinguished (0.003 pg/m(3) TEQ). Other pollutants changed less dramatically. Our findings suggest that airborne concentrations of potentially harmful substances may be elevated during landfill fires even when criteria air pollutants remain largely unchanged.


Bourdon-Lacombe J.A.,Water and Air Quality Bureau | Moffat I.D.,Water and Air Quality Bureau | Deveau M.,Water and Air Quality Bureau | Husain M.,Environmental Health Science and Research Bureau | And 6 more authors.
Regulatory Toxicology and Pharmacology | Year: 2015

Toxicogenomics promises to be an important part of future human health risk assessment of environmental chemicals. The application of gene expression profiles (e.g., for hazard identification, chemical prioritization, chemical grouping, mode of action discovery, and quantitative analysis of response) is growing in the literature, but their use in formal risk assessment by regulatory agencies is relatively infrequent. Although additional validations for specific applications are required, gene expression data can be of immediate use for increasing confidence in chemical evaluations. We believe that a primary reason for the current lack of integration is the limited practical guidance available for risk assessment specialists with limited experience in genomics. The present manuscript provides basic information on gene expression profiling, along with guidance on evaluating the quality of genomic experiments and data, and interpretation of results presented in the form of heat maps, pathway analyses and other common approaches. Moreover, potential ways to integrate information from gene expression experiments into current risk assessment are presented using published studies as examples. The primary objective of this work is to facilitate integration of gene expression data into human health risk assessments of environmental chemicals. © 2015 .


Chepelev N.L.,Environmental Health Science and Research Bureau | Chepelev N.L.,Environmental Health Center | Moffat I.D.,Environmental Health Science and Research Bureau | Moffat I.D.,Environmental Health Center | And 10 more authors.
Critical Reviews in Toxicology | Year: 2015

The use of short-term toxicogenomic tests to predict cancer (or other health effects) offers considerable advantages relative to traditional toxicity testing methods. The advantages include increased throughput, increased mechanistic data, and significantly reduced costs. However, precisely how toxicogenomics data can be used to support human health risk assessment (RA) is unclear. In a companion paper (Moffat et al. 2014), we present a case study evaluating the utility of toxicogenomics in the RA of benzo[a]pyrene (BaP), a known human carcinogen. The case study is meant as a proof-of-principle exercise using a well-established mode of action (MOA) that impacts multiple tissues, which should provide a best case example. We found that toxicogenomics provided rich mechanistic data applicable to hazard identification, dose-response analysis, and quantitative RA of BaP. Based on this work, here we share some useful lessons for both research and RA, and outline our perspective on how toxicogenomics can benefit RA in the short- and long-term. Specifically, we focus on (1) obtaining biologically relevant data that are readily suitable for establishing an MOA for toxicants, (2) examining the human relevance of an MOA from animal testing, and (3) proposing appropriate quantitative values for RA. We describe our envisioned strategy on how toxicogenomics can become a tool in RA, especially when anchored to other short-term toxicity tests (apical endpoints) to increase confidence in the proposed MOA, and emphasize the need for additional studies on other MOAs to define the best practices in the application of toxicogenomics in RA. © 2015 Informa UK Ltd.


Cakmak S.,Environmental Health Science and Research Bureau | Dales R.,Environmental Health Science and Research Bureau | Kauri L.M.,Environmental Health Science and Research Bureau | Mahmud M.,Environmental Health Science and Research Bureau | And 7 more authors.
Environmental Pollution | Year: 2014

Background Studying the physiologic effects of components of fine particulate mass (PM2.5) could contribute to a better understanding of the nature of toxicity of air pollution. Objectives We examined the relation between acute changes in cardiovascular and respiratory function, and PM 2.5-associated-metals. Methods Using generalized linear mixed models, daily changes in ambient PM2.5-associated metals were compared to daily changes in physiologic measures in 59 healthy subjects who spent 5-days near a steel plant and 5-days on a college campus. Results Interquartile increases in calcium, cadmium, lead, strontium, tin, vanadium and zinc were associated with statistically significant increases in heart rate of 1-3 beats per minute, increases of 1-3 mmHg in blood pressure and/or lung function decreases of up to 4% for total lung capacity. Conclusion Metals contained in PM2.5 were found to be associated with acute changes in cardiovascular and respiratory physiology. © 2014 Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND.


