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Background: As smoking prevalence has decreased in Canada, particularly during pregnancy and around children, and technological improvements have lowered detection limits, the use of traditional tobacco smoke biomarkers in infant populations requires re-evaluation., Objective: We evaluated concentrations of urinary nicotine biomarkers, cotinine and trans-3'-hydroxycotinine (3HC), and questionnaire responses. We used machine learning and prediction modeling to understand sources of tobacco smoke exposure for infants from the CHILD Cohort Study., Methods: Multivariable linear regression models, chosen through a combination of conceptual and data-driven strategies including random forest regression, assessed the ability of questionnaires to predict variation in urinary cotinine and 3HC concentrations of 2017 3-month-old infants., Results: Although only 2% of mothers reported smoking prior to and throughout their pregnancy, cotinine and 3HC were detected in 76 and 89% of the infants' urine (n = 2017). Questionnaire-based models explained 31 and 41% of the variance in cotinine and 3HC levels, respectively. Observed concentrations suggest 0.25 and 0.50 ng/mL as cut-points in cotinine and 3HC to characterize SHS exposure. This cut-point suggests that 23.5% of infants had moderate or regular smoke exposure., Significance: Though most people make efforts to reduce exposure to their infants, parents do not appear to consider the pervasiveness and persistence of secondhand and thirdhand smoke. More than half of the variation in urinary cotinine and 3HC in infants could not be predicted with modeling. The pervasiveness of thirdhand smoke, the potential for dermal and oral routes of nicotine exposure, along with changes in public perceptions of smoking exposure and risk warrant further exploration., (© 2021. The Author(s).)

Background: Few studies have examined phthalate exposure during infancy and early life, critical windows of development. The Canadian Healthy Infant Longitudinal Development (CHILD) study, a population-based birth cohort, ascertained multiple exposures during early life., Objective: To characterize exposure to phthalates during infancy and early childhood., Methods: Environmental questionnaires were administered, and urine samples collected at 3, 12, and 36 months. In the first 1578 children, urine was analyzed for eight phthalate metabolites: mono-methyl phthalate (MMP), mono-ethyl phthalate (MEP), mono-butyl phthalate (MBP), mono-benzyl phthalate (MBzP), mono-2-ethylhexyl phthalate (MEHP), mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP), mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), and mono-3-carboxypropyl phthalate (MCPP). Geometric mean (GM) concentrations were calculated by age, together with factors that may influence concentrations. Trends with age were examined using mixed models and differences within factors examined using ANOVA., Results: The highest urinary concentration was for the metabolite MBP at all ages (GM: 15-32 ng/mL). Concentrations of all phthalate metabolites significantly increased with age ranging from GM: 0.5-15.1 ng/mL at 3 months and 1.9-32.1 ng/mL at 36 months. Concentrations of all metabolites were higher in the lowest income categories except for MEHP at 3 months, among children with any breastfeeding at 12 months, and in urine collected on dates with warmer outdoor temperatures (>17 °C), except for MBzP at 3 months and MEHP at 3 and 12 months. No consistent differences were found by gender, study site, or maternal age., Conclusions: Higher phthalate metabolite concentrations were observed among children in lower income families. Examination of factors associated with income could inform interventions aimed to reduce infant phthalate exposure.

The Canadian Healthy Infant Longitudinal Development birth cohort was designed to elucidate interactions between environment and genetics underlying development of asthma and allergy. Over 3600 pregnant mothers were recruited from the general population in four provinces with diverse environments. The child is followed to age 5 years, with prospective characterization of diverse exposures during this critical period. Key exposure domains include indoor and outdoor air pollutants, inhalation, ingestion and dermal uptake of chemicals, mold, dampness, biological allergens, pets and pests, housing structure, and living behavior, together with infections, nutrition, psychosocial environment, and medications. Assessments of early life exposures are focused on those linked to inflammatory responses driven by the acquired and innate immune systems. Mothers complete extensive environmental questionnaires including time-activity behavior at recruitment and when the child is 3, 6, 12, 24, 30, 36, 48, and 60 months old. House dust collected during a thorough home assessment at 3-4 months, and biological specimens obtained for multiple exposure-related measurements, are archived for analyses. Geo-locations of homes and daycares and land-use regression for estimating traffic-related air pollution complement time-activity-behavior data to provide comprehensive individual exposure profiles. Several analytical frameworks are proposed to address the many interacting exposure variables and potential issues of co-linearity in this complex data set.