PubMed | Water and Air Quality Bureau, Public Health Agency of Canada and University of Waterloo
Type: Journal Article | Journal: Epidemiology and infection | Year: 2016

Waterborne illness related to the consumption of contaminated or inadequately treated water is a global public health concern. Although the magnitude of drinking water-related illnesses in developed countries is lower than that observed in developing regions of the world, drinking water is still responsible for a proportion of all cases of acute gastrointestinal illness (AGI) in Canada. The estimated burden of endemic AGI in Canada is 205 million cases annually - this estimate accounts for under-reporting and under-diagnosis. About 4 million of these cases are domestically acquired and foodborne, yet the proportion of waterborne cases is unknown. There is evidence that individuals served by private systems and small community systems may be more at risk of waterborne illness than those served by municipal drinking water systems in Canada. However, little is known regarding the contribution of these systems to the overall drinking water-related AGI burden in Canada. Private water supplies serve an estimated 12% of the Canadian population, or ~41 million people. An estimated 14 million (41%) people in Canada are served by small groundwater (26%) and surface water (15%) supplies. The objective of this research is to estimate the number of AGI cases attributable to water consumption from these supplies in Canada using a quantitative microbial risk assessment (QMRA) approach. This provides a framework for others to develop burden of waterborne illness estimates for small water supplies. A multi-pathogen QMRA of Giardia, Cryptosporidium, Campylobacter, E. coli O157 and norovirus, chosen as index waterborne pathogens, for various source water and treatment combinations was performed. It is estimated that 103 230 AGI cases per year are due to the presence of these five pathogens in drinking water from private and small community water systems in Canada. In addition to providing a mechanism to assess the potential burden of AGI attributed to small systems and private well water in Canada, this research supports the use of QMRA as an effective source attribution tool when there is a lack of randomized controlled trial data to evaluate the public health risk of an exposure source. QMRA is also a powerful tool for identifying existing knowledge gaps on the national scale to inform future surveillance and research efforts.


Liu L.,Healthy Environmental | Kauri L.M.,Healthy Environmental | Mahmud M.,Healthy Environmental | Weichenthal S.,Water and Air Quality Bureau | And 8 more authors.
International Journal of Hygiene and Environmental Health | Year: 2014

Background: Iron and steel industry is an important source of air pollution emissions. Few studies have investigated cardiovascular effects of air pollutants emitted from steel plants. Objective: We examined the influence of outdoor air pollution in the vicinity of a steel plant on cardiovascular physiology in Sault Ste. Marie, Canada. Methods: Sixty-one healthy, non-smoking subjects (females/males. = 33/28, median age 22 years) spent 5 consecutive 8-hour days outdoors in a residential area neighbouring a steel plant, or on a college campus approximately 5 kilometres away from the plant, and then crossed over to the other site with a 9-day washout. Mid day, subjects underwent daily 30-minute moderate intensity exercise. Blood pressure (BP) and pulse rate were determined daily and post exercise at both sites. Flow-mediated vasodilation (FMD) was determined at the site near the plant. Air pollution was monitored at both sites. Mixed-effects regressions were run for statistical associations, adjusting for weather variables. Results: Concentrations of ultrafine particles, sulphur dioxide (SO2), nitrogen dioxide (NO2) and carbon monoxide (CO) were 50-100% higher at the site near the plant than at the college site, with minor differences in temperature, humidity, and concentrations of particulate matter ≤2.5μm in size (PM2.5) and ozone (O3). Resting pulse rate [mean (95% confidence interval)] was moderately higher near the steel plant [+1.53bpm (0.31, 2.78)] than at the college site, male subjects having the highest pulse rate elevation [+2.77bpm (0.78, 4.76)]. Resting systolic and diastolic BP and pulse pressure, and post-exercise BP and pulse rate were not significantly different between two sites. Interquartile range concentrations of SO2 (2.9ppb), NO2 (5.0ppb) and CO (0.2ppm) were associated with increased pulse rate [0.19bpm (-0.00, 0.38), 0.86bpm (0.03, 1.68), and 0.11bpm (0.00, 0.22), respectively], ultrafine particles (10,256count/cm3) associated with increased pulse pressure [0.85mmHg (0.23, 1.48)], and NO2 and CO inversely associated with FMD [-0.14% (-0.31, 0.02), -0.02% (-0.03, -0.00), respectively]. SO2 during exercise was associated with increased pulse rate [0.26bpm (0.01, 0.51)]. Conclusion: Air quality in residential areas near steel plants may influence cardiovascular physiology. © 2013 Elsevier GmbH.


PubMed | Helmholtz Center Munich, Healthy Environmental, Technical University of Denmark, Copenhagen University and Water and Air Quality Bureau
Type: Journal Article | Journal: Toxicology and applied pharmacology | Year: 2015

Inhalation of carbon black nanoparticles (CBNPs) causes pulmonary inflammation; however, time course data to evaluate the detailed evolution of lung inflammatory responses are lacking. Here we establish a time-series of lung inflammatory response to CBNPs. Female C57BL/6 mice were intratracheally instilled with 162 g CBNPs alongside vehicle controls. Lung tissues were examined 3h, and 1, 2, 3, 4, 5, 14, and 42 days (d) post-exposure. Global gene expression and pulmonary inflammation were assessed. DNA damage was evaluated in bronchoalveolar lavage (BAL) cells and lung tissue using the comet assay. Increased neutrophil influx was observed at all time-points. DNA strand breaks were increased in BAL cells 3h post-exposure, and in lung tissues 2-5d post-exposure. Approximately 2600 genes were differentially expressed ( 1.5 fold; p 0.05) across all time-points in the lungs of exposed mice. Altered transcript levels were associated with immune-inflammatory response and acute phase response pathways, consistent with the BAL profiles and expression changes found in common respiratory infectious diseases. Genes involved in DNA repair, apoptosis, cell cycle regulation, and muscle contraction were also differentially expressed. Gene expression changes associated with inflammatory response followed a biphasic pattern, with initial changes at 3h post-exposure declining to base-levels by 3d, increasing again at 14 d, and then persisting to 42 d post-exposure. Thus, this single CBNP exposure that was equivalent to nine 8-h working days at the current Danish occupational exposure limit induced biphasic inflammatory response in gene expression that lasted until 42 d post-exposure, raising concern over the chronic effects of CBNP exposure.


PubMed | Water and Air Quality Bureau, Healthy Environmental and Algoma University
Type: Journal Article | Journal: International journal of hygiene and environmental health | Year: 2014

Iron and steel industry is an important source of air pollution emissions. Few studies have investigated cardiovascular effects of air pollutants emitted from steel plants.We examined the influence of outdoor air pollution in the vicinity of a steel plant on cardiovascular physiology in Sault Ste. Marie, Canada.Sixty-one healthy, non-smoking subjects (females/males=33/28, median age 22 years) spent 5 consecutive 8-hour days outdoors in a residential area neighbouring a steel plant, or on a college campus approximately 5 kilometres away from the plant, and then crossed over to the other site with a 9-day washout. Mid day, subjects underwent daily 30-minute moderate intensity exercise. Blood pressure (BP) and pulse rate were determined daily and post exercise at both sites. Flow-mediated vasodilation (FMD) was determined at the site near the plant. Air pollution was monitored at both sites. Mixed-effects regressions were run for statistical associations, adjusting for weather variables.Concentrations of ultrafine particles, sulphur dioxide (SO2), nitrogen dioxide (NO2) and carbon monoxide (CO) were 50-100% higher at the site near the plant than at the college site, with minor differences in temperature, humidity, and concentrations of particulate matter 2.5 m in size (PM2.5) and ozone (O3). Resting pulse rate [mean (95% confidence interval)] was moderately higher near the steel plant [+1.53 bpm (0.31, 2.78)] than at the college site, male subjects having the highest pulse rate elevation [+2.77 bpm (0.78, 4.76)]. Resting systolic and diastolic BP and pulse pressure, and post-exercise BP and pulse rate were not significantly different between two sites. Interquartile range concentrations of SO2 (2.9 ppb), NO2 (5.0 ppb) and CO (0.2 ppm) were associated with increased pulse rate [0.19 bpm (-0.00, 0.38), 0.86 bpm (0.03, 1.68), and 0.11 bpm (0.00, 0.22), respectively], ultrafine particles (10,256 count/cm(3)) associated with increased pulse pressure [0.85 mmHg (0.23, 1.48)], and NO2 and CO inversely associated with FMD [-0.14% (-0.31, 0.02), -0.02% (-0.03, -0.00), respectively]. SO2 during exercise was associated with increased pulse rate [0.26 bpm (0.01, 0.51)].Air quality in residential areas near steel plants may influence cardiovascular physiology.