The independent and joint effects of within- and between-city contrasts in air pollution on mortality have been investigated rarely. To examine the differential effects of between- versus within-city contrasts in pollution exposure, we used both ambient measurements and land use regression models to assess associations with mortality and exposure to nitrogen dioxide (NO2) among ~735,600 adults in 10 of the largest Canadian cities. We estimated exposure contrasts partitioned into within- and between-city contrasts, and the sum of these as overall exposures, for every year from 1984 to 2006. Residential histories allowed us to follow subjects annually during the study period. We calculated hazard ratios (HRs) adjusted for many personal and contextual variables. In fully-adjusted, random-effects models, we found positive associations between overall NO2 exposures and mortality from non-accidental causes (HR per 5 p.p.b.: 1.05; 95% confidence interval (CI): 1.03-1.07), cardiovascular disease (HR per 5 p.p.b.: 1.04; 95% CI: 1.01-1.06), ischaemic heart disease (HR per 5 p.p.b.: 1.05; 95% CI: 1.02-1.08) and respiratory disease (HR per 5 p.p.b.: 1.04; 95% CI: 0.99-1.08), but not from cerebrovascular disease (HR per 5 p.p.b.: 1.01; 95% CI: 0.96-1.06). We found that most of these associations were determined by within-city contrasts, as opposed to by between-city contrasts in NO2. Our results suggest that variation in NO2 concentrations within a city may represent a more toxic mixture of pollution than variation between cities.

Continuous monitors can be used to supplement traditional filter-based methods of determining personal exposure to air pollutants. They have the advantages of being able to identify nearby sources and detect temporal changes on a time scale of a few minutes. The Windsor Ontario Exposure Assessment Study (WOEAS) adopted an approach of using multiple continuous monitors to measure indoor, outdoor (near-residential) and personal exposures to PM₂.₅, ultrafine particles and black carbon. About 48 adults and households were sampled for five consecutive 24-h periods in summer and winter 2005, and another 48 asthmatic children for five consecutive 24-h periods in summer and winter 2006. This article addresses the laboratory and field validation of these continuous monitors. A companion article (Wheeler et al., 2010) provides similar analyses for the 24-h integrated methods, as well as providing an overview of the objectives and study design. The four continuous monitors were the DustTrak (Model 8520, TSI, St. Paul, MN, USA) and personal DataRAM (pDR) (ThermoScientific, Waltham, MA, USA) for PM₂.₅; the P-Trak (Model 8525, TSI) for ultrafine particles; and the Aethalometer (AE-42, Magee Scientific, Berkeley, CA, USA) for black carbon (BC). All monitors were tested in multiple co-location studies involving as many as 16 monitors of a given type to determine their limits of detection as well as bias and precision. The effect of concentration and electronic drift on bias and precision were determined from both the collocated studies and the full field study. The effect of rapid changes in environmental conditions on switching an instrument from indoor to outdoor sampling was also studied. The use of multiple instruments for outdoor sampling was valuable in identifying occasional poor performance by one instrument and in better determining local contributions to the spatial variation of particulate pollution. Both the DustTrak and pDR were shown to be in reasonable agreement (R² of 90 and 70%, respectively) with the gravimetric PM₂.₅ method. Both instruments had limits of detection of about 5 μg/m³. The DustTrak and pDR had multiplicative biases of about 2.5 and 1.6, respectively, compared with the gravimetric samplers. However, their average bias-corrected precisions were <10%, indicating that a proper correction for bias would bring them into very good agreement with standard methods. Although no standard methods exist to establish the bias of the Aethalometer and P-Trak, the precision was within 20% for the Aethalometer and within 10% for the P-Trak. These findings suggest that all four instruments can supply useful information in environmental studies.