Personal exposure studies of air pollution generally use self-reported diaries to capture individuals' time-activity data. Enhancements in the accuracy, size, memory and battery life of personal Global Positioning Systems (GPS) units have allowed for higher resolution tracking of study participants' locations. Improved time-activity classifications combined with personal continuous air pollution sampling can improve assessments of location-related air pollution exposures for health studies. Data was collected using a GPS and personal temperature from 54 children with asthma living in Montreal, Canada, who participated in a 10-day personal air pollution exposure study. A method was developed that incorporated personal temperature data and then matched a participant's position against available spatial data (i.e., road networks) to generate time-activity categories. The diary-based and GPS-generated time-activity categories were compared and combined with continuous personal PM2.5 data to assess the impact of exposure misclassification when using diary-based methods. There was good agreement between the automated method and the diary method; however, the automated method (means: outdoors = 5.1%, indoors other =9.8%) estimated less time spent in some locations compared to the diary method (outdoors = 6.7%, indoors other = 14.4%). Agreement statistics (AC1 = 0.778) suggest 'good' agreement between methods over all location categories. However, location categories (Outdoors and Transit) where less time is spent show greater disagreement: e.g., mean time "Indoors Other" using the time-activity diary was 14.4% compared to 9.8% using the automated method. While mean daily time "In Transit" was relatively consistent between the methods, the mean daily exposure to PM2.5 while "In Transit" was 15.9 μg/m3 using the automated method compared to 6.8 μg/m3 using the daily diary. Mean times spent in different locations as categorized by a GPS-based method were comparable to those from a time-activity diary, but there were differences in estimates of exposure to PM2.5 from the two methods. An automated GPS-based time-activity method will reduce participant burden, potentially providing more accurate and unbiased assessments of location. Combined with continuous air measurements, the higher resolution GPS data could present a different and more accurate picture of personal exposures to air pollution.


Wheeler A.J.,Water and Air Quality Bureau
Environmental health : a global access science source | Year: 2014

Naphthalene exposures for most non-occupationally exposed individuals occur primarily indoors at home. Residential indoor sources include pest control products (specifically moth balls), incomplete combustion such as cigarette smoke, woodstoves and cooking, some consumer and building products, and emissions from gasoline sources found in attached garages. The study aim was to assess naphthalene exposure in pregnant women from Canada, using air measurements and biomarkers of exposure. Pregnant women residing in Ottawa, Ontario completed personal and indoor air sampling, and questionnaires. During pregnancy, pooled urine voids were collected over two 24-hour periods on a weekday and a weekend day. At 2-3 months post-birth, they provided a spot urine sample and a breast milk sample following the 24-hour air monitoring. Urines were analyzed for 1-naphthol and 2-naphthol and breast milk for naphthalene. Simple linear regression models examined associations between known naphthalene sources, air and biomarker samples. Study recruitment rate was 11.2% resulting in 80 eligible women being included. Weekday and weekend samples were highly correlated for both personal (r = 0.83, p < 0.0001) and indoor air naphthalene (r = 0.91, p < 0.0001). Urine specific gravity (SG)-adjusted 2-naphthol concentrations collected on weekdays and weekends (r = 0.78, p < 0.001), and between pregnancy and postpartum samples (r = 0.54, p < 0.001) were correlated.Indoor and personal air naphthalene concentrations were significantly higher post-birth than during pregnancy (p < 0.0001 for signed rank tests); concurrent urine samples were not significantly different. Naphthalene in breast milk was associated with urinary 1-naphthol: a 10% increase in 1-naphthol was associated with a 1.6% increase in breast milk naphthalene (95% CI: 0.2%-3.1%). No significant associations were observed between naphthalene sources reported in self-administered questionnaires and the air or biomarker concentrations. Median urinary concentrations of naphthalene metabolites tended to be similar to (1-naphthol) or lower (2-naphthol) than those reported in a Canadian survey of women of reproductive age. Only urinary 1-naphthol and naphthalene in breast milk were associated. Potential reasons for the lack of other associations include a lack of sources, varying biotransformation rates and behavioural differences over time.

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