We evaluated the impact on personal exposure to air pollutants of following advice which typically accompanies air quality advisories and indices. Scripts prescribed the time, location, duration and nature of activities intended to simulate daily activity patterns for adults and children. Scripts were paired such that one individual would proceed with usual activities (base scenario), whereas the other (intervention scenario) would alter activities as if following advice. Other than commuting, where the intervention group walked or used public transportation rather than riding in personal vehicles, this group generally spent less time outdoors. Ultra-fine particles (UFPs), particulate matter of median aerodynamic diameter less than 2.5 mum (PM(2.5)) and total volatile organic compounds (VOCs) were measured using samplers carried by individuals during the course of daily activities. During daytime activities (e.g., work, daycare) constituting the largest share of sampling time (approximately 6 h per day), the intervention group experienced a 14% reduction in exposure to UFPs (P=0.01), a 21% reduction in exposure to PM(2.5) (P=0.08), and an 86% increase in exposure to VOCs (P=0.02). Other findings included an 89% increase in exposure to UFPs (P=0.02) and a threefold increase in exposure to VOCs (P=0.08) in the intervention group during evening cooking. Following smog advisory advice results in reduced exposures to some pollutants, while at the same time increasing exposure to others. Advice needs to be refined giving consideration to overall personal exposure.

In this paper, the pooled NO2 association with nonaccidental mortality is examined across 10 cities in Canada in single- and two-pollutant time-series models. The results reaffirm that NO2 has the strongest association with mortality, particularly in the warm season. Although attributing such effects to NO2 cannot be ruled out, it is plausible that NO2 is acting as an indicator for some other exposure affecting the population. This could include PM2.5, as has been suggested from some personal exposure data, but it could also be indicating a more specific type of PM2.5, such as traffic-related particles, given that in cities the main source of NO2 is motor vehicle exhaust. NO2 could also be acting as a surrogate for other pollutant(s) originating from motor vehicles or high-temperature combustion, such as volatile organic compounds (VOCs) or polycyclic aromatic hydrocarbons. Another possibility is other oxidized nitrogen species ("NO(z)") or photochemically produced pollutants that can co-vary with NO2, especially during urban stagnation events. Data to test these different possibilities across several Canadian cities are examined. The focus is on correlations in time or space between NO2 and other pollutants that are more strongly linked to vehicle emissions. The results support the hypothesis that NO2 is a better indicator than PM2.5 of a range of other toxic pollutants. This includes VOCs, aldehydes, NO(z) and particle-bound organics in motor vehicle exhaust. Thus, overall, the strong effect of NO2 in Canadian cities could be a result of it being the best indicator, among the pollutants monitored, of fresh combustion (likely motor vehicles) as well as photochemically processed urban air.

A longitudinal study investigating personal exposures to PM(2.5), nitrogen dioxide (NO(2)), and carbon monoxide (CO) for cardiac compromised individuals was conducted in Toronto, Canada. The aim of the study was (1) to examine the distribution of exposures to PM(2.5), NO(2), and CO; and (2) to investigate the relationship between personal exposures and fixed-site ambient measurements of PM(2.5), NO(2), and CO. In total, 28 subjects with coronary artery disease wore the Rupprecht & Patashnick ChemPass Personal Sampling System one day a week for a maximum of 10 weeks. The mean (SD) personal exposures were 22 microg m(-3) (42), 14 p.p.b. (6), and 1.4 p.p.m (0.5) for PM(2.5), NO(2), and CO, respectively. PM(2.5) and CO personal exposures were greater than central fixed-site ambient measurements, while the reverse pattern was observed for NO(2). Ambient PM(2.5) and NO(2) were correlated with personal exposures to PM(2.5) and NO(2) with median Spearman's correlation coefficients of 0.69 and 0.57, respectively. The correlations between personal exposures and ambient measurements made closest to the subjects' homes or the average of all stations within the study were not stronger than the correlation between personal exposures and central fixed-site measurements. Personal exposures to PM(2.5) were correlated with personal exposures to NO(2) (median Spearman's correlation coefficient of 0.43). This study suggests that central fixed-site measurements of PM(2.5) and NO(2) may be treated as surrogates for personal exposures to PM(2.5) and NO(2) in epidemiological studies, and that NO(2) is a potential confounder of PM(2.5).